- 10 year old mn lab mix with 2 week history of decreased appetite and intermittent vomiting
- PE shows jaundice and abominal pain
- Chem prof shows ALT=714 U/L, ALKP=351 U/L, GGT=26 U/L, TBil=3.6mg/dl, Na=163 mmol/L, Cl=123mmol/L
- CBC is wnl although HCT=53% (N: 37-61%).
- Abdominal ultrasound shows diffuse, coarse, micronodular, echogenic hepatic parenchyma with small pockets of anechoic fluid seen between the liver lobes and the liver and the diaphragm, and a very small gallbladder with a thickened, echogenic wall.
- 10 year old mn lab mix with 2 week history of decreased appetite and intermittent vomiting
- PE shows jaundice and abominal pain
- Chem prof shows ALT=714 U/L, ALKP=351 U/L, GGT=26 U/L, TBil=3.6mg/dl, Na=163 mmol/L, Cl=123mmol/L
- CBC is wnl although HCT=53% (N: 37-61%).
- Abdominal ultrasound shows diffuse, coarse, micronodular, echogenic hepatic parenchyma with small pockets of anechoic fluid seen between the liver lobes and the liver and the diaphragm, and a very small gallbladder with a thickened, echogenic wall.
- It was difficult to identify the gallbladder intially, but after the dog was sedated and placed on his back, it was more obvious (sorry no pics saved). No CBD obstructions seen. No masses at the level of the pancreas or duodenum.
- Ultrasound guided fna of the effusion yielded a yellow tinged transparent fluid-cytology and fluid analysis are pending.
- Ultrasound guided fna of the hepatic parencyma was also done. I had to go up to a 20 gauge needle in order to get the liver cells to exfoliate (22 gauge corkscrew technique did not work)…..firm tissue?
- My primary differentials are cholangiohepatitis/cholecystitis, Lepto, neoplasia
- This is not a surgical case, yet, right? The gallbladder appears small and abnormal but with the diffuse liver pathology, my recommendation is to treat aggressively for cholangihepatitis while awaiting cytology results. No coag panel so I did not biopsy.
Comments
Chronmic hepatitis pattern
Chronmic hepatitis pattern mostly fibrous which is why the fna even corkscrew didn’t work. Needs core bx 14-16 gauge or so and copper staining if applicable. Ascites likely from portal hypertension see if you can get pv velocities < 18 cm/sec would confim but just on presentation bili and architecture likely port hyper here. Chronic Lepto can do this. Once port hyper starts though tough to keep non clinical. Watch BUN Glucose Albumin and cholesterol dropping as those bring bad px. Have to hope for lepto here to potentially be somewhat treatable.
Emerging LSA also possible sometimes sneaks up on core bx in these CAH looking cases… suspect transition from LP hepatitis to LSA just like occurs in the Gi with IBD and LSA. Have to see what the infiltrates are doing to the portal triads whether lined up alongside or destroying them as in LSA.
See the basic search for similar portal hypertension:
cases: http://sonopath.com/members/case-studies/search?text=portal+hypertension&species=All
Chronmic hepatitis pattern
Chronmic hepatitis pattern mostly fibrous which is why the fna even corkscrew didn’t work. Needs core bx 14-16 gauge or so and copper staining if applicable. Ascites likely from portal hypertension see if you can get pv velocities < 18 cm/sec would confim but just on presentation bili and architecture likely port hyper here. Chronic Lepto can do this. Once port hyper starts though tough to keep non clinical. Watch BUN Glucose Albumin and cholesterol dropping as those bring bad px. Have to hope for lepto here to potentially be somewhat treatable.
Emerging LSA also possible sometimes sneaks up on core bx in these CAH looking cases… suspect transition from LP hepatitis to LSA just like occurs in the Gi with IBD and LSA. Have to see what the infiltrates are doing to the portal triads whether lined up alongside or destroying them as in LSA.
See the basic search for similar portal hypertension:
cases: http://sonopath.com/members/case-studies/search?text=portal+hypertension&species=All
Thanks Eric. In descriptive
Thanks Eric. In descriptive terms, how would you define a chronic hepatitis pattern? Micronodular? Echogenic?
Thanks Eric. In descriptive
Thanks Eric. In descriptive terms, how would you define a chronic hepatitis pattern? Micronodular? Echogenic?
Increased portal markings,
Increased portal markings, coarse architecture progressing to micronodular (<3 mm) (up to here describes your case) or macronodular (>3mm) changes that can then progress to cirrhosis which gets big first from swelling and nodular production then shrivels into a raisin. Portal hypertension can start at any phase past fibrosis which takes about 28 days according to Twedt (visible scarring). So my rule of thumb is if there are increased portal markings then the process has been going on at least 28 days…
Increased portal markings,
Increased portal markings, coarse architecture progressing to micronodular (<3 mm) (up to here describes your case) or macronodular (>3mm) changes that can then progress to cirrhosis which gets big first from swelling and nodular production then shrivels into a raisin. Portal hypertension can start at any phase past fibrosis which takes about 28 days according to Twedt (visible scarring). So my rule of thumb is if there are increased portal markings then the process has been going on at least 28 days…
Here are some CAH cases some
Here are some CAH cases some of which progressed to cirrhosis as well form the basic search:
http://sonopath.com/members/case-studies/search?text=chronic+hepatitis&species=All
Coarse architecture needs core Bx. FNA will not give solid samples typically…need to cut the scar.
Here are some CAH cases some
Here are some CAH cases some of which progressed to cirrhosis as well form the basic search:
http://sonopath.com/members/case-studies/search?text=chronic+hepatitis&species=All
Coarse architecture needs core Bx. FNA will not give solid samples typically…need to cut the scar.
Will need core biopsy samples
Will need core biopsy samples to stain for copper. Apparently copper will accumulate as a primary cause of the liver problem or secondary to chronic inflammatory changes.
I recently received this information from one of the internal medicine specialists from IDEXX.
“(copper quantification)- level helps determine whether copper presence is related to primary copper hepatopathy (very high levels–definite copper chelation) or secondary to chronic hepatitis (moderate levels—initial treatment likely for inflammatory disease and not necessarily copper chelation therapy)”
I never knew this.
Will need core biopsy samples
Will need core biopsy samples to stain for copper. Apparently copper will accumulate as a primary cause of the liver problem or secondary to chronic inflammatory changes.
I recently received this information from one of the internal medicine specialists from IDEXX.
“(copper quantification)- level helps determine whether copper presence is related to primary copper hepatopathy (very high levels–definite copper chelation) or secondary to chronic hepatitis (moderate levels—initial treatment likely for inflammatory disease and not necessarily copper chelation therapy)”
I never knew this.
From my Twedt notes:
Copper
From my Twedt notes:
Copper breeds: Terriers, dobies, labs dalmations. Need bx of 1.6 mm diameter to dx….
i.e. 14-16g Bx by 1.8 cm length of sample…. which is the largest US-guided sample but they push lapscope samples for this but I haven’t had any issue with this size liver bx and quantification when sending to CSU.
Copper quantification is ideal but if you have a good pathologist relationship they will give you a gut feeling as to primary or secondary copper but if going by th ebook need to quantify, if primary then chelate and rebx in 3 months to see if improving.
From my Twedt notes:
Copper
From my Twedt notes:
Copper breeds: Terriers, dobies, labs dalmations. Need bx of 1.6 mm diameter to dx….
i.e. 14-16g Bx by 1.8 cm length of sample…. which is the largest US-guided sample but they push lapscope samples for this but I haven’t had any issue with this size liver bx and quantification when sending to CSU.
Copper quantification is ideal but if you have a good pathologist relationship they will give you a gut feeling as to primary or secondary copper but if going by th ebook need to quantify, if primary then chelate and rebx in 3 months to see if improving.
Ok, thanks. Do you just
Ok, thanks. Do you just submit the sample in a red top tube? And please remind me, who does staining for copper on a slide sample?
Ok, thanks. Do you just
Ok, thanks. Do you just submit the sample in a red top tube? And please remind me, who does staining for copper on a slide sample?
Double check with the lab but
Double check with the lab but I always use formalin unless considering a sample for PCR for LSA then just saline or if culturing.
Double check with the lab but
Double check with the lab but I always use formalin unless considering a sample for PCR for LSA then just saline or if culturing.
Copper levels can be
Copper levels can be determined from the formalin samples. I know because I just checked. Let me know if you hear something different.
Copper levels can be
Copper levels can be determined from the formalin samples. I know because I just checked. Let me know if you hear something different.