Surgery Small Intestine And Appendix T G

Surgery Small intestine and appendix Dr. Teresa Galdona PA-C

Small intestine Most common surgical emergencies, acute appendicitis, mechanical SBO, paralytic ileus, Crohn’s Ds. Functions: digestive, nutritional, immunological, and endocrine. ANATOMY: 3 segments: duodenum, yeyunum and ileum. Ligament of Treitz separates duodenum from yeyunum and ileum, also separates upper GIT from Lower GI track. Duodenum is mostly retroperitoneal and is encircling pancreas. Duodenum is divided in 4 segments: one of most important segments is descending there is located duodenal papilla or ampulla of Vater, also 2 small papillas, one small papilla for accesory pancreatic duct (Santorino duct) and mayor papilla for main pancreatic duct (Wirsung duct) 40% is yeyunum and 60% is ileum.

Small intestine 40% is jejunum and 60% is ileum. Blood supply: SMA for SB Duodenum blood supply by gastroduodenal art. Venous drainaje is parallel to arterial drainaje with majority of veins draining at SM vein which joins splenic vein and Inf Mesenteric that drains into Portal vein. Terminal ileum has abundant lymphatic tissue (Peyer patches) and ileum terminates at ileocecal valve. Besides this lymphatic tissue there are other 2 lymphatic tissues. One is called GALT (gut associated lymphoid tissue) located at the lamina propia and mucosa of ileum.

Small intestine The other lymphatic tissue is called MALT (mucose associated Lymphoid tissue) form by B cells from periphery of Peyer’s patches that migrate to mesenteric nodes to bloodstream then these cells return to mucosa adjacent to Peyer’s patches as B2 memory cells forming MALT. Nerve supply: Through CNS 2 systems: extrinsic and intrinsic neural plexus Pain fibers activated by intestinal distension communicate primarily by sympathetic visceral afferent fibers

Small intestine Appendix arises from cecum Blood supply via appendiceal art. terminal branch of ileocolic art. Rich in lymphatic tissue. Variable positioned called atypical like retrocecal, retroperitoneal in relation with cecum. PHYSIOLOGY: Main function is: 1) digestion of food through digestive enzimes, secretion of digestive juices, absorption of water, electrolytes, and nutrientes. 2) Motility 3) propulsion 4) storage

Small intestine Nerve innervation is given by: Enteric nervous system 1) Intrinsic neural plexus ------ Submucosal (Meissner) ------ Auerbach or Myenteric (Mucosa + smooth muscle) Ach ------ excitatory neurotransmitter at the Myenteric VIP + Somatostatin ------- inhibitory neurotransmitter These plexus determine pattern of contraction 2) Extrinsic neural plexus ------ Parasympathetic (Vagus) (giving by CNS to ANS) and pelvic parasympathetic nerves (excitatory) ------ Sympathetic (Splachnic nerves) (inhibitory) These plexus determine contraction (no type of contract. like fast or slow)

Small intestine Daily we produce about 5 to 10 Lt of digestive fluids by salivary glands, stomach, biliary tree, pancreas, and intestine which is handle by SB which absorbs about 80% of it. Na is major ion b/c it regulates osmotic gradient promoting H2O absorption. Cl ion regulates secretion of H2O. SB absorbs: fat, carbs and proteins. Triglycerides and cholesterol absorption: Fats are broken down to ---- FFA + monoglicerides + Ca Bile salt act as detergens allowing formation of micelles (smaller substrates + fat soluble Vit) micelles dissociate at the enterocyte apical membrane delivering FA, Colesteroland and monoglycerides where they cross the membrane into the cell

Small intestine Inside the enterocyte, triglycerides are reconstructed and form a new form or molecule called chylomicrons transported by lymphocytes to portal system Fat absorption occur mostly at duodenum and upper jejunum Bile salts are reabsorbed in terminal ileum Carbohydrates digestion start in the mouth by salivary amylasa and it is complete in jejunum by pancreatic amylasa and converted into glucosa, galactose and fructose Proteins are absorbed like fats in duodenum and upper jejunum Digestion of proteins star in stomach with gastric pepsin. CCK is secreted by intestinal endocrine cells and stimulated by polypeptides in intestinal lumen that in turn stimulates pancreatic secretion of peptidases (like trypsin, chymotripsin, elastase and carboxipeptidase) which breaks proteins to AA

Small intestine Certain substances are absorbed in specific segments of SB For Vit B12 + IF absorbed at terminal ileum Fat soluble Vit ADEK + bile salts are absorbed at terminal ileum Ca, Fe are absorbed at duodenum. Small intestine is rich in hormone production some of them are these: Secretin ---- produce by duodenal S cell in response to bile or acid that stimulates pancreatic production of HCO3 and H2O CCK ---- release by proximal SB mucosa in response to FA and AA and stimulates emptying of gallbladder and pancreatic enzymes

Small intestine Small intestine is rich in hormone production some of them are these: Secretin ---- produce by duodenal S cell in response to bile or acid that stimulates pancreatic production of HCO3 and H2O CCK ---- release by proximal SB mucosa in response to FA and AA and stimulates emptying of gallbladderand pancreatic enzymes

Small intestine Motilin ---- produced in jejunum and it coordinates stomach and esophageal function with SB activity during fasting. Gastric Inhibitory peptide (GIP) ---- produced by jejunal K cells and stimulates insulin release in response to carbohydrates and fat. Neurotensin ----- secreted in response to fat, stimulates pancreatic exocrine secretion that facilitates fat absorption. Glucagon like peptide 2 (GLP2) ------ potent SB trophic hormone VIP (vasoactive intestinal peptide) ---- stimulates pancreatic and intestinal secretion, inhibits gastric secretion. Gastrin releasing peptide ----- stimulates release of all intestinal hormones except secretin, helps regulate gastric acid and gastrin secretion.

Small intestine Somatostatin ----- acts as an on and off switch for intestinal hormones, gastric and pancreatic secretion and intestinal motility. It stimulates parietal cells to decrease HCL acid production, inhibits gastrin release, reduces Histamine released from ECL cells. Peptide YY---- produce in distal SB and proximal colon, affects gastric and pancreatic secretion. Small Bowel Ds: Meckel’s diverticulum It is MC congenital abnormality of SB Remnants of embryonic vitelline or omphalomesenteric duct Present in 2% of population 2:1 / male:female

Small intestine 2 types of mucosa: 1) gastric Most common) 2) pancreatic or colonic Located 2 feet of ileocecal valve S/S: Symptoms are rare, and they tend appear as the patient increases in age. ANATOMY: Caused by incomplete obliteration of vitelline duct (from midgut) Which should close between 8 th and 10 th weeks of gestation. Blood supply is from the vitelline vessels.

Small intestine Pathophysiology: Cells of vitelline duct are pluripotential ( they have multiple capabilities) and it is not rare to find different types of mucosa in there. MC mucosa find is gastric (50%), less frequent pancreatic or colonic mucosa. Because gastric mucosa can produce acid in the proximity of SB mucosa, it can cause ulceration and hemorrhage of adjacent SB. Benigns tumors like lipomas, leiomyomas, neurofibromas, and angiomas have been describe also in the diverticula, and they can act as lead point for intossusception and Bowel obstruction. Another consequence of the diverticula is that persistence of vitelline duct can cause a sinus from umbilicus to ileum, presenting as an enteric fistula at the umbilicus

Small intestine An umbilical sinus can develops when the umbilical end of the duct remains patent. It also can happen that the duct obliterates but leaves a fibrous cord remnant that can act as a fixation point of SB to abdominal wall and cause BO. Finally the diverticula can be occluded by fecal material and become inflamed, presenting like an appendicitis. It can present as: 1) Obstruction: intestinal obstruction can happen b/c of volvulos of SB around the diverticula or a constrictive effect of a mesodiverticular band.

Small intestine 2) hemorrhage: can present as BRBPR, mostly painless, in infants <than 2 years of age. Dx: 90% with radionuclide scanning using Technetium 99m which is pick up by ectopic gastric mucosa that delineates the diverticula 3) intossusception: when diverticula acts as a lead point. It presents as a palpable (R) sided mass and passaje of “ jelly current” stools. Air or contrast enema in pediatric population helps to reduce the intossusception in the acute setting. If no bowel compromise has occurred then resection of diverticula should be accomplished. 4) diverticulitis: it mimics appendicitis and Meckel’s diverticula should be suspected if a pt specially a young one is being explored for suspected appendicitis and is found to have a normal appendix 5) ileus 6) inflamation

Small intestine 7) Umbilical fistula 8) Perforation 9) Miscellaneous (fistula, tumor) Less common complications: Deficiency anemia Malabsorption Foreign body Perforation Incarceration in an hernia (Littre’s hernia) including inguinal, femoral and umbilical hernia.

Small intestine D/D: 1) Acute appendicitis, SBO from other causes, Regional enteritis, all these 3 present similarly to and are more common than Meckel’s diverticulum. 2) Lower GI bleeding, except in very young pts, is most commonly due to diverticulitis or angiodysplasia 3) Think of Meckel’s in small children that develop lower abdominal pain, obstruction, lower GI bleeding or umbilical drainaje and should be considered as a secondary diagnosis in older pts in whom other pathologies are far more likely. Dx of Meckel’s: particularly in older pts should include endoscopy and GIT series, other pts may have their Dx when in surgery and other pts with atypical presentation and negative work-up will get benefits from Meckel’s scan, SB series, or even laparoscopy.

Small intestine Tx: Resection of Diverticula is curative Incidentalomas happened, it is when an asymptomatic diverticulum is found at time of surgery for other purposes. In younger pts --- low morbidity of resection is justified as a preventive measure. in no that young pts ----- it is indicated when they have a narrow base, or when a mesodiverticular band is present, or when there evidence of a heterotopic tissue, also resection may be appropiated in pts with hostile abdomen in whom would be difficult to re-explore for example in presence of multiple adhesions, in recurring SBO and in pending radiation.

Small intestine Crohn Ds 7 to 10 cases per 100,000 population Underlying genetic, environmental factors and microflora act together inducing events First degree relatives have increased risk of having Crohn’s than regular population. Genetic relation: increased disease in monozygotic twins than in dizygotic ones. IBD 1 locus chromosome 16 has been associated with Crohn’s Ds. Most common environment factors associated with Crohn’s are: NSAID’s and smoking The disease has a bimodal presentation: 1) late teens and early twenties 2) late in six or seven decades

Small intestine Crohn Ds Distribution of disease goes from any part from the mouth to the anus, although, SI and colon are most commonly involved. Involvement by %: 1) ileocecal area 40% to 50% 2) Small intestine 30% to 40% 3) Colon 20% Ds: It is not curable It can go on remission for long time Flares and exacerbations occur

Small intestine Crohn Ds Crohn’s involvement in SI and colon tend to be segmental with sparing areas between involved mucosa which is different than with UC, “skip areas”. Also Crohn’s is a chronic, transmural inflammatory disease, because of that fistulas can happen and histological it is characterized by non caseating granulomas There are a few extraintestinal manifestations like in skin (pioderma), eyes (iritis, conjunctivitis,uveitis, iridocyclitis, episcleritis) mouth (ulcers), joints (arthritis), biliary tract (sclerosing cholangitis,pericholangitis, granulomatus hepatitis), vasculitis and aphtous stomatitis. These pts have altered imune responses that stimulate continuosly the mucosal epithelium explained by an increased surface adherent and intracellular bacteria (in the mucosal epithelium)

Small intestine Crohn Ds Constant and continue inflammatory and immunological stimulation induces release of cytokines,arachidonic acid (prostaglandines), and nitric oxide that in turn destroys mucosa and causes damage. Due to continue inflammation an remission these pts develop strictures and obstruction on SI and colon Adherences is also another type of presentation it can happen to adherence to another loops or to bladder that can lead to fistulas formationand when that happen then abcesses develop. There are few different types of fistulas: retroperotoneal, intraabdominal, perianal (mostly seen in colorectal involvement) S/S: Triad of abdominal pain,diarrhea, and weight loss. Progressive, waxing and wanning symptoms

Small intestine Crohn Ds RLQ location most common due to ileocecal involvement Bleeding is not as common. Associated Signs and symptoms like anorexia, weight loss, fever, malaise. Perianal involvement with fistulas, fissures and abcesses is common. Note: surgical intervention unaware of this disease in perianal abcesses or an anal fistula can cause difficulty healing and that should alert the clinician that something else is going on. Nutritional malnourish due to decreased oral intake and malabsorption when terminal ileum is involved, hypoalbuminemia ADEK deficiency. Course of Ds is urgent or slow (indolent)

Small intestine Crohn Ds Dx: No specific lab study H/P can lead to suspect Crohn’s. Endoscopy help with Dx. Colonoscopy, Barium enema and SB contrast studies. (visualization of terminal ileum) MC used to Dx ulceration, fistulas, stricture. CT scan for abscesses, masses, obstruction and fistulas. Enteroclisis (air and contrast injection to see mucosa outline) Bx’s Cystography / Cystoscopy/ vaginal exam (urinary, vaginal fistulae)

Small intestine Crohn Ds Dd: dificcult ito differentiate between Crohn’s and colitis also when Ds present in acute fashion. Also difficult to differentiate from acute appendicitis, acute regional ileitis, PID, or TB. Tx: Medical Analgesics, decrease motility of bowel, wound care for fistulae, hydration, nutritional (parenteral) due to decreased oral intake and malabsorption particularly at terminal ileum disease vitamins (ADEK). For chronic diarrhea use of lactose, loperamide, diphenoxylate, codeine, cholesteramine ( bile salt induce diarrhea) (induced paralitus ileus, toxic magacolon, bacterial overgrowth.

Small intestine Crohn Ds Serum phosphate and K levels in malnurish pts Sulfasalazine two components 1) sulfonamide moiety of sulfasalazine (Bacteriostatic) 2) 5-aminosalicylate Anti-inflammatory action, by limiting production of prostaglandins and leukotriens. New product is mesalamine (no sulfonamide moiety part) Corticosteroides: Topical Prednisone (60 mgs/day) oral Hydrocortisone IV in pts with oral intolerance Budenoside (luminal steroid) Keep in mind side effects of steroids. (HTN, weight gain, striae, osteoporosis)

Small intestine Crohn Ds Immunossupressive therapy: azathioprine, 6 mercaptopurine, MTX cyclosporine, new ones are monoclonal antibodies like Infliximab. Surgical Tx: Mostly when pt has fistulae, obstruction, perforation, hemorrhage is not treated surgically in Crohn’s, because there is a great recurrence of Crohn’s after surgery. Complications: Malnutrition, electrolyte imbalance, fistulae, perforation, steroids side effects (osteoporosis, cataract, weight gain, striae, HTN), wound healing in pts taking immunossupressive medications (MTX, Infliximab)

Small Bowel Tumors Tumors of SB are not common. They may present as SBO , GI bleeding, sometimes they show metastasis S/S as a form of presentation, also intossusception can be another presentation. Dx: endoscopy, capsule endoscopy is another method based on a capsule size device swallow by pt that produces some emissions like a chip that transmits 2 images that later are read, this is a good one b/c small tumors can be diagnosed.

Small Bowel Tumors These tumors are more common than malignants. Asymptomatic. 1:1 / man/female, sixth decade. MC one is leiomyoma, in jejunum. Lipomas can also present as benign tumors in duodenum and ileum, Hemangiomas, Hamartomas, Lymphangiomas, Schwanomas, neurofibromas. Peutz-Jeghers syndrome assotiated with multiple hamartomas and mucocutaneous hyperpigmentation.

Small Bowell Malignant tumors Malignant TU’s of SB represent about 2% of all GIT. More common in men than in females, sixth decade. MC TU’s are: ADC: Represent ½ of SB TU’s. MC location is duodenum. Obstruction presentation in a pt without hernia or previous abdominal surgery with probably adhesions should make the clinician to think of neoplasia. Also associated S/S of anemia, occult GI bleeding and weight loss may indicated malignancy. When tumor is located in the ampullar area jaundice and pancreatitis may first S/S. Tx: Surgical with resection + lymphatic removal Carcinoid Tumors Lymphoma GI Stromal/ Leiomyosarcoma

Small Bowell Malignant tumors Carcinoid Tumors: Develop from Kulchistky cells in cryps of Lieberkuhn which are cells that form part of the APUD(amine precursor uptake and decarboxilation) system or argentaffin cells. Size of tumor is proportional to malignancy, the bigger the tumor the bigger the possibility of malignancy. 1 cm tumors have only 2% possibilities of mets >2 cm tumors have 90% possible mets. Almost 50% of all carcinoids are located in appendix as in 1 st place, SB carcinoids are in 2 nd place mostly in ileum. Presentation is usually SB obstruction. Dx: Laparoscopy

Small Bowell Malignant tumors Tx: Surgical with excition of bowell + hemicolectomy. Carcinoid Syndrome is manifestation of metastatic intestinal carcinoid. It is characterized by attacks of flushing (head, trunk), bronchospasm, abdominal cramping and diarrhea, pellagra like symptoms,(R ) side vavular HD.Alcohol, exertion, excitement, anesthesia, can trigger these S/S. Serotonin (5-hydroxitryptamine) produced by the tumor ---- in the liver it becomes 5-HIAA, and with other susbstances like kallikrein, histamine, ACTH, causes S/S.

Small Bowell Malignant tumors Dx: urinary 5-HIAA (5-hydroxiindole acetic acid) TX: resection Lymphoma: SI MC place for them. 10%-15% of all lymphomas are located in SB 5 th and 6 th decades. Ileum MC place (Peyer’s patches). MALT lymphomas more common in stomach associated to H.pyloris are also seen in SB. S/S: vague abdominal pain, fatigue, weight loss Perforation, GI bleeding, obstruction, intussusception.

Small Bowell Malignant tumors Dx: CTscan. Tx: Surgical resection.+ chemo and radiation.Poor prognosis. GI Stromal (GIST)/ Leiomyosarcoma: Mesenchimal TU’s of GIT known as leiomyosarcomas are now known as GIST tumors. Benign show the c-kit protein, malignant ones don’t have that marker. Poor prognosis. 6 th decade, presentation can be as any of the previous presentatons like perforation, bleeding or obstruction.

Surgery Small Intestine And Appendix T G

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Surgery Small Intestine And Appendix T G