Hepatic Encephalopathy Hepatic Encephalopathy

Dr Muzaffar MehdiSenior Resident MD Gastroenterology Shaikh Zayed Hospital Lahore

PIMA CONVENTION MARCH 2010 AIMC

Definition

Hepatic encephalopathy (HE) is a complex metabolic mental state disorder with a spectrum of reversible neuropsychiatric abnormalities seen in patients with severe acute or chronic liver dysfunction after exclusion of other brain diseases

Epidemiology

•Exact data regarding incidence and prevalence is lacking• 70% of patients with liver cirrhosis, while clinically unremarkable have pathologic changes on EEG and psychometric tests.MHE•Prevalence of minimal HE is 53.3% in patients with extra hepatic portal vein obstruction•Approximately 50% of patients with liver cirrhosisdevelop HE after surgical portosystemic bypass procedures•After placement of a TIPS approximately one third of patients develops HE.

Type Description Subcategory Subdivision

A Encephalopathy associated with acute liver failure

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B Encephalopathy with porto-systemic bypass and nointrinsic hepatocellular disease

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C Encephalopathy associated with cirrhosis or portalhypertension ⁄ porto-systemic shunts

Episodic

Persistent

Minimal

•Percipated •Spontaneous •Recurrent •Mild •Severe•Treatment dependent

Classification

Clinical Detection Relationship Of HE Subtypes

Etiology and Pathogenesis

• liver cirrhosis with reduced functional hepatic mass underlies the development /HCC

• Triggered by precipitating factors

Incresed NH3• Increased

protien intake • Constipation• GI bleeding • Blood TX • Infections • Sepsis• Renel failure

Hypovolumia /hepatic hypoxia •Overdiuresis •Large volume paracentesis •Diarrhoea vomiting •Circulatory shock

Drugs •Tranqulizers•Narcotic analegesics•Diuretics •Electrolyte Imbalance •Hypokalemia •Hyponateremia •Metabolic acidosis / alkolosis

Portosytemic shunts

•Spontaeous •Surgical•TIPS

•Neurotoxins (Ammonia,GABA,Maganese )•Impaired astrocyte functions •Dysfunction of blood brain barrier •Imbalance of amino acids •False neurotransmitters

Factors Involved In HE development

Ammonia Theory

Clinical Manifestations & Diagnosis :MHE

•Clinically normal•No mental deficit •Normal verbal ability • Deficit in attention ,visual perception, memory function, and learning •Impaired daily activities / driving•Only sophisticated tests such as EEG,CFF,ICT,NCT,DST,BDT,CDR,RBANS• Neuroimaging : SPECT ,MRI,MRS.DWI

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Number Connection Test (NCT)Number Connection Test (NCT)

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Manifestations & Diagnosis :MHE

Clinical Manifestations : OHE

Detailed physical examination to place according to WHC for management •R/O FND •Hypereflexia •Positive Babinski’s sign•Asterixis•Parkinsonian symptoms •Hepatic mylopathy spastic paraparesis

Stage Consciousness Intellect and behaviour

Neurological findings

0 Normal Normal Normal examination; if impaired psychomotor testing, then MHE

1 Mild lack of awareness Shortened attention span; impaired addition or subtraction

Mild asterixis or tremor

2 Lethargic Disoriented; inappropriate behaviour

Obvious asterixis; slurred speech

3 Somnolent but arousable

Gross disorientation; bizarre behaviour

Muscular rigidity and clonus; Hyper-reflexia

4 coma Coma Decerebrate posturing

West-Haven criteria for HE: OHE

Stages of Hepatic Encephalopathy

Differential Diagnosis

Metabolic encephalopathies•Hypoxia •Ethonol •Electrolyte imbalance•Ketoacidosis •CO2 narcosis •Psychoactive drugs •Salicylate toxicity•Wilson disease

Intracranial lesions

•Bleeding subdural

subarachnoidal intracerebral

•Tumor •Abscess •Vascular accident

Meningeal irritation

•Meningitis•Encepalitis

•Seizure disorders

Psychiatric diseases

Course And Prognosis

•Develops rapidly few hours – 1-2 days•Mortality in grade IV is 80% •Death usually due to brain herniation / edema ICH•Type C develops slowly – undulating course / recurrence •Neuropsychiatric manifestations are reversible•Can lead to permanent damage with dementia, extra pyramidal signs, cerebellar degeneration,myelopathy with spastic paraplegia, peripheral polyneuropthy•Liver TX can reverse all changes

Treatment Objectives

1.Normalization of neurological functions2.Elimination of precipitating factors 3. lowering ammonia level

Hepatic Encephalopathy Precipitants

Treatment option

Chronic encephalopathy Acute encephalopathy

Lactulose 15-45ml 2-4 times Oral /NG until 2-3 bowel movements /day

30-45 ml /hourly Oral /NG until bowel movement and clinical improvement Retention Enema 300 ml + water2-6 hrly/improvement

Rifaxamin NeomycinMetronidazole

1100 –1200 mg/day oral 8-12hrly 1-4 gm /day oral 250 mg oral 12 hrly Oral

1100 –1200 mg/day 8-12hrly 1-2 gm 4-6 /hrly oral/NG 250 mg oral 12 hrly O/NG

Sodium benzoateBromocriptine

5 gm / oral twice a day

Surgery Obliteration of portosystemic anastomosis ,Surgical shunt LIVER TRANSPLAANT

LIVER TRANSPLANT

Treatment Options for Hepatic Encephalopathy

BRAIN

KIDNEY

GUT LIVER

MUSCLE

NH3

Glutamine

Lactulose AcarboseABX

LOLA

UREA

Mechanism Of Action of Drugs

Actions Of Lactulose

First line options• Identify precipitating

factor• Nutrional management• Reduce dietry protiens • Enterl nutrtion• Zinic supplementation• Lactulose/lactitol2nd line options • ABX• LOLA • Acarbose, probiotics,• l –carnitine • Flumazinal

Exclude other causes Nutritional support 1. Dairy and vegetable

based diet2. Consider BCAA3. Lactulose/Lactitol4. Zinc supplementation5. Interventional radiology

search large portosytemic shunts occlud / reduce TIPS diameter

NH3 lowering agents1. ABX2. LOLA3. BromocriptineOLT evaluation

1. No established indication for treatment

2. Consider changes daily activeties (avoid driving)

3. In selected patients Lactulose /lactitol Dietry intervention

vegetable based diet .probiotics

Episodic encephalopathy Persistent Encephalopathy Minimal encephalopathy

Management of Hepatic Encephalopathy

Prophylaxis Of New Episodes

1. Control of precipitating factors2. Nutritional support 3. Adequate protein intake with dairy and

vegetable based diets 4. Vitamins 5. Zinc supplementation 6. Lactulose /lactitol as needed 7. OLT evaluation

Nutritional measures in patient with acute HE

SUFFICENT CALORIC SUPPLY 30 k cal /kg body weight /day RESTRICTION OF DIETRY PROTIEN Day 1-5 20-30 g/day Then 1-2 g/kg body weight /day INCREASED OF GLUCOSE (LIPID) CALORIES 10% glucose 1-2 L/day BRANCHED CHAINED AMINO ACID ( BCAA)0.2-1.2 G/KG body weight i.v/day REPLACEMENT OF VITAMINS AND TRACE ELEMENTS Vitamin B complex Vitamin K Zinc

Thanks