Page 137 - Clinical Small Animal Internal Medicine

13 Hypoglycemia in Patients without Diabetes Mellitus 105

Polycythemia vera: an 87% decrease in blood glucose tested with paired serum bile acids. Therefore, the most
●
VetBooks.ir ● Hypovolemic shock: poor capillary circulation leads to reliable tests for detection of a portosystemic shunt are
levels over four hours has been reported.
paired fasting and postprandial bile acid (100% detec­
increased glucose transit time, promoting increased
glucose extraction by the tissue. Capillary blood sam­ tion), 80% demonstrate low protein C activity (this test
reflects the severity of shunting), >60% show microcyto­
pling from the ear or paw pads is low compared to cen­ sis, low total protein and cholesterol, and a urine specific
tral venous glucose levels which are normal. gravity <1.025, and biurate crystalluria occurs in approx­
imately 33% and 22% of PSVA‐E and PSVA‐I respec­
tively. It is important to remember that usually, biopsy
Congenital Hepatic Disease: Portosystemic alone cannot differentiate PSVA and MVD and that
Vascular Shunts, Microvascular Dysplasia, MVD alone is not associated with signs of illness (e.g.,
and Glycogen Storage Disease
clinical hypoglycemia).
The most common congenital cause of hepatic‐induced
hypoglycemia is portosytemic vascular anomalies Other Diagnostics
(PSVA). PSVA is really an “umbrella term” which includes Imaging studies are needed to differentiate PSVA‐E from
dogs with extrahepatic shunting (PSVA‐E) or intrahe­ PSVA‐I and MVD and are important for surgical and
patic shunting (PSVA‐I). In addition, many small‐breed medical treatments. These include transsplenic micro­
dogs with PSVA have concurrent microvascular dyspla­ bubble studies, transsplenic and colorectal technetium‐
sia (MVD). The prevalence of hypoglycemia in dogs with 99m scintigraphy. However, the gold standard of imaging
PSVA varies from 5% to 10%. The hypoglycemia associ­ studies is contrast multisector CT imaging and three‐
ated with PSVA is presumably caused by chronic hepatic dimensional image reconstruction, which provides
hypoperfusion which leads to insufficient glycogen optimal comprehensive information for diagnosis and
stores and inadequate hepatocellular function to support surgical planning for PSVA.
gluconeogenesis.
Treatment
Signalment It is inarguable that optimal therapy for symptomatic
There is no gender predilection while the average age at PSVA is shunt attenuation. However, it is important to
presentation is 1.5 years for PSVA‐E and 1.0 year for remember that all symptomatic PSVA dogs will benefit
PSVA‐I, although dogs can be as young as 1 month or as from medical management, yet all dogs do not require all
old as 12 years. Significant difference in body weight forms of therapy. For example, a wide spectrum of PSVA
between PSVA‐E and PSVA‐I correlates with the long‐ patients at Cornell University have been managed medi­
recognized propensity for PSVA‐E to occur in small‐ cally with survival outcome and survival duration no dif­
breed dogs and PSVA‐I to occur in large‐breed dogs. ferent than for shunt ligation.
Breed prevalence for PSVA‐E implicates high risk in the
Yorkshire terrier and several other small breeds includ­ Glycogen Storage Diseases
ing shih tzu, Maltese, pug, miniature schnauzer, West
Highland white terriers, bichon frise, miniature and toy Glycogen storage diseases (GSD) are rare congenital
poodles, Havanese, cairn terriers, silky terriers, and mix­ hepatic disorders in which hypoglycemia results from
tures of these breeds. The most prevalent breed with the inability to convert glycogen to glucose because of
PSVA‐I is the Labrador retriever, followed by mixed‐ the absolute or relative deficiency of the enzymes neces­
breed dogs and Siberian huskies. sary for the breakdown of glycogen stores in the liver.
Type III GSD (Cori disease), a deficiency of amylo‐1,6‐
History glucosidase, was documented in puppies with massive
Historical features of PSVA include pediatric hypoglyce­ hepatomegaly caused by glycogen accumulation, failure
mia, small body stature (runt of the litter), episodic inap­ to thrive, and muscle weakness. Type I GSD (von Gierke
petence, vomiting, salivation, polyuria and polydipsia, disease) has been documented in the Maltese breed.
and signs associated with ammonium biurate urolithiasis This uncommon disorder is a deficiency of glucose‐6‐
(hematuria, stranguria, and pollakiuria). Neurobehavioral phosphatase caused by a defect in the glucose‐6‐phos­
signs of hepatic encephalopathy may be unapparent or phatase gene. Affected puppies develop progressive
may include ataxia, obsessive circling, and head pressing. hepatomegaly characterized by diffuse hepatocellular
vacuolization, tremors, weakness, and neurologic signs
Laboratory Findings when hypoglycemic. Biochemical abnormalities include
In a cohort of 610 dogs with PSVA at Cornell University, fasting hypoglycemia, hypercholesterolemia, hypertri­
no dog with a portosystemic shunt was undetected when glyceridemia, and elevated uric acid levels. Confirmatory