Eunice¹, Ayisha Sheerin S^2*, Gayathri³, Karthick Subash S⁴

¹Assistant Professor, ^2,3,4Post Graduates Department of General Medicine, Kanyakumari Medical College, Tamil Nadu, INDIA.

Email: ayishasheerin@gmail.com

Peradeniya organophosphorus poisoning scale (POP scale)­­­

RESULTS

100 cases of OPC poisoning admitted to Kanyakumari Medical College were considered. Commonest age group involved were between 26 to 35 years. Males were the most common victims (65%).Suicide was the most common motive of poisoning (90%) and ingestion was the most common mode of poisoning (90%). Majority of patients admitted within 5 hours of exposure. Chlorpyrifos was the most common compound in poisoning. The percentage of population in 0 to 3(mild), 4 to 7(moderate) and 8 to 11(severe) POP scores were 55% ,42% and 3% respectively. Our study showed that the Hyperglycemic patients had more severe poisoning followed by the hypoglycemic patients and the majority of euglycemics had mild (0 to 3) poisoning. The ventilator requirements were 92.5%, 52% and 100% among hypoglycemics, euglycemics and hyperglycemics respectively. The mortality in hypoglycemics, euglycemics and hyperglycemics where 55.6% ,11.3% ,65% respectively. Further, the RBS was compared with the scores POP scale to look for statistically significant association between the extremes of glycemic status and higher grades of these clinical severity scores using Chi-square test.. The results were statistically significant (p=0.0001, Chisquare=18.643, DF=2 for POP scale.

Table 1: Age Distribution Of Study Subjects

Table 2: Gender Distribution Of Study Subjects

Table 3: Glycemic status (RBS) at presentation - severity and its relation to ventilator support requirement and mortality

Table 4: POP score at the time of presentation - Severity and its relation to ventilator support and mortality

Table 5: Association of glycemic status (RBS) of patients with different grades of POP score

DISCUSSION

In addition to neurotoxicity and oxidative stress, alterations in glucose homeostasis often culminating hyperglycemia is increasingly being reported as characteristic outcome of OPC poisoning. Numerous experiments have been conducted with experimental animals that reveal hyperglycemia as a characteristic outcome of OPC poisoning. Acute exposure of rats to malathion resulted in hyperglycemia with peak increase occurring at 2.2h after administration followed by decrease after 4h. This reversible phase of hyperglycemia was associated with increased glycogen deposition in liver, indicating that glucose may have come from gluconeogenesis. Malathion induced hyperglycemia was associated with AChE inhibition in pancreas.

• Pancreatic dysfunctions : OPC possess propensity to elicit structural and functional alterations in pancreatic milieu that may be associated with disruptions in euglycemic conditions. From the animal studies, it may be argued that OPC may present a great threat to pancreatic functions in human beings and such threats may have far-reaching consequences on gluco-regulation in human beings.
• HPA AXIS DYSFUNCTION : Acetylcholine exerts strong influence on functioning of hypothalamus-pituitary-adrenal (HPA) axis. Acetylcholine has been found to increase corticotrophin releasing hormone (CRH) activity of hypothalamus in vitro as measured by effect on corticosteroidogenesis, an effect that was antagonized by atropine.Given the importance of ACh in excitation of HPA axis, assessment of cholinergic stress in activation of HPA axis in monocrotophos treated rats becomes important.
• Adrenal involvement: Adrenals are an important part of the endocrine system and play a key role in glucose homeostasis by secreting glucocorticoid and amine hormones. Glucocorticoid hormones (GCs) (mainly cortisol in man and corticosterone In rodents) are secreted by the adrenal cortex under the control of hypothalamic pituitary-adrenal axis. Glucocorticoid hormones, along with other key hormones, act to maintain blood glucose levels within narrow limits. GCs, glucagon and epinephrine raise blood glucose by inhibiting glucose uptake in the periphery and stimulating hepatic glucose release. Increased glycogenolysis and gluconeogenesis appear to be the two chief mechanisms underlying OPC-induced hyperglycemia. OPC and other AChE inhibiting organophosphate compounds exert strong influences on functioning of hypothalamic-pituitary-adrenal (HPA) axis, leading to increased circulating levels of corticosteroid hormones in vivo. Further, hypercorticosteronemia was associated with decrease in adrenal cholesterol pools, which is the precursor for corticosterone synthesis. Depletion in adrenal cholesterol pools may therefore be attributable to increased synthesis and secretion of corticosterone. Interestingly, both OPC did not cause depletion in hepatic glycogen content. At time points that represented normalization of blood glucose levels, there was phenomenal increase in liver glycogen levels. The data presented above clearly demonstrates co-existence of hypercorticosteronemia and induction of liver gluconeogenesis enzyme activities with hyperglycemia in OPC treated rats, indicating that OPC may trigger induction of liver gluconeogenesis machinery as result of hypercorticosteronemia , leading to hyperglycemia.
• RISK FOR DIABETES: Oxidative stress in pancreatic milieu and glucose intolerance, up regulated gluconeogenesis machinery and hyperglycemia are critical factors in diabetes etiology. With the ability to induce the above-mentioned dysregulations, OPC may have far reaching consequences on diabetic outcomes.
• Likewise,hypoglycemia is an independent marker of severity and mortality in critical illnesses . The FOUR cause death categories in patients with critical illness and hypoglycemia are 1. Neurologic 2. Cardiovascular 3. Hypoxic respiratory failure and 4. Liver related .
• Individual hypoglycemic episodes are associated with biologic toxicity by increasing the systemic inflammatory response, inducing neuro-glycopenia, inhibition of corticosteroid stress response and cerebral vasodilation. Hence we urge that the management of both the extremes of glycemic status and their fluctuation is of prime importance in acute OPC poisoning like any other critical illness for better outcomes.

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