A 28-year-old woman, 8 weeks pregnant, developed acute severe asthma, with a short non-infective prodrome, and a hypoxic cardiac arrest. Her initial rhythm in the emergency department was ventricular fibrillation. Resuscitation to sinus tachycardia required 10 min, including endotracheal intubation. On transfer to the ICU, she was therapeutically cooled to 33°C for 24 h.
Management included salbutamol (inhaled and intravenous), ipratropium, aminophylline, hydrocortisone, magnesium, ketamine and inhalation anesthesia with 1 MAC isoflurane. Severe hypercapnic acidosis from inadequate minute ventilation required neuromuscular blockade (NMB). With ventilation improving over 48 h, we intentionally ceased thhe intravenous sedatives and NMB, and used 0.25–0.5 MAC isoflurane as the sole sedative to avoid residual sedation from long-acting intravenous agents and facilitate early neurological assessment.
She developed generalised status myoclonus (GSM) by 48 h, when the neuromuscular blockers were stopped. When isoflurane was stopped on day 4, she was comatose, with absent motor response to painful stimulus, preserved pupillary, corneal, cough and gag reflexes and spontaneously breathing, with severe GSM, refractory to three antiepileptic medications. Electroencephalography showed generalised periodic discharges with no discernable background rhythm. Reversible causes of coma (biochemical, metabolic, septic and drugs) were eliminated by clinical examination, specific investigations and duration of action of sedative medications.
By day 8, there was no agreement about her neurological outcome among the clinicians. Additional social issues due to the interethnic marriage and the pregnancy required intensive social work support to help a disparate family understand the complicated process of neurological prognostication.
GSM (despite delayed onset at 48 h) was interpreted by some as a poor prognostic marker in a deeply comatose patient and by others as possible Lance Adams Syndrome (LAS) in the setting of a respiratory cause of cardiac arrest.[3
] The plasma neuron-specific enolase (NSE) was 51 mcg/L (indicating poor prognosis), but the results were delayed by 10 days.[2
] Somatosensory-evoked potential (SSEP) was unhelpful due to myoclonus motion artefacts.
On day 10, brain magnetic resonance imaging (MRI) using fluid attenuation inversion recovery and diffusion weighted imaging (DWI) was performed, which showed bilateral basal ganglia and frontoparietal cortex infarction “consistent with severe hypoxic encephalopathy” .
T2- fluid attenuation inversion recovery image showing basal ganglia infarction
Medical consensus regarding poor prognosis was finally reached following discussions between two intensivists and two neurologists. She was extubated with family agreement, and died in 24 h with comfort measures.