Download - Hepatic Encephalopathy
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DR DR . E. SENTHIL KUMAR M.B.B.S
NATIONAL HOSPITAL
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57 YEARS OLD MALE PATIENTADMITTED ON 8 / 2 / 09 WITH HISTORY OF
ALTERED SENSORIUM
NOT TAKING FEEDS 2 MONTHS
DROWSINESS ….. PAST ONE DAY
H / O ICU ADMISSION FOR SIMILAR COMPLAINTS …. LAST MONTH
HE WAS FULLY EVALUATED & TREATED .
AT THE TIME OF DISCHARGE …
PATIENT ABLE TO WALKSPEECH AND HIGHER FUNCTIONS .. NORMALICTERIC
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PERSONAL HISTORY
ALCOHOLIC FOR THE PAST 37 YEARS
FAMILY HISTORY :
NOT CONTRIBUTORY
PAST HISTORY
INTERMITTENT JAUNDICE FOR THE PAST 4 YEARS (TREATED WITH NATIVE MEDICINES)
K / C / O CIRRHOSIS FOR PAST TWO YEARS AND ON RX
K / C / O HYPERTENSION FOR PAST 2 MONTHS AND ON RX
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CLINICAL FINDINGS :
ICTERIC +++ PALLOR +
BILATERAL PITTING PEDAL EDEMA +
RS : BILATERAL CREPITUS +
CNS : GLASGOW COMA SCALE - E1 V 2 M 3 - 6 / 15
PUPILS ….. 4mm , PERLA
PLANTAR ….. WITHDRAWAL RESPONSE
B / L LIMB SPASTICITY ++ , REFLEXES
VITALS :
PULSE : 86 / minBP : 148 / 92 mm HgRR : 22 / minTEMP : N
spO2 : 98 %U / O : ADEQUATEBLOOD SUGAR : 209 mg %
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NO INTUBATION DONE @ THE TIME OF ADMISSION
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INVESTIGATIONS (9 / 2 / 09 )
TOTAL BILIRUBIN : 5.4 DIRECT : 2.3 INDIRECT : 3.1
URINE UROBILINOGEN : INCREASED
BLOOD AMMONIA : 79
PLATELETS : 1.02 LAKHS
INR : ELEVATED
SR POTASSIUM : REDUCED
CT BRAIN
GROSS AGE RELATED CEREBRAL ATROPHY
FEATURES S / O SMALL VESSEL ISCHEMIC CHANGE
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USG ABDOMEN
COARSE ECHOGENIC LIVER S / O CIRRHOSIS
SPLENOMEGALY
MODERATELY DISTENDED BLADDER WITH DEBRIS (CYSTITIS)
CXR – PA VIEW
INHOMOGENEOUS OPACITIES IN RT UPPER AND MIDZONE
CARDIOMEGALY
ATHEROMATOUS AORTA
ECG : SB
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DIFFERENTIAL DIAGNOSIS :
1. HYPOGLYCEMIA ….. RULED OUT { SUGAR @ ADMN – 209 }
2. HYPOXIA ….. RULED OUT { NO CYANOSIS , SATURATION – N }
3. UREMIA …. RULED OUT { NORMAL RFT }
4. KETO ACIDOSIS …. RULED OUT { SUGAR – NEAR NORMAL & URINE KETONE NEGATIVE }
5. ELECTROLYTE IMBALANCE …. POSSIBLE { LOW POTASSIUM }
6. HEPATIC COMA …. POSSIBLE { HIGH BILIRUBIN , RAISED INR HYPOKALEMIA LOW UREA LOW ALBUMIN MILDLY ELEVATED AMMONIA USG ABDOMEN .. S/O CIRRHOSIS }
7. ALCOHOL / OTHER INTOXICATION …. NO CONTRIBUTORY HISTORY
8. INTRA CRANIAL CAUSE { SDH, SOL,NEUROPSYCHIATRIC STATE, POST ICTAL ENCEPHALOPATHY , MENINGITIS, ENCEPHALITIS }
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COURSE IN HOSPITAL : 8/2/09 … DATE OF ADMISSION
TREATMENT GIVEN :
PROTEIN RESTRICTION
TAB SPIRONOLACTONE , POTASSIUM INFUSIONS
INJ RANITIDINE
INJ MANNITOL
INJ VIT K
LACTULOSE
TAB RIFAXIMIN
RESOURCE HEPATIC POWDER
HEPAMERZ INFUSIONS
BACLOFEN , PHYSIOTHERAPY
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14/2/09 … DROWSINESS TO HYPOTENSION18/2/09 HYPOKALEMIA (3.3) FEBRILE ++DAY 6 - 10 CRP , INR INCREASED BLOOD AMMONIA INCREASED ( 110 )
CLINICAL PICTURE :
PATIENT DEVELOPED
MILD NECK STIFFNESS SPASTIC QUADRIPARESIS
NEURO CALL OVER GIVEN
EEG :
BACKGROUND ACTIVITY NORMALRESPONSE TO EYE OPENING NORMAL DURING HYPER VENTILATION SLOW WAVES PRESENT IN ANTI HEAD REGION
ed
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CSF ANALYSIS :
PROTEIN – 31
GLUCOSE – 90
CHLORIDE – 117
APPEARANCE – CLEAR
AFB – NEGATIVE
CULTURE – NO GROWTH
VDRL - NEGATIVE
HIV - NEGATIVE
NORMAL CT BRAIN , NORMAL EEG , NORMAL CSF PROFILE , NORMAL VDRL & HIV
RULES OUT INTRA CRANIAL CAUSES , MENINGO ENCEPHALITIS , POST ICTAL STATES
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BASED ON THESE , A DIAGNOSIS OF HEPATIC COMA WAS MADE
“ HEPATIC ENCEPHALOPATHY - ESSENTIALLY A DIAGNOSIS OF EXCLUSIONHEPATIC ENCEPHALOPATHY - ESSENTIALLY A DIAGNOSIS OF EXCLUSION “
BUT DESPITE H.E. DIRECTED INTENSIVE MEDICAL CARE
28 / 2 /09 … FURTHER DETERIORATION IN GCS ( E 1 V2 M 1)DAY 20
1/3/09 … CENTRAL VENOUS LINE SECURED
2/3/09 … PATIENT INTUBATED AND PLACED IN MECHANICAL VENTILATORDAY 22 FALLING PLATELET COUNT
TREATMENTTREATMENT RESISTANTRESISTANT HEPATIC HEPATIC COMA …COMA …
??? CAUSE
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CAUSES OF PERSISTENT HEPATIC COMA DESPITE TREATMENTCAUSES OF PERSISTENT HEPATIC COMA DESPITE TREATMENT
INFECTION ….. SBP , LRI { VAP } , SEPTICEMIA , UTI
ELECTROLYTE IMBALANCE … PERSISTENT HYPOKALEMIA
ASSOCIATED RENAL FAILURE …. RULED OUT { NORMAL RFT , OUTPUT }
HYPOGLYCEMIA …. RULED OUT { PATIENT WAS ON > 2000 Kcal / Day SUGARS WERE STABLE }
UPPER GI BLEED …. RULED OUT { RT ASPIRATES – NOT BLOOD STAINED STOOL NEGATIVE FOR BLOOD , HB % - N }
CONSTIPATION …. RULED OUT { PT ON LACTULOSE & PASSING 2-4 STOOLS PER DAY}
DEHYDRATION ….. RULED OUT { ADEQUATE FLUID INTAKE PULSE , BP , U / O – NORMAL }
ACID BASE IMBALANCE …. POSSIBLE ( ABG NOT DONE )
DRUGS ….. POSSIBLE { BDZ GIVEN FOR SEDATION IN EARLY STAGES LASIX , PSYCHOTROPIC MEDICINES , NARCOTICS WERE AVOIDED}
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FEVER WORK UP DONE :
BLOOD C/S … NON FERMENTING GNB
SPUTUM C/S … KLEBSIELLA
URINE C/S … ENTEROCOCCI & PNEUMOCOCCI
TREATMENT :
DOPAMINE DRIP STARTED
POTASSIUM INFUSIONS MAINTAINED
APPROPRIATE ANTIBIOTICS ADDED ( MEROPENEM , VANCOMYCIN , PIPERACILLIN – TAZOBACTAM )
BACLOFEN AND PHYSIOTHERAPY GIVEN
BDZ STOPPED
OTHER TREATMENT CONTINUED
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12/3/09 … TRACHEOSTOMY DONEDAY 32
18/3/09 … PATIENT IMPROVED AND WEANED OFF THE VENTILATORDAY 38 ON NOR ADRENALINE DRIP (DUE TO PERSISTENT HYPOTENSION)
AS ON 25/3/09 : …DAY 45
ICTERIC ++
AFEBRILE
VITALS … STABLE
BLOOD NH3 … STABLE
SERUM K + … STABLE
INR , PLATELETS … STABLE
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DISCHARGE BEING PLANNED ON 30 / 3 / 09 ….. DAY 50
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SUMMARY SUMMARY
57 YEARS OLD MALE ADMITTED WITH
FLUCTUATING CONSCIOUSNESS LEVEL (FOR WHICH TREATED AT OUTSIDE HOSPITALS FOR PAST FEW MONTHS)
SEVERE HEPATIC DYSFUNCTION AS EVIDENCED BY
HIGH BILIRUBIN & AMMONIA ,HIGH BILIRUBIN & AMMONIA , LOW ALBUMIN , POTASSIUM & UREA LOW ALBUMIN , POTASSIUM & UREA VIT K RESISTANT COAGULOPATHYVIT K RESISTANT COAGULOPATHY
ADMITTED WITH STAGE 3 H.E. WHICH WAS RESISTANT TO TREATMENT
COMPLICATED BY MULTI FOCAL SEPSIS , ELECTROLYTE IMBALANCE , ? BDZ USE PROGRESSED TO STAGE 4 - PATIENT PLACED IN MV
AFTER SUSTAINED TREATMENT WITH DIETARY MGT , ANTIBIOTICS ,HEPAMERZ , VIT K , POTASSIUM INFUSIONS , LACTULOSE , BACLOFEN AND PHYSIOTHERAPY PATIENT IMPROVED TO PRESENT CONDITION
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THIS IS THE FIRST CASE OF SEVERE TREATMENT RESISTANT STAGE 3 / 4 HEPATIC COMA ADMITTED IN NATIONAL HOSPITAL
PATIENT – IN ICU FOR NEARLY 50 DAYS WITH CONSTANT MONITORINGAND MANAGEMENT OF THE ENCEPHALOPATHY , MULTI FOCAL SEPSIS, PERSISTENT HYPOTENSION , HYPO KALEMIA , HYPER AMMONEMIA ,HYPER BILIRUBINEMIA & COAGULOPATHY
PATIENT – IN VENTILATOR FOR 14 DAYS
PATIENT - SUCCESSFULLY REVIVED AFTER NEARLY 50 DAYS OF INTENSIVE MEDICAL CARE
ALL OF THIS POSSIBLE ONLY BECAUSE HIS COMPANY AGREED TO PAY FOR THE EXPENSES
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HEPATIC ENCEPHALOPATHY
Hepatic encephalopathy is defined as a spectrum of neuropsychiatric abnormalities in patients with liver dysfunction characterized bypersonality changes, intellectual impairment, and a depressed level ofconsciousness
Type A hepatic encephalopathy associated with A cute liver failure.
Type B hepatic encephalopathy associated with portal-systemic B ypass
Type C hepatic encephalopathy associated with C irrhosis and portal hypertension or portal-systemic shunts.
Type C hepatic encephalopathy is, in turn, subcategorized as episodic, persistent, or minimal.
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PATHOGENESIS
Endogenous Neurotoxins
AmmoniaMercaptansPhenolsShort-medium fatty acids
Increased Permeability of Blood-Brain Barrier
Change in Neurotransmitters and Receptors
GABAMet enkephalin
Altered BCAA/AAA ratio
Zinc deficiency
Manganese deposits
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PRECIPITATING FACTORS
DrugsBenzodiazepinesNarcotics, opioidsAnti psychoticsAnti depressantsAlcoholdiuretics
Portosystemic ShuntingRadiographic or surgically placed shuntsSpontaneous shuntsVascular OcclusionPortal or Hepatic Vein Thrombosis
DehydrationVomitingDiarrheaHemorrhageDiureticsLarge volume paracentesis
Increased Ammonia Production, Absorption or Entry Into the BrainExcess Dietary Intake of ProteinRenal failureGI BleedingInfectionElectrolyte Disturbances (ie., hypokalemia)ConstipationMetabolic alkalosisPrimary Hepatocellular
Carcinoma
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CLINICAL PICTURE
MINIMAL H.E.
EARLY SYMPTOM ….. ALTERATION OF SLEEP PATTERNEARLY SIGN ….. CONSTRUCTIONAL APRAXIA
OTHER FEATURES …
UNAWARENESS OF CLINICAL SUBJECTIVE SYMPTOMS
ABSENT EEG FINDINGS
PSYCHOMETRIC/NEUROSPYCHOLOGICAL TESTS CAN DISCLOSE DEFICITS
HYPER VENTILATION
REDUCED BODY TEMPERATURE
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NEJM Volume 337:473-479
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ASTERIXIS IS ABSENT IN STAGES 0 & 4
IT IS SEEN IN OTHER ORGANFAILURES ALSO
EG : RENAL FAILURE PULMONARY FAILURE
ALSO OBSERVED IN BARBITURATETOXICITY
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LAB DIAGNOSIS :
PSYCHOMETRIC / NEUROPSYCHOLOGICAL TESTSPSYCHOMETRIC / NEUROPSYCHOLOGICAL TESTS
ELECTRO PHYSIOLOGIC STUDIESELECTRO PHYSIOLOGIC STUDIES
IMAGE TECHNIQUESIMAGE TECHNIQUES
CLINICAL LABORATORY TESTSCLINICAL LABORATORY TESTS
PSYCHOMETRIC / NEUROPSYCHOLOGICAL TESTS
Retelling and interpretation a fable
Forward / backward digit span
Reproduction of simple figures
Block design test
Critical flicker test
WAIS performance IQ
Line tracing tests: LTT
Number connecting test: NCT
Digital-symbol test: DST
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EEG :
Classic EEG changes associated with hepatic encephalopathy are high-amplitude , low-frequency waves and tri phasic waves
VEP …. Useful in detecting early H.E.
BRAIN IMAGING
MRI / CT are used mainly to rule out other causes . MRI has the additionaladvantage of being able to demonstrate hyperintensity of the globus palliduson T1-weighted images, a finding that is commonly described in hepatic encephalopathy
LAB PARAMETERS
RENAL FUNCTION DISORDERSELECTROLYTE IMBALANCE { ESP SR POTASSIUM LEVELS }ACID-BASE EQUILIBRIUMLIVER FUNCTIONINFLAMMATORY PARAMETERS
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BLOOD AMMONIA LEVELS
Clinical assessment more reliable than serial ammonia estimation
Arterial sample is preferable
Blood drawn from an extremity to which a tourniquet has been appliedmay provide a falsely elevated ammonia level
NORMAL RANGE : 18 TO 60
May also be elevated in other states of hyper ammonemia such as
uretero sigmoidostomyurea cycle disorders
AMMONIA HAS NO RELATION TO CLINICAL STATUS
THIS PATIENT HAD ONLY MILD ELEVATION ( < 120 ) INSPITE OF SEVERE ENCEPHALOPATHY
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MANAGEMENT OF H.E.
TREATMENT OF PRECIPITATING FACTORS
DIETARY MANAGEMENT
INTESTINAL CLEANSING
ROLE OF FLUMAZENIL , ZINC , MANGANESE
AMMONIA DETOXIFICATION
TRANSPLANTATION
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TREATMENT OF PRECIPITATING FACTORS :
ADEQUATE HYDRATION
HYPOGLYCEMIA : ADEQUATE CARBOHYDRATE SUPPLEMENT
GI BLEEDINGS : STOP BLEEDING AND AVOID ANEMIA
INFECTIONS { ESP. SBP } : ANTIMICROBIALS
ACIDOSIS / ALKALOSIS : TO BE CORRECTED
DIURETICS : ESP LASIX TO BE AVOIDED
SEDATIVES : DISCONTINUED
CONSTIPATION : TO BE CORRECTED WITH LACTULOSE
UREMIA : TO BE CORRECTED
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DIETARY MANAGEMENT :
ENSURE ADEQUATE CALORIE & FLUID INTAKE
RESTRICT PROTEINS TO LESS THAN 30 gm PER DAY
PLANT PROTEIN IS BETTER THAN ANIMAL PROTEIN
BRANCHED CHAIN AMINO ACID SUPPLEMENTATION
ZINC SUPPLEMENTATION
INTESTINAL CLEANSING :
LACTULOSE
NEOMYCIN , METRONIDAZOLE , AMPICILLIN , PAROMOMYCIN
RIFAXIMIN
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ROLE OF FLUMAZENIL , ZINC , MANGANESE :
FLUMAZENIL IS HIGHLY USEFUL IN THOSE CASES TREATED WITH BDZ
EVEN IN OTHER CASES , IT MAY HAVE A ROLE
ZINC DEFICIENCY IS IMPLICATED IN THE PATHOGENES OF H.E. AND HENCE ITS SUPPLEMENTATION IS HELPFUL IN SOME CASES
MANGANESE EXCESS IS ALSO A PRESUMED PREDISPOSING FACTOR AND THIS IS SAID TO BE RESPONSIBLE FOR THE HYPER DENSITY OF GLOBUS PALLIDUS ON MRI
SO MANGANESE CHELATORS MAY BE USED IN FUTURE
Others :
Modification of intestinal flora : (replacing ammoniagenic coliforms with non ammoniagenic bacilli)
Methionine sulfoximine.
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AMMONIA DETOXIFICATION :
Protein restriction
Lactulose
Neomycin , metronidazole , Ampicillin , paromomycin , Rifaximin
L-ornithine L-aspartate (LOLA)
Sodium benzoate, sodium phenylbutyrate, sodium phenylacetate
L-carnitine
Dialysis
LIVER TRANSPLANTATION
SEVERE AND TREATMENT REFRACTORY H.E.
ACUTE LIVER FAILURE WITH H.E.
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APPROACH TO A PATIENT WITH H.E.
Exclude nonhepatic causes of altered mental function.
Periodic estimation of blood ( preferably arterial ) ammonia
Precipitants of hepatic encephalopathy, such as metabolic disturbances, gastrointestinal bleeding, infection, and constipation, should be corrected.
Avoid CNS depressants especially BENZODIAZEPINES{ but they may be used in co existing alcohol withdrawal + H.E.}
Prophylactic intubation for grade 3 & 4 H.E. cases to prevent aspiration
Treatment of hyper ammonemia
Zinc , Vit K supplementation
Supportive care & nutrition