Anatol J Clin Investig 2008:2(1):45-46.
CENTRAL ANTICHOLINERGIC SYNDROME ASSOCIATED WITH ATROPINE: CASE REPORT F.Ozlem Orhan1, Nimet ŞENOĞLU2, Erman BAĞCIOĞLU1, Hilmi DEMİRKAN 1 1 2
Kahramanmaraş Sütçüimam Üniversitesi Tıp Fakültesi, Psikiyatri Ad, Kahramanmaraş Kahramanmaraş Sütçüimam Üniversitesi Tıp Fakültesi, Anestezi Ve Reanimasyon Ad, Kahramanmaraş
Abstract We report a case of anticholinergic syndrome after Atropine treatment for organophosphate poisoning in a young patient. Manifestations of anticholinergic syndrome may range from excitatory symptoms, including delirium and agitation, to central nervous system depression, stupor and coma. These reactions are related to the considerable interpersonal variation in susceptibility to Atropine, to the extent that toxic effects may occur at the usual therapeutic doses. Clinicians should watch for symtoms in patients with altered mental status following therapy with Atropine. (Anatol J Clin Investig 2008:2(1);45-46).
Introduction Organophosphate poisoning is frequently used as a method for suicide in Turkey (1-3). Atropine is used to counteract the symptoms of organophosphate poisoning. Reduction in cholinergic activity in the central nervous system (CNS) because of atropine can result in anticholinergic syndrome. Central manifestations of the syndrome range from excitatory symptoms, including delirium and agitation, to central nervous system depression, stupor and coma. Peripheral signs of anticholinergic syndrome can include decreased secretions, dry, warm and flushed skin, tachycardia, cardiac dysrhythmias, mydriasis, loss of ocular accommodation, photophobia, decreased peristalsis and urinary retention (4-6). These reactions are related to the considerable interpersonal variation in susceptibility to Atropine (idiosyncrasy), to the extent that toxic effects may occur at the usual therapeutic doses (7). Central anticholinergic syndrome (CAS) cases have been reported in the literature but to our knowledge, there was only a few report about the syndrome secondary to Atropine treatment of organophosphate poisoning. We report a case of CAS in a young patient to draw attention to the possibility of developing a serious side effect while trying to correct an otherwise potentially fatal problem (organophosphate poisining). Case report An 18-year-old male was admitted to the emergency department after ingesting 100 ml of an organophosphate insecticide in a suicide attempt. Although the patient appeared dull, gloomy and inactive, he was conscious and well oriented at admission. There were no clinical symptoms of organophospate ingestion. His blood pressure was 110/70 mmHg, pulse rate was 110/min and other vital signs were normal. Laboratory findings were as follows: WBC
12000/uL; Hb 16 g/dL; Hct 49%; Plt 248.000 L; neither liver and kidney function tests nor serum electrolytes showed any abnormalities. Based on his medical history the psychiatry department in the emergency unit diagnosed him as having major depression. The rest of his medical history was unremarkable. He underwent general antioverdose treatment including gastric lavage, activated charcoal and cathartics. During the follow up, his secretions increased and pupillary examination showed bilateral miosis. In addition to gastric lavage and standard therapy, intravenous Atropine and pralidoxime (PAM) were administered as his plasma cholinesterase level was 2,7 U/mL, confirming the clinical diagnosis of organophosphate poisoning. In all, 1600 mg PAM and 32 mg Atropine were administered over two days via intravenous infusion during which time the patient was noted to be agitated, confused, swearing intermittently, mumbling incoherently and trying to get out of his restraints. He also pulled out his nasogastric tube and intravenous lines. He presented hyperprexia (38ºC) and tachycardia (120/min) but his laboratory tests were unremarkable. Psychiatric evaluation was requested a second time. He was also disoriented, and had problems with delayed recall, difficulty sustaining attention and delusions of persecution. Although he was able to follow simple commands, he was unable to cooperate in a formal mental status examination. According to these signs and symptoms he was diagnosed with delirium using the diagnostic and statistical manual, 4th ed (DSM-IV) criteria for delirium. It was concluded that the delirium was a result of Atropine treatment. For this reason all medications including Atropine and PAM were stopped and Olanzapine 10 mg/day was given. Delirium regressed and his neurological examination was normal after 24 h. He was discharged from the hospital on the 7th day with an elevated plasma cholinesterase of 7 U/mL,
F.Ozlem Orhan Kahramanmaraş Sütçüimam Üniversitesi Tıp Fakültesi, Psikiyatri Ad, Kahramanmaraş e-mail:
[email protected]
AJCI, 2008;2(1):45-46.
ORHAN et al.
and his psychiatric symptoms resolved without any neurological deficit in 15 days.
Peripheral anticholinergic signs and symptoms such as decreased secretions, dry, warm and flushed skin, tachycardia, mydriasis and hyperprexia were also noted in this case.
Discussion CAS is sometimes overlooked, although anticholinergic drugs are frequently prescribed. Unfortunately, there are no definitive criteria defining the diagnosis. Because of the variability of symptoms and the lack of a specific test to definitively diagnose anticholinergic syndrome, the diagnosis of the syndrome involves excluding other possible causes of the altered mental status (8). There currently are no laboratory tests that can confirm the presence or absence of CAS. The differential diagnosis for CAS includes metabolic disorders, respiratory disorders, neurological disorders, psychiatric disorders, and iatrogenic causes (5,8).
In the past, CAS occurred frequently as a result of the routine administration of the preoperative medications scopolamine and/or atropin. But the available literature on systemic adverse reactions to atropine is limited, with most reports relating to the use of eye drops containing atropine. Erol et al. reported a case of CAS secondary to atropine treatment of organophosphate poisoning in an elderly patient, and pointed out to consider the syndrome in patients with altered mental status following therapy with atropine (13). A high index of suspicion and prompt recognition is important. Delays in diagnosis and treatment may lead to costly specialist consultations, costs associated with intensive nursing care, unnecessary tests, and potential patient morbidity (14,15). CAS has different characteristics compared with other forms of delirium. Clinicians should take these characteristics into account and should be especially aware of patients with altered mental status following therapy with Atropine in deciding diagnosis and treatment.
The syndrome may manifest as a hyperactive state or a depressed central nervous system. Hyperactive manifestations, often associated with Atropine, may include: agitation, hallucinations, delirium, excitement, convulsions, ataxia and myoclonus. The depressed form of CAS, often associated with scopolamine, may present with signs and symptoms such as coma, somnolence, stupor, and respiratory depression (5, 8-12). In our case, hyperactive manifestations associated with Atropine such as agitation, delirium, and hallucinations were prominent.
References 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15.
Kara IH, Guloglu C, Karabulut A, Orak M. Sociodemographic, clinical, and laboratory features of cases of organic phosphorus intoxication who attended the Emergency Department in the Southeast Anatolian Region of Turkey. Environ Res 2002; 88: 82-83. Aygun D, Doganay Z, Altintop L, Guven H, Onar M, Deniz T et al. Serum acetylcholinesterase and prognosis of acute organophosphate poisoning. J Toxicol Clin Toxicol 2002; 40: 903-910. Sahin HA, Sahin I, Arabaci F. Sociodemographic factors in organophosphate poisonings: a prospective study. Hum Exp Toxicol 2003; 22: 349-353. Schneck HJ, Rupreht J. Central anticholinergic syndrome (CAS) in anesthesia and intensive care. Acta Anaesthesiol Belg 1989; 40: 219–228. Rupreht J. The central muscarinic transmission during anaesthesia and recovery—the central anticholinergic syndrome. Anaesthesiol Reanim 1991; 16: 250–258. Barkin RL, Stein ZLG. Drugs with anticholinergic side effects. South Med 1989; 82: 1547–1549. Economacos G, Kanakis J. A case of hypersensitivity to atropine. Anesth Analg Reanim 1981; 38: 748. Brown DV, Heller F, Barkin R. Anticholinergic syndrome after anesthesia: a case report and review. Am J Ther 2004; 11: 144-53. Cook B, Spence AA. Post-operative central anticholinergic syndrome. Eur J Anaesthesiol 1997; 14: 1-2. Torline RL. Extreme hyperpyrexia associated with central anticholinergic syndrome. Anesthesiology 1992; 76: 470-471. Elias MA, Abouleish E. Scopolamine patch can be confusing to the patient and anesthesiologist: A case report. Anesthesiology 1997; 86: 743-744. Ezri T, Szmuk P, Konichezky S, Abramson D, Geva D. Central anticholinergic syndrome complicating management of a difficult airway. Can J Anesth 1996; 43: 1079. Erol DD, Gecici O. Central anticholinergic syndrome secondary to atropine treatment of organophosphate poisoning. Psychogeriatrics 2006; 6: 145–146. Katsanoulas K, Papaioannou A, Faidakis O, et al. Undiagnosed central anticholinergic syndrome may lead to dangerous complications. Eur J Anaesthesiol 1999; 16: 803-809. Ries CR. Physostigmine in 1999: Tolerability, indications and availability. Can J Anaesth 1999; 46: 707.
44
