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Liver Failure PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Liver Failure”.

This medical PowerPoint presentation talks about liver failure, a medical condition in which the liver loses its ability to function properly. It can occur suddenly, known as acute liver failure, or over a longer period of time, known as chronic liver failure.

The liver is responsible for many vital functions in the body, including detoxifying harmful substances, producing bile to help with digestion, storing vitamins and minerals, and regulating blood clotting. When the liver fails, it can lead to a range of serious complications.

Symptoms of liver failure can include jaundice (yellowing of the skin and eyes), abdominal pain and swelling, nausea and vomiting, fatigue, confusion or disorientation, and bleeding easily. Treatment depends on the underlying cause of liver failure and may involve medication, lifestyle changes, or in severe cases, liver transplant.

Common causes of liver failure include chronic hepatitis B or C, long-term alcohol abuse, nonalcoholic fatty liver disease, autoimmune disorders, and certain medications or toxins. It is important to seek medical attention if you experience any symptoms of liver failure, as early diagnosis and treatment can improve outcomes.

Tags : liver failure, Gastroenterology, Gastroenterology PowerPoint presentation

Published on : Apr 26, 2023 | Views : 832 | Downloads : 0

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Slide 1-

Liver Failure Mackay Memorial Hospital Department of Internal Medicine Division of Gastroenterology R4 陳泓達 97/6/22
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Liver failure: Clinical syndrome: sudden loss of liver parenchymal and metabolic function Manifest as coagulopathy and encephalopathy
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Acute liver failure : Defined as interval between onset of the illness and appearance of encephalopathy < 8 weeks
Slide 4-

Etiology: Western countries: heterogenous, drugs (acetaminophen, NSAID), viruses Developing countries: viruses, regional Difference (endemic area ?)
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Journal of Gastroenterology and Hepatology(2002)17, S268–S273
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Acetaminophen toxicity Idiosyncratic drug toxicity Hepatotropic viruses Miscellaneous causes Indeterminate acute liver failure (viruses can not be demonstrated ? )
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Uncommon causes: Wilson’s disease, other infections (CMV, HSV, EBV), vascular abnormality, toxin, acute fatty liver of pregnancy, antoimmune hepatitis, ischemia, malignant infiltration
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Symptoms and signs: Jaundice, altered mental status, nausea/ vomiting, anorexia, fatigue, malaise, myalgia/arthralgia Most of them present hepatoencephalopathy and icteric appearance.
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Non-specific Management Hypoglycemia Encephalopathy Infections Hemorrhage Coagulopathy Hypotension(hypovolemia, vascular resistance ↓) Respiratory failure Renal failure Pancreatitis
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Hypoglycemia: monitoring blood glucose, IV glucose supplement. Infection: aseptic care, high index of suspicion, preemptive antibiotic. Hemorrhage (i.e. GI): NG placement, H2 blocker or PPI. Hypotension: hemodynamic monitoring or central pressures, volume repletion
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Respiratory failure (ARDS): mechanical ventilation. Renal failure (hypovolemia, hepatorenal syndrome, ATN): hemodynamic monitor, central pressure, volume repletion, avoid nephrotoxic agent
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Encephalopathy major complication precise mechanism remains unclear Hypothesis: Ammonia production Treatment toward reducing ammonia production Watch out airway, prevent aspiration
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Encephalopathy Stage 1: day-night reversal, mild confusion, somnolence Stage 2: confusion, drowsiness Stage 3: stupor Stage 4: coma
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Encephalopathy Predisposing factor of hepatic encephalopathy: GI bleeding, increased protein intake, hypokalemic alkalosis, hyponatremia, infection, constipation, hypoxia, infection, sedatives and tranquilizers
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Encephalopathy TX upon ammonia hypothesis Correction of hypokalemia Reduction in ammoniagenic substrates: cleansing enemas and dietary protein restriction. Lactulose: improved encephalopathy, but not improved outcome. Dose 2-3 soft stools per day
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Encephalopathy Oral antibiotics: neomycin  lack of evidence nephrotoxicity  limited use.
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Cerebral Edema Cerebral edema develops in 75 - 80 % of patients with grade IV encephalopathy. precise mechanism : not completely understood Possible contributing factor: osmotic derangement in astrocytes changes in cellular metabolism alterations in cerebral blood flow
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Cerebral Edema Clinical manifestations: ↑intracranial pressure (ICP) and brainstem Herniation  the most common causes of death in fulminant hepatic failure ischemic and hypoxic injury to the brain hypertension, bradycardia, and irregular respirations, ↑ muscle tone, hyperreflexia
Slide 20-

Cerebral Edema Monitoring of ICP: routinely used by more than one-half of liver transplantation programs in the United States Tx: to maintain ICP below 20 mmHg and the CPP above 50 mmHg.
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Coagulopathy diminished capacity of the failing liver to synthesize coagulation factors. The most common bleeding site: GI tract. Prophylactic administration of FFP: not recommended.  performed before transplant or invasive procedure
Slide 22-

Specific Treatment ACT intoxication: charcol followed by NAC Drug induced hepatotoxicity: discontinue drugs supportive treatment Viral hepatitis: HBV: anti-HBV treatment, lamivudine HSV/varicella zoster: acyclovir others: supportive care
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Wilson’s disease: early diagnosis  liver transplant autoimmune hepatitis: confirm diagnosis (liver biopsy), corticosteroid liver transplant acute fatty liver of pregnancy or the HELLP syndrome: obstetrical services, and expeditious delivery are recommended
Slide 24-

Acute ischemic injury (shock liver): cardiovascular support Malignant infiltration: liver biopsy for diagnosis treat underlying disease. Indeterminate etiology: consider biopsy for diagnosis and further guide of treatment
Slide 25-

Liver transplant Liver transplant: remain backbone of treatment of fulminant hepatic failure reliable criteria to identify these patients who really need transplant.  remain unresolved in fulminant hepatic failure.
Slide 26-

At King’s College hospital in London (not due to ACT) either PT>100 second or the presence of any three of the following variables: 1. age < 10 or > 40 years ; 2. an etiology of non-A, non-B hepatitis, halothane, drug induced liver failure; 3. duration of jaundice before onset of encephalopathy > 7 days, prothrombin time >50 s, and serum bilirubin > 300 mmol/L.
Slide 27-

Encephalopathy Coagulopathy (PT)
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Liver transplant Criteria: In chronic liver disease most commonly used prognostic model MELD score (Model for End-stage Liver Disease ) 3.8[Ln serum bilirubin (mg/dL)] + 11.2[Ln INR] + 9.6[Ln serum creatinine (mg/dL)] + 6.4 Ln: natural logarithm.
Slide 29-

Liver transplant CONTRAINDICATIONS: Cardiopulmonary disease can not be corrected, or preclude surgery. Malignancy outside of the liver within 5 years of evaluation, or can not be cured. Active alcohol and drug use
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Advanced age and HIV disease: relative contra-indication (site-specific management)
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Liver support system Non-cell-based: plasmapheresis and charcoal-based hemoabsorption Cell-based systems : known as bioartificial liver support systems
Slide 32-

Liver support system Non-cell-based: not improved survival. Available systems: molecular adsorbents recirculation system (MARS) Cell-based systems: undergoing trial.