Rajendrasingh Pruthvirajsingh Rajput¹, Shital Rathod^2*

¹III^rdJunior Resident, ²Associate Professor, Department of Medicine, Dr Shankarrao Chavan Government Medical College, Vishnupuri, Nanded, Maharashtra, INDIA.

Email: drraj16dec@gmail.com

RESULTS

Majority of the patients (61.0%) were in the age group of 21 to 40 years. The age group of 41-60 years had 31 (31.0%) cases. Male patients (73.0%) were more than female patients (27.0%). Maximum number of patients were laborer (41.0%), followed by farmer (40.0%), housewives (13.0%), and only 6(6.0%) were students.

Table 1: General characteristic

DM was most commonly used OP agent in 37patients (37.0%) followed by CP 21 (21.0%) and MC among 10 (10.0%) of the cases.

Table 2: Distribution of patients according to OP agents used

The commonest route of exposure was ingestion (96.0%) followed by inhalational route which was observed in 3 (3.0%) of the patients and least common was topical among 1(1.0%) of the cases. Maximum patients reported ICU stay of 5-6 days (68.0%) followed by 17 (17.0%) patients who stayed at the ICU for over 6 days and 15.0% who stayed for less than 5 days. The mean duration of stay in the ICU was 5.49 ± 1.72days.

Table 3: Distribution of cases according to Route of Exposure and ICU stay

Fasciculations was the most common clinical feature (71.0%), followed by excess secretions and miosis in 65 (65.0%) each respectively, absent neck holding (22.0%), altered mental status (15.0%), bradycardia (12.0%) and hypotension (6.0%). Only 2 (2.0%) cases were observed to have Intermediate syndrome and both the cases died during the course of the treatment.

Table 4: Distribution of patients according to clinical features at presentation

Maximum cases 34 (34.0%) suffered from respiratory failure as the main complication in the present study. IMS and convulsions each were observed among 4 (4.0%) of the cases respectively. There were 3 deaths among those with IMS, thus becoming the complication with highest mortality.

Table 5: Distribution of cases according to complications

In present study 18 (18.0%) patients died and 82 (82.0%) of the patients survived.

Table 6: Distribution of patients according to Outcome

The quantity of OP compound consumed (p=<0.0001) posed an 11 times higher risk of mortality (p=<0.0001). Similarly, absence of neck holding posed a 7 times higher risk of mortality (p < 0.0001). Other factors that were significantly associated with a higher risk of mortality were low mean serum cholinesterase levels(p=0.003), later presentation at hospital (p=<0.0001) and absence of altered mental status at presentation (p=0.004). Conversely, greater duration of ICU stay was inversely associated with mortality as recovering cases tend to stay longer at the ICU.

Table 7: Predictors of mortality in OP poisoning cases (Univariate logistic regression)

*p<0.05 was statistically significant

On multivariate logistic regression analysis, the factors that were independently associated with mortality in OP poisoning cases were age more than 40 years (p=0.038) and time interval between consumption and admission (p=0.044). Whereas, the higher mean duration of ICU stay (p=0.014) was found to be inversely related to mortality which might be due to the ventilator support and adequate treatment received by the patients who stayed for longer duration.

Table 8: Predictors of mortality in OP poisoning cases (Multivariate logistic regression)

*p<0.05 was statistically significant

DISCUSSION

The incidences of organophosphorus pesticide poisonings are common in the developing world.⁹ Suicidal and non-suicidal organophosphate poisoning is one of the major problems in rural areas of India, with rapidly rising incidence rate.¹⁰ Toxicity of these compounds may result insignificant mortality and morbidity. About 99% of fatal cases occur in developing countries, especially in agricultural workers.¹¹ Mortality rates have been reported ranging from 10 to 22%.¹² In the Kashmir valley Malik et al. revealed that 33.5% of the cases of Organophosphorus compound poisoning were under the age of 25 years.¹³ In Mangalore, Karnataka the most common age group to be affected was between 20-30 (36.6%).¹⁴ The age affliction reported by the present study was similar to that from the other studies as mentioned above.^15-16 The reason could be that this age group by all probability is vulnerable to various emotional conflicts that occur during this phase of life. Problems leading to psychological stress may induce the youths for taking the drastic steps to end their life by consuming toxic substances. Males were affected more than females (73.0% versus 23.0% respectively) in the present study. A similar pattern was observed by other studies by Padmanaba et al.,¹⁷ and Joshi et al.,¹⁸ Where the male to female ratio ranged from1.2:1 to 4:1. The reason behind this may be due to the fact that males constitute the main work force in the fields, as they are more involved in spraying crops and handling pesticides. There may be a regional difference in the gender association of Organophosphorus compound poisoning as in some Northern regions of India like Jammu that have a female preponderance in Organophosphorus compound poisoning due to their role in spraying pesticides in the apple orchards.¹³ It was observed that nearly 80.0% of the affected population was farm labourers and farmers. This was also observed in several studies and may be attributed to their easy accessibility to the Organophosphorus as a part of their occupations. In the present study, Dimethoate was most commonly used OP agent (37.0%) followed by Chlorpyrifos (21.0%). Study by Gagarin et al.,²⁰ also reported Methyl parathion was the most common poison consumed (27%) followed by Chlorpyrifos (22%). It was also the most common poison detected in the study by Banerjee et al.,²¹ Dimethoate was most commonly consumed OPC in the study of Banday et al.,²² This variation in the type of poison consumed can be attributed to the regional availability of pesticides in different regions. In the present study, fasciculations was the most common clinical feature (71.0%), followed by excess secretions and miosis in 65 (65.0%) each. This shows that muscarinic effects predominate and appear first as compared to the nicotinic effects. Similarly, the study by Emerson et al.²³ showed that muscarinic symptoms were found in 92% of the cases. Miosis as observed in our study was found to be a good clinical sign to diagnose Organophosphorus poisoning, which is also comparable with other studies that showed similar rates of miosis. We found that miosis was found in nearly two-third of the cases and in 91% cases in the study done by Banerjee et al.,²¹ which was higher than that observed in our study. In the present study respiratory failure was observed among 34 % cases as the predominant complication. Respiratory failure was similarly reported by other studies as the main complication of Organophosphorus poisonining.²⁴ Other complications were Intermediate syndrome and convulsions each in 4.0% of the cases respectively. Intermediate syndrome and convulsions were observed in four cases, out of which three died eventually during the course of treatment. Similar complications were reported by previous studies.^24,2 In our study, mortality was 18 %, maximum in the age group of 41-50 years (41.2%). The deaths were slightly higher among females (18.5%) as compared to males (17.8%). Most of the deaths resulted from consumption of Monochrotophos and Chlorpyrifos. The commonest clinical feature observed on admission among the cases that died during the course of the study was hypotension (83.3%). Other studies have also reported similar mortality rates following OP poisoning varying from 4-30%.^24,26 In study by Safdar et al.²⁵ 4% of the patients died. Mortality was higher in those cases that had consumed large amount of OP substances (50-100 ml) and was highest in cases who consumed >100 ml (p <0.05). As observed in the present study, morbidity and mortality was proportionately higher in majority of patients who developed single/mutli-organ failure and required prolonged ventilatory support. Frequency of mortality due to organophosphates given by Yamashita, et al. ²⁷ varied between 4% and 30% and 5.5% in a study by Malik et al.¹³ In our study, it became evident also that most of patients who expired, there was a delay between consumption of Organophosphorus substance and initiation of treatment of more than nine hours, which is also supported by study done by Suleman MI et al.²⁴ Majority of the patients with a lag time less than 6.5 hrs recovered and survived, whereas the recovery and survival of patients decreased with the increase in lag time. Moreover, the patients with increased lag time required increased duration of mechanical ventilation.²⁸ The reason for higher mortality rates may be due to late arrival, not receiving any treatment at periphery before arrival to the hospital, poverty and illiteracy, unawareness regarding mortality rate of Organophosphorus poisoning and non-availability of intensive care unit (ICU) facilities.²⁹ In our study the mean Sr. cholinesterase level was higher among the survivors as compared to the deaths. This difference in the mean Sr. cholinesterase levels and outcome was statistically significant. According to Turabi A et al.,³⁰ out of 1999 patients, 899 (44.97%) showed lower levels of serum cholinesterase. Mortality in the present study was less as compared to study conducted by Agarwal S B et al.,³¹ Lower serum cholinesterase levels were associated with higher requirement for ventilatory support (p= 0.02) as well as longer average duration of ICU stay(p<0.001) among the cases that experienced mortality. Overall, in our study the factors that independently predicted mortality among the Organophosphorus poisoning patients included greater time interval from consumption to hospitalization (p = 0.035) and higher quantity of the OP compound consumed. New policies for educating the public especially of rural areas about the dangerous life-threatening effects of Organophosphorus compounds could help ameliorate the harmful effects of such poisoning and be an effective prevention strategy for reducing its incidence.

CONCLUSION

Mortality was higher cases, present late, delay in initiation of treatment and consumed larger amounts of Organophosphorus compounds. Lower serum cholinesterase levels correlated well with requirement of ventilatory support, increased duration of Intensive care unit stay and outcome.

REFERENCES

1. Zhao X,WuC, WangY, CangT, Chen L, Yu R,etal.Assessment oftoxicity risk of insecticides usedin riceecosystem on TrichogrammaJaponicum, an egg parasitoid of rice lepidopterans. J Econ Entomol. Feb2012;105(1):92-101.
2. Chen SW, Gao YY, Zhou NN, LiuJ, Huang WT, Hui L, et al. Carbamates of4'-Bioorg MedChemLett.Dec152011;21(24):7355-8.
3. WHO 2008 Clinical Management of Acute Pesticide Intoxication: Prevention of Suicidal Behaviours. Accessed 04^th Oct 2020 Available at: https://www.who.int/mentalhealth/prevention/suicide/pesticidesintoxication.pdf?ua=1
4. Ferrando F. Pesticide poisoning in the Asia-Pacific region and the role of a regional information network. Clinical toxicology 1995;33:677-682.
5. Massoulié J, Pezzementi L, Bon S, Krejci E, Vallette F-M. Molecular and cellular biology of cholinesterases. Progress in neurobiology.1993;41(1):31-91.
6. Gaspari RJ, Paydarfar D. Pathophysiology of respiratory failure following acute dichlorvos poisoning in a rodent model. Neurotoxicology. 2007;28(3):664-71.
7. Barr D B, Allen R, Olsson A O, Bravo R, Caltabiano L M, Montesano A, et al. Concentrations of selective metabolites of organophosphorus pesticides in the United States population. Environmental research. 2005;99(3):314-26.
8. Indira M, Andrews MA, Rakesh TP. Incidence, predictors, and outcome of intermediate syndrome in cholinergic insecticide poisoning: a prospective observational cohort study. Clinical toxicology (Philadelphia, Pa).2013;51(9):838-45
9. Rodgers M L.OP poisoning. Am J Emerg Med. 2006 :22:335-44.
10. Gupta SK, Peshin SS, Srivastava A, Kaleekal T, Pandian TV. An epidemiological pattern of poisoning in India. Pharmacoepidemiol Drug Saf. 2002;11:73-4.
11. Patil Virendra C. Clinical Profile and Outcome of Organophosphorus Poisoning at Tertiary Care Centre in Western Maharashtra. Indian J Forensic Med Toxicol. 2012; 6 (2) :23.
12. Peter JV, Sudarsan TI, Moran JL. Clinical features of organophosphate poisoning: A re view of different classification systems and approaches. Indian J Crit Care Med. 2014;18(11):735-745.
13. Malik G.M., Organophosphorus Poisoning in the Kashmir Valley, 1994 to 1997 , NEJM, 1998 Vol. 338:1078-1079, No.15.
14. Tanuj K, Mnezes RG. Suicidal poisoning in southern India : gender differences. Journal of forensic and legal Medicine 2008;15(7)10-18.
15. Kar SM, Timsinha S, Agrawal P. An Epidemiological study of Organophosphorus Poisoning at Manipal Teaching Hospital, Pokhara, Nepal. Journal of Indian Academy of Forensic Medicine. 2010;32(2):108-9.
16. Gannur D G, Maka P, Narayan Reddy KS. Organophosphorus compound poisoning in Gulbarga region -A five-year study. Indian Journal of Forensic Medicine and Toxicology. 2008;2(1).
17. Padmanabha TS, Gumma K, Kulkarni GP. Study of profile of organophosphorus poisoning cases in a tertiary care hospital, North Karnataka, Bidar, India. Int J Pharma Bio Sci. 2014;5(1):332-9.
18. Joshi SC, Prakash C, Joshi A, Joshi G. Profile of organophosphorus poisoning at tertiary care hospital in Uttarakhand. J Indian Academy Forensic Med. 2013; 35(4):346-8.
19. Shah N, Mundhra S. Clinical profile of organophosphate poisoning at a tertiary care center. Int J Med Sci Public Health. 2016; 5(8):1621-5.
20. Gagarin P, Rajagopal R. Clinical role and outcome of organophosphorus poisoning in a tertiary care centre, a prospective observational study. International Journal of Medical Research and Review 2020; 8(2):148-53.
21. Banerjee I, Tripathi S, Roy AS. Clinico-epidemiological characteristics of patients presenting with organophosphorus poisoning. N Am J Med Sci.2012;4(3):147-150
22. Banday TH, Tathineni B, Desai MS, Naik V. Predictors of Morbidity and Mortality in Organophosphorus Poisoning: A Case Study in Rural Hospital in Karnataka, India. Nam J Med Sci. 2015;7(6): 259-265.
23. Emerson GM, Gray NM, Jelinek GA, Mountain D, Mead HJ. Organophosphate poisoning in Perth, Western Australia, 1987– 1996. JEmergMed1998;17(2):273–7.
24. Suleman MI, Jibran R, Rai M. The analysis of organophosphate poisoning case treated at Bhawal Victoria Hospital, Bahawalpur 2000-2003. Pak JMedSci.2006;22:244–9.
25. Safdar A, Saeed A, Muhammad NR. Organophosphorus poisoning: Emergency management in intensive care unit. Prof . 2003;10:308–14.
26. Chugh SN, Aggarwal N, Dabla S, Chhabra B. Comparative evaluation of “atropine alone” and “atropine with pralidoxime (PAM)” in the management of organophosphorus poisoning. J Indian Acad Clin Med2005;6(1):33–7.
27. Yamashita M, Yamashita M, Tanaka J, Ando Y. Human mortality in organophosphate poisonings. Vet HumToxicol 1997;39:84-5.
28. Wadia RS. Treatment of organophosphate poisoning. Indian J Crit Care Med. 2003;17:85–7.
29. Numidasa UA, GawarammanaI B, Kularatne SA, Kumarasiri PV, Goonasekera CD. Survival pattern in patients with acute organophosphate poisoning receiving intensive care. J Toxicol Clin Toxicol. 2004;42:343–7.
30. Turabi A. Poisoning cases in and around Karachi and their Management along with Medico legal Aspects. University of Karachi. 2004.
31. Agarwal SB, Bhatnagar VK, Agarwal A, Agarwal U, Venkaiah K, Nigam SK,et al. Impairment in clinical indices in acute organophosphate insecticide poisoning Patients in India. The Internet Journal of Toxicology.2007;4(1).