Gastrointestinal and Abdominal: Small Intestine Flashcards

1
Q

Anatomy and Physiology

A
  • comprises the duodenum, jejunum, and ileum and extends from the pylorus proximally to the cecum distally
  • is to digest and absorb nutrients
  • Absorption is achieved by the large surface area of the small intestine, secondary to its long length and extensive mucosal projections of villi and microvilli.
  • A broad-based mesentery suspends the small intestine from the posterior abdominal wall once the retroperitoneal duodenum emerges at the ligament of Treitz and becomes the jejunum.
  • Arterial blood is supplied from branches of the superior mesenteric artery, and venous drainage is via the superior mesenteric vein (Fig. 4-1).
  • The mucosa has sequential circular folds, called plicae circulares.
    • are more numerous in the proximal bowel than in the distal bowel.
  • The mucosal villi and microvilli create the surface through which carbohydrates, fats, proteins, and electrolytes are absorbed (Figs. 4-2 and 4-3).
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2
Q

Small Bowel Obstruction

A
  • causes progressive proximal accumulation of intraluminal fluids and gas.
  • Peristalsis continues to transport swallowed air and secreted intestinal fluid through the bowel proximal to the obstruction, resulting in small bowel dilation and eventual abdominal distention.
  • Depending on the location of the obstruction, vomiting occurs early in proximal obstruction and later in more distal blockage (Fig. 4-4).
  • Crampy abdominal pain initially occurs as active proximal peristalsis exacerbates bowel dilation.
  • With progressive bowel wall edema and luminal dilation, however, peristaltic activity decreases and abdominal pain lessens.
  • exhibit abdominal distention and complain of mild diffuse abdominal pain
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3
Q

Small Bowel Obstruction: Etiology

A
  • first and second most common causes:adhesions and hernias, respectively (Table 4-1).
  • adhesions are caused by postoperative internal scar formation.
  • Discovering the actual mechanism of obstruction is important for therapeutic planning, because the mechanism of obstruction relates to the possibility of vascular compromise and bowel ischemia.
    • a closed-loop obstruction caused by volvulus with torsion is at higher risk for vascular compromise than an SBO from a simple adhesive band (Fig. 4-5).
    • incarceration in a fixed space
      • Incarceration and subsequent strangulation impedes venous return, causing edema and eventual bowel infarction.
    • intraluminal obstruction by a gallstone or bezoar and intussusception caused by an intramural or mucosal lesion at the leading edge
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4
Q

Small Bowel Obstruction: History

A
  • complaints of intermittent crampy abdominal pain, abdominal distention, obstipation, nausea, and vomiting. Vomiting of feculent material usually occurs later in the course of obstruction
  • Constant localized pain or pain out of proportion to physical findings may indicate ischemic bowel and is a clear indication for urgent surgical exploration
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5
Q

Small Bowel Obstruction: Physical Examination

A
  • A distended abdomen with diffuse midabdominal tenderness to palpation
  • Typically, there are no signs of peritonitis.
  • If constant localized tenderness is apparent, indicating localized peritonitis, then ischemia and gangrene must be suspected.
  • An essential aspect of the physical examination is to check for abdominal wall hernias, especially in postsurgical patients.
  • Elevation in temperature should not be present in uncomplicated cases.
  • Tachycardia may be present from hypovolemia secondary to persistent vomiting or from toxemia caused by intestinal gangrene.
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6
Q

Small Bowel Obstruction: Diagnostic Evaluation

A
  • Upright radiographs classically demonstrate distended loops of small bowel with multiple air–fluid interfaces.
    • Occasionally, the radiograph shows the etiology of the obstruction, the site of obstruction, and whether the obstruction is partial or complete.
    • Dilated small bowel in the presence of a dilated colon suggests the diagnosis of paralytic ileus, not SBO.
    • A small bowel contrast study may be necessary to demonstrate transit of contrast into the colon, thereby ruling out SBO.
    • Free air indicates perforation of the intra-abdominal gastrointestinal tract, whereas biliary gas and an opacity near the ileocecal valve indicate gallstone ileus.
  • Abdominal computed tomography (CT) scans can often demonstrate the transition point, where the dilated bowel proximal to the point of obstruction transitions to the decompressed bowel more distally.
    • Also, in cases where the bowel has twisted on its mesentery, a “swirl sign” can be seen as the mesenteric vasculature twists on itself, creating a distinctive swirling radiographic pattern.
  • Laboratory examination often reveals a hypokalemic alkalosis owing to dehydration from repeated emesis.
    • White blood cell count and amylase may be mildly elevated.
    • Lactic acidosis is cause for concern and may indicate intestinal necrosis.
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7
Q

Small Bowel Obstruction: Treatment

A
  • In decades past, most patients were taken directly to the operating room for exploration to rule out intestinal necrosis
  • over the past few decades it became apparent that most patients can be safely managed medically in the absence of peritonitis or other worrisome clinical findings
  • Supportive therapy allows for spontaneous resolution of the obstruction and return of normal bowel function.
  • For patients who are candidates for a trial of nonsurgical therapy, initial treatment consists of nasogastric decompression to relieve proximal gastrointestinal distention and associated nausea and vomiting.
  • Fluid resuscitation and supportive hydration is necessary because patients are typically intravascularly depleted from diminished oral fluid intake and vomiting.
  • The decision to operate is based on the nature of the obstruction and the patient’s clinical condition.
  • On initial presentation, if ischemia or perforation is suspected, immediate operation is necessary. Otherwise, patients can be observed with serial physical examinations, serum tests, and abdominal radiographs for evidence of resolution. If the patient’s condition worsens or fails to improve with supportive therapy, operative intervention is indicated.
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8
Q

Crohn’s Disease

A
  • a transmural inflammatory disease that may affect any part of the gastrointestinal tract, from the mouth to the anus.
  • Ileal involvement is most common.
  • characterized by skip lesions that involve discontinuous segments of abnormal mucosa.
  • Granulomata are usually seen microscopically, but not always.
  • Areas of inflammation are often associated with fibrotic strictures, enterocutaneous fistulae, and intra-abdominal abscesses, all of which usually require surgical intervention.
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9
Q

Crohn’s Disease: Epidemiology

A
  • occurs throughout the world,
  • The incidence in the United States is approximately 10 times that of Japan. Ashkenazi Jews have a far higher incidence of disease than do African Americans.
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10
Q

Crohn’s Disease: Etiology

A
  • cause remains unknown
  • Because of the presence of granulomata, mycobacterial infection has been postulated as the causative agent
  • An immunologic basis for the disease has also been advanced; however, although humoral and cellular immune responses are involved in disease pathogenesis, no specific immunologic disturbance has been identified.
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11
Q

Crohn’s Disease: Pathology

A
  • small intestine is affected in at least 70% of all patients with Crohn’s disease
  • ileum is typically diseased, with frequent right colon involvement.
  • On gross inspection, the serosal surface of the bowel is hypervascular, and the mesentery characteristically shows signs of “creeping fat.”
  • The bowel walls are edematous and fibrotic. The mucosa has a cobblestone appearance, with varying degrees of associated mucosal ulceration (see Color Plates 2 and 3).
  • Histologically, a chronic lymphocytic infiltrate in an inflamed mucosa and submucosa is seen.
  • Fissure ulcers penetrate deep into the mucosa and are often associated with granulomata and multinucleated giant cells.
  • Granulomata are seen more frequently in distal tissues, which explains why granulomata are seen more often in colonic disease than in ileal disease.
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12
Q

Crohn’s Disease: History

A
  • complaining of diarrhea, abdominal pain, anorexia, nausea, and weight loss.
  • diarrhea is usually loose and watery, without frank blood
  • Dull abdominal pain is usually in the right iliac fossa or periumbilical region.
  • Children often present with symptoms of malaise and have noticeable growth failure.
  • Strictures may cause partial SBO, resulting in bacterial overgrowth and subsequent steatorrhea, flatus, and bloating.
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13
Q

Crohn’s Disease: Physical Examination

A
  • appear to be either generally healthy or may have significant cachexia.
  • Abdominal examination may reveal right iliac fossa tenderness.
  • In acutely ill patients, a palpable abdominal mass may be present, indicating abscess formation.
  • Enterocutaneous fistulae may be present.
  • Oral examination may reveal evidence of mucosal ulceration, whereas perianal inspection may show skin tags, fissures, or fistulae.
  • Extraintestinal manifestations include erythema nodosum, pyoderma gangrenosum, ankylosing spondylitis, and uveitis.
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14
Q

Crohn’s Disease: Diagnostic Evaluation

A

Blood studies often show a mild iron-deficiency ane-

mia and a depressed albumin level. If hypoalbumine-

mia is severe, peripheral edema may be present.

Small intestine Crohn’s disease is diagnosed by

bariumcontrast enteroclysis. This small intestine enema

technique provides better mucosal definition than stan-

dard small bowel follow-through studies. This tech-

nique illustrates aphthoid ulcers, strictures, fissures,

bowel wall thickening, and fistulae. Fistulograms are

helpful to define existing fistula tracks, and CT can

localize abscesses. Once radiographic evidence of

disease is found, colonoscopy should be performed to

evaluate the colonic mucosa and to obtain biopsies of

the terminal ileum

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15
Q

Crohn’s Disease: Differential Diagnosis

A

In addition to the diagnosis of Crohn’s disease, one

should consider the possibility of acute appendicitis,

Yersinia infection, lymphoma, intestinal tuberculosis,

and Behçet disease.

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16
Q

Crohn’s Disease: Complications

A

Crohn’s disease carries a high morbidity and low mor-

tality. Small bowel strictures secondary to inflam-

mation and fibrosis are common complications that

present as obstructions. Fistulae from small bowel to

adjacent loops of small bowel, large bowel, bladder,

vagina, or skin also occur. Ileal Crohn’s disease can

result in gallstone formation because of the interrup-

tion of the enterohepatic circulation of bile salts.

Kidney stones may also form because of hyperox-

aluria. Normally, calcium and oxalate bind in the

intestine and are excreted in the feces. With ileal

Crohn’s disease, steatorrhea causes ingested fat to bind

intraluminal calcium, thus allowing free oxalate to be

absorbed. Finally, adenocarcinoma is a rare complica-

tion that usually arises in the ileum.

17
Q

Crohn’s Disease: Treatment

A

Mild disease can be controlled with a 4- to 6-week

course of sulfasalazine or mesalazine. Alternatively, oral

corticosteroids can be used with equivalent results.

Metronidazole may also be useful. Patients with bile

salt–induced diarrhea after ileal resection may benefit

from cholestyramine.

Severe disease is treated with hospitalization, bowel

rest, hydration, intravenous nutrition, corticosteroids,

and metronidazole. Patients with chronic active disease

may benefit from a course of mercaptopurine.

Surgery for Crohn’s disease should only be per-

formed for complications of the disease (Table 4-2).

Operation should be conservative and should address

only the presenting indication, using gentle surgical

technique. Resections should be avoided, as overly

aggressive intervention can produce surgically induced

short bowel syndrome and malnutrition. Some com-

mon surgical problems encountered in Crohn’s disease

and its treatments include ileocolic disease, which is

managed by conservative ileocecal resection to

grossly normal margins (Fig. 4-6); stricture, managed

by stricturoplasty, which entails incising the antime-

senteric border of the stricture along the intestinal

long axis and then closing the enterotomy trans-

versely (Fig. 4-7); and abscess/fistula, which is man-

aged by open or percutaneous drainage of the abscess

and resection of the small bowel segment responsible

for initiating the fistula with primary anastomosis

(Fig. 4-8)

18
Q

Crohn’s Disease: Treatment: Picture

A

Crohn’s Disease: Treatment: Picture

19
Q

Meckel’s Diverticulum

A

This most common congenital anomaly of the small

intestine is an antimesenteric remnant arising from a

failure of vitelline duct obliteration during embryonic

development. Meckel’s diverticula are true diverticula

affecting all three intestinal muscle layers. Diverticula

are usually 12 cm in length and are found within

100 cm of the ileocecal valve.

Associated abnormalities of the vitelline duct

depend on the degree of duct obliteration that occurs

during development. Complete ductal obliteration

leaves a thin fibrous band connecting ileum to umbili-

cus, whereas complete duct persistence results in a

patent ileoumbilical fistula. Partial obstruction results

in cyst or blind sinus formation (Fig. 4-9). Heterotopic

tissue (gastric, pancreatic) is found in 30% to 50% of

diverticula.

In the United States, Meckel’s diverticulum is

associated with the “Rule of 2s”: it occurs in 2% of the

population, is located within 2 ft of the ileocecal

valve, is usually 2 in long, contains two types of het-

erotopic tissue (gastric, pancreatic, duodenal, or intes-

tinal), and is the most common cause of rectal

bleeding in infants younger than 2 years.

20
Q

Meckel’s Diverticulum: Complications

A

Bleeding within the diverticulum may occur from pep-

tic ulceration arising from heterotopic gastric mucosa.

In infants, Meckel’s diverticulum is the most common

cause of major lower gastrointestinal bleeding.

Bowel obstruction may result from one of two mech-

anisms. Intussusception can occur when an inverted

diverticulum functions as a lead point, or small bowel

volvulus can occur around a fixed obliterated vitelline

duct extending from the ileum to the umbilicus.

21
Q

Meckel’s Diverticulum: Diagnostic Evaluation

A

For Meckel’s diverticula containing heterotopic gastric

mucosa, the technetium 99 (99Tc) scan is helpful for

diagnosis: pertechnetate anions are taken up by ectopic

gastric parietal cells and indicate diverticulum loca-

tion. Diverticula that do not contain heterotopic gas-

tric tissue can occasionally be visualized using standard

barium-contrast studies.

22
Q

Meckel’s Diverticulum: Treatment

A

Definitive treatment for Meckel’s diverticulum compli-

cations is surgical resection. In adult patients inci

dentally found to have an asymptomatic Meckel’s diverticu-

lum during laparotomy, the diverticulum should be

left in situ, as the chance of producing surgical mor-

bidity and mortality are respectively 23 and five times

higher for resection than when only symptomatic

diverticula are removed.

23
Q

Small Bowel Tumors

A

Tumors of the small bowel are rare, accounting for 1%

to 5% of all gastrointestinal tumors. Most tumors are

benign. Common benign neoplasms of the small bowel

include tubular and villous adenomas, lipomas, leiomy-

omas, and hemangiomas. Telangiectasias of R

endu-Osler-Weber syndrome, neurofibromas of neurofibro-

matosis, hamartomatous polyps of Peutz-Jeghers

syndrome, and heterotopic tissue as in Meckel’s diver-

ticulum are also found. Possible explanations for this

lack of malignancy include short exposure to ingested

carcinogens secondary to rapid transit time, low bac-

terial counts resulting in fewer endogenously pro-

duced carcinogens, and the intraluminal secretion of

IgA by small bowel mucosa.

Benign lesions are usually asymptomatic and are

incidental findings. Of symptomatic lesions, obstruc-

tion is the most common presentation, followed by

hemorrhage. In the workup of gastrointestinal bleed-

ing, however, unless other evidence exists, small bowel

lesions should be low on the list of differential diag-

noses, because >90% of bleeding lesions occur between

the esophagus and distal duodenum and between the

ileocecal valve and anus. Small bowel lesions should

be suspected if careful skin examination reveals café-

au-lait spots (neurofibromatosis), telangiectasia (Rendu-

Osler-Weber syndrome), or mucocutaneous

pigmentation (Peutz-Jeghers syndrome).

Malignant tumors of the small bowel typically

present with obstruction or bleeding. The four major

malignant tumors are adenocarcinoma, gastrointesti-

nal stromal tumors, carcinoid, and lymphoma.

24
Q

Small Bowel Tumors: Diagnostic Evaluation

A

Visual endoscopic identification of small bowel

tumors is usually possible for lesions of the proximal

duodenum and terminal ileum. The remainder of the

small bowel requires examination by barium-contrast

studies. For larger lesions, CT may be helpful.

In situations involving active hemorrhage,

99 Tc sulfur colloid or 99 Tc-labeled red blood cell studies may

show the bleeding site. However, a bleeding rate of

1 mL/min is required for accurate localization.

When available diagnostic modalities are insuffi-

cient, exploratory laparotomy may be necessary. In

addition to external inspection at laparotomy, operative

endoscopy can be used for intraluminal evaluation.

25
Q

Carcinoid Tumors

A

Carcinoid tumors are the most common endocrine

tumors of the gastrointestinal tract, constituting more

than half of all such lesions. They account for up to

30% of all small bowel tumors. Carcinoid tumors arise

from neuroendocrine enterochromaffin cells. Hence

tumors can secrete serotonin and other humoral sub-

stances, such as histamine, dopamine, tachykinins,

peptides, and prostaglandins. The metabolite of sero-

tonin, 5-hydroxyindoleacetic acid, is excreted in the

urine and is easily detected.

All carcinoids are considered malignant because of

their potential for invasion and metastasis. Patients

with metastatic disease manifest the carcinoid syn-

drome,

which consists of the systemic effects (flush-

ing, diarrhea, sweating, and wheezing) of secreted

vasoactive substances. Presence of the carcinoid syn-

drome indicates hepatic metastasis, because systemic

effects occur when venous drainage from a tumor

escapes hepatic metabolism of vasoactive substances.

Approximately 85% of carcinoid tumors are found

in the intestine; of these, approximately 50% are found

in the appendix, making it the most common site of

occurrence, followed by the ileum, jejunum, rectum,

and duodenum (see Color Plate 4). Other sites of dis-

ease include the lungs and occasionally the pancreas

and biliary tract. Appendiceal carcinoids rarely metas-

tasize, whereas lesions of the ileum have the highest

association with carcinoid syndrome. Jejunoileal carci-

noids are frequently multicentric.

26
Q

Carcinoid Tumors: History

A

The clinical presentation of patients with carcinoid

tumors differs depending on tumor location. Primary

tumors may present as SBO, because tumors can incite

an intense local fibrosis of the bowel that causes angu-

lation and kinking of the involved segment. As noted,

metastatic disease with hepatic spread manifests as the

carcinoid syndrome. Occult primary lesions do not

cause systemic effects because 5-hydroxytryptamine

(serotonin) is metabolized by the liver. Other present-

ing symptoms can include abdominal pain, upper intes-

tinal or rectal bleeding, intussusception, weight loss, or

a palpable abdominal mass.

27
Q

Carcinoid Tumors: Diagnostic Evaluation

A

Laboratory studies should include plasma and urine

analysis to evaluate for elevated levels of plasma

serotonin and urinary 5-hydroxyindoleacetic acid.

Barium-contrast studies are also useful for diagnosing

carcinoid tumors. Barium enemas can demonstrate

lesions of the rectum and large bowel, whereas small

bowel enteroclysis may show a discrete lesion or a

stricture secondary to fibrosis. Because primary

tumors are usually small, CT is usually helpful only

for detecting hepatic metastases. Colonoscopy can

show tumors from the terminal ileum to the rectum.

Because neuroendocrine tumors often express func-

tional receptors, radiolabeled octreotide imaging can be

useful in detecting occult disease. Octreotide scanning is

based on physiologic function, rather than on detectable

anatomic alterations, and may have better diagnostic

sensitivity than conventional imaging modalities.

28
Q

Carcinoid Tumors: Treatment

A

Surgical resection of the primary tumor is always

undertaken, even in cases of metastatic disease. If the

tumor is left in situ, bowel obstruction and intussus-

ception ultimately result. At laparotomy, adequate

bowel and mesenteric margins must be obtained, as

with any cancer-related operation. Depending on tumor

size and the degree of spread, lesions can be treated

with simple local excision for small primaries to wide

en bloc resection for metastatic disease.

Patients who have carcinoid syndrome can achieve

symptomatic relief with subcutaneous injections of

somatostatin analogs (e.g., octreotide). Induction with

general anesthesia may provoke a life-threatening

carcinoid crisis characterized by hypotension, flushing,

tachycardia, and arrhythmias. Intravenous somatostatin

or octreotide rapidly reverses the crisis.

29
Q

Carcinoid Tumors: Prognosis

A

Carcinoid tumors are relatively indolent, slow-growing

neoplasms. Prognosis for patients with carcinoid

tumors is directly related to the size of the primary

tumor and to the presence of metastasis.

For noninvasive lesions of the appendix and rectum

less than 2 cm in size, the 5-year survival rate nears 100%. As

the tumor size increases, the survival rate decreases. The

presence of muscle wall invasion and positive lymph

nodes are poor prognostic signs.

Patients with hepatic metastases have an average

survival of approximately 3 years. Liver lesions are usu-

ally multiple. Because incapacitating symptoms of the

carcinoid syndrome are proportional to tumor bulk,

cytoreductive surgery can ameliorate symptoms, as well

as prolong survival. Nonsurgical palliation is achieved

with somatostatin analog therapy or chemoemboliza-

tion of the tumor.

30
Q

Key points

A
  • Small bowel obstruction is commonly caused by

adhesions and hernias. Bowel infarction occurs with

closed-loop obstruction and strangulation. Patients

with peritonitis require immediate surgery. Many

patients are successfully managed with supportive

therapy alone. Surgery is indicated if the obstruction

fails to resolve spontaneously.

  • Crohn’s disease is a transmural inflammatory process

that affects any part of the gastrointestinal tract,

from mouth to anus. The ileum is most commonly

involved. Surgical treatment is reserved mainly for

complications.

  • Meckel’s diverticulum is the most common congenital

abnormality of the small intestine and arises from a

failure of vitelline duct obliteration. It is a true divertic-

ulum and may contain heterotopic gastric and pancre-

atic tissue. Peptic ulceration with hemorrhage may

develop. It is the most common cause of major lower

gastrointestinal bleeding in infants.

• Small bowel tumors are rare and usually benign,

often presenting as small bowel obstructions. Benign

tumors include adenomas, lipomas, leiomyomas, and

hemangiomas. Malignant tumors include adenocar-

cinoma, gastrointestinal stromal tumors, carcinoid,

and lymphoma.

• Carcinoid tumors are the most common endocrine

tumors of the gastrointestinal tract and most

frequently occur in the appendix. All carcinoid tumors

are considered malignant because of their potential

for invasion and metastasis.

• Carcinoid tumors secrete serotonin, which is broken

down in the liver to the metabolite 5-hydroxyin-

doleacetic acid, which is, in turn, excreted in the urine.

Carcinoid syndrome, manifested by flushing, diarrhea,

sweating, and wheezing, invariably indicates hepatic

metastases, because vasoactive substances have

escaped hepatic metabolism.

• Carcinoid syndrome is treated with somatostatin

analogs and chemoembolization to provide sympto-

matic relief