First Aid For Surgery - Small Intestine

Front 1

Is all of the small bowel midgut?

Back 1

No! All of the small intestine is derived from the midgut except for the proximal duodenum, which is derived from the foregut. The junction between the foregut and midgut is immediately distal to the opening of the common bile duct.

Front 2

Origin of a Meckel's diverticulum

Back 2

Initially, the primitive gut tube communicates with the yolk sac. This communication narrows by the sixth week to form the vitelline duct. If the vitelline duct fails to obliterate by the end of gestation, it persists as a Meckel’s diverticulum seen in 2% of the population.

Front 3

Ligament of Treitz

Back 3

Site where duodenum ends and jejenum begins! This is the tissue that connects the duodenum of the small intestines to the diaphragm. It is also known as the suspensory ligament of the duodenum.

Front 4

Anterior vs Posterior ulcers of duodenum

Back 4

Anterior ulcers tend to perforate, causing leakage of duodenal contents into the peritoneal cavity, leading to peritonitis. Ulcers that result in massive bleeding are posterior ulcers that have penetrated the gastroduodenal artery.

Front 5

SMA contribution to small bowel

Back 5

The entire small bowel is supplied by branches of the SMA except the proximal duodenum (which is supplied by branches from the celiac trunk).

Front 6

Small bowel obstruction

Back 6

Cessation, impairment, or reversal of physiologic transit of intestinal contents 2/2 mechanical or functional cause; MCC is ADHESIONS from PRIOR ABDOMINAL SURGERY (75%). The second MCC is incarcerated hernia!

Front 7

Etiology of SBO

Back 7

(1) Extrinsic: adhesions, hernia, cancer, abscess, congenital; (2) Intraluminal: gallstone ileus, foreign body, intussusception; (3) Intramural: Crohn's, lymphoma, radiation enteritis; (4) Functional [Paralytic ileus]: Postop, hypokalemia/electrolyte abnormalities, peritonitis, medications [anticholinergics, opiates], hemoperitoneum/retroperitoneal hematoma

Front 8

Definition of steatorrhrea

Back 8

>6g of fecal fat/24hr with 100g lipid ingested. Normally, more than 93% of ingested fat is absorbed

Front 9

Pathophysiology of SBO

Back 9

(1) Gas and fluid begin to accumulate in lumen, proximal to site of obstruction; (2) Bowel distends as intraluminal contents builds up, and intramural and intraluminal pressure rise; (3) If intramural pressure exceeds pressure in microvasculature, then perfusion of the intestine is decreased, resulting in small bowel ischemia, and ultimately necrosis; (4) Impairment of perfusion is termed strangulation

Front 10

Closed loop obstruction

Back 10

Blockage of both proximal and distal segments of the small intestine; seen with incarcerated hernia, torsion, adhesions, volvulus. Requires EMERGENT surgery because progression to strangulation is quite rapid

Front 11

SBO vs LBO

Back 11

As opposed to large bowel obstruction, SBO is rarely caused by neoplasm. If neoplasm is the cause, it is most likely secondary to extrinsic compression as opposed to large bowel obstruction.

Front 12

S&S of SBO

Back 12

Colicky abdominal pain, abdominal distention, nausea, vomiting, obstipation, hyperactive bowel sounds, signs of decreased intravascular volume 2/2 decreased PO intake, vomiting, and accumulation of fluid in bowel lumen and wall (third spacing)

Front 13

Features associated with strangulated SBO

Back 13

(1) Tenderness; (2) Tachycardia; (3) Fever; (4) Markedly elevated WBC count; (5) Acidosis with elevated lactate level. BEWARE: these indicators are not present in 5-15% of patients with intestinal infarction, especially the elderly

Front 14

Abdominal Series findings with SBO

Back 14

Supine: dilated loops of small intestine with paucity of air in colon; Upright: multiple air-fluid levels in a "stepladder"

Front 15

Use of CT in suspected SBO

Back 15

CT is more sensitive and specific; Findings include: (1) Transition Zone, with dilation of bowel proximally and decompression of the bowel distally, no contrast present to transition point, and paucity of gas and fluid in colon

Front 16

Treatment of SBO

Back 16

If patient is stable of has partial SBO, give trial of non-operative management: (1) NPO; (2) IV hydration to counter third-spacing; (3) NGT for gastric decompression; decreases nausea, vomiting, distention; (4) Foley to monitor UOP; (5) Monitor lytes for hypokalemia, base deficit/metabolic acidosis (signs of ischemia)

Front 17

Typical scenario: A 5-year-old child presents with increasing irritability, colicky abdominal pain, and rectal bleeding with stools that have a currant jelly appearance. A tubular mass is palpated in the right lower quadrant. Upright abdominal x-ray shows airfluid levels with a stepladder pattern.

Back 17

Think: Intussusception. Barium enema is both diagnostic and therapeutic

Front 18

Crohn's Disease

Back 18

Inflammatory bowel disease characterized by transmural inflammation involving any part of the GI tract, from mouth to anus, of unknown etiology. The inflammation is discontinuous, resulting in skip lesions, and often leads to fibrosis and ultimately obstruction, as well as to the formation of fistulae.

Front 19

Differential diagnosis of RLQ pain

Back 19

(1) Appendicitis; (2) Crohn's disease; (3) Infectious colitis - Yersinia, Campylobacter; (4) Gynecologic pathology in females (ovarian torsion, abscess, ectopic); (5) Ischemic colitis

Front 20

S&S of Crohn's Disease

Back 20

(1) Crampy abd pain in RLQ, diarrhea, wt loss are most common symptoms; (2) Fever, fatigue; (3) Bleeding (hemoccult+ stools common, but gross lower GI bleeding less common than in UC; (4) Perianal disease including skin tags, anal fissures, perirectal abscesses, and anorectal fistula; (5) S&S of intestinal perforation and/or fistula formation [localized peritonitis, fever, abdominal pain, tenderness, and palpable mass on physical exam]; (6) Extraintestinal manifestations: aphthous ulcers, arthritis, uveitis, erythema nodusum/pyoderma gangrenosum, sclerosing cholangitis

Front 21

Diagnosis of Crohn's disease

Back 21

C-scope with biopsies demonstrating transmural inflammation, focal ulcerations visualized in terminal ileum, cobblestone appearance of mucosa

Front 22

Benign Neoplasms of Small Intestine

Back 22

Adenomas > leiomyomas > lipomas (but leiomyomas most likely to cause symptoms); Most small intestinal benign neoplasms are found in the duodenum; MCC of adult intussusception!

Front 23

Risk Factors for small bowel neoplasm

Back 23

(1) Hereditary syndromes: Peutz-Jeghers (hamartomatous polyps), Gardner syndrome (adenoma), FAP (adenoma); (2) Consumption of red meat and salt-cured foods

Front 24

Intermittent obstruction

Back 24

Most common presentation in a symptomatic patient with a small bowel neoplasm. It can be caused by either narrowing of the small bowel lumen or secondary to intussusception, with the neoplasm serving as the lead point

Front 25

Test of choice for detection of tumors in small bowel

Back 25

Enteroclysis; a double-contrast study that involves passing a tube into the proximal small bowel and injecting barium + methylcellulose. It can detect tumors missed on conventional SBFT. Extended small bowel enteroscopy is much like push enteroscopy, but involves the advancement of the enteroscope by peristalsis and allows for visualization up to 70% of the small bowel mucosa and tumors missed by enteroclysis

Front 26

Typical scenario: A patient presents with pigmented spots on his lips and a history of recurrent colicky abdominal pain. What is the cause of his abdominal pain?

Back 26

Think: Peutz-Jeghers syndrome. The hamartomatous polyps are likely causing intermittent intussusception

Front 27

Malignant Neoplasms of Small Intestine

Back 27

Rare; adenocarcinoma > carcinoid > GIST > lymphoma

Front 28

Treatment of malignant neoplasm of small bowel

Back 28

(1) Wide en bloc resection of involved intestine; (2) For adenocarcinomas, wide local excision of intestine with its accompanying mesentery is performed along with regional lymph nodes. (2) GISTs usually treated with segmental resection of affected intestine and Gleevec, a TK-inhibitor; (3) Patients with duodenal lesions may requite pancreaticoduodenectomy; (4) Bypass may be required for palliation; (5) Diffuse lymphoma --> chemotherapy should be primary therapy

Front 29

Small bowel mets

Back 29

Small bowel is frequently affected by metastasis or invasion from cancers originating in other organs, particularly melanoma.

Front 30

GIST

Back 30

CD-117 (c-kit) positive; associated with hemorrhage

Front 31

Carcinoid tumors

Back 31

Malignant tumor of enterochromaffin cell origin, part of Amine Precursor Uptake and Decarboxylation (APUD) system; MC in the appendix, followed by small bowel and then rectum

Front 32

Small bowel and colonic carcinoids

Back 32

Associated with highest degree of malignant potential

Front 33

S&S of carcinoid tumors

Back 33

(1) Slow-growing, frequently asymptomatic, usually found incidentally; (2) Intermittent obstruction; (3) Rectal bleeding (from rectal carcinoid), pain, weight loss; (4) Carcinoid syndrome - approximately 10% of cases: due to production of serotonin, bradykinin, or tryptophan by tumor and exposure of these products to systemic circulation prior to breakdown by the liver; (5) Characterized by cutaneous flushing, sweating, watery diarrhea, wheezing, dyspnea, valvular lesions. REMEMBER: FDR (flushing, diarrhea, regurgiation [tricuspid])

Front 34

Carcinoid Syndrome

Back 34

Develops when the tumor produces amines and peptides outside of the portovenous circulation. Classically, appendiceal and small intestinal carcinoids cause the carcinoid syndrome only after they have metastasized to the liver. Patients who present with carcinoid syndrome are often not surgical candidates because they already have extensive metastatic disease

Front 35

Diagnosis of Carcinoid

Back 35

(1) Most found incidentally during radiographic studies, appendectomy, or surgery for SBO; (2) 5-HIAA in 24hr urine; (3) Plasma chromogranin A; (4) Pentagastrin provocation test - pentagastrin induces flushing (used in Pts with marginally elevated 5-HIAA, but who describe flushing symptoms); (5) Otherwise, diagnosed as any other SBO

Front 36

Treatment of carcinoid

Back 36

(1) MEDICAL: serotonin antagonists: cyproheptadine or somatostatin analogues (octreotide); (2) SURGICAL: appendiceal carcinoid < 2cm: appendectomy; if >2cm, right hemicolectomy; for small intestine, resect carcinoid and mesenteric lymph nodes

Front 37

Fistula

Back 37

A communication between two epithelialized surfaces. Can form btw two parts of GI or GU tract, an internal fistula (choledocho-duodenal or colovesical), or between an internal organ and epithelialized surface (enterocutaneous), an external fistula. If there is no preceeding iatrogenic injury, fistula formation is most likely 2/2 progression of Crohn's or cancer

Front 38

Risk factors for fistula formation

Back 38

(1) Previous abdominal surgery [MC - 80%!]; (2) Diverticular disease; (3) Crohn's disease; (4) Colorectal cancer

Front 39

S&S of fistula

Back 39

(1) Iatrogenic fistulae usually occur 5-10 days postop; (2) If associated with abscess, can be accompanied by fever and leukocytosis; (3) Drainage of succes entericus (bowel contents) from skin (enterocutaneous fistula); (4) Diarrhea 2/2 malabsorption (entero-enteric fustula); (5) Pneumaturia and symptoms of UTI (colovesicular fistula)

Front 40

What's worse: proximal or distal fistula?

Back 40

Proximal fistulas cause more problems than distal fistulas because the draining contents are more acidic, more fluids and electrolytes are lost, and more absorptive area is lost.

Front 41

Treatment for fistula

Back 41

(1) Stabilization: manage electrolytes, fluids, nutritional status; (2) Drainage of abscesses; (3) Allow time for spontaneous closure: bowel rest, TPN, octreotide for high-output and pancreatic fistulas; (4) If 6-8wks pass w/o improvement, then surgery should be performed to resect fistula tract, together with the segment of small bowel from which is originates

Front 42

Prognosis of fistulas

Back 42

(1) Enterocutaneous fistulas have a 15-20% mortality related to complications of sepsis and underlying disease; (2) Surgery is associated with considerable morbidity and a high recurrence rate

Front 43

High output vs Low output fistulas

Back 43

High output fistulas drain > 500 mL/24 hrs and are proximal (stomach, duodenum, proximal small bowel). Low output fistulas drain < 500 mL/24 hrs and are distal (distal small bowel and colon).

Front 44

Mesenteric Ischemia

Back 44

Reduction in blood flow to small bowel 2/2 variety of mechanisms; can result in two conditions: (1) acute mesenteric ischemia and (2) chronic mesenteric ischemia

Front 45

Factors that keep a fistula tract open

Back 45

FRIENDS: (1) Foreign body; (2) Radiation; (3) Inflammation/Infection; (4) Epithelialization; (5) Neoplasm; (6) Distal obstruction; (7) Short segment fistula (<2.5cm fistula tract)

Front 46

Acute Mesenteric Ischemia

Back 46

Rapid onset of intestinal hypoperfusion; can be caused by arterial occlusion (usually single artery): (1) SMA embolism - 50% of all AMI; (2) SMA thrombosis (acute) 15-25% of all AMI; (3) Vasospasm (nonocclussive mesenteric ischemia) - 20-30% of all AMI; (4) Venous obstruction (either thrombosis or strangulation usually of SMV) - 5% of all AMI. Regardless of cause, AMI can lead to mucosal sloughing within 3 hours of onset, and to intestinal infarction 6hr after onset

Front 47

MC vessel involved in acute mesenteric ischemia

Back 47

SMA is the most common vessel involved in AMI. Most emboli that cause AMI originate in the heart (left atrial or left ventricular thrombi). Ninety-five percent of patients with AMI will have a history of cardiovascular disease (atrial fibrillation or myocardial infarction).

Front 48

S&S of acute mesenteric ischemia

Back 48

(1) Abd pain OUT OF PROPORTION to tenderness on physical exam (HALLMARK); (2) Pain is colicky and diffuse, typically in mid-abdomen; (3) Can be associated with nausea, vomiting, and diarrhea; (4) Following infarction, peritonitis (rebound and rigidity), abdominal distention, and passage of bloody stools occur

Front 49

Best test for acute mesenteric ischemia

Back 49

Mesenteric angiography: most sensitive and specific method for diagnosing AMI, albeit invasive

Front 50

CT for AMI

Back 50

CT has somewhat of a low sensitivity for detecting arterial AMI. Therefore, if a patient has high suspicion for AMI, then patient should undergo angiography despite negative CT results. CT has a high sensitivity (<90%) for detectign acute mesenteric venous thrombosis

Front 51

Treatment for AMI

Back 51

(1) Midline laparotomy with assessment of intestinal viability; for embolic causes: intraoperative embolectomy. For CA/SMA thrombosis: bypass site of obstruction using saphenous vein graft (from supreaceliac aorta to distal SMA)

Front 52

Chronic Mesenteric Ischemia

Back 52

Insidious, episodic, or constant state of intestinal hypoperfusion; rarely leads to infarction of small bowel 2/2 development of collateral circulation over time. May be caused by (1) Arterial ischemia [most common]; associated with atherosclerosis of more than one mesenteric and splanchnic vessels; (2) Venous thrombosis: thrombosis of portal or splenic veins, leading to portal HTN with subsequent development of esophageal varices and splenomegaly; (3) Vasculitis

Front 53

Risk factors for chronic mesenteric ischemia

Back 53

(1) Atherosclerotic vascular disease; (2) Smoking

Front 54

S&S of chronic mesenteric ischemia

Back 54

(1) 'Intestinal angina': dull, crampy postprandial abdominal pain leading to food aversion and weight loss (hallmark); (2) Patients with chronic venous thrombosis may be asymptomatic due to collateral formation, or may present with esophageal variceal bleeding

Front 55

Diagnosis of CMI

Back 55

(1) Angiography is gold standard; (2) CT and MR angiography: good initial tests b/c can identify whether a stenosis is present and serve as a guide for angiography

Front 56

Celiac artery compression

Back 56

Infrequent cause of CMI; celiac artery compression syndrome or median arcuate ligament syndrome. Treatment is release of the arcuate ligament and bypass of persistent stricture.

Front 57

Treatment of Arterial CMI

Back 57

(1) Surgical revascularization with either aortomesenteric bypass graft or mesenteric endarterectomy; (2) Percutaneous transluminal angioplasty with or without stent placement; (3) For CHRONIC venous mesenteric thrombosis: anticoagulation

Front 58

Typical scenario: A 70-year-old male with a history of peripheral vascular disease and hyperlipidemia presents to the emergency department with severe, diffuse abdominal pain. His blood pressure is 170/100 and his pulse is 90 bpm. Supine abdominal radiograph shows free air in the abdomen and within the wall of the small intestine. What is the most likely diagnosis?

Back 58

Think: Small Bowel infarction

Front 59

Short Bowel Syndrome

Back 59

Presence of <200cm of small bowel in adult patients, resulting in decreased absorption, diarrhea, malnutrition, and dehydration

Front 60

Etiology of Short Bowel Syndrome

Back 60

ADULTS: acute mesenteric ischemia, Crohn's, malignancy; KIDS: Volvulus, intestinal atresia, NEC

Front 61

Pathophysiology of Short Bowel Syndrome

Back 61

Malabsorption occurs 2/2 resection of small bowel; presence of intact colon and ileocecal valve decreases severity of malabsorption; Resection of ileum associated with increased malabsorption 2/2 inability to reabsorb bile salts and B12

Front 62

Medical Treatment of Short Bowel Syndrome

Back 62

(1) TPN, Fluids, Electrolytes; (2) PPI; (3) Antimotility agents to decrease transit through small bowel; (4) Octreotide may be used to decrease intestinal secretions

Front 63

Surgical Treatment of Short Bowel Syndrome

Back 63

(1) Restoration of intestinal continuity in patients with stomas; (2) Segmental reversal of small bowel; (3) Placement of colon between two segments of small bowel; (4) Creation of artificial small bowel valves; (5) Surgeries to lengthen bowel; (6) Small Bowel Transplant