HEMORRHOIDS. RECTAL FISSURES. PARAPROCTITIS. RECTAL FISTULAS. EPITHELIAL PARACOCCIDIOIDAL CANALS
EMBRYOLOGY AND ANATOMY
The embryonic gastrointestinal tract begins developing during the fourth week of gestation. The primitive gut is derived from the endoderm and divided into three segments: foregut, midgut, and hindgut. Both midgut and hindgut contribute to the colon, rectum, and anus.
The midgut develops into the small intestine, ascending colon, and proximal transverse colon, and receives blood supply from the superior mesenteric artery. During the sixth week of gestation, the midgut herniates out of the abdominal cavity, and then rotates 270 degrees counterclockwise around the superior mesenteric artery to return to its final position inside the abdominal cavity during the tenth week of gestation.
The hindgut develops into the distal transverse colon, descending colon, rectum, and proximal anus, all of which receive their blood supply from the inferior mesenteric artery. During the sixth week of gestation, the distal-most end of the hindgut, the cloaca, is divided by the urorectal septum into the urogenital sinus and the rectum.
The distal anal canal is derived from ectoderm and receives its blood supply from the internal pudendal artery. The dentate line divides the endodermal hindgut from the ectodermal distal anal canal.
The large intestine extends from the ileocecal valve to the anus. It is divided anatomically and functionally into the colon, rectum, and anal canal. The wall of the colon and rectum comprise five distinct layers: mucosa, submucosa, inner circular muscle, outer longitudinal muscle, and serosa. In the colon, the outer longitudinal muscle is separated into three teniae coli, which converge proximally at the appendix and distally at the rectum, where the outer longitudinal muscle layer is circumferential. In the distal rectum, the inner smooth-muscle layer coalesces to form the internal anal sphincter. The intraperitoneal colon and proximal one third of the rectum are covered by serosa; the mid and lower rectum lack serosa.
The colon begins at the junction of the terminal ileum and cecum and extends 3 to
The arterial supply to the colon is highly variable (Fig. 28-1). In general, the superior mesenteric artery branches into the ileocolic artery (absent in up to 20% of people), which supplies blood flow to the terminal ileum and proximal ascending colon, the right colic artery, which supplies the ascending colon, and the middle colic artery, which supplies the transverse colon. The inferior mesenteric artery branches into the left colic artery, which supplies the descending colon, several sigmoidal branches, which supply the sigmoid colon, and the superior rectal artery, which supplies the proximal rectum. The terminal branches of each artery form anastomoses with the terminal branches of the adjacent artery and communicate via the marginal artery of Drummond. This arcade is complete in only 15 to 20% of people.
Colon Lymphatic Drainage
The lymphatic drainage of the colon originates in a network of lymphatics in the muscularis mucosa. Lymphatic vessels and lymph nodes follow the regional arteries. Lymph nodes are found on the bowel wall (epicolic), along the inner margin of the bowel adjacent to the arterial arcades (paracolic), around the named mesenteric vessels (intermediate), and at the origin of the superior and inferior mesenteric arteries (main). The sentinel lymph nodes are the first one to four lymph nodes to drain a specific segment of the colon, and are thought to be the first site of metastasis in colon cancer. The utility of sentinel lymph node dissection and analysis in colon cancer remains controversial.
The colon is innervated by both sympathetic (inhibitory) and parasympathetic (stimulatory) nerves, which parallel the course of the arteries. Sympathetic nerves arise from T6-T12 and L1-L3. The parasympathetic innervation to the right and transverse colon is from the vagus nerve; the parasympathetic nerves to the left colon arise from sacral nerves S2-S4 to form the nervi erigentes.
The rectum is approximately 12 to
In the distal rectum, the inner smooth muscle is thickened and comprises the internal anal sphincter that is surrounded by the subcutaneous, superficial, and deep external sphincter. The deep external anal sphincter is an extension of the puborectalis muscle. The puborectalis, iliococcygeus, and pubococcygeus muscles form the levator ani muscle of the pelvic floor.
Anorectal Vascular Supply
The superior rectal artery arises from the terminal branch of the inferior mesenteric artery and supplies the upper rectum. The middle rectal artery arises from the internal iliac; the presence and size of these arteries are highly variable. The inferior rectal artery arises from the internal pudendal artery, which is a branch of the internal iliac artery. A rich network of collaterals connects the terminal arterioles of each of these arteries, thus making the rectum relatively resistant to ischemia
The venous drainage of the rectum parallels the arterial supply. The superior rectal vein drains into the portal system via the inferior mesenteric vein. The middle rectal vein drains into the internal iliac vein. The inferior rectal vein drains into the internal pudendal vein, and subsequently into the internal iliac vein. A submucosal plexus deep to the columns of Morgagni forms the hemorrhoidal plexus and drains into all three veins.
Lymphatic drainage of the rectum parallels the vascular supply. Lymphatic channels in the upper and middle rectum drain superiorly into the inferior mesenteric lymph nodes. Lymphatic channels in the lower rectum drain both superiorly into the inferior mesenteric lymph nodes and laterally into the internal iliac lymph nodes. The anal canal has a more complex pattern of lymphatic drainage. Proximal to the dentate line, lymph drains into both the inferior mesenteric lymph nodes and the internal iliac lymph nodes. Distal to the dentate line, lymph primarily drains into the inguinal lymph nodes, but can also drain into the inferior mesenteric lymph nodes and internal iliac lymph nodes.
Both sympathetic and parasympathetic nerves innervate the anorectum. Sympathetic nerve fibers are derived from L1-L3 and join the preaortic plexus. The preaortic nerve fibers then extend below the aorta to form the hypogastric plexus, which subsequently joins the parasympathetic fibers to form the pelvic plexus. Parasympathetic nerve fibers are known as the nervi erigentes and originate from S2-S4. These fibers join the sympathetic fibers to form the pelvic plexus. Sympathetic and parasympathetic fibers then supply the anorectum and adjacent urogenital organs.
The internal anal sphincter is innervated by sympathetic and parasympathetic nerve fibers; both types of fibers inhibit sphincter contraction. The external anal sphincter and puborectalis muscles are innervated by the inferior rectal branch of the internal pudendal nerve. The levator ani receives innervation from both the internal pudendal nerve and direct branches of S3 to S5. Sensory innervation to the anal canal is provided by the inferior rectal branch of the pudendal nerve. While the rectum is relatively insensate, the anal canal below the dentate line is sensate.
Perturbation of the embryologic development of the midgut and hindgut may result in anatomic abnormalities of the colon, rectum, and anus. Failure of the midgut to rotate and return to the abdominal cavity during the tenth week of gestation results in varying degrees of intestinal malrotation and colonic nonfixation. Failure of canalization of the primitive gut can result in colonic duplication. Incomplete descent of the urogenital septum may result in imperforate anus and associated fistulas to the genitourinary tract. Many infants with congenital anomalies of the hindgut have associated abnormalities in the genitourinary tract.
Normal Physiology
Fluid and Electrolyte Exchanges
Water, Sodium, Potassium, Chloride, Bicarbonate, and Ammonia
The colon is a major site for water absorption and electrolyte exchange. Approximately 90% of the water contained in ileal fluid is absorbed in the colon (1000 to 2000 mL/d), and up to 5000 mL of fluid can be absorbed daily. Sodium is absorbed actively via a Na-K ATPase. The colon can absorb up to 400 mEq of sodium per day. Water accompanies the transported sodium and is absorbed passively along an osmotic gradient. Potassium is actively secreted into the colonic lumen and absorbed by passive diffusion. Chloride is absorbed actively via a chloride–bicarbonate exchange.
Bacterial degradation of protein and urea produces ammonia. Ammonia is subsequently absorbed and transported to the liver. Absorption of ammonia depends in part upon intraluminal pH. A decrease in colonic bacteria (e.g., broad spectrum antibiotic usage) and/or a decrease in intraluminal pH (e.g., lactulose administration) will decrease ammonia absorption.
Short-chain fatty acids (acetate, butyrate, and propionate) are produced by bacterial fermentation of dietary carbohydrates. Short-chain fatty acids are an important source of energy for the colonic mucosa, and metabolism by colonocytes provides energy for processes such as active transport of sodium. Lack of a dietary source for production of short-chain fatty acids, or diversion of the fecal stream by an ileostomy or colostomy, may result in mucosal atrophy and “diversion colitis.”
Colonic Microflora and Intestinal Gas
Approximately 30% of fecal dry weight is composed of bacteria (1011 to 1012 bacteria/g of feces). Anaerobes are the predominant class of microorganism, and Bacteroides species are the most common (1011 to 1012 organisms/mL). Escherichia coli are the most numerous aerobes (108 to 1010 organisms/mL). Endogenous microflora are crucial for the breakdown of carbohydrates and proteins in the colon and participate in the metabolism of bilirubin, bile acids, estrogen, and cholesterol. Colonic bacteria also are necessary for production of vitamin K. Endogenous bacteria also are thought to suppress the emergence of pathogenic microorganisms, such as Clostridium difficile. However, the high bacterial load of the large intestine may contribute to sepsis in critically ill patients and may contribute to intra-abdominal sepsis, abscess, and wound infection following colectomy.
Intestinal gas arises from swallowed air, diffusion from the blood, and intraluminal production. Nitrogen, oxygen, carbon dioxide, hydrogen, and methane are the major components of intestinal gas. Nitrogen and oxygen are largely derived from swallowed air. Carbon dioxide is produced by the reaction of bicarbonate and hydrogen ions, and by the digestion of triglycerides to fatty acids. Hydrogen and methane are produced by colonic bacteria. The production of methane is highly variable. The gastrointestinal tract usually contains between 100 and 200 mL of gas and 400 to 1200 mL per day are released as flatus, depending upon the type of food ingested.
Motility, Defecation, and Continence
Unlike the small intestine, the large intestine does not demonstrate cyclic motor activity characteristic of the migratory motor complex. Instead, the colon displays intermittent contractions of either low or high amplitude. Low-amplitude, short-duration contractions occur in bursts and appear to move the colonic contents both antegrade and retrograde. It is thought that these bursts of motor activity delay colonic transit and thus increase the time available for absorption of water and exchange of electrolytes. High-amplitude contractions occur in a more coordinated fashion and create “mass movements.” Bursts of “rectal motor complexes” also have been described. In general, cholinergic activation increases colonic motility.
Defecation is a complex, coordinated mechanism involving colonic mass movement, increased intra-abdominal and rectal pressure, and relaxation of the pelvic floor. Distention of the rectum causes a reflex relaxation of the internal anal sphincter (the rectoanal inhibitory reflex) that allows the contents to make contact with the anal canal. This “sampling reflex” allows the sensory epithelium to distinguish solid stool from liquid stool and gas. If defecation does not occur, the rectum relaxes and the urge to defecate passes (the accommodation response). Defecation proceeds by coordination of increasing intra-abdominal pressure via the Valsalva maneuver, increased rectal contraction, relaxation of the puborectalis muscle, and opening of the anal canal.
The maintenance of fecal continence is at least as complex as the mechanism of defecation. Continence requires adequate rectal wall compliance to accommodate the fecal bolus, appropriate neurogenic control of the pelvic floor and sphincter mechanism, and functional internal and external sphincter muscles. At rest, the puborectalis muscle creates a “sling” around the distal rectum, forming a relatively acute angle that distributes intraabdominal forces onto the pelvic floor. With defecation, this angle straightens, allowing downward force to be applied along the axis of the rectum and anal canal. The internal and external sphincters are tonically active at rest. The internal sphincter is responsible for most of the resting, involuntary sphincter tone (resting pressure). The external sphincter is responsible for most of the voluntary sphincter tone (squeeze pressure). Branches of the pudendal nerve innervate both the internal and external sphincter. Finally, the hemorrhoidal cushions may contribute to continence by mechanically blocking the anal canal. Thus, impaired continence may result from poor rectal compliance, injury to the internal and/or external sphincter or puborectalis, or nerve damage or neuropathy.
Clinical Evaluation
A complete history and physical examination is the starting point for evaluating any patient with suspected disease of the colon and rectum. Special attention should be paid to the patient’s past medical and surgical history to detect underlying conditions that might contribute to a gastrointestinal problem. If patients have had prior intestinal surgery, it is essential that one understand the resultant gastrointestinal anatomy. In addition, family history of colorectal disease, especially inflammatory bowel disease, polyps, and colorectal cancer, is crucial. Medication use must be detailed as many drugs cause gastrointestinal symptoms. Before recommending operative intervention, the adequacy of medical treatment must be ascertained. In addition to examining the abdomen, visual inspection of the anus and perineum and careful digital rectal exam are essential.
The anoscope is a useful instrument for examination of the anal canal. Anoscopes are made in a variety of sizes and measure approximately
The rigid proctoscope is useful for examination of the rectum and distal sigmoid colon and is occasionally used therapeutically. The standard proctoscope is
Flexible Sigmoidoscopy and Colonoscopy
Video or fiberoptic flexible sigmoidoscopy and colonoscopy provide excellent visualization of the colon and rectum. Sigmoidoscopes measure
Plain X-Rays and Contrast Studies
Despite advanced radiologic techniques, plain x-rays and contrast studies continue to play an important role in the evaluation of patients with suspected colon and rectal diseases. Plain x-rays of the abdomen (supine, upright, and diaphragmatic views) are useful for detecting free intra-abdominal air, bowel gas patterns suggestive of small or large bowel obstruction, and volvulus. Contrast studies are useful for evaluating obstructive symptoms, delineating fistulous tracts, and diagnosing small perforations or anastomotic leaks. While Gastrografin cannot provide the mucosal detail provided by barium, this water-soluble contrast agent is recommended if perforation or leak is suspected. Double-contrast barium enema has been reported to be 70 to 90% sensitive for the detection of mass lesions greater than
Computed tomography (CT) is commonly employed in the evaluation of patients with abdominal complaints. Its utility is primarily in the detection of extraluminal disease, such as intra-abdominal abscesses and pericolic inflammation, and in staging colorectal carcinoma, because of its sensitivity in detection of hepatic metastases. 2 Extravasation of oral or rectal contrast may also confirm the diagnosis of perforation or anastomotic leak. Nonspecific findings such as bowel wall thickening or mesenteric stranding may suggest inflammatory bowel disease, enteritis/colitis, or ischemia. A standard CT scan is relatively insensitive for the detection of intraluminal lesions.
Virtual colonoscopy is a new radiologic technique that is designed to overcome some of the limitations of traditional CT scanning. This technology uses helical CT and three-dimensional reconstruction to detect intraluminal colonic lesions. Oral bowel preparation, oral and rectal contrast, and colon insufflation are used to maximize sensitivity. Early evaluation of virtual colonoscopy suggests that accuracy may approach that of colonoscopy for detection of lesions
The main use of magnetic resonance imaging (MRI) in colorectal disorders is in evaluation of pelvic lesions. MRI is more sensitive than CT for detecting bony involvement or pelvic sidewall extension of rectal tumors. MRI also can be helpful in the detection and delineation of complex fistulas in ano. The use of an endorectal coil may increase sensitivity.
Positron emission tomography (PET) is used for imaging tissues with high levels of anaerobic glycolysis, such as malignant tumors. 18 F-fluorodeoxyglucose (FDG) is injected as a tracer; metabolism of this molecule then results in positron emission. PET has been used as an adjunct to CT in the staging of colorectal cancer and may prove useful in discriminating recurrent cancer from fibrosis. At present, the efficacy and utility of PET in the detection of recurrent and/or metastatic colorectal cancer remains unproven.
Angiography is occasionally used for the detection of bleeding within the colon or small bowel. To visualize hemorrhage angiographically, bleeding must be relatively brisk (approximately 0.5 to 1.0 mL per minute). If extravasation of contrast is identified, infusion of vasopressin or angiographic embolization can be therapeutic.
Endorectal and Endoanal Ultrasound
Endorectal ultrasound is primarily used to evaluate the depth of invasion of neoplastic lesions in the rectum. The normal rectal wall appears as a five-layer structure (Fig. 28-6). Ultrasound can reliably differentiate most benign polyps from invasive tumors based upon the integrity of the submucosal layer. Ultrasound can also differentiate superficial T1-T2 from deeper T3-T4 tumors. Overall, the accuracy of ultrasound in detecting depth of mural invasion ranges between 81 and 94%. 3 This modality also can detect enlarged perirectal lymph nodes, which may suggest nodal metastases; accuracy of detection of pathologically positive lymph nodes is 58 to 83%. Ultrasound may also prove useful for early detection of local recurrence after surgery.
Endoanal ultrasound is used to evaluate the layers of the anal canal. Internal anal sphincter, external anal sphincter, and puborectalis muscle can be differentiated. Endoanal ultrasound is particularly useful for detecting sphincter defects and for outlining complex anal fistulas.
Physiologic and Pelvic Floor Investigations
Anorectal physiologic testing uses a variety of techniques to investigate the function of the pelvic floor. These techniques are useful in the evaluation of patients with incontinence, constipation, rectal prolapse, obstructed defecation, and other disorders of the pelvic floor.
Anorectal manometry is performed by placing a pressure-sensitive catheter in the lower rectum. The catheter is then withdrawn through the anal canal and pressures recorded. A balloon attached to the tip of the catheter also can be used to test anorectal sensation. The resting pressure in the anal canal reflects the function of the internal anal sphincter (normal: 40 to
Neurophysiologic testing assesses function of the pudendal nerves and recruitment of puborectalis muscle fibers. Pudendal nerve terminal motor latency measures the speed of transmission of a nerve impulse through the distal pudendal nerve fibers (normal: 1.8 to 2.2 msec); prolonged latency suggests the presence of neuropathy. EMG recruitment assesses the contraction and relaxation of the puborectalis muscle during attempted defecation. Normally, recruitment increases when a patient is instructed to “squeeze,” and decreases when a patient is instructed to “push.” Inappropriate recruitment is an indication of paradoxical contraction (nonrelaxation of the puborectalis). Needle EMG has been used to map both the pudendal nerves and the anatomy of the internal and external sphincters. However, this examination is painful and poorly tolerated by most patients. Needle EMG has largely been replaced by pudendal nerve motor-latency testing to assess pudendal nerve function and endoanal ultrasound to map the sphincters.
Rectal evacuation studies include the balloon expulsion test and video defecography. Balloon expulsion assesses a patient’s ability to expel an intrarectal balloon. Video defecography provides a more detailed assessment of defecation. In this test, barium paste is placed in the rectum and defecation is then recorded fluoroscopically. Defecography is used to differentiate nonrelaxation of the puborectalis, obstructed defecation, increased perineal descent, rectal prolapse and intussusception, rectocele, and enterocele. The addition of vaginal contrast and intraperitoneal contrast is useful in delineating complex disorders of the pelvic floor.
Fecal occult blood testing (FOBT) is used as a screening test for colonic neoplasms in asymptomatic, average-risk individuals. The efficacy of this test is based upon serial testing because the majority of colorectal malignancies will bleed intermittently. FOBT has been a nonspecific test for peroxidase contained in hemoglobin; consequently, occult bleeding from any gastrointestinal source will produce a positive result. Similarly, many foods (red meat, some fruits and vegetables, and vitamin C) will produce a false-positive result. Patients were counseled to eat a restricted diet for 2 to 3 days prior to the test. Increased specificity is now possible by using immunochemical FOBT. These tests rely on monoclonal or polyclonal antibodies to react with the intact globin portion of human hemoglobin. Because globin does not survive in the upper gastrointestinal tract, the immunochemical tests are more specific for identifying occult bleeding from the colon or rectum. Dietary restrictions are not necessary. Any positive FOBT mandates further investigation, usually by colonoscopy.
Stool studies are often helpful in evaluating the etiology of diarrhea. Wet-mount examination reveals the presence of fecal leukocytes, which may suggest colonic inflammation or the presence of an invasive organism such as invasive E. coli or Shigella. Stool cultures can detect pathogenic bacteria, ova, and parasites. C. difficile colitis is diagnosed by detecting bacterial toxin in the stool. 4 Steatorrhea may be diagnosed by adding Sudan red stain to a stool sample.
Specific laboratory tests that should be performed will be dictated by the clinical scenario. Preoperative studies generally include a complete blood count and electrolyte panel. The addition of coagulation studies, liver function tests, and blood typing/cross-matching depends upon the patient’s medical condition and the proposed surgical procedure.
Carcinoembryonic antigen (CEA) may be elevated in 60 to 90% of patients with colorectal cancer. Despite this, CEA is not an effective screening tool for this malignancy. Many practitioners follow serial CEA levels after curative-intent surgery in order to detect early recurrence of colorectal cancer. However, this tumor marker is nonspecific, and no survival benefit has yet been proven. Other biochemical markers (ornithine decarboxylase, urokinase) have been proposed, but none has yet proven sensitive or specific for detection, staging, or predicting prognosis of colorectal carcinoma. 5
Although familial colorectal cancer syndromes, such as familial adenomatous polyposis (FAP) and hereditary nonpolyposis colon cancer (HNPCC) are rare, information about the specific genetic abnormalities underlying these disorders has led to significant interest in the role of genetic testing for colorectal cancer. 6 Tests for mutations in the adenomatous polyposis coli (APC) gene responsible for FAP, and in mismatch repair genes responsible for HNPCC, are commercially available and extremely accurate in families with known mutations. Although many of these mutations are also present in sporadic colorectal cancer, the accuracy of genetic testing in average-risk individuals is considerably lower and these tests are not recommended for screening. Because of the potential psychosocial implications of genetic testing, it is strongly recommended that professional genetic counselors be involved in the care of any patient considering these tests.
Abdominal pain is a nonspecific symptom with a myriad of causes. Abdominal pain related to the colon and rectum can result from obstruction (either inflammatory or neoplastic), inflammation, perforation, or ischemia. Plain x-rays and judicious use of contrast studies and/or a CT scan can often confirm the diagnosis. Gentle retrograde contrast studies (barium or Gastrografin enema) may be useful in delineating the degree of colonic obstruction. Sigmoidoscopy and/or colonoscopy performed by an experienced endoscopist can assist in the diagnosis of ischemic colitis, infectious colitis, and inflammatory bowel disease. However, if perforation is suspected, colonoscopy and/or sigmoidoscopy are generally contraindicated. Evaluation and treatment of abdominal pain from a colorectal source should follow the usual surgical principles of a thorough history and physical examination, appropriate diagnostic tests, resuscitation, and appropriately timed surgical intervention.
Pelvic pain can originate from the distal colon and rectum or from adjacent urogenital structures. Tenesmus may result from proctitis or from a rectal or retrorectal mass. Cyclical pain associated with menses, especially when accompanied by rectal bleeding, suggests a diagnosis of endometriosis. Pelvic inflammatory disease also can produce significant abdominal and pelvic pain. The extension of a peridiverticular abscess or periappendiceal abscess into the pelvis may also cause pain. CT scan and/or MRI may be useful in differentiating these diseases. Proctoscopy (if tolerated) also can be helpful. Occasionally, laparoscopy will yield a diagnosis.
Anorectal pain is most often secondary to an anal fissure or perirectal abscess and/or fistula. Physical examination can usually differentiate these conditions. Other, less common causes of anorectal pain include anal canal neoplasms, perianal skin infection, and dermatologic conditions. Proctalgia fugax results from levator spasm and may present without any other anorectal findings. Physical exam is critical in evaluating patients with anorectal pain. If a patient is too tender to examine in the office, an examination under anesthesia is necessary. MRI may be helpful in select cases where the etiology of pain is elusive.
Lower Gastrointestinal Bleeding
The first goal in evaluating and treating a patient with gastrointestinal hemorrhage is adequate resuscitation. The principles of ensuring a patent airway, supporting ventilation, and optimizing hemodynamic parameters apply and coagulopathy and/or thrombocytopenia should be corrected. The second goal is to identify the source of hemorrhage. Because the most common source of gastrointestinal hemorrhage is esophageal, gastric, or duodenal, nasogastric aspiration should always be performed; return of bile suggests that the source of bleeding is distal to the ligament of Treitz. If aspiration reveals blood or nonbile secretions, or if symptoms suggest an upper intestinal source, esophagogastroduodenoscopy is performed. Anoscopy and/or limited proctoscopy can identify hemorrhoidal bleeding. A technetium-99 (99mTc)-tagged red blood cell (RBC) scan is extremely sensitive and is able to detect as little as 0.1 mL/h of bleeding; however, localization is imprecise. If the 99mTc-tagged RBC scan is positive, angiography can then be employed to localize bleeding. Infusion of vasopressin or angioembolization may be therapeutic. Alternatively, a catheter can be left in the bleeding vessel to allow localization at the time of laparotomy. If the patient is hemodynamically stable, a rapid bowel preparation (over 4 to 6 hours) can be performed to allow colonoscopy. Colonoscopy may identify the cause of the bleeding, and cautery or injection of epinephrine into the bleeding site may be used to control hemorrhage. Colectomy may be required if bleeding persists despite these interventions. Intraoperative colonoscopy and/or enteroscopy may assist in localizing bleeding. If colectomy is required, a segmental resection is preferred if the bleeding source can be localized. “Blind” subtotal colectomy may very rarely be required in a patient who is hemodynamically unstable with ongoing colonic hemorrhage of an unknown source. In this setting, it is crucial to irrigate the rectum and examine the mucosa by proctoscopy to ensure that the source of bleeding is not distal to the resection margin
Occult blood loss from the gastrointestinal tract may manifest as iron-deficiency anemia or may be detected with fecal occult blood testing. Because coloeoplasms bleed intermittently and rarely present with rapid hemorrhage, the presence of occult fecal blood should always prompt a colonoscopy. Unexplained iron-deficiency anemia is also an indication for colonoscopy.
Hematochezia is commonly caused by hemorrhoids or fissure. Sharp, knife-like pain and bright-red rectal bleeding with bowel movements suggest the diagnosis of fissure. Painless, bright-red rectal bleeding with bowel movements is often secondary to a friable internal hemorrhoid that is easily detected by anoscopy. In the absence of a painful, obvious fissure, any patient with rectal bleeding should undergo a careful digital rectal examination, anoscopy, and proctosigmoidoscopy. Failure to diagnose a source in the distal anorectum should prompt colonoscopy.
Constipation and Obstructed Defecation
Constipation is an extremely common complaint, affecting more than 4 million people in the United States. Despite the prevalence of this problem, there is lack of agreement about an appropriate definition of constipation. Patients may describe infrequent bowel movements, hard stools, or excessive straining. A careful history of these symptoms often clarifies the nature of the problem.
Constipation has a myriad of causes. Underlying metabolic, pharmacologic, endocrine, psychologic, and neurologic causes often contribute to the problem. A stricture or mass lesion should be excluded by colonoscopy or barium enema. After these causes have been excluded, evaluation focuses upon differentiating slow-transit constipation from outlet obstruction. Transit studies, in which radiopaque markers are swallowed and then followed radiographically, are useful for diagnosing slow-transit constipation. Anorectal manometry and electromyography can detect nonrelaxation of the puborectalis, which contributes to outlet obstruction. The absence of an anorectal inhibitory reflex suggests Hirschsprung’s disease and may prompt a rectal mucosal biopsy. Defecography can identify rectal prolapse, intussusception, rectocele, or enterocele.
Medical management is the mainstay of therapy for constipation and includes fiber, increased fluid intake, and laxatives. Outlet obstruction from nonrelaxation of the puborectalis often responds to biofeedback. 7 Surgery to correct rectocele and rectal prolapse has a variable effect on symptoms of constipation, but can be successful in selected patients. Subtotal colectomy is considered only for patients with severe slow-transit constipation (colonic inertia) refractory to maximal medical interventions. While this operation almost always increases bowel movement frequency, complaints of diarrhea, incontinence, and abdominal pain are not infrequent, and patients should be carefully selected. 8
Diarrhea and Irritable Bowel Syndrome
Diarrhea is also a common complaint and is usually a self-limited symptom of infectious gastroenteritis. If diarrhea is chronic or is accompanied by bleeding or abdominal pain, further investigation is warranted. Bloody diarrhea and pain are characteristic of colitis; etiology can be an infection (invasive E. coli, Shigella, Salmonella, Campylobacter, Entamoeba histolytica, or C. difficile), inflammatory bowel disease (ulcerative colitis or Crohn’s colitis), or ischemia. Stool wet-mount and culture can often diagnose infection. Sigmoidoscopy or colonoscopy can be helpful in diagnosing inflammatory bowel disease or ischemia. However, if the patient has abdominal tenderness, particularly with peritoneal signs, or any other evidence of perforation, endoscopy is contraindicated.
Chronic diarrhea may present a more difficult diagnostic dilemma. Chronic ulcerative colitis, Crohn’s colitis, infection, malabsorption, and short gut syndrome can cause chronic diarrhea. Rarely, carcinoid syndrome and islet cell tumors (vasoactive intestinal peptide-secreting tumor [VIPoma], somatostatinoma, gastrinoma) present with this symptom. Large villous lesions may cause secretory diarrhea. Collagenous colitis can cause diarrhea without any obvious mucosal abnormality. Along with stool cultures, tests for malabsorption, and metabolic investigations, colonoscopy can be invaluable in differentiating these causes. Biopsies should be taken even if the colonic mucosa appears grossly normal.
Irritable bowel syndrome is a particularly troubling constellation of symptoms consisting of crampy abdominal pain, bloating, constipation, and urgent diarrhea. Work-up reveals no underlying anatomic or physiologic abnormality. Once other disorders have been excluded, dietary restrictions and avoidance of caffeine, alcohol, and tobacco may help to alleviate symptoms. Antispasmodics and bulking agents may be helpful.
The incidence of fecal incontinence has been estimated to occur in 10 to 13 individuals per 1000 people older than age 65 years. Incontinence ranges in severity from occasional leakage of gas and liquid stool to daily loss of solid stool. The underlying cause of incontinence is often multifactorial and diarrhea is often contributory. In general, causes of incontinence can be classified as neurogenic or anatomic. Neurogenic causes include diseases of the central nervous system and spinal cord along with pudendal nerve injury. Anatomic causes include congenital abnormalities, procidentia, overflow incontinence secondary to impaction or neoplasm, and trauma. The most common traumatic cause of incontinence is injury to the anal sphincter during vaginal delivery. Other causes include anorectal surgery, impalement, and pelvic fracture.
After a thorough medical evaluation to detect underlying conditions that might contribute to incontinence, evaluation focuses on assessment of the anal sphincter and pudendal nerves. Pudendal nerve terminal motor latency testing may detect neuropathy. Anal manometry can detect low resting and squeeze pressures. Defecography can detect rectal prolapse. Endoanal ultrasound is invaluable in diagnosing sphincter defects.
HEMORRHOIDS
Hemorrhoids from Greek mean bleeding. Nowadays hemorrhoids are volume increase or dilation of cavernous bodies in rectum.
Ishiorectal space (1), pelviorectal space (2), perianal space (3).
Etiology and Pathogenesis
Appearance of hemorroids is connected with such factors as functional insufficiency of connective tissue, increase of venous pressure at constipation, hard physical work, low-active life style, pregnancy, alcoholism, spicy food. Mechanism of hemorrhoids’ development is connected with disorder of blood outflow by venules from cavernous bodies and their hyperplasia in distal part of rectum. Cavernous bodies are usually situated in basal part of anal columns (Morgagni’s). Presence of direct arteriovenous anastomoses conditions in hemorrhoids bleeding of arterial character.
Pathomorphology
External hemorrhoids have their origin from veins of lower hemorrhoidal plexus, internal – from upper. External hemorrhoids are soft, of bluish color, they have not smooth surface and are filled with blood. Sometimes they are dense and filled with thrombs. Sometimes external hemorrhoids are prolapsed internal nodes. They have long leg deeply in anal canal.
Histologically they observe wall atrophy, anomalies of development, often – signs of thrombophlebitis.
Hemorrhoids are cushions of submucosal tissue containing venules, arterioles, and smooth-muscle fibers that are located in the anal canal (see Fig. 28-4). Three hemorrhoidal cushions are found in the left lateral, right anterior, and right posterior positions. Hemorrhoids are thought to function as part of the continence mechanism and aid in complete closure of the anal canal at rest. Because hemorrhoids are a normal part of anorectal anatomy, treatment is only indicated if they become symptomatic. Excessive straining, increased abdominal pressure, and hard stools increase venous engorgement of the hemorrhoidal plexus and cause prolapse of hemorrhoidal tissue. Outlet bleeding, thrombosis, and symptomatic hemorrhoidal prolapse may result.
External hemorrhoids are located distal to the dentate line and are covered with anoderm. Because the anoderm is richly innervated, thrombosis of an external hemorrhoid may cause significant pain. It is for this reason that external hemorrhoids should not be ligated or excised without adequate local anesthetic. A skin tag is redundant fibrotic skin at the anal verge, often persisting as the residual of a thrombosed external hemorrhoid. Skin tags are often confused with symptomatic hemorrhoids. External hemorrhoids and skin tags may cause itching and difficulty with hygiene if they are large. Treatment of external hemorrhoids and skin tags are only indicated for symptomatic relief.
Internal hemorrhoids are located proximal to the dentate line and covered by insensate anorectal mucosa. Internal hemorrhoids may prolapse or bleed, but rarely become painful unless they develop thrombosis and necrosis (usually related to severe prolapse, incarceration, and/or strangulation). Internal hemorrhoids are graded according to the extent of prolapse. First-degree hemorrhoids bulge into the anal canal and may prolapse beyond the dentate line on straining. Second-degree hemorrhoids prolapse through the anus but reduce spontaneously. Third-degree hemorrhoids prolapse through the anal canal and require manual reduction. Fourth-degree hemorrhoids prolapse but cannot be reduced and are at risk for strangulation.
Combined internal and external hemorrhoids straddle the dentate line and have characteristics of both internal and external hemorrhoids. Hemorrhoidectomy is often required for large, symptomatic, combined hemorrhoids. Postpartum hemorrhoids result from straining during labor, which results in edema, thrombosis, and/or strangulation. Hemorrhoidectomy is often the treatment of choice, especially if the patient has had chronic hemorrhoidal symptoms. Portal hypertension was long thought to increase the risk of hemorrhoidal bleeding because of the anastomoses between the portal venous system (middle and upper hemorrhoidal plexuses) and the systemic venous system (inferior rectal plexuses). It is now understood that hemorrhoidal disease is no more common in patients with portal hypertension than in the normal population. Rectal varices, however, may occur and may cause hemorrhage in these patients. In general, rectal varices are best treated by lowering portal venous pressure. Rarely, suture ligation may be necessary if massive bleeding persists. Surgical hemorrhoidectomy should be avoided in these patients because of the risk of massive, difficult-to-control variceal bleeding.
Classification
Hemorrhoids by etiological signs are divided onto innate and acquired, by localization – internal (submucosal), external and mixed (combined).
By clinical course hemorrhoids are: acute and chronic, not complicated and complicated (thrombosis, strangulation of hemorrhoids). There also define primary and secondary hemorrhoids (at liver cirrhosis, diseases of circulatory system, tumors).
Symptoms and clinical course
Early signs of hemorroids are rush feeling in asnal region that appears due to skin maceration by mucous excretions from rectum. This sign is increased in diet violations that may be a consequence of constipation or diarrhea.
There define three degrees of hemorrhoids. At I degree nodes prolabe from anus during defecation, but they replace independently and are painful during palpation. At II degree there is a need to replace nodes. There is edema in perianal region and pain. At III degree nodes prolabe at very low physical loading, edema and pain are severe. The speciality of chronic hemorrhoids is that there are conditions for appearance of mucosal fissures, polipes and paraproctitis.
Variants of clinical course and complications
Initial part of hemorrhoids is characterized by gradual beginning and low reflected clinical signs – presence of hemorrhoidal nodes. Duration of this period may be different – from several months to years. Chronic course of hemorrhoids is characterized by periodical acute conditions and remissions. Difference of clinical course of hemorrhoids is only in complications.
Bleeding from hemorrhoids appears mostly during or after defecation and may be as profuse as moderate. Blood is bright red (arterial).
Acute thrombosis of hemorrhoidal nodes is mostly seen in III degree of hemorrhoids. Thrombosis is a complication of as external as internal nodes. At this there appear edema of bluish color, severe pain. Progress of disease course sometimes may be conditioned by thrombosis of inferior vena cava.
Such complication as prolapse and strangulation in anal sphincter of internal hemorrhoidal nodes appear not so often. Nodes swell, become bluish, sometimes there occur necrosis that spreads on external nodes. Edema of anal region spreads to
Diagnostic program
1. Anamnesis and physical data.
2. Examination of anal region.
3. Finger investigation of rectum.
4. Examination of rectum by rectal mirror.
5. Rectoromanoscopia.
6. General analysis of blood and urine.
7. Coagulogram.
8. Sedimentation reactions (Reaction of Wassermann).
Digital examination of the rectum:
a) examination of the perianal region; b) examination of the anus; c) examination of the ampula.
Digital examination of the rectum
Differential diagnostics
Anal fissure is characterized by severe pain during of after defecation, spasm of sphincter and small bleeding during defecation.
The cancer of rectum at the beginning of disease, usually, is painless, a blood in the first portions of excrement appears. At the examination of rectum hard formation or ulcers with a dense bottom is observed. Histological examination of biopsy specifies a diagnosis.
Single or multiple polyps of rectum may be combined with polyposis of colon. Revealed symptoms are disorder of defecation and blood in feces. Examination of rectum lets us verify the diagnosis.
Incomplete prolapse or prolapse of rectal mucosa differs from hemorrhoids of III degree by combination with low reflected incontinention.
Tactics and choice of treating method
Conservative treatment is provided in patients with not complicated hemorrhoids (I degree of disease). Treatment must be complex and include diet therapy, remedies and physioprocedures.
For treatment of such patients they use massage through Diet therapy means excluding from ration spicy and salty food. rectum, recommend carrying of bandages. They also prescribe enemas (micro enemas with warm water, oils, antiseptics), warm as sitting bath, perineal shower, warming compresses.
In acute period they use bandages with cold water, cooling bandages with plumbum water or furacilinum.
Medicamentous therapy includes prescription of anti bleeding remedies and analgetics, antiseptics, anti-inflammatory remedies (orally, intravenously and locally as rectal suppositoria).
They also use physiotherapeutic methods (UHF, darsonvalization), treating physical training for strengthening of abdominal muscles and diaphragm, pelvis, spa treatment (H2S baths, mud and radon sanatoria).
Indications for surgical treatment are frequent bleedings from hemorrhoidal nodes that are accompanied with anemia, big nodes that worsen defecationm inflammation, prolapse and strangulation of nodes.
There are known more than 30 methods of hemorrhoids’ extraction. The main moments of operation are divulsion of sphincter, extraction and ligation of hemorrhoidal nodes situated in zones on 3, 7, and 11 hours at position of patient on back. Hemorrhoidal nodes are cut from external area to internal, leg is ligated by silk ligature and extracted. The most wide spread method is by Milligan-Morgan – extraction of nodes with renewal of mucosa in anus (Pic. 4.1.1).
In patients with complication of secondary hemorrhoids by bleeding that may not be treated by conservative therapy as a rule there is provided only ligation of bleeding areas.
Medical Therapy
Bleeding from first- and second-degree hemorrhoids often improves with the addition of dietary fiber, stool softeners, increased fluid intake, and avoidance of straining. Associated pruritus may often improve with improved hygiene. Many over-the-counter topical medications are desiccants and are relatively ineffective for treating hemorrhoidal symptoms.
Rubber Band Ligation
Persistent bleeding from first-, second-, and selected third-degree hemorrhoids may be treated by rubber band ligation.
Mucosa located 1 to
Infrared Photocoagulation
Infrared photocoagulation is an effective office treatment for small first- and second-degree hemorrhoids. The instrument is applied to the apex of each hemorrhoid to coagulate the underlying plexus. All three quadrants may be treated during the same visit. Larger hemorrhoids and hemorrhoids with a significant amount of prolapse are not effectively treated with this technique.
Sclerotherapy
The injection of bleeding internal hemorrhoids with sclerosing agents is another effective office technique for treatment of first-, second-, and some third-degree hemorrhoids. One to 3 mL of a sclerosing solution (5-phenol in olive oil, sodium morrhuate, or quinine urea) are injected into the submucosa of each hemorrhoid. Few complications are associated with sclerotherapy, but infection and fibrosis have been reported.
Excision of Thrombosed External Hemorrhoids
Acutely thrombosed external hemorrhoids generally cause intense pain and a palpable perianal mass during the first 24 to 72 hours after thrombosis. The thrombosis can be effectively treated with an elliptical excision performed in the office under local anesthesia. Because the clot is usually loculated, simple incision and drainage is rarely effective. After 72 hours, the clot begins to resorb, and the pain resolves spontaneously. Excision is unnecessary, but sitz baths and analgesics are often helpful.
Operative Hemorrhoidectomy
A number of surgical procedures have been described for elective resection of symptomatic hemorrhoids. All are based on decreasing blood flow to the hemorrhoidal plexuses and excising redundant anoderm and mucosa.
Closed Submucosal Hemorrhoidectomy
The Parks or
Open Hemorrhoidectomy
This technique, often called the Milligan and Morgan hemorrhoidectomy, follows the same principles of excision described above, but the wounds are left open and allowed to heal by secondary intention.
Whitehead’s Hemorrhoidectomy
Whitehead’s hemorrhoidectomy involves circumferential excision of the hemorrhoidal cushions just proximal to the dentate line. After excision, the rectal mucosa is then advanced and sutured to the dentate line. While some surgeons still use the Whitehead hemorrhoidectomy technique, most have abandoned this approach because of the risk of ectropion (Whitehead’s deformity).
Stapled Hemorrhoidectomy
Stapled hemorrhoidectomy has been proposed as an alternative surgical approach. 81–83 Unlike excisional hemorrhoidectomy, stapled hemorrhoidectomy does not aim to excise redundant hemorrhoidal tissue. Instead, stapled hemorrhoidectomy removes a short circumferential segment of rectal mucosa proximal to the dentate line using a circular stapler. This effectively ligates the venules feeding the hemorrhoidal plexus and fixes redundant mucosa higher in the anal canal. Critics suggest that this technique is only appropriate for patients with large, bleeding, internal hemorrhoids, and is ineffective in management of external or combined hemorrhoids. Although stapled hemorrhoidectomy has not been widely accepted at this time, it remains a promising new technique.
Milligan-Morgan operation
After operation hemorrhoidectomy may appear early (bleeding from the wound) and later (stricture of anal canal) complications. With the aim of prevention of bleeding at hemorrhoidectomy leg is ligated with silk ligation, and the wound – by node ligations to bottom. For prevention of stricture of anal canal there makes sense to extract nodes not more than in 4 places. During this between extracted nodes there must stay not injured mucosa. When indicated, if after operation surgeon revealed the stricture of entrance into anal canal, hemorrhoidectomy is finished by dosed sphincterectomia.
During appearance of stricture of anal canal by posterior comissure scar in extracted, there is provided dosed sphincterectomia, and then mucosa is connected with perianal skin with further fixation by separate ligations.
Complications of Hemorrhoidectomy
Postoperative pain following excisional hemorrhoidectomy requires analgesia usually with oral narcotics. Nonsteroidal anti-inflammatory drugs, muscle relaxants, topical analgesics, and comfort measures, including sitz baths, are often useful as well. Several studies show that stapled hemorrhoidectomy is associated with a significant decrease in postoperative pain. Other complications are similar to those seen with excisional hemorrhoidectomy. Urinary retention is a common complication following hemorrhoidectomy and occurs in 10 to 50% of patients. The risk of urinary retention can be minimized by limiting intraoperative and perioperative intravenous fluids, and by providing adequate analgesia. Pain can also lead to fecal impaction. Risk of impaction may be decreased by preoperative enemas or a limited mechanical bowel preparation, liberal use of laxatives postoperatively, and adequate pain control. While a small amount of bleeding, especially with bowel movements, is to be expected, massive hemorrhage can occur after hemorrhoidectomy. Bleeding may occur in the immediate postoperative period (often in the recovery room) as a result of inadequate ligation of the vascular pedicle. This type of hemorrhage mandates an urgent return to the operating room where suture ligation of the bleeding vessel will often solve the problem. Bleeding may also occur 7 to 10 days after hemorrhoidectomy when the necrotic mucosa overlying the vascular pedicle sloughs. While some of these patients may be safely observed, others will require an exam under anesthesia to ligate the bleeding vessel or to oversew the wounds if no specific site of bleeding is identified. Infection is uncommon after hemorrhoidectomy; however, necrotizing soft-tissue infection can occur with devastating consequences. Severe pain, fever, and urinary retention may be early signs of infection. If infection is suspected, an emergent examination under anesthesia, drainage of abscess, and/or débridement of all necrotic tissue are required.
Long-term sequelae of hemorrhoidectomy include incontinence, anal stenosis, and ectropion (Whitehead’s deformity). Many patients experience transient incontinence to flatus, but these symptoms are usually short-lived and few patients have permanent fecal incontinence. Anal stenosis may result from scarring after extensive resection of perianal skin. Ectropion may occur after a Whitehead’s hemorrhoidectomy. This complication is usually the result of suturing the rectal mucosa too far distally in the anal canal and can be avoided by ensuring that the mucosa is sutured at or just above the dentate line.
RECTAL FISSURES
Rectal fissures are linear or triangle shaped defects of anal mucosa. This disease takes 3rd place after hemorrhoids and paraproctitis by frequency.
Etiology and pathogenesis
The most wide spread theories of appearance of fissures are mechanic and infectious. Due to the first, appearance of fissures is conditioned by injury of anal mucosa by dense feces in combination with constipation and diarrhea. Diseases that promote formation of fissures are proctosigmoiditis, enterocolitis and hemorrhoids. Often fissures accompany gastritis, gastric and duodenal ulcers.
By infectious theory fissures appear at inflammation of anal glands (criptitis) that lead to tissue fibrosis and decrease of their elasticity. Appearance of disease also may be promoted by syphilis, tuberculosis, homosexualism.
Classification
Rectal fissures by clinical course are divided onto acute and chronic. They may be complicated (paraproctitis, malignization, bleeding, pectenosis) and combined with other diseases of anal canal (hemorrhoids, criptitis, polypus).
Rectal fissures
Symptoms and clinical course
Such disease is seen mostly in women of middle age. Fissures are mostly situated in area of posterior comissure on 6 hours by clock dial in patient’s position laying on back. More rarely fissures are situated on anterior and lateral walls. On posterior wall of anal canal conditions of bleeding are worse, that’s why there is more danger of mucosal injury during defecation, it is connected with pressure of feces during their motion onto posterior and anterior commissures. Fissure mostly has longitudinal direction and hides between skin folds in anal area. In chronic course near external edge of fissure there appear skin fold with undermined edges, so called terminal tuberculum. On internal edge of fissure there is tuberculum of smaller size. In rare cases there are seen two fissures at the same time.
Clinical picture of anal fissure includes triad of symptoms: pain during or after defecation, spasm of sphincter, and low bleeding during defecation.
Pain in patients with rectal fissures has burning character connected with moving of volumatic dense feces through anal canal. It depends also on degree of reflection of sphincter spasm, irradiates into perineum, genitalia, urinary bladder, back, and conditions disuric signs in males and dysmenorrhea in females.
Sphincter spasm during the onset of the disease may be small. In chronic course it may lead to proliferation of connective tissue.
Blood in feces appears during or after defecation, it has bright red color and is excreted mostly in small quantity.
After examination of patient with such pathology you should ask him to exert himself in relaxed sphincter, it is like defecation. In such conditions anus lowers and deep areas of skin, terminal fold and mucosa become visible. It lets us examine external area of fissure. In incredible spasm of sphincter patient is moved onto table in position on side with legs near abdomen or in “knee-elbow” position, with the help of napkins they carefully move tissues of anus toward different sides. During this in that region of anal ring where is predicted localization of fissure they examine deep skin folds. In careful investigation there may be found fissure without severe pain for patient.
Variants of clinical course and complications
Acute fissure is characterized by acute onset, presence in anal area of linear longitudinal wound with soft bottom and length 1-
Chronic fissures may disturb patients from two months to 1 year and more. In prolonged existence fissure transforms into chronic ulcer with dense sclerozing bottom. In patients with chronic fissures there may appear complications.
Bleeding at rectal fissures is mostly low. There is observed excretion of bright red blood during or after defecation. In extraordinary cases even low but frequent bleeding from rectal fissures leads to revealed anemia.
Pectenosis is revealed in chronic fissures. At this pathology sphincter muscles are replaced by connective tissue and the patient gets coprostasis. Any examination of rectum is impossible because of narrowing of rigid anal ring.
At paraproctitis as a complication of fissure the entrance for infection is crypt through which inflammatory process is spreaded. The patient suffers from pain of pulsing character in area of rectum and perineum, fever. During palpation of perianal region there appear severe pain. Punction lets reveal purulent focus.
Malignization is characteric for prolonged fissure. In such cases pain decreases, there is observed ulcer with dense bottom with grey covering. In first portions of feces there appears blood with bad smell. Excisional biopsia with further histological investigation helps to find out the malignization of fissure.
Diagnostic program
1. Anamnesis and physical data.
2. Examination of canal by stretching of anal tissues.
3. Finger examination of rectum.
4. investigation of rectum by rectal mirror.
5. Rectoromanoscopia (contraindicated in pectenosis).
6. General analysis of blood and urine.
7. Coagulogram.
8. Sedimentation reactions (reaction of Wassermann).
Differential diagnostics
Chronic fissures of rectum should be often differentiated with other diseases that may have the same local signs.
Proctalgia. Pain is localized in the area of rectum. Consider, that the reason of proctalgia is pathology of the higher nervous system (neuroses, hysteria). At objective examination the visible organic changes are not exposed.
The anal form of non specific ulcerous colitis is characterized by the superficial damage of rectum – hyperemia and edema of mucus, formation of shallow ulcers and erosions. As a rule, non specific ulcerous colitis with all its signs begins from the distal part of rectum.
Kron’s disease of rectum begins from submucosal layer, ulcers do not spread much, they mostly are like fissures that penetrate onto all depth of intestinal wall, have longitudinal and transversal directions, and may cause formation of fistules and abscesses. At histological investigation during Kron’s disease there is revealed granuloma.
Cancer of rectum. Presence in anal canal of formation with not smooth edges and additions of blood in feces gives a possibility to suspect malignization of fissure. Morphological investigation of bioptates with presence of atypical cells proves malignant process.
Tactics and choice of treating method
Acute fissures are treated conservatively.
Treatment includes diet therapy, prescription of remedies and physiotherapeutic procedures.
Diet therapy means excluding from ration spicy and salty food, introduction of oral-oil substances that regulate feces.
They use warm procedures (baths, hot water bottles), physiotherapeutic measures (darsonvalization, UHF, diathermia).
Medicamentous therapy means prescription of anti-spasmatic (spasmalginum, no-spa, spasmolytinum) and analgetics (promedolum, baralginum).
Rectally they use micro enemas (oily, antiseptic), rectal suppositoria (with belladonna, anaesthesinum and their standard forms – proctosedylum, G preparation). Under the fissure by injection they introduce hydrocortizonum with novocainum.
Transverse cut of the mucosa above the upper merge of the Rectal fissures
End view of the operation
Indications for surgical treatment are chronic ulcer complicated by pectenosis, fistule, bleeding, and also non effective conservative treatment. From radical methods we recommend cutting of fissure in longitudinal direction including all the fissure into deleted part. Operation is added by dosed sphincterectomia. Defect of mucosa is closed in transversal direction by ligation of rectal mucosa to perianal skin.
POLYPS OF COLON AND RECTUM
Polyps are non malignant tumors on legs that grow from mucosa.
Etiology and pathogenesis
Reasons of polyp’s appearance are disorders in embryonal development , inflammatory processes of mucosa and also viral infection.
Pathomorphology
Polypus of inflammatory origin differ from adenomatous ones by their incorrect form and size variety. They are soft, filled with blood, often with ulceration and hematomas. Such polypus usually combine with other signs of inflammation in intestine.
Adenomatous polypus are often part of syndromes. Thus, combination with non malignant tumors of bones, skin and soft tissues is characteric for Gardner’s syndrome, combination with focal melanosis of mucosa – for Peitz-Eggers’ syndrome, combination with brain tumors – for Turco’s syndrome.
Classification
By etiology:
· Innate (hereditary, family)
· Acquired (at inflammatory processes)
Separately they define also children (juvenile, innate and acquired).
By process’ spreading:
· Single
· Multiple
· Total (injury of all intestines).
By external appearance and microscopic structure:
· True (glandular, fleesy, from multi layer epithelium)
· False (hypertrophic at ulceric colitis, fibrose).
Symptoms and clinical course
Men get this disease in 2-3 times more than women. Single polypus of colon and rectum have usually latent course and are often revealed accidentally.
Multiple polypus may lead to diarrhea, bleeding, changes in morphological and biochemical blood composition. At this children do not devlop properly. At distal localization in some patients polypus prolapse and strangulate in anal ring causing pain. Low situated polypus irritate rectum and cause tenesmas, sometimes they cause prolapse of intestinal wall.
Among disease’s symptoms first palce belongs to disorders of defecation and blood in feces with further anemia, hypoproteinemia, decrease of workability. Fleesy polypus leads to disorders of water-salt and protein metabolism, because mucus’ excretion at defecation may achieve
At multiple polyposis they define triad of symptoms:
1. Pigment spots (on the face, lips, mucosal membranes of cheeks, fingers, and other areas of covering epithelium).
2. Polyposis of digestive tract.
3. Hereditary character of disease.
Finger examination of rectum and observation with rectal mirror give a possibility to investigate its lower part. During this procedures you can reveal polypus of different size situated on jucosa of rectum and also polypus prolapsed with invaginate of sygmoid colon.
Irigography reveals single and multiple defects of filling (Pic. 4.1.13), so called symptom of “shooted aim” that may be seen in different parts of colon. At presence of invaginate as complication of polypus there is charactering defect of filling.
With the help of rectoromanoscope you can examine rectum and sigmoid colon on average height
Variants of clinical course and complications
Polypus of small size at the onset have latent course. With their growth during moving of feces may occur disorder of their completeness with further possible complications. More often is bleeding that in most cases occur defecation. Depending on the height of polypus’ localization in intestine blood may be dark red to bright red color. Blood loss may be from small, light to severe, with signs of small and incredible anemia.
In most patients polypus have a tendense to malignization. Provided biopsia in pre operation period with morphological investigation reveals malignant transformation of tissues and proves this diagnosis not in all cases. It depends on that in what part polypus becomes malignant. Final diagnosis may be put after the operation during histological investigation of all polypus.
Polypus of big size situated in rectum usually strangulate. During this strangulation takes place on the level of anal ring and is accompanied with severe pain. Not reducible polypus may necrotize.
Polypus are situated in caecum, colon and sigmoid colon. In the most motile areas they may lead to intestinal invagination. In this case there appear spastic pain, blood excretion with feces. During abdominal palpation they reveal painful infiltrate. Invagination may prolapse into rectal lumen.
Diagnostic program
1. Anamnesis and physical data.
2. Finger investigation of rectum.
3. Investigation by rectal mirror.
4. Rectoromanoscopy.
5. Irigography.
6. Fibrocolonoscopy.
7. General analysis of blood and urine.
8. Coagulogram
Differential diagnosis
Polypus of colon and rectum should be differentiated with malignant and non epithelial tumors, non specific ulcer colitis and rectal fissures.
Cancer of right part of colon ahs a course with incredible anemia (toxicoanemic form) due to absorption of tumor’s toxic products, their action on hemopoetic organs.
Cancer of left part of colon is usually accompanied with signs of obturative intestinal impassability. Additional examination (finger rectal examination, irigography, endoscopic methods) give a possibility to prove the diagnosis.
At chronic course of non specific ulcer colitis there is injured mucosa of intestine, and little islands of not injured mucosa between multiple big ulcers look like polypus, so called pseudopolyposis. Detailed anamnesis, specialities of clinical course of the disease, irigography and colonoscopy exclude presence of true polypus.
Not epithelial tumors (leyomyoma, lipoma) are situated under intestinal mucosa and at their small size do not cause any symptoms. With their growth mucosa is injured, there occurs bleeding with its signs. X-ray and endoscopic methods of investigation, and also histological investigation prove the final diagnosis.
Chronic fissure of rectum with not smooth edges and terminal tuberculum often simulates true polypus. Removal of this formation both with fissure and provided histological investigation help in proving of diagnosis.
Tactics and choice of treating method
Conservative method of treatment is rarely used. For this is used solution of green greater celandine for its introduction in enemas (3-
Because of polypuses of small intestine and rectums are inclined to malignization, the basic method of its treatment is surgical .
Methods of operative treatment at polypus are divided into two groups:
1. Local operations (endoscopic electrocoagulation, polypus’s removal). Indication for electrocoaguclation is presence of single polypus oarrow leg, rarely – multiple polypus. Depending on the localization polypus on wide leg are removed through rectum of by laparotomy with further colotomy.
2. Radical operations as resection of separate segments of colon, right-side, left-side, subtotal colectomy or coleproctectomy are provided at multiple polypus.
PARAPROCTITIS
Acute paraproctitis is acute inflammation of pararectal cellular tissue. They take near 30% of all diseases of rectum.
Etiology and pathogenesis
In most cases paraproctitis is caused by polymicrobial flora. During inoculation of purulent content there are usually revealed staphylococci, E. coli, Gram positive and Gram negative rods. Causative agents of tuberculosis, actinomycosis, syphilis are rare causative agents of paraproctitis. Clostridial infection causes occurance of gas gangrene of pelvis cellular tissue. In etiology of paraproctitis the great role belongs to penetration of infection into pararectal cellular tissue, status of organism’s immunity, presence of additional diseases (diabetes mellitus). Infection may penetrate through ana glands, injured rectal mucosa, and also by hematogenic and lymphogenic way from neighbour organs injured by inflammatory process. Every anal crypt collects openings from 6-8 anal glands. Thus, anal crypt is opened gate for infection. After that follow swelling and obturation of duct connecting anal gland with anal crypt. Due to that there forms purulent cyst that opens and infection gets into perianal and perirectal spaces.
Pathomorphology
Morphologically there is defined purulent inflammation of crypts with further spreading to perirectal, ischiorectal and pelvis cellular tissue. Purulent inflammation usually is as phlegmone or (rarely) abscess.
Classification
1. By etiology – usual, anaerobic (gangrenous-putrefactive, ascendent anaerobic lymphangitis, anaerobic sepsis), specific, traumatic paraproctitis.
2. By localization – submucosal, subcutaneous, oschiorectal, pelviorectal, retrorectal paraproctitis
Separately there is defined secondary paraproctitis at which inflammatory process spreads to pararectal cellular tissue from prostate gland or female genitalia.
Symptoms and clinical course
Paraproctitis has as local as general symptoms. The most often are pain in anal region of rectum, swelling, hyperemia, fluctuation, constipation, sometimes – disuria, increase of body temperature, loss of appetite and workability.
During general blood analysis there are leukocytosis with left disposition of leukocyte formula, SES increase. If in-time operative treatment shouldn’t be provided, period of disease may increase to 10 days and more. After that there comes independent opening of abscess into rectum (chronic paraproctitis), formation of recurrent paraproctitis or reconvalescense.
Variants of clinical course and complications
Subcutaneous, submucoal and ischiorectal paraproctitis ar characterized mostly by typical course, there usually are no difficulties in putting of diagnosis. Pelviorectal paraproctitis as the most severe form is not revealed exactly. At first pain in inflammated area is not felt, disease starts from headache, fever, increase of body temperature. Sometimes on this stage of disease there is put such diagnosis as influenza. After that appears pain in lower part of pelvis that irradiates into uterus, urinary bladder causing disorders of urination. Patients get treatment in urologist, gynecologist and therapeutist for a long time. If inflammatory infiltrate of pelviorectal cellular tissue transforms into abscess, disease becomes acute. External signs are revealed at spreading of purulent process onto ischiorectal and subcutaneous cellular tissue. It lasts in limits of one place. At the same time, processes may spread onto other pelvis part and form horseshoe shaped paraproctitis. Retrorectal paraproctitis as a kind of pelviorectal from the very beginning is accompanied with pain. During this pain is concentrated in rectum, coccygeal area, it is increased in sitting position of patient and during defecation. At this localization of abscess there may be two-side horseshoe shaped injury. Paraproctitis with clostridial infection is characterized from the beginning with sever intoxicaton, high temperature.
Palpatory in this regions there is felt crepitation. Acute paraproctitis may be complicated by fistulas, phlegmones, lymphangitis, sepsis. At clostridial infectioot in time and incomplete treatment may lead to death.
Diagnostic program
1. Anamnesis and physical data.
2. Examination of anal area and anal canal.
3. Finger examination.
4. Investigation by rectal mirror.
5. Rectoromanoscopy.
6. X-ray examination of ischial areas in lateral position.
7. Bacteriogram of purulent content.
8. General analysis of blood and urine.
9. Biochemical analysis of blood.
10. Coagulogram.
11. Sedimental reactions (reaction of Wassermann).
Differential diagnosis
Paraproctitis is differentiated with hemorrhoids, purulent dermoid cysts, suppuration of epithelial paracoccygeal canals, cancer of rectum, tumors and inflammatory diseases of sacral bone.
Acute hemorrhoids are accompanied with severe pain, swelling of perianal area, formation of thrombs iodes, nodes’ necrosis.
Suppurated presacral dermoid cyst has no connection with rectum, and paraproctitis usually does. Pararectal abscess is always connected with rectum in area of anal crypts. If suppurated cyst empties into intestine, then fistula’s direction is beyond the linea dentate.
Suppurated epithelial pericoccygeal canals are characterized by presence of point openings on coccygeal level, fistula’s direction is beyond rectum.
Cancer of rectum at the onset of the disease is usually accompanied with no pain. During examination of rectum there is revealed dense formation. Data of punctional biopsia help to prove the diagnosis.
Diseases of sacral bone as tumoral as inflammatory of the basis of osteomyelitis with injury of bone tissue structure are revealed by X-ray examination.
Tactics and choice of treating method
Method of choice for treatment of acute paraproctitis is surgical. But on early stages of pelviorectal paraproctitis with deep infiltration of tissues surrounding rectum, without signs of softening there is indicated conservative treatment (warming compress on area of perineum with 20% spiritus aethylicus, antibioitics of wide spectrum of stion, lumbal novocainum blocade, strict bed regime, exclusion of cellulose from food, usage of cleaning enemas). Surgical treatment means early operation by opening of abscess by semilunar incision with dreanging and liquidation of its inner opening (removal of crypt) through which abscess’ cavity is connected with rectum.
Opening ischiorectal paraproctitis.
At paraproctitis there may be observed transsphincter and extrasphincter directions of fistulas, at pelviorectal and retrorectal – extrasphincter. Important thing is choice of way of big abscess’ opening: through skin or mucosa from rectum. With this aim before opening of abscess by thick needle you should provide punction of infiltrated area and if exudates is got you should provide the incision. If pus of ischiorectal area is spreaded on subcutaneous cellular tissue and there are changes in shape of buttock, fluctuation, question of surgical operation has no doubt. At retrorectal paraproctitis there makes sense to open the abscess from rectal lumen. If in this case there functions inner fistule, it usually brings no troubles for patients (Pic. 4.1.7).
At signs of anaerobic infection they provide wide multiple incisions, necrectiomia, wound cavity is washed by solutions of oxidants (permanent washing), you should use antibiotics of wide action spectrum, polyvalent anti-gangrenous serum (250-300,000 units 1 time per 2-3 days), desintoxicative therapy, oxygen barotherapy (10 procedures at pressure 2 atmospheres), introduction of fresh blood blood, albumine, plasma, hemodes, rheopolyglucinum. At diabetes mellitus they provide insulin therapy and introduction of metrogilum.
After the operation there may appear early complications: bleeding from wound bottom, especially at anaerobic paraproctitis, and late – insufficiency of distal part of rectum, recidivum of paraproctitis, formation of fistules. If bleeding occurs, they provide tamponade of these areas, and if it does not stop – bleeding places are ligated. At insufficiency of sphincter there should be provided one more operation: renewal of sphincter completeness by П-like ligations.
RECTAL FISTULAS
(CHRONIC PARAPROCTITIS)
Rectal fistulas are tubular purulent canals in cellular tissue surrounding rectum and anus.
Etiology and pathogenesis
Rectal fistulas occur mostly on the basis of acute paraproctitis. Reasons of chronic fistulas are:
– opening of purulent paraproctitis without cutting of crypt;
– shortening of external anal sphincter at which fistula’s canal is pressed and excretion of its content stops;
– decreased resistance to infection and low tissue regeneration;
– epithelization of coccygeal canals.
Classification
I. By etiology and pathogenesis:
1. Innate.
2. Acquired (traumatic, inflammatory, tumoral).
II. By infection character:
1. Vulgaric.
2. Anaerobic.
3. Specific (tuberculous, syphilitic, actinomycotic etc.)
III. By anatomical signs:
1. Depending on connection with intestinal lumen (complete, incomplete, internal, external).
2. By correlation to external sphincter (intrasphincter, extrasphincter, transsphincter).
3. Depending on primary localization of inflammatory process (subcutaneous, submucosal, ischiorectal, pelviorectal).
4. Depending on localization of external and internal fistula’s canals (cutaneous, marginal, on crypt level).
5. By fistula’s shape (simple – direct, complex – curve and containing cavities).
There define 4 degrees of extrasphincter fistulas:
I degree – scar and inflammatory changes are absent.
II degree – scar process around inner fistula’s opening without inflammatory changes in pararectal cellular tissue.
III degree – purulent cavities or infiltrates in pararectal cellular tissue without scars around inner opening.
IV degree – incredible infiltrates or pururlent cavities inpararectal cellular tissue and big scar process around inner opening.
Symptoms and clinical course
Self feeling and general status of patient with chronic course of paraproctitis in most cases is satisfacting. At long time existing inflammatory focus workability decreases, increased irritability appears, sleep becomes worse. Depending on activity of inflammatory process, character of excretions fro fistula changes. After abscess opening pain decreases and may be back when process becomes acute. In most patients with rectal fistulas there are observed signs of proctosigmoiditis and chronic recurrent paraproctitis. When process becomes acute pain appears and temperature increases. There is formed purulent focus with formation of new fistula’s canals.
In most patients fistula situated near anal ring goes inside the sphincter. Fistula situated 4-
Variants of clinical course and complications
Patients with fistulas feel rush and heaviness in areas of rectum and anus. Long existing fistulas are accompanied with scar changes of anal ring (pectenosis) that difficults defecation. After fistula’s closing (between acute periods) patients have no troubles and feel healthy. In some patients there stay painful infiltrates where inflammatory process may renew. The most dangerous and rare complication of chronic paraproctitis is malignant transformation of rectal fistulas.
Diagnostic program
1. Anamnesis and physical data.
2. Examination of anal area and anal canal.
3. Finger examination of rectum.
4. Investigation by rectal mirror.
5. Rectoromanoscopy.
6. Bacteriogram of purulent content.
7. General analysis of blood and urine.
8. Biochemical analysis of blood.
9. Sedimental reactions (reaction of Wassermann).
10. Contrast fistulography.
11. Introduction of catheter into fistula’s canal.
Differential disagnosis
Chronic paraproctitis are differentiated with suppuration of epithelial paracoccygeal canals, diseases of sacral bone, fissures of rectum and suppurated presacral dermoid cysts.
Suppurated epithelial paracoccygeal canals are primary openings of fistulas in area of intergluteal folds, and fistula’s canals are situated behind the dental line and are not connected with rectum.
Diseases of sacral bone on the basis of osteomyelitis are recognized by X-ray method. At this there are revealed disorders of bone structure.
Fissures of rectal mucosa are acaompanoed with severe pain, bleeding and spasms of sphincter. Presence of wound mostly on posterior comissure proves the diagnosis.
Suppurated presacral dermoid cyst has no connection with rectum. Even if it empties into rectum, fistula’s canal is always situated beyond the linea dentata.
Tactics and choice of treating method
At conservative treatment of chronic paraproctitis (fistulas) they use sitting baths and warming compresses with 20% spiritus aethylicus. They also prescribe physiotherapeutic procedures (ultraviolet radiation, local darsonvalization, electrophoresis with 1% solution of potassium iodide, 1% novocainum solution), lavage of fistula with diluted solutions of antiseptics.
Operative treatment is indicated if fistula is present for a long time or closes for some time and then opens again after acute inflammatory period. In patients with intrasphincter fistulas there is used operation by Gabriel. Its basis is that fistula is cut from inner to external opening. Skin that covers the fistula is cut as triangle. Its peak includes internal opening, and basis is situated outside (Pic. 4.1.8).
In case of fistula going through inner parts of sphincter (transsphincter fistula) during canal removal there are injured fibers of sphincter. For renewal of cut sphincter there are used node of П-like ligations. At extrasphincter fistulas there are used such operations:
Ryzhykh-I – they remove fistula’s canal in perineal wound to rectal wall and cut in basis. Stump of fistula’s canal is emptied with Folkmann’s spoon, cleaned with iodine solution and ligated with two or three layers of catgut ligations. During this ligated stump of fistula’s canal is covered by surrounding tissues. Operaiton is finished with dosed sphincterotomia of inner fibers. This method is used when inner fistula’s opening is localized in posterior crypt.
Ryzhykh-II (second variant) is used when inner fistula’s opening is localized in anterior crypt or on lateral wall. Removal offistula in perineal wound is provided the same as in the first variant. Further, upon the inner fistula’s opening there is separated piece of mucosa (width 1-
By Blinnitchev, opening in rectal mucosa is closed by catgut ligations in two stairs. There is separated mucosa upon the ligated opening, it should be fixed including submucosal layer to muscular membrane and ligated by silk ligations to perianal skin. Sometimes mobilized piece is moved downwards. Mobilized mucosal-muscular piece is ligated in such a way that needle should go near the edge of terminal fold to the basis of mobilized piece. After that by separate silk ligations they fix piece’s edge to perianal skin.
Ligation method (by Hippocrates). On the wall of anal canal there should be cut inner fistula’s opening and perianal skin together with narrow stripe of mucosa. Into this layer there are put ligations No.6 and sphincter fibers are tightened. Thus, thread stretches with 1-
At extrasphincter fistulas of I degree there is used operation of Ryzhykh of Blinnitchev, or removal of fistula with ligation of sphincter. At fistulas of II degree fistulas are removed with ligation of sphincter, at III degree – operation of Blinnitchev or ligation method. At fistulas of IV degree there is used ligation method.
EPITHELIAL PARACOCCIDIOIDAL CANALS
The reasons of origin of paracoccidioidal ducts are: innate defect of development, remain of spinal chord, violation of reduction of coccygeal vertebras with stretching of tail ligament, theory of moving cells. In the mechanism of occurrence of canal inflammation there play role as trauma as infection penetration. In most cases beginning of inflammatory process in epithelial canals occurs at the same time with period of sexual development (hormonal-endocrine rebuilding of organism).
Classification
There define such stages of course of epithelial paracoccygeal canals (by Yu.V. Dooltsev and L.V. Ryvkin, 1988):
I. Epithelial paracoccygeal canals without any clinical findings.
II. Acute inflammation of epithelial paracoccygeal canals:
(a) infiltrative stage;
(b) abscess formation.
III. Chronic inflammation of epithelial paracoccygeal canals:
(a) infiltrative stage;
(b) recurrent abscess;
(c) purulent fistula.
IV. Remission of inflammation of epithelial paracoccygeal canals.
Symptoms and clinical course
Epithelial paracoccygeal canals may have no clinical findings, that’s why they are often revealed accidentally during medical examination. In such cases I distal part of intergluteal fold near occygeal apex upon the edge of anal region there are seen one or several point openings where sometimes hair grows. Diameter of those openings is from 1 to
Variants of clinical course and complications
At non complicated epithelial paracoccygeal canals patients suffer from dull pain, feeling of pressing in coccygeal region, especially during long time walking. Increased sweating in intergluteal region is accompanied with rush, sometimes there appears painful infiltrate that disappears independently.
Acute stage of the disease is characterized by changes of general and local character. Body temperature, as a rule, increases to 39-40 degrees centigrade and is accompanied with chilling. Local symptoms are severe pain in coccygeal region, sometimes with irradiation into rectum. At the same time there appear swelling, infiltration of intergluteal region, skin upon the place of inflammation becomes bluish-violet. Further, abscess is formed. During independent opening of abscess there goes purulent content of dark color with bad smell. Sometimes abscess from coccygeal region spreads to pararectal and even pelviorectal spaces, but as a rule it does not open into rectal lumen.
Diagnostic program
1. Anamnesis and physical data.
2. Examination of coccygeal and anal regions.
3. Finger examination of rectum.
4. Investigation by rectal mirror.
5. Rectoromanosopy.
6. Bacteriogram of purulent content.
7. General analysis of blood and urine.
8. Biochemical analysis of blood.
9. Sedimental reactions (reaction of Wassermann).
10. Contrast fistulography.
11. X-ray examination of pelvis bones.
Differential diagnosis
Presacral cyst teratoma both with epithelial paracoccygeal canal at the initial stage and period of complications’ absence are differentiated easily, because when teratoma is present, finger examination of rectum gives a possibility to reveal tumor-like formation in presacral region. Complication of cyst teratoma with fistulas is differentiated with suppurated paracoccygeal canal with incredible difficulties. Provided contrast fistulography of fistula’s canals at cyst teratoma gives a possibility to define its localization in presacral region, and epithelial canal may often be branched and ends blindly in soft tissues behind the coccygeum.
At paraproctitis epithelial opening in intergluteal fold is usually absent, and fistula’s canal in most cases is connected with rectal lumen and is revealed during finger examination or investigation by rectal mirror. At pressing on pararectal region from fistula’s canals there appears purulent content. Preliminarly introduced tampon is stained by methylene blue at the moment of its getting into external opening of fistula.
Osteomyellitis of pterygoideal bone and coccygeum is often connected with injury of this region. On observing X-ray grams there is revealed characteristic picture of injured bone (foci of osteoporosis and sequesters). Fistulography helps in proving of diagnosis. Two independent diseases – epithelial paracoccygela canals and osteomyelitis of sacral bone and coccygeum – at the same time may be combined in one patient extremely rarely.
Tactics and choice of treating method
In treatment of epithelial paracoccygela canals surgical method is preferred. Only in stage of infiltrate with the aim of stopping of further inflammation development they provide novocainum blockade (100 ml of 0.25% solution with antibiotics). Every day during 5-6 days there should be applied compresses with Vishnevskiy’s ointment, physiotherapeutic methods are used (UHF, diathermia, ultraviolet rays).
Important meaning in preparation to operation belongs to sanation of purulent fistula’s canals. After inoculation of excretion from canals, determination of microflora and sensibility to antibiotics they provide pre operational sanation by some remedies.
In case of abscess formation of paracoccygeal canals abscess is opened in urgent order. During this they use two main positions of patient on operation table: on the abdomen and on the side. When patient lays on back (by Depage) feet end of the table is moved downwards on 45 degrees. Angle corresponds to projection of coxal articulations. Legs are moved to the sides and feet are situated on the support. Such position in most cases is used during operations under local anesthesia. General anaesthesia is used in position on the side. Patient lays on right side with legs bended in coxal articulations. Left leg is situated on the right, during this left thigh is near abdomen. After anesthesia by two semilunar incisions along the middle line surgeon opens the abscess. If it spreads laterally from intergluteal fold it should be opened and removed too. In average 10% of patients where abscess included epithelial canal and got proteolytic action of pus, after not palliative operation of abcess opening there was no recurrent and reconvalescence became. Thus in 90% cases during abscess opening there stay walls of epithelial canal and its branches, there is formed secondary fistula, but after lowering of inflammatory process there is needed one more radical surgical operation. It includes removal of epithelial canal, its branches together with infiltrated surrounding tissues, purulent formations, with this aim they introduce methylene blue preliminary. Further, depending on presence or absence of infiltrate and abscesses, quantity of fistulas, radical operation is finished by one of methods: complete closing of wound, opened wound tamponade, ligation of wound edges to the bottom. When epithelial canals are revealed accidentally or in small symptoms of inflammation, absence of infiltrates, abscesses wound is closed completely including its bottom (Pic. 4.1.10).
In rare cases when after opening and removal of abscesses there stays big wound surface, wound should be treated by opened method. For sanation of such wounds, except usual remedies, they use laser and ultrasound.
At abscesses and secondary fistulas in most cases there should be provided radical operation: wound edges are to be ligated to its bottom. During removal of lateral fistula’s canals because of absence of fossa in this region there are applied rare situational ligations onto wound edges not including the bottom.
In surgical practice in treatment epithelial paracoccygeal canals there should be taken into account anatomical variants of structure of sacral-coccygeal-gluteal region. In most patients there may be high position of buttocks, deep intergluteal fold, acute angle between buttocks and middle line of sacrococcygeal region, close position of primary epithelial opening from anus.
After incision of suppurated paracoccygeal canal before ligation of wound edges to its bottom there appears need to remove subcutaneous cellular tissue through all length from both wound sides. During this narrow skin pieces easily and closely situate during their ligation to wound bottom. The last in this case is healed with narrow scar.
In patients with middle and low localization of buttocks with more dull angle of position, less depth of intergluteal fold, higher position of epithelial paracoccygeal canal after its removal wound edges are ligated to the bottom in such a way that ligation includes skin, cellular skin, bottom and go outside through cellular tissue on the opposite side 1-
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