University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
UNIVERSITY OF SANTO TOMAS
FACULTY OF MEDICINE AND SURGERY
DEPARTMENT OF MEDICINE
PULMONARY and CRITICAL CARE
MEDICINE 2
AY 2023-2024
SECTION OF PULMONARY AND CRITICAL CARE MEDICINE
TABLE OF CONTENTS
General Description
2
Case Discussions
5
SGD 1: Asthma and COPD
SGD 2: CAP and Pleural Effusion
SGD 3: Lung Cancer and VTE
Ward Work
9
Interview check list
10
Physical Examination of the Respiratory System
11
Lectures
Basic Chest Imaging
13
ABG
16
Spirometry
17
Community Acquired Pneumonia (CAP)
20
COPD
27
Bronchiectasis
39
Tuberculosis
40
Sleep Disorders
47
Lung Cancer
49
Venous Thromboembolism
52
Emergency
Acute Respiratory Failure / ARDS
58
Hemoptysis
59
Massive Pulmonary Embolism
61
WS 1 Clinico Radiologic Correlation
62
WS 2 ABG / Clinico Radiologic Correlation
65
WS 3 Spirometry / Inhaler Gadget / Peakflow
74
WS 4 Ultrasound
80
Workshops
Team-Based Learning for Third Year Medical Students
TBL 1 Asthma
82
TBL 2 Dyspnea (Cardio-Pulmo Integration)
83
Additional Notes:
1
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
Bronchial Asthma
84
Pulmonary Arterial Hypertension (PAH) / Pulmonary Hypertension (PH)
96
UNIVERSITY OF SANTO TOMAS
FACULTY OF MEDICINE AND SURGERY
DEPARTMENT OF MEDICINE
PULMONARY and CRITICAL CARE MEDICINE
AY 2023-2024
GENERAL DESCRIPTION
• Pulmonary Medicine: Tuesday and Thursday
• 7:00 am to 12:00 nn
CHAIRMAN, Department of Medicine:
Melvin Marcial, MD, MHPEd
CHIEF OF SECTION of Pulmonary Medicine: Julie Christie G. Visperas, MD, MHPEd
PULMONARY MEDICINE LEADER:
Julie Christie G. Visperas, MD, MHPEd
PULMONARY AND CRITICAL CARE MEDICINE
ENTRY COMPETENCIES:
• Basic Anatomy and Physiology of the Respiratory System
PULMONARY AND CRITICAL CARE MEDICINE
ENTRY COMPETENCIES:
• Basic Anatomy and Physiology of the Respiratory System
TERMINAL COMPETENCIES:
At the end of the module, the third year students should be able to:
• review the pathophysiologic aspects of the Respiratory system as found in disease states
• correlate the patient manifestations with the pathophysiology involved in Respiratory diseases
• arrive at a logical diagnosis based on signs and symptoms
• formulate a logical, rational, and cost effective medical plan for patients, to include both diagnostic
and therapeutic aspects
• apply ethical principles in the approach to the diagnosis and management of patients with
Respiratory diseases
LEARNING ACTIVITIES:
LECTURES
• teacher / specialist oriented activity
• most common diseases of the Respiratory system will be presented to the students, with focus on
clinical application of basic concepts, as well as updates on diagnosis and treatment
• an interactive/ student oriented approach will be utilized as much as possible to enhance learning
CLINICAL CASE CONFERENCE
This is the venue for presenting cases admitted in the UST Hospital, which will illustrate any or all of the
following:
- interesting / rare cases in Respiratory Medicine, as this may be the only opportunity for the students
to be exposed to such problems
- cases with complicated/ multidisciplinary courses- so that the students may be made aware of the
complex interactions among the various organ systems and specialties
- classical textbook cases so that the students may appreciate further the clinical applications of what
they may have been given as didactics
2
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
-
Revised August 2023
diagnostic dilemmas, so that the students may observe how the various consultants dissect the
patient’s problems in order to come up with a logical diagnosis.
Ethical issues which may be encountered.
Question and answer formats and Interactive key pads/polls will be used to encourage the medical students
to participate in the discussion.
CASE DISCUSSIONS
1. student lead and facilitator guided
2. cases are prepared before-hand
3. students will:
3.1. formulate learning objectives relevant to the case
3.2. present a concept map ( this will be their guide for the management of the patient)
3.3. submit simple and processed problem list
WARD WORK
- self directed and tutor-guided activity
- provides an opportunity for the students to handle actual patients in the ward - to get a complete
medical history and physical examination, identify the pertinent problems of the patient, arrive at a
logical diagnosis, and plan a management scheme
- the students may also be asked to accompany their patients to certain procedures as this will
enhance their learning experience
- one written history with case discussion will be submitted per module
WORKSHOP
- student - oriented, facilitator guided
- provides an opportunity for the students to have hands-on training in/ with
skills/procedures/algorithms used in the respiratory system
the various
EXAMINATIONS
- short quizzes will be given per week, based on the reading assignments as well as the previous
workshops/ Clinical Case Discussion
- module examinations will be given at the end of each shift
STUDENT EVALUATION
MODULE/Shifting Grade =
98% (70% from the Class Standing + 30% from the Shifting Examination)
2% (Attendance Grade)
Class Standing = 70%
25% from Cluster Exams/Quizzes (12.5% Cardio; 12.5% Pulmo)
45% Module Specific Gradable Activities
Cardio-Pulmo Module Gradable Activity:
Interactive Case Discussion/SGD (5 Cardio + 3 Pulmo)= 15% Cardio; 15% Pulmo
History (Patient Write Up: 1 Cardio and 1 Pulmo) = 15% CARDIO; 15% PULMO
Ward/ Simulated Patient Encounter = 10%
TBL in Pulmo
iRAT = 5%
tRAT/tAPP = 10%
Attitude = 10%
Peer Evaluation = 5%
REFERENCES:
Harrison’s Principles of Internal Medicine 21st Edition
Pleural Diseases 6th edition by Richard Light
Global Strategy for the Diagnosis, Management, and Prevention of Chronic
3
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
Obstructive Pulmonary Disease (updated 2022)
IDSA and ATS Guidelines on Community Acquired Pneumonia 2019
Philippine Clinical Practice Guidelines on the Diagnosis, Empiric. Management, and
Prevention of Community-acquired (CPG 2016)
Manual of Procedures for the National TB Control Program (Philippines, 6th Edition,
2020),
Clinical Practice Guidelines for the Diagnosis, Treatment, Prevention and Control of
Tuberculosis in Adult Filipinos: 2016 Update, International Standards for
Tuberculosis Care 3nd Edition (ISTC 3rd ed., 2014
WHO’s Guidelines for the Treatment of Drug-susceptible Tuberculosis and Patient Care
Global Initiative for Asthma updated 2023
Philippine COVID-19 Living Recommendations, Institute of Clinical Epidemiology, National
Institutes of Health, UP Manila; PSMID; DOH. January 3, 2022
SGD1: Breathless in bed
Gene Ehica, a 52 year old, married Filipino male, casino dealer consulted because of
dyspnea.
Three weeks before consultation, the patient experienced awakenings around 3 am
where he would have dyspnea that would resolve spontaneously initially and later with
the use of a blue inhaler that was prescribed a years ago for and emergency room visit.. This
would be associated with a high-pitched sound as he exhaled. He used to walk to work
as he lived just one kilometer. away but now takes a tricycle. He would experience
some cough and shortness of breath while dealing cards so he would use 2 puffs of the
inhaler before working, which he did five days weekly.
4
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
Review of systems revealed he had daily morning nasal stuffiness.
Family history: Father - COPD and CAD, died at the age of 76. Mother and brother have
asthma
Past medical history - recall being told to have childhood asthma but has been relatively
symptom-free except for some easy fatiguability starting three years ago.
Treated for TB for 6 months 5 years ago under DOTS.
Hypertensive on maintenance medications
Personal history: Non-smoker, non-alcoholic
Occupational history: card dealer at the casino for 25 years
Physical examination:
Conscious, coherent, cooperative
BP: 120/80 RR: 20 cpm CR: 100 bpm T: 37 C
Skin is warm and moist
No alar flaring, no circumoral cyanosis, no sternocleidomastoid muscle retractions.
Symmetrical chest expansion, no retractions, equal tactile fremitus, resonant, no
adventitious lung sounds. On forced expiration, a wheeze could be appreciated.
Other examinations were normal.
1. Make a summary statement/ illness script of the case above.
2. What is your most likely diagnosis? What information in the history and physical
examination findings are contributory?
3. What are your differential diagnoses?
4. What are the contributing factors to dyspnea?
5. Which is a diagnostic examination of choice? How is it expected to help in the
diagnosis?
6. Interpret the spirometry results which will be shown to you by your facilitator. Is it
compatible with the patient presented?
7. What other tests may be helpful in disease management?
8. What is the pharmacological management approach?
9. What non-pharmacological approaches can we employ?
10. How do we know the disease is under control?
11. Construct a follow-up program for the patient.
12. What are the indicators that a patient should seek medical attention?
13. When should the patient be referred to a specialist?
14. Construct a concept map.
SGD 2
YOU TAKE MY BREATH AWAY
CASE DISCUSSION 2 / SGD 2
YOU TAKE MY BREATH AWAY
OBJECTIVES:
• Recognize the most common signs and symptoms of patients with Pneumonia and
Pleural effusion
• Correlate the manifestations with the pathophysiology of the disease/s
• Recommend procedures that will aid in the diagnosis and management of Pneumonia
and Pleural effusion
• Classify Pneumonia patients according to current guidelines
• Know the most common organisms involved in each classification
• Prescribe management for Pneumonia and Pleural effusion
• Recognize complications associated with management of pleural effusion; recommend
interventions for these complications\
5
•
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
Make simple and processed problem lists
CASE: Vina Vahasia, a 50 year old teacher, consulted for dyspnea.
Eight days prior to admission, the patient started having cough with yellowish phlegm, as well as
fever with a temperature range of 37.5- 38.6C. Three days ago, she also started experiencing
sharp left upper quadrant pain which intensified whenever she would cough. She also mentions
that around this time, she also started having exertional dyspnea when going up to the second
floor of her apartment. She had a chest x-ray done, was told she had pneumonia, and was
prescribed antibiotics, However, she discontinued the antibiotics after taking only 1 dose because
of nausea and vomiting.
Two days ago, she started dyspnea even on activities of daily living. She also felt short of breath
when lying down on her right side, and was only comfortable when she used 3 pillows at night.
The persistence of the cough and worsening of the dyspnea prompted consultation.
(-) weight loss; (-) anorexia; (-) chest heaviness; (-) PND; (+) nocturia.
She is a known Diabetic since 2004, with irregular intake of Glibenclamide. Her CBG results
range from 160-180 mg/dl.
She does not smoke nor drink alcoholic beverages. Family history is (+) for DM.
GS: conscious, alert, aware, speaks in short sentences, but prefers a semi-upright
position; prominence of the SCM.
VS: BP 110/70, CR 100/min, RR 24/min, T 37.9C; O2 sats 93% at RA
Funduscopic exam: (+) exudates OU
Chest: Lagging of the left hemithorax, decreased fremiti, dullness, and decreased breath
sounds from T6 downwards
Cardio: apex beat was at the 5 th LICS, parasternal area; heart sounds normal; JVP and
CAP normal; peripheral pulses ++
Abdomen: unremarkable
Ext: no edema
NE: 20% sensory deficit both feet
GUIDE QUESTIONS:
1. Make a summary statement/ illness script of the case above.
2. Correlate the manifestations of the patient with the possible pathophysiology of the
disease/s
a. Eight days fever, cough, dyspnea, pleuritic pain
b. Shortness of breath when lying on her right side
c. Progressive shortness of breath
d. Nocturia, CBG results, retinopathy, neuropathy
e. Speaks in short sentences, prefers semi upright position, SCM prominence, RR 24;
O2 sats 93%
f. Lagging of L, decreased fremiti, dullness and decreased BS T6 downwards, apex
beat displaced to the contralateral side
6
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
g. Nausea and vomiting
3. What is our admitting impression? Make a simple and processed problem list.
4. How do we classify our patient (what guidelines do we use)? What is the
classification of our patient?
5. What is the importance of classifying the patient?
6. What are the most common organisms involved in CAP? What are the recommended
antibiotic coverage?
7. What labs/ procedures will we request for? Why? What are the expected results?
8. Interpret the chest imaging and ultrasound which will be shown to you by your
facilitator on the day of the SGD.
9. Does our patient have a transudate or an exudate? Is it possible to differentiate them
based on clinical manifestations?
10 Ultrasound guided Thoracentesis was done. 800 cc of slightly turbid amber colored
fluid was obtained . Interpret the test results for the pleural fluid which will be shown
to you on the day of the SGD.
11. When do we expect response to treatment? What if the patient is not improving?
12. Is there any way to prevent Pneumonia?
SGD 3
Intended Learning Outcomes:
1. Recognize the common risk factors and manifestations of lung cancer.
2. Discuss the approach to the evaluation of a pulmonary mass.
3. Discuss the approach to the management of lung cancer.
4. Discuss the risk factors for VTE.
5. Discuss the approach to the diagnosis and management of VTE.
Case Scenario Part 1:
A 51-year-old female consulted because of an incidental finding of a pulmonary
mass noted on her routine annual physical examination chest x-ray. She is currently
7
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
asymptomatic. She denies cough, hemoptysis, dyspnea, chest pain, unexplained weight
loss and fever.
Other than the usual seasonal flu and common childhood illnesses, she had no
history of previous illness. She is not hypertensive nor diabetic. She had no history of
previous PTB diagnosis nor treatment. Her obstetric history is G1P1 (1001), with no
history of oral contraceptive use. Her family medical history is likewise unremarkable.
She does not smoke. She is a businesswoman residing in a high-rise condominium in
BGC.
Her physical examination was likewise unremarkable. Her vital signs were as
follows: BP 120/80 CR: 72 RR: 18 Temp. 36.7 O2 sat: 98% on room air. Her neck was
supple with no palpable cervical lymph nodes. There was symmetrical chest expansion,
no retraction, equal tactile and vocal fremitus, resonant on percussion of both lungs,
lung sounds were normal. There was no edema. Other physical examination findings
were normal.
A chest CT scan with contrast was done and representative cuts are shown
below.
Chest X-ray:
Chest CT scan with contrast:
GUIDE QUESTIONS:
1. Make a summary statement/ illness script of the case above.
2. What other data in the history and PE should you look for? Describe the chest xray.
3. Which of her clinical features are compatible with a benign disease, and which
ones are compatible with a malignant process?
4. Give your presumptive diagnosis, presumptive cell type and presumptive staging
based on the given clinical data.
5. How would you establish the diagnosis and clinical stage?
8
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
6. Discuss the approach to pre-treatment planning?
Continuation…
After your clinical evaluation and pre-treatment planning, you diagnose her to have
Adenocarcinoma of the Lungs, Stage 3a (T3N0M0). Her performance status is generally
good (ECOG 0).
7. What are the goals of treatment for this case? What treatment options will you
recommend for her?
8. What are the goals for follow-up care?
Part 2:
After a course of neo adjuvant therapy, she underwent VATS with left lower lobectomy.
She tolerated the procedure well, there was no immediate post-operative complication
noted. She was apparently recovering well from surgery until, on her 5th post-op day
when she suddenly complained of dyspnea with right-sided pleuritic pain. Her vital signs
were as follows: BP = 120/80, CR 120, RR 28, Temp 36.8, O2 Sat 92% while on 5lpm
O2 supplementation via nasal canula. You are considering the possibility of pulmonary
embolism.
GUIDE QUESTIONS:
1. What are her risk factors for pulmonary embolism?
2. What is the clinical probability of pulmonary embolism in this case? What other
symptoms and signs should you look for to strengthen your diagnosis?
3. How will you manage the patient?
WARD WORK / Virtual Patient Encounter/Telemedicine:
INTENDED LEARNING OUTCOME:
WEEK 1 - History and PE - review of IPPA
1. Discuss clinical manifestations of patients manifesting with respiratory distress and
with respiratory failure
2. Correlate the various manifestations with pathophysiology involved
3. Review the physical examination techniques (IPPA) in patients with pulmonary
diseases
WEEK 2 - Case
1. Identify patients with Pulmonary disorders
2. Obtain significant data—subjective and objective—from patients
3. Correlate the data obtained and formulate a logical diagnosis
4. Discuss differentials, diagnostic and therapeutic plans
WEEK 3 - clinical correlation, discussion of case
1. Critique the patient history / PE obtained the previous week
2. Discuss x-rays / ABGs / Mechanical ventilator management bedside
9
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
INTERVIEW CHECK LIST
ITEM
A. OPENING
1. Initial greeting
a. verbal introduction
b. shakes hands of patient
c. addresses patient appropriately—
Mr., Mrs, Tatay, Nanay, Lola
2. puts patient at ease
B. INFORMATION GATHERING
3. questioning: uses open-to-closed
ended questions
4. expounds on problem(s)
5. establishes a narrative thread
6. problem survey
7. clarification
C. CLOSING
8. encourages patient’s questions
DEFINITION
SCORE
States name and role on team
Greets patient and companions warmly
Minimizes distractions; attends to patient’s
comfort and privacy
MAXIMUM SCORE: 10
Focuses by starting with open questions
and ending with closed questions.
Avoids multiple and leading questions
Asks and verifies problem(s) appropriately
Maintains a chronological account. Lets the
patient tell the story without interrupting and
listens attentively. Follows significant leads
Asks “what else?” until all major concerns
are expressed. Goes over review of
systems
Restates the content (paraphrases patient’s
answers) and checks for accuracy, i.e. “Let
me see if I have this right?”
MAXIMUM SCORE: 50
Does not avoid questions and answers
clearly
9. states appreciation for patient’s
efforts
MAXIMUM SCORE: 10
D. FACILITATION SKILLS
10. eye contact
11. invites/ reinforces patient’s
responses with nods, and repeating
patient’s last statement
Conveys interest and attentiveness
MAXIMUM SCORE: 10
E. FLOW
12. overall feeling is that the interview
moves smoothly from one component
to another with key points summarized
and ending with a smooth closure
MAXIMUM SCORE: 20
TOTAL SCORE:
10
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
PHYSICAL EXAMINATION OF THE RESPIRATORY SYSTEM
RULE OUT THE PRESENCE OF RESPIRATORY DISTESS/ IMPENDING RESPIRATORY FAILURE
1.
2.
Mentions if the following are present: (at least 4)
4 points
Abdominal paradox
Central cyanosis
Altered sensorium
Preference for the upright position/ tripod position
Prominence of the SCM
Retractions
Speaks in phrases (ask the patient a question and note how he responds
States if there is respiratory distress/ failure, or if we can now proceed with
the rest of the physical examination
1 point
5 points
DONE
NOT DONE
ONCE RESPIRATORY DISTRESS / FAILURE HAS BEEN RULED OUT, PROCEED WITH THE
STRUCTURED PE OF THE CHEST
NOT
DONE
1.
DONE
INCOR
RECTLY
DONE
PREPARATION
Washes hands
Greets patient, introduces self
Explains procedure, asks for permission/ consent
Asks patient to remove shirt/ blouse- provides drapes if necessary
4 points
2.
INSPECTION
3.
Describes the appearance of the chest- symmetry/ masses/ bulges/ scars/
lesions- both anterior and posterior
Compares antero-posterior to lateral diameter
States which is wider- antero-posterior or lateral diameter
3 points
INSPECTION/ PALPATION
3.1.
3.2.
3.3.
TRACHEA
While facing the patient, inspects the position of the trachea
Inserts index fingers on the spaces on either side of the trachea
Observes whether the spaces on either side are equal
States if trachea is midline
4 points
CHEST EXPANSION
While facing the patient, places thumbs along costal margins and xiphoid
processes with palms resting on the anterior chest
Asks patient to take a deep breath
Observes for movement of his/ her hands
Describes if chest wall movement is symmetrical/ asymmetrical
Moves toward back of patient
Locates inferior angle of the scapula
Palpates for the 10th ICS along the midscapular line
Puts both palms flush against the chest wall along the 10th ICS, grasping
the posterior chest
Moves both hands medically (towards the vertebral line) so as to form a
crease along the mid-back
Asks the patient to take a deep breath
Observes for movement of his/her hands with the chest wall movement
Describes if the chest wall movement is symmetrical/ asymmetrical
12 points
PALPATION FOR TACTILE FREMITI
Palpates gently across anterior and posterior chest
Describes if there are any points of tenderness/ bulges/ masses
Asks patient to cross his arms across his chest
Moves toward back of patient
11
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
4.
4.1.
4.2.
5.
5.1.
5.2.
6.
Revised August 2023
Rests the ulnar surface of his/her hand in the upper posterior chest, medial
to the scapula
Asks patient to say “ninety-nine” or “tres-tres”
Feels for vibration in the area (tactile fremiti)
Moves hand to other side and does same procedure
Moves hand to a lower position in the chest, and does same procedure
Always compares one side to the other while moving from upper to mid
chest area, initially always medial to the scapula
Once below the level of T7/ 7th ICS, examines for tactile fremiti along the
scapular lines and posterior axillary lines, always comparing one side to
the other
States if the tactile fremiti are equal
12 points
PERCUSSION
PERCUSSION OF LUNGS
Reminds patient to keep his arms crossed
Beginning at the upper lung field, aligns finger (of pleximeter hand) along
intercostal space along the paravertebral line, making sure that it is only
the distal 3rd of the finger resting on the chest wall
Strikes the distal 3rd of the finger with the tips of the fingers of the free hand
(plexor)
Listens for percussion sound produced
Does same procedure, moving from one side of the chest to the other,
from the upper to the lower lung fields
5 points
DIAPHRAGMATIC EXCURSION
Asks the patient to take a deep breath and hold it
Percusses along the scapular line and locate the area of dullness which is
the level of the diaphragm
Marks that level
Asks patient to do normal breathing
Instructs patient to exhale as much as possible
Percuss upward from marked point and locate the area of dullness
States positions of both levels
Moves to opposite side and repeats procedure
8 points
AUSCULTATION
BREATH SOUNDS
Makes sure that patient still has his arms crossed over his chest
Asks patient to take slow deep breaths through his mouth
Auscultates with the diaphragm of the stethoscope in the same areas used
in palpation and percussion (moving from upper lung field to lower, always
comparing one side to the other)
Listens to 2-3 respiratory cycles before moving to next position
States if there are adventitious breath sounds
5 points
VOCAL FREMITI
Repeats the same procedure but asks patient to say “tres-tres” or “ninetynine” instead of taking deep breaths
Listens for vocal fremiti
States if vocal fremiti are equal
3 points
ENDING THE PHYSICAL EXAMINATION
Informs patient that examination is done
Asks patient if he needs help dressing
Thanks patient
3 points
TOTAL POINTS
PERFECT SCORE 64 points
12
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
LECTURES :
LECTURE 1 : BASIC CHEST IMAGING
INTENDED LEARNING OUTCOME:
1. Review normal chest radiograph
2. Assess the quality of the chest radiograph
3. Identify and interpret radiograph abnormalities
4. Correlate radiographic result of clinical manifestations
5. Identify normal chest ultrasonography findings
6. Interpret abnormal chest ultrasonography findings
1. QUALITY OF FILM
1.
2.
3.
4.
5.
PA view
Position
Penetration
full Picture
full insPiration
2. BASIC CHEST X-RAY INTERPRETATION
Are There Many Lung Lesions?
A
1.
2.
3.
4.
costophrenic sulci
contour of hemidiaphragm
level of hemidiaphragm
Right usually higher than left
T
1. symmetry of thoracic cage / ICS
2. rib fractures
M
1. trachea
2. heart
3. hila (L usually higher than left)
LL
1. compare one lung to the other lung
NORMAL CHEST ULTRASOUND
-
bat sign
lung sliding
comet tails
sea shore sign
LUNG PATHOLOGIES
PLEURAL EFFUSION – sonolucency- usually above the diaphragm
– loculated effusion
PNEUMOTHORAX – absence of lung sliding, identification of lung point; bar code sign
13
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
PNEUMONIA – dynamic air bronchograms
Emphysema
A – flat/depressed hemidiaphragm; low set
T – widened interspaces
M – dropped heart – investigate for Pulmonary hypertension (look at Pulmonary
arteries)
LL – hyperluscent lungs, +/- bullae, pruning of blood vessels
Pneumothorax
A – +/- flattening of one hemidiaphragm on the side of the pathology; +/blunting of costophrenic sulcus (secondary to bleeding)
T – +/- widened interspaces on affected side
M – +/- shifting of midline structures contralaterally
LL – presence of visible visceral pleural line- radiographic hallmark
Consolidation
A – may be normal
T – normal
M – +/- silhouette sign depending on the lobe involvement
LL – presence of air bronchograms
Obstructive Atelectasis
A – hemidiaphragm may be affected depending on the size of atelectasis
T – +/- narrowed interspaces on affected side with compensatory widening on
opposite side
M – +/- shifting of midline structures ipsilaterally
LL – homogenous opacification of affected area
Cicatricial Atelectasis
A – hemidiaphragm may be affected depending on the size of atelectasis
T – +/- narrowed interspaces on affected side with compensatory widening on
opposite side
M – +/- shifting of midline structures ipsilaterally
LL – inhomogenous opacification of affected area, with air bronchograms
Effusion
A – blunting of costophrenic sulcus, or non visualization of hemidiaphragm, due
to presence of fluid
T – +/- widened interspaces on affected side (may be hard to visualize because
of the presence of fluid)
M – +/- shifting of midline structures contralaterally depending on amount of fluid
as well as presence of any other underlying lung pathology
LL – homogenous opacification with a lateral upward curve (meniscus sign)
-on lateral decubitus view – the homogenous density (fluid) occupies the
most dependent portion of the chest wall (layering) if it is FREE within the
pleural space
Cavitary Tuberculosis
A – costophrenic sulci not affected unless there is concomitant effusion or
thickening
T – interspaces not affected unless there is also volume loss/ atelectasis
M – +/- shifting of midline structures depending on volume loss
LL – lucency within the lung parenchyma usually with an irregular margin.
14
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
Bronchiectasis
A – costophrenic sulci not affected unless there is concomitant effusion or
thickening
T – interspaces not affected unless there is also volume loss/ atelectasis
M – +/- shifting of midline structures depending on volume loss
LL – honeycomb densities
Metastatic lesions
A – costophrenic sulci not affected unless there is concomitant effusion or
thickening
T – interspaces not affected unless there is also volume loss/ atelectasis
M – +/- shifting of midline structures depending on volume loss
LL – cannon ball appearance; brocnhoalveolar spread; multiple nodules
REFERENCES:
Harrison’s Principles of Internal Medicine 20thEdition
Chest Radiography (Felson)
Module on Pulmonary Medicine Workbook
NOTES:
15
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
LECTURE 2 : ARTERIAL BLOOD GAS (ABG)
INTENDED LEARNING OUTCOME:
1. Learn the usefulness of the arterial blood gas
2. Know the normal values
3. Interpret arterial blood gases
4. Present a simple algorithm in the interpretation of ABG results
5. Apply various equations to blood gas interpretation and clinical management
NOTES:
16
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
LECTURE 3 : SPIROMETRY
INTENDED LEARNING OUTCOME:
1. Define ventilation
2. Enumerate the organs involved in ventilation
3. Describe the physiologic changes during ventilation
4. Define the different ventilatory defect (obstructive, restrictive and mixed)
5. Show how a spirometry testing is done
6. Enumerate the parameters measured and define its normality
7. Show and rationalize an algorithm of how a spirometry report in interpreted
8. Interpret several spirometry report and correlate with the possible diagnosis of
clinical cases
9. Enumerate and show examples of how spirometry is used in clinical practice
REFERENCES:
Harrison’s Principles of Internal Medicine 21st Edition
American Thoracic Society Statement on Pulmonary Function Testing
Module on Pulmonary Medicine Workbook
NOTES:
17
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Concept of Ventilatory Defect
Site of Pathology
Ventilatory
Defect
Airways
Obstructive
P: Pleura
A: Alveoli (lungs)
I: Interstitium
(lungs)
N: Neuromuscular
apparatus
T: Thoracic cage
Restrictive
Primary
Loop
Manifestation
Low air flow
Short
exaggerated
concavity
Low lung
Narrow
volume
Revised August 2023
FEV1/FVC FVC
Almost
always
low
Always
low
1. Breathing Maneuver/ Parameters Measured/ Interpretation Algorithm
1.1. Forced Vital Maneuver: After several tidal breathing, subject inhale to TLC then
forcefully, rapidly, completely expire to RV for at least 6 seconds and then forcefully and
rapidly inspire back to TLC
1.2. Parameters Measured
1.2.1. Forced Expiratory Volume in one Second (FEV1): From TLC, it is the volume
forcefully expired by patient for one second. It is considered as an airflow
parameter
1.2.2. Forced Vital Capacity (FVC): The volume forcefully expired from TLC to RV.
Considered as an airflow parameter
1.2.3. FEV1/FVC: Considered as an airflow parameter
1.3. Parameters for Normality
1.3.1. GOLD Standard: Lower Limit of Normality is the 5 th percentile
1.3.2. Alternative Standard
1.3.2.1. FEV1/FVC: anything below 0.7 or 70 is considered abnormally low
1.3.2.2. FEV1 or FVC: anything below 80% of the predicted is considered
abnormally low
1.4. Significant response to Bronchodilator: Labelling requires 2 conditions: FEV1 or FVC
increase of at least 12% from baseline: FEV1 or FVC increase of at least 200 ml from
baseline
2. Sequence of Interpretation
2.1. Is it a good quality test?
2.2. Is there an obstructive ventilatory defect?
2.3. Is there a probable restrictive ventilatory defect?
2.4. If a ventilatory defect is present, what is the severity?
2.5. Is there a significant response to bronchodilator?
18
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
FLOW CHART FOR THE INTERPRETATION OF A SPIROMETRY RESULT
FLOW CHART FOR THE INTERPRETATION OF A SPIROMETRY RESULT
19
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
LECTURE 4 : COMMUNITY ACQUIRED PNEUMONIA (CAP)
INTENDED LEARNING OUTCOME:
1. Recognize the most common signs and symptoms of patients with Community
Acquired Pneumonia
2. Correlate the manifestations with the pathophysiology of the disease
3. Recommend procedures that will aid in the diagnosis and management
4. Classify patients according to current guidelines
5. Know the most common organisms involved in each classification
6. Prescribe initial management based on the classification of the patient
7. Provide differentials for patients who do not respond to medications
REFERENCES:
Harrison’s Principles of Internal Medicine 21st Edition
IDSA and ATS Guidelines on Community Acquired Pneumonia 2019
Philippine Clinical Practice Guidelines on the Diagnosis, Empiric. Management, and
Prevention of Community-acquired (CPG 2016)
Module on Pulmonary Medicine Workbook
NOTES:
20
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
Clinical Practice Guidelines for Community Acquired Pneumonia
Reference Card: Pneumonia Severity Index
Calculation of the patient’s PSI allows classification of the severity of pneumonia using the
scaled rankings in the following table:
Table: severity of Pneumonia Scale
Class
Class I
Class II
Class III
Class IV
Class V
Description of severity
Exhibit no severe clinical signs and aged less than 50 yrs. old. This class ha a
30-day mortality rate of 0.1%, however, it is not relevant to residents of RACFs.
PSI score 1-70. This class has a 30-day mortality rate of 0.6% and are usually
treated in the RACF home.
PSI score 71-90. This class has a 30-day mortality rate of 0.9% and should be
assessed for appropriateness of IV treatments in the facility of hospital.
PSI score 91-130. This class has a 30-day mortality rate of 9.3% and I usually
treated in hospital.
PSI score >130. This class has a 30-day mortality rate of 29.2% and should be
treated in hospital
PSI risk class I – Patient age ≤50 years and patient has none of the following:
History of:
Clinical signs:
• Neoplastic disease
• Acutely altered mental state
• Liver disease
• Respiratory rate ≥30 per minute
• Congestive cardiac failure
• Systolic blood pressure <90 mm Hg
• Cerebrovascular disease
• Temperature <35oC or ≥40oC
• Renal disease
• Pulse rate ≥125 per minute
PSI risk classes II, III, IV and V – calculate score using the following information:
Factor
PSI score
Resident’s score
Patient age
Age in years (male)
or age in years
(female) -10
Nursing home (but not hostel) resident
+10
Coexisting illness
- Neoplastic disease
- Liver disease
- Congestive cardiac failure
- Cerebrovascular disease
- Chronic renal disease
Signs on examination
+30
+20
+10
+10
+10
- Acutely altered mental state
- Respiratory rate ≥30 per minute
- Systolic blood pressure <90 mm Hg
- Temperature <35oC or ≥40oC
- Pulse rate ≥125 per minute
Results of investigation
+20
+20
+20
+15
+10
21
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
PNEUMONIA SEVERITY INDEX
Identifying the level of risk in CAP patients: The risk factors and how they are scored:
Patient Characteristic
Males
Females
Nursing home residents
Comorbid Illness
Neoplastic disease
Liver disease
Congestive heart failure
Cerebrovascular disease
Renal disease
Physical Examination Findings Altered mental status
Respiratory rate 30 breaths per minute or more
Systolic blood pressure < 90 mm Hg
Temperature < 35oC or 40oC or more
Pulse 125 beats per minute or more
Laboratory Findings
pH< 7.35
BUN > 10.7 mmol/L
Sodium less than 130 /L
Glucose > 30 percent
Hematocrit < 30 percent
Partial pressure of arterial oxygen < 60 mm Hg
Pleural effusion
Demographic Factors (Age)
Points Assigned*
Age (in years)
Age (in years) -10
+10
+30
+20
+10
+10
+10
+20
+20
+20
+15
+10
+30
+20
+20
+10
+10
+10
+10
*A risk score (total point score) for a given patient is obtained by summing the patient age in years (ago
minus 10 for females) and the points for each applicable patient characteristics.
*Oxygen saturation < 90 percent was considered abnormal in the Pneumonia PORT cohort study. The
application of the PSI to the initial site of treatment decision (translation research) combines the PSI risk
score and in addition considers the status of arterial oxygenation when used to guide the initial site of
treatment.
How Risk Levels Are Scored
Risk Level
30-Day Mortality
Risk
Class
Based on:
Low
Less 0.5 percent
I
Algorithm
Low
Greater than or equal to 0.5 and less than 1.0 percent
II
70 or fewer points
Low
Greater than or equal to 1.0 and less than 4.0 percent
III
71-90 points
Moderate
Greater than or equal to 4.0 and less than 10.0 percent
IV
91-130 points
High
Greater than or equal to 10.0 percent
V
Greater than 130 points
Source: Fine MJ, Auble TE, Yealy DM, et al. A prediction rule to identify low-risk patients with
community-acquired pneumonia.NEngl J Med 1997;336(4):242-50.
22
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
CURB-65 AND CRB-65 SEVERITY SCORES FOR COMMUNITY-ACQUIRED PNEUMONIA
Clinical factor
Points
Confusion
1
Blood urea nitrogen > 19 mg per dL
1
Respiratory rate ≥ 30 breaths per minute
1
Systolic blood pressure < 90 mm Hg
or
Diastolic blood pressure ≤ 60 mm Hg
Age ≥ 65 years
1
1
Total points:
0
Deaths/total
(%)*
7/1,223 (0.6)
1
31/1,142 (2.7)
2
69/1,019 (6.8)
Short inpatient hospitalization or closely supervised outpatient treatment
3
79/563 (14.0)
Severe pneumonia; hospitalize and consider admitting to intensive care
4 or 5
44/158 (27.8)
CURB-65 score
Recommendation†
Low risk; consider home treatment
0
Deaths/total
(%)*
2/212 (0.9)
Very low risk of death; usually does not require hospitalization
1
18/344 (5.2)
Increased risk of death; consider hospitalization
2
30/251 (12.0)
3 or 4
39/125 (31.2)
CRB-65 score‡
Recommendation†
High risk of death; urgent hospitalization
CURB-65 = Confusion, Urea nitrogen, Respiratory rate, Blood pressure, 65 years of age and older.
CRB-65 = Confusion, Respiratory rate, Blood pressure, 65 years of age and older.
* - Data are weighted averages from validation studies.1-2
† -Recommendation are consistent with British Thoracic Society guidelines.3 Clinical judgment may
overrule the guideline recommendation.
‡ - A CRB-65 score can be calculated by omitting the blood urea nitrogen value, which gives it a point
range 0 to 4. This score is useful when tests blood tests are not readily available.
1.
2.
3.
Aujesky D, Auble TE, Yealy DM, Stone RA, Obrosky DS, Meehan TP, et al. Prospective comparison of three
validated prediction rules for prognosis in community-acquired pneumonia. Am J Med. 2005; 118-384-392.
Lim WS, van der Eerden MM, Laing R, Boersma WG, Karalus N, Town Gl, et al. Defining community acquired
pneumonia severity on presentation to hospital: an international derivation and validation study. Thorax.
2003;58:377-382.
British Thoracic Society Pneumonia Guidelines Committee. BTS guidelines for the management of communityacquired
pneumonia
in
adults
–
2004
update.
Available
at
http://www.britthoracic.org.uk/c2/uploads/MACAPrevised apr04.pdf. Accessed March 20, 2006.
23
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
FOR LOW RISK PATIENTS - ADMIT WHEN:
- complications of pneumonia
- exacerbation of underlying disease
- inability to take oral medications or receive out patient care
- multiple risk factors
- PLUS
o hypoxemia O2 sat < 90% or PaO2 < 60mmHg
o shock
o decompensated co-existing disease
o pleural effusion
o inability to take oral medications
o social problems
o lack of response to previous antibiotic treatment
WHERE SHOULD WE ADMIT PATIENTS?
ADMIT TO ICU IF:
- septic shock requiring vasopressors
- ARF requiring intubation or MCV
- 3 of the ff minor criteria:
o RR > 30/min
o P/F < 250
o Multilobar infiltrates
o Confusion/ disorientation
o Uremia (BUN > 19 mg/dl)
o Leucopenia (< 4000 cells / mm3)
o Thrombocytopenia (< 100,000 cells / mm3)
o Hypothermia (< 36C)
o Hypotension requiring aggressive fluid resuscitation
MOST PROBABLE ORGANISMS
- OUTPATIENT - S pneumonia, M pneumonia, H influenza, C pneumonia, respiratory viruses
- IN PATIENT NON ICU - S pneumonia, M pneumonia, H influenza, C pneumonia, Legionella spp,
anaerobes (aspiration), respiratory viruses
- IN PATIENT ICU - S pneumonia, S aureus. Legionella, Gram (-) bacilli, H influenza
EMPIRIC THERAPY
OUTPATIENT
- previously healthy, no use of antibiotics in previous 3 monthso Macrolide, Doxycycline
- with co-morbidities
o respiratory FQ, B lactam + macrolide
- high probability of macrolide resistant Strep even in patients with no co-morbiditieso respiratory FQ, B lactam + macrolide
INPATIENT NON ICU - respiratory FQ, B lactam + macrolide
INPATIENT ICU - B lactam + either azithromycin or a respiratory FQ
INPATIENT ICU with Psedomonas infection - antipseudomonas B lactam + cipro or levofloxacin
or B-lactam + aminoglycoside + azithromycin or
B-lactam + aminoglycoside + antipneumococcal
fluoroquinolone (penicillin allergy - substitute
aztreonam for the B-lactam)
INPATIENT ICU with community acquired MRSP - add vancomycin or linezolid
24
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
25
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
26
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
LECTURE 5 : CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
INTENDED LEARNING OUTCOME:
1. Classify the different severities and stages of COPD
2. Develop an appropriate pharmacological and non-pharmacological regimen for
patients with COPD based on disease severity, as well as for exacerbations of
COPD
3. Create a proper prescription, treatment monitoring plan, and the treatment regimen
for a COPD patient
27
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
28
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
29
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
30
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
31
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
32
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
33
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
34
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
35
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
36
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Revised August 2023
37
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
38
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
LECTURE 6 : BRONCHIECTASIS
INTENDED LEARNING OUTCOME:
1. Define bronchiectasis
2. Recognize common signs and symptoms of bronchiectasis
3. Identify common causes of bronchiectasis
4. Apply treatment principles in a given case
REFERENCES:
Harrison’s Principles of Internal Medicine 21st
Edition
NOTES:
39
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
LECTURE 7 : TUBERCULOSIS
INTENDED LEARNING OUTCOME:
1. Familiarize students on the clinical signs and symptoms, risk factors and laboratory
evidence associated with active TB disease.
2. Review current local (DOH-NTP Manual of Procedures) and international (ISTC 2014
and WHO Guidelines) recommendations for TB diagnosis and management for drugsusceptible and drug-resistant TB, even in cases of TB/HIV co-infection – including
disease classification, registration group, treatment regimens and outcomes.
Int’l Std for TB Care:
• To ensure early diagnosis, providers must be aware of individual and group risk factors for tuberculosis and perform
prompt clinical evaluations and appropriate diagnostic testing for persons with symptoms and findings consistent
with tuberculosis.
• All patients, including children, with unexplained cough lasting two or more weeks or with unexplained findings
suggestive of tuberculosis on chest radiographs should be evaluated for tuberculosis
WHO 2018:Standards for early TB detection
• For persons with signs or symptoms consistent with TB, performing prompt clinical evaluation is essential to ensure
early and rapid diagnosis.
• All persons who have been in close contact with patients who have pulmonary TB should be evaluated. The highest
priority contacts for evaluation are those:
o with signs or symptoms suggestive of TB;
o aged <5 years;
o with known or suspected immunocompromising conditions, particularly HIV infection;
o who have been in contact with patients with MDR-TB or XDR-TB.
• All persons living with HIV and workers who are exposed to silica should always be screened for active TB in all
settings. Other high-risk groups should be prioritised for screening based on the local TB epidemiology, health system
capacity, resource availability and feasibility of reaching the risk groups.
• CXR is an important tool for triaging and screening for pulmonary TB, and it is also useful to aid diagnosis when
pulmonary TB cannot be confirmed bacteriologically. CXR can be used to select individuals for referral for
bacteriological confirmation and the role of radiology remains important when bacteriological tests cannot provide a
clear answer.
Standards for TB diagnosis
• All patients with signs and symptoms of pulmonary TB who are capable of producing sputum should have as their
initial diagnostic test at least one sputum specimen submitted for Xpert MTB/RIF Ultra assay. This includes children
who are able to provide a sputum sample and patients with EPTB. A second Xpert MTB/RIF Ultra assay may be
performed for all patients who initially test negative by Xpert MTB/RIF Ultra but whose signs and symptoms of TB
persist.
• The Xpert MTB/RIF Ultra assay should be used in preference to conventional microscopy and culture as the initial
diagnostic test for cerebrospinal fluid specimens from patients being evaluated for TB meningitis. The Xpert MTB/RIF
Ultra assay is recommended as a replacement test for usual practice (including conventional microscopy, culture or
histopathology) for testing specific nonrespiratory specimens (lymph nodes and other tissues) from patients suspected
of having EPTB.
• For persons living with HIV, the Xpert MTB/RIF Ultra assay should be used as an initial diagnostic test. LF-LAM can be
used to assist in the diagnostic process for HIV-positive patients who are seriously ill.
• DST using WHO-recommended rapid tests should be performed for all TB patients prior to starting therapy, including
new patients and patients who require retreatment. If rifampicin resistance is detected, rapid molecular tests for
resistance to isoniazid, fluoroquinolones and second-line injectable agents should be performed promptly to inform the
treatment of MDR-TB and XDR-TB.
• Culture-based DST for selected second-line anti-TB agents should be performed for patients enrolled in individualised
(longer) MDR-TB treatment.
Standard for diagnosing LTBI
• Either TST or IGRA can be used to test for LTBI. TST is not required before initiating IPT in persons living with HIV.
40
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
NTP-MOP:
• All presumptive TB should undergo DSSM unless it is not possible due to the following situations o mentally incapacitated as decided by a specialist or medical institution
o debilitated or bedridden
o children unable to expectorate
o patients unable to produce sputum despite sputum induction
Int’l Std for TB Care:
• All patients, including children, who are suspected of having pulmonary tuberculosis and are capable of producing
sputum should have at least two sputum specimens submitted for smear microscopy or a single sputum specimen
for Xpert MTB/RIF testing in a quality-assured laboratory. Patients at risk for drug resistance, who have HIV risks,
or who are seriously ill, should have Xpert MTB/RIF performed as the initial diagnostic test.
Blood-based serologic tests and interferon-gamma release assays should not be used for diagnosis of active
tuberculosis.
41
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
•
•
For all patients, including children, suspected of having extrapulmonary tuberculosis, appropriate specimens from
the suspected sites of involvement should be obtained for microbiological and histological examination. An Xpert
MTB/RIF test is recommended as the preferred initial microbiological test for suspected tuberculous meningitis because
of the need for a rapid diagnosis.
In patients suspected of having pulmonary tuberculosis whose sputum smears are negative, Xpert MTB/RIF and/or
sputum cultures should be performed. Among smear- and Xpert MTB/RIF negative persons with clinical evidence
strongly suggestive of tuberculosis, anti-tuberculosis treatment should be initiated after collection of specimens
for culture examination.
WHO Guidelines:
• Sputum should be obtained, as well as appropriate specimens for culture and histopathological examination in
cases of extrapulmonary TB, depending on the site of disease. Examination of sputum and a chest radiograph are
also suggested, in case patients have concomitant pulmonary involvement.
• For HIV-negative patients, if broad-spectrum antibiotics are used in the diagnosis of smear-negative pulmonary TB,
anti-TB drugs and fluoroquinolones should be avoided. A trial of broad-spectrum antibiotics is no longer
recommended to be used as a diagnostic aid for smear-negative pulmonary TB in persons living with HIV.
WHO 2018: Standards for HIV infection and other comorbid conditions
• HIV testing should be routinely offered to all patients with presumptive TB and those who have been diagnosed with
TB.
• Persons living with HIV should be screened for TB by using a clinical algorithm.
• ART and routine CPT should be initiated among all TB patients living with HIV, regardless of their CD4 cell count.
• A thorough assessment should be conducted to evaluate comorbid conditions and other factors that could affect the
response to or outcome of TB treatment. Particular attention should be given to diseases or conditions known to affect
treatment outcomes, such as diabetes mellitus, drug and alcohol abuse, undernutrition and tobacco smoking.
WHO 2018: Standards for treating drug-susceptible TB
• While awaiting DST results, patients with drug-susceptible TB and TB patients who have not been treated previously
with anti-TB agents and do not have other risk factors for drug resistance should receive a WHO-recommended firstline treatment regimen using quality assured anti-TB agents. The initial phase should consist of 2 months of isoniazid,
rifampicin, pyrazinamide and ethambutol. The continuation phase should consist of 4 months of isoniazid and
rifampicin. Daily dosing should be used throughout treatment. The doses of anti-TB agents should conform to WHO’s
recommendations. FDC anti-TB agents may provide a more convenient form ofadministration.
• In patients who require retreatment for TB, the category II regimen should no longer be prescribed and DST should be
conducted toinform the choice of treatment regimen.
• In patients with tuberculous meningitis or tuberculous pericarditis, adjuvant corticosteroid therapy should be used in
addition to anappropriate TB treatment regimen.
Standards for treating drug-resistant TB
• In patients with rifampicin-susceptible, isoniazid-resistant TB, 6 months of combination treatment with rifampicin,
ethambutol, pyrazinamide and levofloxacin, with or without isoniazid, is recommended.
• Patients with MDR/RR-TB require second-line treatment regimens. MDR/RR-TB patients may be treated using a 9–11month MDR-TB treatment regimen (the shorter regimen) unless they have resistance to second-line anti-TB agents or
meet other exclusion criteria. In these cases, a longer (individualised) regimen with at least five effective anti-TB
agents in the intensive phase and four agents in thecontinuation phase is recommended for ⩾20 months. Partial
resection surgery has a role in treating MDR-TB.
Standard for treating LTBI
• Persons living with HIV and children younger than 5 years who are household or close contacts of persons with TB and
who, after anappropriate clinical evaluation, are found not to have active TB but to have LTBI should be treated.
Disease Classification Based on Anatomical Site and Bacteriologic Status
Anatomical
Site
Bacteriological
status
Definition of Terms
Smear-positive
Bacteriologicallyconfirmed
Pulmonary
(PTB)
Clinicallydiagnosed
Culturepositive
Rapid
Diagnostic
Test-positive
A patient with at least one (1) sputum specimen positive for AFB, with or without
radiographic abnormalities consistent with active TB
A patient with positive sputum culture for MTB complex, with or without radiographic
abnormalities consistent with active TB
A patient with sputum positive for MTB complex using rapid diagnostic modalities such as
Xpert MTB/RIF, with or without radiographic abnormalities consistent with active TB
A patient with two (2) sputum specimens negative for AFB or MTB, or with smear not done due to specified
conditions but with radiographic abnormalities consistent with active TB; and there has been no response to
a course of empiric antibiotics and/or symptomatic medications; and who has been decided (either by the
physician and/or TBDC) to have TB disease requiring a full course of anti-TB chemotherapy
OR
42
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Extrapulmonary
(EPTB)
Bacteriologicallyconfirmed
Clinicallydiagnosed
A child (less than 15 years old) with two (2) sputum specimens negative for AFB or with smear not done, who
fulfills three (3) of the five (5) criteria for disease activity (i.e., signs and symptoms suggestive of TB, exposure
to an active TB case, positive tuberculin test, abnormal chest radiograph suggestive of TB, and other laboratory
findings suggestive of tuberculosis); and who has been decided (either by the physician and/or TBDC) to have
TB disease requiring a full course of anti-TB chemotherapy
OR
A patient with laboratory or strong clinical evidence for HIV/AIDS with two (2) sputum specimens negative for
AFB or MTB or with smear not done due to specified conditions but who, regardless of radiographic results,
has been decided (either by physician and/or TBDC) to have TB disease requiring a full course of anti-TB
chemotherapy.
A patient with a smear/culture/rapid diagnostic test from a biological specimen in an extra-pulmonary site (i.e.,
organs other than the lungs) positive for AFB or MTB complex
A patient with histological and/or clinical or radiologic evidence consistent with active extra-pulmonary TB and
there is a decision by a physician to treat the patient with anti-TB drugs
TB Disease Registration Groups
Registration Group
New
Retreatment
Relapse
Treatment After
Failure
Treatment After Lost
to Follow-up (TALF)
Previous Treatment
Outcome Unknown
(PTOU)
Other
Definition of Terms
A patient who has never had treatment for TB* or who has taken anti-TB drugs for less than one (<1) month.
A patient previously treated for TB, who has been declared cured or treatment completed in their most recent treatment episode, and
is presently diagnosed with bacteriologically-confirmed or clinically-diagnosed TB.
A patient who has been previously treated for TB and whose treatment failed at the end of their most recent course.This includes:
•
A patient whose sputum smear or culture is positive at 5 months or later during treatment.
•
A clinically diagnosed patient (e.g., child or EPTB) for whom sputum examination cannot be done and who does not show
clinical improvement anytime during treatment.
A patient who was previously treated for TB but was lost to follow-up for two months or more in their most recent course of treatment
and is currently diagnosed with either bacteriologically-confirmed or clinically-diagnosed TB.
Patients who have been previously treated for TB but whose outcome after their most recent course of treatment is unknown or
undocumented.
Patients who do not fit into any of the categories listed above.
Recommended Category of Treatment Regimen
Category of
Treatment
Category I
Category Ia
Category II
Category IIa
Classification and Registration Group
Pulmonary TB, new (whether bacteriologically-confirmed or
clinically-diagnosed)
Extra-pulmonary TB, new (whether bacteriologically-confirmed or
clinically-diagnosed) except CNS/ bones or joints
Extra-pulmonary TB, new (CNS/ bones or joints)
Pulmonary or extra-pulmonary, previously treated drug-susceptible
TB (whether bacteriologically confirmed or clinically-diagnosed)
•
Relapse
•
Treatment After Failure
•
Treatment After Lost to Follow-up (TALF)
•
Previous Treatment Outcome Unknown
•
Other
Extra-pulmonary, Previously treated drug susceptible TB (whether
bacteriologically confirmed or clinically diagnosed - CNS/ bones or
joints)
Standard Shorter
MDR-TB Regimen
(SSTR)
RR-TB or MDRTB
Standard Regimen
Drug-resistant
(SRDR)
RR-TB or MDRTB
Regimen for XDR
XDR-TB
Treatment Regimen
2HRZE/4HR
2HRZE/10HR
2HRZES/1HRZE/5HRE
2HRZES/1HRZE/9HRE
4-6 Km-Mfx-Pto-Cfz-Z-Hhigh-dose-E /
5 Mfx-Cfz-Z-E
Treatment duration for at least 9-12
months
ZKmLfxPtoCs
Individualized once DST result is
available
Treatment duration for at least 18-24
months
Individualized based on DST result and
history of previous treatment
Note: H=Isoniazid, R=Rifampicin, Z=Pyrazinamide, E=Ethambutol, S=Streptomycin
43
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
NTP-MOP:
• DOT can be done in any accessible and convenient place for the patient (e.g., DOTS facility, treatment partner’s house,
patient’s place of work, or patient’s house) as long as the treatment partner can effectively ensure the patient’s intake of
the prescribed drugs and monitor his/her reactions to the drugs. Any of the following could serve as treatment partner:
a) DOTS facility staff, such as the midwife or the nurse; or b) a trained community member, such as the barangay health
worker (BHW), local government official, or a former TB patient.
• Trained family members may be assigned to administer oral medications during weekends and holidays; or as the sole
treatment partner in special/exceptional cases, such as:
o Poor access to a DOTS facility due to geographical barriers (including temporarily displaced populations)
o Debilitated and/or bed-ridden patients
o DOT schedule is in conflict with the patient’s work/school schedule and unable to access other DOTS facilities
o Cultural beliefs that limit the choice of a treatment partner (e.g., indigenous people)
o Treatment of children
• In such cases where a family member is the treatment partner, drug supply is to be distributed on a weekly basis or as
agreed by the health worker and the family member.
• Streptomycin intramuscular injections are to be administered only by trained and authorized health personnel. Patients
with no access to such services during weekends/holidays may forego streptomycin doses during weekends/holidays
provided they still complete the recommended number of doses (i.e., 56 doses).
• A TB patient diagnosed during confinement in a hospital may start treatment using NTP drug supply upon the
approval of the hospital TB team. Once discharged, the patient shall be referred by the hospital TB team to a DOTS
facility for registration and continuation of the assigned standard treatment regimen.
Treatment response is monitored through follow-up sputum exams – only 1 specimen required. The schedule generally follows
this principle: follow-up DSSM shall be done at the end of intensive phase, at the end of the 5th month and at the end of
treatment.
Category
I/Ia
Category
II /IIa
Note:*If the patient belongs to Category I or Ia and baseline DSSM is negative, no need to repeat DSSM in succeeding months.
**For Category I or Ia patients who remain positive after the intensive phase, follow the DSSM schedule of Category II patients
without changing the treatment regimen.
Int’l Std for TB Care:
•
Response to treatment in patients with pulmonary tuberculosis (including those with tuberculosis diagnosed by a rapid molecul ar test)
should be monitored by follow up sputum smear microscopy at the time of completion of the initial phase of treatment (two
months). If the sputum smear is positive at completion of the initial phase, sputum microscopy should be performed again at 3
monthsand, if positive, rapid molecular drug sensitivity testing (line probe assays or Xpert MTB/RIF) or culture with drug
susceptibility testing should be performed. In patients with extra-pulmonary tuberculosis and in children, the response to treatment
is best assessedclinically.
•
An assessment of the likelihood of drug resistance, based on history of prior treatment, exposure to a possible source case
having drug-resistant organisms, and the community prevalence of drug resistance (if known), should be undertaken for all patients.
Drug susceptibility testing should be performed at the start of therapy for all patients at a risk of drug resistance. Patients
who remain sputum smear-positive at completion of 3 months of treatment, patients in whom treatment has failed, and patients who
have been lost to follow up or relapsed following one or more courses of treatment should always be assessed for drug resistance.
For patients in whom drug resistance is considered to be likely an Xpert MTB/RIF test should be the initial diagnostic test. If rifampicin
resistance is detected, culture and testing for susceptibility to isoniazid, fluoroquinolones, and second-line injectable drugs should be
performed promptly. Patient counseling and education, as well as treatment with an empirical second-line regimen, should begin
immediately to minimize the potential for transmission. Infectioncontrol measures appropriate to the setting should be applied.
•
Patients with or highly likely to have tuberculosis caused by drug-resistant (especially MDR/XDR) organisms should be treated with
specialized regimens containing quality-assured second-line anti-tuberculosis drugs. The doses of anti-tuberculosis drugs should
conform to WHO recommendations. The regimen chosen may be standardized or based on presumed or confirmed drug susceptibility
patterns. At least five drugs, pyrazinamide and four drugs to which the organisms are known or presumed to be susceptible, including
an injectable agent, should be used in a 6–8 month intensive phase, and at least 3 drugs to which the organisms are known or
presumed to be susceptible, should be used in the continuation phase. Treatment should be given for at least 18–24 months
44
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
beyond culture conversion. Patient-centered measures, including observation of treatment, are required to ensure adherence.
Consultation with a specialist experienced in treatment of patients with MDR/XDR tuberculosis should beobtained.
WHO Guidelines:
•
A positive smear at the end of intensive phase has a very poor ability to predict relapse or pretreatment isoniazid resistance. However,
it is useful in detecting problems with patient supervision and for monitoring program performance. For smear-positive pulmonary
TB patients (whether Category 1 or 2) treated with first-line drugs, sputum smear microscopyMAY be performedat completion of
the intensive phase of treatment.Then for new cases, sputum smear microscopy is to be repeated at the end of the fifth and sixth
months.However,if the specimen obtained at the end of the intensive phase (month 2) is smear-positive in new patients, sputum smear
microscopy should be obtained at the end of the third month; and if it is still positive, sputum culture and drug susceptibility
testing (DST) should be performed. This will allow a result to be available earlier than the fifth month of treatment.In previously
treated patients, sputum culture DST should be performed if follow-up smear after the intensive phase is positive. In patients treated
with the regimen containing rifampicin throughout treatment, if a positive sputum smear is found at completion of the
intensive phase, the extension of the intensive phase is not recommended.
•
If a patient is found to harbour a multidrug-resistant strain of TB at any time during therapy, treatment is declared a failure and
the patient is re-registered and should be referred to an MDR-TB treatment programme.It is unnecessary, unreliable and wasteful
of resources to monitor the patient by chest radiography. Pulmonary TB patients whose sputum smear microscopy was negative
(or not done) before treatment and whose sputum smears are negative at 2 months need no further sputum monitoring. They shoul d
be monitored clinically; body weight is a useful progress indicator. For patients with extrapulmonary TB, clinical monitoring is
the usual way of assessing the response to treatment.
Int’l Std for TB Care:
•
HIV testing and counseling should be conducted for all patients with, or suspected of having, tuberculosis unless there is a
confirmed negative test within the previous two months. Because of the close relationship of tuberculosis and HIV infection, integrated
approaches to prevention, diagnosis, and treatment of both tuberculosis and HIV infection are recommended in areas with high HIV
prevalence. HIV testing is of special importance as part of routine management of all patients in areas with a high prevalence of HIV
infection in the general population, in patients with symptoms and/or signs of HIV-related conditions, and in patients having a history
suggestive ofhigh risk of HIV exposure.
•
In persons with HIV infection and tuberculosis who have profound immunosuppression (CD4 counts less than 50 cells/mm3),
ART should be initiated within 2 weeks of beginning treatment for tuberculosis unless tuberculous meningitis is present. For all
other patients with HIV and tuberculosis, regardless of CD4 counts, antiretroviral therapy should be initiated within 8 weeks of
beginning treatment for tuberculosis. Patients with tuberculosis and HIV infection should also receive co-trimoxazole as
prophylaxis for other infections.
•
Persons with HIV infection who, after careful evaluation, do not have active tuberculosis should be treated forpresumed latent
tuberculosis infection with isoniazid for at least 6 months.
•
All providers should conduct a thorough assessment for co-morbid conditions and other factors that could affect tuberculosis
treatment response or outcome and identify additional services that would support an optimal outcome for each patient. These
services should be incorporated into an individualized plan of care that includes assessment of and referrals for treatment of other
illnesses. Particular attention should be paid to diseases or conditions known to affect treatment outcome, for exampl e, diabetes
mellitus, drug and alcohol abuse, undernutrition, and tobacco smoking. Referrals to other psychosocial support services or to
such services asantenatal or well-baby care should also be provided.
•
All providers should ensure that persons in close contact with patients whohave infectious tuberculosis are evaluated and managed
in line with internationalrecommendations. The highest priority contacts for evaluation are:
o Persons with symptoms suggestive of tuberculosis
o Children aged <5 years
o Contacts with known or suspected immunocompromised states,particularly HIV infection
o Contacts of patients with MDR/XDR tuberculosis
45
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
WHO Guidelines:
• The first priority for HIV-positive TB patients is to initiate TB treatment, followed by co-trimoxazole and ART.
• Drug susceptibility testing is now recommended at the start of TB therapy in all people living with HIV, to avoid mortality due
to unrecognized drug-resistant TB), and strongly encourages the use of rapid DST in sputum smear-positive persons living with
HIV.
Treatment Outcomes for Drug-susceptible TB Cases
Outcome
Cured
Treatment
completed
Treatment
failed
Died
Lost to
follow-up
Not
Evaluated
Definition
A patient with bacteriologically-confirmed TB at the beginning of treatment and who was smear- or culture-negative in the
last month of treatment and on at least one previous occasion in the continuation phase.
A patient who completes treatment without evidence of failure but with no record to show that sputum smear or culture
results in the last month of treatment and on at least one previous occasion were negative, either because tests were not
done or because results are unavailable.This group includes:
• A bacteriologically confirmed patient who has completed treatment but without DSSM follow-up in the last month of
treatment and on at least one previous occasion
• A clinically diagnosed patient who has completed treatment
A patient whose sputum smear or culture is positive at 5 months or later during treatment.
OR
A clinically diagnosed patient (child or EPTB) for whom sputum examination cannot be done and who does not show
clinical improvement anytime during treatment.
A patient who dies for any reason during the course of treatment.
A patient whose treatment was interrupted for 2 consecutive months or more.
A patient for whom no treatment outcome is assigned. This includes cases transferred to another DOTS facility and whose
treatment outcome is unknown.
LECTURE 8 : SLEEP RELATED BREATHING DISORDERS
46
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
OBSTRUCTIVE SLEEP APNEA (OSA)
INTENDED LEARNING OUTCOME:
1. Discuss respiratory physiology during sleep
2. Recognize the symptoms attributable to a sleep related disorder of breathing
3. Present the clinical evaluation of a patient with SDB
4. Describe the natural course of the disease and the systemic consequences
5. Discuss options for treatment
5.1. lifestyle changes
5.2. oral appliances
5.3. continuous positive airway pressure
5.4. surgical options
Physiologic Impact of sleep on breathing
• minimal in normal individuals
• significant consequences in those with disturbances of respiratory structure or
function
o decreased metabolic drive
o decreased diaphragmatic strength
o decreased intercostal and accessory muscle function activity (in those with
structurally small oropharynx)
Sleep Disordered Breathing (SDB)
• Apnea: Cessation of airflow for at least 10 seconds
• Hypopnea: Reduction in airflow with resultant desaturation of ≥4%
Definitions of SDB
• Apnea-Hypopnea Index (AHI): Averaged frequency of apnea and hypopnea events
per hour of sleep
Types of Sleep Studies
• Type I -in-laboratory, technician-attended, overnight polysomnography (PSG)
• Type II -can perform full PSG outside of the laboratory without a technologist
• Type III -do not record the signals needed to determine sleep stages or sleep
disruption
• Type IV -continuous single or dual bioparameter devices
Obstructive Sleep Apnea
• AHI or RDI ≥15 from portable monitors
• AHI or RDI ≥5 and associated with symptoms (excessive daytime sleepiness,
impaired cognition, mood disorders, insomnia, hypertension, ischemic heart disease,
or history of stroke)
• The presence of respiratory efforts during these events suggests that they are
predominantly obstructive
Treatment
• Oral appliance
• CPAP
• Surgical approach
• Medications
• Risk factor directed treatments (weight reduction, sleep hygiene)
REFERENCES:
47
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Harrison’s Principles of Internal Medicine 20th Edition
Principles of Sleep Medicine, Kryger, Roth and Dement, 4 th Edition
NOTES:
48
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
LECTURE 9 : LUNG CANCER
INTENDED LEARNING OUTCOME:
1. Enumerate the risk factors in the development of lung cancer
2. Discuss the etiopathogenesis of lung cancer
3. Present an algorithm in the evaluation of patient with lung cancer
4. Discuss the advances in the diagnosis and staging of Lung Cancer
5. Discuss the standard treatment of Non-Small Cell and Small Cell Lung Cancer
6. Elaborate on the role of palliative care in the management of patient with Lung Cancer
vis-à-vis standard treatment
Lung Cancer
Lung cancer causes 1.37 million deaths per year worldwide, which represents 18% of all
cancer deaths. Within the European Union, lung cancer is the most frequently fatal
cancer, leading to over 266,000deaths yearly and accounting for 20.8% of all cancer
deaths. Definitive surgery in the early stages is themost effective treatment for lung
cancer. However, most patients are diagnosed at an advanced, and thusnon-curable,
disease stage.
Survival time decreases significantly with progression of disease, with a 5-yearsurvival
time declining from 50% for clinical stage IA to 43%, 36%, 25%, 19%, 7% and 2% for
stages IB, IIA, IIB, IIIA, IIIB and IV, respectively. Moreover, Shi et al.reported a 5-year
survival rate of morethan 80% in 185 surgically treated patients with peripheral smallsized lung cancers (2 cm or less) afterlobectomy and lymph node dissection. In particular,
the 5-year survival rate increased with smallertumour size: 80% in tumours1.6–2.0 cm,
85% in tumours 1.0–1.5 cm and 100% in tumours<1.0 cm indiameter, respectively. It is
49
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
therefore crucial to detect lung cancer early, before symptoms occur and whilecurable
therapy is still achievable.
50
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
REFERENCES:
ESR/ERS Lung Cancer White Paper April 2015.
American Cancer Society. AJCC Lung Cancer Staging 8th Edition.
Harrison’s Principles of Internal Medicine 20thEdition
American College of Chest Physicians (ACCP) Evidence-based Clinical Practice
Guidelines in the Diagnosis and Treatment of Lung Cancer (2nd Edition). Chest 2007:
132
Clinical Practice Guidelines in the Diagnosis and Treatment of Lung Cancer, UST
Benavides Cancer Institute, Thoracic Unit (2007)
51
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
LECTURE 10 : VENOUS THROMBOEMBOLISM (VTE)
INTENDED LEARNING OUTCOME:
1. Define burden of illness and provide a clear definition of terms: Deep vein thrombosis
(DVT), Pulmonary Embolism (PE) and VTE
2. Enumerate the risk factors (Virchow’s Triad) for the development of VTE and cite
predisposing clinical conditions.
3. Discuss the etiopathogenesis of VTE (formation of blood clots from the leg veins to
the lungs) and its consequences on the cardiorespiratory system.
4. Enumerate the clinical manifestations of DVT-PE
5. Discuss the objective evaluation and diagnostic work-up for DVT-PE
5.1. applying the "clinical decision/prediction rule" (Well’s Criteria)
6. Discuss briefly the current and recommended management for VTE using:
6.1. Pharmacologic modalities: a) anticoagulants e.g. heparins (UFH, LMWH),
warfarin, pentassacharides; b) thrombolytics; c) new oral anticoagulants (NOA)
6.2. Non-pharmacologic modalities eg. IVC filter, IPC, GCS, and anti-embolic
stockings (AES).
6.3. PROPHYLAXIS using either pharmacologic or non-pharmacologic
REFERENCES:
Harrison’s Principles of Internal Medicine 21st Edition
Textbook of Respiratory Medicine 5th edition. Murray-Nadel, 2021; 7th Edition
Antithrombotic Therapy for VTE Disease: Antithrombotic Therapy and Prevention of
Thrombosis, 2nd Update to 9th ed: American College of Chest Physicians EvidenceBased Clinical Practice Guidelines. Chest August 2021
Wells (2001) Annals of Intern Med, 135: 98-107; July 2001
NOTES:
52
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
1. DEFINITION
•
•
•
•
Venous Thromboembolism
Venous thromboembolism (VTE) includes deep venous thrombosis (DVT) and pulmonary embolism (PE).
Pulmonary Embolism (PE)- a complication of an underlying disease
▪ It commonly results from venous thrombosis occurring in the deep veins of the lower extremities.
It is the number one preventable cause of death in the hospital.1,2
The incidence of VTE in Asia is perceived to be low compared to Western countries. However, Asian studies
report an incidence of fatal PE ranging from 0.2% to 6%.3
Basic risk factors- Virchow’s triad-stasis, hypercoagulability, and Intimal wall or endothelial injury.
2. ETIOLOGY – ETIOPATHOGENESIS
•
•
•
•
•
•
Venous thrombi start to form either in the vicinity of a venous valve, where eddy currents arise, or at the site
of intimal injury.
Platelets start to aggregate with release of mediators that initiate the coagulation cascade, causing the
formation of a red thrombus.
At any time during the formation of a venous thrombus, a portion or all of the thrombus can detach as an
embolus.
Once embolism occurs, it can trigger very serious pulmonary and cardiac effects (impaired gas exchange;
increased pulmonary vascular resistance), depending on the extent of the reduction of the cross sectional
area of the pulmonary vascular bed as well as the preexisting status of the cardiopulmonary system.
Over 90 percent of cases of acute PE are due to emboli emanating from the proximal veins of the lower
extremities.
Thrombus formed above the popliteal vein e.g. iliofemoral,(above-the-knee, thigh or proximal thrombi) appear
to be the source of most clinically recognized pulmonary embolus.
3.CLINICAL MANIFESTATIONS
•
•
•
•
•
•
Dyspnea / tachypnea
Syncope, hypotension or cyanosis indicates a massive PE
Pleuritic pain, cough, or hemoptysis- small embolism located distally near the pleura.
Physical examination- non specific; may have tachypnea and tachycardia, accentuated P2 component of S2;
recent onset RVH; elevated JVP
No clinical findings are universal and the absence of specific findings does not rule out the diagnosis.
Wells Criteria relies on a carefully taken history and physical examination which consists of seven variables,
namely: (see Appendix)
1-signs-symptoms of DVT
2-PE more likely than alternative diagnosis
3-tachycardia (>100 bpm)
4-surgery or immobilization in last 4 weeks
5-prior DVT or PE
6-hemoptysis
7-active malignancy
4. LABORATORY/ANCILLARY PROCEDURES (see algorithm in Appendix)
•
•
•
Blood tests
▪ A complete blood count(CBC)– may show leukocytosis.
▪ Arterial blood gases (ABGs)–may reveal low oxygen and carbon dioxide levels.
▪ new generation D-dimer assay in combination with the Wells clinical prediction rule is effective in
ruling out clinically significant PE. A negative test using the ELISA technique (e.g. Vidas d-dimer less
than 500 ng/ml) may rule out PE in patients with a low to moderate pretest probability and a
nondiagnostic VQ scan.
Electrocardiography –tachycardia and nonspecific ST-T wave changes.
▪ classic finding of an “S1-Q3-T3” pattern is observed in only 20% of patients with proven PE.
Chest radiography –nonspecific, may be normal
53
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
•
•
•
•
•
•
•
•
•
▪ A peripheral wedge shaped infiltrate (Hampton’s hump)- PE with infarction
▪ Localized decrease in pulmonary vascular markings (Westermark’s sign)
Ventilation-Perfusion Lung Scan – A normal perfusion lung scan virtually excludes PE
▪ high probability lung scan indicates a high likelihood of emboli (95 percent) particularly in patients
with a high pretest probability of pulmonary emboli.
Magnetic Resonance –sensitivity of 85% and specificity of 96% for central, lobar, and segmental emboli.
▪ inadequate for the diagnosis of subsegmental emboli.
Echocardiography –can be used to rule out AMI, tamponade, aortic dissection.
▪ Transesophageal echocardiography (TEE) can show indirect evidence of PE in 80% of patients with
massive PE and central emboli in 70% of cases.
Computed Tomography - can visualize the main, lobar, and segmental pulmonary emboli with a reported
sensitivity of >90%.
CT Pulmonary angiography – remains the gold standard for diagnosis and will be needed in up to 20 percent
of patients with suspected PE and inconclusive noninvasive evaluations. A positive result consists of a filling
defect or sharp cutoff of small vessels. A negative test appears to exclude clinically relevant PE.
Leg studies
Contrast venography – has long been considered the "gold standard" for the diagnosis of DVT (MRA is
emerging as a safe and reliable imaging test for both PE and DVT). In a study of 160 patients suspected
clinically of having DVT in whom contrast venography was negative, only 1.3 % developed DVT during a six
month follow-up.
Impedance plethysmography(IPG) – a noninvasive test which measures venous outflow from the lower
extremity and can detect proximal vein thrombosis with sensitivity and specificity of 91 and 96 percent,
respectively. The IPG has been well validated against the gold standard. Detection of calf vein thrombosis is
poor.
Duplex scan – is the most widely used modality for evaluating patients with suspected DVT. Also known as
Color-flow Doppler imaging or Compression ultrasonography (CU), this noninvasive test is operator
dependent and does not distinguish between old from new clot. In one study of consecutive outpatients with
clinically suspected DVT, CU had a sensitivity and specificity of 100% and 99%, respectively. Like all tests,
ultrasonography for DVT is most useful when the results are combined with an assessment of pretest
probability.
5.MANAGEMENT
PHARMACOLOGIC
Anticoagulants- main treatment regimen; administered to avoid further clot formation in the lower extremities
▪ Unfractionated heparin (UFH) IV or SQ- initial drug of choice
o bolus of 80 IU/kg IV and maintenance infusion at 18 IU/kg.
o duration is usually 7-10 days (5 days is just as effective
o partialthromboplastin time (aPTT) of the patient maintained between 2-3 times the upper limit of the
laboratory normal
▪ Oral anticoagulation with warfarin - may be started on the first day of heparin therapy (usual overlap is 3 - 5 days,
as full effect of warfarin requires 5 days.
o Prothrombin time (PT) should be monitored and the international normalized ratio (INR) target of 2.5, with
a range of 2.0-3.0.
▪ Low molecular weight heparin (LMWH)e.g. enoxaparin.
o Recommended dose is 1 mg/kg of given subcutaneously every 12 hours for up to 3 months in VTE
patients with reversible risk factors.
o For recurrent emboli and nonreversible risk factors, therapy may have to be given indefinitely.
o less bleeding complications from LMWH than UFH
Thrombolytic Therapy
• Streptokinase, Urokinase, and recombinant Tissue Plasminogen activator (rTPA).
• accelerate the resolution of the pulmonary artery clot and may be used especially in patients with massive
embolism and systemic hypotension.
• must be followed by a standard course of heparin treatment
• increased incidence of bleeding.
Newly developed anticoagulant/Antithrombotic Drugs.
• Most are monotherapeutic(specific factor Xa inhibitors e.g.Fondaparinux) in contrast to the LMWH which are
polytherapeutic.
54
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
New oral anticoagulants (NOAC)
• Dabigatran, and rivaroxaban have already been approved for prophylaxis after hip and knee surgery in the US
while, apixaban has been approved in Europe; Rivaroxaban have been approved for VTE treatment as well
Non-Pharmacologic
• IVC filter, intermittent pneumatic compression device (IPC), graduated compression stockings (GCS), and antiembolic stockings (AES).
• Inferior vena cava (IVC) interruption, via filter placement may be used as an alternative therapy for VTE when
absolute contraindications (eg, recent surgery, hemorrhagic stroke, or significant active or recent bleeding) or failure
of anticoagulation are present.
6. PROPHYLAXIS
Pharmacologic
• Unfractionated heparin –SQ, every 8 hrs; needs aPTT monitoring
• Low molecular weight heparin –for both prophylaxis and treatment of patients who present primarily with DVT
with or without concomitant PE.
o Dalteparin and fondaparinux was approved for prophylaxis only but not VTE treatment.
Fondaparinux- Factor Xa inhibitor, pentasaccharide, given for prophylaxis medical patients at 2.5 mg/
subcutaneous q 24hours.
Rivaroxaban- FactorXa inhibitor given for prophylaxis in patient who underwent orthopedic surgery;
dose 10mg/tab per orem once a day.
Non-pharmacologic
• Early ambulation, especially for post-operative patients.
• Graduated elastic compression stockings – provide pressure on the lower extremities, to prevent venous stasis.
• Intermittent pneumatic compression – is a mechanical device attached to the extremities, which provides some
form of passive leg exercises, therefore stimulating muscle contraction.
• Inferior vena caval interruption – a most popular and widely used device is the Greenfield filter.
APPENDIX:
❖ VTE Diagnostic Algorithm (A Practical Approach)
Suspect DVT or PE
Assess Clinical probability
(Wells or Geneva criteria)
DVT
Low-Mod
PE
High
D-dimer
D-dimer
ELISA or Latex
Normal
no DVT
High
Low-Mod
ELISA or Latex
Increased
do ImagingDuplex
Normal
Increased
do ImagingCTPA or VQ
no PE
th
*Algorithm modified by Dr. Villespin from Harrison’s Internal Med 18 ed. 2011_Feb 14, 2013
55
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
I. Wells scoring system for DVT
CLINICAL VARIABLE
Score
Active Cancer
1
Paralysis, paresis, or recent cast
1
Bedridden >3d; major surgery <12 weeks 1
Localized tenderness along the deep veins 1
Unilateral calf swelling>3cm
Unilateral pitting edema
Collateral superficial nonvaricose veins
Alternate dx at least as likely than DVT
1
1
1
-2
Original criteria: (Lancet, 1997; 350: 1795-98)
Score
< 1 point
1-2 points
> 3 points
Risk
Low probability
Moderate probability
High probability
Probability of DVT
3%
17%
75%
Simplified Criteria: (CMAJ, 2006)
1 point- DVT is likely
< 1 point- DVT is unlikely
II. A. Wells Score for PE
CLINICAL FEATURE
Signs &Sx of DVT
PE most likely dx
Hear rate >100
Immobilzation or surgery 4 wks prior
Previous DVT or PE
Hemoptysis
Active Cancer
Total
Points
3.0
3.0
1.5
1.5
1.5
1.0
1.0
12.5
Wells Criteria for PE (Original, 3-tiered)
Risk
Points % Patients with these features Probability of PE (%)
Low
0-2
40
3.6
Moderate ate 3 - 6
53
20.5
High
>6
7
66.7
Wells’ Criteria: (Modified, 2-tiered)
> 4 PE is likely
≤ 4 PE is unlikely
56
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
II. B. Geneva Score(Original, 3-tiered))
The original Geneva score is calculated using 7 risk factors and clinical variables:
Variables
•
•
Score
Age
60 - 79 years
1
80+ years
2
Previous venous thromboembolism
Previous DVT or PE
•
2
Previous surgery
Recent surgery within 4 weeks
•
3
Heart rate
Heart rate >100 beats per minute
•
•
•
•
•
•
1
PaCO2
< 35mmHg
2
35 – 39 mmHg
1
PaO2
< 49 mmHg
4
49 – 59 mmHg
3
60 – 71 mmHg
2
72 – 82 mmHg
1
Chest X-ray
Plate-like atelectasis
1
Elevation of hemidiaphragm
1
< 5 points indicates a low probability of PE
5 - 8 points indicates a moderate probability of PE
> 8 points indicates a high probability of PE
Risk
Points
Low
Moderate
High
0-4
5-8
9 - 12
% Patients with Probability of PE
these features
(%)
49
44
6
10
38
81
EMERGENCY :
57
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
EMERGENCY : RESPIRATORY FAILURE / ARDS
INTENDED LEARNING OUTCOME:
1. Define acute respiratory failure and ARDS
2. Recognize signs and symptoms for the diagnosis of acute respiratory failure and
Acute respiratory distress syndrome
3. Discuss approach to patients with ARF and ARDS
REFERENCES:
Handbook of Medical and Surgical Emergencies, UST
Harrison’s Principles of Internal Medicine 21st Edition
NOTES:
58
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
EMERGENCY : HEMOPTYSIS
INTENDED LEARNING OUTCOME:
1. Define massive hemoptysis
2. Enumerate etiology and differential diagnosis for patients presenting with massive
hemoptysis
3. Discuss approach to patients with massive hemoptysis
Definition
Hemoptysis is defined as the expectoration of blood from the respiratory tract. Massive
hemoptysis is variably defined as the expectoration of 100-600 mL o blood over a 24 hour
period. Varied conditions may present with hemoptysis such as bronchitis, pneumonia,
tuberculosis or bronchogenic carcinoma.
Etiology
Blood may originate from the nasopharynx or the gastrointestinal tract. If the blood is dark
red in appearance with an acidic pH it is a clue that its origin is the GI tract. True
hemoptysis is bright red in appearance and alkaline in pH.
Differential Diagnosis
Source other than the lower respiratory tract
Upper airway bleeding
GI bleeding
Tracheobronchial source
Neoplasm
Bronchitis
Bronchiectasis
Foreign body
Pulmonary parenchymal source
Lung abscess
Pneumonia
TB
Lupus pneumonitis
Pulmonary vascular source
AV malformation
Pulmonary embolism
Miscellaneous
Pulmonary endometriosis
Systemic coagulopathy
59
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Approach to a patient with Hemoptysis
REFERENCES:
Harrison’s Principles of Internal Medicine 21st Edition
Murray and Nadel’s Textbook of Respiratory Medicine
60
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
EMERGENCY : MASSIVE PULMONARY EMBOLISM
INTENDED LEARNING OUTCOME:
1. Define massive pulmonary embolism.
2. Utilize algorithms in the diagnosis of massive pulmonary embolism.
3. Discuss the use of thrombolytic therapy in massive pulmonary embolism.
Massive pulmonary embolism is defined as an acute pulmonary embolism(PE) with
sustained systemic arterial hypotension.1 Proposed definition according American Heart
Association is acute PE with sustained hypotension (systolic blood pressure <90 mm Hg
for at least 15 minutes or requiring inotropic support, not due to a cause other than PE,
such as arrhythmia,hypovolemia, sepsis, or left ventricular [LV] dysfunction),
pulselessness, or persistent profound bradycardia (heart rate <40 bpm with signs or
symptoms of shock).1Of the number of cases of Venous Thromboembolism (VTE), 10%
is estimated to be classified as massive pulmonary embolism.2 This makes it pertinent to
be able to diagnose and manage massive PE adequately.
Only confirmed venous thromboembolism should receive thrombolytic therapy since this
is coupled with major risks. Thrombolytics in addition to heparin anticoagulation as
treatment for Massive PE requires individualized assessment of the balance of benefits
versus risks.2 Potential benefits include rapid resolution of symptoms (eg, dyspnea, chest
pain, and psychological distress), stabilization of respiratory and cardiovascular function
without need for mechanical ventilation or vasopressor support, reduction of RV damage,
improved exercise tolerance, prevention of PE recurrence, and increased probability of
survival. Risks include disabling or fatal hemorrhage in the form ofintracerebral
hemorrhage, and increased risk of minor hemorrhage, which results in prolonged hospital
stay and need for blood transfusions.2Once it is decided that thrombolytic therapy is
warranted, it is recommended that the thrombolytic agent be administered by a peripheral
venous catheter, rather than a pulmonary arterial catheter (Grade 2C). The thrombolytic
regimen infusion time should be short (ie, ≤2 hours), rather than a regimen with a more
prolonged infusion time (Grade 2C).1
Aside from medical management, either catheter embolectomy and fragmentation or
surgical embolectomy is reasonable for patients with massive PE and contraindications
to fibrinolysis (Class IIa; Level of Evidence C). Offering these would depend upon the
expertise of the medical institution.1Another indication for catheter embolectomy and
fragmentation or surgical embolectomy is in massive PE who remain unstable after
receiving fibrinolysis (Class IIa; Level of Evidence C). 2
REFERENCES:
1
Christophe Marti et al. Eur Heart J 2015;36:605-614
2Jaff, M. et al. Circulation. 2011; 123: 1788-1830
3Vyas and Donato& Thrombolysis in Acute Pulmonary Thromboembolism
Southern Medical Journal & Volume 105, Number 10, October 2012
4Kearon C, Akl EA, Comerota AJ, et al. Antithrombotic therapy for VTE disease:
Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of
Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest 2012; 141:e419S.
61
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
WORKSHOP :
WORKSHOPS 1 : CLINICO-RADIOLOGIC CORRELATION
INTENDED LEARNING OUTCOME:
1. Interpret chest radiographs using ATMLL approach
2. Correlate the radiographic findings with historical data and physical examination findings
with emphasis on IPPA
3. Recommend initial management
1.
2.
3.
4.
5.
6.
7.
8.
9.
Emphysema
Pneumothorax
Consolidation
Obstructive Atelectasis
Cicatricial Atelectasis
Effusion
Cavitary TB
Bronchiectasis
Metastatic lesions
Clinico-Radiologic Correlation
Are There Many Lung Lesions?
A
1. costophrenic sulci
2. contour of hemidiaphragm
3. level of hemidiaphragm (R usually higher than left)
T
1. symmetry of thoracic cage / ICS
2. rib fractures
M
1. trachea
2. heart
3. hilar (L usually higher than left)
LL
1. compare one lung to the other lung
Emphysema
A – flat/depressed hemidiaphragm; low set
T – widened interspaces
M – dropped heart – investigate for Pulmonary hypertension (look at Pulmonary
arteries)
LL – hyperluscent lungs, +/- bullae, pruning of blood vessels
62
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Pneumothorax
A – +/- flattening of one hemidiaphragm on the side of the pathology; +/- blunting of
costophrenic sulcus (secondary to bleeding)
T – +/- widened interspaces on affected side
M – +/- shifting of midline structures contralaterally
LL – presence of visible visceral pleural line- radiographic hallmark
Consolidation
A
T
M
LL
– may be normal
– normal
– +/- silhouette sign depending on the lobe involvement
– presence of air bronchograms
Obstructive Atelectasis
A – hemidiaphragm may be affected depending on the size of atelectasis
T – +/- narrowed interspaces on affected side with compensatory widening on opposite
side
M – +/- shifting of midline structures ipsilaterally
LL – homogenous opacification of affected area
Cicatricial Atelectasis
A – hemidiaphragm may be affected depending on the size of atelectasis
T – +/- narrowed interspaces on affected side with compensatory widening on opposite
side
M – +/- shifting of midline structures ipsilaterally
LL – inhomogenous opacification of affected area, with air bronchograms
Effusion
A – blunting of costophrenic sulcus, or non visualization of hemidiaphragm, due to
presence of fluid
T – +/- widened interspaces on affected side (may be hard to visualize because of the
presence of fluid)
M – +/- shifting of midline structures contralaterally depending on amount of fluid as
well as presence of any other underlying lung pathology
LL – homogenous opacification with a lateral upward curve (meniscus sign)
-on lateral decubitus view – the homogenous density (fluid) occupies the most
dependent portion of the chest wall (layering) if it is FREE within the pleural space
Cavitary Tuberculosis
A
T
M
LL
– costophrenic sulci not affected unless there is concomitant effusion or thickening
– interspaces not affected unless there is also volume loss/ atelectasis
– +/- shifting of midline structures depending on volume loss
– lucency within the lung parenchyma usually with an irregular margin.
Bronchiectasis
A
T
M
LL
– costophrenic sulci not affected unless there is concomitant effusion or thickening
– interspaces not affected unless there is also volume loss/ atelectasis
– +/- shifting of midline structures depending on volume loss
– honeycomb densities
63
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Metastatic lesions
A
T
M
LL
– costophrenic sulci not affected unless there is concomitant effusion or thickening
– interspaces not affected unless there is also volume loss/ atelectasis
– +/- shifting of midline structures depending on volume loss
– cannon ball appearance; brocnhoalveolar spread; multiple nodules
Insp
+/- lagging
Palp
Inc TF
Perc
Dull
Auscult
Inc BS
Bronchophony,
egophony,
whispered
pectoriloquy
shift
None
Obstructive
atelectasis
+/- lagging
Dec TF
Dull
Dec BS
Ipsi
Pleural
effusion
+/- lagging
Dec TF
Dull
Dec BS
Contra
Pneumothorax
+/- lagging
Dec TF
Hyper
resonant
Dec BS
Contra
Emphysema
Minimal chest
movement
Dec TF
Hyper
resonant
Dec BS
bilaterally
None
Cicatricial
atelectasis
+/- lagging
Inc TF
Dull
Inc BS
Ipsi
Consolidation
NOTES:
64
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
WORKSHOP 2 : ABG / CLINICO-RADIOLOGIC CORRELATION
INTENDED LEARNING OUTCOME:
1. Learn the usefulness of the arterial blood gas
2. Know the normal values
3. Interpret arterial blood gases
4. Present a simple algorithm in the interpretation of ABG results
5. Apply various equations to blood gas interpretation and clinical management
Mechanics: The students will be divided into 3 groups. Each facilitator will discuss the
2 cases of ABG with the chest x-rays.
CASE 1
A 79 y.o male, smoker came in because of dyspnea. There was use of accessory
muscles of respiration. BP 120/80 CR 90/min RR 14/min.
ABG RESULT: (at 4 LPM oxygenation)
7.33
63
100
29
98
78
0.56
278
0.26
QUESTIONS:
1. Interpret the ABG. Look at –
a. pH
b. PCO2
c. PaO2
d. HCO3
ANSWER:
2. Is the patient hypoxemic?
ANSWER:
3. What is the oxygenation status?
a. P/F ratio of the patient?
b. Expected P/F of the patient?
c. a/A
pAO2 = 713 x FiO2 – pCO2/0.8
65
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
pAO2 =
a/A = paO2/pA02
ANSWER: a/A =
d. AaDO2
AaDO2 = pAO2 – paO2
AaDO2 =
4. What is the cause of the hypoxemia? (Refer to the algorithm)
CASE 2
A 60 y.o male was rushed to the emergency room because of 3 day history of dyspnea,
increased cough and sputum production. He had BP 130/80mmHg, HR 110 regular, RR
32, T 36.6C, oxygen saturation 70% at room air. He had supraclavicular retractions,
paradoxical breathing and peripheral cyanosis, rhonchi and wheezes on both lung fields.
He was intubated and hooked to the mechanical ventilator with the following set up: TV
400, RR 12 (with actual RR of 25) FIO2 of 50%. Chest x-ray done one day ago (show xray to students, ask them to
1.
Interpret using ATMLL: Diagnosis: ______________________
2.
A –
T –
M –
LL –
What are the expected IPPA findings?
Insp
Palp
Perc
Auscult
3.
Explain PE based on sound transmission principles
4.
What in the cxr is pathognomonic of lobar consolidation?
5.
What is the most common organism involved?
shift
66
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
ABG RESULT: (at 50% FIO2)
QUESTIONS:
1. Interpret the ABG. Look at –
a. pH
b. PCO2
c. PaO2
d. HCO3
ANSWER:
2. What is the oxygenation status?
a. P/F ratio of the patient?
ANSWER:
b. Expected P/F of the patient?
ANSWER:
c. a/A
pAO2 = 713 x FiO2 – pCO2/0.8
ANSWER:
d. AaDO2
AaDO2 = pAO2 – paO2
AaDO2 =
ANSWER:
3. What is the desired Fio2 of this patient?
dFio2 = expected pO2 + pCO2
a/A
0.8
713
67
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
dFiO2 =
=
ANSWER:
4. How would we correct the hypoventilation?
Remember:
●
●
●
VA = Ve - Vd
●
Ve = Vt x RR
ANSWER:
5. Which caused the hypoxemia of the patient?
a. Shunt
b. Hypoventilation plus another mechanism
c. VQ mismatch
d. Diffusion
ANSWER:
68
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Reference:
Harrison’s Principles of Internal Medicine 19thEdition
Notes:
69
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
70
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
ARTERIAL BLOOD GAS
MAIN INDICATIONS
1. to know the ventilatory status of the patient (acid base balance)
2. to know the oxygenation status of the patient
1. Ventilatory status / acid base
• pH pCO2
• HCO3
2. Oxygenation status
a. PaO2
b. O2 sat
c. aAO2
d. p(A-a)O2
e. P/F
IMPORTANT EQUATIONS:
1. Henderson - Hasselbach
pH= 6.1 + log HCO3 / PaCO2 x 0.03
2. Alveolar Equation
VA = VCO2 / PaCO2 x K
VA = 1 / PaCO2
3. Alveolar Gas Equation
PAO2 = FiO2 (PB – PH2O) – PACO2 / R
PAO2 = FiO2 (713) – PACO2 / 0.8
4. Alveolar–arterial oxygen difference normal p(A-a)O2 = 15 +/- 5 torr
P(A-a)O2
P(A-a)O2 = PAO2 – PaO2
PAO2 is computed for using equation #3
PaO2 is derived from ABG results
5. Arterial alveolar ratio
aAO2
normal aAO2 = 0.75
PaO2 is derived from the ABG result
PAO2 is computed for using equation #3
6. P/F ratio
PaO2 / FiO2
PaO2 is derived from the ABG result
FiO2 is the fraction of inspired oxygen being
given to the patient
Normal values
for patients < 60 y.o.
for patients > 60 y.o.
expectedP/F = 400
expected P/F = 400 – (years above 60 x 5)
7. LPMto FiO2
8. Desired FiO2
LPM x 4 + 20
- compute for PAO2 (equation # 3)
- compute for aAO2 (equation # 5)
- compute for desired FiO2
desired PaO2*
+
aAO2
PaCO2
0.8
desired FiO2 =
713
• desired PaO2 is usually 80-100
71
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
INTERPRETING THE ARTERIAL BLOOD GAS
1. IS THE ABG NORMAL OR ABNORMAL?
Normal values:
pH
7.35 – 7.45
pCO2 35- - 45
pO2*
80 – 100
HCO3
22 – 27
O2 sat > 95%
2. IF THE ABG IS NORMAL, GREAT!
3. IF THE ABG IS ABNORMAL, PROCEED WITH INTERPRETATION OF THE ACID BASE
BALANCE AND OXYGENATION
VENTILATORY/ ACID BASE STATUS
1. Is the problem ACIDEMIA or ALKALEMIA?
pH< 7.4 = acidemia
pH> 7.4 = alkalemia
2. Is the primary disturbance RESPIRATORY or METABOLIC?
• correlate the pH with the pCO2 and HCO3
• a high pCO2 leads to acidemia, while a low pCO2 leads to alkalemia
• a high HCO3 leads to alkalemia, while a low HCO3 leads to acidemia
3. Is it UNCOMPENSATED, PARTIALLY, OR FULLY COMPENSATED?
Respiratory acidosis
Alkalosis
Metabolic acidosis
Alkalosis
Primary disturbance
high pCO2
low pCO2
Compensation
HCO3 will increase
HCO3 will decrease
low HCO3
high HCO3
pCO2 will decrease
pCO2 will increase
UNCOMPENSATED - there is no movement of either the pCO2 or the HCO3 in response to the
primary disturbance
PARTIALLY COMPENSATED - there is movement of the pCO2 or HCO3 in an attempt to
correct the primary disturbance, but the movement is not enough to normalize the pH
COMPENSATED - there is movement of the pCO2 of HCO3 to correct the primary disturbance,
and the increase or decrease is enough to normalize the pH
72
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
OXYGENATION STATUS
1. Is the patient HYPOXEMIC?
• a normal pO2 DOES NOT MEAN that there is no hypoxemia in a patient on
supplemental oxygen
• the other indices of oxygenation have to be considered
• any time a patient has a pO2 > 100, he is probably receiving supplemental oxygen
OXYGENATION
AT ROOM AIR FiO2 = 21%
1. patients< 60 y.o. expected PaO2 = 80 – 100
2. patients> 60 y.o. expected PaO2 = 80 – years above 60
3. compare PaO2 value in ABG to the expected
4. if actual < expected, patient is hypoxemic
ON SUPPLEMENTAL OXYGEN
1. check aAO2, p(A-a)O2 and P/F ratio
expected aAO2 > 0.75
expected p(A-a)O2 = 15 + 5
expected P/F
for patients < 60 years old = 400
for patients > 60 years old = 400 – (yrs above 60 x 5)
2. Is the patient receiving the desired FiO2?- compute for desired FiO2 using equation #8 in
previous page
73
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
WORKSHOP 3: SPIROMETRY / INHALER GADGETS / PEAK FLOW
STATION 1: SPIROMETRY
INTENDED LEARNING OUTCOME:
At the end of the session the participants will:
1. Know how a spirometry test is performed.
2. Be able to generate a good spirometry test.
3. Be able to discern whether a spirometry test is of good quality.
Acceptability Criteria:
1. Good start (extrapolated volume < 150 ml)
2. Good end [FET > 6 sec. & Plateau (< 25 ml/ sec)]
3. No artifacts (smooth curve)
Reproducibility Criteria:
1. There should be at least 3 acceptable trials
2. Two largest acceptable FVC: 150 ml with each other
3. Two largest acceptable FEV1: 150 ml with each other
74
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
STATION 2: INHALER GADGETS
INTENDED LEARNING OUTCOME:
At the end of the session, the participants will:
1. Be familiar with the different inhaler gadgets, their uses, advantages and
disadvantages.
2. Be able to demonstrate proper use of the different inhaler gadgets.
I.
Types of inhaler gadgets.
1. Metered dose inhalers
a. Pressurized Metered Dose Inhaler (pMDI)
i. Rapihaler
ii. Ventolin pMDI
b. Soft-mist pMDI
i. Respimat
2. Dry powder inhalers
a. Single unit dose
i. Rotahaler
ii. Breezhaler
b. Multi-dose reservoir
i. Turbohaler
ii. Nexthaler
c. Multi-unit dose
i. Diskus
ii. Elipta
II.
Proper inhalation technique for each type of device.
• pMDI
1. Shake 4 or 5 times if suspension formulation.
2. Take the cap off.
3. Prime the inhaler.
4. Exhale slowly, as far as comfortable.
5. Hold the inhaler in an upright position.
6. Immediately place the inhaler in the mouth between the teeth, with the tongue
flat under the mouthpiece
7. Ensure that the lips have formed a good seal with the mouthpiece
8. Start to inhale slowly, through the mouth and at the same time press the
canister to actuate a dose.
9. Maintain a slow and deep inhalation, through the mouth, until the lungs are
full of air. This should take an adult 4-5 secs.
10. At the end of the inhalation, take the inhaler out of the mouth and close the
lips.
11. Continue to hold breath for as long as possible, or up to 10 sec before
breathing out.
12. Breathe normally.
13. If another dose is required, repeat steps 4-12.
•
1.
2.
3.
DPI
Take the cap off (some do not have a cap).
Follow the dose preparation instructions in the PIL.
Do not point the mouthpiece downwards once a dose has been prepared for
inhalation because the dose could fall out.
75
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
4. Exhale slowly, as far as comfortable (to empty the lungs). Do not exhale into
the DPI.
5. Start to inhale forcefully through the mouth from the very beginning. Do not
gradually build up the speed of inhalation.
6. Continue inhaling until the lungs are full.
7. At the end of inhalation, take the inhaler out of the mouth and close the lips.
Continue to hold breath for as long as possible or up to 10s.
III.
Controller and Reliever medications.
•
CONTROLLER MEDICATIONS
o ICS/ LABA▪ Salmeterol + Fluticasone
• Diskus/ Accuhaler
• Metered dose inhaler
▪ Formoterol + Budesonide
• Turbuhaler (may also be used as rescue medication)
o LABA/LAMA
▪ Umeniclidium + Vilanterol
•
o Long acting anticholinergic (for COPD)
▪ Tiotropium
• Handihaler
• Soft-mist inhaler
•
RESCUE/RELIEVER MEDICATIONS
o Short acting B agonists
▪ Salbutamol
• Metered dose inhaler
• Rotacap
• Nebules
▪ Terbutaline
• Metered dose inhaler
• Turbuhaler
o Anticholinergic/ SABA
▪ Salbutamol / ipratropium
• Metered dose inhaler
76
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
STATION 3: PEAK FLOW
INTENDED LEARNING OUTCOME:
At the end of the session, the students will be able to:
1. Enumerate indications for peak flow monitoring
2. Demonstrate proper technique for doing peak flow
3. Compute for peak flow variability
4. Interpret results of peak flow values
PEAK FLOW MONITORING
• May help confirm the diagnosis of asthma
•
60 L/min (or 20% or more pre-BD PEF) post BD
•
diurnal variation > 20% (for bid values > 10%)
•
Improves control of asthma specially in patients with poor perception of
symptoms
•
May help identify environmental (including occupational) causes of asthma
symptoms
•
Advantages: portable, simple to use, may be used at home
•
Disadvantage: may not correlate directly with FEV1- may underestimate degree
of airflow limitation
PEAK FLOW VARIABILITY COMPUTATIONS
• maximum – minimum divided by mean daily average
•
minimum am pre-BD divided by recent best- most useful clinically
NOTES:
77
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
PEAK FLOW RESULTS 1
PATIENT A – 20-year-old college student complaining of episodes of chest tightness
and exertional dyspnea, especially during the “ber” months. She does not smoke, but
her boyfriend is a chain smoker. FH is (-) for Asthma but her sister has Allergic Rhinitis.
PE is unremarkable.
She could not schedule her spirometry as she was in the middle of exam week so was
asked to monitor her peak flow for 1 week and bring back the results
PEAK FLOW VALUES*
AM
Pre BD
Post BD
PM
Pre BD
Post BD
Day 1
300
300
320
340
Day 2
300
310
300
330
Day
3`
Day 4
310
320
340
350
300
310
340
350
Day 5
310
310
330
350
Day 6
300
310
340
360
Day 7
310
310
350
360
RESULT
AVERAGE
* These tests can be repeated during symptoms or in the early morning. Daily diurnal PEF variability is
calculated from twice daily PEF as ([day’s highest minus day’s lowest]/mean of day’s highest and lowest)
and averaged over a week.
Excessive variability in twice-daily PEF over 2 weeks
• Adults: average daily diurnal PEF variability > 10%
• Children: average daily diurnal variability > 13%
Notes:
USE COMPUTATION #1
78
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
PEAK FLOW RESULTS 2
PATIENT B – 37-year-old pharmacist, diagnosed to have Asthma 3 years ago. She
denies any shortness of breath and says that she hasn’t had any significant Asthma
attacks in the past 2 years. She takes Montelukast prn.
She consults because she has been having non-productive cough for the past 2 weeks,
which wakes her up at night. PE is normal. She was asked to monitor her peak flow for
1 week.
PEAK FLOW VALUES personal best = 350
AM
PM
Pre BD
Post BD
Pre BD
Day 1
250
270
300
Post BD
320
Day 2
260
270
300
330
Day 3`
250
280
310
320
Day 4
290
290
320
330
Day 5
280
290
330
330
Day 6
280
290
320
340
Day 7
270
300
320
340
RESULT
AVERAGE
Notes:
USE COMPUTATION #2
79
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
WORKSHOP 4: LUNG ULTRASOUND
INTENDED LEARNING OUTCOME:
1. Identify normal lung ultrasound findings on B mode and M mode
2. Note for movement of the diaphragm on normal respiration
3. Visualize movement of diaphragm on ultrasound on normal, deep inspiration and
shallow inspiration
Instructions: Students will be grouped by subsection. Their respective facilitators with a
faculty lead will help the students during the session, which will last for 30 minutes. There
will be 2-3 subsections at a time which will be scanning the standardized patient, taking
note of the following:
1. Lung Sliding
a. Position of standardized patient/ subject: Supine
b. Ultrasound probe: high frequency 12L/ Linear
c. Mode: B mode (brightness mode)
d. Note for Bat sign
e. Note for lung sliding on inspiration and expiration
f. Note for a “somewhat” disappearance of this lung sliding when you ask the
subject to hold his/her breath
g. Note for:
• A lines
• B lines
• Comet tails
• Bat sign
h. Mode: M mode (motion mode)
• Sea-shore sign: normal
• Bar code sign/ stratosphere sign: pneumothorax
i. Output: An image of the normal sliding of your standardized patient
2. Diaphragm movement on inspiration and expiration
a. Position of standardized patient/ subject: Supine
b. Ultrasound probe: Low frequency/ curvilinear probe
c. Mode: B mode (brightness mode)
d. How to scan: Anterior-axillary line on the right; Mid-Posterior axillary line; 5th8th ICS on the left; use spleen or liver as acoustic window and angle probe
toward the spine
e. Note for diaphragm moving on inspiration- caudad movement of mirror image
artifact
f. Note for diaphragm moving on expiration- cephalad movement of mirror image
artifact
g. Note for difference of motion of diaphragm on deep, normal and shallow
inspiration. Freeze a good image of each of the three maneuvers.
h. Output: Image of the diaphragm during normal, deep and shallow inspiration.
3. Femoral and Popliteal Vein Scanning
a. Position the Standardized patient/subject: supine or sitting
b. Ultrasound Probe: High Frequency/ Linear probe
c. Mode: B Mode (Brightness Mode)
d. How to Scan: Femoral Area: With the probe indicator oriented to the right
of the patient, on transverse orientation from the inguinal area lightly scan
to visualize the Mickey Mouse sign which comprise: the Femoral Artery
(appears round in cross section with strong pulsations and non
compressible); saphenous vein (compressible) and Femoral vein
80
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
(compressible). Patient should be in a supine position with legs relaxed or
internally rotated.
Popliteal Area: With the probe indicator oriented to the right of the patient,
on transverse orientation from the popliteal crease, lightly scan to visualize
the popliteal vein and artery with the popliteal vein which is compressible.
Patient may be in a sitting position with legs hanging from the edge of the
bed.
REFERENCES:
Ultrasound Institute, University of South Carolina, USA
You may access: Overview of Lung Ultrasound
https://www.youtube.com/watch?v=WOlz8-km6hE
81
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
TBL 1
ASTHMA: TEAM-BASED LEARNING FOR THIRD YEAR MEDICAL STUDENTS
PURPOSE:
This team-based learning (TBL) module focuses on the diagnosis and management of
patients with asthma in the primary care and ER settings. The students will work as a
group in discussing the case.
EDUCATIONAL OBJECTIVES:
By the end of this session, learners will be able to:
1. Complete a structured clinical assessment of a patient with symptoms suggestive of
asthma, identifying the likelihood of asthma diagnosis.
2. Consider alternate diagnoses for patients presenting with respiratory symptoms.
3. Assess asthma control and asthma severity.
4. Apply stepwise approach to asthma therapy.
5. How to identify patients who are at high risk of a life-threatening asthma attack
6. Manage asthma in the primary care and ER setting.
FORMAT:
1. Individual Readiness Assessment Test (iRAT)
2. Team Readiness Assessment Test (tRAT)
3. Discussion of Answers
4. Team Application (Tapp)
5. Discussion of Case Application
6. Post Test
REFERENCES:
Barnes, P. (2018). Asthma In: Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo
DL, Loscalzo J. eds.Harrison's Principles of Internal Medicine, 20e (pp. 19571969) New York, NY: McGraw-Hill;
http://0-accessmedicine.mhmedical.com.ustlib.ust.edu.ph/content.aspx?
bookid=2129&sectioned=159313747. Accessed August28, 2019.
2020 GINA Report, Global Strategy for Asthma Management and Prevention.
(https://ginasthma.org/gina-reports/)
82
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
TBL 2
DYSPNEA (CARDIO-PULMO INTEGRATION):
TEAM-BASED LEARNING ON FOR THIRD YEAR MEDICAL STUDENTS
PURPOSE:
To enhance the ability of third-year medical students to assess the causes of and
treatments for common causes of dyspnea
OBJECTIVES:
1. To create a differential diagnosis (>1 possible etiology) for causes of dyspnea from
common illness scripts representative of typical patients encountered on Internal
Medicine services
2. To infer a differential diagnosis to guide initial testing to evaluate for common causes
of dyspnea
3. To associate what types of initial therapy are required for the common causes of
dyspnea
4. To demonstrate critical thinking skills in coming up with management of the case
presented based on physical exam findings, imaging modalities, and laboratory
studies.
FORMAT:
1. Individual Readiness Assessment Test (iRAT)
2. Team Readiness Assessment Test (tRAT)
3. Discussion of Answers
4. Team Application (Tapp)
5. Discussion of Case Application
6. Post Test
ADVANCED PREPARATION:
Cardio and Pulmo Module Notes / Workbooks
83
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
ADDITIONAL NOTES:
BRONCHIAL ASTHMA
Clinical Presentation
Asthma is a heterogeneous clinical syndrome affecting the lower respiratory tract. It
presents as episodic or persistent symptoms of wheezing, dyspnea, air hunger, and
cough. Symptoms may be precipitated or exacerbated by exposure to allergens and
irritants, viral upper respiratory tract infections, bacterial sinusitis, exercise, and cold air.
Nocturnal symptoms indicate more severe disease, causing awakening in the early
morning hours (for those with a normal diurnal schedule). The clinical presentation of
asthma is variable with respect to severity, underlying pathogenic mechanisms, effect on
quality of life, and responsiveness to treatment.
Risk Factors
Risk factors for asthma include heredity, exposure to environmental tobacco smoke, viral
infections in the first 3 years of life, and socioeconomic factors such as income level, the
presence of cockroach or rodent infestations in the home, and access to medical care.
Heritable factors include genes regulating IgE-related mechanisms, glucocorticoid
response, airway smooth muscle development (ADAM33) and components of the
immune system (HLA-G).Tobacco smoke is a common exacerbating factor in patients
with asthma.
Physical Examination
Physical findings in stable asthma are nonspecific, and physical examination findings can
be normal when the patient is well. Poorly controlled asthma may exhibit auscultatory
wheezing or rhonchi, but the intensity of wheezing is a poor indicator of the severity of
either airflow obstruction or disease pathology. In an acute exacerbation of asthma,
tachypnea, pulsus paradoxus, cyanosis, and use of accessory muscles of respiration may
be evident.
Differential Diagnosis
Upper respiratory tract Vocal cord dysfunction
Congestive rhinopathy
Obstructive sleep apnea syndrome
Lower respiratory tract Chronic obstructive pulmonary disease
Occupational bronchitis
Cystic fibrosis
Bronchiectasis
Pneumonia
Gastrointestinal tract
Gastroesophageal reflux disease
Cardiovascular system
Congestive heart failure
Pulmonary hypertension
Chronic thromboembolic pulmonary disease
Central nervous system
Habitual cough
Diagnosis
Spirometry is the most important diagnostic procedure for evaluating airway obstruction
and its reversibility. It should be performed in all patients in whom asthma is a diagnostic
consideration. The maximal volume of air forcibly exhaled from the point of maximal
inhalation (forced vital capacity, FVC), the volume of air exhaled during the first second
84
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
of this maneuver (FEV1), and FEV1:FVC ratio are 3 key measures. An FEV1:FVC ratio
less than the lower limit of normal (0.7-0.8 in adults, depending on age) indicates airway
obstruction. Reversibility of airway obstruction is indicated by an increase in FEV1 of 200
mL or greater and 12% or greater from baseline after inhalation of short-acting β2agonists.
Management
Please refer to pages 76-85 for relevant algorithms, treatment options and management
steps based on the Global Initiative for Asthma.
REFERENCES:
Global Initiative for Asthma 2019.
McCracken JL. Et. al; Diagnosis and management of Asthma in Adults: A Review. JAMA
2017;318(3):279-290
Diagnostic flowchart for diagnosing asthma
Reference:
1. 2020 GINA Report, Global Strategy for Asthma Management and Prevention
(https://ginasthma.org/gina-reports/)
2. Philippine Consensus Report on Asthma Diagnosis and management 2019
85
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Table 1 (Australian Asthma Handbook v1.1 Section 1.1 asset ID: 4)
Investigating asthma-like symptoms
Taking a History
Type
Recommendation
Consensus
Consider asthma in adults with (any of):
recommendation*
• episodic breathlessness
• wheezing
• chest tightness
• cough
Consensus
Ask about:
recommendation*
• current symptoms (both daytime and night-time)
• pattern of symptoms (e.g. course over day, week or year)
• precipitating or aggravating factors (e.g. exercise, viral infections,
ingested substances, allergens)
• relieving factors (e.g. medicines)
• impact on work and lifestyle
• home and work environment
• smoking history (tobacco, cannabis, exposure to other people’s
smoke)
• past history of allergies including atopic dermatitis (eczema) or
allergic rhinitis
(“hay fever”)
• family history of asthma and allergies
Consensus
When respiratory symptoms are not typical, do not rule out the possibility
recommendation* of asthma without doing spirometry, because symptoms of asthma vary
widely from person to person
*Based on clinical experience and expert opinion (informed by evidence, where available)
Table 2 (Australian Asthma Handbook v1.1 Section 1.1 asset ID: 4)
Findings that increase or decrease the possibility of asthma in adults
Asthma is more likely to explain the symptoms if any of
these apply
Asthma is less likely to explain the symptoms if any of
these apply
More than one of these symptoms
•
wheeze
•
breathlessness
•
chest tightness
•
cough
Symptoms recurrent or seasonal
Symptoms worse at night or seasonal
History of allergies (e.g. allergic rhinitis, atopic dermatitis)
Dizziness, light headedness, peripheral tingling
Symptoms obviously triggered by exercise, cold air, irritants,
medicines (e.g. aspirin or beta-blockers), allergies; viral
infections, laughter)
Family history of asthma or allergies
Symptoms began in childhood
Widespread wheeze audible on chest auscultation
FEV1 or PEF lower than predicted without other explanation
Isolated cough with no other respiratory symptoms
Chronic sputum production
No abnormalities on physical examination of chest when
symptomatic (over several visits)
Change in voice
Symptoms only present during respiratory tract infections
Heavy smoker (now or in past)
Cardiovascular disease
Normal spirometry or PEF when symptomatic (despite
repeated tests)
Eosinophilia or raised blood IgE level without other
explanation
Symptoms rapidly relieved by a SABA bronchodilator
Table adapted from:
Respiratory Expert group. Therapeutic guidelines Limited. Therapeutic Guidelines: Respiratory Version4. Therapeutic Guidelines Limited. Melbourne, 2009.
British Thoracic Society (BTS) Scottish Intercollegiate Guidelines Network (SIGN). British Guidelines on the Management of Asthma. A national clinical
guideline. BTS. SIGN. Edinburgh; 2012
86
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Australian Asthma Handbook v1.1 asset ID:2
Table 3 Confirmed variable airflow limitation
Documented excessive variability in lung
function* (one or more of the tests below)
AND documented expiratory flow limitation*
Positive bronchodilator (BD) reversibility test*
(more likely to be positive if BD medication is
withheld before test: SABA ≥4 hours, LABA≥15
hours)
Excessive variability in twice-daily PEF over 2
weeks*
Significant increase in lung function after 4
weeks of anti-inflammatory treatment
Positive exercise challenge test*
Positive bronchial challenge test
(usually performed only in adults)
The greater the variation or the more occasions
excess variation is seen, the more confident the
diagnosis
At a time when FEV1 is reduced, confirm FEV1/FVC is
reduced (it is usually >0.75 – 0.80 in adults)
Adults: increase in FEV1 of > 12% and > 200 mL from
baseline, 10-15 minutes after 200-200 mcg Albuterol
(Salbutamol) or equivalent (greater confidence if
increase is > 15% and > 400 mL)
Children: increase in FEV1 of > 12% predicted
Adults: average daily diurnal variability > 10%**
Children: average daily diurnal PEF variability > 13%**
Adults: increase in FEV1 by 12% and > 200 mL (or PEF
by 20%) from baseline and after 4 weeks of treatment,
outside respiratory infections
Adults: fall in FEV1 of >10% and >200 mL from baseline
Children: fall in FEV1 of > 12% predicted or PEF > 15%
Fall in FEV1 from baseline of ≥20% with standard dose
of methacholine or histamine, or ≥15% with
standardized hyperventilation, hypertonic saline or
mannitol challenge
BD: bronchodilator (short-acting SABA or rapid-acting LABA); FEV1: forced expiratory volume in 1 second; LABA:
long-acting beta2-agonist; PEF: peak expiratory flow (highest of three readings); SABA: shirt-acting beta2-agonist.
* These tests can be repeated during symptoms or in the early morning. Daily diurnal PEF variability is calculated
from twice daily PEF as ([day’s highest minus day’s lowest]/mean of day’s highest and lowest) and averaged over a
week. For PEF, use the same meter each time as PEF may vary by up to 20% between meters. BD reversibility may
be lost during severe exacerbations or viral infections, and airflow limitation may become persistent over time. If
bronchodilator reversibility is not present at initial presentation, the next step depends on the availability of other
tests and the urgency of the need for treatment. In a situation of clinical urgency, asthma treatment may be
commenced and diagnostic testing arranged within the next few weeks, but other conditions that can mimic
asthma should be considered and the diagnosis of asthma confirmed as soon as possible.
Table 4
GINA assessment of asthma control in adults
Asthma symptom control
In the past 4 weeks, has the patient had
Daytime asthma symptoms more than twice/week?
Any night waking due to asthma?
SABA reliever for symptoms
More than twice a week?
Any activity limitation due to asthma?
Level of symptom control
Uncontrolled
WellPartly
Controlled Controlled
YES
NO
YES
NO
YES
NO
YES
NO
None
of these
1-2
of these
3-4
of these
87
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Risk Factors for Poor Asthma Outcome
Assess risk factors at diagnosis and periodically, particularly for patients experiencing exacerbations.
Measure FEV1 at start of treatment, after 3–6 months of controller treatment to record the patient’s personal
best lung function, then periodically for ongoing risk assessment
Having uncontrolled asthma symptoms is an important factor for exacerbations.
Additional, potentially modifiable risk factors for flare-ups (exacerbations), even in patients
with few symptoms, include:
Having any of
• High SABA use (with increased mortality if > 1 x 200-dose canister/month)
these risk
• Inadequate ICS: not prescribed ICS; poor adherence, incorrect inhaler technique
factors
• Low FEV1, especially if < 60% predicted
increases the
• Higher bronchodilator reversibility
patient’s risk of
• Major psychological or socioeconomic problems
exacerbations
• Exposures: smoking, allergen exposure if sensitized
even if they
• Comorbidities: obesity, chronic rhinosinusitis, confirmed food allergy
have few
• Sputum or blood eosinophilia
asthma
• Elevated FENO (in adults with allergic asthma)
symptoms
• Pregnancy
Other major independent risk factors for flare-ups (exacerbations)
• Ever intubated or in intensive care unit for asthma
• ≥ severe exacerbations in the last 12 months
Risk factors for developing fixed airway obstruction
• Preterm birth, low birth weight and greater infant weight gain
• Lack of ICS treatment
• Exposure tobacco smoke; noxious chemicals; occupational exposures
• Low initial FEV1; chronic mucous hypersecretion; sputum or blood eosinophilia
Risk factors for medication side-effects
• Systemic: frequent OCS; long-term, high dose and/or potent ICS; also taking P450 inhibitors
• Local: high-dose or potent ICS; poor inhaler technique
FEV1: forced expiratory volume in 1 second; ICS: inhaled corticosteroids; OCS: oral corticosteroid; P450 inhibitors: cytochrome
P450 inhibitors such as ritonavir, ketoconazole, itraconazole; SABA: short-acting beta2-agonist.
Reference:
0. 2020 GINA Report, Global Strategy for Asthma Management and Prevention
(https://ginasthma.org/gina-reports/)
1. Philippine Consensus Report on Asthma Diagnosis and management 2019
88
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Figure 1
Asthma Control Test
Score: 25 – Congratulations!
You have TOTAL CONTROL of your asthma.
You have no symptoms and no asthma-related
limitations. See your doctor if this changes.
Score: 20 to 24 – On Target
Your asthma may be WELL CONTROLLED but not
TOTALLY CONTROLLED. Your doctor may
be able to help you aim for TOTAL CONTROL.
Score: less than 20 – Off Target
Your asthma may NOT BE CONTROLLED.
Your doctor can recommend an
action plan to help improve your
asthma control.
89
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Figure 2: Stepwise Management
Global Initiative for Asthma Global Strategy for Asthma Management and Prevention, 2020.
Available from: https://ginasthma.org/gina-reports/
90
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Table 5
Initial Asthma Treatment: recommended options in adolescents and adults
Presenting symptoms
Preferred INITIAL TREATMENT
All patients
• SABA-only treatment (without ICS) is not
recommended
Infrequent asthma
•
As needed low dose ICS-formoterol
symptoms, e.g. less than
(Evidence B)
twice a month
Other options include ICS whenever SABA is taken,
in combination or separate inhalers
*
Asthma symptoms or
•
Low dose ICS with as needed SABA (Evidence
need for reliever twice a
A), or
month or more
• As-needed low dose ICS-Formoterol (Evidence A)
Other options include LTRA (less effective than ICS,
Evidence A), or taking ICS whenever SABA is taken
either in combination or separate inhalers
(Evidence B). Consider likely adherence with
controller if reliever is SABA.
**
Troublesome asthma
• Low does ICS-LABA as maintenance and reliever
#
symptoms most days; or
therapy with ICS-formoterol (Evidence A) or as
waking due to asthma
conventional maintenance treatment with asonce a week or more,
needed SABA (Evidence A), OR
especially if any risk
• Medium dose ICS**with as needed SABA
factors exist
(Evidence A)
Initial asthma
• Short course of oral corticosteroids AND start
presentation is with
regular controller treatment with high-dose ICS
severely uncontrolled
(Evidence A) or
#
asthma, or with
medium-dose ICS-LABA (Evidence D)
exacerbation
ICS: inhaled corticosteroids; LABS: long-acting beta2-agonist; LTRA: leukotriene receptor antagonist; OCS:
oral corticosteroids; SABA: short-acting-beta2-agonist
*
Corresponds to starting at Step 2
** Corresponds to starting at Step 3
#
Not recommended for initial treatment in children 6-11 years
Global Initiative for Asthma Global Strategy for Asthma Management and Prevention, 2020.
Available from: https://ginasthma.org/gina-reports/
91
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Figure 3
SUGGESTED INITIAL CONTROLLER TREATMENT IN ADULTS WITH A DIAGNOSIS OF ASTHMA
FIRST ASSESS:
Confirmation
of diagnosis
Symptom control &
modifiable risk factors
(including ling function)
Comorbidities
IF
:
Symptoms most days,
waking at night
≥ once a week
and low lung function?
START
WITH:
YES
Medium dose
ICS-LABA (MART or
maintenance-only)
STEP 4
Low dose
ICS-LABA (MART or
maintenance-only)
STEP 3
Daily low dose
ICS or as-needed
low dose
ICS-Formoterol
STEP 2
Daily low dose
ICS or as-needed
low dose
ICS-Formoterol
STEP 1
NO
Symptoms most days,
or waking at nigh
≥ once a week ?
YES
NO
Inhaler technique
& adherence
Symptoms twice a
month or more?
Patient preferences
& goals
YES
NO
Global Initiative for Asthma Global Strategy for Asthma Management and Prevention, 2020.
Available from: https://ginasthma.org/gina-reports/
92
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
ASSESSMENT OF SEVERITY
MANAGEMENT-COMMUNITY SETTINGS
The severity of the exacerbation (Figure 4.4-1)
determines the treatment administered.
Indices of severity, particularly PEF (in patients
older than 5 years), pulse rate, respiratory rate,
and pulse oximetry, should be monitored
during treatment.
Most patients with severe asthma
exacerbations should be treated in an acute
care facility (such as a hospital emergency
department) where monitoring, including
objective measurement of airflow obstruction,
oxygen saturation, and cardiac function, is
possible. Milder exacerbations, defined by a
reduction in peak flow of less than 20%,
nocturnal awakening, and increased use of
Table 6 Severity of Asthma Exacerbations*
Breathless
Talks in
Alertness
Respiratory rate
Accessory muscles and
suprasternal retractions
Wheeze
Pulse/min.
Pulsusparadoxus
PEF
after initial
bronchodilator
% predicted or
% personal best
PaO2 (on air)┼
and/or
PaCO2 ┼
Mild
Moderate
Severe
Walking
Talking
Infant – softer shorter
cry; difficulty feeding
At rest
Infant stops feeding
Can lie down
Prefers sitting
Sentence
Phrases
May be agitated
Usually agitated
Increased
Increased
Normal rates of breathing in awake children:
Age
< 2 months
2-12 months
1-5 years
6-8 years
Usually not
Usually
Hunched forward
Words
Usually agitated
Often >30/min
Normal Rate
< 60/min
< 50/min
< 40/min
< 30/min
Usually
Moderate , often only
Loud
end expiratory
< 100
100-120
Guide to limits of normal pulse rate in children:
Infants
2-12 months-Normal Rate
Preschool
1-2 years
School age
2-8 years
Absent
May be present
< 10mm Hg
10-25 mm Hg
Over 80%
Approx. 60-80%
Normal
Test not usually
necessary
> 60 mm Hg
< 45 mm Hg
< 45 mm Hg
Respiratory arrest
imminet
Drowsy or confused
Usually loud
Paradoxical thoracoabdominal movement
Absence of wheeze
> 120
Bradycardia
< 160/min
< 120/min
< 110/min
Often present
> 25 mm Hg (adult)
20-40 mm Hg (child)
< 60% predicted or
personal best
(< 100 l/min adults)
or
response lasts < 2hrs
< 60 mm Hg
Absence suggests
respiratory muscle
fatigue
Possible cyanosis
> 45 mm Hg;
Possible respiratory
failure (see text)
SnO2%(on air)┼
> 95%
91-95%
< 90%
Hypercapnea (hypoventilation) develops more readily in young children than
in adults and adolescents.
*Note: The presence of several parameters, but not necessarily all, indicates the general classification of the exacerbation.
┼Note: Kilopascals are also used internationally; conversion would be appropriate in this regard.
93
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Figure 4
Management of Asthma Exacerbations in Acute Care Setting
Initial Assessment (see Figure 4.1-1)
• History , physical examination (auscultation, use of accessory muscles, heart rate, respiratory rate, PEF or FEV1,
oxygen saturation, arterial gas if patient in extremis)
Initial Treatment
• Oxygen to achieve O2 saturation ≥ 90% (95% in children)
• Inhaled rapid-acting β2-agonist continuously for one hour.
• Systemic glucocorticosteroids if no immediate response, or if patient recently took oral glucocosteroid, or if episode
is severe.
• Sedation is contraindicated in the treatment of an exacerbation.
Reassess after 1 hour
Physical examination, PEF, O2 saturation and other tests as needed.
Criteria for Moderate Episode:
• PEF 60-80% predicted/personal best
• Physical exam: moderate symptoms, accessory muscle use
Treatment:
• Oxygen
• Inhaled β2-agonist and inhaled anticholinergic every 60min
• Oral glucocorticosteroids
• Continue treatment for 1-3 hours, provided there is
improvement
Criteria for Severe Episode:
• History of risk factors for near fatal asthma
• PEF< 60%;predicted/personal best
• Physical exam: severe symptoms at rest, chest retraction
• No improvement after initial treatment
Treatment:
• Oxygen
• Inhaled β2-agonist and inhaled anticholinergic
• Systemic glucocorticosteroids
• Intravenous magnesium
Reassess after 1-2 Hours
Good Response within 1-2 Hours:
• Response sustained 60 min after last
treatment
• Physical exam normal: No distress
• PEF > 70%
• O2 saturation > 90% (95% children)
Incomplete Response within 1-2
Hours:
• Risk factors for near fatal asthma
• Physical exam: mild to moderate signs
• PEF < 60%
• O2 saturation not improving
Poor Response within 1-2 Hours:
• Risk factors for near fatal asthma
• Physical exam: symptoms severe,
drowsiness, confusion
• PEF < 30%
• PCO2> 45 mm Hg
• PO2< 60 mm Hg
Admit to Acute Care Setting
• Oxygen
• Inhaled β2-agonist ± anticholinergic
• Systemic glucocorticosteroid
• Intravenous magnesium
• Monitor PEF, O2 saturation, pulse
Admit to Intensive Care
• Oxygen
• Inhaled β2-agonist + anticholinergic
• Intravenous glucocorticosteroids
• Consider intravenous β2-agonist
• Consider intravenous theophylline
• Possible intubation and mechanical
ventilation
Reassess at intervals
Improved: Criteria for Discharge Home
• PEF > 60% predicted/personal best
• Sustained on oral/inhaled medication
Home Treatment:
• Continue inhaled β2-agonist
• Consider, in most cases, oral glucocorticosteroids
• Consider adding a combination inhaler
• Patient education: Take medicine correctly
Review action plan
Close medical follow-up
Poor Response (see above):
• Admit to Intensive Care
Incomplete response in 6-12 Hours (see
above):
• Consider admission to Intensive Care if no
improvement within 6-12 hours
Improved (see opposite)
94
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Figure 5
Global Initiative for Asthma Global Strategy for Asthma Management and Prevention, 2020.
Available from: https://ginasthma.org/gina-reports/
95
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
PULMONARY ARTERIAL HYPERTENSION (PAH) / PULMONARY HYPERTENSION
(PH)
Intended Learning Outcomes:
• Recognize the signs and symptoms of pulmonary hypertension
• Define diagnostic modalities applicable to the clinical presentation of a patient
suspected to have pulmonary hypertension
• Interpret test results for the diagnosis of pulmonary hypertension.
• Know possible treatment regimen depending on the diagnosis and severity of
pulmonary hypertension.
Definition:
• Pulmonary Hypertension (PH): a hemodynamic and pathophysiological condition
defined as mean PAP >25 mmHg at rest assessed by RHC
• Pulmonary Arterial Hypertension (PAH): a clinical condition characterized by
presence of pre-cap PH in the absence of other causes of pre-cap PH
• In recent journals (ERJ), AmPAP of 20 mmHg should be considered as the upper
limit of normal value. This new definition has been recently proposed by other.
However, this abnormal elevation of mPAP in isolation is not sufficient to define
PVD as it can be due to an increase in CO or PAWP.
• Pre-capillary PH is best defined by the concomitant presence of mPAP>20
mmHg, PAWP ≤15 mmHg and PVR ≥3 WU emphasizing the need for RHC with
mandatory measurement of CO and accurate measurement of PAWP
Updated clinical classification of pulmonary hypertension (PH)
1 PAH
1.1 Idiopathic PAH
1.2 Heritable PAH
1.3 Drug- and toxin-induced PAH (table 3)
1.4 PAH associated with:
1.4.1 Connective tissue disease
1.4.2 HIV infection
1.4.3 Portal hypertension
1.4.4 Congenital heart disease
1.4.5 Schistosomiasis
1.5 PAH long-term responders to calcium channel blockers (table 4)
1.6 PAH with overt features of venous/capillaries (PVOD/PCH) involvement (table 5)
96
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
1.7 Persistent PH of the newborn syndrome
2 PH due to left heart disease
2.1 PH due to heart failure with preserved LVEF
2.2 PH due to heart failure with reduced LVEF
2.3 Valvular heart disease
2.4 Congenital/acquired cardiovascular conditions leading to post-capillary PH
3 PH due to lung diseases and/or hypoxia
3.1 Obstructive lung disease
3.2 Restrictive lung disease
3.3 Other lung disease with mixed restrictive/obstructive pattern
3.4 Hypoxia without lung disease
3.5 Developmental lung disorders
4 PH due to pulmonary artery obstructions (table 6)
4.1 Chronic thromboembolic PH
4.2 Other pulmonary artery obstructions
5 PH with unclear and/or multifactorial mechanisms (table 7)
5.1 Haematological disorders
5.2 Systemic and metabolic disorders
5.3 Others
5.4 Complex congenital heart disease
PAH: pulmonary arterial hypertension; PVOD: pulmonary veno-occlusive disease; PCH: pulmonary capillary
haemangiomatosis; LVEF: left ventricular ejection fraction.
Pulmonary Hypertension Symptoms:
- Breathlessness
- Fatigue
- Weakness
- Chest pain/angina
- Syncope/presyncope
- Abdominal distention
97
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
-
Raynaud’s in about 10% (worse prognosis)
Hemoptysis (rare)
Pulmonary Hypertension Physical Signs:
- Left parasternal lift /RV heave
- Loud P2 of 2nd Heart sound
- Pansystolic murmur of Tricuspid regurgitation
- Diastolic murmur of Pulmonary insufficiency
- Right-sided 3rd heart sound
Pulmonary Hypertension Physical Signs (Advanced State):
- Jugular vein distention
- Hepatomegaly
- Peripheral edema
- Ascites
- Cool extremities
Clues for Classification of Pulmonary Hypertension:
- clear lungs (Normal breath sounds)
- no clubbing(except in CHD, PVOD)
- central and peripheral cyanosis
- hoarseness (Ortner syndrome)
- stigmata of secondary causes of PAH:
o scleroderma, cirrhosis, HIV, OSA
ACCF/AHA Diagnostic Approach to PAH 2
98
University of Santo Tomas Faculty of Medicine and Surgery
Department of Medicine
Section of Pulmonary & Critical Care Medicine
Four stage approach to diagnosis (Galiè N et al. Eur Heart J 2009)
•
•
•
•
Clinical suspicion of PAH
o symptoms, known risk factors
Exclusion of Group 2 (left heart disease) and Group 3 (lung disease) PH
o ECG, chest radiograph, echocardiography, PFTs, HRCT
Exclusion of Group 4 (CTEPH) PH
o ventilation/perfusion lung scan
PAH evaluation and characterisation
o CT pulmonary angiography, CMRI, haematology, biochemistry,
serology, and ultrasonography
o functional class and exercise capacity
o right heart catheterisation (RHC)
Treatment of PAH
Stage A
Stage B
Stage C
Stage C
Stage D
High risk with
no symptoms
PAH with
+ VDC
PAH with
- VDC
PAH with
- VDC
Low Risk
High Risk
Refractory
symptoms
requiring
special
intervention
Hospice
Transplantation
Inotropes, atrial septostomy
Consider multidisciplinary team
Combination therapy
IV meds (Flolan or Trepostonil)
Aldactone and digoxin
Dietary sodium restriction, diuretics
Bosentan +/- Sildenafil +/- Ventavis
Calcium Channel Blockers
Risk factor reduction, patient and family education
Sleep apnea, Obesity, Uncontrolled hypertension and/or depress LVEF, drug abuse
REFERENCES:
Harrison’s Principles of Internal Medicine 20th Edition; Chapter 304
ESC/ERS Guidelines 2009
Haemodynamic definitions and updated clinical classification of pulmonary
hypertension.Gérald Simonneau, David Montani, David S. Celermajer, Christopher
P. Denton, Michael A. Gatzoulis, Michael Krowka, Paul G. Williams, Rogerio Souza
European Respiratory Journal 2019 53: 1801913; DOI: 10.1183/13993003.01913-2018
99