I By Dr PUSHYA A GAUTAMA Dissertation submitted to Rajiv ...

I

A CLINICAL STUDY TO EVALUATE THE SHWASAHARA KARMA OF PARNAYAVANI

(COLEUS AROMATICUS BENTH.) ARKA NEBULIZATION IN THE MANAGEMENT OF

TAMAKA SHWASA WITH SPECIFIC REFERENCE TO ACUTE EXACERBATION OF

BRONCHIAL ASTHMA

By

Dr PUSHYA A GAUTAMA

Dissertation submitted to

Rajiv Gandhi University Of Health Sciences,

Karnataka, Bengaluru

In partial fulfillment of the requirement for the award of the degree of

Ayurveda Vachaspati (Doctor of Medicine)

In Dravya Guna

Under the Guidance of

Dr HARINI A M D (Ayu.)

Associate Professor

DEPARTMENT OF DRAVYA GUNA SRI DHARMASTHALA MANJUNATHESHWARA

COLLEGE OF AYURVEDA AND HOSPITAL

HASSAN, KARNATAKA -573201

2018

II

RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES,

KARNATAKA, BENGALURU

DECLARATION BY THE CANDIDATE

I hereby declare that this dissertation entitled “A Clinical Study To Evaluate The Shwasahara

Karma Of Parnayavani (Coleus aromaticus Benth.) Arka Nebulization In The Management Of

Tamaka Shwasa with specific reference to acute exacerbation of Bronchial Asthma” is a

bonafide and genuine research work carried out by me under the guidance of Dr Harini A.,

Associate Professor Department of Dravya Guna, Shri Dharmasthala Manjunatheshwara

College of Ayurveda and Hospital, Hassan – 573201.

Date: 3.3.2018 Signature of the candidate

Place: Hassan Dr. Pushya A. Gautama

III

RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES,

KARNATAKA, BENGALURU

CERTIFICATE BY THE GUIDE

This is to certify that the dissertation entitled “A Clinical Study To Evaluate The Shwasahara

Karma Of Parnayavani (Coleus aromaticus Benth.) Arka Nebulization In The Management

Of Tamaka Shwasa with specific reference to acute exacerbation of Bronchial Asthma” is a

bonafide research work done by Dr. Pushya A. Gautama in partial fulfillment for the degree of

Ayurveda Vachaspati in Dravya Guna.

Date : 3.3.2018 SIGNATURE OF GUIDE Place: Hassan Dr. Harini A. M D (Ayu.),

Associate Professor Dept.of Dravya Guna

Shri Dharmasthala Manjunatheshwara College of Ayurveda, Hassan - 573 201

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V

COPYRIGHT

DECLARATION BY THE CANDIDATE

I Dr. Pushya A. Gautama of Shri Dharmasthala Manjunatheshwara college of Ayurveda and

Hospital, Hassan hereby declare that Rajiv Gandhi University of Health Sciences, Bengaluru,

Karnataka. Shall have the perpetual rights to preserve, use, and disseminate this dissertation /

thesis in print or electronic format for academic / research purpose.

Signature by the Candidate Date: 3.3.2018 Place: Hassan Dr. Pushya A. Gautama

© Rajiv Gandhi University of Health Sciences, Karnataka

VI

ACKNOWLEDGEMENT

This thesis is the culmination of two years effort in my journey towards

obtaining a Masters degree in Ayurveda. I am extremely grateful to everyone

without whom this could not have been possible.

First of all, I bow my head to Lord Ganapathi, Lord Dhanvantari and

Lord Manjunatha for their blessings.

I am grateful to Padmavibhushana Dr. D Veerendra Heggade,

Dharmadhikari Shri Kshetra Dharmasthala and President SDM Education Society,

for his legendary vision that led to the establishment of such a centre for Ayurveda

in the country.

I am deeply grateful to my beloved Principal, Dr. Prasanna N. Rao,

Principal SDMCAH, Hassan for his support, guidance, and his extraordinary

leadership.

Above all, I am extremely grateful to my guide, Dr. Harini A, Asso.

Professor, Dept of Dravyaguna, SDMCAH, for her wisdom, support and guidance in

everthing – academically and in life. Without her, this thesis would not have been

possible. It is with utmost reverence that I thank mam for making me the person I

am today, and showing me the way ahead on countless occasions.

VII

I am extremely grateful to the dynamic and amazing HOD of my

Department, Dr. Prakash L Hegde for embodying the perfection he expects from

students. Thank you sir for being a living example of excellence with humility.

I offer my sincerest thanks to the esteemed teachers of my department – Dr.

Pradeep, Dr. Anuradha K N, and Dr. Tejaswi Kiran who have taught me

everything I know, and whose guidance will always shine like a beacon.

I am sincerely grateful to Dr. Girish K J and Dr. Suhas Kumar Shetty for

their constant support and valuable suggestions.

I am grateful to my loving friends and colleagues Dr. Puneshwar Keshari,

Dr. Kopila Adhikari, Dr. Ahana Nambiar, Dr. Anju C, Dr. Supriya Araganji, –

Dr. Udayshankar, Dr. Chithira V Babu, and Dr. Shyamasundaran K. I thank all

other colleagues, seniors and juniors who were involved in the study.

Any endeavor in my life would be incomplete without the mention of my the

foundation stones of my life – my parents and brother. I am extremely grateful to

them for their constant and unwavering love.

Lastly, I would like to specially thank my patients for believing in me, and

cooperating. Without them, this study could not have taken place.

DATE:

PLACE: Hassan Dr. PUSHYA A GAUTAMA

VIII

ABBREVIATIONS

A.H. Ashtanga Hridaya

A.S. Ashtanga Sangraha

A.T. After Treatment

C.S. Charaka Samhita

S.S. Sushruta Samhita

M.N. Madhava Nidana

Y.R. Yoga Ratnakara

B.P. Bhavaprakasha

G.N. Gada Nigraha

PEFR Peak expiratory flow rate

IPD In-‐patient department

OPD Out-‐patient department

WHO World Health Organization

API Ayurvedic Pharmacoepia of India

BT Before Treatment

AT After Treatment

IX

LIST OF TABLES

Sl. No. TABLES PAGES

1. Synonyms Of Parnayavani 7

2. Vernacular Names Of Parnayavani 7

3. The Known Volatile Constituents Of Parnayavani 15

4. The Known Non-Volatile Constituents Of Parnayavani 19

5. Rasa Panchaka and Karma Of Parnayavani 21

6. Pharmacological Activity Of Different Parts Of C. Aromaticus 27

7. Nidana Classification Based On Dosha Prakopa 35

8. Vyadhi Avastha Sambandi Nidana In Tamaka Shwasa 36

9. Agantu Nidana In Tamaka Shwasa 37

10. Poorvarupa Of Tamaka Shwasa 38

11. Rupa Of Tamaka Shwasa 39

12. Samprapti Ghatakas In Tamaka Shwasa 45

13. Upashaya And Anupashaya In Tamaka Shwasa 47

14. Group Allocation In Clinical Study 78

15. Subjective Assessment Parameters (Gina) Of Acute Asthma 79

16. Gina Grading Of Subjective Parameters In Acute Asthma 79

17. Trial drug authentification, processing and manufacture 81

18. Results Of Physicochemical Analysis 88

19. Result Of Preliminary Phytochemical Tests 88

20. Summarized Results Of Preliminary Phytochemical Tests 90

X

21. Results Of Parnayavani Arka Evaluation 91

22. Ms Of Compounds Identified From Arka Of Coleus Aromaticus 92

23. Gender Distribution Of 60 Patients Of Tamaka Shwasa 93

24. Age Distribution Of 60 Patients Of Tamaka Shwasa 94

25. Marital Status Distribution Of 60 Patients Of Tamaka Shwasa 95

26. Place Wise Distribution Of 60 Patients Of Tamaka Shwasa 96

27. Religion Wise Distribution Of 60 Patients Of Tamaka Shwasa: 97

28. Socio-Economic Status Wise Distribution Of 60 Patients Of Tamaka

Shwasa

98

29. Education Wise Distribution Of 60 Patients Of Tamaka Shwasa 99

30. Presenting Complaints Of 60 Patients Of Tamaka Shwasa 100

31. Duration Of Onset In 60 Patients Of Tamaka Shwasa 101

32. Mode Of Onset In 60 Patients Of Tamaka Shwasa 102

33. Trigger Factors In 60 Patients Of Tamaka Shwasa 103

34. History Of Previous Illness In 60 Patients Of Tamaka Shwasa 104

35. History Of Previous Treatment In 60 Patients Of Tamaka Shwasa 105

36. Family History In 60 Patients Of Tamaka Shwasa 106

37. Occupation Of 60 Patients Of Tamaka Shwasa 107

38. Agni Of 60 Patients Of Tamaka Shwasa 108

39. Ahara Of 60 Patients Of Tamaka Shwasa 109

40. Nidra Of 60 Patients Of Tamaka Shwasa 110

41. Rasa Preference Of 60 Patients Of Tamaka Shwasa 111

42. Alcohol And Smoking Consumption In Patients Of Tamaka Shwasa 112

XI

43. Tea And Coffee Consumption In 60 Patients Of Tamaka Shwasa

113

44. Wheezing In 60 Patients Of Tamaka Shwasa 114

45. Nature Of Wheezing Sounds In 43 Patients Of Tamaka Shwasa 115

46. Timing Of Wheezing Sounds In 43 Patients Of Tamaka Shwasa 116

47. Rhonchi In 60 Patients Of Tamaka Shwasa 117

48. Crepitations In 60 Patients Of Tamaka Shwasa 118

49. Timing Of Crepitation In 21 Patients Of Tamaka Shwasa 119

50. Friedman’s Test To Assess Breathlessness Within Parnayavani Arka

Nebulization Group

120

51. WSR Post Hoc Test With Bonferroni’s Correction To Assess

Breathlessness Within Trial Group

121

52. Friedman’s Test To Assess Wheezing Within Parnayavani Arka

Nebulization Group

121


Wheezing Within Trial Group

122

54. Friedman’s Test To Assess Speech Difficulty Within Parnayavani

Arka Nebulization Group

123


Speech Difficulty Within Trial Group

123

56. Friedman’s Test To Assess Cough Within Parnayavani Arka

Nebulization Group

124

57. WSR Post Hoc Test With Bonferroni’s Correction To Assess Cough 125

XII

Within Trial Group

58. Friedman’s Test To Assess Sputum Expectoration Within

Parnayavani Arka Nebulization Group

125


Sputum Expectoration Within Trial Group

126

60. Friedman’s Test To Assess Tightness In Chest Within Parnayavani


127

61. WSR Post Hoc Test With Bonferroni’s Correction To Assess Chest

Tightness Within Trial Group

128

62. Friedman’s Test To Assess Pulse Rate Within Parnayavani Arka

Nebulization Group

128

63. WSR Post Hoc Test With Bonferroni’s Correction To Assess Pulse

Rate Within Trial Group

129

64. Friedman’s Test To Assess Respiratory Rate Within Parnayavani


130


Respiratory Rate Within Trial Group

130

66. Mann Whitney –U Test For Between The Groups Analysis 132

67. Anova With Repeated Measures With A Greenhouse-Geisser

Correction In Parnayavani Arka Nebulization Group

138

68. Tests Of Within Subjects Effects Of Pefr For Parnayavani Arka Group 138

69. Independent Samples T- Test Between The Groups Analysis Of Pefr

Immediately After Nebulization

139

XIII

70. Independent Samples T- Test Between The Groups Analysis Of Pefr

One Hour After Nebulization

140

XIV

LIST OF FIGURES

Sl. No. FIGURES PAGE NO.

1. Flow chart of Tamaka Shwasa Samprapti 46

2. Octadecane, 3-ethyl-5-(2 ethylbutyl) 92

3. Dodecyl acrylate 92

4. Octadecanal, 2-bromo- 92

5. Gender Distribution of 60 patients of Tamaka Shwasa 93

6. Age distribution of 60 patients of Tamaka Shwasa 94

7. Marital status Distribution of 60 patients of Tamaka

Shwasa

95

8. Place wise distribution of 60 patients of Tamaka Shwasa 96

9. Religion wise distribution of 60 patients of Tamaka

Shwasa:

97

10. Socio-economic status wise distribution of 60 patients of

Tamaka Shwasa

98

11. Education wise distribution of 60 patients of Tamaka

Shwasa

99

12. Presenting complaints of 60 patients of Tamaka Shwasa 100

13. Duration of onset in 60 patients of Tamaka Shwasa 101

14. Mode of onset in 60 patients of Tamaka Shwasa 102

15. Trigger factors in 60 patients of Tamaka Shwasa 103

16. History of previous illness in 60 patients of Tamaka 104

XV

Shwasa

17. History of previous treatment in 60 patients of Tamaka

Shwasa

105

18. Family History in 60 patients of Tamaka Shwasa 106

19. Occupation of 60 patients of Tamaka Shwasa 107

20. Agni of 60 patients of Tamaka Shwasa 108

21. Ahara of 60 patients of Tamaka Shwasa 109

22. Nidra of 60 patients of Tamaka Shwasa 110

23. Rasa preference of 60 patients of Tamaka Shwasa 111

24. Alcohol and Smoking consumption in patients of Tamaka

Shwasa

112

25. Tea and Coffee consumption in 60 patients of Tamaka

Shwasa

113

26. Wheezing in 60 patients of Tamaka Shwasa 114

27. Nature of Wheezing sounds in 43 patients of Tamaka

Shwasa

115

28. Timing of Wheezing sounds in 43 patients of Tamaka

Shwasa

116

29. Rhonchi in 60 patients of Tamaka Shwasa 117

30. Crepitations in 60 patients of Tamaka Shwasa 118

31. Timing of crepitation in 21 patients of Tamaka Shwasa 119

32. Macroscopy of coleus aromaticus leaf 213

33. T.S of midrib of Coleus aromaticus leaf 213

XVI

34. Midrib portion enlarged – Coleus aromaticus leaf 214

35. T.S. of lamina of Coleus aromaticus leaf 214

36. Lamina portion enlarged – coleus aromaticus leaf 215

37. Upper midrib – Coleus aromaticus leaf 216

38. Lower epidermis – Coleus aromaticus leaf 216

39. Coleus aromaticus 217

40. Shredding of leaves 217

41. Weighing of leaves 217

42. Soaking of leaves 217

43. Soxhlet distillation 217

44. Clear Arka obtained 217

1

ABSTRACT

A CLINICAL STUDY TO ASSESS THE EFFICACY OF PARNAYAVANI

(Coleus aromaticus Benth.) ARKA NEBULIZATION IN THE MANAGEMENT

OF TAMAKA SHWASA W.S.R. TO ACUTE EXACERBATION OF

BRONCHIAL ASTHMA

Background and Objectives:

Global incidence of Tamaka Shwasa, Bronchial asthma is estimated to be

around 334 million. In India, 15-20 million population are asthmatics. It is of utmost

importance to find ways to combat this disease. Parnayavani is a commonly used

folklore remedy for Tamaka Shwasa. With this perspective, the objective of the study

was to assess the Shwasahara Karma of Parnayavani Arka when administered

through nebulization and compare it with the Standard drug – Theophylline

nebulization.

Methods:

Subjects were divided in to two groups, Trial group consisting of 30 subjects

received a single dose of Parnayavani Arka nebulization (5ml). Standard group

consisting of 30 subjects received a single dose of Theophylline nebulization (5ml).

Before administration and after administration assessment was done using the

following criteria - Subjective parameters as per GINA guidelines and objective

parameter – i.e. Peak Expiratory Flow Rate, both within and between the groups.

2

Results:

With respect to subjective and objective parameters, (p=0.05), this study

found that Parnayavani Arka nebulization showed equivalent action to Theophylline

immediately after nebulization. However, there was no significant difference

between the groups (p=0.05).

Interpretation and Conclusion:

Parnayavani Arka nebulization showed equivalent action to Theophylline

immediately after nebulization, but did not show sustained action till the end of one

hour, with almost all parameters showing a non-significant decrease by the end of one

hour.

It has proven bronchodilatory, antispasmodic, tracheal and bronchial muscle

relaxant properties. Parnayavani has Katu Tikta Rasa and Ushna Veerya. Hence, it

counteracts the effects of Kapha in the Pranavaha Srotas. This proves the

Shwasahara Karma of Parnayavani Arka nebulization immediately in acute

exacerbation of bronchial asthma.

Keywords – Coleus aromaticus, Shwasahara, Parnayavani, Theophylline,

Nebulization, Bronchial asthma

3

INTRODUCTION

A CLINICAL STUDY TO ASSESS THE EFFICACY OF PARNAYAVANI (Coleus aromaticus Benth.) ARKA NEBULIZATION IN THE MANAGEMENT OF TAMAKA SHWASA W.S.R. TO ACUTE EXACERBATION OF BRONCHIAL ASTHMA

The drug Parna Yavani (Coleus aromaticus Benth.) is a large succulent herb,

fleshy and highly aromatic, much branched, possessing short, soft erect hairs, with

distinctive smelling leaves. It is Teekshna, Ushna and Laghu in Guna, Katu Tikta in

Rasa, and is said to have Deepana, Pachana, Ruchya, Malasangraha Karmas. It is

indicated in disorders such as Agnimandya, Yakrudroga, Grahani, Udarraroga,

Krimi, Visoochika, Ashmari, and Mootrakricchra, Kasa and Shwasa. (1)

Shwasa is commonly understood to mean ‘difficulty in breathing’ –

‘Shwasanaat Shwasaha’. (2) It is broadly divided into five – Kshudra Shwasa, Maha

Shwasa, Chinna Shwasa, Urdhva Shwasa and Tamaka Shwasa.

Bronchial Asthma is one of the oldest recorded respiratory disorders. It may

be correlated with Tamaka Shwasa due to similarity in their signs and symptoms.

Asthma is a common long term inflammatory disease of the airways of the lungs,

characterized by variable and recurring symptoms, reversible airflow obstruction and

bronchospasms (3)

According to the WHO, over 180,000 deaths world wide are caused due to

asthma annually. (4) India, as of 2015, is the country with the highest number of

deaths caused by respiratory causes. There has been an overall increase of incidence

of respiratory disorders in India, with a marked increase in all the metropolis,

especially Delhi. (5). Modern drugs used in the treatment of bronchial asthma are

selected on the basis of symptom frequency, severity, chronicity etc. These

medications are associated with a number of side-effects. Theophylline, the most

4

commonly used bronchodilator can be associated with nausea, diarrhea, palpitations,

tachycardia, cardiac arrhythmia and insomnia. (6) Hence, it is obvious that safer

efficacious, easily available ad affordable medication is the need of the hour. In this

regard, ParnayavaniArka (Coleus aromaticus), a drug commonly used in folklore

practice in the treatment of Kasa and Shwasa, has been selected for administration

through nebulization, to analyze its efficacy in the management of Tamaka Shwasa.

The Shwasahara karma of ParnaYavani has been well documented. (1)

A nebulizer is a drug delivery device used for the administration of medication

as mist inhaled into the lungs, commonly used in the treatment of asthma, COPD,

cystic fibrosis, and other respiratory disorders. Advantages of nebulization over

metered dose inhalers are: their ability to deliver larger doses at a greater rate,

especially in conditions of acute asthma, as well as lower doses required for clinical

result. (7)

5

OBJECTIVES OF THE STUDY

1. To evaluate the Shwasahara (bronchodilatory) Karma of

Parnayavani (Coleus aromaticus Benth. Arka nebulization in

Tamaka Shwasa.

2. To carry out pharmacognostic study of Parnayavani (Coleus aromaticus

Benth.)

3. To carry out preliminary phytochemical analysis of Parnayavani (Coleus

aromaticus Benth.)

4. To compare the Shwasahara action of Parnayavani Arka nebulization

(Coleus aromaticus Benth.) with the standard Theophylline nebulization.

6

DRUG REVIEW

In Ayurveda, a drug is called Bheshaja, or Aushadha - that which

overcomes Bhesham or Osha, i.e. disease or even fear of disease and includes any

material or means used for this purpose. Classical texts of Ayurveda have little

mention of Parnayavani, although abundant folklore uses of this drug have been

documented.

CLASSICAL REFERENCES OF PARNAYAVANI:

Literature on Parnayavani that has been obtained from various authentic texts of

Ayurveda can be presented under the following headings.

§ VEDIC PERIOD, SAMHITA PERIOD, NIGHANTU KALA:

No references are found in texts belonging to these periods.

§ CONTEMPORARY TEXTS:

Parnayavani has been mentioned in Priya Nighantu by Vaidya P V Sharma. This

drug is said to be Teekshna, Ushna and Laghu in Guna, Katu Tikta in Rasa, and is

said to have Deepana, Pachana, Ruchya, Malasangraha Karma. It is indicated in

disorders such as Agnimandya, Yakrudroga, Grahani, Udarraroga, Krimi,

Visoochika, Ashmari, and Mootrakricchra. (8)

Books of modern botany have identified this drug as follows (9),(10),(11) –

Coleus aromaticus Benth.

7

Parnayavani was initially considered as the Yavani Vishesha mentioned in

Dhanvantari Nighantu, which was eventually proven to be Khurasani Yavani

(Hyoscymus niger) – an entirely different drug. (9)

SYNONYMS: (8)

Due to its limited mention in classical texts, few synonyms of Parnayavani are

available.

TABLE 1: SYNONYMS OF PARNAYAVANI

SYNONYMS D.G.V.

Parnayavani +

Yavani +

Gandhaparnika +

Table 2: VERNACULAR NAMESOF PARNAYAVANI(8, 10-12)

S.N. Language Name

1. Hindi Patta ajwain, Amroda, Patherchur, Pathercheer

2. English Country borage, Indian mint, Indian borage

3. Bengali Patharchoor, Patechur, Amakuchi

4. Gujarati Ovapan

5. Kannada Doddapatre, Sambrani, Sambrani soppu

6. Malayalam Panikoorka

7. Marathi Panova

8. Tamil Karpooravalli, Kurpuravallai

9. Telugu Karuvacru, Suganda vallekam, Karpooravalli

8

10. French Coleus d’Afrique, Plectrianthus aromatique

11. German Cubanischer oregano, Jamaican Thymian

12. Japanese Koreusu amboinikusu, Kuuban oregano

13. Malay Daun kucin, Daun Kambing

14. Russian Plektrantus aromatryi

15. Spanish Oregano

16. Vietnamese Tan ay le

17. Mah Panova

18. Gujarathi Ovapana

19. Chinese Zuo Shou Xiang

TAXONOMICAL NOMENCLATURE:

The name is derived from the Greek word koleos meaning sheath, referring to the

manner in which the stamens are united (10); while aromaticus refers to the

aromatic volatile oils present in the leaves. (11)

Kingdom-Plantae

Phylum: Tracheophyta

Division – Magnoliopsida

Class – Eudicots

Subclass – Gamopetalae

Family- Lamiaceae

Subfamily: Nepetoideae

Genus – Coleus

9

Species – aromaticus

Botanical name – Coleus aromaticus

Synonyms:

• Plectranthus aromaticus

• Plectranthus amboinicus

• Coleus amboinicus

GEOGRAPHICAL DISTRIBUTION:

It is unclear whether the origin of this drug is Africa or India. However, this drug

is now cultivated and available pantropically. (12, 13)

The drug is found throughout India from the upper Gangetic plane to Bihar,

Orissa, West Bengal, Tripura, Gujarat, Deccan, Konkan plateau, Karnataka

plains, Andhra Pradesh, Tamil Nadu, Kerala and Lakshadweep.

FAMILY FEATURES OF LAMIACEAE (14-15)

The broad family features of Lamiaceae are as follows:

• Labiateae refers to the labia shaped petals- fused into an upper lip and a

lower lip. Although this is considered acceptable, most botanists

nowadays use the term Lamiaceae in reference to this family.

• This family consists of about 236 genera with 6900-7200 species.

Among these, the largest genera are:-

Salvia (900), Scutellaria (360), Stachys (300), Plectranthus(300), Hyptis

(280), Teucrium (250), Vitex (250),

Thymus (220), and Nepeta (200).

• It is a family of flowering plants, most of which are aromatic in nature.

10

• The flowers are bilaterally symmetrical with 3 petals united to form an

upper lip, and 2 united to form a lower lip, and 5 united sepals. They are

usually bisexual and verticillate.

• Leaves are opposite, decussate or whorled.

• The stem is frequently square in cross section.

Macroscopic Description of Coleus aromaticus Benth. (16-18)

• General description: A large succulent herb, fleshy and highly

aromatic, much branched, possessing short, soft erect hairs, with

distinctive smelling leaves.

• Stem: Fleshy, about 30-90 cm, either hispidly villous, or tomentose.

Leaves: Simple, broadly ovate to suborbicular in shape, thick, thickly

pubescent, with the lower surface possessing numerous glandular hairs

giving it a frosted appearance.

• Flowers: Shortly pedicelled, pale, purplish in dense whorls at distant

intervals in a long slender raceme. The flowers have a bell shaped calyx

and the throat is smooth inside with two lips, the upper lip being ovate

and thin, the lower lip having four narrow teeth. The corolla is pale

purplish and five times longer than the calyx, with a short tube, inflated

throat and short lips.

• Fruit – Nutlets; smooth, pale brown in colour, 0.7 mm long and 0.5mm

wide.

Microscopic Description – (19)

Leaves -

• Petiole: Transverse section of petiole of Coleus aromaticusBenth.. is

concave on the upper side and convex on the lower side. Trichomes of both

11

glandular and nonglandular type are present all over the surface. The outer

layer epidermis consist of a single layer of laterally elongated cells,

followed by 3-4 layers of cortical cells which are round &

collenchymatous. The rest of the cortical cells are polygonal to round. The

vasculature comprises of a ring of eight collateral vascular bundles, of

which the two are larger in size. The ground tissue consists of thin walled

parenchymatous cells.

• Midrib: Transverse section of leaf passing through the midrib appears

hemispherical on the ventral side and slightly depressed on the dorsal side.

Upper epidermis is single layered and consists of compactly arranged

rectangular cells. Below this layer there is palisade parenchyma which is

also continuous with the midrib. Vascular bundles are solitary, collateral

and consist of 4-6 rows of xylem and a thin arc of phloem runs along the

midrib. Lower epidermis is similar to upper epidermis and is discontinuous

due to the presence of diacytic stomata On the upper and lower epidermal

surface numerous glandular and non glandular trichomes are present.

• Lamina: Transverse section of leaf shows dorsiventral character. Upper

Epidermis consists of single layer of rectangular cells along with a thin

layer of cuticle on it. Numerous Trichomes of both glandular and non

glandular nature are present on both upper and lower epidermis.

• Mesophyll: The Mesophyll is differentiated into 2 parts – palisade

parenchyma and spongy parenchyma. The palisade parenchyma lies toward

the upper epidermis and consist of single layer of elongated columnar

parenchymatous cells. Towards the lower epidermis there lies the spongy

parenchyma which consists of 5-6 layers of loosely arranged spherical

12

cells. Beside these numerous oil globules and prismatic calcium oxalate

crystals were present in the ground tissue. Coursing through the mesophyll

vascular bundles surrounded by parenchymatous cells is present.

• Hairs: The plant is densely covered with hairs of both glandular and non

glandular type. The glandular trichomes are of capitates type which

consists of a basal epidermal cell, unicellular to bicellular stalk of variable

lengh, a neck cell and a large globular unicellular secretory head. The non

glandular trichomes are 3-6 celled, variable length uniseriate, unbranched

and progressively tapering with pointed apex.

• Powder characteristics: The moderately coarse leaf powder(40 mesh size)

is dark green in colour and when studied under different magnifications

show the presence of diacytic stomata, epidermal cell, glandular and

uniseriate trichomes etc.

PART USED:

Generally, the leaves are the used part of this plant, though the whole

plant may also be used.

PHYTOCHEMISTRY:

The literature survey has emphasized the occurrence of different classes of

phytocompounds including 76 volatiles and 30 non-volatile compounds

• Volatile Composition of C. aromaticus (20)

The essential oil obtained from the leaves and stem explants contain a total of

76 volatile constituents. The essential oil contains copious quantity of the two

13

major phenolic compounds, namely, carvacrol and thymol, which are

pharmaceutically appreciated for various properties. The quality as well as quantity

of chemical compounds occurring in the essential oil is directly related to its

biological functions.

GC and GC-MS techniques have indicated the occurrence of Thymol (94.3%),

followed by Carvacrol (1.2%), 1,8-Cineole (0.8%), p-Cymene (0.3%), Spathulenol

(0.2%) and Terpinen-4-ol (0.2%) as the major constituents of Indian C. aromaticus

leaf essential oil. Investigation of volatiles of C. aromaticus collected from

Mysore, Karnataka, India showed the existence of Carvacrol (70%), -

Caryophyllene (6.2%), p-Cymene (5.6%) and -Terpinolene (5.3%) as the main

components. (21) The volatile composition of aerial parts and flowers of C.

aromaticus growing in Belgaum, Western Ghats region of North West Karnataka,

revealed the occurrence of 12 components from aerial parts oil and 4 constituents

from flower oil and represented 94.29% and 90.25% of the total oil, respectively.

In both the essential oils, the major compound observed was Carvacrol (50.98% in

flowers and 77.16% in aerial parts oils). Yet, the presence of chemical variation in

the leaf essential oils was evident from the plants collected from the same state. A

total of 10 volatile compounds were identified with dominant constituents as

Carvacrol (50.7%), -caryophyllene (13.1%) and patchoulane (8.7%). (22-27).

The leaf essential oil obtained from Martinique, France was found to contain

Carvacrol (72%) as a chief phenolic component along with newly identified

compounds such as (Z)-1,3-Hexadiene (0.1%), (E,Z)- -Farnesene (0.2%), (Z)-3-

Hexenol (0.6%), -Muurolene (0.2%) and (E,E)- -Farnesene (0.2%) (28) C.

14

aromaticus oil from Cambodia was shown to contain largely Thymol (57.4%). (29)

Similarly, Velasco et al. (30) identified 15 volatile constituents in the essential oil

of C. aromaticus collected from Venezuela and the major component observed was

Carvacrol (65.2%). The essential oil from Uganda consisted of Linalool (50.3%),

Carvacrol (14.3%), Nerol acetate (11.6%) and Geranyl acetate (11.7%) as the

major components as revealed by GC-MS analysis (31) Essential oil of C.

aromaticus leaves from Serdang, Malaysia was shown to contain Carvacrol

(19.29%), 3-Carene (20.78%) and Camphor (17.96%) as the major volatile

constituents. (32)

The essential oil yield and its main chemical constituents are also influenced

by the environmental factors and different seasons. Mallavarupu et al. have

revealed that the quality of essential oil will be superior when collected during

September. The oil content was found to be higher in the plants harvested during

September in comparison to the plants harvested during May. Moreover, the

compositions also differed among the two harvest times. About 68% of

oxygenated monoterpenes, 11% of sesquiterpenes and 3.3% oxygenated

sesquiterpenes were found in the oil distilled from the September harvest time,

whereas, the oil obtained from the May harvest comprised higher amounts of

monoterpenes (35.7%). The major compounds such as Carvacrol (67.0%), -

Caryophyllene (7.4%), -Humulene (2.1%) and Caryophyllene oxide (2.2%) were

found to be higher in oil obtained during September, while the oil distilled during

May showed the presence of p-Cymene (12.6%), -Terpinene (15.5%), Carvacrol

(53.0%) and -Caryophyllene (4.3%). (33)

15

Table 3: The known volatile constituents of Coleus aromaticus Benth. (34)

Compound

Name Formula Plant Origin/Part

Monoterpene hydrocarbons

-3-Carene C10H16

India, Malaysia, Morocco,

Mauritius/Leaf

p-Cymene C10H14

Brazil, India, Cambodia, Malaysia,

Venezuela/Aerial parts, Leaf

Limonene C10H16 India, Mauritius/Leaf

-Myrcene C10H16 Cambodia, India, Venezuela /Leaf

Ocimene C10H16 Morocco/Leaf

-Phellandrene C10H16

India, Comoros, Mauritius,

Venezuela/Leaf

-Phellandrene C10H16 India/Leaf

-Pinene C10H16 India, CambodiRa /Leaf

-Pinene C10H16 India/Leaf

Sabinene C10H16 Cambodia,India, Morocco /Leaf

-Terpinene C10H16 India, Mauritius/Leaf

-Terpinene C10H16

Brazil, Cambodia, Malaysia,

Mauritius India, /Leaf

-Terpinolene C10H16 Morocco, Brazil/Leaf

-Thujene C10H16 India, Comoros, Venezuela/Leaf

Oxygenated monoterpenes

Camphor C10H16O Comoros, Malaysia, Mauritius/Leaf

Carvacrol C10H14O

Cambodia, India, Malaysia,

Mauritius, Venezuela/Aerial parts,

16

Leaf, Flower

Carvone C10H14O India/Leaf

1,8-Cineole C10H18O India/Leaf

Eugenol C10H12O2 Cambodia, India/Leaf

Geraniol C10H18O Mauritius/Leaf

Linalool C10H18O Comoros, Mauritius /Leaf

Methyl carvacrol C11H16O India/Leaf

Methyl eugenol C11H14O2 Cambodia/Leaf

-Terpineol C10H18O India, Comoros, Venezuela /Leaf

Terpinen-4-ol C10H18O Brazil, India, Mauritius /Leaf

Thymol C10H14O

Brazil, Cambodia, India,

Venezuela/Aerial parts, Leaf

Thymol methyl

ether C11H16O Brazil/Leaf

Sesquiterpene hydrocarbons

-Amorphene C15H24 Cambodia/Leaf

Aromadendrene C15H24 Brazil, India/Leaf

trans- -

Bergamotene C15H24

Brazil, Comoros, India, Venezuela

/Leaf, Aerial parts, Flower

trans- -

Bergamotene C15H24 Cambodia/Leaf

-Cadinene C15H24 Cambodia/Leaf

-Cadinene C15H24 India, Cambodia/Leaf

-Calacorene C15H20 India/Aerial parts

cis-Calamenene C15H22 Cambodia/Leaf

-Caryophyllene C15H24 Brazil, India, Venezuela /Leaf,

17

Flower

-Caryophyllene C15H24 India/Leaf

-Copaene C15H24 Comoros, India /Leaf

-Cubebene C15H24 India/Leaf, Aerial parts

(E,Z)- -

Farnesene C15H24 France /Leaf

Germacrene D C15H24 Cambodia/Leaf

-Gurjunene C15H24 India/Aerial parts

Humulene C15H24

Brazil, Cambodia, India, Morocco,

Venezuela/Leaf, Aerial parts

-Muurolene C15H24 Cambodia, France, Mauritius/Leaf

Patchoulene C15H24 India, Mauritius/Leaf

-Selinene C15H24 India, Comoros/Leaf

-

Sesquiphellandre

ne C15H24 Cambodia/Leaf

Compound

Name

Formula Plant Origin/Part

Oxygenated sesquiterpenes

Caryophyllene

oxide C15H24O

India, Cambodia, Venezuela /Leaf,

Aerial parts

-Cedrene

epoxide C15H24O India/Aerial parts

-Copaen-4- -ol C15H24O India/Aerial parts

1-Epi-cubenol C15H26O India/Aerial parts

18

-Eudesmol C15H26O India/Leaf

-Himachalene

oxide C15H24O India/Aerial parts

Humulene oxide C15H24O India/Leaf

Spathulenol C15H24O India/Leaf

Others (Terpenes,

phenylpropanoids, esters, fatty

acids, alcohols, aldehyde)

1,2-Benzenediol

4-(1,1

C10H14O2 India/Leaf dimethylethyl)

Chavicol C9H10O India/Leaf

Methyl chavicol C10H12O India/Aerial parts

-Corocalene C15H20 India/Aerial parts

Dihydro carveol C10H18O India/Aerial parts

Durohydroquino

ne

C10H14O

2 India/Leaf

1,4 Eicosadiene C20H38 India/Leaf

Ethyl Salicylate C9H10O3 India/Leaf

(Z)-1,3-

Hexadiene C6H10 France /Leaf

(Z)-3-Hexen-1-

ol C6H12O France/Leaf

19

Methyl

octanoate C9H18O2 India/Aerial parts

1-Octen-3-ol C8H16O India, Mauritius, Venezuela/Leaf

Oleic acid

C18H34O

2 India/Leaf

2-Phenyl ethyl

tiglate

C13H16O

2 India/Aerial parts

Phytol C20H40O India/Leaf

Squalene C30H50 India/Leaf

Tetradecanal C14H28O India/Aerial parts

3,7,11,15–

Tetramethyl-2-

hexadecen-1-ol C20H40O India/Leaf

Thymol acetate

C12H16O

2 India/Leaf

Trans-sabinene

hydrate

C12H20O

2 India/Aerial parts

Undecanal C11H22O India/Aerial parts

Table 4: The known non-volatile components of Coleus aromaticus (34)

A total of 30 non-volatile constituents have been identified from C. aromaticus

according to our literature survey (27). These non-volatile chemical components

included phenolic acids, flavonoids, monoterpene hydrocarbons, sesquiterpene

hydrocarbons, oxygenated monoterpenes and esters

20

Compound Name Plant Origin/Part

Phenolic acids

Caffeic acid India, Egypt/Leaf, stem, root (Methanol extract)

Gallic acid India/Stem (Methanol extract)

p-Coumaric acid

India, Egypt/Leaf, stem, root (Methanol and ethyl

acetate fraction)

Rosmarinic acid

India, Egypt, Thailand/Leaf, stem, root (Methanol

and ethyl acetate fraction)

Salvianolic acid A Thailand/Aerial parts (Water extract)

Shimobashiric acid Thailand/Aerial parts (Water extract)

21

Flavonoids

Table 5: RASA PANCHAKA AND KARMA OF PARNAYAVANI (8)

RASA

PANCHAKA PARNAYAVANI

Rasa Katu, Tikta

Guna Teekshna, Ushna, Laghu

Virya Usna

Vipaka Katu

Chrysoeriol Leaf, stem, root (Chloroform extract; Ethyl acetate fraction) –

Philippines/Egypt Cirsimaritin Philippines/Leaf (Chloroform extract)

Eriodictyol Egypt/Leaf, stem, root (Ethyl acetate fraction)

Luteolin Egypt/Leaf, stem, root (Ethyl acetate fraction)

Rutin India/Stem (Methanol extract)

Salvigenin Philippines/Leaf (Chloroform extract)

Thymoquinone Thailand/Aerial parts (Water extract)

Quercetin Egypt/Leaf, stem, root (Ethyl acetate fraction)

5,41 -Dihydroxy-6,7-

dimethoxy flavone

Egypt/Leaf, stem, root (Ethyl acetate fractions)

5,41 -Dihydroxy-

3,7-dimethoxy flavone


5-O-Methyl-luteolin Egypt/Leaf, stem, root (Ethyl acetate fractions)

3,5,7,31 ,41 -Pentahydroxy

flavanone Egypt/Leaf, stem, root (Ethyl acetate fractions)

41 ,5,7-Trihydroxyflavone

(apigenin)


22

Doshaghnata Kapha Vata Shamaka

Karma Deepana, Pachana, Ruchya, Malasangrahaka

Rogaghnata

Agnimandya, Yakridroga, Grahani, Udara, Krimi, Visoochika,

Ashmari, Mootrakricchra

TRADITIONAL USES:

C. aromaticus is among the most widely used herbs by traditional medicine

practitioners due to widespread availability in India and other countries. A brief

summary of its traditional uses is given below:

§ Respiratory Disorders

amboinicus is frequently cited in the treatment of chronic coughs, asthma,

bronchitis and sore throat in India and the Caribbean Islands (35). In Eastern Cuba,

essential oil from aerial parts of C. aromaticus is used to treat asthma (36).

Decoction or juice made from leaves together with other herbs is also taken orally

to control asthma. This decoction is also used to treat catarrhal infections where it

clears the excessive build-up of thick phlegm or mucus in an airway or cavity of

the body. In Brazil, a drink or a bath of C. aromaticus juice/decoction is used to

treat influenza, cough, bronchitis and throat problems (37).

• Digestive system Diseases

C. aromaticus is a popular treatment for dyspepsia, indigestion and diarrhea, and a

carminative in India and Africa. C. aromaticus juice obtained from pounded leaves

is used as a drink to cure constipation in Indonesia and Malaysia. (38) In India, the

23

leaves of C. aromaticus are consumed along with buttermilk, yogurt, or any other

probiotic sources during pathogen-induced diarrhea. (39)

• Epilepsy:

In Cuba, it is used as an anticonvulsive and antiepileptic drug (40)

§ Skin diseases

C. aromaticus has been used in Brazil since the early days for the treatment of

skin ulcerations caused by Leishmania braziliensis (41) In India, the juice of the

leaves is used to treat skin allergies. It is also used to treat burns in Asian regions

(42) When the leaf paste is baked on a flame and applied to cuts or burns, it acts as

an antiseptic and promotes healing (42)

• Animal and insect bites

Leaves of C. aromaticus are also used as a poultice for centipede and scorpion

bites in Asian regions, including Malaysia (38)

§ Lactogenic Activity

In Indonesia, C. aromaticus is used as a traditional food in soup to stimulate

lactation for the month or so following childbirth. The leaves are commonly

consumed by mothers who have given birth in North Sumatra, in particular the

Batak tribe. The leaves of this herb are believed to increase the production of

breast milk due to the high content of nutrients, especially iron and carotene.

Consumption of leaves significantly increases minerals such as iron, potassium,

zinc and magnesium in milk, thus, improving the infant’s weight and health

holistically (43)

24

• Cardiac diseases:

C. aromaticus is also used in the Caribbean, to treat congestive heart failure

(44)

§ Genitourinary diseases:

§ The leaves of C. aromaticus are frequently utilized in the treatment of

urinary diseases in the Amazon and India. (45) This species is also

reported to relieve kidney troubles and treat vaginal discharges, and is

taken as a drink after childbirth (46). The juice of C. aromaticus has been

used as a natural remedy to dilute the crystals in the urinary tract in India

from ancient times (47)

§ Analgesic activity

In Africa, C. aromaticus is used as a remedy for headaches (48)

§ Activity against Other Diseases

C. aromaticus is an important herb in Asia and South America for the

treatment of infectious diseases such as fevers cholera and meningitis. It also used

to treat sensory disorders associated with ear and eye problems. In India its leaves

are rubbed into the eyes to alleviate conjunctivitis (48).

RESEARCH PROFILE:

C. aromaticus is a widely researched herb – both for its culinary as well as

therapeutic usage. A brief research profile of the drug C. aromaticus is as follows:

§ Digestive disorders:

25

The leaves are known to have a prebiotic effect on the probiotic bacteria

Lactobacillus plantarum. They utilize the phytoconstituents of the leaves by

producing necessary metabolic enzymes. A detailed examination by Shubha and

Bhatt describes the mode of hot water extract (HWE) of C. aromaticus leaves on

growth inhibition of Escherichia coli and Salmonella typhimurium (pathogens)

while stimulating the growth of Lactobacillus plantarum. Sodium dodecyl sulfate

polyacrylamide gel electrophoresis (SDS-PAGE)gel showed the presence of

phenolic acid decarboxylase enzyme induced in the presence of HWE, which

indicated the utilization of polyphenols by the bacteria. Cells grown on HWE also

showed -galactosidase activity, indicating their ability to utilize sugars present in

HWE. This provides evidence in the traditional use of the leaves in the alleviation

of diarrhea by accelerating microbial gut balance during infection.(49)

§ Epilepsy:

Bhattacharjee and Manjumder tested the anticonvulsant activity of the leaf,

stem and root alcoholic extract separately on Swiss albino mouse models by

maximal electric shock-induced seizures and pentylenetetrazole-induced seizures.

They found significant anticonvulsant activity in both the models with alcoholic

leaf extract recording the highest activity. (50)

§ Scorpion bites:

It is reported that aqueous extracts (0.706 mg/mL and 0.406 mg/mL) of C.

aromaticus to be more than 70% efficient when tested against fibroblast cell lysis

(51) This implies the aqueous extracts to have a tendency to be scorpion

(Heterometrus laoticus) venom antidotes.

26

§ Cardiac diseases:

The aqueous extracts of the fresh leaves of C. aromaticus exhibited dose-

dependent positive inotropic activity in the isolated frog heart without affecting

the heart rate. This may be attributed to the increase in sodium influx thereby

causing greater intracellular availability of calcium. In this report the bioactivity of

the tissue-cultured extracts of C. aromaticus to the parent plant was also described.

Both extracts from tissue-cultured and parent plant produced a comparable

significant effect indicating that they both can be used as a source of biochemical

production. (52)

§ Genito-urinary diseases:

The antilithiotic activity of the concentrated fresh juice of the leaves of C.

aromaticus is proved by Jose et al. The said study on urine analysis revealed

significant reduction in calcium, oxalates and total protein level compared to the

control. Further histopathological results showed an absence of crystal and normal-

sized tubules with a single epithelial lining. He suggested this antilithiotic activity

could be associated with calcium oxalateorigin. The diuretic properties of ethanolic

and aqueous extracts of C. aromaticus were evaluated by determination of urine

volume and electrolyte concentration in male albino rats. Furosemide (10 mg/kg)

was used as a standard, while normal saline (0.9%) was used as a control. Both

ethanolic and aqueous extracts (500 mg/kg) have shown a significant increase in

the volume of urine and urinary concentration of Na, K and Cl ions and were

comparable to furosemide. This study concludes that the leaves of C. aromaticus

possess diuretic activities (53)

27

§ Analgesic activity:

The aqueous extract of C. aromaticus leaves showed an analgesic and anti-

inflammatory property, mainly modulated by controlling inhibition of

proinflammatory mediators (54).

Table 6: Pharmacological activity of different parts of C. aromaticus: (55)

Pharmacological

activity Bioactive compound Research profile

Antibacterial activity

Biogenic zinc oxide

nanoparticles

Pam-ZnO NPs control the growth of

methicillin-resistant

Staphylococcus aureus biofilm;

inhibits growth of Escherichia coli,

Salmonella typhimurium &

Mycobacterium tuberculosis.

Antiviral activity -

Exhibited antiviral activity against

viruses (VSV, HSV1 & HIV).

Activity against

Respiratory diseases -

Expectorant, smooth muscle relaxant,

bronchodilator

Lavicidal potential

Pam-ZnO NPs (zinc

oxide nanoparticles)

Exhibited up to 100% mortality in

Anopheles stephensi, Culex

Quinquefasciatus & Culex

tritaeniorhynchus.

Oral Diseases Carvacrol Antagonistic effect when used with

28

mouthwash.

Digestive diseases

(Diarrhea,

Constipation,

dyspepsia, indigestion

& as carminative) -

Stimulates growth of Lactobacillus

plantarum and inhibits growth of

selected food-borne pathogens

(Escherichia coli & Salmonella

typhimurium); relieves constipation

troubles; prevents formation of

gas in the gastrointestinal tract &

facilitates expulsion of gas

Antitumor activity

Flavone (Luteolin),

flavonols

Inhibited the growth of sarcoma 180 &

Ehrlich ascite carcinoma

tumors in mice; showed significant

anticancer activity through

inducing apoptosis in A549 (human lung

cancer) cell line.

Antiinflammatory

activity

Rosmarinic acid L, Rutin,

Thymoquinone,

Quercetin

Concentration of 0.1 mg/mL inhibited

10%–50% DNA binding to its consensus

sequence; decreased carrageenan-induced

paw edema up to 40%;

significantly increased IgG, IgM &

lysozyme activity in rats.

Analgesic activity -

Analgesia in musculo-skeletal disorders

proven

Wound healing

activities -

Increased wound healing activity in

experimentally induced

29

diabetic mice & againt murrels.

Cardiovascular

disorders -

Positive inotropic activity in the isolated

frog heart; effective for

treating congestive heart failure.

Skin disease (Anti-

dandruff, Cuts,

Skin Allergy; Burns)

Thymol, 1,8-Cineole, -

Pinene, -pinene,

phenolic compounds

Inhibits the growth of Malassezia furfur;

applied on cut as antiseptic

promoted better healing; paste was

effective against skin allergies,

skin burns.

Insect bites -

Potency as antidote for scorpion

(Heterometrus laoticus) venom

with>50% efficiency.

Lactogenic properties

Nutrient content (iron &

carotene)

Increased breast milk production in new

mothers.

Anti-epileptic activity

Alkaloids, flavonoids &

saponins

Effective as an anticonvulsive and/or

antiepileptic medicine.

Activity against

Genitourinary diseases -

Showed increased urine volume &

electrolyte concentration in

male albino rats.

Antioxidant activity Carvocrol & Thymol

Exhibited significant inhibition in DPPH

free radical & hydroxyl

radical formation.

Other diseases - Reduced free radical formation in

30

Xerophathalmia.

PROPAGATION, CULTIVATION AND COLLECTION

(56-57)

PROPAGATION:

Coleus aromaticus is propagated by terminal stem cuttings, approximately 10 cm

in size. It is rarely propagated by roots or seeds.

CULTIVATION:

It grows well in subtropical and tropical climates – especially well drained, red

loamy soil, semi shaded positions. Care should be taken to avoid water stagnation.

Ideally, the crop grows in areas receiving 70cm annual rainfall. 60 X 45cm spacing

is required for planting. Around 37,000 plants may be planted in one hectare. In

soils with low fertility, 60 X 30 cm spacing may be done. Immediatetly after

planting, irrigation should be done, and continued ideally once every week for

optimum yield. 15t/hectare of farmyard manure is added during the last ploughing.

NPK fertilizers at 30:60:50 kg/hectare is applied in two split doses. The first dose

is administered at 30 days, while the second dose is administered at 45 days after

planting. 10kg Zinc sulfate is also aopplied per hectare to avoid micronutrient

deficiency.

Likely sources of crop d estruction are : Nematode infection, Root rot, and

Bacterial wilt. 200kg of neem cake and 20kg carbofuran is applied to each hectare

before planting to prevent nematode infection.

31

COLLECTION:

The plant is collected at maturity i.e. after complete flowering and fruiting.

Usually, it is collected 5-6 months after planting. Care should be taken to avoid

damage to leaves while harvesting. For every hectare, the yield is around 15-20

tons of fresh leaves.

TRADE AND COMMERCE (58)

Rate in Indian market is Rs. 260/kg. Major drug dealers are in Karnataka,

Chandigarh, Amritsar, Delhi, Gujarat, Punjab, Tamilnadu, Maharashtra and

Orissa.

32

DISEASE REVIEW

HISTORICAL REVIEW OF SHWASA:

VEDIC AND UPANISHAD PERIOD

Available literature from the Prevedic and Vedic periods reveals the

physiology of respiration from an Indian perspective. In the Rig Veda, the terms

Prana and Vayu are used interchangeably. The term Shwasa was first used during

the Upanishad Kala. The Garuda Purana contains the earliest attempts to

scientifically assess Shwasa – and mentions the Nidana of Shwasa. (59)

SAMHITA PERIOD:

Charaka Samhita, Sushruta Samhita, Ashtanga Hridaya, Ashtanga Sangraha,

Madhava Nidana, Bhavaprakasha, Yogaratnakara etc. and all major treatises

elaborately describe the types, Nidana, Poorvaroopa, Roopa, Samprapti, Upashaya,

Anupashaya, Chikitsa and the variable presentations of Shwasa. (60-67)

ETYMOLOGICAL DERIVATIONS (NIRUKTI)

ETYMOLOGY OF TAMAKA SHWASA

The term Tamaka Shwasa consists of two words - Tamaka and Shwasa

ETYMOLOGY OF TAMAKA:

The word Tamaka is derived from Tama + Va. According to Shabda

Kalpa Druma it is defined as Tamyatyasmat anena va. Tamaka means -

oppression of the chest, to choke, to be suffocated, to be exhausted, to be

uneasy, or distressed. (68)

ETYMOLOGY OF SHWASA:

The word Shwasa is derived from the root - Shwas + Karane gnanj.

Shabda Kalpa Druma defines Shwasa as follows - Shvasiti anena iti Shwasa

which refers to the act of respiration. This derivation details the physiology of

33

breathing. But rapid or interrupted breathing is a disease, also known as

Shwasa. In the context of disease, it refers to ‘panting respiration’. (68)

TAMAKA SHWASA:

Tamaka Shwasa is defined as

· ‘Visheshat Durdine Tamyeth Shwasa sa Tamako Mataha’

Shwasa which occurs especially during Durdina is called Tamaka Shwasa.

(69).

· ‘Tamakascha Asou Shwasascha Tamaka Shwasa’

The attack of Shwasa, which occurs mainly during the Tamah kala - night

time, is called Tamaka Shwasa.

NIDANA PANCHAKA OF TAMAKA SHWASA

The Nidana Panchaka ie, Nidana, Poorvaroopa, Roopa, Samprapti,

Upashaya, Anupashaya of Tamaka Shwasa have been elaborated in various

Samhitas as mentioned above.

NIDANA

Tamaka Shwasa has been described as a Yapya Vyadhi by Charaka.

As Nidana is the Vyadhi Karana (67), Nidana Parivarjana plays an important

role in the management of diseases like Tamaka Shwasa in order to prevent

the further vitiation of Doshas. (67)

Various authors (61-68) have mentioned general etiological factors of

Shwasa These are the same for Tamaka Shwasa as well.

34

According to Chakrapani, the Nidanas of Tamaka Shwasa may be

classified into two: (69)

b) Vata Prakopaka Nidanas

c) Kapha Prakopaka Nidanas

Vata Prokopaka Nidanas: The Nidanas which cause the vitiation of Vata.

These include - Sheetapana and Sheeta Ashana, Ruksha Bhojana, Sheetavata

Sevana, Raja Sevana, Vyayama and Vegadharana, etc.

Kapha Prakopaka Nidanas: The Nidanas which cause the vitiation of Kapha.

These include - Gurubhojana, Adhyashana, Shleshmala Ahara Sevana,

Sheetapana, etc.

Another classification of Shwasa Roga Nidana is as follows :- (68)

� Bahya (extrinsic)

� Abhyantara ( intrinsic)

Bahya nidanas (69-73) like Rajas, Dhuma etc. are factors from the

external environment responsible for causation of the disease.

Abhyantara Nidanas are the Doshas. Kapha and Vata are the main

Doshas responsible for the manifestation of Tamaka Shwasa.

The vitiation of Vata and Kapha Dosha in Tamaka Shwasa, is referred

to as Sannikrista Nidana. It is the outcome of exposure to Viprakrista Nidanas

in the form of Ahita Aharas and Viharas. A summary of etiological factors of

Tamaka Shwasa are presented below:

35

Table 7: Showing Nidana classification based on Dosha Prakopa

Nidana Factors C.S74 S.S75 A.H76 A.S77 M.N78

Ahara Vatakara

Rukshanna + + + + +

Vishamashana + + - - -

Adhyashana - + - - -

Samashana - + - - -

Sheetashana - + - - +

Sheetapana + + + + +

Pittakara

Tila taila + - - -

Vidahi + + - - +

Katu - - + +

Ushna - - + + -

Amla - - + + -

Vihara Kaphakara

Jalaja Mamsa + - - - -

Anupa

Mamsa + + - - +

Dadhi + - - - -

Abhishyandi + + + + +

Vishtambhi + + - - +

Vatakara

36

Raja + + + + +

Dhuma + + + + +

Prag vata + + + + +

Sheeta Sthana + + - - +

Sheeta Ambu + + + + -

Ativyayama + + + + +

Gramya

Dharma/ Stree + + + + -

Apatarpana + + - - +

Kantha Ura

Pratighata + - - - -

Bharakarshita - + - - +

Adhwahata - + - - +

Vega nirodha - + + + +

Abhighata - + - - -

Marmabhigata - - + + -

Pittakara

Ushna Vayu - + - - +

Kaphakara

Abhishyandi

upachara + + - - -

Table 8: Showing Vyadhi Avastha Sambandi Nidana in Tamaka Shwasa

Sl. No Nidana C.S S.S A.S A.H Y.R B.P M.N G.N

37

1. Pratishyaya + + - - - - - -

2. Kasa - + + + + - - -

3. Jwara + - + + + + + -

4. Chardi + - + + + - - -

5. Kshata Ksheena + - - - - - - -

6. Atisara + - + + + + + -

7. Visuchika + - - - - - - -

8. Vibandha + - - - - - - -

9. Dourbalya + - - - - - - -

10. Udavarta + - - - - - - -

11. Raktapitta + - - - - - - -

12. Anaha + - - - - - - -

13. Pandu + - + + + - - -

14. Rukshata + - - - - - - -

15. Apatarpana + + - - + + + -

Table 9: Showing Agantu Nidana in Tamaka Shwasa

Sl. No Nidana C.S S.S A.S A.H Y.R B.P M.N G.N

1. Marmaghata + + + + + - - -

2. Visha + - + + + - - -

3. Kantorasa Pratighata + - - - - - - -

38

POORVA RUPA

The Lakshanas which appear before the onset or manifestation

of actual signs of a disease are considered as Poorva Rupa (79). No

specific Poorva Rupas have been explained for Tamaka Shwasa.

However, the general Poorva Rupas explained for Shwasa are

applicable in Tamaka Shwasa as well.

Table 10: Showing Poorvarupa of Tamaka Shwasa

Poorvarupa C.S80 S.S81 A.H82 M.N83

Anaha + + + +

Parshva Shula + + + +

Hrit pidana + + + +

Pranasya Vilomata + - + -

Adhmana - - - +

Mukha Virasata - + - +

Shankha Nistoda - - + +

Arati - + - -

Bhakta Dvesha - + - -

RUPA

The signs and symptoms which exhibit as a result of disease

manifestation in the body are called Roopas. Vata and Kapha Dosha,

Rasa Dhatu and Pranavaha srotas are the main factors concerned in the

pathogenesis of Tamaka Shwasa. Other features such as the mode of

39

onset, course, aggravating factors, and relieving factors are very typical

and are hence diagnostic of Tamaka Shwasa.

Table 11: Showing Rupa of Tamaka Shwasa

Rupa C.S84 S.S85 A.H86 M.N87

Griva Parigraha + - + +

Shira Parigraha + - + +

Shwasa + + + +

Peenasa + - + +

Ghurghuraka Shabda + + + +

Prana Prapeedaka Shwasa + - - +

Kasena Pratamyati + - - +

Kasat Pramohanam + - + +

Shleshmana Vimokshane

Sukham + - - +

Shamyati Kaphe Heena - + - -

Krichchra Bhashitam + - - +

Anidra/ Svapata Vivardhate + + - +

Asino Labhate Saukhyam + - - +

Ushnabhinandati + - - +

Ucchritaksha + - + +

Lalata Sveda + + + +

Mukha Shosha/Trishna + - + +

Muhurmuhu Shwasa + - + +

40

Sakapha Kasa - + - -

Vamana - + - -

Aruchi - - + -

Roopa of Pratamaka Shwasa

Jwara + + + +

Murcha + + + +

Udvarta Rajo Ajeerna Klinnakaya

Nirodha + - - +

Sheete shamyet - - + -

Rupa of Santamaka Shwasa

Tamasa vardhate + - - +

Sheeta prashamyati + - - +

Majjata Tamasi + - - +

Among the numerous Rupas of Tamaka Shwasa mentioned in

the table, Ati-Teevra Vega Shwasa, Ghurghura Shabda, and Sakapha

Kasa are considered to be the chief symptoms of Tamaka Shwasa.

Ghurghurkam: It is a typical sound produced, when excessive secretion of

the Kapha, causes Avarodha in the Pranavaha Srotas and thereby obstructs the

free flow of Pranavayu.

Ati Teevra Vega Shwasa: The excess secretion of mucus & sputum clogs the

path of the Pranavayu, i.e., it results in difficulty in breathing due to

obstruction to the flow of air in and out of the lungs.

41

Kasa: The excess secretion of mucus & sputum clogs the path of Pranavayu

causing Kasa. When unable to expectorate, the thick sticky sputum further

aggravates the coughing and sense of suffocation.

Greeva - Shiraso- Uraso Sangraham: These features are due to the hyper

inflation of the lungs. The subject experiences discomfort, or aching pain on

bilateral aspects of the chest.

Sleshmanam vimokshante muhurtham labhathe sukham: Once the

sputum has been expectorated, the frequency of breathlessness and coughing

reduces and there is momentary relief due to the easy flow of Prana Vayu. The

subject prefers hot things, which liquefy Kapha, and make Kapha

expectoration easier.

Kanthodhvamsa: Because of repeated coughing the patient develops

hoarseness of voice.

Shayanasya Shwasa Peeditha: When the patient lies in a recumbent position,

the space for air exchange reduces in the lungs which causes a sudden

decrease in the volume of the thoracic cavity. The air trapped cannot easily

escape and severe pain occurs.

42

Asinolabhate Saukhyam: On sitting the diaphragm is lowered and the space

for air exchange increase, and the volume of the thoracic cavity increases.

This facilitates the flow of Pranavayu.

Kricchrena Bhashate: During an episodic attack of Tamaka Shwasa the

patient can hardly speak. This is due to Shwasa Krucchrata and also due to

tenacious mucous coated in the throat including the vocal cords.

When the condition becomes severe, certain life threating symptoms or

Asadhya Lakshanas of Tamaka Shwasa will be seen in patients like -

Pramoham Kasamanashcha. The patient may go into syncope during bouts of

coughing. Other symptoms like increased respiratory distress which can be

correlated to the term Pratamyati, may also be seen. The patient becomes

motionless -Sannirudhyate.

Sometimes the patient may develop loss of consciousness – Pramoham. Some

have their eyes wide open - Ucchrita Akshata, sweating on the forehead -

Lalata Sweda, dryness of the mouth due to air hunger – Vishukasyata etc.

PRABHEDA OF TAMAKA SHWASA

2 types of Tamaka Shwasa have been explained (88).

· Pratamaka Shwasa: If Tamaka Shwasa is associated with Jvara and

Murcha, it is called Pratamaka. Udavarta, Rajas, Ajeerna, Klinnakaya and

43

Veganirodha are mentioned as the etiological factors. According to Vagbhatta,

this type of Shwasa subsides by giving Sheetala Upachara.

· Santamaka Shwasa: This type aggravates due to Tamas and is alleviated by

Sheetala Upachara. A patient with this condition feels as if he/she is being

submerged in Tamas. Some authorities correlate this condition to Cardiac

arrhythmia.

SAMPRAPTI

Samprapti is the process from Dosha Vaishamya till the expression of

the disease. Shwasa is a disease caused due to the simultaneous vitiation of

Vata and Kapha wherein either both are independent, or vitiate each other

(89). Among the two Doshas, Kapha Dosha is primarily involved in the

Tamaka Shwasa Samprapti. (90).

Samanya Samprapti

The morbid Vata which gets obstructed by Kapha, causing the vitiation

of the Prana, Udaka, and Annavaha srotas. The Vata then finally gets lodged

in the Ura pradesha causing Shwasa and Hikka. (91)

Vishista Samprapti of Shwasa

In the common Samprapti of all the five types of Shwasa, when the

Kapha and Vata obstruct the Srotas, the hindered Vayu, trying to overcome

the obstacle, moves in all directions results in Shwasa. The term

‘Vishawakvrajati’ denotes this.

44

Samprapti of Tamaka Shwasa:

Vata moving in the Pratiloma Gati pervades the Srotas (channel),

afflicts the Shiras and Griva, stimulates Kapha and causes Tamaka Shwasa.

This Kapha causes obstruction at the site of the throat Ghurguraka Shabda is

produced when Vata passes through the same region. This results in an

increase in the respiratory rate. (92)

Sthana Samshraya in Tamaka Shwasa

During this Kriyakala, the Purvarupavastha of Tamaka Shwasa is

manifested. In this stage, Khavaigunya occurs due to the already aggravated

Doshas circulating throughout the body which in turn affects the tissues of the

Pranavaha Srotas. Due to Sthana Samshraya of Doshas in the Pranavaha

Srotas, it becomes obstructed (Srotosanga) and Vata moves in all directions.

Vyakta in Tamaka Shwasa

Srotosanga due to Kapha and Ama Dosha in Pranavaha Srotas causes

Vimarga Gamana of Pranavata, results in the manifestation of the Lakshanas

of Tamaka Shwasa.

Bhedavastha in Tamaka Shwasa

The pathological process which is already ongoing in a patient reaches

this stage if the patient is a chronic sufferer, or if the disease is uncontrolled.

In long term permanent irreversible air flow obstruction, other Dhatus and

Srotas are vitiated, resulting in complications.

45

Table 11: Samprapti Ghatakas in Tamaka Shwasa

SAMPRAPTI GHATAKAS

Dosha Prana Vayu, Udana Vayu, Pachaka Pitta,

Avalambaka Kapha

Dushya Rasa

Agni Jataragni, Rasadhatwagni

Ama Jataragnijanya, Rasa dhatwagnijanya

Srotas Pranavaha Srotas, Udakavaha, Annavaha,

Rasavaha Srotas

Srotodushti Prakara Sanga, Vimargagamana

Udbhava Sthana Pitta Sthana (Adhoamasaya)

Sanchara Sthana Urah, Kanta, Shiras.

Adhishtana Uras

Vyakta Sthana Uras

Roga Marga Abhyantara

[Type the document title]

46

Figure 1: Flow chart of Samprapti in Tamaka Shwasa

Nidana Sevana

Vata Prakopaka

Vata prakopa

Kapha prakopaka

Kapha prakopa

Agnimandya

Kapha prakopa, Amotpa8

Sarva shareera

sancharana

Doshas lodge in Pranavaha

Srotas

Obstruct the movement of Prana Vayu

PraAloma gaA of Vayu

Tamaka Shwasa

Raja, Dhooma

Kha vaigunya in pranavaha

srotas

Pranavaha srotas

vaigunya


47

UPASHAYA – ANUPASHAYA

Upashaya

Any Dravya (Oushadhi, Ahara) or Adravya (Vihara) Upacharas which lead to

Sukhanubandha areUpashaya (93).

Anupashaya

Anupashaya is the opposite of Upashaya i.e. Ahara, Vihara and Oushadhis which

aggravate the condition of the disease are Anupashayas.

Table 13: Showing Upashaya and Anupashaya in Tamaka Shwasa (94)

Upashaya Anupashaya

Ushna Ahara Vihara.

Sheeta Ahara Vihara, Sheeta Ambu-

cold water

Aseeno Labhate Soukhyam – feels

comfortable to breath in a sitting

position.

Shayanasya Shwasa Piditaha –

discomfort worsens on lying.

Vimokshante Sukham –slight relief in

breathlessness on spitting out of the

sputum.

Presence of Kapha in the Pranavaha

srotas worsens difficulty in breathing.

Sunny weather relieves the symptoms.

Meghaihi Abhivardhate – cloudy

weather worsens the attack.

Quiet atmosphere is favorable. Pragvata – breeze.


48

Clear atmosphere, devoid of smoke and

dust helps in reducing the symptoms.

Exposure to dust or smoke worsens the

attack of Tamaka Shwasa.

Factors that reduces the Kapha vitiation

bring relief.

Sleshmala - Kapha increasing factors

aggravate the disease.

SADHYASADHYATA

Sadhyasadhyata refers to the prognosis of a disease i.e., whether the

disease is easily curable, difficult to cure or incurable. In Charaka Samhita it is

clearly mentioned that Tamaka Shwasa which is of recent origin is considered as

Sadhya and when it becomes chronic it is considered as Yapya. (95)

Vagbhata also supports the opinion of Charaka. He adds that if the disease

persists for less than a year in a Durbala Rogi, the disease is Kricchra Sadhya. (96)

Some authors consider Tamaka Shwasa to be Asadhya in Durbala Rogis. (97).

CHIKITSA

The term Chikitsa is derived from the root Kit Rogaapanayane.ie, the

measures adopted to remove causative factors. This also includes the break down

of the pathology involved and maintenance of Doshic equlibirum. Among the five

varieties of Shwasa - Urdhva, Maha and Chinna Shwasa are Asadhya and hence

treatment of these is not fruitful. Kshudra Shwasa is a trivial condition and does

not require any energetic treatment.

As the pathology of Tamaka Shwasa involves multiple changeable factors,

effective treatment of this illness cannot be standardized beyond a point. Vitiated

Vata and Kapha Doshas stemming from the Pitta Sthana, afflict the Rasa Dhatu

and Hridaya marma in the Pranavaha Srotas to produce the illness. Thus, the


49

procedures which aim to correct imbalance in Vata or Kapha Dosha form the main

aim of treatment in Tamaka Shwasa. (98)

Thus, drugs having Ushna veerya and which are Vatanulomaka are given

to Shwasa patients. Tamaka Shwasa is identified as a Yaapya /Kashtasaadhya

Vyadhi in which treatment has to be continued for prolonged periods with

meticulous care of the patient. (99)

NIDANA PARIVARJANA: (100)

The main Chikitsa for any disease is Nidana Parivarjana- avoidance of

causative factors. Being a Yapya Roga, avoidance of triggering factors and

provision of good quality of life with minimum medication is the aim of Tamaka

Shwasa management.

Treatment modalities used in Tamaka Shwasa may broadly be divided into two:

1. Management of Vegavastha

2. Management of Avegavastha

VEGAVASTHA

In the Vegavastha, all Acharyas have highlighted the importance of

Shodhana Chikitsa. After Poorvakarma of Snehana and Swedana, Vamana Karma

is advocated.


50

Vamana Karma in Tamaka Shwasa (101)

Vamana Karma expels the accumulated Kapha which has been liquefied by

Snehana and Swedana, thus clearing the air passages. Thus the free movement of

Vayu is restored. This is followed by Dhoomapana. In weak patients who cannot

undergo Shodhana, Dhoomapana alone can be adviced.

Nasya Prayoga in Tamaka Shwasa (102-103)

Different Yogas such as Rasona, Palandu, Grinjanaka Svarasa, and

Madhura Varga Dravya Siddha Ghrita are indicated for Nasya Karma.

AVEGAVASTHA

In between attacks treatment is given to prevent further vitiation of

Doshas.

1. Virechana Karma

2. Brimhana Chikitsa

3. Rasayana Chikitsa

Virechana Karma (104)

Virechana drugs which are Vatanulomaka, Ushna, and Kaphavataghna are

beneficial in setting right the Pratiloma Gati of Vayu. The Udbhava Sthana of

Tamaka Shwasa is the Pittasthana. Thus, Virechana which is Pittahara in nature,

cleanses the Pitta Sthana. Nityavirechana is an important therapeutic measure in

Tamaka Shwasa.


51

Brimhana and Rasayana Chikitsa (105)

Brimhana and Rasayana Chikitsa enhance the vital capacity and resistance

of the lungs, and can also act as adjuvants to the present modern treatments by

improving the quality of life of affected patients. Further, in the long run, this

disease causes emaciation of the body, which can be corrected by Brimhana

Chikitsa.

CONTEMPORARY VIEW:

HISTORICAL REVIEW OF ASTHMA:

Asthma is a Greek word derived from the verb aazein, meaning to exhale

with an open mouth, to pant, to gasp, or breathe sharply. The word first appeared

in Homer‘s Iliad. (106)

Hippocrates (460-367 B.C): He was the first person to use the term with reference

to a medical condition in his text Corpus Hippocraticum. (106)

The signs and symptoms of Tamaka Shwasa resemble those of Bronchial

Asthma in contemporary science.

DEFINITION

Bronchial Asthma is an inflammatory airway disease with episodic

occurrence of dyspnoea with wheezing. (107) The Global Initiative for Asthma has

proposed a descriptive definition of Asthma as follows - Asthma is a chronic

inflammatory disorder of the airways in which many cells and cellular elements

play a role‘.

The chronic inflammation is associated with airway hyper responsiveness

that leads to recurrent episodes of wheezing, breathlessness, chest tightness and


52

coughing, particularly at night or in the early morning. These episodes are usually

associated with widespread but variable airflow obstruction within the lung that is

often reversible either spontaneously or with treatment.

EPIDEMOLOGY (108)

The prevalence of asthma increased steadily over the latter part of the last

century, first in the developed and then in the developing countries. Current

estimates suggest that Asthma affects 300 million people worldwide, with a

predicted additional 100 million people affected by 2025. The socio-economic

impact is enormous, as poor control leads to days lost from school or work,

unscheduled health-care visits and hospital admissions.

Although the development and course of the disease, and the response to

the treatment, are influenced by genetic determinants, the rapid rise in prevalence

implies

that environmental factor are critically important in the development and

expression of the disease. To date, studies have explored the potential role of

indoor and outdoor allergens, microbial exposure, seasonal changes, diet, vitamins,

breastfeeding, tobacco smoke, air pollution and obesity but no clear consensus has

emerged. (109)

PATHOPHYSIOLOGY (110)

Airway hyper-reactivity (AHR) – the tendency for airways to narrow

excessively in response to triggers that have little or no effect in normal individuals

– is integral to the diagnosis of asthma and appears to be related, although not

exclusively, to airway inflammation. Other factors likely to be important in the

behavior of airway smooth muscle include the degree of airway narrowing and


53

neurogenic mechanisms. The relationship between atopy (the propensity to

produce IgE) and asthma is well established, and in many individuals there is a

clear relationship between sensitization and allergen exposure, as demonstrated by

skin prick reactivity or elevated serum specific IgE.

Common examples of allergens include house dust mites, pets such as cats

and dogs, pests such as cockroaches, and fungi. Inhalation of an allergen into the

airway is followed by an early and late-phase Bronchoconstrictor response.

In exercise-induced asthma, hyperventilation results in water loss from the

pericellular lining fluid of the respiratory mucosa, which, in turn, triggers mediator

release. In Persistent Asthma, a chronic and complex inflammatory response

ensues, characterized by an influx of numerous inflammatory cells, the

transformation and participation of airway structural cells, and the secretion of an

array of cytokines, chemokines and growth factors. Examination of the

inflammatory cell profile in induced sputum samples demonstrates that, although

asthma is predominantly characterized by airway eosinophilia, neutrophilic

inflammation predominates in some patients, while, in others, scant inflammation

is observed: so-called ‗pauci-granulocytic‘ asthma. With increasing severity and

chronicity of the disease, remodeling of the airway may occur, leading to fibrosis

of the airway wall, fixed narrowing of the airway and a reduced response to

bronchodialator medication.

CLINICAL FEATURES (111)

Typical symptoms include recurrent episodes of wheezing, chest tightness,

breathlessness and cough. Classical precipitants include exercise, particularly in

cold weather, exposure to airborne allergens or pollutants, and viral upper


54

respiratory tract infections. An inspection for nasal polyps and eczema should be

performed. Patients with mild intermittent asthma are usually asymptomatic

between exacerbations.

Individuals with persistent Asthma report ongoing breathlessness and

wheeze, but these are variable, with symptoms fluctuating over the course of one

day, or from day to day or month to month. Asthma characteristically displays a

diurnal pattern, with symptoms and lung function being worse in the early morning

or night. Particularly when poorly controlled symptoms such as cough and wheeze

disturbs sleep and have led to the term Nocturnal Asthma. Cough may be the

dominant symptom in some patients, and the lack of wheeze or breathlessness may

lead to a delay in reaching the diagnosis of so-called cough-variant Asthma. Some

patients with Asthma have a similar inflammatory response in the upper airway.

Careful enquiry should be made as to a history of Sinusitis, Sinus headache, a

blocked or runny nose, and loss of sense of smell.

Symptoms may occur in certain seasons or without any pattern; some

patients may remain symptomatic throughout the year. Cough is paroxysmal and

may be

accompanied by expectoration of thick and sticky sputum. Sneezing and running

nose are common and may precede and accompany with the attacks of wheezing.

The frequency and severity of symptoms and exacerbations varies from patient to

patient and also within the same patient from time to time.

AETIOLOGY (112)

Although the etiology of asthma is often elusive, an attempt should be

made to identify any agents that may contribute to the appearance or aggravation

of the condition. Particular enquiry should be made about potential allergens, such


55

as exposure to a pet cat, guinea pig, rabbit or horse, pest infestation, exposure to

moulds following water damage to a home or building, and any potential

occupational agents. In some circumstances, the appearance of asthma is triggered

by medications. Beta-blockers, even when administered topically as eye drops,

may induce bronchospasm, as may aspirin and other non-steroidal anti-

inflammatory drugs (NSAIDs). Other medications implicated include the oral

contraceptive pill, cholinergic agents and prostaglandin F2α. Betel nuts contain

arecoline, which is structurally similar to methacholine and can aggravate asthma.

Etiological factors of bronchial asthma are of two types. Some factors

called inducing factors can set initial development of asthma, whereas some other

factors provoke an episode in predisposed individuals suffering from asthma and

these are called provoking or trigger factors.

v Inducing Factors

Genetic factors are important to determine why asthma occurs in a particular

individual. Asthma occurs more commonly in relatives of atopic individuals. A

distinct gene for atopy on chromosome 11 has been identified. The frequent

clinical observation that asthma runs in families has been supported by many more

formal investigations. The genetics of production of total serum IgE have studied.

A correlation was found between the total serum IgE of parents and children,

suggesting the involvement of one or more genes. A gene for IgE response with

maternal inheritance was identified at chromosome. High level of IgE in cord

blood appears to be strong indicator of subsequent development of atopic disease.


56

v Precipitating Factors (Triggers) for Asthma (113)

1. Allergic triggers

· Indoor and outdoor moulds

· Pollen

· Insects

· Animal dander

· Dust mite particles

· Cockroach particles

· Some food and drug additives, preservatives and coloring agents (sulphites

used as a preservatives in some foods)

2. Non-allergic triggers

· Irritants: Tobacco smoke, indoor fuel (biomass) smoke, room deodorants,

fresh paint, household cleaning products, cooking odors

· Work place chemicals (occupational asthma, perfumes and cosmetics)

· Outdoor air pollution (zone, oxides of nitrogen, sulphur dioxide)

· Respiratory viral infections (para influenza in children, rhinovirus and

influenza in adults) can lead to prolonged destabilization of chronic

asthma.

· Exercise: especially in cold and dry air (free running, cycling, jogging);

swimming is least likely to precipitate

· Micro aspiration of gastric secretions (Gastro eosophageal reflux)


57

· Non-steroidal anti inflammatory drugs (aspirin, ibuprofen, indomethacin,

mefanmic acid)

· B-adrenergic antagonists (even selective agents can trigger asthma at high

doses; eye drops containing these drugs can precipitate asthma)

· Change in atmospheric conditions (pressure, humidity, temperature)

· Psychological factors; also alter perception of airways obstruction.

·

FEATURES THAT INCREASE THE PROBABILITY OF ASTHMA

(114)

More than one of the following symptoms: Wheeze, Breathlessness, Chest

tightness and Cough, particularly if:

· Symptoms worse at night and in the early morning

· Symptoms in response to exercise, allergen exposure and cold air

· Symptoms after taking aspirin or beta blockers

· History of atopic disorder

· Family history of asthma and/or atopic disorder

· Widespread wheeze heard on auscultation of the chest

· Unexplained low FEV1 or PEF

· Unexplained increased peripheral blood Eosinophilia

FEATURES THAT LOWER THE PROBABILITY OF ASTHMA (115)

· Prominent dizziness, light-headedness, peripheral tingling sensation

· Chronic productive cough in the absence of wheeze or breathlessness

· Repeatedly normal physical examination of chest when symptomatic

· Voice disturbance


58

· Symptoms with colds only

· Cardiac disease

· Normal PEFR or spirometry when symptomatic

EXACERBATIONS OF ASTHMA (116)

The course of Asthma may be punctuated by exacerbations with increased

symptoms, deterioration in lung function, and an increase airway inflammation.

Exacerbations are most commonly precipitated by viral infections, moulds

(Alternaria and Cladosporium), pollens and air pollution is also implicated. Most

attacks are characterized by a gradual deterioration over several hours to days but

some appear to occur with little or no warning: so-called Brittle Asthma. An

important minority of

patients appear to have a blunted perception of airway narrowing and fail to

appreciate the early signs of deterioration.

PROGNOSIS (117-118)

The outcome from Acute Severe Asthma is generally good. Death is

fortunately rare but a considerable. Failure to recognize the severity of an attack,

on the part of either the assessing physician or the patient, contributes to delay in

delivering appropriate therapy and to under-treatment.


59

INVESTIGATIONS (119)

Some physical examination findings increase the probability of asthma.

Nasal mucosal swelling, increased nasal secretions, and nasal polyps are often seen

in patients with allergic asthma. Eczema, atopic dermatitis, or other manifestations

of allergic skin disorders may also be present. Wheezing during normal breathing

or a prolonged forced expiratory phase correlates well with the presence of air flow

obstruction. Chest examination may be normal between exacerbations in patients

with mild asthma. During severe asthma exacerbations, airflow may be too limited

to produce wheezing and the only diagnostic clue on auscultation may be globally

reduced breath sounds with prolonged expiration. Hunched shoulders and use of

accessory muscles of respiration suggest an increased work of breathing.

PULMONARY FUNCTION TESTS (120)

The diagnosis of Asthma is predominantly clinical and based on a

characteristic history. Supportive evidence is provided by the demonstration of

variable airflow obstruction, preferably by using Spirometry to measure FEV1 and

VC. This identifies the obstructive defect, defines its severity, and provides a

baseline for bronchodilator reversibility.

PEAK EXPIRATORY FLOW RATE (121)

Definition:

Peak expiratory flow rate (PEFR) is the maximum rate at which the air

can be expired after a deep inspiration.


60

PEAK EXPIRATORY FLOW MONITORING (122)

PEF should be recorded as the best of three forced expiratory blows from

total lung capacity with a maximum pause of two seconds before blowing. The

patient can be standing or sitting. Further blows should be done if the largest two

PEF are not within 40 l/min.

PEF is best used to provide an estimate of variability of airflow from

multiple measurements made over at least two weeks. Increased variability may be

evident from twice daily readings. More frequent readings will result in a better

estimate but the improved precision is likely to be achieved at the expense of

reduced patient compliance.

OTHER INVESTIGATIONS (122)

Measurement of allergic status: The presence of atopy may be

demonstrated by skin prick tests. Similar information may be provided by

the measurement of total and allergen-specific IgE. A full blood picture

may show the peripheral blood Eosinophilia.

· Radiological examination: Chest X-ray appearances are often normal or

show hyperinflation of lung fields. Lobar collapse may be seen if mucus

occludes a large bronchus and, if accompanied by the presence of flitting

infiltrates, may suggest that Asthma has been complicated by allergic

Bronchopulmonary aspergillosis. An HRCT scan may be useful to detect

Bronchiectasis.


61

· Assessment of Eosinophilic airway inflammation: An induced sputum

differential Eosinophil count of greater than 2% or exhaled breath nitric

oxide concentration (FENO) may support the diagnosis but is non-specific.

MANAGEMENT (123)

Asthma is a chronic condition but may be controlled with appropriate

treatment in the majority of patients. Whenever possible, patients should be

encouraged to take responsibility for managing their own disease. A full

explanation of the nature of the condition, importance of key symptoms such as

nocturnal waking, the different types of medication, and, if appropriate, the use of

PEF to guide management decisions, should be given.

AVOIDANCE OF AGGRAVATING FACTORS (123)

This is particularly important in the management of Occupational Asthma

but may also be relevant in atopic patients. Smoking cessation is particularly

important, as smoking not only encourages sensitization, but also induces a

relative corticosteroid resistance in the airway.

THE STEPWISE APPROACH TO THE MANAGEMENT OF ASTHMA

(123)

· Step 1: Occasional use of inhaled short-acting β2-Adreno receptor agonist

Bronchodilators

· Step 2: Introduction of regular preventer therapy

· Step 3: Add-on therapy


62

· Step 4: Poor control on moderate dose of inhaled steroid and add-on

therapy: addition of a fourth drug

· Step 5: Continuous or frequent use of Oral Steroids

· Step-down therapy

NEBULIZATION

For treating acute symptoms, fast drug delivery and disposition is often

beneficial. Metered dose inhalers for asthma provide a prototype for rapid delivery

of drug to its site of action, as they produce beta agonist aerosols that deposit

directly onto the target tissue of the pulmonary airways. (124)

A nebulizer is a device which turns an aqueous solution of a drug into a

mist of fine particles for inhalation. (124). The aim of nebulizer therapy is to

deliver a therapeutic dose of the desired drug within a short delivery time, usually

10 minutes.

This is most beneficial when:

• Large inhaled drug doses are required

• Patients are too unwell or are unable to co-ordinate drug delivery devices

• Drugs are unavailable in hand held inhalers and a wider choice is needed

• Direct pulmonary therapy is required

A nebulizer delivers the liquid form of medication. Nebulized medications

are generally safe, as the amount of medication the child is prescribed and actually

receives is relatively small. This way of delivering the medication is relatively

easy for all age groups. The medication can be either pre-mixed or require the user


63

to dilute the medication with saline solution that is specifically manufactured for

use in the lungs. (125)

Aim of nebulizer therapy (125)

The aim of nebuliser therapy is to deliver a therapeutic dose of the desired

drug as an aerosol in the form of reparable particles within a fairly short period of

time, usually 5–10 minutes.

PROPER USE OF NEBULIZERS FOR THE PERFECT OUTPUT (126)

Driving gas:

In acute asthma while giving Salbutamol, Terbutaline, Ipratropium or

Duovent, use oxygen as the driving gas. In all other situations use air. Patients

with severe asthma are often hypoxic. Giving a bronchodilator via air may worsen

hypoxaemia. The appropriate gas should be indicated by the prescriber.

Diluents & fill volumes

All nebulizer chambers leave a residual volume of between 0.5 and 1.0ml.

The residual volume in the Intersurgical Cirrus Chamber is 0.9ml. This means that

0.9ml of the drug does not reach the patient, and this should be considered when

the dose is calculated. Increasing the fill volume by adding a diluents leads to a

decrease in the amount of active drug wasted.

Flow rates

Gas flow rate influences both nebulization time and the size of the droplets

being dispersed. An increased flow rate means that although nebulization time is


64

shorter, the size of the droplets is smaller. For efficient drug delivery to the

bronchial tree, the optimum droplet diameter is 1-5 microns.

Delivery time

The nebulizer will never run dry due to the residual volume. Dependent

upon the drug and nebulizer, up to 80% of the total dose is administered within the

first five minutes of delivery. But compliance drops with longer administration

time. The nebulizer chamber should be tapped when spluttering occurs.

Patient position

The patient should be comfortable and sitting upright. Ensure the mask fits

properly and is comfortable and encourage the patient to breathe steadily through

the mouth (not nose) where possible. The patient should avoid talking as this

reduces the efficiency of drug delivery. Leaning slightly forwards gives maximum

expansion of the lungs. It is important that the nebulizer chamber remains upright

at all times.

DRUGS USED VIA A NEBULISER (126-127)

Beta agonists, anti-cholinergics, corticosteroids and antibiotics are the main

drugs commonly administered by nebulizer. If a diluent is required, unless

otherwise stated, only Sodium Chloride 0.9% for injection should be used, as

hypotonic solutions can cause bronchospasm.


65

ARKA AS A DOSAGE FORM: (127-128)

Arka Kalpana can be defined as a liquid preparation obtained by

distillation of certain liquids or of drugs soaked in water using the Arkayantra, or

any convenient modern distillation apratus. The concept of Arka as a dosage form

is dealt with mainly in Ravana’s Arka Prakasha. Seven different types of Arka

have been mentioned in classical literature – based on contents, part used, duration

of preparation, action on the doshas, Manogunas, Rutus and Rogas.

General Method of Arka preparation:

A required quantity of water is added to the particular drug which is soaked and

kept overnight. The following day morning, it is poured into the Arka Yantra and

the remaining water is added to it and it is boiled. Recent authors add that eight

times the quantity of water must be added to the raw drug. The vapors produced

therein get condensed and are collected in a receiver. Recent authors have once

again specified that only 2/3rds of the condensed liquid must be collected.

Specifications for Arka preparation with respect to the nature of the Agni

(Deeptagni, Kharagni etc.), the concentration of the Arka required (Atyanta

Kathina, Kathina etc.), the part of the plant used (Patra, Kanda etc.), have been

mentioned.

Aim of Arka Kalpana:

The Arka kalpana is frequently used today due to its reduced dose, increased

patient compliance and increased potency. Contemporary texts provide standard

preparation methods and evaluation techniques for Arkas extracted from different

plants.


66

The main aim in this Kalpana is to extract the maximum number of active and

volatile principles from the raw ingredients. Hence, it is suitable for use as a

nebulizing agent.

67

METHODOLOGY

The objectives of the study were to evaluate the Shwasahara Karma of

Parnayavani Arka nebulization and compare its efficacy with a standard drug

– Theophylline - nebulization and carry out a preliminary phytochemical and

pharmacognostic study of Parnayavani (Coleus aromaticus Benth.). In

fulfillment of these, the study has been carried out in two phases as follows:

• Preliminary pharmacognostic and physico-chemical analysis

• Clinical study

Ø PHARMACOGNOSTIC ANALYSIS :

1. Macroscopy: The external features of the test sample was documented

using Canon IXUS digital camera.

2. Microscopy: Sample was preserved in fixative solution. The fixative used

was FAA (Formalin-5ml + Acetic acid-5ml + 70% Ethyl alcohol-90ml).

The materials were left in FAA for more than 48 hours. The preserved

specimens were cut into thin transverse section using a sharp blade and the

sections were stained with saffranine. Transverse sections were

photographed using Zeiss AXIO trinocular microscope attached with Zeiss

AxioCam camera under bright field light. Magnifications of the figures are

indicated by the scale-bars.

3. Powder microscopy: A pinch of powder was warmed with drops of

chloralhydrate on a microscopic slide and mounted in glycerine. Slides

observed under microscope and diagnostic characters were observed and

photographed using Zeiss AXIO trinocular microscope attached with Zeiss

68

AxioCam camera under bright field light. Magnifications of the figures are

indicated by the scale-bars.

Ø PHYSICO-CHEMICAL ANALYSIS:

I. PHYSICAL ANALYSIS

1) Loss on drying at 105oC

10 g of sample was placed in tarred evaporating dish. It was dried at 105˚C for 5

hours in a hot air oven and weighed. The drying was continued until the

difference between two successive weights was not more than 0.01g after

cooling in a desiccator. The percentage of moisture was calculated with

reference to the weight of the sample.

2) Total Ash

2 g of sample was incinerated in a tarred platinum crucible ata temperature not

exceeding

450˚C until carbon free ash was obtained. The percentage of ash was calculated

with reference to the weight of the sample.

3) Acid insoluble Ash:

To the crucible containing total ash, 25ml of dilute HCl was added and boiled.

The insoluble matter was collected on ashless filter paper (Whatmann 41) and

washed with hot water until the filtrate became neutral. The filter paper

containing the insoluble matter was then transferred to the original crucible,

dried on a hot plate and ignited to a constant weight. The residue was allowed

to cool in a suitable dessicator for 30 min and weighed without delay.

69

Thepercentage of acid insoluble ash was calculated with reference to the air

dried drug.

4) Water soluble ash

The ash obtained from the Total Ash experiment was boiled for 5 min with 25

ml of water; insoluble matter collected on an ashless filter paper, washed with

hot water, and ignited for 15 min at a temperature not exceeding 450˚C. The

weight of the insoluble matter was subtracted from the weight of the ash. The

difference in weight represents the water soluble ash content with reference to

the air-dried sample.

5) Alcohol soluble extractive

4 g of the sample was accurately weighed and taken in a glass stoppered flask.

100 ml of distilled Alcohol (approximately 95%) was added, and shaken

occasionally for 6 hours. It was then allowed to stand for 18 hours. It was then

filtered rapidly taking care not to lose any solvent. 25ml of the filtrate was

pipetted out in a pre-weighed 100 ml beaker and evaporated to dryness on a

water bath. It was then kept in a hot air oven at 105°C for 6 hours, cooled in a

desiccator for 30 minutes and weighed. The percentage of Alcohol extractable

matter of the sample was then calculated. The experiment was repeated twice,

and the average value taken.

6) Water soluble extractive:

4 g of the sample was accurately weighed and taken in a glass stoppered flask.

100 ml of distilled water was added and shaken occasionally for 6 hours. It

was then allowed to stand for 18 hours, then filtered rapidly taking care not to

70

lose any solvent. 25ml of the filtrate was pipetted out in a pre-weighed 100 ml

beaker and evaporated to dryness on a water bath. It was then kept in a hot air

oven at 105°C for 6 hours, cooled in a desiccator for 30 minutes and weighed.

The percentage of water extractable matter of the sample was then calculated.

The experiment was repeated twice, and the average value taken.

II. PHYTOCHEMICAL ANALYSIS

Preliminary phytochemical tests:

Preliminary Phytochemical tests are used to detect the presence of various

organic functional groups, which is indicative of the type of phytochemicals

present in the plant. These tests indicate the presence of different classes of

constituents present in the extract. Tests were performed as per the

methodologies mentioned by Harborne JB, 1973 (Phytochemical Methods.

Jackman H. (Ed.), London, p. 70.)

The following tests were carried out for the aqueous extract of the drug:

1. Tests for alkaloids

a. Dragendroff’s test: To a few mg of extract dissolved in alcohol, a few drops

ofacetic acid and Dragendroff’s reagent were added and shaken well. An

orange red precipitate formed indicates the presence of alkaloids.

b. Wagners’s test: To a few mg of extract dissolved in acetic acid, a few drops

of

Wagner’s reagent was added. A reddish brown precipitate formed indicates

the presence of alkaloids.

71

c. Mayer’s test: To a few mg of extract dissolved in acetic acid, a few drops of

Mayer’s reagent was added. A dull white precipitate formed indicates the presence of

alkaloids.

d. Hager’s test: To a few mg of extract dissolved in acetic acid, 3 ml of Hager’sreagent

was added, the formation of yellow precipitate indicates the presence of alkaloids.

2. Tests for carbohydrates

a. Molisch’s test: To the extract, 1 ml of α-naphthol solution and conc. sulphuricacid

were added along the sides of test tube. Violet colour formed at the junction of the two

liquids indicates the presence of carbohydrates.

b. Fehling’s test: A few mg of extract was mixed with equal quantities of

Fehling’s solution A and B. The mixture was warmed on a water bath. The

formation of a brick red precipitate indicates the presence of carbohydrates.

c. Benedict’s test: To 5 ml of Benedict’s reagent, a few mg of extract was added,and

boiled for two minutes and cooled. Formation of a red precipitate indicates the

presence of carbohydrates.

3. Test for steroids

a. Libermann-Burchardtest:To the extract was dissolved in chloroform, 1 ml ofacetic

acid and 1 ml of acetic anhydride were added, then heated on a water bath and

cooled. Few drops of conc. Sulphuric acid were added along the sides of the test tube.

Appearance of bluish green colour indicates the presence of steroids.

72

b. Salkowski test: The extract was dissolved in chloroform and equal volume ofconc.

Sulphuric acid was added. Formation of bluish red to cherry red colour in chloroform

layer and green fluorescence in the acid layer indicates the presence of steroids.

4. Test for saponins: To a few mg of extract, distilled water was added andshaken.

Stable froth formation indicates the presence of saponins.

5. Test for tannins: To the extract, a few drops of dilute solution of ferric chloridewas

added, formation of dark blue colour shows the presence of tannins.

6. Test for flavonoids

Shinoda’s test: To the extract in alcohol, a few magnesium turnings and fewdrops of

conc. hydrochloric acid were added and heated on a water bath. Formation of red to

pink colour indicates the presence of flavonoids.

7. Test for phenols

To the extract in alcohol, added two drops of alcoholic ferric chloride. Formation of

blue to blue black indicates the presence of phenol.

8. Test for coumarins

To the extract in alcohol, a few drops of 2 N sodium hydroxide solution was added.

Dark yellow colour formation indicates the presence of coumarins.

73

9. Test for triterpenoids

The extract was warmed with tin bits and few drops of thionyl chloride. Formation

of pink colour indicates the presence of triterpenoids.

74

CLINICAL STUDY

AIM:

To evaluate the efficacy of Parnayavani Arka nebulization in the management of Tamaka

Shwasa with special reference to Bronchial Asthma.

ETHICS:

The study was initiated after obtaining Institutional Ethics Committee (SDM/IEC/22/2015-

2016) Approval and written informed consent from participants. The study was registered

with the Clinical Trial Registry of India (CTRI/2018/03/012339)

SOURCE OF DRUG:

Parnayavani was cultivated in the Shri Dharmasthala Manjunatheshwara College of

Ayurveda and Hospital, Hassan herbal garden.

PLACE OF WORK:

(a) Parnayavani Arka was prepared at the Dept. of Dravyaguna and Rasashastra and

Bhaishjyakalpana, Shri Dharmasthala Manjunatheshwara College of Ayurveda and

Hospital, Hassan.

(b) Preliminary pharmacognostic and physic-chemical analysis was carried out at Shri

Dharmasthala Manjunatheshwara College of Ayurveda and Hospital, Kuthpady,

Udupi

(c) Clinical study was carried out at Shri Dharmasthala Manjunatheshwara College of

Ayurveda and Hospital, Hassan.

76

DESIGN OF THE STUDY:

A single blind double arm, active control clinical trial with pre-test - post-

test design.

Plan of Study:

The clinical study was done as follows:

Patients falling under the inclusion criteria were randomly allocated to the

study and pre and post PEFR was done to evaluate change in lung function.

Nebulization was given at a dose of 5 ml, once.

SOURCE OF DATA:

Patients of either sex diagnosed with Tamaka Shwasa, who fulfilled inclusion criteria

for the study were taken from the OPD and IPD of Shri Dharmasthala

Manjunatheshwara College of Ayurveda and Hospital, Hassan.

Methods of collection of data:

A clinical case proforma was prepared with all points of history taking,

physical signs and symptoms of Tamaka Shwasa. Accordingly patients were

subjected to detailed clinical examinations. Selected patients were randomly

allocated into one of two intervention groups based on chit method - Parnayavani

Arka nebulization group, or Theophylline nebulization group.

77

Design of the study:

The present clinical study was a double arm, active control, randomized

clinical study conducted in a tertiary Ayurveda healthcare center attached to a

teaching institute, situated at the district headquarters in Hassan, Karnataka. 60

patients suffering from Tamaka Shwasa w.s.r. to Bronchial Asthma, who signed

the informed consent form, and who fulfilled the inclusion criteria for the study

were randomly allocated into two groups – one with the trial drug of Parnayavani

Arka nebulization, and the other with the standard drug, Theophylline

nebulization.

Diagnosis

Diagnosis was made on the basis of Lakshanas of Tamaka Shwasa w.s.r. to

bronchial asthma like wheezing, tightness of chest, breathlessness and cough,

followed by a detailed respiratory system examination.

Inclusion criteria:

• Peak Expiratory Flow Rate (PEFR) 60% - 90%

• Conscious and well oriented

• Age 16 – 60 years

• Either gender

• Previously diagnosed cases of bronchial asthma

• Those patients who are ready to sign the informed consent form

78

Exclusion criteria:

• PEFR < 40%

• Patients with a history of Tuberculosis, Emphysema, Chronic airway

limitation

• History of Cardiac involvement

• Other complicated respiratory diseases having any organic lesions such as a

tumor or any anatomical defect in the airway

• Cyanosis

• Uncontrolled Hypertension,

• Uncontrolled Diabetes mellitus

Table 14: Group allocation in clinical study

Group No. Patients Drugs Dose

Dose

administration

T (Stand. Group) 30 Theophylline respule nebulization 5 ml Single time

PA (Trial Group) 30 Parnayavani Arka nebulization 5ml Single time

Assessment criteria:

1. The effect of the therapy was assessed on the basis of relief in the

following signs and symptoms of Tamaka Shwasa w.s.r. to bronchial asthma as

per GINA guidelines which were assigned suitable scores.

• Breathlessness

• Wheezing

79

• Difficulty in speech

• Chest tightness

• Cough

• Sputum expectoration

• Pulse rate

• Respiratory rate

Table 15: Subjective assessment parameters (GINA) of Acute asthma

Signs and Symptoms BT IMMEDIATELY AT 1 HOUR AT

1. Breathlessness

2. Wheeze

3. Talks in

4. Cough

5. Sputum

6. Chest Tightness

7. Pulse Rate

8. Respiratory Rate

Table 16: GINA Grading of Subjective Parameters in Acute Asthma

SL

No

ASSESSMENT

CRITERIA 0 1 2 3

80

2. Objective parameter for assessment was PEFR done before treatment,

after treatment, and one hour after treatment.

1 . Breathlessness Absent

Mild- while

walking

Can lie down

While at rest-

prefers sitting

While at rest-sits

upright

2. Wheeze Absent

Moderate -

often only at

end expiration

Loud-

throughout

expiration

Usually loud-

throughout

inhalation &

exhalation

3. Talks in Sentences Sentences Phrases Words

4. Cough Absent After exercise Continuous,

disturb work

Continuous,

disturbs normal

activity

5. Sputum Absent 1-3 times 4-5 times Continuously

6. Chest tightness Absent Mild Moderate Severe

7. Pulse/min <80 80-100 100-120 >120

8. Respiratory

rate/min 18-23 24-30 31-40 >40

81

Table 17: Table showing trial drug authentication, processing and manufacture :

Raw materials and authentication Cultivated and collected from the herb

garden of Shri Dharmasthala

Manjunatheshwara College of Ayurveda,

Hassan, and validated at the Dept. of

Dravyaguna, Shri Dharmasthala

Manjunatheshwara College of Ayurveda,

Hassan.

Parnayavani Arka preparation

To 50gms of raw Parnayavani Patra, 2

times water was added and kept for 24

hours. This mixture (drug and water)

was continuously heated in the

ArkaYantra (distillation apparatus) till

60% of distillate was collected. After

cooling, the collected Arka (distillate)

was filtered and preserved in an air

tight container.

Packaging and labelling The prepared medicine was stored in a

properly labeled airtight container,

labeled with the Name, Batch no.,

82

manufacturing date, and expiry date.

Withdrawal Criteria

The participants were allowed to withdraw from the trial if there were any

major ailments necessitating the institution of new modalities of treatment. The

decision to withdraw a participant from the trial was taken by the principal

investigator with proper justification and formal information to the Ethics Committee

within two working days.

Drop-Outs

An attempt was made to record the reason for drop outs, if any during the clinical trial.

STATISTICAL METHODS

§ Statistical analysis was done using SPSS VER. 20

§ Completed 60(30+30) patients were taken for statistical analysis.

§ Friedman’s test with Bonferroni correction was applied to analyze the

significance of change in Subjective parameters (within the group).

§ Wilcoxon sign rank test was done for post Hoc analysis with

Bonferroni correction on parameters which show significance in

Friedman’s test, to interpret the time of significant change.

§ Mann-Whitney U was done to assess the differences in time points

within the groups.

83

§ Repeated measures ANOVA was done for analyzing the different

time of significant changes between the groups.

The obtained results were interpreted in statistical terms as:

§ Significant (S): P <0.05

84

SAMPLE SIZE OF ESTIMATION

Mean population (µ0): 8

Mean, study group (µ1): 5

Probability of type I error (α) : 0.05

Probability of type II error (β): 0.2

Power: 0.8

Sample Size group 1 (N1): 29

Sample Size group 2 (N2): 29

Total: 58

N1 = (σ21 + σ2

2 / K) (z1- α/2 + z1- β)2 ∆2

= (4.12 + 4.12/1)(1.96 + 0.84)2

32

N1 = 29 N2 = K * N1 = 29 Hence, a sample size consisting of 60 volunteers was selected.

85

RESULTS

1. PHARMACOGNOSTIC ANALYSIS

2. CLINICAL STUDY

PHARMACOGNOSTIC STUDY:

Leaf of Coleus aromaticus Benth.

• Macroscopy:

Leaf:

The leaves are simple, opposite, long petioled, broadly ovate or cordate,

with an acute apex. They have a dentate margin, are very fleshy, thick and

very aromatic. They are thickly studded with hairs. On the lower surface,

glandular hairs are more numerous.

Stem:

The stem is fleshy, tomentose, hispidly villous and is about 30 cm.

• Microscopy:

• Petiole:

Transverse section of petiole is concave on the upper side and convex on

the lower side. Trichomes of both glandular and nonglandular type are

present all over the surface. The outer layer epidermis consist of a single

layer of laterally elongated cells, followed by 3-4 layers of cortical cells

which are round & collenchymatous. The rest of the cortical cells are

polygonal to round. The vasculature comprises of a ring of eight collateral

vascular bundles, of which the two are larger in size. The ground tissue

consists of thin walled parenchymatous cells.

86

• Midrib:

Transverse section of leaf passing through the midrib appears

hemispherical on the ventral side and slightly depressed on the dorsal side.

Upper epidermis is single layered and consists of compactly arranged

rectangular cells. Below this layer there is palisade parenchyma which is

also continuous with the midrib. Vascular bundles are solitary, collateral

and consist of 4-6 rows of xylem and a thin arc of phloem runs along the

midrib. Lower epidermis is similar to upper epidermis and is

discontinuous due to the presence of diacytic stomata On the upper and

lower epidermal surface numerous glandular and non glandular trichomes

are present.

• Lamina:

Upper Epidermis consists of single layer of rectangular cells along with a

thin layer of cuticle on it. Numerous trichomes of both glandular and non

glandular nature are present on both upper and lower epidermis.

The Mesophyll is differentiated into 2 parts – palisade parenchyma and

spongy parenchyma. The palisade parenchyma lies toward the upper

epidermis and consist of single layer of elongated columnar

parenchymatous cells. Towards the lower epidermis there lies the spongy

parenchyma which consists of 5-6 layers of loosely arranged spherical

cells.

87

Beside these numerous oil globules and prismatic calcium oxalate crystals

and starch cells were present in the ground tissue. Coursing through the

mesophyll vascular bundles surrounded

• Trichome:

The plant is densely covered with hairs of both glandular and non

glandular type.

The glandular trichomes are of capitates type which consists of a basal

epidermal cell, unicellular to bicellular stalk of variable lengh, a neck cell

and a large globular unicellular secretory head.

The non glandular trichomes are 3-6 celled, variable length uniseriate,

unbranched and progressively

Powder:

The powder is green, bitter to taste and has a characteristic odour. It shows

epidermal cells in the surface view with slightly wavy walls; diacyctic

stomata; both uneseriate as well as glandular trichomes; broad and narrow

vessel elements also seen, collapsed trichomes seen in the surface view of

the epidermis.

88

Table 18: RESULTS OF PHYSICOCHEMICAL ANALYSIS:

Table 19: RESULT OF PRELIMINARY PHYTOCHEMICAL TESTS:

Sl No Tests Color if positive Parnayavani

1. Alkaloids

Dragendrof’s test Orange precipitate Red precipitate

Wagners test Red precipitate Red precipitate

Mayers test Dull white precipitate Dull white precipitate

Hagers test Yellow precipitate

2. Steroids

Liebermann- buchard

test Bluish green

Greenish white at the chloroform

layer and colorless at the acid layer

Salkowski test Bluish red to cherry

red

Green solution at the upper layer and

clear at the base layer

Physico-chemical result (w/w)%

Test Parnayavani Standard (API)

Foreign matter None Not more than 2%

Loss on drying 6.24% -

Total ash 7.5% Not more than 16%

Acid insoluble acid 1.4% Not more than 2 %

Water soluble ash 2.8% -

Alcohol soluble extractive 15.2% Not less than 7%

Water soluble extractive 19.2% Not less than 23%

89

3. Carbohydrate

Molish test Violet ring Violet ring

Fehlings test Brick red precipitate Ink blue solution

Benedicts test Red precipitate Dark green solution

4. Tannin

With FeCl3 Dark blue or green or

brown Green

5. Flavanoids

Shinoda’s test Red to pink White solution

6. Saponins

With NaHCO3 Stable froth Stable froth

7. Triterpenoids

Tin and thionyl

chloride test Red White precipitate

8. Coumarins

With 2 N NaOH Yellow Brownish green

9. Phenols

With alcoholic ferric

chloride

Blue to blue black,

brown Green

10. Carboxylic acid

With water and

NaHCO3 Brisk effervescence no effervescence

11. Resin

With aqueous acetone Turbidity Turbidity

90

12. Quinone

5% NaOH Pink/purple/red Brownish green

13. Amino acids

Ninhydrine reagent Purple color Green solution

Table 20: Summarized results of preliminary phytochemical tests

Test Parnayavani

Alkaloid +

Carbohydrate +

Carboxylic acid -

Coumarins -

Flavanoids -

Phenol +

Quinone -

Resins +

Steroid -

Saponins +

Tannin +

Terpenoid -

Amino acids -

91

Table 21: RESULTS OF PARNAYAVANI ARKA EVALUATION:

Test Parnayavani

pH 6

Refractive index 1.33229

Specific gravity 63.89

Viscosity 63.89

Volatile matter

(%)

0.21

Boiling point 1000C

Total acidity 0.36

% acidity 0.021

92

RESULTS OF GC-MS EVALUATION OF ARKA:

Table 22: MS of compounds identified from Arka of Coleus aromaticus

Fig.2: Octadecane, 3-ethyl-5-(2 ethylbutyl)

Fig 3: Dodecyl acrylate

Fig 4: Octadecanal, 2-bromo-

RT Name Formula MF RMF

6.311 Octadecane, 3-ethyl-5-(2

ethylbutyl)

C26H54 882 897

6.981 Dodecyl acrylate C15H28O2 811 847

7.077 Octadecanal, 2-bromo- C13H35BrO 770 770

93

CLINICAL STUDY:

Table 23: Gender Distribution of 60 patients of Tamaka Shwasa

Gender analysis of 60 patients of Tamaka Shwasa in the current study showed that

there were 12 males and 17 females in the trial group, and 16 males and 15 females in

the control group. Totally there were 28 males and 32 females.

Figure 5: Gender Distribution of 60 patients of Tamaka Shwasa

12

16 18

14

Trial Control

Male Female

Gender Group Total Percentage (%)

Trial Control

Male 12 16 28 46.7

Female 18 14 32 53.3

Total 30 30 60 100

94

Table 24: Age distribution of 60 patients of Tamaka Shwasa:

Age-wise analysis of 60 patients of Tamaka Shwasa in the current study showed that

there was highest incidence of patients in the age group between 40-60 years, and 20-

30 years.

Figure 6: Age distribution of 60 patients of Tamaka Shwasa:

0

2

4

6

8

10

12

14

10-‐20 yrs 20-‐30 yrs 30-‐40 yrs 40-‐50 yrs 50-‐60 yrs

Trial

Control

Age Group Total Percentage (%)

Trial Control

10-20 yrs 0 0 0 0

20-30 yrs 5 8 13 21.7

30-40 yrs 2 8 10 16.7

40-50 yrs 13 5 18 30

50-60 yrs 10 9 19 31.6

Total 30 30 60 100

95

Table 25: Marital status Distribution of 60 patients of Tamaka Shwasa:

Marital status analysis of 60 patients of Tamaka Shwasa in the current study showed

that there were 2 unmarried and 28 married subjects in the trial group, and 4

unmarried and 26 married subjects in the control group. Totally, there were 6

unmarried and 54 married subjects. There were no divorced or widowed subjects.

Figure 7: Marital status Distribution of 60 patients of Tamaka Shwasa

2 4

28 26

Trial Control

Unmarried Married

Marital status Group Total Percentage (%)

Trial Control

Unmarried 2 4 6 10

Married 28 26 54 90

Total 30 30 60 100

96

Table 26: Place wise distribution of 60 patients of Tamaka Shwasa

Place wise distribution of 60 patients of Tamaka Shwasa in the current study showed

that there were 12 subjects from urban areas and 18 subjects from rural areas in the

trial group. There were 25 subjects from urban areas and 5 subjects from rural areas in

the control group.Totally, there were 37 subjects from urban areas and 23 subjects

from rural areas.

Figure 8: Place wise distribution of 60 patients of Tamaka Shwasa

12

25

18

5

Trial Control

Urban Rural

Place Group Total Percentage (%)

Trial Control

Urban 12 25 37 61.6

Rural 18 5 23 38.4

Total 30 30 60 100

97

Table 27: Religion wise distribution of 60 patients of Tamaka Shwasa:

Religion wise distribution of 60 patients of Tamaka Shwasa in the current study

showed that there were 29 Hindu subjects and 1 Muslim subject in the trial group.

There were 26 Hindu subjects, 2 Muslim subjects and 2 Christian subjects in the

control group. Totally, there were 55 Hindu subject, 3 Muslim subjects and 2

Christian subjects.

Figure 9: Religion wise distribution of 60 patients of Tamaka Shwasa

0

5

10

15

20

25

30

35

Hindu Muslim Christian

Trial

Control

Religion Group Total Percentage (%)

Trial Control

Hindu 29 26 55 91.7

Muslim 1 2 3 5

Christian 0 2 2 3.3

Total 30 30 60 100

98

Table 28: Socio-economic status wise distribution of 60 patients of Tamaka

Shwasa:

Socio-economic status wise distribution of 60 patients of Tamaka Shwasa in the

current study showed that there were 3 from poor backgrounds, 27 from lower middle

class backgrounds, 21 from middle class backgrounds, and 9 from upper middle class

backgrounds.

Figure 10: Socio-economic status wise distribution of 60 patients of Tamaka

Shwasa

3

20

7

0 0

7

14

9

Poor Lower middle class Middle Class Upper middle class

Trial Control

Socio-economic status Group Total Percentage (%)

Trial Control

Poor 3 0 3 5

Lower middle class 20 7 27 45

Middle Class 7 14 21 35

Upper middle class 0 9 9 35

Total 30 30 60 100

99

Table 29: Education wise distribution of 60 patients of Tamaka Shwasa

Education status wise distribution of 60 patients of Tamaka Shwasa in the current

study showed that there were 17 subjects who had completed Lower Secondary

education, 1 subject who had completed SSLC, 9 subjects who had completed

Undergraduation, and 3 subjects who had completed Postgraduation in the trial group.

There were 8 subjects who had completed lower secondary education, 6 subjects who

had completed SSLC, 1 subject who had completed PUC, 21 who had completed

Undergraduation and 6 who had completed Postgraduation in the control group.

Totally, there were 25 subjects who had completed Lower Secondary education, 7

subjects who had completed SSLC, 1 subject who had completed PUC, 21 subjects

who had completed Undergraduation, and 6 subjects who had completed

Postgraduation.

Figure 11: Education wise distribution of 60 patients of Tamaka Shwasa

17

1 0

9

3 8 6

1

12

3

Lower Secondary

SSLC PUC UG PG

Trial Control

Education Group Total Percentage (%)

Trial Control

Lower Secondary 17 8 25 41.7

SSLC 1 6 7 11.7

PUC 0 1 1 1.6

UG 9 12 21 35

PG 3 3 6 10

Total 30 30 60 100

100

Table 30: Presenting complaints of 60 patients of Tamaka Shwasa

In the current study, it was found that maximum number of patients presented with

Wheezing during the night (60), Chest tightness (50), Dyspnoea on exertion (42), and

cough (35).

Figure 12: Presenting complaints of 60 patients of Tamaka Shwasa

25

5 12

9

30

21

11

0

9

17 13

23

8

30 29

3 0

6

Trial Control

Presenting complaints Group Total

Trial Control

Dyspnoea on exertion 25 17 42

Dyspnea on rest and exertion 5 13 18

Cough 12 23 35

Wheezing during the day 9 8 17

Wheezing during the night 30 30 60

Chest tightness 21 29 50

Difficulty in speech 11 3 14

Confusion 0 0 0

Rhinitis 9 6 15

101

Table 31: Duration of onset in 60 patients of Tamaka Shwasa:

Analysis of duration of onset in 60 patients of Tamaka Shwasa in the current study

showed that there were 9 who complained of onset less than 5 years ago, 2 who

complained of a duration of onset between 5-10 years ago, 7 who complained of onset

between 10-15 years ago, and 5 who complained of a duration of onset between 20-25

years ago in the trial group. There were 10 who complained of onset less than 5 years

ago, 11 who complained of a duration of onset between 5-10 years ago, 13 who

complained of onset between 10-15 years ago, and 0 who complained of a duration of

onset between 20-25 years ago in the control group. Totally, there were 19 who

complained of onset less than 5 years ago, 13 who complained of a duration of onset

between 5-10 years ago, 12 who complained of onset between 10-15 years ago, 11

who complained of a duration of onset between 15-20 years ago, and 5 who

complained of a duration of onset between 20-25 years ago.

Figure 13: Duration of onset in 60 patients of Tamaka Shwasa

9

2

7 7 5

10 11

5 4

0

0-‐5 years 5-‐10 years 10-‐15 years 15-‐20 years 20-‐25 years

Trial Control

Duration Group Total Percentage (%)

Trial Control

0-5 years 9 10 19 31.7

5-10 years 2 11 13 21.7

10-15 years 7 5 12 20

15-20 years 7 4 11 18.3

20-25 years 5 0 5 8.3

Total 30 30 60 100

102

Table 32: Mode of onset in 60 patients of Tamaka Shwasa:

Analysis of mode of onset in 60 patients of Tamaka Shwasa in the current study

showed that there was no subject complained of gradual onset while all subjects

complained of sudden onset.

Figure 14: Mode of onset in 60 patients of Tamaka Shwasa

0

5

10

15

20

25

30

35

Trial Control

Gradual

Sudden

Onset Group Total Percentage (%)

Trial Control

Gradual 0 0 0 0

Sudden 30 30 60 100

Total 30 30 60 100

103

Table 33: Trigger factors in 60 patients of Tamaka Shwasa:

Analysis of trigger factors in 60 patients of Tamaka Shwasa in the current

study showed that there were 12 subjects who complained of dust as a trigger, 28

subjects who complained of cold as a trigger, 18 subjects who complained of both

dust and cold as triggers, and 2 who complained of other specific allergens.

Figure 15: Trigger factors in 60 patients of Tamaka Shwasa

7

20

3 0

5 8

15

2

Dust Cold Dust and Cold Other allergen

Trial Control

Trigger Group Total Percentage (%)

Trial Control

Dust 7 5 12 20

Cold 20 8 28 46.7

Dust and Cold 3 15 18 30

Other allergen 0 2 2 3.3

Total 30 30 60 100

104

Table 34: History of previous illness in 60 patients of Tamaka Shwasa

Analysis of trigger factors in 60 patients of Tamaka Shwasa in the current

study showed that there were 12 subjects who complained of dust as a trigger, 28

subjects who complained of cold as a trigger, 18 subjects who complained of both

dust and cold as triggers, and 2 who complained of other specific allergens.

Figure 16: History of previous illness in 60 patients of Tamaka Shwasa

10

15

0

5 5

1

6

18

Diabetes Hypertension DM and HTN Nothing signiNicant

Trial Control

Previous illness Group Total Percentage (%)

Trial Control

Diabetes 10 5 15 20

Hypertension 15 1 16 46.7

DM and HTN 0 6 6 30

Nothing significant 5 18 23 3.3

Total 30 30 60 100

105

Table 35: History of previous treatment in 60 patients of Tamaka

Shwasa:

Analysis of previous medication in 60 patients of Tamaka Shwasa in the

current study showed that there were 27 subjects who had a history of use of B2

adrenoreceptor bronchodilators such as Salbutamol or Terbutaline. 16 subjects had a

history of use of Anti-inflammatory therapy of inhaled corticosteroids such as

Beclometasone, Budesonide etc. 9 subjects had a history of use of Long acting B2

agonists such as Salmoterol, Formoterol etc. 5 subjects had a history of oral steroid

use. 3 subjects did not have significant previous treatment history.

Figure 17: History of previous treatment in 60 patients of Tamaka Shwasa

12

8

3 4 3

15

8 6

1 0

Trial Control

Treatment Group Total Percentage (%)

Trial Control

B-2 adrenoreceptor bronchodilators 12 15 27 45

Anti-inflammatory therapy - ICS 8 8 16 26.7

Long acting B2 agonists - Add on therapy 3 6 9 15

Oral steroid therapy - Prednisolone 4 1 5 8.3

Nothing significant 3 0 3 5

Total 30 30 60 100

106

Table 36: Family History in 60 patients of Tamaka Shwasa:

Analysis of family history in 60 patients of Tamaka Shwasa in the current

study showed that there were 16 subjects whose father (father’s relatives) suffered

from asthma, 11 subjects whose mother suffered from asthma (or mother’s relatives),

1 subject whose son suffers from asthma, 2 subjects whose daughter suffers from

asthma, and 30 subjects who have no significant history of asthma.

Figure 18: Family History in 60 patients of Tamaka Shwasa

5

8

0

2

15

11

3

1 0

15

Father Mother Son Daughter Nothing signiNicant

Trial Control

Family history Group Total Percentage (%)

Trial Control

Father 5 11 16 26.7

Mother 8 3 11 18.3

Son 0 1 1 1.6

Daughter 2 0 2 3.4

Nothing significant 15 15 30 50

Total 30 30 60 100

107

Table 37: Occupation of 60 patients of Tamaka Shwasa:

Analysis of occupation in 60 patients of Tamaka Shwasa in the current study

showed that 15 subjects were housewifes/homemakers, 9 were independent

businessmen, 16 were agriculturalists, 6 were students, and 14 belonged to other

occupations such as drivers, construction workers etc.

Figure 19: Occupation of 60 patients of Tamaka Shwasa

4

8

12

1

5

11

1

4 5

9

Housewife Business Agriculture Student Other

Trial Control

Occupation Group Total Percentage (%)

Trial Control

Housewife 4 11 15 25

Business 8 1 9 15

Agriculture 12 4 16 26.7

Student 1 5 6 10

Other 5 9 14 23.3

Total 30 30 60 100

108

Table 38: Agni of 60 patients of Tamaka Shwasa

Analysis of Agni in 60 patients of Tamaka Shwasa in the current study

showed that 19 subjects had Sama Agni and 41 subjects had Manda Agni.

Figure 20: Agni of 60 patients of Tamaka Shwasa

0

5

10

15

20

25

Sama Manda Teekshna Vishama

Trial

Control

Agni Group Total Percentage (%)

Trial Control

Sama 8 11 19 31.7

Manda 22 19 41 68.3

Teekshna 0 0 0 0

Vishama 0 0 0 0

Total 30 30 60 100

109

Table 39: Ahara of 60 patients of Tamaka Shwasa:

Analysis of Ahara in 60 patients of Tamaka Shwasa in the current study

showed that 19 subjects were consumed only vegetarian food, while 41 subjects

consumed a mixed diet.

Figure 21: Ahara of 60 patients of Tamaka Shwasa

7

23

0 0

12

18

0 0

Vegetarian Mixed Teekshna Vishama

Trial Control

Ahara Group Total Percentage (%)

Trial Control

Vegetarian 7 12 19 31.7

Mixed 23 18 41 68.3

Teekshna 0 0 0 0

Vishama 0 0 0 0

Total 30 30 60 100

110

Table 40: Nidra of 60 patients of Tamaka Shwasa

Analysis of Nidra in 60 patients of Tamaka Shwasa in the current study

showed that 53 of subjects reported disturbed sleep, while 7 reported sound sleep.

Fig. 22: Nidra of 60 patients of Tamaka Shwasa

26 27

4 3

Trial Control

Disturbed Sound

Nidra Group Total Percentage (%)

Trial Control

Disturbed 26 27 53 88.4

Sound 4 3 7 11.6

Total 30 30 60 100

111

Table 41: Rasa preference of 60 patients of Tamaka Shwasa

Analysis of Rasa preferred in 60 patients of Tamaka Shwasa in the current

study showed that 27 subjects preferred Madhura Rasa, 6 preferred Amla Rasa and 27

preferred Katu Rasa.

Fig. 23: Rasa preference of 60 patients of Tamaka Shwasa

14

1

15 13

5

12

Madhura Amla Katu

Trial Control

Rasa Group Total Percentage (%)

Trial Control

Madhura 14 13 27 45

Amla 1 5 6 10

Katu 15 12 27 45

Total 30 30 60 100

112

Table 42: Alcohol and Smoking consumption in patients of Tamaka Shwasa:

Analysis of Alcohol and Smoking in in 60 patients of Tamaka Shwasa in the

current study showed that 17 subjects were regular smokers, 2 were habituated to

regular alcohol intake (beer, whiskey), 7 to both, and 34 to neither.

Fig. 24: Alcohol and Smoking consumption in patients of Tamaka Shwasa

4 2

5

21

13

0 2

13

Smoking Alcohol Both None of the above

Trial Control

Habits Group Total Percentage (%)

Trial Control

Smoking 4 13 17 28.4

Alcohol 2 0 2 3.3

Both 5 2 7 11.6

None of the above 21 13 34 56.7

Total 30 30 60 100

113

Table 43: Tea and Coffee consumption in 60 patients of Tamaka Shwasa:

Analysis of Alcohol and Smoking in in 60 patients of Tamaka Shwasa in the

current study showed that 17 subjects were regular smokers, 2 were habituated to

regular alcohol intake (beer, whiskey), 7 to both, and 34 to neither.

Fig. 25: Tea and Coffee consumption in 60 patients of Tamaka Shwasa

28 30

2 0

Trial Control

Tea/Coffee Neither

Habits Group Total Percentage (%)

Trial Control

Tea/Coffee 28 30 58 96.7

Neither 2 0 2 3.3

Total 30 30 60 100

114

Table 44: Wheezing in 60 patients of Tamaka Shwasa

Analysis of wheezing sounds in 60 patients of Tamaka Shwasa in the current study

showed that 43 had wheezing sounds, while 17 subjects did not show wheezing

sounds.

Fig. 26: Wheezing in 60 patients of Tamaka Shwasa

27

16

3

14

Trial Control

Present Absent

Wheezing Group Total Percentage (%)

Trial Control

Present 27 16 43 71.6

Absent 3 14 17 28.4

Total 30 30 60 100

115

Table 45: Nature of Wheezing sounds in 43 patients of Tamaka Shwasa

Among the 43 subjects who had wheezing sounds, 41 had polyphonic wheezes

while 2 had monophonic wheezes.

Fig. 27: Nature of Wheezing sounds in 43 patients of Tamaka Shwasa

27

16

3

14

Trial Control

Present Absent

Wheeze Group Total Percentage (%)

Trial Control

Polyphonic 26 15 41 95.3

Monophonic 1 1 2 4.7

Total 27 16 43 100

116

Table 46: Timing of Wheezing sounds in 43 patients of Tamaka Shwasa

Among the 43 subjects who had wheezing sounds, 17 showed inspiratory

wheezes and 26 showed expiratory wheezing sounds.

Fig. 28: Timing of Wheezing sounds in 43 patients of Tamaka Shwasa

10

7

12

14

Trial Control

Inspiratory Expiratory

Wheeze time Group Total Percentage (%)

Trial Control

Inspiratory 10 7 17 39.5

Expiratory 12 14 26 60.5

Total 22 21 43 100

117

Table 47: Rhonchi in 60 patients of Tamaka Shwasa

Analysis of rhonchi in 60 patients of Tamaka Shwasa in the current study

showed that 17 patients had rhonchi, while 43 did not.

Fig. 29: Rhonchi in 60 patients of Tamaka Shwasa

2

15

28

15

Trial Control

Present Absent

Rhonchi Group Total Percentage (%)

Trial Control

Present 2 15 17 28.4

Absent 28 15 43 71.6

Total 30 30 60 100

118

Table 48: Crepitations in 60 patients of Tamaka Shwasa

Analysis of rhonchi in 60 patients of Tamaka Shwasa in the current study

showed that 17 patients had rhonchi, while 43 did not.

Fig. 30: Crepitations in 60 patients of Tamaka Shwasa

13

8

17

22

Trial Control

Present Absent

Ralls Group Total Percentage (%)

Trial Control

Present 13 8 21 35

Absent 17 22 39 65

Total 30 30 60 100

119

Table 49: Timing of crepitation in 21 patients of Tamaka Shwasa

Among the 21 patients who had crepitations, it was found that 16 had coarse

ralls, while 5 had fine ralls.

Fig. 31: Timing of crepitation in 21 patients of Tamaka Shwasa

4

12

0

5

Trial Control

Coarse Fine

Ralls Group Total Percentage (%)

Trial Control

Coarse 4 12 16 76.2

Fine 0 5 5 23.8

Total 4 17 21 100

120

RESULTS OF SUBJECTIVE PARAMETERS:

a. Within the group analysis :

Table 50: FRIEDMAN’S TEST TO ASSESS BREATHLESSNESS WITHIN

PARNAYAVANI ARKA NEBULIZATION GROUP

Parameters Mean

Rank

N Chi-

Square

Value

P-

Value

Breathlessness

BT

3.00

30

59.363

0.000 Breathlessness

– AT

1.48

Breathlessness

– AT (1hr)

1.52

121

Table 51: WSR Post hoc test with Bonferroni’s correction to assess

Breathlessness within trial group

There was a statistically significant difference in breathlessness before and after

intervention. Post-hoc analysis with WSR was conducted with a Bonferroni correction

applied, resulting in a significance level p<0.017. There was a significant decrease in

breathlessness between the BT and AT groups (Z = 4.928a a, p=0.000), and between

the BT-AT1 group (Z=-4.940a, p=0.000). There was a non-significant increase in

breathlessness between the AT-AT1 group (Z=-1.000b, p=0.157).

Table 52: FRIEDMAN’S TEST TO ASSESS WHEEZING WITHIN


Parameters Mean

Rank

N Chi-

Square

Value

P-Value

Wheezing

–

BT

2.98

30

57.022

0.000 Wheezing

– AT

1.45

Wheezing 1.57

Parameters Breathlessness

(BT-AT)

Breathlessness

(BT-AT1)

Breathlessness

(AT-AT1)

Z-Value -4.928a -4.940a -1.000b

P-value 0.000 0.000 0.317

a. Based on positive ranks

b. Based on negative ranks

122

– AT (1hr)


Wheezing within trial group

•

•

There was a statistically significant difference in wheezing before and after



wheezing between the BT and AT groups (Z = -4.998a, p=0.000), and between the

BT-AT1 group (Z=--4.939, p=0.000). There was a non-significant increase in

wheezing between the AT-AT1 group (Z=-1.604, p=0.083).

Parameters Wheezing

(BT-AT)

Wheezing

(BT-

AT1)

Wheezing

(AT-

AT1)

Z-Value -4.998a -4.939a -1.604b

P-value 0.000 0.000 0.083



123

Table 54: FRIEDMAN’S TEST TO ASSESS SPEECH DIFFICULTY WITHIN


Parameters Mean

Rank

N Chi-

Square

Value

P-Value

Speech

difficulty

– BT

3.00

30

60

0.000 Speech

difficulty

– AT

1.50

Speech

difficulty

– AT (1hr)

1.50

Table 55: WSR Post hoc test with Bonferroni’s correction to assess Speech

difficulty within trial group

Parameters Cough

(BT-AT)

Cough

(BT-

AT1)

Cough

(AT-

AT1)

Z-Value -5.007a -5.0079a -0.000b

P-value 0.000 0.000 1.000



124

There was a statistically significant difference in cough before and after intervention.

Post-hoc analysis with WSR was conducted with a Bonferroni correction applied,

resulting in a significance level p<0.017. There was a significant decrease in speech

difficulty between the BT and AT groups (Z = -5.007a, p=0.000), and between the

BT-AT1 group (Z=-5.007, p=0.000). There was no change in speech between AT-

AT1 groups. (Z=-0.000, p=1.000).

Table 56: FRIEDMAN’S TEST TO ASSESS COUGH WITHIN


Parameters Mean

Rank

N Chi-

Square

Value

P-Value

Cough –

BT

3.00

30

60.00

0.000

Cough –

AT

1.50

Cough –

AT (1hr)

1.50

125

Table 57: WSR Post hoc test with Bonferroni’s correction to assess Cough

within trial group

•

•

There was a statistically significant difference in cough before and after intervention.

Post-hoc analysis with WSR was conducted with a Bonferroni correction applied,

resulting in a significance level p<0.017. There was a significant decrease in Cough

between the BT and AT groups (Z = -4.932a, p=0.000), and between the BT-AT1

group (Z=-4.932, p=0.000). There was no change in cough between the AT-AT1

group (Z=-0.000, p=1.000).

Table 58: FRIEDMAN’S TEST TO ASSESS SPUTUM EXPECTORATION

WITHIN PARNAYAVANI ARKA NEBULIZATION GROUP

Parameters Mean

Rank

N Chi-

Square

Value

P-Value

Sputum

expectoration

2.98

Parameters Cough

(BT-AT)

Cough

(BT-

AT1)

Cough

(AT-

AT1)

Z-Value -4.932a -4.932a -0.000

P-value 0.000 0.000 1.000



126

–

BT

30

51.784

0.000

Sputum

expectoration

– AT

1.60

Sputum

expectoration

– AT (1hr)

1.42

Table 59: WSR Post hoc test with Bonferroni’s correction to assess Sputum

expectoration within trial group

•

There was a statistically significant difference in sputum production before and after



sputum production between the BT and AT groups (Z = -4.800a, p=0.000), and

between the BT-AT1 group (Z=-4.922, p=0.000). There was a non-significant

decrease in sputum production between the AT-AT1 group (Z=-1.387, p=0.166).

Parameters Sputum

expectoration

(BT-AT)

Sputum

expectoration

(BT-AT1)

Sputum

expectoration

(AT-AT1)

Z-Value -4.800a -4.922a -1.387a

P-value 0.000 0.000 0.166



127

Table 60: FRIEDMAN’S TEST TO ASSESS TIGHTNESS IN CHEST WITHIN


Parameters Mean

Rank

N Chi-

Square

Value

P-Value df

Tightness

in the

Chest –

BT

3.00

30

57.532

0.000

2

Tightness

in the

Chest –

AT

1.47

Tightness

in the

Chest –

AT (1hr)

1.53

128

Table 61: WSR Post hoc test with Bonferroni’s correction to assess Chest

tightness within trial group

Parameters Tightness

in the

chest

(BT-AT)

Tightness

in the

chest

(BT-

AT1)

Tightness

in the

chest

(AT-

AT1)

Z-Value -4.920a -4.922a -1.000b

P-value 0.000 0.000 0.317

There was a statistically significant difference in Chest Tightness before and after



chest tightness between the BT and AT groups (Z = -4.920a, p=0.000), and between

the BT-AT1 group (Z=-4.922a, p=0.000). There was a non-significant increase in

chest tightness between the AT-AT1 group (Z=-1.000b, p=0.025)

Table 62: FRIEDMAN’S TEST TO ASSESS PULSE RATE WITHIN


Parameters Mean

Rank

N Chi-

Square

Value

P-Value

Pulse rate

–

BT

2.92



129

Pulse rate

– AT

1.52 30 54.071 0.000

Pulse rate

– AT (1hr)

1.57

Table 63: WSR Post hoc test with Bonferroni’s correction to assess Pulse

rate within trial group

•

•

There was a statistically significant difference in pulse rate before and after



pulse rate between the BT and AT groups (Z = -5.013a, p=0.000), and between the

BT-AT1 group (Z=-4.916, p=0.000). There was a non-significant increase in pulse

rate between the AT-AT1 group (Z=-1.000, p=0.317).

Parameters Pulse

rate

(BT-AT)

Pulse

rate

(BT-

AT1)

Pulse

rate

(AT-

AT1)

Z-Value -5.013a -4.916a -1.000b

P-value 0.000 0.000 0.317



130

Table 64: FRIEDMAN’S TEST TO ASSESS RESPIRATORY RATE WITHIN


Parameters Mean

Rank

N Chi-

Square

Value

P-Value

Respiratory

rate –

BT

2.60

30

36.000

0.000 Respiratory

rate – AT

1.70

Respiratory

rate – AT

(1hr)

1.70


Respiratory rate within trial group

Parameters Respiratory

rate (BT-

AT)

Respiratory

rate (BT-

AT1)

Respiratory

rate (AT-

AT1)

Z-Value -4.243a -4.243a -0.000b

P-value 0.000 0.000 1.000



131

There was a statistically significant difference in respiratory rate before and after



respiratory rate between the BT and AT groups (Z = -4.243a, p=0.000), and between

the BT-AT1 group (Z=-4.243, p=0.000). There was a no change in respiratory rate

between the AT-AT1 group (Z=-0.000, p=1.000).

132

b. Between the groups:

Table 66: MANN WHITNEY –U TEST FOR BETWEEN THE GROUPS

ANALYSIS

DEPENDANT

VARIABLE

INDEPENDENT

VARIABLE

N MEAN

RANK

ASYMP.

SIG. (2

TAILED)

P-value

INFERENCE

Breathlessness

immediately after

nebulization

Parnayavani Arka 30 30

Theophylline 30 31

Total 60 -0.399 0.690**

Breathlessness one

hour after

nebulization


Theophylline 30 32

Total 60 -0.993 0.321**

Wheezing

immediately after

nebulization


Theophylline 30 31

Total 60 -0.463 0.643**

Wheezing one

hour after


133

nebulization

Theophylline 30 31

Total 60 -0.000 1.000**

Speech difficulty

immediately after

nebulization

Parnayavani 30 30.50

Theophylline 30 30.50

Total 60 -0.000 1.000**

Speech difficulty

one hour after

nebulization

Parnayavani Arka 30 31.5


Total 60 -0.493 0.624**

Cough

immediately after

nebulization

Parnayavnai Arka 30 30.5


Total 60 -0.000 1.000**

Cough 1 hour after

nebulization


Theophylline

nebulization

30 29.50

Total 60 -0.753 0.451**

Sputum Parnayavani arka 30 31.5

134

expectoration


Total 60 -0.853 0.393**

Sputum

expectoration 1

hour after

nebulization



Total 60 -0.753 0.451**

Tightness in the

chest immediately

after nebulization


30 31.00

Total 60 -0.331 0.741**

Tightness in the

chest 1 hour after

nebulization


Theophyllinel 30 30

Total 60 -0.296 0.767**

Pulse rate

immediately after

nebulization



Total 60 -0.853 0.393**

135

Pulse rate one hour

after nebulization



Total 60 -0.753 0.451**

Respiratory rate

immediately after

nebulization


Theophylline 30 31

Total 60 -0.587 0.557**

Respiratory rate

one hour after

nebulization



Total 60 -0.000 1.000**

On comparing breathlessness immediately after nebulization in the

Parnayavani Arka nebulization group and the Theophylline nebulization group, it was

found the two groups did not differ significantly, U(29) = 435.000, W(29) = 900.000,

Z = -0.399, p = 0.690.On comparing breathlessness one hour after nebulization in the



Z = -0.993, p = 0.321.

On comparing wheezing immediately after nebulization in the Parnayavani

Arka nebulization group and the Theophylline nebulization group, it was found the

two groups did not differ significantly, U(29) = 435.000, W(29) = 900.000, Z = -

136

0.463, p = 0.643. On comparing wheezing one hour after nebulization in the


found that there was no significant change between the groups. U(29) = 450.000,

W(29) = 915.000, Z = 0.000, p = 1.000.

On comparing speech difficulty immediately after nebulization in both groups,

no significant difference was found between the two groups. U(29) = 450.000, W(29)

= 915.000, Z = -0.000, p = 1.000. On comparing speech difficulty one hour after

nebulization in both groups, there was no significant difference between the groups.

U(29) = 450.000, W(29) = 915.000, Z = -0.0001, p = 1.000

On comparing cough immediately after nebulization in both groups, there no

significant difference between the groups. U(29) = 450.000, W(29) = 915.000, Z = -

0.0001, p = 1.000. On comparing cough one hour after nebulization in the



Z = -0.753, p = 0.451.

On comparing the sputum expectoration immediately after nebulization in the



Z = -0.853, p = 0.393. On comparing sputum expectoration one hour after

nebulization in the Parnayavani Arka nebulization group and the Theophylline

nebulization group, it was found the two groups did not differ significantly, U(29) =

420.000, W(29) = 885.000, Z = -0.753, p = 0.451.

On comparing the chest tightness immediately after nebulization in the



137

Z = -0.331, p = 0.741. On comparing the chest tightness one hour after nebulization in

the Parnayavani Arka nebulization group and the Theophylline nebulization group, it

was found the the two groups did not differ significantly, U(29) = 435.000, W(29) =

900.000, Z = -0.296, p = 0.767.

On comparing the pulse rate immediately after nebulization in the Parnayavani

Arka nebulization group and the Theophylline nebulization group, it was found the

two groups did not differ significantly, U(29) = 420.000, W(29) = 885.000, Z = -

0.853, p = 0.393. On comparing pulse rate one hour after nebulization in the



Z = -0.753, p = 0.451.

On comparing respiratory rate immediately after nebulization in the



Z = -0.587, p = 0.557. On comparing the respiratory rate one hour after nebulization

in the Parnayavani Arka nebulization group and the Theophylline nebulization group,

it was found the two groups did not differ significantly, U(29) = 450.000, W(29) =

915.000, Z = -0.000, p = 1.000.

138

OBJECTIVE PARAMETER: (PEFR)

a. Within the group :

Table No. 67: ANOVA WITH REPEATED MEASURES WITH A

GREENHOUSE-GEISSER CORRECTION IN PARNAYAVANI ARKA

NEBULIZATION GROUP

b.

c.

Table 68: TESTS OF WITHIN SUBJECTS EFFECTS OF PEFR FOR

PARNAYAVANI ARKA GROUP:

Source Correction df F-Value P-Value

Greenhouse-

Geisser

56.678 1.954 349.055 0.000

Parameters Mean

Difference

(I-J)

Standard

Error

Significancea I J

1 2

3

-85.000

-80.667

3.888

3.521

0.000

0.000

2 1

3

85.000

4.333

3.888

3.447

0.000

0.656

3 1

2

80.667

-4.333

3.521

3.447

0.000

0.656

a. Adjustment for multiple comparisons: Bonferroni

139

A RM-ANOVA with a Greenhouse-Geisser correction determined that mean PEFR

values differed statistically significantly between timepoints F (1.954, 56.678) =

349.055, p < 0.000). Post hoc tests using the Bonferroni correction revealed that

PEFR After Treatment was significantly increased as compared to PEFR Before

Treatment. (p=0.000). PEFR after 1 hr (AT1hr) was significantly increased as

compared to PEFR Before Treatment. (0.000). PEFR after 1hr (AT1hr) showed a non-

significant decrease in PEFR as compared to PEFR After Treatment. Hence, we can

conclude that the intervention elicits a statistically significant increase in PEFR, both

immediately after and 1 hour after nebulization.

b. Between the groups:

Table No. 69: INDEPENDENT SAMPLES T- TEST BETWEEN THE GROUPS

ANALYSIS OF PEFR IMMEDIATELY AFTER NEBULIZATION

Intervention N Mean Std. Deviation

Parnayavani Arka 30 199.67 13.514

Theophylline 30 196.67 14.70

F P T Df Std. Error

0.341 0.562 0.823 58 3.63571

Analysis of PEFR immediately after nebulization in the Parnayavani Arka group and

Theophylline nebulization group showed a non-significant difference.

140

Table 70: INDEPENDENT SAMPLES T- TEST BETWEEN THE GROUPS

ANALYSIS OF PEFR ONE HOUR AFTER NEBULIZATION

Intervention N Mean Std. Deviation

Parnayavani Arka 30 189.33 12.57

Theophylline 30 192.33 14.54

F P T Df Std. Error

1.079 0.303 -0.855 58 3.51079

Analysis of PEFR one hour after nebulization in the Parnayavani Arka group and

Theophylline nebulization group showed a non-significant difference.

141

DISCUSSION

REGARDING DRUG, DOSAGE FORM AND MODE OF ADMINSITRATION:

Microscopy and Macroscopy:

• The findings from the micro and macroscopic studies were corroborated by

similar findings from other studies, thus proving the authenticity of the drug

sample.

Preliminary phytochemical and physicochemical analysis:

• The results from study showed that the leaves of C. aromaticus possess

alkaloids, carbohydrates, phenols, resins, tannins and saponins.

• The drug is a proven source of many volatile principles. In the current study, it

was shown that the volatile oil content in the Arka sample was 0.21%.

GC-MS:

• Three volatile compounds were elicited from the current Arka sample.

• Among these, Dodecyl acrylate (C10H28O2) was found to possess structural

similarity to Thymol and Carvacrol (C10H14O2) as per the PubChem indexing

tool.

• Thymol and Carvacrol are the chief active principles in the drug C.

aromaticus.

142

ON DEMOGRAPHIC DATA:

1. Age:

A study revealed the prevalence of asthma has been found to be maximum in children

below the age of 5 and adults above the age of 70 years. (129) An ICMR report from

2009 states the prevalence of ever-asthma in adults over 15 years of age in India to be

2.4%, while a recent report suggests that it could be as high as 3.5%. (130) An

independent study found that elderly patients were more likely to suffer from asthma

due to psychological stress and perceived lack of social support systems. (131)

However, the observations in the present study do not correlate to previous works as

patients between the age group of 16-60 years were included. In the current study, it

was found that the age group between 40-60 years, and 20-30 years showed

maximum prevalence.

2. Marital status:

In the current study, 54 subjects were married and 6 were unmarried. It has been

found that there are more reported cases of asthma in India among

divorced/widowed/separated/deserted people as compared to married or unmarried

people. (131)

3. Occupation:

There are more than 400 substances that are currently known to induce asthma in the

workplace. (132) However, the occupations that show the highest prevalence of

asthma are region specific and cannot be generalized – they include factory workers,

drug manufacturers, farmers, grain handlers etc. In India, there are relatively few

studies that attempt to evaluate preventable occupation induced causes of asthma.

143

(133) A relatively recent study found that out of 62725 men and 52995 women

surveyed, the prevalence of ‘workplace induced’ asthma was 1.9%. Men who worked

as machine operators, or in the mining, construction, manufacturing or transport

categories were found to be most prone to developing asthma, while those in trade

and business were least prone. (131) The current study found that housewives and

agriculturalists were most prone to asthma.

4. Place(Urban/Rural):

Contrary opinions exist regarding prevalence of bronchial asthma in rural and urban

areas. In 2013, Agarwal reported that there was a higher prevalence of asthma in rural

adults and children as compared to industrialized countries. (131) The same article

also states that asthma was one among the leading causes of death in rural areas, with

rural North Eastern States and Tripura having the highest prevalence. Iverson 2005

suggests that rural dwellers have ‘fewer disabilities and long term limiting illnesses’,

and are also less drug-dependent. (134) Another meta-analysis study found that

globally there was minimal difference in the incidence of asthma between urban and

rural areas.(135) Urban factors that cause bronchial asthma include indoor air

pollutants, airborne microbes, air pollution, traffic, pollen, high temperatures and

humidity etc. Rural factors that directly or indirectly cause bronchial asthma include

biomass fuel combustion, airborne microbes, pest allergens, endotoxins, and a limited

access to health care (134, 135). In this study, it was found that there were a larger

number of subjects from urban areas (61.6%) as compared to rural areas. This might

be because many of the subjects who attended the study were from Hassan city.

5. Religion

144

Two independent studies – a cohort (Agarwal 2013) (131) and a meta-analysis

(Prakash, 2017) (136) found that Muslim men and women were more likely to report

cases of asthma as compared Hindus and other sects. The reason for this has been

proposed to be a difference in dietary habits – with Muslims tending to have a higher

proportion of non-vegetarian components in their food. (131) The relationship

between a non-vegetarian diet and asthma has been independently established. (137)

In the current study, there were 55 Hindu subjects, 3 Muslim subjects and 2 Christian

subjects. This is probably because Hassan has a greater Hindu population as

compared to other religions – over 50% of subjects who enrolled for the trial were

from Hassan city.

6. Economic status:

The current study found that the highest percentage (45%) of subjects belonged to a

lower middle class background. It has been found that in India, families with the

lowest wealth quintile had a higher asthma prevalence, as compared to wealthier

families (131) – with the highest prevalence in Eastern and North-Eastern states

(136). Lower economic status households have poorer nutrition, longer work hours

for manual labour and diminished access to health care, especially in rural areas.

7. Education:

The current study found that those over 50% of enrolled subjects had studied only

upto SSLC (10th Standard). (138) Various studies have shown that the prevalence of

asthma is inversely proportional to the number of years of schooling. (139) People

who are less educated tend to be more prone to developing asthma. This is possibly

because of a greater health awareness both at home and in the work place, in more

educated groups.

145

DISCUSSION ON PATIENT HISTORY:

1. Chief complaints:

The most common clinical presentations during an episode of asthma are

breathlessness, cough and wheezing most often during the night or early hours of the

morning with or without chest tightness. (140) The wheezing is attributed to dynamic

lung hyperinflation on exposure to a specific/non-specific trigger. It tends to be

polyphonic due to its origin from diverse lung airways. (141) The cough may be dry

or expectorant with small quantities of sticky sputum – whitish/greenish in colour.

(142) However, while minimal, or asymptomatic presentations have been known, they

are beyond the purview of the current study. The current study considered only cases

which presented with exacerbation of symptoms which include use of accessory

respiratory muscles, wheezing, breathlessness etc. It was found that maximum

patients reported wheezing during the night (60), chest tightness (50), Dyspnoea on

exertion (42) and cough (35). These are the main symptoms used to diagnose

bronchial asthma.

2. History of illness:

• Duration

In the current study, it was found that maximum patients reported onset less

than 5 years ago. However, 60% of the study population mentioned a duration

of onset between 10-20 years back. One study that compared 50 patients with

146

asthma of comparable severity found that childhood-onset asthmatics showed

significantly greater sensitivity to allergens, while adult-onset asthmatics

showed worse lung function despite a shorter duration of disease. (131)

• Mode of onset

While the exact mechanism underlying the development of an acute asthma

attack is unknown, there are two phenotypes which are commonly seen

clinically: (143)

a. Gradual onset – Associated with eosinophilic infiltration, gradual

attacks are seen over 48 hours, and show slower response to

treatment.

b. Sudden onset – Associated with significant exposure to allergens.

Such attacks tend to present in the late night or early morning, is

associated with neutrophilic inflammation, and shows a swifter

response to therapy.

The following study showed that 98% of the subjects showed sudden onset of

asthma.

• Trigger factors

The following trigger-induced phenotypes of asthma have been proposed:

(144)

a. Allergic asthma

147

Most asthma attacks are caused due to allergens. While onset is

usually in childhood, a number of adult asthmatics demonstrate this

phenotype as well. Common allergens include dust, pollen, animal

dander etc. The current study showed that 20% of the subjects cited

dust as a triggering factor for asthma. While study is ongoing to

better understand the inflammatory cascade in allergic asthma, it

has been found that IgE is an important mediator of inflammatory

reactions. Anti-IgE therapy has shown significant reduction in

exacerbations. This study found that

b. Occupational asthma

‘Work-aggravated asthma’ refers to asthma that is exacerbated by

work place conditions, while ‘occupational asthma’ refers to

asthma that was caused due to workplace exposure. The current

study found that the highest percentage of subjects were

agriculturalists, where exposure to dust, and natural allergens is

high. Subjects belonging to other occupations – such as drivers,

construction and building workers, coolie workers constituted 23%

of the sample population. All of these have high exposure to

occupational triggers such as dust, rubble, extreme temperatures

etc.

c. Others:

a. Aspirin induced asthma – not seen in the current study

148

b. Exercise induced asthma – not seen in the current study.

c. Menses related asthma – not seen in the current study.

3. History of past illnesses and treatment history:

• Hypertension:

In the following study, it was found that 46.7% of patients suffered from hypertension

and were under medication for the same. Commonly seen Hypertension medication

was Amlodipine (Ca Channel Blocker), Losartan and Olmesartan (ACE inhibitor),

Atenolol (B-Blocker), While asthma has been known to increase predisposition for

adult hypertension (145) , a history of diagnosed hypertension with medication is

significant when coming to the prescription of asthma medication. Beta blockers have

been known to induce bronchial obstruction and airway reactivity, even on topical

administration. (146) Angiotensin converting enzyme (ACE) inhibitors induce cough

and airway hyperresponsiveness in certain patients (147). However, Calcium channel

blockers have been shown to have a mildly relaxant effect on bronchial tone, and

small protective effect against allergens, and exercise induced broncho-

constriction.(148)

• Diabetes:

In the current study, 20% of the patients were diabetic and under medication for the

same. Microangiopathy of the lungs is seen as a chronic complication in patients of

both Type 1 and Type 2 diabetes. (149) One cohort that examined the risk of

pulmonary disease in patients of diabetes in 1,811,288 members found that

individuals with diabetes were at increased risk of asthma. (150) Few studies exist

149

that examine the relationship between Diabetes medication and asthma. However, it

has been proven that Metformin use in Diabetes patients was associated with

significantly reduced risk of asthma exacerbations and hospitalisations. (151)

4. Family History:

Genetic predisposition is a significant cause of asthma – and plays a major role in

asthma pathogenesis in over 50% of asthma cases. Five main asthma genes and gene

complexes have been identified that predispose for asthma – ADAM33, PHF11,

DPP10, GRPA AND SPINK5. (152) The complete functions of these genes are still

being investigated. Other genes such as IL13 that modify mucus production and

FCERI-B which modify the allergic trigger on mast cells and microbial pattern

recognition receptors of the innate immune system play a significant role in the

asthma pathogenesis. (153) In the current study,

5. Ahara:

Mixed diet was the most common Ahara taken in the current study (68%).

Previous studies have shown that a non-vegetarian diet increases the likelihood of

asthma in childhood and adults.(137) Mamsahara is Guru, Manda and Kapha

Prakopakara – thus playing an important role in the Samprapti of Tamaka Shwasa.

6. Rasa:

Madhura and Katu Rasa Ahara was the most preferred in this study. The

intake of Madhura Rasa results in Kapha Prakopa which is an important factor in the

150

Samprapti of Tamaka Shwasa. The intake of Katu Rasa Ahara may be have been

observed due to Kapha predominance in the body, and a natural desire for Vipareeta

Guna.

7. Nidra:

In the current study, 88% of subjects had disturbed sleep. Mid night nocturnal

dyspnoea is one of the cardinal features in asthma diagnosis. In asthmatic patients, in

the supine position, the alveoli become obstructed by secretions due to which

respiration becomes labored. Reflex cough and dyspnea are hence observed. (154)

Classically, Charaka has corroborated that disease aggravation is observed on lying

down - ‘Na chaapi labhate nidra shayane shwasa piditam’.

8. Habits:

Tea and Coffee:

Caffeine which is the main ingredient in both tea and coffee has been proven to be a

weak bronchodilator that also transiently reduces fatigue of the respiratory muscles.

(155) In the current study, 98.7% of the subjects were regular consumers of tea and

coffee. A meta-analysis on the effect of caffeine on asthma shows that even at low

doses (less than 5 mg/kg body weight) caffeine transiently improves lung function for

upto two hours. (156) Caffeine is also chemically related to Theophylline, a drug

commonly used in the treatment of asthma. (155, 156) However, it is not

recommended to undergo a lung function test for upto 4 hours after consumption of

caffeine as the results might be influenced by it. (155)

151

Smoking:

Smoking has severe detrimental effects on asthma – it has been known to accelerate

decline of lung function (157), and alter inflammatory mechanisms in asthma to

resemble those in COPD (158) . It is also associated with a poor response to inhaled

corticosteroids which are recommended as first line anti-inflammatory medication in

asthma. (159) In this study, it was found that 28.4% of the subjects were regular

smokers.

Alcohol:

The effect of alcohol on asthma has been contradictorily described by clinical and

experimental studies – with some claiming that alcohol is beneficial while others

claim that it worsens symptoms. (160) Some studies claim that the additives in

alcoholic beverages such as Sulfite cause bronchoconstriction, while pure ethanol by

itself is a broncho-relaxant. (161) Among alcoholic beverages, wine drinkers have

maximum alcohol sensitivity. (162) In the current study 3.3% were regular drinkers –

with the most common drinks being rum, whiskey and beer. 11.6% of the subjects

were regular drinkers and smokers.

152

DISCUSSION REGARDING RESULTS:

SUBJECTIVE PARAMETERS: (GINA)

Chest Tightness:

It has been widely believed that chest tightness is only one of the cardinal

symptoms of asthma. However, recent findings suggest that chest tightness

may be the only symptom that asthmatic patients experience. (163)

Inflammation of the airways and resultant bronchoconstriction is the cause of

chest tightness. (164) Inhaled Arka was found produce to produce a

significant decrease in chest tightness in both the groups in the current study.

There was no significant difference in chest tightness immediately after

nebulization and 1 hour after nebulization between the groups showing that

both drugs have equivalent efficacy. However, in the trial group, there was a

non-significant increase in chest tightness after one hour, showing that perhaps

the action of the drug at a dose of 5 ml does not last beyond a temporary

period. Further dose dependent clinical and experimental studies will need to

be carried out to establish this.

The proven tracheo-relaxant properties, and anti-inflammatory activity

of both the chief active constituents of Parnayavani – Thymol and Carvacrol –

might be responsible for this action. Also, previous studies have proven that

inhalation is the most superior method of drug administration in acute asthma

– both in terms of efficacy of drug delivery to the lung field as well as in terms

of desired action.

153

Breathlessness:

Breathlessness is one of the cardinal symptoms of Bronchial asthma. This also

takes place due to airway inflammation and resulting bronchoconstriction.

(165) Inhaled Arka was found produce to produce a significant decrease in

breathlessness – both at rest and on exertion, in the current study. There was

no significant difference in breathlessness immediately after nebulization and

1 hour after nebulization between the groups showing that both drugs have

equivalent efficacy.

However, there was a non-significant increase in breathlessness after

one hour in the trial group, showing that perhaps the action of the drug at a

dose of 5 ml does not last beyond a temporary period. Further dose dependent

clinical and experimental studies will need to be carried out to establish this.

The proven tracheo-relaxant properties, and anti-inflammatory activity of both

the chief active constituents of Parnayavani – Thymol and Carvacrol – might

be responsible for this action. Also, previous studies have proven that

inhalation is the most superior method of drug administration in acute asthma

– both in terms of efficacy of drug delivery to the lung field as well as in terms

of desired action

154

Wheezing:

Wheezing is such a common presentation in Bronchial Asthma, that the

symptom is often used synonymously with the disease by laymen. It is

attributed to dynamic lung hyperinflation on exposure to a specific/non-

specific trigger. It tends to be polyphonic due to its origin from diverse lung

airways. (166) The current study showed a significant decrease in wheezing in

both groups. 43 out of 60 subjects complained of wheezing, while 41 of the 43

had polyphonic wheeze. There was no significant difference in wheezing

immediately after nebulization and 1 hour after nebulization between the

groups showing that both drugs have equivalent efficacy.

However, there was a non-significant increase in wheezing after one

hour in the trial group, showing that perhaps the action of the drug at a dose of

5 ml does not last beyond a temporary period. Further dose dependent clinical

and experimental studies will need to be carried out to establish this. Thymol,

a major active principle in Arka has proven antispasmodic and anti-

inflammatory effects. It has been shown to decrease recruitment of

inflammatory cells and inflammatory mediators (such as IL-13, IL-5 and IL-4)

into the airways as well as reduce airway hyperresponsiveness, both of which

play an important role in the genesis of wheeze. Carvacrol is a phenolic

monoterpene that is known to be bronchial smooth muscle relaxant. It has also

been shown to selectively reduce the release of IL-4 (cytokine that is an

inflammatory mediator released by Th2 helper cells), while stimulating INF-

gamma (IL that naturally counteracts the action of inflammatory mediators,

produced by Th1 helper cells).

155

Cough

Generally in asthma, variable airflow obstruction leads to symptoms such as

cough and dyspnea. In the current study, 35 out of 60 patients complained of

cough associated with other symptoms. There was no significant difference in

cough immediately after nebulization and 1 hour after nebulization between

the groups showing that both drugs have equivalent efficacy. Cough in asthma

is typically dry or minimally productive, but may also be associated with

hyper-secretion of mucus. In such cases, cough is a respiratory defense

mechanism to expel the accumulated mucus. Many active constituents of the

Arka are antitussive (alpha-pinene, eugenol etc.) and spasmolytic (thymol,

carvacrol etc.). Hence, the drug was found to reduce cough and sputum

production in all asthma subjects.

Pulse rate

Transient hypoxia induced by bronchoconstriction in asthma is responsible for

tachycardia in asthma. (167) This is relieved on bronchodilation. In the current

study most subjects showed mild to moderate tachypnea that significantly

reduced after nebulization. The trial group showed a significant decrease in

pulse rate before and after treatment, that persisted till the one hour followup.

This demonstrates that bronchodilatory effects of the drug last for upto an

hour after drug administration. There was no significant difference in pulse

rate immediately after nebulization and 1 hour after nebulization between the

trial and control group showing that both drugs have equivalent efficacy at

both time points.

156

Sputum expectoration

The airway epithelium is normally covered by a mucus gel layer, that, under

pathological conditions such as asthma may show hypersecretion and

manifests as increased intracellular mucin, or increased mucus in the airway

lumen. (168) In case of excessive luminal mucus, cough clearance facilitates

ciliary clearance of the airways. In asthma, the distal airways become

impacted with mucus produced by surface epithelium, thus showing minimal

sputum expectoration. (169) In the current study, it was shown that there was a

significant decrease in mucous production post nebulization, possibly due to

the reduction in cough associated with bronchodilation.

There was a further non-significant decrease in sputum expectoration

after 1 hour. This might be because after nebulization, there is usually a

residual expectoration of exudate that increases in volume with rehydration.

This is expectorated immediately, or a few minutes after nebulization. This is

however absent an hour after nebulization. There was no significant difference

in sputum expectoration immediately after nebulization and 1 hour after

nebulization between the trial and control group showing that both drugs have

equivalent efficacy at both time points.

157

Speech difficulty

Speech difficulty as a result of hyperventilation is a common finding in

asthma. (142) It reduces with bronchodilation induced by medication. In the

current study, Post nebulization, there was a significant decrease in speech

difficulty in the trial group which remained unchanged uptil the one hour

follow up. This demonstrates that the therapeutic effects of the drug last for

upto an hour after drug administration. There was no significant difference in

respiratory rate immediately after nebulization and 1 hour after nebulization

between the trial and control group showing that both drugs have equivalent

efficacy at both time points.

Respiratory rate

Subjects of acute asthma generally tend to display tachypnea born of

hyperventilation due to bronchoconstriction. It has been shown in several

studies that in asthma, the average rate of respiration is between 20-25

cycles/min. (167) This was corroborated in the current study, with most

subjects displaying moderate tachypnea. Post nebulization, there was a

significant decrease in respiratory rate, which remained unchanged uptil the

one hour follow up. This demonstrates that bronchodilatory effects of the drug

last for upto an hour after drug administration. There was no significant

difference in respiratory rate immediately after nebulization and 1 hour after

nebulization between the trial and control group showing that both drugs have

158

equivalent efficacy. As mentioned previously, the main active ingredients of

this drug have proven antispasmodic and muscle relaxant properties.

Bronchoconstriction induced hyperventilation and tachypnea will

automatically be relieved on bronchodilation.

OBJECTIVE PARAMETERS:

PEFR:

Peak flowmetry is used to measure peak velocity of air streams in forced

expiration, and is intended to determine the condition of bronchial patency.

Asthma, being an obstructive type of disordered ventilation (because of

bronchoconstriction, compression of the trachea etc.), shows a markedly

increased load on the respiratory muscles. The ability of the respiratory

apparatus to perform additional functional load decreases. Hence, fast

expiration and rapid breathing become impossible. However, after

nebulization with Arka, which is known to have bronchodilatory and anti-

inflammatory properties, and also reduce airway hyperresponsiveness, the

PEFR significantly increased. In the current study, significant increase in the

PEFR in both groups was observed immediately after treatment.

However, in the trial group, there was a non-significant decrease in

PEFR after one hour, showing that perhaps the action of the drug at a dose of

5 ml does not last beyond a temporary period. Further dose dependent clinical

and experimental studies will need to be carried out to establish this.

159

There was no significant difference in PEFR immediately after nebulization

and 1 hour after nebulization between the groups showing that both drugs have

equivalent efficacy at both time points.

160

DISCUSSION REGARDING MODE OF ACTION OF PARNAYAVANI ARKA

NEBULIZATION :

As mentioned in the drug review section, two main volatile principles in

Parnayavani are Thymol and Carvacrol. Thymol is a naturally occurring monocyclic

phenolic compound derived from the herb Thymus vulgaris, which has widely

documented antioxidant, antispasmodic and anti-inflammatory effects. It has been

shown to decrease recruitment of inflammatory cells and inflammatory mediators

(such as IL-13, IL-5 an IL-4) into the airways as well as reduce airway

hyperresponsiveness, both of which play an important role in the pathogenesis of

bronchial asthma. Carvacrol is a phenolic monoterpene that is known to be a tracheal

smooth muscle relaxant. It has also been shown to selectively reduce the release of

IL-4 (cytokine that is an inflammatory mediator released by Th2 helper cells), while

stimulating release of INF-gamma (interleukin that naturally counteracts the action of

inflammatory mediators, produced by Th1 helper cells). A double blind clinical study

of Carvacrol in asthma patients was shown improve LFTs, and reduce subjective

parameters of asthma such as dyspnea and tightness of chest, and objective parameters

such as infiltration of inflammatory cells into airways.

Thus, when administering an aqueous distillate of the drug through

nebulization – which directly targets the airways and lung fields, instantaneous relief

is observed due to its anti-inflammatory and bronchodilatory action.

In Tamaka Shwasa, there is Avarana of Vata by Kapha. So in this condition,

Vata is in Moodavastha. Parnayavani Arka does Kapha Vilayana, due to its

Teekshna, Ushna and Laghu Gunas, which helps break Avarana of Kapha. As Vata

161

attains its Prakrutavastha, and resumes its normal course in the Pranavaha Srotas, the

patient obtains relief from Shwasa Kruchrata.

162

CONCLUSION

• Parnayavani Arka nebulization at a dose of 5ml was administered in 30 subjects

who presented in Vegavastha of Tamaka Shwasa w.s.r. to acute exacerbation of

bronchial asthma.

• Parnayavani Arka nebulization showed significant decrease in chest tightness,

breathlessness, wheezing, speech difficulty, cough, sputum production, pulse rate

and respiratory rate. (p=0.05), immediately after administration. It also showed a

significant decrease in PEFR (p=0.05) immediately after nebulization proving that

it increases lung expiratory flow.

• However, there was a non-significant increase in chest tightness, breathlessness,

wheezing and respiratory rate by the end of one hour indicating that the effect at a

dose of 5 ml on single time administration does not last for one hour. Further dose

dependent studies, and studies after repeated periodic administration will need to

be done to evaluate it’s long term efficacy.

• There was a non significant difference between the two groups in both subjective

and objective parameters, indicating that Parnayavani Arka has equivalent action

to Theophylline in acute exacerbation immediately after administration.

• The pharmacognostic study helped confirm the identity of Parnayavani. Three

volatile compounds were elicited from the Arka sample on GC-MS evaluation.

Among these, Dodecyl acrylate (C10H28O2) was found to possess structural

similarity to Thymol and Carvacrol (C10H14O2) as per the PubChem indexing tool.

Thymol and Carvacrol are the chief active principles in the drug C. aromaticus.

163

• Thus, the study concludes that Parnayavani arka nebulization at a dose of 5 ml

was effective in Vegavastha of Tamaka Shwasa w.s.r. to acute exacerbation of

bronchial asthma immediately after administration.

164

SUMMARY

Title:

A Clinical Study To Evaluate The Shwasahara Karma Of Parnayavani (Coleus

Aromaticus Benth.) Arka Nebulization In The Management Of Tamaka Shwasa with

specific reference to acute exacerbation of Bronchial Asthma

Introduction:

Global incidence of Tamaka Shwasa, Bronchial asthma is estimated to be around

334 million. In India, 15-20 million population are asthmatics. It is of utmost importance

to find ways to combat this disease. Parnayavani is a commonly used folklore remedy for

Tamaka Shwasa. With this perspective, the objective of the study was to assess the

Shwasahara Karma of Parnayavani Arka when administered through nebulization and

compare it with the Standard drug – Theophylline nebulization.

Review of Literature:

Drug Review:

The drug Parna Yavani (Coleus aromaticus Benth.) is a large succulent herb,

fleshy and highly aromatic, much branched, possessing short, soft erect hairs, with

distinctive smelling leaves. It is Teekshna, Ushna and Laghu in Guna, Katu Tikta in

Rasa, and is said to have Deepana, Pachana, Ruchya, Malasangraha Karmas. It is

indicated in disorders such as Agnimandya, Yakrudroga, Grahani, Udarraroga, Krimi,

Visoochika, Ashmari, and Mootrakricchra, Kasa and Shwasa.

165

Disease Review:

Tamaka Shwasa is defined as - ‘Visheshat Durdine Tamyeth Shwasa sa

Tamako Mataha’. Shwasa which occurs especially during Durdina is called Tamaka

Shwasa. Bronchial Asthma is an inflammatory airway disease with episodic occurrence

of dyspnoea with wheezing.

Materials and Methods:

The study was carried out in two parts:

a. Physico-Chemical Analysis:

b. Clinical study

Physico-Chemical analysis: The drug was subjected to physical evaluation, chemical

investigations, and the Arka was subjected to GC-MS evaluation.

Clinical study: For the clinical study, the subjects were divided randomly into two groups

comprising of 30 patients each.

Group No. Patients Drugs Dose

T (Stand. Group) 30 Theophylline respule nebulization 5 ml

PA (Trial Group) 30 Parnayavani Arka nebulization 5ml

The duration of the study was for a single hour, with analysis done before

nebulization, immediately after nebulization and one hour after nebulization.

166

Observations and Results:

With respect to subjective and objective parameters, (p=0.05), this study found

that Parnayavani Arka nebulization showed equivalent action to Theophylline

immediately after nebulization. However, there was no significant difference between

the groups (p=0.05).

Discussion and Conclusion:

Parnayavani Arka nebulization showed significant decrease in chest tightness,

breathlessness, wheezing, speech difficulty, cough, sputum production, pulse rate and

respiratory rate. (p=0.05), immediately after administration. It also showed a significant

decrease in PEFR (p=0.05) immediately after nebulization proving that it increases lung

expiratory flow.

However, there was a non-significant increase in chest tightness, breathlessness,

wheezing and respiratory rate by the end of one hour indicating that the effect at a dose of

5 ml on single time administration does not last for upto one hour. Further dose

dependent studies, and studies after repeated periodic administration will need to be done

to evaluate it’s long term efficacy.

There was a non significant difference between the two groups in both subjective

and objective parameters, indicating that Parnayavani Arka has equivalent action to

Theophylline in acute exacerbation immediately after administration.

This proves the Shwasahara Karma of Parnayavani Arka nebulization

immediately in acute exacerbation of bronchial asthma.

167

References:

A list of sources referred to in the completion of this work is given.

169

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186

CONSENT FORM 1.Title of synopsis:

A CLINICAL STUDY TO EVALUATE THE SHWASAHARA KARMA OF PARNAYAVANI (Coleus aromaticus Benth.) ARKA NEBULIZATION IN THE

MANAGEMENT OF TAMAKA SHWASA (BRONCHIAL ASTHMA) 2. Participant enrollment ID for this trial: ___________________________________

3. Name of the Investigating Physician (Research Scholar): Dr. Pushya A. Gautama

4. Name of the Guide: Dr. Harini A. M.D. (Ayu)

5. I confirm that I have read/the study has been explained to me adequately and I have

understood the information sheet for the above study and had the opportunity to ask

questions.

6. I hope to complete the study, but I understand that my participation is voluntary

and that I am free to withdraw at any time, without giving a reason, and without my

medical care or legal rights being affected.

7. I understand that my doctor will provide information about my progress, in

confidence, to the related authorities. I understand that the information held by the

Investigators and researchers and records maintained by the concerned authorities

might be used to follow up my health status.

8. I understand that the information will be used for medical research only and that I

will not be identified in any way in the analysis and reporting of the results. I

understand that sections of any of my medical notes may be looked at by the

authorities or responsible individuals from the members of the IEC, Regulatory

authorities or Court, if necessary. I give permission for these individuals to have

access to my records.

9. I understand what is involved in this trial and agree to take part in the clinical trial

for a period of 3 days.

Signature of the Subject:

Name of the Subject: Date:

Signature of the Witness:

Name of the Witness: Date:

Signature of the Research Scholar:

Name of the Research Scholar: Dr. Pushya A. Gautama Date:

Signature of the Guide:

Name of the Guide: Dr.Harini A. M.D. (Ayu) Date:

Scanned by CamScanner187

188

CLINICAL CASE PROFORMA:

Name: Serial No.

Age: yrs OPD No.

Marital status: M/UM/W/D Address

Place: U/R

Religion: H/M/Ch/Other Mob. No.

Occupation: Date of commencement:

Economic status: VP/P/L/M/U/R Date of completion

Education: L/SSC/PUC/UG/PG

MAIN COMPLAINTS:

Symptoms Duration

Dyspnoea on rest/ dyspnoea on exertion

Cough

Wheezing during the day

Wheezing during the night

Use of accessory muscles

Diffculty in speech

Confusion

Rhinitis

ASSOCIATED COMPLAINTS:

Symptoms Duration

Thirst

Fever

Anorexia

Vomitting

Fainting

189

Pain in the chest/flanks

HISTORY OF THE PRESENT ILLNESS:

HISTORY OF PAST ILLNESSES:

TREATMENT HISTORY:

FAMILY HISTORY:

Symptoms Age/Yrs Health Status

D/L

Disease Notes

Father

Mother

Brother

Sister

Son

Daughter

SOCIAL HISTORY:

OCCUPATIONAL HISTORY: Dust/Smoke/Smell/Extreme temperatures

Type of

work……………………………………………………………………………………

….Working hours………../Night

Shift………Resting day………….

Exercise: Minimum/Moderate/Heavy

PERSONAL HISTORY:

Agni: Sama/Tikshna/Vishama/Manda

Koshta: Mridu/Madhyama/Kroora

Aahara: Type: Veg/Non Veg/ Mixed

Matra: Alpa/ Madhyama/ Atipramana

190

Rasa preferred: Madhura/ Amla/ Lavana/ Katu/ Tikta/ Kashaya

Nidra: ……… Hrs. Disturbed/ Sound/ Excess

Mala: Formed/ Unformed/ Hard/ Smooth/ Regular/ Constipated

…….. Times/ Day

Mootra: Frequency: ………. /day

Regular/Increased/Incontinence/ Retention

Habit Duration Quantity

Tea

Coffee

Smoking

Alcohol

Tobacco

Snuff

Others

OBSTETRIC HISTORY:

No delivery/ Normal / Surgical intervention/ Abortion/ Last delivery

GYNAECOLOGICAL HISTORY:

Menstrual cycle: Regular/ Irregular

Menarche age:

Metrorrhagia/Dysmenorrhoea/Leucorrhoea

Menopause age:

ROGI PAREEKSHA:

Dashavidha Pareeksha;

• Prakriti

• Vikruti

• Sara

• Samhanana: P/M/A

• Vyayama shakti: P/M/A

• Vaya

• Pramana: Height……… cm. Weight …………….. kg

191

• Satva

• Abhyavaharana shakti: P/M/A

• Jarana shakti : P/M/A

• Desha: Jata J/A/S

Samvruddha: J/A/S

Vyadhita: J/A/S

Ashta sthana pareeksha:

• Nadi: Regular/Irregular/Full/Low volume/ V/P/K/VP/PK/VK

• Mala

• Mootra

• Jihva

• Shabda

• Sparsha

• Drik

• Akruti

GENERAL EXAMINATION:

• Pulse: /min. Regular/Irregular/Full/Weak

• BP: ………………… mm of Hg

• Temperature:

• Respiratory rate

• Build: Slender/ Muscular/ Obese

• Nourishment: Good/Poor

• Nails: Pink/Pallor/ Bluish

• Conjunctive: Pink/Pallor/Bluish

• Cyanosis: Extremities: Upper/Lower, Buccal mucosa, Lips, Conjunctiva

• Oedema: Foot/Ankle/Leg/Sacral region/ Hands/ Face/Pitting/ Non pitting

• Skin –

• Lymph nodes:

192

Pranavaha Sroto Pareeksha:

Inspection:

• Size and shape of the chest –

o Bilaterally symmetrical, elliptical, conical, long and flat, funnel chest,

barrel chest, kyphosis, scoliosis, local bulging

• Movement of the chest: Symmetrical, reduced in the right/left side,

Synchronicity of movement, Delayed movement in Left/Right

• Inspiratory retraction of interspaces – Exaggerated, Diminished to the

right/left.

• Movement of coastal margins during inspiration: Outward, Inward, Use of

accessory muscles

• Rate of respiration: ………./min

• Rhythm: Regular/Irregular/Periodic breathing/ Prolonged

inspiration/Prolonged both phase/Kussmauls respiration/ Ataxic breating/

Apnoetic breating/ Catch in breathing

• Type of respiration: Abodminal – thoracic, Thoraco – abdominal, Pursed lip

breathing, Shallow breathing

• Sternomastoid sign – Absent/Present

• Distended chest veins: Absent/Present

• Oedema: Unilateral/Bilateral

Palpation:

• Trachea: Slightly shifted to right/ Centrally located/ Shifted to the left

• Apex impulse

• Expansion of the chest – Unilateral/ Bilateral masses/ Sinus tract/ Tenderness/

Lymph node enlargement

• Tactile fremitus: Decreased/ Absent/ Normal in …….. lung

Percussion:

• Resonant/Hyperesonant/ Dull/ Stony dull

Auscultation:

• Breath sounds – Vesicular/Bronchovesicular/ Bronchial

193

• Adventitious sounds – rhonchi – High pitched/ low pitched/ Inspiratory,

Expiratory/ Short/ Long

• Crepitation – Early inspiratory/ Late inspiratory/ Mid inspiratory/ Expiratory

• Pleural rub site -

…………………………………………………………………………………

………

• Vocal resonance- Increased/ Decreased/ Absent/ Normal

INVESTIGATIONS:

Parameters BT AT

Hb gm%

TC

DC

Total Eosinophil count

ESR

Urine

CXR

Sputum/AFB

Spirometry

SEVERITY OF ILLNESS:

Parameters BT 1st day 2nd day 3rd day After 1

week

Attack per week

Duration of the

attack

Tightness in the

chest

Cough – Dry or

Expectorant

Dyspnoea on

rest

Dyspnoea on

exertion

Wheezing

194

Use of

accessory

muscles

Sputum colour

Sputum

quantity

Sputum

consistency

Pulse

BP

Temperature

Respiratory rate

Appetite

Digestion

Sleep

Weight /kg

PEAK FLOW METER TEST:

Parameters BT 1st day 2nd day 3rd day After 1

week

PEF

Gradings

RESULTS:

Signature of Scholar Signature of Guide Signature of HOD

195

GINA – SEVERITY OF ASTHMA EXACERBATION

Signs and Symptoms BT IMMEDIATELY AT 1 HOUR AT

1. Breathlessness 2. Wheeze 3. Talks in 4. Cough 5. Sputum 6. Chest Tightness 7. Pulse Rate 8. Respiratory Rate

1 – Mild asthma exacerbation 2 – Moderate asthma exacerbation 3 – Severe asthma exacerbation

SL No

ASSESSMENT CRITERIA 0 1 2 3

1 . Breathlessness Absent Mild-‐ while walking

Can lie down

While at rest-‐prefers sitting

While at rest-‐sits upright

2. Wheeze Absent Moderate -‐ often only at end expiration

Loud-‐throughout expiration

Usually loud-‐throughout inhalation & exhalation

3. Talks in Sentences Sentences Phrases Words

4. Cough Absent After exercise Continuous, disturb work

Continuous, disturbs normal

activity

5. Sputum Absent 1-‐3 times 4-‐5 times Continuously

6. Chest tightness Absent Mild Moderate Severe

7. Pulse/min <80 80-‐100 100-‐120 >120

8. Respiratory rate/min 18-‐23 24-‐30 31-‐40 >40


196


201


207


210


211


212

213

Figure1:Macroscopy of Coleus aromaticus

Fig 32. Macroscopy of Coleus aromaticus

Figure2: Microscopy of Coleus aromaticus

Fig 33. T.S of midrib

Pa→ Ph→

GT→

Xy→

VB→

Pal→

LE→

T→

SG→

UE↓

cavity; E

–

epidermis

; GT –

ground

tissue; Ph

–

phloem;

RC -

rosette

crystal;

VB –

vascular

bundle;

Xy –

xylem.

SP→

214

Fig 34. midrib portion enlarged

GT –glandular trochomes; LE – lower epidermis; Me – mesophyll;Pa – parenchyma; Pal –

palisade; Ph – phloem; SG-starch rains; SP – spongy parenchyma; UE – upperepidermis; VB –

vascular bundle; XY – xylem.

Fig 35. T.S of lamina

Pal→

↑Me↓

SP→

E→

T→

Pa→ Ph→

GT→

Xy→ VB→

Pal→

LE→

T→ UE↓

cavity; E

–

epidermis

; GT –

ground

tissue; Ph

–

phloem;

RC -

rosette

crystal;

VB –

vascular

bundle;

Xy –

xylem.

215

Fig 36.Lamina enlarged

E – epidermis; Col – collenchymas; LE – lower epidermis; Me – mesophyll;Pa – parenchyma;

Pal – palisade; Ph – phloem; ; SG-starch grains; SP – spongy parenchyma; . GT –glandular

trichomes; UE – upperepidermis; VB – vascular bundle; XY – xylem.

Pal→

↑Me↓

SP→

GT→

SG→

LE→

UE→

216

Fig 37. Upper midrib

Fig 38. Lower epidermis

GT –glandular trichomes; LE – lower epidermis;Pa – parenchyma; Ph – phloem; SG-starch

grains; SP – spongy parenchyma; UE – upperepidermis; VB – vascular bundle; XY – xylem.

Pa→

VB→

Ph→

UE↓

cavity;

E –

epider

mis;

GT –

groun

d

tissue;

Ph –

phloe

m; RC

-

rosette

crystal

; VB –

vascul

ar

bundle

; Xy –

xylem.

Xy→

LE→

T→

VB→

SG→

GT→

217

PROCESS OF ARKA PREPARATION

Fig. 39. Coleus aromaticus Benth. Fig. 40. Shredding the leaves

Fig. 41. Weighing the leaves

Fig.43. Soxhlet distillation

Fig.42. Soaking the leaves

Fig.44. Clear Arka obtained

I By Dr PUSHYA A GAUTAMA Dissertation submitted to Rajiv ...

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