an evaluation of antifungal properties of mouth …
TRANSCRIPT
“A 5 YEAR RETROSPECTIVE STUDY OF POISONING CASES IN
PAEDIATRIC AGE GROUP AT THE DISTRICT HOSPITAL,
BELGAUM”
By
DR. RAVINDRA. S. HONNUNGAR.
DISSERTATION Submitted to the Rajiv Gandhi University of Health Sciences,
Karnataka, Bangalore
In partial fulfillment of the requirements for the degree of
MD (FORENSIC MEDICINE)
Under the Guidance of DR. B. S. YADWAD.
M.D.
DEPARTMENT OF FORENSIC MEDICINE J. N. MEDICAL COLLEGE, NEHRU NAGAR,
BELGAUM-590010.
2003-2006
i
RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES,
KARNATAKA.
DECLARATION BY THE CANDIDATE
I hereby declare that this dissertation entitled “A 5 YEAR RETROSPECTIVE
STUDY OF POISONING CASES IN PAEDIATRIC AGE GROUP AT THE
DISTRICT HOSPITAL, BELGAUM” is a bonafide and genuine research work carried
out by me under the guidance of Dr. B. S. YADWAD. MD Professor and Head,
Department of Forensic Medicine, J. N. Medical College, Nehru Nagar, Belgaum-
590010.
Date: Signature of the Candidate Place: Belgaum. (Dr. Ravindra. S. Honnungar.)
ii
RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, KARNATAKA.
CERTIFICATE BY THE GUIDE
This is to certify that the dissertation entitled “A 5 YEAR RETROSPECTIVE
STUDY OF POISONING CASES IN PAEDIATRIC AGE GROUP AT THE
DISTRICT HOSPITAL, BELGAUM” is a bonafide research work done by
Dr. Ravindra. S. Honnungar in partial fulfillment of the requirement for the degree of
MD (Forensic Medicine).
Date: Signature of the Guide Place: Belgaum. Dr. B. S. YADWAD. MD Professor & Head, Department of Forensic Medicine, J. N. Medical College, Nehru Nagar, Belgaum-590010.
iii
RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, KARNATAKA.
ENDORSEMENT BY THE HOD, PRINCIPAL/HEAD OF
THE INSTITUTION
This is to certify that the dissertation entitled “A 5 YEAR RETROSPECTIVE
STUDY OF POISONING CASES IN PAEDIATRIC AGE GROUP AT THE
DISTRICT HOSPITAL, BELGAUM” is a bonafide research work done by
Dr. Ravindra. S. Honnungar under the guidance of Dr. B. S. Yadwad. MD Professor
and Head, Department of Forensic Medicine, J. N. Medial College, Nehru Nagar,
Belgaum-590010.
Seal & Signature of the Seal & Signature of the
HOD Principal Dr. B. S. Yadwad MD (BHU) Dr.V. D. Patil MD Professor and Head, Principal, Department of Forensic Medicine J. N. Medical College, J. N. Medical College,Nehru Nagar, Nehru Nagar, Belgaum-590010. Belgaum-590010. Date: Date: Place: Belgaum. Place: Belgaum.
iv
COPYRIGHT
DECLARATION BY THE CANDIDATE
I hereby declare that the Rajiv Gandhi University of Health Sciences, Karnataka
shall have the rights to preserve, use and disseminate this dissertation in print or
electronic format for academic / research purpose.
Date: Signature of the Candidate Place: Belgaum. Dr. Ravindra. S. Honnungar.
© Rajiv Gandhi University of Health Sciences, Karnataka
v
Acknowledgement
At outset, I wish to thank my all mighty GOD for his guidance and
blessings in every step of my life.
I am very much thankful to my Parents who have supported a lot and are
always with me.
I am indebted to my guide Dr. B.S. Yadwad M.D. Professor And Head,
Department of Forensic Medicine, J. N. Medical College, Belgaum. For his able
and expert guidance and constant encouragement during the preparation of this
dissertation.
I am extremely thankful to Dr. V.D. Patil, M.D., Principal, J.N. Medical
College, Belgaum, for permitting me to carry out this study.
My sincerest gratitude to the District Surgeon and Staff of the Medical
Record Section, District Civil Hospital, Belgaum for permitting me to undertake
this study.
I am, also thankful to Late Dr. F.S. Kuligod, Professor,
Dr. Manjulabai K.H., Associate Professor, Dr. Prasanna S. Jirli, Dr.
Ashokkumar Shetty, Assistant Professors, Dr. Ravi, N., Dr. Vijaykumar
Nair, Dr. Harishgouda, Dr.Gurudutt, Dr.Santosh C.S., Dr. Sunil
Aramani and Dr. Raju K. and postgraduate colleagues of various departments,
for their timely advice and encouragement.
I am also very thankful to my wife Vani, and my children Lohit &
Likhita for always being with me.
I am also grateful to Mr. Prakash Pathak, Mr. Basavaraj
Horaginmani and Mr. Babaji, Department of Forensic Medicine.
Date: Signature of the candidate Place: Belgaum. Dr Ravindra. S. Honnungar.
vi
ABSTRACT
Poisoning comprises a significant bulk of hospital admissions at tertiary care
centres. The technological advance, with its social and mental pressures has further
worsened the picture. Because it is pediatric emergency, a thorough knowledge about the
nature and magnitude of the problem is necessary.
Background and Objectives:
Accidental ingestion of poisons and household products is a potential source of
morbidity and mortality in children all over the world. Despite a fair assumption of the
magnitude of the problem, we found lack of concrete data with respect to poisoning in
children. We decided to undertake this study with the objective of quantifying the
problem.
1) To know prevalence of poisoning and mortality
2) To know the commonest type of poison encountered
3) To know the common age involved in paediatric age group.
4) To elicit seasonal variation if any.
5) To know the manner of poisoning (accidental/ suicidal/ homicidal).
Methods:
Retrospective analysis of case records of all childhood poisonings in District
Hospital, Belgaum over 5 years from January 1999 to December 2003 were studied. All
cases of poisoning in the 1 to 15 years age group were studied in detail with respect to
age, sex, type of poison and outcome. Food poisoning and idiosyncratic reactions to
drugs were excluded from the study.
vii
Results:
A total of 116 cases formed the basis for the study, the prevalence of poisoning
was observed to be 1.9%. The most common amongst ingested poisons was
organophosphorus compounds (38.16%) followed by kerosene (21.16%) and seeds
(18.42%). Most common age group involved was 1-3 yrs. The study showed male
predominance. There was no significant season-wise variation observed. Manner of
poisoning in 92% cases was accidental in nature. 2 female cases died due to consumption
of organophosphorus compounds.
Amongst 116 cases, 40 cases were due to snake and insect bites. In this, 30 cases
were due snakes and 10 were due to insect and scorpion bite. Maximum number of cases
observed was in the age group 4 and 12 years. The study showed male predominance
than females. Maximum number of snake and insect bites occurred in rainy and summer
season. All the reported cases of snake bite and insect bites during the present study were
accidental in nature. 3 cases died due to snake bite. The data was compared with the
studies of Indian and Western authors.
Interpretation and Conclusion:
Male children predominate over females as they display a greater degree of
activity. Most common age group involved is 1-3 years. At this age the child’s motility
and ingenuity allow him access to any unlocked drawer or cupboard at home, despite
apparent hurdles, and the impulsiveness characteristic of that age may lead to disaster.
Efforts should be made to contain accidental poisoning in toddlers that are largely
preventable by parent education, stacking away chemicals in closets under lock and key.
Keywords: Accidental ingestion; Prevalence; Retrospective analysis; Organophosphorus
compound.
viii
CONTENTS
PARTICULARS PAGE
1. INTRODUCTION 1
2. OBJECTIVES 5
3. REVIEW OF LITERATURE 6
4. METHODOLOGY 63
5. RESULTS 66
6. DISCUSSION 82
7. CONCLUSION 87
8. SUMMARY 89
9. BIBLIOGRAPHY 91
10. ANNEXURES 96
ANNEXURE – I (PHOTOGRAPHS)
ANNEXURE – II (PROFORMA)
ANNEXURE – III (MASTER CHART)
ix
LIST OF TABLES
TABLE NO. TITLE PAGE
NO.
1 Yearwise Distribution of Poisoning Cases 66
2 Pattern of Poisoning Cases in Paediatric Age Group 67
3 Common Types of Poison Consumed 68
4 Age Wise Distribution of ingested poisons 69
5 Sex Wise Distribution 70
6 Seasonal Variation 71
7 Urban and Rural Variation 72
8 Manner of Poisoning 73
9 Year wise distribution of sake and insect bite cases 74
10 Type of Snake Bite 75
11 Age Wise Distribution of Snake and Insect Bites 76
12 Sex Wise Distribution 77
13 Seasonal Variation 78
14 Site of Bite 79
15 Urban and Rural Distribution 80
16 Manner of Snake Bite 81
x
LIST OF GRAPHS
GRAPH NO. TITLE PAGE
NO.
1 Yearwise Distribution of Poisoning Cases 66
2 Pattern of Poisoning Cases in Paediatric Age Group 67
3 Common Types of Poison Consumed 68
4 Age Wise Distribution of ingested poisons 69
5 Sex Wise Distribution 70
6 Seasonal Variation 71
7 Urban and Rural Variation 72
8 Manner of Poisoning 73
9 Year wise distribution of sake and insect bite cases 74
10 Type of Snake Bite 75
11 Age Wise Distribution of Snake and Insect Bites 76
12 Sex Wise Distribution 77
13 Seasonal Variation 78
14 Site of Bite 79
15 Urban and Rural Distribution 80
xi
INTRODUCTION
Toxicology is the branch of medical science, which deals with the sources,
pharmacokinetics and pharmacodynamics of poisons, the clinical manifestations
produced by them, their lethal doses and the therapeutic measures to be employed to
counter them.1
A poison is a substance (solid, liquid or gaseous), which if introduced in the living
body or brought into contact with any part thereof, will produce ill health or death by its
constitutional or local effects or both.2
It is difficult to draw a boundary line between medicine and poison because
medicine in large doses acts as poison and that a poison in a small dose is a medicine.
The only real difference in the legal sense is the intent with which they are purposely and
not accidentally given.
Poisons are as old as mankind or perhaps even older. Their description can be
found in the ancient Egyptian, Babylonian, Hebrew and Greek literature. Poisons have
been described in Atharva Veda (1500 BC), Kalpasthana. Chikitsaathana and
Uttarasthana of the Shastras have described symptoms and antidotes of poisons in detail.
Susruta (350 BC) described the procedures for incorporating poisons into foods, drinks,
perfumes, medicine, bathing water, snuffer sprinklers (The ancient Indian's had mastered
the art of turning dazzling damsels into beings capable of delivering death kisses, known
as the Vishkanya)1. Suicide and homicide by poisoning is considered less grave a crime
than causing death by violence in India.
The exact incidence of poisoning in India is uncertain due to lack of data of
central level as majority of cases are not reported, and as mortality data are a poor
1
indicator of incidence of poisoning. This varies from country to country depending on the
kind of poisons encountered, the extent of awareness about poisoning, the availability of
treatment facilities. While in developed countries the rate of mortality from poisoning is
as low as 1 to 2%, in India it varies from a shocking 15 to 35%. Children under 15 yrs of
age account for most cases of accidental poisoning, but fortunately they are associated
with relatively low mortality. On the other hand, most suicidal exposures are seen in
individuals over 15 years of age but are associated with high mortality.3
Accidental poisoning, a common paediatric emergency is one of the important
causes of morbidity and mortality in children especially in developing countries.
Thousands of innocent children under the age of five years are poisoned accidentally
every year throughout the world, mainly due to their innovative and exploratory nature
and mouthing tendencies.4,5 Here, the term "Accidental Poisoning" in childhood may be
used loosely as a designation for all such cases, but many children are not actually
poisoned, either because the substance was not toxic or because it was not swallowed or
was lost during swallowing.
There are six basic modes of exposure to poisoning:
i. Ingestion
ii. Occular exposure
iii. Topical exposure
iv. Environmental
v. Inhalation
vi. Transplacental exposure
Poisonings may be the result of acute or chronic exposures. Most poisonings are
acute and the victims are typified by the child who surreptitiously invades the medicine
cabinet or the storage area for household cleaners. Chronic poisoning refers to toxicity
2
produced over a period of time where a substance accumulates in the body, producing
toxic results; it is best exemplified by environmental exposure to lead or other heavy
metals.6
There is no significant reduction in the number of poisoning accidents but the
pattern of poisoning has shown a great change over the last decade. New hazards are
constantly appearing with the introduction of new products for domestic use, new
chemicals in farming and industry and easier availability of some drugs and abuse of
some others. Great changes have taken place in our pattern of living and social customs
also. There is break down of joint families. In many families both the parents live away
from the child for the entire day and the child is left in the care of an older sibling.
Apart from poisons those are ingested, poisoning due to animal bites especially
snake bite is a common medical emergency and an occupational hazard, more so in
tropical India, where farming is a major source of employment. Children of fieldworkers
forced into child labour are in a life risking occupation. The number of deaths due to
snake bite in India is estimated to be about 15000 – 20000 per year.7
There are a number of hospital based epidemiological studies on childhood
poisoning in India implicating different agents and all studies emphasize the
implementation of improvement in prevention programmes. Childhood poisonings are
usually accidental unlike in adults where they are more frequently suicidal or homicidal.
This makes childhood poisoning amenable to prevention with some simple but intelligent
measures. Potentially noxious substances should never be stored in containers normally
used for storing food or beverages. Kerosene oil and caustic soda in particular should
never be kept in tumblers and beverage bottles.
3
Despite a fair assumption of the magnitude of the problem, we found lack of
concrete data with respect to poisoning in children. We decided to undertake this study
with the objective of quantifying the problem.
The present study is undertaken to find out the prevalence of accidental poisoning
in children due to different categories of poisons and incidence of fatalities.
4
OBJECTIVES OF THE STUDY
The present study is a retrospective study of pediatric poisoning cases admitted
and autopsied at District Hospital, Belgaum undertaken with the following aims and
objectives.
1) To know the prevalence of poisoning and mortality.
2) To know the commonest type of poison encountered.
3) To know the common age group involved.
4) To elicit seasonal variation if any.
5) To know the manner of poisoning (accidental/ suicidal/ homicidal).
5
REVIEW OF LITERATURE
HISTORICAL REVIEW
“A poison in a small dose is a medicine and a medicine in a large dose is a
poison.” Said Alfred Swain Taylor, the 19th century toxicologist.
No other form of murder in the history of homicide has been as dramatized,
documented, romanticized, disparaged or has achieved such a high level of art as
poisoning, which was described as the coward’s weapon by the Jacobean dramatist John
Fletcher. Dating all the way back to the ancient Sumerians who, in 4500 BC, were
probably among the first to document its effects. The ancients initially used plant
substances like curare and aconite to poison their hunting arrows and darts; somewhere
along the line, somebody figured that what could bring down a beast would kill a man as
well.8
The early history of poisoning is very much intertwined with mythology and
belief. As early as 2500 BC, the Sumerians worshiped a goddess of poisons called Gula,
who was also regarded as the mistress of charms and spells. Many references are to be
found in Greek mythology as well, among which is the story of Medea, grand daughter of
Helios the sun God, who made a failed attempt to trick her husband Aegeus into killing
her stepson Theseus (Aegeus’s son) with poisoned wine by claiming the latter was an
enemy and pretender to the throne. At the last moment, however, Aegeus recognized
Theseus sword and dashed the goblet from his sons lips. Many ancient civilizations were
intimately acquainted with poisons and their effects. The earliest records of poisoning in
Egypt date back to around 3000 BC, as per the research of Menes, on the subject of
poisonous plants. Although the documentation and release of detailed accounts were
punishable by death at the time, it is now known that the Egyptians were among the first
masters of distillation, knew about many classical poisons and were no strangers to the
6
extraction of poisons (probably cyanide) from peach kernels – a papyrus translated by
Duteuil records the preparation of poisonous substances for the purpose of killing.8
The Greeks were certainly conversant with poisons as well, being the ones who
introduced poisoning as a form of capital punishment they called ‘state poison’ – it was
by this method that the philosopher Socrates was executed. During the age of the Roman
Empire, poisoning became a common activity at the dinner table, especially in the high
circles of society. It was certainly a convenient way of getting rid of unwanted family
members, as Nero demonstrated.
Around 246 BC, the Chinese developed a drama form known as the Chou Ritual,
which comprised six ceremonial dancers carried out with feathers. The ritual involved the
burning of five poisons; Cinnabar (mercury), realger (arsenic), green vitriol (copper
sulphate), lodestone and an unknown poison and the catching of the fumes on a bunch of
feathers for external use. The Persians were similarly interested in poisons, as shown by
Queen Parysatis who, during the reign of Artaxerxes II (405-359 BC), demonstrated her
love for her daughter-in-law Statira by poisoning the knife used to carve a bird at her
dinner table. By 82 BC, poisoning had apparently become so much of a scourage in the
Roman Empire that the Roman dictator and constitutional reformer Lucius Cornelius
Sulla found it necessary to issue the world’s first law against poisoning, called the Lex
Cornelia. A fat lot of good it did. The incidences of poisoning continued to escalate at an
alarming rate to their peak in the 1st Century AD, when the Julio-Claudian emperors
reigned. Among the emperors who were subsequently murdered by poison were Vitellius,
Domitian, Hadrian, Commodus, Caracalla and Alexander Severus.8
In the 8th century AD, poisoning took another step forward when an Arab chemist
successfully transformed arsenic into an odourless, tasteless powder that would elude
7
detection for at least ten centuries, thus providing the sinister world of poisoners with the
convenient and deadly inheritance powder.
The Victorian era is generally regarded as the heyday of poisoners. Indeed, it is
the period from which many of the world’s most notorious poisoners hail. While people
who poisoned for personal gain are to be found through the ages, now that poison was
readily available to commoners, potential poisoners now had a new incentive; life
insurance. In fact, poison was so popular as a homicide weapon, and so readily available
in various forms, that laws such as the Arsenic Act of 1851 had to be introduced to bring
the crime under control. Interestingly, one of the most well known contemporary deaths
by arsenic may not have been homicide after all. When Napoleon became ill in the
autumn of 1820, he was convinced that he was the target of poisoning. For years it was
believed that he had been poisoned by French and British conspirators. It was not until
recently that it was shown that the wallpaper in his house contained arsenic, and that the
metabolism of mould on the wall paper was likely to have caused release of the poison in
gaseous form. It should also be pointed out that many medicines of the period contained
arsenic, which could have also contributed to Napoleon’s demise.9
One of the earliest classifications of poisons was done by the Greek Physician
Dioscorides (AD 40-80) who categorized poisons into 3 groups – animal, vegetable, and
mineral. Experimental toxicology perhaps began with Nicander (BC 204-135), another
Greek physician who experimented with animal treatise on plant poisons is De Historia
Plantarum, by Theophrastus (BC 370-286). The Greeks used some plant toxins as poisons
of execution. Socrates (BC 740-399) was executed by the administration of hemlock.10
In ancient India, the poisons – arsenic, aconite and opium we known. They were
used by women to get rid of oppressive husbands. The Mahabharat, which is usually
8
ascribed to the fifth or sixth century B.C. mentions that Bhimsen, the Hindu Samson was
poisoned by his cousin Duryodhan whom he had defeated in a duel. In a semi-historical
legend of mid-India, it is narrated that the grand father of Asoka, Chandra Gupta, a
contemporary of Alexander the Great, sent to latter monarch in the guise of a present, a
fascinating girl who was a ‘poison maiden’ fed on poison until she was so saturated with
venoum that her embrace would prove fatal to an ordinary mortal. The mere conception
of the idea of such a Borgia-like siren would imply considerable familiarity with
poisoning. In Mohamedan times, poisoning was recognized form of capital punishment
and was unusually rife in harem intrigues and against political foes and prisoners.11
In Kalpasthan, Chikitasasthana and Uttarasthana of the Shastras, symptoms and
antidotes of poisons are given in detail. Susruta (350 BC) described how the poisons were
mixed with food and drink, ointment oils, perfumes, medicines, bathing water, snuff, or
sprinkled over clothes, shoes, beds, jewellary or put in the ears, eyes, etc. Kautilya in his
Arthashastra (about 2 century BC) states that the art and science of poisoning was
extensively studied as a separate branch, and used both as an offensive and defensive
measure against the enemy. Gradually, there arose a class of professional poisoners, who
could ingeniously mask the bitter taste or strange odours of the poisons with sweet tasting
and pleasant substances.2
Development of toxicology as a distinct speciality began in earnest in the 18th and
19th centuries with the pioneering work of Bonaventure Orfila (1787-1853), who is
generally regarded as the father of modern toxicology. He advocated the practice of
autopsy followed by chemical analysis of viscera to prove that poisoning had taken place.
His treatise Traite des poisons published in 1814 laid the foundations of forensic
toxicology. In 1829, one of his students, Robert Christian (1797-1882) published a
simplified English version tilted “A Treatise on Poisons”. The first published work on
9
clinical toxicology was “A Practical Treatise on Poisons” written by O Costill, and
published in 1848.10
By the 20th century, literature concerning the manufacture of poisons had left its
cobwebby corners in the apothecary for the bookshelves of those who sought the
knowledge and it was not just about getting rid of unwanted family any more by using
poisons as weapons. On the other hand, the growth of the field of toxicology also brought
about the controlled use and circulation of poisonous substances.
In the mean time, new and obscure poisons were beginning to emerge in the
market, many of them legal medical drugs such as fentanyl, insulin, and various muscle
relaxants including succinyl choline and Pavulon. New methods of poisoning were
introduced, as well the resourceful use of common household chemicals such as
antifreeze. Antifreeze was introduced as a murder weapon in the 1980s by Shirley Allen,
who used it to kill her husband for insurance money.
The race between the quest for the perfect poison and advances in toxicology
keeping pace with new poisons continues. Today, we can be sure that, no matter what
poison, a method can and will be developed to trace it. The question is how much damage
can be done before the perpetrator is caught. But while the progress of toxicology will
guarantee apprehension of the poisoner every time, it is doubtful that it would put an end
to the crime altogether.
Human poisoning both suicidal and homicidal cases of poisoning are more
common in India than in western countries owing to the ease with which poisons can be
obtained in any bazaar inspite of certain restrictions that have been imposed regarding
their sale. Accidental poisoning is also increasing due to greater use of these chemicals
10
for industrial, agricultural and domestic purposes. Accidental cases of bites by venomous
snakes frequently occur in India.
In India pattern of poisons has changed from the old common poisons like opium,
arsenic, datura, oleander etc. to new poisons like insecticides, barbiturates, diazepam etc.
During the last three decades, the study on pattern of accidental poisoning cases in
paediatrics has become an important subject for the forensic pathologists and the
toxicologists worldwide. The commonest type of the poison encountered, the age and sex
incidence, the manner of poisoning, the socioeconomic relation with poisoning, the
mortality following poisoning and many other parameters have been the subjects of study
of several workers.
A study on pattern of poisoning in children carried out in Safdarjang Hospital
over 5 years revealed prevalence of poisoning was 1.4% of the total admission. 60% of
the children were below the age of 3 yrs and that for all poisoning the ratio of males to
females was 2:1. Poisoning due to opium was mostly in children below the age of one
year. 79% of poisoning cases were accidental, either the mother gave the medicine by
mistake or the child picked it up but 21% were as a result of toxicity to overdosage of
drugs. 8% of cases were due to phenothiazine toxicity. The incidence of kerosene oil
poisoning was 36.3%. The children were below the age of three years and only two were
above the age of five years and one of these was a mentally retarded child. 2% children
admitted for kerosene oil poisoning died. Incidence of aspirin poisoning was less than 2%
in this study while in U.S.A. it is the commonest poison encountered.12
A study conducted in pediatric wards of Ispat General Hospital, Rourkela.
Diagnosis of poisoning was made mainly from history. The prevalence of poisoning was
0.33 percent. Eleven cases (11.22%) belonged to the age group of 0 to 1 year, 59
11
(60.18%) were of 1 to 4 years and 28 (28.6%) belonged to the age group of 4 to 14 years.
Sixty-three children were male and thirty-five were female. Household chemicals were
the major offending agents (42.84%), next common were the seeds (26.58%) and drugs
(24.485). Respiratory complication was common in kerosene poisoning (48.02%). Of the
total 98 cases, 2 deaths occurred, one due to kerosene poisoning and other due to opium.
Fatality, non-fatality ratio was 1:48.13
Pattern of accidental poisoning in children was conducted over three years during
the period between 1977-79. The study was carried out in Paediatric Department of
Calcutta National Medical College and Hospital. It revealed the prevalence of childhood
poisoning to be 1.98% with kerosene oil poisoning (44%) at the top of the list followed
by poisoning due to medicaments and chemicals (35.7%), pesticides (9.5%), poisonous
seeds (6%) and corrosives (4.76%). There was no fatality and no definite seasonal
prevalence of any categories of poisoning in this study. About 62% of poisoning occurred
in 1-3 years age group and for all poisoning cases incidence in male was higher than
female.14
A retrospective study of all the children, with accidental poisoning admitted under
pediatric care of the Nehru Hospital attached to post-graduate institute of Medical
Education and Research, Chandigarh between 1970 and 1979. Eighty-three children were
diagnosed as accidental poisoning due to chemicals or drugs. These constituted 0.64
percent of total pediatric admissions during the period. Kerosene oil poisoning was the
commonest (43%) followed by barbiturates (13%) and phenothiazines (8%) in order of
frequency. Children belonging to lower income groups constituted 97.5% of all cases.
Sixty-one children (73.5%) came from urban areas. There was a mortality rate of 4.8%,
the majority of deaths were due to corrosives.15
A study of 499 cases of poisoning admitted to Sir Padamat Mother and Child
Health Institute, Jaipur during 3 years (1982-1984), the prevalence of accidental
12
poisoning accounted for 1.9%. 85% of these cases belonged to urban and urban-slum
areas while the rest were from rural areas. 70.7% of the cases were under the age of 5 yrs
(7.4% below 1 year, 61.3% in the age group of 1-4 years). The male-female ratio was
3.2 : 1. Food poisoning (32.2%) was the commonest followed by kerosene oil ingestion
(22.8%), medicament and chemicals (17.7%), plant poison (11.2%), corrosives (6.6%)
and pesticides (6.2%) respectively. The overall mortality rate was 2.4%. Five of the 12
fatalities were due to kerosene, 3 due to food poisoning, 2 due to pesticides and 1 each
due to opium and diesel oil ingestion.16
A study of two hundred twenty five cases of poisoning in children over a period
of 2 ½ years at KEM Hospital, Bombay, were studied. The prevalence was 2.68%, with
male : female ratio of 1.7 : 1. Maximum cases occurred in the preschool age group, i.e., 0
– 5 years (82.6%). Kerosene poisoning accounted for 49% cases, next major group being
drugs (12.4%) and local medicaments (9.3%). Other poisons were pesticides (8.9%),
animal bites (6.7%) and dyes (4.9%).17
A retrospective study was carried out in Krishna Hospital and Medical Research
Centre, Karad, in South-West India over five years (1984-1988). Overall prevalence of
accidental poisoning in children was 1.8% (oral 1%, parenteral 0.8%). Mean age of
children was 6.5 yrs, with male-female ratio 2:1. Oral poisoning was more common in
children below 5 years whereas parenteral poisoning was common in children above 5
years. Kerosene was the commonest oral poison (30%). Oral poisoning was more
common in summer (61%) and parenteral in the rainy season (51%). Rural children were
more commonly involved than urban children (ratio being 5 : 2). Gastro-intestinal
symptoms were commoner with oral poisons. No mortality was noted with oral poisons;
whereas 3% children died due to snake bite.18
A retrospective analysis from January 1996 to May 1999 on children admitted
with poisoning to the pediatric ward of Government R.M. Hospital, Thanjavur. The total
13
pediatric admissions during this period were 15141 and poisoning was diagnosed in 1056
(6.9%). 203 (19.2%) had chemical poisoning and 853 (80.8%) had biological poisoning.
125 children were less than 2 years of age, 570 were between 2 to 5 years of age and 361
were above 5 years of age. The male to female ratio was 1.5 : 1 in chemical and 1.2 : 1 in
biological poisoning. The mortality rate was 5.4% in chemical and 3.5% in biological
poisoning. Kerosene poisoning topped the list.19
A study conducted on pediatric poisoning in Government Hospital, Srinagar, the
major referral hospital for pediatrics catering to the whole of Kashmir Valley. During 4
years period, accidental poisoning accounted for a total of 650 cases (0.96%), out of
which 130 cases (0.75%) were in 1997, 90 (0.58%) in 1998, 180 (1.2%) in 1999 and 250
(1.25%) in 2000. Maximum number of cases (49.8%) were in the age group of 1-5 years
and least (4.2%) were below 1 year of age. 46% of cases were above the rural : urban
ratio was 1 : 6. Kerosene oil was the leading poison consumed in all the four comparative
years (39.25%) whereas food poisoning was the least encountered poisoning (2.4%).
Overall mortality rate was 6%. A total of eleven patients died during hospital stay.
Highest number of deaths were in 1997 (4 out of 130) and lowest in 2000 (2 out of 250
cases).20
Pattern of acute poisonings in childhood in Ankara was studied. They took
poisoned patients under 17 year of age, presenting to the Emergency Department (ED)
from January 1995 to December 2000. The clinical data were obtained for 489 patients.
Three-hundred and thirty-one children, forming 63.6% of all patients, were under 5 years
of age. Slightly more, boys (52.3%) than girls were intoxicated at ages less than 10 years,
after which girls (79%) than boys were involved. The majority of all cases were due to
accidental poisoning (78.1% of all poisonings) which occurred mostly in children under
five years of age (73.3%). While accidental poisonings (97.1%) were the most common
mode of poisoning between 1-5 yrs, self poisonings (67.3%) had the highest ratio in cases
14
over 10 yrs of age. Drugs were the most frequent offending agent (57.7%), followed by
ingestion of a caustic/ corrosive substance (16.8%) and carbonmonoxide intoxication
(9.4%). Analgesics were the most common agents, forming 23.7 % of all poisonings due
to drugs.21
A seven-year review of accidental poisoning in children at the King Khalid
Military City Hospital (KKMCH), Hafr Al Batin, Saudi Arabia conducted retrospectively
during the period from January 1992 to December 1998. Of the 9951 single admissions in
the pediatric ward, 168 (1.7%) were identified as cases of accidental poisoning. There
were 90 males and 78 females, giving a male to female ratio of 1.2 : 1. Majority of the
children were between 1 to 3 years. Drugs accounted for 108 cases (64.3%) and other
household substances accounted for 60 (35.7%). Although no deaths were recorded in
this study.22
A retrospective study based on hospital admissions due to poisoning in three
districts in the western province of Sri-Lanka-Colombo, Gampaha and Kalutara carried
out. Approximately, 25% of the total population of Srilanka resides in these districts. Out
of total 4556 patients admitted with a history of poisoning, 540 were below 15 years thus
contributing 11.4% of the total group. There was a male preponderence (66%). A higher
proportion (60%) was under 5 years of age. Only 12% of the group was under 1 year of
age. Kerosene oil poisoning accounted for nearly half the cases among the children below
5 years of age. Medicinal agents and pesticides were the other toxic agents of importance.
The mortality due to poisoning among children was 3.2.23
A retrospective study on accidental poisoning in children at J.L.N. Medical
College and Hospital, Ajmer was conducted. Records of all poisonings cases admitted in
children ward during period June 1987 to May 1993 were analysed. Of 20,011 patients
admitted, 223 were of accidental poisoning amounting to 1.1%. The commonest age
group was 0-5 years constituting 81.2% of total patients of poisonings, followed by 5-10
15
years (16.1%). There was an overall male predominance, with male to female ratio of 1.6
: 1. Accidental ingestion of kerosene was the commonest poisoning (48.8%), followed by
accidental ingestion of drugs (11.7%), and Snake bite (11.2%). Other causes included
dhatura poisoning (8.1%), food poisoning (7.2%) and ingestion of Paris Green (3.1%). Of
all the cases, 3 patients, two of snake bite and one from severe dhatura poisoning died. In
this study, snake bite was commonest among parenteral poisoning. Out of total 20 cases,
15 (75%) were due to non-poisonous snakes. Out of 5 poisonous snake bites, 3 cases
presented with haemorrhagic manifestations and one each with paralytic features and
local cellulitis. The incidence of poisoning was 41.7% in summer, 33.6% in rainy and
24.7% in winter season. Kerosene poisoning occurred throughout the years, peaking in
summer while maximum cases of snake bite were seen in rainy season with no case
recorded during winter.24
A study was conducted on paediatric poisoning over a period of six months. The
stdy was conducted among the children admitted to the Paediatric ward of the Institute of
Maternal and Child Health, Calicut. This is considered as a referral hospital in the
Malabar area of Kerala. All patients admitted with alleged history of poisoning were
studied in detail. In the study, out of total of 3423 admissions, 160 cases (4.67%) were
poisoning cases. The majority of the cases were accidental (96.8%), while 2.5% of cases
were homicidal. There was male preponderance of 2.13 : 1. Kerosene was the commonest
poison ingested (42.5%). Kerosene poisoning was substantially more common among
toddlers aged 1 to 3 years. Among those aged more than nine years, bites and stings were
the commonest kinds of poisoning. Two children died due to snake bite, one due to food
poisoning and one case of ammonium dichloromate ingestion.25
A prospective study of all the patients below 18 years with snake venom
poisoning admitted to C.G. Hospital, Davangere, during the period January 1985 to
December 1992, was studied. During this period six hundred and thirty three cases of
16
snake bite were admitted, which contributed to 2.2% of total admission. Maximum cases
(40.4%) were in the age group 11-15 years. The youngest patient recorded was a 9
months old female baby bitten at home. Four hundred and thirty three cases were males
and 200 females. In 33.2% cases, snake bite occurred in the months of October,
November and December and 31.4% in the month of April, May and June. Thirty three
(5.2%) cases died in the hospital with a male : female ratio of 3:1.26
During 1985-1989, a retrospective study conducted on scorpion sting in pediatric
age group in Calcutta Medical College Hospitals. Total of 152 children in the age group
between 0 and 6 were admitted to the hospital. 82 were males and 70 were females. The
parts where the stings were inflicted were the fingers, back of heads, palms, wrists,
forearms, upper arms, toes, soles, feet, ankles, legs, thighs, buttocks, back, chest etc.
Season wise distribution indicated 19, 70 and 63 children were stung in the winter,
summer and rainy months respectively. Eighteen (11.8%) of the total admitted children
died of scorpion sting.27
EPIDEMIOLOGY OF POISONING:
Magnitude of Poisoning:
Poisoning is mostly a medical emergency. The number of patients admitted to
hospitals due to poisoning is increasing day-by-day throughout the world. Owing to the
vast development in the filed of chemistry, a significant number of new compounds have
appeared as new poisonous substances in trade, industry and medicine. For this reason,
poisoning is no longer restricted to industrial medicine and toxicology but has spread to
internal medicine also.
17
Poisoning as a World Problem:
In U.S.A. acute poisoning is the fourth common cause of accidental deaths, of
which a majority are reported to be from the pediatric hospitals. Sixty four percent of
poisoning involve children under 6 years. In majority of these cases, it is found that
substances used in the household are most commonly ingested by these children. Each
year in the United states, well over a million children are reported poisoned.28 In 2002,
the nation’s 62 Poison Control Centers received 2.3 million incident reports, including
adults and children. More than half the poisoning involved kids under the age of 6.
Tragically, 23 children died from poisoning that year.29
In Great Britain alone the incidence of poisoning is over 30,000 cases per year. Of
this, about 10.30% cases receive treatment in emergency wards of the hospital. About
40% of the rest, though reported to hospital are sent back home with just outpatient
measures only, as they have none or very mild symptoms. Another 30% of the total are
never reported to the hospital at all, but were treated at home. However, remaining 10%
(about 4000) cases are estimated to succumb fatally on the whole.30
Problem in India:
In India, while the most pressing and commonest problems remain those related
to infectious diseases and malnutrition, accidental poisoning is one of the important
emergencies encountered in children. Poisoning causes 0.03% of deaths in children
below 1 year of age, 0.16% in 1-4 year age group and 0.37% in the 5-14 years age group
according to the official report submitted to the Government of India.13 Hospital statistics
reported periodically from different parts of the country, indicate an incidence varying
from 0.33% to7.64% of total admissions.31
18
The young preschool child is most susceptible to accidental poisoning. Data from
various socio-cultural groups indicate that 2 to 3 year old children account for over half
of the reported cases and 80 to 90% are under 5 yrs of age. Usually, this pattern of
occurrence is related to the developmental stage of the child. As the infant starts crawling
and walking around one year of age, his activity and curiosity increase and lead him to
explore unfamiliar objects by putting them into his mouth. Later, by about 2 ½ - 3 yrs of
age the child’s motility and ingenuity allow him access to any unlocked drawer or
cupboard at home. By the age of 4 years, the incidence of accidental poisoning begins to
decline despite a further increase in motor development and co-ordination, as the older
child tends to select things that taste good for purposes of ingestion.32
However, it is very difficult to find out the exact incidence of poisoning cases in
India and the number of people who die due to poisoning. This is because of not
reporting to the authorities in cases of survival. However, the magnitude of the poisoning
cases in India can be observed by the number of cases reported based on the annual
reports of the chemical examiners laboratories from various states which is only a tip of
the iceberg.
Incidence of Snakebites in India:
Snakes are found all over the world except Arctic, New Zealand and Ireland.
There are about 3000 species of snakes in the world known to date out of which 216
species are found in India alone, out of which 52 species are reported to be poisonous.
Thus only about one-fourth of snakes are poisonous and this is the factor which boosts
the success of the witch-craft in treating snake-bites in India.33
In India, no definite statistics are maintained of snake bites, leave alone of the
snake-bite deaths. This is because of the fact that many of the victims, prefer to be treated
by traditional healers, do not reach the hospitals. In a study in 1954 reported that about
19
2,00,000 people were bitten every year by snakes in India and about 15,000 of them
died.34 It is important to note that over half of the human victims bitten by potentially
lethal venomous snakes escape with only slight or even no poisoning. It is believed that
in India, the largest number of snake-bites are recorded in the states of West Bengal,
Uttar Pradesh, Maharashtra, Tamilnadu and Kerala. It is usually at the beginning of the
rainy season that the higher incidence of snake bite is seen.35
CLASSIFICATION 36
Poisons may be classified according to the chief symptoms which they produce as
follows:
I) Corrosives:
i) Strong acids:
a. Mineral acids – Sulphuric, nitric, hydrochloric acid.
b. Organic acids – Carbolic, oxalic, acetic, salicylic acids.
ii) Strong alkalies – Hydrates and carbonates of sodium, potassium and
ammonia.
iii) Mechanical – Powdered glass, diamond dust etc.
II) Irritants:
i) Inorganic:
a. Non-metallic - phosphorus, chlorine, bromine, iodine
b. Metallic - arsenic, antimony, mercury, copper, lead, zinc, silver.
ii) Organic
a. Vegetable - Abrus precatorius, castor, croton, calotropis etc.
b. Animal - Snake and insect bites, cantharides.
20
iii) Systemic
a. Cerebral - opium, barbiturates, alcohol, ether, chloroform, datura,
belladonna, cannabis etc.
b. Spinal - Nux vomica, gelsemium
c. Peripheral - Conium, curare
d. Cardiovascular - Aconite, quinine, oleander, tobacco, hydrocyanic acid.
e. Asphyxiants - Carbon monoxide, carbon dioxide, hydrogen sulphide.
iv) Miscellaneous
a. Food poisoning and others
b. Analgesics and antipyretics – Aspirin, Antifebrin, Phenacetin.
c. Neuroleptics - Chlorpromazine, trifluoperazine, thioridazine
d. Transquilizers - Meprobanate, chlordiazepoxide
e. Antidepressant:
• Thymoleptics, Imipramine, Amitryptaline,
• MAO incubators, Nialimid, Phenoxypropazine, Isoxcurboxazid,
Phenylazine, Tranylcypromine
f. Stimulants - Amphetamine, Methidrine, Dexidrine
g. Antihistamine - Benadryl, Periactin, etc.
h. Insecticides:
• Chlorinated hydrocarbon compounds - aldrin, Endrin, D.D.T.,
Dieldrin, Lindane
• Aryl phosphates - araoxan, Parathion, Methyl parathion, chlorothion,
diazinon etc.
21
TYPE OF POISONING:
1) Fulminant:- Produced by a massive dose of poison. Death occurs very rapidly,
sometimes without preceding symptoms, i.e., the patient appears to collapse
suddenly.
2) Acute:- Produced by a single large dose or several small doses taken in a short period.
Onset of signs and symptoms is usually abrupt.
3) Chronic:- Produced by small doses taken over a long period. Onset is usually
insidious.
4) Subacute:- Some poisons also show a subacute type of poisoning which lies
somewhere between the latter two extremes mentioned above.
Indian Law on Drugs and Poisons:37
Several legal acts have been passed regulating and controlling the manufacture,
distribution and sale of drugs and poisons. The principal ones include;
a) Poisons Act (1919)
b) Drugs and Cosmetics Act (1940)
c) Drugs and Cosmetics Rules (1945)
These rules have classified all therapeutic drugs into various schedules.
Schedule C: Biological products
Schedule E: List of poisons
Schedule F: Vaccines and Sera
Schedule G: Hormonal preparations
Schedule H: Drugs with special restrictions. They are to be sold only on
prescription.
Schedule J: List of diseases, the drugs for which should not be advertised.
22
Schedule L: Antibiotics, antihistamines and other chemotherapeutic agents (like
schedule H drugs, these are also required to be sold only on prescription)
d) Pharmacy Act (1948)
e) Drugs Control Act (1950)
f) Drugs and Magic Remedies Act (1954)
g) Narcotic Drugs and Psychotropic Substances Act (1985, Amended 1988).
As per the act, a narcotic drug could be an opiate a true narcotic), cannabis (a non-
narcotic), or cocaine (the very antithesis of a narcotic, since it is a stimulant). The term
“psychotropic substance” is with reference to mind-altering drugs such as phencyclidine,
amphetamines, barbiturates, methaqualone and benzodiazepines etc.
The Act imposes complete prohibition on the cultivation, manufacture, sale,
purchase, use, or transport of any of the mentioned drugs except for medical or scientific
purpose. The minimum punishment for any offence committed under the Act is 10 yrs
rigorous imprisonment and a fine of Rs.1 lakh, while the maximum punishment is 20 yrs
and Rs.2 lakhs. There is also scope for enhanced punishment for repeat offences, which
includes the imposition of even the death penalty.
Toxicology and the Indian Penal Code:37
There is no exact definition of the term “poison” mentioned in any of the sections
of the IPC. The following sections deal with offence relating to toxicology.
Section 284 Lays down the penalty for any person causing harm to somebody through
rash or negligent handling of a poison. Punishment; up to 6 months in
prison, or payment of a fine, or both.
Section 299 Culpable homicide (by any method including poisoning)
23
Section 300 Murder (by any method including poisoning). Punishment; life
imprisonment or death.
Section 304A Rash or negligent homicide (By any method including poisoning).
Punishment; Up to 2 years or fine or both.
Section 324 Causing hurt by dangerous weapons or means (including poisoning).
Punishment: Up to 3 years or fine or both.
Section 326 Causing grievous hurt by dangerous weapons or means (including
poisons). Punishment: Up to 10 years or life imprisonment with or
without fine.
Section 328 Causing hurt by means of poison with intent to commit on offence.
Punishment: Up to 20 yrs, with or without fine.
Duties of the Doctor in a Case of Poisoning:37
Clinical:
a) Assess the patient’s condition, pay attention to life threatening problems of
airway, breathing, circulation and CNS depression.
b) Try to identify the nature of the incriminating poison; interrogate the patient, the
family or friends; try to obtain a sample, appraise its toxicity (by consulting the
toxicity rating), etc. If the identity is not clear, have someone describe the
substance (colour, odour, physical form, etc.).
c) Determine the route of exposure; oral, inhalation, skin contact, injection, etc.
d) Try to deduce the dosage consumed.
e) Find out how much time has elapsed since the incident.
f) Obtain history of allergies and hypersensitivity to drugs, cosmetics and foods.
24
g) Obtain psychiatric history and enquire as to previous suicide attempts, use of
illicit drugs, etc.
h) Consider associated problems (head injury, concurrent illness).
i) Subject blood, urine, aspirated gastric contents, etc. to laboratory analysis.
j) Assess the status of hepatic and renal functions.
k) Carry out all necessary investigations; electrolyte profile, blood gas analysis,
ECG, EEG, chest and abdominal x-rays, esophagoscopy, etc., depending on the
nature of poisoning.
l) Lay emphasis on supportive measures.
Forensic:
a) If it is a case of food poisoning originating from a public eatery (canteen, care,
hotel, etc.)
b) If a case of poisoning is definitely accidental or suicidal in nature, the attending
doctor is under no legal obligation to notify the police. But if the patient dies, the
police must be informed. Death certificate should not be issued.
c) All cases of homicidal poisoning (definite or suspected), must be reported to the
police as per section 39 of the criminal procedure code (CRPC). Failure to do so
will make him culpable under section 176 of the Indian Penal Cod (IPC).
d) Doctors working in Government run hospitals are required to report every case of
poisoning (accidental, suicidal and homicidal) to the police.
e) If the police require information on a case of poisoning (suicidal or homicidal),
the doctor must divulge it. There is no scope for professional secrecy (section 175
CrPC). If no information is given or wrong information is deliberately supplied,
the doctor becomes culpable under section 202 and 193 IPC respectively.
25
f) Every effort must be made to collect and preserve evidence suggestive of
poisoning. Deliberate omission to do so can attract punishment under section 201
of IPC.
g) If a poisoned patient is conscious but on the verge of death, record a dying
declaration relating to the circumstances.
h) If a patient dies while being treated or was brought dead to the doctor, death
certificate must not be issued. Instead, notify the police and make arrangements
for a postmortem examination.
i) Maintain detailed, written records of every case of poisoning.
j) Collect vomitus, faeces, stomach washings, contaminated food, incriminating
substance, etc., and dispatch the same for chemical analysis to the nearest
Forensic Science Laboratory.
GENERAL APPROACH TO THE POISONED CHILD:6
The poisoned patient often represents an acute onset emergency with a broad
spectrum of multi-organ system pathophysiology that shares many features with the
multiple trauma victim. In fact, poisoning might be viewed as a multiple chemical
trauma. The concept of a brief window of opportunity to make critical diagnostic and
management decisions is like-wise analogous. Thus, with a nod toward the widely
acclaimed advanced trauma life support model of the American College of Surgeons, one
may conceptualize a management approach that attempts to prioritize critical assessment
and, at times, simultaneous, management interventions.
26
General Approach to the Known or Suspected Intoxication:
Initial life – Support phase:
Airway: Usual signs with emphasis on protective reflexes
Breathing: Adequate tidal volume?
Circulation: Secure IV access
Disability: Level of consciousness
Pupillary size, reactivity
Drugs: Dextrose (± Rapid bedside test)
Oxygen
Naloxone
Decontamination: Ocular – copious saline lavage
Skin – copious water, then soap and water
GI – consider options
Evaluation and Detoxification Phase:
History – Brief, focused
Known toxin, Estimate amount
Elapsed time
Early symptoms
Home treatment
Significant underlying conditions but unknown toxin –
consider if
Suspected Patient: Acute onset
Pica-prone age
Past history pica, ingestions
Current household “stress”
27
Multiorgan system dysfunction
Significantly altered mental status
Puzzling clinical picture
Family: Medications at home
Recent illness (under treatment)
Social: Grandparents visiting
Holiday parties etc.
Physical Examination:
Vital signs
Level of consciousness, neuromuscular status
Eyes, pupils, extraocular movements, fundi
Mouth – Corrosive lesions, odours
Cardiovascular – Rate, rhythm, purfusion
Respiratory – Rate, chest excursion, air entry
Gastrointestinal – Motility, corrosive effects
Skin odours – Colour, bullae or burns, autonomic signs
Laboratory (individualize):
CBC: Cooximetry
ABG: Serum osmolarity
ECG: Cardiac monitor
Chest X-ray: Abdominal x-ray
Electrolytes, BUN/ creatinine, glucose, calcium, liver function panel
Rapid overdose toxicologic screen
Quantitative toxicology tests (especially acetaminophen)
28
Assessment of Severity / Diagnosis:
Clinical findings
Laboratory abnormalities (with consideration of anion, osmolar gaps)
Toxidromes
Specific Detoxification:
Re-assess ABCDs
Institute appropriate GI decontamination (if not already underway)
Urgent antidotal therapy
Consider excretion enhancement
Continue supportive care
CLUES TO DIAGNOSIS OF UNKNOWN POISON:38
I) Vital Sign Changes:
A) Pulse
Bradycardia Tachycardia
Narcotics Alcohol
Organophosphates Amphetamines
Cyanide Tricyclic antidepressants
Carbon monoxide Salicylates
β-blockers Cocaine
B) Respiration
Bradypnea Tachypnea
Alcohol Amphetamine
Barbiturates Methanol
Narcotics Salicylates
Sedative-Hypnotics Carbon monoxide
29
C) Blood Pressure
Hypotension Hypertension
Antidepressants Amphetamine
Antihypertensives Sympthomimetics
Antipsychotics Tricyclic antidepressants
Cyanide Antihistamines
D) Temperature
Hypothermia Hyperpyrexia
Ethanol Strychnine
Barbiturates Anticholinergics
Phenothiazines Monoamine oxidase inhibitors
Cyclic antidepressants Sympathomimetics
II) Neuromuscular:
A) Coma
Narcotic depressants
Sedative-hypnotics
Alcohols
Organophosphate insecticide
Clonidine
B) Delirium/ Psychosis
Steroids
Heavy metals
Cocaine
Heroin
Methaqualone
C) Convulsions
Aminophylline
Organophosphates
Camphor
Amphetamine
Phencyclidine
30
D) Ataxia
Diphenylhydantoin
Organic solvents
Alcohol
Carbon monoxide
Hydrocarbons
E) Paralysis
Botulism
Ticks
Paralytic shelfish poisoning
Heavy metals
Poison hemlock
III) Eyes
A) Pupils
Pinpoint (miosis) Dilated (mydriasis)
Opium Datura
Organophosphates Amphetamine
Ethanol Cocaine
Barbiturates Methanol
Phenothiazines Meperidine
Phenyclidine Antihistamines
B) Nystagnus:
Sedative-hypnotics
Carbamazepine
Phencyclidine
Barbiturates
Glutethimide
31
IV) Skin:
A) Jaundice:
Carbon tetrachloride
Naphthalene
Acetaminophen
Heavy metals
B) Cyanosis (Unresponsive to oxygen, as a result of methemoglobinemia)
Anilinedyes
Benzocaine
Phenacetin
Nitrobenzene
C) Pinkness to redness:
Alcohol
Cyanide
Boric acid
Antihistamines
V) Odours:
A) Acetone: Acetone, phenol and salicylates
B) Alcohol: Ethanol (alcoholic beverages)
C) Bitter almond: Cyanide
D) Garlic: Heavy metals (arsenic, phosphorus and thallium), organophosphates
E) Oil of wintergreen: Methylsalicylates
F) Hydrocarbons: Hydrocarbons (gasoline turpentine etc.)
32
CLASSIFICATION OF SNAKES
There are more than 3500 known species of snakes, but only 300 are venomous.39
The poisonous snakes are divided into five main groups.
1) Elapidae Cobras, kraits, mamas and coral snake, tiger snake, death adder
2) Viperidade True viper
3) Hydrophidae Sea snakes
4) Crotalidae Pit viper, rattle snakes, copper heads, pit viper, bush master
5) Colubridae Boomslang, bird snakes
The poisonous variety commonly found in India are king cobra, common cobra,
common Krait, Russel’s viper and saw scaled viper. The most common poisonous snake
is the common krait.
MORPHOLOGY: 40
1) Cobra:
Has hood with a mark like spectacle. There is a white band at the junction of body
and hood. The underside of hood bears 2 dark round spots and 3 dark bands.
Colour – Brown, length – 2mts.
2) King Cobra:
Has hood but no mark on it.
Colour – yellow, green, brown or black and has yellowish white cross-bands on
the body. Length – 3-4 mts.
3) Common Krait:
It has alternating black and yellow bands on the back. There is a black mark on
the neck. The tail ends bluntly and is swollen at its tip.
Length = 1.5 – 2mts.
33
4) Russel’s Viper:
Has a ‘V’ shaped mark on its head. Belly is white and has 3 rows of black spots
along its back.
Colour – light brown
Length – 1.5 mts
5) Saw-Scaled Viper:
It has a wavy white line on each flank of the back with diamond shaped areas
between these two lines.
Colour – Brown
Length – Less than 1 mt
Poison Gland:
There is one pair of poison glands situated behind the eyes on either side. It is a
modified salivary gland.
Fangs:
All poisonous snakes have 2 fangs. These are cannulated curved teeth situated on
the maxillary bones and are connected with the sac of the gland. When snakes bite,
poison is poured through fangs in to the wound.
Pathophysiology:
Snake venom is a complex mixture of proteins having enzymatic activities. Some
important enzymes present in the venom are,
Proteinase Phosphodiesterase
Transaminase 5-Nucleotidase
Hyaluronidase ATPase
Phospholipase ABC and D Alkaline phosphatase
34
Ribonuclease Acid phosphatases
Deoxyribonuclease Endonucleases
Cholinesterases
Crotalidae venom is rich in proteolytic enzyme activity.
Viperidae venom is scanty in amount and others have venom with little or no
proteolytic activity.
Elapidae venom is neutroxic and produces a curare-like effect and flaccid
paralysis
Crotalidae venom produces local tissue injury, haemorrhage and haemolysis.
Systemic absorption of venom occurs through the lymphatics. The action of the
venom leads to pooling of blood in the microcirculation and subsequent loss of plasma
due to increased capillary permeability leading to fall in circulating blood volume. This in
turn causes circulatory collapse and death.
Effects of Snake Venom:
A) Local Effects:
- Direct cytotoxic
- Secondary to ischemia, compression of nerves and infection
B) Haematotoxic Effects:
i) RBC
- Activation of phospholipase of RBC membrane
- Formation of lecithin and isolecithin (haemolysis).
ii) Platelets:
- Activation of coagulation system [Schwarzman like phenomenon]
- Increased adhesiveness (micro-angiopathy)
35
iii) Effects on coagulation:
- Coagulant effect (viper), conversion of prothrombin to thrombin, fibrinogen to
fibrin.
- Anticoagulant effect – consumptive coagulopathy (fibrinogen)
C) Neurotoxic effects:
- Post-synaptic block (cobra)
- Pre-synaptic block (krait)
D) Cardiotoxic effect (cobra):
- Cardiac asystole
E) Renal effect:
- ATN (50-75 percent)
- ARF (11-15 percent)
- Glomerular disease (Rare)
- Renal infarction
- Acute cortical necrosis
Factors Affecting Severity of Snake Bite:1
1) Age: Younger the age, more serious will be the outcome.
2) Location of bite: Bite on face and trunk is more dangerous than those of
extremities.
3) Size of snake: Larger the snake, worse the prognosis.
4) Secondary infection: Presence or absence of clostridia and/or anaerobic organisms
in the wound or the skin of the victim.
5) Post-snake bite activity: Exercise or running after the bite increases the rate of
absorption of toxins.
36
Manifestation:1
Cobra:
Bite is painful. A small wheal develops at the site of bite. Swelling may be
minimal or absent, constitutional symptoms appear after about half an hour. The patient
feels sleepy, appears slightly intoxicated and experiences weakness in legs followed by
excessive salivation or vomiting. This is followed by paralysis of the tongue and larynx.
There may be ptosis and strabismus due to paralysis of extraocular muscles. Within two
hours of bite paralysis is complete, coma sets in and respiration ceases. Convulsions may
or may not occur and finally the heart stops.
Krait:
Symptoms resemble those of cobra bite but the feeling of drowsiness and
intoxication is more intense. Albumin appears in urine.
Viper:
Following injection of venom severe pain develops at the site. Local swelling
develops which spreads in all directions, accompanied by the appearance of ecchymoses
and bullae over the involved area and tender enlargement of regional lymphnodes.
Serosanguinous fluid oozes from the wound followed by the gangrene of the skin and
subcutaneous tissue. The systemic absorption of venom leads to development of fever,
nausea and vomiting, circulatory collapse, low grade jaundice, neuropathic muscle
cramping. The most dreaded manifestation is haemorrhagic signs including bleeding
from fang puncture sites, venipuncture sites and into the skin and subcutaneous tissue.
Also observed are epistaxis, haematuria, hemoptysis, hematemesis and subconjunctival,
subperitoneal and intracranial haemorrhage.
Death occurs within 24-48 hrs and is usually secondary to intracranial
haemorrhage. If the patient survives, he may develop acute renal failure secondary to
37
disseminated intravascular coagulation (DIC) and cortical or tubular necrosis following
circulatory collapse.
Sea Snakes:
Bite leads to development of polymositis with a limbgirdle distribution. Muscle
enzyme levels are increased in blood and myoglobinuria with renal failure ensues.
Laboratory Abnormalities:
In severe case, Anemia, Leucocytosis, Thrombocytopenia, Hypofibrinogenemia,
Protenuria, Azotemia.
ECG Findings:
Bradycardia, ST segment depression or elevation, T-wave inversion, prolongation
of QT interval and various types of arrhythmias.
Immunodiagnosis ELISA is widely used to detect specific snake venom
antigen in wound aspirate, serum, urine, CSF and other body fluids.
Treatment:41
It is of prime importance to determine whether the patient has been actually bitten
by a poisonous snake. Look for fang marks, presence of local pain, oedema, numbness or
weakness. Their absence speaks against snake venom poisoning. Treatment can be
divided in to two parts.
i) First and
ii) Immediate management
First-Aid:
Assure the patient to prevent exertion and vagal syncope, allay anxiety.
Immobilize the limb. Apply a tourniquet above the bite mark about 5cms above the upper
38
limit of oedema or fang mark and shift it proximally every 15 minutes, if swelling
spreads further. Tourniquet should be tight enough only to obstruct lymphatic flow but
not the venous drainage. A tourniquet can only be applied if snake bite occurs on the
limbs. Clean the wound with sterile dressing. Incision and suction does not help in
removal of venoum or improve the outcome, so this is no longer recommended.
Cryotherapy is not of much use.
Immediate Management:
Establish i.v. line and administer fluids and plasma expanders or blood
transfusion to restore intravascular volume. Care of airways and breathing should be
given first priority, if there is any evidence of respiratory failure early intubation and
assisted ventilation may be used. Inject tetanus toxoid, 1st dose, if child is immunized
previously. Appropriate antibiotics must be given to patient to cover both gram positive
and gram negative organisms because secondary infection of necrotizing wound may lead
to septicaemia. In case of viper bite sedative may be given. Pain may be relieved by
NSAID. Surgical debridement and immediate split skin grafting is indicated if there are
signs of necrosis and gangrene. Irritation of eyes with large volume of water is indicated
if there is snake venom ophthalmia due to contact of cobra venom with eyes.
Glucocorticoids may be given for prevention of allergic reactions.
Specific Therapy:
Species specific anti-venom is the specific therapy but due to high cost and non-
availability and difficulty in identifying the species, polyvalent antivenom is commonly
used. Polyvalent anti-venom is derived by hyperimmunizing horses with venoms of four
common poisonous snakes; cobra, common krait, Russel’s viper and saw-scaled viper.
Indication of Antivenom:
39
1) Patients with serious manifestations of envenomation like impaired
consciousness, neurotoxicity, hypotension, shock, abnormal ECG, bleeding
diathesis, DIC, rhabdomyolysis and acute renal failure.
2) Local swelling, at the site of snake bite, involving more than half of the bitten
limb with extensive blistering or bruising.
Reconstitution of Antivenin:
The antivenin is diluted with 10ml of distilled water or isotonic saline and given
at the rate of 4ml/minute. Reconstituted antivenin can, however, also be diluted with 3
volumes of normal saline and infused very slowly and then with increased rate if well
tolerated over next 1-2 hrs.
Therefore depending on clinical response 3-5 vials may be added every 2 hrs till
all systemic signs and symptoms disappear or the progression of swelling ceases.
Dosage Guidelines for Antivenin Administration:
Severity of Envenomation
Clinical Features Amount of Antivenin
1. Mild Progressive local swelling with or without lymphadenitis and local purpura / ecchymosis
5 vials
2. Moderate Mild systemic signs or coagulation defect or haematological changes or nausea, vomiting and bradycardia.
5-15 vials
3. Severe Rapidly progressive swelling with extensive local effect, systemic signs and symptoms, DIC, encephalopathy, shock, paralysis.
15-20 vials
Stop the antivenin for same period till the reaction subsides, and if the
envenomation is severe, antivenin can be readministered even in the presence of reaction.
Clinical improvement is often seen immediately after administration of antivenin. There
is improvement in Glassgow coma scale of patient and normalization of blood pressure.
40
The neurological manifestation may improve either within 30 min, or may take hours.
Bleeding stops by 15-30 minutes and coagulation profile returns to normal within 6 hrs.
Neurotoxic envenomation leading to respiratory paralysis is managed by anti-
cholinesterases. Patients who respond to atropine sulphate (50μg/kg) and edrophonium
chloride (0.25 mg/kg i.v.) should be given neostigmine methyl sulphate (50-100μg/kg)
and atropine 4 hrly or by continuous intravenous infusion.
Contraindications to Antivenin Therapy:
1) History of atopic disorders
2) Sensitive to equine antiserum
Antivenin Reactions:
Patients with antivenin reactions, manifest with anaphylaxis, hypotension,
bronchospasm and angioneurotic oedema. Antivenin reactions occur in 3-4 percent
patients treated with antivenin within 10-180 minutes. Antivenin reactions should be
managed with SC or IM adrenaline, anti-histamine injection, steroids and dopamine as
Vasopressor. As a precautionary measure a small test dose should precede the full
therapeutic dose.
Desensitization:
For descensitisation, subcutaneous injection of 0.1, 0.2 and 0.5 ml of a 1:100
dilution of antivenin at 15 minute intervals. Subsequently a 1:10 dilution is given in the
same manner, followed by undiluted antivenin. If no sever reaction occurs, the usual dose
is given intravenously.
Supporative Management:
IV crystalloids, fresh blood, fresh frozen plasma and dopamine infusion should be
used to combat hypotension and shock. Acute renal failure should be managed with
41
restriction of fluid and electrolytes. If respiratory failure develops, it should be managed
with assisted ventilation and 100% oxygen.
Postmortem Appearance:
Poisonous snakes leave two or occasionally one fang mark. Non-poisonous
snakes leave a semicircular set of tooth marks. The punctures are 1.2 cm deep in
colubrine and 2.5 cm deep in viperine bites. In colubrine bite the site of bite contains
fluid and haemolysed blood causing staining of the vessels. In viperine bite there is
discolouration, swelling and cellulitis about the mark and haemorrhage occur from the
puncture and mucous membranes. Haemorrhages into the bowel, purpuric spots on
pericardium and haemorrhages in the lungs and in many tissues may be seen. Kidneys are
inflamed. However, there will not be any specific changes in the viscera in cases of snake
bites.
SCORPION STING1
Scorpion sting is very common in tropical countries particularly in rural and
coastal areas such as Maharashtra, Tamil Nadu, Bihar etc. India harbours 99 species of
scorpions but only two species, mesobuthus tamulus (the common red scorpion) and
palamnieus swammerdani are poisonous. Scorpions have crab-like appearance with long,
fleshy, five segmented, tail like post-abdomen, ending in a broad sac and a prominent
hollow sting. The venom containing glands are present in telson, the last tail segment and
the venom passes by a duct attached to these glands. Envenomation is usually harmless in
adults but causes toxicity in children. Maximum incidence of scorpion bite occurs in
summer and rainy season (breeding season).
The venom of scorpion is acidic and it contains toxalbumin(neurotoxic),
proteinases, phospholipases (both haematotoxic and myotoxic), cardiotoxins and
42
charybdotoxin which is a specific inhibitor of high conductance calcium activated
potassium channel.
Pathophysiology:
Scorpino venom, in addition to local irritant effect, acts as a powerful stimulus
for;
1) Massive release of catecholamines
2) Suppression of insulin secretion
3) Elevation of plasma angiotensin II level.
Scorpion Envenomation
Autonomic Storm↓ ↓ Insulin Secretion Stimulation ofrenin-angiotensin
systemDIC
Pancratitis
LipolysisCatecholamine release
↑ Angiotensin-II
Peripheralvasoconstriction
Hypertension
↑ ECF Volume↑ Myocardial OxygenConsumptionCoronary vasoconstriction Pulmonary
oedema↑ ↑ Free FattyAcids
CoronaryVasoconstriction
Myocardial ischemia
Arrythmias
Heart Failure
↑↑ Oxygen Acidosis
Consumption
(Pathophysiology of Scorpion Sting)
The pathological changes, metabolic disturbances and cardiovascular
manifestations produced by scorpion venom toxicity can be explained with these above
events. Excess of catecholamines results in increased myocardial oxygen consumption
43
due to its positive inotropic and chronotropic effect, coronary and peripheral
vasoconstriction, increased after load.
Reduction of insulin secretion leads to hyprglycemia, lipolysis and increased free
fatty acids concentration, altered RBC ATPase activity and osmotic fragility, DIC,
depletion of glycogen store of atria, ventricle, skeletal muscle and liver.
Elevation of plasma angiotensin II level is responsible for reduced arterial partial
pressure of oxygen and HCO3, changes in pH due to increased lactic and ketoacids. It
also causes coronary and peripheral vasoconstriction and potentiates the effect of
catecholamines.
Increased free fatty acids concentration is an important factor for arrhythmias and
heart failure in scorpion sting victims. Utilization of excess free fatty acids results in
increased oxygen consumption which could aggravate the ischemic injury to
myocardium. It increases the susceptibility of the ventricles to the disorganized electrical
behaviour and ectopic beats. It also produces inhibition of sodium and potassium
stimulated ATPase activity and sarcolemmal defects. Free fatty acids alter the function of
platelets leading to an increased tendency for intravascular thrombosis and DIC.
Clinical Manifestations:
The clinical manifestations are either local or systemic. The local manifestations
are intense local pain, swelling, ecchymosis and rarely tissue or bone necrosis.
Neurological:
I. Autonomic Nervous System:
These are the earliest and most prominent manifestations, also known as the
“autonomic storm”.
44
• Profuse perspiration
• Tachypnoea
• Excessive salivation
• Vomiting
• Lacrimation
• Mydriasis
• Frequent passage of stool and urine
• Priapism and ejaculation
II. CNS:
• Encephalopathy
• Convulsions (focal or generalized)
• Hemiplegia and other focal neurological deficits
• Transient blindness (amaurosis fugax)
Cardiovascular:
• Hypertension / hypotension
• Arrhythmia
• Gallop rhythm
• Varying degrees of condition-block
• Apical systolic murmer
• Focal myocardial infarction
• Myocarditis
• Congestive heart failure
• Shock
45
ECG Changes:
In children with myocarditis, serial ECG is helpful, changes may be as follows:-
• ST segment – normal or depressed
• T wave – flat or inverted
• Deep Q-wave in lead I and avL
• Various degrees of heart block
• Arrhythmia (Atrial or ventricular)
Echocardiography; Myocardial dysfunction either focal or generalized and ventricular
dilatation.
Respiration:
• Dyspnoea
• Cyanosis
• Haemoptysis
• Pulmonary oedema
Gastro-intestinal:
• Abdominal pain
• Hematemesis
• Malena
• Puncreatitis
• Pseudopancreatic cyst
• Raised serum amylase
Metabolic:
• Metabolic acidosis
• Hyperglycemia, hyperkalemia
• Increased free fatty acids
46
• Increased cholesterol and triglycerides
• Increased PaCO2
• Reduced PaO2
• Reduced pH
• Reduced HCO3
• Increased serum lactate
Renal:
• Hematuria
• Oliguria
• Acute renal failure
Hematological:
• Increased erythrocyte fragility
• Disseminated intravascular coagulation
Hepatobiliary:
• Raised transaminases (increased AST, ALT)
• Raised bilirubin
• Dilatation of branches of hepatic artery and vein
• Intravascular thrombosis
• Subcapsular haemorrhage
• Focal hydropic degeneration and
• Focal necrosis
Miscellaneous:
• Muscle fasciculation
• Tetany like contractures
47
Diagnosis:
Scorpion envenomation is diagnosed on the basis of;
2) History of scorpion sting
3) Clinical features
4) Lab investigations
• Urine analysis
• Blood glucose
• Estimation of serum amylase, lactic acid, AST, ALT and LdH
• Blood gas analysis
• ECG
Management of Scorpion Sting:
Management of scorpion sting has been divided into two groups; i.e., local
management and systemic management.
Local Management:
A ligature should be applied immediately proximal to the site of sting to delay
absorption of toxins. The ligature should be released at frequent intervals in order to
allow small amounts of toxin to reach the circulation which can be eliminated by the
detoxifying mechanism of the body. The wound should be washed with plain water,
ammonia, borax or potassium permanganate followed by cooling of the affected part with
ice. Immobilisation of affected part should be done. The affected area should be
infiltrated with a local anaesthetic agent preferably 2% xylocaine hydrochloride to
alleviate pain. If the child has been previously immunized against tetanus one dose of
tetanus toxoid should be administered.
48
Systemic Management:
The management of scorpion sting envenomation is chiefly directed at
neutralizing the toxin by anti-serum and supportive therapy for complications. Anti-
venom therapy has been differently advocated by many workers. though majority of
investigators consider anti-venom the only specific treatment, there are a few who deny
its efficacy in the prevention and abolition of cardiovascular manifestations.
Administration of anti-venom effectively neutralizes, prevents and reverses the
cardiovascular, haemodynamic, metabolic and electrocardiographic changes induced by
scorpion venom. As the venom accumulates in cardiac tissues and act indirectly through
the release of autopharmacological substances, treatment with sympatholytic agents
(α and β-blockers) may be more effective and rapid.
In the past the most widely used lytic cocktail consisted of chlorpromazine
(50mg), promethaxine (50mg) and pethidine (100mg) in 50 ml of 5% dextrose in a dose
of 0.3ml/kg/hr i.v. It was once considered to be the animation, thereby reducing the
cerebral metabolism and further ensuing complications. It is no longer used for managing
scorpion stings. This is mainly due to a greater frequency of complications observed
during lytic cocktail therapy such as hypotension, respiratory depression and convulsions.
Since cardiovascular and pulmonary complications following scorpion bite are
due to excessive release of catecholamines, the α and β-blockers can prevent myocardial
damage. Although β-blocker (propranolol) protects against sinus tachycardia, it does not
prevent either A-V block or pulmonary oedema.
Alpha-blocker (prazosin) antagonizes the effects of catecholamines and thus
prevents further damage of myocardium but it cannot reverse the damage. Prazosin,
0.4mg/kg/day orally in two-three divided doses, is used either alone or along with sodium
49
bicarbonate and/or insulin. Prazosin stimulates gastric acid secretion, thus aggravating the
existing subclinical or clinical acute pancreatitis.
Recently insulin has been recommended for the treatment of scorpion sting, and is
being widely used. The dose of insulin is 0.1 to 0.2 IU/kg/day sub-cutaneously in three
divided doses with frequent monitoring of blood sugar to prevent hypoglycemic attacks.
Administration of insulin antagonizes the metabolic changes produced by excessive
catecholamines and it increases the glycogen content of heart thereby protecting the heart
from the effects of hypoxia. It helps to restore the myocardial contractility after ischemic
insult and increases the cardiac output. Insulin also stimulates sarcolemmal Na+-K+-
ATPase activity, inhibits Ca+-K+-ATPase activity and stabilizes lysosomal membrane.
Since insufficient surfactant is one of the possible cause of pulmonary oedema and
ARDS, insulin, by increasing the surfactant synthesis in alveoli, can counter the
development of these complications. Thus the use of insulin is justified in the effective
management of scorpion sting.
Cardiac glycosides are not effective in pulmonary oedema in the presence of sinus
tachycardia and normal cardiac size since both cardiac glycosides and venous inhibit
Na+-K+-ATPase activity in myocardium.
Diuretics should not be used in scorpion bite even in the presence of pulmonary
oedema because of their dehydrating effect, alteration in blood viscosity and stimulation
of rennin-angiotensin system.
Atropine should not be given routinely for profuse perspiration, vomiting and
increased salivation because it may aggravate the tachycardia and other sympathetic
effects of venom. It also aggravates hypertension and the severity of pulmonary oedema.
The only real indication of atropine is the presence of severe bradycardia with or without
hypertension.
50
Glucocorticoids are contraindicated in the treatment of scorpion envenomation
because of their catabolic and anti-insulin action, which only aggravates the
complications. It also stimulates rennin-angiotensin system, hence glucocorticoids are
contraindicated in non-cardiogenic pulmonary oedema.
Hypertension should be controlled with calcium channel blockers, vasodilators
and ACE inhibitors. ACE inhibitors are particularly effective because of elevated
angiotensin-II level in patients with scorpion sting. Peripheral circulatory failure should
be effectively managed with low dose dopamine (5-20 μg/kg/ml) along with supportive
therapy. If the patient has developed pulmonary oedema, it should be managed with
100% oxygen, insulin, vasodilator therapy and ventilatory support. Intravenous calcium
gluconate is indicated, if fasciculations and tetany like muscular contractions develop.
Convulsions are managed as per convention children who have developed
defibrination syndrome, acro-osteolysis or encephalopathy should be managed
conservatively.
DIAGNOSIS OF POISONING:42
Diagnosis has to be made in the living as well as in the dead.
Diagnosis of Poisoning in the Living:
There is no single symptom, and no definite group of symptoms, which are
absolutely characteristic of poisoning. A medical practitioners task becomes very difficult
in diagnosing a case of poisoning as, in order to avoid police investigation, nobody is
willing to supply him with a true and correct history of the case. However, one can, to
certain extent, diagnose a case of poisoning, from the following characters of the
symptoms exhibited by the patient.
51
1) The onset is usually sudden in a previously healthy child except in chronic
poisoning, where the symptoms develop gradually, and may be easily mistaken
for disease, also it should be suspected if repeated similar attacks of vomiting or
diarrhea occur in a person after a meal, drink or medicine. In chronic poisoning
patient’s habits, daily activities, etc., must be carefully investigated.
2) The symptoms usually commence within about an hour after the poison has been
taken in a particular kind of food, drink or medicine.
3) The symptoms are uniform in character and rapidly increase in severity followed
either by death or recovery. Sometimes, remissions may occur, and certain
poisons may leave sequele of long duration.
4) Children taking at the sometime, the same kind of food or drink containing poison
suffer from similar symptoms of poisoning at or about the same time.
5) The detection of poison in food, medicine, vomit, urine or faeces is strong proof
of poisoning.
While diagnosing a case of poisoning the causes modifying the action of poisons
should be considered as these factors influence the presentation of signs and symptoms.
Causes Modifying Action of Poisons:
I) Quantity:
The natural presumption is that large dose of a poison will produce death more
rapidly by causing severe symptoms than a smaller one, but in some cases, evil effects
are mutigated by vomiting excited by a large dose of poison, such as copper sulphate.
Moreover, the action of a poison varies with quantity of its dose.
52
II) Form:
a) Physical state:
Poisons administered in the form of gases or vapours act at once and most
energetically. Poisons in the form of solutions act much more rapidly than powders.
Poisons in the form of solids act very slowly, because they are difficult to be absorbed
and in some cases may prove quite harmless.
b) Chemical combination:
The action of poison depends upon the solubility or insolubility resulting from a
chemical combination. Thus, silver nitrate and hydrochloric acid are both strong poisons
when taken separately but when combined, form an insoluble salt of silver chloride which
is almost innocuous. It should be borne in mind that certain poisons which are almost
insoluble in water may be dissolved in the acid secretion of the stomach, and are then
readily absorbed into blood, as in the case of lead carbonate or copper arsenite.
c) Mechanical combination:
The action of a poison may be altered very much if combined mechanically with
inert substances.
III) Modes of Administration:
The rapidity of the action of a poison depends upon the mode in which it is
introduced into the system. In order to rapidity of action,
a) Inhaled in gaseous or vapourous form
b) Injection into blood vessels
c) Intramuscularm subcutaneous and intradermal injection
d) Application to a wound
53
e) Application to a serous surface
f) Application to bronchotracheal mucous membrane
g) Introduction into stomach
h) Introduction into natural orifices e.g. Lectum, Vagina, Urethra, etc.
i) Application to unbroken skin
IV) Condition of the body:
a) Age:
It has a considerable bearing upon the dosage of drugs. Poisons have greater
effect at the two extremes of age. A child under two years of age has not yet fully
developed the drug metabolizing enzymes of the liver and does not have an effective
blood brain barrier and as such is more susceptible to the effect of most drugs.
b) Idiosyncracy:
It is an abnormal response to a drug due to an inborn peculiarity. Intolerance of
varying degree is exhibited by certain people for certain drugs and even articles of diet.
E.g. shellfish, eggs, fruits, etc.
c) Habit:
The effect of certain poisons decreases with habitation. Tolerance results from a
decreased reaction between the chemical and the biologic effector substance. Hence,
addicts can tolerate quantities of the drug which would endanger life if they had been
initial doses.
d) State of Health:
In general, a healthy and vigorous person is less likely to succumb to the effects
of poison than one who is enfeebled with general debility, senility, chronic or disabiling
disease.
54
e) Sleep and intoxication:
During sleep all the bodily functions are reduced. Hence the action of a poison is
delayed, if a person goes to sleep soon after taking it. The action is also retarded, if one
takes a poison when in an intoxicated condition.
Diagnosis of Poisoning in the Dead:
Diagnosis in the dead has to be made from:-
I) Postmortem Appearances:-
In order to make a probable guess of the poison and to look for its characteristic
postmortem appearances, it is necessary to read the police report and also get as much
information as possible from the relatives of the deceased regarding the quality and
quantity of the poison administered, the character of the symptoms with reference to their
onset and the time that elapsed between the taking of the poison and the development of
its first symptoms, the duration of illness, nature of the treatment adopted, and the time of
death.
External Examination:
1) The surface of the body and the clothes may show stains or marks of vomit,
faeces or the poison itself.
2) In some cases the colour of the postmortem staining may give a clue regarding the
type of poison used. The colour of PM staining in some of the poisons are as
follows.
Colour Poison
a) Bright red Hydrocyanic acid
b) Cherry pink Carbon monoxide
c) Red brown/ Deep blue Nitrates, potassium, chlorates, nitrobenzene
d) Dark brown Phosphorus
e) Black Opium
55
3) Some poisons impart a peculiar and specific smell from the mouth and nose.
Smell Poison
a) Garlicky
b) Bitter almond
c) Kerosene
d) Alcoholic
e) Urine
Phosphorus
Cyanides
Organophosphorus compound
Alcohol
Ammonical compounds
4) Injection marks over the skin and the natural orifices, e.g., mouth, nostrils, rectum
and vagina may show the presence of poisonous material or the signs of its having
being used.
Internal Examination:
There is no special routine peculiar to poisoning cases. All organs must be
examined and all contents preserved.
1) The tongue, mouth, gullet, oesophagus, upper respiratory tract and stomach
should be examined for any evidence of inflammation, erosion or staining.
Stomach in particular may show any of the following features:-
a. Hyperemia
b. Softening
c. Ulcers
d. Perforation
2) A strongly acid reaction in the duodenum and intestines is of greater significance
than that in the stomach contents. Diphtheritic colitis is a peculiar feature in
mercuric salt poisoning.
3) Substances such as chloroform, carbon tetrachloride trinitrotoluene etc., may
produce liver necrosis where as arsenic, amanita phalloides, yellow phosphorus
etc. produce a fatty yellow liver.
56
4) Parenchymatous degenerative changes in kidneys are found in irritant metal
poisoning and in cantharidian poisoning.
5) Subendocardial haemorrhages in the left ventricle of the heart is seen in acute
arsenical poisoning.
6) In cases of cranial abortion it may be necessary to send the vagina and uterus for
analysis.
All other viscera situated in the three main cavities of the body should be
examined thoroughly on the merit.
II) Chemical Examination:
In all suspected cases of poisoning the respective viscera are to be sent for
chemical analysis. In certain cases of poisoning the following articles are specifically
preserved for chemical analysis.
Organ Poison
a) Heart Digitalis, Quinine, Aconite
b) Brain Organophosphorus compounds and volatile organic
compounds
c) Spinal cord Strychnine
d) Lung Gaseous poisons, HCN, alcohol, chloroform
e) Uterus Drugs and chemicals when used for criminal abortion
Toxicity of the chemicals have been devised depending on the quantity which
produce them.
1) Relatively harmless 15gm/kg
2) Practically non-toxic 5-11 gm/kg
3) Slightly toxic 0.5 – 5gm/kg
57
4) Moderately toxic 50-500 mg/kg
5) Highly toxic 1-50 mg/kg
6) Extremely toxic 1mg/kg or less
III) Experiments on Animals:
This is not an ideal test, for signs and symptoms may be due to insusceptibility of
the animal to the particular poison, e.g., rabbits are unsusceptible to belladonna,
hyocyamus and stramonium, pigeons are not affected by opium. Cats and dogs are
affected by poisons almost in the same way as man. They may be fed with the suspected
food, or with the poison after it is separated from the viscera and the symptoms noted.
IV) Moral and circumstantial evidence:
Such evidence may consist of motive, the evidence of witness about the recent
purchase of the poison, his behaviour before and after the commission of the offence, and
the recovery from the possession of the accused or the premises of poison.
GENERAL TREATMENT OF POISONING:43
Poisoning is a medical emergency. The treatment should be instituted at the
earliest to save the life of the patient. First aid and emergency therapeutic measures are
most significant before any specific therapy is given.
The treatment of the patient consists of:-
I) Removal of unabsorbed poison from the body
a. Inhaled poisons:- If the poison is inhaled as a gas, the patient must be removed to
fresh air, artificial respiration and oxygen should be given. The air passages
should be kept free from mucous by postural drainage or by aspiration.
58
b. Injected poisons:- If the poison is introduced subcutaneously into a limb from a
bite or an injection, apply a ligature above the wound and loosen it every 10 or 15
minutes for 20 or 30 seconds to prevent the formation of gangrene. The wound
should be excised, the poison sucked out and poison neutralized by suitable
chemical substance.
c. Contact poisons:- If the vagina is applied to the skin or a wound, or is inserted
into the vagina, rectum or urinary bladder it should be removed by thorough
lavage of the affected parts with copious amounts of water or should be
neutralized by a specific chemical solvent.
d. Ingested poisons
Gastric Lavage:-
If the poison is swallowed, it should be removed by gastric lavage, most effective
if done within 2 to 5 hrs of ingestion, using a stomach pump or an ordinary, non-
collapsible rubber tube.
Gastric lavage may be done with water 1:5000 potassium permanganate, 5%
sodium bicarbonate, 4% tannic acid, 1% sodium thiosulphate, 1 to 3% calcium lactate or
starch solution depending upon the type of ingested poison.
The gastric lavage is repeated till clear and odourless fluid comes out of the
stomach. At the end, a small quantity of the fluid containing the antidote is left behind in
the stomach, so that it neutralizes whatever small quantity of the poison is left behind.
Contraindications for gastric lavage:
In certain conditions gastric lavage is contraindicated,
1) Corrosive poisoning
2) Convulsant poisons
3) Comatose patients
59
4) Upper alimentary disease, e.g., oesophageal varices
5) Marked hypothermia
Emetics:
Emetics should be used only if difficulty in obtaining or using a stomach tube
occurs. The following emetics may be administered depending upon the situation.
1) Copious amounts of warm water.
2) A table spoon full (15gms) of ground mustard or two table spoonfuls of common
salt in number (200 ml) of warm water.
3) Zinc sulphate 1 to 2 gm in a tumbler of water.
4) About 1 to 2 gm of ammonium carbonate dissolved in water
5) Ipe cacuanha powder or syrup etc.
II) Administration of Antidotes:
Antidotes are substances which counteract or neutralize the effects of poisons.
a) Mechanical Antidotes:
These antidotes neutralize poisons by mechanical action or prevent their
absorption, e.g. Animal charcoal, demulscents like milk, starch, egg whites, milk of
magnesia, aluminium hydroxide gel and bulky foods etc.
b) Chemical antidotes:
These antidotes counteract the action of poison by forming harmless or insoluble
compounds or by oxidizing poison when brought into contact with them. The examples
are weak acids for alkalies, alkaline carbonates and magnesium for mineral acids, lime
for oxalic acid, sodium sulphate for lead and tannin and albumin for alkaloids.
60
c) Physiological antidotes:
They act on the tissues of the body and produce symptoms exactly opposite to
those caused by the poison action on them or the enzymes. E.g. atropine and
physiostigmine, digitalis and aconite, chloroform and amylnitrite, strychnine and
barbiturates etc.
For treatment of some of the heavy metal poisonings, chelating agents like
B.A.L., E.D.T.A., Penicillamine, Desferriosamine etc., may be used which inactivate the
metallic ions and dislodge the metals from its combination with the sulphhydral radicals
in the tissue enzymes.
When the exact poison is not known or when a combination of two or more
poisons had been taken, universal antidote is given which consists of two parts of
powdered animal charcoal which adsorbs alkaloids, one part of the magnesium oxide
which neutralizes acids without gas formation and one part of the tannic acid which
precipitates alkaloids, glucosides, and many of the metals.
III) Elimination of Poison by Excretion:
When the poison is already absorbed into the systemic circulation, the excretion
from the body may be enhanced by following procedures.
a) Renal Excretion:- It may be improved by maintaining an adequate diuresis
through the administration of ample amount of fluids. Manipulation of urinary pH
can enhance renal excretion of drugs.
b) Purging:- Sodium sulphate with copious amounts of water, hastens the
elimination of poison in the stool.
c) Peritoneal dialysis and haemodialysis:- It is very useful for removing barbiturates,
bromides, salicylates, alcohols, sodium chlorite etc.
61
d) Diaphoretics:- In most cases, it is doubtful whether this speeds up the excretion of
toxic agents. In most cases application of heat (blankets hot water bottles), and
administration of hot beverages (hot tea, hot milk) will cause increased
perspiration. Profuse perspiration will be produced by five milligram of
pilocarpine nitrate, s.c. and a less marked effect may be produced by cutaneous
irritation and cutaneous vasodilatation produced by alcohol, salicylates and
antipyretics.
IV) Symptomatic Treatment:
It refers to the adoption of general measures to support the life of the patient and
to alleviate distress. The symptoms should be treated on general lines.
62
METHODOLOGY
The data was collected from cases of poisoning in paediatric age group admitted
to the District Hospital, Belgaum from the year Jan 1999 to December 2003. 116
poisoning cases admitted to paediatric wards in District Hospital, Belgaum, during this
period formed the material for this study. Even though some cases have come from
Belgaum city proper, majority of the patients were from the nearby rural areas.
Broadly the patients were divided into following two groups:-
1) Poisoning cases due to ingested poisons
2) Poisoning cases due to snake and insect bites
Poisoning cases due to ingested poisons:
Inclusion Criteria:
a) All patients with history of consumption of poison having positive and significant
signs and symptoms, accompanied or unaccompanied by container or poison.
b) Patients with doubtful history of consumption of poison but with definite signs
and symptoms of acute poisoning.
Exclusion Criteria:
a) Food poisoning
b) Idiosyncratic reactions to drugs
While reviewing the case papers, the important features like type and quantity of
poison consumed, duration between consumption and onset of symptoms, occupation and
monthly income of parents are noted and also evaluation of the patients symptoms like
abdominal pain, loose motions, vomiting, haemateuresis, malaena, dizziness, vertigo and
any other general symptoms. In most of the cases history regarding the manner of
poisoning is elicited.
63
Clinical examination was done under the following headings:-
• General physical examination:
The vital signs like pulse rate, blood pressure, respiratory rate and level of
consciousness were noted in all cases of poisoning.
The state of the eyes, pupils, tongue and skin are checked. A thorough search was
made for the presence of any suicidal or homicidal injuries over the body in all cases.
• Systemic examination:
A detailed examination of central nervous system, cardiovascular system,
respiratory system and per-abdomen was noted.
Once the diagnosis of poisoning is made treatment is instituted on general lines
followed by specific therapy according to individual cases. The treatment of the patient
carried out under the following guidelines.
1) Removal of unabsorbed poison from the body
2) Administration of antidotes
3) Elimination of poison by excretion
4) Symptomatic treatment
Whenever death of the patient occurred, the body was subjected to post-mortem
examination.
Poisoning cases due to snake and insect bites:
The inclusion criteria:
a) All patients with history of bites having positive and significant signs and
symptoms due to poisonous creatures like snakes, scorpions, bees and insects.
b) Patients with doubtful history of bites due to poisonous creatures but with definite
acute onset of signs and symptoms locally or systemically.
64
Exclusion criteria:
a) Patients with history of bite but having no signs and symptoms either locally or
systemically.
Details about the type of snake, site of bites, time of bite and the manner of snake
bite.
The presence of two definite puncture wounds with progressive swelling and
tenderness with persistent bleeding was taken as poisonous bite, whereas inverted ‘U’
shaped or multiple teeth marks with mild non-progressive swelling confined to the site of
bite with minimum bleeding which stopped on its own were considered to be due to non-
poisonous snake bite.
The presence of pain, numbness, tenderness, neuroparalytic and haematoxic signs
and symptoms were also considered for differentiating poisonous and non-poisonous
snake bites.
Once the diagnosis of poisonous snake bite was made, first aid treatment followed
by specific antivenin therapy was instituted for all the cases.
65
RESULTS
PREVALENCE OF POISONING:
In an analysis, 116 poisoning cases admitted to paediatric wards in District
Hospital, Belgaum, during January 1999 to December 2003 which include both ingested
poisons and poisons due to snake and insect bites, the prevalence of poisoning was
observed to be 1.9%. The total number of hospital admissions to paediatric wards during
this period was 5972.
Table No.1: Yearwise Distribution of Poisoning Cases
Feature 1999 2000 2001 2002 2003 Total
Total number of admission to paediatric department
1422 1337 930 1110 1173 5972
Total number of poisoning cases
38 26 19 17 16 116
Prevalence = 1.9%
0
200
400
600
800
1000
1200
1400
1600
No.
of C
ases
1999 2000 2001 2002 2003
Graph No.1: Yearwise Distribution of Poisoning Cases
Total admissions to pediatric department No. of piosoning cases
66
Table No.2: Pattern of Poisoning Cases in Paediatric Age Group
Type of Poison 1999 2000 2001 2002 2003 Total Percentage
Ingested poisons 23 16 15 10 12 76 65.51
Snake and insect bites
15 10 4 7 4 40 34.48
116 100
0
5
10
15
20
25
No.
of C
ases
1999 2000 2001 2002 2003
Graph No.2: Pattern of Poisoning Cases in Paediatric Age Group
Ingested poisons Snake and insect bites
For the purpose of better study, the cases were divided into following two groups:-
i) Poisoning cases due to ingested poisons
ii) Poisoning cases due to snake and insect bites
The total number of poisoning cases in paediatric age group were 116. Out of
which 76 were ingested poisons and 40 were poisoning due to snake and insect bites
which accounted for 65.51% and 34.49% respectively.
67
POISONING CASES DUE TO INGESTED POISONS
Table No.3: Common Types of Poison Consumed
Poison No. of Cases Percentage
Organophosphorous compound
Kerosene
Seeds
Drugs
Rodenticide
Carbamate
Corrosives
Organochlorine
Miscelleneous
29
16
14
5
2
2
2
1
5
38.16
21.06
18.42
6.58
2.63
2.63
2.63
1.31
6.58
Total 76 100.00
0
5
10
15
20
25
30
No.
of C
ases
Op. compounds Kerosene Seeds Drugs Rodenticide Carbamate Corrosives Organochlorine Miscellaneous
Graph No.3: Common Types of Poison Consumed
The present study shows that 44% of the total poisoning were due to insecticides
which included organophosphorus compounds, carbamate and chlorinated hydrocarbon
compounds. The second commonest poison was kerosene (21.05%). The third
commonest poison was seeds (18.42%).
68
Table No.4: Age Wise Distribution of ingested poisons
Age (Yrs) No. of Cases Percentage
1-3
4-6
7-9
10-12
13-15
36
17
11
10
2
47.36
22.36
14.47
13.15
2.63
Total 76 100
0
5
10
15
20
25
30
35
40
No.
of C
ases
'1 - 3 '4 - 6 ' 7 - 9 '10 - 12 '13 - 15
Age (Yrs)
Graph No.4: Age Wise Distribution of Ingested Poisons
The present study shows that the maximum number of patients were in the age
group between 1 and 3 yrs, approximately two-thirds of the patients were between 1 and
6 years.
69
Table No.5: Sex Wise Distribution
Males Females Age (Yrs)
No. Percentage No. Percentage
1-3
4-6
7-9
10-12
13-15
22
12
5
5
0
50
27.28
11.36
11.36
0
14
5
5
6
2
43.75
15.62
15.62
18.76
6.25
44 100.00 32 100.00
0
5
10
15
20
25
No.
of C
ases
'1 - 3 4 - 6' '7 - 9 '10 - 12 '13 - 15
Age (Yrs)
Graph No.5: Age and Sex wise Distribution of Cases
Males
Females
The sex ratio shows males were more involved than the females. The ratio of
male : female was 1.3 : 1.
70
Table No.6: Seasonal Variation
Season No. of Cases Percentage
Rainy season
Summer season
Winter season
29
25
22
38.15
32.90
28.95
76 100.00
0
5
10
15
20
25
30
No.
of C
ases
Rainy Season Summer Season Winter Season
Graph No.6: Seasonal Variation
In the present study no significant season-wise variation was observed. 38.15% of
the cases were recorded in rainy season, 32.90% of the cases were recorded in summer
season and 28.95% of the cases were recorded in winter season.
71
Table No.7: Urban and Rural Variation
Areas No. of Patients Percentage
Rural
Urban
52
24
68.42
31.58
76 100.00
Graph No.7: Urban and Rural Variation
Rural, 52
Urban, 24
The study showed that 68% of the patients were from the rural and the remaining
32% from urban areas.
72
Table No.8: Manner of Poisoning
Males Females Manner
Cases Percentage Cases Percentage
Suicidal
Homicidal
Accidental
0
1
43
0.00
2.28
97.72
2
2
28
6.25
6.25
87.5
44 100.00 32 100.00
0
5
10
15
20
25
30
35
40
45
No.
of C
ases
Suicidal Homicidal Accidental
Graph No.8: Manner of Poisoning
Males
Females
The present study showed that the manner of poisoning in 92% cases was
accidental in nature. The suicidal poisoning was seen in 2 females who had failed in the
exams. There were 3 homicidal cases, where parents frustrated in life had given poison to
their 3 children (1 male and 2 female) and also consumed themselves.
Mortality:
In this study, it was found that 2 female cases died due to consumption of
organophosphorus compound which accounted for 2.6% of the total reported cases.
73
POISONING DUE TO SNAKE AND INSECT BITES:
Out of 116 cases of poisoning admitted to paediatric wards in District Hospital,
Belgaum during January 1999 to December 2003, the total number of poisoning cases
due to snake and snake bites were 40. This constituted 34.48% of the total studied.
Table No.9: Year wise distribution of sake and insect bite cases
Cases Types
1999 2000 2001 2002 2003 Total
Snakes 12 9 4 1 4 30
Insect and scorpion bite 3 1 0 6 0 10
Total cases = 40
0
2
4
6
8
10
12
No.
of C
ases
1999 2000 2001 2002 2003
Graph No.9: Year wise Distribution of Snake and Insect bite cases
Snakes Insect and scorpion bite
74
Table No.10: Type of Snake Bite
Snake Cases Percentage
Poisonous
Non-poisonous
8
22
26.66
73.34
30 100.00
Graph No.10: Type of Snake Bite
Poisonous, 8
Non-poisonous, 22
Non-poisonous snakes constituted 73.34% of all the snake bite cases whereas
poisonous snake bite was only 26.66%.
75
Table No.11: Age Wise Distribution of Snake and Insect Bites
Age (Yrs.) No. of Patients Percentage
1-3
4-6
7-9
10-12
13-15
5
9
3
19
4
12.5
22.5
7.5
47.5
10
Total 40 100
0
2
4
6
8
10
12
14
16
18
20
No.
of C
ases
'1 - 3 '4 - 6 '7 - 9 '10 - 12 '13 - 15
Age (Yrs)
Graph No.11: Age Wise Distribution of Snake and Insect Bites
The present study showed that the maximum number of patients was in the age
group between 10 and 12 years (47.5%). More than 85% of the cases were between the
age group 4 and 12 years. Decline in the incidence of snake and insect bites was noticed
after 13 years of age.
76
Table No.12: Sex Wise Distribution
Males Females Age (Yrs.)
No. Percentage No. Percentage
1-3
4-6
7-9
10-12
13-15
2
5
2
15
2
7.7
19.20
7.7
57.7
7.7
3
4
1
4
2
21.42
28.58
7.14
28.58
14.28
Total 26 100.00 14 100.00
0
2
4
6
8
10
12
14
16
No.
of C
ases
'1 - 3 '4 - 6 '7 - 9 '10 - 12 '13 - 15
Age (Yrs)
Graph No.12: Age and Sex Wise Distribution of Cases
Males
Females
Our study showed that males were slightly more affected than the females. The
males constituted 65% of the total snake and insect bite cases whereas in females it was
35%. The maximum number of male victims was observed in the age group between 4
and 12 yrs (84.6%) whereas in females it was 64.3% in the same age group.
77
Table No.13: Seasonal Variation
Season No. of Cases Percentage
Rainy season
Summer season
Winter season
18
13
9
45%
32.5%
22.5%
40 100
Graph No.13: Seasonal Variation of Cases
Summer season, 13
Winter season, 9 Rainy season, 18
Maximum number of snake and insect bites occurred in rainy and summer season.
78
Table No.14: Site of Bite
Body site No. of Cases Percentage
Upper limbs
Lower limbs
Others
9
26
5
22.5
65
12.5
40 100
Graph No.14: Site of Bite
Lower limbs, 26
Others, 5 Upper limbs, 9
The maximum number of bites (65%) occurred in the lower extremities while in
the upper extremities it was 22.5%.
79
Table No.15: Urban and Rural Distribution
Area No. of Cases Percentage
Rural
Urban
28
12
70
30
Total 40 100.00
Graph No.15: Urban and Rural Distribution of Cases
Urban, 12
Rural, 28
The present study showed that 70% of patients were from rural areas whereas
30% of them from urban areas.
80
Table No.16: Manner of Snake Bite
Males Females Manner
Cases Percentage Cases Percentage
Suicidal
Homicidal
Accidental
0
0
26
0.00
0.0
65.00
0
0
14
0.00
0.00
35.00
All the reported cases of snakebite and insect bites during the present study were
accidental in nature involving more number of male victims.
Mortality:
Among the 40 reported cases of snake bite and insect bite, 3 cases died. 2 cases on
the way to hospital from the rural areas and 1 case died in the hospital due to severe
internal haemorrhage and respiratory failure. This accounted for 7.5% of the total
reported cases.
81
DISCUSSION
PREVALENCE OF POISONING:
In our study, the prevalence of poisoning was observed to be 1.9%. In a study
conducted in J.L.N. Medial College, Ajmer, the prevalence was reported to be 1.1%.24 A
study was conducted in the department of pediatrics, King George’s Medical College,
Lucknow, Uttar Pradesh in three alternate calendar years i.e., 1989, 1991 and 1993 were
screened. The Indian literature on poisoning in children was reviewed and decade wise
data from a total of 22 studies were used to determine the changing trend. They noticed
childhood poisoning constituted 2.1% of the total paediatric admissions.44 So prevalence
of our study is within the narrow range of the previous results.
POISONING CASES DUE TO INGESTED POISONS:
a) Commonest type of poison consumed:
In our study, it was observed that 44% of the total poisoning were due to
insecticides which includes organophosphorous compounds, carbamate and chlorinated
hydrocarbon compounds. The second commonest poison was Kerosene (21.05%). The
third commonest poison was seeds (18.42%). A similar study done in Calicut, South
India shows that kerosene was the commonest poison involved (42.5%).25 As per the
study conducted in Srinagar, Kerosene oil was the leading poison consumed which
accounted for 39.25%.20 Another study done in Thanjavur also showed kerosene
poisoning to be most common which accounted for 76.5%.19 Insecticides were the most
common in our study, mainly because agriculture is the main occupation in and around
Belgaum and most of the farmers keep the insecticides in their home. This mainly
accounted for accidental poisoning in the children.
82
b) Commonest age group and sex involved:
The present study shows that the maximum number of patients were in the age
group between 1 and 3 years, approximately, two-thirds of the patients were between 1
and 6 yrs. The sex ratio shows males were more involved than females. The ratio of male
: female was 1.3 : 1. A retrospective analysis of the telephone calls received by the
National Poisons Information Centre, AIIMS, New Delhi reveals, children below the age
of 6 yrs to have been affected more than other groups which accounted for 64.75% and
there was a higher ratio of poisoning in males (63.11%) than in females (36.88%).45
Similar study was done in Sri Lanka and the results were almost similar to our studies in
which, children below 5 years have been affected more (60%) compared to others. There
was a male preponderance (66%).23 In another study, retrospective data on childhood
poisoning from eight regional hospitals in India has been reviewed. It showed 70%
children were below 5 yrs and male outnumbered female in the ratio of 1.6 : 1.46 So our
results are almost similar to the previous studies.
c) Seasonal Variation:
In the present study, no significant season-wise variation was observed. 38.15%
of the cases recorded in rainy season, 32.9% of the cases were recorded in summer
season and 28.95% of the cases were recorded in winter season. In a study conducted in
South West Maharashtra, 43% cases seen in Summer, 37% in the rainy season and 20%
in winter.18 So not much significant seasonal variation is observed.
d) Manner of poisoning:
The present study shows that the manner of poisoning in 92% cases were
accidental in nature. Similar results were seen in a study conducted in Ankara, which
showed 97.1% accidental poisoning in children.21 In another study conducted in Accident
and Emergency Department, at the Children’s University Hospital, Ireland, a total of 148
83
cases were recorded, out of them, 86% were accidental poisoning.47 So manner of
poisoning in children is almost always accidental in nature.
e) Mortality Rate:
In our study, out of 76 ingested poisoning, 2 female cases died due to
consumption of organophosphorous compound which accounted for 2.6% of the total
reported cases. According to WHO, mortality due to poisoning in children up to 4 years
age varies between 0.3 to 7.0 per 1,00,000 population in various countries. However, no
such information is available from India, though in hospitalized children, accidental
poisoning accounts for 0.68% to 7.6% of admissions.48
POISONING DUE TO SNAKE AND INSECT BITES:
a) Type of snake-bite:
In our study, non-poisonous snakes constituted 73.34% of all the snake bite cases
whereas poisonous snake bite was only 26.66%. In a study conducted in J. L.N. Medial
College, and Hospital, Ajmer, they found out, 75% of the total bites were due to non-
poisonous snakes and 25% were due to poisonous snakes.24 In another study conducted in
Central Research Institute, Himachal Pradesh, non-poisonous snakes were the most
common (90.5%). Although snake bites are a cause for concern, most of them are caused
by non-poisonous snakes.49 So our results are almost similar to the previous published
results.
b) Commonest age group and sex involved:
In the present study, more than 85% of the cases were between the age group 4
and 12 years. The males constituted 65% of the total snake and insect bites, whereas in
females it was 35%. A similar study done in Government Children Hospital, Jammu
during January 1975 to May 1980. In this, seventy seven cases were in the age group of
5-10 years. Male outnumbered female in the ratio of 55:45.50 In another retrospective
84
study conduced in department of pediatrics of the Royal Victoria Hospital, Banjul, the
Gambia over a 3-year period. The age range was 2-14 years and the male : female ratio
was 2.1 : 1.51 So our results are almost consistent with the previous published results.
Seasonal Variation and Site of Bite:
In our study, maximum number of snake and insect bites occurred in rainy and
summer season. The maximum number of bites (65%) occurred in the lower extremities
while in the upper extremities it was 22.5%. A prospective study in C.G. Hospital,
Davangere during the period January 1985 to December 1992 was undertaken. They
studied six hundred and thirty three cases of snake bite over a period of 8 yrs. Most of the
cases were seen during two periods, i.e. October, November, December (210 cases) and
April, May, June (199 cases). Most cases (506) were encountered in the lower limbs.26 In
another retrospective study on scorpion sting was done in a hospital in Calcutta. They
noticed maximum number of cases were seen during summer and rainy season. The parts
where the stings were inflicted were the fingers, back of the hands, palms, soles, ankles
and legs.27 A similar study done in rural Zimbabwe also showed that most of the bites
occurred on the leg, below the knee.52 Another study done in B.P. Koirala Institute of
Health Sciences, Nepal also showed sixty percent of the bites in the lower limb.53 So
overall our result are similar to the previous ones.
Urban and Rural Distribution:
In our study, 70% of the patients were from rural areas whereas 30% of them
from Urban areas. A retrospective study done in Postgraduate Institute of Medical
Education and Research, Chandigarh, also showed urban to rural ratio was 1 : 4.7. They
came to conclusion that snakebites are common in the rural population of developing
countries.54 So previous study results are similar to ours.
85
Manner of snake bite:
All the reported cases of snake and insect bite in our study were accidental in
nature involving more number of male victims. No reported cases are available for
homicidal or suicidal poisoning due to snake bites in India.
Mortality Rate:
In our study 3 cases died due to snake and insect bites which accounted for 7.5%
of the total reported cases. The morbidity and mortality can be reduced substantially by
increasing and maintaining confidence in victims, good medical care and providing
health education.
86
CONCLUSION
Poisoning is a pediatric emergency and a thorough knowledge about the nature
and magnitude of problem especially when associated with regional peculiarities is
necessary. Pediatric reports from various centres reveal the much needed information and
changing spectrum. This study was conduced retrospectively in District Hospital,
Belgaum, the major tertiary hospital in the area.
The advent of various social and environmental changes has brought about a
noticeable alteration in the pattern of poisoning seen now-a-days. Fresh hazards are
constantly appearing with the introduction of newer chemicals for domestic, agricultural
and industrial usage.
In developing countries, a combination of factors contributing to accidental
poisoning among children is likely to exist in households of lower socio-economic
groups. Such a family is likely to have lower standards of housing, hence inadequate
space. The mother has to cope with difficult and time consuming household work which
minimizes the time for supervision of young children. Other factors such as family stress
and behavioural problems of children, may also be related to the above circumstances.
The data available from the present study does not enable the assessment of risk
factors. However, by identifying the importance of childhood poisoning as a cause of
morbidity as well as the relative importance of different poisoning agents may help in
channeling the intervention programmes and further research in the right direction.
87
Preventive Measures:
Accidental poisoning in children is preventable. Early detection and first aid
measures at the site of poisoning need to be stressed. Public education to keep toxic
substances out of reach of children is important. Similarly, outdoor games or walking in
fields and jungles barefoot should be discouraged, specially during summer and rains.
More community surveys must be planned to find the magnitude of the problem in
different areas. Regional toxicological centres with well equipped laboratories to treat,
guide and conduct research in the problem will be helpful.
Mass media such as television, radio and newspaper should be harnessed for
creating awareness about the potential hazards and their prevention. Flow charts for
emergency management and necessary facilities and medicines should be made available
at all health centres so that treatment may be promptly instituted.
88
SUMMARY
116 poisoning cases admitted to Pediatric wards in District Hospital, Belgaum
during January 1999 to December 2003 were studied retrospectively for the various
parameters like prevalence of poisoning, commonest type of poison encountered, the
common age group involved, the seasonal variation, the manner of poisoning and
mortality rate.
The prevalence of poisoning which include both ingested poisons and snake and
insect bites was 1.9%, and the mortality rate was 4.3%.
I) Poisoning Cases due to Ingested Poisons:
• The commonest poisons consumed were due to insecticides (44%) which included
organophosphorus compounds, carbamate and chlorinated hydrocarbon
compounds. The second commonest poison was kerosene (21.05%). The third
commonest poison was seeds (18.42%).
• Maximum number of patients was in the age group between 1 and 3 yrs (47.36%).
• Males were more frequently affected than the females as shown by ratio of 1.3 : 1.
• There was no significant month wise variation in number of poisoning cases.
However, maximum number (29) of cases occurred in the rainy season.
• Children from rural areas were most affected (68%) than from urban (32%) areas.
• The manner of poisoning in 92% cases was accidental in nature. Females were
more vulnerable for suicidal poisonings than females.
• 2 female cased died due to consumption of organophosphorus compound which
accounted for 2.6% of the total reported cases.
89
II) Poisoning due to snake and insect bites:
• Poisoning due to snake and insect bites was 34.48% of the total cases studied.
• Non-poisonous snake bites constituted 73.33% of all the snake bite cases whereas
poisonous snake bites were only 26.66%.
• Maximum number of patients was in the age group between 10 and 12 yrs
(47.5%). Males were affected more compared to females.
• Maximum number of snake and insect bites occurred in rainy (45%) and summer
(32.5%) season.
• The maximum number of bites (65%) occurred in the lower extremities while in
the upper extremities it was 22.5%.
• Children from rural areas (70%) were commonly affected than urban areas (30%).
• All the reported cases of snake bites were accidental in nature involving more
number of male victims (65%).
• 3 cases died due to snake bite which accounted for 7.5% of the total reported
cases.
90
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QUESTIONNAIRE (Proforma used to collect data)
1. Sl. No.: Hospital Admission No:
2. Name:
3. Age: Informant :
4. Sex:
5. Address: Monthly Income of Parent/:
Guardian
6. Occupation of the Father:
7. Occupation of the Mother:
8. Occupation of the Guardian:
9. Date and time of admission:
10. Date of discharge (if recovered) :
11. Date and time of expiry:
12. Manner of poisoning : Suicidal/ Homicidal/ Accidental
13. H/o. Presenting Complaints:
i) Type and quantity of poison consumed/
Type of animal bite
ii) Duration between consumption of poison/ bite
and onset of symptoms
iii) Duration between consumption of poison /bite
and admission / treatment
14. Pedigree chart
15. General Physical Examination:
Pulse rate
Resp rate
Temperature
Smell of breadth/ vomitus/ aspirated matter
Eyes – Pale/ congested
Pupils – constricted/ dilated/ normal
Cyanosis – present/ absent
Site of animal bite
15. Systemic examination:
CNS
CVS
Resp
P/A
16. Lab diagnosis:
17. Diagnosis
18. Treatment
19. In Case of Death:
- Cause
- Autopsy features
KEY TO MASTER CHART
S. No. - Serial Number
Hosp No - Hospital Number
Yrs - Years
M - Male
F - Female
DOA - Date of Admission
DOD - Date of Discharge
DOE - Date of Expiry
R - Rural
U - Urban
UL - Upper limb
LL - Lower limb
OP - Organophosphorus compounds
NPS - Non-poisonous snake
PS - Poisonous snake
Photographs
Commonest agricultural poisons – accidentally consumed
Commonly ingested accidental poisons and drugs
Drugs and equipments used in treatment of paeditric poisoning
S. No. Hosp. No. Name Age
(Yrs)Sex
(M/F) DOA DOD DOE Informant Areas (R/U)
Poison consumed
Site of Bite
Manner of poisoning
1 2177 Rajashree 10 F 10/2/1999 12/2/1999 - Father U OP - Accidental2 2185 Iranna 12 M 10/3/1999 12/3/1999 - Father R NPS UL Accidental3 2389 Gangawwa 4 F 8/4/1999 10/4/1999 - Father R Kerosene - Accidental4 2459 Raju 5 M 14/5/99 19/5/99 - Mother R Kerosene - Accidental5 2701 Paan 5 M 23/6/99 27/6/99 - Mother R Seed - Accidental6 2778 Rahul 12 M 15/7/99 17/7/99 - Mother R OP - Accidental7 2779 Praveen 6 M 17/8/99 18/8/99 - Mother R OP - Accidental8 2940 Siddlingappa 10 M 2/8/1999 3/8/1999 - Neighbour R NPS UL Accidental9 5421 Anushya 13 F 6/8/1999 7/8/1999 - Neighbour U Drugs - Accidental10 9615 Saritha 1 F 6/8/1999 7/8/1999 - Neighbour R NPS UL Accidental11 9980 Raju 12 M 15/8/99 16/8/99 - Mother R Seed - Accidental12 9921 Holewwa 11 F 16/8/99 18/8/99 - Mother U Drugs - Accidental13 10745 Raju 4 M 31/8/99 1/9/1999 - Mother R Kerosene - Accidental14 10558 Yallawwa 2 F 27/8/99 29/8/99 - Mother R OP - Accidental15 10559 Bharanama 4 F 1/9/1999 3/9/1999 - Mother U OP - Accidental16 10502 Salekha 2 F 3/9/1999 5/9/1999 - Mother R OP - Accidental17 10498 Nagaraj 3 M 5/9/1999 8/9/1999 - Father U PS LL Accidental18 10555 Ramesh 12 M 9/9/1999 11/9/1999 - Father R Seed - Accidental19 10638 Rajashree 3 F 13/9/99 15/9/99 - Mother U OP - Accidental20 11038 Yellappa 6 M 17/9/99 18/9/99 - Mother R Carbamate - Accidental21 12069 Shivaraj 8 M 20/9/99 23/9/99 - Father R Kerosene - Accidental22 12074 Nagendra 8 M 21/9/99 23/9/99 - Father R Seed - Accidental23 12075 Geeta 7 F 4/10/1999 5/10/1999 - Father R Seed - Accidental24 12079 Abinandana 6 M 7/10/1999 9/10/1999 - Father R NPS UL Accidental25 12080 Maheboob 7 M 9/10/1999 11/10/1999 - Father R Kerosene - Accidental26 12138 Aswini 14 F 10/10/1999 - 12/10/1999 Father R OP - Suicidal27 13814 Arati 15 F 10/10/1999 - 13/10/1999 Father R OP - Suicidal28 14537 Adarsh 5 M 5/11/1999 7/11/1999 - Mother R OP - Homicidal29 14538 Ayesha 1 F 8/11/1999 9/11/1999 - Mother R OP - Accidental30 14540 Anand 9 M 10/11/1999 11/11/1999 - Mother R Kerosene - Accidental
MASTER CHART
S. No. Hosp. No. Name Age
(Yrs)Sex
(M/F) DOA DOD DOE Informant Areas (R/U)
Poison consumed
Site of Bite
Manner of poisoning
31 14838 Ambrish 12 M 13/11/99 16/11/1999 - Mother R NPS UL Accidental32 14902 Manjunath 3 M 15/11/99 18/11/1999 - Mother U Seed - Accidental33 15204 Satish 2 M 17/11/99 19/11/1999 - Mother R Carbamate - Accidental34 15205 iyaz 2 M 20/11/99 24/11/1999 - Mother R NPS UL Accidental35 15432 Nazma 3 F 5/12/1999 7/12/1999 - Mother R OP - Accidental36 15549 Sweta 2 F 9/12/1999 12/12/1999 - Mother U OP - Accidental37 15909 Malik 6 M 19/12/9 - 20/12/1999 Mother U PS UL Accidental38 15986 Ramesh 4 M 29/12/99 30/12/1999 - Mother R Kerosene - Accidental39 984 Balappa 10 M 24/1/00 29/1/2000 - Neighbour R Kerosene - Accidental40 3681 Sagar 11 M 27/1/00 29/3/2000 - Neighbour R Seed - Accidental41 3573 Ayesha 5 F 25/3/00 27/3/2000 - Mother U DDT - Accidental42 3898 Lata 12 F 1/4/2000 2/4/2000 - Mother R NPS LL Accidental43 5346 Arshad 2 M 4/5/2000 4/5/2000 - Mother U OP - Accidental44 5430 Narayan 12 M 29/5/2000 29/5/2000 - Father R Seed - Accidental45 6631 Jyotiba 11 M 30/5/2000 31/5/2000 - Father R NPS LL Accidental46 6988 Prashant 7 M 5/6/2000 7/6/2000 - Mother R Seed - Accidental47 6989 Sunil 5 M 6/6/2000 8/6/2000 - Mother U Seed - Accidental48 6990 Pramod 5 M 6/6/2000 8/6/2000 - Father U OP - Accidental49 9413 swar 1 M 31/7/2000 1/8/2000 - Father R NPS LL Accidental50 4781 Akash 2 M 21/8/2000 21/8/2000 - Father R OP - Accidental51 6228 Bharamappa 4 M 23/9/2000 25/9/2000 - Father R NPS LL Accidental52 10560 Prasad 2 M 24/9/2000 27/9/2000 - Father U OP - Accidental53 10597 Reshma 9 F 26/10/2000 28/10/2000 - Mother R Seed - Accidental54 12073 Sohel 7 M 29/10/2000 29/10/2000 - Mother R NPS LL Accidental55 12077 Kamala 10 F 1/1/2000 4/11/2000 - Mother U Carbamate - Accidental56 12110 Phalavathi 12 F 5/11/2000 8/11/2000 - Neighbour U Drugs - Accidental57 13537 Ravindra 10 M 8/11/2000 10/11/2000 - Neighbour R Seed - Accidental58 13710 Parvathi 10 F 9/11/2000 10/11/2000 - Mother R PS LL Accidental59 13911 Jyotiba 9 M 25/11/2000 30/11/2000 - Mother U Drugs - Accidental60 13963 Sudhakar 12 M 2/12/2000 5/12/2000 - Mother R Seed - Accidental
S. No. Hosp. No. Name Age
(Yrs)Sex
(M/F) DOA DOD DOE Informant Areas (R/U)
Poison consumed
Site of Bite
Manner of poisoning
61 14737 Nagawwa 9 F 5/12/2000 10/12/2000 - Mother R NPS LL Accidental
62 14837 Sangeeta 1 F 8/12/2000 10/12/2000 - Mother R OP - Accidental63 14963 Santosh 6 M 17/12/2000 19/12/2000 - Mother R NPS LL Accidental64 14997 Anand 9 M 31/12/2000 31/12/2000 - Father U Carbamate - Accidental65 3319 Asia 12 F 5/1/2001 6/1/2001 - Father R Drugs - Accidental66 3476 Shilpa 1 F 24/3/2001 30/3/01 - Father R Insect Neck Accidental67 4670 Komal 3 F 5/4/2001 12/4/2001 - Mother R OP - Accidental68 4781 Akash 3 M 7/4/2001 - 11/4/2001 Neighbour U PS LL Accidental69 4800 Sudhir 11 F 8/5/2002 10/5/2001 - Neighbour R Seed - Accidental70 6021 Rekha 2 F 10/6/2001 14/6/2001 - Neighbour R Kerosene - Accidental71 6715 Jayant 14 M 18/6/2001 19/6/2001 - Father R Insect Face Accidental72 6732 Sharada 12 F 20/7/201 22/7/2001 - Father R Drugs - Accidental73 9200 Anand 12 M 27/7/2001 29/7/2001 - Father R NPS UL Accidental74 9796 Kajol 3 F 1/8/2001 5/8/2001 - Mother U Turpentine - Accidental75 9800 Shoba 14 F 8/8/2001 16/8/2001 - Mother U Insect Forehead Accidental76 9816 Mahadevi 14 F 28/8/01 30/8/2001 - Mother R Datura - Accidental77 9825 Maulahusen 13 M 2/9/2001 5/9/2001 - Mother R Turpentine - Accidental78 9901 Raman 1 M 7/9/2001 8/9/2001 - Mother R NPS LL Accidental79 9920 Balesha 12 M 10/9/2001 14/9/2001 - Mother U Kerosene - Accidental80 9929 Inayat 4 M 20/9/01 23/9/2001 - Father U Insect Back Accidental81 9947 Manjunath 5 M 30/10/01 2/11/2001 - Father U OP - Accidental82 10028 Supriya 10 F 5/12/2001 15/12/2001 - Father U Insect Back Accidental83 10128 Gopal 12 M 23/2/2001 28/1201 - Father R Kerosene - Accidental84 660 Harish 1 M 5/1/2002 7/1/2002 - Mother R OP - Accidental85 866 Sonamma 1 F 8/1/2002 13/1/02 - Mother R NPS UL Accidental86 889 Arati 2 F 2/2/2002 4/2/2002 - Mother R NPS UL Accidental87 984 Rahul 1 M 13/3/2002 16/3/02 - Mother R Rodenticide - Accidental88 1142 Ajaya 1 M 17/4/2002 19/4/02 - Father R OP - Accidental89 1162 Arif 4 M 19/5/2002 20/5/02 - Father U NPS LL Accidental90 1413 Priyanka 6 F 14/6/2002 18/6/02 - Father U OP - Accidental
S. No. Hosp. No. Name Age
(Yrs)Sex
(M/F) DOA DOD DOE Informant Areas (R/U)
Poison consumed
Site of Bite
Manner of poisoning
91 1802 Sweta 6 F 19/6/2002 21/6/02 - Neighbour R NPS UL Accidental92 1804 Aswini 5 F 20/7/2002 23/7/02 - Mother R OP - Accidental93 1865 Sneha 3 F 21/7/2002 22/7/02 - Mother U Kerosene - Accidental94 2444 Mahantesh 10 M 23/8/2002 24/8/02 - Father R PS LL Accidental95 2973 Jayed 2 M 25/8/2002 27/8/02 - Mother U Kerosene - Accidental
96 3071 Deepa 3 F 29/9/2002 30/9/02 - Mother R Insect LL Accidental97 3231 Malanogonda 4 M 30/9/2002 4/10/2002 - Father R Rodenticide - Accidental98 3232 Sukhadev 2 M 30/9/2002 5/10/2002 - Father R OP - Accidental99 3458 Sandeep 5 M 25/10/2002 - - Neighbour U PS LL Accidental
100 3563 Mahammed 12 M 4/11/2002 5/11/2002 - Father R Seed - Accidental101 151 Nilesh 2 M 6/1/2003 8/1/2003 - Father U Kerosene - Accidental102 251 Mamin 1 M 29/1/2003 31/1/2003 - Father R PS LL Accidental103 252 Chetan 3 M 29/1/2003 31/1/2003 - Father U Kerosene - Accidental104 296 Sanjana 1 F 4/2/2003 7/2/2003 - Neighbour R NPS LL Accidental105 297 Dezum 2 M 5/2/2003 7/2/2003 - Father R Insect LL Accidental106 562 Basavant 2 M 2/3/2003 4/3/2003 - Father U Insect LL Accidental107 877 Kstopher 1 M 8/4/2003 11/4/2003 - Neighbour R PS - Accidental108 1393 Deepak 5 M 20/5/2003 21/5/2003 - Mother U Insect LL Accidental109 1422 Malanogonda 3 M 23/5/2003 24/5/2003 - Mother R OP - Accidental110 1707 Kallappa 11 M 17/6/2003 17/6/2003 - Mother U NPS LL Accidental111 1808 Mahadeva 12 M 24/6/2003 14/7/2003 - Mother R Kerosene - Accidental112 1910 Sanju 2 M 6/7/2003 6/7/2003 - Mother R Insect Forehead Accidental113 2088 Nikheta 4 F 29/7/2003 5/8/2003 - Neighbour R DP - Accidental114 2089 Mahadevi 12 F 29/7/2003 9/8/2003 - Neighbour R NPS LL Accidental115 2090 Sarikha 6 F 29/7/2003 5/8/2003 - Father R NPS LL Accidental116 2091 Kusuma 9 F 29/7/2003 5/8/2003 - Father U OP - Accidental
End Result
ImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImproved
DeadDead
ImprovedImprovedImproved
End Result
ImprovedImprovedImprovedImprovedImprovedImproved
DeadImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImproved
End Result
Improved
ImprovedImprovedImprovedImprovedImprovedImproved
DeadImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImproved
End Result
ImprovedImprovedImprovedImprovedImproved
ImprovedImprovedImproved
DeadImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImprovedImproved