158. Cirrhosis Complications

Question 1

What are the signs of decompensated cirrhosis?

Answer 1

Fluid Overload, coagulopathy
Jaundice, fatigue, malnutrition
High risk of spontaneous hemorrhage

Question 2

Portal HTN

• subtypes
• pathophys
• sx
• exam
• labs
• imaging
• when is biopsy indicated

Answer 2

Subtypes: Intrahepatic (most common - alcohol HCV)
Post-Hepatic (Budd Chiari - hypercoagulable state), Pre- Hepatic (PV thrombosis)
PPhys: fixed fibrosis +/- inflammation +/- blood volume
sx: cognitive errors/slowness, abd fullness, leg swelling, weight gain, fatigue
Exam: memory testing, asterixis (halt traffic), ascites, lower extremity edema, muscle wasting
Labs: low Na, platelets, albumin, cholesterol, BUN; HIGH INR, ammonia
imaging: nodular liver, ascites, varices, splenomegaly
Biopsy: indicated if fibrosis assessment/etiology are unclear

Question 3

Ascites

• sx
• exam
• why do a paracentesis
• pathophys
• tx

Answer 3

Sx: abd fullness, early satiety
exam: distended abd, shifting dullness
Paracentesis: shows cause (Portal HTN has serum to ascites gradient >1.1), Portal HTN, infection, malignancy
PPhys: 1. PHTN = high NO and VD = low renal perfusion
2. High RAAS, SNS, ADH = more fluid retention = more PHTN
3. Liver filtrates fluid into peritoneum = ascites

Tx: Low Na Diet (<2g/day)
diuretics: NKCC inhibitor (Furosemide - lowers K), Aldo inhibitor (spironolactone - raises K) - balance K/euvolemia
Paracentesis: assess etiology, immediate volume reduction/sx relief
TIPS: liver shunt from PV to HV to reduce intrahepatic resistance and reduce PHTN (only in refractory ascites)

Question 4

Spontaneous Bacterial Peritonitis

• what is it
• dx (sx, exam, paracentesis)
• pathophys
• tx
• prophylaxis

Answer 4

Infected ascites
Sx: vary from asx to abd pain
exam: abd distention, guarding
Paracentesis: >250 neutrophils/mm3 (may or may not have positive cultures)
PPhys: enteric bacteria = lymphatics, cross intestinal wall = ascites (and ascites = malnutrition = less opsonin production = less ability to fight infection)

Tx: ABx - G+ and G- coverage (Ceftriaxone) w/ oncotic support (IV albumin), check paracentesis for response after 3 days (less neutrophil count)

Prophylaxis: long term G+/G- coverage (ciprofloxacin)

Question 5

Hepatic Hydrothorax

• what is it
• dx (sx, exam, labs, CXR, thoracentesis)
• pathophys
• tx

Answer 5

increase in pleural fluid (mostly R sided)
sx: dyspnea
exam: diminished breath sounds
labs: hypoxemia
CXR: lung opacity
thoracentesis: PHTN etiology, infections, malignancy
PPhys: PHTN = ascites = high pos intraabd pressure + Neg intrathoracic pressure = draws fluid through diaphragm rents

TX: same as ascites (low Na Diet, Double diuretics, thoracentesis, TIPS if refractory)

Question 6

Hepatopulmonary Syndrome

• what is it
• dx (sx exam labs echo)
• pathophys
• tx
• type I vs Type II

Answer 6

PHTN induced pulmonary shunting
Sx: dyspnea (platypnea - while sitting up)
exam: spider angiomata
labs: low PaO2 on ABG (orthodexia - hypoxemia on pulse ox)
echo: positive bubble sign (bubbles travel to left side of heart due to pulm VD)
PPhys: PHTN = VD and angiogenesis = vascular shunts = O2 mismatch
Tx: mild - O2 supplement
severe- liver tx

Type 1: diffusion-limitation = VD causes larger diffusion distance = hypoxemia
Type 2: R->L shunt = angiogenesis causes shunt = hypoxemia

Question 7

Portopulmonary HTN

• what is it
• dx (sx exam labs echo)
• Pathophys
• Tx

Answer 7

PHTN induced pulm HTN (can co-exist with HPS)
Sx: dyspnea
exam: digital clubbing
labs: hypoxemia on pusle ox
echo: suggests increased pulm artery pressure
Perform R Heart Cath!
PPhys: PHTN = more VC in lung = VC, arterial thickening, thrombosis, fibrosis = high pulm artery pressure = Rheart failure
Tx: Mild - O2 support, VD therapies (endothelin receptor antagonist - bosentan; cGMP PDE inhibitor - Sildenafil), LIVER TX
severe - same as mild but NO liver tx (too high risk of morbidity/mortality)

Question 8

Hepatorenal Syndrome

• what is it
• dx (sx exam labs)
• Pathophys
• tx

Answer 8

renal hypoperfusion in severe PHTN = AKI
sx: weight gain, dyspnea
exam: cirrhotic pt with ascites and edema
Labs: high creatinine, urine studies show oliguria (prerenal AKI)
Dx of exclusion - r/o other AKI causes
PPhys: PHTN = splanchnic VD = renal hypoperfusion = renal VC and RAAS activation = increase in CO (compensation) = increase in PHTN (cycle!) = renal ischemia = renal failure with anuria to uremia

TX:
meds - VCs for splanchnics (midodrine - a1 agonist), VD inhibitor (octreotide - glucagon inhibitor, epinephrine - a/b agonist), oncotic support (IV albumin)
renal replacement therapy: hemodialysis
Liver +/- kidney tx: kidney fx sometimes improves after liver tx

Question 9

Esophageal Varices

• what is it
• dx (sx exam labs, test for definitive dx)
• pathophys
• tx

Answer 9

PHTN induces large/new veins
Normal flow hepatopetal (esophageal - gastric - portal)
Sx: vary from asx to hematemesis
exam: tachycardia, hypotension (if bleeding)
labs: low hemoglobin, high BUN (if bleeding)
EGD: definitive dx with direct view
PPhys: PHTN - reversal of flow (hepatofugal) into esophageal veins - engorged veins - increased bleeding risk

Tx:

• volume resuscitation (IV Fluids)
• Coagulopathy (platelet replacement - FFP)
• Meds: acid suppression (PPIs), Infectious prophylaxis (G+/G- coverage - ceftriaxone, ciprofloxacin), PHTN control (VD inhibitor/decreasing CO - nonselective B Blocker [propranolol] - cause VC by blocking B2; VD inhibitor/glucagon inhibitor - [octreotide])
• EGD: varix ligation (banding)
• TIPS: for recurrent/refractory variceal bleeding

Question 10

Hepatic Encephalopathy

• what is it
• dx (sx, exam, labs, imaging)
• pathophys
• tx
• tests

Answer 10

Altered mentation in cirrhosis due to endogenous toxin build-up (often ammonia)
Sx: altered mentation, constipation (less toxin excreted)
Exam: memory tests (36 cents), asterixis (hand flap)
Labs: r/o toxins, infections, electrolyte problems (do NOT check NH3)
CT brain to r/o other causes

PPhys: 1. high NH3 influx from intestines (bacteria), kidneys, muscle

2. Cirrhosis: impaired NH3 detoxification, PHTN shunting
3. Precipitants: constipation, GI bleed, infection, volume depletion (all increase toxin buildup)
4. High NH3 = brain cell swelling (high osmotic pull), abnormal neural signaling

TX: ammonia control and precipitant mgmt

• ammonia control (LACTULOSE: converts NH3 to NH4+ and catharsis - increases bowel movement for constipation precipitant)
• ABx (Rifaximin - tx infectious precipitant)
• IV fluids if volume deplete precipitant
• EGD/Banding if GI bleed precipitant

Question 11

HCC

• when does it occur
• dx (sx, exam, labs, imaging, biopsy)
• Pathophys
• tx

Answer 11

Common in setting of cirrhosis EXCEPT for (HBV, PBC males)
Sx: most asx
Exam: palpable in late stages
Labs: AFP - not always elevated in HCC
Imaging: CT with ARTERIAL enhancement (perfused by HA)
Biopsy: uncommon due to risk of tumor spread/seeding

PPhys: chronic liver inflammation, regeneration + background of cirrhosis (except HBV, PBC in men)

Tx: Liver directed (radio-ablation, trans-arterial embolization for local chemo/radiotherapy)
Resection (recurrence common)
transplant (recurrence uncommon)
chemotherapy for metastatic disease (poor outcomes)