Friday, October 28, 2011

Dr. OZ Adhesions

Dr. Oz Small Bowel Obstruction | Bloating-Vomiting-Pain

Dr. Oz Small Bowel Obstruction: A mysterious condition making you bloated, its more serious than you may realize. Have you ever been warned of the possibility of a small bowel obstruction, it is something that may happen in one third of all people after belly surgery and it is more serious than you may even realize. It is not only uncomfortable but is also life threatening!
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Tagged as: belly surgery small bowel obstruction, dr. oz bloating small bowel obstruction, Dr. Oz Small Bowel Obstruction, SBO, small bowel obstruction causes, small bowel obstruction symptoms, unable to pass gas sbo, what is a small bowel obstruction

Thursday, October 27, 2011

Health director defends handling of Penan child’s birth ~ C Section Adhesions

Health director defends handling of Penan child’s birth

MIRI: The State Health Department yesterday said standard care and management were provided to a Penan mother Seri Yung and her baby by its staff in Limbang and Miri hospitals but apologised for not waiving the charges.
In a statement, its state director Dr Zulkifli Jantan said complications due to lack of oxygen supply (hypoxic ischaemic encephalopathy) was the cause of the infant’s death. It was brought about by the extra long time needed in the ceasarian operation due to massive adhesions present.

“The department would like to state that all reasonable care and management have been duly provided to both Seri Yung and her infant while in Limbang and Miri hospitals,” he said.

The statement was in response to a letter highlighted through Batu Lintang assemblyman See Chee How that a Penan couple from Limbang was requesting an inquest into the death of their infant and case management.

The couple also alleged that they were verbally abused, and were forced to borrow money to pay the RM180 hospital charges.

The department apologised over the flap (on hospital charges), saying it was due to miscommunication. The patient had described herself as a Rela staff and not as a Penan, and therefore was charged accordingly.

“If she had presented herself as a Penan who could not afford the charges, the fee exemption could have been activated on the spot. For this (misunderstanding), we would like to tender our sincere apologies,” Dr Zulkifli said.

He said Seri had a previous Ceasarian operation to deliver her first baby in 2006, and in the recent case, an emergency operation was needed due to the prolonged labour.

She came to Limbang hospital at the early stage of her labour, diagnosed as a high risk patient and was sent by an ambulance to Miri Hospital on Oct 15 as her condition warranted it.

Labour commenced spontaneously in Miri Hospital and normal delivery trial was planned as previous Ceasarian operation did not contraindicate such, and the condition of mother and infant were monitored accordingly throughout.

“However, progress was slow and the infant began showing signs of distress, and a Ceasarian section was carried out but it was 30 minutes longer than normal due to extensive adhesions affecting the uterus and abdominal wall as a result of previous Ceasarian operation, “ he added.

The patient recovered from the operation without complications, and doctors at the Miri Hospital explained to her and her husband the whole incident, including about the infant.

The infant showed poor oxygenation upon birth at 4/10 in the first minute assessment and improved to 5/10 in five minutes. Emergency and intensive care was provided from birth until the infant girl passed away on Oct 17 caused by lack of oxygen due to longer than expected operation.

“The situation could not have been dealt with in a different way. Although it is common to have some adhesions from a previous Ceasarian operation, it is not common to have the extensive adhesions that this unfortunate patient had,” he added.

Dr Zulkifli said that the care and management of the mother and infant from Limbang to Miri hospitals were correct and appropriate.

The date mentioned by See (Chee How) contradicted with the department’s chronology of event. The infant was reported to have died on Oct 15 after Seri Yung was transferred to Miri hospital on Oct 13.

The Batu Lintang assemblyman said nothing short of a public apology from Miri Hospital would suffice as the couple was hurt and disappointed for losing their baby girl and also subject to needless criticism and humiliations for their financial hardships.

Meanwhile, on the imposition of RM180 hospital charges, the Miri Hospital director Dr Jack Wong said a breakdown in communication could be the cause.

He said the hospital could not ascertain at that point of time, the status of the patients (Seri and daughter) – whether they were entitled to a waiver of the hospital charges.

“However, we are prepared to waive the charges and to meet Seri and her husband, Roy Dumani. We will work out a mechanism to help solve the problems,” said Dr Wong.

On allegations of verbal abuse by the hospital staff, Dr Wong said investigation was being carried out.

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Wednesday, October 26, 2011

Adhesion-Prevention Strategy in C-Sections: Focus on Risk Reduction

Adhesion-Prevention Strategy in C-Sections: Focus on Risk Reduction
By Victor Hugo Gonzalez-Quintero, M.D., M.P.H. Interim Director, Division of Maternal Fetal Medicine Associate Professor of Clinical Obstetrics and Gynecology Director, Residency Program | October 26, 2011
University of Miami/Jackson Memorial Medical Center


Cesarean deliveries are now the most commonly performed abdominal surgery in the United States.1 In 2005, an estimated 30.3 % of all births involved C-section procedures2, and preliminary estimates from the Centers for Disease Control and Prevention indicate that the incidence of C-sections will continue to rise in the coming decade.3

The increased use of C-section procedures presents some important health considerations for specialists in maternal fetal medicine. According to the results of a study published in the American Journal of Obstetrics & Gynecology in May 20071:

Among women who underwent a second C-section, 46% (100 out of 217), developed pelvic adhesions.
Among women treated with a third C-section, 75% (48 out of 64) developed adhesions.
Among women treated with a fourth C-section, five out of six (83%) developed pelvic adhesions.
The development of adhesions was also shown to have an impact on time-to-delivery. On average, infant delivery was delayed 5.6 minutes among women who had a second C-section as compared to an average primary C-section. The comparative delay increased to 8.5 minutes and 18.1 minutes, respectively, for third and fourth C-sections
The Rationale for Proactive Strategies to Prevent Adhesions in C-Sections

Time to infant delivery once anesthesia has been administered and risk of surgical complexity at repeat C-section are of critical concern, particularly in cases of emergent C-section. Based on these findings and continuing trends in the incidence and impact of C-sections, obstetrical practices are increasingly considering strategies to help reduce the risk of adhesions. In some practices, strategies focus on restrictions in the use of C-section procedures among patients. The availability of proven adhesion prevention strategies has also built support for a more proactive strategy to reduce risk, especially among patients treated with multiple C-section procedures. Following a comprehensive review of options, our division led a practice-wide initiative to incorporate adhesion prevention strategies to reduce the risk of adhesions in most C-section procedures.

In considering this plan, which was introduced in 2005, we identified several factors in support of a more proactive adhesion prevention strategy:

As a busy obstetrical practice performing several thousand C-section procedures each year, our department is clearly positioned to be affected by trends in surgery that might increase the risk of adhesions among our patients. Based on available data it became apparent that an increased risk of post-surgical adhesions among our patients could have a significant impact in terms of treatment complications and delayed delivery time.
The use of an adhesion barrier was already in place in formulary at the hospital and was widely used in gynecologic oncology procedures where the risk of post-operative adhesions is well-established.
Based on established familiarity with adhesion prevention strategies in gynecologic oncology, support for a preventative strategy in obstetrics was in place among labor and delivery management teams familiar with both the proven efficacy of adhesion prevention strategies and the potential impact of adhesion development on our patients.
The introduction of an adhesion prevention strategy would require only minimal additional staff training and monitoring.
Data related to the safety and efficacy of adhesion prevention barriers was widely available.
Importantly, to deliver maximum benefit we determined that a preventative strategy to reduce the risk of adhesions in C-sections must be positioned as a complement to superior surgical technique at every stage.
The availability of more conclusive data related to the risk of adhesions among C-section patients will help to shape even more effective prevention strategies in the years ahead. In this area, however, the rapid increase in C-section procedures challenges us to identify the optimal strategies to reduce patient risk as quickly as possible. While available data related to the morbidity associated with C-section adhesions are limited, we concluded that available data are sufficient at this stage to support a broad preventative intervention strategy as outlined. We are continuing to monitor results based on this strategy to draw more precise conclusions related to treatment experience.

1. Morales KJ, Gordon MC, Bates GW Jr. Post cesarean delivery adhesions associated with delayed delivery of infant. Am J Obstet Gynecol 2007;196:461.e1-461.e6.
2. Martin JA, Hamilton BE, Sutton PD, Ventura SJ, Menacker F, Kirmeyer S, Munson ML. Births: Final data for 2005. National vital statistics reports; vol 56 no 6. Hyattsville, MD: National Center for Health Statistics 2007.
3. Hamilton BE, Martin JA, Ventura SJ. Births Preliminary data for 2006. National vital statistics reports; vol 56 no 7. Hyattsville, MD: National Center for Health Statistics. 2007.

Monday, October 24, 2011

The inpatient burden of abdominal and gynecological adhesiolysis in the US

BMC Surg. 2011; 11: 13.
Published online 2011 June 9. doi: 10.1186/1471-2482-11-13 PMCID: PMC3141363

Copyright ©2011 Sikirica et al; licensee BioMed Central Ltd.
The inpatient burden of abdominal and gynecological adhesiolysis in the US
Vanja Sikirica,1 Bela Bapat,2 Sean D Candrilli,2 Keith L Davis,2 Malcolm Wilson,3 and Alan Johns4
1Shire Pharmaceuticals, Wayne, PA 19087 USA
2RTI Health Solutions, 200 Park Offices, Research Triangle Park, NC 27709 USA
3The Christie NHS Foundation Trust, Manchester, M20 4BX, UK
4Texas Health Care, Fort Worth, TX 76109 USA
Corresponding author.
Vanja Sikirica:; Bela Bapat:; Sean D Candrilli:; Keith L Davis:; Malcolm Wilson:; Alan Johns:
Received January 5, 2011; Accepted June 9, 2011.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Other Sections▼
AbstractBackgroundMethodsResults and DiscussionConclusionsCompeting interestsAuthors' contributionsFundingPre-publication historyReferencesAbstractBackground
Adhesions are fibrous bands of scar tissue, often a result of surgery, that form between internal organs and tissues, joining them together abnormally. Postoperative adhesions frequently occur following abdominal surgery, and are associated with a large economic burden. This study examines the inpatient burden of adhesiolysis in the United States (i.e., number and rate of events, cost, length of stay [LOS]).Methods
Hospital discharge data for patients with primary and secondary adhesiolysis were analyzed using the 2005 Healthcare Cost and Utilization Project's Nationwide Inpatient Sample. Procedures were aggregated by body system.Results
We identified 351,777 adhesiolysis-related hospitalizations: 23.2% for primary and 76.8% for secondary adhesiolysis. The average LOS was 7.8 days for primary adhesiolysis. We found that 967,332 days of care were attributed to adhesiolysis-related procedures, with inpatient expenditures totaling $2.3 billion ($1.4 billion for primary adhesiolysis; $926 million for secondary adhesiolysis). Hospitalizations for adhesiolysis increased steadily by age and were higher for women. Of secondary adhesiolysis procedures, 46.3% involved the female reproductive tract, resulting in 57,005 additional days of care and $220 million in attributable costs.Conclusions
Adhesiolysis remain an important surgical problem in the United States. Hospitalization for this condition leads to high direct surgical costs, which should be of interest to providers and payers.Keywords: Adhesions, adhesiolysis, abdominal, gynecological, burden of illness, hospitalizations.
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Young carers ~ taking care of Parents

Supporting the county’s young carers
Mark Shields
Friday, October 21, 2011
12:21 PM
CHILDHOOD is a time for having fun, making friends and gaining confidence. But for more than 1,300 young carers across the county, those years are filled with looking after sick or disabled parents or siblings – which is where Crossroads Care Cambridgeshire comes in.

WHEN Shannon O’Neill gets home from school, the first thing she does is check how her mum Michelle is.

Michelle, 39, suffers from fibromyalgia and adhesion-related disorder (ARD), a condition which causes her constant abdominal pain.

There are times when she is able to look after Shannon as she would like to but, on her bad days, the pain is so intense that 11-year-old Shannon must look after her.

That could mean flushing out the feeding peg that was used in the past to connect Michelle’s colostomy bag, or giving her a massage to soothe her aching muscles.

Then it’s on to the household chores: making dinner, cleaning, washing, drying, and locking the house up for the night – before she sits down to begin her homework.

Even when Michelle is having a good spell, the unpredictability of her condition means she is always in Shannon’s thoughts.

“I’m always thinking of coming back at the end of the day and seeing how my mum is,” said Shannon. “I don’t like going to groups or after school clubs any more, because I’m scared to see what’s going to happen.”

Young carers are often the victims of bullying as they struggle to handle school, homework and their caring duties. As adults, they are twice as likely not to be in education or training as their peers, because caring has affected their education or would mean leaving their parent or sibling without care.

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Saturday, October 22, 2011

Prolonged (longer than 3 hours) laparoscopic cholecystectomy: reasons and results.

Am Surg. 2011 Aug;77(8):981-4.


Department of Surgery, Providence Hospital and Medical Centers, Southfield, Michigan, USA.


For the experienced surgeon, the average operative time for a laparoscopic cholecystectomy is less than 1 hour. There has been no study documenting the causes and results of prolonged (longer than 3 hours) surgery. A retrospective study was done of patients who underwent cholecystectomy between January 2003 and December 2007. A total of 3126 cholecystectomies were done. After excluding patients who had a planned open cholecystectomy and patients who had additional laparoscopic surgeries, we identified 70 patients who had a planned laparoscopic cholecystectomy with operative time exceeding 3 hours. Multivariate stepwise logistic regression was performed analyzing the various factors leading to prolonged surgery. Of the 70 patients, ranging in age from 21 to 92 years (mean, 57 years), most (n = 53) were female. Operative time ranged from 3 hours to 6 hours 40 minutes (mean, 3 hours 37 minutes). Emergency:elective admission ratio was 9:5 and acute cholecystitis (n = 40) was the most common indication. Common characteristics were obesity (n = 44, P = 0.031), intra-abdominal adhesions (n = 43, P = 0.004), and previous abdominal surgeries (n = 40, P = 0.002). Intraoperative complications included spillage of stones (n = 6), bile duct injury (n = 3), and bleeding (n = 3). The possibility of prolonged laparoscopic cholecystectomy should be anticipated in patients with obesity and previous abdominal operations. Prolonged surgery increases the risk of complications (bile duct injury, bleeding) and prolongs the postoperative hospital stay.

[PubMed - in process]

Thursday, October 20, 2011

Asherman's Syndrome

Asherman's Syndrome
"It's no longer a question of WHAT IF, but with knowledge it's answering WHAT NOW"
Welcome to our Web Site
Welcome to our site. If you are looking for information and support for Asherman's Syndrome, intrauterine adhesions/scarring, or related problems, you've found the right place.

What is Asherman's Syndrome?
Asherman's Syndrome, or intrauterine adhesions or synechiae, is an acquired uterine condition, characterized by the formation of adhesions (scar tissue) inside the uterus. In many cases the front and back walls of the uterus stick to one another. In other cases, adhesions only occur in a small portion of the uterus. The extent of the adhesions defines whether the case is mild, moderate or severe. The adhesions can be thin or thick, can be spotty in location, or can be confluent. They are usually not vascular, an important attribute that helps in treatment. Click here for more on Asherman's Syndrome grades.

Most patients with Asherman's have scanty or absent periods (amenorrhea) but some have normal periods. Some patients have no periods but feel pain at the time each month that their period would normally arrive. This pain may indicate that menstruation is occurring but the blood cannot exit the uterus because the cervix is blocked by adhesions. Recurrent miscarriage and infertility could also be symptoms (1).

Asherman’s syndrome occurs when trauma to the endometrial lining triggers the normal wound-healing process, which causes the damaged areas to fuse together. Most commonly, intrauterine adhesions occur after a D&C(dilation and curettage) that was performed because of a missed or incomplete miscarriage, because of retained placenta with or without hemorrhage after a delivery, or elective abortion. Pregnancy-related D&Cs have been shown to account for 90% of Asherman’s cases (2). Adhesions sometimes also occur following other pelvic surgeries such as cesarean section, surgery to remove fibroids or polyps, or in the developing world, as a result of infections such as genital tuberculosis (3) and schistosomiasis (4).

The risk of developing Asherman’s from a D&C is 25% 2-4 weeks after delivery (5-8). D&Cs also lead to Asherman’s in 30.9% of procedures for missed miscarriages(17) and 6.4% for incomplete miscarriages (2). Asherman’s risk increases with the number of D&Cs performed; after a single termination the risk is 16% however after 3 or more D&Cs the risk jumps to 32% (9). Each case of Asherman's Syndrome is different, and cause must be determined on a case-by-case basis. In some cases, Asherman's may have been caused by an "overly-aggressive" D&C. However, this is not often considered to be the case. The placenta may have attached very deeply in the endometrium or fibrotic activity of retained products of conception could have occurred both of which make it difficult to remove retained tissue without causing injury to the basal endometrium. For the most comprehensive information about D&Cs and Asherman's Syndrome, please click here to visit

There is a variant of Asherman's Syndrome that is more difficult to treat. This is a so-called "unstuck Asherman's" or endometrial sclerosis. In this condition, which may coexist with the presence of adhesions, the uterine walls are not stuck together. Instead, the endometrium has been denuded. Although curettage can cause this condition, it is more likely after uterine surgery, such as myomectomy. In these cases the endometrium, or at least its basal layer, has been removed or destroyed.

Asherman’s is thought to be under-diagnosed because it is usually undetectable by routine diagnostic procedures such as ultrasound scan. The condition is estimated to affect 1.5% of women undergoing HSG (10), between 5 and 39% of women with recurrent miscarriage (11-13), and up to 40% of patients who have undergone D&C for retained products of conception following childbirth or incomplete abortion (14) (see Causes above).

Direct visualization of the uterus via Hysteroscopyis the most reliable method for diagnosis. Other methods are sonohysterography (SHG) and hysterosalpingogram (HSG).

Ideally, prevention is the best solution. It was suggested as early as in 1993 (9) that the incidence of IUA might be lower following medical evacuation (eg. Misoprostol) of the uterus, thus avoiding any intra-uterine instrumentation. So far, one study supports this proposal, showing that women who were treated for missed miscarriage with misoprostol did not develop IUA, while 7.7% of those undergoing D&C did(15). The advantage of misoprostol is that is can be used for evacuation not only following miscarriage, but also following birth for retained placenta or hemorrhaging. Alternatively, D&C could be performed under ultrasound guidance rather than blindly. This would enable the surgeon to end scraping the lining when all retained tissue has been removed, avoiding injury. Early monitoring during pregnancy to identify miscarriage can prevent the development of, or as the case may be, the reoccurrence of Asherman’s as adhesions are more likely to occur after a D&C the longer the period after fetal death (2). Therefore immediate evacuation following fetal death may prevent IUA. There is no evidence to suggest that suction D&C is less likely to result in adhesions than sharp D&C. Cases of Asherman’s have been reported even following manual vacuum aspiration (16) and the rate of Asherman’s has not dropped since the introduction of suction D&C.

Asherman’s must be treated by a very experienced surgeon via hysteroscopy (sometimes assisted by Laparoscopy) Those few surgeons experienced enough in treating severe Asherman’s Syndrome recommend the avoidance of energy sources inside the uterus (this means removing scars with scissors rather than with energy-generating instruments such as resectoscopes or lasers, although not all surgeons agree with this). Adhesions have a tendency to reform especially in more severe cases. There are different methods to prevent re-scarring after surgery for Asherman´s Syndrome. Many surgeons prescribe estrogen supplementation to stimulate uterine healing respectively the growth of endometrium and place a splint or balloon to prevent apposition of the walls during the immediate post-operative healing phase. Other surgeons recommend weekly in-office hysteroscopy after the main surgery to cut away any newly formed adhesions. As yet, studies have not confirmed which method of treatment is most likely to have a successful outcome, that is one where the uterus/cervix remain scar free and fertility is restored.

This site is for a growing community of women who suffer or have suffered with Asherman's Syndrome. This site will provide information about Asherman's Syndrome, as well as personal support and shared experiences. Here, we share our hopes and despairs and talk about other options available for building our families, such as surrogacy and adoption. We will share medical and legal information, including any valuable links to other sites on the World Wide Web. We will also share our own stories as means of providing encouragement and hope.

Visit our YouTube channel to view videos about the experiences of women who have Asherman's Syndrome and the specialized doctors who treat them. We are continuously adding more videos to this channel so check it out often.

Contact Us
If you would like to join us or have any questions answered please visit our Contacts page.

If you are a medical professional and are interested in getting in touch with us, please email us for further communication. Please include the following information in your email: Name, Profession, Country, and Area of Interest in our group.

References (please click here for a complete list)

Wednesday, October 19, 2011

Intra-abdominal adhesions: Cellular mechanisms and strategies for prevention.

Int J Surg. 2011 Sep 23. [Epub ahead of print]
Intra-abdominal adhesions: Cellular mechanisms and strategies for prevention.
Maciver AH, McCall M, James Shapiro AM.
SourceDepartment of Surgery, University of Alberta Hospitals, 2000 College Plaza, 8215 112th Street, Edmonton, Alberta, Canada T6G 2C8.

Postoperative intra-abdominal adhesions represent a serious clinical problem. In this review, we have focused on recent progress in the cellular and humoral mechanisms underpinning adhesion formation, and have reviewed strategies that interfere with these pathways as a means to prevent their occurrence. Current and previous English-language literature on the pathogenesis of adhesion formation was identified. As the burden of surgical disease in the world population increases, and the frequency of reoperation increases, prevention of adhesion formation has become a pressing goal in surgical research.

Copyright © 2011. Published by Elsevier Ltd.

Idiopathic encapsulating peritonitis: Report of two cases.

Surg Today. 2011 Dec;41(12):1644-8. Epub 2011 Oct 4.
Idiopathic encapsulating peritonitis: Report of two cases.
Da Luz MM, Barral SM, Barral CM, Bechara Cde S, Lacerda-Filho A.
SourceDivision of Coloproctology and Small Bowel, Alfa Institute of Gastroenterology, Federal University of Minas Gerais Hospital, Av. Alfredo Balena 110 - 2° andar, Belo Horizonte, MG 30130-100, Brazil.

This report presents two cases of young males who developed the rare idiopathic form of sclerosing encapsulating peritonitis (SEP) presented as partial bowel obstruction, both diagnosed during surgical treatment, with satisfactory outcomes. Sclerosing encapsulating peritonitis is a rare and enigmatic condition, characterized by intraperitoneal fibrosclerosis, which causes intestinal obstruction. It is a chronic entity with a poorly elucidated pathophysiology, leading to the constitution of a thick white nacreous fibrosis membrane that wraps the bowel in a concertina-like fashion with some adhesions configuring an intra-abdominal cocoon. Sclerosing encapsulating peritonitis is reported in a wide variety of patients, including those who have undergone peritoneal dialysis, young adolescent girls, cirrhotic patients after peritoneal-venous shunting, and patients treated with β-blockers. Nevertheless, the etiology of SEP remains obscure. This entity presents many difficulties in preoperative diagnosis because of its peculiar characteristics. Recognition of the SEP results in proper management and prevents unnecessary bowel resection. Regardless of cause, the treatment of the obstruction is surgical, with dissection of the encasing membrane from the intestine and separation of adherent loops of small bowel until they are laid free and returned to their normal configuration. The prognosis after appropriate surgical therapy is good, but depends on coexisting diseases.

PMID:21969199[PubMed - in process]

Monday, October 17, 2011

Functional Bowel Disorders

Functional Bowel Disorders
Michael Snyder, MD
Clinical Instructor
Colon and Rectal Surgery
University of Texas at Houston Health Center
Clinical Associate Professor
Baylor College of Medicine
Houston, Texas

Functional bowel disorders are syndromes characterized by chronic gastrointestinal tract symptoms in patients without significant infectious, metabolic or anatomical abnormalities. Functional gastrointestinal disorders can affect the entire digestive tract from the mouth to the anus. The two most common functional disorders seen by the colon and rectal surgeon are irritable bowel syndrome (IBS) and functional constipation which affect the mid to lower gastrointestinal tract.

Irritable Bowel Syndrome

Irritable Bowel Syndrome (IBS), the most frequent condition diagnosed in most gastroenterology practices, is responsible for over three million office visits annually. Depending on the diagnostic inclusion criteria, the prevalence of IBS in the United States is between six and twenty percent (1). Female predominance is as high as 2:1 in some studies. While it is primarily a disorder of younger people in the third or fourth decade of life, up to 23% of patients with IBS have symptoms that persist into old age. A new diagnosis of IBS should be made cautiously in patients older than 60, however, because this age group has an increased incidence of other colonic disorders with similar symptoms. Since there has never been a well-designed study on the natural history of IBS, the reasons for the female predominance are unclear. Whether this represents a true difference or is secondary to health care seeking behavior is uncertain. IBS is a chronic disorder with at least 75% of patients having persistent symptoms five years or more after the diagnosis is first considered (2).

The understanding of the pathophysiology of IBS has evolved significantly over the past half century. Originally IBS was thought to represent a nervous disorder with augmented gastrointestinal motility occurring in patients under stress. Recent research has shown that IBS is a complex multifaceted disorder. Abnormalities in intestinal motility in conjunction with heightened visceral sensory input and processing are important aspects of the disease. In many patients with IBS, abdominal pain in the immediate postprandial period is associated with either rhythmic contractions or high amplitude prolonged contractions. These alterations in the migratory motor complex can either delay or accelerate intestinal transit (3). In addition, increased sensitivity to pain in the gastrointestinal tract has been demonstrated in patients with IBS. Several studies have suggested that patients with IBS may process sensory input from the gastrointestinal tract differently and have an exaggerated response to intestinal distention (4). Finally, two studies have demonstrated that infectious gastroenteritis may increase the possibility of developing IBS later in life (5,6), presumably by damaging the enteric nerves responsible for peristalsis.

IBS is defined by abdominal discomfort associated with altered bowel habits. As there are no biochemical or structural markers, IBS is diagnosed by the absence of organic disease and the presence of a constellation of symptoms. The Rome II diagnostic criteria divide IBS into three relatively equal groups depending on the presence of diarrhea, constipation, or alternating diarrhea and constipation. These criteria for IBS require at least twelve weeks duration of symptoms in one year that need not be consecutive. Symptoms defining IBS are abdominal pain or discomfort relieved with defecation or associated with a change in the frequency or appearance of the stool. Nine symptoms supporting the diagnosis of IBS include (a greater than 25% occurrence of): 1) Fewer than three bowel movements per week, 2) More than three bowel movements per day, 3) Hard or lumpy stools, 4) Loose (mushy) or watery stools. 5) Straining during bowel movement, 6) Urgency, 7) Passing mucous during bowel movement, 9) Abdominal fullness, bloating or swelling. IBS with diarrhea is associated with one or more of the supportive symptoms numbered 2,4 or 6 and none of 1, 3 or 5. IBS with constipation is associated with one or more of the supportive symptoms numbered1,3 or 5 and none of 2, 4 or 6 (7). An individual patient may change from one diagnostic group to the other during the treatment of this, so symptom based management is currently recommended.

Patients prone to diarrhea find that the first stool in the morning is usually normal in consistency. Subsequent bowel movements, however, become more watery and mucoid, and are associated with intestinal cramps, rectal urgency and bloating. Symptoms are relieved with the passage of stool but often quickly return. Patients prone to constipation also note mucous either in the stool or separately. The stool consistency is often hard, and/or rocky. Many patients strain to complete defecation or experience incomplete evacuation. Fecal incontinence occurs in up to 20% of patients with IBS, primarily in those with concomitant diarrhea. This is possibly due to repetitive reflex relaxation of the sphincter mechanism associated with colonic spasms.

The evaluation of patients who fall into one of the Rome II criteria is limited as long as no "alarm" symptoms or signs are noted. These "alarm" symptoms or signs include hematochezia, weight loss greater than ten pounds, family history of colon cancer, recurring fever, anemia, and severe chronic diarrhea. Routine colonoscopy for colon cancer screening is no different than the general population. Based on the best current data, the probability of colorectal cancer, inflammatory bowel disease and infectious diarrhea is less than 1% among IBS patients without "alarm" symptoms or signs (8). As this is similar to that of healthy patients undergoing screening, the routine use of endoscopy, radiologic tests, or microbiological evaluation is unnecessary. The only exception occurs in those patients with IBS and diarrhea. The incidence of celiac sprue in these patients is 5% and routine testing of these patients should certainly be considered (9).

Because the precise etiology of IBS is unknown, and there is a lack of objective biochemical markers, treatment of IBS has focused upon the relief of symptoms. Treatment of IBS is indicated when the symptoms of IBS significantly decrease the quality of life. It should result in improvement of global IBS symptoms such as abdominal pain, bloating and altered bowel habits.

For patients with IBS and constipation initial treatment involves increasing both the amount of daily fiber to 25-30gms and water intake to 64oz a day. For many patients with mild symptoms this may be all that is required. If dietary changes are insufficient, fiber supplements such as methylcellulose or psyllium are added. While these products act as hydrophilic agents to bind water and prevent excessive dehydration, they do not relieve abdominal pain and may accentuate bloating. Other laxatives such as polyethylene glycol solutions have been used with some success, but also do not address the abdominal discomfort. Tegaserod, a selective serotonin type 4 receptor agonist, binds to the enteric receptors initiating the peristaltic reflex. Four randomized controlled trials have compared tegaserod 6mg b.i.d. to placebo and found significant global symptom relief in women with IBS and constipation. The use of tegaserod in men or in patients with alternating diarrhea and constipation is not established (10).

For patients with IBS and diarrhea, loperamide has been studied in randomized control trials and found to decrease stool frequency, improve stool consistency, but have no effect on abdominal pain or bloating. Low doses of tricyclic antidepressants may also decrease the frequency of diarrhea. In those women who fail to respond to this conservative therapy and who have severe diarrhea predominant IBS, the serotonin type 3-receptor antagonist alosetron may be used. Five randomized controlled studies have demonstrated efficacy. Side effects include constipation (25%) and ischemic colitis (84 cases in the literature)(10).

Therapy for the abdominal discomfort associated with IBS has been disappointing until recently. Traditionally, antispasmodic agents have been prescribed. Dicyclomine and hyoscyamine are the two agents available in the United States. The only trial to demonstrate efficacy of either medication was associated with a 70% rate of anticholinergic side effects (10). Since these side effects include constipation, the two antispasmodic medications should be used cautiously in IBS patients with constipation. Antispasmodic medications should be taken 30-60 minutes prior to a meal to prevent postprandial abdominal pain and bloating. Currently, however, the most effective and preferred medication for abdominal pain and bloating is the previously mentioned serotonin type 4 receptor agonist, tegaserod.

Other therapies for IBS include behavioral modification and investigational drugs. Anxiety and depression are noted in up to 20% of IBS patients. Behavioral therapy for IBS has been evaluated in sixteen randomized controlled studies. While none of these examined global IBS improvement, most studies demonstrated that attenuation of individual IBS symptoms correlated with a reduction in anxiety and depression. In patients with sleep disorders, the administration of melatonin significantly diminished abdominal pain and rectal urgency (11). Other medications with visceral analgesic properties are being investigated to include the kappa opioid agonist fedotozine and neurokinin receptor antagonists. Probiotics are also being evaluated because of promising results controlling flatulence in a controlled trial.


Constipation, a common disorder seen by both primary care and specialty physicians, is responsible for more than 2.5 million annual office visits. Many people do not seek medical care and instead self medicate with a multitude of over the counter and alternative medications. Constipation is a symptom of many diseases and the medications used to treat them. It is interchangeably used to describe patients with stool that is difficult to pass, passes infrequently, or has a hard consistency. Because of a lack of consensus defining constipation in the literature, the International Congress of Gastroenterology formulated the Rome II criteria. They defined constipation as abdominal discomfort of at least twelve weeks duration in the previous twelve months (need not be consecutive) having two or more of the following symptoms; 1) Straining more than 25% of the time, 2) Lumpy or hard stools more than 25% of the time, 3) Anorectal blockage, 4) Incomplete evacuation, 5) Need for manual maneuvers, and 6) Less than three stools per week. In these patients loose stools may not be present and there should not be sufficient criteria for the diagnosis of irritable bowel syndrome (12).

The physiology of constipation primarily encompasses the transit of stool through the colon, rectum and anus. Stool enters the colon as a liquid and becomes solid during passage to the rectosigmoid. Segmental and high amplitude propagating contractions are the two major contractile activities in the colon. The propagating contractions are responsible for the movement of stool to the anal sphincter, which regulates eventual stool evacuation. These propagating contractions originate from pacemakers found in the muscle layer of the colon called the interstial cells of Cajal (13). The loss or inactivity of these cells may play a role in patients with slow transit constipation.

Defecation is the evacuation of stool from the rectum and is determined by the propulsive force of the stool and the resistance of the anus. It is triggered by distention of the rectum by stool. Propulsive force consists of voluntary increases in intra-abdominal pressure and involuntary high amplitude contractions of the rectum. Resistance to defecation decreases with voluntary straightening of the anorectal angle in conjunction with relaxation of the external sphincter and involuntary relaxation of the internal anal sphincter.

The etiology of constipation may be primary or secondary. The more common secondary causes of constipation are listed in Table 1. Many patients have multiple factors that may contribute to their constipation. Notably, medications, including over-the-counter and herbal preparations, are a factor in up to 40% of patients (14).

The evaluation of constipated patients begins with a thorough history and physical exam to identify one of the numerous secondary causes of constipation. A colonoscopy or combined sigmoidoscopy and barium enema should be considered to identify malignant or anatomical abnormalities in the colon and rectum. A careful examination of the perineum and anus will help exclude anatomical outlet obstruction, the presence of a rectocele and abnormal perineal descent. Laboratory testing includes thyroid functions and electrolytes to help diagnose metabolic and endocrine abnormalities contributing to the constipation.

If the initial evaluation does not reveal a secondary cause for the constipation, a transit study is recommended to objectively measure the severity, and helps establish the primary cause of the constipation. The initial study called a SitzMark test is performed with radio-opaque markers that are swallowed. Abdominal radiographs are obtained on days 3 and 5. The radiograph on day 3 confirms the patient ingesting the markers. The presence of more than 25% of the markers in the colon at day 5 is indicative of a positive test. Markers evenly spread throughout the colon are consistent with slow transit constipation, while those that congregate in the rectosigmoid are indicative of an outlet obstruction. A negative SitzMark test with fewer than 25% of the markers on day 5 is suggestive of normal transit constipation or a patient who is not compliant with the instructions regarding no laxative use during the testing.

Further evaluation of outlet obstruction consists of anal manometry and defecography. Anal manometry permits documentation of the anorectal inhibitory reflex to rule out a short segment Hirschrprung’s disease. In addition, normal manometric sphincter pressures during simulated defecation are useful in excluding outlet obstruction. Defecography is particularly useful in the diagnosis of intra-anal prolapse, rectoceles, and other pelvic floor abnormalities. Barium paste is placed into the rectum and the act of defecation is visualized. Anorectal angle visualization, perineal descent and the nonemptying of rectoceles can be objectively measured.

There are three types of primary constipation that are important to recognize. The first type, colonic inertia, is associated with a lack of urgency and intractability resulting in many patients having several days to weeks between bowel movements. Daily use of stimulant laxatives is typical and evacuation is uncommon without medication. While the etiology is idiopathic in nature, the patients are overwhelmingly young women. Increasing dietary fiber or fiber supplements may make symptoms of bloating and abdominal cramps worse. SitzMark studies are often markedly positive demonstrating a characteristic pattern of markers relatively evenly spaced throughout the colon. It is important to rule out coexisting outlet obstruction with defecography and/or anal manometry. The second type, normal transit constipation, is characterized by evacuation frequency and stool consistency that is within the normal range, but the patients feel constipated. Bowel management regimens and reassurance are often all that is necessary to treat these patients. The third type, anismus or obstructed defecation, is characterized by the sensation of incomplete evacuation and the need to strain to produce a stool. SitzMark studies may be positive with most markers present in the rectosigmoid. Physical examination along with defecography and/or anal manometry is critical in determining both the exact etiology and response to therapy.

Treatment of functional constipation begins with dietary manipulation consisting of a high fiber diet (25-30gm/day) and augmented water intake (64oz/day). Most patients can be effectively managed with dietary measures alone or in conjunction with occasional laxative or enema use. For those patients who fail dietary measures, treatment with mild stimulating or osmotic laxatives can be safely done. Polyethylene glycol (PEG) is a poorly absorbed large polymer with substantial osmotic activity. When used in a solution that does not contain any salt, PEG can be ingested in large amounts without any harmful effect. PEG also binds water to the stool improving the consistency in many constipated patients. Other osmotic agents include non-absorbed carbohydrates such as lactulose. These agents also bind water and soften the stool. Complications include fermentation with consequent bloating, flatus and abdominal cramping.

Additional therapies for refractory constipation have attempted to address the lack of normal high amplitude contractions in the colon found in patients with slow transit constipation. The selective serotonin type 4 receptor agonist, tegaserod, is currently recommended for women with IBS and constipation. It acts by stimulating the serotonin type 4 receptors with a pronounced enterokinetic effect. Constipation was improved in 5-19% of women compared to placebo (15). Previous serotonin type 4 agonists such as cisipride and prucalopride also induced strong contractions of the proximal colon, but because of cardiac arrhythmias and carcinogenesis respectively, they have been withdrawn from the market. Another way to recreate the high amplitude contractions appears to be colonic pacing. In a small study pacing induced rectal evacuation in two-thirds of patients with total colonic inertia (16). Further studies will determine if it will become a replacement for extirpative surgical intervention.

Other medical approaches to stimulating the enteric neural plexuses include serotonin reuptake inhibitors, cholecystokinnin antagonists, antimuscarinic agents and serotonin type 1-receptor agonists. All these agents are currently being investigated and are not yet commercially available.

The surgical approach to constipation is one of last resort. Obstructive defecation is initially treated with biofeedback that improves symptoms in up to 70% of patients, although a rare patient may benefit from internal sphincterotomy. In patients with slow transit constipation refractory to medical therapy, attempt at segmental resection of the colon is unsuccessful. Total abdominal colectomy with ileorectal anastomosis is the preferred operation. Relief of abdominal pain and return to normal bowel function occur in up to 90% of patients with total abdominal colectomy. Risks of the surgery include ileus in approximately one-third of patients, small bowel obstruction, diarrhea, and possible incontinence (17).


Functional bowel diseases such as IBS and constipation are common disorders. The Rome II criteria permit more objective diagnosis and patient stratification. Therapy is determined by the major symptom or symptom complex. Therapy is often simply dietary modification, but may require medications, biofeedback and rarely surgery. As more knowledge about the enteric neural pathways and the influence of various neurotransmitters on bowel motility is discovered, focused treatment regimens with fewer side effects should be possible.

Table 1. Common Causes of Constipation

Low fiber diet, inadequate fluid intake, ingestion of stool hardening foods.

Inadequate toilet facilities, depression, psychosis, ignoring need for bowel movement, immobility.

Endocrine, Metabolic
Diabetes mellitus, hypothyroidism, hypoparathyroidism, pregnancy, hypopituitarism, hypokalemia, hypercalcemia.

Cerebrovascular accident, Parkinson’s disease, multiple sclerosis, trauma, cerebral or spinal tumors, colonic inertia, Ogilvie’s syndrome, Hirschprung’s disease, Chagas’ disease.

Analgesics, anticonvulsants, antihistamines, antihypertensives, diuretics, chemotherapeutics, anticholinergics, metal ions and minerals.

Neoplasm, diverticular disease, inflammatory bowel disease, volvulus, ischemic colitis, endometriosis, anastomotic stricture.

Anal Outlet
Thrombosed hemorrhoids, anal fissure, rectal prolapse, proctitis, rectocele, nonrelaxing puborectalis, hypertrophic internal anal sphincter.


1.Olden, KW. Diagnosis of irritable bowel syndrome. Gastroenterology. 2002;122:1701-14.
2.Harvey RF, Mauad EC, Brown AM. Prognosis in the irritable bowel syndrome: a five year prospective study. Lancet. 1987;1:963-5.
3.Kellow JE, Phillips SF, Miller IJ, et al. Dysmotility of the small intestine in irritable bowel syndrome. Gut. 1988;29:1236-43.
4.Mertz H, Morgan V, Tanner G, et al. Regional cerebral activation in irritable bowel syndrome and control subjects with painful and non-painful rectal distention. Gastroenterology. 200;118:842-8.
5.Gwee KA, Leong YL, Graham C, et al. Psychometric scores and the persistence of irritable bowel after infectious diarrhoea. Lancet. 1996;347:150-3.
6.Rodriguez LA, Ruigomez A. Increased risk of irritable bowel syndrome after bacterial gastroenteritis. BMJ. 1999;318:565-6.
7.Thompson WG, Longstreth GF, Drossman DA, et al. Functional bowel disorders and functional abdominal pain. Gut.1999;45(suppl II):1143-7.
8.American College of Gastroenterology Functional Gastrointestinal Disorders Task Force. Evidence-based position statement on the management of irritable bowel syndrome in North America. Am J Gastroenterol. 2002;97:11(suppl):S1-5.
9.Sanders DS, Carter MJ, Hurlstone DP, et al. Association of adult celiac disease with irritable bowel syndrome: a case control study in patients fulfilling ROME II criteria referred to secondary care. Lancet. 2001;358:1604-8.
10.Brandt LJ, Bjorkman D, Fennerty MB, et al. Systematic review on the management of irritable bowel syndrome in North America. Am J Gastroenterol. 2002;97:11(suppl):S7-26.
11.Bowser A. Melatonin relieves IBS symptoms in patients with sleep disorders. Gastroenterology & Endoscopy News. 2005;56:12.
12.Thompson WG, Longstreth GF, Drossman DA, Heaton KW, et al. Functional bowel disorders and functional abdominal pain. Gut. 1999;45(suppl 2):1143-7.
13.Ward SM. Interstial cells of Cajal in enteric neurotransmission. Gut. 2000;47(suppl 4):iv40-3.
14.Adeniji OA, DiPalma JA. Prevalence of medication-associated constipation. Am J Gastroenterol. 2001;96:SI40.
15.American Gastroenterological Association Clinical Practice Committee. AGA technical review on irritable bowel syndrome. Gastroenterology 2002;123:2108-31.
16.Shafik A, Shafik AA, El-Sibai O, Ahmed I. Colonic pacing; a therapeutic option for the treatment of constipation due to total colonic inertia.
17.Lubowski DZ, Chen FC, Kennedy ML, King DW. Results of colectomy for slow transit constipation. Dis Colon Rectum. 1999;39:23-9.

Friday, October 14, 2011


URL: (дата обращения: 14.10.2011).
№ 1 for 2010 year

Medical and Biological sciences


Zasyadkina N.E., Vorobyov A.A., Dvoretskaya J.A.

PDF (128 K)
стр. 18-19

Last years , the quantity of surgically treated gynaecological diseases, used to be progressively increased. The most frequent surgical intervention is the total or subtotal hysterectomy with or without adnexa ( in occasion of myoma and adenomyosis).

The percent of this operations is about 38% in Russia, 25% in Great Britain, 36% in USA, 35% in Sweden. The middle age of such a surgically treated women is about 40.5 years old. Its about 76.8% of hysterectomy with ovariectomy were realized to a women of 40-45 years old in Great Britain. In USA the quantity of hysterectomy is about 60000 per year, in 60% of cases accompanied with bilateral ovariectomy.

In fact, the problem of adhesiogenesis is especially actual in operative gynaecology, because in the most cases, gynaecological surgery may attend a high risk of peritoneal adhesions forming, expanding beyond the bounds of pelvis. The rate of morphogenesis pelvic and peritoneal adhesions after obstetrical and gynaecological surgery is about 60-100%. For example, 92.6% - after supravaginal amputation of uterus, 95% - after uterine extirpation.

Postoperative adhesions has a great negative influence on a patients health condition , causes an intestinal obstruction, chronic pelvic pain syndrome, different surgical complications as an injuring of viscera and etc.

Main aim: An assessment of adhesiogenesis level under condition of hormonal insufficiency in the dynamics of a postoperative injury in the experiment.

Materials and Methods

The new experimental method of Adhesiogenesis modelling in a case of hormonal insufficiency was designed to determine the level of adhesive process.This model is reproducible on different kind of experimental animals. It were 30 nubilous female rats (Wistar Line)used in experiment. Their middle age was about 3 month, the weight was near 200 -350 grams. The method was realized by comparison of results of simultaneously provided experiments(a standard operational injury, uterine amputation without ovaries, uterine amputation with ovaries )were assessed under the experiment.

The level of adhesiogenesis in absolute numbers (TVA -total volume of adhesions) was assessed by us on the grounds of received macromorphometric data ( length, diameter, thickness, area of adhesions) and devised formula. It is possible to determine and objectively compare the process of adhesiogenesis in different groups.

In accord of earliest classification, all adhesions that were founded were devided on chordal, filiform, arachnoidal, scarious or planar morphological types. Each adhesion was described with a special parameters : diameter and length of a chordal and filiform adhesions, thickness and the area of scarious and planar adhesions.

Taking into account of the chordal and filiform adhesions middle diameter is about 5 and 1.5mm and scarious adhesion thickness is near 1mm, it is enough to define its length( for chordal and filiform adhesions) or area ( for scarious adhesions ) to identify their volume.

The formula for calculating of the TVA (Total Volume of Adhesions) was:

Vadh = Slchord.p(dchord/2)2 + Slfilif.p(dfilif./2)2 + + Slarachn.p(darachn./2)2 + SSscar.hscar. + SSплоск.hplanar.,

V - volume, l - adhesive length, d - diameter of adhesive transversal section, S - area of adhesion, h - thickness of adhesion, p = 3,14.


The data was processed by statistical calculation of arithmetical mean.

In the first group ( with a standard operational injury ) TVA was 0.45 cm3. In the second group (amputation of the uterus without ovaries) TVA was 0.73 cm3. In the third group (amputation of the uterus with ovaries ) TVA was 0,92 сm 3.


TVA depends of the operational injury, so the widening of operational injury volume in a condition of attendant postoperational hormonal insufficiency activates the elevation the TVA.

The data was obtained by experiment allows to suppose the possible importance of such a clinical researches, including the reasonability of substitutive hormonal treatment of the patients with surgical menopause.


Surgical anatomy of abdomen after operative intervension and laparoscopic surgery of adhesions. A.A. Vorobjov, A.G.Beburishvili Volgograd "Izdatel" 2001

Postoperational adhesions V.I.Kulakov , L.V.Adamyan, O.A.Minbaev Moscow 1998

Hysterectomy and the female health V.I.Kulakov , L.V.Adamyan, S.I.Ascolskaya Moscow "Medicina" 1999

Gynaecology. National guidance. V.I.Kulakov, I.B.Manukhin, G.M.Savelieva Moscow "Geotar-Media´ 2009

Prophylaxis of postoperational adhesions in abdominal cavity. Surgical and morphological aspects. S.V.Poroyskiy diss.сand. of medicine. Volgograd 2004.


Bibliographic reference


URL:  (дата обращения: 14.10.2011).

Thursday, October 13, 2011

Adhesion Related Disorder International Human Rights Team IHRT: So you want to go to Germany and have surgery with Kruschinski based on false hopes offered by Karen Steward??

Adhesion Related Disorder International Human Rights Team IHRT: So you want to go to Germany and have surgery with Kruschinski based on false hopes offered by Karen Steward??

Intestinal ischemia and infarction

Intestinal ischemia and infarction

Intestinal ischemia and infarction is damage to (ischemia) or death of (infarction) part of the intestine due to a decrease in its blood supply.

Causes There are several possible causes of intestinal ischemia and infarction.

Hernia: If the intestine moves into the wrong place or becomes tangled, this can lead to intestinal ischemia.

Adhesions: The intestine may become trapped in scar tissue from past surgery (adhesions). This can lead to ischemia if left untreated.

Embolus: A blood clot from the heart or main blood vessels may travel through the bloodstream and block one of the arteries supplying the intestine. Patients with previous heart attacks or with arrhythmias, such as atrial fibrillation, are at risk for this problem.

Arterial thrombosis: The arteries that supply blood to the intestine may become so narrowed from atherosclerotic disease (cholesterol buildup) that they become blocked. When this happens in the arteries to the heart, it causes a heart attack. When it happens in the arteries to the intestine, it causes intestinal ischemia.

Venous thrombosis: The veins carrying blood away from the intestines may become blocked by blood clots. This blocks blood flow into the intestines. This is more common in people with liver disease, cancer, or blood clotting disorders.

Low blood pressure: Very low blood pressure in patients who already have narrowing of the intestinal arteries may also cause intestinal ischemia. This typically occurs in patients who are very ill for other reasons. It can be compared to losing water pressure in a hose with a partial blockage.

SymptomsThe hallmark of intestinal ischemia is abdominal pain. Other symptoms include:

Exams and TestsLaboratory tests may show a high white blood cell (WBC) count (a marker of infection) and increased acid in the bloodstream.

Other tests include:

•CT scan of the abdomen
None of these tests are foolproof, however. Sometimes the only sure way to diagnose intestinal ischemia is with a surgical procedure.

TreatmentTreatment usually requires surgery. The section of intestine that has died is removed, and the healthy remaining ends of bowel reconnected.

In some cases, a colostomy or ileostomy is necessary. A blockage of arteries supplying the intestine is corrected if possible.

Outlook (Prognosis)Intestinal ischemia is a serious condition that can result in death if not treated promptly. The outlook depends on the cause. A good outcome may be achieved with prompt treatment.

Possible Complications Intestinal infarction may require a colostomy or ileostomy, either temporary or permanent. Peritonitis is common in such cases.

Severe illness with fever and bloodstream infection (sepsis) can result.

When to Contact a Medical ProfessionalCall your health care provider if you have any severe abdominal pain.

PreventionPreventive measures include:

•Control risk factors, such as heart arrhythmias, high blood pressure, and high cholesterol
•Do not smoke
•Eat a nutritious diet
•Quickly treat hernias
Alternative NamesIntestinal necrosis; Ischemic bowel; Dead bowel; Dead gut

ReferencesFry RD, Mahmoud N, Maron DJ, Ross HM, Rombeau J. Colon and rectum. In: Townsend CM Jr, Beauchamp RD, Evers MB, Mattox KL, eds. Sabiston Textbook of Surgery. 18th ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 50.

Hauser SC. Vascular diseases of the gastrointestinal tract. In: Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 146.

Update Date: 1/20/2010Updated by: David C. Dugdale, III, MD, Professor of Medicine, Division of General Medicine, Department of Medicine, University of Washington School of Medicine; and George F. Longstreth, MD, Department of Gastroenterology, Kaiser Permanente Medical Care Program, San Diego, California. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.

Wednesday, October 12, 2011

Diagnosis and management of chronic radiation enteritis

Diagnosis and management of chronic radiation enteritis

INTRODUCTION — Chronic radiation enteritis is a complication of radiation therapy for cancer, most commonly for rectal, prostate and pelvic malignancies. It can affect both the large and small intestine, is often progressive, and may lead to a variety of clinical consequences (such as diarrhea, nausea, weight loss, abdominal pain, intestinal obstruction, and perforation) depending upon the extent of the injury. It usually develops six or more months after radiation therapy (mean approximately 5 years, range two months to as long as 30 years. This contrasts with the timing of acute radiation enteritis (characterized by diarrhea and abdominal pain), which develops during or shortly after radiation therapy and resolves within two to six weeks.

The incidence has not been well defined, in part because of the large number of patients who died or were lost to follow-up in major studies involving radiation therapy, and because of the variability in the field size and dose of radiation. One literature review estimated that the incidence ranged from 1.2 to as high as 15 percent in patients with rectal cancer

This topic review will focus on the diagnosis and management of chronic radiation injury to the small intestines and proximal colon. Issues related to the prevention and treatment of chronic radiation proctitis (usually encountered following treatment of cancers of the rectum, cervix, uterus, prostate, urinary bladder, and testes) are presented separately.

PATHOGENESIS — Chronic radiation enteritis usually develops only after large doses of radiation therapy have been delivered (4500 to 5500 cGY); it is uncommon at lower doses. In addition to the dose of radiation, several other predisposing conditions have been described including:

Older age
Combined chemotherapy
Poor radiation technique
Postoperative radiation; in this setting, bowel loops fixed together by adhesions may prolapse into the pelvis, leading them to receive excessive radiation exposure. Adhesions due to past surgical procedures can have the same effect.
Intestinal injury is believed to be related to oxidative damage caused by the formation of free radicals. The end result is an obliterative endarteritis that leads to intestinal ischemia resulting in stricturing with ulceration and fibrosis and occasionally fistula formation. The physiologic consequences may include altered intestinal transit, reduced bile acid absorption, increased intestinal permeability, bacterial overgrowth and lactose malabsorption The resulting clinical manifestations may include nausea, vomiting, lactose intolerance, obstructive symptoms, diarrhea, weight loss, malnutrition, and bleeding (usually in patients with colonic involvement).

The prominent histopathologic features are those of an occlusive vasculitis with diffuse collagen deposition and fibrosis. The arteriolar walls may show a hyaline ring-like thickening and large foams cells beneath the intima. Mucosal ulceration, necrosis and perforation may develop as the disease progresses. Progressive fibrosis leads to stricturing with dilation of proximal segments. The intestinal segments and their associated serosa appear grossly thickened. Telangiectasias may be seen.

The precise mechanisms leading from oxidative damage to the histologic and morphologic abnormalities described above are incompletely understood. Several theories have been proposed, all of which are probably interrelated:

One model suggests that fibrosis develops from the initial mucosal injury
Another theory suggests that fibrosis develops in connective tissues where radiation has caused a decrease in cell turnover and a low rate of proliferation.
A third model focuses on the cellular responses to vascular damage caused by paracrine mediators. The signals leading to the developing of fibrosis are a topic of intensive ongoing investigation.
One study found that intestinal webs forming after radiation therapy demonstrated an impaired vasodilatory response in vitro to acetylcholine treatment. This microvascular dysfunction may lead to the formation of the abnormal tissue response seen in the wall of the intestine post-radiation therapy.
CLINICAL MANIFESTATIONS — The classical features of radiation enteritis are abdominal pain, nausea, vomiting, and diarrhea. Patients with severe disease may develop intermittent, partial, or complete small bowel obstruction

As noted above, bacterial overgrowth may lead to malabsorption and contribute to the nausea, abdominal pain and diarrhea. Bacterial overgrowth should be suspected in patients with intestinal strictures. Another clue may be the development of new lactose intolerance. Nonspecific symptoms include diarrhea, bloating, excessive gas, borborygmi, and nausea. Most such patients have only subtle laboratory or clinical findings pointing toward the diagnosis; thus a high index of suspicion is required. Rare patients with severe malabsorption may present with a more fulminant clinical and laboratory profile

DIAGNOSIS — The diagnosis is usually established by suggestive radiologic findings in patients with compatible clinical features who have a history of prior radiation exposure. The patient's previous radiation treatment record should be reviewed to determine the total dose and distribution of the radiation field. This may help to determine which intestinal segments may have received excessive radiation exposure, information that can be correlated with the radiologic findings and the clinical presentation.

We usually obtain an abdominal CT scan followed by an upper gastrointestinal series with small bowel follow through in patients with suspected small bowel disease. Additional imaging is reserved for patients in whom the diagnosis remains unclear. We generally perform a colonoscopy in patients with suspected colonic involvement.

Upper gastrointestinal series — An upper gastrointestinal series with small bowel follow-through is a useful initial test for evaluating the extent of disease although it is not as sensitive as enteroclysis.

Enteroclysis — Enteroclysis involves the instillation of contrast material (usually administered through a nasoenteric tube) into the small bowel using a pump (making it considerably less comfortable than a standard small bowel follow-through). It provides more detailed visualization of the small bowel compared with a standard upper gastrointestinal series. Suggestive findings include submucosal thickening, single or multiple stenoses, adhesions, and sinus or fistula formation. Its sensitivity and specificity for radiation enteritis have not been well-defined.

CT scan — Computed tomography may show thickening of bowel segments, but the findings are nonspecific. CT may be helpful in narrowing the differential diagnosis, particularly in distinguishing strictures due to radiation enteritis from those arising from abdominal metastases or a local recurrence

CT enteroclysis (in which a CT is performed after instilling contrast into the intestine using a nasoenteric tube) produces superior bowel opacification compared with conventional CT, and may therefore be useful for identifying low-grade or intermittent obstruction (reported sensitivity and specificity of approximately 88 and 82 percent, respectively). However, the technique is still used only in a few specialized centers. Similarly, other improvements in CT imaging of the small bowel (such as three-dimensional imaging) will likely also have a role in diagnosis of radiation enteritis but are not yet widely available

Magnetic resonance enteroclysis — Magnetic resonance enteroclysis permits visualization of the small bowel using similar principles as described above for CT enteroclysis. Initial studies suggest the results are comparable to (and possibly more sensitive than) CT enteroclysis. However, only small numbers of patients have been studied and the technique is not yet widely available.

Enteroscopy — Enteroscopy (peroral endoscopy of the small bowel using specialized endoscopes) has a limited role in the diagnosis of radiation enteritis although it may help to narrow the differential diagnosis. Enteroclysis can be performed following enteroscopy by leaving a tube inserted in the intestine upon withdrawal of the enteroscope.

Capsule endoscopy — There is no published experience with capsule endoscopy specifically for diagnosing radiation enteritis, although there is some clinical experience. However, it should probably not be performed in patients in whom there is a strong clinical suspicion for radiation enteritis because the capsule may become lodged in a strictured segment, requiring surgical removal.

Colonoscopy — Colonoscopy is helpful in evaluating colonic involvement and can also visualize the terminal ileum. Mucosal features consistent with radiation injury include pallor with friability and telangiectasias, which can be multiple, large, and serpiginous; these changes tend to be continuous. Although mucosal biopsies are not diagnostic, they can help to exclude other causes of proctitis such as infection or inflammatory bowel disease.

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of chronic radiation enteritis is broad. Other diagnostic possibilities include post-surgical adhesions, malabsorption syndromes, abdominal metastases, lymphoma, Crohn's disease, infectious, ischemic or ulcerative colitis, and intestinal pseudo-obstruction.

MEDICAL MANAGEMENT — Prevention is the key to avoiding chronic radiation enteritis. Once established, treatment should be as conservative as possible focusing on relief of symptoms. Experience with specific medical treatments has been derived largely from small clinical trials and case series. Approaches used to treat small bowel disease will be summarized below while specific treatments aimed at radiation proctitis are discussed separately.

Dietary recommendations — There does not appear to be a clear-cut diet that reliably alleviates symptoms. A high fiber diet should probably not be recommended specifically since it may worsen diarrhea and urgency. Some patients may develop lactose intolerance, which may be due to bacterial overgrowth, and may improve following antibiotic treatment (see below). Others may require avoidance of lactose. Enteral formulas supplemented with glutamine may have a benefit but studies are limited

Antidiarrheal agents — Judicious use of antidiarrheal agents (such as loperamide) can help improve diarrhea, although it should not be used in patients with suspected small or large bowel obstruction. The efficacy of loperamide was evaluated in a crossover trial involving 18 patients with diarrhea due to radiation enteritis who were randomly assigned to loperamide or placebo for 14 days separated by a 14 day washout period. Loperamide was associated with a significant reduction in the frequency of bowel movements, slower intestinal transit, and improvement in the absorption of bile acids.

Antibiotics — Antibiotics may reduce symptoms in patients in whom bacterial overgrowth has developed. Specific testing for bacterial overgrowth is preferable to empiric therapy. A major drawback to empiric therapy is that treatment may require more than one antibiotic, and repeated and sometimes cyclic treatment. Because antibiotics may be associated with adverse effects, some of which may mimic symptoms of bacterial overgrowth (such as diarrhea and abdominal discomfort), establishing a firm diagnosis is important. This can usually be accomplished with a breath test.

5-ASA drugs — A case report (published nearly three decades ago) suggested a possible benefit from sulfasalazine with or without oral prednisone. There is no large published experience with either of these drugs. Discordant results have been obtained from controlled clinical trials evaluating mesalazine or sulfasalazine in the prevention of acute radiation enteritis

Hyperbaric oxygen — HBO has been used for treatment of refractory foot ulcers in diabetes and in other conditions [39]. The theoretical benefit of hyperbaric oxygen therapy (HBO) may be via inhibition of bacterial growth [40], preservation of marginally perfused tissue, and inhibition of toxin production [41].

A benefit in chronic radiation enteritis was suggested in a case report of a patient in whom 20 treatments over a one month period brought about objective improvements in symptoms and absorption of D-xylose. However, this anecdote did not give the results of long-term follow-up. Other reports have also suggested a benefit for patients with chronic radiation proctitis.

The equipment needed for hyperbaric oxygen treatment is expensive and not widely available. Thus, at the present time, it is not a practical means of treating chronic radiation enteritis outside of centers specializing in this approach, particularly since its effectiveness has not been well-studied.

Parenteral nutrition — A mainstay of the medical therapy of severe chronic radiation enteritis has been total parenteral nutrition (TPN), the success of which is similar for other intestinal disorders requiring TPN. One of the largest series included 54 patients who required home TPN mostly because of intestinal obstruction (27 patients), short bowel syndrome (17 patients), malabsorption (five patients), fistula formation (three patients), and dysmotility (two patients). TPN was initiated a median of 20 months after radiation therapy and was administered for a median of 20 months. Cumulative 5-year survival was 64 percent. Most early deaths were due to recurrent cancer. Similar survival estimates were reached in other series .

SURGERY — As noted above, surgery for radiation enteritis should be avoided if possible because of several inherent difficulties in operating on patients with chronic radiation injury

Diffuse fibrosis and adhesions between bowel loops can make resection technically challenging.
The risk of a leak is high when creating an anastomosis between irradiated tissues. Furthermore, it can be difficult to distinguish healthy tissue for irradiated tissue by gross inspection alone; intraoperative endoscopy may be helpful in this setting, but experienced is limited.
Extensive resection may be required, potentially leading to short bowel syndrome.
Despite attempts at conservative management, approximately one-third of patients progress to the point where surgery is required. Most surgical series of patients treated for radiation enteritis are small; the most common indications for surgery have been persistent ileus, intestinal fistulization, and massive adhesions. Surgical mortality rates are as high as 10 to 22 percent and many patients require more than one laparotomy

An illustrative series focused on 109 patients who underwent surgery during a 10 year period. Five patients died postoperatively (all of whom had undergone resection) while 33 (30 percent) had postoperative complications. Complications were more likely in patients who underwent emergency surgery. Repeat surgery was required in 40 percent of patients during a 40 month follow-up period. Overall survival in patients without a cancer recurrence was 85 percent at year one, and 69 percent at year five.

Strictureplasty may offer a less invasive approach to the management of strictures, but experience is limited. The role of small bowel transplantation in this setting is still being determined; its role, if any, will probably be only in children

SUMMARY AND RECOMMENDATIONS — Chronic radiation enteritis may lead to a variety of clinical consequences (such as diarrhea, nausea, weight loss, abdominal pain, intestinal obstruction and perforation) depending upon the extent of the injury. It usually develops six or more months after radiation therapy (mean approximately 5 years, range two months to as long as 30 years).

The diagnosis is usually established by suggestive radiologic findings in patients with compatible clinical features who have a history of prior radiation exposure. The patient's previous radiation treatment record should be reviewed to determine the total dose and distribution of the radiation field. This may help to determine which intestinal segments may have received excessive radiation exposure, information that can be correlated with the radiologic findings and the clinical presentation. We usually obtain an abdominal CT scan and an upper gastrointestinal series with small bowel follow-through. Further testing with an enteroclysis (standard, CT, or MRI depending upon local expertise) can be performed if the above is unrevealing and clinical suspicion remains.

Management should be conservative, addressing the predominant symptoms.

Patients with diarrhea, abdominal pain, nausea or bloating should undergo breath testing for bacterial overgrowth and treated with antibiotics if bacterial overgrowth is confirmed. Avoidance of lactose may benefit other patients while antidiarrheal agents (such as loperamide) may also be helpful. Loperamide should be avoided in patients with obstructive symptoms.
Patients with intermittent obstructive symptoms may benefit from a low residue diet, although dietary tolerance is variable. Radiologic evaluation may help to identify the strictured segment, information which may be critical should strictureplasty or surgery be ultimately required. The narrowed segment may not always be visible with an upper gastrointestinal series, particularly in patients with intermittent symptoms. Such patients may require enteroclysis as described above.
Despite conservative measures, surgery will be required in approximately 30 percent of patients. This is usually due to persistent ileus, intestinal fistulization, and massive adhesions.
Prognosis is variable since the disease is progressive. Early mortality is usually due to cancer recurrence. Five-year survival is approximately 70 percent in those without cancer recurrence, although many patients continue to have troubling digestive symptoms for the remainder of their lives.

Intensive, ongoing research on mechanisms related to fibrogenesis may eventually produce effective means to prevent or reverse disease progression once it has been established. However, at the present time, prevention during radiation therapy is central to reducing the risk of developing chronic radiation enteritis.

Adhesions, and what can be done about them

Adhesions, and what can be done about them

Pelvic Adhesions

Pelvic adhesions cause many problems for millions of women. From obstructed tubes associated with infertility, to pelvic tenderness, and painful intercourse, to chronic pelvic pain. Curiously, adhesions can be very extensive, yet relatively silent. They may remain silent indefinitely, or long after the causative event, become symptomatic. The causes of adhesions are multiple but basically the tissue irritation that produces the adhesive process arises from an inflammatory event, or from trauma (i.e. post surgical).

Examples of an inflammatory event would be a tubal infection from a sexually transmitted disease (e.g. Gonorrhea), a post surgery infection, or appendicitis. Chronic "irritation" of the pelvic tissues from a common disease process such as endometriosis, may also incite adhesions. A very significant proportion of symptomatic pelvic adhesive disease arises from previous necessary pelvic surgery ( removal of an ovarian cyst would be a good example).

What are "pelvic adhesions" anyway?? In the process of trying to repair injured tissue, a series of normal healing events may cause some structures in the pelvis to become unintentionally "stuck" to another tissue or structure. In a normal healthy pelvis (or the whole abdominal cavity for that matter) this large space is lined with a tissue called peritoneum, which also covers the outside of organs located in the abdomen and pelvis. In an non-injured or irritated state, the peritoneum can be likened to slippery cellophane wrap…. the organs and structures lying immediately adjacent to each other just slip off each other and do not become bonded together. Given a tissue injury, the healing process initiates a sequence of events that can result in a certain tissue becoming "stuck" to its neighbor, and when this happens certain undesirable results occur.

The ovary for example is a very sensitive structure, much like the testis. If as a consequence of an ovarian cystectomy,( the removal of the cyst from the ovary) the ovary becomes "attached' to the pelvic sidewall, or the top of the vagina, the patient may experience persistent pelvic pain and/or painful intercourse. The diagnosis is suspected by a history of ovarian surgery, and subsequent persistent pain or tenderness unrelated to her menstrual cycle.

After a large abdominal incision (e.g. a hysterectomy for large fibroids) the bowel or an associated fatty structure called the omentum may become adherent to the abdominal wall. Adhesions begin to develop within hours of surgery. If by chance it is a loop of bowel, the patient may experience intermittent bouts of crampy pain, perhaps associated with some nausea, bloating, or even vomiting. The intestinal symptoms are related to some degree of bowel obstruction that inhibits the passage of the bowel contents or gas through the partially obstructed area. When the obstruction is severe then the patient will be very ill with nausea, distention and vomiting, and may not be passing any gas rectally. Xray studies may confirm the severe obstruction, and treatment may require decompression of the bowel by means of a tube passed through the stomach to the intestine, or even exploratory surgery.

More often in my experience, the symptoms are troublesome and annoying, and the obstruction is not severe enough to make any of the Xray tests informative. Often the patient will be sent to the gastroenterologist , and endoscopoic evaluation of both the upper and lower bowel will be performed . Frequently, the diagnosis is "irritable bowel syndrome". It should be remembered that intra-abdominal and pelvic adhesions rarely if ever show up on Xray or ultrasound. Unfortunately, every time an abdominal incision is performed, the risk is present for recurrent adhesion problems. The good news is however that most patients will not develop serious post-operative adhesions causing further problems. Those unfortunate to do so may ultimately undergo repeated surgeries, always hoping that "this will do it!!"

Does everybody develop adhesions?? No they do not, but it is not understood why one person develops very extensive adhesions, and the next individual none at all. The nature of the traumatic tissue event, the duration of the inflammatory insult, the nature of the preceding surgery, the operative technique of the surgeon, and the unknown healing characteristics of a given individual all interplay in the final outcome.

What can be done to minimize pelvic adhesions from forming? Early treatment of an infectious process if identified, utilization of safe sex practices to minimize the transmission of sexually transmitted disease, meticulous surgical technique to minimize unnecessary tissue trauma, and perhaps using barrier products where appropriate. The latter may be helpful in reducing the extent or severity of the post operative adhesion development.

What to do if symptomatic adhesions develop, what are the patients options? The first option in any situation is don't do anything. Pain is a relative experience, and the degree of severity will vary from individual to individual. Minor, or even moderately severe discomfort can often be lived with, or controlled by medication, acupuncture, or medical hypnosis. Not infrequently pelvic pain is not helped by conventional treatment such as hormones, pain medicine, or even surgery. In those circumstances, non-conventional treatment with acupuncture or hypnosis can sometimes be very helpful.

Given significant symptomatic pelvic adhesions being suspected from the history and physical exam, a thorough workup is indicated , which may include special xray studies and ultrasound. Ultimately, laparoscopy may be utilized to allow visual inspection of the intra-abdominal organs. What to do surgically depends on the findings. If an ovary is bound down with adhesions from previous surgery, the extent of the adhesive process may indicate a simple cutting of the adhesions or if necessary, removal of the ovary. If the patient has completed her fertility requirements, and if the pelvic adhesive process is very extensive, a complete hysterectomy with removal of both tubes and ovaries may be indicated. Obviously, the patient and her gynecologist need to have had a very comprehensive and detailed discussion about what might be encountered, and what options might be exercised.

What about abdominal wall adhesions resulting from prior abdominal surgery? These can usually be taken down laparoscopically, thus minimizing tissue injury, as opposed to a conventional large incision. Multiple tiny incisions may be necessary in order for the surgeon to see well, and from different angles the area of dense adhesions. Nonetheless, several tiny 1/2 inch incisions are far less uncomfortable than a conventional laparotomy incision.

If the adhesions are extensive, and the patient has undergone previous adhesion surgery that failed, I have taken an unorthodox approach to such individuals. Because adhesions begin to form almost immediately, along with the healing process involving the raw anterior abdominal wall, I have in special situations recommended a repeat laparoscopy in one week. At this point, the "new" adhesions are flimsy, soft, do not contain a blood supply, and can be swept away with minimal tissue injury, compared to a conventional adhesiolysis (freeing the adhesions surgically) of old adhesions that are dense, very adherent, and bloody. This is performed in an outpatient setting, and usually takes but a few minutes, compared to the time involved dealing with extensive, dense old adhesions.

It is important that patients inquire about their surgeon's experience with extensive adhesions, because what might be viewed as "not possible laparoscopically" by one gynecologist, may be very familiar territory for another. Because bowel may be intimately involved with the adhesive process the patient has to be aware that the worst case scenario may require bowel surgery, and a conventional laparotomy incision.

Pelvic adhesions can be a serious detrimental quality of life issue. Some patients are total pelvic cripples because of this problem. Once formed, they do not disappear with time. If you are suffering from some of the medical complaints outlined earlier, do consider a consultation with an experienced laparoscopic gynecologist and hopefully your adhesive problems can be solved.

J. Glenn Bradley, MD Correspondent for Laparoscopy and Hysteroscopy and Alternatives to Hysterectomy Advisory Board Member

Monday, October 10, 2011

What you don't know can hurt you: Knowledge is Power in a Doctor/Patient Relationship

Meet Jennifer Lewis, a long time sufferer of endometriosis and vocal advocate for those who suffer the disease.

What you don't know can hurt you: Knowledge is Power in a Doctor/Patient Relationship
By Jennifer Lewis | October 7, 2011

I was intimidated from the get-go. I was a 23 year old woman going on her fourth Laparoscopy for endometriosis. I had been experiencing severe pain and abnormal bleeding with and w/o my periods since I was fifteen, diagnosed with endometriosis at eighteen and already had three surgical laparoscopies to remove the endometial growths. This time the doctor wanted to try a different technique called a LUNA or uterine ablation. This procedure severs the ligaments in the uterus thus reducing pain created by cramping during menstruation. By this time I was having varying degrees of bleeding throughout the month as well as pain that did not correlate with my periods. I thought, "what the heck, maybe the fourth times’ a charm". I didn’t research the fact that LUNA’s are only of considerable benefit to women with pain DIRECTLY associated with their periods. At the time of the surgery I was in pain 75% of the time, and it was NOT only related to what by now had become unbearable menstruation. By the time I was 25 I had two more similar surgeries to relieve pain and abnormal bleeding caused by the regrowth of the endometrial tissue. I inquired on more than one occasion about a hysterectomy but was told by the heroes in white coats that I was either too young, I would regret it, menopause at my age would be ghastly, maybe I should seek therapy and learn to "live" with the pain"(that was a good one!) or that I should, as one of my FORMER GYN’s put it, "Swallow the pain medication and Buck Up". Essentially, I let my doctor be the ringmaster of the circus inside my body. I was intimidated by the number of degrees on his walls and the various snapshots of smiling new mothers and newborns; all having had complete faith in this physician to lead them down the path to a better life. Why should I think any different? I mean, who am I, Jennifer, to question a man who spent half his life learning how to practice medicine? But my gut and my instinct were pulling me in another direction; a direction that saved my life.

Only after seven surgical procedures, years on addictive narcotic medications, high doses of mind altering hormones, ER visits, catheterizations and mental anguish did I learn how to learn about being a patient. After experiencing fear and abandonment along with complete lack of faith in both the field of medicine and the doctors who practice it did I begin my true healing. Essentially, I became my own health advocate, and it changed my life.

Knowledge is power, plain and simple. Whether you are stricken with a life threatening illness or dealing with a persistent problem that affects the quality of your life you must take your health and any problems associated with it and ATTACK it with knowledge. In being your own advocate, it is essential that you approach your provider with sense of self and dignity; a competent individual who is aware of her own body. Your own research on and about the issue at hand is vital as well as your own personal ammunition; use it! As much as your physician would like to be, she/he may not be current on all of the cutting edge research and experimental trials that you may be eligible for. Go to the local University or college and research the medical section. The local hospital will also have up to date periodicals and medical journals that may contain useful information. In doing your own research, you become better able to understand your options. Only then can you make an informed consent on the treatment best suited for you. Utilize your provider as you would a consultant. This will enable a mutually effective exchange and your doctor will not only respect your interest in your own healthcare but respond to it.

It took me ten years of chasing white coats until I sat still enough to see my pattern. Be it intimidation, laziness or apathy, I had no regard for my most precious gift, my health. This is a society where we are inherently trained to entrust our healthcare in the hands of doctors. Asking for a second opinion, questioning a test result or inquiring about or expressing concerns over medications you may be taking can be difficult at best. When I was faced with the option of having my seventh surgery I began to really sit and think about my body, my goals (realistic) of the outcome of the surgery as well as the quality of my life. I was not comfortable speaking freely and easily with my current provider so I changed doctors. Instead of walking in her office uninformed, I confidently presented her with a list of questions I had, similar case studies and outcomes of the treatments and my realistic goals. I was able to weigh the pros and the cons intelligently and make an informed decision based on both my research and her professional experience. Less than two weeks later I had a total hysterectomy, something I had wanted and inquired about many times before only to be told that I could not possibly know for certain that was what I wanted because I was too young, too disillusioned or just too naïve about the consequences. Only after ten years did I find restitution in having the total hysterectomy and the ironic thing is that I was fought all that time by the doctors who proclaimed they wanted to help me. I got better when I finally decided to help myself.

Questions to ask your doctor include:

What are the benefits of doing this?
What are the risks involved?
What are my other options?
What should I do first?
What are the probable outcomes of each of these options?
What are the probable outcomes if I decide NOT to do this?
How many times have you performed/administered this drug before and what were the outcomes?

Remember, this is your body, your healthcare and your decision. Every woman has the potential to be her own powerhouse when it comes to her body, seize the opportunity or someone in a white coat will.

Jennifer Lewis
Author, Endometriosis: One Womans Journey
Freelance writer