title: A comparison of physostigmine and benzodiazepines for the treatment of anticholinergic poisoning.
abstract: To compare the efficacy and safety of physostigmine with benzodiazepines for the treatment of agitation and delirium associated with anticholinergic poisoning.
  
  
  
  We conducted a retrospective study of 52 consecutive patients referred to a university hospital toxicology consultation service who were treated with physostigmine, benzo-diazepines, or both for anticholinergic agitation and delirium. Patients treated with physostigmine were compared with those treated with benzodiazepines with respect to demographics, severity of poisoning, response to treatment, side effects of treatment, and complications.
  
  
  
  Physostigmine controlled agitation and reversed delirium in 96% and 87% of patients, respectively. Benzodiazepines controlled agitation in 24% of patients but were ineffective in reversing delirium. Initial treatment with physostigmine (n=30) resulted in a significant decrease in the incidence of agitation (P <.001) and level of central nervous system stimulation (P <.001), whereas initial treatment with benzodiazepines (n=22) did not (P =.03 and P =.05, respectively). Patients treated initially with physostigmine had a significantly lower incidence of complications (7% versus 46%; P <. 002) and a shorter time to recovery (median, 12 versus 24 hours; P =. 004) than those treated initially with benzodiazepines. There were no significant differences between these groups in the incidence of side effects (7% versus 14%; P =0.6) and length of stay (median, 32 versus 39 hours; P =.15).
  
  
  
  Results suggest that physostigmine is more effective and safer than benzodiazepines for the treatment of anticholinergic agitation and delirium. A prospective controlled study is necessary to confirm such findings.
authors.affiliation: Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. mburns@caregroup.harvard.edu
authors.forename: M J
authors.initials: MJ
authors.lastname: Burns
authors.forename: C H
authors.initials: CH
authors.lastname: Linden
authors.forename: A
authors.initials: A
authors.lastname: Graudins
authors.forename: R M
authors.initials: RM
authors.lastname: Brown
authors.forename: K E
authors.initials: KE
authors.lastname: Fletcher
mesh_terms: D000284:Administration, Oral; D000328:Adult; D017109:Akathisia, Drug-Induced / Q000188:drug therapy; D001569:Benzodiazepines / Q000008:administration & dosage / Q000627:therapeutic use*; D002490:Central Nervous System / Q000187:drug effects; D018680:Cholinergic Antagonists / Q000097:blood / Q000506:poisoning*; D002800:Cholinesterase Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D003693:Delirium / Q000139:chemically induced / Q000188:drug therapy; D006801:Humans; D007273:Injections, Intramuscular; D007275:Injections, Intravenous; D010830:Physostigmine / Q000008:administration & dosage / Q000627:therapeutic use*; D011041:Poisoning / Q000188:drug therapy; D012189:Retrospective Studies
chemical_list: D018680:Cholinergic Antagonists; D002800:Cholinesterase Inhibitors; D001569:Benzodiazepines; D010830:Physostigmine