Non Conventional Poisoning - PowerPoint Presentation

Slide1

Non Conventional Poisoning

HAM Nazmul AhasanProfessor of MedicineDhaka Medical College

Slide2

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.

Slide3

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.

Slide4

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.

 

Slide5

Slide6

Examination

He was found ill-looking with respiratory distress.He was moderately anaemic, severely icteric and mildly dehydrated.

Epigastrium

was tender.

Slide7

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

Slide8

Ingredients of Poisoning varies from country to country and even from one region to another within the same country.

Slide9

Poisoning in different regions

Source: Davidson’s Principal and Practice of Medicine 22nd Edition

Slide10

Distribution of registered patients according to place and name of agents

Place of case0

Name of pesticide

Total

Pesticide

Sedatives

Kerosine

Snake bite

Cu-

Sul

phate

Methanol

Potka fish

Others

OP

Carmate

Others

Benzodiazepine

Other sedative

DMCH

27923276018977310251212982318CMCH299781119343830313005051390Coxsbazar90044017000013119HathazariUHC26013511600074126Jenaida4453681713114039537Sitakund UHC290420712010863Total116833123737954139434720193745531324 (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

Slide11

Nonconventional poisoning

Copper sulphate poisoningPuffer fish poisoningMethanol poisoningAluminum

phosphide

Common household corrosives poisoning

Nitric

acid,

Hydrochl

oric

acid

,

Sulfuric

acids

Barium Carbonate poisoning

Slide12

‘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

Slide13

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 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

Slide14

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 ulcers

The Greeks

sprinkled a dry powder composed of copper oxide and copper sulfate on the wound.

Slide15

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

Slide16

Easily available in the local market

It is found in almost every houses in this localityCommon 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

Slide17

Copper

Sulphate poisoning in Khulna division :Age and Gender Distribution Sex

No. of cases (%)

Male

11 (26.19)

Female

31 (73.81)

Total

42 (100)

Age range

No. of cases

< 20

11

20

– 29

2430 – 3901

40 – 49

00

50 – 59

00

> 60

06

Slide18

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

Slide19

Copper

Sulphate ToxicityGIT Erosion, cramp, melenaeLiver Hepatocellular damage

RBC

Hemolysis

,

methaemoglobinaemia

Kidney

Hemoglobinuria

,

oligura

, AKI

Slide20

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.

Slide21

Clinical feature of Copper

Sulphate PoisoningFirst Day: Strong metallic taste, abdominal pain and burning, nausea, vomiting, diarrhea, salivationSecond 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

Slide22

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.

Slide23

Diagnosis:

Diagnosis is based on history of ingestion of copper sulphate.

Slide24

Lab investigation

CBC and PBF: Anaemia and Features of HaemiolysisLiver 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.

Slide25

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

Slide26

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 stage

Treat hepatic failure & Acute Kidney Injury

Hospital Management of Copper

Sulphate

Poisoning

cont.

Slide27

A Common aphorism in Khulna

Taka 2/=

Taka 3/=

Taka 5/=

Treatment c

ost (approximate)

Taka 20,000

Treatment c

ost (approximate)

Taka 30,000

No Treatment

is effective

Slide28

Puffer Fish Dishes

Looking Delicious!!

Slide29

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

Slide30

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

Fugu

It is the second most poisonous vertebrate in the world (275 times

deadlier than cyanide

poison).

Slide31

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

Slide32

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

Slide33

Puffer-fish Poisoning Outbreaks in

Bangladesh Year Place Victim

Death

1998 (November)

Cox’s

bazar

08

05

2002 (April)

Khulna

37

08

2005 (July)

Khulna

06

00

2008 (April)

Kishoreganj

03

02

2008 (April)

Norshingdi45052008 (June)Dhaka10032008 (June)Dhaka1003In addition from 1988-96 55 patient was reported. Out of them 16 died through out country.

Slide34

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

Slide35

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 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

Tetrodotoxin

(TTX)

Slide36

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

Slide37

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

Slide38

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.

Slide39

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

Slide40

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.

Slide41

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

Slide42

Aluminium

Phosphide Rat killer : for protection of grain and as fumigant

Slide43

Aluminium

PhosphideForms 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

Slide44

Clinical feature of ingested

phosphideNausea Vomiting Abdominal painHeadache Agitation chest tightness

Dyspnoea

Ologuria

Jaundice

Bleeding

Metabolic acidosis

Hypokalaemia

cardiac arrhythmia

Convulsion

Shock persistent

hypotension

Slide45

Clinical feature of

phosphide inhalationMild and moderate toxicitySevere toxicity

Eye and Nasal Irritation

Cough

Chest tightness

Headache

Nausea

Vomiting

Abdominal pain

Ataxia

dizzinesss

Hypotension

Metabolic acidosis

Hypokalaemia

Severe

dyspnoeaGI bleedingCardiac arrhythmiaCardiac failurePulmonary oedemaComa seizure

Slide46

Emergency monitoring

Pulse Blood PressureCadiac rhythmECG

Level of consciousness

Respiration

Pulse

Oxymetry

Acid base balance

Serum electrolyte

Serum

creatinine

Serum CPK

Serum

Trop

I

Slide47

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

Slide48

Household poisoning

Slide49

Household poisoning

DisinfectentHarpicDichlorometoxylenolCresol

Detergent

Soap

Washing liquids

Cosmetics

Cologne

Perfume

Lotions, nail polish

Bleach

Sodium Hypochlorite

Hydrogen peroxide

Petroleum products

Kerosene

Paraffin

TurpentinePaint thinnerFurnitures and floor polish

Slide50

Detergents and Disinfectants

Clinical feature nausea, vomiting, diarrhoea. corrosive effects to mucousaNail polish (acetone)-Irritation of mucous membrane, Metabolic acidosis, comaManagement

No specific antidote

Supportive treatment as

corrosive poisoning

Slide51

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

Slide52

Acids and corrosives

Skin: blister, pain, necrosis, ulceration, scarring after healingIngestion: 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

Slide53

Management

Do not induce emesisGastric 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

Slide54

Methanol poisoning

Methanol Poisoning in Bangladesh- a Fatal case series: Robed Amin , Ariful

Basher, F R

Chowdhury

, M A

Faiz

Slide55

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

Slide56

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

Slide57

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

Slide58

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)4536610412Visual disturbance-+--+-+-Respiratory distress-+++---+Abdominal Pain-++++--Diarrhoea-----+--Lag period3hrs48 hrs 7hrs6hrs48hrs6hrs7hrs3hrsSymptoms analysis of methanol poisoning

Slide59

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

6

38812457Pulse84/m100/m80/m90/m100/m96/mNP72/m BP80/60120/80100/60100/70110/7090/60NR100/70 OpthalmoscopyDisc OedemaOptic AtrophyDisc OedemaOptic AtrophyHyperemiaDisc CongestionOptic AtroophyHyperemiaLungs Crackles-+++---+ Acidotic Breathing++++++++ Shock+----++-Sign analysis of methanol poisoning

Slide60

Rapidly developing optic atrophy in methanol poisoning

Slide61

Management of Methanol poisoning

Stomach wash, Oxygen inhalationIntravenous 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

Slide62

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

Slide63

For Preservation of Vision

Eye protection against light, Consultation with ophthalmologistInj. Folinic acid 50mg IV- 4 hourly for 24-48 hours

Inj. B12 1000 micro-gram IV daily for 5 days

Inj. Methyl

Prednisolone

1gm daily for 3 days may help

Slide64

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

Slide65

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

Ghose

1

*

, 

Abdullah Abu Sayeed

1

, 

Amir Hossain

1

, Ridwanur Rahman2, Abul Faiz3 and Gofranul Haque1 

Slide66

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 intestine

Produce

hypokalaemia

direct effect on the muscles.

Slide67

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

Slide68

Motive Behind Suicidal Poisoning

Familial Disharmony 73%Failure in examination 5.7%Disappointment of Love affairs 5.1%Poverty 4.9%Physical illness 2.3%Psychiatric illness 2.2%

Miscellaneous 2.6%

Unidentified 4.1%

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, 197-199

Slide69

Take Home Message

Poisoning is a common medical emergencySome are conventional and Some are NonconventionalDoctors 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

Slide70

‘..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

Slide71

“..You've taken away my looks, my identity, by just a glance.

By making me drink the wine from the distillery of loveYou'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)

Slide72

Messi

with his childDr. X who had Copper

Sulphate

poisoning

Love for precious life

All living being want to live through offspring

Slide73

Love for precious life

Shahrisabz

Samarkand

Emir

Taimur

 (

April 9, 1336 -  February 18, 1405) 

Slide74

Acknowledgement

Late Professor Dr AKM RafiqueddinProfessor Dr M A Faiz

Dr Robed

Amin

Dr

Fazle

Rabbi

Chowdhury

Dr Chandra

Shekhar

Bala

Slide75

Thank

you