Chapter 41
Common Gastrointestinal
Disorders
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Acute Gastrointestinal Bleeding
Upper gastrointestinal bleeding
• Peptic ulcer disease
– Primary factor is H. pylori, ingestion of ASA, NSAIDs,
smoking
• Stress-related erosive syndrome
– Decreased perfusion of stomach mucosa, related to
physiologic stress
• Esophageal varices
– Collateral circulation as a result of portal hypertension,
rising pressure causes tortuous distended veins or
varices
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Acute Gastrointestinal Bleeding (cont.)
• Mallory–Weiss tears
– Laceration of the distal esophagus, gastroesophageal
junction, and cardia of the stomach
– Heavy alcohol use, binge drinking, forceful
vomiting/retching, or violent coughing
• Dieulafoy’s lesions
– Vascular malformations, usually in the
proximal
stomach
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Clinical Presentation
• Presentation depends on the amount of blood loss.
• Slight anemia to shock
• Orthostatic changes imply volume depletion of 15% or
more.
• Hallmark of GIB is hematemesis, hematochezia, and
melena.
• Upper GIB—hematemesis, “coffee ground,” melena
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Assessment
• History
– History of PUD, dyspepsia, alcohol, smoking,
vomiting/retching, NSAIDs or ASA
• Physical examination
– Hemodynamic stability, VS, orthostatics, tissue
perfusion, LOC
– Abdominal exam, rectal exam
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Laboratory Studies
• Low H & H
• Mild leukocytosis and hyperglycemia
• High BUN
• Hypernatremia, hypokalemia
• Prolonged PT/PTT
• Thrombocytopenia
• Hypoxemia
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Management
• Volume resuscitation with IVF or blood products,
vasopressors
• Oxygen, central line
• NPO, NGT
• Electrolyte repletion
• Acid-suppressive therapy—PPIs or H2 antagonistic drugs
• Pharmacotherapy for decreasing portal hypertension
– Vasopressin, octreotide, somatostatin
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Definitive Diagnosis
• Endoscopy within 12 to 24 hours to identify the site
– Can be done at bedside
• Angiography—locates the site or abnormal vasculature,
insensitive in venous bleeding
• Barium studies are often inconclusive, and risk
of retained barium.
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Therapeutic Intervention
• Endoscopy—hemostasis 90% of cases but 25% of high
risk sites may rebleed
• Angiography
• Balloon tamponade—with esophageal varices
• Transjugular intrahepatic portosystemic shunt (TIPS)
• Surgery
– Rarely indicated; severe hemorrhage unresponsive to
initial resuscitation, unavailable/failed endoscopy,
perforation, obstruction, malignancy
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Medical Management
• Eradication of H. pylori, stop NSAIDs.
• PPIs or PPI and COX-2 inhibitor (if ASA or NSAIDs are
unavoidable)
• Beta-blockade reduces portal pressure.
• Prophylactic antibiotics
• Alcohol cessation
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Lower Gastrointestinal Bleeding
• Diverticulosis
– Sac-like protrusions in the colon; arteries are prone
to injury.
– Risk factors: diet low in fiber, ASA/NSAIDs, advanced
age, and constipation
• Angiodysplasia/AV malformation
– Dilated, tortuous submucosal veins, small AV
communications, or enlarged arteries
– Occurs anywhere in the colon and can be
venous or
arterial bleed
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Clinical Presentation
• Hemodynamic instability and hematochezia
• Diverticular bleeding is often painless, may complain of
cramping.
• Angiodysplasia presents with painless hematochezia.
• Chronic lower GIB presents with iron deficiency anemia.
• Hemorrhoids can present with massive bleeding from
rectal varices from portal hypertension.
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Assessment
• History
– Peptic ulcer disease, inflammatory bowel disease,
renal/liver disease
– Medication, color and consistency of stool, abdominal
pain, fever, rectal urgency, weight loss
– Change in bowel habits
• Physical examination
– VS, palpable mass, rectal exam
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Laboratory Studies
• CBC
• Electrolytes
• BUN and creatinine
• PT/PTT
• Type and cross-match
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Management
• Fluid resuscitation, NGT
• Colonoscopy for diagnosis and treatment
• Upper endoscopy distinguishes the source.
• Radionucleotide imaging—locates the site of bleed
• Angiography—for diagnosis and embolization
• Surgical intervention
– Exploratory lap, segmental bowel resection, total
colectomy
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Small Bowel Obstruction
• Adhesions are the most common cause after laparotomy,
radiation, ischemia, infection, or foreign body.
• Hernias—strangulated
• Tumors—uncommon in the small bowel
• Pathophysiology
– Fluid and air accumulate proximal to obstruction
causing distention.
– Bowel wall becomes edematous and distended.
– Peristalsis decreases and normal function halts.
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Clinical Presentation
• Severity of symptoms is proportionate to severity of
ischemia.
• Acute onset of intermittent, crampy, periumbilical pain
• Vomiting often relieves the pain.
• In strangulated SBO, the pain is localized, steady,
severe.
• Fever, constipation, obstipation
• Hemodynamic instability
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Assessment
• History of abdominal surgery/trauma, inflammatory
bowel disease, diverticulitis, radiation, PUD, pancreatitis
– Medication history, psychiatric history
• Physical examination
– Visible peristalsis and distention,
epigastric/periumbilical/diffuse abdominal
tenderness, hyperactive BS early then high-pitched
tinkling
– S & S of dehydration, palpable mass; palpate for
inguinal hernia.
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Diagnostic Studies
• Labs for differential
• Radiography
– Dx of obstruction, perforation, barium
• Computed tomography
– Obstructive lesions, neoplasms, hernias, and
ischemia
• Endoscopy
– Direct visualization of obstruction in colon or
proximal SB
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Management
• Medical management
– NPO, NGT, IVF, electrolyte repletion, I & Os, TPN,
central line
– Monitor for S & S of sepsis, perforation, ischemia,
necrosis, gangrene
• Surgical management
– Strangulated bowel, volvulus, incarceration, or
closed
loop obstructions need immediate surgery.
– Lysis of adhesions, resection, ostomy, bowel
decompression
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Colonic Obstruction
• Carcinoma, sigmoid diverticulitis, and volvulus
• Cecum does not allow decompression of fluid/gas into
the small bowel.
• Fluid and gas accumulate, increasing intraluminal
pressure.
• Colonic wall becomes ischemic.
• Normal colonic flora then produces methane and
ammonia, which add to distention.
• Changes in normal flora and translocation of
bacteria can
cause septic complications.
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Clinical Presentation
• Abdominal pain, distention, progressive obstipation
• Colicky/severe unremitting pain in peritonitis, severe
constant pain in gangrenous bowel
• Vomiting may occur late.
• Changes in bowel habits
• Dehydration
• Diarrhea may be present if stool is leaking past an
obstruction.
• Dyspnea from abdominal distention
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Assessment
• History of altered bowel movements, bloody stool,
iron deficiency anemia, weigh loss, anorexia, fever,
pain
• Physical examination
– Abdominal distention, tympany, ascites
– S & S of dehydration, hyperactive then hypoactive
BS, mass, diffuse abdominal tenderness with
guarding or rebound
– Rectal exam
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Laboratory Studies
• Iron deficiency, leukocytosis
• Imaging
– Abdominal films identify site of obstruction.
– CT distinguishes anatomic and pseudo-obstruction.
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Management
• Fluid and electrolytes, NPO, NGT, rectal tube
• Surgical management
– Left colon—decompression with primary anastomosis
– Right colon—primary resection and anastomosis
• Endoscopic therapy
– Stents as a palliative measure until surgery
– Used to debulk obstructing tumors
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Ileus
• Often called paralytic ileus or adynamic ileus
• Failure of intestinal contents to pass because of decreased
peristalsis activity in the absence of mechanical obstruction.
• Can have intra-abdominal or extra-abdominal causes
• Post-op, metabolic abnormalities, medications, local/systemic
inflammation, spinal cord injury, blood-borne toxins
• Pathophysiology
– Poorly understood
– Peristalsis decreased or ceases; distention occurs as
gas/fluid/electrolytes accumulate.
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Clinical Presentation
• Diffuse abdominal pain, nausea/vomiting, constipation,
hiccups, bloating
• History of thyroid/parathyroid disease, heavy metal
exposure, diabetes, scleroderma
• Physical examination
– Abdominal distention, decreased/absent BS,
resonant to percussion, tachycardia, orthostatic, S &
S of dehydration
• Labs—electrolyte abnormalities
• Abdominal radiography shows colonic dilation; CT
identifies causes of ileus.
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Management
• Treat the underlying cause.
• NPO, IVF, electrolyte repletion, NGT
• Hold medications that affect motility (narcotics).
• Neostigmine, prokinetic medications
• Colonoscopy
• Surgery for perforation
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Acute Pancreatitis
• Gallstones are responsible for 40% of cases.
• Alcoholism is the second leading cause of pancreatitis and accounts
for 35% of the cases.
• Hypercalcemia and hypertriglyceridemia, medications, infectious
processes
• Pathophysiology
– Pancreatic enzymes become prematurely activated.
– Results in autodigestion of the pancreas and peripancreatic
tissue
– Substances released from injured pancreas cause a cascade of
events that lead to systemic sequelae.
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Clinical Presentation
• Deep, boring midepigastric or periumbilical pain
• Nausea/vomiting without pain relief, tachycardia,
hypotension, abdominal distention, low-grade fever
• History of biliary disease, alcohol use, diabetes,
medications, location of pain, weight loss, N/V
• Physical examination
– Diffuse abdominal tenderness and
guarding, tympanic
to percussion
– Hypoactive BS, jaundice, ascites, S & S of
dehydrations
or hypovolemic shock
– Grey Turner’s Copyright
or Cullen’s sign
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Diagnostic Studies
• Labs
– Elevated serum amylase and lipase, electrolyte
imbalance, hyperglycemia, LFTs elevated with
concurrent liver disease, elevated ALT and alkaline
phosphatase with biliary disease
• Imaging studies
– Radiographs exclude other causes.
– CT is the preferred test.
– MRCP for bile duct stones, ERCP locates and
removes
stones.
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Ranson’s Criteria
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Complications
• Local—pacreatic necrosis, pseudocyst, abscess
• Pulmonary—atelectasis, ARDS, pleural effusion
• Cardiovascular—shock states
• Renal—ARF
• Hematologic—DIC
• Metabolic—hyperglycemia, hypertriglyceridemia,
hypocalcemia, metabolic acidosis
• Gastrointestinal—GIB
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Management
• IVF, electrolyte repletion, pain management, rest
pancreas with NGT to suction
• NPO, TPN, bed rest
• Surgical management
– With massive necrosis, pancreatic resection
is done.
– Broad-spectrum antibiotics
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Hepatitis
• Noninfectious hepatitis
– Excessive alcohol use
– Autoimmune disorders
– Metabolic or vascular disorders (right-sided HF)
– Acute biliary obstruction
– Medications (Tylenol, isoniazid, HMG-CoA reductase
inhibitors, anticonvulsants, antimicrobials, alpha-
methyldopa, amiodarone, and estrogens)
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Infectious Hepatitis
• Highly contagious
• Classified according to specific infecting agent and
corresponding serology markers
– Hepatitis A, B, C, D, and E
• HSV, EBV, CMV, adenovirus, coxsackievirus B, VZV
• Present with nonspecific flu-like symptoms
• Systems more severe in hepatitis B
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Pathophysiology
• Hepatocytes, blood vessels, and Kupffer cells are
responsible for uptake and degradation of foreign and
potentially harmful substances in the body.
• In mild disease, hepatocytes may regenerate.
• In severe disease, regeneration is incomplete and fibrosis
leads to cirrhosis and impediment of blood flow through
the liver.
• Fulminant liver failure can progress to cerebral edema,
coma, and death.
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Assessment
• History of alcohol use, drug use, medications, herbal
supplements, surgery and transfusion history,
occupational and travel history, sexual history
• Physical examination
– Jaundice, hepatomegaly, splenomegaly
– Muscle wasting, ascites, peripheral edema
– Vitamin deficiencies, bruising, telangiectasis, spider
nevi
– Abdominal wall vein dilation, bruit over the liver
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Laboratory Studies
• Tests for evaluating hepatocellular injury
– AST, ALT
• Tests for evaluating liver synthetic function
– Albumin, total protein, and PT
• Tests for evaluating cholestasis (excretory function)
– Serum bilirubin
– Alkaline phosphatase and GGT
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Management
• Treatment is supportive.
• Rest, hold harmful medications.
• Monitor hemodynamic status.
• Monitor hepatic enzymes, electrolytes.
• Strict I & O, daily weight, abdominal girth
• High-calorie, low-protein diet
• Monitor for bleeding.
• Avoid alcohol, narcotics, barbiturates.
• Treat encephalopathy.
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Cirrhosis
• Complication of liver disease
• Caused by chronic HCV, alcohol abuse, nonalcoholic
steatohepatitis, hereditary hemochromatosis, Wilson’s
disease, and alpha1-antitrypsin deficiency
• Inflammation, fibrotic changes, and increased
intrahepatic vascular resistance cause compression of the
liver lobule, leading to increased resistance or
obstruction of normal blood flow through the liver, which
is normally a low-pressure system
• Results in splenomegaly, varices, hemorrhoids, cardiac
dysfunction
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Assessment
• H & P reveals altered liver function.
• Altered glucose, carbohydrate, fat, and protein
metabolism
• Decreased synthesis of albumin leads to interstitial
edema and decreased plasma volume.
• Clotting dysfunction
• Ascites, lower extremity edema, hypotension
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Management
• Monitor nutrition, fluid balance, urine output,
electrolytes, PT/PTT, platelet function, hematocrit.
• Monitor LOC, abdominal girth.
• Manage ascites—paracentesis or VP shunt.
• TIPS procedure to decompress portal venous
system
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Complications of Hepatitis
• Hepatic encephalopathy
– Caused by accumulation of toxic agents absorbed in
intestinal tract
– Limit protein intake, lactulose, neomycin, or
metronidazole.
• Hepatorenal syndrome
– Often fatal: treatment is supportive.
• Spontaneous bacterial peritonitis
– Infected ascitic fluid, treat with broad-
spectrum
antibiotics.
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Obesity
• Overweight defined as body mass index [BMI] between 25
and 30 kg/m2
• Obese defined as BMI greater than 30 kg/m2
• Etiology is genetic as well as environmental.
• Weight loss of just 10% is often enough to bring down
high blood pressure, HbA1c levels, and lipid parameters.
• Comorbidities include but not limited to diabetes,
hypertension, obstructive sleep apnea, and
osteoarthritis
• No single laboratory study is diagnostic of obesity.
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Obesity—Management
• Bariatric surgery produces better weight loss than the
conventional diet and exercise.
• Most bariatric surgeries worldwide are now performed
laparoscopically.
• The goal of bariatric operations is restriction of food
intake, restriction of food absorption, or both to promote
weight loss.
– laparoscopic adjustable gastric band (LAGB)
– Roux-en-Y gastric bypass
– sleeve gastrectomy (SG)
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