Gastroenterology — Severe Colitis

109. Severe Colitis

broad syndrome: infectious vs ischemic vs IBD flare · stabilize + find cause · imaging + stool studies + scope · watch for toxic megacolon · Super Compact

Sx: frequent bloody/mucoid diarrhea + crampy abdominal pain + urgency/tenesmus · fever · dehydration/tachycardia · exam: abdominal tenderness, distension (distension + systemic toxicity → toxic megacolon — emergency)

Neg: denies pain out of proportion + AF/vascular hx (acute mesenteric ischemia) · denies recent abx/hospitalization + watery diarrhea (C. diff — still test) · denies chronicity + extraintestinal sx (IBD vs acute infection) · denies marked distension + systemic toxicity (toxic megacolon)

SHx: recent antibiotics/hospitalization (C. diff) · travel/sick contacts/food exposure (infectious) · vascular disease/hypotension/cocaine (ischemic) · IBD history/NSAIDs/smoking

Etiology: infectious (C. difficile, Shigella, Salmonella, Campylobacter, EHEC/STEC, CMV in immunosuppressed, E. histolytica) · ischemic (watershed — splenic flexure/rectosigmoid; low-flow, vascular, cocaine) · IBD flare (UC or Crohn colitis)

RF: recent antibiotics (C. diff) · age/atherosclerosis/hypotension (ischemic) · known IBD · immunosuppression (CMV) · NSAID use

Data: CBC (leukocytosis; anemia from bleeding; low albumin in IBD) · CMP (K, dehydration, AKI; bicarbonate) · lactate (↑ → ischemia/severe; serial) · CRP/ESR (severity, IBD activity) · C. difficile NAAT/toxin · stool culture + ova/parasites + E. histolytica Ag · stool PCR panel · CMV testing if immunosuppressed · blood cultures · CT abdomen/pelvis w/ contrast (colonic wall thickening, distribution, megacolon, pneumatosis/portal gas=ischemia, abscess/perforation) · flexible sigmoidoscopy (unprepped, cautious — diagnostic for IBD/CMV/ischemia; avoid full colonoscopy in severe/toxic — perforation risk) · AXR (colonic dilation, thumbprinting in ischemia)

DDx: acute mesenteric ischemia (small bowel, pain out of proportion, AF) · C. diff colitis (abx hx, +toxin/NAAT) · IBD flare (chronicity, endoscopic/histologic features) · ischemic colitis (watershed, post-hypotension, usually self-limited)

Home Meds: hold antimotility agents — loperamide (Imodium)/opioids (precipitate toxic megacolon, prolong infection) · hold NSAIDs · hold/adjust immunosuppressants pending dx (may need escalation in IBD, caution if infection) · hold antihypertensives if hypotensive

Plan

CONSULT: GI (scope, IBD management) · Surgery (early if toxic megacolon, perforation, ischemia, or no improvement) · ID (complex/immunosuppressed infectious colitis) · Vascular/IR (mesenteric ischemia)

– Stabilize: IV crystalloid resuscitation, correct electrolytes (K, Mg), NPO or bowel rest if severe, strict I&Os; avoid antimotility agents
– VTE prophylaxis: enoxaparin (Lovenox) 40 mg SC daily — IBD flare is prothrombotic, prophylaxis indicated even with rectal bleeding
– Workup-driven therapy — treat the cause:
  • C. difficile: oral vancomycin 125 mg PO q6h (fulminant: 500 mg PO/NG q6h + IV metronidazole (Flagyl) 500 mg q8h ± vancomycin enema)
  • Other infectious: targeted antibiotics by organism; avoid empiric antibiotics in suspected EHEC/STEC (↑HUS risk); supportive care for most viral/self-limited
  • Ischemic colitis: supportive — IV fluids, bowel rest, optimize perfusion, stop vasoconstrictors; antibiotics (ceftriaxone + metronidazole) if moderate-severe; surgery for gangrene/perforation/peritonitis
  • IBD flare (acute severe UC): IV methylprednisolone (Solu-Medrol) 60 mg/day or hydrocortisone 100 mg IV q6h; assess response at day 3 (stool frequency + CRP); nonresponse → rescue infliximab (Remicade) 5 mg/kg IV or cyclosporine + surgery consult
– Exclude/screen infection before escalating IBD immunosuppression (esp. C. diff and CMV)
– Marked colonic dilation (>6 cm) + systemic toxicity = toxic megacolon — stop antimotility agents, surgery consult now.
– PT/OT: mobilize as tolerated
– Trend daily: stool frequency/blood, abdominal exam + girth, WBC/CRP, lactate, electrolytes, albumin, daily AXR if megacolon risk
– Escalation triggers: colonic dilation, peritoneal signs, rising lactate, hemodynamic instability, or steroid-refractory severe UC at day 3 → urgent surgery/rescue therapy + ICU
– Discharge checklist: cause-specific treatment completed/transitioned (PO antibiotics, steroid taper + maintenance biologic for IBD); colonoscopy follow-up to confirm healing/exclude malignancy; hydration/diet plan; GI/surgery follow-up; return precautions (worsening bleeding, fever, distension, pain)

109. Severe Colitis

complete reference · infectious + ischemic + IBD flare · stool/imaging/endoscopy workup · cause-specific therapy · Full Card

Symptoms / Associated Sx

• Frequent bloody or mucoid diarrhea, crampy abdominal pain, urgency and tenesmus; nocturnal diarrhea suggests an organic/inflammatory cause

• Systemic features: fever, dehydration, tachycardia, fatigue; extraintestinal manifestations (joints, eyes, skin) point toward IBD

• Exam: abdominal tenderness and distension; significant distension with systemic toxicity raises concern for toxic megacolon

Neg

• Pt denies abdominal pain out of proportion to exam + atrial fibrillation/vascular disease — argues against acute mesenteric ischemia (a small-bowel arterial emergency distinct from colitis)

• Pt denies recent antibiotics/hospitalization + watery diarrhea — lowers but does not exclude C. difficile (always test in severe colitis)

• Pt denies marked colonic distension + systemic toxicity — argues against toxic megacolon (reassess with serial exams and films if deteriorating)

Social History (SHx)

• Recent antibiotic exposure or hospitalization (C. difficile)

• Travel, sick contacts, undercooked food, daycare exposure (infectious colitis)

• Vascular disease, recent hypotension/hypovolemia, cocaine/sympathomimetic use (ischemic colitis)

• Known inflammatory bowel disease, NSAID use, smoking status (smoking worsens Crohn, paradoxically protective in UC)

Main Etiology

• Infectious: C. difficile, Shigella, Salmonella, Campylobacter, enterohemorrhagic/Shiga-toxin E. coli (STEC), Yersinia, CMV (immunosuppressed), Entamoeba histolytica

• Ischemic: typically non-occlusive low-flow injury at watershed zones (splenic flexure, rectosigmoid); precipitated by hypotension, vascular disease, vasoconstrictors, cocaine

• IBD flare: acute severe ulcerative colitis or Crohn colitis

RF

• Modifiable: antibiotic stewardship, NSAID avoidance, blood pressure/perfusion optimization, medication adherence in IBD

• Non-modifiable: age and atherosclerosis (ischemic), established IBD, immunosuppression (CMV)

Data

• CBC with differential (leukocytosis; anemia from bleeding; low albumin reflects severity/chronic inflammation)

• CMP (potassium and magnesium, dehydration, AKI, low bicarbonate)

• Lactate (elevation suggests ischemia or severe systemic illness; trend serially)

• CRP/ESR (severity and IBD disease activity, steroid-response monitoring)

• C. difficile NAAT/toxin assay (test all severe colitis regardless of antibiotic history)

• Stool culture, multiplex GI PCR panel, ova and parasites, E. histolytica antigen (identify treatable pathogens)

• CMV studies (blood PCR and tissue staining in immunosuppressed or steroid-refractory IBD)

• Blood cultures (febrile/toxic patients)

• CT abdomen/pelvis with contrast (colonic wall thickening and distribution, megacolon, pneumatosis or portal venous gas indicating ischemia, abscess or perforation)

• Flexible sigmoidoscopy (unprepped, cautious) (distinguishes IBD, CMV inclusions, ischemic mucosa; avoid full colonoscopy in severe/fulminant disease due to perforation risk)

• Plain abdominal radiograph (colonic dilation, thumbprinting of submucosal edema in ischemia, serial monitoring for megacolon)

DDx

Acute mesenteric ischemia (small-bowel, pain out of proportion, embolic source) · C. difficile colitis (antibiotic exposure, positive toxin/NAAT) · IBD flare (chronicity, endoscopic and histologic features) · ischemic colitis (watershed distribution, post-hypotensive, often self-limited)

Home Meds

• Hold: antimotility agents — loperamide (Imodium) and opioids (can precipitate toxic megacolon and prolong infectious colitis)

• Hold: NSAIDs (worsen colitis and bleeding)

• Hold/adjust: immunosuppressants pending diagnosis — may need escalation for an IBD flare but caution if infection is present

• Hold: antihypertensives/diuretics if hypotensive or volume depleted

Plan

CONSULT: GI (endoscopy and IBD management) · Surgery (early involvement for toxic megacolon, perforation, ischemic gangrene, or failure to improve) · Infectious Disease (complex or immunocompromised infectious colitis) · Vascular surgery/IR (if mesenteric ischemia identified)

• Stabilize: IV crystalloid resuscitation, correct potassium and magnesium, bowel rest in severe disease, strict intake/output; avoid antimotility agents throughout

• VTE prophylaxis: enoxaparin (Lovenox) 40 mg SC daily — IBD is prothrombotic and prophylaxis is indicated even with rectal bleeding

• Treat the identified cause:

• • C. difficile: oral vancomycin 125 mg PO q6h (fulminant disease: vancomycin 500 mg PO/NG q6h plus IV metronidazole (Flagyl) 500 mg q8h, with vancomycin enemas if ileus)

• • Other infectious colitis: pathogen-directed antibiotics; avoid empiric antibiotics when STEC/EHEC is suspected (antibiotics increase hemolytic uremic syndrome risk); most viral and many bacterial colitides are self-limited and need only supportive care

• • Ischemic colitis: supportive care with IV fluids, bowel rest, perfusion optimization, and withdrawal of vasoconstrictors; antibiotics (ceftriaxone (Rocephin) 1 g IV q24h + metronidazole (Flagyl) 500 mg IV q8h) for moderate-to-severe disease; surgery for gangrene, perforation, or peritonitis

• • Acute severe ulcerative colitis: IV corticosteroids — methylprednisolone (Solu-Medrol) 60 mg/day or hydrocortisone 100 mg IV q6h; assess response at day 3 using stool frequency and CRP; steroid nonresponse warrants rescue therapy with infliximab (Remicade) 5 mg/kg IV or cyclosporine, with early surgical consultation

• Screen for and exclude infection (especially C. difficile and CMV) before escalating IBD immunosuppression

• PT/OT: mobilize as tolerated

• Trend daily: stool frequency and blood, abdominal exam and girth, white count and CRP, lactate, electrolytes and albumin, and daily abdominal radiograph if there is any megacolon risk

• Escalation triggers: colonic dilation, peritoneal signs, rising lactate, hemodynamic instability, or steroid-refractory severe UC at day 3 → urgent surgery or rescue therapy and ICU-level care

• Discharge checklist: cause-specific treatment completed or transitioned (oral antibiotic course, or steroid taper with a maintenance biologic for IBD); follow-up colonoscopy to confirm mucosal healing and exclude malignancy where appropriate; hydration and diet plan; GI and/or surgery follow-up; return precautions for worsening bleeding, fever, distension, or pain

Red Flags

• Toxic megacolon: colonic dilation >6 cm + systemic toxicity → stop antimotility agents, urgent surgery consult

• Peritoneal signs, free air, or pneumatosis/portal venous gas → perforation or transmural ischemia → emergent surgery

• Rising lactate with pain out of proportion → consider mesenteric ischemia

• Steroid-refractory acute severe UC at day 3 → rescue therapy or colectomy decision

• Hemodynamic instability or massive lower GI bleeding → ICU, transfusion, urgent intervention

Senior IM Resident Pearls

• Stop the Imodium. Antimotility agents in severe colitis (especially C. diff or IBD) can precipitate toxic megacolon — discontinue them on admission.

• Don't give antibiotics for suspected EHEC/STEC (bloody diarrhea, no fever, after undercooked beef) — they raise the risk of hemolytic uremic syndrome.

• Test for C. diff and CMV before escalating IBD therapy. A "refractory flare" is often a superimposed infection, and steroids/biologics will make it worse.

• Day 3 is the decision point in acute severe UC (Oxford/Travis criteria): >8 stools/day or 3–8 stools with CRP >45 predicts steroid failure — line up rescue therapy and surgery early.

• Avoid full colonoscopy in fulminant colitis — limited unprepped flex sig gets the diagnosis with far less perforation risk.

• Common mistake: attributing all bloody diarrhea to IBD without stool studies — infectious mimics are common and change management entirely.

Gastroenterology — Inflammatory Bowel Disease

110. Inflammatory Bowel Disease Flare

UC vs Crohn · acute severe UC = Truelove-Witts · IV steroids → day-3 assessment → rescue (infliximab/cyclosporine) or colectomy · exclude infection · Super Compact

Sx: UC: bloody diarrhea + urgency/tenesmus + cramping, continuous from rectum · Crohn: abdominal pain (often RLQ) + diarrhea ± blood, weight loss, fistula/perianal disease · fever, fatigue, extraintestinal (arthritis, uveitis, erythema nodosum, pyoderma)

Neg: denies recent abx + positive C. diff toxin (C. diff superinfection — test always) · denies immunosuppression + CMV inclusions (CMV colitis) · denies pain out of proportion + lactate (ischemia) · denies marked distension/toxicity (toxic megacolon)

SHx: tobacco (worsens Crohn; UC often ex-smokers) · NSAID use (triggers flares) · medication adherence/recent taper · family history IBD

Etiology: chronic immune-mediated intestinal inflammation; UC — continuous colonic/rectal mucosal inflammation · Crohn — transmural, skip lesions, any GI site (terminal ileum classic), strictures/fistulae; flare triggers: nonadherence, NSAIDs, infection (C. diff/CMV), smoking (Crohn), stress

RF: medication nonadherence · NSAID use · intercurrent infection · smoking (Crohn) · recent steroid taper

Data: CBC (anemia, leukocytosis, thrombocytosis) · CMP/albumin (low albumin = severity; electrolytes; K) · CRP/ESR (activity, steroid-response) · fecal calprotectin (mucosal inflammation marker) · C. difficile toxin/NAAT + stool studies (always exclude infection) · CMV (if refractory/immunosuppressed) · Truelove-Witts criteria (acute severe UC: ≥6 bloody stools/day + ≥1 of: temp >37.8, HR >90, Hgb <10.5, ESR >30) · AXR/CT (megacolon, complications, Crohn abscess/fistula/stricture) · flexible sigmoidoscopy (confirm + biopsy CMV; avoid full colonoscopy in severe) · iron studies/B12/vit D

DDx: infectious colitis incl C. diff (stool studies) · CMV colitis (refractory, immunosuppressed, inclusions) · ischemic colitis (watershed, vascular) · IBS/functional (no inflammation, normal calprotectin/CRP)

Home Meds: continue/optimize mesalamine (Asacol/Lialda) for UC maintenance · hold NSAIDs · continue biologics — infliximab (Remicade)/adalimumab (Humira)/vedolizumab (Entyvio)/ustekinumab (Stelara) (check levels; may dose-escalate) · hold antimotility agents in severe disease

Plan

CONSULT: GI (urgent — disease assessment, scope, biologic decisions) · Colorectal surgery (early in acute severe UC, complications) · ID (if CMV/complex infection) · Nutrition

– Stabilize: IV fluids, correct electrolytes (K, Mg), transfuse if needed; VTE prophylaxis — enoxaparin (Lovenox) 40 mg SC daily (give despite bleeding — IBD is highly prothrombotic); avoid antimotility agents/opioids/NSAIDs
– Exclude infection FIRST: C. diff and CMV before/with escalating immunosuppression
– Acute severe UC (Truelove-Witts): IV corticosteroids — methylprednisolone (Solu-Medrol) 60 mg IV daily or hydrocortisone 100 mg IV q6h ×3 days
– Day-3 assessment (Oxford/Travis): >8 stools/day, OR 3–8 stools/day + CRP >45 → predicts steroid failure → rescue therapy
– Rescue: infliximab (Remicade) 5 mg/kg IV (may need accelerated/higher dosing in severe) OR cyclosporine 2 mg/kg/day IV infusion; colectomy if no response to rescue within 4–7 days or any deterioration
– Crohn flare: corticosteroids (prednisone 40 mg or IV equivalent; budesonide (Entocort) 9 mg for ileocecal); escalate/optimize biologic (anti-TNF, vedolizumab, ustekinumab, risankizumab); drain abscess (IR) + antibiotics before immunosuppression; manage stricture/fistula surgically as needed
– Steroid-sparing maintenance: initiate/optimize biologic ± immunomodulator (azathioprine/methotrexate); steroid taper once improving — do not use steroids as maintenance
– Don't escalate immunosuppression into an undiagnosed infection — a C. diff– or CMV-driven "refractory flare" gets dramatically worse on steroids/biologics.
– PT/OT: mobilize; nutrition optimization (correct iron/B12/vit D, consider EEN in Crohn)
– Trend daily: stool frequency/blood, abdominal exam/girth, CRP, Hgb, albumin, electrolytes, daily AXR if megacolon risk
– Escalation triggers: day-3 steroid failure → rescue/surgery; toxic megacolon, perforation, uncontrolled hemorrhage → emergent colectomy; rescue failure by day 4–7 → colectomy
– Discharge checklist: steroid taper schedule + maintenance biologic/immunomodulator plan; confirm infection cleared; bone protection (calcium/vit D) if steroid course; vaccinate (avoid live vaccines on biologics); GI follow-up + scope to confirm healing; colorectal surgery follow-up if relevant; return precautions (worsening bleeding, fever, distension, severe pain)

110. Inflammatory Bowel Disease Flare

complete reference · ulcerative colitis + Crohn disease · Truelove-Witts + day-3 rescue algorithm · biologics + surgery · Full Card

Symptoms / Associated Sx

• Ulcerative colitis: bloody diarrhea, urgency, tenesmus, lower abdominal cramping; disease is continuous and begins at the rectum

• Crohn disease: abdominal pain (often right lower quadrant), diarrhea with or without blood, weight loss, perianal disease and fistulae; transmural and segmental ("skip lesions")

• Systemic and extraintestinal: fever, fatigue, peripheral and axial arthritis, episcleritis/uveitis, erythema nodosum, pyoderma gangrenosum, primary sclerosing cholangitis (UC)

Neg

• Pt denies recent antibiotics + positive C. difficile toxin/NAAT — a C. difficile superinfection must always be excluded before treating a "flare" with immunosuppression

• Pt denies immunosuppression + CMV inclusions on biopsy — CMV colitis must be excluded in steroid-refractory or immunosuppressed patients

• Pt denies pain out of proportion + elevated lactate — argues against ischemia; denies marked colonic distension + systemic toxicity — argues against toxic megacolon

Social History (SHx)

• Tobacco: worsens Crohn disease; ulcerative colitis patients are frequently ex-smokers (smoking is paradoxically associated with lower UC risk)

• NSAID use (well-recognized flare trigger)

• Medication adherence, recent corticosteroid taper or biologic interruption

• Family history of IBD

Main Etiology

• Chronic immune-mediated intestinal inflammation in genetically susceptible individuals with environmental triggers

• UC: continuous mucosal inflammation limited to the colon, extending proximally from the rectum

• Crohn: transmural inflammation with skip lesions anywhere from mouth to anus (terminal ileum classic), prone to strictures, fistulae, and abscesses

• Flare precipitants: medication nonadherence, NSAIDs, intercurrent infection (C. difficile, CMV), smoking (Crohn), psychological stress

RF

• Modifiable: medication adherence, NSAID avoidance, smoking cessation (Crohn), prompt infection treatment

• Non-modifiable: established IBD phenotype/extent, genetic predisposition, prior severe flares

Data

• CBC (anemia from blood loss/chronic disease, leukocytosis, reactive thrombocytosis)

• CMP and albumin (low albumin indicates severity and protein loss; electrolytes including potassium)

• CRP/ESR (disease activity and steroid-response monitoring)

• Fecal calprotectin (sensitive marker of mucosal inflammation; distinguishes flare from functional symptoms)

• C. difficile toxin/NAAT and stool studies (always exclude infectious triggers)

• CMV testing — blood PCR and tissue immunostaining (steroid-refractory or immunosuppressed)

• Truelove-Witts criteria for acute severe UC (≥6 bloody stools/day plus at least one of: temperature >37.8°C, heart rate >90, hemoglobin <10.5 g/dL, ESR >30)

• Abdominal radiograph / CT (toxic megacolon, perforation; in Crohn — abscess, fistula, stricture, and disease extent)

• Flexible sigmoidoscopy with biopsy (confirm diagnosis, assess severity, obtain CMV histology; avoid full colonoscopy in severe disease due to perforation risk)

• Iron studies, vitamin B12, vitamin D (nutritional deficiencies common, especially in Crohn)

DDx

Infectious colitis including C. difficile (stool studies positive) · CMV colitis (refractory disease, immunosuppression, viral inclusions) · ischemic colitis (watershed distribution, vascular risk) · irritable bowel syndrome/functional disease (normal calprotectin and CRP, no mucosal inflammation)

Home Meds

• Continue/optimize: mesalamine (Asacol/Lialda) for UC maintenance and mild flares

• Continue/escalate: biologics — infliximab (Remicade), adalimumab (Humira), vedolizumab (Entyvio), ustekinumab (Stelara), risankizumab (Skyrizi); check drug levels and consider dose escalation

• Hold: NSAIDs (flare trigger) and antimotility agents in severe disease

• Adjust: immunomodulators (azathioprine, methotrexate) — continue maintenance but recognize they are not flare rescue agents

Plan

CONSULT: GI (urgent — disease assessment, endoscopy, biologic/rescue decisions) · Colorectal surgery (early in acute severe UC and for Crohn complications) · Infectious Disease (CMV or complex infection) · Nutrition (deficiency correction, enteral support)

• Stabilize: IV fluids, correct potassium and magnesium, transfuse for symptomatic anemia; VTE prophylaxis with enoxaparin (Lovenox) 40 mg SC daily given despite rectal bleeding (IBD is strongly prothrombotic); avoid antimotility agents, opioids, and NSAIDs

• Exclude infection first: C. difficile and CMV must be assessed before or alongside escalating immunosuppression

• Acute severe UC (Truelove-Witts): IV corticosteroids — methylprednisolone (Solu-Medrol) 60 mg IV daily or hydrocortisone 100 mg IV q6h for 3 days

• Day-3 assessment (Oxford/Travis criteria): >8 stools/day, or 3–8 stools/day with CRP >45 mg/L, predicts corticosteroid failure and triggers rescue therapy

• Rescue therapy: infliximab (Remicade) 5 mg/kg IV (accelerated or intensified dosing may be needed in severe disease with high inflammatory burden/low albumin) or cyclosporine 2 mg/kg/day IV infusion; proceed to colectomy if there is no response to rescue within 4–7 days or any clinical deterioration

• Crohn flare: corticosteroids (prednisone 40 mg PO daily or IV equivalent; budesonide (Entocort) 9 mg daily for ileocecal disease); escalate or optimize biologic therapy (anti-TNF, vedolizumab, ustekinumab, risankizumab); drain any abscess (IR) and treat with antibiotics before immunosuppression; surgical management of strictures and fistulae as indicated

• Steroid-sparing maintenance: initiate or optimize a biologic with or without an immunomodulator (azathioprine or methotrexate); taper steroids once improving — corticosteroids are never appropriate as maintenance therapy

• PT/OT: early mobilization; nutritional optimization including iron, B12, and vitamin D repletion, with consideration of exclusive enteral nutrition in Crohn

• Trend daily: stool frequency and blood, abdominal exam and girth, CRP, hemoglobin, albumin, electrolytes, and a daily abdominal radiograph if megacolon risk exists

• Escalation triggers: day-3 steroid failure → rescue therapy or surgery; toxic megacolon, perforation, or uncontrolled hemorrhage → emergent colectomy; failure of rescue therapy by day 4–7 → colectomy

• Discharge checklist: corticosteroid taper schedule with a defined maintenance biologic/immunomodulator plan; confirmation that infection has been excluded/treated; bone protection (calcium and vitamin D) for steroid courses; vaccination review (avoid live vaccines while on biologics); GI follow-up with endoscopy to confirm mucosal healing; colorectal surgery follow-up if relevant; return precautions for worsening bleeding, fever, distension, or severe pain

Red Flags

• Acute severe UC meeting Truelove-Witts → admit, IV steroids, surgical consult on board from day 1

• Toxic megacolon (colonic dilation >6 cm + toxicity) → emergent surgery

• Perforation, uncontrolled hemorrhage, or peritonitis → emergent colectomy

• Steroid-refractory disease at day 3 → rescue therapy or colectomy; do not simply continue steroids

• Superimposed C. difficile or CMV → infection driving the flare; escalating immunosuppression alone worsens outcomes

Senior IM Resident Pearls

• Surgery is on the team from day 1 in acute severe UC — early colorectal involvement improves outcomes; colectomy is a treatment, not a failure.

• Day 3 decides. The Oxford criteria (>8 stools/day or 3–8 with CRP >45) identify steroid failures who need rescue — don't drift past day 3 hoping steroids will work.

• Always exclude C. diff and CMV before blaming the IBD — they masquerade as refractory flares and worsen with immunosuppression.

• Give VTE prophylaxis despite the bleeding. Hospitalized IBD patients have a high thrombosis risk; the rectal bleeding is not a contraindication.

• Low albumin lowers infliximab levels — severe, hypoalbuminemic patients clear the drug faster and may need accelerated/intensified dosing.

• Common mistake: using steroids as maintenance — they don't maintain remission, cause harm, and signal the need for a steroid-sparing biologic.

• Budesonide for ileocecal Crohn gives high first-pass metabolism and fewer systemic steroid effects, but it is for mild-to-moderate disease, not severe flares.

Gastroenterology / Surgery — Colonic Diverticulitis

111. Diverticulitis

LLQ pain + fever · CT to stage uncomplicated vs complicated · selective antibiotics · drain abscess / surgery for perforation · Super Compact

Sx: left lower quadrant pain (sigmoid) + low-grade fever · change in bowel habit (constipation/diarrhea) · nausea · localized LLQ tenderness ± mass (diffuse peritonitis/rigidity → perforation)

Neg: denies diffuse peritonitis + free air (perforation — complicated) · denies pain out of proportion + lactate (ischemia) · denies weight loss + anemia + obstruction (colon CA — confirm with interval colonoscopy) · denies dysuria/pneumaturia (colovesical fistula)

SHx: low-fiber diet · obesity/sedentary · NSAID use · prior diverticulitis · smoking

Etiology: micro-perforation of a colonic diverticulum → localized inflammation/infection; uncomplicated (~75% — inflammation only) vs complicated (~25% — abscess, perforation, obstruction, fistula); sigmoid most common in Western patients

RF: low-fiber diet · obesity · NSAID/opioid use · age · prior episodes · smoking

Data: CBC (leukocytosis/left shift) · CMP (dehydration, renal fxn) · CRP (severity; >150 → complicated more likely) · lactate (sepsis/ischemia) · blood cultures (if toxic) · UA (sterile pyuria/fistula clue) · CT abdomen/pelvis w/ IV (± oral) contrast (diagnostic + staging — wall thickening, fat stranding, abscess, free air, fistula; Hinchey classification) · defer colonoscopy acutely (perforation risk) → interval colonoscopy 6–8 wks after first complicated/uncertain episode to exclude malignancy

DDx: colorectal cancer (can mimic/coexist — interval scope) · acute colitis (infectious/IBD/ischemic) (diarrhea, distribution) · perforation/other acute abdomen (free air, peritonitis) · gynecologic (ovarian/PID/ectopic) (in women — pelvic exam, β-hCG, US)

Home Meds: hold NSAIDs (associated with perforation) and opioids where possible · hold oral meds if NPO · continue essentials · hold immunosuppressants caution (worse outcomes — lower threshold to treat/admit)

Plan

CONSULT: Surgery (complicated disease, perforation, failure of medical therapy, recurrent) · IR (percutaneous drainage of abscess ≥3–4 cm) · GI (interval colonoscopy)

– Stage by CT (Hinchey): I — pericolic abscess/phlegmon · II — pelvic/distant abscess · III — purulent peritonitis · IV — feculent peritonitis
– Uncomplicated diverticulitis: bowel rest/clear liquids advancing as tolerated, analgesia, IV fluids; antibiotics are now selective — immunocompetent, mild, no systemic signs may be managed without antibiotics (AGA); when treated/inpatient: ceftriaxone (Rocephin) 1–2 g IV q24h + metronidazole (Flagyl) 500 mg IV q8h, or piperacillin-tazobactam (Zosyn) 3.375 g IV q6h; step down to PO — amoxicillin-clavulanate (Augmentin) 875 mg PO BID, or ciprofloxacin (Cipro) 500 mg PO BID + metronidazole 500 mg PO q8h ×4–7 days
– Complicated — abscess: antibiotics + percutaneous drainage (IR) if ≥3–4 cm; smaller → antibiotics alone; failure/large → surgery
– Complicated — perforation (Hinchey III/IV) / peritonitis: resuscitation, broad-spectrum antibiotics, emergent surgery (Hartmann procedure or primary anastomosis ± diversion)
– Obstruction/fistula: manage obstruction; elective resection for symptomatic fistula (e.g. colovesical)
– Elective resection: consider after complicated episode, recurrent disease, or immunosuppression — individualized, not by episode count alone
– Always arrange interval colonoscopy 6–8 weeks after a complicated or first uncertain episode — diverticulitis can mask an underlying colon cancer.
– PT/OT: mobilize; high-fiber diet education for prevention once recovered
– Trend daily: abdominal exam, fever curve, WBC/CRP, diet tolerance, drain output if placed
– Escalation triggers: worsening pain/peritonism, rising WBC/lactate, free air, or failure to improve on antibiotics by 48–72h → CT + surgery; sepsis → ICU
– Discharge checklist: complete oral antibiotic course (if prescribed); tolerating diet; interval colonoscopy scheduled (complicated/first uncertain episode); high-fiber diet + lifestyle counseling; surgery follow-up if complicated; return precautions (worsening pain, fever, inability to eat, abdominal distension)

111. Diverticulitis

complete reference · uncomplicated vs complicated (Hinchey) · selective antibiotics · drainage/surgery · interval colonoscopy · Full Card

Symptoms / Associated Sx

• Left lower quadrant pain (sigmoid colon most commonly involved), often constant and progressive, with low-grade fever

• Altered bowel habits (constipation or diarrhea), nausea, occasionally vomiting; anorexia

• Exam: localized LLQ tenderness, possible palpable mass; diffuse peritonitis or rigidity suggests free perforation

Neg

• Pt denies diffuse peritonitis + free air on imaging — argues against perforated (complicated) diverticulitis requiring emergent surgery

• Pt denies weight loss + iron-deficiency anemia + obstructive symptoms — lowers concern for colorectal cancer, but interval colonoscopy is still required to exclude it after a complicated/first episode

• Pt denies pneumaturia/fecaluria/recurrent UTIs — argues against a colovesical fistula (a complication of recurrent disease)

Social History (SHx)

• Low-fiber, high-red-meat Western diet

• Obesity and sedentary lifestyle

• NSAID and opioid use (associated with perforation/complications)

• Prior episodes of diverticulitis; smoking

Main Etiology

• Micro-perforation of a colonic diverticulum leads to localized inflammation and infection of pericolic tissue

• Uncomplicated (~75%): inflammation/phlegmon without abscess or perforation

• Complicated (~25%): abscess, free or contained perforation, obstruction, or fistula

• Sigmoid colon predominates in Western populations; right-sided disease is more common in Asian populations

RF

• Modifiable: low dietary fiber, obesity, physical inactivity, NSAID/opioid use, smoking

• Non-modifiable: increasing age, prior diverticulitis, underlying diverticulosis extent

Data

• CBC with differential (leukocytosis with left shift)

• CMP (dehydration, renal function for contrast and dosing)

• CRP (severity marker; high values, particularly >150 mg/L, increase the likelihood of complicated disease)

• Lactate (sepsis or ischemia)

• Blood cultures (toxic-appearing/septic patients)

• Urinalysis (sterile pyuria can hint at a colovesical fistula or bladder irritation)

• CT abdomen/pelvis with IV (and often oral) contrast (diagnostic and staging — bowel wall thickening, pericolic fat stranding, abscess, free air, fistula; basis for Hinchey classification)

• Pregnancy test in women of childbearing age (exclude ectopic and guide imaging)

• Interval colonoscopy 6–8 weeks after resolution (exclude colorectal malignancy after a complicated or first/uncertain episode; defer in the acute phase due to perforation risk)

DDx

Colorectal cancer (can mimic or coexist — mandates interval colonoscopy) · acute colitis (infectious, IBD, or ischemic) (diarrhea, distribution on imaging) · perforated viscus / other acute abdomen (free air, generalized peritonitis) · gynecologic pathology (ovarian torsion/cyst, PID, ectopic — pelvic exam, β-hCG, ultrasound)

Home Meds

• Hold: NSAIDs (associated with perforation) and opioids where feasible (worsen ileus/constipation)

• Hold: oral medications if NPO; convert essentials to IV

• Caution: immunosuppressants are associated with worse outcomes — lower the threshold to treat with antibiotics and admit

Plan

CONSULT: Surgery (complicated disease, perforation, medical failure, recurrent disease, fistula) · Interventional Radiology (percutaneous drainage of abscesses ≥3–4 cm) · GI (interval colonoscopy)

• Stage by CT (Hinchey classification): I — confined pericolic abscess/phlegmon; II — pelvic, distant, or retroperitoneal abscess; III — generalized purulent peritonitis; IV — generalized feculent peritonitis

• Uncomplicated diverticulitis: bowel rest with clear liquids advancing as tolerated, analgesia, IV fluids; antibiotics are now used selectively — immunocompetent patients with mild disease and no systemic signs may be managed without antibiotics per AGA guidance; when antibiotics are indicated or the patient is admitted: ceftriaxone (Rocephin) 1–2 g IV q24h plus metronidazole (Flagyl) 500 mg IV q8h, or piperacillin-tazobactam (Zosyn) 3.375 g IV q6h; step down to oral amoxicillin-clavulanate (Augmentin) 875 mg PO BID, or ciprofloxacin (Cipro) 500 mg PO BID plus metronidazole 500 mg PO q8h, for a total of 4–7 days

• Complicated — abscess: antibiotics plus percutaneous (IR) drainage for collections ≥3–4 cm; smaller abscesses often resolve with antibiotics alone; failure of drainage or large/multiloculated collections warrant surgery

• Complicated — perforation (Hinchey III/IV) or generalized peritonitis: resuscitation, broad-spectrum antibiotics, and emergent surgery (Hartmann procedure, or primary anastomosis with or without diverting ostomy in selected patients)

• Obstruction or fistula: manage obstruction supportively; symptomatic fistulae (e.g. colovesical) typically require elective resection

• Elective sigmoid resection: considered after a complicated episode, for recurrent or smoldering disease, or in immunosuppressed patients — decision is individualized rather than based on episode count alone

• PT/OT: mobilization; dietary fiber education for secondary prevention once recovered

• Trend daily: abdominal exam, fever curve, white count and CRP, diet tolerance, and drain output if a percutaneous drain is placed

• Escalation triggers: worsening pain or peritoneal signs, rising WBC/lactate, free air, or failure to improve on antibiotics within 48–72h → repeat CT and surgical evaluation; sepsis → ICU

• Discharge checklist: complete the oral antibiotic course if prescribed; tolerating diet; interval colonoscopy scheduled for complicated or first/uncertain episodes; high-fiber diet and lifestyle counseling; surgical follow-up for complicated disease; return precautions for worsening pain, fever, inability to tolerate oral intake, or abdominal distension

Red Flags

• Generalized peritonitis or free air (Hinchey III/IV) → emergent surgery

• Large or enlarging abscess, or failure of percutaneous drainage → surgery

• Sepsis/hemodynamic instability → ICU, resuscitation, source control

• Immunosuppressed patient → atypical/blunted presentation, higher complication risk, lower threshold to admit and operate

• New colonic obstruction or fistula → surgical evaluation; exclude underlying malignancy

Senior IM Resident Pearls

• Antibiotics are now selective, not automatic. Mild uncomplicated diverticulitis in an immunocompetent patient can often be managed without antibiotics (AGA) — reserve them for systemic signs, complicated disease, or comorbidity.

• Always close the loop with interval colonoscopy 6–8 weeks after a complicated or first uncertain episode — a "diverticulitis" that doesn't fully resolve can be a perforated colon cancer.

• CT both diagnoses and stages. The Hinchey class drives the decision between antibiotics, drainage, and surgery.

• Abscess size guides the approach: roughly ≥3–4 cm gets percutaneous drainage; smaller often resolves on antibiotics.

• Surgery is individualized. The old "operate after two episodes" rule is gone — decisions weigh complications, immune status, and quality of life.

• Common mistake: reflexively keeping patients NPO and on broad IV antibiotics for mild disease — many do well with early oral intake and selective, narrower therapy.

Hepatology — Acute Liver Failure

112. Acute Liver Failure (ALF)

coagulopathy (INR ≥1.5) + ANY encephalopathy + no prior cirrhosis · NAC for all · ICU + early transplant center contact · cerebral edema is the killer · Super Compact

Sx: jaundice + altered mental status/encephalopathy + coagulopathy · nausea/malaise/RUQ pain · in acetaminophen: nausea/vomiting early then hepatic phase; asterixis, signs of cerebral edema (advanced HE) (rapid onset over days–weeks in someone without known liver disease)

Neg: denies known cirrhosis/chronic liver disease (defines ALF vs acute-on-chronic) · denies isolated cholestatic obstruction (biliary) · denies primary sepsis/hypotension as sole cause (ischemic/shock liver — different course) · denies alcohol pattern AST:ALT >2 modest (alcoholic hepatitis)

SHx: acetaminophen — intentional OD or staggered/therapeutic misadventure (quantify total + timing) · alcohol/other hepatotoxins · herbal/supplement use · viral risk factors · recent new drugs (DILI)

Etiology: acetaminophen (#1 in US — dose-dependent, treatable) · viral (hep A, B, E; HSV; in endemic/pregnant) · DILI (idiosyncratic — antibiotics, anti-TB, herbals, antiepileptics) · autoimmune · ischemic/shock liver · Wilson disease · Budd-Chiari · acute fatty liver of pregnancy/HELLP · amanita mushroom · idiopathic

RF: acetaminophen exposure (chronic alcohol/malnutrition lower threshold) · viral exposure · new hepatotoxic medications · pregnancy (HEV, AFLP)

Data: INR/PT (≥1.5 defines coagulopathy; do NOT correct prophylactically — tracks severity/prognosis) · LFTs (very high AST/ALT in acetaminophen/ischemic; pattern by cause) · bilirubin · ammonia (very high >150–200 → cerebral edema/herniation risk) · acetaminophen level (plot on Rumack-Matthew nomogram; level can be undetectable in late/staggered — treat clinically) · CMP (glucose — hypoglycemia common/dangerous; Cr — AKI; phosphate) · ABG/lactate (acidosis + lactate are King's College criteria) · CBC · viral serologies (HAV IgM, HBsAg/anti-HBc IgM, HEV, HSV PCR) · ceruloplasmin/autoimmune markers · ammonia trend · ICP considerations · pregnancy test · CT head (rule out other causes of AMS; cerebral edema)

DDx: acute-on-chronic liver failure (known cirrhosis — different management/prognosis) · severe alcoholic hepatitis (alcohol, AST:ALT >2) · sepsis with hepatic dysfunction (infection-driven) · ischemic/shock liver (hypotension, massive transient transaminitis)

Home Meds: stop all hepatotoxins + the culprit drug · avoid sedatives (mask HE) where possible · hold nephrotoxins · do NOT routinely correct INR with FFP (removes prognostic marker; only for active bleeding/procedures)

Plan

CONSULT: Hepatology + TRANSPLANT CENTER (contact early — ALF can progress to need for emergent transplant) · ICU/Critical care · Toxicology/Poison control (acetaminophen) · Neurology (if cerebral edema/ICP concerns)

– Definition: coagulopathy (INR ≥1.5) + any degree of hepatic encephalopathy + illness <26 weeks + NO pre-existing cirrhosis
– ICU admission for all; frequent neuro checks (grade of HE), glucose monitoring
– N-acetylcysteine (NAC) for ALL causes: IV regimen — 150 mg/kg over 1h, then 50 mg/kg over 4h, then 100 mg/kg over 16h (continue if acetaminophen or per protocol); NAC improves transplant-free survival even in non-acetaminophen ALF with early-grade HE
– Acetaminophen-specific: activated charcoal if <1–2h post-ingestion; NAC dosed by Rumack-Matthew nomogram / clinical suspicion — when in doubt, treat
– Viral: HSV → acyclovir; HBV → tenofovir/entecavir; supportive for HAV/HEV
– Cerebral edema (leading cause of death): elevate head 30°, avoid stimulation; hypertonic saline (target Na 145–155) or mannitol for raised ICP; hyperventilation as temporizing; consider ICP monitoring at experienced centers; ammonia >150–200 = high risk
– Supportive: treat hypoglycemia (D10/D50 — check frequently), correct electrolytes/phosphate; lactulose role limited/controversial in ALF (risk of ileus/distension) — used cautiously; stress ulcer prophylaxis; low threshold for empiric antibiotics given high infection risk; vasopressors for hemodynamics
– Prognosis/transplant — King's College Criteria: acetaminophen — arterial pH <7.3, OR all of (INR >6.5 + Cr >3.4 + grade 3–4 HE); non-acetaminophen — INR >6.5, OR ≥3 of (age, etiology, jaundice-to-HE interval, bilirubin, INR) → list for emergent transplant
– Do not "fix" the INR with FFP — it is your prognostic compass and transplant criterion; correct only for active bleeding or a planned invasive procedure.
– PT/OT: limited in acute phase; per ICU protocol
– Trend: serial neuro exam/HE grade, INR, ammonia, glucose (frequent), Cr, lactate, ABG, infection surveillance
– Escalation triggers: grade 3–4 HE → intubate for airway protection; signs of raised ICP/herniation → osmotherapy + neuro; meeting King's College criteria → emergent transplant listing/transfer
– Discharge checklist (survivors): hepatology follow-up; address etiology (mental health/substance treatment if intentional overdose, avoid culprit drug, vaccinate for hepatitis); medication counseling re: acetaminophen limits; return precautions

112. Acute Liver Failure (ALF)

complete reference · acetaminophen + viral + DILI · NAC for all · King's College criteria · ICU + transplant · Full Card

Symptoms / Associated Sx

• Jaundice, altered mental status/hepatic encephalopathy, and coagulopathy developing rapidly (days to weeks) in a patient without known chronic liver disease

• Nonspecific prodrome: nausea, vomiting, malaise, anorexia, RUQ discomfort

• Acetaminophen toxicity has phases: early GI symptoms, a deceptive latent phase, then hepatic injury at 24–72h; advanced disease brings asterixis and signs of cerebral edema

Neg

• Pt denies known cirrhosis or chronic liver disease — this distinction defines acute liver failure versus acute-on-chronic liver failure (different management and prognosis)

• Pt denies an isolated cholestatic/obstructive picture with biliary dilation — argues against biliary obstruction as the cause of jaundice

• Pt denies a clear AST:ALT >2 alcoholic pattern with modest transaminase values — helps separate from severe alcoholic hepatitis

Social History (SHx)

• Acetaminophen exposure — intentional overdose or unintentional "therapeutic misadventure" (staggered supratherapeutic dosing, often with alcohol or fasting); quantify total dose and timing

• Alcohol and other hepatotoxin use; herbal and dietary supplements (a frequently overlooked cause)

• Viral exposure risks; recent new prescription medications (idiosyncratic DILI)

• Pregnancy (HEV, acute fatty liver of pregnancy, HELLP)

Main Etiology

• Acetaminophen — leading cause in the US; dose-dependent and treatable with NAC

• Viral hepatitis — hepatitis A, B, and E; HSV (especially immunocompromised/pregnant); hepatitis E carries high mortality in pregnancy

• Drug-induced liver injury (idiosyncratic) — antibiotics (amoxicillin-clavulanate, anti-tuberculous drugs), antiepileptics, herbals/supplements

• Other: autoimmune hepatitis, ischemic ("shock") liver, Wilson disease, Budd-Chiari syndrome, acute fatty liver of pregnancy/HELLP, Amanita mushroom poisoning, malignant infiltration; a significant proportion remain indeterminate

RF

• Modifiable: acetaminophen dosing (chronic alcohol use and malnutrition/fasting lower the toxic threshold), avoidance of hepatotoxic combinations

• Non-modifiable: viral exposure, pregnancy-related causes, genetic predispositions to idiosyncratic DILI

Data

• INR/PT (≥1.5 defines the coagulopathy of ALF and is a key prognostic and transplant criterion — do not correct prophylactically)

• LFTs (markedly elevated AST/ALT in acetaminophen and ischemic injury; pattern helps identify etiology)

• Bilirubin (severity and prognostic scoring)

• Ammonia (arterial levels >150–200 µmol/L correlate with cerebral edema and herniation risk)

• Acetaminophen level (plot on the Rumack-Matthew nomogram for single acute ingestions; may be low/undetectable in late or staggered ingestions, so treat on clinical suspicion)

• CMP (glucose — hypoglycemia is common and dangerous; creatinine for AKI/hepatorenal; phosphate — hypophosphatemia paradoxically suggests regeneration)

• ABG and lactate (acidosis and elevated lactate are components of the King's College criteria for acetaminophen ALF)

• CBC (anemia, thrombocytopenia, leukocytosis)

• Viral serologies (HAV IgM, HBsAg and anti-HBc IgM, HEV, HSV PCR)

• Ceruloplasmin, autoimmune markers, pregnancy test (Wilson disease, autoimmune hepatitis, pregnancy-related causes)

• CT head (exclude other causes of altered mental status and assess for cerebral edema)

DDx

Acute-on-chronic liver failure (underlying cirrhosis — different trajectory and management) · severe alcoholic hepatitis (alcohol history, AST:ALT >2) · sepsis with hepatic dysfunction (infection-driven multiorgan illness) · ischemic/shock liver (preceding hypotension, very high but rapidly improving transaminases)

Home Meds

• Stop: all hepatotoxic agents and the suspected culprit drug

• Avoid: sedatives and benzodiazepines where possible (they mask and worsen encephalopathy)

• Hold: nephrotoxins

• Do not routinely transfuse FFP to correct the INR — it removes a critical prognostic and transplant-listing marker; reserve correction for active bleeding or invasive procedures

Plan

CONSULT: Hepatology and a TRANSPLANT CENTER early (ALF can progress rapidly to needing emergent transplantation) · ICU/Critical care · Toxicology/Poison control (acetaminophen) · Neurology (cerebral edema/intracranial pressure)

• Definition: coagulopathy (INR ≥1.5) plus any degree of hepatic encephalopathy, with an illness duration <26 weeks and no pre-existing cirrhosis

• ICU care for all: frequent neurologic assessments (encephalopathy grade), continuous glucose monitoring, and meticulous supportive care

• N-acetylcysteine for all causes: IV regimen — 150 mg/kg over 1h, then 50 mg/kg over 4h, then 100 mg/kg over 16h, continued per protocol for acetaminophen; NAC improves transplant-free survival even in non-acetaminophen ALF with early-grade encephalopathy

• Acetaminophen-specific: activated charcoal if presenting within 1–2h of ingestion; dose NAC by the Rumack-Matthew nomogram or clinical suspicion — when uncertain, treat

• Viral: acyclovir for HSV; tenofovir or entecavir for HBV; supportive care for HAV/HEV

• Cerebral edema (the leading cause of death): elevate the head of bed to 30°, minimize stimulation; treat raised intracranial pressure with hypertonic saline (target sodium 145–155 mmol/L) or mannitol; brief hyperventilation as a temporizing measure; consider invasive ICP monitoring at experienced centers; an arterial ammonia >150–200 marks high risk

• Supportive care: treat hypoglycemia aggressively with dextrose (check glucose frequently); correct electrolytes and phosphate; use lactulose cautiously given the risk of ileus and bowel distension in ALF; stress-ulcer prophylaxis; a low threshold for empiric antibiotics given high infection susceptibility; vasopressors for hemodynamic support

• Prognosis and transplant listing — King's College Criteria: for acetaminophen ALF — arterial pH <7.3, or the combination of INR >6.5, creatinine >3.4 mg/dL, and grade 3–4 encephalopathy; for non-acetaminophen ALF — INR >6.5, or any 3 of 5 (unfavorable age, etiology, jaundice-to-encephalopathy interval >7 days, bilirubin, INR) → list for emergent transplantation

• PT/OT: limited in the acute phase; follow ICU mobility protocols as tolerated

• Trend: serial neurologic exams and encephalopathy grade, INR, ammonia, frequent glucose, creatinine, lactate, arterial blood gas, and infection surveillance

• Escalation triggers: grade 3–4 encephalopathy → intubate for airway protection; signs of raised ICP or impending herniation → osmotherapy and neurology/neurosurgery; meeting King's College criteria → emergent transplant listing or transfer to a transplant center

• Discharge checklist (survivors): hepatology follow-up; address the underlying cause (mental health and substance use treatment after intentional overdose, avoid the culprit drug, hepatitis vaccination); counseling on safe acetaminophen limits; return precautions for recurrent jaundice, confusion, or bleeding

Red Flags

• Progressive encephalopathy (grade 3–4) → intubate; high risk of cerebral edema and herniation

• Arterial ammonia >150–200, rapidly rising INR, or worsening acidosis → impending decompensation, escalate and contact transplant center

• Meeting King's College criteria → emergent transplantation is the only proven life-saving intervention

• Severe hypoglycemia → can be fatal and is easily missed; check glucose frequently

• Acetaminophen ingestion with rising transaminases/INR → time-critical NAC; do not wait for a "toxic" nomogram level in staggered/late presentations

Senior IM Resident Pearls

• Call the transplant center early. ALF can outpace your workup — the window to transfer and list closes fast as encephalopathy progresses.

• NAC for everyone. It's not just for acetaminophen — IV NAC improves transplant-free survival in non-acetaminophen ALF with early encephalopathy, and it's low-risk.

• Don't correct the INR reflexively. It's your prognostic marker and transplant criterion; FFP only for active bleeding or procedures. Cirrhosis-style "rebalanced hemostasis" thinking applies.

• Watch the glucose. The failing liver stops gluconeogenesis — profound hypoglycemia is common, dangerous, and quietly mimics worsening encephalopathy.

• Ammonia >150–200 flags cerebral edema risk — unlike chronic HE, in ALF the ammonia number genuinely informs intracranial risk.

• Common mistake: withholding NAC because the acetaminophen level is "undetectable" in a late or staggered ingestion — treat on the clinical picture, not just the nomogram.

Gastroenterology — Esophageal Emergency

113. Severe Dysphagia / Food Impaction

acute esophageal obstruction · can't handle secretions = emergency · urgent EGD (within 6–24h) · find underlying cause (often EoE/stricture/ring) · Super Compact

Sx: acute inability to swallow + sensation of food stuck (often meat) · drooling/inability to handle secretions (complete obstruction — emergency) · chest pain/pressure, odynophagia, retching · respiratory distress if aspiration (history of progressive solid-food dysphagia → structural cause)

Neg: denies cardiac substernal pain + exertional + ECG changes (ACS — must exclude, mimics) · denies neck crepitus/sepsis (perforation from impaction/instrumentation) · denies fluctuating dysphagia to solids+liquids w/ regurgitation (achalasia/motility) · denies globus w/o true obstruction (functional)

SHx: known EoE/atopy/allergies · GERD/stricture/prior dilation · alcohol/tobacco (malignancy) · poor dentition/rapid eating · prior food impactions

Etiology: structural: peptic stricture, Schatzki ring, eosinophilic esophagitis (esp younger men, recurrent impaction), esophageal cancer, web · motility: achalasia, scleroderma · foreign body; meat bolus most common impaction

RF: EoE/atopy · GERD/peptic stricture · esophageal malignancy risk (smoking, alcohol, Barrett's) · prior impaction/dilation · neuromuscular/motility disorder

Data: clinical diagnosis — do not delay EGD for extensive imaging if complete obstruction · CBC/BMP (pre-procedure, dehydration) · coags (pre-EGD) · CXR / CT neck-chest (if perforation suspected — pneumomediastinum, free air, or to localize; avoid barium if perforation/aspiration risk — use water-soluble or none) · ECG/troponin (exclude cardiac cause of chest pain) · EGD (diagnostic + therapeutic — disimpaction + biopsy esophagus for EoE)

DDx: ACS (cardiac chest pain — ECG/troponin) · esophageal perforation (post-impaction/retching — crepitus, sepsis, pneumomediastinum) · achalasia/motility (progressive dysphagia solids+liquids) · globus/functional (no true obstruction on exam/EGD)

Home Meds: hold oral meds (NPO) · hold/reverse anticoagulants pre-EGD if feasible · continue essentials IV · start PPI (esp for likely peptic stricture/EoE)

Plan

CONSULT: GI (URGENT EGD for disimpaction + biopsy) · Anesthesia/airway (if aspiration risk, complete obstruction) · ENT/Thoracic surgery (if perforation or proximal/foreign body) · Allergy (if EoE confirmed, longitudinally)

– Airway first: assess ability to handle secretions; if drooling/aspirating → keep upright, suction, NPO, prepare for protected EGD/intubation
– Timing of EGD: emergent (within 6h) if complete obstruction or unable to manage secretions; urgent (within 24h) for all food impactions even if able to swallow saliva — don't let it sit (mucosal pressure necrosis/perforation risk)
– Endoscopic management: push (gentle) or retrieve the bolus; do NOT blindly push if resistance/known stricture; obtain esophageal biopsies at the same setting to evaluate for EoE (proximal + distal)
– Avoid: meat tenderizer (papain — esophageal injury/perforation risk); glucagon may be tried (1 mg IV to relax LES) but low efficacy and should not delay EGD
– After disimpaction — treat the cause: peptic stricture → PPI + dilation; EoE → high-dose PPI ± topical steroids (swallowed fluticasone/budesonide) + dietary therapy + allergy referral; Schatzki ring/web → dilation; malignancy → staging + oncology; achalasia → motility workup
– Supportive: IV fluids while NPO; antiemetics; PPI — pantoprazole (Protonix) 40 mg IV
– A patient who cannot swallow their own saliva has a complete obstruction and needs emergent EGD — this is airway-adjacent, not a "morning scope."
– PT/OT: speech/swallow eval after resolution if dysphagia persists; aspiration precautions
– Trend: ability to tolerate secretions/diet, signs of perforation (fever, chest pain, crepitus, leukocytosis) post-procedure
– Escalation triggers: respiratory distress/aspiration → airway management; post-EGD chest pain + fever + subcutaneous emphysema → suspect perforation → CT + surgery; failure of endoscopic removal → surgical/ENT
– Discharge checklist: underlying cause identified + treatment started (PPI, EoE therapy, dilation plan); biopsy results follow-up; dietary modification education (chew well, avoid large meat boluses); GI follow-up + repeat EGD/dilation as planned; return precautions (recurrent impaction, chest pain, fever, inability to swallow)

113. Severe Dysphagia / Esophageal Food Impaction

complete reference · structural + motility causes · urgent EGD + biopsy · EoE recognition · Full Card

Symptoms / Associated Sx

• Acute inability to swallow with the sensation of food (often a meat bolus) lodged in the chest/throat

• Drooling and inability to handle oral secretions indicate complete obstruction — a true emergency with aspiration risk

• Chest pain or pressure, odynophagia, retching; respiratory distress if aspiration occurs

• A background of progressive solid-food dysphagia points to a structural cause (stricture, ring, malignancy)

Neg

• Pt denies exertional substernal chest pain + ECG changes + troponin rise — argues against acute coronary syndrome, which can mimic esophageal chest pain and must be excluded

• Pt denies neck crepitus, fever, and systemic toxicity — argues against esophageal perforation (a feared complication of impaction, retching, or instrumentation)

• Pt denies fluctuating dysphagia to both solids and liquids with regurgitation — argues against a primary motility disorder such as achalasia

Social History (SHx)

• Known eosinophilic esophagitis, atopy, food allergies, or asthma (EoE is a leading cause of impaction in younger men)

• GERD, peptic stricture, prior esophageal dilation

• Alcohol and tobacco use (malignancy risk), Barrett's esophagus

• Poor dentition, rapid eating, prior food impactions

Main Etiology

• Structural: peptic (reflux) stricture, Schatzki ring, eosinophilic esophagitis, esophageal carcinoma, esophageal web

• Motility: achalasia, scleroderma/systemic sclerosis esophageal dysmotility

• Foreign body or food bolus (meat most common); often the impaction unmasks a previously undiagnosed structural lesion

RF

• Modifiable: eating habits, GERD control, alcohol/tobacco

• Non-modifiable: EoE/atopy, prior stricture or dilation, esophageal malignancy, neuromuscular/motility disorders

Data

• Primarily a clinical diagnosis — do not delay endoscopy for extensive imaging when there is complete obstruction

• CBC/BMP (pre-procedure assessment, dehydration from inability to swallow)

• Coagulation studies (pre-endoscopy)

• CXR or CT neck/chest (if perforation suspected — pneumomediastinum, subcutaneous/free air; avoid barium when perforation or aspiration is a concern, using water-soluble contrast or none)

• ECG and troponin (exclude a cardiac cause of chest pain)

• EGD (both diagnostic and therapeutic — relieves the impaction and allows esophageal biopsies to evaluate for eosinophilic esophagitis)

DDx

Acute coronary syndrome (cardiac chest pain — ECG and troponin) · esophageal perforation (after impaction/retching — crepitus, sepsis, pneumomediastinum) · achalasia or other motility disorder (progressive dysphagia to solids and liquids) · globus/functional dysphagia (no true obstruction at endoscopy)

Home Meds

• Hold: oral medications (NPO)

• Hold/reverse: anticoagulants before endoscopy where feasible

• Start: a proton pump inhibitor, particularly when a peptic stricture or eosinophilic esophagitis is likely

Plan

CONSULT: GI (urgent EGD for disimpaction and biopsy) · Anesthesia/airway (aspiration risk or complete obstruction) · ENT/Thoracic surgery (perforation, proximal or sharp foreign body) · Allergy (longitudinal EoE management)

• Airway first: assess the ability to manage secretions; if drooling or aspirating, keep the patient upright with suction, NPO, and prepare for a protected endoscopy or intubation

• Timing of endoscopy: emergent (within 6h) for complete obstruction or inability to handle secretions; urgent (within 24h) for all food impactions even if saliva can be swallowed — prolonged impaction risks pressure necrosis and perforation

• Endoscopic management: gentle advancement or retrieval of the bolus; avoid blind forceful pushing against resistance or a known stricture; obtain proximal and distal esophageal biopsies in the same session to evaluate for eosinophilic esophagitis

• Pharmacologic adjuncts: avoid meat tenderizer (papain) due to esophageal injury/perforation risk; glucagon 1 mg IV may be attempted to relax the lower esophageal sphincter but has limited efficacy and should not delay endoscopy

• After disimpaction, treat the underlying cause: peptic stricture → PPI plus dilation; eosinophilic esophagitis → high-dose PPI with or without swallowed topical corticosteroids (fluticasone or budesonide), dietary therapy, and allergy referral; Schatzki ring/web → dilation; malignancy → staging and oncology; suspected achalasia → formal motility evaluation

• Supportive care: IV fluids while NPO, antiemetics, and a PPI such as pantoprazole (Protonix) 40 mg IV

• PT/OT: speech/swallow evaluation after resolution if dysphagia persists; aspiration precautions

• Trend: ability to tolerate secretions and diet, and post-procedure signs of perforation (fever, chest pain, crepitus, leukocytosis)

• Escalation triggers: respiratory distress or aspiration → airway management; post-endoscopy chest pain with fever and subcutaneous emphysema → suspect perforation, obtain CT and involve surgery; failure of endoscopic removal → surgical or ENT intervention

• Discharge checklist: identified underlying cause with treatment initiated (PPI, EoE therapy, dilation plan); follow-up on biopsy results; dietary education (thorough chewing, avoiding large unchewed meat boluses); GI follow-up with planned repeat endoscopy/dilation as needed; return precautions for recurrent impaction, chest pain, fever, or inability to swallow

Red Flags

• Inability to handle secretions/drooling → complete obstruction, emergent EGD and airway protection

• Respiratory distress or aspiration → immediate airway management

• Post-impaction or post-procedure chest pain + fever + crepitus/pneumomediastinum → esophageal perforation

• Sharp object, battery, or proximal foreign body → emergent removal (button battery is a corrosive emergency)

• Underlying malignancy on endoscopy → staging and oncology referral

Senior IM Resident Pearls

• Can't swallow spit = emergency. Inability to manage secretions means complete obstruction and aspiration risk — that's an emergent scope, not an overnight wait.

• Biopsy the esophagus at the index endoscopy. Food impaction in a younger man is EoE until proven otherwise — taking biopsies then spares a second procedure.

• Don't push blindly. Forcing a bolus past resistance or a known stricture can perforate; retrieve or advance only under direct vision.

• Skip the meat tenderizer. Papain can cause esophageal necrosis and perforation — it's an old, dangerous remedy.

• Glucagon is a weak adjunct. It occasionally relaxes the LES but shouldn't delay definitive endoscopy.

• Common mistake: treating the impaction and discharging without addressing the cause — recurrence is high unless the stricture, ring, or EoE is managed.

Gastroenterology — Refractory Nausea & Vomiting

114. Severe Nausea/Vomiting with Dehydration

gastroparesis vs cyclic vomiting vs gastric outlet obstruction · rehydrate + correct electrolytes · find the mechanism · exclude obstruction · Super Compact

Sx: persistent nausea + recurrent vomiting + inability to tolerate PO · signs of dehydration (tachycardia, orthostasis, dry mucosa, ↓UOP) · gastroparesis: early satiety, bloating, postprandial fullness · CVS: stereotyped severe episodes w/ well intervals · GOO: vomiting undigested food, succussion splash, weight loss

Neg: denies obstipation + distension + mechanical obstruction on imaging (SBO/LBO) · denies headache/neuro deficit/papilledema (central/raised ICP cause) · denies pregnancy (hyperemesis — check β-hCG) · denies DKA/uremia/hypercalcemia (metabolic causes)

SHx: diabetes (gastroparesis) · cannabis use — heavy/chronic (cannabinoid hyperemesis, mimics CVS) · alcohol · opioid use (slows motility) · prior gastric/bariatric surgery; PUD/malignancy hx (GOO)

Etiology: gastroparesis (diabetic, post-surgical, idiopathic; meds — opioids/GLP-1) · cyclic vomiting syndrome (stereotyped episodes; cannabinoid hyperemesis variant) · gastric outlet obstruction (malignancy — gastric/pancreatic; PUD with scarring); also central, metabolic, drug-induced

RF: diabetes (poor control) · chronic cannabis use · opioid/anticholinergic/GLP-1 use · prior gastric surgery · PUD/malignancy

Data: BMP (hypokalemia, hypochloremic metabolic alkalosis from vomiting; BUN/Cr — dehydration/AKI; glucose) · CBC (hemoconcentration, infection) · Mg/phosphate · lipase (pancreatitis) · LFTs · β-hCG (all women of childbearing age) · TSH · upright AXR / CT abdomen (exclude mechanical obstruction; GOO — dilated stomach; retained food) · EGD (GOO — obstructing lesion/ulcer; biopsy for malignancy) · gastric emptying scintigraphy (confirms gastroparesis — delayed emptying at 4h; do AFTER excluding obstruction, off opioids/anticholinergics) · consider cannabinoid history/urine tox

DDx: mechanical bowel obstruction (SBO/LBO/GOO) (imaging, obstipation) · central/raised ICP (neuro signs) · metabolic (DKA, uremia, hyperCa, adrenal) · cannabinoid hyperemesis (chronic cannabis, relief w/ hot showers)

Home Meds: hold opioids, anticholinergics, GLP-1 agonists (slow gastric emptying) · hold oral meds if not tolerating · convert essentials IV · review meds that cause N/V

Plan

CONSULT: GI (EGD, gastroparesis/GOO management) · Surgery (GOO — malignancy or refractory PUD) · Endocrine (diabetic gastroparesis optimization) · Nutrition (if prolonged poor intake)

– Resuscitate & correct: IV crystalloid (NS or LR) to restore volume; aggressively replete potassium and magnesium; correct hypochloremic metabolic alkalosis (volume + chloride/KCl); strict I&Os
– Symptom control: antiemetics — ondansetron (Zofran) 4–8 mg IV q8h; caution QT; add metoclopramide (Reglan) 10 mg IV q6h (prokinetic + antiemetic — limit duration, tardive dyskinesia risk) or promethazine; for CVS — supportive + triptans/abortive per protocol
– Exclude mechanical obstruction first (imaging ± EGD) before diagnosing gastroparesis
– Gastroparesis: dietary modification (small, low-fat, low-fiber meals); prokinetics — metoclopramide (Reglan) first-line, erythromycin 3 mg/kg IV q8h (motilin agonist, short-term); optimize glycemic control; stop offending meds; severe/refractory → GI for further therapy (gastric stimulator, G-POEM, jejunal feeding)
– Cyclic vomiting syndrome: abortive (triptans, antiemetics, sometimes IV fluids + sedation in a quiet dark room); prophylaxis (TCAs — amitriptyline, or topiramate); if cannabinoid hyperemesis → cannabis cessation is definitive, topical capsaicin abdominal cream as adjunct
– Gastric outlet obstruction: NG decompression, NPO, IV fluids/PPI; EGD to define cause; malignancy → staging + stent vs surgery; PUD-related → high-dose PPI, treat H. pylori, dilation or surgery
– Ask about cannabis: chronic heavy use with compulsive hot-shower relief is cannabinoid hyperemesis, not refractory gastroparesis — endless prokinetics won't fix it; cessation does.
– PT/OT: mobilize as tolerated; nutrition consult if intake poor >5–7 days (enteral access)
– Trend: volume status/UOP, electrolytes (K, Mg, bicarbonate), weight, ability to tolerate PO, glucose
– Escalation triggers: refractory vomiting with severe electrolyte derangement → ICU/closer monitoring; mechanical GOO not relieved → endoscopic/surgical intervention; inability to maintain nutrition → enteral/parenteral support
– Discharge checklist: mechanism identified + treated; antiemetic/prokinetic regimen; dietary plan; glycemic optimization (diabetic); cannabis cessation counseling if applicable; offending meds discontinued; GI/endocrine follow-up; return precautions (intractable vomiting, dehydration signs, inability to keep fluids down)

114. Severe Nausea/Vomiting with Dehydration

complete reference · gastroparesis + cyclic vomiting + gastric outlet obstruction · electrolyte correction · mechanism-directed therapy · Full Card

Symptoms / Associated Sx

• Persistent nausea with recurrent vomiting and inability to tolerate oral intake; signs of dehydration — tachycardia, orthostasis, dry mucous membranes, reduced urine output

• Gastroparesis: early satiety, bloating, postprandial fullness, epigastric discomfort

• Cyclic vomiting syndrome: stereotyped, severe, discrete episodes separated by symptom-free intervals

• Gastric outlet obstruction: vomiting of undigested food, succussion splash, weight loss, early satiety

Neg

• Pt denies obstipation + distension + a mechanical transition point on imaging — argues against small or large bowel obstruction

• Pt denies headache, focal neurologic deficits, or papilledema — argues against a central or raised-intracranial-pressure cause of vomiting

• Pt denies pregnancy + metabolic derangements (DKA, uremia, hypercalcemia) — these common systemic causes must be excluded (check β-hCG, glucose, BMP, calcium)

Social History (SHx)

• Diabetes mellitus, particularly with poor glycemic control (diabetic gastroparesis)

• Chronic heavy cannabis use (cannabinoid hyperemesis syndrome mimicking cyclic vomiting)

• Opioid, anticholinergic, or GLP-1 receptor agonist use (delayed gastric emptying)

• Prior gastric or bariatric surgery; peptic ulcer disease or malignancy history (gastric outlet obstruction)

Main Etiology

• Gastroparesis: diabetic, post-surgical (vagal injury), or idiopathic; medication-induced by opioids and GLP-1 agonists

• Cyclic vomiting syndrome: recurrent stereotyped episodes; the cannabinoid hyperemesis variant is increasingly common

• Gastric outlet obstruction: malignancy (gastric or pancreatic) or peptic ulcer disease with scarring/stenosis

• Also consider central, metabolic (DKA, uremia, hypercalcemia, adrenal insufficiency), and drug-induced causes

RF

• Modifiable: glycemic control, cannabis use, offending medications (opioids, anticholinergics, GLP-1 agonists)

• Non-modifiable: prior gastric surgery/vagal injury, underlying malignancy, established motility disorder

Data

• BMP (hypokalemia and hypochloremic metabolic alkalosis from vomiting; BUN/creatinine for dehydration/AKI; glucose)

• CBC (hemoconcentration, infection)

• Magnesium and phosphate (commonly depleted, important before refeeding)

• Lipase and LFTs (pancreatitis, hepatobiliary causes)

• β-hCG (all women of childbearing age — exclude pregnancy/hyperemesis)

• TSH and calcium (metabolic contributors)

• Upright abdominal radiograph / CT abdomen (exclude mechanical obstruction; gastric outlet obstruction shows a dilated stomach with retained food)

• EGD (identify and biopsy an obstructing gastric outlet lesion or ulcer)

• Gastric emptying scintigraphy (confirms gastroparesis with delayed emptying at 4h — performed only after mechanical obstruction is excluded and off opioids/anticholinergics)

• Cannabis history / urine toxicology (cannabinoid hyperemesis)

DDx

Mechanical bowel/gastric outlet obstruction (imaging, obstipation, retained food) · central or raised-ICP cause (neurologic signs) · metabolic causes (DKA, uremia, hypercalcemia, adrenal insufficiency) · cannabinoid hyperemesis syndrome (chronic cannabis, compulsive hot-shower relief)

Home Meds

• Hold: opioids, anticholinergics, and GLP-1 receptor agonists (delay gastric emptying and worsen symptoms)

• Hold: oral medications if not tolerating intake; convert essentials to IV

• Review: all medications for emetogenic or motility-impairing effects

Plan

CONSULT: GI (endoscopy, gastroparesis or gastric outlet obstruction management) · Surgery (gastric outlet obstruction from malignancy or refractory PUD) · Endocrinology (diabetic gastroparesis optimization) · Nutrition (prolonged inadequate intake)

• Resuscitate and correct: IV crystalloid (normal saline or lactated Ringer's) to restore intravascular volume; aggressively replete potassium and magnesium; correct the hypochloremic metabolic alkalosis with volume and chloride/potassium chloride; strict intake/output

• Symptom control: ondansetron (Zofran) 4–8 mg IV q8h (monitor QT); metoclopramide (Reglan) 10 mg IV q6h as a combined prokinetic/antiemetic (limit duration given tardive dyskinesia risk) or promethazine; for cyclic vomiting, supportive care with abortive triptans and antiemetics

• Exclude mechanical obstruction with imaging and, if needed, endoscopy before diagnosing gastroparesis

• Gastroparesis: dietary modification (small, frequent, low-fat, low-fiber meals); prokinetics — metoclopramide (Reglan) first-line, erythromycin 3 mg/kg IV q8h as a short-term motilin agonist; optimize glycemic control; discontinue offending medications; refer refractory cases to GI for gastric electrical stimulation, gastric per-oral endoscopic myotomy (G-POEM), or jejunal feeding

• Cyclic vomiting syndrome: abortive therapy (triptans, antiemetics, IV fluids, and a calm low-stimulation environment) and prophylaxis (tricyclic antidepressants such as amitriptyline, or topiramate); if cannabinoid hyperemesis, cannabis cessation is curative and topical capsaicin can serve as an adjunct

• Gastric outlet obstruction: nasogastric decompression, NPO, IV fluids, and a PPI; EGD to define the cause; malignancy managed with staging plus stenting or surgery; PUD-related obstruction managed with high-dose PPI, H. pylori treatment, and dilation or surgery

• PT/OT: mobilize as tolerated; nutrition consult with enteral access if inadequate intake persists beyond 5–7 days

• Trend: volume status and urine output, electrolytes (potassium, magnesium, bicarbonate), weight, oral tolerance, and glucose

• Escalation triggers: refractory vomiting with severe electrolyte derangement → closer monitoring/ICU; unrelieved mechanical gastric outlet obstruction → endoscopic or surgical intervention; inability to maintain nutrition → enteral or parenteral support

• Discharge checklist: identified and treated mechanism; antiemetic/prokinetic regimen; dietary plan; glycemic optimization for diabetics; cannabis cessation counseling where relevant; discontinuation of offending medications; GI/endocrinology follow-up; return precautions for intractable vomiting, signs of dehydration, or inability to keep fluids down

Red Flags

• Severe electrolyte derangement (profound hypokalemia, alkalosis) → arrhythmia risk, aggressive repletion and monitoring

• Mechanical gastric outlet obstruction with a dilated stomach → decompress and define cause; exclude malignancy

• Vomiting with neurologic signs → central cause/raised ICP → neuroimaging

• New gastric outlet obstruction with weight loss → malignancy until proven otherwise

• Refeeding risk after prolonged poor intake → monitor phosphate, magnesium, potassium

Senior IM Resident Pearls

• Always ask about cannabis. Chronic heavy use with compulsive hot-shower relief is cannabinoid hyperemesis — no amount of prokinetics fixes it, but cessation does.

• Exclude obstruction before scintigraphy. A gastric emptying study in someone with a mechanical block is meaningless — image and scope first.

• Stop the opioids and GLP-1 agonists before labeling someone a "refractory gastroparetic" — both profoundly slow emptying and are reversible causes.

• Vomiting buys you a hypochloremic, hypokalemic metabolic alkalosis — volume and chloride/potassium repletion, not just antiemetics, correct it.

• Limit metoclopramide duration — tardive dyskinesia risk rises with prolonged use; it carries a black-box warning.

• Common mistake: escalating antiemetics without identifying the mechanism — gastroparesis, CVS, and outlet obstruction need entirely different treatments.

Gastroenterology / Surgery — Colonic Obstruction

115. Partial Large Bowel Obstruction

colon cancer vs stricture vs volvulus · check competent ileocecal valve (closed-loop risk) · CT to find cause/level · decompress + treat cause · Super Compact

Sx: abdominal distension + crampy pain · constipation/obstipation (partial may still pass some gas/stool) · nausea ± feculent vomiting (late) · change in stool caliber/bleeding (cancer) · exam: distension, tympany, ± mass (sudden severe distension + peritonism → volvulus/ischemia)

Neg: denies diffuse dilation incl small bowel w/o transition (ileus/pseudo-obstruction) · denies pain out of proportion + lactate (ischemia/strangulation) · denies acute small-bowel pattern (SBO) · denies systemic toxicity + megacolon (toxic megacolon)

SHx: colorectal cancer risk (age, family hx, prior polyps, no screening) · diverticular disease (stricture) · constipation/laxative use, institutionalized/elderly (sigmoid volvulus) · prior surgery/radiation

Etiology: colorectal cancer (#1 cause of LBO — often left-sided) · stricture (diverticular, ischemic, IBD, anastomotic, radiation) · volvulus (sigmoid — elderly/constipated; cecal — younger); also fecal impaction, extrinsic compression

RF: age/colorectal cancer risk factors · diverticular disease · chronic constipation (volvulus) · IBD/prior radiation (stricture) · prior abdominal surgery

Data: CBC (anemia → occult cancer; leukocytosis → ischemia) · CMP (electrolytes, dehydration, renal fxn) · lactate (ischemia/closed-loop) · CEA (baseline if cancer) · type & screen · CT abdomen/pelvis w/ contrast (level + cause — mass vs stricture vs volvulus "whirl/coffee-bean" sign; competence of ileocecal valve → closed-loop; ischemia signs; cecal diameter — >10–12 cm = perforation risk) · upright AXR (colonic dilation; sigmoid volvulus coffee-bean; cecal volvulus) · contrast enema / flex sig (define obstruction; sigmoid volvulus detorsion) · colonoscopy (diagnostic/biopsy, stent placement — cautious if near-complete)

DDx: acute colonic pseudo-obstruction (Ogilvie) (massive dilation, no mechanical cause) · SBO (small-bowel pattern) · ileus (diffuse, post-op/metabolic) · toxic megacolon (colitis + toxicity)

Home Meds: hold oral meds (NPO) · hold opioids/anticholinergics (worsen colonic motility) · convert essentials IV · hold antihypertensives if hypotensive

Plan

CONSULT: Surgery (obstructing cancer, volvulus failing endoscopic detorsion, ischemia, perforation) · GI (colonoscopic decompression/stent, biopsy) · Oncology (malignant cause) · IR (if applicable)

– Stabilize: NPO, IV fluids, correct electrolytes, NG tube if vomiting/proximal distension, Foley, strict I&Os; serial abdominal exams
– Assess closed-loop risk: a competent ileocecal valve with distal obstruction = closed loop → progressive cecal distension → ischemia/perforation (cecal diameter >10–12 cm is concerning) → more urgent intervention
– Colorectal cancer (obstructing): CT staging + CEA; options — emergent surgical resection (± diversion/Hartmann) vs self-expanding metal stent as a bridge to elective surgery or palliation (GI/surgery decision); biopsy to confirm
– Sigmoid volvulus: endoscopic detorsion + rectal tube decompression (first-line if no ischemia/perforation) → followed by elective sigmoidectomy (high recurrence without surgery); peritonitis/ischemia → emergent surgery
– Cecal volvulus: usually surgical (right hemicolectomy or cecopexy) — less amenable to endoscopic detorsion
– Benign stricture: treat underlying cause (IBD, ischemic, diverticular); dilation or resection as appropriate
– Antibiotics: broad-spectrum if ischemia/perforation/peri-op
– In distal colonic obstruction with a competent ileocecal valve, the cecum is the pressure relief that can't pop — watch cecal diameter; >10–12 cm signals impending perforation and the need to decompress urgently.
– PT/OT: mobilize once stable/post-op
– Trend: abdominal exam/girth, cecal diameter on serial imaging, WBC/lactate, bowel function, electrolytes
– Escalation triggers: rising lactate/WBC, peritoneal signs, progressive cecal dilation, free air, or failed endoscopic detorsion → emergent surgery; instability → ICU
– Discharge checklist: definitive cause addressed (oncologic plan/resection, elective surgery for volvulus, stricture management); stoma teaching if created; oncology follow-up + staging complete; bowel regimen; surgery/GI follow-up; return precautions (distension, no stool/flatus, pain, vomiting, bleeding)

115. Partial Large Bowel Obstruction

complete reference · colon cancer + stricture + volvulus · closed-loop physiology · stent vs surgery · Full Card

Symptoms / Associated Sx

• Abdominal distension with crampy pain; constipation or obstipation (partial obstruction may still permit some passage of gas/stool)

• Nausea and, in late/proximal disease, feculent vomiting

• Change in stool caliber, hematochezia, or unexplained anemia suggest an underlying colorectal cancer

• Exam: distension, tympany, possible palpable mass; sudden severe distension with peritoneal signs suggests volvulus or ischemia

Neg

• Pt denies diffuse dilation including small bowel without a transition point — argues against ileus or acute colonic pseudo-obstruction (Ogilvie)

• Pt denies pain out of proportion to exam + elevated lactate — argues against ischemia/strangulation (a closed-loop or volvulus complication)

• Pt denies a small-bowel obstructive pattern — distinguishes large from small bowel obstruction

Social History (SHx)

• Colorectal cancer risk factors: age, family history, prior adenomatous polyps, inadequate screening, IBD

• Diverticular disease (stricture)

• Chronic constipation, laxative use, institutionalization, neurologic/psychiatric disease (sigmoid volvulus)

• Prior abdominal surgery or pelvic radiation (stricture, adhesions)

Main Etiology

• Colorectal cancer — the most common cause of large bowel obstruction, frequently in the left/sigmoid colon

• Stricture — diverticular, ischemic, inflammatory (IBD), anastomotic, or radiation-induced

• Volvulus — sigmoid (elderly, chronically constipated, institutionalized) or cecal (younger patients, abnormal fixation)

• Other: fecal impaction, extrinsic compression by tumor or mass

RF

• Modifiable: colorectal cancer screening adherence, constipation management

• Non-modifiable: age, IBD/radiation history, diverticular disease, anatomic predisposition to volvulus

Data

• CBC (iron-deficiency anemia raises suspicion for occult colorectal cancer; leukocytosis suggests ischemia)

• CMP (electrolyte derangement, dehydration, renal function)

• Lactate (ischemia or closed-loop obstruction)

• CEA (baseline tumor marker if malignancy is found)

• Type and screen (pre-operative)

• CT abdomen/pelvis with contrast (identifies the level and cause — mass vs stricture vs volvulus with a whirl/coffee-bean sign; assesses ileocecal valve competence and closed-loop physiology; detects ischemia; cecal diameter >10–12 cm signals perforation risk)

• Upright abdominal radiograph (colonic dilation; sigmoid volvulus coffee-bean sign; cecal volvulus appearance)

• Water-soluble contrast enema or flexible sigmoidoscopy (define the obstruction; flexible sigmoidoscopy can detorse a sigmoid volvulus)

• Colonoscopy (diagnosis and biopsy of an obstructing lesion; stent placement; performed cautiously in near-complete obstruction)

DDx

Acute colonic pseudo-obstruction (Ogilvie syndrome) (massive colonic dilation without mechanical cause) · small bowel obstruction (small-bowel pattern) · paralytic ileus (diffuse, post-operative/metabolic) · toxic megacolon (underlying colitis plus systemic toxicity)

Home Meds

• Hold: oral medications (NPO)

• Hold: opioids and anticholinergics that impair colonic motility

• Convert: essential medications to IV

• Hold: antihypertensives/diuretics if hypotensive or volume depleted

Plan

CONSULT: Surgery (obstructing cancer, volvulus failing endoscopic detorsion, ischemia, perforation) · GI (colonoscopic decompression/stenting, biopsy) · Oncology (malignant cause) · Interventional Radiology where applicable

• Stabilize: NPO, IV fluids, electrolyte correction, nasogastric tube for vomiting or proximal distension, Foley with strict intake/output, and serial abdominal exams

• Assess closed-loop risk: a competent ileocecal valve combined with a distal obstruction creates a closed loop, leading to progressive cecal distension and risk of ischemia/perforation; a cecal diameter >10–12 cm is concerning and prompts more urgent intervention

• Obstructing colorectal cancer: CT staging and baseline CEA; management options include emergent surgical resection (with diversion or a Hartmann procedure) or a self-expanding metal stent as a bridge to elective surgery or for palliation, decided jointly by GI and surgery; biopsy to confirm the diagnosis

• Sigmoid volvulus: endoscopic detorsion with rectal tube decompression as first-line therapy in the absence of ischemia or perforation, followed by elective sigmoidectomy given the high recurrence rate without surgery; peritonitis or ischemia mandates emergent surgery

• Cecal volvulus: usually managed surgically (right hemicolectomy or cecopexy), as it is less amenable to endoscopic detorsion

• Benign stricture: treat the underlying cause (IBD, ischemic, diverticular) with endoscopic dilation or resection as appropriate

• Antibiotics: broad-spectrum coverage if ischemia, perforation, or perioperative

• PT/OT: mobilize once stabilized or post-operatively

• Trend: abdominal exam and girth, cecal diameter on serial imaging, white count and lactate, return of bowel function, and electrolytes

• Escalation triggers: rising lactate/WBC, peritoneal signs, progressive cecal dilation, free air, or failed endoscopic detorsion → emergent surgery; hemodynamic instability → ICU

• Discharge checklist: definitive cause addressed (oncologic treatment plan and resection, elective surgery for volvulus, stricture management); stoma teaching if an ostomy was created; oncology follow-up with completed staging; a bowel regimen; surgery/GI follow-up; return precautions for distension, obstipation, pain, vomiting, or bleeding

Red Flags

• Closed-loop obstruction with progressive cecal dilation (>10–12 cm) → impending perforation → urgent decompression/surgery

• Peritoneal signs, free air, rising lactate → perforation or ischemia → emergent surgery

• Cecal volvulus or sigmoid volvulus with ischemia → operative management

• Obstructing mass → underlying colorectal cancer until proven otherwise → staging and tissue

• Failed endoscopic detorsion of sigmoid volvulus → surgery

Senior IM Resident Pearls

• The cecum is the pressure valve that can't pop. With a competent ileocecal valve and a distal obstruction, the cecum dilates dangerously — watch its diameter, because >10–12 cm heralds perforation.

• LBO is colon cancer until proven otherwise. A new large bowel obstruction in an adult needs tissue and staging, not just decompression.

• Stent as a bridge. A self-expanding metal stent can convert an emergent obstructed resection into an elective, better-prepared operation — or palliate unresectable disease.

• Detorse the sigmoid, then schedule surgery. Endoscopic decompression fixes the acute volvulus, but recurrence is high without elective sigmoidectomy.

• Cecal volvulus is surgical. Unlike sigmoid volvulus, it rarely responds to endoscopic detorsion.

• Common mistake: mistaking Ogilvie pseudo-obstruction for mechanical LBO — there's no transition point, and the treatment (neostigmine, correcting electrolytes, stopping opioids) is entirely different.

Hepatology — Acute Viral Hepatitis

116. Acute Viral Hepatitis

A, B, occasionally E (also C, D) · hepatocellular transaminitis · mostly supportive · watch for ALF · serologies define the virus · Super Compact

Sx: prodrome (malaise, anorexia, nausea, low-grade fever, RUQ pain) → icteric phase (jaundice, dark urine, pale stool, pruritus); ± arthralgias/rash (HBV serum sickness-like) (most self-limited; watch for AMS/coagulopathy → ALF)

Neg: denies acetaminophen/toxin exposure + AST/ALT in thousands (acetaminophen/toxic — different) · denies AST:ALT >2 alcohol pattern (alcoholic hepatitis) · denies biliary dilation + cholestatic-only pattern (obstruction) · denies encephalopathy + INR ≥1.5 (progression to ALF — escalate)

SHx: HAV: travel, contaminated food/water, fecal-oral, sick contacts · HBV: sexual exposure, IVDU, perinatal, occupational · HEV: travel/endemic, undercooked pork/game, pregnancy · alcohol/other hepatotoxins

Etiology: HAV (fecal-oral, acute only, no chronic) · HBV (blood/sexual/perinatal; can become chronic) · HEV (fecal-oral; severe in pregnancy, chronic in immunosuppressed) · HCV (often subclinical acute, high chronicity) · HDV (only with HBV); also EBV/CMV/HSV

RF: travel to endemic areas · unprotected sex/multiple partners · IVDU · occupational/needlestick exposure · pregnancy (HEV severity) · immunosuppression

Data: LFTs (hepatocellular pattern: AST/ALT often in hundreds–thousands, ALT > AST typically; ↑bili) · INR/PT (≥1.5 + encephalopathy = ALF — critical) · CBC · viral serologies: anti-HAV IgM · HBsAg + anti-HBc IgM + HBeAg/HBV DNA · anti-HEV IgM + HEV RNA · anti-HCV + HCV RNA · anti-HDV (if HBV+) · also EBV/CMV/HSV if atypical · acetaminophen level + autoimmune/Wilson workup (exclude mimics) · RUQ US (exclude obstruction, baseline)

DDx: acute liver failure (coagulopathy + encephalopathy) · acetaminophen/toxic/DILI (exposure, very high AST/ALT) · alcoholic hepatitis (AST:ALT >2) · autoimmune hepatitis (autoantibodies, ↑IgG) · biliary obstruction (cholestatic, ductal dilation)

Home Meds: stop alcohol + hepatotoxins · limit acetaminophen (≤2 g/day) · review all meds for hepatotoxicity · hold nephrotoxins

Plan

CONSULT: Hepatology (severe/atypical, HBV needing antivirals, any ALF features) · ID/Public health (reportable diseases — report HAV/HBV/HEV) · OB (HEV in pregnancy) · Transplant center (if ALF criteria develop)

– Diagnose by serology and exclude non-viral causes (acetaminophen level, alcohol history, autoimmune/Wilson markers, obstruction on US)
– Mostly supportive (most cases self-limited): rest, hydration, antiemetics, nutrition; avoid alcohol and hepatotoxins; treat pruritus (cholestyramine/antihistamines)
– HAV: supportive; no specific antiviral; report to public health; post-exposure prophylaxis for contacts (vaccine ± immunoglobulin)
– Acute HBV: usually supportive (most adults clear spontaneously); antiviral therapy — tenofovir (Viread/Vemlidy) or entecavir (Baraclude) — for severe acute hepatitis, fulminant course, or immunocompromised; monitor for chronicity; report; vaccinate/PEP contacts (HBIG + vaccine)
– HEV: supportive; ribavirin for severe or chronic (immunosuppressed); high mortality in pregnancy — OB co-management
– HCV acute: often progresses to chronic — refer for direct-acting antiviral therapy; HDV — requires HBV management
– Monitor for ALF (INR ≥1.5 + any encephalopathy in a patient without cirrhosis): serial INR + mental status; if it develops → ICU + contact transplant center early, start N-acetylcysteine (NAC) IV (150 mg/kg over 1h → 50 mg/kg over 4h → 100 mg/kg over 16h; improves transplant-free survival even in non-acetaminophen ALF), treat hypoglycemia (frequent glucose checks, D10/D50), manage cerebral edema if ammonia >150–200 (head of bed 30°, hypertonic saline/mannitol), intubate for grade 3–4 HE; do not correct INR with FFP (prognostic marker); list per King's College criteria (acetaminophen: pH <7.3, or INR >6.5 + Cr >3.4 + grade 3–4 HE; non-acetaminophen: INR >6.5, or 3 of 5 adverse factors)
– The single most important inpatient task is detecting progression to acute liver failure — trend the INR and mental status; a climbing INR with new confusion changes everything.
– PT/OT: activity as tolerated
– Trend: LFTs/bilirubin, INR, mental status, glucose; resolution over weeks
– Escalation triggers: INR ≥1.5 + encephalopathy → ALF pathway + transplant center; intractable vomiting/dehydration → IV support; worsening synthetic function → hepatology/ICU
– Discharge checklist: serology/diagnosis documented; counseling on transmission prevention; vaccinate susceptible contacts; HBV/HCV follow-up to assess for chronicity + link to care; avoid alcohol/hepatotoxins; public health reporting done; return precautions (confusion, bleeding, worsening jaundice, persistent vomiting)

116. Acute Viral Hepatitis

complete reference · hepatitis A, B, E (and C, D) · serologic diagnosis · supportive care + monitoring for ALF · Full Card

Symptoms / Associated Sx

• Prodromal phase: malaise, anorexia, nausea/vomiting, low-grade fever, RUQ discomfort, distaste for cigarettes (classic for HAV)

• Icteric phase: jaundice, dark urine, pale stools, pruritus, tender hepatomegaly

• Extrahepatic: arthralgias, urticarial rash, or serum sickness-like syndrome (notably with acute HBV)

• Most cases are self-limited; vigilance for altered mental status and coagulopathy signals progression to acute liver failure

Neg

• Pt denies acetaminophen or other toxin exposure with transaminases in the thousands — helps separate viral hepatitis from acetaminophen/toxic injury

• Pt denies an AST:ALT >2 alcoholic pattern — argues against alcoholic hepatitis

• Pt denies encephalopathy + INR ≥1.5 — their presence indicates progression to acute liver failure and changes management entirely

Social History (SHx)

• HAV: travel to endemic regions, contaminated food/water, fecal-oral exposure, sick contacts, men who have sex with men

• HBV: sexual exposure, injection drug use, perinatal transmission, occupational/needlestick

• HEV: travel/endemic exposure, undercooked pork or game meat, pregnancy (severe disease)

• Alcohol and other hepatotoxin use; medications and supplements

Main Etiology

• Hepatitis A: fecal-oral transmission; causes acute hepatitis only, never chronic

• Hepatitis B: blood, sexual, and perinatal transmission; most immunocompetent adults clear it, but a minority develop chronic infection

• Hepatitis E: fecal-oral; usually self-limited but causes severe disease in pregnancy and chronic infection in the immunosuppressed

• Hepatitis C: often subclinical in the acute phase with high rates of chronicity

• Hepatitis D: occurs only as co-infection or superinfection with HBV

• Other viruses: EBV, CMV, HSV (especially immunocompromised/pregnant)

RF

• Modifiable: travel precautions, safe sex, injection practices, vaccination (HAV, HBV)

• Non-modifiable: pregnancy (HEV severity), immunosuppression (HEV chronicity), occupational exposure

Data

• LFTs (hepatocellular pattern — AST and ALT often in the hundreds to thousands, typically ALT > AST; elevated bilirubin)

• INR/PT (a value ≥1.5 with any encephalopathy defines progression to acute liver failure — the critical monitoring parameter)

• CBC (may show atypical lymphocytes with EBV/CMV; cytopenias)

• Viral serologies (anti-HAV IgM; HBsAg, anti-HBc IgM, HBeAg, HBV DNA; anti-HEV IgM and HEV RNA; anti-HCV and HCV RNA; anti-HDV if HBV positive; EBV/CMV/HSV testing for atypical cases)

• Acetaminophen level, autoimmune markers, ceruloplasmin (exclude common mimics)

• RUQ ultrasound (exclude biliary obstruction and establish a baseline)

DDx

Acute liver failure (coagulopathy plus encephalopathy) · acetaminophen/toxic/drug-induced injury (exposure, very high transaminases) · alcoholic hepatitis (AST:ALT >2) · autoimmune hepatitis (autoantibodies, elevated IgG) · biliary obstruction (cholestatic pattern with ductal dilation)

Home Meds

• Stop: alcohol and hepatotoxic agents

• Limit: acetaminophen to ≤2 g/day

• Review: all medications and supplements for hepatotoxicity

• Hold: nephrotoxins

Plan

CONSULT: Hepatology (severe or atypical disease, HBV requiring antivirals, any features of ALF) · Infectious Disease/Public Health (reportable conditions) · Obstetrics (HEV in pregnancy) · Transplant center (if ALF criteria develop)

• Diagnose by serology and exclude non-viral causes (acetaminophen level, alcohol history, autoimmune and Wilson workup, obstruction on ultrasound)

• Supportive care (most cases are self-limited): rest, hydration, antiemetics, adequate nutrition; avoid alcohol and hepatotoxins; manage pruritus with cholestyramine or antihistamines

• Hepatitis A: supportive only; report to public health; provide post-exposure prophylaxis to contacts (vaccine with or without immunoglobulin)

• Acute hepatitis B: usually supportive as most adults clear spontaneously; antiviral therapy with tenofovir (Viread/Vemlidy) or entecavir (Baraclude) for severe acute hepatitis, a fulminant course, or immunocompromised patients; monitor for transition to chronic infection; report; vaccinate and give HBIG to exposed contacts

• Hepatitis E: supportive; ribavirin for severe or chronic disease (immunosuppressed); high mortality in pregnancy warrants obstetric co-management

• Hepatitis C (acute): frequently becomes chronic — refer for direct-acting antiviral therapy; hepatitis D requires management of the underlying HBV

• Monitor for acute liver failure (the development of coagulopathy with INR ≥1.5 plus any degree of encephalopathy in a patient without underlying cirrhosis): obtain serial INR and mental status checks; if it develops, admit to the ICU and contact a transplant center early, start IV N-acetylcysteine (150 mg/kg over 1h, then 50 mg/kg over 4h, then 100 mg/kg over 16h — it improves transplant-free survival even in non-acetaminophen ALF with early encephalopathy), treat hypoglycemia aggressively with frequent glucose monitoring and dextrose, manage cerebral edema when arterial ammonia exceeds 150–200 µmol/L (elevate the head of bed to 30°, hypertonic saline targeting sodium 145–155 or mannitol), and intubate for grade 3–4 encephalopathy; do not correct the INR with FFP because it is the key prognostic and transplant-listing marker; apply the King's College Criteria to list for emergent transplantation (acetaminophen: arterial pH <7.3, or the combination of INR >6.5, creatinine >3.4 mg/dL, and grade 3–4 encephalopathy; non-acetaminophen: INR >6.5, or any 3 of 5 adverse factors — unfavorable age, etiology, jaundice-to-encephalopathy interval >7 days, bilirubin, and INR)

• PT/OT: activity as tolerated

• Trend: LFTs and bilirubin, INR, mental status, and glucose, with resolution expected over weeks

• Escalation triggers: INR ≥1.5 with encephalopathy → acute liver failure pathway and transplant center; intractable vomiting/dehydration → IV support; worsening synthetic function → hepatology and ICU involvement

• Discharge checklist: documented serologic diagnosis; transmission-prevention counseling; vaccination of susceptible contacts; follow-up for HBV/HCV to assess for chronicity and link to care; avoidance of alcohol and hepatotoxins; completed public health reporting; return precautions for confusion, bleeding, worsening jaundice, or persistent vomiting

Red Flags

• INR ≥1.5 + any encephalopathy → acute liver failure → ICU and transplant center

• HEV in pregnancy → high mortality → obstetric and hepatology co-management

• Fulminant acute HBV → antiviral therapy and transplant evaluation

• Rapidly rising bilirubin and falling synthetic function → impending liver failure

• Severe dehydration from vomiting → IV resuscitation

Senior IM Resident Pearls

• Your main job is catching ALF. Most acute viral hepatitis is supportive — the inpatient value-add is trending INR and mental status to detect the few who progress to liver failure.

• Anti-HBc IgM makes the acute HBV diagnosis — it's positive in acute infection (and the window period) when HBsAg and anti-HBs may be confusing.

• Think HEV in the returning traveler or pregnant patient — it's underdiagnosed, severe in pregnancy, and chronic in the immunosuppressed.

• Most acute HBV in adults self-resolves — reserve antivirals for severe, fulminant, or immunocompromised cases rather than treating everyone.

• These are reportable. Notify public health and arrange contact prophylaxis/vaccination — it's part of the treatment, not an afterthought.

• Common mistake: anchoring on "viral hepatitis" and missing acetaminophen co-ingestion or autoimmune hepatitis — always exclude the treatable mimics.

Hepatology — Infection of Ascites

117. Spontaneous Bacterial Peritonitis (SBP)

infected ascites in cirrhosis · ascitic PMN ≥250 = diagnosis · tap BEFORE antibiotics · cefotaxime + albumin · often asymptomatic · Super Compact

Sx: fever + diffuse abdominal pain/tenderness in a cirrhotic with ascites · OR often subtle/absent — new/worsening encephalopathy, AKI, hypotension, ileus, or unexplained decompensation may be the only clue (low threshold to tap — many are minimally symptomatic)

Neg: denies surgical abdomen + free air + polymicrobial ascites (secondary peritonitis — different management) · denies localized peritoneal source (perforation/abscess) · denies prior abdominal surgery as cause · denies hemorrhagic tap (not the source)

SHx: cirrhosis etiology (alcohol/viral/MASH) · prior SBP (recurrence) · low ascitic protein (predisposes) · recent GI bleed (risk) · PPI use (associated)

Etiology: bacterial translocation from gut into ascitic fluid in portal hypertension; usually monomicrobial — E. coli, Klebsiella, Streptococcus (GNR most common); polymicrobial/anaerobes → suspect secondary peritonitis

RF: cirrhosis with ascites · low ascitic fluid protein <1.5 g/dL · prior SBP · GI bleeding · advanced liver disease/high MELD · PPI use

Data: diagnostic paracentesis (before antibiotics) — ascitic PMN ≥250/mm³ = SBP (corrected count if bloody: subtract 1 PMN per 250 RBC) · ascitic culture in blood culture bottles at bedside (↑ yield) · ascitic total protein + glucose + LDH (distinguish secondary peritonitis: protein >1, glucose <50, LDH high, polymicrobial → Runyon criteria) · SAAG (≥1.1 confirms portal HTN) · CBC · CMP (Cr — AKI/HRS risk) · blood cultures · lactate · INR/bili (severity)

DDx: secondary bacterial peritonitis (perforation/abscess — polymicrobial, ↑protein, surgical) · other infection (UTI/pneumonia) driving decompensation · bowel perforation · ascites from non-cirrhotic cause (SAAG <1.1)

Home Meds: hold nonselective β-blocker during SBP/AKI/hypotension (worsens outcomes) · hold diuretics if AKI/hypotensive · hold nephrotoxins (NSAIDs) · review PPI necessity (deprescribe if not indicated)

Plan

CONSULT: Hepatology (cirrhosis management, transplant assessment) · GI (if secondary peritonitis or GI source) · Surgery (if secondary peritonitis/perforation suspected)

– Diagnose: diagnostic paracentesis with cell count + differential before antibiotics; PMN ≥250/mm³ confirms SBP (treat empirically while culture pends)
– Empiric antibiotics: cefotaxime (Claforan) 2 g IV q8h (or ceftriaxone (Rocephin) 2 g IV q24h) ×5 days; adjust to culture; broaden to carbapenem if healthcare-associated, recent β-lactam exposure, or nosocomial/resistant risk
– IV albumin (reduces HRS + mortality): 1.5 g/kg on day 1 and 1 g/kg on day 3 (especially if Cr >1, BUN >30, or bili >4)
– Hold nonselective β-blockers during the acute episode (associated with worse outcomes/AKI in SBP); hold diuretics if AKI
– Evaluate for secondary peritonitis if: ≥2 of (ascitic protein >1, glucose <50, LDH > serum upper limit), polymicrobial culture, or failure to improve → CT abdomen + surgery
– Secondary prophylaxis (after first SBP — indefinite): ciprofloxacin (Cipro) 500 mg PO daily or TMP-SMX DS daily; primary prophylaxis if low ascitic protein + advanced disease, or during/after GI bleed (ceftriaxone then norfloxacin/cipro)
– Any cirrhotic with ascites who deteriorates in ANY way — fever, encephalopathy, AKI, hypotension, or just "off" — gets a diagnostic tap. SBP is frequently silent and missing it is lethal.
– PT/OT: mobilize; nutrition (don't protein-restrict)
– Trend: repeat paracentesis at 48h if not improving (expect ≥25% PMN drop), Cr/renal function, mental status, hemodynamics, cultures
– Escalation triggers: rising Cr/HRS → albumin + vasoconstrictor + nephrology; no PMN improvement at 48h → reassess for resistant organism or secondary peritonitis; septic shock → ICU; encephalopathy/airway → ICU
– Discharge checklist: complete 5-day antibiotic course; indefinite secondary SBP prophylaxis prescribed; β-blocker decision documented; transplant evaluation referral (SBP is a transplant trigger); hepatology follow-up; HCC surveillance (ultrasound ± AFP q6 months) + endoscopic varices surveillance; return precautions (fever, abdominal pain, confusion, decreased urine)

117. Spontaneous Bacterial Peritonitis (SBP)

complete reference · diagnostic paracentesis · cefotaxime + albumin · secondary peritonitis differentiation · prophylaxis · Full Card

Symptoms / Associated Sx

• Fever, diffuse abdominal pain and tenderness in a cirrhotic patient with ascites

• Often subtle or absent symptoms — new or worsening hepatic encephalopathy, acute kidney injury, hypotension, ileus, or unexplained clinical decompensation may be the only manifestations

• A high index of suspicion is essential because many patients are minimally symptomatic

Neg

• Pt denies a surgical abdomen with free air and polymicrobial ascitic culture — argues against secondary bacterial peritonitis, which requires source control rather than antibiotics alone

• Pt denies a localized intra-abdominal source (perforation, abscess) — supports primary/spontaneous rather than secondary peritonitis

• Pt denies a non-portal-hypertensive cause of ascites (SAAG <1.1) — confirms the cirrhotic, portal-hypertensive substrate in which SBP occurs

Social History (SHx)

• Etiology of cirrhosis (alcohol, viral, MASH)

• Prior episodes of SBP (recurrence risk)

• Recent gastrointestinal bleeding (a precipitant)

• Proton pump inhibitor use (associated with increased SBP risk)

Main Etiology

• Bacterial translocation from the gut lumen into ascitic fluid in the setting of portal hypertension and impaired immune defenses

• Usually monomicrobial; most common organisms are gram-negative enterics (E. coli, Klebsiella) and streptococci

• Polymicrobial or anaerobic growth should raise concern for secondary peritonitis from a perforation or abscess

RF

• Modifiable: PPI deprescribing when not indicated, prophylaxis after GI bleed or prior SBP

• Non-modifiable: cirrhosis with ascites, low ascitic fluid protein <1.5 g/dL, advanced liver disease/high MELD, prior SBP

Data

• Diagnostic paracentesis before antibiotics (ascitic PMN ≥250 cells/mm³ establishes SBP; for a bloody tap, subtract 1 PMN per 250 RBCs to correct)

• Ascitic fluid culture inoculated into blood culture bottles at the bedside (substantially improves yield)

• Ascitic total protein, glucose, and LDH (Runyon criteria to distinguish secondary peritonitis: protein >1 g/dL, glucose <50 mg/dL, LDH above the serum upper limit)

• Serum-ascites albumin gradient (SAAG) (≥1.1 g/dL confirms portal hypertension)

• CBC (leukocytosis; baseline cytopenias)

• CMP (creatinine — acute kidney injury and hepatorenal syndrome risk drives albumin therapy)

• Blood cultures (frequently concordant with ascitic culture)

• Lactate, INR, bilirubin (severity and prognosis)

DDx

Secondary bacterial peritonitis (perforation/abscess — polymicrobial, high protein, low glucose, surgical) · another infection (UTI, pneumonia) driving decompensation · bowel perforation (free air, surgical abdomen) · non-cirrhotic ascites (SAAG <1.1 — malignancy, TB)

Home Meds

• Hold: nonselective beta-blockers during the acute SBP episode, AKI, or hypotension (associated with worse outcomes)

• Hold: diuretics if AKI or hypotensive

• Hold: nephrotoxins (NSAIDs)

• Review: the indication for any PPI and deprescribe if not needed

Plan

CONSULT: Hepatology (cirrhosis management and transplant assessment) · GI (suspected GI source or secondary peritonitis) · Surgery (if secondary peritonitis/perforation is suspected)

• Diagnose: perform a diagnostic paracentesis with cell count and differential before starting antibiotics; an ascitic PMN ≥250/mm³ confirms SBP and warrants empiric treatment while cultures are pending

• Empiric antibiotics: cefotaxime (Claforan) 2 g IV q8h or ceftriaxone (Rocephin) 2 g IV q24h for 5 days, narrowed to culture results; broaden to a carbapenem for healthcare-associated, nosocomial, or recent beta-lactam-exposed patients at risk for resistant organisms

• IV albumin: 1.5 g/kg on day 1 and 1 g/kg on day 3 to reduce hepatorenal syndrome and mortality, particularly when creatinine >1, BUN >30, or bilirubin >4

• Hold nonselective beta-blockers during the acute episode (associated with renal injury and worse outcomes in SBP); hold diuretics with AKI

• Evaluate for secondary peritonitis when there are ≥2 Runyon criteria (ascitic protein >1, glucose <50, LDH above serum upper limit), polymicrobial cultures, or failure to improve → CT abdomen and surgical evaluation

• Prophylaxis: indefinite secondary prophylaxis after a first SBP with ciprofloxacin (Cipro) 500 mg PO daily or TMP-SMX DS daily; primary prophylaxis for low ascitic protein with advanced disease, and short-course antibiotic prophylaxis during and after GI bleeding (ceftriaxone transitioning to an oral fluoroquinolone)

• PT/OT: mobilize; nutritional support without protein restriction

• Trend: repeat paracentesis at 48h if not improving (expect a ≥25% fall in PMN count), renal function, mental status, hemodynamics, and culture results

• Escalation triggers: rising creatinine/hepatorenal syndrome → albumin, vasoconstrictor, and nephrology; failure of PMN count to fall at 48h → reassess for a resistant organism or secondary peritonitis; septic shock or encephalopathy with airway risk → ICU

• Discharge checklist: complete the 5-day antibiotic course; prescribe indefinite secondary SBP prophylaxis; document the beta-blocker decision; refer for transplant evaluation (SBP is a transplant-listing trigger); hepatology follow-up; HCC surveillance with ultrasound (± AFP) every 6 months and endoscopic varices surveillance; return precautions for fever, abdominal pain, confusion, or decreased urine output

Red Flags

• SBP with rising creatinine → hepatorenal syndrome risk → albumin and close renal monitoring

• Septic shock → ICU and resuscitation

• Criteria suggesting secondary peritonitis → CT and surgery; antibiotics alone are insufficient

• Hepatic encephalopathy/airway compromise → ICU

• Failure of PMN count to improve at 48h → resistant organism or wrong diagnosis

Senior IM Resident Pearls

• Tap first, ask questions later. Any cirrhotic with ascites who deteriorates in any way gets a diagnostic paracentesis before antibiotics — SBP is often silent and the cell count is the diagnosis.

• Albumin is part of the treatment, not a volume expander afterthought — 1.5 g/kg then 1 g/kg reduces hepatorenal syndrome and death (Sort 1999).

• Inoculate culture bottles at the bedside — sending fluid to the lab in a syringe dramatically lowers culture yield.

• Polymicrobial = think secondary peritonitis. True SBP is monomicrobial; multiple organisms or the Runyon criteria point to a surgical source.

• Hold the beta-blocker during the acute episode — in this setting it can drop cardiac output and worsen renal perfusion.

• Common mistake: giving antibiotics before tapping — once treated, the ascitic culture and cell count are confounded and the diagnosis becomes murky.

• SBP is a transplant trigger. It marks advanced disease with high one-year mortality — refer for evaluation.

Vascular / Surgical Emergency — Bowel Ischemia

118. Acute Mesenteric Ischemia

pain out of proportion to exam · CT angiography fast · embolic vs thrombotic vs NOMI vs venous · time = bowel · revascularize + resect · Super Compact

Sx: sudden severe diffuse/periumbilical abdominal pain out of proportion to a benign exam · nausea/vomiting/diarrhea (early) · later: distension, peritonism, bloody stool, shock ("pain out of proportion" early; peritonitis = late/transmural infarction)

Neg: denies localized colitis pattern + watershed distribution (ischemic colitis — usually less catastrophic) · denies SBO/LBO mechanical pattern (obstruction) · denies pancreatitis (↑lipase) · denies AAA/dissection (vascular catastrophe — image)

SHx: atrial fibrillation (embolic — #1) · atherosclerosis/PAD/prior CAD (thrombotic) · low-flow states/pressors/heart failure/dialysis (NOMI) · hypercoagulable/cirrhosis/prior VTE (venous) · cocaine

Etiology: arterial embolic (~50% — SMA embolus, AF/cardiac source) · arterial thrombotic (~15–25% — on atherosclerotic SMA, often prior chronic mesenteric angina/weight loss) · nonocclusive (NOMI) (~20% — splanchnic vasoconstriction in shock/low-flow, pressors) · mesenteric venous thrombosis (~5–10% — hypercoagulable, subacute)

RF: atrial fibrillation/cardiac emboli · atherosclerosis · low cardiac output/vasopressors/dialysis · hypercoagulable state · age

Data: do NOT delay imaging · lactate (↑ but LATE/insensitive — normal does not exclude; rising = transmural) · CBC (leukocytosis, often marked) · CMP (metabolic acidosis, AKI) · ABG/base deficit · amylase/lipase (can be mildly ↑; exclude pancreatitis) · coags/lactate trend · type & screen · CT angiography (arterial + venous phase) — test of choice (arterial occlusion/embolus, venous thrombosis, bowel wall changes, pneumatosis, portal venous gas, lack of enhancement; do NOT wait for oral contrast) · ECG (AF source) · catheter angiography (diagnostic + therapeutic option)

DDx: ischemic colitis (colonic, watershed, usually self-limited) · bowel obstruction (mechanical pattern) · perforated viscus/pancreatitis (lipase, free air) · AAA rupture/aortic dissection (vascular — CT)

Home Meds: hold oral meds (NPO, likely surgery) · hold vasoconstrictors/digoxin if NOMI (worsen splanchnic flow) · continue/start anticoagulation per type (heparin) · hold nephrotoxins (but don't delay CTA for renal concern in this emergency)

Plan

CONSULT: EMERGENT Vascular surgery + General surgery · Interventional radiology (endovascular revascularization) · ICU · GI (post-op/chronic)

– This is a time-critical emergency — bowel viability falls with every hour. Resuscitate and image simultaneously; don't wait for lactate to rise
– Immediate measures: aggressive IV fluid resuscitation, correct acidosis/electrolytes, NPO, NG decompression; broad-spectrum antibiotics — piperacillin-tazobactam (Zosyn) 4.5 g IV q6h (translocation/perforation risk); systemic anticoagulation — IV unfractionated heparin (bolus + infusion) unless contraindicated/active bleeding
– Embolic (SMA embolus): emergent surgical embolectomy or endovascular thrombectomy/thrombolysis + heparin; laparotomy to assess bowel viability and resect infarcted segments
– Thrombotic (atherosclerotic SMA): revascularization — open bypass or endovascular stenting; resect nonviable bowel
– NOMI: treat the underlying low-flow state (optimize cardiac output, withdraw vasopressors/digoxin where possible); intra-arterial vasodilators (papaverine) via angiography; surgery for peritonitis/infarction
– Venous (MVT): systemic anticoagulation is primary therapy; surgery only for peritonitis/infarction
– Second-look laparotomy at 24–48h if bowel viability uncertain after initial resection
– Peritonitis / transmural infarction at any point → emergent laparotomy regardless of cause
– Severe pain with a soft, unimpressive abdomen and an AF history is mesenteric ischemia until proven otherwise — go straight to CT angiography; waiting for a high lactate or peritonitis means waiting for dead bowel.
– PT/OT: ICU rehab post-op; nutrition (may need TPN if extensive resection/short gut)
– Trend: lactate, base deficit, abdominal exam, urine output, hemodynamics, repeat imaging as needed
– Escalation triggers: peritoneal signs, rising lactate, hemodynamic collapse → emergent OR; multi-organ failure → ICU; short-gut after massive resection → nutrition/TPN planning
– Discharge checklist: long-term anticoagulation plan (esp embolic/venous — treat AF, hypercoagulable workup for venous); address embolic source (AF — rate/rhythm + anticoagulation); secondary prevention (statin/antiplatelet for atherosclerotic); nutrition plan if resected; vascular surgery/hematology follow-up; return precautions (recurrent severe pain, bleeding, fever)

118. Acute Mesenteric Ischemia

complete reference · embolic + thrombotic + NOMI + venous · CT angiography · emergent revascularization · Full Card

Symptoms / Associated Sx

• Sudden, severe, diffuse or periumbilical abdominal pain that is classically out of proportion to a relatively benign abdominal exam (the hallmark early finding)

• Early nausea, vomiting, and diarrhea (gut emptying); an urge to defecate

• Late findings: abdominal distension, peritoneal signs, bloody stools, and shock — these indicate transmural infarction and a poor prognosis

Neg

• Pt denies a localized colitic pattern in a watershed distribution — argues for acute mesenteric (small-bowel arterial) ischemia rather than the typically less catastrophic ischemic colitis

• Pt denies a mechanical small or large bowel obstructive pattern — distinguishes from obstruction

• Pt denies markedly elevated lipase or free air — argues against pancreatitis or a perforated viscus as the primary process

Social History (SHx)

• Atrial fibrillation or a cardiac embolic source (the leading cause — embolic AMI)

• Atherosclerosis, peripheral arterial disease, prior coronary disease (thrombotic AMI; may have preceding chronic mesenteric angina with post-prandial pain and weight loss)

• Low-flow states — heart failure, shock, vasopressor use, dialysis (non-occlusive mesenteric ischemia)

• Hypercoagulable states, cirrhosis, prior venous thromboembolism (mesenteric venous thrombosis); cocaine use

Main Etiology

• Arterial embolism (~50%): embolus lodging in the superior mesenteric artery, usually from a cardiac source such as atrial fibrillation

• Arterial thrombosis (~15–25%): acute thrombosis on a pre-existing atherosclerotic SMA stenosis, often with a history of chronic mesenteric ischemia

• Non-occlusive mesenteric ischemia (NOMI, ~20%): splanchnic vasoconstriction during low-flow states, shock, or vasopressor therapy without a fixed occlusion

• Mesenteric venous thrombosis (~5–10%): typically subacute, in hypercoagulable patients

RF

• Modifiable: cardiac output optimization, judicious vasopressor use, anticoagulation for AF, atherosclerosis risk-factor control

• Non-modifiable: atrial fibrillation, established atherosclerosis, hypercoagulable states, advanced age

Data

• Do not delay imaging — early diagnosis before infarction is the single most important determinant of outcome

• Lactate (elevation supports ischemia but is late and insensitive; a normal lactate does not exclude early AMI, and a rising lactate suggests transmural injury)

• CBC (leukocytosis, often marked)

• CMP and ABG (metabolic acidosis, base deficit, acute kidney injury)

• Amylase/lipase (may be mildly elevated; primarily to exclude pancreatitis)

• Coagulation studies, type and screen (pre-operative and anticoagulation planning)

• CT angiography (arterial and venous phases) — the test of choice (identifies arterial occlusion/embolus, venous thrombosis, bowel wall thickening or non-enhancement, pneumatosis intestinalis, and portal venous gas; do not delay for oral contrast)

• ECG (atrial fibrillation as an embolic source)

• Catheter mesenteric angiography (both diagnostic and a therapeutic platform for endovascular intervention)

DDx

Ischemic colitis (colonic, watershed, usually self-limited) · bowel obstruction (mechanical pattern with transition point) · perforated viscus or pancreatitis (elevated lipase, free air) · ruptured AAA or aortic dissection (vascular catastrophe — defined on CT)

Home Meds

• Hold: oral medications (NPO, likely operative)

• Hold: vasoconstrictors and digoxin if NOMI is suspected (they worsen splanchnic perfusion)

• Start/continue: systemic anticoagulation appropriate to the mechanism (heparin)

• Hold: nephrotoxins — but do not delay CT angiography over renal concerns in this emergency

Plan

CONSULT: EMERGENT vascular surgery and general surgery · Interventional radiology (endovascular revascularization) · ICU · GI (post-operative and chronic management)

• Treat as a time-critical emergency — bowel viability declines hourly; resuscitate and image simultaneously rather than waiting for lactate to rise or peritonitis to develop

• Immediate measures: aggressive IV fluid resuscitation, correction of acidosis and electrolytes, NPO with nasogastric decompression; broad-spectrum antibiotics — piperacillin-tazobactam (Zosyn) 4.5 g IV q6h for bacterial translocation/perforation risk; systemic anticoagulation with IV unfractionated heparin unless contraindicated

• Embolic (SMA embolus): emergent surgical embolectomy or endovascular thrombectomy/thrombolysis with heparin, plus laparotomy to assess bowel viability and resect infarcted segments

• Thrombotic (atherosclerotic SMA): revascularization by open bypass or endovascular stenting, with resection of nonviable bowel

• NOMI: treat the underlying low-flow state by optimizing cardiac output and withdrawing vasopressors/digoxin where possible; intra-arterial vasodilators (papaverine) via angiography; surgery for peritonitis or infarction

• Mesenteric venous thrombosis: systemic anticoagulation is the primary therapy, with surgery reserved for peritonitis or infarction

• Second-look laparotomy at 24–48h when bowel viability is uncertain after the initial resection

• Peritonitis or transmural infarction at any point mandates emergent laparotomy regardless of the underlying mechanism

• PT/OT: ICU rehabilitation post-operatively; nutrition support, with parenteral nutrition if extensive resection produces short-gut syndrome

• Trend: lactate, base deficit, serial abdominal exams, urine output, hemodynamics, and repeat imaging as indicated

• Escalation triggers: peritoneal signs, rising lactate, or hemodynamic collapse → emergent operation; multi-organ failure → ICU; massive resection → nutrition/parenteral support planning

• Discharge checklist: a defined long-term anticoagulation plan (especially embolic and venous disease); treatment of the embolic source (AF rate/rhythm control plus anticoagulation); secondary prevention with statin and antiplatelet therapy for atherosclerotic disease; a hypercoagulable workup for venous cases; nutrition plan after resection; vascular surgery and hematology follow-up; return precautions for recurrent severe pain, bleeding, or fever

Red Flags

• Pain out of proportion to exam in an at-risk patient → presume mesenteric ischemia and image emergently

• Peritoneal signs, rising lactate, or shock → transmural infarction → emergent laparotomy

• Pneumatosis intestinalis or portal venous gas on CT → advanced ischemia

• Normal lactate is falsely reassuring early → do not use it to rule out

• Metabolic acidosis with a large base deficit → significant ischemic burden

Senior IM Resident Pearls

• Pain out of proportion is the whole diagnosis early on — a patient writhing in pain with a soft belly and an AF history needs CT angiography now, not serial exams.

• Don't wait for the lactate. It rises late; by the time it's high, the bowel is often infarcted. Imaging beats biomarkers here.

• Match the mechanism to the fix: embolic → embolectomy; thrombotic → bypass/stent; NOMI → fix the low-flow state and vasodilate; venous → anticoagulate.

• NOMI hides in the ICU. The hypotensive, pressor-dependent patient who develops a distended, acidotic abdomen may have non-occlusive ischemia — ease the vasoconstrictors if you can.

• Anticoagulate early unless there's a contraindication — it limits clot propagation across all arterial and venous subtypes.

• Common mistake: ordering a non-contrast CT or waiting for oral contrast — you need CT angiography with arterial and venous phases, and time spent waiting is bowel lost.

Geriatrics / Gastroenterology — Fecal Impaction

119. Severe Constipation / Fecal Impaction

esp elderly/immobile · overflow diarrhea is a clue · disimpact + clear + maintain · find & fix reversible causes · exclude obstruction · Super Compact

Sx: no BM for days–weeks, abdominal distension/discomfort, straining · paradoxical overflow ("spurious") diarrhea — liquid stool leaking around impaction (mistaken for diarrhea) · anorexia, nausea · in elderly: delirium, agitation, urinary retention, functional decline · DRE: hard stool in rectal vault

Neg: denies mechanical obstruction features (mass, stricture, no flatus + dilated bowel) · denies red flags: weight loss, bleeding, anemia, new-onset older age (colorectal cancer — needs scope) · denies neuro/cord signs (cauda equina/cord compression) · denies metabolic cause unaddressed (↓K, ↑Ca, hypothyroid)

SHx: immobility/bedbound · opioids/anticholinergics/iron/CCBs · low fiber/fluid intake · dementia/Parkinson's · prior constipation · institutionalized

Etiology: slow colonic transit + dehydration + immobility + constipating meds (esp opioids) → hard stool bolus in rectum/sigmoid; contributors: hypothyroidism, hypercalcemia, hypokalemia, neurologic disease, outlet dysfunction; complications: overflow incontinence, stercoral ulcer/colitis, perforation, urinary retention

RF: advanced age/immobility · opioid + anticholinergic use · low fiber/fluid · neurologic disease (Parkinson's, dementia, spinal) · metabolic (↑Ca, ↓K, hypothyroid)

Data: DRE (confirm impaction, vault stool, tone, masses) · BMP (K, Ca, glucose, renal) · calcium/Mg · TSH · CBC (anemia → CRC concern) · abdominal X-ray (fecal loading, megacolon/megarectum, exclude obstruction/free air) · CT (if obstruction, perforation, stercoral complication, or mass suspected) · colonoscopy (non-urgent — for red flags/age-appropriate CRC screening after resolution)

DDx: mechanical large bowel obstruction (mass/stricture/volvulus) · colorectal cancer (red flags — scope) · ileus/pseudo-obstruction (Ogilvie) (dilation, no mechanical cause) · metabolic/endocrine causes (↑Ca, hypothyroid, ↓K)

Home Meds: minimize/stop opioids, anticholinergics, iron, verapamil where possible · start bowel regimen with any opioid · review all constipating agents · continue essentials

Plan

CONSULT: GI (refractory, red flags, suspected obstruction/megacolon) · Surgery (stercoral perforation, complications) · Geriatrics (frail elderly, polypharmacy)

– Exclude obstruction/perforation (exam + AXR ± CT) before aggressive oral purgatives
– Disimpact (distal/rectal impaction): manual disimpaction (gentle, ± lubricant/local anesthetic) + enemas — warm tap water or mineral oil retention enema to soften, then saline/sodium phosphate enema (avoid phosphate enemas in renal failure/elderly — hyperphosphatemia risk) ± glycerin/bisacodyl suppository
– Clear proximal stool: once distal obstruction relieved → osmotic laxative — polyethylene glycol (MiraLAX) 17 g (or high-dose PEG-electrolyte solution for severe loading) ± stimulant (bisacodyl/senna); avoid bulking agents (fiber) during acute impaction (worsens)
– Supportive: IV fluids/hydration, correct electrolytes (K, Ca), mobilize, treat reversible causes (hypothyroid, hypercalcemia)
– Maintenance regimen (prevent recurrence): scheduled PEG (MiraLAX) daily + stimulant PRN; adequate fluid/fiber once resolved; toileting routine; for opioids → start scheduled osmotic + stimulant laxative prophylactically, add PAMORA (methylnaltrexone/naloxegol) for opioid-induced constipation refractory to laxatives
– "Diarrhea" in an immobile elderly patient is often overflow around a fecal impaction — do a rectal exam before giving antidiarrheals, which would make it dramatically worse.
– PT/OT: mobilization is therapeutic + preventive; toileting assessment
– Trend: bowel movements, abdominal exam/distension, electrolytes, delirium/comfort, resolution on repeat AXR if severe
– Escalation triggers: peritoneal signs/free air → stercoral perforation → emergent surgery; megacolon/megarectum or failure to clear → GI; worsening distension → reassess for obstruction
– Discharge checklist: effective maintenance bowel regimen in place; constipating meds minimized + opioid prophylaxis if continued; reversible causes treated; mobility/fluid/fiber plan; colonoscopy arranged if red flags or due for screening; geriatrics/GI follow-up; return precautions (no BM, distension, vomiting, severe pain, bleeding)

119. Severe Constipation / Fecal Impaction

complete reference · elderly/immobile · disimpaction + clearance + maintenance · opioid-induced constipation · Full Card

Symptoms / Associated Sx

• Absence of bowel movements for days to weeks, abdominal distension and discomfort, straining, sensation of incomplete evacuation

• Paradoxical overflow ("spurious") diarrhea — liquid stool leaking around a hard impaction, frequently misinterpreted as diarrhea

• Anorexia, nausea; in older adults, delirium, agitation, urinary retention, and functional decline may dominate

• Digital rectal exam reveals hard stool in the rectal vault (or an empty vault with more proximal impaction)

Neg

• Pt denies features of mechanical obstruction (palpable mass, no flatus, dilated bowel with a transition point) — argues against large bowel obstruction

• Pt denies alarm features — weight loss, rectal bleeding, iron-deficiency anemia, new symptoms at older age — whose presence mandates colonoscopy to exclude colorectal cancer

• Pt denies neurologic signs of cord compression or cauda equina (saddle anesthesia, urinary retention with weakness) — a reversible neurologic cause of bowel dysfunction

Social History (SHx)

• Immobility or bedbound status

• Opioids, anticholinergics, iron, calcium-channel blockers (especially verapamil)

• Low dietary fiber and fluid intake

• Neurodegenerative disease (dementia, Parkinson's), institutionalization, prior chronic constipation

Main Etiology

• Slow colonic transit compounded by dehydration, immobility, and constipating medications (opioids prominent) producing a hard stool bolus in the rectum or sigmoid

• Contributing metabolic and neurologic factors: hypothyroidism, hypercalcemia, hypokalemia, diabetes, Parkinson's, spinal cord disease, pelvic floor/outlet dysfunction

• Complications: overflow incontinence, stercoral ulceration and colitis, bowel perforation, urinary retention

RF

• Modifiable: medication burden (opioids, anticholinergics), fiber and fluid intake, mobility

• Non-modifiable: advanced age, neurologic disease, metabolic disorders

Data

• Digital rectal exam (confirms impaction, assesses vault stool, sphincter tone, and rectal masses)

• BMP (potassium, calcium, glucose, renal function)

• Calcium and magnesium, TSH (hypercalcemia and hypothyroidism as reversible contributors)

• CBC (anemia raises concern for colorectal cancer)

• Abdominal radiograph (fecal loading, megacolon/megarectum, and exclusion of obstruction or free air)

• CT abdomen (when obstruction, perforation, stercoral complication, or an underlying mass is suspected)

• Colonoscopy (non-urgent — for alarm features or age-appropriate colorectal cancer screening after the acute episode resolves)

DDx

Mechanical large bowel obstruction (mass, stricture, volvulus) · colorectal cancer (alarm features — colonoscopy) · acute colonic pseudo-obstruction (Ogilvie) (colonic dilation without mechanical cause) · metabolic/endocrine causes (hypercalcemia, hypothyroidism, hypokalemia)

Home Meds

• Minimize/stop: opioids, anticholinergics, iron, and verapamil where clinically feasible

• Start a bowel regimen alongside any opioid

• Review: all constipating agents; continue essential medications

Plan

CONSULT: GI (refractory disease, alarm features, suspected obstruction or megacolon) · Surgery (stercoral perforation and complications) · Geriatrics (frail older adults with polypharmacy)

• Exclude obstruction and perforation with exam, abdominal radiograph, and CT if needed before giving aggressive oral purgatives

• Disimpaction of a distal/rectal impaction: gentle manual disimpaction with lubricant and local anesthetic as needed, plus enemas — a warm tap water or mineral oil retention enema to soften, followed by a saline enema; avoid sodium phosphate enemas in older adults and renal impairment given hyperphosphatemia risk; glycerin or bisacodyl suppositories as adjuncts

• Clear proximal stool once the distal obstruction is relieved with an osmotic laxative — polyethylene glycol (MiraLAX) 17 g, or a high-dose PEG-electrolyte solution for severe loading — with a stimulant (bisacodyl or senna); avoid fiber/bulking agents during acute impaction as they worsen it

• Supportive care: IV hydration, correction of electrolytes (potassium, calcium), mobilization, and treatment of reversible causes (hypothyroidism, hypercalcemia)

• Maintenance regimen to prevent recurrence: scheduled polyethylene glycol (MiraLAX) daily with a stimulant as needed; adequate fluid and fiber once resolved; a regular toileting routine; for patients on opioids, start scheduled osmotic plus stimulant laxatives prophylactically and add a peripherally acting mu-opioid antagonist (methylnaltrexone or naloxegol) for opioid-induced constipation refractory to laxatives

• PT/OT: mobilization is both therapeutic and preventive; toileting and functional assessment

• Trend: bowel movements, abdominal exam and distension, electrolytes, delirium/comfort, and resolution on repeat radiograph in severe cases

• Escalation triggers: peritoneal signs or free air → stercoral perforation → emergent surgery; megacolon/megarectum or failure to clear → GI; worsening distension → reassess for obstruction

• Discharge checklist: an effective maintenance bowel regimen in place; constipating medications minimized with opioid prophylaxis if opioids continue; reversible causes treated; a mobility, fluid, and fiber plan; colonoscopy arranged for alarm features or due screening; geriatrics/GI follow-up; return precautions for no bowel movement, distension, vomiting, severe pain, or bleeding

Red Flags

• Stercoral perforation (peritonitis, free air) → surgical emergency with high mortality

• Alarm features (weight loss, bleeding, anemia, new onset in older age) → colonoscopy to exclude colorectal cancer

• Neurologic signs (saddle anesthesia, retention with weakness) → cord compression/cauda equina

• Megacolon/megarectum with systemic toxicity → consider toxic megacolon

• Sodium phosphate enema in renal failure/elderly → dangerous hyperphosphatemia — avoid

Senior IM Resident Pearls

• Do the rectal exam. "Diarrhea" in an immobile elderly patient is often overflow around an impaction — antidiarrheals would be exactly the wrong move.

• Disimpact distally before purging proximally. Pouring oral PEG above a hard rectal plug causes cramping and distension without relief — clear the outlet first.

• No fiber during an acute impaction. Bulking agents need water and motility to work and will worsen a true impaction; save fiber for maintenance.

• Every opioid order needs a bowel regimen — prophylactic osmotic plus stimulant laxatives, escalating to a PAMORA for refractory opioid-induced constipation.

• Avoid phosphate enemas in the elderly and in renal failure — they cause life-threatening hyperphosphatemia and hypocalcemia.

• Common mistake: treating the constipation and ignoring the cause — missed hypercalcemia, hypothyroidism, or a colon cancer turns a "simple" impaction into a recurring or dangerous problem.

Gastroenterology / Surgery — Gastric Outlet Obstruction

120. Gastric Outlet Obstruction (GOO)

malignancy vs peptic ulcer disease · vomiting undigested food + succussion splash · decompress + correct alkalosis · EGD to define cause · Super Compact

Sx: recurrent vomiting of undigested food (non-bilious) · early satiety, epigastric fullness/bloating, weight loss · succussion splash (retained gastric contents >3h after eating) · dehydration (malignancy: progressive, weight loss, anorexia; PUD: pain history, may have ulcer symptoms)

Neg: denies bilious vomiting + distal obstruction pattern (SBO) · denies normal gastric emptying study off opioids (functional gastroparesis) · denies acute presentation w/o weight loss (less likely malignant) · denies neuro/metabolic emetic cause

SHx: PUD history / H. pylori / chronic NSAID use (benign cause) · smoking/alcohol (malignancy + PUD) · weight loss/anorexia (malignancy) · prior gastric surgery

Etiology: malignancy (now the leading cause — gastric adenocarcinoma, pancreatic head cancer, duodenal/ampullary, lymphoma) · peptic ulcer disease (chronic/scarring pyloric/duodenal ulcer with stenosis ± acute edema; historically #1, now less common with PPI/H. pylori treatment); also Crohn, caustic stricture, bezoar

RF: chronic PUD/H. pylori/NSAIDs · smoking · gastric/pancreatic malignancy risk · prior caustic ingestion

Data: BMP (hypokalemic, hypochloremic metabolic alkalosis from vomiting; dehydration/AKI; paradoxical aciduria) · CBC (anemia → malignancy/chronic ulcer) · Mg/phosphate · albumin/nutrition (chronic — malnutrition) · LFTs/lipase (pancreatic/biliary cause) · upright AXR / CT abdomen w/ contrast (dilated stomach + retained food, transition at pylorus/duodenum, mass, staging) · EGD (key test) (directly visualize + biopsy obstructing lesion — malignant vs benign; rule out/confirm) · H. pylori testing · CEA/CA 19-9 if malignancy

DDx: gastroparesis (functional delayed emptying, no mechanical lesion) · SBO (bilious, distal) · proximal small bowel obstruction · functional/cyclic vomiting (no obstruction)

Home Meds: hold oral meds (NPO) · convert essentials IV · start high-dose IV PPI (pantoprazole) esp if PUD-related · hold NSAIDs · hold antihypertensives if hypotensive/dehydrated

Plan

CONSULT: GI (EGD + biopsy, dilation/stent) · Surgery (definitive — resection, gastrojejunostomy, bypass) · Oncology (malignant cause) · Nutrition (malnutrition common)

– Stabilize: NPO, NG tube decompression (relieve retained contents/vomiting), IV fluid resuscitation; correct hypokalemic hypochloremic metabolic alkalosis — normal saline + aggressive KCl repletion (volume + chloride restore it); replete Mg/phosphate; strict I&Os
– High-dose IV PPI: pantoprazole (Protonix) 40 mg IV BID (or continuous) — reduces ulcer edema; test + treat H. pylori if PUD-related
– EGD: define and biopsy the lesion (distinguish malignant from benign); therapeutic options at scope
– Benign (PUD-related) GOO: medical therapy (PPI, H. pylori eradication, stop NSAIDs) often improves edematous component; persistent mechanical stenosis → endoscopic balloon dilation (± repeat) or surgery (pyloroplasty, antrectomy, gastrojejunostomy) if refractory
– Malignant GOO: staging CT; options — endoscopic self-expanding metal stent (good for poor surgical candidates / shorter life expectancy, faster recovery) vs surgical gastrojejunostomy (durable, better for longer life expectancy/good performance status); EUS-guided gastrojejunostomy at expert centers; treat underlying malignancy per oncology
– Nutrition: malnutrition is common — early nutrition support; enteral (post-obstruction feeding tube) or parenteral if prolonged
– The vomiting drives a hypokalemic, hypochloremic metabolic alkalosis with paradoxical aciduria — fix it with saline and potassium chloride (a chloride-responsive alkalosis), not just antiemetics.
– PT/OT: mobilize; nutrition optimization pre-intervention
– Trend: electrolytes (K, Cl, bicarbonate), volume status/UOP, NG output, nutrition, ability to tolerate PO after intervention
– Escalation triggers: severe electrolyte derangement/arrhythmia risk → closer monitoring; failure of medical/endoscopic therapy → surgery; malignant obstruction → expedite stent/bypass + oncology
– Discharge checklist: cause defined (biopsy result); definitive treatment done/planned (dilation, stent, surgery); H. pylori eradication + PPI for PUD; oncology pathway + staging for malignancy; nutrition plan; diet advancement instructions; GI/surgery/oncology follow-up; return precautions (recurrent vomiting, inability to eat, dehydration, weight loss)

120. Gastric Outlet Obstruction (GOO)

complete reference · malignancy + peptic ulcer disease · decompression + alkalosis correction · stent vs surgery · Full Card

Symptoms / Associated Sx

• Recurrent vomiting of undigested, non-bilious food; early satiety, epigastric fullness and bloating

• Weight loss, anorexia, and dehydration; a succussion splash on exam (retained gastric contents heard >3h after eating)

• Malignant causes tend to present with progressive symptoms, weight loss, and anorexia; peptic ulcer-related obstruction often has a prior ulcer/pain history

Neg

• Pt denies bilious vomiting with a distal obstructive pattern — argues against small bowel obstruction

• Pt denies normal gastric emptying off opioids — a mechanical lesion distinguishes GOO from functional gastroparesis

• Pt denies an acute presentation without weight loss — chronicity and weight loss raise concern for a malignant cause

Social History (SHx)

• Peptic ulcer disease history, H. pylori infection, chronic NSAID use (benign etiology)

• Smoking and alcohol (both malignancy and PUD)

• Weight loss and anorexia (malignancy)

• Prior gastric surgery or caustic ingestion

Main Etiology

• Malignancy — now the leading cause: gastric adenocarcinoma, pancreatic head cancer, duodenal/ampullary tumors, lymphoma

• Peptic ulcer disease — chronic pyloric or duodenal ulceration with fibrotic stenosis, often with superimposed acute edema; historically the most common cause but less frequent with widespread PPI use and H. pylori eradication

• Other: Crohn disease, caustic stricture, gastric bezoar

RF

• Modifiable: NSAID use, H. pylori infection, smoking

• Non-modifiable: gastric/pancreatic malignancy, prior caustic injury

Data

• BMP (classic hypokalemic, hypochloremic metabolic alkalosis from loss of gastric acid; dehydration/AKI; paradoxical aciduria)

• CBC (anemia suggests malignancy or chronic ulceration)

• Magnesium and phosphate, albumin/prealbumin (chronic obstruction causes malnutrition; important before refeeding)

• LFTs and lipase (pancreatic or biliary cause)

• Upright abdominal radiograph / CT abdomen with contrast (dilated stomach with retained food, a transition point at the pylorus/duodenum, an obstructing mass, and staging information)

• EGD (key diagnostic test) (direct visualization and biopsy of the obstructing lesion to distinguish malignant from benign and to permit therapeutic intervention)

• H. pylori testing; CEA/CA 19-9 if malignancy is identified

DDx

Gastroparesis (functional delayed emptying without a mechanical lesion) · small bowel obstruction (bilious vomiting, distal) · proximal small bowel obstruction · functional or cyclic vomiting (no obstruction on imaging/endoscopy)

Home Meds

• Hold: oral medications (NPO); convert essentials to IV

• Start: high-dose IV PPI (pantoprazole), particularly for PUD-related obstruction

• Hold: NSAIDs

• Hold: antihypertensives/diuretics if hypotensive or dehydrated

Plan

CONSULT: GI (EGD with biopsy, dilation or stenting) · Surgery (definitive resection, gastrojejunostomy, or bypass) · Oncology (malignant cause) · Nutrition (malnutrition is common)

• Stabilize: NPO with nasogastric decompression to relieve retained contents and vomiting; IV fluid resuscitation; correct the hypokalemic hypochloremic metabolic alkalosis with normal saline and aggressive potassium chloride repletion (a chloride-responsive alkalosis corrected by volume and chloride); replete magnesium and phosphate; strict intake/output

• High-dose IV PPI: pantoprazole (Protonix) 40 mg IV twice daily or as a continuous infusion to reduce ulcer-related edema; test and treat H. pylori if PUD-related

• EGD: define and biopsy the lesion to distinguish malignant from benign disease and to enable therapeutic options

• Benign (PUD-related) obstruction: medical therapy with PPI, H. pylori eradication, and NSAID cessation often resolves the edematous component; persistent mechanical stenosis is treated with endoscopic balloon dilation (sometimes repeated) or surgery (pyloroplasty, antrectomy, gastrojejunostomy) if refractory

• Malignant obstruction: staging CT, then either an endoscopic self-expanding metal stent (favored for poor surgical candidates or shorter life expectancy, allowing faster recovery) or surgical gastrojejunostomy (more durable, favored for longer life expectancy and good performance status); EUS-guided gastrojejunostomy at expert centers; manage the underlying malignancy with oncology

• Nutrition: address the common malnutrition early with enteral feeding beyond the obstruction or parenteral nutrition if prolonged

• PT/OT: mobilization; nutritional optimization before intervention

• Trend: electrolytes (potassium, chloride, bicarbonate), volume status and urine output, nasogastric output, nutritional status, and oral tolerance after intervention

• Escalation triggers: severe electrolyte derangement with arrhythmia risk → closer monitoring; failure of medical/endoscopic therapy → surgery; malignant obstruction → expedite stenting or bypass with oncology

• Discharge checklist: defined cause with biopsy result; completed or planned definitive treatment (dilation, stent, surgery); H. pylori eradication and PPI for PUD; oncology pathway and staging for malignancy; nutrition plan and diet advancement instructions; GI/surgery/oncology follow-up; return precautions for recurrent vomiting, inability to eat, dehydration, or weight loss

Red Flags

• Severe hypokalemic, hypochloremic metabolic alkalosis → arrhythmia risk → aggressive saline and potassium repletion

• Obstructing mass → underlying malignancy until biopsy proves otherwise

• Significant weight loss and malnutrition → nutritional support before any major intervention

• Aspiration from retained gastric contents → decompress and protect the airway

• Failure of medical/endoscopic therapy → surgical referral

Senior IM Resident Pearls

• Fix the alkalosis with chloride, not antiemetics. GOO vomiting causes a chloride-responsive hypokalemic hypochloremic metabolic alkalosis with paradoxical aciduria — saline plus KCl corrects it.

• Malignancy now leads. The teaching that PUD is the top cause is dated — with modern acid suppression, cancer is the most common etiology, so biopsy the lesion.

• Decompress first. An NG tube empties the obstructed stomach, relieves vomiting, reduces aspiration risk, and improves the subsequent endoscopic view.

• Stent vs surgery is a prognosis decision: stents suit shorter life expectancy and poor operative candidates; gastrojejunostomy is more durable for fitter patients with longer expected survival.

• Treat the ulcer fully. PPI plus H. pylori eradication and NSAID cessation can resolve the edematous component and avoid surgery in benign disease.

• Common mistake: diagnosing "gastroparesis" without excluding mechanical GOO — always image and scope before attributing vomiting to a motility disorder.

Thoracic / Surgical Emergency — Esophageal Rupture

121. Esophageal Perforation

high-acuity, high-mortality · Boerhaave vs iatrogenic · chest pain + subcutaneous emphysema + sepsis · CT + water-soluble esophagram · time-critical · Super Compact

Sx: severe acute chest/epigastric/back pain (often after vomiting/retching or instrumentation) · odynophagia, dysphagia · dyspnea · subcutaneous emphysema (crepitus neck/chest), Hamman's crunch · rapidly → fever, tachycardia, sepsis/mediastinitis · Mackler triad (vomiting + chest pain + subcutaneous emphysema) for Boerhaave

Neg: denies cardiac ischemia pattern + ECG/troponin (ACS — must exclude, mimic) · denies aortic dissection (tearing pain, CT) · denies PE · denies simple food impaction w/o perforation · denies pancreatitis/PUD perforation (lipase, free air pattern)

SHx: recent endoscopy/dilation/TEE/intubation (iatrogenic — most common cause) · forceful vomiting/retching (Boerhaave, often alcohol/binge) · foreign body/caustic ingestion · esophageal disease (cancer, stricture, EoE)

Etiology: iatrogenic (most common — endoscopy/dilation/instrumentation) · spontaneous (Boerhaave) (barogenic rupture from forceful vomiting — usually distal left posterolateral) · foreign body/food impaction · caustic injury · trauma · malignancy; leads to mediastinal/pleural contamination → mediastinitis, sepsis

RF: recent esophageal instrumentation · forceful emesis/binge alcohol · esophageal pathology (stricture/cancer/EoE) · caustic/foreign body ingestion

Data: do not delay resuscitation/surgery for diagnostics · CBC (leukocytosis) · CMP/lactate (sepsis) · type & screen, coags · blood cultures · CXR (pneumomediastinum, pleural effusion — often left, hydropneumothorax, subcutaneous/mediastinal air) · CT chest/neck/abdomen w/ contrast (best initial) (extraluminal air/contrast, mediastinal fluid, effusion, perforation site) · water-soluble (Gastrografin) esophagram (confirms + localizes leak; avoid barium — mediastinal irritant) · pleural fluid (↑amylase, low pH, food particles if thoracentesis) · EGD (selective — can extend perforation; sometimes therapeutic)

DDx: ACS/MI (ECG, troponin) · aortic dissection (CT angio) · PE · perforated peptic ulcer (free air below diaphragm) · pancreatitis (lipase) · pneumonia/pneumothorax

Home Meds: strict NPO · hold all oral meds → IV · hold/reverse anticoagulants (surgery likely) · start IV PPI · hold nephrotoxins

Plan

CONSULT: EMERGENT Thoracic/Esophageal surgery · ICU · GI (endoscopic stent/clip in selected cases) · IR (drainage of collections)

– This is a surgical emergency with high mortality that rises with delay — resuscitate, image, and involve surgery simultaneously
– Immediate measures: strict NPO; aggressive IV fluid resuscitation; broad-spectrum antibiotics + antifungal — piperacillin-tazobactam (Zosyn) 4.5 g IV q6h (or carbapenem) + fluconazole (mediastinal/pleural contamination, cover oral flora + Candida); IV PPI — pantoprazole (Protonix) 40 mg IV; analgesia; NG tube only under guidance (risk of worsening); drain pleural collections (chest tube)
– Determine management by stability, location, time, and contamination:
  • Operative (most, esp Boerhaave / late / sepsis): surgical primary repair (buttressed) + wide drainage; if late/unstable → drainage, diversion, esophageal exclusion, or esophagectomy in extreme cases
  • Endoscopic (selected — contained, iatrogenic, early, stable): covered self-expanding metal stent or endoscopic clipping/vacuum + drainage
  • Nonoperative (highly selected — small contained leak, minimal contamination, stable, good drainage): NPO, antibiotics, drainage, nutrition support, serial imaging
– Nutrition: early enteral access (jejunal/feeding tube) or parenteral — patient is NPO for a prolonged period
– Chest pain + subcutaneous emphysema after vomiting or a recent endoscopy is esophageal perforation until proven otherwise — every hour of delay raises mortality; image with CT + water-soluble study and call surgery now.
– PT/OT: ICU rehab; aspiration/airway precautions
– Trend: hemodynamics, lactate, WBC, fever curve, chest tube output, repeat imaging/esophagram before resuming PO, nutrition
– Escalation triggers: septic shock/mediastinitis → ICU + emergent source control; ongoing leak/contamination → reoperation/diversion; respiratory failure → intubation
– Discharge checklist: documented healing (contrast study) before diet advancement; underlying cause addressed (treat esophageal pathology); stent removal plan if placed; nutrition plan/access; thoracic surgery + GI follow-up; return precautions (chest pain, fever, dysphagia, dyspnea)

121. Esophageal Perforation

complete reference · iatrogenic + Boerhaave · CT + water-soluble esophagram · operative vs endoscopic vs nonoperative · Full Card

Symptoms / Associated Sx

• Severe acute chest, epigastric, or back pain — classically after forceful vomiting/retching (Boerhaave) or recent esophageal instrumentation

• Odynophagia, dysphagia, dyspnea; subcutaneous emphysema with neck/chest crepitus and occasionally a Hamman's crunch (mediastinal air)

• Rapid progression to fever, tachycardia, and sepsis from mediastinitis

• Mackler triad (vomiting, chest pain, subcutaneous emphysema) is the classic but incomplete presentation of Boerhaave syndrome

Neg

• Pt denies an ischemic ECG and troponin rise — acute coronary syndrome is a key mimic that must be excluded

• Pt denies a tearing pain with aortic dissection findings on CT — another vascular catastrophe to exclude

• Pt denies a simple food impaction without perforation and denies the free-air pattern of a perforated peptic ulcer or elevated lipase of pancreatitis

Social History (SHx)

• Recent endoscopy, esophageal dilation, transesophageal echocardiography, or intubation (iatrogenic — the most common cause)

• Forceful vomiting or retching, often in the context of binge alcohol use (Boerhaave)

• Foreign body or caustic ingestion

• Underlying esophageal disease (carcinoma, stricture, eosinophilic esophagitis)

Main Etiology

• Iatrogenic — the most common cause, from endoscopic instrumentation, dilation, or intubation

• Spontaneous (Boerhaave syndrome) — barogenic transmural rupture from a sudden rise in intraesophageal pressure during forceful vomiting, typically at the distal left posterolateral esophagus

• Foreign body/food impaction, caustic injury, trauma, and malignancy

• The resulting mediastinal and pleural contamination drives mediastinitis, empyema, and sepsis

RF

• Modifiable: careful instrumentation technique, avoidance of forceful retrieval through strictures

• Non-modifiable: underlying esophageal pathology, episodes of forceful emesis

Data

• Do not delay resuscitation and surgical consultation for diagnostics

• CBC (leukocytosis); CMP and lactate (sepsis and perfusion)

• Type and screen, coagulation studies, blood cultures (operative and sepsis workup)

• Chest radiograph (pneumomediastinum, pleural effusion — often left-sided, hydropneumothorax, subcutaneous or mediastinal air)

• CT chest/neck/abdomen with contrast (best initial test) (extraluminal air or contrast, mediastinal fluid, pleural effusion, and the perforation site)

• Water-soluble (Gastrografin) esophagram (confirms and localizes the leak; barium is avoided because it is a mediastinal irritant)

• Pleural fluid analysis if thoracentesis performed (elevated amylase, low pH, food particles)

• EGD (used selectively — it can extend the perforation but is sometimes therapeutic)

DDx

Acute coronary syndrome (ECG, troponin) · aortic dissection (CT angiography) · pulmonary embolism · perforated peptic ulcer (free air below the diaphragm) · pancreatitis (elevated lipase) · pneumonia or pneumothorax

Home Meds

• Strict NPO

• Hold: all oral medications — convert to IV

• Hold/reverse: anticoagulants (surgery is likely)

• Start: IV PPI

• Hold: nephrotoxins

Plan

CONSULT: EMERGENT thoracic/esophageal surgery · ICU · GI (endoscopic stenting or clipping in selected cases) · Interventional radiology (drainage of collections)

• Treat as a surgical emergency in which mortality rises with every hour of delay — resuscitate, image, and involve surgery simultaneously

• Immediate measures: strict NPO; aggressive IV fluid resuscitation; broad-spectrum antibiotics plus antifungal coverage — piperacillin-tazobactam (Zosyn) 4.5 g IV q6h (or a carbapenem) with fluconazole to cover oral flora and Candida in the contaminated mediastinum/pleura; IV pantoprazole (Protonix) 40 mg; analgesia; nasogastric tube placement only under guidance given the risk of extending injury; chest tube drainage of pleural collections

• Choose management by stability, perforation location, time since injury, and degree of contamination:

• • Operative (most cases, especially Boerhaave, late presentation, or sepsis): surgical primary repair with tissue buttressing and wide drainage; late or unstable patients may require drainage, esophageal diversion/exclusion, or esophagectomy in extreme cases

• • Endoscopic (selected — contained, iatrogenic, early, stable): covered self-expanding metal stent or endoscopic clip/vacuum therapy with drainage

• • Nonoperative (highly selected — small contained leak, minimal contamination, hemodynamically stable, well drained): NPO, antibiotics, drainage, nutritional support, and serial imaging

• Nutrition: establish early enteral access (jejunal feeding tube) or parenteral nutrition given the prolonged NPO course

• PT/OT: ICU rehabilitation with aspiration and airway precautions

• Trend: hemodynamics, lactate, white count and fever curve, chest tube output, repeat contrast imaging before resuming oral intake, and nutritional status

• Escalation triggers: septic shock or mediastinitis → ICU and emergent source control; ongoing leak or contamination → reoperation/diversion; respiratory failure → intubation

• Discharge checklist: documented healing on a contrast study before advancing diet; treatment of the underlying esophageal cause; a stent-removal plan if a stent was placed; nutrition plan and access; thoracic surgery and GI follow-up; return precautions for chest pain, fever, dysphagia, or dyspnea

Red Flags

• Sepsis/mediastinitis → ICU and emergent source control; mortality climbs sharply with delayed treatment

• Subcutaneous emphysema + pneumomediastinum after vomiting or instrumentation → perforation until proven otherwise

• Hemodynamic instability → operative management, not conservative

• Hydropneumothorax/empyema → chest drainage plus definitive repair

• Barium use → avoid; it intensifies mediastinal inflammation

Senior IM Resident Pearls

• Time is mortality. Esophageal perforation outcomes hinge on early diagnosis and source control — the longer the contamination sits, the worse the prognosis, so call surgery before the workup is "complete."

• Pain + subcutaneous emphysema after vomiting or a scope = perforation until imaging says otherwise.

• Use water-soluble contrast, not barium. Barium causes a severe mediastinal inflammatory reaction; Gastrografin localizes the leak more safely.

• Cover fungi too. The mediastinum is contaminated with oral flora including Candida — add an antifungal to broad-spectrum antibiotics.

• Stents are for selected leaks. Contained, early, iatrogenic perforations in stable patients may be managed endoscopically; Boerhaave and septic patients usually need the OR.

• Common mistake: anchoring on ACS for chest pain and missing the perforation — always reconcile the story (recent endoscopy, retching) and look for mediastinal air.

Gastroenterology / Surgical Emergency — Toxic Megacolon

122. Toxic Megacolon

colonic dilation + systemic toxicity · severe UC or C. diff · stop antimotility agents · treat cause + serial imaging · colectomy if no improvement/perforation · Super Compact

Sx: severe colitis (bloody diarrhea — may paradoxically decrease as colon dilates/atonic) + abdominal distension + systemic toxicity (fever, tachycardia, hypotension, AMS) · abdominal pain/tenderness · signs of dehydration/sepsis (sudden drop in stool frequency + worsening distension = ominous, not improvement)

Neg: denies mechanical obstruction (mass/transition point) · denies simple ileus w/o toxicity (post-op/metabolic) · denies pseudo-obstruction w/o colitis (Ogilvie) · denies isolated dilation w/o systemic signs (not "toxic")

SHx: known IBD (esp UC) · recent antibiotics/C. diff · antimotility/opioid/anticholinergic use (precipitant) · recent colonoscopy/barium · hypokalemia · immunosuppression (CMV)

Etiology: transmural inflammation extending to smooth muscle → colonic dilation + paralysis + systemic toxicity; causes — severe UC (classic), fulminant C. difficile, other infectious (CMV, Salmonella, Shigella), ischemic; precipitants — antimotility agents, opioids, anticholinergics, hypokalemia, barium enema, colonoscopy

RF: severe IBD flare · C. difficile · antimotility/opioid use · hypokalemia · recent instrumentation

Data: CBC (leukocytosis, anemia) · CMP (hypokalemia — worsens atony, correct; dehydration) · lactate (ischemia/severity) · CRP/ESR · albumin (low = severe) · blood cultures · C. difficile toxin/NAAT + stool studies · CMV if immunosuppressed · abdominal X-ray (key) (colonic dilation — transverse colon >6 cm; thumbprinting, mucosal islands, loss of haustra; serial films to monitor) · CT (dilation, wall changes, perforation, abscess, megacolon complications) · avoid colonoscopy (perforation risk)

Diagnosis (Jalan criteria): radiographic colonic dilation (>6 cm) PLUS ≥3 of: temp >38, HR >120, WBC >10.5, anemia — PLUS ≥1 of: dehydration, AMS, electrolyte disturbance, hypotension

Home Meds: STOP antimotility agents (loperamide/Imodium), opioids, anticholinergics (precipitate/worsen) · correct hypokalemia · hold oral meds (NPO) · hold NSAIDs

Plan

CONSULT: Surgery (early/urgent — co-manage from admission) · GI · ICU · ID (if infectious)

– This is a surgical emergency-in-waiting — surgery on board from the start; the decision point is improvement vs deterioration over 24–72h
– Resuscitate: aggressive IV fluids, correct electrolytes (especially potassium and Mg), transfuse as needed; NPO + NG decompression; strict I&Os, ICU monitoring; VTE prophylaxis (enoxaparin 40 mg SC daily — prothrombotic)
– Stop all precipitants: antimotility agents, opioids, anticholinergics
– Treat the underlying cause:
  • Severe UC: IV corticosteroids — methylprednisolone (Solu-Medrol) 60 mg/day or hydrocortisone 100 mg IV q6h; broad-spectrum antibiotics added (translocation/perforation risk) — piperacillin-tazobactam (Zosyn) 4.5 g IV q6h
  • C. difficile: oral vancomycin 500 mg PO/NG q6h + IV metronidazole (Flagyl) 500 mg q8h ± vancomycin enema
  • CMV: ganciclovir if confirmed
– Adjuncts: position changes (rolling/knee-elbow) to redistribute gas; correct K aggressively; avoid opioids for pain
– Serial monitoring: abdominal exam + girth + serial AXR (q12–24h); assess response over 24–72h
– Surgery (subtotal colectomy with end ileostomy) for: perforation, progressive dilation, worsening toxicity, hemorrhage, or failure to improve within 24–72h of maximal medical therapy
– Falling stool output with rising distension is NOT improvement — the colon is becoming atonic and dilating; trust the abdominal film and the systemic signs, not a "better" stool count.
– PT/OT: per ICU; nutrition (don't protein-restrict in UC)
– Trend: serial AXR/colonic diameter, abdominal exam/girth, vitals/toxicity, WBC/lactate, electrolytes (K), Hgb
– Escalation triggers: perforation/free air, peritonitis, hemodynamic instability, progressive dilation, or no improvement by 24–72h → emergent colectomy; septic shock → ICU
– Discharge checklist (post-recovery/post-op): underlying disease maintenance (IBD biologic plan or completed C. diff therapy); ileostomy teaching if colectomy; avoid future antimotility agents during flares; GI/colorectal surgery follow-up; return precautions (distension, fever, bleeding, pain)

122. Toxic Megacolon

complete reference · severe UC + fulminant C. difficile · Jalan criteria · medical therapy with surgical backstop · Full Card

Symptoms / Associated Sx

• A background of severe colitis (bloody diarrhea) on which abdominal distension and systemic toxicity (high fever, tachycardia, hypotension, altered mental status) supervene

• Abdominal pain and tenderness, signs of dehydration and sepsis

• Stool frequency may paradoxically decrease as the colon becomes dilated and atonic — a deterioration that can be mistaken for improvement

Neg

• Pt denies a mechanical obstruction with a mass or transition point — argues against large bowel obstruction

• Pt denies a simple post-operative or metabolic ileus without systemic toxicity

• Pt denies acute colonic pseudo-obstruction (Ogilvie) without underlying colitis, and denies isolated colonic dilation without systemic signs — toxic megacolon requires both dilation and systemic toxicity

Social History (SHx)

• Known inflammatory bowel disease, particularly ulcerative colitis

• Recent antibiotics or C. difficile infection

• Use of antimotility agents, opioids, or anticholinergics (precipitants)

• Recent colonoscopy or barium enema; hypokalemia; immunosuppression (CMV)

Main Etiology

• Transmural inflammation extending into the colonic smooth muscle layer causes loss of motility, dilation, and systemic toxicity

• Causes: severe ulcerative colitis (the classic association), fulminant C. difficile colitis, other infectious colitides (CMV, Salmonella, Shigella), and ischemic colitis

• Precipitants: antimotility agents, opioids, anticholinergics, hypokalemia, barium enema, and colonoscopy

RF

• Modifiable: avoidance of antimotility/opioid/anticholinergic agents during severe colitis, correction of hypokalemia, caution with instrumentation

• Non-modifiable: severity of the underlying colitis, C. difficile or CMV infection

Data

• CBC (leukocytosis, anemia)

• CMP (hypokalemia worsens colonic atony and must be corrected; dehydration)

• Lactate (ischemia and severity); CRP/ESR and albumin (low albumin indicates severe disease)

• Blood cultures (systemic toxicity/sepsis)

• C. difficile toxin/NAAT and stool studies; CMV testing if immunosuppressed

• Abdominal radiograph (key) (colonic dilation, classically the transverse colon >6 cm; thumbprinting, mucosal islands, loss of haustration; serial films to monitor progression)

• CT abdomen (dilation, wall changes, perforation, abscess, and other complications)

• Avoid colonoscopy (high perforation risk in the dilated, inflamed colon)

• Diagnostic framework (Jalan criteria) (radiographic colonic dilation >6 cm plus at least 3 of: temperature >38°C, heart rate >120, WBC >10.5, or anemia; plus at least one of: dehydration, altered mental status, electrolyte disturbance, or hypotension)

DDx

Mechanical large bowel obstruction (mass/transition point) · acute colonic pseudo-obstruction (Ogilvie) (dilation without colitis or toxicity) · ileus (post-operative/metabolic, no toxicity) · severe colitis without dilation (precursor state)

Home Meds

• STOP: antimotility agents (loperamide), opioids, and anticholinergics (they precipitate and worsen the condition)

• Correct: hypokalemia aggressively (potassium and magnesium)

• Hold: oral medications (NPO) and NSAIDs

Plan

CONSULT: Surgery (early/urgent — co-manage from admission) · GI · ICU · Infectious Disease (infectious etiology)

• Manage as a surgical emergency-in-waiting with surgery involved from the outset; the pivotal question is whether the patient improves or deteriorates over 24–72h of maximal medical therapy

• Resuscitate: aggressive IV fluids, correction of electrolytes (especially potassium and magnesium), transfusion as needed; NPO with nasogastric decompression; strict intake/output and ICU-level monitoring; VTE prophylaxis with enoxaparin (Lovenox) 40 mg SC daily given the prothrombotic state

• Stop all precipitants: antimotility agents, opioids, and anticholinergics

• Treat the underlying cause:

• • Severe UC: IV corticosteroids — methylprednisolone (Solu-Medrol) 60 mg/day or hydrocortisone 100 mg IV q6h — with broad-spectrum antibiotics such as piperacillin-tazobactam (Zosyn) 4.5 g IV q6h for translocation/perforation risk

• • C. difficile: oral vancomycin 500 mg PO/NG q6h plus IV metronidazole (Flagyl) 500 mg q8h, with vancomycin enemas if ileus

• • CMV colitis: ganciclovir if confirmed

• Adjuncts: repositioning maneuvers (rolling to prone or knee-elbow position) to help redistribute colonic gas; aggressive potassium correction; avoid opioids for analgesia

• Serial monitoring: abdominal exam and girth with serial abdominal radiographs every 12–24h, assessing the response over 24–72h

• Surgery (subtotal colectomy with end ileostomy) for: perforation, progressive colonic dilation, worsening systemic toxicity, significant hemorrhage, or failure to improve within 24–72h of maximal medical therapy

• PT/OT: per ICU protocols; nutritional support without protein restriction in UC

• Trend: serial radiographs and colonic diameter, abdominal exam and girth, vital signs and toxicity, white count and lactate, electrolytes (potassium), and hemoglobin

• Escalation triggers: perforation or free air, peritonitis, hemodynamic instability, progressive dilation, or no improvement by 24–72h → emergent colectomy; septic shock → ICU

• Discharge checklist (after recovery or surgery): maintenance therapy for the underlying disease (an IBD biologic plan or completed C. difficile treatment); ileostomy teaching if colectomy was performed; counseling to avoid antimotility agents during future flares; GI/colorectal surgery follow-up; return precautions for distension, fever, bleeding, or pain

Red Flags

• Perforation or free air → emergent colectomy; carries very high mortality

• Progressive colonic dilation or worsening toxicity despite therapy → operative management

• Falling stool output with rising distension → worsening atony, not improvement

• Hemodynamic instability/septic shock → ICU and likely surgery

• Continued antimotility/opioid use → ongoing precipitant; must be stopped

Senior IM Resident Pearls

• Less stool can be worse, not better. As the colon dilates and goes atonic, diarrhea decreases — interpret a falling stool count with rising distension as deterioration, guided by the abdominal film.

• Surgery is co-managing from day one. Toxic megacolon can perforate suddenly; early surgical involvement and a clear 24–72h decision window save lives.

• Hunt down and correct the potassium. Hypokalemia worsens colonic atony and is a fixable contributor — and stop every antimotility/opioid/anticholinergic agent.

• No colonoscopy. Insufflating a dilated, inflamed colon risks perforation; serial plain films are your monitoring tool.

• Don't forget antibiotics in steroid-treated UC megacolon — bacterial translocation across the compromised wall justifies broad coverage.

• Common mistake: continuing maximal medical therapy past the window — failure to improve in 24–72h, or any perforation/progression, means the colon comes out.

Infectious Disease / GI — Severe C. difficile

123. Fulminant Clostridioides difficile Colitis

severe/fulminant CDI (hypotension, ileus, megacolon) · oral vancomycin 500 + IV metronidazole · early surgery consult · stop the inciting antibiotic · Super Compact

Sx: profuse watery diarrhea + crampy abdominal pain + fever · fulminant features: hypotension/shock, ileus (paradoxically little diarrhea), toxic megacolon, marked leukocytosis · dehydration (↓ diarrhea + distension/ileus in known CDI = ominous, not better)

Neg: denies alternative infectious colitis (stool panel) · denies IBD flare as primary (though can co-occur) · denies ischemic colitis (vascular/watershed) · denies mechanical obstruction

SHx: recent antibiotics (clindamycin, fluoroquinolones, cephalosporins, broad-spectrum — key history) · recent hospitalization/healthcare exposure · PPI use · advanced age · immunosuppression · prior CDI (recurrence)

Etiology: C. difficile toxin-producing overgrowth after antibiotic disruption of gut flora → toxins A/B → colitis; fulminant = CDI + hypotension/shock, ileus, or megacolon; risk of perforation, sepsis, death

RF: recent/current antibiotics · healthcare exposure · age >65 · PPI · immunosuppression/comorbidity · prior CDI

Data: C. difficile testing (NAAT + toxin EIA, or GDH + toxin algorithm; test only if ≥3 unformed stools/24h unless ileus) · CBC (marked leukocytosis — WBC ≥15 = severe; very high or leukemoid suggests fulminant) · CMP (Cr ≥1.5 = severe; K, dehydration) · lactate (↑ lactate ≥2.2 / rising = fulminant/ischemia) · albumin (low = severe) · CT abdomen/pelvis (colonic wall thickening, megacolon, ascites, perforation — for severe/fulminant/ileus) · AXR (megacolon, ileus) · lactate trend · avoid colonoscopy unless diagnostic uncertainty

Severity (IDSA/SHEA): non-severe WBC <15 + Cr <1.5 · severe WBC ≥15 OR Cr ≥1.5 · fulminant hypotension/shock, ileus, OR toxic megacolon

DDx: other infectious colitis (stool panel) · IBD flare (can coexist — test both) · ischemic colitis (vascular, watershed) · toxic megacolon from other cause (dilation + toxicity)

Home Meds: STOP the inciting antibiotic if at all possible (or narrow) · STOP antimotility agents (loperamide — risk of megacolon) · review/stop PPI if not needed · hold nephrotoxins · contact + enteric precautions

Plan

CONSULT: Surgery (early/urgent in fulminant — co-manage) · GI · ID · ICU (if shock/megacolon)

– Stop inciting antibiotics + antimotility agents; contact precautions; soap-and-water hand hygiene (spores resist alcohol gel)
– Resuscitate: IV fluids, correct electrolytes (K, Mg), pressors if shock, ICU for fulminant
– Antibiotic therapy by severity (IDSA/SHEA + ACG):
  • Non-severe / severe (non-fulminant): oral vancomycin 125 mg PO q6h ×10 days, OR fidaxomicin 200 mg PO BID ×10 days (preferred for reduced recurrence)
  • FULMINANT: oral (or NG) vancomycin 500 mg q6h + IV metronidazole (Flagyl) 500 mg q8h; add vancomycin retention enema 500 mg in 100 mL saline PR q6h if ileus (oral may not reach colon)
– Surgical evaluation (early) — colectomy (subtotal colectomy + end ileostomy) or diverting loop ileostomy with colonic vancomycin lavage for: perforation, toxic megacolon, peritonitis, end-organ failure, or clinical deterioration/failure to improve on medical therapy; lactate ≥5 and marked leukocytosis (≥50k) portend poor surgical outcomes — operate before that point
– Recurrence (after this episode): fidaxomicin or vancomycin taper-pulse; consider bezlotoxumab (anti-toxin B monoclonal) to reduce recurrence; fecal microbiota transplant (FMT) for multiply recurrent CDI
– In fulminant CDI with ileus, oral vancomycin may never reach the colon — that's why you both raise the dose to 500 mg, add IV metronidazole, and give vancomycin per rectum; and why surgery must be at the bedside early.
– PT/OT: as tolerated; nutrition support
– Trend: WBC, Cr, lactate, hemodynamics, stool output AND abdominal distension (watch for ileus/megacolon), serial AXR/CT if fulminant
– Escalation triggers: rising lactate/WBC, hypotension, megacolon, perforation, or no improvement in 3–5 days → emergent surgery; shock → ICU
– Discharge checklist: complete 10-day course (vancomycin/fidaxomicin); recurrence-prevention plan (fidaxomicin/bezlotoxumab/FMT pathway if recurrent); avoid unnecessary future antibiotics + PPIs; document CDI for future antibiotic decisions; ID/GI follow-up; return precautions (recurrent diarrhea, fever, distension, dehydration)

123. Fulminant Clostridioides difficile Colitis

complete reference · severity stratification · vancomycin + metronidazole + rectal vancomycin · early surgery · Full Card

Symptoms / Associated Sx

• Profuse watery diarrhea, crampy lower abdominal pain, and fever

• Fulminant features: hypotension or shock, ileus (with paradoxically little diarrhea), toxic megacolon, and marked leukocytosis

• Dehydration; a decrease in diarrhea accompanied by distension and ileus in known CDI signals deterioration, not recovery

Neg

• Pt denies an alternative infectious colitis on stool panel — confirm CDI rather than another pathogen

• Pt denies a primary IBD flare (though CDI can coexist with and complicate IBD — test for both)

• Pt denies an ischemic (watershed/vascular) pattern and denies mechanical obstruction

Social History (SHx)

• Recent antibiotic exposure — clindamycin, fluoroquinolones, cephalosporins, and other broad-spectrum agents (the key historical risk factor)

• Recent hospitalization or healthcare exposure

• Proton pump inhibitor use, advanced age, immunosuppression, multiple comorbidities

• Prior CDI (recurrence risk)

Main Etiology

• Antibiotic disruption of normal colonic flora permits overgrowth of toxin-producing C. difficile; toxins A and B drive colonic inflammation and injury

• Fulminant disease is defined by CDI with hypotension/shock, ileus, or toxic megacolon, and carries risks of perforation, sepsis, and death

RF

• Modifiable: antibiotic stewardship, PPI deprescribing, infection-control practices

• Non-modifiable: advanced age, immunosuppression, comorbidity, prior CDI

Data

• C. difficile testing (NAAT plus toxin EIA, or a GDH-plus-toxin algorithm; test only patients with ≥3 unformed stools in 24h unless ileus is present)

• CBC (marked leukocytosis — WBC ≥15 defines severe disease; a very high or leukemoid count suggests fulminant disease)

• CMP (creatinine ≥1.5 mg/dL defines severe disease; potassium and dehydration)

• Lactate (elevated or rising lactate indicates fulminant disease or ischemia; markedly elevated values predict poor surgical outcomes)

• Albumin (hypoalbuminemia indicates severe disease)

• CT abdomen/pelvis (colonic wall thickening, megacolon, ascites, perforation — for severe, fulminant, or ileus presentations)

• Abdominal radiograph (megacolon, ileus)

• Avoid colonoscopy unless there is diagnostic uncertainty (perforation risk; pseudomembranes can confirm but are rarely needed)

• Severity classification (IDSA/SHEA) (non-severe: WBC <15 and creatinine <1.5; severe: WBC ≥15 or creatinine ≥1.5; fulminant: hypotension/shock, ileus, or toxic megacolon)

DDx

Other infectious colitis (stool panel) · IBD flare (may coexist — test both) · ischemic colitis (vascular, watershed distribution) · toxic megacolon from another cause (colonic dilation + systemic toxicity)

Home Meds

• STOP the inciting antibiotic whenever possible, or narrow the spectrum

• STOP antimotility agents (loperamide) — they increase the risk of toxic megacolon

• Review/stop PPI if not clearly indicated

• Hold nephrotoxins; institute contact/enteric precautions

Plan

CONSULT: Surgery (early/urgent in fulminant disease — co-manage) · GI · Infectious Disease · ICU (shock or megacolon)

• Foundational measures: stop the inciting antibiotics and all antimotility agents; institute contact precautions with soap-and-water hand hygiene (alcohol gel does not kill spores)

• Resuscitate: IV fluids, correction of electrolytes (potassium, magnesium), vasopressors for shock, and ICU admission for fulminant disease

• Antibiotic therapy by severity (IDSA/SHEA and ACG):

• • Non-severe or severe (non-fulminant): oral vancomycin 125 mg PO q6h for 10 days, or fidaxomicin 200 mg PO BID for 10 days (preferred where available for lower recurrence)

• • Fulminant: oral or nasogastric vancomycin 500 mg q6h plus IV metronidazole (Flagyl) 500 mg q8h; add a vancomycin retention enema (500 mg in 100 mL saline per rectum q6h) when ileus is present, since oral drug may not reach the colon

• Early surgical evaluation — subtotal colectomy with end ileostomy, or a diverting loop ileostomy with antegrade colonic vancomycin lavage — for perforation, toxic megacolon, peritonitis, end-organ failure, or clinical deterioration/failure to improve on medical therapy; markedly elevated lactate (≥5 mmol/L) and severe leukocytosis (≥50,000) predict poor surgical outcomes, so operate before reaching that point

• Recurrence management (for after this episode): fidaxomicin or a vancomycin taper-and-pulse regimen; consider bezlotoxumab (anti-toxin B monoclonal antibody) to reduce recurrence; fecal microbiota transplantation for multiply recurrent CDI

• PT/OT: as tolerated; nutritional support

• Trend: white count, creatinine, lactate, hemodynamics, and both stool output and abdominal distension (watching for ileus/megacolon), with serial abdominal radiographs or CT in fulminant disease

• Escalation triggers: rising lactate or white count, hypotension, megacolon, perforation, or no improvement within 3–5 days → emergent surgery; shock → ICU

• Discharge checklist: complete the 10-day course (vancomycin or fidaxomicin); a recurrence-prevention plan (fidaxomicin, bezlotoxumab, or FMT pathway for recurrent disease); avoidance of unnecessary future antibiotics and PPIs; clear documentation of CDI to guide future antibiotic decisions; ID/GI follow-up; return precautions for recurrent diarrhea, fever, distension, or dehydration

Red Flags

• Fulminant disease (hypotension/shock, ileus, toxic megacolon) → ICU and early surgery

• Rising lactate and severe leukocytosis (leukemoid reaction) → impending deterioration; operate before lactate ≥5 / WBC ≥50k

• Ileus → oral vancomycin may not reach the colon → add rectal vancomycin and IV metronidazole

• Perforation or peritonitis → emergent colectomy

• Decreasing diarrhea with rising distension → developing megacolon

Senior IM Resident Pearls

• Fulminant CDI changes the regimen. It's high-dose oral vancomycin (500 mg) plus IV metronidazole — and rectal vancomycin if there's ileus, because oral drug can't reach a paralyzed colon.

• IV vancomycin does nothing for CDI — it isn't secreted into the gut lumen. The route matters: oral/NG and rectal deliver drug to the colon; IV is only for metronidazole here.

• Soap and water, not gel. C. difficile spores survive alcohol-based sanitizer — hand-washing and contact precautions prevent transmission.

• Get surgery involved early. Operating before lactate and white count climb to the extremes improves outcomes; waiting for frank perforation is too late.

• Stop the antimotility agents and the culprit antibiotic. Both drive progression to megacolon; narrowing or stopping the inciting antibiotic is itself therapeutic.

• Common mistake: reassurance from decreasing stool output — in a deteriorating patient that often means ileus and impending megacolon, not improvement.

Hepatology / Vascular — Splanchnic Vein Thrombosis

124. Budd-Chiari Syndrome / Portal Vein Thrombosis

hepatic venous outflow (BCS) vs portal inflow (PVT) thrombosis · Doppler/CT-MR venography · anticoagulate + hunt myeloproliferative cause · Super Compact

Sx: BCS: classic triad — abdominal pain + ascites + hepatomegaly; ± jaundice, lower-extremity edema (IVC), can be fulminant or chronic · PVT: abdominal pain, variable; acute — pain, ileus, ± mesenteric ischemia if extension; chronic — portal HTN (varices/bleed, splenomegaly, ascites) often well-compensated (acute extensive PVT with mesenteric extension → bowel ischemia)

Neg: denies cirrhosis-only ascites w/o vascular occlusion (decompensated cirrhosis) · denies SBP as cause of ascitic decompensation · denies right heart failure/constrictive pericarditis (hepatic congestion mimic) · denies pure cardiac/renal ascites

SHx: myeloproliferative neoplasm (#1 — esp JAK2 V617F+; PV, ET) · OCP/pregnancy/hormones · inherited thrombophilia (factor V Leiden, prothrombin, protein C/S, antithrombin) · PNH, antiphospholipid syndrome · Behçet's · intra-abdominal infection/inflammation/malignancy/cirrhosis (PVT); ETOH

Etiology: BCS — thrombotic obstruction of hepatic venous outflow (hepatic veins/IVC) → sinusoidal congestion, portal HTN, hepatocyte injury · PVT — thrombosis of portal vein (± SMV/splenic); underlying prothrombotic state in most non-cirrhotic cases; cirrhosis/malignancy/local inflammation common in others

RF: myeloproliferative neoplasm/JAK2 · inherited/acquired thrombophilia · hormonal (OCP, pregnancy) · cirrhosis (PVT) · intra-abdominal malignancy/inflammation · PNH/APS/Behçet's

Data: LFTs (variable — congestive pattern in BCS, may be near-normal in chronic) · INR/bilirubin/albumin (synthetic fxn/severity) · CBC (cytopenias from hypersplenism; or polycythemia/thrombocytosis → MPN clue) · Doppler ultrasound (first-line) (absent/reversed hepatic vein or portal flow, thrombus, collaterals, "spider-web" in BCS) · CT/MR venography (confirm + define extent, hepatic vein/IVC vs portal/SMV, exclude malignancy/cavernoma) · thrombophilia + MPN workup: JAK2 V617F (+ CALR/MPL), antiphospholipid antibodies, PNH flow cytometry, protein C/S, antithrombin, factor V Leiden, prothrombin gene, homocysteine · ascitic fluid (SAAG high; exclude SBP) · AFP if HCC concern

DDx: decompensated cirrhosis (no outflow/inflow occlusion) · right heart failure / constrictive pericarditis (hepatic congestion) · malignant portal/hepatic vein invasion (HCC tumor thrombus) · sinusoidal obstruction syndrome (post-HSCT/toxin)

Home Meds: start anticoagulation (heparin → warfarin/LMWH; DOAC in selected) · hold OCP/hormonal agents (prothrombotic) · caution bleeding risk w/ varices (treat/prophylax varices alongside AC) · hold nephrotoxins

Plan

CONSULT: Hepatology (management, transplant assessment in BCS) · Hematology (thrombophilia/MPN workup + long-term AC) · IR (TIPS, angioplasty/thrombolysis) · Surgery/Transplant (fulminant BCS); GI (variceal management)

– Anticoagulation is the cornerstone (both BCS and non-cirrhotic PVT): start therapeutic LMWH/heparin → transition to warfarin (or LMWH); manage varices first/concurrently to mitigate bleeding risk; long-term/indefinite AC given underlying thrombophilia
– Identify & treat the underlying cause: full thrombophilia + MPN workup (JAK2 etc.); refer hematology — MPN-directed therapy (e.g. hydroxyurea, cytoreduction), treat APS/PNH/Behçet's accordingly; stop estrogen
– BCS — stepwise (escalate if no response): (1) anticoagulation + treat ascites (diuretics, sodium restriction, paracentesis); (2) angioplasty/stenting of short-segment hepatic vein/IVC stenosis, or thrombolysis in selected acute cases; (3) TIPS for refractory cases (decompress); (4) liver transplant for fulminant BCS or failure of other measures
– PVT — by acuity: acute non-cirrhotic → anticoagulate promptly (recanalization more likely early); consider thrombolysis if mesenteric extension/ischemia; chronic / cavernous transformation → manage portal HTN (variceal screening/prophylaxis), anticoagulate selectively (esp if prothrombotic state, SMV involvement, or transplant candidate)
– Watch for mesenteric extension → bowel ischemia — surgical emergency if infarction
– Variceal management: screen/treat per portal HTN (nonselective β-blocker or banding) before/with AC to reduce bleeding risk
– Splanchnic vein thrombosis is a flag for an occult myeloproliferative neoplasm — JAK2 V617F can be positive even with normal blood counts (masked by hypersplenism/hemodilution); always send the MPN workup.
– PT/OT: as tolerated; nutrition
– Trend: LFTs/synthetic function, ascites/volume, signs of bleeding, mental status (HE), Hgb/platelets, response/recanalization on imaging
– Escalation triggers: fulminant hepatic failure (BCS) → transplant center; mesenteric ischemia (PVT extension) → emergent surgery; refractory ascites/variceal bleed → TIPS/banding; deterioration → ICU
– Discharge checklist: long-term anticoagulation plan + INR/monitoring; hematology follow-up with MPN/thrombophilia results + cause-directed therapy; variceal surveillance/prophylaxis; hepatology follow-up (± transplant pathway); stop estrogen-containing agents; return precautions (GI bleeding, worsening ascites/abdominal pain, confusion, jaundice)

124. Budd-Chiari Syndrome / Portal Vein Thrombosis

complete reference · hepatic outflow vs portal inflow thrombosis · anticoagulation + MPN workup · stepwise BCS therapy · Full Card

Symptoms / Associated Sx

• Budd-Chiari syndrome (BCS): the classic triad of abdominal pain, ascites, and hepatomegaly; jaundice and lower-extremity edema (with IVC involvement); presentations range from fulminant hepatic failure to insidious chronic disease

• Portal vein thrombosis (PVT): acute disease causes abdominal pain and ileus and, with mesenteric extension, bowel ischemia; chronic disease presents with portal hypertension (variceal bleeding, splenomegaly, ascites) and is often well-compensated

Neg

• Pt denies cirrhosis-only ascites without vascular occlusion — distinguishes these vascular disorders from decompensated cirrhosis

• Pt denies SBP as the driver of ascitic decompensation

• Pt denies right heart failure or constrictive pericarditis — hepatic congestion from cardiac causes mimics BCS

Social History (SHx)

• Myeloproliferative neoplasm — the leading underlying cause, frequently JAK2 V617F-positive (polycythemia vera, essential thrombocythemia)

• Estrogen exposure (oral contraceptives, pregnancy, hormone therapy)

• Inherited thrombophilias (factor V Leiden, prothrombin gene mutation, protein C/S or antithrombin deficiency)

• Paroxysmal nocturnal hemoglobinuria, antiphospholipid syndrome, Behçet's disease; for PVT also cirrhosis, intra-abdominal malignancy, infection/inflammation; alcohol use

Main Etiology

• BCS: thrombotic obstruction of hepatic venous outflow (hepatic veins and/or IVC) producing sinusoidal congestion, portal hypertension, and hepatocyte injury

• PVT: thrombosis of the portal vein, sometimes extending to the superior mesenteric or splenic veins; an underlying prothrombotic state underlies most non-cirrhotic cases, while cirrhosis, malignancy, and local inflammation predominate in others

RF

• Modifiable: estrogen-containing medications, treatment of the underlying hematologic disorder

• Non-modifiable: myeloproliferative neoplasms, inherited and acquired thrombophilias, cirrhosis (PVT), intra-abdominal malignancy or inflammation

Data

• LFTs (variable — a congestive pattern in BCS, sometimes near-normal in chronic disease)

• INR, bilirubin, albumin (synthetic function and severity)

• CBC (cytopenias from hypersplenism, or polycythemia/thrombocytosis pointing toward a myeloproliferative neoplasm)

• Doppler ultrasound (first-line) (absent or reversed hepatic vein/portal flow, visible thrombus, collaterals, and the "spider-web" pattern of hepatic vein collaterals in BCS)

• CT or MR venography (confirm the diagnosis, define the extent — hepatic vein/IVC versus portal/SMV — and exclude malignancy or portal cavernoma)

• Thrombophilia and MPN workup (JAK2 V617F and, if negative, CALR/MPL; antiphospholipid antibodies; PNH flow cytometry; protein C/S, antithrombin; factor V Leiden and prothrombin gene mutation; homocysteine)

• Ascitic fluid analysis (high SAAG; exclude SBP); AFP if hepatocellular carcinoma is a concern

DDx

Decompensated cirrhosis (no outflow/inflow vascular occlusion) · right heart failure or constrictive pericarditis (hepatic congestion) · malignant venous invasion (HCC tumor thrombus) · sinusoidal obstruction syndrome (post-transplant/toxin-related)

Home Meds

• Start: anticoagulation (heparin/LMWH transitioning to warfarin; DOACs in selected patients)

• Hold: estrogen-containing/hormonal agents (prothrombotic)

• Caution: bleeding risk in the presence of varices — treat and prophylax varices alongside anticoagulation

• Hold: nephrotoxins

Plan

CONSULT: Hepatology (management and transplant assessment in BCS) · Hematology (thrombophilia/MPN workup and long-term anticoagulation) · Interventional radiology (TIPS, angioplasty, thrombolysis) · Surgery/Transplant (fulminant BCS) · GI (variceal management)

• Anticoagulation is the cornerstone for both BCS and non-cirrhotic PVT: start therapeutic LMWH or unfractionated heparin and transition to warfarin (or maintain LMWH); manage varices first or concurrently to reduce bleeding risk; anticoagulation is generally long-term or indefinite given the underlying thrombophilia

• Identify and treat the underlying cause: a full thrombophilia and MPN workup (JAK2 and others), with hematology referral for MPN-directed therapy (such as hydroxyurea/cytoreduction) and management of antiphospholipid syndrome, PNH, or Behçet's; discontinue estrogen

• BCS — stepwise escalation: (1) anticoagulation plus ascites management (diuretics, sodium restriction, paracentesis); (2) angioplasty/stenting of a short-segment hepatic vein or IVC stenosis, or thrombolysis in selected acute cases; (3) TIPS for refractory disease to decompress the congested liver; (4) liver transplantation for fulminant BCS or failure of other measures

• PVT — management by acuity: acute non-cirrhotic PVT is anticoagulated promptly (recanalization is more likely with early treatment), with thrombolysis considered for mesenteric extension or ischemia; chronic PVT with cavernous transformation is managed by treating portal hypertension (variceal screening and prophylaxis) and anticoagulating selectively, particularly with a prothrombotic state, SMV involvement, or transplant candidacy

• Monitor for mesenteric extension leading to bowel ischemia — a surgical emergency if infarction develops

• Variceal management: screen for and treat varices per portal hypertension guidance (nonselective beta-blocker or endoscopic banding) before or alongside anticoagulation to reduce bleeding risk

• PT/OT: as tolerated; nutritional support

• Trend: LFTs and synthetic function, ascites and volume status, signs of bleeding, mental status (encephalopathy), hemoglobin and platelets, and imaging response/recanalization

• Escalation triggers: fulminant hepatic failure in BCS → transplant center; mesenteric ischemia from PVT extension → emergent surgery; refractory ascites or variceal bleeding → TIPS or banding; clinical deterioration → ICU

• Discharge checklist: a long-term anticoagulation plan with INR/monitoring; hematology follow-up with MPN/thrombophilia results and cause-directed therapy; variceal surveillance and prophylaxis; hepatology follow-up with a transplant pathway where relevant; discontinuation of estrogen-containing agents; return precautions for GI bleeding, worsening ascites or abdominal pain, confusion, or jaundice

Red Flags

• Fulminant BCS with acute liver failure → transplant center evaluation

• PVT extending to the mesenteric veins with bowel ischemia → surgical emergency

• Variceal hemorrhage → endoscopic and portal-hypertension management, balanced against anticoagulation

• Refractory ascites or hepatic decompensation → TIPS or transplant evaluation

• Underlying myeloproliferative neoplasm → may be masked by hypersplenism; missing it leaves the thrombotic driver untreated

Senior IM Resident Pearls

• Splanchnic vein thrombosis = hunt for an MPN. JAK2 V617F can be positive even with normal counts, because hypersplenism and hemodilution mask the polycythemia/thrombocytosis — always send the workup.

• Anticoagulate even with varices. The thrombotic driver usually outweighs bleeding risk — treat the varices in parallel rather than withholding anticoagulation.

• Early anticoagulation recanalizes acute PVT. The sooner you start in acute non-cirrhotic PVT, the better the chance of restoring flow and preventing cavernous transformation.

• BCS is a ladder. Anticoagulation → angioplasty/stent → TIPS → transplant; escalate based on response rather than jumping to the most invasive option.

• Watch the SMV. PVT that propagates into the superior mesenteric vein threatens the bowel — new pain out of proportion means possible venous mesenteric ischemia.

• Common mistake: attributing the ascites and portal hypertension to cirrhosis and stopping there — vascular occlusion on Doppler/venography changes the entire management and demands a thrombophilia workup.