Dr. Spiegel: Factors that can result in false positive scores on the CIWA-Ar
Clinicians often use the symptom-triggered Clinical Institute Withdrawal Assessment for Alcohol Scale, Revised (CIWA-Ar)1 to assess patients’ risk for alcohol withdrawal because it has well-documented reliability, reproducibility, and validity based on comparison with ratings by expert clinicians.2,3 The CIWA-Ar commonly is used to determine when to administer lorazepam to limit or prevent morbidity and mortality in patients who are at risk of or are experiencing alcohol withdrawal. Refined to a list of 10 signs and symptoms, the CIWA-Ar is easy to administer and useful in a variety of clinical settings. The maximum score is 67, and patients with a score >15 are at increased risk for severe alcohol withdrawal.1 For a downloadable copy of the CIWA-Ar, click here.
Despite the benefits of using the CIWA-Ar, qualitative description of certain alcohol withdrawal symptoms is prone to subjective misinterpretation and can result in falsely elevated scores, excessive benzodiazepine administration, and associated sequelae.4 This article describes such a scenario, and examines factors that can contribute to a falsely elevated CIWA-Ar score.
CASE REPORT: Resistant alcohol withdrawal
Mr. J, age 24, is referred to the consultation-liaison service at our teaching hospital for “overall psychiatric assessment and help with alcohol withdrawal.” When brought to the hospital, Mr. J was experiencing diaphoresis and tachycardia. During the interview, he says he “experiences withdrawal symptoms all the time, so I am familiar with the signs.”
Mr. J is cooperative with the interview. Psychomotor agitation or retardation is not noted. His speech is goal-directed, his mood is “calm,” and his affect is within normal range. His thought content is devoid of psychoses or lethal ideations. On Mini-Mental State Examination, Mr. J scores 28 out of 30, which indicates normal cognitive functioning. He reports drinking eight 40-oz bottles of beer daily for the past 3 months. He started drinking alcohol at age 14 and has had only one 1-year period of sobriety. He denies using illicit drugs and his urine drug screen is unremarkable. Mr. J has a history of delirium tremens (DTs), no significant medical history, and was not taking any medications when admitted. His psychiatric history includes generalized anxiety disorder (GAD) and antisocial personality disorder and his family history is significant for alcohol dependence.
Laboratory workup is unremarkable except for a blood alcohol level of 0.23%. Review of systems is significant for mild tremor but no other symptoms of alcohol withdrawal. Physical examination is within normal limits.
Mr. J is started on a symptom-trigger alcohol detoxification protocol using the CIWA-Ar. Based on an elevated CIWA-Ar score of 33, he receives lorazepam IV, 11 mg on his first day of hospitalization and 8 mg on the second day. On the third day, Mr. J is agitated and pulls his IV lines in an attempt to leave. Over the next 24 hours, his blood pressure ranges from 136/90 mm Hg to 169/92 mm Hg and his pulse ranges from 94 to 115 beats per minute. He is given lorazepam, 30 mg, and is transferred to the intensive care unit (ICU).
At this time, Mr. J’s Delirium Rating Scale (DRS) score is 20 (maximum: 32). He remains in the ICU on lorazepam, 25 mg/hr. After 3 days in the ICU, lorazepam is titrated and stopped 2 days later. After lorazepam is stopped, Mr. J’s DRS score is 0, his vital signs are stable, and he no longer demonstrates signs or symptoms of DTs or alcohol withdrawal. He is discharged 1 day later.
Symptom-triggered treatment
Alcohol withdrawal symptoms mainly are caused by the effects of chronic alcohol exposure on brain γ–aminobutyric acid (GABA) and glutamate systems; benzodiazepines are the standard of care (Box).5,6 Mr. J had a history of DTs, which is a risk factor for more severe alcohol withdrawal symptoms and recurrence of DTs.7 Some authors report that fixed dosing intervals are the “gold standard therapy” for alcohol withdrawal, and may be preferable for patients with a history of DTs.8 However, Mr. J was placed on a symptom-triggered protocol, which is standard at our hospital. The decision to implement this protocol was based on concerns of oversedation and possible respiratory suppression. Clinical trials have demonstrated that compared with fixed scheduled therapy for alcohol withdrawal, symptom-triggered protocols result in a reduced need for benzodiazepines (Table).
This treatment strategy requires frequent patient reevaluations—particularly early on—with attention to signs and symptoms of alcohol withdrawal and excessive sedation from medications. Additionally, although most patients with alcohol withdrawal respond to standard treatment that includes benzodiazepines, optimal nutrition, and good supportive care, a subgroup may resist therapy (resistant alcohol withdrawal). Therefore, Mr. J—and others with resistant alcohol withdrawal—may require large doses of benzodiazepines and additional sedatives and undergo complicated hospitalizations.9 Nonetheless, as exemplified by Mr. J, symptom-triggered protocols for alcohol withdrawal can result in potential morbidity and mortality.