Acute Liver Failure Group 3

 

Acute liver failure

 

Group 3 Leader: Sibay Kyla Assistant Leader: Dejesus, Janszen Castillo Members:

● ● ● ●

Gillian mae Dolosa  Nicka marice Majadora Aaron khan Nadduha Donna joy Perez

● Sittienor hannah Sarip ● Gabriel Villegas

 

Case Scenario

 

A 64-year-old man, Mr. Koko Melo, with a significant medical history of chronic obstructive  pulmonary disease, alcohol alcoh ol abuse, and depression presented pres ented to the intensive intens ive care unit(ICU)of FUMC as a transfer from the emergency department for acute hepatic failure. Melohad reportedly ingested 50 tablets of hydrocodone/acetaminophen (10-325 mg; 16.2 g of acetaminophen)in an attempted suicide 6 hours before arrival at HospitalM. His initial laboratory evaluation was notable for the following: •Ethanol level: 320 mg/dL •Acetaminophen level: 430 μg/mL •Aspartate aminotransferase (AST) level: 2066 U/L •Alanine aminotransferase (ALT) level: 1321 U/L •Potassium level: 5.6 mEq/L •Creatinine phosphokinase (CPK) level: 62,530 IU/L Orders at the ED was to place Mr. Meloon a continuous norepinephrine infusion at 20 μg/h. He was intubated secondary to being obtunded. He underwent treatment for hyperkalemia and was started on intravenous N-acetylcysteine (NAC)200mg/mL as follows: -Loading dose of 150 mg/kg IV; mix in 200 mL of 5% dextrose in water and infuse over 1hour  -Dose 2:50 mg/kg IV in 500 mL D5W over 4 hours -Dose 3: 100 mg/kg IV in 1000 mL D5W over 16 hours

 

Upon admission at the ICU, the patient was afebrile, blood pressure was 94/57mmHg, heart rate of92  bpm, and respiratory rate rat e at22 breaths/min. breaths/min . He weighs 87 kg. His oxygen saturation satu ration was 96% on the ventilator. On examination, Mr. Mel exhibited diffuse jaundice, smelled of alcohol and tobacco, and appeared much older than his stated age. He was in no acute distress. He had bilateral scleral icterus. His cardiopulmonary examination findings were unremarkable for any acute changes. His abdominal examination revealed a fluid wave with the absence of any peritoneal signs. On his 2nd hospital day, laboratory evaluation findings included the following: •Hemoglobin level: 10.5 g/dL •Platelet: 110 x 103/L •Sodium level: 146 mmol/L •Potassium level: 4.6 mmol/L •Blood urea nitrogen level: 26 mg/dL •Creatinine level: 3.02 mg/dL •AST level: 2094 U/L •ALT level: 1685 U/L •Totall bilirubin level: 0.4 mg/dL •Tota •INR: 2.11 •Troponin level: 35.25 ng/mL (increasing to 44.66 ng/mL) •Acetaminophen level: 237 μg/mL •Acetaminophen •CPK level: 57,000 IU/L •ABG: pH = 7.03, paCO2= 41.26 mmHg, HCO3= 6.0 mmol/L, paO2= 112.53mmHg, and a BE =–22.6 mmol/L

 

Ultrasonography of the abdomen revealed an increased hepatic echogenicity suggesting diffuse hepatocellular disease, cirrhosis, and small amount of perihepatic ascites. Given the Melo’ Melo’ss condition, conservative treatment was recommended. He was started on a low-intensity heparin infusion(UFH 50,000units/5mLinfusion rateof 12 units/kg/hr)for 48 hours. By day 3, Melo’screatinine Melo’screatinine level rose to 4.18 mg/dL, and he was anuric. His AST level level increased to 3895 U/L, and his ALT ALT level increased to 3215 U/L, despite intravenous  NAC administration. administration. His lactic acid level increased increased from 2.2 to 8.2 mmol/L, mmol/L, with an an anion gap of 25. He subsequently underwent dialysis. By day 4, vancomycin and piperacillin/tazobactam were initiated for healthcarehealthcareassociated pneumonia. Chest radiography revealed revealed hazy opacities in the lung lun g bases. The transplant surgery team deemed him to be a poor candidate from a surgical  perspective for a liver transplant.

 

Background Background of  of the study

 

Acute liver failure (ALF) is a devastating syndrome that triggers a cascade of events, leading to multiple organ failure and often death. ALF is a syndrome defined by the occurrence of encephalopathy, coagulopathy and jaundice in an individual with a previously normal liver. Patients with high grades of encephalopathy, the chances of survival are less than 20% with medical management alone. Early deaths in ALF are often caused by cerebral oedema or cardiovascular collapse, whereas late deaths tend to result from sepsis and multiple organ failure. O’Grady System Hyperacute (0 - 1 week  Acute (From 1 week - 4 weeks) Subacute (From 4th week - 12 weeks)

 

Causes of Acute Liver Failure

Symptoms

Complications

1. Viral Hepatitis   - Hepatitis A, B, C, D, E   - CMV, EBV EBV,, VZV   2. Drugs/T Drugs/ Toxins   -Acetaminophen   -Herbal supplements

Signs and symptoms of acute liver failure may include:  Yellowing of your skin and eyeballs (jaundice)  Pain in your upper right abdomen  Abdominal swelling

Acute liver failure often causes complications, including: Excessive fluid in the brain (cerebral edema). Bleeding and bleeding disorders.

  -Antibiotics   -Mushroom poisoning 3. Shock/ ischemic liver  4. Alcoholic hepatitis 5. Autoimmune disease 6. Cryptogenic

      

(ascites)  Nausea Vomiting A general sense of feeling unwell (malaise) Disorientation or confusion Sleepiness Breath may have a musty or sweet odor  Tremors

Infections. Kidney failure.

 

ETIOLOGY

 

Etiology Drug induce (acetaminophen) Risk Factors:

Risk Factors: Modifiable

 Non-modifiable -Alcohol abuse  -Obesity (patient: 87 kg)

-Age (67 years old) - Gender (male)

Other risk factors: Prescription medications. - Antibiotics - Non steroidal -anti inflammatory drugs - Anticonvulsants - Hepatitis A, B, E

 

Pathophysiology

 

Acute Liver Failure

Acetamenophen hepatotoxicty

Damage to the Liver 

Lost of Metabolic Function

Loss of parenchyma Liver shrinking to small

 ammonia clearance

Hepatic encephalopathy

Change of behavior, reduced alertness, confused, anxiety

hyperammonaemia Cerebral edema Cytotoxic Impaired cellular osmoregulation  Astrocyte edema

Intracranial pressure

Hypertension, bradycardia

Massive hepatic necrosis Serum transaminases

Vasogenic Disruption of cerebral autoregulation

Intracranial blood volume & cerebral blood flow.

Elevated systemic concentration of nitric Acid.

 Act as potent vasodilator 

 

Clinical manifestation • Jaundice & Bilateral scleral ictus • Ascites

Others •Right abdominal pain •Nausea •Vomiting •Malaise •Disorientation or confusion •Breath may have a musty or sweet odor •Tremors

 

Pertinent findings ●

Medical history of COPD, alcohol abuse, and depressionDiabetes depression Diabetes testing blood  background..  background

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BP was 94/57 mmHgSet mmHgSet of diabetes symptoms with flat design

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HR of 92 bpm RR at 22 bpm

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O2 was 96% on the ventilator 

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Diffuse jaundice

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Smelled of alcohol and tobacco

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Bilateral scleral icterus

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Cardiopulmonary examination findings were unremarkable for any acute changes

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Abdominal examination revealed a fluid wave with the absence of any peritoneal signs

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Increase hepatic echogenicity

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Diffuse hepatocellular disease, cirrhosis, and small amount of perihepatic ascites Chest radiography revealed hazy opacities in the lungs

 

Thank you