Fever, atropine

Atropine suppresses thermoregulatory sweating. Sympathetic cholinergic fibers innervate eccrine sweat glands, and their muscarinic receptors are readily accessible to antimuscarinic drugs. In adults, body temperature is elevated by this effect only if large doses are administered, but in infants and children even ordinary doses may cause "atropine fever."... 

The rise In body temperature due to the belladonna alkaloids is usually significant only after large doses. Nevertheless in infants and small children, moderate doses induce "atropine fever."... 

Atropine fever Hyperthennia induced by antimuscarinic drugs caused mainly by inhibition of sweating... 

Atropine suppresses sweating, which is tolerable in adults, but can cause atropine fever in children, even at ordinary doses. Urinary retention and gastric hypomoti-lity, usually expected post surgery, are exacerbated with antimuscarinic use. 

Aspirin does not alter the normal body temperature, which is maintained by a balance between heat production and dissipation. In a fever associated with infection, increased oxidative processes enhance heat production. Aspirin acts by causing cutaneous vasodilation, which prompts perspiration and enhances heat dissipation. This effect is mediated via the hypothalamic nuclei, as proved by the fact that a lesion in the preoptic area suppresses the mechanism through which aspirin exerts its antipyretic effects. The antipyretic effects of aspirin may be due to its inhibition of hypothalamic prostaglandin synthesis. Although aspirin-induced diaphoresis contributes to its antipyretic effects, it is not an absolutely necessary process, because antipyresis takes place in the presence of atropine. 

Ext. Belladonna (extract of belladonna) The active agent Is atropine. In neuralgia. It was preferred over opium. Used In cases of whooping cough, scarlet fever, spasmodic asthma, and other Instances calling for an antlspasmodic. 

The unwanted peripheral effects of all atropine-like drugs include flushing of the skin, dryness of the mucous membranes with fever, tachycardia, reduced salivary secretion and dryness of the mouth, drying up of the gastrointestinal secretions and decreased gastric acidity, and reduced muscle tone in the gut and constipation. Bladder tone and frequency of micturition are reduced and acute urinary retention is a risk, especially in older men with prostatic hyperplasia. Nasal, bronchial, and lacrimal secretions are reduced. 

Only six of 36 children who took overdoses of co-phenotrope had signs of atropine overdose (central nervous system excitement, hypertension, fever, flushed dry skin) (1). Opioid overdose (central nervous system and respiratory depression with miosis) predominated or occurred without any signs of atropine toxicity in 33 cases (92%). Diphenoxylate-induced hjrpoxia was the major problem and was associated with slow or fast respiration, hypotonia or rigidity, cardiac arrest, and in three cases cerebral edema and death. Respiratory depression recurred 13-24 hours after the ingestion in seven cases and was probably due to accumulation of difenoxine, an active metabolite of diphenoxylate. Recommended treatment is an intravenous bolus dose of naloxone, followed by a continuous intravenous infusion, prompt gastric lavage, repeated administration of activated charcoal, and close monitoring for 24 hours. 

Most antihistamines have anticholinergic atropine-like actions and cause a dry mouth and similar side-effects. The clinical uses of H, antihistamines are extensive, particularly for the symptomatic relief of allergy, such as hay fever and urticaria, and (together with corticosteroids) in the acute treatment of anaphylactic shock. Many antihistamines also have antinauseant properties and are used, for instance, to prevent travel sickness (though this property may well result from their anticholinergic actions). The older antihistamines produce drowsiness and this sedative action may be used to help sleep (e.g. promethazine). 

The acute poisoning that occurs with most antihistaminics does not cause severe CNS depression as would be expected based on their sedative properties, but is manifested by mydriasis, fever, flushing, CNS excitement, hallucinations, ataxia, athetosis, and convulsions. Some of these effects, which resemble those of atropine poisoning, may be due to their anticholinergic properties. Diazepam is an effective antidote to poisoning and should be used to reverse the CNS excitement and convulsions. 

Inferior-wall Ml or ischemia, hypoxia, vagal stimulation, and sick sinus syndrome. Acute rheumatic fever. Valve surgery. Digoxin toxicity. Correction of underlying cause. Atropine for symptomatic slow rate. Pacemaker insertion if patient doesn t respond to drugs. Discontinuation of digoxin if appropriate. 

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