Emma Holt

Replying to scott@vtx-cpd.com 02/11/2021 - 17:07

It’s pretty amazing how much information they can gain from a few slides, which they describe as predominantly harvesting fresh blood and having low to moderate cellularity.

Do you have a preference of how many hepatic FNA’s you take/submit generally for an ultrasound that shows diffuse, non-specific hepatic changes?

I normally aim for a minimum of three slides/FNA that look like they are good samples, but I don’t think I’ve based this on any specific evidence.

Thanks again

Emma

Replying to Liz Bode 23/09/2021 - 20:05

This sounds like a fun medicine case 🙂

Is the murmur new or had it previously been noted?

Looking at the images, I think that the left atrium looks subjectively enlarged, with a thickened mitral valve leaflet and some prolapse of the valve. Could this be a vegetative bacterial endocarditis lesion?

For further investigations I would want a blood culture, urine culture and I would want to examine the lame leg to look for a wound/source that could cause a blood borne infection (if anything was found then I would sample/culture if possible). After this I would be looking at imaging abdo ultrasound and CT looking for any other lesions (primary or secondary).

Replying to Liz Bode 01/09/2021 - 08:20

I saw this in a case last year, and I think it was not long after I’d done the anaemia course with Scott, which had referenced the paper you mentioned Liz (I’m not sure if I would paid too much attention to it otherwise, so I may have missed it in previous cases).

The case I saw was a 13yo FN dashund, with a history of chronic GI signs (variable appetite, vomiting, diarrhoea and weight loss). On ultrasound there were diffuse gastric and small intestinal changes (increased wall thickness and increased mucosal echogenicity), with mild mesenteric lymphadenopathy and some non-specific hepatic changes. Sadly the owner didn’t want to investigate further so no samples were taken and the dog was managed with Pred which improved the clinical signs for a month or so, before further deterioration.

Based on the imaging and progression of clinical signs my main Ddx were chronic enteropathy or neoplasia (lymphoma), but I was more suspicious that this was neoplastic.

I’m not sure how significant the reticulocytosis without anaemia was in this case, but there was definitely underlying pathology present.

Hi Scott,

There’s a lot of information you’ve given us here!

Bloods:
-Neutrophilia:Most likely an inflammatory response (due to infection/inflammation etc)
-HCT: Low end of normal, but still within normal limits.

-Mild increase in ALP: Causes could be secondary (GI, pancreatitis, endocrinopathies, cholestasis (GB disease, bile duct neoplasia, cholelithiasis) etc) or primary hepatic (hepatitis, cholangiohep, neoplasia)
-Marked ALT elevation: Primary hepatic disease (hepatitis, hepatic toxicity, hepatic trauma, neoplasia (adenocarcinoma),) or extra hepatic causes including cholestasis will cause an increase in ALT, but I would expect ALP to be higher than ALT if the primary pathology was due to cholestasis.

So I would be suspicious of primary hepatic disease, the degree of elevation doesn’t give me any information about severity of damage and so I would want to follow the trend of ALT and consider re-testing in 5-7days to see if its trending up or down.

-Marked Tbil elevation: I think pre-hepatic causes are unlikely based on the current HCT levels and the degree of hyperbilirubinaemia and so this elevation is either due to primary hepatic disease or secondary EHBO (could be due to cholelithiasis if obstructing the CBD but a dilated CBD would be noticed on ultrasound) or could be due to pancreatitis.

-Amylase is a non-specific test so I wouldn’t read too much into this.
-In light of the hyperbilirubinaemia the bile acids are not useful.

Ultrasound:
-Hepatomegaly is non-specific, differentials could include hepatitis, steroid hepatopathy, vaculolar hepatopathy,lipidosis, neoplastic infiltration (round cell: lymphoma/MCT or diffuse adenocarcinoma), amyloidosis
-Localised lymphadenopathy could be due to inflammatory changes or neoplastic infiltration.
-Splenomegaly: Sedation, EMH, lymphoid hyperplasia, neoplastic infiltration and unlikely splenic torsion (as you would expect to see other changes, lack of Doppler, hyperechoic mesentery and change in splenic echogenicity).
-Splenic infarct is likely an incidental finding, however underlying disease creating a hypercoagulable state is possible.
-Splenic nodule: Likely incidental finding ddx include EMH,benign lymphoid hyperplasia, haematoma, granuloma, neoplasia.
-Gallbladder sludge is an incidental finding if gravity dependent. Cholelithiasis could be incidental or clinically significant depending on location etc, could be associated with cholangitis, cholangiohep, cholestasis.

Cytology:
I’m rubbish at cytology so will attempt these

First image I think is a vaculolar hepatopathy, lipid type.
Second image: Hepatocytes with bile casts indicative of cholestasis.
Third: Are these hepatocytes and some spindle cells. I don’t think I see any criteria of malignancy so maybe it’s fibrosis…But I could be completely wrong.

Based on all of the above I would be suspicious that there was pancreatitis present (CPLi would be nice to add info), but I would also wonder about a primary hepatic process going on because of the degree of ALT elevation (but I think cytology report might help give more information on this compared to my guess)and your bile aspirate may shed light on if there is any infectious/inflammatory process within the GB too.

Replying to Areti Tsioka 22/07/2021 - 07:39

Hi Areti,

How did you get on with this case? Did the haematological abnormalities improve once the Phenobarb was stopped?

I came across my first case of phenobarb induced hepatoxocity a couple of weeks ago, (progressive elevation of ALT/ALP and dropping ALB, and acute onset PU/PD. Liver biopsies had histological changes which were consistent with phenobarb toxicity), so he is currently coming of his phenobarbitone and monitoring to see how his liver parameters respond.

I hope your patient is responding well.

Emma

Hi Areti,

I haven’t seen thrombocytopaenia associated to phenobarb, but I did have a case of phenobarbital induced neutropenia a few years ago. The dog improved on both haematology and clinical signs after stopping the medication initially, but sadly relapsed (despite not re-starting phenobarb) and was diagnosed with immune-mediated neutropenia on a bone marrow biopsy and steroids were started, but she didn’t do very well in the long run.

I found this article which may be of use, I’ve just read the abstract, but it looks like median resolution of haematological abnormalities was 17 days post phenobarb withdrawal.

Phenobarbitone-induced haematological abnormalities in idiopathic epileptic dogs: prevalence, risk factors, clinical presentation and outcome
E Bersan 1, H A Volk 2, C Ros 3, L De Risio 3

Abstract
The aim of this retrospective study was to assess prevalence, risk factors, clinical presentation and outcome of phenobarbitone induced haematological abnormalities (PBIHA) in dogs. The medical records of two veterinary referral institutions were searched for dogs diagnosed with idiopathic epilepsy and treated with PB as monotherapy or polytherapy between March 2003 and September 2010. Sixteen dogs had PBIHA; the median age at diagnosis was 69.5 months. Phenobarbitone was administered at a median dose of 3 mg/kg twice a day for a median period of 100.5 days and the median serum phenobarbitone level was 19 μg/ml. Two dogs had neutropenia, three had anaemia and thrombocytopenia, two had anaemia and neutropenia; the remaining nine had pancytopenia. All dogs were referred for non-specific clinical signs. Phenobarbitone was discontinued after diagnosis, and the median time to resolution of PBIHA was 17 days. The prevalence and risk factors for PBIHA were evaluated from a questionnaire survey of referring practices to obtain more detailed follow-up on cases diagnosed with idiopathic epilepsy. The prevalence rate of PBIHA was 4.2%, and the condition occurred in dogs treated with standard therapeutic doses often within the first three months after starting treatment. Serial haematological evaluations should be therefore considered from the beginning of phenobarbitone therapy to allow early diagnosis and treatment of PBIHA.

This is really interesting to read. I have always used a glucocorticoid, some times alongside chlorphenamine and often sent home with oral Piriton/Preds if concerned. I’ve never just used Chlorphenamine on it’s own, but maybe I should from now on.