Status Epilepticus Due to Organophosphate Poisoning in an Infant

We report a case of a three months old female presented with status epilepticus who was diagnosed as organophosphate (OP) poisoning. She was from rural area with agricultural background. Typical clinical features and history of exposure to organophosphate compound were absent. The infant was successfully treated with atropine, pralidoxime and supportive management. Safety and efficacy data of pralidoxime in infants are limited in literature and was found safe in our case.


Introduction
U ninten onal organophosphate (OP) poisoning in children is common 1 . Exposure can occur via skin and mucous membranes, inhala on or inges on.
OP poisoning is usually diagnosed by characteris c clinical features, low serum or red blood cell cholinesterase level and a history of exposure to a known OP compound 2 . Clinical features of organophosphate poisoning in children are diff erent from those in adults 1 and history of exposure may not be found in some children 3 . Diagnosis of OP poisoning may be missed in such cases. Treatment of OP poisoning includes suppor ve therapy and atropine, oximes, benzodiazepines, gastrointes nal decontamina on and experimental therapies 2 . Usefulness and safety of oximes in acute OP poisoning have been ques oned recently 4 and data for paediatric pa ents are even fewer.
We report a three month old female presen ng as status epilep cus who developed pinpoint pupils and excessive bronchial secre ons a er 12 hours of admission. She was diagnosed OP poisoning. Source and route of exposure was not known a er detailed inquiry of parents. The pa ent was treated successfully with suppor ve treatment and intravenous atropine and pralidoxime.

The Case
A three month old female was presented with sudden onset of excessive crying for three hours and generalized tonic clonic seizures for last one hour. There was no history of fever, feeding diffi culty, respiratory or gastrointes nal complaints, bleeding tendency or trauma. Her father was a farmer and was residing in a village. She was born of a non-consanguineous marriage with uneven ul birth history and her birth weight was 2.5 kg. She was exclusively breas ed and her growth and development were normal. She was not on any medica on. Her weight was 5.6 kg and head circumference was 39 cm. On examina on, she was afebrile, pulse rate was 132/minute, and respiratory rate was 42/minute. On systemic examina on, both pupils were constricted and reac ve to light and rest of the examina on was uninforma ve. A er taking relevant samples, she was treated with intravenous calcium gluconate, dextrose, an bio cs, phytomenadion, loading dose of phenobarbitone and maintenance intravenous fl uids.
Inves ga ons on the fi rst day of admission were as follows: Hemoglobin 8.7 gm/dL, total white blood cell count 16000/mm 3 with 58% neutrophils and 40% lymphocytes, platelet count 8.7 lacs/mm 3 , plasma glucose 157 mg/dL, prothrombin me 15.5 seconds with INR 1.15, ac vated par al thromboplas n me 26.7 seconds, serum ionized calcium 1.15 mmol/L. Examina on of cerebrospinal fl uid showed 3-5 lymphocytes/mm 3 and culture was nega ve for bacterial organism.
During the hospital stay, the pa ent developed increasing tachypnoea with respiratory secre ons. At 12 hours of admission, pulse rate was 146/minute, respiratory rate was 64/minute with bilateral secretory sounds in lung fi elds. There was no recurrence of seizure but the pa ent did not regain consciousness. Both pupils were pinpoint with rest of the central nervous system examina on uninforma ve. Chest X-ray was normal. Organophosphate poisoning was suspected and serum cholinesterase level by enzyma c method was 99 U/L (normal range: 5900-12220 U/L) confi rming diagnosis of organophosphate poisoning.
In addi on to suppor ve management, the pa ent was treated with intravenous atropine and pralidoxime chloride. Atropine was given as 0.05 mg/kg/dose intravenously every 15 minutes un l clearing of bronchial secre ons and then as needed. Pralidoxime was given as 2 intermi ent doses of 50 mg/kg at interval of 12 hours as intravenous infusion over 30 minutes each. The pa ent showed clinical improvement within 90 minutes of ini a on of specifi c therapy and atropine was safely tapered a er 48 hours. There was no untoward reac on. The source of organophosphate was not found a er detailed history.

Discussion
Common presen ng symptoms and signs of OP poisoning in children are pinpoint pupils, excessive respiratory secre ons, diarrhea, vomi ng, altered sensorium, respiratory failure, 'garlic odor' from body, shock, apathy, muscle weakness, etc 3 .
As our pa ent presented with excessive crying and status epilep cus only, meningi s, metabolic abnormali es, and intracranial hemorrhage were suspected ini ally. Presence of constricted pupils on admission was not suffi cient to suspect OP poisoning. It was suspected a er 12 hours of admission when pa ent developed pinpoint pupils and excessive bronchial secre ons. Although diarrhea is an important feature in OP poisoning in children less than 5 years of age 5 , our pa ent did not develop diarrhea during the course.
No source was found a er making detailed enquiry for possible exposures. No insec cide or any spray was used inside the house or in vicinity of house in last week. There was no history of any inges on or applica on over skin and mucous membranes. No soap or shampoo 6 was used for bathing.
Children of agricultural workers are at high risk for development of both acute and chronic neurological symptoms 7 . The father being a farmer and residence in rural area were important clues.
Unusual presenta ons of OP poisoning such as presenta on as diabe c ketoacidosis 8 , transplacentally acquired OP poisoning in a newborn 9 , OP poisoning complica ng as extrapyramidal parkinsonism 10 , etc have been reported in literature. In our case, age of the pa ent and her clinical presenta on were unique.
There are no well-controlled clinical trials to establish eff ec veness and safety of pralidoxime chloride in infants is as OP poisoning in this age group is not common. Our pa ent did not develop any side eff ect with use of intermi ent infusion dosing of pralidoxime.
Major limita on in our case report is that we do not know whether it was a carbamate poisoning. So we cannot comment about eff ec veness of pralidoxaime in our case.
To summarize, we report a three month old pa ent from agricultural family background who presented with status epilep cus. She was diagnosed OP poisoning a er 12 hours of admission due to presence of pinpoint pupils and excessive bronchial secre ons. Source and mode of exposure was not known. She improved with suppor ve therapy with intravenous atropine and intermi ent infusion dosing of pralidoxime. Pralidoxime was safe in the infant.

Conclusion
This report emphasizes importance of high index of suspicion to diagnose OP poisoning in infants, especially those coming from agricultural or rural areas. Presence of pinpoint pupils and bronchial secre ons are a strong clue. History of exposure may not be present. Intermi ent infusion dosing of pralidoxime was safe in our case.