History

The morphology of endometriosis ranges from the spectacular to the extremely subtle. Spectacular manifestations of any disease are most easily found, so the earliest descriptions of endometriosis naturally focus on cases with the maximal anatomic derangement and the most obvious physical and surgical findings. Endometriosis did not have a name at first because no one really knew much about it. Early cases of what might have been severe rectovaginal endometriosis were called 'posterior paravaginitis and parametritis with proliferation of epithelium' [1]. Surgeons finding extreme disease did not know by looking at it whether the nodular adhesive process they found was benign or malignant. The histological appearance, however, resembled a benign adenomyoma such as could be found diffusely or discretely in the uterine myometrium. Therefore, the earliest papers on endometriosis, including cases involving the intestinal tract, speak of the disease as an 'adenomyoma' to reflect the specific rubbery nodular morphology and microscopic appearance. 'Adenomyoma', 'deep endometriosis', 'severe endometriosis' and 'invasive endometriosis' are often used synonymously today which can seem confusing. The most impressive presentation of intestinal endometriosis is associated with obliteration of the cul-de-sac and associated rectal and vaginal involvement.

Early case reports

Stevens in 1910 presented to the Obstetrical and Gynaecological Section of the Royal Society of Medicine a case of adenomyoma of the posterior vaginal fornix [2]. On digital examination, the patient had two small hard nodules each about 6mm in diameter. Excision was accomplished vaginally and was accompanied by 'some difficulty'. The histology was of interlacing bands of smooth muscle surrounding glandular structures resembling endometrium. There was no mention of accompanying severe rectal symptoms and the pelvic contents were not surveyed.

Cuthbert Lockyer in 1913 presented to the Royal Society two cases of adenomyomas invading the posterior vaginal fornix, one with 'teat-like' projections [3]. One patient was taken to surgery. Obliteration of the cul-de-sac with invasion of the anterior rectal wall by a benign adenomyomatous growth was found. The patient was treated by en bloc resection of the uterus still attached to the affected bowel segment, followed by diverting sigmoid colostomy. Illustrations of the gross and microscopic features of this case show unequivocally that this would be considered severe invasive endometriosis today. The rectal mucosa was intact. Lockyer guessed that this tumor must arise from rests of Wolffian duct origin, although he was to change his mind within two years. This must be one of the first reports in the English-speaking literature of endometriosis involving the intestinal tract.

DeJong, also in 1913, published a report of small bowel obstruction due to adenomyoma of the ileum [4].

In 1914, Griffith presented a case of a pregnant woman with polyhydramnios and a tumor between the cervix and rectum, with invasion of the posterior vaginal fornix [5]. The tumor grew in size during pregnancy, and a vaginal biopsy showed glandular epithelium surrounded by decidual change which was surmised to arise from Müllerian duct rests. The tumor, as well as the uterine size, shrunk considerably after local implantation of radium for 20 hours.

Also in 1914, Leitch presented a case of an endometriotic nodule on the antimesenteric wall of the mid-sigmoid colon, 'the size of a Barcelona nut' which was found at surgery to be adherent to the posterior uterus, apparently without any rectal involvement [6]. After lysing the adhesions, the intestinal nodule was removed by segmental resection and anastomosis and microscopy clearly showed what today would be considered endometriosis invading the bowel wall to the submucosa. The area of the uterus to which the sigmoid had been adherent showed a fibrotic plaque which was removed and this also showed endometriosis. Leitch proposed that endometrium had migrated through the wall of the uterus and into the bowel wall, carrying with it the potential for formation of surrounding fibromuscular metaplasia. In the discussion that followed, Lockyer disavowed his former support of origin from Wolffian rests and introduced the concept of peritoneal epithelial metaplastic heteroplasia resulting from an inflammatory process, such as parametritis or 'pelvo-peritonitis'. Dr Leitch was unconvinced, having never seen any gross or microscopic evidence of inflammation. Leitch was also not swayed by Lockyer's previous argument for transformation from embryonic rests, stating that although fetal cells have some degree of totipotentiality: '(t)he cells composing (rests) manifestly age just the same as normal cells, and the embryonic potentialities for growth depart with their youth.' Leitch mentioned four cases of a similar condition which were reported by Sitzenfrey in 1909, but gave no reference.

Cullen published several papers between 1914 and 1920 which clearly illustrated and defined adenomyomas of the rectovaginal septum with obliteration of thecul-de-sac, rectal wall involvement and variable invasion of the cervix [7, 8, 9, 10, 11]. His usual treatment was by hysterectomy. This was performed by separation of the uterus from its lateral attachments followed by en bloc resection of the affected segment of rectum, with the uterus still adherent at the cervix to the anterior bowel wall, followed by colostomy. Occasionally, he would do staged procedures: a colostomy first, followed later by en bloc resection of the uterus and affected bowel segment. After performing this surgery on several patients, he concluded that: 'The removal of an extensive adenomyoma of the rectovaginal septum is infinitely more difficult than a (Wertheim) hysterectomy for carcinoma of the cervix.' This statement remains true today.

By 1922, Sampson had described adenomyoma of the appendix [12]. Sampson postulated, incorrectly, that intestinal adenomyomas occurred due to rupture of ovarian endometrioma cysts, with secondary seeding of the bowel, and that the cysts themselves were the result of reflux menstruation of endometrium first seeding the ovary resulting in a cyst. The existence of a leiomyomatous or adenomatous change in the bowel wall that could not be explained by implantation of endometrial epithelium apparently did not concern him, nor was he aware at that time of the multiple and often profound differences between endometrium and endometriosis which preclude consideration of endometriosis as an autotransplant [13].

Endometriosis of the cecum is uncommon and the cecum is so large that obstructive symptoms are rare. This may explain why endometriosis of the cecum apparently did not enter the literature until much later [14].

Sites of intestinal involvement

The sigmoid colon is most commonly involved, followed by the rectum, ileum, appendix and cecum (Table 1). There has been only one mention of endometriosis of the transverse colon, illustrated in schematic form [15].

† Some patients had previous appendectomy.
‡ The total of the column exceeds the total number of patients with intestinal disease because 200 patients had more than one intestinal site of involvement.

Symptoms

Symptoms due to lesions of intestinal endometriosis are related to their anatomic locations, depth of invasion of the endometrial-like glands and stroma with surrounding fibromuscular metaplasia ('adenomyoma'), and degree of distortion of the bowel wall and lumen. Since most patients with intestinal endometriosis frequently have endometriosis in multiple pelvic locations, it is sometimes difficult to know what symptoms are caused by the intestinal disease versus the pelvic disease.

Some intestinal endometriosis is asymptomatic. Superficial disease of the bowel wall in any site does not typically produce symptoms, nor typically do small nodules less than 1cm in diameter. Most disease of the appendix is asymptomatic, although cyclic catamenial right lower quadrant pain may rarely occur if the appendix is enlarged and hemorrhagic due to the effects of the disease. Intussusception of the appendix involved by endometriosis is a rare cause of abdominal pain, nausea and diarrhea [, 17, 18, 19, 20].

Endometriosis involving the cecum only occasionally produces right lower quadrant pain [21] and will not cause symptoms of obstruction because the cecal diameter is so large. Endometriosis of the ileum can cause crampy right lower quadrant pain if the lumen is distorted, or symptoms of complete bowel obstruction and malnutrition in extreme cases. Bowel obstruction due to endometriosis is almost always due to ileal obstruction [22], occasionally involving the ileocecal valve, although rare cases of rectosigmoid obstruction have been reported [23].

Pain or intestinal cramping in the left lower quadrant before bowel movements can be caused by nodular endometriosis of the rectosigmoid colon, either because of partial mechanical obstruction or perhaps by impeding the transmission of peristaltic waves. Symptoms can worsen prior to and during menses and complete obstruction is rare [24].

Rectal nodules of endometriosis occur most commonly in association with obliteration of thecul-de-sac (Table 1) and can cause rectal pain with each bowel movement throughout the month as well as rectal pain with flatus, intercourse, or sitting. In contrast, endometriosis of thecul-de-sac or uterosacral ligaments without rectal involvement may cause painful bowel movements primarily during menses. Some patients can be quite specific in their description of 'something between the vagina and rectum'. Occasionally, a woman may be so bothered by pain that they have examined themselves vaginally and felt tender nodularity. Some with obliteration of thecul-de-sac and rectal wall involvement may complain of low grade fever, particularly with menses. Alternating constipation and diarrhea may affect some [25], with aggravation of either symptom possible during menses. Cyclic rectal bleeding during menses is highly suggestive of significant intestinal endometriosis, but is uncommon. With increasing severity of intestinal endometriosis, there is an increase of the clinical diagnosis of irritable bowel syndrome.

Intestinal perforation associated with endometriosis, sometimes fatal, has occurred in pregnant and non-pregnant patients [26, 27, 28, 29].

Diagnosis

Barium enemas, ultrasound exams, colonoscopy and magnetic resonance imaging (MRI) or computed tomography (CT) scans are only occasionally positive in cases of intestinal endometriosis. This is because the disease begins on the serosal surface and either remains there or invades the muscularis to some varying extent but rarely involves the mucosa. Positive preoperative scans or endoscopy depends on a sufficient degree of distortion of the affected intestinal site [24, 30, 31, 32, 33]. Occasionally, endoscopy may reproduce the patient's pain when an intestinal nodule is reached.

Physical examination can suggest the possibility of intestinal involvement by the presence ofcul-de-sac nodularity associated with exquisite tenderness that may reproduce the patient's pain. Not all nodularity that may be found during surgery will be palpable on pelvic examination [34, 35]. In some patients, the posterior vaginal fornix is invaded by endometriosis advancing from an underlying nodule of the rectum or uterosacral ligament. When present, vaginal endometriosis can manifest simply as epithelial piling (the 'teat-like' structures of Lockyer) without discoloration, epithelial piling with bluish papules, or full-thickness involvement with a reddish polypoid surface which sometimes is bleeding. These manifestations of vaginal endometriosis are frequently missed on vaginal speculum examination in the office because the speculum has been used solely to examine the cervix and obtain cytology. The speculum should be directed posteriorly to examine the posterior fornix in all patients.

The most accurate diagnosis of intestinal endometriosis occurs during surgery and each potential area of intestinal involvement can usually be seen easily with the laparoscope. After examining the upper abdomen and diaphragm, the cecum and appendix are viewed.

Endometriosis of the appendix most commonly manifests as a whitish scarred area, either in the mid-portion of the appendix or near its tip, which causes the appendix to curl toward the scarring. Hemorrhagic changes are uncommon. One of the first impressions the surgeon may get is that the appendix cannot be straightened out even with traction (Fig. 1) as it appears to be curled upon itself.

Endometriosis of the cecum is the rarest site of intestinal involvement and is frequently manifest by an area of yellowish fibrosis of the anterior wall of the cecum, sometimes immediately adjacent to the base of the appendix. Cecal endometriosis is usually associated with some hemorrhagic changes associated with superficial sheets of adhesions which trap blood and cause the formation of hemorrhagic blebs (Fig. 2), and must be distinguished from the rare case of cecal hemangiomas (Fig. 3).

The small bowel should be examined from the cecum proximally for about 40cm. This can frequently be done with one atraumatic grasper to run the bowel, although some cases may require two atraumatic graspers for efficient investigation. Like intestinal endometriosis in other sites, endometriosis of the ileum primarily occurs on the antimesenteric border (Fig. 4), sometimes in a linear pattern which is the result of embryologic patterning. In cases where certain areas are very biologically active, the ileum folds upon itself and can produce constriction of the lumen (Fig. 5). Occasionally, there are several discrete areas of such fibrotic folding, with normal bowel immediately adjacent to the nodules. There is usually no hypertrophy of the adjacent fatty mesentery. Frequently, there are associated smaller whitish plaques of superficial disease which can also be located on the antimesenteric surface of the bowel, although some cases may display such small plaques on the sides of the ileal wall or on its mesentery. It is important to distinguish endometriosis of the ileum from Crohn's disease since both occur in the same region of bowel, although apparently never simultaneously. Crohn's disease manifests as an entire segment sometimes 15-20 cm in length of indurated, straight, hyperemic ileum with associated 'fat creeping' of the adjacent fatty mesentery completely along the length of the inflamed segment (Fig. 6). In either endometriosis or Crohn's disease of the ileum, mesenteric lymphadenopathy can be observed in the arc of mesentery draining the affected segment (Fig. 7).

Endometriosis of the sigmoid can be present as asymptomatic small superficial whitish or grayish macules with rare hemorrhagic change (Fig. 8). Like nodular ileal endometriosis, sigmoid nodules are located on the antimesenteric or anterior bowel wall and occur most commonly either immediately adjacent to thecul-de-sac reflection or in the mid-sigmoid several centimeters away. Rarely will two sigmoid nodules be present in the same patient. Sigmoid nodules are whitish due to the underlying fibromuscular hyperplasia and may have little or no hemorrhagic change. More commonly, the area of maximal fibrotic retraction of the anterior bowel wall in the center of the nodule will have hemorrhagic change and superficial sheets of hemorrhagic adhesions. There can be localized hypertrophy of the adjacent appendix epiploica on one or both sides of the bowel (Fig. 9).

Obliteration of thecul-de-sac occurs when the lower rectosigmoid colon is adherent to the posterior cervix and uterosacral ligaments. This condition is commonly associated with ovarian endometriomas which may hide the severe underlying pathology (Fig. 10). Although the morphology is one of adhesive change with slight overlying hemorrhagic changes along the line of adherence, obliteration of thecul-de-sac signifies the presence of invasive disease of the hidden surfaces, including the uterosacral ligaments, posterior cervix, and usually the anterior bowel wall. When the bowel is involved by nodular disease, the rectum will be rounded (Fig. 11). When the bowel wall is involved by little or no disease, the rectum will be flat as it joins the cervix (Fig. 12). Endometriosis of the vagina can occasionally be present with obliteration of thecul-de-sac. 'Endometriosis of the rectovaginal septum' may actually represent a slight misnomer which has been around for almost a century [2, 36]. While extensive disease, such as can be found with obliteration of thecul-de-sac, can frequently be palpated between the fingertips during combined vaginal and rectal examination, the areolar tissue of the septum is rarely extensively involved. Only at the end of the rectovaginal septum where the large nodule is physically intruding by its expansive growth will there be slight involvement by fibrosis associated with the advancing disease. Like endometriosis in many other pelvic areas, expanses of fatty tissue are largely spared from invasion by endometriosis.

Surgical treatment

Intestinal endometriosis may be treated by resections that are superficial, partial thickness, full-thickness or segmental. Most women with intestinal endometriosis will not require a segmental bowel resection. If bowel surgery is anticipated a preoperative bowel prep is given and prophylactic antibiotics are used. As the number of intestinal areas involved by endometriosis increases, the likelihood of a full-thickness or segmental bowel resection increase (Fig. 13). It is unnecessary to remove the pelvic organs to treat intestinal endometriosis successfully.

Figure 13. As the number of intestinal areas involved by endometriosis increases, the likelihood of a full-thickness or segmental bowel resection increases.

The wall of the intraperitoneal colon is composed of four layers: serosa, outer longitudinal muscularis, inner circular muscularis, and mucosa. Beneath the peritoneal reflection of thecul-de-sac, the serosal layer is absent. The wall of the small bowel is similar but thinner. Thus, the muscularis of the small bowel behaves surgically as one layer. These layers of the bowel wall can be used to the surgeon's advantage during treatment of intestinal endometriosis since frequently a layer involved by endometriosis can be peeled away from underlying layers, resulting in a partial-thickness bowel resection which may denude the mucosa in some cases. The techniques described below can be performed most effectively with a triple-puncture technique using 3mm scissors passed down the operating channel of a 10mm operating laparoscope, using either sharp dissection or high current density electroexcision using 90 watts of pure cutting current [37]. Surgery for intestinal endometriosis is dictated by the depth of invasion and the geographic distribution of disease, so various techniques are necessary, all guided in part by palpation of the bowel wall for nodularity.

Superficial lesions

Scissors cut perpendicularly into the normal bowel wall adjacent to the lesion, first entering only the outer layer of muscularis. The lesion is grasped and undermined, with the scissors working in a layer of muscularis. The dissection can quickly proceed beyond the lesion, so care must be taken to decide when to cut back out of the bowel wall. Suture reinforcement of the bowel wall with 2-0 silk is wise. Valuable practice can be gained by suturing even small defects in the bowel wall. To make internal suturing easy, two points must always be kept in mind: (1) The long end of the suture should be held in order to form an arch pointing toward the port through which the tying instrument is passed. (2) The short end of the suture should be placed immediately beneath where the knot will be tied (Fig. 14). This avoids reaching for the end of the suture, which can pull the suture through the tissue.

Mucosal skinning

Occasionally, a larger lesion will require dissection down to the mucosa for complete removal. If there is no submucosal fibrosis, both layers of muscularis can easily be peeled off the mucosa using sharp and blunt dissection (Fig. 15), a technique sometimes referred to as 'mucosal skinning'. Once the lesion has been completely undermined, the scissors are used to cut back out to the surface of the bowel. Be careful not to pass too far beyond the nodule before cutting back out. Interrupted 2-0 silk suture is used to close the serosa and muscularis in one layer. Antibiotic prophylaxis is optional.

Ileal resection

The ileum is most commonly involved in its terminal portion. A bulky mass effect of a nodule in the bowel wall may not be suggested by visible surface changes, but may be appreciated by palpation with graspers. Laparoscopic surgery on the ileum is possible, but is difficult due to the typical placement of accessory trocars for pelvic surgery. Scissors can be used to sharply excise the nodule within the muscularis by a mucosal skinning technique. With care, many nodules can be removed without penetrating the lumen. Most defects of the ileum should be closed with interrupted 3-0 silk since the bowel wall is thin to begin with.

Since the ileum is frequently involved by several lesions which may be superficial or deep, laparoscopic surgery can be tedious, even if additional appropriately placed trocars are inserted. In many cases, it is more efficient to mobilize laparoscopically the peritoneal attachments of the ileum and cecum so that the ileum can be delivered through a minilaparotomy incision where partial-thickness, full-thickness, or segmental bowel resections can be performed (Figs. 16-18). This minilaparotomy incision may be an enlargement of the right lower quadrant or umbilical trocar site. Occasionally, the ileum can be reached through a transvaginal approach if there is sufficient mobility (Fig. 19).

Full thickness disc resection of colon

If submucosal fibrosis is present, or if the nodule is large, entry into the lumen of the bowel may be inevitable. Entry into the bowel lumen allows palpation of the lesion through the mucosa as well, so the point at which the dissection begins to exit the bowel wall can be determined accurately. The mucosa can be closed with continuous 3-0 vicryl and the seromuscularis can be closed with interrupted 2-0 silk. The pelvis is filled with irrigation fluid and air can be injected into the sigmoid colon through a sigmoidoscope to check for air leaks. If leakage occurs, it must be stopped with more sutures.

Appendectomy

Monopolar appendectomy is simple and rapid. The appendiceal tip is grasped as the 3mm monopolar scissors with 50 watts of coagulation current shave along the wall of the appendix where the vessels are quite small (Fig. 20). This cuts and coagulates the vessels simultaneously until the cecum is reached (Fig. 21). Three endoloops are applied around the base of the bare appendix and the scissors cut between the suture (Fig. 22). The scissors grasp the appendix and extract it out the 10 mm umbilical sheath. The appendiceal stump can be lightly electrocoagulated and buried beneath the surface of the cecum with a purse-string suture if desired.

Conversion to laparotomy

While many cases of intestinal endometriosis can be managed successfully laparoscopically, laparotomy can still play an important role in treating intestinal endometriosis if the surgeon lacks the necessary laparoscopic skills [38]. Since patients with intestinal endometriosis frequently have extensive pelvic disease, bowel surgery for endometriosis may follow one to two hours of pelvic surgery for removal of invasive endometriosis and mobilization of the bowel. As the length of laparoscopic surgery increases, the energy level of the surgeon decreases, and surgery seems interminably long. Laparotomy may be selected if a lengthy surgery (i.e., over 4 hours) is anticipated. Also, laparotomy is far more efficient if two or more segmental resections are required in a single patient. In such patients, laparoscopic excision of all pelvic endometriosis and laparoscopic mobilization of the large bowel or ileum can allow the use of very small incisions for the remaining bowel surgery (Fig. 23).

In lengthy cases or cases involving extensive dissection or increased blood loss, a surgical drain left in thecul-de-sac can be helpful. Excess bloody irrigation fluid may otherwise drain messily out of laparoscopy puncture sites for up to 18 hours following surgery, to the consternation and concern of the nursing staff. If such bloody irrigation fluid remains in the abdomen, it can be an occasional cause of mild postoperative temperature elevation which can confuse the postoperative clinical picture. A drain can also help detect postoperative bleeding or infection.

Postoperative care

No change in routine orders is necessary following partial-thickness bowel resection, and patients can be discharged the day of surgery if tolerating oral liquids and pain pills without vomiting, and if they are able to void and have stable vital signs. In patients with one or two full-thickness disc resections, clear liquids can be started the morning after surgery, and the patient can be discharged in the afternoon if stable. She should stay on a light diet until passing gas.

Following segmental bowel resection, the patient is given only ice chips by mouth until passing gas. Routine nasogastric suctioning is unnecessary. Flatus usually occurs on about the fourth postoperative day. Clear liquids are then begun. If this is tolerated, the patient can advance to full liquids and be discharged. At home, carbohydrates are added for a day or two, followed by white meat, then diet as tolerated. Such a diet provides low residue foods which are easily processed in the stomach and small intestine. The main dietary items to avoid in the early postoperative period are foods that are high in roughage, such as salads and vegetables, or foods that are high in protein, such as meat and beans. The volume of oral intake in the early postoperative period is also important, since even water in large volumes can challenge the intestines too much. Most patients will be on a regular diet by 10 days after surgery.

Complications

If significant postoperative gas pain or nausea occur, the patient should resume clear liquids until better and try to avoid narcotic pain pills. Narcotic pain pills can cause gastritis or stimulate the nausea center and may be the main problem in some patients. The patient should inform the doctor of unusual circumstances such as persistent vomiting, worsening pain or bloating, or fever so the possibility of complications can be considered. Dehydration due to decreased oral intake can sometimes confound the picture since the patient may have weakness or nausea on this basis. If the patient reports concerns by telephone, clinical information about presence of intestinal activity can sometimes be gained by having a family member listen for bowel sounds by pressing an ear against the patient's abdomen and by taking the patient's temperature. Information about dehydration can be gained by asking about urinary output over the last day or two.

If there is sufficient concern of a significant complication, the patients should be brought to the hospital for tests including blood tests, cultures if infection seems possible, as well as tests for integrity of the intestinal and urinary tracts. For rectal, sigmoid, cecal and some ileal resections, barium or water-soluble contrast enemas will give the fastest information about bowel leaks. Some radiologists may express concern that if a leak is present, the patient may be made sicker by the procedure, and may be hesitant to perform such a procedure. This concern is unfounded. Such a leak must be identified since it can be eventually fatal and if identified would lead to immediate surgery anyway to fix the problem and clean out the extravasated contrast material. Spiral CT scans with oral or intravenous contrast or intravenous pyelograms may be helpful in identifying urinary tract or small bowel problems. Simple upright x-rays of the abdomen can identify ileus with excess gas in the small bowel and excess air-fluid levels. Free air under the diaphragm could potentially be related to recent surgery but could indicate an intestinal leak.

Some patients might be so ill that extensive testing is pointless and urgent surgical evaluation is the best choice. If the patient is taken to surgery urgently with no imaging tests, indigo carmine should be injected intravenously during surgery since some patients might have simultaneous urinary tract damage. Underwater air pressure examination can help identify small leaks of the rectosigmoid colon. Larger leaks will be obvious by the presence of malodorous fecal-contaminated liquid. Occasionally, a suspected intestinal complication will not be found and the patient's clinical picture could actually be due to a urinary complication. If the surgeon focuses on the somewhat more worrisome possibility of an intestinal leak, the excess watery, cloudy fluid encountered during surgery could be misinterpreted as an early abscess.

During surgery, the actual repair to the bowel or urinary tract will frequently be in the hands of a general surgeon or urologist and such repairs are beyond the scope of this article. Small intestinal leaks operated quickly may require simple oversewing with sutures. Larger leaks may be treated by temporary diverting colostomy. Ureteral damage may respond to insertion of a stent, although small defects created by sharp injury may be stitched laparoscopically or at laparotomy. Larger ureteral defects may require reimplantation into the bladder, sometimes with a psoas hitch if a length of ureter must be resected. Bladder injuries can be oversewn at laparoscopy or laparotomy, or sometimes treated with a urinary catheter only. A surgical drain left in postoperatively can help identify what is happening in the abdomen after surgical repair of a complication. This can also be used to obtain intraperitoneal cultures later, or for postoperative irrigation. A drain allows simple bedside detection of ongoing urinary tract leaks by the injection of indigo carmine intravenously or through a catheter in the bladder.

The patient going through a surgical complication needs all the support she can get from family, friends and the treating staff. Although the surgeon responsible for a complication will naturally feel embarrassment and sometimes will want to avoid the patient and family, this is not helpful to anyone. The surgeon should not withdraw from the patient unless asked. Time at the patient's bedside will help provide an important part of the emotional support which will be helpful in the psychological healing which must accompany the physical healing. The patient will appreciate that her original surgeon is with her at every step of the process and has not abandoned her. Expressions of genuine concern and sorrow over what she is going through are entirely appropriate human responses. Concern over possible medicolegal action may cause some treating physicans to appear to withdraw, withhold information, and seem cold and uncaring. This escalates the possibility of legal action since it is easier to sue a boor than a friend. The facts of the case and what led to the complication can be fully and freely discussed with the patient without jeopardizing a legal defense later. The occurrence of a complication does not always signify medical negligence. Some complications are unavoidable and unrecognizable at surgery. Embarrassment and a desire for immediate self-punishment should not cause the surgeon to claim that the surgical care which preceded the complication was against the standard of care. The standard of care does not require perfection, since it is universally recognized by doctors, lawyers, judges and juries that perfection is impossible to obtain. The standard of care requires simply that the doctor has done what other reasonable physicians might do with the same disease process, or to have done what has repeatedly worked successfully in previous personal experience. It implies that certain guidelines or rules (not necessarily those that have been published) have been observed, that a rational game plan was developed and followed. The majority of medical and surgical practice is not supported by randomized controlled trials and never will be. Judgment, experience and flexibility are some of the hallmarks of the standard of care, and these are more important in surgical treatment than published journal articles or books. Publications represent opinions based on either the experience of an author or evidence usually from some type of observational study. As such, there will be many opinions possible about every step of a procedure, beginning with placement of incisions and trocars to postoperative feeding. Therefore, the standard of care does not exist in any book. The standard of care is not dictated by the practice of the majority, with the same thing done to every patient. This would ignore the fact that patients can be different. If the surgeon's judgment is to use one approach instead of another because of training, experience or the surgical problem at hand, then the standard of care is being fulfilled by consideration of the pertinent facts in choosing and performing a surgical step or an entire surgical procedure in accordance with basic surgical principles.

References

1. Meyer R. Quoted by Culbertson C, in Discussion of Cullen TS. Adenomyoma of the rectovaginal septum. JAMA 1916;67:401-6.
2. Stevens TG. Adenomyoma of the vaginal wall. Proc Roy Soc Med 1910;3:57-8.
3. Lockyer C. Adenomyoma in the rectouterine and rectovaginal septa. Proc Roy Soc Med 1913; 4:112-16 (plus Discussion).
4. DeJong RJ. Subserose Adenomyomatose des Dunndarms. Virchows Arch (Path Anat) 1913; 211:141-156.
5. Griffith WSA. Pregnancy with utero-rectal adenomyoma, with extensive decidual meaplasia. Proc Roy Soc Med 1914;6:389-92.
6. Leitch A. Migratory adenomyomata of the uterus. Proc Roy Soc Med 1914;6:393-8 (plus Discussion).
7. Cullen TS. Adenomyoma of the rectovaginal septum. JAMA 1914;62:835-9.
8. Cullen TS. Adenomyoma of the rectovaginal septum. JAMA 1916;67:401-6.
9. Cullen TS. Adenomyoma of the rectovaginal septum. Johns Hopkins Hosp Bull 1917;28; 343-67.
10. Cullen TS. The distribution of adenomyomata containing uterine mucosa. Am J Obstet Gynecol 1919;80:130-8.
11. Cullen TS. The distribution of adenomyomas containing uterine mucosa. Arch Surg 1920;1: 215-83.
12. Sampson JA. Intestinal adenomas of endometrial type. Arch Surg 1922;5:217-80.
13. Redwine DB. Was Sampson wrong? Fertil Steril 2002;78:686-93.
14. Henriksen E. Endometriosis. Am J Surg 1955;90: 331-6.
15. Weed JC, Ray JE. Endometriosis of the bowel. Obstet Gynecol 1987;69:727-30.
16. Nissen ED, Goldstein AI. Intussusception of the appendix associated with endometriosis. Int J Gynaecol Obstet 1973;11:184-9.
17. Mann WJ, Fromowitz F, Saychek T, Madariaga JR, Chalas E. Endometriosis associated with appendiceal intussusception. A report of two cases. J Reprod Med 1984;29:625-9.
18. Sonnino RE, Ansari MR. Intussusception of the appendix and endometriosis. Henry Ford Hosp Med J 1986;34:61-4.
19. Panzer S, Pitt HA, Wallach EE, Thuluvath PJ. Intussusception of the appendix due to endometriosis. Am J Gastroenterol 1995;90: 1892-3.
20. Case 13-2000. Case records of the Massachusetts General Hospital. N Engl J Med 2000;342: 1272-8.
21. Aronchick CA, Brooks FP, Dyson WL, Baron R, Thompson JJ. Ileocecal endometriosis presenting with abdominal pain and gastrointestinal bleeding. Dig Dis Sci 1983;28:566-72.
22. Dmowski WP, Rana N, Jafari N. Postlaparoscopic small bowel obstruction secondary to unrecognized nodular endometriosis of the terminal ileum. J Am Assoc Gynecol Laparosc 2001; 8:161-6.
23. Cattell RB. Endometriosis of the colon and rectum with intestinal obstruction. N Engl J Med 1937;217:9-16 (plus Discussion).
24. Hepburn JJ. Endometriosis as a cause of acute intestinal obstruction. N Engl J Med 1937;217:6-8.
25. Hauck AE. Endometriosis of the colon. Ann Surg 1960;151:896-902.
26. Yelon JA, Green JM, Hashmi HF. Endometriosis of the appendix resulting in perforation: A case report. J Clin Gastroenterol 1993;16:355-6.
27. Gini PC, Chukudebelu WO, Onuigbo WIB. Perforation of the appendix during pregnancy: A rare complication of endometriosis. Br J Obstet Gynaecol 1981;88:456-8.
28. Clement PB. Perforation of the sigmoid colon during pregnancy: A rare complication of endometriosis. Br J Obstet Gynaecol 1977;84: 548-50.
29. Bakri YN, Tayeb A, Amri A. Fatal perforation of endometriotic colon. Int J Gynecol Obstet 1992; 37:301 (Letter).
30. Colcock BP, Lamphier TA. Endometriosis of the large and small intestine. Surgery 1950;28: 997-1004.
31. Graham B, Mazier WP. Diagnosis and management of endometriosis of the colon and rectum. Dis Colon Rectum 1988;31:952-6
32. Harris RS, Foster WG, Surrey MW, Agarwal SK. Appendiceal diseae in women with endometriosis and right lower quadrant pain. J Am Assoc Gynecol Laparosc 2001;8:536-41.
33. Fedele L, Bianchi S, Zanconato G, Tozzi L, Raffaelli R. Gonadotropin-releasing hormone agonist treatment for endometriosis of the rectovaginal septum. Am J Obstet Gynecol 2000;183: 1462-7.
34. Chapron C, Dubuisson J-B, Pansini V, Vieira M, Fauconnier A, Barakat H, Dousset B. Routine clinical examination is not sufficient for diagnosing and locating deeply infiltrating endometriosis. J Am Assoc Gynecol Laparosc 2002;9: 115-9.
35. Redwine DB, Wright J. Laparoscopic treatment of obliteration of thecul-de-sac in endometriosis: Long term followup. Fertil Steril 2001;76: 358-65.
36. Martin DC, Batt RE. Retrocervical, rectovaginal pouch, and rectovaginal septum endometriosis. J Am Assoc Gynecol Laparosc 2001;8:12-17.
37. Redwine DB. Bowel resection for endometriosis. In: Tulandi T (ed) Atlas of laparoscopic technique for gynecologists. London: WB Saunders. 1994:121-9.
38. Coronado C, Franklin RR, Lotze EC, Bailey HR, Valdes CT. Surgical treatment of symptomatic colorectal endometriosis. Fertil Steril 1990;53: 411-16.