Oral Surgery Oral Diagnosis 11 (1998)
Vol 11: 1-368
ORAL SURGERY
ORAL DIAGNOSIS
Published by Osfix Research Centre in co-operation with FREO r.y. and the
Institute of Oral and Maxillo-Facial Surgery, University of Kuopio, Finland
MONITORED INTRAVENOUS
SEDATION WITH LOCAL
ANAESTHESIA FOR DENTAL
OUTPATIENTS.
Clinical Observations
by
Kari Luotio, DDS
Eight studies and
clinical guidelines
AUTHOR’S ADDRESS:
OSFIX OY/LTD
P.O.BOX 14, FIN-47200 ELIMÄKI
OSFIX@SCI.FI
Elimäki 1998
To Kirsti, Johanna, Eero, Lauri and Juha
without whom this book would have been
accomplished many years earlier.
Life is based on rhythms.
From the basic rhythm of the earth around the sun
to the complex rhythms of music.
Thus
we are living in the middle of an endless interplay
of countless rhythms.
This book is inspired by the
continuos rhythm of the monitored heart
.
5
Monitored intravenous sedation with local anaesthesia for dental outpatients
CONTENTS
FOREWORD .......................................................................................................................... 14
PREFACE ............................................................................................................................... 17
ACKNOWLEDGEMENTS..................................................................................................... 19
ABBREVIATIONS ................................................................................................................. 21
PART I:
1 GENERAL INTRODUCTION AND REVIEW OF THE LITERATURE .................. .23
1.1 GENERAL DESCRIPTION OF THE STUDY ................................................... 25
1.2 ABSTRACT......................................................................................................... 27
1.2.1 Part II (Monitoring...): .......................................................................... 27
1.2.2 Part III (Experiences...): ...................................................................... 28
1.2.3 Part IV (Challenges): ........................................................................... 29
1.3 INTRODUCTION TO OXYGEN DELIVERY SYSTEM .................................. 31
1.4 THE STATE OF ART IN THE BEGINNING THE WORK
IN THE YEARS 1992-1993:
REVIEW OF THE LITERATURE................. .................................................... 35
1.4.1 SEDATION WITH LOCAL ANAESTHESIA OR GENERAL
ANAESTHESIA? ........................................................................................... 35
1.4.1.1 Midazolam ............................................................................ 35
1.4.1.2 Midazolam compared to diazepam ....................................... 35
1.4.2 PATIENT MANAGEMENT WITH INTRAVENOUS SEDATION ... 36
1.4.2.1 Dentist’s sight ....................................................................... 36
1.4.2.2 Patient’s opinion ................................................................... 36
1.4.2.3 Antagonist to benzodiazepines.............................................. 36
1.4.3 BENZODIAZEPINES COMBINED WITH OPIATES ...................... 38
1.4.3.1 Healthy patients .................................................................... 38
1.4.3.2 Medically compromised patients .......................................... 38
1.4.4 THE COMPARISON OF ORAL AND INTRAVENOUS
ADMINISTRATION ............................................................................................ 40
1.4.5 THE NECESSITY OF OXIMETRY DURING
INTRAVENOUS SEDATION ....................................................................... 41
1.4.5.1 Hypoxia................................................................................. 41
1.4.5.2 Pulse oximetry ...................................................................... 41
1.4.6 SEVERE COMPLICATIONS DURING PROCEDURE ..................... 44
1.4.6.1 Psychological complications ................................................. 44
1.4.6.2 Other complications .............................................................. 44
7
Contents
1.5 AIMS OF THE STUDY ...................................................................................... 46
1.5.1 MORE DETAILED DESCRIPTION OF THE BACKGROUNDS
AND AIMS OF THE SEPARATE STUDIES ............................................... 48
1.5.1.1 Part II (Monitoring...) ........................................................... 48
1.5.1.2 Part III (Experiences...) ......................................................... 48
1.5.1.3 Part IV (Challenges) ............................................................. 49
1.6 PATIENTS AND METHODS ............................................................................. 50
1.6.1 STUDY DESIGN ................................................................................. 50
1.6.1.1 Patients.................................................................................. 51
1.6.1.1.1 Patients in Part II (Monitoring...) .......................... 51
1.6.1.1.2 Patients in Part III (Experiences...) ........................ 51
1.6.1.1.3 Patients in Part IV (Challenges) ............................ 52
1.6.2 PRE- AND POSTOPERATIVE PATIENT PREPARATION ............. 54
1.6.3 MEDICATION ..................................................................................... 56
1.6.3.1 Medication in Part II (Monitoring...) .................................... 56
1.6.3.1.1 Sedation ................................................................. 56
1.6.3.1.2 Local anaesthesia ................................................... 56
1.6.3.2 Medication in Part III (Experiences...) .................................. 57
1.6.3.3 Medication in Part IV (Challenges) ...................................... 57
1.6.4 MONITORING AND DATA REVIEW............................................... 58
1.6.5 THE WORKING PRINCIPLE OF THE PULSE OXIMETRIC
EQUIPMENT................................................................................................. 59
1.6.5.1 Different equipment philosophies ......................................... 59
PART II:
MONITORING PATIENTS WITH THREE PULSE OXIMETER
EQUIPMENTS ...................................................................................................................... 61
2.1 SURVEY 1: DETECTION OF OXYGEN SATURATION UNDER
INTRAVENOUS SEDATION WITH OHMEDA PULSE OXIMETER AND
REGISTRATION OF OTHER CARDIOVASCULAR PARAMETERS ............ 63
2.1.1 ABSTRACT ......................................................................................... 63
2.1.2 INTRODUCTION ................................................................................ 64
2.1.3 PATIENTS AND METHODS ............................................................. 66
2.1.3.1 Study design .......................................................................... 66
2.1.3.2 Patients.................................................................................. 66
2.1.3.3 Sedation ................................................................................ 67
2.1.3.4 Monitoring and data review .................................................. 68
2.1.3.5 Statistical methods ................................................................ 69
2.1.4 RESULTS ............................................................................................ 70
2.1.4.1 Oxygen saturation of blood .................................................. 70
2.1.4.2 Other remarks........................................................................ 70
2.1.5 DISCUSSION ...................................................................................... 73
2.1.5.1 Desaturation .......................................................................... 73
2.1.5.2 Monitoring ............................................................................ 74
2.1.6 CLINICAL CONCLUSION ................................................................. 77
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Monitored intravenous sedation with local anaesthesia for dental outpatients
2.2 SURVEY 2: DETECTION OF CARDIOVASCULAR RESPONSES
TO LOCAL ANAESTHESIA WITH A DATEX CARDIOCAP
MULTIPARAMETER MONITOR ........................................................................ 79
2.2.1 ABSTRACT ......................................................................................... 79
2.2.2 INTRODUCTION ................................................................................ 79
2.2.3 PATIENTS AND METHODS ............................................................. 82
2.2.3.1 Study design .......................................................................... 82
2.2.3.2 Subjects ................................................................................. 82
2.2.3.3 Local anaesthesia .................................................................. 82
2.2.3.4 Timing of the procedure ........................................................ 83
2.2.3.5 Monitoring ............................................................................ 85
2.2.3.6 Statistical methods ............................................................... 85
2.2.4 RESULTS ............................................................................................ 87
2.2.4.1 Pulse .................................................................................... 87
2.2.4.2 Amplitude of pulse wave ..................................................... 87
2.2.4.3 Blood pressure ..................................................................... 88
2.2.4.4 Oxygen saturation of blood (SaO2) ..................................... 88
2.2.5 DISCUSSION ...................................................................................... 93
2.2.5.1 Amplitude of pulse wave and the measuring equipment ....... 93
2.2.5.2 Oxygen saturation of blood during dental treatment ............ 93
2.2.5.3 Toxic reactions ...................................................................... 94
2.2.5.4 Pulse and blood pressure after local anaesthesia ................... 94
2.2.6 CLINICAL CONCLUSIONS ............................................................... 97
2.3 SURVEY 3: DETECTION OF MAXIMAL PULSE AND PERIPHERAL
BLOOD FLOW UNDER INTRAVENOUS SEDATION WITH A DATEX
SATTLITE TRANS PULSE OXIMETER ............................................................. 99
2.3.1 ABSTRACT ......................................................................................... 99
2.3.2 INTRODUCTION .............................................................................. 100
2.3.2 1 Monitored sedation ............................................................. 100
2.3.2.2 Local anaesthesia ................................................................ 100
2.3.2.3 Amplitude of pulse wave (A.P.W.) ..................................... 101
2.3.2.4 Aim of the study.................................................................. 101
2.3.3 PATIENTS AND METHODS ........................................................... 102
2.3.3.1 Study design ........................................................................ 102
2.3.3.2 Monitoring .......................................................................... 102
2.3.3.3 The working principle of the pulse oximetric equipment .... 102
2.3.3.4 Patients................................................................................ 103
2.3.3.5 Sedation .............................................................................. 103
2.3.3.6 Statistical methods .............................................................. 104
2.3.4 RESULTS .......................................................................................... 106
2.3.4.1 Maximal pulse rate .............................................................. 106
2.3.4.2 Amplitude of pulse wave (A.P.W.) .................................... 106
2.3.4.3 Other observations .............................................................. 107
2.3.5 DISCUSSION .................................................................................... 114
2.3.5.1 False alarms ........................................................................ 114
2.3.5.2 Reactions to local anaesthesia ............................................. 114
2.3.5.3 Clinical monitoring ............................................................. 115
2.3.6 CLINICAL CONCLUSIONS ............................................................. 117
9
Contents
PART III:
PATIENTS’ EXPERIENCES DURING AND AFTER SURGERY UNDER
INTRAVENOUS SEDATION ............................................................................................ 119
3.1 STUDY 4: PEROPERATIVE EXPERIENCES ........................................... 121
3.1.1 INTRODUCTION .............................................................................. 122
3.1.1.1 Fear ..................................................................................... 122
3.1.1.2 Sedation ............................................................................. 122
3.1.1.3 Aims of the study ................................................................ 124
3.1.2 PATIENTS AND METHODS ........................................................... 125
3.1.2.1 Patients................................................................................ 125
3.1.2.2 Questionnaire ...................................................................... 127
3.1.2.3 Medication .......................................................................... 128
3.1.2.4 Statistical methods .............................................................. 130
3.1.3 RESULTS .......................................................................................... 131
3.1.3.1 All patients (n=108) ............................................................ 131
3.1.3.2 Phobia group (n=53) ........................................................... 131
3.1.3.3 Operation group (n=38) ...................................................... 132
3.1.3.4 Differences .......................................................................... 132
3.2 STUDY 5: POSTOPERATIVE EXPERIENCES ......................................... 141
3.2.1 INTRODUCTION .............................................................................. 141
3.2.1.1 Postoperative recovery ........................................................ 141
3.2.1.2 Aim of the study.................................................................. 142
3.2.2 PATIENTS AND METHODS ........................................................... 143
3.2.2.1 Statistical methods .............................................................. 143
3.2.3 RESULTS .......................................................................................... 144
3.2.3.1 All patients (n=108) ............................................................ 144
3.2.3.2 Phobia group (n=53) ........................................................... 145
3.2.3.3 Operation group (n=37) ...................................................... 146
3.2.3.4 Differences ............................................................... 147
3.3 GENERAL DISCUSSION OF PART III ....................................................... 155
3.3.1 The anxious patient ................................................................. 155
3.3.2 Amnesia .................................................................................. 156
3.3.3 Sedation and confusion ........................................................... 156
3.3.4 Postoperative pain ................................................................... 157
3.4 CLINICAL CONCLUSIONS ......................................................................... 160
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Monitored intravenous sedation with local anaesthesia for dental outpatients
PART IV:
CHALLENGES ................................................................................................................... 163
4.1 SURVEY 6: ADVANCED MONITORING: HOLTER ECG AND
ANALYSIS OF THE STATUS OF THE AUTONOMIC
NERVOUS SYSTEM ............................................................................................. 165
4.1.1 ABSTRACT ....................................................................................... 165
4.1.2 INTRODUCTION .............................................................................. 165
4.1.2.1 Autonomic nervous system and fear ................................... 165
4.1.2.2 Aim of the study.................................................................. 167
4.1.3 PATIENTS AND METHODS ........................................................... 168
4.1.3.1 Patient: preparation, sedation and local anaesthesia ........... 168
4.1.3.1.1 1. Study group: ................................................... 168
4.1.3.1.2 2. Reference group............................................... 169
4.1.3.2 Monitoring .......................................................................... 170
4.1.3.3 Statistical methods .............................................................. 171
4.1.4 RESULTS .......................................................................................... 172
4.1.5 DISCUSSION .................................................................................... 180
4.1.5.1 Cardiac occurrences ............................................................ 180
4.1.5.2 Pulse ................................................................................... 180
4.1.5.3 Heart rate variability ........................................................... 181
4.1.6 CLINICAL CONCLUSIONS ............................................................. 183
4.2 STUDY 7: STRESS INDEX ........................................................................... 185
4.2.1 ABSTRACT ....................................................................................... 185
4.2.2 INTRODUCTION .............................................................................. 185
4.2.3 PATIENTS AND METHODS ........................................................... 187
4.2.3.1 Study design........................................................................ 187
4.2.3.2 Monitoring .......................................................................... 187
4.2.3.3 Patients................................................................................ 188
4.2.3.4 Sedation .............................................................................. 189
4.2.3.5 Local anaesthesia ................................................................ 189
4.2.3.6 Timing of the procedure ...................................................... 190
4.2.3.7 Statistical methods .............................................................. 190
4.2.4 OBSERVATIONS.............................................................................. 192
4.2.5 DISCUSSION .................................................................................... 200
4.2.5.1 Stress during treatment ....................................................... 200
4.2.5.2 Amplitude of pulse wave (A.P.W.) ..................................... 200
4.2.5.3 Amplitude of pulse wave and the measuring equipment ..... 201
4.2.5.4 Stress index ......................................................................... 202
4.2.6 CLINICAL CONCLUSIONS ............................................................. 205
11
Contents
4.3 STUDY 8: COMPLICATED CASES............................................................ 207
4.3.1 ABSTRACT ....................................................................................... 207
4.3.2 INTRODUCTION .............................................................................. 208
4.3.3 PATIENT MANAGEMENT AND METHODS ................................ 209
4.3.4 OBSERVATIONS.............................................................................. 210
4.3.4.1 CASE 1. FIG. 1 ................................................................... 210
4.3.4.2 CASE 2. FIG. 2 ................................................................... 211
4.3.4.3 CASE 3. FIG. 3 ................................................................... 212
4.3.4.4 CASE 4. FIG. 4 ................................................................... 213
4.3.4.5 CASE 5. FIG. 5 ................................................................... 214
4.3.5 DISCUSSION .................................................................................... 218
4.3.5.1 Respiratory problems and oxygen ....................................... 218
4.3.5.2 Antidote for correction of hypoxia ...................................... 219
4.3.5.3 Wrong detection of hypoxia ................................................ 219
4.3.6 CLINICAL CONCLUSION ............................................................... 223
PART V:
5 GENERAL DISCUSSION AND CONCLUSIONS ...................................................... 227
5.1 DETECTION OF ADVERSE REACTIONS .................................................... 227
5.2 EFFECTS OF LOCAL ANAESTHETIC PREPARATIONS ........................... 228
5.3 THE USE OF TWO LOCAL ANAESTHETIC PREPARATIONS
IN COMBINATION .......................................................................................... 229
5.4 EFFECTS OF BENZODIAZEPINES VS. LOCAL ANAESTHETICS ............ 229
5.5 PATIENTS' REACTIONS TO TREATMENT UNDER INTRAVENOUS
SEDATION WITH LOCAL ANAESTHESIA .................................................. 230
5.6 THE PATIENT’S CONDITION AFTER TREATMENT UNDER
INTRAVENOUS SEDATION WITH LOCAL ANAESTHESIA. .................... 231
5.7 ARRHYTHMIAS AND THE STATUS OF AUTONOMIC
NERVOUS SYSTEM ........................................................................................ 231
5.8 FALSE ALARMS IN PULSE OXIMETRY ..................................................... 232
5.9 COMPLICATED CASES ................................................................................. 233
5.10 STATISTICAL VIEW VS. CLINICAL VIEW ............................................... 234
5.11 CONCLUSIONS ............................................................................................. 235
PART VI:
6 CLINICAL GUIDELINES .............................................................................................. 237
INTRAVENOUS SEDATION PROTOCOL............................................................ 239
6.1 Introduction ....................................................................................................... 243
6.2 The Patient for Sedation .................................................................................... 245
6.2.1 Examining the Patient ........................................................................ 245
6.2.2 Clinical Anatomy ............................................................................... 245
6.3 Benzodiazepines ................................................................................................ 247
6.3.1 Operating mechanism ......................................................................... 247
6.3.2 Half-life .............................................................................................. 247
6.3.3 Pharmacodynamics ............................................................................. 248
6.3.4 Pharmacokinetic anomalies ................................................................ 248
6.4 The Commercial Drugs ...................................................................................... 249
6.4.1 Selecting a suitable drug..................................................................... 249
6.4.2 Diazepam ............................................................................................ 249
6.4.3 Midazolam .......................................................................................... 250
6.4.4 Administration equipment .................................................................. 251
6.4.5 First aid equipment ............................................................................. 252
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Monitored intravenous sedation with local anaesthesia for dental outpatients
6.5 Monitoring the Patient ....................................................................................... 254
6.5.1 Blood pressure monitors ..................................................................... 254
6.5.2 Pulse oximetry .................................................................................... 254
6.5.2.1 The monitoring principle and equipment ........................................ 255
6.5.2.2 Monitoring during sedation ............................................................. 256
6.5.2.3 Emergency situation ....................................................................... 256
6.5.2.4 Sources for defaults ......................................................................... 257
6.5.3 Pulse wave oximetry........................................................................... 257
6.6 Intravenous Sedation in Practice ........................................................................ 259
6.6.1 Cannulating the vein in the crook of the arm ..................................... 259
6.6.2 Administering the drug and observing the effects .............................. 260
6.6.3 Recovery from sedation ...................................................................... 261
6.6.3.1 Oxygen saturation............................................................................ 261
6.6.3.2 Flumazenil ....................................................................................... 261
6.7 Complications ..................................................................................................... 264
6.7.1 Local complications ........................................................................... 264
6.7.2 Hypoxia .............................................................................................. 264
6.7.3 Fainting .............................................................................................. 265
6.7.4 Psychogenic complications ................................................................ 265
6.7.5 Other complications ........................................................................... 265
6.8 Legal aspects ...................................................................................................... 267
6.9 Conclusions ....................................................................................................... 268
6.10 Instructions to patients ..................................................................................... 269
1.11 Pictures ............................................................................................................ 270
7 APPENDICES
7.1 APPENDIX I
DESCRIPTION OF THE DRUGS USED AND STUDIED ..................................... 283
7.2 APPENDIX II
QUESTIONS AND PATIENTS’ COMMENTS FOR STUDIES 4 AND 5 ............. 309
7.3 APPENDIX III
PLETYSTOMOGRAFIC PULSE WAVE ............................................................... 331
7.4 APPENDIX IV
COMMUNICATION BETWEEN PC AND OXIMETER ...................................... 353
7.4 APPENDIX V
CRITICAL THOUGHTS .......................................................................................... 361
REFERENCES...................................................................................................................... 369
13
FOREWORD
In dental practice, monitors are still used extremely
seldom although technical possibilities already exist. In
fact there is an abundance of equipment. Fatal
complications in a dental chair are so uncommon that the
use of monitors cannot be mandatory. But it is certain that
some dangerous episodes and threatening situations
nevertheless occur. It is not so much a question of "life or
death" but of the quality of care in general. Many of the
principles of monitoring accepted in anaesthesia for
general surgery can also be applied in dental operative
care. Patient monitoring is used in order to detect
dangerous deviations from normal in circulation and
respiration. These complications can be due to therapeutic
procedures or the medication used, but they can result as a
deterioration of the patient’s own organic disease. It
should be extremely important to recognise these
occurrences in due time, to be able to make the right
conclusions to begin the correct therapeutic manoeuvres.
On the basis of these observations and conclusions, the
surgeon is also able to adequately inform the patient on
the occurrence. Without appropriate monitoring these
goals cannot be reached with certainty.
14
Monitored intravenous sedation with local anaesthesia for dental outpatients
Some patients may have such a fear for dental
procedures that they need to be sedated. This study
describes treatment models which have been widely
accepted and reported during the last decade, but North
European tradition has preferred psychological methods,
nitrous oxide inhalation sedation and general anaesthesia
to the intravenous sedation with local anaesthesia.
However, intravenous sedation with local anaesthesia is a
pleasant, efficient and safe means to treat anxiety
problems both for the dentist and his patient. To reach an
adequate and accurate effect, these drugs have to be
administered to the vein but not at the level of general
anaesthesia. The patient always remains conscious. Even
intravenous sedation includes risks which must
imperatively be recognised, and due precautions must be
made for treating eventual complications. The basis for a
secure intravenous sedation is the appropriate skills of the
staff.
15
Monitored intravenous sedation with local anaesthesia for dental outpatients
PREFACE
The present series of eight independent studies divided into three chapters in this
publication describes methods of intravenous sedation, monitoring, and the
experiences of the patients. These are follow-ups with modern equipment, and the
studies are descriptive reconstructions of the treatments. Each study contains a short
independent introduction, review of literature, description of material, aims,
observations, analyses and a discussion of the results. The first two studies and
survey 6 are more statistical and analytical than descriptive. Studies 3, 7, 8, the
review of the literature in part I and the appendices are written from a viewpoint of
a clinician and they are mainly descriptive. Studies 4 and 5 display a double
structure: a clinical descriptive view and a statistical view. Moreover, the opinions
expressed are the authors’ own/personal opinions.
Part II consists of two studies which are descriptive reviews of patient records
during sedation, and one study which is an on-line recording of cardiovascular
parameters during local anaesthesia. There were many differences in patient
preparation, cannulation and intravenous infusion, sedative drugs and local
anaesthesia i.e. in the underlying factors. It is important to understand that these
studies were not controlled clinical experiments but clinical follow-ups of normal
treatment or local anaesthesia periods. Therefore there were no reference groups in
two of these works, and findings were compared with the literature. Part III
describes the patients’ experiences: An anonymous questionnaire was mailed to
patients previously treated with intravenous sedation with local anaesthesia at the
author’s private practice. This chapter is further divided into two parts: per- and
postoperative findings i.e. memories. Part IV describes some challenges and
applications which arose from earlier studies. There are more sophisticated methods
of monitoring, such as the Holter ECG, and a new index for stress as well as a
description of difficulties in treatment, such as complications. The whole work is
mainly descriptive because the statistics of real life treatments are quite complex as
the material used originated from the dentist’s practical work and not a statistically
perfect sample. Part V is the vertebrae of the book: It gives clinical quidelines for
sedation. These quidelines are based both on authors’ clinical experience and on the
studies in parts II-IV: The use of monitoring, and sedation methods, have been
clinically applied in dentistry and oral surgery, methods which are widely used in
anaesthesiology and critical care: the main concern is always patient safety.
The topic of this book is quite unknown to dentists, then again clinicians and
scientists have quite different needs. Thus the book itself can be read in three ways:
1) browsing bold prints, abstracts and clinical conclusions; 2) reading only the parts
interesting for the reader, e.g. the patients’ experiences; 3) thoroughly going into the
whole works. Moreover, there is quite a few various appendices at the end of this
book but I am positive that their presence is justified as I hope that this book will
live long as a brief introduction for intravenous sedation practice.
17
Monitored intravenous sedation with local anaesthesia for dental outpatients
ACKNOWLEDGEMENTS
This study is carried out primarily at the author’s private practice in Elimäki, and
secondly in the department of Oral and Maxillofacial Surgery, University of
Kuopio, during the years 1992-1997.
I would like to thank Oral Surgeon, Associate Professor Risto Kotilainen and
Anaesthesiologist, Docent Matti Mattila for supervising this study.
Anaesthesiologists, Professor Matti Salo and Docent Kari Korttila has given me
remarkable comments during finalishing this book. It would not have been possible
to complete this work without their professional advice and guidance through the
whole study. Moreover, I wish to thank Doctor Tomi Laitinen and Professor Esko
Länsimies for co-operation and advice in a study dealing with the Holter ECG.
I express my gratitude to my research group in the department of Oral and
Maxillofacial Surgery: Janne Ryhänen, Outi Hyyppä, Sinikka Navari, Tapani
Hyppönen, Marika Vainio and Hannu Vesanen. They all have helped me with
reviewing the literature and performing parts of these studies with me. When we
began, they were all candidates but during these years they have professionally
graduated.
I thank Tiina Vuori, translator for the revision of English, and Tuija Poussa, MSc
for the revision and further analysis of statistical methods. Moreover, I thank Irja
Virolainen for helping with the layout.
I am very grateful to doctors Osmo Hiltunen, Hannu Kokki and Matti Mattila for
helping me with the first Finnish intravenous sedation course in summer 1996.
Special thanks goes to my oldest son Juha who has helped me so many times
with computers and developed the communication program between PC and pulse
oximeter for me.
Last but not least, my gratitude goes to my whole family: my wife Kirsti, my
sons Juha, Lauri, Eero and my daughter Johanna for their irreplaceable support.
19
Monitored intravenous sedation with local anaesthesia for dental outpatients
ABBREVIATIONS
SaO2
BP
APW
ECG
HRV
VAS
Blood oxygen saturation
Blood pressure
Amplitude of pulse wave
Electrocardiogram
Heart rate variability
Visual analogy scale
21
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part I
PART I
GENERAL INTRODUCTION
AND REVIEW OF THE
LITERATURE
23
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part I
1.1 GENERAL DESCRIPTION
OF THE STUDY
Our knowledge of patients’ cardiovascular and pulmonar
parameters in dental chair, in real-life conditions, is still
limited. It is most important that the therapy as well as
premedication do not harm the patient. Thus this study was
performed and specially focused on the cardiovascular and
pulmonar parameters before, during and after sedation and on
the methods observing them. -Main observations were:
Low oxygen saturation before sedation constitutes a risk for
oxygen desaturation during sedation. Pulse oximetric
monitoring allows early intervention in ventilation problems.
No cardiovascular problems were found when the two most
commonly used local anaesthesia were used in combination.
There was little need for general anaesthesia. Most patients
preferred intravenous sedation.
Amplitude of pulse wave was the most responsive but only
descriptive measurable single parameter indicating stress.
The amount of cardiac occurences were within normal limits
during sedation.
The maximum pulse of sedated patients was suggestively
lower and the high and low frequency components of heart rate
variability were higher indicating stress relief.
To estimate the value of generic stress a new index was
developed, which is called the stress index.
25
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part I
1.2 ABSTRACT
saturation were found (SaO2 under
90 %), and all problems related to
sedation
were
resolved
by
administering supplementary oxygen
or a benzodiazepine antagonist. Blood
pressure and pulse rate were slightly
lower after treatment than before it
(mean change in systolic blood
pressure. -6.9 % units - p=0.04).
Pulse oximetric monitoring was
found extremely sensitive as a
predictor for desaturation and it also
allows
early
intervention
in
ventilation problems.
1.2.1 Part II (Monitoring...)
In the first study part of the
patients were monitored with three
pulse oximeter equipment: oxygen
saturation was detected with Ohmeda
pulse
oximeter,
cardiovascular
responses to the local anaesthesia
with Datex Cardiocap multiparameter
monitor and Amplitude of pulse wave
with Datex Sattlite Trans pulse
oximeter. In the first study of this
part, 41 patients were monitored with
a pulse oximeter, and blood pressure
values were measured during major
or protracted dental operations under
intravenous sedation with local
anaesthesia. The most important
finding was that there seems to be a
risk that low oxygen saturation (SaO2
< 90%) before sedation constitutes a
risk for oxygen desaturation during
sedation.
Before beginning the
procedure, the oxygen saturation
level (SaO2) was found to be 98%.
The lowest SaO2 levels were found a
few minutes after injection or later
during the treatment when the
average level was 92 % (p<0.0001).
The patients who had preoperative
SaO2 over 98% declined to a
minimum saturation at the average
level of 94%. The patients with the
initial saturation under 98% showed
signs of measurable desaturation mean
level
88%.
However,
desaturation did not correlate with the
dose of the sedative agent when this
was used at the therapeutic level.
Only five cases of low arterial oxygen
In the second study the
cardiovascular effects of the two local
anaesthetic agents (lidocaine and
prilocaine) and two vasoconstrictors
(epinephrine and phelypressine) were
observed. There were no radical
changes of systolic or diastolic blood
pressure. The mean blood oxygen
saturation values were within normal
limits and the displayed SaO2 values
were between 96 - 98 percent during
the measuring period in 96 percent of
detected values. Heart rate slightly
decreased after the injection of
prilocaine - phelypressine, but pulse
rate increased after the epinephrinecontaining lidocaine injection. Both
the prilocaine and lidocaine injections
resulted in statistically significant
(p=0.001) changes in heart rate.
Amplitude of pulse wave was the
most
responsive
measurable
parameter. Amplitude of pulse wave
diminished just before and during the
injection as a result of psychological
27
General introduction and review of the literature
stress. Blood flow showed the
smallest values during the injection of
local anaesthetic. No cardiovascular
problems were found when the two
most
commonly
used
local
anaesthesia
preparations
(epinephrine-containing lidocaine and
phelypressine-containing prilocaine)
were
used
in
combination.
Consequently, if the effect of one
local anaesthesia preparation is not
sufficient it is possible to increase the
effect
by adding the
other
preparation.
the injection due to psychological
stress. The blood flow showed
decreasing values during and after the
injections of local anaesthetic.
Moreover, poor A.P.W. caused
measuring artefacts into the levels of
blood oxygen saturation, which can
be avoided by covering the patients
with a blanket. The nature of this
descriptive parameter is discussed.
1.2.2 Part III (Experiences...)
In study 4 of this part, 108 patients
who had experienced major or
protracted dental operations under
intravenous sedation with local
anaesthesia were asked questions
concerning their experiences of the
treatment using an anonymous
questionnaire, and the findings are
divided into two chapters according
to their occurrence in time, i.e.
peroperative
and
postoperative
periods. Two clear subgroups were
formed (by excluding 17 patients)
according to indication for treatment:
for 38 patients the main reason for
undergoing intravenous sedation with
local anaesthesia was a major surgical
treatment (operation group), and for
53 patients the fear of any dental
treatment, i.e. dental care phobia
(phobia group). The operation group
served as a reference group.
In the third study of this part, 26
patients were monitored with pulse
oximeter during major or longstanding dental operation under
intravenous sedation with local
anaesthesia.
The
cardiovascular
effects
of
benzodiazepine
(midazolam) and the local anaesthetic
agent (lidocaine) and vasoconstrictor
(epinephrine)
were
observed.
Maximal pulse rate increased both
during and after the injection of
midazolam as well as the injection of
epinephrine containing lidocaine. The
increase was very slight after
midazolam but notable after local
anaesthesia. As a result of stress
relief, pulse rate was lower after
treatment than before it (p<0.05). The
highest level of pulse level was
recorded during local anaesthesia
(p<0.005). There was no significant
difference in pulse rate before
treatment and during sedation. During
our retrospective review of patient
records, amplitude of pulse wave
(A.P.W.) was the most responsive but
only descriptive measurable single
parameter indicating stress. In
general, A.P.W. decreased towards
Peroperatively the most important
finding was that the patients later felt
there was little need for general
anaesthesia. Most patients (87%)
preferred intravenous sedation with
local anaesthesia. The patients were
nearly unanimous in recommending
intravenous sedation with local
28
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part I
anaesthesia for others. These
subgroups showed no statistical
difference in unpleasant experiences
during
treatment,
though
the
operation group was slightly more
satisfied with the intravenous
sedation with local anaesthesia than
the phobia group (p= 0.05). Eight
patients in the phobia group felt that
they could undergo the procedure
with local anaesthesia alone the next
time, while only 1 patient in the
operation group preferred the
procedure with local anaesthesia
alone. The need for general
anaesthesia was low, the patients (5
cases) reporting the need for general
anaesthesia belonging to the phobia
group. The patients in both groups
reported that pain, fear, anxiety,
confusion and drowsiness had not
disturbed them during the treatment.
on the next day. The patients felt
healthy after intravenous sedation
with local anaesthesia and the feeling
increased during the following days
(p=0.0001). Patients felt confusion
for approximately three hours, and
most patients felt ready for daily
work the next morning. However,
sedative premedication increases the
need of sleep and the patients need
more rest than normally on the first
day after treatment.
1.2.3 Part IV (Challenges)
This part again consists of three
chapters. The first describes advanced
monitoring: Holter ECG and the
analysis of the status of the
autonomic nervous system. The
second chapter introduces a new
stress index, and the last chapter
some complicated cases. Survey 6
comprises 23 study group patients
undergoing dental procedure under
intravenous sedation, and 12 control
registrations of the University Clinic
outpatients who underwent dental
surgical
operations
without
intravenous sedation. Patients were
monitored with a Holter ECG
recorder until next morning. The
tapes were reviewed with an
arrhythmia analysis program allowing
the detection of normal sinus beats
and supraventricular and ventricular
extrasystoles.
The
heart
rate
variability analysis (HRV) was
performed both during and after
surgery. The amount of cardiac
occurences were within normal limits
in both groups; the maximum pulse
was suggestively lower in the study
Postoperatively (study 5), pain
was the primary symptom after
treatment under intravenous sedation
with local anaesthesia. Patients
reported that the pain was not a result
of sedation with local anaesthesia but
a result of the operation itself. The
incidence of confusion and tiredness
reduced after the first night. The
possibilities to avoid pain and
confusion are discussed. Some other
disorders were detected but they were
rare: headache and nausea but no
vomiting.
Subgroups
showed
statistically significant differences
with the incidence of confusion
immediately after the treatment. The
phobia group felt more confused than
the operation (control) group
(p=0.05). No statistical difference
appeared in unpleasant experiences
29
General introduction and review of the literature
group and the high and low frequency
components of heart rate variability
were systematically and, in recovery
stage, even statistically higher
(p=0.05) in the study group, all
indicating stress relief.
which is called the stress index.
When a subject suffers from generic
stress, we can measure the most
significant cardiovascular changes,
such as a rising pulse rate and a
diminishing amplitude of pulse wave.
By dividing the pulse rate by the
amplitude of pulse wave (pulse /
blood flow) we get a sensitive
indicator for stress, or the stress
index.
Study 7 is a combination of parts
of two previous studies: survey 2 and
survey 6, both describing amplitude
of pulse wave. This study describes
cardiovascular parameters indicating
stress during treatment under
intravenous sedation, and local
anaesthetic alone. Moreover, two
local anaesthetic agents (lidocaine
and
prilocaine)
and
two
vasoconstrictors (epinephrine and
phelypressine)
were
observed.
Amplitude of pulse wave was the
most
responsive
measurable
parameter. Amplitude of pulse wave
diminished just before and during the
injection
as
a
result
of
vasoconstriction due to psychological
stress. Blood flow showed the
smallest values during the injection of
local anaesthetic. Similarly, heart rate
slightly decreased after the injection
of prilocaine and phelypressine, but
pulse rate increased after the
epinephrine-containing
lidocaine
injection.
Controversially,
both
parameters increased after the
injection of sedative agent: pulse rate
only slightly but amplitude of pulse
wave showed a remarkable increase.
To estimate the value of generic
stress a new index was developed,
The last study (8) describes cases
where remarkable and long-standing
hypoxia were detected with pulse
oximeter during intravenous sedation.
Diazepam with soybean oily solvent,
midazolam and in some cases
fentanyl were used as intravenous
sedative agents in these cases. The
first signs of hypoxia were seen
through pulse oximetry. External
oxygen was added for all of these
patients during the dental treatment
period to avoid more complications as
a result of hypoxia. Attempts were
made to solve the problems related to
hypoxia
by
administering
supplementary
oxygen,
benzodiazepine
antagonist,
and
ventilation. Some of the patients
needed further follow-up but none of
these
patients
developed
any
additional complications. The lowest
SaO2 levels of these patients were
found during the postoperative period
and the role of poor amplitude of
pulse wave in these cases is
discussed.
30
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part I
1.3 INTRODUCTION TO
OXYGEN DELIVERY SYSTEM
The oxygen delivery system must
provide oxygen at adequate rates to
all body tissues to support their
oxygen consumption for survival. In
large
animals,
two
physical
constraints to transport have been
solved physiologically. First, the rate
of gas diffusion in liquids is
extremely slow. It takes hours for
oxygen to diffuse through a
centimeter of water. Even though
animals have increased dramatically
in size from single celled to large
mammals, the diffusion distance from
the
oxygen
source
to
the
mitochondrion
has
not
much
increased. The vast microvascular
circulatory system has solved the
diffusion problem by supplying an
oxygen tension source near all cells.
The tissue capillary density is roughly
matched to the metabolic oxygen
demands of the tissues. The second
physical problem is that oxygen is
relatively insoluble in water, the
medium of cellular life. The
haemoglobin molecule has effectively
increased
the
blood's
oxygen
solubility by reversibly binding
oxygen. The addition of haemoglobin
to the water-based oxygen transport
fluid (blood) increases the carried
oxygen approximately 60-fold.
Oxygen is taken up by blood in the
lungs, transported by blood to all
organs and tissues, and within microcirculation released by blood into
tissues. The driving force behind
oxygen uptake as well as oxygen
release is the partial pressure
difference of oxygen; in other words,
oxygen diffuses from alveolar space
into blood and from blood into tissue.
In addition to this necessary transport
by diffusion, oxygen is transported by
convection from the lungs to the
organs. The amount of oxygen
transported to all organs is called
oxygen supply and it is determined by
the product of cardiac output and the
arterial oxygen concentration.
31
General introduction and review of the literature
The principal aim of monitoring
during procedures is patient safety.
Oxygen is the most acutely
necessary substrate of aerobic life.
Oxygen
saturation is
life-maintaining
and
pulse oximetry
is therefore
obligatory
when
a patient has
a treatment
under
intravenous
sedation.
120
100
% Hb SATURATION
80
60
40
20
0
0
32
20
40
60
80
PaO2 mmHg
100
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part I
Any change in arterial tension,
arterial saturation, the oxygen binding
curve and the oxygen binding power
of Hb, haemoglobin concentration or
the physically dissolved oxygen leads
to an alteration in the oxygen content
of blood. As a consequence of a
disturbance
in
lung function,
hypoxaemia may be produced by a
decrease in oxygen tension. In such
circumstances all values, namely
tension or partial pressure (PaO2),
saturation (SaO2) and content or
concentration (CoO2), are decreased.
This is hypoxic hypoxaemia. Carbon
monoxide
poisoning
or
methaemoglobin formation decreases
two variables, SaO2 and CoO2 where
the PaO2 remains normal and results
in toxaemic hypoxaemia. Anaemia
hypoxaemia with a decrease in the
haemoglobin concentration (anaemia)
lowers CoO2 only while PaO2 and
SaO2 remain normal. Thus, the
necessary terms to understand are:
blood flow and electrocardiogram),
they are only useful devices and can
never
replace
human
senses,
observation skills and the measured
value of blood oxygen saturation.
Intravenous sedation has proved
helpful in avoiding cardiovascular
reactions during oral surgical
operations, but there is a risk of
provoking respiratory depression.
This adverse effect can easily be
detected at an early stage, where the
pulse wave and / or a drop in
saturation is signalled visually with
pulse oximeter and can be corrected
by administering supplementary
oxygen. Monitors as well as
intravenous sedation are still very
seldom used in dental practice in
North Europe despite their low cost.
Fatal complications in the dental
chair are so uncommon that the use of
monitors is not obligatory, and is not
recommended by the Finnish
authorities. This is in contrast to the
situation in United States, Japan,
Canada and many other parts of the
world. There the monitors are in
widespread use for conscious
intravenous sedation; in fact, they are
mandated by laws and practice
standard. Our tradition relies on the
high education level of the medical
and dental surgeons, and no precise
rules exist.
 The amount of haemoglobin in
blood (depends on individual
variation)
 Oxygen
tension
(partial
pressure) in blood (depends on
atmospheric
pressure
and
oxygen
concentration
in
atmosphere)
 Oxygen saturation of blood
(depends on the dissociation
curve. See figure on next page)
 Oxygen concentration in blood
(depends on haemoglobin and
oxygen tension)
The selection of a correct monitor
must originate from essential needs in
each
particular
situation
and
circumstances. On the basis of
experiences from surgical anaesthesia
there are some clear priorities among
monitored parameters and these
Although this book introduces
some other methods and parameters
to monitor (e.g. blood pressure, pulse,
33
General introduction and review of the literature
experiences can easily be applied also
to dental practice. The use of
monitors must rise from risk analysis.
They should be used in situations
which include the most concrete
dangers. The selection of monitored
parameters should lead to conclusions
on how dangers could be surely
detected. When we monitor a patient
who is having a treatment under
intravenous sedation, the most
important factor to monitor is the
amount of oxygen in blood because
every sedative agent will cause some
depression
in
the
respiratory
parameters.
34
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part I
1.4 THE STATE OF ART
AT THE BEGINING OF THE WORK
IN THE YEARS 1992-1993:
REVIEW OF THE LITERATURE
1.4.1 SEDATION WITH LOCAL ANAESTHESIA OR GENERAL
ANAESTHESIA?
Intravenous conscious sedation with local analgesia is associated with less
patient stress than is general anaesthesia. When intravenous sedation is used, only
the levels of the plasma growth hormone and prolactin rise significantly. General
anaesthesia will significantly increase heart rate, systolic blood pressure, mean
arterial pressure, and the levels of plasma epinephrine, cortisone, prolactin, blood
glucose; all indicative of a stress response. Conscious sedation can be used
correspondingly to reduce measurable parameters of stress, such as serum cortisone
levels and systolic blood pressure that patients would develop during operation.
(Shepherd et al. 1988, Hempenstall et al. 1986) A cost comparison showed that it
was twice as expensive to have the same procedure done in an outpatient surgical
suite under general anaesthesia as it was in a private office under Intravenous
sedation (Van-Sickels and Tiner 1992).
1.4.1.1 Midazolam
1.4.1.2 Midazolam compared to
diatsepam
Intravenous
midazolam
administered in conscious sedation
doses reduces significantly the
affection and motivational component
of the pain experience (Coulthard and
Rood 1992), and midazolam produces
at least 20 minutes of profound
amnesia for all stimuli (Hupp and
Becker 1988) A bolus injection
followed by the continuous infusion
of midazolam shows good safety and
better amnesia during procedure than
a bolus injection of midazolam, but it
prolonged recovery time (Luyk et al.
1992)
Midazolam has more advantages
for the patient than diazepam; quicker
onset of sedation, less pain during
injection,
profound
anterograde
amnesia and fewer postoperative
complications being the main features
(Clark et al. 1987, Clark and Rodrigo
1986, Rodrigo and Clark 1986). Also
a more rapid return to normal
activities is seen with midazolam.
Psychometric testing, however, has
failed to show any objective
differences between the treatments
(Barker et al. 1986).
35
General introduction and review of the literature
1.4.2 PATIENT MANAGEMENT WITH INTRAVENOUS SEDATION
1.4.2.1 Dentist’s sight
1.4.2.2 Patient’s opinion
Patient management and general
anaesthesia are the most commonly
employed techniques. The frequency
of the use of intravenous and
inhalation sedation varies according
to the age of the patient. Only 55% of
dentists in general practice have any
training in a sedative technique in the
UK (Edmunds and Rosen 1989).
Intravenous conscious sedation in
combination with local anaesthesia is
an alternative during unpleasant
surgical and dental procedures, and in
several cases it can replace general
anaesthesia. Monitoring as well as a
trained staff make the methods safe
and allow to reduce complications
(Zoller and Zoller 1992). The length
of certain implant surgery operation
as well as their precision requires the
complete co-operation of patients
(Charlton et al. 1991). Many mentally
and/or physically handicapped and
anxious dental patients do not receive
adequate dental treatment because
effective
ways
of
supportive
treatment are insufficiently known
and/or available to dentists (BouvyBerends and Makkes 1990). The
predominantly favourable response of
the patients leads to the suggestion of
using intravenous sedation even in
minor oral surgery (Kingon 1990).
The majority of the patients has
never heard of the availability of
intravenous sedation to supplement
local anaesthesia during dental
surgery; and when given the chance
to experience this method the
majority will find it highly
acceptable: 85 % of the patients
prefer surgery under sedation and
local anaesthesia to local anaesthesia
alone.
None
prefers
general
anaesthesia for dental surgery.
(Rodrigo and Clark 1986, Lundgren
1988) Postoperatively, many patients
have complete amnesia for operative
events, most are satisfied with the
monitored anaesthesia care and would
desire a similar anaesthetic technique
for
future
procedures
when
intravenous midazolam and fentanyl
have been used as primary
pharmacological
agents
in
intravenous sedation (Lind et al.
1990).
1.4.2.3 Antagonist to
benzodiazepines
Flumazenil appears to be a
promising
drug
for
reversing
midazolam conscious sedation. A
patient who receives flumazenil after
intravenous
midazolam
is
significantly more alert at 5 min
following drug administration (Clark
et al. 1991). In cases of undue
sedation persisting after dental
treatment, flumazenil may be used
36
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part I
with minimal risk for resedation.
Flumazenil in doses from 0.5 to 1.0
mg rapidly reverses the sedative and
amnesic effects of midazolam without
the apparent evidence of subsequent
resedation (Davies et al. 1990).
Flumazenil almost totally reverses the
effects of mental sedation for
approximately 2 hours, but not
physical sedation or memory. A
number of central nervous systemrelated side effects have been
observed but none of these is
considered serious (Davies et al.
1990, Ghoneim et al. 1989, Cooper et
al. 1991).
Flumazenil recipients are less
sedated
postoperatively,
better
oriented and more co-operative. The
patients cannot remember operative
events. The dental surgeons feel that
flumazenil makes recovery in the
supine position unnecessary and postoperative
monitoring
easier.
Flumazenil is a drug that should be
included in the armamentarium of any
emergency
drug
kit
when
benzodiazepines
are
used
intravenously. (Reed et al. 1989)
37
General introduction and review of the literature
1.4.3 BENZODIAZEPINES COMBINED WITH OPIATES
anaesthesia care, and 94% would
desire a similar anaesthetic technique
for
future
procedures
when
intravenous midazolam and fentanyl
were
used
as
primary
pharmacological
agents
in
intravenous sedation during dental
implant surgery (Lind et al. 1990).
When nalbuphine and fentanyl were
compared as analgesic components of
intravenous conscious sedation with
diazepam, 88% who received
nalbuphine and 87% treated with
fentanyl indicated complete pain
relief. No statistically significant
differences were observed between
nalbuphine and fentanyl treatments.
(Dolan et al. 1988)
1.4.3.1 Healthy patients
The mean consumption of local
anaesthetics is significantly lower
with intravenous anxiolytics than
with intravenous analgesics. The
postoperative subjective assessment
of the operation by the patients is
better under anxiolytic than under
analgesic sedation, too. (Breier 1992)
However, opiates allow for a
significant reduction in the mean
dosage of midazolam required to
produce satisfactory sedation when
compared with experiments where
midazolam
alone
was
used.
Postoperatively 95 % of the patients
are able to walk unaided after 2
hours. At this time, significantly more
patients who received opiates were
pain free. (Hook and Lavery 1988)
Diazepam and midazolam with
fentanyl produce a both safe and
acceptable sedation. Diazepam causes
more venous sequels. The patients
who had recieved midazolam had
better amnesia effects with no
incidence of venous sequels. (Bakaeen et al. 1987) Adequate amnesia
associated with midazolam/fentanyl
intravenous
sedation
in
the
intraoperative period is displayed
using a dosage of midazolam 0.10 0.13 mg/kg (Miller et al. 1989).
Moreover, midazolam produces at
least 20 minutes of profound amnesia
for all stimuli (Hupp and Becker
1988). 65% of patients had complete
amnesia for operative events, 96%
were satisfied with monitored
1.4.3.2 Medically compromised
patients
The narcotic analgesics fentanyl
or alfentanil and the local anaesthetic
4% articaine with epinephrine
(1:200,000) have been used for
medically compromised patients aged
between 32 and 80 years, with an
ASA physical status of III and IV.
Surgical procedures included multiple
dental extraction, cystectomy and the
removal of impacted teeth. All
patients completed the surgery
without deeper anaesthesia and
mostly enjoyed a comfortable
intraoperative period. Only one
respiratory depression was observed,
but quickly reversed. Other adverse
effects were few and without
38
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part I
consequences,
haemodynamic
changes remained in tolerable limits.
In conclusion this anaesthetic
technique can be a suitable alternative
for general anaesthesia in oral surgery
for high- risk patients. (Lefevre 1991)
Similarly, intramuscular butorphanol
was shown to be a safe and effective
agent for dental premedication for
institutionalised
severely
and
profoundly
retarded
patients.
Vomiting (2.6%) was the most
frequent adverse effect observed
when sedation was carried over with
opiates. (Jann et al. 1987)
39
General introduction and review of the literature
1.4.4 THE COMPARISON OF ORAL AND INTRAVENOUS
ADMINISTRATION
Rapidly
acting
oral
benzodiazepines such as midazolam
provide safe and effective alternatives
to intravenous diazepam (Hosie et al.
1988). Although surgeons' ratings
indicated
that
sublingual
lormetazepam was comparable to
intravenous
diazepam,
patients'
ratings indicated greater satisfaction
with and preference for intravenous
diazepam (O-Boyle et al. 1988).
temazepam. (Skelly et al. 1992)
Patients who were given temazepam
per os showed wide variations in
plasma concentrations. Patients with
low
plasma
temazepam
concentrations at the time of surgery
showed no significant reduction in
anxiety scores. The intravenous
diazepam caused greater amnesia
during surgery, but showed also a
significant slowing of reaction time at
the time of discharge. (Hosie et al.
1988) Another non parentheral
alternative is the rectal sedation
method which is equally efficient
with a double dose compared to
intravenous administration (Lundgren
1988).
Per os temazepam elixir provided
a useful sedative for oral surgery,
avoiding the complications of
intravenous administration. However,
for equivalent levels of sedation,
intravenous midazolam had greater
anxiolytic and amnesic effects than
40
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part I
1.4.5 THE NECESSITY OF OXIMETRY DURING INTRAVENOUS
SEDATION
administered; only 3% of patients
who received supplemental oxygen
had episodes of hypoxia. The use of
supplemental
oxygen
is
recommended for all patients
undergoing intravenous sedation.
(Hardeman et al. 1990) However, in
some patients undergoing a third
molar removal with local anaesthetic
alone, oxygen saturations in the range
of 93-89% were recorded. The results
suggest that all patients undergoing
the removal of third molars are at risk
of hypoxia. Short episodes of hypoxia
may be of insignificant consequence
in
healthy
patients,
but
in
compromised patients early detection
may avoid serious complications.
(Lowe and Brook 1991, Rodrigo and
Rosenquist 1988) Careful dosage and
the use of an ultra slow technique
indicates that a continuous oxygen
supplement would not appear
necessary routinely (Read-Ward
1990).
1.4.5.1 Hypoxia
The arterial saturation of oxygen
(SaO2) will decrease abruptly after
the administration of sedative agents
in each case but there are always
individual variations. (Sugiyama et al.
1991) The decrease in saturation may
appear during surgery and in the
period
immediately
following
surgery. It is suggested that it may be
necessary to observe and selectively
monitor some patients in the
immediate post-surgical period as
well as during the period of
operation. This would be the case
particularly
with
medically
compromised patients and the elderly
(Zacharias et al. 1992). A comparison
of patients sedated with intravenous
lorazepam, diazepam, or midazolam
during oral surgery shows that the
midazolam
group
had
higher
respiratory rates than those of the
other two drugs (van-der-Bijl et al.
1991). During the induction of both
midazolam and fentanyl or diazepam
and fentanyl respectively, the patients
had significantly lower average O2
saturation values than receiving either
midazolam or diazepam alone.
Patients receiving midazolam and
fentanyl had lower O2 saturation than
the midazolam or the diazepam and
fentanyl group. (Tucker et al. 1986)
1.4.5.2 Pulse oximetry
There are various technical
problems involved in estimating
oxygen saturation non-invasively
from a light signal transmitted
through tissue. The light is absorbed
and scattered by tissue, dark skin, and
other blood haemoglobin (capillary
and venous blood haemoglobin). For
these and some other reasons,
spectophotometric principles and
calculations do not strictly apply for
20% of patients experienced
hypoxic
episodes
in
the
postanaesthetic recovery unit when
no
supplemental
oxygen
was
41
General introduction and review of the literature
non-invasive oximeters. Because
SaO2 cannot be theoretically
calculated, it is estimated by an
empirically derived algorithm based
on clinical data. For example the
Hewlett Packard ear oximeter
accurately estimated SaO2 using
eight wavelengths of light. Although
this device has been useful in
pulmonary function laboratories, it is
too cumbersome and too expensive to
be practical for intraoperative use.
Two technological advances and an
ingenious
idea
allowed
the
development of a new generation of
oximeters. The two technological
developments were the availability of
light emitting diodes (LEDS) and
microprocessors. LEDs provide a
stable, lightweight light source.
Microprocessors
allow
the
programming of complex empirical
functions into relatively inexpensive
devices. The remaining problem was
how to discriminate the arterial
haemoglobin saturation from the
transilluminated
tissue
signal.
(Temper and Barker 1986)
60% saturation. The pulse oximeter is
designed to be insensitive to
haemodynamics although extreme
hypotension or vasoconstriction may
produce a signal that is too weak to
process and the oximeter will read a
default message (Tremper et al.
1985). The pulse oximeter gives
incorrect SaO2 readings in the
presence of abnormal haemoglobin
due to medication with nitrites or a
smoking habit (Sugiyama et al. 1991).
In hospitals, monitoring is more
regularly used for patients undergoing
for example endoscopy than in
private offices. During endoscopic
procedures, which are comparable to
short acting unpleasant dental
procedures,
most
endoscopists
monitor vital signs before and after
procedures but less often during
procedures. However, pulse oximetric
and electrocardiographic monitoring
is in common use and is also used in
most cases during endoscopic
procedures. There is a significant
relationship between the awareness of
oxygen saturation and the timing of
nursing interventions e.g. oxygen or
antagonist therapy. Because advanced
cardiac life support training is not
common among endoscopists and
gastrointestinal assistants(Keeffe and
O-Connor 1990), the use of pulse
oximetry is in these circumstances
essential (Hinzmann et al. 1992).
The solution was to analyse the
changes of the light signal produced
by arterial pulsation. The signal is
then empirically correlated to SaO2
values obtained from an invasive
blood sampling which has been
demonstrated to be a correct
calculation (Tremper et al. 1985;
Mihm and Halperin 1985; Yelderman
and New 1983). This equipment is
able to predict Sao2 with a 3%
standard error of the estimate
(Tremper et al. 1985). Mihm and
Halperin (1985) reported patients
with respiratory failure showing
about the same standard , even below
Some authors are of the opinion
that oximetry monitoring may not be
clinically useful because the largest
mean decrease in oxygen saturation
observed during procedures under
intravenous sedation is less than that
considered normal during sleep.
42
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part I
Likewise the high incidence of
desaturation do not cause adverse
outcomes or complications (Berg et
al. 1991 and Bilotta et al. 1990).
However, pulse oximetry is highly
valuable because it will immediately
react for any progressive oxygen
desaturation and therefore an early
correction is possible. As the use of
pulse oximetry should be considered
obligatory for all endoscopic or
paediatric patients during intravenous
sedation (Casteel et al. 1990), it is
useful as a respiratory monitor during
oral surgery (Sugiyama A et al.
1991).
43
General introduction and review of the literature
1.4.6 SEVERE COMPLICATIONS DURING PROCEDURE
The most numerous complications
are hypoxia and venous irritation. The
first is handled in previous chapters,
and venous irritation only in the
appendixes of this book.
1.4.6.2 Other complications
Other possible complications are
cardiac dysrhythmias (Rodrigo et al.
1990):
During
an
extraction
procedure under local anaesthesia
with intravenous sedation using
diazepam, a 14 year-old girl patient
showed many multifocal premature
ventricular contractions in ECG. This
patient had the history of a radical
operation for tetralogy of Fallot.
(Himuro et al. 1989)
1.4.6.1 Psychological
complications
Fantasies during sedation have
been reported with I.V. midazolam or
diazepam: most of them had some
sexual element and a minority were
unpleasant experiences. Some led to
litigation against the sedationist. Out
of verified reports made by 25
patients of incidents occurring during
sedation, 17 did not happen and in
9/13 clear descriptions there was a
relation
between
fantasy
and
something that really happened under
sedation. All occurred with what are
now considered large doses of the
drugs. Benzodiazepines have proven,
in appropriate doses, to be among the
safest in medicine for short term use.
There have, however, been a few
cases of what can be described as
fantasies occurring during sedation:
events occurring in a logical sequence
which are very real to the patient and
yet, on the evidence of two or more
independent witnesses, did not occur.
Many of these have had an element of
sexual trespass. (Dundee 1990)
The increasing use of intravenous
and inhalation sedation in the dental
office has the potential of increasing
the
incidence
of
malignant
hyperthermia which is documented in
two cases (Cantin et al. 1986).
Paradoxical excitement associated
with intravenous conscious-sedation
in a patient undergoing dental surgery
was successfully reversed with 1.0
mg physostigmine (Milam and
Bennett 1987).
44
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part I
The most important fact
is that
without general anaesthesia
the amnesic effects of
benzodiazepines
are available in a
real-life stress situation.
(File et al. 1986)
45
General introduction and review of the literature
1.5 AIMS OF THE STUDY
The principal aims of this study were to describe or
determine if possible:
1. whether peroperative monitoring by pulse oximetry can
detect adverse reactions during intravenous sedation.
2. whether vasoconstrictor containing local anaesthetic
preparates have any effects on the blood oxygen
saturation and cardiac parameters available when
observed with pulse oximetry.
3. the problems related in the use of two local anaesthetic
preparations in combination
4. the differences in measurable pulse oximetric
recordings of commercial local anaesthetics from the
effects of benzodiazepines.
46
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part I
5. patients' reactions to treatment under intravenous
sedation with local anaesthesia i.e. whether the patients
experiences of the procedure under sedation were
positive or negative.
6. the patient’s condition during the hours and days
following dental operations under sedation; i.e. to study
how the patients felt after the treatment under
intravenous sedation with local anaesthesia.
7. some false alarms of pulse oximetry, and complicated
cases during intravenous sedation with local
anaesthesia, and their reasons.
8. arrhythmias and the status of amplitude of pulse wave
and sympatho-vagal balance during operation and the
following day.
47
General introduction and review of the literature
1.5.1 MORE DETAILED DESCRIPTION OF THE BACKROUNDS
AND AIMS OF THE SEPARATE STUDIES
intravenous sedation with local
anaesthesia. Also changes in the
values of blood pressure and pulse
were
searched
from
patient
monitoring data.
1.5.1.1 Part II (Monitoring...)
The background of the studies has
been the necessity to find an ideal
relation of pain and anxiety relief
when anxious patients are treated
under intravenous sedation with local
anaesthesia.
The final reason for this article
was the need to describe some false
alarms in the oxygen saturation of
blood during intravenous sedation,
and to find explanations thereto.
As benzodiazepines alone do not
create pain relief, it is obligatory to
also use local anaesthetics in certain
cases. An experiment was made with
local anaesthetics to differentiate the
measurable cardiovascular effects of
two commercial vasoconstrictor
containing
local
anaesthetic
preparations commonly used worldwide
from
the
effects
of
benzodiazepines. A lot of information
concerning certain parameters which
have previously been poorly detected
emerged during the course of this
study.
1.5.1.2 Part III (Experiences...)
Another reason was to find out
whether local anaesthetic agents, and
sedative vasoconstrictors, have any
effects on the cardiac parameters
indicating stress when observed with
pulse oximetry. Moreover, any
undesirable cardiac parameters when
two commonly used local anaesthetic
agents are used in combination were
searched by monitoring.
Before the treatments, a number of
criteria were considered for the
selection
for
treatment
and
anaesthesia: who needs sedation, for
whom diazepam alone would not be
sufficiently effective, and whether
there might be any difference in the
effectiveness of one type of
anaesthesia for different types of
operations. Postoperatively, in the
cases where the decision is made to
use intravenous sedation, many
patients have complete amnesia of
operative events and typically express
the desire for a similar anaesthetic
technique in the future. However, it
remains unclear how the patients
would react to diazepam sedation if
used in amounts which would not
essentially produce total amnesia.
It was also necessary to determine
whether peroperative monitoring by
pulse oximetry can detect adverse
reactions in oxygen saturation during
The present study attempts to
resolve whether the patients had had
positive or negative experiences of
the procedure under sedation. Patient
48
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part I
evaluation would thus indicate
whether sedation had any effect on
the patient's phobia, i.e. had the
phobia been relieved, remained
unchanged or even worsened.
could be differences between patients
who suffered from dental care phobia
and those whose treatment was a
major oral surgery. Similarly,
information was needed on how much
time the patient needs for recovery.
Moreover, the condition of the
patient during the hours and days
following dental operations were
described. There was a clinical
interest to study how the patients felt
after the treatment under intravenous
sedation with local anaesthesia. In
out-patient practice, the only way to
find out the patients' condition after
the treatment is to make direct
questions or to make different
psychological measurements to the
patients after treatment. In this study,
an anonymous questionnaire was sent
to resolve the main question, "did the
patient have complications after the
procedure under sedation" i.e. is the
procedure as superior as it seems to
be from the point of view of the
dentist. It was known very well that
postoperatively many patients incur
complete amnesia for operative
events but it was not known how the
patients felt after the procedure when
they recovered from the therapy.
There was also a need to define if the
treatment itself was the main source
for the symptoms, and whether there
1.5.1.3 Part IV (Challenges)
The purpose of this study is to
define the safety of dental procedures
under intravenous sedation by
recording the arrhythmias during the
operation and the following day.
Another purpose is to evaluate the
sympatho-vagal balance using a
frequency-domain analysis of heart
rate variability. Since we know that
powerful sympathetic activation may
increase the risk for arrhythmias, one
aim of this study was to clarify the
changes in ECG and in the function
of the autonomic nervous system
during and after oral surgery. A
further reason for this article was the
need to describe complicated cases
during intravenous sedation with
local anaesthesia, and their reasons.
Moreover, a new prospective index the stress index- is introduced.
49
General introduction and review of the literature
1.6 MATERIALS AND PATIENS
for the revision of databases was to
get an answer to a very important
clinical question: How did the
patients feel? The later revised
databases formed the study material
(retrospective review of patient
records). These records included
subsequent findings, for instance that
the use of a monitor enabled the
determination of the correct sedation
level earlier and easier than the
normally used ptosis i.e. eye closure
reaction does. Further questions
appeared later on and were attempted
to answer through study designs, but
in every case the treatment of the
patient has been in the first place and
the study in the second. Although the
monitoring equipment was changed to
detect more sophisticated parameters,
all the studies have only been clinical
follow-ups. Because there was no
reference group in every study, all of
the parameters were compared with
the literature on corresponding
studies.
1.6.1 STUDY DESIGN
This publication includes three
parts of which the first and the last
are retrospective descriptive reviews
of patient records. There were many
differences
between
patient
preparation,
cannulation
and
intravenous infusion, sedative drugs
and local anaesthesia i.e. in the
underlying factors.
It is important to
understand that
these studies were
not controlled
clinical trials but
clinical follow-ups
i.e. observational
studies of normal
treatment periods.
Part III (Experiences...) differs
from the other study parts because it
does not include monitored findings,
but the opinions of treated patients. It
is carried out with an anonymous
questionnaire which was mailed to
the
patients
who
previously
underwent intravenous sedation with
local anaesthesia. The patients were
divided into two main groups:
patients to whom the main purpose
for the treatment under intravenous
sedation with local anaesthesia was
the major surgical procedure itself
(operation group), and to patients
One study comprises course
exercises which gave the author an
opportunity to allow the students to
practice
local
anaesthesia,
to
demonstrate cardiovascular effects
thereto, and to collect objective
measurable findings. Thus there was
no indication of approval by an
institutional review board governing
human experimentation in any of
these studies. During treatments and
clinical
follow-up
with
pulse
oximeter, there was no study design
in the first study that would answer
any particular question but the aim
50
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part I
who were scared of dental treatment,
i.e. they had dental care phobia
(phobia group).
corresponding to the ASA I or II
groups. The study was done during an
ordinary local anaesthesia course for
students. Every subject had to come
twice to the test on separate days.
Part IV is called ”Challenges”
because it contains some advantages
for monitoring and case studies which
have showed poor performance and
caused therefore further questions.
Survey 3 i.e. the last study of this
part is a retrospective review of
patient records comprising 26
registrations of the author's private
outpatients who underwent dental
operations with intravenous sedation.
The patients were 16 (62%) males
and 10 (38%) females. Mean age was
42 years (SD 15). The patients had
some oral surgical operations or they
underwent large conservative dental
treatment or extraction under sedation
because of dental care phobia.
1.6.1.1 PATIENTS
1.6.1.1.1 Patients in Part II
(Monitoring...)
Survey 1 comprised 41 of the
author's private outpatients who
underwent dental operations between
January and September 1993 with
intravenous sedation and local
anaesthesia. 44 % of the patients were
males and 56 % females. Mean age
was 47 years (SD 14). Twenty-three
of the patients had surgical operations
primarily for implantological reasons,
and 18 patients underwent large
conservative dental treatment or
extraction under sedation because of
dental care phobia. They were in
good health and had no severe
systemic
diseases
(in
the
classification of American Society of
Anaesthesiology ASA I - II i.e. no
systemic diseases or only a moderate
disease which do not limit activity).
1.6.1.1.2 Patients in Part III
(Experiences...)
The research group for studies 4
and 5 consisted of 108 patients
undergoing dental procedure with
intravenous sedation at the author’s
private practice. They were 46 %
males and 54 % females. Mean age
was 42 years (SD 13). Patients
underwent surgery primarily for
implantological
reasons,
major
conservative dental treatment, or
extraction under sedation due to
dental care phobia. The subjects were
unselected private practice dental
patients in a good state of health or
suffering from systemic disease
which may moderately limit their
activity, i.e. they conformed to groups
I-III of the ASA (American
Association of Anaesthesiologists)
classification. None of the patients
Survey 2 consisted of twenty
dental students. The students were
between 19 and 31 years of age with a
mean age of 22 years (SD 3); 80 %
were females. Each person accepted
in the test group had to be healthy and
free
of
any
surgical
risk,
51
General introduction and review of the literature
corresponded
to
the
ASA
classification for groups IV - V. The
patients were within the limits of
generally accepted indications and
contraindications as mentioned in the
text books for dental anaesthesia.
were within the limits of generally
accepted
indications
and
contraindications as mentioned in the
text books for dental anaesthesia and
oral surgery.
2. The reference group
1.6.1.1.3 Patients in Part IV
(Challenges)
The reference group consisted of
12 patients undergoing dental
procedure
without
intravenous
sedation. Sexual distribution was
balanced between females and males,
i.e. 50 % and 50 %. Mean age was 45
years (SD 15). Subjects were
unselected University clinic patients,
who were transmitted to the
department of oral surgery. They
were all voluntary for study and they
conformed to groups I-II of the ASA
(American
Association
of
Anaesthesiologists). None of the
patients corresponded to the ASA
groups IV - V. Thus the patients were
within the limits of generally
accepted
indications
and
contraindications for dental treatment.
This part includes three studies.
The first of them is survey 6; it is the
only one which has an independent
study group. The later two study
groups are formed by combining the
study groups of previous works, and
only reorganizing the question or aim.
Survey 6 combines two groups of
patients, of which the author’s private
practice patients are called ‘the study
group’ and the university clinic
patients ‘the reference group’.
1. The study group:
The research group consisted of
23 patients undergoing dental
procedure under intravenous sedation
at the author's private practice. They
were 35 % males and 65 % females.
The mean age was 48 years (SD 17).
The patients underwent surgery
primarily for implantological reasons,
major conservative dental treatment,
or extraction under sedation due to
dental care phobia. The subjects were
ordinary, unselected private practice
dental patients, who conformed to
groups I-III of the ASA (American
Association of Anaesthesiologists).
None of the patients corresponded to
the ASA groups IV - V. The patients
Study 7 includes a part of patients
and subjects from studies 2 and 3.
Study 8 is a study of complicated
cases.
There were differences between
patient
preparation
(eating
instructions),
cannulation
and
intravenous infusion as well as local
anaesthesia i.e. in the underlying
factors. Thus these studies are mainly
non-randomised studies to compare
two types of patient care.
52
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part I
Table 1. Patients
Study number:
Number of subjects
Indication
1
41
23 surgery
18 phobia
Males %
44
Females %
56
Age years,
mean 47
SD
15
range 23-76
Parameters measured
SaO2
BP
Pulse
Main sedative agent
Time
Lidocain (mg)
Mean
SD
Cases
Prilocain (mg)
Mean
SD
Cases
Midazolam (mg) Mean
SD
Cases
Diazepam (mg)
Mean
SD
Cases
Fentanyl (mg)
Mean
SD
Cases
Midazolam
1993
154
80
39
241
111
38
5.38
1.93
32
22.5
8.3
7
0.079
0.019
7
2
20
course
exercise
20
80
22
3
19-31
SaO2
BP
Pulse
A.P.W.
1995
180
20
270
20
-
-
* Not available on collected data
** See text
53
3
26
surgery
phobia
62
38
42
15
18-76
SaO2
Pulse
A.P.W.
4-5
108
38 surgery
53 phobia
46
54
42
13
16-78
-
6
35
surgery
phobia
40
60
47
16
21-81
SaO2
Pulse
ECG
Midazolam
1994
155
54
26
203
118
17
5.02
1.72
26
-
Diazepam
1992
177
86
100
234
108
88
6.2
2.7
24
12
5
85
0.065
0.025
7
Midazolam
1996
*
*
**
-
-
General introduction and review of the literature
1.6.2 PRE- AND POSTOPERATIVE PATIENT PREPARATION
In all studies except studies 4-6,
patient preparation was identical:
During the first examination, all
patients completed a questionnaire
about previous and present illnesses,
allergies and medications. A dental
care plan was drawn up and all the
patients were referred to radiological
examination (orthopantomography).
All the patients who underwent major
surgical operation e.g. sinus-lift
procedure, were also referred to
laboratory
blood
evaluations
(Sedimentation rate, B-Hb, B-leuk,
fB-glu). The patients were advised
both verbally and in writing how to
prepare for intravenous sedation (for
example, no food or drink for four
hours prior to treatment).
and medication for cardiopulmonary
resuscitation. All treatments were
carried out by the same dentist, i.e.
the author.
After treatment blood pressure
was recorded again and the venous
cannula removed.
The patients stayed
in the dental chair,
and pulse oximetric
monitoring was
continued until
bleeding after
extraction had
stopped and until the
patients felt well and
were able to walk
and get dressed
without help.
The patients left the
clinic with an adult
escort.
Patients were not given oral
premedication,
sedatives
nor
antibiotics on the day of the operation
or the previous day. Blood pressure
was recorded and monitoring with a
pulse oximeter initiated before the
insertion of a peripheral venous
cannula. After the insertion of the
cannula, an infusion of 0.9% sodium
chloride solution was started, and
then the sedative agent was applied
with disposable syringe using the
slow injection technique. After
sedation local anaesthesia was
performed.
The treatment room was equipped
with dental unit, pulse oximeter,
oxygen supplement unit and some
resuscitation facilities, including
endotracheal intubation equipment
In survey 6, patient preparation
was similar to the study group but for
the reference group the written
instructions on how to prepare for the
54
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part I
operation
it
was
particularly
mentioned that they should eat before
operation. This was a result of
different preparation practices of the
University clinic and the author's
private office.
analgesic drug) before operation.
Blood pressure was recorded and
Holter ECG initiated in the operation
theatre before operation. The
treatment room was equipped in the
same way as the other studies but the
treatment procedures were carried out
by several surgeons.
Neither in reference group patients
were given oral premedication (e.g.
55
General introduction and review of the literature
1.6.3 MEDICATION
for sedation (Dormicum 5 ml inj. 1
mg/ml Roche), with mean amounts
5.02 mg SD 1.72 mg. Fentanyl
(Fentanyl 2 ml inj. 50 microgram/ml
Orion R) was not used for additional
pain relief preoperatively, only in 1
case for analgesia postoperatively
(0.05 mg).
1.6.3.1 Medication in Part II
(Monitoring...)
1.6.3.1.1 Sedation
In survey 1 an infusion of 0.9%
sodium chloride solution was started,
and then the sedative agent was
applied with a disposable syringe
using the slow injection technique.
Diazepam with soybean oily solvent
was used for sedation in 7 treatment
periods (Stesolid Novum 2 ml inj. 5
mg/ml Dumex/KabiVitrum) and
midazolam in 32 cases (Dormicum 5
ml inj. 1 mg/ml Roche), with mean
amounts 22.5 mg SD 8.3 mg and 5.4
mg SD 1.9 mg respectively. Fentanyl
(Fentanyl 2 ml inj. 50 microgram/ml
Orion R) was used for additional pain
relief in only 3 cases (mean 79
microgram SD 19 microgram) and
only if there was insufficient level of
local anaesthesia. The author used
intravenous agents divided into small
parts (2 mg diazepam and 1 mg
midazolam). This almost barely
effective dose was repeated every 2
or 3 minutes until a minor decrease (2
- 3 %) in blood oxygen saturation is
detected. Extra doses after the initial
saturation fall were not normally used
with patients aged over 60 years. The
benzodiazepine antagonist used was
flumazenil (Lanexat 5 ml inj. 0.1
mg/ml Roche).
1.6.3.1.2 Local anaesthesia
In survey 1 local anaesthesia was
performed with lidocaine (Xylocain
adrenalin 1.8 ml inj. 20 mg/ml+12.5
microgram/ml ASTRA, mean 7.74 ml
SD 4.23 ml) and prilocaine (Citanest
Octapressin 1.8 ml inj. 30
mg/ml+0.54 microgram/ml ASTRA,
mean 8.01 ml SD 3.91 ml). The same
protocol to combine two agents was
performed in every study of this
publication. Because the dentist’s
(author’s) normal practice is to avoid
high epinephrine amounts he always
uses two different local anaesthetics.
Thus the method is used in these
studies, too.
In survey 2 the mentioned
practice was further studied and local
anaesthesia was performed with a
lidocaine - epinephrine solution
(Xylocain adrenalin 1.8 ml inj. 20
mg/ml+12.5 mcg/ml ASTRA) and
prilocaine - phelypressine solution
(Citanest Octapressin 1.8 ml inj. 30
mg/ml+0.54 mcg/ml ASTRA). The
site of injection was the upper jaw,
the buccal sulcus just distal of the
second upper molar. Both sides of the
maxilla were anaesthetised. This site
In survey 2 no sedation was used.
In survey 3 after starting an
infusion, only midazolam was used
56
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part I
was chosen because there is room for
a large enough volume of local
anaesthetic, and the trifurcation of the
trigeminal nerve is near the
anaesthetised area.
Local anaesthesia was performed in
combination with lidocaine (Xylocain
adrenalin 1.8 ml inj. 20 mg/ml+12.5
mcg/ml ASTRA) mean 8.8 ml SD 4.3
ml
and
prilocaine
(Citanest
Octapressin 1.8 ml inj. 30
mg/ml+0.54 mcg/ml ASTRA) mean
8.6 ml SD 3.6 ml.
In survey 3 local anaesthesia was
performed
with
a
lidocaineepinephrine combination (Xylocain
adrenalin 1.8 ml inj. 20 mg/ml +
0.0125 mg/ml, ASTRA, mean 155 mg
SD 54.3 mg lidocaine and 0.097 mg
SD 0.034 mg epinephrine) and
prilocaine-phelypressine combination
(Citanest Octapressin 1.8 ml inj. 30
mg/ml+0.54 microgram/ml ASTRA,
mean 203 mg SD 118 mg prilocaine
and 0.0036 mg SD 0.0021 mg).
1.6.3.3 Medication in Part IV
(Challenges)
In the study group of survey 6 an
infusion of 0.9% sodium chloride
solution was started, and then the
sedative agent was applied with a
disposable syringe using the slow
injection technique. Midazolam was
used for sedation (Dormicum 5 ml
inj.
1
mg/ml
Roche).
The
benzodiazepine antagonist used when
needed was flumazenil (Lanexat 5 ml
inj. 0.1 mg/ml Roche). Local
anaesthesia was performed with
lidocaine (Xylocain adrenalin 1.8 ml
inj. 20 mg/ml+12.5 microgram/ml
ASTRA) and prilocaine (Citanest
Octapressin 1.8 ml inj. 30
mg/ml+0.54 microgram/ml ASTRA).
1.6.3.2 Medication in Part III
(Experiences...)
In studies 4 and 5 diazepam with
soybean oil solvent was used for
sedation in 85 cases (Stesolid Novum
2
ml
inj.
5
mg/ml
Dumex/KabiVitrum) or midazolam in
24 cases (Dormicum 5 ml inj. 1
mg/ml Roche) with the mean amounts
corresponding to 12 mg SD 5.0 mg
and 6.2 mg SD 2.7 mg, respectively.
For pain relief, fentanyl (Fentanyl 2
ml inj. 50 microgram/ml Orion) was
rarely used (only in 7 cases,
combined with some of the sedative
agent mentioned above); when used it
was administered in the slightest
amounts (mean 1.3 ml SD 0.5 ml).
The benzodiazepine antagonist which
was available, and used when needed
in these cases, was flumazenil
(Lanexat 5 ml inj. 0.1 mg/ml Roche).
No sedatives were used in the
reference
group,
only
local
anaesthesia was performed with
lidocaine (Xylocain adrenalin 1.8 ml
inj. 20 mg/ml+12.5 microgram/ml
ASTRA) or/and prilocaine (Citanest
Octapressin 1.8 ml inj. 30
mg/ml+0.54 microgram/ml ASTRA).
Medication in studies 7 and 8 are
described solely in these studies.
57
General introduction and review of the literature
1.6.4 MONITORING AND DATA REVIEW
In part II (Monitoring...) of the
first study the patients were
monitored with an Ohmeda Biox
3740
(Ohmeda,
USA)
Pulse
Oximeter, in the second study with a
CARDIOCAP II CH-S (Datex,
Helsinki Finland) multiparameter
physiological monitor, and in the
third study with SATLITE TRANS
TM (Datex, Helsinki Finland) pulse
oximeter. The monitors were
connected to the serial port of
Toshiba T1000SE portable computer
for the trend collection of data by a
collection program. In the first study
the program was Ohmeda's own
program: 37XX, but in the other
studies custom-made programs were
used for the real-time collection of
data. Later programs recorded
numerical values from pulse oximeter
after the whole treatment and followup period. The data on blood
pressure, pulse, initial and minimal
SaO2 were collected from patient
history files which were formed as
on-line
registerations
during
operations and parameters were
further analysed using the computer.
In the second study, blood pressure
was measured and the data collected
automatically every two minutes from
the subjects' left upper arm.
Ohmeda pulse oximeter but no data
collection was done.
In
Part
III
(Challenges),
monitoring was a combination of
pulse oximetry (Ohmeda) and ECG
which was performed with Holter
recordings. All of the Holter tapes in
the study population were analysed
using the Marquette 8500 scanner
running version 5.7 of the Marquette
arrhythmia analysis program allowing
the detection of normal sinus beats
and supraventricular and ventricular
extrasystoles. After an automatic
analysis of the tape, the data file was
visually reviewed and manually
corrected. Heart rate variability
analysis was performed by running
the Marquette heart rate variability
analysis program. The HRV analyses
were
performed
using
four
consecutive minutes’ periods during
surgery and the three following hours
after the operation. Total power (TP)
between 0 - 0.40 Hz along with the
power in the low-frequency band (LF,
0.04 to 0.15 Hz) and in the highfrequency band (HF, 0.15 to 0.40 HZ)
were calculated and logarithmically
transformed. In addition to spectral
components, also LF to HF ratios and
normalised units were used as
markers of sympatho-vagal balance
during the different stages of
operation and recovery period.
In Part III (Experiences...) the
patients were monitored with
58
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part I
1.6.5 THE WORKING PRINCIPLE OF THE PULSE OXIMETRIC
EQUIPMENT
A pulse oximetry probe includes a
light emitter and detector (finger
probe), which are connected to the
monitor. The emitter emits red and
infrared light, which passes through
the tissue to the detector. The pulse
wave is derived from the detected
infrared signals so that the actual
pulse wave is displayed as a mirror
image of the intensity wave form. In
pulse oximetry a photoelectric
measures the absorption of light using
two different wave lengths. In the
area of infrared light the absorption is
not affected by the changes in the
oxyhemoglobin concentration and so
the changes in infrared absorption
essentially reflect only changes in
local blood volume. The pulsation of
the arterial blood flow modulates the
light passing through it, and the
oximeter converts this light intensity
information into pulse rate values,
which are presented together with
SaO2 values on a monitor screen. The
pulse wave is derived from the
intensity of the transmitted light. The
pulsating blood flow in the finger is
the result of the left ventricle
contraction of the heart, which fills
the vascular bed of the finger with
arterial blood. It is important to
understand that the pulse wave
reflects changes in blood volume, not
changes in blood pressure. The
oximeter converts this light intensity
information into pulse rate values
which are presented with SaO2 value
in a liquid crystal display or on the
screen. The microprocessor calculates
the SaO2 e.g. 25 times per second.
These calculations are averaged by
running-weighted-average
method
which allows erroneous SaO2 values
to be discarded when the displayed
value is determined.
1.6.5.1 Different equipment
philosophies
Ohmeda
Biox
3740
Pulse
Oximeter is a stand-alone, noninvasive, arterial oxygen saturation
monitor, providing continuous, realtime SaO2 and pulse rate readings.
The light generated in the finger
probe passes through the tissues. The
oximeter measures the relative
absorption of red light at 660 nm and
infrared light at 940 nm by Hb and
HbO2. Two different forms of
haemoglobin, oxyhemoglobin and
reduced haemoglobin allow different
amounts of light to pass at these wave
lengths. Similarly, the pulsation of
the arterial blood flow modulates the
passing light. The oximeter converts
these changes in information into
pulse rate and SaO2 value.
Similarly Datex pulse oximetric
equipment (Cardiocap and Satlite
Trans) function using the light which
is generated in the finger probe, and
the light passes through the tissues.
The total absorption of the light
depends on the absorbing components
59
General introduction and review of the literature
again: tissues, venous blood and the
pulsating arterial blood. Different
amounts of light are absorbed by
oxygenated haemoglobin (HbO2) and
unoxygenated
or
reduced
haemoglobin (Hb). These oximeters
measure the relative absorption by Hb
and HbO2 of red light at 660 nm and
infrared light at 910 nm.
automaticaly correct the amount of
amplitude of pulse wave when
represented on screen. This gives one
additional measurable parameter for
analysis: the level of vasoconstriction
which is controlled by autonomic
nervous system.
The main difference between the
equipment is that Datex do not
60
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
PART II
MONITORING THE PATIENTS
WITH THREE PULSE
OXIMETER EQUIPMENT
61
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
2.1
Survey 1
Detection of oxygen saturation
under intravenous sedation
with Ohmeda pulse oximeter
and registration of other
cardiovascular parameters
2.1.1 ABSTRACT
In this survey 41 patients were monitored with a pulse oximeter giving oxygen
saturation and pulse values. Blood pressure values were measured separately during
major or protracted dental operations under intravenous sedation with local
anaesthesia. The most important finding was that there seems to be a risk that low
oxygen saturation (SaO2 < 90%) before sedation constitutes a risk for oxygen
desaturation during sedation. Before starting the procedure, the mean of oxygen
saturation level (SaO2) was found to be 98,1%. The lowest SaO2 levels were found
some minutes after injection or later during the treatment when the average level
was 92,7 % (p<0.0001). For patients who had preoperative SaO2 over 98% the
minimum saturation was at the average level of 94%. The patients with the initial
saturation under 98% showed signs of measurable desaturation - mean level 88%.
However, desaturation did not correlate with the dose of the sedative agent when
this was used at the therapeutic level. Only five cases with low arterial oxygen
saturation were found (SaO2 under 90 %), and all the problems related to sedation
were resolved by administering supplementary oxygen or a benzodiazepine
antagonist. Blood pressure and pulse rate were slightly lower after the treatment
than before it. In systolic blood pressure the difference was significant (p=0.04).
Pulse oximetric monitoring was found to be extremely sensitive as a predictor for
desaturation and it also allows early intervention in ventilation problems.
63
Monitoring the patients with three pulse oximeter equipments
arterial blood oxygenation, as
measured
by
pulse
oximetry
(Matthews et al. 1992). Arterial
oxyhemoglobin saturation (SaO2)
drops
regularly
after
the
administration of a notable amount of
a sedative agent. There is also a
significant decrease in the saturation
level of oxygen as sedation
progresses from light to deep. Age is
positively
correlated
with
desaturation, but a history of disease
or medications have failed to be
sensitive predictors of desaturation
(Bilotta et al. 1990). The protracted
half-lives of some benzodiazepines,
and drug interactions, if opioids are
used
in
combination
with
benzodiazepines, appear to be
potential hazards in the elderly.
Desaturation slightly below 90% may
be clinically insignificant since no
complications have been noted at this
level (5,4). As it is impossible to
identify patients at risk for
hypoxaemia beforehand, it is
recommended that supplemental
oxygen should be given to all patients
and that monitoring should be
performed by pulse oximetry.
2.1.2 INTRODUCTION
Intravenous sedation has been
shown
helpful
in
avoiding
cardiovascular reactions in oral
surgical operations, but there is a risk
of provoking respiratory depression.
This adverse effect can easily be
detected at an early stage, where the
pulse wave and / or a drop in
saturation is signalled visually and
can be corrected by administering
supplementary oxygen. Monitors as
well as intravenous sedation are still
very seldom used in Europe in dental
practice despite their low cost. Fatal
complications in the dental chair are
so uncommon that the use of
monitors is not obligatory, and is not
recommended by the local authorities.
This is in contrast to the situation in
United States, Japan, Canada and
many other parts of the world. There
the monitors are in widespread use
for conscious intravenous sedation; in
fact, they are mandated by laws and
practice standard. Our tradition relies
on the high education level of the
medical and dental practicians and no
exact rules exist. However, episodes
involving some degree of risk or
discomfort do occur, and changes in
the patients’ cardiovascular status
also occur regularly .
It is not so much a question of
"life or death" but of the quality of
care in general. Many of the basic
principles of monitoring accepted in
anaesthesia for general surgery can
also be applied in dental surgery. The
method of early detection of hypoxia
with
pulse
oximetry
during
intravenous sedation has been
previously described by the author.
When the decrease of SaO2 is
observed, external oxygen or
alternatively
an
injection
of
The administration of diazepam
until ptosis is observed is a safe
procedure and although changes in
SaO2 and pulse rate do occur, these
alterations are not significant and
SaO2 remains above 95% (Gallon et
al. 1992). Similarly, intravenous
sedation with midazolam causes a
statistically
significant
but
physiologically insignificant fall in
64
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
benzodiazepine antagonist can be
used.
peroperative monitoring by pulse
oximetry can detect adverse reactions
in
oxygen
saturation
during
intravenous sedation with local
anaesthesia. Also information on
changes in the values of blood
pressure and pulse was needed from
patient monitoring data.
The aim
The aim of this survey was to
determine the usefulness of pulse
oximetry during intravenous sedation
in dental practice i.e. whether
65
Monitoring the patients with three pulse oximeter equipments
2.1.3 PATIENTS AND METHODS
2.1.3.1 Study design
This survey consisted of all (i.e.
41) of the author's private outpatients
who underwent dental operations
between January and September 1993
with intravenous sedation. The
patients were 44 % males and 56 %
females. Mean age was 47 years (SD
14). Twenty-three of the patients had
surgical operations primarily for
implantological reasons, and 18
patients underwent large conservative
dental treatment or extraction under
sedation because of dental care
phobia (Table 1). Some patients had a
second sedated and monitored
treatment period later. These later
treatments are excluded from the
study material.
This study is a retrospective
descriptive review of patient records
which were formed with on-line
registeration program. The method is
still retrospective because the
recordings were not made for study
but for normal careful patient and
treatment follow-up and notes. There
were many differences between
patient preparation, cannulation and
intravenous infusion, sedative drugs
and local anaesthesia i.e. in the
underlying factors. It is important to
understand that this study was not a
controlled clinical trial but a clinical
follow-up of normal treatment
periods. Thus there was no indication
of approval by an institutional review
board
governing
human
experimentation. During treatments
and the clinical follow-up with pulse
oximeter there was no study design
that would answer a particular
question. The later revised databases
formed
the
study
material
(retrospective review of patient
records). These records included
subsequent findings, for instance that
the use of a monitor made it possible
to determine the correct sedation
level earlier and easier than the
normally used ptosis i.e. eye closure
reaction does. Because there was no
reference group, e.g. the appearance
of oxygen desaturation (Sao2 < 90%)
was compared with the literature.
During the first examination, the
patients completed a questionnaire
about previous and present illnesses,
allergies and medications. A dental
care plan was drawn up and all the
patients were referred to radiological
examination
(orthopantomograph)
and all the implantological patients
except patients aged under 50 years
requiring a single tooth replacement
were also referred to laboratory blood
evaluations (B-Se, B-Hb, B-leuk, fBglu). The patients were advised both
verbally and in writing on how to
prepare for intravenous sedation (for
example, no food or drink for four
hours prior to treatment). They were
in good health and had no severe
systemic
diseases
(in
the
classification of American Society of
Anaesthesiology ASA I - II i.e. no
2.1.3.2 Patients
66
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
systemic diseases or only a moderate
disease which do not limit activity).
2.1.3.3 Sedation
Patients were not given oral
premedication,
sedatives
nor
antibiotics on the day of the operation
or the previous day. Blood pressure
was recorded and monitoring with a
pulse oximeter initiated before the
insertion of a peripheral venous
cannula. After the insertion of the
cannula, an infusion of 0.9% sodium
chloride solution was started, and
then the sedative agent was applied
with disposable syringe using the
slow injection technique. The
treatment room was equipped with
dental unit, pulse oximeter, oxygen
supplement
unit
and
some
resuscitation facilities, including
endotracheal intubation equipment
and medication for cardiopulmonary
resuscitation. All treatments were
carried out by the same dentist, i.e.
the author.
Diazepam with soybean oily
solvent was used for sedation for 7
patients (Stesolid Novum 2 ml inj. 5
mg/ml Dumex/KabiVitrum) and
midazolam in 32 cases (Dormicum 5
ml inj. 1 mg/ml Roche). Table 2
presents the doses of the agents used.
Fentanyl (Fentanyl 2 ml inj. 50
microgram/ml Orion R) was used as
an additional pain relief in only 3
cases (mean 79 microgram SD 15.5
microgram), and only if there was an
insufficient level of local anaesthesia.
Intravenous agents were divided into
small parts (2 mg diazepam and 1 mg
midazolam). This almost barely
effective dose is repeated every 2 or 3
minutes until a minor decrease (2 - 3
%) in blood oxygen saturation is
detected. Extra doses after the initial
saturation fall were not normally used
with patients aged over 60 years. The
benzodiazepine antagonist used was
flumazenil (Lanexat 5 ml inj. 0.1
mg/ml Roche).
Table 1. Distribution of patients
according to sex and type of
treatment. Number of patients.
MALE
FEMALE
Local anaesthesia was performed
with lidocaine (Xylocain adrenalin
1.8 ml inj. 20 mg/ml+12.5
microgram/ml ASTRA, mean 7.74 ml
SD 4.23 ml) and prilocaine (Citanest
Octapressin 1.8 ml inj. 30
mg/ml+0.54 microgram/ml ASTRA,
mean 8.01 ml SD 3.91 ml). There was
no particular reason for the use of two
different local anaesthetics; it was
only the author’s normal practice to
avoid high epinephrine amounts.
TOTAL
Conservative
treatment
8
10
18
Surgical
operation
10
13
23
Total
18
23
41
After treatment, blood pressure
was recorded again and the venous
cannula removed. The patients stayed
67
Monitoring the patients with three pulse oximeter equipments
in the dental chair and pulse
oximetric monitoring was continued
until bleeding after extraction had
stopped, and until patients felt well
and were able to walk and get dressed
without help.
Table 2B. The average amounts
and standard deviations of the
medications used in this survey.
Quantities of the agents are expressed
in milligrams.
Table 2A. The average amounts
and standard deviations of the
medications used in this survey.
Quantities of the sedative agents are
expressed in millilitres and those of
the local anaesthetics in 1.8 ml
syringe ampoules.
MEDICATION
Dormicum
MEAN
SD
5.38
1.93
32
4.50
1.66
7
1.58
0.38
3
4.21
2.22
39
4.47
2.06
38
ml
Xylocain
1.8 ml ampoules
Citanest
SD
CASES
Midazolam mg
5.38
1.93
32
Diatzepam mg
22.5
8.3
7
Fentanyl mg
0.079
0.019
3
Lidocaine mg
154
80
39
Prilocaine mg
241
111
38
Patients were monitored with an
Ohmeda pulse oximeter and the data
was collected with Ohmeda's own
program (37XX) using a Toshiba
T1000SE computer. The 37XXprogram do not allow exact notes
from the patients, it is mainly visual.
Thus in many case maximum or
minimum values had to exclude
because of unvaluable data. Ohmeda
Biox 3740 Pulse Oximeter is a standalone, non-invasive, arterial oxygen
saturation
monitor,
providing
continuous, real-time SaO2 and pulse
rate readings.
ml
Fentanyl
MEAN
2.1.3.4 Monitoring and data
review
CASES
ml
Stesolid
MEDICATION
1.8 ml ampoules
The monitor was connected to the
serial port of Toshiba T1000SE
portable computer for the trend
collection of data by a collection
program (The Ohmeda program
37XX). The program recorded
numerical values from pulse oximeter
after the whole treatment and followup period.
68
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
Blood pressure values were
measured with a separate noninvasive
automatic meter (Omron, model-hem
700CP), and the values were saved in
the patient history files.
saturation was associated with the
change in other variables. The
correlation coefficient (r) was
calculated using the analysis of a
variance table, i.e. in the case of
oxygen saturation and systolic blood
pressure, the correlation (Bland and
Altman 1995) was calculated using
the formula:
The collected data was reviewed
and every registration with oxygen
saturation under 90% or pulse rate
over 120 per minute was printed out
for further investigations. The data on
blood pressure, pulse, initial and
minimal SaO2 was collected from
patient history files and parameters
were further analysed using the
Microsoft Works-2 and MedStat
programs
and
the
previously
mentioned Toshiba AT personal
computer.
r=

Sum of squares for systolic BP
Sum of squares for systolic BP + residual
sum of squares
A stepwise multiple regression
analysis was performed to find the
possible
preoperative
indicator
variables on minimal oxygen
saturation during a dental operation.
The variables introduced to the model
were preoperative diastolic and
systolic blood pressure, pulse and
oxygen saturation.
2.1.3.5 Statistical methods
Paired t-test was used to compare
response variables before and after a
dental operation. The changes were
described as means and 95%
confidence intervals. Analysis of
covariance (ref) was used to study
whether the change in oxygen
The data were analysed using
SPSS statistical package (Version
6.1.3).
69
Monitoring the patients with three pulse oximeter equipments
2.1.4 RESULTS
certain period of time between 8589%. In three cases, SaO2 fell below
85% and hypoxia was severe. The
lowest detection in the collected data
was, however, higher: 82%. Pulse
rate over 120 was detected only in
two cases. In some cases, very short
periods of extrasystoles (which were
impossible to diagnose precisely with
pulse oximeter) were detected but no
severe arrhythmias or cyanoses were
found, and the oxygen desaturation
could be corrected in every case with
supplementary oxygen or with
flumazenil,
a
benzodiazepine
antagonist.
2.1.4.1 Oxygen saturation of the
blood
The highest oxygen saturation of
arterial blood (SaO2) detected in the
patients were at the beginning of
measuring. The average of these
levels was 98.1 % (SD 1.4 %). The
lowest SaO2 levels were found some
minutes after the injection of sedative
agents or later during the treatment
period (mean 92.7 % SD 3.3%). The
maximal effects of the midazolam on
oxygen saturation are shown in Fig. 2
as a function of dose. Significant is
the correlation between initial SaO2
and minimum saturation, as shown in
Fig. 1. Patients who had preoperative
SaO2 over 98% had the minimum
saturation at the average level of
94%, and when the initial saturation
was exactly 98% the average
minimum saturation was 93%.
Patients with the initial saturation
under 98% showed signs of
measurable desaturation - mean level
88%. This means that low oxygen
saturation before sedation constitutes
a risk for oxygen desaturation during
sedation. However, it was impossible
to
show
any
sensitivity
to
desaturation because the percent
decreases of SaO2 were identical in
each group. Desaturation did not
correlate with the dose of sedative
agent if used at therapeutical level.
2.1.4.2 Other remarks
Blood pressure and pulse rate
were also measured before and after
treatment, and they are shown in
Table 3. Both values were slightly
lower after treatment but there was no
statistical significance in pulse rate
and diastolic blood pressure but,
however, in the systolic blood
pressure the decrease was significant
(p=0.04). Cardiovascular reactions to
medication are shown in Fig. 2 as
function of the dose of sedative
agents. No significant changes were
seen in blood pressure or in pulse
rate. A multiple regression analysis of
preoperative variables on minimal
oxygen saturation (SaO2) during a
dental operation shows that only low
initial oxygen saturation predicts
desaturation during the treatment
under sedation (table 5).
Desaturation (SaO2 below 90%)
was detected only in five cases. In
two of these the hypoxia was mild,
i.e. oxygen saturation remained for a
70
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
Table 3. Blood pressure, (mmHg), pulse rate and oxygen saturation (%) before
and after a dental operation.
Before
After
Change
Mean
SD
Mean
SD
Mean
p-value
95 % CI
Systolic BP
148.6
24.8
141.6
21.3
-6.9
0.04
(-13.4 to -0.4)
Diastolic BP
91.0
16.8
87.9
13.7
-3.1
0.12
(-11.0 to +1.3)
Pulse rate
77.8
16.1
72.9
12.2
-4.9
0.12
(-11.0 to +1.3)
Oxygen
saturation
98.1
1.4
92.7
3.3
-5.4
<0.0001
(-6.3 to -4.5)
Table 4. Correlation between individual changes in oxygen saturation and
changes in blood pressure and pulse rate.
Changes in oxygen
saturation vs. changes in
Correlation coefficient
p-value
Systolic BP
0.37
0.05
Diastolic BP
0.30
0.13
Pulse rate
0.21
0.31
Table 5. A multiple regression analysis of preoperative variables on minimal
oxygen saturation (SaO2) during a dental operation.
Coefficient
Constant
Preoperative Sa02
-21.7
(SE)
25.2
1.190
0.255
Model R2=0.44
71
p-value
0.40
0.0001
Monitoring the patients with three pulse oximeter equipments
Figure 1. The relation between SaO2 before and after or during (minimum value)
the dental operation. The values were determined from the screen as a clinical
dentist will see it.
Figure 1
Minimum saturation %
100
98
96
94
92
90
88
86
84
82
80
94
95
96
97
98
99
100
Preoperative oxygen saturation %
Figure 2. The relationship of midazolam dose to minimum
oxygen saturation. Only the cases who had recieved only midazolam
are represented.
Figure 2
100
Minimum saturation %
98
96
94
92
90
88
86
84
82
80
1
2
3
4
5
6
7
8
Dose of m idazolam (m g)
72
9
10
11
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
2.1.5 DISCUSSION
previously mentioned, large amounts
of sedatives were used in the present
survey but the desaturation (< 90 %)
incidence was only slightly over 10
%.
2.1.5.1 Desaturation
Arterial oxyhemoglobin saturation
(SaO2)
is
lower
after
the
administration of a notable amount of
sedative agents. There is also a
significant decrease in the saturation
level of oxygen as the patient
progresses from light to deep
sedation. The intravenous diazepam
and midazolam have been shown to
decrease oxygen saturation by 3% as
compared to the preoperative level
when administered in the average
dosages of 6.4 mg and 3.3 mg
respectively. (Matthews et al. 1992)
In this survey, much greater amounts
of sedative agents were used (three
times the previously mentioned
amount of diazepam and 1.5 times
that of midazolam, and consequently
the decrease in saturation was greater
(approx. 5%). However, even
unsedated patients who only have
local anaesthesia have a small
postoperative
fall
in
oxygen
saturation (Matthews et al. 1992), but
the decrease as a result of local
anaesthesia is under 1% (survey 2).
Ventilation hazards of intravenous
midazolam may appear in the elderly,
and the use of benzodiazepines with
lower
hypnogenic
effects
is
recommended (Heinze and Rohrbach
1992). The incidence of saturation
falling to less than 90% have
reported to have been between 4%
and 40% depending of the level of
sedation (Tay et al. 1991, McKee et
al. 1991, Hardeman et al. 1990)
which is an interesting finding. As
Premedication with a combination
of fentanyl and diazepam until eye
closure is induced leads to a more
significant reduction of SaO2. In
most of the patients, minimum SaO2
has been lower than 90%, and it has
been lower than 85% in more than
every third patient (Castillo et al.
1990). No effect of the opiate and
sedative combination on oxygen
saturation was seen in the present
survey, because fentanyl was used so
rarely (in only three patients) and in
normal amounts (79 microgram).
However, extreme care is essential if
this combination is used. It is
possible that the relatively low
incidence of desaturation in this
survey is a result of early
recognition of initial 2-3% SaO2
decrease with pulse oximetry during
the initiation of the sedation.
Patients at risk for hypoxaemia
cannot be identified definitely prior to
the initiation of the procedure (Visco
et al. 1989). However, if dental
patients are monitored with pulse
oximetry, and an ultra-slow technique
is used with careful dosage in the
administration of sedative agents, no
continuous oxygen supplement is
necessary routinely (Read-Ward
1990), although it should be
available. No routine oxygen
supplement was used with the
73
Monitoring the patients with three pulse oximeter equipments
patients in this survey. The minor
decrease in SaO2 was used as a sign
of sufficient sedation during the
initiation of medication and oxygen
was added only if the 90% level
lasted a long time. However, Lowe
and Brook (1991) have reported
oxygen saturation in the range of 9389% in some patients undergoing
third molar removal with local
anaesthetic alone! They concluded
that all patients undergoing removal
of third molars are at risk of hypoxia.
Short episodes of hypoxia may be of
little consequence in healthy patients,
but with compromised patients early
detection
may
avoid
serious
complications
(Rodrigo
and
Rosenquist 1988). Moreover, there is
some information available that a
cardiac patient might develop a
decrease in oxygen delivery that may
be due to increased pulmonary
vascular resistances (Nishida et
al.1996, Slater et al. 1995, Francoise
et al. 1996). However, no negative
correlation between diastolic blood
pressure and minimal oxygen
saturation could be shown in this
survey. This finding is important to
remember in patient selection:
sedation is often used to reduce the
stress of cardiac patients.
the medication used, and they can
lead to a deterioration of the
patient's own organic disease. It is
extremely important to recognise
this in good time, so that the right
decisions can be made on
appropriate therapeutic actions.
The patients in this survey
accepted this non-invasive monitoring
method quite easily. For the dentist,
the machine was easy to use. The size
of the monitor is small, and sufficient
in dental chair surroundings. Without
these features the device is useless in
the dental office. Moreover, the
monitor should react dynamically to
changes and give a clear warning if
any problems arise. It should monitor
the arterial oxygen saturation and the
continuous pulse wave should be
visible on the screen. The review of
the follow-up immediately after
treatment is recommendable, and an
internal trend memory makes it
possible to review and document the
patient's
reactions
during the
treatment period.
Monitoring is more regularly used
in hospitals than in private offices.
During endoscopic procedures, which
are comparable to short acting
unpleasant dental procedures, most
endoscopists monitor vital signs
before and after the procedure.
Moreover, pulse oximetric and
electrocardiographic monitoring are
in common use. There is a significant
relationship between the knowledge
of oxygen saturation and the timing
of nursing interventions like oxygen
or
antagonist
therapy.
Since
knowledge of advanced cardiac lifesupport is not common among
2.1.5.2 Monitoring
Sugiyama et al (1991) have
reported that a pulse oximeter is
useful as a respiratory monitor during
oral surgery. Patient monitoring is
used to detect dangerous deviations
from normal in circulation and
respiration. Such deviations may be
due to therapeutic procedures or to
74
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
endoscopists and gastrointestinal
assistants (Keeffe et al. 1989), the use
of pulse oximetry in these
circumstances is essential (Hinzmann
et al. 1992). The experience of the
author as well as that expressed in the
literature suggests that electronic
monitoring is very uncommon in
dental practice. However, clinical
experience shows that not only a
good resuscitation education but also
the use of pulse oximetry could
increase patient safety in dental
offices. Pulse oximeter, oxygen
supplement unit and resuscitation
facilities were available for the
patients in this survey. The author has
been educated in the use of
endotracheal intubation and the use of
medication for cardiopulmonary
resuscitation. Probably as a result of
the use of pulse oximetric monitoring,
there has never been any use for these
skills, although the described
intravenous method was used long
before and after this survey.
another; i.e. sedation correlates with
respiratory depression. Oxygen was
added when the 90% level lasted a
long time. The pulse oximeter is
valuable because it will react
immediately to any progressive
oxygen desaturation, making early
correction possible. Hence the use of
pulse oximetry should be obligatory
for all endoscopic or paediatric
patients during intravenous sedation
(Casteel et al. 1990) and it is also
useful as a respiratory monitor during
oral surgery (Sugiyama et al. 1991).
A pulse oximeter primarily
monitors arterial oxygen saturation.
This, of course, is an essential safety
factor. It also provides a continuous
display of pulse rate and, in some
advanced pulse oximeters like
Ohmeda, also a visible pulse wave on
the screen. An internal trend-memory
greatly increases the benefit of
monitoring. The monitoring period
can be reconstructed, printed,
analysed and reported. This feature is
very
valuable
in
case
of
complications. A pulse oximeter with
these internal features has the first
priority among the vital function
monitors. These findings are a
justification for recommending its use
in dentistry and in oral surgery for all
patients who are sedated regardless of
venous or oral route.
Since the largest mean decrease in
oxygen saturation observed during
procedures
under
intravenous
sedation is less than that considered
normal
during
sleep,
some
researchers are of the opinion that
oximetry monitoring is not needed.
Likewise the high incidence of
desaturation does not cause adverse
outcomes or complications. (Berg et
al. 1991, Bilotta et al. 1990)
However, in this survey a small
decrease of SaO2 was found to be a
sign of sufficient sedation during the
initiation of medication. This is very
understandable because it is more
than probable that one central
nervous effect correlates with
In
conclusion,
low
initial
saturation may be a warning signal of
hypoxia and the use of a monitor may
help to determine the correct sedation
level earlier and easier than the
normally used ptosis i.e. eye closure
reaction. This survey was not a
clinical trial: there were differences
75
Monitoring the patients with three pulse oximeter equipments
in the underlying factors and no
reference group exists. Therefore it is
not justified to conclude that low
initial oxygen saturation might be a
contraindication for sedation or that
the sedationist should use the pulse
oximeter to estimate the sufficient
level of sedation before local
anaesthesia. This is mainly a question
of clinical experience indicating the
need for randomised clinical trial.
76
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
2.1.6 Clinical conclusions
Peroperative pulse oximetric monitoring detects adverse
reactions such as hypoxia and high pulse level during
intravenous sedation.
Low initial oxygen saturation may be a warning signal
of hypoxia during sedation.
The use of a monitor may help to determine the correct
sedation level - when the venous route is used - earlier
and easier than the normally used ptosis i.e. eye closure
reaction.
77
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
2.2
Survey 2
Detection of cardiovascular
responses to local anaesthesia with
Datex Cardiocap
multiparameter monitor
2.2.1 ABSTRACT
In this survey the cardiovascular effects of two local anaesthetic agents
(lidocaine and prilocaine) and two vasoconstrictors (epinephrine and phelypressine)
were observed. There were no radical changes in systolic or diastolic blood
pressure. The heart rate slightly decreased after the injection of prilocainephelypressine, but increased after the epinephrine-containing lidocaine injection.
Both prilocaine- phelypressine and lidocaine- epinephrine injections resulted in
statistically significant (p=0.001) changes in heart rate. Amplitude of pulse wave
was the most responsive measurable parameter. Amplitude of pulse wave
diminished just before and during the injection as a result of psychological stress.
The blood flow showed the smallest values during the injection of local anaesthetic.
Mean blood oxygen saturation values were within normal limits and the displayed
SaO2 values were between 96 - 98 percent during the measuring period in 96
percent of detected values. No cardiovascular problems were found when these
preparations were used in combination. Consequently, if the effect of one local
anaesthesia preparation is not sufficient it is possible to increase the effect by
adding the other preparation without a danger of adverse reactions.
safety of epinephrine with dental
local anaesthesia is well known.
Epinephrine-containing lidocaine has
little effect on haemodynamics, while
norepinephrine-containing lidocaine
causes more changes in the
2.2.2 INTRODUCTION
It is important to identify the ideal
balance of pain and anxiety relief
when anxious patients are treated
under intravenous sedation. The
79
Monitoring the patients with three pulse oximeter equipments
cardiovascular system (Hirota et al.
1992). Most studies have not noted
any severe changes in heart rate or
blood pressure when a local
anaesthetic is used with epinephrine
(Davenport
et
al.
1990).
Montebugnoli et al. (Montebugnoli et
al. 1990) found that there were no
significant
differences
in
cardiovascular response when a group
of patients under non-specific stress
were given an anaesthetic with or
without
epinephrine.
The
cardiovascular response during dental
stress may not be associated with the
use of epinephrine in an anaesthetic
solution. Individual reactions seem to
dominate
in
certain
cases
(Montebugnoli et al. 1990, Meyer
1990).
injection, but during the real
operative
procedure
the
cardiovascular parameters do not
correlate with the level of epinephrine
derived from the solution of local
anaesthetic (Knoll-Kohler et al.
1989). Although there are some
changes in cardiovascular parameters,
the mean oxygen saturation does not
change when local anaesthetics are
used (Daublander et al. 1992).
Toxic reactions may appear in
cases of intravascular injection of
local anaesthetics with epinephrine or
norepinephrine (Tsirlis and Iakovidis
1989). Bachmann et al. (Bachmann et
al. 1988) showed that there is a risk
of systemic side effects in
experimental infiltration anaesthesia
if an amount near but slightly below
maximum is used. In this survey, the
amount of each agent was 1/3 of the
known maximum which is enough to
cause cardiovascular changes but far
less than enough to induce toxic
reactions.
Exact
reactions
in
the
cardiovascular system caused by local
anaesthetics and vasoconstrictors are
only partially and controversially
documented. Salonen et al. (Salonen
et al. 1988) reported that a lidocaineepinephrine solution elevates heart
rate but does not affect systolic or
diastolic blood pressure. The increase
in heart rate is reported to be rare and
never by more than 10 beats per
minute (Frabetti et al. 1992).
However,
every
clinically
experienced dentist knows that
sometimes patients will develop
unpleasant
tachycardia
if
an
anaesthetic containing epinephrine is
used. Moreover, other reports show a
sharp decrease in the diastolic blood
pressure (Montebugnoli et al. 1990,
Meyer 1990). Lidocaine with
epinephrine has been shown to cause
a doubling of the plasma epinephrine
concentration two minutes after
The aims
This experiment was performed
with local anaesthetics to differentiate
the measurable cardiovascular effects
of two commercial local anaesthetics
commonly used world-wide, to be
able to differentiate the same
reactions if sedatives are used with
local anaesthetics.
Another aim was to find any
undesirable cardiac parameters when
two commonly used local anaesthetic
agents are used in combination.
80
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
Thirdly there was a need to see if
the Datex pulse oximeter allows the
measuring of changes in amplitude of
pulse wave as a result of local
anaesthesia.
The final aim of this survey was to
discover whether local anaesthetic
agents and vasoconstrictors have any
effects on blood oxygen saturation
values when observed with pulse
oximetry.
81
Monitoring the patients with three pulse oximeter equipments
2.2.3 PATIENTS AND METHODS
measurable findings. Every subject
had to come twice to the test on
separate days. There were two dropouts who left the study after the first
day, thus a total of 38 registration
periods were obtained for analysis.
During every registration period local
anaesthetics was injected into both
sides of the upper jaw, hence
obtaining 76 injection periods. In one
case the test had to be discontinued
during the second injection as a result
of a sinus tachycardia reaction.
2.2.3.1 Study design
This paper is a retrospective
descriptive review of follow-up
records. It is important to understand
that this survey was not a controlled
clinical trial but a clinical follow-up
of a normal course exercise and a
demonstration.
Later
revised
databases formed the study material.
Thus there was no indication of
approval by an institutional review
board
governing
human
experimentation.
2.2.3.3 Local anaesthesia
2.2.3.2 Subjects
Local anaesthesia was performed
with a lidocaine - epinephrine
solution (Xylocain adrenalin 1.8 ml
inj. 20 mg/ml+12.5 mcg/ml ASTRA)
and prilocaine - phelypressine
solution (Citanest Octapressin 1.8 ml
inj. 30 mg/ml+0.54 mcg/ml ASTRA).
The site of injection was the upper
jaw, the buccal sulcus just distal of
the second upper molar. Both sides of
the maxilla were anaesthetised. This
site was chosen because there is room
for a large enough volume of local
anaesthetic, and the trifurcation of the
trigeminal nerve is near the
anaesthetised area.
The study group consisted of
twenty dental students. The students
were between 19 and 31 years of age
with a mean age of 22 years (SD 3);
80 % were females. Each person
accepted in the test group had to be
healthy and free of any surgical risk,
corresponding to the ASA (American
Society of Anaesthesiologist) I or II
groups. Oral contraceptives were the
commonest medication (three of
females). One subject was undergoing
a thyroxin substitution therapy for
hypothyreosis. No other illness or
permanent medication was reported.
Patients were in a horizontal
position during the infiltration of
local anaesthetic.
The survey was done during a
normal local anaesthesia course for
students.
This
provided
an
opportunity to allow the students to
practice
local
anaesthesia,
to
demonstrate cardiovascular effects
thereto and to collect objective
82
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
time taken for the injection of the 4
cartridges was 2 min 11 seconds (SD
24.6 seconds) (Table 1).
2.2.3.4 Timing of the procedure
During the first appointment
(method 1), the subjects received 4
cartridges (4 x 1.8 ml) of CitanestOctapressin, corresponding to 216 mg
of prilocaine and 3.89 mcg of
phelypressine, injected submucosally
5 minutes after beginning the pulse
oximetric measurement. The area of
injection was the upper right buccal
sulcus. Ten minutes later they
received a similar injection to the left
side of the maxilla, but the local
anaesthetic this time was Xylocain
adrenalin. The dose was also 4 x 1.8
ml. The amount of anaesthetic
corresponded to 144 mg of lidocaine
and 90 mcg of epinephrine. The mean
During the second appointment
(method 2) after two days wash-out,
the subjects received two cartridges
of Citanest-Octapressin to the right
side and two cartridges of the same
agent to the left side 5 minutes after
beginning the pulse oximetric
measurement. Ten minutes later, they
received two cartridges of Xylocain
adrenalin to both sides of the maxilla,
so every subject had two measuring
sessions. The injection sites were the
same in both sessions (Table 2).
83
Monitoring the patients with three pulse oximeter equipments
Table 1. Timing of the procedure with each patient in method 1:
Preparations injected into separate areas
Time(min)
0 min
start of measurement
5 min
onset of injection into right upper jaw, 4 cartridges of
Citanest- Octapressin
15 min
initiating injection into left upper jaw, 4 cartridges of
Xylocain adrenalin
25 min
end of measurement
Two days wash-out before method 2
Table 2. Timing of the procedure with each patient in method 2:
Both preparations injected into same areas.
Time (min)
0 min
start of measurement
5 min
onset of the first injection: 2 cartridges of Citanest-Octapressin into
both sides of maxilla (total 4 cartridges)
15 min
initiating the second injection: 2 cartridges of Xylocain adrenalin
into both sides of maxilla (total 4 cartridges)
25 min
end of measurement
84
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
flow in the finger is the result of left
ventricle contraction of the heart,
which fills the vascular bed of the
finger with arterial blood. It is
important to understand that the pulse
wave reflects changes in blood
volume, not changes in blood
pressure.
2.2.3.5 Monitoring
Subjects were monitored using a
CARDIOCAP II CH-S (Datex,
Helsinki Finland) multiparameter
physiological monitor. This pulse
oximeter is a stand-alone, noninvasive, arterial oxygen saturation
monitor which can monitor ECG and
blood pressure. It gives continuous,
real-time SaO2 and pulse rate
readings. Follow-up information is
available through both the analog and
digital output ports.
The monitor was connected
directly to the serial port of a Toshiba
T1000SE portable computer for realtime collection of data by a collection
program ("KERÄÄ" by Dr Matti
A.K. Mattila). The program recorded
numerical values from Cardiocap at
10 seconds intervals.
The pulse oximetric equipment
works using light which is generated
in the finger probe and passes through
the tissues. The total absorption of
the light depends on the absorbing
components: tissues, venous blood
and the pulsating arterial blood.
Different amounts of light are
absorbed by oxygenated haemoglobin
(HbO2) and unoxygenated or reduced
haemoglobin (Hb). The oximeter
measures the relative absorption by
Hb and HbO2 of red light at 660 nm
and infrared light at 910 nm. These
two different forms of haemoglobin
allow different amounts of light to
pass through at these wave lengths.
The oximeter converts this relative
light intensity information into
arterial oxygen saturation values.
Blood pressure was measured
automatically every two minutes from
the subjects' left upper arm. A finger
probe was used for pulse oximetric
registration, i.e. blood oxygen
saturation (SaO2). The probe was
placed on the subject's right middle
finger. The data from the Cardiocap
were further analysed using at first
the Microsoft Works-2 and MedStat
programs
and
the
previously
mentioned Toshiba AT personal
computer.
2.2.3.6 Statistical methods
The total of 6840 numerical values
of pulse, amplitude of pulse wave,
systolic and diastolic blood pressure
and oxygen saturation of blood were
first reduced to averages for each
minute and for the five-minute pretreatment period (0-4 min), and for
two ten-minute periods after the first
and the second injections (5-14 min;
15-24 min). The pre-treatment five-
The pulsation of the arterial blood
flow modulates the light passing
through it, and the oximeter converts
this light intensity information into
pulse rate values, which are presented
together with SaO2 values on a
monitor screen. The pulse wave is
derived from the intensity of the
transmitted light. The pulsating blood
85
Monitoring the patients with three pulse oximeter equipments
minute average was used as a
baseline value.
Pre-treatment baseline-values were
compared between method 1 and 2
using paired t-test. To test whether
the site of the injection had any effect
(method 1 vs. method 2), the twentyminute averages (5-24 min) were
calculated and tested using paired ttest. The data were analysed using
STATISTICA
(StatSoft,
Tulsa,
USA).
Analysis of variance (ANOVA)
for repeated measurements was
applied using the successive periods
0-4 min, 5-14 min and 15-24 min. In
cases where the ANOVA gave a
significant (p<0.05) result, paired
contrasts were made in order to
identify which injections accounted
for the significant overall p-value.
86
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
2.2.4 RESULTS
minute (p=0.0004, 2 to 5) in method 1
and method 2 respectively. Then,
after the second injection the heart
rate increased 6 beats per minute
(p<0.0001, 4 to 8) and 10 beats per
minute (p<0.0001, 6 to 13) during
method 1 and 2 respectively (Table
3).
2.2.4.1 Pulse
At the beginning of the
measurement, the heart rate was quite
stable. After the first injection
(prilocaine and phelypressine), the
heart rate slightly decreased in both
methods. The injection with lidocaine
- epinephrine (Xylocain adrenalin)
increased the heart rate, because of
the epinephrine. In method 2, when
both preparations were injected into
the same areas, the results were very
similar to those in method 1, where
injection areas were separated. After
the second injection (lidocaine epinephrine), the heart rate increased
faster with method 2 than with
method 1, but heart rate levels were
very similar. Towards the end of the
measurement, the heart rate increased
about 10/min from base level in both
methods. However, a prilocainephelypressine combination (CitanestOctapressin)
affects
the
cardiovascular system less than a
lidocaine-epinephrine
combination
(Xylocain adrenalin). The results of
heart rate measurements are presented
in Fig. 1. The two days with methods
1 and 2 were comparable with respect
to the baseline values (0-4 min).
During the 24-minute periods, heart
rates
changed
significantly
(p<0.0001, ANOVA of repeated
measurements). Compared to the
baseline, the heart rate decreased
after the first injection approximately
4 beats per one minute (p<0.0001,
95% confidence interval 3 to 6 beats
per one minute) and 4 beats per
2.2.4.2 Amplitude of pulse wave
Amplitude of pulse wave was the
most
impressionable
of
the
measurable parameters during the
survey. (Fig. 2) Amplitude of pulse
wave observations are subject not
only to biologic and measurement
variation but also to temporal
variation in clinical circumstances.
Standardising the circumstances to
reduce the environmental variation
(e.g. room temperature) was not
possible during a local anaesthesia
course, and therefore the findings
should be regarded as tentative.
Blood flow showed the smallest
values during and immediately after
the injection of local anaesthetic in
both methods. In baseline blood flow
levels there was a considerable
difference (p=0.02) between days.
The difference in baseline-levels,
decrease of 8 units, can be interpreted
as the consequence of reduced stress.
During the first session, employing
method 1, no significant changes in
blood flow could be observed. During
the second session, employing
method 2, the blood flow level differs
87
Monitoring the patients with three pulse oximeter equipments
significantly across time (p=0.0001,
ANOVA of repeated measurements).
After the first injection the blood
flow decreased 9 units (p=0.005, 95%
confidence interval 3 to 15) compared
to the baseline. After the second
injection, the level of blood flow
further decreased by 6 units (p=0.01,
2 to 10). The total effect of the two
injections was approximately 15 units
(p=0.002, 6 to 23) compared to the
baseline (Table 3).
2.2.4.4 Oxygen saturation of
blood (SaO2)
Oxygen
saturation
slightly
decreased towards the end of the
measurement
period,
but
so
marginally that the differences caused
by injections or methods were less
than one percent. (Fig. 5) During the
first session, however, the level of
oxygen
saturation
decreased
statistically significantly (p=0.04,
ANOVA of repeated measurements).
This significant result was caused by
the difference between baseline level
and the level after the second
injection (p=0.05). This finding,
although statistically significant, has
no clinical significance. The mean
saturation values after the first
injection varied between 94 % and
98.8% and 95.7 % and 98.5 %, during
methods 1 and 2 respectively (Table
3).
2.2.4.3 Blood pressure
There were no clinically or
statistically significant changes in
systolic (Fig. 3) or diastolic (Fig. 4)
blood pressure in either of the study
methods (Table 3). It seems that the
local anaesthetics used in this survey
only have a very small effect on
blood pressure when used lege artis in
dentistry, although the doses used
were considerable.
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
Figures 1 – 5. Cardiovascular responses after local anaesthesia are presented
below.
Fig 1. Pulse
90
PULSE (1 min)
85
80
75
70
prilocainphelypressin
65
lidocain
epinephrine
Method 1
Method 2
60
0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24
MINUTES
Fig 2. Amplitude of pulse wave
AMPLITUDE OF PULSE WAVE
45
40
35
30
25
20
15
10
5
lidocain
epinephrine
prilocainphelypressin
Method 1
Method 2
0
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24
MINUTES
89
Monitoring the patients with three pulse oximeter equipments
SYSTOLIC BLOOD PRESSURE (mmHg)
Fig 3. Systolic blood pressure
130
125
120
115
110
105
100
95
90
85
80
75
70
65
lidocain
epinephrine
prilocainphelypressin
1
2
4
6
8
10
12
14
16
Method 1
Method 2
18
20
22
24
MINUTES
DIASTOLIC BLOOD PRESSURE (mmHg)
Fig 4. Diastolic blood pressure
130
125
120
115
110
105
100
95
90
85
80
75
70
65
prilocainphelypressin
1
2
4
6
Method 1
Method 2
lidocain
epinephrine
8
10
12
14
MINUTES
90
16
18
20
22
24
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
BLOOD OXYGEN SATURATION (SaO2)
Fig.5. Blood oxygen saturation
98
97
prilocainphelypressin
lidocain
epinephrine
Method 1
Method 2
96
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24
MINUTES
91
Monitoring the patients with three pulse oximeter equipments
Table 3. Cardiovascular responses during the follow-up of 24 minutes.
Prilocaine-phelypressine was injected five minutes after starting the follow-up, and
lidocaine-epinephrine ten minutes later.
Method 1 = subjects received prilocaine-phelypressine injections in the right
upper jaw and lidocaine-epinephrine injections in the left side.
Method 2 = two days later the same subjects received prilocaine-phelypressine
injections in both sides of the upper jaw and lidocaine-epinephrine injections in the
same areas.
Method
Before
anaesthesia
(0-4 min.)
After
prilocaine
(5-14 min.)
After lidocaine
(15-24 min.)
Effects of
agents
Difference of
methods
Mean SD
Mean SD
Mean SD
p-value*
p-value**
Pulse
1
79.2 15.2
74.8 14.3
80.9 14.1
<0.0001 ab
2
77.5 12.5
74.0 11.5
83.6 9.8
<0.0001 abc
0.74
SaO2
1
97.3 0.8
97.2 0.7
97.1 0.7
0.04 c
2
97.2 0.5
97.2 0.5
97.2 0.5
0.94
0.84
A.P.W.
1
27.8 28.7
26.0 22.3
23.3 18.5
0.25
2
36.3 29.7
27.3 22.1
21.5 17.5
0.0001 abc
0.73
Syst. BP
1
125.0 10.3
125.0 12.2
124.4 11.8
0.71
2
122.8 8.7
122.6 8.8
123.5 8.7
0.66
0.73
Diast. BP
1
86.8 8.3
86.6 8.0
86.3 7.3
0.60
2
85.3 6.6
85.7 7.0
85.6 6.6
0.08
*) ANOVA of repeated measurements. Significant (p<0.05) contrasts are between:
a) 0-4 min vs. 5-14 min.
b) 5-14 min vs. 15-24 min.
c) 0-4 min vs. 15-24 min.
**) Paired t-test to compare method 1 vs. method 2 (5-24 min)
92
0.79
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
2.3.5 DISCUSSION
patients undergoing surgical removal
of a third molar with local
anaesthesia experienced hypoxic
periods during surgery. Breath
holding was suggested to be
responsible for the observed falls in
SaO2. Their conclusion was that
other types of dental care which cause
breath holding or restrict the upper
airway may also cause changes in
SaO2 levels.
2.3.5.1 Amplitude of pulse wave
and the measuring equipment
The regulation of peripheral
arterial circulation is in the control of
the autonomic nervous system.
Vasoconstriction is induced by the
stimulation of the smooth muscles of
arterioles. This decreases the
amplitude of the pulse wave and may
be due to some discomfort such as
pain, fear, low temperature or
hypovolaemia. Rapid and strong
vasodilatation is often seen after the
injection of a sedative agent, as a
result of feeling good. The amplitude
of the pulse wave is the most
informative indicator of changes in
circulation, and CARDIOCAP II CHS allows us to observe this parameter.
Hypoxia may also be related to
underlying medical problems (White
et al. 1989). A considerable portion
of these desaturations might be due to
patient movement or movement of the
photodetector probe. Wilson (Wilson
1990) found that 87 % of the
desaturations in child patients under
sedation resulted from patient
movement.
2.3.5.2 Oxygen saturation of
blood during dental treatment
There is some evidence that even
unsedated patients develop small
postoperative falls in oxygen
saturation (Matthews et al. 1992).
The study by White et al. (White et
al. 1989) showed that nearly half of
the patients developed clinically
significant desaturation during minor
oral surgery under local anaesthesia.
White et al. assumed that this might
be due to breath holding or peripheral
vasoconstriction as a response to
anxiety or fear.
Moreover, the influence of local
anaesthetics on oxygen saturation is
not clear. In this survey, the
saturation values were not more
than 0.5 % lower at the end of the
measurement than the base level.
The displayed readings also stayed
stable between the values of 96 and
98% during the test period. We may
conclude that local anaesthesia is not
a possible source of measuring
failures, and that the agents used in
local anaesthesia do not affect the
level of the patients' oxygen
saturation.
Lowe and Brook (Lowe and Brook
1991) noticed that one fifth of the
2.3.5.3 Toxic reactions
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Monitoring the patients with three pulse oximeter equipments
(Gortzak et al. 1992a) studied
subjects during routine restorative
dental treatment and found that
patients showed considerable blood
pressure variation. Those treated
without local anaesthesia showed a
significant mean blood pressure
increase, while patients treated under
local anaesthesia with articaine
showed no significant changes in
blood pressure during treatment.
Cioffi et al. (Cioffi et al. 1985)
concluded that routine restorative
dental care with lidocaine and
epinephrine local anaesthesia did not
produce
clinically
important
haemodynamic responses despite an
increase in epinephrine levels.
Too large plasma concentrations
of a local anaesthetic may result in
toxic reactions. Systemic toxicity may
occur either in the presence of
excessive volumes of anaesthetic or
during inadvertent
intravascular
injections (Fiset et al. 1985). In this
survey, the amount of each agent was
one-third that of the known
maximum, which is enough to cause
cardiovascular changes but far too
little to induce toxic reactions. Also,
slow biotransformation or elimination
may be the cause of toxic reactions in
some patients. Those with decreased
renal function or with advanced liver
disease are at risk of the accumulation
of anaesthetic or its by-products
(Laskin 1984). The unpleasant
subjective experiences (CNS effects)
reported by the subjects in this survey
after the administration of local
anaesthetics were not seen as
measurable registrations in pulse
oximetry or in blood pressure values.
This is at variance with the view that
blood pressure and heart rate should
be seen as unreliable indices of the
onset of systemic local anaesthetic
toxicity (Pateromichelakis 1992).
Moreover, it is possible to reduce the
amount of one local anaesthetic agent
using a combination of two agents,
which will even enhance the effect
(Luotio et. al 1997).
Frabetti et al. (Frabetti et al. 1992)
found that patients undergoing
surgical treatment had higher heart
rate values than patients undergoing
conventional
therapy.
Patients
undergoing muco-gingival surgery
had the mean heart rate values of one
hundred per minute, while the group
undergoing scaling had the mean
heart rate values of 78 beats per
minute. In this survey, the mean
pulse rate of the patient rose from 70
to 86 beats per minute after the
injection of local anaesthetics
containing
epinephrine.
Meyer
(Meyer 1987) also found that the
increases in heart rate and alterations
of blood pressure were different in a
group undergoing extraction from a
group to whom local anaesthesia only
had been administered, and these
differences are possibly rather an
expression of an endogenous
catecholamine release as a result of
stress than a pharmacological effect.
He also concluded that endogenous
2.3.5.4 Pulse and blood pressure
after local anaesthesia
Considerable controversy exists in
the
literature
regarding
the
haemodynamic changes caused by
local anaesthetics. Gortzak et al.
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
alternations always take place in the
same way. It has also been found that
there is a temporary blood pressure
increase during the injection of local
anaesthetic (21,19) and at the time of
extraction of a tooth (Meyer 1987).
Also, the heart rate had two peak
values during the extraction of the
tooth: the first during the injection of
the local anaesthetic, and the second
during the extraction phase (Meyer
1987). There may also be some
increase in systolic blood pressure
(Gortzak et al. 1992a). However, no
clinically significant change could be
detected in either systolic or diastolic
blood pressure.
during a normal local anaesthesia
course for students. There were
differences in the underlying factors
i.e. the survey was non-randomised:
the order of the injections of
lidocaine and prilocaine were the
same in both methods; external
conditions were not constant because
there was even a difference in the
base level of the stress between the
methods which were performed in
separate days without randomization.
Moerover, the order of methods 1 and
2 was not randomized. This causes
the problem that a comparison of
methods 1 and 2 is not valid.
Therefore it is not justified to
conclude that one method of local
anaesthesia is better than another.
However, this survey showed that the
common clinical practice to combine
different local anaesthetic agents do
not obviously harm a healthy patient.
It may be concluded that no
reasons to avoid the combination of
lidocaine and prilocaine were found.
However, the study design was very
complex because this was not a
clinical trial but a monitory period
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
2.3.6 Clinical conclusions
Changes in pulse rate were possible to detect with pulse
oximetry: Heart rate slightly decreased after the injection
of prilocaine with phelypressine, but pulse rate increased
after the epinephrine-containing lidocaine injection.
There is no reason to avoid the combination of
lidocaine and prilocaine, if needed, because no increase in
a non-desired effect can bee seen. Consequently, if the
effect of one local anaesthesia preparation is not sufficient
it is possible to add the other preparation.
Amplitude of pulse wave was the most reactive
parameter during injection.
Local anaesthesia does not affect blood oxygen
saturation to a degree that should be taken into account
clinically.
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
2.3
Survey 3
Detection of maximal pulse and
amplitude of pulse wave
under intravenous sedation with a
Datex Sattlite Trans pulse oximeter
2.3.1 ABSTRACT
In this survey 26 registrations of 26 patients were monitored with pulse oximeter
during major or long-standing dental operation under intravenous sedation with
local anaesthesia. This survey was not a controlled clinical trial but normal
treatment periods and a clinical follow-up with pulse oximeter. Later revised
databases formed the survey material (retrospective review of patient records). The
cardiovascular effects of benzodiazepine (midazolam) and the local anaesthetic
agent (lidocaine) and vasoconstrictor (epinephrine) were observed. Pulse rate
increased both during and after the injection of midazolam as well as epinephrine
containing lidocaine injection. The increase was very slight after midazolam but
after local anaesthesia it was notable. As a result of stress relief, pulse rate was
lower after the treatment than before it (p<0.05). The highest level of pulse level
was recorded during local anaesthesia (p<0.005). There was no significant
difference in pulse rate before treatment, during sedation and during treatment.
During the retrospective review of patient records, amplitude of pulse wave
(A.P.W.) was the most responsive measurable single parameter indicating stress. In
general A.P.W. decreased towards the injection due to psychological stress. Blood
flow showed decreasing values during and after injections of local anaesthetic.
Moreover, poor A.P.W. caused measuring artefacts into the levels of blood oxygen
saturation, which can be avoided by covering the patients with a blanket. The nature
of this descriptive parameter is discussed.
99
Monitoring the patients with three pulse oximeter equipments
2.3.2 INTRODUCTION
2.3.2.2 Local anaesthesia
2.3.2.1 Monitored sedation
Epinephrine containing lidocaine
has little effect on haemodynamics
(Hirota et al. 1992). Most study
groups have not noted significant
changes in heart rate or blood
pressure if local anaesthetic is used
with epinephrine (Davenport et al.
1990).The increase in heart rate is
reported to be rare and never by more
than 10 beats per minute (Frabetti et
al. 1992). Cardiovascular parameters
have been documented to increase as
early as after the one minute waiting
period after injection; after two and
three minute waiting periods the
increases were far less pronounced
(Daublander et al. 1992). Lidocaine
with epinephrine has shown to cause
a doubling of the plasma epinephrine
concentration two minutes after
injection, but during the treatment
procedures which cause emotional
stress, the cardiovascular parameters
do not correlate with the level of
epinephrine derived from the solution
of local anaesthetic (Knoll-Kohler et
al. 1989). However, every clinically
experienced dentist knows that
patients
sometimes
develop
unpleasant tachycardia reactions if
epinephrine containing anaesthetic is
used.
In dental practice monitors are still
extremely seldom used despite the
fact that simple and low-cost
technical solutions, such as pulse
oximeters, already exist. The pulse
oximeter primarily monitors arterial
oxygen saturation, which is of course
an essential safety factor. Secondarily
a continuous display of pulse rate is
obtained and in some advanced pulse
oximeters also a visible pulse wave
on the screen. The information of the
pulse wave can be widely utilised in
the monitoring of circulation and
patient's reactions to pain and
discomfort. The correct monitor
should, however, be selected on the
basis of the essential needs in each
particular
situation
and
circumstances. The methodology of
the early detection of hypoxia with
pulse oximeter during intravenous
sedation
has
been previously
described by the author.
Intravenous
sedation
with
midazolam causes a statistically
significant
but
physiologically
insignificant fall in arterial blood
oxygenation, as measured by pulse
oximetry (Matthews et al 1992).
Desaturation slightly below 90% may
be clinically insignificant since no
complications have been noted (Berg
et al. 1991 and Bilotta et al. 1990) but
because patients at risk for
hypoxaemia cannot be predetermined
it is recommended that the patients be
monitored with a pulse oximeter
(McKee et al. 1991).
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
because they are very similar in
shape. Their information is, however,
totally different. A visible pulse wave
means practically that blood is
circulating at the site of measurement.
During
normal
sinus
rhythm
consecutive pulse waves are uniform,
but during arrhythmia they can
continuously vary in size and shape.
In fact, these observations can be
applied also to evaluate the
importance
of
that
particular
arrhythmia for circulation (Mattila et
al 1989, Mattila 1990).
2.3.2.3 Amplitude of pulse wave
(A.P.W.)
Observing the A.P.W. enables the
dentist to notice constriction in the
peripheral arteries as a result of
psychological stress: The blood flow
of the finger shows diminishing
values before the injection of local
anaesthetic i.e. before any possible
cardiovascular effect. A pulse
oximeter probe is usually placed on a
finger; other alternatives are toes or
earlobes. These alternative locations
are equally suitable as a finger when
measuring oxygen saturation and
pulse rate, but they do not indicate
the reactions in the pulse wave
amplitude. In general, peripheral
arteries in fingers react to painful
stimuli much stronger than arteries in
other places (Mattila et al 1990).
2.3.2.4 Aim of the study
The background for this survey
has been a necessity to find the ideal
relation of pain and anxiety relief
when anxious patients are treated
under intravenous sedation with local
anaesthesia.
Quite naturally, the absorption of
infrared light is relative and
dependent on the thickness of the
finger, being different in individual
fingers. Consequently, the reliability
of the pulse wave amplitude
recording requires that the recording
site is not changed. Because of the
relativity of amplitude it is important
to have a basis for comparison
(Mattila et al 1989). In practice this
means that when monitoring sedation,
the recording should be started before
cannulation. Some confusion seems
to exist between direct arterial blood
pressure and visible pulse wave
The aim of this retrospective
review of patient records was to
evaluate the effect of intravenous
sedatives and local anaesthetic agents
with vasoconstrictors to pulse rate
and amplitude of pulse wave when
observed with pulse oximetry.
Another reason for this article was
the need to describe some false
alarms of the oxygen saturation of
blood during intravenous sedation,
and find explanations thereto.
101
Monitoring the patients with three pulse oximeter equipments
2.3.3 PATIENTS AND METHODS
The program recorded numerical
values from SATLITE at every 10
seconds. A finger probe was used for
pulse oximetric registration i.e. blood
oxygen saturation (SaO2). The probe
was placed to the patient's right
middle finger. The data from
Cardiocap was further analysed using
the Microsoft Works-2 and MedStat
programs and the above mentioned
computer.
2.3.3.1 Study design
This survey is a retrospective
descriptive review of patient records.
There were many differences between
patient preparation, cannulation and
intravenous infusion as well as local
anaesthesia, i.e. in the underlying
factors. It is important to understand
that this survey was not a controlled
clinical trial but a clinical follow-up
of normal treatment periods. Later
revised databases formed the survey
material. During the treatments there
was no survey design to answer any
particular question. Thus there was
no indication of approval by an
institutional review board governing
human experimentation.
2.3.3.3 The working principle of
the Datex pulse oximetric
equipment
Light is generated in the finger
probe and it passes through the
tissues. The total absorption of light
can be derived into absorbing
components: tissues, venous blood
and the pulsating arterial blood.
Different amounts of light are
absorbed by oxygenated haemoglobin
(HbO2) and unoxygenated or reduced
haemoglobin (Hb). The oximeter
measures the relative absorption of
red light at 660 nm and infrared light
at 910 nm by Hb and HbO2. These
two different forms of haemoglobin
allow different amounts of light to
pass at these wave lengths. The
oximeter converts this information on
relative light intensity into arterial
oxygen saturation values.
2.3.3.2 Monitoring
During the measuring, patients
were monitored with SATLITE
TRANS TM (Datex, Helsinki
Finland). This pulse oximeter is a
stand-alone, non-invasive, arterial
oxygen saturation monitor which can
also monitor ECG and blood
pressure. It gives continuous, realtime SaO2 and pulse rate readings.
Follow-up information is available
through both the analog and digital
output ports.
The monitor was connected
directly to the serial port of Toshiba
T1000 SE portable computer for the
real-time collection of data by a
collection program.
The pulsation of the arterial blood
flow modulates the passing light. The
oximeter converts this light intensity
information into pulse rate values
which are presented by SaO2 value
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
on a monitor screen. The pulse wave
is derived from the intensity of
transmitted light. The pulsating blood
flow in the finger is the result of left
ventricle contraction of the heart
which fills the vascular bed of the
finger with arterial blood. It is
important to understand that the pulse
wave-form reflects changes in blood
volume, not changes in blood
pressure.
laboratory blood evaluations (B-Se,
B-Hb, B-leuk, fB-glu). The patients
were advised both verbally and in
writing on how to prepare for
intravenous sedation (for example, no
food or drink for four hours prior to
treatment).They were in good health
and had no severe systemic diseases
(in the classification of American
Society of Anaesthesiology ASA I - II
i.e. no systemic diseases or only a
moderate disease which does not
limit activity).
2.3.3.4 Patients
Patients were not given oral
premedication,
sedatives
nor
antibiotics on the day of the operation
or the previous day. Blood pressure
was recorded and monitoring with a
pulse oximeter initiated before the
insertion of a peripheral venous
cannula. After the insertion of the
cannula, an infusion of 0.9% sodium
chloride solution was started, and
then the sedative agent was applied
with disposable syringe using the
slow injection technique (Table 1).
The treatment room was equipped
with dental unit, pulse oximeter,
oxygen supplement unit and some
resuscitation facilities, including
endotracheal intubation equipment
and medication for cardiopulmonary
resuscitation. All treatments were
carried out by the same dentist, i.e.
the author.
This retrospective review of
patient records comprised 26
registrations of 26 of the author's
private outpatients who underwent
dental operations under intravenous
sedation with local anaesthesia. The
survey was carried out between
October 1993 and February 1994 and
included all the patients treated under
intravenous sedation with local
anaesthesia at the clinic during that
period of time. Patients were 16
(62%) males and 10 (38%) females.
Mean age was 42 years SD 15 years.
The patients had some oral surgical
operations or they underwent large
conservative dental treatment or
extraction under sedation because of
dental care phobia.
During the first examination, the
patients completed a questionnaire
about previous and present illnesses,
allergies and medications. A dental
care plan was drawn up and all the
patients were referred to radiological
examination (orthopantomography).
All the patients who underwent major
surgical operation e.g. sinus-lift
procedure, were also referred to
2.3.3.5 Sedation
Midazolam was used for sedation
(Dormicum 5 ml inj. 1 mg/ml Roche),
with mean amounts 5.02 mg SD 1.72
mg. Table 2 presents the doses of the
agents used.
103
Monitoring the patients with three pulse oximeter equipments
in the dental chair, and pulse
oximetric monitoring was continued
until bleeding after extraction had
stopped and until the patients felt
well and were able to walk and get
dressed without help. The patients
left the clinic with an adult escort.
Fentanyl (Fentanyl 2 ml inj. 50
microgram/ml Orion R) was not used
for
additional
pain
relief
preoperatively, only in 1 case for
analgesia postoperatively (0.05 mg).
(Table 2)
Local anaesthesia was performed
with
a
lidocaine-epinephrine
combination (Xylocain adrenalin 1.8
ml inj. 20 mg/ml + 0.0125 mg/ml,
ASTRA, mean 155 mg SD 54.3 mg
lidocaine and 0.097 mg SD 0.034 mg
epinephrine) and a prilocainephelypressine combination (Citanest
Octapressin 1.8 ml inj. 30
mg/ml+0.54 microgram/ml ASTRA,
mean 203 mg SD 118 mg prilocaine
and 0.0036 mg SD 0.0021 mg).
2.3.3.6 Statistical methods
Paired t-test was used to compare
maximal pulse readings during
different parts of the survey. Changes
in maximal pulse from baseline, and
from the previous part of the survey
were described as means and 95%
confidence intervals. Fisher's exact
test was used to study the association
between
room
temperature
(covered/uncovered patient) and
amplitude
of
pulse
wave
(satisfactory/unsatisfactory
p.b.f).
The data were analysed using SPSS
statistical package (Version 6.1.3).
After treatment, most of the
patients (16 cases) received 30 mg
ketorolak (Toradol inj. 30 mg/ml,
Syntex) injection for analgesics via
venous cannula. Blood pressure was
recorded again and the venous
cannula removed. The patients stayed
104
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
Table 1. The treatment was divided into five periods as described in this table.
The maximal pulse rate was determined during every period.
Treatment periods in which cardiovascular
parameters were observed.
Name of period
Description
Duration
1. Waiting (Before)
Patient in the chair
before cannulation
5 - 10 minutes
2. Sedation
After cannulation but
before local anaesthetic
injections
5 - 10 minutes
3. Local anaesthesia
Injections of local
anaesthetic agents
5 - 10 minutes
4. Treatment
Operative period:
incisions, drilling,
extraction, sealing,
fillings, etc.
15 - 120 minutes
5. After
Intravenous-cannula
removed, patient still in
the chair
Table 2. The premedications used in this survey. Quantity of the agents is
expressed in milligrams and local anaesthetics also in 1.8 ml ampoules (in brackets).
Medication
No. of patients
Mean
Midazolam (mg)
26
5.02
Lidocaine (mg)
26
155 (4.31)
Prilocaine (mg)
17
203 (3.76)
105
SD
1.72
54.3
118
Monitoring the patients with three pulse oximeter equipments
2.3.4 RESULTS
per minute, SD 14.4, p<0,001) as a
result of stress relief (Tables 4-6).
2.3.4.1 Maximal pulse rate
Pulse alone was a good indicator
for stress but the maximal pulse rate
during a period reflects the highest
discomfort better. There were no
considerable differences between the
waiting period (89.8 beats per minute,
SD 14.4), the sedation period (91.3
SD 13.6), and the treatment period
(91.4 SD 11.5) compared to pulse
measurements recorded during the
waiting period before cannulation:
89.8 beats per minute (Table 4).
As a conclusion, maximal pulse
rates before operation, during
sedation and during treatment were
constant but were increased by local
anaesthesia and decreased by the end
of the procedure.
2.3.4.2 Amplitude of pulse wave
(A.P.W.)
A.P.W. will rise after the injection
of benzodiazepine and afterwards the
local anaesthesia will cause some
vasoconstriction. A single dose of
benzodiazepine produced effective
vasodilatation which remained for 45
minutes (fig 2). In general, P.B.F
decreased towards the injection due
to psychological stress. The blood
flow showed decreasing values
during and after the injections of
local anaesthetic.
Maximal pulse rate increased
slightly both during and after the
injection the midazolam, but after the
epinephrine containing lidocaine
injection the increase from base level
was notable (8.8 beats per minute,
p<0.005, Table 5, Fig. 1). Injection
with
lidocain
epinephrine
(Xylocain-adrenalin) increased the
heart rate because of epinephrine.
The heart rate increased about 10/min
from base level (Tables 5 and 6).
The effect of low room
temperature to the A.P.W. was
notable. The difference in A.P.W.
between the patients who were
covered with a blanket and the
patients who were not is both
clinically and statistically significant.
(p=0.07 using Fisher’s exact test,
Table 3).
The higher pulse level was
detectable for 20 minutes although
the injection period for local
anaesthesia only took 10 minutes (Fig
3). During the treatment period itself
the pulse rate decreased into the level
of 91.4 (SD 11.5). Moreover,
maximal pulse rates were lower after
the treatment (80.8 beats per minute,
SD 13.2) than before it (89.8 beats
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
Table 3. The effect of low room
temperature to the amplitude of pulse
wave (A.P.W.).
Covered
patients
1. satisfactory
A.P.W.
2. unsatisfactory
A.P.W.
Total
feel cold. Low temperature has also
closing effect in A.P.W. and this may
often cause measuring failures
because of low signal. Thus pulse
oximetric measuring works properly
only in cases where the patient has
comfortable conditions. Figure 4
combines the patients whose A.P.W.
was under 20 (in relative scale) all the
time. The upper line presents the
measured SaO2. There is a great
amount of artefacts (*) on this line.
An artefact is described as an
extensive fall in SaO2 readings
without any organic reasons such as
breathing failure or obstructed
airways. Good A.P.W. allows the
right detection of SaO2 during the
sedation and treatment period (Fig.
5).
Uncovered Total
patients
12 (92%)
7 (54%)
19
1 (8%)
6 (46%)
7
13 (100%)
13 (100%)
26
13 patients were covered with a
blanket an 13 were not. The decision
to cover the patient with a blanket or
not
was
not based on a
randomisation, the dentist only
realised that some of the patients felt
cold. Therefore all the uncovered
patients had their treatment earlier
than the covered patients. This
vasoconstriction occurs if the
treatment is carried out in a cool
operation room where patients may
2.3.4.3 Other observations
False alarms were observed during
momitoring as represented in fig 4.
107
Monitoring the patients with three pulse oximeter equipments
Fig 1. Pulse rate in the different stages of treatment.
The boxplots are formed from "boxes", which contain 50% of the values falling
between the 25th and 75th percentiles, and the "whiskers", lines that extend from
the box to the highest and lowest values, excluding outliers. A line across the box
indicates the median. (Four patients were excluded from this figure because of
missing values.)
P u ls e
120
110
100
90
80
70
60
50
N=
22
B e fo r e
22
S e d a tio n
22
L o c a l a n e sh t.
22
T r e a tm e n t
22
A fte r
T r e a tm e n t p e r io d
Table 4. Maximal pulse values during the survey
Before
Sedation
Mean
89.8
91.3
98.6
91.4
80.8
SD
14.4
13.6
12.5
11.5
13.2
72.8-121.8
72.8-113.4 54.6-105.0
Range 64.4-120.4 71.4-116.2
Local anaesthesia Treatment After
108
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
Table 5. Maximal pulse. Changes from baseline.
Change from
baseline
(=before) to
Mean
SD
95% confidence interval p-value*
Sedation
+1.5
10.2
-2.6 to +5.6
0.46
Local anaesthesia
+8.8
8.8
+5.2 to +12.3
<0.001
Treatment
+1.6
11.7
-3.2 to +6.3
0.50
After
-9.0
11.9
-13.8 to -4.2
0.001
*) paired t-test
Table 6. Maximal pulse. Changes from the previous part of treatment.
Change from
previous part of
treatment
Mean
SD
95% confidence interval p-value*
Baseline to sedation
+1.5
10.2
-2.6 to +5.6
0.46
Sedation to local
anaesthesia
+7.2
9.1
+3.6 to +10.9
<0.001
Local anaesthesia to
treatment
-7.2
6.6
-9.9 to -4.5
<0.001
-10.6
7.6
-13.6 to -7.5
<0.001
Treatment to after
*) paired t-test
109
Monitoring the patients with three pulse oximeter equipments
Fig 2. Pulse rate (A) and amplitude of pulse wave (B) after the injection of
midazolam. The figure consists of five (n=5) patients. Only the cases in which the
quality of detections was most excellent were accepted to this figure. These five
measurements are in combination so that the injections of midazolam occur at the
same time; two minutes after beginning i.e. at the left corner of the 60 minutes
scale. The line itself is the mean of the five registrations.
PULSE RATE
A
100,0
90,0
80,0
70,0
60,0
50,0
40,0
30,0
20,0
10,0
0,0
Injection of
sedative
agent
sedation
local anesthesia
treatment
0 MIN < TIME IN MINUTES > 60 MIN
AMPLITUDE OF PULSE WAVE
B
100,0
90,0
80,0
70,0
60,0
50,0
40,0
30,0
20,0
10,0
0,0
Injection of
sedative
agent
sedation
local anesthesia
treatment
0 MIN < TIME IN MINUTES > 60 MIN
110
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
Fig 3. Pulse rate (A) and amplitude of pulse wave (B) after local anaesthesia
with lidocaine - epinephrine. The figure consists of five (n=5) patients. Only the
cases in which the quality of detections was most excellent were accepted to this
figure. These five measurements are in combination so that the first injections of
lidocaine - epinephrine occur at the same time; two minutes after beginning i.e.
some millimetres from the left corner of the 30 minutes scale. The line itself is the
mean of the five registrations.
PULSE RATE
A
100,0
90,0
80,0
70,0
60,0
50,0
40,0
30,0
20,0
10,0
0,0
0 MIN < TIME IN MINUTES > 30 MIN
AMPLITUDE OF PULSE WAVE
B
100,0
90,0
80,0
70,0
60,0
50,0
40,0
30,0
20,0
10,0
0,0
0 MIN < TIME IN MINUTES > 30 MIN
111
Monitoring the patients with three pulse oximeter equipments
Fig 4. The oxygen saturation readings (A) and amplitude of pulse wave (B) in
cases where the patients were treated in a cool operation room without blanket
covering. The figure consists of five (n=5) patients. Only the cases in which the
quality of detections was worst were accepted to this figure. These five
measurements are in combination so that the injections of midazolam occur at the
same time; two minutes after beginning i.e. at the left corner of the 1 hour and 20
minutes scale. There are three major areas of the artefacts (*) in the oxygen
saturation readings. The line itself is the mean of the five registrations.
A
SaO2
*****
****
100
90
80
70
60
50
40
30
20
10
0
0 MIN < TIME IN MINUTES > 1 H 20 MIN
AMPLITUDE OF PULSE WAVE
B
100
90
80
70
60
50
40
30
20
10
0
0 MIN < TIME IN MINUTES > 1 H 20 MIN
112
******
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
Fig 5. The oxygen saturation readings (A) and amplitude of pulse wave (B) in
cases where the patients were treated with a blanket covering. Figure consists of
five (n=5) patients (the same as in figures 2 and 3). Only the cases in which the
quality of detections was most excellent were accepted to this figure. These five
measurements are in combination so that the injections of midazolam occur at the
same time; two minutes after beginning i.e. at the left corner of the 60 minutes
scale. The line itself is the mean of the five registrations. No artefacts are available.
SaO2
A
100,0
90,0
80,0
70,0
60,0
50,0
40,0
30,0
20,0
10,0
0,0
0 MIN < TIME IN MINUTES > 60 MIN
AMPLITUDE OF PULSE WAVE
B
100,0
90,0
80,0
70,0
60,0
50,0
40,0
30,0
20,0
10,0
0,0
0 MIN < TIME IN MINUTES > 60 MIN
113
Monitoring the patients with three pulse oximeter equipments
2.3.5 DISCUSSION
patient warm covering him or her
with a blanket. Of course it is
possible to block this autonomic
vasoconstriction reaction with local
anaesthetic injected into the patient's
finger (Eastwood 1992 and Sakurada
1995) but when we are treating a
scared patient, it is wise to avoid such
painful procedures. Moreover, an
alarm delay lasting 12 to 30 seconds
would prevent most false alarms (Pan
and Gravenstein 1994).
2.3.5.1 False alarms
An SaO2-artefact or false alarm is
here described as extensive fall in
SaO2 readings without any organic
reasons like breathing failure or
obstructed airways (Fig. 4). The study
of White et al. (1989) have showed
that nearly half of the patients
developed
clinically
significant
desaturation during minor oral
surgery under local anaesthesia. They
assumed that this might be due to
breath-holding
or
peripheral
vasoconstriction as a response to
anxiety or fear (White et al. 1989).
This retrospective review of patient
records explains those observations:
poor amplitude of pulse wave
(A.P.W.) has caused false alarms.
Even Lowes and Brooks' (1991)
finding, that every fifth patient
undergoing the surgical removal of
third molar with local anaesthesia
alone experienced hypoxic periods
during surgery, is explained by false
alarms. The influence of local
anaesthetics to oxygen saturation has
been studied by the author. In a
previous study the saturation values
were no more than 0,5 % lower
(statistically insignificant) than the
base level at the end of the
measurement. Local anaesthesia is a
possible source of measuring
failures (Fig. 4) because it causes
vasoconstriction but the agents used
in local anaesthesia do not affect the
level of the patient’s oxygen
saturation. The easiest way to avoid
these false alarms is to keep the
2.3.5.2 Reactions to local
anaesthesia
Considerable controversy exists in
the
literature
regarding
the
haemodynamic changes caused by
local anaesthetics. Previous studies
have shown that there are no radical
changes in blood pressure after local
anaesthesia but the pulse rate will rise
approximately 10 beats per minute if
epinephrine containing lidocaine is
used. Octapressin containing agents
do not affect the pulse rate (previous
article). Gortzak (et al. 1992b)
studied subjects during routine
restorative dental treatment. They
found that all patients showed
considerable blood pressure variation.
Patients treated without local
anaesthesia showed a significant
mean blood pressure increase while
patients treated with articaine as an
agent of local anaesthesia showed no
significant changes in blood pressure
during treatment. Cioffi et al. (1985)
concluded that routine restorative
114
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
dental care with lidocaine epinephrine local anaesthesia did not
produce
clinically
important
haemodynamic response despite an
increase in epinephrine levels.
Frabetti et al. (1992) found also that
patients who underwent surgical
treatment had higher heart rate values
than
patients
that
underwent
conventional therapy. According to
this retrospective review of patient
records the maximal pulse of the
patient elevates from 91.3 beats to
98.6 beats per minute after the
injection of epinephrine containing
local anaesthetics but if prilocainephelypressine injection is used only
one stress point is found: at the
moment of injection (Study 7). .After
the
injection
of
lidocaineepinephrine there was an additional
period of high pulse 5 - 10 minutes
later when the epinephrine began to
spread to the blood stream from the
injection area. These new findings
will explain also why the maximum
st-segment
depression
in
electrocardiogram was recorded 11
minutes after infiltration (Veit et al.
1993): the effect of epinephrine takes
20 minutes and that is the time during
which the patient may have subjective
disorders. If the patient has dental
care phobia the situation may
become frightful to the patient when
the operative manoeuvres are begun
before these epinephrine derived
disorders have disappeared. If it is
obligatory to use epinephrine
containing lidocaine to avoid pain it
is possible to reduce the amount of
epinephrine by combining it with
prilocaine - phelypressin. The
combination does not cause adverse
effects (Luotio et. al 1996) and may
even enhance the local anaesthetic
effect (Luotio et. al 1997).
2.3.5.3 Clinical monitoring
The light generated in the finger
probe of the pulse oximeter passes
through the tissues. Different
amounts of light are absorbed by
oxygenated haemoglobin (HbO2) and
unoxygenated
or
reduced
haemoglobin (Hb). The pulsation of
the arterial blood flow modulates the
passing light. The pulse wave is
derived from the intensity of the
transmitted light. The total absorption
of the light can be derived into
absorbing
components:
tissues,
venous blood and the pulsating
arterial blood. The pulse wave-form
reflects changes in blood volume and
is the result of left ventricle
contraction of the heart which fill the
vascular bed of the finger with
arterial blood (Mattila et al. 1989).
Patients show vasoconstriction if
the treatment is carried out in a cool
operation room where they may feel
cold. This also has a closing effect in
A.P.W. which may often cause
measuring failures because of low
signal.
Thus
pulse
oximetric
measuring is reliable only in cases
where the patient has comfortable
surroundings.
Without
capillary
pulsating blood flow, the pulse
oximeter cannot compute the
saturation value and the equipment
will lose its proper function.
However, possible measuring failures
do not allow us to leave the patients
without monitoring in the operation
theatre.
115
Monitoring the patients with three pulse oximeter equipments
A.P.W. will increase after the
injection of benzodiazepine, and
afterwards the local anaesthesia will
cause some vasoconstriction. The
regulation of peripheral arterial
circulation is controlled by the
autonomic
nervous
system.
Vasoconstriction is induced by the
stimulation of smooth muscles of
arterioles. This decreases the
amplitude of the pulse wave and may
be due to some discomfort such as
pain, fear, low temperature, as well as
hypovolaemia (Mattila et al 1990).
Vasodilatation is often seen after the
dosage of sedative agent as a result of
feeling good. The amplitude of the
pulse wave is the most informative
indicator of the changes in
circulation. In most equipment these
changes
in
amplitude
are
automatically
corrected
before
expressed in display. This of course
helps the operator as no manual
correction is needed but at the same
time one very informative parameter
is lost if anxious patients are treated
or if the patient is going to develop a
vasoconstriction
due
to
uncomfortable
conditions
or
situations.
116
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part II
2.3.6 Clinical conclusions
The main difference in the measurable pulse oximetric
effects of local anaesthetics from benzodiazepines lies in
amplitude of pulse wave. That will rise after the injection
of benzodiazepine and afterwards local anaesthesia will
cause some vasoconstriction: Vasodilation is often seen
after the dosage of sedative agent as a result of feeling
good. The decreases of the amplitude of pulse wave may
be due to some discomfort such as pain, fear or low
temperature and these may cause artefacts into the
measuring values.
The amplitude of the pulse wave is the most
informative indicator of changes in circulation. In most
equipment these changes in amplitude are automatically
corrected before the pulse wave is expressed in display.
At the same time one very informative parameter is lost.
117
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part III
PART III
PATIENTS’ EXPERIENCES
DURING AND AFTER
SURGERY UNDER
INTRAVENOUS SEDATION
119
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part III
3.1
Study 4
Peroperative experiences
In this study 108 patients who had experienced major or protracted dental
operations under intravenous sedation with local anaesthesia were asked questions
concerning their experiences, using an anonymous questionnaire. The most
important finding was that the patients felt there was little need for general
anaesthesia. Most patients (87%, 95% concidence interval 81% to 94%) preferred
intravenous sedation with local anaesthesia. The patients were nearly unanimous in
recommending intravenous sedation for other patients. Two clear subgroups were
formed (by excluding 17 patients) according to their reasons: for 38 patients the
main reason for undergoing intravenous sedation with local anaesthesia was a major
surgical treatment (operation group), and for 53 patients the fear of any dental
treatment, i.e. dental care phobia (phobia group). These subgroups showed no
statistical difference in unpleasant experiences during treatment, though in the
operation group the general impression of the treatment was slightly higher than in
the phobia group (p= 0.05). Eight patients in the phobia group felt that they could
undergo the operation next time with local anaesthesia alone, while only 1 patient in
the operation group preferred the operation with local anaesthesia alone. The need
for general anaesthesia was low, the patients (5 cases) reporting the need for general
anaesthesia belonging to the phobia group. Local anaesthesia alone, as well as
general anaesthesia, had somewhat higher preference in the phobia group than in the
operation group (p=0.05). The patients in both groups reported that pain, fear,
anxiety, confusion and drowsiness had not disturbed them during the treatment
although the phobia group reported more confusion and fear during the operation
than others (p<0.05).
121
Patients’ experiences
3.1.1 INTRODUCTION
through sedation, since it is a rapid
way to control fear and does not
require any activity from the patient.
This contrasts with the view of
Krochak and Rubin (1992) who argue
that
although
antianxiety
pharmacological agents have their
indications, they do not always treat
the psychological needs of the
patient.
3.1.1.1 Fear
Fear activates the autonomic
nervous system causing many clinical
problems. Notable changes occur in
the patient's heart rate, peripheral
pulse volume, sweat activity and
muscle tension as well as steroid
levels in blood (Schahachter and
Singer 1962, Berggren 1984).
However, subjective feelings do not
always correlate with measured
physiological reactions (Tuutti 1986).
Moreover, in many cases the adverse
reactions to local anaesthetic are
psychogenic in nature. Fear of
injection, or of dental treatment in
general, may lead to some of the most
frightening "allergic" reactions tachycardia
and
vasodepressor
syncope (Kleinhauz and Eli 1993).
3.1.1.2 Sedation
Both types of patients, those
presenting with only phobias and
those with psychiatric disorders, can
be treated in the dental office.
However, a patient who suffers from
dental care phobia can also be a
source of stress for the dentists. Many
dentists feel uncomfortable having to
ease the patient's anxiety, nor do they
want to spend the extra time required
to treat this type of patient (Milgrom
and Weinstein 1993). An anxious
patient poses a problem for the dentist
because the fear can prevent the
dentist from working effectively.
Moreover, insufficient knowledge
and
understanding
of
the
psychological
and
emotional
reactions caused by fear may affect
the dentist's sense of professional
satisfaction (Berggren 1984).
Several
factors
have
been
discussed as causing dental fear:
patients may have a phobic or
psychopathological syndrome, they
may suffer from neurosis or high
general anxiety levels (Berggren
1984). Excessive levels of presurgical
fear are even harmful to postoperative
recovery (Edelman 1992 ). Fear is a
learned behaviour, and can therefore
be unlearned to be substituted by
another way of behaviour (Krochak
and
Rubin
1992).
However,
psychological treatment is an
extremely long way and of little use if
the patient suffers from an acute
disorder. For the dentist, the easiest
way to control the patient's fear is
A number of both psychological
and pharmacological techniques are
available to the dentist to reduce fear.
Such
pharmacological
methods
122
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part III
include premedication with sedative
drugs or nitrous oxide, and general
anaesthesia. Alternatively, the use of
intravenous, inhalation or oral
sedation
have
been
reported
(Lemasney et al. 1989). Intravenous
conscious sedation with local
anaesthesia has been shown to
produce less patient stress than does
general anaesthesia. Indeed, the use
of intravenous sedation produces no
clinically meaningful physiological
changes in the patient's condition.
Conversely,
general
anaesthesia
increases heart rate and blood
pressure as well as the levels of
plasma epinephrine and cortisone,
which are all indicative of a stress
response. Thus, conscious sedation
can be used to reduce the measurable
parameters of stress that patients
would develop during operations or
other dental procedures (Shepherd et
al. 1988, Hempenstall et al. 1986).
Moreover, cost comparison has
showed that it is twice as expensive
to have the same procedure conducted
under general anaesthesia as it is
under intravenous sedation (Van
Sichels and Tiner 1992). A further
argument in favour of intravenous
sedation is that though general
anaesthesia
may
resolve
the
immediate dental problem, the phobia
still remains (Lemasney et al. 1989).
Despite its advantages, the
majority of patients have never heard
of the availability of intravenous
sedation
to
supplement
local
anaesthesia during dental surgery.
Nevertheless, earlier studies reveal
that when given the opportunity to
experience this method, the majority
of patients have found it highly
acceptable. (Rodrigo et Clark 1986,
Lundgren 1988) Lind (et al. 1990) has
previously
reported
that
postoperatively many patients have
complete amnesia of operative events
and typically express the desire for a
similar anaesthetic technique in future
procedures
when
intravenous
midazolam and fentanyl have been
used in combination. However, it
remains unclear how the patients
would react to diazepam sedation if
used in amounts which would not
essentially produce total amnesia.
An easy way to find out the
patients' subjective feelings towards
the use of sedation is to pose direct
questions or to use different
psychological measurements (precise
instruments for the measurement of
dental fear) made to the patient after
treatment. However, a patient may
sometimes lie and we can thus not
always be sure about the real truth
(Bernstein 1976).
123
Patients’ experiences
patients had had positive or negative
experiences of the procedure under
sedation. Patient evaluation would
thus indicate whether the sedation
had any effect on the patient's phobia,
i.e. had the phobia been relieved,
remained unchanged or even become
worse.
3.1.1.3 Aims of the study
The aim of this study was to
determine patients' reactions to
treatment under intravenous sedation
and to compare different patient
groups with respect to subjective
experiences and opinions. The
present study attempts to resolve this
question by determining whether the
124
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part III
3.1.2 PATIENTS AND
METHODS
or whose subgroup was difficult to
determine, i.e. no answer in this
question (1 patient) or double ticks (2
patients). These patients are still in
the whole material as members of
the”others” group. For 37 patients,
the main reason for treatment under
intravenous sedation was the major
nature of the surgical procedure itself
(operation group). 53 patients were
scared of the dental treatment, i.e.
they had dental care phobia (phobia
group). The groups were comparable
with respect to gender distribution
(Chi-square test, p=0.66). The
patients in the phobia group were
significantly younger than the
patients in the operation group (37.0
vs. 48.9; p<0.0001), and also younger
than the other patients (37.0 vs. 43.5;
p=0.05). The phobia group differed
significantly from other patients also
with respect to the time lag between
the operation and the questionnaire
and the time between the last
appointment at the dentist and the
operation (Tables 1-2)
3.1.2.1 Patients
The research group consists of 108
patients undergoing dental procedure
with intravenous sedation at the first
author’s private practice. The
material comprises all the patients
who had their treatment under
intravenous sedation before the
mailing of the questionnaire. Patients
underwent surgery primarily for
implantological
reasons,
major
conservative dental treatment, or
extraction under sedation due to
dental care phobia. The subjects were
private practice dental patients, who
are mostly in a good state of health,
though there is always a minority of
patients suffering from systemic
disease which may limit their activity,
i.e. they conformed to groups I-III of
the ASA (American Association of
Anaesthesiologists)
classification.
None of the patients corresponded to
the ASA classification for groups IV V. No patients were excluded. The
patients were within the limits of
generally accepted indications and
contraindications as mentioned in the
text books for dental anaesthesia.
Before the treatments, a number of
criteria were considered for treatment
and anaesthesia selection: who needs
sedation, for whom would diazepam
alone not be sufficiently effective and
whether there might be any difference
in the effectiveness of one type of
anaesthesia for different types of
operations.
The mean age was 42 years (SD
13). The patients were divided into
two main groups by the dentist
according to their main reason for the
treatment: phobia or oral surgery
(question 1.). These subgroups were
formed or refined by excluding 17
patients who answered ”other reason”
125
Patients’ experiences
Table 1. Types of treatments in the different clinical groups of patients
All patients
Subgroups
Type of treatmens
(108)
Phobia (53)
Operation (38)
restorative works
52 (48%)
39 (74%)
4 (10%)
extraction
47 (44%)
32 (60%)
7 (18%)
scaling
38 (35%)
26 (49%)
5 (13%)
oral surgery
44 (41%)
8 (15%)
30 (79%)
Table 2. Patient characteristics in the phobia group, the operation group and in
”others”.
All
(n=108)
46%
54%
Phobia
(n=53)
43%
57%
Operation
(n=38)
46%
54%
Others
(n=17)
56%
44%
Gender
males
females
Age (years)
mean
SD
range
42.1
12.8
16-78
37.0
9.9
16-63
48.9
12.9
19-78
43.5
13.9
22-67
Time (months)
from operation
mean
SD
range
11.4
8.3
1-30
13.6
8.5
1-30
7.9
6.9
1-30
11.8
8.0
4-30
Previous visit
mean
before operation range
4.9
0-30
7.3
0-30
2.1
0-10
126
3.6
0.2-15
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part III
years for the phobia and operation
groups respectively.
3.1.2.2 Questionnaire
An anonymous questionnaire was
mailed to the 136 patients who had
previously undergone intravenous
sedation with local anaesthesia. The
response rate to the mailed survey
was 79.4% (108 patients). Two
patients could not be located by
postal authorities and 26 declined to
respond. Of the patients who
responded, 49 (46 %) were found to
be males and 57 (54 %) females,
yielding a total sample of 108 (2
patients did not answer this question).
The whole study group received
the following treatments: restorative
work in 52 cases (48%), extraction in
47 cases (44%), scaling in 38 cases
(35%) and a surgical procedure in 44
cases (41%). For the operation group,
the corresponding figures were:
restoration 4 (10%), extraction 7
(18%), scaling 5 (13%) and surgery
30 (79%), and for the phobia group
39 (74%), 32 (60%), 26 (49%) and 8
(15%), respectively. Almost all
patients underwent treatments (e.g.
extraction or major surgery) after
which postoperative pain was to be
expected.
The mean period of time between
the treatment and answering the
questionnaire was 11.4 months (SD
8.2) for the whole study group. For
the phobia group and the operation
group, this period was 13.1 (SD 8.4)
and 7.9 (SD 6.8) months respectively.
(There is no particular explanation for
the difference of response delay
between the groups: these patients
were the whole material of the
intravenously sedated patients of the
clinic during one period of time.)
Previous contact with a dentist prior
to this treatment was 4.9 (SD 5.9)
years for the whole study group, and
7.0 (SD 7.0) years and 2.1 (SD 2.7)
The questionnaire used a vertical
visual analogy scale (V.A.S.) which
plumbed the patients’ subjective
opinions about experiences during
treatment (peroperative). The patients
were asked to mark the point on a
100-millimetre
scale
between
satisfying and displeasing. The lower
end indicated a lack of the asked
experience and the upper end a strong
presence of the experience.
127
Patients’ experiences
3.1.2.3 Medication
For sedation, diazepam with
soybean oil solvent were used in 85
cases (Stesolid Novum 2 ml inj. 5
mg/ml
Dumex/KabiVitrum)
or
midazolam in 24 cases (Dormicum 5
ml inj. 1 mg/ml Roche), with the
mean amounts corresponding to 12
mg SD 5.0 mg and 6.2 mg SD 2.7 mg,
respectively. For pain relief, fentanyl
(Fentanyl 2 ml inj. 50 microgram/ml
Orion) was rarely used (only in 7
cases, combined with some of the
sedative agents mentioned above);
when used, it was administered only
in low amounts (mean 1.3 ml SD 0.5
ml). The benzodiazepine antagonist
which was available and used in
cases, when needed, was flumazenil
(Lanexat 5 ml inj. 0.1 mg/ml Roche).
Local anaesthesia was performed in
combination with lidocaine (Xylocain
adrenalin 1.8 ml inj. 20 mg/ml+12.5
mcg/ml ASTRA) mean 8.8 ml SD 4.3
ml
and
prilocaine
(Citanest
Octapressin 1.8 ml inj. 30
mg/ml+0.54 mcg/ml ASTRA) mean
8.6 ml SD 3.6 ml (Table 3).
At the first examination, the
patients completed a questionnaire
about previous and present illnesses,
allergies and medications. A dental
care plan was prepared. All patients
were
referred
to
radiological
examination (orthopantomography)
and
the
majority
of
the
implantological patients were also
referred
to
laboratory
blood
evaluations (B-Se, B-Hb, B-leuk, fBglu). Patients were advised both
verbally and in writing on how to
prepare for intravenous sedation (for
example, no food or drink during the
four hours prior to treatment).
No oral premedication was given
to the patients on either the day of the
operation or the preceding day.
Before the insertion of peripheral
venous cannula, blood pressure was
recorded, and monitoring with a pulse
oximeter was initiated if midazolam
was used as the sedative agent. These
patients were followed up with an
Ohmeda pulse oximeter and the data
collected with the program supplied
by Ohmeda (37XX) using a Toshiba
T1000SE computer. After canulation,
an infusion of 0.9% sodium chloride
solution was started and a sedative
agent was applied with a disposable
syringe using the slow injection
technique. The surgery was equipped
with a dental unit, pulse oximeter,
oxygen
supplement
unit
and
resuscitation facilities including
endothracheal intubation equipment
and medication for cardiopulmonary
resuscitation.
After treatment, blood pressure
was recorded again and the venous
cannula removed. The patients
remained in the dental chair until the
bleeding following extraction had
subsided and the patient felt well and
was able to walk and dress without
help.
128
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part III
Table 3. Medication (mg) in groups
Midazolam
n
Mean
Range
All
(n=108)
24
6.2
2.5-15
Diazepam
n
Mean
range
8.5
12.0
5-40
Fentanyl
n
Mean
Range
Lidocain*
n
Mean
range
100
177.1
36-468
53
194.4
36-360
31
146.3
72-360
16
180
72-468
Prilocain**
n
Mean
range
88
234
54-648
47
261
54-648
27
196.2
54-378
14
212.4
108-432
7
0.065
0.025-0.1
Phobia
(n=53)
9
8.1
5-15
Operation Others
(n=38)
(n=17)
11
4
5. 1
5. 1
2.5-10
3.5-25
45
13.2
7.5-40
27
10.3
5-20
2
0.065
0.025-0.1
4
0.065
0.05-0.1
13
11.7
5-25
1
0.065
* the amount of vasoconstrictor (epinephrine) not expressed on this table
** the amount of vasoconstrictor (phelypressine) not expressed on this table
129
Patients’ experiences
used to compare the VAS values
between phobia group and other
groups.
3.1.2.4 Statistical methods
The answers were measured from
the VAS-scale and represented as
boxplots which are made up of
"boxes" which contain 50% of the
values falling between the 25th and
75th percentiles, and the "whiskers",
lines that extend from the box to the
highest and lowest values, excluding
outliers. A line across the box
indicates the median.
The patients in the phobia group
were significantly younger compared
to the other patients. It was also
discovered that age was significantly
(negatively) correlated with most of
the experiences and symptoms. For
that reason, an analysis of covariance
(ANCOVA) was performed to
compare the phobia group to other
patient groups. In the ANCOVA
model, age was included as a
covariate to control the differences in
age distributions between groups.
A visual analoque scale (VAS)
was used to describe the experiences
(0=unpleasant, 100=pleasant) and
symptoms (0=none, 100=extreme)
during the treatment. These VAS
values are depicted in Box-andwhisker plots. The box indicates the
lower and upper quartiles (25th and
75th percentiles) and the central line
is the median. The points at the ends
of the whiskers indicate the lowest
and highest values (excluding
outliers). Mann-Whitney U test was
Chi-square test was used to test
the differences in preferences
between patient groups if the therapy
had to be repeated. The data were
analysed using SPSS statistical
package (Version 6.1.3).
130
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part III
3.1.3 RESULTS
therapy under intravenous sedation
with local anaesthesia for other
patients. Only one patient left this
question unanswered. Most of the
patients (78 cases, 72%) subsequently
made a new appointment with the
dentist (Fig. 4, Table 6).
3.1.3.1 All patients (n=108)
The results for the whole study
group indicated that the patients felt
the experience of treatment under
intravenous sedation with local
anaesthesia to be more pleasant than
unpleasant (Mean 62, SD 16 in the
VAS-scale) and were more satisfied
than displeased (76, SD 13) with the
treatment. When asked about their
unpleasant experiences, the responses
for the whole study group were the
following (scale 100 = extreme, 0 =
none): low pain (18, SD 16), some
fear (26, SD 23), low anxiety (17, SD
19), low confusion (18, SD 20), and
some drowsiness (28, SD 24).
(Medians and ranges are expressed in
table 4)
3.1.3.2 Phobia group (n=53)
In the phobia group, the patients
felt that the experience of the
treatment under intravenous sedation
with local anaesthesia was more
pleasant than unpleasant (Mean 62,
SD 17 in the VAS-scale) and were
more often satisfied than displeased
(75, SD 14) with the treatment. When
asked about unpleasant experiences,
these patients reported experiencing
the following (scale: 100 = extreme, 0
= none): low pain (17, SD 14),
moderate fear (33, SD 25), low
anxiety (19, SD 21) low confusion
(22, SD 22) and some drowsiness (29,
SD 24). (Medians and ranges are
expressed in table 4)
In addition, the patients were
asked which type of anaesthesia they
would prefer if the therapy had to be
repeated. For the whole study group,
the perceived need for general
anaesthesia was very low (5 patients,
5%), with most patients preferring
intravenous sedation and local
anaesthesia (94 patients, 87%) and
only 11 patients (10%) reporting they
could repeat the operation with local
anaesthesia alone. (Some of the
patients made several ticks for each
question in the questionnaire)
However, none of the patients felt
that they could undergo the treatment
without local anaesthesia. With only
one exception all patients (99%)
stated that they could recommend
In response to which type of
anaesthesia would be preferred if the
therapy had to be repeated, even the
phobia group felt little need for
general anaesthesia (5 patients,
9.4%). Interestingly, all patients who
had sought general anaesthesia were
in this group. Most patients expressed
a preference for intravenous sedation
with local anaesthesia (43 patients,
81%). Eight patients (15%) stated
131
Patients’ experiences
they would repeat the operation with
local anaesthesia alone. (Some of the
patients made several ticks for each
question in the questionnaire). None
of the patients, however, felt they
could undergo the treatment without
local anaesthesia. All patients, except
one, (98%) reported they could
recommend the therapy under
intravenous sedation with local
anaesthesia for other patients. One
patient did not respond to this
question. Most of the patients in the
phobia group (28 patients, 52%) were
found to make a new appointment
with the dentist later(Fig. 4, Table 6).
anaesthesia was expressed by those in
the operation group. Almost all these
patients
preferred
intravenous
sedation with local anaesthesia (36
patients 95%). Only one patient
(2.6%) reported that the operation
could be repeated with local
anaesthesia alone. None of the
patients felt that they could withstand
the
treatment
without
local
anaesthesia. All patients reported that
they could recommend the therapy
under intravenous sedation with local
anaesthesia for other patients. All,
except one patient, (36 patients 95%)
later made a new appointment with
the dentist (Fig. 4, Table 6).
3.1.3.3 Operation group (n=38)
3.1.3.4 Differences
In the operation group, the patients
reported feeling that the experience of
treatment under intravenous sedation
with local anaesthesia was more
pleasant than unpleasant (Mean 58,
SD 16 in the scale 100-0) and were
more often satisfied than displeased
(73, SD 14) to the treatment. When
questioned concerning unpleasant
experiences, patients in the operation
group reported experiencing low
levels of the following (scale: 100 =
extreme, 0 = none): pain (19, SD 19),
fear (17, SD 17), anxiety (13, SD 14),
confusion (15, SD 17). Only
drowsiness (28, SD 26) was reported
at a moderate level. (Medians and
ranges are expressed in table 4)
There was a statistical difference
(p=0.05) between the operation and
phobia groups in the general
impression on the treatment; the
phobia group felt the treatment a little
bit more pleasant than the operation
group but the difference was minimal
(1 VAS unit). Satisfaction with the
treatment showed a similar or even
higher tendency but the statistical
significance was not so strong
(p=0.09). Fear and confusion during
the operation were the only
parameters which were higher in the
phobia group than in both of the other
groups (table 4), but in confusion the
statistical analysis failed to show any
high significance between the
operation and the phobia group. The
patients’ age did not correlate with
fear (Table 5) but there was, however,
a correlation with confusion. A
When the patients were asked
which type of anaesthesia they would
prefer if the therapy were to be
repeated, no need for general
132
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part III
preference (if the therapy had to be
repeated) comparison showed that
intravenous sedation had the highest
preference in the operation group
(95%). The phobia group also
preferred intravenous sedation in the
first place (81%) but the preferences
for local anaesthesia alone or general
anaesthesia were higher in this group
(p=0.05). Although there were some
statistically significant differences
between the groups, the values of
those differences were minimal.
133
Patients’ experiences
Table 4. Subjective experiences during the treatment in the phobia group,
operation group and ”others” group.
Experiences:
General
impression*
(0=unpleasant
100=pleasant)
Range**
Satisfaction with
treatment*
( 0=displeased
100=satisfied)
**
Symptoms during
treatment:
Pain*
**
Fear*
**
Anxiety*
**
Confusion*
**
Drowsiness*
**
All
Phobia
patients group
Operation
group
Others
p-values***: p-values:
phobia vs.
phobia
operation
vs. others
67
0.05
0.77
(54-68) (51-71) (52-67)
69
78
68
(67-68)
68
0.09
0.26
(67-87) (67-92) (67-85)
(68-72)
15
15
(4-33) (4-33)
22
34
(4-37) (14-50)
7
9
(2-33) (2-35)
8
20
(2-35) (3-38)
30
31
(5-39) (6-43)
17
(4-22)
10
(3-33)
2
(2-19)
3
(1-5)
22
(5-34)
0.73
0.64
0.004
0.04
0.37
0.12
0.18
0.009
0.54
0.33
67
67
66
15
(4-33)
12
(4-34)
7
(2-29)
8
(3-30)
26
(4-50)
*) Visual Analogue Scale (VAS) values were used. In symptoms a higher value
denotes a more extreme disorder, i.e. pain, fear, anxiety, confusion or drowsiness.
The figures are median (IQR).
**) IQR = inter-quartile range (25th centile - 75th centile).
***) Mann-Withney U-Test
134
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part III
Table 5. Comparison of study groups with respect to subjective experiences and
symptoms during the treatment. The results based on the analysis of co-variance,
where the groups' experiences are being compared and age is included as a covariance.
Experiences *
Phobia vs.
Operation
p-value
Phobia vs.
Others
p-value
effect of age
beta-coefficient
p-value
General impression
0.17
0.36
0.24
0.07
Satisfaction
0.08 *
0.12
-0.09
0.43
Pain
0.33
0.70
-0.29
0.04
Fear
0.0007
0.02
-0.25
0.20
Anxiety
0.16
0.16
-0.20
0.24
Confusion
0.06 *
0.008
-0.38
0.03
Drowsiness
0.77
0.26
-0.54
0.01
135
Patients’ experiences
Figure 1 a and b. General impression (0=unpleasant, 100=pleasant) in all
patients and in phobia group, operation group and in others.
Figure 1a
All patients (n=108)
0
20
40
60
80
100
V.A.S: Unpleasant - Pleasant
Figure 1b
Subgroups
Phobia (n=53)
Operation (n=38)
Others (n=17)
0
20
40
60
V.A.S: Unpleasant - Pleasant
136
80
100
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part III
Figure 2 a and b. Satisfaction with treatment (0=unpleasant, 100=pleasant) in all
patients and in phobia group, operation group and in others.
Figure 2a
All patients (n=108)
0
20
40
60
80
100
V.A.S: Displeased - Satisfied
Figure 2b:
Supgroups
Phobia (n=53)
.
Operation (n=38) .
Others (n=17)
.
0
20
40
60
V.A.S: Displeased - Satisfied
137
80
100
Patients’ experiences
Figure 3 a-d. The level of unpleasant experiences in the study groups.
Unpleasant experiences are presented as a visual analogy scale: a higher value
denotes a more extreme disorder, i.e. pain, fear, anxiety or confusion.
Figure 3a
All patients (n=108)
Fear
.
Anxiety
.
Confusion
.
Pain
.
Disorder
0
20
40
60
80
100
V.A.S. No symptom - severe symptom
Figure 3b
Phobia subgroup (n=53)
Fear
.
Anxiety
.
Confusion
.
Pain
.
Disorder
0
20
40
60
80
V.A.S. No symptom - severe symptom
138
100
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part III
Figure 3c
Operation subgroup (n=38)
Fear
.
Anxiety
.
Confusion
.
Pain
.
Disorder
0
20
40
60
80
100
V.A.S. No symptom - severe symptom
Figure 3d
Other (n=17)
Fear
.
Anxiety
.
Confusion
.
Pain
.
Disorder
0
20
40
60
80
V.A.S. No symptom - severe symptom
139
100
Patients’ experiences
Figure 4. The preference for the different types of peroperative anaesthesia. The
patients were asked: "Which type of anaesthesia would you prefer if the treatment
had to be repeated."
100
90
80
PERCENTS OF PATIENTS
70
60
50
40
30
20
10
0
GENERAL ANESTH.
I.V. SEDATION
WHOLE GROUP
LOCAL ANESTH.
OPERATION GROUP
NO ANESTHESIA
PHOBIA GROUP
Table 6. Preferences (%) if the therapy had to be repeated.
Groups: All
Phobia
Oper.
Others
p-values *
Phobia vs.
Operations
Preferences:
Phobia vs.
Others
Intravenous
sedation with
local anaesthesia
87%
81%
95%
88%
0.06
0. 50
Local anaesthesia
alone
10%
15%
3%
12%
0.05
0.73
Without local
anaesthesia
0%
0%
0%
0%
General
anaesthesia
5%
9%
0%
0%
0.05
0.19
*) Chi-square test
140
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part III
3.2
Study 5
Postoperative experiences
In this study, 136 patients had major or protracted dental operations under
intravenous sedation with local anaesthesia. They were later mailed an anonymous
questionnaire. The most important finding was that pain was the primary symptom
after treatment under intravenous sedation with local anaesthesia. Patients reported
that the pain was not a result of sedation but the result of the operation itself. The
incidence of confusion and tiredness reduced after the first night. The possibilities
to avoid pain and confusion are discussed. Some other disorders were detected but
they were rare: headache and nausea but no vomiting. Two clear subgroups were
formed (by excluding 17 patients) according to their reasons: for 38 patients the
main reason for undergoing intravenous sedation with local anaesthesia was a major
surgical treatment (operation group), and for 53 patients the fear of any dental
treatment, i.e. dental care phobia (phobia group). The operation group served as a
reference group. These subgroups showed statistically significant differences with
the incidence of confusion immediately after the treatment. The phobia group felt
more confused than the operation group (p= 0.05) and were more often incapable of
daily work or driving a car (p<0.05). No statistical difference appeared in
unpleasant experiences on the next day. The patients felt healthy after intravenous
sedation with local anaesthesia and the feeling increased during the following days
(p<0.0001). The patients felt confusion for approximately three hours and most
patients felt ready for the daily work in the next morning. However, sedative
premedication increases the need of sleep and the patients need more rest than
normally on the first day after treatment.
example the duration of the operation,
cannot explain the wide variations in
postoperative morbidity after oral
surgery (Berge and Boe 1994).
Common side effects such as nausea
and vomiting may occur in up to one
third of the patients if opioids are
used. However, the incidences of
emetic symptoms in the postoperative
3.2.1 INTRODUCTION
3.2.1.1 Postoperative recovery
There is some evidence available
that excessive levels of presurgical
fear are even harmful to postoperative
recovery (Edelman RJ 1992 ), but
commonly used predictors, for
141
Patients’ experiences
period have failed to show any
difference although benzodiazepines
are used (Bonazzi et al 1994).
Similarly, the proper combination of
two differently acting sedative agents
have not prolonged the recovery time
(Taylor et al. 1992). Thomson (et al.
1993) have found that, although
initial postoperative recovery to a
'fully awake' state occurred more
rapidly if benzodiazepine antagonist
(flumazenil) had been used, objective
psychomotor testing have revealed
even poorer performance if compared
with
spontaneously
recovering
patients. They believed that the
patients need at least 1 h before the
discharge home. There have been
only
minor
differences
in
postoperative recovery time between
the methods of sedation, even in the
cases
when
patient-controlled
sedation was used (Osborne et al.
1994).
3.2.1.2 Aim of the study
This article attempts to describe
the condition of the patient during the
hours and days following dental
operations. The aim for this study was
a clinical interest to find out how the
patients felt after treatment under
intravenous sedation with local
anaesthesia.
An
anonymous
questionnaire was sent to resolve the
main question, "did the patient have
complications after the procedure
under sedation" i.e. is the procedure
as superior as it seems to be from the
point of view of the dentist.
Moreover, it was tried to define if the
treatment itself was the main source
for the symptoms, and if there could
be differences between patients who
suffered from dental care phobia and
those whose treatment was a major
oral surgery. There was also a need to
find out how much time the patient
needs for recovery.
142
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part III
3.2.2 PATIENTS AND METHODS
The study group is the same as in
the previous study 4.
test, pairwise comparisons were made
using Wilcoxon test for matched
pairs. Mann-Whitney U test was used
to compare the VAS values and
duration of confusion between phobia
group and other groups. Chi-square
test was used to compare the patient
groups with respect to nominal data.
The data were analysed using SPSS
statistical package (Version 6.1.3).
3.2.2.1 Statistical methods
A visual analoque scale (VAS)
was
used
to
describe
the
postoperative general condition (0 =
awful, 100 = wonderful). Friedman's
nonparametric analysis of variance
was performed to compare the VAS
values from three successive periods:
before sleep, next day and next week.
Following a significant Friedman's
143
Patients’ experiences
3.2.3 RESULTS
decrease of most postoperative
disorders from the time before sleep
to the time after sleep. Tiredness was
the primary symptom, caused mainly
by diazepine, and therefore it was the
most rapidly decreasing disorder.
However, it was impossible to show
the decrease of the pain and "the
other symptoms" (Table 2).
3.2.3.1 All patients (n=108)
The patients in the whole study
group felt more healthy (wonderful
feeling) than unhealthy (awful
feeling) after intravenous sedation
with local anaesthesia. This question
was further divided into three time
limits: before sleep, from the
following morning to the following
night, and the following week. In the
visual analog scale 0-100 (awful wonderful) the answers were (Mean
and standard deviation, medians and
ranges are expressed in table 1):
before sleep 67 (SD 18.8), next day
73 (SD 19.1) and following week 80
(SD 19.8). The time effect (Table 1)
was
significant
(p=0.0001).
Interpreted into words this means that
the patients felt well all along and the
feeling was enhanced with time. (Fig.
1a )
As a whole, patients felt that they
were confused for 2.7 hours (SD 3.5);
the escorts thought that the patients
were confused 2.6 hours (SD 3.8).
Most patients (64 cases, 59%) felt
capable of daily work the next
morning. The opinion of the escort
was similar (59 cases, 54%).
Respectively they felt capable of
driving a car the next morning:
patients themselves in 69 cases (64%)
and in the escorts' opinion in 62 cases
57%. The remainder of the patients
answered in the negative or left the
question unanswered. In 40 cases
(37%) the patients believed that the
main reason for disorders was the
treatment itself. 34 patients (32%) felt
that sedation caused the main
disorders and 16 (15%) felt local
anaesthesia was responsible for
disorders. 8 patients (7%) expressed
that there was "some other reason"
for those disorders.
The patients in the whole
examination group suffered following
major postoperative disorders after
treatment but before going to sleep:
16 patients felt to be confused (15%),
39 felt tired (36%), 29 felt pain
(27%). Other disorders were rare:
headache in 5 cases (5%), nausea in 3
cases (3%), no vomiting, other
disorder in 8 cases (7%). (Fig.2) After
sleep the disorders were at a lower
level: confused 6 cases 6%, tiredness
13 cases 12%, pain 23 cases 21%,
headache 3 cases 3%, nausea 1 case
1%, no vomiting, other disorder 9
cases 8%. (Fig.3). There was a
The following questions were
made to the patients: At which time
did the treatment begin, when was it
over; when did they sleep the next
time; when did they wake up? On the
144
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part III
basis of the answers the sleeping
behaviours
could
be
divided
according to the treatment time.
Three subgroups were formed:
1."aftrnoon nap group" which
comprises the patients who slept and
woke up before the actual night. 2.
"evening group" which comprises
patients who went into bed before
midnight and woke up the next
morning. 3."night group" contains the
rest of the patients, who had their
night's sleep after midnight. It was
found that if the treatment was before
or at noon (mean at 11:09), the
patients had a sleeping period in the
afternoon. The duration of the sleep
varied considerably on this day. If the
treatment was carried out in the
afternoon (mean at 5:20 p.m.) the
patients went to sleep early evening
(mean at 7:58 p.m.) and they had an
extended period of sleep. The patients
who were treated in the evening
(mean at 7:00 p.m.) got to sleep late
at night (mean at 00:37 a.m.). The
sleeping patterns are presented in
tables 3a and 3b.
23). Pairwise comparisons showed a
significant (p=0.05) increase in VAS
values (Table 1). In other words they
felt well all the time and the feeling
intensified with time. (Fig. 1b)
After treatment but before going to
sleep the patients in the phobia group
suffered the following postoperative
disorders: 13 patients felt confused
(24%), 18 felt tired (34%), 15 felt
pain (28%). Other disorders were
again rare: headache in 1 case (2%),
nausea in 3 cases (6%), no vomiting
at all, other disorders in 3 cases (6%).
(Fig.2, table 2). After sleep the
disorders were at a lower level:
confusedness 4 cases 8%, tiredness 8
cases 24%, pain 13 cases 24%,
headache 1 cases 2%, nausea 1 case
2%, no vomiting, other disorders 5
cases 9%. The most important
disorders were the pain from the
operation and the tiredness from the
sedative. (Fig.3, table 2)
The patients (phobia group) felt
that they were confused for 2.3 hours
(SD 2.8), and the escorts thought that
the patients were confused 2.2 hours
(SD 3.9). Most patients felt (29 cases
55%) capable of daily work the next
morning. The opinion of the escort
was similar (27 cases 51%).
Respectively, they felt capable of
driving a car the next morning:
patient’s opinion 29 cases (55%) and
escort’s opinion in 27 cases (51%).
The patients believed that the main
reason for the disorders was the
treatment itself in 18 cases (34%). 13
patients (25%) felt that sedation
caused the main disorders and 8
3.2.3.2 The phobia group (n=53)
In the phobia group, as in all
groups, the patients felt more healthy
(wonderful feeling) than unhealthy
(awful feeling) after intravenous
sedation with local anaesthesia. In the
visual analog scale 0-100 (awful wonderful) the answers were (Mean
and standard deviation, medians and
ranges are expressed in table 1):
before sleep 65 (SD 22), next day 70
(SD 23) and following week 77 (SD
145
Patients’ experiences
(15%) felt that local anaesthesia was
responsible for disorders. 4 patients
(8%) expressed that there was "some
other reason" for the disorders. Pain
was the most important disorder in
this group.
The patients (operation group) felt
that they were confused 3.5 hours
(SD 4.7), the escorts thought that the
patients were confused 3.2 hours (SD
4.1). Most patients felt (25 cases
66%) capable of daily work the next
morning. The opinion of the escort
was similar (23 cases 60%).
Respectively, they felt capable of
driving a car the next morning:
patient’s opinion in 31 cases (82%)
and escort’s opinion 27 cases 71%.
The remaining patients answered in
the negative or left the question
unanswered. Nearly half of the
patients believed that the main reason
for the disorders was the treatment
itself (in 14 cases = 37%). The same
number of patients (14 patients =
37%) felt that sedation caused the
main disorders and 5 (13%) felt that
local anaesthesia was responsible for
disorders. 3 patients (8%) expressed
that there was "some other reason"
for those disorders i.e. the patients
felt pain equally disturbing as
tiredness.
3.2.3.3 Operation group (n=37).
In the operation (control) group
the patients felt healthy after
intravenous sedation with local
anaesthesia. In the visual analog scale
0-100 (awful - wonderful) the
answers were (Mean and standard
deviation, medians and ranges are
expressed in table 1): before sleep 66
(SD 15), next day 72 (SD 14) and
following week 78 (SD 15). Pairwise
comparisons
showed significant
increase in VAS again (p<0.05). This
means in practice that they felt well
all the time and the feeling was
intensified with time. (Fig. 1c)
After treatment but before going to
sleep the patients in the operation
(control) group suffered from the
following
major
postoperative
disorders: 13 patients felt tired (35%),
12 felt pain (32%). Other disorders
were rare: headache in 3 cases (8%),
2 patients felt confused (5%), no
nausea nor vomiting at all, other
disorders in 1 case (3%). (Fig.2, table
2) After sleep the disorders were at a
lower level: confused 2 cases 5%,
tiredness 5 cases 13%, pain 8 cases
22%, headache 1 case 3%, no nausea
nor vomiting, other disorders 2 cases
5%. (Fig.3, table 2)
146
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part III
3.2.3.4 Differences
groups when all symptoms were
investigated.
The
statistically
significant
difference between the groups was in
the
incidence
of
confusion
immediately after the treatment. The
phobia group was more confused than
the operation (control) group
(p=0.01). Likewise there were
differences between the groups in the
capability of driving or daily works
(p<0.05, table 5). However, a
statistical analysis failed to show any
differences in disorders between these
If the treatment took place in the
morning or at noon, the patients had a
sleeping period in the afternoon. The
duration of this afternoon nap varied
considerably. If the treatment was
carried out in the afternoon, the
patients went to sleep early in the
evening and they had an extended
sleep. The patients who were treated
in the evening went to sleep late at
night. (Table 3)
147
Patients’ experiences
Table 1. General condition (VAS* values) before sleep, the next day and the
next week in the phobia group, the operation group and others group.
Groups: All
Phobia
Oper.
Others
p-values***
Median
(IOR)
Median
(IQR)
Median
(IQR)
Median
(IQR)
Phobia
vs. Oper.
Phobia
vs.
Others
Before
sleep
68
(57-72)
68
(58-75)
68
(58-70)
70
(54-72)
0.83
0.89
Next day
70
(66-93)
68
(56-97)
70
(67-75)
74
(70-82)
0.77
0.41
Next
week
83
(70-97)
87
(69-99)
77
(70-91)
90
(82-98)
0.33
0.56
P<0.0001
P=0,0001
P<0.001
Time:
p-value of P<0.0001
time
effect***
*) Visual Analoque Scale was used. 0=awful and 100=wonderful.
**) Mann-whitney U-test
***) Friedman*s test. In all three groups the time effect is significant (p<0.0001),
and in the phobia and operation groups all the pairwise comparisons (before sleep
vs. next day and next day vs, next week) showed a significant (p<0.05) increase in
VAS values. In the ”others” group the increase of VAS values from next day to next
week was significant (p<0.05).
148
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part III
Figure 1a -d. Postoperative feeling (0=unpleasant, 100=pleasant) in all patients
and in phobia group, operation group and in others.
Figure 1a:
All patients (n=108)
Next evening
Next day
Next week
0
20
40
60
80
100
80
100
V.A.S: unpleasant - pleasant
Figure 1b:
Phopia subgroup (n=53)
Next evening
Next day
Next week
0
20
40
60
V.A.S: unpleasant - pleasant
149
Patients’ experiences
Figure 1c:
Operation subgroup
(n=38)
Next evening
Next day
Next week
0
20
40
60
80
100
80
100
V.A.S: unpleasant - pleasant
Figure 1d:
Other (n=17)
Next evening
Next day
Next week
0
20
40
60
V.A.S: unpleasant - pleasant
150
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part III
Figure 2. Postoperative disorders after treatment on the day of the treatment. The
phobia group felt more confused than the operation (control) group.
100
Incidence (%) of dissorder
90
80
70
60
50
40
30
20
10
0
w hole group
Confusion
Tiredness
operation group
Pain
Headache
phobia group
Nausea
Other
2)
Figure 3. Postoperative disorders after treatment and first sleep. No differences
between the groups.
100
Incidence (%) of dissorder
90
80
70
60
50
40
30
20
10
0
w hole group
Confusion
Tiredness
operation group
Pain
151
Headache
phobia group
Nausea
Other
Patients’ experiences
Table 2. The occurrence (%) of different symptoms before (B) and after (A) the
first sleep at home in the phobia group, operation group and ”others” group… and
reasons for those disorders.
Groups:
All
Phobia
Oper. Others
15%
6%
36%
12%
27%
21%
5%
3%
3%
1%
0%
0%
7%
8%
25%
8%
34%
15%
28%
25%
2%
2%
6%
2%
0%
0%
6%
9%
5%
5%
34%
13%
32%
21%
8%
3%
0%
0%
0%
0%
3%
5%
6%
0%
47%
0%
12%
12%
6%
6%
0%
0%
0%
0%
24%
12%
34%
15%
25%
37%
13%
37%
8%
8%
Disorder:
Confusion
Tiredness
Pain
Headache
Nausea
Vomiting
Other
Reason for
disorder:
treatment itself
sedation
local
anaesthesia
other reason
B
A
B
A
B
A
B
A
B
A
B
A
B
A
152
p-values
Phobia
Phobia
vs.
vs.
Operation Others
0.09
0.01
0.67
0.24
0.98
0.33
0.79
0.09
0.74
0.17
0.70
0.26
0.17
0.39
0.81
0.39
0.14
0.32
0.39
0.57
0.49
0.39
0.03
0.78
47%
18%
41%
0.79
0.79
0.20
0.33
0.80
0.19
6%
0.95
0.82
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part III
Table 3 A. Sleeping behaviour after treatment. This table consists of patients
(N=76) who went into bed before midnight and woke up the next morning. The
patients who had a previous afternoon nap or who had their night's sleep after
midnight are excluded.
Treatment began
5:20 p.m.
(SD 2:42)
Treatment completed
7:16 p.m.
(SD 2:44)
Patient fell asleep
7:58 p.m.
(SD 6:51)
Patient woke up
7:05 a.m.
(SD 1:22)
Table 3 B. Sleeping behaviour after treatment. This table consists of previously
excluded patients.
AFTERNOON NAP
GROUP
Treatment began
11:09 a.m.
(SD 3:03)
This group (N=10)
consists of those
Treatment completed
12:37 p.m.
(SD 2:45)
patients who slept
Patient fell asleep
3:27 p.m.
(SD 2:44)
and woke up before the
actual night.
Patient woke up
3:56 p.m.
(SD 5:52)
LATE NIGHT GROUP
Treatment begun
7:00 p.m.
(SD 0:37)
(N=5) contains the rest
of the patients
Treatment completed
9:15 p.m.
(SD 0:50)
who had their night's
Patient fell asleep
00:48 a.m.
(SD 0:24)
sleep after midnight.
Patient woke up
08:06 a.m.
(SD 0:48)
153
Patients’ experiences
Table 4. Duration of confusion (hours) in the phobia group, the operation group
and others group
Group:
All
Phobia
Oper.
Others
p-values
Phobia vs.
Opinion: Mean
SD Mean
SD Mean SD Mean
SD Oper.
Others
Patient’s
2.8
3.5
2.6
2.8
3.5
4.8
2.3
2.2
0.91
0.96
Escort’s
2.7
3.9
2.4
4.0
3.2
4.2
2.5
2.9
0.86
0.82
Table 5. Capability (%) of daily work or driving
Group:
Phobia Operation Others
Daily work:
p-value
Phobia vs. Phobia vs.
Operation Others
patient’s opinion
55%
66%
59%
0.29
0.77
escort’s opinion
53%
64%
64%
0.31
0.45
Driving:
patient's opinion
60%
82%
56%
0.03
0.77
escort's opinion
57%
79%
53%
0.04
0.78
154
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part III
3.3 GENERAL DISCUSSION OF PART III
types of therapy: drugs or behavioural
treatment. Even when sedative agents
are used, patient preparation will
influence the effectiveness. The
determination to use a sedative is
often a reflection of the personal style
of the dentist. Some patients strongly
believe in the power of drugs. Others
fear the effects of the drugs
themselves, or fear the loss of control
if they take a psychoactive drug. For
example, some do not want their
minds clouded by a mind altering
drug. If the patient feels that dental
treatment will be safe, and overall
trust is high, but the patient is still
scared, he or she is a good candidate
for drug therapy. Patients who worry
about the treatment not being safe, or
exhibit a low level of trust, are again
poor candidates (Milgrom and
Weinstein 1993). This is in harmony
with our finding that the phobia
group’s acceptance for treatment
under intravenous sedation with local
anaesthesia was not as high as the
others’.
3.3.1 The anxious patient
Since its introduction in the late
1800s, the use of local anaesthesia
has revolutionised the field of
surgery. Today, local anaesthesia
stands alone as the method of choice
for pain control in dentistry. There
are many reports on the relationship
between fear and pain, but in general
there are no mentions in the literature
on other psychological factors that
may influence the inadequacy of local
anaesthesia. Because there is a close
association between the memory of
pain and expected pain, dental
procedures causing pain - in
connection with anxiety - constitute a
major barrier to seeking dental care
for some people (Vassend 1993). The
patients in this study could not
remember
any
significant
unpleasant experiences, such as
pain, during treatment. As a result,
as many as half of the patients, even
in the phobia group, subsequently
made a new appointment with the
dentist following this major and
frightening
operation.
Previous
studies have documented that
patients' memories of dental pain
may later turn into consistent
anxiety (Kent 1984, 1985). The
author believes that intravenous
sedation may have prevented this as
well as caused some relief from
anxiety.
If the dentist chooses drug
therapy, it is still important to discuss
the treatment with the patient:
patients might be told that the drug is
a relaxant and will make them feel
more comfortable, and that the patient
will loose cognition of time, and that
after treatment, most patients do not
remember any unpleasant episodes of
the therapy. According to the author's
clinical experience, many patients
will decide after a few appointments
Many clinicians believe they must
choose between two quite different
155
Patients’ experiences
that they no longer need the drug.
This is extremely important: we can
break the circulus vitiosum of
anxiety.
Clark et Rodrigo 1986, Rodrigo et
Clark 1986). Previous psychometric
studies, however, have failed to show
any objective differences between
these treatments (Barker et al. 1987).
3.3.2 Amnesia
3.3.3 Sedation and confusion
Intravenous
benzodiazepine
administered in conscious sedation
doses reduces significantly the
affection and motivational component
of the pain experience (Coulthard et
Rood 1992) and will produce
approximately
20
minutes
of
profound amnesia (Hupp et Becher
1988). Common experience shows
that the injections of local
anaesthetics form the only painful
procedures during dental treatment.
The author used the 20-minute period
to perform local anaesthesia, and
results show that the patients had no
memory of this painful period.
Although a continuous infusion of
sedative produces better amnesia
during the procedure than a bolus
injection, it also prolongs the
recovery time (Luyk et al. 1992). In
private practices, rapid recovery is
crucial. Most of the patients in this
study received diazepam, and a
minority midazolam. They did not
receive a continuous infusion, though
additional boluses were available in
case of need. Midazolam has been
shown to offer more advantages for
the patient than diazepam, with a
more rapid onset of sedation, less
pain during injection, profound
anterograde amnesia and fewer
postoperative complications being the
main features (Clark et al. 1987,
Patient management and general
anaesthesia are the techniques most
commonly employed in the cases of
dental care phobia and the frequency
of the use of inhalation sedation
varies according to the age of the
patient as it is mainly used for
treating children. Only 55% of
dentists in general practice have any
training in sedative techniques in the
UK (Edmunds and Rosen 1989).
Intravenous conscious sedation in
combination with local anaesthesia is
an alternative during unpleasant
surgical and dental procedures, and in
several cases can replace general
anaesthesia. Monitoring as well as a
trained staff make the methods safe
and enable to reduce complications
like hypoxia (Zoller and Zoller 1992,
Luotio et al. 1993) The length and
precision of certain implant surgery
operations require the complete cooperation of patients (Charlton et al.
1991). Many mentally and/or
physically handicapped and anxious
dental patients do not receive
adequate dental treatment because
effective
ways
of
supportive
treatment are insufficiently known
and/or available to dentists (BouvyBerends and Makkes 1990). The
predominantly favourable response of
the patients leads to the suggestion of
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part III
using intravenous sedation with local
anaesthesia even in minor oral
surgery. (Kingon 1990)
with
spontaneously
recovering
patients, and they concluded that they
could not allow the discharge of
patients sooner than 1 hour after the
injections. Moreover, the clinical
experience of the author of this study
has shown that, although the patients
who suffer from dental care phobia
are more confused after treatment
than others and may need flumazenil,
these very patients are possible
candidates for the central nervous
system-related side effects of this
drug. However, the confusion will be
relieved by itself during the hours to
come: The patients felt confused for
three hours only and did not need
any observation the next morning
(Tables 4 and 5 in study 5).
Sedation and confusion are the
two sides of the same patient
management: we call it sedation when
we want to relax the patient but
confusion when we want to send him
or her back home... It is possible to
remove confusion or sedation with
flumazenil, which appears to be a
promising drug for reversing the
conscious sedation by midazolam.
The patient who receives flumazenil
after intravenous midazolam is
significantly more alert as early as
after 5 min following drug
administration. (Clark et al 1991) In
cases of undue sedation persisting
after dental treatment, flumazenil in
doses from 0.5 to 1.0 mg rapidly
reverses the sedative and amnesic
effects of midazolam without
apparent evidence of subsequent
resedation. (Davies et al 1990)
Flumazenil reverses almost totally the
effects of mental sedation for
approximately 2 hours but not
physical
sedation
or
memory
(Ghoneim et al 1989, Cooper et al
1991). Flumazenil makes recovery in
the supine position unnecessary and
hence is a drug that should be
included in the armamentarium of any
emergency
drug
kit
when
benzodiazepines
are
used
intravenously
(Rosenbaum
and
Hooper 1988). Thomson (et al. 1993)
have controverted this in their study
where they found that psychomotor
testing after flumazenil have revealed
even poorer performance if compared
3.3.4 Postoperative pain
The main disorders after the
operation under intravenous sedation
were tiredness and pain. The first
does not require anything else but
sufficient sleep. However, pain is a
more complicated symptom and
often overlooked by the doctor but
easily relieved with more effective
analgesics. At the time of this study
the patients got a prescription for
some non-steroidal anti-inflammatory
drugs (NSAIDs) which inhibit
peripheral prostaglandins. Today
these drugs are the framework in the
treatment of postoperative pain.
Analgesic agents, with do not operate
against peripheral prostaglandin
synthesis (e.g. paracetamol), may also
provide some pain relief. However,
long-acting NSAIDs like piroxicam
157
Patients’ experiences
have proved to be superior to
paracetamol, which does not induce a
complete relief from pain (Dolci et al.
1993). Because the patients are
canulated, the use of parentheral
analgesic is simple and advisable.
The
intramuscular
dosage
of
ketorolac, a new NSAID, has shown a
similar degree of pain relief to that of
parentheral diclofenac. This safe and
effective drug is an important new
addition
to
the
available
intramuscular NSAIDs preparations.
(Walton et al. 1993) Moreover, it is
possible to enhance pain relief by
combining analgesic agents with
different drugs like opioids and
NSAIDs (Dionne et al 1994).
within dental surgery, although they
are very effective. Local anaesthetics
are not only effective for the
termination of intraoperative pain but
postoperative pain as well. They are
useful for lengthy dental treatments
and for the prevention of severe pain
following many types of surgical
procedures. However, the timing of
normal short-acting local anaesthesia
does not reduce the postoperative
pain experience (Zacharias et al.
1993).
It is an interesting point that the
American patients of European origin
have felt the pain less severe than
those of American African or Latin
origin (Faucett et al. 1994). More
understandable is the fact that the
increased rates of postoperative
complications and a tendency for
increased postoperative pain were
found when the patients were treated
by a general practitioner and not an
oral surgeon. Even the number of
days off work have been higher in
these cases (Berge and Gilhuus
1993).
Baxendale (et al.1993) have
reported that the use of prophylactic
oral dexamethasone is useful in
reducing postoperative analgesia
requirements. Similarly the injection
of a slow-release methylprednisolone
have reduced the frequency and
intensity of postoperative pain
(Kaufman et al. 1994). Neither of
these corticosteroids nor long-acting
local anaesthetics are in common use
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part III
Parentheral medication
with local anaesthetics
is every-day practice in dentistry,
but there must be
a psychological barrier
to prohibit the use of
other parentheral drugs,
although they could
significantly reduce the patients'
unpleasant experiences.
159
Patients’ experiences
3.4 Clinical
There was more confusion in the
phobia group than in the operation
(control) group perhaps because the
patients in this group received more
sedative agents. It is possible to
remove the sedation with flumazenil
but the relatively high price of the
product limits the use. Moreover, half
of the patients felt both ready for
work and vehicle driving, but because
a great deal of them felt they were not
capable of these activities, it is more
than advisable to
The most important
reason for the
disorders was
the treatment itself (i.e.
pain).
After getting the results expressed
in this study, the author changed the
protocol of analgesic drugs. The
previous tolfenamic acid - ibuprofen
type therapy was abandoned and a
single dose of intravenous ketorolac
after operation and a subsequent
prescription of long-acting piroxicam
was introduced. After oral surgery the
patients should also receive an opiate
addition. Since the pain needs to be
relieved and the most effective
medications against pain contain
opioids, the need for resting days may
continue for several days.
forbid all the
patients to drive or
work on the next
day.
Sedative premedication increases
the need of sleep and the patient will
rest more than normally on the first
day after the treatment.
As a conclusion it can be
expressed that there are no severe
problems after treatment under
intravenous sedation if the problems
are provided against during the
procedure, the patient is domesticated
with an adult escort and the patient is
well
medicated
against
pain.
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part III
conclusions
However,
even in these
cases, the author could carry the
therapy through to the end without
any objective difficulties. Most of the
According to this study, the
recollection of the treatment by the
patients seems to be rather positive.
Patients prefer sedation in major
operations.
patients felt only
minimally
uncomfortable
experiences
during the therapy
under intravenous
sedation.
Some of the
patients showing
dental care phobia
may need general
anaesthesia.
However, such patients accounted
for only 10% of the phobia group.
The authors' clinical experience has
shown that mental problems, such as
a previously diagnosed panic disorder
or some psychiatric medications, may
form relative contraindications for
intravenous sedation.
Nevertheless, if the patient is
extremely scared, there is little that
we could or can do to remove all
anxiety.
161
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
PART IV
CHALLENGES
163
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
4.1
Survey 6
Advanced monitoring: Holter
ECG and analysis of the status of
autonomic nervous system
4.1.1 ABSTRACT
This survey comprised 23 study group patients undergoing dental procedures
under intravenous sedation and 12 control registrations of the University Clinic
outpatients who underwent dental surgical operations without intravenous sedation.
Patients were monitored with a Holter ECG recorder until the next morning. The
tapes were reviewed with an arrhythmia analysis program allowing the detection of
normal sinus beats and supraventricular and ventricular occurences. The heart rate
variability analysis (HRV) was performed during surgery and also after the
operation. The amount of cardiac occurences were within normal limits in both
groups; the maximum pulse was suggestively lower in the study group and the high
and low frequency components of heart rate variability were systematically and in
recovery stage even statistically higher (p=0.05) in the study group, all indicating
stress relief.
Moreover, in many cases, the adverse
reactions to local anaesthetic are
psychogenic in nature. Fear of
injection, or of dental treatment in
general, may lead to some of the most
frightening pseudo-allergic reactions tachycardia
and
vasodepressor
syncope (Kleinhauz and Eli 1993).
There is no oral surgical procedure
without fear, pain and drugs, all of
which may cause changes in the
balance of the autonomic nervous
system. The autonomic nervous
4.1.2 INTRODUCTION
4.1.2.1 Autonomic nervous
system and fear
The autonomic nervous system is
activated by fear, which causes many
clinical problems. There are changes
in the patient’s heart rate, peripheral
pulse volume, sweat activity and
muscle tension as well as in steroid
levels in blood (Berggren 1984).
165
Challenges
system controls the visceral functions
of the body e.g. body temperature,
cardiac muscle, arterial pressure and
respiratory function. Oral surgical
procedures may change the balance to
the activation of the sympathetic
system and may also cause changes in
respiratory habits. The activation of
the sympathetic system prepares the
body for physical activities through
increasing heart rate and blood
pressure (fight or flight). We also
know that a powerful sympathetic
activation may increase the risk for
arrhythmias.
and the function of cardiac branches.
Holter also allows the studying of
ischemic occurrences, which is the
most promising character because for
the dentist the easiest way to control
the patient’s fear i.e. autonomic
responses is sedation, but sedation
always causes a risk of hypoxia.
Arterial oxyhemoglobin saturation
(SaO2) decreases regularly after the
administration of a notable amount of
any sedative agent. The decrease in
the saturation level of oxygen is
significant if sedation progresses
from light to deep level. Age is
positively
correlated
with
desaturation, but a history of disease
or medications have failed to be
sensitive predictors of desaturation
(Bilotta et al. 1990). The protracted
half-lives of some benzodiazepines,
and drug interactions, if opioids are
used
in
combination
with
benzodiazepines, appear to be
potential hazards in the elderly.
Desaturation slightly below 90% may
be clinically insignificant since no
complications have been noted at this
level (Berg JC et al. 1991, Bilotta et
al. 1990). The use of Holter makes it
able to detect real cardiac problems
like ST-depressions derived from
desaturation.
Heart rate variability analysis has
been documented to be a method for
evaluating a risk of arrhythmia; it has
also created interest for use as a
monitoring method during and after
surgery (Marsch et al 1994), but no
method for simultaneous heart rate
variability analysis is available.
Moreover, more information is
required on the relationship between
the detected changes of autonomic
status using HRV and real
arrhythmia. At this moment the study
of HRV as well as the documentation
of brady- and tachycardias are most
exclusively done on 24 hours Holter
recordings. This makes it easy to
evaluate the basal rhythm, heart rate
and its changes as well as ectopias
166
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
recording the arrhythmia during
operation and the following day.
4.1.2.2 The aim of the study
The backroud of this survey was
that powerful sympathetic activation
may increase the risk for arrhythmias;
the purpose of this survey was to
analyse the changes in ECG and in
the function of autonomic nervous
system during and after oral surgery.
The second aim is to define the
need for ECG monitoring during
operations
under
intravenous
sedation.
The third purpose is to evaluate
the sympatho-vagal balance using a
frequency-domain analysis of heart
rate variability.
The first aim of this survey is to
investigate the safety of dental
procedures
under
intravenous
sedation with local anaesthesia by
167
Challenges
4.1.3 PATIENTS AND METHODS
previous and present illnesses,
allergies and medications. A dental
care plan was drawn up and all the
patients were referred to radiological
examination
(orthopantomograph)
The patients were advised both
verbally and in writing on how to
prepare for intravenous sedation (for
example, no food and no drink for
four hours prior to treatment).
4.1.3.1 Patients: preparation,
sedation and local anaesthesia
1. Study group:
The research group consisted of
23 patients undergoing dental
procedure under intravenous sedation
at the author's private practice. The
mean age was 48 years (SD 17). The
patients underwent surgery primarily
for implantological reasons, major
conservative dental treatment, or
extraction under sedation due to
dental care phobia. The subjects were
ordinary, private practice dental
patients, who conformed to groups IIII of the ASA (American Association
of Anaesthesiologists). None of the
patients corresponded to the ASA
groups IV - V. The patients were
within the limits of generally
accepted
indications
and
contraindications as mentioned in the
text books for dental anaesthesia and
oral surgery.
Patients were not given oral
premedication,
sedatives
nor
antibiotics on the day of the operation
or the previous day. Blood pressure
was recorded and monitoring with a
pulse oximeter and Holter ECG
initiated before the insertion of a
peripheral venous cannula. After the
insertion of the cannula, an infusion
of 0.9% sodium chloride solution was
started, and then the sedative agent
was applied with a disposable syringe
using the slow injection technique.
Midazolam was used for sedation
(Dormicum 5 ml inj. 1 mg/ml Roche).
The benzodiazepine antagonist used
was flumazenil (Lanexat 5 ml inj. 0.1
mg/ml Roche). Local anaesthesia was
performed with lidocaine (Xylocain
adrenalin 1.8 ml inj. 20 mg/ml+12.5
microgram/ml
ASTRA)
and
prilocaine (Citanest Octapressin 1.8
ml inj. 30 mg/ml+0.54 microgram/ml
ASTRA). After treatment the blood
pressure was recorded again and after
follow-up the venous cannula
removed. The patients remained in
the dental chair until the bleeding
The patients were monitored with
an Ohmeda pulse oximeter and with a
Holter ECG recorder. The data from
the pulse oximeter was collected with
a Microsoft Works program using a
Toshiba T1000SE computer. The
analysis
of
the
24-hour
electrocardiographic recordings is
based on the Holter recordings.
During the first examination, the
patients completed a questionnaire on
168
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
following extraction had subsided and
the patient felt well and was able to
walk and dress without help.
Patient preparation was similar
than in the study group but when the
patients were advised in writing on
how to prepare for the operation it
was mentioned that they should eat
before the operation. This was the
result of different preparation
practices in the University clinic and
the author's private office.
The treatment room was equipped
with dental unit, pulse oximeter,
oxygen supplement unit and some
resuscitation facilities, including
endotracheal intubation equipment
and medication for cardiopulmonary
resuscitation. Both treatment periods
were carried out by the same dentist,
i.e. the author.
Patients were not given oral
premedication (e.g. analgesic drug)
before operation. Blood pressure was
recorded and Holter ECG initiated in
the operation theatre immediately
before operation. Local anaesthesia
was performed with lidocaine
(Xylocain adrenalin 1.8 ml inj. 20
mg/ml+12.5 microgram/ml ASTRA)
or/and
prilocaine
(Citanest
Octapressin 1.8 ml inj. 30
mg/ml+0.54 microgram/ml ASTRA).
2. Reference group
The reference group consisted of
12 patients undergoing dental
procedure
without
intravenous
sedation. The mean age was 45 years
(SD 15). Subjects were unselected
University clinic patients, who were
transmitted to the department of oral
surgery with normal indications. They
were all voluntary for survey and they
conformed to groups I-III of the ASA
(American
Association
of
Anaesthesiologists). None of the
patients corresponded to the ASA
groups IV - V. Thus the patients were
within the limits of generally
accepted
indications
and
contraindications
for
dental
treatment.
There were differences between
patient
preparation
(eating
instructions),
cannulation
and
intravenous infusion and local
anaesthesia i.e. in the underlying
factors, but it is important to
understand that this survey was not a
controlled clinical trial but a clinical
follow-up to compare two types of
patient care i.e. a non-randomised
survey.
The treatment room was equipped
with dental unit, pulse oximeter,
oxygen supplement unit and some
resuscitation facilities, including
endotracheal intubation equipment
and medication for cardiopulmonary
resuscitation. These treatment periods
were carried out by several surgeons.
The patients were monitored only
with a Holter ECG recorder. The
analysis
of
the
24-hour
electrocardiographic recordings were
based on the Holter recordings.
169
Challenges
4.1.3.2 Monitoring
There
are
no
statistically
significant differences in patient
characteristics between the groups:
Age had an effect on variables, but it
is not a confounding factor in this
survey.
All of the Holter tapes in the study
population were analysed using the
Marquette 8500 scanner running
version 5.7 of the Marquette
arrhythmia analysis program allowing
the detection of normal sinus beats
and supraventricular and ventricular
extrasystoles. After an automatic
analysis of the tape, the data file was
visually reviewed and manually
corrected.
Table 1. Patient characteristics in
patients undergoing dental procedure
under intravenous sedation (study
group) and in patients without
intravenous
sedation
(reference
group)
Study
group
(n=23)
Sex (%) males
Age
(years)
ASA
Heart rate variability analysis was
performed by running the Marquette
heart rate variability analysis
program. HRV analyses were
performed using four consecutive
minutes’ periods during surgery and
the three following hours after the
operation. Total power (TP) between
0 - 0.40 Hz along with the power in
the low-frequency band (LF, 0.04 to
0.15 Hz) and in the high-frequency
band (HF, 0.15 to 0.40 HZ) were
calculated
and
logarithmically
transformed. In addition to spectral
components, also LF to HF ratios and
normalised units were used as
markers of sympatho-vagal balance
during the different stages of
operation and recovery period.
Reference
group
(n= 12)
35%
50%
females
65%
50%
mean
48
45
SD
17
15
range
21-81
28-80
1
57%
83%
2
43%
17%
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
independent samples or MannWhitney U, test when appropriate,
was used to compare the groups with
respect to heart rate and HRV
variables at the baseline, and with
respect to the changes from baseline.
4.1.3.3 Statistical methods
Mann-Whitney U test was used to
compare the groups with respect to
the number of cardiac occurences.
Heart rate variability (HRV)
analysis includes four variables to be
analysed; total power (TP), lowfrequency band (LF) high-frequency
band (HF), and the ratio LF/HF.
These variables are expressed and
analysed
using
logarithmic
transformed values. T-test for
Fisher's exact test was used to
compare the patient groups with
respect to nominal data. The data
were analysed using SPSS statistical
package (Version 6.1.3).
171
Challenges
4.1.4 RESULTS
There was no depression of the
heart rate variability (HRV) during or
after the treatment. In the study group
HRV was afterwards even at a higher
level (Figure 1). At the baseline, there
was a remarkable difference between
the groups (table 6). The differences
at the baseline were controlled by
forming variables to express changes
from baseline. The difference
between the groups was significant in
recovery stage (p<0.05) in HF and
LF. The TP differed in all stages
(p<0.05)
except
during
local
anaesthesia (table 7).
None of the patients in either
group had any meaningful arrhythmia
during or after the treatment. The
amount of extrasystoles were within
normal limits. There is no significant
difference between groups with
respect to the occurrence or number
of cardiac incidents (Tables 2,4 and
5).
No ST-depressions indicating the
hypoxia of cardiac muscle were
detected, not even in the cases where
pulse oximeter reported oxygen
saturation under 85% (Table 3).
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
Table 2. The number of unknown but registered cardiac occurrences in both
groups
Study group
Reference group
Peroperative atrial
premature complexes
1.9 SD 0.9
1.3 SD 0.6
Postoperative atrial
premature complexes
2.4 SD 0.7
1.2 SD 0.5
Peroperative atrial
tachycardias
Postoperative atrial
tachycardias
0.04 SD 0.04
0.08 SD .08
0.17 SD 0.14
-
Peroperative ventric.
prem. complexes
Postoperative ventric.
prem. complexes
0.17 SD 0.14
3.0 SD 2.0
1.2 SD 0.6
7.3 SD 7.3
Peroperative
ventricular tachycardias
Postoperative
ventricular tachycardias
-
-
-
-
ST-decrease
-
-
T-inversion
-
-
Table 3. The number of correction manoeuvres for respiratory problems:
Oxygen delivery:
peroperatively
postoperatively
Intravenous flumazenil:
peroperatively
postoperatively
Long term recovery
postoperatively
Study group
Reference group
(n=23)
(n=12)
3
2
-
5
-
2
-
173
Challenges
Table 4. Peroperative and postoperative cardiac occurrences (%) in groups of
patients undergoing dental procedure under intravenous sedation (study group) and
in patients without intravenous sedation (reference group)
Extra systoles
Period
arterial
peroperative
43%
50%
0.74
postoperative
70%
50%
0.29
peroperative
9%
33%
0.15
postoperative
22%
50%
0.13
83%
92%
0.65
ventricular
At least one cardiac
incident (peroperative
/ postoperative)
Study
group
(n=23)
*Fisher's exact test
174
Reference p-value*
group
(n= 12)
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
Table 5. Total number of peroperative and postoperative cardiac occurrences in
groups of patients undergoing dental procedure under intravenous sedation (study
group) and in patients without intravenous sedation (reference group)
Study group
Reference group
(n=23)
(n= 12)
1
1
IQR
0-2
0-5
range
0-21
0-30
2
1
IQR
0-6
1-3
range
0-14
0-50
2
2
IQR
1-11
1-8
range
0-23
0-80
p-value*
Number of preoperative
cardiac occurrences:
Median
0.40
Number of postoperative
cardiac occurrences:
Median
0.60
All cardiac occurrences:
Median
* Mann-Whitney U- test
175
0.99
Challenges
Table 6. Heart rate variability: HF, LF, TP and LF/HF during different periods of
follow-up in patients undergoing dental procedure under intravenous sedation (study
group) and in patients without intravenous sedation (reference group).
Frequency Period
Study
group
(n=23)
Reference
group
(n= 12)
pvalue
HF*
before operation
local anaesthesia
surgery
recovery
the next morning
Mean
4.63
4.45
5.19
5.23
5.84
LF*
before operation
local anaesthesia
surgery
recovery
the next morning
5.63
5.20
5.87
6.38
6.37
1.20
1.32
1.13
1.20
1.29
6.25
5.77
6.16
6.40
6.54
0.60
0.97
0.61
0.82
0.92
0.05
TP*
before operation
local anaesthesia
surgery
recovery
the next morning
7.36
7.21
7.52
7.95
7.93
0.70
0.64
0.64
0.67
0.75
7.71
7.43
7.56
7.86
7.87
0.56
0.89
0.58
0.54
0.58
0.14
Median
3.73
2.83
2.51
3.63
1.77
IQR
1.33-4.93
1.47-4.57
1.40-3.54
1.74-5.04
1.16-4.34
Median
3.03
3.06
2.68
4.06
2.59
LF/HF** before operation
local anaesthesia
surgery
recovery
the next morning
SD
1.30
1.30
1.25
1.25
1.41
Mean
5.13
4.68
5.37
5.11
5.48
SD
0.77
0.96
0.79
0.79
1.02
IQR
2.36-4.23
2.30-4.47
2.17-3.74
3.16-5.09
1.71-5.69
* logarithmic transformed values, t-test for independent samples
** in LF/HF, LF and HF are in original units, Mann-Whitney U-test.
176
0.07
0.78
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
Table 7. Heart rate variability: Mean in HF, LF, TP and LF/HF from baseline
during follow-up in patients undergoing dental procedure under intravenous
sedation (study group) and in patients without intravenous sedation (reference
group).
Frequency
Period
Study
group
(n=23)
Reference
group
(n=12)
pvalue
H F*
local anaesthesia
surgery
recovery
the next morning
Mean
-0.18
0.56
0.59
1.21
SEM
0.18
0.14
0.17
0.31
Mean
-0.45
0.24
-0.02
0.35
SEM
0.24
0.19
0.23
0.20
0.40
0.19
0.05
0.07
LF*
local anaesthesia
surgery
recovery
the next morning
-0.43
0.25
0.75
0.74
0.21
0.15
0.17
0.25
-0.48
-0.08
0.16
0.29
0.24
0.19
0.22
0.19
0.88
0.20
0.05
0.24
TP*
local anaesthesia
surgery
recovery
the next morning
-0.15
0.16
0.59
0.57
0.10
0.08
0.10
0.17
-0.27
-0.14
0.16
0.16
0.22
0.09
0.13
0.10
0.56
0.03
0.02
0.05
LF/HF**
local anaesthesia
surgery
recovery
the next morning
Median
-0.19
-0.72
0.23
-0.38
IQR
-0.86-0.46
-2.03-0.02
-0.72-1.02
-2.79-0.18
IQR
-0.91-0.87
-1.32-0.79
0.10-1.58
-1.62-2.34
0.89
0.31
0.14
0.09
Median
-0.16
-0.26
0.63
0.26
* logarithmic transformed values, t-test for independent samples
** in LF/HF, LF and HF are in original units, Mann-Whitney U-test.
SEM= standard error of mean
IQR= inter quartile range
177
Challenges
Table 8. Pulse rate during and after the operation in patients undergoing dental
procedure under intravenous sedation (study group) and in patients without
intravenous sedation (reference group).
Heart rate
Study group
Reference group
(n=23)
(n=12)
Mean
SD
Mean
SD
p-value*
Maximum pulse:
during operation
98.4
15.5
100.8
17.5
0.68
109.0
17.4
121.7
23.5
0.08
during operation
59.9
7.7
60.6
10.7
0.82
after operation
54.3
7.6
56.5
8.1
0.43
after operation
Minimum pulse:
*t-test for independent samples
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
Fig 1. The difference between the groups in total power. Higher score indicates
the relief of symphatic activity (expressed in logarithmic scale: ln(ms2/Hz)). The
non- sedated control patients are the first 12 patients on the left corner of the figure.
The sedated patients are found on the right side. The time is expressed in z-axis:
S1-S3;
before operation
S4-S5;
local anaesthesia
S6-S10; surgery
S11-S15; recovery
S16-;
the next morning
Heart rate variability (total power)
10
9-10
9
8-9
7-8
7
6-7
6
5-6
5
S19
4
S13
3
33
25
29
17
21
9
patients
4-5
3-4
2-3
S7
13
1
2
5
total pover
8
S1
179
Challenges
4.1.5 DISCUSSION
reference group. The anxiety of nonsedated patients was a possible cause
for the poorer performance of the
reference group, but because this
survey was not a controlled clinical
trial and no statistical significance
could be detected, the result is mainly
suggestive. Moreover, no ST-segment
depression indicating hypoxia was
detected although several correction
manoeuvres of oxygen level were
performed in the study group, not
even in cases who needed long-term
recovery postoperatively. Thus no
need for ECG monitoring during
dental treatment under intravenous
sedation was discovered.
4.1.5.1 Cardiac occurrences
Psychological and physiological
changes
and
pharmacological
treatments during dental surgery have
effects on circulatory and respiratory
functions.
The
regulatory
mechanisms,
especially
the
autonomic nervous tone, are altered.
Pain and anxiety can cause direct
sympathetic activation. Changes in
the normal breathing frequency and
the tidal volume affect cardiac vagal
input, which can be observed in
reduced respiratory sinus arrhythmia.
Local anaesthetic drugs containing
epinephrine have direct systemic
effects on the autonomic nervous
system changing the balance toward
sympathetic activation. Also, sedative
drugs have significant effects on the
regulation
of
respiration
and
circulation. Since the impairment of
cardiac vagal modulation has been
found to be associated with the
electrical instability of the heart, also
in dental surgery, susceptibility to
arrhythmias is in theory increased.
However, this survey shows that
sedation rather
prevents
than
provokes arrhythmias, especially the
amount of ventricular premature
complexes. Although no statistical
significance could be found between
the groups, not even in the
peroperative occurrences (p=0.15),
the most important finding is that the
study group did not show any signs of
poorer
performance
than
the
4.1.5.2 Pulse
Cioffi et al. (1985) concluded that
routine restorative dental care with
lidocaine and epinephrine local
anaesthesia did not produce a
clinically important haemodynamic
response despite an increase in
epinephrine levels. Frabetti et al.
(1992) also found that patients who
underwent surgical treatment had
higher heart rate values than patients
who underwent conventional therapy.
Patients with muco-gingival surgery
had the mean heart rate values of one
hundred per minute while a group
with scaling and root planing had the
mean heart rate values of 78 beats per
minute. According to a previous
study by the author, the mean pulse of
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
the patient elevates from 70 beats to
86 beats per minute after the injection
of epinephrine containing local
anaesthetics (Survey 2). Meyer
(1987) also found that the increase of
heart rate and the alterations of blood
pressure were different in a group
with extraction than in a group
undergoing local anaesthesia only,
and that they are possibly an
expression of an endogenous
catecholamine release as a result to
stress and not to a pharmacological
effect. He also concluded that
endogenous alternations always take
place in the same way.
1985). The development of the
equipment and analysis programs has
enabled the increased importance of
autonomic nervous tests in clinical
cardiology during the last decade.
Today most cardiologists prefer the
heart rate variability analysis or
baroreflex sensitivity testing to
classical methods when they have to
evaluate the risk for arrhythmia
(Farrel et al. 1992). Clinical studies
have shown that decreased heart rate
variability will forecast higher risk
for sudden cardiac death. This
appears not only in the cases of
medically compromised patients
(Kleiger et al. 1987, Töyry et al.
1996) but healthy people as well
(Tsuji et al. 1994).
Similarly, as in during local
anaesthesia a high heart rate indicates
stress; when we are investigating the
effect of sedation, a lower heart rate
indicates stress relief. In this survey
there was no statistical significance
between the study and reference
groups,
although
there
were
informative differences in the
maximum pulse after surgery. The
stress relief decreased the maximum
pulse of the study group 13 counts
per minute (p=0.08). This is in
harmony with the other finding that
intravenous sedation causes a
decrease in sympathetic activation.
The heart is well-supplied with
both
sympathetic
and
parasympathetic nerves which affect
cardiac pumping in to ways: by
changing the heart rate and through
the strength of contraction. This
stimulation on the S-N node
illustrates the antagonism of these
two systems. Norepinehrine released
from sympathetic nerve endings
stimulates an increase in the
spontaneous rate of forming of the SA
node.
Controversially
the
acethylcholine decreases this rate. If
the heart rate was constant at 72 beats
per minute it could easily be
described at a frequency of 1.2 Hz i.e.
833 ms. Since it is not truly constant,
multiple
frequency
components
comprise its make-up.
4.1.5.3 Heart rate variability
The immediate influence of
sympathetic activation has been
directly linked to a higher risk for
cardiac
arrest
as
has
been
documented with an animal model
(Schwartz et al. 1984, Bilman et al.
In HRV the measurements are
derived from the R-R intervals of the
181
Challenges
ECG, and the connection of these
intervals creates a rhythmic pattern.
Research has demonstrated three
discrete components in the frequency
domain. The first is a low-frequency
component (0.02-0.09 Hz) which
constitutes
the
functions
of
thermoregulation and vasomotor tone
and the renin-angiotensin control
system all mediated by autonomic
nervous
system
(Kitney
and
Rompelman 1977). The increase of
the LF component appears as a
result of parasympathetic activation
(Kamath and Fallen 1993, Malliani et
al. 1991). The second one is a midfrequency component (0.09-0.15 Hz)
as a result of the baroreceptor reflex
and regulation of blood pressure, and
not of interest in this survey. The last
one is a high-frequency (HF)
component (0.15-49 Hz) and derived
from respiration. These frequencies
are present when the heart rate
changes suddenly or as a result of
respiration. Normal respiration rate is
10/min which is 0.17 Hz and this
frequency will transfer into the highfrequency component. Moreover this
frequency seems to be a marker of
sympathetic function (Paganini et al.
1986, Hirsch and Bishop 1981). New
methods for the quantification of
autonomic nervous functions and the
measuring of sympatho-vagal balance
have made it possible to analyse the
significance of these reactions: In this
survey there
were systematic
differences between groups in both of
these parameters and the difference
was even statistically significant in
the
recovery period
(p=0.05)
immediately
after
treatment.
Moreover, there were significant
differences in total power (TP) at all
stages except during local anaesthesia
(p=0.05).
These
observations
indicated that there was a remarkable
increase in parasymphatic and/or
decrease in symphatic activity in the
study group. Moreover, the stress
from local anaesthesia in both groups
and the later stress relief especially in
the study group is visible in figures 24, and in harmony with the finding
that during local anaesthesia the
groups did not differ from each other.
182
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
4.1.6 Clinical conclusions
Intravenous sedation decreases the activation of the
sympathetic component, increases heart rate variability
and decreases maximum pulse, indicating the need of
sedation when cardiac patients are under dental surgery.
The decrease of SaO2 as a result of intravenous
sedation does not cause per- or postoperative
unsatisfactory cardiac occurrences.
No need for ECG monitoring during dental treatment
under intravenous sedation was discovered.
The safety of medically comprimised patients will
increase as a result of stress relief.
183
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
4.2
Study 7:
Stress index
4.2.1 ABSTRACT
In this descriptive study cardiovascular parameters indicating stress during
treatment under intravenous sedation and local anaesthetic alone are described.
Moreover the two local anaesthetic agents (lidocaine and prilocaine) and two
vasoconstrictors (epinephrine and phelypressine) were observed. Amplitude of
pulse wave was the most responsive measurable parameter. Amplitude of pulse
wave diminished just before and during the injection as a result of vasoconstriction
due to psychological stress. Blood flow showed the smallest values during the
injection of local anaesthetic. Similarly, heart rate slightly decreased after the
injection of prilocaine and phelypressine, but pulse rate increased after the
epinephrine-containing lidocaine injection. Controversially both parameters
increased after the injection of sedative agent: Pulse rate a little but amplitude of
pulse wave showed a remarkable increase. To estimate the value of generic stress, a
new index, the stress index was developed. When a subject suffers from generic
stress, we can measure most significant cardiovascular changes, such as rising pulse
rate and diminishing amplitude of pulse wave. By dividing the pulse rate by the
amplitude of pulse wave (pulse / blood flow), a sensitive estimator for the stress is
acquired, namely the stress index.
causes more changes in the
cardiovascular system (Hirota et al.
1992). Most studies have not noted
any severe changes in heart rate or
blood pressure when a local
anaesthetic is used with epinephrine
(Davenport
et
al.
1990).
Montebugnoli et al. (1990) found that
there were no significant differences
in cardiovascular response when a
group of patients under non-specific
4.2.2 INTRODUCTION
It is important to identify the ideal
balance of pain and anxiety relief
when anxious patients are treated
under intravenous sedation. The
safety of epinephrine with dental
local anaesthesia is well known.
Epinephrine-containing lidocaine has
little effect on haemodynamics, while
norepinephrine-containing lidocaine
185
Challenges
stress were given an anaesthetic with
or
without
epinephrine.
The
cardiovascular response during dental
stress may not be associated with the
use of epinephrine in an anaesthetic
solution. Individual reactions seem to
dominate
in
certain
cases
(Montebugnoli et al. 1990, Meyer
1990). The increase in heart rate is
reported to be rare and never by more
than 10 beats per minute (Frabetti et
al. 1992). However, every clinically
experienced dentist knows that
sometimes patients will develop
unpleasant
tachycardia
if
an
anaesthetic containing epinephrine is
used.
effects of surgical stress on changes
in polymorphonuclear leukocyte
elastase (PMNE) levels; Poon (et al.
1995) have studied plasma corticol
levels as well as catecholamine and
glucose levels. Even beta-endorphin
release has been found to indicate
stress during surgery (Acosta et al.
1995). All of these methos need a
blood sample and are therefore not
suitable for dental practice because of
lack of hospital blood laboratory. An
example of noninvasive methods is
the ascorbyl free radical monitored by
electron spin resonance spectroscopy
(Pietri et al. 1994). This method
could be of great value in clinical
practice in hospitals during e.g. open
heart surgery, but it is absolutely
impossible to apply in a dental
practice.
But how to measure the level of
stress? We do have many indicators
for stress. High systolic blood
pressure, high pulse, and cold fingers
(peripheral vasoconstriction) have
been the most frequently used signs
of stress. However, they are
sometimes contradictory because the
body tries to keep the homeostasis: a
change in one parameter will cause a
compensatory change in another
parameter. Thus many attemps have
been made to develop indicators for
stress even during the last years.
Noshima (et al. 1997) examined the
Aim of the study
The aim of this study was to
discover whether sedative agents or
vasoconstirctor
containing local
anaesthetic agents have any effects on
cardiac parameters indicating stress
when observed with pletysmographic
pulse oximetry.
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
4.2.3 PATIENTS AND METHODS
4.2.3.1 Study design
4.2.3.2 Monitoring
This paper is a retrospective
descriptive review of patient records
of two individual study groups.
There were many differences between
patient preparation, cannulation and
intravenous infusion and local
anaesthesia i.e. in the underlying
factors. The first study group
comprised the authors’ private
practice patients who had an
operation under intravenous sedation
with local anaesthesia. These patients
were monitored with Datex Satlite
Trans pulseoximeter. The second
study group is formed of dental
students who had a course exercise of
local
anaesthesia.
Their
cardiovascular
parameters
are
monitored with Datex Cardiocap.
Both
equipment
allowed
the
monitoring of the level of amplitude
of pulse wave. It is important to
understand that this study was not a
controlled clinical trial but a clinical
follow-up of normal treatment or
exercise periods. Later revised
databases formed the study material.
Thus there was no indication of
approval by an institutional review
board
governing
human
experimentation. Moreover, this
study is completely descriptive, no
statistical analysis in performed.
During measuring the patients of
the first group were monitored with
SATLITE TRANS TM (Datex,
Helsinki Finland) This pulse oximeter
is a stand-alone, non-invasive, arterial
oxygen saturation monitor. It gives
continuous, real-time SaO2 and pulse
rate readings. Follow-up information
is available through both the analog
and digital output ports.
The subjects of the second group
were
monitored
using
a
CARDIOCAP II CH-S (Datex,
Helsinki Finland) multiparameter
physiological monitor. This pulse
oximeter is a stand-alone, noninvasive, arterial oxygen saturation
monitor which can also monitor ECG
and blood pressure. It gives
continuous, real-time SaO2 and pulse
rate readings. Follow-up information
is available through both the analog
and digital output ports.
Both pulse oximetric equipment
function using light which is
generated in the finger probe and
passes through the tissues. The total
absorption of the light depends on the
absorbing
components:
tissues,
venous blood and the pulsating
arterial blood. Different amounts of
light are absorbed by oxygenated
haemoglobin
(HbO2)
and
unoxygenated
or
reduced
haemoglobin (Hb). The oximeter
187
Challenges
measures the relative absorption by
Hb and HbO2 of red light at 660 nm
and infrared light at 910 nm in
Cardiocap. Ohmeda uses 660 and 949
nm wavelengths. These two different
forms of haemoglobin allow different
amounts of light to pass through at
these wave lengths. The oximeter
converts this relative light intensity
information into arterial oxygen
saturation values.
4.2.3.3 Patients
The first study group is based on
the retrospective review of patient
records comprising 26 registrations of
26 of the author's private outpatients
who underwent dental operations
under intravenous sedation with local
anaesthesia. Patients had some oral
surgical operations or they underwent
large conservative dental treatment or
extraction under sedation because of
dental care phobia. From this base
group five patients were selected and
their parameters combined to
represent the changes. These cases
were selected because the time table
of the different parts of their
treatments were identical enough and
their amplitude of pulse wave was on
a sufficient level. The treatment was
divided into five periods as described
in table 1. The maximal pulse rate
was determined during every period.
The pulsation of the arterial blood
flow modulates the light passing
through it, and the oximeter converts
this light intensity information into
pulse rate values, which are presented
together with SaO2 values on a
monitor screen. The pulse wave is
derived from the intensity of the
transmitted light. The pulsating blood
flow in the finger is the result of left
ventricle contraction of the heart,
which fills the vascular bed of the
finger with arterial blood. It is
important to understand that the pulse
wave reflects changes in blood
volume, not changes in blood
pressure.
During the first examination, the
patients completed a questionnaire on
previous and present illnesses,
allergies and medications. A dental
care plan was drawn up and all the
patients were referred to radiological
examination (orthopantomography).
The patients were advised both
verbally and in writing on how to
prepare for intravenous sedation (for
example, no food or drink for four
hours prior to treatment).They were
in good health and had no severe
systemic
diseases
(in
the
classification of American Society of
Anaesthesiology ASA I - II i.e. no
The monitors were connected
directly to the serial port of a Toshiba
T1000SE portable computer for realtime collection of data by a collection
program ("KERÄÄ" by Dr Matti
A.K. Mattila). The program recorded
numerical values from Cardiocap at
10 seconds intervals.
A finger probe was used for pulse
oximetric registration, i.e. blood
oxygen saturation (SaO2). The probe
was placed on the subject's right
middle finger.
188
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
systemic diseases or only a moderate
disease which does not limit activity).
pulse oximeter initiated before the
insertion of a peripheral venous
cannula. After the insertion of the
cannula, an infusion of 0.9% sodium
chloride solution was started, and the
sedative agent was then applied with
disposable syringe using the slow
injection technique. The treatment
room was equipped with dental unit,
pulse oximeter, oxygen supplement
unit and some resuscitation facilities,
including endotracheal intubation
equipment and medication for
cardiopulmonary resuscitation. All
treatments were carried out by the
same dentist, i.e. the author.
The
second
study
group
consisted of twenty dental students.
The students were between 19 and 31
years of age with a mean age of 22.5
years (SD 3.22); 80 % were females.
Each person accepted in the test
group had to be healthy and free of
any surgical risk corresponding to the
ASA
(American
Society
of
Anaesthesiologist) I or II groups. Oral
contraceptives were the commonest
medication (three of females). One
subject was undergoing a thyroxin
substitution
therapy
for
hypothyreosis. No other illness or
permanent medication was reported.
4.2.3.5 Local anaesthesia
The study was done during a
normal local anaesthesia course for
students.
This
provided
an
opportunity to allow the students to
practice
local
anaesthesia,
to
demonstrate cardiovascular effects
thereto and to collect objective
measurable findings.
In the first study group local
anaesthesia was performed with a
lidocaine-epinephrine
combination
(Xylocain adrenalin 1.8 ml inj. 20
mg/ml + 0.0125 mg/ml, ASTRA) and
a
prilocaine-phelypressine
combination (Citanest Octapressin
1.8 ml inj. 30 mg/ml+0.54
microgram/ml ASTRA). Lidocain
mean 88 mg (range 40-100) and
additional prilocain 60 mg only in
one case.
4.2.3.4 Sedation
Sedation was performed only in
the first study group and midazolam
was used for sedation (Dormicum 5
ml inj. 1 mg/ml Roche), Midazolam
mean 5.7 mg, (range 7-5 mg).
After treatment, most of the
patients (16 cases) received 30 mg
ketorolak (Toradol inj. 30 mg/ml,
Syntex) injection for analgesics via
venous cannula. Blood pressure was
recorded again and the venous
cannula removed. The patients stayed
in the dental chair, and pulse
oximetric monitoring was continued
until bleeding after extraction had
Patients were not given oral
premedication,
sedatives
nor
antibiotics on the day of the operation
or the previous day. Blood pressure
was recorded and monitoring with a
189
Challenges
stopped and until the patients felt
well and were able to walk and get
dressed without help. The patients
left the clinic with an adult escort.
maxilla; the dose was also 4 x 1.8 ml.
The
amount
of
anaesthetic
corresponded to 144 mg of lidocaine
and 90 mcg of epinephrine. The mean
time taken for the injection of the 4
cartridges was 2 min 11 seconds (SD
24.6 seconds) (Table 2).
In the second study group local
anaesthesia was performed with a
lidocaine - epinephrine solution
(Xylocain adrenalin 1.8 ml inj. 20
mg/ml+12.5 mcg/ml ASTRA) and a
prilocaine - phelypressine solution
(Citanest Octapressin 1.8 ml inj. 30
mg/ml+0.54 mcg/ml ASTRA). The
doses were 80 mg lidocaine and 120
mg prilocaine. The site of injection
was the upper jaw, the buccal sulcus
just distal of the second upper molar.
Both sides of the maxilla were
anaesthetised. This site was chosen
because there is room for a large
enough volume of local anaesthetic,
and the trifurcation of the trigeminal
nerve is near the anaesthetised area.
Patients were in a horizontal position
during the infiltration of local
anaesthetic.
4.2.3.7 Statistical methods
The values of amplitude of pulse
wave (A.P.W.) are not suitable for a
statistical analysis in real life
treatment conditions, since they are
too sensitive to external conditions,
e.g. room temperature. Because there
is no solid base level of that
parameter measured from individual
patients, only the means were
calculated and these values are
represented in the graphics, but no
statistical
analysis
has
been
performed. The scheme for the stress
index (S.I.) is:
S.I. = pulse / amplitude of pulse
wave
4.2.3.6 Timing of the procedure
During the appointment, the
subjects received 4 cartridges (4 x
1.8 ml) of Citanest-Octapressin,
corresponding to 216 mg of
prilocaine and 3.89 mcg of
phelypressine, injected submucosally
5 minutes after beginning the pulse
oximetric measurement. The subjects
received two cartridges of CitanestOctapressin to the right side and two
cartridges of the same agent to the
left side. Ten minutes later, they
received two cartridges of Xylocain
adrenalin to both sides of the
Systolic and diastolic BP, pulse,
and SaO2 were measured before,
during and after injection. The
changes were tested using paired ttest or Wilcoxon matched pairs test,
when appropriate. Spearman rank
correlations were calculated to study
whether the individual change in
stress index (=pulse/APW) is
correlated with the change in other
variables. The data were analysed
using SPSS statistical package
(Version 6.1.3).
190
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
Table 1. Treatment periods in which cardiovascular parameters were observed in
the first study group.
Name of period
Description
Duration
1. Waiting (Before)
Patient in the chair before
cannulation
5 - 10 minutes
2. Sedation
After cannulation but before
local anaesthetic injections
5 - 10 minutes
3. Local anaesthesia
Injections of local anaesthetic
agents
5 - 10 minutes
4. Treatment
Operative period: incisions,
drilling, extraction, sealing,
fillings, etc.
15 - 30 minutes
Table 2. Timing of the procedure with each patient in the second study group.
Time (min)
Intervention
0 min
start of measurement
5 min
starting of the first injection: 4 cartridges of Citanest-Octapressin
15 min
starting of the second injection: 4 cartridges of Xylocain adrenalin
25 min
end of measurement
191
Challenges
4.2.4 OBSERVATIONS
In both study groups, amplitude of
pulse wave (A.P.W.) was the most
reactive
of
the
measurable
parameters. Amplitude of pulse wave
observations depend not only on
biological
and
measurement
variations but also on temporal
variations in clinical circumstances.
Standardising the circumstances to
reduce the environmental variations
(e.g. room temperature) or to include
these circumstances as covariates was
not possible during the treatments or
during a local anaesthesia course, and
therefore the findings should be
regarded as tentative.
by amplitude of pulse wave (pulse /
blood flow), and a new index, the
stress index was obtained. This is a
very responsive estimator for stress.
The stress index (pulse rate/A.P.W.)
shows the maximal effect of stress
relief 5- 15 minutes after the injection
of benzodiazepine in the first study
group. Local anaesthesia and
treatment will increase stress. After
the injection of lidocaine-epinephrine
there was an additional stress period
5 - 10 minutes later as the
epinephrine began to spread to the
blood stream from the injection area.
Epinephrine induced stress relieved
approximately 20 minutes after first
injection. Three stress peaks were
found: cannulation, the epinephrine
reaction and the treatment. (fig 1,
table 3) Similarly, in the second study
group the prilocaine-phelypressine
injection had only one stress point: at
the moment of injection, but after the
injection of lidocaine-epinephrine,
there was an additional stress period
5 - 10 minutes later, when the
epinephrine began to spread to the
blood stream from the injection area
(fig 2, table 4). No end point of
epinephrine induced stress is visible
in the figure, because the measuring
was stopped 10 minutes after the
lidocaine-epinephrine injection.
A.P.W. will rise after the injection
of benzodiazepine and afterwards the
local anaesthesia will cause some
vasoconstriction. A single dose of
benzodiazepine produced an effective
vasodilatation which remained for 45
minutes in the first study group. In
general A.P.W. decreased towards the
injection due to psychological stress.
Blood flow showed decreasing values
during and after the injections of
local anaesthetic. Similarly, in the
second study group the blood flow
showed the smallest values during the
injection of local anaesthetic with
both methods (fig 2). The difference
in baseline-levels, a decrease of 8
units, can be interpreted as a
consequence of reduced stress.
The statistical test of the stress
indicating parameter (tables 5-7)
showed
that
no
statistically
significant indicator is available.
To estimate the value of stress, the
pulse rate (fig 1 and 2) was divided
192
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
Only the stress index may be trend
setting. Although there is a
correlation in changes in other
parameters vs. stress index (table 8),
the level of change is without clinical
significance.
193
Challenges
Fig 1. Stress index after the injection of midazolam. Stress index is calculated by
dividing the pulse rate by the amplitude of pulse wave. Five measurements are in
combination so that the injections of midazolam occur at the same time; two
minutes after the beginning. The cannulation is clearly visible at the left corner.
Lidocaine and epinephrine are injected 15-30 minutes later i.e. in the left mid
portion of the 46 minutes scale. The effect of treatment remains for 30-46 minutes.
Stress
Figure 1
4,5
4,0
3,5
3,0
2,5
2,0
1,5
1,0
0,5
0,0
sedation
2
4
6
local anaest.
treatment
8 10 12 14 16 18 20 22 24 26 28 30 32 34 36 38 40 42 44 46
Time
194
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
Fig 2. Stress index during local anaesthesia. Prilocaine-phelypressin is injected
five minutes and lidocaine-epinephrine 15 minutes after the beginning. Both
injections are visible in the curve but the later injection caused a constant elevation
of the value.
F ig u r e 2
Stress
4 ,5
4 ,0
3 ,5
3 ,0
2 ,5
2 ,0
1 ,5
1 ,0
0 ,5
0 ,0
0
1
2
3
4
5
6
7
8
9
10 11 12 13 14 15 16 17 18 19 20 21 22 23 24
T im e
195
Challenges
Table 3. Heart rate, amplitude of pulse wave and stress index after the injection
of midazolam. Stress index is calculated by dividing the pulse rate by the amplitude
of pulse wave.
Time
(Min)
2
4
6
8
10
12
14
16
18
20
22
24
26
28
30
32
34
36
38
40
42
44
46
Period and effect
Cannulation
Injection of sedative
Sedative effect
Sedative effect
Sedative effect
Sedative effect
Sedative effect
Sedative effect
Local anaesthesia
Epinephrine effect
Epinephrine effect
Epinephrine effect
Epinephrine effect
Epinephrine effect
Treatment begins
Operation effect
Operation effect
Operation effect
Operation effect
Operation effect
Operation effect
Operation effect
Operation effect
Pulse
Mean
79,0
86,8
88,0
86,3
84,2
84,1
85,0
83,2
85,7
86,0
86,7
87,2
85,5
86,2
89,4
90,0
90,3
89,1
87,5
87,2
86,9
84,0
83,0
196
A.P.W.
Mean
28,5
46,5
65,7
74,3
83,7
82,7
84,1
80,9
66,0
52,0
48,8
55,9
52,7
52,5
33,3
36,4
43,9
37,5
40,5
38,2
30,8
30,5
27,3
Stress
Index
Mean
2,8
2,0
1,3
1,2
1,0
1,0
1,0
1,0
1,3
1,7
1,8
1,6
1,7
1,7
2,7
2,5
2,1
2,4
2,2
2,3
2,9
2,8
3,1
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
Table 4. Heart rate, amplitude of pulse wave and stress index during local
anaesthesia. Stress index is calculated by dividing the pulse rate by the amplitude of
pulse wave.
Time
(Min)
0
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
Period and effect
Waiting
Waiting
Waiting
Waiting
Waiting
Injection of prilocaine
Phelypressine effect
Phelypressine effect
Phelypressine effect
Phelypressine effect
Phelypressine effect
Phelypressine effect
Phelypressine effect
Phelypressine effect
Phelypressine effect
Injection of lidocaine
Epinephrine effect
Epinephrine effect
Epinephrine effect
Epinephrine effect
Epinephrine effect
Epinephrine effect
Epinephrine effect
Epinephrine effect
Epinephrine effect
Pulse
Mean
A.P.W.
Mean
76
77
76
79
79
76
74
72
73
74
74
73
74
75
76
76
77
82
86
88
87
86
85
84
84
40
40
37
34
32
22
25
32
35
32
27
28
27
25
20
20
21
21
22
23
23
22
21
22
20
197
Stress
index
Mean
1,9
1,9
2,1
2,4
2,5
3,5
3,0
2,3
2,1
2,3
2,7
2,6
2,8
3,0
3,9
3,9
3,7
3,9
3,9
3,8
3,8
4,0
4,0
3,8
4,2
Challenges
Table 5. Systolic and diastolic blood pressure, pulse, Sao2, APW, and stress
index 2-3 minutes before injection, during injection and after injection.
A:
B:
C:
Before injection of During injection of After injection of
local anaesthetics local anaesthetics
local anaesthetics
Systolic BP
125 SD 10.9
125 SD 14.5
126 SD 13.2
Diastolic BP
71.3 SD 8.4
71.0 SD 7.8
70.7 SD 7.1
Pulse
76.5 SD 16.1
76.2 SD 15.1
72.4 SD 15.1
SaO2
97.4 SD 0.99
97.1 SD 1.2
97.4 SD 0.8
APW
23.0 SD 22.7
22.9 SD 23.9
27.3 SD 25.7
3.3 SD 11.7
7.8 SD 8.4
5.6 SD 4.3
Stress index
Table 6. Mean changes in systolic and diastolic BP, pulse, Sao2, APW, and
stress index from A to B and B to C.
From A to B
p-value
From B to C
p-value*
Systolic BP
-0.05
0.98
+0.65
0.79
Diastolic BP
-0.35
0.86
-0.25
0.89
Pulse
-0.30
0.93
-3.75
0.38
SaO2
-0.25
0.43
+0.30
0.33
APW
+0.1
0.99
-4.4
0.43
Stress index
+4.5
0.43
-2.2
0.12
*) Paired T-test
A, B, C as in Table 5.
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
Table 7. Changes in APW and stress index from A to B and B to C
From A to B
p-value
Median IQR
From B to C
p-value*
Median IQR
APW
-0.50 -13 to 9
0.78
+1.00 -5 to 13
0.45
Stress index
-0.22 -5 to 3
0.77
-1.06 -3 to 0.2
0.09
*) Wilcoxon matched pairs test
A, B, C as in Table 5.
Table 8. Correlation (r, Spearman rank correlation) between the changes in stress
index versus the changes in other variables
Stress index vs. from A to B
p-value
r
from B to C
p-value
r
Systolic BP
-0.12
0.63
+0.61
0.004
Diastolic BP
-0.48
0.03
+0.44
0.05
Pulse
-0.33
(0.15)
+0.22
(0.21)
SaO2
+0.15
0.53
-0.07
0.78
APW
-0.74
-0.78
(<0.0001)
(0.0002)
(In brackets: result of the scheme of the stress index: Pulse/APW)
A, B, C as in Table 5.
199
Challenges
4.2.5 DISCUSSION
induced
stress
is
visible
approximately 20 minutes after the
first injection. It can be concluded
that local anaesthesia and treatment
increase stress.
4.2.5.1 Stress during treatment
Under generic stress of any
subject we can measure the most
significant changes in a rising pulse
rate and the decrease of A.P.W. A
good indicator for evaluating stress
during operation is the "stress index"
i.e. pulse rate per A.P.W.. The stress
index shows the maximal effect of
stress relief 5- 15 minutes after
injection of benzodiazepine. A single
dose of benzodiazepine produced
effective
vasodilatation
which
remained for 45 minutes. This amount
of time is sufficient for unpleasant
manoeuvres in dental treatment.
Observing the A.P.W. enables the
dentist to notice that there is
constriction in the peripheral arteries
as a result of psychological stress:
The elevation in the heart rate due to
exogenic as well as endogenic
epinephrine during and after the local
anaesthetic injection was clearly
visible.
Blood
flow
showed
diminishing values during the
injection of local anaesthetic before
any possible cardiovascular effect,
and similarly later after the injection
as a result of these cardiovascular
occurrences. It is assumed that the
reason for the first change was the
psychological stress before injection.
After the injection of lidocaineepinephrine there was an additional
stress period 5 - 10 minutes later
when the epinephrine began to spread
to the blood stream from the injection
area. The end point of epinephrine
4.2.5.2 Amplitude of pulse wave
(A.P.W.)
Observing the amplitude of pulse
wave enables the dentist to notice
constriction in the peripheral arteries
as a result of psychological stress:
The blood flow of the finger shows
diminishing values before the
injection of local anaesthetic i.e.
before any possible cardiovascular
effect. A pulse oximeter probe is
usually placed on a finger; other
alternatives are toe or earlobe. These
alternative locations are equally
suitable as a finger when measuring
oxygen saturation and pulse rate, but
they do not indicate the reactions in
the pulse wave amplitude. In general,
peripheral arteries in fingers react to
painful stimuli much stronger than
arteries in other places (Mattila et al
1990). However, the finger causes
serious problems as a site for
measuring because the deviations of
the detected values will increase to a
levels which fade out of statistical
significance (table 5).
Quite naturally, the absorption of
infrared light is relative and
dependent on the thickness of the
finger being different in individual
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
fingers. Consequently the reliability
of the pulse wave amplitude
recording requires that the recording
site is not changed. Because of the
relativity of amplitude it is important
to have a basis for comparison
(Mattila et al 1989). In practice this
means that when monitoring sedation,
recording should be started before
cannulation.
injection of a sedative agent, as a
result of feeling good. The amplitude
of the pulse wave is the most
informative indicator of changes in
circulation, and CARDIOCAP II CHS allows us to observe this parameter.
An observation of the amplitude
of pulse wave might reveal that there
is a constriction in the peripheral
arteries resulting from psychological
stress. The blood flow in this study
showed the smallest values during the
injection of local anaesthetic, before
any possible cardiovascular effect.
The
author
has
observed
vasoconstriction in patients if the
treatment is carried out in a cool
operation room, where patients may
feel cold. This also has a closing
effect on peripheral arteries, which
may often cause measuring failures
due to a low signal (Survey 3). Pulse
oximetric measuring seems to work
properly only in cases where the
patient is comfortable. However, a
few false desaturation registrations in
pulse oximetry obviously do not harm
the patient, and possible measuring
failures do not allow us to abandon
patient monitoring in the operation
theatre.
Some confusion seems to exist
between direct arterial blood pressure
and visible pulse wave because they
are very similar in shape. Their
information is, however, totally
different. A visible pulse wave means
practically that blood is circulating in
the site of measurement. During
normal sinus rhythm consecutive
pulse waves are uniform, but during
arrhythmia they can continuously
vary in size and shape. In fact, these
observations can be applied also to
evaluate the importance of that
particular arrhythmia for circulation
(Mattila et al 1989, Mattila 1990).
4.2.5.3 Amplitude of pulse wave
and the measuring equipment
The regulation of peripheral
arterial circulation is under the
control of the autonomic nervous
system. Vasoconstriction is induced
by a stimulation of the smooth
muscles of arterioles. This decreases
the amplitude of the pulse wave and
may be due to some discomfort such
as pain, fear, low temperature or
hypovolaemia. Rapid and strong
vasodilatation is often seen after the
In most other pulse oximeters
these changes in amplitude are
automatically corrected before being
shown in the display. This, of course,
helps the operator, because no manual
correction is needed, but at the same
time one very informative parameter
is lost when anxious patients are
being treated. Other parameters, for
example the crest time and closing
201
Challenges
time of the aortic valve, are available
on screen, and even some arrhythmia
can be verified.
the finding of Veit et al. (Veit et al.
1993) where maximum ST-segment
depression (indicating hypoxia in
cardiac
muscle)
in
the
electrocardiogram was recorded 11
minutes after infiltration. Moreover,
in survey 2 there was different baselevel in the stress index in methods 1
and 2. This can be explained with the
reduced level of fear on the second
exercise appointment.
4.2.5.4 Stress index
There was a clear elevation in the
heart rate due to exogenic and
endogenic epinephrine during and
after the local anaesthetic injection. It
is assumed that the reason for this
was psychological stress before
injection and the relief of the stress
after injection. To estimate the value
of the physiological stress, a new
index, the stress index was developed.
When a subject suffers from generic
stress,
the
most
significant
cardiovascular changes can be
measured, such as rising pulse rate
and diminishing amplitude of pulse
wave. However, the values of
amplitude of pulse wave are too
sensitive to external conditions and to
the variation of the basic levels of this
indicator
between
patients.
Consequently the "the stress index" is
only a descriptive indicator and it is
useful only when we want to measure
the changes of the sympathetic status
of one individual patient. The
prilocaine-phelypressine injection had
only one stress point: at the moment
of injection. After the injection of
lidocaine-epinephrine, there was an
additional stress period 5 - 10 minutes
later, when the epinephrine began to
spread to the blood stream from the
injection area. The end point of
epinephrine induced stress could not
be determined because the follow-up
time was too short. This may explain
During treatment the stress index
shows the maximal effect of stress
relief 5- 15 minutes after the
injection of benzodiazepine. A single
dose of benzodiazepine produced an
effective
vasodilatation
which
remained for 45 minutes. This time
is
sufficient
for
unpleasant
manoeuvres in dental treatment.
Observing the A.P.W. enables the
dentist to notice the constriction in
the peripheral arteries as a result of
psychological stress: The elevation in
the heart rate due to exogenic as well
as endogenic epinephrine during and
after the local anaesthetic injection
was clearly visible. Blood flow
showed decreasing values during the
injection of local anaesthetic before
any possible cardiovascular effect,
and similarly later after injection as a
result of these cardiovascular
occurrences. It could be assumed that
the reason for the first change was the
psychological stress before injection.
After the injection of lidocaineepinephrine there was an additional
stress period 5 - 10 minutes later
when the epinephrine began to spread
to the blood stream from the injection
area. The end point of epinephrine
202
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
an operation or treatment with the
stress index, i.e. pulse rate per
amplitude of pulse wave. But the
equipment itself does not express this
parameter. Thus it needs calculations
during treatment, which decreases the
clinical value of this parameter.
induced
stress
is
visible
approximately 20 minutes after the
first injection. But is it possible to
conclude the self-evident fact that
local anaesthesia and treatment
increase stress when observed with
some cardiovascular parameter? To
test this hypothesis, a statistical test
of the stress indicating parameter
(tables 5-7) was performed. The test
included three observation periods:
before, during and after injection. It
could be assumed that there should be
some increase of stress during
injection and some relief after it. The
test showed that no statistically
significant indicator for stress is
available. Only the stress index may
be trend setting (p=0.09). Although
there is correlation in changes in
other parameters vs. stress index
(table 8), the level of change is
without clinical significance.
This study was not a clinical trial,
but two clinical follow ups with two
individual study designs. Moreover,
there were differences in the
underlying factors and the study was
non-randomised. Therefore it is not
justified to conclude that we should
always monitor the stress of the
patient. However, this study showed
that it is possible measure the level of
stress, and this may be necessary
when
medically
compromised
patients
are
under
treatment.
Therefore further research is needed
to validate the new stress index.
It can be concluded that it might
be possible to evaluate stress during
203
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
4.2.6 Clinical conclusions
The best indicator for evaluating stress with pulse
oximeter during an operation or treatment is amplitude of
pulse wave or stress index, i.e. pulse rate per amplitude of
pulse wave. The problem is that there is no constant base
level; during the operation the elevation of the index is
only an indicator.
This study showed that it is possible to measure the
level of stress, and this may be necessary when medically
compromised patients are treated. Stress itself is not an
adverse reaction but often predominates them.
205
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
4.3
Study 8:
Complicated cases
4.3.1 ABSTRACT
This case study describes cases of the early detection of hypoxia with pulse
oximeter during intravenous sedation with local anaesthesia. These patients are
selected from previous two study groups which are further described in studies 1
and 6. The first signs of hypoxia were seen through pulse oximetry.
In the first study group, two of the patients were treated with a surgical operation
and one patient underwent a large conservative dental treatment under sedation
because of dental care phobia. During the dental treatment period, external oxygen
was added for all the three patients to avoid more complications as a result of
hypoxia. Two of the patients also received an injection of benzodiazepine
antagonist. One patient needed further follow-up but none of the patients developed
additional complications. As a conclusion, pulse oximetric monitoring was
discovered extremely sensitive as a predictor for coming complications as well as
allowing early intervention in ventilation problems.
In the last study group, five cases were found who developed long-standing low
oxygen saturation levels which were detected with pulse oximeter. Three cases were
solved by administering supplementary oxygen and/or benzodiazepine antagonist.
However, two cases needed a long period of recovery afterwards. The lowest SaO2
levels of these patients were found during the postoperative period. Attempts were
made to solve the problems related to hypoxia by administering supplementary
oxygen, benzodiazepine antagonist and ventilation stimulates but without any
improvement. The role of poor amplitude of pulse wave in these cases is discussed.
207
Challenges
4.3.2 INTRODUCTION
Hardeman et al (1990) have found
that twenty percent of sedated
patients
experienced
hypoxic
episodes in the postanaesthetic
recovery unit when no supplemental
oxygen was administered. Only three
percent of patients who received
supplemental oxygen had episodes of
hypoxia. They recommended the use
of supplemental oxygen for all
patients undergoing intravenous
sedation. Short episodes of hypoxia
may be of little consequence in
healthy patients (Rodrigo and
Rosenquist
1988),
but
in
compromised patients early detection
may avoid serious complications.
The principal aim of monitoring
during procedures is patient safety. It
is not so much a question of "life or
death" but of the quality of care in
general. Many of the principles in
monitoring
accepted
in
the
anaesthesia for general surgery can be
applied also in dental operative care.
Patient monitoring is used in order to
detect dangerous deviations from
normal in circulation and respiration.
These complications may be due to
therapeutic procedures or the
medication used, but they can also
result from a deterioration of the
patient’s own organic disease. It
should be extremely important to
recognise these occurrences in due
time, to be able to make right
conclusions for beginning correct
therapeutic manoeuvres. On the basis
of these observations and conclusions
the surgeon is also able to adequately
inform the patient on the event.
Without appropriate monitoring these
goals can certainly not be reached.
Aim of the study
The aim of this study was to
describe hypoxia cases, their causes
and the necessary treatments after this
most recurrent complication.
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
4.3.3 PATIENT MANAGEMENT AND METHODS
The three first cases were selected
from the material of the first study.
The other cases are from the original
unselected patient material of survey
6. Two years fall between these
treatment periods, and much had been
learned but the complications were
there like they always are. However,
pulse oximetric equipment was still
the same: Ohmeda Biox 3740.
detected with pulse oximeter and
which forced the sedationist to make
corrective manoeuvres. In most cases
mild respiratory depression was
corrected with intravenous flumazenil
postoperatively (five patients). Three
of the subjects had received
supplementary oxygen previously
during the procedure. Two of these
needed
a
long-term
recovery
afterwards.
Five cases in the last study group
(survey 6) developed long-standing
low oxygen saturation which was
209
Challenges
4.3.4 OBSERVATIONS
4.3.4.1 CASE 1. FIG. 1
The patient was a 28 years old female student who had a medication of
amitriptylin hydrochloride (Pertriptyl, ORION) and tematsepam (Tenox, ORION)
for depression. She also had atopic eczema without any medication. Moreover, she
was highly overweight (160 cm, 98 kg) and a cigarette smoker. She underwent a
large cariological and periodontological therapy with intravenous sedation. At first
she received 20 mg diazepam without any sedative effect. The dose was duplicated
with a low sedation effect. Before medication the SaO2 was 95%, and after 92%.
External oxygen (3 l/min) was added during the dental treatment period. After
treatment the nasal oxygen cannula was removed and the SaO2 fell to the level of
88%. As a result, the patient received a 0,5 mg injection of flumazenil and another
0,5 mg with isotonic NaCl infusion during the following hours. After the patient had
received the previously mentioned amount of benzodiazepine antagonist, SaO2
remained within normal limits. The patient spent the following night under nurse
supervision and connected into the pulse oximeter.
Figure 1
210
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
4.3.4.2 CASE 2. FIG. 2
The next patient was a 45-year old female housekeeper, 56 kg in weight, without
any disease or medication. The treatment was an implantation into the right side of
the upper jaw with a sinus lift operation, and into the molar area in the right side of
the mandible with a revision of the mandible nerve. 7,5 mg midazolam was used for
sedation. After 10 minutes the SaO2 fell under 90%. 40 minutes late, external
oxygen was added and 0,5 mg flumazenil was injected. 40 minutes later again,
while the mandibular nerve was prepared, the saturation suddenly decreased to a
level under 80%. The patient was again medicated with 0,5 mg flumazenil; as a
result the SaO2 rose extremely quickly back to 100%. The patient left the clinic
with adult supervisor after the treatment.
Figure 2
211
Challenges
4.3.4.3 CASE 3. FIG. 3
The last patient was a 81-year old female pensioner ( 64 kg ) without any
medication or known disease. Some previous operations had been done. The
operation this time (1993) was an implantation into the anterior area of the lower
jaw. The dose of the sedative agent was 2.5 mg midazolam. The patient fell
immediately into deep sleep. External oxygen was added again; as a result, the
saturation of oxygen in blood rose from 83% to 97%. After one hour the operation
was over and the oxygen cannula removed without any complications.
Figure 3
212
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
4.3.4.4 CASE 4 FIG 4
The patient was a 24-year old female barkeeper, 60 kg in weight, suffering from
some undiagnosed chronic nasal problems without medication. She expressed a fear
of the operation. She underwent a third molar surgery combined with an upper front
teeth implantation under intravenous sedation. At first she received 8.0 mg
midazolam with normal sedative effect. During the dental treatment period, one and
a half hours after premedication, external oxygen (3 l/min) was added. After the
treatment the SaO2 fell under the level of 90%. As a result, the patient received a
0,5 mg injection of flumazenil and another dose of 0,5 mg with an isotonic NaCl
infusion during the following hour. After the patient had received the previously
mentioned amount of benzodiazepine antagonist, SaO2 still remained below normal.
She was then given a slow injection of 0.25mg salbutamol with no effect. The
patient spent the following 8 hours under nurse supervision, connected into the
pulse oximeter in the local hospital. She was domesticated before night. The
possibility of peripheral vasoconstriction remained open.
Case 4
100
90
Pulse and SaO2
80
70
60
SaO2
50
Pulse
40
30
20
10
0
Tim e
213
Challenges
4.3.4.5 CASE 5 FIG. 5
The patient was a 20-year old female student, 54 kg in weight, without any
disease or medication, but she had considerable dental care phobia. The treatment
was a third molar operation. 8 mg midazolam was used for sedation. There were no
problems or complications during the treatment. After the operation, one hour later,
the SaO2 fell under 90% and external oxygen was added. 0,5 mg flumazenil was
injected and another dose of 0,5 mg with an isotonic NaCl infusion during the
following hour, without any improvement of measured low oxygen saturation level.
She was then given a slow injection of 20 mg doxapramic hydrochloride
(respiratory stimulant) without any effect. A diagnosis of peripheral
vasoconstriction was done because the equipment showed a low signal and neither
the flumazenil nor doxapramic corrected the saturation values. Although the SaO2
remained at 86-87%, the patient was fully ordinated and felt in good condition of
health. In conclusion, the symptoms appeared after operation but they did not
complicate the procedure. The only real problem was the need of long-term
recovery. After the treatment the patient stayed in the dental chair, and pulse
oximetric monitoring was continued until all attempts to correct the oxygen
saturation were shown to be ineffective. The patient desired to be sent home and she
left the clinic under adult supervision.
Case 5
140
Pulse and SaO2
120
100
80
SaO2
60
Pulse
40
20
0
Tim e
214
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
It is possible to cancel sedation
with flumazenil
and a fall in saturation
can be corrected by administering
supplementary oxygen.
215
Challenges
Figure 6. The range of saturation in the described cases as a percentage of total
time.
Figure 6
35 %
30 %
20 %
15 %
Case
Case
4
Case
3
Case
2
5
84
86
88
90
94
0%
92
SaO2
96
5%
98
100
10 %
216
Case
1
Percent
25 %
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
Table 1. The range of saturation in the described cases as a percentage of total time.
SaO2
Case 1
Case 2
Case 3
Case 4
Case 5
100
0%
31 %
12 %
4%
6%
99
0%
8%
33 %
14 %
12 %
98
0%
2%
10 %
6%
8%
97
2%
3%
9%
4%
4%
96
6%
10 %
5%
8%
6%
95
6%
9%
11 %
3%
4%
94
16 %
5%
11 %
2%
2%
93
16 %
6%
3%
1%
2%
92
10 %
6%
2%
3%
6%
91
10 %
5%
2%
5%
6%
90
10 %
4%
2%
3%
4%
89
6%
5%
1%
2%
8%
88
11 %
4%
1%
17 %
9%
87
6%
1%
0%
21 %
11 %
86
2%
1%
0%
8%
4%
85
0%
0%
0%
0%
6%
84
0%
0%
0%
0%
4%
217
Challenges
4.3.5 DISCUSSION
the intravenous agent divided into
small parts (1 mg midazolam). This
almost barely effective dose is
repeated every 2 or 3 minutes until a
minor decrease (2 - 3 %) in blood
oxygen saturation is detected. The
incidence of saturation falling to less
than 90% have been between 4% and
40%, depending on the level of
sedation (Tay et al. 1991, Hardeman
et al. 1990).
4.3.5.1 Respiratory problems
and oxygen
Intravenous sedation has been
shown
helpful
in
avoiding
cardiovascular reactions in oral
surgical operations, but there is a
risk of provoking respiratory
depression. This adverse effect can
easily be detected at an early stage,
where the pulse wave and / or a fall
in saturation is signalled visually
and
can
be
corrected
by
administering
supplementary
oxygen. There is also a significant
decrease in the saturation level of
oxygen as the patient progresses from
light to deep sedation. The
intravenous diazepam and midazolam
have been shown to decrease oxygen
saturation by 3% compared to the
preoperative level, when administered
in the average dosages of 6.4 mg and
3.3 mg respectively. (Matthews et al.
1992). However, even unsedated
patients who only have treatment
under local anaesthesia have a small
postoperative
fall
in
oxygen
saturation (Matthews et al. 1992).
Lowe and Brook (1991) have
reported oxygen saturation in the
range of 93-89% in some patients
undergoing third molar removal with
local anaesthetic alone. Ventilation
hazards of intravenous midazolam
may appear in the elderly, and the use
of benzodiazepines with lower
hypnogenic effects is recommended
(Heinze et al. 1992). The author used
Hardeman et al. (1990) found that
20% of sedated patients experienced
hypoxic
episodes
in
the
postanaesthetic recovery unit when
no supplemental
oxygen was
administered, while only 3% of
patients who received supplemental
oxygen had such episodes. They
recommend the use of supplemental
oxygen for all patients undergoing
intravenous sedation in oral surgery.
However, if dental patients are
monitored with pulse oximetry, and
an ultra-slow technique is used with
careful dosage in the administration
of sedative agents, no continuous
oxygen supplement is necessary
routinely
(Read-Ward
1990),
although it should be available. No
routine oxygen supplement was used
with the patients in this study. The
minor decrease in SaO2 was used as a
sign of sufficient sedation during the
initiation of sedation, and oxygen was
added when the 90% level lasted a
long
time.
However,
this
supplementary oxygen did not correct
218
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
the "hypoxia" in every case. In fact,
only in one case of five it was alone
effective.
suffer from dental care phobia are
more confused after treatment than
others and may need flumazenil, the
very patients are possible candidates
for central nervous system related
side effects of this drug. The
confusion will relief by itself during
the following hours but flumazenil
should mainly be used in the cases
of low pulse oximeter values to
diagnose the real condition of the
patient. In these five cases, it was
used four times. In one case the
corrective treatment was successful
and in three cases it enabled to
suspect the wrong detection of
hypoxia.
4.3.5.2 Antidote for correction
the hypoxia
It is possible to cancel sedation
with flumazenil, which appears to be
a promising drug for reversing
midazolam conscious sedation. The
patient who receives flumazenil after
intravenous
midazolam
is
significantly more alert as early as at
5 min following drug administration
(Clark et al 1991). In cases of undue
sedation persisting after dental
treatment, flumazenil in doses from
0.5 to 1.0 mg rapidly reverses the
sedative and amnesic effects of
midazolam without an apparent
evidence of subsequent resedation
(Davies et al 1990). Flumazenil
reverses almost totally the effects of
mental sedation for approximately 2
hours, but not physical sedation or
memory. (Ghoneim et al 1989,
Cooper et al 1991) Flumazenil makes
recovery in the supine position
unnecessary and moreover it is a
drug that should be included in the
armamentarium of any emergency
drug kit when benzodiazepines are
used intravenously (Rosenbaum and
Hooper 1988). This study showed
that flumazenil is needed to remove
confusion in the cases of low oxygen
saturation and to diagnose real
hypoxia from other, vasoactive
problems. However, the clinical
experience of the author has already
shown that, although the patients who
4.3.5.3 Wrong detection of
hypoxia
The highest oxygen saturation of
arterial blood (SaO2) detected in the
patients were of course at the
beginning of measuring. The lowest
SaO2 levels were found some
minutes after the injection of sedative
agents or later during the treatment
period.
The study of White et al. (1989)
showed that nearly half of the
patients
developed
clinically
significant desaturation during minor
oral surgery under local anaesthesia.
They assumed that this might be due
to breath-holding or peripheral
vasoconstriction as a response to
anxiety or fear.
This study may explain those
observations. There may have been
219
Challenges
false alarms as a result of poor
amplitude of pulse wave. False
alarms may explain even Lowe's and
Brook's (1991) finding that every fifth
patient undergoing surgical removal
of third molar with local anaesthesia
alone experienced hypoxic periods
during surgery. The easiest way to
avoid these alarms is to keep the
patient warm by covering him or her
with a blanket which allows better
amplitude of pulse wave. Of course it
is possible to block this autonomic
vasoconstriction reaction with local
anaesthetic
injected
into the
patient’s finger (Eastwood 1992,
Sakurada et al. 1995) but when
treating a scared patient it is
advisable to avoid such painful
operations. Moreover, an alarm delay
lasting 12 to 30 seconds would
prevent most false alarms (Pan and
Gravenstein 1994).
of the pulse wave is the most
informative indicator of the changes
in circulation. (Part I, article 3) In
most equipment - as in this case the
Ohmeda pulse oximeter - these
changes
in
amplitude
are
automatically
corrected
before
expressed in display. This of course
helps the operator as no manual
correction is needed, but at the same
time one very informative parameter
is lost if anxious patients are treated.
And we know that the equipment
needs the pulsating component of the
pulse to work properly. Automatic
correction of the amplitude of pulse
vawe may prevent us to find the
decrease in amplitude of pulse wave
and create wrong trust in the
equipment. This was the problem in
these cases because Ohmeda pulse
oximeter was used. This equipment
does not express the level of A.P.W.,
it only indicates the low quality of
signal.
The regulation of peripheral
arterial circulation is controlled by
the autonomic nervous system.
Vasoconstriction is induced by the
stimulation of smooth muscles of
arterioles. This decreases the
amplitude of pulse wave and may be
due to some discomfort like pain,
fear, low temperature as well as
hypovolaemia. (Mattila et al. 1990)
Vasodilation is often seen after the
dosage of sedative agent as a result of
feeling good. This reveals one
alternative to correct low-signal
problems: To add sedative. But there
is no sedationist who will do this
while the oximeter is warning about
low saturation values. During pulse
oximetric observation the amplitude
In order to reach the quality level
of the individual tailoring of
premedication a simple monitoring
method is needed for the monitoring
and evaluation of patients' anxiety,
the efficacy of premedication as well
as the influences of premedication on
the course of anaesthesia. Michael
Johnstone showed already in 1976 in
his monograph named "Adult
preoperative medication" that pulse
plethysmography can well be applied
for the estimation of premedicant
effects. Despite of its obvious
advantages, plethysmographic pulse
wave was practically used only by
few.
Since
that
time
220
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
plethysmographic
pulse
wave
registration has become available for
most instances, because pulse wave is
an intrinsically essential part of pulse
oximetry recording.
haemoglobin due to medication with
nitrites or even due to smoking habits,
but the described cases, with one
exception (Case 1), did not smoke or
have any medication.
Patients who have higher anxiety
score have smaller pulse wave
amplitude. This difference is seen
also during maximal vasodilatation.
(Mattila et al. 1990) Does this mean
that patients who are anxious of
anaesthesia have different (more
vasoconstriction)
vasomotor
behaviour also during their normal
life? Saumet et al (l986) observed that
changes in skin thermal clearance
correlated well with the amplitude of
the plethysmographic wave. A cold
surrounding can of course partly
account for the vasoconstriction
detected in the patients, but
environmental circumstances were
similar for all patients. The pulse
oximeter may give incorrect SaO2
readings in the presence of abnormal
One explanation for the false
positive detection of hypoxia in
dental operations is the so-called
peripheral cyanosis or Raynaud's
disease; a condition in which the
mechanism
is
peripheral
vasoconstriction
and
delayed
peripheral
circulation
due
to
sympathetic activation. This leads to
the
desaturation
of
capillary
haemoglobin
although
central
circulation is well maintained.
Women are affected five times more
often than men and the age of
presentation is between 20 and 40
years (Wilson et al 1991). This is in
harmony with the authors’ experience
and the fact that all these cases have
been females.
221
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part IV
4.3.6 Clinical conclusion
Intravenous sedation may be helpful in avoiding cardiac
reactions during oral surgery, but there is a risk of
provoking respiratory depression. This reaction can be
corrected by administering supplementary oxygen and/or
flumazenil.
Wrong positive detection of hypoxia appears in
particular situations. Flumazenil should be available in the
cases of low pulse oximeter values to diagnose the real
condition of the patient.
223
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part V
PART V
225
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part V
5 GENERAL DISCUSSION AND
CONCLUSIONS
5.1 Detection of adverse
reactions
recognition of initial 2-3% SaO2
decrease with pulse oximetry during
the initiation of the sedation.
The main purpose in evaluating
the patient with pulse oximeter is to
detect the changes in blood oxygen
level early, which is a life
maintaining
function.
Adverse
reactions in this parameter is hypoxia.
Arterial oxyhemoglobin saturation
(SaO2)
is
lower
after
the
administration of a notable amount of
sedative agents. There is also a
significant decrease in the saturation
level of oxygen as the patient
progresses from light to deep
sedation. The incidence of saturation
falling to less than 90% have been
reported to have been between 4%
and 40%, depending on the level of
sedation (Tay et al. 1991, McKee et
al. 1991, Hardeman et al. 1990),
which is an interesting finding. Large
amounts of sedatives were used in
survey 1 but the desaturation
incidence was only slightly over 10
%. It is possible that the relatively
low incidence of desaturation in this
study is a result of the early
Since the largest mean decrease in
oxygen saturation observed during
procedures
under
intravenous
sedation is less than that considered
normal
during
sleep,
some
investigators are of the opinion that
oximetry monitoring is not needed.
Likewise the high incidence of
desaturation does not cause adverse
outcomes or complications. (Berg et
al. 1991, Bilotta et al. 1990)
However, in this study a small
decrease of SaO2 was found to be a
sign of sufficient sedation during the
initiation of medication. Oxygen was
added when the 90% level lasted a
long time. The pulse oximeter is
valuable because it will react
immediately to any progressive
oxygen desaturation, making early
correction possible. Hence the use of
pulse oximetry should be obligatory
for all endoscopic or paediatric
patients during intravenous sedation
(Casteel et al. 1990), and it is also
227
General discussion and conclusions
useful as a respiratory monitor during
oral surgery (Sugiyama et al. 1991). It
can be said that low initial saturation
may be a warning signal of hypoxia
and that the use of a monitor may
help to determine the correct sedation
level earlier and easier than the
normally used ptosis i.e. eye closure
reaction.
hundred per minute, while the group
undergoing scaling had mean heart
rate values of 78 beats per minute. In
this study, the mean pulse rate of the
patient rose from 70 to 86 beats per
minute after the injection of local
anaesthetics containing epinephrine.
Meyer (Meyer 1987) also found that
the increases in heart rate and
alterations of blood pressure were
different in a group undergoing
extraction and in a group to whom
only only local anaesthesia had been
administered, and these differences
are possibly an expression of an
endogenous catecholamine release as
a result of stress rather than a
pharmacological effect. He also
concluded
that
endogenous
alterations always take place in the
same way. It has also been found that
there is a temporary blood pressure
increase during the injection of local
anaesthetic (21,19) and at the time of
extraction of a tooth (Meyer 1987).
Also, heart rate had two peak values
during the extraction of the tooth; the
first during the injection of the local
anaesthetic, and the second during the
extraction phase (Meyer 1987). There
may also be some increase in systolic
blood pressure (Gortzak et al. 1992a).
However, no clinically significant
change could be detected in this study
in either systolic or diastolic blood
pressure. This means that the only
parameter necessary to monitor after
local anaesthesia is pulse, and the
pulse oximeter is the equipment of
first choice for this purpose.
5.2 Effects of local anaesthetic
preparations
Local anaesthetic preparations do
not affect blood oxygen saturation in
the clinical meaning but it was quite
astonishing that in survey 2 there was
a statistically significant decrease (0.1
- 0.3%) in this parameter. It is most
important to understand in this
particular case that the statistical
significancy depends on the amount
of measurements, it does not have any
clinical meaning. The study by White
et al. (White et al. 1989) showed that
nearly half of the patients developed
clinically significant desaturation
during minor oral surgery under local
anaesthesia. White et al. assumed that
this might be due to breath holding or
peripheral vasoconstriction as a
response to anxiety or fear. This
study at least excluded the effect of
local anaesthesia.
Frabetti et al. (Frabetti et al. 1992)
found that patients undergoing
surgical treatment had higher heart
rate values than patients undergoing
conventional
therapy.
Patients
undergoing muco-gingival surgery
had mean heart rate values of one
228
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part V
parameters were found, whether the
agents were combined or not. Thus
there is no reason to avoid this
combination which does not harm a
healthy patient anyhow.
5.3 The use of two local
anaesthetic preparations in
combination
This is a subject which has almost
completely been ignored in previous
studies. Simcock (et al. 1994) studied
this with a combination of lidocaine
2% and bupivacaine 0.5%, and a
combination of lidocaine 2% and
prilocaine 1%. Patient evaluation of
discomfort during the administration
of the anaesthetic and during
operation was assessed on a visual
analogue scale but no statistically
significant difference between groups
was found. Similarly the subject is
studied concerning the quality of
motor block: the mixture of
bupivacaine and lidocaine was less
effective than the other combinations,
of which the mixture of bupivacaine
and prilocaine showed the best motor
block. The combination of the two
long-acting
local
anaesthetics
bupivacaine and etidocaine had the
longest effect (Keckeis et al. 1994).
The most interesting point in these
findings is that the lidocaineprilocaine combination had an equal
effect to bupivacaine combination,
although bupivacaine is a long-acting
local anaesthetic preparation. This is
in synergy with the author’s finding
that combining lidocaine and
prilocaine enables the time increase
of local anaesthesia (Luotio et al.
1997). Moreover, the existence of
EMLA (Astra®), the only ointment
for skin surface anaesthesia which
contains
this
combination,
is
indicating potentiation. In the present
study no differences in cardiovascular
5.4 Effects of benzodiazepines
vs. local anaesthetics
Benzodiatzepines
cause
the
decrease of SaO2 and the epinephrine
in local anaesthetics increase the
heart rate. Thus they do not affect the
same parameter. Moreover, the
different
local
anaesthetic
preparations have different actions:
according to the retrospective review
of patient records in survey 2, the
maximal pulse of the patient elevates
from 91.3 beats to 98.6 beats per
minute after the injection of
epinephrine
containing
local
anaesthetics but if a prilocainephelypressine injection is used only
one stress point is found: at the
moment of injection. After the
injection of lidocaine-epinephrine
there was an additional period of high
pulse 5 - 10 minutes later when the
epinephrine began to spread to the
blood stream from the injection area.
The parameter which was affected
by both sedation and local
anaesthesia was amplitude of pulse
wave (A.P.W.). Observing the
amplitude of pulse wave enables the
dentist to notice a constriction in the
peripheral arteries as a result of
psychological stress: the blood flow
of the finger shows diminishing
values before the injection of local
229
General discussion and conclusions
anaesthetic i.e. before any possible
cardiovascular effect. A pulse
oximeter probe is usually placed on a
finger; other alternatives are toe or
earlobe. These alternative locations
are equally suitable as a finger when
measuring oxygen saturation and
pulse rate, but they do not indicate the
reactions in the pulse wave
amplitude. In general, peripheral
arteries in fingers react to painful
stimuli much stronger than arteries in
other places (Mattila et al 1990).
Therefore a pulse oximeter with a
finger probe and a possibility to
observe this parameter allows to
observe the main difference: local
anaesthetic preparations will cause
vasoconstriction and diminishing
values of A.P.W. but sedatives cause
vasodilatation and elevating values.
However, such patients accounted for
only 10% of the phobia group. The
authors' clinical experience has
shown that mental problems, such as
a previously diagnosed panic disorder
or some psychiatric medication may
form relative contraindications for
intravenous sedation. However, even
in these cases, the therapy could be
carried through without any objective
difficulties. Most patients felt only
minimally uncomfortable experiences
during therapy under intravenous
sedation with local anaesthesia.
Nevertheless, if the patient is
extremely scared, there is little that
can be done to remove all anxiety.
Intravenous
benzodiazepine
administered in conscious sedation
doses reduces significantly the
affection and motivational component
of the pain experience (Coulthard et
Rood 1992) and will produce
approximately 20 minutes profound
amnesia (Hupp et Becher 1988).
Common experience shows that the
injections of local anaesthetics form
the only painful procedures during
dental treatment. The author used this
period of time to perform the local
anaesthesia, and results show that the
patients had no memory of this
painful period. As a result, as many as
half of the patients - even in the
phobia group - subsequently made a
new appointment with the dentist
following this major and frightening
operation. Previous studies have
documented that patients' memories
of dental pain may later turn into
consistent anxiety (Kent 1984, 1985).
There is a strong indication in this
5.5 Patients' reactions to
treatment under intravenous
sedation with local anaesthesia
Afterwards the level of preference
for intravenous sedation with local
anaesthesia among the different types
of peroperative anaesthesia was
extremely high, over 80% in every
group. The reason for this was that
the patients could not remember any
significant unpleasant experiences,
such as pain, during treatment.
According to this study, the
recollection of the treatment of the
patients treated under intravenous
sedation with local anaesthesia seems
to be rather positive but some of the
patients showing severe dental care
phobia may need general anaesthesia.
230
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part V
study that intravenous sedation may
have prevented this as well as caused
some relief from anxiety.
Moreover, it is possible to enhance
pain relief by combining analgesic
agents with different drugs like
opioids and NSAIDs (Dionne et al
1994). After getting the results
expressed in study 5 the author
changed the protocol of analgesic
drugs. The previous tolfenamic acid ibuprofen
type
therapy
was
abandoned and a single dose of
intravenous ketorolac after operation
and a subsequent prescription of longacting piroxicam was introduced.
After oral surgery the patients should
also receive on opiate addition. Since
pain needs to be relieved and the most
effective medications against pain
contain opioids, the need for resting
days may continue for several days.
5.6 The patient’s condition after
treatment under intravenous
sedation with local anaesthesia
The main disorders after an
operation under intravenous sedation
with local anaesthesia were tiredness
and pain. The first does not require
anything but sufficient sleep.
However, pain is a more complicated
symptom and often overlooked by the
doctor, but easily relieved with more
effective analgesics. At the time of
this study the patients got a
prescription for some non-steroidal
anti-inflammatory drugs (NSAIDs)
which
inhibit
peripheral
prostaglandins. Today these drugs are
the framework in the treatment of
postoperative pain. Analgesic agents,
which do not operate against
peripheral prostaglandin synthesis
(e.g. paracetamol), may also provide
some pain relief. However, longacting NSAIDs like piroxicam have
proved to be superior to paracetamol
which does not induce a complete
relief from pain (Dolci et al. 1993).
Because the patients are canulated,
the use of parentheral analgesic is
simple and advisable. Intramuscular
dosage of ketorolac, a new NSAID,
has shown a similar degree of pain
relief to that of parentheral
diclofenac. This safe and effective
drug is an important new addition to
the available intramuscular NSAIDs
preparations (Walton et al. 1993).
5.7 Arrhythmias and the status
of autonomic nervous system
This study shows that sedation
rather prevents than provokes
arrhythmia, especially the amount of
ventricular premature complexes.
Although no statistical significance
could be found between the groups,
not even in the peroperative
occurrences (p=0.15), the most
important finding is that the study
group did not show any signs of
poorer
performance
than
the
reference group. The anxiety of nonsedated patients was a possible cause
for the poorer performance of the
reference group but because this
study was not a controlled clinical
trial and no statistical significance
could be detected, the result is mainly
suggestive. Today most cardiologists
231
General discussion and conclusions
prefer the heart rate variability
analysis or baroreflex sensitivity
testing to classical methods when
they have to evaluate the risk for
arrhythmia (Farrel et al. 1992).
Clinical studies have shown that
decreased heart rate variability will
forecast higher risk for sudden
cardiac death. This appears not only
in
the
cases
of
medically
compromised patients (Kleiger et al.
1987, Töyry et al. 1996) but healthy
people, too (Tsuji et al. 1994). The
increase of the low frequency
component appears as a result of
parasympathetic activation (Kamath
and Fallen 1993, Malliani et al.
1991). Moreover, high frequency
seems to be a marker of sympathetic
function (Paganini et al. 1986, Hirsch
and Bishop 1981). New methods for
the quantification of autonomic
nervous function and measuring
sympatho-vagal balance have made it
possible
to
investigate
the
significance of these reactions: in this
study
there
were
systematic
differences between the groups in
both of these parameters, and the
difference was even statistically
significant in the recovery period
(p=0.05) immediately after treatment.
These observations indicated that
there was a remarkable increase in
parasymphatic and/or decrease in
symphatic activity in the study group.
term recovery postoperatively. Thus
no need for ECG monitoring during
the
dental
treatment
under
intravenous sedation was found.
5.8 False alarms in pulse
oximetry
An SaO2-artefact or false alarm is
here described as extensive fall in
SaO2 readings without any organic
reason such as breathing failure or
obstructed airways (Fig. 4). The study
of White et al. (1989) has showed that
nearly half of the patients developed
clinically significant desaturation
during minor oral surgery under local
anaesthesia. They assumed that this
might be due to breath-holding or
peripheral vasoconstriction as a
response to anxiety or fear (White et
al. 1989). This retrospective review
of patient records explains those
observations: poor amplitude of pulse
wave (A.P.W.) has caused false
alarms. Even Lowes and Brooks'
(1991) finding that every fifth patient
undergoing surgical removal of third
molar with local anaesthesia alone
experienced hypoxic periods during
surgery, is explained by false alarms.
The influence of local anaesthetics to
oxygen saturation has been studied by
the author. In a previous study the
saturation values were no more than
0,5
%
lower
(statistically
insignificant) than the base level at
the end of the measurement. Local
anaesthesia is a possible source of
measuring failures (Fig. 4) because it
causes vasoconstriction but the agents
used in local anaesthesia do not affect
Moreover,
no
ST-segment
depression indicating hypoxia was
detected although in the study group
several correction manoeuvres of
oxygen level were performed; not
even in the cases that needed long232
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part V
the level of the patient’s oxygen
saturation. The easiest way to avoid
these false alarms is to keep the
patient warm.
5.9 Complicated cases
The most important complication
resulting from intravenous sedation is
too low level of SaO2 and it is treated
by correcting respiratory function
with supplementary oxygen and
removing sedation with antidote.
Hardeman et al. (1990) found that
20% of sedated patients experienced
hypoxic
episodes
in
the
postanaesthetic recovery unit when
no
supplemental
oxygen
was
administered, while only 3% of
patients who received supplemental
oxygen had such episodes. They
recommend the use of supplemental
oxygen for all patients undergoing
intravenous sedation in oral surgery.
An interesting alternative is that
the level of sedation is too light and
psychological stress keeps the
periphery closed. If this is correct, it
shoud be possible to remove false
alarms by increasing the amount of
sedatives. But it is hardly likely that
any sedationist would give more of an
agent which may cause respiratory
depression while the oximeter is
warning about possible hypoxia!
One explanation for the false
positive detection of hypoxia in
dental operations is the so-called
peripheral cyanosis or Raynaud's
disease; a condition in which the
mechanism
is
peripheral
vasoconstriction
and
delayed
peripheral
circulation
due
to
sympathetic activation. This leads to
the
desaturation
of
capillary
haemoglobin
although
central
circulation is well maintained.
Women are affected five times more
often than men and the age of
presentation is between 20 and 40
years, which is in harmony with the
authors’ experience (Wilson et al
1991).
Sedation can be cancelled with
flumazenil, which appears to be a
promising
drug
for
reversing
midazolam conscious sedation. The
patient who receives flumazenil after
intravenous
midazolam
is
significantly more alert as early as at
5 mins following drug administration
(Clark et al 1991). In cases of undue
sedation persisting after dental
treatment, flumazenil in doses from
0.5 to 1.0 mg rapidly reverses the
sedative and amnesic effects of
midazolam without apparent evidence
of subsequent resedation (Davies et al
1990). Flumazenil reverses almost
totally the effects of mental sedation
for approximately 2 hours, but not
physical sedation or memory.
(Ghoneim et al 1989, Cooper et al
1991)
233
General discussion and conclusions
groups have only been too limited in
those cases. More important is that
we should not believe all differences
which could be shown to have
statistical significance, e.g. in these
studies there was statistically
significant decreases in SaO2 after
local anaesthesia: 0.5 percent units!
Nevertheless, even the dentist’s
experience brings the indication in
proportion with real life conclusions.
However, many of the results have
been so marked that they indicate
further studies.
5.10 Statistical view vs. clinical
view
The whole work is mainly
descriptive because the statistics of
real life treatments is quite complex.
Because the material used originated
form the dentist’s practical work and
not a statistically perfect sample, the
data in every case is distorted. The
further analysis of an underlying
factor does not bring any further
benefit because the possibility of the
effect of these underlying factors can
never be excluded within this study
framework.
Clinically the author has reached a
high level in patient monitoring in
European dental tradition: the use of
monitoring and sedation methods
have been applied in dentistry and
oral surgery which are widely used in
anaesthesiology and critical care.
These methods will cause an
elevation in patient safety which is, of
course, the main issue.
In medical science the clinical
view should always be in the first
place and the statistics giving support
to the observations. It is not that
much the question of occurrences or
symptoms when we are not able to
show statistical significance although
some difference might have a high
clinical significance: The study
234
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part V
5.11 Conclusions
A pulse oximeter is very sensitive in detecting adverse reactions. High pulse, if
not detected, cause most of the problematic conditions of the patient in the dental
office. When sedatives are used, the main deorientation is hypoxia and
oversedation. Pulse oximetry often prevents them. Controversially, local
anaesthetics are not causing the decrease in blood oxygen saturation but especially
epinephrine in these preparations may cause high pulse levels which, combined with
fear as mentioned, may lead to vasovagal problems or even harm a medically
compromised patient. However, the high level of pulse rate can be avoided e.g. by
combining the lidocaine and prilocaine preparations when epinephrine containing
preparations do not produce sufficient anaesthesia in therapeutical doses. Moreover,
an early detection of rising pulse with pulse oximeter will prevent complications.
However, fear, cold and external epinephrine together and alone cause peripheral
vasoconstriction whereas sedatives open the periphery. This controversial effect of
sedatives and symphatomimetics should be remembered during sedation because the
vasoconstriction will cause artefacts to measurements.
Intravenous sedation is the method of patients’ choice in oral surgery and even in
cases of dental phobia, although the preference is a little bit lower among the latter.
After treatment the only seriously disturbing disorder was pain, which should be
avoided with proper analgesia. The studied sedative method is simple to monitor
with pulse oximeter alone because it does not cause cardiac problems but rather
prevents them by decreasing the activity of the symphatetic component of
autonomic nervous system. During the sedation the main problem is the low level of
oxygen saturation which in certain cases may be long-standing but can be corrected
with external oxygen and/or flumazenil. There is also a risk of false detection of
hypoxia i.e. the condition of patient is good but the monitor indicates problems.
This condition can be diagnosed from cold fingers and the ineffectiveness of
correction manoeuvres, and it is most easily avoided by preventing the patient from
shivering with cold.
235
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part VI
PART VI
6. CLINICAL GUIDELINES
237
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part VI
INTRAVENOUS SEDATION
PROTICOL
239
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part VI
LIST OF CONTENTS:
CLINICAL GUIDELINES ................................................................................................. 237
INTRAVENOUS SEDATION PROTOCOL............................................................ 239
6.1 Introduction ....................................................................................................... 243
6.2 The Patient for Sedation .................................................................................... 245
6.2.1 Examining the Patient ........................................................................ 245
6.2.2 Clinical Anatomy ............................................................................... 245
6.3 Benzodiazepines ................................................................................................ 247
6.3.1 Operating mechanism ......................................................................... 247
6.3.2 Half-life .............................................................................................. 247
6.3.3 Pharmacodynamics ............................................................................. 248
6.3.4 Pharmacokinetic anomalies ................................................................ 248
6.4 The Commercial Drugs ...................................................................................... 249
6.4.1 Selecting a suitable drug..................................................................... 249
6.4.2 Diazepam ............................................................................................ 249
6.4.3 Midazolam .......................................................................................... 250
6.4.4 Administration equipment .................................................................. 251
6.4.5 First aid equipment ............................................................................. 252
6.5 Monitoring the Patient ....................................................................................... 254
6.5.1 Blood pressure monitors ..................................................................... 254
6.5.2 Pulse oximetry .................................................................................... 254
6.5.2.1 The monitoring principle and equipment ........................................ 255
6.5.2.2 Monitoring during sedation ............................................................. 256
6.5.2.3 Emergency situation ....................................................................... 256
6.5.2.4 Sources for defaults ......................................................................... 257
6.5.3 Pulse wave oximetry........................................................................... 257
6.6 Intravenous Sedation in Practice ........................................................................ 259
6.6.1 Cannulating the vein in the crook of the arm ..................................... 259
6.6.2 Administering the drug and observing the effects .............................. 260
6.6.3 Recovery from sedation ...................................................................... 261
6.6.3.1 Oxygen saturation............................................................................ 261
6.6.3.2 Flumazenil ....................................................................................... 261
6.7 Complications ..................................................................................................... 264
6.7.1 Local complications ........................................................................... 264
6.7.2 Hypoxia .............................................................................................. 264
6.7.3 Fainting .............................................................................................. 265
6.7.4 Psychogenic complications ................................................................ 265
6.7.5 Other complications ........................................................................... 265
6.8 Legal aspects ...................................................................................................... 267
6.9 Conclusions ....................................................................................................... 268
6.10 Instructions to patients ..................................................................................... 269
1.11 Pictures ............................................................................................................ 270
241
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part VI
6.1 INTRODUCTION
Some patients may have such a
fear for dental procedures that they
need to be sedated. To reach an
adequate and accurate effect these
drugs have to be administered to the
vein. This is called intravenous
sedation (sedative medication given
through the vein). It is not general
anaesthesia.
Even
intravenous
sedation includes risks which must
imperatively be recognised, and due
precautions for treating eventual
complications must be made.
with these doses, to the effect that
they are practically in a very deep
anaesthesia during the whole
procedure, which severely impairs the
dentist's work. Also recovery from
the procedure takes several hours,
which will then paralyse the
operations of the dental surgery for
the remaining hours.
Although the basic doses for
intravenous sedation are 10 mg of
diazepam and 5 mg of midazolam
(notice the difference in the
efficiency ratio of midazolam), the
individual amount for the patient is
titrated to the exact point through
intravenous
dosage.
Hence
oversedation or undersedation will be
extremely rare. There will be no
problems with the procedures and the
patient's recovery is swift.
Why should we use intravenous
sedation, recognizing all its intrinsic
risks, instead of oral sedation?
This is a typical question made by
dentist colleagues to the author of this
study. To answer it we need to look at
some principles: orally, a useful
dosage of diazepam is 10 mg for
young and adults, 5 mg for children.
Smaller doses will not produce a
useful sedation. The dosages per os
for midazolam are 7,5 to 15 mg.
For the patient, intravenous
sedation is a necessary alternative in
dental care. It should nevertheless not
include risks that are greater than the
advantages. The dentist and the dental
surgery assistant must acquire
sufficient training for and a good
command of this procedure. The
skills must also be regularly sustained
and developed. This is the way to
avoid emergencies and complaints.
Given orally, for the majority of
patients these doses create a good
sedation sufficient for a normal
procedure. The problem is that a
minority of patients will not get any
sedative effect with these doses. In a
case of a frightened patient, the
experience of the treatment will be
most unpleasant. Another minority of
patients will become oversedated
The purpose of these instructions
is to provide a theoretical basis for
the understanding of intravenous
243
Clinical guidelines
sedation, but the practical application
of the procedure necessitates manual
training and displayed skill of
commanding the subject.
244
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part VI
6.2 The Patient for Sedation
 a serious muscular weakness,
Myastenia gravis
 a serious neurological illness
 an alcohol problem or a drug
addiction
 advanced age or underage
 sensitivity to benzodiazepine
(extremely rare)
 pregnancy, also extreme care
should be taken with breastfeeding mothers
6.2 1 Examining the Patient
A careful recording of the medical
history is the precondition of safe
intravenous sedation. An example of
an easily filled medical history form
is enclosed. This form will be further
complemented by an interview, as it
gives the best contact with the
patient. It is important to define the
patient's weight and length so that the
drug dosages can be correctly chosen.
The interview also gives an
opportunity to draft a psychological
profile of the patient. The dentist
should aim at establishing the level of
anxiety and the level of self-control in
the patient. If the patient is extremely
frightened and he/she reacts to the
slightest
stimulus
during
the
examination, it should be seriously
considered
whether
intravenous
sedation is the right method of
treatment. Besides a consent from the
patient, intravenous sedation requires
also the surgeon's command of this
method of treatment and its
complications. Intravenous sedation
is not suitable for a patient who has:
In case of any doubt that this
treatment might be unsuitable to the
patient, it is advised to consult his/her
practising general physician. Despite
the consultation it must be
remembered, though, that the
responsibility for the sedation lies
with the treating dentist.
6.2.2 Clinical anatomy
When undertaking intravenous
sedation it is important to know the
anatomy of the vascular system in the
hand. Suitable sites of injection for a
dental sedation are the cubical fossa
and the dorsum of the hand. The
advantages of the cubical fossa are
the large veins that are easy to
punctuate, and the fact that the
injection is less painful than when
punctuating the dorsum of the hand.
Also eventual haematomas caused by
the injection are less visible in the
cubical fossa than the dorsum of the
 acute lung disorder
 a serious disorder in the liver
functions
 operating disorder of the kidneys
 steroid medication
 psychiatric medication, including
benzodiazepines
245
Clinical guidelines
 tenderness of the site of injection
 the possibility of puncturing the
cannula into an artery and
 the possibility of injecting the
drugs into arterial circulation
hand, and they are easily covered
with clothes. The dorsum of the hand
may at times be the only possibility
when the patient's clothing prevents
the use of the cubical fossa or when
no visible vein is found in the cubical
fossa.
The complications of an intraarterial injection are very severe; in
the worst case they may lead to the
loss of the whole limb or a serious
circulation
disorder
therein.
Therefore
patients
sedated
intravenously shall always be
connected into the open line.
There is a risk at the cubical fossa
of accidentally punctuating the
cannula into an artery, or of causing
an arterial bleeding into the tissues.
There may also be problems in the
liquid flow of the cannula when the
patient is bending his arm.
When a free-flowing liquid
infusion tube is connected to the
cannula which is placed in an artery,
a fast and powerful blood intrusion to
the infusion tube and upwards all the
way to the infusion bottle or bag can
be observed. At this point there is no
doubt about the cannula being
misplaced. When the cannula alone is
placed in the vein there is never an
absolute certainty that it is securely in
the vein and not in an artery.
The disadvantages of the dorsum
of the hand are above all smaller
veins, more sensitive site of injection
and the visibility of the bruises.
The complications of cannulation
are:
 bleeding from the injection area to
the tissues (haematoma)
 thrombus and infection of the vein
(thromboflebite)
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part VI
6.3 Benzodiazepines
that this is not the time the drug takes
to disappear from the body, nor is it
the time when the drug's effect can be
seen in the body. The terms 'long
half-time', 'short half-time' may
sometimes be confused with 'longacting' and 'short-acting', and
therefore the meaning of each should
be kept clearly in mind. For instance
the half-time of diazepam is several
dozens of hours (24-48), whereas its
active sedation time is only a few
dozen minutes.
6.3.1 Operating mechanism
It is important to know the
operating mechanisms of the applied
drugs. In the clinical pharmacology of
benzodiazepines the main issue is
pharmacodynamics or how the drug
works in the body. Although it is easy
to measure the drug plasma levels for
most drugs, estimating the drug's
concentration at the receptor sites is
extremely difficult. Many drugs are
attached to receptors and their plasma
levels do not necessary correlate with
their effect. This often causes
problems in defining the correct
dosage. This is also the case for
benzodiazepines. Nevertheless it is
clear that there is no clear correlation
between benzodiazepine plasma
levels and their clinical effect. Hence
follows that the calculation of
pharmacokinetic parameters from
plasma levels is not clinically
relevant. This applies e.g. to the halflife of benzodiazepines. The very
effect of benzodiazepines is based on
their connecting to receptors in the
brain. Therefore their clinical effect
have a very vague correlation with
their plasma levels.
The following steps shall be
observed when dosing intravenous
drugs:
1. The uptake or absorption phase
which is the time taken to inject
the drug, in the case of drugs
dosed straight into the vein. The
absorption phase of oral drugs is
long and it depends on the uptake
of the drug.
2. The distribution phase, where the
drug is distributed into tissue
components according to its
properties, e.g. the liquid system
or fatty tissues.
3. The elimination phase which
begins when a balance between
plasma and the other tissues of the
body
has
been
reached.
Subsequently,
the
drug
is
6.3.2 Half-life
Half-life means the time taken for
the plasma concentration to decrease
by 50 per cent. It is important to note
247
Clinical guidelines
eliminated
through
liver
metabolism or kidney secretion
according to the drug's half-life.
The patient will recover clinically
considerably better when the drug
is eliminated from his body.
dose), plasma levels are extremely
high for several days. The patient
will, however, recover clinically to
the extent that he is fully alert and fit
to leave the hospital considerably
faster than what would be the
elimination time of the drug.
It is important to understand that
the clinical maximum effect of a drug
does not have a correlation with its
plasma level. This is quite apparent
when a drug is administered
intravenously: when the drug's
plasma level is still increasing, the
patient is much more sedated and
tired than when the plasma level is
already decreasing (compare with
getting drunk and coming down).
6.3.3 Pharmacodynamics
All diazepines has the following
four characteristics:
1. Hypnotic or sleep inducing
2. Anxiolytic (sedative, eliminating
anxiety, calming)
3. Muscle relaxant effect
4. Prevention and reduction of
convulsions.
The lack of correlation between
drowsiness and drug plasma levels is
also evident when the patient is
prescribed diazepam for continued
use. The patients tend to be tired
during the first few days even though
the plasma level is still rising over the
following days. The steady state level
where the elimination and further
administration is in balance, is
reached much later. The effect of a
given dose depends more on the
speed of increase of the plasma level
than the plasma level itself.
The action of benzodiazepines is
based on the stasis of benzodiazepine
receptors. These receptors are found
in the central nervous system. The
receptors are very specific to the
agonists
and
antagonists
of
benzodiazepine. They are not
receptive to other sedative agents
such as barbiturates.
6.3.4 Pharmacokinetic
anomalies
In overdose cases where the
patient has taken massive amounts of
diazepam (even 400 times the usual
248
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part VI
6.4 The commercial drugs
combination does irritate veins, and
in an oil-water emulsion which does
not carry the irritating effect and
which is the only acceptable solution
in intravenous sedation. In Finland
the trade name of the latter is Stesolid
Novum 5mg/ml injection liquid and it
is packed in 2 ml ampoules, which
means that one ampoule contains 10
mg diazepam. In Stesolid Novum the
diazepam is solved in an oil phase.
The organic solvents used in
conventional parentheral diazepam
products have been found to cause
unpleasant symptoms and pain in 78
% and thrombophlebitis in 30 %
when injected in the vein and thus
they may be considered unsuitable for
intravenous
sedation.
The
corresponding frequencies for the
Stesolid Novum injections are 5.3 and
1.1 %. Stesolid Novum is ready for
injection and it may also be
administered to small peripheral
veins. Diazepam should never be
injected in the muscle because of very
insecure absorption.
6.4.1 Selecting a suitable drug
The ideal sedating agent should
possess the following properties:
1. Sufficient sedative and anxiolytic
properties
2. Amnesia or cutting off memory
for the duration of the procedure
3. Easy administration
4. No irritating effects on veins or
tissues
5. Short and speedy recovery
6. No effects on cardiovascular or
respiratory systems
7. Low toxicity
8. No side-effects
9. Compatibility with other drugs.
Both diazepam in an emulsified
form and midazolam come very close
to the above principles. Therefore
they are widely used in the world in
connection with dental procedures as
well as e.g. with gastroenterological
procedures. The most common drugs
used in dental procedures are
diazepam, midazolam and flumazenil.
The official indication of the drug
is
premedication
before
the
procedure. Dosage for premedication
is
intravenously
0.1-0.2
mg
diazepam/kg. A rule of thumb for the
maximum dosage of diazepam in
dental procedures is that doses over
20 mg may only be used for
exceptionally lengthy procedures.
The initial dose of diazepam should
6.4.2 Diazepam
Diazepam is available in 2 ml
ampoules
containing
10
mg
diazepam.
Diazepam is available both in a
water-alcohol
solution,
which
249
Clinical guidelines
never exceed 20 mg. It should also be
borne in mind that the clinical effect
for elderly and weak patients is
usually reached with smaller doses.
This means in practice that elderly
persons should be administered only
ca. 2.5 mg diazepam at a time and
allowed a few minutes for the effects
to become apparent after each dose.
Other facts to remember are the
contraindications and the fact that
diazepam impairs the tolerance for
alcohol, sedatives and sleeping
tablets.
cause an exceptionally strong reaction
if other sedatives are taken before
complete elimination, and this carries
a risk of danger. On the other hand
these problems occur quite rarely
even though diazepam is a very
common drug.
After
oral
administration
diazepam is absorbed rapidly. A
single dose of 10-15 mg gives a
plasma concentration of 0.2-0.3
micrograms/ml within 2 hours. The
elimination of the drug is initially
rapid but it slows down into a total
half-life of 1-2 days.
The effect of diazepam to the
central nervous system is localised in
the subcortical areas and the reflexes.
Its half-life in the plasma is 24-48
hours. The long half-life causes a risk
of drug accumulation in the body if
the doses are repeated before an
earlier drug has been eliminated. If a
patient uses diazepam daily for his
medication, a dose given in the vein
may lead to respiratory depression.
Recording the drugs used by the
patient is therefore imperative in the
medical history.
Following
an
intravenous
administration (10-15 mg), the
plasma
concentration
of
1
microgram/ml is reached within 4
minutes and a strong sedative effect is
immediate. The concentration then
falls to 0,25 micrograms/ml per hour
and the clinical effect is reduced at
the same rate. The main effect of the
intravenous dose falls within the first
hour, whereafter the effect resembles
that of an oral dose. To reach the
same concentrations orally as are
created intravenously for the first
hour, extremely high doses of the
drug would be needed.
The main metabolite of diazepam
is desmethyldiazepam, which has a
half-life of 100 hours. Yet diazepam
may interact with any drug that has
depressant effects on the central
nervous system. It can potentiate the
effect of other hypnotics and
sedatives on the brain. It may also
increase the effects of alcohol. The
use of diazepam is also problematic if
the patient has anti-depressant
medication. The slow elimination of
diazepam and its metabolites may
6.4.3 Midazolam
Midazolam is available in 5 ml
ampoules containing 5 mg midazolam
or a content of 1 mg/ml, and in 3 ml
ampoules
containing
15
mg
midazolam or a content of 5 mg/ml.
The latter have been intended solely
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part VI
for general anaesthesia use and are
not suitable for dental applications.
The former, dilute solution should be
used for dental procedures as it
enables the safe titration of the dose.
not needed to create the desired
response. The easiest means of
dosage is to titrate 1 mg of the drug
through a cannula every second
minute and then follow up for the
response.
Midazolam is sold under the trade
name Dormicum. Midazolam can
form water-soluble salts with acids
which provide a well-tolerated watersoluble injection liquid. The drug has
a short duration and is well suited for
premedication. Midazolam typically
shows a rapid action on the onset and
a short duration due to a fast
metabolism. Due to its low toxicity,
the therapeutical scale of midazolam
is wide. A short-term anterograde
amnesia is seen after intravenous
dosage, and patients show a clear
tendency of drowsing off after the
desired sedation level has been
reached. The elimination half-life is
1.5-3 hours.
The effect of midazolam is so
strong and individual that there is risk
for serious side effects. A respiratory
depression may turn into the
discontinuation of respiration which,
undetected, leads to cardiac arrest.
This is a great risk with elderly or
weak patients, and resuscitation
equipment
should
always
be
available.
Midazolam interacts with the
following drugs: analgesics, sleeping
drugs, anxiolytes, antidepressants,
neuroleptics,
simeditine
and
erythromycin. All these drugs
contribute to a longer active period or
a stronger response. It must especially
be noted that midazolam should be
administered with special caution to
elderly people and weak patients, and
to patients suffering from an
obstructive
pulmonary
disease,
chronic kidney deficiency or cardiac
insufficiency.
The elimination half-life of the
principal metabolite, alfahydroxy
midazolam, is shorter than that of
midazolam. With elderly people, the
half-life of midazolam may become
even three times longer. Therefore an
intravenous dosage should be titrated
against the patient's response.
The
official
indication
of
midazolam is intravenous basic
sedation
in
connection
with
diagnostic or surgical procedures
carried out in local anaesthesia. The
initial dose is 2.5 mg 5-10 minutes
before the operation. Additional
doses of 1 mg may be given in case of
need. Over 5 mg doses are generally
6.4.4 Administration equipment
Disposable
syringe:
for
premedication with midazolam, the
most practical size is 5 ml and with
diazepam 2 ml.
Needle: needles are needed for the
suction of the drug from the ampoules
251
Clinical guidelines
to the syringe. Ideal needles are as
wide and long as possible, e.g. ones
with a Luer connector 20 g x 1" or 0.9
x 40 mm.
the infusion may be set to one drop
per 2-3 seconds (=1 ml/min).
Surgical tape: The cannula is
attached without allowing any
movement for it. A strong adhesive
tape, preferably in a y-form bandage.
Pharmacies have a wide range of
various surgical tape materials packed
in rolls so finding a suitable one for
attaching the cannula should cause no
problems.
Cannula: in intravenous sedation,
the patient should also have a venal
cannula. Ideal would be one with
three entrances, which facilitates the
possible change of infusion bag. The
cannula needle may be very thin as
only salt solution needs to be
transferred through the cannula, and a
thin needle will also make the
cannulation procedure much more
pleasant. A suitable width of cannula
is 20 G (Gauge) which corresponds to
a diameter of 1 mm, and a sufficient
length for the needle is 30 mm. This
size of cannula will allow the transfer
of 50 ml liquid per minute which is
quite sufficient for this need. With a
thin cannula the injection is painless
and succeeds well. Also venal
irritation is much smaller than when
using a larger cannula.
Venous stasis: A venous stasis is
attached above the cannulation site to
bring up the veins. It should direct the
pressure to prevent the return of the
blood through the veins but to let the
blood pressure to fill the limb.
6.4.5 First aid equipment
Additional oxygen is the most
frequent supplement needed in
intravenous sedation. An oxygen
cylinder is absolutely necessary and
no procedures should be started if
there is not enough oxygen for
several hours' administration. Nasal
cannula are ideal for administering
oxygen during the procedure as an
oxygen mask cannot be used.
Infusion tube: The simplest
transfer tube with an infusion
chamber, restriction valve and a Luer
lock for connecting the cannula.
Infusion liquid: A physiological
sodium chloride liquid (0.9 %),
available at the pharmacy, is used in
intravenous sedation. It comes in both
glass and plastic holders. A volume of
half a litre is quite sufficient for
sedation purposes. The rate of the
infusion should be fast at the
beginning of sedation, and when the
sedation level is sufficient the rate of
Precautions against respiratory
arrest shall be made with a
emergency resuscitator, "Ambu", that
is connected to the oxygen. During
the procedure the sedationist must
have both the possibility and the
ability to perform an endothracheal
intubation for the patient when
needed. This makes intravenous
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Monitored intravenous sedation with local anaesthesia for dental outpatients
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sedation a suitable next step after
getting experienced with nitrous
oxide.
The
above
mentioned
resuscitation methods must be
acquired for the permit to use nitrous
oxide.
ampoules. They contain 0.5 mg of the
drug or 0.1 mg/ml. It is important
always to have the antagonist within
reach in case any problems should
arise during the procedures.
-doxazepram; (Dopram®), which
stimulates the respiratory center in
the brain;
-salbutamol (Ventoline®) opens the
pulmonary tubes e.g. in connection
with status asthmaticus;
-etilephrine (Effortil®) which is used
to increase the volume per minute of
the heart and to increase blood
pressure.
The resuscitation drugs listed in
the general dental studies shall
naturally be found at the surgery.
These are 1) epinephrine, 2)
diazepam, 3) atropine, 4) cortisone,
and various liquids to solve the
above, as well as the syringes and
needles to administer them. In
addition to these, intravenous
sedation procedures require certain
drugs primarily intended to cure
respiratory depression and to support
the cardiovascular system. These
drugs are:
All the above mentioned drugs are
in injection form and require the
acquiring of due training in addition
of learning their properties from
books. It is of utmost importance that
all necessary emergency/resuscitation
drugs are within reach for the dental
surgeon making the procedure, and
that the expiry dates of ampoules are
duly followed. Moreover, the
ampoules should not be opened until
immediately before use as an opened
ampoule will not keep.
-nalorphin (Nalorfin®), which cures
the respiratory depression caused by
opiates;
-flumazenil (Lanexat®) to impede the
benzodiazepine receptors and thus
cure the respiratory depression
caused
by
benzodiazepines.
Flumazenil is a benzodiazepine
antagonist and it is available in 5 ml
253
Clinical guidelines
6.5 Monitoring the patient
The safety and well-being of the
patient is the responsibility of the
operating dental surgeon. All sedated
patients must be monitored. The price
of monitoring equipment is no excuse
for not monitoring the patient. Also
monitoring findings should be
carefully registered. The most
important monitors of all are the eyes
and ears of the person carrying out
the procedure, which means that the
patient must be observed closely
during the whole procedure. This is
the way to avoid unnecessary
problems. If the data gained through
electronic
monitoring
is
in
contradiction
with
clinical
observations, human intelligence and
observation skills are needed to solve
the situation. Even if monitoring is
essential, it will never replace the
human senses, only complete them.
so monitoring need not be
continuous. The basic requirement is
the possibility to measure and record
the pressure before and after the
procedure, and also during the
procedure according to the patient's
symptoms.
6.5.2 Pulse oximetry
The functions of the body depend
on a continuous intake of oxygen.
This vital supply has been secured by
many means, the most important of
which is the ability of haemoglobin to
bind oxygen. The amount of oxygen
tied in haemoglobin depends on the
prevailing oxygen pressure, but an
essential fact is that the dependence is
not linear but creates a co-ordination
curve of a gentle S. The amount of
oxyhaemoglobin,
oxygenated
haemoglobin in the total amount of
haemoglobin is called oxygen
saturation, measured as a percentage.
The flat ending of the oxygen
dissociation curve of haemoglobin
ensures a good oxygen saturation on a
wide variation scale of the oxygen
pressure. On the other hand the steep
fall of the curve enables quick
delivery of oxygen in the areas with
oxygen pressure characteristic to
certain tissues.
6.5.1 Blood pressure monitors
There is a variety of pulse and
blood pressure monitors on the
market, the simplest of which
measure
the
blood
pressure
automatically at the pressing of a
button, the more complicated ones
measuring the blood pressure
independently at
pre-set minute
intervals. All monitors should enable
recording the results with a printer.
There are no drastic changes in blood
pressure during intravenous sedation
Oximetry
saturation or
254
measures
oxygen
the percentage of
Monitored intravenous sedation with local anaesthesia for dental outpatients
Part VI
oxyhaemoglobin. It can also be
measured in a laboratory test from an
arterial blood sample, but nowadays
oximetry means a non-invasive
monitoring system where the
monitoring
occurs
continually
through the skin. The oximeter is
usually connected to a finger, but
other monitoring sites such as the
earlobe are also suitable.
6.5.2.1 The monitoring principle
and equipment
Oximetry is based on the fact that
the light absorption characteristics of
haemoglobin and oxyhaemoglobin
are different, and they also vary
according to different wavelengths of
light. The oximeter has a sensor with
diodes steadily pulsating two
different
wave-lengths.
The
equipment measures the variation in
the absorption of red (R ) and infrared
(IR) light during systole and diastole,
and on the basis of these quantities it
calculates the value of oxygen
saturation. Typically the sensor is
connected to a finger. It is important
that the sensor stays steadily in place.
It causes no pain or disturbance to the
patient so this method is an ideal case
of non-invasiveness. The equipment
works very quickly after the sensor
has been placed and no calibration is
needed.
Pulse
oximetry
has
been
developed for clinical use in the mid1970's in Japan. During 1980's this
monitoring system has become
extremely popular and during the last
few years it has in many countries
even been considered compulsory in
the control of general anaesthesia.
Since 1986 pulse oximetry has
become so popular also in Finland
that it is considered by many as the
most important monitoring system in
anaesthesia.
Pulse wave oximetry also utilizes
the information contained in the pulse
wave. Even though it only used to
function in the monitoring of the
timing of the saturation, the pulse
wave printed on the screen is
becoming a normal feature in the
equipment. The size of the pulse
wave easily shows great variation
according to various factors and thus
it reflects the changes in blood flow
at the monitoring site.
Several pulse oximeters on the
market operate in the above
mentioned principle, some of which
may be called pulse wave oximeters.
The equipment may be designed
solely for pulse oximetry but it may
also be an integrated part of the
monitoring
equipment.
Pulse
oximeters are small in size. Some of
them have a video display, some LCD
display. Typically they display
oxygen saturation and pulse rate in
numerical values, and the pulsating
wave-form beat by beat. Adjustments
are usually limited to setting alarm
limits. Modern technology has also
brought an output for data recording.
255
Clinical guidelines
Even if this property is not used as a
routine, it is irreplaceable when
carrying out clinical studies on pulse
oximetry. Many equipment offer the
possibility to follow the development
of monitoring quantities in a specific
trend memory.
This information
gives a learning basis for a secure
intravenous sedation. The equipment
usually works on ordinary current but
they are secured with a built-in
battery.
most changes in saturation occur.
Even extensive local anaesthesia
creates more decreases in saturation
than
is
commonly
believed.
Saturation may decrease in cases
where anaesthesia has to be
complemented
with intravenous
analgesics or sedatives. The situation
is usually relieved with a dosage of
oxygen.
In many countries the pulse
oximeter has been considered such an
essential safety factor that its use is
compulsory or close to compulsory
during general anaesthesia. In Finland
its use is recommended, but the
decision still lies in the consideration
of the anaesthesia team.
The range of application of pulse
oximetry covers the whole of
anaesthesiology and the intensive
care related thereto. It is always
applicable when there may be
exceptions
in normal oxygen
saturation. Pulse wave oximetry may
also be used to monitor changes in
peripheral circulation when no
changes in oxygen saturation are
expected.
6.5.2.3 Emergency situations
There would be plenty of use for
pulse oximetry in estimating the
danger of sudden emergencies and the
corresponding
efficiency
of
correcting measures. Lack of oxygen
is connected with many acute
illnesses and damages and with them
creates a concrete risk factor. A pulse
oximeter also immediately displays
the effectiveness or inefficiency of
the corrective measures. If the patient
is transferred to a hospital, the
monitoring should be continued as
unexpected changes in the patient's
condition may arise in emergencies.
6.5.2.2 Monitoring during
sedation
The most feared of possible
emergencies in connection with
sedation is a sudden lack of oxygen.
Therefore pulse oximetry is a safety
factor which enables the quick
perception of sudden lack of oxygen
and the counteraction of its
consequences. Attention must be paid
to a continual decrease of
the
saturation already before it reaches
the stage of actual lack of oxygen.
Pulse oximetry is particularly
applicable in the beginning of
sedation as this is the phase where
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part VI
method before, but with pulse
oximetry it has acquired a new
renaissance.
6.5.2.4 Sources for default
There are certain sources of
default within pulse oximetry and
pulse wave oximetry although as such
they are quite reliable methods.
The photoelectric pletysmography
measures the absorption of infrared
light and prints the mirror image as a
pulse wave. The shape and height of
the pulse wave depend on the volume
increase caused by the pulsation of
the heart at the site of monitoring.
Thus the value of infrared light
absorption (IR) correlates to blood
flow but does not give an absolute
value for the volume of circulation,
only a relative value. The pulse curve
resembles in shape the direct arterial
pressure curve, but should not be
confused to it. In general most
attention is paid to the height of the
curve, which is indeed its most
informative feature.
The absorption of red light is not
specific to oxyhaemoglobin but the
same phenomenon is created by the
setting of carbon monoxide to
haemoglobin. This is visible e.g. in
the case of extensive smoking.
Pulse oximetry measures oxygen
saturation which only decreases a
little although there would be a
considerable decrease in the venal
oxygen pressure. Therefore the shape
of the dissociation curve should
always
be
considered
when
interpreting the oxygen saturation
values!
The smooth muscles of the finger
veins are very sensitive towards
sympathetic nervous stimuli. When
the patient is anxious, his hands are
cold and pale. Also pain creates a
reaction of strong venal contraction.
Many drugs used in anaesthesia, and
in fact the anaesthesia itself, enlarge
peripheral veins. If due to bleeding
the amount of blood is insufficient,
circulation in fingers decreases
drastically. If the circulation in a limb
is disturbed due to pressure on an
artery, the pulse wave is significantly
decreased. In fact there is much more
variation in the pulse wave than in the
pulse rate or the oxygen saturation.
In pulse oximetry the saturation
and pulse rate values require a
pulsating circulation but the values
remain reliable even during poor
peripheral circulation.
6.5.3 Pulse wave oximetry
The pulse wave was originally
only assisting the timing of oxygen
saturation monitoring. A visible
pulsating wave-form has, however,
such an important information value
that it deserves its visibility. A visible
pulse wave changing in volume gives
the equipment an additional feature
of pulse wave oximetry. The pulse
wave has been used as a monitoring
A precondition for using the
height of the pulse wave for
257
Clinical guidelines
monitoring is that it is visible and that
only changes in volume at the
monitoring site affect its size. In some
equipment the pulse wave is
maintained at the same size by
changing the amplification, thus
losing its informative value. The size
of the pulse wave often changes to
such an extent that the amplification
has to be changed but this should be
done in progressive steps rather than
in a sliding fashion. The visibility of
the pulse wave also confirms the
reliability of the saturation and pulse
rate values. Usually the pulse wave
needed for a reliable monitoring is
suprisingly small, but without a
smallest pulsation no value is
obtained.
the pulse wave shows a regular
increase. Depending on the starting
point, its height is increased four to
five times. In a peaceful phase the
pulse wave is high, but a procedure
will again contract it. During
anaesthesia the pulse wave will react
to painful stimuli and superficial
anaesthesia.
The height of the pulse wave is
not an absolute but only a relative
quantity. In different fingers the
height of the pulse wave is different;
in the right hand it is usually higher
than in the left hand, and in the
middle finger it is the highest. The
height of the pulse wave has no
quality, but its changes in the same
patient are significant. As the pulse
wave is so sensitive and the changes
in its height can be due to many
causes, learning to interpret the
height of the pulse wave should be
done taking into account the other
simultaneous monitoring methods.
When the patient has been given
premedication and is transferred to
the operation room, the height of the
pulse wave gives an indication on the
sufficiency
of
the
given
premedication. The pulse wave of an
anxious patient is minute. In sedation
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part VI
6.6 Intravenous sedation in
practice
Before beginning intravenous
sedation the dentist should make sure
that all necessary resuscitation
equipment and drugs are close at
hand and also, that there is oxygen in
the oxygen cylinder and that the
expiry dates of the drugs have been
followed.
The patient is placed into an
almost supine position, his blood
pressure is taken and the probe for the
pulse oximeter is attached, and the
initial values for blood pressure and
oxygen saturation are recorded.
The cannulation can also be done
completely without pain with an
emulsion ointment or plaster (Emla
®) to numb the skin for the
cannulation procedure. The plaster is
evidently
more
practical
for
cannulation purposes as it is
individually packed and can be
attached by the patient or his parent
to an agreed place. The anaesthetic
effect begins after 1 hour and thus to
be useful the product should be given
beforehand for the patient to apply at
home. More detailed information of
the product can be found in the
national Pharmaca.
6.6.1 Cannulating the vein in
the crook of the arm
Before the patient arrives, the
following equipment should be made
available:
 a 5 ml syringe
 a large needle (G 21) for the
suction of the drug
 intravenous cannula
 alcohol swab
 drugs
 venous stasis
 infusion fluid package
 infusion tube
A venous stasis is placed at the
patient's arm to provide good
visibility of the veins. When fitting
the venous stasis it should be
remembered that the pressure should
not be so great that arterial circulation
in the arm is obstructed. After this the
cannula is attached and fixed to the
skin with plaster.
The patient's weight should be
found out beforehand or, if it has not,
it should be verified at the latest at
this point. The drug is nevertheless
dosed
primarily according to
individual reactions and only
secondarily in accordance with the
patient's weight.
259
Clinical guidelines
 the patient closes his eyes or
seems to be somnolent
 the value in the pulse oximeter
decreases by 2-3 % of the initial
value as a result of decreased
respiration rate.
The salt solution is placed in the
infusion stand and the chamber of the
intravenous-line is filled with the
liquid. The whole length of the tube
is checked carefully for air bubbles.
The infusion tube is attached to the
cannula and for a while the infusion
restrictor is set to allow maximum
flow. This is to ensure that the flow is
free and the surrounding tissue is not
swelling as a sign of paravenous
infusion. At this point it will be
evident if the injection has hit an
artery as blood will then rush up the
injection tube.
Sedation is commenced, and
especially for anxious patients, local
anaesthetics containing epinephrine
should be avoided as a possible
tachycardia reaction caused by
epinephrine may disturb a good
sedation. Calmness should always be
prevalent when handling the patient
as he is awake and by no means
anaesthetised.
6.6.2 Administering the drug
and observing the effects
After the sedation phase it is
possible to give additional doses of
midazolam if the patient's bearing
would indicate a need for further
medication. However, the pulse
oximeter should be observed before
every additional dose, and no further
doses should be given if the pulse
oximeter value is equal to or lower
than 95 %.
When the infusion is working
normally, the administration of
midazolam is commenced. With a
disposable syringe, midazolam (1
mg/1 ml) is given in 1 mg doses. The
doses are repeated every 2 minutes. A
conversation is held with the patient
throughout the administration, on any
subject, to observe the impairment of
the motor co-ordination of speech.
Other motor disorders can be
observed e.g. by asking the patient to
touch his nose before every new dose
of drugs. When the patient closes his
eyes is also noted, and pulse oximeter
values are observed. An appropriate
level of sedation is reached when one
of the following observations is
made:
 the patient's
slurred
speech
If sedation is followed by a
surgical procedure, it is worth
reminding the patient that he may
freely sleep while the team is
preparing the operating room ready
for surgery. The patient will usually
fall asleep a few minutes after the
conversation with him has been
stopped.
Before surgical procedures it is
always good to give the patient a
small dose of fentanyl (50
microgram/ml) immediately before
becomes
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Monitored intravenous sedation with local anaesthesia for dental outpatients
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the surgery, e.g. some 25 micrograms
of fentanyl is usually sufficient. The
advantage of this is that the patient
reacts less to small sensations of pain
which may arise despite of sedation.
As fentanyl is also a powerful
respiration depressant, the value in
the pulse oximeter must be checked
before administering the drug. In
conventional
treatment
(e.g.
extraction, root treatments etc.) the
treatment
should
be
initiated
immediately after the sedation
becomes effective. An additional 1
mg of midazolam (see the pulse
oximeter)
is
recommended,
whereafter the saliva aspirator is
placed on site. A recommendable
suction fan is the short loop-form
aspirator. These aspirators work like
a string thus helping the patient to
keep his mouth open.
to another finger, but only after the
exclusion of real oxygen desaturation.
In case you suspect the malfunction
of probe, use your own finger to test
the function of the probe.
If the value remains unchanged,
airways are open and patient is
breathing, additional oxygen should
immediately be given to the patient.
Nasal cannula and a regular 3-10 l
oxygen cylinder (e.g. AGA) is
suitable, when checked that there is
enough oxygen for several hours'
need.
The
administration
of
additional oxygen will repair almost
without exception a beginning
hypoxia. If the respiratory depression
is caused by benzodiazepines and the
low oxygen saturation is not
increased by oxygen administration,
the patient should be administered
intravenously
some
flumazenil
(Lanexat 0.1 mg/ml à 5 ml). This
drug can be dosed in 0.1 mg i.e. 1 ml
portions which are repeated every
minute until the oxygenation has
returned to normal. The dosage may
at a maximum rise up to 1 mg (10
ml).
6.6.3 Recovery from sedation
6.6.3.1 Oxygen saturation
Oxygen saturation is monitored
closely both during the procedure as
well as during the reversal of
sedation. If oxygen saturation falls
under 90 %, it is important to check
immediatelly the patient’s respiration
movements and openess of airways. It
is also diagnostic to know if the
decrease is sudden or slow. In some
cases the reason can be local at the
measuring finger: it should be
checked that the probe does not give
so much pressure to the monitoring
site that circulation is obstructed. In
this case the probe should be moved
If respiration depression is caused
by benzodiazepines, return to normal
oxygenation is very fast and will
occur during the very first doses.
As flumazenil is a benzodiazepine
antagonist, it blocks the same
receptors where benzodiazepines are
attached. Therefore flumazenil may
be given in a sufficiently small
amount to revert an eventual
respiration depression, but not to lose
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Clinical guidelines
the sedation. The procedure may then
be carried out normally.
1. an efficient emergency drug for
oversedated patients
2. full co-operation of the patient
3. a safer recovery period
6.6.3.2 Flumazenil
The possibility of using flumazenil
as an antagonist in overdose cases
makes it an extremely important drug
for securing the sedation process. It
must be kept within reach whenever a
patient is sedated. A part of the
patients are very sensitive to
benzodiazepines and in these cases an
antagonist may even prove to be a
life-saving drug. Elderly patients are
much more sensitive than the young
to the effect of benzodiazepines. In
the cases where general anaesthesia is
contraindicated due to the patient's
respiratory
illness,
intravenous
sedation is the only possibility to
enable certain procedures, and
flumazenil ensures that the sedation is
safe. A general rule for elderly
patients is not to send them home
immediately after treatment with
intravenous sedation, but rather to
arrange for an overnight monitoring
for them at the ward.
Besides treating complications,
flumazenil may be used to end the
sedation of a patient after a short
procedure. The patient may be given
0.05 mg per 5 minutes of flumazenil,
until he can walk without assistance.
As the half-time of flumazenil is
shorter than that of benzodiazepine, a
resedation may occur within 2-3
hours, and this should be notified to
the patient and his escort.
The initial dose of 0.2 mg
flumazenil is administered through
the cannula while it is still in place in
the cubical fossa. It must be noted
here that the cannula should remain in
place during the whole procedure and
must not be removed until the patient
is fully recovered. A few seconds
after being given flumazenil, the
patient is likely to open his eyes.
When the patient is fully awake he is
given permission to sit up and, after a
few further minutes, he is also given
written instructions for recovery
which are referred to orally. The
instructions should essentially forbid
driving and the use of alcohol. At this
stage there is no point in explaining
too complicated things to the patient.
The instructions will order the patient
to rest for the following day.
The
advantages
of
benzodiazepine antagonist are:
When the patient is sedated, his
level of consciousness has decreased
and this may encumber complicated
procedures, e.g. the preparation of a
dental crown. What can be done is to
make the unpleasant procedures
immediately in the beginning of
sedation. When the stage is reached
when the patient should no longer be
sedated but co-operative, he is given
flumazenil until he can contribute to
the procedure (e.g. the fitting of
occlusion and dentures).
the
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Part VI
The
patients
which
have
undergone
treatment
under
intravenous sedation and have been
given flumazenil to eliminate the
sedation, can sit and stand up
normally. It must, however, be
remembered that they still remain
sedated and cannot fully look after
themselves. It is crucial to know that
the effective time of flumazenil is
shorter than that of midazolam and in
theory the sedation with eventual
respiration depressions may return,
even though the long duration of
dental procedures makes it highly
unlikely. The presence of an escort is
even in these cases absolutely
necessary. The escort gives the
patient a feeling of security and
someone to talk to about the
experience.
After the procedure, the patient
may be sent home 3 hours after the
last dose of midazolam. He should be
sent with an adult escort. Both the
patient and his escort should be
reminded of the written instructions
which the patient received already on
his previous call; the main points
being that the patient's ability to
observe traffic is not sufficient in the
12 hours to follow, and that he should
not take alcohol during this time, as it
would increase the effect of the drugs
and vice versa. Some people may
show
unpredictable
individual
reactions. The patient should be made
aware of the dentist's office and home
telephone numbers in case any help
might be needed after the treatment.
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Clinical guidelines
6.7 Complications
cannula ending up in circulation. The
breaking of a venal cannula and the
drifting of a loose part into
circulation is without exception poor
medical practice caused by the
cannulation technique, and it will
lead to prosecutions and claims.
6.7.1 Local complications
Intravenous
injections
may
produce a reaction at the injection
site,
later
turning
into
a
thrombophlebitis.
This
is
an
inflammatory reaction found at the
injection site: redness of skin,
swelling and pain. The vein may be
blocked due to the infection
(thrombus), but although painful, this
is not a dangerous condition. Also
haematomas are found at the injection
site. They are generally a result of a
damage occurred in the vein, and the
consequent
bleeding
into
the
surrounding tissues. To avoid
paravenous injections please make
sure that the needle really is in the
vein. The most reliable way to control
this is to connect the infusion bottle
to the cannula. If the cannulation has
failed, do not try the same vein again
but use another vein which should be
as large as possible. With appropriate
technique, an extravenous injection
will be observed almost as soon as it
has occurred. The cannula is then
taken out and a compression bandage
is tied on the site, eventually even
lifting the hand slightly to avoid
swelling. If a thrombophlebitis is
developing, it will heal itself in a few
days, or one to two weeks.
6.7.2 Hypoxia
A serious hypoxia is a most rare
complication
of
diazepam
or
midazolam, and it occurs most likely
as a consequence of an obstruction in
the respiratory passages. When the
sedation is too strong, the airways are
not held open naturally. The patient
will perform breathing movements
but no air is going through. During a
partial obstruction the patient's
breathing sounds like snoring. Drugs
may interact to emphasise the
respiratory depression effect of
diazepam. Oversedation and overdose
will also cause respiratory depression.
It is important to titrate the sedation
dose to the exact point. As mentioned
above, pulse oximetry of the patient
is of utmost importance.
There are descriptions in medical
literature of the broken tip of a
metallic needle or plastic parts of the
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part VI
intravenous sedation have had
sexually coloured illusions, the worst
of which have even led to prosecution
against the sedating physician. This is
why it is very important that all
monitoring is set up before the
sedation. This applies especially to
EKG monitoring; the patient should
not under sedation undergo such
procedures which he would not
expect a dentist to do. For security
reasons it is also vital that another
member of the staff is present during
the whole of the treatment process: in
the initiating of sedation, during the
procedure and during the recovery
period. A good precaution for the
dentist's legal protection is taking a
video of the procedure and filing the
tapes.
6.7.3 Fainting
An extremely fearful patient may
produce a vasovagal collapse, either
before or during the administration of
the drug. In this case the procedure
will be immediately discontinued and
normal instructions against fainting
are followed. First the limbs are lifted
up. No dental procedure should be
done at that time. The patient is given
a new appointment and it should be
considered whether part of the
diazepam or midazolam should be
given beforehand per os for instance
1-2 hours before the appointment.
6.7.4 Psychogenic complications
Patients who are under psychiatric
medication or treatment are not
suitable for intravenous sedation.
There are some descriptions on
paradoxical excitement which is
mainly found in children, but in
single cases there has been evident
aggressive reactions even with adults.
The only way to deal with the
situation seems to be to discontinue
the procedure. A more common
reaction is the decrease of the
patient's conscious inhibition, where
the patient becomes very talkative
and would say things he would
normally not
mention. When
initiating sedation it is good to lead
the conversation into harmless topics
as the amnesia caused by the drug
may further distort the recollection on
the contents of the conversation.
Some cases have been recorded
where
patients
undergoing
6.7.5 Other complications
There is a small group of patients
which, after being given a few
milligrams
of
diazepam
or
midazolam, will fall into deep sleep
as the dose does not depend on the
patient's weight. A large patient may
reach a deep sedation while a small
patient with not much weight may
take considerable doses. The latter
group may look the dentist in the eye
after a 10 mg dose and say, "It doesn't
feel at all". What must be
remembered, however, is that the
patient may be sedated even though
he might claim otherwise. This case
would call for psychomotor tests such
as asking the patient to touch his
nose. It is likely that he cannot
perform this trick. Also a signature on
265
Clinical guidelines
a piece of paper would easily reveal
the depth of the sedation. Increasing
the dose for an extremely resistant
patient may lead to a quick and deep
fall into oversedation. Therefore a
key rule is not to give the patient
more than 10 mg midazolam or 20 mg
diazepam intravenously.
infusion and when giving the first
drugs. Ask whether he can feel
any local pain and if not, all is
well.
An intra-arterial infection may
cause an ischemy and necrose of the
distal part of the whole arm. In case
of acute respiratory or oral infection
causing the obstruction of airways,
intravenous
sedation
is
contraindicated. Acute dental patients
are ill suited for intravenous sedation.
Thus acute processes must first be
brought in control through draining or
antibiotics, and only thereafter can
the procedure be undertaken in local
anaesthesia and intravenous sedation.
The intravenous administration of
midazolam
has
only
few
cardiovascular effects. The problems
i.e. intra-arterial injections are easily
avoided when the following is kept in
mind:
 Only use a vein that is clearly
visible, and after placing the
cannula connect the infusion tube.
 Always ask how the patient feels
both at the beginning of the
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Part VI
6.8 Legal aspects
Sedation
creates
operational
disorders in the patient's memory
which may cause misunderstandings
leading at their worst into prosecution
against the dentist. Therefore certain
principles shall be adopted:
-if teeth need to be extracted during
the procedure, the patient must be
informed about this beforehand,
before the procedure
-no payments shall be made at the
sedation appointment
-the most important principle is to
explain all procedures diligently to
the patient, and to give him written
instructions.
-the patient shall be told what
preparations the procedure will
require and what he has to observe
after the procedure.
-careful recording of the patient's
medical history
When these instructions are
followed, everything is likely to go
fine. If problems would arise with the
patient, they can mostly be solved in
a quiet and informative discussion
with the patient. If not, it might be
useful for the dentist to contact a
more experienced colleague. Also the
patient should be offered a meeting
with this more experienced colleague.
If legal procedures must be taken, the
primary task is to contact the lawyer
of the dentist or the dentists' union.
-the patient must come with a reliable
escort
-the procedure must be suitable for
intravenous sedation
-the staff must be trained
-emergency equipment and drugs
close at hand and effective
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Clinical guidelines
6.9 Conclusions
Intravenous sedation is both for the dentist and his
patient a pleasant, efficient and safe means to treat anxiety
problems. The basis for the security is, however, the
appropriate skills of the staff. Therefore in the conditions
prevailing in the area of North European dental education
tradition, instructions could be given where the dentist
should first be qualified in using nitrous oxide, thus
having a command and practice of patient handling,
intravenous injections and endothracheal intubations from
before. Thereafter the dentist could attend an intravenous
sedation course and start apprenticeship with a colleague
who is experienced in sedation. Individual sedation
should be commenced only when the dentist has thorough
knowledge on this anesthesiological method. The skill
should also be continuously maintained. Endothracheal
intubation exercises should not be left at one time but this
life-saving procedure in a severe complication should be
practised annually at a central hospital. Also intravenous
sedation should not remain a measure to be taken only
when the treatment cannot be done in any other way. The
skills to carry out the sedation would then be too weak
and the object could be an extremely difficult patient that
would test the skills of even an experienced sedationist.
The best way to maintain sedation skills is to use the
method constantly.
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Part VI
6.10 Instructions to patients
 You should be followed by an
adult escort who will see to your
safe journey home and who will
be available for you until the
following morning.
 During the 24 hours after the
procedure YOU MUST NOT:
 leave home alone
 take alcohol
 drive a vehicle
 go to work
 Please also make sure that you
have informed the operating
dentist of all your possible
illnesses and medications.
 A feverish cold or cough as well
as other feverish illnesses, until
they have been cured, will prevent
any treatments. Also in the case of
an open labial herpes the treatment
cannot be carried out.
 If you have to cancel your
appointment, please do so 2 weeks
before the agreed time
 Immediately before coming to the
appointment please use the toilet.
Instructions for an extensive
dental procedure:
 Please have an X-ray and the
laboratory tests taken within a
week
from
the
control
appointment. Please take the X-ray
pictures and laboratory results to
the next appointment.
 The procedure will be made in
local anaesthesia and using a
sedative premedication. Therefore
no pain or fear is experienced
during the treatment.
 Please dress lightly: a shortsleeved shirt and loose-fitting
trousers. Do not use make-up or
other chemicals in the face. Nail
enamel should be removed. Wrist
watch, rings, necklaces and other
jewellery should be left at home if
you are entering a surgical
procedure. Remember to take the
X-ray picture with you.
 EATING AND DRINKING IS
FORBIDDEN 4 HOURS PRIOR
TO
THE
APPOINTMENT.
Therefore
please
take
the
medication you may have been
prescribed at exactly 4 hours
before the appointment.
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Clinical guidelines
6.11 Pictures
The most feared of possible emergencies in connection with sedation is a sudden
lack of oxygen. Therefore pulse oximetry is a safety factor which enables the quick
perception of sudden lack of oxygen and the counteraction of its consequences.
Attention must be paid to a continual decrease of the saturation already before it
reaches the stage of actual lack of oxygen. Pulse oximetry is particularly applicable
in the beginning of sedation as this is the phase where most changes in saturation
occur. Saturation may decrease in cases where anaesthesia has to be complemented
with intravenous analgesics or sedatives. The situation is usually relieved with a
dosage of oxygen.
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part VI
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Clinical guidelines
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part VI
The simplest transfer tube with an infusion chamber, restriction valve and a Luer
lock for connecting the cannula is the best for dental use. A physiological sodium
chloride liquid (0.9 %), available at the pharmacy, is used in intravenous sedation. It
comes in both glass and plastic holders. A volume of half a litre is quite sufficient
for sedation purposes. The rate of the infusion should be fast at the beginning of
sedation, and when the sedation level is sufficient the rate of the infusion may be set
to one drop per 2-3 seconds (=1 ml/min).
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Clinical guidelines
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part VI
Suitable sites of injection for a dental sedation are the cubical fossa and the dorsum
of the hand. The advantages of the cubical fossa are the large veins that are easy to
punctuate, and the fact that the injection is less painful than when punctuating the
dorsum of the hand. Also eventual haematomas caused by the injection are less
visible in the cubical fossa than the dorsum of the hand, and they are easily covered
with clothes. The dorsum of the hand may at times be the only possibility when the
patient's clothing prevents the use of the cubical fossa or when no visible vein is
found in the cubical fossa.

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Clinical guidelines
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Monitored intravenous sedation with local anaesthesia for dental outpatients
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When the infusion is working normally, the administration of midazolam is
commenced. With a disposable syringe, midazolam (1 mg/1 ml) is given in 1 mg
doses. The doses are repeated every 2 minutes. A conversation is held with the
patient throughout the administration, on any subject, to observe the impairment
of the motor co-ordination of speech.
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Clinical guidelines
An appropriate level of sedation is reached when one of the following observations
is made:
 the patient's speech becomes slurred
 the patient closes his eyes or seems to be somnolent
 the value in the pulse oximeter decreases by 2-3 % of the initial value as a result
of decreased respiration rate.
After the sedation phase it is possible to give additional doses of midazolam if the
patient's bearing would indicate a need for further medication. However, the pulse
oximeter should be observed before every additional dose, and no further doses
should be given if the pulse oximeter value is equal to or lower than 95 %.
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Monitored intravenous sedation with local anaesthesia for dental outpatients
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Clinical guidelines
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Part VI
Besides treating complications, flumazenil may be used to end the sedation of a
patient after a short procedure. The initial dose of 0.2 mg flumazenil is administered
through the cannula while it is still in place in the cubical fossa. It must be noted
here that the cannula should remain in place during the whole procedure and must
not be removed until the patient is fully recovered. A few seconds after being given
flumazenil, the patient is likely to open his eyes. After that, infusion of rest
flumazenil is recommended. When the patient is fully awake he is given permission
to sit up and, after a few further minutes, he is also given written instructions for
recovery which are referred to orally. As the half-time of flumazenil is shorter than
that of benzodiazepine, a resedation may occur within 2-3 hours, and this should be
notified to the patient and his escort.
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
7.1 APPENDIX I
DESCRIPTION OF THE
DRUGS USED AND STUDIED
Published with permissions of
Roche, Dumex and Astra
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
MIDAZOLAM
International Standard Prescribing Information
November 30 1995
DORMICUM, ampoule
RO 21-3981
Dormicum
Midazolam
Short-acting benzodiazepine for the premedication, sedation, induction and
maintenance of anesthesia
Ampoules for intravenous, intramuscular and rectal administration
of Dormicum to form water -soluble
salts with acids. These produce a
stable and well tolerated injection
solution.
Composition
Active ingredient: midazolam as
hydrochloride.
The pharmacological action of
midazolam is characterized by rapid
onset and, because of rapid metabolic
transformation,
short
duration.
Because of its low toxicity,
midazolam has a wide therapeutic
range.
Ampoules 5 mg/1 ml, 15 mg/3 ml,
5 mg/5 ml and 50 mg/10 ml for i.v.,
i.m. and rectal administration.
Excipients:
sodium
chloride,
hydrochloric acid, sodium hydroxide,
water for injection.
Midazolam has a very rapid
sedative and sleep -inducing action of
pronounced intensity. It also exerts an
anxiolytic, an anticonvulsant and a
muscle-relaxant effect.
Properties and effects
Midazolam, the active ingredient
of Dormicum, is a derivative of the
imidazobenzodiazepine group. The
free base is a lipophilic substance
with low solubility in water.
After parenteral administration
anterograde amnesia of short duration
occurs (the patient does not recall
events that occurred during the peak
of activity of the compound).
The basic nitrogen in position 2 of
the
imidazobenzodiazepine
ring
system enables the active ingredient
285
Appendix I
drugs, this has been confirmed in vivo
(see Interactions)
Pharmacokinetics
Absorption after intramuscular
injection
Absorption of midazolam from the
muscle tissue is rapid and complete.
Maximum plasma concentrations are
reached
within
30
minutes.
Bioavailability is over 90%.
Elimination
In
healthy
volunteers,
the
elimination half -life is between 1.5
and 2.5 hours. Plasma clearance is in
the range of 300-400 ml/min. When
midazolam is given by i.v. infusion,
its elimination kinetics do not differ
from those following bolus injection.
The elimination half -life of the main
metabolite, -hydroxy-midazolam, is
shorter than that of the parent
substance. It is conjugated with
glucuronic acid (inactivation). The
metabolises are renally excreted.
Absorption
after
rectal
administration
Midazolam is absorbed quickly.
Maximum plasma concentration is
reached
within
30
minutes.
Bioavailability is about 50%.
Distribution
When midazolam is injected
intravenously,
the
plasma
concentration -time curve shows two
distinct phases of distribution. The
volume of distribution calculated
under steady -state conditions is
Pharmacokinetics
in
special
clinical situations
In adults over 60 years of age, the
elimination half -life may be
prolonged up to three times and in
some
intensive
-care
patients
requiring midazolam by i.v. infusion
for long -term sedation, up to six
times. In these patients infusion at an
unchanged rate results in higher
plasma levels at steady state.
0.7-1.2 l/kg bodyweight. Studies
show a protein binding of 96 -98%.
In
animals
and
humans,
midazolam has been shown to cross
the placenta and to enter fetal
circulation. Small quantities of
midazolam are found in human milk.
The elimination half -life may also
be prolonged in patients with
congestive heart failure and with
reduced hepatic function.
Metabolism
Midazolam is metabolized rapidly
and
completely. The primary
metabolise is (-hydroxy-midazolam.
The fraction of the dose extracted by
liver has been estimated at 40-50%.
Many medicaments have been found
to inhibit the production of this
metabolite in vitro; for some of these
In children (3-10 years) the
elimination half-life is between 1 and
1.5 hours.
In neonates the half-life of
elimination is prolonged with a mean
of 6 hours (3-12 hours) due to liver
immaturity.
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
the dose should be determined with
caution, the special factors relating to
each patient being taken into
consideration.
Indications and usage
Conscious
sedation
before
diagnostic or therapeutic procedures
with or without local anesthesia (i.v.
administration).
a) Intravenous conscious sedation
The intravenous injection of
Dormicum should be given slowly at
a rate of approximately 1 mg in 30
seconds. The drug takes effect in
about 2 minutes after the injection has
been given.
Premedication before induction of
anesthesia
(i.m.
or
rectal
administration in children). Induction
and maintenance of anesthesia. As an
induction
agent
in
inhalation
anesthesia or a sedative component in
combined anesthesia, including total
intravenous anesthesia (i.v. injection,
i.v. infusion).
In adults below the age of 60 the
initial dose is 2.5 mg given 5 - 10
minutes before the beginning of the
procedure.
Ataralgesia in combination with
ketamine
in
children
(i.m.
administration).
Further doses of 1 mg may be
given as necessary.
A total dose greater than 5 mg is
usually not necessary.
Long-term sedation in intensive
care units (i.v. administration as bolus
injection or continuous infusion).
In adults over 60 years of age,
debilitated or chronically ill patients,
the initial dose must be reduced to 11.5 mg and given 5-10 minutes before
the beginning of the procedure.
Further doses of 0.5-1 mg may be
given as necessary.
A total dose greater than 3.5 mg is
usually not necessary.
Dosage and administration
Midazolam is a potent sedative
agent
which
requires
slow
administration and individualization
of dosage.
The dose should be individualized
and titrated to the desired state of
sedation according to the clinical
need, physical status, age and
concomitant medication.
In adults over 60 years of age,
debilitated or chronically ill patients
287
Appendix I
b) Anesthesia
Rectal administration in children:
The total dose of Dormicum ranging
from 0.3-0.5 mg/kg bodyweight
should be administered 20-30 minutes
before induction of anesthesia.
Pre-medication: Pre-medication
with Dormicum given shortly before a
procedure does produce sedation
(induction of sleepiness or drowsiness
and relief of apprehension) and
preoperative impairment of memory.
Rectal administration of the
ampoule solution is performed by
means of a plastic applicator fixed on
the end of the syringe.
Dormicum
can
also
be
administered in combination with
anticholinergics.
If the volume to be administered is
too small, water may be added up to a
total volume of 10 ml.
The pre-medication is usually
administered 20-60 minutes before
induction of anesthesia. Intramuscular
administration: In adults below the
age of 60 the dose of Dormicum
ranges from
Induction: The desired level of
anesthesia is reached by stepwise
titration.
The intravenous induction dose of
Dormicum should be given slowly in
increments. Each increment of not
more than 5 mg should be injected
over 20-30 seconds allowing 2
minutes
between
successive
increments.
0.07-0.1 mg/kg according to the
general condition of the patient.
The usual dose is 5 mg.
In adults over 60 years of age,
debilitated and chronically ill, the
dose ranges from 0.025-0.05 mg/kg.
In pre-medicated adults below the
age of 60 the dose can range from
0.15-0.2 mg/kg but a total dose
greater than 15 mg is usually not
necessary.
The usual dose is 2-3 mg.
In children between ages of 1 and
15 proportionally higher doses are
required than in adults in relation to
body weight. The dose range from
0.08-0.2 mg/kg bodyweight has been
shown to be effective and safe.
In non pre-medicated adults below
the age of 60 the dose may be higher
(0.3-0.35 mg/kg bodyweight), but a
total dose greater than 20 mg is
usually not necessary.
Dormicum should be administered
deep into a large muscle mass 30-60
minutes prior to the induction of
anesthesia.
In adults over 60 years of age,
debilitated and chronically ill
patients, lower doses will be required.
288
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
Maintenance: The maintenance of
the desired level of unconsciousness
can be achieved by either further
intermittent doses or continuous
infusion of intravenous Dormicum
typically in combination with
analgesics.
allowing
2
minutes
successive increments.
between
The maintenance dose usually
ranges from 0.03-0.1 mg/kg/hr when
used in combination with narcotics or
ketamine.
In hypovolemic, vasoconstricted
or hypothermic patients the loading
dose should be reduced or omitted.
The intravenous loading dose can
range from 0.03-0.3 mg/kg but a total
dose greater than 15 mg is usually not
necessary.
The maintenance dose can range
from 0.03-0.2 mg/kg/hr.
In adults over 60 years of age,
debilitated or chronically ill patients,
lower maintenance doses will be
required.
The level of sedation should be
assessed regularly if permitted by
patient's condition.
In children receiving ketamine for
anesthesia
(ataralgesia),
an
intramuscular dose of Dormicum of
0.15 - 0.20 mg/kg is recommended.
In hypovolemic, vasoconstricted
or
hypothermic
patients
the
maintenance dose should be reduced,
at times to as low as 25 % of the
usual dose.
A sufficiently deep level of sleep
is generally achieved after 2-3
minutes.
When Dormicum is given with
potent analgesics, the latter should be
administered first so that the sedative
effects of Dormicum can be safely
titrated on top of any sedation caused
by the analgesic.
c) Intravenous sedation in the
intensive care unit
The desired level of sedation is
reached by stepwise titration of
Dormicum followed by either
continuous infusion or intermittent
bolus.
Special dosage instructions
Compatibility
with
infusion
solutions: The Dormicum ampoule
solution can be diluted with sodium
chloride 0.9 %, dextrose 5 % and 10
%, levulose 5 %, Ringer's solution
and Hartmann's solution in a mixing
ratio of 15 mg midazolam per 100 1000 ml infusion solution. These
solutions remain physically and
chemically stable for 24 hours at
The intravenous loading dose
should be given slowly in increments.
Each increment of 1-2.5 mg
should be injected over 20-30 seconds
289
Appendix I
room temperature, or 3 days at 5 C
(see also Special remarks).
involuntary movements (including
tonic/clonic convulsions and muscle
tremor) have also been observed.
Should such symptoms suggestive of
a paradoxical reaction occur, the
response to Dormicum should be
evaluated before proceeding.
The Dormicum Ampoule solution
should not be diluted with Macrodex
6 % in Dextrose or mixed with
alkaline injections.
Convulsions have been reported in
premature infants and neonates.
Contraindications
Known
hypersensitivity
benzodiazepines.
to
Dormicum ampoules should be
used only when resuscitation facilities
are available, as i.v. administration of
Dormicum may depress myocardial
contractility and cause apnea. After
receiving Dormicum parenterally,
patients should not be discharged
from hospital or consulting room for
at least 3 hours and then only if
accompanied by an attendant. Prior to
receiving Dormicum, the patient
should be warned not to drive a
vehicle or operate a machine for at
least 12 hours.
Precautions
Special
caution
should be
exercised
when
administering
Dormicum parenterally to patients
representing a higher risk group:
adults over 60 years of age,
debilitated or chronically ill, patients
with obstructive pulmonary disease,
with chronic renal failure, impaired
hepatic function or with congestive
heart failure. These higher risk
patients require lower dosages (see
Dosage and administration) and
should be continuously monitored for
early signs of alterations of vital
functions.
After prolonged i.v. administration
of Dormicum, abrupt discontinuation
of the product may be accompanied
by withdrawal symptoms. Therefore,
a gradual reduction of Dormicum is
recommended.
As with any substance with CNS
depressant and/or muscle-relaxant
properties, particular care should be
taken when administering Dormicum
to a patient with myasthenia gravis,
owing to pre-existing muscle
weakness.
Pregnancy, nursing mothers
Dormicum - like other drugs should not be used in the first three
months
of
pregnancy
unless
considered absolutely necessary by
the physician. Special care must be
taken when benzodiazepines are used
during labour and delivery, as high
In rare cases paradoxical reactions
such as agitation, hyperactivity and
aggressivity
have
occurred;
290
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
single doses may produce respiratory
depression, hypotonia, hypothermia
and poor sucking in the neonate.
Midazolam passes into breast milk
and in general, should not be
administered
to
breastfeeding
mothers.
In rare cases paradoxical reactions
such as agitation, hyperactivity and
aggressivity
have
occurred;
involuntary movements (including
tonic/clonic convulsions and muscle
tremor) have also been observed.
Undesirable effects
Local effects on veins (pain on
injection and thrombophlebitis) can
occur.
Dormicum is well tolerated. Slight
decrease in arterial blood pressure
and slight changes of heart rate and
respiration are fairly common.
In isolated cases, generalized
hypersensitivity, from skin reactions
to anaphylactoid reactions, have been
reported.
Severe cardiorespiratory adverse
events have occurred on rare
occasions. These have included
respiratory
depression,
apnea,
respiratory arrest and/or cardiac
arrest. Such life-threatening incidents
are more likely to occur in adults
over 60 years of age and those with
pre-existing respiratory insufficiency
or impaired cardiac function,
particularly when the injection is
given too rapidly or when a high
dosage is administered. Dormicum
ampoules should be used only when
resuscitation facilities are available.
Convulsions have been reported in
premature infants and neonates.
After prolonged i.v. administration
of Dormicum, abrupt discontinuation
of the product may be accompanied
by withdrawal symptoms.
After rectal administration,
slight euphoria has been observed.
a
Interactions
Enhancement of the central
depressive effect may occur when
Dormicum is used concomitantly with
antipsychotics, hypnotics, anxiolytics
/sedatives, antidepressants, narcotic
analgesics,
antiepileptic
drugs,
anesthetics
and
sedative
antihistamines.
The following adverse events have
also
been
observed:
Nausea,
vomiting,
headache,
hiccoughs,
laryngospasm, dyspnea, hallucination,
oversedation, drowsiness, ataxia.
Anterograde amnesia may still be
present at the end of the procedure
and in isolated cases prolonged
amnesia has been reported.
There is a potentially relevant
interaction between midazolam and
compounds which inhibit certain
291
Appendix I
hepatic
enzymes
(particularly
cytochrome P 450 III A).
Overdosage
The symptoms of overdose are
mainly an intensification of the
pharmacological effects; central
depression (from oversedation to
coma), mental confusion, lethargy
and muscle relaxation or paradoxical
excitation. In most cases only
observation of vital functions is
required.
Data clearly indicate that these
compounds
influence
the
pharmacokinetics of midazolam and
that this may lead to prolonged
sedation. At present this reaction is
known to occur in vivo with
ketoconazole,
itraconazole,
erythromycin, diltiazem, verapainil
and cimetidine, but not with
cyclospon'n and nitrendipine.
Extreme overdosage may lead to
coma, areflexia, cardiorespiratory
depression and apnea, requiring
appropriate
countermeasures
(ventilation, cardiovascular support).
The effects of overdosage can be
controlled with the benzodiazepine
antagonist
Anexate
(active
ingredient: flumazenil).
Therefore patients receiving the
above compounds or others which
inhibit P 450 III A together with
midazolam should be monitored
carefully for the first few hours after
administration of midazolam. (Studies
have shown that ranitidine has no
significant
effect
on
the
pharmacokinetics of intravenously
given midazolam.)
Special remarks
One study in-vitro has shown the
hydroxylation of midazolam to be
inhibited by a number of other
substances
(e.g.
amiodarone,
neuroleptics); accordingly, interaction
with a whole range of medicaments is
theoretically possible. However, there
is no evidence that these results are of
clinical relevance.
Incompatibilities
Do not dilute Dormicum ampoule
solutions with macrodex 6% in
Dextrose.
Alcohol may enhance the sedative
effect of midazolam.
Storage
Dormicum ampoules should not be
frozen because they can burst.
Furthermore, precipitation can occur
which dissolves on shaking at room
temperature.
Do not mix Dormicum ampoule
solutions in alkaline injections.
Midazolam precipitates in sodium
bicarbonate.
Stability
292
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
This medicine should not be used
after the expiry date (EXP) shown on
the pack.
Medicine: Keep out of reach of
children
Current at November 1995
Packs
Ampoules 5 mg in 1 ml
Ampoules 15 mg in 3 ml
Ampoules 5 mg in 5 ml
Ampoules 50 mg in 10 ml
Rectal applicators
F. Hoffmann-La Roche Ltd, Basel,
Switzerland
10
5
10
5
50
293
Appendix I
FLUMAZENIL
International Standard Prescribing Information
November 1993
ANEXATE
RO 15-1788
Anexate (Lanexat in Finland)
Flumazenil
Benzodiazepine antagonist
In animal experiments the effects of
compounds showing not affinity for
benzodiazepine
receptors,
e.g.
barbiturates, ethanol, meprobamate,
GABA mimetics, adenosine receptor
agonists, were not affected by
Anexate,
but
those
of
nonbenzodiazepine
agonists
of
benzodiazepine receptors, such as
cyclopyrrolones (e.g. zopiclone) and
triazolopyridazines, were blocked.
The
hypnotic-sedative
benzodiazepine effects are rapidly
reversed by Anexate after its i.v.
injection (within 30-60 seconds) and
may reappear gradually within the
next few hours, depending on the
half-life and dose ratio of the agonist
and antagonist. In animal toxicity
studies, Anexate proved to be of low
toxicity and devoid of mutagenic
activity. Anexate may possess some
weak
intrinsic
agonistic,
e.g.
anticonvulsant, activity.
Composition
Active ingredient: flumazenil.
Ampoules containing 0.5 mg
active ingredient in 5 ml aqueous
solution and 1 mg active ingredient in
10 ml aqueous solution (for i.v.
administration).
Excipients:
ethylenediaminetetraacetic
acid,
acetic acid, sodium chloride, sodium
hydroxide, water for injections.
Properties and effects
Anexate,
an
imidazobenzodiazepine, is a benzodiazepine
antagonist which, by competitive
inhibition, specifically blocks the
central nervous effects of agents
acting
through
benzodiazepine
receptors. The antagonistic effect was
documented in studies involving 17
different benzodiazepine derivatives.
294
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
In animals pretreated with high
doses of benzodiazepines over several
weeks, Anexate elicited symptoms of
withdrawal.
Indications and usage
Anexate is indicated for reversal
of the centrally sedative effects of
benzodiazepines. It is therefore used
in anesthesia and intensive care in the
following indications:
Pharmacokinetics
Distribution
Flumazenil, a weak lipophilic
base, is about 50% bound to plasma
proteins. Albumin accounts for two
thirds of the plasma protein binding.
The mean volume of distribution at
steady state (Vss 0.95 l/kg) is similar
to that of structurally related
benzodiazepines.
In anesthesia: Termination of
general anesthesia induced and
maintained with benzodiazepines in
inpatiens.
Metabolism
The carboxylic acid in free and
conjugated form is the main
metabolite in human urine. In
pharmacological tests, this main
metabolise was inactive as a
benzodiazepine agonist or antagonist.
In intensive care: Anexate
provides diagnostic indications of
intoxication with benzodiazepines or
rules such intoxication out.
Reversal
of
benzodiazepine
sedation in short diagnostic and
therapeutic procedures in both
inpatients and outpatients.
As a diagnostic measure in
unconsciousness of unknown origin
to differentiate between involvement
of benzodiazepines, other drugs or
brain damage.
Elimination
Flumazenil is almost completely
(99%) nonrenally eliminated. 'The
mean total plasma clearance of
flumazenil is 1 1/min and can be
attributed almost entirely to hepatic
clearance. The low renal clearance
rate suggests effective reabsorption of
the drug after glomerular filtration.
The average elimination half-life of
the drug is 50-60 minutes.
As specific reversal of the central
effects of benzodiazepines in the drug
overdose (return to spontaneous
respiration and consciousness in order
to render intubation unnecessary or
allow extubation).
Dosage and administration
Standard dosage
Anexate should be administered
i.v. by an anesthesiologist or
experienced physician. For infusion,
295
Appendix I
Anexate may be diluted with dextrose
5% or sodium chloride 0.9%; it may
also be used concurrently with other
resuscitative procedures.
Restrictions on use
Contraindications
In anesthesia: The recommended
initial dose is 0.2 mg administered i.v.
over 15 seconds. If the desired degree
of consciousness is not obtained
within 60 seconds, a second dose (0.1
mg) can be injected, and this may be
repeated at 60-second intervals where
necessary, up to a total dose of 1 mg.
The usual dose is 0.3-0.6 mg.
Anexate is contraindicated in
patients with known hypersensitivity
to the drug.
In mixed intoxications with
benzodiazepines
and
cyclic
antidepressants, the toxicity of the
antidepressants can be masked by
protective benzodiazepine effects. In
the
presence
of
autonomic
(anticholinergic), neurological (motor
abnormalities) or cardiovascular
symptoms of severe intoxication with
tricyclics/tetracyclics, Anexate should
not be used to reverse benzodiazepine
effects.
In the intensive care unit: The
recommended initial dose is 0.3 mg
i.v. If the desired degree of
consciousness is not obtained within
60 seconds, Anexate may be injected
repeatedly until the patient awakes or
up to a total dose of 2 mg. If
drowsiness recurs, an i.v. infusion of
0.1-0.4 mg per hour has been shown
to be useful. The rate of infusion
should be individually adjusted up to
the desired level of arousal.
Precautions
The use of Anexate is not
recommended in epileptic patients
who
have
been
receiving
benzodiazepine treatment for a
prolonged period. Although Anexate
exerts a slight intrinsic anticonvulsant
effect, its abrupt suppression of the
protective effect of a benzodiazepine
agonist can give rise to convulsions in
epileptic patients.
In the intensive care unit, in
patients treated for a long time with
high doses of benzodiazepines, the
individually titrated injections of
Anexate, slowly administered, should
not produce withdrawal syndromes. If
unexpected signs of overstimulation
occur, 5 mg diazepam or 5 mg
midazolam should be given i.v.
Patients with severe head injury
(and/or unstable intracranial pressure)
treated with Anexate to reverse the
effects of benzodiazepines may
develop raised intracranial pressure.
If a significant improvement in
consciousness or respiratory function
is not obtained after repeated doses of
Anexate,
a
nonbenzodiazepine
etiology must be assumed.
Effect on driving and other
psychomotor skills in outpatients
296
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
Although after i.v. administration
of Anexate the patients are awake and
conscious, they should be warned
against engaging in hazardous
activities requiring complete mental
alertness
(such
as
operating
dangerous machinery or driving a
motor vehicle) during the first 24
hours after administration since the
effect of the originally ingested or
administered benzodiazepine may
return.
injection
of
Anexate.
These
undesirable effects usually did not
necessitate special treatment.
Very rarely, seizures have been
reported, particularly in patients
known to suffer from epilepsy.
Rapid injection of Anexate in
patients with long-term exposure to
benzodiazepines ending at any time
within the weeks preceding Anexate
administration
may
produce
withdrawal symptoms and should
therefore be avoided. If such
symptoms arise, a slow i.v. injection
of 5 mg diazepam or 5 mg midazolam
should be given.
Pregnancy, nursing mothers
Although studies in animals given
high doses of Anexate have not
shown evidence of embryotoxicity or
teratogenicity, no controlled studies
involving pregnant women have been
conducted. Attention is therefore
drawn to the general medical
principle that no drugs should be
administered in the early stages of
pregnancy except where absolutely
necessary.
Interactions
Anexate blocks the central effects
of benzodiazepines by competitive
interaction at the receptor level. The
effects of nonbenzodiazepine agonists
at benzodiazepine receptors, such as
zopiclone, triazolopyridazines and
others, are also blocked by Anexate.
Parental administration of Anexate
in emergencies is not contraindicated
during lactation.
Particular caution is necessary
when using Anexate in cases of
mixed drug overdose since the toxic
effects (such as convulsions and
cardiac dysrhythmias) of other drugs
taken in overdose (especially cyclic
antidepressants) may emerge with the
reversal of the benzodiazepine effects
by Anexate.
Undesirable effects
Anexate was well tolerated even at
high parenteral doses of up to 100
mg.
In rare cases during use in
anesthesia, flush, nausea and/or
vomiting have been reported.
Complaints such as feeling of
anxiety, palpitations and fear have
been infrequently observed after rapid
The
pharmacokinetics
of
benzodiazepine agonists are unaltered
297
Appendix I
in the presence of Anexate and vice
versa.
Stability
This medicine should not be used
after the expiry date (EXP) shown on
the pack.
Overdosage
Even when given at a dosage of
100 mg i.v., no symptoms of
overdosage were observed. For
withdrawal symptoms attributable to
the agonist, see under Standard
dosage.
Packs
Ampoules 0.5 mg in 5 ml
Ampoules 1 mg in 10 ml
5,25
5,25
Medicine: keep out of reach of
children
Special remarks
Current at November 1993
Please note
When used in anesthesiology at
the end of an operation, Anexate
should not be injected until the effect
of peripheral muscle relaxants has
subsided.
F. Hoffmann-La Roche Ltd, Basel,
Switzerland
298
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
DIAZEPAM
The national board of health
Summary of product characteristics for Stesolid Emulsion, injection
26 October 1995
1.
Trade name of the medicinal product
Stesolid Emulsion
2.
Qualitative and quantitative composition
Diazepam 5 mg/ml
3.
Pharmaceutical form
Injection
4.
4.1
CLINICAL PARTICULARS
Therapeutic indications
Conditions of anxiety and restlessness. Attacks of convulsions. Spasticity.
Alcohol withdrawal symptoms. Pre-anaesthetic medication. Induction of
anaesthesia and short-acting anaesthesia.
4.2
Posology and method of administration
Convulsions:
Adults: 10-20 mg by slow intravenous injection, repeated if necessary.
Children: 0.25-0.5 mg/kg by intramuscular or slow intravenous injection.
Pre-anaesthetic medication: 0,2 mg/kg intramuscularly, or 0.1-0.2 mg/kg by
slow intravenous injection.
Reduce the dose for elderly patients.
4.3
Contra-indications
Myasthenia gravis. Sleep apnoea. Severe liver insufficiency. Acute
respiratory depression.
4.4
Special warnings and precautions for use
Very slow intravenous injection, owing to the danger of respiratory
depression. Reduced dose for elderly patients. Habituating.
299
Appendix I
4.5
Interaction with other medicaments and other forms of interaction
Alcohol, hypnotics, neuroleptics, antihistamines, clonidine, and opioids
potentiate the sedative effect. Cimetidine, disulfiram, and oestrogen reduce
the rate of metabolism. Omeprazole may prolong the elimination time of
diazepam. Theophylline counteracts the sedative and psychomotor actions of
diazepam.
4.6
Pregnancy and lactation
Pregnancy: May be used, but not in the last trimester.
Lactation: Should not be used.
4.7
Effect on ability to drive and use machines
Warning symbol.
4.8
Undesirable effects
Tiredness. Drowsiness. Dizziness. Loss of memory, Ataxia. Disturbance of
the balance. Anterograde amnesia. Confusion. Paradoxical reactions, such as
confusion, excitation, and dysphoria, may occur (particularly in children and
elderly patients). Respiratory depression. Phlebitis.
4.9
Overdose
Loss of consciousness rising to come. Respiratory depression.
Treatment: Symptomatic, possibly flumazenil.
4.10
Dispensing category
A.
5. PHARMACOLOGICAL PARTICULARS
5.0
Therapeutic classification
N 05 BA 01
5.1
Pharmacodynamic properties
Pharmacotherapeutic group: Anxiolytic, belonging to the benzodiazepine
group.
Mode of action: Diazepam is an agonist, which binds to specific
benzodiazepine receptors in the brain, thereby potentiating the normal
transmission of the signal substance, GABA. GABA inhibits the
transmission of important signal substance, thus resulting in neuronal
inhibition. The muscle-relaxing effect is mediated via spinal synaptic
reflexes.
300
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
Pharmacodynamic effects: Diazepam is an anxiolytic, which acts by
suppressing the symptoms of anxiety, restlessness, and tension. Moreover,
diazepam possesses sedative and muscle-relaxing actions.
5.2
Pharmacokinetic properties
Distribution: The maximum plasma concentration sets in within 30-60
minutes of intramuscular injection of diazepam. Intravenous injection of
diazepam 10 mg produces a maximum plasma concentration of about 600
ng/ml within a few minutes. Further distribution brings about a marked fall
in the plasma concentration lasting for 2-4 hours. Protein binding: 96-98%.
Diazepam is lipid-soluble, penetrates tissue well, and crosses the blood-brain
barrier.
Metabolism: Diazepam is metabolised chiefly in the liver by hydroxylation
and glucuronidation. The half-life of N-desmethyldiazepam, the
metabolically active metabolite, is 2-4 days.
Elimination: Diazepam is eliminated chiefly with the urine in the form of
metabolites and about 10% is excreted with the faeces. Half-life: Adults: 2050 hours, elderly patients 70-100 hours. Children: premature infants 40-110
hours; new-born full-term infants about 30 hours; up to 1 year of age about
10 hours; and above 1 year of age about 20 hours.
5.3
Preclinical safety data
6.
PHARMACEUTICAL PARTICULARS
6.1
List of excipients
Diazepam, fractionated soya bean oil, diacetylated monoglycerides,
fractionated egg phospholipids, glycerol, sterile water.
6.2
lncompatibilities
Miscibility:
Intralipid in all concentrations.
Glucose solutions 55-300 mg/ml in glass infusion bottles.
May be injected through an infusion tube while the infusion is being given.
Adsorption of diazepam to polyvinyl chloride infusion containers may occur.
6.3
Shelf life
18 months.
6.4
Special conditions for storage
Room temperature.
301
Appendix I
6.5
Nature and contents of container
Glass ampoules.
6.6
Instructions for use/handling None.
7.
Marketing authorisation holder
A/S Dumex (Dumex Ltd)
Prags Boulevard 37,
DK-2300 Copenhagen S.
8.
9.
Marketing authorisation No. 9850
Date of authorisation/revision of summary of product characteristics
26 October 1995.
302
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
LIDOCAINE
CATALOGUE TEXT
23.3.1981
XYLOCAIN ADRENALIN 20 mg/ml + 12,5 microg/ml solution for injection
(Declaration)
Dosage
Lidocaine
hydrochloride
anhydrous 20 mg, adrenaline tartrate
corresp. to adrenaline 12,5 microg
(1:80 000), sodium chloride, sodium
metabisulphite, methylparahydroxybenzoate 1 mg, water for injection to
1 ml.
Usually 1-2 ml (20-40 mg
lidocaine chloride). With surgery 2-35 ml (40-60-100 mg lidocaine
chloride). Larger doses may be used
in special cases. Larger dose than 25
ml = 13 cylinder ampoules (500 mg
lidocaine chloride) should not be
exceeded. Dose for children and
debilatated has to be lower.
(Description)
In infiltration anesthesia the
duration of analgesia in pulpa is 60
minutes when Xylocaine Adrenalin
20 mg/ml + 12,5 microg/ml is used.
Due to the long duration of analgesia
and remarkable ischemic effect this
preparation is effective and gives
good visibility to the site of
operation.
Adverse events
Undesirable reactions are very rare
in the doses used in dental
procedures. Vertigo and drowsiness
may occur now and then followed by
overdosage or in connection with
decreased tolerance. Symptoms do
not usually require special treatment.
Serious undesirable reactions may
occur followed by clear overdosage,
accidental i.v. injection or in
connection with decreased tolerance.
The nature of complications
depends on the volume of the dose,
the administration route and the status
of the patient. Undesirable reactions
Indications
Local analgesia (anesthesia) with
odontological surgery, complicated
extractions and gingival surgery. The
preparation has a good ischemic
effect.
303
Appendix I
are mainly CNS and/or cardiovascular
reactions.
CNS
effects
cause
depression of the cerebral cortex and
medulla oblongata. Cerebral cortex
effects manifested in anxiety,
drowsiness,
blurred
vision,
difficulties to speak, tremor and
convulsions.
Medulla
oblongata
effects induce vomiting, paleness,
cold sweat and finally apnoea
(respiratory depression). Hypotension
is a sign of cardiovascular effect and
it may occur after, concomitantly or
also
before
CNS
excitation.
Myocardial depression may lead to
cardiovascular collapse and possible
cardiac arrest.
affecting the child at therapeutic
levels.
Serious reactions have to be
treated rapidly by ventilation,
(resuscitation),
administrating
barbiturates or muscular relaxants.
2 years. Keep cool but free from
frost.
Reactions caused by an overdose
of adrenaline see professional
literature.
Metal ions may dissolve e.g. from
cannules and syringes containing
metal parts. Solution must not be kept
long in contact with metal surfaces,
since dissolved metal ions may cause
severe local irritation (swelling) at the
site of injection.
There is no data if adrenaline
excreted in the breast milk, but it is
very unlikely that adrenaline has
absorption in the gastrointestinal
channel of the child.
Interactions
Adrenaline may increase the effect
of tricyclic antidepressants.
Storage and shelf-life
Sensitive to light, keep in box.
Pregnancy and lactation
Lidocaine has been used in large
number of pregnant women. An
increased incidence of malformations
or direct or indirect harmful effects
on the foetus have not been reported.
Lidocaine is excreted in the breast
milk, but there is generally no risk of
Packages
Cylinder ampoules 100 x 1,8 ml
Self-aspiriting cylinder ampoules 100
x 1,8 ml
304
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
PRILOCAINE
CATALOGUE TEXT
CITANEST OCTAPRESSIN 30 mg/ml + 0,54 microg/ml solution for injection
toxicity and it is well tolerated. It is
suitable as a routine localizing agent
provided that local ischemia is not
essential in the injected area.
(Declaration)
Prilocaine hydrochloride 20 mg,
felypressin 0,54 microg, sodium
chloride, water for injection to 1 ml.
Felypressin is tissue friendly and it
has a very low toxicity. Animal
studies has shown that felypressin in
low concentrations effects only
capillars in veins when adrenaline
and noradrenaline effect capillars
both in veins and in arteries. The
localizing effect of felypressin
increases local anaesthesia without
causing ischemia in the injected area.
(Description)
Citanest Octapressin contains
local anaesthetic, prilocaine, and
vasopressin analogue, felypressin.
Felypressin has a local effect
differently from adrenaline. Thus
Citanest Octapressin gives an optimal
local analgetic effect without any
significant
ischemia.
Citanest
Octapressin 30 mg/ml + 0,54
microg/ml solution has the same
anaesthesia frequence, reaction time,
distribution
and
potency
of
anaesthesia as Xylocain Adrenaline
20 mg/ml + 12,5 microg/ml solution
has.
Duration
of
infiltration
anaesthesia is a little shorter when
used Citanest Octapressin than when
used Xylocain Adrenaline. Duration
of mandibular anaesthesia is as long
as when used Xylocain Adrenaline 20
mg/ml + 12,5 microg/ml solution.
Citanest Octapressin has a low
Indications
(In
dentistry)
Infiltration
anaesthesia, where there is no need
for ischaemia in the injected area.
Regional nerve block anaesthesia.
Duration of infiltration anaesthesia in
pulp is about 45 minutes.
305
Appendix I
events (vertigo, drowsiness) may
sometimes occur followed by
moderate
overdosage,
or
in
connection with decreased tolerance.
Usually in these cases there is no
need for special treatment. Serious
undesirable reactions in dental
procedures are very rare but they may
occur followed by clear overdosage,
accidental i.v. injection or in
connection with decreased tolerance.
The nature of complications depends
on the volume of the dose, the
administration route and the status of
the patient. Undesirable reactions are
mainly CNS and/or cardiovascular
reactions.
CNS
effects
cause
depression of the cerebral cortex and
medulla oblongata. Cerebral cortex
effects manifested in anxiety,
drowsiness,
blurred
vision,
difficulties to speak, agitation and at
last tremor and convulsions. Medulla
oblongata effects induce vomiting,
paleness, cold sweat and finally
apnoea (respiratory depression).
Hypotension is a first sign of
cardiovascular effect and it may occur
after, concomitantly or also before
CNS
excitation.
Myocardial
depression may lead to cardiovascular
collapse and possible cardiac arrest.
Dosage
Usually 1-2 ml (30-60 mg
lidocaine chloride). Maximum dose
600 mg = 20 ml = 11 cylinder
ampoules. Dose for children and
debilatated have to be lower.
Contraindications
Hypersensitivity
anaesthetic agents.
to
local
Pregnancy and lactation
Citanest Octapressin has been
administered to a large number of
pregnant women. An increased
incidence of malformations or direct
or indirect harmful effects on the
foetus have not been reported.
Prilocaine is excreted in breast milk,
but there is generally no risk of
affecting the child at therapeutic
levels.
It is not known whether
felypressin is excreted in breast milk.
Adverse events
Undesirable reactions are very rare
in the doses used in dental
procedures.
Allergic
reactions.
Allergic
reactions (in the most severe
instances anaphylatic shock) to local
anaesthesia of the amide type are rare.
When larger doses are used it may
in some cases occur paleness in face
due to the effect of Octapressin in
veins and it is not a symptom of
reduced blood pressure. Mild adverse
Serious reactions have to be
treated rapidly by ventilation,
(resuscitation),
administrating
barbiturates, diazepam or muscular
relaxants.
306
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
Packages
Methemoglobin.
Increase
of
methemoglobin or clinical symptoms
of methemoglobinemia has not been
reported with recommended doses.
However, methemoglobin may form
when used high doses. Prilocaine 600
mg (= 11 cylinder ampoules) may
increase methemoglobin level from
about 1 % (normal value) to 4 - 6 %.
Hemolysis does not follow this.
Cylinder ampoules (clear) 100 x 1,8
ml
Self-aspiriting cylinder ampoules 100
x 1,8 ml
Cylinder ampoules have been
hygienically packed in blisters. They
are for single-use. Preparation does
not contain preservatives. Discard
residue.
Special warnings
ATC-code
Studies has shown that there is no
interaction
between
Citanest
Octapressin
and
tricyclic
antidepressants.
N01BB04
Storage and shelf-life
3 years in room temperature.
Avoid freezing.
Sensitive to light, keep in box.
Metal ions may dissolve e.g. from
canules and syringes containing metal
parts. Solution must not be kept long
in contact with metal surfaces, since
dissolved metal ions may cause
severe local irritation (swelling) at the
site of injection.
307
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
7.2 APPENDIX II
QUESTIONS AND
PATIENTS COMMENTS OF
STUDIES 4 AND 5
309
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
According to my patient files I have performed a dental procedure for you
using sedative premedication. I am presently collecting scientific data
concerning these procedures. Therefore I am asking you to please kindly fill
in the enclosed questionnaire concerning your dental care, and return it to me
in the enclosed envelope. I would appreciate it if you could answer the
questions as soon as possible and return the questionnaire within a week
The study is a part of my thesis “Premedication in Dental Care” supervised
by Mr. Risto Kotilainen, Professor (oral surgery) and Mr. Matti Mattila,
Docent (Anaesthesiology) in the University of Kuopio.
The questionnaire will not reveal your name, nor is there any chance that
your person would be disclosed at any stage of the study. This ensures that
you can make your answers as honest as possible. The study material is
divided into two patient categories: those who seeked this treatment mainly
because of fear and those who were applied sedative medication because of
the nature of the procedure. This is why there may be points in the questions
that seem difficult or impossible to answer. In such a case you may simply
ignore the question. You may write your answer next to the question if
“yes/no” answers or the “tick the right box” method does not seem natural for
a question. It is always possible to tick several boxes. In the “yes/no”
alternatives, please strike out what is not appropriate.
I want to thank you in advance for your trouble. Your help is invaluable in
my work.
Elimäki, 7th June 1993
Kari Luotio
Dentist
tel. 951-77126
P.S. If you have any questions, please do not hesitate to phone me. The best
time to reach me is after 8 o’clock P.M.
311
Appendix II
The first group of questions define the reasons which made you seek this method of
treatment.
1. Primary division
a. I wanted this treatment primarily because of fear
b. I needed other treatment that was carried out in premedication
c. Other alternative, which? _____________________________
If you chose alternative “b” in the first point, please do not answer the four
following questions but continue directly from point 6.
2. Why did you seek treatment in premedication?
a. I wanted my teeth treated within one appointment
b. I am afraid of the pain involved in dental procedures
c. I am afraid of local anaesthesia
d. I have painful experiences of dentistry
e. My dentist - patient relationships always end at the start
f. Other reason, what? __________________________________
3. What has been the main reason for the discontinuation of previous dentist patient relationships? __________________________________________
4. Why did you not seek dental care in sleep (general anaesthesia)?
a. I am afraid of anaesthesia
b. Anaesthetic treatment is much more expensive
c. No anaesthetic treatment was available
d. Other reason, what? ___________________________________
5. What was the real initiative for you this time as you seeked treatment?
a. Another person’s recommendation of a dentist
b. The pressure from my spouse or some other next of kin
c. Disadvantageous changes in appearance
d. Bad smell/taste in the mouth or in breath
e. Pain, infection or other such symptom
f. Other reason, what? ___________________________________
312
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
6. What procedures were made this time?
a. Denture or a traditional bridge
b. A denture fitted in the jawbone
c. Surgical procedure, e.g. extraction
d. Filling
e. Gingivitis treatment
7. How long time was it since your previous appointment to the dentist?
__________ years
8. Did you at that time seek treatment because of toothache?
Yes / no
9. Was the treatment then discontinued? (Please strike out what is not appropriate)
Yes / no
10. When were your teeth last fully treated, or the treatment was finished?
_______ years earlier
The second group of questions deals with your socio-economic background and the
answers should be given according to the situation you were in at the time of the
treatment.
11. How old were you when the procedure was carried out?
__________ years
12. Are you male / female
(please strike out what is not appropriate)
13. Were you at that time
a. married
b. living together
c. divorced
d. single
313
Appendix II
14. How many children did you have at that time?
__________ children
15. What was your education?
a. Comprehensive school
b. Vocational college
c. College
d. University
16. Did you then live
a. in your own apartment
b. in a rented apartment
c. as a subtenant
d. with your parents
e. in another form of housing
Did you then work
17.
a. as an employee
b. as private entrepreneur
c. I was not working
d. I was unemployed
e. I was student
18.
a.
b.
c.
d.
in a leading position
in a supervisory position
as a qualified worker
as unskilled labour
19. What was your profession? ____________________________
20. What was the level of income (rounded in the nearest thousand marks) of your
family (the household you lived in at the time)?
Gross earnings ca. _________ FIM/month
21. What was your personal level of income at that time?
Gross earnings ca. _________ FIM/month
314
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
22. Did you have difficulties in covering the expenses of the treatment? Yes / no
23. Did you receive any reimbursements for the treatment costs from the National
Pensions Institute?
Yes / no
How much? Some _______ %
24. Did you receive other reimbursements?
Yes / no
From where? _______________
How much? _______________
25. Do you feel that this type of treatment should be
a. Free of charge (100 % reimbursement)
b. With nominal charge (90 % reimbursement)
c. Partly reimbursed (50 %)
d. Society should not participate in the costs of this type of treatment.
315
Appendix II
This page is an example to explain for you how to answer the questions in the
following pages.
Question:
Was there any pain during the procedure?
The purpose is that you imagine a scale where one end is marked by
“the greatest imaginable pain” and the other end is marked by “not the
slightest feeling of pain”. You would then think where in this scale
your experience concerned would be situated. You will find vertical
lines in the following pages and next to them words to help identify
the feelings. To this scale you should insert a cross line or a cross at
the point where you think your feelings would fit in.
Model answer in words: “I faintly remember a slight pain towards the
end of the treatment, but I cannot even remember what it was
connected to.”
You would then draw a cross somewhere between “no pain” and
“slight pain”.
Model answer drawn on the scale:
Immense
Severe
Slight
Insignificant
(or none at all)
316
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
The next group of questions deals with how you experienced the treatment itself.
26. Please insert a line to the scale below at places that in your opinion best
describe your experience of the treatment.
General impression of the treatment
Satisfaction to treatment
Wonderful
Happy
Pleasant
Pleased
Unpleasant
Unsatisfied
Objectionable
Disappointed
27. Which procedures where made at that time?
a. filling
b. excavation
c. scaling tartar from teeth
d. surgery
28. If the procedure were to be made again, would it be done?
a. in the same way, or with premedication
b. conventionally with local anaesthesia
c. even without local anaesthesia
d. in sleep (general anaesthesia)
317
Appendix II
29. Could you recommend this method of treatment to others?
Yes / no
30. Have you been able to personally make an appointment or make ordinary
consultation calls to the dentist after this treatment?
Yes / no
31. Please insert lines to the scale below at places that in your opinion best describe
your sensations during treatment.
Pain
Fear
Drowsiness
Anxiety
Confusion
Immense
Strong
Slight
Insignificant
The last group of questions will deal with the consequences of the treatment.
32. Did you have any of the following symptoms between end of the dental
procedure and falling asleep back home, and if yes, how much?
a. Confusion
____________
b. Drowsiness
____________
c. Pain
____________
d. Headache
____________
e. Nausea
____________
f. Vomiting
____________
g. Other, what? __________________________
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Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
33. After you woke up, did you have any of the following symptoms, and how
much?
a. Confusion
____________
b. Drowsiness
____________
c. Pain
____________
d. Headache
____________
e. Nausea
____________
f. Vomiting
____________
g. Other, what? __________________________
34. Again, please draw a line that describes your general condition at the following
stages:
From end of
treatment to
falling asleep
at night
From the
following morning
to the following
night
Excellent
Good
Poor
Miserable
319
During the week
following
treatment
Appendix II
35. How many hours after the treatment did you consider yourself sleepy or
confused?
_____________ hours
36. What is your escort’s view on the above question?
____________ hours
37. What time did the procedure begin?
At _____________
38. What time did the procedure end?
At _____________
39. What time did you fall asleep after the procedure?
At _____________
40. What time did you then wake up?
At _____________
41. Did you consider yourself able to work the following morning?
Yes / no
42. What is your escort’s / spouse’s view of the above?
Yes / no
43. Did you consider yourself able to drive a car the following morning? Yes / no
44. What is your escort’s /spouse’s view of the above question?
Yes / no
45. What do you think the symptoms you experienced came from?
a. From the procedure itself
b. From local anaesthesia
c. From premedication
d. Other, what? __________________________________
46. What symptoms do you think followed the premedication?
________________________________________________________
________________________________________________________
47. How many months is it since the procedure was made? (Please answer in
months, not in years)
_____________ months
320
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
Here I have reserved some space in case you would like to share your ideas on the
procedures and your experiences. Please feel free to use also the back of the page
when needed.
________________________________________________________
________________________________________________________
________________________________________________________
________________________________________________________
________________________________________________________
________________________________________________________
Finally I have marked your medication below with a code. Your person will not be
disclosed from this.
do
st
fe
mu
xy
ci
321
ta
dg
co
Appendix II
Answers to question 3:
1:
5:
6:
7:
9:
13:
14:
15:
16:
17:
19:
21:
22:
23:
26:
27:
29:
31:
35:
37:
39:
40:
41:
43:
44:
46:
48:
51:
52:
53:
94:
95:
96:
99:
102:
106:
108:
Fear of pain
Previous appointment 15 years earlier, fainting in the middle of the
procedure, scolded by dentist in addition to all the pain
Have not been allowed to seek treatment before pains
Fear, getting bored of the many appointments
Change of address
Dentist’s lack of consideration, did not use enough anaesthetic
Timidity
Fear
The dentist moved away from the district
Moving away from the areas
A long trip
Fear
Fear, fainting, nausea
Fear
Pain
A renewing pain under old fillings
Pain during treatment
Lack of time, fear, financing
Financial situation
Fear
Moving away from the area
The previous dentist, Mr. Mönkkönen, discontinued his surgery
Pain, fear
Fear
Fear
I was afraid of pain the previous dentists had been harsh and hurt me
Fear
Too painful procedures
Indifference, carelessness
Fear
Neglected teeth - carelessness, fear
Cannot easily leave from work (long distances)
Have not had so-called treatment plan before (now own financing)
Extremely long intervals between treatments
Poor result of treatment
The patient - dentist relationship did not end but I changed dentist.
Bad experiences
322
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
Comments written at the end:
Patient 1:
Maybe (I will make a new appointment) if I will get toothache, but I do not think
I will go to a dentist voluntarily.
I’m really happy as my teeth were done in one single appointment. I recommend
to all who are afraid of going to the dentist.
Patient 2:
My childhood experiences (of the dentist are) really bad. All milk teeth were
excavated and that caused my present fear.
I will recommend to all who suffer from fear of dentist. The procedure was so
painless and, I think, a simple thing. Maybe next time I can agree to treatments
without premedication, and to get all done at once is in my opinion a positive thing,
and the fact that I was being informed all the time on what was being done in my
mouth.
Finally. With the school scale from 4 to 10 I give 10+ for my own experience! I
was so pleased. I wish you a nice summer.
Patient 5:
(My) previous appointment (was) 15 years ago, fainting in the middle of
procedure, I was scolded by the dentist in addition to all the pains (and this ended
all my previous patient - dentist relationships).
Patient 6:
During the procedure (towards the end, if I can remember it correctly) I was cold
and shaky. I don’t know if this would have been caused by end of effect of
medication, the situation was remedied in due course. The pains I experienced
afterwards were caused mainly by the many fillings done, and they were mild.
323
Appendix II
Patient 7:
(My earlier dentist - patient relationships were discontinued due to) fear, getting
bored to the many appointments. I knew there were many large holes. I had gone
through general anaesthesia many times in previous surgeries (so I did not wish
general anaesthesia). I have shared my positive experiences on premedication, and
many people have been interested in this. Even a stranger once called me and asked
how he could get such a treatment and where.
Patient 8:
I did not feel the excavation. The surgery felt like milling, but I felt no pain. If I
had known before what the procedure would be like, I would not have had to fear so
much.
Patient 12:
I recommend to all who suffer from fear.
Patient 13:
I was pleased with the procedures and will recommend to others who are afraid
of going to the dentist.
Patient 14:
I am pleased with the procedure and from my experience I can recommend this
to others.
Patient 16:
Despite anticipating fear, the procedure was painless. The symptoms that
followed were caused by the number of teeth that were being excavated. The pain
killers I received were efficient.
Patient 17:
I have discussed dental care in premedication with another person who suffers
panic disorders. Our experiences were similar, or the premedication takes away the
feeling of pain (anaesthesia) but a strong mental anxiety remained. The need to
escape - typical for a panic disorder patient - (you’ve got to get away) was immense.
(The muscles were relaxed but not the mind.) Thinking about it afterwards, it was
an unpleasant experience for me mentally. But I was very pleased with the result.
324
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
Patient 19:
The procedures I felt were very appropriate and pleasant. No unpleasant sideeffects. I warmly recommend this method of treatment for everyone.
Patient 20:
A sister of my late husband’s she cannot take pain either in connection with
dental care, and therefore she cannot get herself to the dentist she has been very
interested in this treatment of mine she is 30 years old. In my case this is the only
method of treatment as far as oral treatment is concerned.
Patient 21:
The premedication was probably so mild that no symptoms followed the
treatment. During the procedure the filling caused some pain, but not disturbingly.
All in all the most pleasant dental appointment I’ve had.
Patient 22:
I think the procedure should have been done with less premedication. Is it
possible that the tachycardia of the heart could be caused by anaesthesia? Also my
blood pressure rose, whether this is normal I do not know. All in all a good
experience as I felt no fear, the resulting drunkenness was a little unpleasant. This
may be caused also because I have not felt well for a year.
Patient 23:
(answer to question 5) The advertisement that gave the image that fear and its
causes are accepted, not underestimated. Also the feeling that people care.
Patient 26:
The procedures were painless and fast.
Patient 29:
If I had guessed this was so painless I would have had my teeth treated earlier.
Patient 33:
I am fully satisfied myself, and relieved of many years’ pain; fast and careless,
even a pleasant experience. I recommend to people easily scared or with weak teeth.
325
Appendix II
Patient 34:
I am a panic disorder patient. Dispite the premedication I was still anxious.
Panic! The premedication during procedure was not strong enough? I was
disappointed with the effects of premedication. It was not effective enough, that’s
why I was afraid during the procedure. And had to take painkillers astonishingly
many days, ca. one week. Then at first the pain was relieved. Next time I have a
tooth excavated, I would like to undergo general anaesthesia.
Patient 35:
The experience of the procedure most positive, can recommend to others!
Patient 36:
In all ways a pleasant and polite experience!
Patient 41:
I recommend and have already recommended the treatment in question for my
friends/relatives. I understand fear for dentist is very common.
Patient 42:
The procedure was a pleasant experience. I have recommended also for other
“cowards”.
Patient 43:
A very good treatment cannot be blamed really good
Patient 45:
It was all over in one go, beautifully.
Patient 46:
In my opinion the use of a sedative or premedication is excellent for patients
who are genuinely afraid of the pains experienced at the dentist’s, and afraid of the
suspense which for me is very intense. My experiences at Mr. Kari Luotio’s surgery
have been excellent. I think Mr. Luotio always shows personal consideration of the
patient, and I could not imagine going to any other dentist. I recommend
premedication also for others who suffer pain and fear, and I have told many people
about it and many have asked for the place from me, where you may have it, even
from other regions. A really good method of treatment.
326
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
Patient 47:
The procedure was quite pleasant the days that followed were awful the pain
indescribable.
Patient 48:
A pleasant experience, at first I was a little scared. The fear went away after
medication. Time just flied (3,5 hours). No consequences the following morning.
Patient 50:
It is a relief to know that there is such a possibility, if there will be other major
procedures with anaesthesia. I was aware of what was happening and I recall our
talks but I felt nicely like “who cares!”.
Patient 51:
Otherwise I’m most pleased to the procedure being done with premedication, but
at some stage I felt a severe pain, fortunately only for a moment. Too little
medication? I cannot remember a thing of the procedure, or it felt like general
anaesthesia. I am pleased.
Patient 54:
Painkilling medication immediately (0-0,5 hours) after procedure, or even the
first painkiller from the dentist!
Patient 57:
I am a worrier by nature all new things make me wonder. As I get to know them
the suspense disappears. I felt quite calm before the procedure.
Patient 58:
There was no effect to the ability to work the next morning; the procedure as
such was so large that it had an effect e.g. to the ability to speak and eat.
Patient 62:
No negative comments about premedication.
Patient 64:
The experience did not cause anxieties, even though one might think so at first.
When needed I will recommend this also to others.
327
Appendix II
Patient 65:
I was prejudiced at first, that fitting the implant would be painful. I am surprised
the procedure went quite painlessly in my opinion.
Patient 70:
“Through difficulties to victory!”
Patient 73:
By far the biggest problems were those caused by temporary loose dentures.
Patient 75:
The most unpleasant thing after the procedure was a quite marked swelling in the
cheek on the side that was operated, and it lasted a few days.
Patient 76:
A week after the procedure I was more tired than usually, otherwise I felt really
good.
Patient 77:
Taking the medicine caused quite a strong pain in the stomach. The results up to
now are good.
Patient 79:
Drilling the denture into the jawbone was a suprisingly painless procedure. The
only disadvantage here is a seemingly lengthy process.
Patient 82:
The experience was pleasant and painless, I did not need any painkillers. Healing
was fast but due to the nature of my work 3 days off work was adequate. The
stitches had melted some 9 days from procedure. I can recommend this to others!!
THANK YOU!
Patient 83:
I am very pleased with the result.
Patient 85:
I have told about this to many people and I warmly recommend premedication in
dental care.
328
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
Patient 86:
Through this procedure I have been greatly helped with my teeth. I am really
happy that I found the person who committed himself to look after these teeth. Here
in the country possibilities are very weak and getting information on this kind of
treatment is quite difficult. I am disappointed with public dental care if their
resources or skills run out. Continuation or advice for additional care are bleak. The
only advice I have got was that we’ll wait and then fit in dentures.
Patient 88:
The experience of the operation was painless and pleasant. I felt calm and safe. I
can recommend this to everyone. The resulting pains healed fast.
Patient 92:
I have been very pleased with the treatment given, and the general attitude. I
have also recommended the treatment to my friends and openly told them what I
have been able to.
Patient 93:
My best experience on a dentist appointment!
Patient 96:
You know for yourself “where you are” and may partly participate in the
treatment. Feel quite calm during the procedure. Not confused after the procedure.
Patient 97:
During the two-hour operation I felt good. Time passed surprisingly quickly.
Patient 98:
If painkiller is injected in the vein during treatment the procedure is pleasant this
was the case the first time.
The second time, as far as I know, I did not receive a painkiller injection and the
procedure was a little more painful.
Patient 100:
After the operation I felt a little drowsy, but the most annoying thing was only a
somewhat “strange feeling” in the mouth.
329
Appendix II
Patient 106:
I sat with an open mouth for two hours but it seemed short, I felt no pain. I felt a
little tipsy. It was an altogether nice experience. I sat in the chair with confidence
and did not feel the anxiety I usually feel at the dentist’s. I can recommend (and
have already recommended) the same treatment for others (if their wallet can take
it).
Patient 107:
The treatment was a most pleasant experience, painless, and in today’s busy life
a fine thing as you do not need to run back and forth to the dentist’s. This method of
treatment should be increased, I mean more of these dentists who make procedures
all in one time.
Patient 108:
I was pleased with the procedure, such a large “redecoration” done with
suprisingly little pain. I felt no confusion and quickly recovered from the
premedication. I can recommend it.
330
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
7.3 APPENDIX III
PLETYSTOMOGRAFIC PULSE
WAVE
Published with permission of
Datex
331
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
CONTENTS
1
2
3
4
5
ARTERIAL FINGER CIRCULATION
REGULATION OF ARTERIAL CIRCULATION
REGISTRATION OF THE PULSE WAVE
SHAPE AND COMPONENTS OF THE PULSE WAVE
TYPICAL VARIATIONS IN THE PULSE WAVE DURING
ANAESTHESIA
6 CONCLUSIONS BASED ON CHANGES IN THE AMPLITUDE OF
THE PULSE WAVE DURING ANAESTHESIA
7 DIFFERENTIAL DIAGNOSIS
8 THE PLETHYSMOGRAPHIK WAVEFORM DISPLAYED BY
DATEX-ENGSTROM MONITORS
9 BENEFITS OF THE PLETHYSMOGRAPHIC WAVEFORM
10 DETERMINATION OF THE PULSE WAVE
11 TREND DISPLAY
12 SUMMARY
333
Appendix III
1 ARTERIAL FINGER CIRCULATION
Pulsatile blood flow causes
distinct variations in the amount of
blood in the vascular bed of the finger
due to the relatively large number of
arterioles near to the skin.
the vascular bed of the finger with
arterial blood. Photoelectric finger
plethysmography registers the volume
changes in arterial blood, and a
positive deflection denotes blood
volume increase at the place of
measurement (finger).
Pulsatile blood flow in the finger
is the result of left ventricle
contractions of the heart, which fill
Fig. 1. The effect of blood volume changes on the plethysmogram. The diameter
of the blood vessel increases when the local blood volume increases following heart
contractions.
334
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
2 REGULATION OF PERIPHERAL ARTERIAL CIRCULATION
Vasoconstriction is induced by
sympathetic stimulation of the
smooth muscle of the peripheral
arterial bed. This results in a decrease
in pulse wave amplitude (Fig. 2).
lists some factors which affect
vasodilatation and vasoconstriction.
The decrease in pulse wave amplitude
is very often related to discomfort,
pain or other stress-related stimuli
(Table 1).
The effect of the sympathetic tone
varies greatly in the individual. Fig. 3
Fig. 2. The effect of vasoconstriction and vasodilatation on pulse wave
amplitude.
335
Appendix III
Fig. 3. Factors influencing
vasoconstriction and vasodilatation .
Table 1. Typical
discomfort and pain.
causes
of
DISCOMFORT OR PAIN
DURING ANAESTHESIA
• Preoperative anxiety
• Endotracheal intubation
• Skin incision
• Periods of superficial anaesthesia
• Supefficial level of anaesthesia
• Postoperative discomfort
• Postoperative pain
VASODILATATION
Changes in the pulse wave
amplitude during anaesthesia are
normally related to neurogenic- or
humorally-determined changes in the
smooth muscular tonus of the arterial
walls.
• Anaesthetics
• Sedation
• Hypercarbia
VASOCONSTRICTION
• Fear
• Pain
• Low temperature
• Hypovolemia
• Hypocarbia
336
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
3 REGISTRATION OF THE PULSE WAVE
Photoelectric
plethysmography
measures the absorption of incident
light at an infrared wavelength (910
nm in Datex-Engstrom pulse wave
oximeters). The absorption of
infrared light is not significantly
affected by changes in the
oxyhemoglobin concentration, see
Fig. 4, so changes in light absorption
essentially reflect only changes in
local blood volume.
Fig. 4. Absorption coefficients of hemoglobin.
Measurement is made optically
with an infrared light source and a
photo-sensitive detector which are
attached to an appropriate part of the
skin, normally to a finger. In the
transmission method the detector is
positioned opposite to the emitter,
(Fig. 5)
Fig. 5. Attachment of a finger
probe.
337
Appendix III
the pulsating arterial blood, see Fig.
6.
The plethysmographic pulse wave
is derived from the intensity of the
transmitted light. The total absorption
of the incident light can be divided
into
components,
which
are
equivalent to compartments in the
substance: tissue, venous and arterial
blood and the pulse added volume of
Note: The pulse waveform reflects
changes in blood volume and
movements of the blood vessel walls,
not changes in blood pressure.
Fig. 6. Absorption of infrared light in thefinger.
338
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
4 SHAPE AND COMPONENTS OF THE PULSE WAVE
The amplitude of the pulse wave is
the most informative indicator of
changes in circulation of the vascular
bed. Other parameters, for example
crest time and the dicrotic notch can
also be identified from the pulse
wave, see Fig. 7. The dicrotic notch is
caused by the closing of the aortic
valve.
Fig. 7. Analysis of the peripheral
pulse wave.
339
Appendix III
5 TYPICAL VARIATIONS IN THE PULSE WAVE DURING
ANAESTHESIA
Fig.
8
shows
how
the
plethysmographic
pulse
wave
amplitude changes during general
anaesthesia. The following different
phases can be identified, see Fig. 8:
Following intubation, the patient
is prepared for surgery. There are no
strong external stimuli in this quiet
phase, thus maximum vasodilatation
can be seen.
1. Preanaesthetic phase
5. Skin incision
The patient is afraid of the
operation and the anaesthesia despite
premedication.
Relative
vasoconstriction and hence a small
pulse amplitude are normal during
this phase.
Skin incision is very strong
stimulus which appears as a
significant decrease in pulse wave
amplitude with or without other
changes in monitored parameters (for
example increasing blood pressure
and heart rate).
2. Induction
During the induction phase, the
patient loses consciousness, and
marked vasodilatation causing a
significant increase in pulse wave
amplitude can be seen. This is
partially
due
to
the
direct
vasodilatatory effect of different
anaesthetics.
6. Maintenance phase
In most patients, the pulse wave
amplitude recovers to its previous
level in a short period of time. During
the maintenance period, the pulse
wave reacts to different surgical
stimuli with minor reflectory
decreases in amplitude. During a
prolonged operation, the pulse wave
amplitude
may
progressively
decrease.
3. Laryngoscopy and intubation
Laryngoscopy and endotracheal
intubation are strong stimuli which
cause sudden vasoconstriction and a
decrease in the pulse wave amplitude.
4. Surglcal preparation phase
340
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
7. End of anaesthesia
8. Recovery
The patient begins to regain
consciousness and is more sensitive
to the various stimuli during this
phase - resulting in vasoconstriction
and a decrease in the pulse wave
amplitude.
During recovery from anaesthesia,
the pulse wave amplitude is often
relatively low because the patient
experiences postoperative pain and
other discomfort.
Fig. 8. Typical plethysmographic pattern during anaesthesia.
341
Appendix III
6 CONCLUSIONS BASED ON CHANGES IN THE AMPLITUDE OF
THE PULSE WAVE DURING ANAESTHESIA
The following conclusions can be
made from the plethysmogram during
anaesthesia (Note: the patient is
basically healthy and the operation
proceeds
without
any
major
complications):
amplitude
indicates
anaesthesia.
too
light
4. Surgical preparation phase
No significant conclusions can
usually be made.
1. Preanaesthetic phase
If the patient has a low pulse wave
amplitude before anaesthesia, it may
be an indication that the patient is
scared of the operation and the
premedication has been insufficient.
5. Skin incision
Skin incision is one of the
strongest stimuli during an operation.
The strong reaction can be avoided by
a booster dose of intravenous or
inhalation
anaesthetics
before
incision.
2. Induction
Strong vasodilatation is very
typical during the induction phase.
This is due to a redistribution of
circulation at the beginning of
anaesthesia. Possible disadvantages
can be counteracted by active
infusion therapy.
6. Maintenance phase
If the pulse wave amplitude stays
low during the operation, it is
normally an indication of light
anaesthesia. Frequent changes in
amplitude
also
indicate
light
anaesthesia in the absence of other
influencing factors.
3. Laryngoscopy and intubation
The
sudden
reaction
to
laryngoscopy and intubation is
common even to a deep anaesthesia.
It is not necessarily a sign of an
unacceptable induction, but is
reflectory in nature and normally
recovers quickly. A slow recovery of
A
progressive,
continuous
decrease in pulse wave amplitude is
usually due to a blood volume deficit
(hypovolemia), decrease of body
temperature or hyperventilation.
Changes in the pulse wave amplitude
should always be considered together
with other variables in order to
342
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
diagnose the real cause of any
changes.
8. Recovery
In the recovery room, the pulse
wave amplitude can be used as a
guide to better patient care.
Vasodilatation is normally associated
with a good quality of recovery and
patient welfare.
7. End of anaesthesia
A normal reaction to the various
stimuli during this phase is
vasoconstriction.
343
Appendix III
7 DIFFERENTIAL DIAGNOSIS
Table 2. Relation of changes in the
pulse wave to other parameters in
various situations.
Clinical
Situation
Pulse
wave
BP
HR
EtCO2
Peripheral
temperature
SpO2
Hypovolemia





-
Too light anaesthesia





-
Too deep anaesthesia





-
Hyperventilation





-
Hypoventilation





()
-





Hypoksia


-
Parameter
indicates increase
indicates decrease
constant or no significant change
344
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
Correct interpretation of changes
in the plethysmographic wave can
only be made by simultaneous
comparison with changes in the
clinical signs and other monitored
parameters.
sensitivity of the pulse wave and the
ECG
to
different
clinical
disturbances.
The following table indicates the
relation
of
other
commonly
monitored parameters to changes in
the pulse wave in different situations.
• ECG is one of the most
commonly monitored physiological
parameters. Table 3 compares the
Table 3. Relative sensitivity of pulse wave and ECG to various disturbances.
ECG (shape)
DISTURBANCE
PLETHYSMOGRAPHIC
PULSE WAVE (amplitude)
+
-
-
Hypovolemia
+
-
Hypercarbia
+
-
Hypocarbia
+
-
Too light anaesthesia
+++
-
Too deep anaesthesia
+++
+
Arrhythmia
+++
-
Low cardiac output
+
+++
Cardiac arrest
+++
+
Primary myocardial ischemia
-
+
Hypoxia
+
indicateschange
indicates no change
+++
++
+
-
345
immediate reaction
fast reaction
slow reaction
no reaction
Appendix III
8 THE PLETHYSMOGRAPHIC WAVE DISPLAYED BY DATEXENGSTROM MONITORS
Datex-Engstrom
pulse
wave
oximeters measure oxygen saturation
from the absorption of incident light
at two wavelengths. In addition, they
display
the
plethysmographic
waveform on the screen. The scale of
the pulse wave indicates the
amplitude factor, and can be changed
manually. The pulse rate, derived
from the pulse wave, is displayed as a
numeric value.
As an example, Datex-Engstrom
Capnomac UltimaTM has an integral
video display, which gives both high
resolution waveform display and
comprehensive
trend
display
capabilities.
Fig. 9. Datex-Engstrom Capnomac UltimaTM with plethysmographic pulse wave
display.
346
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
9 BENEFITS OF THE PLETHYSMOGRAPHIC WAVEFORM
The
plethysmogram
is
a
diagnostically relevant parameter to
monitor:
 The pulse wave also shows
other abnormalities in heart
function, eg arrhythmias. By
inspecting the peripheral pulse
wave,
we
can
make
conclusions
about
the
importance
of
occasional
arrhythmias.
 The waveform amplitude is
related to changes in blood
volume at the monitoring site
 The shape of the pulse wave
and its amplitude give valuable
information about the condition
of the peripheral vascular bed.
The pulse wave indicates
changes in local, peripheral
blood circulation better than
any other parameter.
 Consecutive
pulse
waves
readily show rapid, beat-to-beat
changes in circulation. The
effect of breathing can also
seen from the waveform
baseline fluctuation
 Changes in the plethysmogram
reflect
the
effects
of
premedication, sedation and
depth of anaesthesia
The displayed waveform is an
actual basis of the oxygen saturation
measurement (SpO2). Thus the user
can always check that the SpO2
measurement is not compromised by
motion or other artefacts.
 The amplitude of the pulse
wave is sensitive to stimuli
provoking vasoconstriction, eg
fear, pain, cold, hypocapnia,
etc
347
Appendix III
10 DETERMINATION OF THE PULSE WAVE
During start up, the optimum
display range for the pulse wave is
automatically set, the gain is then
fixed. The user can, however, change
the gain manually during operation to
account for large changes in
amplitude. Thus relative changes in
peripheral circulation are accurately
reproduced
in
the
displayed
waveform.
Fig. 10. Derivation
plethysmographic wave.
of
intensity (increase in absorption) is
recorded as an upward deflection in
the plethysmogram, see Fig. 10. This
variation can be expressed as a
percentage, which we call the
amplitude factor:
I
I
Amplitudefactor = max- min X 100 %
Imax
The amplitude factor reflects
blood volume changes and can thus
indicate the strength of perfusion in
the measuring site. The smaller the
amplitude factor is, the smaller the
blood volume change, and vice versa.
the
Despite the obvious similarity of
the waveform to the arterial blood
pressure waveform, the pulse wave is
not analogous to the blood pressure.
Naturally, the pulse wave amplitude
varies from patient to patient.
The actual pulse wave is displayed
as a mirror image of the intensity
waveform, so that a decrease in
348
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
11 TREND DISPLAY
Fig.
11.
Changes
in
plethysmographic pulse waveform
amplitude and SpO2 during open
heart surgery. The patient underwent
repair of a ventricular septal defect.
After successful emergence from
cardiopulmonary bypass, impaired
function of the left ventricle resulted
in a decrease in cardiac output,
dramatic decrease in SpO2 and
plethysmographic
pulse
wave
amplitude (1). SpO2 decreased to 40
% and the patient experienced a
cardiac arrest (2). During the
successful
cardiopulmonary
resuscitation, sodium nitroprusside
infusion was started (3). SpO2
improved
rapidly
due
to
vasodilatation, release of left
ventricular overload and improved
function of the left ventricle.
349
Appendix III
display a trend is to select the
amplitude value which corresponds to
maximum vasodilatation as a 100 %
reference value, and compare changes
in amplitude with this (Fig. 12). This
kind of approach gives a tool to
compare the trends of different
patients during anaesthesia and
analyze
typical
phases
and
similarities between patients.
Hardcopy
trending
of
the
monitored parameters gives a
permanent, continuous record.
A serial data output gives the
numeric information every 10
seconds. Information is easy to
process further with a personal
computer
and
commercial
spreadsheet and graphic software
packages. An informative way to
Fig. 12. Relative pulse wave amplitude changes of a patient during propofol
short anaesthesia.
350
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
12 SUMMARY
The plethysmographic waveform,
displayed by all Datex-Engstrom
pulse wave oximeters, is a valuable
addition to parameters monitored in
modern anaesthesia. Together with
other clinical signs and parameters, it
supplements the clinical picture of the
patient condition and thus helps
improve patient care and anaesthesia.
The pulse wave is a rapid and
sensitive indicator of various
disturbances during anaesthesia. The
long-term trend information gives an
overall view of the course of the
anaesthesia and is a valuable tool for
teaching and research purposes.
351
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
7.4 APPENDIX IV
COMMUNICATION BETWEEN
PC AND OXIMETER
353
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
The following list is a Q-BASIC program which allows the communication
transferring from the Ohmeda pulse oximeter to the personal computer. The four
first rows form the start file and rest of the list is the program itself. This program
do not only collect the data from the equipment but allows the operator add
comments between the data. The program is done by Juha Luotio and he has granted
permission for its free use; it is also available in disk when requested from the
author’s address.
@echo off
echo.
echo starting MedCom...
qbasic /run MedCom.Bas
LET c = 0
LET g = 10
LET p = 0
CLS
SCREEN 2
LOCATE 10, 30: PRINT "Pulse Oximeter"
LOCATE 11, 30: PRINT "Communication"
LOCATE 12, 33: PRINT "Program"
LOCATE 25, 65: PRINT "Version 1.0"
SLEEP 5
SHELL "a:"
SHELL "cd\"
CONST ESC = 27
kys:
LOCATE 10, 20: INPUT "Where is pulse oximeter? In COM 1 or 2 "; h
nimi:
LOCATE 11, 20: INPUT "Give a name of the file: ", g$
IF g$ = "" THEN LOCATE 13, 20: PRINT "Incorrect file name": GOTO nimi
COLOR 15
CLS
LOCATE 7, 20: PRINT "To start the program press any key."
LOCATE 9, 20: PRINT "DURING THE PROGRAM:"
LOCATE 11, 20: PRINT "To add comments into the collected data press F1."
LOCATE 12, 20: PRINT "To continue collection press ENTER."
LOCATE 13, 20: PRINT "To exit from the program press ESC."
LOCATE 14, 20: PRINT "To clear the screen durin program press F2."
SLEEP 30
IF h = 2 THEN GOTO com2
355
Appendix III
CLS
COM(1) ON
OPEN "COM1:1200,S,7,1,ASC,OP0,LF,RB500" FOR INPUT AS #1
OPEN g$ FOR OUTPUT AS #2
ON COM(1) GOSUB ComHandel
WHILE INKEY$ <> CHR$(ESC)
WEND
COM(1) OFF
CLOSE #2
CLS
LOCATE 10, 20: PRINT "SYSTEM OF COLLECTION. PRESS ANY KEY"
LOCATE 11, 20: PRINT "AND EXIT THE ''MEDCOM.BAS'' USING ''FILE''."
SYSTEM
com2:
CLS
COM(2) ON
OPEN "COM2:1200,S,7,1,ASC,OP0,LF,RB500" FOR INPUT AS #1
OPEN g$ FOR OUTPUT AS #2
ON COM(2) GOSUB ComHandel
WHILE INKEY$ <> CHR$(ESC)
WEND
COM(2) OFF
CLOSE #2
CLS
LOCATE 10, 20: PRINT "SYSTEM OF COLLECTION. PRESS ANY KEY"
LOCATE 11, 20: PRINT "AND EXIT THE ''MEDCOM.BAS'' USING ''FILE''."
SYSTEM
ComHandel:
LOCATE 9, 5: PRINT "Comments:
"
LET c = c + 1
INPUT #1, tieto$
IF c = 1 THEN LET j$ = tieto$
IF c = 2 THEN LET b$ = tieto$
IF c = 3 THEN LET x$ = tieto$
IF c = 4 THEN LET z$ = tieto$
IF c = 5 THEN LET s$ = tieto$
LOCATE 7, 5: PRINT "DATE; "; DATE$; " TIME; "; TIME$; ";"; tieto$; " **
CONNECTION......."
PRINT #2, "; DATE; "; DATE$; "; TIME; "; TIME$; ";"; tieto$
356
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
LOCATE 1, 5: PRINT j$
LOCATE 2, 5: PRINT b$
LOCATE 3, 5: PRINT x$
LOCATE 4, 5: PRINT z$
LOCATE 5, 5: PRINT s$
KEY(2) ON: ON KEY(2) GOSUB Tyhjen
SLEEP 1: KEY(1) ON: ON KEY(1) GOSUB kommentti
RETURN
kommentti:
LET p = p + 1
LET g = g + 1
IF g >= 25 THEN RETURN
LOCATE 9, 5: INPUT "Comments: ", komm$
IF komm$ = "X" OR komm$ = "x" THEN LET komm$ = "Xylocain adr. 1.8 ml"
IF komm$ = "C" OR komm$ = "c" THEN LET komm$ = "Citanest Oct. 1.8 ml"
IF komm$ = "D" OR komm$ = "d" THEN LET komm$ = "Dormicum (1mg/ml) 1
ml"
IF komm$ = "O" OR komm$ = "o" THEN LET komm$ = "Oxygen 3 l/min"
IF komm$ = "T" OR komm$ = "t" THEN LET komm$ = "Toradol 1 ml"
IF komm$ = "F" OR komm$ = "f" THEN LET komm$ = "Fentanyl 0.5 ml"
LOCATE g, 5: PRINT "COMM"; p; "; TIME = "; TIME$; " COMM = "; komm$
PRINT #2, "COMM"; p; "; TIME = "; TIME$; " COMM = "; komm$
IF g = 24 THEN LOCATE 25, 5: PRINT "NO MORE COMMENTS. PRESS ''F2''
TO CLEAN THE SCREEN"
COLOR 15
RETURN
Tyhjen:
CLS
LET g = 10
RETURN
357
Appendix IV
Following list is an example of a real monitored and documented treatment
period:
21.10.1994 12:43
name os the patient removed
extraktioita (extractions)
21.10.1994 12:48 kanyl
kesäajassa vieläkin (still in summer time)
21.10.1994 12:48 1 ml Dormicum 1mg/ml
21.10.1994 12:49 1 ml Dormicum 1mg/ml
21.10.1994 12:49 1 ml Dormicum 1mg/ml
21.10.1994 12:49 1 ml Dormicum 1mg/ml
21.10.1994 12:50 1 ml Dormicum 1mg/ml
21.10.1994 12:51 1,8 ml Citanest Octapressin 30 mg/ml + 0,54
21.10.1994 12:51 1,8 ml Citanest Octapressin 30 mg/ml + 0,54
21.10.1994 12:52 1,8 ml Citanest Octapressin 30 mg/ml + 0,54
21.10.1994 12:52 1,8 ml Citanest Octapressin 30 mg/ml + 0,54
21.10.1994 12:53 1,8 ml Xylocain adrenalin 20 mg/ml + 12,5 mcg/ml
21.10.1994 12:54 1,8 ml Xylocain adrenalin 20 mg/ml + 12,5 mcg/ml
21.10.1994 12:55 1,8 ml Xylocain adrenalin 20 mg/ml + 12,5 mcg/ml
21.10.1994 12:58 1,8 ml Xylocain adrenalin 20 mg/ml + 12,5 mcg/ml
21.10.1994 12:59 ex..,
13:01 8 hammasta pois ja proteesit nyt suussa
( 8 extractions done and prosthesis in the mouth)
21.10.1994 13:03 lanexat lähtee.. (the begin of flumazenil)
21.10.1994 13:04 5 ml meni ( total dose 0.5 mg)
13:11 kylmät sormet vaihdan anturin paikkaa
( Cold fingers. Changing of the place of the probe)
21.10.1994 13:13 loppu ..kan.pois (The end. Cannula removed)
.
:SaO2=--- PR=--- ** PROBE OFF
PATIENT
:SaO2=--- PR=--- ** PROBE OFF
PATIENT
:SaO2=--- PR=--- ** PROBE OFF
PATIENT
:SaO2=--- PR=--- ** PROBE OFF
PATIENT
:SaO2=--- PR=--- ** PROBE OFF
PATIENT
:SaO2=--- PR=--- ** PROBE OFF
PATIENT
WHAT?
:SaO2=--- PR=-WHAT?
:SaO2=--- PR=--- ** PROBE OFF
PATIENT
:SaO2=--- PR=--- ** PROBE OFF
PATIENT
:SaO2=--- PR=--- ** PROBE OFF
PATIENT
358
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
:SaO2=--- PR=--- ** PROBE OFF
PATIENT
:SaO2=--- PR=--- ** PROBE OFF
PATIENT
:SaO2=--- PR=--- ** PROBE OFF
PATIENT
:SaO2=--- PR=--- ** PROBE OFF
PATIENT
:SaO2=--- PR=--- ** PROBE OFF
PATIENT
:SaO2= 93 PR= 72
:SaO2= 93 PR= 71
:SaO2= 95 PR= 68
:SaO2= 97 PR= 71
:SaO2= 97 PR= 70
:SaO2= 96 PR= 70
:SaO2= 96 PR= 68
:SaO2= 95 PR= 69
:SaO2= 95 PR= 74
:SaO2= 95 PR= 75
:SaO2= 95 PR= 74
:SaO2= 95 PR= 75
:SaO2= 95 PR= 76
:SaO2= 95 PR= 76
:SaO2= 96 PR= 78
:SaO2= 95 PR= 79
:SaO2= 95 PR= 78
:SaO2= 95 PR= 78
:SaO2= 96 PR= 78
:SaO2= 95 PR= 80
:SaO2= 95 PR= 77
:SaO2= 96 PR= 74
:SaO2= 96 PR= 73
:SaO2= 96 PR= 74
:SaO2= 96 PR= 74
:SaO2= 95 PR= 77
:SaO2= 95 PR= 82
:SaO2= 95 PR= 79
:SaO2= 97 PR= 79
:SaO2= 98 PR= 79
:SaO2= 97 PR= 80
:SaO2= 96 PR= 80
:SaO2= 96 PR= 81
:SaO2= 97 PR= 78
:SaO2= 96 PR= 79
:SaO2= 96 PR= 79
:SaO2= 95 PR= 79
:SaO2= 95 PR= 79
:SaO2= 95 PR= 78
:SaO2= 95 PR= 79
:SaO2= 95 PR= 82
:SaO2= 96 PR= 82
:SaO2= 96 PR= 81
OHMEDA BIOX 3740 PULSE
OXIMETER
TREND DATA OUTPUT
12 SECONDS PER DATA POINT
:SaO2=--- PR=--:SaO2= 96 PR= 69
:SaO2= 97 PR= 70
:SaO2= 96 PR= 74
:SaO2= 96 PR= 72
:SaO2= 97 PR= 75
:SaO2= 97 PR= 75
:SaO2= 97 PR= 80
:SaO2= 98 PR= 76
:SaO2= 99 PR= 74
:SaO2= 99 PR= 65
:SaO2= 98 PR= 67
:SaO2= 96 PR= 72
:SaO2= 95 PR= 73
:SaO2= 96 PR= 63
:SaO2= 97 PR= 62
:SaO2= 97 PR= 61
:SaO2= 96 PR= 60
:SaO2= 95 PR= 60
:SaO2= 95 PR= 66
:SaO2= 95 PR= 65
:SaO2= 95 PR= 66
:SaO2= 95 PR= 67
:SaO2= 95 PR= 70
:SaO2= 96 PR= 66
:SaO2= 95 PR= 70
12:50 10/21/94
359
12:55 10/21/94
13:00 10/21/94
Appendix IV
:SaO2= 97 PR= 80
:SaO2= 97 PR= 80
:SaO2= 96 PR= 79
:SaO2= 96 PR= 79
:SaO2= 96 PR= 79
:SaO2= 94 PR= 78
:SaO2= 94 PR= 79
:SaO2= 94 PR= 77
:SaO2= 95 PR= 75
:SaO2= 95 PR= 75
:SaO2= 95 PR= 71
:SaO2= 95 PR= 70
:SaO2= 95 PR= 68
:SaO2= 94 PR= 72
:SaO2= 94 PR= 77
:SaO2= 94 PR= 77
:SaO2= 97 PR= 77
:SaO2= 97 PR= 78
:SaO2= 96 PR= 77
:SaO2= 97 PR= 72
:SaO2= 97 PR= 73
:SaO2= 97 PR= 83
:SaO2= 96 PR= 80
:SaO2= 96 PR= 80
:SaO2= 96 PR= 81
:SaO2= 96 PR= 79
:SaO2= 96 PR= 79
:SaO2= 96 PR= 78
:SaO2= 96 PR= 74
:SaO2= 96 PR= 76
:SaO2= 96 PR= 75
:SaO2= 96 PR= 74
:SaO2= 96 PR= 75
:SaO2= 95 PR= 76
:SaO2= 95 PR= 77
:SaO2= 94 PR= 75
:SaO2= 94 PR= 75
:SaO2= 94 PR= 74
:SaO2= 93 PR= 76
:SaO2= 93 PR= 78
:SaO2= 94 PR= 75
:SaO2= 95 PR= 72
:SaO2= 96 PR= 73
:SaO2= 95 PR= 75
:SaO2= 94 PR= 75
:SaO2= 94 PR= 78
:SaO2= 94 PR= 76
:SaO2= 94 PR= 75
:SaO2= 93 PR= 77 13:10 10/21/94
:SaO2= 94 PR= 73
:SaO2= 95 PR= 73
:SaO2=--- PR=--- PO
:SaO2=--- PR=--- PO
:SaO2=--- PR=--- PO
:SaO2=--- PR=--- PO
:SaO2=--- PR=--- PO
:SaO2=--- PR=--- PO
:SaO2=--- PR=--- PO
:SaO2=--- PR=--- PO
:SaO2=--- PR=--- PO
:SaO2=--- PR=--- PO
:SaO2=--- PR=--- PO
:SaO2=--- PR=--- PO
:SaO2=--- PR=--- PO
:SaO2=--- PR=--- PO
:SaO2=--- PR=--- PO
:SaO2=--- PR=--- PO
:SaO2=--- PR=--- PO
:SaO2=--- PR=--- PO
:SaO2=--- PR=--- PO
:SaO2=--- PR=--- PO
:SaO2=--- PR=--- PO
:SaO2=--- PR=--- PO
:SaO2=--- PR=--- PO 13:15 10/21/94
:SaO2=--- PR=--- PO
:SaO2=--- PR=--- PO
:** POWER ON **
:SaO2= 99 PR=214
** PROBE OFF PATIENT
:SaO2=--- PR=---
13:05 10/21/94
** PROBE OFF PATIENT
360
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
7.5 APPENDIX V
CRTICAL THOUGHTS
361
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
A year after the completion of the manuscript:
Critical thoughts from one side and the other
real world: the world is far too
complicated for that. The syntheses
are valid only under special
conditions, devoid of chaotic
components. If we do not complete
the examinations with careful
descriptions of reality as it is, we will
soon believe in our theories rather
than reality.
The Methods: experiments against
observation
The
experimental
method
of
examination which at present is
almost the sole method used in e.g.
medicine, is of fairly young origin,
since Galileo Galilei was claimed to
have made the first experiments in the
natural
sciences.
Until
then,
observation and deduction were the
only methods used, as - rightly interrupting nature’s events with an
experiment would have altered
reality. A case in point of this
alteration is my second extensive
study; the Osfix implant study
(www.osfix.sci.fi) where the test
group consisted of healthy edentulous
adults with a nonresorbed mandible...
Unfortunately, patients in the real
world, or those in my dental practice,
rarely fulfil the criteria. Nevertheless,
the treatment has to be made.
Personally, I think the study plan
approved by the Ethical Board and
the Medical Board distorts reality! Of
course there remains a lot to be said
about
ancient
and
medieval
observational
philosophy,
but
rejecting clinical observation in the
favour of an experimental method
(basing the examination on exclusion
and
randomization)
may
be
parallelled with emptying the baby
out with the bathwater. The fact that
observation seldom leads to a great
synthesis is mainly due to the lack of
counterpart for the synthesis in the
This is why in my most important
study I have wanted to observe my
patients without test arrangements,
i.e. to observe the treatment as such,
and - as was noted in the study plan
submitted to the faculty, the
treatments had already been made and
therefore there seemed to be no sense
in applying for a permission from the
Ethical Board. Thus there was no
study plan when monitoring the
patients, but there was an access to
various monitors for observing the
patient’s well-being, and the sedation
accounts are based on the data stored
on discs by these monitors,
complemented with comments on
medication in the data flow. This is
not a question of making online
information to be used in studies, but
carefully following up sedation which
is routine in my dental practice.
Examining the stored-up information
(the disc is part of the “patient
information card”) retrospectively
and making conclusions from the
examinations - either combining
similar treatment procedures or by
363
Appendix V
statistical means with multi-analysis
of variance, has created the science.
index exist, could upcoming problems
be predicted from this?
A most intriguing facet concerning
my method was the observation
material in the work observing
anesthesia made for medical students,
as the experimental thinking (time
schedule - division into groups) that
has saturated the university also crept
in my work although I had planned to
remain
an
observer.
In
an
afterthought; if I had known from the
beginning what will happen, I would
have either completed a plan with
randomizations and applied for a
permit from the Ethical Board, or
made the work in my dental clinic on
real patients which are solely given
local anesthetics, not sedated. The
local anesthetics given to dental
students only seemed a perfect
occasion to “have the job well done”.
Later on in the Holter study I had
gained knowledge: I made a dental
student in the university operating
theatre to ask the morning patient if
he/she would carry an extra monitor
for 24 hours. I thus prevented the
ordinary staff from distorting the
patient group. The same question was
placed for all patients coming to my
dental practice for a sedation, until
the 23 registrations had been
completed (incidentally, only one
denied). I thus have two different
groups, as they are, in my work. Of
course no firm conclusions may be
made from these kind of groups - only
indicative ones. The purpose of my
method is not to firmly prove
anything - that I leave to others - but
to bring up previously unknown
issues; could it be thus, could such an
364
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
mathematical
system,
which
additionally affects our emotions, but
the notion on what music should be
like, is tied to time, place and social
reference group. Also the assumption
that there is so-called superior and
inferior art reveals the social ties
within art. Furthermore, art clearly
contains an end in itself.
Science, Art and Dentists
In my outlook on life I define science
(and inevitably also its cousin, art) as
follows:
-Science is a method whereby
awareness obtains information on the
outside reality. Humans are part of
this concrete reality as biological
creatures with a basic instinct to
survive and reproduce. Our awareness
is rising from this basis as an
interdepencency through our social
network. This network gives us a
notion of ourselves, of others and of
reality. This is, however, only a
notion. It is not necessarily connected
to reality, it is an agreement made by
our social network. Yet science is
undisputably an interdependency
between awareness and reality, with
an exterior goal. This goal is further
clearly divided into two: to an attempt
to understand reality, and to an
attempt to informatively affect the
reality, the latter being often referred
to as engineering skills or, in case of
medicine, clinical knowhow. The
experimental method again has been
one of the most brilliant means of
getting clear of
the disturbance
caused
by
our
collective
consciousness and reach the first
goal. But overemphasizing the
experiment will lead into a massive
problem: science is thus limited into a
structure between experiment and
awareness...
If we agree on the above, I cannot
resist making a couple of conclusions
which will
greatly irritate our
awareness:
1.Scientific reports are works of art,
since they are socially tied, selfpurposeful products comparable to a
painting. The new, disease resistent
grain is the product of scientific
work, a report thereof is a work of
art...
2.The branches of science that do not
fall into the natural sciences,
e.g.psychology, are pure art, as no
reality exists as an object of their
study. They bear no difference to
committed art.
The polarization of the professioninto unpractial experimentalists who
have created their own, introvert
academic culture, and into practical
dentists, who have to zigzag through
traditions, marketing and study results
- has created a blind faith to the
former being somewhat better
representatives of science. They are
not. Dentistry is part of the medical
sciences and this reveals on which
grounds the treatment should be
based. Treatment is no less scientific
than making experiments. It is a
question of difference in outlook on
-Art again is the processing of
awareness, emotions and the above
mentioned social agreement both in
individual
and
collective
consciousnesses; music is a logical,
365
Appendix V
life: even an university researcher
may believe and create sheer
nonsense in his everyday life. The
scientific outlook on life is no more
anchored into researchers than to
practical doctors. Both are equally a
part of the scientific world, or they
are not. The book in your hand
attempts, however, to be a friendly
gesture from practice towards
academic culture.
I broke the pattern into pieces
small enough for the clinicist to read
one at a time. This is why the book
contains so much repetition, but then
again if you have read the item
“Patients and methods” in Part 1,
there is no need to read them again in
the sections thereafter. My aim has
been to repeat the most essential
points at least three times, as
repetition still is the path to learning.
Furthermore, the book can be read in
three ways: 1) browsing bold prints,
abstracts and clinical conclusions; 2)
reading only the parts interesting for
the reader, e.g. the patients’
experiences; 3) thoroughly going into
the whole works. Thus I have
considered the practical needs of a
professional, yet aimed at waking an
initial
interest,
then
further
introducing to them the interesting
issues, and finally starting a process
that leads to learning. This form has
aroused an enormous opposition in
the pre-examiners - hardly any
criticism has been expressed on the
subject itself - and, surprisingly
enough, a year after the manuscript
was completed, I came across a book
(Dryden and Vos 1994) in which I
could read that in my form-opposing
attitude I might still be right.
The readability of this book
This book would probably be more
readable for those living in academic
culture, if it would obey the
conventional dissertation pattern, but
I have intently wanted to break that
pattern (where form sometimes
replaces contents), as I am writing of
my observations to a dentist who is
making
clinical
work.
The
possibilities of a clinicist to allocate
his time are absolutely such that I
know not of any clinicist colleague
who would have read even one
dissertation from cover to cover! The
reason is not in the “ignorance” of the
clinicists, but the fact that most
dissertations make you wonder if
anyone, save the pre-examiners and
the opponent, ever read them. What
an effort, and usually a waste of time.
This issue cannot be justified by the
traditional outline of a monography.
366
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
The academic world seems at first sight most respectable,
but a closer examination will reveal it
pompous, authoritarian, domineering and offensive.
367
Monitored intravenous sedation with local anaesthesia for dental outpatients
Appendicies
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