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Cirrhosis and its Consequences
Katherine Scott, DVM, DACVIM (SAIM)

VCA Alameda East, 9770 East Alameda Ave, Denver, CO, USA

Etiology/Pathophysiology that results in obstruction of venous return of portal
blood. PH can be classified according to location of the
Cirrhosis increase in blood pressure, including prehepatic, intra­
hepatic, or posthepatic causes. The type of portal hyper­
Development of hepatic fibrosis and subsequent cirrho­ tension caused by cirrhosis is an intrahepatic form of PH,
sis is a common complication of chronic hepatitis (CH). as opposed to prehepatic PH that occurs in disorders of
Cirrhosis is defined histologically by the presence of dif­ the portal vein itself, or posthepatic PH that occurs with
fuse bridging fibrosis and regenerative hepatic nodules. right‐sided heart failure or caudal vena cava disorders.
CH can be caused by a variety of different initial insults With cirrhosis, hepatic sinusoidal endothelial cells have
that include toxins or drugs, breed‐associated metabolic lost normal fenestrae and acquired a collagenous base­
errors, including disorders of copper metabolism, and ment membrane in their place. This change, as well as
infections, although the majority of cases are idiopathic. other remodeling changes in the liver such as regenera­
Regardless of the underlying cause, fibrosis may develop tive nodules and microthrombi, results in distortion of
when CH is severe and/or is present for an extended sinusoids and increases intrahepatic venous resistance,
period of time. with resultant PH.
Fibrosis develops when hepatic myofibroblast‐like cells
become activated secondary to hepatic injury. These cells Ascites
produce factors including transforming growth factor‐ Once PH is present, ascites may also develop as, accord­
beta (TGF‐beta), which upregulate hepatic extracellular ing to Starling’s law, the increased venous resistance and
matrix components such as collagen and glycoaminogly­ increase in portal venous hydrostatic pressure drive fluid
cans. TGF‐beta also upregulates inhibitors of metallopro­ out of the vasculature and into the interstitial space.
teinases, resulting in decreased extracellular matrix Lymphatic drainage of the interstitial space may be able
breakdown. In CH, these changes result in progressive to deal with this extra fluid for some time, but when the
accumulation of extracellular matrix in the liver. Cirrhosis regional lymphatics become overwhelmed and unable to
develops with the diffuse accumulation of fibrous tissue control this increase in interstitial fluid, ascites will
in the liver, resulting in conversion of normal hepatic develop.
architecture into structurally abnormal hepatic nodules Additionally, ascites may develop as a result of hypoal­
(Figure 65.1). With the development of cirrhosis, a variety buminemia secondary to severe liver disease. Albumin is
of adverse consequences develop, and these are predomi­ a plasma protein normally produced by the liver, and
nantly related to the development of portal hypertension significant hepatic dysfunction may result in a clinically
and progression of hepatic dysfunction. important decrease in albumin concentration. Albumin
is the most important blood protein responsible for
maintenance of normal plasma colloid oncotic pressure.
Portal Hypertension
If serum albumin levels decrease to less than approxi­
Portal hypertension (PH) is an increase in blood pres­ mately 1.6 g/dL, plasma colloid oncotic pressure will
sure within the portal vasculature, the vessels responsi­ become too low to maintain intravascular volume and
ble for providing venous drainage to the intestines and fluid will enter the interstitial space. Animals with cir­
spleen. The hypertension can be caused by any disease rhosis will often develop both portal hypertension and

Clinical Small Animal Internal Medicine Volume I, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical