Vous êtes sur la page 1sur 5

Original Article

Morbidity, Mortality and Management of Wheat Pill Poisoning


Rabia Rathore and Muhammad Zafar Ullah Khan

Background: Suicide is one of the leading causes of death worldwide. People adopt different ways to commit suicide. Methods: We enrolled 50 patients presenting to emergency department, Mayo Hospital, Lahore with intake of wheat pills with suicidal intention. The end point was death, discharge or leaving hospital against medical advice. The study was designed to know the effects of wheat pill on various systems of the body and its outcome. Results: Of the total 50 patients studied, 28 (56%) were males and 22 (44%) were females. 35 (70%) patients died, 8 (16%) were discharged and 7 (14%) left against medical advice. Wheat pill containing Aluminium Phosphide is easily available, cheap and without any ban on its sale. General awareness about the lethal effects of its ingestion should be created among masses and efforts be made to impose legal restrictions on its sale. Conclusion: It can be concluded that wheat pill poisoning is becoming very common as a mode of committing suicide. Since wheat pill is highly toxic, mortality is significantly higher and painful. Wheat pill is freely available and very cheap so awareness should be created among rural areas and urban peripheries regarding its toxicity and high mortality. A legal ban should be imposed on its over the counter sales. Its possession should be authorized to personnel trained in proper storage and dispensing. Keywords: Suicide, Wheat pill, poisoning, arrhythmias, Aluminium Phosphide Introduction
Suicide is a Latin word, 'sui' means to kill oneself. It is an act of taking one's own life voluntarily and 1 intentionally. Suicide has been committed by people from all walks of life since the beginning of known history. Suicide is often interpreted as a cry for help and attention or to express despair and the wish to 2 escape rather than a genuine intent to die. Poisoning is a harmful effect that occurs when a toxic substance is swallowed, inhaled, or comes in contact with the skin, eyes or mucous membranes. The damage caused by poisoning depends on the poison, the amount utilized, the age, and the underlying health of the person who takes it. We chose to conduct this study in order to evaluate morbidity, mortality and outcome associated with the intake of wheat pills during the hospital stay.

having previous prostate surgery or history of stricture urethra were excluded from the study.
The parameters studied were patients' age, residual urine, traces of uroflowmetry, maximum flow rate (Qmax), average flow rate (Qave), flow time and voided volume.10-15 ml as equivocal and > 15 ml as unobstructed. SPSS version 15 was used for statistical analysis. For the significance level One sample T test

Wheat Pill Chemical composition


Aluminium Phosphide Inert ingredients Paraffin
3

= =

56 % 44 %

Use
Aluminium phosphide is an inorganic phosphide used to control insects and rodents in a variety of settings. It is mainly used as an indoor fumigant at crop transport, storage or processing facilities.4 It may be used as an out door fumigant for burrowing rodents and mole control.5

Material and Methods Computer record of uroflowmetry between March 2005 and February 2006 was checked. Patients above the age of 50, having IPSS >20 and post void micturitional residual urine less than 100 ml and voided urine volume greater than 150 ml were included in the study. Patients

Availability:
It is available in the form of pellets, tablets, porous 19

blister packs, sachets or powder. Mechanism of Action: Metal phosphides liberate Phosphine gas after coming in contact with moisture of grains or water or HCL of the stomach after ingestion. Other gases liberated are Ammonia (NH3) and Carbon dioxide (CO2).6 Pathophysiology: 1. It causes non-competitive inhibition of cytochrome e-oxidase leading to inhibition of mitochondrial oxidative phos phorylation which in turn leads to multiorgan dysfunction. 2. Once absorbed into the body phosphine can damage cell membranes and enzymes important for respiration and metabolism like decrease in catalases and increase in harmful enzymes like superoxide dismutases etc. 3. It has been seen that phosphine causes decrease in Magnesium intracellularly and its concentration increases extracellularly. 4. When phosphine is inhaled it can react with moisture in the lungs to form phosphoric acid which can cause blistering and edema leading to ARDS. 5. I t a l s o c a u s e s t h e d e n a t u r i n g o f oxyhaemoglobin leading to decreased Oxygen delivery to body tissues. 6. Local trauma to the gastric tissues leading to gastritis. Characteristics of Phosphine Gas: Description colorless gas, odor of garlic or decaying fish. Molecular weight 34.0 Daltons. Melting point: - 209o F (-134o C) Boiling point -126o F (-87.7o C) (at 760 mmHg) Vapour pressure > 760 mmHg at 68o F (20o C) Gas density: 1.17 (air = 1) Water solubility: Slightly water soluble (0.3 % at 68 F (2c) Flammability: Extremely flammable and explosive, may ignite spontaneously on contact with air. Acute Exposure: Phosphine interferes with enzymes and protein synthesis primarily in mitochondria of heart and lungs.7 Metabolic changes in heart muscles

causes cation disturbances that alter transmembrane potentials. Ultimately cardiac arrest, peripheral vascular collapse and pulmonary edema may occur. Pulmonary edema and pneumonitis are believed to result from direct cytotoxicity to pulmonary cells. In fatal cases, centrilobular necrosis of heart has been reported.7 Most deaths occur within first 12-24 hours after exposure and are cardiovascular in origin. After 24 hours usual cause of death is liver failure.8 Chronic Exposure: Chronic exposure to very low concentrations may result in anemia, bronchitis, gastrointestinal disturbances and usually speech and motor disturbances. Carcinogenicity: The EPA has determined that phosphine is not classifiable as to its human carcinogenicity9. Reproductive and Developmental Effects: Phosphine is not included amongst reproductive and developmental toxicants, No teratogenic effects from acute exposure are known. Table: system wise symtomatology pertaining to wheat pill poisoning.
System G.I.T. 100% CVS 100% Symptoms Thirst, nausea, vomiting, burning
epigastrium, abdominal cramps.

Hypotension, shock, brady/tachy-cardia, arrhythmias, myocarditis, congestive cardiac failure and ult-mately cardiac arrest. Respiratory Dyspnoea, crackles/ rales, pulmo50-60% -nary edema (ARDS), chest tight-ness, cough. Hepatobiliary Jaundice, tender hepatomegaly 20-30% raised transaminases, increased bilirubin. Renal 5-10% oliguris, proteinuria, bematuria or acture renal failure. CNS Anxiety, apprehension, restlessness, convulsions, coma, headac= he, dizziness, impaired gaist, double vision. Electrolytes Blood gas analysis reveals combined respiratory and metabolic acidosis. There is hepomagnesaemia

Management Guidelines for Wheat Pill Poisoning There is no specific antidote for wheat pill (Aluminium phosphide). Supportive measures are done till phosphine is excreted. Brush all visible particles from clothes, skin and hair. Thoroughly flush exposed skin and

hair. Thoroughly flush exposed skin and hair with water for 3-5 minutes; then wash with mild soap. If Phosphides have been ingested, do not induce emesis. Confirm the presence of wheat pill poisoning by use of AgNO3 (Silver Nitrate) paper. This can be done by placing Silver Nitrate paper in front of patient's mouth and asking him or her to exhale repeatedly; the colour of the paper will turn black in case the patient is phosphine gas positive.10 Gastric lavage with 1:1000 potassium permanganate till patient is confirmed phosphine gas negative by silver nitrate paper. of activated charcoal at 1 mg/kg (adults 60Slurry 90 gm) orally or through a nasogastric tube. Mineral oil or coconut oil may be used for gastric lavage. Maintain two intravenous lines with wide bore canula.

Adult Respiratory Distress Syndrome


Oxygen is delivered through face mask at moderate flow rates of 5-10 litres/min. 100 percent of oxygen to achieve PaO2 of 60-70 percent with lowest FiO2 Mechanical support is needed if above measures fail.

Steps to reduce systemic toxicity


No agent of proven efficacy as it rapidly binds to enzyme systems and produces cellular dysfunction. ++ However, Mg is thought to have anti peroxidant, anti arrhythmic and membrane stabilizing effects, hence, has been tried with some success.

Dosage Schedule
of Magnesium Sulphate IV stat, then One gm after every hour for next 3 hours and One gm then after every 4-6 hours up to a maximum One gm of 5 days. With this dose, serum Magnesium levels remain between 3.0 to 4.6 mEq/L which is safe. Lower and higher doses have been employed without any success. Another regime for giving MgSO4 is 3 gm of MgSO4 in 500 ml of Dextrose water in first three hours, followed by 6 gm of MgSO4 in 500 ml of Dextrose water over 24 hours starting next day and continued for 3-5 days. Intravenous Sodium Bicarbonate 50-100 meq in 1000 ml normal saline every 8 hours to keep bicarbonate level around 18-20 meq and pH above 7.1 (300 meq/day)

Treatment of Sequel or other related problems Shock


fluids (3-4 liters of fluid out of which Intravenous 50% should be normal saline under CVP guidance. (4-6 ug/kg/min) with Dobutamine to Dopamine keep the systolic blood pressure above 100mmHg. Intravenous hydrocortisone 200-400 mg after every 4-6 hours to be administered a. To reduce the dose of dopamine b. To check capillary leakage in lungs. c. To potentiate responsiveness of shock to endogenous catecholamines. d. To compensate for low levels of cortisol found in cases with severe poisoning.

Steps to Increase Ph3 Excretion


Phosphine is stable and is excreted through breath and partially in the urine. enhance its excretion through urine: Steps to a. Adequate hydration. b. Renal perfusion by IV fluid and c. Low dose dopamine (4-6 ug/kg/min). and dialysis are not employed due to Diuretics haemodynamic instability, however may be used if patient develops acute renal failure and becomes haemodynamically stable.

Hypoxia
Patent airway & Oxygen inhalation through mask. ventilation if needed. Assisted blood gas analysis 4 hourly. Monitor

Arrhythmias
Amiodarone has been claimed to be of some success in a study. sulphate has been tried with success in Magnesium reversion of supraventricular and ventricular arrhythmias. It has anti peroxidant effect and remains stable in hypoxic cell environment. is not effective to combat bradycardia or Atropine bradyarrhythmias of this poisoning.

Post Hospital Management


Admission and Follow-up Monitoring of delayed effects - Pulmonary edema and liver damage may be delayed for 72 hours or more so patients with

significant exposure should be admitted and observed carefully (survival for 4 days usually predicts full recovery). Patient release Asymptomatic patients with normal initial examination, minimal exposure, and no signs of toxicity after observation for 4 to 6 hours may be discharged with instructions to return to the emergency department if symptoms of toxicity develop.

involvement with intense thirst, 5(10%) patients developed pulmonary edema and none of the patient had renal involvement.

Discussion:
Suicide is a leading cause of death world wide.12 There are four major groups of people who commit suicide. By far the greatest number falls into situational problems i.e. patients commit suicide in younger age groups usually due to unsuccessful love affairs and social inhibitions, economic situations due to 13 joblessness and failure in examination. In fourth decade it is usually a fight with spouse or financial problems, whereas in old age usually due to family inattention or chronic illness, otherwise suicidal attempt is clearly a stratagem for controlling or hurting others. Suicide can be attempted due to severe depression or psychiatric illness. The gender ratio in our study is similar to accepted view of male dominance that has been reported in many countries as well as in other local studies.14 Suicide is the second common cause of mortality in 15-34 year olds. The rate increases with age peaking 15 for women in their sixties and men in their seventies. In our study 40 patients were in the age group of 1030 years, 7 patients were in the age group from 30-60 years whereas only 3 patients over the age of 60 years committed suicide. The finding goes against the increasing incidence of suicide with age. Patients presenting to emergency with intake of wheat pills usually belong to rural areas who indulge in out door activities of harvesting, processing and storage of crops. The higher mortality is associated with intake of freshly bought wheat pills from the market (probably freshly prepared), intake of more than one pills and time lapse of more than 4 hours before coming to emergency. It can be concluded that wheat pill poisoning is becoming very common as a mode of committing suicide. Since wheat pill is highly toxic, mortality is significantly higher and painful. Wheat pill is freely available and very cheap so awareness should be created among rural areas and urban peripheries regarding its toxicity and high mortality. A legal ban should be imposed on its over the counter sales. Its possession should be authorized to personnel trained in proper storage and dispensing. Department of Medicine, King Edward Medical College, theesculapio@hotmail.com www.sims.edu.pk/escuplapio.html.

Mortality (50-90 %)
Factors: - Freshness of pills. - Dose consumed. - Onset of symptoms. - Emptiness of stomach i.e. vomiting etc. - Delay in arrival in hospital - Delay in institution of therapy. Mortality - Supportive therapy alone 70-100 % - Supportive therapy & Magnesium Sulphate 25-45 %

Patients and Methods


Fifty patients were enrolled who presented to the emergency of West Medical Ward, Mayo Hospital, Lahore with history of ingesting wheat pills with suicidal intention during the period between August 2006 and April 2007. End point was leaving the hospital either dead, discharged or leaving against medical advice.

Results
Of the total 50 patients studied, 28 (56%) were males and 22 (44%) were females. 35 (70%) patients died, 8 (16%) were discharged and 7(14 %) patients left against medical advice. Age distribution showed 10 patients were in second decade (11-20 years), 22 patients in third decade (21-30 years), 8 patients in fourth decade (31-40 years), 7 in fifth decade (41-50) and 3 in sixth decade (50-60 years). 35 (70 %) out of 50 patients had cardiac involvement i.e. 12 patients had atrial fibrillation, 4 had ventricular fibrillation, 4 had ventricular tachycardia, 5 had complete heart block, 2 developed sinus bradycardia and 8 patients had non specific T wave and ST segment changes. 19 (38%) patients had CNS involvement i.e. became very irritable. 6 (12%) patients had hepatic involvement with raised aminotransferases, 30 (60%) patients had GIT

References
1. 2. Awan NR. Principles and practice of Forensic Medicine, Lahore. Sublime Arts: 2002:25. Bluglass R, Bawden P (eds). Principles and practice of F o r e n s i c P s y c h i a t r y. Edinburgh: Churchill Living Stone; 1990: 213-606. Royal Society of Chemistry. 1991 (as updated). The Agrochemicals Handbook, Royal Society of Chemistry Information Services, Cambridge, UK. Garry VF, Griffith J, Danzl TJ, Nelson RJ, Whorton EB, Krueger LA et al. Human genotoxicity: pesticide applicators and Phosphine. Science 1989;246(35): 251254. Newton PE, Shroeder RE, Sullivan JB, Busey WM, Banas DA. Inhalation toxicity of Phosphine in the rat: acute, sub-chronic and developmental. Inhal Toxicol 1993; 5 (2): 223239. Klimmer OR. Contribution to the study of action of phosphine. Archiv fur Toxikologie, 1969; 24 (23): 164-187. Leuschner F. Evaluation of the acute toxicity of Phostoxin (Active ingredient: aluminum phosphide) to rainbow trout. Laboratory for Pharmacology and Toxicology. Hamburg, German Federal Republic 1984. Waseem T, Bhatti NB, Khan AH, Nasir N. Acute poisoning due to wheat preservative aluminum phosphide. Pak J. Cardiol 1997; 8(3-4): 43-48. U.S. Environmental Protection Agency. 1994. File: Aluminum Phosphide Integrated Risk Information System (IRIS) US EPA, Washington, DC. Chugh SN. Metal Phosphide poisoning. J Ind Acad Clin Med 1999; 4(2):83-9. Gautam CS, Pandhi P, Sharma PL. Beneficial effect of xanthinol nicotinate in experimental aluminium phosphide poisoning. Indian Journal of Pharmacology 1992, 24: 134-137. Maris RW. Suicide. Lancet 2002; 360:319-326. Kim WJ, Singh T. Trends and dynamics of youth suicides in developing countries. Lancet 2004; 363: 1090-1091. Sultana K. Proportion of suicidal deaths among autopsy. Ann Abbasi Shaheed Hosp Khi Med Dent Coll 2002; 7:317-8. Snowdon J. Suicide rates and methods in different age groups: Australian data and perceptions. Int J Geriatr Psychiatry 1997; 12 (2): 253-8.

11.

6.

7.

3.

12. 13.

4.

8.

14.

9.

15.

5.

10.