A 73-year-old male from Kathmandu, a retired physician by profession, presented to the emergency room with generalized weakness associated with fever for one week. He had self-tested for COVID-19 antigen at home which was positive six days prior to presentation. His past medical history included diabetes mellitus and systemic hypertension for 20 years, coronary artery disease (triple vessel disease) for which he had undergone coronary artery bypass grafting and percutaneous coronary intervention six months before this presentation. He had also undergone low anterior resection for mid-rectal carcinoma one month prior. He had received neo-adjuvant chemotherapy (two cycles) with carboplatin-based therapy six months before and 28 sessions of radiotherapy (last session 3 months back). His medications included aspirin 75 mg once daily, clopidogrel 75 mg once daily, metoprolol succinate 25mg once daily, metformin 1 gm twice daily, losartan 50 mg once daily and rosuvastatin 10 mg once daily. He was a social drinker and non-smoker. His family history was unremarkable.
On examination in the emergency room, he was conscious and oriented. His pulse rate was 113/min, regular, blood pressure was 150/80 mmHg, temperature was 97.20F and oxygen saturation was 94% on room air. His respiratory, cardiovascular and abdominal examinations were unremarkable. His nervous system examination was not properly carried out in the emergency room but looked grossly normal. His laboratory tests showed anemia with acute kidney injury with raised inflammatory markers and transaminases (table 1) and his polymerase chain reaction (PCR) for COVID-19 was positive. His chest X-ray was normal. He was admitted with the provisional diagnosis of mild COVID-19 with acute kidney injury. His metformin and losartan were held in view of acute kidney injury. During admission in the ward, he complained of increasing limb weakness. His renal function started getting worse and his urine culture grew Escherichia coli sensitive to meropenem. His serum potassium started decreasing (table 1) after a couple of days, therefore his weakness was assigned to hypokalemia. His thyroid function test was also suggestive of hypothyroidism which was presumed to have contributed to the weakness. At the same time, he was complaining of bowel incontinence which was concluded to be due to his recent rectal surgery.
On the ninth day of admission, he was still complaining of weakness of his limbs and inability to get out of bed. At this time, a full neurological examination was done. The patient was conscious, well oriented to time, place and person, his higher mental function and sensory examinations were intact. However, he had mild atrophy of the proximal muscles bilaterally but no fasciculations, his muscle power was 2/5 in bilateral shoulders (abduction, adduction, flexion, and extension), 1/5 in bilateral hips (flexion, extension, abduction, and adduction) and 2/5 in neck flexors and extensors. He had global areflexia and his plantars were bilaterally flexors. His distal muscle power was normal and he had no history of dysphagia, dysarthria, diplopia or aspiration. Meanwhile his liver transaminases were increasing (table 1) for which no etiology could be found. At this time, Guillaine Barre Syndrome (GBS) was strongly considered as one of the differentials as the patient had proximal weakness with areflexia. Lumbar puncture and nerve conduction test did not show any feature suggestive of GBS. Muscle enzymes including creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) were sent as polymyositis was another possibility. CPK and LDH were markedly elevated (table 1), therefore a working diagnosis of polymyositis was made. A magnetic resonance imaging (MRI) of bilateral thighs showed increased signals in STIR sequence (figure 1) which was also in favour of muscle inflammation. He was then started on prednisolone at 1mg/kg along with other supportive treatment. The patient started feeling better in a couple of days after starting prednisolone. He underwent both active and passive physiotherapy during the ward admission. Finally, he was planned for discharge on the 16th day of admission (seventh day of steroid). His power in left shoulder had improved to 3/5, and bilateral hips to 2/5 and that in other groups was stationary. His CPK had started decreasing and his renal function was normal (table 1). Meanwhile his antinuclear antibody (ANA) and myositis profile came back negative. His muscle biopsy came back showing features of inflammatory myositis with both perimysial and endomysial infiltration of inflammatory cells (figure 2). During follow-up at one week, his power in bilateral upper limbs had improved to 4-/5, bilateral lower limbs to 3/5 and neck muscles to 3/5. His CPK and transaminases had come down to normal (Table1). The patient is currently under tapering steroid along with methotrexate and getting active physiotherapy.