Case Files

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ORGANOPHOSPHATE POISONING WITH  – NO “SLUDGE”

Ashish Kumar Singh*,

*Senior Resident, Department of Medicine, Lady Hardinge Medical College

Organophosphate (OP) poisoning is common in India. We report a case of severe OP poisoning, presenting with seizure, altered sensorium which posed a diagnostic dilemma. Despite nonavailability of history of OP poisoning, he was treated based on strong suspicion and showed a good clinical response to treatment with atropine and pralidoxime, and had a successful recovery. Atypical presentations may be encountered following administration of OP poison, and even a slight suspicion of this, warrants proper investigations and treatment for a favourable outcome. Persistently low plasma cholinesterase level is a useful marker for making the diagnosis.

INTRODUCTION

Organophosphate (OP) poisoning is common in developing countries. Poisoning occurs mostly by voluntary ingestion, inhalation, or by absorption through the skin. The diagnosis of OP poisoning made based on clinical grounds. In the absence of known ingestion/exposure, clinical features of cholinergic excess should indicate the possibility of organophosphorus poisoning. We describe a case of severe OP poisoning presenting with seizure, altered sensorium with no history of exposure to organophosphorus compounds in any form which was successfully treated on clinical judgment.

CASE REPORT

Our patient, a 53-year-old diabetic male, chemist by occupation who presented to ER with sudden onset loss of consciousness of 6 hours duration from early morning. There was history of travel by train for last 24 hours prior to unconscious state. Convulsion was suspected based on history of staring look with spontaneous movements of all limbs lasted for 2-3 minutes and it was noted when relatives tried to wake up the patient. Vitals shows high blood pressure, hyper glycaemia, hypoxia on presentation. Examination showed twitching involving all over face, right sided upper limb fasciculations, no focal neurological deficit found, pupils were normal. Bilateral crackles heard over chest. Diabetic ketoacidosis was ruled out. A provisional diagnosis of Diabetes mellitus with hyper glycaemia with hypertension with GTCS with post ictal confusion with aspiration pneumonitis made and patient managed accordingly. Patient was put on mechanical ventilation. CSF analysis done as patient didn’t show any improvement in sensorium and it turned out to be normal. After 48 hours of hospitalization, patient developed miosis of bilateral eyes with no improvement in sensorium. Spontaneous respiratory efforts were absent suggestive of respiratory muscle paralysis. Brain Imaging done to rule out pontine hemorrhage. History reviewed regarding pesticidal exposure or substance use and found to be negative. Keeping in mind the high possibility of poisoning, toxicological screening was done. As urinary opiate was negative and plasma cholinesterase levels found to be low (less than 25% of normal levels), a strong suspicion of organophosphorus poisoning was made.  Atropine boluses given initially and then started on infusion after achieving signs of atropinisation. Post atropine infusion, patient’s sensorium started improving within 24-48 hours. He initially showed spontaneous eye opening followed by response to verbal commands. Gradually, he showed spontaneous breathing and weaned off from ventilator successfully. Patient kept on atropine infusion, slowly tapered and then stopped. Patient observed in hospital for development of intermediate syndrome and then discharged on 14th day of hospital stay.

DISCUSSION

The typical toxidrome in OP poisoning consists of SLUDGE symptoms. However, some patients might present with atypical presentation, which makes diagnosis difficult like in our case. Most symptoms and signs in OP poisoning are result of excessive muscarinic stimulation via receptors present either centrally or peripherally. Over stimulation of central receptors results in seizure, encephalopathy and coma as observed in our patient. Patients may also present with other neurological manifestations described below.

Three types of paralysis are described in OP poisoning based on time after exposure. Weakness, fasciculations, cramps and twitching can occur acutely with the cholinergic symptoms. 10 to 40 percent of patients poisoned with organophosphorus develop a distinct neurological disorder, 24 to 96 hours after exposure and resolution of cholinergic excess. This disorder is referred to as intermediate syndrome which consists of characteristic neurological findings including neck flexion weakness, decreased deep tendon reflexes, cranial nerve abnormalities, proximal muscle weakness and respiratory insufficiency. Usually, recovery occurs in 1-2 weeks. Exposure of highly fat-soluble OP agents and inadequate treatment with oximes are risk factors for development of intermediate syndrome (1). Organophosphorus agent induced delayed neuropathy (OPIDN) typically occurs 1-3 weeks after exposure. Affected patients present with transient painful stocking glove paraesthesia followed by symmetrical motor polyneuropathy causing flaccid paraparesis, which can progress to quadriparesis. OPIDN can recover in weeks to months, but can cause permanent neurological disability. (2)

Coma is seen in 17-29% of patients and can last for hours to days. (3) Cerebellar ataxia has also been described as a delayed presentation. (4) It has been reported in studies that, survivors of OP poisoning may have neurobehavioral defects such as decreased memory, abstraction, attention and Parkinsonism which may be permanent. (5)

Symptoms of cholinergic toxidrome with superimposed history of OP exposure or ingestion makes the diagnosis straightforward. But atypical presentations in absence of exposure history creates diagnostic dilemma. Reduced plasma cholinesterase level is a useful biochemical tool in such cases to confirm suspected OP poisoning. An assay for plasma cholinesterase activity is more easily performed, but does not correlate with severity of poisoning. Direct measurement of RBC acetylcholinesterase activity provides a measure of the degree of toxicity. Sequential measurement of RBC AchE activity may also be used to determine the effectiveness of oxime therapy. (6)

CONCLUSION

Despite presence of predominant central symptoms in absence of SLUDGE symptoms and exposure history, a strong clinical suspicion and relevant biochemical findings, made it possible to diagnose the OP poisoning and timely and accurate treatment helped the patient to survive. Keeping the atypical clinical manifestations in mind, diagnosis of OP poisoning should not be missed, even if there is no strong history of exposure.

REFERENCES:

  1. Samuel J, Thomas K, Jeyaseelan L, Peter JV, Cherian AM. Incidence of intermediate syndrome in organophosphorous poisoning. J Assoc Physicians India. 1995;43:321–3.
  2. Aygun D, Onar MK, Altintop BL. The clinical and electrophysiological features of a delayed polyneuropathy developing subsequently after acute organophosphate poisoning and it’s correlation with the serum acetylcholinesterase. Electromyogr Clin Neurophysiol. 2003;43:421–7. 
  3. Tsai JR, Sheu CC, Cheng MH, Hung JY, Wang CS, Chong IW, et al. Organophosphate poisoning: 10 years of experience in southern Taiwan. Kaohsiung J Med Sci. 2007;23:112–9.
  4. Fonseka MM, Medagoda K, Tillakaratna Y, Gunatilake SB, de Silva HJ. Self-limiting cerebellar ataxia following organophosphate poisoning. Hum Exp Toxicol. 2003;22:107–9.
  5. Senanayake N, Sanmuganathan PS. Extrapyramidal manifestations complicating organophosphorus insecticide poisoning. Hum Exp Toxicol. 1995;14:600–4. 
  6. Areekul S, Srichairat S, Kirdudom P. Serum and red cell cholinesterase activity in people exposed to organophosphate insecticides. Southeast Asian J Trop Med Public Health. 1981;12:94–8.