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The syndrome of delayed toxic–hypoxic encephalopathy is triggered by a sedating toxin that precipitates a period of cerebral hypoxaemia. The syndrome is rare and has a classic biphasic course with a seemingly complete recovery from the first episode of coma followed by a dramatic deterioration. We describe the diagnostic challenge provided by such a case.
Day 1: A 37-year-old man took 30 ml of methadone, 150 mg diazepam, plus cannabis and alcohol. On waking the next day, he took 20 ml more methadone and spent the afternoon and evening watching DVDs. The following morning, he rose at midday before returning to bed, where his partner found him unrousable at 22:00. He was taken to the emergency department where his Glasgow Coma Score was 3/15 and he had small pupils (see figure 1, time line). On arrival he was hypoxic, tachycardic and hypotensive. Blood tests showed acute renal impairment, hyperkalaemia, with serum creatine kinase of >8000 U/l (24–195) and hypoglycaemia. His blood biochemistry was corrected and two doses of naloxone given to no effect. A CT scan of head was normal. Toxicology screen was positive for methadone, benzodiazepines and cannabinoids. Blood-borne viral serology was negative. He was intubated and spent 4 days in intensive care; on extubation he was confused and paranoid but was discharged after 10 days in hospital (day 12), ‘99% back to normal’.
Seventeen days after discharge (day 28), he lost the ability to walk and was doubly incontinent; 38 days after the initial toxic insult he was re-admitted to hospital. On examination, he had reduced facial expression, spoke words but not full sentences and followed simple commands. He had marked action and rest myoclonus (video 1), with bradykinesia in the upper limbs and hypereflexia. An MR scan of brain (figure 2) showed extensive diffuse, symmetrical …
Patient consent Obtained.
Competing interests None.
Provenance and peer review Not commissioned. Externally peer reviewed. This paper was reviewed by Peter Enevoldson, Liverpool, UK.
Contributors The patient was looked after my three of the co-authors and the other two co-authors reported the neuroimaging and conducted and reported the neuro physiological investigations. All authors contributed to the manuscript.