What's the Take Home?

A 61-Year-Old Man Admitted to the Hospital After a Motor Vehicle Accident

Volume 59 - Issue 9 - September 2019

Author:
Ronald N. Rubin, MD—Series Editor

Citation:
Rubin RN. A 61-year-old man admitted to the hospital after a motor vehicle accident. Consultant. 2019;59(9):278-280.

 

A 61-year-old man was admitted to the inpatient service at a trauma center after having sustained injuries in a motor vehicle accident. He sustained multiple facial lacerations, and radiographs documented fractures of the wrists. These injuries were addressed with facial suturing and casting. A contrast computed tomography (CT) scan of the head was negative for structural pathologies.

He had been kept overnight for observation, and at 10:00 the next morning, approximately 10 hours after presentation and 12 hours after the accident, he had a grand mal seizure. He recovered within 2 hours. At that time, physical examination revealed that he was afebrile, had a pulse of 124 beats/min, was significantly agitated, and was tremulous with bilateral hand tremors. One observer noted fasciculations of the tongue. He also was disoriented as to time and place. There were no focal neurologic abnormalities.

Laboratory results at admission revealed a blood alcohol level of 200 mg/dL, a normal white blood cell count, a low platelet count of 90 × 103/µL, an elevated blood urea nitrogen level of 29 mg/dL, and an elevated alanine aminotransferase (ALT) level of 267 U/dL. All other results, including electrolyte levels, prothrombin time, and albumin level, were normal.

A history was pieced together that the patient was a chronic alcohol drinker who had had several incidents of driving while intoxicated over the years and who had consumed a significant amount of alcohol the evening of the accident, a behavior pattern that was usual for him. He had had inpatient stays related to alcohol abuse in the past.

Answer: C, he manifests at-risk drinking, is at high risk for SAWS, and should be kept in the hospital for supportive care and prophylaxis with benzodiazepines.

This patient’s case serves to open a discussion about the epidemiology, findings, and diagnosis of alcohol withdrawal syndrome. This is a frequently neglected yet very old and common problem in the United States and worldwide. The name alcohol withdrawal syndrome implies pathology that occurs after cessation or withdrawal of alcohol, so the initial issue for discussion is, What does this mean?

First it needs to be established what is high risk or heavy alcohol use, which is defined as the consumption of 4 or more drinks per day or 14 or more drinks per week for men and 3 or more drinks per day or 7 or more drinks per week for women.1 

When alcohol consumption at this level is stopped, a variety of somewhat poorly understood biochemical changes in receptor and catabolic product levels in the brain abruptly reverse; the resulting imbalances cause overall central nervous system (CNS) hyperactivity and lowered seizure thresholds over a reasonably predictable timeframe, yielding the signs, symptoms, and findings of SAWS. Specifically, these include autonomic hyperactivity, psychological symptoms, seizures, and full-blown delirium tremens.2 

The older of us will recall the days when a full 15% mortality rate from full-blown “DTs” was the rule, as complications such as aspiration pneumonia (from sedation and the ubiquitous restraints) and acute myocardial infarction from intense autonomic hyperactivity ensued. Today, far better attention to nursing care, sedation specifics (benzodiazepines rather than barbiturates), and early-recognition risk scales has lowered that number to low single-digits.2

Approximately 50% of heavy users of alcohol who abruptly stop drinking will experience at least some of the manifestations of alcohol withdrawal within 24 hours. These include alcoholic tremulousness, sinus tachycardia, insomnia, and nausea/emesis. Transient visual or tactile illusions, psychomotor agitation, anxiety, and generalized grand mal seizures are seen in combination with delirium (eg, disorientation, disturbed cognition), all within several days after alcohol cessation.2-4

Classical timeframes are 24 hours for seizures and 3 days for delirium tremens; signs and symptoms far outside these parameters suggest other causes—for example, a structural CNS pathology such as subdural hematoma, or the presence of other toxic substances.

A variety of schemes have been developed to help clinicians predict and adjudicate the risk of SAWS in patients. Suffice it to say, no single historical, laboratory, or physical finding has enough specificity or sensitivity for strict clinical use. However, combination schemes seem to be quite helpful and include the Luebeck Alcohol Withdrawal Risk Scale (LARS) and the easier to apply (in this author’s opinion) Prediction of Alcohol Withdrawal Severity Scale (PAWSS).2,5 

The PAWSS evaluates 10 clinical findings and requires the presence of 4 to assign high risk to the situation. Since 3 of these criteria include a history of heavy alcohol use within 30 days; a blood alcohol level greater than 200 mg/dL on admission; and the presence of increased autonomic activity (tachycardia of >120 beats/min, nausea/emesis, tremor, sweating, agitation), the ease of applying this scheme is obvious. The higher the score, the higher is the risk.2,5 Although these risk tables are by no means perfect, their application—along with some good clinical sense—can go a long way in predicting and more accurately diagnosing SAWS, particularly the still very dangerous full-blown delirium tremens. And, stunningly, as alluded to earlier, much of now documented data and schemes were already well-known decades ago!

A few remarkable demographic and epidemiological specifics are as follows:

Although SAWS accounts for less than 1% of admissions to general medical/surgical services, in a study from a large academic medical center, a full 10% of motor vehicle accident cases who were admitted developed SAWS!2 Think about the full meaning of those data. And, in a recent large meta-analysis of studies encompassing MEDLINE and EMBASE search of studies appropriate in diagnostic criteria and size from 1946 to 2018 found sufficient data in only 14 high-quality studies.2 And even then, “only” 53 cases with seizure and 251 cases with delirium tremens were listed.2,6 It seems this author can recall seeing a good percentage of that number in my own 3-year residency at an inner-city academic center. We would have phenytoin syringes (now known to be incorrect) and benzodiazepine syringes drawn up and ready come every Monday morning—the point being how poorly alcohol withdrawal has been systematically studied, considering how common it is.

Regarding how this discussion applies to the case described above, Answers A and B are alternative explanations for his symptoms, which if true would be strong negatives for a SAWS hypothesis. It is quite likely in this day and age that a CT scan would be done for anyone with a new-onset seizure. But, with the history of chronic heavy alcohol intake, a blood alcohol level above 200 mg/dL on admission, and no focal neurological findings before or after the event, acute alcohol withdrawal is far more likely as the cause.

Similarly, despite the patient’s heavy alcohol use history, no signs or symptoms of alcoholic cirrhosis are present, and the key laboratory parameters of serum albumin and international normalized ratio (dependent upon normal hepatic synthetic function) are normal. The isolated ALT elevation is very likely due to alcohol liver damage, but again, by itself not to the degree where hepatic encephalopathy with this level of delirium would be expected.

Alcohol withdrawal with seizure, autonomic hyperexcitability, and early delirium tremens is the most likely explanation for the myriad findings seen in this patient’s case, and Answer C is correct here.

Answer D is incorrect, since by any of the risk schemes, this patient is at very high risk for frank delirium tremens developing with even more severe autonomic and delirium signs, symptoms, and morbidity risk. He needs careful and effective observation and benzodiazepine prophylaxis at least over a several-day period, and perhaps more vigorous management than that. This is true even in the absence of further seizures, and in fact his initial seizure already gives him a roughly 33% risk for developing full-blown delirium tremens.2

PATIENT FOLLOW-UP

The patient remained hospitalized and was started on a regimen of a benzodiazepine over several days. He experienced no further seizures. The signs and symptoms of autonomic hyperactivity abated, allowing a taper of the benzodiazepine.

By the fourth day, his vital signs were normal, and he was awake, alert, and oriented. His platelet count and ALT level were trending back to normal prior to discharge. He received a brief counseling session where the initiation of psychosocial intervention and utilization of a supervised program of disulfiram were discussed.


TAKE-HOME MESSAGE

Alcohol abuse remains very common in the United States. Morbidity from heavy alcohol use includes alcohol withdrawal seizures and frank delirium tremens characterized by autonomic hyperactivity (eg, tachycardia, sweating, insomnia, psychomotor agitations) and the presence of delirium within hours to days after cessation of chronic heavy alcohol consumption. Attendant laboratory risk factors include blood alcohol levels greater than 200 mg/dL, elevated serum ALT values, and lowered platelet counts. Although no single history, sign, symptom, or laboratory value is sufficient to generate or exclude an accurate risk level for SAWS, a variety of predictive scales have been formulated by which a combination of such parameters can predict the onset of SAWS with a high degree of sensitivity and specificity. When such schemes are used, appropriate management decisions such as inpatient care and benzodiazepine prophylaxis can be used to prevent the morbidity and mortality associated with delirium tremens and other manifestations of SAWS.

 

Ronald N. Rubin, MD, is a professor of medicine at the Lewis Katz School of Medicine at Temple University and is chief of clinical hematology in the Department of Medicine at Temple University Hospital in Philadelphia, Pennsylvania.

 

REFERENCES:

  1. Rethinking Drinking: Alcohol and Your Health. National Institutes of Health, National Institute on Alcohol Abuse and Alcoholism. https://www.niaaa.nih.gov/sites/default/files/publications/Rethinking_Drinking.pdf. Revised May 2016. Accessed August 21, 2019. NIH publication 15-3770.
  2. Wood E, Albarqouni L, Tkachuk S, et al. Will this hospitalized patient develop severe alcohol withdrawal syndrome? The rational clinical examination systematic review. JAMA. 2018;320(8):825-833.
  3. Kim DW, Kim HK, Bae E-K, Park S-H, Kim KK. Clinical predictors for delirium tremens in patients with alcohol withdrawal seizures. Am J Emerg Med. 2015;33(5):701-704
  4. Schuckit MA. Recognition and management of withdrawal delirium (delirium tremens). N Engl J Med. 2014;371(22):2109-2113.
  5. Maldonado JR, Sher Y, Das S, et al. Prospective validation study of the Prediction of Alcohol Withdrawal Severity Scale (PAWSS) in medically ill inpatients: a new scale for the prediction of complicated alcohol withdrawal syndrome. Alcohol Alcohol. 2015;50(5):509-518.
  6. Saitz R. Medications for alcohol use disorder and predicting severe withdrawal. JAMA. 2018;320(8):766-767.