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Cardiovascular manifestations in severe falciparum malaria include
mainly hypotension and acute pulmonary oedema. 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. Malaria can
also complicate pre-existing cardiac decompensation and may even prove fatal for patients
with compromised heart.
Myocardial
function is generally well preserved in severe falciparum malaria. The cardiac index may
be elevated with low peripheral vascular resistance and low to normal ventricular filling
pressures. Hypovolumia (due to reduced fluid intake, high grade fever, sweating, vomiting
and diarrhoea) also may contribute to the reduced pressures. There may be reduction in
visceral perfusion. Orthostatic hypotension is common. Septicemia, metabolic acidosis and
hypoxia may result in a drop in cardiac index. The pathophysiology of algid malaria is not
well understood, but it is presumed to be due to septicemia. Cardiac arrhythmias are
uncommon.
See pathology
Acute Pulmonary Oedema:
Acute pulmonary oedema is a grave and
usually fatal complication of severe falciparum malaria with more than 50% mortality. 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: 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.
Shock (Algid malaria):
The blood pressure may be generally low
in malaria due to peripheral vasodilation caused by the pyrogens. However, a systolic
blood pressure of 80 mm Hg or less, defined as shock, indicates complications. This may be
associated with cold and clammy peripheries, cyanosis, venous collapse etc.
Hypotension in malaria could be
due to many reasons:
-
Dehydration due to high-grade fever,
excessive sweating and inadequate fluid intake.
-
Dehydration due to vomiting and/or
diarrhoea.
-
Pulmonary oedema.
-
Metabolic acidosis.
-
Associated Gram negative septicemia.
-
Massive gastrointestinal haemorrhage.
In a given patient, one or more of the
above listed causes may be playing a role.
Dehydration is common and often goes
unnoticed. If untreated, it can cause oliguria and even acute renal failure. Control of
temperature by antipyretics plus tepid sponging and careful management of vomiting and/or
diarrhoea are important in all cases of malaria.
Gram negative septicemia has been blamed
as an important cause of hypotension in some cases of falciparum infection. Gram negative
organisms have been frequently cultured from the blood of patients with cerebral malaria.
Septicemia is restricted to patients with severe falciparum infection and it may be due to
reduced immunity, secondary infections from the gut, indwelling catheters and intravenous
lines and infections in the lung, urinary tract, meninges, etc.
Management:
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Hypovolumia and dehydration should be
properly identified, evaluated and managed with intravenous saline or Ringer’s
lactate. Plasma volume expanders like gelatin or dextran can be used. If the patient has
associated anemia, blood transfusion can be given. The central venous pressure should be
maintained at 0-5 cm of H2O and if needed, Dopamine infusion can be started.
Anti-emetics can be used to control vomiting. Metaclopramide is known to cause
extrapyramidal signs, particularly in children. In such cases, promethazine or other
centrally acting anti-emetics can be tried.
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Blood and urine culture should be done in
all such cases. Soon after collection of the specimen for culture, broad-spectrum
antibiotics should be started. Third generation cephalosporins or Benzyl penicillin with
Gentamicin can be used.
Cardiac arrhythmias: Cardiac
arrhythmias are very rarely observed in severe falciparum malaria. It could be due to
myocardial ischaemia caused by sequestration of red cells in the coronary circulation or
due to the adverse effects of drugs like quinine, quinidine and mefloquine.
Exacerbation of pre-existing cardiac
failure: Malaria may prove fatal for patients with pre-existing cardiac failure due to
valvular stenosis or myocardial disease. High grade fever, parasitemia, fluid overload can
all contribute to the problem. In all such cases, measures should be taken to bring down
the temperature rapidly with anti-pyretics and tepid sponging. Potentially cardiotoxic
drugs like quinine, mefloquine and halofantrine should be avoided.
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