ite review: gi

1/16/2007 UNSOM: EMR

Gastroenterology

UNSOM Emergency Medicine

Review


Dysphagia (1)• Difficulty swallowing• Solids: mechanical/obstructive• Solids/liquids: motility disorder• Oropharyngeal dysphagia (transfer): neuromuscular disorder

(CVA)• Progressive (CA) vs. non-progressive (web)• Strictures 2° reflux (can mimic CA)• Work up

EsophagramEndoscopyEsophageal motility studies


Dysphagia (2)• Infectious: Botulism, diptheria, polio, rabies,

Sydenham’s chorea (rheumatic fever), tetanus• Immunologic: Scleroderma, multiple sclerosis,

myasthenia, ALS, polymyositis, amyloidosis• Motor dysfunction:

CN palsy (posterior CVA), diabetic neuropathyAchalasia (vomit undigested food)

Aperistalsis of esophagus (loss of Auerbach’s plexus in the esophagus)

Tx: CCB (Diltiazem, nifedipine) –Botox, dilation, myomotomy


• A 32-year-old woman presents with chest pain that has worsened over the past 2 months. She says it gets worse when she lies flat or exercises and after she eats or drinks quickly. She has no significant past medical history, but her husband says she has lost about 10 pounds recently and has been throwing up undigested food. What are the expected diagnostic findings?

• A. Diffuse ST-segment elevation and PR-interval depression

• B. Dilated esophagus proximal to a beaklike lower esophageal sphincter

• C. Gastric inflammatory changes• D. White matter plaques in the brainstem


Dysphagia (3)Mechanical

• Zenker’s diverticulum Pharyngoesophageal pouchProximal: above the UESElderly, regurgitation of undigested food

• Cancer: MCC = squamousRisk factors: smoking, achalasia, caustic ingestion

• Extraluminal obstruction / tumor


Dysphagia (4)Mechanical

• StricturesGERD, chronic inflammation, occur in distal

esophagus• Schatzki’s ring

Fibrous structure distal esophagusMCC of intermittent dysphagia, steakhouse

syndrome• Webs (occurs intermittently)

Circumferential mucosal outpouchings Congenital or acquiredPlummer - Vinson Syndrome = symptomatic

hypopharyngeal webs + iron deficiency anemia


Odynophagia• Odynophagia - pain upon swallowing

spasm - painful muscle contraction• Causes of esophagitis

RefluxInfection: candida, herpes, immunosuppression:

(HIV, DM, steroid use, CA)Inflammatory conditions: infection, radiation,

trauma, foreign body• Admit dysphagia, odynophagia

BleedingRuptureSevere dehydrationMalnutrition


• Which of the following patients requires oral fluconazole treatment?

• A. 17-year-old girl with both dysphagia and odynophagia refractory to acid suppression therapy who also has multiple allergies

• B. 27-year-old man with chest pain and severe odynophagia who also has asthma and is HIV positive

• C. 47-year-old man with transport dysphagia for solids initially and now liquids who also smokes

• D. 55-year-old man with halitosis, transfer dysphagia, and neck fullness


Hiccups (Singultus)• Involuntary stimulation of the respiratory reflex

with spastic contraction of inspiratory muscles on closed glottis

• Benign causes: gastric distention, smoking, ETOH, change is environmental temperature

• Persistent: damage to vagus/phrenic nerve/CNS Continue with sleep: organic Relieved with sleep: psychogenic

• OrganicCNS: neoplasm, MS, ICPPUD, tonsillitis, goiter, pericarditis, pacemaker, STEMI


Esophageal Rupture (1)• MCC iatrogenic

#1: Endoscopy#2: Dilation MCC in ED: NG tubeDiagnosis by esophagram

• Mallory - Weiss - partial thickness tearLocation: GE junction5-15 % of UGI bleedsVomiting, retchingRisk factors: ETOH, hiatal herniaSpontaneous resolution common


Esophageal Rupture (2)• Boerhaave’s Syndrome - full thickness tear

Males usually, age 40-60Typically associated with alcohol (50%)Typically left posterior distal ruptureChemical, then infectious mediastinitisSevere chest pain, shock, sepsisAir in mediastinum (Hamman’s crunch) PyopneumothoraxGastrografin (water soluble) UGIFluids, Antibiotics, Surgical consult

• X-ray: mediastinal air, left pleural effusion, pneumothorax, widened mediastinum


Pneumomediastinum / Subcutaneous Emphysema


Esophageal Foreign Bodies• Levels of narrowing

MCC: Cricopharyngeus muscle (C6) (<4 y/o)Aortic arch (T4)Tracheal bifurcation (T6)Gastroesophageal junction (least) (T11)

• Coin x-rays AP orientation = trachea (same plane as vocal

cord orientation)Transverse orientation = esophagus


Foreign Body

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Esophageal Foreign Body


Esophageal Foreign Bodies (3)• 10-20% require some intervention• 1% demand surgical treatment• Most foreign bodies will pass if they traverse

the pylorus • Soft drink pull tabs - may not show up on x-ray


Esophageal Foreign Bodies (4)• Indications for endoscopy

Sharp / elongatedButton batteriesPerforationNickel / quarter at C6 (pediatric)

In esophagus > 24 hours


Esophageal Foreign Bodies (5)• Button batteries

Double density radiographicallyMust always be removed from esophagus immediatelyRapid burns with perforation < 6 hours (Lithium worse)Batteries do not need to be removed:

Passed esophagus, asymptomaticPassed the pylorus <48 hours

Most will pass completely in 48-72 hours, serial radiography• Treatment: broad-spectrum ABX, surgical consultation


Foreign Bodies (6)Sharp objects > 5cm long & 2cm wideMagnet + metalAll others: serial exam / x-raysFish/Chicken bones or plastic CT


Sharp Foreign Body Sharp Foreign Body


Large-corrosive-impacted Foreign Body


Esophageal Food Impaction• Most patients with food impaction have

underlying esophageal pathology• Must evaluate for cause after dislodgement• Treatment options:

Glucagon - relaxes distal esophageal sphincterNifedipine - reduces lower esophageal toneCarbonated beverages - gaseous distention

may push the bolus into the stomachEndoscopyNo papain (meat tenderizer)


Caustic Ingestions (1)• Acids (+/- bad)

Coagulation necrosisNo ongoing tissue necrosis

• Alkali (bad) Liquefaction necrosis (pH 12.5)Ongoing tissue necrosis

• SeverityNature, volume and concentrationTissue contact timePresence or absence of stomach contentsTonicity of pyloric sphincter 5


Caustic Ingestions (2)• Inconsistent relationship between oral signs /

symptoms and esophageal findings• All patients with 2-3° burns are symptomatic• Diluents - water / milk only for solid alkali• No neutralizers = exothermic generation of heat

• Complications

Early: acute airway compromise due to edema, perforation

Late: stricture, perforation

Endoscopy best diagnostic tool


- smoking, alcohol - type O blood- NSAIDs and steroids

Peptic Ulcer Disease• Incidence decreasing in general population and

increasing in the elderly (liberal use of NSAIDs)• MCC Duodenal (80%), gastric (20%)

• Helicobacter pylori responsible for most

• Predisposing factors:

• Treatment:

• Complications:

- antibiotics against H. pylori (amox, clarithro, metro)- histamine blockers (histamines stimulate acid inhibitors) - parietal cell inhibitors (omeprazole) - ulcer surface protectants (sucralfate)

- bleeding - perforation (can cause pancreatitis) (do upright CXR for free air) - obstruction


Bilirubin (1)• Breakdown product of hemoglobin• Hyperbilirubinemia• Unconjugated (> 85%) (“indirect reacting”)

Increased bilirubin load (hemolysis)Inability to conjugate (Gilbert’s, neonatal, sepsis)

• Conjugated (< 30%) (“direct reacting”)Decreased ability to excrete from biliary

tree = cholestasis / obstructionIntrahepatic cholestasis

Hepatocellular damageDamage to biliary endothelium

Extrahepatic cholestasisBiliary outflow obstruction (stones, mass,

congenital inflammation, CHF)


Bilirubin (2)• Conjugated bilirubin in bowel is converted by

gut bacteria to urobilinogen

• Urobilinogen is absorbed from the gut into the circulation and excreted in urine

• If jaundice is present but urine urobilinogen is negative = excess unconjugated hyperbilirubinemia

• If jaundice is present but excess positive urine urobilinogen = excess conjugated bilirubin


Hepatitis (1)• Causes - viral and toxic

Malaise, jaundice, increased SGOT, increased bilirubin

Alcoholic hepatitis Abnormal protime is a marker indicating

significant liver dysfunction if elevated, consider altering or holding doses of liver-metabolized drugs

• Viral Type AFecal - oral, onset 2 weeks post-exposureProphylaxis - immune globulin within 2 weeks of

exposure (travelers, household contacts)


Hepatitis (2)• Viral Type B

Percutaneous, parenteral or sexual exposureOnset 1-6 mo (mean = 75 days) post-exposureComplications = cirrhosis, liver cancer, carrier

state (10%)• Markers

HBsAg: + early (before enzymes increase) InfectiveHBsAb: + 2-6 mo after clearance of HBsAg ImmuneHBcAb: + 2 wks after + HBsAg * persists for lifeHBeAg: + implies high infectivity *May be the only positive marker during the window

when HBsAg declining and HBsAb increasing


Hepatitis (3)• Hepatitis B exposure - source known HBsAg

positive • Unvaccinated

HBIG ASAP + vaccination (0, 1 mo, 6 mo)• Vaccinated

Incomplete series- vaccine boosterKnown responder- test for HBsAb if > 10,

no rx; if < 10 HBIG and vaccine boosterKnown non - responder - HBIG x 2 (0, 30 days)


Hepatitis (4)• Hepatitis B exposure - source unknown

• UnvaccinatedInitiate vaccination

• VaccinatedSame as for HBsAg positive source

• HBIG only recommended if source or situation maybe high risk for exposure


Hepatitis (5)• Viral Type C

Percutaneous, parenteral or sexual exposureUsual cause of non-A, non-B hepatitisHigh carrier rate, higher incidence in HIVCirrhosis / liver cancer (50%)2% seroconversion

• Indications for hospitalization (any hepatitis)Encephalopathy, PT/INR significantly increased,

dehydration, hypoglycemia, bilirubin over 20, age over 45, immunosuppression, diagnosis uncertain


Hepatic Encephalopathy• Precipitants = “LIVER” (Librium [sedatives],

Infection, Volume loss, Electrolytes disorders, Red blood cells in the gut [a major cause])

• Others: dietary protein excess, worsening hepatocellular function

• Early sign = “sleep inversion” - sleeping during the day / awake at night

• Asterixis (“liver flap”)• Ammonia levels: arterial more helpful than venous• Check for hypoglycemia!!!• Treatment: Oral or rectal neomycin / lactulose /

decrease dietary protein / avoid sedatives / avoid bicarbonate (alkalosis can worsen encephalopathy)


Spontaneous Bacterial Peritonitis• Occurs with chronic liver disease

Portal hypertension bowel edema migration and leakage of enteric organisms (E. coli 50%, enterococcus 25%)

• Abdominal tenderness, worsening ascites, encephalopathy, fever, sepsis, shock

• Diagnosis: paracentesis with increased WBCPMN >250/ul

• Tx: Ceftriaxone, ppx: Cipro or Bactrim


• A 57-year-old man with a history of cirrhosis presents with acute renal failure. He denies recent illness and is not taking any nephrotoxic medications. He is well hydrated; his urinalysis is negative. Which of the following is the definitive treatment?

• A. Hydration• B. Liver transplant• C. Renal transplant• D. Transjugular intrahepatic portosystemic

shunt


Gallbladder (1)• Stones = mostly bilirubin / cholesterol -

(radiolucent) • Biliary colic = pain, vomiting, due to obstruction

by stones without inflammation• Cholecystitis (stone-related = calculous)

MCC of abdominal pain in the elderly ORObstruction distention pain / vomiting /

inflammation infection (usually E. coli, Klebsiella) increased WBCs

• Rupture of stone into small bowel with obstruction at ileocecal valve = GALLSTONE ILEUSAir in biliary tree (from bowel) = pneumobilia


Gallbladder (2)• Acalculous cholecystitis

No stones5-10% of casesUsually a complication of another process

(trauma, burn, postpartum, postop, narcotics)Patients often quite sickLikely cause of GB perforation Increased risk with diabetes and elderlyGreater morbidity than calculous variety

• Ascending cholangitis Infection spreading through biliary treeCharcot’s triad = jaundice, fever, RUQ pain


Gallbladder (3)

• Ultrasound initial diagnostic study of choiceUltrasound shows stones, wall thickening, duct dilatation

(not inflammation)HIDA has sensitivity/specificity 97% / 90%HIDA or PIPIDA scan is positive if GB is not visualized =

cystic duct obstruction, best test for cholecystitis

Immediate surgical consultAir in biliary tree, fever, jaundice,

diabetic, elderly, immuno-compromised


Gallbladder Ultrasound


Pancreatitis (1)• Causes

Alcohol or gallstones the most commonDrugs: thiazides / estrogens / salicylates /

acetaminophen / antibiotics [ metronidazole, sulfonamides, erythromycin, nitrofurantoin]

Metabolic disorders [hyperlipidemias, hypercalcemia, DKA, uremia]

Viral infections [mumps, hepatitis, mono, many others]

Bacterial infections [salmonella, streptococcus, mycoplasma, legionella, many others]


Pancreatitis (2)

• On admissionAge > 55Glucose > 200

mg / dlWBC > 16,000SGOT > 250LDH > 350

• At 48 hoursDecreased in HCT >

10%Increase in BUN > 5

mg / dlCa++ below 8 mg / dlpAO2 < 60 mmHgBase deficit > 4 mEq / LRapid fluid sequestration

(over 6L)

• Ranson’s criteria (prognostic)

3 positives = severe disease


Pancreatitis (3)• Amylase

Multiple non-pancreatic sources Height of amylase not necessarily related to

severity• Lipase

May be more sensitive than amylaseMore specific than amylaseClosely follows clinical course

• Plain x-ray Colon cutoff = dilation only over pancreasPancreatic calcificationSentinel loop = small bowel air over pancreasImaging study of choice - contrast CT


Sentinel Loop (Pancreatitis)


Pancreatitis complications• Pseudocyst, necrosis• Hyperglycemia, hypocalcemia• Volume loss, acidosis, GI bleed• ARDS, DIC, renal failure• Death


GI Bleeding Definitions

• Hematemesis - UGI proximal to ligament of Treitz

• HematocheziaMaroon stools

Very rapid UGI bleed (uncommon)Usually colon or small bowel bleed

• Melena - black tarry stools - usually UGI bleed, color from effects of acid and digestion on blood (GI protein breakdown of blood causes increased BUN)


Upper GI Bleeding Sites• A prior site of GI bleeding is often not the site

of subsequent bleeds (best example = variceal bleed, half of subsequent bleeds are from another site)

• UGI sitesMCC PUD (45-50%) usually duodenalGastritis (15-30%) (alcohol, NSAIDS)Varices (10-15%) 1/3 of UGI bleed deathsMallory - Weiss esophageal tears (5-10%)Esophagitis (5-10%) (MCC in pregnancyDuodenitis (less than 5%)


Upper GI Bleeding Risk Factors for Increased Mortality

• Advancing age• SBP < 100 + hr > 100• Hematochezia• Varices• Jaundice• Hemoglobin < 10 g/dl• Co-morbid conditions


• A 67-year-old woman presents after three episodes of hematemesis. She denies significant past medical history and is taking only an over-the-counter medication for osteoarthritis. She appears anxious and diaphoretic. During the interview, she vomits 250 mL of bright red blood. Physical examination is notable for blood pressure 79/58, pulse 122, moderate epigastric abdominal tenderness and bloody stool. Which of the following is most likely to control the bleeding?

• A. Bedside esophagogastroduodenoscopy• B. Nasogastric tube placement with lavage• C. Omeprazole infusion followed by vasopressin drip• D. Sengstaken-Blakemore tube


UGIB Management• PPI (No benefit?)• Octreotide for variceal bleed, decreases

splanchnic flow (No benefit?)• Vasopressin for variceal if delay to endoscopy• Only clear benefit from antibiotics in cirrhotics• Sengstaken-Blakemore/Minnesota tube last

resort for esophageal varices


Lower GI Bleeding (1) Sites

• MCC Upper GI bleed • Diverticulosis• Angiodysplasia (AV malformations), associated with HTN and aortic stenosis - usually right colon• Aortoenteric fistula, esp if previous AAA repair

Erosion of synthetic vascular graft into gut (often preceded by premonitory bleed)

• Cancer / polyps, IBD, rectal disease• Hemorrhoids: MCC of rectal bleeding• Anal fissure – MCC of minor LGI bleeding in infants

to age 5


Low risk LGIB – send home?• No comorbid disease• Normal vitals• Negative or trace positive stool guiac• Negative NG lavage (if performed)• Normal H/H• Good support/reliable• 24 hour follow up


Osler-Weber-Rendu Syndrome• Autosomal dominant vascular anomaly• Multiple small telangiectases of the skin,

mucous membranes, GI tract• Recurrent episodes of GI bleeding, gross and

occult


Pediatric GI Bleeding (1) Under 2 Months• Upper

Bleeding diathesisSwallowed maternal bloodVascular malformation

• LowerMCC is Meckel’s diverticulum (50%)Congenital GI duplicationsIntussusceptionNecrotizing enterocolitis Swallowed maternal bloodVascular malformationVolvulus


Pediatric GI Bleeding (2) Necrotizing Enterocolitis

• Predisposed Premature neonatesHypoxiaHypothermiaPolycythemiaUmbilical catheters

• Mucosal edema to full thickness necrosis• Distention, tenderness, dehydration, vomiting• X-ray - ileus, bowel wall thickening, pneumatosis

intestinalis (late)


Neonatal Necrotizing Enterocolitis

Med-Challenger • EM


Pediatric GI Bleeding (3) Under 2 Years

• UpperBleeding diathesisForeign bodyGastroenteritisTraumatic hemobiliaVascular

malformationMallory-Weiss tear

• LowerAnal fissureCongenital dupl.GastroenteritisHUSHS purpuraInflammatory bowel

diseaseIntussusceptionMeckel’s

diverticulumMilk allergyPolyps


Pediatric GI Bleeding (4) Lower GI Bleeding Sites (1)

• Meckel’s diverticulumCongenital anomaly, 2% of populationTypically diagnosed age < 2Located 40 cm from ileocecal jnx, free or attached to

umbilicusEctopic production of gastric acid (30-50%)Peptic ulceration causes bleedMost common cause of significant LGI bleeding in

childrenCan mimic appy, may initiate intussusception, or

volvulus

Painless “bright red” bleeding(most common clinical presentation)


• A 11-month-old boy is brought in by his mother after she noticed a large amount of dark red blood in his diaper. He appears well and has normal vital signs and a benign abdominal examination. Rectal examination is remarkable for blood without an obvious source. Which of the following is needed to confirm the suspected diagnosis?

• A. Abdominal ultrasound examination• B. Additional history on diet• C. Apt test• D. Nuclear medicine scan


Pediatric GI Bleeding (5) Lower GI Bleeding Sites (2)• Intussusception

Sudden, intermittent pain, vertical sausage mass in 50%

“Currant jelly” stoolSecond most common cause of lower GI

bleeding in childrenMost common cause of bowel obstruction in

first 2 yrs.BE = diagnostic and therapeutic

Lead pointsAdults = polyp, cancer

Child = Meckel’s, lymphoid patch


Hernias (1)• Inguinal - most common

Direct - does not involve passage through the inguinal canal

Indirect - involves inguinal canal (most common)

• Femoral – femoral canal, usually female, below the inguinal ligament, strangulation / incarceration common


Hernias (2)• Umbilical

Congenital: newborns - blacks > whites; females > males, strangulation / incarceration rare

Acquired: women, obesity, pregnancy & ascites, strangulation / incarceration common

• Pantaloon : Indirect + direct at same time• Spigelian (lateral ventral): level of arcuate line lateral

to rectus abdominus, difficult to diagnose, CT / US• Richter - incarceration of a single wall of a

hollow viscus• Incarcerated = irreducible (highest incidence of

inguinal incarceration = 1st year)• Strangulated = irreducible with vascular compromise

(don’t manually reduce)


Ileus• Ileus = cessation of normal peristalsis without

mechanical obstruction

• Continuous pain, distention, decreased bowel sounds, minimal or no tenderness, no flatus or BM, usually self limiting

• Ileus is more common than mechanical bowel obstruction

• X-rays show entire bowel with dilated, fluid-filled loops


Bowel Obstruction• Small bowel

(1) adhesions, (2) hernias, (3) malignancy Generally more intense pain and more vomiting

and less distention than large bowel obstructionX-ray - “step ladder” plicae circulares - traverse

bowel width• Large bowel

(1) cancer, (2) diverticulitis, (3) sigmoid volvulus

X-ray: haustral pattern (doesn’t traverse entire bowel width)

• “Closed-loop” obstruction dangerous = perforationCan occur in colon if ileocecal valve is

competent


Small Bowel Obstruction

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Small Bowel Obstruction


Volvulus• Sigmoid volvulus

Elderly, debilitatedChronic motility

disorderInsidious onset, most

recurX-ray: inverted u, loops

project obliquely to RUQ

Sigmoidoscopy may be therapeutic

• Cecal (15 -20%)Young (35 -55), runnerCongenital freely

mobile cecumAcute onset

X-ray: kidney shaped loop, LUQ,

Requires surgery

Third most common cause of large bowel obstruction behind (diverticular, tumor)

The most common cause in pregnancy


Sigmoid Volvulus


Cecal Volvulus

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Bowel Perforation• Large bowel > small bowel• Mechanism: inflammation, ulceration, trauma,

obstruction• Causes - diverticular disease (the most common

cause), appendicitis (especially at extremes of age), colitis / IBD, ischemia, cancer, foreign body, PUD, radiation

• Cecum the most common site• X-rays – may miss small amount of free air or

retroperitoneal, best view = upright chest x-ray

Ulcers are the most common cause of a visceral perforation


Free Air; Thickened Bowel Wall


Pediatric GI Emergencies• Obstructive GI lesions 1st year

Gut atresiaInguinal herniaMalrotation, +/- volvulusVolvulus around congenital bandIntussusceptionMeconium ileus (associated with CF)Hirschsprung’s diseaseDuplication cysts of intestine

BE is diagnostic study of choice after plain x-ray


Pediatric GI Emergencies Obstructive Newborn GI Lesions 1st Year• Intussusception

MCC surgical abdomen/obstruction 3mo – 6yrIleocolic most common (85%)Peak incidence - age 5 to 9 months / most occur

before 2Classic triad only in 30% (colicky pain, vomiting,

currant jelly stool)Paroxysms of colicky pain is the most specific

symptomKUB: “coiled spring”Infants less than one can have profound

listlessness as wellChildren with Henoch-Schönlein purpura are at

increased riskUltrasound can be diagnostic as well as BE


Intussusception


Intussusception - Barium Enema

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Intussusception - Barium Enema


Pediatric GI Emergencies Obstructive Newborn GI lesions 1st year• Malrotation +/- volvulus

First year of life > first monthEarly diagnosis is crucial to prevent gangrene

of midgutAbnormal rotation & fixationX-ray: loop of bowel over-riding the liver is

suggestive (double bubble)Acute abdomen, shock, rigid / distended

abdomen, bilious vomitingBilious vomiting / signs of obstruction = prompt

surgical consultation


Pediatric GI Emergencies Obstructive Newborn GI Lesions 1st Year

• Pyloric stenosisNon-bilious projectile vomitingHypochloremic metabolic alkalosisFirst born males, familial propensity 50%Third week to third month of lifePalpable “olive”: mass lateral margin right

rectus muscle at liver edgeUltrasound (20%) false negative UGI: delayed gastric emptying, string sign


• What is the most common cause of small bowel obstruction in children?

• A. Adhesions• B. Hernia• C. Intussusception• D. Midgut volvulus


Constipation• Most common digestive complaint in United States,

2.5 million visits • 30-40% > 65 years old• Acute causes: obstruction, medication (narcotics, Ca2+

blockers, psych. meds, Fe, antacids)• Common cause: fiber + fluid intake + exercise• Chronic causes: slow growing tumor, thyroid,

parathyroid, lead, neurologic dysfunction• Rectal exam for: fecal impaction, rectal mass, heme +

stool, anal fissure• Treatment: diet/behavior changes, medical adjuncts,

underlying cause

MUST RULE OUT OBSTRUCTION


Inflammatory Bowel Disease• Crohn’s disease & ulcerative colitis• Idiopathic, chronic• High rate of colon CA with disease > 10 years• Exacerbation / remission pattern• Bimodal age distribution peaks between 20’s

and 60’s• Extracutaneous manifestations - arthritis

(20%), dermatologic (4%), hepatobiliary (4%), vascular (1.3%) - also uveitis

• Tx: sulfasalazine, mesalamine, prednisone, metronidazole, ciprofloxacin


Regional Enteritis - Crohn’s Disease• Chronic inflammatory disease of the entire GI

tract

• Segmental involvement is characteristic = “skip lesions”

• Abdominal pain, cramps, diarrhea (sometimes bloody), fever, perianal fissures, fistulas or abscesses or rectal prolapse (90%), toxic megacolon

• Gross blood uncommon• ↑ oxalate absorption of terminal ilium leads to

nephrolithiasis


Ulcerative Colitis• Chronic inflammatory disease - colon• Similar GI symptoms to Crohn’s disease

Major finding = bloody diarrheaToxic megacolon

Gross distention (over 8 cm)Transverse colon Systemic toxicity Peritonitis

• Rectum, small bowel not affect (unlike Crohn’s)

• Colon cancer = 10 - 30 times greater risk


Mesenteric Ischemia • Risk factors - dysrhythmias (a. fib), low flow &

hypercoagulable states, vascular disease• Deadly / generally elderly / early angiography• Causes:

Embolic *(30%)Arterial thrombus *(10%)Venous thrombus (10%)Nonocclusive (50%)

• Leukocytosis (present in most cases), acidosis, hyperphosphatemia, hyperamylasemia - all inconsistently present

• Avoid digoxin, beta-blockers, vasopressors (decrease splanchnic blood-flow)

*Sudden onset with pain out of proportion

to physical findings


Mesenteric Ischemia Imaging

• Thickened bowel wall• Pneumointestinalis (air in bowel wall)• Air in portal vein• “Thumb printing” = submucosal hemorrhage

All infrequently seen

Mainstay of diagnosis = arteriography


Appendicitis (1)• Luminal obstruction inflammation infection• Anorexia often present• Increased perforation in elderly and small children• Pain migrating periumbilical to RLQ is specific• Late pregnancy - moves lateral and superior• BE - mass effect and non-filling• KUB - appendicolith (1%)• Ultrasound - dilated, non-compressible >6mm• Spiral CT – usually diagnostic

Most common cause of surgical abdomen


Appendicolith

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Appendicitis (2)• Confounders = situs inversus, retrocecal, pregnancy

malrotation, very long appendixResult-uncommon pain location: right upper quadrant,

back, flank, testicular, suprapubic• Rovsing’s sign = LLQ palpation RLQ pain

Psoas sign = RLQ pain on thigh extension while lying in left lateral decubitus positionObturator sign = RLQ pain with internal rotation of the flexed right thigh

• Most common symptom: anorexia, nausea and vomiting• R sided tenderness most common sign• Rebound, rectal and referred tenderness common• Psoas/obturator sign uncommon


Diverticular disease


Diverticulitis (1)• Pain is the most common symptom

Steady, deep, LLQ

• Bowel habits may be altered - diarrhea or constipation

• May mimic appendicitis if copious redundant sigmoid colon

• Intraluminal pressure is greatest in the sigmoid (most diverticula there)


Diverticulitis (2)• Manifestations = pain (inflammation / infection)

and bleeding; pain left side, bleeding right side • Free perforation is rare / most are contained to

the mesentery

• May cause urinary frequency / urgency due to

irritation of underlying GU structures

• Colon cancer may be in the differential

• Tx: fiber, abx (Cipro/Metro), analgesics


Diarrhea• Viral

Most common cause of diarrhea 50-70% of casesMostly winter / spring / children / day careRotavirus, adenovirus calicivirus, enterovirus, Norwalk agent

- “RACE to Norwalk”

Rotavirus MCC pediatric cause of diarrhea 50%Self-limiting / fecal-oral / community outbreak


Diarrhea - Invasive• Invades mucosa inflammation (stool WBCs)

and bleeding (degree varies by pathogen), fever, rash, arthritis, septicemia

• E. coli 0157:HS Hamburger, petting zoo, raw milk, untreated waterCan cause HUS (children) and TTP (elderly)No ABX recommended may increase risk of HUS


Diarrhea - Invasive (2)• Shigella

Very infectious, high fever, febrile seizures, watery - bloody

• Salmonella Very common bacterial diarrhea

(U.S.) Watery / mucoid Pet turtles, amphibians, eggs,

chickens Osteomyelitis can occur in sicklers

(autosplenectomy) and those with splenectomy

Antibiotics increase carrier state (give if sick / septic)

Most commoncause of bloody

diarrheaSystemic toxicity =

typhoid fever (low WBC and relative bradycardia,

abdominal pain, no diarrhea)


Diarrhea - Invasive (3)• Campylobacter

Most common cause of bacterial diarrheaHard to culture / water-borne (raw milk)Invasive enterotoxin60-70% with bloody diarrhea (gross or occult) Erythromycin (children), fluoroquinolone (adults)Acute infection associated with development of

Guillain-Barré syndrome• Vibrio

Parahaemolyticus - oysters, clams, crabs, 2 -12 hour latency

Vulnificus - oysters, shellfish increased morbidity / mortality with pre-existent liver disease


Diarrhea - Invasive (4)• Yersinia enterocolitica

Invasive gram pos bacteriaIncreasing evidence, most common in

childhoodCan mimic appendicitisFeverColicky abdominal pain (may be prolonged)DiarrheaMay be persist 10-14 days

• Diagnosis: fecal WBC stain positive, stool C&S

• Treatment: uncomplicated - supportive only complicated - TMP-SMX, quinolones


Diarrhea - Protozoan (1)• Giardia

Most common US intestinal parasite

Beavers, deer, stream contamination

Stools floating, frothy, foul-smelling, flatulence

Multiple stool specimens may be needed to

identify cysts and / or trophozoites

Metronidazole

Homosexuals, campers, pregnancy


Diarrhea - Protozoan (2)• Amebiasis (entamoeba histolyticus)

Spread between family members and sexual partners

Fecal / oral - anal intercourseDiarrhea can be bloodyExtra-intestinal manifestations (5%)

Liver abscess most common (“chocolate cysts”)Pericarditis, pleuropulm disease, cerebral amebiasis

Wide variety of presentations Asymptomatic cyst passer ColitisCerebral amebiasis


Diarrhea Protozoan (3)• Cryptosporidium

Intestinal protozoan parasitesMCC of chronic diarrhea in AIDSContaminated water supply; recent outbreaksChildren, animal handlers; immunocompromisedIngestion of oocysts; trophozoites attack intestinal

membrane1 week incubation, severe watery diarrhea,

abdominal pain

• Diagnosis: Oocyst in stool• Treatment: Fluid replacement, CDC rec’s

nitazoxanide, or parmomycin plus azithro


Diarrhea - Toxigenic (1)

• Bacteria producing enterotoxin • Food-borne• Diarrhea: watery, voluminous• Minor fever, no septicemia• No WBC or RBC in stool


Diarrhea - Toxigenic (2)• Staph (toxin)

Contaminated foodsGI overgrowth from antibioticsHam, poultry, dairy products, potato saladMCC of food-borne diseaseSymptoms within 6 hours of ingestion Usually afebrile, no abx

• E. coli Water contaminated by fecesMCC Traveler’s diarrhea No readily available diagnostic testsTMP / SMX, cipro


Diarrhea - Toxigenic (3)• Clostridium perfringens

Common, large outbreaksMeat and poultry sourceEnterotoxin mediated6 hours (longer onset)Watery diarrheaSevere abdominal crampsFecal WBC / RBC negativeTreatment: fluids; no abx

• Vibrio – choleraCopious watery diarrhea= “rice water stools”Severe fluid & electrolyte problemsTreatment: fluids, ciprofloxacin, TMP-SMX


Diarrhea – Toxigenic• Bacillus Cereus• Aerobic spore forming pod• Common in rice, especially Chinese

restaurants• Spores germinate when boiled rice is not

refrigerated• Two forms:

Emetic: 2 – 3 hours post ingestion (much like Staph)Diarrheal: 6 – 14 hours (much like Clostridia)

• Also from vegetables and meat• Self limited; no specific therapy or test


Diarrhea - Toxigenic (4)• Scombroid poisoning

Named for fish (suborder) = tuna, mackerel, mahimahi (most frequent cause), related species

Heat - stable toxin from bacterial action on dark - meat fish

Histamine - like toxin / rapid symptom onset (30 min)

Fish - tastes “peppery”Facial flushing, diarrhea, throbbing headache,

abdominal cramps, palpitations Give antihistamines and H2 blockersSuspect when multiple patients have “allergic

reaction”


Diarrhea - Toxigenic (5)• Ciguatera

S.E. US, tropical and subtropical watersGrouper, snapper, king fishFish eat certain dinoflagellates in spring /

summer, that contain toxins harmful to those eating the fish

Muscle weakness, paresthesias (perioral, burning hand / feet), distorted or reversed temperature sensation, vomiting, diarrhea

Neuro symptoms worsened with alcoholNo specific treatment, symptoms can be

permanent


Pseudomembranous Enterocolitis • Varieties = neonatal, postop, antibiotic-related• Due to overgrowth of toxin-producing C. difficile• Begins 7 - 10 days after beginning antibiotics• Patients may be quite sick - fever, toxic, profuse

diarrhea, dehydration• Diagnosis via immunoassay for toxin • Inflammatory disease, membrane - like yellow

plaques• Treatment by stopping precipitating antibiotics • Treat with metronidazole or vancomycin orally• No anti-diarrheals


Botulism• Characteristics

Heat-labile neurotoxin, short onset (half hour)Inadequately processed canned foodsBulbar symptoms / descending paralysis /

anticholinergic findings• Infantile

Floppy baby, constipation, feeble cry Honey can be sourceMost common in breast-fed / also less severe in

this subset• Adult

Diplopia (most common early finding), dysphonia, ptosis, dysarthria, dysphagia

Anticholinergic symptoms - urinary retention, pupil abnormalities, dry mouth, abd. cramps, nausea and vomiting


Rectal Prolapse• Full thickness protrusion of rectum through anal

canal• Sensation of rectal mass• In children, intussusception more likely• Differentiation from internal hemorrhoids &

intussusceptionIntussusception – can place finger between

protruding rectum and anusInternal hemorrhoids – fold of mucosa radiates

out like spoke on a wheelRectal prolapse – folds of mucosa circular


Rectal Prolapse


Hemorrhoids• Engorgement, prolapse, or thrombosis of the

hemorrhoid veins• Internal located at 2, 5, 9 o'clock position• Risk factors: constipation, pregnancy, ascites, portal

hypertension• Painless ,self limited, BRBPR,common presentation• Treatment

Non complicated (nonsurgical): sitz bath, laxatives, topical steroids, fiber

Complicated: large, incarcerated, strangulated, intractable pain require surgery

Thrombosed: elliptical incision to remove clot


Anal Fissure• Most common causes of painful rectal bleeding in

adults and children• 90% posterior midline• Non-midline fissures should suggest more serious

conditionsIBD, CA, sexual abuse

• Sharp cutting pain, especially with bowel movement, blood-streaked stool

• Perianal hygiene, sitz bathsFistula in Ano

Tract between rectum and skin Causes drainage and itchingConsider Crohn’s Disease


Perianal Fissure


Rectal Trauma• Causes:

Penetrating 80%Blunt 10%IatrogenicForeign body

• Must consider GU & colon injuries• Rectal foreign body

60% removed in EDHigh-riding or sharp require general anesthesiaSigmoidoscopy after removal


Rectal Foreign Body


GI Miscellaneous (1)• BE and colonoscopy are relatively

contraindicated in diverticulitis (fear of perforation)

• Hypoglycemia in alcoholics may not respond to glucagon because liver glycogen stores are depleted

• AIDS patients with diarrhea usually have stool specimens positive for pathogens; due to the numerous causes, empiric therapy is not advised


GI Miscellaneous (2)• Extension of a perirectal abscess = ischiorectal

abscess

• Prolapsed, irreducible internal hemorrhoids require urgent surgery

• In most alcoholics with low-grade amylase elevations, the source is non-pancreatic

• Most common serious complication of a Sengstaken - Blakemore tube = aspiration / suffocation

ite review: gi

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