Analytica MedicaISSN:0974-4142

Volume : 13 No: 1 & 2 Jan- Dec. 2010

Journal of Scientifi c & Research Society

BLDE UniversityBijapur-586 103, Karnataka, India

B.L.D.E. UNIVERSITY

Smt. Bangaramma Sajjan Campus, Sholapur Road, Bijapur – 586103, Karnataka, India.University: Phone: +918352-262770, Fax: +918352-263303 ,

Website: www.bldeuniversity.org, E-mail: office@bldeuniversity.org

Analytica MedicaISSN:0974-4142

Volume : 13 No. 1 & 2 Jan- Dec-2010

Journal of Scientific & Research Society

BLDE UniversityBijapur-586 103, Karnataka, India

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ISSN:0974-4142Analytica MedicaAn

alytica

Medic

a

Disclaimer:Statements and opinions expressed in the articles published in the journal are those of authors and not necessarily of the Editor. Neither the Editor nor the Publisher guarantees, warrants or

endorses any product or service advertised in the journal.Published by: Scientific & Research Society

BLDE University, Bijapur-586 103, Karnataka, INDIAPrinted by:BLDEA Offset Printers, Bijapur

Volume: 13 No : 1& 2 Jan-Dec - 2010 Editorial Board Editor Dr J G Ambekar Professor, Dept. of BiochemistryAssociate Editors Dr Aparna Palit - Asso. Prof. Skin & VD Dr Surekha Arakeri - Prof. Pathology Dr Praveen Shahapur - Asso. Prof. MicrobiologyAdvisory Board Dr Satish S Jigjini - Vice-Chancellor Dr R C Bidri - PrincipalMembers Dr D G Talikoti Dr S P Choukimath HOD, Anasthesia HOD, Psychaitry Dr S D Desai Dr Anand Dharwadkar HOD, Anatomy HOD, Physiology Dr O B Pattanashetti Dr Dilip Rathi HOD, Orthopaedics HOD, Biochemistry Dr M M Angadi Dr S V Patil HOD, Comm. Med. HOD, Paediatrics Dr K Yoganarasimha Dr M S Biradar HOD, Forensic Medicine HOD, Medicine Dr B R Yelikar Dr Tejshwini Vallabh HOD, Pathology HOD, Surgery Dr R S Wali Dr S V Reddy HOD, Pharmacology HOD, Obg & Gyne. Dr B V Peerapur Dr Arun Inamdar HOD, Microbiology HOD, Dermatology Dr K Yoganarasimha Dr K P Vallabha HOD, Med. Edn. HOD, Opthalomology Dr N H Kulkarni HOD, Otorhenolyrangeology

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Original ArticlesA COMPARATIVE STUDY OF ECG PATTERNS IN DIFFERENT TRIMESTERS OF PREGNANCYDr.Nandini.B.N, Dr.Manjunath Aithala,Department of Physiology, BLDEU’s Shri B.M.Patil Medical College, Hospital & Research Centre, Bijapur. .................................1A PROSPECTIVE COMPARISION OF NIFEDIPINE WITH RITODRINE FOR TOCOLYSISJaju Purushotham Bankatlal, Veena B. DhabadiDepartment of Obstetrics &Gynaecology, BLDEU’s Shri B.M.Patil Medical College, Hospital & Research Centre, Bijapur. ................10A PROSPECTIVE STUDY TO ASSESS THE ROLE OF AGE AS A FACTOR IN HEALING OF TYMPANIC MEMBRANE FOLLOWING MIDDLE EAR SURGERIESPreety Ninan, S.P.GuggurigoudarDepartment of ENT, BLDEU’s Shri B.M.Patil Medical College, Hospital & Research Centre, Bijapur. ................18Case ReportSCHNEIDERIAN PAPILLOMA OF MIDDLE EAR-A RARE CASE REPORTDr. Savita Shettar , Dr. S. B. Hippargi, Dr.B.R.Yelikar.Department of Pathology, BLDEU’s Shri B.M.Patil Medical College, Hospital & Research Centre, Bijapur. ................25Original ArticlesA STUDY OF PULMONARY FUNCTIONS OF WOMEN AT DIFFERENT TRIMESTERS OF PREGNANCY IN BLDEU’S SHRI B.M.PATIL MEDICAL COLLEGE HOSPITALAnita Teli, Asha.Dharwadkar, Manjunatha. Aithala Department of Physiology, BLDEU’s Shri B.M.Patil Medical College, Hospital & Research Centre, Bijapur. ......................................................................................28ROLE OF EXERCISE AND NUTRITION ON CARDIOPULMONARY FITNESS ON RESIDENTIAL AND NON-RESIDENTIAL SCHOOL CHILDRENDr Jyoti Khodnapur, Dr G B Dhanakshirur, Dr Manjunatha Aithala Department of Physiology, BLDEU’s Shri B.M.Patil Medical College, Hospital & Research Centre, Bijapur. ................36

Analytica MedicaJan-Dec 2010 CONTENTS Volume. 13 Number. 1& 2

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DECREASED PARASYMPATHETIC FUNCTION IN HEALTHYOFFSPRINGS OF TYPE-2 DIABETIC PARENTSSangeeta.D.Tuppad, Anand R Dharwadkar*, Asha A.Dharwadkar*, Manjunath A**Department of Physiology, BLDEU’s Shri B.M.Patil Medical College, Hospital & Research Centre, Bijapur. ................44

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Original ArticleA COMPARATIVE STUDY OF ECG PATTERNS IN DIFFERENT

TRIMESTERS OF PREGNANCYDr.Nandini.B.N, Dr.Manjunath Aithala,

Department of Physiology, BLDEU’s Shri B.M.Patil Medical College, Hospital & Research Centre, Bijapur.

AbstractPR interval reflects the slow conduction of an impulse through the AV node, which is

controlled by the balance between the sympathetic and parasympathetic divisions of the autonomic nervous system. The objective of the study is to investigate the mechanism of electrocardiogram’s short P-R interval during pregnancy. We surveyed 150 pregnant women were chosen for the study, i.e., 50 women in each trimester of pregnancy and were compared with another 50 age matched non-pregnant women as controls who had normal P-R interval. In first, second and third trimesters of pregnancy, there was highly significant rise in heart rate( p<0.001 i.e., 1.12E-12 , 7-05E-12 and 3.49E-16 respectively) as compared to control. There was a statistically significant decrease in PR interval (p<0.001) in all trimesters of pregnancy when compared to control group.Key words: Pregnancy, ECG, PR interval, INTRODUCTION

In pregnant women, large number of local and systemic changes are known to occur. These changes will continue throughout pregnancy1 especially cardiovascular changes such as increase in heart rate, cardiac output and intravascular volume2. The physiological changes during pregnancy facilitate the adaptation of the cardiovascular system to the increased metabolic needs of the mother enabling adequate delivery of oxygenated blood to the peripheral tissues and to the fetus3. In the absence of these adaptations, incidence of gestational complications such as fetal growth restriction and pregnancy induced hypertension are known to increase.4

Hemodynamic changes during pregnancy play a major role in the induction of arrhythmias. The increased incidence of arrhythmias during pregnancy is also reported.5

The anatomical, physiological and biochemical adaptations to pregnancy are profound. Many of these changes begin soon after fertilization and continue throughout gestation.6

During pregnancy and puerperium, there are remarkable changes in the heart and circulation. The most important changes in cardiac function occur in the first eight weeks of pregnancy.6

2

The demands for an increased flow of blood during pregnancy are met mainly by increasing the cardiac output. In an average non pregnant woman, cardiac output is about 4.5 liter per minute. At the eighth month of pregnancy, this rises to about 5.5 L.7

The cardiac output rises to a peak in the middle of pregnancy and thereafter slowly declines thereafter though it still remains 1 L/min above the non pregnant values.8 The decline in cardiac output in late pregnancy might be due to postural changes. In the supine position, the large uterus often impedes cardiac venous return. It can decrease to about 20% less in supine position as compared to the lateral recumbent position.6

Cardiac output depends on the heart rate and on the output of the ventricles at each beat i.e., the stroke volume.The resting pulse rate increases as the pregnancy advances. Non-pregnancy : 70 beats/min,Early pregnancy : 78 beats/min and End of pregnancy : 85 beats/min

The heart rate increases by 10-15 beats per minute more than the pre - pregnant state. There is an increase in both stroke volume and heart rate. The stroke volume increases to 10% more than the non-pregnant value, where as the heart rate increases to 20% more than the non-pregnant value. In the early months of pregnancy, the stroke volume rises rapidly to a peak and then declines, while the pulse rate slowly increases. The mechanisms of increasing the cardiac output have varying importance at the extremes of pregnancy.

There is an increased susceptibility for cardiac arrhythmias during pregnancy. It is manifested by frequent sinus tachycardia, atrial or ventricular premature beats and paroxysmal supraventricular tachycardia.8

MATERIALS AND METHODSA cross sectional study was conducted in the Department of Physiology, Shri B.M.Patil

Medical College, Hospital and Research Centre, Bijapur. Duration of the study was one year from December 2008 to November 2009.Method of Collection of data: Study Group: 150 pregnant women in the age group of 20-35yrs who were attending

the OPD of OBGy of Shri B.M. Patil Medical College were included in the study group. The study group was in turn divided into 3 subgroups. Each sub group was comprising of 50 women in first, second and third trimesters of pregnancy.

Control Group: It was comprising of another apparently healthy age matched 50 non pregnant women.

Recording of ECG:ECG was recorded after giving 5 minutes of rest to the subject to allay anxiety. ECG

was recorded in all 12 leads i.e., 3 Standard Bipolar Limb Leads I: II & III, 3 Unipolar

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augmented limb leads: aVR, aVL, aVF and 6 Precordial leads: V1 to V6, by connecting electrodes to left arm, right arm, left leg and right leg in supine position.STATISTICAL ANALYSIS

The results were expressed as Mean + SD for continuous data and number and percentages for categorical data. Z test was used for comparison between control and study groups and Z test was used for comparison within the study group. Categorical data was analyzed by Chi- square test.

A ‘p’ value of 0.05 or less was considered as statistically significant.Heart Rate:

Heart rate is expressed in terms of beats per minute. Heart rate in control, pregnant women in 1st, 2nd and 3rd trimesters were 75.68 + 3.99, 82.28 + 7.84, 88.24 + 9.10 and 95.52 + 7.04 bpm respectively (Table 1). Heart rate showed a statistically significant increase in 1st, 2nd and 3rd trimesters of pregnant women when compared to non pregnant women (p <0.001) (Table 2). Similarly, there was a statistically significant increase in heart rate in 2nd and 3rd trimesters (p <0.001) when compared to 1st trimester of pregnant women (Table 2). There was a statistically significant increase in heart rate in 3rd trimester (p <0.001) when compared to 1st trimester pregnant women (Table 3). P wave:a. Duration:

P wave duration (sec) in control, pregnant women in 1st , 2nd and 3rd trimesters were 0.08 + 0.01, 0.08 + 0.01, 0.08 + 0.01 and 0.07 + 0.01 respectively (Table 1). The P wave duration among control and study group and within the subgroups of study group were not statistically significant (p>0.05) (Table 2 & 3).b. Amplitude:

P wave amplitude (mv) in controls, pregnant women in 1st, 2nd and 3rd trimesters were 1.00 + 0.17, 1.00 + 0.23, 1.02 + 0.27 and 1.02 + 0.28 respectively (Table 1). The P wave amplitude among control and study group and within the subgroup of study group were not statistically significant (p>0.05) (Table 2 & 3).PR Interval:

PR interval (sec) measured in control, pregnant women in 1st, 2nd and 3rd trimesters were 0.15 + 0.01, 0.14 + 0.02, 0.14 + 0.02 and 0.13 + 0.02 respectively (Table 1). There was a statistically significant decrease in PR interval (p<0.001) in all trimesters of pregnancy when compared to control group. Similarly, a statistically significant decrease in PR interval was observed in 2nd (p< 0.05) and 3rd trimesters (p< 0.001) when compared to 1st trimester of pregnancy (Table 2 & 3).

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Table 1

: Mean

+ SD a

nd Ra

nge of

Heart

rate,

P wave

and P

R Inte

rval of

subje

cts in

Contr

ol and

Study

groups

PARA

METE

RSCO

NTRO

L1ST T

RIMES

TER

2ND TR

IMES

TER

3RD TR

IMES

TER

Mean

+ SD

Range

Mean

+ SD

Range

Mean

+ SD

Range

Mean

+ SD

Range

HR (be

ats/min

)P w

ave

75.68

+ 3.99

68 – 8

482.

28 + 7

.8466

– 100

88.24

+ 9.10

72 – 1

0895.

52 + 7

.0484

– 112

Dur

(sec)

0.08 +

0.01

0.06 –

0.10.0

8 + 0.0

10.0

4 – 0.1

0.08 +

0.01

0.04 –

0.10.0

7 + 0.0

10.0

4 – 0.1

Amp

(mv)

1.00 +

0.17

0.5 – 1

.51.0

0 + 0.2

30.5

– 21.0

2 + 0.2

70.5

– 21.0

2 + 0.2

80.5

– 2P

R Inte

rval

(sec

)0.1

5 + 0.0

10.1

2 – 0.1

60.1

4 + 0.0

20.1

– 0.16

0.14 +

0.02

0.1 - 0

.160.1

3 + 0.0

20.01

4 – 0.1

6

Table 2

: Test o

f Signi

ficance

of He

art ra

te, P w

ave an

d PR I

nterva

l using

Z ati

stics b

/n Cont

rol an

d Stud

y gro

ups.

PARA

METE

RSCO

NTRO

L & 1ST T

RIMES

TER

CONT

ROL &

2ND TR

IMES

TERC

ONTR

OL &

3RD TR

IMES

TER

Z-Valu

eP-V

alue

Z-Valu

eP-V

alue

Z-Valu

eP-V

alue

HR (be

ats/min

)P w

ave5.3

00.0

001***

4.69

0.0001

***5.7

60.0

001***

Dur

(sec)

0.43

0.667

0.39

0.696

0.37

0.711

Amp

(mv)

01

01

01

PR Int

erval

(sec)

2.53

0.0003

**2.5

10.0

003**

2.11

0.0003

** p>

0.05: N

ot Sign

ificant

, *p: <0

.05: Si

gnifica

nt, **

p: <0.0

1: High

ly sign

ificant

, *** p

: <0.00

1: Very

highly

sig

nifican

t.

5

Table 3

: Test o

f Signi

ficance

for He

art ra

te, P w

ave an

d PR I

nterva

l using

Z Sta

tistics

within

the su

bgroup

s of

Study

group.

PARA

METE

RS1ST &

2ND TR

IMES

TERS

1ST & 3RD

TRIM

ESTE

RS2ND

& 3RD

TRIM

ESTE

RS

Z-Valu

eP-V

alue

Z-Valu

eP-V

alue

Z-Valu

eP-V

alue

HR

(beats/ min

)P w

ave

3.50

0.0001

***7.7

90.0

001***

3.99

0.0001

***Du

r (se

c)0.3

9

0.696

1.23

0.218

0.49

0.624

Amp

(mv)

0

10.4

00.6

890

1

PR

Interva

l (se

c)2.5

10.0

12*4.4

60.0

001***

2.93

0.0034

**

p>

0.05: N

ot Sign

ificant

, *p: <0

.05: Si

gnifica

nt, **

p: <0.0

1: High

ly sign

ificant

, *** p

: <0.00

1: Very

highly

sig

nifican

t.

6

7

DISCUSSIONPregnancy is a normal physiological process. It induces widespread circulatory

adaptations in the mothers. The pregnancy induced changes in the cardiovascular system develop primarily to meet the increased metabolic demands of mother & fetus.

Both structural and functional changes are known to occur in the heart and vessels due to pregnancy. Ventricular dimensions, heart rate, cardiac output, vascular compliance and capacitance will increase whereas peripheral resistance and blood pressure decrease during pregnancy. Many of these changes are induced by gestational hormonal milieu which influences vessel structure, basal tone and reactivity via receptors for chorionic gonadotropin, estradiol and progesterone located in vascular endothelium and smooth muscle.9

A cross-sectional study was carried in 150 healthy pregnant women and 50 healthy non pregnant women in the age range of 18-35 years of BLDEA’s Shri B M Patil Medical College, Hospital and Research Centre, Bijapur. The subjects were distributed in two groups, i.e., control group and the study group. The study group was comprising of subjects in 1st , 2nd & 3rd trimesters of pregnancy.Heart Rate:

In our study there was a statistically significant increase in the heart rate in 1st, 2nd and 3rd trimesters of pregnancy as compared to non pregnant women.

A progressive increase in heart rate is observed as age of pregnancy advances. Heart rate increased by approximately 15% in the 5th week. It increased after 8th week to a maximum of approximately 85-90 beats per minute. In the last trimester of pregnancy, there is a chance of an increase of 10-20 beats per min. The heart rate of a pregnant woman steadily increased throughout pregnancy.11 The increase in the heart rate is linked to autonomic nervous system changes that produce alterations in cardiac autonomic modulation. Failure of these adaptations may result in pregnancy related complications.

The increase in heart rate may have been triggered to maintain the cardiac output in a state of relative hypovolemia12. The increase in heart rate was due to a decrease in vagal baroreflex as well as a decrease in parasympathetic tone.13 The increase in heart rate mainly during third trimester of pregnancy compensates for the fall in the stroke volume resulting from caval compression.15

The observations made in our study are in agreement with the findings of studies conducted by Duvekot JJ 11, Schier RW & Briner VA12, Voss A 13, Hytten 7, Clap IF & Capeless E9, EKholm EKM .14

P wave:In our study, there was no statistically significant difference in measurements of P

wave amplitude and duration when compared between the control and the study groups.

8

PR Interval:PR interval was shown to be statistically significantly decreased in 1st, 2nd and 3rd

trimesters of pregnancy as compared to control group. There was also a statistically significant decrease in 2nd & 3rd trimesters of pregnancy compared to 1st trimester of pregnancy and in 3rd trimester of pregnancy when compared to 2nd trimester of pregnancy.

The decrease in PR interval during pregnancy could be due to shortening of A-V conductance with respect to tachycardia that accompanies during pregnancy.16

The PR interval is shortened due to Accelerated atrioventricular node conduction, accelerated atrioventricular conduction may be due to following mechanisms, high sympathetic tone, atrioventricular node bypass, AV acceleration, small atrioventricular node, increased heart rate, individual differences, fever, exercise hypoxia, hyperthyroidism, anemia, and other sympathomimetic drugs can cause PR interval shortened

The results showed, in late pregnancy PR shortening was significantly higher than the incidence of early pregnancy, this maybe duetothe following reasons advanced maternal blood volume, increased oxygen demand, the formation of organizations causing relative hypoxia, the body more sensitive to hypoxia leads to myocardial ATP production in the high-energy phosphate bond reduced sympathetic reflex caused excitement, leading to accelerated conduction atrioventricular junction, leaving PR interval shortened.

Similar report was made by Joseph E Carruth et al. In their study, they found that mean PR interval was shorter at 3rd trimester when compared to 1st and 2nd trimesters of normal pregnancy & it was statistically significant.10

After 2 months of delivery ECG review showed that only 3 cases had PR interval shortened, the other had been returned to normal, indicating that the body changes in neuroendocrine and other physiological recovery. This indicates that shortening of PR interval during pregnancy is benign and no treatment is required.

REFERENCES1) Dawn CS. Maternal physiology during pregnancy. In: Text book of Obstetrics and

Neonatology.16th ed. Calcutta: Dawn books 2003: 51.2) Ozmen N, Cebeci BS, Yiginer O, Muhcu M, Kardesoglu E and Dincturk M. P- wave

dispersion is increased in pregnancy due to shortening of minimum duration of p: Does this have any clinical significance? J International medical research 2006; 34:468-474.

3) Oakeley C, Warnes CA. Physiological changes in pregnancy. J Obstet Gynaecol India 1968;18:34-38.

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4) Carla A, Oppen V, Twell IV, Robert M, Bruinse WH, Heethaar RM. A Longitudinal study of maternal hemodynamics during normal pregnancy. J Obstet and Gynaecol 1996; 88: 40.

5) Nakagawa M, Katou S, Ichinose M, Nobe S, Yonemochi H, Miyakawa I. Characteristics Of New Onset Ventricular Arrhythmias in Pregnancy. J Electrocardiology 2004; 37: 47-53.

6) Cunningham GF, Gant NF. Maternal adaptations to pregnancy. In:Williams Obstetrics. 21st ed. New York: McGraw-Hill; 2001: 167-200.

7) Hyttenn FE, Leitch I. Physiology of human pregnancy. 2nd ed. Oxford: Blackwell; 1971:315-318.

8) Zipes, Libby, Bonow, Braunwald. Pregnancy and cardiovascular disease. In: Braunwald’s heart disease a text book of cardiovascular medicine. 7th ed. Philadelphia: Elsevier; 2004:1965-1967.

9) Clapp III JF, Capeless E. Cardiocavascular function before, during and after the first and subsequent pregnancies. Am J Cardiol 1997; 80: 1469-1473.

10) Carrutn JE, Mirvis SB, Brogan DR, Wenger NK. The electrocardiography in normal pregnancy. Am Heart J 1981; 102: 1075-1078.

11) Duvekot JJ, Cheriex EC, Pieters FA, Meheere PP, Peters LL. Early pregnancy changes in hemodynamics and volume homeostasis are consecutive adjustments triggered by a primary fall in systemic vascular tone. Am J Obstet Gynecol 1993; 169:1382-1392.

12) Schier RW, Briner VA. Peripheral arterial vasodilatation hypothesis of sodium and water retention in pregnancy: implications for pathogenesis of pre eclampsia-eclampsia. Obstet Gynecol 1991; 77:632-639.

13) Voss A, Malberg H, Schumann A, Wessel N, Walther T, Stepan H. Baroreflex sensitivity, heart rate and blood pressure variability in normal pregnancy. Am J Hypertens 2000; 13:1218-1225.

14) Ekholm EMK, Hartialaj, Huikuri HV. Circardian rhythm of frequency-domain measures of heart rate variability in pregnancy. Br J Obstet & Gynecol 1997; 104: 825-828.

15) Julian DG, Wenger NK. Heart disease and heart surgery during pregnancy. In: women and heart disease. United Kingdom: Martin Dunitz; 2000.196.

16) Adamson DL, Piercy CN. Managing palpitations and arrhythmias during pregnancy. Postgraduate M J 2008; 84: 66-72.

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Original ArticleA PROSPECTIVE COMPARISION OF NIFEDIPINE WITH

RITODRINE FOR TOCOLYSISJaju Purushotham Bankatlal, Veena B. Dhabadi

Department of Obstetrics &Gynaecology, BLDEU’s Shri B.M.Patil Medical College, Hospital & Research Centre, Bijapur.

AbstractStructural Abstract:Objectives: To compare the tocolyticefficacy of Nifedipine and Ritodrine, their adverse effects and neonatal outcome.Design : Prospective randomized trial.Methods : One hundred twenty women with clinical features of preterm

labour fulfilling designated inclusion and exclusion criteria were enrolled in the study. They were allocated to eethernifedipine group or Ritodrin group by using simple randomization technique. Tocolytic efficacy, maternal side sffects and neonatal outcomes were evaluated. Tools of statistical analysis used were Epi Info software and Chi square test.

Results: Tocolysis was successful i.e, prolongation of pregnancy for 48 hours in 54% (90%) women in Nifedipine group as compared to 41 (68.3%)women in Ritodrine group (p value =0.003 and chi square = 8.54). The prolongation of pregnancy uoto 37 weeks was in 28 women (46.6%) in Nifedipine group as compared to 16 women (26.6%) in Ritodrine group ( p value = 0.033). 18 women (30%) in Nifedipine group had side effcts as compared to 48 women (80%) in Ritodrine group (p value <0.001). Neonatal outcome was similar in both the groups.

Conclusion: Oral Nifedipine is cheaper and effective alternative which has fewer andless serious side effects as compared to I.V.Ritodrine for suppression of the preterm labour.

Key words: Preterm labour, Nifedipine, Ritodrine, tocolysisIntroduction :

Preterm labour remains one of the unconquered frontiers in the present era of obstetrics. Its incidence is obout 7-9 % of pregnancies accounting for three quarters of the mortality

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and morbidity among newborns without congenital anamalies1. Throughout the years a variety of drugs with different pharmacologic principles are used to suppress preterm labour. The choice is limted by their efficacy safety and side effects. Ritodrine, Beta sympathomimetic, is one such agent which is commonly used tocolytic. It has serious meternal and fetal side effects limiting its use2.therefore it is necessary to search for better tocolytic which should be effective and safe with minimal side effects.

Nifedipune, calcium channel blocker, is an effective smooth muscle relaxant with low toxicity low teratogenicity3. There is growing evidence that nifedipine is effective in suppressing preterm labour with minimum maternal and fetal side effects. It relaxes the uterus by inhibiting inward flow of calcium ions across uterine smooth muscle cells.

In some animal studies the administration of nifedipine has been associated with decrease in uterine blood flow resulting in fetal hypoxia and acidosis4. However studoes in human pregnancies did not show any significant alteration in uterine blood flow.

Question still remain concerning the tocolytic effectiveness and side effects of nifedipine. In this paper we present the result of a prospective randomized study which was designed to compare the efficacyof oral Nifedipine with I.V.Ritodrine.Material and Methods

This study was conducted at Shri . B. M. Patil Medical College Hospital and Research Centre, Bijapur, during October 2006 to September 2008. One hundred and twenty women with preterm labour fulfilling inclusion and exclusion criterion were enrolled . Sixty women were assigned to Nifedipine group and sixty women to Ritodrine group by simple randomization technique. The groups were similar with respect to maternal age, gestational age and parity.

Preterm labour was diagnosed as regular uterine contractions of four in twenty minutes with cervical dilatation of greater than one one cm and effacement of eighty percent or more as proposed by ACOG guidelines.

Inclusion criteria were singleton pregnancy with vertex presentation between 28 wks and 36 wks with cervical dilatation of 1 to 3 cms and intact membranes. Exclusion criteria were antepartum haemorrhage, pregnancy induced hypertension, congenital anomaly, intrauterine growth retardation, bronchial asthma, diabetis mellitus, cardiovascular diseases, severe anemia, hydramnios and chorioamnionitis.

Hospital Ethics committee approved the study. Informed consent was taken from all the participants. Detailed history was taken. Thorough general, systemic, obstetric, per speculum and per vaginal examination was done. Each women was investigated for Hb%, TC, DC, Urine – Routine, Blood group & Rh typing, HIV, HBsAg, USG and High vaginal swab for culture & sensitivity.

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Group ‘A’ comprised of sixty women who were given oral Nifedipine. It was administered as an initial oral loading dose of 30 mg. If uterine contractions persisted after 90 minutes , another 20 mg Nifedipine was given orally . if labour was suppressed after the first or second dose , a maintenance dose of 20 mg Nifedipine was given orally every 8th hourly till 37 wks or till delivery whichever occurs early . However if uterine contractions persisted for 60 minutes after the second dose , the treatment was considered as ‘Nifedipine failure’

Group ‘ B ‘ was constited by 60 women who were given intravenous Ritodrine . 100mg of Ritodrine (two ampoules of Ritodrine each containing 50 mg ) was added to 500 ml of ringers lactate. the infusion was started at the rate of 50 µg / minute and increased by 50 µg every 15 minute until the uterine contractions stopped , upto maximum rate of 350 µg / minute. Infusion was stopped if unacceptable side effects developed like palpitations, chest pain and tachycardia> 120/ min .

I. V. infusion of Ritodrine drip was continued for 24 hours after the cessation of uterine contractions. Oral ritodrine 10 mg tablet was given 30 minutes before stopping IV drip and continued every 6 hrly till 37 wks of pregnancy or delivery whichever occurs early. Tocolysis was considered successful if delivery was deferred for at least 48 hours.

All women in the study were given 12 mg betamethasone I.M. and repeated after 24 hours to enhance fetal lung maturity. Antibiotic prophylaxis in the form of oral 250 mg amoxicillin and 250 mg of cloxacillin 8th hourly was given to all women. Metronidazole was added if there were signs of bacterial vaginosis.

Trestment failure was said to exist if uterine relaxation was not achived despite administration of described maximum dose or development of significant side effects which necessitated discontinuation of therepy. Data regarding mean prolongation of pregnancy ( at 48 hours, 1 week, 37 wks ), side effects, failure of treatment , and gestational age at delivery, Apgar score and neonatal details were recorded. Patient variables, results of tocolysis, side effects and neonstal outcomes were analyzed statistically by Fischer’s exact test wherever appropriate to determine significance (P < 0.05 ), chi-square (X2) analyses with Yate’s correction by Epi-info software.

In this hospital incidence of preterm delivery was 10% during the study period.Results :

As seen in Table 1 there was no significant difference among the various characterstics in both groups (p value >0.05). 85% of Nifedipine group and 90% of Ritodrine group were between 16 years and 25 years of age .Primigravida were in majority in both the group i. e. 75 % in Nifedipine group and 80% in Ritodrine group . 66.6% of Nifedipine group & 58.3% of Ritodrine group were booked cases . More number of women was between gestational age 32 to 34 wks being 60% in Nifedipine group and in Ritodrinegroup .

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Table 2 shows that the prolongation of pregnancy upto 48 hrswas seen more in Nifedipine group as compared to Ritodrine group (p value = 0.004, Chi-Squre = 8.54 and df= 1 ). It is stastically significant. This shows that Nifedipine was more successful in delaying delivery for 48 hours enabling corticosteroids to enhance fetal lung maturity. The prolongation of pregnancy upto 7 days was comparable in both groups. Prolongation of pregnancy till 37 weeks was seen in 46.6% in Nifedipine group as compared to 26.6% in Ritodrinegroup .p value is 0.0371 which is statistically significant .

Table 3 shows that failure was more in Ritodrine group as compared to Nifedipine group, p value is 0.0034 & chi-square = it is statistically significant Table 4 shows comparison of side effects , Out of sixty women treated with Nifedipine 12 ( 20% ) had headache , 5 ( 8% ) had palpitation and 3 ( 5% ) had flushing . These side effects were not severe enough to discontinue therapy. Out of sixty women treated with Ritodrine, 25 ( 41.6% ) women had palpitations, breathlessness in 3 ( 5% ) and pulmonary oedema was seen in 2 (4%) women. In 2 women with pulmonary oedema , therapy was discontinued. In rest of the women drip rate reduced . Fetal tachycardia developed in 24 ( 40% ) women and nausea- vomiting occurred in 6 (10%) women. 48 women (80%) in Ritodrine group had side effects as compared to 18 women ( 30%) in Nifedipine group ( p value < 0.0001). It is statistically significant. Table – 5 shows that the mean gestational age at birth in Nifedipine group was 35 wks 3 days and in Ritodrine group it was 34 wks. the difference is not statistically significant.

Number of admissions to NICU was 55% and 65% in Nifedipine group and Ritodrine group respectively. Perintal deaths in Ritodrine group was 9 (15%) as compared to 6 ( 10% ) in Nifedipine group . Respratory distress syndrome was 13.3% in Nifedipine group and 16.6% in Ritodrine group. The causes of perinatal death were Respiratory Distress syndrome, septicemia, intraventricular hemorrhage . Neonatal outcome are comparable in both the groups. Four women in Ritodrine group had pronounced fall in blood pressure for which reduction of dosage was necessary. Two women developed pulmonary oedema which was managed with stopping the IV drip, oxygen and diuretics . Nausea and vomiting were successfully treated with antacids and antiemetic In Nifedipine group there was fall in systolic blood pressure (BP) by 10mm of Hg in 20 women and Diastolic blood pressure by 10mm Hg below the baseline in 24 women after administration of second dose of drug. This decrease in BP did not necessitate any special treatment. Headache , flushing subsided after few hours without any specific measure.

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TablesTable 1. Characteristics on admission in the two groups.

Values are given in number or mean Characteristics Nifedipine (n = 60) Ritodrine(n = 60)

Maternal age (years) 22 2Gestational age (weeks) 33 33Parity 0 45 (75%) 48 (80%)>_1 15(25%) 12 (20%)Booked 40 (66.6%) 35 (58.3%)Un booked 20 (33.3%) 25 (41.7%)

Table: 2 Prolongation of pregnancy with tocolytic therapy Nifedipine

(n = 60)Ritodrine

(n= 60) P value< 48 hrs 06 (10%) 19 (31.6%) 0.0069

Up to 48 Hrs 54 (90%) 41 (68.3%) 0.0069Up to 7 Days 42 (70%) 36 (60%) 0.338

Up to 37 Weeks 28 (46.6%) 16 (26.6%) 0.0371Table: 3 Outcomes in treatment groups

Nifedipine Ritodrine P valueSuccess n (%) 54 (90%) 41 (68.3%) 0.003Failure n (%) 6 (10%) 19 (31.6%) 0.002

Table: 4 Side effects associated with Tocolytic therapy Side effects NifidipineN = 60 RitodrineN = 60Palpitation 5 (8%) 25 (41.6%)Breathlessness - 3 (5%)Headache 12 (20%) -Flushing 3 (5%) -Pulmonary oedema - 2 (1.1%)Nausea & vomiting - 6 (10%)Fetal tachycardia - 24 (40%)

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Table: 5 Neonatal OutcomeParameters Nifedipine group n = 60 Ritodrine group n = 60

Mean Gestational age at birth 35 weeks 3 days 34 weeks Birth weight 2050 grams 1900 grams NICU Admission 33 (55%) 39 (65%)Perinatal death 6 (10%) 9 (15%)Respiratory DistressSyndrome 8 (13.3%) 10 (16.6%)

Discussion:This study compares the efficacy, side effects, neonatal and safety of NIfedipine with

Ritodrine in the suppression of preterm labour. The survival analysis shows that at 48 hours, which is relevant because it permits use of steroids to promote lung maturity. 90 percent of nifedipine group remain underlivered compared to 68.3 percent in Ritodrine group which is statisticcally significant ( p value 0.003). The prolongation of pregnancy till fetal maturity was seen in 46.6% in Nifedipine group and 26.6% in Ritodrine group which shows significant difference (p. value 0.0371)

The efficacy of nifedipinein the present study is comparable with other study groups of Kupfedipine et al.and Ferguson et al.The efficacy of Ritodrine is comparable to other studies in prolongation of pregnancy upto 7 days but at 48 hrs and upto 36 weeks the number of women who remain underlived was lower when compared to the studies of Kupfermic et al.and Ferguson et al.This study shows the significant difference in the tocolytic of Ritodrine and Nifedipine. Nifedipine caused fewer side effects which subsided after few hours and did not necessitate any special treatment where asRitodrine group had more frequent and serious side effects for which two women had discontinued therapy. In the present study palpitation was commom side effect, seen in 41.6% of women and fetal tachycardia in 40% of women. Most common side effect in Nifedipine group was headache as seen in 20% of women. Ferguson2, Meyer3, Kupfermine1 and Papatsonis4 all found Nifedipine to be associated with significantly fewer maternal side effects as compared to Ritodrine. James2 had to stop therapy in three women because of chest pain in Ritodrinegroup. kedar5 points out in his study that B sympathomimetics are not suitable for women with cardiovascular disease or diabetes where as Nifedipine exhibits greater selectivity for inhibition of uterine activity with very minimum effect on maternal cardiovascular and metabolic changes. Administration of Nifedipine in retard form is equally effective.

We also evaluated hemodynamie side effects in the present study . There was reduction in both systolic and diastolic B. P. following oral administration of second dose of

16

nifebipine in 24 women. However these changes were not significant and were less when compared to decrease in B.P. associated with Ritodrine. Observed fall in B.P. are unlikely to be of physiological importance.

Four women in Ritodrine group had pronounced fall in B. P. for which reduction of dosage of drug was necessary. Maitra6 found both agents to cause increase in pulse rate, fetal heart rate and decrease in B. P. which was statistically significant. Kupferminc1 found that fall in mean arterial and diastolic B.P. and rise in maternal heart rate were significantly greater with Ritodrine than with Nifedipine. Similar decrease of blood pressure was also noted by Reid Wellby7 and Ferguson2 and all of them felt that it was unlikely to be if pathological significance.

James2 also demonstrated Nifedipine treatment to be useful to delay delivery in treatment failures with Ritodrine and vice versa .This is cross over therapy. These two drugs act through different cellular mechanism to achieve uterine quiescence. In his study he could not demonstrate any adverse fetal hemodynamics and cardiprespiratory effects when Nifedipine was used because of minimum changes in maternal hemodynamics . In a study by Kashnian8 et al .in which Atosiban was compared with Nifedipine showed that efficacy in delaying delivery for more than 48 hrs in order to undergo steroid therapy as well as side sffects of both the drugs were similar.

Present study showed comparable neonatal outcomes in both groups . papatson4 in his study showed lower NICU admission in Nifedipine group . Maitra’s6 study observed similsr APGAR scores in both groups . Nifedipine does not interfere with interpretation of fetal heart rate tracing as does Ritodrine , which may be important in timely diagnosis of intra uterine infection in preterm rupture of membranes.Conclusion:

Nifedipine was more successful in delaying the delivery for 48 hours which would enhance fetal lung maturity by use of corticosteroids .The mean prolongation of gestation was higher for Nifedipine group when compared to Ritodrine group. Oral Nifedipine is a cheaper, effective alternative and has fewer, less serious side effects and less hemodynamic compromise when compared to I. V. Ritodrine for suppression of preterm labour.References :1. Kupferminc, et al. Nifedipine versus Ritodrine for suppression preterm labour. B rJ of

Obstet&gynecol, Dec 1993(100), 1090-10942. Ferguson, James E., et al. A comparison of tocolysis with nifedipine or Ritodrine:

Analysis of efficacy and maternal fetal and neonatal outcome. Am J ObstetGynecol, july 1990 (163), 105-112.

3. Meyer WR, Randall HW, Graves, Nifedipine versus Ritodrine for suppressing preterm labour. J Reprod Med, 1990 June; 35(6): 649-53.

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4. Papatsonis, DNM et al. Nifedipine and Ritodrine in the management of preterm labour: A randomized multicenter trial. ObstetGynecol 1997 August; 90: 230-234.

5. Kedar M. Ganla et al. A prospective comparison of Nifedipine and Isoxsuprine for tocolysis. J ObstetGynecol India 1999 April, 259-263.

6. MaitraNandita, Christian Vincent, Verma RN, Desai V A, Maternal and fetal cardiovascular side effects of Nifedipine and Ritodrine used as tocolysis. J ObstetGynecol India, Vol 57(2), March-April 2007, 131-134.

7. Read MD, DE Wellby. The use of calcium antagonist (Nifedipine) to suppress preterm labour. Br J Obstet&Gynecol, 1986; 93:933-937.

8. Kashanian M, AR Akbarian, M Soltanzadeh, Atosiban and Nifedipine for treatment of preterm labour. International Journal of Gynaecology and Obstetrics (2005) June, 91,10-14.

18

Original ArticleA PROSPECTIVE STUDY TO ASSESS THE ROLE OF AGE AS A

FACTOR IN HEALING OF TYMPANIC MEMBRANE FOLLOWING MIDDLE EAR SURGERIES

Preety Ninan, S.P.GuggurigoudarDepartment of ENT,

BLDEU’s Shri B.M.Patil Medical College, Hospital & Research Centre, Bijapur.

AbstractBackground: Age is known to affect all phases of healing Though it is suggested by

many it is not properly documented.in healing of tympanic membrane with ageObjective: This study was carried out to assess the role of age as a factor in healing of

tympanic membrane following middle ear surgeries.Methods: 71 patients were studied and audiograms were recorded pre-operatively and

post-operatively 3rd and 7th week Comparisons were made between two age groups below and above 40 years. Results: Pre operative and post operativeA-B gap were compared by using-t test and chi-square test.Using chi-square test , the p value (0.712) was insignificant.between the two age groups

Interpretation and conclusion: In this study age was not a significant factor affecting healing of tympanic membrane following middle ear surgery.Key words: ages; pure tone audiometry

Chronic Suppurative otitis media (CSOM) is the most common middle ear disease that is encountered in our set up in almost every age group .There are various surgical procedures that are performed in cases of CSOM. The outcome of these surgical procedures depends on various factors .One such important factor is the age of the patient.

It has commonly been reported that healing slows down with increasing age and is known to affect all phases of healing. With increasing age,there is a decrease in inflammatory response and reduction in the rate of epithelialisation. A chief criticism of such findings ,however is that studies have not adequately excluded confounding factors that are more common in aged persons,such as medication use and morbidity. Other studies report no difference in the healing rates of older versus younger patients.Thus it remains controversial whether aging delays wound healing in humans.

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The aim of this study is to examine the effects of age on healing of tympanic membrane following middle ear surgeries while excluding all such confounding factors.Materials and Method:

The study population consisted of 71 patients who were suffering from chronic suppurative otitis media.The study period was one and half years from October 2008 to april 2010

Details of cases will be recorded including history and clinical examination with emphasis on detailed otoscopic examination and examination under microscope preoperatively and postoperatively All patients undergoing middle ear reconstructive surgeries were subjected to pure tone audiometry pre operatively and on 3rd and 7th post operative week. The patients were divided into 2 groups

Group I : patients upto 40 years Group II : patients above 40 yearsPatients with actively discharging ears, diabetes mellitus or hypertension, anaemia,

renal disease ,jaundice or with history of smoking or intake of drugs like corticosteroids or immunosupressants were excluded from study.Results:

In this study, 40 patients were less than 40 years while 31 patients were above 40 years.(table 1)

TABLE -1: AGE DISTRIBUTIONAGE OF PATIENTS [ n=71]

AGE (YEARS) NUMBER OF PATIENTS %≤40 40 56>40 31 44

Of the total 71 patients, 27 were males and 44 were females.(table 2)TABLE-2

Sex distributionSEX NUMBER OF PATIENTS PERCENTAGEMales 27 38%Females 44 62%

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TABLE-3PRE-OPERATIVE DIAGNOSIS [ n=71 ]

DIAGNOSIS NUMBER OF PATIENTS PERCENTAGELEFT CSOM 27 38%RIGHT CSOM 18 25%BILATERAL CSOM 26 37%

TABLE-4Surgical procedures performed [ n=71]

SURGICAL PROCEDURE NUMBER OF PATIENTS PERCENTAGE

Tympanoplasty 63 89%Cortical mastoidectomy with Tympanoplasty 8 11%

TABLE -5 Comparison between preoperative & postoperative resultsVariable Mean ± SD (SE) Paired t test Preoperative Vs Postop 3rd week 28.443 ± 6.932

22.743 ± 7.2780.830.87

t = 15.32p = 0.000 HS

Postoperative 3rd week Vs Postop 7th week 22.743 ± 7.27817.789 ± 7.691

0.870.92

t = 13.15p = 0.000 HS

Preoperative Vs Postop 7th week 28.394 ± 6.89417.789 ± 7.691

0.820.92

t = 18.3p = 0.000 HS

Postoperative hearing improvement between the two age groups was evaluated by air- bone gap closure.The results were catergorised into the following groups:31 i) Group A: remarkable improvement in which air –bone gap closure is 0-10 dB. ii) Group B: moderate improvement in which air –bone gap closure is 11-20dB. iii) Group C: slight improvement indicates air –bone gap closure of 21-30dB. iv) Group D: no improvement indicates air –bone gap of more than 31dB. v) Group E: postoperative air-bone gap within 30 dBTABLE 6 A – B gap at 3rd week following surgery

Age No of PatientsA(0-10 dB) B (11-20 dB) C (21-30 dB) D (> 31 dB) E (0-30 dB)

No % No % No % No % No %≤40 yrs 40 0 0 20 50% 12 30% 8 20% 32 80%> 40 Yrs 31 0 0 18 58% 11 36% 2 6% 29 93%Total 71 0

03854%

2332%

1014%

6186%

Excellent Good Fair Failure Satisfactory

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Using proportion of patients with a postoperative A-B gap of 30 dB as the criterion ,86% of patients achieved their A-B gap closer within 30 dB.TABLE 7 Hearing results at 3rd postoperative week.

Age (Years) Mean A-B gap (dB) ±SD P Value≤40 23.08 ±7.57 t=0.12

P=0.903NS>40 22.87±6.48

No statistically significant difference between the two age groups at 3rd post operative week.Table 8 A – B gap at 7 week following surgery

Age No of Patients A (0-10 dB) B(11-20 dB) C (21-30 dB) D (> 31 dB) E (0-30 dB)

No % No % No % No % No %≤ 40 yrs 40 14 35% 13 32% 11 28% 2 5% 38 95%> 40 Yrs 31 8 26% 15 48% 7 23% 1 3% 30 97%Total 71 22

31%2839%

1826%

34%

6896%

Excellent Good Fair Failure SatisfactoryUsing proportion of patients with a postoperative A-B gap of 30 dB as the criterion ,in

this study 96% of patients achieved their A-B gap closer within 30 dB at 7 th postoperative week .Table- 9 Hearing results at 7th postoperative week.

Age (Years) Mean A-B gap (dB) ±SD P Value≤40 17.80±7.85 t=0.15

P=0.879NS>40 18.06±6.67

There was no statistically significant difference between the results in two age groups at the end of the 7th postoperative week.Table-10 Success in relation to age

Age Success (closure of TM Failure No % No %

≤ 40 Years 38 / 40 95% 2 / 40 5 %> 40 Years 30 / 31 96.7% 1 / 31 3 %

p value= 0.712Differences not significant on Chi-square test (p> 0.05)Hence ,from the above results it can be concluded that age did not significantly influence the results following middle ear surgery.

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Discussion :Despite a rapidly increasing proportion of elderly subjects in society,little is known

regarding the effects of ageing on wound healing. Most studies claiming impaired wound healing with age have invariably been carried out on aged subjects with associated pathology,thus raising doubts about results ranging from the assessment of wound dehiscence rates and tensile strength to invitro fibroblast and keratinocyte studies19.This study exclusively studies effect of age as an independent factor in healing of tympanic membrane following middle ear reconstructive surgeries.

There are different criteria for assessing hearing after chronic ear surgery such as social hearing method,hearing gain method and mean A-Bgap for each frequency but none are universally accepted method. The standard method of comparing postoperative air conduction to preoperative bone conduction appears most frequently in literature4. Thus ,this method has been used for calculating hearing results in this study.

In a study by Radpour S, the instance of graft failure following middle ear surgery did not differ greatly by age. The risk of failure was higher in patients with concomitant diseases ,such as coronary artery disease, diabetes mellitus, hypertension,renal disease, cerebral vascular disease and anaemia10. This study has excluded patients with any of these coexisting conditions. Hence ,outcome of surgery was not found to be different in any age group.Conclusion :

This study confirms that age as an individual factor had no significant role on the outcome of surgery. The presence of coexisting disease is more important than age itself. Hence, careful patient selection was most likely to increase the rate of an intact tympanic membrane with improvement in hearing. Therefore it was concluded that age is not a factor in success or failure of healing of tympanic membrane following middle ear reconstructive surgery.

References :1. Ercan Pinar, Kerim Sadullahoglu, Caglar Calli,Semih Oncel.Evaluation of prognostic

factors and middle ear risk index in tympanoplasty. Otolaryngology Head and Neck Surgery 2008 sep;139(3): 386-390

2. Lin AC ,Messner AH.Pediatric tymanoplasty-factors affecting success.Curr Opin Otolaryngoly Head Neck Surg 2008feb;16(1):64-68

3. Sckolnick et al . Pediatric Myringoplasty: Factors that affect success. Laryngoscope 2008 april; 118: 723-729

4. Shrestha S, Sinha BK. Hearing results after myringoplasty. Kathmandu University Medical Journal 2006;4(16): 455-459

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5. Illana et al .Tympanoplasty: Surgical results and a comparison of the factors that may interfere in their success.Brazilian Journal of Otorhinolaryngology 2006 april;72(2):267-271

6. Albera et al .Prognostic factors in Myringoplasty.Annals of Otology,Rhinology& Laryngology 2006;115(12): 875-879

7. Collins et al .Pediatric Tympanoplasty.Arch Otolaryngology Head Neck Surgery 2003 June ;129:646-651

8. Umapathy N, Dekker PJ. Myringoplasty: is it worth performing in children.2003 oct; 129:1053-1055

9. Fadl A Fadl . Outcome of type 1 tympanoplasty. Saudi Medical Journal 2003;24(1): 58-61

10. Radpour S. Tympanoplasty in geriatric patients : surgical considerations. Ear Nose Throat Journal 1999 Jul ;78(7):484-488

11. Emmett JR.Age as a factor in success of tymanoplasty :a comparison of outcomes in young and old.Ear Nose Throat J1999 Jul;78(7):480-83

12. Vrabec et al .Meta-analysis of Pediatric Tympanoplasty.Arch Otolaryngology Head Neck Surg 1999 May;125:530-534

13. Denoyelle et al .Myringoplasty in children : Predictive factors of outcome.Laryngoscope 1999 Jan ;109:47-51

14. Blakley et al.Preoperative hearing predicts postoperative hearing.Otolaryngology Head Neck Surgery 1998 Dec;119:559-563

15. Bajaj Y, Bais AS, Mukherjee B. Tympanoplasty in children : a prospective study. The Journal of Laryngology and Otology 1998 Dec ;112:1147-1149

16. Caylan et al .Myringoplasty in children: Factors influencing surgical outcome.Otolaryngology Head Neck Surgery 1998;118:709-713

17. Tai CF,HoKY ,Juan KH. Age and the prognosis of tympanoplasty type I.Kaohsiung J Med Sci1998 Sep;14(9):542-7

18. Albu S et al . Prognostic Factors in Tympanoplasty. The American Journal of Otology 1998;19: 136-140

19. Gillian S Ashcroft, Michael A Horan , Mark . The effects of ageing on wound healing : immunolocalisation of growth factors and their receptors in a murine incisional model. J Anat 1997;190: 351-365

20. Podoshin L et al. Type1Tymanoplasty in Children. The American Journal of Otology 1996;17: 293-296

21. Gersdorff et al . Myringoplasty : long term results in adults and children.The American Journal of Otology 1995 July;16(4): 532-535

22. Aoyagi et al. Effects of Aging on Hearing results in tympanoplasty.Acta Oto-laryngologica 1994 S511;114: 81-86

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23. Van PC, Van BB, Spruijit K,Kuiper JP.Age related changes in wound healing .Clin Exp Dermatol 1994 sep;19(5):369-74

24. Gerstein AD,Philips TJ ,RogersGS,Gilchrest BA.Wound Healing and aging.Dermatol Clin1993 oct;11(4):749-57

25. Glenn Issacson. Tympanoplasty in children . Otolaryngologic Clinics of North America 1994 June;27(3):593-605

26. Makota Sakai. Proposal of a guideline in reporting hearing results in middle ear and mastoid surgery.The American Journal of Otology 1994 May;15(3):291-293

27. Ophir et al . Myringoplasty in the pediatric population . Arch Otolaryngol Head Neck Surgery 1987 Dec;113:1288-1290

28. Warren Y Adkins, Benjamin White . Type 1 tympanoplasty : influencing factors. Laryngoscope1984 July;94:916-918

29. Reddy et al. Postnatal risk factors of hearing impairment.Int J of Human Gen 2006;6(3):191-193

30. Stephen R Young,Melissa Calvin. Wound healing- Soft and hard tissue repair.In: Scott Browns Otorhinolaryngology,Head and Neck Surgery.7th ed;Edward Arnold ;2008.P .87-94

31. AristidesSismanis.Tympanoplasty.In:Glasscock-Shambaugh Surgery of the Ear.5thed;Elsevier;2003.P .463-487

32. Anirban Biswas. Pure Tone Audiometry.In:Clinical Audio-vestibulometry for Otologists and Neurologists.3rd ed;Bhalani;2002.P.1-18

33. Barbara E Weinstein. The ageing auditory system.In: Geriatic Audiology.2nd ed;Thieme;2000.P 55-60

34. David Hom. Salient healing features of tympanic membrane.In: Essential tissue healing of face and neck; Poeples;2009.P.150-156

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Original ArticleSCHNEIDERIAN PAPILLOMA OF MIDDLE EAR

-A RARE CASE REPORTDr. Savita Shettar , Dr. S. B. Hippargi, Dr.B.R.Yelikar.

Department of Pathology, BLDEU’s Shri B.M.Patil Medical College, Hospital & Research Centre, Bijapur.

AbstractInverted (Schneiderian) papilloma involving the middle ear as a primary lesion is an

extremely rare occurance.Here is male patient aged 85years ,presented with left ear discharge since 4years. It was blood stained since 3months. H/o giddiness present since 3months.On examination left fascial palsy was present. Otoscopy: showed Granular polyp which bleeds on touch. Audiometry: Mixed type of hearing loss on left. With Post aural incision ,biopsy has been taken.Microscopy showed,multiple finger like projections lined by pseudostratified columnar epithelium, which was showing stratification, mild atypia with central fibrovascular core. On these features diagnosis of Schneiderian papilloma was made.Conclusion

Inverted papillomas of middle ear eventhough rare but rate of reccurance,and association of sqamous cell carcinoma is very common compared to nose and paranasal sinuses. Hence diagnosis and follow up of patient is very important.

Key words: Inverted papilloma, Middle ear, Squamous cell carcinoma.Introduction :

Scheneiderian Papilloma is a benign epithelial tumor that arises from mucous membrane of nasal cavity and paranasal sinuses. Most commonly arises from lateral wall of nose in the region of middle meatus. Extra sinonasal tract sites in which Schneiderian type papilloma have been reported include Pharynx , lacrimal sac, middle ear mastoid1. These neoplasms are readily identified by their histo-morphological features, and are characterized by their tendency to recur if inadequately excised. It is due to its rarity of these tumors in the middle ear, the possibility of misdiagnosis and mismanagement are common. That is why this case has been taken.

26

Case ReportHere is a male patient aged 85 years presented with left ear discharge since 4 years,

it was watery. Since 3 months it is blood stained, H/o giddiness was present since 3 months.

On physical examination: Left fascial palsy was present.On Otoscopic examamination: Granular Polyp was seen in left ear which bleeds on

touch.Audiometry - Moderate to severe hearing loss.Left side – Mixed type,Sever.Right side – Mild & sensoneural type. All other investigations were within normal limits.Clinically - Chronic Suppurative Otitis Media (CSOM) with granulation tissue was

made. With post aural incision, biopsy of the polyp was taken.

PathologyMacroscopy: Pearly white tissue measuring 0.5-0.8cms.Microscopy : Tumor tissue lined by stratified squamous epithelium, composed of papillary fronds

with a fibrovascular core (fig 1). Inverted type of growth pattern was identified (fig 1). Epithelium was showing stratification. There was uniformity in cell maturation with retained polarity. The cells were having round to oval nuclei and a glassy cytoplasm (fig. 2). At places intercellular bridges were seen. Mitotic figures were scanty. Intraepitelial cystic spaces filled with inflammatory cells seen at places.

Fig1:Invertedpapillaryfronds(5x) Fig2:Microcystic spaces(10x) Fig3:Retained polarity,Scantmitosis(40x)

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Discussion :Schneiderian Papilloma is a benign sinonasal tract epithelial neoplasm with characteristic

clinical and pathologic features. Different morphological types of Schneiderian Papilloma are inverted(endophytic), cylindrical and fungiform(exophytic)2.

Multiple factors are believed to cause Schneiderian Papilloma like viral infection by Human Papilloma virus 6/11, allergy, inflammation (i.e. following CSOM), environmental factors 3.

The pathogenesis as indicated by Kaddour and woodhead is due to embryological migration of Schneiderian mucosa from sinonasal tract to middle ear 4.

According to Hymas J, Schneiderian Papilloma follows chronic irritation (eg. due to CSOM) which leads to squamous metaplasia with continued inflammation subsequent development of papilloma 2. Long standing Papillomas may show malignant transformation and develop into non keratinizing type of squamous cell carcinoma2. Patients commonly present with ear discharge, conductive deafness and otalgia 5.Conclusions

Similar to sinonasal counterparts, the middle ear papillomas will recur if not completely excised. Therefore, their specific morphological recognition by the surgical pathologists is essential for initiation of appropriate management5. Another indication for early aggressive surgical management is because longstanding recurrent cases may show malignant transformation to squamous cell carcinoma 5.References1. Stone DM, Berktold RE , Ranganathan C, Weit RJ, Inverted Papilloma of middle ear

and 2. HyamsVJ .Papillomas of nasal cavity and paranasal sinuses. A clinicopathological

study of 315 cases. Ann Otol Rhino Laryngol 1971; 80 : 192 – 206.3. Brandwein M, Steinberg B, Thung S, Biller H, Dilorenzo T, Galli R. Human

Papillomavirus 6/11 and 16/18 in Schneiderian inverted papillomas : in situ hybridization with human papilloma virus RNA probes. Cancer 1989 ; 63: 1708 -13.

4. Kaddour H S, Woodhead CJ. Transitional Papilloma of the middle ear. J Laryngol Otol 1992; 106: 628-9.

5. Wenig B M. Schneiderian type mucosal Papillomas of the middle ear and mastoid. Ann Otol Rhinol Laryngol 1996 Mar; 105 (3) 226 -33.

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Original ArticleA STUDY OF PULMONARY FUNCTIONS OF WOMEN AT

DIFFERENT TRIMESTERS OF PREGNANCY IN BLDEU’S SHRI B.M.PATIL MEDICAL COLLEGE HOSPITAL

Anita Teli, Asha.Dharwadkar, Manjunatha. Aithala Department of Physiology,

BLDEU’s Shri B.M.Patil Medical College, Hospital & Research Centre, Bijapur.

AbstractBackground & Objectives: Pregnancy is characterized by profound changes in the

function of virtually every regulatory system in the human body. The events in pregnancy elicit one of the best examples of selective anatomical, physiological & biochemical adaptation that occur during pregnancy & profound changes in respiratory physiology is a part of the same process. Thus this study is designed to evaluate the pulmonary function tests in 1st, 2nd and 3rd trimesters of pregnancy & compare them with non-pregnant control group.

Methods: A cross-sectional study is carried in 200 healthy women in the age range of 19-35 years attending BLDEA’s Shri B M Patil Medical College, Hospital and Research Centre, Bijapur. The subjects are distributed in four groups, i.e control (non-pregnant) group and 1st, 2nd & 3rd trimester pregnant groups. Number of subjects in each group is 50. We have recorded various physical, physiological & respiratory parameters in control and study groups. Mean + SD of all groups are compared for statistical significance by ‘Z’ test

Results: There is gradual significant increase in Respiratory rate in all trimesters of pregnancy. There is significant decrease in FVC, FEV1, FEV1%, PEFR in all trimesters of pregnancy with maximum decrease in 1st trimester. There is significant decrease in MEP in all trimesters of pregnancy with maximum decrease in 2nd trimester.

Conclusion: The changes in pulmonary function are attributed to major adaptations in the maternal respiratory system. These changes may also be influenced by the mechanical pressure of enlarging gravid uterus, elevating the diaphragm & restricting the movements of lungs thus hampering the forceful expiration & decrease in 1st trimester might be due to decline in alveolar Pco2 caused by hyperventilation which acts as bronchoconstrictor & due to sensitization of respiratory centre due to progesterone.

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This knowledge of pulmonary function changes during pregnancy may be helpful in the prevention of gestational complications associated with an inadequate maternal respiratory adaptation.

Key words: Pregnancy, FVC, PEFR, MEP. Introduction

Pregnancy is characterized by profound changes in the function of virtually every regulatory system in the human body. The events in pregnancy elicit one of the best examples of selective anatomical, physiological & biochemical adaptation that occur during pregnancy & profound changes in respiratory physiology is a part of the same process1 .The changes in the respiratory physiology 2 are due to increasing size of the fetus with advancing gestation which constitutes a mechanical impediment to normal process of ventilation3& due to hormone Progesterone which increases ventilation by increasing respiratory centre sensitivity to carbondioxide as a result the tidal volume and minute ventilation is increased 4-6.

The physiological adaptation of the pregnant woman involve the circulatory, respiratory, digestive, renal, endocrine & metabolic systems. Their precise knowledge allows the clinician to verify the extent of the adaptation in pregnant women & helps to avoid unnecessary treatment of physiology changes misinterpreted as pathological changes in reference to pre pregnancy standards7.

The knowledge of the expected or desired changes in pulmonary parameters is fundamental in understanding of how the disease states affect pregnancy & vice versa8 . Also, information regarding status of pulmonary function is essential for assessment of fitness for anaesthesia.9

The above reviews reveal that there is a sizeable proportion of evidence indicating relationship between pregnancy & respiratory functions from various parts of the world. Although some workers have already studied pulmonary function tests in women during pregnancy in some parts of our country10, there are very few reports involving subjects of South Indian origin in this field. This warrants study on influence of pregnancy on pulmonary functions involving subjects of South Indian origin (Karnataka).Objectives

The aim of this study is to evaluate the changes in the pulmonary functions of women in the age group of 19-35 yrs at 1st, 2nd& 3rd trimesters of pregnancy & compare them with that of healthy non-pregnant age matched controls.Materials and Methods

A cross sectional study was undertaken to determine the pulmonary function changes in

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1st, 2nd & 3rd trimesters of pregnancy. The observations were compared with age matched healthy non pregnant women in the Department of Physiology, Shri B.M.Patil Medical College, Hospital and Research Centre, Bijapur. Duration of the study was one year from December 2009 to May 2011 .150 pregnant women in the age group of 19-35yrs who were attending the OPD of OBGy of Shri B.M. Patil Medical College were included in the study group. The study group was in turn divided into 3 subgroups. Each sub group was comprising of 50 each in all trimesters of pregnancy. Apparently healthy age matched 50 non pregnant women comprised control group.

The nature and purpose of the study were explained to the subjects who had volunteered for the study. From each participant an informed consent was obtained. A proforma was used to record the relevant information from each selected individual who had fulfilled inclusion criteria. The subjects who had exclusion criteria were dropped from the study. A thorough physical & systemic examination of each subject was done (respiratory system).For each test, three readings will be taken. The highest reading will be taken for calculation. All tests will be recorded in a sitting posture at room temperature, in morning hours between 9 am to 12 noon.Inclusion Criteria

Apparently healthy subjects of Indian origin were included in the study. The apparent health status of the subject were determined through thorough clinical examination and history taking.Exclusion Criteria

The Following Subjects with acute respiratory infection in the previous three months, chronic respiratory infection including asthma, cardiovascular diseases, with history of diabetes mellitus, hypertension were excluded from the study.

Respiratory Rate- It is recorded by inspection and palpation of chest and abdomen & is expressed as cycles/minute (cpm).

The following pulmonary parameters are recorded by Computerized Spiropac(Medicad) 11

1. FVC (Forced Vital Capacity in L)2. FEV1 (Forced Expiratory Volume at the end of first second in L)3. FEV1% (Percentage of Forced Expiratory Volume in one second in %)4. PEFR (Peak Expiratory Flow Rate in L/sec)5. MEP (Maximum Expiratory Pressure in mmHg) - Recorded by using modified Black’s apparatus.

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Statistical AnalysisThe results were expressed as Mean + SD. Z test was used for comparison between

control and study groups in consultation with statistician. A ‘p’ value of 0.05 or less was considered as statistically signifi cant.

ResultsRESPIRATORY RATE (CPM):

Mean RR + SD of control & pregnant women in 1st, 2nd and 3rd trimesters are 16 +3, 22 + 3, 23 + 4.3 and 26 + 3.7 cpm respectively. There is statistically very highly signifi cant gradual increase in RR from 1st to 3rd trimester as compared to control (p=0.001) .

Table 1: Mean + SD of FVC, FEV1 & FEV% of subjects in Control and Study groups

PARAMETERSCONTROL I-TRIMESTER II- TRIMESTER III- TRIMESTERMean+ SD Mean + SD Mean + SD Mean + SD

FVC(L) 2.50+ 0.39 1.87+0.37(p=0.001***)

1.85+0.39(p=0.001***) 2.19+ 2.0(p=0.001***)

FEV1(L) 2.24+ 0.39 1.56+0.49(p=0.001***)

1.69+0.39(p=0.001***) 1.78+0.32(p=0.001***)

FEV1(%) 91.94+ 3.68 86.55+17.55(p=0.017**)

92.09+10.91(p=0.482) 90.32+ 10.33(p=0.150)

p>0.05: Not Signifi cant, *p: <0.05: Signifi cant, ** p: <0.01: Highly signifi cant, ***p: <0.001: Very highly signifi cant

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DiscusssionA cross-sectional study was carried in 200 healthy women in the age range of 19-

35 years of BLDEA’s Shri B M Patil Medical College, Hospital and Research Centre, Bijapur. The subjects were distributed in four groups, i.e control (non-pregnant) group and 1st , 2nd &3rd trimester pregnant groups. Number of subjects in each group is 50. We have recorded various physical, physiological & respiratory parameters in control and study groups.Respiratory Rate:

In our study, there is significant increase in respiratory rate from 1st trimester to 3rd trimester of pregnancy as compared to control group which is in agreement with Bernhard H Heidemann, who state that PaCO2 falls and then levels off at 4.1kPa (31mmHg) by the end of the first trimester. This is caused by a 10% increase in the respiratory rate, secondary to progesterone mediated hypersensitivity to CO2, and an increase in alveolar and minute ventilation, secondary to increased respiratory rate and tidal volume12.

Forced vital capacity :Our study showed significant decrease in FVC from 1st trimester to 3rd trimester as

compared to control which is in agreement with other workers. The decrease in FVC is maximum in first trimester which may be attributable to hormonal changes which requires further studies.

A study of forced vital capacity in pregnant women by Dipok Kumar Sunyal and workers showed reduced FVC in all trimesters as compared to control & maximum decrease in third trimester. The decrease in FVC is attributable to the mechanical pressure of enlarging gravid uterus, elevating the diaphragm & restricting the movements of lungs thus hampering the forceful expiration13.

A study by Deepal & workers showed no significant changes in FVC during all trimesters of pregnancy . Hormonal alteration in pregnancy causes a reduction in the tracheo-bronchial smooth muscle tone & the increasing thoracic width may be due to enlarging uterus as a result there is no impairment in large airway function throughout pregnancy14.FEV1 ,FEV1% & PEFR :

Our study showed significant decrease in FEV1,FEV1% & PEFR from 1st trimester to 3rd trimester as compared to control which is in agreement with other workers. The decrease in FEV1, FEV1% & PEFR is maximum in first trimester which may be attributable to hormonal changes, which requires further studies.

A study by Neeraj & workers showed decrease in FEV1, FEV1% & PEFR in third

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trimester as compared to control group. The decrease may be due to a decline in alveolar Pco2 caused by hyperventilation which acts as bronchoconstrictor. Hormonal influences also play a role in altering & compromising the FEV1, FEV1% & PEFR15.

In a study by Mrunal Phatak & others, there was no significant change in FEV1 & FEV1% & they claimed that it was due to progesterone, corticosteroids & relaxin during pregnancy which cause certain degree of bronchodilatation due relaxation of muscles10.MEP:

Our study showed significant decrease in MEP from 1st trimester to 3rd trimester as compared to control with maximum decrease in 2nd trimester.Conlusion : We conclude from our study that• The significant increase in RR by 4 cpm might be due to sensitization of respiratory

centre due to progesterone is compensated by decrease in TV ultimately maintaining the constant MV even during all trimesters of pregnancy.

• The significant decrease in FVC, FEV1, FEV1%, PEFR might be due to the mechanical pressure of enlarging gravid uterus, elevating the diaphragm & restricting the movements of lungs thus hampering the forceful expiration and maximum decrease in 1st trimester due to decline in alveolar Pco2 caused by hyperventilation which acts as bronchoconstrictor.

• The statistical significant decrease in PEFR & MEP in all trimesters might be due to decrease in expiratory muscle power.

References1. Chhabra S, Nangia V, Ingley KN. Changes in respiratory function tests during

pregnancy. Ind J Physiol Pharmacol 1988; 32: 56-602. Pandya KD, Chandwani S, Desai CA, Dadlani AG. Study of vital capacity and timed

vital capacity in normal non-pregnant and pregnant women. J Obst Gynecol Ind 1984; 36 : 1053-1057

3. Saxena SC, Rao VSC , Mudgal SA. Study of pulmonary function tests during pregnancy. J Obst Gynecol 1979; 29 : 993-995

4. Bayliss DA, Millhorn DE. Central neural mechanics of progesterone action: application to the respiratory system. J Appl Physiol 1992; 73(2):393-404

5. Skatrud JB, Dempsey A, Kaiser DG. Ventilatory response to medroxyprogesterone acetate in normal subjects: time course and mechanism. J Appl Physiol 1978; 44(6): 939-944

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6. Lysons HA, Antonio R. The sensitivity of the respiratory centre in pregnancy and after the administration of progesterone. Trans Assoc Am Phys 1959; 72: 173-180

7. Foidart M. Physiology of the pregnant woman and risk factors. Contracept fertile sex 1993; 21: 811-815

8. Elkus R, Popovich J Jr. Respiratory physiology in pregnancy. Clin Chest Med 1992; 13: 555-565

9. Mokkapati R, Prasad EC, Venkatraman, Fatima K. Ventilatory functions in pregnancy . Indian J Physiol Pharmacol 1991; 35: 237-240

10. Phatak MS, Kurhade GA. Longitudinal study of antenatal changes in lung function tests and importance of postpartum exercises in their recovery. Indian journal of physiology pharmacology 2003; 47(3): 352-356.

11. Pal G.K. Textbook of practical physiology 2nd edition Orient Longmann publications Chennai 2005;p:154-161

12. Heidemann B. Changes in maternal physiology during pregnancy. Update in Anaesthesia 2005 ;20: 21-24

13. Sunyal DK, Md Ruhul Amin, MH Molla, Abida Ahmed, Shameena Begum. Forced vital capacity in normal pregnancy. J med. Sci. Res 2007 July; 09(01) : 21-25

14. Weerasekara Deepal S. , Ruberu D.Kusua and S.Sivayogan Pulmonary Functions in Pregnant Sri Lankan Women. Sabaragauwa university journal 1999 ;2(1); pp.57-60

15. Neeraj , Sodhi Candy , John Pramod, Singh Joydeep & Kaur Vaneet, Indian J Physiol Pharmacol 2010 : 54 (1) : 69-72.

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Original ArticleROLE OF EXERCISE AND NUTRITION ON

CARDIOPULMONARY FITNESS ON RESIDENTIAL AND NON-RESIDENTIAL SCHOOL CHILDREN

Dr Jyoti Khodnapur, Dr G B Dhanakshirur, Dr Manjunatha Aithala Department of Physiology,

BLDEU’s Shri B.M.Patil Medical College, Hospital & Research Centre, Bijapur.

AbstractPhysical fitness is the prime criterion for survival, to achieve any goal and to lead

a healthy life. Effect of exercise to have a good physical fitness is well known since ancient Vedas. Our aim is to find out effect of exercise and nutrition on growing children with scientific records. So, we have selected Residential and Non-Residential school children with age between 12 and 16 years. Obviously, Residential school children will get recommended nutritious food and they are undergoing regular physical exercise training. Subjects were divided into two groups. Group I is residential and group II is non-residential each of having 100 students and they were subjected for cardiopulmonary fitness tests and pulmonary function tests.

Physical fitness not only assessed by suitable cardiopulmonary fitness parameters like Physical Fitness Index (PFI in %) and maximal oxygen consumption that is VO2max (ml/kg/min) by using Harvard step test but also by pulmonary function tests like Forced Expiratory Volume in 1 sec (FEV1 in %), Peak Expiratory Flow Rate (PEFR in L/Min) and Maximal Expiratory Pressure (MEP in mmHg). Results were compared and subjected to statistical analysis for Z test. VO2 Max (Mean + SD) in residential was 66.03 + 7.06 & in non-residential school children was 55.24 + 7.53. PFI (Mean + SD) in residential was 54.96 + 8.38 & in non-residential school children was 44.75 + 5.05. FEV1 (Mean + SD) in residential was 91.21+ 7.53 & in non-residential school children was 87.79+9.79. PEFR (Mean + SD) in residential was 499.05+ 95.39 & in non-residential school children was 389.25+ 96.98. MEP (Mean + SD) in residential was 90.1+ 17.05& in non-residential school children was 73.83+ 25.50. So, VO2 Max (p=0.000), PFI (p=0.000), FEV1 (p=0.000), PEFR (p=0.000) and MEP (p=0.000) were significantly higher in residential as compared to that of non-residential school children. So, from above data analysis it is observed that regular exercise and nutritious food increase the cardiopulmonary fitness values in Residential school children.

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Key words: Residential school children, Non- Residential school children, VO2max, PFI, FEV1, PEFR, MEP.Introduction

Physical fitness is defined as ability to carry out daily tasks with vigor and alertness without undue fatigue with ample of energy to enjoy leisure time pursuits, to meet unusual situations and unforeseen emergencies.(1)

For a common man, the physical fitness is ability to withstand stress and pressure under different circumstances where an unfit person would be ineffective or would quit.(1)

Regular physical exercise is known to have beneficial effects on health. As diseases are related to lack of fitness, Americans realized that there is a need to counteract a sedentary lifestyle with planned physical activity through sports and formal exercise. This brought government’s attention to the lack of fitness of its citizenry. This led to the establishment of minimum fitness standards in the country’s public schools.(2)

In our country, we are getting acquainted with the modern amenities at a very fast rate. So, we are neglecting the natural physical activities. The present attractive education system has helped to improve the education standards. But, the non active sedentary stressful life has made the youth physically unfit. Now, the time has come to consider about the physical fitness and exercise in the adolescent age group. Realizing this fact, educationalists have recommended minimal physical exercise in the curriculum.(3)

The physical growth in boys and girls more or less is equal up to adolescence. So, we have selected boys only.

The age between 12 and 16 years, the physique is changing. During this period of growth, height, weight and maximum aerobic capacity will reach their peak. So, to achieve good fitness in children sports programme should be arranged.(4)

The exercise will help to attain maximum physical fitness due to development of muscle and cardiorespiratory strength as well as endurance of the children.(4)

The advantages of physical fitness are many, like increase in the level of intelligence, tolerance, activity and social behavior.

Physically fit children are easily adapt for stress. Their neuromuscular tension is less. They do not suffer from easy fatiguability. Nutrition through diet provide necessary energy substrates including vitamins and minerals which in turn provide enzymes that catalyze energy production.

Physical fitness not only assessed by cardiopulmonary fitness parameters like VO2 max and PFI but also by pulmonary function tests like FEV1, PEFR and MEP.

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The present study was undertaken to show the effects of exercise and nutrition on growing children by comparing the cardiopulmonary test performance of residential and non-residential school children. Materials and Methods

Our study included 200 students in the age range of 12 to 16 years from residential (Sainik) and non-residential (Banjara) schools of Bijapur city, North Karnataka.

Method of collection of data (5): For comparison, we divided the students into two groups.

Group I: It consisted of 100 male students from residential (Sainik) school of Bijapur city, North Karnataka.

Group II: It consisted of 100 male students from non-residential (Banjara) school of Bijapur city, North Karnataka.

The subjects represented almost all socioeconomic sections and religions.Written consent was taken from Principals of both the schools as students were

minor.The ethical clearance for the study was obtained from the ethical committee of BLDE

University.The procedures were explained to children. Through thorough history and detailed

clinical examination, students were selected.Subjects were taken into confidence and data was collected at the school campus during

working hours between 12 noon to 2pm during resting period.Inclusion criteria: 1) Apparently healthy 2) Age: 12-16 yrs Exclusion criteria: 1) Suffering from cardiopulmonary disorders 2) Any chronic

diseases 3) Any endocrine disorders 4) H/O obesity or anemia.Cardiopulmonary fitness parameters:

By using Modified Harvard Step Test (HST): The test was done on Modified Harvard Steps of 33 cms height. PFI and VO2 max were calculated by using following formulae.1) Physical fitness Index (%)(PFI %) (6) PFI = Duration of exercise in secs × 100 2(pulse 1+2+3)2) Maximal aerobic power VO2 Max (ml/kg/min) by Margaria’s equation (7). It was obtained by using the formula. VO2 Max = 111.33 – (0.42×Pmax)

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Recording of Pulmonary Parameters (8,9)

1) FEV1% by using Benedict-Roth’s recording spirometry.2) PEFR by using peak flow meter.3) MEP by using Modified Black’s apparatus (10).

ResultsGroup I: Residential (Sainik) school children = 100 students.Group II: Non-Residential (Banjara) school children = 100 students.

Recording of cardiopulmonary fitness test parameters and pulmonary function test parameters were shown below in table form and in graphical form.

The mean PFI (%) for group I (Residential) was 54.96+8.38, which was significantly higher than that of group II (Non-Residential) which was 44+5.05 (p = 0.000). (Table I)

The mean VO2 max (ml/kg/min) for group I (Residential) was 66.03+7.06, which was significantly higher than that of group II (Non-Residential) which was 55.24+7.53 (p = 0.000). (Table I)

It was observed from Graph I that mean PFI (%) and mean VO2 max (ml/kg/min) were significantly higher in group I (Residential) as compared to those of group II (Non-Residential).

FEV1 (Mean + SD) in residential was 91.21+7.53 & in non-residential school children was 87.79+9.79 (p = 0.000). PEFR (Mean + SD) in residential was 499.05+95.39 & in non-residential school children was 389.25+ 96.98 (p = 0.000). MEP (Mean + SD) in residential was 90.1+ 17.05& in non-residential school children was 73.83+25.50 (p = 0.000). (Table II)

It was observed from Graph II that mean FEV1 (%), mean PEFR (L/min) and mean MEP (mmHg) were significantly higher in group I (Residential) as compared to those of group II (Non-Residential).

Table 1: shows cardiopulmonary fitness parameters.Parameters Group I Group II Z

Values p valuesMean + SD SE Mean + SD SEPFI(%) 54.96 + 8.38 0.838 44.75 + 5.05 0.505 10.44 0.000***VO2 Max(ml/kg/min) 66.03 + 7.06 0.706 55.23 + 7.53 0.753 10.44 0.000***

*p: <0.05: Significant, ** p: <0.01: Highly significant, *** p: <0.001: Very highly significant

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Table 2: shows pulmonary function parameters.Parameters Group I Group II Z

ValuesP Values

Mean + SD SE Mean + SD SEFEV1 (%) 91.21+ 7.53 0.753 87.79 + 9.79 0.979 5.19 0.000***PEFR (l/m) 499.05+ 95.39 9.539 389.25 + 96.98 9.698 8.07 0.000***MEP mmHg 90.1+ 17.05 1.705 73.83 + 25.50 2.550 5.30 0.000***

*p: <0.05: Significant, ** p: <0.01: Highly significant, *** p: <0.001: Very highly significant

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Statistical AnalysisAll the values were presented as mean, standard deviation and standard error.

Comparison of mean values of parameters were done between group I and group II using Z test. (11)Discussion

Several studies have established that physical fitness is necessary to carry out daily task. The effect of regular exercise is known to have beneficial effect on health. Gymnastic activity in school curriculum was introduced by John Bernard. (2)

In our country, there are residential and non-residential schools. Residential schools like Sainik school, Navodaya school and many others have implemented regular exercise training by qualified trained persons for their students. Nutritious food is also provided under the guidance of qualified dieticians and doctors in such schools. In non-residential schools, education is being provided but regular exercises are not monitored regularly and no dieticians are there to guide for the nutrition for the students.

Physical fitness is assessed by cardiopulmonary efficiency tests. Cardiopulmonary fitness parameters included PFI and VO2 max. They are very highly statistically significant in Group I as compared to those of Group II. (p=0.000)

The mean PFI (%) obtained for Group I and Group II were 54.96 + 8.38 and 44.75 + 5.05 respectively, indicating that students of residential (trained) school had higher values than that of students of non-residential (untrained) school due to regular physical activity and training may be one of the contributing factors in attainment of such growth. (12) These values correlated with observations made by Chatterjee et al (2001) (13). Their study also showed higher PFI score in trained (athletics) than those of untrained (non-athletics) but comprising of female subjects only.

Sunil KR. Das et al also studied PFI with modified Harvard test in young men and women. Their study restricted to untrained subjects only. (14)

We found very highly significant increase in VO2 max of the subjects from Group I compared to Group II. The obtained values were 66.03 + 7.06 and 55.23 + 7.53 respectively.

Pulmonary function tests including FEV1%, PEFR and MEP. The values as shown in table II were significantly higher in Group I compared to Group II. (p=0.000)

Similar observations were reported regarding lung function tests by different authors all over the world at different age groups.

Lakhera et al (1994)(15) observed in their study that lung volumes, lung capacities and FEV1 (%) were consistently higher in athletes than those of non-athletes due to lower air way resistance. These observations were very much correlated with those of Group I subjects in our study. It could be concluded that training definitely improves the Lung Volumes and Capacities in growing children.

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The values of MEP obtained in Residential and Non-Residential school children by Choudari D et al (2002)(16) correlate with our present study.

Similar observations were reported regarding cardiopulmonary efficiency and pulmonary functions by different authors all over the world at different age groups.Conslusion

Our study clearly indicates that regular exercise and balanced nutrition supplementation will improve physical fitness and pulmonary functions as indicated in Group I (Residential school) children.Suggestion for further Research

Longitudinal study may be conducted on Non-Residential school children. They may be subjected to regular exercise training and providing nutritious food as per the dieticians advice. The effect may be observed for different duration between the same age groups. Acknowledge

I am thankful to staff members of Dept of Physiology, BLDE University, Principals and school children of Sainik School (Residential) and Banjara School (Non-Residential). References1. 1. Clarke HH. Basic understanding of physical fitness. Physical fitness Research

Digest series 1971;1:2.2. http://exercise.lovetoknow.com/Physical_Fitness_history.3. Sujit K, Choudari. Text book of Concise Medical Physiology. 3rd Ed. Calcutta: New

central book agency Ltd; 2000: p.404. 4. Pansare MS. Physiology of Fitness. Medical J of Western India 1986;14;18-20.5. Sidhu KS, Methodology of Research in Education. Sterling’s Publishers Pvt Ltd, New

Delhi, (1st Edition), 1984, 4th reprint 1990, Page 262-272.6. Meisner JS, Lawrie JA. Human biology- A guide to field methods. Ind Edn, Oxpord

and Edinburg; BlackwellPublishers:325-328,1969.7. Marquaria R, Aghema P, Rovelli E 1965. Determination of maximal oxygen

consumption in man. J Appl Physiol; 20:1070-1073.8. Udwadia FE, Sunawala JD. Lung function studies in healthy Indian subjects. J Ass of

Physicians of India 1987:36(7):491-6.9. Mahajan KK, Mahajan AM. Pulmonary functions in healthy females of Haryana. Ind

J Chest Dis All Sci 1997; 39:163-71.

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10. Jain AK. Manual of Practical Physiology. 2nd ed. Himachal Pradesh: Arya; 2007: p.178-184, 223, 233, 148-151.

11. Dr Mahajan Methods in Biostatistics (5th Edition), Jaypee Brothers, Medical Publishers Ltd, New Delhi 1989; Page 102, 114-119, 125-39.

12. Sharman IM, Down MC. The effect of Vit E and training on physiological function and athletes performance in adolescent swimmers. Brit. J. Nutr. 1971;26:265-276.

13. Chatterjee S, Mitra A. The relation of physical fitness score with different morphological parameters and VO2 Max on adult female Athletes and Non athletes. Ind. J Physiol and Allied Sci 2001;Vol 55(1): 7-11.

14. Das SK, Mahapatra S. Determination of physical fitness index (PFI) with modified Harvard Step Test (HST) in young men and women. Ind J Physiol and Allied Sci 1993; Vol 47(2): 73-5.

15. Lakhera SC, Kain TC, Bandopadhayay P. Lung function in middle distance adolescent runner. Ind J Physiol Pharmacol 1994;38(2):117-20.

16. Choudari D, Aithala M, Kulkarni VA. Maximal expiratory pressure in Residential and Non-Residential school children. Indian Journal of Paed 2002; vol 69.

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Original ArticleDECREASED PARASYMPATHETIC FUNCTION IN HEALTHY

OFFSPRINGS OF TYPE-2 DIABETIC PARENTSSangeeta.D.Tuppad, Anand R Dharwadkar*, Asha A.Dharwadkar*, Manjunath A**

Department of Physiology, BLDEU’s Shri B.M.Patil Medical College, Hospital & Research Centre, Bijapur.

AbstractBackground :

Type-2 Diabetes Mellitus has strong genetic component. Individuals with both the parents with Type-2 Diabetes Mellitus have 40% risk of developing Diabetes. Now a days Type-2 Diabetes Mellitus is diagnosed more frequently in children and young adults.Objective :

To study Parasympathetic Functions in the healthy offsprings of Type-2 Diabetic Parents Study Design & Methods :

Study group: 30 normal healthy medical students (Offsprings of Type-2 Diabetic Parents) in the age group of 18-21years of BLDEU’S Shri B.M.Patil Medical College, Bijapur.

Control group: 30 age matched normal healthy medical students (Offsprings of Nondiabetic Parents).Computerised 4 channel Physiopac (MEDICAID) used for recording the parameters.Results:

Statistical analysis done by unpaired Student’s t-test. The results expressed as means ±SD. Mean Valsalva ratio± SD of Study group is1.28± 0.24. Mean Valsalva ratio±SD of control group is 1.33 + 0.2(p=0.222), Mean Ratio[Immediate heart rate response to standing (30:15 ratio)]+ SD of Control Group & Study Group is 1.34 + 0.20 & 1.31 + 0.2 respectively(p=0.335), Mean HRV[Heart rate variation during Deep Breathing] + SD of Control Group & Study Group is 28.56 + 7.44 & 26.25 + 8.47 respectively(p=0.132).

Gradings according to Ewing & Clarke, 16 out of 30 in study group are graded either borderline/abnormal., whereas 5 in 30 in control group is graded abnormal.

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Conslusion:The above result reveals that there is an impairment Parasympathetic Function in the

offsprings of Diabetic Parents even in presence of normoglycemia. This warrants the study of Cardiovascular autonomic functions in the healthy offsprings of diabetic parents to prevent the complications.Key words: Type-2 Diabetes, Parasympathetic function, Offsprings of diabetic parents.Introduction

The portion of the nervous system that regulates most of the visceral functions of the body is called as Autonomic Nervous System1. Its main aim is to maintain the optimal internal environment (Homeostasis) of the body. It governs various body functions which are normally carried out without conscious control2.

Diabetes Mellitus is a group of common metabolic disorders that share the phenotype of hyperglycemia. Several distinct types of Diabetes Mellitus exist and are caused by a interaction of genetics and environmental factors3.

Individuals with Diabetes Mellitus may develop signs of autonomic dysfunction involving cholinergic, noradrenergic and peptidergic systems. Autonomic neuropathies affecting cardiovascular system cause a resting tachycardia and orthostatic hypotension3.

Type 2 Diabetes Mellitus has a strong genetic component. The concordance of Type 2 Diabetes Mellitus in identical twins is between 70% to 90%. Individuals with a parent with Type 2 Diabetes Mellitus have an increased risk of Diabetes. If both parents have Type 2 Diabetes Mellitus, the risk approaches to 40%. Now a day Type 2 Diabetes Mellitus is being diagnosed more frequently in children and young adults, particularly in obese adolescents3.

Epidemiologic evidence suggests that these complications of diabetes begin early in the progression from normal glucose tolerance to frank diabetes. Early identification and treatment of persons with pre-diabetes have the potential to reduce both the incidence of diabetes and related cardiovascular and microvascular disease3. Objective

To study the Glycemic status and Cardiovascular Parasympathetic Autonomic Functions in the offsprings of Type 2 Diabetic Parents in the age group of 18-21 years of BLDEU’S Shri B.M.Patil Medical College, Bijapur. Methodology

The cross-sectional study was carried out in 30 healthy offsprings of Type 2 Diabetic Parents (Study group) and 30 healthy offsprings of Nondiabetic Parents (Control group) in

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the age range of 18 - 21 years randomly selected among 1st MBBS students of BLDEU’s Shri B M Patil Medical College, Bijapur.

The ECG recordings for these tests were performed on Computerized Physiopac(Medicaid).

Glycemic status of an individual is determined by Oral Glucose Tolerance Test4.1. Fasting blood glucose. 2. Two hours After Glucose Load (Consisting of 75g glucose anhydrate in 300ml of water ingested over the course of 5 minutes).

From each participant an informed consent was obtained. Recordings were taken during morning hours between 9 to 12noon. Stastical Analysis

The results were expressed as mean + SD and range values. Comparisons between study group and control group were done by using unpaired ‘t’ test. The ‘p’ values of 0.05 or less, 0.01 or less and 0.001 or less were considered as statistically significant, highly significant and very highly significant respectively.Results1] Heart Rate response to Valsalva maneuver in Control and Study Group: Mean VR + SD of Control Group- 1.33 + 0.20 Mean VR+ SD of Study Group - 1.29 + 0.24

There is insignificant (p=0.222) decrease in the Valsalva ratio (VR) of subjects in Study Group compared to Control Group(Table 1). 2] Heart rate variation (HRV) during Deep Breathing in Control and Study Group: Mean HRV + SD of Control Group- 28.56 + 7.44 Mean HRV + SD of Study Group- 26.25 + 8.47

There is insignificant (p=0.132) decrease in the heart rate variation during deep breathing in Study Group compared to Control Group(Table 1). 3] Immediate heart rate response to standing (30:15 ratio) in Control and Study Group: Mean Ratio + SD of Control Group- 1.34 + 0.20 Mean Ratio + SD of Study Group- 1.31 + 0.20

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There is insignificant (p=0.335) decrease in the immediate heart rate response to standing in Study Group compared to Control Group(Table 1)Glycemic status of an individual1] Fasting Blood Glucose (mg/dl) of Control and Study Group: Mean FBG + SD of Control Group 85.03+7.81 Mean FBG + SD of Study Group 85.56 +7.03

There is insignificant (p=0.395) increase in the Fasting Blood Glucose in Study Group compared to Control Group(Table 2). 2] Postload Blood Glucose (mg/dl) of Control and Study Group: Mean PLBG + SD of Control Group 96.56+12.55 Mean PLBG + SD of Study Group 99.20 +14.92

There is insignificant (p=0.234) increase in the Postload Blood Glucose in Study Group compared to Control Group(Table 2).Table 1: Autonomic function parameters of subjects in Study and Control Groups.

Autonomic function parameters Control Group Study Group Level of significance

Valsalva Ratio 1.33 + 0.20 1.29 + 0.24 0.222HR variation to deep breathing (Maximum-Minimum) 28.56 + 7.44 26.25 + 8.47 0.132Immediate HR response to standing (30:15) 1.34 + 0.20 1.31 + 0.20 0.335

Parasympathetic Function ScoreParasympathetic Function scores are done according to D.J.Ewing and B.F.Clarke.

No. of subjects expressed as percentage of the total number of the subjects in the groups and compared. Higher the score, more is the dysfunction.

Parasympathetic function scores calculated for each group are presented in Table-2Table 2: Parasympathetic function score in Control and Study Group Parasympathetic

Function Score Groups 0 1 2 3 4 5Control Group 83.3% 6.6% 10% 0 0 0Study Group 43.3% 33.3% 16.6% 6.6% 0 0

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Table 7A: Fasting Blood Glucose and Postload Blood Glucose in Control and Study Group.

Parameters Control Group Study Group Level of signifi canceFasting Blood Glucose(mg/dl) 85.03+7.81 85.56 +7.03 0.395Postload Blood Glucose(mg/dl) 96.56+12.55 99.20 +14.92 0.234

DiscussionThe cross-sectional study is carried in 60 normal healthy medical students (Offsprings

of Type 2 Diabetic Parents n=30; and Nondiabetic Parents n=30) in the age group of 18-21years of BLDEU’s Shri B M Patil Medical College, Bijapur.

Parasympathetic function is assessed by heart rate response to Valsalva maneuver, heart rate response to deep breathing, immediate heart rate response to standing.A. Parasympathetic Function Tests:I. Heart rate response to Valsalva maneuver

A normal response to Valsalva maneuver is characterized by a decrease in the pulse pressure & tachycardia during strain & blood pressure overshoot & bradycardia following

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the strain. The Valsalva maneuver tests the integrity of both parasympathetic & sympathetic divisions of autonomic nervous system. The hemodynamic changes during the maneuver are mediated via baroreceptors. With parasympathetic affection, the baroreceptor mediated reflex bradycardia response to elevated blood pressure will be reduced.

In the present study the mean value of Valsalva ratio (Table no.1) showed a significant (p=0.002) decrease in Subgroup-3 of study group compared to control group still remaining in the normal range (> 1.21, according to Ewing and Clarke grading)5

Our findings are in accordance with earlier studies done by C. Hauerslev Foss et al6. Heart rate response to Valsalva maneuver appear to be more sensitive parameters to detect autonomic dysfunction amongst the three Parasympathetic function tests. II. Heart rate response to deep breathing:

Heart rate response to deep breathing (sinus arrhythmia) is a normal phenomenon & is primarily due to fluctuation of parasympathetic output to the heart.

There is insignificant (p=0.132) decrease in the heart rate variation during deep breathing in Study Group compared to Control Group(Table-1).

Our study is in accordance with studies done by C. Hauerslev Foss et al6.III. Heart rate response to Standing (30: 15 ratio):

Heart rate response to standing in normal subjects consists of tachycardia maximum around 15th beat followed by relative bradycardia around 30th beat after standing7. These hemodynamic responses are mediated by baroreceptors.

In our study we found a insignificant (p=0.335) decrease in the immediate heart rate response to standing in Study Group compared to Control Group(Table-1).

Our study is in accordance with studies done by C. Hauerslev Foss et al6.

Glycemic Status:There is insignificant increase in the Fasting Blood Glucose and Postload Blood

Glucose in Study Group compared to Control Group(Table-2). Our study is in accordance with studies done by I.N.Migdalis et al8,Frontoni S et al9

Our results are not in agreement with Hauerslev Foss et al6.We found significantly lower mean values for the three cardiovascular parasympathetic

reflex tests in study group compared to control. The results indicate that heart rate variation is reduced in study group compared to control. We found a higher prevalence of cardiac autonomic dysfunction in study group compared to control even in presence of normoglycemia.

Our observations indicate that subclinical autonomic dysfunction may develop without

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the presence of long-term hyperglycemia in family members of type 2 diabetic subjects; thus, it is not simply a complication of the hyperglycemia in these patients..

An explanation could be that it is possible to inherit susceptibility genes for autonomic neuropathy, and that these genes could be expressed before—or maybe even without—the subjects developing diabetes. Different factors (including hyperglycemia) could subsequently affect the expression of the genes and influence the progression of neuropathy9.

This cross-sectional study shows autonomic dysfunction in study group indicate that early autonomic dysfunction may be present with normoglycemia , and we suggest that autonomic dysfunction may be part of a genetic syndrome which appears earlier than appearance of dysglycemia which requires further longitudinal study in study group. Conslusion

We conducted a cross-sectional study to evaluate Glycemic status and Cardiovascular Autonomic Functions in 60 normal healthy medical students (Offsprings of Type 2 Diabetic Parents and Nondiabetic Parents in the age group of 18-21years of BLDEU’s Shri B M Patil Medical College, Bijapur. We performed Parasympathetic function tests (heart rate response to Valsalva maneuver, heart rate response to deep breathing, immediate heart rate response to standing).

We conclude from our study that1) Autonomic function tests showed gradual decrease in function in study group compared

to control.2) Heart rate response to Valsalva maneuver & Blood pressure response to Sustained

Hand Grip appear to be more sensitive parameters to detect autonomic dysfunction amongst the three Parasympathetic function tests & the two Sympathetic function tests respectively

3) There is a gradual increase in the abnormal autonomic function score in subgroups of study group based on history of prevalence of diabetes in both parents and in first degree relatives.

4) There is insignificant increase in Fasting blood glucose and Postload blood glucose in study group compared to control group.

5) Though the grading & function scores are accepted no reference in the literature is available following these criteria. So we have tried to present the autonomic function in the form of score which may help to grade the subjects easily rather than expressing the results as pure values of different tests.Further study on insulin levels is needed to determine insulin sensitivity and insulin-

resistance and its relation to autonomic dysfunction.

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References1. Guyton & Hall. Textbook of medical Physiology.11th edition. Pennsylvania:

Elseveir; 2006.P: 748.2. Jain A K. Manual of practical Physiology. 3nd edition. Himachal Pradesh: Arya

Publications; 2008. P: 279-280.3. Alvin CP, Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson

LJ, editors. Harrison’s principles of Internal Medicine. Vol 2.17th edn. New York: McGraw Hill Companies 2008; P:2275- 2289.

4. Fiorentini A, Perciaccante A, Paris A, Serra P, and Tubani L. Circadian rhythm of Autonomic activity in non diabetic offsprings of type 2 diabetic patients. Cardiovasc Diabetol. October 2005. 10.1186/1475-2840-4-15.

5. Ewing DJ, Clarke BF. Diagnosis and management of diabetic autonomic neuropathy. Br Med J 1982 Oct; 285: 916-918.

6. Hauerslev Foss, E. Vestbo,A Froland, H. J. Gjessing, C. E. Mogensen and E. M. Damsgaard. Autonomic Neuropathy in Nondiabetic Offspring of Type 2 Diabetic Subjects Is Associated With Urinary Albumin Excretion Rate and 24-hAmbulatory Blood Pressure. The Fredericia Study. Diabetes.March 2001;50(3):630- 636.

7. Dixit MB. Comparative cardiovascular responses to 70o Head up tilt in pilots and non-pilots. Aviat Med 1983; 27: 38-42.

8. I.N. Migdalis D. Zachariadis, K. Kalogeropoulou,C. Nounopoulos , A. Bouloukos, M. Samartzis. Metabolic Abnormalities in Offspring of NIDDM Patients with a Family History of Diabetes Mellitus. Diabetic Medicine, 1996 May ;13(5):434–440,

9. Frontoni S, Pellegrinotti M, Bracaglia D, Farrace S, Caselli A, Baroni A, et al. Hyperinsulinaemia in offspring of Type 2 diabetic patients: impaired response of carbohydrate metabolism, but preserved cardiovascular response. Diabet Med. 2000 Aug;17(8):606-11