Delirium tremens develops in a minority of patients undergoing acute alcohol withdrawal; however, that minority is vulnerable to significant morbidity and mortality. Historically, benzodiazepines are given intravenously to control withdrawal symptoms, although occasionally a more substantial medication is needed to prevent the devastating effects of delirium tremens, that is, propofol. We report a trauma patient who required propofol sedation for delirium tremens that was refractory to benzodiazepine treatment. Extubed prematurely, he suffered a non-ST segment myocardial infarction followed by an ST segment myocardial infarction requiring multiple interventions by cardiology. We hypothesize that his myocardial ischemia was secondary to an increased myocardial oxygen demand that occurred during his stress-induced catecholamine surge during the time he was undertreated for delirium tremens. This advocates for the use of propofol for refractory benzodiazepine treatment of delirium tremens and adds to the literature on the instability patients experience during withdrawal.
Delirium tremens (DTs), the most feared consequence of acute alcohol withdrawal, can lead to hallucinations, delirium, seizures, myocardial infarction, all of the above, or death [
A 65-year-old male was admitted to the trauma service after a mechanical fall down from five cement stairs. The result was multiple left sided rib fractures and a small lung contusion without loss of consciousness. He was admitted for oxygen therapy and pain control with a patient-controlled-anesthesia unit, along with thiamine and Librium [Valeant Pharmaceuticals, Bridgewater, NJ] once it was evident he had a history of significant alcohol abuse. The patient had no primary care physician so there was no documented past medical history; however, he did not report angina symptoms. Without signs of alcohol withdrawal, he was scheduled for discharge 36 hours after admission. The night before his expected discharge he became tachycardic, hypertensive (systolic to 200 mmHg from baseline of 120 mmHg), and lethargic and was treated by beta-blocker, clonidine patch, nil per os (NPO) and upgraded to the intensive care unit. He was subsequently intubated for lethargy and was started on propofol, fentanyl, and tube feeds. He was stabilized and remained an 11 t on the Glascow Coma Scale and after a successful weaning trial he was extubated less than 24 hours later after intubation.
Once extubated he quickly became tachycardic and hypertensive but responded appropriately. It was decided that he would be treated symptomatically with intravenous BZ even though they proved ineffective previously. Hours later, he underwent rapid sequence intubation after prolonged hypoxia, respiratory distress, and tachycardia. Secondary to his hemodynamic instability, a 2D cardiac echocardiogram was performed which showed a left ventricle ejection fraction of 35%. He went into an episode of ventricular tachycardia as troponin of 22 ng/ml resulted along with electrocardiogram changes diagnosing a non-ST segment myocardial infarction (Figure
Evidence of NSTEMI, along with elevated troponins; the patient underwent cardiac stent placement.
72 hours later, he was persistently oliguric and hypotensive and troponins were elevating (stable at 4 ng/ml then elevating to 32 ng/ml over 12 hours). A repeat electrocardiogram was performed showing an ST segment elevation myocardial infarction in the inferior leads (Figure
ST segment elevation in lead II, III, and aVF with elevation of troponins; additional stent placed 72 hours s/p LAD & LCA stent placement.
Once the patient was stabilized, over the course of a week, his sedation was weaned. It became evident that the patient was not responsive and his pupils were uneven with successful weaning of all sedation/narcotics. A computed tomography of the head was performed showing bilateral cerebral hemispheric infarcts as well as a 20 mm midline shift and partial effacement of the fourth ventricle. Neurosurgery recommended nonoperative care and started the patient on mannitol for cerebral edema, labeling him with a dismal prognosis. He developed Staphlyococcus pneumonia and was started on antibiotics appropriately. Twenty days after admission the patient went into asystole and expired. He never recovered from his myocardial ischemia induced by the catecholamine surge caused by delirium tremens.
Our delirium tremens patient suffered from both NSTEMI and STEMI, which as a combined insult proved to be unrecoverable. He obviously had underlying cardiac stenosis, evident by his catheterization; however, his oxygen demand was exponentially increased during the brief period of time when he was extubated resulting in myocardial ischemia. Prior to being weaned from propofol, his vital signs were stable and he seemed to be enduring his alcohol withdrawal. This supports literature stating propofol should be used in DTs refractory to treatment with BZ. Although it is unproven, it would seem that his premature cessation of propofol resulted in a cascade of events that caused hemodynamic instability, myocardial ischemia, and multiple cardiac catheterization procedures that likely caused his resulting cerebral infarcts.
Alcohol withdrawal symptoms are present in up to 31% of trauma patients, with studies reporting delirium in 4–15% of all patients with alcohol dependence admitted to the hospital [
Benzodiazepine therapy is successful in mimicking the inhibitory effects of GABA, which is unopposed due to the absence of ethanol. Unfortunately, BZ treatment does not have any effect on the upregulated NMDA receptors which are unopposed, as this is the mechanism of BZ treatment failure. The upregulated NMDA receptors are directly treated with propofol sedation, which not only mimics GABA-receptors but also blocks the excitatory NMDA-receptor pathway. Because propofol acts on both receptors, it has been promoted to second line treatment and proven as the leading medication to treat patients who are refractory to BZ treatment [
Propofol’s ability to mediate the hemodynamic instability during alcohol withdrawal is paramount in patients refractory to BZ treatment and should be started promptly when recognized. There is documented variability of QT intervals and ST segment changes associated with withdrawals as well as increases in myocardial oxygen demand secondary to a catecholamine surge [
This is an additional reported case on a very scarcely reported subject documenting myocardial infarction in the setting of delirium tremens. Although cases have shown DTs causing ST segment variability and a propensity towards arrhythmias, our patient seems to have suffered myocardial infarction because of myocardial stress. His myocardial stress was secondary to a catecholamine surge and resulting hemodynamic instability from delirium tremens.
The authors declare that there is no conflict of interests regarding the publication of this paper.