A 68 year-old male was admitted to the hospital for symptoms of congestive heart failure which were not responding to outpatient therapy. His symptoms on admission: orthopnea, shortness of breath on walking on level ground less than 50 yards, leg edema, nocturia, and post-prandial fatigue and dizziness. He was being treated with Lasix (furosemide) 80 mg twice daily, captopril 50 mg three times per day, and digoxin 0.25 mg per day. He was known to his physician as being an immoderate alcohol consumer, and had consumed as much as a case of beer per day for most of his adult life during his employment as a plumber. His wife reports that he was drinking one to two six-packs of beer per day over the past few years prior to admission. He had never been treated for alcohol dependence, and despite a history of blackouts and one seizure occurring after a heavy episode of drinking several years prior to admission, had been gainfully employed until his retirement 4 years before admission. His last drink of alcohol was several hours prior to admission, when he reportedly had consumed two beers with his evening meal, had become very short of breath, and was transported to the ER. He had no history of myocardial infarction, and had been treated for high blood pressure in his forties. He smoked one pack of cigarettes per day.
On examination, he was an obese white male lying in bed and mildly short of breath. His blood pressure was 110/60 with a heart rate of 100, which was regular. He had no fever, and he weighed 120 kilograms. He had a ruddy complexion as well as rhinophyma. Spider angiomas were readily apparent on his neck. Lung examination showed crackles and rales half-way up the lung fields. He had jugular venous distension sitting up at a 45 degree angle. His cardiac sounds were difficult to appreciate. His abdomen was mildly distended, and his liver was normal size. There was no abdominal tenderness. Peripheral pitting edema was noted, and extended to his thighs. His skin was cool and clammy. A chest x-ray showed a fine interstitial reticular pattern consistent with mild congestive heart failure. His heart was enlarged, with a prominent left ventricle. His EKG showed decreased voltage. Laboratory examination showed a potassium of 5.5 meq/l, bicarbonate of 22, magnesium of 1.0 meq/l, a BUN of 110 and a creatinine of 3.5. A blood gas showed a pO2 of 78 and a pCO2 of 30. A blood alcohol level was not obtained.
The clinical impression was that this patient had congestive cardiomyopathy, and the possibility of a pericardial effusion was also entertained. He had mild renal impairment, and was also mildly intravascular volume depleted.
The patient had a cardiomyopathy and a history of hypertension, and alcohol is a risk factor for both conditions. Alcohol is also an acute depressant of cardiac function, and it could be hypothesized that a combination of a high-salt meal along with alcohol might have been directly responsible for tipping him into what is clearly acute congestive heart failure.
This patient had signs and symptoms of congestive heart failure on admission, and a corroborative chest x-ray. He did not have any evidence of a previous myocardial infarction, but did have a history of high blood pressure and alcoholism. The causes of his congestive cardiomyopathy might have included long-standing high blood pressure, which may have been due to alcohol intake, as well as alcoholic cardiomyopathy. The latter may have been the most probable, given his history of heavy chronic excessive alcohol consumption.
The cornerstone of his medical therapy was after-load reduction with an ACE inhibitor, as well as diuretics. In addition, his continued alcohol use, because of its negative impact on his cardiac function, should have been addressed. Clearly, his continued alcohol use may have contributed to his failing cardiac function even if it did not occur at excessive levels.
It would have been useful to obtain an alcohol level on admission, to document alcohol intake with his history, to establish if tolerance was present based on behavioral evidence of intoxication matched to his alcohol level, and to use as evidence to help him understand that continued alcohol use given his failing heart function was a very high risk behavior.
His elevated BUN/Creatinine ratio suggests that he was intravascularly volume depleted, while his overall fluid status suggests that he was total body sodium overloaded. His renal blood flow was compromised by low cardiac output, explaining the decrement in renal function and the high potassium, though the latter may have been an effect of the ACE inhibitors as well.
Dehydration and a failing heart would have called into play stress hormones such as cortisol, aldosterone, and serum catecholamines. Serum catecholamines might also have been elevated due to AWS. The latter would have resulted in a tachycardia, but given the fact that he was after-load reduced and dehydrated, his blood pressure may not have increased, as would have been the case with a patient with normal heart function and normal volume status.
The course over the first day suggests that conservative treatment was moderately successful in causing a natriuresis (loss of sodium in urine). However, he had an elevated heart rate at this point. This could have been due to incipient alcohol withdrawal, or it may have been an appropriate response to loss of intravascular volume, or most likely, some combination of these factors.
Over the next day, the patient was salt restricted and treated with intravenous diuretics (furosemide) 80 mg IV every 12 hours with good response. He diuresed 3 liters and his weight decreased about 2.5 kilograms. A cardiac ultrasound revealed a small pericardial effusion. The captopril was increased to 100 mg every 8 hours. His blood pressure was 122/84 with a heart rate of 120. The patient became increasingly more anxious, had not slept since admission, and was verbalizing severe discomfort to clinical staff. Because of his history of alcoholism, he was begun on Librium 100 mg every 8 hours.
The patient had CHF. Hypoxia could have caused his sympotoms, as would the response to both central and peripheral release of catecholamines. He may have also been suffering from cerbreal hypoperfusion due to low cardiac output.
This patient has a major medical illness, and you can expect his condition to change dynamically over time. For this reason alone, an agent which is metabolized more rapidly than Librium, such as lorazepam (Ativan) might have been chosen. This would have allowed better titration of his symptoms based on response, and should he have become overly sedated, it would not last as long. He was an older patient, and this would have also further decreased his metabolic rate for Librium, making the case for having chosen a shorter acting agent like lorazepam where the metabolism is not appreciably prolonged with age.
Carbamazepine, an anticonvulsant, could have been used to treat Type A AWS. This anti-convulsant does not usually cause sedation at doses required for treatment of Type A AWS. While not commonly used in the US, there is a vast experience with use of this drug to treat AWS in Western Europe. Unlike benzodiazepines, it also does not appreciably alter, as far as is known, stress response hormones such as catecholamines. In this case, it would have been helpful, since even slight decreases in catecholamines may further have impaired his cardiac function.
He slept for a few hours after the first dose of Librium, and it was noted his blood pressure was 100/60 with a heart rate of 100. After the second dose, he again slept for a few hours, and his blood pressure was noted to be 90/40 with a heart rate of 80.
He might be suffering a myocardial infarction or ischemia, thereby further depressing his cardiac function. This possibility was entertained by the clinicians caring for him. However, what was not addressed was the possibility that Librium was depressing his respiration, possibly interfering with gas exchange, and causing a respiratory acidosis because he was not “blowing off” carbon dioxide. In addition, while benzodiazepines do not have a large effect on output of serum catecholamines, there are some mild effects on lowering of catecholamines, probably due to activation of inhibitory GABAergic receptors controlling centrally mediated output. It is therefore also possible that his serum catecholamines were decreased by Librium therapy. This is dangerous, because in this case, the patient’s homeostatic response to falling cardiac output, which would result in rises in serum catecholamines, has been blunted by medication.
Low cerebral blood flow due to a failing heart is one.
Hypoxia due to CHF.
Respiratory acidosis can also cause a mental status change.
Severe electrolyte disturbances.
An arterial blood gas. This would answer the question of whether the patient had a respiratory acidosis, and also whether he had significant hypoxia, all of which could have contributed to his mental status change. Even if you are convinced that the patient’s symptoms are all due to drug effect, in this case, Librium, it is critical to entertain alternate scenarios and to rule them out when appropriate. Unfortunately, in this case, a blood gas was never obtained.
He awoke a few hours after his second dose of Librium. He was agitated but had difficulty making coordinated muscular movements. He threatened the nursing staff with physical harm if they did not immediately call his wife so he could leave the hospital. As a response to this behavior, he was given a third dose of Librium, 100 mg orally.
The patient is exhibiting disinhibited behavior, but it appears he knows he is in the hospital and would like to leave. He is also uncoordinated, perhaps due to cerebellar effects of the benzodiazepine. All of the causes listed previously (hypoxia, acidosis, worsening cerebral blood .ow) could have contributed. He has received a benzodiazepine, which can result in disinhibited behavior. It is also possible that the patient is beginning to exhibit Type C symptoms of AWS.
The therapeutic objective was to sedate the patient.
Four hours after the dose of Librium, a “code blue” was called and the patient was found to be in cardiorespiratory arrest. He underwent electromechanical dissociation and was pronounced dead 30 minutes after cardiopulmonary resuscitation was administered.
Failure to entertain that anxiety and psychomotor agitation can have alternate causes, which need to be considered before instituting therapy for treatment of alcohol withdrawal.
In a patient with severe congestive heart failure, such as the patient in this case, management of the heart failure should have been much more aggressive, especially if concurrent alcohol withdrawal syndrome was suspected.
When his blood pressure and heart rate decreased after the first dose of Librium, the possibility that Librium was inappropriately decreasing circulating catecholamines should have been entertained. The patient was not treated aggressively. The non-aggressive nature of treatment of his heart failure may have been driven by a prejudice against individuals that suffer from alcoholism. This prejudice may have caused the staff to attribute all the patient’s symptoms to alcohol withdrawal, when in reality he had severe congestive heart failure.
Failure to transfer the patient to an intensive care unit for cardiac monitoring. This would have included frequent blood gas determinations, monitoring of urine output, and a Swann-Gantz catheter placement to allow better assessment of cardiovascular function and fluid status. This would have been ideal in any patient, but was especially indicated when the patient may have also had symptoms of alcohol withdrawal, which is known to cause major disturbances in autonomic function.
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