A 45 year old female was transferred from a psychiatric facility, where she was admitted 4 days previously for elective alcohol detoxification after a family intervention. She had a long history of alcohol abuse, having suffered her first alcohol related amnestic episode (blackout) at age 15. She had been gainfully employed as an accountant until approximately age 35, when she was terminated for frequent absence from work. Most recently, her husband reports she has been consuming approximately 1/2 gallon of vodka per day, which she has delivered to the house. She has had 15 admissions to various facilities for alcohol detoxification, and was not able to achieve any lasting (>1 month) period of sobriety. Her alcohol use has escalated over the past 10 years, and she has not been able to find gainful employment. Her last 3 admissions were characterized by severe alcohol withdrawal symptoms which included alcohol withdrawal delirium.
On admission to the psychiatric hospital, she was found to be mildly jaundiced, with moderate right upper quadrant tenderness on exam. Her blood alcohol level on admission was 155 mg.% (0.155g/100dl), 2 hours after self-reported alcohol use. She was mildly disinhibited, had nystagmus, but was oriented in all spheres.
She received 60 mg. phenobarbital when her blood alcohol level was 90 mg.%, to treat increasing anxiety and restlessness. The dose was repeated every four hours for a total of 240 mg. phenobarbital. Four hours after her last dose, the clinical staff withheld additional doses of phenobarbital because the patient could barely be roused. She was disoriented to place and time, but knew her name. Her vital signs showed a blood pressure of 153/100, heart rate was 120, respiratory rate was 22 and rectal temperature was 100.5ºF.
This patient may have very significant liver disease. She may have hepatic encephalopathy, precipitated by an occult GI bleed, use of a sedative-hypnotic (phenobarbital), electrolyte disorder. Other possibilities (especially if she has a bleeding disorder from the liver disease) would include an occult head injury and subsequent subdural hematoma. She has a mild fever, which may be due to hepatitis, but she may also have an occult infection in her lungs or urinary tract. These are some possibilities should be investigated before assuming that her symptoms are due solely to AWS.
The patient has liver disease. This might represent acute or chronic alcoholic hepatitis, or may be due to other reasons. Oral phenobarbital has a very long onset time when given orally, up to four hours, and is very slowly metabolized, with a half-life of up to 120 hours in healthy individuals. The half-life is prolonged in patients with liver disease. Because of its slow onset time, very long half-life, and propensity to sometimes cause long-standing sedation, it should not be used for treatment of AWS.
A shorter acting benzodiazpeine like lorazepam, whose metabolism is not significantly altered by liver disease might have been a better choice. The best choice might have been an anti-convulsant such as carbamazepine, which can treat AWS symptoms but does not cause significant sedation.
The patient is experiencing anxiety and restlessness with a falling blood alcohol level. She has some Type A (anxiety, restlessness) as well as some Type B (hypertension, tachycardia) symptoms. In addition, she has a history of significant AWS on previous admission, and her alcohol history suggests very heavy chronic excessive use.
Over the next 12 hours, she showed no improvement in mental status, her vital signs showed a blood pressure of 110/75, heart rate of 130, RR of 26 and rectal temperature of 101ºF. She was unable to take nutrition. She was transferred to a medical facility.
Physical examination showed her to be jaundiced and heavily sedated. She slurred her words, but was able to slowly answer questions. She winced on right upper quadrant palpation. She was oriented to person, but not to place. She had asterixis (liver flap), and had very uncoordinated movements. She did not realize she had been transferred to a medical facility. Her PT was 3x control, her PTT was 2x control, bilirubin total was 10.3 (normal up to 2.2), WBC was 25K, potassium was 2.1 meq/L (normal 3.5 - 5), magnesium was 0.55 meq/L (normal 1.2 - 3), phosphate was 0.12 meq/l. She had mildly lower serum albumen and total protein. Her SGOT was 10x normal, and SGPT was 7x normal. Her blood ammonia level was 3x normal. Her chest x-ray showed no evidence of infiltrate, and her urinalysis showed no bacteria. Viral hepatitis studies were all negative. A CT scan did not show any evidence of hematoma, but the radiologist commented on the fact that she had markedly widened cortical sulci suggesting a high degree of brain atrophy when adjusted for her age. An EKG showed marked T wave flattening and tachycardia.
An IV was begun, and she was given 1/2 normal saline containing potassium chloride 40 meq/l and magnesium sulfate 8gms/L and was run at 100 cc/hour. She was placed on oral phosphate supplements. She was also placed on Lactulose with a presumptive diagnosis of hepatic encephalopathy.
This patient is at risk for severe injury if she were to attempt to rise out of bed and fall, due to her clotting abnormality and her poor balance. She should have been placed on bedrest. Since it was unclear as to whether she could follow these instructions, it would have been prudent to place her on constant observation.
The phenobarbital was discontinued and over the next 24 hours, she gradually became more awake, and was able to eat dinner. Overnight, she attempted to get out of bed multiple times, and was not responsive to redirection by staff. She then fell from her bed. On exam, she had a large hematoma on her left chest, and was in acute pain. She had no evidence of head trauma. A radiograph of her ribs showed non-displaced rib fractures. She was educated to remain in bed and to call for assistance, but was not pleased that she could not use the bathroom on her own. The clinical staff noted emotional lability, and she became very angry that she could not walk unassisted. She was noted to engage in inappropriate behaviors such as yelling for staff, removing her IV and throwing the IV set on the floor. She seemed completely unconcerned that she was bleeding profusely from the IV site and that she had soiled her bed. She was oriented to person, but not place or time. She could not sequence the events of the past 24 hours.
She is developing worsening Type C symptoms as evidenced by inappropriate behaviors. She has poor short term memory and is partially disoriented. The patient also has hepatic encephalopathy and still has significant amounts of phenobarbital in her system which could have been contributing factors.
Clinical staff discussed the case with a covering physician. Librium 100 mg. was ordered but the dose was held since the patient had gastric upset and refused the medication. Some of the staff were reticent to give a dose of sedative hypnotic in the presence of hepatic encephalopathy. The staff also questioned the recommendation that the patient be restrained.
One of the therapeutic objectives is control of the patient’s self-self-injurious behavior, by changing the level of care and/or drug administration.
The patient is exhibiting behaviors that are harmful to herself and possibly staff and other patients. She still has significant amounts of phenobarbital in her system, and is now exhibiting disinhibited behavior, along with other symptoms that are consistent with Type C AWS. The staff was correct in avoiding additional doses of a sedative hypnotic in the setting of hepatic encephalopathy, as benzodiazepines as a class of drugs can worsen the condition and increase the disinhibited behaviors. Also, the use of restraints in this patient was clearly not appropriate given that no other therapy had been attempted.
At this point, the patient could be placed on 1:1 observation, so that staff can redirect her behavior. In addition, one could choose to treat with neuroleptics that do not result in significant sedation, but would decrease her psychomotor agitation. Clinical staff suggested low dose haloperidol, given at a dose of 0.5 mg. very slow IV push for the first dose, and then orally every hour until behavioral control was achieved.
The patient was placed on one-to-one observation and after two doses of haloperidol, one hour apart, was calmer. She made no further attempts to discontinue her IV, and an EKG obtained one hour after her first dose showed no QT interval prolongation. She was placed on a standing dose of 0.5 mg. haloperidol orally every six hours. Vital signs showed a blood pressure of 160/96, HR 115, and RR 17. She was afebrile. Staff noted some sweating and tremulousness. She continued to have asterixis. She was oriented to person and time, but not to place. She had very poor short-term memory. One-to-one observation was terminated and she was placed back on constant observation.
The patient has an increase in blood pressure, along with some tremulousness and sweating. She may be experiencing Type B AWS symptoms. Other causes might include hypoglycemia, which should be considered in someone with significant liver disease, as the liver glycogen stores may be depleted.
The therapeutic objectives are to decrease the patient’s Type B symptoms. Given the presence of liver disease, and the fact that she is not experiencing significant Type A symptoms, a sympatholytic agent should be considered, which would address the effects of rising levels of catecholamines. Either Catapres (clonidine) or an orally available beta-blocker such as Inderal (propranolol) or Tenormin (atenolol) would be reasonable choices. However, it should be remembered that patients with significant liver disease may already be significantly vasodilated. Hence, they may respond very strongly to any agent that could lower blood pressure. Therefore, whatever agent is chosen, the first dose should be a low test dose, to help assure that the patient does not become hypotensive. In addition, it is reasonable to check for signs of orthostatic hypotension, as this can give a clue to lowered intravascular volume, even if the patient is hypertensive.
The patient was given a dose of 0.05 mg. clonidine orally. After one hour, vital signs showed a blood pressure of 112/83, HR 96. She was afebrile, and she had resolution of tremors and sweating. Blood pressure gradually increased over the next 6 hours.
There are several possibilities for dosing of clonidine. Since the object is to treat Type B symptoms, the agent could be given at the same level as the test dose every 8 hours if any Type B symptoms are present, and held if the blood pressure drops below set parameters. For example, the agent could be held for any blood pressure prior to administration of systolic < 110 and diastolic < 80, which would avoid problems with hypotension. Or, the agent could be ordered on a prn basis more frequently, such as every four hours, and only given if Type B symptoms are present and blood pressure is within set parameters. The objective is to minimize any adverse effects of the drug on blood pressure, while maintaining its effect of decreasing circulating catecholamines, thereby attenuating Type B symptoms.
On Day 4 of the current admission, the patient’s current regimen was close observation, OOB with assistance, haloperidol 0.5 mg. po every 6 hours, and clonidine 0.05 mg. every 6 hours, with blood pressure hold limits. She was also receiving Lactulose, 30 me every 8 hours. Her behavior is more appropriate with staff and other patients. She continues to have mild asterixis, and short term memory is impaired. She is oriented to person and place, and occasionally to time.
Either the frequency of dosing, or the amount of drug given at each dosing interval can be decreased. In the case of clonidine, doses of less than 0.05 mg. are hard to obtain, so the dosing interval can be increased over the next 72 hours from q 6 hours to q 8 hours to q 12 hours, with the patient being observed for any emergent Type B symptoms. Should this occur, the dosing frequency can be increased. The same general theme would apply to haloperidol, where the dose of the drug could be decreased to 0.25 mg. over a 24 hour period, and then dosing frequency decreased to three times and then twice daily again as long as target symptoms do not emerge.
Over the next three days, both haloperidol and clonidine are successfully tapered and then discontinued. However, the patient still exhibits poor short term memory, even though she is now oriented in all spheres. She can now ambulate on her own, and close observation is discontinued, since she does not have any evidence of poor balance. Her asterixis has resolved, her jaundice is resolving and she is eating well. A Folstein mini-mental status screening test was performed, and the patient scored 15/30, with many of the deficits in both memory and mathematical abstraction.
The patient may still have significant levels of phenobarbital in her system. She is also resolving what is likely alcohol withdrawal delirium as well as hepatic encephalopathy. In addition, she may have an alcoholic dementia, as evidenced by poor performance on the Folstein mini-mental status examination, and the results of her CT scan. Women are much more sensitive to the neurotoxic effects of alcohol than males, and her long alcohol use history is consistent with these findings. It is also unclear whether she had at any point in time experienced a Wernicke encephalopathy from thiamine deficiency which may have resulted in permanent memory short-term memory impairments.
A better understanding of her cognitive status would be critical for discharge planning. She requires a complete neurological and neuropsychiatric evaluation to both assess her cognitive capacity as well as to determine her functional status. An occupational therapy consult might also be considered to assess her ability to care for herself. This might be required if long-term placement is contemplated.
IQ measured by Wechsler scale reveals normal verbal performance (105) but severely impaired on Freedom-from-distractibility and Performance scales, as well as markedly slowed processing. This is consistent with an alcoholic dementia.
Since there is a good possibility that the patient may regain some cognitive function over the next 6-12 months, she is discharged to a nursing home, and arrangements are made for an alcohol counselor to visit her. She will be followed by a neurologist.
Note: This patient was almost discharged back to her home. In alcoholic dementia, the relative preservation of verbal ability tends to mask other severe cognitive deficits, as the patient may appear to interact normally with other patients and staff. It is difficult to imagine that this patient would have received any benefit from a cognitively based alcohol treatment program, or that she could perform tasks associated with ADL’s.
Alcoholic dementia is a devastating diagnosis for both the patient and her spouse, and counseling should be offered to the spouse to address issues related to both his spouse’s dependency issues, as well as issues of grief and loss.
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