Problem 6

Emergency Medicine
Group 10
 Tutor: dr. Agus & dr.Haming
• Ketua : Renald Patria Dharmasyah
• Sekretaris : Cindy Claudia
• Penulis :Nikolaus Ronald Karnadi

• Anggota :
– Wenny Agustin Biang
– Farrel Uttu
– Vamelda Agustin
– Melani Nugraha
– Wenny Damayanti
– Nailah Rahmah
– Chyntia Winata
– Yoko Septian Jaya
– Sinta Gotama
 6th problem
Gasping for Air
• A 65 year old male is brought to an ED by ambulance for being unresponsive .He was being
cared for in a nursing facility from previous stroke incident.His breathing is shallow & rapid
when he was brought to the ED .In the past 3 to 4 days ,he had been coughing & there were wet
sounds heard in his cough.Paramedics report that his saturation is 67% when he was found.He
has a history of bronchial asthma & was diagnosed with pulmonary tuberculosis 10 years ago but
have not completed this medication.He was also a heavy smoker in his young age.

• In the ED ,his vital sign are as follow ,temperature is 38.7 C ,BP 100/78 mmHg,heart rate is
118beats/min,RR : 30 breaths /min,& his oxygen saturation is 84% on a non-rebreather face
mask.On his physical throax examination,his breathing is labored with intercostal muscle
retraction visible on inspection.There is an asymmetrical chest wall expansion when he
breathes.On percussion,his thorax sounds sonorous on some part of his chest,and on
auscultation,there are crackles & wheezing .His initial blood gas analysis shows that his pH is
7.26 ,PCO2 is 60 mmHg ,PO2 is 55 mmHg ,his HCO3 is 26 mEq/L
• Discuss the case,assess the patient condition ,plan proper diagnostic procedure & treatment
while considering all possibilities
• References for some supplementary diagnostic examination:
– pH : 7.35-7.45
– pCO2 : 35-45 mmHg
– P02 : 90-100mmHg
 LANGKAH 2
1. Apakah ada hubungan keluhan dengan stroke ?
2. Apakah ada hubungan keluhan riwayat asma dan
TB yg tidak dirawat?
3. Hubungan perokok dengan keluhan sekarang ?
4. Bagaimana intepretasi Pf & PP
5. Apa penyebab wet sound coughing?
6. Mengapa HCO3 ada dibatas atas ?
7. SaO2 84% walaupun ttp diberikan NRM ,apa
yang harus dilakukan?
 Langkah 3
1.Kemungkinan,faktor resiko pneumonia
2.Ada
3.Bisa COPD ( bronikitis kronik & emfisema)
4.Demam( 38.7 c) ,SaO2 : 84% ( N: > 95%)
-PP : asidosis respiratorik ( AGD)
-TD: normal
-RR: takipneu
-retraksi interkostal
-tidak simetris pengembangan kedua
parupneumothorax ( perkusi : hipersonor) /efusi pleura
(perkusi : redup ( hemothorax/pneumonia)
-Crackles : COPD
-wheezing : Asthma
5.Akibat infeksi/TB,pneumonia,COPD
6.Komplikasi asidosis respiratorik sdh mulai terjdi
7.Ditambahkan dengan ventilasi mekanik
 Mind Map
Anamnesa PF
Pulmonary Emergency

1) ARDS Respiratory failure

2) Avian influenza - Type 1 & Type 2
3) Pulmonary tuberculosis
4) COPD exacerbation
5) Status Asthmaticus
6) SARS
7) Aspiration pneumonia
8) Pneumothorax
9) Tracheal aspiration
10) Massive pleural effusion
11) Pulmonary edema
12) Hemothorax

Tatalaksana awal farmako & non farmakoprognosis & komplikasi

LEARNING ISSUES
 Acute Respiratory Distress Syndrome
• A clinical syndrome of
severe dyspnea of rapid
onset, hypoxemia, and
diffuse pulmonary
infiltrates leading to
respiratory failure
• ARDS is caused by diffuse
lung injury (direct/indirect)
from many underlying
medical and surgical
disorders

Harrison’s Principles of Internal Medicine. 18th Ed.

 ARDS
• Etiology
– Severe sepsis syndrome and/or bacterial pneumonia
(~40–50%)
– Trauma
– Multiple transfusions
– Aspiration of gastric contents
– Drug overdose
– Pulmonary contusion
– Multiple bone fractures
– Chest wall trauma/flail chest

http://clinicalgate.com/acute-respiratory-distress-syndrome-2/
ARDS

http://clinicalgate.com/acute-respiratory-distress-syndrome-2/
 ARDS
• Physical examination
– Tachypnea, tachycardia and the need for a high
fraction of inspired oxygen (FiO2) to maintain
oxygen saturation
– Febrile or hypothermic
– Cyanosis of the lips and nail beds
– Sepsis  hypotension and peripheral
vasoconstriction with cold extremities
– Examination of the lungs  bilateral rales
– Manifestations of the underlying cause

http://emedicine.medscape.com/article/165139-clinical#b2
 ARDS
• Differential diagnosis
– Aspiration Pneumonitis and Pneumonia
– Bacterial Pneumonia
– Bacterial Sepsis
– Hypersensitivity Pneumonitis
– Multiple Organ Dysfunction Syndrome in Sepsis
– Hospital-Acquired Pneumonia (Nosocomial
Pneumonia) and Ventilator-Associated Pneumonia
– Perioperative Pulmonary Managemen
– Respiratory Failure
– Transfusion Reactions
– Ventilator-Associated Pneumonia
– Viral Pneumonia

http://emedicine.medscape.com/article/165139-differential
 ARDS
• Test & diagnosis
– Arterial blood gas
– Hematologic
– Renal
– Cytokines
– To exclude cardiogenic pulmonary edema 
obtain a plasma B-type natriuretic peptide
(BNP) value and echocardiogram
– Chest X-ray  bilateral pulmonary infiltrates
– CT-scan
– Bronchoscopy

http://emedicine.medscape.com/article/165139-differential
 ARDS
• Management
– Positive end-expiratory pressure (PEEP) is
empirically set to minimize FIO2 (inspired O2
percentage) and maximize PaO2 (arterial partial
pressure of O2)
– Fluid management
– Neuromuscular blockade
– Glucocorticoids

http://clinicalgate.com/acute-respiratory-distress-syndrome-2/
 COPD: an umbrella term

• Umbrella term used to describe

progressive lung diseases which
include:

– Emphysema
– Chronic bronchitis
– Refractory (irreversible) asthma
– Severe bronchiectasis
 COPD
• Chronic obstructive pulmonary disease
(COPD) is a lung ailment that is characterized
by a persistent blockage of airflow from the
lungs.

• It is an under-diagnosed, life-threatening lung

disease that interferes with normal breathing
and is not fully reversible.
 Understanding COPD
• Critical to first understand normal
lung function

Image courtesy of The National Institute

of health
Lungs with COPD

Image courtesy of The National Institute

of health
 Causes
• Most cases of COPD occur
as a result of long-term
exposure to lung irritants
that damage the lungs and
the airways
• The most common irritant
that causes COPD is
cigarette smoke
• In rare cases, a genetic
condition called alpha-1
antitrypsin deficiency may
play a role in causing COPD
Symptoms
• breathlessness
• abnormal sputum (a
mix of saliva and
mucus in the
airway)
• a chronic cough
• daily activities can
become very
difficult as the
condition gradually
worsens
 Tripod Hoover sign  inward
position movement of lower ribcage
on inspiration
Purse lips breathing

n
 Diagnosis
• A simple diagnostic test
called "spirometry“
measures how much air
a person can inhale and
exhale, and how fast air
can move into and out
of the lungs

• Spirometry can detect

COPD long before its
Symptoms appear.
 Treatment
• COPD has no cure

• Quitting smoking is the most important step an

individual can take to treat COPD

• Other treatments for COPD may include

medicines, vaccines, pulmonary rehabilitation
(rehab), oxygen therapy, and surgery
 Managing COPD
• COPD symptoms usually • Avoid lung irritants
slowly worsen over time
• Get ongoing care
• A cold, the flu, or a lung
infection may cause • Manage the disease and its
symptoms to intensify symptoms
• Prescription antibiotics may • Prepare for emergencies
treat infections and other
medicines, such as
bronchodilators and inhaled
steroids, can help facilitate
breathing
Noninvasive ventilation
 Status Asthmaticus
• extreme form of an asthma exacerbation that
can result in hypoxemia, hypercarbia, and
secondary respiratory failure

Status asthmaticus: severe bronchospasm, doesn’t respond to aggressive therapies

within 30-60 mins.
 Backgro
und
• Acute Exacerbation
• Unresponsive
• Mild to Severe form
• Trend is towards less number of admissions in
intensive care

• Han P, Cole RP. Evolving differences in the presentation of severe asthma requiring intensive care unit
admission. Respiration. Sep-Oct 2004;71(5):458-62.
 Treatment
goals
• Reverse airway obstruction
• Correct Hypoxemia
• Prevent or treat complications like
pneumothorax and respiratory arrest
Etiol
ogy
 Etiology

• Acute Bronchospastic component marked by

smooth muscle
bronchoconstriction.
• Later inflammatory airway swelling and
edema
 Early bronchospastic
response
• Exposure to allergen
• Mast cell degranulation
• Release of histamine, PGD2, LT-C4
• airway smooth muscle contraction, increased
capillary permeability, mucus secretion, and
activation of neuronal reflexes
• Bronchoconstriction typically responds to
bronchodilator therapy like beta 2 agonist adrenergic
 Later inflammatory response
• Inflammatory mediators prime endothelium and
epithelium of
bronchial mucosa.
• Inflammatory cells like eosinophils, neutrophils and
basophils attach to primed endothelium and
epithelium and later enter into the tissues
• Eosinophils release ECP and MBP which induce
desquamation of
airway epithelium and expose nerve endings
• It leads to further hyper responsiveness.
 Later inflammatory response
• Airway resistance and obstruction
• caused by Bronchospasm, mucus plugging,
and edema in the peripheral
• Air trapping
• results in lung hyperinflation,
ventilation/perfusion (V/Q)
mismatch, and increased dead space
ventilation.
 Later inflammatory response
• Increase in pleural and intra alveolar pressure and
distended alveoli
leads to hypoxemia and increase in minute
ventilation.
Complicat
ions
• Slow compartments vs fast compartments
• Respiratory alkalosis vs hypercarbia
• Cardiac arrest
• Respiratory failure or arrest
• Hypoxemia with hypoxic ischemic central nervous
system (CNS) injury
• Pneumothorax or pneumomediastinum
• Toxicity from medications
 Risk
factors
• Genetic
• GERD
• Viral
infections
• Air
pollutants
• Medicatio
ns
• Cold
exposure
 Prognosis
• Generally good except when combined with heart
failure or COPD
• Poor prognostic factors include delay in starting
treatment especially
steroids
 History
• Severe dyspnea or hours
or days.
• Previous intubation and
ventilation
Risk factors for developing status
asthmaticus
• Increased use of home bronchodilators without
improvement or
effect
• Previous intensive care unit (ICU)
admissions, with or without intubation
• Asthma exacerbation despite recent or current
use of corticosteroids
• Frequent emergency department visits and/or
hospitalization
• Less than 10% improvement in peak expiratory flow
rate (PEFR)
 Asthma with No Wheezing
• Silent chest
• Severe
obstruction
• fatigue
 Physical
Examination
• Tachypnea
• Wheezing in early stages
• Initially expiratory
• Later in both phases, may have absent breath sound in
advance stage
• Use of accessory muscles
• Inability to speak more than 1 to 2 words
• Decreased oxygen saturation
• Tachycardia and Hypertension
• Signs of complication, tension pneumothorax,
pneumomediastinum
• Peak expiratory flow meter measurement
 Assessment of severity of asthma
exacerbation
• Moderate asthma exacerbation:
• Increasing symptoms.
• PEFR >50-75% best or predicted.
• No features of acute severe asthma.
• Acute severe asthma - any one of:
• PEFR 33-50% best or predicted.
• Respiratory rate ≥25 breaths/minute.
• Heart rate ≥110 beats/minute.
• Inability to complete sentences in one breath.
• Life-threatening asthma - any one of the
following in a patient with severe asthma:
• Clinical signs: altered conscious level, exhaustion, arrhythmia,
hypotension, cyanosis, silent chest, poor respiratory effort.
• Measurements: PEFR <33% best or predicted, SpO2 <92%, PaO2 <8 6.0
kPa, 'normal' PaCO2 (4.6- kPa).
 Differential
diagnosis
• In children
• Viral infections, bronchiolitis
• Foreign body
• Congestive heart failure
• Extrinsic compression, lymph node,
tumor, blood vessel
• Tracheomalacia, primary or secondary
• Inhalational injury
• Other diagnosis, like cystic fibrosis,
bronchiectasis etc
 Workup
• Blood test
• CBC, ABG, Electrolytes, RBS, Theophillne level
• Chest X-ray
• To rule out pneumothorax, pneumomediastinum, heart
failure, pneumonia
 Complete blood
count
• CBC with differential to evaluate for pneumonia,
ABPA, Churg-Strauss
vasculitis
• It could vary because of treatment as
well with or without neutrophilia
• Serum lactate level
 Arterial blood gases
• If peak expiratory flow rate is less than 30% of
predicted or patient
best
• Signs of fatigue or progressive airflow obstruction
• Stages of progression
4 stages of blood gas progression
with status
asthmaticus
PaCO 2 PaO
2

Stage 1 Decrease Normal

Stage 2 Decrease Decreased
Stage 3 NORMAL Decreased
Stage 4 High Decreased
 Electrolytes and
glucose

• Hypokalemia as a result of
medications
• Hyperglycemia and in infants
hypoglycemia
 Need for
hospitalization
• If after treatment PEF and FEV1 is between
50% to 70%
• If less than 50% then intensive care
admission is indicated

National Heart, Lung, and Blood Institute. Managing exacerbations

of asthma. In: National Asthma Education and Prevention Program
(NAEPP). Expert panel report 3: guidelines for the diagnosis and
management of asthma. National Guideline Clearinghouse
Response to
treatment
• Response to treatment is assessed by Pulse
oximetry and spirometry
 Impulse
Oscillometry Testing
• Almost independent of patient cooperation
• Valid for all ages from 4 years and older children, adult and
geriatric
patients.
• Quite breathing i.e Tidal volume breathing for 30 seconds
• It measures impedance at different frequencies indicative of
central
and peripheral airway resistance.
• Bronchodilator therapy often does not reach the peripheral
airways. IOS can provide objective response to drug
therapy even when FEV1 can't.
 Histologic finding
• Autopsy of patients dying in few hours showed
Neutrophil infiltration
• Those who die in days showed Eosinophilic
infiltration.
• Extensive mucus production and severe
bronchial smooth muscle hypertrophy
 Treatment
• Mainstay of treatment of status asthmaticus are beta
2 agonist, systemic steroids and theophyllines.
• Pregnant and non pregnant are treated in the same
manner
• Fluid replacement, hypokalemia and
hypophosphatemia are important to treat.
• Routine use of antibiotics is discouraged
• Oxygen monitoring and therapy
• Maintain SatO2 above 92% except in pregnant and cardiac
patients where maintain above 95%.
• Endotracheal intubation, ventilation and chest tube
placement as needed.
• ECMO when needed.
 Beta2 Agonists
• Albuterol neubulizer continuously 10 – 15
mg/hour or q5 to 20 min
• Albuterol MDI 4 puff with chamber 15 to 30 minute
interval
• Endotracheal epinephrine has no role.
• Intravenous beta2 agonist when inhalation is not
possible
• Epinephrine 0.3 to 0.5mg subcutaneously (caution
in CHF and history
of arrhythmias)
 Anticholinergics
• Ipratropium bromide every 4 to 6
hours
• Synergistic effect with beta2
agonist.
• Does not cross blood brain barrier
like atropine
 Glucocorticoids
• Most important treatment in status asthmaticus
• decrease mucus production
• Improve oxygenation
• Reduce beta-agonist or theophylline requirements
• Decrease bronchial hypersensitivity
• Help to regenerate the bronchial epithelial cells.
• Oral and IV have same onset of action
• No role of nebulized steroids
• Name any ten Adverse effects of steroids
 Bronchodilators
• Methylxanthines theophylline, aminophylline
• bronchodilatation, increased diaphragmatic
function, and central
stimulation of breathing
• Narrow therapeutic index, needs monitoring
• Smokers and patients on phenytoin need higher
doses
• Side effects, nausea, vomiting, palpitation
• 6mg/kg loading followed by 1mg/kg/hour
 Bronchodilators
• Magnesium Sulfate
• relax smooth muscle and hence cause
bronchodilation
• Usually 1 gm to 2.5gm is administered as
a single dose.
• No studies on repeated doses
• More effective in children. 40mg/kg over
20 minutes
 Sedatives
• Usually reserved for intubated patients
• In very agitated patients on high bronchodilator
therapy a dose of
lorazepam 0.5mg to 1mg intravenous
Therapies for severe and resistant status
despite mechanical ventilation
• Ketamine
• Inhaled anesthetic agents
• NMBA
• Other treatments in case reports and
personal experiences
 Extracorporeal life
support
• high risk of developing refractory status
asthmaticus.
• Patients with a history of multiple incubations
• Respiratory failure requiring intubation within 6 hours of
admission
• Hemodynamic instability
• Neurologic impairment at the time of admission
• Duration of respiratory failure greater than 12 hours
despite maximal medical
therapy.
• Practiced in limited centers of the world
 Non invasive
ventilation
• Limited to weaning from ventilation
• Not effective in most of the acute cases unlike
acute exacerbation of
COPD
 Mechanical ventilation
• Indications --- already discussed
• Considerations
• Low volume, lower rate, I:E 1:3-4, addition of PEEP to
prevent airway collapse during expiration (cautiously)
• Heavy sedation
• Steroids and NMBA can cause prolong paralysis
• Monitor flow volume loop, exhaled tidal volume,
autoPEEP
• Decreased cardiac output due to decreased preload,
diastolic hypotension
• Fluid and judicious use of noradrenaline / phenylephrine
• Arterial line for repeated blood gases
• Replace electrolytes
Heli
ox
• Mixture of Helium and Oxygen
• Effective when percentage of Helium is at least 60%,
so limiting its use
when FiO2 requirement is high
• It has more laminar flow and less turbulence in
small airways so the Oxygen reach to lower
airways besides nebulized aerosols.
• No effect on caliber of bronchi.
Sunil Saharan & Rakesh Lodha
& Sushil K. Kabra.
Management of Status
Asthmaticus in Children. Indian
J Pediatr (2010) 77:1417–1423
DOI 10.1007/s12098-010-
0189-8.
 Avian Influenza
• Penyakit infeksi akibat virus influenza tipe A yg
biasa mengenai unggas
• Virus influenza  famili orthomyxoviruses,
– terdiri dari 3 tipe, yaitu A, B, C
– B dan C  menyebabkan penyakit pd manusia dg
gejala yg ringan dan tdk fatal
– A  dapat mengenai unggas dan manusia (H1, H2,
H3, serta N1 dan N2  human influenza)
– H5N1  Highly Pathogenic Avian Influenza (HPAI)
 Suspected

Probable
•  antibody (min 4x) against H5
with HI test or ELISA
Observation • H5 specific antibody detected (single serum)
Temperature >38oC (neutralization test)
• Severe Pneumonia/ respiratory failure
with one or more: / dead with no other cause
-cough
-sore throat
-cold (pilek )
-shortness of breath
(pneumonia) Confirmed
- Virus culture (+)
- PCR (+)
- IFA test (+)
- H5 specific antibody detected
(paired serum) (neutralization
test)   antibody (min 4x)
 Hospital care
• Suspected
+ shortness of breath with RR ≥ 30x/minutes
+ HR ≥ 100x/minutes with consciousness disorder
• Suspected with leucopenia
• Suspected with pneumonia ( radiology imaging)
• Probable and Confirmed

Treatment

• M2 Inhibitor : Amantadin and Rimantadin (100 mg 2x/day or 5 mg/kgBB for

3-5 days)
• Neuramidase Inhibitor : Zanamivir and Oseltamivir ( 2 x 75mg for a week)

Suspected case  Oseltamivir 2 x 75 mg for 5 days, symptomatic and antibiotic

if indicated
Probable  Oseltamivir 2 x 75 mg for 5 days, large spectrum AB and steroid if
indicated(severe pneumonia, ARDS)
Prophylactic  Oseltamivir 75 mg 1x/day for > 7 days (until 6 weeks)
 Pulmonary Edema

• Mechanism of Fluid favors movement of fluid into

accumulation
– Fluid accumulates in the
interstisium of the lung
depends on the balance of
hydrostatic & oncotic forces
within the pulmonary
capillaries & in the
surrounding tissue.
– Hydrostatic pressure :favours
movement of fluid from the
capillary into the interstisium.
– Oncotic pressure which is
determined by the protein
concentration in the blood
the vessel ( level of albumin
,the primary protein in the
plasma ,may be low in
condition ( such as cirrhosis
& nephrotic syndrome )
• Hypoalbumin favors
movement of fluid into the
tissue for any hydrostatic
pressure in the capillary

Harrison Princples Internal Medicine 19th

 Cardiogenic Pulmonary Edema
• Cardiac abnormalities lead to an increase in pulmonary venous pressure
shift the balance of forces between capillary & the interstisium.

• Hydrostatic is increased  fluid exits the capillary at an increased rate

resulting in interstitial ( more severe cases : alveolar edema )
– Development of pleural effusion may further compromise
respiratory system function & contribute to breathing discomfort.

• Early sign of pulmonary edema :

– Exertional dyspnea
– Orthopnea
– Chest radiograph peribronchial thickening ,prominent vascular
marking in the upper lung zones & kerley B lines

Harrison Princples Internal Medicine 19th

 Cardiogenic pulmonary edema
• As the pulmonary edema worsen alveoli fill
with fluid
– The chest radiograph shows patchy alveolar
filing ( typically in a perihilar distribution
)progress to diffuse alveolar infiltrate

– Increasing airway edema associated with rhonci

& wheezes

Harrison Princples Internal Medicine 19th

Non Cardiogenic pulmonary edema

• Non cardiogenic pulmonary edema

– Lung water increases due to damage of the pulmonary
capillary lining with consequent leakage of proteins & other
macromolecule into the tissue ,fluid follows the protein ( as
oncotic forces are shifted from the vessel to the surrounding
lung tissue) process is associated with dysfunction of the
surfactant lining the alveoli ,increased surface forces &
propensity for the alveoli to collapse at low lung volumes )

Harrison Princples Internal Medicine 19th

Non cardiogenic pulmonary edema
• Non cardiogenic pulmonary edema characterized by
intrapulmonary shunt + hypoxemia & decreased
pulmonary compliancelower functional residual
capacity

• Pathologic examination hyaline membranes are

evident in the alveoli & inflammation leading to
pulmonary fibrosis may be seen
• Clinically : mild dypnea to respiratory failure
• Auscultation : may be realtively normal despite chest
radiograph that show diffuse alveolar infiltrate
Harrison Princples Internal Medicine 19th
http:/ambulance.qld.gov.au/clinical.html
Goldman Cecil 24th edition
 Distinguishing cardiogenic from non
cardiogenic pulmonary edema
• History of cardiac disease ( identification )
• Physical examination in cardiogenic pulmonary edema evidence
increased intracardiac pressure ( S3 gallop,elevated JVP ,peripheral
edema ) & rales & or wheezes on ausculation of chest
– Chest radiograph : enlarged cardiac sillhoute ,vascular redistribution
,interstitial thickening & perihilar alveolar infiltrat ,pleural effusion

• In P.examination in noncardiogenic : pulmonary finding may be

relatively normal in early stage
– Heart size is normal ,alveolar infiltrates are distributed more uniformly
throughout the lungs & pleural effusion are uncommon
 Pulmonary Edema
• Non Cardiogenic
• Cardiogenic Edema Edema

Cardiogenic edema  with severe, Noncardiogenic edema, with

symmetric, basilar-predominant airspace severe,symmetric, more diffuse
opacities,associated with cardiomegaly airspace opacities; however, the cardiac size
and likely small effusions. is normal and no pleural effusions are
present
https://www.ncbi.nlm.nih.gov/pmc/
articles/PMC5408000/figure/f1/
https://www.ncbi.nlm.nih.gov/pmc/articles/PM
C5408000/
 Aspiration Pneumonia

• The development of a radiographic infiltrate and

clinical features consistent with pneumonia in a patient
with risk factors for increased oropharyngeal aspiration
• Any condition that increases the volume and/or
bacterial burden of oropharyngeal secretions in the
setting of impaired host defense mechanism may lead
to aspiration pneumonia
PULMONARY ASPIRATION SYNDROME
• Aspiration of gastric contents will produce a
chemical pneumonitis (Pulmonary Aspiration
Syndrome) similar to that caused by any irritant
that is inhaled or aspirated in significant
quantities.
• Mechanical obstruction by aspirated food
particles will further impair gas exchange.
• Pulmonary aspiration is a frequent cause or
contributor to the development of the acute
respiratory distress syndrome (ARDS).
ASPIRATION PNEUMONIA
• Aspiration of oropharyngeal secretions is typically chronic and
may cause a bacterial pneumonia characterized as aspiration
pneumonia.
• The chest X-ray usually shows consolidation in the lung
segments which were dependent at the time of aspiration.
• If the patient was supine the posterior segments of upper or
apical segments of lower lobes are involved.
• The basal segments of lower lobes particularly the right lower
lobe are involved if the patient was upright.
• In individuals with poor dental hygiene and large amounts of
dental plaque this commonly results in anaerobic lung abscess.
 Risk Factor
• Dysphagia (major)
• Volume of the aspirate
• Colonization of the oropharynx :
especially in elderly that increased
colonization of Staphylococcus
aureus and aerobic gramnegative
bacilli (e.g., Klebsiella pneumoniae
and Escherichia coli)
• lack of oral hygiene care as well as
conditions of peridental and/or
dental disease
• Marked depression of the cough
reflex
 Diagnosis

• There is no “gold standard” test to diagnose

aspiration pneumonia
• The diagnosis is therefore inferred when a
patient with known risk factors for aspiration
develops clinical features compatible with
pneumonia (fever, shortness of breath,
purulent sputum) with an infiltrate in a
characteristic bronchopulmonary segment
• Pulmonary aspiration syndrome occurring in the hospital
may occur during anesthesia, cardiopulmonary resuscitation, or other
procedures.
• Community-acquired cases are usually associated with trauma causing
an alteration of mental status, drug overdose (including pronounced
alcohol intoxication) or seizures.
• Sometimes vomiting and aspiration is a witnessed event.
• Within minutes to hours after aspiration, the patient develops
productive cough; dyspnea; fever; leukocytosis; and rales on chest
auscultation.
• Chest X-ray shows pulmonary infiltrates which are generally diffuse,
although dependent segments of the lung (especially the right lower
lobe) are more commonly involved.
• Food particles may be present on gross examination of sputum. The
condition should be considered at least initially to be an inflammatory
process in the lung not an infectious one.
• Provide respiratory support (eg, supplemental oxygen) as
necessary on the basis of arterial blood gas measurements
(or pulse oximetry) and clinical findings.
• If the patient has significant dyspnea or respiratory distress, immediately establish
airway control with intubation and mechanical ventilation.
• Witnessed aspirations should be treated by prompt oropharyngeal and tracheal
suctioning.
• Acute obstruction of the upper airway should be treated immediately with the
Heimlich maneuver.
• Retained, aspirated foreign bodies (greatest risk in children) often necessitate
bronchoscopy for final diagnosis and removal.
• Corticosteroids have not been demonstrated to be helpful and may increase
susceptibility to infection.
• Antibiotics for aspiration pneumonia should be given if infection occurs and not for
prophylaxis following an episode of aspiration.
 Management
• Antimicrobial therapy
 Streptococcus pneumoniae, S. aureus, and Haemophilus
influenza : narrow spectrum antibiotics
 third generation cephalosporins, fluoroquinolones, piperacillin,
or carbapenems : for aerobic gram (-)
 vancomycin or linezolid should be considered in patients at risk
of infection with methicillin-resistant S. aureus (MRSA)
• ACE-Inhibitor
• Nicergoline & an ergot alkaloid derivative
• Oral hygiene
 Massive pleural effusion
• Result from fluid accumulating in the potential
space between the visceral & parietal pleurae

Tintinalli’s Emergency Medicine: A Comprehensive

 Pathophysiology
• Continous amount of fluid is secrested from the parietal
pleura into the pleura space where it is absorbed by the
visceral pleural microcirculation
• Fluid reduce friction between the pleural layers & allows
for smooth lung expansion & contraction w/ respiration
• Any process that increase fluid production/ interferes w/
fluid absorption accumulation in the pleural space
• Exudative effusions result from pleural disease, usually
inflammation/ neoplasia that produce active fluid secretion/
leakage w/ high protein
• Transudative effusions result from an imbalance
between hydrostatic & oncotic pressures production of an
ultrafiltrate w/ low protein into the pleural space

Tintinalli’s Emergency Medicine: A Comprehensive

• Under normal circumstances pleural fluid
exists in a dynamic equilibrium, with
approximately 1 L of fluid traversing the
pleural space over 24 hours, but the net
accumulation of fluid in the pleural space is
small (≈0.1–0.2 mL/kg body weight) and
clinically insignificant.
• Pleural effusion develops when the influx
of fluid into the pleural space exceeds the
efflux.

Rosen's Emergency Medicine 9th Edition

 Etiology

Rosen's Emergency Medicine 9th Edition

 Differential
Clinical features Diagnosis
• May be silent/ come to detection
from other symptom(mild pleural
effusion)
• Increase in volume of the effusion
w/ the production of dyspnea/
development of inflammation &
associated pain w/ respiration
• Percusion dullness & decreased
breath sounds
• Small/ moderate-size effusion
percusion dullness & decreased
breath sounds at the lung base with
relative normal lung findings above
the level of fluid
• Large/ massive effusions
imposibble to distinguish a fluid
level on clinical examination

Tintinalli’s Emergency Medicine: A Comprehensive

 Diagnosis
• Adult: 150-200 mL of pleural fluid in the hemithorax
• Supine chest radiographs hazy appearance of pleural
fluid in the posterior pleural space
• CT scan chest clarify findings on chest radiograph
• Diagnostic thoracocentesis obtain pleural fluid for
analysis
• Light developed the most widely used criteria to
differentiate transudates from exudates using serum
and pleural fluid protein and lactate dehydrogenase
levels

Tintinalli’s Emergency Medicine: A Comprehensive

Tintinalli’s Emergency Medicine: A Comprehensive
• Small free-flowing pleural effusions better visualized on decubitus
radiographic views
USG
• A significant pleural effusion is large enough to produce a pleural fluid
strip >10mm wide on lateral decubitus radiographic views/ by USG

Tintinalli’s Emergency
Medicine: A
Tintinalli’s Emergency Medicine: A Comprehensive
 Treatment
• Therapeutic thoracentesis w/ drainage of 1.0-1.5 L of
fluid if the patient has dyspnea at rest
• Diuretic therapy resolves >75% of effusions due to HF
within 2-3 days
• Patients w/ pleural empyema (gross pus/ organism on Gram
stain) drainage w/ large bore thoracostomy tubes
• Massive effusions (>1.5-2L) urgent thoracentesis may
stabilize respiratory/ circulatory status
• Empyema chest tube drainage/ operating room to prevent
complications
• Relative contraindications to thoracocentesis
coagulopathy & other bleeding disorders

Tintinalli’s Emergency Medicine: A Comprehensive

Rosen's
Study Guide, 8e Emergency Medicine 9th Edition
Harrison's Principles of
Internal Medicine
 Pneumothorax
Pneumothorax is defined as the presence of air in the pleural
space. Although intrapleural pressures are negative throughout
most of the respiratory cycle, air does not enter into the pleural
space. Hence, net movement of gases from the capillary blood
into the pleural space would require pleural pressures lower than
–54 mm Hg (lower than –36 cm H 2 O), which hardly ever occur
in normal circumstances. Hence, if air is present in the pleural
space, one of three events must have occurred: (1)
communication between alveolar spaces and pleura, (2) direct or
indirect communication between the atmosphere and the pleural
space, or (3) presence of gas-producing organisms in the pleural
space.
 PSP has an incidence of 7.4–18 cases (age-adjusted
incidence)/100,000 population per year in males, and 1.2–6
cases/100,000 population per year in females. PSP typically
occurs in tall, thin subjects. Other risk factors are male gender
and smoking. PSP typically occurs at rest. Precipitating factors
may be atmospheric pressure changes (which may account for the
often observed clustering of PSP) and exposure to loud music.
Almost all patients with PSP report a sudden ipsilateral chest
pain, which usually resolves spontaneously within 24 h. Dyspnea
may be present but is usually mild.
Secondary spontaneous pneumothorax
A multitude of respiratory disorders have been described as a
cause of spontaneous pneumothorax. The most frequent
underlying disorders are COPD with emphysema, cystic fibrosis,
tuberculosis, lung cancer, HIV-associated Pneumocystis carinii
pneumonia, followed by more rare but ‘typical’ disorders such as
lymphangioleiomyomatosis and histiocytosis X. Because lung
function in these patients is already compromised, secondary
spontaneous pneumothorax (SSP) often presents as a potentially
lifethreatening disease, requiring immediate action, in contrast
with PSP which is more of a nuisance than a dangerous condition.
The general incidence is almost similar to that of PSP. Depending
upon the underlying disease, the peak incidence of SSP can occur
later in life, years of age in the emphysema population.
In SSP, dyspnea is the most prominent clinical feature; chest
pain, cyanosis, hypoxemia, and hypercapnia, sometimes
resulting in acute respiratory failure, can also be present.
Diagnosis is confirmed on a posteroanterior chest radiograph;
in bullous emphysema, the differential diagnosis with a giant
bulla can be difficult, necessitating CT confirmation. As in
PSP, air may enter the pleural space through various
mechanisms: direct alveolar rupture (as in emphysema or
necrotic pneumonia) via the lung interstitium, or backward via
the bronchovascular bundle and mediastinal pleura
(pneumomediastinum). Recurrence rates usually are higher as
compared to those for PSP, ranging up to 80% of cases as is
observed in cystic fibrosis.
 Traumatic Noniatrogenic
pneumothorax
Pneumothorax ranks second to rib fracture as the most common
sign of chest trauma, occurring in up to 50% of chest trauma
victims. In half of these cases, pneumothorax may be occult; in
chest trauma patients requiring mechanical ventilation, CT of the
chest should therefore always be performed. Most surgeons and
emergency physicians will place a chest tube in occult and
nonoccult traumatic pneumothoraces. If positive pressure
ventilation is anticipated, placement of a chest tube is mandatory.
Traumatic iatrogenic pneumothorax
Iatrogenic pneumothorax occurs most often following
transthoracic needle biopsy (24%), subclavian vein
catheterization (22%), thoracentesis (20%), transbronchial lung
biopsy (10%), pleural biopsy (8%) and positive pressure
ventilation (7%). Diagnosis of iatrogenic pneumothorax is often
delayed, which should make physicians vigilant. Small and
asymptomatic iatrogenic pneumothoraces often do not need any
treatment, and resolve spontaneously. In larger or symptomatic
pneumothoraces, simple manual aspiration or placement of a
small catheter or chest tube attached to a Heimlich valve usually
is successful. Larger tubes may be necessary in emphysematous
patients or when mechanical ventilation is indicated.
 Tuberculosis
• TB is a disease caused by a bacterium called
Mycobacterium tuberculosis.
• Infection with M tuberculosis  exposure of
the lungs or mucous membranes to infected
aerosols.
• Person with active pulmonary TB, a single
cough can generate 3000 infective droplets,
with as few as 10 bacilli needed to initiate
infection.
 Patophysiology
• Droplet inhaled  nuclei deposited within the
terminal airspaces of the lung  organisms grow
for 2-12 weeks, until they reach 1000-10,000 in
number  sufficient to elicit a cellular immune
response  can be detected by a reaction to the
tuberculin skin test.
• The infection may be cleared by the host immune
system or suppressed into an inactive form called
latent tuberculosis infection (LTBI)
TB lesions
• Epithelioid granuloma with central caseation
necrosis.
• The most common site  within alveolar
macrophages in subpleural regions of the lung.
• Bacilli proliferate locally and spread through
the lymphatics to a hilar node, forming the
Ghon complex.
Early tubercles  spherical, 0.5- to 3-mm nodules
with 3 or 4 cellular zones demonstrating the
following features:
• A central caseation necrosis
• An inner cellular zone of epithelioid macrophages
and Langhans giant cells admixed with
lymphocytes
• An outer cellular zone of lymphocytes, plasma
cells, and immature macrophages
• A rim of fibrosis (in healing lesions)
• Initial lesions may heal and the infection become
latent before symptomatic disease occurs. Smaller
tubercles may resolve completely.
• Fibrosis occurs when hydrolytic enzymes dissolve
tubercles and larger lesions are surrounded by a
fibrous capsule.
• Such fibrocaseous nodules usually contain viable
mycobacteria and are potential lifelong foci for
reactivation or cavitation.
• Some nodules calcify or ossify and are seen easily
on chest radiographs.
• Tissues within areas of caseation necrosis have high
levels of fatty acids, low pH, and low oxygen tension,
all of which inhibit growth of the tubercle bacillus.
• If the host is unable to arrest the initial infection, the
patient develops progressive, primary TB with
tuberculous pneumonia in the lower and middle lobes
of the lung.
• Purulent exudates with large numbers of acid-fast
bacilli can be found in sputum and tissue.
• Subserosal granulomas may rupture into the pleural or
pericardial spaces and create serous inflammation and
effusions.
Lesions that develop around mycobacterial foci can be
either proliferative or exudative.
• Proliferative lesions  the bacillary load is small and
host cellular immune responses dominate. These
tubercles are:
- Compact
- With activated macrophages admixed,
- Surrounded by proliferating lymphocytes, plasma cells,
and an outer rim of fibrosis.
• Exudative lesions  large numbers of bacilli and host
defenses are weak. Without treatment, these lesions
progress and infection spreads.
 Risk factors
The following factors help to determine whether
a TB infection is likely to be transmitted:
• Number of organisms expelled
• Concentration of organisms
• Length of exposure time to contaminated air
• Immune status of the exposed individual
 Clinical features
• Cough
• Weight loss/anorexia
• Fever
• Night sweats
• Hemoptysis
• Chest pain
• Fatigue
• Abnormal breath sounds, especially over the
upper lobes or involved areas.
 Diagnosis: Screening method
• Mantoux tuberculin skin test with purified
protein derivative (PPD)  active and latent
TB
• An in vitro blood test based on interferon-
gamma release assay (IGRA) with antigens
specific for Mycobacterium tuberculosis 
latent TB
 Laboratory test
• Acid-fast bacilli (AFB) smear and culture -
Using sputum obtained from the patient
• HIV serology in all patients with TB and
unknown HIV status
 Work up
• Chest radiograph to evaluate for possible
associated pulmonary findings. If chest
radiography findings suggest TB and a sputum
smear is positive for AFB, initiate treatment
for TB.
• A computed tomography (CT) scan of the
chest may help to better define abnormalities
in patients with vague findings on chest
radiography.
 Treatment

Latent TB
• Recommended regimens  isoniazid and rifampin
• An alternative regimen  isoniazid plus rifapentine as
directly observed therapy (DOT) once-weekly for 12 weeks
 SARS
Definition
• a rapidly progressive illness caused by a coronavirus /
the severe acute respiratory syndrome coronavirus.

• Isolation procedures for suspected SARS patients:

airborne, droplet, and contact isolation.
• Healthcare providers should wear a higher respiratory
facemask when caring for patients with SARS, in
addition to glove, gown, and eye protection.

• RF for death in coronavirus infection include:

– age >60 years, diabetes mellitus, and hepatitis B
infection.
 Clinical Features
• The clinical features of coronavirus infection:
– fever (99% frequency)
– nonproductive cough
– Dyspnea
– myalgias
– headache
– diarrhea
• Many cases progress to a moderate-severe condition
characterized by hypoxia and dyspnea at rest.
• Respiratory failure requiring mechanical ventilation
occurs in 10% to 20% of hospitalized patients with
SARS
http://payload.cargocollective.com/1/3/102448/1513469/SARS_spread02.jpg
• Consider the dx of SARS on clinical reasons
when the patient has been exposed to known
cases or has traveled to regions with SARS
activity.
• Chest radiographs: subtle peripheral
pulmonary infiltrates.
• Chest CT demonstrates ground-glass
consolidation during early phases of illness.
• Lymphopenia, thrombocytopenia, elevated
lactic dehydrogenase, liver enzymes, and
creatine phosphokinase levels
https://www.cdc.gov/sars/
clinical/images/clinicalgu
idance1.gif