Hepatic Problems

• Primary disease process (breakdown of organ itself); SHOCK
• Complication of chronic liver disease
• MODS
• Hypoglycemia (carb metabolism failure)

• Viral infections: Hep A, B, and C; Cytomeglovirus; EVB (mono)
• Hepatoxins: acetaminophen, mushroom toxins, Insoniazid, Hydrocarbons

• Rapid, massive destruction
• Widespread necrosis

• No preexisting liver disease; healthyl iver
• Encelphalopathy level: significant mental status change; stage 3 or 4
• Rate of onset: < 8 weeks

• 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

• Hallmark of AHF
• Altered neuro status caused by build up of ammonia or hepatic origin; breakdown of proteins
• Associated w/ hypoglycemia, cerebral edema

• 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

• 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

• 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

• Coma
• Seizures
• Dilated pupils (still responsive)
• Flaccidity
• ECG: severe, abnormalities and brain problems
• No amt of stimulation will wake them up, no brain interaction

• 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

• Neuro: encelphalopathy
• CV: hypotension
• GI: N/V, diarrhea, constipation, anorexia, ascites
• Hematopoeitic: impaired coags
• Pulm: tachypnea, crackles, pulmonary edema, portal HTN, fluid back up

• Back flow issue
• Caused by cirrhosis
• Over time will devlop varices to help relieve pressure

Hepatic parenchymal damage, increased pressure required to perfuse liver, increased capillary resistance, portal HTN

• Chronic liver disease: development of varices
• Acute liver disease: no varices, congestion in splenic organs

• 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

• Ascites fluid becomes infected
• Translocation of bacteria: bowel to ascites
• Fever, pain

• Prophylaxis: prevent initial bleeding
• Meds: beta blockers, nitrates (if no response from beta blockers)
• 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

• 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

• 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

• Creates pressure in esophagus w/ balloon
• Risk of rupturing esophagus
• Maintain O2