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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

DEPARTMENT OF POST GRADUATE STUDIES IN SHALYA TANTRA

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

2004

DEPARTMENT OF POST GRADUATE STUDIES IN SHALYA TANTRA

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

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.

 

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

Place : Udupi

Guide,Professor and Head of the Department,

Department of Post Graduate studies in

Date : .02.2004

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

ACKNOWLEDGEMENTS

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.

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 & the mean score was reduced to 0.1.

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 the mean score was reduced to 0.6.

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.

Balavat Vigraha,Ativyaama, suppresion

 

 

Katu,Lavana,

of Adhaarniya Vegas, etc.

 

 

Laghuaahara,Sushkasaaka,Valloora,

 

 

 

 

Uddhalaka etc.

 

 

 

PITTA

Pittaprakopakaahaaraas i.e.Katu, Amla,

Krodha, Shoka,Bhaya,Maithuna,Aayasa

 

 

Lavana, Ushna, Vidaahi, Teekshna,

Upavaasa etc.

 

 

Tila, Pinyaka, etc.

 

 

 

KAPHA

Kaphaprakopakaaahaaraas, i.e.

Divaswapna, Avyayaama, Aalasya .

 

 

Madhura, Amla, Lavana, Sheeta,

 

 

 

 

Snigdha Aahara, Maasha etc.

 

 

 

 

 

 

 

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

Sushruta

Charaka

Kashyapa

A.San.

A.H.

M.Ni.

 

as

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Shyaava,

 

 

 

 

 

 

 

Shyaava,

Krushna,

 

 

 

 

Shyaava or

 

 

Aruna,

Aruna,

 

 

 

Varna

Shyaava

-

Krushna,Bh

Bhasma

Shyaava

 

Aruna

 

 

 

 

asma of

kapotha or

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Asthi.

Asthi

 

 

 

 

 

 

 

 

Varna

 

 

 

Vartma

Rooksha

Stabdha,

Stambha,

-

-

Stabdha,

 

Kathina

Kathina

Kathina

 

 

 

 

 

 

 

Todha,

Teevra

 

Sphuruna,T

 

 

 

 

 

Bheda,

 

Todha,

 

 

 

Vedana

Ruk,

Maharuja

odha, Bheda

Maharuja

 

Chatachataya

Bheda etc.

 

 

na etc

Sphurana

 

etc.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Alpa sraava

Alpasraav

 

 

 

 

 

 

 

resembling

a

 

 

 

 

Sheeta,Picchi

Mandhasra

Alpasraav

Mastu,

resemblin

Mandhasr

 

Sraava

la,Alpasraav

Kshaara,

g Mastu,

 

ava

a

aava

 

 

a

Maamsa

Maamsa,

 

 

 

 

 

 

 

 

 

 

 

Dhaavana,

Pulakaam

 

 

 

 

 

 

 

Pulakodaka

bu

 

 

 

 

 

 

 

 

 

 

 

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

 

 

 

 

Peeta, Neela,

Neela,

 

Varna

Peeta,

-

-

Haritha,

Peeta,

-

Neelabha

Krushna,

Kapila

 

 

 

 

 

 

 

 

Pingala

Pingala

 

Utpatti

Kshipra

-

-

Kshipra

Kshipra

-

 

Daaha,

 

 

 

Raaga,

 

 

 

 

 

Paaka

 

 

Paaka,

 

 

 

Trushna,

 

Trushna,

Jwara,

Daaha, Raaga,

pain

Anya

Raaga,

Moha,

Moha,

Daaha,

Paaka,

resembli

lakshana

studded

Jwara,

Jwara,

Moha,

Jwara,Dhoomay

ng Vrana

s

with

Kleda,

Sveda,

Trushna

ana,

caused

 

Peeta

Daaha

 

 

 

 

by

 

Pidaka

 

 

 

 

 

 

 

 

Kshaara

 

 

 

 

 

 

 

 

 

 

 

 

Sraava is

 

 

 

 

 

 

warm,

 

 

 

 

 

Sraava large in

large in

 

 

Sraava

 

 

qty. resembling

qty

 

 

resembli

 

 

Gomootra,

resembli

 

Sraava

ng

Pootisraa

Pootisraa

solution of

ng

Pootisraa

Kimshuk

va

va

Bhasma,

Kimshuk

va

 

 

a flower,

 

 

Kimshuka or

a, Taila

 

 

Ushna.

 

 

Mrudveeka or

or

 

 

 

 

 

Taila

solution

 

 

 

 

 

 

of

 

 

 

 

 

 

Bhasma

 

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

 

Sthoola,

 

 

 

 

 

 

covered

 

 

 

Sthoola,

 

 

with

Snigdha,

Sthaimith

Snigdha,

Katina,

Bahu

 

Stabdha

ya,

covered

piccha,

Vartma

Guru,Bah

Katina,

Sira

Maardhav

with Sira

Guru,

 

u piccha

Sthoola

 

Snaayu

a

Snaayu

Snigdha

 

 

 

 

jaala,

 

 

 

Jaala

 

 

Katina

 

 

 

 

 

 

Mandha

 

 

Mandha

 

 

 

vedana,

Mandha,

Mandha,

vedana,

 

Mandha

Anya

severe

Kandu,

Alparuk,

vedana,

vedana,

vedana

lakshanas

Kandu,

Swaapa,

Kandu

Sthaimith

Chirakaari

Chirakaari

 

feeling of

Sthaimith

 

ya

 

 

 

 

 

heaviness

 

 

ya

 

 

Sraava

 

 

 

Sraava

 

 

 

 

 

 

resemblin

Large

Alpa

 

 

 

 

g

 

Shukla,

 

 

qty. of

Samkleda

 

Alpa

 

Navaneeta

 

Sheeta,

Atisraava

Sveta

,

 

samkleda

, Tila

 

Saandra

 

Ghana

Chirapaak

 

 

 

pishta,

 

 

 

 

sraava

i

 

 

 

 

Naarikelo

 

 

 

 

 

 

 

 

 

 

daka

 

 

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

Pravaala

Raktha

 

(Raktha)

(Raktha)

 

 

 

 

 

 

 

Covered with network of

Covered with

 

 

 

 

Vartma

Krushnasphota,

-

-

 

 

Krushnasphota, Pidaka

 

 

 

Pidaka

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Smells like Turanga

Smells like

Smells like

 

 

Vaaji Sthaana,

Vaaji Sthaana,

 

 

sthaana, Vedanaayuktha,

 

Anyalakshanas

has other

has other

-

Dhoomayana Sheela and

 

features of

features of

 

 

having features of Pitta

 

 

Pitta

Pitta

 

 

 

 

Sraava

Raktha Sraava

Sarakthapooya

Sarakthapooya

Raktha

Sraava

Sraava

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

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Meena

 

Gandha

-

-

-

-

dhaavana

-

 

 

 

 

 

toya

 

 

 

 

 

 

 

 

Varna

Aruna, Peeta

-

-

Rakta,

-

Rakta

Aruna

 

 

 

 

 

 

 

 

 

 

 

 

 

Vedana

Todha,

Todha,

Daaha,

Todha,

-

Kandu

Daaha,Dhoomayana

Kandu

Ushna

Supta

 

 

 

 

 

Sheeta,

Peeta,

Rakta,

Ushna,

Rakta,

Sraava

Peeta, Aruna

Picchila,

Paandu

Aruna

Krishna

Paandu

 

 

Alpa

 

 

 

 

 

 

 

 

 

 

 

 

 

Anya

 

Rooksha,

 

Rooksha,

Mridu,

Guru,

-

Guru,

Guru

Picchila,

Lakshanas

Tanu

Visarpa

 

Dhaaruna

 

Snigdha

 

 

 

 

 

 

 

 

 

 

 

 

Table No.

7- Tridoshaja and

Sannipaataja Vrana Lakshanas13:

 

 

Lakshanas

VPR

VKR

PKR

VPK

VPKR

 

 

 

 

 

Has

 

 

 

Varna

-

-

-

Varna of

-

 

 

 

 

 

 

3 types

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Nirdahana,

 

Sphurana,

 

 

Has

Nirmathana,

Vedana

Todha,

Kandu, Sphurana,

Daaha,

Vedana

Sphurana,

Daaha,

Chumachumayana

Kandu

of 3

Todha,

 

 

Dhoomayana

 

 

types

Daaha,

 

 

 

 

 

Kandu

 

Peeta, Tanu,

Paandu, Ghana,

Paandu,

Has

 

Sraava

Ghana,

Sraava of

Naana Varna

Rakta

Rakta

 

Rakta

3 types

 

 

 

 

 

Anya

-

-

Paaka,

-

Paaka, Raaga

Lakshanas

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

Mentioned 12

Either Atisamvrutha

Either Samvrutha

Discharg

or Ativivrutha

characteristic

or Ativivrutha,

or Vivrutha,

es Pooti

Ati-katina or

features indicating

Atimrudu or Katina,

Katina or Mrudu

Sraava,

 

Mrudu,

the advanced stage of

Atiutsaadha or

Atiutsanna or

or Dushta

 

Utsanna or

morbidity of Vrana.

Avasaadha,

Avasanna,

Ashruk,h

Avasanna. Ati

Svetatva, Avasanna

Atisheeta or Usna

Atiushna or

as

 

sheeta or

Vartmatva,

Rakta, Krushna, or

Atisheeta,

Utsangi

Usna, having

Athisthoola-

Paanduta, covered

Raktatwa or

(sinuses)

 

one of the

Vartmatva,Atipinjara

with Pooti Maamsa,

Paanduta,Dischar

inside,

 

colours

tva, Neelatva,

Sira,Snaayu, etc.

ges Pooti Pooya

Chirastit

Krushna,Rakta

Syaavatva,

Dishcarges Pooti

covered with

ha, emits

, Peeta, Shukla

Atipidakatva, Rakta-

Pooya, Daaha,

Pooti Maamsa,

Pooti

etc,Bhairava,fi

Krushnatva

Paaka,

Sira, Snaayu,

Gandha

 

lled with

Atipootitva,

Kandu,Svayathu,Ve

associated with

&

 

Pootipooya,M

Ropyatva Kumbhi-

dana Pitaka, etc.

Atiruk, Daaha,

doesn’t

 

aamsa, Sira,

Mukhatva,.Vranas

appearing as

Swayathu, Kandu

posses

 

Snaayu etc.

with Pootigandha,

Upadravas, Dheerga

& other

any

 

Moving in

Vivarna, Bahusraava,

Kaalanubandha

complications,

features

oblique track

Maharuja

 

Dheerga Kaalanu

of

 

(Unmargi)

 

 

bandha

Shuddha

 

having

 

 

 

Vrana

 

Amanoghna

 

 

 

 

 

 

Darshana,

 

 

 

 

 

 

Atigandha,

 

 

 

 

 

Vedanayukta,

 

 

 

 

 

 

associated

 

 

 

 

 

 

with Daaha,

 

 

 

 

 

Paaka, Raaga,

 

 

 

 

 

 

Kandu,

 

 

 

 

 

Shopha Pidaka

 

 

 

 

 

 

etc.

 

 

 

 

 

 

Discharging

 

 

 

 

 

 

excessively

 

 

 

 

 

 

Dushta

 

 

 

 

 

 

Shonitha,

 

 

 

 

 

 

Dheerga

 

 

 

 

 

 

 

 

 

 

 

 

Kaalaanuband

hi

Shuddha Vrana16:

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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

Na

Not vitiated by

Resembles Jihva

ResemblesJihva

Tridoshas

Atirakta,

Doshas,

in color,

Talaaba and is

having Shyaava

Paandu,

resembles Jihva

Mrudu,Slakshna

Atimrudu,Slakshna

Oshta,

Shyaava,(n

in color, and is

with Shyaava

,Snigdha,

resembles Jihva

a ati) Ruk,

Slakshna having

Osta,Samapidika,

Suvyavasthitha,

Talaabha & is

Utsanna,

Shyaava Oshta

having Unnata

Alpa Vedana ,

Mrudu, Snigdha

Utsangi.

centre being

Madhya,not

Niraasraava.

not having

 

elevated or even

acommpanied

 

Vedana, Sraava,

 

not having

with any

 

good looking,

 

Vedana, Sraava.

Upadravas.

 

has developed

 

 

 

 

Sama Pidika.

 

 

 

 

 

 

 

 

 

Ruhyamaana vrana18:

Lakshanas:

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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:

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|

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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:

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±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

Injury to Maamsa, Sira, Snaayu,

Saamanya Lakshanas:- Bhrama, Pralaapa,

Sandhi, Asthi

Pathana, Srasthangatha,

 

Vichestana, Pramoha, Glani, Ushnata,

 

Moorcha, Teevraruja, dischrge of Rakta

 

resembling Mamsodaka, loss of functions of

 

Indriyas etc.

 

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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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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e®d¯ddy°dPda £d¤ddííUµdTZ ¯ddyePd£d±Sd Ÿd «ddy´dPd«dŠ |

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£dSddyTy®d I¶°ddSdyPd £dz¬da ¯ddy¥d¦de«d°Sd£dy |

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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,Vaikritaapa ham

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

-

Ropana

 

 

 

 

Ghrita,Ropana

 

Ghrita.

 

 

 

 

Ghrita.

 

 

 

 

Taila

+

Shodhana

-

Ropana

 

 

 

 

Taila,Ropana

 

Taila.

 

 

 

 

Taila

 

 

 

 

Rasakriya

+

-

-

+

 

 

Avachoornana

+

+

-

Choorna.

 

 

Vranadhoopana

+

+ (Kaatinyakara,

-

+

 

 

 

 

Maardhavakara)

 

 

 

 

Utsaadana

+

+

-

+

 

 

Avasaadana

+

+

-

+

 

 

Mrudukarma

+

Maardhavakara

-

+

 

 

 

 

Aalepana.

 

 

 

 

Dhaarunakarma

+

Kaatinyakara

-

+

 

 

 

 

Aalepana

 

 

 

 

Kshaarakarma

+

+ (Daaha)

-

+

 

 

Agnikarma

+

+ (Daaha)

-

+

 

 

Krishnakarma

+

Varnya

Savarneekara

Savarnakara

 

 

 

 

 

na

na

 

 

 

 

 

 

 

 

Paandukarma

+

Varnya

Savarneekara

Savarnakara

 

 

 

na

na

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

-

+

+

-

Utklinnaprakshaal

-

-

+

Prakshaalan

ana

 

 

 

a.

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,

Sandhaana, Peedana, Shonitasthaapana, Nirvaapana, Utkaarika,

Ropana

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

Chinna Vrana is further divided into

----

Vrana is

 

 

oblique

five types

 

oblique/straight,

 

 

/straight,sepera

i.e.Ghrishta,Avakritha,Avagaada,Vila

 

wide, causing

 

 

tion of body

mbita,Paatita.

 

seperation of

 

 

parts.

 

 

body parts.

Bhinna

Perforation/

Mentioned

Vrana

Puncture of

 

 

puncture of

Anubhinna,Bhinnotthundita,Atibhinna

occuring in

Aashayas,dischar

 

 

 

 

 

 

 

 

Aashayas,exud

,Nirbhinna to those Vranas which

Koshtha

ging contents to

 

ing mild

occur in Koshtha.

with small

the exterior.

 

Sraava.

 

orifice.

 

Viddha

Injury to any

Classified into further 8 types-

Vrana with

Injury to any part

 

part of body

Anuviddha,Uttundita,Atividdha,Nirvid

small

of body other

 

other than

dha etc.

orifice

than Aashayas

 

Aashaya,Uttun

 

occuring

and Uttundita.

 

dita.

 

anywhere

 

 

 

 

other than

 

 

 

 

Koshtha.

 

Kshata

Vrana which is

Considered Chinna,Viddha &Picchita

…………

Neither

 

neither Ati

as Kshata because of loss of skin

……..

Atichinna nor

 

Chinna nor Ati

continuity.

 

Ati Bhinna but

 

Bhinna. but

 

 

having mild

 

having

 

 

features of both

 

features of

 

 

& irregular in

 

both and

 

 

shape

 

irregular in

 

 

 

 

shape.

 

 

 

Type

Sushruta

A. San.

A.H.

M.Ni.

 

 

 

 

 

Picchita

Flattening of

Body part with Asthi increasing in size

Mentioned

Flattening of any

 

any part of

by getting soaked in Rakta and Majja.

Vidalita in

part of body

 

body along

it is of two types with Vrana and

which

along with Asthi,

 

with Asthi,

without Vrana.

features are

filled with Rakta

 

filled with

 

similar to

and Majja.

 

Rakta and

 

features

 

 

Majja.

 

mentioned

 

 

 

 

in Sushruta.

 

Ghrista

Peeling of skin

Mentioned it as Twak Chedana.

Exudes

Peeling of skin

 

of any part of

 

Laseeka

of any part of

 

body

 

alone or

body

 

accompanied

 

mixed with

accompanied

 

with watery

 

lttle of

with watery

 

exudation.

 

Rakta

exudation.

 

 

 

associated

 

 

 

 

with

 

 

 

 

burning

 

 

 

 

sensation.

 

Avagaad

………………

Broad and long(Vishaala and

Severe than

………….

a

 

Aayama)mentioned it as a type of

Ghrishta

 

 

 

Chinna Vrana.

Vrana.

 

Vichinn

………………

…………….

Severe than

…………….

a

 

 

Avagaada

 

 

 

 

Vrana.

 

Paatita

………………

Body part getting detached or

Injured

……………….

 

..

seperated completely from body.

body part

 

 

 

 

gets

 

 

 

 

seperated

 

 

 

 

from body.

 

Pravila

………………

…………………

Vrana in

………………

mbhi

 

 

which Asthi

 

 

 

 

remains in

 

 

 

 

place.

 

Vilambit

………………

Vrana in which little of Asthi,Snaayu

…………

……………..

a

 

etc remains as residue.

………

 

Avakrut

………………

Abrasion of Twak and little of

…………

………………

ha

 

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

Family

Useful

Chemical

Rasa

Guna

Veer

Vipaa

Prabha

Karma

 

 

 

 

name

 

part

compositio

 

 

ya

ka

ava

 

 

 

 

 

 

 

 

 

n

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Jaati

Sumana,

Jasmi

Oleaceae

Patra,

Salicylic

Tikta,

Laghu,

Ushn

Katu

-

Kapha,

Pitta,

 

 

Chetika

num

 

Puspha,

acid,

Kashaa

Snigdh

a

 

 

Vaata Hara

 

 

 

officin

 

Moola.

Jasminine

ya

a,

 

 

 

 

 

 

 

 

 

ale

 

 

 

 

Mrudu

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Nimba

Tiktaka,

Azadir

Meliaceae

Panchang

Bark-

Tikta,

Laghu

Sheet

Katu

-

Kapha,

Pitta

 

 

Pichu-

achta

 

as.

nimbine,

Kashaa

 

a

 

 

Shaamaka,

 

 

marda

indica

 

 

Margosine,

ya

 

 

 

 

Pootihara,

 

 

 

 

 

 

nimbidine

 

 

 

 

 

Kushtaghna,

 

 

 

 

 

 

 

 

 

 

 

 

Kandooghna,

 

 

 

 

 

 

 

 

 

 

 

 

Shodhana,

 

 

 

 

 

 

 

 

 

 

 

 

Ropana,

 

 

 

 

 

 

 

 

 

 

 

 

 

Vedana

 

 

 

 

 

 

 

 

 

 

 

 

 

sthaapana

Patola

Kulaka,

Tricho

Cucurbitac

Patra.

Fruit-

Tikta

Laghu,

Ushn

Katu

-

Vaata

 

 

 

Raaji-

santhu

eae

 

protein, fat,

 

Rooks

a

 

 

Pitta

 

 

 

Phala

s

 

 

Calcium,

 

ha,

 

 

 

Kapha

Hara,

 

 

 

dioca

 

 

Mg

 

 

 

 

 

Vrana

 

 

 

 

 

 

 

 

 

 

 

 

 

Shodhana,

 

 

 

 

 

 

 

 

 

 

 

 

Ropana,

 

 

 

 

 

 

 

 

 

 

 

 

 

Vedanasthaa

 

 

 

 

 

 

 

 

 

 

 

 

pana

 

Naktama

Karanja,

Ponga

Legu-

Patra,

Kara-

Tikta,

Laghu,

Ushn

Katu

-

Kapha

 

ala

Snigdha

mia

minosae.

Twak,

njin,

Katu,

Teeksh

a

 

 

Vaatahara,

 

 

patra

pinnat

 

Beeja.

pongamol,

Kashaa

na

 

 

 

Pitta

 

 

 

 

a

 

 

pongamin

ya

 

 

 

 

Vardhaka.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Siktaka

-

-

-

-

-

Madhu

Snigdh

-

-

-

Sand-

 

 

 

 

 

 

 

 

ra

a,

 

 

 

hanakara,

 

 

 

 

 

 

 

 

Picchil

 

 

 

Vrana

 

 

 

 

 

 

 

 

 

a

 

 

 

Ropaka,

 

 

 

 

 

 

 

 

 

 

 

 

 

Bhootaghna

Madhuk

Kleethaka,

Glycy

Leguminos

Moola

Glycyrrhizi

Madhu

Guru,

Sheet

Madh

-

Vaata

 

a

Yashtimadh

rrhiza

ae

 

n.

ra.

Snigdh

a

ura

 

Pittahara,

 

 

u.

glabra

 

 

 

 

a

 

 

 

Vedana

 

 

 

 

 

 

 

 

 

 

 

 

 

sthaapana,

 

 

 

 

 

 

 

 

 

 

 

 

Daahashaam

 

 

 

 

 

 

 

 

 

 

 

 

aka

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Kushta

Vaapya,

Sauss

Composita

Moola

Alkoloids

Tikta,

Laghu,

Ushn

Katu

-

Kapha

 

 

 

Utpala

urea

e

 

inulin,sauss

Katu,

Rooks

a

 

 

Vaatahara,

 

 

 

lappa

 

 

urine

Madhu

ha,

 

 

 

Vedana

 

 

 

 

 

 

 

 

ra

Teeksh

 

 

 

-sthaapana,

 

 

 

 

 

 

 

 

na

 

 

 

Rakshoghna,

 

 

 

 

 

 

 

 

 

 

 

 

Durgandha

 

 

 

 

 

 

 

 

 

 

 

 

naashana,Var

 

 

 

 

 

 

 

 

 

 

 

 

nya.

 

Haridra

Gouri,Nisha

Curcu

Zingiberac

Kandha

Curcumin

Tikta,

Laghu,

Ushn

Katu

-

VPK

 

 

 

 

ma

eae

 

 

Katu

Rooks

a

 

 

Shaamaka

 

 

 

longa

 

 

 

 

ha

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Dravya

Paryaay

Latin

Family

Useful

Chemical

 

Rasa

Guna

Veer

Vipaak

Prabha

Karma

 

a

name

 

Part

Composition

 

 

ya

a

ava

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Dhaaru

Dhaarvi,

Berberi

Berberida

Kaanda,

Berberine

 

Tikta,

Laghu

Ushn

Katu

-

KP

Shaamaka,

haridra

Katankat

s

ceae

Moola,

 

 

Kasha

,

a

 

 

Vedana

 

eri

aristata

 

Phala

 

 

aya

Rooks

 

 

 

Sthaapana,

 

 

 

 

 

 

 

 

ha

 

 

 

Shodhana,

 

 

 

 

 

 

 

 

 

 

 

 

Ropana

Katuro

Katuka,

Picrohi

Scrophula

Moola(Bh

Roots-

 

Tikta

Laghu

Sheet

Katu

-

KP Hara

hini

Tikta

za

riaceae

oumika

Picrorhizin

 

 

,

a

 

 

 

 

 

 

kurroa

 

Kaanda)

 

 

 

Rooks

 

 

 

 

 

 

 

 

 

 

 

 

 

ha

 

 

 

 

 

Manjist

Vikaasa,

Rubia

Rubiaceae

Moola

Manjistin,

 

Tikta,

Guru,

Ushn

Katu

-

KP Hara, Vrana

ha

Yojanav

cordifo

 

 

Rubiadin

 

Kasha

Rooks

a

 

 

Ropana

 

alli

lia

 

 

 

 

aya,

ha

 

 

 

 

 

 

 

 

 

 

 

 

Madh

 

 

 

 

 

 

 

 

 

 

 

 

 

ura

 

 

 

 

 

 

Padmak

Padmaga

Prunus

Rosaceae

Twak,

Prunetin,

 

Kasha

Laghu

Sheet

Katu

Vedana

KP

Shamana,

a

ndhi

cerasoi

 

Beejamajj

Padmakastin

 

aya,

 

a

 

Sthaapa

Daahaprashama

 

 

des

 

a

 

 

Tikta

 

 

 

na

na

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Lodhra

Sthoolav

Sympl

Symploca

Twak

Loturine,

 

Kasha

Laghu

Sheet

Katu

-

KP

Shamana,

 

alkala

ocos

ceae

 

Tannin

 

aya

,

a

 

 

Ropana,

 

 

racemo

 

 

 

 

 

Rooks

 

 

 

Shothahara

 

 

sa

 

 

 

 

 

ha

 

 

 

 

 

Abhaya

Hareetak

Termin

Combreta

Phala

Chebulinic

 

Kasha

Laghu

Ushn

Madhur

Tridosh

VPK Shaamaka,

 

i, Pathya

alia

ceae

 

acid

 

aya

,

a

a

ahara

Shodhana,

 

 

chebul

 

 

 

 

Pradh

Rooks

 

 

 

Ropana, Vedana

 

 

a

 

 

 

 

aana,

ha

 

 

 

Sthaapana

 

 

 

 

 

 

 

Panch

 

 

 

 

 

 

 

 

 

 

 

 

 

arasa

 

 

 

 

 

 

 

 

 

 

 

 

 

Alava

 

 

 

 

 

 

 

 

 

 

 

 

 

na

 

 

 

 

 

 

Neelotp

Utpala

Nymph

Nymphoe

Moola,

Protein,

 

Madh

Laghu

Sheet

Madhur

-

Daahaprashama

ala

 

oea

aceae

Pushpa,

starch

 

ura,

,

a

a

 

na,

 

 

 

stellata

 

Beeja

 

 

Kasha

Picchi

 

 

 

Tridoshahara

 

 

 

 

 

 

 

aya,

la,

 

 

 

 

 

 

 

 

 

 

 

 

Tikta

Snigd

 

 

 

 

 

 

 

 

 

 

 

 

 

ha

 

 

 

 

 

Tuttha

Mayoora

-

-

-

CuSo4.

7

Kasha

Laghu

Ushn

Katu

-

Lekhana,

 

ka,

 

 

 

H2O

 

aya,

,

a

 

 

Bedhana,

 

Tamraga

 

 

 

 

 

Madh

Ushna

 

 

 

Medhohara

 

rbha

 

 

 

 

 

ura,

 

 

 

 

 

 

 

 

 

 

 

 

 

Katu

 

 

 

 

 

 

Saariva

Ananta,

Hemid

Asclepiad

Moola

Roots-oil-P-

 

Madh

Guru,

Sheet

Madhur

-

VPK Shaamaka,

 

Gopavall

esmus

aceae

 

Methoxy

 

ura,

Snigd

a

a

 

Shodhana,

 

i

indicus

 

 

salicylic

 

Tikta

ha

 

 

 

Dourgandha

 

 

 

 

 

aldehyde

 

 

 

 

 

 

Hara

 

Tila

Pavitra,

Sesam

Pedaliacea

Beeja

Seeds-

 

Madh

Guru,

Ushn

Madhur

-

VPK

Shamana,

 

Jatila

um

e

 

Protein, Fat ,

 

ura,

Snigd

a

a

 

Vrana

 

 

indicu

 

 

Oil-Sesamin,

Kasha

ha

 

 

 

Shodhana,

 

 

m

 

 

Oleic acid

 

aya(A

 

 

 

 

Ropana,

 

 

 

 

 

 

 

nurasa

 

 

 

 

 

 

 

 

 

 

 

 

 

),

 

 

 

 

 

 

 

 

 

 

 

 

 

Tikta

 

 

 

 

 

 

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

5 pala

Guggulu

 

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

Floor-gr.tissue is present,

Floor- pale gr.tissue

inflammed,

Edge- bluish outline of

induration- present at

floor-covered with slough

growing

base,edge, surrounding

without any granulation

epithelium & slight serous

skin. Ulcer shows no

tissue.

discharge.

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

Rolled

out

or

 

 

 

 

 

 

 

 

 

 

pearly

white

everted

 

 

 

 

 

 

 

 

 

 

 

 

beaded

 

 

 

 

 

The

disease

The

edge

droops

Every

 

healing

This type of edge

Growing portion at

causing

 

ulcer

down

at rt. angle

ulcer has a sloping

develops

in

the

edge

of

ulcer

spreads

in

and

to skin surface as

edge,

which

is

invasive

cellular

heaps up and spills

destroys

 

the

if it has been cut

reddish

purple

in

disease

and

over

the

normal

subcutaneous

 

out with a

punch

color and

consists

becomes

necrotic

skin

 

 

e.g.

tissue faster than it

e.g.gummatous

of new

healthy

at the centre e.g.

Squamous

cell

destroys

the

skin.

ulcer, deep trophic

epithelium

 

e.g.

rodent ulcer.

carcinoma

 

The over

hanging

ulcer,syphilitic

healing

traumatic

 

 

/epitheloma.

 

skin is thin, friable

ulcer

(vertically

or venous ulcer.

 

 

 

 

 

 

and reddish

blue,

punched out).

 

 

 

 

 

 

 

 

 

 

unhealthy

 

e.g.

 

 

 

 

 

 

 

 

 

 

 

 

 

tuberculosis

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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

presentation

Uses

comments

 

antiseptic

 

 

 

 

Chlorhexidine(H

Alcohol-0.5%

Skin preparation

Has cumulative effect.

 

ibiscrub)

Aqueous-4%

Surgical scrub in

Effective against gram positive

 

 

 

dilute solutions in

organisms & relatively stable in

 

 

 

open wounds

presence of pus, body fluids.

Povidone- iodine

Alcohol-10%

,,

Safe, fast acting broad spectrum.

 

 

Aqueous-

 

Sporicidal activity, anti-fungal.

 

 

7.5%

 

Iodine is not free but combined

 

 

 

 

with polyvinylpyrrolidone.

 

 

 

 

 

 

 

 

 

 

 

 

Cetrimide(savlon

Aqueous

Hand washing,

Pseudomonas species may grow in

)

 

Instrument and

stored contaminated solutions.

 

 

surface cleaning.

 

Alcohols

70% ethyl,

Skin preparation,

Should be reserved for use as

Hypochlorites

isopropyl

instrument &

disinfectant

 

aqueous

surface cleaning

 

 

preparations(e

(debriding agent

 

 

usol, Milton,

in open wounds?)

 

 

chloramine T)

 

 

Hexachlorophan

Aqueous

Skin preparation,

Has action against gram negative

e

bisphenol

hand washing.

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

 

 

Antibiotic

 

 

 

 

 

 

infections

 

 

sensitivity

 

 

Staphylococcus

Lives

in

naso

Infections

 

are

Most

of

the

strains

aureus

pharynx, present in

usually

localized

are

resistant

to

 

infected discharges.

eg: Boils,

Styes,

Penicillin

because

 

Spread

by

contact,

Carbuncle,

Septic

they

 

produce

 

air borne etc.,

hands,

 

wound

penicillinase.

They

 

 

 

 

infections etc.,

are

sensitive

to

 

 

 

 

 

 

 

Flucloxacillin

 

&

 

 

 

 

 

 

 

Methicillin.

 

 

Streptococcus

Lives

in pharynx.

Infections

 

tend to

Highly sensitive

to

 

Spread by air borne

spread

 

eg:

Penicillin.

 

 

 

 

from

respiratory,

Erysipelas,

 

 

 

 

 

 

 

contact.

 

cellulitis,

puerperal

 

 

 

 

 

 

 

 

 

sepsis,

tonsillitis

 

 

 

 

 

 

 

 

 

etc.

 

 

 

 

 

 

 

Table No.23-Gram negative bacilli

Organism

Site & Spread

Infections

 

Antibiotic

 

 

 

 

 

 

sensitivity

 

E.Coli

Normal inhabitant

UTI,

Peritonitis,

Most of them

are

 

of large bowel

Contaminated

 

sensitive

to

 

 

wounds,

 

Intra

ampicillin,

 

 

 

abdominal sepsis.

gentamycin.

 

Klebsiella

’’

’’

 

 

Resistant

to

 

 

 

 

 

ampicillin

 

Pseudomonas

Large bowel

Attacks

damaged

Sensitive

to

aeruginosa

 

and moist

tissues

gentamycin and some

 

 

such

as

burns,

cephalosporins.

 

 

 

urinary

tract and

 

 

 

 

tracheostomy

 

 

 

 

 

wounds

 

with

 

 

 

 

production

of

 

 

 

 

characteristic

blue

 

 

 

 

geen pus.

 

 

 

Table No.24-Anaerobic organisms

 

 

 

 

 

Organisms

Site & Spread

Infections

 

Antibiotic sensitivity

Gram positive cocci

Widely

found in

Abdominal

sepsis,

Sensitive to penicillin

eg:

clostridium

nature

particularly

wound

infections

and metronidazole.

species,

peptococci,

faeces,

colon,

with severe

local

 

 

streptococci.

rectum, oropharynx,

pain

 

 

 

 

 

 

vagina etc,.

 

 

 

 

 

Gram

negative

Large

bowel,

Intra

abdominal

Sensitive

to

bacilli.

Eg;

vagina,

oro

sepsis, pelvic sepsis

metronidazole

and

bacteroides fragilis.

pharynx.

 

 

 

 

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

7

 

6

21-30

5

31-40

4

41-50

3

51-60

2

 

1

 

0

No. of patients

 

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

20

 

15

male

 

female

10

 

5

 

0

No. of patients

 

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

5

house wife

student

 

4

hotel worker

3

labourer

business

 

2

agriculture

1

driver

tailor

 

0

mechanic

no. of patients

 

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

14

 

12

hindu

10

muslin

8

christian

6

 

4

 

2

 

0

No. of patients

 

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

14

12

10

8

6

4

2

0

No. of patients

rich

u-middle class

l-middle class poor

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

20

 

15

married

10

unmarried

 

5

 

0

No. of patients

 

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

14

 

12

urban

10

rural

8

 

6

 

4

 

2

 

0

No. of patients

 

Among 20 patients selected for the study, higher incidence was seen in the patients of rural area.

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

20

 

15

vegetarian

10

mixed

 

5

 

0

No. of patients

 

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

12

10

8

6

4

2

0

No. of patients

up to 1 month

1 to 3 months

3 to 6 months

6 months to 1 year above 1 year

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

20

15

10

5

0

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

No. of patients

%

Vrana

 

 

V-P

10

50

V-K

9

45

K-P

1

5

Figure No.11- Incidence of type of Dushta Vrana

10

 

8

v-p

6

v-k

k-p

 

4

 

2

 

0

No. of patients

 

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

12

10

8

6

4

2

0

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

8

trauma

7

6

varicosity

5

diabetes

4

pressure sore

3

ischaemia

2

 

1

 

0

No. of patients

 

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

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

 

(pain)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

B(n=10)

Mean

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

 

(pain)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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

2.5

 

 

 

 

 

 

 

 

2

 

 

 

 

 

 

 

 

1.5

 

 

 

 

 

 

 

 

1

 

 

 

 

 

 

 

 

0.5

 

 

 

 

 

 

 

 

0

 

 

 

 

 

 

 

 

T

D

D

D

D

 

D

 

D

B

14

28

42

56

0

4

 

7

 

8

 

Table No. 39- Efficacy of treatment on pain

Comparison of effect of treatment on pain in two groups

mean-A mean-B

G

 

Mean

Difference

%

 

Paired ‘t’ test

 

 

 

 

 

In means

 

 

 

 

 

 

BT

 

AT

 

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

 

 

 

 

 

 

Grade

BT

AT

 

 

 

 

G-A

G-B

G-A

G-B

 

 

(n=10)

(n=10)

(n=10)

(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

G

FU

BT

7D

14D

21D

28D

35D

42D

49D

56D

63D

70D

77D

84D

AT

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

A(n=10)

Mean

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

 

(Itc)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

B(n=10)

Mean

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

 

(Itc)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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

1.2

 

 

 

 

 

 

 

 

 

1

 

 

 

 

 

 

 

 

 

0.8

 

 

 

 

 

 

 

 

 

0.6

 

 

 

 

 

 

 

 

 

0.4

 

 

 

 

 

 

 

 

 

0.2

 

 

 

 

 

 

 

 

 

0

 

 

 

 

 

 

 

 

 

T

 

D

28D

 

D

56D

70D

 

D

B

4

2

4

 

1

 

4

 

8

 

mean-A mean-B

Table No. 42- Efficacy of treatment on itching

Comparison of effect of treatment on itching in two groups

G

Mean

 

Difference

%

 

Paired ‘t’ test

 

 

 

 

 

In means

 

 

 

 

 

 

BT

 

AT

 

S.D

S.E.M.

t value

p value

 

 

 

 

 

 

 

 

 

 

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

 

 

 

 

 

 

Grade

BT

AT

 

 

 

 

G-A

G-B

G-A

G-B

 

 

(n=10)

(n=10)

(n=10)

(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

G

FU

BT

7D

14D

21D

28D

35D

42D

49D

56D

63D

70D

77D

84D

AT

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

A

Mean

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

(n=10)

(B.S)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

B

Mean

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

(n=10)

(B.S)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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

1.2

 

 

 

 

 

 

 

 

1

 

 

 

 

 

 

 

 

0.8

 

 

 

 

 

 

 

 

0.6

 

 

 

 

 

 

 

 

0.4

 

 

 

 

 

 

 

 

0.2

 

 

 

 

 

 

 

 

0

 

 

 

 

 

 

 

 

T

D

D

D

D

 

D

 

D

B

14

28

42

56

0

4

 

7

 

8

 

mean-A mean-B

Table No.45- Efficacy of treatment on burning sensation

Comparison of effect of treatment on Burning sensation in two groups

G

 

Mean

Difference

%

 

Paired ‘t’ test

 

 

 

 

 

In means

 

 

 

 

 

 

BT

 

AT

 

S.D

S.E.M.

t value

p value

 

 

 

 

 

 

 

 

 

 

A

1.1

 

0.1

1

90.9

0.816

0.258

3.873

0.004

(n=10)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

B

1.1

 

0.2

0.9

81.8

0.876

0.277

3.250

0.010

(n=10)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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

 

 

No. of patients

 

 

 

 

 

 

Grade

BT

AT

 

 

 

 

G-A

G-B

G-A

G-B

 

 

(n=10)

(n=10)

(n=10)

(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

G

 

FU

BT

7D

14D

21D

28D

35D

42D

49D

56D

63D

70D

77D

84D

AT

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

A

 

Mean

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

(n=10)

 

(L)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

B

Mean

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

(n=10)

(L)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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

8

 

 

 

 

 

 

 

7

 

 

 

 

 

 

 

6

 

 

 

 

 

 

 

5

 

 

 

 

 

 

 

4

 

 

 

 

 

 

 

3

 

 

 

 

 

 

 

2

 

 

 

 

 

 

 

1

 

 

 

 

 

 

 

0

 

 

 

 

 

 

 

T

14D

D

D

D

D

 

D

B

28

42

56

70

4

 

8

 

mean-A mean-B

Table No. 48- Efficacy of treatment on length of ulcer

Comparison of effect of treatment on length in two groups

G

 

Mean

Difference

%

 

Paired ‘t’ test

 

 

 

 

 

In means

 

 

 

 

 

 

BT

 

AT

 

S.D

S.E.M.

t value

p value

 

 

 

 

 

 

 

 

 

 

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

G

FU

BT

7D

14D

21D

28D

35D

42D

49D

56D

63D

70D

77D

84D

AT

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

A

Mean

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

(n=10)

(W)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

B

Mean

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

(n=10)

(W)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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

6

 

 

 

 

 

 

 

5

 

 

 

 

 

 

 

4

 

 

 

 

 

 

 

3

 

 

 

 

 

 

 

2

 

 

 

 

 

 

 

1

 

 

 

 

 

 

 

0

 

 

 

 

 

 

 

T

14D

D

D

D

D

 

D

B

28

42

56

70

4

 

8

 

mean-A mean-B

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

Comparison of effect of treatment on width in two groups

 

G

 

Mean

Difference

%

 

Paired ‘t’ test

 

 

 

 

 

 

 

In means

 

 

 

 

 

 

 

 

BT

 

AT

 

S.D

S.E.M.

t value

p value

 

 

 

 

 

 

 

 

 

 

 

 

 

A

5.325

 

0.92

4.405

82.7

1.692

0.535

8.108

=<0.001

 

 

(n=10)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

B

2.35

 

0.505

1.845

78.5

0.777

0.246

7.513

=<0.001

 

 

(n=10)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

G

FU

BT

7D

14D

21D

28D

35D

42D

49D

56D

63D

70D

77D

84D

AT

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

A

Mean

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

(n=10)

(Dep)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

B

Mean

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

(n=10)

(Dep)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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

0.4

 

 

 

 

 

 

 

 

 

 

0.35

 

 

 

 

 

 

 

 

 

 

0.3

 

 

 

 

 

 

 

 

 

 

0.25

 

 

 

 

 

 

 

 

 

 

0.2

 

 

 

 

 

 

 

 

 

 

0.15

 

 

 

 

 

 

 

 

 

 

0.1

 

 

 

 

 

 

 

 

 

 

0.05

 

 

 

 

 

 

 

 

 

 

0

 

 

 

 

 

 

 

 

 

 

T

D

 

D

 

D

D

 

D

 

D

B

14

8

2

56

0

4

 

2

 

4

 

7

 

8

 

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

G

Mean

Difference

%

 

Paired ‘t’ test

 

 

 

 

In means

 

 

 

 

 

 

BT

AT

 

S.D

S.E.M.

t value

p value

 

 

 

 

 

 

 

 

 

A

0.37

0.04

0.33

89.18

0.164

0.0517

5.854

=<0.001

(n=10)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

B

0.203

0.053

0.149

73.64

0.0804

0.0254

5.883

=<0.001

(n=10)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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

G

FU

BT

7D

14D

21D

28D

35D

42D

49D

56D

63D

70D

77D

84D

AT

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

A

Mean

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

(n=10)

(Td)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

B

Mean

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

(n=10)

(Td)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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

2

 

 

 

 

 

 

 

 

1.8

 

 

 

 

 

 

 

 

1.6

 

 

 

 

 

 

 

 

1.4

 

 

 

 

 

 

 

 

1.2

 

 

 

 

 

 

 

 

1

 

 

 

 

 

 

 

 

0.8

 

 

 

 

 

 

 

 

0.6

 

 

 

 

 

 

 

 

0.4

 

 

 

 

 

 

 

 

0.2

 

 

 

 

 

 

 

 

0