Hi everybody,
Today I scanned a MN 6yo Toy poodle with history of recurrent urates and struvite uroliths (removed surgically in the past), no other clincal signs present. Ultrasound findings: Small liver (as due to peritoneal pericardial hernia) and nephroliths and uroliths present.
It was hard to determine if any shunt was present, but I beleive that PV was small, and cvc look pretty normal to me.
Could it be any relation between PPDH and urates? or should I still think that a shunt is present? and recommend CT or scintigraphy?
Hi everybody,
Today I scanned a MN 6yo Toy poodle with history of recurrent urates and struvite uroliths (removed surgically in the past), no other clincal signs present. Ultrasound findings: Small liver (as due to peritoneal pericardial hernia) and nephroliths and uroliths present.
It was hard to determine if any shunt was present, but I beleive that PV was small, and cvc look pretty normal to me.
Could it be any relation between PPDH and urates? or should I still think that a shunt is present? and recommend CT or scintigraphy?
Bile acids performed today also, results will be available tomorrow. Any suggestions or info will be appreciated. I can post video if needed.
Cheers,
Veronica
Comments
Would wait for the bile acid
Would wait for the bile acid results and if abnormal would recommend CT/scintigraphy and possibly liver biopsy as primary portal vein hypoplasia (microvascular dysplasia) would be a differential diagnosis. However, as the patient is relatively asymptomatic can also consider medical management only. Another possibility would be to rule out UTI as can sometimes result in urate crystals/stones. Unless there is is liver failure probably not associated with PPDH.
Would wait for the bile acid
Would wait for the bile acid results and if abnormal would recommend CT/scintigraphy and possibly liver biopsy as primary portal vein hypoplasia (microvascular dysplasia) would be a differential diagnosis. However, as the patient is relatively asymptomatic can also consider medical management only. Another possibility would be to rule out UTI as can sometimes result in urate crystals/stones. Unless there is is liver failure probably not associated with PPDH.
Hi Veronica!
I´ve never
Hi Veronica!
I´ve never heard about an association between PPDH and urates. I would also consider a shunt or liver failure the most likely differentials. Please keep me updated!
Thx
Peter
Hi Veronica!
I´ve never
Hi Veronica!
I´ve never heard about an association between PPDH and urates. I would also consider a shunt or liver failure the most likely differentials. Please keep me updated!
Thx
Peter
The association would be
The association would be coincidental I would think unless you go by the adage that one good congenital defect begets another…i.e a shunt or pvh being present. When you go back in to scan this dog again if the BA are high, check out our shunt study first and do a path search on sonopath for “shunt.”
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This should help you prepare. The normals dvd has the normal portal hilus pv/cvc/ao ratio and the path CDs have shunts in them as well. These should all help prepare you “down under”… the portal hilus…so to speak:)
The association would be
The association would be coincidental I would think unless you go by the adage that one good congenital defect begets another…i.e a shunt or pvh being present. When you go back in to scan this dog again if the BA are high, check out our shunt study first and do a path search on sonopath for “shunt.”
Click here for Resources Articles
Click here for Search
This should help you prepare. The normals dvd has the normal portal hilus pv/cvc/ao ratio and the path CDs have shunts in them as well. These should all help prepare you “down under”… the portal hilus…so to speak:)
Thank you so much for all
Thank you so much for all this great info!
Got BAST back
Pre-prandial bile acids 53.9 (0-15)
Post-prandial bile acids 8.8 (0-30)
The pathologist has suggested that these results would suggest premature contraction of the gall bladder, and that the results are not typical of a porto-caval shunt.
The issue now is should surgical removal of the stones is indicated or try medical treatment first (I think also depends of owner) but any comments on if suggest just diet or going in to take them out?
I got the CDs yesterday! I will start checking them all!Thanks Eric and Thanks Remo and Peter.
Thank you so much for all
Thank you so much for all this great info!
Got BAST back
Pre-prandial bile acids 53.9 (0-15)
Post-prandial bile acids 8.8 (0-30)
The pathologist has suggested that these results would suggest premature contraction of the gall bladder, and that the results are not typical of a porto-caval shunt.
The issue now is should surgical removal of the stones is indicated or try medical treatment first (I think also depends of owner) but any comments on if suggest just diet or going in to take them out?
I got the CDs yesterday! I will start checking them all!Thanks Eric and Thanks Remo and Peter.
Veronica, here is an exceprt
Veronica, here is an exceprt from the book we are desparately trying to finish. This is from the shunt section of the liver chapter and explains why bile acids can be elevated despite the lack of shunting:
This passage is an excerpt from the upcoming textbook Clinical Approach to Sonographic Pathology, Small Animals & Exotics by Lindquist, Yanik, & Frank offered by http://www.SonoPath.com in 2012.
Non-shunt Pathology That Can Elevate Bile Acids11–13
Nonhepatic Causes
• Inflammatory bowel disease/intestinal dysbiosis
• Spontaneous GB contraction
• Hypertriglyceridemia
• Ursodeoxycholic acid treatment
• Severe disease or resection of the ileum (site of bile acid reabsorption)
• Cholecystectomy
• Prolonged anorexia
• Hyperadrenocorticism
• Pancreatitis
• Other nonhepatic pathology
• Transient elevation in Irish wolfhound puppies, other breeds?
Hepatic Causes
• Diffuse hepatocellular disease
• Cholestatic disease
• Primary portal vein hypoplasia/Microvascular dysplasia
Notes
Fasting plasma ammonium (AMM) and bile acid (BA) profiles were found to be nearly of equal sensitivity in detecting portovenous anomalies (AMM 100 percent versus BA 92.2 percent) in one large study.14 However, AMM determination was found to be much more sensitive in detecting the presence of either congenital or acquired shunting compared with BA testing (AMM 89.3 percent versus BA 17.9 percent) for dogs with confirmed liver disease.14 Most dogs with portosystemic shunts have postprandial BA concentrations of more than 100 µmol/L, but values do not correlate with the severity of disease.6 Dogs with portosystemic shunts have lower clotting factor activity than healthy dogs, and this can cause complications at surgery.15
References
11. Kirk’s Current Veterinary Therapy, Vol XII. Philadelphia: Saunders, 1995:739–740.
12. Willard M, Tvedten H: Small Animal Clinical Diagnosis by Laboratory Methods, 4th ed. St. Louis: Elsevier, 2004241–242.
13. Allen L, Stobie D, Mauldin N, et al: Clinicopathologic features of dogs with hepatic microvascular dysplasia with and without portosystemic shunts: 42 cases (1991–1996). J Am Vet Med Assoc 214, 1999.
14. Gerrizen-Bruning MJ, van den Ingh TS, Rothuizen J: Diagnostic value of fasting plasma ammonia and bile acid concentrations in the identification of portosystemic shunting in dogs. J Vet Intern Med 20:13–19, 2006.
15. Kummeling A, Teske E, Rothuizen J, et al: Coagulation profiles in dogs with congenital portosystemic shunts before and after surgical attenuation. J Vet Intern Med 20:1319–1326, 2006.
Veronica, here is an exceprt
Veronica, here is an exceprt from the book we are desparately trying to finish. This is from the shunt section of the liver chapter and explains why bile acids can be elevated despite the lack of shunting:
This passage is an excerpt from the upcoming textbook Clinical Approach to Sonographic Pathology, Small Animals & Exotics by Lindquist, Yanik, & Frank offered by http://www.SonoPath.com in 2012.
Non-shunt Pathology That Can Elevate Bile Acids11–13
Nonhepatic Causes
• Inflammatory bowel disease/intestinal dysbiosis
• Spontaneous GB contraction
• Hypertriglyceridemia
• Ursodeoxycholic acid treatment
• Severe disease or resection of the ileum (site of bile acid reabsorption)
• Cholecystectomy
• Prolonged anorexia
• Hyperadrenocorticism
• Pancreatitis
• Other nonhepatic pathology
• Transient elevation in Irish wolfhound puppies, other breeds?
Hepatic Causes
• Diffuse hepatocellular disease
• Cholestatic disease
• Primary portal vein hypoplasia/Microvascular dysplasia
Notes
Fasting plasma ammonium (AMM) and bile acid (BA) profiles were found to be nearly of equal sensitivity in detecting portovenous anomalies (AMM 100 percent versus BA 92.2 percent) in one large study.14 However, AMM determination was found to be much more sensitive in detecting the presence of either congenital or acquired shunting compared with BA testing (AMM 89.3 percent versus BA 17.9 percent) for dogs with confirmed liver disease.14 Most dogs with portosystemic shunts have postprandial BA concentrations of more than 100 µmol/L, but values do not correlate with the severity of disease.6 Dogs with portosystemic shunts have lower clotting factor activity than healthy dogs, and this can cause complications at surgery.15
References
11. Kirk’s Current Veterinary Therapy, Vol XII. Philadelphia: Saunders, 1995:739–740.
12. Willard M, Tvedten H: Small Animal Clinical Diagnosis by Laboratory Methods, 4th ed. St. Louis: Elsevier, 2004241–242.
13. Allen L, Stobie D, Mauldin N, et al: Clinicopathologic features of dogs with hepatic microvascular dysplasia with and without portosystemic shunts: 42 cases (1991–1996). J Am Vet Med Assoc 214, 1999.
14. Gerrizen-Bruning MJ, van den Ingh TS, Rothuizen J: Diagnostic value of fasting plasma ammonia and bile acid concentrations in the identification of portosystemic shunting in dogs. J Vet Intern Med 20:13–19, 2006.
15. Kummeling A, Teske E, Rothuizen J, et al: Coagulation profiles in dogs with congenital portosystemic shunts before and after surgical attenuation. J Vet Intern Med 20:1319–1326, 2006.
Great list of Ddx. Thanks
Great list of Ddx. Thanks Eric! Cant wait to get the book!!!good luck
Going back to my previous question, we are considering not doing further investigation in the liver as no clinical sings and BA were not elevated postpandrial (does that makes sense?) or should I still insist on it.
Should the stones in kidney and bladder be removed surgically to evaluate the mineral component again? or keep only diet.
Thanks
Great list of Ddx. Thanks
Great list of Ddx. Thanks Eric! Cant wait to get the book!!!good luck
Going back to my previous question, we are considering not doing further investigation in the liver as no clinical sings and BA were not elevated postpandrial (does that makes sense?) or should I still insist on it.
Should the stones in kidney and bladder be removed surgically to evaluate the mineral component again? or keep only diet.
Thanks
depends if the liver appears
depends if the liver appears small because part of it is in the chest or is it truly small. If the pv cvc ao ratio is largely 1:1 then try medical tx for the urates because the liver will be pv hypoplasia at worse case. Cover uti and appropriate diet (I am at a loss on diet unless we talk fiorentina steak and a glass of taurasi red wine:). But I am sure a nutritional consult from your usual food company can help here. Then rescan in 6 weeks or so to see if you have made any progress.
depends if the liver appears
depends if the liver appears small because part of it is in the chest or is it truly small. If the pv cvc ao ratio is largely 1:1 then try medical tx for the urates because the liver will be pv hypoplasia at worse case. Cover uti and appropriate diet (I am at a loss on diet unless we talk fiorentina steak and a glass of taurasi red wine:). But I am sure a nutritional consult from your usual food company can help here. Then rescan in 6 weeks or so to see if you have made any progress.