GASTROENTEROLOGY

Editor: Alex DeWeerd, MD
Reviewed by: Patrick Yachimski, MD, Robin Dalal, MD, Rishi Naik MD

Acute Abdominal Pain

Author: Mahsima Shabani

General Approach

  • Rule out life threatening causes:
  • Obstruction, volvulus, peritonitis, perforation, acute mesenteric ischemia, aortic dissection or AAA rupture, acute MI, ectopic pregnancy
  • History: pain location/radiation/quality/severity/timing, prior episodes, aggravating and alleviating factors (eating, bowel movements, position), nausea/emesis, changes in urine/stool, gas, constitutional symptoms, LMP, sexual history, Alcohol, NSAID and antibiotic use.
  • Initial work-up: CBC, BMP, POC Gluc, LFTs, INR, lactate, lipase, U/A, urine hCG, abdominal US
System Causes Common features Workup
Esophagus Esophagitis – GERD, EOE, candida, HSV, CMV, pill, functional Epigastric pain, nocturnal reflux, odynophagia, dysphagia, thrush, immunocompromised Trial PPI, nystatin swish and swallow, consider EGD
Intra-abdominal esophageal rupture Upper abdominal pain; recent trauma, endoscopic intervention, severe straining or vomiting (Boerhaave syndrome) CXR (free peritoneal air), CT chest and abdomen
Stomach Peptic ulcer disease Epigastric pain, better or worse w/ food, ± melena; NSAID use, steroid use CBC, EGD, H. pylori testing
Gastritis Burning epigastric pain/discomfort, heartburn, N/V, hematemesis, bloating and fullness after meals; NSAID, ETOH abuse H. pylori testing, Trial PPI, ± EGD
Gastroparesis N/V, early satiety, post-prandial fullness, bloating; hx of DM, dysautonomia, abdominal surgery Scintigraphy after excluding mechanical obstruction or mucosal disease
Liver Hepatitis: Ischemic, Viral, ETOH, trauma, toxins, autoimmune, congestive RUQ pain, malaise, N/V, anorexia ± jaundice, dark urine, light stools; hx of EtOH, herbal supplement, Tylenol, or IVD use LFTs, LDH, Alb, INR, ETOH, Tylenol lvl, viral panel, RUQ U/S + dopplers; CT
Perihepatitis (Fitz-Hugh-Curtis syndrome) RUQ pain and tenderness with pleuritic component, referred pain to the right shoulder; ALT/AST usually normal Bimanual exam, beta-hCG, NAAT for Chlamydia and Gonorrhea, HIV, pelvic US
Liver abscess Fever with RUQ pain; history of DM, hepatobiliary or pancreatic disease, liver transplant, chronic PPI use US, CT abdomen, BCx, empiric Abx, US/CT-guided drainage
Budd-Chiari syndrome Fever, abdominal, ascites, jaundice, GIB, +/- HE; hx of thrombophilia, OCP use, systemic AI disease Doppler US of liver
Malignancy, HCC, mets Upper abdominal pain, weight loss, early satiety Abdominal US, AFP, CT Abdomen (triple phase)
Spleen Splenomegaly LUQ pain, +/- left shoulder pain, early satiety LFT, CBC, smear, CT abdomen
Splenic infarct Severe LUQ pain; hx of hypercoag state, AFib, splenomegaly ECG for AFib, coags, splenomegaly w/u
abscess Fever and LUQ tenderness CT, BCx, broad-spectrum Abx, drainage
Splenic rupture Left shoulder pain worse with inspiration; hx of trauma CT, surgery
Portal vein thrombus Abdominal pain, dyspepsia, or GIB; history of cirrhosis Doppler US, CT abdomen, AC
Biliary Biliary colic RUQ or epigastric discomfort +/- N/V, lasts >30mins, worse with food, abdominal exam usually benign, overweight, ♀, 40's LFTs, RUQ US
Cholecystitis Prolonged >4hrs RUQ or epigastric pain, guarding, Murphy's sign, nausea, emesis with fever LFTs, RUQ US, HIDA scan
Choledocholithiasis/ cholangitis RUQ pain, N/V with jaundice, fever, +/- hypotension, AMS CBC, LFTs, RUQ U/S, BCx
Sphincter of Oddi dysfunction Biliary type pain without other apparent causes with abnormal LFTs (obstructive pattern) during the episode of pain LFTs, RUQ US
Pancreas Acute or chronic pancreatitis Persistent epigastric pain radiating to back, N/V, hx of ETOH use or gallstones, family hx; hx of similar pain weeks prior suggests complications. Lipase, CT A/P (rarely necessary within 24-48 hrs), RUQ US for gallstones
Intestines Gastroenteritis Diarrhea with N/V, abdominal pain; sick contact, undercooked food, travel Supportive care
Diverticulitis Older, h/o diverticulosis, LLQ pain (RLQ common in Asian pts) usually constant and lasted several days +/- N/V, fever based on complications CBC, CT A/P w contrast
SBP Fever, abdominal pain and/or AMS; advanced liver disease and ascites Diagnostic paracentesis
Constipation Hx of IBS, narcotic use, Zofran use, unable to pass stool, straining KUB
Bowel Obstruction/Ileus Prior hernia, abd surgery or malignancy, crampy abdominal pain, N/V, obstipation, distended tympanic abdomen with absent bowel sounds. KUB (air fluid levels), CT is more sensitive. If concerned, page EGS and consider NGT to suction
GI perforation Severe abdominal pain, following procedures; can present indolent in immunosuppressed patients Upright or lateral decubitus KUB/CXR, EGS consult
Acute mesenteric ischemia Rapid onset, severe, diffuse pain (pain out-of-proportion to exam) with N/V, can follow a recent hypotensive episode; hx of vascular (arterial or venous) disease, AFib, dissection, thrombosis CBC (leukocytosis), BMP (metabolic acidosis), lactate, CT A/P w contrast (CTA if high suspicion)
Chronic mesenteric ischemia Post-prandial (intestinal angina) pain with weight loss, N/V, diarrhea Abdominal CTA or mesenteric doppler ultrasound
Peritoneal Dialysis-related peritonitis Diffuse abdominal pain and cloudy peritoneal effluent with fever, N/V, abdominal tenderness KUB, CT abdomen, nephron consult, may require EGS
Celiac disease Diffuse abdominal pain with steatorrhea, flatulence. Ttg-IgA, total IgA, DGP IgG, EGD with duodenal biopsies
Colonic non-occlusive mesenteric ischemia Cramping pain, laterally (most often left), urge to defecate + hematochezia CBC, BMP, Lactate, CT A/P w contrast +/- colonoscopy
Appendicitis Periumbilical to RLQ (occasionally epigastric or generalized) with anorexia, N/V, later fever CBC, CRP, lactate, beta-HCG in women, CT A/P w/contrast
IBD Diarrhea (can be bloody), urgency, tenesmus, bowel incontinence, weight loss, fevers. Associated extraintestinal manifestations (arthritis, uveitis, pyoderma) CBC, lactate, ESR, CRP, C-diff, GIPP, stool O&P if recent travel history. CT enterography.
Infectious colitis including C. diff colitis ABx exposure, diarrhea, abdominal cramping; can present with acute peritoneal signs with perforation and fulminant colitis C-diff PCR, CBC, KUB (megacolon)
Colorectal cancer Can present with obstruction and perforation; older adults, IDA, family history of CRC Colonoscopy
Colonic pseudo-obstruction (Ogilvie's syndrome) Pseudo-obstruction in elderly pt, signs of obstruction w/o mechanical cause CBC, lactate, CT A/P w contrast, if no peritonitis supportive care, can try neostigmine
Volvulus Progressive abdominal pain, nausea, distention, constipation, vomiting CBC, lactate, KUB, CT A/P w contrast
Typhlitis Neutropenia, abdominal pain (often RLQ), fever CBC with diff, CT A/P w/ contrast, blood cx, C-diff; empiric ABx
Helminthic infections Loose stools with mucus or blood, nocturnal BM common with anemia and eosinophilia; CBC-diff (eosinophilia), stool O&P
Eosinophilic gastroenteritis Abdominal pain, N/V, early satiety, diarrhea, weight loss associated with eosinophilia and/or history of food allergy or intolerance CBC-diff, CMP, EGD
Lactose intolerance Cramping abdominal pain, bloating, flatulence, and diarrhea. Hydrogen breath test
OB/Gyn Ectopic pregnancy RLQ or LLQ pain with vaginal bleeding, sexually active, 6-8 weeks after LMP, can present with life-threatening hemorrhage if ruptured Urine hCG, pelvic US, CBC, T&S, OB/Gyn consult
Pelvic inflammatory disease/ Tubo-ovarian abscess Lateralization uncommon, acute onset lower abdominal or pelvic pain, cervical motion tenderness; often with cervical discharge in a sexually active woman; hx of STI Bimanual pelvic exam w/ GC NAAT, pelvic US
Endometriosis Associated with dysmenorrhea, dyspareunia, AUB, pelvic pain and/or infertility; may have bowel or bladder symptoms TA or TV US, OB/Gyn consult for surgical interventions
Leiomyomas (fibroids) Symptoms usually related to bulk effect of tumor; infrequently acute pain from degeneration of torsion of pedunculate tumor, can have uterine tenderness TA or TV US
Ruptured ovarian cyst Sudden-onset severe focal lower quadrant pain after sexual intercourse; not associated with vaginal discharge CBC, T&S, TA or TV US, observe if HDS
Ovarian torsion Acute-onset mod-to-severe localized pain to one side. Often with N/V in a young woman with adnexal mass; usually no vaginal discharge Pelvic US w/ doppler, OB/Gyn consult
Ovarian hyperstimulation Abdominal discomfort/distention, diarrhea, N/V in women undergoing fertility treatment Supportive
Ovarian cancer Abdominal or pelvic pain with bloating, urinary urgency or frequency, difficulty eating/feeling full quickly. Pelvic US, CT A/P
Ovulatory pain (Mittelsmerz) Mid-cycle right or left-sided pain coinciding with timing of ovulation. Supportive
Kidney Nephrolithiasis Usually sharp flank pain but may have back or lower abdominal pain, colicky± hematuria, h/o kidney stones, Crohn's disease U/A, CT A/P w/o contrast
Pyelonephritis Usually, flank pain but can be lower abdominal pain, fever/chills, CVA tenderness, usually with dysuria, frequency, urgency. U/A with culture, BMP, CT A/P w/ and w/o contrast
Cystitis Suprapubic pain associated with dysuria, frequency, urgency, hematuria U/A with reflex culture
Urinary Retention Suprapubic pain with inability to urinate, older man with BPH, anticholinergics Post-void residual
Renal infarct Acute flank pain with N/V, +/- fever, HTN; hx of vascular disease or A-fib, coagulopathies CBC, BMP, UA, ECG (Afib), CT A/P w contrast
Vascular Myocardial infarction CAD risk factors, DoE, epigastric pain, diaphoresis ECG, troponin
Aortic Dissection Vascular Risk factors, sudden onset, tearing pain→ back CT dissection rule out
AAA rupture Vascular risk factors, sudden onset → back, hypotensive, pulsatile abdominal mass; h/o smoking, older man CT A/P w contrast, consult vascular surgery
Abdominal compartment syndrome Critically ill patients; burn, trauma, massive ascites, abdominal surgery, intraperitoneal bleeding, associated with new organ dysfunction. Intra-abdominal pressure measurement (intragastric, intracolonic, intravesical or IVC catheter)
MSK/skin Herpes zoster Immunocompromised, dermatomal rash, burning pain Physical exam, vesicle PCR for zoster
Muscle strain Worse with twisting or bending, h/o trauma, overuse, heavy exercise Physical exam; rest, NSAIDs
Hernia Bulge, worse w/Valsalva CT A/P w/o contrast
Pulmonary Pneumonia Productive cough, fever CXR, CBC, sputum cx
Pulmonary embolus Tachycardia, tachypnea, hypoxemia ECG, trop, BNP CTA chest
Hematologic Paroxysmal nocturnal hemoglobinuria Fatigue, dyspnea, hemoglobinuria, cytopenia UA w/ microscopy, CBC, smear, retic count, DAT, coags, CMP, LDH, hapto
TTP Non-specific pain, N/V/D associated with neurologic and renal injury, MAHA, thrombocytopenia UA, CBC, smear, retic count, DAT, coags, CMP, LDH, hapto; ADAMTS13
Acute intermittent porphyria Severe, poorly localized with motor/sensory neuropathy, red urine, tachycardia Urinary PBG
Lead poisoning "Lead colic", constipation, anorexia and arthralgia/myalgia, excessive fatigue, headache, anemia Exposure history (paint, batteries, welding, ammunition), blood lead level
Endocrine Adrenal insufficiency/crisis Hypotension, fatigue, lethargy, N/V, weight loss, hyperpigmentation BMP (↓Na, ↑K, ↓ Glu), Cort. stim
DKA Diffuse abdominal pain, N/V; h/o DM CBC, BMP, U/A, beta– hydroxy butyrate
Hypothyroidism Accompanied with constipation, fatigue, weakness, and other symptoms of hypothyroidism TSH, fT4
Functional IBS, depression, somatization, functional dyspepsia, anxiety abdominal migraine Imaging and other workup negative Diagnosis of exclusion
Other Intra-abdominal abscess Prior intra-abdominal disease or surgery, fever CBC, BCx, CT A/P w/ contrast
Hypercalcemia N/V, constipation, ↑ thirst, ↑ urination, bone pain, muscle weakness, confusion, fatigue BMP, ionized calcium, PTH, Vit D, PTHrp
Angioedema (hereditary or ACEi-related) Paroxysmal GI colic with N/V/D along with prodromal fatigue, erythematous skin discoloration and angioedema C4, c1-INH, c1q, discontinue ACEi
Familial Mediterranean fever Recurrent acute abdomen w/o identifiable cause (repeated laparotomies) with fever, synovitis, pleuritis, erysipelas-like erythema; 1st degree relative with FMF Genetic testing, colchicine trial

Acute Diverticulitis

Authors: Emily Poellinger, Alex DeWeerd

Background

  • Inflammation and/or infection of a diverticulum, a small out-pouching along wall of colon
  • Presence of colonic flora on urine culture or pneumaturia suggests colovesical fistula
  • Most pts with uncomplicated diverticulitis have significant improvement 2-3 days after antibiotics

Presentation

  • Lower abdominal pain (85% LLQ), tenderness to palpation on exam, decreased appetite, nausea/vomiting, low-grade fever, change in bowel habits (constipation or diarrhea), leukocytosis

Evaluation

  • CBC w/diff, CMP, Lipase, U/A, β - hCG
  • Imaging: CT abdomen/pelvis with oral and IV contrast
  • CT findings: localized bowel wall thickening (>4mm), paracolic fat stranding, presence of colonic diverticula

Management

  • Generally okay to treat in the outpatient setting (no differences in outcomes were found between outpatient and inpatient care in uncomplicated diverticulitis), but inpatient treatment recommended for the following:
  • Complicated diverticulitis (presence of abscess, perforation, obstruction, fistula)
  • Septic, uncontrollable abdominal pain, age >70, significant comorbidities, immunosuppressed, inability to tolerate PO intake
  • Diet: Bowel rest vs. clear liquids (advance diet as tolerated)
  • IVF: give IVF to correct volume deficits from decreased PO intake
  • Antibiotics: should cover GNRs and anaerobic organisms
  • In general, hospitalized patients should be empirically started on IV antibiotics and then transitioned to PO after resolution of abdominal pain/advancing diet for a total 10-14 day course
  • IV regimen: Zosyn, Cefepime + Metronidazole, or meropenem (if high risk for organisms w/ESBL)
  • PO regimen: Ciprofloxacin/Levofloxacin + Metronidazole OR Augmentin
  • If low risk and mild disease, may not need antibiotics
  • Colonoscopy after complete resolution of symptoms (6 – 8 weeks) to definitively rule out presence of underlying colorectal cancer (unless performed in last year)

Complications

  • Patients who fail to improve on IV antibiotics or deteriorate require repeat imaging
  • Abscesses: depends on size of abscess
  • < 4cm: IV antibiotics, if fail to improve percutaneous drainage vs surgery

  • 4cm: IV antibiotics + percutaneous drainage (if possible) vs surgery

  • Obstruction/structuring: radiographic differentiation between acute diverticulitis and colon cancer is difficult; thus, surgical resection of bowel is needed to relieve obstruction and rule out cancer
  • Fistula: most commonly involves the bladder, vagina, small bowel, or uterus. Rarely heal spontaneously, therefore will require surgical correction.
  • Bleeding: most common cause of overt lower GI bleeding in adults, typically resolves spontaneously.
  • If persistent, endoscopic intervention to locate and stop the bleeding; if hemodynamically unstable, angiography is the next step to locate and/or control the bleed. If bleeding persists and patient is unstable, segmental colectomy can be performed if the site of bleeding is clearly located with endoscopy/angiography; if no site is found, subtotal colectomy can be performed.
  • Surgical management for a diverticular bleed is rare and should be a last resort approach.
  • Perforation:
  • Microperforation (contained perforation): Presence of small amount of air bubbles, but no oral contrast outside of colon on CT
    • Most treated with IV antibiotics and bowel rest like uncomplicated diverticulitis
  • Frank perforation (contained perforation): Intraabdominal free air, air under the diaphragm, and diffuse peritonitis requires emergency surgery so consult EGS
  • Recurrent diverticulitis: elective surgery generally not recommended for patients with prior diverticulitis episodes if they were managed medically and uncomplicated.
  • Indications for elective surgery include patients who have had a prior episode of complicated diverticulitis or are immunosuppressed. Surgery typically performed 10-12 weeks after last acute diverticulitis episode

Segmental colitis associated with diverticulosis (SCAD)

  • Definition: chronic mucosal inflammation in a segment of colon with diverticula
  • Pathogenesis: currently unknown, leading hypotheses include fecal stasis, localized ischemia, and mucosal prolapse
  • Symptoms: chronic diarrhea, abdominal pain, intermittent hematochezia
  • Diagnosis: colonoscopy with chronic inflammatory changes on biopsy only in an area of the colon with diverticula (sigmoid colon>>descending colon) and absence of inflammation in the rectum (compared to ulcerative colitis, which always involves the rectum)
  • Rule out other causes: acute uncomplicated diverticulitis (increased paracolic fat stranding/mild colonic wall inflammation, endoscopy shows primary involvement of diverticular orifices and peri diverticular mucosa), infectious colitis (stool studies/tissue biopsy), NSAID-induced colitis (medication exposure), ischemic colitis (acute presentation), IBD (UC involves rectum, CD typically involves other sites in GI tract), radiation colitis (history of radiation, tissue biopsy showing eosinophils)
  • Management: Start with antibiotics (cipro or flagyl x 10-14 days), if unresponsive, add oral mesalamine x 7-10 days with dose escalation if persistent after 2 weeks. If symptoms remain, start prednisone 40 mg and gradually taper over 6 weeks.

Acute Pancreatitis

Author: Kristijan Bogdanovski

Background

  • Common causes: Gallstones (40%), EtOH (30%)
  • Other causes: post-ERCP, pancreatic cancer/obstruction, blunt abdominal trauma, hypertriglyceridemia (TG >1000), hypercalcemia, drugs (thiazides, protease inhibitors, azathioprine, 6MP), mumps, Coxsackie, vasculitis, pregnancy, genetic (PRSS1, SPINK1, CFTR), autoimmune (IgG4), scorpion venom
  • Several scoring systems (all available on MDCalc)
  • BISAP (Evaluate in first 24hours of presentation)
    • Score 3 -5: mortality > 15 %
  • APACHE II (Evaluate in first 24hours of ICU admission)
    • Score> 8: mortality 11 – 18 %
  • Ranson (Evaluate at admission + 48hrs post admission)
    • Score > 3: mortality > 15% (consider ICU admission)
  • Glasgow-Imrie (modified Ranson criteria, used 48h post admission)
    • Score >2 associated with higher mortality (consider ICU admission)

Presentation

  • Must have 2 out of the following 3 criteria:
  • Pain characteristic of pancreatitis (sharp, epigastric, radiating to back)
  • Enzymes (lipase or amylase) >3x ULN (ULN at VUMC = 78)
    • ***Use lipase, much more specific than amylase
  • Imaging characteristic of pancreatitis (US, CT, MRI)
    • If pain is characteristic and lipase > 3xULN, no need for CT A/P (imaging only really useful if either of the 2 criteria above are equivocal)
  • Grading Severity:
  • Mild: no organ failure or systemic complications
  • Moderate: transient organ failure (<48 hours)
  • Severe: persistent organ failure (>48 hours)

Evaluation

  • Lipase, CBC, CMP, lipid panel, lactate, direct bilirubin
  • Obtain RUQ U/S for all pts, evaluates for gallstones
  • CT A/P w/ IV contrast if indicated
  • Reserved for patients not improving at 48-72 hour to assess for complications
  • If performed at onset, underestimates severity (necrosis takes 72 hours from onset)

Management

  • Fluids, Fluids, Fluids:
  • Bolus 10 mg/kg (if clinically hypovolemic) + 1.5mL/kg/hr Maintenance Fluids
  • Follow HCT and BUN as markers for successful fluid resuscitation
  • Persistent hemoconcentration at 24 hr is associated with necrotizing pancreatitis
  • Pain Control:
  • Common starting narcotic regimen is oxycodone 10 mg q6h PRN and hydromorphone 0.5 mg q4h for breakthrough
  • Nutrition:
  • Do NOT have to make NPO at presentation, restarting enteral feeding as early as tolerated is recommended; addressing fluid resuscitation and pain control will help improve appetite and PO tolerance
  • Start with clear liquid diet or mechanical soft and advance as tolerated
  • Low fat diet (Fatty acids ↑ CCK ↑ trypsinogen to trypsin)
  • If NPO > 72 hours, attempt PO and if fail, place Dobhoff for enteral nutrition at latest by day 5… outcomes with NG/NJ >>> TPN
  • Antibiotics:
  • Fever, leukocytosis common, not an indication for ABX as the necrosis is (often) sterile
  • Infection of the necrosis should be suspected with failure to improve 7 days after onset
    • CT A/P w/ IV contrast recommended to assess for pancreatic or extra-pancreatic necrosis or local complications
    • Most likely organisms enteric (E. Coli, Klebsiella, Pseudomonas, Enterococcus)
    • If clinical signs of infection and abdominal imaging demonstrating gas within necrosis, can empirically start ABX without aspirate or culture
    • Use abx with good pancreatic necrotic penetration: Cefepime/FQ + Flagyl or carbapenem
    • EUS or IR guided drain for aspirate: can be done on immature collections for diagnostic purposes but typically only done if collection is walled-off—at least 4 weeks
  • Endoscopic Intervention (cystogastrostomy) has emerged as first-line therapy for symptomatic pseudocysts or walled-off pancreatic necrosis, with step-up therapy to video assisted retroperitoneal debridement (VARD) or surgery when needed

Additional Information

  • Urgent ERCP for choledocholithiasis on imaging, with cholangitis or obstructive jaundice, otherwise elective ERCP (see page on choledocholithiasis)
  • Complications:
  • ARDS, abdominal compartment syndrome, AKI, DIC
  • < 4 weeks after pancreatitis: Peripancreatic fluid collection, acute necrotic collection

  • 6 weeks after pancreatitis: pancreatic pseudocyst, walled-off necrosis (WON)

  • Most fluid collections should be followed over time as acute collections can resolve and are unable to be sampled safely with EUS
  • Gallstone pancreatitis:
  • All pts should have cholecystectomy once recovered (recurrence is 25-30%) with EGS
  • Performed during initial admission in cases of mild acute pancreatitis
    • Consider age or co-morbid illness precludes fitness for surgery

Chronic Pancreatitis

Author: AJ De Witte

Definition

  • A syndrome characterized by irreversible chronic progressive pancreatic inflammation, fibrosis, and scarring, resulting in damage to and loss of exocrine (acinar), endocrine (islet cells), and ductal cells.

Etiology: TIGAR-O mnemonic

  • Toxic Metabolic: EtOH, tobacco use, hyperCa (Ca > 12), HLD (fasting TG > 300, nonfasting > 500), CKD 5, medications, toxins
  • Idiopathic: early onset (age < 35), late onset (age > 35)
  • Genetic: Autosomal dominant (PRSS1 gene), recessive (CFTR, SPINK1, etc.)
  • Autoimmune: IgG4-related (AIP type 1), AIP type 2
  • Recurrent, severe acute pancreatitis
  • Obstructive: pancreas divisum, ampullary stenosis, main duct pancreatic stones or strictures, widespread calcifications, mass causing duct obstruction

Presentation

  • Abdominal pain (most common)
  • Exocrine insufficiency: diarrhea, steatorrhea, weight loss
  • Typically occurs later in disease process
  • Endocrine insufficiency: diabetes
  • Occasionally asymptomatic

Evaluation

  • Imaging: CT or MRI (may be negative early in course of disease)
  • If CT or MRI negative but suspicion for CP remains high, consider EUS +/- biopsy or secretin-enhanced MRCP

Labs: - BMP, LFTs, lipid panel, PeTH - Consider genetic testing, especially in younger patients and/or patients without clear etiology - Pancreatic function testing diagnoses exocrine insufficiency but is not necessary for diagnosis of CP - Gold standard = 72 hour fecal fat (> 7g of fat per 100g stool per day) - rarely done - More practical = fecal elastase (<100 = diagnostic, 100-200 = indeterminate) - Must be performed on formed stool, can be false positive If watery specimen - Do not have to stop pancreatic enzymes to measure - Lipase and amylase levels can be elevated, but are usually normal due to pancreatic scarring and fibrosis

Management

  • Tobacco and EtOH cessation
  • Pancreatic enzyme replacement therapy if evidence/diagnosis of exocrine insufficiency
  • Usual dose: 50,000 units/meal + 25,000 units with snacks
  • Should take with first bite of a meal and consider adding extra enzymes or splitting up dose throughout meal if lasting longer than 15 mins
  • If lack of response: try increasing dose, confirm compliance, add PPI, split up dose throughout meal, look for concurrent GI disorders
  • Pain: Tylenol + NSAIDs > Opioids (Tramadol), consider SSRI/SNRI/TCA or gabapentin
  • For refractory pain, other options include celiac plexus blockade or total pancreatectomy with islet auto transplant
  • Vitamin supplementation + Vit D + Ca
  • Consider antioxidants (selenium, ascorbic acid, β-carotene, and methionine, vitamin E) – mixed evidence but some studies have shown improved pain control
  • Routine testing for osteoporosis and fat-soluble vitamin deficiencies

Anorectal Disease

Author: Ashley Cozart

Background

  • Benign and malignant causes share symptoms, often hemorrhoidal complaints.

Presentation

  • Perianal pain
  • Generalized: pruritis ani, less likely to be malignant
  • Localized: skin trauma, perianal abscess, perianal neoplasms, external hemorrhoids
  • Anal canal pain: anal fissure, anal cancer, anal ulceration (STIs), proctalgia fugax
  • Bleeding: anal fissures, internal hemorrhoids, anal cancer
  • Prolapsing tissue: prolapsing internal hemorrhoids, rectal prolapse
  • Pruritis: most likely idiopathic, inflammatory skin disorders (dermatitis, hidradenitis suppurativa, SCC), infections (STIs and Candida), systemic diseases (usually generalized; DM, cholestasis, thyrotoxicosis, HIV, etc.)
  • Perianal drainage: anal fistula, fecal incontinence, or other skin conditions (i.e. pilonidal cyst)

Evaluation

  • Visual inspection+ DRE + anoscopy/proctoscopy/colonoscopy
  • Anoscopy: eval of anal condylomata, neoplasms, internal hemorrhoids, anal fissures
  • Rigid proctoscopy: eval of rectal neoplasms, proctitis
  • Colonoscopy: eval of anal bleeding

Management

  • Internal hemorrhoids:
  • Low grade (I or II):
    • Dietary: water intake + fiber supplements +/- stool softeners
    • Lifestyle modifications: limiting seated and toilet time
    • Rx: topical anesthetics + steroids (intermittent short-term use), vasoactive agents (Prep H, Nitro), antispasmodic agents (ie. Nifedipine), sitz baths.
    • Refer to GI clinic or colorectal surgery clinic if refractory to 6-8 weeks of medical treatment
  • High grade (III or IV): refer to colorectal surgeon
  • If bleeding refractory to conservative management, refer for banding (colorectal surgery vs GI)
  • External hemorrhoids:
  • Thrombosed external hemorrhoids:
    • <72 hours- bedside incision and thrombectomy

    • 72 hours- operative intervention avoided since discomfort will likely improve.

    • If nonviable skin on exam- urgent surgical intervention
  • If not thrombosed, can treat like low grade internal hemorrhoids as stated above
  • If rectal bleeding associated with any type of hemorrhoid, refer for colonoscopy
  • Perianal abscess: consult surgery for urgent incision and drainage
  • Anal fistula: surgery
  • Anal fissure: treat w/ 1 mo of supportive measures (fiber, sitz bath, topical analgesic), topical vasodilator (nifedipine or nitroglycerin), and resolution of constipation. Surgery if refractory.
  • Anal cancer: treatment based on tumor location/histology
  • Rectal prolapse: Likely surgical repair (indications include sensation of rectal prolapse and fecal incontinence and associated constipation. Pelvic floor exercises (VUMC Pelvic Floor Therapy Clinic) if patients cannot undergo procedure.
  • Proctalgia fugax: reassurance for mild-intermittent, topical nitroglycerin if severe-frequent

Biliary Disease

Author: Braden Vogt, Alex Wiles

Pearls:

  • ERCP is not available at VA: requires fee-basis consult to VUMC, contact GI to arrange
  • Prior cholecystectomy -> CBD normally dilates to 10 mm, not pathologic
  • Pneuomobilia generally indicates performance of prior biliary sphincterotomy and/or biliary stent
  • CBD dilation classically > 6mm, but CBD dilates with age: 70 yo -> 7mm, 80 yo -> 8mm; opiates can also cause biliary dilatation

Acute Acalculous Cholecystitis

  • Inflammation of the GB without obstructing stone (due to stasis and ischemia)
  • Presentation: Seen in critically ill/ICU pts; similar history as above; may present as unexplained fever or RUQ mass (rarely jaundice)
  • Ddx: calculous cholecystitis, pancreatitis, hepatic abscess
  • Evaluation: Same as acute calculous cholecystitis
  • Imaging: GB wall thickening, pericholecystic edema, intramural gas, GB distention

Management: Supportive care, antibiotics, GB drainage - IVF, correct electrolyte abnormalities, NPO - Broad spectrum antibiotic coverage - Place CT-guided procedure consult for cholecystostomy placement vs Endoscopic drainage (transpapillary cystic duct stent via ERCP or cholecystoduodenostomy by EUS) - Consult EGS if necrosis, perforation, or emphysematous changes present

Acute Calculous Cholecystitis

  • Inflammation of the GB from an obstructing stone in the GB neck or cystic duct
  • Ddx: PUD, pancreatitis, choledocholithiasis, ascending cholangitis, IBD, Fitz-Hugh Curtis
  • Presentation: Severe constant RUQ pain, fever/chills, N/V, + Murphy sign
  • Evaluation: CBC (leukocytosis), CMP (mild AST/ALT ↑), Lipase, Lactate, BCx x2
  • Imaging: RUQ U/S: gallstones + GB wall thickening or pericholecystic edema
  • If U/S non-diagnostic (no stones or GB inflammation)→ HIDA Scan (lack of GB filling)

Management: NPO, IVF, IV Abx until resolved or surgical removal - Urgent Cholecystectomy (<72H) with EGS; - If poor surgical candidate: Cholecystostomy with IR; endoscopic drainage options for selected patients (i.e. poor surgical candidates also with ascites) - Complications: gangrenous cholecystitis, perforation, emphysematous cholecystitis, cholecysto-enteric fistula, gallstone ileus

Biliary Colic

  • Transient biliary obstruction typically at the GB neck without GB inflammation (no fever)
  • Presentation: Constant (not colicky) intense, dull RUQ pain and N/V for 30 minutes to 6 hours, then resolves, provoked by fatty foods (CCK), absent Murphy's sign
  • Biliary colic generally consists of discrete episodes separated by weeks to months, and not daily pain
  • Evaluation: Normal (CBC, LFTs, Lipase, Lactate)
  • Imaging: RUQ U/S: cholelithiasis (stones in GB)
  • Management: Elective cholecystectomy as outpatient

Choledocholithiasis

Author: Anton de Witte, Braden Vogt

  • Obstruction of biliary outflow by CBD stone without inflammation (no fever)
  • Impacted cystic duct stone (cholecystitis) with compression of the CBD (Mirizzi syndrome)
  • Presentation: RUQ pain (can be painless), N/V and jaundice
  • Evaluation: CMP and D-bili (Bili/ALP/ GGT ↑↑↑, AST/ALT mild ↑), CBC (Leukocytosis suggests cholangitis), Lipase
  • Imaging: RUQ U/S: dilated CBD (ULN is 6mm) → MRCP/EUS vs ERCP (see below)
  • MRCP preferred given non-invasive but has lower sensitivity for smaller stones (consider EUS if still have suspicion despite negative MRCP or if patient contraindication to/intolerance of MRI)

Approach to Choledocholithiasis:

(Please refer to the physical handbook for algorithm image)

Approach to risk stratification choledocholithiasis:

| Risk Profile | Clinical and Imaging Features | |High|-CBD stone on imaging-Clinical Acute Cholangitis-T.bili > 4 AND dilated CBD (>6mm with GB, >8mm without GB)| |Intermediate|-Abnormal liver enzymes-Age > 55-Dilated CBD on US with T.bili < 4| |Low|No predictors present| |---|---|

Management

  • NPO & IVF, pain control PRN
  • Procedures as per above algorithm
  • See Cholangitis section If concern for acute cholangitis

Acute Cholangitis

  • Bacterial infection of biliary tract 2/2 obstruction (typically stones) or prior instrumentation (ERCP)
  • Pts with malignant obstruction typically do not develop cholangitis
  • Presentation: Charcot triad (RUQ pain, fever, jaundice); Reynolds' Pentad (AMS, Hypotension)
  • Evaluation: CBC, CMP (D bili, ALP ↑↑↑) Blood Cultures, Lipase, Lactate
  • CRP, AST/ALT can be ↑↑ as well
  • Imaging: RUQ U/S: dilated CBD (ULN is 6mm), no need for MRCP/EUS
  • Consider MRCP overnight if ERCP is not being done emergently

Management:

  • NPO, IVF
  • Consult GI for urgent/emergent ERCP (generally within 24 hr)
  • If ERCP not feasible or fails to establish biliary drainage, can consider EUS-guided biliary drainage, percutaneous transhepatic cholangiography, or surgical decompression
  • Antibiotics for Biliary Disease (IDSA Guidelines):
  • Mild to moderate acute cholecystitis (stable):
    • Ceftriaxone 2g daily, Cefazolin 1-2g q8H
  • Cholangitis or Severe acute cholecystitis (unstable or immunocompromised):
    • Zosyn 3.375g q8H, Meropenem 1g q8H or Cipro 500 q12H and Flagyl 500 q8H
    • Healthcare-associated Biliary infections: consider Vancomycin (order w/PK consult)

Clostridioides Difficile Infections

Author: Anton De Witte

Background

  • Clostridioides difficile is the causative bacteria for antibiotic-associated colitis
  • Always consider C. diff in a hospitalized patient with unexplained leukocytosis
  • Microbiology: Anaerobic gram-positive, spore-forming, toxin-producing bacillus
  • Outside colon, exists in spore form – resistant to heat, acid, and antibiotics (why we must wash our hands)
  • Spores are transferred from environment to person, once in intestine convert to functional vegetative, toxin-producing forms → susceptible to antibiotics
  • To be pathogenic, must release toxin (A+B) to cause colitis and diarrhea
  • Risk Factors: Antibiotic use (during use or typically up to 1 month after use), age >65, hospitalization, enteral feeding, obesity, stem cell transplant, chemo, IBD, cirrhosis, +/- PPI use (no clear causal relationship)

Presentation

  • Spectrum from asymptomatic carrier to fulminant colitis with toxic megacolon
  • Asymptomatic carrier: 20% of hospitalized patients (50% of adults in long term care facilities)
  • Non-severe disease: watery diarrhea (>3 unformed stools in 24 hours), lower abdominal pain, nausea, ± fever, leukocytosis (WBC >15,000)
  • Severe disease: diarrhea, diffuse abdominal pain, abdominal distention, fever, lactic acidosis, AKI (Cr > 1.5), marked leukocytosis (sometimes >40,000)
  • Fulminant disease: Severe criteria + hypotension/shock, ileus (rare), or megacolon (>7cm colon diameter and/or >12cm cecum diameter)
  • Recurrent disease (relapse > reinfection): resolution of symptoms on therapy followed by reappearance of symptoms within 2-8 weeks after stopping therapy; (Up to 25% of patients have recurrence)
  • If symptoms never resolve, consider refractory C. diff or alternative diagnosis

Evaluation

  • Stool PCR for toxigenic strains (very sensitive, can detect asymptomatic carriers w/o toxin production); with reflex EIA (enzyme immunoassay) for toxins A and B (specificity of 99%)
  • PCR (+)/Toxin (-) = carrier
  • PCR (+)/Toxin (+) = treat
  • PCR (-) = no treatment
  • Imaging
  • Nonsevere disease: no imaging necessary
  • Severe or fulminant disease: CT a/p with oral and IV contrast
  • Endoscopy: Typically used when alternative diagnosis is suspected; not warranted for classical symptoms, positive laboratory tests, or clinical response to treatment

Management

  • Contact precautions until at least 48 hours after diarrhea resolves
  • Classify patient disease severity to guide treatment algorithm
  • Do not repeat stool testing – 50% remain positive after treatment up to 6 weeks later
Clinical Condition Treatment
Non-fulminant disease
Initial episode (nonsevere or severe) -First line: PO Vancomycin 125mg QID x 10 days OR PO Fidaxomicin 200mg BID x 10 days
-Second line: (only for non-severe disease in low-risk patients): PO Metronidazole 500mg TID x 10-14 days
Recurrent episode
Consult ID +/- GI		 First Recurrence:
-First line: PO Fidaxomicin 200mg BID x 10 days
-Second line: Vancomycin Taper (PO 125mg QID x 14 days → PO 125mg BID x 7 days → PO 125mg QD x 7 days → PO 125mg q72h x 2-8 weeks)
-Adjunctive therapy: IV Bezlotoxumab 10mg/kg x1
Second or Further Recurrence:
-Same as above
-Consider Fecal Microbiota Transplantation (FMT)
Fulminant disease
Consult ID, GI and EGS		 Ileus Absent:
-PO Vancomycin 500mg QID + IV Metronidazole 500mg TID
Ileus Present
-Same as above + consider Vancomycin enemas 500mg q6h
Consider colectomy or FMT

Constipation

Author: Chelsie Sievers

Background

  • Definition: presence of lumpy/hard stools, straining, use of digital maneuvers, sensation of incomplete evacuation, frequency <3 BM per week.
  • Common etiologies: opioid-induced, medications (anti-depressants, iron, anticholinergics) hypothyroidism, hypokalemia, pregnancy, IBS, neurogenic (trauma, MS, Parkinson disease, diabetes, autonomic dysregulation).
  • Always think about risk of obstruction (prior abdominal surgeries, oncology history or risk for GI/GU malignancies, history of IBD/Crohn's).

Evaluation

  • Evaluate etiologies plus lifestyle factors (low fiber intake, low fluid intake, reduced mobility, acute illness)
  • Clinical diagnosis, no need for imaging unless concerned for obstruction → KUB/ CT
  • BMP + Mg to evaluate electrolytes, consider TSH if chronic
  • Rectal exam to exclude rectal mass or fecal impaction (constipation + diarrhea doesn't exclude impaction/obstruction. Overflow around mass = encoparesis)

Management

  • Stop or minimize offending medications if possible
  • Optimize lifestyle factors: out of bed, walking hallways, increase fluid intake, + cup of coffee if appropriate.
  • Escalating pathway: ensure meds are scheduled not PRN
  • MiraLAX (PEG) 17g BID (can give TID) + Senna nightly (can increase to BID and/or 2 tabs) → Bisacodyl suppository → enema (tap water or SMOG) → stronger osmotic laxative (lactulose 20mg once, Mag-citrate, Golytely) → escalate lactulose dosing 20 – 30 mg q2hrs

Other considerations:

  • Avoid Fleet enemas (sodium-phosphate) in CKD and geriatric populations
  • "The hand that writes for opioids also writes a bowel regimen"
  • Generally, start with scheduled MiraLAX (PEG) 17g daily + senna nightly
  • If severe and unrelieved by escalating therapies, can try methylnaltrexone
  • Lactulose can cause severe bloating and cramping
  • In patients unable to take PO: place DHT to deliver meds or rectal lactulose (important for patients with cirrhosis with AMS/HE).
  • In patients with CF (at risk for distal intestinal obstruction syndrome): ensure have pancreatic enzymes ordered, managed more like constipation than true obstruction: PO/ NGT MiraLAX QID or Golytely.
  • Acute colonic pseudo-obstruction (Ogilvie's syndrome): >12cm cecal diameter = severe dilation, risk of perforation. Treated with neostigmine, 2mg IV over 3 to 5 minutes. Monitor for bradycardia, hypotension, and dysrhythmias (relative contraindications: recent MI, asthma, PUD, epilepsy). Decompression with colonoscopy used in some cases.
  • Consider pelvic floor dysfunction, pelvic floor PT may be helpful

Laxatives

Mechanism Examples Effects
Bulking-agent Psyllium seed (Metamucil), methylcellulose (Citrucel) Absorb water and increase fecal bulk
Osmotic Laxatives Polyethylene glycol (PEG = MiraLAX and Golytely), lactulose, mag-citrate Hyperosmotic substances, pull fluid into GI tract
Stimulant Laxative Senna, Bisacodyl (Dulcolax) Stimulates peristalsis
Stool Softener Docusate (Colace) Generally ineffective
Opioid antagonist Methylnaltrexone (Reslistor) Peripheral acting opioid antagonist, inhibits opioid-induced decreased gastrointestinal motility
cGMP Agonist Linaclotide (Linzess), Plecanatide (Trulance) Stimulates intestinal secretion of Cl-/HCO3-
Prostaglandin derivative Lubiprostone (Amitiza) Increases intestinal chloride-rich fluid secretion

Diarrhea

Author: Charles Oertli

Background

  • 3 BM/day OR abnormally loose stool

  • Acute (<2 weeks), persistent (2-4 weeks), or chronic (>4 weeks)
  • 95% of acute diarrhea is self-limited & no additional treatment needed
  • Most cases of acute diarrhea are due to infections
  • Non-infectious etiologies become more common with increasing duration
  • Voluminous watery diarrhea more likely disorder of small bowel
  • Small volume frequent diarrhea more likely disorder of colon
  • Nocturnal diarrhea suggests an inflammatory or secretory etiology

Acute Diarrhea

Etiology

  • Watery diarrhea: viral gastroenteritis (norovirus, rotavirus, enteric adenovirus), C. diff, C. perfringens, S. Aureus, Bacillus cereus, enterotoxigenic E. coli, Cryptosporidium, Listeria, Cyclospora, vibrio cholerae, (Giardia is typically more chronic), Tropheryma whipplei, COVID
  • Inflammatory diarrhea: Salmonella, Campylobacter, Shigella, EHEC, Yersinia, E histolytica, invasive viruses (CMV, HSV), Non-cholera vibrio. Look for red flag symptoms (see below).
  • Medications, specifically antibiotics

Presentation

  • Evaluate for red flags (BATS are Vulnerable vampires)
  • Bloody stools,
  • Antibiotics/Recent hospitalization
    • Any antibiotic can cause C. diff; the longer the treatment, the more likely
    • Most common to cause C. diff: Clindamycin > Penicillins/Cephalosporins/Fluoroquinolones
  • Too many stools: >6 unformed stools/day
  • Sepsis (Fever) or Severe abdominal pain
  • Vulnerable (Age >70 yr, immunocompromised, IVDU, IBD, pregnant, travel)

Evaluation

  • All patients: CBC w/ diff and BMP to eval for leukocytosis (C.diff), AKI, electrolyte abnormalities, thrombocytopenia/anemia (HUS), eosinophilia (parasites)
  • If red flag symptoms or diarrhea > 7d: ESR/CRP, C.diff, GIPP
  • If immunocompromised: consider CMV, MAC, microsporidia
  • If abdominal pain: consider CT A/P with IV contrast
  • If concern for IBD or hx of IBD: CT Enterography with PO and IV contrast
  • Blood Cultures if febrile/septic

Management

  • All patients: supportive care with PO or IVF, electrolyte repletion
  • If C.diff negative or treatment for C.diff started, ok for symptomatic treatment with Loperamide
  • Start with Loperamide 4mg x1 then transition to 2mg QID (AC+HS) (maximum 16mg/day)
  • If fever or inflammatory symptoms and C.diff not back, ok for Bismuth sabsalicylate (Pepto-Bismol) 30mL or 2 tablets q30min x8
  • Indications for antibiotics:
  • GIPP negative for Shigella, 0157:H7 (can precipitate HUS) and salmonella (can prolong carrier state)
  • Empiric antibiotic therapy ONLY if toxic appearance or high concern for progressive illness/decompensation
    • Ciprofloxacin 500 mg BID or levofloxacin 500 mg daily x 3-5 days
    • Azithromycin 500 mg daily x 3 days
  • Ampicillin + gentamicin used for pregnant women to cover for Listeria
  • C. diff positive (see section below)

Approach to Chronic Diarrhea

Causes of Watery Diarrhea

Secretory Motility Osmotic
Microscopic colitis
Bile acid malabsorption
Carcinoid
Crohn's disease
Gastrinoma
VIPoma
Mastocytosis
Addison's disease
Hyperthyroidism		 Diabetes
Amyloidosis
Systemic scleroderma

Meds: macrolides, metoclopramide, bisacodyl, senna, pyridostigmine		 Lactose intolerance
Bile salt diarrhea
Sugar alcohols: sorbitol, mannitol, xylitol
Meds: antibiotics, caffeine, colchicine, NSAIDs, antineoplastics, antiarrhythmics (digoxin), metformin, carbamazepine
Meds: citrates, lactulose, magnesium-containing antacids, mycophenolate, antibiotics, propranolol, hydralazine, procainamide
Functional: IBS

Causes of Fatty Diarrhea (Steatorrhea)

Malabsorption Inflammatory
Celiac disease
Gastric bypass
Short bowel syndrome
Tropical Sprue
Whipple disease
Small intestinal bacterial overgrowth (SIBO)
Post-infectious malabsorptive diarrhea
Maldigestion
Pancreatic insufficiency
Hepatobiliary disorders		 Diverticulitis
Ischemic colitis
Neoplasia
Radiation colitis
Arsenic poisoning
Microscopic colitis
Invasive infections: bacterial (tuberculosis, yersinosis), viral (CMV, HSV),
Parasites (amebiasis, strongyloidiasis)
Inflammatory bowel disease

Evaluation

  • Labs: CBC w/ diff, CMP, ESR/CRP, TSH, celiac serologies if high suspicion (anti-TTG)
  • Spot fecal elastase Steatorrhea (greasy, malodorous stools that float)
  • Colonoscopy indicated if alarm symptoms are present ( >45 yrs and hasn't had one, or <45 yrs and concern for IBD, CMV, ischemic colitis or microscopic colitis)
  • If concern for IBS: Rome IV criteria (see section on "IBS" below)

Management

  • IBS: trial elimination diet/low FODMAP, antidiarrheals
  • Pancreatic insufficiency: enzyme replacement (Creon), consult nutrition for assistance
  • Celiac: eliminate gluten, will need outpatient nutrition follow-up
  • Bile acid malabsorption: can try cholestyramine (can affect absorption of other meds)

Dysphagia

Author: Julie Anne Giannini

Background

  • Oropharyngeal dysphagia- difficulty initiating swallow, experiencing coughing, choking
  • Esophageal dysphagia- difficulty swallowing several seconds after initiation

Presentation

Difficulty swallowing solids, liquids, or both?

Solids only = mechanical

  • Progressive symptoms: esophageal stricture, peptic stricture, or esophageal cancer
  • Not progressive symptoms: eosinophilic esophagitis, esophageal rings or web, external compression (vascular abnormalities)

Solids and Liquids = motility disorder

  • Progressive symptoms: achalasia or systemic sclerosis
  • Not progressive symptoms: esophageal hypercontractility or esophageal outflow obstruction

Evaluation: Esophageal Dysphagia

  • Upper endoscopy +/- biopsy if no previous history of esophageal abnormalities
  • Normal upper endoscopy:
    • Barium swallow for dysphagia to solids only if mechanical obstruction still suspected
    • Esophageal manometry for dysphagia to solids and liquids or suspecting motility disorder
  • Barium swallow if history of prior radiation, caustic injury, surgery, suspicion for proximal esophageal lesion (Zenker's) or complex stricture
  • Do not order if food impaction suspected or imminent endoscopy
  • Order as timed barium esophagram. If barium emptying is normal and tablet passes without issues, it rules out motility abnormality or stricture.
  • Esophageal manometry helps assess intraluminal pressures, peristalsis, and bolus transit.
  • Disorders of EGJ outflow: achalasia, EGJ outflow obstruction
  • Disorder of Peristalsis: absent contractility, distal esophageal spasm, hypercontractile esophagus, ineffective esophageal motility

Evaluation: Oropharyngeal Dysphagia

  • Videofluoroscopic modified barium swallow and fiberoptic endoscopic evaluation of swallowing (FEES)

Management

  • Food impaction: IV glucagon to relax lower esophageal sphincter vs urgent upper endoscopy

Odynophagia

Author: Ahmed Samy

Definition

  • Pain with swallowing, often accompanied by dysphagia and retrosternal discomfort

Etiology: PIECE mnemonic

Pill-induced

  • antibiotics (tetracyclines), NSAIDs, ART, K-Cl, bisphosphonates
  • Diagnosis: clinical, but EGD may be warranted for persistent(> 1wk) or severe symptoms
  • Rx: discontinue culprit med (or substitute with liquid formulation) and start PPI; Can do GI cocktail combination (maalox, benadryl, lidocaine) swish and swallow x 3 days.
  • Prevention: take culprit meds w/ 8 oz water and sit upright for 30 mins after.

Infectious:

  • Candida esophagitis: HIV (CD4 < 100), heme malignancies, chemo, antibiotics, steroids
  • Can exist without OP thrush
  • Diagnosis: consider empiric fluconazole trial (improvement by 3-5 days). If refractory, EGD, biopsy, culture
  • Treatment: fluconazole 400mg PO/IV day 1, then 200-400mg daily x 14-21 days.
  • HSV esophagitis: immunocompromised including transplant recipients
  • Diagnosis: well-circumscribed "volcano-like" ulcers on EGD, biopsy or brushings of ulcer edge; absence of herpes labialis or oropharyngeal ulcers should not preclude diagnosis
  • Rx: acyclovir 400mg PO five times daily x14-21 days (immunocompromised) acyclovir 200mg PO five times daily or 400mg PO tid x 7-10 days (immunocompetent)
  • CMV esophagitis: HIV (CD4 < 50 )
  • Diagnosis: EGD-linear/longitudinal ulcers + confirmed pathology. Generally, PCR/viral load not helpful but negative serology may lower suspicion
  • Rx: begin treatment while path is pending- ganciclovir 5mg/kg IV q12h vs foscarnet (if leukopenia, low plts). Change to PO once able to tolerate- valganciclovir 900mg BIDx 3-6weeks.
  • Confirmed CMV esophagitis warrants optho eval for CMV retinitis

Eosinophilic esophagitis (see section)

Caustic

  • alkali or acid-induced injury (household cleaners, batteries, pool cleaners).
  • Evaluation:
  • ABCs, including fluid resuscitation and intubation if needed.
  • Rule out life-threatening perforation based on exam (mediastinitis, peritonitis), end organ damage (CBC, CMP, lactate, UDS), and imaging (CT-chest/abdomen w/contrast showing transmural necrosis).
  • NPO until evaluation is complete to determine the grade of injury
    • Avoid attempting to reverse ingestion with emetics or neutralizing agents via NG tube
  • Stress ulcer ppx w/ PPI. Conflicting evidence for steroids.
  • EGS consult (preemptively start broad abx) if workup is suggestive of urgent intervention. Otherwise, EGD < 24hrs of ingestion to further grade injury
  • Lower-grade injury: start on liquid and advance to regular diet over 24-48 hours.
  • Higher-grade injury: needs ICU-level monitoring; start PO intake at 48 hrs, based on tolerability (liquids vs enteral vs TPN)
  • Additional information:
  • Subsequent EGD monitoring q2-3 years recommended to monitor for complications (esophageal stricture, SCC)
  • Ingestion is often intentional, consider psych eval if appropriate

GERD (see section)

Gastroparesis

Author: Hashim Hayat

Background

  • Syndrome of objectively delayed gastric emptying in absence of mechanical obstruction
  • Etiology: Diabetes (most common), post-surgical (gastric or bariatric surgery), thyroid dysfunction, autoimmune or neurologic disorders, medication-induced (GLP-1 agonists, narcotics, anticholinergic agents

Presentation

  • Nausea, vomiting (may contain food eaten several hours prior), abdominal pain (dull, crampy; rarely a predominant symptom), early satiety, postprandial fullness, bloating, weight loss in severe cases

Evaluation

  • Exclude mechanical obstruction and mucosal disease with CTE and EGD
  • Scintigraphic gastric emptying study = gold standard for diagnosis (measures gastric retention of solids at 4h)
  • Stop medications that may affect gastric emptying 48 hrs prior to testing
  • Must have blood sugar < 275 (Hyperglycemia delays gastric emptying)

Management

  • Support with IVF and electrolytes – PO intake preferred
  • Glycemic control in diabetics
  • Stop offending medications
  • Nutrition consult for teaching on frequent small volume meals that are low in fat and soluble fiber
  • If continued symptoms after above, try prokinetics and antiemetics
  • Prokinetics
    • Liquid formulations preferred for better absorption
    • Give 15min before meals and at bedtime.
    • First line is Reglan. If no response, try Domperidone and subsequently erythromycin (not good for long term, pts develop tachyphylaxis)
  • Antiemetics: helps symptoms but do not improve gastric emptying
  • In severe cases patients may require enteral feeding (post pyloric preferred) or venting g-tube
  • Emerging endoscopic treatment options: G-POEM (gastric peroral endoscopic myotomy)

GERD

Author: Lindsey Creech

Background

  • Reflux of stomach contents causing symptoms and/or endoscopic complications
  • Severity classified based on appearance of esophageal mucosa on EGD and frequency of symptoms.
  • Erosive esophagitis: endoscopically visible breaks in distal esophageal mucosa + GERD
  • Nonerosive reflux disease: presence of symptoms of GERD without esophageal mucosal injury and positive pH testing

Presentation

  • Esophageal symptoms: heartburn, regurgitation, chest pain, dysphagia, globus sensation, odynophagia
  • Extra-esophageal symptoms: chronic cough, hoarseness, asthma, chest pain, dental erosions, globus sensation
  • Complications: Esophageal stricture, Barrett's esophagus, esophageal adenocarcinoma

Evaluation

  • Clinical diagnosis with classic heartburn and/or regurgitation
  • If dx uncertain, can perform ambulatory pH monitoring
  • EGD indicated for the following:
  • Presence of alarm features (dysphagia, persistent vomiting, GI cancer in 1º relative, odynophagia, GI bleeding, weight loss, iron deficiency anemia, age ≥ 60 y/o with new-onset GERD symptoms)
  • Risk factors for Barrett's esophagus (duration of GERD at least 5-10 years [must be present], >50 yo, male, white, hiatal hernia, obesity, nocturnal reflux, tobacco use, first-degree relative w/ Barrett's and/or adenocarcinoma)
  • Abnormal UGI tract imaging (i.e. luminal abnormalities)
  • Continued symptoms despite adequate PPI therapy

Management

  • First and foremost, Lifestyle and dietary modifications:
  • Weight loss, elevate HOB, avoid large meals or meals within 3 hrs of bedtime, elimination/minimization of chocolate, caffeine, spicy foods, citrus, and carbonated beverages
  • Mild/intermittent symptoms (2x/wk) w/o erosive esophagitis (if had EGD):
  • Trial H2RA (famotidine 10mg) PRN; reassess in 4 wks
  • If persistent sx, increase H2RA BID (famotidine 20mg); reassess in 2 wks. If sx improve, step-down therapy as tolerated
  • If persistent sx on H2RA BID, then PPI qd (omeprazole 10mg), increase to omeprazole 20mg if remaining uncontrolled; reassess in 4-8 wks
  • If sx improve, discontinue PPI
  • If persistent sx, manage as refractory and refer to GI for EGD +/- ambulatory pH testing
  • Frequent symptoms (>2 episodes/wk, and/or severe symptoms that impair QOL):
  • PPI qd (omeprazole 20mg) for 8 wks, if sx improvement, discontinue PPI
  • Recurrent symptoms:
  • 2/3 of patients w/ nonerosive reflux disease relapse when acid suppression is discontinued
  • If ≥3 months after discontinuing, repeat 8-wk course of PPI
  • If <3 months of discontinuing, EGD (if not already performed) to rule out other etiologies or complications
  • Erosive esophagitis and Barrett's esophagus:
  • Require maintenance acid suppression with a standard dose PPI (omeprazole 20mg) daily given likelihood of recurrent symptoms and complications if stopped
  • PPI use:
  • Should be prescribed at lowest dose and for shortest duration appropriate
  • Most effective if taken 30-60min before first meal of the day
  • Taper if taking >6 mo, then transition to H2RA PRN for mild or intermittent sx
  • Long term side effects: Very well tolerated, high-quality RCTs show slightly higher risk of enteric infections (such as C.diff)
  • If pregnant patient, start with antacids or sucralfate
  • If elderly patient, attempt to wean off PPI/H2RA or discontinue with goal of using antacid PRN (due to side effects of H2RA and PPI)

Eosinophilic Esophagitis

Author: Wrinn Alexander

Background

  • Association with atopy (asthma, allergies, eczema, rhinitis)
  • Dysphagia (most commonly to solid foods), food impaction, central chest pain, GERD/refractory heartburn, upper abdominal pain
  • Clinical presentation may vary based on age:
  • Children < 4 years often have feeding concerns and growth issues
  • Children 4-11 years often have frequent regurgitation, abdominal pain, and vomiting
  • Adolescents & adults may present with food impactions, dysphagia, and chest pain

Evaluation

  • Diagnostic criteria
  • Symptoms related to esophageal dysfunction
  • EGD with >15 eos/hpf on biopsy
  • Exclusion of other causes for esophageal eosinophilia
  • 50-60% pts will have elevated serum IgE lvl; peripheral eosinophilia can be seen but is generally mild

Management

  • Management depends on patient's preference
  • Elimination diet: 1FED (animal milk; most common), 2FED (milk and wheat), 6FED (milk, egg, wheat, soy, fish and nut)
  • Standard dose PPI for 8 weeks ± elimination diet. If still symptomatic after 4 weeks, increase PPI to BID. Use lowest PPI dose that maintains symptom remission
  • Alternative treatment is oral budesonide suspension 2mg twice daily x12 weeks or fluticasone propionate (18+ yo: >220 mcg/spray, four sprays daily in divided doses; 12-17yo: 220mcg/spray, eight sprays daily in divided doses; 1-11yo: 110 mcg/spray, eight sprays daily in divided doses)
  • After the above trials, repeat EGD in 8-12 weeks to assess response. If on stricter elimination diets than 1FED, can reintroduce food groups and repeat assessment
  • May require intermittent dilation of strictures to relieve dysphagia
  • Evaluation by an allergist is recommended given strong association with allergies
  • Dupilumab and Eohilia are alternative treatment options and are the only FDA-approved agents for EoE
  • Complications: food impactions, post-endoscopic tears, esophageal rupture (rare)

ACG 2025 Guidelines on EoE: https://gi.org/journals-publications/ebgi/eluri_feb2025/
ACG 2025 Podcast on EoE: https://education.gi.org/podcasts/podcast_207

Peptic Ulcer Disease

Author: Kinsley Ojukwu

Background

  • Peptic ulcer disease (PUD) occurs when there is a break (ulceration) in the lining of the stomach or duodenum.
  • Ulcer is >5mm break in the mucosa, with extension through muscularis mucosa or deeper layers. Erosion is <5mm.

Etiology

  • H-Pylori infection > NSAID use >>> ZES associated gastrinoma
  • Other associated factors: smoking, EtOH, acute stress, malignancy, and glucocorticoids in combination with NSAIDs

Presentation

  • Episodic aching, gnawing, or burning epigastric pain; N/V, heartburn alleviated by antiacids.
  • Gastric ulcers (pain worse w/eating, weight loss); duodenal ulcers (pain better w/eating, worse on empty stomach, worse at night)
  • May be asymptomatic until complications such as hemorrhage or perforation
  • Alarm features: unintentional weight loss, persistent vomiting, melena, unexplained iron deficiency anemia, progressive dysphagia, early satiety, palpable abdominal mass, left supraclavicular lymphadenopathy (Virchow node)

Evaluation

  • EGD for complicated PUD, patients with alarm sx, or dyspepsia w/ age >60
  • CBC, H Pylori testing if no strong NSAID use
  • H. Pylori endoscopic tests (biopsy urease, histology, culture)
  • H. Pylori non-endoscopic tests (Serology – IgG, Urea Breath test, stool antigen)
  • Most H. Pylori tests affected by PPI and/or antibiotic use; stop PPI 1-2 weeks prior to testing; serology testing is not useful post treatment.

Management

  • General: treat underlying cause, encourage smoking cessation, limit ETOH, stop NSAIDs
  • Uncomplicated peptic ulcer (non H. pylori)
  • Oral PPI (e.g., omeprazole 20 to 40 mg daily) x 4 weeks (duodenal ulcers) or 8 weeks (gastric ulcers)
  • Uncomplicated peptic ulcer and + H. Pylori
  • Oral PPI BID x14 days with combination antibiotic regimen
    • Macrolide exposure/resistance: Bismuth Quadruple Therapy
    • No Macrolide exposure/resistance: Clarithromycin Triple Therapy (Amoxicillin)
  • FYI: There is an order set for H pylori regimen in EPIC at VUMC
    • Confirm H. pylori eradication (via stool antigen test, urease breath test, or EGD >4 weeks after completion of therapy. If not eradicated, re-treat:
    • Clarithromycin Triple Therapy -> Bismuth Quadruple Therapy
    • Bismuth Quadruple Therapy -> Levofloxacin Triple Therapy
  • Complicated peptic ulcer (bleeding, perforation, gastric outlet obstruction)
  • Gastric or duodenal ulcer perforation is a surgical emergency; will clinically present as peritonitis, but may be subtle in older/immunocompromised pts
    • Fluid resuscitation, NG decompression, acid suppression, empiric antibiotic therapy, EGS consult
  • EGD is indicated to determine etiology and for possible treatment, however surgery is often indicated.
  • IV PPI (if bleeding: IV PPI for 72 hrs after endoscopic treatment, then oral PPI)

Additional Information

  • Continue maintenance PPI therapy (omeprazole 20 mg daily) for the following:
  • Peptic ulcer >2 cm and age >50 or multiple co-morbidities
  • Frequently recurrent peptic ulcers (>2 in one year)
  • H. pylori-negative, NSAID-negative ulcer disease
  • Failure to eradicate H. pylori (including salvage therapy)
  • Condition requiring long term aspirin/NSAID use
  • Persistent ulcer on repeat EGD (if performed)
  • Indications for repeat EGD (8-12 weeks):
  • Persistent/recurrent symptoms despite medical therapy
  • Complicated ulcer (bleeding), with evidence of ongoing bleeding
  • Giant gastric ulcer (>2 cm) or features of malignancy at initial endoscopy
  • Gastric ulcer that was not biopsied or inadequately sampled on initial EGD
  • Gastric ulcer in pt w/risk factors for gastric cancer (>50 yo, H. pylori, immigrant from high prevalence area [Japan, Korea, Taiwan, Costa Rica], FHx, presence of gastric atrophy, adenoma, dysplasia, intestinal metaplasia)
  • In refractory dyspepsia, consider alternative etiologies: malignancy, infection (CMV), Crohn's, eosinophilic gastroenteritis – all can mimic PUD and present as ulcers in the stomach and duodenum

GI Bleeding

Author: Alex DeWeerd

Background

  • Intraluminal blood loss anywhere from the nasopharynx/oral cavity to the anus
  • Don't forget epistaxis or oropharyngeal bleeding as possible source of melena
  • IV PPI prior to endoscopy may ↓ need for endoscopic therapy but does not impact transfusion requirement, rebleeding risk, need for surgical intervention, or mortality
  • Classification: relative location to the Ligament of Treitz (LoT)
  • Upper = proximal to LoT
    • PUD, gastritis (alcohol, stress, NSAIDs, ASA), esophagitis, variceal bleed, Mallory-Weiss tear, AVM, Dieulafoy's lesion, aorto-enteric fistula, gastric antral vascular ectasias, malignancy
  • Lower = distal to LoT
    • Diverticular bleed, ischemic/infectious/IBD/radiation colitis, malignancy, angiodysplasia, anorectal (hemorrhoids, anal fissure), Meckel's diverticulum, post-polypectomy bleed

Historical factors to consider when trying to identify source of bleeding

  • Cirrhosis or chronic alcohol use: varices or portal hypertensive gastropathy
  • Hx of AAA or aortic graft: aorto-enteric fistula
  • Hx of renal disease, aortic stenosis, HHT: angiodysplasia
  • Hx of H. pylori, NSAID use, tobacco use: PUD
  • Hx of tobacco use, H. pylori, weight loss, early satiety, dysphagia, change in bowel habits: malignancy
  • Painless hematochezia: diverticular bleed
  • Abdominal pain: colitis
  • Look out for false positives: bismuth, charcoal, licorice, and iron

Presentation

  • Hematemesis (very specific for upper GI bleed), hematochezia (usually lower although brisk upper possible), melena (usually upper), coffee-ground emesis, epigastric/abdominal pain, acute or chronic, hx of GI bleed and prior endoscopies.
  • Exam: VITALS – assess hemodynamic stability to determine resuscitation needs, MICU vs. floor; orthostatic vs, rectal exam every time (smear stool on white tissue paper to look for melena), look for signs of cirrhosis (jaundice, palmar erythema, ascites, spider angiomata)
  • Vital signs that may help estimate severity of bleed:
    • Blood loss <15% - resting tachycardia
    • Blood loss 15-40% - orthostatic hypotension
    • Blood loss >40% - supine hypotension

Evaluation

  • CBC, PT/INR, CMP, Lactic Acid, Blood Gas
  • BUN/Crt ratio > 30:1 more predictive of upper GI bleed, <20:1 more predictive of lower GI bleed
  • EGD: usually best
  • Difficulty localizing GIB: pill-capsule, balloon enteroscopy Meckel's scan, tagged RBC scan
  • Massive lower GI bleeds will require arteriography

Management

  • Secure airway (intubation) if comatose, extremely combative, or massive hematemesis
  • At least 2 large bore IV's (> 18 gauge) – ask nurses directly to ensure these are placed
  • Maintain active type and screen
  • Bolus IVF to maintain MAP >65H/H monitoring q6-q12 hours; transfusions as indicated
  • Active bleeding: Start IV PPI (pantoprazole) 40 mg BID if thought to be upper/possible ulcer. If no active bleeding, can start IV PPI 40mg qd
  • If cirrhotic, Ceftriaxone 1g daily for empiric SBP prophylaxis
  • If possibility of variceal bleed: Octreotide IV 50 mcg x1 then 50 mcg/hr drip x 3-5 days
  • NPO if unstable vs. clear liquids (no reds or purples) until morning for EGD
  • Balloon tamponade can be temporizing measure for uncontrolled hemorrhage 2/2 EV (needs to be intubated if device is placed)
  • For massive lower GI bleed: If hemodynamically unstable, consult IR and get a CTA abd/pelvis while doing fluid and blood product resuscitation. If hemodynamically stable, start with upper endoscopy to rule out UGIB. If source not identified on EGD, get CT angiography (if actively bleeding) or colonoscopy (if severe bleeding has stopped). If source not identified, investigate for small bowel bleed.
  • Never give prep to a patient for colonoscopy (GoLytely) without discussing with GI fellow
  • Consult gastroenterology to facilitate endoscopy. Consider consulting hematology if emergent anticoagulant reversal agent is needed.
  • If endoscopy is unable to stop bleeding -> IR is next who can embolize
  • If embolization fails -> EGS for source removal

Ileus

Author: Julie Giannini

Background

  • Non-mechanical decrease or stoppage of flow of intestinal contents.
  • Result of a neuroimmune interaction that consists of the early neurogenic phase (autonomic nervous system) and the inflammatory phase (immune system).
  • Risk factors: critically ill patients, s/p abdominal or retroperitoneal surgery, or perioperative complications (pneumonia or abscess).
  • Other risk factors: opioid use, intra-abdominal inflammation/infection, bleeding, hypokalemia, and delayed enteral nutrition.

Presentation

  • Abdominal distention, bloating, N/V, inability to pass flatus, sparse/absent bowel sounds, often with slower onset than seen in a mechanical bowel obstruction
  • Pain is often diffuse, persistent, and w/o peritoneal signs

Evaluation

  • Plain abdominal films: supine and upright films may show dilated small bowel loops, air in the colon and rectum w/o a transition point.
  • If plain films are not diagnostic, CT w/ oral/IV contrast to help identify presence of transition point
  • BMP

Management

  • Treating the underlying cause, bowel rest, IV fluids, +/- NG decompression, decrease opioids, ambulation
  • Small bowel follow-through with gastrografin or water-soluble contrast does not help ileus

Inflammatory Bowel Disease

Authors: Emily Poellinger, Krissie Lobon

Background

  • Ulcerative colitis (UC): colon only (can have backwash ileitis) and almost always involves the rectum; contiguous lesions; mucosal inflammation
  • Crohn's disease (CD): any part of the GI tract; "skip lesions"; transmural inflammation
  • Important historical considerations to include in your documentation and presentation:
  • Location of disease (CD: LB/SB, LB only, SB only; UC: proctitis, left-sided or pancolitis)
  • Complications: Fistulas, sinus tracts, strictures, perianal disease, microperforation (more commonly in CD)
  • Include previous endoscopy and imaging findings; current and prior IBD treatment and reason for transition (SEs, failure), primary IBD provider

Genetics and Epidemiology

  • First-degree relatives of people with IBD are 20x more likely to be diagnosed with the condition; however, only 15% of patients with IBD have a first-degree relative with the disease
  • Genetic predisposition: CD > UC
  • The number of individuals affected by IBD across the globe has increased from 3.7 mil (1990) to 6.8 mil (2017)
  • Age of onset 15-30, though can present at any age. A bimodal age distribution with second peak between 50-80 is also seen
  • Smoking is a risk factor for CD and increases risk of complications of CD. Does not increase risk for UC.

Presentation

  • UC: frequent diarrhea (often bloody), tenesmus, urgency, abdominal pain; may have fever, malaise, symptomatic anemia, and weight loss
  • Complications: severe bleeding/anemia, fulminant colitis, toxic megacolon, perforation, colorectal cancer
  • CD: abdominal pain, nausea/vomiting, fever, malaise, weight loss; May also have diarrhea (± bloody depending on CD location)
  • Complications: fistulas (entero-enteric, entero-vesicular, entero-cutaneous, rectovaginal, perianal, retroperitoneal), abscesses, strictures, obstruction
  • Small bowel involvement (>100 cm of terminal ileum) can lead to fat malabsorption 2/2 impaired enterohepatic circulation of bile salts
  • Extra-intestinal (EI): arthritis, sacro-iliitis, uveitis, episcleritis, aphthous ulcers, erythema nodosum, pyoderma gangrenosum, PSC (esp. UC), nephrolithiasis (calcium oxalate), thromboembolism, metabolic bone disease
  • Disease severity (mild, moderate, severe) can be objectively measured using different indices, for example the Montreal classification of severity of UC is one such index that stratifies UC and CD. Crohn's Disease Activity Index (CDAI) is also used as a grading system to describe disease activity. The frequency and severity of diarrhea, systemic symptoms, and lab abnormalities are also considerations of classification of IBD.
Ulcerative Colitis Crohn's Disease
Site Colon only, can have ileitis Any part of the GI tract
Distribution Diffusely throughout colon; mucosa and submucosa inflammation only Focal, "skip lesions", transmural inflammation
Histology Crypt abscess Non-caseating granulomas
Complications Toxic megacolon, colorectal cancer Fistulas, strictures, abscesses, obstruction
Perianal disease Rare Common
Extraintestinal Manifestations Common Common

Evaluation

  • CBC w/diff, CMP, CRP, ESR, ± CMV PCR
  • If diarrhea: rule out infection with GI Pathogen panel and C. diff, consider stool cultures, O&P, CMV PCR
  • If anemic: obtain iron studies and type & screen
  • If weight loss or concern for malnutrition: albumin, pre-albumin, Vitamin D, B12, folate
  • Imaging:
  • CT Enterography (oral contrast) preferred in CD, for luminal/extra-luminal complications
  • How to order CTE: "CT abdomen pelvis enterography", order barium (Volumen) 0.1% oral suspension x2, 1st dose to be given by nurse 60 min before study, 2nd study to be given 30 min before (nurse should be in contact with CT tech)
  • Endoscopy: If CD, will depend on the situation, but if acute severe UC, patient will need flex sig/colonoscopy asap (can be unprepped)

Management

Acute Flare

  • Check for infectious etiology for acute flare: Send stool for C.diff and GI pathogen panel
  • Pain control: usually a major component of hospital course
  • Avoid NSAIDs, oral pain medications are preferred
  • If pain is difficult to control, consider Acute Pain Service consult
  • Narcotics and Imodium are contraindicated in toxic megacolon
  • Antibiotics: appropriately treat infections (intra-abdominal or perianal abscess) with antibiotics (consider prior culture data, often use cipro/flagyl), but empiric antibiotics not routinely recommended otherwise
  • VTE Prophylaxis: All IBD patients, even if having blood in stool (unless requiring transfusion) as they are at much higher risk of VTE
  • Nutrition: Nutrition consult for all IBD patients; For severe malnutrition or if prolonged bowel rest is needed, TPN is sometimes initiated
  • Anemia: Ferritin <100 or iron sat <20 with ferritin <300, consider iron infusions (if no bacteremia) or transfuse for severe anemia
  • Smoking Cessation (esp. with CD): discuss smoking cessation & consult tobacco cessation
  • Consult Colorectal Surgery (not EGS): SBO, toxic megacolon, bowel perforation, peritonitis, fistulizing disease
  • Ensure consideration of other causes of colitis as above evaluation suggests (infectious, vascular, drug-induced)

Immunosuppression: (Infections must be ruled out and/or treated before starting)

  • Steroids:
  • IV methylprednisolone (solumedrol) 30 mg BID or hydrocortisone 100 mg TID/QID for 3-5 days
  • If multiple days without improvement, IBD providers will often consider initiation of biologics/immunomodulators
  • Budesonide (Entocort): non-systemic steroid released during intestinal transit
  • Transition to oral (40 mg prednisone daily) once clinically improved/tolerating PO; typically prescribe a prolonged taper on discharge (often down by 5 mg every week)
  • If severe proctitis: consider rectal steroids (hydrocortisone enema/foam)
  • If lack of response to steroids: rescue therapy with advanced therapies (Infliximab, Cyclosporine, JAK) or surgical intervention (colectomy for UC)
  • Infliximab (Inflectra) is available at VUMC
  • If patient fails to respond to steroids, consider possibility of CMV colitis (usually evaluated by biopsy on flex sig or colonoscopy), serum CMV PCR is part of initial workup but if negative it does not rule out CMV colitis
  • Prior to initiating a biologic, all patients must have the following negative studies within the last year: Quantiferon Gold and CXR, Hepatitis B serologies, HIV, urine histoplasma Ag (some providers)
  • Colon cancer screening: IBD that involves at least 1/3 of the colon (UC or CD) is associated with increased colon cancer. Usually not doing CRC screening as an inpatient but important consideration for outpatient care

Induction and Maintenance Therapies for Remission

Mild-Moderate UC:

  • Induction of Remission: Multiple agents approved – advanced therapies preferred for mild/moderate disease. PO budesonide MMX, PO steroids, anti-TNF (adalimumab, golimumab, infliximab), Anti-integrin (Vedolizumab), IL 12/23 (Ustekinumab), IL-12 (Risankizumab, mirikizumab, guselkumab), JAK inhibitors (tofacinitib, upadacinitib), S1P (ozanimod, etrazimod). Avoid monotherapy with thiopurines or methotrexate
  • When infliximab is used for induction often best to pursue combination induction with thiopurine like azathioprine
  • Maintenance Therapy:
  • If remission achieved with advanced therapy, continue for maintenance
  • Corticosteroids are not used for maintenance therapy. The goal is steroid free remission

Moderate-Severe UC:

  • Induction of Remission: multiple agents approved – advanced therapies are preferred for moderate to severe disease. Anti-TNF (adalimumab, infliximab, certolizumab pegol) ± immunomodulator (azathioprine, 6-MP, methotrexate) to prevent antibody development; anti-IL 12/23 (Ustekinumab), anti-IL23 (Risankiaumb, mirikizumab, guselkumab), anti-integrin antibodies (vedolizumab, natalizumab), JAK inhibitor (Upadacitinib)
  • PO steroids for short term use to alleviate symptoms during induction
  • Maintenance Therapy: typically use the same medication used to achieve induction for maintenance and decision to discontinue immunomodulator is individualized based on disease history/complications but often it is discontinued after 12-24 months specifically for younger males, patients >60, or patients with history of recurrent nonmelanoma skin cancer

Intestinal Ischemia

Author: Ashley Ciosek

Acute Mesenteric Ischemia

Presentation

  • Early: Abdominal pain is most common symptom, abdominal distension ("pain out of proportion to exam", meaning pain develops before abd tenderness)
  • Late: As transmural bowel infarction develops, abdomen becomes distended, bowel sounds become absent, and peritoneal signs develop
  • Arterial occlusion: Sudden onset, severe periumbilical pain, nausea and emesis
  • Venous thrombosis: More insidious onset abdominal pain, waxing and waning
  • Non-occlusive mesenteric ischemia: variable location and severity of abdominal pain; often overshadowed by a precipitating disorder

Pathophysiology

  • Sudden onset ↓ or absence of blood flow to the small intestines
  • Mesenteric arterial occlusion:
  • Arterial embolism: Associated with cardiac arrhythmias (atrial fibrillation), valvular disease, endocarditis, ventricular aneurysm, aortic atherosclerosis, and aortic aneurysm
  • Arterial thrombosis: Most commonly from atherosclerotic disease; can also be 2/2 abdominal trauma, infection, or dissection
  • Venous thrombosis:
  • Associated w/ hypercoagulable states, malignancy, prior abdominal surgery, abdominal mass → venous compression, intra-abdominal inflammatory processes
  • Non-occlusive mesenteric ischemia:
  • Intestinal hypoperfusion and vasoconstriction; associated with decreased cardiac output, sepsis, vasopressor use

Evaluation

  • Type and Screen, Lactic acid, BMP, CBC
  • Imaging: KUB: Normal in > 25% of cases
  • Ileus w/ distended bowel loops, bowel wall thickening, ± pneumatosis intestinalis (bowel wall air)
  • Free intraperitoneal air → immediate abdominal ex-lap
  • CT Angiography: no oral contrast, obscures mesenteric vessels, ↓ bowel wall enhancement
  • Focal or segmental bowel wall thickening, intestinal pneumatosis, portal vein gas, porto-mesenteric thrombosis, mesenteric arterial calcification, mesenteric artery occlusion

Management

  • General: IVFs, NPO, hemodynamic monitoring and support (try to avoid vasoconstricting agents), anticoagulation, broad-spectrum antibiotics, pain control
  • If develops peritonitis or evidence of perforation on CT → EGS consult for surgery
  • Mesenteric arterial embolism: Embolectomy vs. local infusion of thrombolytic agent
  • Mesenteric arterial thrombosis: Surgical revascularization vs. thrombolysis with endovascular angioplasty and stenting
  • Venous thrombosis: Anticoagulation; possible thrombolysis if persistent symptoms
  • Non-occlusive disease: Treat underlying cause, stop vasoconstriction meds, consider intra-arterial vasodilator infusion
Acute Mesenteric Ischemia Ischemic Colitis
Abd pain early on, then abd tenderness later ("pain out of proportion") Abd tenderness > abd pain
Acute illness, afib, endocarditis 90% patients are >60 y/o
BRBPR less common overall (>24 hrs after pain starts) BRBPR onset <24 hrs into pain episode
Dx: CT angio abd Dx: colonoscopy

Chronic Mesenteric Ischemia

Background

  • ↓ blood flow to intestines, typically caused by atherosclerosis of mesenteric vessel; risk factors include smoking, diabetes, sedentary lifestyle, age
  • Also known as intestinal angina
  • High-grade mesenteric vascular stenoses in at least two major vessels (celiac, SMA, or IMA) must be established

Presentation

  • Recurrent dull, crampy, postprandial (<60min to onset) abdominal pain
  • Pts develop food aversion and often have associated weight loss

Evaluation

  • CTA abdomen/pelvis is preferred (>90% sensitivity and specificity)
  • Can also consider duplex U/S (NPV ~99%), though less helpful if large habitus or prior abd surgery

Management

  • Conservative management if asymptomatic: smoking cessation and secondary prevention to limit progression of atherosclerotic disease
  • Nutritional evaluation
  • Revascularization (open vs. endovascular) is indicated if symptoms are present
  • Mesenteric angioplasty and stenting is first-line therapy
  • Open revascularization preferred in younger pts and those w/ re-stenosis
  • Goal is to prevent future bowel infarction

Ischemic Colitis

Background

  • Sudden, transient reduction in blood flow to colon
  • Typically at "watershed" regions of colon, such as the splenic flexure and rectosigmoid junction
  • Most often nonocclusive (95% of cases) and affects older adults
  • Risk factors: ACS, hemodialysis, shock, aortoiliac instrumentation, cardiopulmonary bypass, extreme exercise (marathon running)

Presentation

  • Rapid onset, mild cramping abdominal pain, associated with urge to defecate, hematochezia
  • Hematochezia is more commonly indicative of colonic (rather than small bowel) ischemia
  • Tenderness present (typically over left side)

Evaluation

  • Lactic acid (nonspecific but elevated), LDH, CPK, CBC (leukocytosis), BMP (metabolic acidosis)
  • KUB
  • CT A/P with IV contrast (and oral contrast if patient can tolerate)
  • Consider CTA A/P if suspicion for vascular occlusion
  • Colonoscopy confirms diagnosis.
  • Edematous, friable mucosa; erythema; and interspersed pale areas; bluish hemorrhagic nodules representing submucosal bleeding
  • Segmental distribution, abrupt transition between injured and non-injured mucosa

Management

  • General: IVFs, bowel rest, antibiotics (Zosyn vs. CTX/Flagyl)

Ischemic Colitis Management

Classification Management
Mild - No risk factors* Supportive care and observation
Antibiotics can be stopped if no ulceration
Moderate - 1-3 risk factors Same as mild ischemia if no vascular occlusion
Systemic anticoagulation +/- vascular intervention if mesenteric occlusion
Severe - > 3 risk factors, peritoneal signs, pneumatosis, pneumoperitoneum, gangrene or pancolonic ischemia on colonoscopy Consult EGS for abdominal exploration and segmental resection

*Risk factors: male, SBP <90, HR >100, WBC>15k, Hgb <12, Na <136, BUN >20, LDH >350, isolated right-sided colonic involvement, abdominal pain with rectal bleeding

Irritable Bowel Syndrome

Author: Kathryn Welp

Background

  • Diagnose by the Rome IV criteria, no longer a diagnosis of exclusion
  • Recurrent abdominal pain on average at least 1 day/week in the last 3 months with an onset at least 6 months prior, associated with two or more of the following criteria
    • Pain related to defecation
    • Change in frequency of stool
    • Change in form (appearance) of stool
  • Patient has none of the following warning signs: >50yrs, evidence of GIB, nocturnal pain or BMs, unintentional weight loss, family hx of colorectal cancer or IBD, palpable abdominal mass or LAD, IDA, +FOBT
  • Classified based on predominant bowel habits
    • Diarrhea: >25% BMs with Bristol stool types 6 or 7
    • Constipation: >25% BMs with Bristol stool types 1 or 2
    • Mixed: both of above

Evaluation

  • Thorough H&P for alarm symptoms as above
  • Consider limited testing with CBC, CMP, CRP, celiac serology (TTG, anti-gliadin, etc), fecal calprotectin

Management

  • (1) Lifestyle/Dietary Modifications:
  • Increased physical activity, low FODMAP diet (I: Eliminate high FODMAP foods for 4-6 wks, II: Incorporate foods back into diet and see what's tolerable)
  • No evidence for probiotics (can potentially worsen bloating 2/2 SIBO)
  • (2) Psychosocial Treatment:
  • CBT, psychotherapy, therapeutic physician-patient relationship
  • (3) Pharmacologic Treatment:
  • Pain: colicky abdominal pain, avoid opioids
    • Peppermint oil (smooth muscle relaxant) – IBGuard, Iberogast
    • Antispasmodics: Hyosciamine acts faster than Dicyclomine
    • TCAs (slow GI transit): Amitriptyline or nortriptyline (causes less constipation so better in IBS-C)
  • Diarrhea:
    • Ondansetron (8mg TID), Loperamide (up to 16g qd), Rifaximin (550mg BID for 2 wks), Eluxadoline (75-100mg BID); consider Lomotil if refractory
  • Constipation:
    • Fiber (Ispaghula husk orange), Miralax, Linzess (first line but can be expensive), Trulance, or Amitiza
  • Other:
    • SSRIs, SNRIs for concomitant mood disorders
    • Gabapentin, Lyrica

Large Bowel Obstruction

Author: Kathryn Welp

Background

  • Mostly occurs distal to the transverse colon due to decreased colonic lumen diameter.
  • 60% due to colon cancer, often the initial presenting symptom.
  • Ddx: SBO, toxic megacolon, Ogilvie's syndrome, paralytic ileus, ischemic colitis

Etiology

  • Malignancy
  • Benign
  • Volvulus (cecal, sigmoid)
  • Strictures (associated with diverticular disease, IBD, prior colorectal resection)
  • Fecal impaction
  • Less common: adhesions, hernia

Presentation

  • Bloating, infraumbilical crampy abdominal pain, and obstipation
  • Focal tenderness or peritoneal signs is concerning for ischemia
  • N/V can occur with proximal obstructions or in incompetent ileocecal valve
  • In subacute cases: change in bowel patterns over time

Evaluation:

  • CBC w/ diff, BMP, CEA (if imaging concerning for malignancy)
  • Abdominal CT: >90% sensitivity and specificity for detecting LBO. Demonstrates dilated colon proximal to a transition point with collapsed distal colon.
  • 3-6-9 rule (describes normal bowel diameter): small bowel <3 cm, large bowel <6 cm, cecum <9 cm
  • Abdominal XR: nonspecific with poor sensitivity.

Management

  • Oral bowel prep contraindicated.
  • Initial supportive care: bowel rest, electrolyte correction, IVF, and gastric decompression.
  • Unstable: peritoneal signs, closed-loop obstructions → emergency surgery
  • Stable:
  • Endoscopic stenting (more commonly for L-sided obstructions)
  • Malignant obstructions require surgery for definitive management
  • Volvulus:
  • Cecal → surgery
  • Sigmoid → endoscopic detorsion before semi-elective surgery (unless unstable)

Small Bowel Obstruction (SBO)

Author: Alex Wiles

Background

  • Risk Factors: prior abdominal surgeries (adhesions), malignancy, hernia, intestinal inflammation (IBD)/stricture, radiation, abscess, foreign bodies
  • Indicators for bowel ischemia: fever, leukocytosis, tachycardia, peritonitis
  • Ddx: early appendicitis, large bowel obstruction, Ogilvie's, DKA, Pancreatitis, IBD, Gastric outlet obstruction

Presentation

  • Nausea, emesis, intermittent colic, bloating, constipation
  • Obstipation if completely obstructed, loss of flatulence
  • Exam: classically with "tinkling" bowel sounds, tympanic abdomen, distended abdomen

Evaluation

  • CBC, BMP, lipase, hepatic function panel, lactate (sensitive, not specific for ischemia)
  • Start with KUB to rule out perforation but typically will require CT (x-ray only ~80% sensitive)
  • CT abdomen/pelvis with IV contrast is optimal study if adequate renal function
  • No oral contrast (American College of Radiology (ACR) Appropriateness Criteria) as it will not aid diagnosis and can lead to aspiration; IV helps evaluate ischemia
  • Key word: transition point
  • Non-specific signs of bowel inflammation: bowel wall thickening, submucosal edema

Management

  • Consult EGS: if any concern for SBO, evaluate need for urgent surgery
  • Surgical indications → complete obstruction, CT with ischemia, perforation
  • Gastric decompression: place NGT (prevent aspiration)
  • NPO until obstruction relieved and NGT removed
  • Fluids: two large bore IVs (nursing communication); LR bolus + maintenance while NPO
  • If no resolution of partial obstruction at 48 hours:
  • Fluoroscopy Upper GI small bowel ft (follow through)
    • In comments, write "Gastrografin contrast" (water-soluble contrast) which osmotically reduces bowel wall edema and aids peristalsis
    • If gastrografin reaches the colon within 24 hours, it predicts clinical resolution of SBO without surgery
    • Note this can also be therapeutic for pSBO and get bowels moving

Nausea & Vomiting

Author: Taylor Riggs

Etiology: VOMMIIT mnemonic

  • Vestibular: Labyrinthitis, vestibular neuritis, Meniere's disease, cerebellar stroke
  • Obstruction: adhesions, hernia, volvulus, constipation, gastric outlet obstruction
  • Motility: gastroparesis, GERD, autonomic dysfunction
  • Medications: antibiotics, SSRI, opioids, cannabinoid hyperemesis
  • Infection: gastroenteritis, hepatitis, pyelonephritis, cholecystitis
  • Inflammation: PUD, pancreatitis
  • Toxins: uremia, ketoacidosis, hypercalcemia, chemotherapy

Evaluation

  • All patients: CBC (leukocytosis, Hgb), BMP (AG, Ca, lytes, AKI), LFTs, lipase, lactate, UA
  • If risk factors: consider TSH, AM cortisol, troponin, β hCG, UDS
  • EKG to eval for ischemia and baseline QTc
  • Imaging
  • If concern for obstruction (abd distention, decreased BMs) → KUB, consider CT A/P
  • If concern for biliary pathology (RUQ pain, abnl LFTs) → RUQ U/S
  • If vestibular/concern for CNS pathology → CTH vs MRI brain

Management: Address underlying cause and stop medications as appropriate

  • Many antiemetics prolong QTc, however in patients without underlying cardiac conduction abnormality, electrolyte abnormality, or organ failure the risk of QTc prolongation leading to significant arrhythmia is low.
  • Obtain screening EKG in patients with underlying heart disease, electrolyte abnormalities, organ failure or on other QTc prolonging meds (antiarrhythmics, antipsychotics, antibiotics)
  • 4-8 mg of IV Zofran is estimated to prolong QTc by ~6ms
  • Try to pick a medication that will address the underlying etiology of nausea
  • If patient does not respond to a medication in a certain class, try a medication from a different class (see below)

Anti-Emetics

Med (by class) Typical Dose Side Effects Prolongs QT?
Serotonin antagonists
Ondansetron (Zofran) 4-8mg PO/IV q6h Constipation, headache, arrhythmia, serotonin syndrome Yes
Granisetron (Kytril) 1 mg PO BID, 2mg pre-chemo, OR 10mcg/kg IV pre-chemo '' Yes
Dopamine Antagonists
Prochlorperazine (Compazine) 5-10 mg PO/IV q6h, 25 mg PR q6h EPS, less sedation than H-blockers (e.g. Phenergan) Yes
Haloperidol (Haldol) 0.5-1 mg PO/IV q6h EPS, arrhythmia Yes
Zyprexa (Olanzapine) 5 -10mg PO qdaily EPS, constipation, anticholinergic Mild ↑
Dopamine and Serotonin Antagonists
Metoclopramide (Reglan) 10 mg PO/IV q6h EPS/dystonia, arrhythmias, drowsiness/dizziness, diarrhea Yes
GABA-A Agonist
Lorazepam (Ativan) 0.5-1mg PO/IV q6h PRN Sedation, delirium, amnesia, respiratory depression No
H1 Antagonists
Promethazine (Phenergan) 12.5 - 25mg PO /PR /IV q6h (avoid IV use if possible) Sedation, EPS (D2 antagonist also), arrhythmias, blurry vision Yes
Diphenhydramine (Benadryl) 25-50mg PO/IV q6h Sedation, delirium, urinary retention, ileus Yes
Meclizine (Antivert) 12.5-25mg PO q6h Sedation, dizziness, falls, blurry vision Yes
Anticholinergics
Scopolamine 1 mg patch q3day Dry mouth, blurry vision, drowsiness No
Glucocorticoids
Dexamethasone 4-8mg PO/IV prior to chemo or XRT, typically use with other agents Hyperglycemia, fluid retention, delirium No
NK1 Antagonists
Aprepitant Given prior to/with chemo Fatigue, neutropenia No
CBD Agonists
Dronabinol 2.5-5mg BID Dizziness, increased appetite, Tachycardia, hypotension No

Ostomy Complications

Author: AJ De Witte

Definition

  • Nomenclature: segment of the bowel used (sigmoid, colon, ileum), surgical construction (loop, end, reservoir), duration (temporary vs permanent)
  • Highest complication rates: loop ileostomies
  • Lowest complication rates: end ileostomies/colostomies

Presentation/Management

Very Early Complications (days)

  • Operative technical issues (ie, LBO) - return to OR

Early Complications (<3 months)

  • Suboptimal stoma site selection + high risk patient factors (ie, nutrition, age, tobacco use).
  • Stomal Necrosis
  • Stomal Bleeding
  • Stomal Retraction
  • Mucocutaneous Separation
  • Management: EGS/colorectal and ostomy team consult

Late Complications (>3 months)

  • Gas
  • Diet (starch and soluble fiber) vs gas ingestion (drinking straws, chewing gum, smoking)
  • Management: dietary modifications, OTC meds, flatus filters if unresponsive
  • Dehydration/high ostomy output (>1.5 L/day):
  • Common in loop ileostomy
  • Management: psyllium husk (1st line), antimotility agents +/- IVF (2nd line).
  • Additional management: octreotide, cholestyramine, tincture of opium.
  • Parastomal Hernia
  • No action needed unless incarcerated/strangulated/bowel obstruction
  • Stomal Prolapse
  • Telescoping of the intestine out from the stoma with risk of intestinal edema, incarceration
  • Uncomplicated prolapse: cool compresses +/- application of osmotic agent, followed by manual reduction + abdominal binder.
  • Complicated prolapse: ischemia +/- bleeding, urgent EGS consult
  • Stomal Stenosis
  • Mild stenosis: diet (avoidance of insoluble fiber) +/- routine dilation.
  • Severe Stenosis: cramping, explosive output. Surgical correction.
  • Mechanical Trauma
  • Routine peristomal hair trimming and plasticizing skin sealants with pouch removal
  • Dermatitis
  • Severely denuded skin, most common with ileostomy.
  • Management: barrier powder + removal of allergen, nystatin/miconazole powder (if fungal), topical steroids (refractory cases)
  • Granulomas
  • Red, moist, elevated lesions (+/- bleeding) at the mucocutaneous border usually from retained extraneous material.
  • Management: removal of extraneous material + Silver nitrate.
  • Peristomal Pyoderma Gangrenosum (PPG)
  • Neutrophilic dermatosis, pathergy (avoid biopsy), seen in IBD
  • Management: mild (topical steroids vs tacrolimus, wound care); severe (systemic steroids +/- anti TNF, surgery)