Flashcards in Equine Icterus and Hepatic Encepalopahy Deck (59):
What blood results are likely to be seen in pre-hepatic hyperbilibinamia? `
- Primarily UNconjugated bilirubin (+- conjugated if > liver capacity)
What are the most common causes of haemolysis in horses?
- NI (neonatal isoerythrolysis, an IMHA) due to incompatibility beween sire and dam blood type
- Infections eg. EIA
- Drugs eg. Penicillin
- Toxins eg. oion
- True autoimmune HA [rare]
What blood results may be seen with hepatic hyperbilirubinaemia?
Increased unconjugated aswell
What is the most common cause of hepatic icterus in horses?
> Anorexia for >2d (-> shortage of ligandin [release usually stimulated by eating] protein responsible for unconjugated bilirubin uptake into liver)
- Also any acute hepatocellular disease
Why are horses difficult when diagnosing icterus?
10-15% normal horses look mildly icteric
Is post-hepatic icterus common in horses?
Give 2 most common causes of post-hepatic icterus in horses
-> impaired excretion of bilirubin
How is cholestasis defined diagnostically?
Conjugated bilirubin >30%bilirubin
How common are PSS in horses?
What are the firs 3 questions to ask yourself when presented with an icteric horse?
- Anorexic? = do nothing, feed
- Foal? = NI
- Pale? = Heamolyic aneamia
-> If none of these, most likely hepatic causes (liver disease)
Give 6 functions of the liver
1. Bile excretion
2. Protein metabolism
3. Carb metabolism
4. Lipid metabolism
6. Immune system (Kuppfer cells)
How do bile acid tests differ in horses?
No need for pre- and post- prandial as no gall bladder so bile excreted continuously
What does the impressive regeneration and reserve capacity of the liver mean clinically?
- Likely to have dysfunctioned for several days prior to onset of clinical signs
- BUT able to regenerate so hepatic disease is not always followed by hepatic failure
What are common clinical signs of liver dysfunction in horses? Less common signs?
- Colic (mild, due to hepatocellular swelling and biliary obstruction)
- Abnormal behaviour
- Weight loss (chronic disease, v food intake, metabolic dysfunction)
> Bilat laryngeal paralysis
> Haemorhagic diathesis
> Dependent oedema
What is the general pathogenesis of hepatic encephalopathy?
- v ammonia clearance and ^ aromatic AAs (cf. Branched chain AAs) -> false neurotransmitters and neurotoxicity
What causes photosensitisation?
Phylloerythrin - photodynamic agent formed by bacteria in gut - usually absorbed, conjugated and excreted by liver
- liver dysfunction -> ^ phylloerythrin
- exposure to UV -> cell membrane damage and necrosis
Give 4 diagnostics useful for working up liver disease
- Clinical signs
- Blood work
Which 3 blood parameters are most liver specific?
- Bile acids
- GGT (also excreted by kidney and mammary but never into blood stream except from liver)
What can be seen on hepatic ultrasonography?
> Only 20% of liver!!! Lung overlies
- size (estimate)
- changes in echogenicity
- dilated bile ducts, abscesses, neoplasia
What are the general principles of treatment of hepatic disease?
- Supportive, goal to maintain animal until liver regenerates
- Correct acid/base balance and fluid deficit (due to v intake)
- IV glucose if anorectic
- ABs if suspect infection
What change suggests regeneration is unlikely?
How can hepatic encephalopathy be treated?
- Sedation *CAREFUL! Horses unaware of suroundings*
- Manitol/hypertonic saline: cerebral oedema
- Oral lactulose to limit ammonia abdorption long term
- oral BCAAs (no evidence for this but does no harm)
- Dietary modification
How may the diet be modified to minimise effects of hepatic encephalopathy?
- ^ carbs, limited protein BUT DO NOT RESTRICT!! (horses v protein diet anyway so further restriction not helpful)
- Recommended diet
> Beet pulp
> Cracked corn
> Sorghum, bran, milo (instead of beet pulp)
> Oat/meadow hay (not Lucerne or alfalfa)
- BUT if this is all horses will eat then let them
Give 4 anti-inflamatories commonly used for treatment of liver disease. Which are most commonly used?
- NSAIDS (flunixin meglumine)
- Corticosteroids (dexamethasone, prednisolone [care-> laminits])
> DMSO (smelly, carcinogenic, free radical scavenger, used rarely)
> Pentoxyfylline to limit fibrosis (used rarely)
Is liver disease usually diagnosed as a specific pathology?
No [liver has minimal ways to respond to insult and aetiological agent often not seen on biopsy]
- PA toxicity
May be diagnosed definitivel
What is the technical name for ragwort poisoning?
Pyrrolizidine Alkaloid toxicity
Is ragwort poisoning a long or short term effect? Pathogenesis?
Long term - ingested over 4-12 weeks [initially clinically silent]
> Pyrrolizidine alkaloids metabolised by liver to toxic pyrrole derivatives
> Anti-mitotic by crosslinking DNA in hepatocytes
> Megalocyte production, death and fibrosis
How is ragwort ingestion supposedly minimised?
Ragwort control Act 2003
What specific finding indicates pyrrolizidine poisoning?
Megalocytosis of hepatocytes on biopsy.
- clinical signs often non-specific
- history of ingestion may hint
In which breeds is hyperlipaemia common?
- Sheltlands, miniatures, ponies
- Obese animals
When is hyperlipaemic disease seen?
Negatvie energy balance due to disease, stress, pregnancy, lactation etc.
Which enzyme releases fatty acids from adipose tissue?
Hormone sensitive lipase
Which enzyme encourgaes uptake of TG/VLDLs to the tissues?
Why can hyperlipaemia result from a normal physiological process in NEB?
Excess FA delivery and TG production (ponies/miniatures v. good at this!!)
What clinical signs are associated with hyperlipaemia?
- icterus (liver doesn't function as well when full of fat)
- mild colic and D+
+- more severe liver disase signs
How is hyperlipaemia diagnosed?
Bloods - measure TGs in serum by PCV
> also predisposition of breed, history and clinical sign
+- liver biopsy
Which is more severe, hyperlipidaemia or hyperlipaemia?
What is the treatment for hyperlipaemia?
1. Reverse NEB (encourage to eat or force fed)
2. Treat hepatic disease with supportive therapy
3. Eliminate stress/treat concurrent 1* disease (?wean foal)
4. Inhibit further fat mobilisation (restore + energy balance, give INSULIN to inhibit hormone sensitive lipase.
5. ^ TG uptake by peripheral tissues - HEPARIN increases activity of lipoprotein lipase. Probably not that useful as likely to already be maximally active.
What is the prognosis for hyperlipaemia?
Poor once severe clinical signs apparent but good if caught early - always suspect!
> monitor TG levels in sick ponies
> ensure adequate nutrition
> prevent obesity
What is the treatment and prognosis for pyrrolizidine alkaloid toxicity?
No specific treatment
- Poor prognosis
- Death <10d after clinical signs of liver failure
- Regneration NOT possible if fibrosis present and megalocytoisis extensive
Give 5 causes of acute hepatitis
1. Theiller's disease
2. Bacterial - Tyzzers disease
4. Viral - EHV in foals, EIA, EVA adults
5. Parasitic (migration of Parascarus Equorum, Strongylus edentatuseuinus/vulguris)
What is the cause of theillers disease?
> outbreaks or single cases
What other names is Theillers disease known by?
- Serum sickness
- Acute necrotic hepatitis
- Serum associated hepatitis
What is the pathology associated with Theillers disease and how is it diagnosed?
- Widespread hepatic necrosis
- Small liver at PM
- Dx: history, abrupt onset of clinical signs, hepatic insufficiency
What is the treatment and prognosis of Theillers disease?
No specific treatment, prognosis poor if severe HE seen
What is the common name for infectious hepatitis? Which organism is responsible?
> Tyzzers disease
> Clostridium piliformis
What aged horses are seen with Tyzzers disease?
Only foals 7-42d
What clinical signs are assocated with Tyzzers disease?
May be none - found dead
Otherwise non-specific, off suck, depression, recumbency
What is the pathogenesis of Tyzzer's disease?
- Multifocal hepatitis and enteritis
How may Tyzzer's be definitively diagnosed?
Post-mortem: ID microorganism
How is Tyzzer's treated? Prognosis?
ABs, supportive therapy
> Prognosis grave. Only 1 known report of successful treatment
What is the pathogenesis of cholelithiasis/cholangiohepatitis?
- cause for stone formation often unknown
> ascending biliary tract infection/inflammation
> biliary stasis
Why is gallstones never diagnosed in horses?
They have no gallbladder - Instead BILE DUCT stones present
What clinical signs are strongly indicative of cholelithiasis/cholangiohepatitis?
Fever + icterus + colic = strongly suggestive
How may cholelithiasis be more definitively diagnosed?
> Enzymes (GGT, SDH, AST)
> Ultrasound (dilated bile ducts, choleliths)
> Biopsy (histopath for inflammation, culture for ascending infection)
How is cholelithiasis treated?
- Longterm antimicrobials (weeks/months)
- Supportive care
What is the prognosis for cholelithiasis?
- dependant on number and extent of choleliths, fibrosis, severity of clinical signs
What are the 4 main diseases of the liver?
> Pyrrolizine alkaloid toxicity
> Unknown cause!