Pulmonary oedema refers to extravasation of fluid from the pulmonary vasculature into

the interstitium and alveoli of the lung.

The formation of pulmonary oedema may be caused by 4 major pathophysiologic

mechanisms.

Imbalance of starling forces which are

Increased pulmonary capillary pressure

Decreased plasma oncotic pressure

Increased negative interstitial pressure

Damage to the alveolar-capillary barrier

Lymphatic obstruction

Idiopathic or unknown mechanism

Classification of Pulmonary Oedema

Cardiogenic pulmonary oedema (CPE): This is defined as pulmonary oedema due to

increased capillary hydrostatic pressure secondary to elevated pulmonary venous

pressure.

Non-Cardiogenic pulmonary oedema: This includes several clinical conditions that are

associated with pulmonary oedema based on an imbalance of starling forces other than

through primary elevations of pulmonary capillary pressure.

Clinical Features of Pulmonary Oedema

Symptoms

Breathlessness

Anxiety

Profuse diaphoresis

Patients with symptoms of gradual onset CPE (e.g. over 24 h) often report dyspnea on

exertion, orthopnea (respiratory discomfort when supine), and paroxysmal nocturnal

dyspnea (patient awakens gasping for air and must sit up).

Cough is a frequent complaint that may provide an early clue to worsening pulmonary

oedema in patients with chronic left ventricle (LV) dysfunction.

Pink frothy sputum may be present in patients with severe disease.

Chest pain should alert the physician to the possibility of acute myocardial ischemia,

infarction, or aortic dissection with acute aortic regurgitation as the precipitant of

pulmonary oedema.

Physical Findings

Tachypnea and tachycardia

Patients may be sitting upright, they may demonstrate air hunger, and they may become

agitated.

Patients usually appear anxious and diaphoretic

Hypertension is often present because of the hyper adrenergic state.

Hypotension indicates severe LV systolic dysfunction and the possibility of cardiogenic

shock.

Auscultation of the lungs usually reveals fine crepitations, but rhonchi or wheezes may

also be present.

Rales (crepitations) are usually heard at the bases first; as the condition worsens, they

progress to the apices.

Auscultation of murmurs can help in the diagnosis of acute valvular disorders manifesting

with pulmonary oedema.

Another notable physical finding is skin pallor or mottling resulting from peripheral

vasoconstriction and shunting of blood to the central circulation in patients with poor LV

function and substantially increased sympathetic tone.

Patients with concurrent right ventricular (RV) failure may present with hepatomegaly,

positive hepatojugular reflux (seen in the neck region) and peripheral oedema.

Severe cardio pulmonary oedema may be associated with a change in mental status which

may be the result of hypoxia or hypercapnia (a condition where there is too much carbon

dioxide in the blood).

Differential Diagnosis, Investigations and Treatment of Pulmonary

Oedema

Differential Diagnosis

Pneumonia

Pneumothorax

Pulmonary Embolism

Respiratory Failure

Diffuse pulmonary infections

Aspiration

Shock

Acute Respiratory Distress Syndrome (ARDS)

Asthma

Cardiogenic Shock

Chronic Obstructive Pulmonary Disease (COPD)

Emphysema

Myocardial Infarction

Respiratory Failure

Diffuse pulmonary infections

Aspiration

Shock

Acute Respiratory Distress Syndrome (ARDS)

Asthma

Cardiogenic Shock

Chronic Obstructive Pulmonary Disease (COPD)

Emphysema

Myocardial Infarction

Investigations

Laboratory Studies

Blood count

Serum electrolyte measurements

BUN and creatinine determination

Cardiac enzymes if available

Electrocardiogram would be very helpful

Imaging Studies

Chest radiography

Echocardiography

Note: Most of these investigations are done at hospital levels and therefore patients suspected

of having pulmonary oedema must be referred for proper investigations.

Treatment of Pulmonary Oedema

Pulmonary oedema is life-threatening and must be considered a medical emergency

In the treatment of pulmonary oedema attention must be directed to identifying and

removing any precipitating causes

Because of the acute nature of the problem, a number of additional nonspecific measures

are necessary before referring the patient to the hospital, these includes

Oxygen therapy (whenever possible)

Diuretics e.g. furosemide (lasix)

Keep patient in semi sitting position                                                                         

REFFERNCES;

      Braunwald & Fauci (2001). Harrison’s principles of internal medicine 15th Ed.  Oxford: McGraw Hill

      Davidson, S (2006). Principles and practice of medicine 20th Ed.  Churchill: Livingstone.

Kumar & Clark (2003) Textbook of clinical medicine. Churchill: Livingstone.

      Douglas Model (2006): Making sense of Clinical Examination of the Adult patient. 1st Ed. Hodder Arnold

      Longmore, M., Wilkinson, I., Baldwin, A., & Wallin, E. (2014). Oxford handbook of clinical medicine. Oxford

      Macleod, J. (2009). Macleod's clinical examination. G. Douglas, E. F. Nicol, & C. E. Robertson (Eds.). Elsevier Health Sciences.

      Nicholson N., (1999), Medicine of Non-communicable diseases in adults. AMREF

      Stuart and Saunders (2004): Mental health Nursing principles and practice. 1st Ed. Mosby

      Swash, M., & Glynn, M. (2011). Hutchison's clinical methods: An integrated approach to clinical practice.