North American Journal of Medical Sciences

: 2015  |  Volume : 7  |  Issue : 6  |  Page : 259--265

Predictors of morbidity and mortality in organophosphorus poisoning: A case study in rural hospital in Karnataka, India

Tanveer Hassan Banday1, Bharath Tathineni1, Mehul Surendra Desai2, Vikas Naik1,  
1 Department of Medicine, Adichunchanagiri Institute of Medical Sciences and Research, Bangalore, Karnataka, India
2 Vydehi Institute of Medical Sciences and Research Centre, Bangalore, Karnataka, India

Correspondence Address:
Tanveer Hassan Banday
Fellowship in Medical Gastroenterology, Adichunchingiri Institute of Medical Sciences and Research Centre, Mandya - 571 418, Karnataka


Background: Organophosphorus (OP) pesticides poisoning can result from occupational, accidental or intentional exposure. Clinical manifestations include cholinergic syndromes, central nervous (CNS) system and cardiovascular disorders. Death is usually due to cardiovascular and respiratory failure. Aim: To evaluate various parameters that can predict outcome of patients in OP poisoning. Materials and Methods: A prospective study conducted in Department of Medicine, Adichunchingiri Institute Of medical Sciences and Research Centre, Karnataka, over period of 1 year. Diagnosis of OP poisoning was based on clinical history of exposure to OP compound and low serum pseudocholinesterase levels. Results: In the present study 133 patients were enrolled, out of which 98.5% were suicidal cases and only 1.5% had accidental exposure. Majority of cases were young male, with F/M ratio 1:3.2. Mortality rates were higher in younger people and in patients who required prolonged ventilator support. The mortality rate was directly proportional to amount of poison consumed, lag time, organ failure (Acute Renal Failure) and plasma pseudocholinesterase levels. Acute complications were frequently noted and were related to morbidity and mortality. No strict relationship was found between liver dysfunction, electrolyte disturbance and clinical outcome. Conclusion: This case study concluded that mortality is directly proportionate to the lag time, amount of OP substances consumed, clinical severity, pseudocholinesterase levels, Acute renal failure and duration of ventilatory support. This study highlights the importance of rapid diagnosis, and initiation of early and effective treatment, which may result in less number complications and also decreases the mortality rates.

How to cite this article:
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.North Am J Med Sci 2015;7:259-265

How to cite this URL:
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. North Am J Med Sci [serial online] 2015 [cited 2022 May 23 ];7:259-265
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Full Text


Organophosphate compounds are widely used as pesticides in agricultural parts of the world. [1] Toxicity of organophosphates is the result of excessive cholinergic stimulation through inhibition of acetylcholinesterase.

Serum cholinesterase level is depressed after organophosphorus (OP) poisoning, as reported by previous various studies. Confirmation of organophosphate poisoning is based on the measurement of cholinesterase activity. Although red blood cell (RBC) and plasma pseudocholinesterase levels can both be used, RBC cholinesterase correlates better with central nervous system (CNS). Acetylcholinesterase is, therefore, a more useful marker for organophosphate poisoning. [2] The rapid accumulation of acetylcholine in the synaptic junctions of CNS and peripheral tissues results in a cholinergic crisis, characterized by range of muscarinic, nicotinic and central effects. [2]

Gastric mucosa is permeable to organophosphates, and is a classical way of absorption in suicidal cases. Liver is the organ where activation and detoxification of organophosphate compound takes place, but they are eliminated primarily through kidneys. [3]

Clinical manifestations are broadly classified into muscarinic and nicotinic which include; bradycardia, hypotension (Muscarinic), tachycardia (nicotinic), increased salivation/lacrimation, excessive sweating, nausea, vomiting, diarrhea, pain abdomen, fecal and urinary incontinence. [4] CNS manifestations include anxiety, restlessness, convulsion, miosis, insomnia, coma, cheyne-stokes breathing, respiratory and cardiovascular failure. [5]

Intermediate syndrome or type II paralysis usually occurs after 24-96 hours after acute cholinergic crisis. Incidence of Intermediate syndrome varies from 8-50%. [6] Chronic OP poisoning can cause organophosphate-induced delayed neuropathy and is seen mostly in agricultural workers. [7]

The initial management of acute OP poisoning includes cardio respiratory stabilization, decontamination (removal of clothes for possible source of continued exposure in occupational intoxication), irrigation of skin and eyes as well as gastric lavage and activated charcoal to minimize absorption of the OP compound. [8] The mainstay of treatment involves atropine - A central and peripheral muscarinic receptor antagonist and pralidoxime chloride, which reactivates inhibited acetyl cholinesterase. [9] In recent years new adjunct therapy and cheap medications such as sodium bicarbonate, magnesium sulfate as well as antioxidants have been considered for the management of OP poisoning. [10] Death is usually occurs due to cardiovascular and respiratory failure, paralysis of respiratory muscles and obstruction caused by bronchospasm and bronchial secretions. [11]

 Materials and Methods

We enrolled 133 patients in a prospective study which was conducted in Department of Medicine, Adichunchingiri medical college, Bangalore from July 2013 to June 2014. Institute ethical committee approved the study. All patients of OP poisoning were included in this study. However, we excluded those patients in whom OP poisoning was doubtful. Detailed history was taken from all the patients' relatives about the circumstances of poisoning. Detailed clinical examination of the patients was done. Diagnosis of OP poisoning was based on clinical features, history of exposure to a known OP compound and was supported by low serum pseudocholinesterase levels. Patients were treated as per the standard protocol of organophosphate poisoning with respiratory support, atropine and pralidoxime. All patients were dealt up to recovery or death from poisoning. Psychiatric consultation was done in all the cases that recovered, before discharging them from the hospital.

Baseline investigations included complete blood hemogram, urea, creatinine, arterial blood gas values, X-ray chest and serum pseudo-cholinesterase level. Data was retrieved from the files on a structured proforma. Studied variables included gender, age, amount of organophosphate consumed, mode of exposure, time lag in starting treatment, duration of ventilator support and hospital stay, acute complications and outcome of patients .

Type of organophosphorus compound consumed

We could identify the type OP compound in most of the cases, patient attenders would bring the bottle of OP compound, that patient would have consumed, to our Emergency department. The various types of OP substances consumed in the present study are as follows.

Diethomate (N = 33), chloropyrifos (N = 15), Quinalophos (N = 12), Acetamide (N = 1), dichlorrofos (N = 5), Dicofol (N = 1), Emamectin, endosulfan (N = 1), Ethiophos (N = 2), Glycophosate (N = 1), carbosulfan (N = 1), methylparathion (N = 3), Monocrotophos (N = 5), Phorate (N = 1), profens (N = 3), Profenofos (N = 2), Profenofos/cypromethrin (N = 1), Unknown OP compound (N = 45), Dermal exposure (N = 2).


Serum pseudocholinesterase level was estimated at the time of admission in all the patients by DGKC method (LiquiChek). The laboratory reference range of pseudocholinesterase used in the present study was Female = 3930-10800/l, male 4620-11500 u/l. Based on the serum pseudocholinesterase levels, the severity of poisoning was defined as per Kumar et al. [ 12]

Mild poisoning: Pseudocholinesterase level 20-50% of normal or >1,401-3,500 IU/L.

Moderate poisoning: Pseudocholinesterase level 10-20% of normal or 701-1, 400 IU/L.

Severe poisoning: Pseudocholinesterase level is <10% of normal or < 700 IU/L.

Statistical study

Data were presented either as mean ± standard deviation (SD) or as percentage. Probability values of P < 0.05 were considered significant, and all statistical analyses were performed using SPSS version 12.0. Fisher's exact test was used for categorical data.


In present study, 133 cases of OP poisoning were admitted during the study period [Table 1]. One thirty one (98.5%) patients ingested the compound and only two patients (1.5%) had dermal/inhaled exposure while spraying pesticides in rice fields [Table 1]. One hundred two (76.7%) were males and 31 (23.3%) female. Most of the cases were young people 80% (< 40years) predominantly males [Table 1]. There was wide variation in age ranging from a minimum of 13-68 years with mean age of 31.5 years [Table 2].{Table 1}{Table 2}

Forty eight patients (36.1%) out of 133 were stable after gastric lavage. They were kept under observation for the next 3 days and finally discharged. The clinical presentation of acute poisoning was variable as shown in [Table 3]. However, the most consistent feature was miosis (93.2%). Eighteen (13.5%) patients developed episodic convulsions. Transient elevation in liver enzymes were noticed in 13.5% patients [Table 3]. However, no significant increase in morbidity/mortality was seen in patients with hypokalemia or deranged liver function test [P > 0.05, [Table 4]. Patient who developed single /multi-organ failure had increased mortality [P < 0.0001, statistically highly significant [Table 4].{Table 3}{Table 4}

Fifty three patients required ventilatory support, out of which only 11 patients survived [Table 5]. Patients were on ventilator support for minimum 1 day to maximum 22 days with a mean 6.85 ± 4.32 days [Table 2]. Mortality was higher in patients who required ventilator support >7 days [P < 0.05 statistically significant, [Table 5].{Table 5}

The amount of OP compound consumed ranges from 10 ml to maximum 200 ml with mean 77.5 [Table 2]. The mortality rate was directly proportional to the amount of poison consumed [P < 0.00003 statistically significant, [Table 5].

The lag time for initiation of treatment was minimum 1.02 hours to maximum 9.57 hours with mean 4.65 ± 2.4 [Table 2]. Mortality rate was higher in patients with lag time > 6.5 hours [P < 0.05, [Table 5].

Twenty-one out of 133 (15.7%) developed derangement in renal function tests (defined as serum creatinine >1.4). In most of cases, derangement of the renal function was reversible and renal function tests improved within a week. However, increased mortality was seen in patients with serum creatinine >3.5 mg/dl [P < 0.05, [Table 5]. Out of three cases that had irreversible renal failure, one case had serum creatinine of 10.2 mg/dl on day of admission with severe metabolic acidosis and he died on the same day due to cardiac arrest. Rest of the two cases with Acute renal failure died within a week's time.

The overall mortality rate was 33.3% (42 out of 126 patients) and seven cases (5.2%) were discharged against medical advice [Table 1]. Delayed complications like mild sensory loss of lower limbs or weakness of limbs were uncommon in our patients on follow-up.


OP compounds were synthesized by von Hoffman. OP pesticide poisoning is common in developing worlds. [11] The highest incidence is seen in India. [13] Suicidal and non-suicidal organophosphate poisoning is a major problem in rural areas of India, with rapidly increasing incidence rate. [14]

In our study the female to male ratio is 1:3.2. In the present study, the incidence of poisoning was higher in males than in females (76.6% Vs. 23.3%). Similar trend was also observed by Safdar et al., [15] and Aziza et al. [16] However, the female to male ratio given by Ather et al., is 1:1 and Tall et al., is 1:1.8 which is quite different from present study. [17],[18]

The age ranged from 13-68 years with mean age was 31.5 years. However, Hayden et al., [19] showed age range from 13-47 years with a mean age of 23 years. In the present study, the incidence of OP poisoning, was highest in patients aged less than 40 years. Majority of the cases (80%) were young people, predominantly males from the age group 13-40 years, this is comparable to other studies as done by Khan MN et al., [20] in which maximum number of patients were between 15-35 years of age. The people in this age group are described to be the most ambitious and more vulnerable to various emotional conflicts that may occur during this phase of life. Our observation was similar to the previous studies that showed the highest incidence of OP poisoning in people aged between 21-39 years. [21]

In our study, the incidence of suicidal poisoning is 98.6%, probably because it is cheap, easily available and used as a major pesticide in agricultural farming throughout India. This was in agreement with other studies [16],[22] which showed deliberate self-poisoning varying from 68-96%. In the study by Aziza et al., [16] 76.92% cases were suicidal and 23.07% were accidental.

The present study found that the level of serum pseudocholinesterase levels on the day of presentation was reduced in majority of cases of OP poisoning. Also it was observed that the need for intubation and oxygen requirement were more in moderate to severe cases with pseudocholinesterase <1400 U/L. In addition mortality was highest in cases with pseudocholinesterase <700 U/L (P < 0.05). This showed a significant association of rate of mortality with the serum pseudocholinesterase levels. Similar to our finding, Mehta et al., [23] observed lower activity of pseudocholinesterase in more than 70% of cases at presentation. Goswamy et al. [24] , concluded that apart from clinical indicators, low serum cholinesterase levels were of greatest predictive value for ventilation in OP poisoning. However, Nouira et al. [25] did not find any statistically significant difference in mean serum cholinesterase levels in those mechanically ventilated and those do not need ventilator support.

Hypokalemia, hyperglycemia, acute renal failure, transient elevation of liver enzymes can occur in OP poisoning. [26] In our study, hypokalemia and transient elevation of liver enzymes were found in 15.03% and 13.5 % of cases respectively. Wang WZ et al. [27] observed that liver injury was seen in 9.8% and 5.17% of cases and control group, respectively in OP poisoning and mortality was higher in cases than controls (22.5% vs 6.32%). However, we failed to document a strict relationship between derangement of serum potassium and liver enzymes with the severity of OP poisoning and clinical outcome (P > 0.05).

Acute renal failure was reported following exposure to OP poisoning in 15.03% of patients. Eighteen patients out of twenty one cases, had transient reversible acute renal failure and three cases (2.2%) had irreversible renal failure. Mortality was higher in patients with acute irreversible renal failure (serum creatinine >3.5 mg/dl). Arefi M et al. [28] in their study found 16.7% of OP poisoning had renal failure which is similar to our study. Similarly, S panda et al. [29] observed altered renal function between the survivors and non survivors suggesting their importance in predicting mortality. The transient renal injury may be due to both a direct action of the organophosphate, causing tubular cell necrosis or secondary mechanism that followed the cholinergic crisis, causing hypovolemic shock and rhabdomyolysis.

The most frequent signs noted in this study were miosis 93.2%, increased salivation 86.4%, anxiety and restlessness 82.7%, bronchospasm 78.2% and incontinence in 58.6%. Other frequent clinical features noted in this study are mentioned in [Table 3] with percentages, also comparable with other studies. [30],[31] In the present study there were 33.8% cases of presented with altered sensorium or loss of conscious, in majority of cases it was subsequently followed by deep coma. Sequeira et al. [32] showed the frequency of deep coma to be 21%. Acute complications seen in this study were episodic convulsions in (13.5%) patients, severe bradycardia (24.8%), hypotension (11.3%) patients. Serious ventricular arrhythmias were not observed. Acute complications [33] were bradycardia in 29 (93.5%), change in mental status in 10 (32.2%), low oxygen saturation (less than 90%) in 21 (67.8%) and subsequent convulsions in 3 (9.6%).

The duration of mechanical ventilation in our patients was 6.857 ± 4.32 days. In the present study, the mortality was highest in patients requiring mechanical ventilation for more than 7 days (P < 0.05), probably due to lung complications from prolonged mechanical ventilation and increased lag time. The high mortality in patients ventilated for <2 days and between 2-7days is most probably due to the severity of poisoning. [8] The mortality following OP poisoning varies from 4-30%. [34] In a study by Safdar et al., [15] 4% of patients who received mechanical ventilator support ultimately expired. In another study, mortality was 50% in patients requiring mechanical ventilation. [22] In contrast to these observations, Aziza et al. [16] reported 8% mortality in patients who received mechanical ventilation.

In our study, it became evident also that most of patients who expired, there was a delay (maximum 9.57 hours) between consumption of OP substance and initiation of treatment, which is also supported by study done by Suleman MI et al. [35] 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. [8]

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, [Table 5]. In present study, morbidity and mortality was proportionately higher in majority of patients who developed single/mutli-organ failure and required prolonged ventilatory support (P < 0.05, [Table 4]. In our study, overall mortality rate was 33.3%, which is higher than shown in a study done by Numidasa UA et al., [36] and Pandyal BP et al. [37] However, frequency of mortality due to organophosphates given by Yamashita et al., [34] varied between 4% and 30% and 5.5% in a study by Malik et al.[33] 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 OP poisoning and non availability of intensive care unit (ICU) facilities. [36]


OP poisonings is common in developing worlds and is of great concern, since it affects the most productive age group of the society. OP poisoning has become an agent of choice for self-poisoning because of its easy availability and low-cost factor especially in rural India. In OP poisonings, acute complications are seen more frequently than chronic complication. Mortality and morbidity are directly proportionate to the lag time in initiation of treatment and/or amount of OP substances consumed, clinical severity (single/multiorgan failure) and duration of ventilatory support. Mortality is also higher in patients who immediately develop acute complications like severe bradycardia and severe acute renal failure. Although each predictor (age, lag time, severity of poisoning, amount of organophosphate consumed, organ failure, acute kidney injury and duration of ventilation) is associated with mortality, death due to organophosphate poisoning results from overlapping contribution of these factors. No single factor is independently responsible for mortality in these patients. Therefore, the importance of rapid diagnosis, early and effective treatment should not be overlooked because patients who receive early and effective treatment generally do better and have less complications and decreased morbidity and mortality rate. Good supportive and ICU care cannot only reduce the frequency of acute or chronic complications, but will also decrease mortality rate in these cases.


We thank Dr. Vasudav Naik for guiding us throughout the study.


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