Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can affect the respiratory, haematopoietic, immune, cardiovascular, gastrointestinal and neurological systems (central and peripheral nervous). It causes neurological complications by direct or indirect phenomena. The various documented neurological presentations include anosmia/hyposmia, ageusia/hypgeusia, encephalitis, myelitis, meningitis, Guillain–Barre syndrome, ischaemic stroke, intracerebral haemorrhage, ruptured aneurysm and subdural haematoma.6
The SARS-CoV-2 virus has neurotropic and neuroinvasive properties. It gains entry into the human body mainly via angiotensin-converting enzyme 2 (ACE-2) receptor.3,7 This receptor is expressed in several organs in the body, the brain parenchyma inclusive. When these receptors are inhibited by SARS-CoV-2 virus, vascular autoregulation and cerebral blood flow becomes compromised.4,8,9 ACE-2 receptor inhibition leads to decreased angiotensin secretion and thus disruption of the blood pressure autoregulation mechanism and consequently increase risk of brain parenchymal haemorrhage.4,10
SARS-CoV-2 is also known to cause an extensive vascular inflammatory response.6,11 This inflammatory process has been noted to be the initiate of “COVID-19–associated coagulopathy through its effect on platelets, endothelium, coagulation and immune system.12 This has been known to principally contribute to thrombotic events rather than haemorrhagic events; however, there are several described cases of bleeding associated with COVID-19 which are usually non-surgical haemorrhages.4,11−13 It known that endothelial inflammation can increase the probability of intracranial haemorrhage in acute disease processes, including reversible encephalopathy syndrome and reversible cerebral vasoconstriction syndrome.14,15 Similarly, the inflammatory response within the walls of the vasculature in patients with COVID-19 can lead to vascular injury and thus increase the possibility of rupture and associated bleed.
Sweid and his colleagues described COVID-19 and stroke in a retrospective study of 22 adult patients; of these patients, 17 had acute ischemic strokes, 3 had a ruptured cerebral aneurysm, and 2 patients had cerebral venous sinus thromboses.4 Oxley et al. documented that there was an association of large vessel occlusion in young adults with COVID-19.16 Rothstein et al. also demonstrated the occurrence of ischaemic stroke, subarachnoid haemorrhage and intracerebral haemorrhage in patients with COVID-19; this they described as comparatively uncommon.3 Likewise, Nawabi et al. reported cases of patients with COVID-19 and intracranial haemorrhage.11 They studied 18 patients and found that the presence of intracranial haemorrhage characteristically associated with the severity of the patient’s COVID-19 symptoms; only 2 of these patients had a bleed prior to presentation with respiratory symptoms.11 In COVID-19 associated haemorrhagic stroke, the estimated prevalence ranged from 0.4 to 2.4%.17 Different types of intracranial haemorrhage and their risk factors in patients with COVID-19 were described by Altschul and his colleagues.18 Most patients presenting with COVID-19 associated stroke had baseline cardiovascular risk conditions such as hypertension, diabetes mellitus, hyperlipidemia, smoking, or previous stroke history. Numerous factors that make COVID-19 patients prone to intracranial haemorrhage include low platelets, hyperfibrinolytic state, consumption coagulopathy, use of antiplatelets and or anticoagulant medications, prolonged hypoxia of endothelial cells and pro-inflammatory state due to cytokine storm.19
In 2020, Gogia et al. reported a case of COVID-19 associated hyperacute SDH, extensive intracerebral haemorrhage and subarachnoid haemorrhage in a 75-year-old patient. This individual was on double antiplatelet (aspirin and clopidogrel) treatment.20 In a study, among 5227 individuals with COVID-19, 35 (0.7%) were found to have haemorrhage of some kind and 17 (0.3%) were due to acute SDH. Twelve (70.6%) of the patients with SDH had a head trauma before the haemorrhage and five were on anticoagulant drugs.18 Our index patient had chronic SDH with a prior history of use of aspirin but no antecedent history of head trauma. The fact that SARS-CoV-2 binds to ACE2 receptors and associated thrombocytopenia may explain the increased risk of a cerebral haemorrhage. Viraemia and ensuing endothelial injury may make the bridging veins of traversing the subdural space more at risk to haemorrhage after a minor trauma from sneezing, coughing or a Valsalva manoeuvre.10
In addition to the hypercoagulable and thromboembolic complications that occur in patients with COVID-19, surgical acute and chronic intracranial haemorrhagic complications should be considered in diabetics and hypertensive patients with SARS-COV-2 infection who have altered level of consciousness. This highlights the need for early neuroimaging in this group of patients.