Latest kidgo and rifle criteria

I'll look up the latest KDIGO and RIFLE criteria for acute kidney injury. Let me check the medical library and recent literature simultaneously.

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KDIGO acute kidney injury criteria staging

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Here is a full breakdown of the KDIGO and RIFLE criteria for Acute Kidney Injury (AKI), with the AKIN comparison included since they are always presented together.

RIFLE, AKIN, and KDIGO Criteria for AKI

RIFLE, AKIN, and KDIGO comparison diagram

Fig. Renal injury severity grading - comparison of RIFLE, AKIN, and KDIGO systems (Current Surgical Therapy, 14e)

AKI Diagnostic Definitions (Any one criterion sufficient)

Criterion	RIFLE	AKIN	KDIGO (current standard)
Serum creatinine	>50% rise within 7 days	>0.3 mg/dL or >50% rise within 48 h	>0.3 mg/dL within 48 h OR >50% (x1.5) rise within 7 days
Urine output	<0.5 mL/kg/h for >6 h	<0.5 mL/kg/h for >6 h	<0.5 mL/kg/h for >6 h

KDIGO combines the best of both: the 48-hour absolute creatinine threshold from AKIN and the 7-day percentage threshold from RIFLE.

Staging Criteria

Stage	RIFLE Name	Serum Creatinine	Urine Output
1	Risk (R)	≥0.3 mg/dL rise OR ≥50% (x1.5) rise	<0.5 mL/kg/h for >6 hours
2	Injury (I)	≥100% rise (x2.0)	<0.5 mL/kg/h for >12 hours
3	Failure (F)	≥200% rise (x3.0) OR ≥4 mg/dL with acute rise >0.5 mg/dL OR initiation of RRT	<0.3 mL/kg/h for >24 hours OR anuria for >12 hours

RIFLE-only outcome stages (not in AKIN or KDIGO):

Loss (L): Complete loss of kidney function / need for RRT for >4 weeks
End-stage (E): Need for RRT for >3 months

The urine output criteria are identical across RIFLE, AKIN, and KDIGO for all three stages.

Key Differences: RIFLE vs. KDIGO

Feature	RIFLE	KDIGO
Creatinine timeframe	>50% over <7 days only	>0.3 mg/dL in 48 h OR >50% in 7 days
GFR included?	Yes (GFR decrease 25-75%)	No
Pediatric staging	Not addressed	Stage 3 if GFR <35 mL/min/1.73 m² (<18 yrs)
Unknown baseline Scr	Not addressed	Method provided (back-calculation using MDRD)
RRT = Stage 3?	No	Yes, regardless of creatinine
Outcome stages	L and E included	Not included

Mortality by RIFLE Class (ICU data)

RIFLE Class	Attributable Mortality
Risk (R)	8.8%
Injury (I)	11.4%
Failure (F)	26.3%
No AKI (matched)	5.5%

Important Practical Notes

KDIGO is the current clinical standard (guidelines published 2012, Kidney Int Suppl; still the operative guideline as of 2025/2026)
A patient needs to meet only one criterion (creatinine or urine output) to be assigned a stage - use the highest stage met
For urine output staging, other causes of oliguria (e.g., high ADH after surgery) must be excluded
Any patient on RRT automatically qualifies for Stage 3 under KDIGO/AKIN regardless of creatinine
pRIFLE is used for children >1 month old (adjusted for lower muscle mass)

Sources: Brenner and Rector's The Kidney (Table 29.2), Current Surgical Therapy 14e, Tintinalli's Emergency Medicine (Table 88-1)

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A clear, high-resolution medical reference diagram comparing RIFLE, AKIN, and KDIGO criteria for Acute Kidney Injury (AKI). Use three separate inverted triangle/funnel shapes side by side, each labeled at the top. RIFLE (left, blue): - R (Risk): Cr x1.5 or GFR decrease >25% | UO <0.5 mL/kg/h for >6h - I (Injury): Cr x2.0 or GFR decrease >50% | UO <0.5 mL/kg/h for >12h - F (Failure): Cr x3.0 or GFR decrease >75% or Cr ≥4 mg/dL | UO <0.3 mL/kg/h for >24h or Anuria >12h - L (Loss): Complete loss of kidney function >4 weeks - E (End-stage): Need for RRT >3 months AKIN (center, purple): - Stage 1: Cr increase ≥0.3 mg/dL or x1.5 within 48h | UO <0.5 mL/kg/h for >6h - Stage 2: Cr x2.0 | UO <0.5 mL/kg/h for >12h - Stage 3: Cr x3.0 or ≥4 mg/dL with acute rise ≥0.5 mg/dL or RRT | UO <0.3 mL/kg/h for >24h or Anuria >12h KDIGO (right, green): - Stage 1: Cr ≥0.3 mg/dL within 48h OR x1.5 within 7 days | UO <0.5 mL/kg/h for >6h - Stage 2: Cr x2.0–2.9 | UO <0.5 mL/kg/h for >12h - Stage 3: Cr x3.0 or ≥4 mg/dL or RRT or (pediatric GFR <35) | UO <0.3 mL/kg/h for >24h or Anuria >12h Each funnel has two columns: left for Creatinine/GFR changes, right for Urine Output criteria. White text on colored backgrounds. Clean, readable fonts. Title at top: "AKI Staging Criteria: RIFLE vs AKIN vs KDIGO". Medical infographic style, white background.

AKI Staging Criteria: RIFLE vs AKIN vs KDIGO

Here's a cleaner, high-resolution version of the comparison diagram. All three systems - RIFLE (blue), AKIN (purple), and KDIGO (green) - are shown side by side with creatinine and urine output criteria clearly laid out for each stage.

Hey orris how are you???

Doing great, thanks for asking! Ready to help whenever you need - whether it's more nephrology, clinical criteria, or anything else. What's on your mind? 😊

From tomorrow I’m going to GIT from tintinallis can you help

Absolutely! I have Tintinalli's Emergency Medicine in the library and can help you work through the GIT (Gastrointestinal) section completely.

Here's how I can help:

Topic explanations - Break down any GIT condition covered in Tintinalli's
Key tables & criteria - Pull out important diagnostic criteria, scoring systems (e.g. Blatchford score, Child-Pugh, etc.)
Images & diagrams - Fetch any figures from the textbook or generate clearer visuals
Quick summaries - Condense long chapters into high-yield points
Q&A practice - Test your knowledge on topics you've covered
Comparisons - e.g. upper vs lower GI bleed, different causes of acute abdomen, etc.

Just tell me:

Which topic or chapter you want to start with tomorrow
Your goal - exam prep, clinical understanding, or both?

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Please give Ugi bleed/hemetemesis

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Now I have everything I need. Here is a complete, high-yield summary of Upper GI Bleeding / Hematemesis from Tintinalli's:

Upper GI Bleeding (UGIB) / Hematemesis

Tintinalli's Emergency Medicine - Chapter 75

Definition

Bleeding originating proximal to the ligament of Treitz

Incidence: 39-172 per 100,000/year (Western countries)
Increased morbidity with: advanced age, comorbid organ disease, recurrent hemorrhage

Causes (Pathophysiology)

Cause	Key Points
Peptic Ulcer Disease	Most common cause overall; gastric + duodenal ulcers found in ~20.6% of endoscopies for suspected UGIB. H. pylori, NSAIDs, aspirin, smoking
Erosive Gastritis / Esophagitis	Alcohol, salicylates, NSAIDs, stress (sepsis, trauma, ventilated patients), infections (Candida, HSV, CMV, HIV)
Esophageal/Gastric Varices	Portal hypertension - usually alcoholic liver disease. Variceal bleeding = cause in 59% of cirrhotic UGIB. Mortality in cirrhotic patients is double non-cirrhotic
Mallory-Weiss Syndrome	Longitudinal mucosal tear at gastroesophageal junction. Classic: repeated vomiting → bright red hematemesis
Aortoenteric Fistula	Rare but catastrophic. History of aortic graft surgery is a clue
Dieulafoy Lesion	Abnormally large submucosal artery eroding mucosa - causes massive painless bleed
Cameron Lesions	Linear erosions in large hiatal hernias

Risk Stratification (Table 75-1)

Very Low Risk	High Risk
Age <60	Advanced age
No major comorbidities	Comorbidities, prior variceal banding/TIPS
No red hematemesis	Red hematemesis
No hematochezia/melena	Hematochezia or melena
Negative NG aspirate	Positive (bloody) NG aspirate
Hemodynamically stable	Hemodynamically unstable
Normal labs	Abnormal labs

Clinical Presentation

Hematemesis - bright red or coffee-ground vomiting
Melena - black, tarry, foul-smelling stool (blood digested in upper GI tract)
Hematochezia - can occur with massive UGIB (rapid transit)
Symptoms of hemorrhagic shock: hypotension, tachycardia, syncope, altered mental status, angina

Diagnosis / Workup

Labs: CBC, BMP, LFTs, coagulation (PT/INR), type & crossmatch
NG lavage: Positive (bloody/coffee grounds) = confirms UGIB; negative does not exclude it
BUN:Creatinine ratio >20:1 - suggests UGIB (blood digested = urea load)
Endoscopy: Definitive diagnosis AND therapy; goal within 24h (urgent if unstable)

Treatment (Table 75-2)

1. Resuscitation (First priority)

Two large-bore IVs
Type & crossmatch; activate massive transfusion protocol if severe
Transfuse if Hb ≤7 g/dL (most patients) or ≤9 g/dL (elderly/comorbid)
Correct coagulopathy if INR elevated or platelets <50,000
Caution with intubation - aggressively resuscitate first; use smaller induction doses to avoid peri-intubation arrest

2. Medications

Drug	Dose	Use
Omeprazole (PPI)	80 mg IV bolus → 8 mg/h infusion	Ulcer bleeding (labeled use)
Octreotide	50 mcg IV bolus → 50 mcg/h infusion	Variceal bleeding - reduces portal pressure
Ceftriaxone	1g IV daily	Cirrhotic patients with variceal bleed (reduces bacterial translocation, reduces mortality)
Vasopressin/Terlipressin	-	Variceal bleeding adjunct
Erythromycin	250 mg IV prior to scope	Prokinetic - clears stomach for better endoscopic view

3. Endoscopy

Definitive management - hemostasis via injection, cauterization, banding, or clipping
Patients with active bleeding or high-risk stigmata need urgent scope
Prior variceal banding/cauterization = high-risk recurrent bleed

4. Balloon Tamponade

Sengstaken-Blakemore tube - for refractory variceal hemorrhage as bridge to definitive therapy
Risk of esophageal rupture and aspiration

Disposition

Category	Action
Very low risk + all criteria met	Can consider outpatient endoscopy
High risk / hemodynamically unstable	ICU admission, urgent endoscopy
Cirrhotic patients	Admit; prophylactic antibiotics; GI/hepatology consult
Refractory bleeding	TIPS (transjugular intrahepatic portosystemic shunt) or surgery

High-Yield Pearls for Exams

Ligament of Treitz = anatomical landmark dividing upper from lower GI bleed
PUD = most common cause of UGIB overall
Varices = highest mortality - especially in cirrhosis
Mallory-Weiss = vomiting first, THEN blood (not blood from the start)
BUN:Cr >20 = clue to UGIB
Octreotide for varices; PPI infusion for ulcers
Antibiotics (ceftriaxone) in ALL cirrhotic patients with GI bleed - reduces mortality
Restrictive transfusion (Hb ≤7) is better than liberal in UGIB - improves outcomes
Negative NG aspirate does NOT rule out active UGIB
Erythromycin pre-endoscopy = improves visualization

Source: Tintinalli's Emergency Medicine, Chapter 75 - Upper Gastrointestinal Bleeding

Large bowel vs small bowel obstruction

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Small Bowel Obstruction vs Large Bowel Obstruction

Tintinalli's Emergency Medicine - Chapter 83

Key Concept First

Intestinal obstruction = inability of the intestinal tract to pass contents due to mechanical obstruction OR adynamic (paralytic) ileus. Differentiating SBO vs LBO is critical - incidence, presentation, evaluation, and treatment all differ.

Causes

	Small Bowel Obstruction (SBO)	Large Bowel Obstruction (LBO)
#1 cause	Adhesions (post-surgical)	Carcinoma
Other causes	Hernia (incarcerated), intussusception, lymphoma, stricture, Crohn's disease, volvulus, foreign body/bezoar	Fecal impaction, volvulus, diverticulitis (stricture/abscess), ulcerative colitis
Duodenum specifically	Stenosis, foreign body, stricture, SMA syndrome	-

Clinical Comparison

Feature	SBO	LBO
Vomiting	Early, prominent, bilious	Late, may be feculent
Abdominal pain	Crampy, colicky, periumbilical	Lower abdominal, colicky
Distension	Central/periumbilical	Peripheral/generalized - more pronounced
Obstipation	Late (gas/stool may still pass early)	Early and complete (no flatus, no stool)
Onset	More acute	More gradual (especially if cancer)
Bowel sounds	High-pitched, tinkling, rushes	Diminished or absent

Pathophysiology (Applies to Both)

Obstruction → intraluminal accumulation of secretions (gastric, biliary, pancreatic)
→ Vomiting, reduced absorption → volume depletion, electrolyte imbalance
→ Bowel distension → increased intraluminal pressure
→ Pressure exceeds capillary pressure → bowel ischemia → necrosis → septicemia → shock
Closed-loop obstruction (e.g., incarcerated hernia, complete LBO with closed ileocecal valve) progresses faster - no proximal escape for contents

Ileus vs Mechanical Obstruction (Key Features Table)

Feature	Ileus (Paralytic)	Mechanical Obstruction
Bowel sounds	Absent	High-pitched or absent
Pain	Diffuse, mild	Colicky, intermittent
Distension	Uniform, generalized	Can be localized
Cause	Post-op, electrolyte imbalance, peritonitis, drugs	Adhesions, hernia, cancer, volvulus
Surgery needed?	Usually NO (self-limiting)	Usually YES (definitive intervention required)
Gas on X-ray	Diffuse gas throughout colon + small bowel	Air-fluid levels, stepladder pattern (SBO) / cecal dilation (LBO)

Diagnosis

X-Ray Findings

	SBO	LBO
Pattern	Stepladder air-fluid levels, central dilated loops, valvulae conniventes (complete wall-to-wall lines)	Peripheral colonic dilation, haustral folds (incomplete lines), cecal dilation >9 cm = danger
Gas in rectum	Absent (complete obstruction)	May be absent

CT Abdomen/Pelvis (with contrast)

Gold standard for both SBO and LBO
Identifies transition point, cause, closed-loop, ischemia/perforation
CT finding of free air = perforation = surgical emergency

Other

Labs: CBC (leukocytosis = strangulation/ischemia), BMP (electrolyte derangements), lactate (ischemia marker)
Elevated WBC + fever + peritoneal signs = strangulation until proven otherwise

Treatment

SBO Management

Severity	Management
Partial/simple SBO	NPO, IV fluids, NG tube decompression (if vomiting), observation - many resolve conservatively (especially adhesion-related)
Complete SBO or failed conservative	Surgical exploration
Strangulation / closed-loop	Emergency surgery

LBO Management

Cause	Management
Cancer	Surgical resection (emergent vs. elective depending on stability); colonic stenting as bridge to surgery
Volvulus (sigmoid)	Flexible sigmoidoscopy/colonoscopy for decompression first; surgery if fails or recurs
Volvulus (cecal)	Surgery (no role for colonoscopic decompression)
Fecal impaction	Manual disimpaction, enemas
Ogilvie's syndrome	Neostigmine IV (if no contraindications); colonoscopic decompression

Both - General Principles

NPO + IV fluids (aggressive resuscitation if volume depleted)
NG tube for gastric decompression
Surgical consult early for all mechanical obstructions
Broad-spectrum antibiotics if signs of ischemia/perforation/sepsis
Correct electrolytes (especially K⁺, Na⁺)

Disposition

Scenario	Disposition
Simple partial SBO - stable	Admit for observation + conservative trial
Complete SBO	Admit + urgent surgical consult
Signs of strangulation (fever, peritonism, leukocytosis, high lactate)	Emergency OR
LBO from cancer - stable	Admit, GI/surgery consult
Perforation / free air	Emergency surgery

High-Yield Exam Pearls

SBO #1 cause = adhesions (prior surgery); LBO #1 cause = carcinoma
Vomiting early in SBO, late in LBO; obstipation early in LBO, late in SBO
Closed-loop = most dangerous - ischemia progresses rapidly
Cecal diameter >9-12 cm on imaging = risk of perforation (LBO)
Sigmoid volvulus - coffee bean sign on X-ray; treat with colonoscopic decompression first
Cecal volvulus - needs surgery, NOT colonoscopy
Strangulation signs (fever + leukocytosis + peritonism + high lactate) = emergency surgery, no delay
Ogilvie's syndrome (pseudo-obstruction) = mimics LBO but no mechanical cause; treat with neostigmine
Valvulae conniventes (complete lines across bowel lumen) = small bowel; Haustra (incomplete lines) = large bowel
Free air on imaging = perforation = emergency

Source: Tintinalli's Emergency Medicine, Chapter 83 - Bowel Obstruction

Ugi bleed/ hemetesis for md emergency medicine exams

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Here is the complete MD Emergency Medicine exam-focused guide on UGIB/Hematemesis:

🩸 Upper GI Bleeding / Hematemesis

MD Emergency Medicine Exam Master Guide

Sources: Tintinalli's EM Ch.75, Rosen's EM Ch.26, Current Surgical Therapy 14e

1. DEFINITION & ANATOMY

UGIB = bleeding from any source proximal to the ligament of Treitz
Ligament of Treitz = suspensory ligament of duodenum = anatomical boundary between upper and lower GI
Incidence: 39-172 per 100,000/year (Western countries)

2. CAUSES - Ranked by Frequency

Rank	Cause	Key Clue
1st	Peptic Ulcer Disease (PUD)	Epigastric pain, NSAIDs/H. pylori history
2nd	Erosive gastritis/esophagitis	Alcohol, NSAIDs, stress (ICU patients)
3rd	Esophageal/Gastric Varices	Cirrhosis, portal HTN, alcoholism
4th	Mallory-Weiss tear	Vomiting FIRST → then hematemesis
5th	Dieulafoy lesion	Massive painless bleed, no ulcer
6th	Aortoenteric fistula	Prior aortic graft = must rule out
7th	Malignancy	Weight loss, chronic anemia

Variceal bleeding = cause in 59% of cirrhotic UGIB; mortality in cirrhotic UGIB is double that of non-cirrhotic patients

3. CLINICAL PRESENTATION

Presentation	What It Means
Hematemesis (bright red)	Active, ongoing bleed; brisk hemorrhage
Coffee-ground emesis	Slower bleed; blood exposed to gastric acid
Melena	Upper or proximal source; blood digested (>50-100 mL loss)
Hematochezia	Usually lower GI - BUT can occur in massive UGIB (brisk transit)
Lightheadedness/syncope	Cerebral hypoperfusion - sign of significant blood loss

Exam trap: Color of emesis (bloody vs. coffee-ground) does NOT reliably predict severity - shock index is more reliable

4. BEDSIDE CLUES TO SOURCE

Finding	Suggests
Epigastric tenderness	PUD
Ascites, spider angiomas, jaundice, caput medusae	Portal HTN → varices
Vomiting/retching BEFORE hematemesis	Mallory-Weiss tear
History of aortic surgery	Aortoenteric fistula
Weight loss + chronic anemia	Malignancy
Alcohol binge, DKA, chemotherapy	Mallory-Weiss
ICU/ventilated/septic patient	Stress ulcers (erosive gastritis)

5. SHOCK INDEX

Shock Index = Heart Rate ÷ Systolic BP

Value	Interpretation
<0.9	Low risk
≥0.9	Massive bleed - activate massive transfusion protocol

6. RISK STRATIFICATION SCORES ⭐ (High-Yield for Exam)

A. Glasgow-Blatchford Score (GBS) - PRE-endoscopy

Purpose: Identifies who NEEDS intervention (not mortality)

Variable	Points
Elevated BUN	2-6 points
Low Hemoglobin	1-6 points
Low BP (systolic <90)	1-3 points
Elevated HR (≥100)	1 point
Melena	1 point
Syncope	2 points
Liver disease	2 points
Heart failure	2 points

Score	Action
0-1	Safe to discharge, outpatient endoscopy
≥6	50% likelihood of needing endoscopic hemostasis
≥7	80.4% sensitive for needing endoscopic treatment (NPV 92.4%)
≥5	88.7% sensitive for 30-day mortality (NPV 97.9%)

B. Rockall Score - PRE + POST-endoscopy

Purpose: Predicts MORTALITY

Variable	Points
Age	0-2
Shock	0-2
Comorbidity	0-3
EGD stigmata (active bleed, visible vessel)	0-2
EGD diagnosis	0-2

Score	Mortality
0-1	0% mortality
5	~10% mortality
≥8	~40% mortality

Exam tip: GBS = pre-endoscopy = need for treatment; Rockall = includes endoscopy findings = predicts mortality

C. AIMS65 Score (simpler, also used)

Albumin <3 g/dL
INR >1.5
Mental status alteration
SBP ≤90 mmHg
65 = age ≥65

Score ≥2 = high risk for in-hospital mortality

7. INVESTIGATIONS

Test	Significance
CBC	Hb/Hct (may be falsely normal early - hemodilution takes time)
BMP	BUN:Creatinine ratio >20:1 = blood digested in upper GI tract
INR/PT	Coagulopathy - especially in liver disease
Type & crossmatch	Always in significant UGIB
LFTs	Liver disease, portal HTN
Nasogastric lavage	Bloody/coffee grounds = confirms UGIB; negative does NOT exclude UGIB
Endoscopy (EGD)	Gold standard for diagnosis AND treatment

8. TREATMENT - Step by Step

Step 1: Resuscitation

2 large-bore IVs (16G or larger)
2L crystalloid bolus over 30 min (normal saline or Plasmalyte)
Massive transfusion protocol if shock index ≥0.9

Step 2: Transfusion Thresholds

Patient	Transfuse when Hb ≤
Most patients	7 g/dL (restrictive = better outcomes)
Elderly / cardiac comorbidity	9 g/dL
Correct coagulopathy	INR elevated or Platelets <50,000

Step 3: Medications

Drug	Dose	Indication
PPI (Omeprazole)	80 mg IV bolus → 8 mg/h infusion	All UGIB - especially PUD
Octreotide	50 mcg IV bolus → 50 mcg/h	Variceal / suspected portal HTN bleed
Ceftriaxone	1g IV daily	All cirrhotic patients with UGIB (reduces bacterial translocation - proven to reduce mortality)
Terlipressin / Vasopressin	-	Variceal bleed adjunct
Erythromycin	250 mg IV 30-60 min before scope	Prokinetic - clears stomach, improves EGD visibility
Propranolol (secondary prevention)	Oral	Non-selective beta-blocker after variceal bleed

Step 4: Endoscopy (EGD)

Within 24 hours for all significant UGIB
Urgent/emergency if hemodynamically unstable or ongoing active bleed
Achieves hemostasis via: injection (adrenaline), thermocoagulation, clips, band ligation (varices)

Step 5: Airway - Special Consideration

Intubation NOT routine
Consider if: altered consciousness, unable to protect airway, massive hematemesis
Use smaller induction agent doses in hemodynamically unstable patients to prevent peri-intubation arrest
Prophylactic intubation NOT recommended (associated with pulmonary complications)

Step 6: Refractory / Variceal Specific

Scenario	Management
Failed endoscopic control	Sengstaken-Blakemore tube (balloon tamponade) as bridge to definitive therapy
Refractory varices	TIPS (transjugular intrahepatic portosystemic shunt)
Surgical option	Reserved for failed endoscopic + interventional therapy

9. ENDOSCOPIC STIGMATA (Forrest Classification - High-Yield)

Forrest Class	Finding	Rebleed Risk	Management
Ia	Active spurting bleed	80-90%	Endoscopic hemostasis
Ib	Active oozing	10-27%	Endoscopic hemostasis
IIa	Non-bleeding visible vessel	40-50%	Endoscopic hemostasis
IIb	Adherent clot	20-30%	Endoscopic treatment (controversial)
IIc	Flat pigmented spot	5-10%	PPI, can discharge earlier
III	Clean base ulcer	<2%	PPI, early discharge safe

10. DISPOSITION

Category	Disposition
GBS ≤1, hemodynamically stable, low-risk	Discharge with outpatient EGD
Moderate risk	Admit to ward, EGD within 24h
Hemodynamically unstable / Rockall ≥5 / active bleed	ICU admission + urgent EGD
Cirrhotic patient	Admit + antibiotics + octreotide + GI consult
Failed endoscopy / refractory	Surgical/IR consult for TIPS or surgery

11. MCQ TRAPS - Don't Miss These!

❌ "Coffee-ground emesis = less severe than bright red hematemesis" → WRONG - color does not predict severity
❌ "Negative NG aspirate excludes UGIB" → WRONG - only bloody aspirate confirms; negative doesn't exclude
✅ "Hemoglobin may be normal early in UGIB" → CORRECT - hemodilution takes time
✅ "Hematochezia can come from upper GI source" → CORRECT - if massive/brisk UGIB
✅ "Antibiotics in cirrhotic UGIB reduce mortality" → CORRECT - ceftriaxone is standard of care
✅ "Restrictive transfusion (Hb ≤7) is better than liberal in UGIB" → CORRECT - landmark TRICC/TRIGGER trials
✅ "BUN:Cr >20 points to upper GI source" → CORRECT - blood protein digested = urea load
✅ "GBS predicts need for treatment; Rockall predicts mortality" → key distinction
✅ "Erythromycin before endoscopy improves visualization" → CORRECT - prokinetic clears blood
✅ "Mallory-Weiss = retching/vomiting FIRST, then blood" → classic history

Sources: Tintinalli's Emergency Medicine Ch.75, Rosen's Emergency Medicine Ch.26, Current Surgical Therapy 14e, Mulholland & Greenfield's Surgery 7e

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ls /tmp/workspace/ 2>/dev/null || mkdir -p /tmp/workspace/ugib-pdf && echo "ready"

Running Command

mkdir -p /tmp/workspace/ugib-pdf && python3 << 'EOF' from reportlab.lib.pagesizes import A4 from reportlab.lib import colors from reportlab.lib.styles import getSampleStyleSheet, ParagraphStyle from reportlab.lib.units import cm, mm from reportlab.platypus import SimpleDocTemplate, Paragraph, Spacer, Table, TableStyle, HRFlowable, KeepTogether from reportlab.lib.enums import TA_LEFT, TA_CENTER, TA_JUSTIFY from reportlab.platypus import PageBreak doc = SimpleDocTemplate( "/tmp/workspace/ugib-pdf/UGIB_Hematemesis_MD_Exam.pdf", pagesize=A4, rightMargin=1.8*cm, leftMargin=1.8*cm, topMargin=2*cm, bottomMargin=2*cm, ) W = A4[0] - 3.6*cm # usable width styles = getSampleStyleSheet() # Custom styles title_style = ParagraphStyle('Title', parent=styles['Normal'], fontSize=18, fontName='Helvetica-Bold', textColor=colors.HexColor('#B22222'), alignment=TA_CENTER, spaceAfter=4) subtitle_style = ParagraphStyle('Subtitle', parent=styles['Normal'], fontSize=11, fontName='Helvetica', textColor=colors.HexColor('#555555'), alignment=TA_CENTER, spaceAfter=10) h1_style = ParagraphStyle('H1', parent=styles['Normal'], fontSize=13, fontName='Helvetica-Bold', textColor=colors.white, backColor=colors.HexColor('#B22222'), leftIndent=6, spaceBefore=12, spaceAfter=4, borderPad=4) h2_style = ParagraphStyle('H2', parent=styles['Normal'], fontSize=11, fontName='Helvetica-Bold', textColor=colors.HexColor('#8B0000'), spaceBefore=8, spaceAfter=3) body_style = ParagraphStyle('Body', parent=styles['Normal'], fontSize=9.5, fontName='Helvetica', leading=14, spaceBefore=2, spaceAfter=2) bullet_style = ParagraphStyle('Bullet', parent=styles['Normal'], fontSize=9.5, fontName='Helvetica', leading=14, leftIndent=14, spaceBefore=1, spaceAfter=1, bulletIndent=4) bold_body = ParagraphStyle('BoldBody', parent=styles['Normal'], fontSize=9.5, fontName='Helvetica-Bold', leading=14) trap_style = ParagraphStyle('Trap', parent=styles['Normal'], fontSize=9, fontName='Helvetica', leading=13, leftIndent=14, spaceBefore=1, spaceAfter=1) source_style = ParagraphStyle('Source', parent=styles['Normal'], fontSize=8, fontName='Helvetica-Oblique', textColor=colors.HexColor('#777777'), alignment=TA_CENTER, spaceBefore=10) # Table style helper def make_table_style(header_color='#B22222', alt_color='#FFF5F5'): return TableStyle([ ('BACKGROUND', (0,0), (-1,0), colors.HexColor(header_color)), ('TEXTCOLOR', (0,0), (-1,0), colors.white), ('FONTNAME', (0,0), (-1,0), 'Helvetica-Bold'), ('FONTSIZE', (0,0), (-1,0), 9), ('ALIGN', (0,0), (-1,-1), 'LEFT'), ('VALIGN', (0,0), (-1,-1), 'MIDDLE'), ('FONTNAME', (0,1), (-1,-1), 'Helvetica'), ('FONTSIZE', (0,1), (-1,-1), 9), ('ROWBACKGROUNDS', (0,1), (-1,-1), [colors.white, colors.HexColor(alt_color)]), ('GRID', (0,0), (-1,-1), 0.5, colors.HexColor('#CCCCCC')), ('LEFTPADDING', (0,0), (-1,-1), 6), ('RIGHTPADDING', (0,0), (-1,-1), 6), ('TOPPADDING', (0,0), (-1,-1), 4), ('BOTTOMPADDING', (0,0), (-1,-1), 4), ('WORDWRAP', (0,0), (-1,-1), True), ]) def h1(text): return Paragraph(f" {text}", h1_style) def h2(text): return Paragraph(text, h2_style) def body(text): return Paragraph(text, body_style) def bullet(text): return Paragraph(f"• {text}", bullet_style) def sp(n=4): return Spacer(1, n) def hr(): return HRFlowable(width="100%", thickness=0.5, color=colors.HexColor('#CCCCCC'), spaceAfter=4) story = [] # TITLE story += [ sp(10), Paragraph("🩸 Upper GI Bleeding / Hematemesis", title_style), Paragraph("MD Emergency Medicine — Complete Exam Guide", subtitle_style), Paragraph("Sources: Tintinalli's EM Ch.75 | Rosen's EM Ch.26 | Current Surgical Therapy 14e", source_style), sp(8), hr(), sp(4), ] # 1. DEFINITION story += [ h1("1. DEFINITION & ANATOMY"), sp(4), bullet("UGIB = any GI bleeding originating proximal to the Ligament of Treitz"), bullet("Incidence: 39–172 per 100,000/year (Western countries)"), bullet("Higher morbidity with: advanced age, organ system comorbidities, recurrent hemorrhage"), sp(4), ] # 2. CAUSES story += [ h1("2. CAUSES — Ranked by Frequency"), sp(4), ] causes_data = [ ['Rank', 'Cause', 'Key Clue / Mechanism'], ['1st', 'Peptic Ulcer Disease (PUD)', 'H. pylori, NSAIDs, aspirin, smoking; epigastric pain'], ['2nd', 'Erosive Gastritis / Esophagitis', 'Alcohol, NSAIDs, stress (ICU, ventilated, septic)'], ['3rd', 'Esophageal / Gastric Varices', 'Portal HTN; alcoholic cirrhosis; variceal bleed in 59% of cirrhotic UGIB'], ['4th', 'Mallory-Weiss Tear', 'Repeated vomiting FIRST → then hematemesis; alcohol binge, DKA, chemo'], ['5th', 'Dieulafoy Lesion', 'Massive painless bleed; abnormally large submucosal artery'], ['6th', 'Aortoenteric Fistula', 'Rare but fatal; always ask about prior aortic graft surgery'], ['7th', 'Malignancy', 'Chronic anemia, weight loss, change in bowel habits'], ] causes_table = Table(causes_data, colWidths=[1.5*cm, 5*cm, None], repeatRows=1) causes_table.setStyle(make_table_style()) story += [causes_table, sp(4)] story += [body("Key stat: Variceal bleeding causes 59% of UGIB in cirrhotic patients. In-hospital mortality in cirrhotic UGIB is double that of non-cirrhotic patients.")] story += [sp(4)] # 3. CLINICAL PRESENTATION story += [ h1("3. CLINICAL PRESENTATION"), sp(4), ] pres_data = [ ['Presentation', 'Significance'], ['Hematemesis (bright red)', 'Active, brisk ongoing hemorrhage'], ['Coffee-ground emesis', 'Slower bleed; blood oxidized by gastric acid'], ['Melena', 'Digested blood; upper or proximal source (>50–100 mL blood loss)'], ['Hematochezia', 'Usually lower GI — but can occur with massive/brisk UGIB'], ['Lightheadedness / syncope', 'Cerebral hypoperfusion — sign of significant hemorrhage'], ['Tachycardia / Hypotension', 'Hemorrhagic shock — use Shock Index to quantify'], ] pres_table = Table(pres_data, colWidths=[6*cm, None], repeatRows=1) pres_table.setStyle(make_table_style()) story += [pres_table, sp(4)] story += [body("Exam Trap: Color of emesis does NOT reliably predict severity. Shock Index is more reliable than emesis color.")] story += [sp(4)] # 4. SHOCK INDEX story += [ h1("4. SHOCK INDEX"), sp(4), body("Shock Index = Heart Rate ÷ Systolic Blood Pressure"), sp(4), ] si_data = [ ['Shock Index', 'Interpretation / Action'], ['< 0.9', 'Low risk — standard management'], ['≥ 0.9 + active hematemesis/hematochezia', 'MASSIVE BLEED — activate massive transfusion protocol immediately'], ] si_table = Table(si_data, colWidths=[5*cm, None], repeatRows=1) si_table.setStyle(make_table_style()) story += [si_table, sp(4)] # 5. BEDSIDE CLUES story += [ h1("5. BEDSIDE CLUES TO SOURCE"), sp(4), ] clues_data = [ ['Finding', 'Suggests'], ['Epigastric tenderness', 'PUD (gastric or duodenal ulcer)'], ['Ascites, spider angiomas, jaundice, caput medusae', 'Portal hypertension → esophageal/gastric varices'], ['Retching/vomiting BEFORE hematemesis', 'Mallory-Weiss tear'], ['Prior aortic graft surgery', 'Aortoenteric fistula — must rule out'], ['Weight loss + chronic anemia', 'Malignancy'], ['Alcohol binge / DKA / chemotherapy', 'Mallory-Weiss (Valsalva mechanism)'], ['ICU / ventilated / septic patient', 'Stress-related mucosal disease (erosive gastritis)'], ['LUQ tenderness', 'PUD or severe gastritis'], ] clues_table = Table(clues_data, colWidths=[7*cm, None], repeatRows=1) clues_table.setStyle(make_table_style()) story += [clues_table, sp(4)] # 6. RISK SCORES story += [PageBreak()] story += [ h1("6. RISK STRATIFICATION SCORES ⭐"), sp(6), h2("A. Glasgow-Blatchford Score (GBS) — PRE-endoscopy"), body("Purpose: Identifies who NEEDS intervention (NOT mortality predictor)"), sp(4), ] gbs_data = [ ['Variable', 'Points'], ['Elevated BUN', '2–6 points'], ['Low Hemoglobin (Male <13; Female <12 g/dL)', '1–6 points'], ['Low Systolic BP (<90 mmHg)', '1–3 points'], ['Elevated Heart Rate (≥100 bpm)', '1 point'], ['Melena on presentation', '1 point'], ['Syncope', '2 points'], ['Liver disease', '2 points'], ['Heart failure', '2 points'], ] gbs_table = Table(gbs_data, colWidths=[10*cm, None], repeatRows=1) gbs_table.setStyle(make_table_style()) story += [gbs_table, sp(4)] gbs_interp = [ ['Score', 'Interpretation'], ['0–1', 'Safe to discharge — outpatient endoscopy appropriate'], ['≥ 6', '50% likelihood of needing endoscopic hemostatic treatment'], ['≥ 7', '80.4% sensitive for needing endoscopic treatment (NPV 92.4%)'], ['≥ 5', '88.7% sensitive for predicting 30-day mortality (NPV 97.9%)'], ] gbs_interp_table = Table(gbs_interp, colWidths=[3*cm, None], repeatRows=1) gbs_interp_table.setStyle(make_table_style('#2E6DA4', '#EEF4FA')) story += [gbs_interp_table, sp(8)] story += [ h2("B. Rockall Score — PRE + POST-endoscopy"), body("Purpose: Predicts MORTALITY (includes endoscopy findings)"), sp(4), ] rockall_data = [ ['Variable', 'Points'], ['Age', '0–2 points'], ['Shock (HR, BP)', '0–2 points'], ['Comorbidity', '0–3 points'], ['EGD stigmata (active bleed, visible vessel)', '0–2 points'], ['EGD diagnosis (Mallory-Weiss, ulcer, cancer, varices)', '0–2 points'], ] rockall_table = Table(rockall_data, colWidths=[10*cm, None], repeatRows=1) rockall_table.setStyle(make_table_style()) story += [rockall_table, sp(4)] rockall_interp = [ ['Score', 'Mortality'], ['0–1', '0% mortality — very low risk'], ['5', '~10% mortality'], ['≥ 8', '~40% mortality'], ] r_interp_table = Table(rockall_interp, colWidths=[3*cm, None], repeatRows=1) r_interp_table.setStyle(make_table_style('#2E6DA4', '#EEF4FA')) story += [r_interp_table, sp(8)] story += [ h2("C. AIMS65 Score (Simple Pre-endoscopy Score)"), sp(4), ] aims_data = [ ['Letter', 'Variable', 'Threshold'], ['A', 'Albumin', '< 3.0 g/dL'], ['I', 'INR', '> 1.5'], ['M', 'Mental status alteration', 'Any altered mental status'], ['S', 'Systolic BP', '≤ 90 mmHg'], ['65', 'Age', '≥ 65 years'], ] aims_table = Table(aims_data, colWidths=[1.5*cm, 5*cm, None], repeatRows=1) aims_table.setStyle(make_table_style()) story += [aims_table, sp(4)] story += [body("Score ≥ 2 = high risk for in-hospital mortality"), sp(4)] # 7. INVESTIGATIONS story += [PageBreak()] story += [ h1("7. INVESTIGATIONS"), sp(4), ] inv_data = [ ['Test', 'Key Significance'], ['CBC', 'Hb/Hct — may be FALSELY NORMAL early (hemodilution takes time)'], ['BMP / BUN:Creatinine ratio', '>20:1 = blood digested in upper GI tract → strongly suggests UGIB'], ['INR / PT', 'Coagulopathy — critical in liver disease patients'], ['Type & Crossmatch', 'Always in significant UGIB; activate MTP if massive bleed'], ['LFTs + albumin', 'Liver disease, portal hypertension, AIMS65 variable'], ['Nasogastric Lavage', 'Bloody/coffee-grounds = confirms UGIB. NEGATIVE does NOT exclude UGIB'], ['Endoscopy (EGD)', 'Gold standard — diagnosis AND hemostasis. Goal: within 24 hours'], ['Lactate', 'Elevated = poor tissue perfusion, impending shock'], ] inv_table = Table(inv_data, colWidths=[5.5*cm, None], repeatRows=1) inv_table.setStyle(make_table_style()) story += [inv_table, sp(4)] # 8. TREATMENT story += [ h1("8. TREATMENT — Step-by-Step"), sp(6), h2("Step 1: Resuscitation"), bullet("Two large-bore IVs (16G or larger)"), bullet("2L crystalloid bolus over 30 minutes (normal saline or Plasmalyte)"), bullet("Activate Massive Transfusion Protocol if shock index ≥ 0.9"), sp(4), h2("Step 2: Blood Transfusion Thresholds"), sp(4), ] transfuse_data = [ ['Patient Group', 'Transfuse When Hb ≤'], ['Most patients (restrictive strategy)', '7 g/dL'], ['Elderly / cardiac comorbidities', '9 g/dL'], ['Correct coagulopathy if', 'INR elevated OR Platelets < 50,000'], ['Massive bleed / hemodynamic instability', 'Uncrossmatched O-negative blood immediately'], ] t_table = Table(transfuse_data, colWidths=[8*cm, None], repeatRows=1) t_table.setStyle(make_table_style()) story += [t_table, sp(4)] story += [body("Note: Restrictive transfusion (Hb ≤7) is superior to liberal strategy in UGIB — improves outcomes (TRIGGER/TRICC trials).")] story += [sp(6)] story += [h2("Step 3: Medications"), sp(4)] meds_data = [ ['Drug', 'Dose', 'Indication'], ['Omeprazole (PPI)', '80 mg IV bolus → 8 mg/h infusion', 'All UGIB — especially PUD. Labeled use for ulcer bleeding.'], ['Octreotide', '50 mcg IV bolus → 50 mcg/h infusion', 'Variceal / portal HTN bleeding — reduces portal pressure'], ['Ceftriaxone', '1g IV daily', 'ALL cirrhotic patients with UGIB — reduces bacterial translocation and mortality'], ['Terlipressin / Vasopressin', 'Per protocol', 'Adjunct for variceal bleed; reduces splanchnic blood flow'], ['Erythromycin', '250 mg IV 30–60 min pre-scope', 'Prokinetic — clears stomach contents, improves EGD visualization'], ['Propranolol (2° prevention)', 'Oral (after acute phase)', 'Non-selective beta-blocker after variceal bleed — reduces rebleed risk'], ] meds_table = Table(meds_data, colWidths=[4.5*cm, 5*cm, None], repeatRows=1) meds_table.setStyle(make_table_style()) story += [meds_table, sp(6)] story += [ h2("Step 4: Endoscopy (EGD)"), bullet("Perform within 24 hours for all significant UGIB"), bullet("Urgent/emergency scope if hemodynamically unstable or ongoing active bleed"), bullet("Hemostasis methods: injection (epinephrine), thermocoagulation, clips, band ligation (varices)"), sp(6), h2("Step 5: Airway Management"), bullet("Intubation is NOT routine in UGIB"), bullet("Consider intubation if: altered consciousness, unable to protect airway, massive hematemesis"), bullet("Use smaller induction agent doses in unstable patients (prevent peri-intubation arrest)"), bullet("Prophylactic intubation NOT recommended — associated with pulmonary complications"), sp(6), h2("Step 6: Refractory / Salvage Options"), sp(4), ] salvage_data = [ ['Scenario', 'Management'], ['Failed endoscopic hemostasis', 'Sengstaken-Blakemore tube (balloon tamponade) as BRIDGE to definitive therapy'], ['Refractory variceal bleed', 'TIPS (Transjugular Intrahepatic Portosystemic Shunt)'], ['Surgical option', 'Reserved for failed endoscopic + interventional therapy'], ] s_table = Table(salvage_data, colWidths=[6*cm, None], repeatRows=1) s_table.setStyle(make_table_style()) story += [s_table, sp(4)] # 9. FORREST story += [PageBreak()] story += [ h1("9. FORREST CLASSIFICATION — Endoscopic Stigmata"), sp(6), ] forrest_data = [ ['Class', 'Finding', 'Rebleed Risk', 'Management'], ['Ia', 'Active spurting bleed', '80–90%', 'Endoscopic hemostasis'], ['Ib', 'Active oozing bleed', '10–27%', 'Endoscopic hemostasis'], ['IIa', 'Non-bleeding visible vessel', '40–50%', 'Endoscopic hemostasis'], ['IIb', 'Adherent clot', '20–30%', 'Endoscopic treatment (controversial)'], ['IIc', 'Flat pigmented spot', '5–10%', 'PPI, can discharge earlier'], ['III', 'Clean base ulcer', '< 2%', 'PPI alone, early discharge safe'], ] f_table = Table(forrest_data, colWidths=[1.5*cm, 5.5*cm, 3*cm, None], repeatRows=1) f_table.setStyle(make_table_style()) story += [f_table, sp(4)] # 10. DISPOSITION story += [ h1("10. DISPOSITION"), sp(4), ] disp_data = [ ['Category', 'Disposition'], ['GBS ≤ 1, hemodynamically stable, low-risk', 'Discharge with outpatient EGD arranged'], ['Moderate risk / stable', 'Admit to ward; EGD within 24h'], ['Hemodynamically unstable / Rockall ≥ 5 / active bleed', 'ICU admission + urgent/emergency EGD'], ['Cirrhotic patient', 'Admit + antibiotics (ceftriaxone) + octreotide + GI consult'], ['Failed endoscopy / refractory bleed', 'IR consult for TIPS or surgical consultation'], ] d_table = Table(disp_data, colWidths=[7*cm, None], repeatRows=1) d_table.setStyle(make_table_style()) story += [d_table, sp(8)] # 11. MCQ TRAPS story += [ h1("11. MCQ TRAPS — Don't Miss These!"), sp(6), ] traps = [ ("❌ WRONG", "Coffee-ground emesis = less severe than bright red hematemesis", "Color of emesis does NOT predict severity. Shock index is more reliable."), ("❌ WRONG", "Negative NG aspirate excludes UGIB", "Only bloody aspirate CONFIRMS UGIB. A negative aspirate does NOT rule it out."), ("✅ CORRECT", "Hemoglobin may be normal early in UGIB", "Hemodilution takes time. Don't be falsely reassured by an early normal Hb."), ("✅ CORRECT", "Hematochezia can originate from the upper GI tract", "With massive/brisk UGIB, rapid transit → hematochezia despite upper source."), ("✅ CORRECT", "Ceftriaxone in cirrhotic UGIB reduces mortality", "Antibiotics are standard of care in ALL cirrhotic patients with GI bleed."), ("✅ CORRECT", "Restrictive transfusion (Hb ≤7) is better than liberal in UGIB", "Supported by TRIGGER and TRICC trials — liberal strategy worsens outcomes."), ("✅ CORRECT", "BUN:Cr ratio >20:1 points to upper GI source", "Digested blood protein → urea load → elevated BUN disproportionately."), ("✅ CORRECT", "GBS predicts need for treatment; Rockall predicts mortality", "Key distinction — GBS is pre-endoscopy intervention guide; Rockall includes EGD."), ("✅ CORRECT", "Erythromycin before endoscopy improves visualization", "Acts as prokinetic agent — clears gastric blood, reduces need for repeat scope."), ("✅ CORRECT", "Mallory-Weiss = retching/vomiting FIRST, then blood", "Classic history. Mucosal tear at GEJ from sudden intragastric pressure rise."), ("✅ CORRECT", "Variceal bleed in cirrhotic patients → always give antibiotics", "Even without infection — reduces bacterial translocation and early rebleed."), ("✅ CORRECT", "PPI infusion (not just oral) is standard in active ulcer bleed", "80 mg IV bolus then 8 mg/h infusion is the regimen."), ] trap_style2 = ParagraphStyle('Trap2', parent=styles['Normal'], fontSize=9, fontName='Helvetica', leading=13, spaceBefore=2, spaceAfter=4) for tag, wrong, correct in traps: color = '#CC0000' if '❌' in tag else '#006600' p = Paragraph(f'{tag} — {wrong} → {correct}', trap_style2) story.append(p) story += [sp(8), hr()] story += [ Paragraph("Sources: Tintinalli's Emergency Medicine Ch.75 | Rosen's Emergency Medicine Ch.26 | Current Surgical Therapy 14e | Mulholland & Greenfield's Surgery 7e", source_style), Paragraph("Generated by Orris AI — For Educational Use Only", source_style), ] doc.build(story) print("PDF generated successfully!") EOF

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UGIB Hematemesis MD Exam

PDF Document · PDF

The PDF includes all 11 sections:

Definition & Anatomy
Causes (ranked by frequency)
Clinical Presentation
Shock Index
Bedside Clues to Source
Risk Scores (GBS, Rockall, AIMS65) with interpretation tables
Investigations
Treatment (step-by-step with drug doses)
Forrest Classification
Disposition
MCQ Traps (12 high-yield exam traps)

Jaundice ed approach and evaluation

Finding Sources

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That section is neonatal jaundice. Let me search specifically for the adult ED approach chapter:

Finding Sources

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Reading File

Excellent - I now have all the material needed for a comprehensive ED-focused answer. Here it is:

Jaundice — ED Approach & Evaluation

Harrison's 22e + Tintinalli's EM + Sleisenger & Fordtran's

DEFINITION & PHYSIOLOGY

Jaundice (icterus) = yellowing of skin, sclera, and mucous membranes due to hyperbilirubinemia
Scleral icterus becomes visible when serum bilirubin > 2-3 mg/dL
Clinically apparent jaundice usually at bilirubin > 3 mg/dL

Bilirubin Metabolism (The Basis of Classification)

RBC breakdown → Unconjugated bilirubin (indirect, water-insoluble)
      ↓  (liver glucuronyl transferase)
Conjugated bilirubin (direct, water-soluble)
      ↓  (excreted into bile)
Intestine → Urobilinogen (reabsorbed/excreted in urine) OR Stercobilin (feces = brown color)

STEP 1: THE ED FRAMEWORK — 3 KEY QUESTIONS

1. Is this ISOLATED bilirubin elevation OR are other LFTs also abnormal?
2. If isolated — is it UNCONJUGATED or CONJUGATED bilirubin?
3. If LFTs abnormal — is pattern HEPATOCELLULAR or CHOLESTATIC?

Evaluation of the patient with jaundice - Harrison's 22e Algorithm

Fig. 52-1 — Harrison's Principles of Internal Medicine 22e: Evaluation algorithm for jaundice

STEP 2: CLASSIFICATION

A. ISOLATED HYPERBILIRUBINEMIA (LFTs otherwise normal)

Unconjugated (Indirect) — Direct fraction < 15%

Category	Cause
Overproduction	Hemolytic disorders (hereditary spherocytosis, sickle cell, G6PD, thalassemia), ineffective erythropoiesis, massive transfusion, hematoma resorption, malaria
Impaired uptake	Drugs: rifampin, probenecid, atazanavir, some cephalosporins/penicillins
Impaired conjugation	Gilbert's syndrome, Crigler-Najjar types I & II

Gilbert's Syndrome - most common hereditary cause; benign; triggered by fasting, illness, stress. Bilirubin rarely >3-4 mg/dL. Bilirubin UDPGT activity reduced to 10-35% of normal.

In chronic hemolysis, bilirubin rarely exceeds 5 mg/dL - if higher, suspect superimposed choledocholithiasis (pigmented gallstones common in hemolytic disorders)

Conjugated (Direct) — Direct fraction > 15%

Cause
Dubin-Johnson syndrome (benign, inherited, dark liver on gross pathology)
Rotor syndrome (benign, inherited)

B. JAUNDICE WITH ABNORMAL LFTs

Hepatocellular Pattern

ALT/AST elevated out of proportion to Alkaline Phosphatase

Category	Causes
Viral hepatitis	Hep A (IgM), Hep B (HBsAg, HBcIgM), Hep C (RNA), CMV, EBV, Hep E
Drug/toxin-induced	Paracetamol (APAP), alcohol, isoniazid, statins, herbals
Autoimmune	Autoimmune hepatitis (ANA, SMA, LKM antibodies)
Metabolic	Wilson's disease (ceruloplasmin - check if patient <40 years), hemochromatosis
Ischemic hepatitis	"Shock liver" - acute hypoperfusion; dramatic aminotransferase rise, gradual bilirubin peak
Other	Sepsis, heart failure (hepatic congestion/hypoxia)

Cholestatic Pattern

Alkaline Phosphatase elevated out of proportion to ALT/AST

Then subdivide → Is biliary tree dilated on USS?

	Intrahepatic Cholestasis (ducts NOT dilated)	Extrahepatic Cholestasis (ducts DILATED)
Causes	Primary biliary cholangitis (PBC), PSC (intrahepatic), drug-induced (see below), viral, TPN, sepsis, post-op, pregnancy cholestasis, heart failure	Choledocholithiasis (#1 cause), pancreatic cancer, cholangiocarcinoma, ampullary carcinoma, gallbladder cancer, hilar lymphadenopathy
Next test	Serologies (AMA for PBC), review drugs	CT/MRCP/ERCP

STEP 3: HISTORY — What to Ask in the ED

Feature	Suggests
RUQ pain + fever + jaundice (Charcot's triad)	Ascending cholangitis (choledocholithiasis)
Charcot's triad + hypotension + AMS (Reynolds' pentad)	Severe/suppurative cholangitis — emergency biliary drainage
Painless progressive jaundice	Malignancy (pancreatic cancer, cholangiocarcinoma)
Jaundice after prolonged vomiting/retching	Mallory-Weiss or hepatic congestion
Alcohol use / alcoholic binge	Alcoholic hepatitis
Medication history (including herbals/supplements)	Drug-induced liver injury (DILI)
IV drug use, unprotected sex, travel	Viral hepatitis (B, C, E)
Recent travel to endemic areas	Hep A, E; malaria; leptospirosis
Previous biliary surgery / ERCP / stent	Biliary stricture, cholangitis
Weight loss + anorexia + painless jaundice	Malignancy
Young patient + neuropsychiatric symptoms	Wilson's disease
Family history of jaundice	Gilbert's, Crigler-Najjar, hemolytic disorders
Pregnancy (2nd-3rd trimester)	Intrahepatic cholestasis of pregnancy, HELLP, acute fatty liver
ICU/post-op/septic patient	Ischemic hepatitis, TPN-related, sepsis cholestasis

STEP 4: PHYSICAL EXAMINATION

Sign	Suggests
Scleral icterus	Bilirubin >2-3 mg/dL (earliest sign)
RUQ tenderness	Biliary pathology, hepatitis
Murphy's sign	Acute cholecystitis
Palpable gallbladder (Courvoisier's sign)	Malignant obstruction (painless)
Hepatomegaly	Hepatitis, congestive hepatopathy, infiltrative disease
Splenomegaly	Portal hypertension, hemolytic anemia, infiltrative disease
Spider angiomas, palmar erythema, gynecomastia, caput medusae	Chronic liver disease / cirrhosis
Asterixis, confusion	Hepatic encephalopathy
Ascites	Portal hypertension, cirrhosis, malignancy
Cachexia / palpable mass	Malignancy
Kayser-Fleischer rings (slit lamp)	Wilson's disease
Fever + rigors	Ascending cholangitis, hepatic abscess

Courvoisier's Law: Palpable non-tender gallbladder + jaundice = malignant obstruction (NOT choledocholithiasis, because stones cause fibrosis/non-distensible GB)

STEP 5: INVESTIGATIONS

First-Line ED Workup

Test	What it Tells You
Total + Direct (Conjugated) Bilirubin	Fractionation guides classification (indirect vs. direct)
ALT / AST	Hepatocellular injury; >1000 = viral/ischemic/drug
Alkaline Phosphatase (ALP)	Cholestatic pattern if elevated out of proportion
GGT	Confirms hepatic source of elevated ALP; elevated with alcohol
Albumin	Chronic liver function; low = cirrhosis, malnutrition
PT / INR	Acute synthetic function; prolonged = severe hepatocyte dysfunction
CBC	Anaemia (haemolytic), WBC (infection/cholangitis), platelets (hypersplenism)
Blood cultures	If fever present - rule out cholangitis/sepsis
Urinalysis	Dark urine (urobilinogen / conjugated bilirubin) = direct hyperbilirubinaemia
Paracetamol level	In all jaundiced patients — rule out APAP toxicity
Blood glucose	Hypoglycaemia = severe hepatic failure

Pattern Recognition from LFTs

Pattern	AST/ALT	ALP	Likely Diagnosis
Hepatocellular	Very elevated (>10x)	Normal or mildly elevated	Viral hepatitis, DILI, ischemic hepatitis
Cholestatic	Mildly elevated	Very elevated (>3x)	Choledocholithiasis, PBC, malignancy
Mixed	Elevated	Elevated	Sepsis, drugs, PSC
Isolated bilirubin	Normal	Normal	Gilbert's, hemolysis, Dubin-Johnson

AST:ALT ratio > 2:1 — strongly suggests alcoholic hepatitis ALT > 1000 U/L — suggests viral hepatitis, ischemic hepatitis, or APAP toxicity

Second-Line / Targeted Workup

Clinical Suspicion	Test
Viral hepatitis	HBsAg, HBcAb IgM, Hep A IgM, Hep C RNA
Autoimmune hepatitis	ANA, SMA, LKM antibodies, SPEP
Wilson's disease (<40 yrs)	Ceruloplasmin, serum copper, urine copper
Haemochromatosis	Serum ferritin, transferrin saturation
PBC	AMA (antimitochondrial antibodies)
Malignancy / obstruction	USS → CT abdomen / MRCP
Cholangitis	Blood cultures, USS biliary tree
Pregnancy	LFTs + USS, HELLP screen (platelets, LDH)
Haemolysis	Blood film, reticulocyte count, LDH, haptoglobin, Coombs test

Imaging

Modality	Use
Abdominal Ultrasound (FIRST LINE)	Biliary dilation, gallstones, liver size/echotexture, ascites, masses
CT Abdomen	Pancreatic mass, lymphadenopathy, cholangiocarcinoma, extrahepatic cause
MRCP	Non-invasive biliary tree imaging (PSC, choledocholithiasis, strictures)
ERCP	Diagnostic + therapeutic (stone extraction, stenting)
Liver biopsy	When above tests inconclusive

STEP 6: ED MANAGEMENT BY CAUSE

Condition	Management
Ascending cholangitis	IV fluids, broad-spectrum antibiotics (ceftriaxone + metronidazole or piperacillin-tazobactam), urgent GI consult for ERCP biliary drainage
Severe cholangitis (Reynolds' pentad)	ICU admission, emergent ERCP or percutaneous drainage
APAP toxicity	N-acetylcysteine (NAC) immediately; liver transplant referral if severe
Alcoholic hepatitis	Supportive, assess severity (Maddrey score), steroids if severe
Acute viral hepatitis	Supportive; isolate if Hep A; refer hepatology
Malignant obstruction	Palliative stenting via ERCP; oncology referral
Haemolytic crisis (sickle cell)	Transfusion, analgesia, hydration
Fulminant hepatic failure	ICU, monitor ICP, consider liver transplant listing
Drug-induced (DILI)	Withdraw offending drug immediately

STEP 7: DISPOSITION FROM ED

Patient Type	Disposition
Cholangitis / sepsis / coagulopathy	Admit ICU or HDU
Acute liver failure (INR elevated, encephalopathy)	Admit ICU, transplant centre referral
New jaundice with unclear cause	Admit for workup
Suspected malignancy	Admit or urgent outpatient CT + GI referral
Gilbert's syndrome - well, normal LFTs, no haemolysis	Discharge with reassurance
Mild isolated unconjugated, stable - all normal	Outpatient follow-up

HIGH-YIELD EXAM PEARLS

Scleral icterus is the earliest detectable sign (bilirubin >2-3 mg/dL)
Charcot's triad = RUQ pain + fever + jaundice → cholangitis; Add hypotension + AMS = Reynolds' pentad = emergency
Courvoisier's sign = painless palpable gallbladder + jaundice = malignancy (pancreatic cancer)
AST:ALT >2:1 = alcoholic hepatitis
ALT >1000 = viral hepatitis, ischemic, or APAP
Isolated indirect hyperbilirubinaemia + triggered by fasting/illness = Gilbert's syndrome
Painless progressive jaundice + weight loss = pancreatic/biliary malignancy until proven otherwise
Dark urine + pale stools = conjugated (obstructive) jaundice (conjugated bilirubin is water-soluble → excreted in urine; stercobilin absent → pale stools)
Check paracetamol level in EVERY jaundiced patient - DILI is easily missed
AMA positive = Primary Biliary Cholangitis (PBC)
Ceruloplasmin if patient <40 yrs with unexplained liver disease = Wilson's disease
Ultrasound is FIRST imaging in all ED jaundice workups

Sources: Harrison's Principles of Internal Medicine 22e (Ch.52) | Sleisenger & Fordtran's GI and Liver Disease | Tintinalli's Emergency Medicine

Acute cholecystitis

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Acute Cholecystitis — ED Approach

Tintinalli's EM Ch.79 | Rosen's EM Ch.76 | Sleisenger & Fordtran's

DEFINITION & OVERVIEW

Cholecystitis = inflammation of the gallbladder
Calculous (95%) = caused by obstructing gallstone in the cystic duct
Acalculous (5%) = no stone; occurs in critically ill patients (sepsis, burns, trauma, ICU)
Gallstone prevalence: 8% in men, 17% in women in the USA; risk increases with age and BMI

THE SPECTRUM OF GALLSTONE DISEASE (Progression)

Asymptomatic gallstones (1-4% per year become symptomatic)
        ↓
Biliary colic (transient cystic duct obstruction → resolves)
        ↓
Acute cholecystitis (obstruction persists → inflammation)
        ↓
Gangrenous cholecystitis (necrosis of gallbladder wall)
        ↓
Emphysematous cholecystitis (gas-forming organisms; especially diabetics)
        ↓
Gallbladder perforation (life-threatening)

PATHOPHYSIOLOGY

Gallstone obstructs cystic duct → gallbladder distends
Increased intraluminal pressure → mucosal ischemia
Cytotoxic bile products (lysophosphatidylcholine) trigger inflammation
Secondary bacterial infection in ~50% of cases
Organisms: E. coli (most common), Klebsiella, Streptococcus, Enterococcus, anaerobes (Clostridia, Bacteroides) in ~40%

Gallstone Types

Type	Composition	Association
Cholesterol (80%)	Supersaturated cholesterol	Obesity, female, fertile, forty (5 F's), OCP, rapid weight loss
Black pigment	Calcium bilirubinate	Chronic haemolysis (sickle cell, spherocytosis), cirrhosis
Brown pigment	Calcium bilirubinate	Biliary stasis, infection, parasites (Southeast Asia)

RISK FACTORS — The 5 F's (for Cholesterol Stones)

Fat, Female, Fertile, Forty, Fair

Additional: OCP use, rapid weight loss, bariatric surgery, TPN, diabetes, pregnancy

CLINICAL FEATURES

Biliary Colic vs Acute Cholecystitis

Feature	Biliary Colic	Acute Cholecystitis
Pain character	Steady/constant (not truly colicky)	Constant, severe, worsening
Location	Epigastrium / RUQ	RUQ - more localised
Radiation	Back / right shoulder tip / right scapula	Same
Duration	< 6 hours (resolves spontaneously)	> 6 hours and persists
Trigger	Fatty meal (variable)	Often follows biliary colic episode
Nausea/vomiting	Yes	Yes
Fever	No	Present in ~1/3 cases (NOT always!)
Murphy's sign	Absent	Present
Peritoneal signs	Absent	May be present (guarding, rebound)
Circadian pattern	Peak around midnight	-

Key Exam Trap: Fever is present in only ~1/3 of acute cholecystitis cases — absence of fever does NOT rule it out

MURPHY'S SIGN

Definition: Sudden cessation of deep inspiration due to pain when the examiner's fingers press the RUQ/right subcostal region, causing the inflamed gallbladder to descend onto the examiner's hand

Sensitivity: 65%
Specificity: 87%
Sonographic Murphy's sign (pain on USS probe pressure over gallbladder) = higher diagnostic value

COMPLICATIONS

Complication	Key Features
Gangrenous cholecystitis	Necrosis of GB wall; pain may paradoxically decrease; higher mortality
Emphysematous cholecystitis	Gas-forming organisms; especially in diabetics and elderly; gas in GB wall on X-ray/CT; emergency surgery
Gallbladder perforation	Rare but life-threatening; generalised peritonitis
Pericholecystic abscess	Localised perforation; RUQ mass
Gallstone ileus	Fistula → stone erodes into bowel → SBO; Rigler's triad on X-ray
Choledocholithiasis	Stone migrates to CBD; jaundice, elevated LFTs
Ascending cholangitis	CBD obstruction + infection → Charcot's triad / Reynolds' pentad
Mirizzi syndrome	Large stone impacted in cystic duct/Hartmann's pouch compresses CHD → obstructive jaundice

Cholangitis — Must Know

Triad/Pentad	Components
Charcot's Triad	RUQ pain + Fever/rigors + Jaundice
Reynolds' Pentad	Charcot's triad + Hypotension + Altered mental status = Severe cholangitis (emergency)

DIFFERENTIAL DIAGNOSIS

Condition	Distinguishing Feature
Acute pancreatitis	Epigastric radiation to back; elevated lipase
Peptic ulcer disease / perforation	History of PUD; peritonism; free air on X-ray
Hepatitis	Elevated transaminases; no acute RUQ mass
Hepatic abscess	Fever; USS finding; travel history
Right lower lobe pneumonia	Cough, SOB, CXR finding
Pyelonephritis	CVA tenderness; urinalysis positive
Appendicitis	Pain migrates to RIF; positive McBurney's point
Fitz-Hugh-Curtis syndrome	Young female; perihepatitis; PID history
Myocardial infarction	ECG, troponin; referred epigastric pain (inferior MI)

INVESTIGATIONS

Labs

Test	Significance
WBC	Leukocytosis in ~60% — may be absent in nearly half!
LFTs (AST, ALT, ALP)	Mildly elevated or normal in uncomplicated cholecystitis; markedly elevated = choledocholithiasis
Total + direct bilirubin	Elevated if CBD involved
Lipase	Elevated = concurrent pancreatitis
Blood cultures	If fever/sepsis — biliary organisms
CRP	Elevated; useful for severity assessment
PT/INR	If jaundiced or severe disease

Leukocytosis may be absent in up to 50% of cases — don't exclude cholecystitis on WBC alone

Imaging (Table 79-7 — Tintinalli's)

Modality	Key Findings	Comment
Ultrasound (FIRST-LINE)	Gallstones, GB wall thickening >3 mm, pericholecystic fluid, GB distension (short axis >40 mm), sonographic Murphy's sign	Preferred initial test; PPV >90% when multiple findings present; negative exam has high NPV
CT Abdomen	GB wall thickening, pericholecystic fat stranding, GB distension, gas in wall (emphysematous)	Better for complications (gangrene, perforation, abscess); insensitive for gallstones
HIDA Scan	Non-visualisation of GB = cystic duct obstruction	Most sensitive and specific; time-consuming, limited availability; loses sensitivity with bilirubin >5-8 mg/dL
MRCP/MRI	GB wall thickening, pericholecystic fluid, excellent biliary tree visualisation	Best for CBD stones; no radiation; time-consuming

Normal CBD diameter: <5 mm (increases with age and post-cholecystectomy) CBD dilation + stones on USS = indirect evidence of choledocholithiasis

TREATMENT

ED Management of Biliary Colic

NPO temporarily
Antiemetics (ondansetron, metoclopramide)
NSAIDs first-line analgesia (ketorolac IV) — equal efficacy to opioids; also reduce short-term complications
Opioids if NSAIDs insufficient (all opioids cause some Sphincter of Oddi spasm — no clinical significance; no opioid is superior over another)
❌ Anticholinergics (atropine/glycopyrrolate) — do NOT work for biliary colic
Discharge + surgical referral for elective laparoscopic cholecystectomy

ED Management of Acute Cholecystitis

NPO (nil by mouth)
IV fluids + electrolyte replacement
Analgesia (NSAIDs + opioids as needed)
Antiemetics
IV Antibiotics:

Regimen	Agent
Single agent (mild-moderate)	Piperacillin-tazobactam 3.375g IV q6h
Cephalosporin-based	2nd/3rd gen cephalosporin (cefuroxime, ceftriaxone)
Carbapenem (severe/resistant)	Meropenem or ertapenem
Combination	Metronidazole + fluoroquinolone (ciprofloxacin)

Surgical consult — early laparoscopic cholecystectomy (within 72h if fit) is treatment of choice
Percutaneous cholecystostomy — if too unwell for surgery (elderly, comorbid, critically ill)

Special Situations

Situation	Management
Emphysematous cholecystitis	Broad-spectrum IV antibiotics including anaerobic coverage; emergency cholecystectomy
Gangrenous cholecystitis	Emergency surgery
Gallbladder perforation	Emergency surgery + washout
Acalculous cholecystitis (ICU)	Percutaneous cholecystostomy (drainage); cholecystectomy when stable
Ascending cholangitis	IV antibiotics + urgent ERCP for biliary drainage
Severe cholangitis (Reynolds' pentad)	ICU + emergency ERCP or percutaneous drainage
Choledocholithiasis	ERCP + stone extraction + elective cholecystectomy

ACALCULOUS CHOLECYSTITIS

Occurs in 5% of cholecystitis cases
More aggressive course — higher risk of gangrene and perforation
Risk factors: ICU patients, sepsis, burns, major trauma/surgery, TPN, diabetes, immunosuppression
Pathophysiology: bile stasis + gallbladder ischaemia → inflammation without stones
Diagnosis: USS or CT showing GB changes without stones; HIDA confirmatory
Treatment: IV antibiotics + percutaneous cholecystostomy (if too unwell for surgery)

DISPOSITION

Category	Disposition
Biliary colic - stable, symptom controlled	Discharge + surgical OPD referral
Uncomplicated acute cholecystitis	Admit for IV antibiotics + early surgery
Complicated cholecystitis (gangrene, perforation, emphysematous)	Admit ICU + emergency surgery
Ascending cholangitis	Admit + urgent ERCP; ICU if Reynolds' pentad
High-risk surgical patient with acute cholecystitis	Admit for antibiotics + percutaneous cholecystostomy

HIGH-YIELD EXAM PEARLS

Biliary colic pain lasts <6 hours and resolves spontaneously; >6 hours = think cholecystitis
Fever is present in only ~1/3 of cholecystitis — absence does NOT exclude diagnosis
Murphy's sign: 65% sensitive, 87% specific; sonographic Murphy's is more reliable
Leukocytosis absent in up to 50% of acute cholecystitis — don't be falsely reassured
USS is first-line imaging — PPV >90% with gallstones + wall thickening + pericholecystic fluid + sonographic Murphy's
HIDA is most sensitive/specific but impractical in the ED
NSAIDs are first-line analgesia for biliary colic (reduce complication risk too); all opioids equally acceptable
Anticholinergics do NOT work for biliary colic pain
Emphysematous cholecystitis = diabetics + elderly = gas in GB wall = emergency surgery
Acalculous cholecystitis = ICU/critically ill patients = more dangerous = percutaneous drainage
Charcot's triad + hypotension + AMS = Reynolds' pentad = emergency
CBD >5 mm on USS = dilated = suspect choledocholithiasis
Courvoisier's sign (non-tender palpable GB + jaundice) = malignant obstruction, NOT stones
Early laparoscopic cholecystectomy (within 72h) is preferred over delayed surgery

Sources: Tintinalli's Emergency Medicine Ch.79 | Rosen's Emergency Medicine Ch.76 | Sleisenger & Fordtran's GI & Liver Disease

Acute cholangitis

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Acute Cholangitis — Complete ED Guide

Current Surgical Therapy 14e | Sabiston Surgery | Yamada's Gastroenterology | Mulholland & Greenfield's Surgery

Based on Tokyo Guidelines 2018

DEFINITION

Acute cholangitis = ascending bacterial infection of the biliary tree due to obstruction of the common bile duct (CBD) - first described by Jean-Martin Charcot in 1877

EPIDEMIOLOGY & CAUSES

Most common in the 5th-7th decades; equal in men and women
Risk of cholangitis from admitted choledocholithiasis patients: up to 5%
Bactibilia (bacteria in bile) found in up to 90% with stone obstruction

Causes of Acute Cholangitis

Category	Specific Causes	Frequency
Biliary stasis - obstruction	Choledocholithiasis	40-70% (most common)
	Malignancy (pancreatic Ca, cholangiocarcinoma, ampullary Ca)	10-60%
	Benign strictures (PSC, post-op, chronic pancreatitis)	5-30%
Direct seeding	ERCP instrumentation	1-7%
	Indwelling biliary stents / drains	Iatrogenic
	Bilioenteric anastomosis	Post-surgical
Other	Parasitic infection (Ascaris, Clonorchis)	Endemic areas

PATHOPHYSIOLOGY

Normal bile sterility is maintained by:

Sphincter of Oddi - mechanical barrier against ascending duodenal bacteria
Laminar bile flow - continuous flushing of bacteria
Bile salts - bacteriostatic properties
IgA secretion in biliary tree

When obstruction occurs:

Bile stasis → bacterial proliferation
Increased intraluminal pressure → biliary ductule permeability ↑
Bacterial translocation from portal venous system into bile ducts
Septicaemia when bacteria enter systemic circulation

Microbiology

Organism	Frequency
E. coli	25-50% (most common)
Klebsiella spp.	10-20%
Enterococcus	10-30%
Enterobacter	5-10%
Anaerobes (Bacteroides, Clostridia)	Recurrent/post-instrumentation cases
Pseudomonas, Citrobacter	Also seen

Infection is typically polymicrobial and dominated by gram-negative coliforms

CLINICAL FEATURES

The Classic Presentations

Presentation	Components	Sensitivity
Charcot's Triad	RUQ pain + Fever/rigors + Jaundice	< 50-60% (often incomplete)
Reynolds' Pentad	Charcot's triad + Hypotension + Altered mental status	~5% (severe/suppurative cholangitis; mortality approaches 100% without treatment)

Exam Trap: Charcot's triad is present in <50% of patients - absence does NOT rule out cholangitis. Fever + RUQ pain is present in 80%; jaundice in only 60%

Differential Diagnosis in the ED

Condition	Distinguishing Feature
Acute cholecystitis	Murphy's sign; no jaundice (unless Mirizzi)
Acute pancreatitis	Elevated lipase; epigastric radiation to back
Mirizzi's syndrome	Stone impacted in cystic duct compressing CHD
Liver abscess	USS finding; fever; may have no jaundice
Biliary leak	Post-procedural/surgical history
Right lower lobe pneumonia	CXR changes; no jaundice
Peptic ulcer perforation	Free air; sudden onset

STEP 1: DIAGNOSIS — Tokyo Guidelines 2018

TG18 Diagnostic Criteria (Table 8.7)

Diagnosis requires 1 item from A + 1 item from B or C (suspected) or 1 from each of A, B, and C (definite):

Category	Criteria
A. Systemic Inflammation	Fever and/or shaking chills; elevated WBC, CRP
B. Cholestasis	Jaundice (bilirubin ≥2 mg/dL); abnormal LFTs (ALP, GGT, AST, ALT)
C. Imaging	Biliary dilatation on USS/CT; evidence of aetiology (stone, stricture, stent)

STEP 2: SEVERITY GRADING — Tokyo Guidelines 2018

Grade I — Mild

Does not meet criteria for moderate or severe
Responds to antibiotics alone

Grade II — Moderate

Any 2 of the following:

Criterion	Threshold
WBC	>12,000 or <4,000/μL
High fever	≥39°C
Age	≥75 years
Total bilirubin	≥5 mg/dL
Albumin	<lower limit of normal × 0.73

Grade III — Severe

Any 1 organ/system dysfunction:

System	Criteria
Cardiovascular	Hypotension requiring vasopressors
Neurological	Disturbance of consciousness (AMS)
Respiratory	PaO2/FiO2 ratio < 300
Renal	Oliguria, creatinine > 2 mg/dL
Hepatic	PT/INR > 1.5
Haematological	Platelets < 100,000/mm³

STEP 3: INVESTIGATIONS

Labs

Test	Significance
WBC + differential	Leukocytosis; may be absent or reversed (<4000) in severe sepsis
CRP	Elevated; severity marker
Total + direct bilirubin	Elevated (≥2 mg/dL confirms cholestasis)
ALP, GGT	Cholestatic pattern - markedly elevated
AST, ALT	Hepatocellular injury from infection/inflammation
Albumin	Hypoalbuminaemia = Grade II severity marker
PT/INR	Coagulopathy; >1.5 = Grade III (hepatic dysfunction)
Blood cultures x2	Positive in ~21-71% of cholangitis; obtain BEFORE antibiotics
Lactate	Elevated = poor perfusion; sepsis
Creatinine	AKI assessment; >2 mg/dL = Grade III
Blood glucose	Sepsis-related hyperglycaemia; hypoglycaemia in fulminant

Imaging

Modality	Role	Key Findings
Ultrasound (FIRST-LINE)	Screening	Biliary dilatation, CBD >6 mm, gallstones, intrahepatic ductal dilation
CT Abdomen	Site of obstruction; complications	Identifies strictures, masses, ductal dilation; HIDA less reliable in infected bile
MRCP	Non-invasive cholangiography	Excellent CBD/biliary tree visualisation; no radiation; preferred pre-ERCP
ERCP	Diagnostic + therapeutic	Gold standard; allows stone extraction, stenting, sphincterotomy
PTC (Percutaneous Transhepatic Cholangiography)	When ERCP fails/unavailable	Requires dilated ducts; second-line drainage
HIDA	Limited role in cholangitis	Reduced sensitivity as infected bile ↓ tracer secretion

Normal CBD: <6 mm (increases post-cholecystectomy and with age)

STEP 4: MANAGEMENT

Immediate ED Actions (ALL grades)

IV access - two large-bore cannulas
IV fluid resuscitation - aggressive if septic
Blood cultures x2 - BEFORE starting antibiotics
IV antibiotics IMMEDIATELY after blood cultures
Severity assessment (TG18 grading)
NPO
Analgesia + antiemetics
Biliary imaging (USS → CT/MRCP as needed)
Surgical/GI consult early

Antibiotic Regimens

Setting	Regimen
Community-acquired, mild-moderate	Cefazolin, Cefuroxime, or Ceftriaxone
Severe / elderly / immunocompromised / community-acquired	Imipenem/cilastatin, Meropenem, Piperacillin-tazobactam, OR (Ciprofloxacin/Levofloxacin/Cefepime + Metronidazole)
Post-bilioenteric anastomosis (any severity)	Imipenem/cilastatin, Meropenem, Pip-tazo, OR Fluoroquinolone + Metronidazole
Healthcare-associated (any severity)	Above regimens + add Vancomycin (for MRSA/resistant Enterococcus)

Duration: 4-7 days after source control; 14 days if bacteraemia present (endocarditis risk)

Cover for ESBL-producing Enterobacteriaceae if local resistance is a concern

Biliary Drainage — Urgency by Grade

Grade	Urgency	Management
Grade I (Mild)	Early ERCP within 72h if responds to antibiotics	Antibiotics alone may suffice; low threshold for drainage if no improvement
Grade II (Moderate)	Early biliary drainage (<72h)	ERCP preferred; early duct clearance required
Grade III (Severe)	Urgent biliary drainage (<24h)	Stabilise haemodynamic/respiratory status FIRST → ERCP as soon as possible; ICU admission

Drainage Methods (in order of preference)

Method	Details	When Used
ERCP (1st line)	Endoscopic sphincterotomy + stone extraction + stenting	Standard; preferred in all anatomically accessible patients
EUS-guided biliary drainage (EUS-BD)	Hepaticogastrostomy or choledochoduodenostomy via EUS	Ascites, hilar strictures, unresectable malignancy
PTC / PTBD (2nd line)	Percutaneous transhepatic drainage; 90% success	Failed ERCP; post-surgical anatomy (Roux-en-Y, Whipple)
Surgical drainage (last resort)	CBD exploration + T-tube + cholecystectomy if stable; morbidity/mortality 10-50%	All endoscopic/percutaneous methods failed or unavailable

ERCP limited in: Roux-en-Y hepaticojejunostomy, gastric bypass, Whipple's procedure, duodenal obstruction

STEP 5: DISPOSITION

Grade	Disposition
Grade I - responds to antibiotics	Admit ward; ERCP within 72h
Grade II - moderate	Admit; urgent ERCP/drainage <72h; GI/surgery consult
Grade III - severe / Reynolds' pentad	ICU admission; urgent ERCP <24h; vasopressors if needed; MDT

COMPLICATIONS

Complication	Features
Septic shock	Reynolds' pentad; mortality ~100% without drainage
Pyogenic liver abscess	Extension of biliary infection into hepatic parenchyma; treated with antibiotics + percutaneous drainage
Portal vein thrombosis / pylephlebitis	Rare; septic thrombophlebitis
Acute renal failure	Sepsis-related; Grade III criterion
DIC	Platelets <100k; Grade III criterion
Recurrent cholangitis	Especially with indwelling stents; stent occlusion

COMPARISON: Cholecystitis vs Cholangitis vs Biliary Colic

Feature	Biliary Colic	Acute Cholecystitis	Acute Cholangitis
Pain	RUQ/epigastric, <6h	RUQ, constant, >6h	RUQ
Fever	No	In ~1/3	Yes (80%)
Jaundice	No	Rare (Mirizzi)	Yes (60%)
Murphy's sign	No	Yes	Less prominent
WBC	Normal	Often elevated	Often elevated
LFTs	Normal	Mildly elevated or normal	Markedly elevated
Bilirubin	Normal	Mildly elevated/normal	Elevated
USS	Stones in GB	Stones + GB changes	CBD dilation
Treatment	NSAID + outpatient Lap Chole	IV abx + early Lap Chole	IV abx + urgent ERCP
Mortality	Very low	Low (higher if complicated)	High if severe/untreated

HIGH-YIELD EXAM PEARLS

Charcot's triad is present in <50-60% - never a reason to exclude cholangitis
Reynolds' pentad (+ hypotension + AMS) = Grade III / suppurative cholangitis = emergency, mortality approaches 100% without treatment
Choledocholithiasis is #1 cause (40-70%); malignancy is #2
Blood cultures BEFORE antibiotics - positive in up to 71% of cases
ERCP is both diagnostic AND therapeutic - first-line drainage method
Grade III = urgent drainage <24h; Grade II = early drainage <72h
Antibiotic duration = 4-7 days post source control; 14 days if bacteraemic
Add Vancomycin for healthcare-associated cholangitis (MRSA/resistant Enterococcus)
PTC is second-line when ERCP fails or post-surgical anatomy (Roux-en-Y, Whipple)
Surgical drainage has 10-50% morbidity/mortality - absolute last resort
ESBL-producing Enterobacteriaceae increasingly common - consider carbapenems in resistant cases
Tokyo Guidelines 2018 are the current standard for diagnosis and severity grading
Normal CBD = <6 mm — dilation = choledocholithiasis / obstruction
HIDA scan unreliable in cholangitis - infected bile reduces tracer secretion

Sources: Current Surgical Therapy 14e | Sabiston Textbook of Surgery | Yamada's Textbook of Gastroenterology 7e | Mulholland & Greenfield's Surgery 7e | Tokyo Guidelines 2018

Diverticulitis

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Diverticulitis — Complete ED Guide

Rosen's Emergency Medicine Ch.81 | Sabiston Surgery | Mulholland & Greenfield's Surgery

DEFINITIONS

Term	Definition
Diverticulum	Outpouching of the colonic wall (false diverticulum — only mucosa + submucosa herniate through muscular wall)
Diverticulosis	Presence of diverticula without inflammation
Diverticulitis	Inflammation/infection of a diverticulum, usually from microperforation
Diverticular bleeding	Bleeding from diverticula without inflammation (typically painless)

EPIDEMIOLOGY

Diverticulosis: increasingly common with age — rare <40, common >60 years
Sigmoid colon most commonly affected (95% in Western countries)
Right colon diverticula more common in Asian populations
Diverticulosis → diverticulitis in up to 25% of individuals
Recurrent episodes in up to 40% of those who develop diverticulitis
Diverticulosis accounts for 40% of all lower GI haemorrhage; severe bleeding in 3-5%

PATHOPHYSIOLOGY

Why Diverticula Form

Diverticula herniate at sites of vascular penetration (vasa recta) through the circular muscle layer — the weakest points of the colon wall.

Two main factors:

Factor	Details
Weakness of the bowel wall	Non-circumferential muscle layers; insertion of vasa recta causes weak points; collagen disorders (Ehlers-Danlos), localized ischaemia
High intraluminal pressure	Low fibre diet → small faecal volume → increased segmentation contractions → high pressure; chronic constipation; colonic stasis; increased collagen crosslinking with age

Other risk factors: Age, obesity, smoking, alcohol, immunosuppression, altered gut flora, seasonal variation (summer months)

Why Diverticulitis Occurs

Diverticulum obstructed by inspissated faeces (faecolith) or increased intraluminal pressure
→ Localised microperforation of diverticulum
→ Pericolonic inflammation (phlegmon)
→ If contained by mesentery: abscess forms
→ If free perforation into peritoneum: peritonitis

Current evidence suggests diverticulitis is primarily an inflammatory process, not purely infectious — this is why antibiotics are now selective, not routine in uncomplicated disease

CLINICAL FEATURES

Classic Presentation

Feature	Description
Pain	Persistent left lower quadrant (LLQ) pain - constant, >24 hours
Location	LLQ (sigmoid); RLQ (right-sided - mimics appendicitis)
Fever	Low-grade to high (high fever = complicated disease/sepsis)
Nausea/vomiting	Common
Change in bowel habit	Constipation or diarrhoea
Anorexia	Common

Complicated Diverticulitis - Additional Features

Feature	Suggests
High fever, rigors, haemodynamic instability	Sepsis, perforation
Diffuse peritonism (rebound, guarding)	Free perforation / peritonitis
Palpable LLQ mass	Abscess / phlegmon
Dysuria, recurrent UTIs, pneumaturia, fecaluria	Colovesical fistula
Feculent vaginal discharge	Colovaginal fistula (post-hysterectomy females)
Vomiting + abdominal distension	Obstruction (stricture)
RLQ pain	Right-sided diverticulitis - mimics appendicitis

Elderly and immunocompromised patients may present subtly despite severe disease. Perforation is more frequent in this group and carries high mortality. Do NOT be falsely reassured by mild symptoms.

DIFFERENTIAL DIAGNOSIS

Condition	Distinguishing Feature
Appendicitis	RLQ pain + periumbilical migration + Rovsing's; right-sided diverticulitis can mimic
Ectopic pregnancy	Female + amenorrhoea + βhCG positive
Ovarian pathology (torsion, cyst)	Female; USS findings
PID	Female; cervical motion tenderness; bilateral
Ischaemic colitis	Elderly; post-prandial; cardiovascular risk factors
IBD (Crohn's/UC)	Younger patient; bloody diarrhoea; systemic features
Colorectal carcinoma	Weight loss; change in bowel habit; PR bleeding; always consider
Ureteral/renal stone	Flank pain; haematuria; urinalysis
Inguinal hernia	Groin swelling
Psoas abscess	Hip pain; fever; travel history (TB)

Underlying colorectal malignancy must be excluded - but investigation is safe to defer until resolution of the acute episode

INVESTIGATIONS

Labs

Test	Significance
CBC	Leukocytosis (many patients); may be absent - not needed to make the diagnosis
CRP	Elevated; correlates with severity
BMP (U&E)	Electrolyte derangement; renal function
Urinalysis	Pyuria/bacteriuria with colovesical fistula; haematuria if ureter involved
βhCG	All women of reproductive age - exclude ectopic pregnancy
Blood cultures	If septic / systemically unwell
Lactate	Elevated = sepsis/perfusion compromise

A patient with prior known diverticulitis presenting with similar mild symptoms may not need any testing - empirical treatment is acceptable if no concerning features

Imaging

Modality	Role	Sensitivity/Specificity
CT Abdomen/Pelvis with IV contrast (GOLD STANDARD)	Confirms diagnosis, stages severity, identifies complications	98% sensitivity, 99% specificity
CT with IV + enteric contrast	Ideal (oral or rectal contrast added)	Best for fistula, abscess
Ultrasound	Accessible; limited by bowel gas; operator dependent	Lower than CT
Plain X-ray	Non-specific; only useful for free air (perforation)	Low diagnostic yield
Barium/water-soluble enema	No longer recommended in acute phase	Risk of perforation
Colonoscopy	Contraindicated in acute phase (perforation risk); defer until resolution	Follow age-appropriate screening

CT Findings in Diverticulitis

Colonic wall thickening
Pericolonic fat stranding (hallmark)
Diverticulae visible
Localised microperforation
Pericolic abscess
Free air (perforation)
Free fluid

HINCHEY CLASSIFICATION (CT-Based Staging)

Stage	Description	Management
Ia	Pericolic phlegmon and inflammation, no fluid collection	Antibiotics ± admission
Ib	Pericolic/mesenteric abscess <4 cm	IV antibiotics; often responds without drainage
II	Pelvic/distant abscess >4 cm	Percutaneous CT-guided drainage + IV antibiotics
III	Purulent peritonitis (contained perforation)	Emergency surgery
IV	Faeculent peritonitis (free perforation)	Emergency surgery - highest mortality

TREATMENT

Uncomplicated Diverticulitis

Current evidence: Acute diverticulitis is more inflammatory than infectious. Antibiotics are NOT mandatory in all uncomplicated cases (AGA 2015 guidelines - selective use).

Patient	Management
Mild, immunocompetent, tolerating PO, reliable follow-up	Outpatient management: liquid diet advancing as tolerated ± oral antibiotics
Cannot tolerate PO / elderly / immunocompromised / significant comorbidities / poor social support	Admit for IV antibiotics + bowel rest

Oral antibiotic options (if used):

Ciprofloxacin 500 mg PO BD + Metronidazole 500 mg PO q8h
Amoxicillin-clavulanate 875/125 mg PO BD

Studies show no benefit of IV over oral antibiotics for uncomplicated diverticulitis

Complicated Diverticulitis

Complication	Management
Small abscess ≤4 cm	IV antibiotics alone — 80%+ success rate
Large abscess >4 cm (Hinchey II)	Percutaneous CT-guided drainage + IV antibiotics; surgery if fails
Fistula (colovesical, colovaginal)	Broad-spectrum antibiotics; elective surgical resection + fistula repair after acute phase
Obstruction (partial)	NG decompression + IV fluids + antibiotics + bowel rest; elective resection after resolution
Obstruction (complete)	Emergency surgery
Purulent peritonitis (Hinchey III)	Emergency surgery: Hartmann's procedure or primary resection + anastomosis
Faeculent peritonitis (Hinchey IV)	Emergency surgery - Hartmann's; highest morbidity/mortality

IV Antibiotic Regimens (Complicated / Admitted):

Piperacillin-tazobactam
Cefepime + Metronidazole
Ciprofloxacin + Metronidazole
Meropenem/Imipenem (severe/resistant)

Surgical Options

Procedure	Description
Hartmann's procedure	Sigmoid resection + end colostomy (no anastomosis) — used in emergency/contaminated field
Primary resection + anastomosis	With or without diverting loop ileostomy
Laparoscopic lavage	For Hinchey III (purulent) — controversial
Common bile duct exploration (T-tube)	Not applicable here

Surgery for acute diverticulitis indicated for: peritonitis, sepsis unresponsive to medical management, failed percutaneous drainage

Elective Surgery Considerations

After a diverticular abscess (Hinchey Ib/II) - ASCRS recommends considering elective resection after successful non-operative treatment
Recurrence after first uncomplicated episode is only ~13% - routine prophylactic surgery no longer recommended after 2 episodes
Individualise surgical decision-making based on patient factors

COMPLICATIONS OF DIVERTICULITIS

Complication	Key Points
Abscess	Most common complication; <4 cm = antibiotics; >4 cm = percutaneous drainage
Fistula	Colovesical (#1 in males) → pneumaturia + fecaluria; Colovaginal (post-hysterectomy females); Colocutaneous (at drain sites)
Obstruction	Stricture from chronic inflammation/fibrosis; can mimic malignancy
Perforation	Free faecal peritonitis = emergency; high mortality
Haemorrhage	From diverticulosis (NOT diverticulitis - bleeding is painless)

DISPOSITION

Patient	Disposition
Mild uncomplicated, immunocompetent, tolerating PO, reliable follow-up	Discharge with oral antibiotics, liquid diet, GP follow-up in 48-72h
Mild uncomplicated but elderly, immunocompromised, or unable to tolerate PO	Admit for IV antibiotics + bowel rest
Complicated (abscess, sepsis, signs of perforation)	Admit ± surgical consult
Hinchey III/IV, haemodynamic instability, peritonitis	Emergency surgical consult + ICU

HIGH-YIELD EXAM PEARLS

LLQ pain >24h = diverticulitis until proven otherwise (sigmoid = most common site)
RLQ diverticulitis mimics appendicitis - more common in Asian populations
CT with IV contrast is gold standard - 98% sensitivity, 99% specificity
Antibiotics NOT mandatory in mild uncomplicated diverticulitis (inflammatory, not purely infective)
Oral antibiotics = IV antibiotics in uncomplicated diverticulitis - no benefit to IV
Elderly and immunocompromised present subtly but have more severe disease and higher perforation risk
Colovesical fistula = #1 fistula type (especially males) → pneumaturia + fecaluria + recurrent polymicrobial UTIs
Hinchey Ib/II (abscess) → percutaneous drainage if >4 cm
Hinchey III/IV (peritonitis) → emergency surgery (Hartmann's)
Abscess <4 cm → antibiotics alone (80%+ resolution rate)
Colonoscopy is contraindicated in acute phase - defer until resolution
Colorectal malignancy must be excluded - defer colonoscopy to follow age-appropriate screening after recovery
Diverticular bleeding is painless (no inflammation) - accounts for 40% of lower GI bleeds
Routine elective surgery after 2 uncomplicated episodes is no longer recommended - individualise
Free air on CT = perforation = emergency surgery

Sources: Rosen's Emergency Medicine Ch.81 | Sabiston Textbook of Surgery | Mulholland & Greenfield's Surgery 7e | Sleisenger & Fordtran's GI & Liver Disease

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Tintinalli's Block 24 — Contents (Pages 1966–2040)

🦴 Musculoskeletal / Orthopaedic

Chapter	Topics
Ch. 284	Septic Arthritis (bacterial nongonococcal + gonococcal), Crystal-induced synovitis (Gout & Pseudogout), Viral Arthritis, Lyme disease, Hemarthrosis, Rheumatoid arthritis, Osteoarthritis, Reactive arthritis, Bursitis (olecranon, prepatellar)
Ch. 285	Foot disorders — Ingrown toenail, Plantar fasciitis, Tarsal tunnel syndrome, Ganglions, Tenosynovitis, Tendon ruptures, Plantar neuroma, Compartment syndrome of foot

🧠 Psychiatric / Behavioural

Chapter	Topics
Ch. 286	Psychiatric assessment in the ED — medical clearance, history, MSE, capacity vs competency, involuntary patients, disposition
Ch. 287	Acute Agitation — verbal de-escalation, pharmacology (haloperidol, ketamine, atypical antipsychotics), restraints
Ch. 288	Delirium — clinical features, mental status exam, treatment

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Section 24 is psychosocial disorders kindly give some predicted important questions with answers from that chapter for final exam

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Here are the predicted important questions with detailed answers from Tintinalli's Section 24 — Psychosocial Disorders, covering all key chapters:

🧠 Section 24: Psychosocial Disorders

Predicted Final Exam Q&A

Tintinalli's Emergency Medicine, Chapters 286–292

CHAPTER 286 — PSYCHIATRIC ASSESSMENT IN THE ED

Q1. What is meant by "medical clearance" in a psychiatric patient presenting to the ED?

A: Medical clearance refers to an initial medical evaluation performed on patients with psychiatric or behavioural complaints to ensure that no serious organic (medical/surgical) pathology is causing or contributing to the presentation. It is NOT a guarantee that the patient is medically "cleared" — rather it is an assessment of medical stability.

7-10% of patients admitted to psychiatric wards have an organic condition that was missed
Examples of missed organic pathology: meningitis, sepsis, delirium, acetaminophen toxicity, neuroleptic malignant syndrome, hepatic encephalopathy, myxedema coma, DKA, epidural/subdural haematoma
New-onset psychosis or altered mental status = organic cause until proven otherwise — psychiatric diagnosis is a diagnosis of exclusion

Q2. What are the key deficiencies commonly found in medical clearance assessments of psychiatric patients in the ED?

A: Studies have documented the following poor-quality assessment deficiencies:

Over 1/3 of assessments lacked a documented history
8% had no physical examination documented
Vital signs were frequently not complete or not reassessed when abnormal
Mental status examination missing in up to 56% of cases
Neurologic examination components absent:
- Cranial nerve testing absent in 50%
- Motor exam absent in 72%
- Sensory exam absent in 88%
- Gait testing absent in 75%
Failure to develop/refine differential diagnosis
"Anchoring" on psychiatric diagnoses without ruling out organic causes
"Kitchen sink" mentality — ordering unnecessary tests without targeted reasoning

Q3. What are the principles of interviewing a psychiatric patient in the ED?

A: (Table 286-4 - Tintinalli's)

Safety first:

Know exit locations before entering — stand close to the exit
Maintain enough distance to avoid being physically attacked
Wear a badge clip that cannot be used to choke you

Establishing cooperation/rapport:

Always introduce yourself clearly
Establish eye contact; smile if possible
Reuse terms the patient uses before asking for clarification (makes patient feel heard)
Start with open-ended questions (best for rapport)
Transition to close-ended questions if open-ended are unproductive
Last resort: Yes/no and multiple-choice questions

Q4. What are the principles of applying violent restraints in the ED?

Ideally performed by a team of 5 — one team leader + one person per limb
A "show of force" with multiple staff present may subdue the patient without actual restraint
Place patient on bed/stretcher; secure all 4 limbs with leather restraints (soft restraints for non-violent settings)
Elevate the patient's head to minimise aspiration risk
Once restrained: offer medications; if refused → administer involuntarily
Provide ongoing explanation to patient and family throughout
Avoid injury to both patient and personnel

Q5. What distinguishes capacity from competency?

	Capacity	Competency
Determined by	Physician (at the bedside)	Court/legal system
Setting	Clinical / ED	Legal proceeding
Time	Moment-specific; can change	More permanent legal determination
Scope	Decision-specific (can have capacity for one decision, not another)	Global

A patient has decision-making capacity if they can: understand information, appreciate consequences, reason about choices, and communicate a decision
Capacity assessment is the ED physician's responsibility; competency is a judge's determination

CHAPTER 287 — ACUTE AGITATION

Q6. What is the definition of acute agitation in the ED context, and what is the recommended stepwise approach?

A: Agitation is defined as a "temporary disruption of the typical physician-patient collaboration which has unintended consequences for the staff or other patients."

Recommended Best Practice Approach (Tintinalli's):

Approach with safety in mind — plan even before patient arrives
Attempt verbal de-escalation in ALL patients first
If worsens: employ a "show of concern" (presence of calm, assertive team)
Treat underlying medical cause first
Restraints only to protect staff/patient from harm — use sparingly
Target medications to most likely cause
Use oral medications when possible
Use second-generation (atypical) antipsychotics as first-line in most situations (except alcohol intoxication)

The goal is to treat agitation sufficiently to allow a thorough medical evaluation

Q7. What is the Sedation Assessment Tool (SAT) and when is medication given?

A: The SAT is a scale from -3 to +3 used to rate level of agitation:

Score	Description
+3	Combative, violent, out of control
+2	Very agitated, pulling at lines/tubes
+1	Agitated, restless
0	Alert and calm
-1	Drowsy, responds to voice
-2	Light sedation
-3	Deep sedation

Patients who cannot be calmed by verbal de-escalation or oral medication receive parenteral medication at scores of +2 or +3

Q8. Describe the pharmacological management of acute agitation. What are the first-line agents?

Situation	First-line Agent	Notes
Most agitation (psychiatric, unknown cause)	Second-generation antipsychotics (olanzapine, ziprasidone, risperidone)	Safer, fewer EPS, effective
Alcohol intoxication	Benzodiazepines (lorazepam)	Antipsychotics less effective; seizure risk
Rapid/extreme agitation	Ketamine (dissociative dose)	Rapid onset; useful pre-intubation or when other agents fail
Classic option	Haloperidol (typical antipsychotic)	Still widely used; risk of QTc prolongation and EPS
Mild-moderate	Oral olanzapine, oral risperidone	Preferred if patient can take oral meds

Key point: Risperidone injection cannot be given within 1 hour of an IM benzodiazepine (risk of severe respiratory depression)

CHAPTER 288 — DELIRIUM & DEMENTIA

Q9. What are the three types of delirium? Which is most commonly missed?

Type	Features	Frequency
Hypoactive ("quiet delirium")	Decreased psychomotor activity, somnolent, withdrawn	Most common + most commonly missed
Hyperactive	Agitated, anxious, combative, increased psychomotor activity	Easier to recognise
Mixed	Alternates between hyper- and hypoactive states	Also common

Delirium is present in 7-10% of elderly ED patients
Diagnosis missed by providers in 57-83% of cases
Delirium is an independent predictor of 6-month mortality
If missed in ED, likely to be missed on inpatient services as well

Q10. How do you differentiate delirium from dementia (minor neurocognitive disorder)?

Feature	Delirium	Dementia
Onset	Acute (hours to days)	Gradual (months to years)
Course	Fluctuating	Progressive but stable day-to-day
Consciousness	Altered	Usually preserved until late
Attention	Impaired	Less affected early
Reversibility	Often reversible	Generally irreversible
Key feature	Acute + fluctuating	Chronic + gradual

Key exam point: Delirium is more likely to occur in patients with underlying dementia — both can coexist

Q11. What is the Mini-Cog test and how is it scored?

A: A 3-minute bedside cognitive screening tool combining:

Three-word recall (e.g., apple, table, penny)
Clock drawing test

Scoring:

Recalls all 3 words → No cognitive impairment (clock drawing not needed)
Recalls 0 words → Cognitive impairment (clock drawing not needed)
Recalls 1-2 words → Clock drawing required to determine result
Clock drawing normal = negative for impairment; abnormal = positive

Q12. What are the different types of dementia and their key distinguishing features?

Dementia	Onset	Key Features
Alzheimer's disease	Gradual	Primarily memory; personality changes; visual-spatial problems
Vascular dementia	Sudden or stepwise	Symptoms correlate with area of brain ischemia
Lewy body dementia	Gradual	Memory + hallucinations + Parkinsonian features; AVOID typical antipsychotics (very poorly tolerated - can cause severe worsening)
Frontotemporal dementia	<60 years old	Disinhibition, apathy, language difficulties; frontal/temporal atrophy

Lewy body dementia — patients resemble delirium (rapid decline, fluctuating course, perceptual disturbances) and do very poorly with typical antipsychotics

Q13. What is the treatment of delirium? What drugs must be avoided?

Treat the underlying cause (infection, metabolic, drug withdrawal, etc.)
Non-pharmacologic first: reorientation, familiar faces, lighting cues, noise reduction
Low-dose haloperidol or atypical antipsychotics — if pharmacologic treatment needed for safety
AVOID benzodiazepines in delirium (worsen confusion) — EXCEPT in:
- Alcohol withdrawal seizures
- Benzodiazepine withdrawal
- Catatonia
If benzodiazepines needed in elderly: choose agents with lower risk of accumulation — Lorazepam, Oxazepam, Temazepam (LOT - no active metabolites)

CHAPTER 289 — DEPRESSION & SUICIDE

Q14. What are the DSM-5 criteria for Major Depressive Disorder (MDD)?

A: ≥5 symptoms present for ≥2 weeks, with at least one being depressed mood OR anhedonia:

Depressed mood most of the day
Anhedonia (decreased interest/pleasure in activities)
Significant weight loss or gain / appetite change
Insomnia or hypersomnia
Psychomotor retardation or agitation
Fatigue or loss of energy
Feelings of worthlessness or excessive guilt
Difficulty concentrating or indecisiveness
Suicidal ideation (with or without a plan)

Must cause significant functional impairment; not due to substance abuse or medical condition

Q15. What are the PHQ-2 screening questions for depression in the ED?

A: The two validated Patient Health Questionnaire-2 questions:

"During the past month, have you been bothered by feeling down, depressed, or hopeless?"
"During the past month, have you been bothered by little interest or pleasure in doing things?"

A positive answer to either warrants further evaluation with PHQ-9 or other tools.

Q16. How do you assess suicide risk in the ED?

Ask direct, non-judgmental questions about suicidal and homicidal thoughts
Seek corroborative information from family, friends, EMS, law enforcement
Ask specifically about access to firearms/weapons
Place at-risk patients in a safe, monitored environment; remove dangerous items
Cannot adequately evaluate suicidality until patient is no longer intoxicated (not necessarily zero alcohol — return to baseline cognition)
Key comorbidities: alcohol and drug abuse are major suicide risk factors
Consider involuntary hold if imminent risk to self or others
Use the SAD PERSONS scale or Columbia Suicide Severity Rating Scale (C-SSRS)

SAD PERSONS risk factors:

Sex (male)
Age (<19 or >45)
Depression
Previous attempt
Ethanol abuse
Rational thinking loss
Social support lacking
Organised plan
No spouse
Sickness (chronic illness)

CHAPTER 290 — PSYCHOSIS / SCHIZOPHRENIA

Q17. What is the mechanism of action of antipsychotic medications?

Most antipsychotics block D2 dopamine receptors and 5-HT2A serotonin receptors
Typical (first-generation) — classified by potency (referring to degree of D2 blockade, not effectiveness):
- High potency (haloperidol, fluphenazine): less sedating, more extrapyramidal side effects (EPS) — tremors, rigidity, akathisia, acute dystonia
- Low potency (chlorpromazine): more sedating; more hypotension and anticholinergic effects
Atypical (second-generation) (olanzapine, risperidone, quetiapine, aripiprazole): more selective; fewer EPS; treat negative symptoms better; risk of metabolic syndrome

Q18. Which typical antipsychotics are associated with QTc prolongation and what is the clinical concern?

Mesoridazine, Thioridazine — both associated with QTc prolongation (FDA black box warning)
Haloperidol IV — can cause QTc prolongation
Ziprasidone — associated with QT prolongation among atypicals
Clinical concern: QTc prolongation → risk of Torsades de Pointes (TdP), a potentially fatal ventricular arrhythmia
In practice: in emergencies, a priori ECG is often impractical; use clinical judgment and review available ECG data

CHAPTER 291 — BIPOLAR DISORDER

Q19. What are the medications used for bipolar disorder and their key ED-relevant side effects?

Drug	Class	Key Side Effects / ED Considerations
Lithium carbonate	Mood stabiliser	Toxicity: narrow therapeutic window; toxicity with NSAIDs, ACE inhibitors, diuretics; tremor, ataxia, polyuria, renal toxicity; avoid in renal failure; reduce dose in elderly
Valproic acid	Antiepileptic / GABA enhancer	GI upset, hepatotoxicity, thrombocytopaenia, weight gain, hair loss, teratogenic (neural tube defects)
Carbamazepine	Antiepileptic, Na-channel blocker	Monitor LFTs and platelets; drug interactions (P450 inducer)
Lamotrigine	Antiepileptic, Na-channel blocker	Risk of Stevens-Johnson syndrome (especially if dose escalated too quickly); OCP failure
Olanzapine	Atypical antipsychotic	Metabolic syndrome, weight gain, sedation
Risperidone	Atypical antipsychotic	IM form: cannot give within 1 hour of IM benzodiazepine
Quetiapine	Atypical antipsychotic	Sedation; slower titration with valproic acid

Lithium toxicity is triggered by: NSAIDs, ACE inhibitors, diuretics, dehydration, renal impairment

CHAPTER 292 — EATING DISORDERS

Q20. What are the serious medical complications of anorexia nervosa that require ED recognition?

Cardiovascular:

Bradycardia, hypotension, orthostasis
Prolonged QTc → Torsades de Pointes risk
Sudden cardiac death

Electrolyte/metabolic (especially in purging-type):

Hypokalaemia (most dangerous — arrhythmias)
Hypochloraemia, metabolic alkalosis (vomiting)
Hypophosphataemia, hypomagnesaemia, hypoglycaemia (severe starvation)

Refeeding syndrome (after prolonged starvation):

Rapid refeeding → insulin release → shift of K⁺, Phos, Mg into cells
→ Hypokalaemia, hypophosphataemia, hypomagnesaemia
→ Arrhythmias, cardiac arrest, heart failure

Endocrine:

Hypothalamic amenorrhoea (low LH, FSH, oestrogen)
Euthyroid sick syndrome (normal/low TSH, low T3)
Osteoporosis (risk persists years after recovery)

GI:

Mallory-Weiss tear or Boerhaave syndrome (forceful vomiting)
Gastric dilatation, gastroparesis, constipation

Neurological:

Wernicke-Korsakoff encephalopathy (thiamine deficiency) — confusion, ataxia, ophthalmoplegia, nystagmus
Pellagra (niacin deficiency) — diarrhoea, dermatitis, dementia

SUMMARY: TOP 10 EXAM TRAPS

New-onset psychosis/AMS = organic cause until proven otherwise — never assume psychiatric first
Hypoactive delirium is most common AND most missed — can be confused with depression
Delirium = acute + fluctuating; Dementia = gradual + progressive
Lewy body dementia — AVOID typical antipsychotics (catastrophic worsening)
Benzodiazepines worsen delirium — use only for alcohol withdrawal, BZD withdrawal, catatonia
Risperidone IM cannot be given within 1 hour of IM benzodiazepine
Lithium toxicity triggered by NSAIDs, ACE inhibitors, diuretics
Capacity = physician determines (bedside); Competency = court/legal determines
Cannot assess suicidality while patient is intoxicated — wait for return to baseline cognition
Refeeding syndrome — hypophosphataemia → cardiac arrest after re-nutritioning severely starved patients

Source: Tintinalli's Emergency Medicine, Section 24 — Chapters 286-292

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