Browse categories and answer follow-up questions to refine your symptom profile.
Approach to the Critical Patient
Immediate priorities
Initial stabilization
Airway protection triggers
Encephalopathy with loss of protective reflexes
Recurrent emesis with aspiration risk
Circulation targets
Mean arterial pressure 65 mmHg or higher
Urine output 0.5 ml/kg/hour or higher
Point-of-care threats
Hypoglycemia
Active gastrointestinal bleeding
Sepsis physiology
Acute liver failure screen
Acute liver failure definition
Coagulopathy with INR 1.5 or higher
Any hepatic encephalopathy
No known cirrhosis
Illness duration under 26 weeks
High-risk features
Encephalopathy
INR 2.0 or higher
Rapidly rising bilirubin
Severe hypoglycemia
Lactate elevation with shock physiology
Suspected acetaminophen toxicity
Early coordination
Hepatology consultation triggers
Acute liver failure criteria
Severe acute hepatitis with INR 1.5 or higher
Suspected autoimmune hepatitis with coagulopathy
Transplant center referral triggers
Acute liver failure criteria
King’s College criteria met
Progressive encephalopathy
Monitoring
Continuous monitoring set
Cardiac monitoring
Pulse oximetry
Neurologic trend
West Haven encephalopathy grade
Serial mental status documentation
Glucose surveillance
Bedside glucose every 1 to 2 hours in acute liver failure
Key concepts
Syndrome framing
Acute hepatitis pattern
Marked aminotransferase elevation
Variable bilirubin elevation
Cholestatic pattern
Predominant alkaline phosphatase elevation
Predominant direct hyperbilirubinemia
Mixed pattern
Combined hepatocellular and cholestatic features
Time-critical pitfalls
Acetaminophen toxicity without reliable history
Low threshold acetaminophen level
Low threshold N-acetylcysteine if timing unclear
Ischemic hepatitis as shock marker
Profound aminotransferase rise with hypotension episode
Lactate elevation and end-organ hypoperfusion
History
Symptom and timeline
Symptom profile
Onset and duration
Hours to days
Days to weeks
Constitutional symptoms
Fever
Malaise
Anorexia
Hepatobiliary symptoms
Jaundice
Dark urine
Pale stools
Pruritus
Right upper quadrant pain
Gastrointestinal symptoms
Nausea
Vomiting
Diarrhea
Exposure and risk
Viral hepatitis risks
Hepatitis A exposure
Recent travel
Foodborne exposure
Household contact
Hepatitis B risks
Unprotected sex
Needle exposure
Healthcare exposure
Perinatal exposure history
Hepatitis C risks
Injection drug use
Prior transfusion or transplant
Needlestick exposure
Hepatitis E risks
Travel to endemic regions
Undercooked pork or game exposure
Medication and toxin risks
Acetaminophen exposure
Single large ingestion
Repeated supratherapeutic dosing
Combination cold and flu products
Drug-induced liver injury risks
Recent new prescription
Herbal and supplement use
Antibiotics exposure
Antiseizure medication exposure
Alcohol exposure
Heavy recent use
Last drink timing
Autoimmune and metabolic clues
Autoimmune history
Thyroid disease
Inflammatory bowel disease
Other autoimmune diagnoses
Family history
Liver disease
Hemochromatosis
Wilson disease
Severity and complications
Hepatic decompensation symptoms
Confusion or sleep reversal
Easy bruising or bleeding
Hematemesis or melena
Systemic red flags
Persistent hypotension episode
Severe abdominal pain with peritonism
Pregnancy status
Immunocompromised state
Physical Exam
General and vital signs
Global assessment
Mental status
Orientation
Asterixis
Hemodynamic state
Hypotension
Tachycardia
Hydration status
Mucous membranes
Orthostatic symptoms
Skin and mucosa
Jaundice
Scleral icterus
Diffuse jaundice
Rash patterns
Viral exanthem
Drug eruption
Bleeding stigmata
Petechiae
Ecchymoses
Abdominal and liver focused
Abdominal findings
Right upper quadrant tenderness
Murphy sign
Guarding or rigidity
Hepatomegaly
Liver edge tenderness
Splenomegaly
Portal hypertension clue
Ascites
Shifting dullness
Fluid wave
Neurologic complications
Encephalopathy features
Asterixis
Hyperreflexia
Intracranial hypertension concern
Severe agitation
Declining GCS
PITFALLS
Common misses
Early acute liver failure with subtle confusion
Sleep pattern reversal as early clue
Asterixis may be absent early
Alcoholic hepatitis mimic of infection
Fever and leukocytosis without bacterial source
Systemic inflammatory physiology
Differential Diagnosis
Life-threatening and time-sensitive
High-acuity causes
Acetaminophen toxicity (ICD-10 T39.1)
Marked aminotransferase rise
Early normal bilirubin possible
Acute liver failure (ICD-10 K72.0)
INR 1.5 or higher with encephalopathy
Hypoglycemia risk
Ischemic hepatitis (shock liver)
Hypotension trigger
Very high aminotransferases
Acute cholangitis (ICD-10 K83.0)
Fever and jaundice
RUQ pain
Acute biliary obstruction
Prominent cholestatic enzymes
Dilated bile ducts on imaging
Hepatocellular pattern causes
Infectious
Acute hepatitis A (ICD-10 B15)
Fecal oral exposure
Symptomatic jaundice common in adults
Acute hepatitis B (ICD-10 B16)
Sexual or parenteral exposure
Serum sickness like prodrome possible
Acute hepatitis C (ICD-10 B17.1)
Often mild or asymptomatic
Serology timing pitfalls
HSV hepatitis
Pregnancy risk
Immunocompromised risk
EBV or CMV hepatitis
Pharyngitis or lymphadenopathy clues
Inflammatory
Autoimmune hepatitis (ICD-10 K75.4)
Female predominance
Other autoimmune history
Toxic and drug-induced
Drug-induced liver injury (ICD-10 K71)
Recent new medication
Mixed or hepatocellular patterns
Alcoholic hepatitis (ICD-10 K70.1)
AST to ALT ratio over 2
Aminotransferases typically under 500 IU/l
Cholestatic pattern causes
Obstructive
Choledocholithiasis (ICD-10 K80.5)
Dilated common bile duct
Episodic pain
Malignancy obstruction
Painless jaundice
Weight loss
Intrahepatic cholestasis
Primary biliary cholangitis (ICD-10 K74.3)
Pruritus prominent
AMA positivity
Sepsis-associated cholestasis
Critical illness context
Direct hyperbilirubinemia
Laboratory Tests
Core panel
Baseline evaluation set
Liver enzymes
ALT
AST
Alkaline phosphatase
GGT
Bilirubin fractionation
Total bilirubin
Direct bilirubin
Synthetic function
INR
Albumin
Metabolic and renal
Electrolytes
Creatinine
Glucose
Hematology
Complete blood count
Platelets
Toxin and targeted tests
High-yield add-ons
Acetaminophen level
Any acute hepatitis without clear cause
Repeated supratherapeutic dosing concern
Salicylate level
Mixed ingestion concern
Unexplained metabolic acidosis
Ethanol level
Altered mental status
Withdrawal risk planning
Etiology workup
Viral hepatitis testing
Hepatitis A
HAV IgM
HAV IgG for immunity context
Hepatitis B
HBsAg
Anti-HBc IgM
Anti-HBs
HBV DNA when severe or immunocompromised
Hepatitis C
Anti-HCV antibody
HCV RNA when acute infection suspected
Hepatitis E
HEV IgM or HEV RNA when travel or pregnancy risk
Autoimmune and metabolic testing
Autoimmune hepatitis markers
ANA
ASMA
IgG level
Wilson disease consideration
Ceruloplasmin in young patients
Hemolysis markers when suspicion high
Hemochromatosis consideration
Ferritin and transferrin saturation
Acute phase elevation pitfalls
Complications and severity labs
Acute liver failure adjuncts
Ammonia
Encephalopathy correlation imperfect
Trend utility limited
Lactate
Shock marker
Prognostic component in criteria sets
Venous blood gas
pH
pCO2 in mmHg
Pregnancy test
All patients with pregnancy potential
Blood cultures
Fever or sepsis physiology
Diagnostic Tests
Scoring Systems
Prognostic and severity tools
King’s College criteria for acute liver failure
Acetaminophen-related
Arterial pH under 7.30 after resuscitation
OR all three
INR over 6.5
Creatinine over 300 umol/l
Grade III or IV encephalopathy
Non-acetaminophen
INR over 6.5
OR three or more risk features
Age under 10 years
Age over 40 years
Etiology non-A non-B hepatitis
Drug-induced liver injury
Duration jaundice to encephalopathy over 7 days
INR over 3.5
Bilirubin over 300 umol/l
MELD-Na
Short-term mortality estimation in liver disease
Limited validation in isolated acute hepatitis without chronic disease
West Haven encephalopathy grade
Grade I sleep reversal and mild confusion
Grade II lethargy and disorientation
Grade III marked confusion and somnolence
Grade IV coma
MRI
MRI and MRCP roles
MRCP indications
Suspected choledocholithiasis with nondiagnostic ultrasound
Persistent cholestatic pattern without clear cause
MRI liver indications
Focal lesion characterization
Vascular complications evaluation when ultrasound limited
Constraints
Limited ED availability
Longer acquisition time
Motion artifact in ill patients
CT
CT abdomen roles
Indications
Alternative abdominal pathology concern
Suspected malignancy obstruction
Complication concern with severe pain
Limitations
Lower sensitivity than ultrasound for gallstones
Radiation exposure
Contrast considerations
AKI risk assessment
Benefit over risk in unstable patients
Ultrasound
Right upper quadrant ultrasound with Doppler
Biliary evaluation
Gallstones
Common bile duct diameter
Intrahepatic duct dilation
Parenchymal clues
Hepatomegaly
Fatty infiltration
Vascular evaluation
Hepatic vein thrombosis concern
Portal vein thrombosis concern
POCUS adjuncts
Ascites detection
IVC assessment for volume status
Disposition
Level of care
Admission criteria
Acute liver failure features
Encephalopathy
INR 1.5 or higher
Severe acute hepatitis features
INR rising trend
Bilirubin rising trend
Intractable vomiting
Dehydration or AKI
Infectious or obstructive concern
Fever or sepsis physiology
Suspected cholangitis
Social and safety concerns
Unreliable follow-up
Ongoing toxin exposure risk
ICU criteria
Advanced encephalopathy
West Haven grade III or IV
Airway protection need
Coagulopathy severity
INR 2.0 or higher with clinical decline
Metabolic instability
Recurrent hypoglycemia
Worsening acidosis
Hemodynamic instability
Vasopressor requirement
Rising lactate with shock physiology
Discharge criteria
Outpatient management suitability
Normal mentation
No asterixis
No confusion
Stable synthetic function
INR under 1.5 and not rising
Glucose stable
No obstructive emergency
No cholangitis physiology
Imaging without obstructing stone when indicated
Follow-up plan reliability
Repeat labs arranged
Etiology testing pending plan
Treatment
Immediate interventions
Supportive care bundle
Fluids and electrolytes
Isotonic crystalloid for hypovolemia
Potassium replacement as needed
Antiemetics
Ondansetron 4 mg IV or PO
Repeat dosing every 6 to 8 hours as needed
Nutrition
Early oral intake as tolerated
Dextrose-containing fluids if poor intake
Medication avoidance
Alcohol abstinence
Avoid unnecessary hepatotoxic agents
Acetaminophen avoidance unless supervised low-dose plan
Antidotes and etiology-directed therapy
N-acetylcysteine
Acetaminophen toxicity treatment
Initiate immediately when toxic ingestion suspected (Class I)
Initiate when level pending and timing unclear (Class I)
IV protocol (21-hour)
Loading dose 150 mg/kg over 1 hour
Maximum 15 g
Second infusion 50 mg/kg over 4 hours
Third infusion 100 mg/kg over 16 hours
Continuation criteria
Continue beyond 21 hours if ALT rising
Continue beyond 21 hours if INR elevated
Continue beyond 21 hours if acetaminophen detectable
Non-acetaminophen acute liver failure
Consider early use in acute liver failure (Class IIa)
Greatest benefit reported in early encephalopathy grades
Suspected HSV hepatitis
Acyclovir
Initiate empiric acyclovir in fulminant hepatitis with pregnancy or immunocompromised risk (Class IIa)
Dosing 10 mg/kg IV every 8 hours
Renal adjustment required
Severe acute hepatitis B
Nucleos(t)ide analog therapy
Consider tenofovir or entecavir in severe or fulminant acute HBV (Class IIa)
Specialist coordination recommended
Cholangitis or biliary obstruction
Antibiotics for cholangitis physiology (Class I)
Piperacillin-tazobactam 4.5 g IV every 6 hours
Ceftriaxone 2 g IV daily
Add metronidazole 500 mg IV every 8 hours
Severe sepsis option
Meropenem 1 g IV every 8 hours
Source control pathway
ERCP urgency for ascending cholangitis
Surgical consultation for cholecystitis overlap
Coagulopathy and bleeding
Coagulopathy principles
INR elevation without bleeding
No routine correction before low-risk care (Class IIb)
Vitamin K trial when malnutrition or cholestasis possible
Phytonadione 10 mg IV once daily for up to 3 days
Active bleeding or urgent procedure
FFP guided by bleeding risk and procedure plan (Class IIa)
Platelets for severe thrombocytopenia with bleeding
Cryoprecipitate for low fibrinogen with bleeding
Encephalopathy and cerebral edema risk
Encephalopathy management
Lactulose
Initiate for encephalopathy when airway protected (Class I)
Dose 20 to 30 g PO or via NG
Titrate to 2 to 3 soft stools daily
Rifaximin
Add-on for recurrent or persistent encephalopathy (Class IIa)
Dose 550 mg PO twice daily
Avoidance
Minimize sedatives
Avoid NSAIDs
Cerebral edema precautions in acute liver failure
Head of bed elevation
30 degrees
Neutral neck position
Hypercapnia avoidance
pCO2 target 35 to 40 mmHg when intubated
Hyperosmolar therapy triggers
Pupillary changes
Cushing physiology
Rapid mental status decline
Hypertonic saline option
3% saline bolus 2 ml/kg
Sodium target 145 to 155 mmol/l
Mannitol option
0.5 to 1 g/kg IV bolus
Avoid if renal failure or hypotension
Symptom control
Pruritus management
Cholestyramine
4 g PO once to twice daily
Separate from other meds by 4 hours
Antihistamines
Limited efficacy for cholestatic itch
Sedation risk with encephalopathy
Pain management
Avoid NSAIDs in liver failure risk
AKI risk
Bleeding risk
Opioids
Lowest effective dose
Monitor mental status closely
Special Populations
Pregnancy
Pregnancy-specific risks
Hepatitis E
Increased severe disease risk
Increased maternal mortality risk in endemic settings
HSV hepatitis
Higher fulminant risk
Low threshold empiric acyclovir in severe hepatitis
Pregnancy-related liver disease mimics
HELLP syndrome
Acute fatty liver of pregnancy
Intrahepatic cholestasis of pregnancy
Medication considerations
N-acetylcysteine safety
Use when indicated
Antiviral selection
Specialist coordination for HBV therapy
Fetal considerations
Obstetrics consultation triggers
Third-trimester disease
Suspected HELLP or acute fatty liver of pregnancy
Geriatric
Older adult considerations
Polypharmacy
Higher drug-induced liver injury risk
Medication reconciliation priority
Baseline comorbidity
Lower physiologic reserve
Higher dehydration and AKI risk
Atypical presentations
Less fever
Subtle encephalopathy
Disposition bias
Lower threshold admission
Borderline INR
Frailty
Limited support
Pediatrics
Pediatric-specific etiologies
Hepatitis A exposure clusters
Daycare outbreaks
Household spread
Metabolic disease
Wilson disease in older children
Inborn errors with acute decompensation
Accidental ingestion
Acetaminophen dosing errors
Weight-based dosing
N-acetylcysteine dosing by actual weight
Use pediatric infusion protocols
Acyclovir dosing by weight
Renal adjustment required
Referral thresholds
Early pediatric hepatology involvement
Coagulopathy
Encephalopathy
Persistent rising enzymes
Background
Epidemiology
Burden and patterns
Viral hepatitis
Hepatitis A outbreaks linked to contaminated food and close contact
Hepatitis B transmission sexual and parenteral
Hepatitis C transmission primarily blood exposure
Drug-induced liver injury
Common cause of acute hepatitis presentations
Antibiotics and supplements frequent contributors
Acetaminophen toxicity
Leading cause of acute liver failure in many high-income settings
Pathophysiology
Hepatocellular injury mechanisms
Viral-mediated cytotoxicity
Immune-mediated hepatocyte injury
Variable cholestasis
Toxic-metabolic injury
Reactive metabolites and oxidative stress
Mitochondrial dysfunction
Ischemic injury
Centrilobular necrosis
Reperfusion injury component
Jaundice mechanisms
Unconjugated bilirubin
Hemolysis contribution
Reduced conjugation contribution
Conjugated bilirubin
Hepatocellular excretion failure
Bile duct obstruction
Therapeutic Considerations
N-acetylcysteine rationale
Glutathione repletion
Detoxification of NAPQI metabolite
Microcirculatory and antioxidant effects
Rationale for non-acetaminophen acute liver failure trials
Antiviral rationale in severe HBV
Viral suppression to reduce ongoing hepatocyte injury
Bridge to recovery or transplant evaluation
Encephalopathy management rationale
Ammonia reduction
Lactulose reduces intestinal ammonia absorption
Rifaximin reduces ammonia-producing gut flora
Patient Discharge Instructions
copy discharge instructions
Discharge instructions
Activity and diet
Rest as needed
Fluids to maintain light yellow urine
Avoidance
No alcohol until cleared by clinician
No acetaminophen unless specifically instructed
Avoid new supplements or herbal products
Infection control and exposure reduction
Hand hygiene after bathroom use
No sharing razors or toothbrushes
Use barrier protection for sex until cleared
No blood donation until cleared
Follow-up plan
Repeat bloodwork within 48 to 72 hours
Primary care or hepatology follow-up arranged
Review pending hepatitis tests
Return to emergency triggers
Confusion
Excessive sleepiness
New bleeding or black stools
Persistent vomiting
Severe worsening abdominal pain
Fainting or severe weakness
Fever with worsening jaundice
Yellowing rapidly worsening over 24 to 48 hours
References
Clinical guidelines and key sources
Reference set
AASLD guidance on acute liver failure evaluation and management
Early transplant center referral for acute liver failure
Critical care management principles
EASL clinical practice guidance on drug-induced liver injury
Diagnostic framework for DILI
Dechallenge and rechallenge cautions
CDC hepatitis resources
Hepatitis A, B, C testing interpretation
Exposure risk and prevention measures
King’s College criteria source literature
Prognostic criteria for acute liver failure
Limitations and clinical context requirement
Coding and terminology
Standardized terms
ICD-10 acute hepatitis A B15
SNOMED CT acute hepatitis A
ICD-10 acute hepatitis B B16
SNOMED CT acute hepatitis B
ICD-10 acute hepatitis C B17.1
SNOMED CT acute hepatitis C
ICD-10 toxic liver disease K71
SNOMED CT drug-induced liver injury
ICD-10 acute liver failure K72.0
SNOMED CT acute hepatic failure
SymptomDx is an educational tool for medical professionals. It does not replace clinical judgment. Verify all clinical data and drug dosages with authoritative sources.