Y. S. Ravikumar,K. M Srinath,L. S Adarsh, Ashik K Sasidharan, Nagalakshmi, Akash Medicine VI Unit, JSSMC & Hospital, Mysore.
A 29 year old male, a chronic alcoholic and smoker, with history of previous suicidal attempts and repeated head injuries, reported to emergency department with vague chest discomfort, incessant vomiting and severe pain in left upper and lower limbs of one day duration. Patient was irritable and slightly restless. His pulse was 100/min and regular. BP was 120/80 mmHg. Systemic examination was unremarkable and pupils were normal. ECG was normal. A provisional diagnosis of chronic alcoholism with alcoholic gastropathy and delirium tremens (DT) was considered. Psychiatrist also concurred with the diagnosis of DT. He was treated with PPIs, thiamine and IV fluids. There was no history suggestive of poisoning. However, naso-gastric aspiration was done, which was normal.
His general condition worsened over the next few hours. He developed fever, increased tracheobronchial secretions and started to desaturate. His pupils became constricted. He was immediately intubated and put on ventilator. Possibilities of brain stem encephalitis, pontine hemorrhage and organophosphate compound poisoning were considered.
The serum cholinesterase level was significantly low (730U/l). He was then started on atropine and pralidoxime. There was no history of poisoning forthcoming on repeated enquiries with the family members. His serum cholinesterase level continued to be low on the subsequent days.
Two days after admission, he developed blebs over his left upper limb, which progressed to cellulitis. Surgical opinion was taken and incision and drainage was done. Over the next two weeks his general condition improved and he was weaned off the ventilator. Patient denied having taken organophosphate compound in any form. However, his brother recollected that, he had found a syringe in the patient’s pocket while shifting him to the hospital. Patient was discharged after a few days. During follow up, he was stable and his serum cholinesterase had improved.
Clinical features like pin point pupils, increased tracheobronchial secretions supported by low serum cholinesterase levels and patient having developed cellulitis of left upper limb and RT aspiration being normal, prompted the diagnosis of organophosphate poisoning-by non-enteral route.
The other causes of low serum cholinesterase levels like, chronic anemia, malnutrition, surgical shock, blood dyscrasias, radiation, exposure to phenothiazines, uremia, chronic liver disease and malignant states, were excluded in this case. Decreased cholinesterase levels, which can be familial was excluded by checking cholinesterase levels of the patient’s siblings and mother. Hence this was a case of organophosphate compound poisoning by parenteral route. It always pays when we have a high index of suspicion in patients who are alcoholics, those with previous suicide attempts and those with some knowledge of using drugs.
Here is a brief review of mechanism of Organophosphate compound poisoning and their clinical features
Overview of Organophosphate and Carbamate toxicity
Clinical Syndromes
Acute Toxicity
Generally manifests in minutes to hours.
Evidence of cholinergic excess
SLUDGE = Salivation, Lacrimation, Urination, Defecation, Gastric Emptying
BBB = Bradycardia, Bronchorrhea, Bronchospasm
Respiratory insufficiency can result from muscle weakness, decreased central drive, increased secretions, and bronchospasm.
Intermediate Syndrome
Occurs 24-96 hours after exposure
Bulbar, respiratory, and proximal muscle weakness are prominent features
Generally resolves in 1-3 weeks
Organophosphorous Agent-Induced Delayed Peripheral Neuropathy (OPIDN)
Usually occurs several weeks after exposure
Primarily motor involvement
May resolve spontaneously, but can result in permanent neurologic dysfunction
Diagnostic Evaluation of Acute Toxicity
Atropine challenge if diagnosis is in doubt (1 mg IV in adults, 0.01-0.02 mg/kg in children)
Absence of anticholinergic signs and symptoms (tachycardia, mydriasis, decreased bowel sounds, ordry skin) strongly suggests poisoning with organophosphate or carbamate.
Decreased RBC acetylcholinesterase activity confirms diagnosis
RBC cholinesterase less than 50% of normal indicates organophosphate toxicity. Disadvantages of Cholinesterase as an indicator:
Normal cholinesterase level is based on population estimates and there is a wide range of distribution defining the normal levels.
False depression of RBC Cholinesterase level is seen in pernicious anemia, hemoglobinoapthies and antimalarial treatment and blood collected in oxalate tubes.
Though organophosphate poisoning is not a rare event, there are a very few case reports of parenteral OP poisoning. The report by Lyon et al. of a 24-year-old man who injected 1.8 g of malathion intravenously. In that patient serum PChE levels were undetectable for 24 hours after the injection, but the patient had only moderate toxic effects and survived. The apparent half-life of malathion, calculated from the serum concentration data, was of 2.89 hours. There are a few case reports of intramuscular and subcutaneous administration of these insecticides, where in the onset of symptoms would be delayed and persist for a longer duration warranting a longer duration of antidote therapy. An interesting case of intravenous toxicity of OP poisoning with monochrotophos who developed intermediate syndrome and required prolonged ventilation and restarting pralidoxime after the fifth day of intoxication has been reported by Badhe & Sudhakar.
These reports of parenteral intoxication of Organophosphate compound, which usually presents as a sequel of ingestion, cautions the emergency care physician to be on the watch to recognize the systemic manifestations of toxicity, actively look for signs of injection marks, local abscesses on the person. In such cases, the usual practice of gastric lavage or use of activated charcoal takes a backseat. Instead, a debridement of the local collection at the injection site would help eliminating the “depot” of insecticide
References:
1. A Case Report of Intravenous Malathion Injection with Determination of Serum Half-Life. Jack Lyon, Howard Taylor and Bruce Ackerman. Clinical Toxicology 1987, Vol. 25, No. 3, Pages 243-249.
2. Intravenous organophosphate injection: an unusual way of intoxication. Güven M, Unlühizarci K, Göktaş Z, Kurtoğlu S. Hum Exp Toxicol. 1997 May; 16(5):279-80.
3. An intravenous organophosphate poisoning with intermediate syndrome: An unusual way of intoxication. Ashok Badhe, S Sudhakar Indian Journal of Critical Care Medicine 2006: 10: 3: 191-192
4. Parenteral injection of organophosphate insecticide.Apropos of two cases. Sao Paulo Med.J. vol.112 no.2 Apr/June 1994.
5. Pocket book of Pesticide Poisoning for Physicians 1st Ed- V.V.Pillay CBS Publishers.
