I have an 8 month old Chi-Poo (Chihuahua and Poodle mix). At about 3 months he started to lose a bit of hair around the folds of his ears, his elbows and hind legs. His chest hair is a bit thin as well. Because of this wierd behaviour, the vet ran some tests - starting with a skin scrapping to check for parasites. He also took blood from our puppy to run a complete blood test, including a thyroid profile test on him. Something suspicious came back with his thyroid profile test - the results were lower than normal. He said to wait a bit and would like to run the tests again. My puppy continued to gain weight, was happy and playful. Last week we ran the tests again, and this time the results were that his thyroid profile came back as being lower than normal, but higher than the previous test. However, something new showed up - they found alkaline phosphatase in his blood. The vet told me that it could be one of two thing - this is emitted sometimes from growing bones and since he's a growing puppy, that's what it could be; or it could be his liver. If his liver is causing this, it is my understanding that this could be the result of a liver shunt. I'm wondering if anyone has any info about liver shunts, what's involved with procedures and possibly some of the symptoms. Kinda worried about the whole thing.
usually with a liver shunt you will see a none thriving puppy. one who has some neurological problems like walking drink ( ataxic ), seizures etc. its because the liver is the organ to filter toxins from the blood stream. with a shunt the body is not directing the blood thru the liver to detoxify it and the blood then is actually poisoning the dog. if your puppy is happy and thriving and gaining weight and all his symptoms are just loss of hair i would not suspect a liver shunt. alk phos levels are usually higher in pups because of their growing so most higher alk phos levels are dismissed in pups unless clinical signs are present to suggest something else.
Pathophysiology Clinical signs associated with portosystemic shunts commonly involve the nervous system, gastrointestinal tract, and urinary tract. General clinical signs include poor growth rate, weight loss, fever, and anesthetic or tranquilizer intolerance. Neurologic dysfunction is seen in most animals with PSS and includes lethargy and depression, ataxia, seizures, behavioral changes, and blindness. Head pressing, circling, and development of a head tilt have also been reported. Gastrointestinal clinical abnormalities include anorexia, vomiting, and diarrhea. Some dogs have no apparent signs or present with signs of cystitis or urinary tract obstruction. Many cats have hypersalivation and some have unusual copper colored irises.
Abnormalities found on hemograms of animals with PSS include leukocytosis, anemia, and microcytosis. Most animals with congenital PSS have normal coagulation profiles. Biochemical abnormalities associated with PSS include decreases in blood urea nitrogen, protein, albumin, glucose, and cholesterol; and increases in serum alanine aminotransferase and alkaline phosphatase. Increase in alkaline phosphatase is most likely from bone growth, since cholestasis is not usually a problem in animals with shunts. Cats with PSS usually have normal albumin concentrations. Urinalysis abnormalities include low urine specific gravity and ammonium biurate crystalluria. At magnifications of 400x or more, ammonium biurate crystals often have a spikey, thornapple or starfish shape and golden color. Because of increased urinary excretion of ammonia and uric acid, dogs and cats may also develop uroliths. Urate uroliths are often radiolucent and therefore may not be detectable on survey radiographs unless they are combined with struvite. Abnormal urine sediment suggestive of cystitis (hematuria, pyuria, and proteinuria) has been described in animals with PSS and may be associated with crystalluria or urolithiasis.
Hepatic histologic changes in animals with PSS include generalized congestion of central veins and sinusoids, lobular collapse, bile duct proliferation, hypoplasia of intrahepatic portal tributaries, proliferation of small vessels and lymphatics, diffuse fatty infiltration, hepatocellular atrophy, and cytoplasmic vacuolization. These pathology changes can also be seen in dogs with hepatic microvascular dysplasia that do not have single congneital shunts. Pathologic changes may be present in the central nervous system, especially in encephalopathic animals.
Hepatic Encephalopathy Hepatic encephalopathy has been recognized in animals with PSS, end-stage liver disease, and congenital urea cycle enzyme deficiencies. Clinical signs include depression, dementia, stupor, and coma. Muscle tremors, motor abnormalities, and focal and generalized seizures have also been reported. The etiology of hepatic encephalopathy is probably dependent on several factors, including circulating toxins, alterations in amino acid concentrations, and increased cerebral sensitivity to drugs and toxins. Toxins that have been implicated in hepatic encephalopathy include ammonia, mercaptans, short chain fatty acids, indoles, aromatic amino acids, and biogenic amines.
Precipitating factors of hepatic encephalopathy include diuretics, protein overload, hypokalemia, alkalosis, and transfusion of stored red cells, hypoxia, hypovolemia, gastrointestinal hemorrhage, infection, and constipation. Increased cerebral sensitivity to sedative, analgesic, and anesthetic agents may induce coma in animals with PSS, even when normal dosages are used. Protein overload and gastrointestinal hemorrhage provide substrates for bacterial production of ammonia, and constipation can increase retention and absorption of ammonia and other encephalopathic substances. Blood which has been stored for 24 hours contains 170 ug of ammonia/dL, and ammonia concentrations will continue to increase with prolonged storage.
Diagnosis of Portosystemic Shunts: Liver Function Tests Although history, physical examination, and routine laboratory tests may be suggestive of portosystemic shunting, liver function tests such as ammonia tolerance test (ATT) and measurement of fasting and postprandial serum bile acid concentrations are more reliable for diagnosing liver dysfunction.
Serum bile acids are synthesized in the liver from cholesterol. After conjugation with taurine, they are secreted into bile and stored in the gallbladder. During food intake, neurohumoral and hormonal factors such as cholecystokinin stimulate gallbladder contraction and excretion of bile acids into the small intestines where they form micelles that enhance lipid emulsification and absorption. At least 95% of intestinal bile acids are actively reabsorbed in the ileum and are transported by portal blood back to the liver (the "enterohepatic cycle"). Normally postprandial bile acid concentrations are minimally increased because of rapid first-pass hepatic extraction. Serum bile acid concentrations are elevated with cholestasis, jaundice, and portosystemic shunting. They are not significantly affected by dehydration, hypovolemia, or passive hepatic congestion, although they can be falsely increased by lipemia and hemolysis. No special techniques are required for handling and storage of serum for bile acid samples. Prolonged fasting may result in normal bile acid concentrations in animals with PSS; therefore, fasting and 2-hour postprandial samples should be analyzed. If the animal is sensitive to high protein meals, a low protein diet mixed with a few milliliters of corn oil can be used to stimulate gastrointestinal motility and cholecystokinin activity.
Normal hepatic function is essential for conversion of ammonia to urea. Increased resting ammonia concentration indicates decreased hepatic mass or shunting of portal blood. Concentrations of blood ammonia are not well correlated with severity of hepatic encephalopathy, and ammonia levels may be normal in 7% to 21% of dogs with PSS, especially after prolonged fasting. The ammonia tolerance test was developed to provide a more accurate diagnosis of liver dysfunction. A heparinized baseline sample is taken after a 12 hour fast, and ammonium chloride is administered orally by stomach tube or in gelatin capsules (0.1 g/kg, maximum 3 grams), or as an enema (2 ml/ kg of a 5% solution inserted 20 to 35 cm into the colon). A second blood sample is obtained 30 minutes after ammonium chloride administration. Blood samples are transported on ice for immediate plasma separation and analysis. Normal values vary with the method of analysis; results in animals with PSS should be compared to a control sample from a healthy animal to ensure accuracy. Improper sample cooling, incomplete plasma separation, or delays in sample analysis will result in falsely elevated values because of erythrocyte and plasma generation of ammonia. Results are invalid after oral ammonium chloride administration if vomiting occurs, and after rectal administration if diarrhea or shallow rectal instillation occurs.
Diagnostic Imaging Diagnosis of microhepatica from survey abdominal radiographs is usually based on an upright, more cranial stomach position. Renomegaly has been reported in dogs with PSS; its etiology has not been determined. Urate calculi normally are radiolucent but occasionally will be seen in the renal pelvis, ureter, or bladder on survey films.
To accurately diagnose a portosystemic shunt and determine its location, imaging techniques such as angiography, ultrasonography, and scintigraphy should be utilized. Intraoperative mesenteric portography provides excellent visualization of the portal system but usually requires a celiotomy. The dog is anesthetized and a small laparotomy is performed. Water-soluble contrast medium (maximum total dose, 2 ml/kg) is injected into a catheterized jejunal or splenic vein, and one or more radiographs are taken during completion of the injection. Alternatively the spleen can be injected directly and percutaneously in a sedated dog. However, there is a risk of splenic laceration with this technique, and the shunt will not be visible on radiographs if the contrast leaks out of the spleen or the spleen overlies the shunt. Because no dilution of contrast material occurs, intraoperative mesenteric portography provides an excellent image of the shunt if it is not too large. The technique is relatively simple and requires no special equipment. Differentiation of intrahepatic and extrahepatic PSS may be made on most portograms. If the most caudal loop of the shunt or the point where the shunt diverges from the portal vein is cranial to the T-13 vertebra, then the shunt location is probably intrahepatic. The shunt location will vary by one half to three fourths of a vertebral length depending on the phase of respiration.
Diagnosis of PSS may be made with hepatic ultrasonography. Ultrasonographic evidence of PSS includes microhepatica, decreased numbers of hepatic and portal veins, and detection of the anomalous vessel. Extrahepatic PSS are more difficult to diagnose with ultrasonography; their location is often obscured by gas-filled intestines. Overlying ribs and lungs may also interfere with a thorough ultrasonographic evaluation. Colorflow doppler is useful for detecting changes in the direction and rate of blood flow in the portal vein.
Nuclear scintigraphy is a noninvasive means of evaluating dogs for portal venous shunting. In dogs 99mtechnetium pertechnetate is extracted from the circulation primarily by the liver. In animals with shunts, the pertechnetate rapidly circulates to the heart and lungs. Normal dogs have a shunt fraction of less than 15% on scintigraphy; most dogs with shunts have fractions greater than 60%.
Magnetic resonance angiography (MRA) and CT scans have also been used to diagnose portosystemic shunts.
The ultimate diagnostic tool is laparotomy. Once experience is obtained, most extrahepatic shunts and approximately half of intrahepatic shunts can be identified on exploratory.
Differential Diagnoses Single congenital portosystemic shunts must be differentiated from multiple acquired shunts secondary to portal hypertension, and from hepatic microvascular dysplasia. Hepatic microvascular dysplasia (HMD) signifies a disorganization of the liverís microscopic architecture which is similar to that of dogs with single congenital shunts. HMD has been reported in small breed dogs such as the Yorkshire terrier, Cairn terrier, Maltese, cocker spaniel, and poodle. Dogs with HMD display biochemical, hematologic, and clinical changes consistent with portosystemic shunting but lack a macroscopic portosystemic shunt. Definitive diagnosis is by ruling out a macroscopic shunt through exploratory laparotomy, nuclear scan, or portography. Signs of HMD are managed by low protein diet; lactulose is added if necessary.
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I have a Pug that has a shunt. It usually is diagnosed by the vet taking the Bile Acid levels. Depending on the shunt, some may be managed by diet and meds, some have no options but surgery. AND a VERY costly one. we are lucky Holly is doing Excellent on the meds and diet food, I just have to make sure she dosnt get my other 2 girls food. Holly did start shedding way more then usual and it just cleared up on its own-but not to the point where she was losing patches, and the vet told me not to worry. Maybe your poor baby has other things in addition to a shunt, or maybe something else all together. The Bile Acids tests are usually very high in Liver shunts. There is a wonderful liver shunt group support group on Yahoo. I would ask them-they have answers to all the questions you may have. Ill dig out my papers on the info I have to see if I can add anything else lator! I hope its not that though-Good luck to you and your poor baby!
Livershuntchat@Yahoo.com-I think I wrote that write.
***Edited By: 763melani on 4/30/2005 1:52:36 PM*** Reason: Forgot the address for livershunt group!
Thanks Scout and Melani - your information is very helpful. Pepe (my puppy) doesn't seem to have those symptoms so I'm hoping it's just his growing bones! We're gonna do the tests again in August to check on the status. I'll just keep an eye on him for the meantime.
***Edited By: kcarpino on 4/30/2005 9:18:50 PM*** Reason: Add information