Rhabdomyolysis in falciparum malaria – a series of twelve cases (five children and seven adults)

Abstract

There are very few reports in the literature of rhabdomyolysis in falciparum malaria and they mostly consist of single case studies. A report from Sri Lanka described a single patient with myoglobinuria and skeletal muscle necrosis. Taylor and Prosser reported a single case of rhabdomyolysis with renal failure. We report on 12 patients with evidence of skeletal muscle injury in severe malaria from Rourkela, Orissa State, India.

Introduction

Rhabdomyolysis in Plasmodium falciparum malaria is reported occasionally in the literature. One report from Sri Lanka described a single patient with general myalgia, myoglobinuria and histological evidence of inflammatory skeletal muscle necrosis.¹ Miller et al. ² demonstrated in a report of Gambian children that muscle damage was proportional to the severity of the disease. Taylor and Prosser³ reported a single case of rhabdomyolysis with renal failure in an 18-year-old man.

We report on 12 cases (five children and seven adults) of skeletal muscle injury in severe malaria from Rourkela, Orissa State, India. (Orissa, with a population of only 4% of the nation, unfortunately contributes to nearly 40% of the deaths due to falciparum malaria in India.)

Case history

Five children and seven adults were admitted with a history of fever, generalized malaise and highly-coloured urination. Eight had cerebral manifestations. There was no history of multiple intramuscular injections, muscle trauma, other elicitable causes of skeletal muscle injury or any evidence of acute myocardial infarction. Three patients had a seizure prior to their hospital admission. In all cases, an asexual form of P. falciparum malaria was detected. Details of the patient are given in Table 1. We suspected rhabdomyolysis as they each had a history of severe muscle pain or highly-coloured urination. The serum creatinine phosphokinase was estimated and was found to be elevated. None of the patients had myoglobinuria or haemoglobinuria. They were treated with injections of quinine dihydrochloride infusions and intravenous fluids. All recovered completely. Follow-up of these patients revealed no residual deficit or abnormal biochemical parameters.

Table 1

Clinical details of patients with falciparum malaria with rhabdomyolysis

Patient (age, sex)	Fever days	Hb (g/dL)	Urea (mg/dL)	Creatinine (mg/dL)	Bilirubin (mg/dL)	AlT (iu/L)	CPK (iu/L)	Cerebral malaria	Seizure
19, female	4	8.5	124	1.7	16.1	27	1680	No	No
17, male	4	10	120	2.4	6.0	78	1141	Yes	No
34, female	4	7	51	0.6	10.0	23	6100	Yes	No
65, male	2	10.5	28	1.1	2.8	18	5500	No	No
7, male	4	8.0	34	0.5	1.4	77	2550	No	No
4, female	7	2.0	54	0.4	1.7	—	537	Yes	No
3, male	7	7.0	115	1.0	1.3	69	2100	Yes	Yes
3, male	6	6.5	56	0.6	1.0	—	423	Yes	Yes
5, female	3	4.0	52	0.6	5.1	21	535	Yes	No
21, female	3	6.5	67	1.0	2.1	—	710	Yes	No
22, male	3	7.0	75	0.8	7.0	57	706	Yes	Yes
15, male	4	8.5	32	0.8	2.4	74	4900	No	No

Hb, haemoglobin; AlT: alanine aminotransferase CPK: creatinine phosphokinase (normal value < 150 iu/L)

Discussion

The mechanism of rhabdomyolysis in malaria is not clearly understood. One hypothesis is that the sequestration of parasitized erythrocytes in the skeletal muscle capillaries leads to microvascular obstruction.

Rhabdomyolysis is usually overlooked and is not investigated or the entity is not suspected. In patients with falciparum malaria complaining of severe myalgia and black-coloured urine, a diagnosis of rhabdomyolysis may be considered. Acute renal failure may be associated in patients with extensive rhabdomyolysis due to any cause.^3,4 We have not been able to correlate the creatine phosphokinase value with the degree of severity of the malaria reported from Africa. Our patients had various grades of haemolysis but none had acute renal failure needing dialysis support.

References

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, Skeletal muscle necrosis in falciparum malaria. BMJ 1988;296:1039

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. Biochemical evidence of muscle injury in African children with severe malaria. J Infect Disease 1989;159:139–42

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