Severe acute inflammatory myositis and rhabdomyolysis in pae
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A 12-year-old African girl with no known co-morbidities presented with progressive weakness of the lower limbs with associated myalgia and dyspnoea. She indicated that, a week prior to presentation, she had sore throat and fever and noticed weakness in her lower limbs. There was no history of any positive SARS-CoV-2 contacts. Two days prior to admission, she developed diarrhoea and mild dyspnoea and lost the ability to walk due to worsening weakness in her lower limbs and myalgia.

On clinical examination she was noted to be tachypnoeic, with oxygen saturation of 95% in room air. The rest of her vital signs and clinical examination were unremarkable, apart from the neurological examination. Her neurological higher functions were normal and she had a Glasgow Coma Scale (GS) of 15 out of 15. There was no meningism or signs of cranial nerve or cerebellar abnormalities. On motor examination hypotonia in both upper and lower limbs was noted, with diminished reflexes: 1 out of 4 in the upper limbs and absent in the lower limbs. Her power was 3 out of 5 in the upper limbs and 2 out of 5 in the lower limbs, and the weakness was noted to be worse proximally than distally. She had normal sensation to touch and proprioception, and there was no loss of bladder or bowel function.

Initial laboratory investigations revealed raised inflammatory markers. Her admission serum creatine kinase (CK) was 7134?U/L, which subsequently increased to 22?000?U/L. Serum phosphate was elevated, and serum lactate dehydrogenase was markedly elevated, as well as aspartate aminotransferase (2227?U/L), with only a moderately elevated alanine aminotransferase (457?U/L). The rest of liver function tests were normal aside from low serum albumin (23?g/dL). She had myoglobinuria on urinalysis and acute kidney injury.

These biochemical abnormalities were typical of severe muscle injury and rhabdomyolysis. Renal function did not improve with fluid resuscitation and required renal replacement therapy (RRT) and intensive care unit (ICU) admission on day 2. Acute indications for RRT were hyperkalaemia unresponsive to medical management (potassium 7.5?mmol/L), anuria and uraemic encephalopathy. She required intubation due to the low GCS (7 out of 15), presumed to be a consequence of uraemic encephalopathy.

Reverse transcription PCR test for SARS-CoV-2 was positive. Her HIV result was negative, and an autoimmune screen, including anticardiolipin, anti-b2 glycoprotein, anti-sm, Anti nuclear antibody (ANA) and Anti neutrophil cytoplasmic antibody (ANCA), was also negative.

She had normal cerebrospinal fluid result. Blood cultures did not grow any organisms. Radiological investigations included normal chest X-ray, renal ultrasound and CT of the brain. Her echocardiogram showed a structurally normal heart with an ejection fraction of 65% and no coronary artery dilatation.

Her blood urea and creatinine improved, and the encephalopathy resolved with clearance of blood urea. RRT was stopped on day 5 of her ICU admission and she was able to be extubated on day 2 in the ICU. She complained of muscle pain which improved with administration of non-steroidal anti-inflammatory drugs and continuation of prednisone. Muscle weakness persisted, but improved gradually over the course of her hospital stay.

It was not clear in this case whether the severe inflammatory myositis was a consequence of an acute viral inflammatory myositis due to SARS-CoV-2 or as part of MIS-C, which has been recently described. This patient did fulfil all the criteria for the diagnosis of MIS-C and was subsequently treated with intravenous immunoglobulin 2?g/kg, and methylprednisolone 10?mg/kg Intravenous injection (IVI) for 3?days followed by 30?mg/kg for 2?days. Antibiotics were stopped after 72 hours as no organisms were cultured on blood, Cerebrospinal Fluid (CSF), urine or stool.