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656 Microvascular Dysplasia, Hepatic

disorders such as chronic enteropathies, has been used as contrast to highlight absence Drug Interactions
ammonium biurate crystalluria, or seizures. • Plasma protein C activity > 70% (normal) Caution is advised when choosing drugs that
or presence of PSVA.
VetBooks.ir of HMD to clinical signs (if any) when these is supportive of diagnosis HMD in patients Recommended Monitoring
It is difficult to determine the contribution
undergo hepatic metabolism.
with elevated serum TSBA concentrations.
disorders occur concurrently.
HISTORY, CHIEF COMPLAINT Advanced or Confirmatory Testing Depends on clinical presentation, but repeti-
tion of CBC, serum biochemistry profile, and
Severity of signs associated with HMD is • Abdominal computerized tomography (CT) urinalsyis q 6-12 months is often appropriate
reflected as a spectrum of none to severe; scan with angiographic contrast to rule out for minimally affected pets.
most affected animals seem healthy. History PSVA
can include signs found with congenital or • Definitive diagnosis by histopathologic PROGNOSIS & OUTCOME
acquired PSVA (e.g., behavioral abnormalities, findings consistent with portal venous
lower urinary signs related to urate stones hypoplasia/hypoperfusion • Prognosis is good to excellent for asymp-
[p. 814]). ○ Obtain 3-5 wedge or laparoscopic biopsies tomatic patients. Normal life expectancy is
from different lobes. For needle biopsies, common.
PHYSICAL EXAM FINDINGS use 14-gauge needle with full throws of • Prognosis is worse for the rare patients with
Unremarkable sampling notch/depth from different lobes. significant hepatic dysfunction.
○ Findings include arteriolization of central
Etiology and Pathophysiology veins, arteriolar duplication, endothelial PEARLS & CONSIDERATIONS
HMD involves shunting of portal blood to biliary hyperplasia, attenuation of lobular
the hepatic venules and histologic changes size, reduced sinusoidal flow, lipogranu- Comments
consistent with hypoperfusion. lomas, and diminished distance between • HMD is often diagnosed in older patients
terminal branches of portal and hepatic during assessment for other diseases (e.g.,
DIAGNOSIS veins. Zone 3 degenerative hepatocelluar protein losing enteropathies, hypoalbumin-
changes can be found in more severe cases. emia, chronic pancreatitis).
Diagnostic Overview ○ There can be marked differences between • CT angiogram is preferred over ultrasound
Diagnostics are initiated because of suspicion liver lobes with caudate lobe often least to rule out PSVA.
of PSVA or to follow-up on laboratory abnor- affected. These histologic changes are seen • HMD is a diagnosis of exclusion of PSVA,
malities discovered incidentally. Elevation of with any cause of hypoperfusion and are then confirmation with biopsy. Biopsy
total serum bile acid (TSBA) concentrations not specific to HMD. alone cannot achieve a diagnosis as results
without supportive findings of PSVA (acquired • Contrast portography shows diminished are indistinguishable from histopathologic
or congenital) or other causes of PVH or liver contrast filling of affected lobes without changes seen in PSVA.
dysfunction suggest HMD. Abdominal imaging escape to vena cava or azygous vein. • Animals with increased TSBA values
is useful to rule out PSVA. • Transcolonic or transsplenic scintigraphy < 100 mmol/L and normal serum biochemi-
results are normal for HMD (shunt fraction cal profile are more likely to have HMD
Differential Diagnosis < 15%). Largely replaced by contrast CT scan than PSVA.
• PSVA (congenital or aquired) • TSBA concentrations > 100 mmol/L or
• Causes of hepatic encephalopathy (p. 440) TREATMENT decreased serum albumin or blood urea
nitrogen (BUN) concentrations should
Initial Database Treatment Overview prompt continued diagnostic efforts to rule
• CBC: uncommonly, microcytosis (low Most often requires no treatment, but if severe, in or out PSVA or primary hepatic disease.
mean corpuscular volume [MCV]) without the patients can be managed with medical
anemia management similar to that for PSVA Prevention
• Serum biochemical profile: often normal Do not breed affected dogs.
but can have mixed mild/modest patterns Acute General Treatment
of elevations of alanine aminotransferase If present, address hepatic encephalopathy Technician Tips
(ALT) and alkaline phosphatase (ALP), or (p. 440). Ensure patients are fasted for 12 hours before
rarely mild hypoalbuminemia bile acid panel testing or abdominal imaging
• Urinalysis: possibly hyposthenuria, rarely Chronic Treatment intended to look for PSVA.
ammonium biurate crystalluria If severe HMD is suspected, consider use of
• TSBA assay (with most emphasis on S-adenosylmethionine 15-30 mg/kg PO q 24h Client Education
postprandial value): often range of 25-100 (or per product label), use of vitamin E 10 U/ Discuss patient-specific prognosis and breed-
mmol/L. These concentrations can be higher kg PO q 24h, and avoiding high-protein diets, related concerns.
and overlap with concentrations found in with goal of providing an optimal microenviron-
PSVA. Concentrations can vary day to day, ment and reduction of oxidative stresses for SUGGESTED READING
and if results are discordant with clinical hepatocytes over the long term. Christiansen JS, et al: Hepatic microvascular dys-
suspicion, repeat in 2 weeks. plasia in dogs: a retrospective study of 24 cases
• Coagulation profile: normal (assessed before Nutrition/Diet (1987–1995) J Am Anim Hosp Assoc 36:385-389,
liver biopsy) Asymptomatic cases require no adjustments 2000.
• Abdominal radiographs: usually normal, of diet. If symptomatic, consider a moder- AUTHOR: Mark E. Hitt, DVM, MS, DACVIM
sometimes microhepatica ate, restricted-protein diet or as for hepatic EDITOR: Keith P. Richter, DVM, MSEL, DACVIM
• Abdominal sonography: ± microhepatica, encephalopathy.
lack of diminished intrahepatic portal
vascular pattern (look at all lobes) versus Behavior/Exercise
PSVA; absence of PSVA and the PV/A ratio Symptomatic cases of HMD may experience
≥ 0.8; normal renal volume/size. Percutane- periodic atpyical behavior (aggression, passivity,
ous transsplenic injection of agitated saline hunger, confusion, inappropriate eliminations).

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