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A Dissertation on “CLINICAL PROFILE OF RAT KILLER PASTE POISONING ”
Submitted to
THE TAMIL NADU DR.M.G.R.MEDICAL UNIVERSITY
CHENNAI - 600032
In partial fulfillment of the regulations for the award of the degree of
M.D. BRANCH – I (GENERAL MEDICINE)
DEPARTMENT OF GENERAL MEDICINE
GOVERNMENT STANLEY MEDICAL COLLEGE, CHENNAI.
THE TAMIL NADU DR. M.G.R.MEDICALUNIVERSITY
TAMILNADU, INDIA
MAY 2020
CERTIFICATE BY INSTITUTION
This is to certify that this dissertation entitled “CLINICAL PROFILE OF RAT
KILLER PASTE POISONING” submitted by Dr .V.KARTHICK to the faculty of
General Medicine, The Tamil Nadu Dr. M.G.R Medical University, Chennai, Tamil
Nadu, in partial fulfillment of the requirement for the award of M.D DEGREE
BRANCH-I (GENERAL MEDICINE) is a bona fide research work carried out by him
under my direct supervision and guidance.
GUIDE HOD
Prof. Dr .T.B.UMADEVI .MD Prof. Dr.C.HARIHARAN.MD
Professor of Medicine, Head of the Department,
Department of Medicine, Department of Medicine,
Stanley Medical College and Hospital, Stanley Medical College and Hospital,
Chennai - 1. Chennai- 1.
PROF. DR.R.SHANTHIMALAR, M.D., D.A.,
DEAN
Government Stanley Medical College and Hospital, Chennai-1.
CERTIFICATE BY THE GUIDE
This is to certify that Dr. V.Karthick ,Post Graduate student (May2017 to April 2020) in
the Department of General Medicine ,Government Stanley Medical College and
Hospital,Chennai-1,has done this dissertation work titled “CLINICAL PROFILE OF
RAT KILLER PASTE POISONING” under my guidance and supervision in partial
fulfillment of the regulations laid down by The Tamil Nadu Dr. M.G.R.Medical
University, Chennai for M.D.,(General Medicine),Degree examination to be held in May
2020.
Prof. Dr. T.B.UMADEVI M.D.,
Professor of Medicine ,
Department of Medicine,
Stanley Medical College and Hospital,
Chennai - 1.
DECLARATION
I, Dr.V.KARTHICK, solemnly declare that the dissertation titled “CLINICAL
PROFILE OF RAT KILLER PASTE POISONING”is a bona fide work done by me
at Government Stanley Hospital, Chennai during March 2018 to August 2018 under the
guidance and supervision of Prof. Dr. T.B.UMADEVI M.D., Professor of Medicine,
Government Stanley Hospital, Chennai. I also declare that this bona fide work or a part of
this work was not submitted by me or any other for award degree or diploma to any other
university, board either in India or abroad. This dissertation is submitted to the Tamil
Nadu Dr. M.G.R Medical University, towards the partial fulfillment of requirement for
the award of M.D. Degree (Branch – I) in General Medicine.
Place: Chennai Signature of the candidate
Date: (Dr.V.KARTHICK )
CERTIFICATE - II
This is to certify that this dissertation work titled “CLINICAL PROFILE OF RAT
KILLER PASTE POISONING ”of the candidate Dr.V.Karthick with Registration
Number 201711055 for the award of M.D., DEGREE in the branch of BRANCH-I
(GENERAL MEDICINE). I personally verified the urkund.com website for the purpose
of plagiarism check. I found that the uploaded thesis file contains from introduction to
conclusion pages and result shows 6 percentage of plagiarism in the dissertation.
Guide & Supervisor sign with Seal
SPECIAL ACKNOWLEDGEMENT
I gratefully acknowledge and thank
PROF. DR.R. SHANTHI MALAR M.D., D.A.,
DEAN
GOVERNMENT STANLEY MEDICAL COLLEGE AND HOSPITAL, CHENNAI.
For granting me permission to utilize the resources of this
Institution for my study
ACKNOWLEDGEMENT
At the outset I thank our Dean DR.SHANTHI MALAR,M.D.,DA.,
for permitting me to carry out this study in our hospital.
I express my profound thanks to my esteemed Professor and Teacher
Dr. C.HARIHARAN, M.D., Professor and HOD of Medicine, Stanley Medical
College Hospital, for encouraging and extending invaluable guidance to perform
and complete this dissertation.
I immensely thank my unit chief Dr. Nalini Kumaravelu MD, for her
constant encouragement and guidance throughout the study.
I wish to thank Dr. RSA Alexander MD and Dr. Vijayalakshmi MD,
Assistant Professors of my unit, Department of Medicine, Stanley Medical College
Hospital for their valuable suggestions, encouragement and advice. I sincerely
thank the members of Institutional Ethical Committee, Stanley Medical College for
approving my dissertation topic.
I thank all my colleagues, House Surgeons, and Staff nurses and other para
medical workers for their support.
At this juncture I would also want to extend my heartfelt gratitude to my family for
their constant support and care.
I sincerely thank all those patients who participated in this study, for their
co-operation.
ABBREVATIONS :
ALT :ALanine Transaminase (or) ALanine Aminotransferase.
ANTU : Alpha – NaphthylThio Urea.
DIC : Disseminated Intravascular Coagulation.
ECG : Electro CardioGram.
FFP : Fresh Frozen Plasma. 6. GIT : Gastro Intestinal Tract.
INR :Internatinational Normalized Ratio.
LD 50 : Lethal Dose in 50% of individuals.
ppm : parts per million.
.PT :Prothrombin Time. 11.SGPT : Serum Glutamic Pyruvic Transaminase.
DOA : Date Of Admission .
CNS : Central Nervous System .
BP : Blood Pressure .
CVS : Cardio Vascular System . 6) RS : Respiratory System .
RBS : Random Blood Sugar .
SGOT : Serum Glutamic ornithylTransferase.
SGPT : Serum Glutamic Pyruvic Transamnase
PT :Prothrombin Time.
INR : International Normalised Ratio .
TABLE OF CONTENTS
S.No CHAPTERS PAGE NUMBER
1 INTRODUCTION 1
2 AIM AND OBJECTIVES OF THE STUDY 7
3 REVIEW OF LITERATURE 8
4 MATERIALS AND METHODS 27
5 STATISTICAL ANALYSIS 29
6 RESULTS 30
7 DISCUSSION 67
8 CONCLUSION 79
9 BIBLIOGRAPHY 80
10 PROFORMA 88
11 ETHICAL COMMITTEE 92
12 PLAGIARISM CERTIFICATE 93
13. INFORMED CONSENT 94
14. MASTER CHART 96
1
INTRODUCTION
Poisoning is mostly preventable, commonly suicidal and rarely being an accidental form
of death in developing agrarian countries. In rural India, poisoning forms the major share
of emergency health care and of about one – fourth to one – third of intensive care
admissions.Among poisoning, in our region, next to organophosphorus poisoning, rat
killer or rodenticide poisoning remains the second most common ingested poison.
However, as compared to organophosphorus poisoning, there are only few works of
literature available for rodenticide poisoning. [1,2]
Almost every system is affected in rodenticide poisoning and also there are no definite
treatment guidelines available. Regarding its incidence, mode of action and management,
only a few studies are available. Further there are no positive clinical trials available
regarding phosphorus paste poisoning, which remains the deadliest among rodenticide
poisons.[3]
Rodenticides are commonly available in almost every household, to prevent their stored
grains from rodents, which is found everywhere. Since it is easily available and also
cheaper than other 1 pesticides in the markets. Because of its easy availability in every
house, it is often taken with a suicidal indent or ingested accidentally by children. [4]
Rodenticide is available in three different forms in our area.
Among these rodenticides, phosphorus is the most commonly and also most lethal Most
common forms available in market includes
2
Powder
Paste
Cakes
Pellets .
RAT KILLER CAKE
The easily available and the less toxic “cake” form contains warfarins and superwarfarins
acts by inhibiting vitamin K cycle thereby preventing the regeneration of reduced vitamin
K from the oxdised form.
RAT KILLER POWDER
The “powder” form contains zinc phosphide and thallium.
The zinc phosphide release phophine gas on contact with water in gastrointestinal tarct
causing heaptic, renal, gastrointestinal toxicity, acute lung injury, coma , seizures.
Thallium combines with sulfhydryl groups, interferes with oxidative phosphorylation
producing anorexia, abdominal pain, diarrhea, painful neuropathy, alopecia, coma.
RAT KILLER PASTE
Paste forms usually contains elemental phosphorus. The three known phosphorus types
1. Yellow phosphorus
2. White phosphorus
3. Red phosphorus.
Among these three forms Red phosphorus is not absorbed and essentially non toxic.
White phosphorus is used mainly in ammunition and fireworks as an explosive agent.
3
The paste form contains 3 % yellow phosphorus as active ingredient. It is a corrosive
agent damaging all tissues it contacts.
Among these rodenticides, phosphorus is the most commonly and also most lethal
poison, especially after 3-4 days of ingestion, as liver injury sets in. Since there are no
sufficient data available regarding rodenticides, [5]In 1990 it estimated that self‐ harm
resulted in 2million cases of poisoning each year with 200000 deaths. In contrast,
accidental and occupational exposure were estimated to cause 1 million cases with 20 000
deaths. Studies have shown that deliberate self‐ poisoning has far higher mortality than
accidental poisoning.[6]
Organophosphates, pesticides are the most commonly used poisonings for suicide. A
pesticide is usually defined as a chemical substance, biological agent, antimicrobial or
disinfectant used against pests including insects, plant pathogens, weeds, mollusks, birds,
mammals, fish, roundworms and microbes that compete with humans for food, destroy
property, have a propensity for spreading or are a vector for disease or simply a nuisance.
The types of pesticides commonly used are also called 1.Insecticides. 2.Herbicides. 3.
Fungicides. 4. Rodenticides[7,8]
RODENTICIDES:
Rodenticides, pesticides specially designed to kill rodents, pose particular risks for
accidental poisoning for several reasons. Since they have been designed to kill mammals,
they are also toxic to humans. Because rodents usually share human environments, the
4
use of rodenticides poses an inherent risk of exposure to people, particularly children and
their pets, as well as other non-target species. They are among the most toxic compounds
regularly found in homes. Rodenticide poisoning has varied incidence across the country.
The mortality rates also vary significantly. The type and quantity of poison consumed,
lack of a specific antidote for some of the rodenticides and time-lapse in treatment affect
the outcome. [9,10]
CLASSIFICATION OF RODENTICIDES:
Who classification
1. Warfarin
2. Warfarin like compounds (brodifacoum, chlorophacinone, difenacoum, diphacinone,
bromadiolone )
3. Calciferol (cholecalciferol, ergocalciferol)
4.Fluoroacetates (Sodium fluoroacetate, Fluoroacetamide)
5. Metal phosphides (,phosphorus, aluminium phosphide, , zinc phosphide, magnesium
phosphide, yellow phosphorous )
6. Chloralose
7. Others (arsenic, thallium, strychnine) [11,12]
5
CLASSIFICATION OF RODETICIDES BASED ON TOXICITY:
HIGHLY TOXIC RODENTICIDES:
Highly toxic rodenticides are those substances with a single dose LD50 of less than
50mg/kg body weight. Some of these compounds have largely been abandoned because
of serious human toxicity. This group includes
1. Aluminum phosphide
2.Sodium monofluoroacetate
3.Strychnine,
4. Zinc phosphide,
5. Yellow phosphorus
6.Arsenic.
7. Thallium
MODERATELY TOXIC RODENTICIDES:
Among the moderately toxic rodenticides, those with LD50 of more than 500 mg/kg body
weight are
1. alpha-naphthyl-thiourea (ANTU)
2. DDT.
6
Patients who ingest large quantities of ANTU may develop dyspnea, rales, and cyanosis
(secondary to pulmonary edema) and hypothermia. Poisoning from exposure to DDT can
result in symptoms such as vomiting, tremors, and convulsions. How much exposure is
required to cause severe illness or even death is, however, not certain. [13,14,15]
LOW TOXICITY RODENTICIDES:
Low toxicity rodenticides are those with LD50 between 500 and 5,000 mg/kg body
weight and include
1. Red squill.
2. Norbomide.
3. Anticoagulants warfarin-type rodenticides.
1. Red squill: Red squill contains several compounds with chemical and pharmacological
properties similar to those of digitalis glycosides. Because of its emetic properties, poor
gastrointestinal absorption and decreased potency (compared to that of digitalis), red
squill has seldom been associated with human toxicity
2. Norbomide: Norbomide is an irreversible smooth muscle constrictor. It causes
widespread ischemic necrosis and death in rats but does not appear to affect other animals
or humans, presumably due to the presence of a specific smooth muscle norbomide
receptor found only in rats.[16,17]
7
AIM AND OBJECTIVE OF THE STUDY
1.To study the clinical profile of patients admitted with rodenticide poisoning and their
course in the hospital.
2. To correlate various parameters with the mortality.
8
REVIEW OF LITERATURE
Rat killer (Ratol) paste contains yellow phosphorus. White phosphorous with its
impurities is called yellow phosphorus. It is used in the firework industry, in bombs, as
Rodenticide. In South India, it is commonly available as rat killer paste (3%). [18]The
toxic dose of yellow phosphorous is 100 mg/kg body weight and toxicity increases when
taken with a fatty meal. Yellow phosphorus causes hepatotoxicity by the production of
phosphoric acid, which causes free radical damage. This poisoning is associated with
high mortality. The good prognostic factors are survival after 3 days and minimal
elevation of LFT. Bad prognostic signs are altered sensorium, cyanosis, hypotension,
metabolic acidosis, elevated prothrombin time, and hypoglycemia.The first phase consists
of nausea, vomiting, abdominal pain, and smoking stools. Then, in the second phase, the
patient may feel symptomatically better and the third stage consists of systemic organ
damage due to absorbed phosphorous. Hepatotoxicity usually is recognized on the 3rd
day by liver function test (LFT). A large number of early deaths.[19,20]
There was competition between humans and rodents for food since the past. Due to his
super-brain, humans developed some agents to kill the rodents. Rodenticides are
produced in such a way to kill the rodents, which damage the crops in the field , stored
grains in godowns, bite peoples and also capable of spreading deadly diseases such as
plague. It includes variety of chemicals with various actions, which may be organic or
inorganic, may be mild or highly toxic, but they kill them in a cost-effective manner.
Now the problem arises because humans either accidentally or intentionally ingest these
9
chemicals. In earlier days rodenticides were mainly made from plant such as strychnine
or inorganic chemicals as thallium and arsenic trioxide.Now, they are manufactured from
synthetic organic compounds Some agents such as thallium are as dangerous to humans
as rodents. However their use is restricted nowadays to lessen the risk of toxicity in
humans especially. But still, they are regarded as toxic, if they are misused[21,22,23]
Environmental poisoning was also found as a significant cause of poisoning admissions
to the hospital. Reptile bite is one of the major environmental poisoning occurring in
rural areas than the urban area. The present study reports environmental poisoning was
seen more in adult males followed by females and this was due to snake bite, followed by
bee Stings, insect and scorpion bite.[19,20]
Poisoning incidence also varies according to the seasons. Incidence was seen more in the
summer season followed by the winter season. Incidences of poisoning during summer
months are more because as the summer days being longer and during which the person
becomes easily fatigued and exhausted as a result of extreme heat conditions leading to
mental imbalance. Another reason may be the preservation of grains during summer is
more and in order to protect them, pesticides are procured and preserved[19]. Due to the
easy accessibility to pesticides, people may try to consume pesticides to end their life
when they suffer from economic burdens or any emotional conflicts.
The reasons observed for the mortality in poisoned individuals were the delay in
admission to the hospital, improper management of the poisoned patient, lack of
information regarding the poison agent and its antidote. To reduce the poison induced
10
morbidity and mortality following steps such as having a centralized poison information
center, availability of standard treatment protocols for managing various poisons, and
educational programs for rural people may be more appropriate[27,28]
It was first identified in urine by chemist HENNING BRANT in Hamburg in 1669. The
early use of phosphorus was in 1720 in medical books. It was used for colic, tetanus,
gout, and apoplexy. It was popular as a tonic aphrodisiac, impressing onlooker of its
phosphorescent and explosive nature. Inspite of its toxicity, it was found in British
pharmacopeia till 1932. White phosphorus gained importance since it was used as main
ingredient in lucifers or in match industry. It was invented by chemist Charles Sauria of
Paris in 1830. It was mainly used in match industry.[19,20] After some years it was
banned worldwide as of using in striking pad. On the matchbox, and now red phosphorus
has replaced it, in striking pad as well as match head. 6 White phosphorus is now used to
manufacture, insecticide, fertilizer as phosphoric acid and homemade wirework [15]
which contain about 10% phosphorus. Phosphorus isthe 15th element in table, it exists in
3 forms I) black phosphorus →nontoxic, not ignite spontaneously II) red phosphorus
→faily innocuous→ intermediate reactivity iii) white phosphorus →highly reactive and
dangerous compound. White phosphorus in tetramer (D4), water-insoluble, a waxy paste.
It emits pale green glow, due to low reactivity with oxygen. Impurities in white
phosphorus make it as yellow phosphorus.[8,16] Phosphorus on combining with oxygen
gives Phosphorus oxide with liberation of light and dense smoke with Garlic odor, On
dissolving with water, it produces phosphoric acid. It is rapidly absorbed and distributed
11
primarily in the liver, kidney, intestinal mucosa, epidermis, follicles, and pancreas Other
tissues such as lung, myocardium, spleen and renal medulla of moderate distribution,
brain fat and muscle of low distribution[ 39]. 7 In rats, sub-cutaneous lethal dose in 10mg
/kg(8) while in human studies suggest lethal dose as 50mg or 1mg/kg.(9). It is highly
lipid solubility, high absorption occur after skin or mucosal exposure[25,26]
MECHANISM OF TOXICITY
It is a protoplasmic poison.
It has a direct toxic effect over heart causing cardiovascular collapse.
Its spontaneous combustion nature yeilds phosphorus oxide which is a
highly irritating substance
TOXOKINETICS
.White phosphorus is rapidly absorbed from the intestinal tract.
After getting aborbed into the systemic circulation, it is mainly getting
concentrated in th e liver, renal cortex, bowel mucosa, epidermis,
pancrease and adrenal cortex.
Within several hours of ingestion 75 % of the total ingested dose is
concentrated in the liver
12
.DISTRIBUTION OF WHITE PHOSPHORUS BY DIFFERENT BODY TISSUES
UPTAKE
HIGH
MODERATE
LOW
Adrenal cortex
Bowel mucosa
Epidermis
Hair follicles
Liver
Pancrease
Renal cortex
Adrenal
medulla
Endometrium
Lung
Myocardium
Ovary
Renal medulla
Spleen
Bone
Fat
Brain
Myometrium
Skeletal
muscle
TOXIC DOSE
Ingestion : 1 mg/kg is fatal dose
Inhalational : 5 mg/kg ( immediately dangerous to life and death
[ Recommended work place limit-0.1 mg/cubic meters as an 8 hour time weighted
average ]
White phosphorus is highly lipid-soluble so that more absorption after skin or mucosal
exposure.
13
CLINICAL MANIFESTATIONS:
Ingestion of more than 1mg/kg
Severe electrolyte disturbance
mental status changes prolongation of the q-t interval
more than 10 fold rise in alanine aminotransferase
severe coagulopathy
peak liver enzymes reached within three days of ingestion
Old literature describes the course of poisoning in 3 stages (13)
I STAGE-It lasts- hours to days after ingestion manifested as irritation of digestive tracts,
may cause arrhythmias and same neurological manifestations.
II STAGE: The digestive symptoms resolve, lasting for few days patients develop
hepatic, renal and cardiac toxicities, mostly causing death.
If recovery occurs, it takes few weeks However most death occurs as a result of a
fulminant hepatic failure within first week. Some delayed death occurs between 5-8 days
due to cardiotoxic. Few deaths only occur,if patient survives beyond this stage.
14
HEPATIC:
It produces hepatotoxicity in dose-dependent manner (14). Aminotransferase rises in half
of ingested patients, mostly begin to rise within one day of exposure. Time of enzyme
peak and level rise differ significantly between patient who survives and who dies.
Patients who die have average peak of sixteen times of normal, reached in 2-3 days. In
those who survive, alanine aminotransferase (SGOT) rises eight times normal, reaching
peak in six days. Serum triglyceride level fall as toxicity develops, there may be also
increased in serum and urinary ketones It consumes oxygen in liver cells, is a
protoplasmic poison which uncouples oxidative phosphorylation, in turns leads to
decrease in intrahepatocyte ATP levels[27,28] It also affects transition of triglyceride as
betalipoproteins. Massive hepatic steatosis, hallmark of white phosphorus toxicity, rise in
triglyceride level in two hours, peaking in two days. Hepatic necrosis is particularly in
zone 1, distinct from acetaminophen and carbon tetrachloride, hepatic glycogen is
decreased due to increased glucose-6- phosphatase activity.[16,29] A nonspecific finding
of huge increase in rough endoplasmic reticulum is typically found in this poison [30,31]
Liver biopsy showed signs of acute hepatocellular necrosis also showing fibrosis and
piecemeal necrosis
EPIDEMIOLOGY :
World Health Organization (WHO) estimated 0.3 million people die every year due to
various poisoning agents[5]. Acute pesticide poisoning is one of the most common causes
of intentional deaths worldwide[6]. High doses of analgesics, tranquilizers, and
15
antidepressants are the commonly used agents for intentional poisoning in industrialized
countries[7] and agricultural pesticides are used in the Asian region for self-poisoning
particularly in rural areas with a fatality range of 10-20%[8]. The majority of pesticide
exposure is seen more in middle and low-income countries due to increased use of
agrochemicals in agricultural sector[9].
Studies have revealed that pesticides are commonly used poisoning agents for intentional
poisoning in India[10]. As agriculture is a major profession in the rural part of India
farmers stock the pesticides to eradicate the weeds and pests. Due to easy availability of
pesticides, they are commonly used by individuals to end their life in stressful
situations[11].
There are scarce epidemiological data regarding the ingestion of yellow phosphorous in
the subcontinent. Case series of general poisonings from Nepal [24], rodenticide
poisonings from Mysore, India [25,6] and Rajasthan, India [26] all show a predominance
of young adults between ages 15 to 40 years old. The Nepalese study highlighted the
greatest burden among homemakers, laborers, and farmers [27]. Extrapolating from our
experience with organophosphate poisonings and as illustrated in this case, we surmise
these ingestions are impulsive acts in an environment where highly toxic substances are
cheap and readily available. This supposition is supported by previously published data
from Sri Lanka, Karnataka, and Rajasthan; in Karnataka, fully 94% were impulsive acts
of self-harm [28,29].
16
NATURAL HISTORY, TREATMENT, AND PROGNOSTIC FACTORS
The time course of a brief asymptomatic period followed by acute liver failure at 72
hours fits other clinical reports of yellow phosphorus ingestions [30]. We surmise that
patients with yellow phosphorus poisoning should be observed closely for at least 3 days,
given the 72-hour asymptomatic latent period. Other authors suggest a week [31]. Other
toxic manifestations include central nervous system effects (restlessness, irritability,
drowsiness, lethargy, stupor, or coma) [32], acute tubular necrosis, bone marrow toxicity
[33], arrhythmias and hemodynamic instability [34]. Clinical manifestations and outcome
vary in different reports. In one case series, 87% had some hepatic derangement and 27%
developed fulminant hepatic failure and died [35]. Similarly, mortality in a second case
series was 28% [36]. Another series found a range of 23-73% mortality depending on
clinical manifestations, with early central nervous system manifestations portending
poorer prognosis [37]. MELD score has been described as a prognostic indicator in
rodenticide poisoning (including yellow phosphorous): average MELD for those who
died was 40.5 as compared to 11.7 for survivors [38]. The patient’s highest MELD score
was 32 (Creatinine 0.6, Total Bilirubin 6.6, INR 4.1).
Some recommend gastric lavage with 1:5000 potassium permanganate followed by
activated charcoal and mineral oil cathartic [12,13]. Clinical studies in rodenticide
poisoning have conflicting evidence about the use of N-Acetylcysteine (NAC) and
adjunctive therapies. One case series showed no benefit [7]; in contrast, Lovejoy FH:
Thallium et al. suggest that early use of NAC improves outcomes for all rodenticide
17
poisonings with liver failure. In that study, survival rates varied based on timing of NAC
administration after rodenticide ingestion: 76% survival rates if NAC was administered
on Day 1, 40% survival if administered on Day 2 and 23% survival if administered 3 or
more days after ingestion [39] though this data is confounded by early gastric lavage for
those presenting shortly after consumption. In light of NAC’s safety profile and recent
guidelines suggesting a role for NAC in non-acetaminophen based liver failure [40], we
chose to administer this drug. Other adjuncts such as corticosteroids and exchange
transfusion have been studied but have not shown clinical benefit [41].
Mozingo DW Smith et al. [18] case series of acute liver failure secondary to phosphorus
ingestion, the two causes of death were massive upper gastrointestinal bleeding and
cerebral edema. In their series, 73% had prolonged PT time and received FFP while only
40% of patients had signs of bleeding [43]. Current American Association for the Study
of Liver Diseases (AASLD) guidelines for the management of acute liver failure
recommend at least one dose of vitamin K subcutaneously, reserving FFP and platelet
transfusion for those with active bleeding or needing invasive procedures [29,44]. These
same guidelines suggest proton pump inhibitors or H2 receptor antagonists for ulcer
prophylaxis [45]. The patient received 13 units of fresh frozen plasma, intramuscular
vitamin K and pantoprazole during her hospital stay. She did not develop clinically
significant bleeding. Due to India’s strict legislation regarding blood banking, this had to
be procured by the patient’s brother from a hospital in a nearby city. Our inability to
maintain a blood bank has serious implications for the care of critically ill patients like
18
our patients [46]. Few patients have families with the time or financial wherewithal to
travel to and from the local city this frequently
CLINICAL MANIFESTATIONS
SKIN, MUCOSA AND GASTROINTESTINAL TRACT:
Burns produced by this poison is extremely painful with characteristic garlic odor, yellow
color, and necrotic base. it heals slowly like other chemical burns, and also requires
prolonged hospital stay[23,24], which may be of second degree or third-degree burns
involving 15% of body surface area, may result in death[25], due to absorption of
phosphorus. Mucosal erosions were also noted, when they get exposed to mouth, eyes, it
may show bullae, injection. Thus following intake of phosphorus, it may show oral burns,
vomiting, loose stools, abdominal pain and even bleeding, as hematemesis. the vomitus
and stool show typical garlic odor, and it also appears as glistening in dark room, hence it
is also mentioned as smoking stool syndrome.[9,35] The main mechanism is exothermic
reaction. If it penetrates dermis, causes tissue damage, due to production of phosphoric
acid, when reacting with oxygen. The digestive system is less involved than skin,
probably due to low oxygen concentration. Severe mucosal involvement is also explained
due to generation of phosphoric acid.[32,33]
19
CARDIOVASCULAR SYSTEM
Early death within twenty-four hours, after intake of phosphorus, is mainly due to
cardiovascular collapse Electrocardiograph taken during interval hours of admission may
reveal. QT prolongation, atrial fibrillation, ST depression, which may be due to
electrolyte deficiency, mainly of calcium. [22,23] Cardiac arrest also occurs, after few
hours of even dermal exposure, it generally occurs 4-10 hours after absorption. Cardiac
arrest without any rhythm disturbances or myocardial injury is also reported.
hypocalcemia also causes cardiomyopathy and mimics like myocardial
infarction.[18,29]Usually there are no morphological changes, however intestinal edema
and vacuolated cytoplasm urine noted.
NERVOUS SYSTEM:
It produces neurological manifestation such as anxiety, confusion, irritability,
hallucination, epilepsy, loss of consciousness and deep coma. If any patient is found to
have neurological findings initially before the involvement of other systems, it had
increased mortality of 20 %.Hypocalcemia can produce carpopedal spasm,
paraesthesia,tetany or laryngeal stridor. However, neural uptake of phosphorus is only
small quantity there was also no distinct histological change in the brain. Thus
neurological manifestation was mainly due to hypocalcemia, rather than due to direct
effect of phosphorus.[43,44]
20
RENAL:
Half of the cases have shown increase urea and creatinine values, but only a few
developed chronic kidney disease.[45] Rarely acute tubular necrosis also noted. It mainly
causes glomerular injury after absorption in GIT, histological finding shows fatty
degeneration in few cases and fatty deposition with necrotic changes in some. [34,35]
ELECTROLYTE DISTURBANCES:
Due to the absorption of phosphorus and into conversion to phosphoric acid, some
deproteination, hyperphosphatemia were noted. Calcium forms calcium phosphates salts
which lead to hypocalcemia. Hyperkalemia was noted, due to hypocalcemia or due to
renal failure.[36,37]
STAGES OF POISONING
There are 3 stages of clinical manifestations are seen in the poisoning patients.
1. FIRST STAGE
It corresponds with the first 24 hours after ingestion.
Most of the patients are asymptomatic during this period.
Some may have symptoms like vomiting and abdominal pain due to
local gastrointetinal irritation.
Sudden cardiac death may occur dring this period due to cardiac
arrhythmias.
Also seen are neurological manifestations due to hypocalcemia.
21
2. SECOND STAGE
This stage occurs within 2 –3 days of ingestion.
Patients may be asymptomatic during this stage
Acute fulminant hepatic failure may develop and patient will be having
jaundice, vomiting ,abdominal pain, and encephalopathy requiring liver
transplantaion. Caogulopathy symptoms can be seen due to loss of clotting
factor mechanisms.
3. THIRD STAGE
This stage corresponds from 4th day to 8 th day after ingestion.
Death may ensue because of fulminant hepatic failure and delayed acrdiac
toxicity.
4. FOURTH STAGE
Corresponds to 8 th day after ingestion.
This stage correlates with the recovery phase.
DIFFERENTIAL DIAGNOSIS :
Unknown rodenticide exposure may be identified by a few findings Rapid action poisons,
may manifest symptoms within six hours, if it shows more cholinergic findings, it
suggests organophosphorus poisoning. More muscular activity suggests strychnine
poisoning More gastrointestinal symptoms such as mucosal burns, vomiting, abdominal
pain and loose stools, suggests yellow 13 phosphorus poisoning. If it shows respiratory
symptoms suggest zinc phosphide. Delayed poisoning, manifests usually after twelve
22
hours, most commonly due to superwarfarin groups [27,40]The smell also shows some
clue such as phosphorus smell as garlic; while zinc and aluminum phosphide smell as
rotten fish, due to liberation of phosphine gas as it combines with air or water.
MANAGEMENT INITIAL CARE:
Basic life support such as protection of the airway and circulatory status must be
maintained. Complete blood count, liver function test, prothrombin time, international
standardized ratio ( INR), blood urea, serum creatinine, serum electrolytes especially of
calcium phosphates, potassium should be done immediately after admission, On
accessing intravenous line, Frequent recording of vitals and cardiac monitoring should be
done. Urine output should be recorded, if the complaint of irritation of the eye , eyewash
should be given with clean water immediately.
DECONTAMINATION OF DIGESTIVE TRACT:
Early gastric lavage was indicated (31). Due to the high toxicity of phosphorus and since
no specific antidote is available, lavage should be done in all patients. However utmost
care must be taken, since explosion may occur following contact with oxygen, after
inserting ryle’s tube (8). This may also be prevented by placing syringe filled with water
at nasal end of the tube, after confirming the position of the tube, water is being instilled,
instead of air. However there is no data available regarding supportive use of charcoal for
adsorbing phosphorus since due to its highly toxic nature and no oesophageal burns is
23
getting reported, activated charcoal is being administered widely in many centers. Bowel
wash with polyethylene glycol is tried, since it forms non-absorbable material and thus
getting washed away with stool (31) Potassium permanganate wash will convert
phosphorus to least toxic oxide (32). Nowadays it is used worldwide, but anyway there
were no positive results. It is not easily available and huge risk, it was not indicated.
TREATMENT:
No specific antidote is available up to date. But n-acetylcysteine regimen has prevented
death an insignificant number of the patient if it was administered early if it was
continued in full course. Since there is no potential side effect, no detailed study is
available, if it is recommended to use in white phosphorus poisoning.
OTHER MODALITIES:
Steroids were not useful in preventing hepatotoxicity. Ubiquinone and sulfate were
preventing liver toxicity to some extent, no human study is available yet (15).
HAEMODIALYSIS:
Haemodialysis rapidly corrects the electrolyte disturbances such as hyperphosphatemia,
hyperkalemia, and hypocalcemia; but no report was available. However it significantly
reduces mortality by 50%, thus exchange transfusion was beneficial.(10,14).
24
PHOSPHIDES:
Phosphides such as zinc and aluminum are being used as rodenticides in developing
countries to protect grains from rodents (33) because it is cheaper and effective. Zinc
phosphide is dark gray in color, has a rotten fish odor and bad taste, hence it was not used
by other animals except rats. When mixed with tartar emetic, both these phosphides,
release phosphine gas readily, when it comes in contact with water or diluted acids (33).
The exact mechanism is not clear. Phosphine is produced after phosphide reacts with
hydrochloric acid in stomach. It inhibits 18 cytochrome-c oxidases and in turn inhibits
oxidative phosphorylation of electron transport system (34), which in turn leads to
various cellular toxicity, necrosis of gastrointestinal tract, liver and also kidneys.
phosphine, being heavier than air, having rotten fish odor, can be detected even at levels
of 2 ppm.(34) Typical odorcan not be a warning sign since toxicity occurs even below the
level of olfactory threshold. A number of oral exposures had been reported. It was also
identified as one of the most common suicidal agents in India (35). The exact level of
lethal dose is not known since it was reported that even after ingesting a small amount of
5gm, the patient has died. Some patients have survived even after ingesting 50gm.
Inhalation of toxic exposure to phosphine is also reported. It causes severe mucosal
irritation, manifested as nausea, vomiting, and abdominal pain within 15 minutes of
ingestion of aluminum phosphide and 30minutes after ingestion zinc phosphide(35) Other
symptoms being hypotension, palpitation, acidosis, tetany. Systemic toxic symptoms
such as broad QRS complex, jaundice, and pulmonary edema are also reported. However
25
neurological manifestations are rare, but seizures and coma are recorded in expired
patients(36). The majority of death occurs after 24 hours of ingestion, which may be
delayed upto 2 weeks, which was mainly reported due to myocardial damage (35). 19
Long term exposure in industry may reduce psychiatric, pulmonary, hepatic and cardiac
findings.
MANAGEMENT:
Treatment is mainly supportive and also symptomatic. If there is acute ingestion,
activated charcoal is useful, however,the patient should be continuously monitored. The
liver function test, urea, creatinine, electrolytes should be measured. After lavage,
phosphine gas is emitted in lavage solution and stools, hence they must be cleaned and
disposed of properly to prevent inhalation exposure to health care workers by providing
proper face masks. Lavage is tried using sodium bicarbonate, plain water or even milk.
Administration of proton pump inhibitor with antacid is useful. But prognosis is worse if
pulmonary and cardiovascular manifestations arise early. A chest x-ray for identifying
pulmonary toxicity and abdominal x-ray for opacities in gut may help.[43,44]
Importantly, coagulation related to vitamin K antagonist (VKA)/LAAR effect may be
recognized by simultaneous prolongation of the prothrombin time (PT), international
normalized ratio (INR), and partial thromboplastin time (PTT). In patients with otherwise
normal hepatic function, coagulation factor activity demonstrates low levels of Factors II,
VII, IX, and X, but preserved levels of the remainder of (non-vitamin K dependent)
coagulation factors. Mixing studies, if performed, are expected to demonstrate correction.
26
Accumulation of Vitamin K Epoxide may be present and the diagnosis confirmed by
specific testing for the presence of rodenticides. which leading to coagulopathy, bleeding
complications, and death.
27
MATERIALS AND METHODS
This study was conducted at Stanley Medical College Hospital Toxicology IMCU,
Stanley Government Medical College, Chennai, during the period of March 2018 to
August 2018 (6 Months). There were 108 patients admitted with an alleged history of
ingesting rodenticide compounds in our emergency medical ward during the study period.
After applying, the inclusion and exclusion criteria, 170 patients only fulfilled all the
criteria and they were chosen as study subjects (n =170 ).
Inclusion criteria:
1.Patients admitted with the history of consumption of rat killer paste
poisoning with age >18 years
Exclusion criteria:
1.Age less than 18 yrs
2.History of consumption of other compounds with the rat killer paste
3Those with the history of acute or chronic liver disease
4.Those who refuse the study
METHODOLOGY &DATA COLLECTION:
In this study those who get admitted with history of rat killer paste poisoning
(yellow phosphorous , zinc phosphide and aluminium phosphide ) are included in the
study after excluding with the exclusion criteria.
28
The patients are monitored with their complete blood count , liver function test ,
Prothrombin time , INR , renal function test till they got discharged from the hospital
.With the results, parameters like age and sex wise distribution, complications, morbidity
and mortality of rat killer paste poisoning are analyzed.
29
STATISTICAL ANALYSIS
1. Continuous variables are expressed as means and standard deviations and
categorical variables as numbers with percentages in brackets.
2. For comparisons between patient groups, we used Student’s T-test for quantitative
variables and Chi-square or Fisher’s exact tests for categorical variables.
3. P<0.01 was taken as significant. Data analysis and interpretation were done with
IBM SPSS Statistics v20.0.
30
RESULTS
TABLE :1AGE GROUP (n=170)
Agegroup Frequency Percent
Up to 20 Years 13 7.6
21- 30 Years 90 52.9
31- 40 Years 45 26.5
41- 50 Years 19 11.2
Above 50 Years 3 1.8
Table :1& Graph :1 170 cases were included in the study. Up to 20 Years-13 cases
(7.6%),21- 30 Years-90 cases (52.9%),31- 40 Years- 45 cases ( 26.5%), 41- 50 Years-19
(11.2%),Above 50 Years-3 (1.8%)
31
GRAPH :1AGE GROUP (n=170)
Table :1& Graph :1 170 cases were included in the study.
Up to 20 Years-13 cases (7.6%)
21- 30 Years-90 cases (52.9%)
31- 40 Years- 45 cases ( 26.5%),
41- 50 Years-19 (11.2%),
Above 50 Years-3 (1.8%)
7.6
52.9
26.5
11.2
1.8
0
10
20
30
40
50
60
Up to 20 Years 21- 30 Years 31- 40 Years 41- 50 Years Above 50 Years
Age group
32
TABLE :2 SEX DISTRIBUTION
SEX Frequency Percent
MALE 97 57.1
FEMALE 73 42.9
Total 170 100.0
GRAPH :2 SEX DISTRIBUTION
Table :2& Graph :2 Among 170 cases
male were 97(57.1%)
females were 73(42.9%)
57.1
42.9
SEX
MALE FEMALE
33
TABLE :3 AMOUNT CONSUMED
AMOUNT CONSUMED Frequency Percent
3 QUARTERS 19 11.2
DOUBLE 1 0.6
HALF 80 47.1
ONE 23 13.5
QUARTER 45 26.5
TWO 2 1.2
Total 170 100.0
GRAPH :3 AMOUNT CONSUMED
TABLE :3& GRAPH :3 Categorizing the amount consumed in patients included in our
study.
3 quarters- 19 cases (11.2%) Double-1 (4%) Half-80 ( 47.1%) One-23 (13.5%)
11.2
0.6
47.1
13.5
26.5
1.2
0
5
10
15
20
25
30
35
40
45
50
3 QUARTERS DOUBLE HALF ONE QUARTER TWO
AMOUNT CONSUMED
34
Quarter- 45 (26.5%) Two-2 ( 1.2%)
TABLE :4 TIME ELAPSED AFTER CONSUMPTION
GRAPH :4 TIME ELAPSED AFTER CONSUMPTION
TABLE :4 & GRAPH :
4 Up to 6Hrs-68 (40%),
>6Hrs-80 (47.1%),
Not Known was -22 cases (12.9%)
40
47.1
12.9
Time
Up to 6Hrs >6Hrs NOT KNOWN
Time Frequency Percent
Up to 6Hrs 68 40.0
>6Hrs 80 47.1
NOT KNOWN 22 12.9
Total 170 100.0
35
TABLE: 5 STOMACH WASH
STOMACH WASH Frequency Percent
NO 24 14.1
YES 146 85.9
Total 170 100.0
GRAPH :5 STOMACH WASH
TABLE :5& GRAPH :5 shows stomach wash done in 146 cases (85.9%), not done in 24
cases (14.1%)
14.1
85.9
STOMACH WASH
NO YES
36
TABLE: 6 PRESENCE OF VOMITING
VOMITING Frequency Percent
NO 82 48.2
YES 88 51.8
Total 170 100.0
GRAPH :6 PRESENCE OF VOMITING
Table :6& Graph :6 Among 170 cases, 88 cases (51.8%) had vomiting, 82 cases (48.2%)
had no episodes of vomiting
48.2
51.8
VOMITING
NO YES
37
TABLE :7 ABDOMEN PAIN
ABDOMEN PAIN Frequency Percent
NO 96 56.5
YES 74 43.5
Total 170 100.0
GRAPH :8 ABDOMEN PAIN
Table :7& graph :8 shows 74 cases ( 43.5%) had abdomen pain , 96 cases (56.5%) were
free from abdomen pain
56.5
43.5
ABD_PAIN
NO YES
38
TABLE :8 JAUNDICE
JAUNDICE Frequency Percent
NO 162 95.3
YES 8 4.7
Total 170 100.0
GRAPH: 8 JAUNDICE
Table: 8 & Graph:8 Only 8 cases (4.7%) had jaundice, and 162 cases (95.3%) did not
show the incidence of jaundice.
95.3
4.7
NO
YES
0 20 40 60 80 100 120
JAUNDICE
NO YES
39
TABLE :9 MALENA
GRAPH: 9 MALENA
Table :9& graph :9 shows incidence of malena , 16 cases (9.4%) had malena and nil in
154 cases (90.6%)
90.6
9.4
MALENA
NO YES
MALENA Frequency Percent
NO 154 90.6
YES 16 9.4
Total 170 100.0
40
TABLE :10 USG FINDINGS
USG Frequency Percent
ASCITES 6 3.5
GR I FATTY LIVER+
ASCITES 1 .6
NORMAL 163 95.9
Total 170 100.0
GRAPH :10 USG FINDINGS
Table: 10 & graph: 10 shows USG findings in case group, Ascites was present in -6 cases
( 3.5%), GR I Fatty Liver+ Ascites- 1 case (6%), normal findings were observed in 163
cases (95.9%)
3.5 0.6
95.9
0
20
40
60
80
100
120
ASCITES GR I FATTY LIVER+ ASCITES NORMAL
USG
41
TABLE: 10 CAUSE OF DEATH
CAUSE OF DEATH Frequency Percent
COAGULOPAHTY+HE 10 52.6%
HE 7 36.8%
PANCREATITIS 2 10.5%
Total 19 100.0
GRAPH: 10 CAUSE OF DEATH
Table :10& graph :
10 COAGULOPATHY+HE- in 10 cases (52.6%),HE-7 cases (36.8%),Pancreatitis was in
2 cases (10.5%)
52.60%
36.80%
10.50%
0.00%
10.00%
20.00%
30.00%
40.00%
50.00%
60.00%
COAG+HE HE PANCREATITIS
CAUSE_OF_DEATH
42
TABLE :11 AGE GROUP CORRELATION WITH COURSE IN HOSPITAL
COURSE_IN_HOSP Total
DISCHARGE DEATH
Age group Up to 20 Years Count 12 1 13
% within COURSE IN_
HOSP
7.9% 5.3% 7.6%
21- 30 Years Count 81 9 90
% within
COURSE_IN_HOSP
53.6% 47.4% 52.9%
31- 40 Years Count 40 5 45
% within
COURSE_IN_HOSP
26.5% 26.3% 26.5%
41- 50 Years Count 15 4 19
% within
COURSE_IN_HOSP
9.9% 21.1% 11.2%
Above 50 Years Count 3 0 3
% within
COURSE_IN_HOSP
2.0% 0.0% 1.8%
Total Count 151 19 170
% within
COURSE_IN_HOSP
100.0% 100.0% 100.0
%
43
GRAPH: 11 AGE GROUP CORRELATION WITH COURSE IN HOSPITAL
0.00%
10.00%
20.00%
30.00%
40.00%
50.00%
60.00%
Up to 20 Years 21- 30 Years 31- 40 Years 41- 50 Years Above 50 Years
7.90%
53.60%
26.50%
9.90%
2.00%
5.30%
47.40%
26.30%
21.10%
0.00%
DISCHARGE DEATH
44
Age group coorelation with hospital stay
Up to 20 Years-13 cases (7.6%)
o Discharge -12 case, (7.9%)death -1 case (5.3%)
21- 30 Years-90 cases (52.9%)
o Discharge -81 case, (53.6%) death -9 case (47.4%)
31- 40 Years- 45 cases ( 26.5%)
o Discharge -40 case, (26.5%) death -5 case (26.3%)
41- 50 Years-19 (11.2%)
o Discharge -15 case, (9.9%) death -4 case (21.1%)
Above 50 Years-3 (1.8%)
o all are discharged. No incidence of death in this age group
Pearson Chi-Square=2.529p=0.639 which is statically less significant.
45
TABLE: 12SEX CORRELATION WITH COURSE IN HOSPITAL
COURSE_IN_HOSP Total
DISCHARGE DEATH
SEX MALE Count 91 6 97
% within
COURSE_IN_HOSP
60.3% 31.6% 57.1%
FEMALE Count 60 13 73
% within
COURSE_IN_HOSP
39.7% 68.4% 42.9%
Total Count 151 19 170
% within
COURSE_IN_HOSP
100.0% 100.0% 100.0%
Sex Correlation With Course In Hospital
Male were 97(57.1%), 91 discharge and 6 were expired
Females were 73(42.9%) -60 were discharged, 13 were expired.
Pearson Chi-Square=5.668* P=0.017
46
GRAPH: 12SEX CORRELATION WITH COURSE IN HOSPITAL
Sex Correlation With Course In Hospital
Male were 97(57.1%), 91 discharge and 6 were expired
Females were 73(42.9%) -60 were discharged, 13 were expired.
Pearson Chi-Square=5.668* P=0.017
0.00%
10.00%
20.00%
30.00%
40.00%
50.00%
60.00%
70.00%
MALE FEMALE
60.30%
39.70%
31.60%
68.40%
DISCHARGE DEATH
47
TABLE: 13 AMOUNT CONSUMED CORRELATION WITH COURSE IN
HOSPITAL
COURSE IN HOSP Total
DIS CHARGE DEATH
AMT_CONS
UMED
3
QUARTERS
Count 13 6 19
% within
COURSE
IN HOSP
8.6% 31.6% 11.2%
DOUBLE Count 0 1 1
% within
COURSE
IN HOSP
0.0% 5.3% 0.6%
HALF Count 78 2 80
% within
COURSE
IN HOSP
51.7% 10.5% 47.1%
ONE Count 17 6 23
% within
COURSE
IN HOSP
11.3% 31.6% 13.5%
QUARTER Count 43 2 45
% within
COURSE
IN HOSP
28.5% 10.5% 26.5%
TWO Count 0 2 2
% within
COURSE
IN HOSP
0.0% 10.5% 1.2%
Total Count 151 19 170
% within
COURSE
IN HOSP
100.0% 100.0% 100.0%
Categorizing the amount consumed in patients included in our study. 3 quarters-
19 cases (11.2%) -13 were discharged, 6 were expired,Double-1 (4%), only one case, in
the categories which were expired.
48
Half-80 ( 47.1%), 78 were discharged, 2 cases expired.One-23 (13.5%), 17
discharged and 6expired.
Quarter- 45 (26.5%), 43 discharged, 2 expired, Two-2 ( 1.2%) both the cases
expired. Pearson Chi-Square=45.081* P<0.001
GRAPH :13 AMOUNT CONSUMED
0.00%
10.00%
20.00%
30.00%
40.00%
50.00%
60.00%
3 QUARTERS DOUBLE HALF ONE QUARTER TWO
8.60%
0.00%
51.70%
11.30%
28.50%
0.00%
31.60%
5.30%
10.50%
31.60%
10.50% 10.50%
DISCHARGE DEATH
49
TABLE: 14 STOMACH WASH CORRELATION WITH COURSE OF
HOSPITAL
Stomach wash in correlation with hospital stay. It is done in 146 cases (85.9%), among
them 132, discharged and 14were dead. not done in 24 cases (14.1%) 19 were discharged,
5 were expired.Pearson Chi-Square=2.625 p=0.105
COURSE_IN_HOSP Total
DISCHARGE DEATH
STOMACH_
WASH
NO Count 19 5 24
% within
COURSE_IN_HOSP
12.6% 26.3% 14.1%
YES Count 132 14 146
% within
COURSE_IN_HOSP
87.4% 73.7% 85.9%
Total Count 151 19 170
% within
COURSE_IN_HOSP
100.0% 100.0% 100.0
%
50
GRAPH: 14 STOMACH WASH CORRELATION WITH COURSE IN
HOSPITAL
0.00%
10.00%
20.00%
30.00%
40.00%
50.00%
60.00%
70.00%
80.00%
90.00%
MALE FEMALE
12.60%
87.40%
26.30%
73.70%
DISCHARGE DEATH
51
TABLE:15 TIME AFTER CONSUMPTION IN CORRELATION WITH COURSE
IN HOSPITAL
COURSE_IN_HOSP Total
DISCHARGE DEATH
time Up to 6Hrs Count 68 0 68
% within
COURSE_IN_HOSP
50.7% 0.0% 45.9%
>6Hrs Count 66 14 80
% within
COURSE_IN_HOSP
49.3% 100.0% 54.1%
Total Count 134 14 148
% within
COURSE_IN_HOSP
100.0% 100.0% 100.0%
Time After Consumption In Correlation With Course In HospitalUp to 6Hrs-68 (40%),
all the cases were alive and discharged, >6Hrs-80 (47.1%),- 66 were discharged, 14 were
dead.
Pearson Chi-Square=13.143** P<0.001
52
GRAPH: 15 TIME AFTER CONSUMPTION IN CORRELATION WITH
COURSE IN HOSPITAL
0.00%
20.00%
40.00%
60.00%
80.00%
100.00%
Up to 6Hrs >6Hrs
50.70% 49.30%
0.00%
100.00%
DISCHARGE DEATH
53
TABLE: 15 VOMITING IN CORRELATION WITH HOSPITAL COURSE
COURSE_IN_HOSP Total
DISCHARGE DEATH
VOMITING NO Count 70 12 82
% within
COURSE_IN_HOSP
46.4% 63.2% 48.2%
YES Count 81 7 88
% within
COURSE_IN_HOSP
53.6% 36.8% 51.8%
Total Count 151 19 170
% within
COURSE_IN_HOSP
100.0% 100.0% 100.0%
Among 170 cases, 88 cases (51.8%) had vomiting, 81 were discharged, 7 dead. 82 cases
(48.2%) had no episodes of vomiting , 70 discharged,12 dead, Pearson Chi-Square=1.908
p=0.167
54
GRAPH: 15 VOMITING IN CORRELATION WITH COURSE IN HOSPITAL
0.00%
10.00%
20.00%
30.00%
40.00%
50.00%
60.00%
70.00%
NO YES
46.40%
53.60%
63.20%
36.80%
DISCHARGE DEATH
55
TABLE: 16 CORRELATION OF ABDOMEN PAIN WITH COURSE IN
HOSPITAL
COURSE_IN_HOSP Total
DISCHARGE DEATH
ABD_PAIN NO Count 89 7 96
% within
COURSE_IN_HOSP
58.9% 36.8% 56.5%
YES Count 62 12 74
% within
COURSE_IN_HOSP
41.1% 63.2% 43.5%
Total Count 151 19 170
% within
COURSE_IN_HOSP
100.0% 100.0% 100.0%
Shows 74 cases ( 43.5%) had abdomen pain 62 cases were discharged, 12 were dead, 96
cases (56.5%) were free from abdomen pain, 89 were dead and 7 were discharged.
Pearson Chi-Square=3.353 p=0.067
56
GRAPH: 16 CORRELATION OF ABDOMEN PAIN WITH COURSE IN
HOSPITAL
0.00%
10.00%
20.00%
30.00%
40.00%
50.00%
60.00%
70.00%
NO YES
58.90%
41.10% 36.80%
63.20%
DISCHARGE DEATH
57
TABLE: 17 JAUNDICE CORRELATION WITH COURSE OF HOSPITAL
COURSE_IN_HOSP Total
DISCHARGE DEATH
JAUNDICE NO Count 147 15 162
% within
COURSE_IN_HOSP
97.4% 78.9% 95.3%
YES Count 4 4 8
% within
COURSE_IN_HOSP
2.6% 21.1% 4.7%
Total Count 151 19 170
% within
COURSE_IN_HOSP
100.0% 100.0% 100.0%
58
GRAPH 17: JAUNDICE CORRELATION WITH COURSE OF HOSPITAL
Only 8 cases (4.7%) had jaundice, and 162 cases (95.3%) did not show incidence of
jaundice.
In jaundice diagnosed patients, 4 were dead and 4 were alive, in undiagnosed cases 147,
discharged and 15 were dead. Pearson Chi-Square=12.746** p<0.001
0.00%
10.00%
20.00%
30.00%
40.00%
50.00%
60.00%
70.00%
80.00%
90.00%
100.00%
NO YES
97.40%
2.60%
78.90%
21.10%
DISCHARGE DEATH
59
TABLE: 18 CORRELATION OF MALENA WITH COURSE OF HOSPITAL
STAY
COURSE_IN_HOSP Total
DISCHARGE DEATH
MALENA NO Count 143 11 154
% within
COURSE_IN_HOSP
94.7% 57.9% 90.6%
YES Count 8 8 16
% within
COURSE_IN_HOSP
5.3% 42.1% 9.4%
Total Count 151 19 170
% within
COURSE_IN_HOSP
100.0% 100.0% 100.0%
16 cases (9.4%) had Malena among them 8 were dead and 8 were discharged, 154 cases
(90.6%) Malena was found 143, survived, 11 dead. Pearson Chi-Square=26.817**
p<0.001
60
TABLE: 18 CORRELATION OF MALENA WITH COURSE OF HOSPITAL
STAY
0.00%
10.00%
20.00%
30.00%
40.00%
50.00%
60.00%
70.00%
80.00%
90.00%
100.00%
NO YES
94.70%
5.30%
57.90%
42.10%
DISCHARGE DEATH
61
TABLE: 19 HEPATIC ENCEPHALOPATHY [HE] CORRELATION WITH
COURSE IN HOSPITAL
COURSE_IN_HOSP Total
DISCHARGE DEATH
HE 1.00 Count 146 8 154
% within
COURSE_IN_HOSP
96.7% 42.1% 90.6%
2.00 Count 5 11 16
% within
COURSE_IN_HOSP
3.3% 57.9% 9.4%
Total Count 151 19 170
% within
COURSE_IN_HOSP
100.0% 100.0% 100.0%
HE: 1 146 patients discharged, 8 dead. HE:2 5 discharged , 11 expired, Pearson Chi-
Square=58.974** P<0.001
62
GRAPH: 19 HEPATIC ENCEPALOPATHY( HE ) CORRELATION WITH
COURSE IN HOSPITAL
0.00%
10.00%
20.00%
30.00%
40.00%
50.00%
60.00%
70.00%
80.00%
90.00%
100.00%
1 2
96.70%
3.30%
42.10%
57.90%
DISCHARGE DEATH
63
TABLE: 20 ABNORMAL & NORMAL CORRELATION WITH COURSE IN
HOSPITAL
COURSE_IN_HOSP Total
DISCHARGE DEATH
ABN Count 1 2 3
% within
COURSE_IN_HOSP
0.7% 10.5% 1.8%
WNL Count 150 17 167
% within
COURSE_IN_HOSP
99.3% 89.5% 98.2%
Total Count 151 19 170
% within
COURSE_IN_HOSP
100.0% 100.0% 100.0%
ABORMAL1 case discharged, and 2 dead, in WNL 150 were discharged and 17 were
dead Pearson Chi-Square=9.472* p=0.002
64
GRAPH: 20 ABNORMAL & NORMAL CORRELATION WITH COURSE IN
HOSPITAL
0.00%
10.00%
20.00%
30.00%
40.00%
50.00%
60.00%
70.00%
80.00%
90.00%
100.00%
ABN WNL
0.70%
99.30%
10.50%
89.50%
DISCHARGE DEATH
65
TABLE: 21 USG FINDING IN CORRELATION WITH COURSE IN HOSPITAL
COURSE_IN_HOSP Total
DISCHARGE DEATH
USG ASCITES Count 4 2 6
% within
COURSE_IN_HOSP
2.6% 10.5% 3.5%
GR I FATTY
LIVER+ ASCITES
Count 1 0 1
% within
COURSE_IN_HOSP
0.7% 0.0% 0.6%
NORMAL Count 146 17 163
% within
COURSE_IN_HOSP
96.7% 89.5% 95.9%
Total Count 151 19 170
% within
COURSE_IN_HOSP
100.0% 100.0% 100.0%
In USG findings,
Ascites were in 6 patients, among them 4 were discharged and 2 were dead
Fatty liver with ascites 1 cases that were discharged.
In normal usg findings, 146 were discharged, 17 were dead. Pearson Chi-
Square=3.185 P=0.203
66
GRAPH: 21 USG FINDING IN CORRELATION WITH COURSE OF HOSPITAL
0.00%
10.00%
20.00%
30.00%
40.00%
50.00%
60.00%
70.00%
80.00%
90.00%
100.00%
ASCITES GR I FATTY LIVER+ ASCITES NORMAL
2.60% 0.70%
96.70%
10.50%
0.00%
89.50%
DISCHARGE DEATH
67
DISCUSSION
Poisoning directly or indirectly is responsible for more than one million illnesses
worldwide.[11]Deliberate self-poisoning has become an increasingly common response
to emotional distress in young adults, and it is now one of the most frequent reasons for
emergency hospital admission.2 Suicide is an important cause of premature death and the
WHO estimates to be nearly 800,000 in number.3 In industrialized countries, the drugs
people commonly take in overdose-analgesics, tranquilizers, antidepressants are
relatively non-toxic[12,1,14]. The estimated case fatality for overdose in England, for
example, is around 0.5%.5 In developing countries, the situation is quite different.6 The
substances most commonly used for self-poisoning are agricultural pesticides including
rodenticides.1,3,7 Overall case fatality ranges from 10%-20%.[18] For this reason, deaths
from pesticide poisoning make a major contribution to patterns of suicide in developing
nations, particularly in rural areas.[19] Three million cases of pesticide poisoning occur
worldwide annually, with 2,20000 deaths, the majority of which are intentional.10
Rodenticides are a heterogeneous group of compounds
68
Raton paste, a commonly used rodenticide in Indian houses contains 3% yellow
phosphorus. Yellow phosphorus is a general protoplasmic poison causing multiorgan
failure.[20] Doses >1 mg/kg are almost invariably fatal.
Raton paste poisoning is either suicidal or accidental. The clinical course of ratol paste
poisoning is different from that of most other poisons. The patients are usually
asymptomatic during the initial 72 h of ingestion, or they may have signs and symptoms
of gastrointestinal irritation. After 72 h they develop deranged liver function, acute
hepatic failure, coagulopathy. Central nervous system effects include changes in mental
status like confusion, psychosis, hallucinations, and coma. Cardiac toxicity includes
hypotension, tachycardia, arrhythmias, and cardiogenic shock. Some patients may
develop acute tubular necrosis and acute renal failure.[21,22,23] Because of the initial
asymptomatic phase few patients do not reveal about ratol paste ingestion and present
late to the hospital. Patients who present late after consumption of the lethal dose develop
fulminant hepatic failure with mortality of 100%.[24] In severe ingestions of ratol paste,
patients do not have the initial asymptomatic stage, and they die due to shock and
cardiopulmonary arrest in early stages itself.[4]
69
There is no specific antidote for yellow phosphorus poisoning. Treatment is directed at
removal of the poison and supportive therapy.[25,26]
Aluminum phosphide, zinc phosphide are the other rodenticides available. They are
mainly used in agricultural fields[27] in contrast to ratol paste, which is used in houses.
Also, ratol paste is commonly mistaken for toothpaste and consumed by children. And
the product directions suggest that the paste be applied to bread to enable ingestion by
rodents, thus making it appealing to children as well.[28] Hence, accidental poisoning is
more common with ratol paste.
Most of the cases were in the age group of 11-30 years. Acute poisoning was commonly
seen among farmers, homemakers, and students in various national and international
studies. In all the cases, the most common route of exposure was oral. The majority of
cases were in the age group of 11-30 years (42 cases, 75%) which can be explained by
the fact that the persons of this age group are suffering from the stress of the modern
lifestyles, failure in love, family problems, nuclear family concept, etc. Our study does
not correlate with the study done by other studies,8 in which incidence was high among
males. Many cases were found among homemakers (18 cases, 32.1%), male laborers (12
cases, 21.4%), and farmers (16 cases, 28.5%) as these groups are more vulnerable groups
70
and easily exposed to the poisoning agents. Poverty, inadequate income to run the
family.monsoon failure was responsible for higher incidence of poisoning among
laborers and farmers. Factors, such as dowry, cruelty by the in-laws, family quarrels,
maladjustment in married life, and dependence of women on husband, are responsible for
the higher incidence of poisoning among homemakers. Failure in the exams or inability
to cope up the high expectation from parents and teachers has increased the incidence of
poisoning among students. High toxicity and non-availability of any specific antidote are
responsible for higher mortality with rat killer poison.[29] LFT derangements are seen
mostly with yellow phosphorus after 2-3 days of consumption in our study.
Various studies on poisoning were done in India Song ZY et al. [30] noticed most
commonly affected age group was 20-40 years. Our study was compatible with Banerjee
et al. in the age group. A study by Winek CLet al. [31] found that a higher number of
patients ingested rat killer poisoning mixing with alcohol but our study showed that,
many patients ingested either raw or mixed with water.
The new finding in our study was the mean lethal dosage (13.42 ± 7.069 gms) of rat killer
poisoning which will cause damage to the organs once ingested. Another new finding of
our study was manifestation of first chief symptoms which was 5.7 ± 6.3093 hours.
71
“People must seek care in the health facility as soon as they have identified the ingestion
of rat killer poison”. Elizabeth J, et al. [32] found in her study that the patients were
usually asymptomatic during the initial 72 hours of ingestion, or they may have signs and
symptoms of gastrointestinal irritation. Our patients in our study developed symptoms
from 5 to 6 hours and vomiting was found in higher numbers in our patients.
Blotting the biological marker AST and ALT showed a higher elevation in patients
ingested rat killer poison which indicates that the first affecting organ was liver followed
by kidney and other organs. AST was 402.6 on the 2nd
day and on 6th
day AST reduced to
159.0. Alt was 439.7 on the 2nd
day and reduced on 6th
day to 171.0. Stephenson JBP et
al. [33] study showed, the mean admission ALT/AST was 306/451, discharge ALT/AST
was 291/302, and peak ALT/AST was 451/655. A few other new findings in our study
were elevation graphs were shown for T.bill, T.protein, Albumin, AST, ALT, urea,
creatinine, PT, and INR for all the patients who ingested rat killer poisoning. Our study
again found the statistical significant elevation biological elevation between the survivor
and non-survivor.[34,35,36]
We found out of 100% of patients received treatments like NAC, Vit-K, supportive, 82%
of our patients survived and discharged. Watson WAet al. [37] reveals best results seen
72
among patients in whom NAC was started early in the course of illness. Guidelines do
not exist regarding routine use of NAC in non-acetaminophen induced ALF, and
in hepatic failure due to rodenticide consumption. Patients admitted with ALF after
phosphorus ingestion has sometimes been managed with NAC [38]. We strongly
recommend that it is a need of hour to frame proper guidelines of treatment that ingest rat
killer poison. However in spite of manageable treatment, half of our patients developed
Toxic Hepatitis, 1/3 developed Acute Liver Failure and ¼ developed Toxic Hepatitis
along with Acute Kidney Injury / Acute Liver Failure along with Acute Kidney Injury. ¼
developed multiple organ failure which leads them to death. Lipton RAet al. [39] showed
35.7% mortality rate whereas our study showed 19% mortality rate. Survived patients
received psychiatric evaluation and were discharged in a stable condition.
Yellow phosphorous: Of the 26 patients, 61.5% recovered, 7% expired, 11% absconded
and one patient was DAMA. Contrastingly, more harm was seen in patients of Ben-Assa
BM et al, where only 48.8% survived, 27.9% expired and 23.2% DAMA. Fernandez et al
observed very high mortality (27%) and concluded that yellow phosphorus is extremely
lethal when consumed, owing to hepatotoxicity (33%).[41] In line with these findings, 5
out of 7 patients who had bleeding manifestations had consumed yellow
73
phosphorous.[55,59] Encephalopathy was seen in 5 patients with yellow phosphorus
poisoning. Hypotension complicated two patients with yellow phosphorous poisoning,
one had myocarditis and cardiogenic shock. About 10 of 26 (38.46%) patients with
yellow phosphorous intake developed fulminant hepatic failure, and they were given N-
acetyl cysteine. However, only four patients improved while four patients were referred
for liver transplantation and two expired. [42,43 56]
The most common symptom was vomiting (70%), followed by pain abdomen (50%) and
giddiness (30%) respectively. A study was done by Balasubramanian K et at,
Pondicherry, showed 36.67 % patients had nausea and vomiting, followed by giddiness
(20%) and pain abdomen (16.7%).[44,45,57,58]
The study found that hepatitis was common complication (32.14%), followed by
cardiogenic shock (8.9%). Three patients developed hepatic encephalopathy and Three
developed bleeding complication among 18 patients with hepatitis. Yellow phosphorus
was causing hepatitis in 11(19.67%) patients, zinc phosphide in 4 (7.14%) and aluminum
phosphide in 3 (5.35%) patients. Cardiogenic shock was due to aluminum phosphide
poisoning [46,47,48]
74
Prosser PRet al.(noted that the systems affected in their study due to Yellow Phosphorous
were gastrointestinal tract (100%), liver (66.70%), Cardiovascular, Nervous and
respiratory systems along with associated metabolic abnormalities (66.7%). In our study
93% patients had derangement in liver enzymes,10% patients had respiratory depression.
No patient had cardiac or metabolic abnormalities[49,50,51]. Simon FA,stated that in a
series of 15 patients observed mortality of 27% is recorded, confirming that Yellow
Phosphorus is extremely lethal when ingested. The duration of hospital admission and
compound consumption are very important. The lesser the duration the prognosis is good.
This is mainly because of gastric lavage given to those patients presenting early, which
decreases the amount of yellow phosphorous entering circulation and early treatment
with N acetylcysteine.[52,53,60]
75
SUMMARY
1. Poisoning is mostly preventable, commonly suicidal and rarely being an accidental
form of death in developing agrarian countries. In rural India, poisoning forms the
major share of emergency health care and of about one – fourth to one – third of
intensive care admissions.
2. To study the clinical profile of patients admitted with rodenticide poisoning and
their course in the hospital.
3. This study was conducted at Stanley Medical College Hospital Toxicology
IMCU, Stanley Government Medical College, Chennai, during the period of
March 2018 to August 2018 (6 Months). There were 108 patients admitted with an
alleged history of ingesting rodenticide compounds in our emergency medical
ward during the study period.
4. After applying, the inclusion and exclusion criteria, 170 patients only fulfilled all
the criteria and they were chosen as study subjects (n =170 ).
5. 170 cases were included in the study. Up to 20 Years-13 cases (7.6%),21- 30
Years-90 cases (52.9%),31- 40 Years- 45 cases ( 26.5%), 41- 50 Years-19
(11.2%),Above 50 Years-3 (1.8%)
6. Categorizing the amount consumed in patients included in our study. 3 quarters-
19 cases (11.2%) Double-1 (4%), Half-80 ( 47.1%),One-23 (13.5%),Quarter- 45
(26.5%),Two-2 ( 1.2%).Up to 6Hrs-68 (40%), >6Hrs-80 (47.1%), Not Known
was -22 cases (12.9%)
76
7. USG findings in case group, Ascites was present in -6 cases ( 3.5%), GR I Fatty
Liver+ Ascites- 1 case (6%), normal findings were observed in 163 cases
(95.9%).COAG+HE- in 10 cases (52.6%),HE-7 cases (36.8%),Pancreatitis was in
2 cases (10.5%)
8. Up to 20 Years-13 cases (7.6%) Discharge -12 case, (7.9%) death -1 case (5.3%) ,
21- 30 Years-90 cases (52.9%), Discharge -81 case, (53.6%) death -9 case (47.4%)
,31- 40 Years- 45 cases ( 26.5%), Discharge -40 case, (26.5%) death -5 case
(26.3%) ,41- 50 Years-19 (11.2%), Discharge -15 case, (9.9%) death -4 case
(21.1%) ,Above 50 Years-3 (1.8%) all are discharged. No incidence of death in
this age group Pearson Chi-Square=2.529p=0.639 which is statically less
significant.
9. Categorizing the amount consumed in patients included in our study. 3 quarters-
19 cases (11.2%) -13 were discharged, 6 were expired,Double-1 (4%), only one
case, in the categories which were expired.
10. Half-80 ( 47.1%), 78 were discharged, 2 cases expired.One-23 (13.5%), 17
discharged and 6expired.
11. Quarter- 45 (26.5%), 43 discharged, 2 expired, Two-2 ( 1.2%) both the cases
expired. Pearson Chi-Square=45.081* P<0.001.Stomach wash in correlation
with hospital stay.It done in 146 cases (85.9%), among them 132, discharged and
14were dead.not done in 24 cases (14.1%) 19 were discharged, 5 were
expired.Pearson Chi-Square=2.625 p=0.105.Time After Consumption In
77
Correlation With Course In HospitalUp to 6Hrs-68 (40%), all the cases were alive
and discharged, >6Hrs-80 (47.1%),- 66 were discharged, 14 were dead. Pearson
Chi-Square=13.143** P<0.001
12. Among 170 cases, 88 cases (51.8%) had vomiting, 81 were discharged, 7 dead. 82
cases (48.2%) had no episodes of vomiting , 70 discharged,12 dead,Pearson Chi-
Square=1.908 p=0.167.
13. Our Study Shows 74 cases ( 43.5%) had abdomen pain 62 cases were discharged,
12 were dead, 96 cases (56.5%) were free from abdomen pain, 89 were dead and 7
were discharged.Pearson Chi-Square=3.353 p=0.067Only 8 cases (4.7%) had
jaundice, and 162 cases (95.3%) did not show incidence of jaundice.In jaundice
diagnosed patients, 4 were dead and 4 were alive, in undiagnosed cases 147,
discharged and 15 were dead.Pearson Chi-Square=12.746** p<0.001.
14. 16 cases (9.4%) had Malena among them 8 were dead and 8 were discharged, 154
cases (90.6%) Malena was found 143, survived, 11 dead.Pearson Chi-
Square=26.817** p<0.001
15. HE: 1 146 patients discharged, 8 dead. HE:2 5 discharged , 11 expired,Pearson
Chi-Square=58.974** P<0.001.
16. ABN 1 case discharged, and 2 dead, in WNL 150 were discharged and 17 were
dead Pearson Chi-Square=9.472* p=0.002
17. In usg findings, ascites were in 6 patients, among them 4 were discharged and 2
were dead, fatty liver with ascites 1 cases that were discharged. In normal usg
findings, 146 were discharged, 17 were dead Pearson Chi-Square=3.185 P=0.203
78
18. Ratol paste poisoning is either suicidal or accidental. The clinical course of ratol
paste poisoning is different from that of most other poisons.
19. The patients are usually asymptomatic during the initial 72 h of ingestion, or they
may have signs and symptoms of gastrointestinal irritation.
20. After 72 h they develop deranged liver function, acute hepatic failure,
coagulopathy. Central nervous system effects include changes in mental status like
confusion, psychosis, hallucinations, and coma. Cardiac toxicity includes
hypotension, tachycardia, arrhythmias, and cardiogenic shock. Some patients may
develop acute tubular necrosis and acute renal failure.
79
CONCLUSION
1. Rodenticide poisoning is the second most common poisoning in our area.
2. Male to female ratio in our study is 1.5: 1.
3. Majority of the patients were in 20 to 30 years age group.
4. Phosphorus compound (paste) forms the major share of poison.
5. Most common symptom is abdominal pain (90%).
6. Mortality in this study was 20 %.
7. Increased time delay in hospitalisation carries more mortality.
8. Jaundice develop following ingestion of phosphorus, carries most mortality, which
also correlates with elevated serum bilirubin and SGPT level
9. Phosphorus (paste) compound of rodenticide , must be banned , to prevent mortality
in young productive poor patients , who intend to ingest poison in a minute decision .
80
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88
CLINICAL PROFILE OF RAT KILLER PASTE POISONING
PROFORMA
NAME : AGE: SEX:
ADDRESS: CONTACT NO:
COMPLAINTS:
HISTORY :
89
DURATION OF ILLNESS:
PAST HISTORY:
TREATMENT HISTORY:
PERSONAL HISTORY:
DRUGS/ TOXINS/ SUBSTANCE ABUSE
FAMILY HISTORY:
GENERAL EXAMINATION:
Pallor: Pulse: BMI:
Icterus: B.P: Temperature:
Lymphadenopathy : Resp.rate:
Oedema:
90
SYSTEMIC EXAMINATION:
CARDIOVASCULAR SYSTEM:
RESPIRATORY SYSTEM:
GASTRO-INTESTINAL SYSTEM :
CENTRAL NERVOUS SYSTEM :
INVESTIGATIONS
HEMOGLOBIN
TOTAL BILIRUBIN
DIRECT BILIRUBIN
SERUM GLUTAMIC OXALOACETIC TRANSAMINASE
SERUM GLUTAMIC PYURUVIC TRANSAMINASE
SERUM AMYLASE
SERUM LIPASE
91
PROTHROMBIN TIME
INR( INTERNATIONAL STANDARDISED RATIO)
SERUM CREATININE
BLOOD UREA
ULTRASOUND-ABDOMEN AND PELVIS
92
93
94
INFORMED CONSENT
“CLINICAL PROFILE OF RAT KILLER PASTE POISONING”
Place of study: Govt. Stanley medical college, Chennai
I …………………………………….……………………. have been informed about the
details of the study in my own language.
I have completely understood the details of the study.
I am aware of the possible risks and benefits, while taking part in the study.
I agree to collect samples of blood/saliva/urine/tissue if study needs.
I understand that I can withdraw from the study at any point of time and even then, I can
receive the medical treatment as usual.
I understand that I will not get any money for taking part in the study.
I will not object if the results of this study are getting published in any medical journal,
provided my personal identity is not revealed.
I know what I am supposed to do by taking part in this study and I assure that I would
extend my full cooperation for this study.
Volunteer: Witness:
Name and address Name and address
Signature/thumb impression: Signature/thumb impression
95
INFORMED CONSENT
“CLINICAL PROFILE OF RAT KILLER PASTE POISONING”
S NO
A
GE
SEXA
MT
CO
NSU
MED
STOM
AC
H W
ASH
TIME LA
PSE FO
R STO
MA
CH
WA
SHV
OM
ITING
AB
D P
AIN
JAU
ND
ICE
MA
LENA
HE
Hb
-1H
b-3
Hb
-5H
b-7
Hb
-9H
b-11
TB-1
DB
-1TB
-3D
B-3
TB-5
DB
-5TB
-7D
B-7
TB-9
DB
-9TB
-11D
B-11
OT-1
PT-1
OT-3
PT-3O
T-5PT-5
OT-7
PT-7
OT-9
PT-9
OT-11
PT-11
PT-1IN
R-1
PT-3IN
R-3
PT-5IN
R-5
PT-7IN
R-7
PT-9IN
R-9
PT-11IN
R-11
RFT
IF AB
N, U
/CrU
SGC
OU
RSE IN
HO
SPC
AU
SE OF D
EATH
CO
MP
LICA
TION
SD
UR
ATIO
N O
F STAYA
L
12
5M
HA
LFYES
6H
YESYES
NO
NO
NO
14.2
13.6
12.8
2.1
1.3
1.90.2
1.50.2
4522
4032
3528
10.80.7
11.20.7
12.50.9
WN
LN
DISC
H6
22
2M
QU
AR
TERYES
7 H
YESN
ON
ON
ON
O13
.512
.81
31
.20
.11.5
0.31.1
0.120
1528
1430
1711.1
1.0710.9
1.0511.6
1.13W
NL
ND
ISCH
7
32
1M
3 QU
AR
TERSYES
16 H
NO
YESYES
YESN
O12
.311
.811
.511.7
10.52
.51
.45.6
2.68.3
5.111.3
9.215.4
12.6123
96245
136456
289589
326692
36515.3
1.5215.8
1.5716.7
1.6718.6
1.8721
2.14A
BN
52/2.1N
DEA
THC
OA
G+H
E10
43
4F
HA
LFYES
6 H
YESYES
NO
NO
NO
11.2
10.3
11.5
1.5
0.5
1.40.2
1.50.2
4524
3621
2813
10.81.04
11.71.14
10.51.01
WN
LN
DISC
H5
52
8M
HA
LFYES
8 H
NO
NO
NO
NO
NO
12.4
12.6
1.5
0.3
1.10.1
2112
187
10.51.01
10.10.97
WN
LN
DISC
H3
62
3M
QU
AR
TERYES
7 H
YESYES
YESN
ON
O12
.911
.512
.111.2
3.2
1.2
4.63.1
5.13.2
3.11.8
7845
10565
11078
9863
9.90.95
11.11.07
20.42.07
14.71.45
WN
LN
DISC
HC
OA
G8
72
2M
HA
LFYES
11 H
YESYES
NO
NO
NO
11.4
11.6
10.5
11.52
.10
.51.8
0.31.5
0.11.2
0.332
1442
2840
132
2011.1
1.0210.6
1.0211.6
1.131.07
WN
LN
DISC
H7
82
6M
HA
LFYES
8 H
N
OYES
NO
NO
NO
11
10.9
12.3
10
.21.5
0.41.1
0.226
1439
2128
1310.6
1.0212.7
1.2411.9
1.16W
NL
ND
ISCH
6
92
4M
HA
LFYES
5 H
NO
NO
NO
NO
NO
12.9
11.5
0.9
0.2
1.30.05
3413
2811
11.61.12
11.11.02
WN
LN
DISC
H5
10
40
FQ
UA
RTER
YES1
8 HN
ON
ON
ON
OYES
12.2
11.5
11.3
11
11.510.5
1.5
0.4
1.80.2
4.22.1
6.83.5
9.54.1
10.87.8
4521
6532
158104
357123
549254
653414
10.81.04
10.51.01
111.06
13.31.3
15.11.5
15.61.55
WN
LN
DEA
THC
OA
G+H
E12
11
36
MH
ALF
YES1
2 H
YESN
ON
ON
ON
O12
.510
.610
.411.1
2.1
12.8
1.13.4
1.52.5
1.132
1445
1698
5665
4111.6
1.1310.8
1.0417.2
1.7215
1.49W
NL
ND
ISCH
CO
AG
8
12
24
MH
ALF
NO
5 H
YESYES
NO
NO
NO
13.4
12.4
11.9
2.5
1.2
1.90.05
1.50.4
7045
7541
6438
11.21.08
121.17
10.71.03
WN
LN
DISC
H7
13
26
FO
NE
YES1
2 H
YESYES
NO
YESN
O11
.211
.410
.811.1
1.2
0.1
1.80.3
2.41.1
3.51.8
5430
6028
10664
155108
11.11.07
10.51.01
14.21.4
15.31.52
WN
LN
DISC
HH
E10
14
19
F3 Q
UA
RTER
SYES8
H
NO
YESN
ON
ON
O12
.511
.511
.610.8
1.1
0.021.5
0.041.3
0.11.5
1.165
2152
2874
3668
3510.4
19.8
0.9411.2
1.0811.6
1.12W
NL
ND
EATH
PAN
CR
EATITIS
5
15
27
MH
ALF
YES7
HN
ON
ON
ON
ON
O13
.412
.712
.31
0.2
0.90.2
1.30.5
239
3512
248
11.51.11
12.91.26
11.11.07
WN
LN
DISC
H7
16
35
MH
ALF
YES9
H
YESN
ON
ON
ON
O12
.811
.612
.51
.20
.31.5
0.40.9
0.165
2254
2141
2812.7
1.2411.1
1.0212.5
0.9W
NL
ND
ISCH
6
17
32
MH
ALF
YES8
HYES
NY
NO
NO
NO
14.3
12.3
13.5
2.5
11.9
0.51.7
0.336
1248
2548
1813
1.2711.7
1.1412.2
1.19W
NL
ND
ISCH
6
18
28
FH
ALF
YES1
0 H
YESYES
NO
NO
NO
11.6
10.1
11.2
10.91
.81
.12.3
1.31
0.133
1541
1832
1211.1
1.0710.5
1.0112.6
1.22W
NL
ND
ISCH
7
19
25
FQ
UA
RTER
YES1
3 HYES
NO
NO
YESN
O10
.59.5
10.2
11
2.1
1.2
2.91.1
3.51.5
4.82.3
4520
5624
8438
10565
12.21.19
13.51.33
16.11.6
15.41.53
WN
LN
DISC
HC
OA
G8
20
20
MH
ALF
YES5
HN
ON
ON
ON
ON
O13
.512
.212
.12
.50
.62.1
0.31.5
0.136
1242
1545
2312.2
1.1912.4
1.2110.8
1.04W
NL
ND
ISCH
5
21
26
MH
ALF
YES8
HYES
YESN
ON
ON
O13
.212
.912
.50
.90
.21.1
0.21.5
0.445
1548
2446
2111
1.612.1
1.1813.3
1.3W
NL
ND
ISCH
5
22
24
MQ
UA
RTER
YES9
H
NO
YESN
ON
ON
O14
.113
.512
.91
.50
.52.4
1.22.1
1.265
2479
3354
12.51.22
11.71.14
10.91.05
WN
LN
DISC
H7
23
29
FO
NE
YES4
HYES
YESN
ON
ON
O1
211
.610
.510.8
2.1
1.2
3.51.8
5.62.4
4.22.1
7054
8435
10266
9848
11.81.15
12.11.18
131.17
12.11.18
WN
LN
DISC
HH
E8
24
28
FH
ALF
NO
NO
YESN
ON
ON
O11
.510
.510
.61
.80
.51.1
0.21.8
0.732
1245
1250
2413.1
1.2812.2
1.1911.4
1.1W
NL
ND
ISCH
5
25
32
MH
ALF
YES1
3 HN
ON
ON
ON
ON
O12
.611
.310
.411.2
10.91
.10
.23.1
1.45.8
3.18.4
3.911.5
7.426
1254
34157
94204
154304
25411.7
1.1411.3
1.0912.7
1.2410.9
1.0511.9
1.16W
NL
ND
ISCH
HE
12
26
31
MH
ALF
YES1
8 HN
ON
ON
ON
ON
O13
.512
.411
.711.5
12.51
.90
.52.5
1.24.9
2.46.8
314.1
2.256
2168
2494
54170
102102
8410.5
1.0111.5
1.1111.2
1.0712.5
1.111.5
1.12W
NL
ND
ISCH
CO
AG
10
27
35
M3 Q
UA
RTER
SNO
YESYES
NO
NO
NO
12.8
12.1
12.6
0.9
0.1
2.41.1
2.51.2
6631
5428
7231
12.11.18
18.21.83
18.61.87
15.81.57
WN
LN
DISC
HC
OA
G+H
E8
28
24
MH
ALF
YES6
HYES
NO
NO
NO
NO
11.5
10.6
9.51
.50
.42.1
1.22
1.432
925
838
1312.7
1.2411.6
1.1311.9
1.16W
NL
ND
ISCH
7
29
28
MQ
UA
RTER
YES1
2 H
YESYES
NO
NO
NO
13.5
12.6
12.5
13.212.8
12.51
.20
.62.5
1.23.5
1.86.5
2.58.5
3.85.5
2.465
2488
35157
104225
128398
154245
12010.8
1.0414.5
1.4317.1
1.7119.9
2.0214
1.3914.3
1.41W
NL
ND
ISCH
CO
AG
14
30
36
MQ
UA
RTER
YES5
HN
OYES
NO
NO
NO
10
11.5
12
1.8
0.2
2.10.9
1.80.9
7045
6242
6854
11.51.11
12.511.22
12.41.21
WN
LN
DISC
H5
31
19
FH
ALF
NO
YESYES
NO
NO
NO
10.2
1111
.610.8
2.4
1.4
2.81.5
3.82.4
5.82.9
3.42.1
8854
154102
187124
206154
10211.3
1.0910.5
1.0111.2
1.0811.5
1.112.4
1.21W
NL
ND
ISCH
HE
12
32
28
FH
ALF
YES9
H
NO
NO
NO
NO
NO
11.5
12.5
12.4
1.9
0.5
2.51.4
1.82.4
1.254
3248
2436
2112.5
1.2213.4
1.3212.9
1.25W
NL
ND
ISCH
6
33
30
MO
NE
YES6
HYES
NO
NO
NO
NO
12.8
13.5
13.4
12.80
.90
.22.5
1.15.8
2.98.5
5.454
23105
74354
179547
24813.5
1.3317.2
1.7218.6
1.8719
2W
NL
ND
ISCH
CO
AG
+HE
8
34
31
MQ
UA
RTER
YES1
5 HN
OYES
NO
NO
NO
12
12.5
12.3
13.21
.20
.51.8
0.42.9
1.53.4
2.475
54108
65182
104254
14210.5
1.0111.3
0.812.7
1.2311.5
1.11W
NL
ND
EATH
HE
7
35
26
F3 Q
UA
RTER
SNO
YESN
ON
ON
ON
O13
.412
.911
.610.8
11.20
.90
.41.2
0.42.3
1.13.5
2.23.1
2.345
2356
2191
66152
98254
12411.1
1.0213.7
1.3515.4
1.5318
1.8120.6
2.09W
NL
ND
EATH
CO
AG
+ HE
10
36
27
MQ
UA
RTER
YES8
HN
OYES
NO
NO
NO
14.2
14.2
13.4
1.7
0.5
2.11.1
1.90.5
3212
3614
2911
12.31.2
13.51.33
12.21.19
WN
LN
DISC
H7
37
22
FQ
UA
RTER
YES5
HN
ON
ON
ON
ON
O11
.210
.510
.410.5
1.5
0.8
2.51.1
2.81.8
3.51.5
6538
7225
10578
8424
16.11.6
17.11.71
15.31.52
17.81.79
WN
LN
DISC
HC
OA
G+H
E10
38
32
MH
ALF
YES8
HYES
NO
NO
NO
NO
12.8
11.9
10.9
11
1.4
0.7
1.30.4
1.50.2
4519
4221
4818
10.51.01
10.61.02
11.61.3
WN
LN
DISC
H5
39
45
MH
ALF
NO
NO
NO
NO
NO
NO
13.5
12.5
11.6
0.8
0.1
1.90.5
2.41.2
1.91
5423
8839
12584
10875
11.61.12
10.81.04
11.11.02
12.71.24
WN
LN
DISC
HH
E8
40
54
FH
ALF
NO
YESN
ON
ON
ON
O12
.611
.810
.91
.50
.41
.020.3
1.50.5
1.30.4
2512
4523
4836
5624
10.61.02
12.81.25
11.71.14
12.21.19
WN
LN
DISC
H10
41
32
MH
ALF
YES4
HYES
YESN
ON
ON
O1
211
.812
.21
.20
.71.6
0.92.2
1.434
2379
4389
3215.3
1.5215.8
1.5716.7
1.67W
NL
ND
ISCH
6
42
56
MQ
UA
RTER
YES6
HYES
YESN
ON
ON
O11
.412
11.8
0.9
0.4
1.30.7
2.21.3
4227
10289
9865
10.81.04
11.71.14
10.51.01
WN
LN
DISC
H6
43
21
M3 Q
UA
RTER
SYES8
HN
ON
ON
OYES
NO
11
10.2
9.69
.41
.40
.62.1
1.43.4
2.12.9
1.756
21189
103245
189160
10211.5
1.1112.51
1.2212.4
1.21W
NL
ND
ISCH
8
44
18
FH
ALF
YES2
HN
ON
ON
ON
ON
O9
.29.6
9.41
.10
.71.1
0.61.2
0.723
2154
3643
2211.3
1.0910.5
1.0111.2
1.08W
NL
ND
ISCH
5
45
34
FH
ALF
YES6
HYES
YESN
ON
ON
O10
.711
11.3
1.6
0.8
21.3
2.61.5
4240
4740
4342
12.51.22
13.41.32
12.91.25
WN
LN
DISC
H6
46
44
MTW
ON
OYES
YESN
OYES
YES14
.613
.813
.22
.11
.43.2
2.16.4
4.6240
170310
306108
7912.5
1.2211.7
1.1410.9
1.05W
NL
ND
EATH
HE
6
47
32
FO
NE
YES7
HN
ON
ON
ON
OYES
11.6
12.3
12
11.91
.40
.62.2
1.35.6
3.28.1
4.851
38230
1981210
890704
65011.8
1.1512.1
1.1813
1.17W
NL
ND
ISCH
8
48
21
MH
ALF
YES2
HN
ON
ON
ON
ON
O12
.912
.40
.90
.61
0.41.2
0.634
2345
4158
3413.1
1.2812.2
1.1911.4
1.1W
NL
ND
ISCH
4
49
26
MH
ALF
YES2
HN
ON
ON
ON
ON
O13
.213
1.1
0.5
1.10.6
1.20.7
4238
4024
5237
11.81.15
12.11.18
131.17
WN
LN
DISC
H5
50
29
FH
ALF
YES8
HN
ON
ON
OYES
NO
11
11.6
11.4
11.61
.50
.91.9
0.73.1
2.14.2
2.956
45230
179306
27986
4013.1
1.2812.2
1.1911.4
1.1W
NL
ND
ISCH
8
51
31
FQ
UA
RTER
YES4
HYES
YESN
ON
ON
O10
.611
11.2
0.9
0.4
1.30.4
21.3
3420
5138
4024
11.71.14
11.31.09
12.71.24
WN
LN
DISC
H6
52
19
MQ
UA
RTER
YES2
HYES
YESN
ON
ON
O1
111
.51
11
0.5
1.20.4
1.20.5
3621
4027
4125
10.51.01
11.51.11
11.21.07
WN
LN
DISC
H5
53
25
M3 Q
UA
RTER
SNO
NO
NO
NO
YESYES
13.2
11.6
11.2
2.4
1.5
3.52.4
6.84.5
208196
320313
10298
12.11.18
18.21.83
18.61.87
WN
LN
DEA
THH
E7
54
24
MO
NE
YES5
HYES
YESN
ON
ON
O12
.812
.412
.31
.30
.71.9
13.2
1.854
34102
9665
4512.7
1.2411.6
1.1311.9
1.16W
NL
ND
ISCH
6
55
32
MO
NE
YES1
3HN
OYES
NO
NO
YES14
.614
14
13.813.6
132
.21
.24.2
2.87.1
3.911.2
6.412.6
7.413
8.289
56623
5111230
975980
711710
625320
27910.8
1.0414.5
1.4317.1
1.71W
NL
ND
EATH
HE
125
56
45
MH
ALF
YES3
HYES
NO
NO
NO
NO
12.7
12.3
12.4
0.9
0.4
1.20.3
1.50.9
4328
5632
4022
11.51.11
12.511.22
12.41.21
WN
LN
DISC
H6
57
50
FQ
UA
RTER
YES8
HYES
YESN
ON
ON
O10
.911
11
11.21
0.6
1.80.9
2.31.3
3.42
3228
10298
202178
8243
11.31.09
10.51.01
11.21.08
WN
LN
DISC
H6
58
25
MQ
UA
RTER
YES6
HN
ON
ON
ON
ON
O12
.611
.81
21
.60
.72
1.14.5
2.765
2388
2943
3412.5
1.2213.4
1.3212.9
1.25W
NL
ND
ISCH
7
59
27
FH
ALF
NO
YESYES
NO
NO
YES9
.29.8
9.89
.32
.51
.44.4
38.2
5.110.2
6.1121
98356
287789
650210
20713.5
1.3317.2
1.7218.6
1.87W
NL
ND
EATH
CO
AG
+HE
6
60
43
MH
ALF
YES2
HN
ON
ON
ON
ON
O13
.413
.21
30
.80
.41.3
0.91.4
0.643
3463
4542
2113.1
1.2812.2
1.1911.4
1.1W
NL
ND
ISCH
5
61
45
M3 Q
UA
RTER
SYES5
HYES
YESN
OYES
NO
14
13.2
13
1.2
0.6
1.80.8
2.21.5
5138
9073
4835
10.80.7
11.20.7
12.50.9
AB
N68/2.6
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5
62
32
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NE
YES4
HN
ON
ON
ON
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O10
.811
11.3
1.7
0.9
1.81
1.91.2
6447
7865
8966
11.11.07
10.91.05
11.61.13
WN
LN
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H6
63
35
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ALF
YES6
HYES
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ON
ON
O13
.513
.213
.21
.80
.92.2
1.24.5
2.745
34320
278180
10715.3
1.5215.8
1.5716.7
1.67W
NL
ND
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7
64
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.612
.812
.60
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0.61.4
0.832
2345
2843
2111.6
1.1310.8
1.0417.2
1.72W
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8
65
25
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NE
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ON
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O10
.211
11.3
1.1
0.6
1.30.6
1.30.6
5637
4534
4024
11.21.08
121.17
10.71.03
WN
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H6
66
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UA
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9.6
10.2
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10.210
10.22
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1.87.2
4.79.6
5.49
4.99.2
565
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111823
678675
589486
402380
30912.5
1.2211.7
1.1410.9
1.05W
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116
67
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.912
12.4
0.9
0.4
1.20.5
2.10.9
4532
4430
6732
10.61.02
12.71.24
11.91.16
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68
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.611
.411
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10
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0.71.9
0.82.2
1.348
23102
7898
6354
4311.6
1.1211.1
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4
69
29
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.213
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0.91.8
160
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3110.8
1.0410.5
1.0111
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5
70
19
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.812
.612
.81
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.71.1
0.61.3
0.745
2252
3445
3211.6
1.1310.8
1.0417.2
1.72W
NL
ND
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5
71
23
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.612
.812
.61
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12.2
1.472
4370
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1.0812
1.1710.7
1.03W
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6
72
43
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NO
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13.5
13.2
13.2
13.11
.40
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1.15.2
36.4
4.243
32120
98550
450230
18712.5
1.2211.7
1.1410.9
1.05W
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6
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10.7
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111.2
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2.59.2
5.48.4
4.39.6
5.210.2
6.3110
98345
230550
4981290
897875
597320
30811.8
1.1512.1
1.1813
1.17W
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ND
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127
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33
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.210
.71
010.2
2.1
1.3
3.82.1
117.4
10.45.6
9878
14093
220176
10298
13.11.28
12.21.19
11.41.1
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21
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2.654
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1.0111.5
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11.2
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1.8318.6
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11.61.13
11.91.16
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.612
12.6
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11.60
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1.43.1
22.7
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1.42.2
1.410.8
1.0414.5
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116
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0.41.9
0.813.5
1.3317.2
1.7218.6
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0.960
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1.111.4
1.114.5
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11.6
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1.2211.6
1.1314.8
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11.33
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1.32.5
1.11.5
0.6258
156234
144189
13266
5312.6
1.2317.9
1.7915.2
1.5114.6
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.912
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0.6
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1.20.6
4549
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9.40.9
14.31.41
WN
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85
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12.8
12.4
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1.60.7
278234
180160
135121
12.71.24
15.61.55
15.11.5
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86
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10.30.99
151.49
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14.7
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2.616
11.3
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124163
762853
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18.11.82
22.022.27
17.31.73
16.21.61
15.81.57
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1.81.9
0.766
73120
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1.5123.1
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.814
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2.67.6
3.386
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13311.5
1.1114.2
1.414.6
1.44W
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6
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.210
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1.12.4
1.556
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8614.5
1.431.45
1.515.6
1.55W
NL
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7
91
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13.6
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2.6
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4.11.8
2.31.7
6882
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10.30.9
11.21.08
12.61.23
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92
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2.51.4
220261
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16.71.6
222.25
16.21.61
15.81.57
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93
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.212
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2.9
1.4
4.32.4
5.13.2
16.210.6
168189
984789
1240956
1023762
10.41
21.22.16
222.27
181.81
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94
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.613
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11.31
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4.22.8
12
.68.3
18.412.4
16.211.7
99124
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11131256
760659
158143
13.31.3
14.61.4
18.51.86
16.31.62
15.51.54
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95
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1.52.4
1.142
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1.0411
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96
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.815
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1.6
0.8
2.71.8
5.63.1
5.42.7
188163
12581136
690731
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9.40.9
14.61.44
14.11.39
13.81.38
WN
LN
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97
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NE
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14.4
13.9
13.312.8
12.61
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.94.5
2.61
0.6
5.716.4
11.213.6
9.112.5
8.8256
3241620
15731362
1249853
679137
108128
9914.5
1.4318.6
1.8616.2
1.614.9
1.4713.8
1.3614.2
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12
98
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.712
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2.28.4
3.579
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901244
15312.2
1.1913.2
1.2912.6
1.23W
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ND
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HE
6
99
25
FH
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NO
NO
NO
NO
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14.1
13.8
13.4
0.9
0.5
3.51.9
2.31.1
4435
325290
6559
13.11.28
12.71.24
14.11.39
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100
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11
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3.74.2
2.21.9
1.175
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308638
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9214.8
1.4613.4
1.3115.2
1.5113.8
1.36W
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8
101
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NE
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13.6
11.3
10.5
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1.0520.1
2.0419
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102
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.312
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1.32.7
1.264
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1.2912.4
1.2212.7
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5
103
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.111
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2.22.9
1.549
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199140
12112.2
1.1913.6
1.3412.5
1.22W
NL
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5
104
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UA
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11.9
11.4
10.6
10.11
.91
.13.3
1.85.7
3.64.2
2.177
93644
582227
17685
7917.1
1.718
1.816.5
1.613.5
1.33W
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8
105
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.913
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0.72.6
1.351
43294
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6310.9
1.0512.1
1.1812.7
1.24W
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6
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.112
.511
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1.12.4
1.463
52120
11671
6615.3
1.5213.6
1.3412.4
1.21W
NL
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6
107
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FH
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NO
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12.8
12.3
11.8
11.41
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.63.6
1.32.6
1.154
63369
30857
72144
1.4113
1.2713.2
1.29W
NL
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5
108
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.311
.811
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10.11
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3.31
6.8
11.2
20.212.6
21.914.6
13099
699734
16081600
620494
105136
14.21.4
22.62.3
17.41.7
16.612.1
16.111.8
WN
LN
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HH
E10
109
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.314
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.613.1
1.7
0.9
5.63.2
7.74.4
4.32.7
167181
443411
182169
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14.31.41
17.21.72
16.81.68
15.61.55
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110
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1.11.4
0.882
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1.1811.9
1.1611.3
1.09W
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111
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.513
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1.72.5
1.232
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12257
7610.9
1.0511.2
1.0810.1
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5
112
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NE
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.414
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1.9
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4.62.5
181
1.317.5
10.2193
163831
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607152
18513.5
1.319.4
1.916
1.616
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NL
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8
113
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.111
.210
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4.21
2.3
7.914.1
9.111.8
6.5271
2991684
1402622
676118
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2.118.6
1.8115.3
1.514.7
1.4214.1
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1.350
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1.1312.6
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116
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.413
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9.34.2
8.33.9
187202
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351426
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19.92.02
16.41.6
14.51.41
14.31.4
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119
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6182
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12.91.26
11.31.09
11.91.16
WN
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120
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2.81.5
5949
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11.51.11
121.17
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121
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13.8
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0.10.9
0.11.3
0.2178
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1.2211.2
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1.31W
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2.15.5
3.58.5
4.19.5
5.511.5
148114
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467256
546305
12.51.22
13.81.36
14.31.41
15.31.52
16.81.68
15.31.52
WN
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123
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12.5
12.7
11.2
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10.1
2317
2014
1811
13.21.29
11.91.16
10.41
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124
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.312
.211.8
1.2
11.9
1.12.2
1.32.1
0.938
2447
3242
2454
3411.5
1.0612.5
1.213.1
1.2812.4
1.21W
NL
ND
ISCH
8
125
22
FH
ALF
YES8
HN
OYES
NO
NO
NO
11.2
1111
.51
.20
.20.9
0.11.1
0.121
1425
1822
1415.2
1.5113.3
1.311.5
1.1W
NL
ND
ISCH
6
126
24
MH
ALF
NO
NO
NO
NO
NO
NO
14.2
13.8
13.4
2.1
1.1
2.91.5
3.11.9
11085
125110
12395
10.30.9
11.51.11
12.21.19
WN
LN
DISC
H6
127
35
MQ
UA
RTER
NO
YESYES
NO
NO
NO
12.1
1211
.812.3
1.1
0.4
2.31.5
3.61.4
2.51.1
9565
125104
158120
188142
13.31.3
12.71.24
11.51.11
14.61.44
WN
LN
DISC
HC
OA
G8
128
26
MH
ALF
NO
NO
YESN
ON
ON
O1
110
.912
.31
0.2
1.50.4
1.10.2
2614
3921
2813
10.61.02
12.71.24
11.91.16
WN
LN
DISC
H6
129
24
MH
ALF
YES5
HN
ON
ON
ON
ON
O12
.911
.50
.90
.21.3
0.534
1328
1111.6
1.1211.1
1.02W
NL
ND
ISCH
5
130
22
MH
ALF
YES1
1 HYES
YESN
ON
ON
O11
.411
.610
.511.5
2.1
0.5
1.80.3
1.50.2
1.10.3
3214
4228
4012
3220
11.11.02
10.61.02
11.61.13
11.11.07
WN
LN
DISC
H7
131
30
MQ
UA
RTER
YES6
HYES
NO
NO
NO
NO
14.8
12.5
14.5
1.2
0.2
1.60.2
1.10.2
6532
5832
5824
11.51.11
10.81.04
12.511.22
WN
LN
DISC
H6
132
22
FQ
UA
RTER
YES1
0HN
ON
ON
ON
ON
O12
.610
.411
.42
.11
1.80.9
21.1
12575
14792
9458
11.71.14
12.91.26
12.51.22
WN
LN
DISC
H5
133
40
F3 Q
UA
RTER
SYES5
HN
OYES
NO
NO
NO
12.6
10.5
11.5
11.22
.51
.23.5
2.13.8
24
2.5154
102215
120389
124531
35414.1
1.3912.9
1.2614.6
1.4411.6
1.13W
NL
ND
ISCH
9
134
24
MQ
UA
RTER
YES8
HYES
NO
NO
NO
NO
11.5
10.5
10.2
0.9
0.1
10.2
1.40.4
3314
3624
4235
11.61.13
131.27
14.21.4
WN
LN
DISC
H6
135
35
FH
ALF
YES6
HN
ON
ON
ON
ON
O11
.612
.411
.512.1
2.4
1.2
2.81.1
3.41.5
2.61.2
8872
7854
8252
7654
13.51.33
14.91.47
13.31.3
12.51.22
WN
LN
DISC
HH
E8
136
27
MQ
UA
RTER
YES9
H
YESN
ON
ON
ON
O13
.812
.114
.11
.20
.21.1
0.21.3
0.232
2038
2130
2113.6
1.3411.8
1.1511.1
1.07W
NL
ND
ISCH
5
137
22
MO
NE
YES4
HN
ON
ON
ON
ON
O13
.113
.512
.12
.81
.13
1.52.9
1.598
65102
74115
8015.2
1.5112.8
1.2511.5
1.11W
NL
ND
ISCH
7
138
32
MH
ALF
YES1
1 HYES
NO
NO
NO
NO
14.1
13.5
14.1
10
.11.5
0.51.1
0.347
2538
2247
2112.1
1.1811.1
1.0712.5
1.22W
NL
ND
ISCH
6
139
28
MO
NE
YES2
4 HN
OYES
NO
NO
NO
11
12.9
13.7
12.111.2
3.5
2.1
4.52.1
6.23.5
6.64.1
8.14.5
540354
647421
702604
904540
854587
15.41.53
16.51.65
17.61.77
19.82
20.52.08
AB
N78 /2.1
ND
EATH
CO
AG
+HE
14
140
21
FQ
UA
RTER
YES6
HYES
NO
NO
NO
NO
11.7
10.7
11.9
1.9
0.2
1.80.5
2.11.5
7852
6624
8054
12.11.18
11.41.1
12.81.25
WN
LN
DISC
H6
141
32
M3 Q
UA
RTER
SYES9
H
YESYES
NO
NO
NO
13.7
12.9
13.1
14.12
.91
.23
1.53.1
1.93.2
2114
85130
98145
124185
12414.1
1.3911.7
1.1413.1
1.2814.5
1.43W
NL
ND
ISCH
8
142
24
MH
ALF
YES4
HN
ON
ON
ON
ON
O11
.612
.112
.11
.90
.51.8
0.52
1.145
2357
2365
3813.8
1.3611.7
1.1412
1.17W
NL
ND
ISCH
6
143
21
FH
ALF
YES6
HYES
NO
NO
NO
NO
10.2
11.2
10.2
1.2
0.1
1.10.1
1.20.2
7545
6625
8541
13.11.28
12.81.25
10.20.98
WN
LN
DISC
H5
144
22
FQ
UA
RTER
YES4
HYES
NO
NO
NO
NO
11.5
11.1
0.9
0.2
11
.10.1
4520
3821
11.51.11
11.21.08
WN
LN
DISC
H4
145
27
MO
NE
YES8
HN
ON
ON
ON
ON
O13
.213
.112
.81
.30
.11.1
0.21.2
0.355
2348
2668
4213.1
1.2812.8
1.2513.1
1.28W
NL
ND
ISCH
5
146
33
MH
ALF
YES2
4 HYES
NO
NO
NO
NO
13.9
14.2
14.6
2.1
1.1
1.90.8
20.9
6527
7234
8541
11.11.07
11.31.09
12.21.19
WN
LN
DISC
H5
147
30
FO
NE
YES7
2 HYES
YESYES
YESYES
12.9
11.8
12
12.210.8
27.6
13.2
27
.813
.72
8.8
13.4
28.815.6
2914.5
1022798
1098756
1170879
1202978
25.22.6
22.82.33
23.52.41
26.52.75
WN
LN
DEA
THC
OA
G+H
E15
148
33
MQ
UA
RTER
YES1
0 H
YESN
ON
ON
ON
O14
.814
.613
.813.5
2.1
1.1
2.81.5
3.42.1
3.81.7
313240
358245
462220
689354
11.91.16
12.91.26
13.81.36
13.51.33
WN
LN
DISC
HC
OA
G10
149
29
FH
ALF
YES8
HN
OYES
NO
NO
NO
11.8
11.7
12.8
13.13
.11
.83.1
1.72.9
1.42.8
1.2145
112134
10488
5174
5412.1
1.1813.1
1.2812.5
1.2213.5
1.33W
NL
ND
ISCH
HE
7
150
42
MH
ALF
YES1
0 H
YESN
ON
ON
ON
O14
.914
.714
.12
.21
.21.5
0.81.7
0.6446
285354
247254
11011.7
1.1412.4
1.2112.8
1.25W
NL
ND
ISCH
8
151
45
MH
ALF
YES1
1 HYES
YESN
ON
ON
O13
.212
.713
.11
.50
.41.7
0.52.1
1.1145
101124
85114
8410.8
0.712.2
1.1911.7
1.14W
NL
ND
ISCH
6
152
25
M3 Q
UA
RTER
SYES4
HN
OYES
NO
NO
NO
14.2
13.9
14
2.4
1.2
2.31.4
3.11.5
154120
164102
11478
11.51.11
11.11.02
10.81.04
WN
LN
DISC
H7
153
28
MH
ALF
YES1
8 HYES
YESN
ON
ON
O12
.213
.213
.112.9
2.1
12
0.81
3.1
1.412.9
1.4112
85100
7298
63104
6512
1.1710.5
1.0110.9
1.0513.5
1.33W
NL
ND
ISCH
PAN
CR
ETITIS8
154
21
FQ
UA
RTER
NO
10 H
YES
NO
NO
NO
NO
10.2
11.1
10.2
1.7
0.9
1.69
0.81.8
1.149
2545
2156
2811.7
1.1412.2
1.1912.4
1.21W
NL
ND
ISCH
8
155
33
MH
ALF
YES6
HN
OYES
NO
NO
NO
14.2
14.7
14.3
1.2
0.1
10.2
10.3
3314
3518
2911
11.30.8
15.41.53
11.781.14
WN
LN
DISC
H7
156
26
FO
NE
NO
YESYES
YESYES
NO
10.2
10.2
11
10.95
.43
.56.8
3.87.9
3.77.5
3.4546
321629
438854
531845
48717.2
1.7215.1
1.4916.1
1.618.7
1.88W
NL
ND
ISCH
CO
AG
10
157
35
M3 Q
UA
RTER
SNO
YESN
ON
ON
ON
O13
.513
.212
.91
.70
.52.1
1.12.1
1.273
6826
5727
10.61.02
11.11.03
11.11.07
WN
LN
DISC
H5
158
28
FQ
UA
RTER
YES6
HYES
YESN
ON
ON
O12
.913
.113
.21
.50
.51.2
0.41.1
0.265
2456
2154
1810.5
1.0111.2
1.0811.7
1.14W
NL
ND
ISCH
8
159
22
FH
ALF
YES9
H
NO
YESN
ON
ON
O11
.110
.810
.52
.51
.22.3
1.12.8
1.7116
78102
6498
5811.7
1.1411.5
1.1212.7
1.24W
NL
ND
ISCH
7
160
28
MH
ALF
YES1
1 HYES
NO
NO
NO
NO
13.4
13.5
12.8
12.13
.51
.44.5
2.44.9
1.94.1
1.2284
115305
145450
185387
15416.5
1.6517.8
1.7918.4
1.8515.3
1.52W
NL
ND
ISCH
CO
AG
9
161
31
MQ
UA
RTER
YES8
HYES
NO
NO
NO
NO
13.4
12.8
11.8
1.7
1.1
1.90.4
2.10.5
8925
9845
7523
13.11.28
15.41.53
10.51.01
WN
LN
DISC
H5
162
28
MH
ALF
YES1
1 HN
ON
ON
ON
ON
O11
.712
.311
.92
.11
.11.9
0.41.8
0.456
2168
1454
1314.6
1.4411.5
1.1113.1
1.28W
NL
ND
ISCH
5
163
34
F3 Q
UA
RTER
SYES1
8 HYES
NO
NO
NO
YES12
.111
.511
.82
.21
.13.4
1.72.8
1.4154
85198
102187
7413.6
1.3414.1
1.3912.5
1.22W
NL
ND
EATH
HE
6
164
21
FO
NE
YES1
7 HYES
YESN
OYES
YES11
.510
.711
.110.5
11.12
.81
.43.4
2.14.5
2.45.5
2.87.4
3354
124586
184789
205989
3541054
54619.1
1.9318.6
1.8720.7
2.122.9
2.3524.5
2.52W
NL
ND
EATH
HE+C
OA
G11
165
29
MH
ALF
YES6
HN
OYES
NO
NO
NO
12.5
11.9
11.7
2.1
1.4
1.91.1
1.80.4
4218
4611
389
15.41.53
12.11.18
14.71.45
WN
LN
DISC
H5
166
24
MH
ALF
YES8
HN
ON
ON
ON
ON
O11
.410
.511
.71
.10
.11.8
1.12.1
1.4102
6595
6489
5414.2
1.411.5
1.1113.4
1.31W
NL
ND
ISCH
6
167
19
FQ
UA
RTER
YES1
1 HYES
NO
NO
NO
NO
12.4
11.9
13.1
12.51
.10
.41.9
0.42.8
1.42.9
1.578
45125
84168
102204
11414.7
1.4515.3
1.5215.8
1.5718.5
1.86W
NL
ND
ISCH
CO
AG
+HE
8
168
27
FH
ALF
YES8
HN
OYES
NO
NO
NO
12.5
11.4
11
2.5
1.2
2.81.2
3.51.4
15498
12387
204114
14.11.39
13.51.33
12.81.25
WN
LN
DEA
THPA
NC
REA
TITIS5
169
35
M3 Q
UA
RTER
SYES4
HN
ON
ON
ON
ON
O13
.112
.511
.51
.10
.21.8
0.42
1.156
1248
1159
2213.6
1.3412.1
1.1812.5
1.22W
NL
ND
ISCH
5
170
40
MH
ALF
YES9
H
NO
NO
NO
NO
NO
12.4
11.2
11.4
2.4
1.1
2.51.1
1.91
10265
8941
8848
13.91.37
11.51.11
12.21.19
WN
LN
DISC
H6
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