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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.
See pathology
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.
See pathology
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.
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