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wikitox:2.1.11.4.1_anticholinergics [2025/02/17 00:25] – kharriswikitox:2.1.11.4.1_anticholinergics [2025/02/24 21:14] (current) – kharris
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 //Angel's Trumpet (Brugmansia), Belladonna, Datura// //Angel's Trumpet (Brugmansia), Belladonna, Datura//
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 Most anticholinergic toxicity seen in clinical practive, results from ingestion of agents with multiple receptor effects (as apposed to pure anticholinergics) this may also lead to clouding of the classic toxidrome - a common example being miosis in a patient suffering from an anticholinergice delirium secondary to olanzapine or quetipaine, due to their alpha blocking effects. Most anticholinergic toxicity seen in clinical practive, results from ingestion of agents with multiple receptor effects (as apposed to pure anticholinergics) this may also lead to clouding of the classic toxidrome - a common example being miosis in a patient suffering from an anticholinergice delirium secondary to olanzapine or quetipaine, due to their alpha blocking effects.
  
-  * Peripheral effects include - dry skin/mouth, mydriasis, tachycardia, urinary retention, ileus, raised temperature (more connomly seen in children).+  * Peripheral effects include - dry skin/mouth, mydriasis, tachycardia, urinary retention, ileus, raised temperature (more comnonly seen in children).
   * Central effects include - confusion, picking movements, agitation, aggression, delirium, sedation, hallucination (mainly visual), seizure (less frequently)   * Central effects include - confusion, picking movements, agitation, aggression, delirium, sedation, hallucination (mainly visual), seizure (less frequently)
  
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 Anticholinesterase inhibitors slow the breakdown of acetylcholine in the synaptic cleft, The resultant increase in synaptic acetylcholine levels can outcompete the competitive bloackade of the anticholinergic agent and restore cholinergic tone. Anticholinesterase inhibitors slow the breakdown of acetylcholine in the synaptic cleft, The resultant increase in synaptic acetylcholine levels can outcompete the competitive bloackade of the anticholinergic agent and restore cholinergic tone.
  
-Physostigmine is a parenteral agent that was used frequently in the past with reported high efficacy at controlling anticholinergic delirium. Its use fell out of favour following reports of deterioration and mortality following its use in serveral tri-cyclic antidepressant overdoses.+Physostigmine is a parenteral agent that was used frequently in the past with reported high efficacy at controlling anticholinergic delirium. Its use fell out of favour following reports of deterioration and mortality following its use in several tri-cyclic antidepressant overdoses.
  
 On more recent review of these cases, it is evident that these patients were suffering with severe sodium channel blockage and required treatment of this, with alkalinisation and intubation, and it was the lack of providing this that led to their deterioration, rather than the provision of physostigmine. On more recent review of these cases, it is evident that these patients were suffering with severe sodium channel blockage and required treatment of this, with alkalinisation and intubation, and it was the lack of providing this that led to their deterioration, rather than the provision of physostigmine.
  
-Treatment of achicholinergic delirium with anticholinesterase inhibitors has been shown to both reverse the delirium and control agitation, far better then sedation alone. Their use should be avoided in patients with bronchospasm or bradycardia. Use:+Treatment of anticholinergic delirium with anticholinesterase inhibitors has been shown to both reverse the delirium and control agitation, far better then sedation alone. Their use should be avoided in patients with bronchospasm or bradycardia. Use:
  
   * **Physostigmine 0.5mg (Child: 0.01mg/kg up to 0.5mg)**  intravenously by slow push. Repeat every 15mins if there is no or patial response. Maximum 2mg (Child: 1mg) within any 60min period.   * **Physostigmine 0.5mg (Child: 0.01mg/kg up to 0.5mg)**  intravenously by slow push. Repeat every 15mins if there is no or patial response. Maximum 2mg (Child: 1mg) within any 60min period.