Difference between revisions of "Hepatic Microvascular Dysplasia"

Revision as of 20:53, 10 July 2010

Description

Microvascular dysplasia (MD) is a congenital defect of the hepatic vasculature that results in abnormal communication between the portal and systemic venous circulation. Unlike portosystemic shunting, microvascular dysplasia is not grossly evident and occurs due to vascular connections between microscopic blood vessels. However, MD may occur in conjunction with a gross shunting vessel and it does cause clinical signs which are very similar to those observed in animals with portosystemic shunts.

Signalment

MD occurs as a congenital disease in several small breeds of dog, particularly the Yorksire terrier and Cairn terrier. The average age at presentation is 3 years (older than most animals presenting with congenital portosystemic shunts) and the condition is more common in female dogs than males.

Diagnosis

Clinical Signs

Signs are very similar to those observed in animals with congenital portosystemic shunts, as listed here. Briefly, these include:

Stunted growth compared to littermates.
Intermittent gastro-intestinal signs, including vomiting and diarrhoea.
Urinary tract signs resulting from urate urolithiasis.
Prolonged recovery from sedation or anaesthesia due to reduced hepatic metabolism of drugs.

Laboratory Tests

Diagnosis relies on ruling out the presence of a gross shunting vessel by diagnostic imaging. A liver biopsy is then performed and histological analysis of the sample will show a pattern identical to that of a congenital portosystemic shunt:

Arteriolarisation of central veins
Smooth muscle proliferation (segmental) within the walls of central veins
Random distribution of small calibre vessels
Endothelial hyperplasia within portal triads
Dilation of periacinar vascular spaces
Decreased diameter of intrahepatic veins

Blood samples

Higher MCV, serum postprandial bile acid concentrations, serum albumin and cholesterol concentrations when PSS and HMD together, compared to HMD alone.

Treatment

Medical management should be implemented, as for portosystemic shunts.

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-*Small intrahepatic portal vessels and portal endothelial hyperplasia which allows abnormal communication between portal and systemic circulation.
+{{unfinished}}
-*Can develop as a separate entity or in conjunction with a portosystemic shunt.
-*Can cause c/s similar to those of PSS.
-*[[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|Vomiting]], [[Diarrhoea|diarrhoea]], [[Urinary System - Anatomy & Physiology|urinary tract]] changes associated with ammonium biurate urolithiasis, stunted growth, prolonged recovery from anesthesia.
-*Average age of presentation =3yrs.
-*Mainly small dogs, esp. Yorkies
-*Females>males
-===Histology===
-**Arteriolarization of central veins
+==Description==
-**smooth muscle proliferation (segmental) within the walls of central veins
+Microvascular dysplasia (MD) is a congenital defect of the hepatic vasculature that results in abnormal communication between the portal and systemic venous circulation.  Unlike [[Portosystemic Shunt|portosystemic shunting]], microvascular dysplasia is not grossly evident and occurs due to vascular connections between microscopic blood vessels.  However, MD may occur in conjunction with a gross shunting vessel and it does cause clinical signs which are very similar to those observed in animals with portosystemic shunts.
-**random distribution of small calibre vessels
-**endothelial hyperplasia within portal triads
+==Signalment==
-**dilation of periacinar vascular spaces.
+MD occurs as a congenital disease in several small breeds of dog, particularly the Yorksire terrier and Cairn terrier.  The average age at presentation is 3 years (older than most animals presenting with congenital portosystemic shunts) and the condition is more common in female dogs than males.
-**May also see decreased diameter of intrahepatic veins.
-*Can’t be accurately distinguished from PSS alone.
+==Diagnosis==
-*Seen in older dogs than PSS
+===Clinical Signs===
+Signs are very similar to those observed in animals with congenital portosystemic shunts, as listed [[Portosystemic Shunt|here]].  Briefly, these include:
+*'''Stunted growth''' compared to littermates.
+*Intermittent '''gastro-intestinal signs''', including vomiting and diarrhoea.
+*'''Urinary tract signs''' resulting from urate urolithiasis.
+*'''Prolonged recovery from sedation or anaesthesia''' due to reduced hepatic metabolism of drugs.
+===Laboratory Tests===
+Diagnosis relies on ruling out the presence of a gross shunting vessel by diagnostic imaging.  A liver biopsy is then performed and histological analysis of the sample will show a pattern identical to that of a congenital portosystemic shunt:
+*'''Arteriolarisation of central veins'''
+*'''Smooth muscle proliferation''' (segmental) within the walls of central veins
+*'''Random distribution of small calibre vessels'''
+*'''Endothelial hyperplasia''' within portal triads
+*'''Dilation of periacinar vascular spaces'''
+*'''Decreased diameter of intrahepatic veins'''
+Blood samples
 *Higher MCV, serum postprandial bile acid concentrations, serum albumin and cholesterol concentrations when PSS and HMD together, compared to HMD alone.
+==Treatment==
+'''Medical management''' should be implemented, as for [[Portosystemic Shunt|portosystemic shunts]].
 [[Category:Liver_-_Developmental_Pathology]]
 [[Category:To_Do_-_James]]