The most common cause of iron deficiency anemia in the elderly is gastrointestinal blood loss.

The next step in evaluation would be colonoscopy and endoscopy. A single negative occult
blood test does not exclude the possibility of gastrointestinal bleeding.

Splenic abscess is complication of bacteremia from a distant infection (eg, infective endocarditis,
cholecystitis).; Diagnosis is made with CT scan of the abdomen; antibiotic therapy plus
splenectomy is generally required because many patients fail percutaneous aspiration (due to the
presence of occult microabscesses).

Because the risk of incarceration with femoral hernias is high (due to narrow hernia orifice),
patients with asymptomatic femoral hernias are referred for early elective hernia repair. In
contrast, asymptomatic inguinal hernias (hernia located above inguinal ligament) can usually be
managed with watchful waiting because hernia contents pass through a wider orifice.
Intraabdominal injury is less likely with open (as opposed to laparoscopic) hernia repair.

Deep (fascial) wound dehiscences can result in exposure or herniation (ie, evisceration) of
intraabdominal organs (eg, bowel), resulting in possible strangulation. Therefore, patients with
fascial dehiscence require emergency surgery.
Superficial wound dehiscences are separations of the skin and subcutaneous tissue with intact
rectus fascia. These typically develop within the first postoperative week due to an abnormal
subcutaneous fluid buildup (eg, seroma) and can often be managed conservatively with careful
dressing changes.

Serologic studies can distinguish between pyogenic and amebic liver abscesses.

Small intestinal bacterial overgrowth

Etiology  Anatomical abnormalities (eg, strictures, surgery)
 Motility disorders (eg, diabetes mellitus, scleroderma)

Signs/  Abdominal pain, diarrhea, bloating, flatulence

symptoms  Malabsorption, weight loss, anemia, vitamin deficiency

Diagnosis  Jejunal aspirate & culture showing >105 organisms/mL

 Carbohydrate breath testing (eg, lactulose, glucose)

Organisms  Streptococci, Bacteroides, Escherichia, Lactobacillus

Treatment  Antibiotics (eg, rifaximin, amoxicillin-clavulanate)

 Avoid antimotility agents (eg, narcotics)
  Dietary changes (eg, high-fat, low-carbohydrate)
 Promotility agents (eg, metoclopramide)

Rectus sheath hematoma

Risk factors  Abdominal trauma, forceful abdominal contractions (eg, coughing)
 Anticoagulation
 Older age, female sex

Clinical  Acute-onset abdominal pain with palpable abdominal mass

features  Blood loss anemia, leukocytosis
 Tenderness may worsen with abdominal contraction (Carnett sign)
 ± Nausea, vomiting, fever

Management  CT scan confirm the diagnosis

 Hemodynamically stable: serial monitoring of CBC, reverse
anticoagulation and transfuse blood products when appropriate
 Unstable: angiography with embolization, surgical ligation

CBC = complete blood count.

Normal structure:

Retroperitoneal abdominal organs

 Suprarenal (adrenal) glands

 Aorta & inferior vena cava
 Duodenum* (except 1st part)
 Pancreas* (head & body)
 Ureters
 Colon* (ascending & descending)
 Kidneys
 Esophagus
 Rectum (mid-distal)

Mnemonic: SAD PUCKER

*Secondarily retroperitoneal (developed intraperitoneal & migrated retroperitoneal).

The osmotic gap is calculated as 290 - [2 (stool Na + stool K)] and is >75 mOsm/kg in all forms
of osmotic diarrhea. Acid steatocrit is a test for fat malabsorption. Lactose intolerance is
characterized by a positive hydrogen breath test, positive stool test for reducing substances, low
stool pH and increased stool osmotic gap. There is no steatorrhea. upper gastrointestinal
bleeding often have an elevated blood urea nitrogen (BUN) and elevated BUN/creatinine ratio,
possibly due to increased urea production (from intestinal breakdown of hemoglobin) and
increased urea reabsorption (due to hypovolemia). spleen tip is sometimes palpable in
healthy newborns. Decreased hepatic uptake of bilirubin can occur with certain drugs (eg,
rifampin) or reduced hepatic blood flow (eg, congestive heart failure).

Congenital and developmental anomalies

 Gastroesophageal reflux
Pathogenesis  Immature lower esophageal sphincter
 Tobacco smoke, which reduces esophageal sphincter pressure, are at
increased risk.

Clinical  Spit-up
features  Normal weight gain
  No pain/back-arching

Management  Upright positioning after feeds

 Burping during feeds
 Frequent, small-volume feeds

Frequent, small-volume feeds; hold the infant upright for 20-30 minutes after feeds; and
place the infant prone when awake. Activities that increase intraabdominal pressure (eg,
fastening the diaper too tight, bringing the knees to the stomach) should be avoided.
Regurgitation usually improves around age 6 months (when the infant can sit unsupported) and
resolves by age 1 year.
 Delayed passage of meconium
Hirschsprung disease Meconium ileus
Pathophysiology  Failure of neural crest cell  Obstruction by
migration inspissated stool

Level of  Rectosigmoid  Ileum

obstruction
Rectal examination  Increased tone  Normal tone
 Positive squirt sign*  Negative squirt sign*
 Meconium  Normal  Inspissated
consistency
Imaging  Dilated proximal colon ±  Dilated small bowel
small bowel  Microcolon
 Narrow rectosigmoid

Associated disorder  Down syndrome  Cystic fibrosis

*Expulsion of gas/stool on rectal examination.

Intussusception
 Risk  Recent viral illness or rotavirus vaccination
factors  Pathologic lead point
o Congenital malformation of the intestines
(eg, Meckel diverticulum)
o Henoch-Schönlein purpura
o Celiac disease
o Intestinal tumor
o Polyps

Clinical  Sudden, intermittent abdominal pain, episodes of

present inconsolable crying, with legs drawn to the
ation abdomen due to pain
 Currant jelly stools
 Sausage-shaped abdominal mass
 Lethargy or altered mental status

Diagno  Target sign on ultrasound(test of choice)

sis 
 Cresent sign
Treatm  Air or saline enema under fluroscopy/ultrasound
ent  Surgery for removal of lead point

Biliary atresia
Pathogenesi  Extrahepatic bile duct fibrosis
s
Clinical  Asymptomatic at birth
findings  Infants age 2-8 weeks:
o Jaundice, acholic stools (eg, light yellow, clay-colored, white) ,
 dark urine
o Hepatomegaly

Diagnostic  Direct hyperbilirubinemia

evaluation  Ultrasound (initial step):
o Absent/abnormal gallbladder &/or CBD
o Triangular cord sign (fibrous remnants seen above the porta
hepatis).
 Liver biopsy:
o Intrahepatic bile duct proliferation
o Portal tract inflammation & edema
o Fibrosis
 Intraoperative cholangiography (gold standard):
o Biliary obstruction

Treatment  Surgical hepatoportoenterostomy (Kasai procedure)

 Liver transplant

An umbilical granuloma presents in newborns after the umbilical cord has separated with a moist, red,
pedunculated, friable umbilical mass. Treatment is with silver nitrate.

Congenital umbilical hernia

Pathophysiolog  Incomplete closure of abdominal muscles
y
Clinical features  Soft, nontender bulge at umbilicus
 Protrudes with increased abdominal pressure
  Typically reducible

Management  Observe for spontaneous closure

 Elective surgery around age 5

A pathologic lead point should be suspected in patients with the following:

 Recurrent intussusception
 Atypical age for intussusception
 Atypical location of intussusception (eg, small bowel into small bowel)
 Persistent rectal bleeding despite reduction of intussusception
A target sign on ultrasound is diagnostic of intussusception and should prompt immediate
treatment with an air or water-soluble contrast enema. Retrograde pneumatic (ie, air enema) or
hydrostatic (ie, contrast enema) pressure reduces the telescoped bowel in most cases.
Laparotomy is indicated if enema reduction is ineffective, if a pathological lead point is
identified, or if the patient has signs of perforation (eg, free air on x-ray, rigid abdomen).
 Infantile hypertrophic pyloric stenosis
Risk factors  First-born boy
 Erythromycin
 Bottle feeding, formula-fed infants have slower gastric emptying and
typically consume more volume in less time. This increased gastric
burden may stimulate pyloric muscle growth.

Presentation  Projectile nonbilious emesis

 Poor weight gain
 Dehydration
 Olive-shaped abdominal mass

Diagnostic  Hypochloremic metabolic alkalosis

studies  Thickened pylorus on abdominal ultrasound

Treatment  Intravenous rehydration

 Pyloromyotomy
Diagnosis is made by ultrasound.

Although pyloromyotomy is the treatment of choice, infants with signs of dehydration or

laboratory abnormalities should be admitted for intravenous rehydration and normalization of
electrolytes prior to definitive surgical treatment. Normalization of electrolytes and correction of
alkalosis prior to surgery have been shown to decrease the risk of postoperative apnea and
improve overall outcomes.

A soap-bubble gas pattern may be present in the ileum due to mixing of meconium with air.

Malrotation with midgut volvulus

 Failure of normal embryonic gut rotation
 Narrow mesenteric base allows for ↑ small bowel mobility
Pathogenesis  Twisting of small bowel around superior mesenteric artery → gut
ischemia & necrosis

Clinical  Most common in infancy (usually age <1 month)

  Acute: bilious emesis, abdominal distension
 Chronic: intermittent abdominal pain & vomiting, failure to
thrive
features
 Untreated: hematochezia, peritonitis & shock
 Complications include bowel necrosis and perforation.

 Abdominal x-ray: ± dilated bowel, air-fluid levels,

pneumoperitoneum
Diagnosis  Upper gastrointestinal series (gold standard): ligament of Treitz
on right; corkscrew, or bird's-beak, duodenum

 Emergency laparotomy (to relieve volvulus)

Treatment  Ladd procedure (to reposition malrotated bowel)
Malrotation is also associated with other congenital anomalies such as diaphragmatic
hernia, omphalocele and heterotaxy syndrome.
Complications: Midgut volvolus (could be intermittent) duodenal obstruction
Diagnosis is confirmed using upper gastrointestinal series, and treatment is surgical (Ladd
procedure) to divide the peritoneal bands and reposition the bowel.

Hirschsprung disease (congenital aganglionic megacolon)

Pathology  Failed neural crest cell migration to distal colon

Symptom  Neonates: Delayed passage of meconium, bilious vomiting, ± enterocolitis

s  Children/adolescents: Chronic constipation, failure to thrive, thin caliber
stools

Physical  Distended abdomen

examinati  Tight anal sphincter
on  Absence of stool in rectal vault
 Forceful stool expulsion on rectal examination
Diagnosis  Rectal suction biopsy (gold standard)
 Anorectal manometry, contrast enema (adjuncts)


Managem  Surgical resection of aganglionic segment

ent
 IgE- & non–IgE-mediated food allergies
Clinical
Example Age Symptom onset
features
 Urticaria
 Vomiting, wheezing
Immediate
IgE mediated Anaphylaxis Any  Angioedema,
(<1 hr)
hypotension

 Painless, bloody
Food protein–
stools
induced allergic <6 months Insidious
 Well appearing
proctocolitis
Non–IgE
 Profuse vomiting,
mediated Food protein–
diarrhea (± blood),
induced
<12 months Within hours dehydration, lethargy
enterocolitis
 Ill appearing
syndrome
Most breastfed infants respond to maternal elimination of dairy alone, and additional
eliminations (eg, soy) usually are recommended only for persistent symptoms to avoid a severely
restricted maternal diet. For formula-fed infants, switching to an extensively hydrolyzed
formula, which contains predigested cow's milk proteins and is free of potentially cross-reacting
soy proteins, is ideal. In rare cases of persistent bleeding, an amino acid–based (elemental)
formula may be required. Symptoms typically resolve in days to weeks.

Gastroesophageal disorders:
Upright chest x-ray revealing intraperitoneal free air (pneumoperitoneum) confirms the
diagnosis of perforation.

Immediately following diagnosis, the following should be initiated:

 Surgical consultation
 Intravenous proton pump inhibitors and broad-spectrum antibiotics
 Fluid resuscitation and nasogastric suction
Esophagus:
The diagnosis is confirmed with barium swallow or upper endoscopy. Whereas symptomatic
sliding hernias are generally managed with medical treatment of reflux symptoms, PEHs often
require surgical repair.

Mallory-Weiss tear
Etiology  Sudden increase in abdominal pressure (eg, forceful
retching)
 Mucosal tear in esophagus or stomach (submucosal
arterial or venous plexus PAINFUL bleeding)
 Risk factors: Hiatal hernia, alcoholism

Clinical  Vomiting, retching

presentation  Hematemesis
 Epigastric pain

Diagnosis  Longitudinal laceration on endoscopy

Treatment  Most heal spontaneously

 Endoscopic therapy for persistent bleeding
 Esophageal perforation
Etiology  Instrumentation (eg, endoscopy), trauma
 Effort rupture (Boerhaave syndrome)
 Esophagitis (infectious/pills/caustic)

Clinical  Chest/back &/or epigastric pain, systemic signs (eg, fever)

presentation  Crepitus (subcutaneous emphysema), Hamman sign (crunching sound
on auscultation)
 Pleural effusion with atypical (eg, green) fluid, low pH, and high
amylase.

Diagnosis  Chest x-ray or CT scan: widened mediastinum, pneumomediastinum,

pneumothorax, pleural effusion
 CT scan: esophageal wall thickening, mediastinal fluid collection
 Esophagography with water-soluble contrast: leak from perforation
 Barium contrast is more sensitive but can incite a granulomatous
inflammatory response; it is used when water-soluble contrast
esophagography is inconclusive.

Management  NPO, IV antibiotics(ampicilli-sulbactam) & proton pump inhibitors

 Emergency surgical consultation

Achalasia
Clinical  Chronic dysphagia to solids & liquids, regurgitation
presentation  Heartburn, weight loss over years
 Upright position increases the pressure in the esophagus and
results in more effective swallowing.

Diagnosis  Manometry (the most sensetive test; if ambivalent do barium): ↑

LES resting pressure, incomplete LES relaxation, ↓ peristalsis of
distal esophagus
 Barium esophagram: smooth "bird beak" narrowing at
gastroesophageal junction

Management  Upper endoscopy to exclude malignancy

 Laparoscopic myotomy or pneumatic balloon dilation
 Botulinum toxin injection, nitrates & CCB

CCB = calcium channel blocker; LES = lower esophageal sphincter.

 Eosinophilic esophagitis
Pathogenesis  Chronic, immune-mediated esophageal inflammation

Clinical  Dysphagia
features  Chest/epigastric pain
 Reflux/vomiting
 Food impaction
 Associated atopy

Diagnosis  PPIs trial for 2 months, then if symptoms do not reselve go for Endoscopy &
 esophageal biopsy (≥15 eosinophils per high-power field)

Treatment  Dietary modification

 ± Topical glucocorticoids (eg, swallowed) fluticasone.
Magnets identified beyond the stomach can be removed via colonoscopy or followed with serial
x-rays (every 4-6 hr). If symptoms (eg, abdominal pain, gastrointestinal bleeding) develop or if
the magnets do not progress in the gastrointestinal tract, surgical removal is indicated.
Esophageal malignancy.

Endoscopy is recommended to exclude malignancy in all patients with suspected achalasia.

Laparoscopic myotomy and pneumatic balloon dilation are the treatments of choice for patients
with achalasia who are at low surgical risk. Options for patients at high surgical risk include
botulinum toxin injection, nitrates, and calcium channel blockers. However, all these treatments
should be considered only after malignancy is excluded and the diagnosis of achalasia is
confirmed.

Medication-induced esophagitis " It is most common

in the mid-esophagus due to compression by the aortic
arch or an enlarged left atrium. "
Drug class Drug
Antibiotics Tetracyclines (acid effect)
Anti-inflammatory Aspirin & many nonsteroidal
agents anti-inflammatory drugs(disrupt
protective layer)
Bisphosphonates Alendronate, risedronate
Others Potassium chloride (osmotic
effect), iron
 Characteristics of gastroesophageal mural injury
Etiology Mallory-Weiss syndrome Boerhaave syndrome
 Forceful retching  Forceful retching
 Mucosal tear  Transmural tear
 Submucosal venous or  Spillage of esophageal air/fluid into
arterial plexus
 bleeding surrounding tissues

Clinical  Epigastric/back pain  Chest/back/epigastric pain

presentation  Hematemesis (bright  Crepitus, crunching
red or coffee-ground) sound (Hamman sign)
 Possible hypovolemia  Odynophagia, dyspnea, fever,
sepsis

Studies  Upper GI endoscopy  Chest x-ray: pneumothorax,

confirms diagnosis (& pneumomediastinum, pleural
can treat persistent effusion
bleeding)  Esophagography or CT scan with
water-soluble contrast confirms
diagnosis

Management  Acid suppression  Acid suppression, antibiotics, NPO

 Most heal  Emergency surgical consultation
spontaneously

GI = gastrointestinal.
 Eosinophilic esophagitis
Pathogenesis  Chronic, immune-mediated esophageal inflammation

Clinical  Dysphagia
features  Chest/epigastric pain
 Reflux/vomiting
 Food impaction
 Associated atopy

Diagnosis  Endoscopy & esophageal biopsy (≥15 eosinophils per high-power field)
 The endoscopic appearance of EoE includes furrowing; small, whitish
exudates; and multiple stacked, ringlike esophageal indentations
(trachealization of the esophagus)


Treatment  Dietary modification

 ± Topical glucocorticoids (eg, fluticasone, budesonide).
 PPIs for concurrent GERD

Diffuse esophageal spasm: impaired inhibitory innervation in the esophagus

Pathophysiology  Uncoordinated, simultaneous
 contractions of esophageal body

Symptoms  Intermittent chest pain

 Dysphagia for solids & liquids

Diagnosis  Manometry: Intermittent peristalsis,

multiple simultaneous contractions, multiple
nonperistaltic simultaneous contractions of the
middle and lower esophagus. The lower
esophageal sphincter usually shows normal
relaxation.
 Esophagram: "Corkscrew" pattern

Treatment  Calcium channel blockers (Diltiazem)

 Alternates: Nitrates or tricyclics

Achalasia (impaired esophageal motility with incomplete relaxation at the lower esophageal
sphincter) and nutcracker esophagus "hypertensive esophagus" it is just exaggerated
contraction(excessive tone at the lower esophageal sphincter).

Endoscopic variceal ligation is an alternate primary preventive therapy in patients with

contraindications to beta blocker therapy.

Current guidelines suggest keeping the hemoglobin >9 g/dL in variceal hemorrhage. This patient
should have serial blood counts drawn and may require transfusion if the hemoglobin decreases
to <9 g/dL.

Stomach:
Patients with autoimmune metablastic atrophic gastritis often develop dyspepsia
with postprandial abdominal pain, bloating, nausea, heartburn, or regurgitation and Macrocytic
anemia; the pathophysiology may be related to changes in gastroduodenal motility, visceral
sensitivity, or acid secretion. Other laboratory findings include elevated serum gastrin
levels; iron deficiency anemia may occur as hypochlorhydria leads to reduced iron
bioavailability. Because AMAG is associated with an increased risk for gastric adenocarcinoma
and neuroendocrine tumors, routine surveillance endoscopy is indicated. Therefore, patients with
pernicious anemia require esophagogastroduodenoscopy at initial diagnosis and with any
suspicious symptoms (eg, positive fecal occult blood test, mid-epigastric abdominal pain).
Gastric cancer is endemic to Eastern Asia, Eastern Europe, and the Andean portions of South
America due to diets high in salt-preserved food (direct mucosal damage) and nitroso
compounds(carcinogen). Manifestations typically include weight loss and chronic mid-
epigastric pain that worsens with eating. Esophagogastroduodenoscopy is the initial test of
choice to establish the diagnosis.
When perforation is suspected and plain radiographs are negative, CT scan of the abdomen with
intravenous contrast can help detect smaller amounts of free air or free fluid. However, CT scan
should not delay surgical consultation and intervention, especially when peritonitis is present.
\

MALT Lymphoma, As a result, all patients with MALT lymphomas should be tested for H
pylori infection, and patients with a positive result who have early-stage MALT lymphoma
should undergo H pylori eradication therapy (eg, quadruple therapy). The majority of patients
achieve complete remission with antibiotic treatment. Patients with more advanced
malignancies or with H pylori-negative tumors should be considered for radiation therapy,
immunotherapy (eg, rituximab), or single-agent chemotherapy.

Dumping syndrome
Symptoms  Abdominal pain, diarrhea, nausea

 Hypotension/tachycardia
  Dizziness/confusion, fatigue, diaphoresis

Timing  15-30 minutes after meals

Pathogenesis  Rapid emptying of hypertonic gastric contents

Initial  Small/frequent meals

management  Replace simple sugars with complex carbohydrates
 Incorporate high-fiber & protein-rich foods
 Drink fluids between rather than during meals
 With refractory symptoms may benefit from a trial of octreotide or
require reconstructive surgery, but this is not usually needed

DS is a common postgastrectomy complication occurring in up to 50% of patients. It is caused

by loss of the normal action of the pyloric sphincter due to injury or surgical bypass and leads to
rapid emptying of hypertonic gastric contents into the duodenum and small intestine. This
causes fluid shifts from the intravascular space to the small intestine, leading to hypotension,
stimulation of autonomic reflexes, and release of intestinal vasoactive polypeptides.
Intestinal and colorectal disorders:

Acute mesenteric ischemia

Presentatio  Rapid onset of periumbilical pain (often severe)
n  Pain out of proportion to examination findings
 Hematochezia (late complication)

Risk factors  Atherosclerosis (acute or chronic)

 Embolic source (thrombus, cardiac vegetation)
 Hypercoagulable disorders

Laboratory  Leukocytosis
 Elevated amylase & phosphate levels
findings  Metabolic acidosis (elevated lactate)

Diagnosis  CT (preferred) or MR angiography

 Mesenteric angiography if diagnosis is unclear

Patients with evidence of bowel infarction should undergo immediate operative evaluation;
otherwise, diagnosis can be confirmed radiologically by CT angiography. Treatment includes
open embolectomy with vascular bypass or endovascular thrombolysis. In addition, patients
should be started on broad-spectrum antibiotics and, in the absence of active bleeding,
anticoagulation to reduce the risk of clot expansion.

Colonic ischemia
Pathophysiology  Usually nonocclusive, “watershed” ischemia
 Underlying atherosclerotic disease
 State of low blood flow (eg, hypovolemia)

Clinical features  Moderate abdominal pain & tenderness

 Hematochezia, diarrhea
 Leukocytosis, lactic acidosis

Diagnosis  CT scan with IV contrast: Colonic wall thickening, fat stranding, to

exclude perforation or extensive necrosis, if complicated resect if not
do colonoscopy to confirm
 Endoscopy: Edematous & friable mucosa
 Thumbprint sign on X-Ray

Management  Intravenous fluids & bowel rest

  Antibiotics with enteric coverage
 Colonic resection if necrosis develops

CT imaging in Ischemic colitis can show edema and air (pneumatosis) in the bowel wall.
Colonoscopy shows segments of cyanotic mucosa and hemorrhagic ulcerations, with a sharp
transition from affected to unaffected mucosa. Unless the patient has perforation or bowel
gangrene, most cases are managed conservatively with intravenous fluids, bowel rest, and
antibiotics.

Acute colonic pseudoobstruction (Ogilvie syndrome)

largely result from autonomic disruption of the colon
Etiologies  Major surgery, traumatic injury, severe infection
 Electrolyte derangement (↓ K, ↓ Mg, ↓ Ca)
 Medications (eg, opiates, anticholinergics)
 Neurologic disorders (eg, dementia, stroke)

Clinical  Abdominal distension, pain, obstipation, vomiting

findings  Tympanic to percussion, ↓ bowel sounds
  If perforation: guarding, rigidity, rebound tenderness

Imaging  X-ray: colonic dilation, normal haustra, nondilated small bowel

 Diagnosis made by CT scan: colonic dilation without anatomic
obstruction

Managemen  NPO, nasogastric/rectal tube decompression

t  IV Neostigmine if no improvement within 48 hr or if the cecal diameter
on imaging exceeds 12 cm (which is a strong predictor of impending
perforation).

Toxic megacolon
Pathophysiology  Colonic smooth muscle inflammation & paralysis
 Complication of IBD or infectious colitis, which produce NO that
decrease motility
 ↑ Risk with use of antimotility agents (eg, loperamide) or opioids

Clinical features  Systemic toxicity (eg, fever, tachycardia, hypotension)

 Abdominal pain & distension following diarrheal illness

Diagnosis  Colonic dilation (>6 cm) on imaging by X-Ray

Treatment  Bowel rest/decompression, antibiotics

 Corticosteroids if IBD-associated
 Surgery for perforation, peritonitis, clinical deterioration, subtotal
colectomy with end-ileostomy

The diagnosis of TM requires both manifestations of systemic toxicity and radiographic

confirmation of colonic dilatation without evidence of mechanical obstruction. CT scan of the
abdomen with intravenous and oral contrast can identify features typical of TM:

 Colonic dilatation >6 cm (diagnostic)

 Loss of normal haustral pattern
 Irregular mucosal pattern, with areas of ulceration alternating with areas of edema

CT scan can also assess for complications of TM (eg, colonic perforation or necrosis) that may
require surgery. But we obtain basline abdominal X-Ray at admission.

Any agent that contributes to a lack of gastrointestinal motility (eg, opiates, anticholinergics,
antimotility medications) should be discontinued. Lack of response or clinical deterioration
often necessitates further imaging (eg, CT of the abdomen) and, sometimes, surgical intervention
(eg, subtotal colectomy).
Clinical features of irritable bowel syndrome, associated with fibromyalgia, depression, and
 anxiety.
Rome IV diagnostic criteria Recurrent abdominal pain/discomfort ≥1 day/week for past
3 months & ≥2 of the following:

 Related to defecation (improves or worsens)

 Change in stool frequency
 Change in stool form

Alarm features  Older age of onset (≥50)

typically require further  Gastrointestinal bleeding
evaluation with colonoscopy.  Nocturnal diarrhea
 Worsening pain
 Unintended weight loss
 Iron deficiency anemia
 Elevated C-reactive protein
 Positive fecal lactoferrin or calprotectin
 Family history of early colon cancer or IBD

IBD = inflammatory bowel disease.

The purpose of laboratory testing is primarily to exclude an alternative diagnosis.

●In all patients with suspected IBS, we perform a complete blood count.
●In patients with diarrhea, we perform the following:
•Fecal calprotectin or fecal lactoferrin
•Stool testing for giardia (antigen detection or nucleic acid amplification assay)
•Serologic testing for celiac disease
•C-reactive protein levels, only if fecal calprotectin and fecal lactoferrin cannot be performed
Celiac disease:
A false-positive D-xylose test (ie, low urinary D-xylose level despite normal mucosal
absorption) can be seen in the following:

 Delayed gastric emptying

 Impaired glomerular filtration
 Small intestinal bacterial overgrowth (SIBO), characterized by alterations in small
intestinal flora (due to abnormal intestinal anatomy or motility), leading to bacterial
fermentation of the D-xylose before it can be absorbed. SIBO is treated with rifaximin;
therefore, it is unlikely in this patient whose D-xylose test results did not change
following treatment with rifaximin.

Celiac disease
 Risk factors  First-degree relative with celiac disease
 Down syndrome
 Autoimmune disorders (eg, type 1 diabetes, autoimmune
thyroiditis)
 North Europe and increase with age

Classic  ± Abdominal pain, distension, bloating, diarrhea

symptoms
Extraintestinal  General: failure to thrive/weight loss, short stature,* delayed
manifestations puberty/menarche*
(may be sole  Oral: enamel hypoplasia, atrophic glossitis
presentation)  Dermatologic: dermatitis herpetiformis
 Hematologic: iron deficiency anemia (due to malabsorption)
 Neuropsychiatric: peripheral neuropathy, mood disorders (eg,
anxiety, depression)
 Musculoskeletal: arthritis, osteomalacia/rickets* (due to vitamin
D malabsorption),

Diagnosis  ↑ Tissue transglutaminase IgA antibody

 Proximal intestinal biopsy (villous atrophy, crypt hyperplasia,
intraepithelial lymphocytosis)
 The diagnosis of celiac disease is highly correlated with positive
results on serological studies, primarily IgA anti-tissue
transglutaminase and IgA anti-endomysial antibodies.
However, many patients with biopsy-confirmed celiac disease
(as in this case) will have negative results on IgA antibody
testing due to an associated selective IgA deficiency, which is
common in celiac disease. If IgA serology is negative but the
suspicion for celiac disease is high, total IgA should be
measured (or IgG-based serologic testing should be done).

Treatment  Gluten-free diet

 Dapsone for dermatitis herpetiformis

*Pediatric findings.

Clinical manifestations of celiac disease

Gastrointestinal  Diarrhea, ± steatorrhea, weight loss
 Abdominal pain
 Flatulence/bloating
 Late manifestations: ulcerative jejunitis, enteropathy-associated T-
cell lymphoma

Mucocutaneous  Dermatitis herpetiformis

  Atrophic glossitis

Endocrine  Vitamin D deficiency

 Secondary hyperparathyroidism

Bone disorders  Osteomalacia/osteoporosis (adults)

 Rickets (children)

Hematologic  Iron deficiency anemia

Neuropsychiatri  Peripheral neuropathy; symptoms related to malabsorption (eg,

c diarrhea, microcytic anemia, vitamin D deficiency) or autoimmune
inflammation (eg, peripheral neuropathy, atrophic glossitis).
 Depression/anxiety

Features of malabsorption in celiac disease

Nutrients Symptoms
General Bulky, foul-smelling, floating stools
Fat & protein Loss of muscle mass, loss of subcutaneous fat,
fatigue
Iron Pallor (anemia), fatigue
Calcium & vitamin D Bone pain (osteomalacia), fracture (osteoporosis)
Vitamin K Easy bruising
Vitamin A Hyperkeratosis
In individuals at low risk for celiac disease, evaluation begins with serologic testing. Patients
with positive serologic testing, should undergo an upper endoscopy with small bowel biopsy to
diagnose celiac disease. In contrast, in individuals with a high probability of celiac disease, both
serologic testing and small bowel biopsy (regardless of celiac specific serology results) should be
performed
Immunoglobulin A (IgA) anti-tissue transglutaminase (tTG) antibody is the single preferred test
for detection of celiac disease in adults. In addition, we concurrently measure total IgA levels. In
patients with IgA deficiency we perform IgG-based testing with deamidated gliadin peptide
(DGP) IgG.

On patient on gluten free diet we perform HLA genetic testing, if negative we exclude celiac but
if positive we do put the patient on gluten challenge.

IBD
Most immediate step in diagnosing IBD is Colonoscopy and bopsies to diffrentiate between the
two.

There appears to be a bimodal distribution of ulcerative colitis with a 15-40 and second peak at
age 50-80.

Crohn disease Ulcerative colitis

Involvement  Anywhere mouth to anus (mostly  Rectum (always) &

ileum & colon) colon
 Perianal disease with rectal sparing  Continuous lesions
 Skip lesions

Microscopy  Noncaseating granulomas  No granulomas

Gross  Transmural inflammation  Mucosal &

findings  Linear mucosal ulcerations submucosal
 Cobblestoning, creeping fat inflammation
 Pseudopolyps

Clinical  Abdominal pain (often RLQ)  Abdominal pain

manifestations  Watery diarrhea (bloody if colitis) (varying locations)
 Bloody diarrhea
 Males

Intestinal  Fistulae, abscesses  Toxic megacolon

complications  Strictures (bowel
obstruction), Depending on the
location and length of the
stricture, surgical resection may be
required.

RLQ = right lower quadrant.

EN and IBD is well recognized and more commonly occurs in Crohn disease than ulcerative
colitis. EN mirrors IBD disease activity, meaning that it worsens during severe IBD flares and
resolves as those flares improve.
Initial management of both CD and UC involves administration of 5-aminosalicylic acids and,
frequently, corticosteroids (mainly in crohns). Maintenance therapy for both diseases may
involve azathioprine or antitumor necrosis factors.
 Classification & management of mild ulcerative colitis
Clinical features  <4 watery bowel movements per day
 Hematochezia is rare or intermittent

Laboratory  No anemia
findings  Normal ESR & CRP

Treatment  5-Aminosalicylic acid agents (eg, mesalamine,

sulfasalazine)

Initial management for mild UC is with 5-aminosalicylic acid (5-ASA) medications (eg,
mesalamine, sulfasalazine, balsalazide), which are used for both induction and maintenance
therapy. Mesalamine enemas or suppositories are preferred in patients with UC confined to the
rectosigmoid, whereas oral 5-ASA medications are needed for more extensive disease.
Corticosteroids are typically reserved for acute disease flares or severe chronic disease and can
be given topically (eg, hydrocortisone enema) or systemically (eg, prednisone).
Smoking and young age (<30) at diagnosis are significant risk factors for uncontrolled
inflammation and disease progression despite medical therapy in Crohn. >50% require repeat
surgery within 10 years if the disease is not properly controlled.
Calprotectin sometimes used in patients with established CD who have symptoms of a flare.

Microscopic colitis: secretory diarrhea

Clinical  Watery, nonbloody diarrhea; fecal urgency & incontinence
findings  Abdominal pain, fatigue, weight loss, arthralgias

Triggers  Smoking, medications (eg, NSAIDs, PPIs, SSRIs, ranitidine)

Diagnosis  Colonoscopic biopsy with lymphocytic infiltration of lamina propria; it is autoimmune

disease, women
o Collagenous: thickened subepithelial collagen band
o Lymphocytic: high levels of intraepithelial lymphocytes

Management  Remove possible triggers

 Antidiarrheal medications & budesonide
Inflammatory bowel disease is frequently complicated by arthritis, which occurs in up to 45% of
patients and can involve axial or peripheral joints.
There are no specific tests for the diagnosis of IBD-associated arthritis. Nonsteroidal anti-
inflammatory drugs (NSAIDs) can relieve arthritis symptoms but exacerbate the underlying
bowel disease. Consequently, although NSAIDs are frequently tried, many of the medications
(eg, sulfasalazine) used to treat the bowel disease itself are also used to treat joint disease.
Inflammatory bowel disease is associated with both axial spondyloarthritis and peripheral
arthritis. The peripheral arthritis can manifest as a self-limited pauciarticular arthritis (typically
affecting the knee) or a chronic polyarthritis that primarily affects the metacarpophalangeal
joints. Although this second type may resemble RA, it is uncommon and almost always follows
onset of gastrointestinal symptoms.

Intestinal obstruction:
Some degree of ileus occurs following most abdominal procedures; however, persistence of the
signs and symptoms (>3-5 days postoperatively) is termed prolonged (or "pathologic")
postoperative ileus (PPI). Techniques to prevent PPI include epidural anesthesia, minimally
invasive surgery, and judicious perioperative use of intravenous fluids (to minimize
gastrointestinal edema)
 SBO vs ileus
SBO Ileus
 Nausea, vomiting
 Nausea ± vomiting
 Obstipation
 No flatus
Clinical  Acute abdomen
 Abdominal distension
features  Hyperactive or absent
 Decreased or absent bowel sounds
bowel sounds

 No transition point
 Air fluid levels
 Dilated loops of bowel
 Dilated proximal
 Air in colon/rectum
bowel, collapsed distal
X-ray  Conservatively managed with antiemetics,
bowel
findings bowel rest, and serial examinations. Opiates,
 Little/no air in
which further decrease bowel motility, should
colon/rectum
be avoided if possible.

SBO = small bowel obstruction.

 Small-bowel obstruction
 Colicky abdominal pain, vomiting
 Inability to pass flatus or stool if complete (no obstipation if partial)
Clinical
 Hyperactive → absent bowel sounds
presentation
 Distended & tympanitic abdomen

 Dilated loops of bowel with air-fluid levels on plain film or CT scan

 Partial: air in colon
Diagnosis
 Complete: transition point (abrupt cutoff), no air in colon

 Ischemia/necrosis (strangulation)
Complications  Bowel perforation

 Bowel rest, nasogastric tube suction, intravenous fluids

 Complicated SBO with suspected strangulation have increased risk of
intestinal bacterial translocation and sepsis; broad-spectrum antibiotics
can reduce infection risk
Management  Surgical exploration (most immediate) for signs of
complications: clinical or hemodynamic instability, fail to improve after
initial conservative measures, and/or develop symptoms or signs of
ischemia or necrosis
Patients with X-ray indicates perforation or pertonitis(rigid abdomen) the best next step is
laprotomy, but In patients in whom perforation is suspected and plain radiographs are negative
(unlike this patient), CT scan of the abdomen with IV contrast can help detect smaller
amounts of free air or free fluid.

Anastomotic leak is a serious postoperative complication that can present with fever, abdominal
pain, tachypnea, and tachycardia(>120 is the most sensetive), usually within the first week after
bariatric surgery. The diagnosis is best confirmed by oral contrast–enhanced imaging (either
abdominal CT scan or upper gastrointestinal series), and treatment requires urgent surgical repair
(surgery even in negative imaging if high suspicion)

Diverticular diseases
Diverticular disease
 Diverticulosis: ↑ intraluminal pressure causing herniation
through points of weakness (vasa recta penetration)
 Diverticular bleeding: injury to exposed vasa recta
Etiology
 Diverticulitis: trapped food particles & ↑ intraluminal pressure
causing microperforation

 Diverticulosis: none
 Diverticular bleeding: painless hematochezia
Symptoms
 Diverticulitis: left lower quadrant pain, nausea, vomiting, fever

 Diet high in red meat & fat & low in fiber

Risk
 Obesity, physical inactivity, smoking
factors

Diverticulosis is most common in the sigmoid colon, but diverticular bleeding is more common
in the right colon. Diverticular bleeding is typically painless. Low- or moderate-volume
bleeding from the right colon will mix with stool and pass as dark or maroon-colored stools .
Large-volume hemorrhage can lead to passage of frank red blood. Irritation due to bleeding can
cause an urge to defecate. The diagnosis is confirmed on colonoscopy (which is indicated in
management of presumed diverticular bleed but contraindicated in diverticulitis due to inflamed
diverticuli [eg, abdominal pain, low-grade fever]). Most cases of diverticular hemorrhage will
resolve spontaneously, but a minority of patients will require endoscopic or surgical
intervention.
Initial management of divurteculitis includes antibiotics (eg, ciprofloxacin plus metronidazole)
and bowel rest. Because colonic malignancy may mimic the presentation and CT findings seen
in diverticulitis, follow up colonoscopy (typically 4-8 weeks later) is often recommended to rule
out malignancy and evaluate the extent of diverticulosis.

Abscess more than or equal to 3 cm require percutenous drainage, if not possible or

deteriorating, the patient should be operated.

Patients with free perforation of the gastrointestinal tract in the setting of ongoing inflammation
(eg, diverticulitis) often have a classic pain sequence:

 Moment of perforation: sudden, severe pain (± vomiting, lightheadedness or syncope)

 After perforation to 2 hours: temporary relief or decreased pain as the inflamed organ
decompresses
 >2 hours after perforation: generalized, constant pain due to peritonitis (± sepsis/septic
shock)

Unlike diverticular microperforation (ie, contained perforation), which usually responds to

medical management (eg, antibiotics, bowel rest), free perforation is a surgical emergency that
requires abdominal washout and resection of the ruptured bowel segment.

Because chronic constipation, which causes chronic fecal overloading, can lead to dilation and
elongation of the sigmoid colon, it is considered a risk factor for sigmoid volvulus. Colonic
hypomotility (eg, neurogenic bowel in neurologic disorders, diabetic enteropathy) can contribute
to constipation and increase the risk of volvulus
Colostriodosis
Clostridioides (formerly Clostridium) difficile colitis in adults
Risk factors  Recent antibiotics
 Hospitalization
 Advanced age
 PPI

Clinical  Profuse diarrhea (most common)

presentation  Fulminant colitis or toxic megacolon

Diagnosis  Stool PCR for C difficile toxin gene

 Stool EIA for C difficile toxin &
glutamate dehydrogenase antigen

Treatment  Oral vancomycin or fidaxomicin

Infection  Hand hygiene with soap & water

control  Contact isolation
 Sporicidal disinfectants (eg, bleach)

EIA = enzyme immunoassay;

Treatment of Clostridioides difficile infection

Initial episode  In patients with CDI, inciting antibiotics
(eg,fluoroquinolones,penicillins,cephalosporins, and clindamycin )
should be stopped as soon as possible, with patients switched to
antibiotics that are less frequently associated with CDI.
 Vancomycin PO

OR

 Fidaxomicin

Recurrence  First recurrence

o Vancomycin PO in a prolonged pulse/taper course
OR
o Fidaxomicin if vancomycin was used in initial episode
 Multiple recurrences
o Vancomycin PO followed by rifaximin (or above regimens)
 o Fecal microbiota transplant

Fulminant  Metronidazole IV plus high-dose vancomycin PO (or PR if ileus is

(eg, present)
hypotension/shock,  Surgical evaluation
ileus, megacolon)
IV = intravenous; PO = per mouth; PR = per rectum.

Appendicitis
Acute appendicitis
Clinical  Nausea, vomiting, anorexia
presentation  Initially: diffuse abdominal pain (visceral pain)
 Later: localized RLQ pain (somatic pain)
 Mild leukocytosis

Examination  McBurney point tenderness

 Psoas sign: pain with right hip extension
 Obturator sign: pain with right hip internal rotation
 Rovsing sign: RLQ pain with LLQ palpation

Diagnosis  Clinical presentation

 CT scan or ultrasound
 In pregnant women, a graded compression abdominal
ultrasound

Treatment  Surgical appendectomy

LLQ = left lower quadrant; RLQ = right lower quadrant.

 Modified Alvarado score
Points Clinical feature
(each)
1  Migratory RLQ pain
 Anorexia
 Nausea or vomiting
 Fever >37.5 C (>99.5 F)
 RLQ rebound tenderness

2  RLQ tenderness
 Leukocytes >10,000/mm3

9 Total possible score

0-3: Appendicitis unlikely.
≥4: Evaluate for appendicitis.

Patients with a contained appendiceal abscess have a very high complication rate from
immediate surgery due to the mass of inflamed, infected, and friable debris and adhesions. If
they are otherwise clinically stable, these patients should be managed with intravenous
antibiotics, bowel rest, and possibly percutaneous drainage of the abscess. They can return in 6-
8 weeks for appendectomy on an elective basis ("interval appendectomy").
Spleen:
 Atraumatic splenic rupture
Risk factors  Hematologic malignancy (eg, leukemia, lymphoma)
 Infection (eg, CMV"(eg, contact sports) should be avoided for 3-
4 weeks from the time of initial diagnosis.", EBV, malaria)
 Inflammatory disease (eg, SLE, pancreatitis)
 Splenic congestion (eg, cirrhosis, pregnancy)
 Medications (eg, anticoagulation, G-CSF)

Clinical  Diffuse or LUQ abdominal pain, peritonitis

presentation  Referred left shoulder pain (Kehr sign)
 Hemodynamic instability

Diagnosis  Acute anemia

  Intraperitoneal free fluid on imaging

Treatment  Catheter-based angioembolization (stable patients)

 Emergency splenectomy (unstable patients)

.
 Recommended vaccines for asplenic adult patients
Pneumococcus  Sequential PCV13 & PPSV23

 Revaccination with PPSV23 5 years later & at age 65

Haemophilus  1 dose Hib vaccine regardless of previous vaccination status

influenzae because antibody titers tend to decrease over time. Revaccination
(booster) is not required.

Meningococcus  Meningococcal quadrivalent vaccine

 Revaccinate every 5 years

Influenza  Inactivated influenza vaccine annually

Other vaccines  HAV

 HBV
 Tdap once as substitute for Td, then Td every 10 years
All patients should receive vaccines either ≥14 days before scheduled splenectomy or ≥14 days
after splenectomy. Although antibody titers are comparable if vaccines are given within 14 days
of splenectomy, the functional activity of the antibodies is lower in these patients than in those
receiving the vaccines 14 days later.
Fulminant bacterial infection can lead to death within hours of symptoms. Therefore, patients
who undergo splenectomy are prescribed an antibiotic to take immediately when they develop
fever. Amoxicillin-clavulanate is used most often due to its broad spectrum of activity against
common encapsulated pathogens, but those with penicillin allergy can take levofloxacin, which
has similar broad efficacy. Patients should be instructed to proceed to the nearest emergency
department for evaluation of fever after they take the antibiotic.

Anal perianal
 Anal & perianal masses
 Erythematous mass with concentric rings that occurs with Valsalva
Rectal prolapse  Mucus discharge, mild abdominal pain, mass sensation

 Dusky/purple lump or polyp

 Associated itching, bleeding
External  Thrombosis: acute enlargement with pain
hemorrhoid  Risk factors include constipation, abnormal defecation (eg, straining,
prolonged sitting on the toilet), increasing age, and pregnancy.

 Intermittent itching, painless bleeding, leakage of stool

Internal
 Detected with digital rectal exam or anoscopy (unless prolapsed)
hemorrhoid
 Fluctuant mass/swelling with erythema
 Fever
Perianal abscess
 Gradual onset

 Pink or flesh-colored papules, plaques, or cauliflower-shaped masses

 Chronic onset
Anogenital wart
 Mild itching, bleeding

 Squamous cell carcinoma most common

Anorectal  Bleeding, pain
cancer  Ulcerating, enlarging mass

 Small, flesh-colored papules

Skin tags  May represent external terminus of anal fissure (sentinel tag)

Clinical features of rectal prolapse

 Women age >40 with history of vaginal deliveries/multiparity
 Prior pelvic surgery
 Chronic constipation, diarrhea, or straining
Risk factors
 Stroke, dementia
 Pelvic floor dysfunction or anatomic defects

Clinical  Abdominal discomfort (not significant pain)

presentation  Straining or incomplete bowel evacuation, fecal incontinence with mucus
 Digital maneuvers possibly required for defecation
 Erythematous mass extending through anus with concentric rings of rectum
(can be intermittent)
  Medical
o Considered for non–full-thickness prolapse
o Adequate fiber & fluid intake, pelvic floor muscle exercises
o Possible biofeedback for fecal incontinence
Management
 Surgical "Rectopexy"
o Preferred for full-thickness or symptomatic prolapse (eg, fecal
incontinence, constipation, sensation of mass)

Proctalgia fugax
Pathophysiology  Spastic contraction of the anal sphincter
 Pudendal nerve compression

Risk factors  Female sex

 Other functional pathologies (eg, irritable bowel syndrome)
 Psychosocial stress, anxiety

Manifestations  Recurrent rectal pain unrelated to defecation

 Episodes lasting seconds to minutes (≤30 min)
 No pain between episodes

Evaluation  Normal physical examination (eg, rectal, pelvic, prostate)

 No laboratory abnormalities

Management  Reassurance
 Nitroglycerin cream ± biofeedback therapy for refractory
symptoms

Staging evaluation for rectal adenocarcinoma

Tumor markers Carcinoembryonic antigen
Imaging CT scan: chest, abdomen, pelvis
Endoscopy/direct visualization Colonoscopy

Coccydynia
Risk factors  Direct trauma (eg, falling backward)
 Repetitive minor trauma (eg, sitting on a hard surface)
 Vaginal delivery (forceps assisted)

Clinical  Pain localized to coccyx, worse with sitting

  Occasional pain with defecation, dyspareunia
features
 Initial: analgesics, coccyx protection
Management  Persistent symptoms: x-ray, local anesthetics

Radiation proctitis
Acute radiation proctitis Chronic radiation proctitis
Postradiation  ≤8 weeks  >3 months to years
onset
 Obliterative endarteritis & chronic
 Direct mucosal
mucosal ischemia
Pathogenesis damage
 Submucosal fibrosis

 Diarrhea, mucus  Severe bleeding

discharge, tenesmus  ± Strictures with constipation & rectal
Manifestations
 Minimal bleeding pain

 Multiple telangiectasias"Chronic tissue

hypoxia results in neovascularization,
 Severe erythema which can lead to hemorrhage and
Endoscopic
 Edema, ulcerations secondary anemia (eg, conjunctival
appearance
pallor)"
 Mucosal pallor & friability

 Antidiarrheals (eg,
 Endoscopic thermal coagulation
loperamide)
Management  Sucralfate or glucocorticoid enemas
 Butyrate enemas

Gonococcal proctitis
 Receptive anal intercourse
Transmission  Direct spread from the vagina

 Mucopurulent anal discharge, occasional rectal bleeding

 Tenesmus, constipation
Manifestations
 Pruritus, rectal pain, rectal fullness

 Nucleic acid amplification test of rectal swab

Diagnosis
 Ceftriaxone + doxycycline (to cover Chlamydia)
Treatment
Fecal impaction is common in older patients with impaired mobility, chronic constipation, or
decreased sensation of stool in the rectal vault. Obstruction of fecal flow in the rectum can cause
backup of stool; passage of liquid stool around the impaction can lead to incontinence. Initial
management includes manual disimpaction and enemas to clear the rectal vault

Anorectal fistula (fistula in ano)

 Perianal abscess
 Crohn disease
Causes  Malignancy, radiation proctitis
 Infection (eg, lymphogranuloma venereum)

Clinical manifestations  Perirectal pain, discharge

 Inflammatory papule/pustule
 Palpable fistula tract

Management  Assess extent of fistula

 o Gentle probe
o Imaging (endosonography, fistulogram, MRI)
 Surgery (eg, fistulotomy)

External hemorrhoids
 Hemorrhoidal venous plexus distension
 Intravascular inflammation, which leads to hemorrhoid
Pathophysiology
thrombosis

 Constipation, low-fiber diet, prolonged sitting

Risk factors  Pregnancy, advanced age

 Anal pruritus, bleeding, discharge of mucus, fecal

incontinence, sensation of fullness in anorectum
Presentation  Thrombosis (severe anorectal pain)
 Purple or blue bulge on examination

 Conservative management:
o High-fiber diet, stool softeners, sitz baths
o Topical analgesics, anti-inflammatories &
antispasmodics (eg, lidocaine, glucocorticoid
suppositories, nitroglycerin cream)
Management  Refractory or thrombosed hemorrhoids:
o Conservative measures when mild
o Hemorrhoidectomy when severe
o Hemorrhoid incision with thrombus removal for
temporary relief

Thrombosis typically occurs with external hemorrhoids and manifests as excruciating anorectal
pain exacerbated by sitting. Direct visualization of a bluish (or purplish) bulge at the anal verge
confirms the diagnosis. Anoscopy can make visualization easier and is useful if the diagnosis is
in doubt. Initial management of thrombosed hemorrhoids includes sitz baths, stool softeners, and
topical anesthetics (eg, lidocaine). External hemorrhoidectomy is needed for severe cases that
fail to respond to conservative measures.

External anal sphincter injury. On examination, patients typically have decreased anal
sphincter tone and an asymmetric anal wink; patients with a large sphincter injury may have a
palpable defect. The diagnosis is confirmed with anal manometry or endoanal ultrasound. Initial
treatment includes dietary modification, bowel training, and antidiarrheal medication; surgical
repair is based on symptom severity and patient preference.Postpartum fecal or flatal
incontinence can occur due to external anal sphincter injury associated with a third- or fourth-
degree obstetric perineal laceration. Patients typically have weakened anal sphincter tone,
asymmetric sphincter contraction, or a palpable defect on examination. Evaluation is with
endoanal ultrasonography. But if normal tone, reassure because it is due to stretching

Lower GI bleeding

High risk features include prior adenomatous colon polyps, age ≥50 (unless the patient has had a
negative colonoscopy within the last 2-3 years), age 40-49 with a first-degree relative with
colorectal cancer at age <60, or a familial colon cancer syndrome (eg, Lynch syndrome)
Initial management of hemorrhoids
  Increased fluid intake
 Increased fiber intake (foods, fiber supplements)
Dietary factors  Reduced fat intake
 Moderation of alcohol intake

 Limit time sitting on toilet (eg, 3 minutes)

 Limit defecation to once daily
Behavioral factors
 Avoid straining during defecation

 Analgesics (eg, benzocaine)

 Astringents (eg, witch hazel)
 Hydrocortisone
Topical agents
 Phlebotonics (eg, calcium dobesilate)
 Hemorrhoidoctomy or ruber band ligation for 4th degree.

Anal fissures
 Local trauma (eg, constipation, prolonged diarrhea, anal sex)

Etiology  Inflammatory bowel disease (eg, Crohn disease)

 Malignancy

 Pain with bowel movements

 Bright red blood on toilet paper or stool surface
Clinical
 Most common at posterior anal midline
presentation
 Chronic fissure may have skin tag (sentinel pile)at distal end

 High-fiber diet & adequate fluid intake

 Stool softeners
 Sitz baths
Treatment  Topical anesthetics & vasodilators (eg, nifedipine, nitroglycerin)
 Surgical intervention (eg, lateral sphincterotomy, fissure excision) is
indicated for fissures that are refractory to medical management.

Angiodysplasia is more frequently diagnosed in patients with advanced renal disease and von
Willebrand (vW) disease, possibly due to the bleeding tendency associated with these disorders.
Angiodysplasia may also be more common in patients with aortic stenosis (AS), possibly due to
acquired vW factor deficiency (from disruption of the vW multimers as they traverse the
turbulent valve space induced by AS). Angiodysplastic bleeding has been reported to remit
following aortic valve replacement.
(They are thought to form due to recurrent, intermittent obstruction of distal venules in the
muscularis propria, which leads to proximal arterial damage. Symptomatic angiodysplasias are
most common in the GI tract and primarily occur in individuals age >60. Risk of bleeding from
angiodysplasias is increased with end-stage renal disease and aortic stenosis (AS).AS is thought
to trigger bleeding from angiodysplasias due to destruction of circulating von Willebrand factor
(VWF) multimers when they pass through the damaged valve.

Diagnosis is usually made on endoscopic evaluation (eg, upper GI endoscopy, colonoscopy)

However, it is not uncommon for angiodysplasia to be missed on colonoscopy due to poor bowel
preparation or location behind a haustral fold. Asymptomatic patients do not require treatment.
Patients with anemia or gross or occult bleeding can be treated endoscopically, usually with
cautery. bleeding from diverticula is frequently arterial, and typically results in passage of
bright red blood. Maroon-colored stools are more characteristic of right colonic angiodysplasia.

Diverticulosis is most common in the sigmoid colon, but diverticular bleeding is more common
in the right colon. Diverticular bleeding is typically painless. Low- or moderate-volume
bleeding from the right colon will mix with stool and pass as dark or maroon-colored stools.
Large-volume hemorrhage can lead to passage of frank red blood. Irritation due to bleeding can
cause an urge to defecate.

The diagnosis is confirmed on colonoscopy (which is indicated in management of presumed

diverticular bleed but contraindicated in diverticulitis due to inflamed diverticuli [eg, abdominal
pain, low-grade fever]). Most cases of diverticular hemorrhage will resolve spontaneously, but
a minority of patients will require endoscopic or surgical intervention.

Hepatic disorders
Acute liver failure is defined as acute onset of severe liver injury with encephalopathy and
impaired synthetic function (defined as INR >1.5) and elevated aminotransferases in a
patient without cirrhosis or underlying liver disease.

The presence of HE differentiates ALF from acute hepatitis, which has a much better prognosis
than ALF.
Toxicity results from overproduction of the toxic metabolite N-acetyl-p-benzoquinone imine
(NAPQI), which leads to hepatic necrosis. NAPQI is normally safely detoxified through
glucuronidation in the liver, but this pathway becomes overwhelmed in overdose. Chronic
alcohol use is thought to potentiate acetaminophen hepatotoxicity by depleting glutathione levels
and impairing the glucuronidation process. On the other hand, N-acetylcysteine increases
glutathione levels and binds to NAPQI, so it is an effective antidote for acetaminophen overdose
when given early.

Acute renal insufficiency is common in ALF, especially when acetaminophen induced, due to
the drug's direct renal tubular toxicity. Hyperbilirubinemia is common as well, but
acetaminophen hepatotoxicity is characterized by relatively low serum bilirubin compared with
that in other etiologies of ALF.

Ischemic hepatic injury occurs in the setting of hypotension and manifests as acute, massive
increases in the transaminases with milder associated increases in the total bilirubin and alkaline
phosphatase.
 Nonalcoholic fatty liver disease
 Hepatic steatosis on imaging or biopsy
 Exclusion of significant alcohol use
Definition
 Exclusion of other causes of fatty liver

 Mostly asymptomatic, Most patients with NAFLD have hepatomegaly

 Metabolic syndrome
Clinical features  ± Steatohepatitis (AST/ALT ratio <1)
 Ultrasound to confirm the diagnosis; Hyperechoic texture on ultrasound

 Diet & exercise

Treatment  Consider bariatric surgery if BMI ≥35

ALT = alanine aminotransferase; AST = aspartate aminotransferase.

Prednisolone is used to treat severe alcoholic hepatitis.

 Hepatic adenoma
 Benign epithelial liver tumor
Epidemiology  Primarily young women on oral contraception

 Often asymptomatic (incidentally found)

Manifestations  Episodic right upper quadrant pain

 Solitary, solid lesion in right lobe of liver

Imaging  Multiple lesions occasionally occur

 Asymptomatic & <5 cm – stop oral contraception

Treatment  Symptomatic or >5 cm – surgical resection

 Malignant transformation (~10%)

 Rupture & hemorrhagic shock, low-grade fever and mild leukocytosis
Complications also sometimes occur due to peritoneal irritation from blood in the
abdominal cavity.

Initial diagnosis is based on the clinical presentation and imaging studies. Ultrasound most
commonly shows well-demarcated, hyperechoic lesions, and contrast-enhanced CT can show
early peripheral enhancement. Needle biopsy is not recommended for suspected hepatic
adenoma due to the risk of bleeding, and surgical excision is preferred.

Management of chronic liver disease involves both treatment of the underlying cause and
strategies to prevent further liver damage (eg, alcohol avoidance, hepatitis A and hepatitis B
vaccination) and screening for cirrhosis, when appropriate, other associated risk factors (eg,
esophageal varices).
 Reye syndrome
 Aspirin use in children during viral infection (eg, influenza B,
varicella)
Pathophysiology  Microvesicular fat deposits in the liver
 Cerebral edema

Clinical features  Triad of hepatomegaly, hypoglycemia, and encephalopathy

  Acute liver failure
o Hepatomegaly without jaundice
 Rapidly progressive encephalopathy
o Vomiting, lethargy, seizure, coma

 ↑ AST, ALT, ammonia

 ↑ PT, INR, PTT
Laboratory  ↓ Glucose
findings  Metabolic acidosis
 Normal bilirubin

 Supportive
Treatment
HCC usually arises in the setting of chronic liver inflammation due to alcohol abuse,
environmental toxins (eg, aflatoxin, betel nut chewing), or viral hepatitis (eg, hepatitis B virus
[HBV], hepatitis C virus [HCV])
Pyogenic liver abscesses usually present with fever, RUQ pain, and hepatomegaly.
Leukocytosis and elevated liver enzymes are common, typically with greater increases in
alkaline phosphatase and bilirubin than in aminotransferases. When located in the hepatic dome,
a liver abscess can cause diaphragmatic irritation and a sterile right-sided pleural effusion;
occasionally the abscess may rupture, spread through the diaphragm, seed the pleural space, and
create an empyema.

Liver abscesses are diagnosed with abdominal imaging (eg, CT scan of the abdomen,
ultrasound), which can be performed rapidly and noninvasively. Management includes blood
cultures, intravenous antibiotics, and abscess drainage with culture of the aspirated material.

Autoimmune hepatitis
Presentation  Asymptomatic
o Identified by abnormal LFTs
 Symptomatic
o Fatigue, anorexia, nausea, jaundice
o Can progress to fulminant liver failure &/or
cirrhosis
 Often associated with other autoimmune disorders (eg,
vitiligo, autoimmune thyroiditis, celiac disease)

Laboratory  Hepatocellular pattern (↑↑ AST & ALT)

findings  Hypergammaglobulinemia
 Large gamma gap (total protein − albumin = >4 g/dL)
 Elevated autoantibodies
o Anti–smooth muscle
o Anti–liver/kidney microsomal type 1
o Antinuclear (nonspecific)

Histology  Portal & periportal lymphoplasmacytic infiltration

Treatment  Prednisone ± azathioprine

ALT = alanine aminotransferase; AST = aspartate aminotransferase; LFTs = liver

function tests.

Nonabsorbable disaccharides (eg, lactulose, lactitol) are preferred for lowering serum
ammonia. Colonic bacteria metabolize lactulose to short-chain fatty acids (eg, lactic acid,
acetic acid). This acidifies the colon to stimulate conversion of the absorbable ammonia to the
nonabsorbable ammonium (an ammonia trap) and causes bowel movements (which facilitates
fecal nitrogen excretion). The medication is titrated to produce 2 or 3 semiformed stools daily.
Alcoholic hepatitis is generally characterized by a ratio of AST to ALT (thought to be due to
hepatic deficiency of pyridoxal 5'-phosphate, an ALT enzyme cofactor) >2, elevated GGT, and
elevated ferritin. The absolute values of AST and ALT are almost always <500 IU/L in
alcoholic liver disease

In ALF due to acetaminophen toxicity, liver transplantation is firmly indicated in patients with
grade III or IV hepatic encephalopathy, PT >100 seconds, and serum creatinine >3.4
mg/dL. One-year survival following liver transplantation for ALF is approximately 80%.

Budd-Chiari syndrome
 Hepatic venous outflow obstruction
 Usually due to:
o Myeloproliferative disorder (eg, PV)
Etiology o Malignancy (eg, hepatocellular carcinoma)
o Oral contraception use/pregnancy

 Acute
o Jaundice, hepatic encephalopathy, variceal bleeding
o Prolonged INR/PTT; elevated transaminases
 Subacute/chronic
Manifestations o Vague, progressive abdominal pain
o Hepatomegaly, splenomegaly, ascites
o Mild/moderate elevation in bilirubin, transaminases

 Abdominal Doppler ultrasound – ↓ hepatic vein flow

Diagnosis  Investigation for underlying disorders (eg, JAK2 testing for PV)

INR = international normalized ratio; PTT = partial thromboplastin time; PV =

polycythemia vera.
Alpha-1 antitrypsin deficiency is associated with emphysematous lung disease, chronic
hepatitis, cirrhosis, and necrotizing panniculitis (painful, erythematous nodules and plaques on
the thighs or buttocks).

The most common causes of cirrhosis in the United States include viral hepatitis (C more than
B), chronic alcoholism, nonalcoholic fatty liver disease (NAFLD), and
hemochromatosis. Laboratory studies, including viral hepatitis serologies and iron studies,
should be obtained.
dilated arteriole surrounded by smaller radiating vessels
 Overview of cirrhosis management
Treat underlying  HCV, HBV: antiviral therapy
liver disease  NASH: weight loss

Provide  Avoid alcohol & hepatotoxic medications

preventive care  Vaccinate for HAV & HBV (unless already immune)

Manage  Screen for esophageal varices (endoscopy) at diagnosis

complications  Screen for HCC: ultrasound ± serum AFP every 6-12 months
 Frequent clinical assessment for ascites and encephalopathy
(prophylactic treatment not recommended)

AFP = alpha fetoprotein; HAV = hepatitis A virus; HBV = hepatitis B virus; HCC =
hepatocellular carcinoma; HCV = hepatitis C virus; NASH = nonalcoholic steatohepatitis.

Primary prophylaxis can be achieved either with endoscopic variceal ligation (EVL) or
administration of a nonselective beta blocker such as propranolol or nadolol. Nonselective
beta blockers reduce portal venous pressure by blocking the adrenergic vasodilatory response of
the mesenteric arterioles, which results in unopposed alpha-adrenergic tone, vasoconstriction,
and reduced portal blood flow. The choice of beta blocker or EVL depends on patient preference
and the size of the varices (EVL is preferred for larger varices).
A transjugular intrahepatic portosystemic shunt is often used as salvage therapy in patients with
refractory ascites or esophageal varices who have failed endoscopic or medical management.
They managed with decreased protein in diet to decrease hepatic encephalopathy.
Antibiotics: Ceftrixone/fluroquinlone and IV PPIs

Sengstaken-Blckmore, when you are in primary hospital or the other modalitites are not available
and you want to transfere to tertiary hospital.Balloon tamponade may be performed as a
temporizing measure for patients with uncontrollable hemorrhage likely due to varices using any
of several devices (eg, Sengstaken-Blakemore tube, Minnesota tube); tracheal intubation is
necessary if such a device is to be placed; ensure proper device placement prior to inflation to
avoid esophageal rupture

(HCC) is a common complication of cirrhosis, with a risk of 1%-8% per annum in this
population. Therefore, screening with abdominal ultrasound every 6 months is recommended.
Because HCC often presents with liver decompensation (eg, new-onset ascites, variceal
bleeding), this condition should prompt abdominal ultrasound to evaluate for HCC.

Hepatic encephalopathy
 Drugs (eg, sedatives, narcotics)
 Hypovolemia (eg, diarrhea)
 Electrolyte changes (eg, hypokalemia which result in
intracellular acediemia)
Precipitating factors  Metabolic alkalosis which stall H+ renders high NH3
 ↑ Nitrogen load (eg, GI bleeding)
 Infection (eg, pneumonia, UTI, SBP)
 Portosystemic shunting (eg, TIPS)

 Sleep pattern changes

 Altered mental status
Clinical presentation  Ataxia
 Asterixis

 Correct precipitating causes (eg, fluids, antibiotics) or pottasium

repletion
Treatment
 ↓ Blood ammonia concentration (eg, lactulose, rifaximin)

Although advanced cirrhosis is irreversible, many patients have concurrent alcohol-related liver inflammation
and active fibrogenesis that improves with abstinence from alcohol. In addition, abstinence leads to a
reduction in portal pressure, which can make ascites more diuretic-responsive and ultimately aids in its
resolution. Alcohol cessation also carries a significant survival benefit compared with patients who continue
to drink and should be recommended in all patients with cirrhosis. Baclofen has been shown to decrease
alcohol cravings in patients with alcoholic liver disease and can help with cessation.

Hepatorenal syndrome
 Advanced cirrhosis with portal hypertension & edema
 Pathogenesis: splanchnic arterial dilation(nitric oxide), decreased vascular
Risk factors
resistance, and local renal vasoconstriction with decreased perfusion(RAAS)

 Reduced renal perfusion

Precipitating
 GI bleed, vomiting, sepsis, excessive diuretic use, SBP
factors
 Reduced glomerular pressure & GFR
 Ascites fluid characteristics
 Bloody: trauma, malignancy, TB (rarely)
 Milky:chylous
Color  Turbid: possible infection
 Straw color: likely more benign causes

 ≥250/mm3: peritonitis (secondary or spontaneous bacterial)

Neutrophils
 ≥2.5 g/dL (high-protein ascites)
o CHF, constrictive pericarditis, peritoneal carcinomatosis, TB,
Total protein
Budd-Chiari syndrome, fungal
 <2.5 g/dL (low-protein ascites)
 o Cirrhosis, nephrotic syndrome

 ≥1.1 g/dL (indicates portal hypertension)

o Cardiac ascites, cirrhosis, Budd-Chiari syndrome
SAAG
 <1.1 g/dL (absence of portal hypertension)
calculated by
o TB, peritoneal carcinomatosis, pancreatic ascites, nephrotic
subtracting
syndrome

Miscellaneous ascitic fluid tests

(perform when clinically indicated)

 ↑ In biliary or bowel perforation
Bilirubin
 ↓ In infection, malignancy, bowel perforation
Glucose
 ↑ In infection, malignancy, bowel perforation
Lactate dehydrogenase
 ↑ In pancreatic ascites
Amylase
 ↑ In chylous ascites
Triglycerides
 Suspected malignant ascites
Cytology
 Suspected bacterial peritonitis
Gram stain and culture

Hepatocellular carcinoma (HCC) is the most common malignancy to present with bloody ascites
due to tumor growth disrupting and eroding nearby blood vessels. Less frequently, peritoneal metastases from
distant primary sites (eg, ovaries, prostate) can cause bloody ascites. Therefore, patients with bloody ascites
should undergo abdominal imaging, measurement of alpha-fetoprotein blood levels (elevated with HCC),
and cytologic analysis.

Management of ascites in cirrhosis

Initial  Imaging for confirmation (eg, abdominal ultrasound)
evaluation  Diagnostic paracentesis to confirm etiology & rule out infection
o SAAG, cell count & differential, total protein

Medical  Spironolactone with furosemide

therapy  Alcohol abstinence, sodium restriction
  Avoid ACE inhibitors, angiotensin receptor blockers, NSAIDs
 Although spironolactone is occasionally used by itself in patients prone to
hypokalemia, furosemide monotherapy is usually avoided in cirrhosis
because it is less effective in this population and predisposes to
electrolyte wasting.

Refractory  Large-volume paracentesis

ascites  Transjugular intrahepatic portosystemic shunt

Spontaneous bacterial peritonitis, any patient with cirrhosis who develop AMS and fever
should undergo paracentesis to rule out SBP
Clinical presentation  Temperature >37.8 C (100 F)
 Abdominal pain/tenderness
 Altered mental status (abnormal connect-the-numbers test)
 Hypotension, hypothermia, paralytic ileus with severe
infection

Diagnosis from ascitic  PMNs >250/mm3

fluid  Positive culture, often gram-negative organisms (eg,
Escherichia coli, Klebsiella, strep)
 Protein <1 g/dL
 SAAG >1.1 g/dL

Treatment  Empiric antibiotics (After paracentesis) - third-generation

cephalosporins (eg, cefotaxime)
 Fluoroquinolones for SBP prophylaxis

SBP is most likely due to either intestinal bacterial translocation directly into the ascitic fluid or hematogenous
spread to the liver and ascitic fluid (due to other bacterial infections).
Ascites separates the visceral and parietal peritoneal surfaces and prevents development of a rigid abdomen,
even with organ perforation. As a result, presentation of secondary peritonitis (ascitic infection due to a
surgically treatable intraabdominal source such as perforated peptic ulcer) can be difficult to distinguish from
SBP.

Pancreatic ascites is a rare complication of chronic pancreatitis that results from damage to the
pancreatic duct, leading to leakage of pancreatic juice into the peritoneal space. Analysis
showing high amylase (often >1000 U/L)

Hepatic hydrothorax is more commonly on the right side due to the less
muscularhemidiaphragm. Patients have dyspnea, cough, pleuritic chest pain, and hypoxemia.
Diagnosis involves documentation of the effusion (eg, chest x-ray) and testing to exclude other
causes (eg, thoracentesis, echocardiogram).

Treatment involves salt restriction and diuretic administration. Therapeutic thoracentesis could
be attempted in patients with prominent symptoms. Chest tube placement should be avoided as
it can result in large-volume protein, fluid, and electrolyte losses as well as other severe
complications (eg, renal failure). The definitive option for treatment is liver transplantation,
although this may not be appropriate for all patients depending on other factors.

Wilson and hemochromatosis

Hereditary hemochromatosis
 Hyperpigmentation
 Arthropathy
 Hepatomegaly, cirrhosis, hepatocellular carcinoma
Clinical
 Diabetes mellitus
manifestations
 Hypopituitarism, secondary hypogonadism
 Cardiomyopathy

 Elevated liver transaminases

 Elevated serum ferritin, transferrin saturation
 HFE genetic mutations
 The initial evaluation of HH includes serum iron studies, which will
show increased levels of serum iron, ferritin, and transferrin saturation.
The diagnosis can be confirmed with genetic testing for
hemochromatosis-associated mutations (eg, HFE). Liver biopsy is not
Diagnosis
required but may be useful to stage the extent of liver involvement (eg,
in patients with significant liver function test abnormalities) or to
confirm the diagnosis in patients who have iron studies indicating iron
overload but negative results on the classic HFE gene markers. Long-
term management of hemochromatosis involves serial phlebotomy to
deplete excess iron stores.

 Therapeutic phlebotomy (urgent if ferritin >1,000 ng/mL)

Management

Clinical manifestations of hereditary hemochromatosis

Skin Hyperpigmentationrs, genitalia
Arthralgia, arthropathy & chondrocalcinosis
Musculoskeletal
Gastrointestinal Elevated hepatic enzymes with hepatomegaly (early), cirrhosis (later) &
 increased risk of hepatocellular carcinoma(accounting for 45% of deaths in HH
patients.)
Endocrine Diabetes mellitus, secondary hypogonadism & hypothyroidism
Cardiac Restrictive or dilated cardiomyopathy & conduction abnormalities
Infections Increased susceptibility to Listeria, Vibrio vulnificus & Yersinia enterocolitica

Arthropathy of hereditary hemochromatosis

 Onset at age <40
 Chronic pain & bony swelling
Clinical features  Most common at 2nd & 3rd MCP joints
 Occasional acute flare

 Joint space narrowing

 Chondrocalcinosis
 Hook-shaped osteophytes at metacarpal heads, characteristic x-ray
X-ray signs
findings include periarticular bony enlargement and subchondral
lucency.

 Oral analgesics (eg, acetaminophen, NSAIDs)

Management  Therapeutic phlebotomy (to prevent other complications)

MCP = metacarpophalangeal; NSAIDs = nonsteroidal anti-inflammatory drugs.

 Wilson disease
Pathogenesis  Autosomal recessive mutation of ATP7B → hepatic copper
accumulation → leak from damaged hepatocytes → deposits
 in tissues (eg, basal ganglia, cornea)

 Hepatic (acute liver failure, chronic hepatitis, cirrhosis)

 Neurologic (parkinsonism, gait disturbance, dysarthria)
Clinical
 Psychiatric (depression, personality changes, psychosis)
findings
 Hemolytic anemia due to RBCs oxidative stress

 ↓ Ceruloplasmin & ↑ urinary copper excretion

 Kayser-Fleischer rings on slit-lamp examination
Diagnosis
 ↑ Copper content on liver biopsy

 First line-Chelators (eg, D-penicillamine, trientine)

 For maintinance-Zinc (interferes with copper absorption)
Treatment  In addition, first-degree family members should be screened
for Wilson disease mutations.

Biliary tract
Biliary cyst
Pathogenesis  Cystic dilation of biliary tree
  Most common: single, extrahepatic dilation of common bile
duct (type I)

 May be incidental finding on imaging

 Classic triad* in children/adults
o Abdominal pain
o RUQ mass
Presentation
o Jaundice
 Neonates: jaundice, acholic stools, dark urine, hepatomegaly
 ± Nausea, vomiting

 Ultrasound ± CT scan or MRCP

Diagnosis  ERCP(if obstruction is suspected.)

 Cholangiocarcinoma
 Acute cholangitis
Complications  Pancreatitis
 Stone formation

 Cyst resection (to ↓ risk of malignancy)

 ± Roux-en-Y hepaticojejunostomy (to allow for biliary
Treatment
drainage)

*Often, only two-thirds of findings are present.

MRCP = magnetic retrograde cholangiopancreatography; RUQ = right upper

quadrant.
 Primary sclerosing cholangitis
 Asymptomatic
 Fatigue & pruritus
Clinical features
 Associated with IBD, particularly UC (~90% of patients)

Laboratory/imaging  Cholestatic liver injury (↑ alkaline phosphatase, ↑ bilirubin)

 Multifocal stricturing/dilation of intrahepatic &/or
 extrahepatic bile ducts on cholangiography
 MRCP is the diagnostic tool of choice (alternative is ERCP
if metal implants)

 Fibrous obliteration of small bile ducts, with concentric

Liver biopsy replacement by connective tissue in onion-skin pattern

 Biliary stricture
 Cholangitis or cholelithiasis vs PBC which has none of these
complications because it is intrahepatic
Complications
 Cholangiocarcinoma, colon cancer, biliary cancer
 Cholestasis (eg, ↓ fat-soluble vitamins, osteoporosis)

IBD = inflammatory bowel disease; UC = ulcerative colitis.

 Primary biliary cholangitis
Pathogenesis  Autoimmune destruction of intrahepatic bile ducts

Clinical features  Affects middle-aged women

 Insidious onset of fatigue & pruritus
Management of PSC includes endoscopic interventions for strictures, therapy for
coexisting ulcerative colitis, antibiotics for cholangitis (with some patients maintained on
longterm antibiotic therapy), and, in some cases, ursodeoxycholic acid

Gilberts yndrome
Epidemiology  Most common inherited disorder of bilirubin metabolism

Pathogenesis  ↓ Hepatic UDP glucuronosyltransferase activity → ↓ conjugation

of bilirubin

Clinical findings  Recurrent episodes of mild jaundice

 Provoked by stress (eg, febrile illness, fasting, dehydration,
vigorous exercise, menstruation, surgery)
 Diagnosis  ↑ Unconjugated bilirubin (ie, indirect hyperbilirubinemia)
 Normal CBC, blood smear, reticulocyte count
 Normal AST, ALT, alkaline phosphatase

Treatment  Benign; no treatment required

ALT = alanine aminotransferase; AST = aspartate aminotransferase; CBC = complete blood

count; UDP = uridine diphosphogluconurate.

Some patients with cholyescystitis who cannot tolerate surgery undergo gallbladder (eg, percutaneous)
drainage only.

To rule out underlying IBD, a colonoscopy should be performed in all patients with a new diagnosis of PSC.
Patients with both PSC and IBD should have annual colonoscopies because they are at a markedly elevated
risk for colon cancer (~5 times higher than those with IBD alone).
normal-sized (≤15 cm) liver.

Inflammation
Acute cholangitis
Etiology  Ascending infection due to biliary obstruction
 Common etiologies include choledocholithiasis, malignancy, primary
sclerosing cholangitis, and biliary interventions that result in
incomplete bile drainage.

Clinical  Fever, jaundice, RUQ pain (Charcot triad)

presentation  ± Hypotension, AMS (Reynolds pentad)

Diagnosis  Cholestatic liver function abnormalities

o ↑ Direct bilirubin, alkaline phosphatase
o Mildly ↑ aminotransferases
 Biliary dilation on abdominal ultrasound or CT scan

Treatment  Antibiotic coverage of enteric bacteria

 Biliary drainage by ERCP within 24-48 hr, relieves the obstruction by
extracting the gallstone and prevents further obstruction with a biliary
stent placement.

AMS = altered mental status; ERCP = endoscopic retrograde cholangiopancreatography; RUQ

= right upper quadrant.

Acalculous cholecystitis
Risk factors  Severe trauma or recent surgery
 Prolonged fasting or TPN
  Critical illness (eg, sepsis, ICU)

Clinical presentation  Fever, leukocytosis, ↑ LFTs, RUQ pain

 Jaundice & RUQ mass less common

Diagnosis  Abdominal ultrasound (preferred)

 HIDA (cholescintigraphy (hepatobiliary iminodiacetic acid)) or
CT scan if needed

Treatment  Enteric antibiotic coverage

 Cholecystostomy for initial drainage
 Cholecystectomy once clinically stable

HIDA = hepatobiliary iminodiacetic acid; ICU = intensive care unit; LFTs = liver function
tests; RUQ = right upper quadrant; TPN = total parenteral nutrition.

Emphysematous cholecystitis
Risk factors  Diabetes mellitus
 Vascular compromise
 Immunosuppression

Clinical  Fever, right upper quadrant pain, nausea/vomiting

presentation  Crepitus in abdominal wall adjacent to gallbladder

Diagnosis  Air-fluid levels in gallbladder, gas in gallbladder wall on CT (U/S is

underdiagnosing)
 Cultures with gas-forming Clostridium, Escherichia coli
 Unconjugated hyperbilirubinemia (eg, from Clostridium-induced hemolysis),
mildly elevated aminotransferases

Treatment  Emergency cholecystectomy

 Broad-spectrum antibiotics with Clostridium coverage (eg, piperacillin-
tazobactam,ertapenem) and bile culture.

In choledochal cyst; There is still a small risk for developing cancer in the remaining bile ducts after surgery,
and serial laboratory testing with or without imaging is usually recommended postoperatively.
ERCP with manometry can confirm the diagnosis of sphincter of Oddi dysfunction (SOD),
which typically causes biliary-type pain with no obvious etiology.

Gallstones
Features that distinguish biliary colic from cholecystitis are pain resolution within 4-6 hours and
absence of abdominal tenderness, fever, and leukocytosis.
HIDA scan is primarily used to exclude cholecystitis in patients with suggestive symptoms (eg,
severe right upper quadrant pain, fever, tachycardia, leukocytosis with left shift) but no
gallbladder inflammation or biliary obstruction on ultrasound.
Management of gallstones

Gallstones without  No treatment required in most patients, Exceptions to

symptoms this rule is porcelain gallbladder.

Gallstones with typical  Elective laparoscopic cholecystectomy

biliary colic symptoms  Possible ursodeoxycholic acid in poor surgical
candidates

Complicated gallstone  Cholecystectomy within 72 hr

disease*
*Acute cholecystitis, choledocholithiasis, gallstone pancreatitis.
Uncomplicated cholecystitis can cause mild elevations in transaminases, total serum bilirubin
from 1-4 mg/dL, and serum amylase without obvious common bile duct or pancreatic disease.
However, alkaline phosphatase is usually not elevated without associated cholangitis or
choledocholithiasis.
Lithotripsy (laser or mechanical fragmentation) is sometimes used for gallstones in the bile duct
that cannot be removed endoscopically.
Cholecystitis, which predisposes to biliary-enteric adhesions, is the most important risk factor,
and patients are more commonly elderly women, which reflects their higher prevalence of
gallstone disease.

Diagnosis can be confirmed by abdominal CT scan, which may reveal gallbladder wall
thickening, pneumobilia, and an obstructing stone. Treatment is surgical and involves removal
of the stone and either simultaneous or delayed cholecystectomy.

After biliary drainage with ERCP, acute cholangitis due to choledocholithiasis, a diagnosis more
common in adults, warrants cholecystectomy to prevent recurrent episodes.

ERCP is always required for acute cholngitis

Pancreatic disorders

Triglyceride-induced pancreatitis
Risk Triglyceride levels (mg/dL)

 <500: minimal risk

 500-999: mild risk
 1,000-1,999: moderate risk
 ≥2,000: high risk

Other risk factors: pregnancy, alcoholism, obesity, uncontrolled diabetes

Clinical  Acute epigastric pain radiating to back
features  ± Fever, nausea, vomiting
 Elevated serum lipase (>3 times upper limit of normal)

Management  Intravenous fluid hydration, pain control

 Glucose ≥500 mg/dL: consider insulin infusion
 Glucose <500 mg/dL or severe pancreatitis (eg, lactic acidosis,
hypocalcemia): consider apheresis (therapeutic plasma exchange)
Sentinal ileus

Other common drugs associated with pancreatitis include:

1. Diuretics (furosemide, thiazides)

2. Drugs for inflammatory bowel disease (sulfasalazine, 5-ASA)
3. Immunosuppressive agents (azathioprine)
4. HIV-related medications (didanosine, pentamidine)
5. Antibiotics (metronidazole, tetracycline)

Overview of chronic pancreatitis

Etiology  Alcohol use
 Cystic fibrosis (common in children)
 Ductal obstruction (eg, malignancy,
stones)
 Autoimmune

Clinical  Chronic epigastric postprandial

presentation painwith intermittent pain-free intervals
 Malabsorption: steatorrhea, weight loss
 Diabetes mellitus
 Laboratory  Amylase/lipase can be normal &
results/imaging nondiagnostic
 CT scan or MRCP can show
calcifications, dilated ducts & enlarged
pancreas

Treatment  Pain management( 1st line is enzyme

supplementation; pregabalin, nortriptyline,
and amitriptyline)
 Alcohol & smoking cessation
 Frequent, small meals
 Pancreatic enzyme supplements (most
important because it decrease the pain that
result from CCK overstimulation, and
improve absorbtion, lipase, protease and
amylase)

MRCP = magnetic resonance cholangiopancreatography.

 Pancreatic adenocarcinoma
Risk factors  Smoking
 Hereditary pancreatitis
 Nonhereditary chronic pancreatitis
 Obesity & lack of physical activity

Clinical presentation  Systemic symptoms (eg, weight loss, anorexia) (>85%)

 Abdominal pain/back pain (80%)
 Jaundice (56%)
 Recent-onset atypical diabetes mellitus
 Unexplained migratory superficial thrombophlebitis
 Hepatomegaly & ascites with metastasis
 Could present with coursvier sign with diltation of intra- & extra hepatic bile ducts. Also

Laboratory studies  Cholestasis (↑ alkaline phosphatase & direct bilirubin)

 ↑ Cancer-associated antigen 19-9 (not as a screening test)

 Abdominal ultrasound (if jaundiced) or CT scan (if no jaundice)

 A celiac plexus block (with glucocorticoids or alcohol) is useful for pancreatic cancer pa
Approximately 25% of patients with pancreatic cancer are diagnosed with DM <2 years prior to
discovery of the tumor. In particular, atypical DM (eg, DM presenting in a thin, older patient)
should raise suspicion for pancreatic cancer, particularly when accompanied by other suggestive
findings (eg, pain, weight loss). It is unclear whether DM promotes carcinogenesis or whether
DM occurs as a consequence of a paraneoplastic syndrome from adrenomedullin secretion,
leading to pancreatic beta cell dysfunction.
Complications include spontaneous infection, duodenal or biliary obstruction, pseudoaneurysm
(due to digestion of adjacent vessels), pancreatic ascites, and pleural effusion. Abdominal
imaging usually confirms the diagnosis.

In patients with minimal or no symptoms and without complications (eg, pseudoaneurysm),

expectant management (eg, symptomatic therapy, nothing by mouth) is preferred initially.
Endoscopic drainage is typically reserved for those with significant symptoms (eg, abdominal
pain, vomiting), infected pseudocyst, or evidence of pseudoaneurysm (usually embolized before
drainage procedure).

Pancreatic ascites is typically serosanguinous or straw-colored with analysis showing high

amylase (often >1000 U/L), high total protein (≥2.5 g/dL), and low serum-ascites albumin
gradient (SAAG) (<1.1, indicating the absence of portal hypertension).

The tumor likely releases mucins that react with platelets to form platelet-rich microthrombi.That
result in hypercoagulable state.Lipase and amylase rise within several hours of the development
of symptoms whereas CT findings may remain normal for up to 48 hours.

Drugs associated with drug-induced pancreatitis

Analgesics  Acetaminophen
 Nonsteroidal anti-inflammatory drugs
 Mesalamine, sulfasalazine
 Opiates

Antibiotics  Isoniazid
 Tetracyclines
 Metronidazole
 Trimethoprim-sulfamethoxazole

Antiepileptics  Valproic acid

 Carbamazepine

Antihypertensives  Thiazides, furosemide

 Enalapril, losartan

Antivirals  Lamivudine
 Didanosine

Immunosuppressant  Azathioprine, mercaptopurine

s  Corticosteroids

Others  Asparaginase
 Estrogens
 Severe acute pancreatitis
Definition  Acute pancreatitis with organ failure (eg, respiratory, cardiovascular, renal)
persisting >48 hr

Predictors  Patient factors:

o Older age (eg, age >55)
o Comorbidities, including obesity (BMI >30 kg/m2)
  Clinical findings:
o Altered mental status
o SIRS (eg, leukocytes >12,000/mm3, temperature >38 C [100.4 F])
 Laboratory findings of intravascular volume depletion:
o ↑ BUN (>20 mg/dL) and/or ↑ creatinine (>1.8 mg/dL)
o ↑ HCT (>44%)
 Radiologic findings:
o CXR: pulmonary infiltrates, pleural effusions
o Abdominal CT scan: severe pancreatic necrosis

Acute necrotizing pancreastitis, Initially, the resulting necrotic collection is sterile; however, infection with
enteric pathogens (eg, Escherichia coli, Pseudomonas, Enterococcus) occurs in
approximately a third of patients, typically 7-10 days after onset of acute necrotizing pancreatitis.
When this occurs, patients can decompensate clinically (eg, fever, confusion, sepsis), and a CT scan of the
abdomenshould be ordered (even if an initial CT scan was obtained). Gas (produced by microorganisms)
within the necrotic collection on CT scan is diagnostic for infected pancreatic necrosis and prompts initiation
of intravenous antibiotic therapy. If CT findings are equivocal, aspiration and culture of the necrotic
pancreatic material may be necessary to confirm the diagnosis. Débridement (eg, endoscopic, surgical) is
often required but is ideally delayed until the patient has stabilized on antibiotic therapy and the necrotic
collection has become encapsulated (ie, walled off), which facilitates débridement.

Tumors of the GI
The calcium infusion study is usually reserved for patients who have gastric acid hypersecretion
and are strongly suspected of having gastrinoma despite a negative secretin test. Calcium
infusion can lead to an increase in serum gastrin levels in patients with gastrinoma.

If gastrinoma is confirmed, patients should be screened for MEN1 with assays for parathyroid
hormone, ionized calcium, and prolactin.
Gastrinomas are managed with high-dose PPI, with surgery (eg, exploratory laparotomy and
resection) considered in patients with sporadic gastrinoma with no evidence of metastatic
disease.

Colon cancer screening in patients at increased risk

Indication Colonoscopy recommendations
Family history of  Age 40 OR 10 years before the age of diagnosis in
adenomatous polyps or affected relative*
CRC  Repeat every 5 years

 1 first-degree
relative age <60
 ≥2 first-degree
relatives at any age

Inflammatory bowel  Begin 8 years after disease onset

disease  Repeat every 1-3 years
 Specialized staining (eg, chromoendoscopy with indigo
 Ulcerative colitis carmine) may be used to enhance visualization of
 Crohn disease with dysplastic lesions. Patients who have limited UC
colonic involvement involving <1/3 of the colon are at lower risk

Classic familial  Age 10-12

adenomatous polyposis  Repeat annually

HNPCC (Lynch  Age 20-25

syndrome)  Repeat every 1-2 years

CRC = colorectal cancer; HNPCC = hereditary nonpolyposis colorectal cancer.

*Whichever is earlier.
findings that suggest a greater risk of malignant transformation (usually warranting more
aggressive colonoscopic surveillance) include:

 Predominance of villous features (long glands on histologic examination), particularly in

the presence of high-grade dysplasia
 Large size (eg, >1 cm)
 High number (eg, >3 concurrent adenomas)

In addition, sessile (nonpedunculated) adenomatous polyps are associated with an increased risk
of synchronous advanced neoplasia and often require careful follow-up to ensure complete
removal.

Surveillance after colon cancer resection

Stage I  Colonoscopy in 1 yr & then every 3-5 yr

Stages II & III  Colonoscopy in 1 yr & then every 3-5 yr

  Periodic CEA testing
 Annual CT scan of the chest, abdomen (± pelvis)

Stage IV  Individualize
 Consider stage II/III strategy but more frequent CT scans

CEA = carcinoembryonic antigen.

Peutz-Jeghers syndrome
Etiology  Autosomal dominant disorder
 Tumor suppressor gene mutation causes unregulated tissue growth

Clinical  Pigmented macules (eg, lips, buccal mucosa, palms/soles)

features  ≥2 gastrointestinal hamartomatous polyps
o Abdominal pain due to obstruction or intussusception
o Anemia due to acute/chronic bleeding
o Rectal prolapse
 ↑ Cancer risk (eg, gastrointestinal, breast, genital tract)
 Positive family history

Diagnosis  Genetic testing

Management  Annual anemia screening

 Cancer screening (eg, upper/lower endoscopy)

Risk factors for colon cancer

Lifestyle  Frequent consumption of red/processed meat
factors  Tobacco, alcohol use

Medical/  Personal/family history of adenomatous polyps

family history or colon cancer
 Inherited colon cancer syndromes (eg, familial
adenomatous polyposis, Lynch syndrome)
 Ulcerative colitis
 Diabetes/obesity
 Prior abdominopelvic radiation * so we do
colonoscopy at age 30-40 alternatives are
FOBT or Fecal DNA testing.

Protective  High-fiber diet

factors  Aspirin/NSAID use

NSAID = nonsteroidal anti-inflammatory drug.

 DM2/Obesity result in Hyperinsulinemia results in increased
circulating levels of insulin-like growth factor-1, which inhibits
colorectal epithelial cell apoptosis and promotes neoplastic
progression. In addition, obesity is associated with increased
expression of inflammatory cytokines (eg, tumor necrosis factor-
alpha), which may promote development of CRC.

Screening methods include:

 High-sensitivity stool-based testing (eg, fecal occult blood testing [FOBT] or fecal
immunochemical testing [FIT] annually)
 Direct visualization techniques (eg, colonoscopy every 10 years, flexible sigmoidoscopy
every 5 years),
 A combination (eg, flexible sigmoidoscopy every 10 years with FIT annually).
Miscellaneous
Abdominal compartment syndrome
Etiology  ↑ intraabdominal pressure causing organ dysfunction
 Risk factors:
o Massive fluid resuscitation (eg, trauma, sepsis)
o Major intraabdominal surgery or pathology (eg,
pancreatitis)
o Intraabdominal fluid collections (eg, bleeding, ascites)

Clinical  Tense, distended abdomen

manifestations  ↑ ventilatory requirements (diaphragmatic elevation, ↑
intrathoracic pressure)
 ↑ CVP (venous compression but ↓ venous return & cardiac
preload)
 Hypotension, tachycardia (↓ venous return & cardiac output)
  ↓ urine output (↓ intraabdominal organ perfusion)

Management  Temporizing measures:

o Avoid over-resuscitation with fluids
o ↓ intraabdominal volume (eg, NG tube, drain fluid
collections)
o ↑ abdominal wall compliance (eg, sedation, paralysis)
 Definitive management: surgical decompression

CVP = central venous pressure; NG = nasogastric.

Cyclic vomiting syndrome

History  Personal or family history of migraines
 Episodes often have identifiable trigger (eg, infection, stress)

Symptom  Stereotypical vomiting episodes

s o Acute onset of nausea, abdominal pain, headache, vomiting
o Self-limited, lasting 1-2 days
 Between episodes
o Usually asymptomatic
o Often regular intervals (eg, 2-4 weeks)
o Treatment is abortive (eg, triptans) and/or supportive (eg,
antiemetics, rehydration), and most children have gradual resolution
of symptoms during adolescence.
o Marijuana is a major risk factor for cyclic vomiting syndrome

Clostridioides difficileinfection (CDI). Although antibiotic use is the single greatest risk factor
for CDI, other well-established risk factors include recent hospitalization and severe comorbid
illness such as inflammatory bowel disease and advanced age.
Bedside diagnostic peritoneal lavage (DPL) may be considered in patients who remain too
hemodynamically unstable for CT scan despite resuscitation.

For hemodynamically stable (eg, systolic blood pressure >90 mm Hg) patients with a negative
FAST:

 High suspicion of intraabdominal injury, as in this patient with tachycardia, LUQ pain,
and referred shoulder pain, should prompt contrast-enhanced CT scan of the abdomen
and pelvis. Intravenous contrast "blush" (extravasation) can often identify active
bleeding.
 Low suspicion of intraabdominal injury (eg, normal vital signs, nontender abdomen) can
be managed with serial physical examinations, which are performed to rule out occult
injury progression
 Evisceration (ie, externally exposed intestines)
 Impalement (ie, penetrating object still in situ) In contrast, patients without an indication for
immediate laparotomy should undergo further evaluation to determine whether peritoneal
penetration occurred (eg, CT scan, local wound exploration for anterior stab wounds" an
experienced surgeon may perform local wound exploration under local anesthetic to look for
violation of the peritoneum (eg, visualization of intraabdominal contents)") and/or whether
intraabdominal injuries are present (eg, Focused Assessment with Sonography for Trauma, CT
scan). The presence of either typically warrants surgical exploration.
Often, blunt splenic injury can be managed nonoperatively (eg, observation with serial
hemoglobin measurement, embolization). However, continued hemodynamic instability (eg,
despite initial resuscitation) or frankperitonitis are indications for exploratory laparotomy and
potential splenectomy.

Once confirmed, DHs typically are managed with bowel rest, nasogastric decompression, and
parenteral nutrition and are followed with serial CT scans or duodenal ultrasonography.
Most DHs resolve within a few weeks with nonoperative management.
 Psoas abscess
Clinical  Subacute fever & abdominal/flank pain that may
presentation radiate to the groin or hip
 Anorexia, weight loss
 Abdominal pain with hip extension (psoas sign)

Diagnosis  CT scan of the abdomen & pelvis

 Leukocytosis, elevated inflammatory markers
 Blood & abscess cultures

Treatment  Drainage
 Broad-spectrum antibiotics
 Dyspepsia
Symptom  Epigastric pain often described as "burning"
s  ± Nausea, vomiting, epigastric fullness, heartburn

Etiology  Functional (75%)

 Malignancy (eg, gastric, esophageal)
 Peptic ulcer, NSAIDs, Helicobacter pylori infection, GERD
 Workup  Age ≥60: Upper endoscopy
 Age <60:
o Testing and treatment for H pylori
o Upper endoscopy in high-risk patients (eg, overt GI bleeding,
significant weight loss, >1 alarm symptom)

Alarm  Progressive dysphagia

symptoms  Iron deficiency anemia
 Odynophagia
 Palpable mass or lymphadenopathy
 Persistent vomiting
 Family history of GI malignancy

Ligamentum arteriosum ligation is used to treat some patients with vascular ring,
Common symptoms of duodenal ulcers include nocturnal pain (due to circadian rhythm of
gastric acid secretion), worsening of the pain with fasting, postprandial bloating, and nausea.
for H. Pylori In a patient without occult bleeding, noninvasive diagnostic testing, including stool
antigen studies and urea breath testing, can be employed. Serology cannot distinguish between
active and cleared infection and is not preferred.

Drugs
Macrophages inside the lamina propria filled with lipofuscin.

Colonoscopy shows melanosis coli, which suggests anthraquinone (eg, senna) laxative abuse.
Excessive use of anthraquinones causes colonic epithelial damage and the release of a brown
pigment (lipofuscin) into the lamina propria that can be visualized on colonoscopy. It disappear
after discontinuoation.

Laxative abuse is characterized by frequent, watery, nocturnal diarrhea. The diagnosis is

suggested by a positive laxative screen or colonoscopy with characteristic findings of melanosis
coli (dark brown discoloration with pale patches of lymph follicles).

Azithromycin is used to treat travelers' diarrhea, which causes abdominal cramps and self-limited
watery or bloody diarrhea.

Lamivudine (3TC) is a reverse transcriptase inhibitor sometimes used to treat HIV and chronic
HBV co-infection.

RAAS system counteracts the effects of splanchnic vasodilation to prevent systemic

hypotension. Because ACE inhibitors blunt this important compensatory response, they should
be avoided in all patients with cirrhosis.

Older patients with a history of chronic antacid use are at risk for vitamin B12 deficiency due to
achlorhydria. These patients frequently have subtle neurologic findings, including lower
extremity paresthesias and signs of dorsal column injury (eg, diminished light touch/vibration
sensation). A serum vitamin B12 test is usually diagnostic, but methylmalonic acid or
homocysteine testing may be required for confirmation in inconclusive cases.