Department of Nephrology Sanjay Gandhi Post Graduate Institute of Medical Sciences Raebareli Road Lucknow India Email: sgulati{at}sgpgi.ac.in
Sir,
Falciparum malaria is a major public health problem in the tropical developing world including India. The spectrum of malaria may range from simple pyrexia to severe complicated forms including cerebral malaria [1]. Cardiac involvement in malaria is rare and predominantly limited to toxic myocarditis and conduction abnormalities [2,3]. We report here a case with documented falciparum malaria and associated cardiac tamponade.
Case. A 30-year-old male presented to the emergency ward of our institute with a history of intermittent high-grade fever with chills for 10 days, icterus for 5 days, decreased urinary output and headache for 3 days. There was history of meleana for the last 2 days. On examination he was found to have blood pressure of 130/80 mmHg, he had a temperature of 100.8°F. He had pallor and icterus. He had no peripheral oedema. On abdominal examination he had hepato-splenomegaly. Cardiovascular examination did not reveal any abnormality. His laboratory reports showed haemoglobin 9.0 g/dl, TLC 7000/cumm, glucose 51 mg/dl, creatinine 4.6 mg/dl, blood urea nitrogen (BUN) 91 mg/dl, serum bilirubin 34 mg/dl, Na+ 137 mEq/l and K+ 4.0 mEq/l. His peripheral blood film showed significant falciparum parasitaemia (5%).
Based on initial evaluation a diagnosis of acute renal failure, acute tubular necrosis secondary to falciparum malaria with hepatic insufficiency and upper GI bleed was made. The patient started on conservative management with i.v. quinine (10 mg/kg/day), i.v. pantoprazole (400 mg/day) and vitamin K (10 mg/day). On day 2 of admission, the patient developed severe pain in his abdomen associated with constipation and subsequently was diagnosed to have pancreatitis for which conservative management was instituted. The serial biochemical and haematological parameters are depicted in Table 1. An ultrasound of the abdomen carried out on the same day showed bulky head of the pancreas and hypoechoic shadows on the pancreas. Serum amylase on the same day was 1760 U. On day 4 of admission he was noticed to have a pericardial rub. A two-dimensional Echo revealed, evidence of pericardial effusion (Figure 1). The patient had a peak serum creatinine of 4.8 mg/dl and the patient was given 3 h of heparin-free haemodialysis. Gradually the patients general condition started improving and his pancreatitis and oliguria resolved, and his output increased from 600 ml/24 h to >2000 ml/24 h. The serum creatinine decreased to 2.05 mg/dl. However, pericarditis persisted and he had intermittent spikes of fever.
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Comment. Falciparum malaria is one of the most common parasitic diseases causing much morbidity and mortality in the tropics. Pericardial involvement in malaria is rare, described only in a few reports worldwide [2,3]. It is usually in the form of pericarditis. This is an unusual case where a patient of documented falciparum malaria and acute renal failure not only developed periodically but also pericardial effusion. While the acute renal failure improved, the pericardial involvement worsened and he developed tamponade, which responded to anti-malarial therapy.
The issue is whether the effusion was due to malaria or due to uraemia per se. The indirect evidence for the association with malaria include, the development of pericarditis and subsequent effusion during the recovery stage of acute renal failure. The azotaemia was for a short duration and hence unlikely to be solely responsible for development of pericarditis and effusion. There was resolution of effusion with clinical defervescence of malaria. The patient had no peripheral oedema and thus fluid over-load is also not a likely contributing factor for effusion. The confirmatory evidence for this association comes from the isolation of the falciparum antigen from the pericardial fluid. We are not aware of any previous published case in literature reporting this association.
The mechanism of the development of pericardial effusion is not very clear. One possible explanation may be the locally elevated cytokine levels. Day et al. [4] have shown that cytokines produced locally in particular tissue during malarial infection may be regulated by the degree of regional parasitic sequestration. Probably regional sequestration of parasites in pericardium may explain the isolated pericardial effusion in our case. Documentation of parasitic antigen in the pericardial fluid confirms the association of malaria and pericardial effusion.
We conclude that development of pericardial effusion may be seen with falciparum malaria. This is crucial, as tamponade if not diagnosed and managed promptly may be a potentially fatal complication, in what is otherwise a curable disease.
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