DIVERTICULAR DISEASE

DEFINITION
y A common condition of uncertain aetiology in which serosa-covered out-pouchings (diverticula) of mucosa occur through gaps in the muscularis propia Pseudo (false) diverticula : mucosa & serosa only Rarely true diverticula : solitary caecal consisting of all 3 layers. Congenital : Meckel s diverticulum

MECKEL S DIVERTICULUM
y Meckel diverticulum is the most common congenital abnormality of the small intestine it is caused by the failure of the vitelline duct ( ie, omphalomesenteric duct) to completely obliterate at 5-7 weeks' gestation if vitelline duct is full unobliterated, serous sinus discharge will leaks from umbilicus, while if the proximal part of he duct is unobliterated it will lead to a development of Meckel divertiulum

Rules of 2 s y y y y y y y

2% of population 2 feet from ileo-caecal valve 2 inches length 2% symptomatic 2 types of common ectopic mucusa (gastric,pancreatic) 2 years most common age at clinical presentation 2 times boys are more liable than girls

ZENKER S DIVERTICULUM
Zenker's diverticulum, is a diverticulum of the mucosa of the pharynx, just above the cricopharyngeal muscle.Its caused by y increased intraluminal pressure that is caused by incoordination of the the cricopharyngeus muscle (CPM). It occurs in an area of anatomic weakness known as Killian's dehiscence between the lower pharyngeal constrictor and the CPM. y Reflux (the regurgitation of stomach acid and pepsin, a proteolytic enzyme) is thought to result in dysfunction and hypertrophy of the CPM y The development of a ZD is thought to be secondary to prolonged dysfunction of the CPM over many years

DIVERTICULOSIS vs DIVERTICULITIS
y Diverticular disease occurs when pouches (diverticula) in the intestine, usually the large intestine or colon, become inflamed. Most diverticula occur in the sigmoid colon, the curved part of the large intestine closest to the rectum, and they tend to become more numerous as we age. Diverticulosis is the presence of many diverticula along the intestinal wall. It occurs more commonly in countries such as the U.S. where the diet is generally low in fiber. More than 50% of adults over age 70 have diverticula, and 80% have no symptoms. Diverticulitis occurs when one or more diverticula become inflamed. The inflammation may be local (just in the area of the diverticulum), or may spread to the abdominal lining (peritoneum), called peritonitis. Small (microscopic) or large perforations (holes in the intestinal wall) occur in 15 - 20% of people who have diverticula.

Box 1: Factors Involved in the Pathogenesis of Colonic Diverticula Genetic factors (meckel s diverticulum) Environmental factors Low-fiber diet Obesity Decreased physical activity Corticosteroids NSAIDs Alcohol Caffeine intake Cigarette smoking Polycystic kidney disease (structural changes of colonic wall) Epidemiologic factors Age (increasing risk with age) Geography Life style Ethnicity

PATHO ANATOMY
y y Mainly in descending colon (90%), Sigmoid colon (10-15%) L-sided diverticular disease predominates in industrialised western societies. R-sided disease more common in Asians.

AETIOLOGY
The vasa recta penetrating the bowel wall create areas of weakness through which a portion of the colonic mucosa and submucosa (covered by serosa) can herniate. y Segmentation can occur as a result of raised intracolonic pressure in certain areas of the colon. Such segmentation represents strong muscular contractions of the colonic wall, which serve to propel the luminal content or to halt the passage of material. Segmentation in diverticulosis is exaggerated, causing occlusion of both ends of the chamber and resulting in high intrachamber pressure which forcing mucosa to herniate y Mycosis thickened circular muscle layer, shortening of the teniae, and luminal narrowing. y Elastin increased elastin deposition between muscle cells and teniae coli. Elastin is also laid down in a contracted form that causes shortening of the teniae and bunching of THE circular muscle. y Changes in structural components of colonic wall : Collagen connective-tissue diseases such as Ehlers Danlos syndrome, Marfan s syndrome, and autosomal-dominant polycystic kidney

disease result in structural changes in the bowel wall, leading to decreased resistance of the wall to intraluminal pressures and thus allowing protrusion of diverticula Changes in mechanical features of colonic wall with increasing age. Compliance is lowest in the sigmoid and descending colon and greatest in the transverse and ascending colon. This difference in mechanical properties between the right and left sides might partly account for the left-sided predominance of diverticulosis.

SIGNS AND SYMPTOMS

y y y y y y Asymptomatic Pain at any part of abdomen (usually tenderness at left iliac fossa) Bloating, irregular constipation, diarrhea flatulence (expulsion through the rectum of a mixture of gases that are byproducts of the digestion process) altered bowel habits (constipation, but diarrhea at the morning) abdominal cramping

ACUTE DIVERTICULA DISEASE y pain in the lt iliac fossa y severe rectal bleeding y abdominal finding (generalized tenderness, involuntary guarding, or decreased or absent bowel sounds) y severe abdominal distension, nausea, vomiting (bowel obsturtion) y High fever (possibility of advanced disease and sepsis from generalized peritonitis caused by perforation and spreading of inflammation in the peritoneum.) y pneumaturia, fecaluria (colovesical fistula) y Leukocytosis y Urinary manifestation (dysuria, frequency, and urgency)

COMPLICATIONS
y y y y y y intra-abdominal abscess (A collection of pus can develop around the inflamed diverticulum, leading to formation of an abscess, usually in the pelvis) Phlegmon ( persistent localized pain after ruptured of diverticulum) colonic stricture,bowel obstruction, peritonitis (diverticulum ruptures freely into the abdominal cavity causing a life threatening
infection)

Rectal bleeding. Abnormal channels (fistulae) arising from diverticulitis (inflammation) may involve/erode surrounding structures such as the bladder, vagina, uterus, or abdominal wall.

STAGING
Hinchey Classification Scheme. Patients with stage 1 disease have small, confined pericolic or mesenteric abscesses, whereas those with stage 2 disease have larger abscesses, often confined to the pelvis. Stage 3 disease, or perforated diverticulitis, is present when a peridiverticular abscess has ruptured and caused purulent peritonitis. Rupture of an uninflamed and unobstructed diverticulum into the free peritoneal cavity with fecal contamination, the so-called free rupture, signifies stage 4 disease and carries the highest risk of an adverse outcome.

Differential Diagnosis of Symptomatic Diverticular Disease and Diverticulitis

Acute appendicitis Colorectal cancer Complicated ulcer disease Crohn s disease Cystitis Ectopic pregnancy Gallbladder disease Incarcerated hernia Ovarian cyst, abscess, or neoplasm Ovarian torsion Pancreatic disease Pelvic inflammatory disease Peritonitis Pseudomembranous colitis Renal disease Small bowel obstruction

Ischemic colitis Mesenteric infarction

Ulcerative colitis

DIAGNOSIS
y Erect or supine abdominal X-ray : gas under diaphragm - pneumoperitonium (perforated viscous), multiple air-fluid level indicates intestinal obstruction

Upright radiograph: complete small bowel obstruction. Upright radiograph shows multiple air-fluid levels

Supine position : complete small bowel obstruction shows distended small bowel loops in the central abdomen with prominent valvulae conniventes (small white arrow)Bowel wall between the loops is thickened and edematous (large white arrow) Radiograph from a patient with massive sigmoid volvulus shows a distended ahaustral sigmoid loop (white arrow), inferior convergence of the walls of the sigmoid loop to the left of the midline, and approximation of the medial walls of the sigmoid loop as a summation line (black arrow).

Obstructive ileus

Radiograph shows a dilated colon with haustral markings (white arrow) and edematous small bowel loops (black arrow)

y CT scan : Possible CT findings include

pericolic fat stranding due to inflammation, colonic diverticula, bowel wall thickening, soft tissue inflammatory masses, phlegmon, and abscesses. Peritonitis, fistula formation, and obstruction can also be assessed. It can be used to guide percutaneous drainage of an abscess.

Colovesicular fistula

Perforation on abdominal CT y Contrast enema examination : complimentary to CT scan in stable patient only. Avoid barium enema or endoscope to unstable patient to prevent from further complication (eg : perforation of the diverticular site can lead to barium peritonitis) picture Shows diverticulum, with sigmoid narrowing and extravasations Double contrats study to investigate fistula formation which to be the gold standard with Sensitivity: 82% and Specificity: 81% Ultrasonography : In diverticulitis, ultrasonographic
findings include thickening of the bowel wall by more than 4 mm. Inflamed diverticula appear as round or ovoid, highly echogenic structures with a ring-down artifact. Inflammation of the pericolic fat is revealed as an area of increased echogenicity adjacent to the colonic wall. Abscess formation appears as a well-defined hypoechoic mass near the colon, and it may demonstrate shadowing because of the presence of air. The absence of peristalsis is helpful for differentiating abscess from adjacent loops of bowel.

y y

MRI, endoscopy, CT colonoscopy , angiography Nuclear imaging : Scanning with technetium-99m (99m Tc) labeled red blood cells often is performed to locate the site of active gastrointestinal tract bleeding, and it may be helpful in evaluating bleeding due to diverticulosis.

Medical management
Outpatient treatment : Patients with mild abdominal pain/tenderness and no systemic symptoms: Acute low-residue diet, Increase fibers in diet Antibiotics for 7 14 days (amoxicillin/clavulanic acid, sulfamethoxazoletrimethoprim, or quinolone + metronidazole for 7 10 days). After initiation of therapy, expect improvement in 48 72 hours. It is important to cover for Escherichia coli and Bacteroides fragilis. If there is no improvement in 48 72 hours, look for a collection intraabdominally. In-patient treatment: Patients with severe signs/symptoms (1 2% of cases): Admit the patient to hospital. Ensure bowel rest. Intravenous antibiotics (Gram-negative and anaerobic coverage) for 7 10 days Intravenous fluids Analgesia (meperidine). Meperidine is preferable to morphine, as the latter may lead to increased intracolonic pressure in the sigmoid. If there is improvement within 48 hours, then continue management, starting a low-residue diet in the acute period. Antibiotics may be switched to the oral form if the patient is afebrile for 24 48 hours and there is a decreasing white blood cell trend. If there is no improvement, phlegmon or a collection (abscess) should be suspected and investigated accordingly. y Some 15 30% of patients admitted for the management of diverticulitis will require surgery during admission, with an associated mortality rate of 18%.

Surgery management
Urgent surgical intervention is mandatory if complications occur, which include: Free perforation with generalized peritonitis Obstruction Abscess not amenable to percutaneous drainage Fistulas Clinical deterioration or failure to improve with conservative management In advanced stages of peritonitis (Hinchey stage 3,4) Hartmann s procedure, originally described in 1923, was initially intended for the treatment of cancer of the rectum. It represents a staged procedure in which the sigmoid colon is mobilized and resected, with the rectum being closed and a colostomy formed. The colostomy is closed at a later date (often around 3 months postoperatively), with restoration of bowel continuity. This staged procedure posed problems, including a second operation, rectal scarring, and difficulty in completing the anastomosis.