Dusta vruna#shl02 udp

EFFICACY OF JATYADI TAILA IN THE

MANAGEMENT OF DUSHTA VRANA

Dissertation submitted to the Rajiv Gandhi University of Health Sciences,

Bangalore,Karnataka in partial fulfillment of the regulations for the award of the

degree of

MASTER OF SURGERY (Ayu)

By

T. MADHU, B.A.M.S.

GUIDE:

DR. K. R. RAMACHANDRA, M.D. (Ayu)

Professor& H.O.D.

S.D.M. College of Ayurveda, Udupi.

DEPARTMENT OF POST GRADUATE STUDIES IN SHALYA TANTRA

S. D. M. COLLEGE OF AYURVEDA, UDUPI – 574 118

2004

EFFICACY OF JATYADI TAILA IN THE

MANAGEMENT OF DUSHTA VRANA

Dissertation submitted to the

Rajiv Gandhi University of Health Sciences, Bangalore, Karnataka,

in partial fulfillment of the regulations for the award of the degree of

MASTER OF SURGERY (Ayu)

By

T. MADHU, B.A.M.S.

GUIDE:

DR. K. R. RAMACHANDRA, M.D. (Ayu)

Professor& H.O.D.

S.D.M. College of Ayurveda, Udupi



2004



CERTIFICATE

This is to certify that the dissertation work entitled “Efficacy of Jatyadi Taila in

the management of Dushta Vrana” has been carried out by Dr. T. Madhu, under my

direct supervision and guidance as a partial fulfillment for the award of degreeM.S.(Ayu).

He has worked hard and sincerely in carrying out this work and established new

concepts in the management of Dushta Vrana along with bacteriological study of Jatyadi

Taila.

This title has not been awarded degree, diploma associateship, fellowship or

similar honours previously.

Recommended the dissertation for evaluation by adjudicators.

Place : Udupi

Date : .02.2004

Dr. K. R. Ramachandra, M.D. (Ayu)

Guide,Professor and Head of the Department,

Department of Post Graduate studies in

Shalya Tantra,

S. D. M. College of Ayurveda, Udupi

CONTENTS

List of abbreviations

List of tables

List of figures

List of color plates

Chapter No. Contents Page No.

1. Introduction 01 - 04

2. Review of literature

2.1. Ayurvedic review 05 - 12

2.2. Drug review 13 - 40

2.3. Modern review 41 - 81

3. Clinical study

3.1. Materials and methods 91 - 98

3.2. Observations 99 -129

4. Discussion 130 -141

5. Conclusion

6. Summary 142 -144

References Bibliography Appendix

Case Proforma

Master Chart

ABBREVIATIONS

A.H. : Ashtaanga Hrudaya

A. Pr. : Ayurveda Prakaasa

A.San. : Ashtaanga Sangraha

AT : After Treatment

B. & L. : Baily & Love’s Short practice of surgery

B. Pr. : Bhaava Prakaasha

B.R. : Bhaishajya Ratnaavali

BT : Before Treatment

Ch : Charaka

Chakra : Chakradatta

Chapt. : Chapter

Chi. : Chikitsaa Sthaana

D : Days

Dra. Vi. : Dravyaguna Vijnaana

FU : Follow up

G.N. : Gada Nigraha

G : Group

K : Kapha

Ka. : Kaashyapa

M. Ni. : Maadhava Nidaana

Mad. Kh. : Madhyama Khanda

M.M.S Manipal manual of surgery

Ni. : Nidaana Sthaana

P : Pitta

Po. Kh. : Poorva Khanda

Pg Page number

R : Rakta

R.Sa Rasayogasaagara

Sha. : Sharangadhara

Sam. : Samhita

S. : Sushruta

S. Das. Surgery : S. Das concise text book of surgery

Soo. : Sootra Sthaana

Ut. : Uttara Sthaana

V : Vaata

Y.R. : Yoga Ratnaakara

I sincerely express my deep sense of gratitude to my Teacher and Guide

Dr. K.R.Ramachandra for the magnitude of his dynamic and untiresome guidance

throughout the study. I would like to put on record the affection and care with which my

esteemed Guide directed me during the study.

I am thankful to Dr. Muralidhar Sharma, Dr. Subramanya Bhat, Dr. Raghavendra

Acharya, Dr. Jayakrishna Nayak, Dr.Jonah and Dr. Ramadevi for their help,

encouragement and suggestions during the work.

I wish to offer my sincere thanks to Prof. Dr. M. H. Rayabhagi, Principal and

Prof. Dr. D. Krishnamoorthy, Dean for the Post Graduate studies, S.D.M. College of

Ayurveda, for their encouragement and support.

I wish to express my gratitude to the authorities of S.D.M. Educational Society for

providing me all the requisite facilities to carry out this work.

My gratitude due to Dr. Y. Narayana Shetty, Superintendent and

Dr. Deepak S. M., Deputy Superintendent of the S.D.M. Ayurveda Hospital, Udupi for

their valuable support and encouragement.

I express my gratitude to Dr. Mamatha Ballal, Professor, Microbiology

department, K.M.C. Manipal, and the H.O.D., Microbiology department, K.M.C.

Manipal, for their contribution in the bacteriological study of Jatyadi Taila.

ACKNOWLEDGEMENTS

I am grateful to our Librarian Shri Harish Bhat, for providing me with the books I needed.

I am thankful to my seniors Dr. Manjunath Bhat, Dr. Lodha Naresh, Dr. Satish

B.G., Dr. Shilpa, Dr. A. Narayan Nambi and Dr. Ravishankar for their help throughout

the study.

I am indebted to my batch mates Dr. D. M. Patil, Dr. Nagaraj, Dr. Ashok M.L.,

Dr. Vishwas, Dr. Ramachandra, Dr. B.V. Shetty, Dr. Mahesh C.D., Dr. Pradeep will

forever remain in my memories for their tremendous compliance in compiling this study.

I am thankful to my juniors Dr. Jayagopal, Dr. Sudheendra, Dr. Raghavendra, Dr.

Pramod, Dr. Bhargav, Dr. Vinay, and Dr. Anil.

My special thanks to for bringing out quality copies.

Dr. T. Madhu

LIST OF TABLES

Table No. Contents Page No.

1. Nidaana of Vrana 15

2. Lakshanas of Vaataja Vrana 16

3. Lakshanas of Pittaja Vrana 17

4. Lakshanas of Kaphaja Vrana 18

5. Lakshanas of Raktaja Vrana 19

6. Lakshanas of Dvidoshaja Vrana 19

7. Lakshanas of Tridoshaja and Sannipaataja Vrana 20

8. Lakshanas of Dushta Vrana 21

9. Lakshanas of Shuddha Vrana 22

10. Vrana Sthaana and its Lakshanas Acc. to Maadhavakara 22

11. Vrana Varna 23

12. Vrana Vedana 24

13. Vrana Sraava Acc. to involvement of Dosha 24

14. Vrana Sraava Acc. to Sthaana

15. Vrana Upakramas 25

16. Incorporation of 60 Upakramas among 7 Upakramas 26

17. Aagantuja Vrana Lakshanas 27

18. Description of ingredients of Jatyadi Taila 27

19. Ingredients of Triphala Guggulu 28

20. Types of edges 28

21. Classification of commonly used antiseptics 31

22. Gram -Positive cocci 32

23. Gram-Negative bacilli 40

24. Anaerobic organisms 42

25. Distribution of 20 patients of Dushta Vrana Acc. to different age group

77

26. Distribution of 20 patients of Dushta Vrana Acc. to sex 78

27. Distribution of 20 patients of Dushta Vrana Acc. to occupation 78

28. Distribution of 20 patients of Dushta Vrana Acc. to the religion 83

29. Distribution of 20 patients of Dushta Vrana Acc. to socio-economic status

84

30. Distribution of 20 patients of Dushta Vrana Acc. to marital status 85

31. Distribution of 20 patients of Dushta Vrana Acc. to habitat 86

32. Distribution of 20 patients of Dushta Vrana Acc. to dietary habits 89

33. Analysis of chronicity in 20 patients of Dushta Vrana

89 34.

34. Analysis of area involved by the Dushta Vrana in 20 patients 99

35. Analysis of type of Dushta Vrana in 20 patients 100

36. Classification of Dushta Vrana Acc. to Adhishtaana 100

37. Analysis of Dushta Vrana Acc. to the cause 101

38. Assessment of pain 115

39. Efficacy of treatment on pain 115

40. Result of treatment on Pain 116

41. Assessment of Itching 117

42. Efficacy of treatment on Itching 118

43. Result of treatment on itching 118

44. Assessment of burning sensation 116

45. Efficacy of treatment on burning sensation 117

46. Result of treatment on burning sensation 117

47. Assessment of length of the Ulcer 119

48. Efficacy of treatment on length of the Ulcer 119

49. Assessment of width of the Ulcer 120

50. Efficacy of treatment on width of the Ulcer 120

51. Assessment of depth of the Ulcer 120

52. Efficacy of treatment on depth of the Ulcer 121

53. Assessment of tenderness 121

54. Efficacy of treatment on tenderness 122

55. Result of treatment on tenderness 122

56. Assessment of discharge 123

57. Efficacy of treatment on discharge 123

58. Result of treatment on discharge 124

59. Assessment of smell 124

60. Efficacy of treatment on smell 124

61. Result of treatment on smell 125

62. Assessment of surrounding area of ulcer 125

63. Efficacy of treatment on surrounding area of ulcer 126

64. Result of treatment on surrounding area of ulcer 126

65. Assessment of Floor & granulation tissue 127

66. Efficacy of treatment on granulation tissue development 127

67. Result of treatment on granulation tissue development 128

LIST OF FIGURES

Figure No. Contents PageNo.

1. Incidence of age 99

2. Incidence of Sex 100

3. Occupation incidence 101

4. Incidence according to the religion 101

5. Incidence of socio-economic status 102

6. Incidence according to marital status 103

7. Incidence according to the habitat 103

8. Incidence according to the dietary habits 104

9. Incidence of chronicity 104

10. Incidence of site of ulcer 105

11. Incidence of type of Dushta Vrana 106

12. Incidence according to the Adhishtaana 107

13. Incidence according to the cause 107

14. Effect on pain 108

15. Effect on itching 108

16. Effect on burning sensation 109

17. Effect on length of ulcer 110

18. Effect on width of ulcer 110

19. Effect on depth of ulcer 111

20. Effect on tenderness 112

21. Effect on discharge 112

22. Effect on smell 113

23. Effect on surrounding area of ulcer 114

24. Effect on floor and granulation tissue 115

LIST OF COLOR PLATES

Plate No. 1. Efficacy of treatment on healing of ulcer

Plate No. 2. Observation on bacteriological study

History of medical science starts with wound healing. The earliest medical

writings extensively consider wound care. In Edwin smith papyrus (1700

B.C) wounds and their management was described. Empirically, the ancient

physicians of Egypt, Greece, India & Europe developed gentle methods of

treating the wounds.

Treatment of wounds is probably the first medical problem faced by the

human being. Frequency of injuries is more often than any other diseases.

Many a times, non-healing nature of ulcers pose a problem in practice. It

may due to various reasons. One of the reasons is improper debridement.

Healing of Vrana is a natural process, but due to the interference of vitiated

Doshas, Vrana becomes Dushta and normal healing process gets delayed.

So to treat such type of Vranas both internal medication as well as external

application is necessary.

Dushta Vrana is a long standing ailment with profuse discharge and slough

where much importance should be given in removing the debris and

enabling the proliferation of healthy tissue.

Sushruta father of Indian surgery describes 60 therapeutic measures

elaborately for the management of Vrana.

For the purpose of Shodhana and Ropana 7 Kriyakalpas are mentioned.

They are Kashaaya, Kalka, Varthi, Rasakriya, Avachoorna, Taila and Sarpi.

Depending on the combination of drugs the Kriyakalpas may be of

Shodhana or Ropana. Among these Taila is indicated in Vrana which has

Utsanna Maamsa, Alpa Sraava etc.

Debridement is of three types i.e. surgical, chemical and mechanical. In

some conditions dead and devitalized tissue is removed by surgical

excision, but by means of this chance of injuring healthy tissue will be

more. In case of chemical debridement various chemicals (like topical

agents i.e. povidone iodine, eusol, hydrogen peroxide etc.) are used in day

to day practice, but most of them are having limitations i.e. eusol has no role

in the treatment of open wounds that are clean, healing well with no signs of

invasive infection. Povidone iodine should not be used in patients who are

sensitive to it. In case of mechanical debridement flushing therapy or

hydrotherapy etc. are used. Since the chemical substances used for the

purpose of dressing have their own setbacks, in the present study Jatyadi

Taila for external application is taken up to understand its efficacy in the

Shodhana and Ropana Karma.

The patients selected for the trial were divided into two groups. However

both the groups were given Triphala Guggulu & Gandhaka Rasayana

internally. The patients were observed during the course of treatment &

follow up period as well. The observations and results were statistically

analyzed.

From this study it becomes evident that the response in the trial group was

good in terms of reduction of size of Vrana along with other features. The

results are encouraging and it requires further study to explore new facts

and figures.

The patients selected for the study were divided into two groups of 10 each.

Group A was subjected to dressing with Jatyadi Taila and Group B with

sterile dry gauze dressing. However both the groups were administered

Triphala Guggulu(450mg) 1tds & Gandhaka Rasayana(350mg) 1tds

internally during the course of treatment. The course of treatment was 3

months and follow up was done during the same period at weekly intervals.

The observations made and salient features are as follows

Incidence observations:

i) Age: Out of twenty patients selected for the study, maximum

incidence was seen in the age group between 41-60 years. It might be

due to the reduced tissue vitality, immunity power and healing rate.

ii) Sex: Maximum incidence of Dushta Vrana was seen in males.

iii) Socio-economic status: Maximum incidence of Dushta Vrana was

seen in lower middle class. It may be related to improper hygiene &

malnutrition and this is yet to be established.

iv) Area involved: Among 20 patients selected for the study, maximum

incidence of area involved by the Dushta Vrana was seen in lower

limbs. It might be because of less circulation (which plays important

role in the healing) and lower limbs are more prone to trauma.

v) Chronicity: Maximum incidence of chronicity was observed in the

patients having duration upto one month.

vi) Adhishtaana & Type of Dushta Vrana: Maximum incidence of

Adhishtaana involved was Twak-Maamsa and most of them were

diagnosed as Vaata-Pittaja, Vaata-Kaphaja Vranas.

Discussion on the effect of treatment:

Observations were made in twenty patients before treatment and after

treatment with Jatyadi Taila application in group A and sterile dry gauze in

group B with regard to the different subjective and objective criteria listed

in the study proforma.

1) Pain:

Group A: All the patients were complaining of pain before treatment.

The mean (pain) score was 1.5 and after treatment it was reduced to 0.2.

Only two patients had mild pain at the end of the treatment.

Among the types of Dushta Vrana i.e. Vaata- Pittaja & Vaata –Kaphaja,

reduction of pain was observed in both the varieties without any

significant variation.

Among the causes of ulcers efficient reduction of pain in trial group was

seen in varicose as well as traumatic ulcers without any significant

variations.

Group B: All the patients were complaining of pain before treatment.

The mean (pain) was 2.1 & after treatment it was reduced to 0.6. At the

end of the treatment 6 patients had mild pain.

2) Itching:

Group A: Before treatment 6 patients were having itching and the mean

(itching) score was 0.9. After treatment itching was reduced completely

in 5 patients and the mean was reduced to 0.1.

Group B: Before treatment 6 patients were having itching and the mean

(itching) was 1.1. After treatment itching was reduced completely in 3

patients, in remaining patients it was reduced to grade 1&2 and the mean

was reduced to 0.4.

3) Burning sensation:

Group A: Before treatment 7 patients were having burning sensation and

the mean (burning sensation) was 1.1. After treatment in 6 patients it was

reduced completely, in 1 patient it was reduced to grade 1 and the mean

was reduced to 0.1.

Group B: Before treatment 6 patients were having burning sensation and

the mean (burning sensation) was 1.1. After treatment in 4 patients it was

reduced completely, in remaining patients it was reduced to grade 1 and

the mean score was reduced to 0.2.

4) Size of the ulcer:

Group A: Out of 10 patients, ulcer was healed completely in 6 patients

& in remaining 4 patients marked reduction was noticed. Before

treatment the mean score was 7.55(length), 5.325(width) & 0.37(depth).

After treatment mean was reduced to 1.67(length), 0.92(width) &

0.04(depth).

Among the cause of ulcer, reduction in the size of ulcer in trial group was

fast in traumatic ulcers, moderate in case of varicose ulcers and slow in

case of pressure sore.

Group B: Out of 10 patients, ulcer was healed completely in 3 patients.

The mean score before treatment was 3.6(length), 2.35(width) &

0.203(depth). After treatment the mean score was reduced to

0.89(length), 0.505(width) & 0.0535(depth).

5) Discharge:

Group A: Before treatment 9 patients were having discharge from the

ulcer & the mean (discharge) was 1.5. After treatment in 7 patients

discharge was reduced completely, in remaining patients it was reduced

to grade 1 and the mean score was reduced to 0.2.

Group B: Before treatment 6 patients were having discharge from the

ulcer & the mean score was 1.2. After treatment in 4 patients discharge

was reduced completely, in remaining it was reduced to grade 1 and the

mean score was reduced to 0.2.

6) Tenderness:

Group A: Before treatment tenderness was present in 9 patients and the

mean (tenderness) score was 1.5. After treatment in 7 patients tenderness

was reduced completely, in remaining it was reduced to grade 1 and

mean was reduced to 0.2.

Group B: Before treatment tenderness was present in 10 patients and the

mean score was 1.9. After treatment in 6 patients tenderness was reduced

completely, in remaining it was reduced to grade 2&1, mean was reduced

to 0.5.

7) Smell:

Group A: Before treatment 3 patients were having smell from the ulcer

and the mean score was 0.5. After treatment smell was reduced

completely in 3 patients and the mean score was 0.

Group B: Before treatment 3 patients were having smell from the ulcer

and the mean score was 0.3. After treatment in 2 patients smell was

reduced completely, in remaining 1 patient it was reduced to grade 1 &


8) Surrounding area of ulcer:

Group A: Before treatment 4 patients were having swelling and blackish

discoloration (i.e. 3 patients with swelling & blackish discoloration and 1

patient with blackish discoloration only) and the mean score was 1. After

treatment in 4 patients it was reduced to grade 1(only blackish

discoloration with out swelling) and the mean was reduced to 0.4.

Group B: Before treatment 8 patients were having swelling and blackish

discoloration (1 patient with swelling & blackish discoloration, 4 patients

with swelling only, 3 with blackish discoloration only) and the mean

score was 1.4. After treatment in 3 patients swelling & blackish

discoloration reduced completely, in remaining 5 patients it was reduced

to grade 2,1( 4 with blackish discoloration, 1 patient with swelling) and


9) Floor & granulation tissue:

Group A: Before treatment all 10 patients were having irregular floor,

slough and unhealthy granulation tissue, the mean score was 2. After

treatment floor became healthy in 6 patients, in remaining 4 it became

smooth, regular with pale granulation tissue and mean was reduced to

0.4.

Group B: Before treatment all 10 patients were having irregular floor

with pale granulation tissue and the mean was 2. After treatment in 3

patients floor became healthy, in remaining patients it became smooth,

regular with pale granulation tissue and the mean was reduced to 0.7.

Follow up period:

During the follow up period (2nd follow up) in a patient of varicose ulcer

pain was aggravated associated with discharge. This can be attributed to

the unwholesome, unhygienic diets & regimen followed by the patient.

In both the groups even though aseptic & sterile precautions were taken

during dressing, sterile dry gauze dressing in group B may avoid the

external contamination and may not be able to promote the growth

promoting factors of granulation tissue. In group A i.e. application of

Jatyadi Taila in addition to aseptic & sterile precautions might cause

proliferation of granulation tissue which can be assessed or evaluated in

terms of faster reduction in the size of ulcer, amount of discharge, smell

etc.

Probable action of drugs:

Jatyadi Taila:

Most of the ingredients of Jatyadi Taila are having Shodhana, Ropana,

Vedana Sthaapana properties, Tikta, Katu, Kashaaya Rasas and Rooksha,

Laghu Gunas.

Kashaaya Rasa: It does Shoshana there by it might be helpful in Vrana

Ropana.

Tikta Rasa: It does Twak Maamsa Sthireekarana and Lekhana. It might

help in increasing tensile strength of wound & removal of slough.

Katu Rasa: It has Vrana Shodhana & Avasaadhana properties.

Tuttha: It is one of the ingredients of Jatyadi Taila having Lekhana

Karma. So it may help in removing the slough. Even in current surgical

practice CuSO4 is used in the removal of slough from the ulcers. So

Tuttha is one which may have such sort of action.

Tila Taila: It is used in the preparation of Jatyadi Taila and has Ushna,

Teekshna, Madhura, Vaataghna, Vyavaayi, Vikaasi, Sookshma

properties. When it is treated with drugs it takes the properties of those

drugs. So it might help (medicine) in reaching the minute spaces quickly

by means of its Sookshma, Vyavaayi, Vikaasi Gunas & helps in reducing

Vedana( because of Vaataghna property).

Triphala Guggulu:

Guggulu is one of the important ingredients of Triphala Guggulu. It is

having Vedana Shaamaka, Lekhana properties. As Vedana is one of the

important feature of Dushta Vrana, it might help in relieving Vedana.

Triphala Guggulu has Vaataghna, Kaphaghna properties by means of

which it may reduce swelling and promotes the healing.

Gandhaka Rasayana:

It might facilitate the healing (by formation of healthy granulation tissue)

by its Rasayana action and Kleda Hara Guna.

So locally application might normalize the Doshas and Dhaatus in that

particular region. For nourshing Dosha & Dhaatu in whole body

combination of internal as well as local medicines is needed.

Discussion on bacteriological study:

From bacteriological study it becomes evident that Jatyadi Taila is having

mild antibacterial activity in case of Pseudomonas aeruginosa. For other

varieties it is not having antibacterial activity. After 15 days of

incubation, inhibition zone (11mm) was noticed and no contamination

was observed in case of pseudomonas aeruginosa, no zone of inhibition

was observed in other varieties.

Jatyadi Taila is not promoting the growth of bacteria. The wound healing

property is not only limited to the antibacterial activity but other factors

are also responsible which have to be studied further.

From this study the following conclusions can be drawn.

In the trial group the results are of significant value in symptomatologies

like size of ulcer, discharge, smell, burning sensation, tenderness, floor&

granulation tissue, pain & itching.

Even though statistically there is no much significant difference between

the two groups, but by seeing the effect on individual parameters

(subjective&objective) and over all response Jatyadi Taila seems to be

effective when compared to dry gauze. It is having more of Ropana

qualities when compared to Shodhana.

Jatyadi Taila is having slow inhibition zone for pseudomonas aeruginosa

and not having inhibition zone in case of others (like e.coli, streptococci

etc.). It is not promoting the growth of bacteria.

Thus it can be concluded that Jatyadi Taila application externally along

with Triphala Guggulu & Gandhaka Rasayana as oral medication are

effective in Dushta Vrana by their Shodhana, Ropana, Vedana Shaamaka,

Rasayana properties etc.

With the introspection of the literature in the Prevedic & Vedic era,

ample of references are found in the Vedas & in all the literatures later to

that.

Sushruta the father of Indian surgery has given importance to Vrana and

its management. He has mentioned two definitions for the word Vrana.

One definition refers to the breach in the continuity whereas the other

refers to the healing of Vrana with discoloration. The description of

Vrana according to the predominance of the Dosha, Varna, Sraava,

Gandha, Vedana, Aakruthi, Upadravas of Vrana & Vranitha are found in

the classics. For the management 60 therapeutic measures are described

in detail. If the Vrana is not treated properly it becomes vitiated due to

the involvement of Doshas and Dhaatus. The management of Dushta

Vrana can be carried out by Antahparimaarjana and Bahiparimaarjana.

Among the Bahiparimaarjana various Kriyakalpas for Shodhana and

Ropana are mentioned. In the pain dominant Vrana Taila is mentioned as

a superior Kriyakalpa among the others. Depending on the combination

of drugs it can be used either for Shodhana or Ropana.

Ulcer is a defect produced due to the necrotization of the inflammatory

tissue. The repair of injured tissue is an even more fundamental process

than inflammation. Healing is an aspect of repair but it suggests the

closure of some gap as in a wound or an ulcer. A wound of skin may heal

perfectly, but the new tissue is a scar lacking sweat glands, sebaceous

glands and other specialized structures. The damaged or necrotized tissue

liberates the chemical stimulus which in turn triggers the mechanism of

healing. The process of healing is fundamentally the same in all the

wounds, but there are marked quantitative differences depending on the

amount of tissue destruction and to a certain extent on the presence of

sepsis. Removal of inflammatory material and necrotic debris, which

may be much or little replacement or reconstruction of the original tissue

to as great a degree as possible. It involves the invasion and replacement

of dyeing and dead tissue by immature mesenchyme for granulation

tissue. The essential function of granulation tissue is to replace useless

material by living mesenchyme.The process of conversion of

inflammatory debris into granulation tissue and finally into fibrous tissue

is known as organisation. Under conditions of ordinary health repair

proceeds at a uniform rate provided there is no local interference. Some

of the general factors are age, diet, vitamin c deficiency and local factors

are ischaemia, local irritants and systemic effects of trauma inhibit the

process of healing. The debridement of an ulcer can be carried out by

surgical, chemical and mechanical debridement to facilitate the healing

process.

In the present study Jatyadi Taila was used for local dressing of ulcer and

Triphala Guggulu, Gandhaka Rasayana 1tds each was administered

internally. In Jatyadi Taila majority of the ingredients posses the qualities

of Katu, Tikta,Kashaaya Rasa, Rooksha, Laghu Guna etc. Probably these

might have brought about the reduction in discharge, smell, removal of

slough and there by promote healing. Similarly in Triphala Guggulu and

Gandhaka Rasayana the attributes bring about the healing by the

Rasaadhi Panchakaas of the ingredients mainly Kashaaya, Katu Rasas,

Laghu, Rooksha Gunas, Vaata & Kapha Hara properties. They produce

Vedana Shaamaka, Shotha Hara and Rasayana properties.

The patients diagnosed as Dushta Vrana were randomly selected and

divided into two groups i.e. group A & group B. In group A dressing

was done using Jatyadi Taila after taking all the aseptic precautions,

whereas in group B after taking aseptic precautions dressing was done

using dry gauze. However both the groups were internally administered

Triphala Guggulu and Gandhaka Rasayana 1tds each. The general

observations were made on age, sex, occupation, socio-economic status,

chronicity, Adhishtaana, type of Dushta Vrana, area involved by Dushta

Vrana along with subjective parameters (like pain, itching, burning

sensation) and objective parameters(like size of ulcer, tenderness,

discharge, smell, surrounding area of ulcer, floor & granulation tissue).

All the observations were statistically analyzed.

Duration of the treatment was for a period of 3 months and follow up was

done at weekly intervals during this period.

The following conclusions can be drawn from the study. Significant

effect was seen in trial group(group A) in symptomatologies like size of

ulcer, discharge, smell, burning sensation, tenderness, pain, itching,

granulation tissue etc. even though there is no much difference

statistically between the two groups. Jatyadi Taila is having slow

inhibition zone for pseudomonas aeruginosa and it is not promoting the

growth of bacteria. The results are encouraging and leave scope for

further exploration in this field.

Ayurvedic review: Historical review: History of Vrana is as old as mankind. Professionals faced the problem on healing of wounds and ulcers. The review of literature makes it clear that constant research for new techniques and solutions to problems was going on in the annals of history. Hence, the review of literature regarding Vrana from Vedic to recent will not be out of context. Some of them are as follows: The literature can be studied under three headings: 1) Prevedic era 2) Vedic era 3) Postvedic era Prevedic era: During this period no direct references regarding Vrana are available. Vedic era: During this period Rigveda and Atharvaveda are considered as chief sources of medical information Rigveda1: Many references are seen in Rigveda. Sandhaan karma done by Ashwini Kumaaras in case of severed head of Yajna (Daksha), joining the limb of Vishpala the daughter of Khela are worth mentioning.

Atharvaveda2 : Ayurveda is Upaveda of Atharvaveda . Many references are available like administration of Rohini Aushadi in Kshata and Vrana, Sheetalajaladhaara for stoppage of bleeding in Sadhyovrana are important. Post vedic era: Agnipurana3: Surgical wounds are enumerated in Agnipurana. Mahavagga ( Buddhist tradition )4: Vrana with Pooya were drained and later they were treated with bandaging, dusting, fumigation etc. Kautilya Arthashaastra5: When Kautilya defined legal offences he has mentioned these acts as punishable offences, they are 1) Any injury which results in bleeding other than Dushta Vrana

is punishable. 2) Any injury which results in bleeding other than Dushta Rakta

is punishable. Jaatakamala6: Dushta Vranas which are painful along with pocket full of pus, should be carefully opened and drained. The wound becomes painful when it comes in contact with salt.

Harshacharita7: References regarding the difficulty in management and arresting the bleeding in the wounds located in Hruth Pradesha, complications like shock, collapse,and unconsciousness in case of fresh wounds with pain and haemorrhage is mentioned. The bandaging was carried out with cotton cloth and in some cases need for fine bark of the trees to cover the wounds is also mentioned. Kaadambari8: Wounds were produced by constant friction and injury. Sometimes injury was severe which produced disabilities in the organs and after healing of the wound there remained scar. Samhita kaala9:

Detail description of Vrana with its management is mentioned in Brihatrayee and Laghutrayee. 36 therapeutic measures were explained in Charaka where as Sushruta has mentioned 60 therapeutic measures for Vrana . Description about Vrana is also mentioned in Bhela Samhita, Kaashyapa Samhita, Gadha Nigraha, Chakradatta, Yogaratnakara, Bhaishajya Ratnavali. Historical review:

References:

1) Rigveda- 1.112.10; 116, 15; 17, 11, 118, 8; 10.39, 8. 2) Atharveda- 2.3.2 –6; 19.34.10; 8.9.1-10. 3) Agnipurana- 31.18-36. 4) Mahavagga- 14.4-5, 23.6. 5) Kautilyas Arthashastra- 3.67.11.14, 3.73.19.10, 2.43.27.11. 6) Jaatakamala- 8.24, 26.29,112. 7) Harshacharita- 324,454,432. 8) Kaadambari- 102,644, 329. 9) Ch.Sam.soo- 19/7, Ch.chi-25; S.Sam.chi- Chapt 1,2 ; S.soo-Chapt

17, 21, 22, 23; Ka.sam-11/8, 10; A.san. Ut-Chapt 29, 30, 31; A.H.Ut- Chapt 25, 26; M.Ni-Chapt 42, 43; G.N- Vranashopha Dvivraneeya Adhikaara;Chakra- Chapt 44, 45; Sha .Sam. Po.Kh-Chapt 7; B. Pr .Mad .Kh- Chapt 47; B.R-Chapt 47, 48.

Vrana: Derivation1:

®d‚Pd ›ddÎde®dŸdjPd‰¦dy ®d‚PdSd£dfe£d ®d‚PdZ|| ±dg. eŸd. 1/6

The word Vrana is derived from the verb root,"®d‚Pd ›ddÎde®dŸdjPd‰¦dy" | So the destruction or discontinuity of body part or tissue is called as Vrana.

®d‚PdSd£dfe£d ›ddÎd®dz®dPSd‰a I¶Tdy£df£Sd¤d‰Z| Dalhana gives the meaning of verb “Vrana” as causing discoloration of the body (or its parts). Definition2:

®dmPddye£d Sd±«ddQŠ éOyµíe§d ®d‚Pd®d±£dg ¦d ¦d¯Sde£d |

AdQyUµ¥ddTPddÏd±«ddQŠ ®d‚Pd B£SdgŸSd£dy ©dg¥dzZ|| ±dg.±dj.21/40

Sdd®dQdSdg®dm‰Pdf£dy e®d®dmPddye£d ®dd ¯dTfTe«de£d®d‚PdZ|| A.±d.D.29/2

As the scar of the wound never dissappears even after complete healing and as its imprint persists life long it is called as Vrana by the wise. Vrana is that which makes person to pray (to god) till his life exists, or

that which exposes the interior of body. Classification3: Almost all the Acharyas have classified Vrana into two catagories i.e. Nija and Aagantuja depending upon the causative factors. The Doshas get vitiated by their own causative factors or by the external agents. Nija or Shaareeraja vrana: Sushruta has specially mentioned these Nija Vranas to be due to Vaataja , Pittaja, Kaphaja, Raktaja, and Sannipaataja. These are further classified into 15 types on the basis of permutation & combination of Tridoshas along with Rakta. Charaka has described Nija Vrana as only of 3 types i.e.due to Vaata, Pitta and Kapha. Aagantuja vrana: It is caused by trauma from Purusha, Pashu, Pakshi, Vyaala, Prapatana, Peedana, Prahara,Teekshnaoushadha, Agni, Kshaara, Visha, Kapaala, Shringa. Sushuruta classified Sadhyovrana into 6 types based on their featuresThey are Chinna, Bhinna, Viddha, Kshata, Pichita & Ghrista. According to Astanga Sangraha Aagantuja Vrana is of 3 types i.e. Chinna, Viddha, Pichita.

Sadhyo Vrana are of 8 types according to Astaanga Hridaya i.e. Ghrista, Avakrutha , Vichinna , Pravilambita, Paatita, Viddha, Bhinna, Vidalitha. Description of Sadhyo Vrana in Maadhava Nidaana is similar to that mentioned by Sushruta where as Shaarangadhara mentioned 8 types. Though Vaagbhata has also accepted classification given by Sushruta, but has mentioned them along with specific clinical features. Charaka has classified Vrana into 20 varieties depending upon their distinctive features, they are4 Krutya, Akrutya, Dushta, Adushta, Marmasthita, Amarmasthita, Samvrutha, Vivrutha, Daaruna, Adaaruna, Sraavi, Asraavi, Savisha, Avisha, Vishamasthita, Samasthita, Utsangi, Anutsangi, Utsanna, Anutsanna. Sushruta and Charaka have also mentioned Vrana as Dushta and Shuddha but not as a type of classification. Charaka has also described 12 characteristic features indicating the advanced stage of morbidity of Vrana. These morbid conditions are also classified into 24 categories depending upon their causative factors like Snaayu Kleda etc. Shaarangadhara classified Vrana under 4 major groups they are Aagantu, Dehaja, Shuddha, Dushta. These are further classified into 15 types.

Depending upon the stages of healing Vrana is classified into Ruhyamaana Vrana and Roodha Vrana5. Accordinrg to shape Sushruta classified Vrana into 4 types they are: Aayatha, Vrutha, Triputaka, Chaturasra. According to prognosis based on location, type of Vrana and discharge Vrana is classified as Sukhasaadhya, Kruchrasaadhya, Yaapya and Asaadhya. Schematic representation of classification of Vrana: Kaarana --- Nija, Aagantuja. Avastha- -- Dushta, Shuddha,Ruhyamaana,Roodha. Vrana--- Aakruthi--- Aayatha, Chathurasra, Vrutha,Triputaka. Saadhyasaadhyatha--- Sukhasaadhya, Kruchrasaadhya, Yaapya,Asaadhya. Nidaana of Vrana6 : Shareeraja Vrana: The causes for this are same as the causative factors reponsible for the vitiation of Doshas. These are classified as Aaharaja and Vihaaraja Kaaranas. Table No. 1 DOSA KAARANAS

AAHARAJA VIHARAJA VAATA Vaataprakopakaaharaasi.e.

Katu,Lavana, Laghuaahara,Sushkasaaka,Valloora,

Uddhalaka etc.

Balavat Vigraha,Ativyaama, suppresion of Adhaarniya Vegas, etc.

PITTA Pittaprakopakaahaaraas i.e.Katu, Amla, Lavana, Ushna, Vidaahi, Teekshna,

Tila, Pinyaka, etc.

Krodha, Shoka,Bhaya,Maithuna,Aayasa Upavaasa etc.

KAPHA Kaphaprakopakaaahaaraas, i.e.

Madhura, Amla, Lavana, Sheeta, Snigdha Aahara, Maasha etc.

Divaswapna, Avyayaama, Aalasya .

Lakshanas7 : Features of Vrana are of 2 types : 1)Saamanya : pain. 2)Vishesha : consists of signs and symptoms caused by Doshas. Vishesha Lakshanas: Vaataja Vrana Lakshanas: Vrana caused due to Vaata is Stabdha, Katina has Shyaava or Aruna Varna, Alpa Sraava and Vedana Baahulyata. Table No. 2- Lakshanas according to various Acharyas8: Lakshan

as Sushruta Charaka Kashyapa A.San. A.H. M.Ni.

Varna Shyaava or

Aruna Shyaava -

Shyaava, Aruna,

Krushna,Bhasma of Asthi.

Shyaava, Krushna, Aruna, Bhasma

kapotha or Asthi Varna

Shyaava

Vartma Rooksha Stabdha, Kathina

Stambha, Kathina

- - Stabdha, Kathina

Vedana

Todha, Bheda,

Chatachatayana etc

Teevra Ruk,

Sphurana Maharuja

Sphuruna,Todha, Bheda

etc.

Todha, Bheda etc.

Maharuja

Sraava Sheeta,Picchila,Alpasraav

a

Mandhasraava

Alpasraava

Alpa sraava resembling

Mastu, Kshaara, Maamsa

Dhaavana, Pulakodaka

Alpasraava

resembling Mastu, Maamsa, Pulakaam

bu

Mandhasraava

etc.

Pittaja Vrana Lakshanas : Vrana caused due to Pitta will be associated with Daaha, Paaka, Raaga, Jwara, Trishna, Moha etc. has Kshipra Utpatti with Neela, Peeta Varna and Pootisraava. Table No. 3- Lakshanas according to various Acharyas9: Lakshas Sushruta Charaka Ka.S. A.San. A.H. M.Ni

Varna Peeta,

Neelabha - -

Peeta, Neela, Haritha, Krushna, Pingala

Neela, Peeta, Kapila Pingala

-

Utpatti Kshipra - - Kshipra Kshipra -

Anya lakshana

s

Daaha, Paaka, Raaga, studded

with Peeta

Pidaka

Trushna, Moha, Jwara, Sveda,

Jwara, Daaha, Moha,

Trushna

Daaha, Raaga, Paaka,

Jwara,Dhoomayana,

Raaga, Paaka pain

resembling Vrana caused

by Kshaara

Trushna, Moha, Jwara, Kleda, Daaha

Sraava

Sraava resembli

ng Kimshuka flower, Ushna.

Pootisraava

Pootisraava

Sraava large in qty. resembling

Gomootra, solution of Bhasma,

Kimshuka or Mrudveeka or

Taila

Sraava is warm,

large in qty

resembling

Kimshuka, Taila

or solution

of Bhasma

Pootisraava

Kaphaja Vrana Lakshanas: Vrana caused due to Kapha will have Paandu or Shwetha Varna associated with Ugra Kandu, Mandha Vedana, Shukla,

Sheeta, Pichila and Ghana Sraava. Table No. 4- Lakshanas according to various Acharyas10: Lakshanas Sushruta Charaka Ka.sam. A.Sam. A.H. M.Ni.

Varna Paandu Paandu Paandu Paandu Paandu Paandu

Vartma

Sthoola, covered

with Stabdha

Sira Snaayu jaala,

Katina

Snigdha, Guru,Bahu piccha

Sthaimithya,

Maardhava

Snigdha, Katina, Sthoola

Sthoola, Katina, covered with Sira Snaayu Jaala

Bahu piccha, Guru,

Snigdha

Anya lakshanas

Mandha vedana, severe Kandu,

feeling of heaviness

Mandha, vedana,

Chirakaari

Mandha, vedana

Chirakaari

Mandha vedana, Kandu, Swaapa,

Sthaimithya

Alparuk, Kandu

Mandha vedana,

Sthaimithya

Sraava

Shukla, Sheeta, Saandra

Alpa samkleda

Atisraava

Sraava resemblin

g Navaneeta

, Tila pishta,

Naarikelodaka

Large qty. of Sveta Ghana sraava

Alpa Samkleda

, Chirapaak

i

Raktaja Vrana Lakshanas: In general this Vrana will have features similar to that of Pittaja Vrana, has Pravaala (Rakta) Varna, Raktasraava covered with network of Krishna Sphota, smells like Turanga or Vaajisthaana. Table No.5- Lakshanas according to various Acharyas11:

Lakshanas Sushruta A.Sam. A.H. M. Ni.

Varna Pravaala Dhala Nichaya Pravaala (Raktha)

Pravaala (Raktha)

Raktha

Vartma Covered with network of Krushnasphota, Pidaka

Covered with Krushnasphota,

Pidaka - -

Anyalakshanas

Smells like Turanga sthaana, Vedanaayuktha, Dhoomayana Sheela and having features of Pitta

Smells like Vaaji Sthaana,

has other features of

Pitta

Smells like Vaaji Sthaana,

has other features of

Pitta

-

Sraava Raktha Sraava Sarakthapooya

Sraava Sarakthapooya

Sraava Raktha Sraava

Table No.6- Dvidoshaja Vrana Lakshanas12: Sushruta has explained the Lakshanas depending upon combination of Doshas while Vaagbhata and Maadhavakara has also made the similar attempt. Lakshanas VP VK PK VR PR KR

Aakruthi - - - - Ghrita manda

-

Gandha - - - - Meena

dhaavana toya

-

Varna Aruna, Peeta - - Rakta, Aruna

- Rakta

Vedana Todha,

Daaha,DhoomayanaTodha, Kandu

Daaha, Ushna

Todha, Supta

- Kandu

Sraava Peeta, Aruna Sheeta,

Picchila, Alpa

Peeta, Paandu

Rakta, Aruna

Ushna, Krishna

Rakta, Paandu

Anya Lakshanas

- Rooksha,

Guru, Dhaaruna

Guru Rooksha,

Tanu Mridu, Visarpa

Guru, Picchila, Snigdha

Table No. 7- Tridoshaja and Sannipaataja Vrana Lakshanas13: Lakshanas VPR VKR PKR VPK VPKR

Varna - - - Has

Varna of 3 types

-

Vedana

Sphurana, Todha, Daaha,

Dhoomayana

Kandu, Sphurana, Chumachumayana

Daaha, Kandu

Has Vedana

of 3 types

Nirdahana, Nirmathana, Sphurana,

Todha, Daaha, Kandu

Sraava Peeta, Tanu,

Rakta Paandu, Ghana,

Rakta

Paandu, Ghana, Rakta

Has Sraava of 3 types

Naana Varna

Anya Lakshanas

- - Paaka, Raaga

- Paaka, Raaga

Dushta Vrana14:

£dÎdQdy°dQje°d£ddy QgÞZ || A. ±da. D. 29/4 Qdy°dzTe¥deÝ£ddy QgÞZ...............|| A. Umµ. D.

25/2 Dushta is one in which there is localization of Doshas or Dushta means getting vitiated by Doshas. Vrana which smells badly (foul odour), has abnormal color with profuse discharge, intense pain and takes long period to heal is said to be Dushta. The features of Dushta Vrana will vary according to the predominant Dosha present in it. Lakshanas of Dushta Vrana15: Table No.8- Lakshanas depending upon the shape, discharge, consistency and chronicity according to various Acharyas:

Sushruta Charka A.S. A.H. M.Ni.

Atisamvrutha or Ativivrutha Ati-katina or

Mrudu, Utsanna or

Avasanna. Ati sheeta or

Usna, having one of the

colours Krushna,Rakta, Peeta, Shukla etc,Bhairava,fi

lled with Pootipooya,Maamsa, Sira, Snaayu etc. Moving in

oblique track (Unmargi)

having Amanoghna Darshana, Atigandha,

Vedanayukta, associated

with Daaha, Paaka, Raaga,

Kandu, Shopha Pidaka

etc. Discharging excessively

Dushta Shonitha, Dheerga

Mentioned 12 characteristic

features indicating the advanced stage of morbidity of Vrana. Svetatva, Avasanna

Vartmatva, Athisthoola-

Vartmatva,Atipinjaratva, Neelatva,

Syaavatva, Atipidakatva, Rakta-

Krushnatva Atipootitva,

Ropyatva Kumbhi-Mukhatva,.Vranas with Pootigandha,

Vivarna, Bahusraava, Maharuja

Either Atisamvrutha or Ativivrutha,

Atimrudu or Katina, Atiutsaadha or

Avasaadha, Atisheeta or Usna Rakta, Krushna, or Paanduta, covered

with Pooti Maamsa, Sira,Snaayu, etc. Dishcarges Pooti

Pooya, Daaha, Paaka,

Kandu,Svayathu,Vedana Pitaka, etc.

appearing as Upadravas, Dheerga

Kaalanubandha

Either Samvrutha or Vivrutha,

Katina or Mrudu Atiutsanna or

Avasanna, Atiushna or Atisheeta,

Raktatwa or Paanduta,Discharges Pooti Pooya

covered with Pooti Maamsa, Sira, Snaayu,

associated with Atiruk, Daaha,

Swayathu, Kandu & other

complications, Dheerga Kaalanu

bandha

Discharges Pooti Sraava,

or Dushta Ashruk,h

as Utsangi (sinuses) inside,

Chirastitha, emits

Pooti Gandha

& doesn’t posses

any features

of Shuddha

Vrana

Kaalaanubandhi

Shuddha Vrana16:

eÎdeªdQdy‰°dzT¦dd¸¶d¦£dZ ¯Sdd®ddzÝZ e§dNµI¶f ±d«dZ |

A®dyQ¦ddy e¦dTdàd®ddy ®d‚PdZ ¯dg¥Q BUµdyŸSd£dy || ±dg.±dj. 23/18

e¡dæµd£d¬ddªddy «dmQgZ e±¦d›¥dZ ¯¬d´Pddy e®d›d£d®dyQ¦dZ ±dg®Sd®de±¤d£ddy

e¦dTdàd®dÜdye£d ¯dg¥Qdy ®d‚Pd Be£d || ±dg.eŸd.1/7

Shuddha Vrana is one, which is free from the localization of Doshas. Vrana which is not invaded by Tridoshas, having Shyaava Oshta, which has developed Sama Pidaka, not having Vedana and Sraava is said to be Shuddha Vrana. Vrana which resembles Jihwa Talaaba, Mrudu, Snigdha, not having Vedana, Sraava and good looking is said to be Shuddha. Features mentioned by Sushruta and Vaagbhata are almost similar. Table No. 9 - Lakshanas according to various Acharyas17:

Sushruta Charka A.San. A.H. M.Ni

Not invaded by Tridoshas

having Shyaava Oshta,

resembles Jihva Talaabha & is

Mrudu, Snigdha not having

Vedana, Sraava, good looking, has developed Sama Pidika.

Na Atirakta, Paandu,

Shyaava,(na ati) Ruk, Utsanna, Utsangi.

Not vitiated by Doshas,

resembles Jihva in color, and is

Slakshna having Shyaava Oshta

centre being elevated or even

not having Vedana, Sraava.

Resembles Jihva in color,

Mrudu,Slakshna with Shyaava

Osta,Samapidika, having Unnata

Madhya,not acommpanied

with any Upadravas.

ResemblesJihva Talaaba and is

Atimrudu,Slakshna,Snigdha,

Suvyavasthitha, Alpa Vedana , Niraasraava.

Ruhyamaana vrana18:

Lakshanas:

I¶§ddy£d®dPd‰§d‚e£d«dd Sd±Sdd¦£ddZ ™¬dyQ®de¡d‰£ddZ |

e±¤dTdeÜde§deLµI¶d®d¦£ddy TdyUµ£dfe£d £d«ddeQ¯dy£dŠ || ±dg.±dj. 23/19

Vrana which has Kapotha Varna,devoid of Kledha and has Sthira Pitika is said to be Ruhyamaana Vrana. Similar type of description is mentioned by Vaagbhata and in Maadhavanidaana. Samyak Roodha Vrana19: Lakshanas:

éOµ®d£«dd‰¦d«d›d‚e¦¤d«d¯dj¦d«dè¡da ®d‚Pd«dŠ |

£®d™±d®dPd‰a ±d«d£d¬da ±d«Sd›d‚jOµa e®de¦deQ‰¯dy£dŠ || ±dg.±dj. 23/20

Vrana which has healed in its seat (dwelling place) without eruptions (Granthi), pain (Vedana) or swelling, has the colour as that of Twak and is even is said to be Samyak Roodha. Samprapti20: Doshas being aggravated by their respective causative factors gets lodged in any of Vrana Sthaanas to give rise to Vrana. Vaata, Pitta, Kapha being aggravated by their respective causative factors

gets lodged in the exterior of the body to give rise to Nija Vrana. Examination of Vrana21:

°dP«dj¬ddyíÝ§deT›d‚dUµf §d¢Ÿd¬d´dPd¬de´d£dZ| °d°Æd e®d¥dd¦dze¦d‰eQ‰ÝzÜd£dgeªd‰Z

±ddØ£dy ®d‚PdZ || ±dg. eŸd. 1/134

Sushruta emphasizes that before treating the Vrana one should know the Shanmoola i.e. the causative factors (Vaata, Pitta, Kapha, Sannipata, Rakta, Aagantuja),Ashta Parigrahee i.e. 8 Vrana Adhistaanas (Twak, Maamsa, Sira, Snaayu, Asthi, Sandhi, Koshta, Marma),Pancha Lakshana Lakshitaha i.e. features of Vaataja, Pittaja, Kaphaja, Sannipaataja and Agantuja Vranas as well as Varna, Sraava, Gandha, Vedana, Aakruti and also 60 Upakramas for the proper management of Vrana. Further it is said that these four (i.e.Shanmoola, Astha Parigraahi, Pancha Lakshana and Shastya Vidhana) are to be thoroughly understood by the Vaidya before treatment,along with the Chikitsa Chatushpaadha the treatment of ulcer becomes easier. Examination of Vrana & patient suffering from this ailment is to be carried out in 3 different ways. They are Darshana, Sparshana and Prashna.

Darshana: By Darshana Pareeksha age of patient, site of Vrana, Aakruthi, Varna, condition of Vrana, etc. can be elicited.

Sparshana: It helps in eliciting the hardness or softness of Vrana, increase or decrease of local temperature etc. Prashna: By Prashna Pareeksha the cause for Vrana, type of Vedana, Agni Bala, Saatmya etc. are to be examined. Sushruta mentioned Shadvidha Pareeksha for the diagnosis. Darshana and Sparshana should be done by Panchaindriya Pareeksha.

Sthaana of Vrana (Vranavasthu)22: Site of Vrana is to be taken into consideration while examination. Twak, Maamsa, Sira, Snaayu, Asthi, Sandhi, Koshta, Marma - these eight are Vrana Vastu (dwelling seats of Vrana). In these all kinds of Vranas occur. Sushruta & Vaagbhata have mentioned Sandhi as the site instead of Medas which was mentioned by Charaka. Maadhavakara (Maadhavanidaana) explained Samaanya & Vishesha Lakshanas in case of injury to Maamsa, Sira, Snaayu, Sandhi, Asthi,Marma.

Table No. 10- Vrana Sthaana and its Lakshanas according to Maadhavakara

VRANASTHAANA LAKSHANAS

Saamanya Lakshanas:- Bhrama, Pralaapa, Pathana, Srasthangatha, Vichestana, Pramoha, Glani, Ushnata, Moorcha, Teevraruja, dischrge of Rakta resembling Mamsodaka, loss of functions of Indriyas etc.

Injury to Maamsa, Sira, Snaayu, Sandhi, Asthi

Vishesha Lakshanas

Injury to Sira Profuse discharge like Indragopa.

Injury to Snaayu

Decrease in height,drooping,loss of Pain, Vrana takes long time to heal

Injury to Sandhi Increase in Shopha ,severe pain,loss of strength, total loss of function etc

Injury to Asthi

Severe pain continuously throughout the day and night, no relief in any posture.

Injury to Maamsa Marma Pallor,loss of tactile sensation.

Shape of Vrana (Aakruthi)23: Aayatha, Chaturasra, Vrutha, Triputaka. These are the shapes of Vrana, others with abnormal shapes are treatable with difficulty. According to Vaagbhata shape of Vrana is considered according to the shape

of Shalya. Shapes of Aagantuja Vranas are Aayatha, Chaturasra,Trayastra, Mandalina, Ardhachandraakaara, Vishaala and Kutila etc.some resembling Sharaavanimna madhyascha,others with elevation in the centre or Aagantuja Vranas have innumerable shapes. Vrana Gandha24: Examination of Gandha of Vrana is also important. Eight types of Gandha are described by Charaka. i.e.Sarpi,Taila,Vasa,Pooya,Rakta,Shyaava,Amla,Pootika. These have been included in discharges by other Acharyas. Vrana Varna 25: Table No. 11- Colour of Vrana according to the involvement of Doshas

Dosha Colour of Vrana Vaata Bhasma, Kapota, Asthi, Parusha, Aruna, Krushna. Pitta & Rakta Neela, Peeta, Haritha, Shyaava, Krushna, Rakta, Kapila, Pingala. Kapha Sweta, Paandu, Snigdha. Sannipaataja Sarva Varna.

Vrana Vedana26: Table No. 12- Vrana Vedana according to Dosha involvement

Dosha Vedana Vaata Todha, Bhedana, Chedana, Taadana, Manthana, Chumachumaayana,

Nirdahana, Sphotana, Kampana, Vidaarana etc. Pitta Osha, Chosa, Daaha, Dhoomaayana, Vedana as if Kshaara is put in

Vrana. Kapha Kandu, Gurutwa, Suptata, Alpa Vedana. Rakta Similar to that of Pitta. Sannipaata All types of Vedana.

Vrana Sraava27: Sushruta and Vaagbhata have given list of discharges based on location (Vranavastu) or involvement of Doshas. Table No. 13- Vrana Sraava according to involvement of Dosha Dosha Vrana Sraava Vaata Parusha, Shyaava, Dadhimastu, Kshaarodaka, Maamsa-

dhaavana,Pulakodaka. Pitta Gomeda, Gomootra, Shanka, Kashaayodaka, Maadhveeka Taila etc. Kapha Navaneeta, Kaseesa, Majja, Naarikelodaka,Varaahavasa. Raktha Like Pitta but more of Raktha Sraava. Sannipaataja Naarikelodaka, Priyanguphala, Kaanjeeka etc. Table No. 14 - Vrana Sraava according to Sthaana

Sthaana Sraava Twak Salilaprakasha, Peetaavabaasa. Maamsa Sarpiprakasha ,Sheeta, Picchila. Sira Rakta Atipravruthi, Pooya comes out after

Paaka. Snaayu Snigdha, Ghana, Singhanaka pratima, Sarakta. Asthi Discharge mixed with Rakta, Majja. Sandhi Picchila, Saphenarudhira. Kostha Discharges Asruk, Mootra, Pureesha, Pooya,

Udaka. Features of Sraava mentioned Vaagbhata is similar to Sushruta. Charaka has explained 14 types of Sraava they are Laseeka, Jala, Pooya,Asruk, Haridra, Aruna, Pinjara, Kashaaya, Neela, Haritha, Snigdha, Rooksha, Sita, Asita. Saadhyaasadhyatha: Sukha saadhya Vrana28:

Characters:

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±dg. ±dj. 23/3 Vrana arising in Vayah (Vrana heals quickly because of Pratyagra Dhaatus),Dhruda(Body having Sthira,Bahu Maamsa, Shastras even though used in treatment do not cause damage to the Siras, Snaayus etc),Praanavanta(Do not become exhausted by Vedana, Abhighaata etc) and Satwavanta(Do not suffer from Vedana caused by Dhaaruna Kriya).

Vranas arising in Twak, Maamsa as Adhisthaana. Aayatha, Chaturasra, Vrutha, Triputa Aakruthi Vranas. Vranas treated by good Vaidyas & patient who is Aatmavantha. Vranas situated in Sphik, Paayu, Prajanana, Lalaata, Ganda, Oshta, Prusta,Karna,Phalakosha, Udara etc.

Location of Vrana in easily approachable site.

Vranas of recent origin & not associated with Upadravas.

Kruchrasaadhya Vrana29: Characters:

Vranas arising in Vruddha, Krusha,Alpapraana,Bheeru etc.

Vranas having Vikruta Aakruthi.

Vranas situated in Akshi, Dantha, Naasa, Apanga,

Srotra,Naabhi,Jatara,Sevani,Nitamba,Parshwa,Kukshi,

Vaksha,Kaksha etc.

Vranas of those suffering from Kushta, Visha, Shosha,

Madhumeha. Vrana associated with complications. Vranas treated by quacks & patient who is Anaatmavantha. Vranas which exude Phena, Pooya, Anila, having Shalya,elevated, Bhagandara etc. Yaapya Vrana30: Characters: Vranas of Avapaatika, Niruddhaprakasha, Sanniruddha Gudha, Jatara, those suffering from Twak Dosha, Prameha, Kantashaalooka, Dantasharkara etc. Asaadhya Vrana31: Characters: Vrana in spite of being situated in location not near Marma Sthaana, free from Siras, Sandhis, Asthi, spreads all over the body. Vranas which are elevated like Maamsapinda with excessive discharge, containing Pooya inside associated with Vedana, having Oshta like Ashwa Apaana, indurated and protruded like Goshringa, those discharging Dushta Rudhira,Tanu,Sheeta,Picchila Sraava, elevated in centre, some are

Santoolavath contains Snaayu, Jaalas, having Durdarshana, Vranas due to vititated Doshas discharging Vasa, Meda, Majja, Mastulunga, Koshtastha Vrana having discharges of Peeta or Asita Varna, Mootra, Pureesha etc. and also those having discharges of Pooya and Rakta. Vranas situated in all ground materials (Sarvotogatha) with Anumukha and Maamsa Budbudha. Vranas situated in Shira, kantha from which air escapes making sound. Vranas in Heena Maamsa person discharging Pooya, Rakta, associated with Arochaka, Avipaaka, Kaasa, Swaasa like Upadravas. Bhinna Vrana in Shira, Kapaala, followed by appearance of Mastulunga, features of all the 3 vitiated Doshas or Kaasa & Swaasa are incurable. Vranas discharging Vasa, Majja, Mastulunga are curable if caused by Aagantuja Kaaranas, otherwise it is incurable (i.e. those caused by Doshas). Vranas with Pulakodaka like Sraava from Pakvaashaya, Kshaarodaka type of Sraava from Raktaashaya, Kalaaya type of Sraava from Aamaashaya & Trikasandhi Pradesha.

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If proper treatment is not done Saadhya Vrana becomes Yaapya, Yaapya becomes Asaadhya and Asaadhya may kill the patient. Vrana Chikitsa32: Vranithaagaara: Vrana Chikitsa should be done in Vranithaagaara to prevent the invasion of Nishacharas in Vranithasya. It should be auspicious and in accordance with Vaastushaastra etc. Vranitha will not suffer from physical, mental & traumatic disorders by residing in such Aagaara.Rakshakarma should be done along with Dhoopana.

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±dg. eŸd. 1/9

In Dushta Vrana Oordhava and Adaha Shodhana should be done then Apatarpana, Raktamokshana should be employed. Kashaaya of Aaragwadhadi & Surasadi Ghana Dravyas should be used for Dhaavana & Taila prepared with Kashaaya of same Dravyas or with Kshaara Drava is used for Vrana Shodhana. Charaka has mentioned 36 Upakramas for the treatment of Vrana where as Sushruta has mentioned 60 Upakramas among them Kashaaya,Kalka, Varthi, Sarpi, Taila, Rasakriya, Avachoorna these 7 are both Shodhana as well as Ropana. Charaka has explained Samaanya and Vishesha Chikitsa for Vrana33 Samaanya Chikitsa: Vranitasya should be given Shodhana, therapies through Vamana or Virechana.Venesection with help of Shastra and Basti. When body becomes Shuddha Vrana gets healed up spontaneously. Vishesha Chikitsa: Vaataja Vrana Chikitsa: Person suffering from Vaataja Vrana should be treated with Sampoorana, Snehapaana, Swedana,Upanaaha,Pradeha, Parisheka which are of unctuous nature. Pittaja Vrana Chikitsa: Person suffering from Pittaja Vrana should be treated with Pradeha, Parisheka, Sarpipaana, Virechana prepared by

Sheetala, Madhura, Tikta Dravyas. Kaphaja Vrana Chikitsa: Person suffering from Kaphaja Vrana should be treated with Pradeha, Parishechana,prepared of drugs which are Kashaaya, Katu, Rooksha,Ushna and Langhana, Paachana etc. Saptaupakramas 34: These are mentioned in treatment of Vrana Shopha they are Vimlaapana,Avashechana,Upanaaha,Paatana,Shodhana,Ropana,Vaikritaapaham Sushruta has mentioned Trividha Karmas for management of surgical disorders,they are35 1) Poorva Karma 2) Pradhaana Karma 3)Paschat Karma. Poorva Karma: Among 60 Upakramas from Apatarpana to Virechana(mentioned for Vranashopha) these are considered as measures of Poorva Karma. By means of these measures either pacification of Vrana Shopha occurs or it becomes ripened. Among 7 Upakramas of Vranashopha Vimlaapana, Avashechana, Upanaaha these 3 should be employed during the Aama Avastha of Vrana Shopha. Pradhaana Karma: Among 60 Upakramas starting form Chedana to Seevana (Shastrakarma) are considered as Pradhaana Karma.

In addition to Ashtavidha Shastra Karmas, Dharana Karma is mentioned in case of Baala, Vruddha, Bheeru and Vrana Shopha present in Marma Pradesha where Shastra Karma is contraindicated. This is performed by doing Peedana with local application of Dravyas. Among 7 Upakramas of Vranashopha Paatana is considered as Pradhaana Karma. Paschat Karma: Among 60 Upakramas starting from Sandhaana to Rakshavidhaana or among 7 Upakramas Shodhana, Ropana and Vaikrutaapaham are considered under Paschat Karma. 1)Vimlaapana: In case of Sthira, Mandha Ruja Vrana Shopha after doing Snehana and Swedana to the part Peedana should be done with bamboo tube or palm and sole or thumb. 2)Avashechana: In case of Shopha of recent onset, Raktamokshana should be resorted in order to mitigate the Vedana and Paaka. Even in Vranas associated with Shopha, which are Katina, containing Rakta, Vedanayukta, deep seated Rakta Avashechana should be done. In case of Shopha associated with Visha, Rakta Visraavana should be done by using leech or by Shastra Padha in order to mitigate Vedana and prevent Paaka. 3)Upanaaha: It should be applied in Aamaavastha and Vidagdhaavastha of Vrana Shopha.It pacifies the former and ripens the later. 4)Paatana: It should be done in case of Pakwa Shopha only.

5)Shodhana: It is one of the important measures in case of Vrana Chikitsa.Among 60 Upakramas as mentioned earlier Kashaaya, Varti, Kalka, Sarpi, Taila, Rasakriya and Avachoornana are the different methods for Shodhana.In case of Vrana associated with Durgandha, Kledha and Picchila Shodhana should be done using Kashaaya of various Dravyas. Shodhana Taila: In case of Vrana which has Utsanna Maamsa, Alpasraava etc.Shodhana should be done with sesamum oil mixed with musterd oil. 6)Ropana: Ropana Kriya should be adopted in Vranas which are having the features of Shuddha Vrana . Kashaaya, Varthi, Kalka, Sarpi, Taila, Rasakriya and Avachoornana are the different methods for Ropana. Ropana Taila: In case of Vranas which are predominent in Kapha and Vaata Ropana should be done by Taila processed with Dravyas. 7)Vaikrutaapaham: Even after complete healing of Vrana restoration of normal colour, shape are essential. So Vaikrutaapaham is such measure which helps in restoration. For this Krishna Karma, Paandu Karma, Romasanjanana, Lomaapaharana etc are mentioned. Table No.15- Upakramas of Vrana acc.to various Acharyas36:

Uapakrama Sushruta Charaka Kashyapa A.San/A.H Apatarpana + - - - Aalepa + - Pralepa Pradeha Parisheka + - + + Abhyanga + - - + Swedana + + - + Vimlaapana + - - +

Upanaaha + - + - Paachana + - - + Visraavana + - + + Sneha + - + - Vamana + - - + Virechana + - - + Chedana + + - - Bhedana + Paatana - - Dhaarana + - - + Lekhana + + - - Eshana + + - - Aharana + - - - Vyadhana + + - - Sraavana + - - - Seevana + + - - Sandhaana + + - - Peedana + + (Avapeedana) - + Shonitasthaapana + - - - Nirvaapana + + - + Utkaarika + - - - Uapakrama Sushruta Charaka Kashyapa A.San/A.H Kashaaya + Shodhana,Ropa

na Kashaaya. - -

Varti + - - + Kalka + - + - Sarpi + Shodhana

Ghrita,Ropana Ghrita.

- Ropana Ghrita.

Taila + Shodhana Taila,Ropana

Taila

- Ropana Taila.

Rasakriya + - - + Avachoornana + + - Choorna. Vranadhoopana + + (Kaatinyakara,

Maardhavakara) - +

Utsaadana + + - + Avasaadana + + - + Mrudukarma + Maardhavakara

Aalepana. - +

Dhaarunakarma + Kaatinyakara Aalepana

- +

Kshaarakarma + + (Daaha) - + Agnikarma + + (Daaha) - + Krishnakarma + Varnya Savarneekara

na Savarnakara

na

Paandukarma + Varnya Savarneekarana

Savarnakarana

Pratisaarana + - - - Romasanjanana + + (Lomarohana) - + Lomaapaharana + - - - Bastikarma + - - - Uttarabasti + - - - Bandha + + + - Patradhaana + Patrachaadana

(Baahya) Patrachaadana (Abhyantara)

- -

Krimighna + - - - Bhrimhana + - - - Vishaghna + - - - Shirovirechana + - - - Nasya + - - - Kavaladhaarana + - - - Dhooma + - - - Madhu-sarpi + - - - Uapakrama Sushruta Charaka Kashyapa A.San/A.H Yantra + - - - Aahaara + Bhojya - - Rakshavidhaana + - - - Shophaghna - + - - Shamana - + + - Chaadhana - + - - Shodhanalepa - + - + Ropanalepa - + - + Ropana - + + - Utklinnaprakshaalana

- - + Prakshaalana.

Shodhana - - + - Pracchanna - + - -

In Sapta Upakramas also we can incorporate 60 therapeutic measures. Table No. 16

7 Upakramas 60 Upakramas

Vimlaapana Aptarpana, Aalepa, Parisheka, Abhyanga, Swedana, Vimlaapana.

Avashechana Visraavana, Sneha, Vamana, Virechana.

Upanaaha Upanaaha, Paachana.

Paatana Chedana, Bhedana, Dhaarana, Lekhana, Eshana, Aharana, Vyadhana, Visraavana, Seevana.

Shodhana, Ropana

Sandhaana, Peedana, Shonitasthaapana, Nirvaapana, Utkaarika, Kashaaya, Varti, Kalka, Sarpi, Taila, Rasakriya, Choorna, Dhoopana.

Vaikrutaapaham Utsaadhana – Rakshavidhi.

Among 36 Upakramas mentioned by Charaka, Shopaghna i.e. treatment of Vrana Shopha which involves Rakta Avashechana, Langhana, Sneha, Pralepa, Pradeha, Upanaaha etc. can be incorporated under 11 Upakramas mentioned by Sushruta for Vrana Shopha. Shastra Karmas mentioned by Sushruta can be incorporated under 6 measures mentioned by Charaka even though he has told Eshana seperately and Aharana has been covered under 6 surgical measures only. Shodhana, Ropana, Vaikrutaapaham mentioned by Sushruta can also be incorporated under those mentioned by Charaka i.e. like Shodhana- Kashaaya, Taila, Ghrita, Ropana-Kashaaya, Taila, Ghrita, Utsaadana, Avasaadana, Aalepana (Maardhavakara & Kaatinyakara) etc. So from the above it becomes evident that 60 Upakramas mentioned by Sushruta can be incorporated in 7 Upakramas of Vrana Shopha and most of them among 60 can be incorporated under 36 Upakramas mentioned by Charaka. Pathyaapathya37:

Pathya: Vrana patient should consume Jeerna Shaali,Odhana which is made warm unctuous& taken with Jaangala Maamsa. Soup prepared from Tanduliyaka, Jeevanti, Vaartaaka, Patola, Kaaravellaka, Daadima,Aamalaka etc. Vrana person should not sleep during day, should remain inside house devoid of breeze etc. Vrana patient should remain devoid of undesirable nails, hairs should be clean, resort to observance of propitiatory and auspicious rites. Apathya: Vrana patient should not consume Navadhaanya, Maasha, Tila, Kalaaya, Kulattha, Nishpaava, Hareetaka Shaaka, Katu, Amla, Lavana Rasa substances, Guda,Sushka Shaaka,eatables made from Pishta, Ajaa, Avika, Anoopa, Maamsa, Sheeta Udaka, Krushara, Paayasa, Dadhi, Dugdha etc. Person who is habituated to drinking Madhya should avoid using Maireya, Arista, Aasava, Seedhu etc. Vrana person should avoid Vaata, Aatapa, Raja, Dhooma, Atibhojana, Bhaya,Shoka, Krodha,Raatri Jaagarana, Vishamaashana, Vyayaama, Upavaasa,Chankramana etc. Upadravas38: These are mainly classified as Vranasya Upadravas,Vranitasya Upadravas

Vranasya Upadravas :- are five relating to abnormality in Aakruthi, Vedana,Gandha,Sraava, Varna. Vranitasya Upadravas:-Jwara, Atisaara, Moorcha, Hikka, Chardi, Arochaka, Swaasa, Kaasa, Avipaaka, Trushna. Charaka mentioned 16 types of Upadravas they are: Visarpa,Pakshaaghaata, Sirasthamba, Apataanaka, Moha, Unmaada, Vrana Ruk, Jwara, Trushna, Hanugraha, Kaasa, Chardi, Atisaara, Hikka, Swaasa and Vepathu. Aagantuja Vrana 39: These are caused by exogenous factors like physical, chemical, mechanical, trauma etc and produces 6 varieties of Vrana. They are classified on the basis of type,depth of injury, amount of destruction of tissue and macroscopic features. Table No.17- Aagantuja Vrana Lakshanas according to various Acharyas:

Type Sushruta A. San. A.H. M.Ni. Chinna Vrana is

oblique /straight,sepera

tion of body parts.

Chinna Vrana is further divided into five types

i.e.Ghrishta,Avakritha,Avagaada,Vilambita,Paatita.

---- Vrana is oblique/straight,

wide, causing seperation of body parts.

Bhinna Perforation/ puncture of

Mentioned Anubhinna,Bhinnotthundita,Atibhinna

Vrana occuring in

Puncture of Aashayas,dischar

Aashayas,exuding mild Sraava.

,Nirbhinna to those Vranas which occur in Koshtha.

Koshtha with small

orifice.

ging contents to the exterior.

Viddha Injury to any part of body other than

Aashaya,Uttundita.

Classified into further 8 types-Anuviddha,Uttundita,Atividdha,Nirvid

dha etc.

Vrana with small orifice

occuring anywhere other than Koshtha.

Injury to any part of body other than Aashayas and Uttundita.

Kshata Vrana which is neither Ati

Chinna nor Ati Bhinna. but

having features of both and

irregular in shape.

Considered Chinna,Viddha &Picchita as Kshata because of loss of skin

continuity.

………………..

Neither Atichinna nor Ati Bhinna but

having mild features of both & irregular in

shape

Type Sushruta A. San. A.H. M.Ni.

Picchita Flattening of any part of body along with Asthi, filled with Rakta and

Majja.

Body part with Asthi increasing in size by getting soaked in Rakta and Majja.

it is of two types with Vrana and without Vrana.

Mentioned Vidalita in

which features are similar to features

mentioned in Sushruta.

Flattening of any part of body

along with Asthi, filled with Rakta

and Majja.

Ghrista Peeling of skin of any part of

body accompanied with watery exudation.

Mentioned it as Twak Chedana. Exudes Laseeka alone or

mixed with lttle of Rakta

associated with

burning sensation.

Peeling of skin of any part of

body accompanied with watery exudation.

Avagaada

……………… Broad and long(Vishaala and Aayama)mentioned it as a type of

Chinna Vrana.

Severe than Ghrishta Vrana.

………….

Vichinna

……………… ……………. Severe than Avagaada

Vrana.

…………….

Paatita ………………..

Body part getting detached or seperated completely from body.

Injured body part

gets seperated

from body.

……………….

Pravilambhi

……………… ………………… Vrana in which Asthi remains in

place.

………………

Vilambita

……………… Vrana in which little of Asthi,Snaayu etc remains as residue.

…………………

……………..

Avakrutha

……………… Abrasion of Twak and little of Maamsa.

…………….

…………………

Chikitsa40: 1) Saamaanya Chikitsa: Immediate general treatment is to pacify the Ooshma released at the site of injury by Sheetala Kriya’s(cooling measures )[ i.e.like that of Pitta Chikitsa] along with use of Madhu, Ghrita for Shodhana. Sadhyo Vrana which has severe pain should be washed in warm Yashti Ghrita or Bala Taila often in order to mitigate the heat of Vrana. Drugs which posses Kashaaya,Sheeta,Madhura,Snigdha properties should be made use for Lepa. Snehapaana,Parisheka,Swedana,Lepa,Upanaaha,Snehabasti prepared from Vaatahara drugs should be adiministered.

Agatunja Vrana can be cured by Mantra,Agada and external application of drugs in the form of paste. 2)Vishesha Chikitsa: Chinna,Bhinna,Viddha Vranas --- Snehapaana,Seka,Upanaaha with Veshavaara,Krushara,Swedana with cereals, Snigdha lepa,Sneha Basti with Vaataghna Oushadha,Snigdha Sneha is prescribed Ghrishta Vrana -----In order to pacify Ushna, Sheetala Aalepa, Parisheka should be done. These should be treated with Choornas (of Saala,Arjuna etc.) after relieving pain (by applying Madhuka ,cold etc.) Picchita Vrana ---- Sheetala Lepa,Pariskeka should be done. Avakrita Vrana ---– Use of Kalka. Vicchinna and Pravilambita Vrana --- Seevana,Bandhana,Avapeedana should be done. Viddha Vrana---Removal of Shalya.

1) S.Chi. 1/6. 2) S.Soo. 21/40; A.San.Ut. 29/2. 3) S.Chi. 1/3; Ch.Soo. 19/7, Ch.Chi. 25/5,6; A.San.Ut. 29/3; A.H.

25/1,2a. 4) Ch.Chi. 25/20,21. 5) S.Soo.23/19,20. 6) S.Soo. 21/19-23; Ch.Chi. 25/6,7. 7) S.Chi. 1/6. 8) S.Chi.1/7; Ch.Chi.25/11; A.H.Ut.25/5,6; A.San.Ut.29/7; Ka.Sam.Dvivraneeya.Chi.8th sloka; M.Ni.42/2. 9) S.Chi.1/7;Ch.Chi.25/13;A.San.Ut.29/8;A.H.Ut.25/7,8;M.Ni.42/

3;Ka.Sam.Dvivraneeya.Chi.8th sloka. 10)S.Chi.1/7;Ch.Chi.25/15;A.H.Ut.25/9;A.San.Ut.29/9;M.Ni.42/4; Ka.Sam.Dvivraneeya.Chi.8th sloka. 11) S.Chi.1/7;A.San.Ut.29/10;A.H.Ut.25/10;M.Ni.42/4. 12) S.Chi.1/7. 13) S.Chi.1/7.

14) A.San.Ut.29/4;A.H.Ut.25/2a. 15) S.Soo.22/7;Ch.Chi.25/24,25,83;A.San.Ut.29/5;A.H.Ut.25/2- 4;M.Ni.42/7.

16) S.Soo.23/18,S.Chi.1/7. 17) S.Soo.23/18,S.Chi.1/7;Ch.Chi.25/86;A.San.Ut.29/12; A.H.Ut.25/11b-12a;M.Ni.42/8. 18) S.Soo.23/19;A.San.Ut.29/31;A.H.Ut.25/22;M.Ni.42/9. 19) S.Soo.23/20;M.Ni.42/10. 20) Ch.Chi.25/10. 21) S.Chi.1/134;Ch.Chi.25/22,23. 22) S.Soo.22/3,Ch.Chi.25/26;A.San.Ut.29/13;M.Ni.43/18-24. 23) S.Soo.22/5,S.Chi.2/5,6,8a;A.H.Soo.28/18. 24) Ch.Chi.25/27. 25) S.Soo.22/12. 26) S.Soo.22/11. 27) S.Soo.22/8;Ch.Chi.25/28,29a;A.San.Ut.29/13-21. 28) S.Soo.22/4,23/3,5;A.San.Ut.29/22,26;A.H.Ut.25/13,14. 29) S.Soo.22/5,6b,23/4,6,7;Ch.Chi.25/29-35,37; A.San.Ut.29/25-27;A.H.Ut.25/15-17. 30) S.Soo.23/8,A.San.Ut.29/28. 31) S.Soo.23/12,14;Ch.Chi.25/37,A.San.Ut.29/29,30; A.H.Ut.25/19-21. 32) S.Soo.19/3-8,S.Chi.1/9,S.Chi.2/86-88. 33) Ch.Chi.25/38,39a,Ch.Chi.25/12,14,16. 34) S.Soo.17/17,18. 35) S.Soo.5/3. 36) S.Chi.1/8;Ch.Chi.25/39-43;A.San.Ut.Chapt-30; A.H.Ut.Chapt25;Ka.Sam.Dvivraneeya Chi-10th sloka. 37) S.Soo.19/16-20,23,32-36;A.San.Ut.30/88;Ch.Chi.25/97,98. 38) S.Chi.1/138,139;Ch.Chi.25/29b-31a;M.Ni.43/25,26. 39) S.Chi.2/8-11,19-22;A.San.Ut.31/2-5;A.H.Ut.26/1-5; M.Ni.43/2-4,11-14. 40) S.Chi.1/4,S.Chi.2/2327,76b;Ch.Chi.25/8a;A.San.Ut.31/6,7,12; A.H.Ut.26/14b,15,28a,A.H.Ut.26/6,7,12.

In the universe everything is a medicine depending on the user. Due to vividities in the manifestation of Vrana, the various recipes of external application and internal administration are available. In case of external application various formulations for debridement are mentioned such as Kwaatha, Kalka, Choorna, Rasakriya, Varthi, Taila and Ghrita depending on the Avastha of Vrana. In the present study use of Jatyadi Taila for external application, Triphala Guggulu and Gandhaka Rasayana for internal administration were taken up. At this juncture the study of the drugs with regards to its mode of action and ] combination is necessary. Jatyadi Taila1: Ingredients: Jaati,Nimba,Patola,Naktamaala,Siktaka,Madhuka,Kusta,Haridra, Dhaaruharidra,Katurohini,Manjistha, Padmaka, Lodhra, Abhaya, Nilotpala, Tutha, Saariva, Taila (Tila).

Table No.18 - Description of ingredients of Jatyadi Taila:

Dravya Paryaaya Latin name

Family Useful part

Chemical composition

Rasa Guna Veerya

Vipaaka

Prabhaava

Karma

Jaati Sumana, Chetika

Jasminum officinale

Oleaceae Patra, Puspha, Moola.

Salicylic acid, Jasminine

Tikta, Kashaaya

Laghu, Snigdha, Mrudu

Ushna

Katu - Kapha, Pitta, Vaata Hara

Nimba Tiktaka, Pichu- marda

Azadirachta indica

Meliaceae Panchangas.

Bark-nimbine, Margosine, nimbidine

Tikta, Kashaaya

Laghu Sheeta

Katu - Kapha, Pitta Shaamaka, Pootihara, Kushtaghna, Kandooghna, Shodhana, Ropana, Vedana sthaapana

Patola Kulaka, Raaji- Phala

Tricho santhus dioca

Cucurbitaceae

Patra. Fruit-protein, fat, Calcium, Mg

Tikta Laghu, Rooksha,

Ushna

Katu - Vaata Pitta Kapha Hara, Vrana Shodhana, Ropana, Vedanasthaapana

Naktamaala

Karanja, Snigdha patra

Pongamia pinnata

Legu- minosae.

Patra, Twak, Beeja.

Kara- njin, pongamol, pongamin

Tikta, Katu, Kashaaya

Laghu, Teekshna

Ushna

Katu - Kapha Vaatahara, Pitta Vardhaka.

Siktaka - - - - - Madhura

Snigdha, Picchila

- - - Sand- hanakara, Vrana Ropaka, Bhootaghna

Madhuka

Kleethaka, Yashtimadhu.

Glycyrrhiza glabra

Leguminosae

Moola Glycyrrhizin.

Madhura.

Guru, Snigdha

Sheeta

Madhura

- Vaata Pittahara, Vedana sthaapana, Daahashaamaka

Kushta Vaapya, Utpala

Saussurea lappa

Compositae

Moola Alkoloids inulin,saussurine

Tikta, Katu, Madhura

Laghu, Rooksha, Teekshna

Ushna

Katu - Kapha Vaatahara, Vedana -sthaapana, Rakshoghna, Durgandha naashana,Varnya.

Haridra Gouri,Nisha Curcuma longa

Zingiberaceae

Kandha Curcumin Tikta, Katu

Laghu, Rooksha

Ushna

Katu - VPK Shaamaka

Dravya Paryaaya

Latin name

Family Useful Part

Chemical Composition

Rasa Guna Veerya

Vipaaka

Prabhaava

Karma

Dhaaruharidra

Dhaarvi, Katankateri

Berberis aristata

Berberidaceae

Kaanda, Moola, Phala

Berberine Tikta, Kashaaya

Laghu, Rooksha

Ushna

Katu - KP Shaamaka, Vedana Sthaapana, Shodhana, Ropana

Katurohini

Katuka, Tikta

Picrohiza kurroa

Scrophulariaceae

Moola(Bhoumika Kaanda)

Roots-Picrorhizin

Tikta Laghu, Rooksha

Sheeta

Katu - KP Hara

Manjistha

Vikaasa, Yojanavalli

Rubia cordifolia

Rubiaceae Moola Manjistin, Rubiadin

Tikta, Kashaaya, Madhura

Guru, Rooksha

Ushna

Katu - KP Hara, Vrana Ropana

Padmaka

Padmagandhi

Prunus cerasoides

Rosaceae Twak, Beejamajja

Prunetin, Padmakastin

Kashaaya, Tikta

Laghu Sheeta

Katu Vedana Sthaapana

KP Shamana, Daahaprashamana

Lodhra Sthoolavalkala

Symplocos racemosa

Symplocaceae

Twak Loturine, Tannin

Kashaaya

Laghu, Rooksha

Sheeta

Katu - KP Shamana, Ropana, Shothahara

Abhaya Hareetaki, Pathya

Terminalia chebula

Combretaceae

Phala Chebulinic acid

Kashaaya Pradhaana, Pancharasa Alavana

Laghu, Rooksha

Ushna

Madhura

Tridoshahara

VPK Shaamaka, Shodhana, Ropana, Vedana Sthaapana

Neelotpala

Utpala Nymphoea stellata

Nymphoeaceae

Moola, Pushpa, Beeja

Protein, starch

Madhura, Kashaaya, Tikta

Laghu, Picchila, Snigdha

Sheeta

Madhura

- Daahaprashamana, Tridoshahara

Tuttha Mayooraka, Tamragarbha

- - - CuSo4. 7 H2O

Kashaaya, Madhura, Katu

Laghu, Ushna

Ushna

Katu - Lekhana, Bedhana, Medhohara

Saariva Ananta, Gopavalli

Hemidesmus indicus

Asclepiadaceae

Moola Roots-oil-P-Methoxy salicylic aldehyde

Madhura, Tikta

Guru, Snigdha

Sheeta

Madhura

- VPK Shaamaka, Shodhana, Dourgandha Hara

Tila Pavitra, Jatila

Sesamum indicum

Pedaliaceae

Beeja Seeds- Protein, Fat , Oil-Sesamin, Oleic acid

Madhura, Kashaaya(Anurasa), Tikta

Guru, Snigdha

Ushna

Madhura

- VPK Shamana, Vrana Shodhana, Ropana,

Preperation: Jaati Dhaaruharidra Nimba Manjistha Patola Katurohini Naktamaala all equal parts Padmaka all equal parts Siktaka Lodhra Madhuka Abhaya Kushta Neelotpala Haridra Tuttha Saariva Kalka of above drugs: 1 part Tila Taila : 4 parts Dravadravya(water): 16 parts Equal quantities of above drugs are taken and made into Kalka.Then Kwaatha is added to the Taila and Paaka is done. Later the Kalka is mixed with the Sneha and Paaka is done over Mridu Agni till the total water content is evaporated. Jatyadi Taila is benificial in cases of Naadivrana, Spotaka, Kacchu, Visarpa, Dagdha Vrana, Kshata by Nakha, Dhanta, Vranas due to Visha, Sadhyovrana, Kushta etc and other types of Dushta Vrana. By applying Taila on Vrana it does Shodhana and Ropana. Triphala Guggulu2: Table No. 19 - Ingredients:

Drugs Quantity Hareetaki 1 pala Vibheetaki 1 pala Aamalaki 1 pala Pippali 1 pala Shodhita Guggulu

5 pala

Ghritha Sufficient quantity

Preperation: Fine powder of Triphala, Pippali is mixed with Shodhita Guggulu Choorna in Khalva Yantra & made into paste form by adding appropriate quantity of Ghritha & grinded well. Then it is rolled into pills. Wounds which are large, painful, edematous& associated with moisture, suppuration, discharge, foul odour subsides after intake of Triphala Kwaatha mixed with Guggulu. It is also beneficial in Bhagandhara, Naadivrana, Pakva Vidradhi, Gandamaala.It removes Vibandha and acts as Vrana Shodhaka, Ropaka. Gandhaka Rasayana3: This Yoga is helpful in Dhaatu Kshaya, Prameha, Mandagni, Shoola, Koshtagata Roga, Kushta, Rajayakshma, Paama, Kandu, Vishadosha, Vaataroga, Vrana, Mootrakruchra, Jara, Valee, Palitha, Gulma and is Bala prada, Agni deepaka. Depending upon ingredients and results obtained from pilot study Gandhaka

Rasayana is taken up and preperation of same is as mentioned below. Preperation: Ingredients: Shuddha Gandhaka. Bhaavanadravyas: Gokshura, Chaturjaata, Gudoochi (Swarasa),Pathya,Aksha,Dhaatri, Bhringaraaja and Ardraka Swarasa. Shuddha Gandhaka is taken and made into powder. Then three Bhaavana is given out of each one i.e. Gokshura,Chaturjaata,Gudoochi Swarasa. Similarly 8 Bhaavanas are done (i.e with Pathya, Akshi,Dhaatri, Bhringaraaja and Ardraka Swarasa).Then after getting dried equal quantity of Mishri is added. Drug review: References:

1) Sha.Sam.Mad.Kh.9/168-171a; B.Pr.Mad.Kh.47/90-95. 2) Sha.Sam.Mad.Kh.7/82,83;Chakra.44/68,69;B.R.47/51;Y.R.Vrana Shotha Chikitsa-79,80,Vidhradhi Chi-49,50;G.N.Chapt 34.

3) A.Pr.2/46-48;R.Sa Vol -1. 1804-1815.

Modern review: The word wound and ulcer are used synonymously though it has some similar & dissimilar features. An ulcer is a discontinuity of an epithelial surface (skin or mucous membrane). It may follow molecular death of surface epithelium or it’s traumatic removal, there is usually progressive destruction of surface tissue cell by cell, as distinct from death of macroscopic portions (eg. Gangrene/necrosis)1. ] Chronic ulcers are the wounds that fail to heal, in general they have a fibrotic margin and a bed of granulation tissue which may include areas of slough (necrotic tissue). Classification of Ulcers: Two types of classification of ulcers are possible 1) Clinically 2) Pathologically.

Clinically2 Spreading ulcer Healing ulcer Callous ulcer

Surrounding skin of ulcer is inflammed,

floor-covered with slough without any granulation

tissue.

Floor-gr.tissue is present, Edge- bluish outline of

growing epithelium & slight serous

discharge.

Floor- pale gr.tissue induration- present at

base,edge, surrounding skin. Ulcer shows no

tendency towards healing.

Pathologically3 Non-specific ulcers Specific ulcers Malignant ulcers Non-specific ulcers: These are due to infection of wounds or physical, chemical agents, local irritation, as in the case of a dental ulcer or interference with the circulation e.g.: Varicose veins are predisposing causes, so according to the cause these ulcers are classified as below Mechanical e.g.: Dental ulcer of tongue from jagged Traumatic ulcer tooth. Physical e.g.: From electrical/ x ray burn. Chemical e.g.: From application of caustics. Arterial ulcer (occurs in atherosclerosis, burgers disease and raynauds disease), Venous ulcer, Neurogenic ulcer, Infective ulcer, Tropical ulcer, Cryopathic ulcer, Martorells ulcer,Bazins ulcer, Diabetic ulcer, Miscellaneous ulcers. Specific ulcers: These are seen in T.B, syphilis, soft sore and actinomycosis. Malignant ulcers: e.g.: Epithelioma, rodent ulcer and malignant melanoma.

Traumatic ulcer: Occurs due to trauma in the areas where skin is closely applied to bony prominences (shin, malleoli, and back of the heel). Characteristic features: It is circular, small in size and painful. E.g.: Foot ballers ulcer, plaster sores, dental ulcer of tongue. Arterial ulcer/Ischaemic ulcer: Occurs due to inadequate skin circulation (due to atherosclerosis, burgers and raynauds disease) in the limbs which are subjected to repeated pressure and trauma (antero lateral aspect of the leg, toes, dorsum of the foot or heel). Characteristic features: Pain is the main complaint with punched out edge and floor may expose the tendons. Venous ulcers: Occurs due to abnormal venous hypertension in the lower third of the leg, ankle and dorsum of foot (this may be associated with demonstrable varicose veins and such ulceration may follow thrombosis and phlebitis in deep and perforating veins). Characteristic features: Venous ulcers are most common on inner side just above medial malleolus of leg. These ulcers are ovoid in shape, usually single in number with irregular, thin blue margin and pale granulation tissue in the floor. Pigmentation is seen in the vicinity of ulcer. These ulcers are usually shallow and never penetrate deep fascia and are slightly painful in the beginning but gradually pain settles down. Base is fixed to deeper structures associated with seropurulent discharge & occasional trace of blood. Neurogenic ulcers /Neuropathic / Trophic / Penetrating ulcers:

Occurs due to impairment of the nutrition of tissues, inadequate blood supply and neurological deficit or repeated trauma to the insensitive part of the body. Features: These ulcers are commonly seen on the heel and ball of the foot when patient is ambulatory and on buttocks, back of heel when patient is non-ambulatory. Edge is punched out, base is slightly indurated and floor is covered with slough. Surrounding skin has no sensation and these are painless. Eg: Bed sore, perforating ulcers. Infective ulcers:

1) Pyogenic ulcer: Causes: Commonly staphylococcus, and occasionally streptococcus.Predisposing factors are anaemia, poor nutritional status.

Features: These are multiple, small, red, scabbed sores on leg or ankle. Syphilitic ulcer: Ulcers due to syphilis are seen in all 3 stages. Primary Hard chancre is seen (external genitalia) Features: Single, painless, indurated base, oval /round in shape with raised hyperaemic margin. Secondary Ulcer may develop in the form of mucous patches,

snail track or in form of condylomas. Tertiary Typical lesion in this stage is localized gumma or gummatous ulcer. Gummatous ulcer:

Gumma is syphilitic hypersensitivity reaction consisting of granular tissue with central necrosis.

These ulcers are commonly seen over subcutaneous bones (tibia, sternum, ulna and skull). Edges are punched out indolent, painless and floor is covered with wash-leather slough (yellowish gray gummatous tissue). Tropical ulcer: Characteristic feature of this ulcer is callousness towards healing. Edge is slightly raised and exudes copious serosanguineous discharge. Pain is an important symptom. Martorells ulcer: Occurs in patients who are usually hypertensive/ atherosclerotic. Cryopathic ulcer: These results from intense cold & chilly weather. Diabetic ulcer: In this slight injury to the glucose laden tissue may cause chronic infection and ulcer formation. Ulceration in diabetes may be precipitated by ischaemia due to diabetic atherosclerosis, infection or peripheral neuritis. When the ulcer is due to neuropathy a trophic ulcer results (features are same as trophic ulcer but surrounding sensation of skin will be less. When ulcer is due to ischaemia, ischaemic ulcer results but it is less painful than typical arterial ulcer.Toes and feet are normally affected. Tuberculous ulcer: Such ulcer usually develops due to bursting of cold abscess, this cold abscess may form from matted tuberculous lymph node or TB of bone or joint & from submucous lesions eg intestinal TB. Characteristic features: It is oval in shape generally with irregular crescentic border, often multiple in number with thin reddish blue, undermined edge and slightly indurated

base. It is usually shallow, accompanied with slight pain, variable amount of discharge and floor is covered with pale granulation tissue. Soft chancre/chancroid (ducrey’s): It is a contagious disease caused by gram –ve haemophillus ducreyi. 3 to 5 days after exposure multiple acute sores develop on external genetalia. These are often painful, gradually becomes pustular and ulcerate to form soft sores. These are multiple, soft, rounded, painful and readily bleed and edges are undermined. Actinomycosis: This condition causes multiple ulcers. At first area becomes indurated, nodules appear, which soften and later ulcerates in various places. Surrounding skin often looks bluish in color. Rodent ulcer/Basal cell carcinoma: It is locally invasive carcinoma of basal layer of epidermis. It is of low grade malignancy. It is commonly seen on the face, above line from corner of mouth to ear, innercanthus of eye, nose on and around nasolabial fold, has raised and pearly white beaded edge, irregular in shape and floor covered with coat of dried serum, epithelial cells. Epithelioma (squamous cell carcinoma): Occurs commonly in the dorsum of hands, in the face, limbs, lips, vulva, penis etc. It has normal temperature and usually not tender, oval or circular in shape with raised and everted edge, indurated base and floor is covered by necrotic tumour, serum & blood. Marjolins ulcer: It is the name given to a squamous carcinoma which arises in a chronic benign ulcer or scar. It is slow growing malignant lesion, painless and edge is not always raised and everted.

Miscellaneous ulcers: Ulceration of leg may be associated with gross anaemia, leukaemia, polycythemia, systemic sclerosis, RA,ulcerative colitis, poliomyelitis, arteriovenous fistula, acholuric jaundice,various collagen disorders, chronic lymph edema, cortisone ulcers etc. The life history of ulcer consists of 3 phases4

1) Stage of extension 2) Stage of transition 3) Stage of repair Stage of extension: During this stage floor is covered with exudate and slough, while base is indurated. The discharge is purulent and even blood stained. Stage of transition: This prepares for healing. Floor becomes cleaner, slough seperates, induration of base diminishes and discharge becomes more serous. Small reddish areas of granulation tissue appear on the floor. Stage of repair: It consists of transformation of granulation to fibrous tissue which gradually contracts to form a scar. The epithelium gradually extends from the new shelving edge to cover the floor. This healing edge consists of 3 zones. An outer layer of epithelium appears white, middle one appears bluish in color (where granulation tissue is covered by a few layers of epithelium) & inner reddish zone of granulation tissue covered by single layer of epithelial cells. The red color of tissue is due to high density of new capillaries. Clinical examination of an ulcer5: This should be conducted in systemic manner Local examination: The following points should be noted I.e. Site, size, shape,number,edge,floor,discharge, surrounding area etc. Inspection: Site: This is very important and often by itself gives a clue to diagnosis. 95% of rodent ulcers occur in the upper part of the face, carcinoma typically

affects the lower lip, while a primary chancre of syphilis is usually on upper lip. Size: Size of an ulcer is important to know the time required for healing. A bigger ulcer will take a longer time to heal particularly in relation to the length of history eg. A carcinoma extends more rapidly than a rodent ulcer but more slowly than an inflammatory ulcer. Shape: Tuberculous ulcers are generally oval in shape but their coalescence may give an irregular crescentic border, rodent ulcer is usually circular, varicose ulcer is vertically oval in shape, gummatous ulcer is circular or serpiginous due to fusion of multiple circles & carcinomatous ulcer is irregular in shape. Number: Tuberculous, gummatous, varicose ulcers, soft chancres may be more than one in number. Margin: It is the junction between normal epithelium and ulcer. Edge: It is an area between the margin and floor of ulcer. Margin or edge takes a characteristic shape in particular form of ulcer. Edge is an important finding of an ulcer which by itself not only gives a clue to diagnosis of ulcer, but also the condition of ulcer eg.In spreading ulcer edge is inflammed and edematous, in healing ulcer-If the edge is traced from red granulation tissue in the centre towards periphery will show a blue zone (due to thin growing epithelium) and a white zone due to fibrosis of the scar.

Table No.20 Five common types of ulcer edges are seen in surgical practice

Undermined edge Punched out Sloping /shelving Raised and pearly white beaded

Rolled out or everted

The disease causing ulcer spreads in and destroys the subcutaneous tissue faster than it destroys the skin. The over hanging skin is thin, friable and reddish blue, unhealthy e.g. tuberculosis

The edge droops down at rt. angle to skin surface as if it has been cut out with a punch e.g.gummatous ulcer, deep trophic ulcer,syphilitic ulcer (vertically punched out).

Every healing ulcer has a sloping edge, which is reddish purple in color and consists of new healthy epithelium e.g. healing traumatic or venous ulcer.

This type of edge develops in invasive cellular disease and becomes necrotic at the centre e.g. rodent ulcer.

Growing portion at the edge of ulcer heaps up and spills over the normal skin e.g. Squamous cell carcinoma /epitheloma.

Floor: This is an exposed surface of the ulcer. When floor is covered with red granulation tissue ulcer seems to be healthy and healing. In slowly healing ulcer floor is covered with smooth and pale granulation tissue, in gummatous ulcer floor is covered with wash leather slough, trophic ulcers penetrates down even to bone, so bone forms the floor & in malignant melanoma black mass at floor will be seen. Discharge: The character of discharge, smell and amount should be noted. In healing ulcer scanty serous discharge, in spreading and inflammed ulcer purulent discharge & in tuberculous ulcer/ malignant ulcer serosanguinous discharge is seen. Purulent discharge indicates active infection and blue green coloration suggests infection with Pseudomonas pyocyaneus. Surrounding area: In acute inflammed ulcer surrounding area is glossy, red and edematous and in varicose ulcer skin is eczematous and pigmented. Vascular insufficiency: Examination of this should be done when the ulcer

is situated on lower part of the leg. One should always search for varicose veins in upper part of the leg or thigh. Palpation: Edge: During palpation consistency of edge should be noted, marked induration of the edge is characteristic feature of a carcinoma. A certain degree of induration is expected in any chronic ulcer whether it is trophic/ gummatous/syphilitic ulcer. Base: It is better felt than seen. It is that on which the ulcer rests. If an attempt is made to pick up the ulcer between thumb and index finger the base will be felt. Slight induration of base is seen in chronic ulcers, marked induration of base is seen in squamous cell carcinoma and some times it is attached to deep structures eg: varicose ulcer to tibia. Depth: It can be recorded in millimeters. Trophic ulcers are as deep as to reach even the bone. Bleeding: Bleeding to touch is common feature of a malignant ulcer. Relation with deeper structures: Malignant ulcers will obviously be fixed to deeper structure by infiltration. The gummatous ulcer over a subcutaneous bone is often fixed to it. Lymph nodes: In acutely inflamed ulcers the regional lymph nodes becomes enlarged, tender and shows the signs of acute lymphadenitis. In tuberculous ulcer lymph nodes become enlarged, matted and slightly tender.In huntarian chancre regional lymph nodes remain discrete, firm and shotty and in malignant ulcers lymph nodes are stony hard and may be fixed to neighbouring structures in late stages. Tenderness: An acutely inflammed ulcer is equisitely tender. Chronic ulcers

such as tuberculous and syphilitic ulcers are slightly tender. Varicose ulcers may or may not be tender. General examination: Evidence of debility, cardiac failure, all types of anaemia including sickle cell anaemia or diabetes must be sought Pathological Examination: E.g. Biopsy will confirm carcinoma, serological and mantoux test may be of value for syphilis and TB respectively. Bacteriological examination of discharge of ulcer is important in inflammed and spreading ulcers. This will not only give a clue to type of organism present in ulcer but also its sensitivity to particular antibiotic. Examination of urine: Urine sugar to exclude diabetes is important. Routine examination of blood: TC, DC, HB%, RBC, ESR should always be done in a patient with an ulcer.Blood sugar estimation may be performed to exclude diabetes. In tuberculous ulcers- Lymphocyte count and ESR will be high.

General principles of ulcer management6a: The main aim of ulcer management is to ensure the quickest & most durable form of healing with a minimal scar. Debridement: Removal of dead & devitalized tissues or foreign material is called as debridement.It is essential to prevent the bacterial growth. It is of following types 1. Surgical debridement.

2. Chemical debridement. 3. Mechanical debridement.

Surgical debridement: Excision of dead and devitalized tissue. Chemical debridement: Debridement using chemicals like Topical agents: A wide variety of topical wound cleaning agents being

available and bacteriostatic agents being promoted for local wound application. Some of them are: Povidone iodine: Strong bactericidal for gram positive and negative organisms (it has a broad spectrum of activity but its anti bacterial effect is reduced by contact with pus or exudate). It should not be used in patients who are sensitive to iodine. Eusol6b: It is one of the hypochlorite solutions widely used in the management of open wounds left to heal by secondary intention. It consists of chlorinated lime and boric acid solution containing 0.25% Wt./ volume of available chlorine with a pH between 7.5&8.5.In dilute concentrations it kills fibroblasts, neutrophils and endothelial cells in tissue culture. Eusol delays the appearance of hydroxyproline (the amino acid marker of wound collagen content) and prolongs the acute inflammatory response. It has no role in the treatment of open wounds that are clean and healing well with no signs of invasive infection. Chlorhexidine: It is the topical antiseptic which is effective against a wide range of gram positive and negative organisms and some fungi. Hydrogen peroxide: It liberates nascent oxygen which bubbles up and opens up tissue spaces for free oxygenation and helps in separating the slough. But it delays wound healing by separating granulations and can cause haemolysis. PDGF6c: Topical application of PDGF helps to rapidly heal chronic non- healing, non malignant ulcers. It was a pilot study conducted in which PDGF derived from patients own blood was used to treat chronic ulcers. Sucralfate6d: It is basically a sugar that binds and activates fibroblast growth factor and causes it to accumulate in wound areas and stimulate epithelial cell proliferation. It exhibits antimicrobial activity against a range of micro organisms. Its antimicrobial activity is by its macrophage activity. It prevents the release of cytokines from damaged skin cells there by exerting anti-inflammatory and smoothening effect. It is absorbed and does not have any toxic, allergic and systemic effects even after prolonged use. Metronidazole as local adjunct6e: Topical preparation of metronidazole (1%)

along with sucralfate (7%) have been used to overcome the problem of inadequate drug delivery due to poor blood supply. Both of them have shown to promote the accumulation of beta EGF and thus enhance reepithelialization, facilitates angiogenesis and granulation tissue formation. Oxpentifylline6f: It has been found to have fibrinolytic effect and to influence the behaviour of white cells. Experimental studies says that healing rates of venous ulcers of the leg will be increased appreciably by the addition of oxpentifylline to a standard regimen of dressing and compression bandaging. Collagen dressings: They significantly hasten the healing rates and reduction in wound nuisance like discharge, soakage. Mechanical debridement: Debridement by using flushing therapy or hydrotherapy etc. Filling dead space: Dead space promotes anaerobic infection. So in order to achieve healing from the base of a large cavity insert packing which prevents cavity collapse but does not add to the wound tension. Protecting adjacent skin: It is important as a moist environment promotes maceration. Treatment of underlying disease. Table No.21-Classification of commonly used antiseptics in general surgical practice7

Name of antiseptic

presentation Uses comments

Chlorhexidine(Hibiscrub)

Alcohol-0.5% Aqueous-4%

Skin preparation Surgical scrub in dilute solutions in

open wounds

Has cumulative effect. Effective against gram positive organisms & relatively stable in

presence of pus, body fluids. Povidone- iodine Alcohol-10%

Aqueous-7.5%

,, Safe, fast acting broad spectrum. Sporicidal activity, anti-fungal. Iodine is not free but combined

with polyvinylpyrrolidone.

Cetrimide(savlon)

Aqueous Hand washing, Instrument and

surface cleaning.

Pseudomonas species may grow in stored contaminated solutions.

Alcohols Hypochlorites

70% ethyl, isopropyl aqueous

preparations(eusol, Milton,

chloramine T)

Skin preparation, instrument &

surface cleaning (debriding agent

in open wounds?)

Should be reserved for use as disinfectant

Hexachlorophane

Aqueous bisphenol

Skin preparation, hand washing.

Has action against gram negative organisms.

Treatment of different types of ulcers8: It can be dealt under the following headings.

1) Treatment of spreading ulcers: After obtaining pus c/s report appropriate antibiotics are given. Many solutions are available to treat the slough like hydrogen peroxide or eusol.

2) Treatment of healing ulcers: Regular dressings are done for few days

with antiseptic creams like liquid iodine, Zinc oxide or silversulphadiazine preparation. A swab is taken to rule out the presence of streptococcus haemolyticus which is contra indication for skin grafting. If the ulcer is small, it heals by itself with epithelialisation from the cut edge of ulcer. If the ulcer is large, free split skin graft is applied as early as possible.

3) Treatment of chronic ulcers: These do not respond to conventional

methods of treatment. Some special forms of treatment are available, their usefulness is doubtful. They are as follows: infrared radiation, short-wave therapy, u.v-rays decrease the size of ulcer, amnion helps in epithelialisation, chorion helps in granulation tissue.

4) Treatment of non-specific ulcers: Any underlying cause is treated eg:

varicose veins, diabetes arterial disease. Many lotions and nonadhesive applications are used to aid the separation of sloughs, hasten granulation and stimulate epithelialisation.Hypochlorite solution and 0.5% AgNo3 are popular in the earlier stages and later 1% Zinc sulphate solution .Ointments and creams used include Zinc

oxide and 1% hydrocortisone. Excessive granulation needs to be discouraged by excision, curettage or by the application of caustics such as Silvernitrate.

Wound dressings9: Hydrocolloid dressings such as granuflex or comfeel consist of a thin polyurethane foam sheet bonded on to a semi permeable polyurethane film which is impermeable to exudates and microorganisms, when the dressing comes into contact with wound exudates it interacts to form a gel which expands into the wound. The moist conditions produced under the dressing promote angiogenesis and wound healing without causing maceration. A hydrocolloid dressing can be applied to small wounds containing dry slough or necrosis, the dressing prevents the loss of water vapour from the skin surface and this effectively rehydrates the dead tissue which is then removed by autolysis. Hydrogel: Is a pale yellow/colorless transparent aqueous gel, when it comes into contact with wound, the dressing absorbs excess exudates and produces a moist environment at the surface of wound without causing tissue maceration. Lyofoam: Is a low-adherent comfortable polyurethane foam sheet, the side of the dressing that is to be placed in contact with skin has been heat treated to render it hydrophilic, whilst the outer surface remains hydrophobic. The dressing is freely permeable to gases and water vapour but resists the penetration of aqueous solutions and exudates. The dressing maintains the moist warm environment at the surface of the wound, which is conducive to granulation and epithelialisation.

Wound10:

Definition: It is the discontinuity or break of the surface. It is of 1) Simple: When only skin is involved.

2) Complex: When it involves underlying nerves, vessels, tendons etc.

From practical point of view wounds are classified into: 1) Tidy wounds- Contains no devitalized tissues, inflicted by sharp

instruments. 2) Untidy wounds- These result from crushing, tearing, avulsion etc

and contain devitalized tissue. Types of wounds:

1) Incised wounds- Caused by sharp objects, edges of the wound are sharp. Tends to gape and bleed freely.

2) Lacerated wounds- Caused by blunt objects, edges of the wound are

jagged. Causes minimal bleeding because of crushing.

3) Penetrating wounds- (variation of punctured wound)- Stab injuries of

abdomen are notorious, depth is more. 4) Crushed or contused wounds- Caused by blunt trauma. 5) Abrasion- Caused by scraping away of superficial skin layer and is

very painful. Dangers and complications of wounds:

1) Haemorrhage- external or internal. 2) Damage to important deeper structures or vital organs. 3) Swelling- may cause local tissue hypoxia and pain. 4) Infection. 5) Scar-causing dysfunction, deformity or disfiguration.

Infection11: It is a biological accident where in the pathogenic micro organism invades body by contamination of tissues from with in or out side and sets the pathological manifestations. Two factors govern the onset and development of infection- viz.,

1. Virulence of micro organisms: It is markedly enhanced by

toxigenicity (production of toxin).These are of two types:

(i) Exotoxins- Toxin is liberated from the surface of living bacteria. These are produced by gram positive bacteria. (ii) Endotoxins- These are produced by gram negative bacilli only when they die out and liberating there contents.

2. Resistance of host: It is the result of integrated sequential function of

its immune apparatus consisting of polymorphs, lymphocytes etc.

Following are some of the important organisms of infection Table No. 22-Gram positive cocci

Organism Site & Spread Principal infections

Antibiotic sensitivity

Staphylococcus aureus

Lives in naso pharynx, present in infected discharges. Spread by contact, air borne etc.,

Infections are usually localized eg: Boils, Styes, Carbuncle, Septic hands, wound infections etc.,

Most of the strains are resistant to Penicillin because they produce penicillinase. They are sensitive to Flucloxacillin & Methicillin.

Streptococcus Lives in pharynx. Spread by air borne from respiratory, contact.

Infections tend to spread eg: Erysipelas, cellulitis, puerperal sepsis, tonsillitis etc.

Highly sensitive to Penicillin.

Table No.23-Gram negative bacilli Organism Site & Spread Infections Antibiotic

sensitivity E.Coli Normal inhabitant

of large bowel UTI, Peritonitis, Contaminated wounds, Intra abdominal sepsis.

Most of them are sensitive to ampicillin, gentamycin.

Klebsiella ’’ ’’ Resistant to ampicillin

Pseudomonas aeruginosa

Large bowel Attacks damaged and moist tissues such as burns, urinary tract and tracheostomy wounds with production of characteristic blue geen pus.

Sensitive to gentamycin and some cephalosporins.

Table No.24-Anaerobic organisms Organisms Site & Spread Infections Antibiotic sensitivityGram positive cocci eg: clostridium species, peptococci, streptococci.

Widely found in nature particularly faeces, colon, rectum, oropharynx, vagina etc,.

Abdominal sepsis, wound infections with severe local pain

Sensitive to penicillin and metronidazole.

Gram negative bacilli. Eg; bacteroides fragilis.

Large bowel, vagina, oro pharynx.

Intra abdominal sepsis, pelvic sepsis

Sensitive to metronidazole and some cephalosporins.

Types of infection12 :

1. Wound abscess. 2. Cellulitis and lymphangitis. 3. Bacteraemia. 4. Septicaemia.

Wound healing13 : The word healing means replacement of destroyed tissue by living tissue i.e. it is the body response to injury in an attempt to restore the normal structure and function. In the context of wound healing two terms should be understood.

1. Regeneration – When healing takes place by proliferation of parenchymal cells and usually results in complete restoration of the original tissues. 2. Repair – When healing takes place by proliferation of connective tissue elements resulting in fibrosis and scarring. At times, both the processes take place simultaneously. Healing of skin wounds provides a classical example of combination of regeneration and repair. This can be accomplished in one of the following two ways. (i). Healing by first intention (primary union) - This is defined as healing of wound which as following characteristics:

Clean and uninfected wounds, Surgically incised wounds, Wounds with out much loss of cells and tissues, Edges of wounds or approximated by surgical sutures.

i.e. Healing by first intention is one in which healing occurs with minimum scarring. (ii). Healing by second intention (secondary union) - This is defined as

healing of a wound having the following characteristics:

Open wounds with a large tissue defect at times infected, Wounds having extreme loss of cells and tissues, Wound which is not approximated by surgical sutures but is left open.

i.e. Healing by second intention is one in which wound heals with more scar tissue and takes longer time to heal. An ulcer heals in the same way. Factors influencing wound healing14

1. General factors. 2. Local factors.

General factors: 1.Age: Healing is fast in the young. 2.Nutrition15: It is a vital component in optimizing the wound healing

environment. It provides the raw materials needed for the wound repair and

the prevention of infection. Wound healing depends upon the adequate

intake and absorption of nutrients such as vitamins, minerals, proteins and

calories. Delayed wound healing occurs if nutritional supplies are lacking

due to intake (malnutrition), abnormal absorption (GIT disease or Surgery),

increased metabolic demands. Vitamins play significant role in promoting healing. They are given usually to supplement the patient’s diet. Vitamin C plays an important part in wound healing process as it affects collagen synthesis, immune function and

decreases capillary fragility. Vitamin A enhances the process of collagen synthesis and epithelialisation. In addition it counteracts the anti inflammatory effects of steroids and cell membranes.

3) Oxygen and its role in healing16:

Oxygen has a significant role in wound healing being essential to provide

additional energy source for the repairing process. Oxygen may infact be

the rate limiting step in early wound repair. Many other components in

addition to oxygen are interrelated to provide the optimal environment

for healing including nutritional state, immune function, cardio pulmonary function etc.

4) Hormones: Corticosteroids inhibits granulation tissue formation.

5) Other conditions which delay or hamper healing are uraemia,

jaundice, anaemia, diabetes, cytotoxic drugs, and malignant diseases. Local factors:

Position of skin wounds- Skin wounds parallel to lines of Langer heal faster.

Blood supply- Wounds with poor blood supply heal slowly. Tension – Healing is jeopardized if the wound is in tension. Infection& Movement – Delays healing. Necrosis- Obviously retards healing. UV light- Exposure of wounds to UV light accelerates healing. Exposure to ionizing radiation- Affects the vascularity and causes

delay in granulation tissue formation. Lymph drainage- Impairment of lymph drainage causes edema of

part, jeopardizes the process of healing.

Wound healing is the summation of a number of processes which follow injury including coagulation, inflammation, matrix synthesis and deposition, angiogenesis, fibroplasias, epithelialisation, contraction, remodeling and scar maturation. The four basic processes which take place in wound healing are

1. Inflammation. 2. Wound contraction. 3. Epithelialisation. 4. Granulation tissue formation.

Inflammation:

Schematic representation of phases of inflammation.

Injury

Initial haemorrhage

Inflammation starts

Haemostasis

Appearance of polymorphs

Diapedesis

Migration

Phagocytosis

Immediately after disruption of tissue integrity either by accidental trauma

or by surgeon’s knife, inflammation starts.

Sequence in inflammation: The inflammatory phase is triggered by two

classes of mediators (soluble signal factors) - those controlling vessel

permeability and those attracting or trapping cells. The clinical signs of

inflammation are caused by changes in blood vessels with dilatation leading

to erythema and endothelial cell separation allowing plasma extravasation,

producing localized swelling. There are overlapping stages but, in general,

the order of arrival at the wound site from an intravascular space is thought

to occur in the following sequence: plasma with soluble components and

cellular constituents, first platelets, then neutrophils, followed by monocytes

and lymphocytes. The migration of epithelial cells to resurface the injured

tissue begins during this phase, mediated by the above events.

Alterations in microvascular permeability after injury allow both fluid and

plasma components to pass to the tissue. Vasoactive amines and peptides

(including histamine from mast cells, serotonin from platelets, and

bradykinin from neutrophils) cause the reversible opening of junctions

between endothelial cells and allow the passage of neutrophils and

monocytes.

Platelets:

The earliest circulating cell or cell fragment detected in the injury site is the

platelet. Platelets contain three types of organelles involved in haemostasis

and initiation of the inflammatory phase, they are

1. Alpha-Granules

2. Dense body granules

3. Lysosomes

The above substances are released when the platelets are activated by

various factors. When injury occurs, contact is made between platelets and

insoluble components of the subendothelial matrix, particularly collagen,

promoting the release of alpha-granule contents which then trigger the

coagulation process. The activation of platelets is enhanced by some of the

complement factors and by bacterial lipopolysaccharides. The latter produce

a 50-fold increase in the amount of serotonin released.

Activated platelets become sticky and aggregate to form a plug that

temporarily occludes small vessels. Both damaged platelets and tissues

release thrombokinase, which converts prothrombin to thrombin, and this in

turn ensures the conversion of soluble fibrinogen to insoluble fibrin. The

release of serotonin and adenine nucleotides contained in the dense bodies of

the platelets induces the aggregation of platelets, which interact with the

fibrin network to form a clot which is stronger and more durable than the

initial platelet plug. If the clot is allowed to dehydrate, it transforms to a dry

eschar (scab) covering the wound.

Other substances released by the alpha-granules, such as platelet derived

growth factor (PDGF), and by the dense body, such as cyclic adenosine

monophosphate (cAMP) are chemotactic for neutrophils.

Accumulation of neutrophils:

Adhesion: Interaction between damaged tissue and serum releases the

complement factor C3, and the C3e fragment of this provokes the release of

neutrophils from the bone marrow. At the same time, circulating leucocytes

near the wound site, particularly neutrophils, cease to flow and adhere to the

endothelium. It has been shown in vitro that adherence is enhanced by

inflammatory mediators, such as C5a (the fifth component of complement),

platelet-activating factor, and leukotriene. There is a very fast initial

response, with onset of adherence as early as 30 seconds after injury and

with a maximum response at 2 minutes.

The binding of leucocytes to endothelium results from the interaction of

complementary receptors in both cell types. Their expression is enhanced by

cytokines and bacterial lipopolysaccharides. Physical factors, such as

haemodynamic shear stress, also influence adherence. This first stage of

adherence is critical. While there is some evidence that some wounds can

heal without the presence of neutrophils, patients with leucocyte adhesion

deficiency, lacking an essential glycoprotein, are unable to mobilize

neutrophils or monocytes, and exhibit decreased pus formation and impaired

wound healing.

Diapedesis: Vasopermeability factors act on actin microfilaments inside the

endothelial cells and effect the reversible opening of junctions so that

neutrophils are able to pass between the endothelial cells to the extravascular

space. It is suggested that the secretion of elastase and other enzymes by the

neutrophils enables them to degrade elastin and components of the

endothelial basement membrane.

Migration: Molecules released by platelets following disruption of the

blood vessels, e.g. kallikrein (an enzyme that leads to the formation of

vasodilating peptides) and fibrinopeptides, diffuse to the site of the wound

and set up a concentration gradient of chemotactic factors which attract the

neutrophils that have traversed the endothelium through the extracellular

space to the injury site.

Phagocytosis: At the site the neutrophils form the first line of defence

against the invading micro-organisms. The neutrophils phagocytose bacteria,

then kill the ingested cells by the production of microbiocidal substances,

oxygen metabolites such as hydroxyl radicals, hydrogen peroxide, and the

superoxide ion. Release of some of these substances to the outside of the cell

may also lead to tissue damage and prolong the inflammatory phase. Some

bacteria may be killed by non-oxidative mechanisms, but these are not

defined in vivo. If bacterial contamination is low, the density of neutrophils

declines, but if numbers of micro-organisms persist, the bacterial

lipopolysaccharides continue to promote the arrival of further neutrophils.

The neutrophils are unable to regenerate their enzymes and so themselves

decay after phagocytosis.

Accumulation of macrophages:

The macrophage is indispensable in the degradation of injured tissue debris

and in the reparative phase of wound. If the macrophages are inhibited,

wound healing is radically impaired.

Normal tissues contain very few macrophages, but, in response to

chemotactic factors released after injury, circulating monocytes are attracted

to the site of injury several hours after the first neutrophils arrive.

Endothelial cells in wounded tissue also play a role in this process, and have

been shown to regulate the preferential adhesion of monocytes and

lymphocytes to endothelium.

At the injury site, monocytes differentiate into macrophages. One of the

signals promoting this differentiation is the binding of fibronectin to surface

receptors on monocytes, which induces the activation of the receptors for

phagocytosis. Macrophages develop functional complement receptors and

undertake similar operations to the neutrophils. However, further

interactions with the interferons, and subsequently with bacterial or viral

products, induce further differentiation into a fully activated phenotype.

Interferons enhance endocytosis and phagocytosis and modulate the surface

receptor functions of newly migrated macrophages. Ingestion of bacteria by

endocytosis triggers the primary oxygenase which converts molecular

oxygen to the superoxide, which then reacts to produce hydrogen peroxide

and hydroxyl radicals required for microbiocidal activity. Oxygen is

essential. If the partial pressure of oxygen falls below 30 mmHg,

macrophages are inactivated; their phagocytosing potential is reduced. The

relationship between oxygen pressure and healing has been shown to be

linear, explaining the beneficial role of oxygen pressure in repair.

The activated macrophage is the major effector cell for degrading and

removing damaged connective tissue components, collagen, elastin, and

proteoglycans. Initial degradation takes place extracellularly up to several

millimetres from the macrophage. Collagen and other fragments are then

ingested and degraded by the cathepsin enzymes and other peptides. In

contrast to neutrophils, macrophages can continue to synthesize the

necessary enzymes, thus persisting for a longer time. They also phagocytose

the decaying neutrophils.

Apart from their role in debridement, macrophages secrete chemotactic

factors which bring additional inflammatory cells to the wound site.

Macrophages also produce prostaglandins, which are strongly vasodilatory

and affect the permeability properties of microvessels. The macrophages act

after the amines and kinins, and are produced on demand, prolonging the

inflammatory phase. Prostaglandins also augment the adenyl cyclase activity

in T lymphocytes, which accelerates the mitosis of other cells.

The angiogenesis stimulated in the early phase of wound healing has been

shown to be related to the presence of macrophages. Increased levels of

lactate production, up to 15-fold, have been found in wounded tissue, and

have caused macrophages to produce and release angiogenic substances. The

macrophages also produce growth factors, such as platelet-derived growth

factor (PDGF), transforming-growth factor (TGF) and fibroblast growth

factor (FGF), which are necessary for the initiation and propagation of

granulation tissue. In this way the macrophages mediate the transition from

the initial inflammatory response to the early repair phase of wound healing.

Lymphocytes:

B lymphocytes may be absent from the wound site. However, helper T cells

are activated following injury, when they recognize any foreign antigen on

the surface of antigen-presenting cells, e.g. Langerhans cell in skin, and

certain types of macrophage.

The T lymphocytes migrate into the wound along with the macrophages.

Monoclonal antibody staining has permitted the identification of sets and

subsets of lymphocytes, and cell culture and biochemical studies have

identified and characterized some of the lymphokines, molecular messengers

secreted by lymphocytes, which influence other cells, particularly

macrophages and fibroblasts. Thus, lymphocytes can produce macrophage

chemotactic factor (MCF), macrophage inhibiting factor (MIF) regulating

movement, macrophage activating factor (MAF), and interleukin-2 (IL-2)

which enables the T cells to proliferate by an autocrine mechanism.

The colony stimulating factors are very potent, being effective at very low

concentrations (pg/ml). They are involved in the stimulation of proliferation,

and of the commitment of the monocyte to differentiation and maturation.

They stimulate the function of phagocytosis, and the production by

macrophages of substances such as prostaglandins, tumor necrosis factor

(TNF) and further colony stimulating factors. As quantities are very small, it

is not known whether all cells are able to produce colony stimulating factors.

They are induced in vivo by the presence of micro-organisms. Colony

stimulating factors are currently in clinical use for the treatment of

neutropenia, both congenital and induced by cancer therapy. It has been

suggested that there could be a prophylactic role for them in abdominal and

genitourinary surgery, where infections are common.

Macrophages and lymphocytes have been shown to be present from day-1 in

wounds, although lymphocytes are fewer in number than macrophages. In a

study on human wounds by Martin and colleagues, macrophages peaked

between 3 and 6 days and lymphocytes between 8 and 14 days. Thus they

persist into the early repair phase of wound healing. Both macrophages and

lymphocytes disappear from mature wounds by an unknown mechanism, but

in abnormal scars both persist long afterwards. In hypertrophic scars,

macrophages and lymphocyte levels have been found to be very high 4 to 5

months after wounding, and lymphocytes were still present at 40% of the

high level after 2 years. It has been suggested that control of lymphocytes

might be a useful approach to control of scarring. It is of interest that

minoxidil, a drug that has been shown in vitro to inhibit collagen lattice

contraction, has been shown to inhibit DNA synthesis and leucocyte

migration inhibition factor (LIF) production by T lymphocytes.

Clinically inflammation is presented by redness, tenderness, heat, swelling

and loss of function.

Wound contraction: It is an important feature of secondary healing, not

seen in primary healing. It has been noticed in open wounds with tissue loss

for centuries. The wound contraction does not begin immediately and that

about 3-4 days elapse before movement of the edges become measurable.

This period, when no wound contraction is noticed, is called the initial ‘lag

period’. After this period there is a period of rapid contraction, which is

completed by the 14th day. At this time the wound is reduced to

approximately 80% of its original size. (Wound contraction is controlled by

both the fibroblasts and extra cellular matrix, and is due to the fibroblasts

applying tension to the surrounding tissue matrix).

The first step in studying the mechanism of wound contraction is to try to

define precisely where the fundamental process is located. It should be

determined whether a centripetal movement occurs because an energy or

power source located out side the defect, is pushing the skin edges inwards

or whether a centrally located power source is pulling the skin edges to the

centre of the defect.

In order to explain the mechanism of wound contraction, a number of factors

have been proposed. These are as under;

i) Removal of fluid by drying has been suggested as a

cause of diminution in the size of wound. But this has

not been substantiated, as water content of central

wound tissue at the beginning of wound contraction has

not changed significantly as at the end of contraction.

ii) Contraction of collagen has also been incriminated as

the cause of wound contraction, but wound contraction

proceeds at a stage when the collagen content of

granulation tissue is very small.

iii) Discovery of myofibroblasts appearing in active

granulation tissue has resolved the controversy

surrounding the mechanism of wound contraction.

These cells have features intermediate between those of

fibroblasts and smooth muscle cells. Their migration in

to the wound area and their active contraction decreases

the size of defect.

Factors inhibiting wound contraction:

i) Corticosteroid administration

ii) Contraction does not occur normally in burns

iii) Immediate skin grafting

iv) X-irradiation

v) Colchicine and vinblastin also inhibit wound contraction,

as they are inhibitors of microtubule formation in the

myofibroblasts

vi) Cytotoxic agents particularly the cytochrome poisons in

non-lethal doses.

Epithelialisation: Epithelial cells are important in the inflammatory phase

as well as in the later repair aspect of wound healing. In skin wounds, the

epidermis immediately adjacent to the wound edge begins thickening on the

first day. Marginal basal cells loose their firm attachment to the underlying

dermis, enlarge and begin to migrate into the wound. The fixed basal cells in

a zone near the wound edge undergo rapid mitotic divisions and the daughter

cells migrate. Within 48 hours, the entire wound surface is re-epithelialised.

After bridging the wound defect, the migrating epithelial cells loose their

flattened appearance and become more columnar in shape. Layering of the

epithelium starts and surface cells keratinize. The epithelial cells also

migrate down the suture tracts. Subsequent epithelial thickening and

keratinisation may produce marked foreign body reaction and formation of

sterile abscess. In one sentence epithelialisation of wound mainly occurs by

proliferation and migration of the marginal basal cells lying close to the

wound margin.

Granulation tissue formation:

Schematic representation of granulation tissue formation:

Phase of inflammation. Phase of clearance. Phase of ingrowth of granulation tissue.

Angiogenesis (neo vascularisation) Fibrous tissue formation.

The haematoma within the wound is soon replaced by granulation tissue,

which consists of a loose matrix of fibrin, fibronectin, collagen,

glycosaminoglycans, particularly hyaluronic acid, containing macrophages,

fibroblasts and ingrowing blood vessels. Granulation tissue formation

consists of 3 phases.

I. Phase of inflammation

II. Phase of demolition or clearance: Combination of proteolytic enzymes

liberated from neutrophils, autolytic enzymes from dead tissue cells

and phagocytic activity of macrophages clear off the necrotic tissue,

debris etc

III. Phase of ingrowth of granulation tissue

This phase consists of two main processes

1) Angiogenesis or Neovascularisation.

2) Formation of fibrous tissue.

Angiogenesis: Formation of new blood vessels at the injury site takes place by the proliferation of endothelial cells from the margins of the severed blood vessels. Initially the proliferated endothelial cells are solid buds but develop a lumen within few hours and start carrying blood. The newly formed blood vessels are more leaky, accounting for the edematous appearance of new granulation tissue. Soon these blood vessels differentiate into muscular arterioles, thin walled venules and true capillaries.The process of angiogenesis takes place under the influence of endothelial cell growth factors, some components of matrix like type IV collagen. Fibrous tissue formation: The newly formed blood vessels are present in an amorphous ground substance or matrix. The new fibroblasts originate from fibrocytes as well as by mitotic division of fibroblasts. Collagen fibrils began to appear by about 6th day. As maturation proceeds, more and more of collagen is formed while the number of active fibroblasts and new blood vessels decreases. This

results in the formation of the scar known as cicatrisation. Two processes are involved in fibrosis

i) Emigration and proliferation of fibroblasts at the injury site. ii) Deposition of extra cellular matrix by these cells.

Extra cellular matrix:

It is a stable complex of macro molecules that underlies epithelial cells and

surrounds connective tissue cells. It plays an important role in wound

healing through its chemotactic, opsonic and attachment properties.The strength of healed wound and properties of scar depends upon the deposition of an adequate extra cellular matrix. The major components in it are collagen, basement membrane, elastic fibres etc. Collagen: It is an extra cellular secretion from specialized fibroblasts and the basic molecules which fibroblasts synthesize are frequently called as tropocollagen. Several types of collagen are there which differ in the amino acid sequence of constituent chains. Type 1 collagen is found in the tendon, ligament and skin. Type 2 collagen is found mainly in the cartilage. Type 3 collagen is found in foetal dermis and later on is replaced by type 1

at birth.

Tensile strength: The strength of a healing wound is of great practical

importance to the surgeon. It acts as the main safeguard against wound

dehiscence. Experimentally it may be estimated by measuring the force

necessary to disrupt the wound. In the first few days the strength of a wound

is only that of the clot which cements the cut surfaces together. Later on

various changes takes place in the wound healing process and at the end the

tensile strength of the wound corresponds to the increase in amount of

collagen present.

Factors influencing the tensile strength of the wound are

Direction of the wound: Skin wounds parallel to the lines of langer heal

faster. Skin incisions made across langer’s lines tend to gape and their

healing is delayed. Tensile strength of the wound becomes more when this is

parallel to the lines of langer. That is why the transverse abdominal incisions

produce strong scar than the longitudinal ones.

Pull of underlying muscles: The wounds which are parallel to the pull of the

underlying muscles constitute strong scar.

Previous wound: Resutured wounds heal faster than those sutured primarily,

as the repairative process has already commenced.

Abdominal binders: Reduce the rate of gain in strength.

Factors affecting granulation tissue formation:

Cortisone administration: Excess corticosteroid administration inhibits

granulation tissue formation. Fibroblasts remain small with little collagen

formation. This effect is well accepted in experimental animals, but

corticosteroid in normal dosage may not influence wound healing in human

beings.

Scurvy: In this condition though vascular granulation tissue is formed, yet

there is failure of collagen formation. Instead there are thick reticulin fibres.

Maturation to collagen does not occur in the absence of vitamin-C

Protein starvation: Also causes delayed formation of collagen. There

remains excessive accumulation of poorly- sulphated ground substance.

Complications of wound healing:17

1. Implantation cysts

2. Painful scars

3. Cicatrisation – it often produces various deformities

4. Keloid formation

5. Neoplasia.

1) B.&L.3/Pg-36,12/Pg-158;S.Das. Surgery11/Pg-125.

2) S.Das. Surgery-11/Pg-126;M.M.S.6/Pg-44. 3) S.Das.Surgery.11/Pg-126;B.&L.12/Pg-

158;M.M.S.6/Pg-44,45. 4) B.&L.12/158,159. 5) S.Das.Surgery.3/Pg-31-34;B.&L.12/Pg-159. 6a) Hospital Today-vol 3 No.7-July 98. 6b) BMJ vol 8 No.5 July 92. 6c) The Antiseptic vol 99 July 02. 6d) Hospital Today vol 7 No.6 June 02. 6e) Hospital Today vol 7 No.12 Dec 02. 6f) BMJ vol 6 No.6 Aug 90. 7) B.&L.7/Pg-95. 8) M.M.S.6/Pg-48,49;B.&L.12/Pg-159. 9) B.&L. 12/Pg-160; Hospital Today vol 5 No.11 Nov 2000. 10) B.&L. 3/Pg-31,33,34; M.M.S.1/Pg-1; Hand book of surgery-S.C.Atri-1/Pg-1. 11) Hand book of surgery-S.C.Atri-1/Pg- 4,5;B.&L.7/Pg.95-98. 12) B.&L.7/Pg.89-91. 13) S.Das.Surgery.1/Pg.1-5; Text book of pathology-Harshmohan.5/Pg.179-184; B.&L.3/Pg-29;Oxford text book of surgery Chapt 1.1. 14) S.Das.Surgery.1/Pg-6,7. 15) Hospital Today vol 5 No.4-April 2000. 16) Internet reference-Brian A.Youn, M.D.Director, Dept of hyperbaric medicine. 17) S.Das.Surgery.1/Pg-6;Hand book of surgery- S.C.Atri-1/Pg.4.

The clinical study is to evaluate the efficacy of Jatyadi Taila in the

management of Dushta Vrana. It comprises of materials & methods,

observations, statistical analysis, discussion & conclusion. In the present

study the diagnosed cases of Dushta Vrana were randomly selected and

subjected to clinical trial. The methodology of clinical trial & observations

are as follows

Source of data: Patients attending the Shalya I.P.D. & O.P.D. of S.D.M.

Ayurveda Hospital, Udupi were taken as the material for the study.

Method of collection of data:

Patients suffering from Dushta Vrana in the age group of 20 – 60 are selected randomly & are subjected to clinical trial. The selected patients were divided into two groups of 10 each.

Group A: Sterile gauze impregnated with Jatyadi Taila is applied externally

after cleaning the wound surface.

Group B: Sterile dry gauze is applied externally after cleaning the wound

surface.

The signs & symptoms were recorded in the proforma designed specially for

this study.

Inclusion criteria:

Patients aged between 20 -60 years.

Both sexes.

Patients suffering from Dushta Vrana (of all types).

Exclusion criteria:

Tuberculous Ulcers.

Ulcers with gangrenous changes.

Malignant Ulcers.

Pregnant Women.

Investigations and interventions:

Investigations:

Routine examination of blood.

Routine urine examination.

Blood sugar& urine sugar.

Culture& sensitivity of the pus.

Any other necessary investigations.

Intervention:

Jatyadi Taila dressing once daily.

Triphala Guggulu 1 tab (450 mg) three times daily.

Gandhaka Rasayana 1 tab (350 mg) three times daily.

The method of dressing:

The Vrana was cleaned with hydrogen peroxide and eusol. Later the area is

dried by a cotton plug using an artery forceps. Then in Group A- A sterile

gauze impregnated with Jatyadi Taila was kept over the Vrana & over it a

sterile pad was placed and dressing was done. In Group B- A sterile gauze

was kept over the Vrana & over it a sterile pad was placed and dressing was

done.

Bandaging was done every day in the morning. If the bandage becomes wet

completely within 24 hours rebandaging was carried out.

Parameters of assessment:

The patients were assessed on the basis of subjective and objective

parameters before and after treatment.

Subjective parameters:

Pain.

Itching.

Burning sensation.

Objective parameters:

Size (by using sterile blotting paper).

Tenderness.

Discharge.

Smell.

Surrounding area of the ulcer.

Granulation tissue and floor.

All the above parameters were graded arbitrarily as follows:

Subjective parameters:

(1) Pain

0-No pain.

1-Mild (localized feeling of pain during movement but tolerable).

2-Moderate (localized feeling of pain not disturbing sleep).

3-Severe (continuous localized feeling of pain which disturbs sleep).

(2) Itching

0-No itching.

1-Mild (slight localized itching sensation).

2-Moderate (moderate localized itching sensation with out sleep

disturbance).

3-Severe (continuous localized itching which disturbs sleep).

(3) Burning sensation

0- No burning sensation.

1-Mild (slight localized burning sensation).

2-Moderate (moderate localized burning sensation with out sleep

disturbance).

3-Severe (continuous burning sensation which disturbs sleep).

Objective parameters:

(1) Size

It was recorded by using a sterile blotting paper which was placed over the

ulcer and pressed with uniform pressure. The impression was measured

directly and the depth was measured with the help of sterile probe.

(2) Tenderness

0-No tenderness.

1-Mild (tenderness after squeezing).

2-Moderate (tenderness after touching with pressure).

3-Severe (tenderness just touching with soft object).

(3) Discharge

0-No discharge.

1-Mild (the gauze is slightly moist).

2-Moderate (the gauze becomes wet completely after opening bandage).

3-Copious (bandage moist completely in 24 hrs & bandage is changed).

(4) Smell

0-No smell.

1-Mild bad smell.

2-Unpleasant but tolerable smell.

3-Foul smell which is intolerable.

(5) Surrounding area of ulcer

0-No blackish discoloration and swelling.

1-Blackish discoloration with out swelling.

2-Swelling with out blackish discoloration.

3-Blackish discoloration with swelling.

(6) Floor and granulation tissue

0-Smooth, regular floor with healthy granulation tissue.

1-Smooth, pale granulation tissue, slight discharge, with out slough.

2-Irregular floor with less granulation tissue and slough.

3-Rough, irregular floor with more slough and no evidence of granulation

tissue.

Follow up period:

All the cases were treated upto a period of 3 months. Weekly assessment of

the patient was carried out during this period.

The following observations were made during the study

Incidence observations.

Observations made before treatment, during the follow up and

after treatment.

Incidence observations:

As per the prepared proforma, observations were made regarding incidence

of Dushta Vrana with regard to age, sex, occupation, religion, socio-

economic status, marital status, habitat, diet, chronicity, area involved, type

of Dushta Vrana, Adhishtaana and cause of ulcer.

Table No. 25 – Distribution of 20 patients of Dushta Vrana according to different age group

Age (in years) No. of Patients %

21-30 4 20 31-40 3 15 41-50 6 30 51-60 7 35

Figure No.1 - Incidence of age

0

1

2

3

4

5

6

7

No. of patients

21-30

31-40

41-50

51-60

Among 20 patients selected for study, 35% of patients were in the age group

between 51- 60 years, 30% of the patients were in the age group between 41-

50 years, 15% of the patients were in the age group between 31-40 years and

20% of the patients were in the age group between 21-30 years.

Table No. 26- Distribution of 20 patients of Dushta Vrana according to sex

Sex No. of patients %

Male 17 85 Female 3 15

Figure No. 2- Incidence of sex

0

5

10

15

20

No. of patients

male

female

Among 20 patients selected for the study, 17 were male and only three

patients were female.

Table No.27- Distribution of 20 patients of Dushta Vrana according to occupation

Occupation No. of patients % House wife 3 15

Student 2 10 Hotel worker 3 15

Labourer 3 15 Business 5 25

Agriculture 1 5 Driver 1 5 Tailor 1 5

Mechanic 1 5

Figure No.3- Incidence of occupation

0

1

2

3

4

5

no. of patients

house wife

student

hotel worker

labourer

business

agriculture

driver

tailor

mechanic

Among 20 patients selected for the study 5 patients were having occupation

of business and 3 patients each were having occupation of hotel worker,

house wife and labourer.

Table No. 28- Distribution of 20 patients of Dushta Vrana

according to the religion

Religion No. of patients %

Hindu 13 65 Muslim 2 10

Christian 5 25

Figure No.4- Incidence according to the religion

0

2

4

6

8

10

12

14

No. of patients

hindu

muslin

christian

Among 20 patients selected for the study 13 were Hindu, 5 were Christian

and 2 were Muslim.

Table No. 29- Distribution of 20 patients of Dushta Vrana according to socio- economic status

Socio- economic status No. of patients %

Rich 0 0 Upper- middle class 4 20 Lower- middle class 13 65

Poor 3 15

Figure No.5- Incidence of socio-economic status

Among 20 patients selected for the study, maximum incidence was seen in

lower- middle class.

Table No.30—Distribution of 20 patients of Dushta Vrana according to marital status

Marital status No. of patients %

Married 16 80 Unmarried 4 20

Figure No.6- Incidence according to marital status

0

2

4

6

8

10

12

14

No. of patients

rich

u-middle class

l-middle class

poor

0

5

10

15

20

No. of patients

married

unmarried

Among 20 patients selected for the study, maximum incidence was seen in

the married.

Table No. 31- Distribution of 20 patients of Dushta Vrana according to

habitat

Habitat No. of patients % Urban 6 30 Rural 14 70

Figure No.7- Incidence according to the habitat

Among 20 patients selected for the study, higher incidence was seen in the

patients of rural area.

0

2

4

6

8

10

12

14

No. of patients

urban

rural

Table No. 32- Distribution of 20 patients of Dushta Vrana according to the dietary habits

Dietary habits No. of Patients % Vegetarian 2 10 Mixed diet 18 90

Figure No.8- Incidence according to dietary habits

0

5

10

15

20

No. of patients

vegetarian

mixed

Among 20 patients selected for the study, higher incidence was seen in the

patients of mixed diet.

Table No. 33- Analysis of chronicity in 20 patients of Dushta Vrana

Chronicity No. of patients %

Up to 1 month 11 55 1-3 months 4 20 3-6 months 1 5

6 months- 1 year 2 10 Above 1 year 2 10

Figure No.9- Incidence of chronicity

Among 20 patients selected for the study, 55% of the patients had the

duration up to 1 month and 10 % had duration of more than 1 year.

Table No. 34- Analysis of area involved by the Dushta Vrana in 20

patients

Area involved (site) No. of patients %

Lower limb 17 85 Upper limb 1 5

Lumbosacral region 2 10 Figure No.10- Incidence of site of ulcer

0

2

4

6

8

10

12

No. of patients

up to 1 month

1 to 3 months

3 to 6 months

6 months to 1 year

above 1 year

0

5

10

15

20

No. of patients

lower limb

upper limb

lumbosacral

Among 20 patients selected for the study, 85% of the patients were suffering

from lower limb ulcers.

Table No. 35- Analysis of type of Dushta Vrana in 20 patients

Type of Dushta

Vrana No. of patients %

V-P 10 50 V-K 9 45 K-P 1 5

Figure No.11- Incidence of type of Dushta Vrana

0

2

4

6

8

10

No. of patients

v-p

v-k

k-p

Among 20 patients selected for the study, 10 patients were diagnosed as V-P

Vrana and 9 patients as V-K Vrana.

Table No. 36- Classification of Dushta Vrana according to Adhishtaana

Adhishtaana No. of patients %

Twak 7 35 Twak- Maamsa 11 55

Twak- Maamsa- Sira 2 10

Figure No.12- Incidence according to Adhishtaana

0

2

4

6

8

10

12

No. of patients

twak

twak-maamsa

twak-maamsa-sira

Among 20 patients selected for the study, in 55 % of patients Adhishtaana

involved was Twak- Maamsa and in 35 % of patients Adhishtaana involved

was Twak.

Table No. 37- Analysis of ulcers according to the cause

Cause of ulcer No. of patients %

Trauma 8 40 Varicosity 7 35 Diabetes 2 10

Pressure sore 2 10 Ischaemia 1 5

Figure No.13- Incidence according to cause

0

1

2

3

4

5

6

7

8

No. of patients

trauma

varicosity

diabetes

pressure sore

ischaemia

Among 20 patients selected for the study, in 8 patients ulcer was produced

due to trauma, 7 patients were having varicosity, 2 patients were diabetic

and in 1 patient due to ischaemia.

Observations made Before Treatment, during each visit and After

Treatment.

The data observed in BT and AT are compared using paired ‘t’ test and the

effect of treatment is analyzed in each among the subjective and objective

criteria. Statistical analysis was done using the software Jandel Sigma stat

version 2.0.

Subjective criteria:

1) Pain:

Table No.38- Assessment of pain

G FU BT 7D 14D 21D 28D 35D 42D 49D 56D 63D 70D 77D 84D AT

A(n=10) Mean (pain)

1.5 1.3 1.1 0.9 0.7 0.6 0.55 0.50 0.45 0.40 0.35 0.30 0.25 0.2

B(n=10) Mean (pain)

2.1 2 1.9 1.8 1.75 1.65 1.55 1.45 1.35 1.25 1 0.9 0.7 0.6

In group A- Before treatment mean (pain) was1.5& after treatment it was reduced to 0.2. In group B- Before treatment mean (pain) was 2.1 & after treatment it was reduced to 0.6.

Figure No. 14- Effect on pain

0

0.5

1

1.5

2

2.5

BT14

D28

D42

D56

D70

D84

D

mean-A

mean-B

Table No. 39- Efficacy of treatment on pain Comparison of effect of treatment on pain in two groups

Mean Paired ‘t’ test G

BT AT

Difference

In means

%

S.D S.E.M. t value p value

A(n=10) 1.5

O.2

1.3

86.6 0.949 0.3 4.333 =0.002

B(n=10) 2.1

O.6

1.5 71.42 0.972 0.307 4.881 =<0.001

Gradual reduction in the pain was observed during the follow up. The

change in the pain that occured with the treatment is greater than would be

expected by chance in both the groups. There is statistically significant

change in both the groups. (P= 0.002, =< 0.001).

Table No. 40- Result of treatment on pain

No. of patients

BT AT Grade

G-A

(n=10)

G-B

(n=10)

G-A

(n=10)

G-B

(n=10)

3 02 04 00 00

2 01 03 00 00

1 07 03 02 06

0 00 00 08 04

Before treatment all 20 patients of both the groups complained of pain. In

group A out of 10 patients only 2 patients had mild pain at the end of the

treatment. In group B out of 10 patients, 6 patients had mild pain at the end

of the treatment.

2) Itching: Table No.41- Assessment of itching


A(n=10) Mean (Itc)

O.9 O.7 O.6 O.5 O.4 O.35 O.3 O.27 O.25 O.23 O.2 O.15 O.12 O.1

B(n=10) Mean (Itc)

1.1 1 O.9 O.85 O.83 O.8 O.7 O.65 O.63 O.6 O.5 O.45 O.42 O.4

In group A – Before treatment mean (Itching) was 0.9 & after treatment it was reduced to 0.1.

In group B- Before treatment mean (Itching) was 1.1 & after treatment it was reduced to 0.4 Figure No. 15- Effect on itching

0

0.2

0.4

0.6

0.8

1

1.2

BT14

D28

D42

D56

D70

D84

D

mean-A

mean-B

Table No. 42- Efficacy of treatment on itching Comparison of effect of treatment on itching in two groups


BT AT

Difference

In means

%


A(n=10) 0.9 0.1 0.8 88.8 0.919 0.291 2.753 0.022

B(n=10) 1.1 0.4 0.7 63.6 0.789 0.249 3.207 0.011

Gradual reduction in itching was observed during the follow up. The change that occured with the treatment is greater than would be expected by chance. Hence there is statistically significant change in both the groups (p=0.022, 0.011).

Table No.43- Result of treatment on itching

No. of patients

BT AT Grade

G-A

(n=10)

G-B

(n=10)

G-A

(n=10)

G-B

(n=10)

3 01 01 00 00

2 01 03 00 01

1 04 02 01 02

0 04 04 09 07

In group A- Before treatment 6 patients were complaining of itching and after treatment 5 patients completely relieved of itching & in 1 patient it was reduced to grade 1. In group B- Before treatment 6 patients were complaining of itching, after treatment 3 patients relieved completely of itching and in remaining patients it was reduced to grade 2&1. 3) Burning sensation: Table No. 44- Assessment of burning sensation


A (n=10)

Mean (B.S)

1.1 1 0.9 0.8 0.7 0.65 0.60 0.55 0.5 0.4 0.3 0.25 0.2 0.1

B (n=10)

Mean (B.S)

1.1 1 0.9 0.85 0.75 0.70 0.65 0.60 0.5 0.45 0.4 0.35 0.25 0.2

Group A- Before treatment mean (burning sensation) was 1.1& after treatment it was reduced to 0.1.

Group B- Before treatment mean (burning sensation) was 1.1& after treatment it was reduced to 0.2. Figure No.16- Effect on burning sensation Table No.45- Efficacy of treatment on burning sensation Comparison of effect of treatment on Burning sensation in two groups


BT AT

Difference

In means

%


A

(n=10)

1.1 0.1 1 90.9 0.816 0.258 3.873 0.004

B

(n=10)

1.1 0.2 0.9 81.8 0.876 0.277 3.250 0.010

Gradual reduction in burning sensation was observed during the follow up. The change that occured with the treatment is greater than would be expected by chance. Hence there is statistically significant change in both the groups (p=0.004, 0.010). Table No. 46- Result of treatment on burning sensation

0

0.2

0.4

0.6

0.8

1

1.2

BT14

D28

D42

D56

D70

D84

D

mean-A

mean-B

No. of patients

BT AT Grade

G-A

(n=10)

G-B

(n=10)

G-A

(n=10)

G-B

(n=10)

3 00 02 00 00

2 04 01 00 00

1 03 03 01 02

0 03 04 09 08

Group-A: Before treatment 7 patients were complaining of burning sensation and after treatment 6 patients were relieved completely out of seven and in one patient it was reduced to grade 1. Group- B: Before treatment 6 patients were complaining of burning sensation and after treatment 4 were relieved completely out of six, in remaining patients it was reduced to grade 1. Objective criteria:

1) Size of the ulcer: 1.1) Length

Table No. 47- Assessment of length of ulcer


A (n=10)

Mean (L)

7.55 7.24 6.51 5.83 5.18 4.6 4.14 3.62 3.18 2.79 2.44 2.09 1.85 1.67

B (n=10)

Mean (L)

3.6 3.43 3.1 2.77 2.57 2.33 2.09 1.91 1.76 1.57 1.37 1.23 1.06 0.89

Group A- Before treatment mean (Length of ulcer) was 7.55 & after treatment it was reduced to 1.67. Group B- Before treatment mean (Length of ulcer) was 3.6 & after treatment it was reduced to 0.89. Figure No. 17- Effect on length of ulcer

012

3456

78

BT14

D28

D42

D56

D70

D84

D

mean-A

mean-B

Table No. 48- Efficacy of treatment on length of ulcer Comparison of effect of treatment on length in two groups


BT AT

Difference

In means

%


A(n=10) 7.55 1.67 5.88 77.8 3.270 1.034 5.645 =<0.001

B(n=10) 3.6 0.89 2.71 75.2 1.892 0.59 4.530 =0.001

The change that occured with the treatment is greater than would be expected by chance. Hence there is statistically significant change in both the groups (p=<0.001, =0.001).

1.2) Width Table No. 49- Assessment of width of ulcer


A (n=10)

Mean (W)

5.325 5.07 4.67 4.29 3.84 3.45 3.05 2.71 2.33 1.98 1.65 1.41 1.11 0.92

B (n=10)

Mean (W)

2.35 2.35 2.16 1.97 1.63 1.45 1.26 1.16 1.045 0.9 0.8 0.69 0.59 0.505

Group A- Before treatment mean (width of ulcer) was 5.325 & after treatment it was reduced to 0.92. Group B- Before treatment mean (width of ulcer) was 2.35 & after treatment it was reduced to 0.505.

Figure No. 18- Effect on width of ulcer

Table No. 50- Efficacy of treatment on width of the ulcer

0

1

2

3

4

5

6

BT14

D28

D42

D56

D70

D84

D

mean-A

mean-B

Comparison of effect of treatment on width in two groups Mean Paired ‘t’ test G

BT AT

Difference

In means

%


A

(n=10)

5.325 0.92 4.405 82.7 1.692 0.535 8.108 =<0.001

B

(n=10)

2.35 0.505 1.845 78.5 0.777 0.246 7.513 =<0.001

The change that occured with the treatment is greater than would be expected by chance. Hence there is statistically significant change in both the groups (p=<0.001, =<0.001).

1.3) Depth Table No. 51- Assessment of depth of the ulcer


A (n=10)

Mean (Dep)

0.37 0.338 0.314 0.28 0.26 0.24 0.22 0.20 0.17 0.15 0.12 0.10 0.07 0.04

B (n=10)

Mean (Dep)

0.203 0.19 0.17 0.16 0.15 0.148 0.12 0.11 0.10 0.089 0.081 0.07 0.06 0.053

Group A- Before treatment mean (Depth of ulcer) was 0.37 & after treatment it was reduced to 0.04. Group B- Before treatment mean (Depth of ulcer) was 0.203 & after treatment it was reduced to 0.053.

FigureNo.19 - Effect on depth of the ulcer

00.05

0.1

0.150.2

0.250.3

0.350.4

BT14

D28

D42

D56

D70

D84

D

mean-A

mean-B

Table No. 52- Efficacy of treatment on the depth of the ulcer Comparison of effect of treatment on depth in two groups


BT AT

Difference

In means

%


A

(n=10)

0.37 0.04 0.33 89.18 0.164 0.0517 5.854 =<0.001

B

(n=10)

0.203 0.053 0.149 73.64 0.0804 0.0254 5.883 =<0.001

The change that occured with the treatment is greater than would be expected by chance. Hence there is statistically significant change in both the groups (p=<0.001, =<0.001).

The change in the size of ulcer occurred during the course of treatment is summarized as follows. When compared with size of ulcer before treatment in group A, the size was reduced to 83.2% after the treatment in terms of length (77.8%), width (82.7%) and depth (89.18%). In group B the size was reduced to 76 % after the treatment in terms of length (75.2%), width (78.5%) and depth (73.6%).

2) Tenderness: Table No. 53 – Assessment of tenderness


A (n=10)

Mean (Td)

1.5 1.4 1.3 1.2 1.1 1 0.9 0.7 0.6 0.5 0.4 0.3 0.25 0.2

B (n=10)

Mean (Td)

1.9 1.85 1.80 1.75 1.70 1.6 1.55 1.48 1.36 1.25 1 0.8 0.7 0.5

Group A- Before treatment mean (Tenderness of ulcer) was 1.5 and after treatment it was reduced to 0.2. Group B- Before treatment mean (Tenderness of ulcer) was 1.9 and after treatment it was reduced to 0.5. Figure No. 20 – Effect on tenderness

Table No. 54- Efficacy of treatment on tenderness Comparison of effect of treatment on tenderness in two groups


BT AT

Difference

In means

%


A

(n=10)

1.5 0.2 1.3 86.6 0.675 0.213 6.091 <0.001

B

(n=10)

1.9 0.5 1.4 73.6 0.516 0.163 8.573 =<0.001

The change that occured with the treatment is greater than would be expected by chance. Hence there is statistically significant change in both the groups (p=<0.001, =<0.001)

Table No. 55 – Result of treatment on tenderness

00.20.40.60.8

11.21.41.61.8

2

BT14

D28

D42

D56

D70

D84

D

mean-A

mean-B

No. of patients

BT AT Grade

G-A

(n=10)

G-B

(n=10)

G-A

(n=10)

G-B

(n=10)

3 00 02 00 00

2 06 05 00 01

1 03 03 02 03

0 01 00 08 06

Group A-Before treatment 9 patients were having tenderness. After treatment 7 patients relieved completely and in remaining 2 patients it was reduced to grade 1. Group B-Before treatment all patients were having tenderness. After treatment 6 patients relieved completely and in remaining patients it was reduced to grade 1 and 2 respectively. 3) Discharge: Table No. 56- Assessment of discharge


A (n=10)

Mean (Dis)

1.5 1.4 1.3 1.25 1.2 1 0.9 0.8 0.7 0.55 0.45 0.4 0.35 0.2

B (n=10)

Mean (Dis)

1.2 1.1 1.0 0.9 0.85 0.8 0.75 0.7 0.65 0.6 0.5 0.4 0.3 0.2

Group A- Before treatment mean (Discharge) was 1.5 and after treatment it was reduced to 0.2. Group B- Before treatment mean (Discharge) was 1.2 and after treatment it was reduced to 0.2.

Figure No. 21- Effect on discharge

Table No. 57- Efficacy of treatment on discharge Comparison of effect of treatment on discharge in two groups


BT AT

Difference

In means

%


A

(n=10)

1.5 0.2 1.3 87 0.675 0.213 6.091 =<0.001

B

(n=10)

1.2 0.2 1 83.3 1.054 0.33 3 0.015

The change that occured with the treatment is greater than would be expected by chance. Hence there is statistically significant change in both the groups (p=<0.001, =0.015).

Table No. 58- Result of treatment on discharge

00.20.40.60.8

11.21.41.6

BT14

D28

D42

D56

D70

D84

D

mean-A

mean-B

No. of patients

BT AT Grade

G-A

(n=10)

G-B

(n=10)

G-A

(n=10)

G-B

(n=10)

3 00 01 00 00

2 06 04 00 00

1 03 01 02 02

0 01 04 08 08

Group A-Before treatment 9 patients were complaining of discharge. After treatment in 7 patients discharge was reduced completely and in remaining 2 patients it was reduced to grade 1. Group B-Before treatment 6 patients were complaining of discharge. After treatment 4 were relieved completely and in remaining 2 patients it was reduced to grade 1.

4) Smell: Table No. 59 – Assessment of smell

G FU BT 7D 14D 21D 28D 35D 42D 49D 56D 63D 70D 77D 84D ATA (n=10)

Mean (Smell)

0.5 0.48 0.46 0.4 0.35 0.3 0.25 0.2 0.17 0.15 0.13 0.12 0.1 0

B (n=10)

Mean (Smell)

0.3 0.3 0.29 0.25 0.24 0.23 0.2 0.19 0.17 0.16 0.15 0.13 0.1 0.1

Group A- Before treatment mean (Smell) was 0.5 and after treatment it was reduced to 0.

Group B- Before treatment mean (Smell) was 0.3and after treatment it was reduced to 0.1.

Figure No. 22-Effect on smell

0

0.1

0.2

0.3

0.4

0.5

0.6

BT14

D28

D42

D56

D70

D84

D

mean-A

mean-B

Table No. 60- Efficacy of treatment on smell Comparison of effect of treatment on smell in two groups


BT AT

Difference

In means

%


A

(n=10)

0.5 0 0.5 100 0.850 0.269 1.861 0.096

B

(n=10)

0.3 0.1 0.2 66.6 0.422 0.133 1.5 0.16

The change that occured with treatment is not great enough to exclude the possibility that the difference is due to chance (p=0.096, 0.16).

Table No.61 – Result of treatment on smell

No. of patients

BT AT Grade

G-A

(n=10)

G-B

(n=10)

G-A

(n=10)

G-B

(n=10)

3 00 00 00 00

2 02 00 00 00

1 01 03 00 01

0 07 07 10 09

Group A-Before treatment 3 patients were having smell from the ulcer. After treatment they were relieved completely. Group B- Before treatment 3 patients were having smell from the ulcer. After treatment 2 were relieved completely and in 1 patient it was reduced to grade 1.

5) Surrounding area of the ulcer: Table No. 62- Assessment of surrounding of ulcer


A (n=10)

Mean (S.A)

1 0.9 0.85 0.78 0.75 0.7 0.68 0.62 0.6 0.55 0.52 0.48 0.45 0.4

B (n=10)

Mean (S.A)

1.4 1.3 1.25 1.20 1.19 1.15 1.13 1.10 1 0.9 0.8 0.75 0.7 0.6

Group A- Before treatment mean (surrounding area of the ulcer) was 1. After treatment it was reduced to 0.4. Group B- Before treatment mean (surrounding area of the ulcer) was 1.4.After treatment it was reduced to 0.6.

Figure No. 23- Effect on surrounding area of ulcer

Table No. 63 – Efficacy of treatment on surrounding area of ulcer

Comparison of effect of treatment on surrounding area of ulcer in two groups


BT AT

Difference

In means

%


A

(n=10)

1 0.4 0.6 60 0.966 0.306 1.964 0.081

B

(n=10)

1.4 0.6 0.8 80 1.033 0.327 2.449 0.037

Group A -The change that occured with the treatment is not great enough to exclude the possibility that the difference is due to chance (p=0.081). Group B –The change that occured with the treatment is greater than would be expected by chance. There is statistically significant change (p=0.037).

00.20.4

0.60.8

11.2

1.41.6

BT14

D28

D42

D56

D70

D84

D

mean-A

mean-B

Table No. 64- Result of treatment on surrounding area of ulcer

No. of patients

BT AT Grade

G-A

(n=10)

G-B

(n=10)

G-A

(n=10)

G-B

(n=10)

3 03 01 00 00

2 00 04 00 01

1 01 03 04 04

0 06 02 06 05

Group A-Before treatment 4 patients were having swelling and blackish discoloration in surrounding area of ulcer (3 patients with swelling and blackish discoloration, 1 patient with blackish discoloration only).After treatment it was reduced to grade 1. Group B-Before treatment 8 patients were having swelling and blackish discoloration. After treatment in 3 patients it was reduced completely, whereas it was reduced to grade 1 in 4 patients and grade 2 in one patient.

6) Floor and granulation tissue: Table No. 65- Assessment of floor and granulation tissue


A (n=10)

Mean (Floor &Gr)

2 1.5 1.25 1.2 1 0.85 0.75 0.65 0.55 0.5 0.45 0.43 0.42 0.4

B (n=10)

Mean (Floor &Gr)

2 1.98 1.90 1.85 1.8 1.75 1.7 1.65 1.6 1.45 1.30 1 0.9 0.7

Group A- Before treatment mean (floor and granulation tissue) was 2. After treatment it was reduced to 0.4.

Group B- Before treatment mean (floor and granulation tissue) was 2. After treatment it was reduced to 0.7.

Figure No. 24- Effect on floor and granulation tissue

0

0.5

1

1.5

2

2.5

BT14

D28

D42

D56

D70

D84

D

mean-A

mean-B

Table No. 66- Efficacy of treatment on granulation tissue development Comparison of effect of treatment on granulation tissue in two groups


BT AT

Difference

In means

%


A

(n=10)

2 0.4 1.6 80 0.966 0.306 5.237 =<0.001

B

(n=10)

2 0.7 1.3 65 0.483 0.153 8.510 =<0.001

The change that occured with the treatment is greater than would be expected by chance. There is statistically significant change (p=< 0.001, =< 0.001).

Table No. 67- Result of treatment on floor & granulation tissue

No. of patients Grade

BT AT

G-A

(n=10)

G-B

(n=10)

G-A

(n=10)

G-B

(n=10)

3 02 03 00 00

2 06 04 00 00

1 02 03 04 07

0 00 00 06 03

Group A-Before treatment all 10 patients were having irregular floor, unhealthy granulation tissue and slough. After treatment 6 patients were cured completely (floor became healthy) and in 4 patients smooth, regular floor with pale granulation tissue was observed. Group B-Before treatment all 10 patients were having irregular floor, pale and unhealthy granulation tissue. After treatment 3 patients were cured completely (floor became healthy) and in 7 patients smooth, regular floor with pale granulation tissue was observed.

Overall response by the treatment:

Out of 10 patients in group A, 6 patients were cured completely and satisfactory improvement was noticed in remaining 4 patients. In group B, out of 10 patients, 3 were cured completely.

Color plate No.1-Efficacy of treatment on healing of ulcer (Group A)

Ulcer-Before treatment

Ulcer-After treatment

Bacteriological study:

Bacteriological study of Jatyadi Taila was conducted in the microbiology department, KMC, Manipal.The Taila used for the dressing was used for the study.

Procedure:

It was conducted under 3 methods a) Punch well method. b) Trench plate method. c) Agar incorporation method The organisms selected for the study are

1) Gram positive cocci (staphylococcus aureus) 2) Gram negative bacilli (E.coli and pseudomonas aeruginosa) A) Punch well method:

Standard strains of pseudomonas aeruginosa, staphylococcus aureus and . also routine strains isolated from pus were used for this method.

25 ml of muller hinton agar at thickness of 4 mm was poured in 90 mm plates. After solidification, the plates were subjected to sterility check. The inoculum was standardized to 0.5 Mac farland standard and the muller hinton agar plates were swabbed with the standard pseudomonas, standard staphylococcus, routine pseudomonas, routine staphylococcus one each respectively. Wells of 6 mm diameter were punched out with aseptic precautions. Each well was filled with 20 micro litres of Jatyadi Taila.The plates were then incerbated at 37 degrees for 24 hrs. Zone of inhibition of growth around the well incorporated with the extract was looked for at the end of the incubation period. B) Trench plate method: Each half of the muller hinton agar plate was swabbed with the standard as well as the routine isolate, after standardizing the inoculum to 0.5 Mac farlands. A trench of dimension 0.5 cm /7.5 cm was cut using sterile precautions diametrically across the plates. The trench was filled with

500 microlitres of Jatyadi Taila. The plates were then incubated at 37 degrees for 24 hrs. Any zone of inhibition of growth around the trench was looked for after the incubation period. C) Agar incorporation method: To 25 ml of muller hinton agar 1 ml of Jatyadi Taila, 2 ml, 3 ml were prepared and spot inoculated with the organisms. Observations of bacteriological study: In punch well method among the organisms used inhibition zone was observed very slowly in pseudomonas aeruginosa. The inhibition zone was 11 mm and in others no inhibition was observed.

Color plate No.2-Observation on bacteriological study

Punch well method

Inhibition zone for Pseudomonas aeruginosa

Punch well method

Absence of inhibition zone for Staphylococcus aureus

Spot method

o Agnivesha, Charaka Samhita redacted by Charaka and Drudhabala, with

Ayurveda Deepika Commentary by Chakrapaanidatta, edited by Vaidya

Yadavji Trikamji Aachaarya, 5th edition, 2001, Published by

Chaukhambha Sanskrit Sansthaan, Varanasi

o Agnivesha, Charaka Samhita redacted by Charaka and Drudhabala, with

Ayurveda Deepika Commentary by Chakrapaanidatta English translated

edition, 2002, by Ram Karan Sharma & Vaidya Bhagavan Dash,

Published by Chaukhambha Sanskrit Sansthaan, Varanasi.

o Ayurvedeeya Rasa Shaastra by Prof. Siddhinandan Mishra,9th edition

1999, Published by Chaukhambha Orientalia, Varanasi.

o Bailey & Love’s Short Practice of Surgery, edited by R.C.G Russell, N.S.

Williams, C.J.K. Bulstrode, 23rd edition.

o Bhaavamishra,Bhaava Prakaasha with Vidyotini Hindi Teeka by

Bhishak Ratna Sri Shankara Shaastri and Sri. Roopalal Vaishya; 8th

edition, 1997, Published by Chaukhambha Sanskrit Sansthaan, Varanasi.

o Bhela, Bhela Samhita, with English translation Dr. K. H. Krishnamurthy,

edited by Professor Priyavat Sharma, 1st edition, 2000, Published by

Chaukhambha Sanskrit Sansthaan, Varanasi.

o Chakrapaanidatta, Chakradatta with Vaidyaprabha Hindi Commentary

by Dr. Indradeva Tripathi,3rd edition 1997, Published by Chaukhambha

Sanskrit sansthaan,Varanasi.

o Govinda Daasa, Bhaishajya Ratnaavali, redacted by Bhishak Ratna Sri

Brahma Shankara Mishra with Vidyotini Teeka by Kaviraj Sri.

Ambikadatta Shaastri edited by Sri. Rajeshwara Datta Shaastri, 16th

edition 2002, Published by Chaukhambha Sanskrit Samsthaan, Varanasi.

o Harsh Mohan,Text book of Pathology, 3rd edition, 1998, Jaypee

publication.

o Konman E.W., Alles S.D., Janda W.M.; Color atlas and text book of

diagnostic microbiology, 4th edition, 1992, Schreckenberga pc, winn. JB

Lippinocott, Philaelphia.

o K.Rajgopal Shenoy, Manipal Manual of Surgery, 1st edition, 2001, CBS

Publishers, New Delhi.

o Maadhavakara, Maadhava Nidaana with Madhukosha Vyaakhya by

Vijayarakshita and Srikantadatta and Vidyotini Teeka by

Ayurvedaachaarya Sri Sudarshana Shaastri, 30th edition, 2001,


o Maadhava, Ayurveda Prakaasha with Artha Vidyotini and

Arthaprakaashini Sanskrit Hindi Vyaakhya, edited by Sri Gulraj Sharma

Mishra, 1999, Published by Chaukhambha Bharati Academy Varanasi.

o Mahajan B.K,Methods in Biostatistics, 6th Edition, Pub: Jaypee Brothers.

o Morris Peter j., Ronald A. Malt; Oxford Text-book of Surgery, Oxford

CD-ROM, 1995, Oxford University Press.

o P.V.Sharma, Dravya Guna Vignana, vol. 2, 17th edition, 1996,

Chaukhambha Vishva Bharathi Academy, Varanasi.

o P.V.Sharma, Indian Medicine in the classical age, 1st edition 1972,

Published by Chaukhambha Sanskrit Series, Varanasi.

o P.V.Sharma, History of Medicine in India, 2nd edition, 1992, Published

by Indian National Science Academy New Delhi.

o Rasa Shaastra by Dr. Damodhar Joshi, 1st edition 1986, Published by

Publication Division, Ayurveda College Trivandrum.

o Rasayoga Saagara with Sanskrit and English introduction, notes by

Pandit Hariprapannaji vol 1,Reprint edition 1998, Published by Krishna

Das Academy, Varanasi.

o S.Das, A Concise Text book of Surgery, 3rd edition, 2001, Published by

Dr. S. Das., 13, Old Mayors’ Court, Calcutta.

o S.Das, A Manual on Clinical Surgery by, 3rd edition, 1996, Published by

Dr. S. Das. 13, Old Mayors’ Court, Calcutta.

o Sodhala, Gadanigraha with Vidyotini Hindi commentary by Sri

Indradeva Tripathi, 3rd edition 1999, Published by Chaukhambha Sanskrit

Sansthaan, Varanasi.

o S.C.Atri,Hand Book of Surgery,3rd edition, Published by Scientific Book

Company Patna.

o Shaarangadhara, Shaarangadhara Samhita, edited by Pandit

Parashuraama Shaastri, Vidyasagar, 4th edition 2000, Published by


o Singal G.D and Singh L.M, Ancient Indian surgery 1st edition, Published

by Chaukhambha Sanskrit Sansthaan Varanasi.

o Sushruta, Sushruta Samhita with English translation by Prof. K.R.

Srikantha Moorthy, 1st edition 2002, Published by Chaukhambha

Orientalia Varanasi.

o Sushruta, Sushruta Samhita with English translation of text and Dalhana

commentary, edited and translated by P. V. Sharma, 1st edition, 1999,

Published by Chaukhambha Sanskrit Sansthaan Varanasi.

o Sushruta,Sushruta Samhita with Nibandhasangraha Commentary of Sri

Dalhana Aachaarya and Nyaaya Chandrika Panjikaa Vyaakhya of Sri

Gayadaasaachaarya, edited by Vaidya Yadavji, Trikamji Aachaarya, 7th

edition 2002, Published by Chaukhambha Orientalia Varanasi.

o Vaagbhata, Ashtaanga Hrudaya with commentaries Sarvaangasundari of

Arunadatta and Ayurveda Rasayana of Hemaadri, collated by Late Dr.

Anna Moreshwara Kunte and Krishna Raamachandra Shaastri,8th edition

1998, Published by Chaukhambha Orientalia, Varanasi.

o Vruddha Jeevaka, Kaashyapa Samhita, with English Translation and

commentary, edited by P.V.Tewari, 1st edition 1996, Published by

Chaukhambha Visvabharati, Varanasi.

o Vruddha Vaagbhata, Ashtaanga Sangraha, by Kaviraj Atrideva Gupta,

edition 1993, Published by Krishna Das Academy, Varanasi.

o Yogaratnaakara, with Vaidyaprabha Hindi Commentary by Dr. Indradev

Tripathi and Dr. Dayashankar Tripathi,1st edition 1998, Published by

Krishna Das Academy, Varanasi.

DEPARTMENT OF SHALYA TANTRA S.D.M. COLLEGE OF AYURVEDA

KUTHPADY – UDUPI.

PROFORMA OF CASE SHEET FOR THE EFFICACY OF JATYADI TAILA IN

THE MANAGEMENT OF DUSHTA VRANA

Name: Case No:

Age: OPD No:

Sex: M/F IPD No:

Religion: Room No. & bed No.:

Socio- economic status: Date of admission:

Marital status: M/UM Date of discharge:

Occupation: Treatment started on:

Address: Treatment completed on:

I. CHIEF COMPLAINTS:

1) VRANA: a) Kaala ( Duration ):

b) Sthaana:

c) Onset: (Sudden/ Recurrent/ gradual)

d) Number of ulcers:

2) SRAAVA : a) Present/Absent (If present – V,P,K,R)

b) Varna

c) Consistency

3) GANDHA: Present/Absent (If present – V,P,K,R)

4) KANDU: a) Present/Absent

b) Duration

5) DAAHA : Present/Absent 6) VEDANA: a) Present/Absent

If present duration :

7) JVARA: Present/Absent

If present

a) Duration

b) Character

c) Rigors

d) Chills

e) Periodicity

8) ANY OTHER ASSOCIATED COMPLAINTS:

II. HISTORY OF PRESENT ILLNESS:

III. HISTORY OF PAST ILLNESS: IV. FAMILY HISTORY: V. PERSONAL HISTORY:

1) Appetite: Good/Moderate/Poor

2) Diet: Vegetarian/Mixed

3) Bowel: R/IR Constipated/Loose Stools

4) Micturition:

5) Sleep: Sound/Disturbed

6) Habits:

VI. TREATMENT HISTORY:

VII. OBS. HISTORY/GYNAEC HISTORY:

VIII. GENERAL EXAMINATION:

a) Built

b) Gait

c) Vitals: - BP:

P.R:

R.R:

Temp:

d) Lymph nodes:

IX. SYSTEMIC EXAMINATION:

(1) Cardio Vascular System:

(2) Respiratory System:

(3) Central Nervous System:

(4) Gastro Intestinal System:

(5) Other Systems:

X. EXAMINATION OF THE ULCER:

A. Inspection site:

(i) Size and Shape:

(ii) Number:

(iii)Position:

(iv) Edge: Undermined

Sloping

Punched out

Raised and Pearly white beaded

Rolled out

(v) Floor: Covered with slough / not

If slough is present then color of slough:

(vi) Discharge: Present or absent

If present: Color –

Consistency-

(vii) Surrounding area of ulcer : Present/Absent

B. Palpation: i) Size of the ulcer: Length

Breadth

Depth

(ii) Tenderness: Present/Absent

(iii) Bleeding on touch: Present/Absent

(iv) Edge: Indurated / not

C. VISHESHA PAREEKSHA

Assessment of the type of Dushta Vrana:

Vrana Prakaara

Varna Sraava Vedana

V Shyaava, Arunaabha, Bhasma, Kapotaasthi, Parusha, Krushna

Picchila, Alpa, Kshaarodaka, Dadhimastu, Maamsadhaavana,

Sphurana, Aayaama, Todha, Bheda, Chedana, Vedana Bahula

P Peeta, Neela, Harita, Kapila, Pingala

Kimshukodaka, Ushna, Gomeda, Gomootra

Daaha, Osha, Chosha, Dhoomaayana

K Paandu, Shweta Shukla, Sheeta, Saandra, Kaaseesa, Picchila, Navaneeta

Manda Vedana, Kandu, Gurutwa, Suptata, Stambha

R Peeta, Neela, Rakta, Kapila, Pingala, Krushna

Kimshukodaka, Ushna, Rakta, Ativisratva

Sphotha, Daaha, Dhoomaayanasheela, Osha, Chosha

V-P Peeta, Aruna Peeta, Aruna Todha, Daaha, Dhoomaayana

V-K ------ Sheeta, Picchila Kandu, Nistodha, Daaruna

V-R Rakta, Aruna Rakta, Aruna Todhabahula, Supta P-K ------ Peeta, Aruna Daaha P-R ------ Ghruta Manda, Meena

Dhaavana Toya Gandhi, Mrudu, Ushna, Krushna

------

K-R Rakta Rakta, Paandu Kandu V-P-R ------ Peeta, Tanu, Rakta Sphurana, Todha, Daaha,

Dhoomaayana

V-K-R ------ Paandu, Ghana, Rakta Kandu, Sphurana, Chumachumaayana

P-K-R ------ Paandu, Ghana, Rakta Daaha, Kandu

V-P-K Trividha Vedana Trividha Sraava, Naarikelodaka, Ervaruka Rasa, Kaanji, Mudgha Yoosha

Trividha Vedana

V-P-K-R Naanaa Varna Naanaa Varna Sraava Nirdahana, Kandu, Nirmathana, Daaha, Sphurana, Todha,

Dushta Vrana Prakaara:

Assessment of Sraava according to the Adhishthaana:

Sthaana Sraava Twak Salilaprakasha, Peetaavabaasa. Maamsa Sarpiprakasha ,Sheeta, Picchila. Sira Rakta Atipravruthi, Pooya comes out after

Paaka. Snaayu Snigdha, Ghana, Singhanaka pratima, Sarakta. Asthi Discharge mixed with Rakta, Majja. Sandhi Picchila, Saphenarudhira. Kostha Discharges Asruk, Mootra, Pureesha, Pooya,

Udaka. Adhishthaana: XI. Examination of vascularity:

A. Inspection:

Visible color changes: B. Palpation:

(a) (i) Dorsalis pedis Palpable/Not palpable/Feeble

(ii) Tibialis posterior Palpable/Not palpable/Feeble

(iii) Poplitial Palpable/Not palpable/Feeble

(iv) Femoral Palpable/Not palpable/Feeble

(b) Local rise of temperature Present/Absent

(a) Sensation Normal/Altered

C. Varicosity Present/Absent

D. Deep vein thrombosis Present/Absent

E. Any other examination (if required)

XII. Investigations:

XIII. Diagnosis according to the cause:

XIV. Chikitsa:

XV. Complications during the treatment:

XVI. Conclusion: Date: Signature:

FOLLOW UP CHART

Name: O.P.NO/I.P.NO:

Assessment criteria

BT 2nd D

3rd D

4th D

5th D

6th D

7th D

14D 21D 28D 35D 42D 49D 56D 63D 70D 77D 84D AT

Pain

Itching

Burning sensation

Size

(In cms.)

Tenderness

Discharge

Smell

Surrounding area of ulcer

Floor & granulation tissue

.

Incidence Chart Group A:

Sl.

N .

Nam

e

Op

/ Ip

No.

Age

Sex

Occ

upat

ion

Rel

igio

n

Soc

io-e

cono

mic

stat

us

Mar

ital

sta

tus

Hab

itat

Die

t

Chr

onic

ity

Sth

aana

Typ

e

Adh

isht

aana

01 RPG 19605 27 M MCH C LMC UM U V 30 D LL VP T

02 NK 19656 48 M HB H LMC M R V 6 M LL VP TMS

03 BF 70126 45 F HW M LMC M U M 45 D LL VP T

04 ED 21459 60 F HW C LMC M R M 2.5 M LL VP TM

05 MSD 21594 32 M B H UMC M R M 45 D LL VP TM

06 GN 21950 45 M T H LMC M U M 6 Y LL VK TM

07 VS 24039 48 M Lb H P M R M 1 Y LS VK TMS

08 JS 22479 54 M HTW H LMC M R M 9 M LL VK TM

09 RSH 24296 35 M B H LMC M R M 45 D LL VP TM

10 VP 24302 60 M B H UMC M U M 2 Y LS VK T

Incidence Chart: Group. B:

Sl.

No.

Nam

e

\Op

No.

Age

Sex

Occ

upat

ion

Rel

igio

n

Soc

io-e

cono

mic

Sta

tus

Mar

ital

sta

tus

Hab

itat

Die

t

Chr

onic

ity

Sth

aana

Typ

e

Adh

isht

aana

1 RS 22531 57 M HTW H LMC M U M 30 D LL VK TM

2 KMA 20416 26 M Lb C P UM R M 15 D LL VK TM

3 RGS 21255 58 M A H UMC M R M 30 D LL VP TM

4 RKS 21500 22 M S H LMC UM R M 15 D UL VP T

5 MN 21682 32 M HTW H LMC M R M 15 D LL VK T

6 LD 23932 58 M DR C LMC M R M 1 M LL VK TM

7 VK 24256 52 F HW H LMC M R M 15 D LL KP T

8 SF 23905 21 M S M UMC UM R M 20 D LL VP TM

9 BS 24364 48 M B H LMC M R M 25 D LL VK TM

10 RS 24492 60 M Lb C P M U M 20 D LL PV T

Observation Chart Group A

Pai

n

Itc

B.S

Dis

Td Sm

ell

S.A

Flo

or

& G

r

Sl.

No.

Nam

e

I.P

/O.P

.No.

BT

AT

BT

AT

BT

AT

BT

AT

BT

AT

BT

AT

BT

AT

BT

AT

1 RPG 19605 3 0 0 0 2 0 2 0 2 0 2 0 0 0 2 0

2 NK 19656 1 0 0 0 1 0 2 0 2 0 2 0 3 1 3 0

3 BF 70126 1 0 0 0 1 0 2 0 2 0 1 0 0 0 2 0

4 ED 21459 1 0 0 0 2 0 1 0 1 0 0 0 0 0 2 0

5 MSD 21594 2 1 1 0 2 1 1 0 2 1 0 0 1 1 1 0

6 GN 21950 1 0 3 0 0 0 0 0 1 0 0 0 3 1 3 0

7 VS 24039 1 0 2 1 0 0 2 1 1 0 0 0 0 0 2 1

8 JS 22479 1 1 1 0 1 0 2 0 2 1 0 0 3 1 2 1

9 RSH 24296 3 0 1 0 2 0 1 0 2 0 0 0 0 0 1 1

10 VP 24302 1 0 1 0 0 0 2 1 0 0 0 0 0 0 2 1

Group B

Pai

n

Itc

B.S

Dis

Td Sm

ell

S.A

Flo

or

& G

r

Sl.

No.

Nam

e

I.P

/O.P

.No.

BT

AT

BT

AT

BT

AT

BT

AT

BT

AT

BT

AT

BT

AT

BT

AT

1 RS 22531 2 1 2 0 0 0 2 1 1 0 1 0 3 1 3 1

2 KMA 20416 3 0 2 0 1 0 2 0 2 0 0 0 1 1 1 0

3 RGS 21255 1 0 0 0 1 0 0 0 1 0 0 0 1 1 2 1

4 RKS 21500 3 1 0 0 2 0 2 1 2 1 0 0 2 0 2 1

5 MN 21682 2 1 2 1 0 0 2 0 2 0 1 1 2 0 3 1

6 LD 23932 2 1 3 2 0 0 1 0 2 1 1 0 0 0 2 1

7 VK 24256 1 1 1 0 3 1 0 0 3 2 0 0 0 0 2 1

8 SF 23905 3 1 0 0 3 1 3 0 3 1 0 0 2 2 3 1

9 BS 24364 1 0 1 0 0 0 0 0 1 0 0 0 1 1 1 0

10 RS 24492 3 0 0 0 1 0 0 0 2 0 0 0 2 0 1 0

Observation Chart Group A

L o

f

ulce

r

W o

f

ulce

r

Dep

of

ulce

r

Sl.

No.

Nam

e

I.P

/O.P

.No.

BT

AT

BT

AT

BT

AT

1 RPG 19605 14 0 7.5 0 0.5 0

2 NK 19656 7.5 0 6.5 0 0.6 0

3 BF 70126 2.5 0 2 0 0.2 0

4 ED 21459 5 0 3.5 0 0.4 0

5 MSD 21594 4.5 0.4 3 0.1 0.3 0.1

6 GN 21950 4 0 4 0 0.2 0

7 VS 24039 15 10 8.75 4.5 0.3 0.1

8 JS 22479 5 1 4.5 0.8 0.3 0.05

9 RSH 24296 8 0 6 0 0.6 0

10 VP 24302 10 5.3 7.5 3.8 0.3 0.15

Group B

L o

f

ulce

r

W o

f

ulce

r

Dep

of

ulce

r

Sl.

No.

Nam

e

I.P

/O.P

.No.

BT

AT

BT

AT

BT

AT

1 RS 22531 5 2.5 3.5 1.2 0.2 0.06

2 KMA 20416 1.5 0 1 0 0.1 0

3 RGS 21255 2.5 1.2 2 0.75 0.2 0.10

4 RKS 21500 11.5 4 6 2.5 0.03 0.02

5 MN 21682 4 0.5 1.5 0.2 0.1 0.01

6 LD 23932 2.5 0.1 2.5 0.05 0.3 0.09

7 VK 24256 2 0.2 2 0.1 0.2 0.06

8 SF 23905 4 0.4 2 0.25 0.5 0.2

9 BS 24364 2 0 2 0 0.2 0

10 RS 24492 1 0 1 0 0.2 0

Abbreviations for Incidence Chart & Observation:

Sex: M- Male F- Female

Religion: H- Hindu M- Muslim C- Christian

Marital status: M- Married UM- Unmarried

Occupation: HW- House wife S- Student HTW-Hotel worker

MCH- Mechanic B- Business A- Agriculture

Lb- Labourer DR- Driver T- Tailor

Socio- economic

Status: P- Poor LMC- Lower middle class

R- Rich UMC- Upper middle class

Habitat: U- urban R- Rural

Diet: V- Vegetarian M- Mixed

Sthaana: LL- Lower Limb UL- Upper Limb LS-Lumbo sacral

Adhishthaana: T- Twak M- Maamsa S- Sira

Vranaprakaara: V- Vaata P- Pitta K- Kapha

S.A- Surrounding area Gr- Granulation

B.S-Burning sensation Itc-Itching Dep-Depth

Dis-Discharge L- Length W-Width

Td-Tenderness n=number of patients

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