![]() Healthcare workers can reduce their risk of this condition by employing proper hand hygiene practices. Primary prevention is best accomplished by avoidance of exposure to causative agents. Local botulinum toxin overexposure or systemic poisoning leading to mydriasis occurs via presynaptic inhibition of acetylcholine release from the short ciliary nerves innervating the iris sphincter muscles. Common examples of accidental exposure include finger-to-eye contact after handling an anticholinergic agent (e.g., healthcare workers, travelers with motion sickness) and ill-fitting nebulizer treatment masks.Īnticholinergic mydriasis occurs via blockade of parasympathetic muscarinic acetylcholine receptors on the iris sphincter muscle.Īdrenergic mydriasis occurs by overstimulation of the α1-receptors of the iris dilator muscle leading to sustained contraction. The primary risk factor is exposure to causative agents. The mechanism is presynaptic inhibition of acetylcholine release from the short ciliary nerves innervating the iris sphincter muscles.Īgents that may cause mydriasis therapeutically or in overdoses: In almost 50% of cases of systemic botulism, bilateral dilated pupils are seen. Local injection of botulinum toxin to treat various neurologic conditions or accidental systemic exposure can also cause toxic pupil. Adrenergic mydriasis can be distinguished from anticholinergic mydriasis or a cranial nerve III lesion by the presence of blanched conjunctiva, lack of ptosis and motility deficit, and residual light reaction. Cocaine blocks norepinephrine reuptake at the junction and amphetamines stimulate release of norepinephrine at the junction leading to iris dilator muscle contraction. This is also the mechanism of mydriasis caused by indirect acting sympathomimetic drugs like cocaine and amphetamines. The route of exposure to these plant-based mydriatics can include aerosolization of particles from the plant, or direct finger-to-eye contact (e.g., a farmer working in a dusty field, a gardener, or a child picking flowers).Īccidental application of nasal drops or sprays with adrenergic properties may also cause a sustained dilation of the pupil (with relatively preserved light reaction). Several household or garden plants found in North America contain high concentrations of alkaloids including atropine, scopolamine, hyoscine, and hyoscyamine. Topical exposure to environmental toxins such as Jimson weed (Datura stramonium) or bella donna alkaloids can also produce mydriasis. In contrast, the unilateral dilated pupil is usually due to local or topical exposure to an assortment of dilating agents (e.g., mydriatic drops).Īnticholinergic mydriasis, also known as pharmacologic blockade and “atropinic” mydriasis, refers to the absolute or partial paralysis of pupillary constriction unilaterally or bilaterally due to topical advertent or inadvertent exposure to an anticholinergic agent. ![]() This effect is usually accompanied by other signs of central nervous system involvement, such as depression, agitation, and altered level of consciousness. Most commonly, the medications, drugs, and toxins that cause pupillary dilation act via iris parasympathetic receptor blockade (anticholinergic mydriasis) but sympathetic stimulation (e.g., topical epinephrine) can also produce lesser degrees of pharmacologic mydriasis (without impairing the light/near reaction).Īgents that affect the central nervous system such as atropine, scopolamine, amphetamine, marijuana, lysergic acid diethylaminde (LSD), and glutethimide can cause bilateral mydriasis. Clinical differentiation from similar appearing life-threatening pathologies, most notably compressive lesions of cranial nerve III, is vital. It is typically characterized by poor or no pupillary constriction to light or near stimuli. Pharmacologic dilation of the pupil is one of the myriad explanations for unilateral or bilateral pupillary dilation. ![]()
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |