I recently received this question from a solid colleague/client that I read cases for and support in the clinical sonography technical and business curve and he had an interesting question:

SM: I scanned a slightly jaundice dog yesterday. PT was double normal so I did not poke. PTT was WNL. Liver: looked totally norm but GB had double wall. I wanted GB aspirate. Liver values norm and Tbilisi norm. Weird case.

Are the clotting times always going to b high when jaundice? Should I just not consider poking them and also not bother with coags?

I recently received this question from a solid colleague/client that I read cases for and support in the clinical sonography technical and business curve and he had an interesting question:

SM: I scanned a slightly jaundice dog yesterday. PT was double normal so I did not poke. PTT was WNL. Liver: looked totally norm but GB had double wall. I wanted GB aspirate. Liver values norm and Tbilisi norm. Weird case.

Are the clotting times always going to b high when jaundice? Should I just not consider poking them and also not bother with coags?

EL: I only do cholecystocentesis when suspended swirling bile is present in a cholangitis case but never if it looks like a mucocele fyi. That just needs to come out
Re to coag or not: I always do because I want to know where they stand on how long the liver dysfucntion is an issue and surmise how long bile has not been entering the intestine for ADEK (fat soluble) vitamin absorption. This along with the degree of cbd dilation or lobar biliary tree dilation I can imagine how long obstruction has been present if it’s a posthepatic case like a cbd stone or tumor or bile plug. Not always are the PT and APTT too elevated to sample in these jaundice cases. Coag parameters and jaundice are not like bile acids and jaundice. Bile acid profile is useless if jaundiced but coag is useful both clinically and for sampling…depends how fast they got jaundiced and if acute liver failure; lepto for example or stone obstruction with sudden onset or progressive/chronic onset like cirrhosis or cbd tumor or reacutizzation of a chronic mucocele. Chronic depletion of coag factors in liver failure leaves only a little reserve. Second issue is if biliary obstruction is present and bile is not hitting the intestine for K absorption. Factor 7 is depleted first (shortest half life) which is K dependent and would explain why PT is elevated and APTT was not because this patient was at the early coagulopathy stage factor 7 depleted. Once liver function drops and bile isnt sent to the small intestine for vit k to be absorbed vit k is still active for 24-48 hours variably with body stores that are still present and residual absorption may still be occurring. You may still have a solid window to fna at least. I go by this template when sampling by a seasoned sonographer with historically sold sampling techniques.

PT (8-12 normal) aptt (< 87 sec) : PT up to 16, aptt < 100 still bx or fna of solid tissue but not lipidosis or mct suspected livers in cats (fna here 25 gauge). PT > 16 < 30 sec and aptt < 120 FNA ok and go 25 gauge if lipidosis or mct suspected. PT> 30 APTT > 120 sec treat vit k and underlying disease and reassess q 48 hours to reach described levels to sample.

This is just what I do how does the rest of the community approach this?