Acute pulmonary edema is a grave and usually fatal complication of severe falciparum malaria with more than 50% mortality. Acute lung injury is defined as the acute onset of bilateral pulmonary infiltrates with an arterial oxygen tension/fractional inspired oxygen ratio of 300 mmHg or less, a pulmonary artery wedge pressure of 18 mmHg or less, and no evidence of left atrial hypertension. ARDS is defined as acute lung injury and an arterial oxygen tension/fractional inspired oxygen ratio of 200 mmHg or less. Volume overload and hypoalbuminemia may aggravate pulmonary capillary leakage. Chest radiograph abnormalities range from confluent nodules to basilar and/or diffuse bilateral pulmonary infiltrates. Noncardiogenic pulmonary edema rarely occurs with P. vivax and P. ovale malaria.[1]
In addition to severe falciparum parasitemia and sequestration, secondary infections, severe anemia, hyperpyrexia, dehydration/fluid overload, metabolic acidosis, hypoxia and disseminated intravascular coagulation can also contribute to the cardiovascular problems in malaria. Although myocardial function is generally well preserved in severe falciparum malaria, malaria can complicate pre-existing cardiac decompensation and may even prove fatal for patients with compromised heart. Cardiac arrhythmias are uncommon.
Pathology of Acute Pulmonary Oedema: In a few patients it could be due to fluid overload as a result of enthusiastic fluid therapy. In others it develops even with normal or negative fluid balance. Pulmonary oedema develops later compared to other complications and it may even appear several days after treatment for malaria, when the patient is otherwise improving with a reduction in peripheral parasitemia.
The mechanism of pulmonary oedema is not clearly understood. It has a close resemblance to adult respiratory distress syndrome. While over-hydration may be the cause in some cases of pulmonary oedema, it can also develop in patients with normal capillary wedge pressures. Such cases may be due to increased permeability of pulmonary capillaries. Sequestration of red cells and clogging of pulmonary microcirculation and disseminated intravascular coagulation may also play their role. Pulmonary oedema is more common in patients with hyperparasitemia, renal failure and pregnancy and it is commonly associated with hypoglycemia and metabolic acidosis. It may develop suddenly after delivery, due to fluid overload. Pulmonary oedema may be the terminal event in many cases of fatal falciparum infection.
The first sign of impending pulmonary oedema is an increase in the respiratory rate. Tachypnoea may also be the first indicator of aspiration bronchopneumonia and metabolic acidosis and a chest X-ray will help in differentiating these conditions. Then patient develops signs of pulmonary oedema like basal crackles, cyanosis, tachycardia etc. The breathlessness worsens rapidly and the patient may die within a few hours. Hypoxia can cause convulsions and deterioration in the level of sensorium.
Management:
See Treatment of Severe P. falciparum malaria
Pulmonary oedema is the most fatal of the complications of falciparum malaria and therefore calls for careful and energetic management.
Fluid overload should be avoided at all costs, especially in pregnant women. The central venous pressure should be maintained between 0-5 cm of H2O by regulating fluid intake and nursing the patient propped up at 450. All intravenous fluids should be stopped immediately and diuretics may have to be administered.
Initial management of pulmonary oedema includes treatment with oxygen, back-rest and diuretics if there is evidence of fluid overload. Inj. Furoscemide 40 mg should be given intravenously and if there is no desired response, the dose can be progressively increased up to 200 mg. Fluid volume can be further reduced by venesection and letting of 250 ml of blood initially. This blood or its packed cells can be re-transfused once the problem settles down. The procedure can be repeated carefully if needed.
If the patient deteriorates with conservative treatment, mechanical ventilation is indicated. Positive end expiratory pressure ventilation may also be needed. Drugs like corticosteroids are not of any proven benefit in the management of these cases.
Overall, pulmonary oedema carries a poor prognosis.
References:
- Andrej Trampuz, Matjaz Jereb, Igor Muzlovic, Rajesh M Prabhu. Clinical review: Severe malaria Critical Care 2003;7:315-323 Available at http://ccforum.com/content/7/4/315
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