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Causes of Acute Hepatic Failure (AHF)
- Primary disease process (breakdown of organ itself); SHOCK
- Complication of chronic liver disease
- MODS
- Hypoglycemia (carb metabolism failure)
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Causes of Fulminant Hepatic Failure (FHF)
- Viral infections: Hep A, B, and C; Cytomeglovirus; EVB (mono)
- Hepatoxins: acetaminophen, mushroom toxins, Insoniazid, Hydrocarbons
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FHF characteristics
- Rapid, massive destruction
- Widespread necrosis
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FHF Criteria
- No preexisting liver disease; healthyl iver
- Encelphalopathy level: significant mental status change; stage 3 or 4
- Rate of onset: < 8 weeks
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LFTs (trends)
- ALT: increase
- AST: increase
- Alk Phos: decrease initally, will increase as problems persist
- Bilirubin: increase; liver can't break down bile, jaundice; chronic indicator
- Albumin: decrease; liver failure
- PT: increased; liver failure, when vit. K decreases
- Platelet count: decreased; portal HTN and spleen issue
- Serum protein electrophoresis: serum smear; look at cells to see what's going on in liver
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Hepatic Encelphalopathy
- Hallmark of AHF
- Altered neuro status caused by build up of ammonia or hepatic origin; breakdown of proteins
- Associated w/ hypoglycemia, cerebral edema
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Stage 1 of Hepatic encelphalopathy
- Awake but mental clouding
- Restlessness
- Altered sleep pattern
- Impaired computation, handwriting, intellectual abilities; analytical deficits
- Diminished muscle coordination
- ECG: mild to moderate, slowing of brain firing, usually no ECG here
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Stage 2 of Hepatic encelphalopathy
- Decreased LOC
- Lethary (sluggish)
- Drowsiness
- Disorientation to time and place
- Confusion
- Asterixis (jumping of limb when touched)/ Diminished reflexes
- Slurred speech
- ECG: mild to moderate, slowing of brain function, usually no ECG here
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Stage 3 of Hepatic encelphalopathy
- Stupor but able to arouse
- No spontaneous eye opening
- Hyperactive reflexes (jerking, bouncing)
- Seizures
- Rigidity
- Abnormal posturing; flexion and extension
- ECG: severe abnormalities, may or may not see seizure activity
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Stage 4 of Hepatic encelphalopathy
- Coma
- Seizures
- Dilated pupils (still responsive)
- Flaccidity
- ECG: severe, abnormalities and brain problems
- No amt of stimulation will wake them up, no brain interaction
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Metabolic Dysfunction of AHF
- Protein metabolism dysfunction: ascites, hypoalbuminemia, hepatic encelphalopathy, impaired clotting factors
- Cab metabolism dysfunction: hypoglycemia
- Fat metabolism dysfunction: N/V, anorexia, constipation or dirrhea
- Prolonged PT: vit K issue
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Effects of AHF on body systems
- Neuro: encelphalopathy
- CV: hypotension
- GI: N/V, diarrhea, constipation, anorexia, ascites
- Hematopoeitic: impaired coags
- Pulm: tachypnea, crackles, pulmonary edema, portal HTN, fluid back up
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Portal HTN
- Back flow issue
- Caused by cirrhosis
- Over time will devlop varices to help relieve pressure
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Portal HTN pathogenesis
Hepatic parenchymal damage, increased pressure required to perfuse liver, increased capillary resistance, portal HTN
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What does portal HTN result in?
- Chronic liver disease: development of varices
- Acute liver disease: no varices, congestion in splenic organs
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Hepatorenal syndrome
- Renal failure secondary to severe liver failure in absence of renal pathology
- Severe, rapidly progressing renal failure
- Uremia/oliguria
- Cr levels >2.5
- Cr cleareance <20 in less than 2 weeks
- Need to treat liver issue first
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Spontaneous Bacterial peritonitis
- Ascites fluid becomes infected
- Translocation of bacteria: bowel to ascites
- Fever, pain
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Treatment of esophageal varices
- Prophylaxis: prevent initial bleeding
- Meds: beta blockers, nitrates (if no response from beta blockers)
- Hemodynamic resuscitation
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Treatment of Hemorrhage: hemodynamic resuscitation
- Blood products and crystalloids
- Maintain Hct >30%
- Clotting factors: platelet replacement
- Always want current type and screen (expires q 24hrs)
- Initally need fluid for perfusion, CO, and BP; then need blood asap
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Treatment of Hemorrhage: Control Bleeding
- Vasopressin: vasocontrictor; only a bandaid, not permanent
- Nitro: to dilate when vasopressin contricts
- Octreotide (IV): inhibits release of vasodilatory hormones, vasocontriction of splanchnic vessels
- Endoscopic therapy: First line, sclerosing chemical, on Protonix after 3-5 stopped bleeding
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Treatment of Hemorrhage: Preventative
- TIPS: shunt made between hepatic and portal veins, kept open w/ metal shunt; decompresses portal system and controlling bleeding
- Complications: stent dysfunction, thrombosis, retraction, displacement, stenosis
- Put in in the OR
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Sengstaken-Blakemore tube
- Creates pressure in esophagus w/ balloon
- Risk of rupturing esophagus
- Maintain O2
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