inpatient / gastroenterology

Cirrhosis and Decompensations

Last Updated: 12/31/2022

# *** [Compensated/Decompensated] Cirrhosis Due to *** [Alcoholic, Hepatitis B/C, NASH, Autoimmune, PBC, PSC]

-- ABC's: 
life-threatening decompensations include SBP/sepsis, EV bleed, severe HE - ICU for pressor need, intubation, or close monitoring of bleed
-- Chart Check: prior decompensations, last para and studies, meds
-- HPI Intake: EtOH use, adherence to meds, constipation, bleeding
-- Can't Miss: variceal bleed, severe HE, SBP leading to sepsis
-- Admission Orders: Labs - CBC, CMP, coag, infectious workup; RUQUS if c/f clotting, underlying HCC; If AKI, send urine Na; new cirrhosis and transplant workup - viral hepatitis panels, iron studies, ANA, ASMA, AMA, a1aT, ceruloplasmin, SPEP
-- Initial Treatment to Consider: abx, GI bleed from varices pathway (EGD, octreotide, PPI, CTX), lactulose/rifaximin; all decompensations should at least get diagnostic para


Transplant: *** (listed, Hepatologist, prior workup)
MELD Score: ***

Decompensation Hx: (VIBES)
-- Volume/Ascites
: *** prior LVP, frequency, salt restriction on lasix/spironolactone
-- Infection/SBP: *** prior infections, h/o low protein ascites, on ppx
-- Bleeding/EV: *** last EGD, prior bleeds, banding, on nadolol/PPI
-- Encephalopathy/HE: *** prior decompensation, on lactulose/rifaximin, BM/day
-- Screening/HCC: *** last screen, AFP; if nodule >1cm get multiphase CT or MRI

-- Clinical: *** pruritis, distention, anorexia, AMS, fatigue
-- Exam: *** hypotension, jaundice, cachexia, temporal wasting, gynecomastia, asterixis/milkmaid's, ascites, AMS, spider angioma, palmar erythema, petechiae/eccymoses, caput medusa, edema, Terry's nails
-- Data: *** serum Na, Creatinine, TBili, INR, albumin; para - albumin, protein, cell counts, cultures; RUQUS
-- Trigger: *** infection, med adherence, bleed, constipation, new clot, sedative, dehydration, alcohol, procedure, hypokalemia, AKI, metabolic alkalosis

The patient's HPI is notable for ***. Exam showed ***. Labwork and data were notable for ***. Taken together, the patient's presentation is most concerning for ***, with a differential including ***.

-- f/u *** CBC, CMP, coags, UA, ascitic studies - PMN, SAAG, GS/Cx
-- Consider RUQUS to rule out portal vein thrombosis
-- If AKI, send urine Na
-- If c/f EtOH use - sent PEth
-- If first presentation of cirrhosis - to discuss full workup inpatient vs outpatient (viral hepatitis panels, iron studies, ANA, ASMA, AMA, a1aT, ceruloplasmin, SPEP)

-- Volume/Ascites: *** diagnostic vs LVP - albumin 8-10 g/L if >5L, diuresis 100mg spironolactone, 40mg furosemide (5:2 ratio); Refractory ascites - midodrine TID, serial LVPs q2 weeks, or TIPS as a bridge to OLT
-- Infection/SBP: *** CTX 2g/day for 5 days and albumin 1.5g/kg day 1; ppx cipro 500mg BID or bactrim SS daily if h/o SBP, ascitic total protein <1.5 AND impaired renal fx (defined by 1 of: Cr >1.2, BUN >25, Na <130, Tbili >3); ciproflax 400mg q12 is alternative; discontinue BB indefinitely
-- Bleed/EV: *** prior bleed or EV w/ risk bleed - nadolol 20-40mg BID ppx with goal HR 55-60, SBP >90; if c/f bleed - octreotide 50mcg load/gtt 50mcg/hr for 3 days, PPI 80mg load/drip 8mg/hr, CTX 1g for 7 days
-- Encephalopathy/HE: *** infectious w/u; lactulose 30g titrated to 3 BMs/day, rifaximin 550mg BID; maintain K >4
-- HRS: *** 100g albumin, followed by 20-40g daily, midodrine 7.5mg to 15mg TID, octreotide 100mcg TID
-- Nutrition: *** Dobhoff with TEN if altered, consult nutrition, low Na/high protein diet
-- Palliative: *** serna lotion (menthol, camphor) for itching
-- If hyponatremic <125, fluid restrict 1.5L/day; Na restrict >2g/day
-- If AKI, hold diuretics, send urine Na (<10 c/f HRS - volume challenge 1g/kg albumin) 
-- If suspect vitamin K deficiency, give vitamin K 10mg x3d to correct nutritional component
-- If c/f portal vein thrombosis, DOAC for 3-6 months
-- Transfuse for hgb > 7, plt > 50, fibrinogen >100


*** with a history of Cirrhosis due to *** [EtOH, NASH, HCV, Autoimmune, PSC, PBC, etc.] decompensated by *** [HE, EV, Ascites, SBP, HCC] with MELD score on admission of ***, currently [listed/not listed] for transplant at ***, followed by *** [Hepatologist] who presents with *** concerning for ***.

The patient’s current volume exam suggests they are ***. We should [hold/continue/initiate] diuretics ***.

Based on Na level of ***, this patient should have a Na diet and fluid restriction. 

There is currently *** concern for SBP based on history/exam, and ascitic fluid showing ***. Based on this, we should treat with *** (CTX 2g for 5 days), or treat prophylactically with ***. 

The patient [does/does not] have a history of esophageal varices, with bleeding history of ***. There is currently *** concern for a GI bleed based on ***. Based on this, we should treat with *** (PPI, octreotide), plan for EGD ***, treat for SBP prophylaxis with CTX 1g daily, and transfuse as needed for Hgb >7. 

The patient [is/is not] currently altered with an exam showing ***, concerning for hepatic encephalopathy. The etiology of this decompensation is likely ***. We should treat with (lactulose, rifaximin) with a goal of *** BM’s (or 500cc stool) per day. 

Based on patient’s MELD of , they [are/are not] a candidate for transplant and [are/are not] currently listed for transplant at ***. Limitations for transplant include (HCC, sobriety, etc).

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If You Remember Nothing Else

The most common etiologies of cirrhosis are EtOH, HCV, NAFLD/NASH. MELD uses Cr, Tbili, INR, and Na to calculate - ranges from 6-40. Decompensations are ascites, SBP, EV, HE, HCC. Common triggers for decompensation include infection, medication non-adherence, constipation, bleeding, and dehydration from diuretic use. All decompensated patients admitted should have a diagnostic paracentesis. SAAG (serum ascites albumin gradient) > 1.1 suggests the etiology of ascites is related to portal hypertension (if there is a big difference, would be more explained by oncotic pressure)

Clinical Pearls

  • Cirrhosis is irreversible fibrosis leading to nodules that interfere with hepatic architecture, vasculature, and ultimately function - when liver function is impaired, its considered End-Stage Liver Disease (ESLD)
  • Alcohol, HCV/HBV, and NAFLD are the most common causes of cirrhosis
  • MELD Score predicts 90d mortality, used to assess for transplant; uses Cr, Tbili, INR, Na; ranges from 6-40 (should use values within last 48 hours); Child-Pugh assesses cirrhosis severity, predicts 1-2y mortality; uses Bilirubin, albumin, INR, ascites, encephalopathy
  • A biopsy is the gold standard for diagnosis of cirrhosis, but imaging is often more than enough for diagnosis
  • RUQUS can tell us about echogenicity/morphology of the liver, presence and appearance of ascites, vascular patency, the biliary tree morphology, evidence of HCC
  • Decompensations are ascites, encephalopathy, and variceal bleeding; SBP, HCC, and varices that don’t bleed are technically not decompensations but whatever
  • Ascites is the most common decompensation; from development, there is a 44% 5y mortality
  • A majority of complications of cirrhosis are related to portal hypertension (varices, ascites, hydrothorax, HRS) and reduced synthetic function (low albumin and oncotic pressure, immune dysfunction, coagulopathy, portal vein thrombosis)
  • Portal hypertension leads to an increase in NO and prostaglandins leading to splanchnic vasodilation - the body increases RAAS and ADH in response leading to Na and water retention; Hyponatremia severity correlates with survival
  • SAAG (serum ascites albumin gradient) > 1.1 suggests the etiology of ascites is related to portal hypertension (if there is a big difference, it would be more explained by oncotic pressure)
  • 10-30% of patients hospitalized with cirrhosis have SBP; diagnosed with >250 PMN/L; if cultures negative, technically called culture-negative neutrocytic ascites (CNNA); secondary peritonitis is usually polymicrobial
  • SBP - 70% GNR, Klebsiella, E. Coli, 30% GPC Enterococcus, Strep Pneumo
  • In general, the diuretic goal should be net neg 500-1000cc - going too fast runs the risk of AKI since ascites fluid mobilized slower than other compartments
  • UNa/UK can help differentiate between too low diuretic dose vs too much Na in the diet; if UNa/UK <1, likely an ineffective dose; if >1 suggests >2g Na intake
  • Do a therapeutic LVP if tense or refractory ascites or unable to use diuretics; if >5L give 6-8g albumin for every L ascites removed
  • Refractory ascites can be treated with midodrine TID, serial LVPs q2 weeks, or TIPS as a bridge to OLT
  • HE is neurotoxic effects of increased NH3 - leads to abnormal neurotransmission (increased GABA, decreased glutaminergic) leads to depressed AMS, and at worst edema; asterixis and milkmaid’s are signs of the neurotoxicity leading to loss of postural tone but also inattention
  • Grade 1 HE - inattention, altered sleep pattern; Grade 2 - lethargy, disoriented, asterixis; Grade 3 - somnolence, AMS, asterixis; Grade 4 - Coma
  • Ammonia absolute value does not add any diagnostic value - level does not correlate with severity - able to compensate for high levels over a chronic timeline
  • Lactulose works by increasing stool output and maintaining acidic pH (converted to lactic acid by intestinal flora which leads to acidification which turns NH3 (ammonia) to NH4+ (ammonium) which is more easily excreted in feces; rifaximin helps reverse HE by (possibly) killing bacteria that turn NH4+ to NH3, allowing NH4 to be excreted (or just result of pH); in general, add rifaximin if refractory, or 2nd admission for HE
  • Beyond rifaximin, can consider Miralax, branched-chain AA, L-ornithine L-aspartate
  • EGD should be done at diagnosis and every 2 years if ongoing/worsening cirrhosis
  • Gastric varices are treated similarly to EV, but are much more dangerous and have high mortality
  • Window hypothesis - beta blockers have no effect on survival or prevention in early cirrhosis, but have a survival benefit in middle stages, & reduce survival in advanced cirrhosis; stop BB if SBP, refractory ascites, HRS< low BP, sepsis
  • PTT and PT/INR do not correlate with the risk of bleeding or clotting in patients with cirrhosis - there is no benefit to correcting INR pre-procedure, but should shoot for goal Plt >50k if getting a risky procedure
  • Avoid FFP in general unless persistent fibrinogen deficiency - large volume leads to increased portal pressures
  • Can stop screening for HCC if Child-Pugh Class C and not listed for transplant due to low survival
  • HCC treatment - curative surgery if Child-Pugh A and small nodule or liver transplant; can also ablate or do TACE/TARE with IR, sorafenib, immunotherapy, radiation
  • Milan Criteria for transplant with HCC - one lesion <5cm or up to 3 lesions all <3cm, no extra-hepatic involvement, no major vessel involvement
  • Hepatic hydrothorax is more commonly R-sided; comes from small defects in the diaphragm, do not need to have large volume ascites to build up on thoracic cavity - can do thora if the cause of dyspnea, but should avoid chest tubes
  • Hepatopulmonary Syndrome - shunting through vascular dilations, often at the bases of lungs, leads to platypnea (dyspnea when upright); get TTE with late bubbles and PFTs showing decreased DLCO; the only treatment is a transplant 
  • HRS - splanchinic dilation → activation of RAAS → renal vasoconstriction → decreased GFR - need to exclude other causes (prerenal - have lack of improvement after volume expansion - no shock, no exposure to nephrotoxic drugs); goal to cause vasoconstriction of splanchnics by repleting volume and giving midodrine and octreotide - goal to avoid dialysis, as usually doesn't help improve mortality
  • TIPS - if refractory ascites, recurring varices, acute decompensation as bridge to liver transplant; early <72h if high risk of rebleed, “rescue” if uncontrolled bleed despite medical and EGD therapy
  • PEth blood test measures phosphatidylethanol (PEth) which is an alcohol biomarker - if <10 considered negative; if >10, likely ongoing alcohol use; >210 indicates excessive use
  • Palmar erythema and spider angiomata are caused by hyperestrogenism
  • Spironolactone can cause gynecomastia

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