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Haloperidol-Induced Ileus

TO THE EDITOR: Abdominal symptoms associated with antipsychotic treatment have been reported since early experiences with drug treatment for psychosis.¹ However, while nonsurgical ileus associated with haloperidol treatment was described more than 20 years ago,² it is nowadays not specified as an occasional complication of haloperidol treatment of delirium in surgical intensive care units.³ The following clinical vignette of a surgical cardiac patient is presented as a reminder of this side effect and to check total dosage.

Case Report
Mr. A, a 74-year-old patient, underwent a coronary by-pass grafting. Before surgery there was slight renal insufficiency (creatinin level before surgery was 158) and hypertension. He was quickly extubated and needed 3 days to be weaned from dobutamine. On day 1 after surgery he was calm but disoriented and hyperalert to surrounding stimuli. On day 2 he did not recognize relatives. Still confused and incoherent on day 3, he needed hemofiltration for the next 2 days, since he was 8 kg over his admission weight and had a serum creatinin level well over 280; his ejection fraction was measured at 30%. Since he complained of pain, he was maintained on a regimen of narcotics for the first five postoperative days (hydromorphone 7 mg, 6 mg, 5 mg, 4 mg, 2 mg), longer than usually needed for such patients, who are often switched to acetaminophen 48 hours after surgery. For the first 7 days after surgery he remained at first calm but confused, talked to himself as if with people, and was not sure if he had undergone an operation. On days 5 to 7 he became agitated for periods with unreliable cooperation. He would ask for his wallet or car and remained disoriented. In the first 4 days after surgery, since agitation was minimal, he was given light doses of haloperidol (4, 9, 8, and 5 mg/day, respectively) because he was still receiving narcotic analgesia. During that time he did not eat because he felt nauseous. After two sessions of hemofiltration, serum creatinin fell to around 180. Five days after surgery he was tube-fed until he pulled out the nasogastric tube on day 8. From day 5 on he became more restless, with bouts of agitation and poor collaboration to care and mobilization. Haloperidol administration had to be adjusted to a higher dosage from days 5 to 7 (15, 17, and 18 mg, respectively). On day 8 after surgery a cardiology consultant was called in for atrial fibrillation, and a regimen of amiodarone was started, with subsequent cessation of haloperidol administration (after an additional 11 mg) for safeguarding the ECG QT interval. The same day a general surgeon was called to address the patient’s abdominal discomfort and distention. Mr. A was without pain, colic, vomiting, or nausea; no surgical condition was noticed. Films of the abdomen showed distention on the ileal portion of the bowels and subocclusion. A nasogastric tube was inserted, and 1700 cl were collected. Adynamic ileus was diagnosed, although some peristaltic activity was noted. Observation and conservative treatment were recommended. On day 9 and 10, Mr. A recovered gradually both from his abdominal condition and from his delirium. Sensorium became clear, he was calm, witty, and spoke with relatives. He resumed eating and expected to return home. With diuretics the serum creatinin level returned to 170 during that time. During the time span of 8 days the patient received a total of 87 mg of intravenous haloperidol in a context of renal insufficiency without showing any sign of extrapyramidal side effects. Narcotics had been stopped 5 days after surgery, and no other drug could account for such complication.

Discussion
Abdominal subocclusion was related to large amounts of haloperidol administered during the postoperative period as the main factor causing such a symptom. Quick resolution, absence of evidence of a surgical abdominal problem, and the anticholinergic activity of haloperidol were the main factors thought to be involved. Previously, colitis^4,5 or megacolon-like Ogilvie syndrome⁶ have been reported to be associated with neuroleptic treatment. Ileus associated with haloperidol treatment has been so far rarely reported.^2,7 Since the incidence of postcardiotomy delirium is high and the use of high doses of haloperidol in such cases frequent, it is useful to report such cases as a reminder of such complications. It remains to be ascertained whether such occurrence is related to total dosage or to length of administration. Since intravenous administration of haloperidol produces little neurologic side effects, and because such mode of drug delivery is geared more to ECG monitoring, it is easy to overlook such a complication for any patient who stays for an extended period in the intensive care unit and is given haloperidol for sedation or treatment of protracted delirium. It is known that renal failure might account for such a condition,⁸ but here renal insufficiency was transient, secondary to low flow, and corrected promptly with two sessions of hemofiltration. Moreover, hypokalemia was not present. The hypovascularized state of the intestine from low flow would be an alternative hypothesis to account for such a problem; however abdominal tomodensitometry failed to show any vascular deficit pertaining to the intestine. The anticholinergic activity of haloperidol could account for such a complication. Although the plasmatic half-life of the drug is reported not to exceed 24 hours, excretion might be slower and a cumulative effect might be present. Here the patient was administered gradually higher doses for a total of 50 mg over days 5, 6, and 7. Total cumulative amount of haloperidol should be checked for any protracted course of delirium, and possibly reevaluated after 60 mg. The title of the report stresses the probable causality of the association while renal insufficiency was accounted for as a predisposing factor. Another predisposing factor I have noted in other patients was the subcutaneous administration of large amounts of haloperidol in obese patients.

REFERENCES

1. Warnes H, Lehmann HE, Ban TA: Adynamic ileus during psychoactive medication: a report of three fatal cases and five severe cases. Can Med Assoc J 1967; 96:1112–1113[Medline]
2. Maltbie AA, Varia IG, Thomas NU: Ileus complicating haloperidol therapy. Psychosomatics 1981, 22:158–159
3. Stern TA, Fricchione GL, Cassem NH, Jellinek M, Rosenbaum JF: Massachusetts General Hospital Handbook of General Hospital Psychiatry, 5th ed. St Louis, Mosby, 2004
4. Sheikh RA, Prindiville T, Yasmeen S: Haloperidol and benztropine interaction presenting as acute intestinal pseudo-obstruction. Am J Gastroenterol 2001; 96: 934–935
5. Gollock JM, Thomson JP: Ischaemic colitis associated with psychoactive drugs. Postgrad Med J 1984; 60:564–565[Abstract]
6. Nanni G, Garbini A, Luchetti P: Ogilvie’s syndrome. Dis Colon Rectum 1982; 25:157–166[Medline]
7. Gasner G, Kosza P: Paralytic ileus during haloperidol therapy. Neuropsychopharmacol Hung 2004; 6:36–38[Medline]
8. Bailey & Love’s Short Practice of Surgery. London, HK Lewis, 1968, p 950

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