Introduction

Rotavirus gastroenteritis has been rarely reported to cause extra-intestinal symptoms [1, 2] and are usually restricted to one site. The authors report a child with rotavirus gastroenteritis with multisystem involvement in form of encephalopathy, myositis, transaminitis and hypoalbuminemia.

Case Report

A 17-mo-old developmentally normal girl, without any significant past history, reported with complaints of loose stools, vomiting and fever for 7 d along with lethargy and swelling of feet for last 3 d, and an episode of convulsion. Loose stools were watery, 6–8 times per day, and without any associated blood or mucus. The child had received intravenous fluids and medications, including phenytoin. There was no history of abdominal distension, decreased urine output, or any history suggestive of shock or hemodynamic instability during treatment outside the hospital. She had not received rotavirus vaccine.

On examination, child was lethargic but there was no sign of dehydration or shock. Her weight-for-age, length-for-age and weight-for-height were all between −1 and + 1 SD. She had thickened feel of skin, pallor, and periorbital and pedal edema, without any rash or petechiae. There were no signs of meningeal irritation or any cranial nerve involvement. There was hypotonia, decreased power in all limbs, absent deep tendon reflexes, and flexor plantar response. Child exhibited excessive irritability on palpation of limbs suggestive of muscle tenderness and restriction of range of motion due to stiffness of skin and muscle. Liver was palpable 3 cm below the costal margin and spleen tip was palpable. Rest of the systemic examination was normal. Laboratory investigations revealed microcytic hypochromic anemia, thrombocytopenia, hypernatremia, hypokalemia, raised serum transaminases, raised creatine phosphokinase (CPK) (both total and CPK-MB fraction) and hypoalbuminemia (Table 1). Arterial blood gas (ABG) showed normal pH (7.44) and normal bicarbonate level (25.6 mmol/L). Stool for rotavirus antigen was positive by rapid immunochromatgraphic test (EpiTuub). CSF was acellular with protein levels of 12 mg/dl sugar of 104 g/dl and sterile culture. As there was no evidence of acidosis or deranged renal function, and mother was giving oral rehydration fluid in inappropriate dilution before being referred to authors’ hospital, hypernatremia was considered to be iatrogenic. Acute rotavirus gastroenteritis with hypernatremia, myositis, transaminitis and encephalopathy was considered. Hypernatremia and hypokalemia were corrected and phenytoin was continued. Over next three days, fever and loose stools subsided but child was lethargic, and developed increasing stiffness of all four limbs. Power was reduced in all four limbs and reflexes were not elicitable. Thickened feeling of skin and muscles persisted and sensorium did not improve over next 7 d. Repeat serum CPK level was 3540 U/L, and CPK-MB was 367 U/L suggesting falling trend; blood and urine cultures were sterile. Contrast-enhanced computed tomography (CECT) of head was normal. Stool for rotavirus typing revealed G3 + G9P[8] strain of rotavirus. CSF for rotavirus could not be processed because of drying of sample. Child was managed symptomatically and showed improvement. At the time of discharge, child was conscious, oriented, and had normal tone with near-normal (4/5) power in all limbs. During follow-up after six weeks, child had normal tone and deep tendon reflexes, and flexor plantar response. CPK total was 268 U/L and CPK MB was 77 U/L; SGOT was 35 IU/L, SGPT was 18 IU/L, total protein was 6.7 g/dl and serum albumin was 4.2 g/dl.

Table 1 Laboratory parameters of the index child at the time of admission
Full size table

Discussion

Rotavirus gastroenteritis has been reported to cause extra-intestinal symptoms involving various systems; but multisystem involvement is rare. The index child presented with neurological symptoms following acute gastroenteritis, which suggested dyselectrolytemia or acute viral encephalopathy. Persistence of neurological symptoms even after gastroenteritis settled, and serum electrolytes normalized, made authors’ suspect acute viral encephalopathy. Elevation of CPK was consistent with myositis. Finally a diagnosis of rotavirus acute gastroenteritis with encephalopathy with myositis with hepatic involvement (transaminitis with hypoalbuminemia) was made. A concomitant infection such as dengue causing multisystem involvement can cause similar presentation; however, the child had no rash or hemoconcentration, and she presented mainly with acute gastroenteritis during winter season (December) when there was no seasonal outbreak of Dengue in the city. However, as dengue or any other infection causing multisystem involvement was not ruled out by investigations, there remains a possibility of such co-occurrence.

Possible mechanisms of neurological manifestations in rotavirus infection are direct viral invasion, increased nitrites and nitrates in serum and CSF or, change in homeostasis of Ca++ or Cl−, dysregulation of the genes related to immune or stress response [3] or overproduction of cytokines by activated T cells and macrophages [4]. In the present case G3 + G9P[8] serotype was isolated from the stool of patient. To date G1, G3, G4, G5, G9 VP7 antigen and P4, P6, P8 VP4 antigen viruses have been isolated from serum, CSF or stool of patient with rotavirus encephalopathy [5, 6].

Myositis is considered a consequence of direct virus invasion into muscle or an immunological reaction [7]. There are reports showing elevated AST and ALT levels in rotavirus gastroenteritis [8]. However there are no reports showing hypoalbuminaemia in patients with biochemical hepatitis, which was present in index case.

Conclusions

The authors documented a rare presentation of rotavirus diarrhea associated with multisystem involvement in form of encephalopathy, myositis, transaminitis and hypoalbuminemia. Rotavirus should be considered in the differential diagnosis of a child with gastroenteritis presenting with encephalopathy or myositis.