Tozinameran

Author Information

An event is serious (based on the ICH definition) when the patient outcome is:

• * death

• * life-threatening

• * hospitalisation

• * disability

• * congenital anomaly

• * other medically important event

A 37-year-old man developed myocarditis, pulmonary haemorrhage, thrombocytopenia, extensive myositis and rhabdomyolysis following COVID-19 vaccination with tozinameran.

The man presented to the emergency department (ED) with back pain for 3 days, left arm pain, swelling and paresthesia for a day in July 2021. He also informed about sudden onset of shortness of breath along with dry cough, orthopnea and sweating. He denied history of smoking, alcohol consuming and drug abuse. He had received, his first dose of COVID-19 vaccination with tozinameran [BNT162b2 mRNA; Pfizer/BioNTech; route and dosage not stated] 12 days before the current presentation. On admission, he was dehydrated. His vital signs were as follows: BP was 138/87 mmHg, heart rate was 114 bpm, respiratory rate was 32 bpm, oxygen saturation was 78% and required oxygen supplementation; and body temperature was 37.1°C. Subsequently, his chest auscultation demonstrates widespread bilateral fine crepitation, mainly over the left lung. His physical examination of the vaccinated arm demonstrates markedly swollen, stiff, warm and tender, with mild skin erythema and restricted movement at the left shoulder and elbow joints. He also informed about reduction in sensation to fine touch and temperature at the entire left upper limb. His spine analysis showed tenderness at paraspinal muscles along with severe tenderness over the latissimus dorsi muscle. Subsequently, his urine examination revealed tea coloured urine and urine dip stick examination was positive for blood (+4) and protein (+). Also, his laboratory examination showed elevated haemoglobin, C reactive protein, platelet count, haematocrit, WBCs, D-dimer, troponin T, creatine kinase, ProBNP and estimated glomerular filtration rate. His laboratory tests were suggestive for acute kidney injury, hyperkalemia and hypoxemia. Thereafter, his electrocardiography revealed sinus tachycardia. Then, his chest X-ray demonstrates features suggestive of pulmonary oedema. Also, chest ultrasound showed bilateral B lines. His CT of the chest and pulmonary angiogram showed extensive bilateral ground-glass and patchy nodular opacities on the left lung; without pulmonary embolism. His echocardiogram reported mild concentric left ventricular hypertrophy with mild global hypokinesis of the left ventricle and the overall left ventricular systolic function was mildly impaired, with an ejection fraction between 45% and 50%. Therefore, his right ventricular systolic function was mildly impaired. Then, his left upper arm soft tissue ultrasound revealed soft tissue edema and abnormal heterogeneous echogenicity and relatively increased vascularity, which are features suggestive of myositis-myonecrosis. Subsequently, he started receiving treatment with tramadol along with paracetamol. On following day of hospitalisation, his full blood count was significant for thrombocytopenia. Therefore, from the above findings, he was diagnosed with severe myositis complicated with rhabdomyolysis and non-oliguric acute kidney injury, thrombocytopenia, myocarditis with pulmonary edema, and pulmonary haemorrhage. His analysis for potential toxic, infectious, paraneoplastic, and autoimmune disorders were non-significant.

Then, the man started receiving treatment with methylprednisolone along with immune-globulin. This treatment showed good response. Eventually, his condition resolved and he was discharged from the hospital after 16 days on prednisolone for 6 weeks.