|
Algid malaria or hypotension due to peripheral
circulatory failure may develop suddenly in severe malaria or it may
be the presenting feature in some cases of malaria, with a systolic blood pressure less than 80 mmHg (10.7 kPa)
in the supine position [less than 50 mmHg (6.67 kPa) in children], a
cold, clammy, cyanotic skin, constricted peripheral veins and rapid
feeble pulse. In some countries this clinical picture is often
associated with a complicating Gram-negative septicemia and possible sites of associated infection
should be sought in such patients, e.g. lung, urinary tract (especially if there is
an indwelling catheter), meninges (meningitis), intravenous
injection sites, intravenous lines etc.[1] Severe hypotension can also develop
suddenly in patients with
pulmonary edema, metabolic acidosis, sepsis, and/or massive hemorrhage due to splenic
rupture or from the gastrointestinal tract.[1,2] Postural hypotension may be
secondary to autonomic dysfunction.[2]
Most patients with shock exhibit a low peripheral vascular resistance
and elevated cardiac output. Cardiac pump function appears remarkably
well preserved despite intense sequestration of parasitized erythrocytes
in the microvasculature of the myocardium.[1] 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. Septicemia, metabolic acidosis and
hypoxia may result in a drop in cardiac index.
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:
[See Treatment of Severe P.
falciparum malaria]
-
Hypovolumia
and 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. Dehydration should be
managed with intravenous saline or Ringer’s lactate. 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.
However, fluid overload should be avoided at all costs, especially
in pregnant women. 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.
-
Blood and urine culture should be done. 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.[1]
Other Cardiovascular Problems: 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.
|
