Pulmonary oedema is defined as a rapid transudation of fluid out of the pulmonary capillaries into the interstitial spaces, alveoli and bronchioles, beyond the capacity of the drainage system of the lungs.
Classification and causes
Aetiology of pulmonary oedema
Cardiogenic pulmonary oedema (primary abnormality is elevated pulmonary capillary pressure)
Aortic stenosis, aortic regurgitation.
Hypertensive heart disease.
Congenital heart diseases.
Mitral stenosis, mitral regurgitation.
Non-cardiogenic pulmonary oedema (primary abnormality is not elevated pulmonary capillary pressure)
Disruption of alveolar-capillary membranes, e.g. acute respiratory distress syndrome (for causes, refer ARDS).
Increased negativity of the interstitial pressure, e.g. rapid evacuation of a large pneumothorax or pleural effusion, and acute severe asthma.
Impeding lymphatic drainage by lymphatic blockade, e.g, fibrotic and inflammatory diseases of lung and lymphangitis carcinomatosis.
Precise mechanism unknown, e.g. narcotic overdose (morphine, methadone, dextropropoxyphene), exposure to high altitude and neurogenic pulmonary oedema.
Pathophysiology of cardiogenic pulmonary oedema
Cardiogenic pulmonary oedema is transudation of fluid, macromolecules and red blood cells from the pulmonary capillaries into initially the interstitium and later, alveoli and bronchioles.
Normally, pulmonary interstitium is efficiently drained by lymphatics. In pulmonary oedema, the rate of fluid accumulation in the interstitium exceeds the drainage capacity of lymphatics, which results in accumulation of fluid in the interstitium.
Various factors which operate in the development of pulmonary oedema can be summarised as follows:
1.Elevated pulmonary capillary pressure favouring transudation of fluid.
2.Widening of the pulmonary capillary endothelial intercellular junctions, allowing passage of fluid, macromolecules and red blood cells into the interstitium (interstitial oedema).
3.Disruption of the intercellular junctions between the alveolar lining cells, allowing fluid, macromolecules and red blood cells to enter the alveoli (alveolar oedema).
Stages in development
'Interstitial oedema'—This is the early stage where oedema is confined to interstitium.
'Alveolar oedema'—This occurs later, with oedema fluid, macromolecules and red blood cells entering the alveoli.
Clinical features of acute pulmonary oedema
Severe dyspnoea and orthopnoea.
Cough which is initially dry, but later with copious, pinkish, frothy expectoration.
Anxiety, pallor, sweating, cyanosis.
Cold, bluish extremities.
Bilateral scattered rhonchi.
Bilateral crepitations, predominantly basal.
Signs of underlying heart disease.
Without effective treatment, there is progressive hypoxia, hypercapnia and acidosis. Eventually, patient dies of respiratory arrest.
Arterial blood gas studies show hypoxia. Initially, the patient has hypocapnia but in late stages, hypercapnia develops.
Radiological features of acute pulmonary oedema
Kerley A lines—thin non-branching lines radiating from the hilum.
Kerley B lines—transverse thin lines of 1-3 cm, seen at the lung bases, lying perpendicular to the pleura.
Blurring of the outline of the central pulmonary vessels and hilum due to perivascular oedema.
`Endobronchial cuffing'—blurring seen around the end-on view of bronchi.
Bilateral fluffy shadows in the lung fields.
Confluencing of fluffy shadows around hilum giving the `bat's wing' appearance (bilateral perihilar opacity dense at the hilum, fading towards periphery).
Pleural effusions at uncommon sites like lamellar effusion, interlobar effusion and subpulmonic effusion. Interlobar effusion might give the appearance of a tumour, but it disappears with treatment (hence called 'phantom', 'disappearing' or 'vanishing' tumour).
Treatment of acute cardiogenic pulmonary oedema
Monitoring the intra-arterial pressure and pulmonary vascular pressures through a Swan-Ganz catheter.
Propped-up position or sitting position with legs hanging down along the side of bed, to reduce venous return. 100% oxygen, preferably under positive pressure. Oxygen corrects hypoxia and positive pressure raises intra-alveolar pressure reducing transudation of fluid. Non-invasive ventilation may be tried if oxygen saturation remains below 90%.
Morphine 2-5 mg intravenously slowly, and repeated if necessary, reduces anxiety and reduces venous return.
Intravenous loop diuretics, e.g. furosemide 40-100 mg (drug of choice), ethacrynic acid 40-100 mg or bumetanide 1 mg.
By diuresis, they reduce the circulating blood volume and hasten the relief of pulmonary oedema.
Intravenous furosemide has a venodilator action by which it reduces venous return.
Preload reduction with nitrates sublingually (5-10 mg of isosorbide dinitrate) or nitroglycerine intravenously (5-100 ng/minute as infusion).
Afterload reduction with intravenous sodium nitropmsside 20-30 jig/minute, in patients with systolic blood pressure more than 100 mmHg
Intravenous aminophylline 250-500 mg diminishes broncho-constriction, increases renal blood flow and sodium excretion (by diuresis), and increases myocardial contractility.
Inotropic agents: To increase the contractility of the myocardium, inotropic agents have been useful. Intravenous dopamine or dobutamine are most often used for this purpose.
Dobutamine is useful in patients with pulmonary oedema without hypotension.
Dopamine is preferred to dobutamine if shock is also present.
Intravenous digitalis has no role in pulmonary oedema; however, in presence of supraventricular tachycardia with fast ventricular rate, intravenous digoxin (0.5 mg) may be useful.
Milrinone increases the contractile state of the heart and reduces the systemic vascular resistance both of which decrease the left ventricular afterload and filling pressures. The loading dose is 50 jig/kg over 10 minutes followed by a maintenance dose of 0.375-0.5 !ig/minute.
In refractory cases, rotating tourniquets may be applied to the limbs. Tourniquets, with pressure just above the
diastolic, are applied to three of the four limbs and rotated every 15 minutes. However, their efficacy is unproven.
Correction of precipitating causes like infection or arrhythmias.
Treatment of underlying cause.