A 54 year old male was admitted to the orthopedic service for elective R hip replacement as a result of degenerative changes from aseptic necrosis of the femoral head. The patient was gainfully employed as a funeral home director. By self-report, there was no other significant medical history, except for a 40 pack-year history of cigarette use. Alcohol and other substance use history was not reported on admission. Physical examination was also reported as normal. Laboratory examination showed a mild elevation of SGOT, normal SGPT. The rest of the examination was within normal limits.
The patient underwent surgery approximately 18 hours after admission. Clinical staff reported that he did not become drowsy after medication with 10 mg. diazepam (Valium). The dose was repeat x 1 with no effect. Except for insomnia, the patient reportedly had no other complaints.
Surgery was uneventful, though the anesthesiologist did report that the patient required unusually large doses of sodium pentothal during the induction phase. He was transported to the recovery suite, awaiting ET extubation. A this time, VS showed a blood pressure of 100/55, HR 96, RR16, afebrile.
He had a lot of myoclonus during emergence, and began to make grasping attempts at the ET. This was noticed by staff, who reported the behavior, and he was placed in soft restraints. His O2 sat remained within normal limits. Over the next three hours, he began to have episodes where he would struggle violently against the restraints, punctuated by periods of relative calm. During one episode, he successfully removed his ET tube.
The two clues in the rather sparse history on admission were: 1) his mildly elevated liver function test, and 2) his lack of response to two sedative doses of diazepam. The helpful anesthesia note also points to the fact that he was tolerant to a short-acting barbiturate, suggesting that this patient has sedative-hypnotic tolerance of unknown cause. Common causes would include chronic use of alcohol or other sedative-hypnotics, either alone or in combination, failure to absorb the drug from the GI tract (unlikely in this case since he was also tolerant to intravenously administered drug) and very rapid elimination of the drug from his system, also unlikely since you would expect diazepam and its metabolites to remain in his system with a half-life of approximately 24 hours.
The elevated SGOT on admission is the only clue you have that chronic excessive alcohol use may be playing a role in tolerance to sedative-hypnotics. The fact that the SGOT was abnormal and not the SGPT is further evidence that the patient may have very mild alcoholic hepatitis.
His delirium is likely due to sedative-hypnotic withdrawal, but other explanatory factors might include hypoglycemia, electrolyte imbalance, pulmonary embolus, or even an intra-operative cerebral infarction, though this is unlikely since no significant hypotension was noted during surgery.
The patient was sedated with 10 mg. IV diazepam, paralyzed and intubated, and moved to the surgical ICU. At this time, blood pressure was very labile, ranging from 110-180 systolic and 68-100 diastolic. HR was 100-140. Within minutes of arriving to the ICU, the patient began struggling against the soft restraints, and was given an additional 10 mg. of diazepam IV. The sedative effects lasted for 15-20 minutes, after which he would resume struggling. It was also noted that he was now sweating profusely, and exhibited a fine tremor when he attempted purposeful movements. He responded to any loud sensory stimulation with increased struggling attempts. It was unclear to treatment staff why this patient was having such a difficult post-operative course, given his benign initial presentation. He lived alone, and no family or friends were immediately available to develop a better pre-morbid history.
Control of psychomotor agitation is critical at this point, given his post-surgical status and possibility of severe injury if his movement is not constrained.
An argument can be made that while sedative medication is being administered, it is appropriate to restrain the patient. However, all efforts to achieve sedation and control of behavior by other means should be instituted, with the aim of terminating soft restraints as soon as possible.
Sedative-hypnotic tolerance/withdrawal (including AWS), possible emergence delirium.
Over the next 12 hours, the patient receives 120 mg. of IV diazepam, and occasionally requires paralytic agents to prevent struggle. VS show a blood pressure of 160-200/102-130, HR 130. Temp by tympanic probe is 101.5ºF. He continues to be diaphoretic, and occasionally tremulous. An friend/employee at his business is reached, who reports that the patient has been known to be an immoderate alcohol user, consuming as much as 1.5 pints of whiskey per day for a number of years, and that he has been trying to assist him in obtaining treatment.
The patient is likely to be experiencing delirium tremens, which is a combination of Type A, B and C withdrawal. Given his condition, only the Type B sub-scale can be adequately assessed. Major stressors such as surgery can precipitate substantial AWS.
The patient would greatly benefit from addition of a neuroleptic to his regimen. One could use either haloperidol or droperidol.
Type B AWS is characterized by release of catecholamines from the adrenal gland, which results in a hypermetabolic state, and usually rises in blood pressure and heart rate, along with diaphoresis and tremulousness. It is critical that this issue is addressed, since severe cardiovascular morbidity and mortality can occur. The sympatholytic agent chosen was propranolol, a beta-blocker. The therapeutic objectives are normalization of blood pressure and heart rate, and decrease in diaphoresis and tremulousness.
After some discussion, droperidol is chosen, since it is a heavily sedating agent. An EKG shows some non-specific ST-T wave changes, but a normal QT interval. Droperidol 10 mg. IV is given, with some calming effect. After 10 minutes, an additional dose of 10 mg. IV is given, with substantial calming effect which lasts for approximately 90 minutes. EKG rhythm strip after two doses of droperidol does not show any QT prolongation, and the patient is given 10 mg. diazepam alternating with 10 mg. droperidol IV every 2 hours prn to control agitation. The paralytic agent is discontinued. Soft restraints are removed at this time.
Type B symptoms are rapidly controlled with IV propranolol, 2 mg. slow IVP, after arterial blood pressure monitoring was instituted. 20 minutes after the first IV dose of propranolol, EKG shows sinus tachycardia and no PR interval prolongation. Propranolol is given in doses of 1 mg. IVP every hour as needed to maintain blood pressure < 150 systolic and 100 diastolic.
The patient’s fluid status is a major consideration, since his sensory losses of water will be increased.
The room should be brightly lit, but other sensory modalities, especially noise and tactile stimulation should be minimized if possible.
Over the next 48 hours, the dose of diazepam is gradually decreased to 2.5 mg. alternating with 2.5 mg. droperidol every two hours prn agitation. IV propranolol is also decreased to 0.5 mg. IV every 6 hours. The patient is extubated. He is easily aroused, and when awake, does not follow commands. He will occasionally talk nonsense looking around the room, and sometimes has emotional outbursts. His VS show a blood pressure of 130/96 HR100 and RR 18. He is afebrile.
Over the next 72 hours, all medication is tapered and discontinued, as the patient has begun to follow commands. He is oriented to person, but not to place or time. He has no memory of post-operative events. The clinical impression is that of resolving delirium tremens.
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