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HAM Nazmul Ahasan Professor of Medicine Dhaka Medical College.

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Presentation on theme: "HAM Nazmul Ahasan Professor of Medicine Dhaka Medical College."— Presentation transcript:

1 HAM Nazmul Ahasan Professor of Medicine Dhaka 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 by watery 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.

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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 2013 accounts for about 1% of Hospital admissions in the UK Even 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 22 nd Edition

10 Distribution of registered patients according to place and name of agents Place of case0 Name of pesticideTotal PesticideSedatives Kerosi ne Snake biteCu-Sul phateMethanolPotka fish Oth ers OP Carm ate Others Benzodiazepine Other sedativ e DMCH CMCH Coxsbazar Hathazari UHC Jenaida Sitakund UHC Total (29.0%)1691 (37.1%)3.0%9.5%0.15%0.4% 20.6%100% Study of Poisoning at different health facilities:1993 Baseline Survey on Poisoning in six centers

11 Nonconventional poisoning Copper sulphate poisoning Puffer fish poisoning Methanol poisoning Aluminum phosphide Common household corrosives poisoning Nitric acid, Hydrochloric acid, Sulfuric acids Barium Carbonate poisoning

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

13 Poisoning profile in southern Bangladesh DiagnosisTotal number of patients (%) Unknown poisoning82 (22.97) OPC poisoning76 (21.29) Snake bite64 (17.93) Sedative48 (13.45) Copper sulphate42 (11.76) Harpic17 (04.76) Food 9 (02.52) Rat killer 5 (01.40) Insect bite 3 (00.84) Savlon 3 (00.84) Kerosene 2 (00.56) Ascabiol 2 (00.56) Dettol 1 (00.28) Octane poisoning 1 (00.28) Glass cleaner 1 (00.28) Mercury 1 (00.28) Grand Total 357

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 wound In the Hippocratic Collection in 460 to 380 B.C. copper is recommended for the treatment of leg ulcers The 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. 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 gm Fatal period – 4 hours to 3 days

16 Easily available in the local market It is found in almost every houses in this locality Common uses are Antifungal agent among the fishermen and cultivators Also in treating foot ulcer in the cattles as 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 Sex No. of cases (%) Male11 (26.19) Female31 (73.81) Total42 (100) Age rangeNo. of cases < – – – – 5900 > 6006

18 Copper Sulphate poisoning is associated with High Mortality Cause of deathNo. of cases Acute hepatic failure5 Acute renal shutdown4 Total9 Ahasan HAMN, Chowdhury MAJ, Azhar MA, Rafiqeuddin AKM. Copper sulphate poisoning. Tropical Doctor. 1994; 24: 52-53

19 Copper Sulphate Toxicity GIT Erosion, cramp, melenae Liver Hepatocellular damage RBC Hemolysis, methaemoglobinaemia Kidney Hemoglobinuria, oligura, AKI

20 Molecular Mechanism Copper inhibits enzymes G-6-PD and glutathione reductase which are important in protecting the cell from oxygen free radicals, lipid peroxidation Significant increase of copper content in the mitochondrion suggest hepatic mitochondrion to be an important target in hepatic toxicity Hemolysis due to 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, salivation Second Day: abdominal cramps melenae due to extensive corrosion and necrosis of GIT Third 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 anaemic In 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 : Hemoglobinuria Renal Function test: Serum Creatinine Monitor whole blood copper levels in symptomatic patients. Methemoglobin levels in cyanotic patients Arterial blood gases. Chest X ray.

25 Hospital Management Liquid Antacid two t.s.f. 6hourly Intravenous Omeprazole 40 mg daily Inj. Dimercaprol 200mg, Intra Mascular, 4 hourly for 2 days, 12 hourly for 14 days = total 40 amples Blood transfusion incase severe anemia due to haemolysis or melaena

26 Dexamethasone IV for Acute hemolysis Treat methemoglobinemia with methylene blue and humidified oxygen. D–penicillamine which can be given subsequently. It has or no role in acute stage Treat hepatic failure & Acute Kidney Injury Hospital Management of Copper Sulphate Poisoning cont.

27 A Common aphorism in Khulna Taka 2/= Taka 3/=Taka 5/= Treatment cost (approximate) Taka 20,000 Treatment cost (approximate) Taka 30,000 No Treatment is effective

28 Puffer Fish Dishes Looking Delicious!!

29 These dishes are prepared of Puffer fish! Some are worth USD $ 400 ÓAvwg ‡R‡b ï‡b wel K‡iwQ cvb cÖv‡Yi Avkv †Q‡o mu‡cwQ cÖvY..Ó

30 Not new ! The puffer fish is illustrated on an Egyptian tomb of the fifth dynasty dated 2500 BC Captain 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 Fugu It is the second most poisonous vertebrate in the world (275 times deadlier than cyanide poison).

31 Despite careful preparation, the number of annual deaths in Japan from puffer fish poisoning is around 50 Deaths have also been reported in Singapore, Hong Kong, Vietnam and Australia Puffer Fish Poisoning

32 In Bangladesh  It is available both fresh water and sea water  It is affordable & tasty.  Sporadic outbreak of poisoning occurs  No specialist/ licensed cook in Bangladesh Common species in our country: Tetraodonpatoca & Tetraodoncutcutia

33 Puffer-fish Poisoning Outbreaks in Bangladesh YearPlaceVictimDeath 1998 (November)Cox’s bazar (April)Khulna (July)Khulna (April)Kishoreganj (April)Norshingdi (June)Dhaka (June)Dhaka1003 In 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 Tahara The 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 The highest concentration of the toxin is found in the viscera (gonads, especially the ovaries; liver; intestines) and skin. The body musculature is usually free of poison Dangerous 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 Tetrodotoxin (TTX)

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 Features Initial 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 helpful  Maintenance of fluid and electrolyte.

41 Management Cont.  Charcol may adsorb rest of poison.  Injection of Neostigmine 0.05ml/kg with  Atropine 0.025ml/kg six hourly for one day is helpful  Artificial respiration if respiratory paralysis

42 Rat killer : for protection of grain and as fumigant

43 Aluminium Phosphide  Forms Phosphine when hydrolyzed by gastric HCl  Phosphine-non competititive inhibition of the cytochrome oxidase of mitochondria  Energy crisis and hypoxic cell damage  Multi Organ Failure  shock

44 Clinical feature of ingested phosphide Nausea Vomiting Abdominal pain Headache Agitation chest tightness Dyspnoea Ologuria Jaundice Bleeding Metabolic acidosis Hypokalaemia cardiac arrhythmia Convulsion Shock persistent hypotension

45 Clinical feature of phosphide inhalation Mild and moderate toxicity Severe toxicity Eye and Nasal Irritation Cough Chest tightness Headache Nausea Vomiting Abdominal pain Ataxia dizzinesss Hypotension Metabolic acidosis Hypokalaemia Severe dyspnoea GI bleeding Cardiac arrhythmia Cardiac failure Pulmonary oedema Coma seizure

46 Emergency monitoring Pulse Blood Pressure Cadiac rhythm ECG Level of consciousness Respiration Pulse Oxymetry Acid base balance Serum electrolyte Serum creatinine Serum CPK Serum Trop I

47 Management Gastric lavage with K + permanganate or 2% Sodium bicabonate Maintain Fluid balance Correction of shock and electrolyte imbalance IV fluid, dopamine, Hydrocortisone 400mg/ dexamethasone 4mg 4hourly Oxygen inhalation Vitamine K 10mg daily if bleeding tendency/PT is prolonged Renal and hepatic function monitoring

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49 Household poisoning Disinfectent Harpic Dichlorometoxylenol Cresol Detergent Soap Washing liquids Cosmetics Cologne Perfume Lotions, nail polish Bleach Sodium Hypochlorite Hydrogen peroxide Petroleum products Kerosene Paraffin Turpentine Paint thinner Furnitures and floor polish

50 Detergents and Disinfectants Clinical feature nausea, vomiting, diarrhoea. corrosive effects to mucousa Nail polish (acetone)- Irritation of mucous membrane, Metabolic acidosis, coma Management No specific antidote Supportive treatment as corrosive poisoning

51 Domestic use of Acids/Corrosives Harpic (10% HCl & Sodium alkyle benzene sulphonate & sodium alkene sulphonate) Dish washer Metal cleaner Battery fluid Nitric acid Phenol, cresol

52 Acids and corrosives Skin: blister, pain, necrosis, ulceration, scarring after healing Ingestion: pain, mucosal oedema, hoarseness, difficulty in swallow, laryngeal oedema, respiratory distress Ingestion : perforation of oesophagus & stomach, chemical peritonitis, abdominal pain, vomiting, diarrhoea Systemic –circulatory failure hypoxia, metabolic acidosis, respiratory failure, DIC, ATN, AKI Long term: stricture, pyloric stenosis

53 Management Do not induce emesis Gastric lavage contraindicated NSAID for pain Oxygen inhalation Tracheostomy if laryngeal oedema External burn / eye –immediate, repeated wash with water. Silver sulphadiazine ointment26 Management of complication- peritonitis Upper GI endoscopy Surgery-oesophageal sticture and gastric outlet obstruction after 4-6 weeks

54 Methanol Poisoning in Bangladesh- a Fatal case series: Robed Amin, Ariful Basher, F R Chowdhury, M A Faiz

55 Methanol Methanol 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  When 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 Methanol

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 Name Age in yrs TA 30 M.R 35 Mr D 40 J.H 40 M. M 55 B.B 55 A.A 35 B.H 50 Unconsiousness Nausea Vomiting(times) Visual disturbance Respiratory distress Abdominal Pain Diarrhoea Lag period3hrs48 hrs 7hrs6hrs48hrs6hrs7hrs3hrs Symptoms analysis of methanol poisoning

59 Name Age in yrs TA 30 M.R 35 Mr D 40 J.H 40 M. M 55 B.B 55 A.A 35 B.H 50 GCS Pulse84/m100/m80/m90/m100/m96/mNP72/m BP80/60120/80100/60100/70110/7090/60NR100/7 0 OpthalmoscopyDisc Oedem a Optic Atroph y Disc Oedem a Optic Atroph y Hypere mia Disc Conge stion Optic Atroo phy Hype remia Lungs Crackles Acidotic Breathing Shock Sign analysis of methanol poisoning

60 Rapidly developing optic atrophy in methanol poisoning

61 Management of Methanol poisoning Stomach wash, Oxygen inhalation Intravenous fluid, management of dehydration & electrolyte imbalance Injection Sodi-bi-Curb solution if acidosis, pH <7.35 or bicarbonate < 15 mEq/L Renal failure -Hemodialysis, Treat Convulsion with Diazepam

62 Antidote: Ethanol Mild poisoning: 95% Ethanol Orally 0.8 ml/kg loading dose followed by 0.1 ml/kg/hour or, Gin/ Whisky 1.8ml/kg loading dose then 0.2ml/kg/hour for 3 to 4 days diluted in fruit juice Severe cases:I.V. 10% ethanol 7.5ml/kg over 60 min then 1ml/kg/hour in non-drinker, 2ml/kg/hour in drinker 10% ethanol : 60ml 100% alcohol in 500ml 5% Dextrose

63 For Preservation of Vision Eye protection against light, Consultation with ophthalmologist Inj. Folinic acid 50mg IV- 4 hourly for hours Inj. B micro-gram IV daily for 5 days Inj. Methyl Prednisolone 1gm daily for 3 days may help

64 27 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. Date line 17, November 2001

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 series Cases J. 2009; 2: 9069.Published online Sep 1, Aniruddha Ghose 1*, Abdullah Abu Sayeed 1, Amir Hossain 1, Ridwanur Rahman 2, Abul Faiz 3 and Gofranul Haque

66 Accidental Barium carbonate poisoning It was kept in the kitchen as rodentocide, looks similar to flour In stomach Ba Carbonate turns into Ba Chloride (water soluble) BaCl absorbs through small intestine Produce hypokalaemia direct effect on the muscles.

67 Management Supportive Gastric lavage Sodium sulphate introduced to form insoluble Ba sulphate Fluid and Electrolyte correction Mechanical ventilation in case of respiratory failure Renal replacement therapy Haemofiltration Similar event in 1945 in a British Army regiment

68 Motive Behind Suicidal Poisoning Familial Disharmony73% Failure in examination5.7% Disappointment of Love affairs5.1% Poverty4.9% Physical illness2.3% Psychiatric illness2.2% Miscellaneous2.6% Unidentified4.1% 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 Nonconventional  Doctors and nurses are to be equipped with knowledge and logistics to manage the non conventional poisoning cases  Lack of preparedness on our part may result in loss of valuable lives  A 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 “..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..” Not all intoxications are treatable -Hazrat Ameer Khusru 1253–1325, Delhi. Close associate of Hazrat Nizamuddin Awlia (R.A )

72 Messi with his child Dr. X who had Copper Sulphate poisoning Love for precious life All living being want to live through offspring

73 Love for precious life Shahrisabz Samarkand Emir Taimur (April 9, February 18, 1405)

74 Acknowledgement Late Professor Dr AKM Rafiqueddin Professor Dr M A Faiz Dr Robed Amin Dr Fazle Rabbi Chowdhury Dr Chandra Shekhar Bala

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