Dear Editor,
Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is a novel virus first identified in China, that results in coronavirus disease 2019 (Covid-19). Patients with Covid-19 often present with a prodrome of symptoms including fever, cough and dyspnoea following exposure to SARS-CoV-2 [1]. In some individuals the dyspnoea may rapidly progress, culminating in severe hypoxia necessitating mechanical ventilation. To-date, Covid-19 is managed supportively as there are no proven treatments. Infection with SARS-CoV-2 is associated with a number of complications; typically renal insufficiency, venous and arterial thomboembolic, and myocardial complications. In this paper, we describe two patients admitted with confirmed (via reverse transcriptase-polymerase chain reaction (RT-PCR) testing) severe Covid-19 needing mechanical ventilation and renal support during their intensive care admission, who on stepping down were noted to have lower limb weakness.
The first patient was a 75-year old Caucasian never smoker, retired IT recruitment manager with a medical history of ischaemic heart disease and bypass surgery in 2001, chronic kidney disease, hypertension and dyslipidaemia. On 25th of March, he was admitted to a district general hospital with a week’s history of worsening dyspnoea. At admission, he was in respiratory failure and acute (on chronic) kidney injury (AKI), and within a few hours required mechanical ventilation and initiated on intravenous (IV) antibiotics for a left lower zone consolidation (Fig. 1a; Table 1). Due to ICU bed pressures, he was moved, 2 days later, to our hospital (a tertiary centre). He made a good respiratory recovery and was weaned of its support and oxygen over the next 48 h though did have 36 h of continuous veno-venous haemofiltration (CVVHF). Additionally, with high D-dimer levels at admission he was maintained on therapeutic IV unfractioned heparin; a CTPA conducted showed multiple segmental and sub-segmental filling defects, with widespread ground-glass opacities (GGOs) and areas of consolidation/ atelectasis (Fig. 1b). Subsequently, he was changed over to a new oral anti-coagulant (NOAC). Over the next 7 days, despite routine physiotherapy, the patient failed to convalesce with weakness in the lower limbs. Neurological examination of the lower limbs revealed an increased tone and reduced power bilaterally though more pronounced on the left. There was no loss of pulses or any sensory findings in the lower limbs and the Babinski sign was negative; coordination and gait were challenging to assess as the patient needed hoisting to stand. A CT scan of the head showed no acute intracranial abnormality (Fig. 1c). Persistent bilateral lower limb weakness and stiffness prompted a magnetic resonance imaging (MRI) scan of the head; this showed small vessel disease and infarcts in the parietal and occipital lobes, and in the midbrain and basal ganglia (Fig. 1d). The patient was subsequently moved to a neuro-rehabilitation centre on the 27th of April for ongoing management/ convalescence.