Adelaide's Medical Thread

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Zaphy

Post   » Wed Jan 06, 2021 12:15 am


Nope, no gallstones noted on the report- here it is. I do wonder if we’d had her on a longer course of antibiotics if she would’ve lived a while longer yet- but given everything else going on, I suppose it’s hard to say whether the hepatitis was causing the bile backup or resulting from it. Not to mention that after she was pooping normally again, there were no symptoms of all the mess inside her to go off of.

DIAGNOSES:
1. Liver: Severe, multifocal, chronic, intra- and extrahepatic choledochal cysts, with ductal plate dysplasia
and fibroplasia and multifocal distention and stricture of the common bile duct, with severe necrotizing
cholangiohepatitis, and midzonal vacuolar hepatopathy.
2. Adrenal gland: Presumptive adrenocortical adenoma.
3. Stomach: Marked gastric dilation with mild gastric pylorus hypertrophy (gross diagnosis).


REMARKS:
The cystic changes noted on gross examination of the gallbladder coupled with the continuous biliary plates with fibroplasia are suggestive of a ductal plate malformation with secondary cholestatic disease as cause of death of the guinea pig. Adult onset intra and interlobular bile duct dysplasia with mild portal fibroplasia and bile duct reduplication are consistent with Caroli’s-like disease. This type of ductal plate malformation is congenital, and involves inappropriate or defective remodeling of the biliary plate epithelium by oval cells, resulting in continuous biliary epithelium and cystic changes to biliary structures. The changes in structure of the intra- and extra-hepatic bile ducts likely influenced the flow of bile, causing decreased outflow and subsequent cholangiohepatitis. The midzonal vacuolar change is attributable to a steroid hepatopathy secondary to the adrenal tumor. The gastric dilation is presumed secondary to the thickening of the gastric pylorus but a functional ileus cannot be ruled out. Gastric dilation may be related to the ductal plate malformation, as there are reports of Caroli’s disease in human patients with cystic dilation of the gastric pylorus and proximal duodenum.

The adrenal tumor is likely of cortical cell origin, but a poorly differentiated pheochromocytoma cannot be definitively ruled out. If further investigation is desired, please contact the diagnostic laboratory to request immunohistochemistry for synaptophysin, chromogranin A, and Melan A on slide 3.


GROSS NECROPSY DESCRIPTION:
Submitted for necropsy is a 5-year-old female guinea pig in good postmortem condition with minimal autolysis. The body is in good nutritional condition with adequate visceral adipose tissue. There is mild crusting on the palmar aspect of the right front limb.

Upon opening the abdomen, the gallbladder is markedly distended up to 20 times its normal size but remains patent. The gallbladder contains pale green, minimally viscous, opaque bile. The common bile duct has a focal area of marked swelling approximately halfway between the gallbladder and the duodenum that measures approximately 1 cm. The common bile duct enters the duodenum there is a circumferential band of fibrous tissue which creates a stricture at the distal end of the duct. The liver is friable and mottled pale tan to red to brown.

The stomach is markedly distended up to 10-15 times its normal size and contains partially digested, fibrous food material. The gastric pylorus is moderately thickened and the pylorus is subjectively small in diameter and the pyloric outflow is stenotic. The small intestine contains moderate amounts of pale to dark green, opaque liquid ingesta. The colon contains low amounts of soft but formed fecal pellets.

The right adrenal gland is approximately two times the size of the left and is expanded by a multilobulated mass. On cut section the mass is mottled dark brown to pale tan and firm.

All organs are closely examined and no additional lesions are noted.

HISTOPATHOLOGY:
Slides 1-2, 7.
Liver: The hepatic capsule is undulating with variably sized hepatic lobules (lobular atrophy) and there is multifocal inflammation and necrosis affecting approximately 25-30% of the examined sections. Frequently portal regions have continuous biliary plates and numerous small-caliber biliary profiles which are supported by low amounts of fibrous stroma and flanked by oval cells with low numbers of lymphocytes and plasma cells. Occasionally, within the lumen of bile ducts are green to brown bile plugs. Periportal and occasionally midzonal hepatocytes occasionally have round, eosinophilic, cytoplasmic globular material (inclusions). Midzonal hepatocytes often have small, round, fine cytoplasmic vacuoles which do not displace the nucleus. There is both randomly distributed single cell necrosis, characterized by shrunken cellular profiles, hypereosinophilic cytoplasm, and nuclear pyknosis. Occasional clusters of centrilobular hepatocytes are necrotic with low numbers of infiltrating heterophils and patchy areas of hemorrhage.

The wall of the gallbladder is markedly expanded by large amounts of fibrous stroma which supports numerous small-caliber, tortuous biliary profiles and moderate numbers of heterophils. These small bile ductules embedded in the fibrous stroma often contain low amounts of mucinous material and rarely clusters of degenerate heterophils.

Lung: No histologic lesions.

Slides 3–4.
Adrenal mass: Expanding and effacing the adrenal gland with nodular expansion that penetrates the capsule, is an unencapsulated, poorly demarcated neoplasm. Neoplastic cells are densely arranged in cords and streams supported by a fine fibrovascular stroma. Most cells are polygonal with distinct cell borders and occasional fine cytoplasmic vacuoles, but approximately 25% of neoplastic cells have a spindloid morphology. Nuclei are small, round, and centralized with a single central nucleolus and finely stippled chromatin. There are two mitotic figures in 10 400 X fields. There is mild anisocytosis and anisokaryosis. Rarely there are low amounts of yellow–pale green extracellular globular pigment. No vascular invasion is apparent. Scattered throughout the neoplastic cells are moderate to marked numbers of heterophils (extramedullary hematopoiesis)

Slide 5.
Kidney: Glomerular basement membranes are occasionally slightly thickened 1-2 times their normal width and there are rare senescent glomeruli. Occasionally, tubules within the medulla are moderately to markedly dilated between 2-10 times are normal size and rarely contain eosinophilic globular material (proteinosis). No renal cysts are apparent.

Slides 6–7.
Colon: The colonic mucosa is segmentally elevated by significant lipid infiltration which causes nodular expansion of the submucosa. The lamina propria is infiltrated by moderate amounts of mucinous edema with lymphocytes and plasma cells. The lumen contains abundant bacterial organisms and fragments of plant material.

Small intestine: There are mild numbers of lymphocytes and plasma cells within the mucosa.

Slide 8.
Brain: No histologic lesions.

Slide 9.
Eye: No histologic lesions.

User avatar
Lynx
Celebrate!!!

Post   » Wed Jan 06, 2021 9:14 pm


I don't ever recall reading such a detailed necropsy before. Unfortunately, a lot of it went over my head but it was interesting to read none the less. From your description above, it does seem your vet provided a layman's interpretation of the detailed findings. It does appear there were no stones in the gallbladder.

I don't know how often you see your vet or how thorough he/she is but would be curious if he/she felt the results expanded their understanding of what to look for and how to treat an ill guinea pig with the signs you were seeing.

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Zaphy

Post   » Thu Jan 07, 2021 2:24 am


Yeah, that’s CSU’s veterinary teaching hospital for you- I’m always so impressed at how thoroughly they document everything. They’re this detailed with the reports for regular appointments too. A lot of the written report went over my head too, I had to Google so many terms- was very glad they laid things out pretty plainly for me in a phone call accompanying the email :)

I’m not sure exactly how useful this information was as opposed to just very interesting- it sounded like this kind of malformation is extremely rare and hadn’t necessarily been seen before. I have had a couple questions come to mind as I’ve mulled things over- it’s not like guinea pigs have to deal with much fat in their diet so I wonder if they really use their livers much anyway, so maybe it didn’t make much difference to her. But I wonder if I’d fed her on one of those bad pellet mixes with the nut and seed mix-ins, if that would have stressed her liver enough for it to be an issue earlier in her life. Obviously I don’t know anything about the ins and outs of guinea pig nutrition, heh. I also wonder if my force feeding her actually benefited her at all in her case at the end, given how misshapen everything was. Things I might email the vet to ask :)

User avatar
Lynx
Celebrate!!!

Post   » Thu Jan 07, 2021 3:16 pm


I am guessing you don't have to eat fat to have a fatty liver. It would depend on the total number of calories taken in and expended. Starchy foods, calorie filled foods, may have carbs that would be stored in the body as fat while at the same time not having a high fat content.

bpatters
And got the T-shirt

Post   » Thu Jan 07, 2021 4:00 pm


Alcohol can cause extreme fatty liver. In fact, fatty liver disease is divided into alcoholic and nonalcoholic varieties.

The causes of the non-alcoholic variant in human aren't known. Contributing factors include obesity, diabetes, insulin resistance, high blood sugar levels, and high triglyceride levels.

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