Ascending weakness after a diarrhoeal illness — the Guillain-Barré stem

Assessment — this is the Guillain-Barré syndrome with the autonomic instability and the incipient respiratory failure. The clinical picture is classic: the subacute symmetric ascending flaccid paralysis over 4 days, the areflexia, the antecedent Campylobacter-like diarrhoea 2 weeks prior, the bilateral facial weakness, and the paraesthesia. The diagnosis is clinical and made at the bedside. The two dangerous features are the autonomic instability (the bradycardia of 48 and the hypertension of 165/95 are the autonomic storm, and the sudden death from the asystole is recognised) and the respiratory failure (the FVC of 18 mL/kg and the NIF of minus 32 cmH2O are below the ICU thresholds). I assess the ABCDE, establish the continuous cardiac monitoring, and prepare for the ICU.^[1]

Immediate management — the ICU and the airway first, then the disease-modifying therapy. The patient is admitted to the intensive care unit immediately — the FVC under 20 mL/kg and the NIF under minus 30 cmH2O mandate the ICU admission and the probable intubation, and the trend, not the snapshot, decides. I intubate early and electively before the crash: the rapid-sequence intubation with the rocuronium 1 mg/kg (the succinylcholine is contraindicated in the acute denervation — the hyperkalaemic cardiac arrest) and the induction agent (the propofol 2 mg/kg or the ketamine 1 to 2 mg/kg, cautiously for the haemodynamic instability). I institute the continuous cardiac monitoring with the atropine drawn up for symptomatic bradycardia.^[1]

Investigations — confirm and exclude the mimics, but never delay the ICU. The lumbar puncture for the CSF (the albuminocytologic dissociation — the elevated protein with the normal cell count, but this may be absent in the first week); the cell count and the protein, the glucose, the Gram stain, the culture, and the viral PCR. The nerve conduction studies (the prolonged distal latencies, the conduction block, the reduced CMAP — but a normal early NCS does not exclude the GBS). The anti-ganglioside antibodies (the anti-GM1, the anti-GQ1b). The bloods to exclude the mimics — the electrolytes (the hypokalaemic periodic paralysis), the magnesium, the creatine kinase, the lead, the toxicology, the thyroid function, the HIV. The MRI of the spine if the cord lesion is possible (the facial diplegia and the areflexia without a sensory level make the cord lesion unlikely here). The spirometry is repeated every 2 to 4 hours to follow the trend.^[1][2]

Disposition — the ICU for the respiratory and the autonomic monitoring, then the prolonged rehabilitation. The patient is admitted to the ICU under the joint care of the neurology and the intensive care. The serial spirometry Q2 to 4H continues. The DVT prophylaxis, the corneal protection for the facial weakness, the bowel and the bladder care, the analgesia, and the nutrition are started. The patient and the family are counselled about the expected prolonged course (the recovery over months, the possible prolonged ventilation, the early tracheostomy discussion at 10 to 14 days). The neurology and the physiotherapy are involved early.^[1][2]