Neurologic Complications and Manifestations-
SARS-CoV-2 virus enters the nervous system by hematogenous spread or retrograde neuronal transmission via the olfactory bulb and enters neuronal and glial cells by attaching to the angiotensin-converting enzyme 2 (ACE2) receptor, widely expressed in various neuronal populations (15). A wide range of neurologic manifestations have been reported in more than a third of the Covid-19 patients, particularly those with a severe infection (16). In addition, neurologic complications, particularly cerebrovascular diseases, represent a major cause of morbidity and mortality for ECMO patients (17, 18).
All Covid-19 patients on ECMO support underwent routine neurological examination. Sixty percent of the ECMO patients developed significant neurologic complications affecting both central and peripheral nervous systems. The most common neurological complications were encephalopathy, seizures, autonomic dysfunction, and critical illness polyneuropathy (Table 5).
Encephalopathy, defined broadly as an alteration in mental status, was seen in 6 patients and can be attributed to a variety of etiologies. All 9 extubated patients can follow commands and show gradual improvement in mental status. Six patients underwent continuous electroencephalography (EEG) monitoring using leads placed into the subgaleal space. Neurologists with advanced EEG training reviewed both raw and quantitative EEG data in correlation with patients’ neurologic exam and hemodynamic parameters. All six patients showed abnormal epileptiform activity. (Figure 5) In three patients, the epileptiform activity correlated with a change in neurologic exam, and both EEG findings and neurologic exams improved after the administration of antiseizure medication. Two patients, who remain on ECMO support at the time of this report, had epileptiform activity without a clinical correlate that also resolved with antiseizure medication. Seven patients developed wide fluctuations of heart rate and blood pressure out of proportion to known stimuli that was suggestive of autonomic dysfunction. Four of these patients had poorly controlled DM rendering it difficult discern between diabetic autonomic neuropathy versus other etiology. We did not find any clinical or radiographic evidence of brain ischemia or hemorrhage in our patients. Transcranial Doppler, obtained in one patient, did not reveal any high-intensity signal transients suggestive of cerebral micro emboli. Brain MRI obtained in two of the patients with seizure activity did not show any acute intracranial finding.
Six patients developed generalized weakness concerning for critical illness myopathy and or polyneuropathy; however, confirmatory nerve conduction and electromyographic studies were not obtained to limit provider exposure. The four patients who have been discharged from the hospital have shown continued improvement in their muscle strength. As this is a preliminary report, the patients’ functional neurologic outcome remains in evolution. Cerebral Performance Category (CPC) will be obtained during follow up visits after discharge.
The underlying mechanisms of neurological complications in Covid-19 patients is still unclear and may involve both direct and indirect effects of SARS-CoV-2 infection as part of the systemic inflammatory response. Coagulopathy, myocardial injury, and pre-morbid risk factors, such as hypertension and diabetes, may also contribute to the development of neurological complications in these patients.