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CMAAO Coronavirus Facts and Myth Buster: Unusual CNS Manifestations |
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CMAAO Coronavirus Facts and Myth Buster: Unusual CNS Manifestations

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961:  Update on Covid-19

IMA-CMAAO Webinar on “Neurological complications in COVID-19 – Part 2”

27th June, 2020, 4-5pm

Participants: Dr KK Aggarwal, President CMAAO, Dr RV Asokan, Hony Secretary General IMA, Dr Ramesh K Datta, Hony Finance Secretary IMA, Dr Sanchita Sharma

Faculty: Dr MV Padma Shrivastava, Prof & Head, Dept of Neurology, AIIMS, New Delhi

Key points from the discussion

  • COVID-19 is very similar to SARS coronavirus of 2003 as it shares the same ACE2 receptor. The initial clinical manifestations are fever, cough, dyspnea and fatigue. The most important lab parameter is lymphopenia. In severe cases, viral pneumonia may lead to severe acute respiratory syndrome, which may be fatal.
  • Diagnosis: Rapid antigen test, Nucleic Acid Amplification Test (NAAT), which gives results in 2 hours, and RT-PCR test (nasopharyngeal swab), which gives results in 8-12 hours.
  • ACE2 receptors are present in nervous system and skeletal muscles.
  • Coronaviruses go beyond the respiratory tract and may invade the CNS resulting in neurological complications (CNS, PNS and skeletal muscle injury). Although the exact route by which the virus enters the nervous system is not known.
  • A missed diagnosis of patient presenting with neurological manifestations increases the chances of spread of infection to HCWs.
  • The COVID-19 virus may enter the CNS through the hematogenous or retrograde neuronal route (evident by the symptom of anosmia).
  • Patients with severe disease have greater likelihood of developing neurological symptoms compared to patients who have mild or moderate disease.
  • It has been shown that intranasal administration of SARS CoV and MERS CoV led to rapid invasion of the virus into the brain, the likely route being through the olfactory bulb via trans-synaptic route.
  • Neurological damage that follows invasion of the COVID-19 virus in the CNS is partially responsible for the acute respiratory failure seen in these patients.
  • Neurological complications seen include HCoV-related meningitis, encephalitis, acute flaccid paralysis, early onset olfactory and gustatory dysfunction and changes in smell and taste perception. Anosmia, hyposmia and dysgeusia have been added in flu screen now.
  • The first observational case series from Wuhan was published in April this year in JAMA Neurology, where around 40% of hospitalized patients had some neurological complaints. The CNS manifestations were dizziness, headache, impaired consciousness, stroke, ataxia and seizures, while the peripheral nervous system manifestations included aguesia, anosmia, vision impairment, neuropathies, GBS. There were skeletal muscular injury manifestations.
  • Red flags in lab parameters, which increase the chances of neurological complications, are lymphopenia, decreased platelet count and high BUN.
  • Older COVID-19 patients with risk factors are more at risk of developing new onset cerebrovascular accident during hospitalization (did not present with stroke), which is an important negative prognostic factor. Most of the strokes were ischemic stroke (Lancet).
  • Older patients and those with diseases like HT, DM, CVD, and malignancy are more susceptible to COVID-19 and are also more likely to develop serious infection.
  • Nervous system manifestations, which include acute ischemic stroke, intracerebral hemorrhage, encephalopathy, skeletal muscle injury, seizures are more common in patients with severe infections.
  • Patients with severe infection had raised TLC, increased neutrophils, lymphopenia and high CRP; they also had high D-dimer levels (JAMA).
  • Lymphopenia is indicative of immunosuppression in hospitalized patients; high D-dimer levels suggest a consumptive coagulopathy.
  • Another paper published in last week of March has summarized the spectrum of neurological presentations in COVID-19 patients: Headache, malaise, fatigue, imbalance, anosmia/ageusia, cerebral hemorrhage, acute neuropathies, encephalitis, and seizures.
  • Neurological presentations could be a manifestation of hypoxia, metabolic/respiratory acidosis, multiorgan dysfunction and sepsis, and certain medications.
  • Inflammation could potentially be related to stroke occurrence (directly/indirectly) or could follow an acute stroke. Atherosclerosis is an inflammatory process; plaque destabilization and rupture may contribute to stroke.
  • COVID-19 is also a prothrombotic state as high levels of D-dimer have been observed in these patients.
  • Measures of protection for health professionals while managing neurological emergencies like stroke in the time of COVID-19 include PPE (level 2) for all team members, team member role designation, green corridor for stroke; CT scan machines need to be sanitized.
  • Contact and droplet precautions: aerosol generating procedures such as oropharyngeal/nasal suctioning, bag valve mask ventilation, intubation, chest compression, NIPPV, nebulization and CPR are minimized; early extubation is not recommended; avoid CPAP, BiPAP and nasal high flow therapy due to the risk of aerosol formation.

 

Dr KK Aggarwal

President CMAAO, HCFI and Past National President IMA

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