A trauma alert is called for a 36-year-old woman brought in by ambulance after intentionally crashing her car into a tree while intoxicated. On physical examination, her vitals are: T 98.6, BP 165/80, HR 115, RR 16, O2 88% on RA, and 96% with 3 L NC. She is slightly lethargic and disoriented to time, but able to answer simple questions. She complains of acute pain in her chest along with a mild headache. She displays no evidence of diaphoresis or tremor and denies feeling anxious or nauseated. Pupils are reactive, without any evidence of nystagmus. The remainder of the neurological and general examination is normal.
The patient gives a history of binge-type drinking, in which she consumes “a lot” of vodka every weekend. She denies daily drinking, however also reports that alcohol helps her sleep at night. She reports 1 previous detox approximately 1.5 years ago. She also notes losing 1 job in the past due to her alcohol use, along with it affecting past relationships, and legal complications due to assaulting others while intoxicated. She denies a history of past delirium tremens or alcohol withdrawal seizures. She denies any history of benzodiazepine, cannabis, cocaine, heroin, or other drug use.
Her injuries include multiple left-sided rib fractures and a subarachnoid hemorrhage for which she is started on levetiracetam (Keppra) for seizure prophylaxis. She is found to have a blood alcohol level (BAL) of 3600 mg/L in the emergency department, along with an AST of 235 U/L, an ALT of 120 U/L, and a normal mean corpuscular volume (MCV) of 95.
1. Name 4 symptoms or signs of alcohol withdrawal.
2. Is she at high risk of developing alcohol withdrawal syndrome (AWS)? How can you tell?
Long-term exposure to ethanol results in adaptive changes in several neurotransmitter systems. Abrupt withdrawal of ethanol results in nonphysiologic levels of these neurotransmitters, which in turn cause the signs and symptoms of alcohol withdrawal. Understanding the basics of these changes not only can help guide your choice of therapy but also can help you appreciate alarming versus less concerning signs.
The changes in neurotransmitter systems can be clustered as shown in Table 15-1.
Chronic exposure to alcohol results in an increase in glutamatergic reaction and decrease in GABA activity. When alcohol is abruptly removed, decreased GABA activity leads to symptoms of anxiety and restlessness, referred to as uncomplicated AWS. Concomitantly, excess glutamate stimulates an increase in noradrenaline and dopamine, as shown in Figure 15-1. Increased noradrenaline results in Type B symptoms resulting in increased sympathetic activity (see Table 15-1). Increased dopaminergic activity leads to Type C symptoms, a contributor to alcohol hallucinosis and, in conjunction with severe Type B symptoms, delirium tremens (alcohol withdrawal delirium). Seizures, alcoholic hallucinosis, and delirium tremens ...
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