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Small Animal Final Year > SA Acute Liver Disease > Flashcards

SA Acute Liver Disease Flashcards

1
Q

What are some examples of toxic/drug induced causes of acute liver disease (acute hepatitis) in dogs?

A
  • Examples include:
  • phenobarbitone
  • carprofen (esp. Labrador retrievers)
  • potentiated sulphonamides
  • environmental toxins e.g. mushrooms
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2
Q

What are some examples of infectious causes of acute liver disease (acute hepatitis) in dogs?

A
  • Examples include:
  • Leptospira
  • CAV-1. neoneatal canine herpes virus
  • bacteria from the GIT i.e. ascending infection via the bile duct – access point possibility. May never locate the bacteria!
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3
Q

How can the clinical signs severity vary with acute liver disease?

A

Can be low-grade disease: may be mild or non-existent, may miss them and they may come and go – often don’t need treatment, the liver just deals with it

Signs may be due to the underlying cause and/or other body systems involved

As disease progresses or becomes more severe –> more classic signs develop

Clinical signs are often variable and non specific

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4
Q

What are some NON SPECIFIC signs of acute liver disease?

A
  • anorexia
  • vomiting/haematemesis
  • diarrhoea/melaena
  • PU/PD
  • jaundice
  • dehydration
  • fever
  • cranial abdominal pain – may mimic pancreatitis, may have all of these things with pancreatitis or acute liver disease
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5
Q

What are some other clinical signs we can see with acute liver disease?

A
  • hepatic encephalopathy
  • depression
  • seziures
  • coma
  • Hepatomegaly
  • If large and painful, may think more of acute liver diseasae
  • evidence of coagulopathy
  • petechial haemorrhages
  • GI bleeding
  • ascites and portal hypertension
  • more likely in chronic disease, but sometimes if you have acute, significant swelling of hepatocytes, then it might be that this might be enough to cause portal hypertension
  • can occur due to hepatocyte swelling
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6
Q

What are some markers of hepatocellular damage?

A

ALT, AST ­increased first

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7
Q

What are some markers of cholestasis?

A

ALP, GGT increased­ later

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8
Q

What are some markers of liver function?

A
  • bilirubin – sometimes delayed ­
  • bile acids
  • variable and depend on cholestasis
  • only useful when bilirubin is normal or only very mildly elevated
  • ammonia increased­ - ammonia is not an easy test to run –needs careful and rapid processing which means it is rarely useful in practice.
  • +/- hypoglycaemia
  • +/- coagulopathy
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9
Q

How should you manage acute liver disease?

(long one, soz)

A
  • Supportive- very important!
  • intravenous fluid support
  • avoid lactated ringers solution/Hartmanns
  • liver cannot metabolise lactate as the buffer, might be a situation where normal saline might be a better fluid to give than haartmans
  • monitor serum potassium and supplement in iv fluids as necessary
  • monitor blood glucose regularly and supplement if necessary
  • Treat the cause if known, for example:
  • antibiotics for leptospirosis
  • stop hepatotoxic drugs
  • N-acetylcysteine for paracetamol toxicity
  • Treat hepatic encephalopathy
  • Manage coagulopathy as necessary
  • fresh frozen plasma
  • Vitamin K therapy might help
  • Treat any gastrointestinal ulceration
  • GI bleeding can be aggravated by coagulopathy
  • Control vomiting
  • maropitant: use with caution due to hepatic metabolism – use this if we think acute or live failure case
  • consider CRI metoclopramide?
  • Diet:
  • short period of starvation while any vomiting is controlled
  • do not starve for > 24-48 hours – if much beyond this, might need to think about enteral nutrition in these cases
  • Anti-emetics
  • palatable low fat high quality diet
  • do not restrict protein as this may inhibit hepatocyte regeneration – need to keep liver well fed, needs high quality protein
  • Other symptomatic and supportive therapy:
  • e.g. ursodeoxycholic acid, anti-oxidants
  • Antibiotics: broad spectrum agents safe for use in liver disease include:
  • ampicillin, amoxicillin, metronidazole (at ¯ dose) and fluoroquinolones.
  • use iv in the acute stages
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10
Q

When supporting the acute liver disease patient with fluids, which fluids should you use and which should you avoid and why?

A

avoid lactated ringers solution/Hartmanns

liver cannot metabolise lactate as the buffer, might be a situation where normal saline might be a better fluid to give than haartmans

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11
Q

What can you give to manage coagulopathy as necesary with acute liver disease?

A
  • Manage coagulopathy as necessary
  • fresh frozen plasma
  • Vitamin K therapy might help
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12
Q

How can you control vomiting with acute liver disease?

A
  • maropitant: use with caution due to hepatic metabolism – use this if we think acute or live failure case
  • consider CRI metoclopramide?
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13
Q

How can you use diet to manage acute liver disease?

A
  • short period of starvation while any vomiting is controlled
  • do not starve for > 24-48 hours – if much beyond this, might need to think about enteral nutrition in these cases
  • Anti-emetics
  • palatable low fat high quality diet
  • do not restrict protein as this may inhibit hepatocyte regeneration – need to keep liver well fed, needs high quality protein
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14
Q

Why should you not restrict protein when managing acute liver disease?

A

do not restrict protein as this may inhibit hepatocyte regeneration – need to keep liver well fed, needs high quality protein

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15
Q

Which antibiotics should you use for the management of acute liver disease?

A
  • Antibiotics: broad spectrum agents safe for use in liver disease include:
  • ampicillin, amoxicillin, metronidazole (at ¯ dose) and fluoroquinolones.
  • use iv in the acute stages
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16
Q

What is the prognosis for acute liver disease?

A
  • Difficult to predict because varies with extent of damage
  • Full recovery is possible but can progress to chronic disease (hepatitis, fibrosis and cirrhosis)
  • Severe cases can require a high level of intensive care
  • refer to a specialist centre if possible
  • Can take a waxing and waning course despite treatment
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17
Q

What are some negative prognostic indicators with regards to the prognosis of acute liver disease?

A

Negative prognostic indicators include presence of :

  • ascites and splenomegaly
  • suggests portal hypertension has developed
  • can still be reversible in acute disease
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18
Q

How does fibrosis develop with regards to acute liver disease?

A
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19
Q

What are some examples of canine infectious liver diseases?

A
  • Canine infectious liver disease
  • Leptospirosis
  • Canine adenovirus 1
  • (Canine herpesvirus)
  • ((Canine acidophil cell hepatitis))
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20
Q

What is the causal organism of Leptospirosis?

A
  • Causal organism: Leptospirosis interrogans (sensu lato)
  • Leptospira spp are motile spirochaetes
  • Several serovars can cause clinical signs in dogs
  • L. icterohaemorrhagiae (rat host) à liver
  • L. canicola (dog host but almost eradicated) à kidney
  • L. grippotyphosa (rodent host)
  • Others e.g. L. bratislava. L.pomona
21
Q

How can animals get Leptospirosis?

What is the incubation period?

A
  • Passed in urine –> mixture of direct/indirect transmission
  • Organisms penetrate mucosal surfaces and can be absorbed here also
  • Incubation period is usually ~ 4–12 days

•

•Clinical disease usually affects liver and kidneys

22
Q

Where does the clinical disease of Leptospirosis usually affect?

A

Clinical disease usually affects liver and kidneys

23
Q

What organ systems do we need to consider with regards to leptospirosis?

A

•Renal involvement is most common à AKI due to

  • swollen tubular epithelial cells
  • tubular necrosis
  • mixed inflammatory reaction may be seen

•Liver is a target organ

  • can be the only site affected – if kidney parameters are normal does not mean the dog doesn’t have lepto. If you have the 2 together – lepto can be very likely
  • liver involved in approx. 10-20% dogs with AKI
  • gross appearance: swollen and friable
  • icterus is common
  • microscopic findings may include:
  • hepatocytic necrosis,
  • nonsuppurative hepatitis
  • intrahepatic bile stasis
24
Q

With leptospirosis, you get acute kidney injury - why?

A
  • swollen tubular epithelial cells
  • tubular necrosis
  • mixed inflammatory reaction may be seen
25
Q

Liver is a target organ for Leptospirosis.

What damage does it do and what do we see?

A
  • can be the only site affected – if kidney parameters are normal does not mean the dog doesn’t have lepto. If you have the 2 together – lepto can be very likely
  • liver involved in approx. 10-20% dogs with AKI
  • gross appearance: swollen and friable
  • icterus is common
  • microscopic findings may include:
  • hepatocytic necrosis,
  • nonsuppurative hepatitis
  • intrahepatic bile stasis
26
Q

What are the clinical signs of Leptospirosis?

A
  • Vary with dose, serovar and level of immunity
  • Peracute leptospiraemia
  • pyrexia, pain, shock, death
  • Acute disease
  • pyrexia, anorexia, dehydration, PD, V+
  • Petechiae and ecchymoses (due to vascultitis +/- ¯ platelets)
  • Jaundice (common)
  • Oliguric acute renal failure –> anuric renal failure (important to monitor urine output)
  • Arthralgia and myalgia
  • Dyspnoea- consider “atypical disease” –> pulmonary involvement à LPHS
27
Q

If you get disease progression with Leptospirosis - what happens in the body?

A

Disease progression:

  • SIRS and MODS –> fatal
  • Chronic renal or hepatic failure
28
Q

What do you see on haematology and biochemistry with Leptospirosis?

A
  • Clinical presentation: any dog that presents with acute liver or renal disease, especially if unvaccinated
  • Haematology (cell counts and smear):
  • mild to moderate neutrophilia
  • thrombocytopaenia (20% cases)
  • Biochemistry
  • azotaemia
  • hyperkalaemia
  • elevated liver enzymes
  • elevated bilirubin (20% cases)
  • Urinalysis: consistent with AKI (30% cases)
  • active urine sediment
  • Coagulation times normal unless progress to DIC
29
Q

Definitive diagnosis of Leptospirosis can be very challenging.

What do you see with PCR and antibody titres?

A
  • PCR of organism from urine and blood
  • samples collected before antibiotic most helpful
  • Antibody titres (MAT)
  • if high in unvaccinated dogs could be diagnostic
  • need a rising titre in vaccinated dogs
  • most convincing is with rising titre (4 fold increase in 2-4 weeks)
  • low in chronic disease therefore not helpful for carrier state
  • false negative (low) results if antibiotics have been given
30
Q

What are some things you need to do with the management of leptospirosis?

A
  • Supportive treatment is important: symptomatic patients are often critical care cases
  • Supportive
  • IVFT – saline, dextrose saline – saline may be better than haartmans
  • Manage AKI if necessary:
  • to maintain urine output
  • furosemide/mannitol/glucose
  • to manage electrolyte disorders (esp. hyperkalaemia)
  • Control vomiting
  • CRI metoclopramide?
  • ondansetron?
  • low dose maropitant?
  • Provide nutrition
  • Liver support drugs
  • especially SAMe and vitamin E
  • other antioxidants
31
Q

How can you manage AKI with regards to management of Leptospirosis?

A

Manage AKI if necessary:

  • to maintain urine output
  • furosemide/mannitol/glucose
  • to manage electrolyte disorders (esp. hyperkalaemia)
32
Q

What is the specific treatment to kill leptospires?

Which drugs are recommended?

A

Early antibiotic treatment is strongly reccomended

  • Penicillin G, ampicillin or ampxycillin for 2 weeks
  • kill circulating organisms very effectively
  • does not remove the carrier state
  • Doxycycline for 2 weeks
  • elimination of carrier state
  • start with a penicillin
  • may cause vomiting and not always tolerated in acute cases – so tend to reserve doxycycline for during recovery phase
33
Q

Why do you reserve doxycycline for the recovery phase of Leptospirosis?

What shoudl you start with instead?

A
  • start with a penicillin
  • may cause vomiting and not always tolerated in acute cases – so tend to reserve doxycycline for during recovery phase
34
Q

What is the prevention of Leptospirosis with regards to vaccination?

A
  • Inactivated organisms
  • Serovars historically have been Icterohaemorrhagica and Canicola
  • Newer vaccines now include Australis and Grippotyphosa (ie 4 serovars)
  • Duration of immunity variable in different animals
  • probably does need annual vaccination unlike other vaccines
  • Serology to assess vaccination efficacy?
  • correlation between antibody levels and protection is poor
35
Q

What is the prevention of Leptospirosis with regards to lifestyle?

A
  • reduce access to potential sources of exposure
  • avoid drinking from or wading/swimming in fresh or stagnant water sources and marshland
  • control rodent sources
  • avoid hunting or access to wildlife
36
Q

What is arrowed here with regards to canine adenovirus 1?

A
  • Tropism for vascular endothelium and hepatocytes
  • inclusions in hepatocytes are pathognomonic
37
Q

What is the prevalence of Canine adenovirus 1?

What is the transmission?

Where does it have tropism for?

A
  • Very low prevalence due to efficacy of vaccine
  • usually seen in unvaccinated dogs
  • Natural exposure suspected
  • non-vaccinated dogs often carry neutralising antibodies
  • Transmission: faeco-oral route
  • Tropism for vascular endothelium and hepatocytes
  • inclusions in hepatocytes are pathognomonic
38
Q

What are the clinical signs of Canine Adenovirus 1?

(Peracute and Acute)

A
  • Peracute disease
  • non-specific rapidly fatal condition without obvious clinical signs
  • Acute disease
  • clinical signs (5-7 days) associated with hepatic necrosis and diffuse endothelial damage:
  • vomiting, diarrhoea, abdominal pain
  • jaundice
  • petechial or ecchymotic hemorrhages
  • DIC may occur due to
  • failure of hepatic processing of clotting factors
  • endothelial damage
  • CNS signs due to HE or encephalitis
39
Q

What are the ocular clinical signs of Canine Adenovirus 1?

A
  • Ocular signs
  • corneal oedema –> blue eye due to
  • immune complex deposition – eye and kidney are very susceptible to deposition
  • corneal endothelial damage
  • anterior uveitis
40
Q

What is the diagnosis of Canine Adenovirus 1?

A
  • Clinical presentation: any young unvaccinated dog with acute hepatitis
  • DD: include leptospirosis, (parvovirus, distemper)
  • Haematology (cell count and blood smear)
  • leucopenia – early stages neutropenia and lymphopenia
  • leucocytosis – recovery stages
  • Biochemistry: as expected for acute hepatitis
  • ­ ALT, AST> GGT, ALP
  • ­ bilirubin
  • Prolonged coagulation times +/-DIC
  • Confirmation/definitive diagnosis:
  • serology (unvaccinated dog)
  • PCR (sometimes)
41
Q

Histologically, what is the main damage to hepatocytes with regards to Canine Adenovirus 1?

A

Histologically, the main damage is to hepatocytes and endothelium (blood vessels – hence the haemorrhaging).
The liver contains areas of necrosis and adenoviral inclusion bodies are seen in Kupffer cells and parenchymal cells.

42
Q

What is the treatment for Canine Adenovirus 1?

A

Treatment

  • Supportive as for any severe acute hepatitis
  • We have no specific antiviral drugs that would help
  • Outcome depends on
    • severity
    • development of widespread complications such as DIC
43
Q

What can septicaemia and endotoxaemia cause?

What can they progress to?

A
  • Both are recognised causes of acute liver disease
  • Severity of systemic consequences are usually related to the primary condition
  • Cytokines from systemic inflammation/sepsis lead to functional hepatic impairment
  • Various changes histologically – non-specific
  • Clin path – elevated bilirubin and liver enzymes
  • Can progress to SIRS and MODS – liver has blood supply from blood and from normal arterial circulation, therefore double whammy potential of having infectious organisms delivered
  • Liver involvement in septicaemic patient – might well be this is the sort of situation that is happeneing
44
Q

What is hepatic encephalopathy?

A

HE is a neuro-physiologic disorder of the central nervous system (CNS)

45
Q

What is the main aim of therapy for the treatment of hepatic encephalopathy?

A
  • Main aim of therapy:
  • to decrease formation of gut derived encephalotoxins
  • ie decrease ammonia
  • Want to minimise toxins, ammonia main one, but there are others.
46
Q

What is the management of acute hepatic encephalopathy?

A
  • Identify, remove and treat precipitating causes:
  • gastrointestinal bleeding
  • constipation
  • metabolic alkalosis
  • Hypokalaemia – complicated! Will precipitate and aggravate hepatic encephalopathy
  • azotaemia
  • inflammatory disease
  • IVFT
  • crystalloids (avoid lactated ringers (Hartman’s solution))
  • Glucose
  • monitor and supplement as needed
  • Diet:
  • feed a high quality diet little and often ASAP
  • protein/calorie malnutrition will ­increase NH3 formation by catabolism of body protein
  • Warm water/lactulose enemas:
  • to remove any source of ammonia from the faeces
  • can be followed by a neomycin retention enema
  • Ampicillin iv to protect against bacteremias
  • Gastroprotectants if evidence of gastrointestinal bleeding
47
Q

What is the dietary management of chronic hepatic encephalopathy?

A

Dietary management:

  • key to the successful management of HE
  • feed normal to slightly ­ amounts of protein
  • protein source should be high-quality and highly-digestible
  • feed small amounts of food several times per day
  • We used to think protein restriction was important- no evidence to support this and most dogs with PSS or liver disease might need normal to increased protein.
48
Q

What is the medical therapy with lactulose for the management of chronic hepatic encephalopathy?

A

Medical therapy: lactulose

  • is a disaccharide which passes into the colon to be degraded by bacteria into SCFAs
  • this acidifies the colonic environment trapping NH3 as ammonium ions (NH4+)
  • SCFAs (short chain fatty acids) are a preferred energy source for colonic bacteria, causing them to incorporate more ammonia into their own bacterial proteins
  • promotes osmotic diarrhoea
  • decreased time over which colonic contents are acted on by intestinal bacteria
49
Q

What is the medical therapy with antibiotics for the management of chronic hepatic encephalopathy?

A

Medical therapy: antibiotics

  • if diet alone, or diet + lactulose, are not effective
  • use drugs that are effective against anaerobic organisms:
  • metronidazole 7.5mg/kg PO q12h
  • amoxicillin 10mg/kg PO q8-12h

Small Animal Final Year (317 decks)

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