22.ACUTE LIVER DISEASES IN CATS, FELINE HEPATIC LIPIDOSIS.

Question 1

FELINE HEPATIC LIPIDOSIS - FATTY LIVER

OCCUR

Answer 1

• Most common primer hepatopathy in cats in USA (Europe 2.)
• acute-subacute—(chronic)
• Domestic, indoor, shorthair, 4-15 years cats
• No breed or sex predilection
• High mortality without treatment, potentially reversible with agressive treatment
  MULTIFACTORIAL
• Obese cat→ stress, prolonged anorexia (maldigestion)
• If the cause unknown: idiopathic HL (IHL)
• Most common is the secondary hepatic lipidosis (85%):

Question 2

SECONDARY HEPATIC LIPIDOSIS

Answer 2

• Hepatic lipidosis is the consequence of metabolic/infective diseases
• Not necessary obesitas, only stress (anorexia)
  Cause
• FORL
• Diabetes mellitus
• IBD, Pancreatitis
• Cardiomyopathy
• FIP
• Chronic kidney disease
• Neoplastic or neurologic disease
• Hepatopathy (pl. cholangitis)
• Toxins, drugs (tetracyclin)

Question 3

CLINICAL SIGNS OF FELINE HEPATIC LIPIDOSIS

Answer 3

CLINICAL SIGNS OF FELINE HEPATIC LIPIDOSIS
- anorexia, depression, dehydration
- Obese cat loose weight (25%), mostly muscle lost
o Obesity not required by secondary form
- GI signs (nausea! vomitus, diarrhoea, or obstipation)
- icterus, hepatomegaly
- Severe case: coagulopathy
o K vitamin depletion due to cholestasis
o Not able to produce enough factors
- Hepatic Encephalopathy: depression, salivation
o Cat look like zombie and salivate
- Electrolytes ↓ (K, P, Mg) B1: ventroflexion of head/neck
- Secondary HL: ↓ original disease

Question 4

DIAGNOSTICS

LABORATORY FINDINGS

Answer 4

DIAGNOSTICS
LABORATORY FINDINGS
- Mild-moderate non-regenerative anaemia, poikilocytosis
- Intrahepatic CHOLESTASIS (hepatocyte swelling)
o ALT, AST up, ALP upup, but!!! GGT same/up, SBA up
- Acute liver function failure: Br, SBA, BUN
- NH3↑: urea cycle, Arginine! in HE
- Coagulopathy (PIVKA…), PTT (APTT)
- Glucose up: stress, hormones insulin resistance, glucose intolerance
- Electrolyte↓: K, P, Mg
CYTOLOGY, FNA (GIEMSA, DIFF-QUICK, SUDANIII)
- orientating, usually enough to suspected diagnosis
- ” foamy” cytoplasm, lipid accumulation without zonal distribution
- NO necro-inflammatory….
- mild lipid accumulation ≠ severe lipidosis!
o FHL: >70-80% hepatocytes involved!
ULTRASOUND
- Hepatomegaly, hyperechogenic liver (DD: amyloidosis, lymphoma)
LIVER BIOPSY (LAPAROTOMY, LAPAROSCOPY, (US TRUE CUT – OLD METHOD)
Diagnosis, stage of diseases
- Gold standard, but dangerous!
o Dangerous due to coagulopathy – could make haemorrhage
o Anaesthesia is also dangerous for the animal
- anaesthesia, K-dependent coagulopathy, HE
- If not respond to treatment within 3-5 days we should do biopsy
Lipid 50→500 g/kg
Histopathology: hepatocyte vacuolisation
- + min. necrosis BUT! without inflammation
- Necrosis ↔ inflammation
- Necrosis ↔ cholestasis

Question 5

TREATMENT

Answer 5

• Intensive forced feeding  Without it the animal will die
• Avoid re-feeding syndrome – gradual increase of feed
• Treat the background causes
• Treatment of hepatic encephalopathy
• Treatment of coagulopathy
• Glucocorticoid contraindicated
  o ↑ Lipolysis and fat accumulation
  o ↑ Catabolism
• Good quality diet, without protein restriction
  o Hun sier good quality diet with good amount of protein??
  stabilization, parenteral fluid, electrolyte and acid-base correction
• especially before anaesthesia, hepatic encephalopathy
• hypokalaemia: Ringer or Ringer acetat + 20 mEq/l KCl
  o with high amount of potassiumchloride
• Mg, P↓
• no: too much dextrose (CHO↑ fat synthesis of liver, TG accum., osmotic diuresis)
• no: lactate – contraindicated in hepatic issues
  Forced feeding
• 3 days nasogastric tube → stabilization →oesophagostomy/gastrostomy
• 4-6 weeks permanent tube
• Calory requirement: Metabolizated energy Kcal (Kcal=4,18 KJ)
• RER=70 (kg 0.75)
• MER (metabolic energy requiremnt)= 132 (kg 0.75) MER=1,4 (30 x kg+70) or 70 x kg
  o Depends on the activity 60-90 kcal x kg (70-80 kcal/kg)
• Liquid diet 0.9-1,3 Kcal/ml
  o Gradually:(re-feeding) 1.day: 1/3 ME
  o 2.day: 2/3 ME 3.day: ME requirement in 2-3 parts
  o Divide the feed for a gradual build up of the feeding
  Hepatic encephalopathy:
• frequently, small amount
• Not necessary decrease the protein, only in severe signs or high NH3, temporary. Better to increase protein tolerancy
  Diet:
• High protein
• No fat supplementation (fat low)
• Low CHO
• Decrease protein only in severe HE! (k/d)
  Diet supplementation – not as important
• Arginine, Taurine, Carnitine: 250 mg/kg (??)
• K1 vitamin: 0,5 mg/kg 2x sc min. 3 days
• B vitamin: 1-2 ml B vitamin/l Thiamine (B1))-100 mg/cat/day
• B12 ! 250 ug – expensive to test levels, just give anyways as cats are sensitive to low levels
  Gastroparesis 30’ before feeding metoclopramide 0.2-0.5 mg/kg
• Antiemetic: maropitant 1 mg/kg
• Glucocorticoid contraindicated. Apetisers (?)
• Proton pump inhibitor (ROS) omeprazole, pantoprazole 1-2x 1 mg/kg
  Antioxidant Glutathione stores depleted Meth →Gluth
• SAMe 20 mg/kg 1x
• NAC 70 mg/kg iv
• E vitamin 100 NE im (10-20 NE/kg per os)
• silymarin 20 mg/kg

Question 6

IDIOPATHIC HEPATIC LIPIDOSIS

PATHOGENESIS

Answer 6

IDIOPATHIC HEPATIC LIPIDOSIS
PATHOGENESIS
MULTIFACTORAL
- Obligate carnivore, high protein requirement (3,5-4 g/kg; 35-45% DM)
- GNG, resting protein catabolism, can not stop postprandial enzyme activity
- essential amino acids: Arginine! Methionine, Taurine, Carnitine - need arg for urea cycle
Fasting: → Lipid accumulation
- ↑ FFA mobilization from peripheral fat stores (anorexia, stress)
- ↓ lipoprotein synthesis
- Triglycerides accumulate in hepatocytes as it cant be transported
Metabolic factors:
- Fasting → E/protein decreased → lipoprotein synthesis (VLDL)down → TG up → lipid accumulation
- Arg, Meth, Taurine down
- Carnitine down →FFA oxidation down
Arginine↓→urea cycle NH3 metabolism↓→ HE, ammonia↑
Neuroendocrine response: ↓insulin/glucagon (?)
- LPL↓: lipoprotein lipase → fat uptake by adipocytes
- HSL↑: hormone sensitive lipase → lipolysis, FFA mobilization

Question 7

DIAZEPAM, CLONAZEPAM

Answer 7

DIAZEPAM, CLONAZEPAM
-	Acute, fulminant liver failure, with high mortality
-	Idiosyncratic drug reaction 
-	Only in Cat
-	Minimum 5-13 days 1-2.5 mg per os
o	Several days to cause toxicosis
-	Centrolobular necrosis
-	In normal case does not cause liver enzyme ↑
-	toxicosis: ↑↑↑ liver enzymes, especially ALT
Treatment:
-	Stop the drug
-	Intensive therapy
-	Poor prognosis

Question 8

FIP

Answer 8

FIP

• Coronavirus
• Pyogranulomatos hepatitis, multifocal hepatic necrosis
• liver covered by thick layer of fibrin
• immune-complex (IC) vasculitis
• multisystemic: peritoneum, pleura, brain, eyes, parenchymal organs