TOXIC EFFECTS OF ORGANOPHOSPHATE POISONING AND USE OF HEMOPERFUSION WHEN ATROPINIZATION TOXICITY WAS OBSERVED IN THE EMERGENCY ROOM OF A TERTIARY HOSPITAL IN THE PHILIPPINES: A CASE REPORT

Pesticides such as insecticides, herbicides, and rodenticides are widely used in the country, which had caused high case rates of acute poisoning, both accidental and intentional. Most of these substances have no readily available antidotes in the emergency rooms. In the recent years, blood purification technique such as hemoperfusion had been used with success in the management of acute poisoning. Hemoperfusion has a high clearance rate for pesticides such as organophosphorus or organochlorine insecticides, rodenticides, and herbicides (Ke at al. 2023).

A 63 year old male, with no known co-morbidities, working in a pest control company, presented at the emergency room of a tertiary hospital due to a suspected case of pesticide poisoning. The history of present condition started few hours prior to admission, when the patient was found by a relative lying on the floor and unconscious and with an empty pesticide bottle (chlorphytos) beside him. Apparently, this was not the first attempt done by the patient. Upon presentation at the emergency room, patient was noted to have decreased sensorium, with no eye opening and verbal output, but with spontaneous and non – purposeful movements. Blood pressure was 120/70, with noted tachycardia and without desaturation at room air. Pertinent physical examination findings include note of vesicular breath sounds, absence of murmurs, soft abdomen, absence of edema, and absence of oral lesions. Due to his sensorial changes, he was immediately intubated and hooked to mechanical ventilator. Initial work-up showed leukocytosis and increased creatinine. Electrolytes, coagulation parameters, liver function tests were normal. ABG showed pure high anion gap metabolic acidosis. ECG was sinus tachycardia and chest radiograph were normal. 

At the level of emergency room, the patient was given with activated charcoal, sodium bicarbonate, and atropinization was started at 1mg TIV q 5 minutes, with uptitration up to a double dose. Patient was regularly checked for signs of congestion. Once atropinization was reached, atropine drip was then started. However, atropine toxicity was noted 8 hours after atropinization manifested as dilated pupils (5mm), dry buccal mucosa and lips, tachycardia at 120s to 130s, and absence of spontaneous movement. Atropine drip was then discontinued. There was also concomittant correction for metabolic acidosis and Internal Jugular vein access was inserted and the patient underwent hemodialysis with hemoperfusion using HA-230 cartridge. Two consecutive HD/HP sessions were done and atropine drip was resumed once the signs of toxicity waned off. On his 3rd hospital day, his sensorium improved from initial GCS 7 (E1V1M5) upon presentation at the ER, then to GCS 3 post atropinization, and now to GCS 13 (E3V5M4) post hemodialysis and hemoperfusion. 

Organophosphate poisoning affects the nervous system by inhibiting acetylcholinesterase. Hemoperfusion was used as an adjunct to the standard therapy of atropinization, especially that toxicity to atropine was observed in the patient. This blood filtration technique removed the toxic substance in the bloodstream, thereby resulting to clinical improvement in the patient who was critically ill and in cholinergic crisis.