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IJRRMS 2012;2(1)

IJRRMS | VOL-2 | No.1 | JAN - MAR, 2012


Lavlesh Kumar

Binaya Kumar Bastia

Kaushik Mishra Raghavendra D. Kulkarni Swapnil S. Agarwal (Orissa) (Karnataka) (Gujarat)

M. I. Sheikh Nilamadhab Kar Ratnakar Dash (Gujarat) (United Kingdom) (Orissa)

Sheetal Chhaya Senthil Kumaran, Sweta Patel

Mamata Mohapatra

Editor-in-Chief:

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Managing Editor :

Ashwini Mohapatra (Karnataka)Brajesh Sahu (West Bengal)E Ravi Kiran (Andhra Pradesh)Girish Sharma (Himachal Pradesh)K. H. Chavali (Chandigarh)Manoj Kumar Mishra (Bihar)Praveen Yadav (Gujarat)

Prabhat Kumar Thatoi (Orissa)R. P. Garg (Rajasthan)Rajesh Sinha (Chhattisgarh)Roopam Gupta (Gujarat)Sanjay Kumar Mukherjee (Gujarat)Shrabana Kumar Naik (New Delhi)Subrat Akhoury (Uttar Pradesh)Sujeet Jha (New Delhi)

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IJRRMS VOL-2 No.1 JAN - MAR, 2012 | | |

Estd.

Editorial

Original Research Papers

Case Reports

Letters to Editor

Nobel Laureates in Medicine or PhysiologySupplements

What ails the Medical Research Publications in India

1. Experimental animal studies on analgesic and anti-nociceptive activity of Allium sativum

(Garlic) powder. Jayanthi MK, Jyoti MB 1

2. Effect of Savitri Pranayama practice on peak expiratory flow rate, maximum voluntary

ventilation and breath holding time. Mamatha SD, Gorkal AR 7

3. Chronic cor-pulmonale in adults: An experience from a tertiary teaching hospital in

Dharwad. Sindhur JC,Rajoor UG 12

4. Maternal Mortality Rate and its causes– Changing trends in Kolkata, India. Chakraborty S,

Sebanti G 16

5. Predictors of maternal mortality during H1N1 pandemic. Mamatha, Umadevi K,

Sujani BK, Urvashi T, Shruti R 19

Hamid S, Rekha, Raina S 237. Recurrent cold abscess of the chest wall in a young immunocompetent person. Gayathri Devi DR,

Narayanaswamy YV, Areena H 26

8. Beneficial role of amantadine in catatonic schizophrenia: A case report. Srivastava M 29

9. Angiofibroma in an elderly – A Case Report. Panigrahi R 31

10. Cardiac tamponade - An unusual presentation of Pulmonary Adenocarcinoma.

Pathan ZA, Chaudappa JS, Parshawnath HA, Lakshmi DKB 33

11. Primary squamous cell carcinoma of breast. Kaur P, Chauhan A, Singh G, Kataria SP 36

Manuscript submission guidelines 38

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6. An anatomical variation of unilateral higher division of sciatic nerve with bifid piriformis

And its clinical implications.

37

CONTENTS VOLUME-2, ISSUE-1

IJRRMS VOL-2 No.1 JAN - MAR, 2012| | |

IJRRMS 2012;2(1)

IJRRMS2011Estd.

What ails the Medical Research Publications in India?

It was in 1990 that the director of a hospital expressed concern regarding the low output of medical research

from India and the issue was addressed at length by an eminent neurosurgeon. That was two decades ago.

Encouraged by a positive note in an editorial expressing the recent rapid extension in quantity of educational

research, and out of curiosity, I tried to have a cursory glance at the progress since that time.

The publication share and scientific activity of India in the global scenario has been reported to be on the

rise; it is growing at an average rate of 7.76% per annum. India has improved its global scientific publication

share amongst developing countries from 1.86% to 2.11 % but still ranks 12th in the table of 20 countries. At

this juncture it is pertinent to mention that in the world context, India's national publications share in

physical sciences, life sciences, and engineering sciences each has been above the global average in each

discipline but in health sciences its share has been below the global average. Encouraging, but not

substantial if one takes into account its population, the abundance of clinical material, ever increasing

number of medical schools and number of graduates and post graduates qualifying every year. There are

immense opportunities which need to be explored to carry out more and more number of researches and

publication.

Amongst the many reasons responsible for the grim picture, inadequate infrastructure and staff, poor

accessibility to funds earmarked for research, poor administrative support, lack of formal training in

research methodology and bio-ethics, poor expression capabilities and unenthusiastic attitude of the

doctors and the resultant low self-esteem, are probably the topmost.

The path of research and research publication is not rosy. Inadequate infrastructure and funds are

commonly cited reasons for the poor research figures. Honest, dedicated team of workers who can devote

their time and commitment are also essential. In India, the overwhelming figures of patient load dictates

that healthcare take preference over research, and it is not perceived as a possible career opportunity by

many. Simultaneously, research can also not be pursued as a part-time hobby either. Institutions do not give

high priority to research activities.

Research ethics is another matter of concern. Researchers in India do not give due consideration to all the

ethical aspects of research and publication. Thesis writing is an essential part of postgraduate curriculum.

But at many medical colleges, this aspect of postgraduate training is taken as an unavoidable compulsion and

not properly practiced. Thus, the student is not exposed to proper research methodology right from the

beginning of his career. Importance of research planning and protocol writing is not stressed upon, and most

of the students find an easy way out by procuring a readymade protocol for their thesis work. Every year

multiple conferences are held for each specialty in the country wherein a multitude of papers are presented.


IJRRMS 2012;2(1)


IJRRMS 2012;2(1)

But only a small fraction of such presented papers find their way into published literature. The reasons could

be apathy of the researchers towards publication or poor quality of research papers being presented at such

conferences that do not merit publication in peer-reviewed journals.

Government organizations like Indian Council of Medical Research (ICMR), Department of Science and

Technology (DST) and Department of Biotechnology (DBT), etc. are prepared to fund the appropriate

research. In fact, the Government of India has set up a separate department of Health Research and has

appointed a medical man as its Secretary, which is an achievement in itself. Despite various channels put in

place the young scientists find it difficult to obtain the funds. Red tape, complex mandatory requirements,

ignorance and almost zero percolation of the schemes to the grass-root level act as dampeners to access of

funds that are aplenty. Recently, some agencies have come forward with readiness to help, guide and

overcome the obligatory hurdles in getting the grants, but this too demand lot of time and effort and money

in making a proper application. Growing institutions/ universities do not want to be left behind and try

copying the good policies of the established ones in allocation of award in cash or kind to their faculties who

wish to publish and prosper. At the same time, they make the guidelines so stringent and unrealistic that only

few among many qualify to achieve. One has to overlook minor deficiency in the beginning to promote the

policy for encouragement of publication.

Recently, guidelines have been laid down linking personal promotions with research publications. This may

have reinforced the idea of 'publish or perish' in the minds of the young researchers. The result is that there

has been a sudden spurt in the quantity of published literature but quality still remains to be achieved. The

'rush' to publish has lead to further dilution of quality. The 'myth of numbers' should be dispelled and quality

research should be encouraged and preferred.

Being a vast and diverse multi-lingual country, not all students being admitted to medical courses are from

the English medium background. Language and expression is a big barrier to publication. As a result, people

who have the capacity to do research and present the results are not excelling. While countries like China,

Turkey, Germany and Iran have medical publications in their local languages, India still uses English for

imparting medical education and also for publications.

Everyone has a potential to write as there are no special skills, certificates or diplomas required for

publishing. It's imperative to place one's work before the scientific community for appraisal. At the same

time we have to overcome the steadily increasing pressure to publish as evidence of an individual's

performance. Also, the editorial boards need to discharge their duty of improving the quality of standards of

articles published in biomedical journals and find a way to increase the low rates of internationally published

articles. After all, 'publication' is a widely accepted indicator of performance in any academic field, especially

science

Editor-in-ChiefIndian Journal of Research & Reports in Medical Science

References:

1. Pandya S K. Why is the output of medical research from India low? BMJ. 1990 August 11; 301(6747):333.

2. Price PM. Prepare to publish. Dynamics. 2000 Summer;11(2):12-7

Dr. Lavlesh Kumar

11 1

Experimental animal studies on analgesic and anti-nociceptive activity of Allium sativum (Garlic) powder

ABSTRACT

Jayanthi MK, Jyoti MB

Background: Allium sativum has the analgesic and antinociceptive potential to emerge as a safer alternative drug having no troublesome adverse effects.Aims: To estimate the analgesic and anti- nociceptive effects of Allium sativum powder (ASP) in animal models; and to compare the effects between central and peripheral nociceptive models with that of other established analgesic drugs.Materials and Methods: Albino rats and mice were used for studying analgesic and anti-nociceptive activity of Allium sativum powder at doses 75, 150 and 300 mg/kg orally. Various models viz. acetic acid induced writhing model, Eddy's hot plate for analgesic study and formalin-induced paw licking model were used for anti-nociceptive study. Results: In acetic acid induced writhing model, effect of ASP was better than the control. In the hot plate model, maximum effect was observed at 60 min at a dose of 300 mg/kg, which was higher than the control. In formalin-induced paw licking model, ASP completely abolished the early phase at 150 and 300 mg/kg and in the late phase, the effect of ASP (300 mg/kg) was higher than control. Conclusion: ASP is effective in both non-narcotic and narcotic models of nociception, suggesting its possible action via peripheral and central mechanism. It also abolishes the early phase in formalin-induced paw licking model. Hence, ASP can be developed as a potent analgesic and anti-nociceptive agent.

Keywords: analgesic, Allium sativum, acetic acid, Eddy's hot plate, formalin

INTRODUCTION

Pain is an unpleasant sensation that can be either acute or chronic and that is a consequence of complex neurochemical processes in the

1 peripheral and central nervous system. Drugs used to relieve pain are opioid (morphine like) and nonopioid (aspirin like) analgesic group of drugs. The introduction of these drugs has revolutionized the treatment of pain. The amazing efficacy of opioid and NSAIDS in painful inflammatory conditions has paved the way for the introduction and use of newer analgesic agents. However, the safety factor in respect of both the analgesic drugs has been rather intriguing and hence a definite need is visualized for the introduction of safer analgesic drugs having no troublesome adverse effects.

Plants still represent a large untapped source of structurally novel compounds that might serve as lead for the development of novel drugs. 2

Furthermore, it is also interesting to note that several natural products especially indigenous drugs have also been invest igated for antinociceptive potential. In fact, opium has originally been described as one of the ingredients

3of poppy (Papaver somniferum) capsule.

Allium sativum (garlic) is one of the plant substances, used as an indigenous remedy for c e r t a i n a i l m e n t s . I t s e f f e c t a s a n immunomodulatory and anti-inflammatory, antithrombotic, lipid-lowering, antitumoral and

4antioxidant properties have been demonstrated. There are several studies on ethanolic, methanolic extracts of Allium sativum but studies on the Allium sativum powder (ASP) are sparse.

Hence, in the light of the aforementioned development, ASP has been taken up for the investigative study of its analgesic potential. Specific objectives of the study were to estimate the analgesic and anti- nociceptive effects of ASP in

IJRRMS 2012;2(1)Original Research Paper


http://www.hindawi.com/journals/aps/2012/789713/

animal models; and to compare the effects between central and peripheral nociceptive models with that of established analgesic drugs like pentazocine and indomethacin. This study also emphasizes the importance and feasibility of the usage of indigenous preparations in clinical medicine.

ASP obtained from garlic bulbs has been taken up for the investigation of analgesic and anti-nociceptive activity.

Processing of ASP: Garlic bulbs were obtained from Spicex Chemicals Private Ltd, Mysore. Bulbs are separated, deskinned, and dried with the help of an instrument having heating system on one side and a fan on the other side, maintaining hot air current at 50°C for 6 hours, then powdered in a mixer- grinder at 1,850 RPM for 3 min. The fine powder thus obtained is kept in air tight containers. The yield of garlic powder from the garlic bulbs after the processing was found to be 250 gm/kg of garlic bulbs.

Test dose: A pilot study was conducted with different doses (50 mg/kg, 75 mg/kg, 150 mg/kg, 200 and 300 mg/kg) to assess the appropriate dose for the study. The analgesic activity was observed at few doses and the same was used in the study.

Phytochemical test

ASP was subjected to standard phytochemical screening tests for various constituents.

Chemicals: Indomethacin 10mg /kg and pentazocine 10mg/kg, ASP, normal saline and other chemicals were of analytical grade.

Animals: Adult Albino mice of either sex weighing between (20-30 g) or Adult Albino rats of either sex weighing between (120-130 g) were used for the study. The animals were procured from animal research laboratory, National Institute of Mental Health and Neuro Sciences, Bangalore and housed in the animal house of the institute in 5 groups, at an ambient temperature of 25±1°C with ad libitum

MATERIAL AND METHODS

access to food and water. The study protocol was approved by Institutional Animal Ethics Committee.

Treatment schedule: The analgesic and anti-nociceptive activities were examined by using the Acetic acid induced writhing test, Eddy's hot plate model and Formalin-induced paw licking model. Animals were divided into five groups, with each group consisting of six animals. Group 1 received vehicle (normal saline); group 2 received indomethacin / pentazocine (10 mg/kg orally), groups 3, 4 and 5 received ASP -75,150 and 300 mg/kg orally respectively.

Acetic acid induced writhing in rats

Adult albino rats were randomized into five groups of 6 each. The analgesic activity of ASP was

5 assessed using writhing test. Control, standard and test groups were treated with vehicle, indomethacin (10 mg/kg) and ASP (75,150 and 300mg/kg) orally respectively, 60 minutes prior to the test. Acetic acid solutions (10 ml/kg, 0.6% in normal saline) was injected intraperitoneally and were observed for the (writhes) contraction of abdominal muscles for 10 min. Number of writhes were counted to assess analgesic activity of various groups, and was expressed as the percentage inhibition of abdominal constrictions between control group and ASP treated group animals.

Thermally-induced pain in mice

This is one of the most commonly used methods 6

for evaluating central analgesic activity of a drug.

In this method heat was used as a source of pain.

Mice were being divided into 5 groups of six each.

First group served as a control, second group

served as the standard (Pentazocine 10 mg/kg,

intraperitoneally), while the third, fourth and fifth

groups received 75,150 and 300 mg/kg of ASP

respectively. After 1 hour, animals were

individually placed on a hotplate maintained at a 0temperature of 55± 0.5 C, and were placed not

more than 15 seconds (cut off time) on the

hotplate, in order to avoid damage to the paws.

IJRRMS 2012;2(1)Jayanthi MK et al. Experimental animal studies on analgesic and anti-nociceptive activity of Allium sativum(Garlic) powder

IJRRMS VOL-2 No.1 JAN - MAR, 2012| | |2

The time taken to flick the hind paw or lick or jump

from the hot plate was considered as the reaction

time of the particular animal. The reaction time

was recorded at 0, 15, 30, 45, 60, 90, and 120 min.

An analgesic increases the reaction time. Percent

decrease in reaction time was taken as index of

pain perception at each interval.

Formalin- induced paw licking model in mice

Adult albino mice randomized into five groups of 6

each were not fed for a day. The control group

received 10ml/kg of distilled water orally, standard

group received indomethacin (10 mg/kg orally)

and the test groups received ASP at doses 75, 150

and 300 mg/kg, orally respectively. Formalin

solution (20 ìl of 2.5%) was injected

subcutaneously under the surface of the right hind

paw of each mouse and the responses were 7

observed for half an hour. The duration of time

spent licking the injected paw was recorded and

was indicative of pain. The first phase of the

analgesic activity normally peaked at 5 minutes

representing the neurogenic response and the

second phase representing inflammatory pain

response after 15-30 minutes of formalin injection.

This suggests formalin test has two distinctive

phases possibly reflecting different types of pain.

Statistical analysis:

The statistical analysis of data was done using one-

way analysis of variance by using the SPSS software

(version 11.5). P< 0.01 was considered as highly

significant.

Acetic acid induced writhing model in mice

As shown in Table - 1, the ASP produced significant

(P<0.01) reduction in the number of writhing in

mice in dose dependent manner. At 100 and 200

mg/kg, the percent reduction of writhing was

57.44% and 72.10% respectively, as compared to

the control group, whereas the standard drug

indomethacin (10 mg/kg) showed a reduction of

91.38% .

RESULTS

Values are expressed in terms of mean ± SEM, n = 6 in each group, *p< 0.01 statistically highly significant as compared with control group. ASP =Allium Sativum Powder.

Thermally-induced pain in mice

In this model, the reaction time in ASP treated group increased significantly (P<0.01) in comparison to the control group. The maximum effect was observed at the highest dose viz. 200 mg/kg at 60 min which showed a reaction time of 16.5 sec, whereas the standard drug pentazocin (10mg/kg) showed a reaction time of 17.2 sec. The extract also showed dose and time dependent activity -Table 2.

Table 2: Analgesic activity of ASP in Eddy's hot plate model in mice


Formalin- induced paw licking model in mice

Administration of ASP at 50 and 100 mg/kg caused reduction in duration of paw-licking (43.8 and 35.11 sec), as compared to the control group (57.2 sec). Higher doses of ASP at 200 mg/kg showed complete abolishment of the early phase



Table 1: Analgesic activity of ASP in albino mice in acetic acid induced writhing method

Groups

Drugs

Dose mg/kg

(p.o)No. of Writhing Percent reduction (%)

I

Control

-

47±1.57 0.00

II

Indomethacin

10

4.73±1.45* 91.38

III

ASP

75 31.18±0.79 33.65

IV 150 20.00±0.53* 57.44

V 300 13.11±0.82* 72.10

Groups Drugs (p.o)

Dose mg/kg

Reaction time in seconds

0 min 30 min 60 min 90 min 120min

I Control - 3.89±0.15 4.10±0.07 4.60±0.17 4.30±0.25 3.59±0.12

II Indomethacin 10 12.6± 0.42*

14.6±0.81* 17.2±0.64* 14.2±0.47* 13.6±0.53*

III

ASP

75 6.55±0.25* 9.12±0.65* 11.7±0.45* 12.2±0.85* 12.5±0.35*

IV 150 8.80±0.12* 11.7±0.65* 13.7±0.55* 14.0±0.47* 13.2±0.34*

V 300 10.6±0.52* 13.6±0.67* 16.5±0.33* 13.5±0.38* 12.4±0.54*

3

indicated by absence of paw licking after the formalin injection. However, the standard drug- indomethacin (10 mg/kg) exhibited a reduction of paw licking time of 25.4 sec only in the early phase. In late phase, the administration of ASP decreased the duration of paw licking dose dependently from 70.37 sec at 50 mg/kg to 48.84 sec at 200 mg/kg in the late phase. On the other hand, indomethacin (10 mg/kg) exhibited a reduction of paw licking time of 33.84 sec in the late phase. The effect of ASP at 200 mg/kg was comparable to standard drug-Table 3.


Analgesics are medications used to relieve pain without reducing the consciousness of the patient. They work by reducing the amount of pain felt and this is generally achieved by interfering with the way the pain message is transmitted by the nerves. We carried out the study using different experimental models to evaluate peripheral and central analgesic and anti-nociceptive activity of ASP.

ASP showed analgesic activity both centrally or peripherally. The plant is supposed have the phytoconstituents which inhibit cyclooxygenase enzyme for producing analgesia peripherally or act on central opioid receptors for producing analgesia centrally. Standard drug indomethacin act on cyclooxygenase pathway of prostaglandins

8synthesis.

Acetic acid induced writhing response in mice is reliable and affords rapid evaluation of peripheral

DISCUSSION

type of analgesic action. Pain sensation in this writhing method is elicited by triggering localized inflammatory response resulting in release of free arachidonic acid from tissue phospholipids via cyclooxygenase (COX), and prostaglandin

9,10biosynthesis. Acetic acid is believed to act ind i rect ly by induc ing the re lease of prostaglandins and other mediators into the peritoneum which in turn stimulate nociceptive neurons sensitive to analgesic anti-inflammatory drugs. The mechanism of analgesic activity of ASP could be probably due to the blockade of pain mediators, which excite pain nerve endings similar to that of indomethacin and NSAIDs. Thus, the reduction in the number of writhing suggests that ASP might exert anti-nociceptive activity by inhibition of cyclooxygenase in peripheral tissue. The hot-plate method is one of the most common tests considered to be selective for the centrally acting drugs. Thermally-induced pain in mice measures the complex response to a non-inflammatory, acute nociceptive input used for

11studying central nociceptive activity. Nociceptive reaction toward thermal stimuli in mice is a well-validated model for detection of opiate analgesics as well as several types of analgesic drugs from

12spinal origin. An agent that causes a prolongation of the hot plate latency using thermally-induced pain in mice must be acting centrally is an

13established fact. NSAIDs inhibit only peripheral 14,15

pain whereas narcotic analgesics block both. ASP has shown inhibition of both types of pain. The analgesic effect of the plants in both models reveals that they have dual action through central

11and peripheral mechanism.

Normally, the fine afferent C- and A- fibers are activated by brief, high intensity stimuli, which do not induce any tissue damage. However, during inflammation, the afferent fibers can be activated by lower intensity stimuli and the pain produced differs in quality and persistence. Formalin induced pain is caused by peripheral tissue inflammation. It involves a phase of inflammation wherein a variety of chemical mediators alter the

16 functions of peripheral afferent fibers.

In the present study, the formalin-induced paw



Groups

Drugs

Dose mg/kg

(p.o)Early phase(duration of paw licking in seconds)

Late phase(duration of paw licking in seconds)

I Control - 57.2±1.57 135.20± 1.10

II Indomethacin 10 25.4±1.45* 41.85±0.34*

III

ASP

75 43.8±0.79* 70.37±1.12*

IV 150 39.00±0.53* 61.31±1.11*

V 300 0 49.84±0.45*

4

licking model comprises of early phase (immediately after injection) seems to be caused by C-fiber activation due to the peripheral stimulus and late phase (starting approximately 20 min after formalin injection) appears to depend on the combination of an inflammatory reaction. The formalin resulted in a progressive biphasic behavioral response such as licking and biting of the injected paw in all the experimental groups. The beginning time point of the phase 2 response in these experimental groups was 15 min after the formalin injection. ASP completely abolishes the early phase at the dose 200 mg/kg, suggesting complete inactivation of C- fiber in the early phase. ASP decreased the reaction time in dose dependent manner in the late phase also, which might suggest that ASP causes partial inactivation of NMDA and non-NMDA receptors.

Phytochemical screening of ASP: It revealed the presence of tannins, flavonoids, aromatic acids,

17reducing sugars and saponins. One of the most biologically active compounds, allicin (diallyl thiousulfinate or diallyl disulfide) does not exist in garlic until it is crushed or cut; injury to the garlic bulb activates the enzyme allinase, which metabolizes alliin to allicin which is further metabolized to vinyldithiines. Ajoene is another chemical constituent thought to be most important to health. Previous studies have shown the anti-inflammatory, analgesic and anti-convulsant

18activity of methanolic extracts of Allium sativum. In contrast to various extracts, the natural powder form can be easily prepared and can serve as an efficient household remedy for common ailments.

A number of studies on Allium sativum, or its major active principles, have shown an antihyperlipidaemic, antibacterial and anti rheumatic properties. In the present study, ASP has shown promising results in experimental algesia. It can be interpreted that ASP possesses promising analgesic and anti-nociceptive properties, possibly exerts its effect through diverse mechanisms that may involve both central pain inhibitory mechanism as well as peripheral pathways through inhibition of prostaglandin synthesis. ASP may serve as a potential adjuvant for management of various painful conditions. The results obtained by this study cannot be directly extrapolated to humans; further studies are required to establish the effect on pain perception in humans.

, Professor, Contact- 9448978273, Email: [email protected] (Corresponding Author)Department of Pharmacology, JSS Medical College (A constituent college of JSS University),SS Nagar, Mysore- 570015,Karnataka,INDIA.

, Asst. Professor Department of Pharmacology, JN Medical College, Belgaum, Karnataka.

CONCLUSION

AUTHOR NOTE

Jayanthi MK

Jyoti MB

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Effect of Savitri Pranayama practice on peak expiratory flow rate, maximum voluntary ventilation and breath holding time

ABSTRACT

Mamatha SD, Gorkal AR

Background: Yoga, an ancient culture of Indian heritage, regular practice leads to ideal physical, mental, intellectual, and spiritual health. Pranayama is one of the yogic practices. These have a number of beneficial physiological effects on various systems in our body. The present work was taken up as data reported on the effect of Savitri pranayama alone on peak expiratory flow rate (PEFR), maximum voluntary ventilation (MVV) and breath holding time (BHT) is scarce.

Aim: To know whether there is any change in PEFR, MVV & BHT in the subjects practicing savitri pranayama and with that of subjects not practicing any type of yoga.

Materials and methods: Two test groups consisting of 30 male student volunteers from Rama Krishna Institute of Moral and Spiritual Education (RIMSE), Mysore, of age between 18 to 28 years were selected. They practiced savitri pranayama for 30 minutes daily for 16 weeks. The control group consisted of age and sex matched 30 students of JSS medical college. PEFR & MVV were determined by using medspiror, a digital spirometer and BHT was determined by using mercury manometer.

Results: The study group showed significant increase in all the parameters measured when compared to control group.

Conclusion: Present study leads to the supposition that Savitri Pranayamic breathing exercise strengthens respiratory muscles and control it by overriding the usual excitatory stimuli to respiratory centres. Hence there is increase in PEFR, MVV & BHT.

Key words: Savitri Pranayama, PEFR, MVV, BHT

INTRODUCTION

Yogic practices, an ancient culture of Indian heritage, have led to ideal physical, mental, intellectual, and spiritual health. Yoga has a number of beneficial physiological effects on various systems in our body. Regular yogic practices have been shown to cause profound improvement

1 2in cardiorespiratory, thermoregulatory and 3

psychologic functions in healthy individuals . Yogic practices have been also found to be most useful in

4 5alleviating hypertension, bronchial asthma, 6 7diabetes mellitus, and coronary artery disease . A

previous study has shown that there is significant increase in PEFR in pranayama practicing school

8 children. Combination of various type of pranayama including Savitri Pranayama has also led to significant increase in hand grip strength (HGS), hand grip endurance (HGE), maximum expiratory pressure (MEP), maximum inspiratory pressure (MIP), forced expiratory volume (FEV), forced

expiratory volume in first second (FEV1) and peak 9 expiratory flow rate (PEFR). Statistically significant

increasing trend (P<0.01) in percentage predicted peak expiratory flow rate (PEFR), forced expiratory volume in the first second (FEV1), forced vital capacity (FVC), forced mid expiratory flow in 0.25–0.75 seconds (FEF25-75) and FEV1/FVC% in bronchial asthma patients practicing combination

10of pranayama. Fifteen days regular practice of 11

different types of pranayama and practice of 12 asanas, pranayamas & suryanamaskara has led to

increase in the mean breath holding time significantly alone with other parameters.

There is a need to know the effect of Savitri Pranayama (which can be done in Savasana position) training alone on respiratory system, so that benefits, if any, could be obtained by its practice and can be advised in non-ambulatory patients to strengthen respiratory muscles.




Study was carried out at Rama Krishna Institute of Moral & Spiritual Education (RIMSE), Mysore and at department of physiology JSS Medical College, Mysore. Informed and written consent was taken from the subjects of both the groups. Our study did not involve any invasive procedure. Ethical clearance was taken from Institutional Ethical Clearance Committee.

For the present study, 30 male student volunteers were selected randomly from RIMSE, Mysore of aged 18-28 years as the test group. Age matched 30 male student volunteers were selected randomly from JSS Medical College as control group. They did not practice any type of pranayama in the past or during the present study. They were not practicing or involved in any type of sports or gymnastic activities regularly. Study was carried out only in males to avoid the variation in genders. The subjects in the test and control group had no history of allergic disorders, respiratory disorders, and systemic diseases in the past as well as during the present study. There were no drop outs in the test as well as in control groups during the present study.

Test group practiced Savitri Pranayama for 30 minutes in the early morning between 6:00 am to 6:30 am, 6 days per week for 12 weeks under the guidance of trained yoga instructor. They performed initial stretching exercise for 10 minutes before starting pranayama. The details of Savitri Pranayama procedure is as follows:

Posture

Shavasana i.e., lying supine on a flat surface with the head preferably to the north or east so as to be in alignment with the earth's magnetic field. The upper limbs relaxed and placed by the sides of the thighs with the palms facing upwards. Feet were relaxed with heels touching each other lightly. Air was breathed in through the nose for 6 numeral counts and held in for 3 numeral counts. Again air was breathed out through the nose for 6 numeral counts and then held out for 3 numeral counts. Breathing was done in and out through both

nostrils. This was repeated for several rounds.

Method for recording PEFR & MVV

Anthropometric measurement was noted. Peak Expiratory Flow Rate (PEFR) & Maximum Voluntary Ventilation (MVV) were measured using medspiror. The instrument is 'Medispiror' brand by 'Recorders and medicare systems', Chandigarh. It is a type of flow sensing digital spirometer. The instrument is capable of giving reproducible test results and represents the major advancement in computerized pulmonary function testing.

Procedures

The subjects were familiarized with the setup and detailed instructions and demonstrations were given to their satisfaction. The subjects were made to breathe out forcefully following deep inspiration into the mouthpiece attached to the pneumatachometer.

Expiration was maintained for a minimum period of 3-4 seconds. Three to four trails of maximal inspiratory and expiratory efforts were made and only the highest reading was taken for data processing. PEFR expressed in litres/sec was noted. For measuring MVV expressed in litres/min, the mouth piece was placed into the subject's mouth and was instructed to breathe quietly. When the subjects settled, they were asked to breathe in and out as rapidly and deeply as possible for 10 seconds, and then MVV was calculated for one minute.

Method for recording BHT

It was measured by valsalva manoeuvre using mercury monometer.

Procedure

According to the specifications laid down in a 13

previous study a mouth piece was constructed which was required for this study. It consists of a hollow PVC tube 15 cm length, closed by a PVC cap at one end with a 2 mm hole in the centre. The other end was connected to PVC reducer. The thickness of the tube was 2 mm with an internal diameter of 3 cm. The bottom of the tube was

IJRRMS 2012;2(1)Mamatha SD et al. Effect of Savitri Pranayama practice on peak expiratory flow rate, maximum voluntary ventilation and breath holding time.


connected to a three way stop cock and linked by a 50 cm rubber tube to the mercury manometer.

The subject was asked to blow through the mouth piece in sitting posture, after deep inspiration, until the pressure in the mercury manometer raises up to 40 mm and is maintained until the subject can no longer hold the breath voluntarily. The time was noted using a stop watch, this records the BHT.

The term break point is defined as involuntary termination of breath holding in response to the development of net ventilatory stimulus too strong to be further resisted by voluntary effort. Hence, reason for the breaking point is that during breath holding, the pO2 falls and pCO2 rises which stimulates the respiratory centre.

Two recordings were done on both test and control groups. In test group first phase of recording (basal recording) were done before starting pranayama practice & second phase of recording were done after 12 weeks of pranayama practice. Same types of recordings were done on control group also.

To avoid influence of circadian rhythm, the recordings were done between 8.30 am-9.30 am

14 only. The tests were done in a quiet room in order to alleviate the emotional and psychological stresses. During the tests, maximum efforts from the subjects were ensured by adequately motivating them to perform at their optimum level.

Statistical analysis: Data are expressed as Mean ±SD. Data analysis was done using Independent samples't' test to find out the significance of differences between groups selected. Differences in means were considered statistically significant when the two-tailed P value is <0.005.

(NS) – Not significant

I. (b)Physical characteristics of the subjects stduring 1 phase of recordings

RESLUTSFirst phase recording showed no significant differences in any of the tested parameters between Test and Control groups.

Second phase recordings showed significant differences in all the tested parameters between Test and Control groups.

(s) – significant- p value < 0.005

II . (b)Physical characteristics of the subjects

during second phase of recording

DISCUSSION

Yogic asanas and pranayama have shown to reduce the resting respiratory rate. Further, they increase the vital capacity, timed vital capacity, MVV, BHT and maximal inspiratory and expiratory

15 pressures. Respiration is regulated automatically by the neural mechanisms through the respiratory centres (RCs) located in the medulla oblongata and pons. The cyclic waning of sensitivity of RC is


I. (a) Comparison of first phase of readings in test and control groups and results of independent samples 't' test

II. (a) Comparison of second phase of readings in test and control groups and results of independent samples't' test


Age Height Weight BMI

Test 21.06+2.42 164.03+3.10 61.88 +2.38 23.05 +0.84

Control 20.83+2.35 163.66+3.32 62.46+2.52 23.24+1.32

t value 0.379 0.442 -0.919 -0.651

p value 0.706 (NS) 0.660(NS) 0.362(NS) 0.518(NS)

PEFR(L/sec) MVV(L/min) BHT(sec)

Test 4.35+ 0.42 97.83+7.21 23.54+ 0.48

Control 4.35+ 0.42 94.63+ 5.25 23.24+ 0.88

t value 0.000 1.96 1.605

p value 1.000(NS) 0.54(NS) 0.114(NS)

Age Height Weight BMI

Test 21.06+2.42 164.03+3.10 62.41+2.61 23.23+0.79

Control 20.83+2.35 163.66+3.32 62.28+2.78 23.14+1.38

t value 0.379 0.442 0.191 0.312

p value 0.706 (NS) 0.660 (NS) 0.849 (NS) 0.756 (NS)

PEFR (L/sec) MVV (L/min) BHT (sec)

Test 5.872+0.98 119.33+14.95 30.42+2.60

Control 4.32+0.37 98.06+ 7.72 23.45+0.63

t value 8.058 6.92 14.25

P value 0.000 (s) 0.000(s) 0.000(s)

9

determined by impulses from higher centres, afferent rhythmic discharges modified by pO2 and pCO2 in blood, and impulses from stretch receptors in lungs and thorax. Results of our study showed that practice of Savitri pranayama is an effective way to develop the strength of respiratory muscles and to bring respiration under volition.

PEFR is the maximum flow rate attained during forced vital capacity manoeuvre measured in litres. Its measurement helps to assess the degree of opening of small airway passages. Pranayama involves using of lung spaces, which is not used up in normal shallow breathing. Therefore, the increased peak expiratory flow rate might be a

1consequence of small airway opening in lungs.

MVV is the maximum volume of air breathed in and out of lungs with maximum voluntary effort in minute (to avoid the effect of increased pCO2 & decreased pO2 during this procedure, recording is done for 10-15 sec and the value is calculated for 1min). It is a test for overall function of respiratory system. It is influenced by the status of respiratory muscles, the compliance of lung-thoracic system, condition of the ventilatory control mechanism and the resistance offered by airways and tissues. The possible explanation for increased MVV could be that regular deep inhalation and expiration of the lungs for prolonged periods has lead to strengthening of respiratory muscles. Therefore, strengthening of respiratory musculature occur incidental to regular practice of pranayamic breathing, during which the lungs and chest inflate and deflate to the fullest possible extent, the muscles are made to work to maximal extent. The maximum inflation and deflation is an important physiological stimulus for the release of

16surfactant and prostaglandins increasing the

1 7alveolar spaces thereby increasing lung compliance and decreasing bronchial smooth muscle tone activity.

During pranayama, an individual continues the phase of inhalation with his strong voluntary control so that lungs are expanded considerably

and the walls of the alveoli are stretched to the maximum thus the chest continues to get expanded under cortical control. The stretch receptors are thus trained and adopted to withstand increased stretching. This helps an individual to hold the breath for a longer period. The RC as a group is under voluntary control and the respiration can be voluntarily arrested for a variable period during any phase of respiratory cycle by inhibitory impulses from higher centres which are able to balance excitatory effect of other afferents. At the end of breath holding, these excitatory impulses increase the sensitivity of the RC to such a level that the voluntary control finally breaks and respiration commences. Increased tolerance to higher pCO2 and lower pO2 achieved

18due to training could also prolong BHT. The duration of breath holding is gradually increased as RC is gradually acclimatized to withstand higher pCO2 and lower pO2 in blood. With this we can predict that the RC will dominate over other influences. Therefore in many different ways the individual practicing pranayama is training the stretch receptors to withstand more stretching and to tolerate more and more CO2 tension so that breath can be held for a longer duration. Hence, in pranayama practitioners, there is a gradual increase in BHT as there is increased tolerance to higher pCO2 and low pO2 that are achieved due to training. As this pranayama can be done in savasana position, practice of savitri pranayama may be beneficial in non-ambulatory patients to improve respiratory musculature and bronchial tone.

In the test group there is statistically significant increase in PEFR, MVV & BHT after 12 weeks of practice when compared to control group. Savitri pranayama training causes increase in lung and thorax compliance, respiratory muscle strength and tolerance of RC against higher pCO2 and therefore there is significant increase in all the parameters measured.

CONCLUSION



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Pranayama' on selected parameters of cardiovascular, pulmonary, and higher functions of brain. Thai J Physiol Sci. 2005;18(2):10–6.

2. Madanmohan, Sivasubramaniyan KM, Balakrishnan S, Gopalakrishnan M, Prakash ES. Effect of six weeks yoga training on weight loss following step test, respiratory pressures, handgrip strength and handgrip endurance in young healthy subjects. Indian J Physiol Pharmacol. 2008;52(2):164-70.

3. Ray US, Mukhopadhyaya S, Purkayastha SS, Asnani V, Tomer OS, Prashad R, et al. Effect of yogic exercises on physical and mental health of young fellowship course trainees. Indian J Physiol Pharmacol. 2001 Jan;45(1):37-53.

4. Murugesan R, Govindarajulu N, Bera TK. Effect of selected yogic practices on the management of hypertension. Indian J Physiol Pharmacol. 2000 Apr;44(2):207-10.

5. Sathyaprabha TN, Murthy H, Murthy BT. Efficacy of naturopathy and yoga in bronchial asthma—A self controlled matched scientific study. Indian J Physiol Pharmacol. 2001 Jan;45(1):80-6.

6. Telles S, Naveen KV. Yoga for rehabilitation: An overview. Indian J Med Sci. 1997 Apr;51(4):123-7. 7. Manchanda SC, Narang R, Reddy KS, Sachdeva U, Prabhakaran D, Dharmanand S, et al. Retardation

of coronary atherosclerosis with yoga lifestyle intervention. J Assoc Physicians India. 2000 Jul;48(7):687-94.

8. Sivapriya DV, Subamalani S, Shyamala T. Effect of nadi shodhana pranayama on respiratory parameters. Recent Research in Science and Technology. 2010;2(11):32-39.

9. Madanmohan, Lakshmi J, Kaviraja U, Ananda BB. Effect of yoga training on handgrip, respiratory pressures and pulmonary function. Indian J Physiol Pharmacol. 2003;47(4):387–392.

10. Candy S, Sheena S, Dandona PK. A study of the effect of yoga training on pulmonary functions in patients with bronchial asthma. Indian J Physiol Pharmacol. 2009;53(2):169-174.

11. Ankad RB, Balachandra AS, Herur A, Patil S, Chinagudi S, Shashikala GV. Effect of Short Term Pranayama and Meditation on respiratory parameters in healthy individuals. International Journal of Collaborative Research on Internal Medicine & Public Health. 2011;3(6):430-437.

12. Makwana K, Khirwadkar N, Gupta HC. Effect of short term yoga practice on ventilator function tests. Ind J Physiol Pharmacol. 1988;32(3):202-206.

13. Black LF, Hyatt RE. Maximal respiratory pressures: Normal values and relationship to age and sex. Am Rev Respir Dis. 1969;99:696-702.

14. Rodahl A, O'Brien M, Firth RG. Diurnal variation in performance of competitive swimmers. J Sports Med Phys Fitness. 1976 Mar;16(1):72-6.

rd15. Bijalani RL. Understanding medical physiology, 3 edition, Jaypee brothers, Noida.2004; p. 897.16. Hildebran JN, Goerke J, Clements JA. Surfactant release in excised rat lung is stimulated by air

inflation. J Appl Physiol. 1981 Oct;51(4):905-10.17. Smith AP. Prostaglandins and respiratory system prostaglandins; physiological, pharmacological and

pathological aspects. Edited by SMM. Karim. 1976; 83-102.18. Bhargava R, Gogate MG, Mascarenhas JF. Autonomic response to breath holding and its variation

following pranayama. Ind J Physiol Pharmacol. 1988;32(4):257-264.


AUTHOR NOTE

Mamatha SD, Assistant Professor , Contact- 9342049717, Email: [email protected] (Corresponding Author)

Gorkal AR, ProfessorDepartment of Physiology, JSS Medical College, a

constituent college of JSS University, Mysore-570015 , Karnataka, India


Chronic cor-pulmonale in adults: An experience from a tertiary teaching hospital in Dharwad

ABSTRACT

Sindhur JC, Rajoor UG

Background: Cor-pulmonale develops in response to acute or chronic changes in the pulmonary vasculature and/or the lung parenchyma that are sufficient to cause pulmonary hypertension. The true prevalence of cor-pulmonale is difficult to ascertain. However, recent advances in two dimensional echocardiography/Doppler imaging and biomarkers make it easier to screen and detect cor-pulmonale. Aim: To study the etiology of cor-pulmonale, and to correlate it with the clinical, chest x-ray (CXR), electrocardiography (ECG) and echocardiography (ECHO) findings.Methods: Fifty consecutive patients admitted with confirmed diagnosis of cor-pulmonale were included into the study. Detailed history, clinical examination, ECG, CXR and ECHO were carried out in all the cases.Results: Out of the 50 patients, 32 were males and 18 were females. Maximum incidence was seen in 50-69 age group comprising 60% of the cases with mean age being 55.2 years. Majority (56%) of patients had the history of symptoms of more than 10 years duration. Chronic bronchitis was the underlying cause in the largest number (54%) of patients. Majority of patients had evidence of pulmonary hypertension. Q/R ratio in a VR >3 was observed in 60% of cases. On ECHO, right atrial enlargement was evident in 46% of patients and RVH was evident in 94% of cases.Conclusions: In patients with clinical diagnosis of chronic cor-pulmonale, chest x-ray is a poor tool for detection of pulmonary hypertension, but gives information about its etiology. ECG provides information about RVH and right atrial enlargement. Echocardiography is helpful in detecting all cases of cor-pulmonale and to exclude pulmonary hypertension produced by left sided heart disease.

cor-pulmonale, pulmonary hypertension, echocardiography

Keywords:

INTRODUCTION

Chronic cor-pulmonale is usually the end result of long standing pulmonary disease, which results from pulmonary hypertension and subsequently to

1right ventricular hypertrophy (RVH) and failure. The right ventricle (RV) may get hypertrophied without producing right heart failure. Therefore, in chronic cor-pulmonale the mechanisms which leads to RVH ultimately results in right heart

2 failure. Chronic cor-pulmonale as a cause of congestive cardiac failure (CCF) is being recognized in recent years. Therefore recognition of chronic cor-pulmonale is of great importance to physicians, pulmonologists and cardiologists. Analysis of cardiovascular epidemiology in India also reflected that chronic cor-pulmonale forms a significant

3proportion of cardiovascular cases. The high incidence of chronic cor-pulmonale in Dharwad, Karnataka which consists mostly of rural population base prompted this study with a view to elucidate its etiology and also to correlate clinical, x-ray,

electrocardiography(ECG) and echocardiography (ECHO) findings in such patients.

Fifty consecutive patients admitted to a tertiary care hospital in Dharwad, Karnataka with confirmed diagnosis of cor-pulmonale were included into the study. Detailed history, clinical examination, electrocardiography (ECG), chest X–ray (CXR) and echocardiography (ECHO) were carried out in all the cases. The results were analyzed and descriptive statistics was used.

Exclusion criteria: Congenital heart diseases, right heart failure secondary to dysfunction of the left side of the heart, ischemic heart disease and rheumatic heart disease cases were excluded from this study.

Data was collected by using proforma meeting the objectives of the study. Purpose of the study was carefully explained to the patients and informed consent was obtained.




Investigations: Complete haemogram, blood urea, serum creatinine, serum electrolytes like sodium, potassium and chloride, routine urine examination, chest x-ray, ECG and ECHO was done in all these patients.

Socioeconomic status of study population was assessed based on modified Kuppuswami's scale. Class I taken as high class, class II and class III taken as middle class, and class IV and class V taken as low class.Chest x-ray findings: The chest x-rays were analyzed by measuring the Cardiothoracic (CT) ratio, along with the widest diameter of the right descending pulmonary artery. Evidence of pulmonary hypertension was taken if right descending pulmonary artery width was >16mm. This was assessed independently by radiologists who were unaware of clinical and laboratory information.ECG findings: ECG was used to detect and exclude patients with Ischemic Heart Diseases (IHD). A 12 lead ECG was recorded in all the patients. The following ECG signs reflecting chronic cor-

0pulmonale were recorded: 1) P wave axis of +90 or more- right axis deviation, 2) P pulmonale, 3) right bundle branch block (RBBB), 4)RVH defined by one of following pattern, a) Q/R ratio in aVR >3, b) R/S ratio in V1>1.

ECHO findings: 2-D echocardiography was used to measure right ventricular dimensions and the right ventricular wall thickness to assess the presence of right ventricular hypertrophy and/or dilatation. Evidence of right atrial enlargement is confirmed if right atrial size >55mm and RVH if free wall thickness >5mm.Statistical methods: The results were analyzed by calculating percentages, the mean values and standard deviation (SD).

Out of 50 patients of chronic cor-pulmonale studied, 32 were males and 18 were females, male: female ratio being 1.8: 1. The age of patients varied from 28 – 78 years. Maximum incidence was seen in 50-69 age group comprising 60% of the cases,

RESULTS

with mean age being 55.20 years. Majority of the patients were illiterates (65%), belonging to low class, and all of them were from rural/semirural areas.Duration of underlying respiratory disease: Before the onset of cardiac failure, patients furnished a history of symptoms referable to the underlying lung condition for a variable period of time. Symptoms of duration of more than 10 years were given by 56% of cases. The shortest duration in this study was 4 months and the longest was 30 years.Physical findings: All the cases presented primarily as gross CCF, with dyspnea, oedema, liver enlargement, raised venous pressure and ascites, but no significant cardiac signs (Table-1). On the basis of absence of signs of other heart disease and presence of gross pulmonary disease, the diagnosis of chronic cor-pulmonale was made.

Table1: Distribution of signs and symptoms manifested (n=50).

Pulmonary conditions: Chronic bronchitis was the underlying cause in the largest number of patients accounting for 54% of caes(Table-2). Pulmonary tuberculosis formed a low figure despite its high incidence in this part of Karnataka.

Table-2: Underlying pulmonary diseases (n=50).

IJRRMS 2012;2(1)Sindhur JC et al. Chronic cor-pulmonale in adults: An experience from a tertiary teaching hospital in Dharwad.


Symptoms and signs No. of patients Percentage (%)

Dyspnea 100

Cough 100

Orthopnea

Raised venous pressure

Lower limb oedema

Enlarged liver

Ascites

Cyanosis

Mental confusion

Epigastric pulsation

Loud P2

Palpable P2

Left parastrernal heave

50

50

32 64

41 82

36 72

34 68

17 34

30 60

16 32

46 92

35 70

26 52

20 40

Disease No of patient Percentage (%)

Chronic bronchitis 28 54

Emphysema 10 20

Bronchiectasis 06 12

Bronchial asthma 02 04

Pulmonary tuberculosis 03 06

Chest deformity 01 02

Primary pulmonary hypertension 00 00

Total 50 100

13

Laboratory findings: Majority (64%) of cases were anaemic. Table 3 shows the CXR, ECG and Echo findings of the study population.

Table-3: CXR, ECG and Echo findings suggesting RVH and pulmonary hypertension (n=50).

DISCUSSIONThe important aspect of this study was the high incidence of cor-pulmonale in an entirely nonindustrial population. Of the 50 patients, maximum numbers of cases (60%) were seen in the age group of 50-69 years. This correlates well with a similar study wherein the incidence was 65% in

4t h e co r re s p o n d i n g a ge g ro u p . M a l e s outnumbered females which is comparable to

5another study where the ratio was 1.2:1. Chronic bronchitis was found to be commonest etiological factor for the causation of cor-pulmonale. Majority of the males were smokers who smoked >10 beedies/day for more than 20 years. Platts et al., in their study has established the definite role of

6smoking in the causation of cor-pulmonale.

All patients suffering from chronic cor-pulmonale were admitted to hospital with varying degree of dyspnea and cough with expectoration. Patients with cor pulmonale may present with RVH,

7 asymptomatic RV dysfunction or RV failure.Evidence of congestive heart failure was seen in majority of the cases as evident by raised jugular venous pressure, enlarged tender liver and lower limb oedema. Majority of patients had pulmonary hypertension as evidenced by epigastric pulsation (92%), loud P (70%) and palpable P (52%). 2 2

Minority of them had evidence of right ventricular hypertrophy with a parastrernal heave (40%). Hence clinical diagnosis is usually possible only when patients develop right ventricular failure.

While comparing the clinical signs for pulmonary hypertension and RVH in patients with and without chronic obstructive pulmonary disease (COPD), it was found that these clinical signs were seen only in a minority of cases with COPD, which is probably due to hyperinflation of the chest. Thus, majority of them presented with evidence of cardiac failure, since most of the patients sought medical aid only when they got disabled to a great extent by their symptoms. A similar study showed pulmonary hypertension as a common complication of chronic obstructive pulmonary

8disease (COPD). The increase in pulmonary artery pressures is often mild to moderate. However, 5–10% of patients with advanced COPD may suffer from severe pulmonary hypertension and present with a progressively downhill clinical course because of right heart failure added to ventilatory

8handicap.

In our study, 48% of the patients had the changes suggestive of pulmonary hypertension on chest x-ray. Cardiomegaly was seen in 62% and pleural effusion in 40%, both of which were seen in patients with gross failure. Chest x-ray is very helpful in patients presenting with cor-pulmonale due to causes other than COPD like bronchiectasis and extensive fibrosis. It is also very helpful to detect the cause of acute exacerbations. The use of non-invasive imaging techniques to assess the anatomy and function of the pulmonary vessels and heart has taken on added importance with the recent advent of novel therapies. Imaging findings not only constitute a diagnostic tool but have also proven to be essential for prognosis and

9treatment follow-up.

A 12 lead ECG was recorded in all patients. 60% had sinus tachycardia because many patients presented with infective exacerbation, and many patients were on beta agonists. Right axis deviation was present in 72% of cases. Mittal SR et

10al., reported in their study, Q/R ratio in aVR >3, was diagnostic of RVH in chronic cor-pulmonale and it had a specificity of 94%. In our study the specificity using Q/R in aVR was only 60%. Right atrial enlargement by measuring height of p wave in lead II was detected in 44%. Right ventricular



Variables No of patients Percentage (%)

X ray changes 24 48

Right descending pulmonary artery width >16mm

Cardiomegaly (CT ratio >50%) 31 62

ECG changes 36 72

Right axis deviation

Q/R >3 in aVR 21 42

R/S >1 in V1 30 60

Echo findings 23 46

Right atrial size >55mm

Free wall thickness >5mm 47 94

14

enlargement by taking ratio of R/S in lead VI was present in 60%. The reported incidence of RVH in

11such patients varies from 28% to 75%.

By using 2D echocardiography, right atrial enlargement was seen in 46% of patients (right

atrial size ≥ 55mm). Right ventricular hypertrophy

(RVH) was seen in 94% (free wall thickness ≥ 5mm), and pericardial effusion was seen in 20% of patients. A study comparing ECG, vector cardiography (VCG) and ECHO data in 78 patients with chronic bronchitis, allowed the distinction of 4 grades of RVH. Apparent ECG signs of RVH in chronic bronchitis develop much later, usually after the development of secondary pulmonary

12hypertension.

The high incidence of cor-pulmonale in a study population consisting mostly from rural background is the result of chronic bronchitis and

CONCLUSION

emphysema secondary to untreated chronic respiratory infections. Contributing factors include low social class and ill ventilated and overcrowded living conditions. In patients with chronic cor-pulmonale, chest x-ray is a poor tool for detection of pulmonary hypertension, but gives information about the etiology. ECG gives information about RVH and right atrial enlargement, in addition to arrhythmias produced by disease per se or drugs used to treat it. Echocardiography is helpful in detecting all cases of cor-pulmonale and to exclude pulmonary hypertension produced by left sided heart disease.

, Associate Professor, Email:(Corresponding Author)

, Assistant ProfessorDepartment of Medicine, SDM College of Medical Sciences and Hospital, Sattur, Dharwad-580009, Karnataka, India.

AUTHOR NOTE

Sindhur JC

Rajoor UG

[email protected]

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Emphysema: In: Murry JF, Nadel JA. Text Book of Respiratory Medicine, Philadelphia, W B Sunders, 2000:1187-1245.

2. Robert N, Jean LV. Pulmonary hypertension. Clin Chest Med. 2001;22:517-529.3. Padmavati S, Arora R. Sex differences in chronic cor pulmonale in Delhi. Br J Dis Chest. 1976

Oct;70(4):251-9.4. Vakil RJ. Heart disease in India. Am Heart J. 1954 Sep;48(3):439-48. 5. Padmavathi S, Pathak SN. Chronic cor-pulmonale in Delhi- A study of 127 cases. Circulation.

1959;20:343-352. 6. Platts MM, Hammond JD, Stuart-Harris CH. A study of cor pulmonale in patients with chronic

bronchitis. Q J Med. 1960 Oct;29:559-74.

7. Haddad F, Doyle R, Murphy DJ, Hunt SA. Right ventricular function in cardiovascular disease, part II: Pathophysiology, clinical importance, and management of right ventricular failure. Circulation. 2008 Apr 1;117(13):1717-31.

8. Naeije R. Pulmonary hypertension and right heart failure in chronic obstructive pulmonary disease. Proc Am Thorac Soc. 2005;2(1):20-2.

9. Hovnanian A, Menezes E, Hoette S, Jardim C, Jasinowodolinski D, Souza R. The role of imaging techniques in the assessment of pulmonary circulation. J Bras Pneumol. 2011 Jun;37(3):389-403.

10. Mittal SR, Jain SC. Q/R ratio in lead a VR--diagnostic of RVH of chronic cor pulmonale. J Assoc Physicians India. 1984 May;32(5):430-1.

11. Bredikis AJ, Liebson RP. The ECG in COPD – biventricular hypertrophy, voltage, rhythm changes. The Journal of Respiratory Disease. 1998;19:43-47.

12. Kudaiberdiev Z. Diagnosis of right ventricle hypertrophy during pulmonary heart disease in patients with chronic bronchitis. Klin Med (Mosk). 1991 May;69(5):90-3.



Maternal Mortality Rate and its causes– Changing trends in Kolkata, India

ABSTRACT

Chakraborty S, Sebanti G

Background: Maternal mortality is a reflection of the healthcare provided to a woman by its society. It is tragic that deaths occur during the natural process of child birth which is mostly preventable.Aim: To analyze the trends of maternal mortality rate (MMR) and its causes in a tertiary care hospital in Kolkata, India.Methods: Study design: Retrospective study. Data source: Records of maternal deaths from 1989-1991; and from 2006-2008. Maternal mortality rates and causes of death were analyzed and compared. Results: The MMR rate came down from 1051 to 494.33 (change of 47%) over a span of seventeen years, while the causative factors did not change their rank orders. Conclusion: Credit for declining trend of MMR may be attributed to improving skills of health workers, adopting improved standards for the management of pregnancy and childbirth at different levels of health care system.

Key words: maternal mortality, Millennium Development Goal, ICD-10

INTRODUCTION

World Health Organization (WHO)'s 10th revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-10) defines maternal mortality as "the death of a woman while pregnant or within 42 days of termination of pregnancy irrespective of the duration and the site of the pregnancy, from any cause related to or aggravated by the pregnancy or its management but not from accidental or

1incidental causes". Every year, approximately 358,000 women die from complications of pregnancy and childbirth worldwide. Sub-Saharan Africa and South Asia accounted for 87% of global

2maternal deaths.

India is one of the countries with a high maternal mortality ratio (MMR) and the highest (136,000)

3estimated number of maternal deaths. The main causes of maternal mortality in India are hemorrhage, sepsis, abortion, hypertensive

4disorders, and obstructed labor. MMR for India was 407 by Sample registration system (SRS) 1997 estimate and came down to 301 per 100,000 live births by SRS 2003 estimate. Going by this pace we would achieve the MMR of 195 by the year 2012 and of 160 by 2015, far from the NRHM goal of 100 per 100,000 live births by 2012 or Millennium Development Goal of 109 per 100,000 live births by

42015.

Maternal mortality is ascribed usually to complications that generally occur during or around labor and cannot be accurately predicted. The major causes of maternal mortality are mostly preventable through regular ante natal check up, proper diagnosis, and management of labor

5complications.

This study is an attempt to collect the distribution and magnitude of the burden of MMR in our population; and to identify the etiological factors. This research will also add to the existing data that are essential to the planning, implementation and evaluation of services for the prevention, control and treatment of the disease burden amongst the mothers.

Study population and design: The present study was conducted in the department of obstetrics, Medical College Kolkata. Hospital records of all the maternal deaths from 1989-1991; and from 2006-2008 were collected. The total numbers of live births during the corresponding period were also collected. The causes of death ascribed for the maternal deaths were recorded from the copies of the cause of death certificate attached, and were confirmed through cross checking the details recorded in the case files. We then analyzed the data to look for the trends of MMR between the two periods, and observed the possible variations in the pattern of modalities.




CAUSES 1989 1990 1991 2006 2007 2008

DIRECT No % No % No % No % No % No %

Hemorrhage 25 32.89 21 22.82 15 17.44 61 19 30.64 16 27.11 13 28.88 48

Preeclampsia/Eclampsia 15 19.73 33 35.86 30 34.88 78 12 19.35 16 27.11 13 28.88 41

Sepsis 05 6.58 07 7.61 02 2.32 14 03 4.83 02 3.38 02 4.44 8

Unsafe abortion 04 5.26 02 2.17 05 5.81 11 09 14.51 04 6.77 02 4.44 15

Obstructed labor 0 0 03 3.26 0 0 3 0 0 01 1.69 0 0 1

INDIRECT

Anemia 04 5.26 03 3.26 09 10.46 16 05 8.06 03 5.08 03 6.66 11

Jaundice 14 18.42 15 16.34 18 20.93 47 11 17.74 06 10.16 05 11.10 22

Heart disease 02 2.63 02 2.17 03 3.48 7 02 3.22 07 11.86 05 11.10 14

Other medical causes 03 3.97 03 3.26 02 2.32 8 0 0 02 3.38 0 0 2

HIV/AIDS 0 0 0 0 0 0 0 0 0 01 1.69 0 0 1

Pulmonary embolism 04 5.26 03 3.26 02 2.32 9 01 1.61 01 1.69 01 2.22 3

Table 2: Causes of maternal mortality

To analyze the causes of maternal deaths, WHO criteria were followed for the purpose of this study. Accordingly, causes were classified as direct (hemorrhage, preeclmpsia/ eclampsia, sepsis, unsafe abortion and obstructed labor) and indirect (anemia, jaundice, heart disease, pulmonary embolism, other medical causes, and HIV/AIDS).

The total number of maternal deaths in the year

2006, 2007 and 2008 were 62, 59 and 45,

corresponding to the total number of live births of

9898, 11705 and 12735 respectively (Table 1). The

calculated MMR for the above period was 626, 504

and 353 with mean being 494.33. During the year

1989 to 1991 the total number of maternal deaths

was 76, 92 and 86 respectively with the

corresponding number of live births of 7538, 7529

and 7681. Hence the MMR during this period was

915, 1089, 1041; with a mean of 1051. Therefore,

the observed decline in the MMR over a span of

seventeen years was from 1051 to 494.33 (47%).

RESULTS

Table 1: Maternal mortality rate

IJRRMS 2012;2(1)Chakraborty S et al. Maternal Mortality Rate and its causes-Changing trends in Kolkata, India


DISCUSSION

The revised Millennium Development Goal framework agreed by the United Nation General Assembly has set a target for maternal health under section 5A as 'reduction of the MMR by

6three quarters between 1990 and 2015. The recommended indicators to reflect this improvement are MMR and the proportion of births attended by skilled health personnel. Meeting Millennium Development Goal- 5 has become a challenging task worldwide.

Our results showed a 47% decline in MMR over last 17 years. The results are more or less comparable to rates from tertiary care hospitals in

6South Asian countries or developed countries. However, Berg et al., in the United States reported the MMR as low as 10.3 in 1991 and 12.9 in 1997 per 100,000 live births; whereas, in similar studies

YEAR NO. OF NO. OF MMR YEAR NO. OF NO. OF MMRDEATH LIVE BIRTH DEATH LIVE BIRTH

1989 76 7538 915 2006 62 9878 626

1990 92 7529 1089 2007 59 11705 504

1991 86 7681 1041 2008 45 12735 353

Analysis of the causes of maternal death (Table-2) showed that during 2006-2008, the direct causes accounted for 66-69% of the maternal deaths while the indirect causes shared a percentage of 30-33.

Retrospectively, analysis of the data during 1989, 1990, and 1991 reflected that the contribution of direct causes ranged from 60-71%, and indirect causes ranged from 28-39.5%. Amongst the individual causes of maternal deaths, hemorrhage and eclampsia took the major share throughout the entire study period with a mean being 26.6% f o r h e m o r r h a g e a n d 2 7 . 6 3 % f o r preeclampsia/eclampsia. The next important cause was jaundice for which the mean figure was 15.78%. Unsafe abortion contributed to 6.49% and anemia accounted for 6.46% of maternal deaths. Pulmonary embolism has remained almost constant at 2.72% while one death has been reported due to AIDS in 2007.

17

1. World Health Organization. International Statistical Classification of Diseases and Related Health Problems. Tenth Revision, Vol. 1: Tabular list, Vol. 2: Instruction manual. Geneva; 1992.

2. World Health Organization. Trends in Maternal Mortality: 1990 to 2008 Estimates developed by WHO, UNICEF, UNFPA and The World Bank. Geneva; 2010.

3. Maternal Mortality in 2000, Estimates developed by WHO. Geneva: UNICEF and UNFPA; 2004. World Health Organization.

4. Govt. of India (Sample Registration System), Maternal Mortality in India: 1997.2003, Trends, Causes and Risk Factors, Registrar General, India, New Delhi in collaboration with Centre for Global Health Research, Toronto.

5. Begum S, Aziz-un-Nisa, Begum I. Analysis of maternal mortality in a tertiary care hospital to determine causes and preventable factors. J Ayub Med Coll Abottabad. 2003;15(2):49–52.

6. Maternal and Newborn Health where we stand, Edited by Patricia Moccia, The state of the World's Children 2009, New York, UNICEF, December2008:1-24.

7. Berg CJ, Chang J, Callaghan WM, Whitehead SJ. Pregnancy related mortality in the United States, 1991-1997. Obstet Gynecol. 2003;101(2):289–96.

8. Jadav AJ, Rote PG. Maternal mortality- changing trends. J Obstet Gynecol India. 2007;57(5):398-400.9. Verma A, Minhas S, Sood A. A study on maternal mortality. J Obstet Gynecol India. 2008;58(3):226-229.10. Pal A, Ray P, Hazra S, Mondal TK. Review of changing trends in maternal mortality in a rural medical college in

West Bengal, J Obstet Gynecol India. 2005;55(6): 521-524.11. Sharma JB. Nutritional anemia during pregnancy in nonindustrialised countries. Edited by John Studd;

Progress in Obstetrics & Gynecology, London, Elsevier,2008; Vol 15:103-122.

IJRRMS 2012;2(1)Chakraborty S et al. Maternal Mortality Rate and its causes-Changing trends in Kolkata, India


conducted in Ethiopia and Pakistan, MMR was 6,7reported as high as 9.6 to 12.7/1000 live births

Many possible factors either alone or in combination may be the stakeholders for such a variation. The tertiary care hospitals, regrettably, receives usually complicated and referred cases, sometimes, the patients are admitted only during the terminal stages of their illness. This may be the reason for such a high reporting of MMR in our setup. However, the overall decline of MMR over the observed period may be attributed to various factors like substantial investment in midwifery training by the central as well as the state government, free case supportive health and family planning services like free sterilization camp, judicious utilization of Family Planning methods, Manual Vacuum Aspiration training for safe abortion, and Janani Surakshya Yojna, etc.

In our study, two third of maternal deaths were attributed to direct causes. Hemorrhage and preeclampsia/eclampsia were responsible for 50% of total deaths. Although the absolute number has come down over a period of 17 years, the percentage of share of causative factors remained unchanged. These findings are more or less consistent with the causes of maternal deaths

8,9,10observed in different Indian studies.

Anemia and jaundice took the major share among the indirect causes of death. Anemia which is very much prevalent in our country is responsible for

5,.

1

indirect as well as the direct causes of deaths from cardiac failure, hemorrhage, infections and preeclampsia. This alone accounts for almost 40-60% of maternal deaths in non-industrialized

11countries.

Amongst the indirect causes of death, a new addition has come up in 2007 i.e. death of a mother with terminal AIDS. As the prevalence is going up, we can expect increase number of such deaths in coming years.

The hospital-based maternal mortality figures do not reflect the true picture in the community. But it provides a more thorough assessment of the underlying cause of death and contributing factors that are useful in planning various strategies or interventions at various levels. It is concluded that majority of the maternal deaths can be averted by

'proper and timely intervention of 3E s i.e., emergency obstetric care, early risk screening and efficient obstetric services.

,Email:[email protected] (Corresponding Author)

Assistant Professor, OBGYN, Nodal officer EmOC

training, Medical College, Kolkata, Assistant Professor,

OBGYN, Ex- Nodal officer EmOC training, Medical College, Kolkata

CONCLUSION

AUTHOR NOTE

Chakraborty Somajita

Goswami Sebanti

REFERENCES

18

Predictors of maternal mortality during H1N1 pandemic

ABSTRACT

Mamatha, Umadevi K, Sujani BK, Urvashi T, Shruti R

Background: Pandemic influenza A(H1N1) 2009 is a benign disease when infecting healthy adults, but it can lead to severe consequences in pregnant women and the fetus. There is also an increased mortality in pregnant women compared to the general population. The 2009 influenza A(H1N1) pandemic was the first ever to occur in the era of modern obstetric and intensive care management.

To study the maternal and fetal outcome in patients with H1N1 infection and to establish its influence on gestational age, mode of delivery and nutritional status as well as to look into the effect of early initiation of antiviral drug (oseltamivir). Method: Study design- retrospective study (2009-2011). Study population-obstetrics patients (20) admitted to MSR hospital, Bangalore with flu like symptoms and tested positive with H1N1. All the patients were treated with oseltamivir and outcome measured in terms of maternal and perinatal mortality.Result: Out of 20 patients who were tested positive, 14(70%) required ICU admission, 6(30%) women died. There was one intrauterine death and 01(5%) had termination of pregnancy at 18 weeks of gestation. Conclusion: In developing countries like India, H1N1 infection in pregnant women is associated with significant maternal mortality. Delayed presentation to tertiary care centre, lack of awareness, restricted access to treatment might have contributed to high mortality.

: H1N1 influenza, pregnancy, oseltamivir

Aim:

Key words

INTRODUCTION

March 2009 witnessed a series of cases of influenza-like illness in Mexico caused by a novel H1N1 virus containing genes from swine, avian,

1 and human influenza strains. In early April 2009, an outbreak of A(H1N1) influenza spread

2,3 worldwide. On June 11, 2009, the World Health Organization declared that criteria for influenza Pandemic had been met. Concern that this pandemic would rival the 1918 pandemic was high. Fortunately, that was not the case. Influenza-related disease activity peaked in late October to November 2009. By August 2010, the H1N1 influenza virus had moved into the post pandemic period. In contrast to previous seasonal influenza strains, the novel 2009 H1N1 strain preferentially affected young adults, with a clustering of severe and fatal cases in adults between the ages of 30 and 50 years. Additionally, H1N1 displayed a heightened potential for severe lung injury as well as gastrointestinal symptoms. Risk factors for severe disease included morbid obesity, pregnancy, immunosuppression, asthma (in children), chronic obstructive pulmonary disease,

neurological disorders, HIV-infection, poverty, 4

and lack of access to care.

H1N1-infected pregnant women were shown to have increased frequency of complications and

5,6 greater morbidity than the general population.All the lower respiratory infections have poor prognosis in pregnant women, because the growing uterus decreases the lung expansion. H1N1 infection causes rapid deterioration of the lung function mimicking adult respiratory disease leading to hypoxia requiring high ventilator setting revealing high résistance in the lungs.

We aim to analyze the maternal and fetal outcome in patients with H1N1 infection with respect to gestational age, mode of delivery and nutritional status, and to establish the influence of early initiation of antiviral drug (oseltamivir) on its overall outcome.

Present study is a retrospective analysis of medical records of all women (20), pregnant or




post partum, admitted to MRS hospital, Bangalore (2009-2011) who were presented with flu like symptoms and tested positive for H1N1. We documented the information about their obstetric history, length of gestation, management of current pregnancy, any complication encountered during the current pregnancy, the time of onset of labour, and mode of delivery (spontaneous, induced or cesarean section) and any post partum hemorrhage (more than 1500 ml). The data were analyzed and tabulated as frequency tables. Descriptive statistics was calculated for all study variables. Continuous variables are expressed as medians (ranges) and categorical variables as percentages. P values were calculated by using Fischers Exact test.

Twenty women of childbearing age consisting 12 cases of antenatal and 08 cases of post partum were admitted with confirmed H1N1 infection. The age group most affected was 20-30 years (Table-1). None of them were immunocompromised or belonged to positive retoviral status.

Table 1: Distribution of cases as per demographic profile and obstetric history

RESULTS

Majority of the cases (58.3%) delivered during their stay in the hospital through LSCS (Table -2). It was necessitated for the reason of maternal hypoxia leading to fetal heart abnormalities and also to decrease the mechanical restriction of the diaphragmatic movements. MTP was done in one

patient at 18 weeks as she had septicemia and renal failure. Two (16.6%) women died due to Multi Organ Dysfunction (MODS). All babies delivered through LSCS survived. Out of 08 puerperal women delivered outside, 50% got treated and discharged, whereas 50% died during treatment.

Table 2: Distribution of cases as per mode of delivery and birth weight

It was observed that all those who got admitted early to the hospital and treated within one day survived; whereas those who came late (after two days) and received treatment late stayed for a longer duration in ICU and required ventilation.

Table 3: Descriptive statistics of study variables

Early initiation of treatment was instituted in 90% of patients who had survived. The recommended timing for starting antiviral treatment is within 48 hours from the onset of symptoms. None of them had received vaccination.

IJRRMS 2012;2(1)Mamatha et al. Predictors of maternal mortality during H1N1 pandemic.


Age <20 01(5%)

20-30 18(90%)

>30 01(5%)

Gravidity Primi 06(50%)

Multi 06(50%)

Parity <1 04(50%)

<2 04(50%)

Gestational age <37 weeks 08(66.6%)

>37weeks 04(33.3%)

Other illness Diabetes Mellitus 01(5%)

Rheumatic Heart Disease 02(10%)

Anemia 04(20%)

Obstetric problems Preeclampsia 04(20%)

Chorioamnionitis 01(5%)

Mode of delivery Medical Termination of Pregnancy 01(5%)

Pre term vaginal delivery 01(5%)

Lower section cesarean section 07(58.3%)

Birth weight <2.5kg 04(50%)

>2.5kg 04(50%)

Study Variables Expired = 06 &

DAMA= 02 Survived = 12

Interval from onset of symptoms to

admission to intensive care unit 3 to 6 days 1 to 2days

Interval from onset of symptoms

to first positive test result for H1N1 2 to 6 days 1 to 3 days

Suffered secondary bacterial pneumonia 07 11

ARDS 03 0

Require invasive mechanical ventilation 08 0

Require Hemodialysis 01 0

Require Vasopressors 05 03

Initiated Antiviral drugs 06 11

Interval between onset of symptom to

antiviral treatment 0 to 5days 0 to 1 day

Duration of stay in intensive care unit 3 days; 21 days Median stay-1 day

(one patient) 4 patients stayed

for 7days

Duration of stay less than 5 days 02 04

Duration of stay ranging from 5 to10 days 05 06

Duration of stay more than 10days 01 02

20

DISCUSSIONThe data reported herein are consistent with

previous studies which demonstrated that pregnant women with influenza are at increased

7,8,9risk of serious illness and death. In addition, delayed treatment with antiviral therapy was associated with more severe illness and increased mortality, as shown previously for both seasonal influenza and 2009 influenza A(H1N1). Whereas, early treatment initiation has been associated with reduced illness duration, symptom severity, mortality, secondary complications and

10,11hospitalizations.

Present study also showed that among the hospitalized patients, early initiation of treatment (within 1 to 2 days) was associated with much better outcome compared to late treatment. These data are not consistent with other studies which suggest that some benefit might be achieved even if treatment is delayed as many as 4

12days after onset of symptoms. Puvanalingam et al., in a case series study of clinical profile of H1N1 influenza infection concluded that in those individuals with comorbid conditions, pregnancy were found to be severely affected and most common cause of death in

13patients was due to pneumonia. Ventilator requirement was associated with poor prognosis in H1N1 patients. Their observations are very much consistent with the findings of our study. We observed that while making right decision in regard to mode of delivery, one must consider the viability of fetus as well as the inherent risk of intractable maternal hypoxia. Although cesarean section allows more rapid delivery in the critically ill patients, the increased operative stress may be

14associated with higher mortality. Therefore, delivery should not be performed with the sole purpose of improving maternal oxygenation or ventilation. However, it is important that urgent delivery and neonatal resuscitation has to be available in the event of sudden maternal or fetal deterioration. Obstetric indications should always determine the mode of delivery.

Pregnant women especially in the second half of pregnancy had a disproportionately high risk of mortality due to 2009 influenza A (H1N1). Early institution of antiviral treatment with oseltamivir in pregnant women appeared to be associated with fewer admissions to an ICU and fewer deaths.

, Assistant Professor, Contact– 09900377955, E-mail: (Corresponding Author)

, Professor and Head of Department , Professor

, Lecturer , Junior resident

Department of OBG, MS Ramaiah Medical College, Bangalore- 560054, Karnataka, INDIA.

CONCLUSION

AUTHOR NOTE

Mamatha

Umadevi KSujani BKUrvashi ThukralShruti Rammohan

[email protected]



Table 4: Interval from onset of symptoms to admission to intensive care unit

REFERENCES1. LaRussa P. Pandemic novel 2009 H1N1 influenza: what have we learned. Semin Respir Crit Care Med.

2011 Aug;32(4):393-9. 2. Centers for Disease Control and Prevention (CDC). Swine influenza A (H1N1) infection in two

children-Southern California. MMWR Morb Mortal Wkly Rep. 2009;58:400-2. 3. Dawood FS, Jain S, Finelli L, Shaw MW, Lindstrom S, Garten RJ et al. Emergence of novel swine-origin

influenza a (H1N1) virus in humans. N Engl J Med. 2009;360:2605-15.

Interval Survival Death

From onset of symptoms Less than 2 days 09(90%) 01(10%), (P<0.02)

and hospitalization More than 2 days 03(30%) 07(70%)

From onset of symptoms Less than 2 days 10(100%) 00, (P<0.001)

and Admission to ICU More than 2 days 02(20%) 02(20%)

Initiation of ARV treatment Less than 2 days 08(72.7%) 03(27.3%), (P<0.36)

More than 2 days 04(44.4%) 05(55.6%)

21



4. Fraser C, Donnelly CA, Cauchemez S, Hanage WP, Van Kerkhove MD, Hollingsworth TD, et al. Pandemic potential of a strain of influenza A(H1N1): Early findings. Science. 2009;324:1557-61.

5. Fisher B, Gibbs RS. H1N1 Influenza and Pregnancy. Postgrad Obstet Gynecol. 2010;30:1-5. 6. Neuzil KM, Reed GW, Mitchel EF, Simonsen L, Griffin MR. Impact of influenza on acute

cardiopulmonary hospitalization in pregnant women. Am J Epidemiol. 1998;148(11):1094-102. 7. Jamieson DJ, Honein MA, Rasmussen SA, Williams JL, Swerdlow DL, Biggerstaff MS, et al. H1N1 2009

influenza virus infection during pregnancy in the USA. Lancet. 2009;374:451-8.8. Louie JK, Acosta M, Jamieson DJ, Honein MA. California Pandemic (H1N1) Working Group. Severe

2009 H1N1 influenza in pregnant and postpartum women in California. N Engl J Med. 2010;362(1):27–35.

9. Webb SA, Pettila V, Seppelt I, Bellomo R, Bailey M, Cooper DJ et al., ANZIC Influenza Investigators. Critical care services and 2009 H1N1 influenza in Australia and New Zealand. N Engl J Med. 2009;361(20):1925–1934.

10. Louie JK, Acosta M, Jamieson DJ, Honein MA. California Pandemic (H1N1) Working Group. Severe 2009 H1N1 influenza in pregnant and postpartum women in California. N Engl J Med. 2010;362(1):27–35.

11. Kaiser L, Wat C, Mills T, Mahoney P, Ward P, Hayden F. Impact of oseltamivir treatment on influenza-related lower respiratory tract complications and hospitalizations. Arch Intern Med. 2003;163(14):1667–1672.

12. Centers for Disease Control and Prevention. H1N1 flu (swine flu): Resources for pregnant women. http://www.cdc.gov/h1n1flu/pregnancy. Accessed: October 25, 2011.

13. Puvanalingam A, Rajendiran C, Sivasubramanian K, Ragunanthanan S, Suresh S, Gopalakrishnan S. Case series study of the clinical profile of H1N1 swine flu influenza. J Assoc Physicians India. 2011 Jan;59:14-18.

14. Kanagasabai S, Subhra S, Sameera Begaum AK, Renjhen P, Karanth LN, Kumar P. H1N1 Infection in Pregnancy, what the Obstetrician should know before the Next Pandemic. European Journal of Scientific Research. 2010;43(2):241-251.

22

An anatomical variation of unilateral higher division of sciatic nerve with bifid piriformis and its clinical implications

ABSTRACT

Hamid S, Rekha, Raina S

Sciatic nerve shows many variations in its division, especially its high division. This variation (high division of sciatic nerve) may results in sciatica, nerve injury during deep intramuscular injections in gluteal region, piriformis syndrome, and failed sciatic nerve block in anesthesia and so on. A case of high divisions of sciatic nerve on left side in a 28-year-old male cadaver was encountered during routine dissection is presented herewith, along with some proposition in available classifications. Knowledge of these variations in course of sciatic nerve may help surgeons and all those who concerns to avoid complication and plan their intervention in a better and more effective way.

sciatic nerve, piriformis muscle, tibial nerve, common peroneal nerve Key words:

INTRODUCTION

CASE REPORT

Sciatic nerve is the thickest nerve of body, arising from sacral plexus. Normally it emerges through the greater sciatic foramen, leaves pelvis and enters into gluteal region by passing below piriformis as a single nerve encompassed by a single epineural sheath. It then crosses posteriorly to the obturator internus, gamelli & quadratus

femoris muscle. It divides subsequently into two terminal nerves i.e., tibial nerve and common peroneal nerve usually at the lower part of the

1posterior compartment of thigh. But sometimes it divides high, while still in pelvis into its terminal branches that leave pelvis in a number of ways. Accordingly, they are classified into different types in relations to piriformis muscle. High division of Sciatic nerve is usually unilateral and rarely bilateral. In this case report, we discuss a unilateral high division of sciatic nerve and its clinical implications like piriformis syndrome, incomplete block of sciatic nerve during popliteal block anesthesia, sciatica, coccygodynia

2and muscle atrophy.

During routine dissection for teaching purpose, a

variation in a 28-year-old male cadaver was

observed that had unilateral left-sided high

division of sciatic nerve. Also, the piriformis was

divided into superior and inferior divisions. The

common peroneal nerve entered gluteal region by

passing between two divisions of the piriformis,

while tibial nerve emerged below lower border of

inferior piriformis (Figure 1). The level of division of

sciatic nerve was situated 44 cm above the joint line

of the knee and 8 cm above the ischial tuberosity

(hip bone). The thickness of sciatic nerve on left

side was 2.3cm (23mm) while on the normal (right)

side, it was 1.8 cm. Rest of the dissection was

normal.

IJRRMS 2012;2(1)Case Report

PF- Piriformis TN- Tibial nerve, CPN- Common Peroneal nerve


PF(UD) PF

(LD)

TN

CPN

23

DISCUSSION

During embryological development at the base of the limb bud, the nerves contributing to the lower

2limb form two plexuses (lumbar and sacral). Later, as the elements from each of these plexuses grow out into the limb, they are subdivided into dorsal and ventral components, for the dorsal and ventral

3musculatures. The sciatic nerve is formed when the large dorsal component of the sacral plexus (common peroneal nerve) and the ventral component (tibial nerve) move downward close

3together. Hence, based on their previously mentioned developmental formation, it is possible that the common peroneal and the tibial divisions of the sciatic nerve separate from each other at different levels from their origins: within pelvis, in the gluteal region, the posterior compartment of the thigh or the popliteal fossa, as observed in this case. Various studies have reported on the level of sciatic nerve division into tibial and common peroneal nerves.

The reported incidence of sciatic nerve division before its exit in the gluteal region varies from 4% to

4,5,6 20.9% across different studies. In a study to measure the level of terminal division of the sciatic nerve sheath above the knee in 30 cadaver specimens, the estimated range varied from 50 to

7180 mm above the popliteal fossa crease. Güvençer et al., observed high division of sciatic nerve in 48% of the cases with many variations; although in 52 % of the cases, the sciatic nerve

8 exited the pelvis without any division. Smoll found the prevalence of this to be 16.9% in cadavers

9and 16.2% in surgical case series. This high division results in sciatica, nerve injury during deep intramuscular injections, piriformis syndrome, failed sciatic nerve block in anesthesia and injury

10during posterior hip operations.

There are different types of high divisions of sciatic nerve within pelvis, usually bilateral. As cited by Guvencer et al., among the many known classifications, the most popular is Beaton and Anson's classification, who classified all

8 variations under 6 types. However, it needs

modification with addition of Type 7, i.e., divisions of sciatic nerve passing between and below the divided piriformis muscle. Classification by

11 Okraszewska was more suitable and we could assign Type IIB for left side as it doesn't mention divided or undivided piriformis. These classifications are necessary, especially, for they help surgeons in assessing cause and site of compression of sciatic nerve and accordingly the treatment differs. This will also alert them to be more careful during surgeries. It is usually seen that when sciatic nerve shows high branching pattern, one of the branch pierces piriformis, but divided piriformis is not usually seen. The latter is said to be a very important cause of piriformis syndrome, as common peroneal nerve passing between two divisions gets compressed

3and irritated. However studies by Machado et al.,

12 5(100 cases) and Ugrenovic et al., (200 cases) failed to find even a single divided piriformis.

13Incidentally, Jawish et al., found only one case of divided piriformis among 26 cases selected from 3550 cases complaining of sciatica. Demiryurek et al., also mentioned a case of bilaterally divided

3piriformis. Unilateral higher division of sciatic

14nerve is still rare. Diagnosis of unilateral division of piriformis is very important, as this will solve dilemma of surgeons as to why the symptoms, signs and also the effects of treatment of piriformis syndrome differ on two sides in same person. Mas

15et al., have also reported a case of bilateral high division of sciatic nerve but with tibial nerve passing under gemelleus superior, unlike the present case wherein common peroneal nerve is passing between two heads of piriformis. Combinations of these variations– high divisions of sciatic nerve on left side and unilateral divided piriformis makes this case very interesting among its types.

Knowledge of anatomical variations in gluteal region is imperative for surgeons, as this is the area of frequent surgical manipulation. A thorough knowledge of different variations will help surgeon to be careful and serve to plan various surgical

CONCLUSION

IJRRMS 2012;2(1)Hamid S et al. An anatomical variation of unilaterial higher division of sciatic nerve withbifid piriformis and its clinical implications


interventions and management in this region. This also encourage radiologist to repeat MRI on other side, keeping in mind that there can be differences on two sides. This knowledge will also play a vital role in preventing deep intramuscular injection hazards in gluteal region.

, Lecturer, Contact- 9419506978, Email: [email protected]

(Corresponding Author)

, P.G. Scholar , Prof.& HOD

Department of Anatomy, Govt. Medical College, Jammu, Jammu and Kashmir, India.

AUTHOR NOTE

Sajad Hamid

RekhaSunanda Raina

REFERENCES

1. Williams PL, Bannister LH, Berry MM, Collins P, Dyson M, Dussek JE, Ferguson MWJ. Gray's thAnatomy. 38 edn. Churchill Livingstone, Edinburgh. 1995;p 1284.

2. Babinski MA, Machado FA, Costa WS. A rare variation in the high division of the sciatic nerve surrounding the superior gemellus muscle. Eur J Morphol. 2003;41:41-2.

3. Demiryurek D, Bayramoglu A, Erbil M, Aldur MM, Mustafa ES. Bilateral divided piriformis muscle together with the high division of the sciatic nerve. Gazi Med J. 2002;13:41-4.

4. Pokorný D, Jahoda D, Veigl D, Pinskerová V, Sosna A. Topographic variations of the relationship of the sciatic nerve and the piriformis muscle and its relevance to palsy after total hip arthroplasty. Surg Radiol Anat. 2006;28:88-91.

5. Ugrenoviæ S, Jovanoviæ I, Krstiæ V, et al. The level of the sciatic nerve division and its relations to the piriform muscle. Vojnosanit Pregl. 2005;62:45-9.

6. Gabrielli C, Olave E, Mandiola E, et al. Inferior gluteal nerve course associated to the high division of the sciatic nerve. Rev Chil Anat. 1997;15:79-83.

7. Saleh HA, El-fark MM, Abdel-Hamid GA. Anatomical variation of sciatic nerve division in the popliteal fossa and its implication in popliteal nerve block. Folia Morphol. 2009; 68(4):256-9.

8. Güvençer M, Iyem C, Akyer P, Tetik S, Naderi S. Variations in the high division of the sciatic nerve and relationship between the sciatic nerve and the piriformis. Turk Neurosurg. 2009;19:139-44.

9. Smoll NR. Variations of the piriformis and sciatic nerve with clinical consequence: a review. Clin Anat. 2010;23(1): 8-17.

10. Gonzalez P, Pepper M, Sullivan W, Akuthota V. Confirmation of needle placement within the piriformis of a cadaveric specimen using anatomic landmarks and fluoroscopic guidance. Pain Physician. 2008;11(3): 327-31.

11. Okraszewska E, Migdalski L, Jedrzejewski KS, Bolanowski W. Sciatic nerve variations in some studies on the Polish population and its statistical significance. Folia Morphol (Warsz). 2002;61(4):277-82.

12. Machado FA, Babinski MA, Brasil FB, Favorito LA, Abidu-Figueiredo M, Costa MG. Anatomical variations between sciatic nerve and piriform muscle during fetal period in human. Int J Morphol. 2003;21:29-35.

13. Jawish RM, Assoum HA, Khamis CF. Anatomical, clinical and electrical observations in piriformis syndrome. J Orthop Surg Res. 2010;5:3.

14. Arifoglu Y, Surucu HS, Sargon MF, Tanyeli E, Yazar F. Double superior gemellus together with double piriformis and high division of sciatic nerve. Surg Radiol Anat. 1997;19:407-408.

15. Mas N, Ozeksi P, Ozdemir B, Kapakin S, Sargon MF, Celik HH, et al. A case of bilateral high division of the sciatic nerves, together with a unilateral unusual course of the tibial nerve. Neuroanatomy. 2003;2:13–15.

IJRRMS 2012;2(1)Hamid S et al. An anatomical variation of unilaterial higher division of sciatic nerve withbifid piriformis and its clinical implications


Recurrent cold abscess of the chest wall in a young immunocompetent person

ABSTRACT

Gayathri Devi DR, Narayanaswamy YV, Areena H

Tuberculous abscess in chest wall is rare. Diagnosis and treatment of chest wall tuberculosis is difficult as well

as contentious in regard to recommendation of the appropriate therapeutic strategy. We present a case of

recurrent chest wall abscess due to Mycobacterium tuberculosis without any evidence of pulmonary/skeletal

involvement in a young immunocompetent person. He was successfully treated by adopting combination of

surgical and anti-tubercular treatment.

extra pulmonary tuberculosis, recurrent chest wall tubercular abscess, cold abscessKeywords:

INTRODUCTION

CASE REPORT

Cold abscess of the chest wall is a rare extra pulmonary tuberculous site. It is usually seen in cases of severe disseminated form of tuberculosis. Chest wall tuberculosis (CWTB) constitutes 1-5 % of all cases of musculoskeletal tuberculosis, which in

1,2,3,4,5turn represents 1-2 % of all tuberculosis cases. Diagnosis of CWTB poses complexity for the reason of it's clinical presentation, which may resemble a

6,7 pyogenic abscess or a chest wall tumor. In addition, CWTB often fails to respond to antitubercular chemotherapy. A controversy exists regarding the appropriate therapeutic strategy. A case of primary tuberculosis of chest wall without any evidence of pulmonary/skeletal tuberculosis in a young immuno-competent patient is presented herewith.

A 20 year old man presented to the out patients department with an ulcer and swelling over lateral part of left chest wall since two months. Cough with expectoration and loss of weight were evident since one week. There was no history of fever or loss of appetite.Past history revealed that he had swelling in right mandibular region and right upper neck below the mandible for which incision and drainage was done two years back. He also had a mass over right chest wall, which was removed and subjected to

histopathological examination which suggested it to be a tubercular lesion. However no microbiological investigation was done at that time. He was prescribed anti-tubercular drugs, which he discontinued on his discretion after taking for one and half months citing no reason.Naked eye examination revealed a solitary, oval and non-tender growth over left side chest wall measuring about 3 x 2 cm, with smooth and ill defined diffused borders, and a normal overlying skin. On the right side of chest wall, at fourth intercostal space, an oval ulcer was seen with an undermined edge surrounded by a blue zone which was not fixed to the underlying structures (Fig 1). Necessary investigations were done (table-1).


Figure 1: A solitary oval swelling on the left side of the chest wall and an ulcer on the right side


Incision and drainage of the abscess was done under aseptic precautions. About 0.5 - 1 ml of thick yellow pus having no foul smell was present which were sent for cu l ture and sens i t iv i ty. H i sto p ath o lo g ica l examin at io n s h owed tuberculous inflammation (Fig 2).

Figure 2: HPE Showing tuberculous inflammation.

Gram stain showed few pus cells with no organisms. No acid fast bacilli were seen in Ziehl Neelsen stain. Aerobic or anaerobic bacteria were not isolated on routine culture. Growth was seen after three weeks on Lowenstein Jensen media. The isolate was sent for confirmation at Tuberculosis Research Center (TRC), Chennai which reported it as Mycobacterium tuberculosis and was sensitive to streptomycin, isoniazid, rifampicin, ethambutol, kanamycin, ethionamide and ofloxacin. The patient was started with direct

observation treatment (DOTS) category-1 (Isoniazid, Rifampicin, Pyrazinamide and Ethambutol) for 2 months followed by (Isoniazid and Rifampicin) for 4 months along with surgical debridement. On follow up, after 5 months there was no recurrence of swelling or abscess.

Chest wall abscess caused by Mycobacterium tuberculosis are rare and still a diagnostic and

8,9therapeutic challenge. TB abscess of the chest is usually related to pleuritis caused by tuberculosis. It may be secondary to haematogenous or lymphatic dissemination or from direct extension from the underlying pleura of the lung. In the present case there is no involvement of either lungs or skeletal structure. However, the primary infection could have started with local manifestations of cervical lymph node infection as suggested by the past history. Putting the controversy at rest, it is therefore, the authors wish to bring to the notice of clinician that such cases can be treated successfully with combination of surgical debridement and DOTS category-1 regime.

, Professor, Contact- 9449986838; Email id: [email protected], (Corresponding Author)Department of Microbiology, M.S.Ramaiah Medical College, M.S RIT Post, Bangalore-560054

, Associate Professor, Department of General Surgery, M.S.Ramaiah Medical Teaching Hospital Bangolore-54.

(M.D.),Tutor, Department of Microbiology, M.S.Ramaiah Medical College, Bangolore-54.

DISCUSSION

AUTHOR NOTE

Gayathri Devi D.R.

Narayanaswamy Y.V

Areena H.

REFERENCES1. Hulnick DH, Naidich DP, McCauley DI. Pleural tuberculosis evaluated by computed tomography.

Radiology. 1983;149(3):759-65.2. Gayler BW, Donner MW. Radiographic changes of the ribs. Am J Med Sci. 1967;253(5):586-619.3. Eid A, Chaudry N, el-Ghoroury M, Hawasli A, Salot WL, Khatib R. Multifocal musculo skeletal

cystic tuberculosis without systemic manifestations. Scand J Infect Dis. 1994;26(6):761-4.

IJRRMS 2012;2(1)Gayathri Devi DR etal. Recurrent cold abscess of the chest wall in a young immunocompetent person

Table -1: Investigations


Hb 11.8g/dl

TLC 12,300 cells/µl

Neutrophils 85%

Lymphocytes 11%

Eosinophils 3%

Monocytes 1 %

ESR 90 mm/hr

HIV I and II Negative

HbsAg Negative

Chest x-ray Normal

27

4. Garcia S, Combalia A, Segur JM, Ramon R. Unusual locations of osteoarticular tuberculosis. Arch Orthop Trauma Surg. 1997;116(6-7):321-3.

5. Chang DS, Rafii M, McGuinness G, Jagirdar JS. Primary multifocal tuberculous osteomylitis with involvement of the ribs. Skeletal Radiol. 1998;27(11):641-5.

6. Paik HC, Chung KY, Kang JH, Maeng DH. Surgical treatment of tuberculous cold abscess of the chest wall. Yonsei Med J. 2002;43(3):309-14.

7. Hsu HS, Wang LS, Wu YC, Fahn HJ, Huang MH. Management of primary chest wall tuberculosis. Scand J Thorac Cardiovascu Surg. 1995;29(3):119-23.

8. Sakuraba M, Sagara Y, Komatsu H. Surgical treatment of tuberculous abscess in the chest wall. Ann Thorac Surg. 2005;79(3):964-96.

9. Gaude GS, Reyas AK. Tuberculosis of the chest wall without pulmonary involvement. Lung India. 2008;25(3):135-137.

IJRRMS 2012;2(1)Gayathri Devi DR etal. Recurrent cold abscess of the chest wall in a young immunocompetent person


Beneficial role of amantadine in catatonic schizophrenia: A case report

ABSTRACT

Srivastava M

Novel pharmacological agents are being used alternatively to manage schizophrenia. However, a significant number of patients do not achieve full remission and have recurrent episodes. One hypothesis illustrates that as a result of pathological processes in the brain, excess glutamate is produced that leads to sequence of events resulting in damage of neurons. NMDA receptor antagonist is proving to be a viable option. It plays a role in reversing the whole sequence. A case report is being presented to highlight its efficacy in treatment of catatonic schizophrenia.

: amantadine, catatonia, NMDA receptors, receptor antagonistKeywords

INTRODUCTION

The use of typical and atypical antipsychotics has o f fe re d m a r ke d i m p ro ve m e nt i n m a ny schizophrenic patients. However, a significant number of patients do not achieve full remission

1and have recurrent episodes. Adjunctive therapies have emerged in a big way to tackle the magnitude of schizophrenia. NMDA (N-methyl d-aspartate)

2receptors have also been targeted for treatment.

Catatonic schizophrenia forms a subtype of schizophrenia, which is often difficult to manage. It has been reported that the use of amantadine in patients with catatonia who do not respond to

2 lorazepam is encouraging. The NMDA receptor antagonism is considered as the mode of action. Memantine, another NMDA antagonist has also been shown to be beneficial in catatonic

1,3 schizophrenia. Documentation on the beneficial

2results of amantadine is very few. To highlight its beneficial role in catatonia a case report is being presented.

CASE HISTORY

A 24 year old married woman presented to outpatient psychiatry services with mutism, staring, puckering of mouth and ambivalence. She was diagnosed to be case of catatonia and was

4rated on Bush catatonia scale, her score was 16. She responded well to IV lorazepam 2mg, within half an hour. She started talking adequately to the examiner and smiled. The family refused for admission; hence she was prescribed lorazepam 6mg/day in divided doses, and sent home.

Two days later she reported again with recurrence of symptoms and refused to eat and drink, this time the Bush catatonia score was escalated to 18. She was admitted, all necessary investigations like CT scan, EEG, regular biochemical parameters and thyroid estimation was done and found to be within normal limits. She was switched on to 8 mg/day I.V. lorazepam, in four divided doses. The patient showed no change in symptoms rather, after 2 days became excessively sedated. Lorazepam was reduced to 6 mg/day, and resperidone in the dose of 4mg/day was added. One week trial of medication showed no change in the symptoms. ECT was prescribed and four ECTs were given on alternate days, however, no change in the catatonia rating scale score was observed. After 10 days, the patient was put on lorazepam 3mg/day in divided doses, and amantadine in the dose of 100 mg, twice daily was added. Next day the patient started taking oral feeds; Ryle's tube

thcould be removed on the 4 day, the Bush catatonia rating score decreased to 6 in a week's time. One week later the amantadine was increased to 150mg, twice daily. The patient was discharged. Follow ups were regular and the patient integrated well into the family. Six weeks later lorazepam was tapered and withdrawn. She became a productive member of her family within a year and is maintaining well on 200mg/day of amantadine.

Amantadine has NMDA receptor antagonist

DISCUSSION



activity, in addition to its dopamine agonist 2 activity. It is approved for use in Parkinson's

2 disease and extra pyramidal diseases. Its potential efficacy in catatonia may be due to blockade of hyperglutaminergic excitotoxicity activity in

2,3neurons. It is hypothesized that as a result of the pathological process in the brain, excess glutamate

2 is produced. Increase in glutamate leads to hyperexcitation of the respective receptors which indirectly allow the calcium channel to remain open. Calcium influx leads to free radical formation

2,3and therefore causes neuronal damage. This whole process is reversed by amantadine for a

1 longer duration. More researches are required to understand the efficacy of NMDA receptor antagonists as safe treatment options for patients of catatonia.

, Contact- 9336910619, Email: (Corresponding Author)Department of psychiatry, Institute of Medical Sciences, Banaras Hindu University, Varanasi-5

AUTHOR NOTE

Mona [email protected]

REFERENCES

1. Carroll BT, Thomas C, Jayanti K. Amantadine and memantine in catatonic schizophrenia. Ann Clin Psychiatry. 2006 Apr-Jun;18(2):133-4.

2. Goff DC, Coyle JT. The emerging role of glutamate in the pathophysiology and treatment of schizophrenia. Am J Psychiatry. 2001;158(9):1376-77.

3. Northoff G. What catatonia can tell us about “top-down modulation”: a neuropsychiatric hypothesis. Behave Brain Sci. 2002;25(5):555-77.

4. Bush G, Fink M, Petrides G, Dowling F, Francis A. Catatonia. I. Rating scale and standardized examination. Acta Psychiatr Scand. 1996 Feb;93(2):129-36.

IJRRMS 2012;2(1)Srivastava M. Beneficial role of amantadine in catatonic schizophrenia: A case report


Angiofibroma in an elderly – A Case Report

ABSTRACT

Panigrahi R

Nasopharyngeal angiofibroma is a histologically benign but locally aggressive vascular tumor that grows in the

back of the nasal cavity. It most commonly affects adolescent males. Patients with nasopharyngeal

angiofibroma usually present with one-sided nasal obstruction and recurrent bleeding. A case of angiofibroma

is presented herewith in a 52 years old man with history of bilateral nasal obstruction and blood stained nasal

discharge but no epistaxis as expected in angiofibroma. He was treated successfully with transmaxillary

approach.

angiofibroma, epistaxis, nasal obstruction, blood stained discharge, transmaxillary Keywords:

INTRODUCTION

CASE REPORT

Nasopharyngeal angiofibroma is highly vascular,

benign, yet locally destructive neoplasm, first th 1recognized by Hippocrates in 4 Century BC. In

1847, Chelius described fibrous nasal polyp 2growing at the time of puberty. Almost 100 years

later, the term “nasopharyngeal angiofibroma” 3was used initially to describe this rare neoplasm.

Alternative titles such as juvenile angiofibroma,

nasopharyngeal fibroma and bleeding fibroma of

adolescence are also used. These constitute 0.5%

of all neoplasms of head and neck. The incidence

ranges from 1:5000 to 1:60,000 in otolaryngologic 4

patients. It occurs almost exclusively in

aldolescent males with an average age of onset

being 14 years.

As this tumor is almost exclusively found in

adolescent boys, there has always been much

speculation and indirect evidence that sex-

hormone receptors play some role in its

development. Recent immunocytological

techniques have been used to show that

androgen receptors are present in at least 75%

of tumors, these receptors are present in both 5

vascular and stromal elements.

A 52 year old man presented with bilateral

nasal obstruction with history of recurrent

episodes of blood stained nasal discharge since

3 years, but without any profuse bleeding.

Anterior rhinoscopy revealed presence of a fleshy

mass in right nasal cavity almost completely

blocking view of choana. Posterior rhinoscopy

revealed large f leshy mass occupying

nasopharynx and right choana. There were no

other abnormalities in pharynx, larynx and ears.

Plain skiagram of the para nasal sinuses (PNS)

revealed soft tissue shadow in right nasal cavity.

CT scan of PNS (both coronal and axial sections)

revealed a large soft tissue mass occupying right

nasal cavity, nasopharynx, maxillary, sphenoid and

ethmoid sinuses. No intracranial extension of the

tumor was noticed. A punch biopsy using Zero

degree endoscope was taken. Mild bleeding

followed, which was controlled by nasal packing

for 24 hours. Histopathology of the tumor mass

confirmed the diagnosis of nasophayngeal

angiofibroma.

The tumor was accessed by transmaxillary

approach using Weber - Fergusson incision under

general anaesthesia. Anterolateral surface of

maxilla and lateral wall of nose (inferior

turbinate) was removed. It offered excellent

exposure to all parts of the tumor thereby

making subsequent mobilisation of mass easy

and with less blood loss. The base was



attached to postero-superior part of lateral

nasal wall which was dissected out with blunt

dissection from all around and mass was

removed in toto. Bleeding was controlled by post

nasal packing. Post operative period was

uneventful and patient was discharged with an

advice for regular follow-up.

Nasopharyngeal angiofibroma is a benign but a

highly vascular tumor with potential for

extrapharyngeal and intracranial extensions. In

spite of being a highly vascular tumour, there was

no episode of spontaneous epistaxis in this

particular case. Similar finding was reported by 6

Singh et al. Differing the views expressed in the

available literatures, this case belongs to an elderly

man of age 52 years.

DISCUSSION

The present controversy regarding therapy has

two proponents, those favouring sugery and those

favouring radiation. As quoted by Briant et al.,

1970, “Pressman stated that- of all the methods of 7treatment, surgery alone has proven effective". Of

the different techniques available, the

transmaxillary approach offers excellent exposure

making subsequent mobilisation easy, thus,

reducing blood loss and hospitalization to

encouragingly low levels. With this approach,

there are less chances of leaving residual mass and

follow up is easy. Improved results can be

attributed to advances in surgical technique,

coupled with advent of CT PNS with contrast.

, Assistant Professor,

Contact – 09437113636 (Corresponding author)Department of E.N.T, HI TECH Medical College & Hospital, Bhubaneswar, Odisha.

AUTHOR NOTE

Rajlaxmi Panigrahi

REFERENCES

1. Gill G, Rice DH, Ritter FN, Kindt G, Russo HR. Intracranial and extracranial nasopharyngeal angiofibroma.

A surgical approach. Arch Otolaryngol. 1976 Jun;102(6):371-3.

2. Waldman SR, Levine HL, Astor F, Wood BG, Weinstein M, Tucker HM. Surgical experience with

nasopharyngeal angiofibroma. Arch Otolaryngol. 1981 Nov;107(11):677-82.

3. Apostal JV, Frazell EL. Juvenile nasophayngeal angiofibroma: clinical study. Cancer. 1965;18:869-878.

4. De Vincentiis G, Pinelli V. Rhinopharyngeal angiofibroma in the pediatric age group. Clinical-statistical

contribution. Int J Pediatr Otorhinolaryngol. 1980 Jun;2(2):99-122.

5. Hwang HC, Mills SE, Patterson K, Gown AM. Expression of androgen receptors in nasopharyngeal

angiofibroma: an immunohistochemical study of 24 cases. Mod Pathol. 1998 Nov;11(11):1122-6.

6. Singh RK, Nigam AK. Juvenile angiofiroma without epistaxis. Indian journal of Otolaryngology and head

and neck surgery. 1977;29(1):19.

IJRRMS 2012;2(1)Panigrahi R. Angiofibroma in an elderly - A Case report


Cardiac tamponade - An unusual presentation of Pulmonary Adenocarcinoma

ABSTRACT

Pathan ZA, Chaudappa JS, Parshawnath HA, Lakshmi DKB

Cardiac tamponade as the first presenting symptom of metastatic malignancy is very rare. A 45 year male presented with dyspnea and productive cough. Chest X-ray, echocardiogram and ECG showed pericardial effusion with cardiac tamponade. Pericardial fluid cytology revealed metastatic adenocarcinoma probably from lung. CT scan of chest showed collapsed lower lobe of left lung with a 2.4x2cm non enhancing hypodense lesion, along with enlarged mediastinal lymph nodes confirming the cytological diagnosis of pulmonary carcinoma.

ardiac tamponade, cytology, pulmonary adenocarcinomaKeywords: c

INTRODUCTION

CASE HISTORY

Cardiac tamponade a life threatening emergency, is rarely the first presenting

1,2,3 symptom in malignancies. Pericardial

involvement, with subsequent effusion and cardiac tamponade, may be a metastatic complication of advanced cancers such as carcinoma lung and breast, leukemia and lymphomas. These neoplastic effusions are

1 usually asymptomatic. There are very few case

reports of cardiac tamponade as initial manifestation of pulmonary adenocarcinoma. Here we report a case of pulmonary adenocarc inoma present ing as cardiac tamponade.

A 42 year male, cotton mill worker, presented with history of breathlessness and productive cough of 8 months duration. The symptoms aggravated in the last 8 days. Examination revealed tachycardia, systolic hypotension, pulsus paradoxus of 20 mm Hg, raised juglar venous pressure (JVP), crepitations and rhonchi more on right side, and reduced air entry on left lung fields. Cardiac sounds were reduced in intensity.

Investigations: Chest X-ray showed cardiomegaly (figure-1a). An electrocardiogram (ECG) showed low voltage complexes; and echocardiography showed large pericardial effusion with right atrial and ventricular collapse and trivial mitral valve regurgitation. Left ventricular systolic function was adequate. Based on the clinical and echocardiography findings the patient was diagnosed to have cardiac tamponade. Pericardiocentesis was performed and 1000ml of hemorrhagic fluid aspirated. The cytological examination of the fluid showed neoplastic epithelial cells and clusters of reactive mesothelial cells in a hemorrhagic background. The neoplastic cells were arranged in cohesive three dimensional clusters with smooth borders, papillae and acinar formations. These cells were polygonal having moderate amount of homogenous cytoplasm with cytoplasmic vacuolations. The nuclei were round to oval, medium to large in size, with fine to coarsely granular chromatin and variably conspicuous nucleoli [figure-2a, 2b]. The neoplastic cells showed PAS positivity (figure-2c). Based on these features diagnosis of metastatic adenocarcinoma, probably arising from the lung was offered. Later patient was investigated for site of primary malignancy. Ultrasonography of



abdomen was normal; there were no enlarged lymph nodes or mass lesion in the abdomen. CT scan of chest revealed large pericardial effusion, moderate left pleural effusion and partial collapse of left lower lobe of lung with a 2.4x2cm non enhancing hypodense lesion within it. Mediastinal lymph nodes were enlarged. The features were suggestive of pulmonary carcinoma.

Figure2: (a) & (b) showing the tumour cells in cluster and papillae with abundant vacuolated cytoplasm, eccentric nucleus (H&E x400 & Pap x400), (c) cells showing PAS positivity (PAS stain x400)

DISCUSSION

The vast majority of tumours affecting heart are of metastatic rather than of primary

4origin. Approximately 10% of the patients with terminal malignancy have cardiac involvement;

2,5out of these 8.5% have pericardial involvement. Neoplastic pericarditis can present as acute p e r i c a r d i t i s , p e r i c a r d i a l e f f u s i o n , effusive-constrictive pericarditis or cardiac tamponade. Neoplastic effusions are usually

asymptomatic. Cardiac tamponade as the initial 6

manifestation of malignancy is very rare. Most often the underlying malignancy is pulmonary carcinoma (37%), breast carcinoma (22%), leukaemia and lymphoma (17%), sarcomas

1,6 (3.5%) and melanoma (3%). Isolated cases of

cardiac tamponade occurring as an initial manifestation of malignant tumours of the thymus, kidneys, stomach, thyroid and

1 oesophagus have been reported. Non-tumour

related causes like hypoalbuminemia from cachexia, uraemia, idiopathic, infectious pericarditis and radiation or chemotherapy related pericarditis should be considered in the

1,6differential diagnosis.

Pericardial involvement as a result of metastatic lung diseases is usually asymptomatic. Tumour implantation on serosal surfaces leads to augmented fluid production and exudation. In addition, epicardial lymphatic and venous obstruction by tumour cells causes further increase in hydrostatic pressure and

6hence fluid accumulation.

The most common symptoms reported in patients with cardiac tamponade due to malignancy were dyspnoea (79%), cough (47%), chest pain (26%), orthopnea (26%) and dysphasia (18%). The physical signs commonly encountered were tachycardia (50%) and signs of systemic venous congestion, pulsus paradoxus and pericardial rub were present in 30% and 12%

1, 6cases respectively.

Right atrial or ventricular collapse on echocardiography, low voltage ST segment changes and electrical alternans on ECG suggest

1cardiac tamponade.

Ben-Horin S et al., studied 173 cases of pericardial effusions of which 58 cases were of neoplastic aetiology. Among these, 45 cases had known malignancy. Pericardial disease was the

7 presenting feature in 13 cases. Petcu PD et al.,

studied 21 cases of pericardial effusion with cardiac tamponade, among which four cases were of neoplastic etiology. Out of these four

Figure 1: (a) Chest X-ray showing cardiomegaly, (b) CT scan chest showing pericardial effusion and a 2.4x2cm non enhancing hypodense lesion within the collapsed lower lobe of left lung

IJRRMS 2012;2(1)Pathan ZA et al. Cardiac tamponade - An unusual presentation of Pulmonary Adenocarcinoma


cases one case presented as cardiac tamponade 8

as the initial manifestation of malignancy.

The sensitivity of detecting malignant cells in the pericardial fluid has been variable in different studies, ranging from 54% to more than 90%. These differences may be due partly to the amount of fluid examined, number of pericardiocentesis and expertise of the

7examiner.

Sometimes it becomes difficult to differentiate between reactive mesothelial cells and malignant cells. Very rarely the cytological examination may establish the exact origin of malignant cells from

8 the pericardial fluid. In the present case

cytological examination with special stain helped to establish the primary site of malignancy, which was later detected by the CT scan.

Cardiac tamponade implicates advanced disease. The median survival of these patients is reported to be between 7 days to 12 months following initial

1diagnosis.

AUTHOR NOTE

Pathan Zaheer Abbas Ali Khan,

Shakapur Chaudappa J

Parshawnath HALakshmi Devi

Contact- +91 9449973442,E-mail: [email protected](Corresponding Author)Associate Professor, Dept of Pathology, SDM College of Medical Sciences and Hospital, Sattur, Dharwad.

, Consultant CardiologistSDM Narayana Hrudayalaya Heart center,

, Professor, Tutor

Dept of Pathology, SDM College of Medical Sciences and Hospital, Sattur, Dharwad.

REFERENCES

1. Sheikh M, Kanjwal K. Cardiac tamponade as initial manifestation of lung carcinoma. PhysiciansAcademy. 2009;3(12):130-32.

2. Vachhani JH, Jessalpara K, Goswamy B, Santwani PM. Malignant pericardial effusion andcutaneous metastasis – An unusual presentation of adenocarcinoma of lung. J cytol.2007;24:199-200.

3. Ballardini P, Margutti G, Zangirolami A, Tampieri M, Incasa E, Gamberini S et al. Cardiac tamponade as unusual presentation of underlying unrecognized cancer. Am J Emerg Med.2007;25(6):737 e5-e6.

4. Lysitsas DN, Banerjee P, Shiu MF. Cardiac tamponade because of left atrium direct invasion by a large cell neuroendocrine metastatic carcinoma of the lung. Eur J Echocardiogr. 2008;9(3):428–29.

5. Petersen EE, Shamshirsaz AA, Brennan TM, Demetroulis EM, Goodheart EJ. Malignant pericardial effusion with cardiac tamponade in ovarian adenocarcinoma. Arch Gynecol Obstet.2009;280(4):675–78.

6. Letonja M, Debeljak A. Cardiac tamponade as the initial manifestation of pulmonary adenocarcinoma. Radiol Oncol. 2007;41(4):161-65.

7. Ben-horin S, Bank I, Guetta V, Livneh A. Large symptomatic pericardial effusion as the presentation of unrecognized Cancer, a study in 173 consecutive patients undergoing Pericardiocentesis. Medicine(Baltimore). 2006;85(1):49-53.

8. Petcu DP, Petcu C, Popescu CF, Bataiosu C, Alexandru D. Clinical and cytological correlations in pericardial effusions with cardiac tamponade. Rom J Morphol Embryol. 2009; 50(2):251–56.

IJRRMS 2012;2(1)Pathan ZA et al. Cardiac tamponade - An unusual presentation of Pulmonary Adenocarcinoma

CONCLUSION

Cardiac tamponade is a life threatening

emergency. It is an uncommon complication and

a rare initial presenting feature of pulmonary

malignancy. The cytological examination of the

pericardial fluid may help to establish the origin

of primary malignancy and confirm the diagnosis

of malignant cardiac tamponade


Primary squamous cell carcinoma of breast

Kaur P, Chauhan A, Singh G, Kataria SP

A 49 years old premenopausal woman presented with 4x3 cm size, hard, mobile lump in upper inner quadrant of right breast. There was no skin and chest wall involvement. Opposite breast was normal. Axillary lymph nodes were not palpable. There was no history of carcinoma in other parts of body; family and medical history was insignificant.

Mediolateral and craniocaudal mammograms of the right breast demonstrated a spherical lesion with ill-defined margins. The skin-nipple-areola complex was not involved and micro calcification was not seen. Histopathological examination of specimen revealed squamous cell carcinoma (SCC)- Fig 1. Immunohistochemistry showed estrogen and progesterone receptors status negative with positive for cytokeratin.

Figure 1- Photomicrograph showing neoplastic squamous cells infiltrating the breast tissue.

On confirmation of diagnosis of primary SCC of breast, the patient underwent radical surgery in form of modified radical mastectomy. Adjuvant treatment was given in form of six courses of paclitaxel and carboplatin based chemotherapy.

Primary SCC of the breast account less than 0.074% of all primary invasive carcinoma of

1breast. Pure SCC of breast may originate from epidermis, the nipple or the malignant

2 transformation of a deep seated cyst. This multimodality management is recommended at

1the same stage of adenocarcinoma.

, Assistant Professor, Contact- 08901387991,Emai l : drparamj i tkaur@redi f fmai l . com (Corresponding Author) Department of Radiotherapy, Regional Cancer Centre, Pt. B D Sharma PGIMS, Rohtak.

, Senior Professor and Unit Head, Assistant Professor

Department of Radiotherapy, Regional Cancer Centre. Pt. B D Sharma PGIMS, Rohtak

, ProfessorDepartment of Pathology, Pt. B D Sharma, PGIMS, Rohtak, Haryana.

AUTHOR NOTE

Paramjeet Kaur

Ashok ChauhanGajender Singh

Sant P Kataria

REFERENCES

1. Weigel RJ, Ikeda DM, Nowels KW. Primary squamous cell carcinoma of the breast. South Med J. 1996;89:511-5.

2. Parmesh CS, Chaturvedi P, Saklani AP, Badwe RA. Squamous cell carcinoma of breast. J Postgrad Med. 2001;47:270-1.

IJRRMS 2012;2(1)Letter to the Editor Kaur P et al. Primary squamous cell carcinoma of breast


The Nobel Prize in Physiology or Medicine 1902 was awarded to Ronald Ross "for his work on malaria, by which he has

shown how it enters the organism and thereby has laid the foundation for successful research on this disease and

methods of combating it".

Sir Ronald Ross (13 May 1857 – 16 September 1932) was a British doctor, born in India. His grandfather, Lieutenant

Colonel Hugh Ross, had malaria, and as a boy, he resolved to find a cure for the disease. At the age of eight, he was sent to

England for his education. He commenced the study of medicine in London in 1875. He passed his final examination in

1880 and joined the Indian Medical Service in 1881. first posting was at Madras. Ross married Rosa Bessie Bloxam in

1889. They had two sons, Ronald and Charles, and two daughters, Dorothy and Sylvia. His wife died in 1931.

Ross studied malaria between 1882 and 1899. He worked on malaria at the Presidency General Hospital, Calcutta. Ross

built a bungalow with a laboratory at Mahanad village, where he used to stay from time to time collecting mosquitoes in

Mahanad and adjoining villages and conducting research. In 1883, Ross was posted as the Acting Garrison Surgeon at

Bangalore where he noticed the possibility of controlling mosquitoes by controlling their access to water. In 1897, Ross

was posted in Ooty and fell ill with malaria. After this he was transferred to Secunderabad. He discovered the presence

of the malarial parasite within a specific species of mosquito, the Anopheles.

In 1899, Ross went back to Britain and joined Liverpool School of Tropical Medicine as a professor of tropical medicine.

In 1901 Ross was elected a Fellow of the Royal College of Surgeons and also a Fellow of the Royal Society, of which he

became Vice-President from 1911 to 1913. In 1902 he was appointed a Companion of the Most Honourable Order of

Bath by King Edward VII, and discovered how malaria was transmitted. In 1911 he was elevated to the rank of Knight

Commander of the same Order.

The Ross Institute and Hospital for Tropical Diseases was founded and in 1926. The hospital was opened by the then

Prince of Wales, the future Edward VII. It was later incorporated into the London School of Hygiene & Tropical Medicine.

Ross survived until a year later when he died after a long illness and asthma attack in 1932.In India Ross is remembered

with great respect. Because of his relentless work on malaria, the deadly epidemic which used to claim thousands of

lives every year could be successfully controlled. There are roads named after him in many Indian towns and cities. In

Calcutta the road linking Presidency General Hospital with Kidderpore Road has been renamed after him as Sir Ronald

Ross Sarani. The regional infectious disease hospital at Hyderabad was named after him as Sir Ronald Ross Institute of

Tropical and Communicable Diseases. The building where he worked and actually discovered the malarial parasite,

located in Secunderabad near the old Begumpet airport, is a heritage site and the road leading up to the building is

named Sir Ronald Ross Road. In Ludhiana, Christian Medical College has named its Hostel as "Ross Hostel". The young

doctors often call themselves "Rossians".

Nobel Prize winners in Physiology or Medicine- 1902

IJRRMS 2012;2(1)


Sir Ronald Ross

37

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11 45

IJRRMS 2012;2(1)


http://www.hindawi.com/journals/aps/2012/789713/

CONTENTS

IJRRMS 2012;2(1)


VOLUME-2, ISSUE-1

EditorialWhat ails the Medical Research Publications in India

Original Research Papers1. Experimental animal studies on analgesic and anti-nociceptive activity of Allium sativum

(Garlic) powder. Jayanthi MK, Jyoti MB 1

2. Effect of Savitri Pranayama practice on peak expiratory flow rate, maximum voluntary

ventilation and breath holding time. Mamatha SD, Gorkal AR 7

3. Chronic cor-pulmonale in adults: An experience from a tertiary teaching hospital in

Dharwad. Sindhur JC,Rajoor UG 12

4. Maternal Mortality Rate and its causes– Changing trends in Kolkata, India. Chakraborty S,

Sebanti G 16

5. Predictors of maternal mortality during H1N1 pandemic. Mamatha, Umadevi K,

Sujani BK, Urvashi T, Shruti R 19

Case Reports6. An anatomical variation of unilateral higher division of sciatic nerve with bifid piriformis

And its clinical implications. Hamid S, Rekha, Raina S 237. Recurrent cold abscess of the chest wall in a young immunocompetent person. Gayathri Devi DR,

Narayanaswamy YV, Areena H 26

8. Beneficial role of amantadine in catatonic schizophrenia: A case report. Srivastava M 29

9. Angiofibroma in an elderly – A Case Report. Panigrahi R 31

10. Cardiac tamponade - An unusual presentation of Pulmonary Adenocarcinoma.

Pathan ZA, Chaudappa JS, Parshawnath HA, Lakshmi DKB 33

Letter to Editor11. Primary squamous cell carcinoma of breast. Kaur P, Chauhan A, Singh G, Kataria SP 36

Nobel Laureates in Medicine or PhysiologySupplements 37

Manuscript submission guidelines 38

Subscription details

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