Liver

After initiating treatment for a patient with a PSVA with Hill's l/d (no added protein), metronidazole (7.5 mg/kg PO BID), and lactulose at 1 ml of lactulose BID you reassess the patient. The clients note that she seems brighter and has normal stools. Her current weight is 4.5 kg. You examine her urine sediment and observe crystalluria depicted in the accompanying image. What would you consider changing in "Princess Anastasia's" medical treatment plan while awaiting her scheduled surgery?

1. increase the metronidazole dose

2. increase the lactulose dose

3. add shredded cheese to her diet to provide 0.5g/kg of additional protein daily

4. emergency referral for surgery

Increase the lactulose dose

• don’t go above 7.5mg/kg metro PO BID in shunt patients.

A 10-year-old male castrated Pug presents for an annual wellness exam where you perform a chemistry profile. The patient has several abnormal values that you collectively consider indicative of cholestatic disease. Which of the following patterns most strongly supports that deduction?

1. increased total bilirubin, ALT, and low albumin

2. Decreased cholesterol, BUN, and high AST

3. Increased ALP, GGT and cholesterol

4. Increased ALP, ALT, and creatinine.

Increased ALP, GGT, and cholesterol

A 5-year-old mixed-breed dog has a mildly increased ALT on pre-anesthetic lab work. The patient is otherwise asymptomatic. Of the following choices, which is the most appropriate course of treatment and correct rationale?

1. Prescribe SAMe (denosyl) at the manufacturers dose and recheck the patient’s ALT in one month to determine if choleresis was effective.

2. Prescribe SAMe (denosyl) at the manufacturers dose and recheck the patient’s ALT in one month to determine if antioxidant therapy was effective.

3. Prescribe vitamin K at 0.5 mg/kg PO daily to prevent coagulopathy

4. Prescribe vitamin E because you suspect the patient’s ALT may be due to a nutritional deficiency.

Prescribe SAMe (denosyl) at the manufacturers dose and recheck the patient’s ALT in one month to determine if antioxidant therapy was effective.

You work at a three-doctor general practice in Vermont. Which of the following tests that are available in your clinic COULD diagnose "Princess Anastasia's" (9-month-old Yorkshire Terrier with a presumptive EHPSVA) shunt definitively?

1. Paired (fasting and post-prandial) bile acids

2. Protein C

3. Urine sediment

4. Abdominal ultrasound conducted by a traveling radiologist

Abdominal ultrasound conducted by a traveling radiologist

A 7-year-old DSH cat named Professor Shelby presents with abdominal distension, and abdominocentesis provides a sample of effusion with a protein of 0.5 g/dL and is minimally cellular. Which of the following best describes the effusion?

1. modified transudate

2. pure transudate

3. exudate

4. chylous effusion

Pure transudate

An abdominal ultrasound of "Professor Shelby" (7-year-old DSH) discloses no evidence of a portal thrombus but multiple cysts in the liver and renal cortex, leading you to believe the cat has a ductal plate malformation. You deduce the most likely anatomic source of the ascites (protein 0.5 g/dL) is:

1. prehepatic

2. presinusoidal

3. postsinusoidal

4. posthepatic

pre sinusoidal

Which of the following treatments would be the most inappropriate for "Professor Shelby" (7-year-old DSH), a cat with a presumptive ductal plate malformation and ascites (protein 0.5 g/dL)?

1. diuretic therapy with furosemide and spironolactone

2. feeding a low sodium diet

3. fluid support with 0.9% saline

4. a bioavailable S-adenosylmethionine supplement (Denosyl)

Fluid support with 0.9% saline

You examine a 6-year-old female spayed Labrador Retriever and note the patient is icteric. In addition to a minimum database (CBC, Chemistry, UA), you consider several other diagnostic tests. Which of the following tests would be unnecessary to run given what you've already discovered on your physical exam?

1. coagulation testing

2. protein C

3. leptospirosis witness (point of care diagnostic) test

4. bile acids

bile acids

You run pre-anesthetic blood work on your favorite patient, a 9-month-old Yorkshire Terrier named "Princess Anastasia," and become concerned that she could have a PSVA. Which of the following list of abnormalities did she have?

1. decreased albumin, BUN, and cholesterol with microcytosis on the CBC

2. decreased sodium, increased ALP and BG

3. increased ALT and cholesterol, decreased BUN

4. increased total bilirubin and ALT, spherocytosis on the CBC

Decreased albumin, BUN, and cholesterol with microcytosis on the CBC

When is abdominal fluid normal?

0-15mls OR in young animals.

clear or straw colored

pH 7.4 SG <1.016

Protein <3.0 g/dl

nucleated cells <3,000

Non-colloidal solutes =plasma

Abdominal distension could be caused by……

1. Aerophagia

2. Abdominal effusion - hemorrhage, chyle, transudate, exudate, bile peritonitis, uroabdomen

3. Organomegaly = liver, spleen

4. distended viscera = gastric torsion, GI obstruction, uterine enlargement (pregnancy or pyo)

5. Masses

6. Pneumoperitoneum

7. Weak abdominal muscles - cushings

8. Obesity

Define ascites

Ascites is defined as fluid accumulation within the peritoneal cavity. Although any peritoneal fluid accumulation could be classified as ascites, the term is more often used to refer to pure and modified transudates

Distended superficial abdominal veins are a sign of…..

ascites - due to entrapment of femoral triangle OR portal/CVC hypertension

Abdominal effusion with TP >2.5 and TNCC <5.0 × 10³789ioukjhm inmjn n

high protein transudate

low protein = <2.5

Which of the following antimicrobials will effectively clear spirochete organism from the kidney of a dog with leptospira infection?

1. Ampicillin sulbactam (unasyn)

2. baytril

3. doxycycline

4. metronidazole

Doxycycline

Which of the following medications are used in the treatment and prevention of oxidant injury?

1. N-acetylcysteine

2. Vitamin E

3. SAMe

4. All of the above

all of the above

Which of the following have been documented to cause acute liver injury in the dog

1. Carprofen

2. Phenobarbital

3. Azathioprine

4. All of the above

All of the above

Copper-associated hepatopathy may be associated with which of the following clinicopatholofic abnormalities

1. increased ALT activity

2. Hyperbilirubinemia

3. Glucosuria

4. All of the above

All of the above

Which of the following endocrine diseases result(s) in a glycogen-type vacuolar hepatopathy (VH)?

1. Diabetes mellitus

2. Hyperadrenocorticism

3. Hypothyroidism

4. All of the above

all of the above.

Hepatic insufficiency in horses

• >80% liver loss required to impair functions

• Insufficiency - NO clinical signs

• Failure - clinical signs

SIGNIFICANT HEPATIC DISEASE CAN BE PRESENT WITHOUT HEPATIC FAILURE

Clinical signs of liver disease in horses

1. icterus

2. pigmenturia

3. weight loss

4. photosensitization

5. respiratory distress - laryngeal paralysis

6. Ventral edema - with lipidosis

7. Colic

Signs of hepatic encephalopathy in horses

Any stage of liver disease

potentially reversible

Signs

1. yawn

2. playing in water bucket

3. cortical blindness

4. head press

5. compulsive walking

6. depression/hyperresponsiveness

AMMONIA (concentration does not equal clinical sign severity)

If no evidence of liver disease, what are your ddx of intestinal hyperammonemia?

1. Dysbiosis

2. Colic/diarrhea

3. clostridial

treat like hepatic encephalopathy

Hepatocellular enzymes in horses

Can be normal in chronic disease

1. SDH (sorbitol dehydrogenase)

   • liver specific, not inducible, sensitive for mild injury

   • unstable

   • normal within 3-5 days of transient hepatic insult

2. AST

   • muscle

3. GLDH (glutamate dehydrogenase)

   • considered specific (liver » renal, brain, muscle, GI)

   • sensitive for mild injury

4. LDH (lactate dehydrogenase)

   • Not specific (liver, muscle, RBC, GI, renal)

   • stable for 36 hours

5. AST, ALT, ALP, LDH not liver specific

What is the most sensitive test for liver disease in the horse?

GGT

• biliary damage, biliary hyperplasia, cholestasis

• remains elevated with chronic liver disease

Function tests for liver disease in the horse?

Bilirubin

• Direct = conjugated

  • >25% direct = likely cholestasis

  • can spill into urine

  • increases because of hepatic disease

• Indirect = unconjugated

  • hepatocellular

  • or fasting, hemolysis, or idiopathic

  • can increase without hepatic disease

Bile Acids

• most useful test of liver function

• better for chronic disease

• enterohepatic circulation

• no pre/post prandial

• Horses do not have a gall bladder

What would cause increased serum bile acids in the horse?

1. portosystemic shunt - decreased blood to liver

2. liver failure - reduced removal from blood. fail to conjugate for excretion

3. cholestasis - reduced excretion, reabsorbed into plasma.

Most useful indicators of liver disease in horses

• biliary and chronic?

• Hepatocellular?

• Function?

Biliary and chronic: GGT

Hepatocellular: SDH, AST

Function: bile acids

Idiopathic inflammatory - chronic active hepatitis in horses?

Progressive inflammation of the liver

mainly periportal

lymphoplasmacytic

viral? hepacivirus?

Treatment

1. steroids

2. general supportive liver care

Infectious causes of hepatic disease in foals

UNCOMMON!

• tyzzer’s

• EHV-1

• Actinobacillus

• streptococcus

• leptospira pomona

• listeria monocytogenes

• bartonella henselae

• rhodococcus equi

Infectious causes of hepatic disease in adults

Bacterial - cholangiohepatitis

viral

What is tyzzer’s disease?

Epidemiology: foals 1-6 weeks

Pathogenesis: Clostridium piliformis

• ingest contaminated soil

Clinical signs:

• septic shock/liver failure

• parachute onset, often found dead

Diagnosis on necropsy

• antemortem findings are non-specific

• multifocal enteritis, hepatitis

• Silver stain - intracytoplasmic bacilli

Cholangiohepatitis/cholelithiasis in horses

• epidemiology

• pathogenesis

• clinical signs

• diagnosis

• treatment

Epidemiology

• middle age horses

  • broodmares

  • predisposes

  • Hx previous GI disease

• Pathogenesis

  • ascending bacterial infection → bacterial cholangitis

  • ascariasis

  • biliary stasis

  • → sludge → one stone → multiple stones

• Clinical signs

  • icterus, colic, fever

  • photosensitivity

  • weight loss

  • neuro rare

• Diagnosis

  • ultrasound

  • biopsy

  • Culture - E. coli, enterobacter spp., clostridium spp.

• treatment

  • antibiotics (enro/metro, TMP/metro) until GGT is normal

  • fluid therapy to increase bile flow

  • DMSO - dissolves brown stone

  • pentoxifylline

  • ursodiol

  • SAMe

  • NSAIDs

  • surgery

Surgical treatment for cholangiohepatitis

Surgical treatment when -

• common bile duct obstructed

• or lack response to med tx

• visualize stones

• ± limited fibrosis = able to repair

• ± biopsy consistent with obstruction

  • circumferential biliary hyperplasia

Viral hepatitis can be caused by

1. equine parvovirus-hepatits

2. equine hepacivirus

3. EIA, EVA, EHV-1

   • liver disease not the primary complaint

4. NOT - equine pegivirus, theiler’s disease associated virus

What is the most common cause of acute liver failure in horses?

Theiler’s disease = equine parvovirus-hepatitis (EpPV-H)

HEPATOCELLULAR disorder

leads to a subclinical to fatal acute hepatitis

Very high AST

low value on PCR = HIGH VIRAL LOAD

severe acute hepatitis w/ necrosis

no fever

Hepaciviral hepatitis

aka non-primate hepacivirus

• close relative of hepatitis C virus

Very common, subclinical

~40% seroprevalence

chronic infection → chronic hepatitis

• fibrosis

• lymphoplasmacytic

• individual cell necrosis

PCR serum or liver

can be persistently infected

No fever

Equine hepatic neoplasia?

Lymphoma

cholangiocarcinoma

Hepatoblastoma - polycythemia without liver failure

What liver disease is primarily in ponies and miniature horses off feed?

Hyperlipidemia

• consider for ANY ill, pregnant, or lactating pony or miniature horse

clinical signs

• primary disease

• depression, anorexia, ± icterus, ataxia, colic

• ventral edema

Increased triglycerides

<50 normal

<500 hyperlipidemia

>500 hyperlipidemia can see grossly

How do you treat hyperlipidemia in ponies?

Give dextrose and insulin to stop fat mobilization

treat underlying condition

IV and enteral nutrition

abort or wean foal

Give heparin to stimulate LPL

Examples of drug induced hepatic failure in horses?

Iron

• hard to reproduce experimentally

• foals treated for NI with multiple transfusions

• deferoximine mesylate can increase iron elimination

Doxycycline + rifampin combination

• foals treated for R. equi

treatments

• corticosteroids

• discontinue drug

• general supportive liver care

4 toxic causes of liver failure in horses

1. pyrrolizidine alkaloids

2. alsike clover

3. panicum grasses

4. mycotoxins, red fescue rare

Pyrrolizidine alkaloid toxicosis

Clinical signs

• 1-12 months after ingestion

• abrupt onset signs of hepatic failure

epidemiology

• pacific coast and southeastern US

  • senecio (ragwort)

  • Amsinckia (fiddle neck)

  • Crotalaria (rattle box)

  • Helotropium

• chronic low level exposure more common

No effective treatment, prognosis = death within 10 days of onset of clinical signs.

What would you see on a pyrrolizidine alkaloid toxicity biopsy in horses?

biopsy is PATHOGNOMONIC

1. megalocytosis

2. biliary hyperplasia

3. fibrosis

Pathophysiology: PA inhibits cell replication and protein synthesis. Cells can’t divide → megalocytes → cell death → fibrosis

True/false: we should use diazepam in treating encephalopathy in horses

NO - to control behavior, use alpha 2 agonist, pentobarbital, phenobarbital

Reduce cerebral edema with mannitol

Where is ALT found?

cytosol (hepatocellular)

Where is AST found?

Mitochondria and cytosol (hepatocellular)

Where is ALP found?

transmembrane anchored - cholestatic marker

where is GGT found?

Canalicular hepatocyte (cholestatic marker)

biliary ductular cell

Which enzyme in cats do we see the largest increase in with extra hepatic bile duct obstruction and cholangiohepatitis

GGT

Which enzyme in cats do we see the largest increase in with cholestasis

ALP

Describe pre-hepatic, hepatic, and post-hepatic bilirubin

**cholestatic marker

pre-hepatic: extravascular hemolysis

Hepatic: decreased hepatocyte function - decreased transcellular transport (sepsis)

post-hepatic: extra hepatic biliary duct obstruction

When does cholesterol increase?

when bile cannot be excreted

What are the 3 types of cholangitis/cholangiohepatitis in cats

neutrophilic

lymphocytic

chronic cholangitis associated with liver fluke

Etiologies of neutrophilic cholangitis in cats

1. most cases result from ascending bacterial infection from the GI tract

2. or enteric mucosal translocation - entry via portal circulation - hematogenous seeding of biliary tract and liver

associated comorbidities of neutrophilic cholangitis in cats

• increase the risk of infection - ?

• impair normal bile flow - ?

• involve malformation of the biliary tree - ?

• increase the risk of infection - IBD, diabetes mellitus

• impair normal bile flow - cholelithiasis, neoplasia

• involve malformation of the biliary tree - ductal plate malformation

Clinical presentation (history and PE) of cat with cholangitis

History

• often acute illness (sick <2weeks)

• Anorexia, ptyalism, vomiting, diarrhea, recent weight loss, lethargy

• waxing/waning clinical signs with chronic disease

Physical exam

• pyrexia (fever)

• dehydration

• jaundice

• ptyalism (hypersalivation)

• cranial abdominal pain

• hepatomegaly

True/false: increased bilirubin is ALWAYS abnormal in cats

true

true/false: liver biopsy with histopathology is required for definitive diagnosis of cholangitis

true

How do you treat neutrophilic cholangitis in cats

1. Antibiotics

2. Vitamin K - if jaundice, bile flow is inhibited and may not be able to absorb fat soluble vitamins

3. Antioxidants - NAC, denosyl or denamarin, Vitamin E

4. Choleretics - ursodiol, denosyl

   • CONTRAINDICATED if there is extra hepatic bile duct obstruction

CBC, CHEM, ultrasound findings of cholangitis in cats

CHEM: increased liver enzymes and bilirubin

CBC: inflammatory leukogram - neutrophilic with a left shift, anemia less common

Prolonged clotting times

Abdominal ultrasound

1. distention of extra hepatic biliary tract

   • distended gallbladder with thickened wall

   • distended common bile duct, cystic duct

2. liver parenchyma - visible

3. cholelithiasis - occasionally seen

How can mechanical or functional biliary obstruction promote infection in cats?

1. mechanical or functional bile duct obstruction (partial or complete) leads to decreased bile flow and increased intraductal pressure

2. this has adverse effects on normal host defense mechanisms including: kupffer cell (resident macrophage) functions, secretory IgA production, integrity of epithelial tight junctions

3. results in increase quantity of bacteria in the bile and a microenvironment more conducive to bacterial invasion into the bile duct epithelium

Information that can be learned from bile cytology

1. presence and nature of inflammation

2. presence of bacteria

3. occasionally non-bacterial pathogens or neoplastic cells observed

Liver biopsy results of cholangitis in cats

mixed periportal inflammatory infiltrate and intraductal neutrophils

How to treat neutrophilic cholangitis in cats

1. esophageal feeding tube

2. treat comorbidities

   • triaditis = IBD + Pancreatitis + cholangitis

3. Abx according to culture

When is abdominal explore surgery indicated for cholangitis in cats?

When there is a concern for an extra hepatic biliary tract obstruction and/or presumptive cholangitis/cholangiohepatitis that is not responding to medical management

goals

1. receive potential obstruction

2. remove nidus of infection

3. collect samples for culture

4. obtain biopsies

What is lymphocytic cholangitis in cats? History and PE

Nature of inflammatory infiltrate suggests that an immune-mediated mechanism plays a role in the pathogenesis of the liver pathology

History:

• slow progressive illness

• polyphasic or anorexia, weight loss, vomiting, lethargy, PU/PD

• family may not perceive cat as being sick

PE

• BAR

• normal temp

• ± jaundice

• ± hepatomegaly

• ± ascites

CBC Chem Ultrasound results of lymphocytic cholangitis

Chem

• increased liver enzymes

• increased bilirubin

• increased globulins

CBC

• lymphopenia in some, others marked lymphocytosis

• neutrophilia

• anemia

Prolonged clotting times

Abdominal ultrasound

• liver parenchyma may have hyper echoic coarse appearance

• may be complicated by coexisting hepatic lipidosis

• distention of extra hepatic biliary tract uncommon

How to treat lymphocytic cholangitis

1. antibiotics

2. vitamin k

3. antioxidants

4. choleretics (unless there is ductopenia)

5. corticosteroids to suppress immune response (prednisolone or dexamethasone)

What is ductopenia?

a decrease in the amount of small bile ducts.

Bile acids are secreted by hepatocytes and have no where to go. Leads to an increase in bilirubin

Cholerectics are contraindicated if ductopenia - concern for toxicity to hepa

Pathophysiology of hepatic lipidosis

Fatty acids released from robust adipose stores in anorexic cats → increased fatty acids in blood overwhelmed livers ability for fat utilization → hepatocytes become distended with triglycerides inhibiting function and restricting bile flow.

A markedly increased ALP with normal-mildly increased GGT is typical of what in cats?

Hepatic lipidosis

Will also see decreased potassium, phosphorus, and magnesium = increased risk for hemolysis and muscle weakness

Feline hepatic lipidosis cbc results

anemia

poikilocytosis

heinz bodies

prolonged clotting times

How to treat feline hepatic lipidosis

1. correct dehydration + maintain hydration

2. correct electrolyte derangements

3. Nutritional support

   • NG tube

   • high calorie diet

   • taurine for bile acid conjugation

   • carnitine for fatty acid oxidation

4. Management of vomiting

   • metoclopramide

   • ondansetron or cerenia

5. thiamin

6. vitamin b12

7. vitamin K

8. vitamin E

9. antioxidants - NAC, denosyl

Hepatic lipidosis - refeeding syndrome

rapid onset of carbohydrate metabolism and insulin release

cellular uptake of phosphate, magnesium, water

hypokalemia, hypophosphatemia, hypomage\nesemia.

Which livestock species are most susceptible to copper toxicosis?

Sheep - who need at least 4-6ppm CU, however normal food has 8-11ppm.

Excess accumulates gradually in the liver = hemolytic crisis occurs when copper is released from the liver.

Goats are resistant!

Can occur in llamas from concentrate feeds.

Common scenarios of copper toxicosis poisoning

1. eating cattle, horse, chicken, swine feeds

2. spreading chicken manure on pasture.

3. Eating salt mixes with added copper

4. Eating pyrrolizidine alkaloids - liver damage from plants increases copper storage

   • senecium

   • heliotropium

   • echium

Clinical and necropsy signs of copper toxicosis

Clinical signs

1. preceded by stressful episode

2. anorexia, lethargy, weakness

3. fever - hemoglobin is a pyrogen

4. Icteric sclera (not all)

5. methemoglobinemia - muddy yellow

6. arched back from kidney pain

7. coffee colored urine

8. sudden death

9. photosensitization - edema and necrosis of areas unprotected “big head”

Necropsy findings

1. Yellow (-brown) mucous membranes and body fat

2. liver yellow brown or greenish

3. gun metal gray kidneys

4. discolored urine

5. hepatocellular necrosis

6. hemoglobinuria nephrosis

7. increased liver and/or kidney copper

   • MUST test both!!!!

Use PAS stain on histopath of liver.

Kidney - use Prussian blue to see iron damaging kidney.

Common reasons for abscesses in the liver of small ruminants

1. Listeria

2. Omphalitis - infection in umbilical cord - blood travels up umbilical vein and infects liver

3. CLA - Caseous Lymphadenitis caused by Corynebacterium pseudotuberculosis

Which liver flukes affect small ruminants? How do you diagnose and treat?

1. fasciola hepatica - eggs, metacercariae → sheep and goat

   • cycle includes fresh water snails

   • acute peritonitis

   • adults in bile ducts

   • chronic biliary fibrosis

   • hypoproteinemia, anemia (blood leaks into bile ducts)

2. fasciola magna

   • American deer fluke

   • natural parasite of deer and elk

   • sheep and goats abnormal hosts

   • larval stages continue to migrate through liver - not in bile ducts, so hard to kill with drugs excreted in bile)

   • Sheep and goats don’t excrete eggs

   • usually fatal within 6 months

3. dicrocoelium dendriticum

   • snail extrudes cercariae as slime balls - ant eats slime ball - metacercariae in brain - sheep eats ant - no migration, less pathogenic

How to treat copper toxicosis in sheep?

1. IV fluids to flush kidneys

2. blood transfusions in anemic

3. methylene blue if methemoglobinemia severe

   • converts methemoglobin to hemoglobin

4. oral ammonium molybdate

5. oral sodium sulfate

6. oral gypsum (calcium sulfate) in salt

7. penicillamine (an expensive chelator)

How do you treat liver flukes in ruminants?

1. Fence of wet areas - fasciola

2. Albendazole for adults

3. Clorsulon orally - adult fasciola

Can lead to - black disease (infectious necrotic hepatitis)

• Clostridium novyi - anaerobe germinates in liver when migrating flukes cause necrosis

• exotoxins cause rapid death

• coagulative necrosis of liver

• Treat with ivomec plus - 2 doses 8 way clostridial

Hepatic artery supplies ___% of the blood flow and ___% of O2 supply.

Portal vein supplies ___% of blood flow and ___% of O2 supply

Hepatic artery supplies 20% of the blood flow and 50% of O2 supply.

Portal vein supplies 80% of blood flow and 20% of O2 supply

Where does the gall bladder lie?

between quadrate lobe and right medial lobe

Biliary anatomical differences between the cat and dog

Cat: common bile duct conjoins with the pancreatic duct AT the major duodenal papilla

Dog: pancreatic secretions are carried by the accessory pancreatic duct which opens separately from the CBD

How much of the liver can be removed during surgery?

65-70% in HEALTHY liver

• if we don’t leave enough of the liver, we can give the dog portal hypertension

• Complete compensatory hypertrophy and hyperplasia is reached by 6 days post-op

  • impeded by:

    1. age

    2. biliary obstruction

    3. diabetes mellitus

    4. malnutrition

What is a hepatoma?

Well-demarcated, benign homogenous hepatocyte proliferations within the liver parenchyma - often incidental findings

What is the most common malignant liver cancer in the dog? (~50%)

Hepatocellular carcinoma

ALP and ALT are elevated in 90% of cases

massive form treated surgically if amenable to resection - no effective treatment for nodular/diffuse form (poor prognosis)

1460 days MST post resection of massive form.

Primary hepatic metastatic tumors in dogs/cats

• Bile duct carcinoma

  • 90% metastatic rate

  • MST approx. 6 months

• Hepatobiliary cystadenomas

  • Older cats

  • Can be multicentric or solitary

  • Good prognosis if surgical resection feasible

• Hepatic neuroendocrine tumors

  • Tend to be nodular or diffuse

  • Typically not amenable to surgical resection

  • 90% metastatic rate

When TBILI on abdominal fluid is >serum TBIBI or when bile pigment is identified on cytology of abdominal fluid we can diagnose ____________

Bile peritonitis

underlying causes

1. blunt abdominal trauma - may not manifest for 2-3 days

2. necrotizing cholecystitis

3. ruptured gall bladder mucocele

Surgical options

1. biliary re routing surgeries

2. cholecystectomy

What is the Pringle Maneuver?

• Emergency procedure performed intraoperatively to halt or slow major blood loss

• The mesoduodenum is retracted to the left

• The index finger is slid along the ventral wall of the caudal vena cava in a cranial direction

• The thumb of the same hand is used to compress the tissue between it and the index finger, resulting in simultaneous compression of the hepatic artery and portal vein

• Can be maintained for 20 mins if necessary while source of hemorrhage is controlled.

What is the purpose of a hepatic biopsy? How would you perform one?

• Biopsy allows liver disease to be characterized

  • Neoplasia (benign vs malignant)

  • Inflammatory, infection, infiltrative

• Liver cytology vs histopathology

  • Much better chance of definitive diagnosis with biopsy

    • Agreement between ultrasound guided FNA and surgical wedge biopsy is often suboptimal (30-40%)

  • Percutaneous aspirate is usually done with ultrasound guidance

  • Small biopsy device (14g - removes a core of tissue) is preferable to fine needle

• Laparoscopic biopsy permits removal of a larger tissue sample.

• Focal lesions present

  • Periphery of lobe

    • Wedge technique

    • Guillotine technique - crush artifact

  • Center of lobe

    • Skin punch technique

Which liver lobe should you avoid sampling?

Caudate liver lobe - this has the best perfusion, disease in the caudate lobe is underestimating.

Sample 1cm x 1cm x 1cm

at least 3 liver lobes

• Q: 9 yo MN mixed breed with an abdominal mass. You find a large liver mass. You are not comfortable removing it and decide to biopsy. What technique would you use?

  • Guillotine

  • Wedge

  • Skin punch

  • Laparoscopic forceps

Skin punch

Indications of a liver lobectomy? Techniques?

Indications

• Solitary liver masses where resection path does not compromise caudal vena cava (midline), portal vein (right side) or common bile duct (right side)

• Tumorts of left lateral and medial liver lobes are the easiest

• Significant risk of hemorrhage

Techniques

• Blunt fracture through parenchyma and hemoclips/cautery

• Overlapping mattress sutures

• Thoracoabdominal stapler

  • Fires 2 or more rows of staggered titanium staples

  • Available in 3 different widths and different heights of closed staples

  • Greatly simplify liver and lung lobe resection

• Ligasure

• Pre-tied ligating loop

True or false: you always ned to ensure potency of MDP and CBD before cholesytectomy

true

Recommended stoma size for re-routing procedure of CBD?

2.5 cm long to minimize stricture off the stoma and decrease the likelihood of enteric reflux becoming entrapped in liver.

Indications and techniques for splenectomy

Indications

• Neoplasia - Most common

• Hyperplasia

• Torsion

• Abscessation

• IMHA/ITP

Techniques

• Hilar ligation 

  • Clamp vessels within each segment between two Carmalt clamps starting at tail of spleen

  • Ligate patient side and transect between clamps

  • Ligate entire group of vessels with 2-0 or 0 absorbable suture

  • Double ligate splenic artery

• Ligasure

  • Computer regulated cautery device

  • Higher current than normal cautery, current is rapidly turned on and off

  • Melts collagen and elastin and then allows repolymerization

  • Seals vessels up to 7mm in diameter

  • Seal withstands 3x normal systolic pressure

• Three-point ligation

  • Pancreatic vessels to avoid

  • Come really close to hilus

• Laparoscopic assisted (not for hemoperitoneum)

  • Indications

    • Generalized splenomegaly

    • Small medium focal nodules/masses

  • Contraindications

    • Large masses

    • Active hemorrhage

    • +/- ascites

    • Coagulopathy varicosities

• Ventral midline celiotomy 

• Suction blood to improve visualization

• Explore abdomen, look for metastases

• Exteriorize spleen

At least three complications after splenectomy

• Reduced athletic performance - may be significant for working/competition/racing dogs

• Increased tendency to GDV in deep chested dogs - in this situation splenectomy is often combined with gastropexy

• Lifelong risk of blood borne infections (babesia)

• Hemorrhage - rare with good surgical technique

• Portal vein thrombosis - usually fatal

• Arrhythmias - common itnra- and post-op and associated with anemia and hemoabdomen due to myocardial ischemia/hypoxia

• Overwhelming post-splenectomy infection - human phenomenon

Do dogs or cats have a sinusoidal spleen

Dogs = sinusoidal spleen

Cat = nonsinusiodal spleen