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Hepatic Encephalopathy
  • Description
  • Signalment
  • Clinical Features
  • Neurolocalization
  • Genetics
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Hepatic encephalopathy occurs as a result of elevated concentrations of neurotoxins (GABA, aromatic amino acids, mercaptans, ammonia, skatoles) that reach the brain through the general circulation, causing brain dysfunction through primary neurotoxicity and secondary pathophysiologic effects such as edema and ischemia. In dogs, hepatic encephalopathy is most commonly associated with congenital portosystemic shunts or acquired shunts secondary to chronic liver disease; however, acute fulminant hepatic disease can also cause hyperammonemia and encephalopathy.
Age of Onset: Any age can be affected
Dogs with congenital hepatopathies (such as congenital portosystemic shunts) will often present at less than 2 years of age.
Hepatic encephalopathy can also be acquired secondary to acute or chronic liver disease and failure.
Sex Predisposition: Any sex of animal can be affected
Clinical Course: Clinical signs progress over time.
In a subset of dogs, clinical signs may be episodic with increased severity during the post-prandial period
Clinical Signs:
Behavioral/Mental Awareness
*Mentation changes
Seizures
*Lethargy/Depression
Compulsive pacing/circling
Head pressing

Movement
Ataxia
Slight hypermetria
Slight hypertonia

Proprioception
Proprioceptive deficits

Cranial Nerves
*Episodic central blindness
Nystagmus

Special Functions (e.g. respiration; urination)
Gastrointestinal (anorexia, diarrhea, melena, vomiting, ptyalism)
Urinary (Hematuria, *polyuria/polydypsia, stranguria)​
Intracranial- metabolic
Unknown
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References
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