Meckel Diverticulum & Hemorrhoids PDF

Meckel diverticulum Meckel diverticulum The blind pouch is located on the antimesenteric side of the small bowel Clinical picture Generally asymptomatic. Bacterial overgrowth may lead to vitamin B12 deficiency. Heterotopic gastric mucosa may cause peptic ulcer in the adjacent intestinal...

Meckel diverticulum Meckel diverticulum The blind pouch is located on the antimesenteric side of the small bowel Clinical picture Generally asymptomatic. Bacterial overgrowth may lead to vitamin B12 deficiency. Heterotopic gastric mucosa may cause peptic ulcer in the adjacent intestinal mucosa ❑Intestinal bleeding or ❑Symptoms resembling acute appendicitis  Hirschsprung disease (Congenital aganglionic megacolon) Genetics: It is more heterogeneous frequent in 50% of familial Occurs in 1 in 5000 those with cases result from M>F (4:1). inactivating to 8000 live births other mutations in RET congenital genes and RET anomalies. ligands *  Arrest of the migration of neural crest-derived cells OR Premature death of before reaching the anus ganglion cells Pathogenesis Aganglionic segment (in This causes functional rectum usually) is formed obstruction and that lacks both the progressive distention of Meissner and Auerbach the proximal colon. myenteric plexuses Morphology Lack of ganglion cells and ganglia in the muscle wall and submucosa of the affected segment. The affected segment is Undergoes dilation – not distended. sometimes massively The wall may be thinned The proximal segment by distention or thickened (properly innervated): by compensatory muscle hypertrophy. The mucosa may be intact or ulcerated (stercoral ulcers) Hirschsprung disease Clinical Features Neonates with delayed passage of meconium, followed by vomiting in 48 to 72 hours. When involve a very short segment of rectum, manifestations may appear in later infancy: ❑ Alternating constipation & diarrhea. Complications: ❑Superimposed enterocolitis with fluid and electrolyte disturbances. ❑Perforation of the distended colon & peritonitis.  BOWEL OBSTRUCTION Major causes of intestinal obstruction Mechanical Obstruction → Usually affects the small intestine Hernias Adhesions Most common (80%) Intussusception Volvulus Tumors Less common Infarction Inflammatory strictures* Obstructive gallstones, fecaliths, foreign bodies Congenital stricture, atresias Congenital bands Meconium in cystic fibrosis Imperforate anus Hernia A weakness or defect in the wall may permit protrusion of serosa-lined sac of peritoneum (hernial sac). The usual sites of weakness are: ❑The inguinal canal ❑The femoral canals ❑The umbilicus ❑Surgical scars. Segments of viscera (most commonly small bowel*) or omentum intrude and become trapped in the hernial sacs. Inscisional Hernial sac Complications Pressure at the neck of the pouch may impair venous drainage of the trapped viscus. Subsequent stasis & edema leading to permanent entrapment(incarceration). Further compromise of its blood supply lead to infarction of the trapped segment (strangulation).  Adhesions Causes of intra-abdominal adhesions: ▪ Surgical procedures. ▪ Infection (localized or generalized peritonitis). ▪ Endometriosis. The intestines may become trapped within the loops of adhesion (internal herniation).  Telescoping of a proximal segment of bowel (intussusceptum) into the immediate distal segment (intussuscipiens). Causes: ▪ In children, may be due to viral infection. Intussusception ▪ In adults, intraluminal mass or tumors. Complications: Intestinal obstruction. Compromised vascular supply & infarction. Intussusception Volvulus Twisting of a loop of bowel about its mesenteric base of attachment (usually clockwise), constricting the venous ± arterial flow Complications: ❑Intestinal obstruction ❑+ Infarction Intestinal obstruction  May affect small or large Ischemic bowel intestine or both. disease Common in later age of life. VASCULAR Angiodysplasia DISORDERS Hemorrhoids  Predisposing factors Arterial thrombosis: Severe atherosclerosis (at the origin of the mesenteric BVs) Systemic vasculitis Dissecting aneurysm Ischemic Arterial embolism: Cardiac vegetations & mural thrombi (IE, MI, AF) Bowel Aortic atheroembolism Venous thrombosis (rare): Disease Venous stasis & hypercoagulable states Non-occlusive ischemia: Cardiac failure, shock & vasoconstrictive drugs Miscellaneous: Radiation injury, aortic aneurysm, volvulus, stricture, hernias, tumors, portal HTN, & trauma The effect of ischemia Depends on: ❑Acute or insidious onset ❑The vessel involved ❑The presence of collateral circulation Acute occlusion of a major trunk - celiac, superior, & inferior mesenteric arteries-may lead to infarction of extensive segment. Acute bowel Acute ischemia ischemia Transmural infarction Infarction involving all visceral layers Usually caused by acute occlusion of a major mesenteric vessel. Gross appearance: ❑Dark red hemorrhagic appearance ❑Begins in the mucosa and extends to serosa that becomes covered with fibrinous exudate within18 to 24 hours Infarcted small bowel Transmural infarction Microscopic appearance: ❑Hemorrhagic infarction* ❑Marked edema, hemorrhage, necrosis, and sloughing of the mucosa. Complications: ❑Within 24 hours intestinal bacteria produce gangrene** and sometimes perforation.  Sudden onset of severe Clinical abdominal pain Bloody diarrhea. Features Diagnosis requires a high index of suspicion in the May lead to shock and appropriate context (e.g., old vascular collapse within hours. age with recent major abdominal surgery, recent MI, AF, or IE). The mortality rate approaches 90%. Mural and mucosal infarctions Mural infarction: ❑Infarction of the mucosa and submucosa sparing the muscular wall. Mucosal infarction: ❑Infarction of the mucosa no deeper than the muscularis mucosae. Both result from acute or chronic hypoperfusion or more localized anatomic defects. Mucosal infarction of small bowel  Most common site is splenic flexture. Chronic inflammation and ulceration mimicking Inflammatory bowel disease. May lead to fibrous stricture. Chronic bowel Clues to diagnosis: ischemia ❑Preserved or minimal distortion of architecture ❑Hyalinization of lamina propria ❑Hemorrhage  Ischemic colitis Hypremic mucosa covered by fibrinous exudate Ischemic colitis Regenerating epithelium and hyalinization of lamina propria  Unexplained abdominal pain Gastrointestinal bleeding Clinical picture History suggestive of ischemia or hypoperfusion Mucosal and mural infarctions are not fatal and may heal if the cause of hypoperfusion can be corrected Hemorrhoids Definition: “ Variceal dilations of the anal and perianal submucosal venous plexuses” After age of 30 yrs as a result of ⇑ venous pressure within the hemorrhoidal plexus.  Predisposing conditions: ❑Chronic constipation Hemorrhoids ❑Venous stasis of pregnancy ❑Portal hypertension ❑Intra-abdominal tumors  Hemorrhoids Internal hemorrhoids: ❑ Varicosities in the superior and middle hemorrhoidal veins. ❑ Appear above the anorectal line. ❑ Covered by rectal mucosa. External hemorrhoids: ❑ Varicosities of inferior hemorrhoidal plexus ❑ Appear below the anorectal line ❑ Covered by anal mucosa.  Asymptomatic. Bleeding. Thrombosis (pain). Clinical picture Internal hemorrhoids may prolapse during straining at stool, and become trapped by the anal sphincter and lead to: ❑Painful, edematous hemorrhagic enlargement ❑Strangulation  The most common type of acquired diverticulua (False). COLONIC DIVERTICULOSIS 50% of western countries people (DIVERTICULAR older than 60 years. DISEASE) → Consumption of a refined low- fiber diet.  Two important influences: 1. Exaggerated peristaltic contractions with abnormal elevation of intraluminal pressure due to low fiber diet. Pathogenesis 2. Focal defects peculiar to the normal muscular colonic wall (where nerves and arterial vasa recta penetrate the muscular wall).  Low-fiber diet results in: ❑Reduced stool bulk ❑↑difficulty in passage of intestinal contents. Exaggerated Segmentation: peristalsis ❑Exaggerated spastic contractions isolate segments of the colon with high intraluminal pressure Consequent herniation of the bowel wall through the anatomic points of weakness. Morphology Site: In the sigmoid colon in 95% of patients. Gross appearance: Multiple, Small, flask-like or spherical outpouchings. Located in the mesentric & lateral aspect of the bowel along sides of taeniae coli. Prominent taenia coli and circular muscle bundles (due to hypertrophy).  Diverticulosis Section through the sigmoid colon showing multiple saclike diverticula protruding through the muscle wall into the mesentery Diverticulosis  Morphology Microscopic appearance: The walls are very thin, made up of mucosa and submucosa enclosed within fat or peritoneal covering. Protrusion of mucosa and submucosa through the muscle wall  Diverticular disease is usually asymptomatic. In 20% of cases, intermittent cramping or continuous left lower quadrant pain. Clinical Complications: features Diverticulitis & peridiverticulitis* (left lower quadrant tenderness and fever). Stricture formation. Lower GI bleeding (Chronic intermittent or rarely massive). Perforation may lead to pericolic abscess, fistula formation or localized peritonitis.