Dr. Hong Kim is an emergency medicine trained toxicologist who also trained in New York city at the famed Bellevue toxicology program. Â In this week’s core content lecture, Dr. Kim reviews the causes or alcohol withdrawal as well as come of the current treatment strategies. Â The second half of this talk is dedicated to reviewing the elusive diagnosis of cyanide toxicity.
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Summary by Dr. Anju Singhal
Alcohol withdrawal syndrome (AWS)
 The Basics
- 8% of all admissions to hospital related to AWS
- 11% MICU patients
- Â Up to 31% of trauma patients experience AWS during their hospitalization.
Delirium Tremens
- Historical mortality ~35%, now with supportive care <5% mortality.
- Typical onset 2-3 days after last drink.
- Presentation symptoms similar to “sympathomimetic toxidrome”
- “Kindling effect” – h/o of AWS predisposes to future episodes of AWS
- Â Chronic use of EtOH causes conformational change in GABA receptor leading to benzo resistance
Treatment
- Primary Treatment Options
- Chlordiazepoxide – only PO form, active metabolites allow for natural tapering
- Diazepam
- Quick onset, long duration, also has active metabolites
- Preferred benzo to use in AWS
- Lorazepam
- Slower onset, no active metabolites
- Can lead to stacking problems given slow onset of action
- Refractory AWS
- Defined as requiring >200 mg diazepam in 3 hours
- Consider phenobarbital or propofol – both work synergistically with benzos
- Phenobarbital: delayed onset, decreases inotropy – dose 75-130 mg IV, max 390 mg
- Adjunctive treatment
- Dexmedetomidine: some studies show decreases autonomic abnormalities, overall benzo use, and vent days – but still preliminary data.
- Avoid antipsychotics (i.e. Haldol)Â in true AWS as can lower seizure threshold
AWS protocols
- Should be symptom guided.
- Start with 10 mg IV diazepam and double each hour until control reached
- Protocol decreased intubations and hospital stay
 Cyanide Toxicity
The Basics
- Exposures: gas (residential fires), liquid ingestions (i.e. nail polish remover, solvents), certain foods (apricot pits, cherry pits, cassava), lab technicians, jewelrey workers, fumigators
- Risk with use of Nitroprusside drips of >2 mcg/kg/min (can reduce this risk with thiosulfate administration)
- MOA: inhibits aerobic metabolism
Symptoms: Non-specific!
- Headache, seizure, coma, cardiovascular collapse, vague gi sx
Diagnosis
- Lab CN levels (slow)
- Lactate >10 in right clinical setting (i.e. house fire) very suggestive of cyanide toxicitiy
Treatment
- Hydroxycobalamin (side effect: red discoloration of serum, urine, skin can last up to 1 month – this affects lab measurement of saturations, bili, cr, mg, etc.)
- Cyanide antidote kit (induces methhemoglobinemia) – can make concominant CO poisoning worse
- Thiosulfate – slow onset
References
- Isbell H, Fraser HF, Wikler A, Belleville RE, Eisenman AJ. An experimental study of the etiology of rum fits and delirium tremens. Q J Stud Alcohol. 1955;16(1):1-33. [PubMed Link]
- Baud FJ, Barriot P, Toffis V, et al. Elevated blood cyanide concentrations in victims of smoke inhalation. N Engl J Med. 1991;325(25):1761-6. [Free Full Text]
- Baud FJ, Borron SW, Mégarbane B, et al. Value of lactic acidosis in the assessment of the severity of acute cyanide poisoning. Crit Care Med. 2002;30(9):2044-50. [PubMed Link]
