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A COMPREHENSIVE STUDY OF ANATOMICAL LOCATION OF SHAKHAGATA VEDHYA SIRA STHANAS IN PARTICULAR DISEASES, By Dr. R. Annapurna, POST GRADUATE DEPARTMENT OF RACHANA SHAREER N.K.J. AYURVEDIC MEDICAL COLLEGE AND PG CENTRE, BIDAR
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“A COMPREHENSIVE STUDY OF ANATOMICAL LOCATION OF
SHAKHAGATA VEDHYA SIRA STHANAS IN PARTICULAR DISEASES”
By
Dr. R. Annapurna
A dissertation submitted to the
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In partial fulfillment of the requirements for the degree of
AYURVEDA VACHASPATHI - M.D (AYURVEDA)
In
RACHANA SHAREERA
POST GRADUATE DEPARTMENT OF RACHANA SHAREER N.K.J. AYURVEDIC MEDICAL COLLEGE AND PG CENTRE, BIDAR
2006
Co-Guide Dr. Chandrakant Halli
BAMS, MS (Shalya Tantra)
.
Guide Prof. Dr. S.B. Kotur
BAMS, MD (Rachana Shareera)
RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, KARNATAKA, BANGALORE
N.K.J. AYURVEDIC MEDICAL COLLEGE AND PG CENTRE, BIDAR
POST GRADUATE DEPARTMENT
OF RACHANA SHAREER
Certificate by the guide
This is to certify that the dissertation entitled “A Comprehensive
Study on Anatomical Location of Shakhagata Vedhya Sira Sthanas in particular
Diseases” is a bonafide literary research work done by Dr. R. Annapurna in
partial fulfillment of the requirement for the degree of Ayurveda Vachaspathi –
M.D (Ayurveda) in RACHANA SHAREER.
Date: Place: Bidar
Signature of the Guide Prof. Dr. S.B. Kotur
;BAMS, MD (Rachana Shareera) Professor Department of Rachana Shareera
NKJ Ayurvedic Medical College & PG Centre Bidar – 585403
Karnataka.
RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, KARNATAKA, BANGALORE
N.K.J. AYURVEDIC MEDICAL COLLEGE AND PG CENTRE, BIDAR
POST GRADUATE DEPARTMENT
OF RACHANA SHAREER
Endorsement by the HOD, Principal/Head of the institution
This is to certify that the dissertation entitled “A Comprehensive Study on
Anatomical Location of Shakhagata Vedhya Sira Sthanas in particular
Diseases” is a bonafide literary research work done by Dr.R. Annapurna under
the guidance of Prof. Dr. S. B. Kotur, M D (Rachana Shareer), Professor
Department of Post Graduate Studies in Rachana Shareer, N. K. Jabshetty
Ayurvedic College And Post Graduate Centre, Bidar.
Seal and signature of the Principal Prof. Dr. S. B. Kotur
BAMS, MD (Rachana Shareer), NKJ Ayurvedic Medical College & PG Centre
Bidar – 585403 Karnataka
Date: Place: Bidar
Seal and signature of the HOD Prof. Dr. N. G. Mulimani
B.Sc.;BAMS, MD (Rachna Shareer) NKJ Ayurvedic Medical College & PG Centre
Bidar – 585403 Karnataka
Date: Place: Bidar
RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, KARNATAKA, BANGALORE
N.K.J. AYURVEDIC MEDICAL COLLEGE AND PG CENTRE, BIDAR
POST GRADUATE DEPARTMENT
OF RACHANA SHAREER
Declaration by the candidate
I here by declare that this dissertation/ thesis entitled “A Comprehensive
Study on Anatomical Location of Shakhagata Vedhya Sira Sthanas in particular
Diseases” is a bonafide and genuine research work carried out by me under the
guidance of Prof. Dr. S.B. Kotur M.D (Rachana Shareer), Professor, PG
Department of Rachana Shareer.
Date: Place: Bidar
RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES,
KARNATAKA, BANGALORE
N.K.J. AYURVEDIC MEDICAL COLLEGE
AND PG CENTRE, BIDAR
POST GRADUATE DEPARTMENT OF
RACHANA SHAREER
Copyright
Declaration by the candidate
I here by declare that the Rajiv Gandhi University of Health Sciences,
Karnataka shall declare the rights to preserve, use and disseminate this dissertation/
thesis in print or electronic format for academic/ research purpose.
Signature of the candidate Dr. R. Annapurna
Date: Place: Bidar
Signature of the candidate Dr. R. Annapurna
ACKNOWLEDGEMENT
It gives great pleasure in extending my deep sense of gratitude and hearty thanks to my esteemed
Guide Dr. S. B. KOTUR, M. D. (Rachana Shareera.), Prof, Department of P. G. Studies in Rachana
Shareera for his guidance, motivation and encouragement throughout the academic carrier which made me
for the completion of this research work successfully.
I sincerely thank Prof. Dr. Chandrakantha Halli M. S. (Shalya Tantra) for a support and
guidance. I would like to express my profound gratitude towards Prof. Dr. N. G. Mulimani M. D.
(Rachana Shareera.), H.O.D., Dept. of Post Graduate Studies in Rachana Shareera for his timely guidance
help and constant support. I express my holy gratitude to the Chairman and Office bearer of management
committee of ‘CHIDAMBAR SHIKSHANA SAMSTHE’ for giving the opportunity to pressure my
post graduation at this institution.
I take this opportunity to thank all the Post Graduate teaching staff of the institution. And Dr.
T. D. Ksheerasagar, Prof. GAMC Bangalore for his valuable guidance.
I express my sincere, love and gratitude to my batch-mates Dr. Jambagi, Dr. Giritammannavar,
Dr. Gangavathi and Dr. Patil, for their moral support.
I am highly indebted to Dr. A. I. Akki, Dr. S. S. Gangoor, Dr. V. S. Choudhari, Dr. Girish. K. J.,
Dr. Yadahalli, Dr. V. S. Hiremath, Dr. Nagnoor, Dr. Trishaila for the able guidance and inspiration given
at various stages of my work.
I sincerely appreciate the assistance received from librarian and non-teaching staff of this
institution during the course of my study.
I remember with respect my Husband Dr. S. M. Kudari, Asst. Prof. B.V.V.S Ayurvedic College
Bagalkot, for his inspiration and encouragement. I sincerely thank my father Shri. R. VISHWANATH
GOUD, and my mother Smt. R. NIRMALA and mother-in-law, SMT. SUSHILA KUDARI and
FAMILY for their profound and unending love. I am grateful to my brother Mr. R. Prabhu, Mr. R.
Mahesh for their unconditional support. I express great love towards my son SUJAY who has inspired me
by his cuteness and naughty activities. Last but not least I thank Mr. Vidyanand, Mr. Sudhir and Mr.
Sampath, Padma’s Internet Café for their timely co-operation. I offer my sincere apologies to any omission
in the above list and appeal to consider them as fortuitous.
Date : Dr.R. ANNAPURNA Place : Bidar
LIST OF ABBREVIATIONS
Cha. Su. - Charaka Sutrasthana
Atharva - Atharvana Veda
Su. Sha - Sushruta Shareera
Su. Ni. - Sushruta Nidana
Su. Su. - Sushruta Sutrasthana
Su. Chi. - Sushruta Chikitsasthana
A. H. - Astanga Hridaya
A. S. - Astanga Sangraha
Bha. Pra. - Bhava Prakasha
Bhe. Sam. - Bhela Samhita
Note:- 1) Hindi Numbering for Shloka references
Arabic Numbering for Bibliography
2) Serial Numbers of Bibliograph is also a reference number of paragraph.
Abstract
ABSTRACT
Background and Objectives :
The science of Ayurveda is well recognized system of medicine has unique
technique for harmonious living. Ayurveda possess a glorious past with extraordinarily
enriched documentation of medicinal literature. The science has been given holistic status
through out the ages.
Knowledge of Rachana Shareera is mandatory for a student of any system of
medicine. It is a vital subject in pre-clinical studies. The terms used by our ancient
Acharyas in context of Rachana Shareera appears to be vague for a causal observer and
leads to a lot of confusion among the student and teachers, as the concepts of Ayurveda
Shareera evolved 3000 years ago. Because of generation gap concepts appear to be
misinterpreted or not fully passed on to future generation. So we are in cross roads
whether to accept the concepts as it is or not. At this junction it is our moral responsibility
to take up such studies to understand the concepts clearly and to pass on knowledge to
younger generation. So the study taken up here is “A COMPREHENSIVE STUDY ON
ANATOMICAL LOCATION OF SHAKHAGATA VEDHYA SIRA STHANAS IN
PARTICULAR DISEASES” with objectives –
To provide literary information of “SIRA SHAREERA” and “SIRA VYADHA
VIDHI SHAREERA”, And to interpret Shakhagata Siravyadhana Sthanas, with
their clinical applicability.
Material and Methods :
Sources of Data :
A. Authoritative Ayurveedic texts like Brihatrayee and Laghutrayee.
B. Other allied literature like Veda and commentaries of Brihatrayees.
C. Modern medical literature on Anatomy
D. Published latest information from journals
E. Materials from internet.
Methods :
Abstract
The present study is related to literary research. Classical texts, modern literature,
journals and internet information is collected, reviewed and critically analysed to fulfil
the objective of the study.
Raktamokshana :
Raktamokshana is one of the important parasurgical denoting letting of blood
outside the body. Different modalities of Raktamokshana are adopted according to Dosha
Avastha, Rakta Avastha and Atura Avastha. ‘Siravyadha’ is one of the type of
Raktamokshana by Shastravacharana. So as to explain its significance a stanza Su. Sha.
8/23 is sufficient.
Sushruta has given same importance of Dosha to Rakta also, where in many
places he has classified many diseases as Raktaja also. As there is specific line of
Shodhana Chikitsa in Vata, Pitta, Kapha, such as Basti, Virechana, Vamana, likewise
Siravyadha is often recommended as Shodhana Chikitsa. There is an universal rule that
always Prakupita Doshas are expelled from their neartest root, such as Basti in Vata,
Virechana in Pitta, Vamana in Kapha, in general Sameepastha Marga is selected for
Shodhana purpose. When we have reviewed Sushruta Shareera Sthana 8th Chapter, it is
surprising that selected sites are recommended for Siravyadha in particular diseases,
probably Adhisthana Sthanas of Vyadhi.
Of course, it appears surprising and vague, why Sushruta has mentioned
particular site for Siravyadha in different diseases.
Why can’t common site is selected in all diseases? is debatable. As Sushruta is
giving particular anatomical sites in individual diseases, there must be a relation between
disease condition and Siravydha particularly anatomical, physiological, and patho-
physiological. Here it is necessary to take-up such study where in we can trace out any
structural relation, patho-physiological relation between site and disease. So a
comprehensive study is done to locate particular Sira of Vydhana Sthana on the basis of
available literature of Dosha concepts, anatomical and pathological perspective. The
study is limited to upper and lower extremities.
Interpretation and Conclusion :
Abstract
So as to fulfill the objectives, a therough review of literature and analysis is done
on the basis of anatomical, physiological and pathological grounds. As Siravydha is
significant line of treatment where Sushruta has mentioned Siras of particular site in
particular disease. So a creative and logical approach has been done to locate Siras of
Siravydha Sthanas in particular disease with pathophysiological interpretation. By the
present study it can be concluded that Sira means vein, Siravydha is effective modality of
treatment, Siravyadha Sthanas in particular diseases cannot be discarded.
Key Words :
Sira, , Vein, Rachana Shareera, Raktamokshana, Siravyadha, Venesection,
Phlebotomy
CONTENTS Page No.
I. INTRODUCTION 1 - 2 II. OBJECTIVES 3
III. REVIEW OF LITERATURE
PART (A) - 1) Etymology of Sira 4 2) Sirashareera 5 - 11 3) Critics of the term Sira and Dhamani 12 - 14
4) Raktamokshana vidhi 15 - 16
5) Siravyadhavidhi 17 - 23
6) Roganusara Siravyadha Sthana 24 - 59
PART (B) - 1) Venous System 60 - 67
2) Physiology of veins 68 - 76
3) Microcirculation 77 - 83
4) Lymphatic System 84 - 87
5) Local Control of Blood flow 88 - 97
6) Regional Venous Systems 98 - 120
7) Blood Letting 121 - 128
IV. DISCUSSION 129 - 138 V. CONCLUSION 139 VI. SUMMARY 140
VII. REFERENCES I - VII
VIII. BIBLIOGRAPHY VIII - XXII
LIST OF TABLES
Page No.
Table No. 1 - Showing Doshanusara Sirasakhya 9
Table No. 2 - Showing Shakhagata Siras 9
Table No. 3 - Showing Koshtagata Siras 9
Table No. 4 - Showing Urdhvajatrugata Siras 10
Table No. 5 - Showing Classification of Siras According to Varna 14
Table No. 6 - Showing Analysis of Forces of Arterial End of Capillary 20 – 21
Table No. 7 - Showing Roganusara Siravyadha According to Sushruta
& Vagbhata
24
Table No. 8 - Showing Sites for Siravyadha of different Vyadhana
Sthanas of particular Diseases in Lower Limb
39
Table No. 9 - Showing Sites for Siravyadha of different Vyadhana
Sthanas of particular Diseases in Upper Limb
44
Table No. 10 - Showing Details of Kshipra Marma 46
Table No. 11 - Showing Details of Gulpha Marma 50
Table No. 12 - Showing Details of Indrabasti Marma 59
Table No. 13 - Showing Details of Janu Marma 82
Table No. 14 - Showing Classification of According to Varna 130
LIST OF FIGURES
Fig. 1 - Overall Anterior View of Principal Veins
Fig. 2 - Comparative Structure of Blood Vessels
Fig. 3 - Embryonic Development of Cardio-vascular System and
Blood Vessels
Fig 4 (a) - Diffusion of Fluid through Capillary Walls and
Interstitial Space
Fig 4 (b) - General Organization of Circulatory System
Fig 4 (c) - Functional Structure of Spleen
Fig 4 (d) - Capillary Walls
Fig 4 (e) - Blood Distribution
Fig 5 (a) - Lymphatic System
Fig 5 (b) - Relationship of Lymphatic Capillaries to Tissue Cells
and Blood Capillaries
Fig 5 (c) - Direction of Flow of Lymph and Blood
Fig 5 (d) - Lymphatic Capillary
Fig 6 (a) - Superficial Veins of Head and Neck
Fig 6 (b) - Veins of Thorax and Abdomen
Fig 7 (a) - Superficial Veins of Lowerlimb
Fig.7 (b) - Long Saphenous Vein
Fig 7 (c) - Superficial Veins of Hands
Fig 7 (d) - Superficial Veins of Upper Limb
Fig 7 (e) - Deep Veins of Upper Limb
Fig 8 - Sites for Siravyadha in Different Diseases in Lower
Limb
Fig 9 - Sites for Siravyadha in Different Diseases in Upper
Limb
Introduction
1
INTRODUCTION
Ayurveda is not only science of medicine but also the way of life style. It is
well organized system of medicine that has unique techniques for harmonious living.
It is not a stagnant one. It was developing through out its history. The science of
Ayurveda has glorious past with extra-ordinarily enriched documentation of medial
literature. That is nothing but experience and observations of ancients.
As Purusha is the conglomeration of soul, mind and body. These three hold
the life processes by maintaining structural and functional dynamism parallelly. In
real sense, Rachana Shareera is the media either to plan for treatment or to achieve the
ultimate aim of life. Hence the fundamental concept of Rachana Shareera has become
basic necessity for both physician and surgeons. That too specially in pre-clinical
studies.
Knowledge of Rachana Shareera is compulsory to students in pre-clinical
studies. Many of the terms appear to be vague for students and teachers leading to lot
of confusions. Because the concepts of Ayurveda Rachana Shareera were evolved
3000 years ago. Now we are lacking the opportunity to clarify the doubts because of
generation gap. Likewise many other concepts appear to be not properly passed onto
the future generation. No doubt Ayurveda is eternal but in present scientific
advancement, we adopt scientific way to popularize the text of Shareera Sthana, in
‘Brihatrayee’ and ‘Laghutrayee’ enlighten the anatomical perspectives in great way.
Still then we are on cross road in accepting the concepts as it is or not. The
two authorities of Ayurveda ‘Charaka’ and ‘Sushruta’ wrote their treatises based on
medicine and surgery. The Rachana Shareera given in Sushruta Samhita Shareera
Sthana is surgical anatomy and that of Charaka Samhita Shareera Sthana is more
metaphysical. Sushruta used the terms with their technical meaning and Charaka used
the terms with their literary usage.
An ancient work in the field of Rachana Shareera by Sushruta, Charaka are
scientific studies. Charaka contributed medicinal anatomy, where Sushruta
contributed surgical anatomy. When, ‘Sira Shareera’, ‘Siravyadha Vidhi Shareera’ of
Sushruta Shareera Sthana are reviewed. Siravyadha is chief line of treatment in
management of many diseases. But here the study is limited to only ‘Urdhwa’ and
Introduction
2
‘Adha’ Shakhas. Because Sushruta has quoted different Siravyadhana Sthanas in
different diseases. Then a question arises why Sushruta particularly mentioned that
particular Sthana in particular diseases? At this juncture, it has been thought that an
attempt should be made to locate Siras of Siravyadhana Sthanas on the basis of
anatomical, physiological and patho-physiological grounds. Because without proper
interpretation any concept cannot be discarded or accepted.
In present literature, there is gap of knowledge incomplete information
pertaining to Roganusara Siravyadha. To fulfill this gap present study in taken up to
substantiate exact anatomical location of Vedhya Siras in Vyadhana Sthanas of
Urdhwa and Adhah Shakhas in particular diseases conditions with special reference to
phlebotomy in venous system.
Objectives
3
OBJECTIVES OF THE STUDY
1. To provide comprehensive literary information about the concepts of “Sira
Shareera” and “Siravyadha Vidhi Shareera” in general.
2. Co-relative study on anatomical location of Urdhva-Adhah Shakhagata
Vedhya Siras pertaining to particular disease excluding pathological
consideration of diseases.
3. To introspect significance and clinical applicability of Vedhya Siras in clinical
practice based on the knowledge of modern anatomy.
Etymology of Sira
4
1. ETYMOLOGY OF SIRA
Sira Nirukti :
Grammatically Sira Shabda is made up of SZ + k + Tip` = (sri which means Raktavahini Nadi.1
According to Shabdartha Kausthubha, Sira means £ÀgÀ, ±ÀjÃgÀzÀ°ègÀĪÀ £Ár, zÉúÀzÉƼÀV£À £Ár2
Sira Paribhasha :
1. The blood vessels which possess Sarana Karma are called as Siras.1, 3
2. As per the Vedas, the Sira is defined as Hira channel that carries the impure
blood and Dhamani carries pure blood.2, 4.
3. The blood vessels which possess Sarana Karma and circulating throughout
body.5
4. By means of Sarana Karma blood vessels carrying Rasadis from one place to
another place.6
Blood vessels possessing Sarana Karma in Mrudugati are called as
Siras.7 Usually Sira is accepted as vein; in this present day era by transmitter
category of authors even though the term Sira is denoting different meanings
like artery, vessel and nerve. Concerned to this verdict few references we can
quote such as -
1 As per Sushruta and Vagbhata, depending on the nature Sira can be classified
as Sheeta, Shweta, Manda, Kapha.3, 8
2. In Karna 10 types of Siras are present. Three of which should be prevented
from injury.4, 9
3. As the branches of Padminikanda are spreading in Jala, likewise the Siras
from Nabhi are spreading in body in all directions.5, 10
4. Prakupita Vata getting Ashraya in Amsa Sandhi and causing Shoshana of
Sandhi Bandhana resulting into Amsa-shosha that existing Vata causes
Sankocha of Sthanika Siras giving rise to Avabahuka, that means Sira is
considered as ‘Kandara’ [Ligament]. 6,11
5. The circulating blood in Siras causes Dhatu Poorana, Kanti, etc. So may be
considered as Dhamani.7, 12
Sira Shareera
5
2. SIRA SHAREERA
Sira Utpatti :
1. Nabhi is the place of origin for the Siras and from these they are distributed in
all directions. All the Siras of the body are connected to Nabhi, and are
distributed as a network through out the body. The Pranas are located at the
site of Nabhi and are associated with it. The Siras are radiating from the Nabhi
like spokes from the centre of a wheel. 8, 13 2. Mula Siras (Root veins) are ten, located in the Hridaya, they transport the Rasa
and Ojas to the whole of body. On them, all the activities of the body depend.
They are large at their roots and very small at their tips and appear like the
lines of a leaf. Thus divided and become seven hundred in number.
[Nabhi has been said to be the origin point of Siras. In fetus it can be seen also
that number of veins are attached to Nabhi. After birth all the Siras attached to
Nabhi don’t function9, 14
3. Siras are important in Sandhis as well they transport the Dosha and Dhatus.
All these are attached to the Nabhi further they ramify to approach various
structures of the body.10, 15
Sira Swaroopa :
1. Vatavaha Siras are light red in colour, carrying Vata; Pittavaha Siras are warm
and blue in colour; Kaphavaha Siras are white and stable. Raktavaha Siras are
red in colour neither very hot nor very cold moderately warm.11, 16 [Note : The above statement is not pragmatic normally during health all the
veins appear blue in colour. Throughout the body since non-oxygenated blood
which is blue in colour is flowing through them. Veins might assume other
colours slightly when the blood vitiated by the Doshas are flowing in them. It
is very difficult to distinguish other colours unless observed closely by
experience.]
2. There are 700 Siras. As a garden or grain field is made wet by the water
carrying big and small channels, similarly the Siras by their contractility and
dilatory properly, supply nutrition to the body. They spread all over the body
just like small and minute laminas arising from the central core of the leaf.
Sira Shareera
6
They originate from the Nabhi and thereby spread all over the body upwards,
downwards and obliquely.12, 17
[Comments : Modern anatomists have never tried to count the exact number
of veins in human body, whereas Sushruta has given the precise number.
Sushruta includes given the precise number. Sushruta includes arteries and
veins both under one heading ‘Sira’. He has also accepted the theory of
‘Kedara-Kulya Nyaya’ postulated in Ayurveda, in reference to body nutrition.]
3. The veins which are bluish-red in colour, small, full and sometime empty
momentarily and having throbbing (pulsation) are carrying blood mixed with
Vata, those which are warm to touch, of quick moment, bluish-yellow in
colour are carrying blood mixed with Pitta; mixture of these signs indicate
mixture of Doshas. Those which are deep seated, evenly placed, smooth and
of slight red colour are carrying pure blood. 13, 18
4. These are two examples of Prananti and Kulya which are corresponding to the
Sthoola and Sukshma Siras respectively. 14,19
Sira Karya:
I. Vata, circulating in their Siras performs physical functions without any
obstruction, promotes the intellect to work proper and prevents the mental
deviations. 15, 20
[Comments : ‘Acharya Dalhana’ has explained the term ‘Kriyanam’ in the
following way – Ik|yiNi> kiyIk|yiNi> p|sirNik&öcni(dni> vik`
Ik|yiNi> BiIPti(dnim` .. This includes both voluntary action and
involuntary action. The word ‘Buddhi Karma’ is related with the five sense
organs and Manas. The intellect plays its role for taking decision in the normal
state. When there is hindrance in the normal functioning of these sense organs.
It is supposed that there is something wrong with the Buddhi or it has gone
under Moha. The Vatavaha Siras perform other actions along with functions
already described.]
A. Vatavaha Sirakarya :
1. ak&(pt vit (sri kiy< :
Vata, circulating in their Siras performs physical functions without any
obstruction, promotes the intellect to work proper and prevents the mental
deviations.16, 21
Sira Shareera
7
2. k&(pt vit (sri kiy< :
When aggravated Vayu occupies its own Siras, it causes various disorders of
Vata.17, 22
B. Pittavaha Sirakarya :
1. ak&Ipt Ip_i Isri kiy< :
Pitta, circulating in its own Siras, gives glow to the body, taste of food,
maintains the digestive power and increases the immunity against diseases. 18,
23
2. k&Ipt Ip_i Isri kiy< :
Pitta when aggravated, moves in its own Siras, produces various disorders of
Pitta. 19, 24
C. Kaphavaha Sirakarya :
1. ak&Ipt kfvhi Isri kiy< :
Kapha, circulating in its own Siras maintains the viscosity of various parts of
the body, stability to the joints, increases the strength and immunity and
performs its other normal functions. 20, 25
2. k&(pt kfvh (sri kiy< : .
When aggravated Kapha occupies its own Siras, various diseases caused by
Kapha appears. 21, 26
D. Raktavaha Sirakarya :
1. ak&Ipt r±tvh Isri kiy< : .
Rakta circulating in its own Siras, nourishes all Dhatus gives colour to the
body, receives tactile sensations and performs its other normal functions. 22, 27
2. k&Ipt r±tvh Isri kiy< : .
When aggravated blood circulates in its own Siras, various disorders of blood
occurs. 23, 28
Sira Sarvavahatvam :
Even though Vata, Pitta, Kapha and Rakta vaha Siras are described. It is also
further classified that there are no exclusive Vatavaha or Pittavaha or Kaphavaha or
Raktavaha Siras; where as all the Siras carry all of them. In abnormal conditions like
Sira Shareera
8
aggravation of vitiation and vitiation of Dosha, they may circulate in different
direction and different channel. 24, 29
Sira Sankhya :
Doshanusara :
Out of seven hundred Siras, there are forty principal Siras. Out of these 10
carry Vata, 10 carry Pitta, 10 carry Kapha and 10 carry Rakta. The Vata carrying
Siras, situated in the specific receptacle of that principal Vata, branch out in one
hundred and seventy five smaller branches (ramifications). Similarly Pitta carrying
Siras at the site of Pitta, Kapha carrying at the site of Kapha and the blood carrying at
the site of Yakrita and Pleeha are found branching in the same number. In this way
there are seven hundred Siras. 25,30
(I) Vatavaha Siras - 010
Pittavaha Siras - 010
Kaphavaha Siras - 010
Raktavaha Siras - 010
Moola Siras (Total) - 040
(II) Vatasthanagata Siras - 175
Pittasthanagata Siras - 175
Kaphasthanagata Siras - 175
Raktasthanagata Siras - 175
Total - 700
While commenting on this text, Ghanekar has said that the above description
regarding the classification of Siras on the basis of Doshas doesn’t maen that the
forty Siras orginate from Nabhi or Hridaya. By this Sushruta meant that Vatavaha
Siras are thos e which are found in Vata predominating areas, such as Pakvashaya,
Kati, Shroni, Sakti, Asthi, Sparshanendriya (skin). Similarly, Pittavaha and
Kaphavaha Siras are found in Pitta and Kapha predominating areas respectively. To
some extent the above comment seems to be correct, but Sushrutas’ description
regarding classification doesn’t tally with the description given in modern books.
Mula Siras :
Ten Mulasira which are connected to the heart, transport Ojas to all the major
and minor parts of the body. All the activities of the body are dependent on them.
They , dividing themselves to the size of two Angula, one Angula, half Angula, Yava,
half Yava and so on, just like ribs and veins of a leaf become seven hundred. 26,31
Sira Shareera
9
Vagbhatanusara :
TABLE NO. 1 SHOWING DOSHANUSARA SIRA SANKHYA
(I) Raktayukta Vayuvaha Siras - 175
Raktayukta Pittavaha Siras - 175
Raktayukta Kaphavaha Siras - 175
Raktayukta Shuddha Raktavaha Siras - 175
Total - 700 All Doshas with their normal state, they nourish the body, while on
other hand, if they vitiated cause trouble to the body. 27, 32
Anganusara : 28, 33
(I) Shakhagata Siras :
TABLE NO. 2 SHOWING SHAKHAGATA SIRAS
Vatavaha Siras - 25X4 = 100
Pittavaha Siras - 25X4 = 100
Kaphavaha Siras - 25X4 = 100
Raktavaha Siras - 25X4 = 100
Total = 400
(II) Koshtagata Siras :
TABLE NO. 3 SHOWING KOSHTAGATA SIRAS
Vatavaha Siras - 34
Pittavaha Siras - 34
Kaphavaha Siras - 34
Raktavaha Siras - 34
Total = 136
Guda, Shishna, Shroni - 08
Parshwa - 04
Prushta - 6
Udara - 6
Vankshna - 10
Total = 34
Sira Shareera
10
(III) Urdhvajatrugata Siras :
TABLE NO. 4 SHOWING URDHVA JATRUGATA SIRAS
(I) Koshtagata Siras Vatavaha Siras - 41 Pittavaha Siras - 41 Kaphavaha Siras - 41 Raktavaha Siras - 41 Total = 164(II) Karnagata - 04 (III) Jihwagata - 06 (IV) Netragata - 08 (V) Greeva - 14 Total = 41
According to Vagbhata,
Guda and Medhragata Siras – 32, Parshwagata Siras – 16, Prustagata Siras –
24, Udaragata Siras – 24, Chest – 40, Greevagata – 24, Hanugata – 16, Jihwagata–16.
Nasagata– 24, Netragata – 65, Karnagata – 16, Shiragata – 20. 34
Out of 700 Siras, four hundred are in the extremities, of which sixteen are not
to be cut, one hundred and thirty six are in the trunk, of which thirty two are not to be
cut, one hundred and sixty-four are at the top, of which fifty are not to be cut. 29, 35
According to Bhela,
It is from the heart that Rasa issues forth and from this (step onwards), the
latter goes to all the places. Heart is reached by the veins and therefore the veins are
said to be born of heart. [This is a clear conception of the heart-artery, vein-heart
cycle of circulation of blood in the body with heart as its centre]. 30, 36 Ten
Dhamanis are attached to the heart. These after going just four inches becomes
twenty (i.e. every one bifurcates). In this way these ten Dhamanis become sixty (i.e.
every one of these bifurcates once again). There in, these sixty Dhamanis become
three hundred thousand networks of Siras. [Such a counting seems to imply a mere
presumptive surmise and not an actual counting out. It is only at the first level that of
the ten arteries from the heart direct observation must have taken place; for many
Sira Shareera
11
authors agree to this number. To presume that the infinite number of arteries of the
body in hundreds of thousands develops by repetitive forkings from these few initials
of ten is too simplistic]. This is as follows – a tree surrounded by branches comes
down every where by the fruits and the large foliage (Palashas) or as when it gets
stretched or extended down if struck by stones, in a similar way this tree of ramifying
vessels gets extended by the (networks of) Siras (in the body of the person as these
spread out every where). In each and every pit of the hair, there is the exit aperture of
the Sira, from end of which trickles down the sweat. 31, 32, 37
Avedhya Siras :
Those veins which the physician should not puncture, deformity and death are
sure if these are punctured.
The wise physician should know that four hundred veins are present in the
Shakas, 136 in Koshta and 164 in Urdhvajatrugata. Among these 16 in extremities.
Koshtagata-32, Urdhvagata – 50, are to be considered as not suitable for puncturing.
33, 38
Shakhagata Avedhya Siras :
There are hundred Siras in one Sakti, among these one Sira is Jaladhara and 3
internal Siras known as 2 Urvis and one Lohitaksha. They are not fit for venesections.
This description is applicable to the opposite Sakti, in this way Siras in Shakhas are
sixteen. 34, 39
[Comments : Dr Bhaskar Govin Ghanekar has accepted great saphenous vein in
lower extremities and cephalic vein in upper extremity as Jaladhar. Femoral vein in
lower extremity have been considered as Urvi and Lohitaksha Sira. So for as cephalic
and basilar vein are concerned they are superficial structure; therefore, they are to be
protected. Femoral and brachial vein are deep seated structures and should not be
taken for venesection. Venesection is to be performed only where there are minute
veins present. Therefore, Sushruta’s version of contraindicated Siras is practicable.]
Critics of the term Sira-dhamani
12
3. CRITICS OF THE TERM SIRA-DHAMANI
Critics: 40
After the above collection from classics for an instance, it is necessary to
analyze the word Sira and Dhamani. As per the ancient classics and texts of present
day authors. (Atharva Veda 1/17/1)
As per this context the terms “Sira and Dhamani” are as old as Vedas. They
have been used loosely in common so that there is no specific meanings.
ni(D t& Fm(n: Isri .. (Amarakosha)
This statement stands on wrong basis unfortunately many commentators
followed it. At this junction, such confusions should however be avoided by better
information from Sanskrit scholars. Of course, in explaining certain words, no
specific meanings is denoted still then, Ayurvedists accept that Dhamani and Sira are
not synonymous.
It is important to note that the traditional meanings of Dhamani as artery and
Sira as vein were grasped by ancient lexicographers in Bengal and Maharastra. In
Bengal the anatomists of 19th century, a work “Maha Shareera Tattva” [over 60 years
old of unknown author] and other scholars described arteries as Dhamani and veins as
Siras in their Bengali work in anatomy. In old Bengali dictionary also [“Ashubodha
Abhidhan” over 30 years old] the same meanings have been give to the same words.
In Maharastra traditional knowledge can be found in Prof. V. S. Apte’s Sanskrit
dictionary, Madhava Chandeobha’s Marathi dictionary, V.G. Apte’s Shabda Ratnakar
– in all these works the word “Dhamani” has been interpreted as a ‘blow pipe’, pipe,
an artery [Sudha Raktavahini]. According to Yaksha, the ancient writer of Nirukti
[Vedic lexicon] the word Dhamani has been taken as synonym of speech. In
explaining the Vedic passages quoted by him. Dhamani has been interpreted as pipe
in which there is flow of fluids. Macdonall and Keith in their Vedic index understand
the word Dhamani as pipe. In Rigveda, the term Dhamani commonly implies a pipe
through, there is a flow of fluids. Both the terms Sira and Dhamani frequently seen in
Atharvan Veda. (Atharva Veda – 1/17/3, Atharva Veda – 7/35/2)
According to both stanzas the terms have been used clearly in differently
senses has both of them occur in the same passages. Ex: 100 Hiras (Siras), 1000
Dhamanis.
Critics of the term Sira-dhamani
13
The interpretations of above stanzas are elaborated clearly by Sayan.
yi[I±t: (A#iy: sÀbIFºy: am*: Eti: p&Ati[ dZÅymini: si[(hnviss:
si[(ht±t vA#i: edZSi[ yi (hri: (sri: rji[vhiniD`y: yIºtgµC(t eRyi(d .
(Sayan Bhashyam)
1. Dhamanis are channels connected to the heart.
2. Thick blood vessels are called as Dhamanis and thin are called as Siras.
3. It is a pity that more than this information is not available in Ayurvedic text.
Although the two terms are used by Charaka and Sushruta, Charaka says that
these are separate channels for the different substances for the system and the heart
and its Dhamanis are source of flow of Rasa. Sushruta speaks more clearly that Sira-
Dhamanis and Srotas all are the same and he established different on another. Because
of (1) distinct characteristic (2) different sources of origin (3) different functions (4)
their usage in Ayurvedic literature in different senses. He then adds usually they
appear similar owing to the close vicinity and similarity of function. The only
question to determined is what is ‘Sira’. Therefore, Charaka’s dictum “¹minit`
Fmºy: srNit` (sri: s|vNit` s|i[ti>(s ..” (Cha. Su.31/1).
It is more illuminating, it starts from root meanings of the terms. According to
Charaka, “¹mi” means to blow and commentators quote blowing or pumping of Rasa
by heart into Dhamanis.
The word “Srotas” is derived from “At\”means slow discharge of fluid. Ex:
capillaries, lymphatics. The word Sira is derived from “sZ” which means move
slowly therefore Sira means channels in which there slow movement. From these
point of view Dhamanis are arteries, Siras are veins and Srotases are lymphatics. In
many passages, Charaka and Sushruta unanimously quote about plenty of portions.
Sushruta uses the term Sira in various places to imply veins in whole of chapter on
“Sira Vyadhavidhi Adhyaya”. On the basis of this it denotes that the Sira is vein.
Judging thus from majority of instances occurring in various places of Charaka and
Sushruta the traditional meaning of Dhamanis appears to be channels from heart. And
of the term “Sira” may be veins. At the same time the term Dhamani has been imply
nerves in many passages of Sushruta Shareera Sthana 9th chapter.
Critics of the term Sira-dhamani
14
Generally speaking however it is thought Dhamani as artery, Sira as vein
commonly. So it is clear for learned people should over look deliberately to give a
clear statement.
Siravarna Vibhakti :
TABLE NO. 5 SHOWING CLASSIFICATION OF SIRAS ACCORDING TO VARNA
Siraprakara Sirakarya Tridosha Drushtya Vargikaraa
1 Rohinyaha Nourishing body by Upasnehana &
Anugrahana
Artery –
Pittavahi
2 Neela Nourishing body by Upasnehana &
Anugrahana
Veins –
Pittavahinya
3 Gourya Nourishing body by Upasnehana &
Anugrahana
Lymphatics –
Kaphavahinya
4 Aruna Akunchana Prasaranadi Karmas Autonomic Nerves –
Vatavahinya
Transmitter category of author Pandit Gangadhar Shastri shows classification
of Siras. For an instance, he makes the blood vessels identical with Pittavaha Sias and
divides them into two classes, which he calls by two specific terms “Rohini” and
“Neela”. He also includes lymphatics and autonomic nerves in the same table given
above. The Pittavaha Siras have been clearly shown as Raktavahinis. Sushruta divides
the Siras as Vatavahi, Pittavahi, Kaphavahi and Raktavahi.
Raktamokshana vidhi
15
4. RAKTAMOKSHANA VIDHI
Introduction :
Raktamokshana is being one of the Shodhana therapy as per Sushruta and
Vagbhata. Raktamokshana is nothing but letting of blood outside the body, where
alone is equal to all measures described in the treatment of diseases caused by
Raktadusti. Rakta is said to be the base for origin of the body. It is the backbone of
life. Pure blood is the back of the health, colour, pleasure and life span. 35, 41
Shareerasta Ahara Prasada Rasa is getting modification by Ranjaka Pitta
called Rakta. In brief regarding its significance is concerned. 42 Rakta is being
Pradhana Poshaka of body where Shareera existing by Rakta itself. So it is essential to
preserve Rakta. 36, 43
By the above quotations Rakta is very significant in maintaining physiological
well-being, where it’s vitiation causes serious illness. So in many places Sushruta
considers Rakta as also one of the Dosha. Likewise Vagbhata has also given same
preference to Rakta as Sushruta. So also Raktamokshana is considered as one of
Shodhana therapy according to Sushruta and Vagbhata.
Raktamokshana is two types 37, 44
(1) Shastravacharana
(2) Anushastravacharana
Any of the above modalities are adopted according to Dosha, Rakta and Atura
Avasthas.
In Vatadushti Shringavacharana is as Shringa of cow is Ushna, Madhura,
Snigdha which opponents of Sheeta, Rooksha. In Pittadushti Jaloukas are selected as
they are being in Jala. They are Sheeta and Madhura, opponents of Pitta. In
Kaphadusti Alabu is selected as it is having Katu Rasa, Rooksha, Teekshna Gunas.46
According to Rakta-Avastha, So that if it is Avaghada [superficial] then
Pracchanna, Jalouka, Alabu, Shringa etc. can be adopted. If there is Sarvadaihika
Raktadusti Siravyadha can be adopted. 47
Raktamokshana vidhi
16
Depending on Atura Bala also different modalities of Raktamokshana are
selected. So that in Raja, Bala, Vrudha, Sukumara, Nari Anushastravacharana can be
adopted in others. Shastravacharana can be adopted. 48
Out of all types of Raktamokshana as Siravyadha is taken up for study it is
highlighted in detail.
r±tmi[xN 38, 45
SAt\(vs\ivn an&SAt\(vs\ivn
SZ>g p\Cºn (sriÄyF jli]k
lib&
Siravyadha vidhi
17
5. SIRAVYADHA VIDHI
Siravyadha is done to let out the blood without producing any untoward
effects on the individual. The selection of the disease and site of the texts. As the Siras
are ot being in fixed place it needs skilled hand. In addiction to instruments, drugs and
other items should be kept handy. The selection of Yantra-Shastras can be made as
per wisdom of the surgeon according to site, disease and availability of instruments.
Therefore adoption of the development of science and technology on par with proper
utilitzation of advanced instruments is permitted and also necessary for the
implementation of theory and to prevent the complications. 54
Historical Background of Siravyadha :
1. Siravyadha is being one of the effective methods explained by Sushruta for the
letting of blood outside the body.49
2. In Shodhana therapy Raktamokshana has been explained as one of the type of
Panchakarma procedure, under which Siravyadha i.e. also considered as an
effective parasurgical procedure. 50
3. It was also practiced in Vedic period to alleviate the swelling. In Kaushika
Sutra of Atharvana Veda have references regarding Raktamokshana by
Shringana is case of Pravavata has been done under the guidance of Buddha.51
4. It is one of the Shalyatantra technique adopted by most of ancient Ayurvedic
scholars and practiced through ages such as [Vaidya Shatapatha Brahmana,
Oupadenava, Ourabhra, Poushkalavata, Karaveerya, Vaitaran, Bhoja,
Kritavirya, Gopura Rakshita, Bhaluki, Kapila, Goutami etc.]. Moreover
Charaka, Sushruta, Vagabhata and others have explained regarding
Raktamokshana. In period of 1200-600 A D extensive practice of parasurgical
procedures were practiced by Unani practioners and during 1300 A D in
Europe. There is evidence of Raktamokshana are available. During 1200 A. D.
Hakeems and Unani practioners were extensively practicing blood letting in
many skin diseases.King Jahangir was also having the habit of blood letting
once in an year. 52
5. During 18th century blood letting was done to whom it was understood that all
other side said treatments were help less and the blood letting was followed to
Siravyadha vidhi
18
maintain physiological well-being. Auto-haemotherapy is extremely used in
dermatology as it has a marked hyposensitizing effect and promotes the
immunologic reactivity. The blood taken from ulnar vein of the affected
person is injected into gluteal muscles E levi has treated many cases of
typhoid in adults of auto-haemotherapy in which 5-10 cc of blood was
removed from veins of arm and re-injected to subcutaneously at once into
lumbo-sacral region. The injections was being repeated twice or thrice on
every five days. The procedure is quite harmless and resulted in rapid fall in
temperature with improvement of general condition. 53
Poorvakarma :
1. Siravyadha Yogya – Ayogya Atura Vichara
2. Upakarana Siddhata
3. Atura Siddhata
1. Siravyadha Yogya-Ayogya Vichara :
a. Siravyadha Yogya: 39, 55
a. All Raktapradoshaja Vikaras h. Mukharoga
b. Especially Vagbhatokta Vikaras
such as Visarpa
i.
Netraroga
c. Vidhradhi j. Mada
d. Pleeha Vruddhi k. Trushna
e. Gulma l. Kushta
f. Agnimandya m. Raktapitta
g. Jwara n. Shrama
b. Siravyadha Ayogya Purusha: 40
a. Bala j. Garbhini
b. Vruddha k. Kasa
c. Ruksha Shareerayukta l. Shwasa
d. Ksheena m. Shosha
e. Parishramita n. Jwara
f. Madyapeeta o. Akshepa
g. Krusha p. Pakshagata
h. Panchakarma Neyojita q. Moorcha etc.
Siravyadha vidhi
19
i. Klaibya r.
Siravyadha Kala :
In Shubhadivas, when the environment is not too cold and not too hot41
,
especially Sheetakala is recommended for Siravyadha so that in Varsharutu when
there are no clouds, in Greeshmarutu when there is cold environment. In Hemanthrutu
Madhyahna Kala are recommended as Siravyadha Kalas.42, 56
(2) Upakarana Siddhata: 57
According to the situation of Siras, different instruments are used for
Siravydha.
(i). Kutarika : If Sira is just over bones this can be used. This is flat, and like
tooth of cow and edge is ½ Angula. It is hold in middle finger and thumb of
sight hand and by left hand Sira is to be fixed and cut.
(ii). Vrihimukha Shastra : If Siras are in Mamsala Sthana this Vrihimukha
Shastra is used for Siravyadha. It is useful in Udaragata Siravyadha. Its handle
is ½ Angula and its Vrithagrabhaga is hold between finger and used.
(iii). Trikurchika : This is used in Bala, Vriddha, Sukumara, Sthree. Other
materials like Karpasa, Pattika, Tourniquet, Pichu, artery forceps, scissors,
rubber tube, connection tube, Kachapatra, medicated oil like Jatyadi Taila,
Udumbar Choorna and according to the disease and Sthana of Siravyadha
different Anushastras are kept ready.
3. Atur Siddhata:
The patient is made Yogya to Siravyadha prior to the process. He is given
internally Snehasadhyas, externally Abhyanga and Sarvanga Swedana, after which
patient is fed with curd mixed diet, Yavagu, Jangala Mamsa Rasa to cause Utklesha in
Raktadhatu so that it comes out devoid of any hindrance. And in suitable position
according to Sthana of Siravyadha making Sira to become prominent by tourniquet.
43, 58
Pradhana Karma :
1. Siravyadhanarth Asana (Position of patients during Siravedha)
2. Roganusara Vedhya Sira Vichara
3. Observation during Siravydha
4. Observation of Dustaviddha Siras
Siravyadha vidhi
20
1. Siravyadhanartha Asana: 59
(i). Shiragata Siravyadha :
Patient is made to sit on stool facing towards sun knees flexed. And both
elbows should be placed at knee joints and fore hands towards neck. And is
tied. The Sira is made to become dominant. Patient is asked to hold air in
mouth for easy expulsion of blood this is done only in Bahirmukha Siras.
(ii). Padagata Siravyadha:
In Siravydha of legs patient should be in sitting position with one leg stretched
where Siravydha is going to be done and another slightly flexed. Leg is tied to
prevent vibrations and to make the Sira to become dominant at the time of
blood letting Gulfasthana should be gently massaged.
(iii). Hastagata Siravyadha :
Thumb is held inside the wrist and suitable position Hastagata Siravyaha is
done.
(2). Roganusara Siravyadha: 60
TABLE NO. 6 SHOWING SITE OF SIRAVYADHA ACCORDING TO SUSHRUTA AND VAGBHATA
S. N. Disease Sushruta Vedhya Sira Vagbhata Vedhya Sira
1. Padadaha Padaharsha Chippa Vatarakta Vicharchika Padadari Vatakantaka Avabahuka
2 Angula above from Kshipra Marma Except Avabahuka Visarpa, Vicharchika others’ are according to Sushruta
2. Kroshtuka Sheersha, Kanja Pangu
4 Angula above from Gulpha in Jangaha
Except Khanja Pangu others according to Sushruta
3. Grudhrasi 4 Angula above or below from Janu Sandhi
According to Sushruta
4. Moorta Vriddhi Behind Vrishana Sthita Sira - 5. Jalodara 4 Angula behind from Nabhi Vama
Parshwa -
6. Antravidhradhi Parshwashoola
Sira in between Vaksha and Sthana According to Sushruta
7. Bahushosha Avabahuka
Sira in between two Amsas -
8. Truteeyak Jwara Sira in between Trikasandhi According to Sushruta
9. Chaturtaka Jwara
Below Amsa-sandhi According to Sushruta
Siravyadha vidhi
21
10. Apasmara Below Hanusandhi Hanu or Bhroo Madhya Sira
11. Unmada Between Keshanta and Shankha or Urahapradesha or Lalata or Sira of
Apanga
Vraha Apanga and Lalata
12. Jeehwaroga Danta Roga
Sira below Jeehwa -
13. Mukharoga - Sira being in Jeehwa, Ostha, Hanu and Talu
14. Taluroga Talugata Sira - 15. Karnaroga Sira above Karna Karnaga Sira
Vyadhana 16. Nasaroga Nasagra Sira Acc. to Sushruta 17. Peenasa - In between Nasa and
Lalata 18. Timira
Akshipaka Shiraroga Adhimanta
Upanasika Sira Latata Sira
Apanga Sira
According to Sushruta
19. Jatroordhava Granthi
- Greeva Karna, Shiragata Sira
(3) Siravyadha Nireekshana: 61
As the aim of Siravyadha is to let out vitiated blood, just after Siravyadha
Doshita Rakta is only coming out as yellowish liquid comes out where
Kusumbha Pushpa is punctured.
Samyak Srava Lakshana :
Automatic stoppage of blood after certain time is on indication of “Samyak
Siravyadha” and it also indicates that complete vitiated blood is expelled out. Then
patient feels light, pain subsides, Rogalakshanas are decreased called “Samyak
Vriddha” Lakshanas.
Asamyak Srava Lakshana :
“Asamyak Sravita” Rakta will cause Daha, Raga, Pakadi Laxanas when
Siravyadha is done in hot conditions, Adhika Swedana, Atividdhata will cause
Atisrava Laxanas like Shirobhitapa, Adhimanta, Timira, Dhatukshaya, Akshepaka,
Pakshaghata, Yekangaroga, Hikka, Shwasa, Kasa, Pandu and lastly Marana. When
position of the patient is not proper when Sira is not prominent of Shastra is not sharp.
If Swedana is not given properly, just after meals Mada, Moorcha, Shrama. In these
conditions, even though after Samyak Siravyadha also Samyak Rakta Srava is not
taking place.
(i) Upachara :
Siravyadha vidhi
22
If there is Aparavrutta Raktasrava any three of, Karpura, Tagara, Devadaru,
Vidanga, Chitraka, Trikatu, Haridra, Karanja, taken and powdered. Mixing it with
Saindhava Lavana and Tila Taila Vrinamukha is gently massaged to provide Samyak
Pravruttata of Rakta. If there is Atirakta Srava, so as to prevent it different measures
can be taken.
1. Lodhra Yasti, Priyangu, Sarjarasa, Gairika, Rasanjana, Shalmali Pushpa
Choorna of these drugs, is applied over Vranamukha of Siravyadha.
2. Arimeda, Medrasingi, Sala, Sarjarasa Twak Choorna is mixed with Madhu
and applied.
3. Sheetal Bhojana, Sheetal Avachoornana.
4. Kshara-Agni Dahana.
(ii). Raktasrava Niyama: 44, 62
In persons who are strong, who have great accumulation of Doshas and who
are of suitable age, experts desire, one Prastha (640 ml) of blood be allowed to flow
out after venous puncture.
At once completely whole vitiated blood should not be letted out, for
remaining Dosha Shamana Chikitsa may be followed according to Rogabala,
Rogibala the fixed quantity of blood is letted. Uttama – 1 Prastha, Madhyama – ½
Prastha, Vagbhata says that 1 Kudava or 3 Pala or 13 Tola may also be letted out to
prevent the complications.
(4). Dusthaviddha Sira Nirikshana: 45, 63
Dusta Vedhya Laxanas are 20. These are Siravyadha Vyapats. (a) Durviddha
(b). Atividdha (c). Kunchita (d). Picchita (e) Kuttita (f) Aprasoota (g) Atyudeerna (i)
Atividdha (j) Parishuska (k) Kunita (l) Vepita (m) Anushita Viddha (n) Shastrahata
(o) Teeryakviddha (p) Apaviddha (q) Ayadha (r) Vidhruta (s) Dhenuka (t) Punah-
Punah Vidha (u) Sirasnayvasthi Viddha.
Paschat Karma: 64
1. Upadrava Chikitsa
2. Pariharya Vishaya
3. Shamanoushadhi Chikitsa
1. Upadrava Chikitsa : During Siravyadha if any Asrava, Alpasrava or Atisrava
they should be treated.
Siravyadha vidhi
23
2. Pariharya Vishaya : Here Agnirakshaka Vishesha Pathya Yojana is followed
such as Natisheetoshna Bhojana, Rakta Vardhaka Annapana should be taken
Vata Prakopaka activities should be promoted.
3. Shamanoushadha Chikitsa : Afte Rakta Mokshana Vishesha Shamanoushadha
Chikitsa is followed .
a. After this – (1) Weekly once for 3-4 times blood letting may be done
(2) If in first sitting not letted then after 15 days once again blood
letting is followed.
Pradhanyata of Siravyadha :
1. As Basti has been mentioned as dominant line of treatment in Kayachikitsa,
likewise Siravyadha has been mentioned as dominant parasurgical procedure
in Shalya Tantra for the letting of blood outside the body. So it is considered
as 50 % of Shalyachikitsa. As Rogadhisthana primarily being Rakta so
Raktamokshana by Siravyadha has got its own importance in curing the
disease. 46, 65
2. Vagbhata also mentioned that Siravyadha is complete treatment in
Shalyatantra as Basti is the complete treatment in Kayachikitsa. As Rakta
Dhatu is the main causative factor in all Vikaras or disease. So it is to be
treated first by Siravyadha Vidhi. 47, 66
3. Raktamokshana by Siravyadha will be helpful to maintain good health by
causing Vrana, Prasannata, Indriya Prasannata, Agnideepti, proper Vega
Pravruthatha, Pusthi, Tushti etc. 48, 67
4. Siravyadha is the supreme procedure amongst all Shodhana therapies. When
Snehadi, Lepanadi treatments have been failed Siravyadha will be followed. 49,
68
5. Diseases of the skin, tumours, oedema and diseases arising from blood will
never occur in persons indulging in blood letting. 50, 69
6. In Rakta Pradoshaja Vikaras Siravyadha is supreme procedure which gives
complete permanent cure rather than other types of Mokshana and other
Shodhana therapies like Vamana-Virechana etc.70
Roganusar Siravyadha Sthana
24
6. ROGANUSARA SIRAVYADHA STHANA
(I). ADHASHAKHAGATA VEDHYA SIRA STHANAS : [Fig. 8]
In diseases such as Padadaha, Padaharsha (tenderness / tingling in the soles),
Chippa (whitlow), Visarpa (erysipelas), Vatashonita (gout), Vatakantaka (sprain of
the ankle), Vicharchika (a skin disease) and Padadari (fissures of soles) etc., the vein
situated two Angula (4 cm) above the Kshipra Marma should be punctured using
Vrihimukha Shastra. 51, 71
As per the quotation Siravyadha is done in the said diseases 2 Angula above
from Kshipra Marma. The anatomical location of vein that part is interpreted on
available anatomical grounds.
Usually Marma Sthanas are contraindicated for Siravyadha. Regarding
“KSHIPRA” 72 Marma is concerned gives a meaning of quick due to its immediate
effect.
TABLE NO. 7 SHOWING DETAILS OF KSHIPRA MARMA
Measure & Type - 2 in number, Snayu, ½ Anguli
Site - In between the big toe and the first toe. Controls
Rasavaha, Pranavaha, Avalambaka and heart.
Tissues involved
(Anatomical
structures)
- Abductor hallucis brevis, lumbricalis muscles, posterior
tibial nerve, dorsal metatarsal artery, plantar arch and
medial plantar artery, metatarso-phalangeal joint.
Signs if injured - Injury may cause impairment of the function of the
abduction and flexion of the great toe. Damage to the
artery may cause severe bleeding, haematoma, inside the
plantar aponeurosis and septic toxaemia. It is Kalantara
Pranahara type Marma
As the site of Vyadhana is two Angula above from the Kshipra Marma that is
usually the branch of great saphenous vein. Where it is the longest vein in the body,
ascend from foot to the groin in the subcutaneous layer. It begin medial end of the
dorsal venous arches of the foot. The dorsal venous arches are network of veins on the
dorsum of the foot formed by dorsal digital veins draining blood from toes and unite
in pairs to form the dorsal metatarsal veins. As dorsal metatarsal veins approach a foot
Roganusar Siravyadha Sthana
25
they combines to form dorsal venous arch. 73 So as per the above context in all said
diseases Siravyadha is done in dorsal venous arch. The dorsal venous arch above two
Angula of Kshipra Marma is the choice sites for venu-puncture. 74
PADADAHA :
Vayu combined with Pitta and Rakta causes burning sensation in fact
particularly while walking. It is know as ‘Padadaha’. The pain is pronounced while
walking and it is mild when standing. 52, 75
The condition ‘Padadaha’ can be correlated to in one or other way to the
thiamine, pantathenic acid deficiency called burning feet syndrome. Usually thiamine
aspartes in metabolic systems of the body, principally as thiamine pyrophosphate.
Thiamine deficiency causes decreased utilization of pyruvic acid and some
aminoacids by the tissues. But increases the utilization of fats, producing 3 target
tissues : (a). peripheral nerves (b). heart and (c). brain. Decreased utilization of these
nutrients is the responsible factors for many debilities associated with thiamine
deficiency. Pantothanic acid widely distributed in fruits, therefore, existence of
clinical deficiency in human is doubtful. Claims have been made as “burning feet
syndrome”. It is characterized by pain in the feet, burning in character. The symptoms
are worst on walking and night. Previously it was thought to be beri-beri.76 Thiamine
deficiency can also cause degeneration of myelin sheath of nerve fibres both in
peripheral and central nervous system. It can be treated by riboflavin and calcium
pantothenate.
Critics:
As the condition shows involvement of Rakta and Pitta Doshas in the
causation of disease, Raktamokshana by Siravyadha is recommended in Pada itself.
Two Angula above from Kshipra Marma. In Pada that is the site where we get easily
available superficial vein. As Adhisthana is being Pada in ‘Padadaha’, this is the site
of Siravyadha in Padadaha. When pathophysiology of Padadaha is concerned it is
nothing but “burning feet syndrome of thiamine deficiency”, which leads to
incomplete metabolism of carbohydrate resulting accumulation of pyruvic acid, which
is a reason for burning sensation of feet. One of the most fundamental principles of
circulatory function is the aility of each tissue to control its own blood flow in
proportion to its metabolic needs. As the need for blood flow changes, the blood flow
also changes. Some specific needs of the tissue for blood flow are delivery of o2,
nutrients such as protein, glucose, carbohydrate, amino acids, fatty acids, etc. removal
Roganusar Siravyadha Sthana
26
of metabolites, transport of hormones. In general, greater the metabolism greater the
blood flow.
So here, by doing blood letting by Siravyadha, in the site which is nothing but
dorsal venous arch, venous pressure can be relieved, fresh blood is rushed towards the
part. So metabolic activity of the part is increased concurrently accumulated excessive
pyruvic acid is drained by which local homeostatis is maintained. So in Padadaha in
the site two Angula above from Kshipra Marma that is dorsal venous arch which is
superficial and easily accessible. On the basis of these backgrounds the site told by
Sushruta and Vagbhata in Padadaha cannot be discarded.77
PADAHARSHA :
Accoring to Sushruta, Padadaha is nothing but the legs have tingling sensation
(feeling of pain and needle) and gradually numbness occurs. This disease is known as
“Padaharsha” and is caused by aggravation of Kapha and Vata together.53, 78
Padaharsha can be correlated to that of “tingling and numbness”. Common
types of parasthesia, commonly seen in neuropathies due to various causes. Presently
the condition is correlated to peripheral neuropathy due to type-II NIDDM. Here
plasma glucose remains normal, insulin levels are elevated. Insulin resistance tends to
worsen despite of elevated insulin concentrations. At last insulin resistance did not
change, but insulin secretion declines resulting into fasting hyperglycemia. Glucose
uptake and glycosis are impaired. So gradually degenerative changes of nerves,
characteristically symmetrical as tingling, pricking, burning and numbness.
Critics :
Because of the aggravation of Vata and Kapha, Padaharsha is manifested so
that peripheral parts of the lower limbs have got tingling and numbness. It has been
pointed out that by means of Sthanika Siravyadha, Doshas are neutralized and
features relieved. So, Siravyadha is done two Angula above from Kshipra Marma, as
Rogadhisthana is Pada and that site often recommended because of superficially
available veins.
When the concept is correlated to modern science, is a type of parasthesia
commonly seen in neuropathy of various causes. Presently the condition is taken up
as neuropathy due to Type-II NIDDM. Here because of insulin resistance of cells,
fasting hyperglycemia is resulted when glucose uptake and glycolysis are impaired
there is gradually generative changes of nerves, characterized by tingling and
numbness. Glycolysis means splitting of pyruvic acid by different chemical reaction.
Roganusar Siravyadha Sthana
27
This end product is oxidized to release energy. By means of blood letting by
phlebotomy, there is increase in insulin sensitivity in individuals with type-II diabetes.
That results in proper glucose uptake and glycolysis which can prevent degeneration
of nerves by the release of energy.
Overall, by phlebotomy the local cellular metabolism is improved, blood flow
improved, providing required nutrients to the nerves. So in “Padaharsha” or
“neuropathy” , venesection is done in dorsal venous arch. On the basis of this patho-
physiological ground, the site of Siravyadha dealt by Sushruta may be accepted. 79,80
CHIPPA :
Dushita Pitta and Vata is getting Ashraya in “Nakha-Mamsa” resulting into
pain, burning and ripening so called Chippa. 54
Vitiated Vata and Pitta is situating in ‘Nakha-Mamsa’ Pradesha and causes the
Vruna of Nakha Mamsa. It is called as ‘Akshat Roga’. 55, 81
This is correlated with Paronychia This is the most common infectioin of nail
bud of fingers. Sings include redness, tenderness, lymphangitis, lymphadenopathy etc.
After the inflammatory phase, pus is trapped besidest the nail. Sometime it may
become chronic where pus is trapped between fibrous septae, which binds skin to the
underlying bone can get into infection. 82
Critics :
There is involvement of Pitta and Vata getting Ashraya in ‘Nakha-mamsa’
resulting Vruna Shotha Laxanas. Such as pain, burning, ripening. Adhisthana being
‘Nakha’, Siravyadha is done 2 Angula above from ‘Kshipra Marma’, which can help
to resolve Vrunashotha Laxanas. When modern correlation is done, is nothing, but
‘nail bud infection’ of fingers. Blood letting by Siravyadha, venous drainage of part is
increased associated with rush of blood supply where endothelial cells are sensitive to
alteration in blood flow. They undergo certain changes facilitating migration of
lymphocytes through vessel wall subsiding local infection, inflammation, providing
improvement in metabolism of cells.
So here also the same branches of dorsal vein arch is selected for phlebotomy.
VISARPA :
By means of Mithya-ahara-vihara like Adhika Lavana-Amla-Katu-Ushna-
Vidahi and Adhika Madya Sevana, Adhyashana (Divaswapna) Vatadi Doshas get
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28
increased they will enter in the Twacha, Mamsa and Rakta. Vitiation will not persists
in one place but it is spreading in nature. According to Dosha dominancy Shotha is
seen called ‘Visarpa’. 56, 83
Dosha-Dushya Sambandha: 57, 84
Dosha Vata, Pitta, Kapha.
Dushya Rakta, Lasika , Twacha and Mamsa.
All the Doshas are responsible and Twak, Mamsa, Lasika and Rakta are
involved. According to Sushruta it is of 4 types – Vataja, Pittaja, Kshataja and
Kaphaja and Tridoshaja. But the common features can be Vedana, Jwara. Shotha
depending on Doshik, involvement of the features are different. Individual Doshaja
are Sadhya and Tridoshaja, Kshataja Asadhya. 85
The features of Visarpa are correlated with cellulitis, erysipelas and herpes
zoster.
Erysipelas: 86
It is spreading lymphangitis, where the causative organism is streptococcus
pyogenes. Poor hygienic living, recurrent URI, chronic illness are the predisposing
causes. But the lesions starts as a scratch, it commences as a rose pink rash which
extends to the skin, vesicles appear sooner or later over the rash and rupture. A serous
discharge comes out from these vesicles. To distinguish between erysipelas and
cellulitis is that, erysipelas as a typical rosy-red rash, on pressure it feels stiff, the
vesicles of erysipelas contain serum. The common sites are face, upper and lower
extremities.
It is a form of cellulitis characterized by bright red appearance of involved
skin. The region is warm, tender, swollen, shiny. It is almost always due to beta-
hemolytic streptoccus. They tend to develop lymphangitis where lymphatic drainage
is disrupted, commonly affect in lower extremity.
Herpes zoster:
Varicella zoster is a virus causing herpes zoster. It usually develops in more
than 40 years, approximately 5 % of patients experience recurrence. The condition
begins as an infection accompanied by fever, malaise, and anorexia, maculo-papular
rashes, usually on upper trunk and face. It is recurrent painful, vascular eruption
cuased by reactivation of chickenpox. It is self limited disease in young and healthy
persons, but cool compressors, anti histamines, analgesics are sufficient. On
Roganusar Siravyadha Sthana
29
reactivation of the virus produced by ganglia to the sensory nerve and peripheral
nerves. Always it presents as a dermatological vascular rash with pain. Trasmission
likely to take place by respiratory route. The subsequent localization leads to seeding
of reticulo-endothelial system, developing viraemia. Results in difused, scattered skin
lesions involving dermis.
Critics:
When we have reviewed the Samprapti of Visarpa, there is involvement of
Vata, Pitta, and Kapha Doshas, Rakta, Lasika, Twacha, Mamsa causing Visarpavat
Shotha. As per the classical references itself; Ekadoshaja Sadhya, Tridoshaja
Kashtasadhya. By Siravyadha two Angulas from Kshipra Marma, Sthanika Shodhana
occurs, where Rakata, Twacha, Mamsna, Lasika-Dusti is neutralized. So Sthanika
Raktamokshana is recommended from the available vein. When features of Visarpa
are seen most probably it is similar to cellulitis, erysipelas and herpes zoster.
The cellulitis spreading inflammation of subcutaneous tissue by causative
organisms like streptococcus or staphylococcus, resulting in swelling, pain, redness
etc.
By means of the blood letting from the site, venous drainage is improved.
Blood is rushed towards the part, WBCs, macrophages were rushed towards the part
to engulf the infectious agents. So immediately inflammatory changes are neutralized.
As local cellular metabolism is improved. So blood letting by phlebotomy told by
Sushruta may be considered.
Another condition can be taken as erysipelas which is nothing but spreading
lymphangitis (inflammation of lymphatic vessels). Lymphatic system is a accessory
route where 1/10th of interstitial fluid is drained. Almost all tissues of the body have
lymphatic channels which drain excessive fluids directly from interstitial spaces.
Lymph returns proteins from tissue spaces. It removes the bacteria, toxins foreign
bodies. So whenever there is any inflammation in lymphatic channels. The excess
protein are left in interstitial space, bacteria, toxins are also not drained. But when
phlebotomy is done, local intravascular pressure is decreased, where in pressure of
interstitial fluid is also decreased. Lymphatic capillary permeability is increased to
improve lymphatic circulation. And also stimulation by endothelial cells, there is a
release of cytokines, scattering of WBC to neutralized infectious agents. In this way
blood letting in dorsal venous arch may be considered.
Roganusar Siravyadha Sthana
30
As varicella zoster virus is directly affecting reticuloendothelial system and
peripheral nerve routes, definitely local Siravyadha helps. Because by means of local
blood letting, there is a stimulation of reticuloendothelial system to produce
erythropoietin decreasing viraemia. Reactivation of virus is stopped as WBC are
scattering towards the affected part. Nerve inflammation is also decreased by
production of steroid hormones. So blood letting in dorsal venous arch may help in
‘herpes zoster’.
VATARAKTA :
Rakta is severly vitiated by Vata Dosha resulting particular disease condition
called Vatarakta.
Sukumara Prakrutiyukta, Mithya-Ahara-Vihara-Sevita, Shokatapta, Adhika
Stree-Sambhogi, Adhika Vyayama, Madya Sevita, Satmya Vipareeta Ahara-Vihara,
Vishama Prayoga of Sneha, Avyavayita, Sthoolatwa, Ati-Lavana, Amla, Katu,
Kshara, Ushna Padartha Sevana, Ati Sevana of Tila, Moola, Shakha, Masha,
excessive intake of Ikshu, Dadhi, Sura, Asava etc. 58, 87
Samprapti : 59, 88
Vataprakopa immediately leads to vitiation of Rakta Vayu-Margavarodha
again excess Raktadusti by Vata as these Vata dominancy is called Vatarakta.
According to Dosha dominancy features are seen.
Laxanas :
1. Toda
2. Bheda (pricking pain)
3. Cracks
4. Dryness
5. Excess temperature
6. Redness
7. Swelling
Sometimes Sarvadaihika Laxanas can also be seen so that pain in Angustha,
Gulfa Sandhi, Janusandhi, Manibandha Sandhi etc.
The condition may be correlated to metabolic disorders. Where purine
metabolism is impaired and serum uric acid level is high, may be because of
excessive production or inadequate excretion i.e. hyperurecaemia. The pathogenesis is
unclear, certain factors have been implicated to cause this condition such as gout, RA,
OA, achronosis, hyperparathyroidism. The involvement may be non-articular or poly-
Roganusar Siravyadha Sthana
31
articular, but often big joints are affected. Urate crystals are actually irritating and
result in acute pain. The skin is overlapping red, warm oedematous. Crystals of
sodium biureate may be deposited in bone, in cartilage and joints.
Clinical Features :
1. It has abrupt onset particularly pain, swelling, tenderness, temperature of first
meta-tarsal joints
2. Frequent attacks disrupt sleep,
3. Sometimes inflammation is of gross that it may resemble cellulitis.
4. Mild attacks resolve spontaneously within two days. Severe attacks may last
for seven to ten days.
Critics :
In Vatarakta, there is immediate vitiation of Rakta resulting Vayu
Margavarodha again excess Raktadusti called Vatarakta, characterized by Thoda,
Bheda, Raktima and Shotha of Hastha, Pada and Sandhi, especially knee joint. By
Raktamokshana at 2 Angula above from Kshipra Marma will definitely help. Here
Dooshita Rakta is expelled out relieving Vayu Margarodha, where vitiated Vata
becomes neutral resulting into relief from the symptoms.
The condition may be correlated by metabolic disorder, where purine
metabolism is impaired and serum uric acid is high may be because of excessive
production or inadequate excretion, that is ‘hyperuricaemia’. In general an
homeostatic mechanisms are concerned there must be removal of metabolic end
products like carbon dioxide which is abundant of all end product of metabolism.
Passage of blood through the kidneys removes most of other substances
besides co2 from plasma, which are not needed by the cells. The substances include
different end product of cellular metabolism, such as urea and uric acid. If they are in
excess they might have accumulated in extracellular fluid. The kidneys perform their
function by filtering large quantity of plasma and reabsorbing substance needed by the
body like glucose, aminoacids, water etc. Most substances are not need by the body
especially metabolic endproducts urea, uric acid are poorly reabsorbed, instead pass
on through the renal tubules into the urine.
In general local blood letting is done by venesection, certain amount of urea,
uric acid might have taken away and there is a release of ‘angitensin’ hormone,
which has got renal and adreno-cortical stimulatory effect providing excretion of
Roganusar Siravyadha Sthana
32
urea, uric acid by the kidneys. That is why in gouty arthritis, blood letting is done in
branch of dorsal venous arch. 89
VATAKANTAKA :
Walk on the hard roads, surface causes Vata Prakopa and produces pain in the
‘Pada’ called ‘Vatakantaka’. 60, 90
Walking on undue surface, exercise leads to vitiation of Vata in the ankle
joints produces pain in the heel that condition is called as Vatakantaka.91
The condition can be correlated to ‘Heel spurs’ or calcaneum spur. ‘Spur’
means bony growth. Heel spur often occurs in heels i.e. calcaneum bone.
Predisposing Factors :
1. Obesity (Excess weight on heel of feet)
2. Ill fitting shoes wearing for longer duration
3. Pronation – means abnormal movements of the foot.
Pathology :
Bony outgrowth usually extend from the heel bone into the soft tissue
surrounding the bottom of the foot causing inflammation of plantar fascia (fascitis)
and pain through out the heel of the foot. That heel spur is composed of calcium
deposits. This bony deposits develop when the plantar fascia stretches abnormally due
to stress factors and occurs where the ligament attaches and stretches away from the
heel bone. 92
Features:
1. Serious pain in the heel of the foot.
2. Generate aching pain with every step.
3. Sharp – pricking type of pain in heel.
4. More in morning hours. Critics :
According to Ayurveda, because of Vata Prakopa, pain resulting into Pada
especially in Gulfa Sandhi (heel of foot) called Vatakantaka. By means of Sthanika
Raktamokshana by Siravyadha, Vata gets neutralized and pain relieved. So blood
letting is done two Angula above from ‘Kshipra Marma’. When the condition is
correlated, it is nothing but “heel spur”. Especially, calcaneum bone is affected, so
called ‘calcaneum spur’. It is nothing but bony out growth, composed by calcium
deposit, pressing over the plantar fascia.
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When normal mechanism of bone calcification is concerned, it is nothing but
secretion of collagen molecules and ground substances, by osteoblast. These
osteoblast become entrapped called osteocytes. The osteoblasts also secrete a
substance into osteocytes, to neutralize an inhibitor called pyrophosphate. So under
normal conditions, there is limited growth of bone. In abnormal conditions, calcium
salts precipitate in arterial walls called arteriosclerosis. Likewise, calcium salts
frequently deposit in degenerative tissues. The osteoblasts secret large quantity
alkaline phosphatase, when they are actively deposited on bone matrix. This
phosphate is believed either to increase local concentration inorganic phosphate are
active collagen fibres. In such a way they cause deposition of calcium salts. As
alkaline phosphate is defuses in blood its level is indicator of rate of bone formation.
By doing phlebotomy in recommended dorsal venous arch, certain amount of
alkaline phosphate is taken away can also be prevented by increased metabolism and
blood flow. In this way, phlebotomy in dorsal venous arch is beneficial. 93
VICHARCHIKA:
In Vicharchika, there is Rukshata developed in Hasta and Pada i.e. cracks like
associated with excess itching and pain. 61, 94
The condition Vicharchika Kushta may be correlated to ‘Eczema’95. It is one
of the type of skin disease, grouped under non-infectious inflammatory dermatoses.
The pathological term dermatitis is synonym with clinical term eczema. Both
dermatitis, eczema refer to inflammatory response to a variety of agents acting on the
skin from outside or from within the body.
In other words, a chronic relapsing pruritic skin condition of unknown
etiology with personal history and family history.
Predisposing Factors :
1. Chemicals
2. Drugs
3. Irritants
4. Unhygienic states
5. Photosensitivity.
Pathology :
This has been well studied that it is due to contact hypersensitivity. Initially
antigens at the epidermal surface are taken up by dendritic Langerhans cells which
migrate by the dermal lymphatics to draining lymph nodes. Antigens processed by the
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34
Langerhas cells are presented to ‘T’ cells. These ‘T’ cells migrate to affected skin
sites where they release cytokines and numerous inflammatory cells. There is local
cytokines release in the vicinity of dermal post-capillary venules. This results in
endothelial activation, where by endothelial cells become enlarged and express
molecules on their plasma membranes that promote adhesion of circulating T
lymphocytes. Once T cells enter the site of antigen through activated microvessels,
they elaborate large numbers of inflammatory cells to the site resulting structural and
functional integrity of epidermis.
There is acanthosis (thickening of epidermis due to hyperplasia of stratum
Malphighi). Loss of connection between epidermal cells with formation of
intraepidermal space containging odema fluid and detached epithelial cells. There is
thickening of horny layers. Intracellular oedema of the epidermis which may progress
to vesicles formation in the epidermis. Upper dermis shows crusts containing
degenerated leucocytes, bacteria and fibrin.
Morphological features :
1. Erythema
2. Odema
3. Papules
4. Oozing
5. Crusting
6. Fissuring
7. Scaring
8. Pigmentation
9. Thickening.
Critics :
In Vicharchika there is Rookshata developed in Pada. By means of blood
letting in the site two Angula above from the Kshipra Marma by Siravyadha is done
where Vata Gunas are neutralized. So the site may be considered for blood letting.
The condition may be correlated to ‘eczema’, where there is contact
hypersensitivity due to which there is hyperplasia of the skin. Epidermis is thick
containing a fluid in intraepidermal space. Upper dermis showing crusts containing
degenerated bacteria, fibrin. In general, structural and functional integrity is lost.
When blood letting by venesection is done in dorsal venous arch, venous drainage of
that part is improved, fresh blood is rushed providing oxygen and nutrients for proper
Roganusar Siravyadha Sthana
35
growth epidermis layer. And also nor-epinephrine and epinephrine hormones are
released acting as an anti-allergic. Because, these hormones released in local tissue
areas cause local circulatory effects. So the site for Siravyadha may be considered.
PADADARI :
In persons who are in habit of walking too much, Vata becomes aggravated
produces dryness of sole cracks / fissures in the soles which is painful. This is known
as ‘Padadari’. 62, 96
This occurs in persons whose profession is to walk long distance daily or in
persons living in desert areas where there are no facilities of cars, buses etc. In India it
is very common in farmers, labour and villagers. In this, Vayu with its intense
Rooksha Guna, gets aggravated and produces cracks and fissures in soles of the feet.
This can be correlated to Rhagades or Crack or Fissure in Sole it is a vertical
loss of epidermis and dermis with sharply defined walls; crack in skin.97 Rhagades
gets aggravated in cold season and in very hot climate. Disease may constitutional in
some cases. The patient feels unbearable pain on placing foot on the ground. Pain is
reduced on wearing tight shoe and on massaging with oil or ghee on the cracked
portion of the sole of the foot.
Critics :
When Vata is aggravated causing dryness in Pada and also pain known as
Padadari. By Siravyadha two Angula above from Kshipra Marma, Rukshata of Pada
is relieved and pain is reduced. When it is correlated to ‘Rhagades’ or ‘cracks’. As
there is vertical loss of epidermis layer, blood letting by venesection of dorsal venous
arch will improve the venous drainage. Concurrently local tissue metabolism is
improved because of rush of blood and there is release of hormone.
SHLEEPADA:
Vataja Shleepada Chikitsa :
In Vataja Shleepada, after unction and sudation of the patient, the surgeon
should puncture the vein four fingers above the ankle. 63, 98
Pittaja Shleepada Chiktsa :
In Pittaja type, the vein located below the ankle, that should be puncture;
besides Pitta alleviating measures should be employed as in Paittika tumour and
erysipelas. 64, 98
Kaphaja Shleepada Chikitsa :
Roganusar Siravyadha Sthana
36
In Kaphaja type, the physician should puncture the well know vein in the big
toe. 65, 98
Pada becomes Shila Saman Kathina, Sthoola ((Slivt` pd> Ål)pdm` ..)
called Shleepada.
Nidana: 66, 99
Stagnant water, Sheetala Ahara and Vihara and Anupa Desha are the causative
factors for Shleepada.
Samprapti: 67, 100
Nidana Sevana Kaphapradhana Tridosha Prakopa vitiated Dosha get
Ashraya in Vankshana, Uru, Janu, Jangha afterwards takes Ashraya in Pada
produces Ghana Shopha Shleepada.
Dosha Kapha Pradhana Tridosha
Dushya Rasa Dhatu
Sthana Padagata Lasikavahi.
Types It is of three types
(I) Vataja Shleepada Laxana :
(a) Krisha, Rooksha, Sputita Shotha
(b) Teevra Vedana
(c) Mild fever.
(II) Pittaja Shleepada Laxana :
(a) Peeta Sankasha
(b) Daha Jvarayukta
(c) Soft to touch
(III) Shlaishmika Shleepada :
(a) Shweta or Pandu Vrana
(b) Snigdha
(c) Guru
(d) Sthira
The condition can be correlated to filariasis.101 Filariasis is a global problem
where there is no satisfactory treatment. “Wucheraria bancrofti” and “Brugia mallai”
parasites are responsible for filariasis. The clinical course of the disease is
inflammatory. Presence of adult worms in lymphatic vessels induce obstruction or
mechanical blockage of the lymphatic channels, causing ‘lymphoedema’. The tissues
Roganusar Siravyadha Sthana
37
surrounding the blocked lymphatics are infiltrated by chronic inflammatory cells such
as lymphocytes, plasma cells, eosinophills. Chronicity of process causes enormous
thickening and induration of the skin of leg.
Clinical Features :
Acute and Chronic :
Fever, lymphangitis, urticaria, regional lymphadenitis, epididymo-orchitis and
eosinophilia. Lymphoedema, non-pitting edema; skin is dry and thick, contours of
ankle is lost.
Critics :
Here in Shleepada, Kapha Pradhana Tridosha, Rasadhatu are involved where
Adhisthana is Uru, Janu, Pada. Usually it is due to stagnant water, where Kapha
Pradhana, Tridoshadusti takes place, Dosha get aggravated, resulting into Shotha
initially in Vankshana, Jangha, Janu gradually settled at Pada.
In the initial stages, Vata involvement is dominant and the condition may
occur in Vankshana. So Adhahjanghagat Siravyadha is done i.e. four Angulas above
from Gulfa Sandhi in Vataja Shleepada.
In Pittaja, the condition is descending down like Jangha, Janu, Adhahajangha
so Siravyadha is done in 4 Angula, below from Gulfa. Likewise in Kaphaja when the
condition settled down in Pada, the Siravyadha done in the site 4 Angula above from
Kshipra Marma.
By means of Siravyadha Dooshita Kapha and Rasa may be expelled out
neutralizing Shotha. So Siravyadha in particular site might have been dealt by
Sushruta.
When we have reviewed the pathology of filariasis, the obstruction
(mechanical blockage) of lymphatic channels causing lymphoedema. The surrounding
tissues are infiltrated by chronic inflammatory cells such as lymphocytes,
eosinophiles.
1/10th of interstitial fluid is drained by lymphatic channels. On the contrary,
interstitial fluid and lymph are similar but the difference is only location. Lymph
returns proteins from tissue spaces into blood. Through lymph only, certain bacteria,
toxins and other foreign bodies are removed from tissues. lymphatic capillaries are
slightly larger in diameters than blood capillaries. And has unique structure that
permits interstitial fluid to flow into them but not out. The endothelial cells make up
the wall of a lymphatic capillary overlap. When pressure is greater in the interstitial
Roganusar Siravyadha Sthana
38
fluid than in lymph, the endothelial cells separate slightly like the opening of the one
way singing door and interstitial fluid enters the lymphatic capillary. When pressure is
greater inside lymphatic capillaries adhere more closely and lymph can not escape
back into the interstitial fluid.
On the basis of this physiology the venesection will definitely helpful in
filariasis. Because 1/10th fluid is drained by lymphatic capillaries. Wherever
lymphatic channels are blocked; the interstitial fluid is not drained by capillaries when
blood letting is done locally, the somewhat pressure in the lymphatic channels is
decreased and also as there is stimulation of endothelial cells they can cause relieve of
blockage also which may provide opening of lymphatic capillaries and also local
metabolism increased. So according to the condition of situation of swelling
Siravyadha site is selected, So that, four Angula above from Gulfa is long saphenous
vein and tributaries at the junction of upper two third and lower one third of the leg.
Likewise if Shotha is there in Pada, short saphenous vein, dorsal venous arch blood
letting is done.
KROSTUKASHIRSA :
In Kroshtuka Sirsha, Khanja, Pangu and pains produced by Vata, puncturing
should be done in Jangha, four Angula (8 cm) above the ankle joint. 68, 102
As per the above said treatment Siravyadha is done in the said diseases, four
Angulas is done in the said diseases, four Angulas from the Gupha Sandhi. The
anatomical location of vein of that part is interpreted on available anatomical basis. In
Gulpha Sanhi, the Gulpha Marma is located, so, Siravyadhana is done above from the
the Gulpha Marma 103 by protecting the Marma Sthana.
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TABLE NO. 8 SHOWING DETAILS OF GULPHA MARMA
Measure and
Type -
2, Sandhi, 2 Anguli
Site -
Ankle joint and the tibia as well as calcium bone. Controls
Medovaha, Asthivaha, and Shukravaha Srotas
Tissue involved
Anatomical
structures
-
Flexor hallucis longus and brevis, tibialis posterior and flexor
or digiti longus muscles. Posterior tibial nerve. Posterior tibial
artery and vein.
Sign if injured
-
Injury to the joint will cause swelling with impairment of the
functions of flexion, extension etc. It is Vaikalyakara type of
Marma
Treatment
-
Suchi Karma (acupuncture) – For tubercular knee, sever pain
in the groin, paresis of the leg, paralysis of the leg, it should
be done, 4 Anguli above the Marma.
As the site of Vyadhana is Gulpha, that area is drained by long saphenous vein
and its tributaries. It starts on medial border of the foot and passes upwards just
anterior to the medial malleolus. It is very consistent in position at this point and can
usually be easily identified as a site for vein harvest.
The long saphenous vein can often be seen as it runs upwards and backwards
across the medial surfaces of the tibia is little above and in front of the medial
malleleolus. This is a useful site for obtaining surgical venous access.
The long saphenous vein is very prominent and easily marked at the medial
border of the tibia at the junction of the upper two third and lower one third of the
leg.104
In Janusandhi, Vata and Rakta Vikruti leads to pain in the knee joint and
swelling which looks like head of fox.69, 105
The condition can be correlated with Septic Arthritis.106 That is Inflammatory
involvement of the joint due to infectious agents like streptococcus, staphylococcus.
Precipitating Factors :
(1) Immunosuppressive therapy (2) alcoholism (3) drug abuse (4) chronic
arthritis.
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Pathology :
There is direct hematogenous seeding of synovium. The large joints of
extremities are commonly affected (75% knee joints). The synovium is well
vascularized and lacks a limiting basement membrane. The process begins with
hyperaemia, synovial swelling and infiltration by polymorphonuclear and
mononuclear leucocytes along with the development of effusion in joint space. There
may be formation of inflammatory tissues and onset of fibrous affections between the
opposing articular surfaces resulting in permanent ankylosis. And also there is release
chondrolytic enzymes contribute to destruction of articular cartilage.
Clinical Features :
1. Pain
2. Warmth
3. Swelling
4. Restricted movement
5. Co-existence of Rheumatoid arthritis
Critics :
In Janusandhi, Vata and Rakta Nirukti leads to pain in the knee joint and
swelling looks like head of the fox. There is involvement of Vata and Rakta. here is
also letting is done in same site where in Vataja Shleepada is done, i.e. 4 Angula
above from Gulfa. By means of Siravyadha Raktamokshana, Dooshita Rakta may be
expelled out and Vata Margavarodha is relieved. So Sushruta might have told this site
for Siravyadha in Krostukasheersha.
As the condition is similar to that of septic arthritis, by means of blood letting
by phlebotomy in long saphenous vein the hyperuriaemia is relieved, by release of
steroid hormone. The effusion (swelling) is resolved. Fibrous adhesions are relieved.
In this way blood letting may help in septic arthritis. So the particularly site told by
Sushruta can be considered.
KHANJA :
Prakupita Vata is getting Ashraya in ligaments of the limbs, causing an
individual to incapability to walk is called Khanja. 69, 107
This condition can be correlated to Monoplegia or poliomyelitis. This is usually due
to lower motor neuron disease with or without associated sensory involvement. Upper
motor neuron weakness occasionally presents with a monoparesis of distal and non-
anti-gravity muscles (LMNL).108
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41
Poliomyelitis :
Much of what is known about the pathogenesis of enteroviruses has been
derived from studies of Polio virus infection. After ingestion, Polio virus is thought to
infect epithelial cells in the mucosa of the gastrointestinal tract and to spread to and
replicate in the submucosal lymphoid tissues. The virus next spreads to the regional
lymph nodes, and viraemia phase ensues and viruses replicates in organs of
reticuloendothelial system. In some cases, a second viraemia occurs and the virus
replicates further invasions of tissues, sometimes causing symptomatic disease. It is
uncertain whether polio virus reaches the CNS during viraemia or wheather is also
spreads through peripheral nerves.
Enterovirus have worldwide distribution.
Clinical Features :
1. Incubation periods 3 to 6 days
2. The common presentation is paralytic disease
3. Severe back, neck and muscle pain by rapid development of motor weakness.
Critics :
In Khanja, Katisthith Prakupita Vata getting Ashraya in Khandaras of Sakthi
resulting into Khanja where there incapability to walk because of single limb
deformity.
Usually because of Margavarodha the Vata got vitiated when Siravyadha is
done in recommended site i.e. four Angula above from Gulfa (long saphenous vein),
Margavarodha is relieved when Vata may get neutralized.
The condition can be correlated to monoplegia which is usually lower motor
neuron lesion. Blood letting by phlebotomy may help locally and systemically also.
Because if there is any thrombus that will be dissolved by fibrinolytic activity of
blood letting. And locally by blood letting removal of waste products of cellular
metabolism is improved and various hormones are released to maintain homeostasis.
Nerve stimulation can occur. So in particular site, Siravyadha may be told by
Sushruta.
PANGU :
Prakupita Vata is getting Ashraya in ligaments of the limbs, causing an
individual to incapability to walk is called Pangu. 71, 109 This condition can be
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42
correlated to diplegia or paraplegia. Cerebral palsy carries connotation of a
development disorders of motor function, that is present from infancy or early
childhood and that is due to non-progressive cerebral disorders. The most commonly
encountered condition is spastic diplegia (affecting both legs).
Cerebral infarction resulting from hypoxia or ischaemia is one determinant of
these disorders, for most abnormal state has its origin before birth in events that go
unrecognized. The insult may occur perinatally as a result of obstetrical mishap. For
some people encephaloclastic event occurs in early childhood.
Pathology :
Ischaemic necrosis in the brain results from ischaemia caused by considerable
reduction or complete interruption of blood supply to the neural tissue which is
insufficient to meet its metabolic needs. The brain requires sufficient quantities of
oxygen and glucose so as to sustain it’s aerobic metabolism, mainly by citric acid
cycle i.e. Kreb’s cycle which requires oxygen. Moreover, neural tissue has limited
stores of energy reserves so that cessation of continuous supply of o2 and glucose for
3-4 minutes results in permanent damage to neurons and neurological cells.
Deprivation of o2 to the brain may occur in 4 different ways.
1. Anoxic – where there is low inspired Po2
2. Anaemic anoxia – in which o2 carrying haemoglobin is reduced.
3. Histotoxic anoxia – e.g. cyanide poisoning
4. Stagnant anoxia – in which the damage is caused by cessation of blood with
resultant local accumulation of metabolites and changes in pH
In all these different forms of anoxia the end results is ischaemic brain
damage, which may be of two manners – (i) generalized cerebral
hypoperfusion (ii) localized reduction of blood supply.
The brain receives 20% of cardiac output for maintaining its vital aerobic
metabolism. Various factors are responsible for irreversible ischaemic damage, such
as body temperature hypoxic episodes pre-existing cerebral diseases. Normally, brain
continues to be perfused upto arterial pressure below this critical value results, rapid
fall in cerebral perfusion. The pathological appearance of the brain varies depending
upon the duration and severity of hypoxic episode. Microscopically, nerve cells die
and are replaced by reactive fibrillary collagenous tissue.
Critics :
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The condition ‘Pangu’ is same as that of Khanja. But both legs are involved.
Prakupita Vata getting Ashraya in Sakti Kandara, Sira, Snayu, Nadi etc. So
Raktamokshana by Siravyadha at 4 Angula above from Gulpha may cause
neutralization of Doshas. So the local Raktamokshana is dealt.
The condition can be correlated to diplegia, where cerebral palsy of
developmental disorder of motor function. Cerebral infarction resulting from hypoxia.
When there is considerable reduction in blood supply to neural tissue which is
insufficient to meet its metabolic needs. The brain requires sufficient o2 and glucose
so as to sustain metabolism.
Cerebrum is most vascular area of the brain. It is highly related to metabolism
of cerebral tissue. Metabolic factors have potent effect in controlling cerebral blood
flow. They are nothing but co2, hydrogen ion and o2. An increase in co2 or hydrogen
ion concentration increases the cerebral blood flow, where as decrease in o2 increases
the blood flow. By means of dilating the cerebral blood vessels increases the blood
flow, which inturn carries co2 and acidic substances. Oxygen deficiency also increases
the cerebral blood flow. On the basis of this theory, as blood letting in long saphenous
vein may induce higher co2 and hydrogen ion concentration which in turn cause
dilatation of cerebral blood vessels with increased blood flow. Concurrently it is
carrying away the acidic substances from the neural tissue.110
APACHI :
In Apachi, Siravyadha is done at two Angula (4 cm) below the Indrabasti
Marma. 72, 111
In above said disease, the Siravyadhana is done 2 Angula below the
“Indrabasti Marma”. The anatomical location of the vein of that part is interrupted on
the available anatomical basis. Venesection is done 2 Angula below the Indrabasti
Marma in lower part of the back of leg. Here the small saphenous vein is easily
visible and usually it is the choice for the venesection.
TABLE NO. 9 SHOWING DETAILS OF INDRABASTI MARMA
Measure and Type - 2, Mamsa, ½ Angulas Site - The point at the middle of the line, joining the posterior
surface of the calcaneum with the centre of the popliteal
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fossa. Controls Agni, small intestine and Annavaha Srotas Tissue Involved and Anatomical structure
- Gastronemics, soleus and plantaris muscles. Peroneal (branch of posterior tibial) and posterior tibial artery and vein. Drainage of lymph to the popliteal lymph glands. Posterior tibial nerve.
Signs if injured - Injury may cause impairment of the function of the foot. If the artery is damaged, there will be severe bleeding, shock and collapse. It is Kalantara Pranahara type of Marma. (At this vital point, posterior tibial artery is more important than any other muscle or ligament)
The Sthana of Siravyadha is two Angula (4 cm) below the ‘Indrabasti Marma’.
This region comes back side of the leg. Here the Vyadhana is done by protected
Marma and its structure. So it is mentioned that venesection is done below the vital
spot. This area is drained by small saphenous vein, usually it can be selected for
venesection, as this vein is easily visible in its lower part.
The short saphenous vein begin at the lateral aspect of the dorsal venous
arches of the foot, cause along the back of the leg. It is the continuation of the lateral
marginal vein. In the lower third of the calf it ascends only by superficial fascia and
skin. It is easily marked at the point behind the lateral malleolus and just lateral to the
tendocalcaneus above the lateral malleolus it drains the lateral border of the foot, the
heel, and the back of the leg. It is connected with the great saphenous vein at the
middle of the calf region by accessory saphenous vein.
It receives many cutaneous tributaries in the leg. In leg, small saphenous vein
ties near the sural nerve.112 Usually short saphenous vein at lower third of the back of
leg is selected for venipuncture.
Nidana :
Since there is no direct explanation of Nidana of Apachi, Dosha involvement
is considered as Kaphadusti and Meda-dusti. So the factors vitiating Kapha and Meda
are responsible for Apachi. 113
Samprapti :
Kapha and Meda are accumulated in Hanvasthi, Akshikasthi, Bahu, Jangha,
and Manya producing Granthis. They are stiff, round, circular, painful, resembling
seed of Amalaki and Matsyanda Jala.
Dosha Involved :
Dosha : Kapha pradhan Tirdosha
Dushya : Meda
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This condition can be correlated to Lymphadenitis which is an inflammatory
condition of lymph nodes.
Etiologies :
1. Inflammatory
2. Infective
3. Neoplastic
Pathology :
Lymph nodes undergo reactive changes in response to a acute variety of
stimuli which include microbial infections, drugs, tissue injury, neoplasia. The
affected lymph nodes are enlarged three times to their normal size. Microscopically,
sinusoids are congested widely dilated and edematous. But in chronic course lymph
nodes are enlarged, firm, non-tender.
Clinical features :
Firm, movable, round, swelling in all regions of the lymph nodes.
Critics :
Where in Apachi, Kapha Pradhana Tridosha and Meda are involved resulting
in Granthi Samana Shotha called Apachi. If it may occur in Manya, Bahu, Jangha etc,
where ever it is situated in upper or lower extremities, Siravyadha is done 2 Angula
below from Indrabasti Marma. Where there is neutralization of Doshas and
mobilization of Medas, so particular site is selected. As per modern science is
concerned lymphadenitis, that is nothing but reactive changes in response to any
stimuli like infections, injury, drugs, neoplasms. As these are connected to the
channels, lymphatic circulation is meant for drainage of toxins and bacteria engulfed
by lymph nodes causing as lymphadenitis. By means of the blood letting venous
drainage is improved. Automatically, lymphatic drainage is improved resolving
inflammation of lymph nodes by increased blood flow, metabolism and removal of
waste products from the interstitial space. So, local part is selected for Siravyadhana
at median vein in upper limb and short saphenous vein in lower limb.
GRUDHRASI :
In Grudhrasi, it should be done four Angula (8 cm) either above or below the
knee joint. 73, 114
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As per above said quotation the Siravyadha is done, four Angula (8 cm)
Sandhi, Janu Marma 115 is located. So, by protecting the vital point Siravyadha is done
below the Janu Sandhi.
TABLE NO. 10 SHOWING DETAILS OF JANU MARMA
Measure and Type - 2, Sandhi, 8 Anguli Site - On the knee joint, Right Marma controls liver, left
Marma controls spleen. Tissue Involved and Anatomical structure
- Knee joint, posterior cruciate ligament, olique posterior ligament, plantaris and gastronemis muscle. Popliteal artery and vein, femur, tibia and patella bones. Medial popliteal nerve.
Signs if injured - Injury to the knee can cause severe pain, edema, difficulty in walking, disfigurement and impairment of all the functions of the joint. It is Vaikalyakarama type of Marma
Treatment - Agnikarma – In sciatica, as usual select sensitive joint 4 Angulai proximal or distal to the Marma and apply heated gold probe at the point.
Usually the great saphenous vein is easily found in this area for venesection
i.e. four Angula below the Janu Sandhi. It begins on the medial side of the dorsum of
the foot and runs upwards and backwards anterior to medial malleolus and then to the
medial surface of the distal third of the tibia. It then ascends on the medial border of
the tibia to the postero-medial surface of the knee and inclines anteriorly through the
thigh to enter the femoral vein. The vein has several communication through the deep
fasica with deep veins. Just below the knee, this vein communicates with anterior vein
of the leg.
When Kandaras of Parshni Padangulis are vititated by Prakupita Vata then
contraction-relaxation of the limb is restricted called “Grudhrasi”. 74, 116
Nidana :
Sheeta, Rooksha – Ahara, Ati-jagarana, Ati-maithuna, Ati-malapravrutthi, Ati-
Shrama, Dhatuksheenata, Chinta, Shoka, Krodha, Amadosha etc.
Samprapti and Laxanas :
Because of above Hetus vititation of Vata results from Sphik, raditating to
Kati, Prushta, Uru, Janu, Jangha, Vedana. Usually, pricking type of pain exists often
Spandana is felt in these areas. If there is involvement of Kapha there is presence of
Tandra, Jadata, Aruchi. Vagbhata considers Grudhrasi as similar to Vishwachi.75, 117
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This is correlated to Sciatica 118 which means pain in the distribution of sciatic nerve
and its components nerve root. Instead as a disease is accepted as lumbar disc
prolapse, which is a common cause of low back ache.
Etiologies :
1. True sciatica neuritis is leprosy, trauma, post-herpetic neuralgia.
2. Mechanical pressure nerve roots
3. In vertebral column – Fibrocytis
4. Lumbar disc diseases
Clinical features :
1. Pain felt in buttocks radiates down the posterior aspect of the thigh, calf, outer
border of foot.
2. Increased on coughing, sneezing, and excess of walking
3. Parasthesia along the nerve root
4. Calf muscle weakness
Critics :
Because of Prakupita Vata, contraction, relaxation of limb is restricted
resulting into pain from Sphik radiating to Kati, Uru, Janu, Jangha etc. By means of
Siravyadha four Angula above or below Raktamokshana is done, where Vatadushita
Rakta is expelled out and pain is relieved. If the intensity of pain is in Prusta, Kati,
above site is selected, if its intensity is more in Pada, below site is selected. In
sciatica, similar features can seen, where in there is compression of sciatica nerve due
to various causes like unusual stretching, neuritis, fibrositis, lumbar disc prolapse etc.
So there is shooting pain along with distribution of sciatic nerve. Usually pain is
associated with tissue damage, free nerve endings are the pain receptors. There may
be various stimuli like mechanical, chemical, thermal causing pain. This is considered
as mechanical. So that because of compression of nerve, blood supply to the tissue is
blocked, then tissue becomes painful. Pain during blockage of blood supply is due to
accumulation of large amount of lactic acid in tissue. Certain chemical agents formed
such bradykinin and proteolytic enzyme which stimulate at nerve endings. So in any
nerve compression or muscle spasm, there is pain but by means of blood letting,
branch of great saphenous vein, 4 Angula above or below, blood flow to the
compressed part may be increased by angiogenesis, as much as possible aerobic
metabolism is enhanced, where the accumulation of lactic acid can be prevented and
accumulated lactic acid may be drained. By means of blood letting the hormone
Roganusar Siravyadha Sthana
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serotonin is released, believed to cause presynoptic and postsynoptic inhibition,
avoiding pain. So if the pain is situated in back and thigh, then upper site is selected,
if the pain is radiated upto leg, lower site is selected.
GALAGANDA :
In Galaganda that vein present at the root of the thigh should be punctured.
This description is also applicable for opposite Shakti and in both Bahus. 76, 119
In Galaganda, aggravated Vata and Kapha Doshas in Gala Pradesha get
Ashraya in Majja and Meda and then produce symptoms according to their Dosha
dominancy. 77, 120
Types :
1. Vataja Galaganda
2. Kaphaja Galaganda
3. Medaja Galaganda
Laxana :
1. Mushkavat – Shotha in neck region
2. Mobile or immobile Galaganda
3. Cold, smooth in nature
4. Improper speech
5. Difficulty in breathing etc.
This can be correlated to Goitre, the term ‘goitre’ is defined as thyroid
enlargement caused by compensatory hyperplasia and hypertrophy of the follicular
epithelial in response to thyroid hormone deficiency. The end result of this
hyperplasia is generally euthyroid state which may be hypo or hyper thyroidism.
Goiter is of two types – 1. simple non-toxic 2. multinodular – toxic.
Pathogenesis :
The mechanism of both the forms of goiter can be considered together, since
nodular goiter is generally regarded as end stage of long standing simple goiter.
Deficient production of thyroid hormone due to various factors. Most common causes
dietary lack of iodine. Deficient thyroid production causes excessive TSH stimulation
which leads to hyperplasia of follicular epithelium as well as formation of new
thyroid follicles. Cyclical hyperplastic stage followed by involution, leads to simple
goiter. Repeated and chronic changes of hyperplasia result in continued growth of
thyroid tissue while involuted area undergo fibrosis leads to nodular goiter. 121
Critics:
Roganusar Siravyadha Sthana
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In Galaganda, Urumula Samsthita Siravyadhana is done, where there may be
neutralization of Kapha-Meda-Rakta Dusti. Any relevance cannot be interpreted or
elicited here. On the contrary, if that is correlated to goiter, which is hyperplasia of
follicular epithelium of thyroid follicles where there may gradually growth of thyroid
tissue and fibrosis. Probably the condition tends towards non-toxic goiter i.e.
hypothyroidism. Here, blood letting by phlebotomy may help by many ways. It may
directly stimulate pituitary to release TSH. Indirectly improve metabolism of whole
body by release of numerous chemicals and hormones. As the available veins of neck
and abdomen are contraindicated for Siravyadhana, so Urumula Sthita Sira may
accepted for Siravyadha.
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TABLE NO. 11 SHOWING SITES FOR SIRAVYADHA OF DIFFERENT
VYADHANA STHANAS PARTICULAR DISEASES IN LOWER LIMB
Sl. No. Vyadhis Vyadha Sthanas (I).
1. Padadaha 2. Padaharsha 3. Visarpa 4. Chippa 5. Vatarakta 6. Vatakantaka 7. Vicharchika 8. Padadari
Two Angulas (4 cm) Above the Kshipra Marma
(II). 1. Vataja Shleepada Four Angula above the
“Gulfa Sandhi 2. Pittaja Shleepada Four Angula below the
“Gulfa Sandhi 3. Kaphaja
Shleepada Four Angula above the “Kshipra Marma”
(III). 1. Kroshtukashirsha 2. Khanja 3. Pangu
Four Angula above from ‘Gulfa Sandhi’
(IV) Apachi Two Angula below from ‘Indrabasti Marma’
(V) Gridhrasi Four Angula above from ‘Janu Sandhi’
(VI) Galaganda Urumoola Sthita Sira
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(II) URDHVASHAKHAGATA VEDHYA SIRA STHANAS : [Fig. 9]
Pleehodara:
In diseases of Pleeha, puncturing should be done especially in the left arm
either at the inner side of elbow joint in the centre of arm or in the are between the
little and ring fingers. 78, 122 As per above information in Pleehodara Siravyadha is
done in left sided Kurpara Sandhi Sthita Sira i.e. median cubital vein which is situated
above ‘Kurpara Marma’.123 It is a type of Sandhi Marma controlling Raktavaha
Srotas, so that Marma on right controls liver, Marma on left controls spleen.
The prominent medial cubital veins links cephalic and basilic vein. It receives
number of tributaries from the front of forearm and gives off the median vein, which
pierces the facial roof of antero-cubital fossa to join the venae commitants of brachial
artery. So the vein recommended for Siravyadha may be left sided medial cubital
vein.
Or otherwise vein situated in between little finger and ring finger may be used
for Siravyadha. As per context, it may dorsal venous arch lies on the dorsum of the
hand. Its tributaries include dorsal metacarpal veins, dorsal digital veins from the
medial side of the little finger and dorsal digital from the index finger two dorsal
digital veins from the thumb. 124
Because of consumption of Adhika Vidahi, Abhishyanda, Ushna, Lavana,
Gunatmaka, Ahara and Vihara Sambandhi Atiyana, Atichinta, Ativyayama, lifting
heavy weights, improper Panchakarma therapy. 79, 125
Samprapti :
Due to above said causes there is a enlargement of spleen which we call it as
Pleehodara especially on the left side. Dosha involved is Kapha, Dushya is Rakta,
Adhisthana – Pleeha, Srotas – Rasavaha and Raktavaha.
Laxana :
Mandajvara, loss of appetite, indigestion, anaemia, loss of strength.
This can be correlated with Splenomegaly.126 Enlargement of spleen can be an
important diagnostic clue of the underlying disorders, when it is sufficiently enlarged
that causes protuberance on left side and dragging pain in left upper quadrant.
Usually spleen is a large single mass of lymphatic tissue in the body with
multiple functions like formation of blood cells, destruction of blood cells, reservoir
function and role in defense mechanism.
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Etiologies :
1. Infection conditions like malaria, enteric fever, viral hepatitis, tuberculosis,
syphilis.
2. Autoimmune diseases like R A, thrombocytopenia.
3. Altered blood flow to the spleen.
4. Cirrhosis of liver.
5. Portal venous obstruction.
6. C C F
The other rare diseases splenomegaly is seen.
Pathology :
Enlarged spleen is heavy and firm. The capsule is tense and thickened. There
is dilatation of sinusoid with prominence of splenic cord. The white pulp is atrophic.
Critics :
Because of the involvement of Kapha, Rakta, Rasavaha, Raktavaha Srotas,
there is enlargement of spleen resulting into mild fever, loss of appetite, indigestion,
weakness etc. By means of blood letting in Vama Kurpara Sandhista Sira, Rasavaha,
Raktavaha Srotoshodhana can occur and Kapha-Raktadusti is neutralized, resolving
Pleehodara. That is the Sthanika Raktamoksha from the nearest vein of the spleen
(Vama Kurpara Sandhisthita Sira). The condition may be similar to spleenomegaly. In
spleen more than 100 ml of blood is always reserved. Spleen has got turn separate
areas for storage of blood, venous sinuses and pulp. Small vessels flow directory into
venous sinus cause sinuses to swell up. The red cells are expelled by spleen into
general circulation. Blood passing through spleen pulp, before it enters the sinuses
under goes through squeezing. So it is expected that RBC’s would not withstand the
trauma. So many of RBCs destroys in the body have their final demise in spleen.
After cellular rupture, the released hemoglobin through the cell trauma are ingested
by reticuloendothelial cells of the spleen, when blood is invaded by infectious agents,
the reticuloendothelial cells of the spleen are rapidly remove the debris, bacteria,
parasites. Due to any cause when there is spleenomegaly, phlebotomy done in left
medial cubital vein by which reserved blood in the spleen is ejected into general
circulation, so that fragile RBCs are wased off, fresh RBCs are formed, blood
circulation to the spleen is increased, so there is removal of old cells. Splenic vein is
drained effectively, so blood letting in left median cubital vein is done in
splenomegaly.127
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YAKRIDLYUDARA:
In Yakrudalyudara, puncturing should be done especially done in the right arm
at the same space. 80, 128
As per above said quotation in Yakrudotodara and Kaphodara, Kasa Shwasa
Siravyadha is done is right sided ‘Kurpara Sandhisthita’, it is right median cubital
vein, which is situated above Kurpara Marma. It is a type of Sanhi Marma controlling
Raktavaha Srotas, so that it controls functions of liver and spleen.
The prominent median cubital vein links cephalic and basilic vein. It receives
number of tributaries from the front of the forearm and gives off the median vein,
which pierces the fascial roof of anterior cubital fossa to join the venae commitantsof
brachial artery. So the vein recommended for Siravyadha may be right sided medial
cubital vein.
The word ‘Dalana’ means laceration and ‘Bhedana’ means ‘cleavage’ or
splitting. So it becomes apparent that a pathological condition in which ‘Yakrit’ gets
structurally damaged by continued cleavage due to vitiated Doshas especially Rakta
and Kapha, where it often enlarges the liver called “Yakridalyudara”.
Nidana :
1. Excessive intake of Vidahee and Abhishyandi Ahara are the main aetiological
factors of Yakridalyudara.
2. Riding on the animals, vehicles, after taking food causing aggressive
movements of the body.
3. Excessive hard work, excessive and walking, lifting heavy weights.
4. Apart from the above, the quantitative and qualitative vitiation of Rakta
Dhatu is also focused to cause ‘Yakridalyudara’.
Samprapti :
Due to above said pathological factors ‘Rakta’ and ‘Kapha’ get vitiated which
cause Vriddhi of Yakrit called Yakriddalyudara.
Charakacharya stresses on the point that, Yakrit Sthana-chyuti or Vriddhi is
taking place as there is gradual vitiation of Rasa and Rakta. He says further that the
‘Yakritvriddhi’ is Kathina like Astheela in later stages and gets the shape of tortoise
shell in advanced stage.
Laxana :
Roganusar Siravyadha Sthana
54
1. Yakrit Vriddhi
2. Manda Jvara
3. Pandu
4. Mandagni
5. Aruchi
6. Mutraghata
7. Angamarda
8. Moorcha.
Types :
1. Vataja
2. Pittaja
3. Kaphaja
4. Sannipataja
5. Raktaja
Vataja, Pittaja, Kaphaja and Sannipataja are Aushadha Sadhya and Raktaja –
Shastrasadhya. 129
Usually liver is an important solid organ where different chemical reactions
are taking place and acts a blood reservoir, whatever the etiological factor that causes
enlargement of liver is called hepatitis which may correlated to Yakrudalyudara.
Aetiologies :
1. Viral (Hepatitis B)
2. Bacterial
3. Chronic alcoholism
4. Metabolic disorder like hypolypedaemia
5. Hepatotoxic drugs
Pathology :
The liver enlargement takes place in three different stages.
1. Fatty liver : As liver acting on a metabolism of the fatty acids,
macroscopically liver looks like pale or light yellow and feels like greasy.
Hepatocytes are enlarge 2-3 times of their normal diameter. The enlargement
of hepatocytes is not only lipids but also increase in their protein and water
content. Often the mitochondria are dilated and distorted. Sever fatty change
leads fibrosis where there is thickening of wall of some central hepatic vein.
Sometimes minor fibrosis around terminal hepatic vein.
Roganusar Siravyadha Sthana
55
Clinically, it goes undiagnosed later there may be features like
epigastric pain, nausea, vomiting, jaundice and non-tender hepatomegaly.
2. Hepatitis : It is nothing but greater extent of hepatocellular necrosis. Usually
injuries are greater in terminal hepatic vein. Because oxygen tension is
decreased in this part of the liver. And most of enzymes are active in the
hepatocytes around the hepatic veins.
Sometimes, hepaticytes are ballooned and shrinked. Mitochondria are
swollen and distorted. Mitochondria are commonly found in hepatocytes
around central hepatic vein. The adventitia of the terminal hepatic vein is
edematous. As fibrosis developed around terminal hepatic vein narrows or
occludes them.
Clinically, anorexia, nausea, vomiting, fever, fatigue, abdominal
discomfort, tender hepatomegaly, raised SGOT and SGPT levels.
3. Cirrhosis : Liver becomes shrinkened with abnormal architecture. Because of
continues necrosis replaced fibrosis resulting into fibrosis. Collagenous septa
is irregular around the terminal hepatic vein. Clinically anorexia, weightloss,
weakness, malnourishment, jaundice, malnutrition, oesophagial and rectal
bleeding firm hepatomegaly and gynecomastia. 130
Critics :
Because of involvement of Kapha and Raktadusti, there is right upper
abdominal swelling called Yakrutalodara. The Raktamokshana is done in Dakshina
Kurpara Sandhisthita Sira, it has to resolve Rakta and Kapha Doshas. The condition
can be correlated to ‘hepatomegaly’. The blood letting helps to mobilize the fatty
acids deposited in the liver by the secretion of steroid hormones. Liver congestion is
decreased, portal venous tension is decreased. Enzymatic activity of hepatic cells is
increased resulting appetite, lack of nausea, fever etc. Providing the production of
fresh RBCs which are not fragile but active and living their normal life span,
performing their normal functions. In this way phlebotomy in right medial cubital
vein has got direct effect on liver.
KAPHODARA :
Roganusar Siravyadha Sthana
56
Kaphodara is a type of Udara, where predisposing factors are Avyayam,
Divasvapna, Adhika Madhura, Picchila, Dadhi, Dugdha Sevana. Avruta Vata
involving Kapha resulting into enlargement of abdomen outside the intestines.131
Here Laxanas like Aruchi, Angashoonata, Hastapada, Andakosha, Uru,
Shotha, Utklesha, Nidradhikya, Kasa, Shwasa. This condition may be correlated to
obesity. Obesity is nothing but the accumulation of fat in the body. When greater
quantity of energy in the form of food, enter the body than the expenditure, the body
weight increases. The precursor fat cells develop form a fibroblast like cell. The
enzyme glycoprotein lipase is detected in this cell type. Excess fat is associate with
hypertrophy of cell and hyperplasia. Abdominal obesity is more highly correlated
with metabolic complications. The pattern of abnormal adipose tissue development
can be altered by many changes. As the most of fat metabolism is done by liver. In
any impaired liver functions fat embolism is also impaired. 132
Critics :
In Kaphodara also Dakshina Kurpara Adhisthita Sira Siravyadha is done like
Yakrutodara. There is also involvement of Kapha, Rakta, Meda giving rise to
Kaphodara. Raktamokshana by Siravyadha helps in neutralizing Doshadusti.
When the same condition is correlated with obesity and the features are similar
to that of obesity. Where in obesity blood letting from right medial cubital vein helps
to mobilize fatty acids. As they help to improve the hepatocellular function. They
release certain enzymes of fat metabolism. So that might be the site dealt by the
Sushruta may be considered.
KASA ROGA :
Prakupita Pranavata is coming out through mouth producing a sound as if fall
of an utensil called Kasa. 81
Samprapti :
Bahya Nidanas (Dhoomopaghatadi) Pranavaha Srotas Khavaigunya and
Galasrotas Vataprakopa Pranavayudusti Nirgamana from Mukha Shuska
Kasa or Ardra Kasa. 133
Dosha: Dooshya Adhisthana :
Dosha : Vata Pradhana Kapha
Dooshya : Rasa, Swarayantra
Srotas : Rasavaha, Pranavaha
Adhisthana : Urah, Kantha
Roganusar Siravyadha Sthana
57
Srotodusti : Shotha, Sanga
Kasa is nothing but cough, which is reflex action as defense mechanism, may
be due to many causes. Ex : URI, CRI. Whenever there is any vitiation is respiratory
tract then there is cough.
Critics :
Here, Dakshina Kurpara Sandhisthita Siravyadha is done where Sanga in
Pranavaha Srotas may relieved and vititated Doshas may be neutralized. So Dakshina
Kurpara-Abhyantara Sthita Siramokshana is done.
When the site is correlated according to modern medicine. That right medial
cubital vein where pressure is venous tension is decreased pulmonary congestion may
be relieved.
SHWASA :
Urdhvagati of Vayu with Vega is called Shwasa, caused by Vata-Kapha
Prakopaka Ahara-Vihara.134
Samprapti :
By means of Mithyahara-vihara, Prakupita Pranavaha leading to its normal
function, associated with Kapha to cause Shwasa with efforts. 135
The condition may be leads to emphysema, CCF or hyperuraecemia.
By means of phlebotomy in medial cubital vein, the congestion of lungs and
liver is relieved blood flow in necessary fact is increased metabolism is maintained.
So it many help in above conditions. Here the Sushruta’s verdict can be accepted.
VISHWACHI :
When Prakupita Vata involves Bahu, Prushta, Hasta, Tala and Anguli-
Kandaras, then there is Karma Kshaya of Bahu. 82, 136
In Vishwachi (pain in the arms) will be similar to that of Grudhrasi, so four
Angula above or below the Kurpara Sandhi Siravyadha is done.
In Vishwachi Raktamokshana is done four Angula from Kurpara Sandhi
nearer to Bharvi (Urvi) Marma, which is controlling the healthy tissue growth,
Rasavaha, Udakavaha Srotas. Regarding the vein of the site four Angula above from
the Kurpara Sandhi may be basilic vein, which is a post-axial vein of upper limb, that
begins with the dorsal venous arch, runs upwards along the medial border of the
forearm. Ends around the elbow where it pierces the deep fascia and lastly runs
around the medial side of the brachial artery.
Roganusar Siravyadha Sthana
58
The site of Siravyadha may be four Angula below from the Kurpara Sandhi. It
is nothing but cephalic vein that begins from the lateral end of the dorsal venous arch.
It runs upwards winds around the lateral border of forearm, continues upwards along
the lateral border of biceps. It pierces deep fascia of pectoralis major. It pierces the
clavipectoral fascia and joints of axillary veins. 137
This is correlated to Brachial Plexus Neuritis. 138 Pain from the injury to the brachial
plexus of the arm can occasionally mimic pain of cervical origin.
Causes :
1. Neoplastic infiltration Ex: Ca breast
2. Horner’s syndrome
3. Infection by immunization
4. Pancost’s tumor of lung.
Symptoms :
1. Shoulder pain radiating down the arm
2. Numbness of the finger
3. Weakness of muscles, innervated by ulnar median nerve
4. Shoulder pain followed over weeks. By weakness of the proximal arm and
shoulder girdle muscle innervated by the upper brachial plexus
5. Muscle wasting and weakness resulting into flexion deformity.
Critics :
There is involvement of Vata, Which may effect Bahu, Hasta, Tala, Anguli,
when blood letting is done four Angula above or below Kurpar Sanhi, Vata may be
neutralized, giving strength to Kandaras. The condition is similar to brachial plexus
neuritis, where there is pain in arm, numbness in fingers, weakness of muscle,
shoulder pain, muscles wasting with flexion deformity.
Locally when blood letting is done in basilic vein, the pain precipitating
factors like lactic acid are reduced, blood supply to the brachial plexus is improved,
where there is aerobic metabolism in the part. There is provison of release of
serotonin also, which inhibits pain of neuritis. In this way blood letting site may
accepted.
TABLE NO. 12 SHOWING SITES FOR SIRAVYADHA OF DIFFERENT VYADHANA STHANAS PARTICULAR DISEASES IN UPPER LIMB
Roganusar Siravyadha Sthana
59
Sl. No. Vyadhis Vyadha Sthanas (I) Pleehodara Vama Kurpara Sandhisthita Sira
or Sira present in between left Kanishtika and Anamika Angulas
(II) Yakrudalyudara Kasa Shwasa
Dakshina Kurpara Sandhisthita Sira or Sira present in between right and Kanishtika and Anamika Angulis
(III) Vishwachi Four Angula above the ‘Kurpara Sandhi’
(IV) Apachi Two Angula below from ‘Indrabasti Marma’
Venous System
60
1. VENOUS SYSTEM
Veins are characterized by relatively thin wall and large capacitance compare
to arteries. The structural plan of the wall is similar to that of other vessels, where the
amount of muscle is considerably less than in arteries. In most veins, especially in the
limbs, muscle is arranged circularly. Longitudinal muscle is present in iliac, portal,
renal veins and in superior and inferior vena cava. On the contrary, muscular tissue is
absent in placental veins, retinal veins; but these veins are consisting of endothelium
supported by variable amount of connective tissue. Pressure within the venous system
doesn’t exceed 5 mm of Hg. As the vein grows larger it decreases upto zero. Because
they contain small amount of muscle and usually vein have limited influence on blood
flow. (Fig. 1)
Due to any cause when there is sudden fall in blood pressure, there is reflex
constriction in vein to compensate the blood loss and tend to maintain the venous
return to the heart. Most veins have valves to prevent reflux of blood flow. When
blood flow reverses, if the semilunar valves cusps, not close properly, then blood fills
in expanded valve of the vein giving rise to knotted appearance to the distended vein.
Leg venous return is against gravity. Valves are of great importance. Blood is moved
towards the heart by intermittent pressures produced by contractions of the
surrounding muscles are absent in thorax and abdominal veins. 139
General Organization of Circulatory System :
Cells of the peripheral blood suspended in the plasma circulate throughout the
body in blood vascular system. Interstitial fluid from peripheral tissue returns to the
blood vascular system through the lymphatic system, which is preceding a channel for
migration of leucocytes and absorption of certain nutrients from the gut. The
cardiovascular system carries nutrients, oxygen, hormones throughout the body and
disperses heat. As a result of pulse pressure which is a mechanical difference between
systolic and diastolic pressure.
Blood circulates in a closed system where heart is the central pump, arteries
carry the blood to the peripheral part, veins returns to the heart. From the centre to the
periphery, arteries increase in number by repeated bifurcation. The valves of arteries
decrease in thickening towards periphery. Venules which return blood from periphery
progressively increase in size. Arteries are usually deeply situated than vein. Overall
Venous System
61
blood from the heart to all parts of the body carries through a series of tubes. Smooth
muscle is contractile where actin and myosin are organized in regular semilunar
manner. These tubes are composed of smooth muscles. Smooth muscles typically
found in tubular structure and hollow viscera, the actual arrangement of cells varies
with tissue. Smooth muscle has no attachment structure to the fasiae, tendons etc.
Blood supply of smooth muscle is extensive than striated muscles. 140
Composition of Vein : (Fig. 2)
Veins are composed of essentially three coats as that of arteries. But there are
variations in their relative thickness. If arteries are to be distinguished from veins
following reasons may be given
- The wall of a vein is very thin than the artery.
- The tunica media contains much collagen than arteries. The amounts of elastic
tissue are much less.
- In arteries tunica media, usually thicker than the adventitia. In contrast the
adventitia of veins is thicker than the media. In some large veins the adventitia
contains a considerable amount of elastic and muscle fibres which run in a
predominantly longitudinal direction. These fibres facilitate elongation and
shortening of the vena cava with respiration.
- A clear distinction between the tunica intima, media and adventitia cannot be
made out in small veins as all these layers consist predominantly of fibrous
tissue. Muscle is conspicuous by its complete absence in venous spaces of
erectile tissue, in veins of cancellous bone, dural venous sinuses, retinal veins
and placental veins. 141
Microscopic Structure of Vein :
(I) Tunica Intima - Endothelium
The endothelium is a mono-layer extending continuously over the entire
vascular tree. It is a key component of vessel wall playing major physiological roles.
Endothelial cells regulate diffusion of substances and migration of cells out of and
into the circulating blood, as these are in contact with blood stream, so influencing
blood flow. Ex : in the brain, endothelial cells of small vessels actively transport
substance like glucose into the brain parenchyma. In the process of ‘fibrinolysis’ or
clot dissolution by secreting a tissue plasminogen activator by endothelial cells, and
they have got phagocytic activity. Endothelial cells synthesize components of basal
lamina. They proliferate to provide new cells during growth in size of blood vessel to
Venous System
62
replace the damaged cells. Angiogenesis is stimulated by endothelial production in
response to locally low oxygen tension. It is important in wound healing and in
growth of tumors.
So overall, all the blood vessels including vein are lined with endothelial cells.
Cells are polygonal and elongated along the length of vessels. These endothelial cells
are sensitive to alteration in blood pressure, blood flow and oxygen tension in the
blood. They secrete various substances that can produce vasodilation by influencing
the tone of the muscles in vessel wall. They produce factors which controls the
coagulation of blood. Under normal condition clotting is inhibited, when required
clotting is facilitated. Under influence of adverse stimuli [ex : cytokines it has been
seen that T-lymphocytes produce cytokines and affect other cells. The function of the
cytokines is to stimulate the production of blood cells. Apart from T-cells cytokines
are also produced by monocytes, macrophages, endothelial cells. Some cytokines are
identified as interlukins, granulocytes stimulating factors, stem cell factor,
erythropoietin] endothelial cells undergo certain changes which facilitates passage of
lymphocytes through the vessel wall. Ex : in acute inflammation, endothelium allows
neutrophils to pass from blood into surrounding tissue. By influence of histamine
(stimulated by antigen mast cells release histamine into tissue) endothelium becomes
highly permeable allowing proteins and fluid to diffuse into the tissue resulting to
oedema. The changes that they occur in endothelium described above are taking place
very rapidly within fraction of minutes.
(II) Tunica Media :
It consists of concentric layers of circumferentially arranged smooth muscle
cells, with variable amount of elastin and collagen. Smooth muscle forms most of the
media of arteries and arterioles. A thin layer of smooth muscle also found in venules
and veins. Smooth muscle cells synthesize and secrete elastin and collagen which bear
directly on mechanical properties of vessels like distensibility cells support, elasticity,
rigidity. The muscle cells can be regarded as multifunctional mesenchymal cells.
After damaged to the endothelium, muscle cells migrate into the intima and
proliferate to reform the layer. In certain pathological conditions, muscles undergo
fatty degeneration, or participate in formation of atheromatous plaque.
(III) Tunica Adventitia :
Venous System
63
This layer is formed by general connective tissue varying in the thickness.
Vasa Vasorum :
Nourishment of tissue of vessel wall is provided by blood circulating vessels
itself. Large vessels have own vasculae supply within adventitia, in the form of
network of vessels called vasa vasorum. Vasa vasorum orginate from and and drains
into adjacent vessels which are peripheral branches. 142
Developmental Anatomy of Blood Vessels : 143 (Fig. 3)
The human yolksac has little yolk to nourish the developing embryo, blood
and blood vessel. Formation starts as early as 15-16 days in the mesoderm of the
yolksac, chorion, and body stalk. Blood vessels develop from isolated masses and
cords of mesenchyma in the mesoderm called blood islands. Spaces soon appear in
the islands and become the lumens of the blood vessels. Some of the mesenchymal
cells immediately around the spaces give rise to the endothelial lining of the blood
vessels. Mesenchyme around the endothelium forms the tunis of the larger blood
vessels. Growth and fusion of blood islands form an extensive network of blood
vessels throughout the embryo.
Development of Veins : The cardiovascular system is the first major system to function in the embryo.
The primordial heart and vascular system appear in the middle of the third week of
embryonic development. The heart starts to function at beginning of fourth week. This
precocious heart development is necessary because the rapidly growing embryo can
no longer satisfy it’s nutritional and oxygen requirement by diffusion alone.
Consequently, there is a need for an efficient method of acquiring oxygen and
nutrients from the maternal blood and disposing of carbon dioxide and waste
products.
Angiogenesis or blood vessel formation, begins in the extra-embryogenic
mesoderm of the yolksac, connecting stalk, and chorion. Embryonic blood vessels
begin to develop about two days later. The early formation of the cardiovascular
system is correlated with the absence of a significant amount of yolk in oocyte and
yolksac and the consequent urgent need for blood vessels to bring oxygen and
nourishment to the embryo from the maternal circulation through the placenta. At the
end of the second week, embryonic nutrition is obtained from the maternal blood by
diffusion through the extra embryonic coelom and yolksac. During the 3rd week and
Venous System
64
primordial uteroplacental circulation develops. Primordial blood vessels cannot be
distinguished structurally as arteries or veins, but are named according to their future
fates and relationship to the heart.
The formation of the embryonic vascular system involves two processes :
vasculogenesis and angiogenesis. Blood vessel formation in the embryo and
extraembryonic membranes during the 3rd week may be summarized as follows:
- Mesenchymal cells differentiate into endothelial cells precursor - angioblasts
(vessel-forming cells), which aggregate to form isolated angiogenic cell
clusters-blood islands.
- Small arteries appear within the blood islands by confluence of intercellular
clefts.
- Angioblasts flatten to form endothelial cells that arrange themselves around
the cavities in the blood island to form the endothelium.
- These endothelium lined cavities soon fuse to form networks of endothelial
channels. (vasculogenesis).
- Vessels sprout into adjacent areas by endothelial budding and fuse with other
vessels (angiogenesis).
Blood cells develop from the endothelial cells of vessels (hemangioblasts) as
they develop on the yolk sac and allantois at end of the third week. Blood formation
does not begin in the embryo until the 5th week. It occurs first in the various parts of
the embryonic mesenchyme, chiefly the liver and later in the spleen, bone marrow and
lymph nodes. Fetal and adult erythrocytes are derived from the different
hematopoietic progenitor cells. The mesenchymal cells surrounding the primordial
endothelial blood cells differentiate into the muscular and connective tissue elements
of the vessels. The earliest sign of the heart is appearance of pair endothelial strands -
angioblastic cords in the cardiogenic mesoderm during the 3rd week. These cords
canalize to form heart tubes, which fuse to form the tubular heart late in the 3rd week.
The heart begins to beat at 23rd day. An inductive influence from the anterior
endoderm stimulates early formation of the heart. The development of heart and blood
vessels is controlled by a cascade of regulatory genes and signaling molecules.
Three paired veins drain into the tubular heart of a four-week embryo -
- “Vitelline veins” return poorly oxygenated blood from the yolksac.
- “Umbilical veins” carry oxygenated blood from the primordial placenta.
Venous System
65
- “Common cardial veins” return poorly oxygenated blood from the body of the
embryo.
The vitelline veins follow the yolk stalk into the embryo. The yolk stalk is the
narrow tube connecting the yolksac with the midgut. After passing through the
septum transversum, the vitelline veins enter the venous end of the heart - the “sinus
venosus”. As the liver primordium grows into the septum transversum the hepatic
cords anastomose around pre-existing endothelium lined spaces. These spaces, the
primordial of the “hepatic sinusoids”, later become linked to the vitelline veins. The
“hepatic veins” form from the remains of the right vitelline vein in the region of the
developing liver.
The portal vein develops from an anastomosis network formed by the vitelline
veins around the duodenum.
The ‘umbilical veins’ run on each side of the liver and carry well oxygenated
blood from the placenta to the sinus venosus. As the liver develops, the umbilical
veins lose their connection with the heart and empty into liver. The right umbilical
vein disappears during the seventh week, leaving the left umbilical veins as the only
vessel carrying well-oxygenated blood from the placenta to the embryo.
Transformation of the umbilical veins may be summarized as follows ;
- The right umbilical vein and the caudal part of the left umbilical vein between
the liver and sinus venosus degenerate.
- The persistent caudal part of the left umbilical vein becomes the umbilical
vein, which carries all the blood from the placenta to embryo.
- A large venous shunt - the ductus venosus develops within the liver and
connects the umbilical vein with the inferior vena cava.
The cardinal veins constitute the main venous drainage system of the embryo.
The anterior and posterior cardinal veins drain cranial and caudal part of the embryo,
respectively. The anterior and posterior cardinal veins join the common cardinal
veins, which enter the sinus venosus. During the 8th week of embryonic development,
the anterior cardinal vein becomes connected by an anastomosis which shunts blood
from the left to the right anterior cardinal vein. This anastomotic shunt becomes the
left brachio-cephalic vein when caudal part of the left anterior cardinal vein
degenerates. The superior vena cava forms from the right anterior cardinal vein and
the right common cardinal vein.
Venous System
66
The posterior cardinal veins develop primarily as the vessels of the
mesocephalic (interim kidneys) and largely disappears with this transitory kidneys.
The only adult derivatives of the posterior cardinal veins are the root of the azygos
vein and the common iliac veins. The subcardinal and supracardinal veins gradually
replace and supplement the posterior cardinal veins. The sub-cardinal vein appears
first. They are connected with each other through the subcardinal anastomosis and
with the posterior cardinal veins through the nephric sinusoids. The sub-cardinal veins
form the stem of the left renal vein, the suprarenal veins, the gonadal veins and
segment of IVC. The supracardinal veins are the last pair of vessels to develop. They
become disrupted in the region of the kidneys. Cranial to this, they become united by
the an anastomosis i.e. represented in the adult by the azygos and hemi-azygos veins.
Caudal to the kidneys, the left supracardinal veins degenerates, but the right
supracardinal veins becomes the inferior part of the IVC.
Development of Superior Vena Cava : 144
The precardinal veins enlarge as the head and brain develop. They are further
augmented by the subclavian veins from the upper limb buds, and so become the chief
tributaries of the common cardinal veins, which gradually assume an almost vertical
position in association with the descent of the heart into the thorax. That part of the
original precardinal vein rostral to the subclavian is now the internaljugular vein, and
their confluence is the brachio-cephalic vein of each side. The right and left common
cardinal veins are originally of the same diameter. By the development of a large /
transverse connection, the left brachio-cephalic vein carries blood across from the left
to the right. The part of the original right precardinal vein between the junction of the
two brachio-cephalic and azygos veins forms the upper part of the superior vena cava,
the caudal part of the latter vessel is formed by the right common cardinal vein.
Caudal to the transverse branching of the left brachio-cephalic the left precardinal and
left common cardinal veins largely atrophy, the former constituting the terminal part
of the left superior intercostal vein; while the latter is represented by the ligament of
the left vena cava and the oblique vein of the left atrium. The remainder of the left
superior intercostal is developed from the cranial end of the post cardinal vein and
drains the second, third, on occasion the fourth intercostal veins. The oblique vein
passes downwards across the back of the left atrium to open into the coronary sinus
which, as already indicated, represents the persistent left horn of the sinus venosus.
Venous System
67
Right and left superior venae cavae are present in some animal and occasionally in
mankind.
Development of Inferior Vena Cava :
The inferior vena cava (IVC) forms during a series of changes in the
primordial veins of the trunk that occur as blood, returning from the caudal part of the
embryo, is shifted from the left to the right side of the body. The IVC is composed of
four main segments
- A hepatic segment derived from the hepatic vein (proximal part of right
vitelline vein) and hepatic sinusoids.
- A prerenal segment derived from the right subcardinal vein.
- A renal segment derived from the subcardinal-supracardinal anastomosis.
- A postrenal segment derived from the right supracardinal vein.
The early postcardinal veins communicate across the midline via an inter-post-
cardinal anastomosis between the iliac veins, and become the major part of the
definitive left common iliac vein. It diverts an increasing volume of blood into the
right longitudinal veins, which accounts for the ultimate disappearance of the most of
those on the left.
The supracardinal veins receive the larger venous drainage of the growing
body wall. The right supracardinal vein persists and forms the greater part of the post
renal segment of the IVC. The continuity of the vessel is maintained by the
persistence of the anastomosis of between the right supracardinal and right
subcardinal vein in the renal collar.
In summary, therefore, the inferior vena cava is formed from below upwards
by the confluence of common iliac veins; short segment of the right postcardinal vein,
the postcardinal-supracardinal anastomosis, part of the right supra-cardinal vein, a
new anastomotic channel of double origin, the hepatic segment of the inferior vena
cava; and the cardiac termination of the right vitelline hepatocardiac vein.
Physiology of Veins
68
2. PHYSIOLOGY OF VEINS
Usually physiology explains the physical and chemical factors that are
responsible for the origin, development and progression of life. The human
physiology is concerned, we are concerned with specific characteristics and
mechanisms of the human body, that make it a living being.
The basic unit of the body is cell. Each type of cell is specially adopted to
perform functions. About sixty percent of the adult human body fluid inside the cell is
called intra-cellular fluid. About one third is in space outside the cell is called
extracellular fluid. This extracellular fluid is in constant motion throughout the body.
It is rapidly transported in circulating blood and mixed between blood and tissue fluid
by diffusion. In extracellular fluid nutrients needed by the cells for maintenance of the
their life. Extracellular fluid is called internal environment of the body. The
extracellular fluid cells those are capable of living, growing, performing need proper
concentration of o2, glucose, ions, amino acids, fatty acids and other nutrients.
Extracellular fluid contains sodium, chloride, bicarbonate, oxygen, glucose, fatty
acids, amino acids. It also contains carbon dioxide, which is transported from cells to
the lungs. The intracellular fluid differs completely. It contains Potassium, phosphate,
Magnesium etc.
Homeostasis: 145
The term homeostasis is maintenance of constant internal environment so that
all the tissues of the body perform their function to maintain constant conditions;
where lungs provide oxygen to the extracellular fluid, kidneys, maintain ion
concentration, GIT provides nutrition. So collectively all together is homeostasis.
Usually extracellular fluid is transported through all parts of body in two stages : one
is movement of blood in and around circulatory system, movement of fluid between
the capillaries and cells [Guyton Fig. 1.1].
As the blood passes through the capillaries there is continuous exchange of
extracellular fluid, that occurs between plasma of portion of blood and interstitial
fluid, which fills intercellular spaces [Fig. 1.2] Note that capillaries are porous, so that
large amount of fluid and its dissolved constituents can diffuse back between blood
and tissue spaces. This process of diffusion is caused by kinetic motion of molecules
in both plasma and interstitial fluid.
Physiology of Veins
69
Thus the extracellular fluid is continuingly being mixed, there by maintaining
almost homeostasis of the body. When blood passes throughout the body, it passes
through lungs also, blood picks up oxygen in alveoli needed by cells. The oxygen
diffuses by molecular motion through this membrane into the blood. In the same way
water and ions diffuse through tissue capillaries. A large portion of blood pumped by
the heart passes through the walls of the GI tract organs where different dissolved
nutrients are absorbed from the ingested food into the extracellular fluid. All the
substances absorbed from GIT not utilized from the cells. The liver changes the
chemical composition of these substances to more usable from to all tissues. At the
sometime blood picks up o2 from the lungs, CO2 released blood into alveoli, so that
the co2 is most abundant end product of metabolism. Passage of blood through
kidneys removes most of the substances like CO2, urea, uric acid, excess ions and
water. The human body is literally thousands of control systems in it. But the most of
significant of these is genetic controlled system. Many others control system operate
by nervous and humoural regulations (chemical).
Oxygen is one the major substance required for the chemical reactions in the
cells. It is god gift that body has special control mechanism to maintain exact constant
o2 concentration in the extracellular fluid. It is principally depending on chemically
characteristics of hemoglobin present in RBCs. Hemoglobin combines with o2 as
blood passes through the lungs. Then blood passes through the capillaries. Because of
its strong chemical affinity, it doesn’t release the oxygen to tissue fluid, if too much
oxygen is already there. If oxygen concentration is too low there sufficient oxygen is
released for adequate oxygen concentration. Like this carbon dioxide concentration in
the extracellular fluid is also essential. This is end product of the oxidative reaction in
cells. If all carbon dioxide formed in the cells accumulate in tissue fluids, exciting
respiratory centres causing to breath deeply and rapidly. So several systems like baro-
receptor systems, and chemical receptor systems are responsible for it.
An Overview of Circulation: 146 [Fig. 4 (a)]
The function of circulation is to serve the needs of the tissue such as nutrients,
o2, hormones and also to transport waste products away, in general to maintain an
appropriate environment in all the tissue fluids for survival and function of the cells.
Sometimes it is difficult to understand how blood flow is controlled according to
tissue needs.
Physiology of Veins
70
The circulation is divided into (1) systemic circulation and (2) pulmonary
circulation. Systemic circulation supplies all the tissues of the body except the lungs
with blood flow, it is called peripheral circulation. The vascular system in each
separate tissue of the body has its own special characteristics, some general principles
of vascular system apply in all the parts of the body. The function of arteries is to
transport blood under high pressure to the tissues. As arteries have strong vascular
walls, so blood flows rapidly in arteries. The arterioles are the last small branches of
the arterioles system and they act as control valves through which blood is released
into the capillaries. The arteriole has the strong muscular wall, capable of closing and
dilating, having capability of vastly altering blood flow to the capillaries in response
to the need of the tissues. The function of the capillaries is to exchange the fluid
nutrients, fluids, electrolytes, hormones and other substances between the blood and
interstitial fluid. For this purpose the capillary walls are very thin and permeable to
small molecule substances. The venules collect blood from the capillaries, which
gradually coalesce into progressive larger veins. The veins function as conduits for
transport of blood from tissues back to the heart and serve as the major reservoir of
the blood, because the pressure in venous system is very low. The venous walls are
thin. Depending upon the needs of the body they also contract and expound.
Volumes of Blood in Different parts of Body : [Fig.4(b)]
64 % in veins, 13% in arteries, 7% in arterioles and capillaries, 7 % in heart
and 9 % in pulmonary vessels.
Cross Sectional Areas of the Blood Flow :
Aorta 2.5 cm2
Small Arteries 20 cm2
Arteries 40 cm2
Capillaries 2500 cm2
Venuoles 250 cm2
Small veins 80 cm2
Venae cavae 8 cm2
Crosssectional areas of vein are much larger than the arteries which explains
large storage of blood in venous system. The same volume of blood flows through
each segment of circulation each minute. The velocity of blood flow is inversely
proportional to its crossectional area.
Basic Theory of Circulatory Function :
Physiology of Veins
71
When tissues are active, they need more blood flow. Heart normally cannot
increase its cardiac output more than 4-7 times. Therefore, it is not possible to
increase blood flow everywhere in the body. When a particular tissue demands
increased flow. Instead, micro-vessel of each tissue are monitoring the tissue needs,
such as availability of oxygen and other nutrients and the accumulation of waste
products. And these in turn control local blood flow to the level of tissue need. The
cardiac output is controlled mainly by the sum of all local tissue flows. When blood
flows through a tissue it immediately returns by the way of veins to the heart. The
heart responds to this increased inflow by pumping all the blood immediately back to
the arteries.
Vascular Distensibility: 147
The valuable characteristic of blood vessels is that they are distensible. Ex :
when a pressure in arterioles is increased this dilates, the arterioles. Therefore,
decreases their resistance. The result is increased blood flow, not only because of
increased pressure, but also because of decreased resistance.
The distensibility of arteries and veins are different. Anatomically the walls of
arteries are far stronger than those of veins. Consequently, veins are eight times
distensible as the arteries. That means, a given in rise of pressure causes about eight
times much extra blood to fill a vein as to fill an artery.
Effect of Sympathetic Stimulation or Inhibition on Blood Vessels :
Large changes are observed in blood flow caused by increased or decreased
sympathetic stimulation. Because inhibition of sympathetic stimulation greatly dilate
the vessels and can increase the blood flow. Conversely, strong sympathetic
stimulation can constrict the vessels so much that blood flow can be decreased as low
as zero.
Regarding volume, pressure, relations are concerned, sympathetic stimulation
increases vascular smooth muscle tone, where it increases pressure at each volume of
arteries or veins; where as sympathetic inhibition decreases the pressure at each
volume. For an instance, increase in vascular tone throughout systemic circulation
often causes large volume of blood to shift into the heart, which is a reason for
increased heart pumping, sympathetic controls of vascular capacity is especially
important during loss of blood [hemorrhage]. Enhancement of sympathetic tone of
vessels, especially of veins reduces, the vessel sizes, so that the circulation continues
to operate almost normally even when 25% of total blood volume has been lost.
Physiology of Veins
72
Veins and their Functions: 148
For years, the veins have been considered to be nothing more than passage
ways, for flow of blood into the heart. But it is becoming apparent that they perform
many special functions that are necessary to the operation of circulation. They are
capable of constricting and enlarging, there by storing small or large quantity of blood
and making this blood available when it is required by the circulation. Vein can also
propel blood forward by means of which called venous pump, which will regulate
even cardiac output.
To understand various functions of vein is necessary to know the pressures in
the vein and how they are regulated. Blood from all systemic veins flows into right
atrium so the pressure in the right atrium is called central venous pressure. Anything
that affects right atrial pressure definitely affect venous pressure everywhere in the
body. Right atrial pressure is regulated by balance between the ability of the heart to
pump blood out of the right atrium and tendency for blood to flow from the peripheral
vessels back into the right atrium. The normal right atrial pressure is about zero mm
of Hg which is equal to the atmospheric pressure of the body. It can rise to 20-30 mm
of Hg under abnormal condition, where there is serious heart failure and massive
transmission of blood.
Large veins have little resistance to the blood flow, when they are distended.
The large veins usually offer considerable resistance to the blood flow, because of this
the pressure in the peripheral veins is 4-7 mm of Hg. that is greater than the right
atrial pressure. This central pressure is regulated by right atrial pressure, peripheral
venous pressure, pressure of abdominal vein and venous pressure of the leg.
Effect of Hydrostatic Pressure on Volume Pressure :
In any body of water, the pressure at the surface of the water is equal to
atmospheric pressure, but the pressure rises one mm of Hg for each 13.6 mm distance
below the surface. This pressure results from the weight of the water and therefore is
called hydrostatic pressure. Hydrostatic pressure also occurs in the vascular system of
the human being because of the receipt of the blood in the vessels, when a person is
standing, the pressure in the right atrium remains about ‘0’ mm of Hg because the
heart pumps into the arteries any excess blood that attempts to accumulate at this
point. However, in an adult who is standing absolutely still, the pressure in the veins
of the feet is about + 90 mm of Hg. Simply because of the hydrostatic weight of the
Physiology of Veins
73
blood in the veins between the heart and the feet. The venous pressures at other levels
of the body to proportionately between zero and 90 mm of Hg.
In the arm veins, the pressure at the level of the top rib is usually about + 6
mm of Hg, because of compression of the subclavian vein as it passes over the this
rib. The hydrostatic pressure down the length of the arm is then determined by the
distance below the level of this rib. Thus, if the hydrostatic difference between the
level of the rib and the hand is 29 mm of Hg. This hydrostatic pressure is added to the
6 mm of Hg pressure caused by compression of the vein as it crosses the rib, making a
total of 35 mm of Hg pressure in the veins of the hand.
The neck veins of an upright person collapse almost completely all the way to
the skull owing to atmospheric pressure on the outside of the neck. This collapse
causes the pressure in these veins to remain zero along their entire extent. The reason
for this is that any tendency for the pressure to rise above this level opens the veins
and allows the pressure to fall back to zero because of increased flow of the blood. On
the other hand, any tendency for the pressure to fall below this level collapses the
veins still more, which increases their resistance and again returns the pressure back
to zero.
The veins inside the skull, however, are in a non-collapsible chamber and they
will not collapse consequently, negative pressure can exist in the dural sinuses of
head, in the standing position, the venous pressure in the sagital sinus is about – 10
mm of Hg, because of the hydrostatic “suction” between the top of the skull and the
base of the skull. Therefore, if the sagital sinus is opened during surgery, air can be
sucked immediately into this vein; the air may even pass downward to cause air
embolism in the heart, so that the heart valves will not function satisfactorily, and
death can ensue.
Venous Valves and the “Venous Pump” their Effects on Venous Pressure:
Were it not for valves in the veins, the hydrostatic pressure effect would cause
the venous pressure in the feet always to be about + 90 mm of Hg in standing adult.
However, every time one moves the legs, one tightens the muscles and compresses
the veins either in the muscles or adjacent to them, and this squeeze the blood out of
the veins. The valves in the veins, are arranged so that the direction of blood flow can
be only toward the heart. Consequently, every time a person moves the legs or even
tenses the muscles, a certain amount of blood is propelled toward the heart and the
pressure in the veins is lowered. This pumping system is known as the “venous pump:
Physiology of Veins
74
or the “muscle pump”, and it is efficient enough that under ordinary circumstances,
the venous pressure in the feet of a walking adult remains close to or less than 25 mm
of Hg.
If a human being stands perfectly still, the venous pump doesn’t work, and the
venous pressures in the lower part of the leg will rise to the full hydrostatic value of
90 mm of Hg in about in 30 seconds. The pressure in the capillaries also increase
greatly causing fluid to leak from the circulatory system into the tissue spaces. As a
result, the legs swell, and the blood volume diminishes, indeed, 10-20 % of the blood
volume can be lost from the circulatory system within the first 15 minutes of standing
absolutely still, as often occurs when a soldier is made to stand at attention.
Venous Pressure Incompetence and Varicose Veins :
The valves of the venous system frequently become “incompetent” or
sometimes are even destroyed. This is especially true when the veins have been
overstretched by excess venous pressure lasting weeks or months, as occurs in
pregnancy or when one stands most of the time. Stretching the veins increases their
cross-sectional areas, but the leaflets of the valves no longer close completely. When
this develops, the pressures in the veins of the legs increases still more owing to
failure of venous pump; this further increases the size of the veins and finally destroys
the function of the valves entirely. Thus the person develops “varicose veins”, which
are characterized by large bulbous protrusions of the veins beneath the skin of the
entire leg and particularly the lower leg. The venous and capillaries cause constant
edema in the legs whenever these people stand for more than a few minutes. The
edema inturn prevents adequate diffusion of nutritional materials from the capillaries
to the muscle and skin cells, so that the muscles become painful and weak the skin
frequently becomes gangrenous and ulcerates. The best treatment for such a condition
is continual elevation of the legs to a level at least as high as the heart, but tight
binders on the legs are also of considerable aid in preventing the edema and its
sequelae.
Blood Reservoir and Function of Vein :
Venous system serves as blood reservoir for the circulation when blood is lost
from the body and arterial pressure begins to fall, pressure reflexes are elicited from
carotid sinuses and other pressure sensitive areas of circulation. These inturn send
sympathetic nerve signals to the veins causing them to constrict. So even after as
Physiology of Veins
75
much as 20 % of total blood volume has been lost. The circulatory system often
functions almost normally because of reservoir function of veins.
Specific Blood Reservoirs :
Certain portions of circulatory system are extended to some other portions
called blood reservoirs. These include spleen, liver, large abdominal veins, venous
plexus, beneath the skin altogether contribute more than thousand ml of blood.
The Spleen as a Reservoir for Storing Red Blood Cells : [Fig. 4 (c)]
The spleen has two separate areas for storing blood; the venous sinuses and
pulp. Small vessels flow directly into the venous sinuses, and the sinuses can swell the
same as any other part of the venous system and store whole blood. In the splenic
pulp, the capillaries are so permeable that whole blood oozes through the capillary
walls into a trabeculae mesh forming the red pulp. The red cells are trapped by the
trabeculae, where as the plasma returns into the venous sinuses and then into general
circulation. As a consequence, the red pulp of the spleen is as special reservoir of
extra red blood cells that are expelled into the general circulation when the
sympathetic nervous system is excited and contracts the spleen or its vessels. In the
lower animals, this extra-storage of red blood cells is much greater than in humas, but
in even in the human, possibly much as 50 millions of concentrated red blood cells
can be released into the circulation, raising the hematocrit 1-2 %.
In other areas of the splenic pulp are islands of white blood cells, which
collectively are called the white pulp. Here lymphoid cells are manufactured similar
to those manufactured in the lymph nodes. They are part of the body’s immune
system. Blood Cleansing Function of the Spleen - Removal of Old Cells :
Blood passing through the splenic pulp before it enters the sinuses undergoes
thorough squeezing. Therefore, it is to be expected that fragile red blood cells would
not withstand the trauma. For this reason, many of the red blood cells destroyed in the
body have their final demise in the spleen. After the cells rupture, the released
hemoglobin and the cells stroma are ingested by the reticuloendothelial cells of the
spleen.
Reticuloendothelial Cells of the Spleen :
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76
The pulp of the spleen contains many large phagocyte reticuloendothelial cells
and the venous sinuses are lined with similar cells. These cells act as a cleansing
system for the blood, acting in concert with a similar system in the venous sinuses of
the liver. When the blood is invaded by infectious agents, the reticuloendothelial cells
of the spleen rapidly remove debris, bacteria, parasites, and so forth. Also, in many
infectious processes, the spleen enlarges in the same manner the lymph glands enlarge
and then erforms its cleansing function even more adequately.
Microcirculation
77
3. MICROCIRCULATION
The most purposeful function of the circulation occurs by the transport of
nutrients to the tissues and removal of cellular excreta. The small arterioles control the
blood flow to each tissue area. The most instances controls its own blood flow its
relation to its needs.
The capillaries are extremely thin structures with walls of a single layer of
highly permeable endothelial cells. Here interchange of nutrients of cellular excrita
occurs between the tissues and circulating blood. about 10 billion capillary with a
total surface area estimated to be 500-700 mm of sq mt. It is very essential to know
the factors that they affect the transfer of fluid through capillary walls between
circulating blood and interstitial fluid.
Anatomy of Microcirculation149 :
The microcirculation of each part of the body is specifically serve special
needs of that part. In general arteries become small enough to be called arterioles,
which generally have internal diameter less than 20 micrometers. The
microcirculation of each organ specifically organize to serve organ special needs. As
arteries become small enough to become arteries then blood enters from arteriole to
capillaries and leaves by the way of venule, the venules are considerably larger than
the arterioles and have a much weak muscular coat. Blood causally doesn’t flow
continuously through the capillaries. Instead it flows intermittently turning on and off
every few seconds. The most important factor found thus far to affect he degree of
opening closing off meta arterioles and pre-capillaries sphincter (Fig 16.2) is the
concentration of oxygen in tissues. When the rate of oxygen use is great the
intermittent periods of blood flow occur more often there by allowing the blood by
carrying increased qualities of oxygen to the tissues.
There is an average rate of blood flow through tissue capillary bed and an
average rate of transfer of substances between the blood of the capillaries and the
surrounding interstitial fluid. Billions of individuals capillaries are responding to the
local condition to the tissue.
Exchange of Nutrients Blood and Interstitial Fluid :
Microcirculation
78
Diffusion through the capillary membrane : [Fig. 4 (d)]
Substance are transferred between plasma and interstitial fluid is by diffusion.
Blood transverses the capillary, tremendous number of water molecules and dissolved
particles move through the capillary wall. Diffusion results from thermal motion of
water molecules and dissolved substances in the fluid. Different particles moving first
into one direction and then in another direction.
Lipid soluble substances can diffuse directly through the cell walls of capillary
endothelium. If a substance is lipid soluble it can diffuse directly through the cell
membrane of capillary without having to go through the pores. The substances
include oxygen carbon dioxide as great as the rate at which plasma itself flows
linearly along the capillary. That is, the water of the plasma is exchanged with water
of the interstitial fluid 80 times before the plasma can go the entire distance through
the capillary.
Effect of Molecular Size of Passage through Pores :
The width of capillary intercellular cleft-pores, 6-7 nanometer, is about 20
times the diameter of the water molecule, which is the smallest molecule that
normally pass through the capillary pores. On the other hand, the diameters of plasma
protein molecules are slightly greater than the width of the pores. Other substances
such as sodium ions, chloride ions, glucose, and urea, have intermediate diameters.
Therefore, the permeability of the capillary pores for different substances varies
according to their molecular diameters.
The capillaries in different tissues have extreme differences in their
permeabilities. For instance, the membrane of the liver capillary sinusoids is so
permeable that even plasma proteins pass freely through these walls almost as easily
as water and other substances. Theses substances can permeate all areas of the
capillary membrane, the rate of transport through the capillary membrane are many
times the rates for most lipid-insoluble substances such as sodium ions and glucose.
Water-Soluble Substances Diffuse Only through Intercellular “Pores” in the
Capillary Membrane :
Many substances needed by the tissues are soluble in water but cannot pass
through the lipid membranes of the endothelial cells, such substances include water
molecules themselves, sodium ions, chloride ions, and glucose. Despite the fact that
not more than 1/1000 of the surface area of the capillaries are represented by the
intercellular cleft between the endothelial cells, the velocity of thermal molecular
Microcirculation
79
motion in the cleft is so great that even this small area is sufficient to allow
tremendous diffusion of water and water soluble substances through these cleft-pores.
To give one an idea of the rapidity with which these substances diffuse, the rate at
which water molecules diffuse through the capillary membrane is about 80 times.
Also the permeability of the renal glomerulae and muscle permeabilities for protein
are about the same. The degrees of capillary permeability are greater in liver, for
instance, to transfer tremendous amounts of nutrients between the blood and the liver
parenchymal cells and the kidneys to allow filtration of large quantities of fluid for the
formation of urine.
Effect of Concentration of Difference on Net Rate of Diffusion through the
Capillary Membrane :
The ‘net’ rate of diffusion of a substance through any membrane is
proportional to the concentration difference between the two sides of the membrane.
That is, the greater the difference between the concentrations of any given substance
on the two sides of the capillary membrane, the greater will be the net movement of
the substance in one direction through the membrane. Thus, the concentration of
oxygen in the blood is normally greater than that in the interstitial fluid. Therefore,
large quantities of oxygen normally move from the blood toward the tissues.
Conversely, the concentration of carbon dioxide is greater in the tissues than in the
blood which causes carbon dioxide to move into the blood and to be carried away
from the tissues.
The rates of diffusion through the capillary membranes of most nutritionally
important substances are so great that only slight concentration differences suffice to
cause more than adequate transport between the plasma and interstitial fluid. For
instance, the concentration of oxygen in the interstitial fluid immediately outside the
capillary is probably no more than 1 % less than the concentration in the plasma of
blood, and yet this 1 % difference causes enough oxygen to move from the blood into
the interstitial spaces to provide all the oxygen required for tissue metabolism.
The Proteins in the Plasma and Interstitial Fluid mainly Determine the Plasma and
Interstitial Fluid Volume :
The pressure in the capillaries tends to force fluid and its dissolved substances
through the capillary pores into the interstitial spaces. In contrast, osmotic pressure
caused by the plasma protein tends to cause fluid movement by osmosis from the
interstitial spaces into the blood, this osmotic pressure prevents significant loss of
Microcirculation
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fluid volume from the blood into the interstitial spaces. Also important is the
lymphatic system, which returns back to the circulation the small amounts of protein
that do leak into the interstitial spaces.
The Interstitium and Interstitial Fluid :
The about one sixth of the body consists of spaces between cells, which
collectively are called the interstitium. The fluid in these spaces is the interstitial fluid.
The structure of the interstitium has two major type of solid structures :
(1) Collagen fibre bundles and proteoglycan filaments. The collagen fiber
bundles extend long distances in the interstitium. They area extremely strong
and therefore provide most of the tensional strength of the tissues. The
proteoglycan filaments, on the other hand, are extremely thin, coiled
molecules composed by about 98 % hyaluronic acid and 2 % protein. These
molecules are so thin that they can never be seen with a light microscope and
are difficult to demonstrate even with the electronic microscope. Nevertheless,
they form a mat of very fine reticular filaments aptly described as “brush pile”.
(2) ‘Gel’ in the Interstitium - the fluid in the interstitium is derived by filtration
and diffusion from the capillaries. It contains the almost same constituents as
plasma except for much lower concentration of proteins. As proteins don’t
pass the walls of capillaries with ease. The interstitial fluid is mainly entaped
in the minutes spaces among the proteoglycan filaments and the fluid present
within them has characteristics of ‘get’. Therefore, called as tissue gel.
Because of the large number of proteoglycan filaments, it is difficult for fluid
to flow through tissue ‘gel’, but still then it diffuses through the gel only diffusion
through cell occurs 99 % rapidly rather than free fluid. So the diffusion allows rapid
transport of electrolyte nutrients, oxygen, carbon dioxide and cellular excreta.
Interstitial Pressure :
As the body is surrounded by tight encasement, such as cranial vault around
the brain, strong fibrous capsule around the kidney, fibrous sheaths around the
muscles, sclera around the eye, the interstitial fluid pressure is positive in these areas.
One should remember that pressure exerted on skin is atmospheric pressure and
normal interstitial fluid pressure is usually negative, as per previously heard concept,
interstitial fluid pressure is always positive. There is general belief that true interstitial
fluid pressure in the tissues is slightly less than atmospheric pressure.
Lymphatic system is the basic cause of negative pressure :
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81
Lymphatic system plays its role in determining interstitial fluid pressure.
Lymphatic system is scavenger, which removes the excess of fluid, protein, debris etc
and other matter from the tissue spaces. When fluid enters the lymphatic capillaries,
any movement of the tissue propels the lymph forward through the lymphatic system,
eventually emptying back into the circulation. In this way, any time any free fluid
accumulates in the tissue, it is simply pumped away as a consequence of tissue
movement, when the amount of fluid leaking from the blood capillaries is slight, as it
true for most tissues, research evidence suggests that actually pump a slight
intermittent negative pressure that gives an average negatively in the loose tissue.
“Plasma Colloid Osmotic Pressure” - Proteins in the Plasma Cause Colloid
Osmotic Pressure :
The proteins are the only dissolved substances in the plasma and interstitial
fluid, much of these are soon removed from the interstitial spaces by way of the
lymph vessels. Therefore, the concentration of protein in the plasma averages about
three times as much as that in most interstitial fluid; 7.3 gm/dl in the plasma versus 2-
3 gm/dl in the interstitial fluid. Only those molecules or ions that fail to pass through
the pores of semi-permeable membrane exert osmotic pressure. Because the proteins
are the only dissolved constituents that do not readily penetrate the pores of the
capillary membrane. It is the dissolved proteins of the plasma and interstitial fluids
that are responsible for the osmotic pressure at the capillary membrane. To distinguish
this osmotic pressure from that which occurs at he cell membrane, it is called either
colloid osmotic pressure or oncotic pressure. The term “colloid” osmotic pressure is
derived from the fact that a protein solution resembles a colloidal solution despite the
fact that it is actually a true molecular solution.
Exchange of Fluid volume through the Capillary Membrane :
Now that the different factors affecting fluid movement through the capillary
membrane have been discussed, the average capillary pressure at the arterial ends of
the capillaries is 15-25 mm of Hg greater than at the venous ends. Because of this
difference, fluid “filters” out of the capillaries at their arterial ends, and at their
venous ends, fluid is reabsorbed back into the capillaries. Thus a small amount of
fluid actually “flows” through the tissues from the arterial ends of the capillaries to
the venous ends. The dynamics of this flow are as follows :
Analysis of the Forces Causing Filtration at the Arterial End of the Capillary:
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82
The approximate average forces operative at the arterial end of the capillary
that cause movement through the capillary membrane are shown as follow:
TABLE NO. 13 SHOWING ANALYSIS OF FORCES AT ARTERIAL END OF CAPILLARY
Factors mm of Hg
Forces tending to move fluid outward capillary pressure 30
Negative interstitial fluid pressure 03
Interstitial fluid colloid osmotic pressure 08
Total Outward Force = 41
Forces tending to move fluid inward :
Plasma colloid osmotic pressure 28
Total inward force 28
Summation of Force
Outward 41
Inward 28
Net Outward Force 13
Thus the summation of the forces at the arterial end of the capillary shows a
net filtration pressure of 13 mm of Hg, tending to move fluid in the outward direction.
This 13 mm of Hg filtration pressure causes, on the average, about 0.5 % of the
plasma in the flowing blood to filter out of the arterial end of the capillaries into the
interstitial spaces.
Analysis of Re-absorption at the Venous End of the Capillary : [Fig. 2 (c)]
The low pressure at the venous end of the capillary changes the balance of
forces in favour of absorption. The force that causes the fluid to move into the
capillary , 28 mm of Hg, is greater than that opposing reabsorption, 21 mm of Hg. the
difference, 7 mm of Hg, is the reabsorption pressure at the venous ends of the
capillaries. This reabsorption pressure is considerably less than the filtration pressure,
but remember that the venous capillaries are more numerous and more permeable than
the arterial capillaries, so that less pressure is required to cause the inward movement
of fluid.
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83
The reabsorption pressure causes about nine tenth of the fluid that has filtered
out of the arterial ends of the capillaries to be reabsorbed at the venous ends. The
remainder flows into the lymph vessels. Under normal conditions, a state of near
equilibrium exists at the capillary membrane, where by the amount of fluid filtering
outward from some capillaries equals almost exactly the quantity of fluid that is
returned to the circulation by absorption through other capillaries. The slight
disequilibrium that does occur account for the small of fluid that is eventually
returned by way of the lymphatics.
Lymphatic System
84
4. LYMPHATIC SYSTEM
The lymphatic system149 represents an accessory route by which fluid can flow
from the interstitial spaces into the blood. And, most important the lymphatics can
carry the proteins and large particulate matter away from the tissue spaces, neither f
which can be removed by absorption directly into the blood capillary. This removal of
proteins from the interstitial spaces is an essential function, without which we would
die within about 24 hours. The lymphatic system consists of fluid called “LYMPH”.
The vessels called “Lymphatic Vessels” to transport the fluid.
Lymph Channels of the body :
Almost all the tissues of the body have lymphatic channels that drain excess
fluid directly from the interstitial spaces. The exceptions include the superficial
portions of the skin, the central nervous system, deeper portions of peripheral nerves,
the endomysium of muscles, and the bones. Even these tissues have minute interstitial
channels called prelymphatics through which interstitial fluid can flow; this fluid
eventually flows either into lymphatic vessels, in the case of the brain, into the
cerebrospinal fluid and directly back into the blood.
Essentially all the lymph from the lower part of the body flows up the thoracic
duct and empties into the venous system at the junction of the left internal jugular
vein and subclavian vein. Lymph from the left side of the head, the left arm, and parts
of the chest region also enters the thoracic duct before it empties into the veins.
Lymph from the right side of the neck and head, the right arm, and parts of thorax
enters the right lymph duct, which then empties into the venous system at the junction
of the right subclavian vein and internal jugular vein.
Terminal Lymphatic Capillaries And Their Permeability: [Fig. 5 (b) & (d)]
Most of the fluid filtering the arterial capillaries flows among the cells and is
finally reabsorbed back into the venous ends of the blood capillaries. But on the
average probably about one tenth of the fluid enters the lymphatic capillaries instead
and returns to the blood through the venous capillaries. The total quantity of this
lymph is normally only 2-3 liters each day.
The minute quantity of fluid that returns into the circulation by way of the
lymphatics is extremely important because substances of high molecular weight, such
as proteins, cannot be reabsorbed in any other way. Yet they can enter the lymphatic
Lymphatic System
85
capillaries almost unimpeded. The reason for this is a special substance of the
lymphatic capillaries. The endothelial cells of the capillaries attached by anchoring
the filaments to the surrounding connective tissue. At the junctions of the adjacent
endothelial cells, the edge of the adjacent cell in such a way that the overlapping edge
is free to flap inward, thus forming a minute valve that opens to the interior of the
capillary. Interstitial fluid, along with its suspended particles, can push the valve open
and flow directly into the lymphatic capillary. But this fluid has difficulty leaving the
capillary once it has entered because any backflow will close the flap valve. Thus the
lymphatics have valves at the very tips of the terminal lymphatic capillaries as well as
valves along their larger vessels upto the point where they empty into the blood
circulation.
Formation of Lymph :
Lymph is derived from interstitial fluid that flows into the lymphatics.
Therefore, lymph as it first flows from each tissue has almost the same composition as
the interstitial fluid. The position concentration in the interstitial fluid of most tissues
averages about 2 gm/dl, and the protein concentration of lymph flowing from these
tissues is near this valve. On the other hand, lymph formed in the liver has a protein
concentration as high as 6 gm/dl and lymph formed in the intestines has a protein
concentration as high as 3-4 gm/dl because about two thirds of all lymph normally is
derived from the liver and intestines, the thoracic lymph, which s a mixture of lymph
from all areas of the body, usually has a protein concentration of 3-5 gm/dl. The
lymphatic system is also one of the major routes of nutrients from the gastrointestinal
tract, being responsible principally for the absorption of fats. Indeed, after a fatty
meal, thoracic duct lymph sometimes contains as much as 1-2 % fat. Finally, when
large particles, such as bacteria, can push their way between the endothelial cells of
lymphatic capillaries and in this way enter the lymph. As the lymph passes through
the lymph nodes, these particles are removed and destroyed.
Rate of Lymph Flow :
About 100 ml of lymph flows through the thoracic duct of a resting human per
hour, and perhaps another 20 ml flows into the circulation each hour through other
channels, making a total estimated lymph flow of about 120 ml/hr between 2 and 3
lts/day.
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86
Effect of Interstitial Fluid Pressure on Lymph Flow : [Fig. 5 (c)]
The lymph is slight at interstitial fluid pressures more negative than -6mm Hg.
Then, as the pressure rises upto valves slightly greater than 0 mm Hg the flow
increases more than 20 fold. Therefore, any factor that increases interstitial fluid
pressure will normally also increase the lymph flow such factors include the following
Elevated capillary pressure
Decreased plasma colloid osmotic pressure
Increased interstitial fluid protein
Increased permeability of the capillaries.
All of these cause the balance of fluid exchange at the blood capillaries
membrane to favor fluid movement into the interstitium, thus increasing interstitial
fluid volume, interstitial fluid pressure and lymph flow all at the same time. However,
note that when the interstitial fluid pressure becomes 1-2 millimeter greater than
atmospheric pressure (0 mm Hg), lymph flow fails to rise further at still higher
pressures. This probable result from the fact that increasing tissue pressure not only
increases entry of fluid into lymphatic capillaries, but also compresses the outside
surfaces of the larger lymphatics, thus impeding lymph flow. At these higher
pressures, these two factors appear to balance each other almost exactly.
Like veins, lymphatic vessels contain valves, which ensure the one-way
movement of lymph. Ultimately, lymph drains into venous blood through the right
lymphatic junction of the internal jugular and subclavian veins. Thus, the sequence of
fluid flow is blood capillaries interstitial spaces lymphatic capillaries (lymph)
lymphatic vessels lymphatic ducts subclavian veins.
The same two “pumps” that aid return of venous blood to the heart maintain
the flow of lymph.
(1) Skeletal Muscle Pump : The “milking action” of skeletal muscle contractions
compresses lymphatic vessels and forces lymph toward the subclavian veins.
(2) Respiratory Pump : Lymph flow is also maintained by pressure changes that
occur during inhalation. Lymph flows from the abdominal region, where the
pressure is higher, toward the thoracic region, where it is lower, when the
pressures reverse during exhalation, the values prevent backflow of lymph. In
addition, when a lymphatic vessel distends, the smooth muscle, in its wall
contracts, which help move lymph from one segment of the vessel to the next.
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87
Role of Lymphatic System in Controlling Interstitial Fluid Protein Concentration,
Interstitial Fluid Volume, and Interstitial Fluid Pressure :
It is already clear that the lymphatic system functions as an “overflow
mechanism” to return to the circulation excess proteins and excess fluid volume from
the tissue spaces. Therefore, the lymphatic system also plays a central role in
controlling (1) the concentration of proteins in the interstitial fluids, (2) the volume of
interstitial fluid , and (3) the interstitial fluid pressure.
The small amounts of proteins leak continuously out of the blood capillaries
into the interstitium. Only minute amounts if any, of the leaked proteins return to the
circulation by way of the venous ends of the blood capillaries. Therefore, these
proteins tend to accumulate in the interstitial fluid, and this inturn increases the
colloid osmotic pressure of the interstitial fluids. The increasing colloid pressure in
the interstitial fluid shifts the balance of forces at the blood capillary membranes in
favor of fluid filtration into the interstitium. Therefore, fluid is pulled osmotically by
these proteins into the interstitium, thus increasing both the interstitial fluid volume
and the interstitial fluid pressure. The increasing interstitial fluid pressure greatly
increases the rate of lymph flow, as explained earlier. This inturn carries away the
excess volume and excess protein that has accumulated in the spaces.
Thus, once the interstitial fluid protein concentration reaches a certain level
and causes a comparable increase in interstitial fluid volume and interstitial fluid
pressure, the return of protein and fluid by way of the lymphatic system becomes
great enough the balance exactly the rate of leakage of these from the blood
capillaries. Therefore, the quantitative values of all these factors reach a steady state;
they will remain balanced at these levels until something changes the rate of leakage
of proteins and fluid from the blood capillaries.
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88
5. LOCAL CONROL OF BLOOD OF FLOW BY THE TISSUES AND HUMORAL REGULATION
Local Control of Blood Flow in Response to Tissue Need150 :
One of the most fundamental principles of circulatory function is the ability of
each tissue to control its own local blood flow in proportion to its metabolic needs.
Further more, as the need for blood flow changes, the flow follows the changes.
Some of the needs of the tissue for blood flow :
1. Delivery of oxygen to the tissues,
2. Delivery of other nutrients such as glucose, amino acids, fatty acids,
3. Removal of carbon dioxide from the tissues,
4. Removal of hydrogen ions from the tissues,
5. Maintenance of hydrogen ions from the tissues,
6. Maintenance of proper concentrations of other ions in the tissues,
7. Transport of various hormones and other specific substances to the different
tissues.
Variation in Blood Flow in Different Tissues and Oxygen :
In general, the greater the metabolism in an organ, the greater its blood flow.
Very large blood flows in the various glandular organs, for example, several hundred
ml/100 gm of thyroid or adrenal gland tissue and a blood flow of 95 ml/100 gm of
liver. The extremely large blood flow through the kidneys, 360 ml/min/100 gm. This
extreme amount of flow is required for the kidneys to perform their function of
cleansing the blood of the waste products.
On the other hand, most surprising is the low blood to the resting muscles of
the body, even though they constitute between 30-40 % of total body mass. In the
resting state, the metabolic activity of the muscles in very low, and so also is the
blood flow, only 4 ml/min/100 gm. Yet during heavy exercise, muscle metabolic
activity can increase more than 60-fold and the blood flow as much as 20-fold.
Mechanisms of Blood Flow Control :
Local blood flow can be divided into 2 phases :
(1) Acute Control
(2) Long-term Control.
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89
Acute control is achieved by rapid changes in local constriction of the
arterioles meta-arterioles, and precapillary sphincters, occurring within seconds to
minutes to provide a rapid means for maintaining appropriate local tissue blood flow.
Long-term control on the otherhand means slow changes in flow over a period of
days, weeks, or even months. In general, the long term changes provide for better
control of the flow in proportion to the needs of the tissues. These changes come
about as result of an increase or decrease in the physical sizes and numbers of actual
blood vessels supplying the tissues.
Acute Control of Local Blood Flow :
(I) Effect of tissue metabolism on Local Blood Flow :
An increase in metabolism upto 8 times normal increase the blood flow
acutely about fourfold. Once the metabolism rises high enough to remove
most of the nutrients form the blood, further increase in metabolism can occur
only with a concomitant increase in blood flow to supply the required
nutrients.
(II) Local Blood Flow Regulation when Oxygen Availability Changes :
One of the most necessary of the nutrients is oxygen. Whenever the
availability of oxygen to the tissues decreases, such as at high altitude, in
pneumonia, in carbon monoxide poisoning or in cyanide poisoning, the blood
flow through the tissues increases markedly.
There are two basic theories for the regulation of local blood flow when either
the rate of tissue metabolism changes or the availability of oxygen changes. They are
(1) The vasodilatory Theory
(2) The oxygen demand Theory
(1) The Vasodilatory Theory : Special role of adenosine :
According to this theory, the greater the rate of metabolism or the less the
availability of oxygen or some other nutrients to a tissue, the greater becomes
the rate of formation of a vasodilator substance. Most of the vasodilator
theories assume that the vasodilator substance is released from the tissue
mainly in response to oxygen deficiency. The decreased availability of oxygen
can cause both adenosine and lactic acid to be released from the tissues; these
substances can cause intense vasodilation. Some physiologists have suggested
that the substance adenosine is by far the most important of the local
vasodilators far controlling local blood flow. For instance, minute quantities of
Local control of Blood flow
90
adenosine are released from heart muscle, whenever coronary heart flow
becomes too little.
(2) Oxygen Demand Theory for Local Blood Flow Control :
Although the vasodilator theory is accepted by most physiologists, several
critical facts have made a few physiologists favour still another theory, which
can be called either the oxygen demand theory. Oxygen is required to maintain
vascular muscle contraction. Therefore, in the absence of an adequate supply
of oxygen and other nutrients, it is reasonable to believe that the blood vessels
would naturally dilate. Smooth muscle requires oxygen to remain contracted,
one might assume that the strength of contraction of the sphincters would
increase with an increase in oxygen contraction. Consequently, when the
oxygen concentration in the tissue rises above a certain level, the precapillary
and meta-arteriole sphincters presumably would close and remain closed until
the tissue cells consume the excess oxygen. When oxygen concentration falls
low enough, the sphincters would open once more to begin the cycle again.
“Possible Role of Other Nutrients besides Oxygen in the Control of Local Blood
Flow” :
Under special conditions, it has been shown that lack of glucose in the
perfusing blood for longer than a few minutes can cause local tissue vasodilation.
Also it is possible that this same effect occurs when other nutrients, such as amino
acids or fatty acids, are deficient, although this has not been studied adequately. In
addition, vasodilation occurs in the vitamin deficiency disease, beriberi, in which the
patient usually has deficiencies of vitamin B substances thiamine, niacin and
riboflavin. In this disease, the peripheral vascular blood flow all over the body can
increase twofold, threefold. Because these vitamins are all concerned with the
oxidative phosphorylation mechanism for generating ATP in the local tissues. One
could suspect that deficiency of these vitamins leads to diminished smooth muscle
contractile ability and therefore to the local vasodilation.
Special Examples of “Metabolic” Control of Local Blood Flow :
(1) Reactive Hyperaemia
(2) Active Hyperaemia
(1) Reactive Hyperaemia :
When the blood supply to a tissue is blocked for a few seconds to several
hours and then is unblocked, the flow through the tissue usually increases to
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91
four to seven times normal; the increased flow will continue for a few seconds
if the block has lasted only a few seconds but sometimes for as long as many
hours if the blood flow has been stopped for an hour or more. This is called
“reactive hyperaemia”. After short periods of vascular occlusion, the extra
blood flow during the reactive hyperemia phase lasts long enough to repay
almost exactly the tissue oxygen deficit that has occurred during the period of
occlusion. This mechanism emphasizes the close connection between local
blood flow regulation and delivery of oxygen and other nutrients to the tissue.
(2) Active Hyperaemia :
When any tissue become highly active such as an exercising muscle,
gastrointestinal gland during a hyper-secretory period or even the brain during
rapid mental activity, the rate of blood flow through the tissue increases. The
increase in local metabolism causes the cells to devour the tissue fluid
nutrients extremely rapidly and also to release large quantities of vasodilator
substances, that results into dilate the local blood vessels and therefore, to
increase local blood flow.
Autoregulation of Blood Flow :
In any tissue of the body, an acute increase in arterial pressure will cause an
immediate rise in blood flow. Within less than a minute, the blood flow in most tissue
returns most of the way back toward the normal level. This return of flow back toward
normal is called “autoregulation of blood flow”. This is related to arterial pressure of
about 70 mm Hg and 175 mm Hg. The blood flow increases only to explain the acute
autoregulation mechanism - (1) Metabolic theory (2) Myogenic theory.
(1) Metabolic Theory : When the arterial pressure becomes too great, the excess
flow provides too much oxygen and too many other nutrients to tissues, and
these nutrients then cause the blood vessels to constrict and the flow to return
nearly to normal despite the increased pressure.
(2) Myogenic Theory : It is not related to tissue metabolism still it explains the
phenomenon of autoregulation. The sudden stretch of small blood vessels will
cause the smooth muscle of the vessel wall contract. When high arterial
pressure stretches the vessel, this inturn reduces the blood flow nearly back to
normal conversely, at low pressures, the degree of stretch of the vessel is less,
so that the smooth muscle releases and allows increased flow.
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It has been suggested especially that the myogenic mechanism protects the
capillaries form excessively high blood pressure. That is if the pressure in the small
arteriole rises too high, these vessels would simply constrict within seconds and
prevent this high pressure from been transmitted into the capillaries, which are so
weak that excessive pressure could rupture them.
Mechanism for Dilating the Large Vessels when Microvascular Blood Flow
increases the Endothelial Derived Relaxing Factor (Nitric Oxide):
The local mechanisms for controlling tissue blood flow can dilate only the
very small microvessels located in the immediate tissue itself because local feedback
caused by vasodilator substances or oxygen deficiency can reach only these vessels.
Yet, when blood flow through the microvascular portion of the circulation increases,
this entrains secondarily another mechanism that does dilate the larger arteries as
well.
The endothelial cells lining the arterioles and small arteries synthesize several
substances that, when released, can affect the degree of contraction of the arterial wll.
The most important of these is a vasodilator substance called “endothelial-derived
relaxing factor”, which is composed principally, if not entirely of nitric oxide, that has
a half life in blood only 6 seconds. Rapid flow of blood through the arteries causes
“shear-stress” on the endothelial cells because of viscous drag of the blood against the
vascular walls. This stress contorts the endothelial cells in the direction of flow and
causes greatly increased release of nitric oxide. The nitric oxide then releases the
arterial wall, causing it to dilate.
Multiple other stimuli also can cause nitric oxide to be released from the
endothelium. These stimuli include acetyl choline, bradykinin, ATP and others. The
nitric oxide inturn causes the local blood vessel to dilate.
Mechanism of Long Term Regulation change in Tissue Vascularity :
Over a period of hours, days and weeks, a long term type of local blood flow
regulation develops in addition to acute regulation. If a tissue becomes chronically
overactive and therefore, requires chronically increased quantities of nutrients the
blood supply usually increases within a few weeks almost to match the needs of the
tissue.
The mechanism of long term local blood flow regulation is a change in the
degree of vascularity of the tissues. That is if the arterial pressure falls to 60 mm Hg
and remains at this level for many weeks, the physical structural sizes of the vessels in
Local control of Blood flow
93
the tissue increase and under some conditions, even the number of vessels increases.
On the other hand, if the pressure increases to a very high level, the number and sizes
of vessels decreases. If the metabolism in a given tissue is increased for a prolonged
period, vascularity increases, if the metabolism is decreased, vascularity decreases.
Thus there is reconstruction of the tissue vasculature to meet the need of the
tissues. This reconstruction occurs rapidly. It also occurs rapidly in new growth of
tissue, such as in scar tissue and in cancerous tissue. On the other hand, it occurs
slowly in old and well established tissue. Therefore, time required for long term
regulation to take place may be a only a few days in the neonate and years together in
elderly person. So response is greater in younger tissues than in older.
Role of Oxygen in Long Term Regulation :
Oxygen is important not only for acute control of local blood flow, but also
long term control. One of effect of this to increase the vascularity in the tissue of
many animals that live at high altitudes, where atmospheric oxygen is low. The excess
oxygen causes almost immediate cessation of new vascular growth in the retina, even
causes degeneration of capillaries that have already formed. There is explosive
overgrowth of new vessels to makeup for the sudden decrease in available oxygen.
Growth of New Vessels - Angiogenesis and Angiogenic Factors :
The term “angiogenesis” means growth of new blood vessels released from
the factors like
1. Ischaemic tissues
2. Tissue growing rapidly
3. Tissues having excessive high metabolic rate.
Multiple angiogenic factors have been found, where 3 of them have been best
characterized are (1) endothelial cells growth factor (2) fibroblast growth factor and
(3) angiogenin, which have been isolated from inadequate blood supply. So
deficiency of tissue oxygen and other nutrients lead to formation of angiogenic
factors.
They cause new vessels to sprout, either from small venules, occasionally
from capillaries. The first step is discontinuation of basement membrane of the
endothelial cells at point of sprouting, followed by rapid reproduction of new
endothelial cells, then streamout of vessel wall in extended cords directed towards
source of the angiogenic factors. The cells in each cord, continue to divide over into a
tube next. The tube connects with another tube, budding from another donor vessels
Local control of Blood flow
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and forms a capillary tubes through which blood begins to flow. If flow is more
smooth muscle cells eventually invade the wall. So that new vessels grow into small
arterioles are perhaps arteries. Thus angiogenesis explains the manner in which
metabolic factors in local tissue can cause growth of new vessels.
Development of collateral circulation :
When an artery, vein is blocked a new vascular channels develops around the
blockage and allows partial resupply of blood to the affect tissue. First stage in this
process is dilatation of vascular tubes around the point of blockage that already
connect the vessel above the blockage to the vessel below. This dilatation occurs
within the first minute or two initiating that it is simply a metabolic relaxation of
muscle fibres of the small vessels involved. After this initial opening of these
collateral vessels. The blood flow usually less than one quarter that needed to supply
tissue needs. The most important example of collateral vessel is thrombosis of one of
the coronary artery.
Humoral Regulation of the Circulation :
This means regulation of circulation by substances secreted or absorbed into
the body fluid such as hormones and ions. Some of these substances are formed by
special glands and transported into the blood throughout the entire body. There are
other substances formed in local tissue areas and cause only local circulatory effects.
Vasoconstrictor Agents –
Norepinephrine, Epinephrine :
Norepinephrine is powerful vasoconstrictor hormone. Epinephrine is some
what less even in some instances causes vasodilation. When the sympathetic nervous
system is stimulated in all parts of the body during stress or exercise. The sympathetic
nerve ending in individual tissue release norepinephrine that excites the heat, veins
and arterioles. The sympathetic nerves also cause adrenal medullae to cause secretion
both hormones into the blood. These hormones cause almost the same excitatory
effects on the circulation.
Angiotensin :
It is a powerful vasoconstrictor pressure. The effect of this is on small
arterioles real important of this is blood is that it normally act on all arterioles to
increase total peripheral resistance there by increasing the arterial pressure.
“Vasopressin” - it is also called as antidiuretic hormone, more powerful than
angiotensin released by posterior pituitary. It has important function in controlling the
Local control of Blood flow
95
water reabsorption in renal tubules controlling body fluid volume so called anti-
diuretic hormone.
Endothelin :
it is a powerful vasoconstrictor in damaged blood vessels. This substance
present in endothelial cells of all blood vessels. This substance present in endothelial
cells of all blood vessels. The usual stimulus for release is damage to the endothelium
which prevents bleeding. A special function of endothelium might be constriction of
umbilical artery of a neonate immediately after birth.
Vasodilator Agents :
Bradykinin :
Several substances called kinins cause vasodilatation formed in the blood and
tissue fluid. Bradykinin causes powerful arteriolar dilatation and increased capillary
permeability. It is believed that bradykinin play a role in regulating blood flow of
skin. Salivary gland, gastrointestinal glands.
Serotonin :
In can have either vasodilator or vasoconstrictor effect. Depending upon the
condition of are of circulation. Its function is still clear.
Histamine :
It is released by every tissue of body, when it becomes damaged or inflamed.
It is derived from mast cells or basophils. It has got powerful vasodilator effect
allowing leakage of fluid and plasma protein into the tissue.
Prostaglandins :
Almost every tissue of the body contain prostaglandins. These are important
intracellular effects.
Effects of Ions on Vascular Control :
Many different ions have little function in regulation of circulation. An
increase in calcium ion concentration causes smooth muscle contraction. So acts as
vasoconstrictor. An increase in potassium ion contraction inhibits smooth muscle
contraction. Magnesium ions have also get same effect. An increase in sodium ion
concentration causes arteriole dilatation.
Nervous Regulation of Circulation: 53
Local control of Blood flow
96
Nervous control normally adjusts blood flow tissue by. Nervous control
mainly affects more global function such as redistributing the blood flow to different
areas of the body, increasing pumping action of heart and providing rapid control of
arterial pressure. Sympathetic and parasympathetic nervous system are important in
contributing to regulation of heart function.
Sympathetic Nervous System :
Sympathetic vasomotor nerve fibres leave the spinal cord through all thoracic
and first two lumbar spinal nerves. They pass into the sympathetic chain and to the
circulation. Through specific sympathetic nerves innervating vasculature of internal
viscera and heart. And through the spinal nerves which innervates vasculature of
peripheral areas. Sympathetic fibres innervating meta-arterioles. The innervation of
veins makes possible for the sympathetic stimulation to decrease the volume of these
vessels. So it is playing major role in regulation of cardio-vascular function
stimulation markedly increases the heart rate.
Parasympathetic Nervous System :
They play minor role regulation of circulation. Parasympathetic stimulation
causes marked decrease in heart rate and slight decrease in heart muscle contractility.
Role of Nervous System for Rapid Control of Arterial Pressure :
Sympathetic nerve are stimulated to cause entire vasoconstrictor and
cardioaccelator function at the same time. There is inhibition of parasympathetic
nerves. This can occur in these ways :
1. Almost all arterioles of the body are constricted increasing peripheral
resistance concretely arterial pressure to provide run-off of blood
2. The veins are also strongly constricted displacing towards heart, thus
increasing the volume of blood in heart chambers.
3. Sympathetic nerves have direct effect to increase the contractile force of the
heart muscle increasing the capable of heart pump.
Reflex Mechanism for Maintaining Normal Arterial Pressure :
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97
Barareceptor Mechanism :
Baroreceptors are spray type nerve endings lying in the walls of arteries
(Large arteries) stimulated when they are stretched. The baroreceptors respond
extremely, to changes in arterial pressure. Excitation of baroreceptors by pressure in
arteries reflexly causes the arterial pressure to decrease providing decreased
peripheral resistance in cardiac output (Fig 18.5)
Chemoreceptors :
Chemoreceptors are sensitive to oxygen lack, carbon dioxide excess and
hydrogen ion excess. They are located in several organs. The signals transmitted from
chemoreceptors into vasomotor centres elevate arterial pressure. Special Features of Nervous Control of Arterial Pressure :
Skeletal muscles and nerve play important role in controlling circulation.
Abdominal Compression Reflex :
Any factors stimulate sympathetic vasoconstrictor system, nerve signals are
transmitted simultaneously through skeletal nerves through skeletal muscles of the
body. This increases basal tone of the muscle which compresses all venous reservoirs
to translocate blood towards the heart.
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98
6. REGIONAL VENOUS SYSTEM
VEINS OF HEAD AND NECK :
Most blood draining from the head passes into three pairs of veins. The
internal jugular, external jugular, and vertebral veins. With in the brain, all the veins
drain into dural venous sinuses and then into the internal jugular veins. Dural venous
sinuses are endothelial lined venous channels between layers of the cranial dura
mater.
Internal Jugular Veins : [Fig. 6 (a)]
The flow of blood from the dural venous sinuses into the internal jugular veins
is as follows –
The superior sagittal sinus begins at the frontal bone, where it receives a vein
from the nasal cavity, and passes posteriorly to the occipital bone. Along its course, it
receives blood from the superior, medial and lateral aspects of the cerebral
hemispheres, meninges, and cranial bones. The superior sagittal sinus usually turns to
the right and drains into the right transverse sinus. The inferior sagittal sinus is much
smaller that the superior sagittal sinus; it begins posterior to the attachment of the falx
cerebri and receives the great cerebral vein to become the straight sinsus. The great
cerebral vein drains to deeper parts of the brain. Along its course the inferior sagittal
sinus also receives tributaries from the aspects of the cerebral hemisphere.
The “Straight Sinus” runs in the tentorium cerebelli and is formed by the
union of the inferior sagittal sinus and the great cerebral vein. The straight sinus also
receives blood from the cerebellum and usually drains into the left transverse sinus.
The “Transverse Sinuses” begin near the occipital bone, pass laterally and
anteriorly, and become the sigmoid sinuses near the temporal bone. The transverse
sinuses receive blood from the cerebrum, cerebellum and cranial bones.
The “Sigmoid Sinuses”(S shaped) are located along the temporal bone. They
pass through the jugular foramina, where they terminate in the internal jugular veins.
The sigmoid sinuses drain the transverse sinuses.
The “Cavernosus Sinuses” (cave like) are located on either side of the
sphenoid bone. They receive blood from the ophthalmic veins from the orbits, and
from the cerebral hemispheres. They ultimately empty into the transverse sinuses and
internal jugular veins. The cavernous sinuses are unique because they have nerves and
Regional Venous System
99
a major blood vessel passing through them on their way to the orbit and face. The
occulomotor nerve, trochlear nerve, and ophthalmic and maxillary braches of the
trigeminal nerve as well as internal carotid arteries pass through the cavernosus
sinuses. The right and left internal jugular veins pass inferiorly on either side of the
neck lateral to the internal carotid and common carotid arteries. They then unite with
the subclavian veins posterior to the clavicle at the sternoclavicular joints to form the
right and left brachio-cephalic veins. From here blood flows into the superior vena
cava. The general structures drained by the internal jugular veins are the brain, face
and neck.152
External Jugular Veins: 153
The external jugular vein mainly drains the scalp and face, although it also
drains some deeper parts. The vein is formed by the union of the posterior division of
the retromandibular vein with the posterior auricular vein and begins near the
mandibular angle just below or in the parotid gland. It descends from the angle to the
middle clavicle, running obliquely, superficial to the sternocleidomastoid, to the root
of the neck. Here it crosses deeper fascia and ends in the subclavian vein, lateral or
anterior to scalneus anterior. There are valves at its entrance into the subclavian, but
they do not prevent regurgitation. Its wall is adherent to the aim of the fascial
opening. It is covered by platysma, superficial fascia and skin and is separated from
sternocleidomastoid by deep cervical fascia. The vein crosses transverse cutaneous
nerve and lies parallel with great auricular nerve, posterior to its upper half. In size the
external jugular vein is inversely proportional to the other veins in the neck, and may
be double. Between the entrance into the subclavian vein and a point 4 cm above the
clavicle, the vein is often dilated, producing a so called sinus.
Posterior-external Jugular Vein :
The posterior external jugular vein begins in the occipital scalp, and drains the
skin and the superficial muscles which lie posterior superior in the neck. It usually
joins the middle part of the external jugular vein.
Anterior Jugular Vein :
The anterior jugular vein arises near the hyoid bone from the confluence of the
superficial submandibular veins. It descends between the midline and the anterior
border of sterno-cleido mastoid.
Turning laterally, low in the neck, deep to the sternocleidomastoid but
superficial to the infrahyoidstrap muscle, it joins either the end of the external jugular
Regional Venous System
100
vein or may enter the subclavian vein directly. In size it is usually inverse to the
external jugular vein. It communicates with the internal jugular vein. There are
usually two anterior jugular veins, united just above the manubrium by a large
transverse jugular arch, receiving the inferior thyroid tributaries. They have no valves
and may be replaced by a middle trunk.
Venous Drainage of the Brain: 154
The venous drainage of the brain occurs through a complex system of deep
and superficial veins. Theses veins possess no valves and have thin wall devoid of
muscular tissue. They pierce the arachnoid matter and the thinner layer of the dura
mater to open into the dural venous sinuses.
Veins of the Brainstem :
The veins of brainstem form a superficial venous plexus deep to the arteries.
Veins of medulla oblongata drain into the veins of spinal cord or the adjacent dural
venous sinuses or into the variable radicular veins which accompany the last four
cranial nerves to either the inferior petrosal or occipital sinuses, or to the superior bulb
of the jugular vein.
Veins of Cerebellum :
The veins of the cerebellum drain mainly into sinuses adjacent to them or from
the superior surface, into the great cerebral vein. The cerebellar veins course on the
cerebellar surface, and comprise superior and inferior groups.
Veins of the Cerebral Hemisphere :
External and internal cerebral veins drain the surfaces and the interior of the
cerebral hemisphere. External cerebral veins may be divided into three groups,
namely, superior, middle and inferior.
Eight – twelve superior cerebral veins drain the supero-lateral and medial
surfaces of each hemisphere. They mainly follow the sulci, although some do pass
across gyri. They ascend to the super-medial border of the hemisphere, where they
receive small veins from the medial surface, and then open into the superior sagittal
sinus. The larger posterior veins are directed obliquely forwards, against the direction
of flow in the sinus, an arrangement which may resist their collapse when intracranial
pressure is raised.
The internal cerebral vein drains the deep parts of the hemisphere and the
choroids plexuses of third and lateral ventricles. It is formed near the interventricular
foramen, behind the column of the fornix.
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Veins of Vertebrae: 155
Veins of the vertebral column form intricate plexuses along the entire column,
external and internal to the vertebral canal. Both groups are devoid of valves,
anastomose freely with each other, and join the intervertebral veins. Inter-connections
are widely established between these plexuses and longitudinal veins early in fetal
life.
The veins also communicate with cranial dural venous sinuses and with the
deep veins of the neck and pelvis. The venous complexes associated with the vertebral
column can dilate considerably and can form alternate routes of venous return in
patients of with major venous obstruction in the neck, chest or abdomen. The absence
of valves allows pathways for the wide and sometimes para-abdominal spread of
malignant diseases and sepsis. Pressure changes in the body cavities are transmitted
into these venous plexuses and thus to the CSF, though the cord itself may be
protected from such congestion by valves in the small veins which drain from the cord
into the internal vertebral plexus. External vertebral venous plexuses, basi-vertebral
veins and inter-vertebral are the veins found in vertebrae.
Veins of the Face: 156
The veins of the face are subject to considerable variations, and therefore, the
following description concerns those which are relatively constant.
Supratrochlear Vein :
The supratrochlear vein starts on the forehead from a venous network
connected to the frontal tributaries of the superficial temporal vein. Veins from the
network form a single trunk, descending near the midline parallel with its fellow or
single trunk, descending near the midline parallel with its fellow the bridge of the
nose. Each vein is joined by a nasal arch across the nose. The veins then diverge, each
joining a supra-orbital vein to form the facial vein near the medial canthus of the eye.
Supra-orbital Vein :
The supra-orbital vein begins near the zygomatic process of the frontal bone,
connecting with the branches of the superficial and middle temporal veins. It passes
medially above the orbital opening pierces the orbicularis oculi and unites with the
supra-trochlear vein near the medial canthus of the eye to form the facial vein. A
branch passes through the supra-orbital notch to connect with superior ophthalmic
vein. In the notch it receives veins from the frontal sinus and frontal diploe.
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Facial Vein :
The facial vein is the main vein of the face. After receiving the supratrochlear
and supra-orbital veins, it travels obliquely downwards by the side of the nose passes
under zygomaticus major, resorius and platysma, descends to the anterior border and
then passes over the surface of masseter. It crosses the body of the mandible, and runs
in the neck to drain into the internal jugular vein. The uppermost segment of the facial
vein – above its junction with the superior labial vein is also termed the angular vein.
The facial vein initially lies behind the more tortuous facial artery, but crosses it at the
lower border of the mandible. The fact that the vein lacks, and that it is connected
with cavernous sinus of the considerable clinical significance in terms of the spread of
infection.
Tributaries of Facial Vein :
Near its origin, the facial vein connects with superior ophthalmic vein, both
directly and via the supraorbital vein, and so is linked to the cavernous sinus. The
facial vein receives tributaries from the pterygoid venous plexuses. It also receives the
inferior palpebral, superior and inferior labial, buccinator, parotid and masseteric
veins, and other tributaries which join it below the mandible.
Superficial Temporal Vein :
The superficial temporal vein begins in a wide spread network joined across
the scalp to the contra-lateral vein and to the ipsi-lateral supra-trochlear, supra-orbial,
posterior auricular and occipital veins that ll drain the some network. Anterior and
posterior tributaries unite above the zygomatic arch to form the superficial temporal
vein. Accompanying its artery, the vein crosses the posterior root of the zygoma and
enters the parotid gland. Here, the superficial temporal vein joins the maxillar vein, to
form the retro-mandibular vein.
Tributaries :
The tributaries are the parotid veins, rami draining the tempero-mandibular
joint, anterior auricular veins and the transverse facial vein. The middle temporal
veins receives the orbital vein and passes back between layers of temporal fascia,
which it pierces to join the superficial temporal vein just above the level of the
zygomatic arch.
Buccal, Mental and Infra-orbital Veins :
The buccal, menal and infra-orbital veins drain the cheek and chin regions and
pass into the pterygoid venous plexus.
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Posterior Auricular and Occipital Veins :
The posterior auricular vein arises in parieto-occipital network that also drains
into tributaries of the occipital and superficial temporal veins. It descends behind the
auricle to join the posterior division of the retro-mandibular vein in or just below the
parotid gland to form the external jugular vein. It receives a stylomastoid vein and
tributaries from the cranial surface of the auricle, drains the region of the scalp behind
the ear and drains into the eternal jugular vein. The occipital vein begins in a posterior
network in the scalp, pierces the cranial attachment of the trapezius turns into the
suboccipital triangle and joins the deep cervical and vertebral veins.
Lingual Vein: 157
The lingual veins follow two routes. The dorsal lingual vein drain the dorsum
and sides of the tongue, join the lingual vein accompanying the lingual artery between
hypoglossus and genioglossus, and enter the internal jugular near the tip of the tongue
and runs back, lying near the mucous membrane. On the inferior surface of the
tongue, near the anterior border of hypoglossus it joins a sublingual vein, from the
sublingual salivary gland, to form the venae comitans nervi hypoglossi which runs
back between mylohyoid and hypoglossus with the hypoglossal nerve to join the
facial, internal jugular or lingual vein.
Pharyngeal Veins :
The pharyngeal veins begin in a pharyngeal plexus external to the pharynx.
They receive meningeal veins and a vein from the pterygoid canal, and usually end in
the internal jugular vein, but may sometimes end in the facial, lingual or superior
thyroid vein.
Superior Thyroid Vein :
The superior thyroid vein is formed by deep and superficial tributaries
corresponding to the arterial branches in the upper part of the thyroid gland. It
accompanies the superior thyroid artery receives the superior laryngeal and crico-
thyroid veins, and ends in the internal jugular or facial vein.
Middle Thyroid Vein :
The middle thyroid vein drains the lower part of the gland and also receives
veins from the larynx and trachea. It crosses anterior to the common carotid artery to
join the internal jugular vein behind the superior belly of omohyoid.
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Vertebral Vein :
Numerous small tributaries from internal vertebral plexuses leave the vertebral
canal above the posterior arch of the atlas and join small veins from local deep
muscles in the sub-occipital triangle. Their union produces a vessel which enters the
foramen in the transverse process of the atlas and forms a plexus around the vertebral
artery. It descends through successive transverse foramina and ends as the vertebral
vein. The vein emerges from the sixth cervical transverse foramen, where it descends,
at first anterior, then antero-lateral, to the vertebral artery, to open supero-posteriorly
into the brachio-cephalic vein.
As it descends it passes behind the internal jugular vein and in front of the first
part of the subclavian artery. A small accessory vertebral vein usually descends from
the vertebral plexus, traverses the seventh cervical transverse foramen and turns
forwards between the subclavian artery and the cervical pleura to join the brachio-
cephalic vein.
Superficial Veins of Upper Limb: 158
Superficial veins of the upper limb assume importance in medical practice
because these are most commonly used for intravenous injections and for
withdrawing blood for transfusion or for testing. [Fig. 7 (d)]
1. Host of the superficial veins of the limb join together to form the two large
veins, cephalic and basilic. An accessory cephalic vein is often present.
2. The superficial veins run away from pressure points. Therefore, they are
absent in the palm in the ulnar border of the forearm and in the back of the
arm and trapezius region. This makes the course of the veins spiral, from the
dorsal to the ventral surface of the limb.
3. The pre-axial vein is longer than the post axial. In other words, the pre-axial
vein drain into the deep vein more proximally that the post-axial vein which
becomes deep in the middle of the arm.
4. The earlier a vein becomes deep the better the because the venous return is
then assisted by muscular compression. The load of the pre-axial vein is
greatly relieved by the more efficient post-axial (basilica) through a short
circulating channel [median cubital vein] and partly also by the deep veins
through a performator vein connecting the median cubital with deep vein.
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5. The superficial veins are accompanied by cutaneous nerves and superficial
lymphatics, and not by arteries. The superficial lymph nodes lie along the
veins, and the deep lymph nodes along the arteries.
6. The superficial veins are best utilized for intravenous infections.
Cephalic Vein :
The cephalic vein forms over the anatomical snuff-box from the radial
extremity of the dorsal venous plexus. It runs proximally over the distal lateral aspect
of the radius where it is easily visible.
Cephalic vein is the pre-axial vein of the upper limb. It runs upwards through
the roof of the anatomical suff-box winds round the lateral border of the distal part of
the forearm. It continues upwards in front of the elbow and along the lateral border of
the biceps brachis. Then it pierces the deep fascia at the lower border of the pectoralis
major. It pierces the clavipectoral fascia and joins the axiallary vein.
At the elbow, the greater part of its blood is drained into the basilic vein
through the median cubital vein, and partly also into the deeps veins through the
perforator vein.
It is accompanied by the lateral cutaneous nerve of the forearm, and the
terminal part of the radial nerve.
Basilic Vein :
The basilic vein of each upper limb originates in the medial part of the dorsal
venous arch. It is the post-axial vein of the upper limb. It extends along the posterior
surface of the ulna to the point near the elbow where it receives the median cubital
vein.
It runs upwards :
1. Along the back of the medial border of the forearm.
2. Winds around the border near the elbow.
3. Continuous upwards in front of the elbow and along the media margin of the
biceps brachi upto the middle of the arm where it pierces the deep fascia.
4. And runs along the medial side of the brachial artery upto the lower border of
the major where it becomes the axillary vein.
It is accompanied by the posterior brach of the medial cutaneous nerve of the
forearm and the terminal part of the dorsal branch of the ulnar nerve.
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Deep Veins: 159
The venae comitantes running with the radial and ulnar arteries drain the deep
and superficial palmar venous arches respectively. They unite near the elbow as
paired brachial veins. The radial veins are smaller, and receive the deep dorsal veins
of the hand. The ulnar veins drain the deep palmar venous arch, and connect with
superficial veins near the wrist. Near the elbow they receive the venae comitantes and
a large branch connects them to the median cubital vein. [Fig. 7 (e)]
1. Radials : Radial veins receive the dorsal metacarpal veins
2. Ulnars : Ulnar veins receive tributaries from the palmar venous arch. Radial
and ulnar veins unite in the bend of the elbow to form the brachial veins.
3. Brachials : Located on either side of the brachial arteries, the brachial veins
join into the axiallary veins. 4. Axiallary veins : The axiallary vein is the continuation of the basilic vein. The
axillary vein is joined by the venae comitantes of the brachial artery a little
above the lower border of the teres major. It lies on the medial side of the
axillary artery. The outer border of the first rib it becomes the subclavian vein.
In addition, to the tributaries corresponding to the branches of the axillary
artery, it receives the cephalic vein in its upper part.
There is no axiallary sheath around the vein, which is free to expand during
times of increased blood flow. Occasionally a muscular band called the axilary arch
overlies the vein. It may compress the vein and cause spontaneous thrombosis.
Subclavian Vein: 160
Right and left subclavian vein unite with the internal jugular to form the
brachio-cephalic veins. The thoracic duct of the lymphatic system delivers lymph into
the left subclavian vein at the junction with the internal jugular. The right lymphatic
duct delivers lymph into the right subclavian vein at the corresponding.
The subclavian vein is a continuation of the axillary vein. It extends from the
outer border of the first rib to the medial border of scalenus anterior, where it joins the
internal jugular to form brachio-cephalic vein. The clavicle and subclavius are
anterior, and the subclavian artery is postero-superior, separated by scalenus anterior
and the phrenic nerve. The first rib and pleura are inferior. The vein usually has a pair
of valves 0.2 cm from its end. Its tributaries are the external jugular, dorsal scapular
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and anterior jugular veins, and occasionally a small brach from the cephalic vein,
which ascends anterior to the clavicle. At its junction with the internal jugular vein,
the left subclavian receives the thoracic duct; the right subclavian vein receives the
right lymphatic duct.
Medial Cubital Vein: 161
Medial cubital vein is a large communicating vein which shunts blood from
cephalic to the basilic vein. If vein must be punctured for an injection, transfusion, or
removal of a blood sample, the median cubital veins are preferred.
It begins from the cephalic vein 2.5 cm below the bend of the elbow, runs
obliquely upward and medially, and ends in the basilic vein 2.5 cm above the medial
epicondyle. It is separated from the brachial artery by the biciptal aponeurosis.
It may receive tributaries from the front of the forearm and is connected to the
deep veins through a perforator vein which pierces the bicipital aponeurosis. The
perforator vein fixes the median cubital vein and thus makes it ideal for intravenous
injections.
Median Vein of the Forearm :
Median vein of the forearm begins from the palmar venous network, and ends
in any one of the veins in front of the elbow. Sometimes it divides into median
cephalic and median basilic veins which join the cephalic and basilic veins
respectively.
Dorsal Venous Arch :
Dorsal venous arch lies on the dorsum of the hand. Its afferents include :
1. three dorsal metacarpal veins,
2. a dorsal digital vein from the medial side of the little finger.
3. a dorsal digital vein from the radial side of the index finger
4. two dorsal digital veins from the thumb,
5. most of the blood from the palm through veins passing around the margins of
the hand and also by perforating veins passing through the interosseuss spaces.
Superficial Veins of The Hand: 162
Dorsal and Palms Digital Veins : [Fig. 7 (c)]
Dorsal digital veins pass along the sides of the fingers, joined by oblique
braches. They unite from the adjacent sides of the digits into three dorsal metacarpal
veins, which form a dorsal venous network over the metacarpus. This is joined
laterally by a dorsal digital vein from the radial digital veins of the thumb, and is
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prolonged proximally as the cephalic vein. Medially and dorsal digital vein from the
ulnar side of minimus joins the network, which ultimately drains proximally into the
basilic vein. A vein often connects the central parts of the network to the cephalic
vein near midforearm.
Palmar digital veins connect to their dorsal counterparts by oblique
intercapitullar veins which pass between metacarpal heads. They also drain to a
plexus superficial to the palmar aponeurosis, extending over both thenar and
hypothenar regions.
Deep Veins of the Hand :
Superficial and deep palmar venous arches accompany their arterial
counterparts and receive the corresponding braches. Thus common palmar digital
veins join the superficial arch, and palmar metacarpal veins join the deep arch.
Palmar and Dorsal Metacarpal Veins :
Deep veins accompanying the dorsal metacarpal arteries receive perforating
branches from the palmar metacarpal veins. They end in the radial veins and the
dorsal venous network over the metacarpus. This network is joined laterally by a
dorsal digital vein from the radial side of the index finger and by both digital veins of
the thumb. It is prolonged proximally as the cephalic vein.
Veins of the Thorax 163
Superior Vena Cava : [Fig. 6 (b)]
The superior vena cava is 7 cm in length, formed by the junction of the
brachio-cephalic veins. It returns blood to the heart from the superior half of the body.
It begins behind the lower border of the first eight costal cartilage near the sternum,
descends vertically behind the first and second intercostals spaces, and ends in the
upper right atrium behind the third right costal cartilage. Its inferior half is within the
fibrous pericardium, which it pierces level with the second costal cartilage. Covered
antero-laterally by serous pericardium, it is slightly covex to the right. It has no
valves.
Tributaries :
The azygos vein and small veins from the pericardium and other mediastinal
structures.
Inferior Vena Cava :
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The inferior vena cava conveys the blood to the right atrium from all structure
below the diaphragm. The majority of its course is within the abdomen, but a small
section lies within the fibrous pericardium in the thorax. It is formed by the junction
of the common ilial veins anterior to the fifth lumbar vertebral body, a little to its
right.
It ascends anterior to the vertebral column, to the right of the aorta. It is
contained is a deep groove on the posterior surface of the liver or sometimes is a
tunnel completed by a band of liver tissue. It crosses the tendinous part of the
diaphragm between its median and right ‘leaves’ and inclines slightly anteromedially.
Passing through the fibrous pericardium and through a posterior inflexion of the
serious pericardium, it opens into the infero-posterior part of the right atrium. The
abdominal portion of the inferior vena cava is devoid of valves.
The abdominal inferior vena cava usually receives the common iliac veins at
its origin and the lumbar, right gonadal, renal, right supra-renal, inferior phrenic and
hepatic veins during its course.
The thoracic part is very short, partly inside and partly outside the pericardinal
sac. The extrapericardial part is separated from the right pleura and lung by the right
phrenic nerve. The intrapericardinal part is covered, except posteriorly, by inflected
serous pericardium. The venous drainage from the tissues below the diaphragm finally
ends in the inferior vena cava. The inferior vena cava of traverses the diaphragm at
the level of the eight and ninth thoracic vertebra between the right and central tendon
of the diaphragm. It then passes through the pericardium and drains into the right
atrium.
Brachiocephalic Veins: 164
Right Brachio-cephalic veins :
About 2.5 cm long the right brachio-cephalic vein begins posterior to the
sternal ends of the right clavicle, and descends almost vertically to join the left
brachio-cephalic vein, forming the superior vena cava posterior to the lower border of
the first right costal cartilage, near the right sternal border. Its tributaries are the right
vertebral, internal, thoracic, inferior thyroid and sometimes the first right posterior
intercostal veins.
Left Brachio-cephalic vein :
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Some 6 cm long, the left brachio-cephalic vein begins posterior to the sternal
end of the left clavicle, anterior to the cervical pleura. It descends obliquely to the
right, posterior to the upper half of the manubrium sterni, to the sternal end of the first
right costal cartilage, uniting here with the right brachio-cephalic vein to form the
superior vena cava. Its tributaries are the right vertebral, internal thoracic, inferior
thyroid, superior intercostal, sometimes the first left posterior intercostal, thymic and
pericardial veins.
Azygos System :
The azygos system, besides collecting blood from the thorax and abdominal
wall, may serve as bypass for all the inferior vena cava that drains blood from the
lower body. Several small veins directly like the azygos system of the inferior vena
cava or hepatic portal vein becomes obstructed, the azygos system can return blood
from the lower body to the superior vena cava.
Azygos Vein :
The azygos vein is anterior to the vertebral column, slightly to the right of the
midline. It usually begins at the junction begins at the junction of the right ascending
lumbar and right subcostal veins near the diaphragm. At the level of the 4th thoracic
vertebra, it arches over the root of the right lung to end in the superior vena cava.
Generally, the azygos vein drains the right side of the thoracic wall, thoracic viscera
and abdominal wall. Specifically the azygos vein receives blood from most of the
right posterior intercostals, hemiazygos, accessory hemiazygos, oesophageal,
mediastinal, pericardial and bronchial veins.
Hemiazygos vein :
The hemiazygos vein is anterior to the vertebral column and slightly to the left
of the midline. It usually begins at the junction of the left ascending lumbar and left
subcostal veins. It terminates by joining the azygos vein at about the the level of the
ninth thoracic vertebra. Generally the hemiazygos vein drains the left side of the
thoracic wall, thoracic wall, thoracic viscera and abdominal wall. Specifically, the
hemiazygos vein receives blood from the ninth through the eleventh left posterior
intercostals, esophageal, mediastinal and sometimes the accessory hemiazygos vein.
Accessory Hemiazygos Vein :
The accessory hemiazygos vein is also anterior to the vertebral column and to
the left of the midline. It begins at four intercostal space and descends from the fifth
to the eighth thoracic vertebra or ends in the hemiazygos vein. It terminates by joining
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the azygos vein at about the level of the eighth thoracic vertebra. The accessory
hemiazygos vein drains the left side of the thoracic wall. It receives blood from the 4th
through eighth left posterior intercostal veins, left bronchial, and mediastinal veins.
Veins of Abdomen And Pelvis: 165
Blood from the abdominal and pelvic viscera and abdominal wall returns
to the heart via the “inferior vena cava”. Many small veins enter the inferior vena
cava. Most carry return flow from the parietal braches of the abdominal aorta, and
this names correspond to the names of the arteries. [Fig. 7 (b)]
The inferior vena cava doesn’t receive veins directly from the gastro-intestinal
tract, spleen, pancreas, and gall bladder. These organs pass their blood into a common
vein, the hepatic portal vein, which delivers blood to the liver. The superior
mesenteric and splenic veins until to form the hepatic portal vein. This special flow of
venous blood is called hepatic portal circulation.
Inferior Vena Cava :
The two common iliac veins that drain to lower limbs, pelvis and abdomen
unite to form the inferior vena cava. The inferior vena cava extends superiorly
through the abdomen and thorax to the right atrium.
Common Iliac Veins :
The common iliac veins are formed by the union of the internal and external
iliac veins anterior to the sacroiliac joint and represent the distal continuation of the
inferior vena cava at their bifurcation. The right common iliac vein is much shorter
than the left and is also more vertical. Generally, the common iliac veins drain the
pelvis, external genitals, and lower limbs.
Internal Iliac Veins :
The internal iliac veins begins near the superior portion of the greater sciatic
notch and run medial to their corresponding arteries. Generally the veins drain the
thigh, buttocks, external genitals and pelvis.
External Iliac Veins :
The external iliac veins are companions of the internal iliac arteries and begin
at the inguinal ligaments as continuations of the femoral veins. They end anterior to
the sacroiliac joint where they join with the internal iliac veins to form the common
iliac veins. The external iliac veins drain the lower limbs, cremaster muscle in males
and the abdominal wall.
Lumbar Veins :
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A series of parallel lumbar veins, usually four on each side, drain blood from
the both sides of the posterior abdominal wall, vertebral canal, spinal cord and
meninges. Lumbar veins run horizontally with the lumber arteries. The lumbar veins
connect at right angles with the right and left ascending lumbar veins, which form the
origin of the corresponding azygos or hemiazygos vein. The lumbar vein drain blood
into the ascending lumbars and then run to the inferior vena cava, where they release
the remainder of the flow.
Gonadal Veins :
The gonadal veins ascend with gonadal arteries along the posterior abdominal
wall. In the male the gonadal veins are called the testicular veins. The testicular veins
drain the testes. In the female, the gonadal veins are called ovarian veins. The ovarian
veins drain the ovaries. The left ovarian vein empties into the left renal vein, and the
right ovarian vein drains into the inferior vena cava.
Renal Veins :
The renal veins are large and pass anterior to the renal arteries. The left renal
vein is longer than the right renal vein and passes anterior to the abdominal aorta. It
receives the left testicular, left inferior phrenic, and usually left supra-renal veins. The
right renal empties into the inferior vena cava posterior to duodenum. The renal veins
drain kidneys.
Supra-renal veins :
These vein drain the adrenal glands.
Veins of the Lower Limb: 166
The veins of the lower limb can subdivided, like those of the upper limb, into
superficial and deep groups. The superficial veins are subcutaneous and lie in the
superficial fascia; the deep veins accompany the major arteries. Both groups have
valves, which are more numerous in the deep veins and also more numerous than in
the veins of the upper limb. Venous plexuses occur within and between some of the
lower limb muscles. [Fig. 7 (a)]
The principal named superficial veins are the long and short saphenous veins.
Their numerous tributaries are mainly unnamed.
Deep veins of the lower limbs accompany the arteries and their branches.
Plantar digital veins arise from plexuses in the plantar regions of the toes, connect
with dorsal digital veins and unite four plantar meta-tarsal veins. These run in the
intermetatarsal spaces and connect by perforating veins with dorsal veins then
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continue to form a day plantar arterial arch. From this arch, medial and lateral plantar
veins run near the corresponding arteries. They communicate with the long and short
saphenous veins before forming the posterior tibial veins behind medial malleolus.
The posterior tibial veins accompany the posterior tibial artery. They receive
veins from the calf muscles, especially the venous plexus in soleus, and connect the
with superficial veins and with the peroneal veins. The latter, running with their
artery, receive branches from soleus and superficial veins.
The anterior tibial veins are continuations of venae comintantes of the dorsalis
pedis artery. They leave the extensor region between the tibia and fibula, pass through
the proximal end of the interossoeus membrane, and unite with the posterior tibial
veins to form the popliteal vein at the distal border of popliteus.
Considerable of the venous drainage is of great importance because in the
lower limb venous blood has to ascend against gravity. This is aided by a number of
local factors, the failure of which gives rise to varicose veins. The veins of lower limb
may be classified into three groups. 167
I. Superficial Veins
II. Deep Veins
III. Perforating Veins
(I) Superficial Veins :
They include the great and small saphenous veins and their tributaries. They
lie in the superficial fascia, on the surface of the deep surface. They are thick walled
because of the presence of smooth muscle and some fibrous and elastic tissues in their
walls.
(II) Deep Veins :
These are the anterior and posterior tibial, peroneal, popliteal, & femoral veins
and their tributaries. They accompany the arteries, and are supported by powerful
surrounding muscles. The valves are more numerous in deep veins than in superficial
veins. They are more efficient channels than the superficial veins because of the
driving force of muscular contraction.
(III) Perforating Veins :
They connect the superficial with the deep veins. Their valves permit only one
way flow of blood, from the superficial to the deep veins. There are about five
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perforators along the great saphenous vein, and one perforator along the small
saphenous vein.
Superficial Veins of Lower limb :
(1) The dorsal venous arch lies on the dorsum of the foot over the proximal part
of the meta-tarsal bones. It receives four dorsal meta-tarsal veins each of
which is formed by the union of two dorsal digital veins
(2) The great or long saphenous vein is formed by the union of the medial end of
the dorsal venous arch with the medial marginal vein which drains the medial
side of the medial surface of tibia obliquely, and runs along its medial border
to reach the back of the knee. The saphenous nerve runs in front of the great
saphenous vein.
(3) The small or short saphenous vein is formed by the union of the lateral end of
the dorsal venous arch with lateral marginal vein, draining the lateral side of
the little toe. It passes upwards behind the lateral malleolus to reach the back
of the leg. The sural nerve accompanies the small saphenous vein.
Both saphenous veins are connected to the deep veins through the perforating
veins.
Great or Long Saphenous Vein: 168
Saphes Easily seen.
The saphenous vein can be easily seen in the leg. Venous drainage acquires
importance as blood has to flow up against the gravity. [Fig. 7 (b)]
The long saphenous vain, is the largest and longest superficial vein of the
lower limb. It starts on the dorsum of the foot from the medial of the dorsal venous
arch, and runs upwards in front of the medial malleolus along the medial side of the
leg, and behind the knee. In the thigh, it inclines forwards to reach the saphenous
opening where it pierces the cribriform fascia and opens into the femoral vein.
In its course through the thigh the long saphenous vein is accompanied by the
branches of the medial femoral cutaneous nerve. Before piercing the cribriform fascia,
it receives three named tributaries corresponding to the 3 cutaneous arteries and also
many unnamed tributaries.
It contains about 10-15 valves which prevent back flow of the venous blood,
which tends to occur because of gravity. One valve is always present at the saphenous
Regional Venous System
115
femoral junction. Incompetence of these valves makes the vein dilated and tortuous
leading to varicose vein.
In almost its entire extent the vein lies in superficial veins, but it has many
connections with the deep veins, especially in the leg. The veins is also connected to
the deeps veins of the limb by perforating veins. There are three medial perforators
just above the ankle, one perforator just below the knee and another one in the region
of the adductor canal. The perforating veins are also provided with valves which
permit flow of blood only from the superficial to deep vein.
Tributaries :
At the ankle the long saphenous vein drains the sole by medial marginal veins.
In the leg it often connects with the short saphenous vein and with deep veins via
perforating veins. Just distal to the knee it usually receives three large tributaries from
the front of the leg, from the tibial malleolar region and from the calf. The tributary
draining the tibial malleolar region is formed delicate veins overt the medial malleolus
and then ascends the medial aspect of the calf as the posterior arch vein.
It connects with posterior tibial venae comintantes by a series of perforating
veins. These are usually three equally spaced between the medial malleolus and the
mid calf. More than three such perforators are uncommon and an arch vein perforators
above mid calf is only very rarely found.
Above the posterior crural arch vein, perforating veins join the long saphenous
vein, or one of its main tributaries at the two main sites. The first is at a level in the
upper calf indicated by its name, the tibial tubercle. Perforator; the second is in the
lower / intermediate third of the thigh where it perforates the deep fascial roof of the
subsartorial canal to join the femoral vein.
In the thigh the long saphenous vein receives many tributaries. Some open
independently, whilst others converge to form large named channels that frequently
pas forwards the basal half of the femoral triangle before joining the long saphenous
near its termination. These may be grouped as follows : one or mor large postero-
medial tributaries, one or more large antero-medial tributaries, four or more peri-
inguinal veins. The postero-medial vein of the thigh, large and sometimes double,
drains a large superficial region indicated by its name. It has radiological and surgical
Regional Venous System
116
significance. One of its lower radicles is often continuous with short saphenous vein.
The postero-medial vein is sometimes named the accessory saphenous vein, through
some restrict the term accessory to a lower, postero-medial tributary when tow are
present. Another large vessel, the antero-lateral vein of the thigh usually commences
from an anterior network of veins in the distal thigh and crosses the apex and distal
half of the femoral triangle to reach the long saphenous vein. As the latter traverses
the saphenous opening, it is joined by the superficial epigastric, superficial circumflex
iliac and superficial external pudendal veins. Their mode of union varies. Superficial
epiagastric and circumflex iliac veins drain the inferior abdominal wall, the latter also
receiving tributaries from the proximo-lateral region of thigh. The long saphenous
vein is often harvested for grafts used both in peripheral and coronary arterial surgery.
Surface Marking of Saphenous Vein: 169
It can be marked by joining the following points, although it is easily visible in
living subjects :
(a) First point on the dorsum of foot at the medial end of the dorsal venous arch
(b) Second point on the anterior surface of the medial malleolus
(c) Third point on the medial border of the tibia at the junction of the upper two
thirds and lower one third of the leg
(d) Fourth point at the adductor tubercle
(e) 5th point just below the centre of the saphenous opening.
Its formation on the dorsum of the foot, its course along the entire length of
the lower limb, and its termination into femoral vein. It contains about 10-20 valves.
There is one valve that lies just before the vein pierces the cribriform fascia and
another at its termination into the femoral vein.
Short Saphenous Vein:170
The short saphenous vein starts on the lateral side of the foot and ascends up
on the back of the leg to end in the popliteal vein. The vein is formed on the dorsum
of the foot by the union of the lateral end of the dorsal venous arch with the lateral
marginal vein. In lower third of the calf it ascends lateral to the calcaneal tendon,
lying on the deep fascia and covered only by superficial fascia and skin. In the leg it
ascends lateral to the tendocalcaneus, and then along the middle line of the calf, to the
lower part of the popliteal fossa. Here it pierces the deep fascia and opens into the
Regional Venous System
117
popliteal vein. It drains the lateral border of the foot, the heel and the back of the leg.
It is connected with the great saphenous and with deep veins.
Tributaries :
The short saphenous vein connects with deep veins on the dorsum of the foot,
receives many cutaneous tributaries in the leg, and sends several communicating
branches proximally and medially to join the long saphenous vein. Sometimes a
communicating branch ascends medially to the accessory saphenous vein. This may
be main the continuation of the short saphenous vein. In the leg, the short saphenous
vein lies near the sural nerve, it has 7-13 valves one near its termination. Its mode of
ending is variable, it may join the long saphenous vein in the proximal thigh or it may
bifurcate, one branch joining the long saphenous, the other the popliteal or deep
posterior femoral veins. Sometimes, it ends distal to the knee in the long saphenous or
sural muscular vein.
Surface Marking :
It can be marked by joining the following points, although this vein is also
easily visible in its lower part :
(a) A point on the dorsum of the foot at the lateral end of the dorsal venous arch
(b) Second point behind the lateral malleolus.
(c) Third point just lateral to the tendocalcaneous above the lateral malleolus.
(d) Fourth point at the centre of the popliteal fossa.
Its formation on the dorsum of the foot, course along the back of the leg, and
termination into the popliteal vein.
Just before piercing the popliteal fascia, it may give a communicating branch
to the accessory saphenous vein. Sometimes, the whole of the small saphenous vein
opens into the great saphenous vein through the accessory saphenous vein.
Occasionally, the small saphenous vein ends below the knee either in the great
saphenous vein, or in the deep muscular veins of the leg.
Perforating Veins: 171
As already mentioned, they connect the superficial with the deep veins. There
are classified as follows :
(I) Indirectly Perforating Veins :
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118
Indirect perforating veins connect the superficial veins with the deep veins
through the muscular veins.
(II) Direct Perforating Veins :
Direct perforating veins connect the superficial veins directly with deep veins.
The great and small saphenous veins are the large direct perforators.
(a) In the thigh : the adductor canal perforator connects the great saphenous vein
with the femoral vein in the lower part of the adductor canal.
(b) Below the knee : one perforator connects the great saphenous vein or the
posterior arch vein with the posterior tibial vein.
(c) In the leg : (i) a lateral perforator is present at the junction of the middle and
lower third of the leg. It connects the small saphenous vein or one of its
tributaries with peroneal vein. Medially, there are three perforators which
connect the posterior arch vein with the posterior tibial vein.
(d) The upper medial perforator lies at the junction of the middle and lower thirds
of the leg.
(e) The middle medial perforator lies above the medial malleolus.
(f) The lower medial perforator lies posteroinferior to the medial malleolus.
Deep Veins of Lower Limb: 172
(I) Posterior Tibial Veins :
The posterior tibial veins accompany the posterior tibial artery. They receive
tributaries from the calf muscle and connections from the superficial veins and
the peroneal veins. Posterior tibial vein is formed by the union of the medial
and lateral plantar veins posterior to the medial malleolus.
(II) Anterior Tibial Veins :
The anterior tibial vein is the superior continuation of the dorsalis pedis vein
in the foot. It extends between the tibia and fibula and unites with the posterior
tibial to form the popliteal vein at the distal border of the popliteus.
Popliteal Vein: 173
It begins at the lower border of the popliteus by the union of veins
accompanying the anterior and posterior tibial arteries, and posterior tibial arteries. It
is medial to the popliteal artery in the lower part of the fossa; posterior to the artery in
Regional Venous System
119
the middle and postero-lateral to it in the upper part of the fossa. The vein continues
as the femoral vein at the opening in the adductors magnus.
The popliteal vein receives -
(1) the small saphenous vein and
(2) the vein corresponding to the branches of the popliteal artery.
Profunda Femoris Vein :
The profunda femoris vein lies anterior to its artery, and has tributaries
corresponding to the branches of the artery. Through these tributaries it connects
distally with the popliteal and proximally with the inferior gluteal veins. It sometimes
drains medial and lateral circumflex femoral veins. It has a valve just before it
terminates.
Femoral Vein: 174
The femoral vein accompanies its artery beginning at the adductor opening, as
the continuation of the popliteal vein, and ending posterior to the inguinal ligament as
the external iliac vein. In the distal adductor canal, it is postero-lateral to the femoral
artery, more proximally in the canal, and in the distal femoral triangle, it is posterior
to it, proximally, at the base of the triangle, it is medial. The vein occupies the middle
compartment of the femoral sheath, between the femoral artery and canal, fat in the
latter allowing expansion of the vein. It has many muscular tributaries; 4-12 cm distal
the inguinal ligament the profunda femoris vein joins it posteriorly and then the long
saphenous vein, which enters anteriorly. Veins accompanying the superficial
epigastric, superficial circumflex iliac and external pudendal arteries join the long
saphenous vein before it enters the saphenous opening. Lateral and medial circumflex
femoris veins are usually tributaries of the femoral. There are usually four or five
valves in the femoral vein. The two most constant are just the distal to the entry of the
profounda femoris and near the inguinal ligament.
Deep and Superficial Venous Systems of the Foot: 175
Plantar digital veins arise from the plexuses in the plantar regions of the toes,
connecting with dorsal digital veins and uniting into four plantar metatarsal veins. The
latter run in the intermetatarsal spaces and connect by perforating veins with dorsal
veins, then continue to form the deep plantar venous arch that accompanies the plantar
arterial arch. From this venous arch, medial and lateral plantar veins run near the
corresponding arteries and after communicating with the great and small saphenous
veins, from the posterior tibial veins behind the medial malleolus.
Regional Venous System
120
The principal named superficial veins are the great and small saphenous. Their
numerous tributaries are mostly unnamed.
Dorsal digital veins receive rami from the plantar digital veins in the clefts
between the toes and then join to form dorsal metacarpal veins, which are united
across the proximal parts of the metatarsal bones in a dorsal venous arch. Proximal to
this arch, an irregular dorsal venous network receives tributaries from deep veins and
is continuous, proximally with a venous network in the leg. At each side of the foot,
this network connects with medial and lateral marginal veins, which are both formed
mainly by veins from more superficial parts of the sole. In the sole, superficial veins
form a plantar cutaneous arch across the roots of the toes and also drain into the
medial and lateral marginal veins. Proximal to the plantar arch there is a plantar
cutaneous venous plexus, especially dense in the fat of the heel. It connects with the
plantar cutaneous venous arch and other deep veins, but drains mainly into the
marginal veins. The veins of the sole are an important part of the lower limb ‘venous
pump’ system aiding return of the blood up the limb. Intermittent to enhance this flow
and so reduce the risk of deep vein thrombosis during periods of increased risk, e.g.
after surgery.
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7. BLOOD LETTING
The importance of blood letting as medicinal agent, in comparison with other
means of cure in various respects, it is the equivocal of remedies when properly
administered. In short, “blood letting is a remedy which when judiciously employed it
is hardly possible to estimate to highly”. Different methods are in use for taking away
the blood for therapeutic purposes first by (1) phlebotomy – where blood is drawn
from available veins. (2) Arteriotomy – where artery is punctured (3) Scarification –
Scraping of superficial cells with syringe. Venesection or phlebotomy is much more
effective than any other modes of treatment for an instance the object may be to take
away the blood so rapidly to make a great impression on the system. 176
Likewise in modern era also Phlebotomy (Venesection) is part of treatment.
Performed in different conditions like – polycythemia vera, hemochromotosis,
hepatitis B, hepatitis C and C C F. 177
Phlebotomy :
Phlebo vein, tome to cut.
Venesection :
Opening of a vein for withdrawal of blood. Although phlebotomy is a
synonym for venesection in clinical practice, phlebotomy refers to therapeutic blood
letting, such as removing some blood to lower the viscosity of blood of a patient with
polycythemia. 178
Webster’s defines phlebotomy as phle bot omy / Fli-bat-eh-mee\n: The letting
of blood in the treatment of diseases. i.e. VENESECTION.111
Historical Background of Blood Letting Therapy :
The practice of blood letting seemed logical when the foundation of all
medical treatment was based on four body humours blood,, phlegm, yellow bile and
black bile. Health was thought to be restored by purging, vomiting, blood letting etc.
The art of blood letting was familiar before Hippocrates in fifth century B.C. Both
surgeons and barbers were practicing this blood letting. Blood letting came to the U.S.
in 18th and early 19th century. The first U. S. president George Washington died from
throat infection in 1799 where he had been drained of nine pints of blood in 24 hours,
where one pint =16-30 ounces, when patient becomes faint bleeding was often
Blood Letting
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encouraged in large areas of the body by multiple incisions. But by the end of 19
century this phlebotomy was declared. 180
The practice of blood letting or phlebotomy dates back to antiquity. The
followers of Hippocrates in blood letting in th 5th century B.C. strongly believed in
blood letting. Early Egyptian have been inspired by seeing bats and remove blood
from animals. Hyppos scratches on tree until the bleed , and other animals scratching
at diseased part for relief. Additionally many human examples of bleeding such as
nasal bleeding, haemetemesis , rectal bleeding, menstruation – these science in nature
led early civilians to think that bleeding must have some beneficial value.
From these simple observation came increasingly the complex theories as to
why blood letting is necessary and how it worked? In early theory of four bodily
humours, an imbalance in these humours was postulated as need for a blood letting
was used to treat everything from fever, madness, upto anemia as one can imagine
treating an anemic patient by removing more blood was the best of ideas. Through the
middle ages to 18th century. There were many strides in medieval field regarding
diseased state, anatomy and therapeutic majors.
Blood letting in modern medicine referred to as phlebotomy was a popular
medical practice upto the late 19th century. It was one of oldest medical practices in
Greeks, Egyptians, and Mesopotamia. It was theorized by many disease caused by
plethoras (over abundance in the blood), so advised that these plethoras be treated
initially by excessive, sweating, reduced food intake, meeting and blood letting,
Greek physicians practiced phlebotomy extensively and gained reputation. Greek
physician Gallen believed that blood was the dominant humor in the order to balance
the other humors. So he also preferred blood letting, he created a complex system that
how much blood should be removed based on patient age, constitution, season,
symptoms etc. The blood to be let was of a specific nature determined by the disease,
either capillaries or venous, and close area of body was affected the linked different
blood vessels with different organs according to their supposed drainage. Ex: right
medial cubital vein in the right hand would be let for liver problems. 181
Blood Letting in the Last Millennium :
Even after the humoral system fell into disuse, but the practice of blood letting
was often recommended by physican and carried out by surgeons and barbers. Blood
letting was used to treat a wide range of diseases becoming a standard treatment for
Blood Letting
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every element. The practice continued throughout the middle ages. In Northern
Europe, Netherlands, France, physicians advocated frequent phlebotomy throughout
18th century the efficiency of phlebotomy was hotly debated, but in 19th century it has
been restricted to few diseases. 182
Phlebotomy is longest running tradition in medical field, originated in
civilization of Egypt, Greek period flourished in Arabic and Indian medicine practice
continued for 2500 years until it was replaced by modern medicine. There are
references of phlebotomy for pneumonia, fevers, back pain, fractures, wounds. This is
based on ancient Indian medicine in which blood considered as one of the humour
maintaining health. It was not until well into the 19th century that people began to
question a value of blood letting. So later phlebotomy is almost never used any more
except for certain rare conditions; one is hemochromatosis. 183
For many centuries blood letting was considered a tried and true remedy for
certain conditions. It was recommended for fevers, inflammations, a rarity of disease
conditions and ironically for hemorrhage. Although it fell in and out of favour, it
persisted in to the 20th century and was even recommended by Sir William Osler in
1923 edition in his principles and practice of medicines. 184
Preparation :
Patients having their blood drawn for analysis may be asked to continue
medications are avoid food. Patients donating blood will be asked for brief medical
history with hematocrit value Hb%, ESR, etc.
Blood letting was popular practice from antiquity to the late 19th century. This
phlebotomy is act of drawing or removing blood from the circulating system through
a cut or puncture.
Description: 185
Phlebotomy is performed by a technician or phlebotomist, blood is usually
taken from a vein on the back the hand or inside of the elbow. The skin over the area
is wiped with an antiseptic, an elastic band, is tied over the hand. The bands acts like
tourniquet, slowing the blood flow in the arm and making the veins more visible. The
patient is asked to make a first and technician feels. The veins in order to select an
appropriate one. When vein is selected the technician inserts a needle into the vein
and releases the elastic band. The required amount of blood drawn and needle is
withdrawn from the vein. The patients pulse and blood pressure should be monitored.
Blood Letting
124
The amount of blood depends upon the purpose of phlebotomy. Blood donors usually
contribute around 350 ml in a session. But in therapeutic phlebotomy larger amount of
blood is drawn than the blood donation.
General Considerations :
1. Open needle package but don’t remove needle shield thread needle on to
holder.
2. Select needle, tubes appropriate for sample desired and a sterile container.
3. Tubes that contain additives should be gently tapped to dislodge any additive
which may be trapped around the stopper.
4. Inster tube into holder push tube stopper onto needle until leading edge of
stopper meets guidelines of holder. Tubes were retract slightly. Leave in the
position. When using 13 mm diameter tubes, it is important to enter the tubes
in the holder when penetrating the stopper to preclude sidewall penetration
and resultant loss of volume.
5. Select site for venipuncture.
6. Apply tourniquet. Prepare venipuncture site with an appropriate antiseptic.
Don’t palpate venipuncture site after cleansing.
7. Place patients arm in a downward position.
8. Remove needle shield. Perform venipuncture with arm in a downward position
and tube stopper uppermost.
9. Push tube onto holder, puncturing diaphragm of stopper.
10. Remove tourniquet as soon as blood appear in tube. Donot allow content of
tube to contact. The stopper or the end of the needle during procedure. If no
blood flows into tube or ceases to flow before an adequate sample is collected,
the following steps are suggested to complete satisfactorily.
Collection : Confirm correct position of needle cannula in vein.
If a multiple sample needle is being used, remove, the tube and place a new
tube into the holder, if the second tube does not draw, remove the needle and
discard an appropriate disposal device. Repeat procedure from Step-I.
11. When first tube in full and blood flow ceases, remove it from holder.
12. Place succeeding tubes in holer, puncturing diaphragm to initiate flow. Tube
without additives are drawn before tubes with additives.
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125
13. While each successive tube is fillup, invert the previous tube containing
additives 8-10 times don’t flow. Vigorous mixing can cause hemolysis.
14. As soon as blood stops flowing in the last tube, remove needle from vein,
apply pressure to puncture site with dry, sterile swab, until bleeding stops.
15. Applying bandage is desired.
16. After the venipuncture, the top of the stopper may contain residual blood at the
puncture site. Proper precautions should be taken when handling tubes to
avoid contact with blood droplets. Dispose of any holder that becomes
contaminated with blood.
17. Needle disposal.
After Care :
When blood is drawn and needle is removed pressure is placed on punctured
site with a cotton wool, to stop bleeding bandage is applied. It is not uncommon for a
patient to feel dizzy or noisiated during after phlebotomy. The patient may be
encouraged to rest for a short period after completion of procedure. Patients are also
instructed to drink plenty of fluids and to eat regularly to replace lost blood volume.
Patients who experience swelling of the puncture site are continued bleeding after
phlebotomy should get medical help.
Most patients will have a small bruise or mild soreness at the puncture site for
several days. Therapeutic phlebotomy may cause thrombocytosis (a vascular
condition characterized by high platelet count) and chronic iron deficiency, some
patients. The risks can be minimized by use of sterilized equipments, careful
attention, and proper techniques.
Significance of Phlebotomy :
1. Recently, in modern medical science blood letting by venesection
(phlebotomy) advised in the conditions like acute pulmonary oedema,
thrombosis of the cerebral arteries, right heart failure indicated by orthopnoea
with distended jugular veins, cyanosis, venous congestion, in acute
pericarditis, in lobar pneumonia where the patients is cyanosed, uraemia
etc.The venesection is done 5-20 ounces of blood is letted out provided there
should not be severe anaemia. 188
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126
2. In iron over load states blood letting is the choice of treatment such as in
hemochromoatosis, tranferrin, deficiency, porphyria, erythropoeitc siderosis,
after portacaval shunting a large quantities of blood is removed about 500 ml
weekly for one – two years, upto the fall of hemoglobin and serum ferritin
level. 189
3. In an alcoholic iron absorption is increased in small intestine. Multiple factors
contribute to hepatic iron deposition, which is a contributing factor for
development of cirrhosis and hepatitis C is always co-factor for the
development of cirrhosis in an alcoholic.190
4. Blood letting is effective in elimination of amino transferase levels of patients
with chronic hepatitis C and iron overload.191
5. When the circulation of blood was first discovered at the same time effects of
blood letting would be clearly understood. The effects of blood letting were
judged upon certain pimple, as if the blood were removing from the veins. The
contractibility of vessels, vital property is improved. 192
6. Hakim Mohammad Ghyas is one of the practioners of India who is practicing
and appreciated effect of blood letting to cure variety of ailments. He claims
blood letting can cure arthritis, lumbago and cancer. The basic tenet of therapy
is the belief that impure blood is the cause of all ailments, get rid of the bad
blood and get well. Even if several session may be needed to achieve the goal. 193
7. In certain conditions management is replaced by venesection such as CCF,
where there is increased strain on right ventricle. So by phlebotomy total
volume of blood is lessened. The work of heat is lightened for a time. The
some result also we can get in pneumonia, pleurisy and bronchitis. It also
helps to lower blood arterial tension in early stages of cerebral hemorrhage
when heart is working vigorously venesection may lead to lowering the blood
pressure and so giving a blood in ruptured vessels an opportunity to coagulate.
In various convulsive attacks, acute uraemia, blood letting in beneficial.
8. Blood letting, by phlebotomy lead to improvement in peripheral insulin
sensitivity in inviduals with high infertility type-2 diabetes.
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127
9. Formation of blood cells appear in yolk sac of the two week embryo. By 8
weeks in established by liver of embryo, by 16 weeks liver has become major
sight of blood cells formation. Spleen also active during this period. Lymphoid
cells and foetal thymus is the temporary sight of lymphocytes. Highly cellular
bone marrow becomes an active blood making system about 20 weeks. At
birth active blood making red marrow occupies upto 22 years. Adult blood
marrow has a large reserve capacity for cell production, whenever there is
excessive demand liver, spleen make the blood.
10. In old age red marrow is replaced by inactive yellow marrow. So red marrow
forms all types of blood cells and also active in destruction of R.B.C.
Therefore, red marrow is the most active organs of the body. It is generally
accepted that all blood cells made from a relatively few cells capable of
mitosis. The production of R.B.C’s referred as erythropoesis.
In health, erythropoesis is regulated from bone marrow and is
stimulated by hypoxia (lack of oxygen). However, oxygen lack does not act
directly on haemopoetic tissues, where it stimulated production of
erythropoetic hormone. Erythropoetin is fromed in kidney also by the action of
erythropoetic factor “erythrogenin”. It is present in kidneys released into the
blood in response to hypoxia. Thyroid hormones T.S.H, adrenocorticoids,
andreno-corticotrophic hormones, human growth hormone – all promote
erythropoietic formation and enhance R.B.C. formation. So in
hypothyroidism, there is reduced erythropoesis. Polycythemia (excess R.B.C.
production) is feature of Cushing syndrome. However high dose of steroids
inhibit erythropoesis. Male hormones stimulate, female hormone depressed by
erythropoietic response.
11. A physiological secondary polycythemia is as a result of tissue hypoxia. In
diseases like chronic bronchitis, emphysema, C.C.F. and Fallot’s tetrology.
Oxygen carrying capacity of blood is increased by polycythemia, where there
is increased viscosity of blood. Increased viscosity produces raised blood
pressure. Venesection is sometimes employed to reduce the red cell volume. 194
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128
12. Haemochromatosis is an autosomal recessive disease characterized by an
increase in iron absorption relative to body iron stores. It has a prevalence of
one in 300 in the Australian Caucasian community. Symptoms and signs are
related to the amount of body iron stores. Early symptoms include lethargy
and fatigue, whilst late symptoms are related to the organs affected such as
liver, heart, pancreas and pituitary gland. Cirrhosis of liver is a particularly
important complication because it is associated with a 200-fold higher risk of
heptocellular carcinoma. On the other hand, the extra risk is entirely removed
if the patient is diagnosed and treated before cirrhosis develops. 195
Discussion
129
DISCUSSION
Discussion is one of prime importance to constitute, the proper conclusions in
any type of research. Science is always subjected for change. It is always relative
truth, not absolute truth. On the other hand, Ayurved is greatly emphasized on its
classical texts, Aptha Vachanas by ancient Acharyas. These are always truths, as they
have done observations and documented, their experiences for the welfare of
mankind. The concepts are evolved many years ago, because of generation gap and
lack of interpretation, concepts are not passed onto future generation properly. So now
we are lacking the opportunity to understand and to clarify the doubts. So the present
study was carried out to ‘anatomically locate Shakhagata Vedhya Sira Sthanas in
particular diseases (literary research). So that the concepts of Sira Shareera and Sira
Vyadha Vidhi Shareera can be better understood and to pass on knowledge to the
future generation for its practical utility.
Discussion on Sira Shareera :
The term ‘Sira, Dhamani’ are as old as Vedas. They have been generally used
with common meaning. But these are not synonymous. Of course, in general Siras
means blood vessels. But on the basis of interpretation of commentators ‘Dhamanis’
is a channel connected to the heart which is thick and ‘Sira’ is thin blood vessels.
Rather than Sushruta, Charaka in clear about this text with quoting dictum “Dhmanat
Dhamanyaha, Sravanath Srotansi, Saranat Sira”. ‘Dhma’ means pumping of Rasa by
heart into Dhamanis, ‘Sru’ means channels where there is slow discharge of fluid.
‘Sra’ means root of word ‘Sira’ means to move slowly. So with these points view,
Dhamanis are arteries, Siras are veins and Srotas are lymphatics. As per Gangadhar
Shastri, the classification of Sira can be understood like this.
Veins are playing very important role in both pulmonary and systemic
circulation. These are characterized by large capacitance compared to arteries.
Initially they were considered as simply reservoirs of blood. But now it has been
identified as veins are very essential to maintain proper circulation, cardiac output
drainage and venous return in the mechanism of homeostasis. The blood vessels like
arteries, veins and capillaries have got similar structural component with little
difference. Compared to arteries veins are thin walled, elastic tissue is less, but in
Discussion
130
artery walls are thick with excess elastic muscle fibers. Microscopically it has got
three layers – 1. tunica intima; it is made up of endothelium performing diffusion,
fibrinolysis, growth of new cells and circulation of lymphocytes, 2. – tunica media ;
this is a thin layer of smooth muscle in veins with properties like distensibility,
elasticity, rigidity, 3. – tunica adventitia; it is formed by general connective tissue
with varying thickness.
TABLE NO. 14 SHOWING CLASSFICATION OF SIRAS ACCORDING TO VARNA
Siraprakara Sirakarya Tridosha Drushtya
Vargikaraa 1 Rohinyaha Nourishing body by Upasnehana &
Anugrahana
Artery –
Pittavahi
2 Neela Nourishing body by Upasnehana &
Anugrahana
Veins –
Pittavahinya
3 Gourya Nourishing body by Upasnehana &
Anugrahana
Lymphatics –
Kaphavahinya
4 Aruna Akunchana Prasaranadi Karmas Autonomic Nerves –
Vatavahinya
The vein are capable of constricting and dilating, thereby storing small or
large quantity of blood and making this blood available for circulation. Venous return
will regulate cardiac output. The pressure of the veins is very important in circulatory
functions. Usually four to seven mm of Hg. The valves of the veins are arranged in
the direction of blood flow, i.e. towards the heart. As it act as a blood reservoir, when
there is a blood loss, arterial pressure begins to fall, inturn, send sympathetic nerves
signals to the veins causing them to constrict, so that the reserved blood in the vein
comes into the circulation.
Discussion on Siravyadha Vidhi Shareera :
Siravyadha is significant therapeutic tool, when judiciously administered. To
denote its importance, Sushruta has himself explained that ‘Siravyadham
Chikitsardham Shalya Tantra Prakirtitaha Yada Pranitaha Samyak Basti
Kayachikitsite’. Half of the health hazards can be managed by Siravyadha as Rakta is
being chief causative factor in the manifestation of diseases. So Raktamokshana by
Discussion
131
different modalities is much more effective in resolving pathogenesis. There are many
historical evidences where it was extensively practiced. During the procedure
preoperatively, indication and contraindication are analyzed. Instruments are collected
depending on the wisdom of the surgeon, site, disease and available instruments.
Sushruta has encouraged modification of instruments as per necessity. Operatively,
patient is taken in particular position, vein of the site should become prominent.
According to the diseases and their Adhisthana different Siras are selected for
Vyadhana. As per Sushruta’s explanation, as he is expert of Rachana Shareera. In
classics, it has been advocated that the blood letting should be done when
environment should not be too cold or too hot; because environmental stimuli can
cause Heena-Mithya-Ati Srava of Rakta. During the procedure it is necessary to
decide the quantity of blood to be letted out. As per classics, one Prastha (768 ml) has
been advocated which is Uttama Shodhana. But in general condition of the patients,
Hb% of the blood, severity of the diseased condition, quantity may be altered to half
Prastha (384 ml) or quarter Prastha (192 ml). Automatic stoppage of blood after
certain time is an indication of Samyak Siravyadha, associatedly the patient feels light
and severity of illness is decreased.
Siravyadha will be beneficial to maintain good health by causing Varna,
Prasannata, Agnideepti, Vegapravrutti, Tushti, Pushti. All Rakta Pradoshaja Vikaras
are successfully treated. According to present day researches it has been identified
that blood letting by phlebotomy is useful in many diseased conditions like acute
pulmonary oedema, thrombosis of cerebral arteries, orthopnoea, venous congestion,
percarditis, pneumonia, iron overload, hemochromatosis, alcoholic liver diseases,
hepatitis C, lumbago, cancer, arthritis, neuritis, type-II diabetes, CCF etc.
In general, the various probable mechanisms are going to change in body by
blood letting, such as local blood supply is improved, local metabolism is improved,
local drainage system is improved, fresh RBCs are produced which are active.
Hepato-cellular activity is improved by enzymatic activity by release of hormones,
sympathetic nerve function improved, as it directly stimulates bone marrow, immune
related T-lymphocytes are produced. Because of these, Siravyadha Vidhi Shareera has
got its own importance on the basis of scientific background.
Discussion on Correlative Study :
Discussion
132
Raktamokshana is one of the important para-surgical procedure denoting
letting of impure blood outside the body. Different modalities of Raktamokshana can
be adopted, but Siravyadha is one of the Shastravacharana. Of course, it appears to be
surprising that different sites have been advocated in different diseases. Why can’t
common site is selected in all diseases?, is the point interpreted here to analyze this
context, different hypothesis and patho-physiological mechanisms are applicable as
the basic unit of the body is cell. Each cell is especially adopting different mechanism
to perform functions. So the term ‘homeostasis’ is used to denoted maintenance of
constant conditions in internal environment. The function of circulation is to serve the
needs of the tissues such as nutrients, oxygen, hormones and also transport waste
products away. When tissues are active they need more blood flow. Heart normally
cannot increase its cardiac out more than four to seven times. Therefore, it is not
possible to increase the blood flow everywhere in the body. When a particular
demands increased flow, instead micro-vessel of each tissue are monitoring the tissue
needs, such as availability of oxygen and nutrients and the accumulation of waste
products, these inturn control local blood flow to the level of tissue need. The
microcirculation of each type tissue of body is specially organized to serve special
needs. Every cell have got their own microcirculation to maintain its constant internal
environment.
On the basis of this general information, the dictum of Sushruta is found to be
suitable. So that according to Roga Adhisthana, different sites of Siravyadha is
selected in different diseases, such as in Padadaha, Visarpa, Chippa, Vatarakta,
Vatakantaka, Vicharchika, Padadari – ‘Two Angula above from Kshipra Marma’-
medial metatarsal vein (a branch of dorsal venous arch).
In Vataja Shleepada – ‘four Angula above the Gupha Sandhi’- short saphenous vein.
In Pittaja Shleepada – ‘four Angula the Gulpha Sandhi’ – branch of dorsal venous
arch. In Kaphaja Shleepada – ‘four Angula above the ‘Kshipra Marma’ – branch of
dorsal venous arch. In Kroshtuka Shirsha, Khanja and Pangu – ‘four Angula above
from Gulpha Sanhi’- short saphenous vein. In Apachi – ‘two Angula below from
Indrabasti Marma’ – tributaries of short saphenous vein. In Grudhrasi – ‘four Angula
above or below from Janu Sandhi’ – great saphenous vein. In Galaganda – ‘Urumula
Sthita Sira’ – femoral vein.
In Pleehodara – ‘Vama-Kurpara Sandhi Sthita Sira’ or ‘Sira present in Vama
Kanistika and Anamika Angulis’ – left median cubital vein or branch of metacarpal
Discussion
133
vein. In Yakruddalyudara – ‘Dakshina Kurpara Sandhisthita Sira’ – right median
cubital vein. In Vishwachi – ‘four Angula above the Kurpara Sandhi’ – cephalic vein.
In Apachi – ‘two Angula below from Indrabasti Marma’ – basilic vein.
Interpretation on Clinical Applicability of Siravyadha
Sthanas in Lower and Upper limbs :
As per the literary review, the concept of Shodhana therapy in Ayurveda in
concerned, always Doshas should be removed from nearest routes. Example, in
Vatadusti – Basti, in Pittadusti – Virechana, in Kaphadusti - Vamana, which is
depending upon their Mulasthanas. Likewise, as Raktamokshana is also one of the
Shodhana therapy, so it is recommended to remove the vitiated blood from nearest
route of Roga Adhisthana. It has been considered that Rakta is Mula of Shareera,
responsible for health, where its Dusti causes various illness. So Sthanika
Raktamokshana has been advised in different diseases. So different modalities of
Raktamokshana is indicated in many diseases, where Siravyadha is significant of
them.
So the sites of Siravyadha dealt by Sushruta is only with the aim of that
Dushita Rakta should be expelled out from Sameepastha Marga. With this motive he
might have been told particular sites for Siravyadha in particular diseased conditions.
He has recommended only Siras which are superficially situated on the contrary,
contraindicated the Vyadhana of Siras deeply situated Srias as Avedhya Siras. On the
basis of said principles, Sushruta might have been told particular Vyadhana Sthana in
different disease conditions. The truths documented by the practically ancients scholar
Sushruta on the basis of his experiences and superimposed power, can never be
rejected, unless the concepts thought in their point of views, so that, that can be better
understood and analyzed on basis of present existing modern science also.
When we have reviewed anatomy, physiology, circulation, venous systems,
homeostasis on the grounds of literary principles, the sites of Siravyadha dealt by
Sushruta are found to be correct, as blood letting from particular site is effective in
resolving the pathology of diseased conditions and beneficial in neutralizing
physiological mechanisms by various changes in the body. As the body has got its
own capacity to compensate during blood loss, performing many defense actions to
resolve pathology and to maintain homeostasis. Cellular level changes have been
brought by various metabolic changes, neurological changes, hormonal changes. As
the blood is circulating in the closed circuit, providing oxygen, nutrients, hormones
Discussion
134
and carry out metabolic waste products. Every cell has got its own control to fulfill
the needs itself.
Concerned to diseases conditions in ‘Padadaha’ – which is nothing but
burning sensation of feet that is due to decreased utilization of pyruvic acid by tissues
due to any cause. So accumulation of pyruvic acid in tissue spaces leads to Padadaha.
Here, blood letting is done in Padadaha i.e. two Angula above from Kshipra Marma,
which is noting but metatarsal vein of dorsal venous arch. One of the most
fundamental principles of circulatory function is the ability of each tissue to control
its own blood flow in proportion to its metabolic needs. In general, the greater the
metabolism, greater will be blood flow. So hereby, Siravyadha, interstitial pressure is
released, fresh blood rush towards the part, metabolic activity of the part is increased,
concurrently accumulated excessive pyruvic acid is drained. So the particular site may
be told where that dorsal venous arch is easily accessible.
In ‘Padaharsha’ – which is tingling and numbness commonly seen in
neuropathies due to various causes, where glucose uptake and glycolysis is impaired
due to various causes, presenting with tingling, numbness, pricking, burning etc. By
means of blood letting by phlebotomy there is increase in insulin sensitivity resulting
proper glucose uptake and glycolysis which can prevent degeneration of nerves by the
release of energy. So the phlebotomy done in said part i.e. two Angula above from
Kshipra Marma i.e. dorsal venous arch.
In ‘Chippa’, where it is the infection of nail bed of fingers causing redness,
tenderness, lymphangitis, formation of pus. By phlebotomy at dorsal venous arch,
venous drainage of the part and lymph drainage, where interstitial space pressure is
decreased facilitating migration of lymphocytes through vessel wall subsiding
infection, inflammation providing improvement in metabolism of cell.
In ‘Visarpa’, which is spreading lymphangitis or neuritis due to organisms or
viruses. The lesions starts as scratch and commences as rose pink rash which extends
to the skin in spreading nature. Vesicles appear sooner in the neck, face, upper limb
and lower limbs. By means of Siravyadha in two Angula above from Kshipra Marma
i.e. dorsal venous arch. Venous drainage of the part is improved. Blood rushed
towards the part, WBCs, macrophages coming towards the part to engulf the
infectious agents. So immediately inflammatory changes are neutralized as local
cellular metabolism is improved. And another mechanism is pressure in interstitial
fluid is decreased improving lymphatic circulation. By means of local blood letting
Discussion
135
directly bone marrow is stimulated to produce erythropoietin decreasing viraemia.
Reactivation of virus is stopped as WBCs are scattering towards the affected part. So
nerve inflammation may be reduced. So the particular site of Siravyadha may be
considered.
In ‘Vatarakta’, which is a metabolic disorder of impairment of purine
metabolism, serum uric acid level is high and also there is inadequate excretion i.e.
nothing but hyperurecaemia. The pathogenesis is unclear. Blood letting in dorsal
venous arch causes reduction in urea, uric acid. There is release of angiotensin
hormone which has got renal and adreno-cortical stimulatory effect providing
excretion of urea, uric acid by kidneys. That is why in gouty arthritis blood letting
done in site told by Sushruta.
In ‘Vatakantaka’ there is bony out growth usually extends from heal into the
soft tissue causing inflammation of plantar fascia and pain. That heel spur is
composed of calcium deposits. The osteoblasts secrete large quantity of alkaline
phosphate which is believed to increase local concentration of inorganic phosphates.
In such a way, they cause deposition of calcium salts. By doing phlebotomy in
recommended dorsal venous arch certain amount of alkaline phosphate is taken away
and also can be prevented by increased metabolism and blood flow. So the site of
Siravyadha may be accepted.
In ‘Vicharchika’ which is pruritc condition of skin. Because of predisposing
factors like chemicals, drugs irritations, large number of inflammatory cells cause
structural and functional integrity of epidermis resulting hyperplasia. Thickening
horny layer, formation of vesicles in epidermis. So there is erythema, crusting,
fissuring, oozing, pigmentation etc. by means of blood letting, blood is rushed and
provides oxygen and nutrients for proper growth of epidermis. The epinephrine and
nor-epinephrine hormones are released, acting as a anti-allergic. So the site of
Siravyadha may be considered.
In ‘Padadari’, fissure in sole due to scratching and infection i.e. nothing but
vertical loss of epidermis. Blood letting in dorsal venous arch will improve venous
drainage, concurrently local tissue metabolism is improved. Because of rush of blood
towards the part and proper drainage of metabolites and also release of hormones. So
the site can be considered.
In ‘Shleepada’, which is a condition where there is inflammation of lymphatic
vessels including mechanical blockage of lymphatic channels, resulting into
Discussion
136
lymphoedema. On the basis of physiology, venesection will help when blood is letted
out from the dorsal venous arch. So that the pressure in the interstitial fluid is reduced
concurrently pressure in the lymphatic channels is also reduced to provide relief of
blockage and opening of capillaries and also local cellular metabolism is improved.
The site four Angulas above from Gulpha Marma i.e. short saphenous vein is
considered.
In ‘Krostuka Sheersha’, which is an inflammatory involvement of joint due to
infectious agents like streptococci, staphylococci organisms where the predisposing
factors may be alcohol, drug abuse, immune suppressive therapy, causing synovitis.
Synovial swelling and also there is a release of condrolytic enzymes, contribute to
destruction of articular cartilage. By means of blood letting in long saphenous vein,
hyperurecaemia is reduced by the release of steroid hormones, effusion may be
resolved, fibrous adhesions are avoided. So the site of Siravyadha may be considered.
In ‘Khanja’, there is monoplegia, where there is incapability to walk. By
means of blood letting in four Angula above from Gulpha Sandhi done, because if
there is any thrombosis that will be dissolved by fibrinolytic activity of blood and also
there is removal of waste products, cellular metabolism is improved, various
hormones released to maintain homeostasis. So the site of Siravyadha dealt by
Sushruta may be considered.
In ‘Pangu’, there is cerebral palsy, which is ischemic necrosis in the brain to
reduce blood supply to neural tissue which is insufficient to meet the metabolic needs,
rapid fall in cerebral perfusion lead to diplegia. Cerebrum is most vascular area of the
brain. Metabolic factors have potent effect in controlling cerebral blood flow. They
are nothing but CO2, hydrogen, oxygen. An increase in CO2 or hydrogen ion
concentration increases cerebral blood flow, where as decrease in oxygen, that
increases the blood flow. By means of dilating cerebral blood vessels increase the
blood flow, which is inturn carries CO2 and acidic substances. Oxygen deficiency
increases the cerebral blood flow. On the basis of this theory, blood letting in long
saphenous may induce higher CO2 and hydrogen ion concentration which inturn cause
dilation of cerebral blood vessels, with increased blood flow, and also carrying acidic
substances from neural tissues.
In ‘Grudhrasi’, where there is pain along the sciatic nerve distribution, due to
lumbar disc diseases. Mechanical pressure on the nerve roots, the pain felt in the
buttocks, thigh, calf, paraesthesia along the nerve root and calf muscle weakness.
Discussion
137
There may be various stimuli like mechanical, chemical, thermal factors causing pain.
By means of blood letting in branch of great saphenous vein, four Angula above or
below from Janu Sandhi, blood flow to the compressed part may be increased by
angio-genesis. As aerobic metabolism is enhanced, the accumulation of lactic acid
may prevented and reduced. By means of blood letting hormones serotonin is released
which is believed to cause pre-synoptic and postsynoptic inhibition avoiding pain. So
if the pain is situated in back and thigh, the upper site is selected, if pain is radiated up
to the leg, lower site is selected.
In ‘Galaganda’, which is thyroid enlargement due to multiple factors. It may
be toxic or non-toxic, that is nothing but repeated and prolonged changes of
hyperplasia of thyroid tissue where there may be fibrosis. Blood letting in Uru-Mula
Sthita Sira which may directly stimulate pituitary and TSH and indirectly improve
metabolism of whole body by the release of numerous chemicals and hormones. As
the available veins of neck and abdomen are contraindicated for Siravyadha this site
might have been accepted for Siravyadha.
In ‘Pleehodara’, there is enlargement of spleen, due to various causes where
the spleen is heavy and firm. The capsule is tense and thick. By blood letting left
sided medial cubital vein, the reticuloendothelial cell of spleen rapidly remove debris,
bacteria, parasites. Usually reserved blood is ejected into the general circulation. The
fragile RBCs are washed off. Splenic vein is drained effectively. So blood letting
particularly on left sided medial cubital vein is considered.
In ‘Yakrutodara’, where there is enlargement of liver, due to various causes,
there may be fatty deposition of liver, or inflammation of hepatocytes or cirrhosis. By
means of blood letting in right sided medial cubitol vein reserved blood in the liver is
ejected into the general circulation, to cause decongestion. Epinephrine and nor-
epinephrine hormones are released, mobilizing fatty acids deposited in the liver.
Hepatocellular enzymatic activity is improved. Fresh RBCs are produced to utilize the
ferritin. By all these affects the enlargement of liver can be reduced. So the said site is
considered.
In ‘Kaphodara’, where there is accumulation of fat, so that an adipose tissue is
deposited. Blood letting in right medial vein helps to mobilize fatty acids. As they
help to improve the hepatocellular function by release of certain enzymes enhancing
fat metabolism. So that might be site of Siravyadha recommended.
Discussion
138
In ‘Kasa’ which is nothing but cough, as defense mechanism of body, in URI
and LRI or any infections of respiratory tract. When blood letting is done in right
sided medial cubital vein, the venous pressure in the right atrium may be decreased
resolving pulmonary congestion. So the site may be considered.
In ‘Shwasa’, the condition may be considered as breathlessness due to CCF or
emphysema or hyperurecaemia. By means of blood letting in right medial cubital
vein, the congestion of lung and liver is decreased. So the verdict of Sushruta can be
accepted.
In ‘Vishwachi’, that is injury to brachial plexus of the arm may mimic cervical
origin. It is nothing but brachial plexus neuritis. Locally by blood letting four Angula
above from Kurpara Sandhi i.e. basilic vein, the pain precipitating factors like lactic
acids are reduced. Blood supply to brachial plexus is improved, where there is aerobic
metabolism in the part. There is provision to release of hormone serotonin, which
inhibits pain of neuritis. In this way blood letting site may be considered.
In ‘Apachi’ which is an inflammatory condition of lymph nodes called
lymphadenitis. Lymph nodes undergo reactive changes in response to acute variety of
stimuli like infection, injury, neoplasia. They are firm, round swellings. By means of
blood letting venous drainage is improved, automatically lymphatic drainage is
improved, resolving in inflammation of lymph nodes by increased blood flow,
scattered WBCs, removal of waste products. So the part two Angula below from
Indrabasti Marma is selected.
Conclusion
139
CONCLUSION
1. Sira means vein.
2. Veins are not only blood reservoirs, but having their own influence in blood
circulation and lymphatic circulation.
3. Lymphatic drainage is essential to maintain homeostasis.
4. Siravyadha is effective therapeutic tool in many health hazards if judiciously
administered.
5. The efficacy of Siravyadha is appreciated by ancient scholars and present day
modern peoples also.
6. Siravyadha is also beneficial in physiological maintenance of well-being.
7. The sites of Siravyadha told by Sushrutacharya are scientific and can be
adopted.
8. Irrespective of contraverises, the sites can be followed for Siravyadha.
9. Almost all the Siras told by Sushruta for Vyadhana purpose can be adopted in
clinical practice.
Recommendation for Future Study :
As the concept of Sira Shareera and Siravyadha Vidhi Shareera are still
unclear to grasp and adopt. So Shalya Tantra scholars can continue clinical study on
individual site of Siravyadha in individual diseases to evaluate therapeutic efficacy of
Siravyadha.
Summary
140
SUMMARY
Ayurveda is as old as mankind, where the concepts have been evolved three
thousand years ago. It is the document where many Acharyas dedicatedly worked for
the benefit of mankind with the motive of welfare of human beings. On the contrary
the things are not properly passed onto the future generations. Because of this
generation gap, many concepts are unclear.
Regarding Rachana Shareera are concerned there are many technical terms
which are vague for a casual observer, teacher and students. So many lacunas may be
found in concepts of Rachana Shareera. Regarding above said dictum is concerned
there is very little information on ‘Sira Shareera’ and Siravyadha Vidhi Shareera’. So
here in present study comprehensive literary information is collected above the topics.
So regarding Sira Shareera with special reference to venous system is interpreted so
as to elicit meanings of the Sira, Dhamani and Srotas. An attempt has been made to
prove ‘Sira’ as ‘vein’ on literary grounds.
Regarding ‘Siravyadha Vidhi Shareera’ is concerned, it is effective Shodhana
therapy for letting of impure blood outside the body. As Basti is dominant line of
treatment in Kayachikitsa, Siravyadha is dominant line of treatment in Shalya Tantra.
Poorvakarma, Pradhanakarma and Paschatkarma are clearly explained on available
literary sources, because of Significance of Siravyadha is elicited on the basis of
classical references, modern information and internet. Modern people also appreciated
the effect of phlebotomy in various diseases.
The chief aim of the study is concerned it is anatomical location of Vedhya
Sirasthanas in particular diseases. This is clearly analyzed on anatomical,
physiological, patho-physiological grounds. As per Ayurvedic concepts and modern
concepts, an honest and logical interpretation is made to identify Siravyadhana
Sthanas in particular diseases, and have been critically analyzed. So as to fulfill the
objectives the discussions are made and conclusions are drawn and also future study
is recommended.
References
I
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IV
pöcs¼t(tSt> Bv>It tiviRy Ip_ivi(hºy: Ip_iAYin[,kfvi(hºyá kfAYin[,
r±tvi(hºyá ykZt¼l)ði[: Evm[ti(n s¼tIsriSti(n Bv>(t .. (Su. Sha. 7/6) 26. dSm*lIsri ñdyp\(tbÛi: svi<>©p\Ry©[Ovi[ji[ nyIºt tRp\(tbÛi Sr)rc[OTi: .
tiAt& Úvy>g&l> a©&lmFi<©&l> yv> yviF<> c gRvi d\&mp#i s[vn)p\tinv(Ûwmini: s¼tSti(n BvIºt .. (A. S. Sha. 6/2)
27. tisi> yYiAv> t&yi<>S(vBig[n pöcs¼tIºFk> Xitm(nlr±t> vh(t .
EP (vBig: (p_iÅl[Om S&Úr±t[Ov(p . IAYti H[v> d[hnm&gZh`Ni(t di[[Pi: s. ÄyRy[n t& p)Dy(ºt .. (A. S. Sha. 6/7)
28. t#i vitvi(hºy: (sri EkIAmn` sI±¸n pöc(v>S(t:, Et[n[trs(±Y bih& c Äyi²yiti]. (vS[PAt& ki[OT[ ct&IAS>t` tisi> g&dm[QiI~ti: ~i[·yiOTmi] o[ o[ piÅv<yi[: PT` pZOT[ tivºy[ Ev ci[dr[ dS vxIs . (Su Sha. 7/7)
29. tisi> ct&:St) SiKis& . t#i Pi[DSÄyi(Fn)yi: PT`I#i>S> StmºtSCi] t#i
oi(#iS<t` . ct&OPOT`y(Fk> Stm*¹v<> t#ii(p pöcSt` ..
(A.S. Sha. 6/13)
30. ñdi[ rsi[ In:sr(t tAmid[(t c sv<S: . (sri(Bñ<dy> v](t tAmit` p\Bvi: (sri: .. (Bhe. Sam.
Su. 20/3)
31. dS Fmºyi[ ñdy[ (nbÛi BvIºt . ti: p\Bv[ ct&r>g&lmi#i> gRvi (v>S(tB<v<(t . Evm[ti dS Fmºy: PIOTB<v>(t .
References
V
t#i t& Bv>It #)IN Stshs|iIN PIOT(ry> jili(n (sriNim` .(Bhe.Sam. Su. 4/27) 32. twYi – vZx: SiKivZt: fmpliS]Ktr(t sv<#i .
twYi vihºyi[¥Åm(BKtt: tYiy> (sriIBrvtt: . ri[mk*p[ ri[mk*p[ MAy (srim&K> Bv(t, yt: Av[d: xrt)(t .. (Bhe. Sam. Su. 4/27)
33. at U´v<> p\vxiIm n (v´y[wi: Isri IBPk` . v]kÃy> mrN> ci(p ÄyFi_iisi> F\v> Bv[t` .. IsriSti(n cRvi(r (vwiµCiSiKis& b&IÛmin` . PT`I#i>Söc St> ki[Oq[ ct&:POT> c m*F<In .. SiKis& Pi[DS Isri: ki[Oq[ oi(#i>Sd[v t& . pøiS÷#i&Ni> c u¹v<mÄy¹yi: p(rk)It<ti: ..(Su
Sha. 19-21)
34. t#i (sriStm[kIAmn` sI±Y Bv(t tisi> jilFri Rv[ki (ts|ái¿yºri: t#ii[v)<s>X[ o[ li[(htix s>Xi c]ki tiARvÄy¹yi: .. (Su. Sha. 7/23)
35. y(dr[d` b(hdi[<Pin` pöcdi S[Fn> c tt` . (n$hi[ vmn> kiy(Sri[r[ki[ as\(vsZ(t .. (A. H. Su.
14/5)
36. d[hAy @(Fr> m*l> @IFr[N]v Fiy<t[ . tAmit` yRn[n s>rÈy r±t> j)v e(t IAY(t : . (Su.
Su. 14/44)
37. t#i SAt\(vs\ivN> Io(vF> p\Cºn> (sriÄFn> c . (Su. Su. 14/24)
38. aSAt\·y[v SAt\kiy< k&v<Iºt an&SAt\iIN .. (Su.
Su. 8/13)
39. t#i piddihpidhP<(c¼p(vsp< vitSi[INt vitk·Tk (vc(c<kipiddir)p\BZ(tP& Ixp\mm<N up(rOTid` oy>g&l[ v\)(hm&K[n (sri> (v¹y[t`
References
VI
Ål)pd[ tIµc(kIRst[ . yYi vÈyt[ k|i[Oq&k(Sr: Köjp©&lvitv[dnis& j>Giyi> g&ÃfAyi[p(r ct&r©&l[, apµyi(mºd\bAt[rFiAtid` oy>©&l[, jin&sºF[@py<Fip vi ct&r©&l[ gZF\Ayi>, U@m*ls>I~ti> glg·D[, Et[n[trsI±Y bih* c Äyi²yiti]; (vS[PAt& vimbihi] k*p<rsºF[r¿y>rti[------ISri[ri[g(FmºYp\BZ(tP& ri[g[IOv(t .. (Su. Su.
8/17)
40. bilAY(vr$xxtx)NB)@p(r~i>ºt mwpi¹vAt\) k(S<t v(mt(v(r±ti¥AYi(pt an&vi(st jig(rt ±l)bkZSgIB<N)ni> kisÅvisSi[Pp\vZܶvrix[pk pxiGiti[pvis (ppisim*µCi< p\p)(Dtini> c (sri> n (v¹y[t`, yiÅciÄyi¹yi: Äyi¹yiÅcidZOTi dZOTiÅciIº#iti:, yIº#itiÅcin&IRYti eIt .. (Su. Sha. 8/3)
41. n]vi(tS)t[ niRy&ON[ n p\vit[ n ciIB\t[ . (sriNi> ÄyFn> kiy<mri[g[ vi kdicn .. (Su. Sha.
8.7)
42. ÄyB\[ vPi<s& (v¹y[_i& g\)Omkil[ t& S)tl[ . h[mºt[ m¹yið[ SAt\kiliAt\\y: AmZti : (Su. Sha.
8/10)
43. aY kZtAvARyynmit&r> ÄyiIFblisiRÀyiwp[Èy IAn³F ji©l>rs> yvig&> c piyIyRvi m&h*t<mi#imiÅvi(st> p*vi<ð[¥prð[ -------k*p<r smIAtpid> p\Ry(dRym&pv[Åy[t` . (A.
H. Su. 27/18)
44. bIlni[ bh&di[PAy vy: AYAy: Sr)(rN: . pr> p\miNImµCIºt p\AY> Si[INtmi[xN[ .. (Su.
Sha. 8/16)
References
VII
45. d&OTÄyFi (v>S(t: - d&Iv<Üi¥(t(vÜi k&(øti Ipµcti k&IÍti¥p\s\&ti¥Ry&d)Ni<¥ºt[[ (vÜip(rS&Oki k*INti v(pti¥tin&IRYt(r¹yi SAt\htiIty<I³vÜi(v¹yi (vd\&ti F[n&ki p&n: p&n(v<¹yi (sriAniÂvIAYsIºFmm<s& µy[(t .(Su. Sha. 8./18)
46. (sriÄFiIÅc(kRsiF<> SÃytº#i[ p\k)It<t: yYi p\iIN(ht: sÀy³bIAt: kiyIc(kIRst[ .. (Su. Sha.
8/23)
47. (sriÄFIÅc(kRsiF<> sÀp*N< vi Ic(kIRstm` . SÃytº#i[ AmZZti[ yd` bIAt: kiyIc(kIRst[ ..
yYi r±tm(FOTin> IvkiriNi> Ivk(rNim` . anºy (h tYi d\Äy> km<[d> p\Ym> tt: .. (A. Sam.
Su. 36/4-5)
48. p\sºn> vN[<Iºd\yImIºd\yiYi<n` eµCºtmÄywin` s&KiIºvti t&IOT bili[pºn> (vS&Ü r±t p&@P vd>(t .. (Cha. Su. 24/24)
49. An[hi(dIB: (k|yiiyi[g]n< tYi l[pn]r(p. yiºRyiS& ÄyiFy: SiIºt: yYi sÀyk` (sriÄyFit` ..
(Su. Sha. 8/22)
50. Rv³di[P g\ºYy: Si[fi: ri[gi: Si[INtjiÅc y[ . r±tmi[xNSi<lini> n Bv>(t kdicn .. (Su. Su. 14/34)
51. t#i piddihpidhP<(c¼p(vsp< vitSi[INt vitk·Tk (vcIc<ki piddir) p\BZ(tP& Ixp\mmi<IN up(rOTid` H©&l[ v|)h)m&K[n (sri> (v¹y[t` .. (Su. Sha. 8/17)
52. pidyi[: k&@t[ dih> Ip_iis<k`s(hti[¥(nl:. (vS[PtÆc¦k\mNit` piddih> tmi(dS[t`` .. (Su. Ni.
1/80)
53. ñOytÅcirNi]] yAy BvtÅc p|s&¼tvt` . pidhP<: s (vX[y: kfvitp\ki[pj: .. (Su. Ni. 1/31)
References
VIII
54. nKmi>smIFOTiy Ip_i> vitÆc v[dnim` . kri[(t dihpiki[ c t> ÄyiIF> Ic¼pmiIdS[t` .. (Su.
Ni. 13/19)
55. k&y<t[ Ip_ii(nl> pik> nKmi>s@ji> Ic¼pmxtri[g c (vwid&pn> nK> c tm` . (A. S. Ut. 36/5)
56. Rv§mi>sSi[INtgti: k&IptiAt& di[Pi: . svi<©si(rNiImhiIAYtmiRmIl©m` .. k&v<Iºt IvAtZtmn&ºntmiS& Si[f> t> sv<ti> IvsrNiµc (vsp<mih&: ..
(Su. Ni. 10/3)
References
IX
57. r±t> lIski Rv¦`mis> d*Oy> di[PiA#iyi[ mli: .
Ivsp<Ni> sm&Rp_ii] IvX[yi: s¼t Fitv: .. (Ca.
Chi. 21/15)
58. vitr±t> Ih d&OT[n r±t[n c (vISOTs>p|iI¼tk> (vkiriºtrm[v ..
p|iyS: s&k&miriNi> Im¸yihiri(vhi(rNim`. Si[kiÅc p|mdimwÄyiyimiÅciItp)Dnit` .. ât&siRÀy(vpyi<sit` An[hid)ni> c IvB|mit` . aÄyviy< tYi AY*l[ vitr±t> p|k&¼yIt .. (Su. Ni.
1/40-41)
59. Ixp|> r±t> d&IOTmiyiIt tµc viyi[mi<g> s>@Nd`¹yiS& yit: k|&Ûi[¥RyY<> migi<ri[Fit` s viy&rRy&Id\±t> d&Py[d\±tmiS& .. tt` s>pZ±t> viy&ni d&IPt[n tTp\ibÃyid&µyt[ vitr±tm` . tÚt` Ip_i> d*IPt[nisZji¥ä Ål[Omi d&OTi[ d*IPt[nisZji¥ä .. (Su. Ni. 1/43-44)
60. ºyAt[ t& (vPmpid[ @j: k&yi<t` sm)rN: . vitk·Tk: eRy[P: (vX[y: K&DIlkiI~t: .. (Su. Ni.
1/76)
61. ri¶yi[¥(tk·D`vIt@j: s@ji BvIºt gi#i[P& IvcIc<kiyim` .. (Su. Ni. 5/13)
62. P(rk|mNS)lAy viy&rRyY<$xyi[: . Pidyi[: k@t[ dir)> s@ji> tls>I~t: .. (Su. Ni. 13/28)
63. An[hAv[di[pºn[t& Ål)pd[¥Inlj[ (BPk` . kZRvi g&Ãfi[p(r Isri> (v¹y[_i& ct&r©&l[ .. (Su.
Chi. 19/52)
64. g&ÃfAyiF: Isri> (v¹y[t` Ål)pd[ Ip_is>Bv[ .
References
X
Ip_i>G»)> c (k|yi> k&yi<t` Ip_iib<&d(vsp<vt` .. (Su. Chi. 19/55)
65. (sri> s&Iv(dti> (v¹y[d¦`g&Oq[ Ål]IOmk[ IBPk` .. (Su. Chi. 19/56)
66. p&riN[ udkB*IyOTi: sv<t&<P& c S)tli: . y[ d[SiAt[P& jiy>t[ Ål)pdi(n (vS[Pt: .. (Su. Ni.
12/17)
67. k&(ptiAt& di[Pi vit(p_iÅl[OmiNi[¥F p|pºn: v«Ni[@ jin&jªis& avIt¹ymini: kiliºtr[N pidmi(~Ry Sn]: Si[f> jnyIºt tt` Ål)pd> eRyicxt[ .. (Su. Ni. 12/13)
68. k|i[OT&kISr: Köjp©&l:vitv[dnis& jªiyi> g&ÃfAyi[p(r ct&r©&l[ .. (Su. Sha. 8/17)
69. vitSi[(Ntj: Si[fi[ jin&m¹y[mhi@j: . (Sr: k|i[OT&kp*v<> t& AY*l:
k|i[OT&km*F<vt` .. (Su. Ni. 1/76)
70. viy& kT`yi IAYt: sºkY: k·DrimiIxp[wydi .
KöjAtdi Bv[¶jºt&: p©&: sºkYi[oyi[v<Fit` .. (Su.
Ni. 1/77)
71. viy& kT`yi IAYt: sºkY: k·DrimiIxp[wydi . KöjAtdi Bv[¶jºt&: p©&: sºkYi[oyi[v<Fit` .. (Su.
Ni. 1/77)
72. apµyiImºd|bAt[rFAtid` o©&l[ . (Su. Ni. 11/10)
73. Jin&sºF[@py<Fi[ vi ct&r©&l[ gZF|Ayim` . (Su. Sha. 8/17)
74. PiION<p|RyI©&(lni> t& k·Dri yi¥(nli(d<ti sk`¸n: x[p> IngZh`N)yid` gZF|s)It (h si
AmZti .. (Su. Ni. 1/74)
75. IAfk`p*vi< kITpZOTi[@jin&j>Gipid> k|mit` .
References
XI
gZF|s) AÀB@k`ti[d]gZh`Ni(t Ap>dt[ m&h&: ..
vitit` kfit` tºd|igi]rviri[ckiIºvti . (Cha. Chi. 28/56)
76. U@m*ls>I~tini> glg·D[ Et[n[ntrsI±Y bihv Äyi²yiti] : .(Su. Sha. 8/17)
77. vit: kfÅc[v gl[ p\vZÜi[ mºy[ t& s>sZ¶y tY]v m[d: . k&v<>(t g·D> k|mS: AvIl©]: smIºvt> t> glg·Dmih& : .. (Su. Ni. 12/23)
78. (vS[PAt& vimbihi] k*p<rs>F[r¿yºtrti[ bih&m¹y[ ¼l)(ð k(nIOTki aniImkyi[m<¹y[ vi ..(Su. Sha. 8/17)
79. IvdHIBOyIºdrtAy jºti[: p\d&OTmRyY<msZk` kfÅc .
¼l)hiIBvZIÜ> stt> kri[(t ¼l)hi[dr> tt` p\vd>(t t¶zi: ..
vim[ c piÆv<> vZIÜm[(t (vS[Ptis)d(t cit&ri[¥#i .(Su. Ni. 7/14-15)
80. Ev> dIxN bihi] ykZd`diÃy[ Etim[v c kisÅvisyi[r·yi(dSIºt ..
(Su. Sha. 8/17)
81. p|iNi[ Hy&dinin>: p\d&OT: s>IBºnki>AyAvnt&ÃyGi[P : .
Inr[It vk|#iit` shsi sdi[Pi[ mInIPIB: kis eIt p|IdOT: .. (Su. Ut. 52/5)
82. tl> p|Ry>g&l)ni> t& k·Dri bih&pZOTt: biói[: km<xykr) (vÅvic) (h si AmZti .. (Su. Ni.
1/75)
83. gZF\Ayi>Imv (vÅviµyi> .. (Su. Sha. 8/17)
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VIII
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09. Ibid
10. Ibid
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22. Ibid
23. Ibid
24. Ibid
25. Ibid
26. Ibid
27. Ibid
28. Ibid
29. Thatte D. G. :Sushruta Samhita of Sushruta, Vol. III, I Edition, with English
translation, Varanasi; Chaukhambha Orientalia, P B No. 1032, , 1994, p 140.
30. Ibid
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Varanasi ; Chaukhambha Orientalia, P. O. Box, 1032, Gokul Bhavan, Gopal
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35. Ibid
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37. Ibid
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39. Ibid
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Academy, 1993, pp 54-70.
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45. Ibid p 29.
46. Ibid p 43.
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47. Ibid p 68.
48. Ibid p 43.
49. Ibid p 49.
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55. Ibid p 65.
56. Ibid p 64.
57. Ibid p 63.
58. Ibid
59. Ibid p 64.
60. Ibid p 65.
61. Ibid p 54.
62. Ibid p 65.
63. Ibid
64. Shrikanthamurthy K. R.: Astanga Hridaya of Vagbhata with text, English
translation, etc, Vol. I, third edition, Varanasi ;Krishnadas Academy, Oriental
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123. Lele Avinash, Ranade Subash, Frawley David : The most secrets of
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