Presentation on theme: "Non Conventional Poisoning"— Presentation transcript:
1 Non Conventional Poisoning HAM Nazmul AhasanProfessor of MedicineDhaka Medical College
2 A 30 year-old married young doctor, hailing from Jessore, was admitted in MU-4,DMCH on 2/9/14 with the complaints of vomiting and loose motion for 3 days, passage of black tarry stool, red urine and respiratory distress for 2 days, with history of copper sulphate ingestion 3 days back.
3 He took 25 grams of copper sulphate 3 days prior to admission as an attempt to suicide. He developed severe vomiting, vomitus was bluish yellow coloured containing ingested particles followed bywatery diarrhoea. After one day loose motion improved but developed severe abdominal cramping pain with burning sensation from throat to upper abdomen.
4 He noticed yellow colouration of sclera and passage of red urine on the second day. Next day he developed passage of black tarry loose stool.His general condition deteriorated.He was admitted into KMCH from where he was referred to Dhaka.He was admitted to BIRDEM first. He was referred to DMCH for better treatment.
6 Examination He was found ill-looking with respiratory distress. He was moderately anaemic, severely icteric and mildly dehydrated.Epigastrium was tender.
7 Acute poisoning is one of the medical emergencies all over the world It was the second of the top ten diseases dealt in the Medicine ward of Dhaka Medical College Hospital in 2012 and is 2013accounts for about 1% of Hospital admissions in the UKEven in the developed world poisoning is a major cause of death in young adults,Much of these deaths are preventable
8 Ingredients of Poisoning varies from country to country and even from one region to another within the same country.
9 Poisoning in different regions Source: Davidson’s Principal and Practice of Medicine 22nd Edition
10 Baseline Survey on Poisoning in six centers Study of Poisoning at different health facilities:1993Baseline Survey on Poisoning in six centersPlace of case0Name of pesticideTotalPesticideSedativesKerosineSnake biteCu-Sul phateMethanolPotka fishOthersOPCarmateBenzodiazepineOther sedativeDMCH27923276018977310251212982318CMCH29978111934383033005051390Coxsbazar9044013HathazariUHC261674126Jenaida445681739537Sitakund UHC292631168331237379541394342093745531324 (29.0%)1691 (37.1%)3.0%9.5%0.15%0.4%20.6%100%Distribution of registered patients according to place and name of agents
12 ‘Copper sulphate is a common mode of poisoning in the southern part of Bangladesh, and has a high rate of mortality.’Ahasan HAMN, Chowdhury MAJ, Azhar MA, Rafiqeuddin AKM. Copper sulphate poisoning. Tropical Doctor,1994; 24: 52-53
14 The Papyrus is an Egyptian medical text, written between 2600 and 2200 B.C. records the use of copper to sterilize chest wounds and to sterilize drinking water.In ancient India Copper sulphate was used for disinfection of woundIn the Hippocratic Collection in 460 to 380 B.C. copper is recommended for the treatment of leg ulcersThe Greeks sprinkled a dry powder composed of copper oxide and copper sulfate on the wound.
15 Copper sulphate is a blue, crystalline or granular powder Copper sulphate is a blue, crystalline or granular powder. Its anhydrous form is white in colour.It is used as fungicide, algicide, herbicide, molluscide and also in steel and petroleum industry.Fatal dose – 30 gmFatal period – 4 hours to 3 days
16 Easily available in the local market It is found in almost every houses in this localityCommon uses areAntifungal agent among the fishermenand cultivatorsAlso in treating foot ulcer in the cattlesas wound disinfectants, fungicide, ingredient of glues for making paper boxes & packets,Antiseptic wash of feet ,used by the farmers working in the saline water in the southern coastal area.For ripening of Banana and Papaya
17 Copper Sulphate poisoning in Khulna division : Age and Gender Distribution Age rangeNo. of cases< 201120 – 292430 – 390140 – 490050 – 59> 6006SexNo. of cases (%)Male11 (26.19)Female31 (73.81)Total42 (100)
18 Copper Sulphate poisoning is associated with High Mortality Cause of deathNo. of casesAcute hepatic failure5Acute renal shutdown4Total9Ahasan HAMN, Chowdhury MAJ, Azhar MA, Rafiqeuddin AKM. Copper sulphate poisoning. Tropical Doctor. 1994; 24: 52-53
20 Molecular MechanismCopper inhibits enzymes G-6-PD and glutathione reductase which are important in protecting the cell from oxygen free radicals, lipid peroxidationSignificant increase of copper content in the mitochondrion suggest hepatic mitochondrion to be an important target in hepatic toxicityHemolysis due to increase oxidation of hemoglobin sulfhydryl groups, leading to increased red blood cell permeability.Copper inhibits enzymes G-6-PD and glutathione reductase which are important in protecting the cell from oxyen free radicals, lipid peroxidation and significant increase of copper content in the mitochondrion suggest hepatic mitochondrion to be an important target in hepatic toxicity, with an involvement of oxidant damage to the liver.Hemolysis is produced by the increase oxidation of hemoglobin sulfhydryl groups, leading to increased red blood cell permeability.
21 Clinical feature of Copper Sulphate Poisoning First Day: Strong metallic taste, abdominal pain and burning, nausea, vomiting, diarrhea, salivationSecond Day: abdominal cramps melenae due to extensive corrosion and necrosis of GITThird Day onwards: Jaundice due to hemolysis and hepatocellular damage may be produced. Oliguria and renal failure can occur due to direct toxicity as well as intra vascular hemolysis, red urine due to Anaemia
22 Clinical features (Contd….) Patient becomes progressively anaemicIn severe cases seizures, delirium and coma may occur.Methaemoglobiraemia may be produced.Hypotension and hypothermia may occur.Complete paralysis of limbs is rarely observed.It can cause dermal irritation on contact.
23 Diagnosis:Diagnosis is based on history of ingestion of copper sulphate.
24 Lab investigation CBC and PBF: Anaemia and Features of Haemiolysis Liver function tests: Serum Bilirubin, S ALT,Urine : HemoglobinuriaRenal Function test: Serum CreatinineMonitor whole blood copper levels in symptomatic patients.Methemoglobin levels in cyanotic patientsArterial blood gases.Chest X ray.
25 Hospital Management Liquid Antacid two t.s.f. 6hourly Intravenous Omeprazole 40 mg dailyInj. Dimercaprol 200mg, Intra Mascular, 4 hourly for 2 days,12 hourly for 14 days = total 40 amplesBlood transfusion incase severe anemia due to haemolysis or melaena
26 Hospital Management of Copper Sulphate Poisoning cont. Dexamethasone IV for Acute hemolysisTreat methemoglobinemia with methylene blue and humidified oxygen.D–penicillamine which can be given subsequently. It has or no role in acute stageTreat hepatic failure & Acute Kidney Injury
27 A Common aphorism in Khulna Taka 2/=Taka 3/=Taka 5/=No Treatmentis effectiveTreatment cost (approximate)Taka 20,000Treatment cost (approximate)Taka 30,000
29 ÓAvwg ‡R‡b ï‡b wel K‡iwQ cvb cÖv‡Yi Avkv †Q‡o mu‡cwQ cÖvY..Ó These dishes are prepared of Puffer fish!Some are worth USD $ 400
30 Not new ! The puffer fish is illustrated on an Egyptian tomb of the fifth dynasty dated 2500 BCCaptain James Cook mentioned in his log book of second voyage in 1774 AD: his crew men was poisoned after eating it.Known as blowfish, toadfish, globefish, balloon fish, Patka fish and FuguIt is the second most poisonous vertebrate in the world (275 times deadlier than cyanide poison).
31 Puffer Fish PoisoningDespite careful preparation, the number of annual deaths in Japan from puffer fish poisoning is around 50Deaths have also been reported in Singapore, Hong Kong, Vietnam and Australia
32 In Bangladesh It is available both fresh water and sea water Common species in our country: Tetraodonpatoca & TetraodoncutcutiaIt is available both fresh water and sea waterIt is affordable & tasty.Sporadic outbreak of poisoning occursNo specialist/ licensed cook in Bangladesh
33 Puffer-fish Poisoning Outbreaks in Bangladesh YearPlaceVictimDeath1998 (November)Cox’s bazar08052002 (April)Khulna372005 (July)06002008 (April)Kishoreganj0302Norshingdi452008 (June)Dhaka10In addition from patient was reported. Out of them 16 died through out country.
34 Tetrodotoxin (TTX)The toxin was first isolated and named in 1909 by Japanese scientist Dr. Yoshizumi TaharaThe amount of TTX varies widely in different species.Tetrodotoxin blocks voltage sensitive sodium channels in nerve tissue leading to failure of depolarization and propagation of action potential in nerve tissue both the central and peripheral nervous systems.Paralysis and respiratory failure account for the main cause of death
35 Tetrodotoxin (TTX)The highest concentration of the toxin is found in the viscera (gonads, especiallythe ovaries; liver; intestines) and skin.The body musculature is usually free of poisonDangerous to eat immediately prior to and during their reproductive season.H A M N Ahasan, A A Mamun, S R Karim, M A Bakar, E A Gazi, Chandra Shekhar Bala; Paralytic Complications of Puffer Fish (Tetrodotoxin) Poisoning; Singapore Med J 2004 Vol 45(2) : 73
36 H A M N Ahasan, A A Mamun, S R Karim, M A Bakar, E A Gazi, Chandra Shekhar Bala; Paralytic Complications of Puffer Fish (Tetrodotoxin) Poisoning; Singapore Med J 2004 Vol 45(2) : 73
37 HAM Nazmul Ahasan, Abdullah Al Mamun, C H Rasul , PK Roy, GP Paul , Chandra Shekhar Bala; Puffer fish poisoning a clinical analysis; Pak J Med Sci, january-March 2003 Vol.19 No 1, 29-31
38 Clinical FeaturesInitial symptoms include peri-oral tingling and numbness, Salivation, nausea, vomiting, and diarrhea with abdominal pain.Motor dysfunction with weakness and speech difficulties then develop.A rapid ascending paralysis occurs over 4-24 hours.Extremity paralysis precedes bulbar paralysis, which is followed by respiratory muscle paralysis.
39 Clinical Features cont. Deep tendon reflexes are preserved early in the course of paralysis.Finally, cardiac dysfunction with hypotension and arrhythmias (bradycardia),Central nervous system (CNS) dysfunction (e.g. coma), and seizures develop. Patients with severe toxicity may have deep coma, fixed non-reactive pupils, apnea, and loss of all brain stem reflexes.Death can occur within 4-6 hours from respiratory muscle paralysis and respiratory failure.F. R. Chowdhury, H. A. M. Nazmul Ahasan, A. K. M. Mamunur Rashid, A. Al Mamun, and S. M. Khaliduzzaman, “Tetrodotoxin poisoning: a clinical analysis, role of neostigmine and short-term outcome of 53 cases,” Singapore Medical Journal, vol. 48, no. 9, pp. 830–833, 2007
40 Management There is no specific antidote. Treatment is only supportive and symptomatic.Removal of unabsorbed poison by gastric lavage by 2%Sodi-bi-carb solution may be helpfulMaintenance of fluid and electrolyte.
41 Management Cont. Charcol may adsorb rest of poison. Injection of Neostigmine 0.05ml/kg withAtropine 0.025ml/kg six hourly for one day is helpfulArtificial respiration if respiratory paralysis
42 Rat killer : for protection of grain and as fumigant Aluminium PhosphideRat killer : for protection of grainand as fumigant
43 Aluminium Phosphide Forms Phosphine when hydrolyzed by gastric HCl Phosphine-non competititive inhibition of the cytochrome oxidase of mitochondriaEnergy crisis and hypoxic cell damageMulti Organ Failureshock
45 Clinical feature of phosphide inhalation Mild and moderate toxicitySevere toxicityEye and Nasal IrritationCoughChest tightnessHeadacheNauseaVomitingAbdominal painAtaxiadizzinesssHypotensionMetabolic acidosisHypokalaemiaSevere dyspnoeaGI bleedingCardiac arrhythmiaCardiac failurePulmonary oedemaComaseizure
46 Emergency monitoring Pulse Blood Pressure Cadiac rhythm ECG Level of consciousnessRespirationPulse OxymetryAcid base balanceSerum electrolyteSerum creatinineSerum CPKSerum Trop I
47 Management Gastric lavage with K+ permanganate or 2% Sodium bicabonate Maintain Fluid balanceCorrection of shock and electrolyte imbalanceIV fluid, dopamine, Hydrocortisone 400mg/ dexamethasone 4mg 4hourlyOxygen inhalationVitamine K 10mg daily if bleeding tendency/PT is prolongedRenal and hepatic function monitoring
49 Household poisoning Disinfectent Detergent Cosmetics Bleach HarpicDichlorometoxylenolCresolDetergentSoapWashing liquidsCosmeticsColognePerfumeLotions, nail polishBleachSodium HypochloriteHydrogen peroxidePetroleum productsKeroseneParaffinTurpentinePaint thinnerFurnitures and floor polish
50 Detergents and Disinfectants Clinical featurenausea, vomiting, diarrhoea.corrosive effects to mucousaNail polish (acetone)-Irritation of mucous membrane, Metabolic acidosis, comaManagementNo specific antidoteSupportive treatment as corrosive poisoning
52 Acids and corrosivesSkin: blister, pain, necrosis, ulceration,scarring after healingIngestion: pain, mucosal oedema, hoarseness, difficulty in swallow, laryngeal oedema, respiratory distressIngestion : perforation of oesophagus & stomach, chemical peritonitis, abdominal pain, vomiting, diarrhoeaSystemic –circulatory failure hypoxia, metabolic acidosis, respiratory failure, DIC, ATN, AKILong term: stricture, pyloric stenosis
53 Management Do not induce emesis Gastric lavage contraindicated NSAID for painOxygen inhalationTracheostomy if laryngeal oedemaExternal burn / eye –immediate, repeated wash with water. Silver sulphadiazine ointment26Management of complication-peritonitisUpper GI endoscopySurgery-oesophageal sticture and gastric outlet obstruction after 4-6 weeks
54 Methanol poisoningMethanol Poisoning in Bangladesh- a Fatal case series:Robed Amin , Ariful Basher, F R Chowdhury, M A Faiz
55 MethanolMethanol is methyl alcohol commonly used in many home chemicals, duplicating fluids, varnishes, stains, paint thinners and dyes.Methylated spirit is very cheap and frequently available.It becomes highly toxic when it is mixed with ethyl alcohol as it is adulterated
56 MethanolWhen taken with ethyl alcohol, it metabolized only after complete metabolism of ethyl alcohol.In course of oxidation, formaldehyde and finally formic acid are formed which are highly toxic.Mode of poisoning: Accidental, Suicidal, rarely homicidal.Adult alcoholics are affected mostly
57 Clinical features of methanol poisoning Methanol poisoning typically induces nausea, vomiting, abdominal pain, and mild central nervous system depression.There is then a latent period lasting approximately 12–24 hours following which an uncompensated metabolic acidosis develops.visual function becomes impaired, ranging from blurred vision and altered visual fields to complete blindness
58 Symptoms analysis of methanol poisoning NameAge in yrsTA30M.R35Mr D40J.HM. M55B.BA.AB.H50Unconsiousness+-NauseaVomiting(times)45361012Visual disturbanceRespiratory distressAbdominal PainDiarrhoeaLag period3hrs48 hrs7hrs6hrs48hrs
59 Sign analysis of methanol poisoning NameAge in yrsTA30M.R35Mr D40J.HM. M55B.BA.AB.H50GCS63812457Pulse84/m100/m80/m90/m96/mNP72/mBP80/60120/80100/60100/70110/7090/60NROpthalmoscopyDisc OedemaOptic AtrophyHyperemiaDisc CongestionOptic AtroophyLungs Crackles-+Acidotic BreathingShock
60 Rapidly developing optic atrophy in methanol poisoning
61 Management of Methanol poisoning Stomach wash, Oxygen inhalationIntravenous fluid, management of dehydration & electrolyte imbalanceInjection Sodi-bi-Curb solution if acidosis, pH <7.35 or bicarbonate < 15 mEq/LRenal failure -Hemodialysis,Treat Convulsion with Diazepam
62 Antidote: EthanolMild poisoning: 95% Ethanol Orally 0.8 ml/kg loading dose followed by 0.1 ml/kg/houror, Gin/ Whisky 1.8ml/kg loading dosethen 0.2ml/kg/hour for 3 to 4 days diluted in fruit juiceSevere cases: I.V.10% ethanol 7.5ml/kg over 60 min then 1ml/kg/hour in non-drinker, 2ml/kg/hour in drinker10% ethanol: 60ml 100% alcohol in 500ml 5% Dextrose
63 For Preservation of Vision Eye protection against light,Consultation with ophthalmologistInj. Folinic acid 50mg IV- 4 hourly for hoursInj. B micro-gram IV daily for 5 daysInj. Methyl Prednisolone 1gm daily for 3 days may help
64 Date line17, November200127 members of armed police battalion of a remote camp in Bandarban district rushed into Chittagong Medcal College Hospital with abdominal pain, vomiting, diarrhoea, generalized paraesthesia, muscle cramps, weakness of limbs, agitation. All of them had iftar together 2-3 hours before onset. On examination most of them found too have rapid shallow breathing, carpopedal spasm, hypotension and flaccid type of paralysis and loss of tendon jerk.
65 Investigations revealed hypokalaemia, hypogycaemia, flat ST segment and U waves in ECG, raised CPK in some patient. They developed respiratory paralysis and ultimately 12 patients died over the period 16 hours from the onset. Chemical analysis of vomitus, blood, flour from their kitchen revealed presence of Barium.Mass barium carbonate poisoning with fatal outcome, lessons learned: a case seriesCases J. 2009; 2: 9069.Published online Sep 1, 2009. Aniruddha Ghose1*, Abdullah Abu Sayeed1, Amir Hossain1, Ridwanur Rahman2, Abul Faiz3 and Gofranul Haque1
66 Accidental Barium carbonate poisoning It was kept in the kitchen as rodentocide, looks similar to flourIn stomach Ba Carbonate turns into Ba Chloride (water soluble)BaCl absorbs through small intestineProduce hypokalaemia direct effect on the muscles.
67 Management Similar event in 1945 in a British Army regiment Supportive Gastric lavageSodium sulphate introduced to form insoluble Ba sulphateFluid and Electrolyte correctionMechanical ventilation in case of respiratory failureRenal replacement therapyHaemofiltrationSimilar event in 1945 in a British Army regiment
68 Motive Behind Suicidal Poisoning Familial Disharmony 73%Failure in examination 5.7%Disappointment of Love affairs 5.1%Poverty %Physical illness 2.3%Psychiatric illness 2.2%Miscellaneous 2.6%Unidentified %HAM Nazmul Ahasan, MA Jalil Choudhury, AKM Rafiquddin et al; Motive behind acute poisoning; Specialist Pakistan’s Med Sci, April-June,Vol. 11, no.3,
69 Take Home Message Poisoning is a common medical emergency Some are conventional and Some are NonconventionalDoctors and nurses are to be equipped with knowledge and logistics to manage the non conventional poisoning casesLack of preparedness on our part may result in loss of valuable livesA National Poisoning Information and Resource Centre should be strengthened as early as possible
70 ‘..Life is short and the art is long, opportunity is fleeting, judgment is difficult and experiment is dangerous. The Physician must do the right thing at right time..’ Hippocrates: The first aphorism
71 Not all intoxications are treatable “..You've taken away my looks, my identity, by just a glance. By making me drink the wine from the distillery of love You've intoxicated me by just a glance..”-Hazrat Ameer Khusru 1253–1325, Delhi. Close associate of Hazrat Nizamuddin Awlia (R.A)
72 Love for precious life All living being want to live through offspring Messi with his childDr. X who had Copper Sulphate poisoning
73 Love for precious life Emir Taimur (April 9, 1336 - February 18, 1405) ShahrisabzSamarkand
74 Acknowledgement Late Professor Dr AKM Rafiqueddin Professor Dr M A FaizDr Robed AminDr Fazle Rabbi ChowdhuryDr Chandra Shekhar Bala
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