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VOLUME 14 ISSUE 02 JULY-DEC 2018
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CONTENTS
EDITORIAL
Be aware of predators!!
ARTICLES
- Eni-yimini Solomon Agoro, Mieebi Marn Wankas
- Muzzafer Mohammad Mir, Mir Bilal, Zahoor Ahmad Parry, Ursilla Taranum, Mir Inkhab
- Somashekhar S. Pujar, Kashif Ali, Ravindra S. Honnungar, Prasanna S. Jirli,
Khaja Azizuddin Junaidi, Pushpa M.G.
- Varsha Dhurvey, Bhawna Gotmare, Firdos Karim
- Shubneet Kaur, Praveen Kumar Yadav
- Vivekanshu Verma, Prateek Rastogi, Devendra Richhariya, Ajay Thapa, Punidha Kaliaperumal,
Chidrupi Sharma,
- Anita Yadav, Rajkumar Dahiya, Jagdish Ram Bhargav, Adarsh Kumar,
Madhulika Sharma, RK Sarin
- Rajashree Khot, Ameya Bhis, Rakhee Josh, Nilima Pal Ambade
- Anupama Mauskar, Nusrat Inamdar, Carpurgaur Shirsat
IX
EDITORIAL
Be aware of predators!!
X
Editor
The Journal of Indian Society of Toxicology
Consequences
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ISSN: 0973-3558, e-ISSN: 0973-3566
Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
DOI: 10.31736/jist/v14.i2.2018.12-16
Eni-yimini Solomon Agoro
1Department of Biochemistry Federal University, Otuoke Bayelsa State, Nigeria,
2The Department of Medical Laboratory Science, Niger Delta University, Wilberforce Island, Bayelsa State, Nigeria.
Biochemical Parameters in Rabbits
Declared none
ABSTRACT
Carbon monoxide (CO) is a toxic gas that escapes easy detecon
due to its euphoric nature. It ulizes hypoxia in causing
mortality or morbidity. The study was aimed at evaluang the
eect of chronic CO concentraon (>200 ppm) in some liver
biochemical parameters ulizing rabbit as a choice animal
model. A total twenty (20) apparently health albino rabbits
constuted the sample size as validated by mead’s equaon.
The animals were divided into four groups of ve rabbits
each. The rst group constuted the controls, the remaining
groups constuted rabbits exposed thirty minutes daily to
CO for 10th, 20th and 30th respecvely. Blood samples were
extracted from the hearts of the animals for the analysis of
liver enzymes, proteins and bilirubin. One way anova (pos hoc-
LSD) was used for the stascal analysis with level of signicant
considered at > 0.05. The study showed that serum aspartate
aminotransferases (AST), alanine aminotransferases (ALT),
alkaline phosphatase (ALP), total and conjugated bilirubin and
albumin/glibulin rao increased signicantly (p>0.05) across
the duraons of exposure. On the contrary, serum total protein
and globulin decreased signicantly (p>0.05). The ndings
revealed that chronic inhalaon of CO could have a long term
negave consequence on the liver.
AST,
ALT,
ALP,
Bilirubin,
proteins, CO.
Received on 5th October 2018
Accepted on 28th December 2018
Published on 31st December 2018
©2018 The Journal of Indian Society of Toxicology.
Published at JIPMER, Pondicherry, 605006, INDIA Subscripon & payment related
queries at: toxicology@aims.amrita.edu and rest all types of queries related to the
journal to be done at drambika_editor@jist.org.in
ARTICLE INFO
Enis Biomedicals (eBm) LTD, Igbogne
Epie, Yenagoa, Bayelsa State, Nigeria; E-mail: siragoro@yahoo.
com: Tel.: 08037434995.
How to Cite this arcle:Agoro ES, Wankasi MM. The Eects
of Chronic Carbon Monoxide Intoxicaon on some liver
Biochemical Parameters in Rabbits. Journal of Indian Society of
Toxicology 2018;14(2):12-16.
INTRODUCTION
Carbon monoxide (CO) is a poisonous non-irritant gas
produced as a result of incomplete combuson of organic
materials due to insucient supply of oxygen. It displaces
oxygen from binding to haemoglobin in the circulatory
system, hence resulng to asphyxic and subsequent
hypoxia that usually result to the collapse of the respiratory
system. Carbon monoxide not only decreases the oxygen
content of blood, but also decreases oxygen availability
to ssues, thereby producing a greater degree of ssue
hypoxia than equivalent reducon in oxyhaemoglobin
caused by hypoxia.1 Carbon monoxide also binds to other
heme proteins, such as myoglobin and mitochondrial
cytochrome oxidase a3, which limits oxygen use when
ssue paral oxygen pressure (PO2) is very low. Organs
with high oxygen demand, such as the heart and brain,
are most sensive to hypoxia and account for the major
clinical sequelae of carbon monoxide poisoning.2 Others
less impacted are lungs, liver and spleen.2 If concentraon
of CO concentraon exceeds 100 ppm, it can be
dangerous for humans. Symptoms of CO poisoning may
include headache, sweang, dizziness, dim vision, tremor
and loss of consciousness.3 Rabbit was the choice animal
model for the research work. The suitability of rabbit as a
choice animal for this study is aributed to its anatomical
The Eects of Chronic Carbon Monoxide Intoxicaon on some liver Biochemical Parameters in Rabbits
ISSN: 0973-3558, e-ISSN: 0973-3566
Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
and physiological similaries to human.4,5 The liver carries
out several important funcons that involve excretory,
synthec or detoxifying mechanisms. Liver funcon tests
are groups of blood tests that give informaon about
the state of the liver.6 A liver funcon test used for this
study includes total protein, albumin, globulin, aspartate
and alanine aminotransferases, bilirubin and alkaline
phosphatase. These biochemical parameters give a
clearer picture of the hepatocellular and biliary axis of the
liver status. Distorons in these biochemical parameter’s
concentraons and acvies point to a compromised
liver. Nigerians are exposed to varying degrees of CO
due to the high demand for CO-producing machines and
equipment. A deliberate study of the eect of chronic
exposure to CO on liver biochemistry could possibly
open up unknown pathophysiology of some idiopathic
diseases. The products of the ndings could be useful in
policy shaping in combang chronic diseases, prevenng
avoidable epidemics and enhancing Medicare. The
eects of CO on a lot of organs, ssues and cells have
been studied by handful of researchers with ndings
implicang CO.7,8,9,10,11,12 Carbon monoxide mechanism
of acon is primarily through starvaon of organs of
oxygen. Most organs survival is basically depended on
the regular supply of oxygen; hence any denial could be
deleterious. Liver is the center of metabolic processes
and usually need regular supply of oxygen. This study is
aimed basically to reveal the possible eect of chronic CO
intoxicaon on the biochemical parameters that is used
to evaluate the integrity and status of the liver.
MATERIALS AND METHODS
Study Area
The CO intoxicaon aspect of the study was carried out
at the fringe of Epie Creek secon of Igbogene Epie in
Bayelsa State Nigeria. Similarly, the Chemical Pathology
Laboratory of the Niger Delta University Teaching Hospital
Okolobiri, Bayelsa State served the biochemical analysis.
Study Populaon
The strength of the sample size of the study was derived
from Mead’s resource equaon.13 A total of twenty (20)
albino rabbits constuted the sample size. The study
involved a chronic exposure of study animals to daily
thirty minutes of mild concentraon of carbon monoxide
for a minimum of ten days and maximum of 30 days. The
rabbits were divided into four groups. The rst group
constuted the controls which were not exposed to
CO prior to mechanical sacrice. The remaining three
groups (10th, 20th and 30th) were exposed to CO for 30
minutes daily for ten days, twenty days and thirty days
respecvely. The daily exposure of CO concentraon was
pegged not more than 200 ppm as dened by Golden,14
and Strumann et al.15 for chronic CO intoxicaon study.
The carbon monoxide gas was obtained from a portal
Sumac generang set.
Ethical Approval
The ethical clearance and experimental protocol were
approved by the Ethics Commiee of the Bayelsa State
Ministry of Health. The Animal Welfare Act of 1985 of the
United States of America for research and Instuonal
Animal Care and Use Commiee (IACUC) protocols were
stringently adhered to.16
Selecon Criteria
Rabbits used were apparently healthy and acve as
conrmed and approved by a veterinary doctor. Rabbits
showing signs or symptoms of illness were excluded from
the research. Lysed blood samples were also rejected.
The research ulized only male albino rabbits of same
age and weight. The age range was between six to eight
months. The weight brackets were 1.5-2kg.
Collecon of Blood Samples
Blood samples were collected from the heart using the
method postulated by Ness.17 Blood was withdrawn
slowly into the appropriate containers to prevent the
heart from collapsing. The blood samples collected were
dispensed into plain containers, allowed to clot and then
separated for the biochemical analysis.
Laboratory Analysis
Serum total protein and albumin concentraons were
esmated quantavely using Biuret and Bromocresol
(BCG) methods respecvely as modied by Randox
Laboratories (United Kingdom). Serum globulin
concentraon and albumin/globulin (a/g) rao were
derived mathemacally.18
Total Protein = Albumin + Globulin
Hence, Globulin = Total Protein – Albumin.
A/G rao= Albumin/Globulin
Agoro ES, et al.
ISSN: 0973-3558, e-ISSN: 0973-3566
Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
DOI: 10.31736/jist/v14.i2.2018.12-16
Aspartate aminotransaminase (AST), alanine
aminotransferase (ALT) and alkaline Phosphatase (ALP)
acvies were assayed using ELITech Clinical Systems
with the aid Selectra proM.. Malloy-Evelyn modied end
point method was used for the esmaon of total and
conjugated bilirubin.18 The unconjugated bilirubin was
esmated mathemacally by subtracng conjugated
bilirubin from total bilirubin.
Stascal Analyses
Data were analyzed with Stascal Package for Social
Sciences (SPSS) program (SPSS Inc., Chicago, IL, USA;
Version 18-21). One-way ANOVA (Post Hoc- LSD) was
used in comparing the means of the liver biochemical
parameters of the various chronic CO intoxicaon groups
of the study.
DISCUSSION
The pulsale inhalaon of CO by Nigerians is roune due
to the massive use of equipment that releases CO and
the huge gap in power supply. Chronic carbon monoxide
poisoning is the inhalaon of low quanty of CO over a
long duraon. This study revealed a signicant decrease
(p < 0.05) in concentraons of serum total protein and
Legend: TP- Total Protein; ALB-Albumin; GLO- Globulin; A/G- Albumin/Globulin.
Symbols- a: P < 0.05 vs control, b: P < 0.05 vs Day 10, c: P < 0.05 vs Day 20
Data are expressed as mean ± SD; Signicant at 0.05 Condence (p < 0.05)
Concentraon of acute CO intoxicaon= ≤ 200 pm
Parameters Control
Day 30 f-value
47.75 ± 6.24 36.75 ± 4.03 a 33.50 ± 3.11 a 33.50 ± 3.70 a 8.021 0.003
30.25 ± 2.36 28.25 ± 4.92 26.75 ± 3.86 29.25 ± 2.99 0.665 0.590
16.50 ± 6.56 8.50 ± 1.73 a 8.25 ± 4.99 a 4.25 ± 0.96 a 5.870 0.010
2.20 ± 1.23 3.50 ± 1.16 5.00. ± 4.14 7.10 ± 1.49a 3.194 0.063
Legend: AST- Aspartate Aminotransferase; ALT-Alanine Aminotransferase; ALP-Alkaline Phosphatase;
TB-Total Bilirubin; CB- Conjugated Bilirubin; UB- Unconjugated Bilirubin.
Symbols- a: P < 0.05 vs control, b: P < 0.05 vs Day 10, c: P < 0.05 vs Day 20
Data are expressed as mean ± SD; Signicant at 0.05 Condence (p < 0.05). Concentraon of acute
CO intoxicaon= ≤ 200 pm
Parameters Control
14.75 ± 2.06 19.00 ± 4.69 38.50 ± 6.35 ab 44.00 ± 4.32 ab 38.68 0.00
13.75 ± 4.79 42.75 ± 3.10 a 85.50 ± 4.80 ab 115.75 ± 13.07 abc 144.07 0.00
AST/ALT 0.88 ± 0.25 0.45 ± 0.09 a 0.46 ± 0.09 a 0.38± 0.03 a10.83 0.00
18.75 ± 6.99 38.50 ± 5.80 a 96.50 ± 11.82 ab 169.25 ± 19.96 abc 117.84 0.00
2.13 ± 0.22 2.38 ± 0.44 3.80 ± 0.48 ab 4.20 ± 0.88 ab 135.23 0.00
0.93 ± 0.15 0.98 ± 0.15 2.30 ± 0.42 ab 2.50 ± 0.50 ab 24.01 0.00
1.20 ± 0.14 1.40 ± 0.47 1.50 ± 0.79 1.70 ± 0.55 0.598 0.00
RESULTS
The Eects of Chronic Carbon Monoxide Intoxicaon on some liver Biochemical Parameters in Rabbits
ISSN: 0973-3558, e-ISSN: 0973-3566
Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
globulin concentraons across the chronic CO intoxicaon
groups (Table 1). The reducon in serum total proteins
and globulins concentraons could be aributed to
immune-suppression. Globulins are immune proteins
produced in response to infecon and inammaon.
The consistent exposure to CO resulted to the decrease
in concentraon of serum globulin which is indicave of
depression of the immune system. Serum total protein
concentraon decrease as observed in this study is due
to the fall in globulin concentraon as further elucidated
by the increase in A/G rao. An increase in A/G rao is
aributable to immunodepression and compromise19. A
depressed immune system is a path usually ulized by
a lot of diseases. The depression could lead to an ease
acquision of a lot of diseases that could be idiopathic
origin. Furthermore the results of this study revealed
a signicant increase (p < 0.05) in concentraons and
acvies of some of the liver biochemical funcon
parameters (Table 2) as the duraon of CO intoxicaon
increased. The increased acvies of AST and ALT are
proof of the toxicity of CO on the hepatocytes and liver
parenchymal cells. The deterioraon of the liver could
be due to the hypoxic acon of the oending agent (CO).
The liver requires connuous availability of oxygen for its
wide range of funcons. This nding agreed partly with
Nanji et al., 20 that showed a necroc eect on the liver
by the synergisc eect of CO and ethanol. This study also
showed that serum ALP acvity increased markedly as the
duraon of CO exposure increased. The increase showed
that CO hypoxic eect also extended to the biliary tree
and surrounding cells. This report contrasted the work
reported by Niebró et al.,21 that showed a decline in
concentraon of ALP in guinea pigs aer 7 days exposure
with 4-5 percent of CO in the air. Moreover, this study
showed a steady increase in total and conjugated bilirubin
as the duraon of CO exposures increase. The elevaon
of conjugated bilirubin could be aributed to the eect of
CO on the blood cells, hepatocellular insuciency or the
biliary tree reux. Stefan et al.,22 showed that at a low
concentraon of carbon monoxide, bilirubin exerts an
an-oxidave funcon, hence protecng cells and ssues
from injuries and that low concentraon of CO serve as a
protecve shield of various body organs. Unconjugated
bilirubin exhibited no signicant dierence across the
study duraon. This has further shown that CO induced
hyperbilirubinaemia cause be reversible as the liver cells
were sll conjugang and not have completely collapsed
CONCLUSION
The aim of the study was to assess the eect of chronic
CO poisoning on biochemical parameters commonly used
to evaluate the integrity and status of the liver. The nding
showed that chronic inhalaon of CO could cause long liver
damage resulng from the consistent starvaon of the
liver of oxygen. Furthermore, the hypoxia characteriscs
could insgate immune-suppression that may make the
body vulnerable to arrays of diseases.
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Metabolism-Porphyrin, Iron, and Bilirubin, In Fundamentals of
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2. Prockop, L.D. and Chichkova, R.I. (2007). Carbon monoxide
intoxicaon: an updated review. Journal of the
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3. Anderson, J., Menkedick, J.R. and Wooton, M.A. (2005). Healthy
Homes Issues: Carbon Monoxide. US Department of Housing
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4. Gwon, A. (2008). The rabbit in cataract/IOL surgery. In: Tsonis,
P.A. (ed.) Animal models in eye research. Elsevier, pp. 184-204.
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6. Ochei J., Kolhatkar A (2003). Haematology In: Medical
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7. Agoro, E.S., Akubugwo, E.I., Chinyere, G.C., Alabrah, P.W. and
Ombor, J.A. (2018a).The cumulave eects of chronic carbon
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Agi, V.N. (2018b). Some vitreous humour cardiorenal
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V.N. (2017a). Vitreous Humour Lipid Peroxidaon as an Emerging
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(2017b). Lipids levels in Vitreous Humor of Rabbits aer Carbon
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(2017c). Comparison of Vitreous Protein Proles of Rabbits
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animal aer death. J Forensic Sci Res., 1:040-045.
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ISSN: 0973-3558, e-ISSN: 0973-3566
Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
DOI: 10.31736/jist/v14.i2.2018.12-16
12. Agoro, E.S., Azuonwu, O., Abbey, S.D. (2017d). The Forensic
Applicaon of Microbiological Quality of the Vitreous Humor
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13. AKirkwood, J. and Robert, H. (2010). The UFAW Handbook on
the Care and Management of Laboratory and Other Research
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ISSN: 0973-3558, e-ISSN: 0973-3566
Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
1Department of General Medicine, Govt. Medical College, Srinagar.
Declared none
ABSTRACT
Background: In Asia around 50% poisoning are due to
organophosphorus (OP) poisoning. The esmated mortality
from Organophosphates ingeson ranges from 10% to 20%.
Objecve: The present study was undertaken to study
the glycemic changes in acute organophosphorus
(ancholinesterase) poisoning and its relaonship with
severity, morbidity and mortality.
Methods: This prospecve observaonal study was conducted
in Government Medical College, Srinagar; Jammu Kashmir;
India. Two hundred six paents with organophosphorus
poisoning were studied.
Results: In this study, the mortality was 10.2% (21 deaths in 206
paents), and venlaon was required in 29 (14.07%) paents.
In paents who expired, glycosuria was found in 76.2% and
blood glucose levels were 216±61 mg/dl, as compared to
paents who survived in whom glycosuria was found in 9.2%
and blood glucose levels were 136±88 mg/dl(P <0.005).
Conclusion: Glycemic changes (hyperglycemia and glycosuria)
are good markers for predicng morbidity and also assessing
need for venlator support.
Glycemia;
organophosphorus;
glycosuria;
blood glucose,
hyperglycemia.
Received on 10th November 2018
Accepted on 23rd December 2018
Published on 31st December 2018
©2018 The Journal of Indian Society of Toxicology.
Published at JIPMER, Pondicherry, 605006, INDIA Subscripon & payment related
queries at: toxicology@aims.amrita.edu and rest all types of queries related to the
journal to be done at drambika_editor@jist.org.in
ARTICLE INFO
Muzzafer Mohammad Mir Department
of General Medicine, Govt. Medical College, Srinagar.; E-mail:
drmuzzafer@yahoo.co.in: Tel.: 7006250472.
How to Cite this arcle:Mir MM , Bilal M, Parry ZH, Taranum
U, Inkhab M. Correlang glycemic changes in acute
organophosphorus poisoning paents with severity, morbidity
and mortality: a prospecve study at Kashmir valley. Journal of
Indian Society of Toxicology 2018;14(2):17-21.
INTRODUCTION
Organophosphates (OP) are the predominant group
of inseccides employed globally for pest control.
Organophosphates (OPs) are widely used in agriculture
and OP intoxicaon is a global public health problem.
[1– 3] As per World Health Organizaon (WHO), three
million cases of pescide poisoning occur every year
and most of them occur in Asia and at least 50% due
to organophosphorus poisoning.[4] The World Health
Organizaon esmated that the incidence of pescide
poisoning in developing countries doubled during 10
years period from 1990.[5] OP intoxicaon can occur by
accidental occupaonal exposure or suicide aempts.
OP poisoning causes adverse eects on ssues and organ
funcon [6 - 9] and these may lead hyperglycemia. A few
earlier studies have reported glycemic changes ranging
from hypoglycemia to hyperglycemia, glycosuria and
ketoacidosis in OP poisoning. [10, 11] There is 10-20% case
fatality rate in developing countries compared with much
lower fatality in developed countries.[12] A number of
systems have been proposed for predicng outcome in
OP poisoning. Many are reliant on laboratory tests. [13-17]
Others that use clinical parameters have been validated
Mir MM, et al.
ISSN: 0973-3558, e-ISSN: 0973-3566
Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
DOI: 10.31736/jist/v14.i2.2018.17-21
using small numbers of paents. [18] The present study
was undertaken to study the various glycemic changes in
acute ancholinesterase poisoning and their relaonship
with morbidity and mortality.
Aim of study
1) To evaluate glycemic changes in OP poisoning and its
correlaon with severity of organophosphorus
poisoning
2) To evaluate the usefulness of glycemic changes as
predictors of signicant morbidity and mortality in OP
poisoning.
MATERIALS AND METHODS
This prospecve observaonal study was done in
Government SMHS Hospital from March 2015 to January
2016. Two hundred six paents of acute OP poisoning
fullling the inclusion and exclusion criteria were included
in the study.
INCLUSION CRITERIA
Paents of either sex, above 18 yrs of age. Paents with
history of consumpon of organophosphorus compound
presenng within 24 hrs.
EXCLUSION CRITERIA
Age less than 18 yrs.
History of Diabetes.
Mixed poisoning.
Unknown poisoning.
A detailed history regarding age sex, type of compound
consumed, me-lag between consumpon and iniaon
of treatment, thorough clinical examinaon was
undertaken. The severity of the poisoning was graded on
a scale of 0 to 3 based on the classicaon by Bardin et
al. [19]
At the me of admission, complete blood count, random
blood sugar, urinalysis for glycosuria and ketone bodies,
arterial blood gas analysis, renal and liver funcon tests
were performed. Glycated hemoglobin levels were
done to check for undiagnosed diabetes. Glycosuria was
detected using dipscks. The magnitude of glycosuria
was quaned as 0.25g% (1+), 0.5g% (2+), 1g% (3+) and
>2g% (4+). The cases with hyperglycemia were tested at
regular intervals unl their blood sugars were normal. The
duraon of glycosuria was also similarly recorded. The
presence of hyperglycemia or glycosuria or hypoglycemia
or ketosis was correlated with the severity of poisoning,
morbidity in terms of complicaons, hospital stay >7days
and requirement of assisted venlaon, and mortality.
STATISTICAL ANALYSIS
Data were analyzed using SPSS. Results were expressed as
mean ± standard deviaon (SD). Categorical variables were
analyzed using the chi-square test and nonparametric
variables were analyzed using the Mann–Whitney U test.
A level of stascal signicance was established at P <
0.05 for all analyses.
RESULTS
Basic characteriscs of the study populaon.
Age (years) 26.03±15.29
18-30 176 (85.4%)
30-40 21 (10.2%)
>40 9 (4.3%)
Sex
Males 68 (33%)
Females 138 (67%)
Marital status
Married 64(31.06%)
Unmarried 142(68.93%)
Residence
Rural 159(77.18%)
Urban 47(22.81%)
Venlaon required 29 (14.07%)
Hospital stay (days) 3.58±2.49*
Mortality 21 (10.2%)
DISCUSSION
Organophosphate poisoning is a serious clinical enty
and causes considerable mortality and morbidity. The
esmated mortality from OP ingeson ranges from 10%
to 20%. [20-23] In this study, the mortality was 10.2% (21
deaths in 206 paents), and venlaon was required in
29 (14.07%) paents. Few studies have highlighted the
occurrence of glycosuria with or without hyperglycemia in
OP poisoning [10, 11, and 24]. In this study, hyperglycemia
was noted in 78 cases (37.86%) and glycosuria was noted
Correlang Glycemic changes in Acute Organophosphorus poisoning paents with severity, morbidity and mortality
ISSN: 0973-3558, e-ISSN: 0973-3566
Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
Parameter Grade II
Grade III
7060±2014 9160±3124 14200±7426 <0.05 ANOVA
0.90±0.32 1.01±0.40 1.20±0.620 .0013ANOVA
126.32±81.4 161±67 196±77 <0.001ANOVA
13(9.2%) 9(21.9%) 11(45.83%) <0.05 CHI
0 01(2.4%) 3(12.5%) <0.05 CHI
Laboratory values on admission in hospital
*TLC: Total leucocyte cout
Table 3:Comparison of glycemic changes between paents with or without
requirement of mechanical venlaon
Parameter Required
Not
210±64 142±90 <0.05 Unpaired t
test
12(41.37%) 21(11.86%) <0.05 Fischer exact
03(10.34%) 01(0.56%) 0.009 Fischer exact
Table 4:Comparison of the glycemic changes between paents with
hospital stay ≤ 7 days and >7 days.
Parameter
194±87 136±78.56 <0.05 unpaired t test
17(48.5%) 16(9.30%) <0.05 Fischer exact
4(11.42%) 00(0%) <0.05 Fischer exact
Table 5:Comparison of the glycemic changes between paents who expired and survived.
Parameter
216±61 137±88 <0.05unpaired t test
16(76.20%) 17(9.2%) <0.05 Fischer exact
3(14.28%) 01(0.54%) 0.003 Fischer exact
in 33 cases of OP poisoning (16.02%) and ketoneuria
was noted in 4 cases (1.94%). We also observed that
blood glucose levels were more in grade III poisoning
(196±77mg/dl) as compared to grade II (161±67) and
grade I poisoning (126±81).A signicant correlaon
was found between hyperglycemia, glycosuria and the
severity of poisoning. These nding correlated with study
of Sangur et al [25] and Shobha et al [11] and Pendkar
et al [24]. Many mechanisms have been propounded
in the pathogenesis of hyperglycemia following OP
compound poisoning _ marked catecholamine excess
following connuous cholinergic smulaon induced
by the poisoning, persistent cholinergic smulaon
leading to ACTH release from the anterior pituitary[27,
28] and increased glycogen breakdown.[29] Various
studies have tried to idenfy morbidity and mortality
Mir MM, et al.
ISSN: 0973-3558, e-ISSN: 0973-3566
Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
DOI: 10.31736/jist/v14.i2.2018.17-21
predictors in OP poisoning. Goswamy et al. found that
measurement of the serum acetylcholinesterase level is
useful in predicng the prognosis in OP poisoning. [30]
However, Aygun et al. have reported that low levels of
serum acetylcholinesterase support the diagnosis of
acute OP poisoning, but are not useful as prognosc
indicator. [31] Lee P et al reported that APACHE II score
>26 was a poor prognosc indicator in OP poisoning. [32]
Eizadi-Mood N et al reported that APACHE II and modied
APACHE II scores can be used in predicng outcomes in
organophosphate poisoning .[33] Davies JO et al reported
the use of Glasgow coma scale in predicng outcome
in acute organophosphorus poisoning.[34] Rehiman S
reported the usefulness of serum cholinesterase level,
clinical score at presentaon as prognosc indicator in
organophosphorus poisoning. [35] Sam KG et al reported
that GCS, APACHE II, predicted mortality rate (PMR) can
be applied in predicng mortality in OP poisoning [36].
Bhaacharyya et al reported that serum creanine
phosphokinase, erythrocyte cholinesterase level, blood
pH and total atropine dose were strongly correlated
with clinical severity.[37] In this study, glycosuria was
found in 41.37% in paents who required venlaon
as compared to 11.86% in those who did not require
venlaon (P <0.005). Mean blood glucose levels were
210±64 mg/dl in paents who required venlaon and
142±90 mg/dl in paents who did not require venlaon
(P <0.005). Stascally signicant associaon was found
between requirement of mechanical venlaon and
hyperglycemia and glycosuria. Paents whose hospital
stay was more than 7 days, glycosuria was found in 48.5%
as compared to 9.30% in whom hospital stay was less
than 7 days(P <0.005). Mean blood glucose levels were
194±87 mg/dl in paents whose hospital stay was >7 days
and 136±78.56 mg/dl in paents whose hospital stay was
≤7 days (P <0.005). Hospital stay >7 days was signicantly
associated with hyperglycemia and glycosuria. In paents
who expired, glycosuria was found in 76.2% and blood
glucose levels were 216±61 mg/dl, as compared to
paents who survived in whom glycosuria was found
in 9.2% and blood glucose levels were 136±88 mg/dl(P
<0.005). This is in accordance with the study of Goel et al.
[14] Sangur et al. [ 25] Pendkar et al. [24] These results
indicate that hyperglycemia and glycosuria are good
markers for predicng morbidity and also assessing need
for venlator support.
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phosphotriesterases in the prophylaxis and treatment of
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2. Langley R, Sumner D. Pescide mortality in the United States,
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3. Öztürk MA, Keleşmur F, Kurtoğlu S, Güven K, Arslan D.
Ancholinesterase poisoning in Turkey--clinical, laboratory and
radiologic evaluaon of 269 cases. Hum Exp Toxicol 1990; 9:
273–9.
4. Singh S. organophosphorus poisoning: an evidence based
approach. MJAFI 2004; 60; 2-4.
CONCLUSION
Glycemic changes (hyperglycemia and glycosuria) were
observed more in paents of grade II and III OP poisoning
and these were the paents who were associated with
increased morbidity and mortality.
Glycemic changes (hyperglycemia and glycosuria) are
good markers for predicng morbidity and also assessing
need for venlator support.
Glycemic changes (hyperglycemia and glycosuria) can be
used to develop a severity scoring system in acute OP
poisoning cases.
Acknowledgements
We would like to thank the Department of Medicine,
Government Medical College Srinagar.
Compeng Interests
No compeng interest.
Consent for Publicaon
Consent to parcipate is not provided as no individual
data is provided and it is not possible for paents to be
idened from the anonymised data used.
Ethics Approval and Consent to Parcipate
Ethics approval was not required as data were collected
rounely for clinical purposes.
Abbreviaons
OP : Organophosphorus poisoning.
Correlang Glycemic changes in Acute Organophosphorus poisoning paents with severity, morbidity and mortality
ISSN: 0973-3558, e-ISSN: 0973-3566
Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
5. World Health Organizaon. WHO Recommended Classicaon
of Pescides by Hazard and Guidelines to Classicaon 2000-
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6. Hsiao C-T, Yang C-C, Deng J-F, Bullard MJ, Liaw S-J. (1996) Acute
pancreas following organophosphate intoxicaon. Clin
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7. Agosni M, Bianchin A. (2003) Acute renal failure from
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8. Yurumez Y, Ikizceli I, Sozuer EM, Soyuer I, Yavuz Y, Avsarogulları L,
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9. Kerem M, Bedirli N, Gürbüz N, Ekinci O, Bedirli A, Akkaya T,
Sakrak O, Pasaoglu H. (2007) Eects of acute fenthion toxicity on
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10. Meller D, Fraser I, Kryger M. Hyperglycemia in ancholinesterase
poisoning. Can Med Assoc J 1981;124:745-8.
11. Shobha TR, Prakash O. Glycosuria in organophosphate and
carbamate poisoning. J Assoc Physicians India 2000;48:1197-9.
12. Eddleston M, Phillips MR. Self poisoning with pescides. BMJ
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13. Bardin PG, van Eeden SF, Moolman JA, Foden AP, Joubert JR.
Organophosphate and carbamate poisoning. Arch Intern Med
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14. Goel A, Joseph S, Dua TK. Organophosphate poisoning:
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15. Grmec S, Mally S, Klemen P. Glasgow Coma Scale score and QTc
interval in the prognosis of organophosphate poisoning. Acad
Emerg Med 2004;11:925-30.
16. Lee P, Tai DY. Clinical features of paents with acute
organophosphate poisoning requiring intensive care. Intensive
Care Med 2001;27:694-9.
17. Matsumiya N, Tanaka M, Iwai M, Kondo T, Takahashi S, Sato S.
Elevated amylase is related to the development of respiratory
failure in organophosphate poisoning. Hum Exp Toxicol
1996;15:250-3.
18. Senanayake N, de Silva HJ, Karalliedde L. A scale to assess
severity in organophosphorus intoxicaon: POP scale. Hum Exp
Toxicol 1993;12:297-9.
19. Bardin PG, Van Eden SF. Organophosphate poisoning: grading
the severity and comparing treatment between atropine and
glycopyrolate. Crit Care Med 1990;18:956–960
20. Munidasa UA, Gawarammana IB, Kularatne SA, Kumarasiri
PV, Goonasekera CD. Survival paern in paents with acute
organophosphate poisoning receiving intensive care. J Toxicol
Clin Toxicol 2004;42:343-7.
21. Yamanaka S, Yoshida M, Yamamura Y, Nishimura M, Takaesu
Y. A study on acute organophosphorus poisoning - Changes in
the acvity and isoenzyme paerns of serum cholinesterase in
human poisoning. Nihon Eiseigaku Zasshi 1993;48:955-65.
22. Yamashita M, Yamashita M, Tanaka J, Ando Y. Human mortality in
organophosphate poisonings. Vet Hum Toxicol 1997;39:84-5.
23. Wycko DW, Davies JE, Barquet A, Davis JH. Diagnosc and
therapeuc problems of parathion poisonings. Ann Intern Med
1968;68:875-82.
24. Pritee G Pendkar, K S Ghorpade, G S Manoorkar, Amol Shinde
blood glucose level in acute organophosphorus poisoning 15(2):
342-44
25. Sungur M, Guven M. Intensive care management of
organophosphate insecside poisoning, crit.care 2001; 5(4);
211-5.
26. Shobha T R, Prakash O, Glycosuria in organophosphate and
carbamate poisoning. JAPI 2000; 48(12).
27. Ramu A, Slonim AE, London M, Eyal F. Hyperglycemia in acute
malathion poisoning. Isr J Med Sci 1973;9:631-4.
28. Koundinya PR, Ramamurthi R. Eect of organophosphate
pescide Sumithion (Fenitrothion) on some aspects of
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(Tilapia) mossambicus (Peters). Experiena 1979;35:1632-3.
29. Civen M, Leeb JE, Wishnow RM, Wolfsen A, Morin RJ. Eects of
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30. Goswamy R, Chaudhuri A, Mahashur AA. Study of respiratory
failure in organophosphate and carbamate poisoning. Heart
Lung 1994;23:466-72
31. Aygun D, Doganay Z, Alntop L, Guven H, Onar M, Deniz T,
et al. Serum acetylcholinesterase and prognosis of acute
organophosphate poisoning. J Toxicol Clin Toxicol 2002;40:903-
10
32. Lee P, Tai DY. Clinical features of paents with acute
organophosphate poisoning requiring intensive care. Intensive
Care Med 2001;27:694-9.
33. Eizadi-Mood N, Saghaei M, Jabalameli M. Predicng outcomes
in organophosphate poisoning based on APACHE II and modied
APACHE II scores. Hum Exp Toxicol 2007;26:573-8.
34. Davies JO, Eddleston M, Buckley NA. Predicng outcome in
acute organophosphorus poisoning with a poison severity score
or the Glasgow coma scale. QJM 2008;101:371-9.
35. Rehiman S, Lohani SP, Bhaarai MC. Correlaon of serum
cholinesterase level, clinical score at presentaon and severity
of organophosphorous poisoning. JNMA J Nepal Med Assoc
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36. Sam KG, Kondabolu K, Pa D, Kamath A, Pradeep Kumar G,
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organophosphorus poisoning. Toxicol Int 2011;18:117-23.
ISSN: 0973-3558, e-ISSN: 0973-3566
Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
DOI: 10.31736/jist/v14.i2.2018.22-25
Somashekhar S. Pujar34
56
2,5Postgraduate, 1Associate Professor, 3Professor and HOD, 4Professor, Department of Forensic Medicine and Toxicology, J.N.
Medical College, Belagavi
6Assistant Professor, Department of Forensic Medicine and Toxicology, BIMS, Belagavi
Declared none
ABSTRACT
Introducon : Poisoning is a problem throughout the world but
its paern vary from one place to other place. The deaths due
to poisoning can be intenonal or unintenonal. The deaths
due to poisoning is increasing at an alarming rate in developing
countries like India because a large number of pescides
are easily accessible to the people with the development in
industrial and agricultural elds.
Objecves : To know the paern and outcome of poisoning
cases admied in a terary care hospital over a period of 3
years.
Materials and Methods : A retrospecve record based study
of all poisoning samples sent for analyzing to Poison Detecon
Centre (PDC) of KLE hospital, Belagavi from January 2014 to
December 2016. The data regarding paern of poisoning, age,
sex, occupaon, basic demographics prole and outcome were
collected from hospital records.
Results: There were total 521 cases of which 426 were posive
for various poisonous compounds and 95 were negave for the
standard tested. Most of the poisoning cases were observed
in males amounng 257 (60.3%). The commonest age group
was 19-29 years (46.5%) and male to female rao was 1.52:1.
The maximum number of cases reported were among illiterate
(71.8%) and were from rural background (70.6%) involved in
agricultural acvies (42.7%). Organophosphorus (57%) was
commonest compound and least was Amitraz (1.2%). The total
mortality was 39 and the maximum deaths were seen with
Organophosphorus compound (66.6%).
Poisoning, Paern,
Poison Detecon
Centre, Rural,
Organophosphorus
Received on 30th December 2018
Accepted on 31st December 2018
Published on 31st December 2018
©2018 The Journal of Indian Society of Toxicology.
Published at JIPMER, Pondicherry, 605006, INDIA Subscripon & payment related
queries at: toxicology@aims.amrita.edu and rest all types of queries related to the
journal to be done at drambika_editor@jist.org.in
ARTICLE INFO
Kashif Ali, Postgraduate, Department
of Forensic Medicine and Toxicology, Kaher’s J.N. Medical
College, Belagavi-590010. Email: alikashif568@yahoo.in
How to Cite this arcle:Pujar SS, Ali K, Honnungar RS, Jirli PS,
Junaidi KA, Pushpa MG. Paern and Outcome of Poisoning
Cases Analyzed in Poison Detecon Centre of a Terary Care
Hospital: A 3 year Retrospecve Study. Journal of Indian
Society of Toxicology 2018;14(2):22-25.
INTRODUCTION
Poisoning is a major medicosocial and legal problem
all over the world but its morbidity and mortality vary
from one place to other place. Among the unnatural
deaths, death owing to poisoning stand next only to road
trac accident deaths.[1] The deaths due to poisoning is
increasing at an alarming rate in developing countries like
India. A large number of pescides are easily accessible
to the people with the development in industrial and
agricultural elds.The World Health Organizaon (WHO)
esmates that about 3 million cases of poisoning occur
Paern and Outcome of Poisoning Cases Analyzed in Poison Detecon Centre of a Terary Care Hospital
ISSN: 0973-3558, e-ISSN: 0973-3566
Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
every year in the world and about 1,93,460 deaths occur
due to unintenonal poisoning.[2] Of these 90% of fatal
poisoning occurs in developing countries parcularly
among agricultural workers. The commonest cause of
poisoning in India and other developing countries is due to
pescides, the reason being agriculture based economy,
poverty, illiteracy, ignorance and lack of protecve
clothing and easy availability of highly toxic pescides.[3]
A study on the paern of poisoning is important as it will
help us to gain a beer understanding of the current trend
in poisoning cases. The paern or prole of poisoning
in a specic region depends on diverse factors such as
age, gender, place of residence, occupaon, educaonal
status, availability and accessibility of pescides.
MATERIALS AND METHODS
It is a 3 year retrospecve study of all poisoning samples
analyzed at Poison Detecon Centre (PDC) of KLE Hospital
aached to Jawaharlal Nehru Medical College, Belagavi
from January 2014 to December 2016. The study included
data regarding paern of poisoning, age, sex, occupaon
and basic demographics prole were collected along with
the name of poisonous substances and outcome from
hospital records. Stascal analysis was done by using
SPSS soware version 25 and the results were calculated
in percentages.
Ethical Clearance was Taken from Instuonal Ethical
Commiee.
Male Female Total Percentage
05 (1.9%) 05 (3%) 10 2.3
47 (18.3%) 37 (21.9%) 84 19.7
122 (47.5%) 76 (44.9%) 198 46.5
33 (12.8%) 21 (12.4%) 54 12.7
26 (10.1%) 16 (9.5%) 42 9.9
13 (5.1%) 10 (5.9%) 23 5.4
07 (2.7%) 02 (1.2%) 09 2.1
04 (1.6%) 02 (1.2%) 06 1.4
257 169 426 100
Table 1 depicts that males predominated females and the
male to female poisoning rao is 1.52:1. The majority of
cases belonged to age group 19-29 years (46.5%) followed
by age group 2-18 years (19.7%) while least number of
cases were seen with age group >70 years (1.4%).
Distribuon of cases according to place of
residence.
Table 2 depicts that majority of the cases were from
rural background (70.6%) followed by urban populaon
(29.4%)
Place of Residence Number of cases Percentage
301 70.6
125 29.4
426 100
Table 3 depicts that the most common populaon aected
were the people involved in agricultural acvies (42.7%)
followed by housewife (25.6%) and students (19.5%).
Table 3:
Number of cases Percentage
182 42.7
109 25.6
83 19.5
28 6.6
24 5.6
426 100
RESULTS
There were total 521 cases of which 426 were posive for
various poisonous compounds and 95 were negave for
the standard tested.
Table 4:
Table 4 depicts that majority of cases were illiterate (71.8%) as compared to literates (28.2%)
Number of cases Percentage
Illiterate 306 71.8
Literate 120 28.2
Total 426 100
Ali K, et al.
ISSN: 0973-3558, e-ISSN: 0973-3566
Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
DOI: 10.31736/jist/v14.i2.2018.22-25
DISCUSSION
In our study, males (60.3%) predominated females
(39.7%) and the male to female poisoning rao was
1.52:1 which is similar to the study conducted by Kiran et
al.[4] This could be due to risk taking behavior of males and
indulging in outdoor acvies. The present study shows
that most of the cases belong to age group 19-29 years
which constute 46.5%. This observaon is consistent
with the studies conducted by Gupta et al[5], Dash et al
[6] and Srivastava et al.[7] In this study rural populaon
(70.6%) was aected more as compared to urban
populaon (29.4%) which is similar to ndings noted by
Tejas et al[8] and Virendar et al.[9] It could be due to the
fact that rural people are more exposed to pescides as
they are involved in agricultural acvies. In this study it
has been observed that the most vulnerable occupaon
Percentage Mortality Percentage
243 57 26 66.6
75 17.5 08 20.5
31 7.3 02 5.1
25 5.8 01 2.6
16 3.8 01 2.6
12 2.9 00 00
05 1.2 01 2.6
19 4.5 00 00
426 100 39 100
Table 5:
Total cases Mortality Mortality Percentage
116 (27.2%) 05 (12.8%) 26 66.6
121 (28.4%) 09 (23.1%) 08 20.5
108 (25.4%) 11 (28.2%) 02 5.1
81 (19%) 14 (35.9%) 01 2.6
426 39 01 2.6
Table 6:
group was the people involved in agricultural acvies
(42.7%) and people who were illiterate (71.8%) which is
similar to studies done by Sandhu et al[10], Pate et al[11]
and Karamjit et al.[12] According to a study done by Dhanya
et al[13] and Marahaa et al[14] the organophosphorus
poisoning constute maximum number of cases (57%)
followed by unspecied drugs (17.5%) which is similar to
our ndings. It was found in our study that more the me
elapsed since exposure to hospital arrival more was the
mortality which is similar to studies done by Gupta et al[15]
and Ramesha et al.[16]
CONCLUSION
In our study there were total 426 cases in which male
predominated female with rao of 1.52:1 and 19-29
years was the commonest age group. Most of them
Paern and Outcome of Poisoning Cases Analyzed in Poison Detecon Centre of a Terary Care Hospital
ISSN: 0973-3558, e-ISSN: 0973-3566
Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
were illiterate from rural/agricultural background. The
commonest compound was organophosphorus. The
total mortality was 39 and maximum mortality was
seen with organophosphorus compound. Since we are a
developing country its our duty to handle mulfunconal
tasks in providing informaon about the various hazards
of pescides and drugs and by establishing poison
informaon centers. Various health care centers need to
organize mass educaon programs to create awareness
to prevent poisoning and its fatalies. There should be
strict pescide regulaon laws to decrease the burden of
incidence of poisoning. Along with this various training
programs should be organized and proper counseling
should be done.
REFERENCES
1. Global Health Esmates 2016: Death by cause, age, sex by
country and by region 2000-2016 Geneva, World Health
Organizaon;2018. Available at hp://www.who.int. Accessed
on 18 Aug 2018.
2. World Health Organizaon,2016. Prevenng disease through
healthy environments: A global assessment of the burden of
disease from environmental risks;2016. Available at hp://www.
who.int. Accessed on 18 Aug 2018.
3. Reddy KSN. The Essenals of Forensic Medicine and Toxicology.
33rd Ed;2014, p.500
4. Kiran N, Shobha Rani RH, Jaiprakash V, Vanaja K. Paern of
poisoning reported at South Indian terary care hospital. IJFMT.
2008;2(2):17-9.
5. Gupta BD, Vaghela PC. Prole of fatal poisoning in and around
Jamnagar. JIAFM. 2005;27(3):145-8.
6. Dash SK, AluriSR, Mohanty MK, Patnaik KK. Sociodemographic
prole of poisoning. JIAFM. 2005;27(3):133-8.
7. Srivastava A, Peshin SS, Kaleekal T, Gupta SK. An epidemiological
study of poisoning cases reported to the Naonal Poison
Informaon Centre AIIMS, New Delhi. Hum ExpToxicol.
2005;24(6):279-85.
8. Tejas P, Kark P, RN Tandon, Saumil M. A study of acute poisoning
cases excluding animal bites at civil hospital, Ahmedabad. JIAFM.
2013;35(2):120.
9. Virendar PS, BR Sharma, Dasari Harish, Krishnan Vij. A ten year
study of poisoning cases in a terary care hospital. IIJFMT.
2004;2(1).
10. Sandhu SS, Garg A, Gorea RK. Poisoning trends in Faridkot
region: A retrospecve study. J Punjab Acad Forensic Med
Toxicol.2010;10(1):20-3.
11. Pate RS, Rojekar MV, Hire RC. Trends of poisoning cases in
terary care teaching hospital in western Indian populaon.
IJMTFM. 2017;7(3):177-84
12. Karamjit S, Oberoi SS, Bhullar DS. Poisoning trends in the Malwa
region of Punjab. J Punjab Acad Forensic Med Toxicol. 2003;3:26-
9.
13. Dhanya SP, Dhanya TH, Bindulatha RN, Herna CG. A retrospecve
analysis of the paern of poisoning in paents admied to the
Medical College Hospital, Calicut. Medical Journal 2009;7(2):1-
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14. Marahaa SB, Singh J, Shrestha R, Koju R. Poisoning cases
aending emergency department in Dhulikhel Hospital-
Kathmandu University Teaching Hospital. Kathmandu University
Medical Journal. 2009;7(2):152-6.
15. Gupta P, Kumar A, Singh SP, Prakash M, Gupta M, Kumar P.
Paern of cases of Acute Poisoning in a Rural Terary care center
in Northern India. Ntl J Community Med 2016;7(4):307-10.
16. Ramesha KN, Krishnamurthy BH, Kumar GS. Paern and
Outcome of acute poisoning cases in a terary care hospital in
Karnataka, India. IJCCM. 2009;13(3):152-5.
ISSN: 0973-3558, e-ISSN: 0973-3566
Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
DOI: 10.31736/jist/v14.i2.2018.26-29
Varsha Dhurvey
1 Professor, 2 Research Scholar
Department of Zoology, Rashtrasant Tukadoji Maharaj Nagpur University, Nagpur-India
Gland of Wistar rats
All authors state that
there is no conict of interest withthe work done in this study.
ABSTRACT
Introducon: Lead (Pb), a heavy metal, is toxic to both human
and animals. There is evidence in the literature that, lead is
highly toxic metal for human and other mammals. The toxic
eect of lead can manifest in various organs, and the male
reproducve organ is an important target.
Material and methods :The objecve of present study is to
invesgate the eect of lead acetate on seminal vesicle and
prostate gland in Wistar rats. Eighteen adult Wistar rats were
divided into three groups, A, B and C. Group A was control and
provided with normal food and water as well as Group B and
C were received 5mg/kg body weight of lead acetate daily for
15 and 30 days respecvely. Aer the compleon of treatment
body and organs weight and histology of seminal vesicle and
prostate gland were examined.
Result : Results showed that decrease in body weight and
organs weight when compared to control. Histopathology of
seminal vesicle of treated rats showed, destrucon in epithelial
lining, reducon in mucosal fold of anddecrease in secreon
as compared to control. As well as prostate gland of treated
group shows lower secretary acvity of epithelium, reduced
secreon, aening of epithelium lining and increasing
intersal space between alveoli.
Discussion and conclusion : It can be concluded from the
results that lead acetate cause toxic eect on seminal vesicle,
prostate gland and impaired male ferlity.
lead acetate; seminal
vesicle; prostate
gland; body weight;
histopathology; albino rat
Received on 8th August 2018
Accepted on 20th November 2018
Published on 31st December 2018
©2018 The Journal of Indian Society of Toxicology.
Published at JIPMER, Pondicherry, 605006, INDIA Subscripon & payment related
queries at: toxicology@aims.amrita.edu and rest all types of queries related to the
journal to be done at drambika_editor@jist.org.in
ARTICLE INFO
Varsha Dhurvey, Professor, Department
of Zoology, Rashtrasant Tukadoji Maharaj Nagpur University,
Nagpur-India. Email: varshadhurvey@yahoo.com
How to Cite this arcle:Dhurvey V, Gotmare B, Karim F. Lead
Acetate induced Histological alteraons in Seminal-vesicle
and Prostate Gland of Wistar rats. Journal of Indian Society of
Toxicology 2018;14(2):26-29.
INTRODUCTION
Lead is the most toxic and major contaminated heavy
metal in our environment. [1, 2] Lead occurs naturally in
the environment in lile amount. However, most of the
high levels found throughout the environment come
from human acvies. The environmental levels of lead
have increased more than 1000- fold over the past three
centuries as a result of human made acvity. The greatest
increase occurred between the years 1950 and 2000, and
reected increasing world wide use of leaded gasoline. [3]
Lead does not have any detectable benecial biological
role, however on the contrary its detrimental eect on
physiological, biochemical and behavioral dysfuncons
have been documented in animals and humans by several
invesgators.[4, 5] Lead metal is a male reproducve
toxicant. [6] Toxicity is manifested in male reproducve
funcon by deposion of lead in testes, epididymis, vas
deferens, seminal vesicle and seminal ejaculate. Lead has
an adverse eect on sperm count, sperm molity and
retarded the acvity of spermatozoa. [7] The involvement
of heavy metal including lead had been implicated in the
Lead Acetate induced Histological alteraons in Seminal-vesicle and Prostate Gland of Wistar rats
ISSN: 0973-3558, e-ISSN: 0973-3566
Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
eology of male inferlity. Environmental exposure to
toxic levels of lead occurs in a number of industries with
potenal adverse eect on the reproducve capacity. [8]
A very lile informaon is available about eect of lead
acetate on seminal vesicle and prostate gland. Hence, the
present study aimed to nd out the eect of lead acetate
on seminal vesicle and prostate gland in Wistar rat.
MATERIALS AND METHODS
Animal collecon and maintenance: Eighteen adult
male albino rats weighing between 237-310 grams were
brought from the animal house unit in Department
of Biochemistry, RTM Nagpur University Nagpur. The
experimental protocol was approved by Instuonal
Animals Ethical Commiee (IAEC) and animal care was
taken as per the guidelines of Commiee for the Purpose
of Control and Supervision of Experiments on Animals
(CPCSEA), Govt. of India (Registraon No. 478/01/
aCPCSEA). The rats were fed with pellet commercial diet
daily and water was provided regularly.
Treatment: The animals were divided into 3 groups A, B
and C, each group containing 6 animals. Group A was used
as control and provided only with dislled water. Lead
acetate 5mg/kg bw administered daily in group B and C
for15 and 30 days respecvely. At theend of treatment,
animals were sacriced by using anesthec chloroform.
At autopsy, body weight of each animal was recorded
and seminal vesicle and prostate gland were removed,
cleaned, weighed and processed for histology.
Histology: Aer the compleon of treatment, animals
were sacriced; seminal vesicle and prostate gland of
control and experimental animals were removed xed
in Bouin’s uid for 24 hrs. Then dehydrated by passing
through graded series of ethyl alcohol, clear in xylene,
embedding in paran wax, blocks were prepared, and
seconed serially at 5µm. For histological study the
secons were stained with haematoxyline and eosin.
The photomicrographs were taken with the help of
digital camera Nikon COOLPIX 8400 aached to the light
microscope Nikon Eclipse E200.
Stascal analysis: The variance between control and
experimental values was calculated using student’s test
with the help of graph pad calculator.
RESULTS
Evaluaon of body, seminal vesicle and prostate gland
weight: The body weight was signicantly decreased in
both the treated group, but parcularly aer 30 days of
treatment as compared to control. Weight of seminal
vesicle and prostate gland was decreased in both the
groups of experimental animals receiving lead acetate.
There was a slight change in seminal vesicle and prostate
gland weight of animals receiving lead acetate for short
(15 days) duraon (Table 1).
Histology of seminal vesicle: The animal with 15 days
treatment with lead acetate shows lower secretary
acvity of epithelium, degenerave changes occur in
epithelium structure, size and shape of cells. Marked
reducon in mucosal folds, with decrease in secreon
(Fig. 2) compared to control (Fig. 1). The histopathological
alteraons were more obvious in animal treated with
lead acetate 5 mg/kg daily for 30 days. In this treated
animal, destrucon of epithelial lining cells with complete
absence of glandular secreon. There was a decrease
in height of mucosal folds and epithelial cells appeared
with small and dense nuclei. In some alveoli there was a
complete loss or decrease of mucosal folding (Fig. 3).
Histology of prostate gland: Prostate gland of rats with
15 days treatment with lead acetate shows lower
secretary acvity of epithelium, degenerave changes
occur in epithelium structure, size and shape of cells
and reduced secreon(Fig. 5) as compared to control
(Fig. 4).The destrucve changes were more prominent
in animal treated with lead acetate 5mg/kg daily for 30
days.Destrucons of epithelial lining cells with complete
absence of glandular secreon, epithelium is aened
and atrophied,enlargement of prostac alveoli and
aened epithelial lining, damage in epithelial lining,
oozing of prostac secreon into intersal space(Fig. 6).
DISCUSSION
In the present study, body weight and weight of seminal
vesicle and prostate gland were slightly decrease which
might be due to loss of electrolyte the similar results were
reported on sodium uoride,[9] cadmium chloride,[10,11]
nickel sulphate,[12] molybdenum.[13] Reducon of seminal
vesicle weight rao in lead intoxicated rats indicated
seminal damage and impaired funcon.[14]The present
study revealed that the seminal vesicle of treated rat
shows lower secretary acvity of epithelium. Degenerave
changes occur in epithelium structure, size, and shape of
cells, marked reducon in mucosal folds, with decrease
in secreon. The histopathological alteraons were
more obvious in animal treated with lead acetate 5 mg/
Dhurvey V, et al.
ISSN: 0973-3558, e-ISSN: 0973-3566
Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
DOI: 10.31736/jist/v14.i2.2018.26-29
kg body weight daily for 30 days, in this treated animal,
destrucon of epithelial lining cells with complete absence
of glandular secreon. There was a decrease in height of
mucosal folds and epithelial cells appeared with small
and dense nuclei. In some alveoli there was a complete
loss or decrease of mucosal folding. These results are in
agreement with [7] the destrucon of epithelial cell and
low density of seminal plasma, [15] showed the reduced
mucosal fold height and number, lowered secreon in
the lumen. Destrucon and disorganizaon in the lining
epithelium and exfoliaon of some cells in the lumen.
[10, 16] Lead induced seminal vesicle damage such as,
hemorrhage, cell debris, and reduced secreon. [7, 17, 18]
Histopathological study of prostate gland of lead acetate
treated rat showed degenerave changes in epithelium
structure, size and shape of cells, destrucon of epithelial
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toxicity of cadmium and lead on redox cycling in type II
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3. Agency for Toxic Substances and Disease Registry (ATSDR),
Toxicological Prole for Lead, U.S. Department of Health and
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4. R.A. Goyer, M.G. Cherian, Ascorbic acid and EDTA treatment of
lead toxicity in rats, Life Sci. 24 (1979) 433–438.
5. Ru H., Markowitz M., Bijur P., Rosen J. Relaonships among
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6. Winder C., Reproducve and chromosomal eect of occupaonal
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7. Chowdhury A., Recent advances in heavy metals induced eect
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8. El-Zohairy EA, Youssef AF, Abul-Nasr SM, Fahmy IM, Salem D,
Kahil AK. Reproducve hazards of lead exposure among urban
egypan men. ReprodToxicol. 1996; 10:145–151.
9. Chinoy N. and Sharma A. Amelioraon of uoride toxicity by
vitamin’s E and D in reproducve funcon of male mice.
Digital Archive of Fluoride Journal. 1998; 203-216.
10. Hady A, Aal K, Moneim W, Ghafeen (2006) Eect of lead,
cadmium and their combinaon on the tess and seminal
vesicle of rats.Mansoura J. ForensicMed. Clin. Toxicology.2006;
17-37.
lining, in some alveoli enlarged and aened of alveoli
epithelial lining as compared to control. This results
are in agreement with [6] the destrucon of epithelial
cells, disintegraon of the epithelial cells lining,[19] the
boundaries of the cells were not clear,oozing of prostac
secreons into intersal space,[20] lead induced prostate
damage such as hyperplasia, reduced secreon.[7, 17, 18]
CONCLUSION
From the above result it can be concluded that
administraon of 5 mg/kg body weight of lead acetate
daily for 15 days and 30 days duraon in drinking water
could adversely aect the histopathology of seminal
vesicle as well as prostate gland and thus impairs the
reproducve funcons in male albino rat.
11. Saksena S, Dahlgren L, Lau I. Chang M. Reproducve and
endocrinological features of male rats aer treatment with
cadmium chloride. Biology of Reproducon.1977; 609-613.
12. Pandey R. Singh S. Seminal toxicity of nickel sulfate in mice.
Biological Trace Element Research.2001; 211-212.
13. Pandey R. Singh S.Eect of molybdenum on ferlity of male rats.
Bio metal. 2002; 65-72.
14. Farook T, Vanithakumari G, Bhavanewari G, MaliniT,Mononayaki
S. Eect of anethole on seminal vesicle of albino rat. Ancient
Science of Life. 1991; 9-11.
15. Nordberg Eect of long term care cadmium exposure on the
seminal vesicle of mice. Reproducve Ferlity.1975; 165-167.
16. Alaee S, Talaiekhozani A, Rezaei S, AlaeeK,Youseane. Cadmium
and male inferlity. Journal of Inferlity and Reproducve
Biology 2014; 62-69.
17. Mohammed A, Ruquyah S. Jafr A. (2016) Eect of dierent doses
level of silver nanoparcles (AgNPs) on the seminal vesicle and
prostate in albino male rat. Histopathological study. Internaonal
Journal of Scienc and Engineering Research.2016; 980-983.
18. Sitavi Y. Murthy S. Eect of heavy metal stress on the seminal
vesicle of Glossogobiuris. Internaonal Journal of Recent
Scienc Research. 2013; 451-454.
19. Romonyuk A. and Shkryoba A. Morphological changes of
prostate gland due to heavy exposure to heavy metals salts. The
New Armenian Medical Journal 2015; 58-62.
20. Spick C. Hearmn K. Czernin J. Evoluon of prostate cancer with
C-Acetate PET/CT. The Journal of Nuclear Medicine. 2018; vol.
(57).5-10.
Lead Acetate induced Histological alteraons in Seminal-vesicle and Prostate Gland of Wistar rats
ISSN: 0973-3558, e-ISSN: 0973-3566
Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
No. of
animals
Treatment
Seminal
vesicle
Prostate gland
Dislled water(15days) 241.6±1.21 242.20±0.86 0.676±0.0022 0.402±0.0048
Lead acetate (15days) 236.40±1.86 175.20±1.07 0.671±0.0019 0.375±0.0059
Dislled water(30days) 307.80±0.86 309±0.89 0.653±0.0029 0.332±0.0016
Lead acetate (30days) 302.80±1.36 225.20±1.24 0.555±0.0029 0.313±0.0025
Figure 3:
Figure 5
Figure 4:
Figure 6
Values expressed in Mean±SE
ISSN: 0973-3558, e-ISSN: 0973-3566
30 Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
DOI: 10.31736/jist/v14.i2.2018.30-34
1M.Sc. Research Scholar, Department of Forensic Science, Punjabi University, Paala, 147002
Declared None.
ABSTRACT
In developing countries such as India, poisoning is one of
the major causes of deaths. Study of paerns of poisoning
help in ascertaining the prevalent problems associated with
poisoning in India. In the present study, a retrospecve study
has been conducted to study the poisoning cases reported in
Civil Hospital of Moga district of Punjab State of Northern India
during the period of January 2007 to May 2016.
Poisoning cases;
retrospecve study; moga;
Punjab; forensic medicine.
Received on 11th January 2018
Accepted on 23rd November 2018
Published on 31st December 2018
©2018 The Journal of Indian Society of Toxicology.
Published at JIPMER, Pondicherry, 605006, INDIA Subscripon & payment related
queries at: toxicology@aims.amrita.edu and rest all types of queries related to the
journal to be done at drambika_editor@jist.org.in
ARTICLE INFO
Praveen Kumar Yadav, UGC-SRF,
Department of Forensic Science, Punjabi University, Paala,
147002. Email: praveenky15@yahoo.com
How to Cite this arcle:Kaur S, Yadav PK. Poisoning trends in
Moga district of Punjab: A 10 year Record based Observaonal
Study. Journal of Indian Society of Toxicology 2018;14(2):30-
34.
INTRODUCTION
A poisoning episode may be dened as the exposure of
an individual (either by ingeson, injecon or inhalaon)
to a substance(s) associated with the signicant potenal
to cause harm[1]. Poisoning is one of the major causes
of deaths across the world and is a major epidemic
of non-communicable disease in the present century.
Acute poisoning is a global health problem.[2] Poisoning
can either be acute or chronic depending on the me -
period for which poisoning has occurred. Acute poisoning
cases are most commonly encountered by the doctors.
Chronic poisoning can result from various sources
such as environment, food and water supplies, or the
industrial release of waste products.[3].[4] Poisoning
can be accidental, homicidal or suicidal. Accidental
poisonings may be occupaonal hazard as in cases of
pescide poisoning in farmers, etc. Homicidal poisonings
are comparavely rare. The paern of suicidal deaths
can reect the prevailing social set up and psychological
mind-set of the inhabitants of a region[5]. Paerns of
poisoning may vary with geographical locaon. Therefore,
it is important to study the paerns of poisoning in
various parts of world. In developing countries with rural
economies, poisoning by pescides and herbicides is
common. However, the paerns of habitaon and work
can also expose the populaon in warmer countries to
toxins from snakes or spiders. Paerns of poisoning also
Poisoning trends in Moga district of Punjab: A 10 year Record based Observaonal Study
ISSN: 0973-3558, e-ISSN: 0973-3566
Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
reect which type of poisons are readily available or are
important for local tradions. In developed countries,
the epidemiology of poisoning oen reects prescribing
pracce and availability[3]. Therefore, the study of
paerns of poisoning can help in policy making by the
governments of various countries. In this study, we have
done a retrospecve study of various poisoning cases
encountered in a Civil hospital of Moga District of Punjab
state of Northern region of India. From this study, we
hope to uncover the paerns of poisoning prevalent in
the respecve region.
MATERIAL AND METHODS
The present study is a retrospecve study which was
conducted in the Civil Hospital of Moga District of Punjab
state of Northern region of India from January 2007 to
May 2016. Figure 1 illustrates the study area. This study
comprised of the individuals who were admied in the
emergency division dedicated to poisoning cases of the
hospital and were alleged to have been poisoned. The
data was collected from the hospital records. Cases, which
were referred from nearby districts to the central hospital
of Moga district, were not considered. In total 646 case
histories were studied to uncover various paern of
poisoning in the region.
RESULTS
A total 646 individuals were treated for poisoning in the
emergency division of the Civil hospital of Moga District.
433 (67%) paents were males and 213 (33%) were
females. From Fig 2 and Table 1, it is evident that the
incidence of poisoning is maximum in the age group of
21-30 years (278 or 43%) followed by 11-20 years (141
or 21.8%) and 31-40 years (120 or 18.6%) whereas the
minimum numbers of poisoning cases were reported
in age group of less than 10 years (20 or 3.1%). Table 2
illustrates the month wise poisoning case distribuon.
Maximum numbers of paents were admied in July (73
or 11.3%) and September (70 or 10.8%) followed by May
(63 or 9.8%) and April (58 or 8.5%). Minimum numbers
of paents were admied in the month of February and
December (36 or 5.6% paents each). The percentage
of paents admied was maximum in the years of 2014
and 2015 with 89 (13.8) poisoning cases each. This
percentage was followed by 2011 (80 or 12.4%) and 2010
(76 or 11.8%). The minimum numbers of poisoning cases
were observed in year 2007 (39 or 6%) (Table 3). Suicidal
cases (273 or 42.3%) and accidental cases (222 or 34.4%)
were major cause of poisonings followed by addicon
cases (78 or 12.1). Homicidal cases were 19 (2.9%) in
number. 281 paents belonged to poor nancial status
whereas 226 paents belong to good nancial status
(Table 4). Celphos which is the brand name for aluminium
phosphide and is used as pescide was responsible for
maximum numbers of poisoning causalies in the study
area. It resulted in 148 (22.9%) poisoning admissions
followed by drug overdose (12.1%), inseccide poisoning
(11.6%), pescide poisoning (7.1%), and phenyl poisoning
(5.3%) (Table 5). Out of total 646 admissions, 61 (9.4%)
paents died, 368 (57.0%) were treated and discharged,
and 217 (33.6%) were referred to other hospital for
further treatment (Table 6)
DISCUSSION
In the present study, the percentage of males among total
poisoning cases was 67% and 33% were females. These
ndings are strongly supported by and are in convergence
with the naonal and global ndings. A possible
explanaon to these ndings can be the frequent exposure
of males to poisoning agents due to their occupaon.
Males are more prone to the stress which may lead to
the suicidal use of poisoning agents[6]. Similar ndings
were observed by Zia et al[7] (71.4% males), Issa et al[8]
(90.9% males), Singh et al [6] (72.72% males), Prajapa
et al[9] (65.4% males). Kumar and Reddy[10] (65.10%
males), Maskey et al[11] (56.6% males), Aaka et al[2]
(69.3% males). Only minor increments were reported
by Jalali et al[12] (51% males) and Hameed et al [13]
(50.9% males), Jailkhani et al[14] (52% males). Dogan et
al [15], Zohre et al[16] (28.7% males) has reported more
number of poisoning cases in females as compared to
the males. In this study males constuted only 35.3% of
total poisoning cases. In the present study, the age group
having maximum causalies due to poisoning was the
21-30 years age group followed by 11-20 years age group
and 31-40 years age group whereas the least number
of paents belonged to less than 10 year age group and
more than 51 year age group. The age groups of 21-30
years and 31-40 years are the most acve periods of an
individual’s life and result in maximum stress as well.
Various studies (Singh et al[6], Liu et al[17], Escorey
and Shirley[18], Meel[19], Sandhu and Dalal[20], Batra
et al[21], Dash et al[22]duraon of hospitalizaon and
me lapse before arrival at hospital. All OP poisoning
cases admied to the Emergency Department of MKCG
Medical College Hospital and other fatal cases received at
the mortuary between September 1999 and August 2001
were prospecvely studied. Males outnumbered females
and most OP poisoning occurred in the 21-30 year age
group. In 68 (97.1%, Nigam et al[23],Garg and Verma[24])
Yadav PK, et al.
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Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
DOI: 10.31736/jist/v14.i2.2018.30-34
show the vicms are frequently aected in the most
acve periods of their lives i.e. adult age. The vicms
in their extremes of ages were far less aected due to
limited exposure to poisonous substances. Excepon to
this nding was observed by Ahmed et al[25] who reports
that maximum poisoning cases fell within the age group
of 10-20 year age group. In the present study, maximum
numbers of poisoning cases were admied in the months
of July and September followed by the months of May and
April. In the summer months, the agricultural and farming
acvies are on peak which may result in easy availability
of poisonous substances such as organophosphates. This
increase in farming acvity will in return result in the
increase of poisoning cases in summer season. Similar
trends have been proposed by Dash et al[22]duraon of
hospitalizaon and me lapse before arrival at hospital.
All OP poisoning cases admied to the Emergency
Department of MKCG Medical College Hospital and other
fatal cases received at the mortuary between September
1999 and August 2001 were prospecvely studied. Males
outnumbered females and most OP poisoning occurred
in the 21-30 year age group. In 68 (97.1%, Singh et
al[26], and Jalali et al[12].In the present study, maximum
numbers of poisoning cases admied were suicidal cases
followed by accidental cases. The number of homicidal
poisoning is very less as compared to suicidal cases.
Similar results have been reported by Vougiouklakis and
Mitselou et al[1], Aaka et al[2], Liu et al[17], Escoery
and Shirley[18], Batra et al[21], Nigam et al[23], Ahmad
et al[25], Singh et al[26], Soltaninejad et al[27], Zhou
et al[28], and Lee et al[29], Flaganan et al[30], Spiller
et al[31], Gupta and Vaghela[32]. Kiran et al[33], Kar et
al[34]. Homicidal poisoning cases as the major cause of
deaths have been reported by McDowell et al[35] and
Hempstead[36]. Accidental poisoning cases as largest
contributor to poisoning causalies were reported by
Malangu[37].In the present study, maximum of poisoning
cases reported were of organophosphate poisoning. This
may be because, India is an agriculture based country and
in farming oriented states such as Punjab, there is an easy
availability of organophosphates. Organophosphates are
used as pescides to be sprayed on the crops. Similar
paerns have been reported by Aaka et al.[2], Ahmad et
al.[25], Nigam et al.[23].
CONCLUSION
In the present study paerns of poisoning at the Civil
Hospital of Moga District of Punjab state of Northern
region of India from January 2007 to May 2016 were
studies. It was observed that maximum number of
poisoning cases were reported in male populaon of 21-
30 years age group. Moreover, accidental poisoning was
most common cause of poisoning. It was also observed
that poor economic condion was the major cause of
poisoning. Celphos, which is a brand name of aluminium
phosphide was the most frequent substance used for the
poisoning.
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Yadav PK, et al.
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34 Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
DOI: 10.31736/jist/v14.i2.2018.30-34
Months Frequency Percent
49 7.6 7.6
36 5.6 13.2
55 8.5 21.7
58 9.0 30.7
63 9.8 40.4
49 7.6 48.0
73 11.3 59.3
55 8.5 67.8
70 10.8 78.6
49 7.6 86.2
53 8.2 94.4
68 5.6 100.0
646 100.0
Economic
Frequency Percentage
Percentage
226 35.0 35.0
281 43.5 78.5
21 3.3 81.7
118 18.3 100.0
646 100.0
Mortality Frequency Percent
Percentage
61 9.4 9.4
368 57.0 66.4
217 33.6 100.0
646 100.0
Frequency Percent
Percentage
20 3.1 3.1
141 21.8 24.9
278 43.0 68.0
120 18.6 86.5
56 8.7 95.2
31 4.8 100.0
646 100.0
Year Frequency Percentage
Percentage
35 5.4 5.4
89 13.8 19.2
89 13.8 33.0
75 11.6 44.6
72 11.1 55.7
80 12.4 68.1
76 11.8 79.9
47 7.3 87.2
44 6.8 94.0
39 6.0 100.0
646 100.0
Table 3:
Frequency Percent
Percentage
54 8.2 8.2
33 5.1 13.3
3.5 13.8
148 22.9 36.7
4 .6 37.3
78 12.1 49.4
3.5 49.9
75 11.6 61.5
67 10.4 71.9
4 .6 72.5
46 7.1 79.6
31 5.3 84.9
30 4.6 89.5
68 10.5 100.0
646 100.0
Table 5:
Table 4:
Table 6:
ISSN: 0973-3558, e-ISSN: 0973-3566 35
Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
3
4
1 Emergency & Trauma care, Medanta-The Medicity, Gurugram
2 Forensic Medicine & toxicology, Sikkim Manipal Instute of Medical Sciences, Gangtok
3 Emergency & Trauma Care, Grande Internaonale Hospital, Nepal
4 Emergency & Trauma Care. Connental Hospital, Hyderabad
All authors state that
there is no conict of interest withthe work done in this study.
ABSTRACT
Modern Medicine has been at the forefront in the use of
paent simulaon for research, training and performance
assessment. With simulaon, no paents are at risk for
exposure to novice caregivers or unproven technologies. It
becomes very important in eld of toxicological emergencies,
due to its acute onset of presentaon, rapid progression of
symptoms, early deterioraon of vitals and adverse outcomes
in morbidity and mortality of paents in extremes of ages.
Our observaonal study suggests that Forensic Medicine and
Toxicology (FMT) residents have limited exposure to crically
ill paents of trauma and toxicology and the budding forensic
professionals lack the skills to manage them. Simulaon has
the potenal to ll this educaonal void in managing clinical
forensic and toxicological emergencies. The following review
will aempt to answer this call by quanfying the eect of
simulaon-based educaonal intervenons on retenon of
knowledge and clinical performance, as applied to acute care
toxicology.
Poisoning management, Simulaon,
training, Teamwork, Condence, clinical skills,
Resuscitaon, toxicological Emergencies
Received on 30th July 2018
Accepted on 10th December 2018
Published on 31st December 2018
©2018 The Journal of Indian Society of Toxicology.
Published at JIPMER, Pondicherry, 605006, INDIA Subscripon & payment related
queries at: toxicology@aims.amrita.edu and rest all types of queries related to the
journal to be done at drambika_editor@jist.org.in
ARTICLE INFO
Vivekanshu Verma, Emergency &
Trauma care, Medanta-The Medicity, Gurugram. Email:
vivekanshu@yahoo.co.in
How to Cite this arcle:Verma V, Rastogi P, Richhariya D,
Ajay Thapa A, Kaliaperumal P, Sharma C. Mastery learning
of Toxicology life support skills by FMT residents using
simulaon technology in India. Journal of Indian Society of
Toxicology 2018;14(2):35-41.
Simulaon has been used as a teaching tool for nearly 40
years in elds as diverse as aviaon and military training.
However, integraon of this technology into the arenas of
medical educaon and assessment is a relavely recent
development.1 Vision 2015 document of MCI emphasizes
adopon of Contemporary Educaon Technologies - Skills
lab, E-learning, Simulaon.1 Simulaon benets learners
in geng hand’s on experience without causing any
harm to actual casualty.2 Today’s learners have had wide
exposure to communicaon technology through high-
speed computers, the Internet, and smartphones. Given
this exposure and the learners’ experse in its use, they
are recepve and generally excited about educaonal
experiences involving simulated situaons because they
oer a more acve process and employ state-of-the-
art technology.3 The purpose of medical simulaon is
Verma V, et al.
ISSN: 0973-3558, e-ISSN: 0973-3566
36 Journal of Indian Society of Toxicology (JIST) Volume 14, Issue 2, 31 Dec 2018
DOI: 10.31736/jist/v14.i2.2018.35-41
to emulate real paents, anatomic regions, and clinical
tasks, or to parallel real-life situaons in which medical
care is provided.4 The widespread adopon of simulaon
technology marks a divergence from the tradional ‘see
one, do one, teach one’ method of medical training,
which for centuries has relied upon real paents.
Mulple factors have contributed to this revoluon
in training. Changing paerns in healthcare delivery
have resulted in shorter hospital stays and clinic visits.5
Furthermore, the increasing drive to reduce medical
errors and improve paent safety has fueled the impetus
to incorporate simulaon technology into training and
assessment programs.5 Limitaons on trainee work
hours have contributed to decreased clinical experience.6
This has resulted in reduced paent availability for
learning, decreased exposure to crically ill paents, and
decreased me for clinical faculty to teach.7 In addion,
technological advances in diagnosis and treatment, such
as newer imaging modalies and life-saving procedures,
require development of skill sets that dier from
tradional approaches.8 Concurrent progress in simulaon
technology that enables increasingly realisc models
oers advantages for such skill acquision.9 Simulaon
in toxicology educaon can teach the skills needed to
manage rare or crical events, such as cardiopulmonary
arrest or associated trauma.10 Toxicology Trainees can
make errors and learn to recognize and correct them
in the simulated environment without fear of being
penalized or causing harm to paents. And nally, ethical
quesons arise concerning the appropriateness of using
real paents as training resources.11 Much of this debate
centers on sensive tasks (i.e., pelvic examinaons in
females) or those that involve potenal risk of harm
to paents (endotracheal intubaon or other invasive
procedures). All of these factors driving the increased
use of simulaon are part of a paradigm shi toward
outcomes-based medical educaon.12 The consensus
calls for research to explore the methods of assessment
and the correlaon of simulated assessments with clinical
performance.13 One reason for greater use of simulaon
in teaching in Clinical toxicology is that changes in
health care system have shortened hospital stays and
brought sicker paents into the hospital, leaving fewer
opportunies for learners to gain hands-on experience
in managing toxicological emergencies. Simulaon is
currently used as an assessment tool to provide ongoing
feedback during training (formave assessment) and
is gaining popularity as an adjuncve method for
demonstrang competency (summave assessment).14
Recent literature demonstrates increased retenon of
knowledge and skills aer simulaon-based training
in the areas of resuscitaon in intoxicated, associated
trauma, airway management, procedural training, team
training, and disaster management in mass casualty due
to poisoning.15
Conceptual Background
Mannequins come in