21. Acute liver diseases in dogs. Acute hepatic failure Flashcards
Introduction to acute liver disease in general?
Introduction To Acute Liver Disease In General
Determination of hepatic diseases can be quite challenging. Clinical
signs can vary greatly, and those signs don’t usually correlate with
the prognosis or severity of the disease. These signs do, however,
correlate to the following:
§ Breed disposition § Sex
§ General health § Age
§ Speed of the liver disease § Vaccination
§ Degree of portal hypertension § Liver condition
Liver disturbances are more likely to be acute than chronic because
chronic conditions allow for regeneration time & functional
adaptation. Clinical signs during a chronic liver disease only show
unless 70% of the hepatic functional mass has been lost
General Non- Specific and specific clinical signs?
GENERAL NON-SPECIFIC CLINICAL SIGNS
§ Anorexia § Apathy
§ Weight loss § Lethargy
§ Poor coat § Depression
§ Vomiting § Dehydration
§ Diarrhoea § Lethargy
GENERAL SPECIFIC CLINICAL SIGNS
§ Icterus § PU/PD
§ Bilirubinaemia § DIC
§ CNS signs (HE*) § Coagulopathy
§ Enlarged abdomen (hepato-/splenomegaly or ascites) *HE = Hepatic encephalopathy
Liver associated ascites?
LIVER-ASSOCIATED ASCITES
There are 3 possible mechanisms how this can arise:
§ Pre-hepatic
§ Intra-hepatic
§ Post-hepatic
All of which are associated with altered hepatic or portal blood flow
Prehepatic mechanism
§ Arteriovenous fistula
§ Portal vein obstruction
§ Portal vein hypoplasia
Intrahepatic mechanism
§ Portal venule hypoplasia
§ Sinusoidal cellular infiltration
§ Fibrosis: Periportal region; Central vein
Post-hepatic mechanism
Or “passive congestion”
§ Hepatic vein obstruction
§ Cauda vena cava obstruction
§ RS-HF
§ Pericardial disease
Differential diagnosis of ascites
§ HF
§ Peritonitis
§ Protein loss due to AKI/GI problem
§ Liver disorders
Predispositions to liver disease?
PREDISPOSITIONS TO LIVER DISEASE
Cats
§ Liver has less storage & regenerative capacity than dog
§ More likely to suffer a biliary disease or hepatic lipidosis
§ Rarely develop fibrosis, cirrhosis, portal hypertension or
APSS (acquired porto-systemic shunt)
§ Chronic liver disease: Hepatomegaly
§ Better prognosis of chronic disease than dogs
Dog
§ More likely to suffer a parenchymal disease
§ Chronic liver disease: Smaller liver
Diagnosis of AHF?
AHF caused by hepatotoxins?
AHF Caused By Hepatotoxins
The liver is sensitive to toxins and drugs, and plays a central role in
their metabolism.
Toxic effects on the liver are divided into the following:
Intrinsic toxic effect
Reproducible
Dose-dependent
Toxic dose limit
Direct toxic effect
E.g. Paracetamol; Xylitol
Extrinsic toxic effect (rare)
Non-reproducible
Unique (non-calculable)
Not dose-dependent
E.g. Phenobarbital; Lomustine; Itraconazole
Paracetamol?
PARACETAMOL (ACETAMINOPHEN)
Ø Cats!
Rapidly depletes the body’s stores of glutathione (GSH); Produced
toxic metabolites which have an oxidative effect
Erythrocyte methemoglobinemia & hepatocyte necrosis
Clinical signs:
§ Cyanosis § Tachycardia
§ Dyspnoea § Tachypnoea
§ Facial oedema § Brown blood
Lab. D
§ Haemolytic anaemia; Methemoglobinemia
§ Abnormal RBCs: Nucleated; Schistocyte; Acanthocyte;
Heinz body
§ ALT ↑; Br ↑; Haemoglobinuria
Treatment
§ Flush the stomach & give activated charcoal
§ Stabilise patient: IVFT; Oxygen; Mannitol
§ Apply high amounts of antioxidants
§ Key treatment: N-Acetylcysteine
Phenobarbital, Phenytoin. potentiated sulphonamides and other drugs?
PHENOBARBITAL
Rarely causes hepatotoxicity; Idiosyncratic reaction
Dx: ↓ Albumin; ↑Br; Enlarged liver (or smaller if chronic)
Tx: ↓ The dose; Supportive therapy
PHENYTOIN
Very hepatotoxic
Causing: Acute/chronic hepatitis; Fatal intrahepatic cholestasis
Short half-life in dogs
POTENTIATED SULPHONAMIDE
Idiosyncratic effect; Common
Forms of toxicosis:
§ Sulphonamide hypersensitivity: Thrombocytopenia;
fever; polyarthropathy
§ Acute hepatopathy: Liver necrosis & cholestasis
§ Destructive cholangitis: Idiosyncratic hypersensitivity →
Severe intrahepatic cholestasis → Acholic faeces
OTHER DRUGS
§ Phenytoin: Hepatitis; Fatal intrahepatic cholestasis
§ Primidone: Liver necrosis, lipidosis & cholestasis
Xylitol toxicosis?
XYLITOL TOXICOSIS
Quickly absorbed into the liver; Causes very pronounced dosedependent insulin production in dogs (cats tolerate it well)
→ Leads to hypoglycaemia; liver necrosis & acute liver failure
Lab. D
§ Hypoglycaemia
§ Hypokalaemia
§ ↑↑↑ Liver enzymes
§ ↑↑↑ Br
§ Hypophosphataemia → Hyperphosphataemia
Clinical signs
§ Vomiting § Lethargy
§ Weakness § Ataxia
§ Tremor § Seizure
§ AHF: Icterus; HE; Coagulopathy
Treatment
§ Emesis (unless ingestion was >30 mins ago)
§ Ø Activated charcoal → Ineffective
§ Monitor & maintain blood glucose
§ Coagulopathy: Fresh frozen plasma; Blood transfusion
§ Palliative therapy
Adenovirus rubarths disease?
AHF Caused By Pathogens
CANINE ADENOVIRUS-1 (RUBARTH’S DISEASE)
Causes hepatic necrosis; Gall bladder oedema
Ø CSx → 1:500 chance
Chronic hepatitis & cirrhosis → 1:16-500 chance
Centrilobular to bridging hepatic necrosis → 1:4 chance
Pathology: Dark & mottled liver
Complications: HE; DIC; Hypoglycaemia; CN; GI vasculitis;
Tonsillitis; Jaundice
Dx: Inclusion bodies; IF antibody test; Biopsy
Tx
§ Vaccine
§ Symptomatic: Atropine (anterior uveitis); IVFT; Blood
transfusion; Topical Glucocorticoid
Canine herpesvirus?
CANINE HERPESVIRUS
Acute; Afebrile; Rapidly fatal in neonates
Older dogs: Mild upper respiratory signs
Multi-organ failure: Liver; Kidney; Lung etc.
Multi-organ failure: Liver (necrosis); Kidney; Lung etc.
Pathology
Acute, systemic necrosis & haemorrhage; Necrotising vasculitis;
Petechiae; Vesicles; Subcutaneous oedema
Lab. D: Eosinophilic intranuclear inclusion bodies
Leptospirosis?
LEPTOSPIROSIS [ZOONOTIC]
Acute disease; Primarily acute renal failure + cholestatic hepatic
disease; Found in stagnant water and other hosts; Shedding via urine
§ L. icterohaemorrhagie → Icterus; Hepatic damage
§ L grippotyphosa → Chronic hepatitis; Fibrosis
§ L. canicola → Renal failure
Toxin causes:
§ Lysis of tight junctions
§ Intrahepatic cholestasis
§ Vascular damage → Bleeding tendancies
Lab. D
§ ALP ↑↑
§ ALT ↑
§ BA ↑
§ Br ↑
Clinical signs
§ Fever § DIC
§ Myalgia § Oedema
§ Jaundice § Haematemesis
§ Haematochezia § Vomiting
§ Vascular injury § Melena
§ Renal dysfunction § Epistaxis
§ Oliguria/anuria § Uveitis
Diagnosis
§ US: Double layer of the gallbladder: Thickened
§ Serology: Microscopic agglutination test (MAT)
§ PCR
§ Isolation from fresh urine (dark field microscopy)
Clostridium Piliformis tyzzers disease?
CLOSTRIDIUM PILIFORMIS (TYZZER’S DISEASE)
Gram negative; Fusiform bacteria; Immunosuppression
Seen in cats too
Clinical signs
Acute onset; Rapidly fatal (within 24-48 hours)
§ Anorexia
§ Lethargy
§ Abdominal discomfort
Diagnosis → Biopsy
§ Multifocal periportal hepatic necrosis
§ Hepatocyte & intestinal epithelium necrosis
Treatment: Ø Treatment; Palliative
Pathology: Multifocal hepatic necrosis; Necrotising ileitis
Helicobacter canis and hepatic abscess?
HELICOBACTER CANIS
Mostly in young dogs
Located in the periphery of lesions in the bile canaliculi
Pathology: Multifocal hepatic necrosis
HEPATIC ABSCESS (EXTRAHEPATIC LIVER INFECTION)
Focal abscess → Hepatobiliary infection; Ischaemia
Multi-focal abscess → Systemic infection
Bacteria of concern (dog): Staphylococcus spp
Haematogenous spread via: Bile duct; Umbilicus
Hypoxic conditions allow the proliferation of anaerobic bacteria
from normal flora
Clinical signs
§ Anorexia § Ascites
§ Depression § Weight loss
§ Vomitus § Hepatomegaly
§ Fever
Lab. D: Neutrophilia (left shift); Liver enzymes ↑; Br ↑↑
Treatment: Surgery →Drainage →Antibiotics (penicillin +
fluroquinolone)
Mycotic Infection?
MYCOTIC INFECTION
Systemic mycosis → Mononuclear phagocytosis → Hepatic signs
Clinical signs
§ Hepatomegaly
§ Ascites
§ Icterus
§ CSx: from inhalation: Cough; Dyspnoea
Lab. D: Liver enzymes ↑/-; SBA ↑; Br ↑; Albumin↓; DIC
Pathology: Granulomatous/pyogranulomatous inflammation
Histoplasmosis: Affecting: Bone marrow; Lymph nodes; GIT
Coccidiomycosis: Affecting: Bones; Joints; Lymph nodes;
Abdominal organs
