Acute or subacute polyradiculoneuropathy presenting as numbness, tingling and extremities weakness over several days with nadir within 4 weeks; in general, approximately 30% of patients require mechanical ventilation
Incidence and presentation:
Incidence unknown in COVID-19
One case of AMSAN (confirmed on EMG/NCS) treated with IVIG; symptoms of GBS followed respiratory symptoms of COVID-19 by about 9 days 
One case with typical GBS presentation, following respiratory symptoms of COVID-19 by about 8 days (no EMG/NCS or LP) 
Two cases of GBS variants (Miller Fisher, polyneuritis cranialis) with symptoms developing 3 and 5 days after symptoms of COVID-19. Both cases had albuminocytologic dissociation 
Five additional cases with symptoms of GBS developing 5-10 days after symptoms of COVID-19, three axonal, two demyelinating neuropathy; all treated with IVIG; three progressed to respiratory failure; two with "poor outcome" 
One case with questionable temporally: symptoms of GBS (albuminocytologic dissociation, neurophysiologic studies) preceded respiratory symptoms by 8 days, although exposure risk was highest around four days prior to development of symptoms of GBS, so authors question if she could have been initially asymptomatic from respiratory standpoint 
Case reports thus far favor more axonal GBS variants and those involving cranial nerves than the general distribution of AIDP and variants - it is unclear whether this is because the distribution of GBS types differs for patients with COVID-19, or if these cases are easier to diagnosis (axonal variants are generally more severe). It is conceivable that patients with more typical, milder presentations of GBS may not be diagnosed, especially if they are ill from respiratory standpoint.
GBS has been reported in association with MERS-coronavirus – a case series of 4 patients (out of 23 admitted patients with MERS-CoV) that had suspected GBS, with a delay ranging from 7-26 days after onset of pulmonary symptoms 
In above series, none required intubation and only one patient required treatment with intravenous immunoglobulins (IVIg)
GBS has also been reported in human coronavirus 229E and OC43 in one pediatric patient 
Alternatively, human coronovirus OC43 in animal models has been shown to be neurotrophic, neuroinvasive and neuroinflammatory, causing flaccid paralysis and demyelination 
Understand GBS symptoms may be delayed 1-3 weeks after onset of pulmonary symptoms based on above series
Neurology consultation to document initial examination; unless diagnosis is deemed very unlikely, neurology consultants should return in 24h for serial examination to detect subtle changes
Pulmonary function testing (PFT) upon initial encounter
Consider ICU level care and/or intubation for patients with single breath count test < 20, observed/palpated use of accessory muscles (including scalenes, sternocleidomastoid), observed paradoxical breathing and neck flexion weakness
Lumbar puncture for cytological dissociation – may be normal in 1/3-1/2 patients in first week of symptoms so does not exclude diagnosis, may need to repeat; all patients in above series had normal cerebrospinal fluid studies
Nerve conduction studies 1-2 weeks after symptom onset if diagnosis remains unclear; note there is high likelihood of equivocal findings early in course and electromyography machine may serve as fomite
Given that ancillary testing may be equivocal within first week of symptoms, in general, would initiate empiric treatment with sufficient clinical suspicion
IVIg 2g/kg administered over 2-5d; as of April 2020, current supply is likely safe as product was prepared well before outbreak; concern for possible scarcity of IVIg in the near future due to limited donors
Plasmapheresis over 5 cycles is equally efficacious and safe alternative – catheter can be placed on floor and plasmapheresis initiated with approval from charge nurse
Patients with mild symptoms who remain ambulatory may not necessarily need treatment even though studies show it may hasten recovery ; decision will have to be weighed against lengthy hospital stay
Pulmonary function testing:
Serial PFTs at least q8h in first 24 hours (if PFTs become unavailable, rely on nursing examinations with same frequency as below)
Frequency thereafter dictated by clinical progression and should be revisited every 24h, space out if weakness has plateaued to minimize aerosolization of viral particles and respiratory therapist exposure; after day 3 of treatment would consider discontinuing completely
PFTs may not accurately reflect diaphragmatic strength in patients with facial weakness or altered mental status; in these cases, clinical respiratory and neurological examinations supersede to determine if patients truly require intubation or intensive care resources
Should include monitoring for single breath count test < 20 or downtrend, observed/palpated use of accessory muscles (including scalenes, sternocleidomastoid), observed paradoxical breathing, worsening neck flexion weakness/limb weakness; notify clinicians with any of above
May be staggered with PFTs (i.e. deferred if patient had reassuring PFT parameters within prior 2 hours) as purpose is to evaluate for impending respiratory failure
If patient is intubated, high-frequency q1h or q2h neurological examinations are not necessary as these are unlikely to change management
Severe BP or HR fluctuations may be indication for escalation to ICU level care for vasopressors or external pacing
Monitor daily BP range, HR range, sodium, urine output, and date of last bowel movement during plateau phase of motor weakness, may space out when motor recovery is noted 
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