ALPHOS (1)AND HHP-03.pptx

class ppt

1. ALPHOS (Aluminium phosphide)

2. CONTENTS INTRODUCTION MECHANISM &ACTION FATAL DOSE & PERIOD SIGNS AND SYMPTOMS LABORATORY FINDINGS DIAGNOSIS TREATMENT POSTMORTEM FINDINGS MEDICO LEGAL ASPECT SUMMARY & CONCLUSION CASE REPORT

3. INTODUCTION Solid & fumigant pesticide, insecticide and rodenticide Used as Grain preservative in north India, Available as White tablets of Celphos , alphos , Quickphos , Phostoxin , Phosphotex Wt of each tablet 3gms – liberates 1 gm of PHOSPHINE (PH3) Leading cause for death due to poisoning. Phosphine is a colorless and odourless gas But on exposure to air it gives characteristic garlic/decaying fish like odor . It is spontaneously inflammable and violently combines with oxygen and halogen When phosphine burns – dense white cloud of ‘phosphorus pentoxide’

4. MECHANISM & ACTION ALP liberates phosphine when it comes in contact with air and moisture. It reacts with acidic media (HCL) of stomach and release phosphine gas, which is rapidly absorbed from gastrointestinal tract by simple diffusion. Phosphine is a protoplasmic poison interfering with enzymes and protein synthesis. It acts by inhibiting the electron transport resulting from inhibition of Cytochrome Oxidase

5. Fatal Dose – 1 to 3 gm; 1 to 3 tablets Fatal Period – 1 hr to 4 days – majority die within 24hrs

6. SIGNS & SYMPTOMS

7. LABORATORY FINDINGS Chemical analysis for ph3 in blood or urine is not recommended as ph3 is rapidly oxidised Leucopnia Increased Serum glutamic oxaloacetic transaminase(SGOT) and serum glutamic pyruvic transaminase (SGPT) Metabolic acidosis Decreased plasma magnesium and serum cortisol Raised plasma renin levels

8. DIAGNOSIS Altered liver function tests with raised transaminase levels ABG shows metabolic acidosis ECG — sinus tachycardia Silver nitrate test – the patient is asked to breathe through a piece of filter paper impregnated with 0.1 N silver nitrate solution for 5 to 10 minutes. If filter paper becomes black, it suggests presence of phosphine. The blackening is imparted because phosphine reduces silver nitrate to silver.

9. TREATMENT

10. POSTMORTEM FINDINGS Typical garlicky odor Congested organs Bright fluid blood Pleural effusion Pulmonary edema Bleeding Gastric mucosa shows shedding Kidney shows acute tubular necrosis Liver shows fatty change, congestion, edema, inflam-matory infiltrate in portal tract and centrizonal necrosis

11. MEDICO LEGAL ASPECT

12. SUMMARY AND CONCLUSION Toxic effect of alphos is due to liberation of phosphine gas when it comes in contact with hcl of stomach Phosphine acts by inhibhiting cytochrome oxidase and oxidative phosphorylation Phosphine gives characteristic garlic / decayin fish like odour Signs & symptoms:abdominal pain,arrthymia,altered mental state,metabolic acidosis,lung failure,seizures Cause of death in alphos poisoning – metabolis acidosis and acute renal failure Fatal dose 150-500mg (1tablet is fatal) Test for alphos poising : silver nitrate test No antidote Treatment is conservative – for shock , ARDS,metabolic acidosis,arrhythmia It is considered as ideal suicidal poison

13. CASE REPORT A 34-year-old woman was brought to the emergency department with alleged history of taking ALP tablets. Her relatives revealed the aluminium canister of ALP tablets and alleged she had taken 2 tablets 30 min before. On arrival, she was drowsy and was not responding to verbal commands. Her body was cold and hypotonic, and her skin was pale with mottling. Her vital signs were as follows: Pulse rate 110/min regular, blood pressure 70/52 mm Hg, respiratory rate 20/min, shallow and body temperature, 36.1°C. On emergency investigations, the electrocardiogram showed sinus tachycardia, pulse oximetry showed O 2  saturation of 91% on room air and arterial blood gas analysis demonstrated metabolic acidosis with pH of 7.1. Presentation of ALP tablets by the family and symptoms of patient favoured diagnosis of ALP poisoning. The patient was instantly attended to; intubation was carried out, and a nasogastric tube was inserted. Normal saline was administered by infusion intravenously. After gastric washing with sodium bicarbonate, gastric lavage was performed using potassium permanganate (1:10,000) and then activated charcoal (100 g) was administered. Shortly afterwards, she vomited hot charcoal filled with small bubbles covered with white smoke that led to thermal burning of the left side of the her face. A simultaneous cough splashed some vomit on the personnel's clothes. She was immediately transferred to an isolated room and underwent infusion of calcium gluconate and magnesium sulphate. The patient's situation progressively deteriorated. Sensorium decreased and apnoea occured necessitating resuscitation and mechanical ventilation. At 3 h after emergency department admission, the patient had cardiac arrest and died.

14. HOUSEHOLD POISONS

15. CONTENTS DEFINITION ROUTE OF POISONING COMMON HOUSEHOLD POISONS WITH EXAMPLES /CLASSIFICATION HOUSEHOLD BLEACHES Chlorine based Non chlorine based -CLINICAL EFFECTS - TREATMENT SOME EXAMPLES DESSICANTS PYRETHRIN Mechanism Clinical features Management Autopsy findings ML importance - PREVENTIVE MEASURES

16. DEFINITION Household poisons are poisoning that occurby exposure to home products, especially happened by children(because they don't know it is,or mimickers to adults), and by adult (accidental, mistakes) Over 90% of toxic exposure to household product occurs in children under 5 year &usually at time when product is in use rather than storage.

17. ROUTE OF ADMINISTRATION Injestion Inhalation Skin contact

18. Common Household poisonings 1.Medicines sleeping tablets – Barbiturates Headache tablets – aspirin 2. Cosmetics and personal care Suntan lotions –denatured alcohol Nail polish remover – acetone Soaps and shampoo 3.Detergents (bleaching agents,floor cleaner,etc ) 4.Pesticides Rat poison – aluminium phosphide,zinc sulphide Insecticide spray- DDT,gammaxene 5 Hydrocarbon Solvents(kerosene, Thinner,petrol ) 6.Plants 7.Kitchen Baking powder – tartaric acid50% Dish washing compounds-sodium poly phosphates,sodium carbonate

19. 8. Miscellaneous: (1) Insecticide spray: (2) Moth balls: (3) Marking ink: (4) Ink remover: (5) Anti-rust products: (6) Cleaning solvents: (7) Fluorescent lamps: (8) Furniture polish: (9) Paint remover: (10) Shoe polish: (11) Hair bleach: (14) Crayons (chalk): (15) Crayons (wax): D.D.T., Gammexane , etc. Naphthalene. Aniline. Sodium hypochlorite 5%. Ammonium sulphide , hydrofluoric acid Petroleum hydrocarbons; carbon tetrachloride; Beryllium. Turpentine; petroleum hydrocarbons. Sodium hydroxide; lead acetate. Aniline; nitrobenzene. Potassium permanganate: hydrogen peroxide. Salts of arsenic, copper, lead. Paranitroaniline .

20. Household bleaches 1.Chlorine based bleaches - contain chlorine or hypochlorite - general disinfectant and bleaching agent. - The toxicity of bleach is related primarily to the oxidizing capacity of the hypochlorite ion and the pH of the solution

21. 2.Non-chlorine bleaches used in numerous household products, including disinfectants, chlorine free bleaches, fabric stain removers, contact lens disinfectants, hair dyes and tooth whitening products - May contain hydrogen peroxide, sodium perborate, sodium percarbonate

22. 1.Chlorine based (main content Hypochlorite) 1. Most household bleach solutions contain 3% - 5%hypochlorite. *swimming pool disinfectants &industrial bleach : up to 20% hypochlorite 2. Bleaches with a hypochlorite concentration greater than 10% are corrosive while those with a concentration of less than 10% are irritants. 3.Householdd bleach is a mild to moderate irritant which does not cause tissue damage unless ingested in large amounts. Systemic toxicity may occur after a large ingestion. 4.Ingestion of more than 100 mL in a child or 300 mL in an adult of a household bleach (<10% sodium hypochlorite) may cause significant toxicity.

23. Clinical effects of Hypochlorite MILD TO MODERATE *dilute hypochlorite solutions (3%-5%) immediate burning in the mouth & throat. GI upset no further injury SEVERE *concentrated solution significant esophageal & gastric burns dysphagia, drooling, severe throat, chest & abdominal pain. hematemesis & GI perforation

24. 2.Nonchlorine based (main content hydrogen peroxide) Colourless , odourless , acidic oxidizing agent available in a variety of concentrations from 3 to 90% General purpose disinfectants 3% Hair bleach and hair dyes 6% Contact lens disinfectants 3% Chlorine free bleach 6% Fabric stain removers 5-15% Industrial strength up to 90%

25. Treatment

26. Some examples

27. PYRETHRUM, PYRETHRINS & PYRETHROIDS Pyrethrum is extract of the chrysanthemum flower. Pyrethrum contains six active components labeled pyrethrins . Pyrethroids are synthetic derivatives of pyrethrins . Commonly used as insect and mosquito repellants

28. Mechanism of action Pyrethroids prolong the inactivation of the sodium chan-nel by binding to it in the open state. However, in most of the cases, toxicity with these agents occurs because of the allergic reactions to these compounds.

29. CLINICAL FEATURES Fatal dose - Pyrethrum 1 gm/kg Dermal exposure - erythema, dermatitis, blister formation Ocular exposure causes irritation, lacrimation Inhalation causes rhinorrhea, sore throat, wheezing, cough, dyspnea Ingestion - causes nausea, vomiting, paresthesia, vertigo, fasciculation, hyperthermia, altered mental status, convulsions, pulmonary edema and coma

30. MANAGEMENT Decontamination Systemic Poisoning – Ingestion - gastric lavage and administration of activated charcoal Fatty substance should be avoided as they promotes the absorption through GIT Allergic reaction should be treated with epinephrine and antihistamines Bronchospasm should be treated with appropriate bronchodilators Convulsions –diazepam

31. AUTOPSY FINDINGS Insect repellant like smell Froth at mouth and nostrils Cyanosis Congestion of organs Pulmonary edema Cerebral edema. ML IMPORTANCE Accidental poisoning may occur. Suicidal poisoning is rare. Homicidal is also rare

32. Preventive Measures

33. Akash A Kattimani 3 rd year Gamc