01Approach to the Critical Patient/attcp73

Immediate priorities

›Airway and breathing threats

›Active hematemesis with aspiration risk

›Depressed mental status or encephalopathy

›Inability to protect airway during massive emesis

›Oxygenation failure

›SpO2 < 92% on room air

›Desaturation during active emesis

›If unable to protect airway, proceed to early definitive airway management

›Rapid sequence intubation preferred

›Videoassisted laryngoscopy recommended given blood in oropharynx

›Circulation and hemorrhagic shock

›Shock physiology triggers

›SBP < 90 mmHg

›Heart rate > 110 beats/min

›Orthostatic changes (BP drop > 20 mmHg)

›Two large-bore IV access (16G or larger) immediately

›Central venous access if peripheral inadequate

›IO access if emergent resuscitation required

›Massive transfusion protocol activation criteria

›Hemodynamic instability unresponsive to crystalloid

›Active bright red hematemesis with signs of shock

›Resuscitation targets

›MAP > 65 mmHg

›Permissive hypotension SBP 80-90 mmHg until endoscopy control

›Key early resuscitation steps

›Volume resuscitation

›Restrict crystalloid to avoid worsening portal pressure

02History/hx63

Presentation pattern

›Core presenting symptoms

›Hematemesis character

›Bright red blood emesis — most common in variceal bleed (67% of cases)

›Coffee-ground emesis

›Volume and frequency of emesis

›Melena

›Black tarry stools indicating upper GI source

›Duration since onset

›Hematochezia

›Bright red blood per rectum — suggests massive bleed with rapid transit

›Presyncope or syncope

›Lightheadedness on standing

›Transient loss of consciousness

Bleeding context

›Temporal history

›Time of onset and rate of progression

›Acute onset vs. gradual worsening

›Rapidity distinguishes hemodynamic risk

›Prior GI bleeding episodes

›Prior variceal bleeding — strongest predictor of rebleeding

›Prior endoscopic treatments (EVL, sclerotherapy)

›History of TIPS placement

Liver disease history

›Known or suspected cirrhosis

›Etiology of liver disease

›Alcohol-related cirrhosis (most common in North America)

›Chronic hepatitis B or C

03Physical Exam/exam52

Vital signs and hemodynamic assessment

›Hemodynamic status

›Blood pressure

›Hypotension SBP < 90 mmHg indicates class III or IV hemorrhage

›Orthostatic drop > 20 mmHg suggests at least 15% blood volume loss

›Heart rate

›Tachycardia > 100 beats/min in response to hemorrhage

›Relative bradycardia may be blunted by beta-blocker use

›Respiratory rate and SpO2

›Tachypnea in response to anemia or aspiration

›Temperature

›Fever suggests concurrent infection (SBP, pneumonia)

Stigmata of chronic liver disease

›Cutaneous findings (specificity > 90% for cirrhosis)

›Spider angiomas

›> 5 on upper body increases cirrhosis probability

›Palmar erythema

›Terry nails (whitened proximal nail bed)

›Jaundice and scleral icterus

›Gynecomastia (men)

›Decreased body hair, testicular atrophy

›Alcohol-specific findings

›Parotid enlargement

›Dupuytren contracture

›Peripheral neuropathy signs

Abdominal examination

›Ascites assessment

›Shifting dullness

04Differential Diagnosis/ddx39

Portal hypertensive sources

›Esophageal variceal hemorrhage (ICD-10: I85.01)

›Most common cause of UGIB in cirrhosis (~70% of episodes)

›Mortality 10-20% at 6 weeks even with optimal therapy

›Distinguishing feature: painless massive hematemesis in known cirrhotic

›Gastric variceal hemorrhage (ICD-10: I86.4)

›Often more massive and more difficult to control endoscopically

›Fundal varices (GOV2, IGV1) associated with higher rebleeding rates

›Cyanoacrylate glue injection preferred over EVL

›Portal hypertensive gastropathy (ICD-10: K31.89)

›Diffuse mucosal oozing in chronic setting

›Mosaic pattern on endoscopy

›Usually slower bleed, less hemodynamically dramatic

›Ectopic varices

›Duodenal, rectal, stomal, or periumbilical locations

›Consider if EGD is negative in known portal hypertension patient

Non-variceal UGIB sources

›Peptic ulcer disease (ICD-10: K27.0)

›Present in ~38% of cirrhotic patients with UGIB

›Melena-predominant presentation

›Helicobacter pylori and NSAID use are risk factors

›Mallory-Weiss tear (ICD-10: K22.6)

›Post-retching hematemesis

›Typically self-limiting; rarely requires intervention

›Distinguish by history of retching before hematemesis

›Dieulafoy lesion (ICD-10: K31.82)

›Arterial bleeding from submucosal vessel without ulceration

›Proximal stomach, near gastroesophageal junction

05Laboratory Tests/lt59

Blood counts and type and screen

›Complete blood count

›Hemoglobin

›Transfusion threshold 70-80 g/L (7-8 g/dL) per AASLD 2024

›Restrictive strategy reduces 6-week mortality vs. liberal

›Initial Hgb may not reflect acute hemorrhage (dilutional lag)

›Platelet count

›Thrombocytopenia < 110 x 10^9/L associated with clinically significant portal hypertension

›Platelet transfusion threshold < 50 x 10^9/L for active bleeding with procedure

›White blood cell count

›Leukocytosis suggests infection or stress response

›Type and crossmatch

›Minimum 2-4 units packed red blood cells

›Emergency release O-negative if immediate transfusion required

Metabolic and liver panel

›Basic metabolic panel

›Creatinine

›Elevated creatinine used in MELD score calculation

›Baseline essential before contrast administration

›Hepatorenal syndrome risk monitoring

›BUN (blood urea nitrogen)

›Elevated BUN-to-creatinine ratio > 30 suggests upper GI source

›Protein load from blood digestion raises BUN

›Sodium

›Hyponatremia common in decompensated cirrhosis

›Sodium < 130 mmol/L in MELD-Na calculation

›Potassium

›Hypokalemia worsens hepatic encephalopathy

06Diagnostic Tests/dt79

Scoring Systems

›MELD score (Model for End-Stage Liver Disease)

›Formula: 3.78 x ln[bilirubin umol/L / 17.1] + 11.2 x ln[INR] + 9.57 x ln[creatinine umol/L / 88.4] + 6.43

›Score 0-40 scale; higher = worse prognosis

›MELD > 15 associated with significantly higher 6-week mortality in variceal bleeding

›MELD-based model by Reverter et al. (Gastroenterology 2014) validated for acute variceal bleeding mortality prediction

›MELD 3.0 includes sex and sodium

›Validated for variceal hemorrhage outcomes in US multicenter cohort (Buckholz et al. 2023)

›Child-Pugh score

›5 variables: bilirubin, albumin, INR, ascites, encephalopathy

›Class A (5-6): compensated cirrhosis, low mortality

›Class B (7-9): moderate dysfunction

›Class C (10-15): highest mortality; 6-week mortality may exceed 30%

›Child-Pugh class C strongest predictor of 6-week mortality in AVH

›Glasgow Blatchford Score (GBS)

›Predicts need for intervention in UGIB

›Variables: BUN, hemoglobin, SBP, heart rate, melena, syncope, hepatic disease, cardiac failure

›GBS 0 identifies low-risk patients potentially suitable for outpatient management

›GBS >= 12 associated with high probability of needing transfusion or endoscopic intervention

›Validated for discriminating variceal vs. non-variceal UGIB risk (Jamil et al. 2022)

›Preemptive TIPS eligibility criteria

›High-risk criteria for early TIPS consideration

›Child-Pugh C score 10-13

›Child-Pugh B with active bleeding at endoscopy

›HVPG > 20 mmHg

›Early preemptive TIPS (within 72 hours) reduces treatment failure and 6-week mortality

MRI

›Liver MRI applications

›MR elastography for liver stiffness quantification

›Noninvasive assessment of clinically significant portal hypertension (CSPH)

›Liver stiffness > 20-25 kPa suggests CSPH by AASLD 2025 guidelines

›Does not replace endoscopy for variceal detection but useful for risk stratification

›MRI liver for hepatocellular carcinoma evaluation

›LI-RADS classification for characterization of focal liver lesions

›Portal vein tumor thrombus assessment (important for TIPS candidacy)

›MR portography

›Non-invasive portal venous anatomy mapping

›Portal vein thrombosis or cavernous transformation assessment

›Less commonly used in acute setting; role in pre-TIPS planning

CT

›CT angiography abdomen/pelvis

›Role in acute variceal bleed

›Not primary diagnostic tool for active variceal hemorrhage

›Useful if endoscopy unavailable or inconclusive

›CT findings supporting portal hypertension and varices

›Varices visible as enhancing tubular structures in portal venous phase

›CT rule-in criteria for CSPH: liver surface nodularity + spleen size > 13 cm

›CT rule-out criteria: liver surface smooth + spleen < 13 cm (Heo et al. Radiology 2023)

›CT for aortoenteric fistula exclusion

›Mandatory if prior aortic graft and UGIB

›Gas around aortic graft or graft-enteric proximity are concerning features

›CT for ectopic variceal source

›Identifies duodenal, ileostomy, or colonic varices when EGD is negative

›CT liver for complication assessment

›Hepatocellular carcinoma detection

›Arterial enhancement and portal washout (LI-RADS criteria)

›Portal vein thrombosis

›Thrombus affects TIPS candidacy and management

›Ascites quantification

Ultrasound

›Bedside emergency ultrasound

›Portal vein diameter and flow

›Portal vein diameter > 13 mm suggests portal hypertension

›Reversal of portal flow (hepatofugal) confirms portal hypertension

›Portal vein ultrasound predicts variceal etiology of UGIB in ED with AUC 0.83 (Naik et al. 2025)

›Spleen size

›Splenomegaly (> 12 cm craniocaudal) supports portal hypertension

›Ascites detection

›FAST-variant for rapid ascites identification

›Guides paracentesis planning if SBP suspected

›Liver morphology

›Nodular liver surface, caudate lobe hypertrophy in cirrhosis

›Doppler ultrasound of portal system

›Hepatic vein patency (excludes Budd-Chiari syndrome)

›Splenic vein assessment

›TIPS patency post-procedure

›Normal TIPS velocity 90-190 cm/s

›Velocity < 60 cm/s suggests dysfunction

›Noninvasive liver stiffness by elastography

›Liver stiffness measurement (LSM) by transient elastography

›LSM > 20-25 kPa = CSPH by AASLD 2025 guideline

›LSM > 15-20 kPa + platelet count < 110 x 10^9/L = high-risk varices

›Can obviate endoscopy screening in low-risk patients (Baveno VII criteria)

07Disposition/dispo37

ICU admission

›Criteria for ICU-level care

›Hemodynamic instability

›Ongoing hypotension despite resuscitation

›Vasopressor requirement

›Airway compromise

›Intubated patients require ICU

›High aspiration risk with encephalopathy

›Active rebleeding

›Rebleeding within 24 hours post-endoscopy

›Failure of two endoscopic attempts at hemostasis

›Severe hepatic decompensation

›Grade III or IV encephalopathy

›Evolving hepatorenal syndrome

›Child-Pugh class C with active bleeding

General ward admission

›Criteria for monitored ward

›Hemodynamically stable after resuscitation

›No vasopressor requirement

›Tolerating oral or NG medications

›Post-endoscopy surveillance

›After successful EVL for continued monitoring

›Minimum 48-72 hours post-procedure observation

›Continued vasoactive therapy

›Octreotide infusion continuation for 2-5 days total

Transfer criteria

›Transfer indications

›No endoscopy capability at receiving facility

08Treatment/t129

Vasoactive therapy

›Octreotide (somatostatin analogue)

›Dosing protocol

›50 mcg IV bolus immediately on clinical suspicion of variceal bleed

›Then 25-50 mcg/hr continuous IV infusion for 2-5 days

›Most commonly used vasoactive agent in North America

›Mechanism and evidence

›Inhibits splanchnic vasodilation reducing portal pressure

›Class I recommendation; reduces early rebleeding when combined with EVL

›Terlipressin (vasopressin analogue)

›Dosing protocol

›2 mg IV every 4-6 hours for 24-48 hours

›Then 1 mg IV every 4-6 hours for up to 5 days total

›Evidence and limitations

›Only vasoactive drug shown to improve survival in variceal bleeding

›Not approved for this indication in North America

›Preferred agent in Europe and Asia

›Contraindications

›Severe coronary artery disease

›Peripheral vascular disease

›Pregnancy

›Vasopressin (avoid)

›Associated with ventricular arrhythmias and sudden death in cirrhotic patients

›JACC review: high risk of cardiovascular complications

›Replaced by terlipressin and somatostatin analogues

Antibiotic prophylaxis

›Ceftriaxone (preferred)

›Dosing

›1 g IV every 24 hours for up to 5 days

›Start before endoscopy regardless of signs of infection

›Evidence

›Prophylactic antibiotics reduce short-term mortality 18.5% vs. 22.2% with placebo

›AASLD 2024 guideline: strong recommendation for antibiotic prophylaxis in all cirrhotic patients with UGIB

›Mechanism

›Reduces risk of spontaneous bacterial peritonitis post-bleed

›GI bleeding triggers bacterial translocation in cirrhosis

›Norfloxacin (alternative)

›400 mg orally twice daily for 7 days

›Alternative when IV access limited or in low-risk patients

›Less preferred than ceftriaxone due to quinolone resistance patterns

Endoscopic treatment

›Esophagogastroduodenoscopy (EGD)

›Timing

›Within 12 hours of presentation in hemodynamically stable patients

›Within 6 hours if ongoing hemodynamic instability

›AASLD 2024: urgent endoscopy improves outcomes in active variceal bleeding

›Erythromycin pre-treatment

›125-250 mg IV given 30-120 minutes before endoscopy

›Prokinetic improves gastric emptying and visualization

›Reduces need for repeat endoscopy

›Endoscopic variceal ligation (EVL)

›Preferred technique for esophageal varices

›EVL superior to sclerotherapy for primary and secondary hemostasis

›Band placed on varix starting at gastroesophageal junction

›Session frequency

›Repeat every 2-4 weeks until variceal obliteration

›Typically 3-5 sessions required for eradication

›Cyanoacrylate glue injection

›Preferred for gastric fundal varices

›GOV2 (type 2 gastroesophageal varices) and IGV1 (isolated gastric varices)

›Superior to EVL for gastric variceal hemostasis

›Complications

›Glue embolization risk

›Requires experienced endoscopist

›Sclerotherapy

›Alternative when EVL not available

›Sodium tetradecyl sulfate or polidocanol injection

›Higher complication rate than EVL (ulceration, stricture)

Bridge to definitive therapy

›Sengstaken-Blakemore tube (balloon tamponade)

›Indications

›Massive refractory hemorrhage as temporizing measure

›Bridge to TIPS or repeat endoscopy

›Technique

›Gastric balloon inflated to 250 mL first

›Esophageal balloon to 30-40 mmHg if continued bleeding

›Limitations

›Rebleeding > 50% on deflation

›Complications: aspiration, esophageal rupture

›Intubate before placement when encephalopathic

›Self-expandable metal stent (SEMS)

›Alternative to balloon tamponade

›Better tolerated than Sengstaken-Blakemore tube

›Can remain in place up to 7-14 days

›Esophageal stent (SX-Ella Danis device) approved for refractory variceal bleeding

TIPS (transjugular intrahepatic portosystemic shunt)

›Indications and timing

›Preemptive early TIPS (within 72 hours)

›Child-Pugh C score 10-13 with active bleeding

›Child-Pugh B with active bleeding at time of endoscopy

›Reduces treatment failure and 6-week mortality in high-risk patients

›Rescue TIPS

›Failed endoscopic hemostasis (two failed attempts)

›Rebleeding within 5 days despite endoscopic + vasoactive therapy

›TIPS target HVPG < 12 mmHg

›Optimal shunt diameter 8-10 mm (PTFE-covered stent)

›Contraindications

›Hepatic encephalopathy grade III or IV (relative)

›Heart failure or hepatopulmonary syndrome (relative)

›Portal vein thrombosis (relative; requires case-by-case evaluation)

›Hepatocellular carcinoma in shunt path

Secondary prophylaxis

›Non-selective beta-blockers (NSBB)

›Carvedilol (preferred NSBB)

›Starting dose 6.25 mg orally daily; target 12.5 mg daily

›Superior portal pressure reduction vs. propranolol

›Initiate at discontinuation of vasoactive therapy

›Propranolol (alternative)

›Starting dose 20 mg orally twice daily

›Titrate to maximum tolerated dose (HR > 55 beats/min, SBP > 90 mmHg)

›NSBB + EVL combination

›Standard of care for secondary prophylaxis (Class I)

›Combination superior to either modality alone

›Proton pump inhibitor

›Pantoprazole 40 mg IV or orally

›Use if non-variceal source cannot be excluded

›Continue if peptic ulcer co-identified at endoscopy

Transfusion strategy

›Red blood cell transfusion

›Restrictive threshold: target Hgb 70-80 g/L (7-8 g/dL)

›Restrictive strategy reduces rebleeding and 6-week mortality vs. liberal

›Liberal strategy worsens portal pressure

›Villanueva et al. NEJM 2013: landmark RCT supporting restrictive strategy

›Exception: active hemodynamic instability

›Liberal transfusion acceptable during acute resuscitation phase

›Fresh frozen plasma

›Do NOT use routinely in cirrhosis with coagulopathy

›Does not reliably correct hemostasis in cirrhosis

›Worsens portal pressure and volume overload

›Use TEG/ROTEM-guided approach instead

›Platelet transfusion

›Threshold < 50 x 10^9/L for active bleeding or invasive procedures

›Avoid routine transfusion for thrombocytopenia alone in cirrhosis

›Cryoprecipitate

›Use if fibrinogen < 1.5 g/L during active resuscitation

›TEG-guided fibrinogen replacement preferred

09Special Populations/sp68

Pregnancy

›Pregnancy-specific considerations

›Prevalence of varices in pregnancy

›Portal hypertension from pre-existing cirrhosis or non-cirrhotic causes

›Increased plasma volume in pregnancy raises portal pressure

›Second trimester peak bleeding risk (maximum blood volume expansion)

›Diagnosis

›EGD safe in all trimesters with appropriate precautions

›Left lateral decubitus position to avoid aortocaval compression after 20 weeks

›Vasoactive therapy in pregnancy

›Octreotide: use with caution; limited human safety data

›Generally considered safer than terlipressin in pregnancy

›Terlipressin: contraindicated in pregnancy (uterotonic effects, fetal harm)

›Vasopressin: avoid due to uterotonic effect

›Endoscopic treatment

›EVL preferred and safe in pregnancy

›Minimize procedure time and radiation exposure

›Beta-blockers for prophylaxis

›Propranolol used with caution; associated with IUGR and neonatal bradycardia

›Benefits generally outweigh risks for secondary prophylaxis

›Fetal monitoring

›Continuous fetal heart rate monitoring during procedures

›Obstetric consultation mandatory

›TIPS in pregnancy

›Relatively contraindicated; radiation exposure and hemodynamic effects

›Reserved for truly refractory cases after multidisciplinary consultation

Geriatric

›Age-related considerations

›Physiologic reserve

›Reduced hepatic synthetic function complicates coagulopathy management

›Lower cardiac reserve limits hemodynamic compensation

›Higher risk of myocardial injury with acute hemorrhage (36% incidence in cirrhotic UGIB)

›Transfusion thresholds

›Consider higher threshold (Hgb 80 g/L) if coronary artery disease or heart failure

›Individual risk-benefit assessment required

›Medication adjustments

›Beta-blocker caution: risk of masking tachycardic response to hemorrhage

›Octreotide safe with standard dosing

›Avoid terlipressin in severe peripheral vascular disease

›Encephalopathy risk

›Higher baseline risk of delirium

›GI blood as protein load triggers encephalopathy

›Lactulose or rifaximin initiation early

›Functional assessment

›Frailty index impacts TIPS candidacy and procedural risk

›Goals of care discussion regarding transplant candidacy

Pediatrics

›Pediatric variceal bleeding considerations

›Etiology differs from adults

›Extrahepatic portal vein obstruction (EHPVO) most common cause in children

›Biliary atresia, neonatal hepatitis as cirrhotic causes

›Wilson disease in older children and adolescents

›Presentation

›Hematemesis often first presentation in child with previously undiagnosed portal hypertension

›Lower tolerance for blood loss relative to smaller body size

›Vasoactive therapy dosing

›Octreotide: 1-2 mcg/kg IV bolus then 1-2 mcg/kg/hr infusion

›Titrate to hemostasis

›Terlipressin: 0.1-0.2 mg IV every 4-6 hours (weight-based dosing)

›Endoscopic treatment

›EVL feasible in children > 10 kg with appropriate pediatric band ligators

›Sclerotherapy used in smaller children where EVL bands are too large

›TIPS in pediatrics

›Feasible in children > 20 kg

›Reserved for refractory bleeding; high technical demand

›Prophylaxis

›NSBB less commonly used in pediatric EHPVO (no benefit for non-cirrhotic portal hypertension)

›EVL eradication program preferred

›Pediatric hepatology referral

›Mandatory for all pediatric cases

›Transplant evaluation if underlying biliary atresia or advanced cirrhosis

10Background/b65

Epidemiology

›Prevalence and incidence

›Variceal bleeding prevalence in cirrhosis

›~50% of cirrhotic patients develop esophageal varices

›Annual risk of first variceal bleed: 5-15% in those with varices

›Large varices or red wale signs confer highest annual bleeding risk (15-20%)

›Mortality

›6-week mortality 10-20% with optimal modern therapy (AASLD 2024)

›Child-Pugh class C patients: 6-week mortality may exceed 30%

›Myocardial injury in 36% of AVH cases with 21% 6-week mortality vs. 7% without

›Incidence trends

›Declining mortality over past 3 decades due to octreotide, EVL, and antibiotic protocols

›Cirrhosis prevalence increasing due to NAFLD epidemic

›Rebleeding risk

›6-week rebleeding rate 15-20% even with optimal therapy

›Highest risk in first 5 days post-event (early rebleeding period)

›1-year rebleeding risk without secondary prophylaxis: 60-70%

Pathophysiology

›Portal hypertension development

›HVPG (hepatic venous pressure gradient)

›Normal HVPG < 5 mmHg

›CSPH (clinically significant portal hypertension) defined as HVPG >= 10 mmHg

›Variceal formation threshold: HVPG >= 10-12 mmHg

›Variceal bleeding threshold: HVPG >= 12 mmHg

›Increased intrahepatic resistance

›Structural: fibrous tissue, regenerative nodules, architectural distortion

›Functional: hepatic stellate cell contraction, endothelin excess, reduced nitric oxide

›Splanchnic vasodilation

›Nitric oxide and other vasodilators cause splanchnic arterial dilation

›Increases portal venous inflow augmenting portal pressure

›Variceal formation and rupture

›Portosystemic collateral formation

›Gastroesophageal junction collaterals most clinically significant

›Coronary (left gastric) vein is main feeding vessel for esophageal varices

›Variceal wall tension law

›Laplace's law: wall tension = transmural pressure x radius / wall thickness

›Increasing variceal size increases wall tension; risk of rupture rises

›Red wale signs indicate local areas of thinned variceal wall

›Bleeding trigger factors

›Acute HVPG elevation (e.g., after Valsalva, coughing, alcohol binge)

›Bacterial infection increases HVPG transiently

›Erosion from reflux esophagitis

Therapeutic Considerations

›Endoscopy timing evidence

›Within 12 hours standard for all presentations

›Earlier endoscopy (< 6 hours) does not improve outcomes in stable patients

›Very early endoscopy (< 6 hours) recommended if hemodynamic instability

›Erythromycin pre-treatment improves endoscopy quality

›Reduces need for repeat endoscopy

›Number needed to treat approximately 7 patients

›Restrictive transfusion strategy evidence

›Villanueva et al. NEJM 2013

›RCT: restrictive (Hgb < 70 g/L) vs. liberal (Hgb < 90 g/L) strategy

›Restrictive: 6-week mortality 5% vs. liberal 9% (NNT = 25)

›Restrictive: lower portal pressure and lower rebleeding rate

›Mechanism: avoiding overload reduces portal pressure increase

›Antibiotic prophylaxis evidence

›Meta-analyses confirm reduction in bacterial infections and short-term mortality

›Short-term mortality reduction: 18.5% vs. 22.2% with placebo

›Ceftriaxone superior to norfloxacin in advanced cirrhosis (higher proportion of gram-negatives)

›Duration: 5-7 days; discontinue if no infection established

›Preemptive TIPS evidence

›Garcia-Pagan et al. NEJM 2010: landmark RCT

›TIPS within 72 hours vs. vasoactive + EVL in high-risk patients

›1-year treatment failure: 3% vs. 50%

›1-year mortality: 14% vs. 39% in high-risk group

›Subsequent validation in multiple cohorts (Class IIa recommendation)

›High-risk criteria: Child-Pugh C 10-13 or Child-Pugh B with active bleeding at endoscopy

11Patient Discharge Instructions/pdi37

copy discharge instructions

›Diagnosis and what happened

›You were admitted with bleeding from abnormal blood vessels in your esophagus called varices

›These form because of increased pressure in the blood vessels around the liver

›This is related to your liver disease (cirrhosis)

›You received treatment to stop the bleeding

›Medications to lower the pressure in your veins

›A procedure called endoscopy to treat the bleeding vessels

›Medications

›Continue all prescribed medications as directed

›Do not stop your beta-blocker without talking to your doctor

›Take lactulose if prescribed for confusion prevention

›Avoid these medications

›No ibuprofen, naproxen, aspirin, or other NSAIDs

›No blood thinners unless specifically prescribed by your specialist

›Diet and lifestyle

›No alcohol — this is essential to protect your liver and reduce bleeding risk

›Even small amounts of alcohol can cause life-threatening bleeding

›Low-sodium diet if you have fluid in your belly (ascites)

›Less than 2 grams of sodium per day

›Eat small frequent meals; avoid very large meals

›Stay well hydrated with water and non-alcoholic beverages

›Follow-up appointments

›Hepatology or gastroenterology appointment within 1-2 weeks

›You will need a repeat scope procedure to check your varices

›Repeat banding (EVL) every 2-4 weeks until the varices are gone

›Primary care follow-up

›Medication review and bloodwork monitoring

12References/r46

Guidelines and key sources

›AASLD Practice Guidance on Risk Stratification and Management of Portal Hypertension and Varices in Cirrhosis

›Kaplan DE, Ripoll C, Thiele M, et al.

›Hepatology. 2024. doi:10.1097/HEP.0000000000000647

›Primary source for vasoactive therapy, antibiotic protocols, transfusion targets, and TIPS indications

›AGA Clinical Practice Update on the Use of Vasoactive Drugs and Intravenous Albumin in Cirrhosis: Expert Review

›Garcia-Tsao G, Abraldes JG, Rich NE, Wong VW.

›Gastroenterology. 2024. doi:10.1053/j.gastro.2023.10.016

›Diagnosis and Management of Cirrhosis and Its Complications: A Review

›Tapper EB, Parikh ND.

›JAMA. 2023. doi:10.1001/jama.2023.5997

›Source for epidemiology, physical exam findings, risk factors, and dietary recommendations

Landmark trials and prognostic tools

›Restrictive vs. liberal transfusion strategy in acute GI bleeding

›Villanueva C, Colomo A, Bosch A, et al.

›NEJM. 2013. doi:10.1056/NEJMoa1211801

›Established restrictive transfusion as standard of care

›Preemptive TIPS in high-risk variceal bleeding

›Garcia-Pagan JC, Caca K, Bureau C, et al.

›NEJM. 2010. doi:10.1056/NEJMoa0910102

›RCT demonstrating survival benefit of early TIPS in Child-Pugh B/C patients

›MELD-based model for acute variceal bleeding mortality

›Reverter E, Tandon P, Augustin S, et al.

›Gastroenterology. 2014. doi:10.1053/j.gastro.2013.08.023

›MELD 3.0 vs. Child Score in variceal hemorrhage outcomes

›Buckholz A, Wong R, Curry MP, et al.

›Hepatology Communications. 2023. doi:10.1097/HC9.0000000000000273

Evidence & Review