Clinical Pathology CaseBY: ABIGAIL SCHMIDT

Signalment: 2 yr 8 mos M Cairn Terrier

History: 6 wks PU/PD;

Drinking 150-300 mls/kg/day

PU/PD Differentials

• Diabetes Mellitus• Hyperadrenocorticism (Cushing’s)• Hypoadrenocorticism (Addison’s)• Renal Disease (CRF)• Liver Disease• Neoplasia

– lymphoma, anac sac adenocarcinoma, multiple myeloma, pheochromocytoma

• Hypercalcemia• Iatrogenic

– Administration of steroids, diuretics, etc.

• Psychogenic Polydipsia• The list continues…..

Diagnostics I would pursue

• Urinalysis

• Haematology

• Full Biochemistry

Diagnostics Actually Run…

• Urinalysis (cystocentesis)– Mild haematuria, otherwise normal– USG 1.010: Isosthenuric

• Haematology– Mild leukocytosis and mild neutrophilia likely a stress

response/mild inflammation

• Biochemistry…

• ACTH Stimulation Test: normal

Normals

Biochemistry

Sodium

Potassium

Na:K ratio

Chloride

Creatinine

Cholesterol

Triglyceride

Total Bilirubin

ALKP

GGT

Albumin:Globulin Ratio

AbnormalsBiochemistry All results mildly…

Calcium

Phosphate

Urea

AST

ALT

Total Protein

Albumin

Globulin

Interpretation of Abnormals• Hypocalcemia possibly decreased due to low albumin? • Hyperphosphatemia• Hypouremia increased loss (PU)/decreased production**BUN, albumin, glucose, and cholesterol = often first parameters

decreased with liver function

• Elevated Liver enzymes: AST, ALT– AST: can be elevated with muscle inflammation or necrosis (e.g. IM muscle

injection, exercise), red blood cell hemolysis, or with liver disease.– ALT: MOST liver specific enzyme; indicated hepatocellular damage

• Hypoproteinemia– Hypoalbuminemia– Hypoglobulinemia

Test Liver for dysfunction R/O

Protein loss or malfunction in protein production

PU/PD Ddx Rule Outs

• Diabetes Mellitus• Hyperadrenocorticism (Cushing’s)• Hypoadrenocorticism (Addison’s)• Renal Disease (CRF) much less likely• Liver Disease ***• Neoplasia

– lymphoma, anac sac adenocarcinoma, multiple myeloma, pheochromocytoma

• Hypercalcemia• Iatrogenic

– Administration of steroids, diuretics, etc.

• Psychogenic Polydipsia

Further Tests to Run?• BILE ACIDS STIMULATION TEST

– Values mild to moderately elevated pre

– Values severely elevated post

– Values even further elevated 2 hrs post

• WORKING DIAGNOSIS…based on signalment, history, urinalysis, bloods thus far: Liver Disease due to Portosystemic Shunt– Most likely extrahepatic due to breed (small dog and predisposition of

Cairn Terriers)

– Shunts allow portal blood to reach the systemic circulation w/o first passing through the liver. Normally blood exiting the intestines, spleen, and pancreas enters the portal vein, which then takes blood to the liver. The liver metabolizes and detoxifies this blood. If a shunt is present the liver is deprived of factors that allow it to fully develop (hepatic atrophy).

– Hepatic atrophy commonly results in hepatic insufficiency.

Liver Shunt Workup & Treatment• Ultrasound microhepatica• Nuclear scintigraphy non-invasive colonic

administration of a radioisotope, and measurement of blood flow– Computer measures amount of radioactive blood in the

heart and the liver and compares the two

• Portography radiograph highlighting portal system after injection of radio-opaque contrast material

• CT Angiography (3D image; assess hepatic vasculature)

• Extrahepatic Shunt: Surgery to correct; amyloid constrictor bands

Medical Management of Shunt Cases

• Congenital vs. Acquired

• Extrahepatic vs. Intrahepatic

• IV fluids

• Enema to remove intestinal toxins before they can be absorbed

• DIET: low protein

• Lactulose alters pH in LI to decrease ammonia and other toxin absorption; also makes environment unfavorable to bacteria

• ABs: to reduce number of toxin-producing bacteria in intestines; also helpful if patient also has a UTI