Gastrointestinal [CIRRHOSIS AND ASCITES]

Definition and Introduction Cirrhosis Etiologies = “VW HAPPENS”

A cirrhotic liver is one that’s been annihilated, replaced by Viral Hep B/C
extensive fibrosis, and with minimal regenerating nodules. It’s Wilsons Eyes, Liver, Basal Ganglia (Cu)
the end-stage of liver disease - regardless of the etiology. It Hemochromatosis “Bronze Diabetes” (Fe)
Alpha-1 Anti trypsin Emphysema and Cirrhosis
produces a number of complications that become targets of
Deficiency
therapy. Once cirrhotic, the only option is transplant. Knowing Primary Sclerosing Men with Crohn’s
etiology, presentation, and the unique considerations is key to Cholangitis
mastering cirrhosis. Primary Biliary Women, Autoimmune, ANA,
Cirrhosis “Biliary Cirrhosis is for Bitches”
Presentations and Labs Ethanol Drinkers
NASH/NAFLD Fat people
The liver does a lot of things. It clears bilirubin - failure causes
Something Rare
jaundice and sclera icterus. It produces bile - accumulation of
bile causes pruritus. It also produces coagulation factors - a Function Effect of Cirrhosis
deficiency produces bleeding. Because all blood flow from the Bilirubin Jaundice, Scleral Icterus, Dark Urine
visceral organs flows through the liver, a cirrhotic liver, like a Bile Pruritus
plug, ↑resistance, causing portal hypertension. This HTN Coagulation Bleeding = ↑PT, ↑PTT, ↑ INR (coags)
causes porto-caval shunting (hemorrhoids, caput medusa, Protein Hypoalbuminemia ↑Ascites, Edema
esophageal varices) and transudation of fluid (ankle edema and Blood Flow Porto-caval shunt, Ascites
(Portal HTN) (hemorrhoids, caput, esophageal varices)
ascites). Ascites is exacerbated by a ↓protein production
Estrogen Gynecomastia, Palmar Erythema
(hypoalbuminemia, Total protein ↓). Estrogen is degraded and Nitrogen Asterixis and AMS/Coma
converted to testosterone while estrogen excess produces
gynecomastia, palmar erythema, and spider angioma. Finally, **Also: Parotid Enlargement, Dupuytren’s Contracture,
the liver controls ammonium metabolism. Excess ammonium clubbing, axillary hair loss**
can cause asterixis (flapping tremor) and encephalopathy. Get
an Ultrasound (1st, to identify cirrhosis), a CT Scan/MRI to J = K (Part – Pint) + (σint – σart)
evaluate nodules or masses, and finally a biopsy (best) to
confirm the diagnosis and etiology. Acute hepatitis causes an
elevation of liver enzymes. A cirrhotic liver is burned out and
AST/ALT will be low or smoldering just above elevated. The
MELD score (calculated using the bilirubin), INR, and
creatinine show how sick a liver is. 1 is normal, 40 is death. Pint σart σint
Transplant workup starts at 15. Part

The full workup of a liver involves the LFTs (AST, ALT, ALk
Phos, BIli, TP, Albumin), Coagulation Factors, Ultrasound, CT Parterial σint or K
scan, and Biopsy. Portal HTN Related Non-Portal HTN Related
SAAG > 1.1 SAAG < 1.1
Ascites and SAAG Cirrhosis Cancer
Fluid in the abdomen (ascites) has multiple etiologies - one of R-sided CHF Peritoneal TB
Budd-Chiari Nephrotic Syndrome
which is cirrhosis. The patient will have flank dullness, a fluid
Portal/Splenic Thrombosis Protein-Losing Enteropathy
wave, and shifting dullness on physical exam. To detect fluid Schistosomiasis Post-Op Lymphatic Leak
an Ultrasound may be performed. Fluid may also be detected Bowel Obstruction
via CT/MRI (which helps with differentiation). What we worry
about is a 1st time presentation (etiology unknown) or a return Cirrhosis Na < 2g/day
customer with a fever or abdominal pain. For both cases do Ascites H2O < 2L/day
paracentesis first to get a SAAG score (Serum Albumin – Therapy Diuresis with spironolactone 100, Lasix 80
Ascites Albumin) and an AFTP (cirrhosis vs cardiac ascites). If Tap 4-6L off requires Albumin infusion
TIPS ↑ blood flow, ↑NH4, ↑Asterixis, AMS
a SAAG is > 1.1 it’s from portal HTN (cirrhosis, R Heart
Failure, Budd-Chiari) If a SAAG is < 1.1 it’s non-portal HTN
related, with ↑ risk of TB and malignancy. The result will direct
the workup. The goal is to treat the underlying causes. If
secondary to cirrhosis, treat is by restricting fluid + salt and
supplementing with diuretics. Everyone with ascites gets ↓Na
Intake (2g max/day), limiting H2O (2L /day). Some people get

© OnlineMedEd. http://www.onlinemeded.org
 Gastrointestinal [CIRRHOSIS AND ASCITES]

diuretics (high dose spironolactone and furosemide). To treat

the symptoms of distention, repeated therapeutic paracentesis
can be performed. A TIPS procedure can relieve ascites, but 1st Presentation OR Fever
because of the risk of hepatic encephalopathy, it’s often avoided ? Every Hospitalized Pt with Ascites
except for the treatment of refractory varices. Treatment or
vaccination against any Hepatitis virus is critical. The patient Cx
SBP TAP Polymicrobial Secondary SBP
must stop drinking alcohol. Finally, avoid NSAIDs which may >250 PMNs >250 PMNs
↓GFR and ↓Diuresis. Ceftriaxone Ceftriaxone
(FQ) +
Spontaneous Bacterial Peritonitis (SBP) MTZ
Cx <250 PMNs
A whole bunch of fluid sitting in the abdomen is a nidus for
infection. So the first step is rule out infection - especially in a
first time case or a return with fever. Do a paracentesis and get
PPX with FQ or Sterile Imaging + Ex-Lap
a cell count and Gram Stain / Culture / Sensitivity. The cutoff
Bactrim DS Treat
is 250 cells; 250 neutrophils to diagnose SBP. No introduction
site may be present (why it’s called spontaneous) and it’s Ascites
usually 70% GNR (E. coli, Klebsiella) and sometimes 30%
GPC (Strep pneumo). Treat with ceftriaxone for double Laboratory Findings
coverage (fluoroquinolone ok if pen allergy) and prophylax AST/ALT Moderately Elevated in smoldering dz
with fluoroquinolone. Since this disease can go from Normal or Low in cirrhosis
asymptomatic to fatal rather quickly, tap all hospitalized patients Alk Phos Moderately Elevated in smoldering dz
Normal or Low in cirrhosis
with ascites. The MELD goes up, tap. The patient has a fever,
Coags ↑INR deficiency of 2,7,9,10
tap. The patient has pain, tap. Platelets (CBC) Thrombocytopenia most sensitive test
Total Protein Low Total Protein – synthesis failure
If you do the tap and it finds 250 polys, make the diagnosis of Albumin Low Albumin –synthesis failure
SBP. BUT, if the tap then comes back polymicrobial, it means U/S Nodules, Vein Patency, Fatty Liver
the diagnosis is actually a secondary bacterial peritonitis strongly indicative of cirrhosis or not
CT Scan Nodules, Masses, and Ascites, even low
(NOT spontaneous) with inoculation from visceral organs. In
amount undetected by U/S or physical
this case it’s necessary to add metronidazole to Ceftriaxone to Biopsy Definitive Diagnosis by histologic
cover anaerobes. Go find the perforation with an Ex-Lap. The confirmation, evidence of underlying
risk of SBP increases with a Total Protein < 1.0 in fluid, so put etiology, specimen for analysis
these patients on prophylaxis.

If they've had SBP they get fluoroquinolone prophylaxis. If

they haven’t had SBP, but total protein is <1.0, they get
fluoroquinolone prophylaxis.

Other complications of Cirrhosis

These are VERY important to the management of a patient with
cirrhosis, but are likely above the level asked of a medical
student. Pay more attention to the etiologies of cirrhosis

Hepatocellular Carcinoma is screened q6month. Obtaining a

RUQ Ultrasound and AFP will likely alert/flag the potential
diagnosis. A triple phase CT scan is sufficient to diagnose
HCC. No biopsy is needed.

Hepatic Encephalopathy is treated with lactulose. A patient

with hepatic encephalopathy has altered mental status, asterixis,
and cirrhosis.

Hepatorenal syndrome is fatal. Treat a patient with renal

failure and cirrhosis by holding the diuretics, giving albumin
and then octreotide.

© OnlineMedEd. http://www.onlinemeded.org