Understanding Microhepatica in Dogs: Causes, Diagnosis, and Management
Microhepatica, or a small liver, in dogs is often associated with hepatic microvascular dysplasia (MVD), also known as portal vein hypoplasia. This condition reflects a congenital or inherited abnormality impacting the liver’s microscopic vascular system, leading to reduced blood flow through the liver tissue. The liver’s limited access to nutrients and oxygen impairs its ability to filter toxins, synthesize essential proteins, and maintain metabolic functions.
What Is Hepatic Microvascular Dysplasia?
MVD is characterized by underdeveloped or absent small portal veins within the liver. This anomaly results in reduced portal perfusion, ultimately causing the liver to be undersized—clinically presenting as microhepatica. It is a common hepatic disorder in small-breed dogs and is usually nonprogressive.
Breeds Predisposed to MVD
- Yorkshire Terriers
- Cairn Terriers
- Maltese
- Miniature Poodles
- Shih Tzus
- Lhasa Apsos
- West Highland White Terriers
- American and English Cocker Spaniels
- Dachshunds
- Bichon Frises
Although rare in larger breeds and cats, isolated feline cases have been documented.
Clinical Signs of MVD and Microhepatica
Many dogs with MVD and resultant microhepatica show no outward symptoms. However, when clinical signs do present, they may include:
- Stunted growth or delayed development
- Poor weight gain or muscle mass
- Lethargy or unusual behavior
- Gastrointestinal issues (vomiting, diarrhea, anorexia, pica)
- Moistening or blood in urination from stones or infections
- Neurological signs like head pressing or seizures in severe cases
These symptoms often mirror and overlap with those seen in dogs suffering from macroscopic portosystemic shunts (PSS), though MVD signs tend to be milder.
Diagnosing MVD and Microhepatica
Accurate diagnosis involves a multi-tiered approach:
- Blood tests may reveal mild anemia, low albumin, or liver enzyme abnormalities.
- Urinalysis can show dilute urine or ammonium biurate crystals.
- Serum bile acid testing is a vital screening tool. Postprandial levels are usually mildly elevated.
- Protein C activity helps distinguish MVD from larger shunts—normal in MVD but reduced in PSS.
Imaging techniques such as ultrasound, CT, MRI, or nuclear scintigraphy rule out macroscopic shunts. Ultimately, confirming MVD requires a liver biopsy showing characteristic microvascular changes. Samples from multiple lobes yield the best diagnostic accuracy.
Treatment and Management
Most dogs with MVD do not require aggressive treatment. Management depends on symptom severity:
- Asymptomatic dogs with only mild test abnormalities may need no therapy.
- For dogs showing signs of hepatic encephalopathy or other clinical presentations, treatment is medical, not surgical.
- Dietary protein restriction: Use digestible proteins from sources like dairy or soy.
- Specialized liver-formulated prescription diets help ensure nutritional adequacy.
- Lactulose minimizes ammonia absorption in the gut; metronidazole may adjust intestinal flora.
- Supplements (SAMe, milk thistle, vitamin E, ursodeoxycholic acid) are optional and of uncertain benefit.
Monitoring liver enzymes, protein levels, and ammonia is advised over routine bile acid retesting.
Prognosis and Outlook
MVD is typically nonprogressive. Many dogs live long, healthy lives without ever developing symptoms. Owners should monitor for changes in behavior or gastrointestinal upset, especially in predisposed breeds. Veterinary checkups focusing on liver health parameters can help catch any emerging complications early.
Genetics and Breeding Concerns
Because MVD is likely of polygenic inheritance, breeding affected dogs is discouraged. Even dogs with normal bile acid tests can produce affected pups if they carry risk alleles. Genetic elimination of MVD is not feasible without sophisticated testing and responsible breeding practices.
Conclusion
Microhepatica in dogs is most often caused by hepatic microvascular dysplasia, especially in certain small breeds. While some dogs remain asymptomatic, others may show signs of liver dysfunction, poor growth, or GI upset. Diagnosis relies on a combination of breed history, laboratory tests, imaging, and liver biopsy. Most affected animals enjoy good quality of life with appropriate monitoring and dietary management. Avoiding breeding of known or suspected carriers is vital to reduce the incidence of this congenital condition.
