Emergency

Emergency in
in
Respiratory
Respiratory Medicine
Medicine
Handoko MD

Department of Internal Medicine

Pulmonology and Respiratory Medicine Division
dr. Ramelan Navy Hospital, Surabaya
 Emergency in Respiratory medicine
1. Hemoptysis
2. Vena Cava Superior Syndrome (VCSS)
3. Tension Pneumothorax
4. Acute Asthma Exacerbation
5. Acute Exacerbation of COPD
6. Acute Pulmonary Edema- ARDS
7. Respiratory Failure
 Hemoptysis
Definition
Coughing up of blood from the airway distal to glottis
Degree of hemoptysis
Pursel:
Bloodstreak (grade I), 1-30 mL (grade II),
30-150 mL (grade III), 150-500 mL (grade IV),
> 500 mL (grade V/massive)
Massive hemoptysis:
Production of ≥ 600 mL of blood within 24 h, high risk
for asphyxiation and death
Frank hemoptysis:
Blood without sputum
 Hemoptysis
Lung’s blood circulation
* 95% through low-pressure pulmonary arteries and
ends up in the pulmonary capillary bed, where gas is
exchanged
* 5% through high-pressure bronchial arteries, which
originate at the aorta and supply major airways and
supporting structures
In hemoptysis, it generally arises from bronchial circulation,
except when pulmonary arteries are damaged by trauma,
erosion of a granulomatous, calcified lymph node, tumor,
or, rarely by pulmonary arterial catheterization or when
pulmonary capillaries are affected by inflammation
Common causes of hemoptysis
Infectious Cardiovascular
Chronic bronchitis Severe left ventricular heart failure
Bronchiectasis Mitral stenosis
Tuberculosis Pulmonary embolism or infarction
Nontuberculous mycobacteria Septic pulmonary embolism / right-sided endocarditis
Lung abscess Aortic aneurysm or bronchovascular fistula
Necrotizing pneumonia Pulmonary hypertension
Mycetoma
Cystic fibrosis Miscellaneous
Idiopathic pulmonary hemosiderosis
Vasculitic Aspirated foreign body
Wegener's granulomatosis Pulmonary contusion or trauma
Systemic lupus erythematosus Post transthoracic needle biopsy or
transbronchial lung biopsy
Neoplastic
Lung cancer Age distribution
Bronchial adenoma < 20 years 20 - 40 years > 40 years
Metastatic disease Mitral Stenosis Lung TB Lung TB
(osteogenic sarcoma, chorio ca)
Bronchiectasis Bronchiectasis Lung cancer
Lung TB Mitral Stenosis Bronchiectasis
Causes of massive hemoptysis
Common
Bronchiectasis (including cystic fibrosis)
Tuberculosis & Nontuberculous mycobacteria
Lung abscess
Mycetoma (aspergilloma, or fungus ball)
Pulmonary contusion or trauma

Uncommon
Invasive aspergillosis or mucormycosis
Mitral stenosis
Pulmonary AVM, Bronchovascular fistula
Bleeding diathesis
Foreign body, Necrotizing bacterial pneumonia
Idiopathic pulmonary hemosiderosis
Bronchial adenoma
Pulmonary embolism with infarction
Septic embolism from tricuspid endocarditis
Pulmonary-renal syndromes
(Goodpasture's syndrome, SLE, Wegener's granulomatosis)
Pulmonary artery rupture
Etiology
Adults, 70-90% of cases are caused by
* Bronchitis
* Bronchiectasis
* TB
* Necrotizing pneumonia
* Primary LC is an important cause in smokers ≥ 40 yr
Metastatic cancer rarely causes hemoptysis
* Cavitary Aspergillus infection
Massive hemoptysis
The most common causes:
* Bronchogenic carcinoma
* Bronchiectasis
Rasmussen's aneurysm is a pulmonary artery
aneurysm adjacent or within a tuberculous cavity,
occurs in up to 5% of patients with such lesions, may
lead to rupture and haemorrhage
Fritz Valdemar Rasmussen
Pathogenesis
TB (20%)
Bronchial mucosa ulceration,
Hemorrhagic diathesis &  capilary permeability,
Systemic & pulmonal anastomosis,
Rasmussen’s aneurysm rupture
Bronchogenic Ca (9,5 - 50%)
Erosion of intraluminal tumor
Bronchiectasis (44,6%)
Cough & mucosal inflammation  vascular rupture
Systemic & pulmonal anastomosis
Aneurysm
Mitral Stenosis
Pulmonary vascular HT  diapedesis of RBCs to alveoli
Rupture of bronchial surface varices
Systemic & pulmonal anastomosis
Diagnostic
History
* Symptoms
* History of illness
* History of previously drugs used, Smoking
* Trauma
Physical Examination
Laboratory examination
Chest X-ray → 30% normal chest X-ray
Fibro-cavitary lession, Fungus ball, Atelectasis,
Infiltrates, Thickened bronchial walls, Lymphadenopathy,
Tumor, Left atrial enlargement, Kerley B-lines, etc
Treatment
To confirm  Hemoptysis or Hematemesis
Keep airway patency
* Airway management
* Oxygenation
* Localization of the bleeding site
* Position: Semisitting vs Trendelenberg
* Signs of acute respirtory failure 
Intubation: ETT ø >7.5 mm to facilitate suctioning
Exsanguination
Persistant Bleeding +HCT < 25-30% /Hb < 10 g%
Infection control
Surgical intervention
Bronchoscopy, embolization, thoracotomy
Differentiating Features of Hemoptysis and Hematemesis
Hemoptysis Hematemesis
History
- Absence of nausea-vomiting - Presence of nausea-vomiting
- Lung disease - Gastric or hepatic disease
- Asphyxia possible - Asphyxia unusual, hypovolemic
shock
Sputum examination
- Frothy - Rarely frothy
- Liquid or clotted appearance - Coffee ground appearance
- Bright red or pink - Brown to black
Laboratory
- Alkaline pH - Acidic pH
- Mixed with macrophages and - Mixed with food particles
neutrophils
 Vena Cava Superior Syndrome (VCSS)
Anatomy
Pathology of VCSS
Pathology of VCSS

Superior vena cava is a large vein that transmits blood from

the upper body back to the heart, located in the middle of
the chest and is surrounded by rigid structures and lymph
nodes. Compression by disease of any of the structures or
lymph nodes surrounding the superior vena cava can cause
the superior vena cava syndrome.
The Alveoli and Gas Exchange

Vena Cava Superior

Syndrome
Pathology of VCSS
Partial obstruction of blood flow through the
superior vena cava
Pathophysiologic events:
compression, invasion, thrombosis, fibrosis
Clinical evaluation
History
Facial & upper extremity swelling, chest pain,
dyspnea, cough, headache, neurologic complaints
Symptoms & signs
Clinical Pictures
Symptoms
Edema of the face, neck, upper extremities,
dyspnea (> supine position), cough, dizziness, dysphagia,
hoarseness, headache, mental status changes, seizure,
syncope, visual complaints
Signs
Tachypnea, distended neck & upper extremity veins,
facial swelling, plethora, cyanosis, dilated superficial
veins, neck, or sublingual area, stridor, confusion,
disorientation
Treatment
Initial management
 the head of the bed   cerebral edema
Quickly assess gag reflex, cough & breathing
Medical therapy
Diuretic: furosemide
Corticosteroid
Radiotherapy emergency
Surgical emergency
 Tension Pneumothorax
Definition
Pneumothorax that the air accumulates in the pleural
space via one-way valve effect
Pathophysiology
The trapped air pressure restrict ventilation and
displace the mediastinum to the opposite side 
Venous return   Cardiac output 
Clinical evaluation
* History
underlying lung disease, trauma, smoking
past episodes of pneumothorax, family history
* Symptoms & Signs
Pathophysiology and degree of lung collaps
Clinical pictures

* Symptoms
Pleuritic chest pain & difficulty of breathing
* Signs
Tachypnea, tachycardia, cyanosis, hypotension,
hemodynamic collaps
Accessory muscle use, distended neck veins,
tracheal shift toward the opposite lung,
Chest examination
Hyper-inflation, hyperresonant,  sound fremitus,
 breath sounds
Chest X-ray of Pneumothorax

British Thoracic Society (2003)

Treatment
Initial interventions
1. Supplemental O2 to maintain SaO2 ≥ 95%
2. Obtain VS & iv access, continuously monitor
cardiac rhythm & SaO2
3. Needle decompression
Evacuation of the air: chest tube insertion
Treatment
 Acute Asthma Exacerbation-Status Asthmaticus
Definition of Asthma
Chronic inflammatory disorder of the airways in which
many cells and cellular elements play a role.
The chronic inflammation causes an associated increase in
airway hyperresponsiveness that leads to recurrent
episodes of wheezing, breathlessness, chest thightness,
and coughing, particularly at night or in the early
morning.
These episodes are usually associated with widespread
but variable airflow obstruction that is often reversible
either spontaneously or with treatment.
Severity of asthma exacerbation (GINA, 2013)
Parameter Mild Moderate Severe Respiratory arrest imminent
Breathless Walking Talking At rest -----
Lie down Prefer sitting Hunched forward -----
Talks in Sentence Phrases Words -----
Allertness May be Usually Usually agitated Drowsy / confused
agitated agitated
RR / min < 20 20 - 30 > 30
Accessory muscles & Usually not Usually Usually Paradoxical thoraco-
suprasternal retract abdominal movement
Wheeze End of End of Expiration & Absence of wheeze
forced exp. expiration Inspiration
Pulse / min < 100 100 - 120 > 120 Bradycardia
Pulsus Paradoxus Absent May bepresent Often present Absence, suggests
< 10 10 - 25 > 25 respiratory muscle fatique
PEFR after initial > 80% 60 - 80% < 60% (100L/min) or
bronchodilator response last < 2h
PaO2 (on air) > 80 mmHg 60 - 80 mmHg < 60 mmHg
(Psbl. cyanosis)
PaCO2 < 45 mmHg < 45 mmHg > 45 mmHg
(Psbl. resp. failure)
SaO2 (on air) > 95% 91 - 95% < 90%
Status Asthmaticus
Definition
Severe acute asthma that not promptly responsive to
therapy with epinephrine sc or aminophyline iv,
initial unresponsiveness to inhaled -adrenergic
bronchodilators is also apparent.
Characteristics
* Widespread mucus inspissation
* Refractoriness to conventional bronchodilators
* Slow recovery of lung function
* Airway wall edema & inflammatory cell infiltration
(Faling & Snider, 1993)
JET NEBULIZER
Management of asthma exacerbations in acute care setting (GINA, 2013)

Initial assessment : History, PE, PEF or FEV1, SaO2, ABG

Initial Tx: O2 to achieve SaO2  90% (95% in children)

Inhaled rapid-acting 2 agonist continuously for 1 hour
Systemic steroids if no immediate response or if pt recently took
oral glucocorticoid, or if episode is severe
Sedation is contraindicated in the treatment of attacks

Reassess after 1 hour

PE, PEF, SaO2, and other tests as needed

Criteria for moderate episode Criteria for severe episode

PEF 60-80% predicted/personal best
Moderate symptoms, accessory
muscle use
Treatment
Oxygen
Inhaled 2 agonist & anti-Ch q 60 min
Oral glucocorticoids
Continue treatment 1-3 hours,
provided there is improvement
History of risk factors for NFA.
Severe symptoms at rest, chest
retraction
PEF < 60% predicted/personal best
No improvement after initial treatment
Treatment
Oxygen
Inhaled 2 agonist & anti-Cholinergic
Systemic glucocorticoids
Magnesium iv
 Re-assess after 1-2 hour

Good response Incomplete response Poor response within

Response sustained within 1-2 hours 1-2 h
60 min after last Risk factors for NFA Risk factors for NFA
treatment, normal PE, PE: Mild-moderate PE: symptoms severe,
no distress signs drowsiness, confusion
PEF > 70% PEF < 60% PEF < 30%
SaO2 > 90% (95%) SaO2 not improving PaCO2 > 45 mmHg
Admit to acute care PaO2 < 60 mmHg
Improved: criteria for setting Admit to ICU
discharge home Oxygen Oxygen
PEF > 60% predicted/ Inhaled 2 agonist ± Inhaled 2 agonist +
personal best + anticholinergic anti-Cholinergic
sustained on oral/ Systemic Glucocorticoids iv
inhaled medications glucocorticoid Consider iv 2 agonist
Continue tx with Magnesium iv Consider iv theophylline
inhaled 2 agonist Monitor PEF, SaO2, PR Possible intubation & MV
Consider, in most cases,
oral glucocorticoids, add
a combination inhaler
Re-assess at intervals Poor or incomplete
Patient education :
response and
Take medcn correctly,
no improvement in 6-12h:
Review action plan, close
Improved admit to ICU
medical follow up
Near-fatal asthma
Definition
Development of respiratory arrest resulting from asthma
 PaCO2 > 50 mmHg ± altered states of consciousness
Risk factors for near-fatal asthma
* Previous episode of near-fatal asthma
* Hospitalization for asthma within the previous year
* Inadequate long-term management
* Delay in time to medical evaluation
* Psychosocial problems / stress
* Low socioeconomic status
* Impaired self-management
(Goldberg H, Peters J, 2006)
Initial pharmacotherapy for near-fatal asthma
Therapy Comments
Oxygen Hypoxemia usually is corrected with 3 to 4L of O2 via nasal cannula or face
mask at 30 - 50% FiO2
Inhaled β2- Nebulized β2-agonists (salbutamol 2,5 - 5 mg) given q 20 min for 3 doses
agonists (decrease to hourly when FEV1 or PEFR improves by 20%) or
can be administered by continuous nebulization 15 mg/h
SC β2- Consider in pts with exacerbations refractory to inhaled medication.
agonists Epinephrine 0,3 - 0,5 mg of 1 : 1000 solution given sc q 20 min to a maximum
of 3 doses. Terbutaline 0,25 - 0,5 mg given sc q 20 min x 3, then q 2 - 4 h
Systemic Should be initiated within 1h of presentation: methyl prednisolone 125 mg q
cortico 6h for 48h. Once patient is significantly improved, switch to oral prednisone
steroids 1 mg/kgBW/d for 3 to 10 d
Anti Ipratropium may be beneficial when combined with β2-agonists;
cholinergics 4 puffs from MDI with spacer, repeated q 15 - 30 min, or
0,5 mg of 0,02% nebulizer solution, decrease to hourly when FEV 1 or PEFR
improves by 20%; discontinue when the patient is stabilized
 Acute Exacerbation of COPD (AECOPD)
Chronic bronchitis
Chronic productive cough on most days for
≥ 3 months per year for ≥ last 2 successive years
Emphysema
Destructive changes in the alveolar walls with airspace
enlargement distal to the non-respiratory bronchioles
Acute exacerbation may be triggered by tracheobronchial
infection & environmental exposures
Three cardinal symptoms
* worsening of dyspnea
*  sputum purulence
*  sputum volume
(Ann Intern Med, 2001; 134:595-9; Chest, 2001; 119:1185-9)
Two distinc type of COPD
Chest X-ray of COPD

Emphysema Chronic bronchitis

Clinical pictures

Degree of exacerbation
Mild
1 of 3 cardinal symptoms + 1 of the following:
* URI in the past 5 days
* Fever without apparent cause
*  wheezing
*  cough
*  RR / HR by 20% above baseline
Moderate
2 of 3 cardinal symptoms
Severe
All 3 cardinal symptoms
Guidelines Algorithm (AACP/ACP-ASIM, 2001)
Stable COPD 3 criterias Severe AECOPD

 Symptoms CXR,
from baseline inhaled bronchodilators1,
systemic steroids2,
ABs3, O2 prn, NPPV prn
3 dx criteria for Yes,
AE COPD criteria 2 only Moderate AECOPD
present ? present
CXR,
inhaled bronchodilators
No systemic steroids2,
1 only O2 prn, NPPV prn

Consider 1 dx criterion with at least CXR,

other diagnosis 1 of the following above inhaled
bronchodilators

No Yes Mild AECOPD

Guidelines
Guidelines Algorithm (AACP/ACP-ASIM, 2001)
3 dx criteria for
Stable COPD   Symptoms from baseline  AECOPD

Criteria present?
Yes  No
Criteria present Consider other dx

1 only  1 dx criterion with at least 1 of the following above

 No  Yes
Consider other dx Mild AECOPD
(CXR, inhaled bronchodilators1)
2 only  Moderate AECOPD
(CXR, inhaled bronchodilators1,
systemic steroids2, O2 prn, NPPV prn)
3 criterias  Severe AECOPD
(CXR, inhaled bronchodilators1, systemic steroids2,
ABs3, O2 prn, NPPV prn)
Principal medication of AECOPD
Anticholinergic once at max dose, then add 2-agonist
ABG should be measured if FEV1 < 40% pred or signs of RF/RHF
SABA+Anticholinergic in stable COPD produces greater and more
sustained improvements in FEV1 than either alone and does not
produce evidence of tachyphylaxis over 90 days of tx
3 days methylprednisolone iv 125 mg q6h, followed by prednisone
po, tapper to complete the 2-week course (60 mg/d on days 4-7,
40 mg/d 8-11, and 20 mg/d 12-15)
Systemic steroids should not be used > 2 weeks
Narrow-spectrum Antibiotics
Appropriate use of ABs in AECOPD is imperative to help control the
emergence of multidrug-resistant organisms
Risk Classification & Suggested ABs (Baum, Eur Respir J, 2004)
Gr Basic Symptoms & risk factors Probable 1st choice Alternatives for
clinical state pathogens tx. failure
0 Acute Cough & sputum without Usually viral None unless Macrolide or
tracheo previous pulmonary diseases symptoms persist Tetracycline
bronchitis for > 4 - 5 days
I Chronic Cough, increase sputum H influenzae Ampicillin, Fluoroquinolone,
Bronchitis production & purulence M catarrhalis Amoxicillin, -Lactam anti -
without Increased dyspnea S pneumoniae Cefpodoxime, Lactamase
risk factors Cefixime, Cefdinir, inhibitor,
(simple CB) Cefuroxime, New Macrolide or
TMSMZ Cephalosporin G2 / G3
II Chronic = Class I + 1 or more of: = Class I + Fluoroquinolone, Macrolide G2
Bronchitis Severe dyspnea Klebsiella spp + -Lactam anti - Cephalosporin G2 / G3
with risk FEV1 < 50% predicted other gram Lactamase (cefuroxime, cefprozil,
factors > 4 exacerbations / yr negatives inhibitor cefixime)
(complicated) Age  55 years Increased May require parenteral
Co-morbidity probability of - therapy
Malnutrition Lactam resistance
Duration of illness > 12 ys
III Chronic = Class II + = Class II + Ambulatory pts: tailor tx to airway pathogen
suppurative Constant purulent sputum P aeruginosa and P aeruginosa common (Ciprofloxacin)
bronchitis Some have bronchiectasis multiresistant Hospitalised pts:
FEV1 < 35% predicted Enterobacteriaceae Parenteral tx usually required
Multiple risk factors eg. & Klebsiella spp
frequent exacerbations
& FEV1 < 50%
 Respiratory Failure

Definition
Impairment in gas exchange to a level that causes
a significant potential for morbidity & mortality
Rule of fifty
PaO2 < 50 mmHg (while breathing room air)
PaCO2 > 50 mmHg
Manifestation
Acute respiratory failure (ARF)
Chronic Respiratory Failure (CRF)
Clinical presentations

Hypoxic-hypo/normocapnic RF
 PaO2 < 55-60 mmHg, normal/low PaCO2
 V/Q missmatch, Physiologic R-L shunt
 Without prior underlying lung disease
 Eg. ALI, ARDS, P. carinii pneumonia
Hypoxic-hypercapnic RF
 PaO2 < 55-60 mmHg, PaCO2 > 50 mmHg
 Alveolar hypoventilation, V/Q missmatch
 Chronic underlying lung disease
 Eg. COPD, ILD, neuromuscular disease,
drug overdose
Etiology
Alveolar hypoventilation
Hypoxia secondary to inadequate ventilation
P(A-a)DO2 > 20 mmHg
V/Q missmatch
Inhomogeneity in the distribution of V & Q
Hypoxia from underventilated area of the lung
Shunt
Passage of blood from venous to arterial system
without traveling through any ventilated area
Diffusion limitation
PO2 pulmonary capillary blood fails to reach
equilibrium with alveolar gas
Common causes of Acute Respiratory Failure
Airflow obstruction
Status asthmaticus
AECOPD
Foreign body aspiration
Upper-airway obstruction
Acute epiglottitis
Laryngeal edema
Alveolar-Filling processes
Pneumonia
Pulmonary edema
Cardiogenic
Non-cardiogenic
Intra-alveolar hemorrhage
Aspiration
Interstial Lung disease
Pulmonary fibrosis
Sarcoidosis
Collagen Vascular lung disease
Hypersensitivity pneumonitis
Pulmonary Vascular Disease
Pulmonary thromboembolism
Fat embolism
Amniotic fluid embolism
Pulmonary vasculitis
Neuromuscular Disease
Narcotics/sedative drug overdose
GBS, ALS
Phrenic nerve, spinal cord injury
Stroke
Obesity/hypoventilation syndrome
Chest wall/pleural disease
Pneumothorax, Flail Chest
Large pleural effusion, Hemothorax
Miscellaneous
Toxic inhalation injury
Smoke inhalation, CO poisoning
Metabolic dearrangement
Hypophosphatemia, Severe hypothyroidism
R-to-L shunts
Pulmonary AVM, ASD, VSD
Clinical Evaluation
History
1. Assessment of the rapidity of symptom onset
2. Assessment of the presence of underlying lung,
cardiovascular, neuromuscular disorders
3. Information about past episodes of RF
4. Current medications
5. Potential toxic exposures
6. Recent illnesses
7. Recent trauma
Clinical Evaluation
Symptoms
1. Dyspnea, more common in hypoxic RF
2. Hypoxic-hypercapnic RF  Somnolence & lethargy in
the absent of dyspnea
3. Confusion & disorientation in severely hypoxic pts
4. Headache in hypercapnic pts due to cerebral blood
vessel dilatation 2nd to  PaCO2
5. Chest pain, nausea, diaphoresis in LVH dysfunction
6. Pleuritic chest pain in pneumothorax / PE
7. Fever, malaise, purulent sputum in AECOPD
Clinical Evaluation
Signs
1. Vital signs
2. Skin: cyanosis, diaphoresis
3. Nasal flaring, dry mucous membrane
4. Neck: accessory muscles,  JVP
5. Lung: wheezing,  breath sounds, bronchial BS
6. Heart: S3 Gallop, murmur
7. Abdomen: hepatomegaly, ascites, HJR, paradoxical
movement of abdominal muscle
8. Extremities: Clubbing, peripheral edema
9. Mental status: agitated, restless, somnolence,
disoriented
Laboratory studies
* ABG analysis
* CBC
* Electrolyte panel (K, Na, Cl), Ca, Mg, P
* Glucose
* BUN, creatinine levels
* PT / PTT
* Urinalysis
Laboratory studies
* ECG
* Chest X-ray
* CT Scan: chest & head
* Angiography, Radionuclide venography,
Doppler examination
Treatment

Initial priorities
1. Airway
2. Ventilation
3. Oxygenation
4. Circulation
General measures
VS, SaO2, Cardiac monitor, IV access, ECG,
Laboratory analysis (ABG, CBC, RF, Electrolyte panel, Renal
function, glucose test)
Treatment of Respiratory Failure
Disposition
Nearly all patients with evidence of ARF by ABGs in
the ED should be admitted to the hospital for further
evaluation and treatment
Pts should be admitted to the ICU if:
* Intubated
* Clinically unstable requiring close supervision/
continuous SaO2 /ECG monitoring
* High FiO2 requirement: > 0.5 to maintain SaO2 > 90%
* Persistent respiratory acidosis
pH<7.30 & PaCO2 > 50 mmHg despite tx in the ED
Pulmonary Edema (PE)
Pulmonary edema
* Cardiogenic
* Non-cardiogenic
A. PE associated with diffuse alveolar damage (DAD)
→ results from a cytotoxic agent directly contacting
lung parenchyma or a systemic inflammatory
process, both of which cause vascular/alveolar
damage and ↑ permeability
→ initially present with subtle interstitial edema,
progresses to widespread bilateral opacification,
fails to resolve in 1-3 days and can progress to
fluid sequestration with areas of confluent
fibrosis
Cardiogenic Pulmonary Edema

Lung edema in a 71-year old woman with fluid overload and cardiac
failure. Chest X-ray and HRCT scan demonstrate bat wing alveolar
edema with a central distribution and sparing of the lung cortex
Pulmonary Edema (PE)
* Non-cardiogenic PE
B. PE without DAD
→ Diffuse bilateral interstitial pattern, usually
resolves within 3 days and tends to be caused by
increased hydrostatic pressure
* Neurogenic pulmonary edema (Shanahan, 1908)
→ mixed edema (↑ hydrostatic pressure mainly in
pulmonary venules and ↑ permeability by
unknown mechanism) containing elements, occur
in up to 50% of pts. after an intracranial insult:
trauma, hemorrhage, seizure (minute to hour)
CXR shows diffuse bilateral opacities mid to upper
lung predominance
 ThePulmonary
Hydrostatic Pressure Alveoli and GasEdema
Exchange

NPE in a 54-year old woman who was admitted for ICH due to arterial HT.
Chest X-ray shows airspace consolidations predominantly at the apices.
No pleural effusions or Kerley lines, and heart size is normal.
HRCT scan demonstrated confluent alveolar consolidations in the central portions
of the lungs. A few thickened interlobular septa are also seen (arrows)
 The Alveoli and
Non-Cardiogenic Pulmonary Gas Exchange
Edema - ARDS
Clinical Disorders Associated with the Developement of ARDS
Direct Lung Injury
Common causes
Pneumonia
Aspiration of gastric contents
Less common causes
Pulmonary contusion
Fat emboli
Near-drowning
Inhalation injury
Reperfusion PE after lung
transplantation or pulmonary
embolectomy
Indirect Lung Injury
Common causes
Sepsis
Severe trauma with shock and
multiple transfusions
Less common causes
Cardiopulmonary bypass
Drug overdose
Acute pancreatitis
Transfusions of blood products
Non-Cardiogenic Pulmonary Edema - ARDS

Definition or Criteria
* Bilateral infiltrates on CXR
* Pulmonary-artery wedge pressure (PAWP) ≤ 18 mmHg
or the absence of clinical evidence of left atrial
hypertension
* Acute Lung Injury (ALI) considered to be present if
PaO2 / FiO2 ratio ≤ 300
* Acute respiratory distress syndrome (ARDS) considered
to be present if PaO2 / FiO2 ratio ≤ 200
Neurogenic Pulmonary Edema
The Alveoli (NPE)
and Gas Exchange

Patient is a 57-year-old female status post-subarachnoid hemorrhage with dyspnea.

Chest X-ray demonstrates bilateral fine reticulonodular opacifications greater
predominance on the right upper lobe. Chst X-ray 24 hours later demonstrates rapid
increase in the diffuse bilateral reticulonodular opacifications greater on the right.
Neurogenic Pulmonary Edema (NPE)

Hydrostatic pressure edema in a 53-year old man with postoperative fluid overload.
PAWP 20mmHg. HRCT scan demonstrates inter-intralobular septal lines
predominating in the anterior portion of the right lung with some peribronchial
cuffing (arrow). Both lung display diffuse ground glass areas of increased
attenuation with gravitational AP gradient
Treatment of NPE

Supportive-conservative
Focus on the underlying disease, usually resolves 48-72 hs
Oxygen is required in most patients
GCS score ≤ 8 should be intubated
Mechanical ventilation may be necessary
PEEP with hypocarbia may be required to ↓ ICP
TV 5-8 ml/kg to avoid excessively high inflation pressure
Prognosis is determined by the course of underlying
neurological problems
Climbing Mountain: risk for HAPE
High Altitude Pulmonary Edema (HAPE)

HAPE in 30-year old female who

developed acute mountain sickness and
brain edema at an altitude of 4,500m.
Chest X-ray and CT scan demonstrate
numerous small, confluent airspace
consolidations.
No Kerley lines or pleural effusions are
seen.
High Altitude Pulmonary Edema (HAPE)
Definition
Abnormal accumulation of water in lung due to a
breakdown in the pulmonary blood-gas barrier triggered
by hypobaric hypoxia in excess of 2,000 m
Pathophysiology
Maladaptive responses to hypoxia:
poor ventilatory response, ↑ sympathetic tone,
exaggerated and uneven pulmonary vasoconstriction,
inadequate production of endothelial NO,
over production of endothelin
→ patchy accumulation of extravascular fluid in alveolar
space
Pathophysiology of HAPE
Treatment of HAPE
Non pharmacologic
* Rest and descent to a lower altitude
* Oxygenation
* Portable hyperbaric chamber
* Positive airway pressure
Pharmacologic (therapy and prophylactic)
* Nifedipine
* Tadalafil, Sildenafil
* Dexamethasone
* Beta 2 agonist
* Acetazolamide