CHAIRMAN : DIWIL H. HALAWASECRETARY: APRIANI K. W. LAIA

ACHMAD FAWZI ALHOY LESLEY DAVIDSON ALEXANDER ANGKASA CHYNTIA ARISHACICILIA SITORUSDITRA KONEKSI WAOMAFITRI RAHMA JUWITAHAAFIZH ISKANDAR MENAS ASPI LOI RICHARD GUNAWAN RIOWILDA HAYATI

Scenario Mr. Satrio 55 years to come brought by his son to the hospital with complaints of defecation black. The last few weeks by his family Mr. Satrio show attitude change, often laugh carelessly, eyes empty and forgetful, and on inspection found vital signs: blood pressure of 150/100 mmHg, HR: 100x / min, RR: 22x / min, T : 35,8C, found foetor hepaticus, flapping tremor, abdominal examination found the liver is palpable, there are spider nevi. Doctors diagnosed with hepatic encephalopathy. How did this happen? What should we do to Mr. Satrio?

1. Clarification of the term

Foetor hepaticus: Breathing is not pleasant because of the increasing dimethyl sulfidatFlapping tremor: a barrage of motions deviation fingers laterally and tremor occurs when the hand in extensionHepatic encephalopathy: damage to the brain due to an interruption in the liver

2. Determination of the problemMr. Satrio 55 years to come brought by his son to the hospital with complaints of defecation black. The last few weeks by his family Mr. Satrio show attitude change, often laugh carelessly, eyes empty and forgetfulOn inspection found vital signs: blood pressure of 150/100 mmHg, HR: 100x / min, RR: 22x / min, T : 35,8Cfound foetor hepaticus, flapping tremor, abdominal examination found the liver is palpable, there are spider nevi.

3. Analysis of the problem1 - The possibility of esophageal varices that causes bleeding in the gastrointestinal tract -Symptoms of the early stages of the disease encephalopathy hepaticus2Damage to the liver due to the extra work the heart to pump blood around the body and metabolic disorders occur in other organs Symptoms of hepatic encephalopathy3Symptoms of hepatic encephalopathy

4. Temporary conclusionMr. Satrio 55 years is likely to undergo hepatic encefalopati

5. Learning objectiveDefinition, Etiology, Epidemiology of Hepatic EncephalopathyPathophysiology and pathogenesis of Hepatic Encephalopathy Diagnosis and Differential Diagnosis of Hepatic EncephalopathyManagement, Preventive And Procedures of Hepatic EncephalopathyComplication and Prognosis of Hepatic Encephalopathy

Definition, Etiology, Classificationand Epidemiology of Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a neuropsychiatric syndrome generally occurs due to high levels of protein in the digestive tract or because of acute metabolic stress (digestive tract bleeding, infections and electrolyte disturbances in patients with portal-systemic shunting)

b. EtiologyHepatic encephalopathy may occur in fulminant hepatitis caused by: - Virus - Drugs or toxinsIn patients with chronic liver disease, acute episodes of encephalopathy is generally triggered by several factors, among others: - Excessive nitrogen load - Electrolyte or metabolic disorders - Drugs - Infection - Idiopathic - Etc

c. ClassificationBy way of occurrence: - Type of acute hepatic encephalopathy - Type of chronic hepatic encephalopathy Based on the disruption of the liver: - Type A - Type B - Type C d. EpidemiologyOverseas events subclinical hepatic encephalopathy ranging between 30-84%. Faint signs of hepatic encephalopathy was found in 70% of patients with liver cirrhosis. The disease section FKUI for a year found 109 patients with liver cirrhosis patients, including 55 patients with hepatic ensefalo. Ensefalo spontaneous hepatic obtained 13 patients, or 37%, while in 22 patients suspected of precipitating factors of gastrointestinal bleeding paisen 13 or 37%, 6 patients with acute infections or 17%, and 3 patients hipokolemi or 9%.

Pathogenesis and Pathophysiology of Hepatic Encephalopathy

Pathogenesis Several hypotheses have been put forward in the pathogenesis of hepatic encephalopathy are: 1. Hypothesis ammonia 2. Hypothesis synergistic toxicity 3. Neurotransmitters false 4. GABA and benzodiazepines

Diagnosis and Differential Diagnosis of Hepatic EncephalopathyHistorya. T he main complaint:Changes in behavior (mental status)intellectual impairmentAbnormalities in neuromuscularloss of consciousness b. additional complaintsWeak and lethargicDisorientation of time and space that is progressive.Acute confusionfetor hepaticusEye and skin look yellowishDark urine, stool color such as clay.

c. History of previous illnessEver suffered from viral hepatitis, toxic hepatitis drugs (halothane, acetaminophen).Ever suffered from cirrhosis of the liverd. history of drug useConsuming hepatotoxic drugs such as barbiturates, morphine, klorpromazine.e. food historyFrequently consuming foods that are high in protein.consuming alcohol

2. physical examinationinspectionEye and skin appears yellow (jaundice), does not always existSkin looks hyperpigmentationHead hair, armpit or pubic rarely or reducedPalms visible presence of purpuraSpider nevi on the face, neck, upper arms, backs of hands, chest, and backLiver nails Abdomen looks great or there is a protrusion on the right hipokondirumIn men obtained testicular atrophyEdema in legs

b. palpationenlargement of the liverasterixisc. percussionShifting dullness (+)enlargement of the liverObtained a distinctive breath odor (fetor hepaticus)3. supporting investigationElectroencephalography (EEG)Psychometric testsExamination of Blood Ammonia

4. Differential diagnosisComa due to intoxication of drugs and alcoholHead trauma (Komosio cerebral, cerebral contusions, subdural hemorrhage and epideral)brain tumorComa due to other metabolic disorders such as uremia, hypoglycemia comaepilepsy

MANAGEMENT HEAD INJURYType of acute hepatic encephalopathy1) Common actions a. Patients with stage III-IV need intensive supportive care b. Monitoring of consciousness, a state of neuropsychiatric, and renal system kardiopulmunal fluid balance, electrolyte and acid and alkaline. c. Giving calories 2000 cal / day or more in the acute phase protein free gram / day.

2) Special measures a. Reducing protein intake b. Reduce the bacterial population of the colon (urea splitting organisms). c. Other drugs d. radical treatmentType of chronic hepatic encephalopathyThe principles of management of hepatic encephalopathy chronic types are as follows:Low protein dietAvoid constipationIf symptoms of encephalopathy increased, plus neomycin 4x1 g / day.Aksaserbasi arise when acute, like the type of acute hepatic encephalopathy.Need long-term monitoringElective surgery: colon by pass, liver transplantation, particularly for chronic hepatic encephalopathy stage III-IV.

PREVENTION1. Diet with protein in a low amount2. The food is given in the form of sweet fruit juice or glucose IV. Given at the beginning of the trip prakoma and when liver damage is not so continue.3. Do not give diuretics that decrease potassium.4. Efforts supportive by providing enough calories and overcome the complications that may be encountered such as hypoglycemia, gastrointestinal bleeding, and electrolyte balance.

Complication Brain edemaKidney failureAcid-base abnormalitiesHypoxiaHemoestasis function and bleeding disordersMetabolic disorders (hypoglycemia) andElectrolyte balance disorders (hypocalcemia)Susceptibility to infectionCirculatory disordersAcute pancreatitis

prognosisDeath is generally caused by bleeding, circulatory and respiratory system failure. Renal failure, infection, hypoglycemia and pancreatitis. Repair or perfect healing can happen when management is done quickly and accurately.EH patient prognosis depends on:Underlying liver disease.Trigger factors.Age, nutritional state.The degree of damage to the liver parenchyma.SexThe ability of liver regeneration.Degrees coma

CONCLUSIONMr. Satrio 55 years suffering from hepatic encephalopathy. Because of the damage to the liver resulting in disruption of the metabolism, so that high ammonia levels in the blood because it was not able to be changed by the liver into urea making it difficult for the exhaust out of the body through the kidneys, because of high ammonia levels make ammonia can pass through the brain barrier (astrocytes) so that the brain undergoes disfunction.

To investigations carried out: Electroencephalography (EEG) Psychometric Tests Blood tests ammonia

Handling in this scenario: Diets low in protein Provision of Lactulose 30-50 cc per hour oral sufficiently mild diarrhea to occur and strict observation neomycin 4x1-2 g / day, peroal for 5 days, or Rifaximin 1200 mg / day Giving vitamin K Improvement of fluid and electrolyte

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