Fatal Cardiac Tamponade in Malarial Acute Renal Failure

Abstract

Uremic hemorrhagic pericarditis occurs much less frequently in acute than in chronic renal failure, but when it does, it is a potentially fatal complication. The possibility of hemorrhagic pericarditis and cardiac tamponade should be considered in patients with acute renal failure and acute hemodynamic instability. This study reports a case of falciparum malaria complicated by acute renal failure that developed fatal cardiac tamponade in the recovery phase of acute renal failure.

Keywords:

• acute renal failure
• malaria
• pericarditis

INTRODUCTION

Uremic hemorrhagic pericarditis usually complicates chronic renal failure but may also occur in cases of acute renal failure (ARF) that are slow to resolve. When it does occur in ARF, it is a potentially fatal complication.[1] It may present dramatically with cardiac tamponade without antecedent clinical and radiological signs of pericardial effusion. Though it may occur in ARF of any etiology, it is extremely rare in malarial ARF. There is only one reported case of confirmed falciparum malaria associated with cardiac tamponade.[2] This study reports a case of falciparum malaria complicated by ARF who developed fatal cardiac tamponade in the recovery phase of ARF.

CASE REPORT

A 45-year-old male hailing from an area that is endemic for falciparum malaria presented with intermittent fever with chills of five days duration and oliguria of 1 day duration. Examination showed a febrile individual with pallor and icterus, no pedal edema, BP 114/74 mm of Hg, and no hepatosplenomegaly.

Initial investigations showed Hb 10.9 gm/dL, TLC 4100/cmm, schizonts of plasmodium falciparum on peripheral smear, blood urea 161 mg/dL, serum creatinine 2.9 mg/dL, Na 136mEq/L, K 4.8 mEq/L, serum bilirubin 6.0 mg/dL (unconjugated 3.8 mg/dL), AST 32 IU/L, and ALT 34 IU/L. Urinalysis showed trace albuminuria with 2–3 WBCs/HPF and no RBCs. Urine culture was sterile and urine spot sodium was 68 mEq/L. An ultrasound of the abdomen showed hepatosplenomegaly (liver 15.4 cm and spleen 12.4 cm), and both kidneys were normal in size and echogenicity. He was negative for HBsAg, anti-HCV, and HIV. Blood cultures were sterile. His subsequent investigations are shown in Table 1. He was treated with parenteral quinine, artesunate, and ceftriaxone. In view of advance azotemia, he was taken up for hemodialysis two days after admission. He showed gradual improvement in his condition, in that he became afebrile, urine output gradually improved, and liver function tests showed a decline toward normal. However, he continued to remain dialysis-dependent and received 11 sessions of hemodialysis until day 15 of hospitalization. On the 16^th day of hospitalization, he developed acute respiratory distress followed by cardiac arrest from which he could not be revived despite vigorous resuscitative effort.

Table 1 Serum hematological and biochemical parameters

	Day 1	Day 2	Day 3	Day 4	Day 6	Day 8	Day 10	Day 12	Day 14	Day 16
Hemoglobin (g/dL)	10.9	9.0	6.1	6.1	7.0	8.5	9.6	9.3	9.9	9.0
TLC/mm^3	4100	9600	14400	12700	9200	11800	9000	9000	10000	9500
BUN (mg/dL)	62	69	171	156	128	117	110	109	116	105
Creatinine (mg/dL)	2.9	2.8	5.9	4.7	5.9	5.3	7.6	8.5	8.6	8.5
Sodium (mEq/L)	136	137	134	135	130	137	132	135	132	131
Potassium (mEq/L)	4.8	4.6	5.0	4.8	4.7	5.2	4.6	5.0	4.6	4.6
Bilirubin (mg/dL)	6.0	18.2	32.4	36.7	29.2	24.9	9.9	3.7	3.8	2.9
SGOT (IU/L)	32	148	62	78	75	104	68	49	55	100
SGPT (IU/L)	34	316	25	24	33	72	54	56	56	117

*Day 1 being the day of hospitalization.

Autopsy showed approximately 350 mL of hemorrhagic fluid in the pericardial cavity (see Figure 1), and sections from the pericardium and epicardium showed fibrinous material on the surface of the epicardium along with inflammation and fibrin deposits in the epicardium (see Figure 2), centri-lobular necrosis in the liver, congestive splenomegaly, and features of acute tubular necrosis in the kidneys.

Figure 1. Hemorrhagic pericardial effusion.

Figure 2. Serofibrinous pericarditis.

DISCUSSION

Acute renal failure is a common complication of plasmodium falciparum malaria in tropical countries.[3] This case had documented plasmodium falciparum parasitemia and had complications in the form of hemolysis and renal failure. He was treated with quinine and artesunate and showed gradual recovery with clearance of parasitemia. His urine output had progressively improved though the azotemia persisted. He was adequately dialyzed, having received 11 sessions of hemodialysis over a period of 15 days. He had sudden cardiac death 16 days after hospitalization. His serial electrocardiograms and chest skiagram done earlier had been normal. Because he had recovered from malaria and was also recovering from ARF, it was difficult to attribute either of these as the cause for sudden death. Autopsy showed a large hemorrhagic pericardial effusion and serofibrinous pericarditis.

Pericarditis and subsequent cardiac tamponade in this situation can be due to either malaria or uremia. Primary cardiac involvement in malaria is rare and limited to toxic myocarditis, conduction abnormalities, and (rarely) pericarditis.[4] There is only one reported case of hemorrhagic pericarditis with cardiac tamponade associated with falciparum malaria.[2] The authors attributed the hemorrhagic pericarditis in that case to malaria because of the development of pericarditis and subsequent effusion during the recovery stage of acute renal failure, resolution of effusion with clinical defervescence of malaria, and isolation of the falciparum antigen from the pericardial fluid. In this case, though, the cause for pericarditis and tamponade was probably uremia, as he had already recovered from malaria. Yet, the role of malaria in the initiation of pericarditis in this case cannot be definitely excluded. The pathogenesis of pericarditis in malaria is possibly due to locally elevated cytokine levels. Day et al. have demonstrated that the systemic pathologic abnormalities of severe malaria are associated with elevated plasma cytokines.[5]

Though tamponading uremic pericardial effusion usually complicates chronic renal failure, it has been reported to occur in cases of ARF also. Zakynthinos et al. reported tamponade developing late in the course in five cases of ARF of varying etiologies.[6] The causes of cardiac tamponade in uremic pericarditis are pericardial effusion, usually of the serosanguineous type, massive hemorrhage into the pericardial sac, and the collagenization of pericardial exudate. This case had massive hemorrhagic effusion as demonstrated on autopsy.