1/63. cocaine-associated rhabdomyolysis and excited delirium: different stages of the same syndrome.Previous case reports indicate that cocaine-associated rhabdomyolysis and excited delirium share many similar features, suggesting that they may be different stages of the same syndrome. We tested this hypothesis by comparing data from 150 cases of cocaine-associated rhabdomyolysis reported in the medical literature with data from an autopsy registry for 58 victims of fatal excited delirium and 125 victims of fatal acute cocaine toxicity. patients with rhabdomyolysis are similar to victims of fatal excited delirium with regard to age; gender; race; route of cocaine administration; the experiencing of excitement, delirium, and hyperthermia; and the absence of seizures. Compared with victims of fatal acute cocaine toxicity, patients with rhabdomyolysis are different with regard to each of these variables. Compared with victims of fatal acute cocaine toxicity, both victims of rhabdomyolysis and fatal excited delirium are more likely to be black, male, and younger; to have administered cocaine by smoking or injection; and to have experienced excitement, delirium, and hyperthermia; they are also less likely to have had seizures. Because cocaine-associated rhabdomyolysis and excited delirium have similar clinical features and risk factors, occur in similar populations of drug users, and can be explained by the same pathophysiologic processes, we conclude that they are different stages of the same syndrome. It appears that this syndrome is caused by changes in dopamine processing induced by chronic and intense use of cocaine rather than by the acute toxic effects of the drug.- - - - - - - - - - ranking = 1keywords = drug (Clic here for more details about this article) |
2/63. Postoperative delirium indicating an adverse drug interaction involving the selective serotonin reuptake inhibitor, paroxetine?We report a postoperative delirium expressed by a 49-year-old female patient during recovery from anaesthesia. Prominent features of the delirium, which lasted for nearly 2 days, included agitation, confusion, uncontrolled limb movements, abnormal ocular function, hypertension, pyrexia, brisk reflexes, ankle clonus and raised creatine kinase. The delirium did not respond to naloxone, diazepam or flumazenil. The patient had not been prescribed neuroleptics but, before surgery, she had been taking the selective serotonin reuptake inhibitor, paroxetine, to relieve her depression. During surgery, she was given morphine, which increases release of the neurotransmitter, serotonin, and ondansetron, which blunts neuronal release of dopamine. Although there is no clear explanation for the delirium, it had many features in common with problems associated with paroxetine withdrawal, the serotonin syndrome and the malignant neuroleptic syndrome. We offer several alternative explanations for this event, all of which rest on disruption of serotonergic and/or dopaminergic transmission and which could also involve inhibition by paroxetine of the P450 enzyme, CYP2D6, which metabolizes ondansetron.- - - - - - - - - - ranking = 2keywords = drug (Clic here for more details about this article) |
3/63. torsades de pointes secondary to intravenous haloperidol after coronary bypass grafting surgery.PURPOSE: Postoperative delirium occurs in about 2% of patients undergoing major cardiac surgery including coronary artery bypass grafting surgery (CABG). haloperidol (Sabex, Boucherville, canada) is a drug commonly used in the intensive care unit for the treatment of delirium and is usually considered safe even at high doses and is rarely implicated in the development of malignant ventricular arrhythmias such as torsades de pointes. The purpose of this study is to report such a complication of use of haloperidol after myocardial revascularization. CLINICAL FEATURES: The patient reported underwent uneventful triple bypass surgery. Administration of large intravenous doses of haloperidol was necessary for control of psychomotor agitation due to delirium. torsades de pointes occurred in the absence of QT prolongation on the third postoperative day following use of the drug with no other obvious etiological factor. CONCLUSION: awareness of this rare complication is key to judicious use of this drug in the post CABG patient in whom such an arrhythmia may have very deleterious consequences because of the underlying cardiac condition.- - - - - - - - - - ranking = 1.5keywords = drug (Clic here for more details about this article) |
4/63. Acute delirium induced by intravenous trimethoprim-sulfamethoxazole therapy in a patient with the acquired immunodeficiency syndrome.The development of a rash in response to trimethoprim-sulfamethoxazole (TMP-SMX) administration is a frequent adverse reaction in people with the acquired immunodeficiency syndrome (AIDS). In contrast, there are no published reports in the English language literature describing TMP-SMX induced delirium in an AIDS patient. This report describes the development of frank delirium in a person with AIDS receiving TMP-SMX. The episode resolved completely within 72 h of withdrawal of the drug.- - - - - - - - - - ranking = 0.5keywords = drug (Clic here for more details about this article) |
5/63. The interaction of delirium and seizures.The induction of a delirium by medical illness, somatic treatments, or experimental drugs occasionally relieves psychotic, excited, and manic states. An induced delirium is a feature of modern electroconvulsive therapy (ECT), and was a feature of insulin coma therapy and psychosurgery. Case material explores the relationship between psychosis, mania, seizures, and electroencephalogram. From our understanding of the mechanism of ECT in relieving intractable status epilepticus, we suggest a hypothesis for the beneficial interaction between delirium and ECT.- - - - - - - - - - ranking = 0.5keywords = drug (Clic here for more details about this article) |
6/63. Occurrence of mirtazapine-induced delirium in organic brain disorder.Mirtazapine is the first of a new class of antidepressants, the noradrenergic and specific serotonergic antidepressants. Its antidepressant effect appears to be related to its dual enhancement of both noradrenergic neurotransmission and serotonin 5-HT1 receptor-mediated serotonergic neurotransmission. Mirtazapine has demonstrated superior tolerability to the tricyclic antidepressants, primarily on account of its relative absence of anticholinergic, adrenergic and serotonin-related adverse effects. We observed mirtazapine-induced delirium in one organically depressed and two major depressed patients with subclinical brain disease. The appearance of hallucinations, psychomotoric agitation and cognitive changes after initiation of mirtazapine, and their prompt improvement after drug discontinuation, led to the impression that these were drug-induced phenomena. One possible hypothesis for the observed deliria is a central increase of norepinephrine after acute administration of mirtazapine. Subclinical brain disease might have favoured the occurrence of delirium in the three cases.- - - - - - - - - - ranking = 1keywords = drug (Clic here for more details about this article) |
7/63. Gamma-hydroxybutyrate withdrawal syndrome.STUDY OBJECTIVE: Gamma-hydroxybutyrate (GHB) withdrawal syndrome is increasingly encountered in emergency departments among patients presenting for health care after discontinuing frequent GHB use. This report describes the characteristics, course, and symptoms of this syndrome. methods: A retrospective review of poison center records identified 7 consecutive cases in which patients reporting excessive GHB use were admitted for symptoms consistent with a sedative withdrawal syndrome. One additional case identified by a medical examiner was brought to our attention. These medical records were reviewed extracting demographic information, reason for presentation and use, concurrent drug use, toxicology screenings, and the onset and duration of clinical signs and symptoms. RESULTS: Eight patients had a prolonged withdrawal course after discontinuing chronic use of GHB. All patients in this series were psychotic and severely agitated, requiring physical restraint and sedation. Cardiovascular effects included mild tachycardia and hypertension. Neurologic effects of prolonged delirium with auditory and visual hallucinations became episodic as the syndrome waned. Diaphoresis, nausea, and vomiting occurred less frequently. The onset of withdrawal symptoms in these patients was rapid (1 to 6 hours after the last dose) and symptoms were prolonged (5 to 15 days). One death occurred on hospital day 13 as withdrawal symptoms were resolving. CONCLUSION: In our patients, severe GHB dependence followed frequent ingestion every 1 to 3 hours around-the-clock. The withdrawal syndrome was accompanied initially by symptoms of anxiety, insomnia, and tremor that developed soon after GHB discontinuation. These initial symptoms may progress to severe delirium with autonomic instability.- - - - - - - - - - ranking = 0.5keywords = drug (Clic here for more details about this article) |
8/63. death of a psychiatric patient during physical restraint. Excited delirium--a case report.We report the case of a young man with a diagnosis of paranoid schizophrenia and multiple drug abuse who died in hospital following a period of prolonged physical restraint. The literature is reviewed, possible factors contributing to death discussed and measures which may reduce the incidence of such deaths in the future highlighted.- - - - - - - - - - ranking = 0.5keywords = drug (Clic here for more details about this article) |
9/63. Postoperative delirium.delirium is a common postoperative complication that is associated with substantial patient morbidity and mortality. Because of the variability in its presentation, delirium has the potential to be overlooked or misdiagnosed. There are few well-designed prospective studies looking at the incidence of delirium; however, retrospective data reveal it to be highly variable. The cause is multifactorial, with the largest predisposing factors being patient age, cerebral disease, and poor preoperative medical status. Common precipitants of delirium postoperatively include infection, hypoxia, myocardial ischemia, metabolic derangements, and anticholinergic drugs. The pathogenesis of delirium is incompletely understood; cholinergic pathways appear to play a crucial role. physicians evaluating postoperative patients for mental status changes need to identify delirium accurately (the diagnostic criteria for which are clearly set out in the DSM-IV). Further investigations center on searching for organic precipitants, which can be treated effectively. The diagnostic workup is not algorithmic and must be tailored to the specifics of each individual case. If there is no readily identifiable cause, treatment should focus on the disorder itself. Supportive care should consist of a multidisciplinary approach aimed at preventing functional decline. Pharmacologic therapy, usually with haloperidol, may be indicated if patients remain agitated. Investigations have supported the premise that delirium is a potentially preventable condition. This prevention can be accomplished by maximizing the patient's medical status and conscientiously avoiding the conditions that are known to precipitate delirium.- - - - - - - - - - ranking = 0.5keywords = drug (Clic here for more details about this article) |
10/63. delirium following a switch from cimetidine to famotidine.OBJECTIVE: To describe a patient who developed delirium when switched from cimetidine to famotidine. CASE SUMMARY: An 84-year-old Taiwanese woman was hospitalized for tarry stools. Her past medical history revealed only a decrease in renal function. She tolerated both oral and intravenous cimetidine therapy with a daily dose of 400-900 mg intermittently for 20 years. On hospital days 1-3, cimetidine 300 mg was injected intravenously every eight hours without difficulty. Considering the possible existence of a cimetidine-resistant bleeding ulcer, famotidine 20 mg was given twice daily orally on hospital days 4-7 and then injected intravenously. Six days after being switched from cimetidine to famotidine, the woman's mental status deteriorated. A series of clinical tests revealed no apparent causative factors. famotidine was then suspected as a probable cause of her delirium. Discontinuation of the drug resulted in rapid resolution of the patient's delirious status. DICUSSION: famotidine crosses the blood-brain barrier less easily than cimetidine and was taken for a much shorter period in this patient. Thus, we propose that the occurrence of delirium in this patient was associated with famotidine, but not cimetidine, and was idiosyncratic rather than dose related. Furthermore, this case involved an elderly patient with compromised renal function who developed delirium in response to intravenous, but not oral, administration of famotidine. These factors seem to increase the risk for, famotidine-induced delirium. CONCLUSIONS: Clinicians should be aware of the possible occurrence of delirium following a switch from one histamine2-receptor antagonist to another. In rare instances, patients switched to famotidine from cimetidine may experience delirium, particularly elderly patients with poor renal function who receive intravenous famotidine.- - - - - - - - - - ranking = 0.5keywords = drug (Clic here for more details about this article) |
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