Study Guide Emergency Medicine September 2015
INTRODUCTION
The practice of emergency medicine requires both a broad knowledge base and a large
range of technical skills. The effective practice of emergency medicine requires a
thorough comprehension of the assessment and management of conditions that threaten
life and limb; the ability to provide immediate care is fundamental. Although there is a
significant crossover between emergency medicine and other clinical specialties,
emergency medicine has unique aspects, such as the approach to patient care and the
decision making process.
HISTORY OF EMERGENCY MEDICINE
The history of emergency medicine as a distinct medical discipline encompasses the past
60 years. The genesis of emergency medicine involved several elements and stemmed
from recognition of the unique nature of trauma care and emergency transport, increasing
mobility of the population and improvements in emergency care and resuscitation. The
American Board of Emergency Medicine became the twenty-third medical specialty,
following its approval by the American Board of Specialties in September 1979. The first
board examination in emergency medicine was offered in 1980. In the early 1980's, the
Australian Society of Emergency Medicine was formed by a group of doctors committed to
the practice and development of emergency medicine, and in 1993 the discipline was
accepted as a principal specialty. These developments have led to the transformation in the
practice of emergency medicine in most hospitals. However, away from the major centres,
there are many non-specialist doctors playing an important role in the delivery of emergency
care to seriously ill patients. These doctors often do so in relative isolation and without the
benefit of the supervision and back up of specialists. Groups such as rural general
practitioners and hospital based medical officers carry a significant emergency medicine
role.
Emergency Medicine has long been established especially in Australasia, Canada, Ireland,
the United Kingdom and the United States, in Asia othe emergency medicine officially
inauguration of Asian Society of Emergency Medicine in Singapore on the 24th of October
1998 at the first Asian Conference on Emergency Medicine which as Prof.DR.dr. Eddy
Rahardjo,SpAnKIC and dr. Tri Wahyu Murni sat as member of Board Director.
It is thus sometimes seen to be synonymous with emergency medical care and within the
province and expertise of almost all medical practitioners. However, the Emergency
Medicine incorporates the resuscitation and management of all undifferentiated urgent and
emergency cases until discharge or transfer to the care of another physician. Emergency
Medicine is an inter-disciplinary specialty, one which is interdependent with all other clinical
disciplines. It thus complements and does not seek to compete with other medical
specialties.
Basic science concepts to help in the understanding of the phatophysiology and treatment
of disease.The medical curriculum has become increasingly vertically integrated, with a
much greater use of clinical examples and cases to help in the understanding of the
relevance of the underlying basic science, The Emergency Medicine block has been written
to take account of this trend, and to integrate core aspects of basic science,
pathophysiology and treatment into a single, easy to use revision aid.
In accordance the lectures that have been full integrated for studens in 6
semester, period of 2012, one of there is The Emergency Medicine Block.
Th
There are many topics will be discuss as below:
Seizure and mental status changes, acute Psychiatric episode, Acute respiratory distress
syndrome and failure, Bleeding disorders (epistaxis, dental bleeding, vaginal bleeding)
Departement Medical Education Faculty of Medicine Udayana University
1
Study Guide Emergency Medicine September 2015
,Shock, Cardiac critical care (Cardiac arrest and CPR), Emergency toxicology and
poisoning, Pregnancy induce Hypertension, Shoulder dystocia, Urologic concern in critical
care, Phlegmon, Acute Blistering and Expoliative skin, Trauma which potentially disabling
and Life threatening condition and Basic Clinical Skill
Beside those topics, also describes the learning outcome, learning objective, learning task,
self assessment and references. The learning process will be carried out for 4 weeks (20
days).
Due to this theme has been prepared for the second time, so many locking mill is available
on it. Perhaps it will better in the future
Thank you.
Planner
Departement Medical Education Faculty of Medicine Udayana University
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Study Guide Emergency Medicine September 2015
CURRICULUM CONTENTS
Mastery of basic knowledge with its clinical and practical implication include airway,
breathing and circulation management.
Establish tentative diagnosis, provide initial management and refer patient with :
 Seizure and mental status changes
 Acute Psychiatric episode
 Acute respiratory distress syndrome and failure
 Bleeding disorders (epistaxis, dental bleeding, vaginal bleeding)
 Shock
 Cardiac critical care (Cardiac arrest and CPR)
 Emergency toxicology and poisoning
 Pregnancy induce Hypertension, Shoulder dystocia
 Urologic concern in critical and non critical care
 Phlegmon
 Acute Blistering and Expoliative skin
 Trauma which potentially disabling and Life threatening condition
SKILLS
 To implement a general strategy in the approach to patients with critical ill through
history and physical examination and special technique investigations
 To manage by assessing, provide initial management and refer patient with critical ill
PERSONAL DEVELOPMENT/ATTITUDE
Awareness to :
 Ethic in critical care
 Basic principle of critical care
 The importance of informed consent to patient and family concerning critical ill
situations
 Risk of patient with critically ill and its prognosis
COMMUNITY ASPECT :
 Communicability of the critical cases
 Cost effectiveness
 Utilization of health system facilities
 Critical ill patient
Departement Medical Education Faculty of Medicine Udayana University
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Study Guide Emergency Medicine September 2015
PLANNERS TEAM
NO.
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15
NAME
Dr.dr. Tjok Gde Agung Senapathi, Sp.AnKAR
(Chairman)
dr. I Ketut Suyasa, SpB,SpOT(K) (Secretary)
dr. IGN Budiarsa,SpS
dr. Sari Wulan, SpTHT KL, dr. Wayan Sucipta,
SpTHT KL
drg. Putu Lestari Sudirman, M.biomed.
dr. Agus Somya, SpPD, KPTI
dr. Dewa Made Artika, SpP
Dr.dr. Diah Kanyawati, SpA(K)
Dr.dr. Wayan Megadana, SpOG(K)
dr. Hariyasa Sanjaya, SpOG(K)
dr. Megaputra, SpOG(K)
dr. Gd Wirya Kesuma Duarsa, SpU, MKes, dr.
Budisantosa, SpU
dr. Ratep,SpKJ
dr. Nyoman Suryawati, SpKK
dr. Sri Laksminingsih SpR (K)
DEPARTMENT
Anesthesiology and
Intensif Terapy
Surgery
Neurology
ENT
Dentistry
Internal Medicine
Pulmonology
Pediatric
Obstetric-Gynecologic
Obstetric-Gynecologic
Obstetric-Gynecologic
Surgery
Psychiatric
Dermatology
Radiology
LECTURERS
NO.
1.
2.
3.
4.
5.
6.
7.
8.
19.
10.
11.
12.
13.
14.
15
NAME
DEPARTMENT
Dr.dr. Tjok Gde Agung Senapathi, Anesthesiology
and Intensif
Sp.AnKAR (Chairman)
Terapy
dr. I Ketut Suyasa, SpB,SpOT(K) Surgery
(Secretary)
Neurology
dr. IGN Budiarsa,SpS
dr. Sari Wulan,SpTHT KL, dr. ENT
Wayan Sucipta,SpTHT KL
drg. Putu Lestari Sudirman, Dentistry
M.biomed.
Internal Medicine
dr. Agus Somya, SpPD, KPTI
Pulmonology
dr. Dewa Made Artika, SpP
Pediatric
Dr. dr. Diah Kanyawati, SpA(K)
Dr.dr.
Wayan
Megadana, ObstetricGynecologic
SpOG(K)
Obstetricdr. Hariyasa Sanjaya, SpOG(K)
Gynecologic
Obstetricdr. Megaputra, SpOG(K)
Gynecologic
dr. Gd Wirya Kesuma Duarsa, Surgery
SpU,MKes, dr. Budisantosa, SpU
Psychiatric
dr. Ratep,SpKJ
Dermatology
dr. Nyoman Suryawati, SpKK
Radiology
dr. Sri Laksminingsih SpR (K)
PHONE
081337711220
081558724088
0811399673
081237874447(SW)
08125318941 (WS)
08155764446/7494974
08123989353
08123875875
081285705152
08123917002
081558314827
08123636172
081339977799 (BS)
081338333951 (GWK)
08123618861
0817447279
08164745561
Departement Medical Education Faculty of Medicine Udayana University
4
Study Guide Emergency Medicine September 2015
FACILITATORS
(REGULAR CLASS)
NO
GROUP
DEPT
PHONE
VENUE
Dr. dr. I Wayan Putu Sutirta
Yasa, M.Si
dr. Yuliana, M Biomed
1
08123953344
2
Clinical
Pathology
Anatomy
085792652363
3
Neurology
08123800180
4
Interna
081805530196
5
Dr.dr. Anna Marita Gelgel,
Sp.S(K)
dr. Pratihiwi Primadharsini,
M.Biomol, Sp.PD
dr. Ni Luh Putu Ariastuti , MPH
5
Public Health
0818560008
6
dr. Reni Widyastuti, S.Ked
6
Pharmacology
08174742501
7
dr. Ida Bagus Alit, Sp.F, DFM
7
Forensic
081916613459
8
8
Surgery
08123511673
9
dr. Agus Roy Rusly Hariantana
Hamid, Sp.BP-RE
dr. I Ketut Wibawa Nada, Sp.An
9
Anasthesi
087860602995
10
dr. Muliani , M Biomed
10
Anatomy
085103043575
2nd floor:
R.2.09
2nd floor:
R.2.10
2nd floor:
R.2.11
2nd floor:
R.2.12
2nd floor:
R.2.13
2nd floor:
R.2.14
2nd floor:
R.2.15
2nd floor:
R.2.16
2nd floor:
R.2.20
2nd floor:
R.2.23
1
2
3
4
NAME
FACILITATORS
(ENGLISH CLASS)
NO
1
GROUP
1
DEPT
Interna
PHONE
08123810423
2
Neurology
081337667939
3
NAME
dr. Jodi Sidharta Loekman,
SP.PD-KGH-FINASIM
dr. Ida Ayu Sri Wijayanti,
M.Biomed, Sp.S
dr. I Wayan Sugiritama, M.Kes
3
Histology
08164732743
4
dr. I Made Sudipta, Sp.THT- KL
4
ENT
08123837063
5
dr. I Made Oka Negara, S.Ked
5
Andrology
08123979397
6
dr. Jaqueline Sudirman,
GrandDipRepSc, PhD
dr. Dyah Kanya Wati, Sp A (K)
6
Obgyn
082283387245
7
Pediatric
05737046003
Dr.dr. Cokorda Bagus Jaya
Lesmana, Sp.KJ
Dr. dr. Made Sudarmaja, M.Kes
8
Psychiatry
0816295779
9
Parasitology
08123953945
dr. Ida Bagus Kusuma Putra,
Sp.S
10
Neurology
085738534259
2
7
8
9
10
Departement Medical Education Faculty of Medicine Udayana University
VENUE
2nd floor:
R.2.09
2nd floor:
R.2.10
2nd floor:
R.2.11
2nd floor:
R.2.12
2nd floor:
R.2.13
2nd floor:
R.2.14
2nd floor:
R.2.15
2nd floor:
R.2.16
2nd floor:
R.2.20
2nd floor:
R.2.23
5
Study Guide Emergency Medicine September 2015
TIME TABLE
Regular Class
DAY/DATE
1.
Mon,
7 Sept
2015
2.
Tue,
8 Sept
2015
3.
Wed,
9 Sept
2015
4.
Thu,
10 Sept
2015
TIME
LEARNING
ACTIVITY
VENUE
CONVEYER
Class room
Dr.dr. Tjok Gde Agung
Senapathi, Sp.AnKAR
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
Highlight in
Emergency Medicine
(Chairman)
Individual Learning
SGD
Break
Student Project
Plenary
Disc room
Facilitators
Class room
08.00-09.00
Lecture 2.
Class room
Dr.dr. Tjok Gde Agung
Senapathi, Sp.AnKAR
dr. IGN Budiarsa,SpS
Disc room
Facilitators
Class room
Class room
dr. IGN Budiarsa,SpS
dr. Ratep,SpKJ
Disc room
Facilitators
Class room
Class room
dr. Ratep,SpKJ
08.00-09.00
-
Status Epilepticus
and Other Seizure
Disorders
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
08.00-09.00
Individual Learning
SGD
Break
Student Project
Plenary
Lecture 3.
-
Acute Psychiatric
Episodes
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
08.00-09.00
Individual Learning
SGD
Break
Student Project
Plenary
Lecture 4.
Acute Respiratory
Distress Syndrome
and Failure
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
Individual Learning
SGD
Break
Student Project
Plenary
dr Sari Wulan, SpTHT KL (
and ENT Team), Dr. Dewa
Made Artika, SpP, Dr. dr
Diah Kanyawati,SpA (K),
dr. Srie Laksminingsih,
SpR
Disc room
Facilitators
Class room
dr Sari Wulan, SpTHT KL (
and ENT Team)
Pulmo, Pediatric, Radiology
Departement Medical Education Faculty of Medicine Udayana University
6
Study Guide Emergency Medicine September 2015
DAY/DATE
TIME
5.
Fri,
11 Sept
2015
08.00-09.00
6.
Mon,
14 Sept
2015
7.
Tue,
15 Sept
2015
8
Wed,
16 Sept
2015
LEARNING
ACTIVITY
Lecture 5.
VENUE
Class room
dr Sari Wulan, SpTHT
KL, dr. Sucipta, SpTHT
KL ( and ENT Team)
Dr.dr Wayan
Megadhana, SpOG(K)
(and OBGYN Team)
Disc room
Facilitators
Class room
dr Sari Wulan, SpTHT
KL, dr. Sucipta, SpTHT
KL ( and ENT Team)
Dr.dr Wayan
Megadhana, SpOG(K)
(and OBGYN Team)
Class room
dr. IGAG. Utara
Hartawan, SpAn MARS
Bleeding
Disorder(Epistaxis,
Hemorrhage In
Pregnancy) and
Airway
Obstruction
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
Individual Learning
SGD
Break
Student Project
Plenary
08.00-09.00
Lecture 6.
Shock
09.00-10.30
Individual Learning
10.30-12.00
SGD
12.00-12.30
Break
12.30-14.00
Student Project
14.00-15.00
08.00-09.00
-
Disc room
Facilitators
Plenary
Class room
Lecture 7.
Class room
dr. IGAG. Utara
Hartawan, SpAn MARS
dr. IGN. Mahaalit
Aribawa, SpAn KAR
Cardiac Arrest and +
Cardiopulmonary
Resuscitaton
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
Individual Learning
SGD
Break
Student Project
Plenary
08.00-09.00
Lecture 8
Disc room
Facilitators
Class room
dr. IGN. Mahaalit
Aribawa, SpAn KAR
dr. Agus Somya, SpPD
KPTI
Class room
Emergency
Toxicology and
Poisoning
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
CONVEYER
Individual Learning
SGD
Break
Student Project
Plenary
Disc room
Facilitators
Class room
dr. Agus Somya, SpPD
KPTI
Departement Medical Education Faculty of Medicine Udayana University
7
Study Guide Emergency Medicine September 2015
DAY/DATE
9
Thu,
17 Sept
2015
10
Fri,
18 Sept
2015
11.
Mon,
21 Sept
2015
12.
Tue,
22 Sept
2015
TIME
08.00-09.00
LEARNING ACTIVITY
Lecture 9
VENUE
Class room
Pregnancy Induce
Hypertension
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
Individual Learning
SGD
Break
Student Project
Plenary
08.00-09.00
Lecture 10
Shoulder Dystocia
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
Individual Learning
SGD
Break
Student Project
Plenary
08.00-09.00
Lecture 11
Disc room
Class room
Class room
Disc room
Class room
Acute Blistering and
Exfoliative Skin
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
Individual Learning
SGD
Break
Student Project
Plenary
08.00-09.00
Lecture 12.
Individual Learning
SGD
Break
Student Project
Plenary
dr. Megaputra,
SpOG(K)
Facilitators
dr. Megaputra,
SpOG(K)
dr. Hariyasa
Sanjaya, SpOG(K)
Facilitators
dr. Hariyasa
Sanjaya, SpOG(K)
dr. Nyoman
Suryawati Sp.KK
Fasilitator
dr. Nyoman
Suryawati Sp.KK
dr. Ketut Suyasa,
SpB SpOT(K) Spine
dr. IGN Wien
Aryana, SpOT
Trauma Which
Potentially Disabling
and life Threatening
Conditions
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
CONVEYER
Disc room
Departement Medical Education Faculty of Medicine Udayana University
Fasilitators
dr. Ketut Suyasa,
SpB SpOT(K) Spine
dr. IGN Wien
Aryana, SpOT
8
Study Guide Emergency Medicine September 2015
DAY/DATE
13
Wed,
23 Sept
2015
14
Fri,
25 Sept
2015
15
Mon,
28 Sept
2015
TIME
LEARNING
ACTIVITY
VENUE
CONVEYER
08.00-09.00
Lecture 13.
Phlegmon
Class room
Drg. Lestari
Sudirman
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
Individual Learning
SGD
Break
Student Project
Plenary
Disc room
Facilitators
Class room
Drg. Lestari
Sudirman
08.00-09.00
Lecture 14.
Class room
dr. Gede Wirya
Kusuma Duarsa,
M.Kes, SpU(K)
Urologic Concern in
Critical Care for
NonTrauma Case
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
Individual Learning
SGD
Break
Student Project
14.00-15.00
Plenary
Class room
08.00-09.00
Lecture 15
Class room
Disc room
Facilitators
dr. Gede Wirya
Kusuma Duarsa,
M.Kes, SpU(K)
dr. Budi Santosa,
SpU
Urologic Concern in
Critical Care for
Trauma Case
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
Individual Learning
SGD
Break
Student Project
Plenary
Disc room
Facilitators
Class room
dr. Budi Santosa,
SpU
16.
Tue,
29 Sept
2015
08.00-selesai
Basic clinical skill (1)
CPR (Regular Class)
Clinical skill lab
Team
17.
Wed,
30 Sept
2015
08.00-selesai
Basic clinical skill (2)
Basic Trauma Care
(Regular Class)
Clinical skill lab
Team
18.
Thu,
1 Oct
2015
19.
Fri,
2 Oct
2015
08.00-Finish
Basic clinical skill (1)
CPR (English Class)
Clinical skill lab
Team
08.00- Finish
Basic clinical skill (2)
Basic Trauma Care
(English Class)
Clinical skill lab
Team
Departement Medical Education Faculty of Medicine Udayana University
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Study Guide Emergency Medicine September 2015
20.
Sat-SudMon-TueWed,
3-4-5-6-7
Oct
2015
21
Thu,
8 Oct
2015.
Prepare For
Examination
EXAMINATION
Departement Medical Education Faculty of Medicine Udayana University
10
Study Guide Emergency Medicine September 2015
TIME TABLE
English Class
DAY/DATE
1.
Mon,
7 Sept
2015
2.
Tue,
8 Sept
2015
3.
Wed,
9 Sept
2015
4.
Thu,
10 Sept
2015
TIME
LEARNING
ACTIVITY
VENUE
Class room
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
Highlight in
Emergency Medicine
(Chairman)
Student Project
Break
Individual Learning
SGD
Plenary
09.00-10.00
Lecture 2.
Class room
09.00-10.00
CONVEYER
Dr.dr. Tjok Gde Agung
Senapathi, Sp.AnKAR
Facilitators
Disc Room
Class room
Dr.dr. Tjok Gde Agung
Senapathi, Sp.AnKAR
dr. IGN Budiarsa,SpS
Status Epilepticus
and Other Seizure
Disorders
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
09.00-10.00
Student Project
Break
Individual Learning
SGD
Plenary
Lecture 3.
Facilitators
Disc Room
Class room
Class room
dr. IGN Budiarsa,SpS
dr. Ratep,SpKJ
Acute Psychiatric
Episodes
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
09.00-10.00
Student Project
Break
Individual Learning
SGD
Plenary
Lecture 4.
Facilitators
Disc Room
Class room
Class room
Acute Respiratory
Distress Syndrome
and Failure
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
Student Project
Break
Individual Learning
SGD
Plenary
dr. Ratep,SpKJ
dr Sari Wulan, SpTHT KL (
and ENT Team), Dr. Dewa
Made Artika, SpP, Dr. dr
Diah Kanyawati,SpA (K),
dr. Srie Laksminingsih,
SpR
Facilitators
Disc Room
Class room
Departement Medical Education Faculty of Medicine Udayana University
dr Sari Wulan, SpTHT KL (
and ENT Team)
Pulmo, Pediatric, Radiology
11
Study Guide Emergency Medicine September 2015
DAY/DATE
TIME
5.
Fri,
11 Sept
2015
09.00-10.00
6.
Mon,
14 Sept
2015
7.
Tue,
15 Sept
2015
8
Wed,
16 Sept
2015
LEARNING
ACTIVITY
Lecture 5.
VENUE
Class room
Bleeding Disorder
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
Student Project
Break
Individual Learning
SGD
Plenary
09.00-10.00
Lecture 6.
Shock
10.00-11.30
Student Project
11.30-12.00
Break
12.00-13.30
Individual Learning
13.30-15.00
SGD
Disc Room
15.00-16.00
Plenary
Class room
09.00-10.00
Lecture 7.
Class room
-
Disc Room
Class room
Class room
dr Sari Wulan, SpTHT
KL, dr. Sucipta, SpTHT
KL ( and ENT Team)
Dr.dr Wayan
Megadhana, SpOG(K)
(and OBGYN Team)
dr. IGN. Mahaalit
Aribawa, SpAn KAR
Facilitators
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
Student Project
Break
Individual Learning
SGD
Plenary
Disc Room
Class room
09.00-10.00
Lecture 8
Class room
dr. IGN. Mahaalit
Aribawa, SpAn KAR
dr. IGAG. Utara
Hartawan, SpAn MARS
Facilitators
Emergency
Toxicology and
Poisoning
Student Project
Break
Individual Learning
SGD
Plenary
dr Sari Wulan, SpTHT
KL, dr. Sucipta, SpTHT
KL ( and ENT Team)
Dr.dr Wayan
Megadhana, SpOG(K)
(and OBGYN Team)
Facilitators
Cardiac Arrest and +
Cardiopulmonary
Resuscitaton
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
CONVEYER
dr. IGAG. Utara
Hartawan, SpAn MARS
dr. Agus Somya, SpPD
KPTI
Facilitators
Disc Room
Class room
Departement Medical Education Faculty of Medicine Udayana University
dr. Agus Somya, SpPD
KPTI
12
Study Guide Emergency Medicine September 2015
DAY/DATE
9
Thu,
17 Sept
2015
10
Fri,
18 Sept
2015
11.
Mon,
21 Sept
2015
12.
Tue,
22 Sept
2015
TIME
09.00-10.00
LEARNING ACTIVITY
Lecture 9
VENUE
Class room
Pregnancy Induce
Hypertension
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
Student Project
Break
Individual Learning
SGD
Plenary
09.00-10.00
Lecture 10
Shoulder Dystocia
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
Student Project
Break
Individual Learning
SGD
Plenary
Disc Room
Class room
09.00-10.00
Lecture 11
Class room
Disc Room
Class room
Class room
dr. Megaputra,
SpOG(K)
dr. Hariyasa
Sanjaya, SpOG(K)
Facilitators
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
Student Project
Break
Individual Learning
SGD
Plenary
Disc Room
Class room
09.00-10.00
Lecture 12.
Class room
dr. Hariyasa
Sanjaya, SpOG(K)
dr. Nyoman
Suryawati Sp.KK
Fasilitator
Trauma Which
Potentially Disabling
and life Threatening
Conditions
Student Project
Break
Individual Learning
SGD
Plenary
dr. Megaputra,
SpOG(K)
Facilitators
Acute Blistering and
Exfoliative Skin
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
CONVEYER
dr. Nyoman
Suryawati Sp.KK
dr. Ketut Suyasa,
SpB SpOT(K) Spine
dr. IGN Wien
Aryana, SpOT
Fasilitators
Disc Room
Class room
Departement Medical Education Faculty of Medicine Udayana University
dr. Ketut Suyasa,
SpB SpOT(K) Spine
dr. IGN Wien
Aryana, SpOT
13
Study Guide Emergency Medicine September 2015
DAY/DATE
13
Wed,
23 Sept
2015
14
Fri,
25 Sept
2015
15
Mon,
28 Sept
2015
TIME
LEARNING
ACTIVITY
VENUE
09.00-10.00
Lecture 13.
Phlegmon
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
Student Project
Break
Individual Learning
SGD
Plenary
Disc Room
Class room
09.00-10.00
Lecture 14.
Class room
Class room
CONVEYER
Drg. Lestari
Sudirman
Facilitators
Urologic Concern in
Critical Care for
NonTrauma Case
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
Student Project
Break
Individual Learning
SGD
Disc Room
15.00-16.00
Plenary
Class room
09.00-10.00
Lecture 15
Class room
Drg. Lestari
Sudirman
dr. Gede Wirya
Kusuma Duarsa,
M.Kes, SpU(K)
Facilitators
dr. Gede Wirya
Kusuma Duarsa,
M.Kes, SpU(K)
Urologic Concern in
Critical Care for
Trauma Case
dr. Budi Santosa,
SpU
10.00-11.30
11.30-12.00
12.00-13.30
13.30-15.00
15.00-16.00
Student Project
Break
Individual Learning
SGD
Plenary
Facilitators
16.
Tue,
29 Sept
2015
08.00-selesai
Basic clinical skill (1)
CPR
Clinical skill lab
Team
17.
Wed,
30 Sept
2015
08.00-selesai
Basic clinical skill (2)
Basic Trauma Care
Clinical skill lab
Team
18.
Thu,
1 Oct
2015
08.00-Finish
Basic clinical skill (1)
CPR (English Class)
Clinical skill lab
Team
19.
Fri,
2 Oct
2015
08.00- Finish
Basic clinical skill (2)
Basic Trauma Care
(English Class)
Clinical skill lab
Team
Disc Room
Class room
Departement Medical Education Faculty of Medicine Udayana University
dr. Budi Santosa,
SpU
14
Study Guide Emergency Medicine September 2015
20.
Sat-SudMon-TueWed,
3-4-5-6-7
Oct
2015
21
Thu,
8 Oct
2015.
Prepare For
Examination
EXAMINATION
ASSESSMENT METHOD
Assessment will be carried out on Thursday 8 th of October 2015. There will be 100
questions consisting mostly of Multiple Choice Questions (MCQ) and some other types of
questions. The minimal passing score for the assessment is 70. Other than the
examinations score, your performance and attitude during group discussions will be
consider in the calculation of your average final score. Final score will be sum up of student
performance in small group discussion (5% of total score) and score in final assessment
(95% of total score). Clinical skill will be assessed in form of Objective structured clinical
examination (OSCE) at the end of semester as part of Basic Clinical Skill Block’s
examination.
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Study Guide Emergency Medicine September 2015
STUDENT PROJECT
Students have to write a paperwork with topic given by the lecturer. The topic will be
chosen randomly on the first day. Each small group discussion must work on one paperwork
with different tittle. The paperwork will be written based on the direction of respective
lecturer. The paperwork is assigned as student project and will be presented in class. The
paper and the presentation will be evaluated by respective facilitator and lecturer.
Format of the paper :
1. Cover 
Title (TNR 16)
Name
Student Registration Number
Faculty of Medicine, Udayana University 2015
2.
3.
4.
5.
Green coloured cover
Introduction
Journal critism/literature review
Conclusion
References
Example :
Journal
Porrini M, Risso PL. 2005. Lymphocyte Lycopene Concentration and DNA Protection from
Oxidative Damage is Increased in Woman. Am J Clin Nutr 11(1):79-84.
Textbook
Abbas AK, Lichtman AH, Pober JS. 2004. Cellular and Molecular Immunology. 4th ed.
Pennysylvania: WB Saunders Co. Pp 1636-1642.
Note.
Minimum 10 pages; line spacing 1.5; Times new roman 12
Departement Medical Education Faculty of Medicine Udayana University
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Study Guide Emergency Medicine September 2015
STUDENT PROJECT
Students have to write a paperwork with topic given by the lecturer. The topic will be
chosen randomly on the first day. Each small group discussion must work on one paperwork
with different tittle. The paperwork will be written based on the direction of respective
lecturer. The paperwork is assigned as student project and will be presented in class. The
paper and the presentation will be evaluated by respective facilitator and lecturer.
Format of the paper :
6. Cover 
Title (TNR 16)
Name
Student Registration Number
Faculty of Medicine, Udayana University 2012
Green coloured cover
7. Introduction
8. Journal critism/literature review
9. Conclusion
10. References
Example :
Journal
Porrini M, Risso PL. 2005. Lymphocyte Lycopene Concentration and DNA Protection from
Oxidative Damage is Increased in Woman. Am J Clin Nutr 11(1):79-84.
Textbook
Abbas AK, Lichtman AH, Pober JS. 2004. Cellular and Molecular Immunology. 4th ed.
Pennysylvania: WB Saunders Co. Pp 1636-1642.
Note.
Minimum 10 pages; line spacing 1.5; Times new roman 12
Departement Medical Education Faculty of Medicine Udayana University
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Study Guide Emergency Medicine September 2015
LEARNING PROGRAMS
Abstracts of Lectures
LECTURE 1 : HIGHLIGHT
EMERGENCY MEDICINE
Tjok Gde Agung Senapathi
Objective
To describe
1.
2.
3.
4.
Highlight Emergency Medicine
Basic principal of Emergency Medicine
Triad Emergency Medicine
Ethics in critical care
Medical ethics is the art of resolving conflicts that arise around treatment and
treatment decisions. The conflict may involve the patient, family, caregivers, or society. An
approach to these conflicts is as necessary as, say, an approach to hypotension or oliguria.
Without an approach we would be ignoring the mechanism that led the conflict or problem in
the first place. A little preparation will allow one to be more comfortable when confronting
these situations, making responses more likely to be useful (and less likely to make things
worse).
There are four basic principles or medical ethics that give us the tools to begin to
resolve some of these conflicts : autonomy, beneficence, and justice. The weight we give
each of these four different principles is often determined by our individual and societal
morals.
AIRWAY
OBJECTIVES
1. To review basic airway management
2. To review indications for definitive airway management
3. To review rapid sequence intubation
INTRODUCTION
In the resuscitation of any patient, management of the airway is the first priority. One
cannot continue in managing breathing or circulation problems if the patient does not have a
patent airway. Even after airway management has taken place, in any patient who fails to
improve, or who deteriorates, always start again with assessment and management of the
airway.
ASSESSING THE AIRWAY
Before managing any patient‘s airway, it is important to quickly assess and identify those
patients in whom you anticipate difficulty in ventilation and / or intubation. If you do – call for
help.
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Some key predictors of a difficult airway include:
Difficult Bag-valve Mask Ventilation “BOOTS”
B = Beard
O = Obese
O = Older
T = Toothless
S = Snores / Stridor
Difficult Intubation - “MAP the Airway”
M = Mallampati Class and Measurements
Evaluate the Mallampati classification by asking patient to open their mouth ―3-3-2-1 rule‖
 3 fingers mouth opening
 3 fingers distance from hyoid to chin
 2 fingers distance from thyroid cartilage notch to floor of mandible
 1 finger anterior jaw subluxation
A = Atlanto-occipital (neck) extension
 Normal = 35 degrees or more
P = Pathologic conditions
 Tumour, hematoma, trauma, etc.
REVIEW OF AIRWAY TECHNIQUES
Temporizing / Adjunctive Measures







Chin lift/jaw thrust to open airway - caveat: no neck extension if suspected C-spine
injury
Bag-valve-mask ventilation – probably the most important, yet under-appreciated,
skill of airway management. In the ED, when bagging, use a two-hands on the mask
technique for a tight seal, and always use an oral airway
Suctioning/removal of foreign bodies
Nasal airway - generally well-tolerated by the temporarily obtunded patient (e.g.
post-ictal, post-procedural sedation, intoxicated)
Oral airway – aids in peri-intubation ventilation; not to be used in patient with intact
gag reflex
Laryngeal mask airway (LMA) – this device is inserted into the mouth and has a cuff
that occludes the hypopharynx. It has a port through which ventilation can then
occur. A variation is the Intubating LMA – this allows the insertion of an endotracheal
tube via the ventilation port. The LMA is used both as a ―rescue device‖ in failed
intubation, and as a primary airway device
Needle cricothyroidotomy - accomplished by inserting a needle in cricothyroid
membrane, and oxygenating the patient using high pressure oxygen source
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Definitive Airway
A definitive airway is the placement of a cuffed tube in the trachea. A cuffed endotracheal
tube does not ensure that aspiration cannot occur, but does reduce the risk.
 Orotracheal / nasotracheal intubation
 Surgical airway – either percutaneous or open cricothyroidotomy with insertion of a
cuffed tracheal tube
Section One RESUSCITATION
INDICATIONS FOR INTUBATION
The indications for intubation can be broken down into four main categories. These can be
recalled as the four P‟s:
1. Patency - to obtain and maintain a patent airway in the face of obstruction.
Examples include: decreased LOC, airway edema/burns, neck hematoma, tumour
2. Positive-pressure ventilation - to correct deficient oxygenation and/or ventilation.
Examples include: pulmonary edema, COPD exacerbation
3. Protection - to protect the airway from aspiration in the event of decreased LOC
4. Predicted deterioration - in some situations, early intubation may be preferable to the
potential need to urgently intubate in a less favourable environment (e.g. in CT
scan), or when it may be significantly more difficult (e.g. progressive edema)
WHEN INTUBATION SHOULD BE
ANTICIPATED
The following are several situations during which ED patients are commonly intubated:
 Trauma
 Overdoses on medications which cause rapid decrease in level of consciousness
 Severe congestive heart failure, asthma, COPD
 Head injured patients, or those who are comatose for non-traumatic reasons
SPECIAL CONSIDERATIONS IN THE ED
Airway management in the ED usually occurs on an urgent or emergent basis. The
following are some things to keep in mind, as they will modify the plan of airway
management:
 less time to assess airway, obtain past history, etc.
 less controlled than in the elective setting
 patients are frequently hemodynamically unstable
 all must be considered to have full stomachs, with the attendant risk of aspiration
 patients often have altered mental status, from markedly decreased to
fighting/agitated due to alcohol, drugs, or head injury
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Cervical spine injury and instability must be assumed in patients who have experienced
major trauma, falls, or have an unknown history of injury.
 this consideration requires modification of airway techniques, both basic and
advanced
 when intubating a patient with a known or suspected c-spine injury, remove the front
of the cervical collar and have an assistant manually stabilize the neck (‗in-line
manual stabilization‘). The collar can be replaced once tube placement is confirmed.
RAPID SEQUENCE INTUBATION
Rapid sequence intubation is defined as the simultaneous administration of a powerful
sedative (induction) agent and a paralytic agent to facilitate intubation and decrease the risk
of aspiration.
Although a detailed discussion of RSI is beyond the scope of this chapter, the basic steps
are reviewed below. These can be recalled as the six P‟s.
1. Preparation – prepare all equipment, personnel, and medications
2. Pre-oxygenation – patient breathing 100% oxygen for 3-5 minutes or asking the
patient to take 4-8 full breaths on 100% oxygen will wash out the nitrogen in the lungs,
and prolong the time available for intubation before desaturation occurs.
3. Pretreatment – pretreatment with medications such as atropine in children,
defasciculating doses of a non-depolarizing muscle relaxant prior to the administration
of succinycholine, and lidocaine in the setting of head injury is considered optional,
given the lack of evidence for their benefit
4. Paralysis with induction – administration of a sedative agent (e.g. ketamine, propofol,
etomidate) followed rapidly by the administration of a muscle relaxant (e.g.
succinylcholine or rocuronium)
5. Place the tube with proof – intubate the patient, and confirm tube placement with endtidal capnometry
6. Post-intubation management – chest x-ray, analgesia and sedation, further
resuscitation
Relative contraindications to rapid sequence intubation include:



anticipated difficult airway, especially difficult bag-valve mask ventilation. In this
situation, an ―awake‖ intubation with the patient maintaining respirations is
preferred
inadequate familiarity and comfort with the technique
unnecessary (e.g. the patient in cardiac arrest or near-arrest)
THE TECHNIQUE OF LARYNGOSCOPY
Ensure that the proper preparations have been made, and the patient is positioned
correctly in the ―sniffing position‖. The laryngoscope is held in the left hand,
and introduced into the mouth on the right side of the tongue. Advance the
laryngoscope slowly to the base of the tongue. Identification of the epiglottis is crucial.
A common novice error is to rapid insert the blade too deeply, missing identification of
the epiglottis.
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Once the epiglottis is identified, seat the tip of the blade in the vallecula. Lift can now
be applied to the laryngoscope in the direction of the handle. Do not lever the blade
back. Once the epiglottis is lifted, the vocal cords should come into view. Without
losing sight of the vocal cords, ask an assistant to hand you the endotracheal tube in
your right hand. The tube is introduced into the right side of the patient‘s mouth without
obscuring your view of the cords. It is important to visualize the tip of the tube as it
passes through the cords. As the tip passes, ask the assistant to remove the stylet,
and place the tube in its final position. Inflate the cuff, and confirm end-tidal CO2.
Routine post-intubation care including chest x-ray, analgesia and sedation, and further
resuscitation will now follow.
For an excellent laryngoscopy video, go to http://emcrit.org/airway/laryngoscopy
TIPS AND TOOLS TO FACILITATE INTUBATION
A number of tips and tools exist that can make intubation easier, even in patients for
whom a clear visualization of the vocal cords is not possible. Some of those commonly
used in the ED include:



‗BURP‘ technique – refers to application of ‗backward, upward, rightward pressure‘
on the larynx to facilitate visualization of the cords during laryngoscopy. It is
important to understand how this differs from ‗cricoid pressure‘ which is applied in
order to prevent aspiration
Bougie or tracheal tube introducer – long, thin, flexible device inserted under the
epiglottis during laryngoscopy. As it enters the trachea, ―clicks‖ are felt as
thebougie passes over tracheal rings, and it STOPS when it reaches a mainstem
bronchus. If esophageal, no clicks are felt and the bougie advances into stomach.
Once in trachea, advance ET tube over bougie.
Video laryngoscopy (Glidescope) – a laryngoscope with a camera mounted on a
more sharply-angled blade allows for improved visualization of the anterior larynx
SUMMARY




Most patients' airways can be managed, at least temporarily, with simple airway
maneuvers and a bag-valve mask device
Familiarize yourself with assessing an airway
Emergency patients have a number of special considerations regarding airway
management
In any patient who fails to improve, or who deteriorates, always start again with
assessment and management of the airway
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REFERENCES
1. Canadian Association of Emergency Physicians
Airway Interventions and
Management Education (AIME) manual.
2. Kovacs G, Law JA. Airway Management in Emergencies. 2008; McGraw-Hill.
3. Blanda M, Gallo UE. Emergency airway management. Emerg Med Clin North Am
2003;21(2):1-26.
4. Reynolds SF, Heffner J. Airway Management of the Critically-Ill Patient: Rapid
Sequence Intubation. Chest 2005;127(4):1397-412.
5. McGill J. Airway Management in Trauma: An Update. Emerg Med Clin N Am
2007;25:603–622
BREATHING
OBJECTIVES
1. To develop an organized approach to breathing problems
2. To use the history and physical examination to help identify the cause of breathing
problems
3. To understand the utility of various investigations for breathing problems
4. To know the various treatment modalities related to breathing problems
INTRODUCTION
After airway, the next priority in resuscitation (ABC‘s) is assessment and management of
breathing problems. The label ‗Breathing‘ encompasses all problems related to shortness
of breath (SOB) and respiratory dysfunction, and these are among the most common clinical
problems encountered in the Emergency Department (ED).
Airway and breathing problems can be difficult to distinguish from each other initially, and
are frequently assessed in tandem. Of course, airway management always comes first.
‗Breathing‘ comes before ‗Circulation‘ in resuscitation because there is no point in working
on the pump part of the equation unless that pump is delivering oxygenated blood to the
tissues.
APPROACH
The causes of respiratory distress or dyspnea are myriad. Rather than learn long lists of
possible diagnoses, it is better to have a clear approach in which to organize all the
information gathered from your history and physical exam. However, the following is a short
list of immediately life-threatening diagnoses that must be rapidly identified and treated:
 Pulmonary Embolus
 Pulmonary Edema (CHF)
 Acute exacerbation of COPD
 Acute severe Asthma
 Tension Pnuemothorax
Mnemonic: Breathing Poorly Can Cause Alot of Tension
After considering these immediately life-threatening diagnoses, an anatomical approach can
be used to identify other causes of breathing difficulties:
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Bronchi and Bronchioles
Asthma, COPD, Bronchiectasis
Lung Parenchyma
The etiologies listed with clinical examples cause problems by filling or blocking the alveoli
and thus preventing gas exchange. Alveoli can be blocked by pus (infection), fluid (edema),
blood and gastric contents (aspiration).
Blood: Pulmonary Contusion, Goodpasture‘s Syndrome, Bleeding Carcinoma
Fluid/Edema: CHF, ARDS, Neurogenic Pulmonary Edema, Toxin/Drug Induced Pulmonary
Edema, High Altitude Pulmonary Edema
Pus/Infection: Bacterial Pneumonia, TB, Fungal Gastric Contents: Aspiration Diffusion
Diseases: Amyloidosis, Interstitial Pulmonary Fibrosis
Vasculature and Blood
This category includes blockage of the pulmonary circulation and disorders of the
content/chemistry of the blood.
Emboli: Clot, Fat, Air, Amniotic Fluid
Metabolic: Acidosis, Thyroid disease
Anemia
Methemoglobinemia
Pleural Space
The pleural space is a potential space between the lung pleura and the chest wall, usually
devoid of any significant fluid/substance. Accumulation of exogenous material in the pleural
space impedes normal respiratory function.
Air: Tension Pneumothorax, Simple Pneumothorax
Blood: Hemothorax
Fluid: Pulmonary Effusion
Pus/Infection: Empyema
Chest Wall & Diaphragm
When the chest wall, intercostal musculature or diaphragm is either damaged or nonfunctioning, the result is breathing impairment. Trauma, neurologic disease and congenital
deformity are potential culprits.
Trauma: Flail Chest, Spinal Cord injury, Diaphragmatic Rupture
Neurogenic Causes: Guilliane-Barré, Myasthenia Crisis and ALS
Congential: Kyphosis, Scoliosis
Cardiac Causes
While many cardiac causes of dyspnea cause pulmonary edema, some cardiac disease
increase pulmonary vascular pressures and decrease lung compliance, thus producing
dyspnea. These include:
 Myocardial Infarction
 Cardiac Tamponade
 Valvular and Congenital Heart Disease
Central Causes
 Hypoventilation: over-sedation or CO2 retainers
 Fever
 Psychogenic/Anxiety
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HISTORY
Try to ascertain, even in the sickest patients, some historical features of the disease
process. Important features of the history are:
 Onset of Symptoms
 Progression of Symptoms
 Severity of Symptoms
 Presence of Associated Symptoms – especially
 chest pain, fever, cough
 Exposure to Noxious Substances
 Exposure to Allergens
 Possible FB ingestions
 Past Medical History: This is particularly
 important as many respiratory and cardiac
 diseases like asthma, COPD, and CHF have a
 recurrent course.
 Risk Factors: It is also imperative to assess for the
 risk factors of such diseases as ischemic heart
 disease and pulmonary embolus.
PHYSICAL EXAMINATION
The physical exam can be very revealing and is based on the classic components of the
physical examination: inspection, palpation, percussion, and auscultation.
Once the airway is controlled, the rate and pattern of breathing are important clues to
underlying diseases. Tachypnea is usual for most conditions - both intrapulmonary and
extrapulmonary. Bradypnea is classic of opiate intoxication (as well as some, usually
catastrophic, CNS events). Certain patterns of breathing, (eg. Kussmaul's or apneustic
breathing) may be indicators of metabolic and neurogenic causes of respiratory dysfunction.
Both hypoxia and hypercarbia may cause agitation, anxiety, and obtundation. Carefully
observe the mechanics of breathing such as chest expansion, accessory muscle use,
paradoxical breathing, indrawing, and number of words spoken per breath (if applicable).
These signs indicate significant respiratory dysfunction and the need for prompt treatment.
Cyanosis is a late and ominous sign (except in chronic intrapulmonary and intracardiac
shunts). Look for surgical scars over the chest as clues to underlying pulmonary disease
and impairment.
Palpation may reveal subcutaneous emphysema over the neck or chest, suggesting
pneumomediastinum or pneumothorax. Check the position of the trachea; if it is not midline
then something is causing it to shift, such as air, fluid or a mass lesion in the chest.
Percussion helps to define what this could be. Hyperresonance is due to air and
pneumothorax (+/- tension) is the likely cause. Percussion that is dull may be due to a
pleural effusion or a hemothorax.
Auscultation may reveal normal, absent, or diminished breath sounds that help to delineate
some of the underlying causes of respiratory dysfunction. Wheezing may be due to
bronchospasm secondary to asthma, COPD, CHF or aspirated foreign body. Crackles may
indicate CHF, pneumonia or chronic underlying lung pathology. Pleural friction rubs suggest
pneumonia or pulmonary embolism.
Although clinical assessment of respiratory function is invaluable, adjunctive tests are often
employed. These tests include pulse oximetry, blood gas determination, and pulmonary
function testing.
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PULSE OXIMETRY
Pulse oximetry provides continuous, immediate and non-invasive assessment of arterial
oxygenation. It is of great value at the bedside in rapidly determining the patient‘s
oxygenation status, and usually obviates an immediate need for blood gas testing. Pulse
oximetry measures hemoglobin saturation, rather than
6 Section One RESUSCITATION
pO2, via spectrophotometric determination of the relative proportions of oxygenated versus
deoxygenated hemoglobin in blood coursing through an accessible pulsatile capillary bed
(usually the nailbed). Using the oxyhemoglobin dissociation curve, it is possible to estimate
the pO2 for any given oxygen saturation. An SaO2 of 90% equals a pO2, of 60 mmHg.
Below this level of saturation you have hit the steep portion of the curve and pO2 drops off
precipitously. For this reason, we strive to keep the oxygen saturation well above 90%.
The accuracy of pulse oximetry is dependent on adequate pulsatile blood flow. Therefore,
shock states, severe anemia, hypothermia, and use of vasopressor agents impairs accurate
measurements. Jaundice, skin pigmentation and nail polish may also interfere with
readings.
INVESTIGATIONS
The following investigations are valuable adjuncts to the assessment of the respiratory
status of a patient:
 CBC- looking for evidence of infection or severe anemia
 Electrolytes- looking for evidence of anion gap acidosis
 Cardiac Enzymes- in patients with risk factors for ischemia
 D-dimer- frequently used to rule out the diagnosis of pulmonary embolism
 CXR- visualizes many forms of lung pathology
 Blood Gas - to assess oxygenation and ventilation
Arterial or Venous Blood Gases
Blood gases are a useful adjunct for a precise assessment of respiratory function, notably
providing information on the adequacy of alveolar oxygenation (pO2), ventilation (pCO2),
the acid-base status of the patient, and whether the respiratory condition is acute or chronic.
Venous blood gases (VBG) provide a close approximation of pH, CO2 and bicarbonate to
the arterial blood gas. While arterial blood gases are slightly more accurate, they cause a
great deal of pain to the patient and require more time to perform. Therefore a VBG is often
measured first and may be sufficient in the clinical asessment.
Pulmonary function tests (PFT)
The most commonly used PFT in the ED is peak expiratory flow rate (PEFR). This is easily
measured with a hand held peak flow meter, in the patient who is co-operative, to assess
the severity of airflow limitation and response to treatment in asthma and COPD. Forced
expiratory volume in one second (FEV1) is another test sometimes used for this purpose.
ACUTE RESPIRATORY FAILURE
This is defined as hypoxia (pO2<50 mmHg) with or without associated hypercapnia
(pCO2>45 mmHg). It is divided into two types:
Type I: respiratory failure without pCO2 retention.
This is characterized by marked V/Q mismatch and intrapulmonary shunting. Examples
include diffuse pneumonia, pulmonary edema, ARDS.
Type II: respiratory failure with pCO2 retention.
This involves V/Q mismatch and inadequate alveolar ventilation. There are two categories of
this type of respiratory failure:
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A. Patients with intrinsically normal lungs but with inadequate ventilation due to
disorders of respiratory control (e.g. overdose, trauma, CNS disease),
neuromuscular abnormalities (e.g. muscular dystrophy, Guillain-Barre, myasthenia),
and chest wall trauma.
B. Patients with intrinsic lung disease with V/Q mismatch and alveolar hypoventilation.
Respiratory failure is precipitated by additional clinical insult, usually infection, which
worsens the underlying disease. Examples include COPD, asthma, cystic fibrosis.
INDICATIONS FOR INTUBATION
1. Airway Protection
 decreased level of consciousness (ie. CNS bleed or overdose)
 general rule of thumb is ―GCS Eight – Intubate‖
 prevent aspiration
2. Respiratory Failure
 this may be a clinical assessment with bedside adjuncts such as pulse oximetry
(blood gases NOT necessary to proceed to intubation)
 examples include hypoxic OR hypercarbic failure
3. Anticipated Course (Prophylactic Intubation)
 airway burn or significant neck trauma (airway compromise likely)
 ill patient that is CT or O.R.-bound
 transfer of critically ill patient to another facility
SPECIFIC TREATMENT MODALITIES
Nasal Prongs
Nasal prongs are usually a well-tolerated method of administering oxygen to the
spontaneously breathing patient. With O2 flows of 2-6 L/minute FiO2 of 25-40% can be
attained.
Face Mask
Use of a face mask requires a spontaneously breathing patient and can deliver up to 5060% FiO2 with a flow rate of 10L/minute. This FiO2 may vary depending upon how well the
mask fits, and what the patient‘s minute ventilation is; i.e. how much room air is entrained
through the mask.
CLINICAL PEARL
In the severely dyspneic and hypoxic patient in
whom you believe you can treat the underlying
problem without intubation and ventilation, (the
classic example being the CHF patient who has
been given diuretics and afterload reducers) one
can use a double-flush system. With this system a
face mask is hooked up to two O2 outlets, thus
delivering up to 30L/minute of pure O2 and FiO2
of nearly 100%.
Oxygen Reservoir Mask
Oxygen reservoir mask is essentially the same as the above set-up, except the mask has an
attached inflatable bag that stores O2 during expiration and from which O2 is inspired. With
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a tight fit and low entrainment, FiO2 of up to 90% can be obtained with O2 flow of
>10L/minute.
Bag-valve Mask Devices
These masks can be used to manually supplement the patient's respiratory effort in patients
who are breathing spontaneously, but require respiratory assistance. The mask comes in
various styles with the most common being the ‗AMBU bag‘. It consists of a rubber or
inflatable plastic facemask, a connector bag which contains O2, and an O2 reservoir
attached to the bag and to the O2 outlet. These devices can deliver up to 100% O2 with
high flow O2 and proper bagging procedure. If tolerated, an oral or nasal airway can help
facilitate ventilation of the patient.
Bag-valve mask ventilation can temporize patients in respiratory arrest until other
therapeutic modalities take effect. However, the majority of patients needing this type of
intervention will require intubation and mechanical ventilation. The decision to mechanically
ventilate the patient in the ED is usually a clinical one. For patients in severe respiratory
distress, do not wait for the blood gas to confirm what you should already know.
CPAP Masks/ BiPAP Masks
CPAP (continuous positive airways pressure masks) are a therapeutic modality option being
increasingly used to treat patients in respiratory distress. The commonest and most studied
uses are in the patient with CHF or severe COPD. This non-invasive mechanical ventilation
temporizes the need for intubation, and may reduce the incidence of patients that need
invasive respiratory support.
Other Therapeutic Modalities
Needle thoracostomy can relieve tension pneumothorax prior to chest tube insertion. Tube
thoracostomy can relieve pneumo-/hemo- thoraces and drain pleural effusions.
Pharmacologic Therapy
Certain medical therapies may assist in specific diseases.
Examples include
bronchodilation (ie. salbutamol) in asthma/COPD, diuretics in CHF, antibiotics in
pneumonia, anticoagulation/thrombolysis in MI/PE.
Summary
The prompt recognition of respiratory dysfunction, including the respective clinical signs and
adjunctive testing, is critical in the ED. Knowledge of specific oxygenation/ventilation and
pharmacologic therapies is paramount to prevent further clinical deterioration.
CIRCULATION
OBJECTIVES
1. To recognize shock utilizing the physical examination
2. To understand the causes of shock
3. To review the management of different types of shock
INTRODUCTION
The circulatory system exists in order to supply cells with oxygenated blood and nutrients,
and to remove waste products. Shock is defined as ‗an abnormality of the circulatory
system causing inadequate tissue perfusion which, if not corrected, will result in cell death.‘
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CAUSES OF SHOCK
The circulatory system consists of two pumps connected in series (right and left heart), a
system of conduits (blood vessels), and circulating fluid (blood). The causes of shock can
be understood by looking at the various components of the circulatory system, and the
disorders that affect them. The following table lists some of the circulatory disorders that
may result in shock.
Table 1. Causes of Shock
The mnemonic ―SSHOCK‖ commonly used for remembering the causes of shock can be
reviewed in chapter 43.
RECOGNIZING SHOCK
Shock has many causes, and the clinical presentation varies. However, many features of
hypoperfusion can be easily recognized by the bedside examination of the patient.
Mental Status
Early: Agitation due to increased sympathetic tone
Late: Obtundation due to decreased CNS perfusion
Pulse
Tachycardia is generally sensitive for acute losses in excess of 12-15% blood volume.
Exceptions occur in primary bradyarhythmias, in patients on beta blockers, and in some
cases of intraperitoneal bleeding.
The presence of palpable pulses may give a rough indication of systolic blood pressure. If
the radial pulse is palpable, systolic pressure exceeds 80mm Hg. If the femoral pulse is
palpable, systolic pressure exceeds 70mm Hg. If the carotid pulse is palpable, systolic
pressure exceeds 60mm Hg.
Blood Pressure
Hypotension is an insensitive marker for tissue hypoperfusion. In the case of hemorrhagic
shock, a fall in blood pressure may not occur until there is blood loss in excess of 30% of
total blood volume. (Similarly, hypotension can occur without shock.)
Orthostatic Vital Signs
An assessment of the change in pulse and blood pressure as a patient is moved from a
supine to sitting or erect position has been used to identify mild degrees of hypovolemia.
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There is no consensus as to what changes constitute a ‗positive response‘ and the test is
insensitive and nonspecific in the assessment of volume status. Orthostatic vital signs
should never be performed in a potentially unstable patient.
Respiratory Rate
Tachypnea occurs in response to increased sympathetic tone and metabolic acidosis. It is
an early sign of hypovolemic shock. The tachypneic response may be blunted in response
to CNS depressants or head trauma.
Skin
The skin is cool and pale early on as blood is shunted to vital organs. Peripheral cyanosis
may
appear later. The exception to this rule is in vasogenic shock, when the skin may be warm
and possibly flushed due to peripheral vasodilatation. In later stages of vasogenic shock,
depression of cardiac output may cause the usual changes of skin hypoperfusion to become
manifest.
Capillary Blanch Test: A positive test occurs when a compressed nail bed takes >2 seconds
to
‗pink up‘ and is said to occur when there is acute blood loss in excess of 15% of total blood
volume.
Heart Sounds
Muffled heart sounds may be noted in cardiac tamponade.
Jugular Venous Pressure
Low: Hypovolemia, Sepsis
High: Left Ventricular Failure, Right Heart Problem
RESUSCITATION
Table 2. Assessment of Hemorrhagic Shock According to Presentation
BEDSIDE ULTRASOUND
ED ultrasound can be a useful tool in identifying the cause of shock. It can rapidly detect
intraabdominal hemorrhage, hyovolemia (IVC filling), pericardial tamponade, or RV
dysfunction (PE).
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GENERAL MANAGEMENT
ABCs + Monitoring
 Airway and breathing assessment occurs first
 Oxygen and saturation monitor
 Cardiac monitor
 Intravenous access and send blood to lab (crossmatch if hemorrhage is suspected);
Lactate
 Control any external bleeding by applying pressure to the wound
 Foley catheter - monitor urine output
 Ongoing assessment of clinical parameters of tissue perfusion include:
◦ Blood pressure, pulse, respirations, level of consciousness, skin
◦ Invasive Monitoring: CVP measurement, Arterial line, ScvO2
SPECIFIC MANAGEMENT
Treatment of Hemorrhagic Shock
 ABCs
 If active control of internal hemorrhage is needed, consult surgery (or occasionally
GI) while you resuscitate - don't wait until the patient is stabilized and the blood work
is back
 Restore circulating blood volume: Prompt restoration of circulating blood volume is
felt to be a critical factor in the reversal of shock. In hemorrhagic shock, as in most
other types, fluid resuscitation begins with aggressive intravenous infusions of
(warmed) crystalloid. Use at least two short, large bore catheters (flow is inversely
proportional to the length of the catheter, and proportional to the 4th power of the
catheter radius). Pressure infusion devices may be used to increase flow rates. The
chart above provides some guidelines for appropriate fluid management.
Peripheral access (preferred):
Equipment: 16-gauge angiocath or larger
Sites: forearm, antecubital
Central access:
Equipment: 8FR introducer inserted via Seldinger technique
Sites: femoral vein, internal jugular vein, subclavian vein
Fluids:
 Ringers lactate or normal saline
 1-2 litres administered rapidly (20ml/kg in children)
 Expect to need approximately 3 times the estimated blood loss (3:1 rule)
Blood (packed RBC‘s):
 if no response or transient response to 2-3L fluids
Platelets and FFP
 In patients with significant blood loss, early transfusion of platelets and FFP may
improve outcome. Many institutions have a ―massive transfusion protocol‖.
Adequacy of fluid resuscitation is assessed by following the clinical parameters of tissue
perfusion as well as urine output. Measurement of central venous pressure may be helpful.
Adequate volume replacement is important, but administration of volume in excess of need
is harmful. Watch for development of pulmonary edema (cardiogenic and non-cardiogenic).
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Under investigation:
 Delayed volume resuscitation in acute hemorrhagic shock - immediate surgery
SPECIFIC MANAGEMENT
NON-HEMORRHAGIC SHOCK
Anaphylactic Shock
Epinephrine (IM; IV if cardiovascular collapse) Intravenous crystalloid
Antihistamines (H1 and H2 blockers) Corticosteroids
Wheezing: Nebulized beta2 agonists
Stridor: Nebulized epinephrine
Cardiogenic Shock
Inotropes, intra-aortic balloon pump, emergency angioplasty
Tension Pneumothorax
Needle thoracostomy followed by chest tube
Septic Shock
Intravenous crystalloid
Antibiotics
Goal directed therapy in the ED decreases mortality in sepsis:
urine output >0.5 mL/kg/h
CVP 8 to12 mm Hg
MAP 65 to 90 mm Hg
ScvO2 >70%
Definitive therapy (drainage of closed space infections, sugery).
Cardiac Tamponade
Intravenous crystalloid, pericardiocentesis
Massive Pulmonary Embolus
Intravenous crystalloid, inotropes, thrombolysis or surgery
Arrhythmias
Specific anti-arrhythmic therapy
SUMMARY





The causes of shock can be understood by looking at the various components of the
circulatory system, and the disorders that affect them (pumps, vessels, blood)
Many features of shock can be easily identified on physical examination by
assessing mental status, pulse, blood pressure, respiratory rate, skin, jugular venous
pressure and capillary refill
Hemorrhagic shock can be classified into 4 categories depending on the estimated
amount of blood lost and some of the above mentioned physical examination
findings
In fluid resuscitation of hemorrhagic shock, expect to need approximately 3 times the
estimated blood loss (3:1 rule)
It is important to rapidly identify the cause of shock and institute specific treatment as
soon as possible
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REFERENCES
1. Marx: Rosen's Emergency Medicine, 7th ed. Mosby, 2009.
2. Tintinalli J. et al, editors. Emergency medicine: A comprehensive study guide. 7th
ed. New York: McGraw-Hill, 2011.
3. Rivers E, Nguyen B, Havstad S, et al: Early goal-directed therapy in the treatment of
severe sepsis and septic shock. N Engl J Med 345: 1368, 2001.
Lecture 2 : SEIZURE AND MENTAL CHANGES DISORDER
STATUS EPILEPTICUS
IGN Budiarsa
Status epilepticus is defined as a condition in which epileptic activity persists for 30 minutes
more.
The seizures can take the form of prolonged seizures or repetitive attacks without recovery
in between. There are various types of status epilepticus and a classification :
(Table below)
Status epilepticus confined to early childhood
1. Neonatal status epilepticus
2. Status epilepticus in specific neonatal epilepsy syndrome
3. Infantil spasms
Status epilepticus confined to later childhood
1. Febrile status epilepticus
2. Status in childhood partial epilepsy syndrome
3. Status epilepticus in myoclonic – static epilepsy
4. Electrical status epilepticus during slow wave sleep
5. Landau – Kleffer syndrome
Status epilepticus occurring in childhood and adult life
1. Tonic – clonic status epilepticus
2. Absence status epilepticus
3. Epilepsia partialis continua
4. Status epilepticus in coma
5. Specific form of status epilepticus in mental retardation
6. Syndrome of myoclonic status epilepticus
7. Simple partial status epilepticus
8. Complex partial status epilepticus
In clinical practice status epilepticus classified :
A. Convulsive status epilepticus
B. Non convulsive status epilepticus
Principle of management of status epilepticus
1. Lifesaving (ABC)
2. Stop seizures immediately
3. Manage in ICU
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COMA AND DECREASE OF CONCIOUSNESS
DPG Purwasamatra
IGN Budiarsa
Objectives : To diagnosis and manage patients with decrease of conciousness
Conciousness is the state of awareness of the self and the enviroment and coma its
opposite, i.e. the total absence of awareness of self and enviroment even when the subject
is externally stimulated.
Conciousness is maintened by each cerebral hemisphere with constant prodding from the
reticular activating system within the central core of the brainstem tegmentum. Disruption of
the reticular activating system or extensive damage to both cerebral hemispheres impairs
conciousness.
The five basic physiologic explanation for loss of conciousness are:
Bilateral cerebral hemisphere disease, unilateral cerebral hemisphere lesion with
compression of the brainstem, primary brainstem lesion, cerebellar lesion with secondary
brainstem compression and non organic or feigned stupor.
Coma, however, is an emergency that the physician must treat before pursuing a diagnosis.
LECTURE 3 : ACUTE PSYCHIATRIC EPISODE
Ratep
Objective :
1. To describe etio-pathogenesis and pathophysiology of acute psychiatric episodes
2. To implement a general strategy in the approach to patients with acute psychiatric
episodes through history and special technique investigations
3. To manage by assessing, provide initial management and refer patient with acute
psychiatric episodes
4. To describe prognosis patient with acute psychiatric episodes
Emergency occur in psychiatric just as we do in every field of medicine. However,
psychiatric emergencies are often particularly disturbing because we do not just involve the
body’s reactions to an acute disease state, as must as actions directed against the self or
others. These emergencies, such as suicidal acts, homicidal delusions, or a serve in ability
to care for oneself, are more likely than medical ones to be sensationalized when they are
particularly dramatic or bizarre.
Psychosis is difficult term to define and is frequently misused, not only in the
newspaper, movies, and on television, but unfortunately among mental health professionals
as well. Stigma and fear surround the concept of psychosis and the average citizens
worries about long-standing myths of mental illness, including psychotic killers, psychotic
rage, and equivalence of psychotic with the pejorative term crazy. Aggressive and hostile
symptoms can overlap with positive symptoms but specifically emphasize problems in
impulse contro
For example, a mother killing her five children in the belief that they are inhabited by
Satan, a famous poet killing herself, the delusional murder of legendary musician, the son of
prominent family found wondering confused and malnourished in a city park, all of these are
psychiatric emergencies that can and up on the front pages of newspaper.
Psychiatric emergencies occur everyday to people. Psychiatric emergencies arise
when mental disorders impair people’s judgment, impulse control, and reality testing. Such
mental disorders include all the psychotic disorders, manic and depressive episodes in
mood disorders, substance abuse, borderline, and antisocial personality disorders and
dementias. There may also be emergencies related to particularly severe reactions to
psychiatric medications, such as neuroleptic malignat syndrome or acute granulocytosis,
that must be recognize, diagnosed and treated immediately.
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LECTURE 4 : ACUTE RESPIRATORY DISTRESS SYNDROME AND FAILURE
Dewa Artika
ARDS is an emergency in the lung area due to disturbance in alveolocapiler
membrane permeability by a number of thing causing liquid accumulation/build up inside
alveoli or bronchus oedema. While ARF is a kind of ARDS complication which is a distability
of lung to do respiration function causing accumulation of CO2 and decrease in O2 inside the
artery. Incident of ARDS is high. In the USA, 150.000 cases were found per year and 50%
of them died due to breathing failure.
Diagnosed based on : complaint, sudden breathing difficulties, coughing, tiredness
and decrease in consciousness and usually preceded by basic illness and triggering factors.
On the thorax photo it was found infiltrate diffuse in the two lungs region, while in ARF
depend on basic illness. The important thing is examination of blood gas analyses where
there is a decrease on PaO2 until below 50 and PaO2 above 50 or refer to as rule of fifty.
Principle of procedure is to give the Oxygen, CO2 removal either with or without
ventilator, liquid restriction, clearing of breathing pathway, overcoming obstruction using
bronchodilator, etc.
Learning Objective
Students are able to describe pathogenesis, to set diagnoses, propose examination, give
medication and evaluate ARDS and ARF patients.
ACUTE UPPER AIRWAY OBSTRUCTION
Wayan Sucipta,
Abstract
Acute upper airway can result from a variety of disorders including trauma, neoplasm,
infection, inflammatory process, neurologic dysfunction, presence of a foreign body.
Affected site can include the oral cavity, oropharynx, larynx and trachea.
Emergency airway management principles include the determination of the site and degree
of obstruction, airway control by ventilation, intubation or surgical bypass of the obstructed
site with a crico thyroidectomy or tracheostomy and treatment of the precipitating cause of
obstruction.
NEONATAL RESUSCITATION and ELECTROLITE IMBALANCE
Diah Kanyawati
Abstract
Ninety percent of asphyxia insults occur in the antepartum or intrapartum periods a a result
of placental insufficiency. After delivery, the baby’s ineffective respiratory effort and
decrease cardiac output. Hypoxic tissues begin anaerobic metabolism, producing metabolic
acids that are initially buffered by bicarbonate.
The incidence of perinatal asphyxia usually related to gestational age and birth weight. The
basic goal of resuscitation are : to expend the lungs and maintain adequate ventilation and
oxygenation, to maintain adequate cardiac output and tissue perfusion. Neonatal
resuscitation equipment and emergency medications should be immediately available.
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RADIOLOGY
Srie Laksminingsih
Learning Objective
At the end of meeting, the student will be able to :
1. Describe the radiology imaging of thorax photo for IRDS (Idiopathic Respiratory
Distress Syndrome) case, Bronchopneumonia, CHD, Pericardial Effusion, Lung
Edema, Pneumothorax, Pleural Effusion, Vena Cava Superior Syndrome.
2. Describe the imaging of abdominal plain photo in : Illeus Obstruction, Paralytic Illeus,
Stone in the Urinary Bladder, Peritonitis, NEC, Cholelithiasis & Acute Cholecystitis.
LECTURE 5 : BLEEDING DISORDER
HEMORRHAGE IN PREGNANCY : ANTEPARTUM AND POST PARTUM
Wayan Megadhana
ANTEPARTUM HEMORRHAGE
Objectives :
1.
Recite the incidence of antepartum hemorrhage
2.
List the etiology of antepartum hemorrhage
3.
Distinguish the differences in the diagnosis of placenta previa and abruption
placenta
4.
Apply the principles of fetal and maternal stabilization in the management of
anterpartum
Antepartum haemorrhage (APH) is defined as bleeding from or in to the genital tract,
occurring from 28 weeks of pregnancy and prior to the birth of the baby. The most important
causes of APH are placenta praevia and placental abruption, although these are not the
most common. APH complicates 3–5% of pregnancies and is a leading cause of perinatal
and maternal mortality worldwide.Up to one-fifth of very preterm babies are born in
association with APH, and the known association of APH with cerebral palsy can be
explained by preterm delivery. Bleeding during various times in gestation may give a clue as
to its cause. Uterine bleeding, however, coming from above the cervix, is concerning. It may
follow some separation of a placenta previa implanted in the immediate vicinity of the
cervical canal, or it may be from a placental abruption or uterine tear. Rarely, there may be
velamentous insertion of the umbilical cord, and the involved placental vessels may overlie
the cervix—vasa previa. Clearly, second- and third-trimester bleeding are associated with a
poor pregnancy prognosis.
POSTPARTUM HEMORRHAGE
Objectives :
1.
2.
3.
4.
Devine postpartum hemorrhage
Recognize etiologic factors for postpartum hemorrhage
Apply appropriate preventive strategies
Employ the principles of resuscitation in management of postpartum
hemorrhage
Traditionally, the definition of postpartum hemorrhage has been blood loss in excess of 500
cc in vaginal delivery and in excess of 1000cc in abdominal delivery. In most cases, the
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cause of postpartum hemorrhage can and should be determined. Frequent causes are
uterine atony with bleeding from the placental implantation site, genital tract trauma, or both.
Postpartum hemorrhage is usually obvious. Important exceptions are unrecognized
intrauterine and intravaginal blood accumulation and uterine rupture with intraperitoneal
bleeding. Initial assessment should attempt to differentiate uterine atony from genital tract
lacerations. Atony is identified by a boggy, soft uterus during bimanual examination and by
expression of clots and hemorrhage during uterine massage. Persistent bleeding despite a
firm, well-contracted uterus suggests that hemorrhage most likely is from lacerations.Bright
red blood further suggests arterial bleeding. To confirmthat lacerations are a source of
bleeding, careful inspectionof the vagina, cervix, and uterus is essential. Sometimes
bleeding may be caused by both atony and trauma, especially after forceps or vacuumassisted vaginal delivery. Importantly, if significant bleeding follows these deliveries, then
the cervix and vagina are carefully examined to identify lacerations. This is easier if
conduction analgesia was given. If there are no lower genital tract lacerations and the
uterus is contracted, yet supracervical bleeding persists, then manual exploration of the
uterus is done to exclude a uterine tear.
EPISTAXIS
SARI WULAN
ENT TEAM
Abstract
Epistaxis is an acute bleeding from nasal cavity and or nasopharynx, due to alteration of
normal hemostasis within the nose. Hemostasis is compromised by mucosal abnormalities,
vascular dissorder or disorders of coagulation. Afek at 2-10 yo and 50-80 yo. Etiology of
epistaxis may be local or systemic. Most epistaxis can stop spontaneously. The local
epistaxis caused by trauma, foreign body, infection, iatrogenic factors and chemical agent.
Meanwhile the systemic can caused by cardiovascular ds, endocrine disorders, systemic
infection, haematologic ds, drug induced, hereditary haemmorhagiec teleangiectasis, Vit C
and K deficiency.
Principle of managing of epistaxis are stop the bleeding, avoid complication and prevent
reccurence.
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Management Epistaxis Algorithm
Epistaxis
Vital Sign Evaluation
General condition
not stabil
General condition
stabil
Identify bleeding point
(suction, tampon adrenalin &
lidocain)
Location not known :
tampon ant 2x24 hr, if
needed tampon
posterior
 manage etiologi
& complication
Location identify
 Cautery /
AgNO3
caustic
Aff tampon
Bleeding (-)
Bleeding (+)
 retampon (E/)
 surgery
intervention
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LECTURE 6 : SHOCK
IGAG Utara Hartawan
Objective :
1. To describe the term, etio-pathogenesis and pathophysiology of shock
2. To implement a general strategy in the approach to patients with shock through
history, physical examination and special tehnique investigations.
3. To manage by assesing, differential diagnosis, provide initial management and
refer patient with shock
4. To describe prognosis patient with shock
Abstracts
Shock is a clinical syndrome due to deficiency of cell perfusion or failure of oxygen intake
by cells which leads to hypoxia and oxygen debt that causes cellular dysfunction. Deficiency
of cell perfusion can be caused by (1) failure of heart contraction (shock cardiogenic) (2)
reduction in blood volume (shock hypovolemic) (3) disturbance in blood volume distribution
(shock distributive) (4) heart function restriction due to tamponade and pericarditis and
blood flow restriction due to pulmonary artery emboli (shock obstructive) (5) a state of
vasomotor instability resulting from impairment of the descending symphatetic pathways in
the spinal cord, or simply a loss of symphatetic tone (neurogenic shock). In traumatic
situations, shock is the result of hypovolemia until proven otherwise.
Hypoxia and cell oxygen debt causes cellular metabolism changes, that leads to cellular
dysfunction and finally it becomes a multiple organ dysfunction syndrome.
General strategy to obtain a diagnosis is done by subjective approach or anamnesis and
objective approach by physical examination and a few other diagnostic examination to find
the primary signs and symptoms of shock and the secondary signs and symptoms from
other organ system perfusion disturbance. X-rays of the chest, pelvis, and lateral cervical
spine usually occur concurrently with early resuscitative efforts; however their procedure
shoulde never interrupt the resuscitative process.
The basic shock managements are: hemodynamic support, optimal oxygen distribution to
cell and treating organ system disfuntion. Then, by overcoming the underlying cause by
medical/surgical approach after media consultation followed by referral if necessary.
Fluids used for volume resuscitation are : (1) blood product (these fluids increase the O2
carrying capacity of blood, their ability to flow and augment CO are limited by the viscosity
effects of the cells); (2) Colloids (these fluids preferentially increase intravascular volume
and are the most effective fluids for increasing CO); (3) crystaloids ( these fluids distribute
evenly in the extracellular space and preferentially increase interstitial fluids volume).
Crystalloids fluids are primarily sodium chloride solutions, and because sodium is
distributed evenly in the extracellular fluid. Because plasma represents only 20% of the
cellular fluids, only 20% of the infused volume of crystalloids fluids will remain in the
vascular space and add to the plasma volume, while the remaining 80% will add to the
instertitial fluids volume. Cooloids fluids, on the other hand, will add primarily to the plasma
volume because the large moleculs in colloids fluids do not readly escape from the vascular
compartment. As much 75-80% of the infused volume of colloids fluids will remain in the
vascular space and add to the plasma volume, at least in the first few hours after infusion.
Once the diagnostic management and early treatment and definitive treatment is done
optimally especially in shock hypovolemic good prognosis is obtained but for other shocks
the prognosis are uncertain.
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CARDIAC ARREST AND CARDIOPULMONAR RESCUSTATION
IGN Mahaalit Aribawa
Objective
:
1. To describe etio-pathogenesis and pathophysiology of cardiac arrest
2. To know how to identify patients with cardiorespiratory arrest
3. To understand the chain of survival
4. To Understand the principles of treating cardiac arrest incorporate basic life support and
advance life support
5. To describe the need for continued resuscitation after return of spontaneous circulation (
ROSC )
6. To describe the role of the resuscitation team
Abstract
Cardiac arrest is the cessation of clinically detectable cardiac output. It is
unpredictable and rarely occurs with doctors in attendance, can occur anywhere, anytime
and to anybody. Cardiac arrest can be because of a disease or due to drowning, poisoning
and others that are capable of causing respiratory and cardiac arrest.
The initial rhythm found may be ventricular fibrillation ( VF ), ventricular tachycardia (
VT ), asystole, and pulseless electrical activity ( PEA ). Bystanders need to commence
cardiopulmonary resuscitation ( CPR ) immediately if the victim is to survive.
Permanent brain damage can occur if blood circulation has stopped for more than a few
minutes (now it has been agreed more than 4-6 minutes) or after a trauma with severe
hypoxia or loss of lots of blood which are not corrected. If resuscitation / CPR is given
immediately and correctly brain death can be avoided and the patient recovers completely.
Resuscitation can be done anywhere, anytime, with or without equipment by trained
whether public or health personnel. CPR (cardiopulmonary resuscitation) is an effort of
medical emergency to cure respiratory function and circulation which has failed drastically
on a patient that has the chances of living. CPR incorporates basic life support ( BLS ), that
is, making use of basic equipment or without equipment and advanced life support (ALS),
that is, using advanced equipment including drugs, defibrillators and advanced airway
management.
The “chain of survival” describes the events needed to achieve a good outcome :
early access to emergency services, early bystander CPR, early defibrillation and early ALS.
In performing advanced life support, the role of ressucitation team is very important and to
achieved good team needed to done routine practical simulation of the team.
LECTURE 8 :EMERGENCY TOXICOLOGY AND POISONING
Agus Somia
Learning objective
:
1.
To describe Approach to general the management of the poisoned patient
a. History
b. Clinical evaluation
c. The toxicology laboratory
2. To describe general Management of the poisoned patient
a. Decontamination procedures
i. Terminating topical exposures
ii. Decreasing exposure to ingested toxins
iii. Gastro-intestinal
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3.
4.
5.
6.
b. Increasing elimination
i. Multi-dose activated charcoal (Gut dialysis) ]
ii. Urine alkalinisation
iii. Extracorporeal elimination
c. Antidotes
d. Pearls and pitfalls of managing poisonings and respective antidotes
To describe management of methanol intoxication
To describe management of opiate intoxication
To descripe management of organophospate poisoning
To describe management of caustic posoning
Abstract
General management of acute intoxication/poisoning
Acutely poisoned patients are commonly encountered in Emergency Centres. Acute
poisoning (accidental or intentional) requires accurate assessment and prompt therapy.
Early identification of the involved toxin/s is crucial and the majority will be identified by a
thorough history and physical examination. An ABC-approach should be followed ensuring
a protected airway, adequate ventilation and hemodynamic stability. Supportive and
symptomatic care remains the cornerstone of treatment. A stepwise approach may be
followed to decrease the bioavailability of toxins. Indications, contra-indications, risks and
dosage regimens are describe for decontamination procedures including both termination of
topical exposures and decreasing exposure to ingested toxins. Furthermore, procedures to
increase the elimination of toxins and a short section covering specific toxins and their
antidotes are also included
Organophosphat poisoning
Organophosphorus pesticide self-poisoning is a major clinical and public-health
problem across much of rural Asia.1–3 Of the estimated 500 000 deaths from self-harm in
the region each year,4 about 60% are due to pesticide poisoning.3 Many studies estimate
that organophosphorus pesticides are responsible for around two-thirds of these deaths5—
a total of 200 000 a year.3 Deaths from unintentional organophosphorus poisoning are less
common than those from intentional poisoning6
Organophosphorus
pesticides
inhibit
esterase
enzymes,
especially
acetylcholinesterase (EC 3.1.1.7) in synapses and on red-cell membranes, and
butyrylcholinesterase (EC 3.1.1.8) in plasma.17 Although acute butyrylcholinesterase
inhibition does not seem to cause clinical features, acetylcholinesterase inhibition results in
accumulation of acetylcholine and overstimulation of acetylcholine receptors in synapses of
the autonomic nervous system, CNS, and neuromuscular junctions.17 The subsequent
autonomic, CNS, and neuromuscular features of organophosphorus poisoning are well
known
Clinical features of organophosphorus pesticide poisoning including:
-
-
overstimulation of muscarinic acetylcholine receptors in the parasympathetic system
Bronchospasm, Bronchorrhoea, Miosis, Lachrymation, Urination, Diarrhoea,
Hypotension, Bradycardia, Vomiting, Salivation.
overstimulation of nicotinic acetylcholine receptors in the sympathetic system:
Tachycardia, Mydriasis, Hypertension, Sweating.
overstimulation of nicotinic and muscarinic acetylcholine receptors in the CNS:
Confusion, Agitation, Coma, Respiratory failure.
overstimulation of nicotinic acetylcholine receptors at the neuromuscular junction:
Muscle weakness, Paralysis and Fasciculations
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Treatment includes resuscitation of patients and giving oxygen, a muscarinic
antagonist (usually atropine), fluids, and an acetylcholinesterase reactivator (an oxime that
reactivates acetylcholinesterase by removal of the phosphate group) (panel 3).35
Respiratory support is given as necessary. Gastric decontamination should be considered
only after the patient has been fully resuscitated and stabilised. Patients must be carefully
observed after stabilisation for changes in atropine needs, worsening respiratory function
because of intermediate syndrome, and recurrent cholinergic features occuring with fatsoluble organophosphorus.
Caustic agent intoxication
Caustic ingestions may cause widespread injury to the lips, oral cavity, pharynx, and
the upper airway. The effect that these agents have on the esophagus accounts for most of
the serious injuries and long-term complications. The nature of the injury caused by caustic
ingestion is determined by a number of factors including the identity of the agent, the
amount
consumed, the concentration, and the length of time the agent is in contact with a given
tissue. Caustic materials cause tissue injury by chemical reaction. These materials are
generally acidic or alkali. Usually, acids with pH less than 3 or bases with pH greater than
11 are of the greatest concern for caustic injury.
The esophagus is the site of most long-term sequelae from caustic ingestion. Injury
to the esophagus is rapid, as described above, for both acids and alkalis, but this acute
tissue
disintegration and deep tissue penetration may continue for hours. Injury progresses within
the first
week after ingestion, with inflammation and vascular thrombosis. A developing ulcer with
fibrin crust will be seen in a few days. Granulation tissue develops between 2 to 4 days and
is revealed under shed necrotic tissue by days 15 to 20.
After caustic ingestion, patients may present with a combination of many symptoms
or none at all depending on the nature of the agent, the specifics of the ingestion (quantity,
intent, timing), and what tissues were affected.
Induction of emesis should be avoided to prevent further injury as the agent is
vomited. Neutralization of the caustic material should be avoided because of the potential
for causing an exothermic injury, which may worsen an existing injury. When the patient is
stable, the pH of any
Opioid intoxication
Opioid analgesic overdose is a preventable and potentially lethal condition that results from
prescribing practices, inadequate understanding on the patient's part of the risks of
medication misuse, errors in drug administration, and pharmaceutical abuse. Three features
are key to an understanding of opioid analgesic toxicity. First, opioid analgesic overdose
can have life-threatening toxic effects in multiple organ systems. Second, normal
pharmacokinetic properties are often disrupted during an overdose and can prolong
intoxication dramatically.3 Third, the duration of action varies among opioid formulations,
and failure to recognize such variations can lead to inappropriate treatment decisions,
sometimes with lethal results
Opioids increase activity at one or more G-protein–coupled transmembrane
molecules, known as the mu, delta, and kappa opioid receptors. The presence of hypopnea
or apnea, miosis, and stupor should lead the clinician to consider the diagnosis of opioid
analgesic overdose, which may be inferred from the patient's vital signs, history, and
physical examination. In patients with severe respiratory depression, restoration of
ventilation and oxygenation takes precedence over obtaining the history of the present
illness or performing a physical examination or diagnostic testing
Naloxone, the antidote for opioid overdose, is a competitive mu opioid–receptor
antagonist that reverses all signs of opioid intoxication. Dosing of naloxone is empirical. The
effective dose depends on the amount of opioid analgesic the patient has taken or received,
the relative affinity of naloxone for the mu opioid receptor and the opioid to be displaced, the
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patient's weight, and the degree of penetrance of the opioid analgesic into the central
nervous system
Metanol Intoxication
Methanol (methyl alcohol, CH3OH) is the simplest type of alcohol, very light, volatile,
colorless, flammable, distinctive smell a little sweeter than etanol.3 methanol is used for
industrial products, and also as a mixture with ethanol to drink Traditional hard. Industrial
products that use methanol is a liquid car cleaner, solvent paints, cleansers, perfumes, car
fuel and other industrial products.
Methanol poisoning is a major disruption to the central nervous system, the optic
nerve and basal ganglia. The formic acid acts cause toxicity to the eye by inhibiting
cytochrome oxidase in the optic nerve, interrupting the flow axoplasma. While substances
that contribute to the occurrence of metabolic acidosis and decreased plasma bicarbonate
is formaldehyde, formic acid and lactic acid.
Toxic doses of methanol ranges between 15-500 cc of methanol solution containing
40% to 60-600 cc of methanol murni.3 methanol poisoning begins with mild drunk and
sleepy. Followed by a latent phase (40 minutes - 72 hours) which is the period without
symptoms, due to the slow production of formaldehyde and formic acid. This phase was
followed by the appearance of metabolic acidosis, anion gap and impaired vision.
Pendangan visual disturbances such as blurred to decrease visual acuity. In the later phase
of seizures, coma and kematian.3,5,11 slower onset of methanol poisoning if the patient is
also taking ethanol simultaneously. In the alcoholic drink various types of alcohol will give a
clinical picture that is not typical.
On laboratory examination found an increase in serum osmolality, anion gap, serum
lactic acid and metabolic acidosis. Definitive diagnosis and monitoring of treatment
response based on the examination of serum methanol levels.
Specific Management of acute methanol poisoning include:
Inhibitors of alcohol dehydrogenase
Treatment with Co-factor: folinic acid 50 mg IV or folic acid 50 mg IV every 6 hours.
Sodium Bicarbonate
Hemodialis: Hemodialis is the fastest way of issuing metabolic toxic acid and
methanol
References
Eddleston M. Buckley NA, Eyer P, AH. Management of acute organophosphorus pesticide
poisoning. Lancet. 2008 Feb 16; 371(9612): 597–607.
Lupa M, Magne J, Guarisco JL, Amedee R. Update on the Diagnosis and Treatment of
Caustic Ingestion. The Ochsner Journal. Volume 9, Number 2, Summer 2009.
Boyer EW. Management of Opioid Analgesic Overdose. N Engl J Med 2012; 367:146-155
Agus somia IK. Keracunan Alkohol. In: Siti Setiati : Buku Ajar Ilmu Penyakit Dalam. Interna
Publishing. 2014.p: 1037-1046.
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LECTURE 9 :
PREGNANCY INDUCED HYPERTENSION
Megaputra
OBGYN Team
Objective :
1. Define pregnancy induced hypertension
2. Review appropriate fetal/maternal assessment
3. Discuss appropriate management of pregnancy induced hypertension
4. Recognize when and how to transport patient with pregnancy induced hypertension
How pregnancy incites or aggravates hypertension remains unsolved despite decades of
intensive research. Indeed, hyper- tensive disorders remain among the most significant and
intriguing unsolved problems in obstetrics.
Hypertensive disorders complicate 5 to 10 percent of all pregnancies, and together they are
one member of the deadly triad—along with hemorrhage and infection—that contributes
greatly to maternal morbidity and mortality. Of these disorders, the preeclampsia syndrome,
either alone or superimposed on chronic hypertension, is the most dangerous. As
subsequently discussed, new-onset hypertension during pregnancy—termed gestational
hypertension—is followed by signs and symptoms of preeclampsia almost half the time, and
preeclampsia is identified in 3.9 percent of all pregnancies.
The World Health Organization (WHO) systematically reviews maternal mortality worldwide,
and in developed countries, 16 percent of maternal deaths were reported to be due to
hypertensive disorders. This proportion is greater than three other leading causes that
include hemorrhage—13 percent, abortion—8 percent, and sepsis—2 percent. In the United
States from 1998 to 2005, Berg and colleagues (2010) reported that 12.3 percent of 4693
pregnancy-related maternal deaths were caused by preeclampsia or eclampsia. The rate
was similar to that of 10 percent for maternal deaths in France from 2003 through 2007
(Saucedo, 2013). Importantly, more than half of these hypertension-related deaths were
preventable (Berg, 2005).
In this country for the past two decades, pregnancy hypertension was considered using the
terminology and classification pro- mulgated by the Working Group of the National High
Blood Pressure Education Program—NHBPEP (2000). To update these, a Task Force was
appointed by President James Martin for the American College of Obstetricians and
Gynecologists (2013b) to provide evidence-based recommendations for clini- cal practice.
The basic classification was retained, as it describes four types of hypertensive disease:
1. Gestational hypertension—evidence for the preeclampsia syndrome does not
develop and hypertension resolves by 12 weeks postpartum
2. Preeclampsia and eclampsia syndrome
3. Chronic hypertension of any etiology
4. Preeclampsia superimposed on chronic hypertension. Importantly, this
classification differentiates the preeclampsia syndrome from other hypertensive
disorders because it is potentially more ominous. This concept aids interpretation of
studies that address the etiology, pathogenesis, and clinical management of
pregnancy-related hypertensive disorders.
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LECTURE 10 :
SHOULDER DYSTOCIA
Hariyasa Sanjaya
OBGYN Team
Objective
Use a systematic approach to the reduction of shoulder dystocia based upon the
physical mechanism of impact and disimpaction.
Shoulder dystocia is one of emergency problems during delivery. Following the
delivery of the head, there is impaction of the anterior shoulder on the symphysis pubis in
the AP diameter, in such a way that the remainder of the body cannot be delivered in the
usual manner. More than 50% of cases shoulder dystocia occur in the absence of any
identified risk factor. The student will discuss the assessment of shoulder dystocia, the
complication for fetus and mother, identification of risk factor, diagnosis and management
LECTURE 11 : NON TRAUMA UROLOGIC EMERGENCY
UROLOGYC CONCERN IN CRITICAL CARE
Gede Wirya Kusuma Duarsa
Budi Santosa
Objectives
1. To understand the basic principles of non trauma urologic emergency
2. Comprehend the definition, etiology, special investigation and basic management
the acute urinary retention, acute scrotum, penile emergencies.
3. Comprehend the definition, etiology, special investigation and basic management of
colic, urosepsis, hematuri,
Abstract
The primary care physician plays a key role in the diagnosis and initial management
of most urologic emergencies. It is critical to stratify patients into those who require urgent
care (eg, phimosis, epididymitis) and those who require emergent care (eg, Fournier's
gangrene, testis torsion), because the time to therapy may significantly impact on outcome
between these two groups. Mismanagement of these conditions may result in significant
sequelae, which are preventable in most cases. Fortunately, most urologic emergencies are
precisely diagnosed with a combination of clinical acumen and appropriate radiologic or
adjunctive studies. This article reviews the diagnosis and management of the most common
urologic emergencies, and highlights pragmatic information of use to the general practitioner
Acute urinary retention is defined as the sudden inability to void despite a distended
bladder (urine volume in the bladder more than its capacity). It is usually preceded by a
history of progressively decreasing force of stream. The most common obstructive cause of
acute urinary retention is benign prostatic hyperplasia. Prostate cancer, urethral strictures,
bladder stones or bladder tumors may also cause obstructive urinary retention, hematuria
and clots should be suspected of harboring an underlying bladder tumor. Less common
obstructive etiologies include urethral foreign bodies, penile constricting bands, and meatal
stenosis. The most common infectious cause for acute retention is acute prostatitis. Other
infectious causes of retention include urethral herpes, periurethral abscesses, and
tuberculous cystitis. There are many pharmacologic agents that may contribute to urinary
retention. Neurogenic causes of urinary retention may be broadly categorized into upper
motor neuron lesions, lower motor neuron lesions, and peripheral nerve lesions.
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The initial diagnosis of the patient who presents with acute scrotal pain may be
challenging. Although testis torsion is the least common cause of the acute scrotum, it
should be high in the differential diagnosis because testicular salvage rates correlate
inversely with time to exploration. Most patients suffer from epididymitis, torsion of a
testicular appendage. The availability of more accurate radiologic imaging studies has
helped to reduce the incidence of negative scrotal explorations, but the importance of the
initial evaluation and clinical findings still remains the most powerful tool in correctly treating
the acute scrotum.
Testis torsion may occur in the neonatal period secondary to lack of fixation of the
tunica vaginalis to the scrotal wall. This is known as extravaginal torsion. Neonatal torsion
has a low salvage rate. If the tunica vaginalis inserts in an abnormally high position on the
spermatic cord (the “bell clapper deformity”), the testis may freely rotate on the cord. Testis
torsion may occur in the neonatal period secondary to lack of fixation of the tunica vaginalis
to the scrotal wall. This is known as extravaginal torsion. Neonatal torsion has a low salvage
rate. If the tunica vaginalis inserts in an abnormally high position on the spermatic cord (the
“bell clapper deformity”), the testis may freely rotate on the cord. This is known as
“intravaginal torsion,” and testis ischemia is dependent on the number of rotations of the
cord. The spermatogenic cells are the most sensitive to ischemia, whereas the testosteroneproducing Leydig's cells are more resistant. Salvage of testicular function is close to 100% if
detorsion occurs within 6 hours of pain onset, but this drops to less than 20% beyond 12
hours. Successful treatment is time dependent in this case
Epididymitis arises from pain and swelling of the epididymis. It usually arises
secondary to infection or inflammation from the urethra or bladder. If the process remains
untreated, it may involve the adjacent testis and scrotum, and eventually result in abscess
formation. Fever and leukocytosis are present in between 30% and 50% of cases. Antibiotic
treatment for epididymitis depends on patient age and probable underlying pathogen.
Neisseria gonorrhoeae and Chlamydia trachomatis account for most cases in men under
35, and these may be treated with intramuscular ceftriaxone plus a course of doxycycline. In
men over 35, urine culture usually reveals Escherichia coli, and treatment consists of an oral
fluoroquinolone for 21 days.
Necrotizing fasciitis of the scrotum and perineum (Fournier's gangrene) is a rare but
life-threatening cause of acute scrotal pain. It is typically found in debilitated or
immunocompromised patients with significant medical comorbidities, particularly diabetes
and alcoholism. The infection usually originates from a perianal or periurethral source, and
includes multiple pathogens, including E coli, Bacteroides, and Streptococci. Patients
present with early systemic toxicity, and genital examination typically reveals erythema,
tenderness, induration, and crepitus. The perineum may appear frankly necrotic and foul
smelling.
Phimosis results from stenosis of the distal aspect of the foreskin, preventing it from
being successfully retracted over the glans. It is a physiologic finding in uncircumcised
infants, and physiologic adhesions typically prevent complete retraction of the foreskin in
this age group. Forcible retraction of the foreskin should not be attempted because it may
actually tear the adhesions and create pathologic phimosis. Phimosis is rarely an emergent
condition, but it may rarely cause urinary retention if the foreskin has sealed off. In this case,
the preputial sac balloons out with each void. Temporary or emergent management of this
condition includes hemostat dilation of the stenotic foreskin. Topical steroids have been
successful in progressively reducing phimosis, but circumcision should be considered in
chronic or refractory cases.
Paraphimosis arises when the foreskin has been retracted proximal to the glans, and
cannot be returned to its normal position secondary to a tight, constricting ring of skin. With
time, the retracted prepuce becomes edematous because of impaired venous and lymphatic
drainage. Treatment of paraphimosis is urgent reduction of the foreskin.
Priapism is defined as a prolonged, painful erection that is unrelated to sexual
arousal. Although the corpora cavernosa are typically rigid and filled with stagnant blood,
the glans and corpus spongiosum remain flaccid. Stuttering priapism refers to recurrent
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painful erections with intervening detumescence, whereas malignant priapism implies a
locally invasive malignant condition in the corpora, and is frequently a preterminal event.
Penile fracture (or rupture) implies disruption of the tunica albuginea surrounding the
corpora cavernosa. This injury typically occurs during vigorous intercourse, when the rigid
penis is misdirected against the partner's pubic bone, and results in buckling trauma. This
injury may also be self-inflicted by abrupt bending of the erect penis during masturbation.
The classic history involves the scenario described previously, with patients usually
reporting a popping sound as the tunica tears, followed by pain, swelling, and rapid
detumescence.
Blood in urine is a common symptoms in urology. There are many causes of
Haematuria including medical bleeding and surgical bleeding. Prompt diagnosis and good
management will prevent further damage or complication.
Case 1 An Old man that unable to void
A 73-year-old man with multiple medical problems presented with complaints that he could
not void and had pain in the lower abdomen. He had a mild dementia, so much of the
history was from his wife, who accompanied him to the clinic. She stated that he had neither
incontinence, fever, nausea, nor vomiting, and he had not had any recent acute illnesses.
The patient had not had any recent change in medications, doses, or frequency of dosing of
his pain medication. He had similar problems in the past, but the symptoms had resolved
after he underwent a transurethral resection of the prostate (TURP) 2 years ago. His wife
also stated that he had been able to void normally up until earlier this morning. Since that
time he had complained frequently about the urge to void and being unable to do so.
The patient's medical history was extensive. Of particular note, he had metastatic
squamous-cell lung cancer and was placed in hospice care 2 weeks before presentation.
He had type 2 diabetes, hypertension, glaucoma, and benign prostatic hypertrophy (BPH).
His medications included an extended-release morphine tablet for pain, rosiglitazone for his
diabetes, and recently discontinued ramipril and hydrochlorothiazide, which he had taken in
the past for his hypertension. On examination, he was mildly tender over the bladder, which
was palpably distended. He attempted to void for a urinalysis specimen and was unable to
do so. A Foley catheter was placed, and 240 mL of urine was collected. The urinalysis
showed a trace of protein, and results were otherwise negative; the pH was 7.3.
Question Learning Task
1. What are some causes of acute urinary retention?
2. What are some typical symptoms of acute urinary tract obstruction?
3. What tests would be helpful in determining the cause of this patient's urinary retention?
4. What treatments would be useful in relieving the symptoms?
5. What are some complications of untreated acute urinary retention?
LECTURE 12 : DERMATO - EMERGEMENCIES
Nyoman Suryawati
Objective
 To understand the basic principle of dermato-emergencies
 Able to identify of dermato-emergencies
 Able to mange of emergencies skin diseases
 Able to refferral of dermato-emergencies
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Stevens – Johnson Syndrome and Toxic Epidermal Necrolysis
Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) are acute life
threatening mucocutaneous reactions characterized by extensive necrosis and detachment
of the epidermis. This two condition are now considered severity variant of an identhical
process that differs only in the final extend of body surface involved. Stevens-Johnson
Syndrome if the skin lesion involve less than 10% of the body surface area (BSA), SJS/TEN
overlap between 10-30% BSA and TEN if more then 30% BSA. Nearly all cases of
SJS/TEN are induced by medications, and the mortality rate can approach 40%.
These reaction clinically begins within 8 weeks (usually 4-30 days) after the onset of
drug exposure for the first time. Nonspecific symptoms such as fever, headache, rhinitis,
cough, or malaise, may precede the cutaneous lesions by 1-3 days. Pain on swallowing and
burning or stinging of the eyes progressively develop, heralding mucous membrane
involvement. The initial skin lesions are characterized by erythematous, dusky red, purpuric
macules, irregularly shaped, which progressively coalesce. Nikolsky’s sign (dislodgement of
the epidermis by lateral pressure) is positive on erythematous zones. At this stage, the
lesions evolve to flaccid blisters, which spread with pressure and break easily. The necrotic
epidermis is easily detached at pressure points or by frictional trauma, revealing large areas
of exposed, red, sometimes oozing dermis.
SJS/TEN are life-threatening disease that requires optimal management: early
recognition and withdrawal of the offending drugs and supportive care in an appropriate
hospital setting. The broad principles of management are fluid replacement, nutritional
supplementation, sterile technique, and wound care. Sterile technique is essential to
prevent complications from endogenous and exogenous sources. Broadspectrum
prophylactic antibiotics are not recommended or still debate according the condition. In
severe condition can be treated in an ICU or burn unit under the coordinated care of an ICU
team and consultants.
Staphylococcal Scalded Skin Syndrome
Staphylococcal scalded skin syndrome (SSSS) is a generalized, confluent, superficially
exfoliative disease, occurring most commonly in neonates and young children. It was known
in the past as Ritter’s disease or dermatitis exfoliativa neonatorum. SSSS is a febrile, rapidly
evolving, generalized, desquamative infectious disease, in which the skin exfoliates in
sheets. Exfoliative toxins (ETs) are made by certain strains of S. aureus (usually phage
group 2). Exfoliatin A and B (ETA and ETB) are two serologically distinct proteins produced
by S. aureus.2 ETs are serine proteases that bind to the cell adhesion molecule desmoglein
1 and cleave it, resulting in a loss of cell–cell adhesion
Its clinical manifestations begin abruptly with fever, skin tenderness, and erythema
involving the neck, groins, and axilla. There is sparing of the palms, soles, and mucous
membranes. Nikolsky sign is positive. Generalized exfoliation follows within the next hours
to days, with large sheets of epidermis separating.
Therapy for SSSS should be directed toward eradication of S. aureus, which
generally requires hospitalization and intravenous antistaphylococcal antibiotics. For
uncomplicated cases, oral antibiotics can usually be substituted after several days. The use
of suitable antibiotics, combined with supportive skin care and management of potential
fluid, and electrolyte abnormalities due to the widespread disruption of barrier function, will
usually be sufficient to ensure rapid recovery.
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LECTURE 13 : TRAUMA WHICH POTENTIALLY DISABLING AND LIFE THREATENING
CONDITIONS
I Ketut Suyasa, IGN Wien Aryana
Objectives :
 To implement a general strategy in the approach to the patient with trauma which
potentially disabling and life threatening condition through history, physical
examination and special technique investigation
 To manage by assessing, provide initial management and refer patient with trauma
which potentially disabling and life threatening condition.
 To describe prognosis patient with trauma which potentially disabling and life
threatening condition.
There is trimodal distribution of death due to trauma. Death due to injury occurs in 1
of 3 time periods of peak. The first peak occurs within seconds to minutes of injury. During
this period, deaths generally result from apnea due to severe brain or high spinal cord
injury, or rupture o the hearth, aorta or other large blood vessels. Very few of these patients
can be salvage.
The second peak occurs within minutes to several hours following injury. Deaths
occurring during these period are usually due to subdural and epidural hematomas,
hemopneumothorax, ruptured spleen, laceration of the liver, pelvic fracture and/or other
multiple injuries associated with significant blood loss. The golden hour of care after injury is
characterized by the need for rapid assessment and resuscitation.
The third peak occurs several days to weeks after the initial injury, is most often due
to sepsis and multiple organ system dysfunction. Care provided during each of the
preceding periods impact on patient outcome during this stage.
The first and every subsequent person to care for the injured patient has a direct
effect on long term outcome.
LECTURE 14 : PHLEGMON / LUDGIG’S ANGINA
drg. Putu Lestari Sudirman, M.biomed.
Objective
:
1. To describe etio-pathogenesis and pathophysiology of phlegmon
2. To implement a general strategy in the approach to patients with phlegmon, physical
examination and special technique investigations.
3. To manage by assessing and refer patient phlegmon
4. To describe prognosis patient with phlegmon
Abstract
Phlegmon / Ludwig's angina is a serious infection and cause death if not get a fast and
precise handling. First introduced by Fredrick Wilhelm Von Ludwig (1836).
Etiology:
Generally begins with orofacial infection can be either acute periapical abscess up with
bilateral facial cervical cellulitis. The natural history of odontogenic infection usually begins
with the death of the pulp, bacterial invasion and expansion process toward periapical
infection.
Pathogenesis:
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Ludwig's angina is a bilateral classical infection that can spread rapidly meet submandibulla
space, sublingual and submentale. Causes are often encountered bacteria (Streptococcus
hemoliucus, streptococcus non hemolicus, stapilococcus, pneumococcus, Eescherichia
choli, Actinomyces), odontogenic infection (infection of the periapical tissues M2, M3 lower
jaw, odontogenic cyst and other causes (infection of the gland sub mandible, tonsils,
osteomyelitis)
with
predisposing
conditions
of
poor
oral
hygiene.
Clinical
features:
Intra Oral: Oral Hygiene bad, there odontogenic infection (caries in M1, M2 lower jaw,
pericorinitis M3, impacted M3 mandibular, odontogenic cyst) of the tongue raised, there was
swelling
under
the
tongue
up
to
the
buccal
fold
trismus,
droolin.
Extra oral: temperature rise, swelling hard as a board under the mandible to the front of the
neck.
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LEARNING TASK
Learning Task 1
Highligt in Emergency Medicine
SELF ASSESMENT:
1. Explain briefly about the scope of “Emergency Medicine”
2. Explain the “basic principals of Emergency Medicine”
3. Elaborate briefly about the details in “Triad Emergency Medicine”
4. Male 24-year-old, previously healthy, athletic male who presents with sharp fleeting
chest pain lasting 5 minutes without shortness of breath while jogging earlier today.
In the emergencydepartment, he is without complaints. His ECG shows sinus rhythm
with T-wave inversions V1–V3. Another patient is a 63-year-old man. He smokes
cigarettes and has a history of poorly controlled hypertension.Earlier today, he
experienced 20 minutes of left-sided chest pain with exertion, radiating to his left
shoulder,associated with shortness of breath and diaphoresis. His ECG shows
normal sinus rhythm and is unchangedfrom an earlier ECG. The first patient has a
relatively low pretest probability for cardiac chest pain. His ECG is not normal, but in
a healthy young man, the T-wave inversions are nonspecific at best.
Please describe whats the specific Problem of this patient (Anamnesis,
Physical Examination, ECG finding and what laboratory Examination you
will perform )
5.
Male 71-years-old who slipped in the bathroom, striking his head.The care provided
should entail a rapid evaluation of his airway, breathing, and circulation while,
simultaneously applying cervical spine stabilization, obtaining vital signs, inserting a
peripheral IV line, and performing a focused secondary examination looking to
uncover other potential traumatic injuries or neurologic impairment. A brief medical
history may uncover information that can have a profound effection how this patient
would be initially cared for. GCS = E4V5M6 he is taking warfarin every day.
Please describe the emergency management spesifically according to the
problem of this patients
Is his airway patent
Does his breathing and circulation normal
Does he need an urgent CT scan of the head or cervical spine
Does he need an ECG, cardiac monitoring
6.
a 64-year-old male patient with a history of diabetes and hypercholesterolemia who
presents to the emergency department with chest pain and shortness of breath. He
is in conscious, his face look pale and the acral feel cold and the skin sweaty , BP
180/100, RR18 x /min, HR 100x /min.
Please describe :
Monitoring Management differential diagnosis, diagnostic workup,
therapeutic management
Learning Task 2
SEIZURE AND MENTAL CHANGES DISORDER
1. Please explain the definition, risk factors, and classification of status epilepticus!
2. Please discuss and explain the pathophysiology of status epilepticus!
3. Please explain and elaborate the management of status epilepticus!
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4. Please define the state of refracter status epilepticus, the management and the drug
of choice of the treatment!
5. Please define the non-convulsive status epilepticus and elaborate with the
management and the therapy of choice!
6. As a general practitioner who works in public health centre, you were visited by a 40
years old man, who brought his brother 35 years old with seizure all over his body
and bubbles in his mouth.
a) As a doctor what would you do?
b) After the first aid the seizure has stopped but the patient is still
unconscious. What do you do next?
After a while the patient has seizure again, even before gaining
consciousness.
c) What caused the patient to seizure again?
d) If u were working in the emergency room at the hospital, what would
your action be?
e) When would you suggest a surgical intervention to an epileptic
patient?
Learning Task 3
ACUTE PSYCHIATRIC EPISODES
1. The patient was a 25-year old female graduate student in physical chemistry who
was brought to the emergency room by her roommates, who found her sitting in her
car with the motor running and the garage door closed at 1.00 AM. She was crying,
looked tiredness, and difficulty in falling a sleep.
What is the working diagnosis and differential diagnosis of this patient?
What is the considerable of the patient treatment?
What about the prognosis of this patient after the treatment
LEARNING RESOURCES
1. Kaplan & Saddock’s Synopsis of Psychiatry, 10th ed
Kaplan & Saddock’s Study Guide and Self Examination Review in Psychiatry,
7th ed.
Learning Task 4
ACUTE RESPIRATORY DISTRESS SYNDROME AND FAILURE
A patient was brought to emergency unit by their family with complaint for sudden
breathing difficulties and decrease in consciousness. Five days before the patient suffered
from high temperature until shivering together with purulent cough and breathing difficulties.
During physical examination it was found T. 100/70, N. 120/m, RR. 30 times/m temp.39 oC.
in the lung it was found ronki diffuse, wheezing. On the thorax photo it was found homogen
covering on the two lung areas and consolidation in the center – right side part. During
examination of blood gas analyses it was found PaO2, 45 mmHg while PaCO2 65 mmHg.
SELF ASSESSMENT
1. Discuss about that case assessment
2. Other recommended examination
3. What is the procedure
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4.
5.
6.
7.
How is the pathophysiology of ARDS
Explain etiopathogenesis of ARF
Distinguish between ARF Hypoxemia and Hyperkapnea
Objective of ventilator installation
RESOURCES
Polly E. Parson, MD. Acute Respiratory Distress Syndrome in Michael E. Hanley, Carolyn
H. Welsh, Lange Current Diagnosis & Treatment in Pulmonary Medicine 2003, 161 – 166.
NEONATAL RESUSCITATION
A baby born at 33 weeks gestation following a caesarean section present with respiratory
distress soon after birth with bradypnoea (RR : 18 times/minutes). Heart rate 80
times/minutes regulary. The baby is requiring oxygen, an intravenous line inserted to
provide maintenance fluids. The mother had a temperature of 380 C.
TASK :
1. What is the diagnosis?
2. What investigation should be carried out?
3. What treatment would you institute of this condition?
4. Despite your effort above the baby has a cardio – respiratory arrest with the ECG
monitor, what is the immediate management?
5. what is the prognosis?
SELF ASSESSMENT :
1. To describe definition of perinatal asphyxia
2. To describe pathophysiology and etiology of asphyxia
3. To describe :
 Perinatal management
 Delivery room management
 Postnatal management
4. To describe prognosis of perinatal asphyxia
RADIOLOGY
1. Describe the radiology imaging of thorax which is specific for :
a. IRDS
b. Bronchopneumonia
c. Congenital Heart Disease
d. Lung Edema
e. Pneumothorax
f. Pleural Effusion
g. Vena Cava Superior Syndrome.
SELF ASSESMENT :
1. A mother who have a new born baby complaint that her baby’s lips is blue and
always breathing so fast.
a. What kind of congenital anomalies do you think about this case ?
b. What kind of simple radiology examination that you suggest to do ?
c. What kind of radiology imaging you can find in this case ?
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2. An old man, complaint cough with sputum every morning, suddenly feel shortness
of breath and suffered from ches pain in his right chest, Patient also complaint that
he did’nt got a fever.
a. What do you think about this case ?
b. What kind of radiology examination that you suggest to do ?
c. What kind of radiology imaging you can find in this case ?
Learning Task 5
BLEEDING DISORDERS
CASE 1 :
♂, 66 years old come to hospital with profuse bleeding in both of his nose and can not stop
spontaneusy. He never had nasal blocked symptom and he commonly complained head
ache and fluctuated blood pressure
QUESTION
1. What is the initial disease/disorder of the patient ?
2. How to manage the patient ?
3. What is the complication of the epistaxis and after managed the patient ?
SELF ASSESSMENT
1. Describe and discuss of causes of epistaxis
2. Describe kind of epistaxis
3. Manage and provide initial management and how to refer the patient
REFERENCE
1. Byron Bailey J., M.D, Epistaxis. In : Head and Neck Surgery Otolaryngology
Third Edition, Volume One. Philadelphia, London : LIPPINCOTT WILLIAMS &
WILKINS, Company ; 2001, p. 415-428
2. Eisele D W, MC Quone S.J.,Epistaxis. In : Emergencies of the Head and Neck.
Philadelphia, London : MOSBY. INC copyright 2000, p 239-262.
CASE 2 :
A 25 years old G3 woman presents to the maternity unit with vaginal bleeding. Fetal heart
rate is 140 per minute and her blood pressure is 110/60 and her HR is 85/minute. Fundal
height is 28 cm. she has been given nothing. What are the possible diagnosis?
CASE 3 :
You have just delivered a 37 weeks twins pregnancy pervaginam. The third stage is
complicated by postpartum hemorrhage unresponsive to uterine massage and use of
oxytocin. What would your next management steps be ?
Case Scenario I
A male patient, aged 34 years old comes to the PUSKESMAS with chief complaint of
having cough and flu since 3 days. After examination, the doctor prescribed the
medicine and as usual, the PUSKESMAS nurse gave the injection. After a few seconds,
the patients collapses suddenly, unconscious, looking pale and sweaty, fast and deep
breath, weak and fast pulse.
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Task:
1. Based on immediate observation, what is the patient going through and what
examination actions should be done to obtain the working diagnosis.
2. Describe briefly the immediate act of first aid that should be done to overcome the
emergency and what is the next step/therapy?
3. Based on your analysis what would have caused this emergency and explain its
pathogenesis and pathophysiology.
4. Explain the patient’s prognosis.
Case Scenario II
A male patient, 46 years old was brought to the PUSKESMAS by so many people after
being attacked by a fighter cock on his right leg. Blood splashing out of the back of his
knees was noted and it had been bandaged using normal cloth. At an early exam, the
patient was alert but anxious, complained of pain, looked pale, breathing increased and
his pulse were weak and fast.
Task:
1. Based on immediate observation, what is the patient going through and what
examination actions should be done to obtain the working diagnosis.
2. Describe briefly the immediate act of first aid that should be done to overcome the
emergency and what is the next step/therapy? Should this patient be referred? If
yes, where?
3. Based on your analysis what would have caused this emergency and explain its
pathogenesis and pathophysiology.
4. Explain the patient’s prognosis.
Case Scenario III
A girl aged 21 years was sent to the PUSKESMAS by family after having fever, vomiting
and refuses to drink-eat since 3 days ago. At an initial examination, patient was
conscious but quite anxious, complained of pain, looked pale, body felt hot, breath fast
and deep, pulse weak and fast, and stomach looked stretched. Extra informations were
that the patient was not married, delayed menses and have gotten treatment from
“dukun beranak”
Task:
1. Based on immediate observation, what is the patient going through and what
examination actions should be done to obtain the working diagnosis.
2. Describe briefly the immediate act of first aid that should be done to overcome the
emergency and what is the next step/therapy? Should this patient be referred? If
yes, where?
3. Based on your analysis what would have caused this emergency and explain its
pathogenesis and pathophysiology.
4. Explain the complication and prognosis of this patient.
SELF ASSESSMENT
1. Explain the etiopathogenesis and pathophysiology of shock
2. Explain the diagnosis step of hypovolemic, cardiogenic, distributive and obstructive.
3. Elaborate briefly about the first aid to shock patient and what should the next
action/treatment be? Should this patient be referred? If yes where to?
4. Explain the complication and prognosis of shock
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RESOURCES
1.
2.
3.
Diagnosis and Management Of Shock, in Critical Care Support Fundamental Book,
1996, p.69-80
Approach to Shock, in The Hand Book of Critical Care, 2001, p55-70.
Pathophysiology and Classification of Shock State, in Textbook of Critical Care, 9 th
Edition, 2005, p.887-910.
Case Scenario I
One Sunday morning, you are enjoying the fine morning at the Sanur Beach. At a
distance, you could see people looking panicked, is screaming for help. There was
young couple being dragged by a wave while they were bathing. The lady managed to
safe herself, where else the man at the beginning who are trying to safe his friend, was
dragged into the water. Then the life guard managed to safe the man and immediately
gave him first aid. You as a medical personnel, coincidently being there, should also
give first aid.
Task:
1. Based on immediate observation, what is the patient going through and what
examination actions should be done to obtain the working diagnosis.
2. Describe briefly the immediate act of first aid that should be done to overcome the
emergency and what is the next step/therapy?
3. Based on your analysis what would have caused this emergency and explain its
pathogenesis and pathophysiology.
4. Explain the complication and prognosis of this patient.
Case Scenario II
Once you were riding your personal car on the road. At one of the junctions you find a
stopping suddenly in the middle of the road, the driver was a male, age around 60 years
old, looked quiet, not moving and his right hand on his left chest. You as a medical
personnel, coincidently being there, should also give first aid.
Task:
1. Based on immediate observation, what is the patient going through and what
examination actions should be done to obtain the working diagnosis.
2. Describe briefly the immediate act of first aid that should be done to overcome the
emergency and what is the next step/therapy?
3. Based on your analysis what would have caused this emergency and explain its
pathogenesis and pathophysiology.
4. Explain the prognosis of this patient.
SELF ASSESSMENT
1. Explain the etiopathogenesis and pathophysiology of cardiac arrest
2. Explain the diagnostic steps of cardiac arrest
3. Elaborate briefly the first aid on cardiac arrest patient at the incident place, during
transportation and after reaching the emergency ward. Since the heart beat is stable,
where should the patient be referred?
4. Explain the complication and prognosis of cardiac arrest.
RESOURCES
1. Cardiopulmonary Resuscitation, in Critical Care Support Fundamental Book,
Chapter 2, 1996, p.15-25
2. Buku Panduan Resusitasi Jantung Paru-Otak, Bantuan Hidup Lanjut, Diterbitkan
oleh DEPKES RI 2000
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3. Resuscitation, in Perioperative Care Book, Anesthesia, Pain Management and
Intensive Care, 2003.
PPH (Post Partum Haemorrhagica)
1. Female patient referred by midwife, with decrease of consciousness after delivery 2
hours ago. She has lost more than 1,5 lt of blood, even after active management of
third of labor. She came to midwife complaining labor pain, vaginal examination
revealed 3 cm of cervical dilatation. After 1,5 hours, she delivered the baby, without
any abnormality. Placenta was completely born, not found any birth canal laceration.
This is her fifth pregnancy, all children are still alive and the youngest is 1 year old.
 What is the most possible diagnosis for this patient? Explain!
 What is the cause of abnormality in this patient?
 What action should be done in this case?
2. Female patient delivered a baby in your clinic 2,5 hours ago, and is still experiencing
vaginal bleeding which is not decreasing after uterotonics administration. History of
delivery was fine, active phase was 4 hours, second stage was 30 minutes, and
placenta was born complete after 10 minutes. 2 hours post partum evaluation shows
fundal height is 2 fingers below umbilicus, uterine contraction (+) good. Vaginal
evaluation reveals no laceration on birth canal.
 Which examination should be done to diagnose this patient?
 Explain treatment management in this patient!
3. If you are a doctor on duty at local Public Health Center, and is facing a case of
uterine atonia, while the nearest referal facility is located 1 hour from your place,
what is your action? Explain!
4. Explain prevention strategies you could apply to avoid 4 most common cause of
primary post partum hemorrhage!
APB (Antepartum Bleeding)
1. Female patient, 40 yo, come to your clinic complaining vaginal bleeding since 1 hour
ago. The blood is fresh colored, and flowing out continously, without abdominal pain.
Patient tell tou that she is 6 months pregnant, but has never visited healthcare
provider. She tested herself for pregnancy with self-urine test twice at home, after
knowing that she had missed her period for a month, and the result was positive.
Patient has delivered 4 times, the youngest was born by C-section in hospital, due to
arrest of labor. She has never had the same complain before. History of previous
medical problem is denied. Petient’s general condition is good, vital signs and
general phisical condition is within normal limit.
 What has possibly happened to this patient?
 According to your analysis, what are the risk factors in this patient? Explain!
 What is the pathogenesis of this patient’s condition?
2. After obstetric examinations are done, found fundal height is ½ umbilikus- prosesus
xifoideus, his (-), FHB 90x/mnt, left sided back, head presentation. Vaginal
examination shows fresh colored blood flowing out of vagina, and vaginal toucher
reveals 1 finger cervical dilatation, head palpated, unclear denominator, cushion
palpated. Bleeding hasn’t stopped and tends to increase; Cito c-section then carried
out.
 In your opinion, are the above treatment correct?
 If not, explain the appropriate actions!
 What are the differential diagnosis for this patient’s condition?
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 What are the complication that possibly happen?
3. A man come to you, carrying his unconscious wife to ER. He told that his wife
complained sudden abdominal pain after falling on the bathroom floor this morning.
The pain was severe and very sudden. No other complain. Patient is 8 months
pregnant, and has routinely visit obstetrician for her pregnancy. This is her first
pregnancy, and never had miscarriage before.
 What is the most possible diagnosis of this patient?
 If obstetric examinations and diagnostic work-ups are done, what are the
expected results to support that diagnosis?
 How is the treatment management fot this patient?
4. Explain the differences between placenta previa, solusio placnta, and vasa previa!
ACUTE UPPER AIRWAY OBSTRUCTION
LEARNING TASK :
Case 2.
Male, 9 month years old complained by his parent with dyspneu, stidor and cough,
immediately after choking peanut without history of upper respiratory infection.
QUESTION
1. What you should ask to complete the anamnesis?
2. What will you find from the physical examination?
3. What kind of other examination to support the diagnosis?
4. What possibility diagnosis of this patient?
5. How to manage and provide initial management and when do tou refer the patient?
SELF ASSESSMENT
1. Describe and discuss of specific symptoms of upper airway obstruction
2. Describe etiology and pathophysiology of each symptoms of upper airway
obstruction
3. Manage and provide initial management or refer patient with upper airway
obstruction
REFERENCE
1. Boies LR, Laryngeal Obstruction. In : Fundamentals of Ofolaryngology Third Edition.
Philadelphia, London : W. B. Saunders, Company ; 1984, p. 396 – 406
2. Adams GL, Boies LR, Hilger PA, Foreign Body Aspiration In : Fundamental of
Ofolaryngology Sixth Edition. Philadephia, London : W.B. Saunders, Company ;
1989, p. 483 – 489.
3. Eisele D. W, MC Quone S.J. in : Emergencies of the Head and Neck. Philadelphia,
Lomdon : MOSBY. INC copyright 2000, p. 111 – 163
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Learning Task 6
SHOCK
1. A 55-year-old man with a long standing history of coronary artery disease is admitted to
ER with a 24-hours episode of intermitten chest pain. On physical examination his
temperature is 38,2ºC, heart rate 140 beats/minute, blood pressure 75/45 mmHg, and
respiration rate 35 breaths/minute. Auscultation of the lung reveals bilateral rales. The
cardiac examination reveals regular rhythm, a normal S1 and accentuated S2, and a new
S3 gallop. The legs are noted to have bilateral pitting edema and palpations reveals cool
extremities and weak pulses.
a. What laboratory examination are you doing for that patient? And also what other
examination for that patient?
b. What working diagnose possible for that patient?
c. What are you doing for the first time to the patient?
2. A 59-year-old woman with a history of type 2 diabetes mellitus was found unconscious at
home by her family members. In the ER, she was noted to have temperature of 38,8ºC,
pulse rate of112 beats/minute, blood pressure of 96/50 mmHg, and respiratory rate of 26
breath/minute. Laboratory values reveal WBC 26.000/mm3, hemoglobin 12 g/dL, normal
platelet count and showed return of concentrated and cloudy urine. The urinalysis
revealed 50 WBC per high power field. A ct scan of the abdomen without contras
revealed no free fluid in the abdomen and an inflamed right kidney.
a. What is the most likely diagnosis?
b. What are the priorities in this patient’s management?
c. How would you monitor and support this patient’s status?
3. A 23-year-man with no known medical history is brought to the ER with gun shot to the
abdomen. The patient is restless and combative, though he has no sign of rerpiratory
distress. His blood pressure 89/37 mmHg, heart rate 112 beats/minute, respiratory rate
26 breaths/minute and his SpO2 is 100% on 10 L by face mask.
a. What laboratory examination are you doing for that patient? And also what other
examination for that patient?
b. What working diagnose possible for that patient?
c. What are you doing for the first time to the patient?
4. A man, 40-years-old, admitted to emergency room after he get traffic accident. He
complain pain at left chest, difficult breathing. There are haematoma at his chest. At
inspection exam, movement of his left chest keep remaining and on auscultation exam,
breathing sound become weak. He become restless an combative. Blood pressure is
70/34 mmHg, pulse rate is 140 beats/ minute, respiratory rate is 36x/minute, and perifer
oxygen saturation 85% with face mask 15 liter/minute. Suspicious fracture of rib bone.
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a. What working diagnose possible for that patient?
b. What are you doing for the first time to the patient?
c. What laboratory examination are you doing for that patient? And also what other
examination for that patient?
d. What definitive action for that patient ? what are you prepare for that action?
Learning Task 7
CARDIAC ARREST AND CARDIOPULMONAR RESCUSTATION
Case Scenario 1
As on duty doctor at hospital, you are received emergency call from 2nd floor hospital.
The nurse said that there is a 70 yo male patient, diagnose as stable angina, suddenly
suffered SOB after eating, getting worse shortly, but still concious. After 10 minute, the
patient became unconcious.
5. Describe briefly the immediate act of first aid that should be done to
overcome the emergency and what is the next step/therapy?
2. What happen to her?
3. Can we prevent this patient became unconcious?
Case Scenario 2
A 30 year old woman attends your clinic with asthma attack. She has a long history of
asthma, with severe attacks requiring hospitalisation. Despite continuous nebulised
salbutamol, she rapidly gets worse over about ten minutes with severe respiratory
distress, she is unable to talk and is becoming increasingly confused and unconcious.
From the monitor you already attach, the ECG shown takikardi and became bradikardia
and continue to asystole.
1. Based on immediate observation, what is the patient going through and what
actions should be done ?
2. Based on your analysis what would have caused this emergency and explain
its pathogenesis and pathophysiology.
3. Can you prevent this patient from asystole? Explain it.
4. Explain the management of asystole.
Case Scenario 3
85 year old man is delivered by car to your clinic. He was found collapsed 10 minute ago
by his family in the garden. At Physical examination, no pulse at a.jugularis, no heart
sound. A monitor is attached and the rhytm is VF.
1. What are you going to do?
2. How long we need to do CPR at this patient?
3. Explain the algorithm of Shockable cardiac arrest
Case Scenario 4
As doctor on duty at emergency room, you received a 50 years old man with history of
chest pain and suddenly unconscious in front of you. After doing fast examination, you
diagnose the patient as cardiac arrest with VT pulseless
1. Explain about the resuscitation team to perform good CPR on this patient.
2. How would you build a good resuscitation team?
3. Explain how would you doing defibrillation on this patient.
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SELF ASSESSMENT
5. Explain the etiopathogenesis and pathophysiology of cardiac arrest
6. Explain the Guideline of BLS and ALS
7. Explain about “shockable” and “non shockable” cardiac arrest.
8. Explain the complication and prognosis of cardiac arrest.
LEARNING RESOURCES
4. Adult Cardiopulmonary resuscitation, in Oh’s Intensive Care Manual, 5th edition,
2003.
5. Cardiopulmonary Resuscitation, in Critical Care Support Fundamental Book,
Chapter 2, 1996, p.15-25
6. Buku Panduan Resusitasi Jantung Paru-Otak, Bantuan Hidup Lanjut, Diterbitkan
oleh DEPKES RI 2000.
7. Resuscitation, in Perioperative Care Book, Anesthesia, Pain Management and
Intensive Care, 2003.
Learning Task 8
EMERGENCY TOXICOLOGY AND POISONING
BASIC MANAGEMENT OF INTOXICATION
LEARNING TASK
1. Able to known intoxication cases by Toxic Syndrome
2. Able to to manage intoxication cases by ABCDE Prosedure
3. Able to treatment the patient by antidote
CASE 1 :
The patient is Mr. Agus , 28-year old hospitalized, refered from his family because of
decreas of consiousness, 6 hours previously look like healthy and done his job as a
salesmen. There are no history of Diabetes , Hypertension, Liver and Kidney Disease.
Some time He drink alcohol and as a smoker. The patient shown pale, sweaty, blood
pressure 90/60 mmHg, Respiratory rate 10 time/mnt with alcohol like smell, pulse rate is
weak about 50 time/mnt, and pupil miosis. In the forearm shown nedle steak injury.The
patient than refered to High care Unit for ventilator machine procedure.
ASSIGNMENT :
1. If you are a Doctor, do you think this case is Intoxication or organic Disease with
severe manifestation ?
2. What the sign of toxic syndrome in this cases.
3. If this patient do you diagnosis as intoxication , what the basic procedure should be
done.
4. When should be treatment the patient whit antidote ?
SELF ASSESSMENT :
1. Describe sign of toxic syndrome
2. Describe basic management of intoxication
3. The kind of antidote, indication and point of moment to giving antidote
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ORGANOPHOSPHAT INTOXICATION
LEARNING TASK
1. Able to diagnosis organophosphate intoxication by toxic syndrome.
2. Able to manage organophosphate intoxication by basic prosedure treatment of
intoxication (Decontamination and Elemination)
3. Able to use specific antidote atropin and monitoring of side effect.
CASE 2 :
The patient was Miss. Lina, whit progressive vomiting after drink one cup of liquid (in after
that is known as organophosforus) unintensionaly, 2 hours after hospitalized. The patient
shown weak and the breathing was Baygon in smell. Pupil miosis, blood pressure 100/70
mmHg, pulse rate 60 time/ mnt, respiratory rate 18 time / mnt, in auscultation shown rale in
all of chest field and defication. The patient there are no history of health disease,
neurologic disease, Diabetes mellitus and Pulmonary disease.
ASSIGNMENT :
1. If you are a docter, what do you do for helping this patient.
2. Do you insert NG tube, but you were knowed that organophosphate diluted by
hydrocarbon
3. Do you washing all of bodies exposure ?
4. What is the technic to used atropin as a antidote, and how to known atropinisation
5. When the patient should be refered to the ward.
SELF ASSESSEMENT :
1. Describe sign of organophosphate intoxication
2. Basic treatment of organophosphate intoxication
3. Describe of severety of organophosphate intoxication
4. Describe technic to used atropin as antidote, an monitoring
CAUSTIC INTOXICATION
LEARNING TASK
1. Able to differentiate clinical manifestation of alkali or acid injury
2. Able to manage alkali and acid injury, by basic intoxication procedure
3. Able to monitor and early detection of serious complication and urgent consultation.
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CASES 3 :
The patient was Miss. Ayu, 25 year-old, hospitalized because of bloody vomiting and chest
pain, the patient refered by her boy frend to emergency room Sanglah Hospital, after
ingestion of liquid for washing the metal, she was needed fo suicide, previously she same
problem with her friend, she come with multiple erotion in her mouth, tongue, pharyng and
bowel meteorism with rebound of pain. Rectal examination shown melena (blacky stool).
Urgent endoscopic shown multiple erotion in area upper spincter of esophagus and in area
antrum of stomach grade II B, blood pressure 90/mm Hg, Respiration rate 26 time/ mnt,
body temprature 37.8 C, Hb 7 mg/dl, WBC 12.000, rale/ ronchy in left chest, Chest X-ray
shown infiltrate in lower lobe of the left lung.
ASSIGNMENT :
1. If you are a doctor, what are you doing for help this patient
2. Do you insert NG tube for decontamination prosedure ?
3. Do you give the patient with active charcoal ?
4. When should consultation for endoscopic examination ?
5. Do you treat the patient with corticosteroid and antibiotic ?
6. What your planing to care this patient for prevent serious complication ?
SELF ASSESSEMENT :
1. Describe sign and symptom alkali and acid intoxication
2. Describe spesific management of caustic injury
3. Describe basic care and prosedure follow up the patient with caustic intoxication.
REFERENCES :
1. Tamaszewski CA., Caustic , In: Emergency Medicine,Second ed, Mc Graw Hill,
2004, 392
2. Tamazszewski CA., Insecticides, Herbicides,and Rodenticides, In: Emergency
Medicine,Second ed, Mc Graw Hill, 2004, 394
3. Phillips SD., Organoclorin, Pyrethrin, and Pyrethroid Insecticides, In : Critical Care
Toxicology, Diagnosis and Managemnent of the critically Poisoned Patient, Ed:
Brent, Wallace et al, Elsevier Mosby, 2005, 929
4. Rella JG and Hoffman RS.,Caustic, In : Critical Care Toxicology, Diagnosis and
Managemnent of the critically Poisoned Patient, Ed: Brent, Wallace et al, Elsevier
Mosby, 2005, 1035
5. Gregus Z and Klaassen CD., Mechanism of Toxicology, In : Essentias of Toxicology,
Ed: Klaassen, Watkins, Mc GrawHill, 2003,
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Learning Task 9
HYPERTENSION IN PREGNANCY
1. A Woman 38 y.o aged, and she is in third pregnancy with twice obstetric history
were term pregnancy, spontaneous delivery and also both child still alive today.
There was no past medical history. Estimated due date in next 15 days. She was
complained headache and epigastric pain. Fetal movement was good and no labor
pain. Physical examination found composmentis consciousness, BP 170/110 mmHg,
pulse 90 x/minute, respiration rate 24 x/minute. General examination: there were no
cardiac and pulmonary abnormality. Obstetric examination: head presentation, FHB
11.11.12 and no uterine contraction.
a. As a doctor on duty, what is additional examination to confirm diagnosis and what
next management will perform firstly?
b. What is suitable diagnosis for above case?
c. What is possible complication to this patient?
2. A woman 31 y.o aged, and she is in second pregnancy, with history of preterm
pregnancy (her first child delivered by cesarean section cause by impending
eclamptic status), body weight 88 kg, height 147 cm, 26 weeks of pregnancy. Visited
outpatient clinic with history of high blood pressure (BP 150/90 mmHg). History of
hypertension, known since 21 y.o and took irregular antihypertensive drug.
a. What are additional physical examination and laboratory testing will perform to
confirm the diagnosis?
b. What is suitable diagnosis for above case?
c. Appropriate management for this case is?
d. Possible complication for the mother and fetus are?
3. A woman 40 y.o aged, and she is in forth pregnancy (gravid 4, para 3), 36-37 weeks
of pregnancy, admitted to the emergency department by her family with history of
seizure (3 times) and then unconscious after the seizure. Brief examination: patient
unconscious, BP 190/110 mmHg.
a.
As emergency Doctor on duty, appropriate initial management for this patient is?
b.
What is additional history taking and physical examination will perform to build
diagnosis?
c.
What is the diagnosis for above case?
d.
Correct management for this case is?
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4. A woman 18 y.o aged and she’s in first pregnancy (gravid 1, para 0). Body weight
was 85 kg, height 146 cm, 32 weeks and 3 days of pregnancy, referred by midwife to
the your hospital due to severe headache and blurry vision, and also vomited since
this morning. Patient in conscious state, BP 180/100 mmHg.
a.
What is additional history taking and physical examination will perform to build
diagnosis?
b.
What is the diagnosis for above case?
c.
What is risk factor for this case?
d.
How about the appropriate management for this case?
Learning Task 10
SHOULDER DYSTOCIA
CASE :
In the labor ward, you as a intern help a pregnant woman in second stage of labor.
Following and easy application, after two time maternal pushing, there is moderately good
descent during the first pull but this slows down as the head is half out. What are potential
causes for this and what is your plan of action at this point?. If shoulder dystocia is
confirmed, what is your management?
Learning Task 11
Dermato – emergencies
Case 1
A 25 years old male come to emergency unit sanglah hospital with blistering skin rash. He
had fever, cough and malaise 5 days before and get medication such us amoxicillin,
parasetamol, and mucopect tablets from general practitioner. Two days later, he developed
erythematous lesions over his extremities, face and trunk. Patient with weak condition, BP
120/80 mmHg, temp 40°C, RR 20x/menit. From eye examination there is redness on
conjungtiva, from mouth and genetalia examination we find multiple erosion with
hemmoragic crust. From his extremities, face and trunk we find multiple purpuric lesion and
some part of rash with bullous and erotion that involve 45% BSA
LEARNING TASK
1. According this case, what is the most likely diagnosis?
2. What other information do you need to support the diagnosis?
3. What other examination you should do to this patient?
4. What monitoring should you do to this patient?
5. How do you manage this patient?
6. What is the complication of this condition?
SELF ASSESSMENT
1. Describe the principle clinical features of SJS, TEN
2. Describe the pathogenesis of SJS, TEN
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3. Explain more detail the basic principle of management of SJS, TEN
4. Describe the prognosis and complication of SJS, TEN.
Case 2
A 8 months baby come to dermatology polyclinic sanglah hospital with skin rash all over the
body. She had fever, cough and rhinitis 6 days before. Two days later, she developed
erythematous rash around the nose and the rash widespread all over her body with the skin
peel easyly. Patient with weak condition, temp 38.5°C, RR 28x/menit. Skin effloresence
from face, trunk, back, and extremities, we find erythematous macule, some part of the
lesion with multiple vesicle and desquamation skin.
LEARNING TASK
1. According this case, what is the most likely diagnosis?
2. What other information do you need to support the diagnosis?
3. What other examination you should do to this patient?
4. What monitoring should you do to this patient?
5. How do you manage this patient?
6. What is the complication of this condition?
SELF ASSESSMENT
1. Describe the principle clinical features of SSSS.
2. Describe the pathogenesis of SSSS
3. Explain more detail the basic principle of management of SSSS
4. Describe the prognosis and complication of SSSS
Learning Task 12
TRAUMA WHICH POTENTIALLY DISABLING AND LIFE THREATENING CONDITIONS
Case1
Male, 55 years old, came to our hospital after traffic accident, with difficulty to take breath,
on primary survey air way was clear, bruising on the right hemithorax, and asymmetrically
thoracic cage movement, breathing sound disappear on the right side and dullness on
percussion.
BP ; 90/60 mmHg, RR : 32 x/Minute, Pulse Rate : 120 x/ minute
1. What is your initial assessment ?
2. How to manage this patient ?
Case 2
Male 60 years old, came to ER after felt down from coconut tree about 8 meter height, he
feel weakness on the both hand and leg. On physical examination BP : 100/60 mmHg, PR :
90 x/mt, RR: 30 x/mt ( thoracoabdominal type)
1. What is your initial assessment ?
2. How to manage this patient ?
Case 3
Female, 20 years old, she was riding motor bike, and felt down by herself. Bruising on the
abdominal right upper quadrant, BP 80/60 mmHg. PR : 120 x/minute: RR 24x/minute. No
deformity on upper and lower extremity
1. What is your initial assessment?
2. Can you describe the probability organ damage in this case ?
3. How to manage this patient?
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Case 4
Male, 21 years old, unconcious patient after traffic accident, he came to our ER, with cepal
hematoma on the right temporoparietal region and pupil anisocor with hemiparesis, GCS
E2V3M5
BP : 120/90 mmHg, PR : 90x/mt, RR : 24 x/ mt
1. What is your initial conclusion ?
2. How to manage this patient ?
Case 5.
Female, 27 years old came to ER with right lower leg painful after traffic accident. On
physical examination : Right lower deformity (+), swollen ad tense, pulsation a. dorsalis
pedis decrease and stretch pain (+)
1. What is your conclusion ?
2. According to anatomy, describe the pathologic region can be happen!
3. How to treat the patient?
Learning Task 13
PHLEGMON / LUDWIG’S ANGINA
1. Patient male, aged 35 years old cames to the UGD RSPTN Bukit Jimbaran, with
complaints of pain in the lower chin, up to the front of the neck feel hard when
touched, fever, difficulty swallowing and difficulty breathing, the patient appears
weak. Intra-oral examination is difficult because patients with difficulty opening the
mouth, tongue looks lifted and swelling of the gums behind that cover most of the
right mandibular M3. Pain in the gums behind the perceived than 5 days ago, the
patient just gargling with warm salt water when not withstand the pain.
a.
What
you
should
ask
to
complete
the
anamnesis?
b. What examinations will you do for this case?
c. What is the diagnosis?
d.
What
does
your
planning
for
management
in
this
case?
e. . Describe the prognosis in this case?
2. Patient male, 27 years old come to RSPTN with dread because of the pain that is felt
in mandibulla left with swelling to the left cheek, intra oral condition appears to exist
in the dental caries with mobillity o2 M2 and M3 residual roots on the left, buccal fold
appears elevated, palpation there is fluctuation exudate. Dental pain is felt starting
from 3 days ago but have not had time to check to the dentist, just buy painkillers to
reduce
the
pain.
a
What
you
should
ask
to
complete
the
anamnesis?
b. What is the diagnosis?
c. What does your planning for management in this case?
3.
Patient woman, 38 years old, came to the Polyclinic RSPTN Bukit Jimbaran with
complaints mandibulla swollen and hard when touched on the lower jaw side since a
few months ago, seemed teeth no complaints. There is no pain and illness but the
patient had never examined the situation to the doctor or dentist.
a
What
you
should
ask
to
complete
the
anamnesis?
b. What is the diagnosis?
c.
What
does
your
planning
for
management
in
this
case?
Self
Departement Medical Education Faculty of Medicine Udayana University
Assassment:
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Study Guide Emergency Medicine September 2015
1. Explain the difference between mandibulla with phlegmon abscess?
2. In addition to any abscess mandibulla differential diagnosis of phlegmon?
3. Discuss with your group the most important management of phlegmon?
Learning Task 14
UROLOGYC EMERGENCY
Case 1 An Old man that unable to void
A 73 years – old man with multiple medical problems presented with complaints that he
could not void and had pain in the lower abdomen. He had a mild dementia, so much of the
history was from his wife, who accompanied him to the clinic. She stated that he had neither
incontinence, fever, nauses, nor vomiting, and he had any recent acute illnesses. The
patient had not had any recent change in medication, doses or frequency of dosing of his
pain medication. He had similar problems in the past, but the symptoms had resolved after
he underwent a transurethral resection of the prostate (TURP) 2 years ago. His wife also
stated that he had been able to void normally up until earlier this morning. Since that time
he had complained frequently about the urge to void and being to do so.
The patient’s medical history was extensive. Of particular note, he had metastatic
squasmous – cell lung cancer and was placed in hospice care 2 weeks before presentation.
He had type 2 diabetes, hypertension, glaucoma, and benign prostatic hypertrophy (BPH)
His medication included an extended – release morphine tablet for pain, rosiglitazone for his
diabetes, and recently discontinued ramipril and hydrochlorothiazide, which he had taken in
the past for his hypertension.
On examination, he was midly tender over the bladder, which was palpably distended. He
attempted to void for a urinalysis specimen and was unable to do so. A Foley catheter was
placed, and 240 ml of urine was collected. The urinalysis showed a trace of protein, and
results were otherwise negative; the pH was 7,3.
Question :
1. What are some cuases of acute urinary retention?
2. What are some typical symptoms of acute urinary tract obstruction?
3. What tests would be helpful in determining the cause of this patient’s urinary
retention?
4. What treatments would be useful in relieving the symptoms?
5. What are some complications of untreated acute urinary retention?
NB:
THERE WILL BE SOME LEARNING TASK WILL BE GIVEN BY THE LECTURERS AND
TEAM IF IT'S NECESSASY PLEASE BE CONFIRM THE LECTURERS AND TEAM.
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~ CURRICULUM MAP ~
Smstr
Program or curriculum blocks
10
Senior Clerkship
9
Senior Clerkship
8
Senior clerksh
ip
7
Medical
Emergency
(3 weeks)
Special Topic:
-Travel medicine
(2 weeks)
Elective Study III
(6 weeks)
Clinic Orientation
(Clerkship)
(6 weeks)
6
BCS (1 weeks)
The Respiratory
System and
Disorders
(4 weeks)
The
Cardiovascular
System and
Disorders
(4 weeks)
The Urinary
System and
Disorders
(3 weeks)
The Reproductive
System and
Disorders
(3 weeks)
BCS (1 weeks)
Alimentary
& hepatobiliary systems
& disorders
(4 Weeks)
BCS (1 weeks)
The Endocrine
System,
Metabolism and
Disorders
(4 weeks)
BCS (1 weeks)
Clinical Nutrition
and Disorders
(2 weeks)
BCS (1 weeks)
BCS (1 weeks)
Musculoskeletal
system &
connective
tissue disorders
(4 weeks)
Neuroscience
and
neurological
disorders
(4 weeks)
Behavior Change
and disorders
(4 weeks)
BCS (1 weeks)
Hematologic
system & disorders & clinical
oncology
(4 weeks)
BCS (1 weeks)
Immune
system &
disorders
(2 weeks)
BCS(1 weeks)
Infection
& infectious
diseases
(5 weeks)
BCS
(1 weeks)
The skin & hearing
system
& disorders
(3 weeks)
BCS (1 weeks)
Medical
Professionalism
(2 weeks)
BCS(1 weeks)
Evidence-based
Medical Practice
(2 weeks)
BCS (1 weeks)
Health Systembased Practice
(3 weeks)
BCS(1 weeks)
Community-based
practice
(4 weeks)
-
Medical
communication
(3 weeks)
BCS (1 weeks)
The cell
as biochemical machinery
(3 weeks)
Growth
&
development
(4 weeks)
BCS (1 weeks)
BCS(1 weeks)
BCS: (1 weeks)
BCS (1 weeks)
Elective Study
II
(1 weeks)
5
4
3
2
1
BCS (1 weeks)
Studium
Generale and
Humaniora
(3 weeks)
BCS (1 weeks)
Special Topic :
- Palliative
medicine
-Compleme
ntary &
Alternative
Medicine
- Forensic
(3 weeks)
Elective
Study II
(1 weeks)
Special Topic
- Ergonomi
- Geriatri
(2 weeks)
Elective
Study I
(2 weeks)
The Visual
system &
disorders
(2 weeks)
Pendidikan Pancasila & Kewarganegaraan (3 weeks)
Departement Medical Education Faculty of Medicine Udayana University
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Study Guide Emergency Medicine September 2015
Departement Medical Education Faculty of Medicine Udayana University
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