Download Rajiv Gandhi University Of Health Sciences, Karnataka

RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, KARNATAKA
BANGALORE
ANNEXURE – II
PROFORMA FOR REGISTRATION OF SUBJECTS FOR DISSERTATION
1.
NAME OF THE
CANDIDATE AND
ADDRESS (IN BLOCK
LETTERS)
Dr. NAGENDER SHARMA
DEPT.OF MEDICINE,
M.R.MEDICAL COLLEGE,
GULBARGA.
PERMANENT ADDRESS
44A, OLD HOUSING BOARD COLONY,
NEAR KAMLA BHAWAN, BHIWANI
(HARYANA) 127021
2.
NAME OF THE
INSTITUTION
H.K.E.SOCIETY’S
MAHADEVAPPA RAMPURE MEDICAL
COLLEGE,
GULBARGA-585105
3.
COURSE OF STUDY AND
SUBJECT
DATE OF ADMISSION TO
COURSE
TITLE OF TOPIC
4.
5.
M.D. (GENERAL MEDICINE)
1st JUNE 2008
STUDY OF CLINICAL PROFILE OF
ORGANOPHOSPHATE COMPOUND
POISONING WITH SPECIAL REFERENCE
TO ELECTROCARDIOGRAPHIC
CHANGES AND ELECTROLYTE
DERANGEMENTS
6. Brief resume of the intended work
6.1 Need for the study
The widespread use of organophosphates and carbamates as
agricultural insecticides has increased the likelihood of poisoning with
these compounds. Cardiac complications often accompany poisoning
with these compounds, which may be serious and often fatal. These
complications are potentially preventable if they are recognised early
and treated adequately. Organophosphate poisoning has been
postulated both in animal and human studies to cause myocardiotoxic
damage (myocardial necrosis). Electrocardiographic changes in
organophosphate compound poisoning have been reported along with
the associated structural myocardial damage. Organophosphate
compound poisoning itself causes diarrhoea and vomiting which can
lead to electrolyte derangements.
Thus, this study is undertaken to study the clinical profile of
organophosphate poisoning and evaluate the importance of
electrocardiographic changes and electrolyte derangements in
organophosphate compound poisoning.
6.2
Review of literature
Dalvi CP, Abraham PP, Iyer SS et al stated that Abnormal ST-T wave
changes and progressive fall in voltage or low voltage were the
commonest ECG changes encountered. Other ECG abnormalities,
like prolongation of QIT interval, Ectopic Beats, conduction defects
and peaked P waves were seen less frequently. The dose of atropine
required was highest and the rate of normalization of ECG and clinical
recovery slowest, in the group with severe poisoning. The mortality
was higher in moderate and severe groups, death was sudden and
clinically unexpected in patient who were appearing to be recovering
normally clinically. Abnormal ECG changes were present in 40% of
mild cases, 87% of moderate cases, 100% of severe
organophosphate poisoning cases .Patient with ECG changes should
be monitored carefully till these changes revert back to normal
because even after transient apparent clinical recovery, these patients
are prone for sudden death1.
A M Saadeh, N A Farsakh, M K Al-Ali et al studied the frequency,
extent and pathogenesis of cardiac complications accompanying
organophosphate and carbamate poisoning. They concluded that
cardiac complications often accompany poisoning with these
compounds particularly during first few hours. 46 cases records (24
females and 22 males) were reviewed. ECG manifestations were,
prolonged QTc interval (67%), Elevated ST segment (24%), inverted
T waves (17%) Prolonged PR interval (9%), Atrial fibrillation (9%),
Ventricular tachycardia (9%), Extrasystoles (6%), Venticular fibrillation
(4%). Other cardiac manifestations were noncardiogenic pulmonary
oedema (43%), sinus tachycardia (35%), Sinus Bradycardia (28%),
Hypertension (22%) and hypotension (17%). Hypoximea, Acidosis
and electrolyte derangements are major predisposing factors2.
S.B Agarwal, V.K Bhatnagar, Amol Agarwal, Usha Agarwal
,K.Venkaiah, S.K Nigam , S.K Kashyap et al studied complete clinical
profile of organophosphate compound poisoning. In there study, sinus
tachycardia, ST Segment depression and T wave Inversion followed
by sinus bradycardia were the most common ECG abnormalities3.
P. Karki, J.A Ansari, S.Bhandary, S Koirala studied extent, frequency
and pathogenesis of cardiac and electrocardiographic manifestation
of acute organophosphate poisoning. They also studied clinical profile
of organophosphate poisoning in terms of age, sex, intension,
symptoms and signs, time interval between compound consumption
and hospitalization, total dose of atropine given, duration of treatment
with atropine, cardiac and electrocardiographic manifestations.
Cardiac manifestations and electrcardiographic changes were
recorded before administration of any medications
ECG
manifestations in there study were prolonged QTc interval (37.8%),
ST/T changes i.e. , Elevated ST segment (16.2%), inverted T waves
(13.5%), Prolonged PR Interval (5.4%) Atrial fibrillation (5.4%),
Ventricular tachycardia (10.8%), Extrasystole (5.4%). Other cardiac
manifestations were sinus tachycardiac (40.5%), Sinus bradycardiac
(18.9%), non cardio genic pulmonary edema (21.6%), hypertension
(13.5%), hypotension (10.8%). In there study cardiac complications
developed in 62.2% of patients, most common were Sinus
tachycardia (40.5%), Prolonged QTc interval (37.8%)4.
Ismail Hamdi kara, Cahfer Guloglu, Aziz Karabulut, Murat Orak et al
studied sociodemographic, clinical and laboratory features of cases of
organophosphorus intoxication and found mean age of
cases24+/_11years, M/F ratio 1/3.8, mostly from low socioeconomical
class and of suicidal intension, most common ECG changes were
sinus tachycardia in 58.3%, ST changes in 54.2 % and T changes in
12.5%. Hypokalemia followed by hyponatremia were the most
common Electrolyte Derangements seen in there study5.
Kumiko Taira,Yoshiko Aoyama and Miwako Kawamata studied
relationship between ECG manifestations and subjective symptoms
accompanying organophosphate pesticide exposure caused by aerial
spray was investigated6.
Yurumez Y, Yavuz Y, Saglam H, Durukan P, Ozkan S, Akdur O,
Yucel M evaluated 85 patients who presented to emergency
department with Organophosphate poisoning and found QTc
prolongation(55.5%) followed by sinus tachycardia (31.8%) were the
most common Elecrocardiographic changes7.
6.3
Objective(s) of the study
1. To study the clinical profile of organophosphate compound
poisoning.
2. To evaluate the importance of electrocardiographic changes
and electrolyte derangements in organophosphate poisoning.
7.
Material and methods
7.1 Source of Data
Patients admitted with history of organophosphate poisoning in
Basaveshwar Teaching and General Hospital, attached to
Mahadeveppa Rampure Medical College, Gulbarga.
7.2 Methods of collection of data(including sampling procedures, if
any)
By using simple random method,100 cases of organophosphate
poisoning admitted over a period of 2 years in Basaveshwar teaching
and General Hospital, Gulbarga will be studied. The patients will be
divided into mild, moderate & severe cases on the basis of modified
criteria of V.N Kabaravala, S.V Solanki &S.C Charterji (1967).
a. Mild cases: Giddiness, headache, vomiting, diarrhoea,
excessive sweating, salivation, abdominal pain, mild to
moderate constriction of pupils. Pulse rate <110/min, normal
BP & no abnormal CVS, RS & CNS findings.
b. Moderate cases: Drowsiness, Bradycardia or tachycardia,
hypo or hypertention &mild pulmonary edema, general
weakness, difficulty in talking, Irritability, fasciculation Or
combination of these.
c. Severe cases: Coma, Cyanosis, Respiratory paralysis,
extensive Fasciculation, pin point pupils, bladder &bowel
incontinence, convulsions Or combination of these. Under any
circumstances.
Treatment will not be withheld for the purpose of study.
Inclusion criteria:
•
All adults with history of consumption &/or exposure to OPC of
either sex, admitted in hospital within 12 hrs of ingestion and
not having been treated outside.
Exclusion criteria:
•
•
•
•
All patients with poisoning due to compounds other than OPC.
Patients with prior H/o consumption of OPC.
Patients who received partial treatment outside and referred
later to this hospital.
Patients having H/o cardiac diseases.
ECG will be recorded in 100 cases before administering atropine,
pralidoxime or any other medications in casuality and ECG will be
repeated in all cases before discharge following recovery from
poisoning to study the possible abnormalities which could have been
from organophosphate compound poisoning.
Blood samples will be drawn for electrolyte estimation (Na+, K+,
Ca+2) before starting treatment for poisoning in all cases and same
investigation will be repeated after recovery before discharge Or
before expiry of those expired.
7.3
Does the study require any investigation or intervention to be
conducted on patients or other humans or animals? if so please
describe briefly
Yes, the study requires investigation like ECG and serum electrolytes
(Na+, K+, Ca+2) serum cholinesterase.
7.4
Has ethical clearance been obtained from your institution in case
of 7.3?
Yes. Ethical clearance has been obtained from “Ethical clearance
committee” of the institution.
8
List of References
1. Dalvi
CP,
Abraham
PP,
Iyer
SS.
Correlation
of
Electrocardiographic
changes
with
prognosis
of
Organophosphate poisoning.JPGM1986; Vol.32/3 :115-119
2. Saadeh AM, Farsakh NA, Al-Al MK. Cardiac manifestations of
acute carbamate and Organophosphate poisoning. Heart
1997;77:461-464
3. Agarwal SB, Bhatnagar VK et al. Impairment in Clinical Indices in
Acute Organophosphate Insecticide poisoning Patients in
India. The Internet Journal of Toxicology. 2007; Vol 4: No.1
4. P Karki, JA Ansari et al. Cardiac and Electrocardiographical
manifestations of Acute Organophosphate poisoning.
Singapore Med J 2004 Vol 45(8);385-389
5. Ismail Hamdi Kara, Cahfer Gulog LU et al. Sociodemographic,
Clinical, and laboratory features of cases of organic
phosphorus Intoxication who attended the Emergency
Department in the Southeast Anatolialian Region of Turkey.
Environment Research. Feb 2002; Vol 88 Issue2: 82-88.
6. Kumiko Taira, Yoshiko Aoyama, Miwako Kawamata. Long QT and
ST-T Change Associated With Organophosphate Exposure
By Aerial
Spray.
Environmental Toxicology
and
Pharmacology July 2006; Vol 22: Issue1:40-45.
7. Yurumez Y, Yavuz Y et al. Electrocardiographic findings of Acute
Organophosphate Poisoning. J Emergency Med. 2008
Feb23; Doi: 10.1016/j.jemer,Med.2007; 08.063.
8. Singh S, Balkrishnan S, and Malhotra V. Parathion Poisoning in
Punjab (A clinical and electrocardiographic study of 20
cases) J. Assoc Phys. India 1969; 17: 181-187.
9. Kiss Z and Fazekas, T. Organophosphate poisoning and complete
heart block (letter). K. Roy. Soc Med. 1982; 75: 85-86,
138-139.
10. Kabrawala VN and Solanki SV. Pralidoxime chloride as an
adjuvant in the treatment of diazinon poisoning. JAPI, 1971;
19: 278.
11. DE and SC Chatterjee. Poisoning with organophosphorus
compounds. JIMA, 1967; 48: 153.
12. Ludomirsky A, Klein H, Sarelli P, Becker B, Hottman S, Taitelman
U et al. Q.T prolongation and polymorphous (torsades de
pointes)
ventricular
arrhythmias
associated
with
organophosphorus insecticide poisoning. Am J Cardiol 1982;
49: 1654-8.
9
Signature of Candidate
10
Remarks of guide
11
11.1 Name and designation
of the
Guide
A good study helps in treatment and
outcome of the patient
Dr. B. MANGSHETTY
M.D.
ASSOCIATE PROFESSOR
DEPARTMENT OF MEDICINE,
M.R. MEDICAL COLLEGE, GULBARGA
11.2 Signature
11.3 Co- guide (if any)
Dr. JAGADISH B. INGIN
M.D (Biochemistry)
PROFESSOR & HOD
DEPARTMENT OF BIOCHEMISTRY ,
M.R. MEDICAL COLLEGE, GULBARGA
11.4 Signature
11.5 Head of the
Department
11.6 Signature
12
12.1 Remarks of the
Chairman and
Principal
12.2 Signature
Dr. G. VEERANNA
M.D., DM (Cardiology)
PROFESSOR AND HOD
DEPARTMENT OF MEDICINE
M.R.MEDICAL COLLEGE, GULBARGA