Hepatobiliary diseases IV

Question 1

Neoplasia of the Liver and Biliary tree: Prevalence

Answer 1

May be primary or metastatic in dogs and cats.
Primary tumors uncommon
* 0.6-1.5% of all tumors in dogs
* 1-3% of all tumors in cats. Primary tumors are more common than metastatic tumors in the cat.

Metastatic tumors
* 3 times more frequent than primary liver tumors in dogs. More commonly originate from the spleen, gastrointestinal (GI) tract and pancreas.

Benign tumors are more common in cats, but in dogs are usually malignant.

Peak incidence of primary hepatobiliary cancer at 10-12 years in both species.

Cats develop malignant hepatic tumors at a younger age than benign tumors.

Question 2

Neoplasia of the Liver and Biliary tree: Tisse of origin and morphology

Answer 2

Four general tissue types from which primary hepatic tumors may be derived:
* Hepatocellular
* Bile duct
* Neuroendocrine
* Mesenchymal

Morphological types of primary hepatic tumor are
* Massive (Large solitary mass confined to one liver lobe)
* Nodular (Multifocal and may involve multiple lobes)
* Diffuse (Includes multifocal or coalescing nodules affecting all lobes or diffuse effacement of the hepatic parenchyma)

Liver can also be involved in other neoplastic processes, including lymphoma, systemic mastocytosis and malignant histiocytosis.

Question 3

An Important Differential Diagnosis for Any Liver Mass

Answer 3

Nodular Hyperplasia

Relatively common and is identified in 15-60% of older dogs.

Also occurs in cats, in around 1% of histopathology submissions.

Diffuse with a “classic appearance” of liver cancer but is NOT cancer.

Histology must be performed before condemning a dog or cat.

Question 4

Describe Hepatocellular carcinoma

Answer 4

One of the most common primary hepatic tumor in dogs Accounting for >50%.

Second most common tumor in cats.

Average age of affected dogs is 12 years (80% of dogs are >10 years of age).

Etiological factors in the development of HCC are largely unknown but Link between progressive vacuolar hepatopathy and HCC in Scottish Terriers at least.

Morphology of the cancer:
53-83% massive, 16-25% nodular and up to 19% diffuse

Question 5

Describe Hepatocellular Adenomas (Hepatomas)

Answer 5

Another most commonly reported primary hepatic tumors in dogs. In dogs rarely cause clinical signs unless they rupture and hemorrhage.

In cats, hepatocellular adenoma occurs more frequently than Hep.CellularCarcinoma.

Solitary adenomas can become quite large and compress to other organs.

Question 6

Describe Bile Duct Carcinoma (Cholangiocarcinoma)

Answer 6

Most common malignant hepatic tumor in cats; second most common in dogs.

Female Labrador Retrievers predilection is suggested but no apparent breed or sex predispositions for cats.

Morphology:
37-46% are massive, up to 54% are nodular and 17-54% diffuse in cats

Can be intrahepatic, extrahepatic or within the gallbladder. Intrahepatic locations more common in dogs.

Equal distribution of intrahepatic to extrahepatic tumors in cats.

Behave aggressively, and metastasis is very common.
67-80% of cats with diffuse intraperitoneal metastasis and carcinomatosis. Metastatic rates of 90% in dogs.

yikes

Question 7

Describe Bile Duct Adenoma (Cystadenomas)

Answer 7

Single or multiple

Usually do not cause clinical signs until they become large and compress adjacent organs.

More than 50% of all feline primary hepatobiliary tumors.

No biliary adenomas were noted among 106 dogs with primary hepatic tumors.

Question 8

Describe Neuroendocrine tumors, Also called hepatic carcinoids.

Answer 8

Arise from neuroectodermal cells.
Infrequently reported in dogs and cats.

Occur at a younger age than other hepatobiliary tumors. Mean of 7 years of age.

Biologically aggressive and due to their diffuse nature not usually surgically resectable.

Nodular in 33% and diffuse in the remaining cases.
Usually intrahepatic.

Question 9

Hepatic Tumors of mesenchymal origin (sarcomas) are rare in cats and dogs. Describe them.

Answer 9

Hemangiosarcoma, leiomyosarcoma and fibrosarcoma most commonly identified.

Hemangiosarcoma in cats and leiomyosarcoma in dogs most commonly.

BUT Liver is a very common site for metastatic hemangiosarcomas in dogs.

Massive and nodular morphology reported in 33% and 67% of cases.

Males predisposed to mesenchymal tumors with no known breed associations. Mesenchymal tumors are biologically aggressive.

Pulmonary and splenic metastasis reported in 86-100% of dogs.

Myelolipomas are benign hepatobiliary tumors of cats which can be single or multifocal.

Histologically composed of adipose tissue intermixed with normal hematopoietic elements. Benign in behavior.

Question 10

Neoplasia of the Liver and Biliary tree: Clinical signs

Answer 10

Usually vague and nonspecific: Lethargy, inappetence, weight loss, vomiting, polyuria/polydipsia, pyrexia and ascites.

Uncommonly, neurological signs may develop due to paraneoplastic hypoglycemia, hepatic encephalopathy or central nervous system metastasis.

Icterus is more common in dogs with bile duct carcinomas and diffuse neuroendocrine tumors.

In cats, only 33% have icterus with biliary neoplasia.
Approximately 50% of cats and 25% of dogs show no clinical signs.

Question 11

Neoplasia of the Liver and Biliary tree Diagnosis: CBC and Coagulation

Answer 11

May reveal a mild nonregenerative anemia, Anemia of chronic disease red blood cell (RBC) sequestration, RBC destruction or iron deficiency.

Neutrophilic leukocytosis may be seen with neoplasia-associated inflammation or necrosis.

Prolonged coagulation times are a potential consequence of any liver disease.

Rarely clinically significant unless liver failure has occurred as a result of diffuse disease.

Question 12

Neoplasia of the Liver and Biliary tree Diagnosis: Biochemistry

Answer 12

Liver enzyme activities commonly increased in dogs and cats. Indicative of hepatocellular or biliary epithelial damage or biliary stasis. Not specific for hepatic neoplasia and does not reflect degree of hepatic neoplastic involvement.

Primary hepatic tumors are More likely to cause hypoproteinemia, hypoglycemia and increases in ALP and ALT activities.
* Less likely to cause hyperbilirubinemia

Hypoglycemia due to Paraneoplastic effect due to a large tumor mass consuming glucose, or reflect production of an insulin-like substance.

Hypoalbuminemia More common in dogs than cats.
May reflect a negative acute phase response, catabolism and poor nutritional intake, or hepatic insufficiency.

Hypercalcemia, Hyperglobulinemia As a paraneoplastic syndrome.

Question 13

Neoplasia of the Liver and Biliary tree Diagnosis: abdo and thoracic xrays

Answer 13

Abdominal radiographsMay identify a cranial abdominal mass with caudal and lateral displacement of the stomach.
* Ascites may interfere with visualizing a mass.
* Occasionally mineralization of mass lesions or the biliary tree is identified.

Thoracic radiographs are Critically important to exclude metastatic disease.

Question 14

Neoplasia of the Liver and Biliary tree Diagnosis: abdominal U/S

Answer 14

Determining presence of a hepatic mass and for identifying if it is massive, nodular or diffuse.

Determine mass size, location and its relationship to surrounding structures.

Doppler (color flow) assessment of mass lesions may demonstrate vascularization patterns helping to distinguish tumors from other benign processes.

Diffuse tumors usually having hypoechoic, heterogeneous, or multifocal parenchymal nodules or masses.

A cystic component may be seen in biliary cystadenomas or hepatic hemangiosarcomas.

Caution! Marked variability in US appearance for all types of liver disease, with no associations between US appearance and histologic diagnosis.

Appearance of hepatic nodular hyperplasia and metastatic disease can be similar!

Question 15

Neoplasia of the Liver and Biliary tree Diagnosis: CT and MRI

Answer 15

Triphasic CT had more than 90% accuracy in differentiating benign from malignant masses in a study with 44 dogs. Superior to US but Could not differentiate the histologic type of malignant tumor.

MRI of focal hepatic lesions in dogs was reported to have high sensitivity (100%) and specificity (90%) in differentiating malignant from benign masses.

Question 16

Neoplasia of the Liver and Biliary tree Diagnosis: FNA and Biopsy

Answer 16

Biopsy and histopathology of lesions is crucial for a definitive diagnosis. Exceptions may be made for solitary and massive hepatic masses. Surgical resection is performed without a preoperative histologic diagnosis because surgery can provide both diagnosis and treatment.

Agreement between cytology and histopathology about 30% in dogs and 50% in cats.

Cytology has the highest positive predictive value when the lesion is neoplastic (87%).

FNA for the diagnosis of diffuse hepatic neoplasia is generally more reliable.

Question 17

Neoplasia of the Liver and Biliary tree: Prognosis and Treatment When Solitary Hepatocellular carcinoma:

Answer 17

Surgical resection, usually lobectomy is recommended for Tumors that have not metastasized.

Mortality rate 5%.
Complication rate 30% (hemorrhage, vascular compromise, reduced hepatic function and hypoglycemia).
Local tumor recurrence is reported in 0-13% of dogs with massive HCC after lobectomy.

Traditional radiation therapy has little place in the management of hepatic tumors. HCC is usually considered chemoresistant.

Prognosis for dogs and cats with massive HCC is good. Primarily because it is more likely they can be completely resected .

The Mean survival time of 42 dogs after liver lobectomy 1460 days of follow-up vs MST of 270 days for dogs managed conservatively!

Question 18

Neoplasia of the Liver and Biliary tree Prognosis and Treatment when Nodular or Diffuse Hepatocellular carcinoma:

Answer 18

Surgical resection is not usually possible and Prognosis is poor.

Radtion therapy also has no place in their management, Primarily because the liver cannot tolerate the significant doses required.

There is limited evidence for the use of chemotherapy for these.

Question 19

Neoplasia of the Liver and Biliary tree Prognosis and Treatment when Biliary duct tumors:

Answer 19

Nodular or diffuse bile duct carcinomas have No known effective management option. Surgical resection is not possible. Not sensitive to radiation or chemotherapy.

When Single bile duct adenoma or multiple lesions confined to one or two lobes, Liver lobectomy is recommended.

When Massive bile duct carcinoma, Lobectomy is also recommended.

Cats with surgically resectable bile duct adenomas prognosis is excellent.

Cats and dogs with massive bile duct carcinoma managed by surgical resection - Survival times are poor, majority dying within 6 months due to local recurrence or metastatic disease.

Question 20

Neoplasia of the Liver and Biliary tree Prognosis and Treatment when Neuroendocrine tumors.

Answer 20

Most are nodular or diffuse and behave aggressively.

Generally not amenable to surgical resection.

No reports of the use of RT or chemotherapy.

Prognosis for poor.

Metastasis to regional lymph nodes, peritoneum and lungs has usually occurred by the time of diagnosis.

Question 21

Neoplasia of the Liver and Biliary tree Prognosis and Treatment when Mesenchymal and other tumors.

Answer 21

For Solitary and massive mesenchymal tumors,
Lobectomy is recommended.

Many have metastasized at the time of diagnosis so Prognosis is poor.

RT with limited efficacy

Chemotherapy – primary mesenchymal hepatic tumors will respond poorly.

Hepatic lymphoma, systemic mastocytosis, malignant histiocytosis May all be managed by systemic chemotherapy.

Question 22

Vascular liver diseases:
describe Portosystemic shunts.

Answer 22

Congenital or acquired vascular anomalies connecting the portal vein with the systemic circulation, bypassing the liver.

CONGENITAL:
Macrovascular portosystemic shunts (PSSs)
* Intrahepatic (IHPSSs)
* Extrahepatic (EHPSSs)
Primary portal vein hypoplasia (PVH)
* PVH with portal hypertension (e.g., noncirrhotic portal hypertension [NCPH])
* PVH without portal hypertension (formerly microvascular dysplasia [MVD])

Disturbances in outflow

AQUIRED:
Multiple, extrahepatic shunts:
* Secondary to hepatic fibrosis (either congenital ductal plate abnormality or acquired chronic hepatitis and cirrhosis).
* Secondary to hepatic arteriovenous malformations (HAVMs)
* Secondary to portal vein thrombosis

Question 23

Describe Congenital PortoSystemicShunts

Answer 23

Commonly occurs as a single intrahepatic or extrahepatic communication (80%).

Single ExtraHepatic PSSs, with a major solitary portocaval shunt being the most common, constitute 66-75% in both species.

25-33% of congenital PSSs are IntraHepatic PSSs in dogs; the condition is less common in cats.

• Most IntraHepatic PSSs occur in larger-breed dogs.
• Most ExtraHepatic PSSs occur in smaller breeds.

Question 24

Describe Acquired PSSs

Answer 24

Commonly occur secondary to chronic portal hypertension.
* Hepatic fibrosis (cirrhosis)
* Portal Vein Hypoplasia with portal hypertension (congenital NCPH)
* Congenital ductal plate abnormalities in dogs and less commonly cats
* Congenital hepatic arteriovenous malformations (HAVMs)

Usually are multiple, tortuous, extrahepatic, and located near the kidneys.

(e.g., noncirrhotic portal hypertension [NCPH])

Question 25

Describe Vascular liver disease: Primary portal vein hypoplasia with Portal Hypertension, or NCPH (e.g., noncirrhotic portal hypertension)

Answer 25

Incompletely developed smaller portal vein branches. Increased resistance that results in portal hypertension and multiple EHPSSs.

Question 26

Vascular liver diseases: Describe Primary portal vein hypoplasia Without Portal Hypertension, Formerly MVD (microvascular dysplasia).

Answer 26

Small intrahepatic portal vessels, portal endothelial hyperplasia, portal vein dilation, random juvenile intralobular blood vessels, and central venous hypertrophy and fibrosis. The above, allow abnormal communications between the portal and systemic circulation at a microvascular level, thus avoiding the increase in portal pressure. Can occur as an isolated disease, or in combination with macroscopic PSS. * 58% of dogs and 87% of cats with Portal Vein Hypertension have concurrent congenital macroscopic PSS.

Question 27

Hepatic Arteriovenous Malformation (HAVM) =

Answer 27

Multiple high-pressure arterial and low-pressure venous communications. Branch of the hepatic artery communicates directly with the portal vein via multiple (dozens to hundreds of) aberrant shunting vessels. Resulting portal hypertension which opens multiple extrahepatic shunts to decompress this system.

Question 28

ExtraHepatic PPSs Signalment versus IntraHepaticPPSs Signalment versus HAVMs

Answer 28

ExtraHepatic PPSs Signalment: * Yorkshire Terrier, Havanese, Maltese, Dandie Dinmont Terrier, Pug, and Miniature Schnauzer Domestic Shorthair, Persian, Siamese, Himalayan, and Burmese IntraHepatic PPSs Signalment: * Irish Wolfhound, Retrievers (Labrador, Golden), Australian Cattle Dogs, and Australian Shepherds Cairn Terriers are likely to have an autosomal inherited Portal Vein Hypoplasia. HAVMs do not have breed predispositions. * Extrahepatic arterioportal malformation have only been reported in unrelated Pembroke Welsh Corgis. ## Footnote Hepatic Arteriovenous Malformation (HAVM)

Question 29

Vascular liver diseases: patient History shows...

Answer 29

Most animals with congenital PSSs have signs (acute or chronic) before 1-2 yrs of age. Multiple acquired EHPSSs in dogs diagnosed at a median age of 3 yrs and median age of dogs diagnosed with portal vein hypoplasia is 3.25 yrs. “Failed to thrive” since birth, small in stature, failure to gain weight, anesthetic intolerance, dull or lethargic at times, and displays “bizarre behavior. Stargazing, head pressing, staring into walls or corners, random barking, intermittent blindness, pacing or aggression. Some pets have a history of dysuria or hematuria (PU/PD) is common in dogs with cPSS. ## Footnote EHPSS = extra hepatic portosystemic shunt

Question 30

Vascular liver diseases: Clinical signs

Answer 30

CNS, GI, and urinary systems are commonly affected. Signs of HE can be obvious or subtle and associated with aberrant behavior. * More obvious CNS signs include ataxia, unresponsiveness, pacing, circling, blindness, seizures, random barking, and coma. GI signs (vomiting, diarrhea, anorexia, pica, and/or GI bleeding/melena/hematemesis) occur in about 30% of dogs; less frequent in cats. * Ptyalism is common in cats (75%) Some pets (20-50%) have signs of lower urinary tract disease: hematuria, stranguria, pollakiuria, or urethral obstruction. * Decreased urea production, increased ammonia excretion, and decreased uric acid metabolism -> formation of ammonium urate calculi or debris!

Question 31

Vascular liver diseases Laboratory findings: CBC

Answer 31

Often include a mild to moderate, microcytic, normochromic, nonregenerative anemia. Due to defective iron transport and metabolism. Microcytosis, reported with or without anemia in 60-72% of dogs and in ∼30% of cats.

Question 32

Vascular liver diseases Laboratory findings: biochemistry.

Answer 32

Abnormalities are common in dogs and cats with PSSs. Decreased hepatic synthesis: low albumin (50%), low BUN (70%), hypocholesterolemia, and hypoglycemia. In cats, hypoalbuminemia is uncommon but low BUN and creatinine are common. Mild to moderate increases in ALP and ALT activities are common.

Question 33

Vascular liver diseases Laboratory findings: Urinalysis

Answer 33

Common abnormalities are low urine specific gravity and ammonium biurate crystalluria. Ammonium biurate crystalluria can be seen in 26-75% of affected dogs and 16-42% of affected cats.

Question 34

Vascular liver diseases Laboratory findings: blood ammonia

Answer 34

Plasma separation and laboratory analysis must be completed within 20 minutes of sample collection! The 6-hr postprandial blood ammonia has been reported as more sensitive (91%) than fasting concentrations (62%). Both false-positive and false-negative baseline ammonias have been documented. Hyperammonemia in young animals not associated with PSS. e.g. instead due to Congenital cobalamin deficiency, methylmalonic acidemia, other urea cycle enzyme deficiencies and urethral obstruction–induced hyperammonemia.

Question 35

Vascular liver diseases Laboratory tests: Bile Acids (BAs) findings.

Answer 35

Fasting (12-hr) and 2-hr postprandial serum BAs are tests of choice for evaluating liver function when suspecting PSSs. Increased postprandial SBAs have been reported as being 100% sensitive for detecting PSSs in dogs and cats. False positives: * Maltese dogs without evidence of liver dysfunction * Inappropriate sample timing * Other hepatobiliary diseases/cholestasis, glucocorticoid or anticonvulsant therapy, tracheal collapse, seizures, and GI disease. False negatives: * Delayed intestinal absorption * Lack of gallbladder contraction * Inadequate food intake/delayed gastric emptying, or malabsorption or maldigestion.

Question 36

Vascular liver diseases Laboratory findings: coag profile

Answer 36

Prolonged coagulation times common in dogs with PSS. Spontaneous bleeding is rare and excessive bleeding does not usually occur during surgical intervention.

Question 37

Vascular liver diseases Diagnostic imaging: radiographs

Answer 37

Often demonstrate microhepatica (60-100% of dogs, 50% of cats). Marginally radiopaque calculi may be seen in the bladder, urethra, ureters, and/or kidneys.

Question 38

Vascular liver diseases Diagnostic imaging: U/S

Answer 38

Widely used diagnostic tool for PSS. Decreased numbers of hepatic and portal veins, a subjectively small liver, and an anomalous vessel are most often seen with cPSS. ExtraHepatic PSSs generally are more difficult to diagnose via US due to small patient size, small vessel size, variable location, and presence of gas in the bowel and lungs. Sensitivity for detection of shunts has ranged from 74-95% and specificity from 67-100%. Sensitivity is higher for IntraHepatic PSS (95-100%) than EHPSS due to the presence of liver parenchyma surrounding the shunting vessel, and the typically large diameter of the intrahepatic shunting vessel and associated portal vein. NB! Results are operator- and experience-dependent.

Question 39

Vascular liver diseases diagnostic imaging: Computed Tomographic Angiography (CTA)

Answer 39

Dual-phase CTA provides a complete evaluation of portal and hepatic vasculature. * Non-contrast * Arterial * Portal * (Late Venous) CTA is helpful in preprocedural planning for surgery.

Question 40

Vascular liver diseases Medical treatment

Answer 40

Should begin in all animals at the time of diagnosis. Controls clinical signs but does not treat the underlying disease. Bacterial translocation/decreasing bacterial byproduct absorption (ammonia): * If comatose patient, Cleansing enemas with warm water or 30% lactulose solution at 5-10 mL/kg * If conscious, Oral lactulose: 0.5-1 mL/kg PO q6-8h to effect of 2-3 soft stools per day. Antibiotics: * Metronidazole 7.5 mg/kg IV or PO q12h * Ampicillin 22 mg/kg IV q6h * Amox+clav 20mg/kg IV q8h Coagulopathy (with evidence of bleeding; postoperative) * Fresh frozen plasma 10-15 mL/kg over 2-3 h * Vitamin K1 1.5-2 mg/kg SC or IM q12h for 3 doses, then q24h Gastrointestinal ulceration (begin treatment before intervention; very common with IntraHepaticPPS, and HAVM due to portal hypertension) * Omeprazole 0.5-1 mg/kg PO q12-24h * Esomeprazole 0.5 mg/kg IV q12-24h * Sucralfate: 1 g/25 kg PO q8h * Correct coagulopathy ## Footnote HAVM = Hepatic arteriovenous malformations

Question 41

Vascular liver diseases Medical treatment for seizure control:

Answer 41

Avoid benzodiazepines due to lvier metabolism. Phenobarbital (4 mg/kg IV q3-6h for 4 doses) KBr: * Loading: 400-600 mg/kg/day divided over 1-5 days PO with food; can be given per rectum if needed. * Maintenance: 20-30 mg/kg PO q24h * Should be avoided in cats due to bronchospasm. Sodium bromide can be used if an IV form is necessary. Propofol 1-3.5 mg/kg IV bolus, followed by CRI of 0.01-0.25 mg/kg/min. Levetiracetam 20 mg/kg (up to 60 mg/kg) PO or IV q8h. ## Footnote Decrease cerebral edema with Mannitol: 0.5-1 g/kg slow IV bolus over 20-30 min

Question 42

Vascular liver diseases nutritional support

Answer 42

Normal (not high) protein diets: 18-22% for dogs and 30-35% for cats; dairy or vegetable proteins preferred. Hepatoprotective therapy (for chronic conditions that are unable to be fully corrected-MVD, NCPH, MEHPSSs, etc.) * S-adenosyl-L-methionine: 17-22 mg/kg/day PO * Ursodeoxycholic acid: 10-15 mg/kg/day PO * Vitamin E: 15 IU/kg/day PO * Milk thistle (silymarin): 3-7 mg/kg PO q8h * L-carnitine: 250-500 mg/day PO (cats) ## Footnote MVD = Primary portal vein hypoplasia without portal hypertension (formerly microvascular dysplasia [MVD]) NCPH = PVH with portal hypertension (e.g., noncirrhotic portal hypertension [NCPH]) MEHPSSs = macrovascular extrahepatic portosystemic shunts

Question 43

Vascular liver diseases: Surgery

Answer 43

No ideal time for surgery, preferably treated medically to minimize clinical signs first. Goal is to attenuate the abnormal vessel to re-establish hepatic parenchyma blood flow from the portal system. ExtrahepaticPSS * Ameroid Constrictor vs Cellophan Bands IntraPSS * Surgical dissection and attenuation with suture, AC, CB or Hydraulic occluder (HO) HAVM - Hepatic arteriovenous malformations * Liver lobectomy, ligation of the nutrient artery, fluoroscopically-guided glue embolization of abnormal arterial vessels.

Question 44

Vascular liver diseases Surgery, Post-operative complications

Answer 44

Seizures * due to Acute removal of endogenous benzodiazepines or changes in brain amino acid concentrations or ratios Portal Hypertension * Some degree of PH can occur following acute partial or complete shunt attenuation. Life-threatening conditions are uncommon though. Hypoglycemia and hypothermia Persisting or recurring clinical signs * Original shunt has remained patent, another shunt was present originally, an incorrect vessel was attenuated, multiple acquired shunts have developed, concurrent hepatic parenchymal disease is present, concurrent neurologic disease is present. Severe GI bleeding * Abnormal GI blood flow, hypoprostaglandinemia, poor mucosal integrity, abnormal mucus production, abnormal cell turnover.

Question 45

Vascular liver diseases Surgery Post-operative care

Answer 45

IV fluids until they are eating and drinking * Dextrose is added to the fluids when blood glucose is <4.4 mmol/L. Monitoring for hypothermia, delayed anesthetic recovery, hemorrhage, seizures, and signs of portal hypertension. Animals usually require opioid analgesics . A high-quality digestible vegetable or dairy protein diet, antibiotics, and lactulose are continued after surgery until liver function improves. Biochemical panels are evaluated 1 month after surgery. If liver parameters are normal, medical management is weaned over 2-4 weeks. Starting with AB, then lactulose, then transitioning to an adult food.

Question 46

Vascular liver diseases Prognosis

Answer 46

Medical management: * Prognosis varies. Studies show a shorter median survival time for dogs managed medically rather than surgically. ExtraHepatic PSS: * Mortality rates: 2-32% (ligation), 7% (ameroid constrictor placement), 6-9% (cellophane banding) Intra PSS: * Median survival 1 to 3 years * Mortality rates 23-63.6% HAVM / Hepatic arteriovenous malformations: * Long-term outcome 38-57% of dogs (surgery) alone and closer to 70% (glue embolization) Microvascular dysplasia/Portal Vein Hypoplasia: * 92% have good long-term survival with medical management Primary portal vein hypoplasia with noncirrhotic portal hypertension * 40% have survived long term Feline PSS * Medical management: prognosis unknown * Postoperative complications are reported in up to 75% of cats * Of surviving cats good or excellent long-term outcome has been reported in 66-80% Acquired PSS * Medical management can result in long term survival in animals with non- progressive disease. * Treatment should be aimed at controlling the clinical signs of HE and slowing the progression of the liver disease.

Question 47

Describe Ductal Plate Abnormalities.

Answer 47

Complex spectrum of pathological abnormalities arising from abnormal development of the biliary ductal system. Ductal Plate abnormalities refers to a lack of remodeling of the ductal plate, resulting in the persistence of embryonic bile duct structures.

Question 48

When Ductal Plate Abnormalities can occur in Extrahepatic and large intrahepatic ducts, you get 2 syndromes. What are they?

Answer 48

Choledocal cyst * Segmental dilatations of extrahepatic and/or intrahepatic biliary ducts. * Most cats presented at the age of 5 to 11 years * Clinical signs of cholangitis and choledochitis. Also may be discovered as incidental findings in abdominal imaging. Caroli disease and Caroli syndrome * Multifocal segmental dilatation of large intrahepatic bile ducts. * Disease when bile ductular dilatation in the absence of other abnormalities. * Syndrome when bile duct dilatation with congenital hepatic fibrosis. Clinical presentation variable, depending on the extent and severity of biliary dilation and hepatic fibrosis. Abdominal ultrasound (US) or computed tomography (CT) can be used to visualize Multiple cystic dilations of intrahepatic bile ducts which communicate with the biliary tree.

Question 49

When Ductal Plate Abnormalities in Medium-sized intrahepatic ducts its called Polycystic liver disease. Describe it.

Answer 49

Progressive expansion of fluid-filled cysts that gradually replace liver parenchyma. Clinical consequences are dependent on the number, size, growth rate, and location of the hepatic cysts -> no signs to hepatic failure. Persian cats or related cross breeds are most commonly affected. Thin-walled, anechoic or fluid filled cysts identified within the hepatic parenchyma on US which do not communicate with the biliary tract. Histopathologic evaluation of tissue is required to definitively exclude other differentials (parasitic, neoplastic).

Question 50

When Ductal Plate Abnormalities occur in Small intrahepatic ducts, its called Congenital hepatic fibrosis. Describe it.

Answer 50

Result of abnormal ductal plate remodeling of the small interlobular bile ducts. Fibrosis is generally progressive and portal hypertension occurs. Most cats and dogs present at a young age (2 months to 2 years) with signs relating to portal hypertension: ascites, anorexia, vomiting, and neurological signs. On US, ascites and evidence of Aquired PSS may be noted but the liver may appear normal. Definitive diagnosis requires histopathology. Periportal to bridging fibrosis, numerous small irregular bile ducts, diminished portal venous vasculature and hyperplastic arterioles. Treatment of affected dogs and cats is limited to supportive.

Question 51

Ductal Plate Abnormalities: Von Meyenburg Complexes

Answer 51

Also known as Biliary hamartomas - rare benign nodular lesions suspected to arise from abnormal remodeling of peripheral interlobular bile ducts. Rarely in dogs and cats. Typically diagnosed as incidental imaging or necropsy findings. Variably sized nodular cystic lesions which may occur multifocally or in isolation. Histologic evaluation of tissue samples is required for definitive diagnosis. No specific treatment is required and an excellent prognosis is expected.