Allam S, Noble JS. Cocaine-excited delirium and severe acidosis.
Anaesthesia (England), Apr 2001, 56(4) p385-386.
Cocaine-Excited Delirium and Severe Acidosis
S. Allam and J. S. Noble
We would like to report a case of cocaine-excited delirium in which the patient survived despite extreme acidosis.
A 25-year-old male patient jumped from a first-floor window to escape his pursuers who were allegedly chasing him with swords. Whilst giving a statement to the police, he suddenly ran off and was apprehended. Although initially conversant with the paramedics, he became drowsy, and in the ambulance had a clonic seizure lasting 1 min.
On arrival in casualty at 13:30 h, there was no eye opening, he was flexing to pain and making incomprehensible sounds. His pulse was 116 beats.min, blood pressure 100/40 mmHg, respiratory rate 28 breaths.min and temperature 38.3 C.(1) The initial blood gases revealed a hydrogen ion concentration of 292 nmol.l (pH 6.53), PaCO2 of 13.13 kPa, base deficit of 35.6 mmol.l and a PaO2 of 25.61 kPa on 10 l of oxygen via a trauma mask. Because the 12-lead ECG demonstrated tall, peaked T waves, he was assumed to be hyperkalaemic. He was intubated with a rapid sequence induction and manual in-line stabilisation of the head with 2 mg of alfentanil and 100 mg of propofol. Hyperventilation was instituted; he was given 10 ml of 10% calcium gluconate and 50 ml of 8.4% sodium bicarbonate. He had 1.5 l of 0.9% saline over 90 min. The initial plasma potassium level was 7 mmol.l, sodium 153 mmol.l, bicarbonate 12 mmol.l, anion gap 44 mmol.l, urea 8.4 mmol.l, creatinine 202 Ámol.l.(1)
By 14:00 h, his temperature had risen to 39.7 C. He was given a total of 2 mg.kg of dantrolene in two separate aliquots within 20 min. Ice packs and a fan were employed as cooling measures. Blood gases taken at 14:47 h revealed a hydrogen ion concentration of 40.1 nmol.l (pH 7.4), PaCO2 of 4.28 kPa, base deficit of 3.8 mmol.l and a PaO2 of 42.92 kPa on an FIO2 of 0.6. Repeat electrolytes showed a potassium of 5.1 mmol.l and an anion gap of 30 mmol.l. By 15:00 h, his temperature had decreased to 37.6 C. X-rays of pelvis, cervical spine, chest and CT scan of head were normal. Bacteriological and biochemical analysis of the CSF was unremarkable.(1)
He was admitted to the ICU and extubated at 20:00 h. Clotting studies were normal and the creatinine phosphokinase level peaked at 8460 mol.l the following day. He was discharged from the ICU the day after admission and from the hospital on the succeeding day with normal renal function. On further questioning, he admitted drinking heavily on the night preceding hospital admission, and to taking cocaine. Toxicological analysis of his urine showed no trace of opioids, benzodiazepines or amphetamines. Cocaine was omitted from the toxicological screen.(1)
The paranoia, agitation and rapidly progressive pyrexia with which this patient presented are features of cocaine-excited delirium.(1) This condition occurs within 24 h of cocaine ingestion in habitual users. Coma and death result without intervention. The prompt administration of hyperventilation, passive cooling, sodium bicarbonate and dantrolene led to a remarkably swift correction of the acidosis and a successful outcome in this case. Survival after such a severe acidosis illustrates that the arterial hydrogen ion concentration gives a restricted view of what is happening at the intracellular and mitochondrial level.
We are reporting this case to increase awareness of cocaine-excited delirium and to suggest one potential management strategy for this potentially fatal syndrome.
(1) Henry JA. Metabolic consequences of drug misuse.
British Journal of Anaesthesia 2000; 85: 136-42.