Gastroenterology

Abdominal Pain: Systematic Evaluation by Location

Anatomical Approach to Chest Pain Differential

A systematic approach to location-based differential diagnosis narrows the possibilities and guides targeted workup:

Organ-Specific Differential by Location

Right Upper Quadrant (RUQ)

Condition	Key Features	Workup
Acute cholecystitis	RUQ pain + fever + Murphy's sign (+)	RUQ US, elevated WBC, elevated LFTs
Biliary colic	RUQ/epigastric pain; fatty food trigger; no fever	RUQ US; normal labs
Hepatitis	RUQ pain + jaundice + malaise	LFTs (elevated transaminases), viral serology
Right lower lobe (RLL) pneumonia	RUQ pain + cough + fever	CXR with RLL infiltrate
Fitz-Hugh-Curtis	RUQ pain in young female + vaginal discharge	History of PID; laparoscopy shows perihepatitis

Epigastric Region

Condition	Key Features	Workup
Acute pancreatitis	Epigastric pain radiating to back	Elevated lipase/amylase; CT abdomen if complications
Peptic ulcer disease	Epigastric pain; relief with antacids; NSAID or H. pylori hx	EGD for diagnosis; H. pylori testing
GERD	Epigastric/substernal burning; positional; food-related	Clinical diagnosis; EGD if alarm symptoms
Acute MI	Epigastric discomfort with dyspnea/diaphoresis	EKG, troponin, CXR
Gastritis	Epigastric pain + nausea; NSAID/alcohol use	EGD; clinical diagnosis often sufficient

Left Upper Quadrant (LUQ)

Condition	Key Features	Workup
Splenic infarction	LUQ pain; sickle cell or hypercoagulable state	CT abdomen with contrast
Splenic rupture	LUQ pain + hemodynamic instability; trauma history	CT abdomen; surgical consultation
Gastritis	LUQ epigastric pain; similar to RUQ	EGD if concerning features
LLL pneumonia	LUQ pain + cough/fever	CXR with LLL infiltrate

Right Lower Quadrant (RLQ)

Condition	Key Features	Workup
Acute appendicitis	RLQ pain; McBurney's point tenderness; migration from periumbilicus	CT abdomen/pelvis; elevated WBC
Ovarian pathology	RLQ pain in female; may correlate with cycle	Pelvic US; β-hCG
Ectopic pregnancy	RLQ pain + vaginal bleeding in pregnant female	Serum β-hCG; pelvic US
Mesenteric adenitis	RLQ pain; viral prodrome; self-limited	CT may show enlarged mesenteric nodes; supportive care
Meckel's diverticulitis	RLQ pain (can mimic appendicitis)	Technetium scan (Meckel's scan); CT

Left Lower Quadrant (LLQ)

Condition	Key Features	Workup
Diverticulitis	LLQ pain + fever; older age; constipation history	CT abdomen/pelvis with oral/IV contrast
Sigmoid volvulus	LLQ pain + severe constipation; abdominal distention	Abdominal X-ray (bird's beak appearance); CT
Ovarian pathology	LLQ pain in female	Pelvic US; β-hCG
Ectopic pregnancy	LLQ pain + vaginal bleeding + pregnancy	β-hCG; pelvic US

Diffuse Abdominal Pain

Condition	Key Features	Workup
Small bowel obstruction	Diffuse colicky pain; vomiting; constipation; distention	Abdominal X-ray (air-fluid levels); CT abdomen
Mesenteric ischemia	Severe diffuse pain; pain out of proportion to exam	CT angiography; lactate; elevated WBC; Doppler US
Peritonitis	Diffuse severe pain; rigid abdomen; rebound/guarding	Imaging (look for free air); labs (elevated WBC, lactate)
Diabetic ketoacidosis	Abdominal pain + metabolic illness signs	Serum/urine ketones; glucose; electrolytes; ABG
Acute gastroenteritis	Diffuse pain + diarrhea/vomiting; prodrome	Supportive diagnosis; stool studies if bloody

Acute Liver Failure: Recognition and Management

Definition and Etiologic Classification

Acute liver failure (ALF) is a rare syndrome of severe hepatic dysfunction developing over less than 26 weeks in a patient with previously normal liver function. Onset of coagulopathy (INR ≥1.5) without cirrhosis defines the condition.

Time-Critical Diagnosis

ALF requires urgent hospitalization in an intensive care setting with transplant capability. Contact a transplant center immediately upon suspicion.

Common Etiologies by Frequency

Etiology	Frequency	Notes
Acetaminophen toxicity	50% (US)	Most common; dose-dependent; N-acetylcysteine (NAC) very effective if given early
Viral hepatitis	10–15%	HAV (fulminant in 0.1–1% of cases), HBV, HEV (high risk in pregnancy)
Drug-induced	10–15%	Isoniazid, phenytoin, NSAIDs, statins, antibiotics (amoxicillin-clavulanate)
Autoimmune hepatitis	5–10%	Young women; responds to steroids
Pregnancy-related	1–3%	HELLP, acute fatty liver of pregnancy; worse in 3rd trimester
Wilson's disease	5% (young patients)	Copper accumulation; Kayser-Fleischer rings; ceruloplasmin low
Budd-Chiari syndrome	2–5%	Hepatic vein thrombosis; hypercoagulable state
Ischemic hepatitis	5–15%	Severe shock/hypoxemia; rapid transaminase rise

Fulminant Hepatic Encephalopathy

Development of hepatic encephalopathy within 8 weeks of symptom onset defines fulminant ALF and indicates worst prognosis; >80% mortality without transplant.

Initial Diagnostic Workup

Essential labs to assess severity and identify etiology:

Test Category	Specific Tests	Interpretation
Synthetic function	PT/INR, albumin	INR ≥1.5 defines ALF
Hepatocellular injury	AST, ALT	Marked elevation (>3000) typical in ALF
Cholestasis	ALP, bilirubin, GGT	Assess pattern of injury; bilirubin tracks severity
Metabolic	CMP (glucose, electrolytes, creatinine)	Hypoglycemia, hyperammonemia, coagulopathy common
Renal function	BUN, creatinine, urine electrolytes	HRS (hepatorenal syndrome) develops in ~50%
Encephalopathy assessment	Blood ammonia, arterial blood gas	Ammonia correlates with severity; guides lactulose dosing
Etiologic workup	Acetaminophen level, viral serology (HAV/HBV/HCV/HEV), autoimmune markers, ceruloplasmin, imaging	See table below for specific tests by suspected etiology

Etiology-Specific Testing

Suspected Cause	Key Tests
Acetaminophen	Serum acetaminophen level (Rumack-Matthew nomogram for toxicity)
Viral hepatitis	Anti-HAV IgM, HBsAg + anti-HBc, anti-HCV (HCV RNA if positive), anti-HEV
Autoimmune	Anti-smooth muscle antibody (ASMA), anti-nuclear antibody (ANA), anti-liver-kidney microsomal (LKM)
Wilson's disease	Ceruloplasmin (low <20 mg/dL), slit-lamp exam for Kayser-Fleischer rings, 24-hr urine copper
Budd-Chiari	Doppler US of hepatic veins, contrast CT/MRI abdomen
Ischemic	Lactate, troponin, EKG, consider echocardiography

King's College Criteria for Transplant Evaluation

Use these criteria to identify patients requiring urgent transplant evaluation:

For acetaminophen-induced ALF:

Arterial pH <7.30, OR
INR >6.5, OR
Creatinine >3.4 mg/dL

For non-acetaminophen ALF:

INR >6.5, OR
ANY three of the following:
Age <10 or >40 years
Etiology: NANB hepatitis, halothane, idiosyncratic drug reaction
Duration of jaundice >7 days before encephalopathy
Bilirubin >17.5 mg/dL
PT >100 seconds (INR >7)

Transplant Listing

Patients meeting King's College criteria should be urgently listed for orthotopic liver transplantation if willing and medically suitable.

Medical Management

Supportive Care Principles

ICU admission with continuous monitoring
Avoid all hepatotoxic medications (acetaminophen, NSAIDs, statins, etc.)
Discontinue oral intake until mental status improves
Total parenteral nutrition if prolonged NPO status
Maintain glucose >100 mg/dL (hypoglycemia worsens encephalopathy)

N-Acetylcysteine (NAC) Therapy

Highly Effective in Acetaminophen Toxicity

NAC dramatically improves outcomes if given early (<24 hours), even with improvement in INR.

Standard NAC protocol:

Phase	Dose	Route	Duration
Loading	150 mg/kg	IV over 60 min	Single dose
2nd phase	50 mg/kg	IV over 4 hours	Single dose
3rd phase	100 mg/kg	IV over 16 hours	May repeat if INR remains elevated

Mechanism: Replenishes hepatic glutathione stores; reduces oxidative injury

Benefit: Works best if given within 24 hours but has been shown to benefit even up to 72 hours in some cases

Management of Complications

Hepatic Encephalopathy

Mechanism: Ammonia and other neurotoxins accumulate with loss of hepatic detoxification

Treatment:

Intervention	Mechanism	Dosing
Lactulose	Reduces ammonia absorption; osmotic laxative	Start 15–30 mL PO BID–TID; titrate to 2–3 soft stools daily
Rifaximin	Non-absorbed antibiotic; reduces ammonia-producing bacteria	550 mg TID
Zinc supplementation	Cofactor for ammonia metabolism	150–300 mg daily in divided doses
L-ornithine L-aspartate (LOLA)	Enhances ammonia metabolism	10 g daily in divided doses (if available)
Restrict protein	Reduces nitrogen load, but must maintain adequate calories	Start at 20–30 g/day; advance as tolerated

Avoid: Sedating medications (benzodiazepines), which worsen encephalopathy

Coagulopathy and Bleeding

Fresh frozen plasma (FFP) — replace only before invasive procedures (does not improve outcomes)
Vitamin K 10 mg IV daily × 3 days if deficient
Platelets if <50 and invasive procedure planned
Proton pump inhibitor (pantoprazole 40 mg IV BID) for stress ulcer prophylaxis

Acute Kidney Injury / Hepatorenal Syndrome

Volume status assessment: Prerenal azotemia vs. HRS vs. acute tubular necrosis
Supportive care: Avoid nephrotoxins
Renal replacement therapy (RRT) if oliguria/uremia develops

Infections

Prophylactic antibiotics often empirically given due to high infection risk
Selective bacterial decontamination with cefotaxime or other agents
Fungal prophylaxis (fluconazole) in high-risk patients

Cirrhosis and Portal Hypertension Complications

Severity Stratification: Child-Pugh Score

Predicts mortality and guides management urgency:

Parameter	Points 1	Points 2	Points 3
Bilirubin (mg/dL)	<2	2–3	>3
Albumin (g/dL)	>3.5	2.8–3.5	<2.8
PT prolongation (seconds)	<4	4–6	>6
Ascites	None	Mild	Moderate/Severe
Encephalopathy	None	Grade 1–2	Grade 3–4

Total score interpretation:

Score	Class	1-Year Mortality
5–6	A	~5%
7–9	B	~20%
10–15	C	~50%

MELD Score

More objective than Child-Pugh; used for transplant listing priority:

Components:

Bilirubin (mg/dL)
INR (PT ratio)
Creatinine (mg/dL)

Calculation involves logarithmic formula; use online calculator. Higher MELD = worse prognosis and higher transplant priority.

Variceal Bleeding

Acute Management

When variceal bleeding is suspected (hematemesis in cirrhotic patient):

Two large-bore IVs and type & crossmatch
Goal Hgb 7–9 g/dL (no over-transfusion; hypervolemia worsens portal pressure)
Octreotide 50 mcg IV bolus, then 50 mcg/hr infusion × 48 hours
Variceal ligation (VL) or sclerotherapy via urgent EGD (within 12 hours)

Prophylaxis for Rebleeding

After successful variceal band ligation, initiate propranolol or carvedilol to reduce portal pressure and prevent rebleeding.

Secondary Prophylaxis

After variceal bleeding, reduce rebleeding risk:

Non-selective beta-blockers: Propranolol (titrate to heart rate reduction of 20–25%) or carvedilol 6.25–12.5 mg daily
Repeat variceal ligation: Every 2–4 weeks until all varices obliterated
Target: Complete variceal eradication

Spontaneous Bacterial Peritonitis (SBP)

Diagnosis

Clinical suspicion: Cirrhotic patient with ascites + fever, abdominal pain, or unexplained deterioration (encephalopathy, renal failure)

Diagnostic paracentesis:

Send fluid for: cell count, protein, culture (preferably in blood culture bottles), glucose
SBP diagnostic criteria: PMN count >250 cells/µL in ascitic fluid

Finding	Typical SBP
PMN count	>250 cells/µL (diagnostic threshold)
Total protein	Often <1 g/dL (poor opsonic activity)
Glucose	May be low (<50)
Culture positivity	~50% with standard technique; higher with blood culture bottles

Treatment

Antibiotic coverage:

Agent	Dosing	Notes
Ceftriaxone	1 g IV Q12H × 5 days	First-line; excellent GI flora coverage
Cefotaxime	2 g IV Q4H × 5 days	Alternative
Fluoroquinolone	Norfloxacin 400 mg BID × 5 days	If allergy to beta-lactams

Albumin supplementation:

1.5 g/kg on day 1 (max 100 g)
1 g/kg on day 3 (max 100 g)
Reduces renal failure and mortality significantly

Repeat paracentesis: At 48 hours if clinical deterioration; should show PMN reduction

SBP Prophylaxis

Indicated in cirrhotic patients with:

Low albumin (<1.5 g/dL) AND low opsonic activity (ascitic protein <1 g/dL)
Previous SBP (indefinite prophylaxis)
Variceal hemorrhage (prophylactic antibiotics during acute bleed and 7 days after)

Prophylactic agents:

Trimethoprim-sulfamethoxazole (TMP-SMX) 1 DS tablet daily
Norfloxacin 400 mg daily (used if sulfa allergy)

Hepatic Encephalopathy Management

Precipitants

Always identify and treat underlying cause:

Infection (SBP, UTI, pneumonia, spontaneous bacteremia)
GI bleeding (increased nitrogen load)
Medications (diuretics, benzodiazepines, opioids)
Dehydration/electrolyte abnormalities
Renal failure
Portal vein thrombosis
High protein intake

Treatment

First-line:

Agent	Mechanism	Dosing
Lactulose	Osmotic laxative; reduces ammonia absorption	15–30 mL BID–TID; titrate to 2–3 soft stools daily
Rifaximin	Non-absorbed antibiotic; inhibits ammonia-producing flora	550 mg TID

Second-line:

Agent	Mechanism	Dosing
Zinc acetate	Cofactor for urea cycle	220–660 mg daily in divided doses
L-ornithine L-aspartate	Enhances ammonia metabolism	10 g daily (if available; used more in Europe)

Hepatorenal Syndrome (HRS)

Definition and Types

Progressive renal failure in advanced cirrhosis without primary kidney disease. Two types:

Type	Presentation	Prognosis
HRS-AKI (Type 1)	Rapid increase in Cr (>2.5 fold over 2 weeks); median survival <2 weeks without treatment	Often triggered by SBP, variceal bleed; high mortality
HRS-CKD (Type 2)	Gradual Cr elevation (1.5–2.5 mg/dL); associated with refractory ascites	Chronic; allows time for transplant evaluation

Diagnostic Criteria

Serum creatinine >1.5 mg/dL in cirrhotic patient
No improvement after 48 hours of albumin and vasoconstrictor therapy
Absence of parenchymal kidney disease (check urine sediment, proteinuria)
No nephrotoxin exposure (NSAIDs, aminoglycosides)

Treatment

Involves vasoconstrictors + albumin:

Agent	Dosing	Mechanism
Midodrine	7.5–15 mg PO TID	Alpha-adrenergic agonist; systemic vasoconstriction
Octreotide	100–200 mcg SQ TID	Splanchnic vasoconstriction
Albumin	1 g/kg (max 100 g) on day 1; 25 g on days 2–14	Expands plasma volume; improves renal perfusion
Terlipressin	0.5–1 mg IV Q6H	Vasopressin analog (used more in Europe/Canada)

Prognosis: HRS-AKI has poor prognosis without liver transplantation. Transplant evaluation should be urgent.

Ascites Management

Diagnostic Paracentesis

Perform to:

Establish diagnosis of ascites etiology (SAAG, protein, cultures)
Therapeutic benefit (remove >5 L relieves symptoms)

SAAG (serum-ascites albumin gradient):

SAAG ≥1.1: Portal hypertension (cirrhosis, Budd-Chiari, portal vein thrombosis)
SAAG <1.1: Non-portal hypertensive (peritoneal TB, malignancy, peritonitis)

Conservative Management

First-line for uncomplicated ascites:

Sodium restriction to <2 g daily (most important dietary measure)
Fluid restriction to 1.5–2 L daily if hyponatremia (<120) develops
Daily weights to monitor fluid balance

Diuretics

If sodium restriction alone insufficient:

Spironolactone (potassium-sparing) + furosemide (loop diuretic) in combination:

Ratio	Starting Doses	Goal	Notes
100:40	Spironolactone 100 mg daily + Furosemide 40 mg daily	Increase by 100 mg spiro + 40 mg furo Q3–5 days as needed	Maintains K+ balance; max spironolactone 400 mg, furosemide 160 mg daily

Weight loss target: 0.5–1 lb daily (maintains intravascular volume)

Avoid: NSAIDs (renal failure risk); ACE-I/ARBs (hyperkalemia risk)

Refractory Ascites

Ascites refractory to sodium restriction + maximum-dose diuretics:

Paracentesis with albumin infusion (8 g per liter removed)
Transjugular intrahepatic portosystemic shunt (TIPS) — reduces portal pressure; complications (encephalopathy, shunt thrombosis)
Liver transplantation — definitive therapy

Gastrointestinal Bleeding: Initial Management and Stratification

Classification and Location

Upper GI Bleeding (UGIB)

Anatomy: Bleeding proximal to the ligament of Treitz (junction of duodenum and jejunum)

Source	Frequency	Characteristics
Peptic ulcer disease	30–40%	Often H. pylori or NSAID-related
Esophageal varices	15–20%	In portal hypertension; high mortality if massive
Mallory-Weiss tear	5–10%	Mucosal tear from forceful vomiting/retching
Malignancy	5–10%	Primary esophageal or gastric cancer
Portal hypertensive gastropathy	5%	Diffuse mucosal bleeding in cirrhosis
Dieulafoy lesion	1–5%	Abnormal arterial branch; high-risk for rebleeding
Other	5–10%	Cameron lesions (GERD), hemobilia, aortic fistula

Lower GI Bleeding (LGIB)

Anatomy: Bleeding distal to ligament of Treitz

Source	Frequency	Characteristics
Diverticulosis	20–30%	Often painless; colonoscopy may not identify bleeding site
Internal hemorrhoids	20–30%	Bright red blood on toilet paper; visible on external exam/anoscopy
Angiodysplasia	10–15%	Vascular malformations; associated with renal failure, aortic stenosis
Malignancy	10–15%	Colon/rectal cancer; may have weight loss, anemia, change in bowel habits
Inflammatory bowel disease	5–10%	Ulcerative colitis or Crohn's; bloody diarrhea; abdominal pain
Ischemic colitis	5%	Usually left-sided; elderly with vascular risk factors
Other	5–10%	Meckel's diverticulum, small bowel angiodysplasia, colitis (infectious)

Risk Stratification

Glasgow-Blatchford Score (for UGIB)

Predicts need for intervention and mortality:

Variable	Points
Blood pressure (SBP <100)	1
Pulse (>100)	1
Melena (presence)	1
Syncope (presence)	2
Hepatic disease (presence)	2
Cardiac failure (presence)	2
Hemoglobin (men: <100 g/L, women: <100 g/L)	1–3
Urea (>50 mg/dL)	1

Score 0 = Very low risk; consider outpatient management Score ≥1 = Hospitalization recommended

AIMS65 Score

Predicts in-hospital mortality:

Variable	Points
Age ≥65 years	1
INR ≥1.5	1
Mental status (confusion/lethargy)	1
Shock (SBP <90 or heart rate >100 with abnormal perfusion)	1
Endoscopy findings (hematin/spurting)	1

Score 0–1 = <1% mortality Score 2–3 = 5–10% mortality Score 4–5 = >20% mortality

Initial Stabilization

ABCs First

Assess airway patency, breathing adequacy, and circulation before proceeding with specific GI intervention.

Resuscitation Protocol

Two large-bore IVs (16–18 gauge if possible) or central line if unstable
Type & screen initially; type & crossmatch 2–4 units PRBC
Baseline labs: CBC, CMP, PT/INR, fibrinogen, lactate
Continuous monitoring — vital signs, SpO2, cardiac rhythm
NPO pending endoscopy/evaluation
Foley catheter to monitor urine output (goal >0.5 mL/kg/hr)
Supplemental oxygen to maintain SpO2 >90%

Blood Product Transfusion Strategy

Product	Threshold	Rationale
Packed RBCs	Hgb <7 g/dL	Liberal transfusion (Hgb 8–9) increases rebleeding risk in variceal bleeding
Fresh frozen plasma	INR >1.5 with active bleeding	Corrects coagulopathy; use only if endoscopy planned
Platelets	<50,000 with active bleeding	Particularly if HAS-BLED score indicates high bleeding risk
Cryoprecipitate	Fibrinogen <100 mg/dL	Needed if massive transfusion (>4 units PRBCs)

Pharmacologic Therapy

Upper GI Bleeding

Proton pump inhibitor (PPI):

High-dose IV pantoprazole 80 mg bolus, then 8 mg/hr infusion (for 72 hours)
Reduces rebleeding risk; particularly important pre-endoscopy

For suspected variceal bleeding:

Octreotide 50 mcg IV bolus, then 50 mcg/hr infusion × 48 hours
Reduces splanchnic blood flow and portal pressure
Continue regardless of endoscopic findings

Antibiotic Prophylaxis (Varices)

Ceftriaxone 1 g IV daily (or norfloxacin 400 mg PO BID) × 7 days
Reduces bacterial translocation and SBP risk in cirrhotic with bleeding

Endoscopic Therapy

Upper Endoscopy (EGD) Timing

Urgent EGD (within 12 hours) for all acute UGIB unless patient not suitable for intervention
Earlier if massive bleeding or hemodynamic instability (consider intubation for airway protection)

Endoscopic interventions by bleeding source:

Source	Technique	Success
Peptic ulcer	Epinephrine injection ± cautery ± clip placement	~90%
Varices	Endoscopic variceal ligation (VL) or sclerotherapy	~90%; VL superior for rebleeding prevention
Mallory-Weiss	Cautery, injection, or clip; usually self-limited	~80%
Dieulafoy	Injection, cautery, clip, or endoscopic band	~95%

Lower Colonoscopy

Colonoscopy within 24 hours for nonmassive LGIB to identify source
During active bleeding: Direct injection, thermal coagulation, or clip placement
Angiodysplasia: Thermal coagulation or argon plasma coagulation (APC)
Diverticular bleeding: Usually no intervention needed (hemostasis achieved endoscopically if actively bleeding)

Small Bowel Evaluation

If UGIB and LGIB workups unrevealing, consider video capsule endoscopy or double-balloon enteroscopy for small bowel source.

Intervention Escalation

Rebleeding Despite Endoscopy

Repeat endoscopy — success decreases with each attempt
Interventional radiology: Angiography with arterial embolization
Surgical evaluation — if persistent bleeding uncontrolled by endoscopy/IR

Acute Pancreatitis: Diagnosis and Management

Definition and Etiologic Spectrum

Acute pancreatitis is inflammation of the pancreas with sudden onset of epigastric pain. Two leading causes account for ~80% of cases: biliary obstruction and alcohol.

Common Etiologies

Category	Causes
Gallstone-related	Biliary obstruction; highest-risk if stone <5 mm (passage into CBD)
Alcohol	Acute intoxication or chronic heavy use; dose-related
Drug-induced	L-asparaginase, azathioprine, sulfonamides, pentamidine, didanosine, valproate, steroids, diuretics, sulfonamides
Metabolic	Hypertriglyceridemia (>1000 mg/dL), hypercalcemia, hypothermia
Infectious	Mumps, Coxsackie B, Mycoplasma (rare in developed countries)
Structural	Pancreatic cancer, PCP, sphincter of Oddi dysfunction
Idiopathic	~20% of cases; diagnosis of exclusion

Memory aid: "GET SMASHED"

Gallstones, Ethanol
Trauma, Tumor, Toxins
Steroid use, Sphincter of Oddi dysfunction, Superbug (infection)
Metabolic (HTG, hypercalcemia)
Autoimmune
SED (smoking-related?)
Hyperlipidemia, Hypertriglyceridemia
END (endoscopy-related), Ethanol
Drugs, Deficiency (nutritional)

Diagnostic Criteria

Diagnosis requires TWO of THREE:

Characteristic abdominal pain: Epigastric, radiating to back, gradual onset (hours), peak at 6–12 hours
Elevated pancreatic enzymes:
Amylase >3× upper limit normal (more nonspecific; rises/falls within days)
Lipase >3× upper limit normal (more specific; elevated longer than amylase)
Characteristic imaging findings: CT abdomen (pancreatic edema, necrosis, peripancreatic fat stranding)

Lipase Preferred

Lipase is more specific and sensitive than amylase for pancreatitis and remains elevated longer (up to 14 days vs. 3–5 days for amylase).

Prognostic Scoring

Ranson's Criteria

Predicts mortality and complications:

At Admission	At 48 Hours
Age >55 years	Hematocrit drop >10%
WBC >16,000/µL	BUN rise >5 mg/dL
Glucose >200 mg/dL	Serum calcium <8 mg/dL
LDH >350 IU/L	Alb drop >1 g/dL
AST >250 IU/L	PaO2 <60 mmHg

Score interpretation:

Score	Mortality
<3	<1%
3–4	15–20%
5–6	30–40%
>6	>50%

BISAP Score

Simpler; calculated at admission:

Variable	Points
BUN >25 mg/dL	1
Impaired mental status	1
SIRS (≥2 criteria)	1
Age >60 years	1
Pleural effusion	1

Score 0–2 = <2% mortality Score ≥3 = Increased mortality and complications

Workup and Imaging

Initial labs:

Amylase, lipase — diagnosing pancreatitis
Comprehensive metabolic panel — glucose (may rise), electrolytes, renal function, calcium
Liver enzymes, bilirubin — if biliary pancreatitis suspected
Triglycerides, cholesterol — if metabolic cause suspected
Albumin, lactate — assess severity
CBC — baseline Hgb/Hct for transfusion triggers

Imaging:

Test	Indication	Findings
Abdominal ultrasound (RUQ focus)	Rule out gallstones; assess for CBD dilation	Stones, wall thickening, pericholecystic fluid
CT abdomen/pelvis with contrast	If not improving by 48–72 hours OR severe pancreatitis	Pancreatic edema, fat stranding (interstitial edema), pancreatic necrosis (20–30% of cases), fluid collections
MRCP	Suspected CBD obstruction or cholangitis	Direct visualization of biliary tree; therapeutic ERCP can be performed

Management Strategy

Supportive Care (Universal)

The foundation of treatment; most mild pancreatitis resolves with supportive care:

NPO status initially; advance diet as tolerated (see below)
Aggressive fluid resuscitation:
Lactated Ringer's preferred (normal saline associated with hyperchloremic acidosis)
Goal: Urine output 0.5–1 mL/kg/hr; may require 150–300 mL/hr initially
Continue fluids until clinical improvement (reduced pain, oral intake tolerated)
Pain control:
IV opioids (morphine, hydromorphone)
Avoid IM injections (risk of abscess/loculation)
Meperidine less preferred (spasms sphincter of Oddi)
Prophylactic measures:
No role for antibiotics in uncomplicated, mild pancreatitis
PPIs if PUD risk factors

Diet Advancement

Start oral intake as soon as tolerated (goal: within 24 hours if possible):

Mild pancreatitis: Advance to regular diet as tolerated; no specific diet restriction needed
Severe pancreatitis: Start with clear liquid diet; advance slowly if tolerating
If unable to eat: Consider enteral nutrition (nasogastric feeding) — improves outcomes vs. total parenteral nutrition

Specific Therapy by Etiology

Biliary pancreatitis with cholangitis: Urgent ERCP with sphincterotomy

Alcohol-related: Nutritional support; thiamine; folate; magnesium replacement

Diverticulitis: Uncomplicated vs. Complicated

Definition and Pathophysiology

Diverticulitis is inflammation of one or more colonic diverticula (outpouchings through the muscular wall). Inflammation can be uncomplicated (simple inflammation) or complicated (perforation, abscess, fistula).

Epidemiology

Incidence increases with age (rare <50 years in US, higher prevalence in Western countries with low-fiber diets). Right-sided diverticulitis more common in Asia.

Clinical Presentation and Diagnosis

Typical Presentation

LLQ pain (RLQ if right colon involved)
Fever (variable; may be absent in mild disease)
Altered bowel habits (constipation or loose stools)
Nausea/vomiting (if complicated)

Diagnostic Imaging

CT abdomen/pelvis with IV and oral contrast is gold standard:

Finding	Interpretation
Colonic wall thickening (>5 mm)	Indicative of colitis
Diverticula with surrounding inflammation	Diagnostic of diverticulitis
Pericolic fat stranding	Indicates degree of inflammation
Localized abscess	Suggests complicated disease; may require drainage
Free air	Suggests perforation; consider surgical consultation
Fistula tract	Communication with bladder (colovesical), small bowel (coloenteric), or other organ

Laboratory findings:

Elevated WBC (may be normal in mild disease)
Elevated CRP/procalcitonin
No pathognomonic lab tests

Uncomplicated Diverticulitis

Definition: Simple inflammation without abscess, perforation, or fistula

Outpatient Management (Select Patients)

Can manage at home if:

Immunocompetent
Tolerating oral intake
No signs of sepsis
Reliable follow-up
Pain well-controlled

Prescribe:

Bowel rest (clear liquid diet)
Oral antibiotics covering gram-negative and anaerobes:
Cipro 500 mg BID + metronidazole 500 mg TID × 7–10 days, OR
Amoxicillin-clavulanate 875 mg BID × 7–10 days
(Can defer antibiotics in mild, uncomplicated disease if no fever/elevated WBC)
Analgesia (acetaminophen preferred; avoid NSAIDs if possible due to increased perforation risk)
Follow-up: Call or visit in 24–48 hours; if worsening, go to ED

Hospitalization Indications

Fever >102°F or signs of sepsis
Inability to tolerate oral intake
Immunocompromised (diabetes, immunosuppression, age >50 with comorbidities)
Intractable pain
Failed outpatient therapy (symptoms worsening after 48–72 hours of oral antibiotics)
First episode in some centers (controversial; if uncomplicated, outpatient is reasonable)

Inpatient protocol:

NPO
IV fluid resuscitation
IV antibiotics: Ceftriaxone 1 g IV Q12H + metronidazole 500 mg IV Q8H (or piperacillin-tazobactam 4.5 g IV Q6H)
Advance diet as tolerated (usually within 48–72 hours if improving)

Complicated Diverticulitis

Diverticulitis with Abscess

CT findings: Localized fluid collection with enhanced rim

Management:

IR-guided percutaneous drainage if abscess >4 cm
IV antibiotics
Delayed elective colectomy (6–8 weeks after resolution) to prevent recurrence

Diverticulitis with Perforation and Peritonitis

Presentation: Severe pain, rigid abdomen, signs of peritonitis

CT findings: Free air, free fluid, wide pericolic stranding

Management:

Immediate surgical consultation
NPO, IV fluids, broad-spectrum antibiotics
Operative intervention: Primary resection with anastomosis (if patient stable and proximal adequate) vs. Hartmann procedure (resection with colostomy) if unstable

Diverticulitis with Fistula

Colovesical fistula (colon-bladder communication; most common):

Presentation: Pneumaturia, fecaluria, recurrent UTIs
Diagnosis: CT with fecal material in bladder, barium enema showing fistula tract
Management: Elective surgical resection of affected bowel segment

Coloenteric or colouterine fistulas: Similar principles; surgical consultation for timing and approach

Biliary Tract Disease: From Colic to Cholangitis

Spectrum of Acute Biliary Illness

Understanding the progression from simple gallstones to life-threatening cholangitis guides urgency of intervention:

Biliary Colic

Presentation

Sudden RUQ or epigastric pain lasting 30 minutes to several hours
No fever (distinguishes from cholecystitis)
No peritonitis (no Murphy's sign)
Often triggered by fatty meal

Workup

Test	Finding
RUQ ultrasound	Gallstones present; normal GB wall and no pericholecystic fluid
Labs	Normal; WBC normal, LFTs normal

Management

Conservative management; stone will typically pass
Elective cholecystectomy if recurrent symptoms (prevents progression to cholecystitis)

Acute Cholecystitis

Presentation

RUQ pain >6 hours (prolonged compared to biliary colic)
Fever (present in ~70% of cases)
Murphy's sign positive (inspiratory arrest during RUQ palpation with deep breath)
Elevated WBC

Diagnostic Criteria

Tokyo Guidelines for Acute Cholecystitis Diagnosis:

Definite: 1 + 1 from below:

RUQ tenderness + fever or elevated inflammatory markers
Imaging findings:
Gallstones + pericholecystic edema/fluid OR
Wall thickening (>4 mm) + pericholecystic fluid OR
Sonographic Murphy's sign

Imaging

Modality	Finding
RUQ US (first-line)	Gallstones + pericholecystic fluid; positive Murphy's sign; GB wall thickening
CT abdomen	Increased GB wall enhancement; pericholecystic stranding; useful if complications suspected
HIDA scan	Nonvisualization of GB (cystic duct obstruction); used if ultrasound nondiagnostic

Management

NPO
IV fluids and electrolyte correction
IV antibiotics: Cefotaxime 2 g IV Q4H + metronidazole 500 mg IV Q8H (covers gram-negative + anaerobes)
Analgesia: IV opioids
Definitive: Cholecystectomy (laparoscopic preferred) within 24–48 hours of diagnosis
Early cholecystectomy (within 72 hours) reduces complications and length of stay
Percutaneous cholecystostomy if patient too ill for surgery (bridge to definitive treatment)

Common Bile Duct Obstruction / Choledocholithiasis

Presentation

Jaundice (scleral icterus, dark urine)
Abdominal pain (epigastric or RUQ)
Elevated conjugated bilirubin and alkaline phosphatase
May be asymptomatic (discovered incidentally on imaging)

Diagnosis

Modality	Use
RUQ ultrasound	Dilated CBD (>6 mm), may show stone
MRCP	Gold standard for imaging CBD; can visualize stones, strictures, masses
ERCP	Therapeutic: stone extraction via sphincterotomy

Management

Uncomplicated choledocholithiasis:

ERCP with endoscopic sphincterotomy + stone extraction (success >90%)
Followed by cholecystectomy if symptomatic GB disease

Mirizzi syndrome (external CBD compression by impacted stone):

ERCP with stone extraction (relief of compression)
Cholecystectomy

Acute Cholangitis (Charcot's Triad)

Clinical Presentation

Charcot's triad (present in only ~50% of cases):

Fever (>38.5°C)
Right upper quadrant pain
Jaundice

Mortality increases with Reynolds' pentad (adds):

Altered mental status
Hypotension

Medical Emergency

Acute cholangitis is a medical/surgical emergency with mortality ~5–10% if untreated, higher if septic shock develops.

Pathophysiology

Bacterial infection of obstructed biliary system. Obstruction (stone, stricture, malignancy) + bacteria (often gram-negative or anaerobes from intestine) + stasis = infection.

Diagnostic Workup

Test	Finding
Labs	Elevated bilirubin, elevated ALP/GGT, elevated transaminases, elevated WBC, elevated lactate (if septic)
Blood cultures	Positive in 50–80% (draw before antibiotics)
RUQ ultrasound	Dilated intrahepatic/extrahepatic bile ducts; may show stone or mass
MRCP	Definitive; shows obstruction site and cause

Management (URGENT)

Immediate broad-spectrum IV antibiotics:
Cefotaxime 2 g IV Q4H (or cefepime/ciprofloxacin if cephalosporin allergy)
+ Metronidazole 500 mg IV Q8H (anaerobic coverage)
± Vancomycin if immunocompromised or recent hospital exposure (MRSA risk)
IV fluid resuscitation — may have sepsis; target urine output 0.5–1 mL/kg/hr
Urgent ERCP with endoscopic sphincterotomy (within 24 hours, sooner if septic or unstable):
Extract stone(s) or relieve obstruction
Success rate >90%
If ERCP fails: percutaneous transhepatic cholangiography (PTC) or surgical intervention

Do Not Delay

Do NOT delay ERCP to await imaging confirmation if clinical suspicion is high and patient deteriorating.

Diarrhea: Classification, Evaluation, and Management

Temporal Classification

Duration-based classification guides workup strategy:

Category	Duration	Typical Causes
Acute	<14 days	Viral (norovirus, rotavirus), bacterial (Salmonella, Shigella, E. coli, Campylobacter), toxins, medications
Persistent	14–30 days	Protozoal (Giardia, Entamoeba), bacterial overgrowth, IBD (early presentation), bile acid malabsorption
Chronic	>30 days	IBD (UC, Crohn's), IBS, malabsorption, medication effect (PPIs, antibiotics), functional causes

Pathophysiologic Classification

Understanding the mechanism guides diagnostic testing:

Osmotic Diarrhea

Mechanism: Unabsorbed osmotically active substances in bowel lumen

Characteristics: - Improves with fasting - Stool osmotic gap >125 mOsm/kg - Examples: Lactose intolerance, magnesium-containing laxatives, polyol malabsorption

Secretory Diarrhea

Mechanism: Active ion secretion exceeds absorption

Characteristics: - Persists with fasting (distinguishes from osmotic) - Stool osmotic gap <125 mOsm/kg - High stool output (often >1 L/day) - Examples: Cholera, VIP-secreting tumor, bile acid malabsorption, certain medications (SSRIs)

Inflammatory Diarrhea

Mechanism: Mucosal inflammation → exudation + increased motility

Characteristics: - Blood/mucus in stool - Fever, abdominal pain - Elevated fecal calprotectin/lactoferrin - Examples: IBD (UC, Crohn's), infectious colitis (C. difficile, Salmonella), ischemic colitis

Mechanism: Abnormal colonic motility

Characteristics: - Often small-volume, frequent stools - Often associated with abdominal pain/cramping - Examples: IBS, diabetic neuropathy, scleroderma

Acute Diarrhea Workup

Most acute diarrhea is viral and self-limited; selective testing indicated:

Indication	Test
Bloody stool or fever	Stool culture (Salmonella, Shigella, Campylobacter, STEC O157:H7)
Abdominal pain + fever >38.5°C	Fecal leukocytes or lactoferrin (suggests inflammatory); stool culture
Recent antibiotics	C. difficile toxin/GDH (if diarrhea onset during or within 10 days of antibiotic)
Immunocompromised (HIV CD4 <200)	Ova & parasites, stool culture, consideration of special stains
Bloody diarrhea + thrombocytopenia	Stool culture for STEC; consider HUS; no antimotility agents

First-line supportive care:

Oral rehydration solution (glucose-electrolyte solutions; WHO formulation preferred)
Antimotility agents contraindicated if fever/bloody stool (risk of toxic megacolon/HUS)
Antidiarrheals (loperamide, diphenoxylate) safe in nonbloody, afebrile diarrhea

Chronic Diarrhea Workup

Initial approach:

History: Onset, duration, stool frequency, presence of blood/mucus, timing (nocturnal vs. daytime), relation to food/stress
Physical exam: Signs of dehydration, weight loss, abdominal examination
Labs: CBC, CMP (electrolytes, renal function), thyroid function, tissue transglutaminase (celiac screening)
Imaging: Consider CT abdomen if weight loss or alarm symptoms

Further testing guided by classification:

Stool osmolality, electrolytes (osmotic gap calculation)
Fecal fat (72-hour collection to assess for steatorrhea)
Fecal calprotectin/lactoferrin (screen for IBD/inflammatory causes)
Colonoscopy (if alarm features, bloody stool, age >50, family history of colorectal cancer)

Clostridioides difficile Infection (CDI)

Epidemiology and Risk Factors

Risk factors:

Antibiotic use (fluoroquinolones, clindamycin, cephalosporins; risk increases with duration)
Advanced age
Severe underlying illness
Immunosuppression
Prior CDI
PPI use (reduces gastric acid barrier)

Clinical Presentation

Spectrum ranges from asymptomatic colonization to fulminant colitis:

Mild-moderate: Watery diarrhea (≥3 unformed stools/24 hr), abdominal cramping, low-grade fever
Fulminant: Toxic megacolon, sepsis, shock, high mortality

Diagnosis

NAAT (nucleic acid amplification test) or enzyme immunoassay (EIA) for C. difficile toxins A/B:

Testing Pitfalls

Do NOT retest during treatment or for 4 weeks after treatment ends (test of cure not recommended; toxin can persist).

Treatment

First-line therapy:

Severity	Agent	Dosing	Duration
Initial, non-severe	Vancomycin (oral only; doesn't get absorbed systemically)	125 mg PO QID	10 days
Severe (Cr >1.5× baseline or fever/leukocytosis)	Vancomycin	125 mg PO QID	10 days
Fulminant	Vancomycin	500 mg PO/NG QID + IV metronidazole 500 mg Q8H	10 days
Recurrent (first or second)	Fidaxomicin	200 mg PO BID	10 days

Second-line agents:

Fidaxomicin 200 mg BID × 10 days (superior for preventing recurrence vs. vancomycin; higher cost)
Metronidazole (only if vancomycin unavailable; inferior outcomes for non-severe CDI)

Adjunctive measures:

Discontinue offending antibiotic if possible
Avoid antimotility agents (risk of toxic megacolon)
Fecal microbiota transplantation (FMT) for multiple recurrences

Last update: April 20, 2026