01Approach to the Critical Patient/attcp50

Hemodynamic instability

›Shock recognition

›HR >= 100 beats/min with SBP <= 100 mmHg

›Associated with higher transfusion requirements and worse outcomes

›Immediate large-bore IV access x2 and fluid resuscitation

›Hypovolemic shock features

›Altered mental status

›Oliguria

›Cool, clammy extremities

›Orthostatic vitals if hemodynamically borderline

›Drop in SBP >= 20 mmHg or HR rise >= 20 on standing

›Indicates significant volume depletion

Airway and resuscitation priorities

›Airway protection

›Active hematemesis with altered mental status

›High aspiration risk

›Rapid sequence intubation if unable to protect airway

›Massive ongoing hemorrhage

›Call for emergent endoscopy and GI consultation

›Activate massive transfusion protocol if required

›Resuscitation targets

›IV crystalloid 1-2 L bolus for initial volume replacement

›Reassess after each bolus

›pRBC transfusion threshold Hgb < 7 g/dL (< 8 g/dL with active cardiac ischemia)

›Avoid over-transfusion in cirrhotic patients

›Over-transfusion worsens portal hypertension

Monitoring and escalation

›Monitoring bundle

02History/hx74

Presentation pattern

›Classic presentation

›Nonbloody emesis or retching followed by hematemesis

›Classic sequence occurs in only approximately 29% of cases

›Blood with first episode of vomiting is more common

›Hematemesis characteristics

›Volume estimation

›Bright red vs coffee-ground appearance

›Vomiting context

›Onset, frequency, severity, and triggers

›Alcohol binge most common precipitant in approximately 44% of cases

›Other triggers: food bolus, coughing, straining, hiccups, seizures

›Duration of retching before bleeding onset

›Prolonged retching increases tear risk

Alarm features

›High-risk symptoms

›Hemodynamic symptoms

›Lightheadedness and dizziness

›Syncope or presyncope

›Severe chest or back pain

›Subcutaneous emphysema or crepitus

›Suspect Boerhaave syndrome if present

›Hematochezia in setting of UGIB

›Indicates brisk severe hemorrhage

›Associated GI symptoms

›Melena

›Indicates slower or more proximal bleeding

›Abdominal pain character

03Physical Exam/exam56

Vital signs and hemodynamic assessment

›Hemodynamic stability assessment

›Blood pressure

›SBP <= 100 mmHg indicates significant hemorrhage

›Orthostatic drop >= 20 mmHg indicates volume depletion

›Heart rate

›HR >= 100 beats/min correlates with worse outcomes

›Shock index (HR/SBP) > 1 predicts transfusion need

›Oxygen saturation

›Baseline room air value

›Aspiration risk screening

General and HEENT exam

›General appearance

›Pallor and diaphoresis

›Acute blood loss indicators

›Dry mucous membranes

›Volume depletion indicator

›Altered mental status

›Hypovolemia or alcohol intoxication

›HEENT findings

›Subcutaneous emphysema in the neck

›Critical finding for Boerhaave syndrome

›Palpate supraclavicular fossae and anterior neck

Chest and abdominal exam

›Chest examination

›Hamman sign (mediastinal crunch on auscultation)

›Pathognomonic for pneumomediastinum

›Boerhaave syndrome indicator

04Differential Diagnosis/ddx41

Life-threatening diagnoses

›Cannot-miss diagnoses

›Boerhaave syndrome (transmural esophageal rupture)

›ICD-10: K22.3

›Mackler triad: vomiting, chest pain, subcutaneous emphysema

›Mortality 20-50%; requires immediate surgical intervention

›Esophageal varices

›ICD-10: I85.11

›Known liver disease or cirrhosis

›Typically more massive hemorrhage

›Aortoenteric fistula

›ICD-10: I77.2

›History of aortic graft

›Herald bleed followed by massive hemorrhage

Common upper GI bleeding causes

›Peptic ulcer disease

›ICD-10: K25-K27

›Most common cause of UGIB overall

›Epigastric pain and NSAID or H. pylori history

›Forrest classification guides endoscopic management

›Erosive esophagitis

›ICD-10: K20.0

›Heartburn, dysphagia

›Usually less severe bleeding than MWT

›GERD history

›Mallory-Weiss tear

›ICD-10: K22.6

›Mucosal laceration at gastroesophageal junction

05Laboratory Tests/lt45

Initial hemorrhage workup

›Complete blood count

›Hemoglobin and hematocrit

›Initial value may not reflect true blood loss for hours

›Trend is more meaningful than single value

›Platelet count

›Thrombocytopenia increases rebleeding risk

›Target > 50 x 10^9/L before endoscopy

›Coagulation studies

›PT and INR

›Coagulopathy predicts complicated course

›INR > 1.5 associated with worse outcomes

›aPTT

›Heparin monitoring if relevant

›Fibrinogen

›Disseminated intravascular coagulation screen in massive hemorrhage

Metabolic and renal assessment

›Basic metabolic panel

›BUN to creatinine ratio

›Ratio > 20:1 suggests upper GI source from digested blood

›Highly specific for UGIB

›Electrolytes

›Hypokalemia and hypochloremia from vomiting

›Metabolic alkalosis from HCl loss

›Liver function tests

›AST, ALT, alkaline phosphatase, bilirubin

›Screen for underlying liver disease

›Cirrhosis affects management significantly

06Diagnostic Tests/dt79

Scoring Systems

›Glasgow-Blatchford Score (GBS)

›Validated for risk stratification in UGIB

›GBS of 0-1 identifies patients safe for outpatient management

›Components: BUN, hemoglobin, SBP, HR, melena, syncope, hepatic disease, cardiac failure

›Clinical utility

›Higher sensitivity than Rockford Score for need for intervention

›Level B evidence for risk stratification in UGIB

›AIMS65 Score

›Predicts in-hospital mortality in UGIB

›Components: albumin < 30 g/L, INR > 1.5, altered mental status, SBP <= 90 mmHg, age >= 65 years

›Score >= 2 associated with significantly higher mortality

›Score 0-1: low mortality risk

›Score >= 2: high mortality risk requiring ICU consideration

›Shock Index

›Heart rate divided by systolic blood pressure

›Shock index > 1 predicts transfusion need in MWT

›Useful at initial presentation for rapid triage

›Normal shock index 0.5-0.7

›Index > 1 requires immediate resuscitation

›Rockford (Forrest) Classification

›Endoscopic risk stratification for active bleeding

›Class Ia: spurting hemorrhage; highest rebleeding risk

›Class Ib: oozing hemorrhage

›Class IIa: visible vessel; intermediate risk

›Class IIb: adherent clot

›Class IIc: flat pigmented spot

›Class III: clean ulcer base; lowest rebleeding risk

MRI

›MRI role in Mallory-Weiss tear

›Generally not indicated for acute MWT diagnosis

›Time-prohibitive in acute hemorrhage setting

›EGD is definitive diagnostic and therapeutic tool

›Potential role in complex or subacute presentations

›Esophageal wall assessment when radiation exposure is a concern

›Post-treatment evaluation of esophageal integrity

›MRI for Boerhaave syndrome assessment

›Not first-line due to time constraints

›CT with oral contrast preferred for acute evaluation

›MRI may characterize mediastinal involvement in stable patients

CT

›CT chest with oral contrast

›Indicated when Boerhaave syndrome is suspected

›Pneumomediastinum identification

›Pleural effusion with esophageal wall thickening

›Extraluminal contrast leak

›ACR Appropriateness Criteria 2024

›CT angiography for massive UGIB when endoscopy not feasible

›Sensitivity for active bleeding > 0.5 mL/min

›CT angiography

›Role in massive UGIB

›When endoscopy is not feasible or fails to localize bleeding

›Can guide transcatheter arterial embolization

›Sensitivity for active GI bleeding

›Requires bleeding rate > 0.3-0.5 mL/min for detection

›Chest X-ray

›Initial screen for Boerhaave complications

›Pneumomediastinum

›Subcutaneous emphysema

›Left-sided pleural effusion

Ultrasound

›Point-of-care ultrasound applications

›Volume status assessment

›IVC collapsibility index

›IVC diameter < 2 cm with > 50% collapse indicates volume depletion

›Pleural effusion detection

›Left-sided effusion in Boerhaave syndrome

›Felipe et al. 2021: bedside ultrasound aids Boerhaave diagnosis

›Abdominal POCUS

›Free peritoneal fluid assessment

›FAST exam for free fluid in perforation concern

›Significant free fluid suggests esophageal perforation

›Hepatic and portal assessment

›Liver texture and portal vein Doppler

›Splenomegaly suggesting portal hypertension

›Upper endoscopy (EGD)

›Gold standard for diagnosis and therapy

›Longitudinal mucosal lacerations at the GEJ

›Most commonly on lesser curvature and left lateral wall of gastric cardia

›Timing recommendations

›Within 24 hours for all UGIB requiring admission

›Urgent or emergent for hemodynamically unstable patients

›NEJM 2020: urgent vs non-urgent endoscopy timing data

07Disposition/dispo43

Discharge criteria

›Safe discharge criteria

›Hemodynamically stable

›GBS of 0-1 for outpatient management

›No active bleeding at endoscopy

›No high-risk features

›No coagulopathy

›No portal hypertension

›No significant comorbidities

›Reliable follow-up available

›GI follow-up within 1-2 weeks

›Patient able to understand return precautions

Admission criteria

›Floor or general ward admission

›Transfusion requirement

›Active bleeding controlled endoscopically

›Significant comorbidities requiring monitoring

›Known liver disease with stable coagulation

›Anticoagulant use requiring reversal monitoring

›GBS >= 2 without high-risk features

›Observation for rebleeding

›Rebleeding typically occurs within 24 hours if it occurs

›ICU or high-dependency admission

›Hemodynamic instability despite resuscitation

›Massive hemorrhage

›Hypovolemic shock

›Need for intubation

›Airway protection failure

08Treatment/t93

Initial resuscitation

›Vascular access and volume

›Two large-bore IV lines

›18-gauge or larger

›Antecubital or forearm preferred

›IV crystalloid resuscitation

›1-2 L normal saline or lactated Ringer as initial bolus

›Reassess after each bolus for response

›Blood product transfusion

›Packed red blood cells

›Threshold Hgb < 7 g/dL in stable patients

›Threshold Hgb < 8 g/dL with active cardiac ischemia

›Avoid over-transfusion in cirrhotic patients

›Fresh frozen plasma

›INR > 1.5 with active bleeding

›10-15 mL/kg

›Platelets

›Platelet count < 50 x 10^9/L with active bleeding

›Clopidogrel effect reversal consideration

Acid suppression therapy

›Proton pump inhibitor

›Pantoprazole 80 mg IV bolus then 8 mg/hr continuous infusion

›Initiate on presentation in all UGIB

›IV infusion for 72 hours then transition to oral

›Mechanism

›Raises gastric pH > 6 to stabilize clot formation

›Reduces pepsin activation and clot lysis

›Evidence

›Class I recommendation for PPI in acute UGIB

›Reduces rebleeding rates and need for surgery

›Transition to oral PPI

›Omeprazole 40 mg orally twice daily or pantoprazole 40 mg once daily

›Continue for 4-8 weeks post-discharge

›Promotes mucosal healing

Antiemetic therapy

›Ondansetron

›4 mg IV or 8 mg IV

›Reduces further retching and vomiting

›Prevents extension of tear or new tear formation

›Alternative agents

›Metoclopramide 10 mg IV

›Prochlorperazine 10 mg IV

›Rationale

›Ongoing vomiting perpetuates mucosal injury

›Aggressive antiemetic therapy is a key management priority

›Reduces transfusion requirements indirectly

Endoscopic therapy

›Indications for endoscopic intervention

›Active bleeding at endoscopy (Forrest Class I or IIa)

›Non-bleeding tears with clean base do not require intervention

›Approximately 90% stop bleeding spontaneously

›Epinephrine injection

›1:10,000 concentration

›Primary hemostasis approximately 94% efficacy

›Most commonly used first-line technique

›Mechanism

›Local vasoconstriction and tamponade effect

›Hemoclipping

›Effective mechanical hemostasis

›Widely used and widely available

›Class I recommendation for endoscopic hemostasis

›Band ligation

›100% primary hemostasis in prospective RCT

›Comparable to epinephrine injection

›Park et al. 2004: prospective randomized trial EBL vs epinephrine

›Preferred technique by some endoscopists

›Particularly for longer lacerations

›Combination therapy

›Injection plus clipping

›Used for refractory cases

›Reduces rebleeding rates vs monotherapy

Salvage therapies

›Transcatheter arterial embolization

›Interventional radiology approach

›When endoscopy fails to control bleeding

›Left gastric artery embolization most common target

›Success rates

›Technical success approximately 85-90%

›Clinical success approximately 60-80%

›Surgical intervention

›Exceedingly rare; less than 0.1% of cases

›Oversewing of the laceration via gastrotomy

›Reserved for endoscopy and IR failure

Coagulation reversal

›Warfarin reversal

›Vitamin K 10 mg IV slow infusion

›Effect in 6-24 hours

›4-factor PCC (Kcentra) for rapid reversal

›Dose based on INR and weight

›Immediate reversal within minutes

›DOAC reversal

›Dabigatran: idarucizumab 5 g IV

›Complete reversal

›Factor Xa inhibitors: andexanet alfa

›Dose based on agent and last dose timing

›Antiplatelet management

›Hold acutely

›Restart timing individualized based on thrombotic risk

›Cardiology consultation for high thrombotic risk patients

09Special Populations/sp71

Pregnancy

›Physiologic considerations in pregnancy

›Hyperemesis gravidarum

›Severe nausea and vomiting in first trimester

›Primary precipitant of MWT in pregnant patients

›Hemodynamic changes

›Physiologic tachycardia and lower baseline blood pressure

›May mask severity of hemorrhage

›Diagnostic approach

›Endoscopy safety in pregnancy

›EGD generally safe in all trimesters when clinically indicated

›Position in left lateral decubitus to reduce aortocaval compression

›Imaging considerations

›Avoid CT if possible, especially first trimester

›Ultrasound preferred for volume status assessment

›Treatment modifications

›PPI use in pregnancy

›Omeprazole and pantoprazole: FDA Category C

›Benefits outweigh risks in active hemorrhage

›Antiemetic therapy

›Ondansetron: use with caution; first trimester cardiac defect concern

›Metoclopramide: preferred in first trimester

›Fetal monitoring

›Continuous fetal heart rate monitoring if viable gestation

›Obstetric consultation for all cases in second and third trimester

Geriatric

›Physiologic considerations

›Blunted hemodynamic response

10Background/b74

Epidemiology

›Incidence and prevalence

›Mallory-Weiss tear accounts for 3-14% of acute UGIB cases

›Second most common cause of non-variceal UGIB after PUD

›Mertens et al. 2024: large systematic German registry analysis

›Demographic distribution

›Male-to-female ratio approximately 3.6:1

›Median age 51 years

›Peak incidence in fifth to sixth decade

›Outcomes data

›Spontaneous cessation in approximately 90% of cases

›Majority managed without endoscopic intervention

›In-hospital mortality approximately 2.7%

›Higher in cirrhotic patients and those with coagulopathy

›Complications

›Bleeding anemia: 26%

›Hypovolemic shock: 2.9%

›Progression to Boerhaave syndrome: rare case reports

›Rebleeding

›Uncommon in uncomplicated cases

›Typically occurs within 24 hours if it occurs

›Higher risk with portal hypertension and coagulopathy

Pathophysiology

›Mechanism of injury

›Sudden increase in intra-abdominal or intragastric pressure

›Forceful vomiting or retching most common mechanism

›Pressure transmitted to gastroesophageal junction

›Mucosal tear formation

›Longitudinal mucosal lacerations at or near GEJ

›Most commonly on lesser curvature and left lateral wall of gastric cardia

›Role of hiatal hernia

›Present in approximately 20% of cases

›Alters pressure dynamics at GEJ

›Watts 1976: hiatal hernia effect on injury site

›Vascular anatomy

›Submucosal vessels at GEJ

›Rich vascular plexus susceptible to shear forces

›Arterial bleeding more common than venous

›Portal hypertension effect

›Increased mucosal blood flow and venous engorgement

›Higher severity and rebleeding risk

›Additional precipitants beyond vomiting

›Hiccups, seizures, straining

›Any mechanism causing abrupt intra-abdominal pressure elevation

›CPR

›Mechanism: chest compressions with gastric distension

›Severe coughing paroxysms

›Chronic obstructive lung disease risk

Therapeutic Considerations

›Endoscopic timing evidence

›NEJM 2020 (Lau et al.)

›Urgent endoscopy within 6 hours vs within 24 hours

›Urgent endoscopy did not improve outcomes in stable patients

›Standard approach: within 24 hours for stable patients

›Unstable patients

›Emergent endoscopy after initial resuscitation

›GI consultation trigger threshold is hemodynamic instability

›Endoscopic therapy evidence

›Park et al. 2004 RCT

›Band ligation vs epinephrine injection for active MWT bleeding

›Band ligation achieved 100% primary hemostasis

›Epinephrine injection: primary hemostasis approximately 94%

›Approximately 35% of patients have a second bleeding lesion identified at endoscopy

›Systematic complete endoscopic evaluation is mandatory

›Bharucha et al. 1997: clinical and endoscopic risk factors

›Transfusion strategy

›Restrictive transfusion strategy (threshold Hgb 7 g/dL)

›Reduces all-cause mortality vs liberal strategy in UGIB

›Avoid over-transfusion in cirrhotic patients

›Exception: cardiac ischemia risk

›Threshold 8 g/dL for cardiovascular disease

›Natural history

›Most tears heal within 48-72 hours without intervention

›Long-term prognosis excellent in absence of underlying liver disease

›Alcohol cessation

›Most impactful modifiable risk factor

›Reduces recurrence risk significantly

11Patient Discharge Instructions/pdi27

copy discharge instructions

›Discharge instructions for Mallory-Weiss Tear

›What happened

›You had a small tear in the lining of the esophagus or stomach where they meet

›This was caused by forceful vomiting or retching

›Most tears heal on their own within 2-3 days

›Medications

›Take your acid-reducing medication (proton pump inhibitor) exactly as prescribed

›Continue for 4-8 weeks to allow complete healing

›Avoid NSAIDs such as ibuprofen and naproxen; use acetaminophen for pain

›Do not restart blood thinners until cleared by your doctor

›Diet and activity

›Start with clear liquids and advance to a bland diet as tolerated

›Avoid alcohol completely; alcohol was the main cause in many cases

›Avoid spicy, acidic, or irritating foods for 2 weeks

›Small frequent meals reduce pressure on the stomach

›Stay well hydrated

›Follow-up

›See your gastroenterologist within 1-2 weeks

›Report any return of symptoms promptly

›Return to the emergency department immediately if you experience

›Vomiting blood again or seeing blood in the toilet

›Black or tarry stools

›Lightheadedness, dizziness, or fainting

›Severe chest or back pain

›Shortness of breath

›Severe abdominal pain

›Rapid heart rate or feeling that your heart is racing

12References/r46

Guidelines and key sources

›Primary evidence sources

›Mertens A et al. J Clin Gastroenterol 2024

›Systematic analysis of incidence, therapeutic strategies, and in-hospital mortality of Mallory-Weiss syndrome in Germany

›PMID: 37668412

›Graham DY, Schwartz JT. Medicine 1978

›The spectrum of the Mallory-Weiss tear; foundational epidemiology

›PMID: 307105

›He L et al. Medicine 2019

›Prediction value of scoring systems in Mallory-Weiss syndrome patients

›PMID: 31145291

›Bharucha AE, Gostout CJ, Balm RK. Am J Gastroenterol 1997

›Clinical and endoscopic risk factors in Mallory-Weiss syndrome

›PMID: 9149189

›Park CH et al. Gastrointest Endosc 2004

›Prospective randomized trial: endoscopic band ligation vs epinephrine injection for actively bleeding MWT

›PMID: 15229420

›Management guidelines

›Lau JYW et al. NEJM 2020

›Timing of endoscopy for acute upper gastrointestinal bleeding

›Urgent vs non-urgent endoscopy outcomes

›Laine L. NEJM 2016

›Upper GI bleeding due to peptic ulcer; applicable management framework for UGIB

›Long B, Gottlieb M. Am J Emerg Med 2024

›Emergency medicine updates: upper gastrointestinal bleeding

›PMID: 38723362

›Shung DL, Laine L. Aliment Pharmacol Ther 2024

›Upper gastrointestinal bleeding: review of current evidence and management implications

Evidence & Review

Evidence & Review