Pulmonary Oedema

Mohammed Mohiey El-Din Fouad

Department of Internal Medicine
Aswan University
 Definition
Pulmonary Oedema is a condition
characterized by fluid accumulation in the
lungs caused by extravasation of fluid from
pulmonary vasculature in to the interstitium
and alveoli of the lungs
The extent to which fluid accumulates in the
interstitium of the lung depends on the balance
of hydrostatic and oncotic forces within the
pulmonary capillaries and in the surrounding
tissue.
Hydrostatic pressure
-favors movement of fluid from the capillary into
the interstitium
Oncotic pressure
-favors movement of fluid into the vessel
Maintenance
-lymphatics in the tissue carry away the small
amounts of protein that may leak out
-tight junctions of endothelium are impermeable
to proteins
 Epidemiology
 Pulmonary edema occurs in about 1% to 2%
of the general population.
Between the ages of 40 and 75 years, males
are affected more than females.
 After the age of 75 years, males and females
are affected equally.
The incidence of pulmonary edema increases
with age and may affect about 10% of the
population over the age of 75 years.
 Pathophysiology
 Imbalance of starling force
-increase pulmonary capillary pressure
-decrease plasma oncotic pressure
-increase negative interstitial pressure
 Damage to alveolar- capillary barrier
lymphatic obstruction
Disruption of endothelial barrier allow
protein to escape capillary bed and enhance
movement of fluid in to the tissue of the lung
Idiopathic or unknown
 Classification
Based on inciting mechanism
1. Imbalance of Starling force
A. Increased pulmonary capillary pressure
-left ventricular failure
-Volume overload
B. Decreased plasma oncotic pressure
- Hypoalbuminemia due to different cause
C. Increased negativity of interstitial pressure
-Rapid removal of pneumothorax with large applied
negative pressures (unilateral)
 Classification
Based on inciting agent
2. Altered alveolar-capillary membrane permeability
 Infectious pneumonia
 Inhaled toxins
 Circulating foreign substances
 Aspiration
 Endogenous vasoactive substances
 Disseminated intravascular coagulation
 Immunologic—hypersensitivity pneumonitis, drugs
Shock lung in association with non-thoracic trauma
Acute hemorrhagic pancreatitis
 Classification
Based on inciting agent
3. Lymphatic insufficiency
• After lung transplant
• Lymphangitic carcinomatosis
• Fibrosing lymphangitis
4. Unknown or incompletely understood
• High-altitude pulmonary edema
• Neurogenic pulmonary edema
• Narcotic overdose
• Pulmonary embolism
• Eclampsia
• After anesthesia
• After cardiopulmonary bypass
 Classification
Based on underlying cause
o Cardiogenic pulmonary edema
o Non-cardiogenic pulmonary edema
 Cardiogenic Pulmonary
Oedema
Cardiogenic pulmonary edema is Pulmonary
edema due to increased pressure in the
pulmonary capillaries because of cardiac
abnormalities that lead to an increase in
pulmonary venous pressure.
Hydrostatic pressure is increased and fluid
exits capillary at an increased rate.
 Cardiogenic Pulmonary
Oedema
Basic pathophysiology:
A rise in pulmonary venous and pulmonary
capillary pressures pushes fluid into the
pulmonary alveoli and interstitium.
CXR:
Bilateral perihilar bat’s wing appearance
Symmetric opacification of lung fields
 Pathogenesis of Cardiogenic
Pulmonary Oedema
Left sided heart failure Decrease pumping
ability to the systemic circulation Congestion
& accumulation of blood in the pulmonary
area Fluid leaks out of the intravascular
space to the interstitium Accumulation of fluid
Pulmonary edema `
 Risk Factors
Vary by cause
Leading risk factor is clearly underlying
cardiac disease.
 Causes of Cardiogenic
Pulmonary Oedema
1.LV failure is the most common cause.
2.Dysrhythmia
3.LV hypertrophy and cardiomyopathy
4.LV volume over load
5.Myocardia infarction
6. left ventricular outflow obstruction
Non-cardiogenic pulmonary
oedema
It is defined as the evidence of alveolar fluid
accumulation without hemodynamic
evidence that suggests a cardiogenic
etiology.
Hydrostatic pressure is normal
Leakage of protein and other molecules into
the tissues occurs.
 Non-Cardiogenic
Pulmonary Oedema
Associated with dysfunction of surfactant
lining the alveoli, increased surface force
and a propensity for the alveoli to collapse
at low volume.
Characterized by intra-pulmonary shunt
with hypoxemia and decrease lung
compliance
 Non-Cardiogenic Pulmonary
Oedema
Mechanism includes:
 Increased alveolar–capillary membrane
permeability
 Decreased plasma oncotic pressure
 Increased negativity of pulmonary
interstitial pressure
 Lymphatic insufficiency or obstruction
 Non-Cardiogenic
Pulmonary Oedema
Causes:
I. Direct injury to the lung
II. Hematogenous injury to the lung
III. possible lung injury plus elevated
hydrostatic pressure
 Staging of Pulmonary
Oedema
Three stages of Pulmonary Oedema can be
distinguished based on the degree of fluid
accumulation:
Stage-1 : all excess fluid can still be cleared
by lymphatic drainage.
Stage-2 : characterized by the presence of
interstitial edema.
Stage-3 : characterized by alveolar edema
due to altered alveolor- capillary
permeability
Mild: Only engorgement of pulmonary
vasculature is seen.
Moderate: There is extravasation of fluid into
the interstitial space due to changes in
oncotic pressure.
Severe: Alveolar filling occurs.
 Unusual types of pulmonary
Oedema
Neurogenic pulmonary oedema
Patients with central nervous system disorders
and without apparent preexisting LV dysfunction
Re-expansion pulmonary edema
Develops after removal of air or fluid that has
been in pleural space for some time, post-
thoracentesis.
Patients may develop hypotension or oliguria
resulting from rapid fluid shifts into lung.
 Unusual types of
Pulmonary Oedema
High altitude pulmonary oedema :
Occurs in young people who have quickly
ascended to altitudes above 2700 m and who
then engage in strenuous physical exercise
at that altitude, before they have become
acclimatized.
Reversible (in less than 48 hours).
 Pathophysiology
On ascending to high altitude, falling level of
PO2 triggers hypoxic pulmonary
vasoconstriction.
This directs blood flow away from hypoxic
areas of lung towards areas that are well
oxygenated.
This results in a rise in mean pulmonary
artery pressure & a heterogeneous blood
flow to different parts of the lung
In areas that receive high blood flow, the
capillary trans-mural pressure rises & walls of
the capillary & alveolus are exposed to stress
failure.
Extensive damage to alveolar capillary
membrane.
Oedema which is rich in high molecular weight
proteins & RBCs to pass freely in to the alveoli &
impair oxygenation.
Patient presents with Headache, Insomnia, Fluid
retention, Cough and Shortness of breath
Symptoms of Pulmonary Oedema
Shortness of breath, orthopnea
Feeling of suffocation
Anxiety, restlessness
Cough with frothy sputum that may be tinged
with blood
Excessive sweating
Pale skin
Chest pain
Palpitations
Signs of pulmonary oedema
Tachycardia
Tachypnea
Agitation
Cold extremities
Sweating
Coarse crepitations
Wheezes
Special considerations
Unilateral pulmonary oedema:
Findings may appear in radiography only
Lymphatic blockade:
Both clinical and radiological manifestations are
dominated by the underlying disease
Neurogenic pulmonary oedema:
Symptoms usually appear within minutes to
hours after the injury
Complications of Pulmonary
oedema
Dysrhythmias

Cardiogenic shock

Respiratory arrest and death

Differential diagnoses
Pneumothorax
Pulmonary embolism
Cardiogenic shock
Cardiac tamponade
Pneumonia
Investigations
Chest X-ray

Arterial blood gases

ECG
Management
Initial treatment: Supportive
measures
Morphine
Oxygen
Nitrates
Definetive treatment: According to
the cause
Cardiogenic pulmonary oedema
Admission into the CCU
Strict monitoring of haemodynamic parameters
IV diuretics
Ultrafilteration
Mechanical ventilation
Nephrogenic Pulmonary
oedema
Haemodialysis with ultrafilteration
Mechanical ventilation
Indications of mechanical
ventilation
Refractory Hypoxia
Excessive work of breathing
Haemodynamic instability
Thank you