1. health and fitness
2. disease
3. chronic pain

The 6th Annual Conference of
Indian Society for
Study of Pain
(West Bengal Branch)
ISSPWBCON
2012
SOUVENIR
w w w . w b i s s p . o r g
The 6th Annual Conference of
Indian Society for
Study of Pain
(West Bengal Branch)
Scientific Sessions:
Neuropathic Pain
Acute Pain
Cancer Pain
Back Pain Neuromodulation
Workshops:
USG Guided Blocks
Pain Research and Publication
ISSPWBCON 2012
8th & 9th December’12
Venue: Bellevue Clinic
Organizing Chairperson
Dr. Santanu Tripathi
Organizing Secretary
Dr. Krishna Poddar
Scientific Secretary
Dr. Subrata Ray
Souvenir Secretary
Dr. Suman Chatterjee
w w w. w b i s s p . o r g
Indian Society for Study of Pain
West Bengal Branch
Executive Committee
President
Dr. Santanu Tripathi 9230566771
Vice President
Dr. J.S.Rudra 9830172590
Dr. Subrata Pahari 9831239910
Secretary
Dr. Krishna Poddar 9830048445
Ex-Officio Secretary
Dr. Gautam Das 9163357246
Joint Secretary
Dr. Subrata Ray 9830021157
Treasurer
Dr. Subrata Goswami 9830430430
Scientific Secretary
Dr. D. J. Bhowmick 9836326113
Executive Committee
Dr. Avijit Banerjee 9830137404
Dr. Suman Chatterjee 9830234881
Dr. Gaurav Maitra 9830791952
Dr. Saikat Sengupta 9830179539
Dr. Trinanjan Sarangi 9831828389
Dr. Sanjay Patawari 9830032420
Dr.Jayanta Bhattacharya 9830022753
Dr Sarbari Swaika 9434021722
Dr Tulsi Bhattacharya 9830110639
Dr. Debabrata Sanyal 9830042928
Indian Society for Study of Pain
West Bengal Branch
Organizing Committee
Chairperson
Dr. Santanu Tripathi
Organizing Secretary
Dr. Krishna Poddar
Patrons
Mr. P Tandon (CEO, Belle Vue Hospital)
Dr. Bibhukalyani Das
Dr. Manjusree Ray
Dr. Amitava Rudra
Dr. Amna Goswami
Advisory Board
Dr. Anjan Dutta
Dr. Arabindo Ray
Dr. S Dasgupta
Dr. Rita Pal
Dr. Gautam Das
Dr. Dipasari Bhattacharya
Joint Secretary
Dr. Sanjay Patawari
Treasurer
Dr. Subrata Goswami
Scientific Secretary
Dr. Subrata Ray
Souvenir Secretary
Dr. Suman Chatterjee
Executive Committee
Dr. J. S. Rudra
Dr. Subrata Pahari
Dr. Avijit Banerjee
Dr. D. J. Bhowmick
Dr. Gaurav Maitra
Dr. Saikat Sengupta
Dr. Trinanjan Sarangi
Dr. Jayanta Bhattacharya
Dr. Sarbari Swaika
Dr. Tulsi Bhattacharya
Dr. Debabrata Sanyal
Mob.: 9914209504
ई मेल/ email:[email protected]
फ़ैक्स/Fax: 0172–2744401, 2745078
0091-172-2744401 (Foreign)
संवेदना हरण एवं गहन चिकित्सा विभाग
Department Of Anaesthesia & Intensive Care
स्नातकोत्तर चिकित्सा शिक्षा एवं अनुसंधान संस्थान, चंडीगढ़ १६००१२ (भारत)
Postgraduate Institute Of Medical Education And Research, Chandigarh – 160012 (India)
National President’s Message
I am delighted to know that the 6th state conference of ISSP West Bengal
Branch will be held on 8th and 9th of December 2012 at Kolkata. The
organising committee have put together an interesting array of topics
for discussion at the conference with a galaxy of speakers. The scientific
programme provides a unique opportunity for debate and exchange of
ideas and information in all fields of pain medicine among pain
specialists. It would be very stimulating for young pain physicians to
interact with experts in the field and expand their knowledge. Clearly,
organizations are looking toward the bigger picture of how pain care
will be delivered in the future.
I offer my best wishes to all the delegates and hope that the conference will not only stimulate
new thinking but also new action in our endeavour to work for a better and healthier planet free
of pain.
Here’s wishing this conference a well deserved grand success.
Y.K.Batra
(President, Indian Society for Study of Pain)
Indian Society for Study of Pain
West Bengal Branch
Message from Editor, Ind J Pain
Dear friends,
It is our great pleasure and we feel proud too that we are organizing state conference
(WBISSPCON) successfully in each year after the first state conference organized in 2006. It
proves dynamicity, enthusiasm of state body members and able leadership of present body. This
enthusiasm is also reflected in Indian Journal of Pain, as we are getting lots of articles from
members of West Bengal chapter. I expect this to increase further with this conference.
I wish every success of this conference.
Long live ISSP.
Gautam Das
Chief Executive Editor: Indian Journal of Pain
(Official journal of ISSP)
Indian Society for Study of Pain
West Bengal Branch
State President's Message
Ever since the dawn of civilization man has always struggled to conquer pain. In
the last few decades phenomenal advances have occurred not only in the
understanding of the cause and genesis of pain but also in making newer
techniques and technologies available to mitigate and control pain. Yet, an
optimum management of pain remains ever elusive, and millions of people
around the world continue to suffer from pain. There is thus a compelling need to
address the subtle yet debilitating effects of pain and to elevate it as a key agenda
among our health professionals, public or private healthcare facilities, and
beyond.
Established as a multidisciplinary organization in the field of pain medicine,
Indian Society of Study of Pain, West Bengal (ISSPWB), ever since the founding
days, has remained a reliable and active voice of pain researchers and care
givers in West Bengal. Today, our members include around 200 pain
researchers, physicians, nurses, psychologists, physiotherapists and other healthcare professionals from all
corners of West Bengal. Through our Society we need to continue our work towards improving awareness
and management of pain in our region through research collaboration, education, skills development, as
well as resource and knowledge exchange. The International Association for the Study of Pain (IASP)
declared the Year 2012 October – 2013 October, as the Global Year Against Visceral Pain. While registering
our solidarity to this call, let me on behalf of ISSPWB pledge that we shall put our best to reverse the dismal
situation of pain care and management in this part of the world.
Finally, it is my pleasure and privilege to solicit your valued participation in the 6th Annual Conference of the
Indian Society of Study of Pain (West Bengal) that is going to take place at Belle Vue Clinic, Kolkata during
December 8-9, 2012. The two-day event will be attended by hundreds of doctors and other health
professionals of West Bengal. Nuances and advances in pain management and research will be discussed
and deliberated on. The ambitious and challenging scientific program will hopefully provide new insights
into basic science, clinical research and therapeutic interventions. Important aspects of pain care and
research will be highlighted with state-of-the-art lectures by leading experts. Presentations and deliberations
will encourage an interactive and inspiring exchange between participants. The carefully crafted
programme schedule will make the Conference a highly innovative and informative venue for clinical
research and a desired destination for the practicing physician. I am sure participants of the Conference will
bring back practical knowledge and solutions that will help improve their practice. Aside from the scientific
exchange, delegates will also have the opportunity to network with colleagues while enjoying the wonderful
ambience of the season’s vibrant climate and colours, cultural and culinary delights. The Conference indeed
promises to be a great meeting!
As the President of the Society, I am very honoured to invite you all to this august event. Let us all make it
a memorable function.
Long Live Our Society !
Jai Hind !!
Dr Santanu K Tripathi
President, ISSP – West Bengal
Indian Society for Study of Pain
West Bengal Branch
Secretary’s Message
Dear All,
It gives me immense pleasure and joy to welcome all distinguished guests, faculties and
delegates to participate in ISSPWBCON 2012 - The 6th Annual Conference of Indian Society for
Study of Pain (West Bengal Branch).
In India each year millions of people suffer from pain even though the awareness and
management of pain is still poorly developed here. This conference will offer to all participants a
comprehensive scientific program featuring renowned experts, symposia, workshops, poster
sessions, and networking opportunities. The academic programme will be facilitated by the best
speakers and clinicians. We are having a special session on Visceral Pain as this year IASP is
celebrating Global year against visceral pain (Oct 2012-2013).
I convey my gratitude to Mr P Tandon, CEO of Belle Vue Clinic, for his kind support. I also thank
all staff of Belle Vue Clinic, who have worked hard to make this conference a success.
My sincere thanks to all the members of the organizing committee for their co-operation and
valuable advices, without whom, organizing this conference would not have been possible.
Long live ISSP
Dr Krishna Poddar
Organizing Secretary, ISSPWBCON 2012;
Secretary, ISSP (West Bengal Branch);
E.C. member ISSP (National).
Indian Society for Study of Pain
West Bengal Branch
Message from the Director, AHRCC, Cuttack
Prof Sukdev Nayak,
MD, LLB, PGDM, DPM
Director
“The greatest evil is physical pain.” Saint Augustine (354-430)
Pain is an unpleasant feeling which motivates the individual to withdraw from
damaging situations, to protect a damaged body part while it heals, and to avoid similar
experiences in the future. A multi modal and multi disciplinary approach is the key to successful
pain management. A lot has been done to address this greatest malady of Human life but
optimum management of pain remains elusive.
I am happy to learn that the Indian Society for Study of Pain (ISSP) West Bengal is organizing the
state level conference, ISSPWBCON 2012 on the 8th and 9th of December 2012 at Belle Vue
Clinic, Kolkata. It is also a great pleasure that a souvenir will be published with valuable inputs
from doyens of Indian Pain Physicians to commemorate this occasion. I am privileged to be
associated with this endeavor.
I wish great success to the conference.
Indian Society for Study of Pain
West Bengal Branch
Programme Schedule
December 8, 2012
Belle Vue Clinic, Kolkata
1030 h
1100 h
1330 h
1415 h
Reception & Registration
Workshop I: Pain Research Methods and Publication Issues
Resource Faculty: Dr S K Tripathi, Dr A Hazra, Dr C Bagchi, Dr. A
Biswas, Dr I Banerjee, Dr S Sen
Co-ordinator: Dr. S Goswami
Working LUNCH
Workshop II: USG-Guided Nerve Block on Mannequin
Resource Faculty: Dr. Sunil Waghmare, Dr Goutam Das
Co-ordinators: Dr. Subrata Ray, Dr. Sanjay Patowari
December 8, 2012
Saturday Club, Kolkata
1800 h
1830 h
2000 h
Inauguration
Panel Discussion: Awareness and Education in Pain Care
Moderator: Dr. S K Tripathi
Panelists: Dr. Manoj Ghosh (Pro-VC, WBUHS), Ms Swati Bhattacharjee
(Sr Journalist, ABP), Dr M Ray (Principal, BMC-Bardhaman), Dr Bibhu
K Das (Veteran Pain Clinician), Dr. Goutam Das (Editor IJP and
Chairman WIP India Chapter)
BANQUET DINNER
December 9, 2012
Belle Vue Clinic, Kolkata
0900 h
Opening Lectures for 2012: The IASP Global Year Against Visceral
Pain Pathophysiology and Management of Visceral Pain
Chairs: Dr. J S Rudra, Dr. S Pahari
Speakers: Dr. Abhijit Paul, Dr. Dipashri Bhattacharya
0935 h
1025 h
1100 h
1110 h
1145 h
1215 h
·
·
·
1300 h
1345 h
·
·
1420 h
1500 h
·
·
1535 h
1600 h
1650 h
Symposium on Neuropathic Pain
Chairs: • Dr. Rita Paul, Dr. Sarbari Swaika, Dr. Manjushree Ray
• Phantom Limb Pain – Dr. Abhijit Banerjee
• Post-Surgical Pain Syndrome – Dr. Sanjay patowari
• Botox in Pain Management – Dr. Debjyoti Dutta
Symposium on Acute Pain Management (Sponsered By Smith Medical)
Chairs: • Dr. Sampa Dutta, Dr. Chumki Dutta
• USG in Nerve Block – Dr. Sunil Waghmare
• Acute Pain Management : Current Status – Dr. Udayan Bakshi
TEA BREAK
Twin Lectures on Back Pain
Chairs: • Dr. Sakuntala Chakraborty, Dr Sucharita Chakraborty
• Back Pain Rehab – Dr. K M Das
• Evidence Based Management Algorithm for Back Pain
– Dr. Trinanjan Sarangi
Past President's Oration
Chairs: Dr. Santanu Tripathi, Dr. S M Basu
Speaker: Dr. Rita Paul
Symposium on Advanced Pain Management
Chairs: • Dr. A Rudra, Dr. Supratik Sen ,Dr D Sanyal
• Radiofrequency in Pain Management – Dr. Chinmoy Roy
• Intrathecal Drug Delivery System – Dr. Bibhu Kalyani Das
• Spinal Stimulators – Dr. Gautam Das
LUNCH
Special Lectures:
Chairs: • Dr. Jayanta Bhattacharya, Dr Ashrukana Mitra
• Medical Errors in Pain Care : Implications for Professional
- Practice and Patient Safety - Dr Santanu K Tripathi
• Obesity and Pain – Dr B Ramana
Panel Discussion: Multidisciplinary Pain Management
Moderator: Dr Trinanjan Sarangi
Panelists: Dr R Rajput (Orthopedic Surgeon), Dr Vijay Kumar (Neurosurgeon), Dr G S Bhattacharya (Oncologist), Dr Krishna Poddar (Interventional Pain Specialist), Dr Uday Mukherjee (Consultant Faciomaxillary
Surgeon)
Interactive Session : How To Do It
Chairs: • Dr. Sumanta Dasgupta, Dr G Mitra
• Cervical Epidural Block – Dr. Subrata Goswami
• Percutaneous Disc Procedures – Dr. Krishna Poddar
Free Paper Session
Chairs: Dr Sujit Chatterjee, Dr. T Bhattacharya
TEA BREAK1610 hAGM and Election of Executive Committee Members
of ISSP - WB
Valediction
Indian Society for Study of Pain
West Bengal Branch
From The Secretary’s Desk
Dear Friends,
Greetings from the ISSP WB secretariat. It gives me great pleasure to put forward this last report in my tenure
as secretary. I express my sincere gratitude and thanks to members of ISSP West Bengal branch who have
given me full support. I would like to summarize the achievements of my journey which began in March of
2009.
Our state branch has progressed by leaps and boundaries in last 3 years. Special thanks and appreciation to
my predecessor Dr. Gautam Das, the pioneer in pain management in Eastern India, who revived not only
our branch but also guided our branch to reach this status.
Directory- ISSP WB also achieved the successful consolidation of all membership records into one master
data base directory. My first initiative was to update mailing list, a herculean task, as there were only a few
phone numbers. Now I have updated correct addresses, phone numbers and E-Mail id of more than half of
members.
Membership- From December 2011, 10 new members have been added to society. Now we are 175
members, making Indian Society for study of Pain West Bengal branch one of the largest branch of ISSP. From
2006 till now our membership has doubled.
I-Card It is my earnest request to you all to get I-Card. Please send two passport photos, your ISSP no., along
with Rs 100 cash/cheque to me or national secretary for ID card (essential for election).
Website One more great achievement for our society is launching our own Website of ISSP (WB)
w.w.w.wbissp.org in 2008. For two years we are continuously updating and maintaining our website. So
please visit our website and, give your feedback and valuable suggestions to [email protected].
It is my great privilege to inform you that Dr Gautam Das, has been elected as Editor of Indian Journal of
Pain, the official journal of ISSP. With Dr Bibhu Kalyani Das, I have attended IASP World Congress at Milan on
Aug 27-1st Sep 2012. There were 75 Indian delegates with total 7000 delegates from all over world.
I am feeling proud to say that ISSP WB is not only one of the largest branch in India but also only state branch
having regular CME’s, Nurses training and pain awareness programme and annual state conference and
workshops. This has been made possible only by the untiring efforts of our entire executive committee.
In my tenure WBISSPCON 2010 held at Medical college attended by more than 150 doctors with
fantastic scientific programme, kudos to Dr Suman Chatterjee. Thanks to Dr Trinanjan Sarangi
for organizing WBISSPCON 2011 at Hotel Kelinworth in style and making it great success.
Scientific activities since January 2011 CME -In year 2011-2012 we had organized four CMEs and three
Nurses education and training programmes. First CME was organized on at Medica Hospital in May 2012.
Co-ordinator –Dr S Tripathi. Topic-1- Update on Pharmacotherapy of Chronic Pain Management ,Speaker :
Dr Subhrojyoti Bhowmick, ,Moderator-Dr S K Tripathi Topic 2. Tapendatol in Post Operative Pain
Management ,Speaker : Dr Amiya Kr Mishra, Senior Consultant, Moderator : Dr Abhijit Paul Attended by 35
doctors.
2nd CME was organized at INK, Institute of Neuroscience Kolkata on 7TH July 2012 ,Co-ordinator - Dr
Chinmoy Roy. Chairpersons- Dr. S. Tripathi, Dr. B. K. Das, Dr. Krishna Poddar Topic-1- A resistant case of
CRPS - case presentation, speaker- Dr. Chinmoy Roy, Topic-2- Approach to a chronic arthritis pain patient,
speaker- Dr. Parashar Ghosh Topic-3 Encountering a major complication following radiofrequency thermal
ablation of gasserian ganglion- DR. B. K. Das Attended by 39 doctors.
3rdCME was organized at Medical College, Kolkata on 8.9.12; Co-ordinator- Dr Suman Chatterjee ;
Chairpersons-Dr A Rudra and Dr Rita Pal Topics-1 Basics of interventional Pain Management; Speaker-Dr
Subrata Ray Topic-2 Pediatric Pain Management; Speaker-Suman Chatterjee Attended by 40 doctors
,including good number of PGT’s.
4thCME was organized at Bellevue on 7th November 2011, Co-ordinator –Dr Krishna Poddar,
Chairpersons-Dr Dr B K Das and Dr S K Tripathi Topic 1Hydrodiscectomy by Dr Krishna Poddar Topic 2
Failed Back syndrome by Dr Subrata Goswami; Attended by 25 doctors.
Nurses Training Programme- First Nurses Training programme was organized at Bellevue Hospital . Coordinotor – Dr Krishna Poddar. Attended by 35 nurses. Topic 1-Dr Krishna Poddar-Introduction to Pain
Management Topic 2-Assesment of Acute pain –Dr S Patwari Topic 3-Opioids-Dr S K Tripathi
2nd Nurses Programme was organized at Fortis Hospital, Rasbehari Avenue. Co-ordinator Dr Krishna
Poddar,attended by 25 Nurses. Topic 1-Pain Assessment-Dr Krishna Poddar Topic 2-Post operative Pain
management-Dr Suchrita Chakraborty 3rd Nurse programme was organized at ESI Sealdah on 28-7-2012
Co-ordinator-Dr Subrata Goswami.
The first session was on Nurse Training on Pain Management. An overview with the types of pain, evaluation
with scoring tools, management with different modalities for both acute and chronic pain sufferers including
Medical Officer and in charge of Pain Management Unit of Sealdah ESI Hospital. 28 senior Nursing Staff of
the Hospital attended the program with great enthusiasm.
The second session was on Headache: Evaluation and Management by Dr Biman Kanti Ray, Associate
Professor, Neurology, Bangur Institute of Neurology, Kolkata. There were interactive case discussions after
the presentation. This CMEwas attended by many senior members of ISSP West Bengal.
Executive Meetings-In year 2011-2012 five EC meetings were done, many issues were discussed, and
scientific programme was planned. Some important issues are• Registration and PAN CARD of the branch
• Our bank account name was same of national bank account name. So our state account name has been
modified to “Indian Society for study of Pain West Bengal Branch “
• CME will be organized every alternate month mimimum 4 CME will be done
• Planning for regular nurses training programme
• Any peer reviwed publication or International presentation can be presented in ISSPWB CME and will be
published in society’s website and society’s year book on Pain . Please send your publications and
presentations.
• Annual conference will be organized on first week of December.
The financial structure of ISSP WBP has been revised on a more professional basis. With balance of Rs
30,000 I started my journey as treasurer in 2006 , and then as secretary on 2009. Now I am proud to say we
are rich of more than one lakh in Fixed deposit and more than a lakh in saving account. We had applied for
our state branch registration and Pan card , I hope very soon we will be successful in having both.
Through these activities, ISSP aim remains to demonstrate that collectively and individually those affiliated
with ISSP share a common vision, which is to provide better education for pain physicians and deliver better
relief for all pain patients. Even though we have made great strides in achieving these goals, there is much
more work to be done. I would like to thank to all members of the Executive Board and Council of Indian
Society for Study of Pain West Bengal, for their understanding, cooperation and teamwork during my term.
My special thanks go to two past presidents, Dr Rita pal and Dr S K Tripathi and all my senior members and
Past Presidents for their great wisdom and cooperation during this term in which we have accomplished all
these achievements.
It is a great pleasure that I am able to say to you today, that Indian Society for Study of Pain West Bengal, has
flourished and I look forward to the future.
Thank you all. Long live ISSP.
Dr Krishna Poddar,
Secretary, ISSP (WB).
Indian Society for Study of Pain (West Bengal)
Report from Hony. Treasurer, ISSP (WB)
Receipts and Payments for the year ending 31.03.2012 , A/C No 20259441419,
Allahabad Bank, Salt Lake
DATES
PARTICULARS BALANCE
RECEIPTS
PAYMENTS
31.03.11
Opening Balance - ` 82,720
16.05.11
Balance closure WBISSPCON2008 - ` 84,470
1,750
16.05.11
Balance closure WBISSPCON2009 - ` 86,290
1,820
25.07.11
N.Bose, caterer (YPP at KPCMC) - ` 76,290
10,000
24.08.11
Kreative Fingers (Website) - ` 69,630
06,660
27.08.11
Monalisa Dutta (Mem.) - ` 73,130
3,500
27.08.11
Mohona Mukherjee (Mem.) - ` 76,630
3,500
27.08.11
Neon (YPP at KPCMC) - ` 91,630
15,000
27.08.11
Parthasarathi Ray(Mem) - ` 95,130
3,500
27.08.11
? (New member) - ` 98,630
3,500
31.08.11
Interest - ` 1,00,239
1,609
06.09.11
National share - ` 94,989
5,250
06.09.11
National Share - ` 89,739
5,250
15.11.11
CME at Bankura - ` 81,739
8,000
16.11.11
Vygon , Bankura (909641) - ` 89,739
07.01.12
To Krishna Poddar - ` 89,039
700
25.01.12
National Share (4 members & I card for 2) ` 77,339
11,700
02.02.12
S Dutta & I card for 2 members - ` 81,039
3,700
03.02.12
Sudipta Mondal - ` 84,539
3,500
03.02.12
Saikat Majumdar - ` 88,039
3,500
03.02.12
Suryabrata Chhatterjee - ` 91,539
3,500
09.02.12
National Share (3 persons) - ` 83,664
29.02.12
Interest - ` 85,433
1,769
27.03.12
Shabnam Agarwal - ` 88,933
3,500
27.03.12
Janmejoy Sengupta - ` 92,433
3,500
8,000
7,875
27.03.12
Manirujjaman - ` 95,933
31.03,12
Closing Balance - ` 95,933
3,500
Fixed Deposits at Allahabad Bank, Salt Lake
(Dr Subrata Goswami, Hony.Treasurer)
DATE OF INVESTMENT
(A/C NO.)
MATURITY AMOUNT
AMOUNT
DATE OF MATURITY
Renewal
09.03.12
20259420919
13,442
12,234 @ 9.5%
10.03.13
09.03.12
20259375806
16,803
15,293 @ 9.5%
10.03.13
27.10.11
50046545621
56,589
53,374 @ 8%
23.07.12
Total
86,834/-
80,901/-
Indian Society for Study of Pain
West Bengal Branch
Obituary
Prof. Shyamal Kumar Roy
(Born 17/08/47 –Died 03/11/12)
Prof. Shyamal Kumar Roy, ISSP Life Member (R 43) passed away on 3rd November ’12 following
a massive intra-cerebral haemorrhage. He served ISA as President, WB State Branch (2005),
Hon. Secretary, ISA WB State Branch (1992-2001)as well as Organising Chairman, ISACON
2005.
He was very popular as teacher, examiner and leader to his students. He delivered & chaired
many scientific sessions, orations, symposia etc; last being at Eastern Zonal Conference (ISAJAC
2012) at Bhubaneswar. He was an MCI Inspector.
He retired as HOD Anaesthesiology, NRS Medical College, Kolkata in 2008. Prior to that, he
worked as Professor & HOD of Burdwan Medical College. After his superannuation, he joined
M.G.M. Medical College, Kishanganj, Bihar where he was associated till his death.
His schooling was from Ramakrishna Mission Vidyapith, Deoghar & Purulia. He graduated from
R G Kar Medical College in 1969 and completed MD in Anaesthesia in 1977. He was an active
Rotarian and Vice-President of Sree Ramakrishna Sarada Welfare Association. He is survived by
his wife and daughter.
WBISSPCON 2011 (Hotel Kenilworth)
Our Other Activities
Organizing Committee Meeting
ISSPWBCON 2012 at Belle Vue Clinic
Workshop
GB Meeting 2011
Nurses Programme At Belle Vue Clinic
DECLARATION OF MONTREAL
Declaration that Access to Pain Management Is a Fundamental Human Right
We, as delegates to the International Pain Summit (IPS) of the International Association for the
Study of Pain (IASP) (comprising IASP representatives from Chapters in 64 countries plus
members in 129 countries, as well as members of the community), have given in-depth attention
to the unrelieved pain in the world,
Finding that pain management is inadequate in most of the world because:
• There is inadequate access to treatment for acute pain caused by trauma, disease, and
terminal illness and failure to recognize that chronic pain is a serious chronic health problem
requiring access to management akin to other chronic diseases such as diabetes or chronic
heart disease.
• There are major deficits in knowledge of health care professionals regarding the
mechanisms and management of pain.
• Chronic pain with or without diagnosis is highly stigmatized.
• Most countries have no national policy at all or very inadequate policies regarding the
management of pain as a health problem, including an inadequate level of research and
education.
• Pain Medicine is not recognized as a distinct specialty with a unique body of knowledge and
defined scope of practice founded on research and comprehensive training programs.
• The World Health Organization (WHO) estimates that 5 billion people live in countries with
low or no access to controlled medicines and have no or insufficient access to treatment for
moderate to severe pain.
• There are severe restrictions on the availability of opioids and other essential medications,
critical to the management of pain.
And, recognizing the intrinsic dignity of all persons and that withholding of pain treatment is
profoundly wrong, leading to unnecessary suffering which is harmful; we declare that the
following human rights must be recognized throughout the world:
Article 1. The right of all people to have access to pain management without discrimination
(Footnotes 1-4).
policies, and systems is unethical and a breach of the human rights of people harmed as a result.
2. The obligation of all health care professionals in a treatment relationship with a patient,
within the scope of the legal limits of their professional practice and taking into account the
treatment resources reasonably available, to offer to a patient in pain the management that
would be offered by a reasonably careful and competent health care professional in that field of
practice. Failure to offer such management is a breach of the patient's human rights.
Note: This Declaration has been prepared having due regard to current general circumstances
and modes of health care delivery in the developed and developing world. Nevertheless, it is the
responsibility of: governments, of those involved at every level of health care administration, and
of health professionals to update the modes of implementation of the Articles of this Declaration
as new frameworks for pain management are developed.
Footnotes
• This includes, but is not limited to, discrimination on the basis of age, sex, gender, medical
diagnosis, race or ethnicity, religion, culture, marital, civil or socioeconomic status, sexual
orientation, and political or other opinion.
• International Covenant on Economic, Social and Cultural Rights (ICESCR) (1966). The State
parties of the ICESCR recognize "the right of everyone to the highest attainable standard of
physical and mental health" (Art. 12), creating the "conditions which would assure to all
medical service and medical attention in the event of sickness."
• Universal Declaration of Human Rights (1948): Rights to Health (Article 25); Convention on
the Rights of a Child (Article 24); Convention on the Elimination of All Forms of Discrimination
Against Women (Article 12); Convention on the Elimination of All Forms of Racial
Discrimination (Article 5(e) (iv)).
• The Committee on Economic, Social and Cultural Rights. General Comment No.14, 22nd
Session, April-May 2000 E/C 12/2000/4. "Core obligations" of all signatory nations
included an obligation to ensure access to health facilities, goods, and services without
discrimination, to provide essential drugs as defined by WHO, and to adopt and implement a
national health strategy.
• Committee on Economic, Social and Cultural Rights. General Comment No.14, 22nd
Session, April-May 2000, E/C 12/2000/4, para. 12. General Comment No. 14 stated that
health accessibility "includes the right to seek, receive and impart information and ideas
concerning health issues."
• Appropriate assessment includes recording the results of assessment (e.g., pain as the "5th
vital sign," can focus attention on unrelieved pain, triggering appropriate treatment
interventions and adjustments). Appropriate treatment includes access to pain medications,
including opioids and other essential medications for pain, and best-practice
interdisciplinary and integrative nonpharmacological therapies, with access to professionals
skilled in the safe and effective use of these medicines and treatments and supported by
health policies, legal frameworks, and procedures to assure such access and prevent
inappropriate use. Given the lack of adequately trained health professionals, this will require
providing educational programs regarding pain assessment and treatment in all of the
health care professions and programs within the community for community care workers
delivering pain care. It also includes establishment of programs in pain medicine for the
education of specialist physicians in pain medicine and palliative medicine. Accreditation
policies to assure appropriate standards of training and care should also be established.
• Failure to provide access to pain management violates the United Nations 1961 Single
Convention on Narcotic Drugs declaring the medical use of narcotic drugs indispensable for
the relief of pain and mandating adequate provision of narcotic drugs for medical use.
• The UN Universal Declaration of Human Rights (1948) (Article 5) states: "No one shall be
subjected to torture or to cruel, inhuman or degrading treatment..." Comment: Deliberately
ignoring a patient's need for pain management or failing to call for specialized help if unable
to achieve pain relief may represent a violation of Article 5.
• The UN Special Rapporteur on the Right to Health and the UN Special Rapporteur on the
question of torture and other cruel, inhuman, and degrading treatment stated: "The failure to
ensure access to controlled medicines for the relief of pain and suffering threatens
fundamental rights to health and to protection against cruel, inhuman and degrading
treatment.”
References
• ANZCA. Statement on patients' rights to pain management. ANZCA PS 45; 2001. Available
at: www.anzca.edu.au.
• Brennan F, Carr DB, Cousins MJ. Pain management: a fundamental human right. Anesth
Analg 2007;105:205-21.
• Cousins MJ, Brennan F, Carr DB. Pain relief: a universal human right. Pain 2004:112:1-4.
• FEDELAT. Proclamation of pain treatment and the application of palliative care as human
rights, May 22,2008.
• IAHPC. Joint declaration and statement of commitment on palliative care and pain treatment
as human rights. Available at www. Hospicecare.com.
• Scholten W, Nygren-Krug H, Zucker HA. The World Health Organization paves the way for
action to free people from the shackles of pain. Anesth Analg 2007;105:1-4.
• Somerville M. Death of pain: pain, suffering, and ethics. In Gebhart GE, Hammond DL,
Jensen TS, editors. Proceedings of the 7th World Congress on Pain. Progress in Pain Research
and Management, Vol. 2. Seattle: IASP Press; 1994. p. 41-58.
Contact: Karen Smaalders | T : +1.206.283.0311 x225 | [email protected]
IASP Sponsors Global Year Against Visceral Pain
Initiative promotes better visceral pain management through increased awareness
SEATTLE, October 15, 2012 – The Global Year Against Visceral Pain launches today, bringing
global attention to pain that originates in or near the internal organs of the body. Visceral pain is
the most frequent form of pain, felt by most people at one time or another, and the number one
reason for patients to seek medical attention. Sponsored by the International Association for the
Study of Pain (IASP), the 12‐month campaign focuses on education for health care professionals
and government leaders as well as public awareness.
Visceral pain associated with ailments such as gallstones, acute pancreatitis, acute appendicitis,
and diverticulitis are the most common reasons for visits to outpatient and inpatient
gastrointestinal (GI) clinics, but visceral pain may also include chronic chest pain, bladder pain,
gynecological pain, and pelvic pain. Up to 25% of the population report visceral pain at any one
time, leading to substantial health care costs.
Led by urogenital pain and gastroenterology experts Timothy Ness, MD, PhD (USA), and Qasim
Aziz PhD, FRCP (UK), the IASP initiative will mobilize IASP's 8,000+ members and 88 national
chapters, and forge partnerships with other organizations, to:
disseminate information about visceral pain worldwide;
• educate pain researchers as well as health care professionals who see the issues associated
with visceral pain firsthand in their interactions with patients;
• Increase awareness of visceral pain among government officials, members of the media,
and the general public worldwide; and
• Encourage government leaders, research institutions, and others to support policies that
result in improved pain treatment for people with visceral pain.
As part of the Global Year Against Visceral Pain, IASP offers a series of fact sheets for clinicians
and health care professionals that cover specific topics related to visceral pain. These fact sheets
are translated into multiple languages and available for free download. Also available on the
web is a page of resources including links and free posters promoting the Global Year.
Throughout the coming year, IASP and its chapters sponsor meetings, symposia, media
interviews, publications, and other efforts to promote education on issues surrounding visceral
pain. For more information, visit: www.iasp‐pain.org/GlobalYear/VisceralPain.
Epidemiology of Abdominal Pain
Abdominal pain is a common symptom that leads to millions of outpatient visits. National
statistical surveys of the burden of gastrointestinal (GI) disease [2,5,6] have consistently
identified abdominal pain as the most common symptom prompting an outpatient clinic visit.
Furthermore, abdominal pain was the leading physician diagnosis for GI disorders in outpatient
clinic visits in the United States in 2004 and the second most common diagnosis in 2009. In the
United Kingdom, 25% of the population report abdominal pain at any one time [3].
Abdominal pain is also the major symptom associated with the most common inpatient GI
diagnoses in the United States. Statistical surveys from both 2004 and 2009 [2,5,6] demonstrate
that the four most common diagnoses among patients admitted for GI complaints are
gallstones, acute pancreatitis, acute appendicitis, and diverticulitis. Abdominal pain is often the
cardinal and presenting symptom in each of these conditions. The management of these
conditions leads to considerable health care costs, with both diverticulitis and acute pancreatitis
costing more than US$2 billion in the United States alone.
Abdominal pain is the reason for referral for about 20% of patients receiving
esophagogastroduodenoscopy [2]. Approximately 280,000 such procedures are performed
each year in the United States, leading to substantial costs.
Abdominal pain is also the most common feature of functional gastrointestinal disorders such as
irritable bowel syndrome and functional dyspepsia. The population prevalence of these
disorders is reported to be 15-25%. Functional GI disorders are one of the most common
presentations in primary care and secondary care GI clinics. Approximately 5% of patients in
primary care and 40% in secondary care GI clinics have a functional GI disorder, and pain is the
most common and difficult to manage symptom [1]. Such patients require considerable health
care resources, with annual treatment costs of US$16.6 billion in the United States [7] and € 28.4
billion across Europe [4].
In summary, abdominal pain is one the most common reasons for presentation to outpatient and
inpatient GI clinics and leads to substantial health care costs. Both organic and functional
disorders of the GI tract can cause abdominal pain.
References
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•
•
•
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Drossman DA. Rome III: the new criteria. Chin J Dig Dis 2006;7:181-5.
Everhart JE, Ruhl CE. Burden of digestive diseases in the United States part I: overall and
upper gastrointestinal diseases. Gastroenterology 2009;136:376-86.
Haider SL, McBeth J, Si!man AJ, Thompson DG, Macfarlane GJ. Psychosocial risk factors for
the onset of abdominal pain. Results from a large prospective population-based study. Int J
Epidemiol 2002;31:1219-25.
Hillila MT, Farkkila NJ, Farkkila MA. Societal costs for irritable bowel syndrome: a population
based study. Scand J Gastroenterol 2010;45:582-91.
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MT, Stizenberg K, Morgan DR, Ringel Y, Kim HP, Dibonaventura MD, Carroll CF, Allen JK,
Cook SF, Sandler RS, Kappelman MD, Shaheen NJ. Burden of gastrointestinal disease in the
United States: 2012 update. Gastroenterology 2012; Aug 8 [Epub ahead of print].
Sandler RS. Digestive and liver diseases statistics, 2004. Gastroenterology 2004;126:144853.
Shih YC, Barghout VE, Sandler RS, Jhingran P, Sasane M, Cook S, Gibbons DC, Halpern M.
Resource utilization associated with irritable bowel syndrome in the United States 1987-1997
Dig Dis Sci 2002;47:1705-15.
Copyright © 2012 International Association for the Study of Pain
Neurobiology of Visceral Pain
Definition
Pain arising from the internal organs of the body:
• Heart, great vessels, and perivascular structures (e.g., lymph nodes)
• Airway structures (pharynx, trachea, bronchi, lungs, pleura)
• Gastrointestinal tract (esophagus, stomach, small intestine, colon, rectum)
• Upper-abdominal structures (liver, gallbladder, biliary tree, pancreas, spleen)
• Urological structures (kidneys, ureters, urinary bladder, urethra)
• Reproductive organs (uterus, ovaries, vagina, testes, vas deferens, prostate)
• Omentum, visceral peritoneum
Clinical Features of Visceral Pain
Key features associated with pain from the viscera include diffuse localization, an unreliable association
with pathology, and referred sensations. Strong autonomic and emotional responses may be evoked with
minimal sensation.
Referred pain has two components: (1) a localization of the site of pain generation to somatic tissues with
nociceptive processing at the same spinal segments (e.g., chest and arm pain from cardiac ischemia) and
(2) a sensitization of these segmental tissues (e.g., kidney stones may cause the muscles of the lateral torso
to become tender to palpation).
These features are in contrast to cutaneous pain, which is well localized and features a graded stimulusresponse relationship.
Anatomy of Neurological Structures
Pathways for visceral sensation are diffusely organized both peripherally and centrally. Primary afferent
nerve fibers innervating viscera project into the central nervous system via three pathways: (1) in the vagus
nerve and its branches; (2) within and alongside sympathetic efferent fiber pathways (sympathetic chain
and splanchnic branches, including greater, lesser, least, thoracic, and lumbar branches); and (3) in the
pelvic nerve (with parasympathetic efferents) and its branches.
Passage through the peripheral ganglia occurs with potential synaptic contact (e.g., celiac, superior
mesenteric, and hypogastric nerves). The gastrointestinal tract and peripheral ganglia form extensive
neuronal plexuses that control autonomic functions. Their role in pain sensation is unknown.
Primary afferent cell bodies traveling to the central nervous system reside primarily in the nodose ganglion
(vagal) and in the T2—L2 and S1-5 dorsal root ganglia (sympathetic-associated and pelvic-nerveassociated). There may be a role of vagal afferents in nociceptive sensation. Some, but not all, spinal
afferents are unequivocally associated with pain sensation.
Visceral primary afferents have been demonstrated to enter the spinal cord and to arborize extensively,
including within Lissauer's tract, to enter multiple spinal segments above and below the segment of entry.
These afferents form synaptic contact with both superficial and deep dorsal horn neurons ipsilateral and
contralateral to the side of entry. The result is extensive, diffuse central nervous system activation.
Spinal pathways for visceral sensation. Abbreviations: ARP: aortorenal plexus, CP: celiac plexus, DRG:
dorsal root ganglia, HN: hypogastric nerve, ICN: inferior cardiac nerve, GSN: greater splanchnic nerve,
LSN: lesser splanchnic nerve, LeSN: least splanchnic nerve, LuSN: lumbar splanchnic nerves, MCG:
middle cervical ganglion, PN: pelvic nerve, PP: pelvic plexus, PuN: pudendal nerve, SCG: superior cervical
ganglion, SG: stellate ganglion, SHP: superior hypogastric plexus, SMP: superior mesenteric plexus, SP:
sacral plexus, TSN: thoracic splanchnic nerves. Adapted from a figure by E.C. Ness in Chin M, et al.
(editors). Pain in Women. Oxford University Press; 2013.
Second-order processing of visceral stimuli occurs at spinal segments and brainstem sites receiving
primary afferent input. Spinal dorsal horn neurons that respond to pain-generating visceral stimuli have
received the most extensive study. Intraspinal nociceptive processing occurs, as well as relay to other
central nervous system sites.
Visceral nociceptive information travels by both traditional spinothalamic pathways (the contralateral
ventrolateral quadrant) as well as by ipsilateral and dorsal spinal pathways. Relay sites for ascending
information have been identified at medullary, pontine, mesencephalic, and thalamic levels. Cortical
processing of visceral information has been noted in the insular cortex, anterior cingulate cortex, and
somatosensory cortex.
Unreliable Nature of Visceral Sensation
Healthy visceral tissues evoke minimal sensations. Acutely inflamed tissues are more likely to produce
painful sensations, but chronic inflammation has unreliable effects.
Electrophysiological studies have identified primary afferent nerve fibers that encode mechanical and/or
chemical stimuli. Many, if not most, primary afferent nerve fibers are "silent" and unresponsive or
minimally responsive to mechanical stimuli at baseline, but they become very mechanically sensitive and
highly responsive to other stimuli in the presence of inflammation. Subsets of neurons respond only to
high intensities of stimulation.
References
• Al-Chaer ED, Traub RJ. Biological basis of visceral pain: recent developments. Pain 2002;96:2212-25.
• Cervero F, Laird JMA. Visceral pain. Lancet 1999;353:2145-8.
• Giamberardino MA. Recent and forgotten aspects of visceral pain. Eur J Pain 1999;3:77-92.
• McMahon SB, Dimitrieva N, Koltzenberg M. Visceral pain. Br J Anaesth 1995;75:132-44.
• Ness TJ, Gebhart GF. Visceral pain: a review of experimental studies. Pain 1990;41:167-234.
• Sengupta JN. Visceral pain: the neurophysiological mechanism. Handbook Exp Physiol 2009 ;194 : 31
-74.
Acute vs. Chronic Presentation of Visceral Pain
Visceral pain is by definition pain sensed as arising from the internal organs of the body. There
are multiple etiologies for pain sensed in internal organs, including:
• Inflammation (acute and chronic), including inflammation caused by mechanical
irritants (e.g., kidney stones)
• Infection
• Disruption of normal mechanical processes (e.g., gastrointestinal dysmotility)
• Neoplasms (benign or malignant)
• Alterations in nerves carrying sensations from the viscera
• Ischemia
Visceral pain may take many different forms, and so processes that may be associated with lifethreatening or readily reversible conditions need to be considered with all presentations.
However, isolated events with an acute presentation and spontaneous resolution are not
uncommon. The level of investigation needs to be guided by prudence and by the persistence or
recurrence of symptoms.
Traditionally, chronic visceral pain has been categorized as either "organic," caused by a
pathological lesion that is detectable by standard diagnostic measures, or "functional," where
the etiology remains obscure and may be due to as yet undefined changes in visceral
hypersensitivity at either the peripheral or central level.
A patient history and physical examination are sufficient to determine a functional diagnosis in
most cases. An appropriate work-up may include laboratory tests for infectious and
inflammatory processes, as well as imaging of sites that are not readily assessed by physical
examination. Treatment of visceral pain disorders should not be delayed unless such treatment
would obscure the diagnostic work-up.
When pains of similar quality and location recur that have been previously investigated for lifethreatening processes, they may not need further investigation. Treatment of these symptoms as
if they resulted from a reversible process (e.g., infection) may be inappropriate. However, failure
to address new symptoms may be equally inappropriate.
Pain is distressing, and underlying psychological and psychiatric processes alter responses to
painful events. Reassurance and behavioral interventions are appropriate for all painful
disorders, but may be of particular benefit when symptoms are recurrent or persistent. Sensory
modulators may be appropriate for a therapeutic trial in cases in which no pathological cause is
apparent.
Painful Functional Bowel Disorders: Psychological Factors
Painful functional bowel syndromes such as irritable bowel syndrome and functional dyspepsia
(FD) are characterized by unexplained persistent or recurrent pain in the abdomen. These
syndromes are common across the world, affecting up to 15-20% of the population [3,10,12,15].
A number of mechanisms have been suggested to explain this syndrome, with two major themes
dominating the clinical literature [10]. First, visceral hypersensitivity to mechanical distension is
found in a significant subset of patients and appears to correlate with postprandial pain
[14,18,22]. Second, psychological and psychiatric problems are very common and are widely
held to have a pathogenic role, given that patients with FD are more anxious and depressed than
healthy controls [3,12,15,21]. In a clinical study that included structured psychiatric interviews, the
investigators found that 87% of patients with FD, compared to 25% of patients with organic
dyspepsia, had a psychiatric diagnosis [15]. Psychological factors related to FD patients included
major depressive disorders, anxiety disorders, and somatization [10,12].
Psychological Factors as Drivers of Gastrointestinal Symptoms
Anybody who has experienced "butterflies in the stomach" or stress-related changes in bowel
habits can attest to the fact that the brain can influence gut function and sensation. Several clinical
studies have suggested that psychosocial comorbidity is a major contributor to the severity of
functional dyspepsia and its impact on quality of life [19]. These findings are reinforced by a
considerable volume of experimental research that links stress and depression to altered
gastrointestinal sensory and motor function [1,5,6,9,17]. Together, these findings have led to the
widespread belief that the physical symptoms of FD reflect either somatization or stress-induced
disturbance of upper-gastrointestinal physiology. Indeed, successful management of patients with
functional bowel disorders requires careful attention to these psychosocial factors, often in
consultation with mental health professionals.
Gastrointestinal Problems as Drivers of Psychological Symptoms
Despite the studies reviewed above, it is still unclear whether the association between functional
bowel disorders and psychological symptoms represents a cause or effect. This question will
require rigorously conducted longitudinal studies that document the onset of psychosocial
dysfunction in relationship to visceral symptoms. Indeed, recent studies indicate that the
relationship may be bidirectional—symptoms in the gut can lead to psychological issues, and vice
versa. For example, investigators in Australia followed a cohort of patients prospectively for 12
years and found that among people free of a functional gastrointestinal disorder (FGID) at
baseline, higher levels of anxiety at baseline represented a significant independent predictor of
developing new-onset FGIDs 12 years later. Conversely, among people who did not have
elevated levels of anxiety and depression at baseline, those with a FGID at baseline had
significantly higher levels of anxiety and depression at follow-up [7]. These results are reinforced
by experimental findings that suggest that minor, transient irritation of the gut in neonatal
animals can lead to features of depression and anxiety that persist into adulthood [11].
The Brain-Gut Axis and Underlying Biological and Neural Circuits
The biological basis of these phenomena is only just beginning to be understood. The gut and
brain communicate with each other by multiple means, including hormonal and neural
mechanisms. An important example of hormonal involvement is CRF (corticotropin-releasing
factor), a hormone secreted by the hypothalamus. Experimental alterations in secretion of CRF
and expression of its receptor, CRF1, have been implicated in the pathophysiology of stressrelated phenomena as well as anxiety, depression, and changes in in gastrointestinal motility
and visceral sensation [16,20]. A variety of CRF-receptor antagonists have also demonstrated
the ability to block increased colonic activity and painful sensations induced by acute or chronic
stress [13].
The gut also relays information to various important nuclei in the brain via ascending fibers in the
vagus nerve, with potentially far-reaching consequences. The central amygdala, for instance,
transforms noxious and stressful signals into behavioral and autonomic responses that include
anxiety and depression. A recent report showed that a probiotic (Lactobacillus rhamnosus) can
reduce stress-induced corticosterone and anxiety- and depression-related behavior in mice, but
this beneficial effect can be prevented by vagotomy [2,8]. Electrical modulation of the vagus
nerve has been approved by the U.S. Food and Drug Administration for the treatment of
depression [4]. Thus, the vagus nerve can modulate emotional responses to gastrointestinal
stimulation.
Facts and Fallacies
It is clear that psychological morbidity is common in patients with functional visceral pain
conditions, and an understanding of this issue is crucial to the optimal management of these
disorders. What is not clear is how much of this comorbidity is cause and effect. Nevertheless,
recognition of this association has led to many unintended consequences, including the
stigmatization of this syndrome as being "all in the head," dismissal of patients' suffering, and a
lack of an organized approach to drug development. Much remains to be learned about the
complex relationship between the "big brain" in the head and the "little brain" in the gut and how
pathology in one can lead to changes in the other. Research in this area could significantly alter
our clinical approach and treatment of these disorders.
References
• Aro P, Talley NJ, Ronkainen J, Storskrubb T, Vieth M, Johansson SE, Bolling-Sternevald E,
Agreus L. Anxiety is associated with uninvestigated and functional dyspepsia (Rome III criteria)
in a Swedish population-based study. Gastroenterology 2009;137:94— 100
• Bravo JA, Forsythe P, Chew MV, Escaravage E, Savignac HM, Dinan TG, Bienenstock J, Cryan
JF. Ingestion of Lactobacillus strain regulates emotional behavior and central GABA receptor
expression in a mouse via the vagus nerve. Proc Natl Acad Sci USA 2011108:16050-5.
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2006;12:673-7.
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Rev Neurother 2010;10:87-92.
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Psychopathology and personality trait in subgroups of functional dyspepsia based on Rome Ill
criteria. Am J Gastroenterol 2009;104:2534-42.
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2006;130:1412-20.
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functional gastrointestinal disorders is bidirectional: a 12-year prospective population-based
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depression, but not fever, in response to peripheral immune signals; a functional anatomical
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cause: a comparison with peptic ulcer disease. J Psychosom Res 1990;34:215-22.
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Gastroenterol 2004;18:707-16.
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the neonatal rats leads to changes in hypothalamic CRF expression, depression- and anxietylike behavior as adults. PLoS One 2011;6:e19498.
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dyspepsia of unknown cause. Am J Psychiatry 1987;144:1222-3.
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Pharm Des 2006;12:4071-88.
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functional and organic dyspepsia. Gut 1998;42:814-22.
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alterations of gut motor function: role of brain corticotropin-releasing factor receptors. Am J
Physiol Gastrointest Liver Physiol 2001;280:G173-7.
• Tack J, Caenepeel P, Fischler B, Piessevaux H, Janssens J. Symptoms associated with
hypersensitivity to gastric distention in functional dyspepsia. Gastroenterology 2001;121:
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• Trimble N, Johnson AC, Foster A, Greenwood-van Meerveld B. Corticotropin-releasing factor
receptor 1-deficient mice show decreased anxiety and colonic sensitivity. Neurogastroenterol
Motil 2007;19:75460.
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Pancreatitis
Definition
Pancreatitis is pain caused by inflammation of the pancreas. Acute pancreatitis is associated with
acute tissue destruction in the pancreas. Chronic pancreatitis is persistent damage of pancreatic
tissue and impairment of pancreatic function and is associated with fibrosis. Symptom flares are
common, with intensification of symptoms for hours, days, or weeks; common triggers include
consumption of alcohol or fatty foods.
Pathophysiology
Acute pancreatitis has three phases: (1) premature activation of trypsin within the pancreas, (2)
intrapancreatic inflammation, and (3) extrapancreatic inflammatory processes. Recurrent bouts
of pancreatitis result in fibrosis and chronic pancreatitis. Apart from the risk of dehydration and
malnutrition, chronic pancreatitis is not typically life- threatening.
Theories related to pain generation include ductal obstruction, fibrotic encasement of the
pancreas, and complex neuropathic-inflammatory interactions. Etiologies include alcohol
abuse, hyperlipidemia, gallstones or congenital pancreatic abnormalities, hereditary factors,
autoimmune disease, and hyperparathyroidism. Between 10% and 30% of cases are idiopathic.
Complications include diabetes mellitus, pseudocysts, pancreatic fistulae, obstruction of biliary
or gastrointestinal portal systems, and malabsorption.
Diagnosis
Diagnosis is based on a careful history, physical examination, and laboratory tests, including
amylase/lipase. Pain is typically localized to the abdomen, the epigastric area, and the back.
Nausea and vomiting are often more problematic than pain. Weight loss, steatorrhea, and
malabsorption are common. Calcification of the pancreas may be visible on abdominal
radiographs. Endoscopic procedures with retrograde cholangiopancreatography or ultrasound
are useful.
Management Options
Most episodes of pancreatitis are mild and resolve themselves with fluid and electrolyte
replacement, food restriction, and abstinence from alcohol and other triggering events. With
evidence of significant pancreatic necrosis (high amylase/lipase), infection, and/or other
systemic metabolic processes, acute pancreatitis may be a life-threatening condition requiring
aggressive surgical and medical intervention. Pancreatic enzymes are needed for exocrine
insufficiency. Ductal decompressive therapy is commonly performed with surgery or use of
stents. Opioids are commonly administered, with caution if the patient has a history of substance
abuse. There is a potential role for antioxidants, gabapentinoids, anesthetic block (celiac plexus
or splanchnic nerves), endoscopic procedures, biliary stents, or surgical excision.
References
• Andren-Sandeberg A, Hoem D, Gilason H. Pain management in chronic pancreatitis. Eur J
Gastroenterol Hepatol 2002;14:957— 70.
• Banks PA, Freeman ML; Practice Parameters Committee of the American College of
Gastroenterology. Practice guidelines in acute pancreatitis. Am J Gastroenterol
2006;101:2379-400.
• Fruloni L. Italian consensus guidelines for chronic pancreatitis. Dig Liver Dis 2010;42(Suppl
6): S381-406.
• Isaji S, Takada T, Kawarada Y, Hirata K, Mayumi T, Yoshida M, Sekimoto M, Hirota M, Kimura
Y, Takeda K, Koizumi M, Otsuki M, Matsuno S. JPN guidelines for the management of acute
pancreatitis: surgical management. J Hepatobiliary Pancreat Surg 2006;13:48-55.
• Loveday BP, Srinivasa S, Vather R, Mittal A, Petrov MS, Phillips AR, Windsor JA. High quality and
variable quality of guidelines for acute pancreatitis: a systematic review. Am J. Gastroenterol
2010;105:1466-76.
• Mullady DK, Yadav D, Amann ST, O'Connell MR, Barmada MM, Elta GH, Scheiman JM,
Wamsteker EJ, Chey WD, Korneffel ML, Weinman BM, Slivka A, Sherman S, Hawes RH, Brand
RE, Burton FR, Lewis MD, Gardner TB, Gelrud A, Disario J, Baillie J, Banks PA, Whitcomb DC,
Anderson MA. Type od pain, pain-associated complications, quality of life, disability and
resource utilisation in chronic pancreatitis: a prospective cohort study. Gut 2010;60:77-84.
• Pancreas Study Group, Chinese Society of Gastroenterology. Guidelines for the diagnosis and
treatment of chronic pancreatitis (Nanjing 2005). Chin J Dig Dis 2005;6:198-201.
• Warshaw AL, Banks PA, Fernandez-Del Castillo C. AGA technical review: treatment of pain in
chronic pancreatitis. Gastroenterology 1998;115:765-76.
Interstitial Cystitis/Bladder Pain Syndrome
Definition
Interstitial cystitis/bladder pain syndrome (IC/BPS) is defined as chronic pain, pressure, and
discomfort (with a duration of more than 3 months) associated with urinary urgency or frequency
without any readily explainable cause (infection, neoplasm, or structural abnormality).
Clinical Findings
Clinical findings include pain, discomfort, and unpleasant symptoms, perceived to be related to
the bladder (localized to suprapubic, urethral, vaginal, and perineal areas and associated with
bladder filling and/or emptying), and urinary frequency and urgency. Common findings include
frequent low-volume voiding when awake, nocturia, and cystoscopic evidence of
glomerulations (submucosal petechial hemorrhages) or mucosal lesions or ulcers (Hunner's
lesions).
Epidemiology
IC/PBS is more prevalent in women than in men (estimates range from a ratio of 2:1 to 10:1).
Self-report studies indicate diagnosis of IC/BPS in 800-900 per 100,000 women; symptoms are
present in 0.5-11% of women depending on the definitions used. IC/PBS is most commonly
diagnosed in the fourth decade of life, but symptoms can predate diagnosis by many years.
Symptom flares are common, with intensification of symptoms for hours, days, or weeks.
Common comorbidities include fibromyalgia, irritable bowel syndrome, headaches, allergies,
rheumatological disorders, vulvodynia, depression, and anxiety disorders.
Pathophysiology
The pathophysiology of IC/BPS is still incompletely understood and is likely to be complex and
multifactorial. Theories include, but are not limited to, the following: an incomplete barrier lining
of the bladder, abnormal mast cells, other immunological factors, a hypersensitive nervous
system (peripheral/central components), genetic factors, and pelvic floor muscle spasm.
Diagnosis
Careful patient history, physical examination, and laboratory tests are necessary to rule out
confusable diagnoses. Useful measures include urinalysis or urine culture, post-voiding
residual measures, and cytology if there is a history of smoking. Voiding symptoms and pain
scores should be gathered as part of the history and to assess response to treatment. Cystoscopy
and urodynamics are useful when diagnosis is in doubt.
Management Options
Conservative options include education, behavioral modification, stress management, lowimpact exercise (walking, stretching, or yoga), and manual physical therapies (including focused
pelvic physiotherapy and/or trigger point release). Systemic medical therapies include
antihistamines, pentosan polysulfate, cyclosporine A, opioids, and neuropathic pain
medications (gabapentinoids or tricyclic antidepressants). Intravesical medical therapy includes
dimethylsulfoxide (DMSO), lidocaine, and heparin. Surgery includes hydrodistension and
fulguration of mucosa! lesions. Other options include neurostimulation (for frequency/urgency),
intradetrusor botulinum toxin injection, pain management interventional procedures (anesthetic
injections), cystoplasty, urinary diversion, and cystectomy.
Interventions that are not recommended except in studies include long-term antibiotics; systemic
corticosteroids; high- pressure, long-duration hydrodistension; and intravesical resiniferatoxin
or bacille Calmette-Guerin.
References
• Fall M, Baranowski AP, Elneil S, Engeler D, Hughes J, Messelink EJ, Oberpenning F, Williams
ACdeC. EAU guidelines on chronic pelvic pain. Eur Urol 2010;57:35-48.
• Hanno PM, Burks DA, Clemens J, Dmochowski RR, Erickson D, Fitzgerald MP, Forrest JB,
Gordon B, Gray M, Mayer RD, Newman D, Nyberg L Jr, Payne CK, Wesselmann U, Faraday
MM. Diagnosis and treatment of interstitial cystitis/bladder pain syndrome. American
Urological Association (AUA) guideline. American Urological Association;2011. Available at:
http://www.auanet.org/content/guidelines-and-quality-care/clinical-guidelines/mainreports/ic-bps/diagnosis_andtreatment_ic¬bps.pdf.
Male Chronic Pelvic Pain Syndrome
Definition
Male chronic pelvic pain syndrome is defined as chronic pain, pressure, or discomfort localized
to the pelvis, perineum, or genitalia of males lasting more than 3 months that is not due to readily
explainable causes (infection, neoplasm, or structural abnormality). Other names for the
disorder include prostatodynia and chronic nonbacterial (abacterial) prostatitis, although it is
unclear how the symptoms relate to the prostate.
Clinical Findings
By definition, this syndrome occurs only in men. Common symptoms include pain or discomfort
in the perineum, suprapubic area, penis, and testicles, as well as dysuria and ejaculatory pain.
Patients may also have urinary symptoms, both obstructive (slow, intermittent stream) and
irritative (increased frequency or urgency). Sexual dysfunction is common. Systemic symptoms
include myalgia, arthralgia, and unexplained fatigue. Some patients may have a variant of
interstitial cystitis/bladder pain syndrome with predominant bladder-related pain associated
with voiding problems.
Epidemiology
Self-report studies indicate diagnosis in 0.5% of males; symptom-based evaluations of the
general population suggest an incidence of symptoms in males ranging from 2.7% to 6.3%. The
syndrome is commonly diagnosed in young to middle- aged men, but is prevalent in all ages.
Symptom flares are common, with intensification of symptoms for hours, days, or weeks.
Common comorbidities include depression, stress, and anxiety disorders.
Pathophysiology
The pathophysiology is still incompletely known and is probably a complex and multifactorial
process that eventually results in a chronic neuropathic and/or muscular pain syndrome.
Initiators of this condition are believed to include infection (including sexually transmitted
diseases and possibly non-culturable organisms and viruses), trauma (including perineal and
urethral trauma), neurological upregulation, non-infection-related inflammation (auto-immune
or neurogenic), dysfunctional voiding, and pelvic floor dysfunction/muscle spasm. In genetically
and/or anatomically susceptible men, these initiators may result in chronic neuropathic and
neuromuscular pain.
Diagnosis
A careful history, physical examination, and laboratory tests should rule out confusable
diagnoses. Useful measures include urinalysis or urine culture and for selected patients,
urodynamics, cystoscopy, and lower urinary tract/pelvic imaging studies.
Management Options
Management is usually multimodal and should be personalized according to the patient's
clinical phenotype. The impact of pain and its treatment on sexual function needs to be assessed
and addressed. Conservative measures include local heat therapy, low-impact exercise
(walking, swimming, stretching, and yoga), diet and lifestyle modifications, and physiotherapy.
Medical therapies may include a trial of antibiotics, alpha-adrenergic blockers, antiinflammatories, muscle relaxants, and herbal preparations.
Pain management includes neuropathic pain medications such as tricyclic antidepressants or
gabapentinoids. Opioids are typically a late medical option. Pain intervention procedures such
as directed injection of local anesthesia may be helpful for patients with defined and localized
pain sites. Bladder-directed therapy is appropriate for patients with an interstitial cystitis/bladder
pain phenotype. Psychotherapy (in particular cognitive-behavioral therapy) may be helpful in
learning
beneficial pain-coping techniques. Surgery should be avoided unless there is a specific
indication (e.g., a urethral or bladder neck obstruction).
References
• Anothaisintawee T, Attia J, Nickel, JC, Thammakraisorn S, Numthavaj P, McEvoy M,
Thakkinstian A. Management of chronic prostatitis/chronic pelvic pain syndrome : a systematic review and network meta-analysis. JAMA 2011;305:78-86.
• Fall M, Baranowski AP, Elneil S, Engeler D, Hughes J, Messelink EJ, Oberpenning F, Williams
ACdeC. EAU guidelines on chronic pelvic pain. Eur Urol 2010;57:35-48.
• Nickel JC. Prostatitis. Can Urol Assoc J 2011;5:306-15.
• Nickel JC, Shoskes D. Phenotypic approach to the management of the chronic
prostatitis/chronic pelvic pain syndrome. BJU Int 2010;106:1252-63.
• Strauss AC, Dimitrakov JD. New treatments for chronic prostatitis/chronic pelvic pain
syndrome. Nat Rev Urol 2010;7:127-35.
• Wagenlehner FM, Naber KG, Bschleipfer T, Brahler E, Weidner W. Prostatitis and male pelvic
pain syndrome. Dtsch Arztebl Int 2009;106:175-83.
Chronic Chest Pain
The Clinical Problem
Angina-like chest pain is an alarming symptom. It is a common reason for presentation to
emergency departments and forms the bulk of the workload for cardiologists. Clinical
evaluation ranges from simple investigations such as electrocardiograms (ECG) (both at rest
and after exercise) and echocardiograms to more expensive and invasive investigations such as
coronary angiography and pharmacological stress tests. In patients with recurrent symptoms
without an obvious cause, further evaluation excludes cardiomyopathies, microvascular
disease, and pericardial disease. However, 10-50% of patients presenting with angina-like chest
pain sufficiently severe to warrant invasive cardiac investigations do not have cardiac disease
[30] and are classified as having noncardiac chest pain (NCCP).
Epidemiology and Social and Economic Impact
NCCP is frequent in the Western world. Up to 30% of patients undergoing coronary angiography
for chest pain have normal coronary arteries [15]. A recent meta-analysis in 14 separate
populations, containing 25,000 subjects, showed a pooled prevalence of NCCP of 13% (95%
Cl, 9-16). Prevalence was similar in women vs. men but was markedly higher in subjects who
also reported gastroesophageal reflux disease (GORD) [19]. Other risk factors include obesity, a
family history of GORD, smoking, and analgesic use [13]. Prognosis of patients with NCCP is
favorable. Myocardial infarction occurs in at most 1% of cases [31,44], and cardiac death occurs
in only 0.6% after follow-up of up to 10 years. In contrast, patients with coronary disease
confined to a single vessel have a mortality of 15% at 48 months and 35% at 11 years [10]. The
economic burden is significant. In one American study, the health care costs were estimated to be
more than US$315 million annually; because of multiple clinic and emergency room visits,
hospitalizations, and prescriptions [36]. In Australia, NCCP accounts for at least $30 million of
the health care budget annually [14].
Clinical Characteristics of Cardiac and Esophageal Causes of Chest Pain
In patients with NCCP, gastrointestinal, pulmonary, musculoskeletal, infectious, drug-related,
and psychological disorders are considered. However, esophageal conditions are considered to
be the most common contributing factor for angina-like chest pain of non-cardiac origin [16].
Interestingly, the clinical history often does not distinguish between cardiac and esophageal
causes of chest pain because pain of esophageal origin can also be located retrosternally with
radiation to the arms, neck, jaws, or back. The pain is often described as squeezing or burning
and can be triggered by swallowing, but also by exercise. In patients with angina, the presence of
heartburn or dysphagia may increase the likelihood of an underlying esophageal condition [2];
however, as many as 50% of patients with a cardiac cause of chest pain may also have
heartburn, regurgitation, or dysphagia [7]. Furthermore, cardiac and esophageal disease may
overlap; for instance in patients with coronary artery disease, gastroesophageal reflux may
trigger ST segment changes on ECG and chest pain [29]. Hence, the existence of cardiac or
esophageal disease cannot be assumed on the basis of clinical presentation alone. Despite
these confounding factors, patients with NCCP are usually younger and are more likely to have a
normal resting ECG compared to patients with cardiac angina [11].
Pathophysiology of NCCP
Common causes of chest pain of esophageal origin are GORD, visceral hypersensitivity, and
esophageal dysmotility. Of these, GORD is the most common esophageal cause of NCCP.
Esophageal pH testing has demonstrated that about half of NCCP patients have abnormal
esophageal acid exposure [9,41]. It is unclear why esophageal acid exposure causes heartburn
in some patients and chest pain in others. Visceral hypersensitivity is a phenomenon in which
conscious perception of visceral stimuli is enhanced. Patients with NCCP, in comparison to
healthy control subjects, demonstrate higher pain sensation scores on exposure to a range of
esophageal stimuli including balloon distension, acid infusion, and electrical and thermal
stimulation [28,35].
Mechanisms proposed to be responsible for esophageal hypersensitivity in patients with NCCP
include sensitization of peripheral afferent nerves (peripheral sensitization) and sensitization of
spinal dorsal horn neurons (central sensitization [25]). Patients with motility disorders such as
symptomatic diffuse esophageal spasm and achalasia may experience retrosternal angina-like
pain, and 30% of NCCP patients have abnormal esophageal manometric findings [8,24]. The
relationship, however, between the manometric findings and the chest pain is complex. Patients
are generally asymptomatic at the time when the motility abnormalities are identified. Finally,
pharmacotherapy with motility-modifying drugs does not correlate with improvement of
symptoms [37]. Several studies report a high incidence of psychiatric diagnoses, such as panic
disorder, generalized anxiety disorder, depression, and somatization disorder, in patients with
NCCP [6,23].
Diagnostic Evaluation
Gastrointestinal work-up is aimed at demonstrating pathological gastroesophageal reflux,
hypersensitivity of the esophagus, or esophageal motor abnormalities.
Gastroesophageal reflux tests: (i) Proton pump inhibitors: Empirical PPI therapy (the "PPI test") is
recommended prior to any invasive testing to diagnose GORD-related NCCP. The onneprazole
doses used in the PPI test range from 40 mg to 80 mg daily over a duration of 7 to 28 days
[17,21]. If the symptom score improves by more than 50-75% relative to baseline, the test is
considered positive. In different studies, the sensitivity of the PPI test for GORD-related NCCP
ranges from 69% to 95%, and the specificity of the test ranges from 67% to 86% [18]. The PPI test
is a cost-saving approach that significantly reduces the number of invasive diagnostic tests. (ii) Re
flux monitoring: Esophageal pH monitoring demonstrates pathological GORD in up to 62% of
the patients with NCCP [9,32]. A group of patients may have normal acid exposure, but still have
a significant temporal relationship between reflux episodes and chest pain events. These patients
are considered to have an acid-hypersensitive esophagus [39]. (iii) Endoscopy: Gastrointestinal
endoscopy reveals reflux esophagitis in up to 31% of patients with noncardiac chest pain [43].
Endoscopy should be reserved for patients with NCCP and alarm symptoms including
dysphagia, odynophagia, weight loss, or anemia.
Esophageal sensitivity tests: (i) Acid perfusion tests: Hydrochloric acid, infused into the middle
third of the oesophagus, is able to induce chest pain. The acid infusion test is positive in 10-38%
of patients with NCCP [3,32]. The sensitivity and specificity for the acid perfusion test is 57% and
62%, respectively [20]. (ii) Balloon distension tests: A small balloon is placed in the lower
esophagus and inflated until patients report pain [351. Richter et al. and other investigators have
observed that balloon distension reproduces chest pain at lower volumes in patients with NCCP
than in controls [28,34]. The sensitivity of the test has been reported to vary between 5% and 50%
Esophageal motility tests: (i) High-resolution manometry (HRM) is the gold standard for
recognition and classification of esophageal motility disorders. A significant percentage (4864%) of patients with achalasia experience chest pain [12]. A recent study using HRM showed
that acid-sensitive NCCP patients have a distinct hypermotility pattern in the smooth muscle
portion of the esophagus [26]. (ii) Pharmacological provocative tests: Provocative tests with
edrophonium, ergonovine, bethanechol, and pentagastrin have been developed to identify
patients with NCCP of esophageal origin [38]. Overall, pharmacological provocative tests are
invasive, are associated with adverse events, are not standardized, have low diagnostic
sensitivity for NCCP, and fail to predict therapeutic outcome.
Treatment of NCCP
Treatment of noncardiac chest pain is challenging because of the heterogenous nature of the
disorder. (i) Acid suppression: Several open-label studies have demonstrated efficacy of acid
suppression with either PPIs or histamine H2-receptor antagonists following the first description
by DeMeester et al. in 1982 [9]. Since the first double-blind, placebo-controlled study of acid
suppression in NCCP by Achem et al. [1,5], similar controlled studies have consistently shown
efficacy of PPI treatment in NCCP. (ii) Smooth muscle relaxants: Nitrates, phosphodiesterase-5
inhibitors, anticholinergic drugs, and calcium channel brockers have been used in the treatment
of NCCP with dysmotility. Most studies included small numbers, and few were placebo
controlled, which prevents us from making any firm conclusions about the efficacy of these
agents. (iii) Tricyclic antidepressants (TCAs): A few clinical trials have evaluated the effect of TCAs
in NCCP. In a double-blind, placebo-controlled trial [4] in 60 patients, imipramine (50 mg)
significantly reduced chest pain episodes in 52% of patients. Prakash and Clouse [33]
demonstrated that 75% of NCCP patients experience symptomatic relief during long-term use of
TCAs for up to 3 years. (iv) Selective serotonin reuptake inhibitors: In a double-blind, controlled
study of sertraline versus placebo in 30 NCCP patients for 8 weeks, sertraline demonstrated a
significant reduction in pain score compared with placebo [42]. However, another study [40]
found no differences between paroxetine and placebo. (v) Serotonin-norepinephrine reuptake
inhibitors (SNRls): Recently, Lee et al. evaluated venlafaxine vs. placebo in a double-blind
controlled study in NCCP, reporting that 52% of patients experienced symptom improvement in
comparison to 4% of those taking a placebo [27]. (vi) Miscellaneous treatments: Symptomatic
improvement has been reported in NCCP patients taking adenosine intravenously as well as
orally. Small-scale studies have shown improvement with endoscopic injection of botulinum
toxin, cognitive-behavioral therapy, and hypnotherapy [22].
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Functional Abdominal Pain Syndrome
Clinical Problem
Functional abdominal pain syndrome (FAPS) is a state of chronic recurrent abdominal pain that
is not due to structural, organic, or metabolic diseases, as far as can be detected by current
routine clinical examinations [7]. Abdominal pain in FAPS is unrelated to provocation,
exaggeration, or relief by everyday physiological stimuli such as eating, exercise, defecation, or
menstruation [7]. FAPS is one of the functional gastrointestinal disorders (FGIDs) and is distinct
from other categories of FGIDs such as irritable bowel syndrome (IBS), unspecified functional
bowel disorder, epigastric pain syndrome in functional dyspepsia, functional chest pain of
presumed esophageal origin, functional gallbladder and sphincter of Oddi disorders, and
functional anorectal pain in adults [10]. Infant colic in neonates and toddlers, as well as IBS,
abdominal migraine, functional dyspepsia, and FAPS in children and adolescents, can also be
related to pain [10]. For instance, IBS is characterized by abdominal pain or discomfort that is
perceived as a weak sensation of abdominal pain and is characterized by more than two of the
following three conditions: relief by defecation, onset associated with changes in stool frequency,
and onset associated with changes in stool form [19]. Epigastric pain syndrome in functional
dyspepsia is defined by chronic pain or burning localized to the epigastrium of at least moderate
severity, at least once per week, and by intermittent pain, not generalized or localized to other
abdominal or chest regions, that is not relieved by defecation or passage of flatus and does not
fulfill the criteria for gallbladder or sphincter of Oddi disorders [25]. The gastrointestinal
symptoms of these pain-related FGIDs have different features. However, the basic mechanisms
of pain may not be mutually exclusive among these disorders.
Epidemiology and Social and Economic Impact
The reported prevalence of FAPS in North America ranges from 0.5% to 2% [9] and does not
differ from rates reported in other countries [8,15]. In contrast, the prevalence of IBS is
approximately 10-20%, that of functional dyspepsia is 20-30% [6], and that of functional
gallbladder and sphincter of Oddi disorders is 7.6-20.7% [3]. Therefore, FAPS is a less common
FGID than IBS, functional dyspepsia, or functional gallbladder and sphincter of Oddi disorders
[7]. However, the prevalence of FAPS is still greater than that of ulcerative colitis (0.0076%) [18]
or chronic pancreatitis (0.0041%) [27], which represent nonmalignant organic diseases that
usually cause chronic abdominal pain. FAPS is more common in women, with a female : male
ratio of 3:2, with prevalence peaking in the fourth decade of life [4,11]. Patients with FAPS have
high work absenteeism and health care utilization, and thus the syndrome imposes a significant
economic burden [11,22].
Clinical Characteristics
The primary feature of FAPS is abdominal pain. However, many diseases can cause chronic abdominal
pain. Therefore, any structural, organic, or chemical disease should be excluded. Patients with FAPS often
have pain-related behaviors [7]. First, they often deny a role for psychosocial stressors. However, pain may
diminish when patients are engaged in distracting activities but increase when they are discussing a
psychologically distressing issue. Second, they express pain through verbal and nonverbal methods. They
urgently report intense symptoms disproportionate to the available clinical and laboratory data. Third,
they seek health care frequently. They often visit the emergency room and request opioid analgesics.
Fourth, they request diagnostic studies or even exploratory surgery to determine the organic origin of their
condition. Fifth, they focus attention on complete relief of pain rather than on adapting to having a
disease. Sixth, they take on limited personal responsibility for self-management. In addition to these
features, distinct psychopathologies are usually found in patients with FAPS, including depressive
disorders, anxiety disorders, and somatoform disorders (axis-I disorders in the Diagnostic and Statistical
Manual of Mental Disorders [1]). Some forms of personality disorders categorized as axis-II disorders may
also be identified. As is the case for other chronic pain conditions, some patients with FAPS may have
catastrophizing thoughts [7] or a history of early life trauma, including physical or sexual abuse [24].
Pathophysiology
The precise etiology and pathophysiology of FAPS are poorly understood. However, brain-gut interactions
play a crucial role in most of the pain-related FGIDs, especially IBS [14,20,21]. Among IBS patients, a
subgroup with severe symptoms have a pathophysiological similarity to patients with FAPS [24].
Physiologically, signals originating from the gastrointestinal tract are conducted to the brain via visceral
afferent pathways, which are mainly classified into parasympathetic afferent and sympathetic afferent
fibers [14,21]. Parasympathetic afferent fibers within the vagus nerve end at the nucleus of the solitary
tract, which also sends signals to the various corticolimbic structures [20]. Sympathetic afferent fibers
converge into the dorsal root ganglia and are connected to secondary sensory neurons in lamina I of the
dorsal horn of the spinal cord. This visceral afferent signal ascends to the spinothalamic tract and relays
the stimuli to the thalamus. The signal then spreads to the insula, cingulate cortex, and the other structures
of the pain neuromatrix. The lamina I neurons also send signals to the limbic system and paralimbic
sensorimotor cortex (including the amygdala and hypothalamus) via the parabrachial nucleus [14].
Therefore, visceral pain signals are directly related to homeostatic regulation, which is mediated by
corticotropin-releasing hormone (CRH) [13]. For instance, activation of the CRH-expressing neurons in the
paraventricular nucleus of the hypothalamus stimulates colonic motility via sacral parasympathetic
outflow [13]. Unlike in IBS, there are no brain-imaging studies of FAPS. However, the fact that abdominal
pain in FAPS is unrelated to physiological events strongly suggests sensitization or associative learning of
the pain-related area of the brain rather than peripheral sensitization. In fact, FAPS patients have
hyposensitivity to non-noxious physiological rectal distension by barostat [23]. Descending pain
modulation systems (opioidergic and noradrenergic pathways) originate in distinct brainstem regions and
are activated automatically in a reflex-like fashion in response to a noxious stimulus [7]. Tonic descending
pain modulation systems originate from serotonergic nuclei in the brainstem and play a role in the central
control of baseline spinal cord excitability [7]. Together with descending pain modulation systems of the
periaqueductal gray, cortical networks on pain modulation circuits (including the insula, amygdala,
anterior cingulate cortex, orbitofrontal cortex, medial and dorsolateral prefrontal cortex, and parietal
cortex) are suggested to be involved in the pathophysiology of FAPS. In patients with chronic back pain, a
decreased volume of gray matter of the whole brain was related to pain duration, and the decrease was
prominent in the bilateral dorsolateral prefrontal cortex [2]. A strong negative correlation was identified
between the thickness of the right dorsolateral prefrontal cortex and ratings on a pain catastrophizing
scale in IBS patients [5]. Thus, functional and structural changes in the brain may underlie the
pathophysiology of FAPS.
Diagnostic Evaluation
The present diagnosis of FAPS is based on the Rome III criteria [10]. Diagnostic criteria for FAPS must
include all of the following: (a) continuous or nearly continuous abdominal pain, (b) no or only an
occasional relationship of pain with physiological events (e.g., eating, defecation, or menses), (c) some
loss of daily functioning, (d) an indication that the pain is not feigned (e.g., malingering), (e) insufficient
symptoms to meet criteria for another FGID that would explain the pain, and (f) criteria fulfilled for the last
3 months with symptom onset at least 6 months prior to diagnosis [7]. Moreover, any structural, organic, or
chemical diseases should be excluded. Differential diagnosis should include malignant neoplasm of the
gastrointestinal tract, biliary tract, pancreas, and liver; ulcerative colitis; Crohn's disease; peptic ulcer;
ulcer of the small intestine; stenosis of the gastrointestinal tract; colonic diverticulitis; ischemic colitis;
cholelithiasis; cholangitis; cholecystitis; pancreatitis; chronic intestinal pseudo-obstruction; megacolon;
colonic inertia; food allergy; allergic or eosinophilic gastroenteritis; parasites; arteriosclerosis in the
abdomen; aortic aneurysm; peritonitis; Fitz-Hugh-Curtis syndrome; Henoch-Schoenlein purpura;
porphyria; endocrine, metabolic, or hematological diseases; collagen diseases; abdominal wall pain;
gynecological and urological diseases; and so on. A precise medical interview and careful physical
examination can greatly contribute to an accurate diagnosis, but urinalysis, fecal examination, complete
blood count, blood chemistry, abdominal ultrasonography, and plain X-ray film of the abdomen are
routinely examined. Upper- gastrointestinal endoscopy, an upper-gastrointestinal series, colonoscopy,
barium enema, capsule endoscopy, small- intestinal endoscopy, barium fluoroscopy of the small intestine,
abdominal computed tomography, abdominal magnetic resonance imaging, endoscopic retrograde
cholangiopancreatography, abdominal angiography, and gastrointestinal manometry and/or barostat
may also be examined, depending on the clinical situation.
Treatment
A cure is not possible, so in caring for patients with FAPS, the aims of treatment are to reduce suffering and
improve the quality of life [24]. Treatment relies on a biopsychosocial approach with a therapeutic patientphysician partnership at its base [10]. Pharmacotherapy for FAPS is centered on antidepressants [7,24].
Tricyclic antidepressants (amitriptyline, imipramine, or desipramine), tetracyclic antidepressants
(mianserin), selective serotonin reuptake inhibitors (fluoxetine, paroxetine, fluvoxamine, sertraline, or
escitalopram), serotonin-norepinephrine reuptake inhibitors (duloxetine, milnacipran, or venlafaxine),
and a noradrenergic and specific serotonergic antidepressant (mirtazapine) are used on the basis of our
understanding of the neurotransmission of visceral pain [7,24]. Antipsychotics (e.g., quetiapine) are
sometimes prescribed [24]. Antidepressants suppress the activities of the pain matrix, facilitate descending
pain modulation systems, and possibly help neurogenesis via brain-derived neurotrophic factor [7,24]. In
a systematic review in children and adolescents with pain-related FGIDs, however, 59% of participants
reported feeling better in the amitriptyline group compared with 53% in the placebo group (relative risk:
1.12; 95% confidence interval: 0.77 to 1.63), which was not a significant difference [17]. Psychotherapy is
a reasonable approach for FAPS patients [7,24]. Especially in children with IBS or FAPS, hypnotherapy has
proven to be highly superior, with a greater reduction in pain scores compared with standard medical
treatment [26]. Moreover, a 1-year follow-up found that treatment was successful in 85% of the
hypnotherapy group and only 25% of the standard medical treatment group. A systematic review also
supports evidence that cognitive-behavioral therapy may be a useful intervention for children with
recurrent abdominal pain [16]. Finally, if patients with FAPS have narcotic bowel syndrome due to a
paradoxical increase in abdominal pain associated with continued or escalating dosages of opioids,
detoxification treatment is beneficial for patients [12].
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of Oddi disorders. Gastroenterology 2006;130:1498-509.
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abdominal pain syndrome. Gastroenterology 2006; 130: 1492-7.
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and long-term outcome. Clin Gastroenterol Hepatol 2004; 2: 395-9.
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2006; 130:1377-90.
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Funch-Jensen P, Corazziari E. U.S. householder survey of functional gastrointestinal disorders.
Prevalence, sociodemography, and health impact. Dig Dis Sci 1993;38:1569-80.
• Drossman DA, Morris CB, Edwards H, Wrennall CE, Weinland SR, Aderoju AO, Kulkarni-Kelapure RR,
Hu YJ, Dalton C, Bouma MH, Zimmerman J, Rooker C, Leserman J, Bangdiwala SI. Diagnosis,
characterization, and 3-month outcome after detoxification of 39 patients with narcotic bowel
syndrome. Am J Gastroenterol 2012; Epub ahead of print.
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Physiology of the gastrointestinal tract. Oxford: Academic Press; 2012. p. 791-816.
• Fukudo S, Kanazawa M. Gene, environment, and brain-gut interactions in irritable bowel syndrome. J
Gastroenterol Hepatol 2011;26(Suppl 3):110-5.
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validity and costs. Dig Dis Sci 1994;39:1935-41.
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abdominal pain (RAP) and irritable bowel syndrome (IBS) in childhood. Cochrane Database Syst Rev
2008;1:CD003014.
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abdominal pain-related functional gastrointestinal disorders in children and adolescents. Cochrane
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in Olmsted County, Minnesota, 1940-1993:incidence, prevalence, and survival. Gut 2000;46:336-43.
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disorders. Gastroenterology 2006;130:1480-91.
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treatment of functional GI disorders. Gastroenterology 2006;131:1925-42.
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abdominal pain. Br J Med Econ 1992;2:75-9.
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:122 -7.
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with functional abdominal pain or irritable bowel syndrome: a randomized controlled trial.
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Anterior Approach Coeliac Plexus Block
Sukdev Nayak, MD, LLB, PGDM, DPM
Director, AH Regional Cancer Centre, Cuttack
Prof & HOD, Deptt of Anaesthesiology, Pain Relief & Palliative Care,
History of Neurolytic Pain Relief:
Nerve destruction using chemicals to promote analgesia had been extensively used in the early
part of the 20th century for management of pain. With the advent of newer analgesics and the
development of safer techniques for pain management, its use has markedly diminished.
However, recent neurodestructive techniques for pain management such as cryoablation,
neurosurgical procedures and the use of radiofrequency lesioning resulted in a surge of interest
in this method of pain relief. However clear cut guidelines for indications, report of long term
outcome, and uniformity in techniques for this type of therapeutic modality are yet to be
standardised. These procedures are available as part of the management option for chronic
pain mainly on the expertise of the pain specialist and the felt need of a selected group of
patients.
Severe chronic abdominal pain including cancer pain may be due to advanced cancers,
especially from tumours originating from upper abdominal viscera such as pancreas, stomach,
duodenum, proximal bowel, liver and biliary tract, compressing enlarged lymph nodes or
chronic pancreatitis. Neurolytic procedure is one of the options when the pain is not relieved by
routine medications or other conservative measures. The initial diagnostic local anaesthetic
block is followed by neurolysis with agents like 50% alcohol or 6% Phenol, giving long-term relief
for 3 months or more. CP block may also be effectively performed for pain relief in patients with
chronic pancreatitis although with less effectiveness. Some authors adopt this procedure for
relief of acute post operative pain as well, using long acting local anaesthetic during surgery.
Anatomy of celiac plexus:
The Celiac Plexus (CP), referred as Plexus Cœliacus or Solar Plexus (Figs. ***) is the largest of the
three visceral sympathetic plexuses in the human body. It is located bilaterally, deep in the
retroperitoneum, over the anterolateral surface of the aorta and just caudal to the origin of the
celiac trunk at the level of T12 –L1 interspaces. It surrounds the celiac artery and the root of the
superior mesenteric artery. It lies behind the stomach & the omental bursa, in front of the crura of
the diaphragm ; the commencement of the abdominal aorta and between the suprarenal
glands. These are two large irregularly shaped masses having the appearance of lymph glands
and are placed one on either side of the middle line in front of the crura of the diaphragm close
to the suprarenal glands, that on the right side being placed behind the inferior vena cava. The
plexus and the ganglia receive the greater and lesser splanchnic nerves of both sides and some
filaments from the right vagus; and give off numerous secondary plexuses along the
neighbouring arteries. The lower part, which is segmented off and named the aortico-renal
ganglion; receives the lesser splanchnic nerve and gives off the greater part of the renal plexus.
The CP serves as the main junction and a relay centre for autonomic nerves and nociceptive
impulses from the upper abdominal viscera i.e. liver, gall bladder, spleen, stomach, pancreas,
kidneys, small bowel, and 2/3 of the large bowel. CP neurolysis, with agents such as ethanol, is
an effective means of diminishing pain that arises from these structures. The sympathetic supply
of CP consists of Greater splanchnic nerve (T5/6 to T9/10), lesser splanchnic nerve (T10/11) and
least splanchnic nerve (T11/12). The upper abdominal organs receive their parasympathetic
supply from the left and right vagal trunks, which pass through the coeliac plexus but do not
connect there.
Image Guidance:
Initially CP blocks were performed without imaging guidance. It was reported later that much
higher success and lower complication rates of CP block can be achieved under imaging
guidance. Hence X-Ray, Ultrasound, fluoroscopy, angiography and Computed tomography
(CT) is now widely used to locate the exact level of the coeliac artery origin.
The use of multidetector CT for imaging guidance has superseded other modalities and allows
direct visualization of the spread of the neurolytic agent in the antecrural space ( Avinash et al ).
Accurate depiction of the retroperitoneal anatomy and the position of the needle tip help avoid
crucial anatomic structures such as the pancreas, aorta, celiac artery, and superior mesenteric
artery. Proper patient education, meticulous pre-procedure planning & counselling, use of
optimal multidetector CT techniques, adjunctive CT manoeuvres, and post-procedure care are
integral to successful celiac plexus neurolysis. Celiac plexus neurolysis does not completely
abolish pain; rather, it diminishes pain, helping to reduce opioid requirements & their related
side effects and improving survival in patients with upper abdominal malignancy.
Technique:
Both anterior and posterior approaches under CT guidance may be employed, depending on
the operator’s preferences. The major advantage of the anterior approach, the preferred
method of the author, is the reduced risk of neurologic complications because the tip of the
needle is anterior to the spinal arteries and spinal canal. Other advantages of anterior approach
are single puncture resulting in less discomfort to the patients, reduced procedure time and use
of a smaller volume of neurolytic agent. It also avoids puncture of the aorta and permits the
patients to remain supine during the whole procedure, thus avoiding the pain due to the prone
position with a mass in the abdomen. The CP block is performed by some authors under
intravenous sedation, but local anaesthetic infiltration of the superficial layers is mandatory to
reduce procedural pain.
Intravenous fluids are required pre-block to reduce the risk of hypotension after the procedure.
Some authors take two needle insertions, one on each side to block both of the coeliac ganglia,
but commonly good spread to both sides is achieved just using one needle. In case the spread is
unilateral, the needle is partly withdrawn, manipulated and repositioned on the other side,
without coming out of the percutaneous puncture, thus avoiding the pain of two pricks. The
needle entry point is just below the tip of the 12th rib, and using X-ray screening in two planes, the
needle is advanced until it is in front of the aorta.
Once in place, a test dose of dye is used to confirm that the injected medication will spread in an
appropriate area. If this is okay, the injection is given gradually over several minutes and
aspirating after every two ml of the neurolytic agent. This ensures that the needle has not
advanced inadvertently, to the aorta or any other vessels during the procedure. The physician
uses the image guidance to evaluate the spread of the injected neurolytic agent.
20 to 30ml of ethanol in concentrations of 50–100% is the most commonly used neurolytic agent
in clinical practice, but many centres use 6% Phenol. Ethanol or Phenol as nerve destructive
agents and bupivacaine or lidocaines as local anesthetics have been used for CP block in cancer
patients. Depot preparation of steroid is used in non-malignant cases.
The degree of pain relief should be evaluated by using subjective and objective criteria. All
patients should be interviewed before the procedure to obtain a baseline pain score for
subjective criteria. Visual analogue scale (range: 0–10) with “0” corresponding no pain and
“10” corresponding the worst pain may be used. Numbers and doses of pain medication are
taken as objective criteria. Patients should be hydrated with normal saline for the risk of
hypotension during or after the procedure.
Immediate effects:
Immediately after the injection, there is a feeling of warmth and awkwardness in abdomen, due
to parasympathetic overacivity. In addition, the abdominal pain may be gone or quite less with
temporary weakness or numbness in the abdominal wall or leg, although this is actually not a
desired effect of a CP block.
After the procedure is completed, bed rest is recommended for 12 hours, with hourly monitoring
of blood pressure, heart rate, and vital signs. Intravenous fluid is recommended pre- and postprocedure because of the risk of hypotension.
Neurolysis does not usually provide complete pain relief but helps to reduce the requirement for
opioid analgesics and improves the patient’s quality of life. Pain relief is long-lasting in 70-90%
of patients who undergo CP neurolysis and the procedure may extend life by enhancing patients’
ability to eat and perform day-to-day activities; by lowering the incidence of drug-related
adverse effects.
Figure of coeliac plexus block technique:
The needle is withdrawn slightly and then redirected forwards until it is in the area of the coeliac
plexus, avoiding the aorta and inferior vena cava. Radio-opaque dye is injected to confirm the
correct placement of the needle, and then the appropriate mixture is injected:
• For non-malignant pain: 10 ml 0.5% bupivacaine on each side
• For malignant pain: 10 ml 6% aqueous phenol + 5 ml 0.5% bupivacaine on each side.
As the block causes dilatation of the upper abdominal vessels, venous pooling can occur,
leading to hypotension. This can be exacerbated by pre-existing dehydration, hence the need for
IV hydration before performing the block.
Complications:
• Neurological complications, vascular injury, or chemical peritonitis (Rare)
• Orthostatic hypotension - may be detected less commonly due to loss of sympathetic
tone and dilated abdominal vasculature. It is usually transient (few hours) and can be manaed with IV hydration. Severe hypotension has been reported even after unilateral block.
• Bleeding due to aorta or inferior vena cava injury by the needle.
• Intravascular injection (should be prevented by checking the needle position with radioopaque dye).
• Upper abdominal organ puncture with abscess/cyst formation.
• Paraplegia from injecting phenol into the arteries that supply the spinal cord (prevented by
checking the needle position with radio-opaque dye).
• Sexual dysfunction (injected solution spreads to the sympathetic chain bilaterally).
• Intramuscular injection into the psoas muscle.
• Lumbar nerve root irritation (injected solution tracks backwards towards the lumbar plexus).
• Paraplegia
• loss of anal and bladder sphincter function
• Transient pain from the procedure and diarrhoea. Transient pain from the procedure Local
posterior abdominal and back pain during or immediately after a CP block has been reporrted; commonly because of the ablative effect of the neurolytic agent .
• Diarrhoea is another common self-limiting complication and occurs due to sympathetic
blockade and unopposed parasympathetic efferent influence after the block; and usually resolves over approximately 48 hours.
• Neurologic complications (e.g. paraplegia, leg weakness, sensory deficits, and paresthesias)
have been reported rarely.
• Paraplegia is attributed to either direct injury of the spinal cord during the procedure or to
injection into the anterior spinal artery, which supplies the lower two thirds of the spinal cord.
• Puncture complications include injury to liver, stomach, pancreas and bowel but are rare.
• Other rare complications include impotence, gastroparesis, superior mesenteric vein thrombosis, chylothorax,pneumothorax, chemical peritonitis, aortic pseudoaneurysm, aortic dissection, haemorrhage and retroperitoneal fibrosis.
Contraindications:
1. Bleeding and infection risks.
2. Where the source of the pain is no longer being transmitted through the autonomic
nerves.
3. It is dangerous to perform the block in the presence of a large aortic aneurysm.
4. allergic to any of the medications to be injected,
5. Patients on blood thinning medications,
6. Active infection and poorly controlled diabetes or heart disease,
7. Should not have the injection or at least consider postponing to improve the overall general medical condition.
Conclusion:
Interventional pain management has taken a front seat in patient care. Old methods are
modified and polished, and new techniques are being developed to produce effective prolonged
analgesia for chronic pain syndromes. Neurolysis, or destruction of nerves either by the
application of chemicals, heat, cold, or surgical disruption gain renewed interest and are now
commonly used as one of our armamentarium in the management of previously recalcitrant
chronic pain conditions. However, these techniques require specialized training, in depth
knowledge of neural anatomy and understanding of chronic pain physiology. Their application
should be reserved only in painful conditions where conventional conservative management
fails.
References:
• Akhan O, Ozmen MN, Basgun N, et al. "Long-term results of celiac ganglia block:correlation of grade of tumoral invasion and pain relief." Am J Roentgenol 2004;182:891–6.
• Avinash Kambadakone, Ashraf Thabet, Debra A. Gervais, Peter R. Mueller, Ronald S.
Arellano, 2011 , CT-guided Celiac Plexus Neurolysis: A Review of Anatomy, Indications,
Technique, and Tips for Successful Treatment, RadioGraphics,31, 1599-1621.
• Caraceni A, Portenoy KR. "Pain management in patients with pancreatic carcinoma."
Cancer 1996;78:639–53.
• D D Davies, 1993, Incidence of major complications of neurolytic coeliac plexus block.J R
Soc Med. May; 86(5): 264–266.
• Davies DD. "Incidence of major complications of neurolytic celiac plexus block." J R Soc
Med 1993;86:264–6.
• Devrim Akinci, Okan Akhan."Celiac ganglia block." European Journal of Radiology 55
(2005) 355–361
• Gimenez A, Martinez-Noguera A, Donoso L, Catala E, Serra R. "Percutaneous neurolysis
of the celiac plexus via the anterior approach with sonographic guidance." Am J
Roentgenol 1993;161:1061–3.
• Janet C Miller, 2012, Radiology Rounds, Masachusetts general Hosptital, Deptt of
Radiology, 10 1http://www.mghradrounds.org/index.php?src=gendocs&ref=2012_
january
• Lee MJ, Mueller PR, van Sonnenberg E, et al. "CT-guided celiac ganglion block with
alcohol." Am J Roentgenol 1993;161:633–6.
• Romanelli DF, Beckmann CF, Heiss WF. "Celiac plexus block: efficacy and safety of the
anterior approach." Am J Roentgenol 1993;160:497–500.
• Whiteman M, Rosenberg, Haskin P, Teplick S. "Celiac plexus block for interventional
radiology." Radiology 1986;161:831–6.
• www.dcmsonline.org/jax-medicine/1998journals/.../neurolytic.htm
STELLATE GANGLION BLOCK
Dr. Subrata Goswami
Medical Officer and In-charge of
The Pain Management Unit
Sealdah ESI Hospital,
Department of Labour, Government of West Bengal
The stellate ganglion block was made popular by Selheim and Kappis (1), Brumm and Mandl (2)
in the early 19th century. White (3) from USA and Leriche and Fontaine (4) from Europe futher
confirmed the fairly predictable results and techniques.
Preganglionic sympathetic fibres destined for head and neck originate from the cell bodies of
intermedio-lateral and intermedio-medial horn cells (5) at 1st and 2nd thoracic spinal cord
segments whereas preganglionic fibres for upper extremity originates at T2 – T8 and
occasionally T9 segments.The preganglionic cholinergic sympathetic B fibres coming out along
the somatic motor Aα fibres (6); reaching the intervertebral foramen, the preganglionic
sympathetic fibres leave the motor root as white rami communicans to enter sympathetic
ganglion near the antero -lateral aspect of the respective thoracic vertebral bodies.
Some post ganglionic cholinergic C fibres leave the sympathetic ganglion to join the motor root
again as gay rami and travel with those spinal segmental nerves to reach the blood vessels of the
muscles, sweat glands and piloerector muscles of the skin. But most of the preganglionic fibres
for head and neck do not relay in the thoracic segmental sympathetic ganglion and rather
ascend up along the sympathetic chain to relay in inferior, middle and superior cervical
ganglion. From those ganglions post ganglionic adrenergic C fibres form plexus around the
nearby blood vessels e.g. vertebral, carotid, subclavian etc to reach the destinations. Plexus
around vertebral artery from stellate reach intracranially as far as posterior cerebellar artery,
where it meets the plexus from internal carotid artery (Lazorthes 1949, Mitchell 1952) (7) (8).
Few post ganglionic cholinergic C fibres join the cervical segmental nerves as gray rami
communicans to reach the blood vesels of muscles, and skin. The inferior cervical ganglion often
fuse with the 1st thoracic ganglion approximately in 80% cases (Jit & Mukherjee,1960) (9),
resembling a star shaped appearance, hence the cervicothoracic ganglion popularly called as
the “stellate ganglion”, situated at the anterolateral aspect of body of the C7, T1, space in
between and in front of the neck of the first rib.
The stellate ganglion is about 2.5 cm long, 1 cm wide and 0.5 cm thick (10). The boundary of the
ganglion may be described as : medially- longus coli muscle, laterally- scalene muscles,
anteriorly- subclavian artery, posteriorly transverse process and prevertebral fascia and
inferiorly posterior aspect of pleura. Other important relations are :- a) vertebral artery , passes
anteriorly after arising from subclavian artery which ascends through he vertebral foramen in the
transverse process of C6 and thus lies posterior to C6 tubercle (Chassaignac’s tubercle).b)
phrenic nerve( C3,4,5) laterally and c) recurrent laryngeal nerve lies anterolmedial to the stellate
ganglion d) costocervical trunk branches near the inferior pole (10).
Post ganglionic fibres from the stellate ganglion supplies different parts of head & neck both via
the plexus around blood vessels and as gray rami of C7, C8, T1, and also sometimes C5 & C6 to
travel along brachial plexus. Blocking the stellate ganglion at this location also blocks the
preganglionic fibres of middle (C5,6) and superior ganglion (C1,-4) , thus blocking the
sympathetic conduction for the whole head-neck and the upper extremities.
However, only blockade of stellate at this level, can not block also the Kuntz’s fibres i.e., post
ganglionic sympathetic fibres from T2 and T3, hence T2 & T3 sympathetic ganglions are to be
blocked for getting predictable successful results.
Pic 1. Raynaud’s phenomenon
Pic 2. SGB at C6 anterior approach
Stellate ganglion block (SGB) using local anaesthetics has
been used mainly as diagnostic
and repeated blocks for short term therapeutic benefits to manage - complex regional pain
syndromes, vascular insufficiencies of head, neck, upper extremities and upper thoracic
dermatomes.
Pic 3. Phantom Limb Pain
Pic 4. Advanced Ca breast, continuous SGB
Pain due to herpes zoster, post herpetic neuralgia, cancer pain, phantom limb pains, atypical
facial pains, vasculopathy associated with miniere syndrome, vasospasm, arterial embolism are
also indications of SGB. It can be used also in post traumatic syndromes associated with swelling,
cold sweats and cyanosis. Frost bite of nose, face or digits of upper extremities can also be
managed effectively with SGB.(11) Chest pain from angina pectoris is another indication too.
SGB has also diagnostic, prognostic and prophylactic value prior to vascular surgery of upper
linb.
Hyperhydrosis of face and upper extremeties can be managed adequately with SGB. Pulmonary
embolism is the only indication for bilateral stellate ganglion block otherwise only one side is
adviced for fear of life threatening complications e.g.
bilateral pneumothorax, phrenic or recurrent laryngeal
nerve palsy!
Horner’s syndrome (“miosis, enopthalmos & ptosis”
alongwith facial anhydration, nasal congestion and
conjunctival injection) due to unopposed
parasympathetic activity are frequently observed with
SGB. Ptosis due to permanent horner’s syndrome after
neurolytic block can be managed with surgical
suspension of the upper eye lid.
Pic 5.Horner's Syndrome after SGB
Anterior blind approach at C6 tubercle (retracting the
carotid vessels laterally with with index finger of non dominant hand during injection) is a very
popular technique for years. A large amount (6-12 ml usually) local anaesthetic solution can
bathe even the upper thoracic ganglions and thus resulting very effective short duration blocks.
Serious complication like vertebral artery puncture are not common with this anterior approach
as vertebral artery lies posterior to C6 tubercle.
Right sided SGB had minimal effects on systemic blood pressure or heart rate, where as it did
increase QT interval, QTc interval and QTcD after head up tilt. These changes did not occur after
left sided SGB- hence right sided SGB associated with potentially increased risk of ventricular
disrythmias and cardiac events in distinction to the absence of these findings after left sided SGB.
Neurolytic blockade has been done eith CRPS when diagnostic block has been given short term
relief. However, permanent complications like- horner's syndrome, brachial plexus block (12) ,
hoarseness (13), epidural or subarachnoid spread , spinal cord infarct – made nurolysis with
alcohol or phenol less popular.
Radiofreequency lesioning with 5 mm 20 G curved blunt tipped canula using conventional RF
(80 degrees / 60 secs) at 3 locations after a sensory (50 Hz/ 0.9 V) and motor (2Hz/2V)
stimulation trial near the junction of transverse process and vertebral body of C7 vertebra (14)
under fluoroscopic /CT- guidance and confirmation
of the needle placement with non- ionic radio
opaque iodinated and low osmolar contrast media
like iohexol 300 mg/ml rapidly gaining popularity
due to least side effects and longer relief.
Pic 6. Satisfactory spread of contrast before SGB
RF lesioning of T2 & T3 sympathetic ganglion is
replacing thoracoscopic thermocoagulation at this
level as relatively less invasive procedure and also
fairly predictable good results particularly for the
upper limbs and upper chest wall.
Anticoagulant therapy (fear of life threatening retropharyngeal/cervico-mediastinal hematoma)
(15), pneumonectomy on the contralateral side( fear of pneumothorax in the healthy side also)
(16) and recent myocardial infarction (fear of suppression of fascilitatory sympathetic drives)
are absolute while glaucoma and AV blocks are relative contraindications of SGB.
Efficacy of a successful block is assessed by visible engorgement of veins of forearm and hands
and diminution of psycho-galvanic reflex, plethysmographic and thermographic changes of the
upper extremity.
References :
• Kappis M: Weitere Erfahrungen mit der Sympathektomie./ Kim Wehr 2:1441,1923
• Brumm F,Mandl F: Die paravertebrale Injektion zur Bekaempfung visceraler Schmerzen.Wien
Klin Aschsch 37:511,1924
• White J C, Sweet W: Pain : Its mechanisms and neurosurgical treatment, Springfield, IL,
Charles C.Thomas,1955.
• Leriche R: / La Chirugie de la Douleur. Paris, Masson et Cie,1949
• Gray / Nervous system, P - 1298, Gray’s Anatomy / 38th Edn, ELBS with Churchill
Livingstone , 1995
• Excitable tissue: Nerve, Page 61,/ Review of Medical Physiology, W. F. Gannong, Mc graw
Hill, 22nd Edn, 2005
• Gray / Nervous system, P - 1303, Gray’s Anatomy / 38th Edn, ELBS with Churchill
Livingstone , 1995
• Bonica JJ , editor: The management of pain, Philadelphia, Lea & Febiger, 1953
• Gray / Nervous system, P - 1298, Gray’s Anatomy / 38th Edn, ELBS with Churchill
Livingstone , 1995
• Gray / Nervous system, P - 1298, Gray’s Anatomy / 38th Edn, ELBS with Churchill
Livingstone , 1995
• Raj’s Practical management of pain, 4th edition, page 866, / Mosby, Elsevier, 2008
• Abdi S, Zhou, Y, Doshi R, et al: stellate ganglion block: emphasis on the new oblique
fluoroscopic approach, / Tech Regional anaesth pain Management 9:73-80, 2005
• Sluijter ME: Radiofreequency Lesions in the treatment of Cervical Pain syndromes: Burlington,
MA, Radionics,1990, pp 1-19
• Racz G: Techniques of Neurolysis. Boston, Kluwer Academic,1989
• Okuda Y, Urabe K, Kitazima T: Retropharyngeal or cervicomediastinal hematomas following
stellate ganglion block./ Eur J Anaesthesiol 20:757-759, 2003
• P. Prithvi Raj et al, Sympathetic blocks of head and neck, page 115, Interventional Pain
Management, Image guided procedures, 2nd Edition, Sauders, Elsevier2008
• Fujii K, Yamaguchi S, Egawa H, et al: Effects of head up tilt after stillate ganglion block on QT
interval and QT dispersion.Reg Anaesth Pain Medicine 2004, 29: 317-322.
Indian Society for Study of Pain
West Bengal Branch
Informed Consent Form
Interventional Pain Management Procedure
Clinic : ........................................................................................................................
Procedure Prescribed : .................................................................................................
Patient’s Name : ............................................................ Age : .............. Sex : .............
Patient’s Address : .......................................................................................................
...................................................................................... Phone no : ...........................
Pain Specialist : .............................................................. Phone no : ...........................
Know Your Procedure
You are about to undergo an invasive procedure for the purpose of diagnosis and/or
treatment of persistent pain. The procedure we are recommending requires placement of
needles into the body and injections of medicines, anesthetics and/or chemicals into the
body. In addition, if you are undergoing a nerve destruction procedure such as radio
frequency nerve ablation or chemical neuroablation, nerve-destroying heat current and/or
nerve-destroying chemicals may be delivered to your body. We believe that the procedure
you are about to receive will help you to become more pain free. However, there is no
guarantee that the procedure will relieve your pain and there is a possibility that your pain
may be the same or worse afterward. Persistent pain is often very difficult to diagnose and
treat, and we can only use our best judgment and medical expertise to recommend and
perform interventions that we hope will help you. As with most interventions in medicine,
there is considerable risk to invasive pain therapies.
Although uncommon, complications can occur with any pain management procedure. All
procedures have risks of allergic reactions to the antibiotics used, steroids, or other injection
agents. Steroids cause temporary water gain, increase in blood pressure, and less control
over diabetes, emotional lability. In general, risks include but are not limited to the
following: bleeding, infection, damage to nerves or spinal cord, damage to blood vessels or
other body tissues, toxic or allergic reactions to medications or chemicals injected,
accidental injection into the blood vessels or spinal fluid, paralysis. Any interventional
procedure, although rarely, can lead to permanent neurologic impairment, and emergent
surgery to correct a problem that arises from the procedure. An extreme unfortunate (and
extremely rare too) outcome is death.
Risks associated with different clusters of procedures are as follows:
Class I: Sacroiliac and medial branch facet blocks, low back trigger point injections, caudal
epidural steroid injections, prolotherapy
Risks associated: Bleeding, infection, nerve injury, steroid effects, increased pain
Class II Intra-articular facet injections, mid and upper back trigger point injections, neck
trigger point injections, intercostal (rib) blocks, piriformis muscle and neck muscle blocks,
peripheral nerve blocks, lumbar transforaminal or interlaminar
epidural steroid
injections,peripheral nerve cryoneurolysis, radiofrequency and laser peripheral nerve
denervations, lumbar sympathetic block.
Risks associated: Class I risks (bleeding, infection, nerve injury, steroid effects,
increased pain) plus local anesthetic toxicity, pneumothorax (punctured lung), bowel
perforation and abscess (lumbar sympathetic block), epidural abscess or blood clot or
extremely rare paralysis (epidural injections)
Class III: Discogram (discography), interscalene and stellate ganglion blocks, celiac plexus
blocks, supraclavicular blocks, intercostal cryoneurolysis, spinal cord stimulator
implantation, intrathecal infusion pump implantation, intradiscal electrothermal
annuloplasty, coblation nucleoplasty, dekompressor, cervical transforaminal steroid
injections, hypogastric plexus block
Risks associated: Class I risks (bleeding, infection, nerve injury, steroid effects, increased
pain) plus hoarseness, paralysis of vocal cords, abdominal or neck infection,
pneumothorax or bleeding into lungs, meningitis, disciitis (infection of the disc),
paralysis or stroke (cervical transforaminal epidural steroid injection)
Class IV: Vertebroplasty, kyphoplasty, laser endoscopic discectomy, selective endoscopic
discectomy, epiduroscopy, peridural adhesiolysis (Racz procedure), cervical discectomy,
thoracic discectomy.
Risks associated: Class I risks (bleeding, infection, nerve injury, steroid effects, increased
pain) plus dysesthesia (uncomfortable or painful radiation down arm or leg),
pneumothorax, hoarseness, difficulty in swallowing, tear of the dural sac requiring
further surgery, weakness, vertebral infection, embolization of cement to lungs or spine
(vertebroplasty/kyphoplasty), paralysis
Special Notes : ............................................................................................................
Please ask any questions you may have prior to signing this consent.
Physician’s Signature : ......................................................... Date : ...............................
Informed Consent
I have been told and explained in detail, the purpose and steps of and the risks involved with
the procedure to be undertaken on me. I understand the medical necessity of the procedure
and the potential risks associated with it as well as the possible benefits. All my questions in
regard to the procedure, are answered to my satisfaction.
I accept the risks and consent to procedure.
Patient’s Signature: ......................................................................... Date: ...................
Witness’s Signature: ......................................................................... Date: ...................
Physician Signature: ......................................................................... Date: ...................
INDIAN CHAPTER OF INTERNATIONAL ASSOCIATION FOR THE STUDY OF PAIN
Reg. No.: U.P./470/84-85
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Tomorrow is the day When Idlers work and Fools reform…
Smith