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False Positives on the Clinical Institute Withdrawal Assessment for Alcohol—Revised: Is This Scale Appropriate for Use in the Medically Ill?

Presented as a poster at the 48th annual meeting of the Academy of Psychosomatic Medicine, San Antonio, Nov. 15–18, 2001. Received March 18, 2003; revision received Sept. 17, 2003; accepted Oct. 17, 2003. From the Department of Psychiatry and Psychology, Mayo Clinic. Address reprint requests to Dr. Bostwick, Department of Psychiatry and Psychology, Mayo Clinic, 200 First St., S.W., Rochester, MN 55905; bostwick.john{at}mayo.edu (e-mail).

General hospital teams increasingly rely upon symptom-triggered protocols like the Clinical Institute Withdrawal Assessment for Alcohol—Revised (CIWA-Ar) to manage alcohol withdrawal syndrome. Although serious illness can exacerbate alcohol withdrawal syndrome, the CIWA-Ar, validated only in detoxification centers and in patients with uncomplicated illness, is used in patients with condition validation trials excluded.

We report on four medically complicated patients with presumed alcohol withdrawal syndrome who were unresponsive to help provided by the CIWA-Ar. A careful history taking revealed two who were not drinking alcohol at admission. A third had active alcoholism that was unappreciated until withdrawal complications ensued. In none did alcohol withdrawal syndrome fully explain their behavioral dyscontrol. Before initiating the CIWA-Ar, we recommend 1) a careful medical review and 2) a reassessment of CIWA-Ar's appropriateness if the behavior worsens or a new alcohol history emerges. With up to 21% of general hospital inpatients shown to have alcohol-related diseases, alcohol withdrawal syndrome (suspect or actual) is common in general hospital settings.¹

Alcohol withdrawal syndrome typically begins 6 to 48 hours after the reduction or cessation of alcohol use. The spectrum of alcohol withdrawal syndrome includes four levels of increasing intensity,² starting with 1) tremulousness, often accompanied by nausea and vomiting; advancing to 2) hallucinations, most often visual, but potentially auditory, tactile, or olfactory; or 3) withdrawal seizures, usually within the first 48 hours; and culminating in 4) frank delirium tremens. Usually beginning 3–5 days after decreased alcohol intake, delirium tremens comprise any or all of the first three categories, plus disorientation, confusion, agitation, and a hyperadrenergic syndrome characterized by a temperature greater than 101°F, a blood pressure greater than 140/90 mm Hg, and a pulse greater than 100 bpm. About 5% of the patients with alcohol withdrawal syndrome progress to delirium tremens, normally lasting days but rarely extending to weeks.^3–5

While common in alcohol withdrawal syndrome, sympathetic hyperactivity is not required for the diagnosis. Such withdrawal symptoms as tremors, diaphoresis, tachycardia, and hypertension result from elevated brainstem levels of noradrenaline (norepinephrine) and high levels of plasma catecholamines.⁵ Despite a positive correlation between alcohol withdrawal severity and increasing autonomic activity, all patients experiencing severe alcohol withdrawal do not have the elevated vital signs more common with advanced age or comorbid acute medical illness.⁶ Despite one study that found a low statistical correlation between vital signs and alcohol withdrawal syndrome,⁷ changes in blood pressure, pulse, and temperature were deemed important enough to be included in the DSM-IV as diagnostic criteria.⁸

Over the last 30 years, a series of rating scales have been developed to measure alcohol withdrawal severity systematically and objectively. With the use of a cluster analysis of signs and symptoms, the Total Severity Assessment and the Selected Severity Assessment scales became the basis for the 18-item Clinical Institute Withdrawal Assessment for Alcohol,⁹ which was revised and shortened into the current 10-item CIWA-Ar scale, which excludes vital sign abnormalities. In a psychiatric hospital population, Stuppaeck and colleagues¹⁰ found such abnormalities to have a low statistical correlation with alcohol withdrawal states. A recent DSM-IV revision of the CIWA-A scale includes autonomic parameters,^5,10,11 but the CIWA-Ar remains the most widely used and studied alcohol withdrawal monitoring scale.

While the CIWA-Ar has demonstrated validity, reliability, and sensitivity in certain situations,⁷ these studies emanate almost exclusively from detoxification facilities whose patients had neither acute medical nor surgical comorbidity.^12,13 The few studies on CIWA-Ar's use in the medically ill have exclusion criteria severely restricting their generalizability to many general hospital patients.

One such study by Reoux and Miller¹⁴ recruited medical patients with alcohol withdrawal, drug withdrawal, delirium tremens, and alcoholic hallucinosis, finding that those followed with the CIWA-Ar required less benzodiazepines for a shorter duration than a control group. Of 172 potential subjects, only 40 (24%) were eligible for the study; however, the other 132 were excluded because of severe liver disease, simultaneous opiate and alcohol withdrawal, concurrent benzodiazepine or anticonvulsant use, or acute medical or surgical problems. These are the patients whose alcohol-related difficulties are managed by consultation-liaison psychiatrists. These were the patients excluded "to reduce the possible effect that concurrent acute medical problems may contribute to the severity of withdrawal symptoms or medication metabolism rates."¹⁴ Sullivan and colleagues¹⁵ had earlier demonstrated essentially the same findings, likewise limiting their retrospective case control study to 133 patients with a principal diagnosis of alcohol dependence.¹⁵

In 2001, Jaeger and colleagues¹⁶ advocated "symptom-triggered therapy for alcohol withdrawal syndrome in medical inpatients." While they showed that the CIWA-Ar's use of general medical services reduced the frequency of delirium tremens,¹⁵ it is instructive to review their exclusion criteria. Among others, those deemed ineligible were patients beginning hospitalization in the intensive care unit, patients on specialty medical or surgical units, and patients admitted after a multiple drug overdose. Moreover, they excluded patients with alcohol withdrawal seizures, since aggressive benzodiazepine treatment had usually already been initiated in the emergency room.¹⁶ The very groups that they excluded—those with concurrent complicated medical or surgical illnesses—embody the "single greatest predictor of delirium tremens development."⁶ These groups are also the ones about which the least is known. A 1997 evidence-based practice guideline by the American Society of Addiction Medicine¹⁷ noted that "no studies were identified which reported on clinical experience in managing alcohol withdrawal in patients with specific coexisting medical or substance abuse disorders."

In our institution, the same one in which Jaeger and colleagues conducted their study, the CIWA-Ar has become the standard throughout the medical center for monitoring potential alcohol withdrawal, regardless of medical and surgical comorbidity. The CIWA-Ar in our institution is paired with a treatment protocol that outlines a management strategy: pharmacological intervention with benzodiazepines for patients with suspected or established alcohol withdrawal, with doses keyed to CIWA-Ar score. We describe four cases of inappropriate reliance on the CIWA-Ar to manage symptoms falsely attributed to alcohol withdrawal syndrome. All four patients had alcohol abuse histories, although only two ultimately proved to have been drinking at hospital admission. After nurse-raters determined that they had elevated scores on the CIWA-Ar, all four received benzodiazepines according to protocol, although in none did primary physicians give consideration to alternate explanations for the "withdrawal" symptoms.

These cases illustrate the importance of distinguishing delirium due to medical causes from delirium due to alcohol withdrawal, the limitations of available diagnostic tools for making this distinction, and potential complications arising from an incorrect diagnosis. Even more important, they highlight the danger of reflexively adopting a clinical instrument not validated for the population being assessed. They underscore various untoward outcomes that can result when careful history taking and ongoing physician assessment are neglected in caring for patients with alcohol dependence.

Case Report

Case A: Does Infection and Bacteremia in a Patient With Chronic Alcohol Dependence Equal Alcohol Withdrawal Syndrome?
Mr. A, a 59-year-old man, was transferred to our medical center for further management of an infected pancreatic pseudocyst, gram-negative bacteremia, and worsening delirium. He had had abdominal pain, nausea, vomiting, diarrhea, a high fever, and chills for at least a week and had received intravenous fluids, calcium gluconate, and broad-spectrum antibiotics during a 4-day admission at the referring facility. His past medical history included longstanding alcoholism and repeated hospitalizations for exacerbations of chronic alcoholic pancreatitis. He reported no alcohol use in the past 2 months.

At admission, he showed waxing and waning alertness, slurred speech, agitation, confusion, and disorientation. He was picking at things in the air that only he could see. Despite multiple potential explanations for his altered mental state, the medical team decided that delirium tremens was the most likely cause and initiated the CIWA-Ar protocol. He had CIWA-Ar scores in the 20's, so he received lorazepam, thiamine, and folate per the protocol. When the medical psychiatry team examined him, he was afebrile, but his pulse and blood pressure were in the normal range. He was somnolent but arousable, without neck rigidity or tremors. He was confused and completely disoriented. His blood gas level was normal, cranial magnetic resonance imaging showed no evidence of mass lesions or intracranial hemorrhage, and a chest X-ray was clear. The psychiatry team suggested electroencephalography to differentiate the fast activity of delirium tremens from the slow activity of delirium. His EEG showed generalized dysrhythmia consistent with toxic metabolic encephalopathy.

Despite the EEG findings, lorazepam was continued for several days for persistently high CIWA-Ar scores based on Mr. A's ongoing anxiety, headache, nausea, vomiting, and confusion. In the absence of strong evidence for alcohol withdrawal, the consultation-liaison team recommended discontinuing lorazepam, a potential contributor to the delirium. Not until Mr. A's pseudocyst was drained and his bacteremia was treated with antibiotics and hydration did his mental status improve.

Case B: If You Have Not Been Drinking, Can You Have Alcohol Withdrawal Syndrome?
Mr. B, a 57-year-old man with known hypertension, coronary artery disease, and type 2 diabetes mellitus, was hospitalized for a sudden onset of chest pain. His admission note listed both alcohol and nicotine dependence but no details about current use. A medical work-up revealed Q waves on his ECG, elevated cardiac enzyme levels, and three-vessel coronary artery disease on coronary angiography. A day after emergent bypass graft surgery on a coronary artery, he became agitated in the coronary care unit, with intermittent confusion and combativeness. After pulling out his urinary catheter and repeatedly attempting to climb out of bed and kick the nursing staff, he was physically restrained. Assumed to be in alcohol withdrawal, he was administered the CIWA-Ar and given large doses of intravenous lorazepam—as much as 30 mg in 24 hours—without any effect other than slurred speech and increased somnolence in between his bouts of agitation. On the fifth postoperative day, the medical psychiatry team was asked to help with his persisting agitation. The team found a barely arousable man who was unable to open his eyes to command, had slurred and unintelligible speech, and prominent ataxia. He appeared inebriated. When a psychiatrist contacted the patient's son, he said that his father had indeed once been a heavy drinker but had quit years ago. The psychiatry team recommended a delirium workup, which showed Mr. B to have a pseudomonas urinary tract infection. The coronary care unit's staff also agreed that postcardiotomy delirium and lorazepam intoxication were likely contributing to his behavioral symptoms.

The psychiatry team suggested that lorazepam be discontinued, and intravenous haloperidol be rapidly titrated, with Mr. B receiving 50 mg over the next 24 hours before achieving a state of calm. Over the next several days, his agitation was resolved, and his cognition cleared. He left the hospital taking no psychotropic agents.

Case C: Frustration and Nicotine Withdrawal Can Complicate Alcohol Withdrawal Syndrome
Mr. C, a 41-year-old man, was hospitalized on a specialized surgical unit for resection of a laryngeal tumor. A longtime heavy drinker and smoker, he had been consuming up to 12 beers and two packs of cigarettes a day until his hospitalization. He had never had chemical dependency treatment.

After a laryngectomy and a tracheostomy, he required nasogastric tube feedings because of prominent facial and neck edema. For a week after surgery, he was monitored for alcohol withdrawal syndrome with use of the CIWA-Ar. He consistently received intravenous lorazepam for mild to moderate scores of 6–12, resulting from ongoing irritable behavior, anxiety, and headaches.

Eventually, a psychiatric consultation was sought to assess his labile behavior. A chart review showed that he had never had elevated vital signs. He was alert and exhibited neither tremors nor abnormal movements. Although he was unable to speak, he communicated by scrawling furiously on a pad and banging his fist on his bedside table for emphasis. His affect was impressively irritable and frustrated. During one of his frequent coughing fits, he jumped to his feet, grabbed his intravenous stand, and lurched into the bathroom, where he expelled secretions violently through his tracheostomy. Despite the challenge of interviewing him, he showed impairments in neither thought form nor content. His notes were angrily on target. He reported no suicidality.

Since his behavior had persisted essentially unchanged for more than a week, the psychiatry team felt that his outbursts likely resulted from longstanding impulsivity and poor coping, consistent with a personality disorder. His agitation was likely intensified by nicotine withdrawal, given his abrupt cessation of a two-pack-a-day habit. Psychiatric hospitalization was proposed to taper his lorazepam and help with postoperative adjustment to his tracheostomy and feeding challenges. Nicotine replacement was also suggested. Mr. C refused all recommendations and was discharged with a tapering dose of lorazepam.

Case D: Delirium May Indicate More Than Alcohol Withdrawal Syndrome
Mr. D, a 59-year-old man, had tolerated the removal of his cancerous bladder without incident. On the first postoperative day, however, he became severely agitated, and a psychiatric consultation was obtained. A collateral history from his son revealed previously unappreciated heavy alcohol use with a history of severe alcohol withdrawal syndrome and multiple inpatient chemical dependency treatments. His last drink had been on the day of admission. By the time the medical psychiatry team was consulted, Mr. D was in florid delirium tremens. He was restless, tremulous, and diaphoretic. Arousable but confused, he mumbled, had slurred speech, and gave incoherent answers to simple questions. He was febrile, with a pulse >100 bpm and blood pressures as high as 180/100 mm Hg. He had pulled out his intravenous tubes and lines, and his nurses had seen him pointing into space while conversing with unseen persons. After treatment with thiamine, folate, lorazepam, and chlordiazepoxide, according to the CIWA-Ar protocol, his fever initially resolved, and his vital signs normalized. His level of consciousness continued to fluctuate from awake and agitated incoherence to unresponsiveness. However, the results of an extensive delirium workup showed that a WBC count, electrolyte levels, a chest X-ray, cardiac enzyme levels, a blood gas level, and a urinalysis were normal.

During an agitated episode, Mr. D vomited and breathed in his stomach contents, developing an aspiration pneumonia severe enough to require temporary mechanical ventilation. Electroencephalography revealed both diffuse nonspecific slow-wave abnormalities and prominent fast activity. Increasing doses of intravenous lorazepam were given, resulting in further agitation. Not until haloperidol was added was his intermittent combativeness fully suppressed.

When he was closely followed by the psychiatry team during a 3-week postoperative hospitalization, his cognition slowly improved as benzodiazepines were tapered. Given his acute postoperative decompensation and superimposed pneumonia, the psychiatric team opined that the delirium was multifactorial rather than simply the result of alcohol withdrawal syndrome. At discharge, he refused further assessment of his alcohol dependence.

Discussion

The preceding cases share many commonalities. Based on the combination of suggestive histories and high scores on the CIWA-Ar, all of the patients were reflexively treated with benzodiazepines for presumed pure alcohol-related withdrawal, despite inadequate medical review. All four patients had alcohol histories that were comorbid with other conditions. Three were delirious in the context of acute medical or surgical conditions, and one had unrecognized nicotine withdrawal. Failure to identify underlying medical and surgical conditions may have complicated or lengthened the hospital courses. In all four cases, only when treatment strategies were revised to deal with complications other than alcohol-related conditions alone did the deliria and agitation resolve.

Routine deployment of the CIWA-Ar in the general hospital is inadequate to manage hospitalized patients with alcohol dependence. The CIWA-Ar has well-established usefulness in assessing the presence and severity of alcohol withdrawal syndrome when uncomplicated by other illnesses. However, in general medical inpatients with alcohol histories, our cases suggest that assessment with the CIWA-Ar alone fails to take into consideration delirium from potential etiologies other than alcohol withdrawal syndrome. Unless they have been hospitalized solely for withdrawal management, alcohol-dependent individuals are, by definition, comorbid for alcohol dependence and an acute medical or surgical condition. Such patients risk receiving inadequate or inappropriate treatment if falsely diagnosed with alcohol withdrawal syndrome by CIWA-Ar criteria alone.¹⁸ Our cases illustrate the assertion by Foy and colleagues¹⁹ that "in general hospitals, where alcohol withdrawal is usually accompanied by a serious acute illness, signs and symptoms may not be as clear-cut, assessment may be difficult, and yet the consequences of inadequate or excessive treatment are likely to be much more serious."

Before instituting the CIWA-Ar in a delirious medically ill patient with comorbid alcoholism, careful attention must be paid to potential delirium other than alcohol withdrawal. Jaeger and colleagues¹⁶ reported an association between symptom-triggered therapy for alcohol withdrawal in medical inpatients and a reduced rate of delirium tremens. While we do not dispute their findings in a carefully circumscribed cohort, we do challenge routine CIWA-Ar deployment in populations they did not study. While we salute efforts to standardize treatment regimens, where appropriate, we also assert that patients with complicated medical and surgical comorbidities—the bread and butter of medical psychiatry's purview—are frequently inappropriate for such protocols, particularly when 1) adequate medical review before initiation and 2) frequent physician reassessment during deployment are not routine.

Our cases exemplify what can happen when these two principles are not followed. In the first two cases, recent alcohol ingestion was assumed without corroboration and without consideration of alternate explanations. In case A, the medical team continued to follow CIWA-Ar protocol for presumed alcohol withdrawal, despite the patient's report of no recent alcohol ingestion and the mounting evidence of pancreatic sepsis. Likewise, in case B, the team assumed a diagnosis of alcohol withdrawal syndrome in a patient who had not been drinking and intoxicated him with lorazepam before considering such alternate explanations for his confusion as postcardiotomy delirium and urinary tract infection. In case C, the patient's agitation was assumed to stem entirely from alcohol withdrawal when there were several alternate contributors, particularly when it extended into the hospitalization's second week. Finally, alcohol dependence in the patient in case D was unappreciated until he was desperately ill. A "cookbook" CIWA-Ar approach then led to undertreatment of alcohol withdrawal, continued extreme agitation, and a complication of aspiration pneumonia requiring mechanical ventilation. What began as alcohol withdrawal after recent surgery quickly advanced to delirium tremens, with a life threatening complication of inadequately managed alcohol withdrawal syndrome.

In summary, we assert that existing alcohol withdrawal assessment protocols are inadequate for treating patients with comorbid alcoholism and medical or surgical illnesses. Acute conditions, such as intense pain, shock, and sepsis can cause extensive catecholamine release that yields the picture of sympathetic overstimulation that results in an elevated CIWA-Ar score, even if vital signs are not taken.¹⁹ Many conditions mimic or intensify the phenotype of alcohol withdrawal syndrome. To identify these subpopulations, we advocate creation of a screening instrument to draw attention to comorbid medical conditions contraindicating routine CIWA-Ar implementation. All potential withdrawal patients in the general hospital deserve customized medical screening that is tailored to their particular situations, rather than one-size-fits-all tools like the CIWA-Ar that are indiscriminately applied.

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