1. Non Conventional Poisoning
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.

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 22nd Edition

10. Baseline Survey on Poisoning in six centers
Study of Poisoning at different health facilities:1993
Baseline Survey on Poisoning in six centers
Place of case0
Name of pesticide
Total
Pesticide
Sedatives
Kerosine
Snake bite
Cu-Sul phate
Methanol
Potka fish
Others OP
Carmate
Benzodiazepine
Other sedative
DMCH
279 23 27
601
897 73
102 5 12 1
298
2318
CMCH
299 7 81
119 34 38
303 3 00
505
1390
Coxsbazar 90 4 40 13
Hathazari
UHC 26 16 74
126
Jenaida
445 6 8 17 39
537
Sitakund UHC 29 2 63
1168 33
123
737
954
139
434 20
937
4553
1324 (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

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
Diagnosis
Total number of patients (%)
Unknown poisoning
82 (22.97)
OPC poisoning
76 (21.29)
Snake bite
64 (17.93)
Sedative
48 (13.45)
Copper sulphate
42 (11.76)
Harpic
17 (04.76)
Food
9 (02.52)
Rat killer
5 (01.40)
Insect bite
3 (00.84)
Savlon
Kerosene
2 (00.56)
Ascabiol
Dettol
1 (00.28)
Octane poisoning
Glass cleaner
Mercury
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
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
Age range
No. of cases
< 20 11
20 – 29 24
30 – 39 01
40 – 49 00
50 – 59
> 60 06
Sex
No. of cases (%)
Male
11 (26.19)
Female
31 (73.81)
Total
42 (100)

18. Copper Sulphate poisoning is associated with High Mortality
Cause of death
No. of cases
Acute hepatic failure 5
Acute renal shutdown 4
Total 9
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.
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, 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. Hospital Management of Copper Sulphate Poisoning cont.
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

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

28. Puffer Fish Dishes Looking Delicious!!

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 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. Puffer Fish Poisoning
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

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

33. Puffer-fish Poisoning Outbreaks in Bangladesh
Year
Place
Victim
Death
1998 (November)
Cox’s bazar 08 05
2002 (April)
Khulna 37
2005 (July) 06 00
2008 (April)
Kishoreganj 03 02
Norshingdi 45
2008 (June)
Dhaka 10
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. Tetrodotoxin (TTX)
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

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
Aluminium Phosphide
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

48. Household poisoning

49. Household poisoning Disinfectent Detergent Cosmetics Bleach
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
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. Methanol
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

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
Name
Age in yrs TA 30
M.R 35
Mr D 40
J.H
M. M 55
B.B
A.A
B.H 50
Unconsiousness + -
Nausea
Vomiting(times) 4 5 3 6 10 12
Visual disturbance
Respiratory distress
Abdominal Pain
Diarrhoea
Lag period
3hrs
48 hrs
7hrs
6hrs
48hrs

59. Sign analysis of methanol poisoning
Name
Age in yrs TA 30
M.R 35
Mr D 40
J.H
M. M 55
B.B
A.A
B.H 50
GCS 6 3 8 12 4 5 7
Pulse
84/m
100/m
80/m
90/m
96/m NP
72/m BP
80/60
120/80
100/60
100/70
110/70
90/60 NR
Opthalmoscopy
Disc Oedema
Optic Atrophy
Hyperemia
Disc Congestion
Optic Atroophy
Lungs Crackles - +
Acidotic Breathing
Shock

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. Date line
17, November
2001
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.

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, 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 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 Similar event in 1945 in a British Army regiment 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 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 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. 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 child
Dr. X who had Copper Sulphate poisoning

73. Love for precious life Emir Taimur (April 9, 1336 - February 18, 1405)
Shahrisabz
Samarkand

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

75. Thank
you