A Dissertation on THE TAMIL NADU DR.M.G.R.MEDICAL

A Dissertation on “CLINICAL PROFILE OF RAT KILLER PASTE POISONING ”

Submitted to

THE TAMIL NADU DR.M.G.R.MEDICAL UNIVERSITY

CHENNAI - 600032

In partial fulfillment of the regulations for the award of the degree of

M.D. BRANCH – I (GENERAL MEDICINE)

DEPARTMENT OF GENERAL MEDICINE

GOVERNMENT STANLEY MEDICAL COLLEGE, CHENNAI.

THE TAMIL NADU DR. M.G.R.MEDICALUNIVERSITY

TAMILNADU, INDIA

MAY 2020

CERTIFICATE BY INSTITUTION

This is to certify that this dissertation entitled “CLINICAL PROFILE OF RAT

KILLER PASTE POISONING” submitted by Dr .V.KARTHICK to the faculty of

General Medicine, The Tamil Nadu Dr. M.G.R Medical University, Chennai, Tamil

Nadu, in partial fulfillment of the requirement for the award of M.D DEGREE

BRANCH-I (GENERAL MEDICINE) is a bona fide research work carried out by him

under my direct supervision and guidance.

GUIDE HOD

Prof. Dr .T.B.UMADEVI .MD Prof. Dr.C.HARIHARAN.MD

Professor of Medicine, Head of the Department,

Department of Medicine, Department of Medicine,

Stanley Medical College and Hospital, Stanley Medical College and Hospital,

Chennai - 1. Chennai- 1.

PROF. DR.R.SHANTHIMALAR, M.D., D.A.,

DEAN

Government Stanley Medical College and Hospital, Chennai-1.

CERTIFICATE BY THE GUIDE

This is to certify that Dr. V.Karthick ,Post Graduate student (May2017 to April 2020) in

the Department of General Medicine ,Government Stanley Medical College and

Hospital,Chennai-1,has done this dissertation work titled “CLINICAL PROFILE OF

RAT KILLER PASTE POISONING” under my guidance and supervision in partial

fulfillment of the regulations laid down by The Tamil Nadu Dr. M.G.R.Medical

University, Chennai for M.D.,(General Medicine),Degree examination to be held in May

2020.

Prof. Dr. T.B.UMADEVI M.D.,

Professor of Medicine ,

Department of Medicine,

Stanley Medical College and Hospital,

Chennai - 1.

DECLARATION

I, Dr.V.KARTHICK, solemnly declare that the dissertation titled “CLINICAL

PROFILE OF RAT KILLER PASTE POISONING”is a bona fide work done by me

at Government Stanley Hospital, Chennai during March 2018 to August 2018 under the

guidance and supervision of Prof. Dr. T.B.UMADEVI M.D., Professor of Medicine,

Government Stanley Hospital, Chennai. I also declare that this bona fide work or a part of

this work was not submitted by me or any other for award degree or diploma to any other

university, board either in India or abroad. This dissertation is submitted to the Tamil

Nadu Dr. M.G.R Medical University, towards the partial fulfillment of requirement for

the award of M.D. Degree (Branch – I) in General Medicine.

Place: Chennai Signature of the candidate

Date: (Dr.V.KARTHICK )

CERTIFICATE - II

This is to certify that this dissertation work titled “CLINICAL PROFILE OF RAT

KILLER PASTE POISONING ”of the candidate Dr.V.Karthick with Registration

Number 201711055 for the award of M.D., DEGREE in the branch of BRANCH-I

(GENERAL MEDICINE). I personally verified the urkund.com website for the purpose

of plagiarism check. I found that the uploaded thesis file contains from introduction to

conclusion pages and result shows 6 percentage of plagiarism in the dissertation.

Guide & Supervisor sign with Seal

SPECIAL ACKNOWLEDGEMENT

I gratefully acknowledge and thank

PROF. DR.R. SHANTHI MALAR M.D., D.A.,

DEAN

GOVERNMENT STANLEY MEDICAL COLLEGE AND HOSPITAL, CHENNAI.

For granting me permission to utilize the resources of this

Institution for my study

ACKNOWLEDGEMENT

At the outset I thank our Dean DR.SHANTHI MALAR,M.D.,DA.,

for permitting me to carry out this study in our hospital.

I express my profound thanks to my esteemed Professor and Teacher

Dr. C.HARIHARAN, M.D., Professor and HOD of Medicine, Stanley Medical

College Hospital, for encouraging and extending invaluable guidance to perform

and complete this dissertation.

I immensely thank my unit chief Dr. Nalini Kumaravelu MD, for her

constant encouragement and guidance throughout the study.

I wish to thank Dr. RSA Alexander MD and Dr. Vijayalakshmi MD,

Assistant Professors of my unit, Department of Medicine, Stanley Medical College

Hospital for their valuable suggestions, encouragement and advice. I sincerely

thank the members of Institutional Ethical Committee, Stanley Medical College for

approving my dissertation topic.

I thank all my colleagues, House Surgeons, and Staff nurses and other para

medical workers for their support.

At this juncture I would also want to extend my heartfelt gratitude to my family for

their constant support and care.

I sincerely thank all those patients who participated in this study, for their

co-operation.

ABBREVATIONS :

ALT :ALanine Transaminase (or) ALanine Aminotransferase.

ANTU : Alpha – NaphthylThio Urea.

DIC : Disseminated Intravascular Coagulation.

ECG : Electro CardioGram.

FFP : Fresh Frozen Plasma. 6. GIT : Gastro Intestinal Tract.

INR :Internatinational Normalized Ratio.

LD 50 : Lethal Dose in 50% of individuals.

ppm : parts per million.

.PT :Prothrombin Time. 11.SGPT : Serum Glutamic Pyruvic Transaminase.

DOA : Date Of Admission .

CNS : Central Nervous System .

BP : Blood Pressure .

CVS : Cardio Vascular System . 6) RS : Respiratory System .

RBS : Random Blood Sugar .

SGOT : Serum Glutamic ornithylTransferase.

SGPT : Serum Glutamic Pyruvic Transamnase

PT :Prothrombin Time.

INR : International Normalised Ratio .

TABLE OF CONTENTS

S.No CHAPTERS PAGE NUMBER

1 INTRODUCTION 1

2 AIM AND OBJECTIVES OF THE STUDY 7

3 REVIEW OF LITERATURE 8

4 MATERIALS AND METHODS 27

5 STATISTICAL ANALYSIS 29

6 RESULTS 30

7 DISCUSSION 67

8 CONCLUSION 79

9 BIBLIOGRAPHY 80

10 PROFORMA 88

11 ETHICAL COMMITTEE 92

12 PLAGIARISM CERTIFICATE 93

13. INFORMED CONSENT 94

14. MASTER CHART 96

1

INTRODUCTION

Poisoning is mostly preventable, commonly suicidal and rarely being an accidental form

of death in developing agrarian countries. In rural India, poisoning forms the major share

of emergency health care and of about one – fourth to one – third of intensive care

admissions.Among poisoning, in our region, next to organophosphorus poisoning, rat

killer or rodenticide poisoning remains the second most common ingested poison.

However, as compared to organophosphorus poisoning, there are only few works of

literature available for rodenticide poisoning. [1,2]

Almost every system is affected in rodenticide poisoning and also there are no definite

treatment guidelines available. Regarding its incidence, mode of action and management,

only a few studies are available. Further there are no positive clinical trials available

regarding phosphorus paste poisoning, which remains the deadliest among rodenticide

poisons.[3]

Rodenticides are commonly available in almost every household, to prevent their stored

grains from rodents, which is found everywhere. Since it is easily available and also

cheaper than other 1 pesticides in the markets. Because of its easy availability in every

house, it is often taken with a suicidal indent or ingested accidentally by children. [4]

Rodenticide is available in three different forms in our area.

Among these rodenticides, phosphorus is the most commonly and also most lethal Most

common forms available in market includes

2

Powder

Paste

Cakes

Pellets .

RAT KILLER CAKE

The easily available and the less toxic “cake” form contains warfarins and superwarfarins

acts by inhibiting vitamin K cycle thereby preventing the regeneration of reduced vitamin

K from the oxdised form.

RAT KILLER POWDER

The “powder” form contains zinc phosphide and thallium.

The zinc phosphide release phophine gas on contact with water in gastrointestinal tarct

causing heaptic, renal, gastrointestinal toxicity, acute lung injury, coma , seizures.

Thallium combines with sulfhydryl groups, interferes with oxidative phosphorylation

producing anorexia, abdominal pain, diarrhea, painful neuropathy, alopecia, coma.

RAT KILLER PASTE

Paste forms usually contains elemental phosphorus. The three known phosphorus types

1. Yellow phosphorus

2. White phosphorus

3. Red phosphorus.

Among these three forms Red phosphorus is not absorbed and essentially non toxic.

White phosphorus is used mainly in ammunition and fireworks as an explosive agent.

3

The paste form contains 3 % yellow phosphorus as active ingredient. It is a corrosive

agent damaging all tissues it contacts.

Among these rodenticides, phosphorus is the most commonly and also most lethal

poison, especially after 3-4 days of ingestion, as liver injury sets in. Since there are no

sufficient data available regarding rodenticides, [5]In 1990 it estimated that self‐ harm

resulted in 2million cases of poisoning each year with 200000 deaths. In contrast,

accidental and occupational exposure were estimated to cause 1 million cases with 20 000

deaths. Studies have shown that deliberate self‐ poisoning has far higher mortality than

accidental poisoning.[6]

Organophosphates, pesticides are the most commonly used poisonings for suicide. A

pesticide is usually defined as a chemical substance, biological agent, antimicrobial or

disinfectant used against pests including insects, plant pathogens, weeds, mollusks, birds,

mammals, fish, roundworms and microbes that compete with humans for food, destroy

property, have a propensity for spreading or are a vector for disease or simply a nuisance.

The types of pesticides commonly used are also called 1.Insecticides. 2.Herbicides. 3.

Fungicides. 4. Rodenticides[7,8]

RODENTICIDES:

Rodenticides, pesticides specially designed to kill rodents, pose particular risks for

accidental poisoning for several reasons. Since they have been designed to kill mammals,

they are also toxic to humans. Because rodents usually share human environments, the

4

use of rodenticides poses an inherent risk of exposure to people, particularly children and

their pets, as well as other non-target species. They are among the most toxic compounds

regularly found in homes. Rodenticide poisoning has varied incidence across the country.

The mortality rates also vary significantly. The type and quantity of poison consumed,

lack of a specific antidote for some of the rodenticides and time-lapse in treatment affect

the outcome. [9,10]

CLASSIFICATION OF RODENTICIDES:

Who classification

1. Warfarin

2. Warfarin like compounds (brodifacoum, chlorophacinone, difenacoum, diphacinone,

bromadiolone )

3. Calciferol (cholecalciferol, ergocalciferol)

4.Fluoroacetates (Sodium fluoroacetate, Fluoroacetamide)

5. Metal phosphides (,phosphorus, aluminium phosphide, , zinc phosphide, magnesium

phosphide, yellow phosphorous )

6. Chloralose

7. Others (arsenic, thallium, strychnine) [11,12]

5

CLASSIFICATION OF RODETICIDES BASED ON TOXICITY:

HIGHLY TOXIC RODENTICIDES:

Highly toxic rodenticides are those substances with a single dose LD50 of less than

50mg/kg body weight. Some of these compounds have largely been abandoned because

of serious human toxicity. This group includes

1. Aluminum phosphide

2.Sodium monofluoroacetate

3.Strychnine,

4. Zinc phosphide,

5. Yellow phosphorus

6.Arsenic.

7. Thallium

MODERATELY TOXIC RODENTICIDES:

Among the moderately toxic rodenticides, those with LD50 of more than 500 mg/kg body

weight are

1. alpha-naphthyl-thiourea (ANTU)

2. DDT.

6

Patients who ingest large quantities of ANTU may develop dyspnea, rales, and cyanosis

(secondary to pulmonary edema) and hypothermia. Poisoning from exposure to DDT can

result in symptoms such as vomiting, tremors, and convulsions. How much exposure is

required to cause severe illness or even death is, however, not certain. [13,14,15]

LOW TOXICITY RODENTICIDES:

Low toxicity rodenticides are those with LD50 between 500 and 5,000 mg/kg body

weight and include

1. Red squill.

2. Norbomide.

3. Anticoagulants warfarin-type rodenticides.

1. Red squill: Red squill contains several compounds with chemical and pharmacological

properties similar to those of digitalis glycosides. Because of its emetic properties, poor

gastrointestinal absorption and decreased potency (compared to that of digitalis), red

squill has seldom been associated with human toxicity

2. Norbomide: Norbomide is an irreversible smooth muscle constrictor. It causes

widespread ischemic necrosis and death in rats but does not appear to affect other animals

or humans, presumably due to the presence of a specific smooth muscle norbomide

receptor found only in rats.[16,17]

7

AIM AND OBJECTIVE OF THE STUDY

1.To study the clinical profile of patients admitted with rodenticide poisoning and their

course in the hospital.

2. To correlate various parameters with the mortality.

8

REVIEW OF LITERATURE

Rat killer (Ratol) paste contains yellow phosphorus. White phosphorous with its

impurities is called yellow phosphorus. It is used in the firework industry, in bombs, as

Rodenticide. In South India, it is commonly available as rat killer paste (3%). [18]The

toxic dose of yellow phosphorous is 100 mg/kg body weight and toxicity increases when

taken with a fatty meal. Yellow phosphorus causes hepatotoxicity by the production of

phosphoric acid, which causes free radical damage. This poisoning is associated with

high mortality. The good prognostic factors are survival after 3 days and minimal

elevation of LFT. Bad prognostic signs are altered sensorium, cyanosis, hypotension,

metabolic acidosis, elevated prothrombin time, and hypoglycemia.The first phase consists

of nausea, vomiting, abdominal pain, and smoking stools. Then, in the second phase, the

patient may feel symptomatically better and the third stage consists of systemic organ

damage due to absorbed phosphorous. Hepatotoxicity usually is recognized on the 3rd

day by liver function test (LFT). A large number of early deaths.[19,20]

There was competition between humans and rodents for food since the past. Due to his

super-brain, humans developed some agents to kill the rodents. Rodenticides are

produced in such a way to kill the rodents, which damage the crops in the field , stored

grains in godowns, bite peoples and also capable of spreading deadly diseases such as

plague. It includes variety of chemicals with various actions, which may be organic or

inorganic, may be mild or highly toxic, but they kill them in a cost-effective manner.

Now the problem arises because humans either accidentally or intentionally ingest these

9

chemicals. In earlier days rodenticides were mainly made from plant such as strychnine

or inorganic chemicals as thallium and arsenic trioxide.Now, they are manufactured from

synthetic organic compounds Some agents such as thallium are as dangerous to humans

as rodents. However their use is restricted nowadays to lessen the risk of toxicity in

humans especially. But still, they are regarded as toxic, if they are misused[21,22,23]

Environmental poisoning was also found as a significant cause of poisoning admissions

to the hospital. Reptile bite is one of the major environmental poisoning occurring in

rural areas than the urban area. The present study reports environmental poisoning was

seen more in adult males followed by females and this was due to snake bite, followed by

bee Stings, insect and scorpion bite.[19,20]

Poisoning incidence also varies according to the seasons. Incidence was seen more in the

summer season followed by the winter season. Incidences of poisoning during summer

months are more because as the summer days being longer and during which the person

becomes easily fatigued and exhausted as a result of extreme heat conditions leading to

mental imbalance. Another reason may be the preservation of grains during summer is

more and in order to protect them, pesticides are procured and preserved[19]. Due to the

easy accessibility to pesticides, people may try to consume pesticides to end their life

when they suffer from economic burdens or any emotional conflicts.

The reasons observed for the mortality in poisoned individuals were the delay in

admission to the hospital, improper management of the poisoned patient, lack of

information regarding the poison agent and its antidote. To reduce the poison induced

10

morbidity and mortality following steps such as having a centralized poison information

center, availability of standard treatment protocols for managing various poisons, and

educational programs for rural people may be more appropriate[27,28]

It was first identified in urine by chemist HENNING BRANT in Hamburg in 1669. The

early use of phosphorus was in 1720 in medical books. It was used for colic, tetanus,

gout, and apoplexy. It was popular as a tonic aphrodisiac, impressing onlooker of its

phosphorescent and explosive nature. Inspite of its toxicity, it was found in British

pharmacopeia till 1932. White phosphorus gained importance since it was used as main

ingredient in lucifers or in match industry. It was invented by chemist Charles Sauria of

Paris in 1830. It was mainly used in match industry.[19,20] After some years it was

banned worldwide as of using in striking pad. On the matchbox, and now red phosphorus

has replaced it, in striking pad as well as match head. 6 White phosphorus is now used to

manufacture, insecticide, fertilizer as phosphoric acid and homemade wirework [15]

which contain about 10% phosphorus. Phosphorus isthe 15th element in table, it exists in

3 forms I) black phosphorus →nontoxic, not ignite spontaneously II) red phosphorus

→faily innocuous→ intermediate reactivity iii) white phosphorus →highly reactive and

dangerous compound. White phosphorus in tetramer (D4), water-insoluble, a waxy paste.

It emits pale green glow, due to low reactivity with oxygen. Impurities in white

phosphorus make it as yellow phosphorus.[8,16] Phosphorus on combining with oxygen

gives Phosphorus oxide with liberation of light and dense smoke with Garlic odor, On

dissolving with water, it produces phosphoric acid. It is rapidly absorbed and distributed

11

primarily in the liver, kidney, intestinal mucosa, epidermis, follicles, and pancreas Other

tissues such as lung, myocardium, spleen and renal medulla of moderate distribution,

brain fat and muscle of low distribution[ 39]. 7 In rats, sub-cutaneous lethal dose in 10mg

/kg(8) while in human studies suggest lethal dose as 50mg or 1mg/kg.(9). It is highly

lipid solubility, high absorption occur after skin or mucosal exposure[25,26]

MECHANISM OF TOXICITY

It is a protoplasmic poison.

It has a direct toxic effect over heart causing cardiovascular collapse.

Its spontaneous combustion nature yeilds phosphorus oxide which is a

highly irritating substance

TOXOKINETICS

.White phosphorus is rapidly absorbed from the intestinal tract.

After getting aborbed into the systemic circulation, it is mainly getting

concentrated in th e liver, renal cortex, bowel mucosa, epidermis,

pancrease and adrenal cortex.

Within several hours of ingestion 75 % of the total ingested dose is

concentrated in the liver

12

.DISTRIBUTION OF WHITE PHOSPHORUS BY DIFFERENT BODY TISSUES

UPTAKE

HIGH

MODERATE

LOW

Adrenal cortex

Bowel mucosa

Epidermis

Hair follicles

Liver

Pancrease

Renal cortex

Adrenal

medulla

Endometrium

Lung

Myocardium

Ovary

Renal medulla

Spleen

Bone

Fat

Brain

Myometrium

Skeletal

muscle

TOXIC DOSE

Ingestion : 1 mg/kg is fatal dose

Inhalational : 5 mg/kg ( immediately dangerous to life and death

[ Recommended work place limit-0.1 mg/cubic meters as an 8 hour time weighted

average ]

White phosphorus is highly lipid-soluble so that more absorption after skin or mucosal

exposure.

13

CLINICAL MANIFESTATIONS:

Ingestion of more than 1mg/kg

Severe electrolyte disturbance

mental status changes prolongation of the q-t interval

more than 10 fold rise in alanine aminotransferase

severe coagulopathy

peak liver enzymes reached within three days of ingestion

Old literature describes the course of poisoning in 3 stages (13)

I STAGE-It lasts- hours to days after ingestion manifested as irritation of digestive tracts,

may cause arrhythmias and same neurological manifestations.

II STAGE: The digestive symptoms resolve, lasting for few days patients develop

hepatic, renal and cardiac toxicities, mostly causing death.

If recovery occurs, it takes few weeks However most death occurs as a result of a

fulminant hepatic failure within first week. Some delayed death occurs between 5-8 days

due to cardiotoxic. Few deaths only occur,if patient survives beyond this stage.

14

HEPATIC:

It produces hepatotoxicity in dose-dependent manner (14). Aminotransferase rises in half

of ingested patients, mostly begin to rise within one day of exposure. Time of enzyme

peak and level rise differ significantly between patient who survives and who dies.

Patients who die have average peak of sixteen times of normal, reached in 2-3 days. In

those who survive, alanine aminotransferase (SGOT) rises eight times normal, reaching

peak in six days. Serum triglyceride level fall as toxicity develops, there may be also

increased in serum and urinary ketones It consumes oxygen in liver cells, is a

protoplasmic poison which uncouples oxidative phosphorylation, in turns leads to

decrease in intrahepatocyte ATP levels[27,28] It also affects transition of triglyceride as

betalipoproteins. Massive hepatic steatosis, hallmark of white phosphorus toxicity, rise in

triglyceride level in two hours, peaking in two days. Hepatic necrosis is particularly in

zone 1, distinct from acetaminophen and carbon tetrachloride, hepatic glycogen is

decreased due to increased glucose-6- phosphatase activity.[16,29] A nonspecific finding

of huge increase in rough endoplasmic reticulum is typically found in this poison [30,31]

Liver biopsy showed signs of acute hepatocellular necrosis also showing fibrosis and

piecemeal necrosis

EPIDEMIOLOGY :

World Health Organization (WHO) estimated 0.3 million people die every year due to

various poisoning agents[5]. Acute pesticide poisoning is one of the most common causes

of intentional deaths worldwide[6]. High doses of analgesics, tranquilizers, and

15

antidepressants are the commonly used agents for intentional poisoning in industrialized

countries[7] and agricultural pesticides are used in the Asian region for self-poisoning

particularly in rural areas with a fatality range of 10-20%[8]. The majority of pesticide

exposure is seen more in middle and low-income countries due to increased use of

agrochemicals in agricultural sector[9].

Studies have revealed that pesticides are commonly used poisoning agents for intentional

poisoning in India[10]. As agriculture is a major profession in the rural part of India

farmers stock the pesticides to eradicate the weeds and pests. Due to easy availability of

pesticides, they are commonly used by individuals to end their life in stressful

situations[11].

There are scarce epidemiological data regarding the ingestion of yellow phosphorous in

the subcontinent. Case series of general poisonings from Nepal [24], rodenticide

poisonings from Mysore, India [25,6] and Rajasthan, India [26] all show a predominance

of young adults between ages 15 to 40 years old. The Nepalese study highlighted the

greatest burden among homemakers, laborers, and farmers [27]. Extrapolating from our

experience with organophosphate poisonings and as illustrated in this case, we surmise

these ingestions are impulsive acts in an environment where highly toxic substances are

cheap and readily available. This supposition is supported by previously published data

from Sri Lanka, Karnataka, and Rajasthan; in Karnataka, fully 94% were impulsive acts

of self-harm [28,29].

16

NATURAL HISTORY, TREATMENT, AND PROGNOSTIC FACTORS

The time course of a brief asymptomatic period followed by acute liver failure at 72

hours fits other clinical reports of yellow phosphorus ingestions [30]. We surmise that

patients with yellow phosphorus poisoning should be observed closely for at least 3 days,

given the 72-hour asymptomatic latent period. Other authors suggest a week [31]. Other

toxic manifestations include central nervous system effects (restlessness, irritability,

drowsiness, lethargy, stupor, or coma) [32], acute tubular necrosis, bone marrow toxicity

[33], arrhythmias and hemodynamic instability [34]. Clinical manifestations and outcome

vary in different reports. In one case series, 87% had some hepatic derangement and 27%

developed fulminant hepatic failure and died [35]. Similarly, mortality in a second case

series was 28% [36]. Another series found a range of 23-73% mortality depending on

clinical manifestations, with early central nervous system manifestations portending

poorer prognosis [37]. MELD score has been described as a prognostic indicator in

rodenticide poisoning (including yellow phosphorous): average MELD for those who

died was 40.5 as compared to 11.7 for survivors [38]. The patient’s highest MELD score

was 32 (Creatinine 0.6, Total Bilirubin 6.6, INR 4.1).

Some recommend gastric lavage with 1:5000 potassium permanganate followed by

activated charcoal and mineral oil cathartic [12,13]. Clinical studies in rodenticide

poisoning have conflicting evidence about the use of N-Acetylcysteine (NAC) and

adjunctive therapies. One case series showed no benefit [7]; in contrast, Lovejoy FH:

Thallium et al. suggest that early use of NAC improves outcomes for all rodenticide

17

poisonings with liver failure. In that study, survival rates varied based on timing of NAC

administration after rodenticide ingestion: 76% survival rates if NAC was administered

on Day 1, 40% survival if administered on Day 2 and 23% survival if administered 3 or

more days after ingestion [39] though this data is confounded by early gastric lavage for

those presenting shortly after consumption. In light of NAC’s safety profile and recent

guidelines suggesting a role for NAC in non-acetaminophen based liver failure [40], we

chose to administer this drug. Other adjuncts such as corticosteroids and exchange

transfusion have been studied but have not shown clinical benefit [41].

Mozingo DW Smith et al. [18] case series of acute liver failure secondary to phosphorus

ingestion, the two causes of death were massive upper gastrointestinal bleeding and

cerebral edema. In their series, 73% had prolonged PT time and received FFP while only

40% of patients had signs of bleeding [43]. Current American Association for the Study

of Liver Diseases (AASLD) guidelines for the management of acute liver failure

recommend at least one dose of vitamin K subcutaneously, reserving FFP and platelet

transfusion for those with active bleeding or needing invasive procedures [29,44]. These

same guidelines suggest proton pump inhibitors or H2 receptor antagonists for ulcer

prophylaxis [45]. The patient received 13 units of fresh frozen plasma, intramuscular

vitamin K and pantoprazole during her hospital stay. She did not develop clinically

significant bleeding. Due to India’s strict legislation regarding blood banking, this had to

be procured by the patient’s brother from a hospital in a nearby city. Our inability to

maintain a blood bank has serious implications for the care of critically ill patients like

18

our patients [46]. Few patients have families with the time or financial wherewithal to

travel to and from the local city this frequently

CLINICAL MANIFESTATIONS

SKIN, MUCOSA AND GASTROINTESTINAL TRACT:

Burns produced by this poison is extremely painful with characteristic garlic odor, yellow

color, and necrotic base. it heals slowly like other chemical burns, and also requires

prolonged hospital stay[23,24], which may be of second degree or third-degree burns

involving 15% of body surface area, may result in death[25], due to absorption of

phosphorus. Mucosal erosions were also noted, when they get exposed to mouth, eyes, it

may show bullae, injection. Thus following intake of phosphorus, it may show oral burns,

vomiting, loose stools, abdominal pain and even bleeding, as hematemesis. the vomitus

and stool show typical garlic odor, and it also appears as glistening in dark room, hence it

is also mentioned as smoking stool syndrome.[9,35] The main mechanism is exothermic

reaction. If it penetrates dermis, causes tissue damage, due to production of phosphoric

acid, when reacting with oxygen. The digestive system is less involved than skin,

probably due to low oxygen concentration. Severe mucosal involvement is also explained

due to generation of phosphoric acid.[32,33]

19

CARDIOVASCULAR SYSTEM

Early death within twenty-four hours, after intake of phosphorus, is mainly due to

cardiovascular collapse Electrocardiograph taken during interval hours of admission may

reveal. QT prolongation, atrial fibrillation, ST depression, which may be due to

electrolyte deficiency, mainly of calcium. [22,23] Cardiac arrest also occurs, after few

hours of even dermal exposure, it generally occurs 4-10 hours after absorption. Cardiac

arrest without any rhythm disturbances or myocardial injury is also reported.

hypocalcemia also causes cardiomyopathy and mimics like myocardial

infarction.[18,29]Usually there are no morphological changes, however intestinal edema

and vacuolated cytoplasm urine noted.

NERVOUS SYSTEM:

It produces neurological manifestation such as anxiety, confusion, irritability,

hallucination, epilepsy, loss of consciousness and deep coma. If any patient is found to

have neurological findings initially before the involvement of other systems, it had

increased mortality of 20 %.Hypocalcemia can produce carpopedal spasm,

paraesthesia,tetany or laryngeal stridor. However, neural uptake of phosphorus is only

small quantity there was also no distinct histological change in the brain. Thus

neurological manifestation was mainly due to hypocalcemia, rather than due to direct

effect of phosphorus.[43,44]

20

RENAL:

Half of the cases have shown increase urea and creatinine values, but only a few

developed chronic kidney disease.[45] Rarely acute tubular necrosis also noted. It mainly

causes glomerular injury after absorption in GIT, histological finding shows fatty

degeneration in few cases and fatty deposition with necrotic changes in some. [34,35]

ELECTROLYTE DISTURBANCES:

Due to the absorption of phosphorus and into conversion to phosphoric acid, some

deproteination, hyperphosphatemia were noted. Calcium forms calcium phosphates salts

which lead to hypocalcemia. Hyperkalemia was noted, due to hypocalcemia or due to

renal failure.[36,37]

STAGES OF POISONING

There are 3 stages of clinical manifestations are seen in the poisoning patients.

1. FIRST STAGE

It corresponds with the first 24 hours after ingestion.

Most of the patients are asymptomatic during this period.

Some may have symptoms like vomiting and abdominal pain due to

local gastrointetinal irritation.

Sudden cardiac death may occur dring this period due to cardiac

arrhythmias.

Also seen are neurological manifestations due to hypocalcemia.

21

2. SECOND STAGE

This stage occurs within 2 –3 days of ingestion.

Patients may be asymptomatic during this stage

Acute fulminant hepatic failure may develop and patient will be having

jaundice, vomiting ,abdominal pain, and encephalopathy requiring liver

transplantaion. Caogulopathy symptoms can be seen due to loss of clotting

factor mechanisms.

3. THIRD STAGE

This stage corresponds from 4th day to 8 th day after ingestion.

Death may ensue because of fulminant hepatic failure and delayed acrdiac

toxicity.

4. FOURTH STAGE

Corresponds to 8 th day after ingestion.

This stage correlates with the recovery phase.

DIFFERENTIAL DIAGNOSIS :

Unknown rodenticide exposure may be identified by a few findings Rapid action poisons,

may manifest symptoms within six hours, if it shows more cholinergic findings, it

suggests organophosphorus poisoning. More muscular activity suggests strychnine

poisoning More gastrointestinal symptoms such as mucosal burns, vomiting, abdominal

pain and loose stools, suggests yellow 13 phosphorus poisoning. If it shows respiratory

symptoms suggest zinc phosphide. Delayed poisoning, manifests usually after twelve

22

hours, most commonly due to superwarfarin groups [27,40]The smell also shows some

clue such as phosphorus smell as garlic; while zinc and aluminum phosphide smell as

rotten fish, due to liberation of phosphine gas as it combines with air or water.

MANAGEMENT INITIAL CARE:

Basic life support such as protection of the airway and circulatory status must be

maintained. Complete blood count, liver function test, prothrombin time, international

standardized ratio ( INR), blood urea, serum creatinine, serum electrolytes especially of

calcium phosphates, potassium should be done immediately after admission, On

accessing intravenous line, Frequent recording of vitals and cardiac monitoring should be

done. Urine output should be recorded, if the complaint of irritation of the eye , eyewash

should be given with clean water immediately.

DECONTAMINATION OF DIGESTIVE TRACT:

Early gastric lavage was indicated (31). Due to the high toxicity of phosphorus and since

no specific antidote is available, lavage should be done in all patients. However utmost

care must be taken, since explosion may occur following contact with oxygen, after

inserting ryle’s tube (8). This may also be prevented by placing syringe filled with water

at nasal end of the tube, after confirming the position of the tube, water is being instilled,

instead of air. However there is no data available regarding supportive use of charcoal for

adsorbing phosphorus since due to its highly toxic nature and no oesophageal burns is

23

getting reported, activated charcoal is being administered widely in many centers. Bowel

wash with polyethylene glycol is tried, since it forms non-absorbable material and thus

getting washed away with stool (31) Potassium permanganate wash will convert

phosphorus to least toxic oxide (32). Nowadays it is used worldwide, but anyway there

were no positive results. It is not easily available and huge risk, it was not indicated.

TREATMENT:

No specific antidote is available up to date. But n-acetylcysteine regimen has prevented

death an insignificant number of the patient if it was administered early if it was

continued in full course. Since there is no potential side effect, no detailed study is

available, if it is recommended to use in white phosphorus poisoning.

OTHER MODALITIES:

Steroids were not useful in preventing hepatotoxicity. Ubiquinone and sulfate were

preventing liver toxicity to some extent, no human study is available yet (15).

HAEMODIALYSIS:

Haemodialysis rapidly corrects the electrolyte disturbances such as hyperphosphatemia,

hyperkalemia, and hypocalcemia; but no report was available. However it significantly

reduces mortality by 50%, thus exchange transfusion was beneficial.(10,14).

24

PHOSPHIDES:

Phosphides such as zinc and aluminum are being used as rodenticides in developing

countries to protect grains from rodents (33) because it is cheaper and effective. Zinc

phosphide is dark gray in color, has a rotten fish odor and bad taste, hence it was not used

by other animals except rats. When mixed with tartar emetic, both these phosphides,

release phosphine gas readily, when it comes in contact with water or diluted acids (33).

The exact mechanism is not clear. Phosphine is produced after phosphide reacts with

hydrochloric acid in stomach. It inhibits 18 cytochrome-c oxidases and in turn inhibits

oxidative phosphorylation of electron transport system (34), which in turn leads to

various cellular toxicity, necrosis of gastrointestinal tract, liver and also kidneys.

phosphine, being heavier than air, having rotten fish odor, can be detected even at levels

of 2 ppm.(34) Typical odorcan not be a warning sign since toxicity occurs even below the

level of olfactory threshold. A number of oral exposures had been reported. It was also

identified as one of the most common suicidal agents in India (35). The exact level of

lethal dose is not known since it was reported that even after ingesting a small amount of

5gm, the patient has died. Some patients have survived even after ingesting 50gm.

Inhalation of toxic exposure to phosphine is also reported. It causes severe mucosal

irritation, manifested as nausea, vomiting, and abdominal pain within 15 minutes of

ingestion of aluminum phosphide and 30minutes after ingestion zinc phosphide(35) Other

symptoms being hypotension, palpitation, acidosis, tetany. Systemic toxic symptoms

such as broad QRS complex, jaundice, and pulmonary edema are also reported. However

25

neurological manifestations are rare, but seizures and coma are recorded in expired

patients(36). The majority of death occurs after 24 hours of ingestion, which may be

delayed upto 2 weeks, which was mainly reported due to myocardial damage (35). 19

Long term exposure in industry may reduce psychiatric, pulmonary, hepatic and cardiac

findings.

MANAGEMENT:

Treatment is mainly supportive and also symptomatic. If there is acute ingestion,

activated charcoal is useful, however,the patient should be continuously monitored. The

liver function test, urea, creatinine, electrolytes should be measured. After lavage,

phosphine gas is emitted in lavage solution and stools, hence they must be cleaned and

disposed of properly to prevent inhalation exposure to health care workers by providing

proper face masks. Lavage is tried using sodium bicarbonate, plain water or even milk.

Administration of proton pump inhibitor with antacid is useful. But prognosis is worse if

pulmonary and cardiovascular manifestations arise early. A chest x-ray for identifying

pulmonary toxicity and abdominal x-ray for opacities in gut may help.[43,44]

Importantly, coagulation related to vitamin K antagonist (VKA)/LAAR effect may be

recognized by simultaneous prolongation of the prothrombin time (PT), international

normalized ratio (INR), and partial thromboplastin time (PTT). In patients with otherwise

normal hepatic function, coagulation factor activity demonstrates low levels of Factors II,

VII, IX, and X, but preserved levels of the remainder of (non-vitamin K dependent)

coagulation factors. Mixing studies, if performed, are expected to demonstrate correction.

26

Accumulation of Vitamin K Epoxide may be present and the diagnosis confirmed by

specific testing for the presence of rodenticides. which leading to coagulopathy, bleeding

complications, and death.

27

MATERIALS AND METHODS

This study was conducted at Stanley Medical College Hospital Toxicology IMCU,

Stanley Government Medical College, Chennai, during the period of March 2018 to

August 2018 (6 Months). There were 108 patients admitted with an alleged history of

ingesting rodenticide compounds in our emergency medical ward during the study period.

After applying, the inclusion and exclusion criteria, 170 patients only fulfilled all the

criteria and they were chosen as study subjects (n =170 ).

Inclusion criteria:

1.Patients admitted with the history of consumption of rat killer paste

poisoning with age >18 years

Exclusion criteria:

1.Age less than 18 yrs

2.History of consumption of other compounds with the rat killer paste

3Those with the history of acute or chronic liver disease

4.Those who refuse the study

METHODOLOGY &DATA COLLECTION:

In this study those who get admitted with history of rat killer paste poisoning

(yellow phosphorous , zinc phosphide and aluminium phosphide ) are included in the

study after excluding with the exclusion criteria.

28

The patients are monitored with their complete blood count , liver function test ,

Prothrombin time , INR , renal function test till they got discharged from the hospital

.With the results, parameters like age and sex wise distribution, complications, morbidity

and mortality of rat killer paste poisoning are analyzed.

29

STATISTICAL ANALYSIS

1. Continuous variables are expressed as means and standard deviations and

categorical variables as numbers with percentages in brackets.

2. For comparisons between patient groups, we used Student’s T-test for quantitative

variables and Chi-square or Fisher’s exact tests for categorical variables.

3. P<0.01 was taken as significant. Data analysis and interpretation were done with

IBM SPSS Statistics v20.0.

30

RESULTS

TABLE :1AGE GROUP (n=170)

Agegroup Frequency Percent

Up to 20 Years 13 7.6

21- 30 Years 90 52.9

31- 40 Years 45 26.5

41- 50 Years 19 11.2

Above 50 Years 3 1.8

Table :1& Graph :1 170 cases were included in the study. Up to 20 Years-13 cases

(7.6%),21- 30 Years-90 cases (52.9%),31- 40 Years- 45 cases ( 26.5%), 41- 50 Years-19

(11.2%),Above 50 Years-3 (1.8%)

31

GRAPH :1AGE GROUP (n=170)

Table :1& Graph :1 170 cases were included in the study.

Up to 20 Years-13 cases (7.6%)

21- 30 Years-90 cases (52.9%)

31- 40 Years- 45 cases ( 26.5%),

41- 50 Years-19 (11.2%),

Above 50 Years-3 (1.8%)

7.6

52.9

26.5

11.2

1.8

0

10

20

30

40

50

60

Up to 20 Years 21- 30 Years 31- 40 Years 41- 50 Years Above 50 Years

Age group

32

TABLE :2 SEX DISTRIBUTION

SEX Frequency Percent

MALE 97 57.1

FEMALE 73 42.9

Total 170 100.0

GRAPH :2 SEX DISTRIBUTION

Table :2& Graph :2 Among 170 cases

male were 97(57.1%)

females were 73(42.9%)

57.1

42.9

SEX

MALE FEMALE

33

TABLE :3 AMOUNT CONSUMED

AMOUNT CONSUMED Frequency Percent

3 QUARTERS 19 11.2

DOUBLE 1 0.6

HALF 80 47.1

ONE 23 13.5

QUARTER 45 26.5

TWO 2 1.2

Total 170 100.0

GRAPH :3 AMOUNT CONSUMED

TABLE :3& GRAPH :3 Categorizing the amount consumed in patients included in our

study.

3 quarters- 19 cases (11.2%) Double-1 (4%) Half-80 ( 47.1%) One-23 (13.5%)

11.2

0.6

47.1

13.5

26.5

1.2

0

5

10

15

20

25

30

35

40

45

50

3 QUARTERS DOUBLE HALF ONE QUARTER TWO

AMOUNT CONSUMED

34

Quarter- 45 (26.5%) Two-2 ( 1.2%)

TABLE :4 TIME ELAPSED AFTER CONSUMPTION

GRAPH :4 TIME ELAPSED AFTER CONSUMPTION

TABLE :4 & GRAPH :

4 Up to 6Hrs-68 (40%),

>6Hrs-80 (47.1%),

Not Known was -22 cases (12.9%)

40

47.1

12.9

Time

Up to 6Hrs >6Hrs NOT KNOWN

Time Frequency Percent

Up to 6Hrs 68 40.0

>6Hrs 80 47.1

NOT KNOWN 22 12.9

Total 170 100.0

35

TABLE: 5 STOMACH WASH

STOMACH WASH Frequency Percent

NO 24 14.1

YES 146 85.9

Total 170 100.0

GRAPH :5 STOMACH WASH

TABLE :5& GRAPH :5 shows stomach wash done in 146 cases (85.9%), not done in 24

cases (14.1%)

14.1

85.9

STOMACH WASH

NO YES

36

TABLE: 6 PRESENCE OF VOMITING

VOMITING Frequency Percent

NO 82 48.2

YES 88 51.8

Total 170 100.0

GRAPH :6 PRESENCE OF VOMITING

Table :6& Graph :6 Among 170 cases, 88 cases (51.8%) had vomiting, 82 cases (48.2%)

had no episodes of vomiting

48.2

51.8

VOMITING

NO YES

37

TABLE :7 ABDOMEN PAIN

ABDOMEN PAIN Frequency Percent

NO 96 56.5

YES 74 43.5

Total 170 100.0

GRAPH :8 ABDOMEN PAIN

Table :7& graph :8 shows 74 cases ( 43.5%) had abdomen pain , 96 cases (56.5%) were

free from abdomen pain

56.5

43.5

ABD_PAIN

NO YES

38

TABLE :8 JAUNDICE

JAUNDICE Frequency Percent

NO 162 95.3

YES 8 4.7

Total 170 100.0

GRAPH: 8 JAUNDICE

Table: 8 & Graph:8 Only 8 cases (4.7%) had jaundice, and 162 cases (95.3%) did not

show the incidence of jaundice.

95.3

4.7

NO

YES

0 20 40 60 80 100 120

JAUNDICE

NO YES

39

TABLE :9 MALENA

GRAPH: 9 MALENA

Table :9& graph :9 shows incidence of malena , 16 cases (9.4%) had malena and nil in

154 cases (90.6%)

90.6

9.4

MALENA

NO YES

MALENA Frequency Percent

NO 154 90.6

YES 16 9.4

Total 170 100.0

40

TABLE :10 USG FINDINGS

USG Frequency Percent

ASCITES 6 3.5

GR I FATTY LIVER+

ASCITES 1 .6

NORMAL 163 95.9

Total 170 100.0

GRAPH :10 USG FINDINGS

Table: 10 & graph: 10 shows USG findings in case group, Ascites was present in -6 cases

( 3.5%), GR I Fatty Liver+ Ascites- 1 case (6%), normal findings were observed in 163

cases (95.9%)

3.5 0.6

95.9

0

20

40

60

80

100

120

ASCITES GR I FATTY LIVER+ ASCITES NORMAL

USG

41

TABLE: 10 CAUSE OF DEATH

CAUSE OF DEATH Frequency Percent

COAGULOPAHTY+HE 10 52.6%

HE 7 36.8%

PANCREATITIS 2 10.5%

Total 19 100.0

GRAPH: 10 CAUSE OF DEATH

Table :10& graph :

10 COAGULOPATHY+HE- in 10 cases (52.6%),HE-7 cases (36.8%),Pancreatitis was in

2 cases (10.5%)

52.60%

36.80%

10.50%

0.00%

10.00%

20.00%

30.00%

40.00%

50.00%

60.00%

COAG+HE HE PANCREATITIS

CAUSE_OF_DEATH

42

TABLE :11 AGE GROUP CORRELATION WITH COURSE IN HOSPITAL

COURSE_IN_HOSP Total

DISCHARGE DEATH

Age group Up to 20 Years Count 12 1 13

% within COURSE IN_

HOSP

7.9% 5.3% 7.6%

21- 30 Years Count 81 9 90

% within

COURSE_IN_HOSP

53.6% 47.4% 52.9%

31- 40 Years Count 40 5 45

% within

COURSE_IN_HOSP

26.5% 26.3% 26.5%

41- 50 Years Count 15 4 19

% within

COURSE_IN_HOSP

9.9% 21.1% 11.2%

Above 50 Years Count 3 0 3

% within

COURSE_IN_HOSP

2.0% 0.0% 1.8%

Total Count 151 19 170

% within

COURSE_IN_HOSP

100.0% 100.0% 100.0

%

43

GRAPH: 11 AGE GROUP CORRELATION WITH COURSE IN HOSPITAL

0.00%

10.00%

20.00%

30.00%

40.00%

50.00%

60.00%

Up to 20 Years 21- 30 Years 31- 40 Years 41- 50 Years Above 50 Years

7.90%

53.60%

26.50%

9.90%

2.00%

5.30%

47.40%

26.30%

21.10%

0.00%

DISCHARGE DEATH

44

Age group coorelation with hospital stay

Up to 20 Years-13 cases (7.6%)

o Discharge -12 case, (7.9%)death -1 case (5.3%)

21- 30 Years-90 cases (52.9%)

o Discharge -81 case, (53.6%) death -9 case (47.4%)

31- 40 Years- 45 cases ( 26.5%)


41- 50 Years-19 (11.2%)


Above 50 Years-3 (1.8%)

o all are discharged. No incidence of death in this age group

Pearson Chi-Square=2.529p=0.639 which is statically less significant.

45

TABLE: 12SEX CORRELATION WITH COURSE IN HOSPITAL


DISCHARGE DEATH

SEX MALE Count 91 6 97

% within

COURSE_IN_HOSP

60.3% 31.6% 57.1%

FEMALE Count 60 13 73

% within

COURSE_IN_HOSP

39.7% 68.4% 42.9%


% within

COURSE_IN_HOSP

100.0% 100.0% 100.0%

Sex Correlation With Course In Hospital

Male were 97(57.1%), 91 discharge and 6 were expired

Females were 73(42.9%) -60 were discharged, 13 were expired.

Pearson Chi-Square=5.668* P=0.017

46

GRAPH: 12SEX CORRELATION WITH COURSE IN HOSPITAL

Sex Correlation With Course In Hospital

Male were 97(57.1%), 91 discharge and 6 were expired

Females were 73(42.9%) -60 were discharged, 13 were expired.

Pearson Chi-Square=5.668* P=0.017

0.00%

10.00%

20.00%

30.00%

40.00%

50.00%

60.00%

70.00%

MALE FEMALE

60.30%

39.70%

31.60%

68.40%

DISCHARGE DEATH

47

TABLE: 13 AMOUNT CONSUMED CORRELATION WITH COURSE IN

HOSPITAL

COURSE IN HOSP Total

DIS CHARGE DEATH

AMT_CONS

UMED

3

QUARTERS

Count 13 6 19

% within

COURSE

IN HOSP

8.6% 31.6% 11.2%

DOUBLE Count 0 1 1

% within

COURSE

IN HOSP

0.0% 5.3% 0.6%

HALF Count 78 2 80

% within

COURSE

IN HOSP

51.7% 10.5% 47.1%

ONE Count 17 6 23

% within

COURSE

IN HOSP

11.3% 31.6% 13.5%

QUARTER Count 43 2 45

% within

COURSE

IN HOSP

28.5% 10.5% 26.5%

TWO Count 0 2 2

% within

COURSE

IN HOSP

0.0% 10.5% 1.2%


% within

COURSE

IN HOSP

100.0% 100.0% 100.0%

Categorizing the amount consumed in patients included in our study. 3 quarters-

19 cases (11.2%) -13 were discharged, 6 were expired,Double-1 (4%), only one case, in

the categories which were expired.

48

Half-80 ( 47.1%), 78 were discharged, 2 cases expired.One-23 (13.5%), 17

discharged and 6expired.

Quarter- 45 (26.5%), 43 discharged, 2 expired, Two-2 ( 1.2%) both the cases

expired. Pearson Chi-Square=45.081* P<0.001

GRAPH :13 AMOUNT CONSUMED

0.00%

10.00%

20.00%

30.00%

40.00%

50.00%

60.00%

3 QUARTERS DOUBLE HALF ONE QUARTER TWO

8.60%

0.00%

51.70%

11.30%

28.50%

0.00%

31.60%

5.30%

10.50%

31.60%

10.50% 10.50%

DISCHARGE DEATH

49

TABLE: 14 STOMACH WASH CORRELATION WITH COURSE OF

HOSPITAL

Stomach wash in correlation with hospital stay. It is done in 146 cases (85.9%), among

them 132, discharged and 14were dead. not done in 24 cases (14.1%) 19 were discharged,

5 were expired.Pearson Chi-Square=2.625 p=0.105


DISCHARGE DEATH

STOMACH_

WASH

NO Count 19 5 24

% within

COURSE_IN_HOSP

12.6% 26.3% 14.1%

YES Count 132 14 146

% within

COURSE_IN_HOSP

87.4% 73.7% 85.9%


% within

COURSE_IN_HOSP

100.0% 100.0% 100.0

%

50

GRAPH: 14 STOMACH WASH CORRELATION WITH COURSE IN

HOSPITAL

0.00%

10.00%

20.00%

30.00%

40.00%

50.00%

60.00%

70.00%

80.00%

90.00%

MALE FEMALE

12.60%

87.40%

26.30%

73.70%

DISCHARGE DEATH

51

TABLE:15 TIME AFTER CONSUMPTION IN CORRELATION WITH COURSE

IN HOSPITAL


DISCHARGE DEATH

time Up to 6Hrs Count 68 0 68

% within

COURSE_IN_HOSP

50.7% 0.0% 45.9%

>6Hrs Count 66 14 80

% within

COURSE_IN_HOSP

49.3% 100.0% 54.1%


% within

COURSE_IN_HOSP

100.0% 100.0% 100.0%

Time After Consumption In Correlation With Course In HospitalUp to 6Hrs-68 (40%),

all the cases were alive and discharged, >6Hrs-80 (47.1%),- 66 were discharged, 14 were

dead.

Pearson Chi-Square=13.143** P<0.001

52

GRAPH: 15 TIME AFTER CONSUMPTION IN CORRELATION WITH

COURSE IN HOSPITAL

0.00%

20.00%

40.00%

60.00%

80.00%

100.00%

Up to 6Hrs >6Hrs

50.70% 49.30%

0.00%

100.00%

DISCHARGE DEATH

53

TABLE: 15 VOMITING IN CORRELATION WITH HOSPITAL COURSE


DISCHARGE DEATH

VOMITING NO Count 70 12 82

% within

COURSE_IN_HOSP

46.4% 63.2% 48.2%

YES Count 81 7 88

% within

COURSE_IN_HOSP

53.6% 36.8% 51.8%


% within

COURSE_IN_HOSP

100.0% 100.0% 100.0%

Among 170 cases, 88 cases (51.8%) had vomiting, 81 were discharged, 7 dead. 82 cases

(48.2%) had no episodes of vomiting , 70 discharged,12 dead, Pearson Chi-Square=1.908

p=0.167

54

GRAPH: 15 VOMITING IN CORRELATION WITH COURSE IN HOSPITAL

0.00%

10.00%

20.00%

30.00%

40.00%

50.00%

60.00%

70.00%

NO YES

46.40%

53.60%

63.20%

36.80%

DISCHARGE DEATH

55

TABLE: 16 CORRELATION OF ABDOMEN PAIN WITH COURSE IN

HOSPITAL


DISCHARGE DEATH

ABD_PAIN NO Count 89 7 96

% within

COURSE_IN_HOSP

58.9% 36.8% 56.5%

YES Count 62 12 74

% within

COURSE_IN_HOSP

41.1% 63.2% 43.5%


% within

COURSE_IN_HOSP

100.0% 100.0% 100.0%

Shows 74 cases ( 43.5%) had abdomen pain 62 cases were discharged, 12 were dead, 96

cases (56.5%) were free from abdomen pain, 89 were dead and 7 were discharged.

Pearson Chi-Square=3.353 p=0.067

56

GRAPH: 16 CORRELATION OF ABDOMEN PAIN WITH COURSE IN

HOSPITAL

0.00%

10.00%

20.00%

30.00%

40.00%

50.00%

60.00%

70.00%

NO YES

58.90%

41.10% 36.80%

63.20%

DISCHARGE DEATH

57

TABLE: 17 JAUNDICE CORRELATION WITH COURSE OF HOSPITAL


DISCHARGE DEATH

JAUNDICE NO Count 147 15 162

% within

COURSE_IN_HOSP

97.4% 78.9% 95.3%

YES Count 4 4 8

% within

COURSE_IN_HOSP

2.6% 21.1% 4.7%


% within

COURSE_IN_HOSP

100.0% 100.0% 100.0%

58

GRAPH 17: JAUNDICE CORRELATION WITH COURSE OF HOSPITAL

Only 8 cases (4.7%) had jaundice, and 162 cases (95.3%) did not show incidence of

jaundice.

In jaundice diagnosed patients, 4 were dead and 4 were alive, in undiagnosed cases 147,

discharged and 15 were dead. Pearson Chi-Square=12.746** p<0.001

0.00%

10.00%

20.00%

30.00%

40.00%

50.00%

60.00%

70.00%

80.00%

90.00%

100.00%

NO YES

97.40%

2.60%

78.90%

21.10%

DISCHARGE DEATH

59

TABLE: 18 CORRELATION OF MALENA WITH COURSE OF HOSPITAL

STAY


DISCHARGE DEATH

MALENA NO Count 143 11 154

% within

COURSE_IN_HOSP

94.7% 57.9% 90.6%

YES Count 8 8 16

% within

COURSE_IN_HOSP

5.3% 42.1% 9.4%


% within

COURSE_IN_HOSP

100.0% 100.0% 100.0%

16 cases (9.4%) had Malena among them 8 were dead and 8 were discharged, 154 cases

(90.6%) Malena was found 143, survived, 11 dead. Pearson Chi-Square=26.817**

p<0.001

60

TABLE: 18 CORRELATION OF MALENA WITH COURSE OF HOSPITAL

STAY

0.00%

10.00%

20.00%

30.00%

40.00%

50.00%

60.00%

70.00%

80.00%

90.00%

100.00%

NO YES

94.70%

5.30%

57.90%

42.10%

DISCHARGE DEATH

61

TABLE: 19 HEPATIC ENCEPHALOPATHY [HE] CORRELATION WITH

COURSE IN HOSPITAL


DISCHARGE DEATH

HE 1.00 Count 146 8 154

% within

COURSE_IN_HOSP

96.7% 42.1% 90.6%

2.00 Count 5 11 16

% within

COURSE_IN_HOSP

3.3% 57.9% 9.4%


% within

COURSE_IN_HOSP

100.0% 100.0% 100.0%

HE: 1 146 patients discharged, 8 dead. HE:2 5 discharged , 11 expired, Pearson Chi-

Square=58.974** P<0.001

62

GRAPH: 19 HEPATIC ENCEPALOPATHY( HE ) CORRELATION WITH

COURSE IN HOSPITAL

0.00%

10.00%

20.00%

30.00%

40.00%

50.00%

60.00%

70.00%

80.00%

90.00%

100.00%

1 2

96.70%

3.30%

42.10%

57.90%

DISCHARGE DEATH

63

TABLE: 20 ABNORMAL & NORMAL CORRELATION WITH COURSE IN

HOSPITAL


DISCHARGE DEATH

ABN Count 1 2 3

% within

COURSE_IN_HOSP

0.7% 10.5% 1.8%

WNL Count 150 17 167

% within

COURSE_IN_HOSP

99.3% 89.5% 98.2%


% within

COURSE_IN_HOSP

100.0% 100.0% 100.0%

ABORMAL1 case discharged, and 2 dead, in WNL 150 were discharged and 17 were

dead Pearson Chi-Square=9.472* p=0.002

64

GRAPH: 20 ABNORMAL & NORMAL CORRELATION WITH COURSE IN

HOSPITAL

0.00%

10.00%

20.00%

30.00%

40.00%

50.00%

60.00%

70.00%

80.00%

90.00%

100.00%

ABN WNL

0.70%

99.30%

10.50%

89.50%

DISCHARGE DEATH

65

TABLE: 21 USG FINDING IN CORRELATION WITH COURSE IN HOSPITAL


DISCHARGE DEATH

USG ASCITES Count 4 2 6

% within

COURSE_IN_HOSP

2.6% 10.5% 3.5%

GR I FATTY

LIVER+ ASCITES

Count 1 0 1

% within

COURSE_IN_HOSP

0.7% 0.0% 0.6%

NORMAL Count 146 17 163

% within

COURSE_IN_HOSP

96.7% 89.5% 95.9%


% within

COURSE_IN_HOSP

100.0% 100.0% 100.0%

In USG findings,

Ascites were in 6 patients, among them 4 were discharged and 2 were dead

Fatty liver with ascites 1 cases that were discharged.

In normal usg findings, 146 were discharged, 17 were dead. Pearson Chi-

Square=3.185 P=0.203

66

GRAPH: 21 USG FINDING IN CORRELATION WITH COURSE OF HOSPITAL

0.00%

10.00%

20.00%

30.00%

40.00%

50.00%

60.00%

70.00%

80.00%

90.00%

100.00%

ASCITES GR I FATTY LIVER+ ASCITES NORMAL

2.60% 0.70%

96.70%

10.50%

0.00%

89.50%

DISCHARGE DEATH

67

DISCUSSION

Poisoning directly or indirectly is responsible for more than one million illnesses

worldwide.[11]Deliberate self-poisoning has become an increasingly common response

to emotional distress in young adults, and it is now one of the most frequent reasons for

emergency hospital admission.2 Suicide is an important cause of premature death and the

WHO estimates to be nearly 800,000 in number.3 In industrialized countries, the drugs

people commonly take in overdose-analgesics, tranquilizers, antidepressants are

relatively non-toxic[12,1,14]. The estimated case fatality for overdose in England, for

example, is around 0.5%.5 In developing countries, the situation is quite different.6 The

substances most commonly used for self-poisoning are agricultural pesticides including

rodenticides.1,3,7 Overall case fatality ranges from 10%-20%.[18] For this reason, deaths

from pesticide poisoning make a major contribution to patterns of suicide in developing

nations, particularly in rural areas.[19] Three million cases of pesticide poisoning occur

worldwide annually, with 2,20000 deaths, the majority of which are intentional.10

Rodenticides are a heterogeneous group of compounds

68

Raton paste, a commonly used rodenticide in Indian houses contains 3% yellow

phosphorus. Yellow phosphorus is a general protoplasmic poison causing multiorgan

failure.[20] Doses >1 mg/kg are almost invariably fatal.

Raton paste poisoning is either suicidal or accidental. The clinical course of ratol paste

poisoning is different from that of most other poisons. The patients are usually

asymptomatic during the initial 72 h of ingestion, or they may have signs and symptoms

of gastrointestinal irritation. After 72 h they develop deranged liver function, acute

hepatic failure, coagulopathy. Central nervous system effects include changes in mental

status like confusion, psychosis, hallucinations, and coma. Cardiac toxicity includes

hypotension, tachycardia, arrhythmias, and cardiogenic shock. Some patients may

develop acute tubular necrosis and acute renal failure.[21,22,23] Because of the initial

asymptomatic phase few patients do not reveal about ratol paste ingestion and present

late to the hospital. Patients who present late after consumption of the lethal dose develop

fulminant hepatic failure with mortality of 100%.[24] In severe ingestions of ratol paste,

patients do not have the initial asymptomatic stage, and they die due to shock and

cardiopulmonary arrest in early stages itself.[4]

69

There is no specific antidote for yellow phosphorus poisoning. Treatment is directed at

removal of the poison and supportive therapy.[25,26]

Aluminum phosphide, zinc phosphide are the other rodenticides available. They are

mainly used in agricultural fields[27] in contrast to ratol paste, which is used in houses.

Also, ratol paste is commonly mistaken for toothpaste and consumed by children. And

the product directions suggest that the paste be applied to bread to enable ingestion by

rodents, thus making it appealing to children as well.[28] Hence, accidental poisoning is

more common with ratol paste.

Most of the cases were in the age group of 11-30 years. Acute poisoning was commonly

seen among farmers, homemakers, and students in various national and international

studies. In all the cases, the most common route of exposure was oral. The majority of

cases were in the age group of 11-30 years (42 cases, 75%) which can be explained by

the fact that the persons of this age group are suffering from the stress of the modern

lifestyles, failure in love, family problems, nuclear family concept, etc. Our study does

not correlate with the study done by other studies,8 in which incidence was high among

males. Many cases were found among homemakers (18 cases, 32.1%), male laborers (12

cases, 21.4%), and farmers (16 cases, 28.5%) as these groups are more vulnerable groups

70

and easily exposed to the poisoning agents. Poverty, inadequate income to run the

family.monsoon failure was responsible for higher incidence of poisoning among

laborers and farmers. Factors, such as dowry, cruelty by the in-laws, family quarrels,

maladjustment in married life, and dependence of women on husband, are responsible for

the higher incidence of poisoning among homemakers. Failure in the exams or inability

to cope up the high expectation from parents and teachers has increased the incidence of

poisoning among students. High toxicity and non-availability of any specific antidote are

responsible for higher mortality with rat killer poison.[29] LFT derangements are seen

mostly with yellow phosphorus after 2-3 days of consumption in our study.

Various studies on poisoning were done in India Song ZY et al. [30] noticed most

commonly affected age group was 20-40 years. Our study was compatible with Banerjee

et al. in the age group. A study by Winek CLet al. [31] found that a higher number of

patients ingested rat killer poisoning mixing with alcohol but our study showed that,

many patients ingested either raw or mixed with water.

The new finding in our study was the mean lethal dosage (13.42 ± 7.069 gms) of rat killer

poisoning which will cause damage to the organs once ingested. Another new finding of

our study was manifestation of first chief symptoms which was 5.7 ± 6.3093 hours.

71

“People must seek care in the health facility as soon as they have identified the ingestion

of rat killer poison”. Elizabeth J, et al. [32] found in her study that the patients were

usually asymptomatic during the initial 72 hours of ingestion, or they may have signs and

symptoms of gastrointestinal irritation. Our patients in our study developed symptoms

from 5 to 6 hours and vomiting was found in higher numbers in our patients.

Blotting the biological marker AST and ALT showed a higher elevation in patients

ingested rat killer poison which indicates that the first affecting organ was liver followed

by kidney and other organs. AST was 402.6 on the 2nd

day and on 6th

day AST reduced to

159.0. Alt was 439.7 on the 2nd

day and reduced on 6th

day to 171.0. Stephenson JBP et

al. [33] study showed, the mean admission ALT/AST was 306/451, discharge ALT/AST

was 291/302, and peak ALT/AST was 451/655. A few other new findings in our study

were elevation graphs were shown for T.bill, T.protein, Albumin, AST, ALT, urea,

creatinine, PT, and INR for all the patients who ingested rat killer poisoning. Our study

again found the statistical significant elevation biological elevation between the survivor

and non-survivor.[34,35,36]

We found out of 100% of patients received treatments like NAC, Vit-K, supportive, 82%

of our patients survived and discharged. Watson WAet al. [37] reveals best results seen

72

among patients in whom NAC was started early in the course of illness. Guidelines do

not exist regarding routine use of NAC in non-acetaminophen induced ALF, and

in hepatic failure due to rodenticide consumption. Patients admitted with ALF after

phosphorus ingestion has sometimes been managed with NAC [38]. We strongly

recommend that it is a need of hour to frame proper guidelines of treatment that ingest rat

killer poison. However in spite of manageable treatment, half of our patients developed

Toxic Hepatitis, 1/3 developed Acute Liver Failure and ¼ developed Toxic Hepatitis

along with Acute Kidney Injury / Acute Liver Failure along with Acute Kidney Injury. ¼

developed multiple organ failure which leads them to death. Lipton RAet al. [39] showed

35.7% mortality rate whereas our study showed 19% mortality rate. Survived patients

received psychiatric evaluation and were discharged in a stable condition.

Yellow phosphorous: Of the 26 patients, 61.5% recovered, 7% expired, 11% absconded

and one patient was DAMA. Contrastingly, more harm was seen in patients of Ben-Assa

BM et al, where only 48.8% survived, 27.9% expired and 23.2% DAMA. Fernandez et al

observed very high mortality (27%) and concluded that yellow phosphorus is extremely

lethal when consumed, owing to hepatotoxicity (33%).[41] In line with these findings, 5

out of 7 patients who had bleeding manifestations had consumed yellow

73

phosphorous.[55,59] Encephalopathy was seen in 5 patients with yellow phosphorus

poisoning. Hypotension complicated two patients with yellow phosphorous poisoning,

one had myocarditis and cardiogenic shock. About 10 of 26 (38.46%) patients with

yellow phosphorous intake developed fulminant hepatic failure, and they were given N-

acetyl cysteine. However, only four patients improved while four patients were referred

for liver transplantation and two expired. [42,43 56]

The most common symptom was vomiting (70%), followed by pain abdomen (50%) and

giddiness (30%) respectively. A study was done by Balasubramanian K et at,

Pondicherry, showed 36.67 % patients had nausea and vomiting, followed by giddiness

(20%) and pain abdomen (16.7%).[44,45,57,58]

The study found that hepatitis was common complication (32.14%), followed by

cardiogenic shock (8.9%). Three patients developed hepatic encephalopathy and Three

developed bleeding complication among 18 patients with hepatitis. Yellow phosphorus

was causing hepatitis in 11(19.67%) patients, zinc phosphide in 4 (7.14%) and aluminum

phosphide in 3 (5.35%) patients. Cardiogenic shock was due to aluminum phosphide

poisoning [46,47,48]

74

Prosser PRet al.(noted that the systems affected in their study due to Yellow Phosphorous

were gastrointestinal tract (100%), liver (66.70%), Cardiovascular, Nervous and

respiratory systems along with associated metabolic abnormalities (66.7%). In our study

93% patients had derangement in liver enzymes,10% patients had respiratory depression.

No patient had cardiac or metabolic abnormalities[49,50,51]. Simon FA,stated that in a

series of 15 patients observed mortality of 27% is recorded, confirming that Yellow

Phosphorus is extremely lethal when ingested. The duration of hospital admission and

compound consumption are very important. The lesser the duration the prognosis is good.

This is mainly because of gastric lavage given to those patients presenting early, which

decreases the amount of yellow phosphorous entering circulation and early treatment

with N acetylcysteine.[52,53,60]

75

SUMMARY

1. Poisoning is mostly preventable, commonly suicidal and rarely being an accidental

form of death in developing agrarian countries. In rural India, poisoning forms the

major share of emergency health care and of about one – fourth to one – third of

intensive care admissions.

2. To study the clinical profile of patients admitted with rodenticide poisoning and

their course in the hospital.

3. This study was conducted at Stanley Medical College Hospital Toxicology

IMCU, Stanley Government Medical College, Chennai, during the period of

March 2018 to August 2018 (6 Months). There were 108 patients admitted with an

alleged history of ingesting rodenticide compounds in our emergency medical

ward during the study period.

4. After applying, the inclusion and exclusion criteria, 170 patients only fulfilled all

the criteria and they were chosen as study subjects (n =170 ).

5. 170 cases were included in the study. Up to 20 Years-13 cases (7.6%),21- 30

Years-90 cases (52.9%),31- 40 Years- 45 cases ( 26.5%), 41- 50 Years-19

(11.2%),Above 50 Years-3 (1.8%)

6. Categorizing the amount consumed in patients included in our study. 3 quarters-

19 cases (11.2%) Double-1 (4%), Half-80 ( 47.1%),One-23 (13.5%),Quarter- 45

(26.5%),Two-2 ( 1.2%).Up to 6Hrs-68 (40%), >6Hrs-80 (47.1%), Not Known

was -22 cases (12.9%)

76

7. USG findings in case group, Ascites was present in -6 cases ( 3.5%), GR I Fatty

Liver+ Ascites- 1 case (6%), normal findings were observed in 163 cases

(95.9%).COAG+HE- in 10 cases (52.6%),HE-7 cases (36.8%),Pancreatitis was in

2 cases (10.5%)

8. Up to 20 Years-13 cases (7.6%) Discharge -12 case, (7.9%) death -1 case (5.3%) ,

21- 30 Years-90 cases (52.9%), Discharge -81 case, (53.6%) death -9 case (47.4%)

,31- 40 Years- 45 cases ( 26.5%), Discharge -40 case, (26.5%) death -5 case

(26.3%) ,41- 50 Years-19 (11.2%), Discharge -15 case, (9.9%) death -4 case

(21.1%) ,Above 50 Years-3 (1.8%) all are discharged. No incidence of death in

this age group Pearson Chi-Square=2.529p=0.639 which is statically less

significant.

9. Categorizing the amount consumed in patients included in our study. 3 quarters-

19 cases (11.2%) -13 were discharged, 6 were expired,Double-1 (4%), only one

case, in the categories which were expired.

10. Half-80 ( 47.1%), 78 were discharged, 2 cases expired.One-23 (13.5%), 17

discharged and 6expired.

11. Quarter- 45 (26.5%), 43 discharged, 2 expired, Two-2 ( 1.2%) both the cases

expired. Pearson Chi-Square=45.081* P<0.001.Stomach wash in correlation

with hospital stay.It done in 146 cases (85.9%), among them 132, discharged and

14were dead.not done in 24 cases (14.1%) 19 were discharged, 5 were

expired.Pearson Chi-Square=2.625 p=0.105.Time After Consumption In

77

Correlation With Course In HospitalUp to 6Hrs-68 (40%), all the cases were alive

and discharged, >6Hrs-80 (47.1%),- 66 were discharged, 14 were dead. Pearson

Chi-Square=13.143** P<0.001

12. Among 170 cases, 88 cases (51.8%) had vomiting, 81 were discharged, 7 dead. 82

cases (48.2%) had no episodes of vomiting , 70 discharged,12 dead,Pearson Chi-

Square=1.908 p=0.167.

13. Our Study Shows 74 cases ( 43.5%) had abdomen pain 62 cases were discharged,

12 were dead, 96 cases (56.5%) were free from abdomen pain, 89 were dead and 7

were discharged.Pearson Chi-Square=3.353 p=0.067Only 8 cases (4.7%) had

jaundice, and 162 cases (95.3%) did not show incidence of jaundice.In jaundice

diagnosed patients, 4 were dead and 4 were alive, in undiagnosed cases 147,

discharged and 15 were dead.Pearson Chi-Square=12.746** p<0.001.

14. 16 cases (9.4%) had Malena among them 8 were dead and 8 were discharged, 154

cases (90.6%) Malena was found 143, survived, 11 dead.Pearson Chi-

Square=26.817** p<0.001

15. HE: 1 146 patients discharged, 8 dead. HE:2 5 discharged , 11 expired,Pearson

Chi-Square=58.974** P<0.001.

16. ABN 1 case discharged, and 2 dead, in WNL 150 were discharged and 17 were

dead Pearson Chi-Square=9.472* p=0.002

17. In usg findings, ascites were in 6 patients, among them 4 were discharged and 2

were dead, fatty liver with ascites 1 cases that were discharged. In normal usg

findings, 146 were discharged, 17 were dead Pearson Chi-Square=3.185 P=0.203

78

18. Ratol paste poisoning is either suicidal or accidental. The clinical course of ratol

paste poisoning is different from that of most other poisons.

19. The patients are usually asymptomatic during the initial 72 h of ingestion, or they

may have signs and symptoms of gastrointestinal irritation.

20. After 72 h they develop deranged liver function, acute hepatic failure,

coagulopathy. Central nervous system effects include changes in mental status like

confusion, psychosis, hallucinations, and coma. Cardiac toxicity includes

hypotension, tachycardia, arrhythmias, and cardiogenic shock. Some patients may

develop acute tubular necrosis and acute renal failure.

79

CONCLUSION

1. Rodenticide poisoning is the second most common poisoning in our area.

2. Male to female ratio in our study is 1.5: 1.

3. Majority of the patients were in 20 to 30 years age group.

4. Phosphorus compound (paste) forms the major share of poison.

5. Most common symptom is abdominal pain (90%).

6. Mortality in this study was 20 %.

7. Increased time delay in hospitalisation carries more mortality.

8. Jaundice develop following ingestion of phosphorus, carries most mortality, which

also correlates with elevated serum bilirubin and SGPT level

9. Phosphorus (paste) compound of rodenticide , must be banned , to prevent mortality

in young productive poor patients , who intend to ingest poison in a minute decision .

80

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ClinGastroenterol 1995; 21: 139-142

88

CLINICAL PROFILE OF RAT KILLER PASTE POISONING

PROFORMA

NAME : AGE: SEX:

ADDRESS: CONTACT NO:

COMPLAINTS:

HISTORY :

89

DURATION OF ILLNESS:

PAST HISTORY:

TREATMENT HISTORY:

PERSONAL HISTORY:

DRUGS/ TOXINS/ SUBSTANCE ABUSE

FAMILY HISTORY:

GENERAL EXAMINATION:

Pallor: Pulse: BMI:

Icterus: B.P: Temperature:

Lymphadenopathy : Resp.rate:

Oedema:

90

SYSTEMIC EXAMINATION:

CARDIOVASCULAR SYSTEM:

RESPIRATORY SYSTEM:

GASTRO-INTESTINAL SYSTEM :

CENTRAL NERVOUS SYSTEM :

INVESTIGATIONS

HEMOGLOBIN

TOTAL BILIRUBIN

DIRECT BILIRUBIN

SERUM GLUTAMIC OXALOACETIC TRANSAMINASE

SERUM GLUTAMIC PYURUVIC TRANSAMINASE

SERUM AMYLASE

SERUM LIPASE

91

PROTHROMBIN TIME

INR( INTERNATIONAL STANDARDISED RATIO)

SERUM CREATININE

BLOOD UREA

ULTRASOUND-ABDOMEN AND PELVIS

92

93

94

INFORMED CONSENT

“CLINICAL PROFILE OF RAT KILLER PASTE POISONING”

Place of study: Govt. Stanley medical college, Chennai

I …………………………………….……………………. have been informed about the

details of the study in my own language.

I have completely understood the details of the study.

I am aware of the possible risks and benefits, while taking part in the study.

I agree to collect samples of blood/saliva/urine/tissue if study needs.

I understand that I can withdraw from the study at any point of time and even then, I can

receive the medical treatment as usual.

I understand that I will not get any money for taking part in the study.

I will not object if the results of this study are getting published in any medical journal,

provided my personal identity is not revealed.

I know what I am supposed to do by taking part in this study and I assure that I would

extend my full cooperation for this study.

Volunteer: Witness:

Name and address Name and address

Signature/thumb impression: Signature/thumb impression

95

INFORMED CONSENT

“CLINICAL PROFILE OF RAT KILLER PASTE POISONING”

S NO

A

GE

SEXA

MT

CO

NSU

MED

STOM

AC

H W

ASH

TIME LA

PSE FO

R STO

MA

CH

WA

SHV

OM

ITING

AB

D P

AIN

JAU

ND

ICE

MA

LENA

HE

Hb

-1H

b-3

Hb

-5H

b-7

Hb

-9H

b-11

TB-1

DB

-1TB

-3D

B-3

TB-5

DB

-5TB

-7D

B-7

TB-9

DB

-9TB

-11D

B-11

OT-1

PT-1

OT-3

PT-3O

T-5PT-5

OT-7

PT-7

OT-9

PT-9

OT-11

PT-11

PT-1IN

R-1

PT-3IN

R-3

PT-5IN

R-5

PT-7IN

R-7

PT-9IN

R-9

PT-11IN

R-11

RFT

IF AB

N, U

/CrU

SGC

OU

RSE IN

HO

SPC

AU

SE OF D

EATH

CO

MP

LICA

TION

SD

UR

ATIO

N O

F STAYA

L

12

5M

HA

LFYES

6H

YESYES

NO

NO

NO

14.2

13.6

12.8

2.1

1.3

1.90.2

1.50.2

4522

4032

3528

10.80.7

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11.51.11

12.21.19

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2.31.5

3.61.4

2.51.1

9565

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131.27

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6.23.5

6.64.1

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16.51.65

17.61.77

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7545

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13.11.28

12.81.25

10.20.98

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20.9

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27.6

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28.815.6

2914.5

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25.22.6

22.82.33

23.52.41

26.52.75

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3.42.1

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1.2145

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0.52.1

1.1145

101124

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0.712.2

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6

152

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2.31.4

3.11.5

154120

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11.51.11

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0.81.8

1.149

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2811.7

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8

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3314

3518

2911

11.30.8

15.41.53

11.781.14

WN

LN

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156

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10.2

10.2

11

10.95

.43

.56.8

3.87.9

3.77.5

3.4546

321629

438854

531845

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1.7215.1

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11.11.03

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0.265

2456

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1.7116

78102

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160

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13.4

13.5

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2.44.9

1.94.1

1.2284

115305

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185387

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9

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2.10.5

8925

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7523

13.11.28

15.41.53

10.51.01

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2.122.9

2.3524.5

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165

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12.5

11.9

11.7

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1.91.1

1.80.4

4218

4611

389

15.41.53

12.11.18

14.71.45

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166

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6

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0.42.8

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1.578

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84168

102204

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168

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12.5

11.4

11

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2.81.2

3.51.4

15498

12387

204114

14.11.39

13.51.33

12.81.25

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THPA

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.112

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1.156

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1.3412.1

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5

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11.2

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2.51.1

1.91

10265

8941

8848

13.91.37

11.51.11

12.21.19

WN

LN

DISC

H6

Documents

A Dissertation on THE TAMIL NADU DR.M.G.R.MEDICAL