IJCRR - 10(5), March, 2018
Pages: 39-45
Date of Publication: 15-Mar-2018
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Profile of Poisoning at a Tertiary Care Hospital in Haryana
Author: Navtej Singh, Tarun Arora, Jyotsna Singh
Category: Healthcare
Abstract:Introduction: Poisonings continues to be a frequent reason for admission to hospitals and intensive care units in the developing countries. The fatal issue is often related to delay in diagnosis and improper management.
Aim: The purpose of the study is to report the morbidity, mortality and survival pattern of poisoning cases received at a tertiary care centre at Haryana. The focus was also in depicting the signs and symptoms of various poisoning for early diagnosis.
Methods: This was a retrospective study consisting of patients admitted with poisoning during the period January 2017 to December 2017, in a tertiary care centre in Haryana. Total of 200 patients admitted with poisoning were analyzed. Diagnosis was made on basis of history of exposure and characteristic clinical picture, with emphasis given to age, sex, month of year, motive of poisoning, type of compound, clinical presentation and final outcome of poisoning
Results: Among the 200 cases, 127 (63.5%) cases of aluminium phosphide and 58 (29%) cases of organophosphate poisoning were observed. Few cases of tricyclic antidepressents poisoning (2%), zinc phosphide poisoning (2%) herbicide (2.5%), phenol and transfluthrin (all out) ingestion(0.5%) each were reported. The most common motive of poisoning (95.5%) was with a suicidal intent. Out of the 200 poisoning cases 146(73%) cases admitted survived on treatment and a mortality rate of 27% was reported. 90.7% of the deaths were due to aluminium poisoning ingestion, while mortality due to organophosphate poisoning was just 7.4%. Maximum cases were observed in the age-group of 21-30 years which holds 72 (36%) cases followed by 49 (26%) cases in 31-40 years. Males outnumbered females in every age group. 92.5% of the cases were from rural background, while only 7.5% of the urban inhabitants were affected by poisoning.
Conclusion: Aluminium phosphide ingestion is the leading cause of deaths due to poisonings observed in Haryana, predominantly seen in youths residing in rural areas with male preponderance. Low cost of these compounds, easy availability at peak moments of frustration; due to marital discord, poor economic growth has pushed up the incidence of self poisoning. Hence up gradation of primary health care facilities to render immediate management of these poisoning cases could go a long way in helping to reduce mortality and morbidity.
Keywords: Poisoning, Aluminium phosphide, Organophosphate, Suicidal
DOI: 10.7324/IJCRR.2018.1057
Full Text:
Introduction
Poisoning among all age groups and both sexes is known worldwide. Poisoning accidental or intentional is significant contributor to mortality and morbidity all over the world. According to WHO pesticide self poisoning or accidental exposure is responsible for afflicting 300.000 people every year with 22000 deaths in developing countries especially those from rural background. 1 India being an agriculture based country use of pesticides, rodenticides and herbicides remain the main agent of pest control and crop protection. Low cost, easy availability, efficacy of action and rapid death have made these compounds the agent of choice for self poisoning. 2 It has been estimated that 5-6 persons per lakh of population die due to poisoning every year in India. This figure could just be the tip of the iceberg since most cases of poisoning actually go unreported. High mortality could be due to lack of hospital services in the vicinity, delayed transport ,non availability of specific antidote, and increased patient to care givers ratio or an improper management.3
Aluminium Phosphide (AIP) commonly known as celphos or wheat pill is used to preserve grains all over the world, is one of the dreaded poisons encountered in toxicology. AIP when ingested releases phosphine gas on contact with moist surfaces or HCL that causes cell hypoxia due to inhibition of oxidative phosphorylation leading to circulatory failure.4 Patients can present clinically with gastrointestinal hemorrhage, arrhythmias, shock, renal, and hepatic failure and CNS disturbances. Patients remain mentally clear till cerebral anoxia due to shock supervenes resulting in coma. ECG changes ranging from ST segment elevation or depression, PR and QRS interval prolongation, complete heart block and fibrillation has been observed. Toxic chemical myocardial inflammation manifests as depressed left ventricular ejection fraction. Treatment of AIP poisoning is mainly supportive and there is no specific antidote. Mortality with AIP poisoning is very high, almost100%.5
Organophosphate compound (OPC) a common pesticide used in agriculture for crop protection is implicated in accidental and suicidal poisoning with 4-30% mortality in Indian studies.1 Acetylcholine is a neurotransmitter present at the neuromuscular junction in peripheral and central nervous systems. Acetylcholineesterase (AChE) is an enzyme that hydrolyses and breaks down acetylcholine. Organophosphate compounds cause phosphorylation and inactivation of this enzyme leading to accumulation of acetylcholine. The inhibition of AChE with subsequent accumulation of acetylcholine at synapses results in overstimulation and disruption of neuronal endings in both central and peripheral nervous system. Complications of OPC poisoning include aspiration of gastrointestinal contents, excessive secretions, neuromuscular involvement, intermediate syndrome, septicemia and adult respiratory distress syndrome. 6,7 The fatal issue is often related to delay in diagnosis and improper management. Management is severe poisoning is difficult requires intensive care management with atropine and oxime cholinesterase reactivators. Key to survival lies in early diagnosis followed by rapid decontamination and definitive therapy.
Zinc phosphide a rodenticide, dark grey crystalline compound used to kill field mice and rat. It reacts with water and gets converted to phosphine gas in the body on ingestion in the stomach. Zinc phosphide is used widely by young members of society for suicidal attempts.8 The clinical symptoms arise due to metabolic and non metabolic effects of phosphine gas and manifest as hypotension, shock, pericarditis, pulmonary edema and congestive heart failure.9 The mortality rate varies from 37%-100% as no antidote is currently available nor a specific treatment protocol has been provided. Gastric flushing and charcoal treatment only is recommended. Apart from gastrointestinal symptoms, Chug et al.199810 reported in their studies that oliguria, coma, convulsions, hepatotoxicity and thrombocytopenia could be seen in zinc phosphide poisoning. Due to extent of damage to lungs and heart patients are lost at early stages.
Phenol (carbolic acid) is an oldest antiseptic agent used in households for cleansing floors. Phenol is a protoplasmic poison with corrosive local effects. Phenol when ingested causes extensive local corrosions. Excruciating pain, nausea vomiting, sweating and diarrhea are the presenting symptoms. Severe GIT burns and strictures are its long term complications. Systemic manifestations develop after 5-30 minutes post ingestion producing hypotension, tachycardia/ bradycardia, dysarrythmias , seizures acidosis hemolysis, meth-haemoglobinemia and shock. Dose is between3-30gram is lethal.11 Early medical intervention following immediate medical evaluation helps in survival. Gastric lavage is not recommended if phenol is ingested. Immediate administration of olive oil and activated charcoal by nasogastric tube is necessary. Decontamination of skin and eyes with copius amount of water followed by undiluted polyethylene glycol is recommended. Intravenous fluid administration and dopamine infusions can be lifesaving. Arrhythmias are corrected with lidocaine infusion, convulsions with diazepam.12
Deaths due to tricyclic antidepressant (TCA) poisoning is due to arrhythmias or hypotension mainly due to quinidine like actions on heart tissues.13 TCA are extensively used for management of depression and other psychiatric diseases.TCA poisoning caused by excessive medication accounts for 270 deaths per year in the United Kingdom. Symptoms include elevated body temperature, blurred vision, dilated pupils, sleepiness, confusion seizures and rapid heart rate even cardiac arrest. Seizures and coma are common complications. Fatality is a result of cardiovascular toxicity. Prompt transport of patient to the nearest emergency department is implicit. Sodium bicarbonate is still considered the treatment of choice apart from supportive management.14
Since there is paucity of literature regarding poisoning in Haryana, this particular observational study was undertaken. Aim to predict morbidity, mortality and survival pattern of poisoning. An attempt has been made to provide recommendations for treatment and prevention of death by poisons on rampage in Haryana.
Materials and methods
The study constituted patients with poisoning admitted to intensive care unit between January 2017 to December 2017 at BPS Government Medical College for Women, Sonepat, Haryana a referral tertiary care center. Ethical clearance was obtained from hospital administration for disclosure of record details only for academic purpose. However, confidentiality was maintained as neither name or CR number of the patient was documented. A total of 200 poisoning cases were analyzed during this period. Diagnosis was made on basis of history of exposure and characteristic clinical picture. Plasma cholinesterase levels could not be analyzed because of non-availability in the hospital. Data was collected from all poisoning cases in a detailed performa as per history given by the patient or relatives, with emphasis given to age, sex, month of year, motive of poisoning, type of compound, clinical presentation and final outcome.
Treatment was started as per the hospital protocol for managing patients of poisoning. The body was washed with soap and water after removal of clothes. Nasogastric tube was passed to decompress the stomach and gastric lavage was done in all the patients. Patients of OPC poisoning were treated with atropine, pralidoxime and respiratory support if required. A loading dose of 3 mg of atropine was given immediately followed by a maintenance dose of 8 mg hourly until target end point of atropination was achieved documented by (1) a clear chest on auscultation with no wheeze (2) heart rate of >72 /min and (3) Dilated pupils. PAM was administered with a bolus of 2gm over a period of 4 hours. Patient with Glasgow coma scale of less than 8 with hypoxia were intubated and mechanically ventilated.
Patients with aluminium phosphide poisonings were confirmed by history and typical odour of the compound. Airway protection was given before gastric lavage. Gastric lavage with diluted potassium permanganate, coconut oil, sodium bicarbonate and activated charcoal was performed. Supportive treatment with IV fluids, magnesium sulfate infusion was given. Vasopressors and ionotropic drugs were administered in patients with hypotension. Patients with unstable hemodynamic were mechanically ventilated. Monitoring of hemodynamic parameters, urine output , arterial blood gases and blood pressure was regularly done in all patients of poisoning . All patients were dealt up to recovery or death from poisoning.
Results
A total of 200 cases of poisoning due to various compounds were registered during the study period from January 2017 to December 2017 in the emergency department.
The socio-demographic profile of the patients is as follows. The age of the patients varied from 11 to 75 years. Maximum cases were observed in the age-group of 21-30 years which holds 72 (36%) cases followed by 49 (26%) cases in 31-40 years and 18.5% of poisoning cases in 11-20 years age group. Males outnumbered females in every age group except above 71 years and above. Male to female ratio is 2.33:1. The most striking feature was observed in 51-60 years age group male to female ratio afflicted by poisoning was highest10:1 as given in the Table 1.
The above table shows that meiosis and blurred vision was the most common manifestation found in 101(79.5%) of the total 127 cases of OPC poisoning. The peripheral muscarinic (SLUDGE) symptoms occurred acutely within minutes. Salivation however was observed in only 5.5% of the cases. Lacrimation, Diarrhea, diaphoresis was seen in 15.7% of the cases on presentation. Urination was not found as a presenting symptom in either of the cases. Nausea and vomiting was the next common presenting symptom found among 57 out of the 127 OPC cases. Respiratory symptoms followed next in the table with 40% presentation as wheezing. Nicotinic effects of OPC poison resulted in hypertension in 45(35.4%) and paralysis in 7(5%) cases. 12 cases were received in an unconscious state. Seizures were reported in 5 cases only.
Intermediate Syndrome (IMS) develops 24-96 hours after exposure and reflects a prolonged action of acetylcholine on the nicotine receptors. The clinical features are muscular weakness in the ocular, neck, bulbar, proximal limb and respiratory muscles. The risk of mortality is due to the associated respiratory depression. Most patients with intermediate syndrome develop respiratory failure, which requires mechanical ventilation.10% cases required ventilatory support. OPC poisoning resulted in a mortality rate of 7%. Following atropinization 20% cases reported toxic psychosis after treatment.
Out of the 5 cases of herbicide poisoning received, isopropyl salt of glycophosphate was ingested by 3 cases and 2-D aminosalt 58,52 24-D poisoning was seen in the rest. Herbicides present OPC and carbamate like poisoning. All cases presented with nausea and repeated vomiting. Seizures was observed in one patient who failed to survive on ventilatory support.
Gastrointestinal symptoms are usually first to appear after exposure to celphos or AIP poison. Nausea and vomiting occurred in all the cases however abdominal pain and diarrhea was not reported among any . 76.2% of the cases had hypotension on arrival in emergency along with GI symptoms. 19(32.7%) cases were received in an unconscious state.6 cases presented with respiratory difficulty and had lung crepts. 33(57%) cases had multiorgan dysfunction on hospital presentation. 9 cases were put on ventilator support.
Discussion
Poisoning is a health hazard and the preferred means of committing suicide in males and females in India. The common causative factors which led to self poisoning were marital disharmony, poor economic conditions and disagreement with family members.15
Interesting change in trend and nature of poisoning has been observed. Among the 200 cases of poisoning,127(63.5%) cases of AIP poisoning and 58(29%) cases of OPC poisoning have been observed. New chemicals such as tricyclic antidepressents (2%) and zinc phosphide (2%) herbicide(2.5%), phenol and transfluthrin (0.5%) being consumed with a suicidal intent has been observed in the present study. In contrast other studies1,2,3,7 have reported organophosphates form the largest bulk of pesticide poisoning. Gargi et al 200316, at Amritsar found the poisonings with organophosphate among 17.64% and aluminium phosphide in 38.23% cases. A similar study done in the Haryana-Rohtak belt by Siwach SB et al17 in 1995 observed aluminium phosphide as the most commonly abused substance followed by OPC and zinc phosphide in 67.8,13.9 and 4.3% cases respectively.
In the present study the victims involved were maximum seen in the 3rd decade, 72 cases(36%) followed by 49(24.5%) cases in the 4th , 37 cases in the 1st (18.5%)and 23 cases (11.5%)in the 5th decade. Poisoning cases have been observed in the elderly individuals also 5.5% incidence in the 51-60 and 3.5% incidence in 61-70 year age group. 79% victims are the young population less than 40 years and 21% above 40 years of age in the present study similar to Syed MA et al. 2014,3 who observed 80.2% of the patients less than 40 years and 19.8% above 40 years. Gargi et al 2003,16 reported the incidence of poisoning of 45.5% in the 21-30 years age group and poisoning in younger population of 11-20 years at 18.5% in accordance with the present study.
Most of the poisoning cases were from rural areas of Haryana 92.5%, predominantly in the young population with male preponderance. Mean male female ratio being 2.33:1 a pattern similar to that reported elsewhere in India.1,2,7,15,16.
Villages are more affected by the menace and failure in the life and tolerance to life is better understood by the urban population in the present study in accordance with other studies.1,2,7 In contrast incidence of poisoning was observed higher in urban areas51.4%and lower in rural areas 45.59% by Gargi et al 2003.16
A season wise variation is seen in the present study, distribution is highest during the rainy , followed by summer season and least in winter season. In summer (March-May) 53 cases, Rainy season (June –August) 60 cases, Spring (Sept- Nov) 49 cases and 37 cases in the winter (Jan- Feb) were observed in the present study. Syed et al, 20143 recorded the highest incidence during summer , followed by rainy and least in spring season.
The present study is in unison with other recent studies that suicidal poisoning is the highest among the population.5,17 In the present study 95.5% cases with suicidal motive and 4.5% of accidental exposure to pesticides, have been observed similar to Syed et al 20143. In contrast a study by Gargi et al 200316, maximum cases were of accidental poisoining 44.4%, followed by 40.60% cases of suicidal poisoning and 3% homicidal poisonings were reported.
The overall mortality rate for OPC poisoning varies from 4%- 30%.18 In the present study mortality due to OPC poisoning was 6.8% similar to Safdar et al;200319. These patients had reported late to the tertiary care centre or developed lung complications on ventilator.
Deaths due to aluminium phosphide poisoning is under reported in Indian subcontinent with mortality varying from 37-100%, because of its easy availability since 1992.Mortality due to aluminium phosphide poisoning in the present study is 38.6% consistent with the literature. Out of the 127 cases of aluminium phosphide poisoning 49 cases who consumed fresh tablets of celphos died while remaining 78 cases consumed denatured tablets survived.
Most symptoms and signs in OP poisoning resulted due to excessive muscarinic stimulation in the present study consistent with previous studies. 10% of the patients developed intermediate syndrome in the present study. Reported frequency of intermediate syndrome varies from 8% to 49%. 2
Conclusion: Aluminium phosphide is the leading cause of deaths due to poisonings observed in Haryana, predominantly seen in youths residing in rural areas with male preponderance. Lack of education, poverty, stressful life, cheap and easy availability of these compounds were the reasons behind the poisoning. Hence upgradation of primary health care facilities to render immediate management of these poisoning cases could go a long way in helping to reduce mortality and morbidity. Strict implementation of pesticide act and new laws and legislations can be made by the government regarding the free sales of the chemical compounds. Social awareness regarding handling of these compounds and their lethal consequences is required at grass root level especially the rural population. Psychological counseling and educating the youth about the dangerous effects of poisoning should be undertaken by the government on priority basis. Alternatives to AIP or celphos and OPC which are less toxic should be developed by the horticulture department. The use of bio- pesticides, known for their purity, effectiveness and nontoxic nature should be promoted. Organic pesticides like salt spray, neem enriched sprays, mixture of chrysanthemum flower tea extract, mineral oil and citrus oils with cayenne pepper should be marketed by the government to reduce the health hazards Lab research should be taken to find specific antidote for aluminium phosphide poisoning.
Conflict of interest
The authors declare that they have no conflict of interest concerning this article. . No funding was required for data collection, data analysis and data interpretation of the stud
Acknowledgement
Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are grateful to authors/editors/publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
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