Hepatic Encephalopathy in Adults

Quick Reference

⚠️ Red Flag: ### Critical Alerts

• Identify and treat precipitants immediately: Infection (SBP), GI bleeding, constipation, medications, electrolyte disturbance
• Ammonia level does NOT correlate with severity: Clinical grading is paramount for management decisions
• Risk of cerebral oedema in acute liver failure: Type A HE has different pathophysiology requiring ICP management
• Differentiate from other causes of AMS: Hypoglycaemia, sepsis, stroke, subdural haematoma, Wernicke's
• Lactulose is first-line treatment: Target 2-3 soft stools daily; both under and over-treatment are harmful
• Diagnostic paracentesis mandatory: All cirrhotic patients with ascites and altered mental status require SBP exclusion
• Minimal HE affects driving: All patients should be assessed and counselled regarding driving fitness

Key Diagnostics

Emergency Treatment Algorithm

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Overview

Hepatic encephalopathy (HE) represents a spectrum of potentially reversible neuropsychiatric abnormalities occurring in patients with liver dysfunction, characterised by alterations in consciousness, cognition, behaviour, and neuromuscular function. [1] The syndrome results from the accumulation of gut-derived neurotoxins, primarily ammonia, that bypass hepatic metabolism due to portosystemic shunting or hepatocellular failure. [2]

HE represents one of the most serious complications of cirrhosis and significantly impacts quality of life, hospitalisation rates, and survival. The condition ranges from subtle cognitive deficits detectable only on psychometric testing (minimal or covert HE) to deep coma (overt HE Grade IV). [3] Recognition of the full spectrum is essential, as even minimal HE impairs daily functioning, work performance, and driving ability.

The 2014 joint AASLD-EASL Practice Guideline established the current classification framework distinguishing Type A (acute liver failure), Type B (portosystemic bypass without intrinsic liver disease), and Type C (cirrhosis), with the latter accounting for the vast majority of clinical cases. [1] Management centres on identifying and treating precipitating factors, reducing gut-derived ammonia through non-absorbable disaccharides (lactulose), and preventing recurrence with rifaximin in appropriate patients.

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Epidemiology

Prevalence and Incidence

Hepatic encephalopathy affects a substantial proportion of patients with cirrhosis, though true prevalence varies by detection method and disease severity:

Demographics and Risk Factors

Prognosis and Mortality

The development of overt HE marks a critical milestone in the natural history of cirrhosis with significant prognostic implications:

Exam Detail: Exam Pearl - Prognosis: The development of overt HE indicates decompensated cirrhosis and should prompt consideration of liver transplant evaluation in appropriate candidates. HE is incorporated into the MELD score through bilirubin and INR but is not directly included. Some centres use "MELD-exception" points for recurrent HE.

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Classification

Type Classification (Aetiology)

The 2014 AASLD-EASL guidelines classify HE by underlying liver disease: [1]

West Haven Criteria (Severity Grading)

The West Haven criteria remain the standard clinical grading system for overt HE: [1,3]

Clinical Pearl: Covert vs Overt HE:

• Covert HE = Minimal HE + Grade I (no obvious clinical manifestations)
• Overt HE = Grade II-IV (clinically apparent)
• This distinction is crucial as covert HE significantly impacts quality of life, driving ability, and employment despite appearing "normal" on standard clinical examination.

Classification by Time Course

Classification by Precipitant

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Pathophysiology

The Ammonia Hypothesis

Ammonia is the central neurotoxin in HE pathogenesis, though the syndrome results from complex interactions between ammonia and other factors: [2,8]

Ammonia Metabolism in Health

Normal Ammonia Handling:
┌─────────────────────────────────────────────────────────────────────┐
│  GUT                    PORTAL VEIN           LIVER                 │
│  ───                    ───────────           ─────                 │
│  Bacterial urease  →    Ammonia (NH3)    →    Urea cycle:          │
│  Protein digestion →    absorption       →    NH3 → Urea → Kidney  │
│  Glutamine breakdown                          → Glutamine synthesis │
│                                                                     │
│  MUSCLE (backup pathway):                                           │
│  NH3 + Glutamate → Glutamine (skeletal muscle detoxification)      │
└─────────────────────────────────────────────────────────────────────┘

Ammonia Metabolism in Cirrhosis

In cirrhosis, multiple derangements lead to hyperammonaemia: [2,8]

Astrocyte Swelling and Cerebral Effects

Exam Detail: Molecular Pathophysiology:

The primary target of ammonia in the brain is the astrocyte, the only cell type capable of ammonia detoxification via glutamine synthetase: [2,9]

Step-by-Step Mechanism:

1. Ammonia crosses BBB: NH3 (uncharged) freely crosses blood-brain barrier
2. Astrocyte uptake: Ammonia enters astrocytes
3. Glutamine synthesis: NH3 + Glutamate → Glutamine (via glutamine synthetase)
4. Osmotic swelling: Glutamine accumulation causes osmotic water influx
5. Low-grade astrocyte oedema: "Alzheimer Type II astrocytosis" on pathology
6. Mitochondrial dysfunction: Glutamine enters mitochondria → "Trojan horse" hypothesis
7. Oxidative stress: Mitochondrial permeability transition → ROS generation
8. Neurotransmitter imbalance: Altered glutamate/GABA ratio

Key Differences: Acute vs Chronic Liver Failure:

Gut-Derived Neurotoxins Beyond Ammonia

Multiple gut-derived substances contribute to HE pathogenesis: [2,10]

The Gut-Liver-Brain Axis

Modern understanding recognises HE as a disorder of the gut-liver-brain axis: [10,11]

Gut-Liver-Brain Axis in HE:
┌─────────────────────────────────────────────────────────────────────┐
│                                                                     │
│   DYSBIOSIS ────────→ INCREASED PERMEABILITY ────────→ TRANSLOCATION│
│      ↓                        ↓                           ↓        │
│   ↑ Ammonia            Bacterial products              Endotoxaemia │
│   ↑ Toxins             cross gut barrier               ↓           │
│      ↓                        ↓                    Systemic         │
│   ↓ Metabolism ←────── LIVER DYSFUNCTION ←──────  Inflammation      │
│      ↓                                                 ↓            │
│   HYPERAMMONAEMIA + SYSTEMIC INFLAMMATION → NEUROINFLAMMATION      │
│                                                        ↓            │
│                              ASTROCYTE SWELLING + BBB DYSFUNCTION   │
│                                                        ↓            │
│                              HEPATIC ENCEPHALOPATHY                 │
└─────────────────────────────────────────────────────────────────────┘

Role of Systemic Inflammation

Systemic inflammation significantly modulates HE severity independent of ammonia levels: [11,12]

Clinical Pearl: Why Ammonia Doesn't Correlate with Severity: The poor correlation between serum ammonia levels and HE grade in cirrhosis is explained by:

1. Astrocyte adaptation in chronic disease
2. Variable contribution of inflammation
3. Individual differences in BBB permeability
4. Muscle mass differences affecting peripheral metabolism
5. Sample handling (ammonia rises rapidly ex vivo)

Clinical Bottom Line: Treat the patient, not the ammonia level.

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Precipitating Factors

Identification and treatment of precipitating factors is the cornerstone of HE management. Approximately 90% of overt HE episodes have an identifiable precipitant: [1,4]

Major Precipitants

Additional Precipitants

Medication-Related Precipitants

⚠️ Warning: High-Risk Medications in Cirrhosis:

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Clinical Presentation

Symptoms by Grade

Minimal Hepatic Encephalopathy (MHE)

Patients appear normal on standard clinical examination but have measurable deficits: [3,5]

Overt Hepatic Encephalopathy

Key Physical Examination Findings

Signs of Chronic Liver Disease

Neurological Signs in HE

• negative myoclonus with wrist dorsiflexion | Grade II (best detected); absent in coma | | Fetor hepaticus | Sweet, musty breath odour | Any grade | | Constructional apraxia | Inability to copy star/clock, poor handwriting | Grade I-II | | Hyperreflexia | Increased deep tendon reflexes | Early grades | | Hyporeflexia | Decreased reflexes | Late grades (Grade III-IV) | | Rigidity | Increased muscle tone | Grade III | | Decerebrate posturing | Extensor posturing | Grade IV | | Clonus | Sustained rhythmic contractions | Variable |

Clinical Pearl: Asterixis Technique and Interpretation:

• Technique: Ask patient to extend arms, dorsiflex wrists, spread fingers for 15-30 seconds
• Positive: Bilateral, asynchronous flapping movements
• Not specific: Also seen in uraemia, hypercapnia, sedative intoxication, hypoglycaemia
• Absent in Grade IV: Comatose patients cannot demonstrate asterixis
• Prognostic: Disappearance during treatment suggests improvement

History Taking

Essential History Components

Collateral History (Essential)

Family members often provide critical information as patients may lack insight:

• Timeline of mental status changes
• Baseline cognitive function
• Medication adherence
• Recent falls
• Sleep pattern changes
• Personality changes

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Differential Diagnosis

AMS in Cirrhotic Patients

⚠️ Warning: Do Not Miss:

• Subdural haematoma: Cirrhotic patients are prone to falls and coagulopathic - low threshold for CT head
• Hypoglycaemia: Common in liver failure; always check glucose immediately
• Wernicke's: Give thiamine before glucose in suspected cases
• SBP: Requires paracentesis to diagnose - do not rely on fever/WBC

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Diagnostic Approach

Clinical Diagnosis

Hepatic encephalopathy is fundamentally a clinical diagnosis based on: [1,3]

1. Known liver disease or evidence of portal hypertension/cirrhosis
2. Altered mental status (ranging from subtle to coma)
3. Exclusion of other causes of altered consciousness
4. Response to HE treatment (supports diagnosis retrospectively)

Laboratory Investigations

First-Line Investigations

Ammonia Level Interpretation

Exam Detail: Ammonia - Clinical Utility and Limitations:

Causes of Elevated Ammonia Without HE:

• Sample handling error (most common)
• Urea cycle disorders
• Renal failure
• Valproate therapy
• GI bleeding (protein load)
• Severe infection/catabolism
• TPN without adequate arginine

Practical Points:

• Ice the sample, process within 30 minutes
• Normal ammonia does NOT exclude HE
• Elevated ammonia does NOT confirm HE
• Trends more useful than single values
• Clinical assessment remains paramount

Diagnostic Paracentesis

Neuroimaging

CT Head

MRI Brain

Testing for Minimal/Covert HE

Psychometric Tests

Computerised/Neurophysiological Tests

Clinical Pearl: EncephalApp Stroop Test:

• Free smartphone application for MHE screening
• Validated sensitivity ~80%, specificity ~80%
• Measures time to identify colour of word vs word meaning
• Cut-off: > 190 seconds combined time suggests MHE
• Practical for outpatient screening

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Minimal Hepatic Encephalopathy

Definition and Significance

Minimal hepatic encephalopathy (MHE) represents the mildest form of HE, detectable only through specialised testing: [3,5]

Impact on Daily Life

Driving and MHE

⚠️ Warning: Driving Implications:

Patients with MHE have significantly impaired driving ability, with studies showing:

• 4-7× increased risk of motor vehicle accidents [13]
• Impaired attention, reaction time, and navigation
• Many countries require reporting and driving cessation

Practical Approach:

1. Screen all cirrhotic patients for MHE using psychometric tests
2. Document discussion of driving risk in medical record
3. Advise cessation of driving if MHE confirmed
4. Consider treatment and retest before return to driving
5. Know local regulations - some jurisdictions mandate reporting
6. Commercial driving - generally contraindicated with any HE

UK DVLA Guidance:

• Notify DVLA if confirmed HE (minimal or overt)
• Driving may resume if controlled and no impairment
• Annual review required

Diagnosis of MHE

Treatment of MHE

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Management

Principles of Management

1. Identify and treat precipitating factor(s) - Most important step
2. Reduce ammonia production and absorption - Lactulose, rifaximin
3. Provide supportive care - Airway, nutrition, fluids
4. Prevent recurrence - Long-term lactulose ± rifaximin
5. Evaluate for liver transplantation - Definitive treatment for recurrent HE
6. Avoid deleterious medications - Sedatives, opioids

Acute Management Algorithm

Acute HE Management:
┌─────────────────────────────────────────────────────────────────────┐
│                    OVERT HE IDENTIFIED                              │
│                           ↓                                         │
│  ┌─────────────────────────────────────────────────────────────────┐│
│  │ IMMEDIATE ASSESSMENT                                            ││
│  │ • Airway/Breathing: Intubate if GCS ≤8                         ││
│  │ • Glucose: Treat hypoglycaemia immediately                      ││
│  │ • Thiamine: Give before glucose if alcoholic                    ││
│  └─────────────────────────────────────────────────────────────────┘│
│                           ↓                                         │
│  ┌─────────────────────────────────────────────────────────────────┐│
│  │ IDENTIFY PRECIPITANT                                            ││
│  │ • Infection: Paracentesis, cultures, UA, CXR                    ││
│  │ • GI bleeding: Rectal exam, NG aspirate, Hb                     ││
│  │ • Electrolytes: K+, Na+, Mg2+                                   ││
│  │ • Medications: Review sedatives, opioids, diuretics             ││
│  │ • Constipation: Bowel history                                   ││
│  │ • Renal function: Creatinine                                    ││
│  └─────────────────────────────────────────────────────────────────┘│
│                           ↓                                         │
│  ┌─────────────────────────────────────────────────────────────────┐│
│  │ TREAT PRECIPITANT                                               ││
│  │ • SBP: Ceftriaxone 2g IV daily                                  ││
│  │ • GI bleed: PPI, octreotide, urgent endoscopy                   ││
│  │ • Electrolytes: Replace K+, correct Na+ slowly                  ││
│  │ • Stop offending medications                                    ││
│  │ • Renal: Fluids, hold nephrotoxins                              ││
│  └─────────────────────────────────────────────────────────────────┘│
│                           ↓                                         │
│  ┌─────────────────────────────────────────────────────────────────┐│
│  │ INITIATE HE-SPECIFIC TREATMENT                                  ││
│  │ • Lactulose 25-30 mL q1-2h until bowel movement                 ││
│  │ • Then 15-30 mL TID-QID (target 2-3 soft stools/day)            ││
│  │ • Lactulose enema if unable to take PO                          ││
│  │ • Consider rifaximin 550 mg BID (especially if recurrent)       ││
│  └─────────────────────────────────────────────────────────────────┘│
│                           ↓                                         │
│  ┌─────────────────────────────────────────────────────────────────┐│
│  │ SUPPORTIVE CARE                                                 ││
│  │ • Nutritional support: 1.2-1.5 g/kg/day protein                 ││
│  │ • Avoid sedatives                                               ││
│  │ • DVT prophylaxis (mechanical if bleeding risk)                 ││
│  │ • Fall precautions                                              ││
│  └─────────────────────────────────────────────────────────────────┘│
└─────────────────────────────────────────────────────────────────────┘

Lactulose: First-Line Therapy

Exam Detail: Lactulose (Lactitol) - Detailed Pharmacology:

Mechanisms of Action:

1. pH reduction: Acidifies colonic contents (pH 5-6)
2. Ammonia trapping: NH3 → NH4+ (ionised, cannot cross membranes)
3. Catharsis: Osmotic laxative effect removes nitrogenous material
4. Microbiome modification: Favours non-urease-producing bacteria
5. Reduced absorption: Decreased colonic transit time

Dosing:

Adverse Effects:

• Diarrhoea (excessive dosing)
• Dehydration and electrolyte disturbance
• Abdominal bloating, cramping, flatulence
• Hyponatraemia (from diarrhoea)
• Sweet taste (poor compliance)

Titration Pearl:

• Too few stools → HE not controlled
• Too many stools → Dehydration → Worsening HE
• Goal is 2-3 soft (not watery) stools per day

Rifaximin: Adjunctive Therapy

Evidence Base: [14]

• The landmark RFHE study (Bass et al., NEJM 2010) demonstrated:
  • 58% relative risk reduction in HE recurrence
  • 50% reduction in HE-related hospitalisation
  • NNT = 4 to prevent one HE episode over 6 months

Indications for Rifaximin:

Nutritional Management

⚠️ Warning: Protein Restriction is Harmful:

Historical practice of protein restriction is now contraindicated. Evidence shows: [15,16]

• Protein restriction causes muscle wasting (sarcopenia)
• Sarcopenia reduces peripheral ammonia detoxification
• Protein restriction does NOT improve HE outcomes
• Malnutrition increases mortality in cirrhosis

Current Recommendations:

L-Ornithine L-Aspartate (LOLA)

Other Therapies

Airway Management

Sedation Considerations:

• Avoid benzodiazepines if possible
• Short-acting agents preferred (propofol, dexmedetomidine)
• Opioids: reduce doses significantly
• Expect prolonged half-lives

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Management of Specific Precipitants

Spontaneous Bacterial Peritonitis (SBP)

GI Bleeding

Constipation

Electrolyte Disturbances

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Type A HE (Acute Liver Failure)

Type A HE occurs in acute liver failure and has distinct pathophysiology requiring different management: [1,17]

Key Differences from Type C

Management of Type A HE

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Post-TIPS HE

TIPS (transjugular intrahepatic portosystemic shunt) creates a direct portosystemic shunt, precipitating HE in 25-45% of patients: [6]

Risk Factors for Post-TIPS HE

Management of Post-TIPS HE

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Disposition

Admission Criteria

ICU Admission Criteria

Discharge Criteria

Follow-Up Recommendations

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Prevention of Recurrence

Primary Prevention

Secondary Prevention (After First Episode)

Clinical Pearl: AASLD/EASL Recommendations for Secondary Prevention:

• After first episode of overt HE: Lactulose
• After second episode (recurrent HE): Lactulose + Rifaximin
• Rifaximin reduces recurrence by ~58% when added to lactulose [14]
• Continue indefinitely unless transplanted

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Liver Transplantation

Indications for Transplant Evaluation

Outcomes Post-Transplant

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Prognosis

Survival After Overt HE

Prognostic Factors

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Special Populations

Elderly Patients

Patients with Renal Dysfunction

Pregnancy

Post-TIPS Patients

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Patient and Caregiver Education

Medication Instructions

Lactulose:

• Goal is 2-3 soft bowel movements per day
• Too few = confusion may return; increase dose
• Too many = dehydration may worsen confusion; decrease dose
• Take even when feeling well
• Can mix with juice if taste unpleasant
• Seek medical attention if unable to take orally

Rifaximin:

• Take twice daily with or without food
• Prevents confusion episodes from returning
• Continue even when feeling well
• May be expensive; ask about patient assistance programs

Warning Signs Requiring Medical Attention

• Increasing confusion or sleepiness
• Unusual behaviour or personality changes
• Unable to wake patient
• Blood in stool (black, tarry) or vomiting blood
• Fever, chills, or feeling unwell
• Abdominal pain or increased swelling
• Unable to take medications
• Falls
• Not having bowel movements

Lifestyle Modifications

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Viva Questions and Model Answers

Viva Point: Q1: A 58-year-old man with alcoholic cirrhosis presents with confusion. How would you assess and manage him?

Model Answer: "I would approach this systematically. First, I would ensure airway safety and check glucose to exclude hypoglycaemia, giving thiamine before any glucose if alcohol-related liver disease is suspected.

For clinical assessment, I would grade the encephalopathy using West Haven criteria and examine for stigmata of chronic liver disease, asterixis, and signs of precipitants such as fever indicating infection or melaena suggesting GI bleeding.

My immediate investigations would include fingerstick glucose, basic metabolic panel looking for electrolyte disturbances and renal dysfunction, complete blood count, liver function tests, INR, ammonia level, blood cultures, and urinalysis. Critically, I would perform a diagnostic paracentesis if ascites is present, as SBP is a common precipitant.

Management follows four priorities: First, identify and treat the precipitant - if SBP is confirmed with PMN count above 250, I would start ceftriaxone 2g IV daily plus albumin. Second, initiate lactulose 25-30mL every 1-2 hours until a bowel movement occurs, then titrate to achieve 2-3 soft stools daily. Third, provide supportive care with adequate nutrition at 1.2-1.5g/kg protein daily, avoiding sedatives. Fourth, consider adding rifaximin if this is recurrent HE.

For disposition, I would admit all patients with Grade II or higher HE, with ICU admission if Grade III-IV or requiring airway protection. Following recovery, I would ensure hepatology follow-up and discuss transplant evaluation if indicated."

Viva Point: Q2: What is the pathophysiology of hepatic encephalopathy?

Model Answer: "Hepatic encephalopathy results from accumulation of neurotoxins, primarily ammonia, due to hepatocellular dysfunction and portosystemic shunting.

Regarding ammonia metabolism, ammonia is normally produced in the gut from bacterial urease activity and protein digestion. It enters the portal circulation and is metabolised by the liver via the urea cycle, converting ammonia to urea for renal excretion. In cirrhosis, both reduced hepatocyte mass and portosystemic shunting allow ammonia to bypass hepatic metabolism and enter the systemic circulation.

At the cellular level, ammonia crosses the blood-brain barrier and enters astrocytes, which are the only cells capable of ammonia detoxification via glutamine synthetase. Ammonia is converted to glutamine, which accumulates and causes osmotic swelling of astrocytes, known as low-grade cerebral oedema. This leads to mitochondrial dysfunction through the 'Trojan horse' hypothesis, oxidative stress, and altered neurotransmission.

Beyond ammonia, other factors contribute including systemic inflammation from bacterial translocation, which amplifies ammonia's effects on the brain, manganese deposition in the basal ganglia, altered ratio of branched-chain to aromatic amino acids, and endogenous benzodiazepine-like substances enhancing GABAergic tone.

This explains why ammonia levels correlate poorly with severity in chronic liver disease, as inflammation and other factors modulate the clinical presentation. It also explains why treating precipitants like infection is so important."

Viva Point: Q3: What is minimal hepatic encephalopathy and what are its implications for driving?

Model Answer: "Minimal hepatic encephalopathy, or MHE, represents the earliest stage of the HE spectrum where patients appear clinically normal but have measurable cognitive deficits on psychometric testing. It affects 20-80% of cirrhotic patients depending on the testing method used.

The key features include normal clinical examination, abnormalities in attention, working memory, psychomotor speed, and visuospatial function, which are detectable only on specialised testing. Common manifestations include sleep-wake inversion, difficulty with complex tasks, and impaired work performance.

Regarding diagnosis, several validated tools exist including the Psychometric Hepatic Encephalopathy Score or PHES as the gold standard, Critical Flicker Frequency testing, the computerised Stroop test via the EncephalApp smartphone application, and the Inhibitory Control Test.

The driving implications are significant. Studies demonstrate a 4-7 fold increased risk of motor vehicle accidents in patients with MHE. This impairment affects attention, reaction time, and navigation abilities critical for safe driving.

From a practical standpoint, all cirrhotic patients should be screened for MHE, those with confirmed MHE should be advised not to drive, treatment with lactulose and possibly rifaximin may improve test performance, and retesting can be considered before resuming driving. In the UK, patients should notify the DVLA, and commercial driving is generally contraindicated with any form of HE.

Treatment with lactulose improves psychometric tests and quality of life, and rifaximin has been shown to improve simulated driving performance."

Viva Point: Q4: How does Type A HE differ from Type C HE?

Model Answer: "Type A HE occurs in acute liver failure without pre-existing liver disease, while Type C occurs in the context of cirrhosis. There are critical differences in pathophysiology and management.

The key pathophysiological differences centre on cerebral oedema. In Type A, cerebral oedema is common and life-threatening, with risk of brain herniation. Astrocytes have no time to adapt to hyperammonaemia. In contrast, in Type C, cerebral oedema is rare because astrocytes develop compensatory mechanisms over time, reducing cell swelling.

Clinically, in Type A, ammonia levels correlate better with severity, and intracranial pressure elevation is a major concern. In Type C, ammonia correlates poorly with grade, and ICP is rarely elevated.

Management priorities differ substantially. For Type A, the priorities are ICU admission, consideration of ICP monitoring, head of bed elevation, prophylactic hypernatraemia targeting 145-150 mEq/L, mannitol or hypertonic saline for ICP elevation, and urgent transplant evaluation. For Type C, the priorities are identifying precipitants, treating with lactulose, adding rifaximin for recurrence, and transplant for recurrent episodes.

The mortality mechanism also differs. In Type A, death typically results from brain herniation if not transplanted. In Type C, death is usually from multiorgan failure or complications of end-stage liver disease.

This distinction is critical because an ALF patient with Grade III-IV HE needs aggressive neuroprotective measures and emergency transplant evaluation, while a cirrhotic patient needs precipitant treatment and lactulose."

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Common Examination Mistakes

⚠️ Warning: Mistakes That Fail Candidates:

1. Using ammonia level to grade severity or titrate lactulose

   • Ammonia does NOT correlate with grade in cirrhosis
   • Treat the patient, not the number

2. Restricting dietary protein

   • Outdated practice; now contraindicated
   • Causes sarcopenia and worsens HE

3. Forgetting to do paracentesis in ascitic patient with AMS

   • SBP is a common precipitant
   • Mandatory investigation

4. Not considering alternative diagnoses

   • SDH, hypoglycaemia, Wernicke's can mimic HE
   • Low threshold for CT head if atypical

5. Not giving thiamine before glucose in alcoholics

   • Risk of precipitating Wernicke encephalopathy

6. Using benzodiazepines for sedation

   • Worsen HE and have prolonged half-life
   • Use short-acting agents if sedation essential

7. Forgetting lactulose titration

   • Must achieve 2-3 soft stools/day
   • Under-treatment and over-treatment both harmful

8. Confusing Type A and Type C HE management

   • Type A (ALF) needs ICP management and urgent transplant
   • Different pathophysiology and priorities

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Key Guidelines

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References

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