A 45 yo male is admitted to the coronary care unit from the ER with a presenting complaint of severe chest pain associated with dyspnea and fatigue, which began three hours prior to admission and has increased in intensity. History reveals that the patient, who is a respected partner in a large law firm, drinks between four and six mixed drinks per day, usually in the evening. He has maintained this drinking pattern for at least 10 years. He reports no work-related or family related problems due to alcohol use, and this story is corroborated by his wife. His last drink was two hours prior to admission. The patient has a history of poorly controlled hypertension, for which he is being treated with atenolol, 25 mg. bid. The patient has never experienced this type of pain, and appears quite anxious. He has a 30 pack-year history of cigarette use, but stopped smoking 5 years prior to admission on his physician's advice. Blood pressure is 110/60, heart rate is 60 Oral temperature is 100F. Respiratory rate is 20. Skin is cool and clammy. Lungs are clear, heart exam shows a soft S1. A mild systolic murmur is heard best at the left lower sternal border. Abdomen is benign. No peripheral edema is noted. EKG shows ST depression in leads II, III and AVF. Some ST segment depression is also noted in precordial leads 4,5,6. Blood chemistries show a potassium of 3.0 meq/L, and initial CPK and LDH are within normal range. Blood alcohol level is reported at 70 mg.%.
The alcohol history was verified by the spouse. It is critical to obtain such corroborative evidence to begin to trust the patient’s alcohol history. However, even a spouse may minimize the amount of alcohol used, perhaps because they also are experiencing alcohol-related problems. In addition, clinicians should be aware of co-dependence issues that may result in enabling behaviors, so that the spouse is also intimately involved in the patient’s denial system. So, while this alcohol history may be accurate, the possibility persists that the patient may be consuming larger amounts of alcohol than reported.
The patient is using atenolol, a beta-blocker, which, if the patient is compliant, may be antagonizing the effects of increased serum catecholamines, which are elevated in any case also due to angina. In this case, if one was using the Type Indicator©, Type B symptoms would be partially treated by the beta-blocker.
Hypokalemia is common in alcoholics, due to the fact that alcohol use results in increased potassium losses, increased losses of magnesium which in turn alters the ability of the kidney to hold back potassium, and in some cases, poor dietary intake. In addition, rising serum catecholamines can cause shifts of potassium into cells, which can result in decreases of potassium in serum.
His last intake of alcohol was two hours prior to admission, and his blood alcohol level on admission was 70 mg.%. Assuming an enhanced metabolic rate in a chronic user of 20mg%/hour, and given that his last drink was two hours prior to admission, this would have given him a peak alcohol level of 110mg%. This level of consumption places him at risk for AWS. It also suggests that both he and his spouse may have minimized the amounts of alcohol consumed at his presentation.
All of them. While in this case there may be alternate explanations for these symptoms, the patient is anxious, restless, has chest pain, high blood pressure, EKG changes, and low serum potassium. All of these symptoms may be due to or exacerbated by AWS.
While in the ER, he receives 2 x 1/150 sl NTG with resolution of the chest pain and normalization of the EKG. Admission orders include continuing of atenolol 25 mg. po BID, and addition of diltiazem 60 mg. po QID, PRN sl NTG is also ordered. A cardiology consultation is obtained and the patient is scheduled for cardiac catheterization in the next 48 hours. Over the next 12 hours, the patient is noted to exhibit increasing anxiety. He complains of insomnia, mild gastric upset, and is described as being restless by the nursing staff. Blood pressure is 138/84 and heart rate is 80.
At this point, the patient’s cardiac symptoms have partially resolved with treatment, but the patient is experiencing insomnia, anxiety, and gastric distress. These symptoms are consistent with Type A withdrawal by the Type Indicator©. Blood pressure and heart rate are both increasing even though the patient is receiving both a beta-blocker and a calcium-channel blocker. These symptoms should be judged in the context of medications that the patient receiving. For example, blood pressure and heart rate are partially driven by increased amounts of serum catecholamines. This can be due to AWS, cardiac malfunction or the combination. One clue is that one might have expected the blood pressure and heart rate to be somewhat lower given the therapy the patient is receiving.
The patient is experiencing insomnia and anxiety, as well as gastric distress. The patient is not receiving any sedative/anxiolytic. Anxiety may be contributing to increasing serum catecholamines, which in this setting increases cardiac work load and might be worsening the patient’s cardiac status. The patient should receive an anxiolytic. Since the question of AWS has been raised, it would be appropriate to administer a benzodiazepine. Given the age, and absence of liver problems, diazepam would have been a good choice. The drug could have been administered orally, at a dose of 10 mg. every hour, until the patient was sedated but easily arousable. This also has the advantage of allowing the clinician to assess the tolerance level to sedative hypnotics, which would have provided critical information regarding the level of tolerance to alcohol, and the associated risk of AWS.
No! Treat the symptoms and not the disease at this point. In this case, there are multiple complicating factors which may prevent an astute clinician from being certain that these symptoms are due to AWS. These include use of beta-blockers which can mask symptoms of Type B withdrawal, as well as cardiac problems which could be associated with increased serum catecholamines. By not treating anxiety and insomnia, the patient is suffering, which is also associated with increased serum catecholamines, which may be negatively affecting his cardiac status.
24 hours after admission, the patient develops another episode of chest pain, with similar findings on EKG as on admission. He is very restless, and has not slept since admission. His blood pressure is 150/92 with a heart rate of 90. The chest pain and EKG abnormalities do not respond to 2 sl NTG given ten minutes apart. He is placed on a NTG drip, which is titrated to blood pressure, and has resolutions of anginal symptoms. Two hours after initiation of parenteral NTG, he is observed to have a tonic-clonic seizure lasting approximately 3 minutes, during which time he is apneic. The episode is terminated with diazepam 5 mg. IV. An arterial blood gas after the event shows a pH of 7.20, pO2 of 55, and pCO2 of 60. Blood chemistries reveal a potassium of 2.5 and serum magnesium of 0.5 meq/L. An EKG immediately after the episode shows ST elevations in leads II,III and F.
The patient exhibited increasing Type A symptoms, with increasing restlessness, anxiety and insomnia. The seizure is certainly consistent with AWS. The patient has a severe electrolyte disturbance, which contributed to the seizure, and is associated with AWS as well as with chronic excessive alcohol consumption. It was finally recognized that this patient was exhibiting severe alcohol withdrawal symptoms (Type A symptoms) and also Type B symptoms breaking through the beta-blocker, with increasing blood pressure and heart rate. However, it is too late. He has suffered a myocardial infarction and may have had neurological damage due to prolonged hypoxia.
This patient has had a seizure, and while he received 5 mg. diazepam, he is not sedated. This suggests at least some level of tolerance to sedative hypnotics. Even though he should have received diazepam earlier in the course, the drug should be increased and titrated so that the patient was heavily sedated to address severe type A symptoms.
An IV of 0.45 normal saline containing 40 meq KCL/liter and 8 gm/l magnesium sulfate is begun at 100 cc/hr. He is given an additional 10 mg. diazepam slow IV push, and does not appear sedated immediately after the dose. The same diazepam dose is repeated in two hours, and the patient still shows no sedation, though he appears calmer. An EKG obtained 24 hours after this event shows Q waves in leads II, III, and aVF. Repeat laboratory examination 24 hours after the seizure shows a serum potassium of 3.2 meq/l, magnesium of 0.8 meq/l, and a serum bicarbonate of 19. On exam, he has very soft heart sounds. His blood pressure is found to be 100/50 with a regular rate of 62.
The patient did not respond to two additional doses of diazepam. This establishes that the patient is tolerant, likely due to alcoholism. The seizure episode, along with the previous Type A and emerging Type B symptoms is also supporting evidence for a diagnosis of AWS.
The physician in this case was reticent to administer larger doses of diazepam, being worried about oversedation. Rather than relying on the patient’s response to the sedative hypnotic, which would have been diagnostically revealing, as well as providing critical therapy, the clinician was focusing on a possible side-effect of the drug.
He continues to appear anxious, and has not slept. Nursing staff reports episodes of confusion, where he appears unaware of the time of day, and at times asks inappropriate questions. He appears unaware that he in a coronary care unit, and believes that he is at home. He attempts to leave his bed and accidentally discontinues his IV numerous times, which is restarted. The Cardiology service reports that he has had an inferior wall myocardial infarction, and is concerned about his low blood pressure, which may be due to a right ventricular infarction. He has a Swann-Gantz catheter placed, which reveals high .lling pressures on the right, but a low wedge pressure. IV .uids are increased to 200 cc/hr and urine output is monitored. He becomes more restless over the next 24 hours, and also complains of additional chest pain, and is nauseous. The Cardiology service suggests an emergent cardiac catheterization, but is concerned about the change in mental status and possible severe alcohol withdrawal. They will proceed with a cardiac catheterization as soon as the patient is stabilized. A formal consultation with the Substance abuse Service is obtained On exam, the patient is confused, agitated, and would like to leave the hospital. His blood pressure is now 121/90 with a heart rate of 68. He is tremulous, diaphoretic, and complains of nausea.
The patient has both CNS excitation (Type A symptoms) as well as hyper adrenergic symptoms (Type B AWS) and alcohol withdrawal delirium (Type C symptoms). The context of severe alcohol withdrawal symptoms in a patient with coronary artery disease represents a severe medical emergency.
Type A symptoms could be due to a stress-related response due to cardiac malfunction. Type B symptoms may be due to low cardiac output resulting in increased serum catecholamines. Type C symptoms may be due to hypoperfusion of brain, hypoxia, electrolyte disturbances and diazepam. However, given the information of this case, it is likely that the patient’s symptoms represent a combination of AWS as well as cardiac status and previous therapy. The point here is that it does not matter what the etiology of the symptoms is, they should have been treated much earlier.
The Substance Abuse Service makes the following recommendations regarding treatment, after consultation with the Cardiology Service. The oral beta-blocker, atenolol, is stopped. No conduction defects are found on EKG, and the patient is given 1 mg. IV propranolol. An EKG is repeated, and since there are no conduction defects, the dose is repeated. An additional 5 doses of propranolol are given over the next 60 minutes. At that point, the patient is no longer tremulous, diaphoretic, and the blood pressure is 110/76 with a rate of 56. Swann-Gantz parameters show normal .lling pressures, and it is advised to continue IV propranolol as required every 4-6 hours to avoid any evidence of hyperadrenergic symptoms. It is also advised that an EKG is obtained prior to each dose of propranolol.
The patient has evidence of increased levels of circulating catecholamines, as manifested by severe hyperadrenergic symptoms. Whether or not due to AWS, it is critical that the work load on the heart and the hypermetabolic state are addressed. The advantage of IV propranolol is immediate control of hyperadrenergic symptoms, and a relatively short duration of action so that the dose may be titrated more effectively to match therapeutic. While the blood pressure is not severely elevated, the heart rate and other symptoms such as diaphoresis suggest that catecholamine levels are high. This is not the time to have to worry about the slow onset of an oral dose of atenolol, nor of the possibility that the dose is incompletely absorbed. Immediate control of symptoms is required to save as much myocardium is possible.
Benzodiazepines are stopped, and the patient is treated with 200 mg. carbamazepine every 6 hours orally. EKG does not show any QT interval prolongation, and haloperidol 0.5 - 1 mg. is given slow IV push every 6 hours as needed to control agitation. The dose is increased to 2 mg. IV every 4 hours prn for agitation after the patient fails to respond to smaller doses. The magnesium sulfate in the IV is increased to 8 gms/l along with 40 mew KCl/liter and run at 150 cc/hour. Repeat laboratory examination 12 hours later shows a potassium of 4.2 meq/l and Mg of 1.2 meq/l. The parenteral magnesium is continued at the same dose, and the KCl concentration in the IV is reduced to 20 meq/l
The patient is exhibiting Type A, B and C symptoms at this point, also called “delirium tremens.” Benzodiazepines therapy is associated with cognitive disruption and disinhibited behavior, therefore the drug was stopped. This case illustrates that benzodiazepines do not prevent alcohol withdrawal delirium.
Type B symptoms have been addressed with propranolol, a beta-blocker. These are the symptoms that might result in mortality in this case. However, the patient also has Type A symptoms, which need to be addressed. In addition, the patient needs an anticonvulsant, as he has already had an alcohol withdrawal seizure. Therefore, carbamazpeine was chosen.
Psychomotor agitation associated with confusion may respond to very large doses of benzodiazepines, once a sedative threshold is reached. However, this is at the cost of side-effects such as cognitive disruption, disinhibition, and even respiratory depression and impaired gag re.ex. Neuroleptics, while they have their own sideeffect profile, more directly address the Type C symptoms that the patient is experiencing.
After 24 hours, the patient is stable. He is not agitated, and has required 10 mg. IV propranolol for control of hyperadrenergic symptoms. He has also required 8 mg. IV haloperidol. He continues to take carbamazepine 200 mg. orally every 6 hours. A cardiac catheterization is performed and the patient has balloon angioplasty. He returns to the coronary care unit. Over the next 48 hours, he requires only 2 mg. haloperidol for control of agitation, in the evening. Propranolol is decreased to 1 mg. IV every 6 hours, and carbamazepine is continued at a dose of 100 mg. orally every 6 hours. Over the next 24 hours, he does not require any additional propranolol, and haloperidol is also discontinued. He is mildly confused, but responds well to staff input. He is discharged to the step-down unit on 100 mg. carbamazepine every 6 hours. Carbamazpeine is continued for an additional 24 hours, and then stopped. He is visited by a substance abuse counselor, who reports that the patient is amenable to outpatient counseling for alcoholism-related issues. He is also willing to join AA and help is given in obtaining a sponsor. The family is found to be very supportive, and after an additional 48 hours, is discharged uneventfully.
The clinicians in this case consistently failed to properly control symptoms. The patient’s Type A symptoms (anxiety, insomnia, and gastric distress) went unmedicated in the critical early hours of treatment. Even if these symptoms were nothing more than the result of the patient’s concern for his cardiac symptoms, controlling them would have helped reduce circulating catecholamines, which in turn would have reduced stress on the heart. In addition, the clinician’s ignored the patient’s rising blood pressure and heart rate in the first 24 hours of treatment, which was ominous given that the symptoms emerged even as the patient was receiving a beta-blocker.
In this case, the increased the risk of adverse cardiac events due to severe Type B symptoms of AWS was not appreciated. What is more important however, is that the heart rate and blood pressure should have been brought under control no matter what their etiology.
This patient was admitted for treatment of coronary artery disease and developed severe alcohol withdrawal symptoms. Although an alcohol history was obtained on admission, as well as a blood alcohol level, which is often not the case, the seriousness of alcohol withdrawal symptoms was not initially recognized.
He had been treated with a beta-blocker, atenolol, which tends to decrease the effects of increased catecholamines which can occur in the setting of alcohol withdrawal. The staff may have been looking for more classic hyperadrenergic symptoms, which were in fact partially treated by the beta-blocker. Instead, the patient exhibited increasing anxiety.
The severity of alcohol withdrawal was not appreciated until he has an alcohol withdrawal seizure. Contributing factors may have included a low serum magnesium, as well as a low serum potassium. He would have also been at a very high risk for a cardiac arrhythmia at this point. He had an inferior wall myocardial infarction at the time of the seizure, which shows in the subsequent EKG.
A clue to his high alcohol tolerance would have been his relative lack of response to what would have been an otherwise sedating dose of diazepam. He then became more agitated, as he develops alcohol withdrawal delirium. Cognitive disruption due to diazepam may have also been responsible for his change in mental status. The development of additional chest pain after a myocardial infarction suggested that the patient had more myocardial muscle at risk. However, at this point, he was also very agitated, complicating treatment.
The treatment recommendations of the substance abuse service were based on the pathophysiology of alcohol withdrawal. This patient had high circulating levels of catecholamines, partially but not fully antagonized by treatment with the oral beta-blocker atenolol. In this case, immediate attention to decreasing the effects of circulating catecholamines was of utmost importance in preventing further cardiac compromise. The oral beta-blocker was stopped, since better control of the beta-blocking dose was required. Therefore, after consultation with Cardiology, an IV beta-blocker was started. The therapeutic objective was to therefore stop the peripheral effects of circulating catecholamines using propranolol.
As this was being accomplished, it was also important to address the behavioral consequences of agitation to decrease exercise-related myocardial oxygen consumption. Since benzodiazepines are associated with confusion, and since there is no literature to support the idea that they are effective agents in treating alcohol withdrawal delirium, the agents are stopped. After checking that the QT interval is not prolonged, which can be further prolonged by certain neuroleptics, and in these cases can result in arrythmias, the patient’s agitation was treated with haloperidol in small doses. The therapeutic objective for use of haloperidol was to decrease the patient’s psychomotor agitation. Many times, as in this case, the agitation responds to relatively low doses of haloperidol.
The patient’s magnesium level is addressed aggressively, since low serum magnesium is associated with cardiac arrhythmias, as well as alcohol withdrawal seizures. Treatment with magnesium has also been shown to decrease cardiac arrhythmias in the setting of myocardial infarction.
Patients can still continue to express evidence of CNS excitation from Type A withdrawal even when Type C symptoms emerge. To avoid use of benzodiazepines in the setting of alcohol withdrawal delirium, the patient was treated with carbamazepine. This agent has little effect on cognitive function, and seems to decrease anxiety associated with Type A alcohol withdrawal symptoms. As an anticonvulsant, it may also be of some use in this setting. After the cardiac catheterization, both the haloperidol and the propranolol are tapered while the patient is observed for re-emergent alcohol withdrawal symptoms. Carbamazepine is also tapered The patient is now ready for long-term alcohol treatment. His supportive family, and his willingness to accept a diagnosis of alcoholism are excellent prognostic signs, and he is discharged to outpatient follow-up treatment.
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