Page 913 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

888 CHAPTER 5

VetBooks.ir Aetiology/pathophysiology disease can be found. Hepatic encephalopathy might
be mistaken for conditions including neurotoxicity,
Hepatic insufficiency may result from various dis-
ease processes depending on the magnitude and
nal compression and cerebral and/or spinal trauma.
duration of the hepatic insult. This insult may take infectious myeloencephalitides, developmental spi-
the form of hepatocellular necrosis, toxicity, inflam- Horses discovered with severe central neurological
mation and/or oxidative damage, and fibroplasia is a signs in association with evidence of a traumatic epi-
common hepatic response to these various insults. sode may lead to confusion regarding whether the
Initially hepatic fibrosis may be fine and delicate and trauma caused the neurological signs, or the horse
remain in a dynamic equilibrium between fibroplasia had an accident due to acute development of neuro-
and fibrolysis, a balance controlled by hepatic stel- logical signs from causes such as HE.
late cells. Periportal fibrosis is by far the commonest Enteric hyperammonaemia is also an impor-
pattern of fibroplasia; further insult may eventually tant differential diagnosis of HE, where hyperam-
irreversibly disrupt hepatic architecture, with inter- monaemia arises in the presence of normal hepatic
connection of fibrotic portal areas with porto-portal function due to overwhelming enteric generation
bridging, which signals a low likelihood of resolution of ammonia. Such cases often show accompanying
and correlates well with hepatic insufficiency. signs or history of intestinal disease such as colic or
diarrhoea, and may result from increased luminal
Clinical presentation protein substrate (e.g. intraluminal colonic bleeding)
Hepatic insufficiency may occur alongside gradu- and/or dysbacteriosis with overgrowth of ammonia-
ally progressive appearance of clinical signs such genic bacterial species.
as weight loss and lethargy, although acute decom-
pensation may also be seen in cases where there Diagnosis
has clearly been slow and gradual development of Following recognition of suspicious clinical signs,
hepatic insufficiency. This appears to be especially hepatic insufficiency is generally confirmed by
the case with signs of hepatic encephalopathy, where clinicopathological indicators of hepatic injury and
evidence of severe cerebral dysfunction (depression, abnormal hepatic function. Increased concentrations
circling, head-pressing, blindness) or bilateral laryn- of serum globulins and bile acids are probably the
geal paralysis may develop in an acute fashion. most consistent abnormalities seen, although other
supportive findings may less commonly include
Differential diagnosis hyperammonaemia, hyperbilirubinaemia (direct
Signs of hepatic insufficiency may be confused and/or indirect), hypoalbuminaemia, hypouraemia,
with other causes of insidious weight loss and leth- prolonged clotting times and hypoglycaemia.
argy, such as protein losing enteropathies, chronic Dynamic tests for hepatic function using clearance
inflammatory and neoplastic diseases and chronic of exogenous agents such as bromosulphthalene,
kidney disease. Jaundice may also be seen in cases indocyanine green or radiopharmaceuticals may be
of haemolytic anaemia as well as simple inappetence used to support and quantify the presence of hepatic
in some horses. Hepatic insufficiency causing sec- insufficiency but are rarely employed.
ondary photosensitisation may be confused with
identical skin lesions resulting from ingestion or Management
exposure to primary photosensitising agents such Perhaps the most crucial element when dealing
as plants (e.g. St. John’s Wort [Hypericum sp.], buck- with cases of hepatic disease and/or insufficiency is
wheat [Fagopyrum sp.]) or pharmaceutical and chemi- to address any specific underlying cause of hepatic
cal agents (e.g. phenothiazines, sulphonamides, insult. Unfortunately, this might often remain elu-
chlorhexidine). Other diseases associated with der- sive despite thorough investigation. Further impor-
matitis restricted to unpigmented skin, such as leu- tant considerations include dietary management and
cocytoclastic (photo-aggravated) vasculitis, should specific treatment of HE and hepatic fibrosis as dis-
also be considered where no evidence of hepatic cussed below.