INTRA AURAL SKIN

INTRA AURAL SKIN

Absorption continues as long as the insecticide remains in contact with the skin and hence the need for immediate cleansing. In the ear, the absorptive surfaces are the skin covering the canal, inflamed tympanic membrane, and moist middle ear mucosa in cases of perforated tympanic membrane. The rate of absorption is highest in moist areas, such as eyes, genitals, and armpits. A study comparing the rates of dermal absorption of OP compounds showed that intra-aural absorption is 5.4 times greater than absorption over the forearm. Other factors that may increase absorption are sweating and increased blood circulation. The rate of absorption is dependent on the site of application, skin condition, type of pesticide, and the duration of contact. Most transdermal exposures are occupational and cause delayed manifestations. reported an acute cholinergic crisis and intermediate syndrome requiring mechanical ventilation in a patient who had an accidental spill of monocrotophos over the face. Badhe and Sudhakar described intravenous monocrotophos poisoning resulting in intermediate syndrome requiring ventilator support. There are a few reported cases of intravenous, intramuscular, and subcutaneous administration of insecticides associated with local and systemic symptoms. The most common route of exposure in cases of deliberate self-harm is oral ingestion. The acute oral toxicity for rats (LD50) is 23 mg/kg (males) and 18 mg/kg (females), whereas the acute dermal toxicity is 354 mg/kg.

It is a highly toxic, water-soluble insecticide with a high oral and a moderate dermal absorption. Monocrotophos, which was used by our patient, is one of the most commonly consumed OP compound for deliberate self-harm. Morbidity and mortality from OP poisoning remains high in rural settings where facilities for intensive care are either absent or limited. Death as a result of poisoning is due to respiratory failure and ventilator-related complications. The presentation may be acute (within 24 h) with multisystemic symptoms of cholinergic excess, intermediate (1-4 days) with predominant neurologic symptoms or chronic (2-3 weeks) with polyneuropathy. OP compounds act by irreversible inhibition of cholinesterase enzyme, which results in overstimulation of muscarinic and nicotinic receptors. She did not develop intermediate syndrome and was subsequently discharged after psychiatry counseling. A low-dose atropine infusion was administered for 2 days and the patient was monitored in the ward for 5 days. Bolus doses of atropine were given to maintain the heart rate above 100/min. Multiple aural irrigations with normal saline were performed to decrease further absorption of monocrotophos. Plasma butyrylcholinesterase level was 1141 U/L (reference range 3000-8000 U/L), thus confirming OP poisoning. Rest of the systemic examination was unremarkable. Examination of the ears did not reveal any sign of local inflammation, and bilateral tympanic membrane appeared intact. She did not have neck muscle weakness or fasciculations. Her heart rate was 100/min, blood pressure was 100/70 mmHg, respiratory rate was 22/min, and pupil size was 2 mm bilaterally. On examination she was drowsy, restless, and disoriented to time, place, and person. She also complained of burning sensation in both the ears.

She had gastric cramps and loose stools with no other SLUDGE symptoms (SLUDGE–salivation, lacrimation, urination, defecation, gastric cramps and emesis). The daughter witnessed her pouring the OP compound into her ears as an impulsive act with no oral consumption. A 51-year-old housewife with no premorbid illness presented to the emergency department within 2 h of allegedly pouring monocrotophos (WHO Class Ib OP compound) into both her ears with the intention of deliberate self-harm after a family dispute.

Intra aural