25. Vascular liver diseases, portosystemic shunt in dogs and cats. Hepatic encephalopathy Flashcards

1
Q

Portal hypertension causes?

A

Portal Hypertension

Elevated blood pressure in the portal system

Normal range: 5-10 mmHg

Portal hypertension is defined as when the portal blood pressure is 5

mmHg higher than the BP in the inferior vena cava

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2
Q

Composition of the portal system?

A

COMPOSITION OF THE PORTAL SYSTEM

§ Portal vein § Splenic vein

§ Superior mesenteric vein § Left gastric vein

§ Inferior mesenteric vein § Umbilical vein

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3
Q

Aetiology of portal hypertension?

A

AETIOLOGY

When blood flowing from the portal system → inf. vena cava meets resistance

The causes of portal hypertension can be categorised by their aetiology

Pre-hepatic causes

Occurs before blood arrives to the liver

§ Portal vein thrombosis

§ Splenic vein thrombosis

§ Arteriovenous malformation

§ Splenomegaly

Intra-hepatic causes

Occurs due to causes affecting the liver specifically

§ Cirrhosis by viral hepatitis; metabolic disease; (alcohol)

§ Primary sclerosing hepatitis

§ Schistosomiasis

§ Nodular regenerative hyperplasia

Post-hepatic causes

Due to problems involving the vena cava

§ Inferior vena cava obstruction

§ RS-HF

§ Hepatic vein thrombosis

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4
Q

Clinical signs of portal hypertension?

A

CLINICAL SIGNS

May be asymptomatic; CSx are usually related to the underlying disease (usually cirrhosis)

§ Hepatosplenomegaly § Fatigue

§ Nitric oxide release § Pruritis

§ Swollen capillaries § Oedema

§ Caput medusae § Ascites

§ Palmar erythema § Jaundice

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5
Q

Portosystemic shunt(PSS)?

A

Portosystemic shunt (PSS)

Abnormal vascular communication between the portal & systemic venous systems

May be acquired or congenital; Intrahepatic or extrahepatic

Consequences

↑ In toxins in the systemic circulation

§ Mercaptan § NH3

§ Benzodiazepine § GABA

§ SCFA (short chain fatty acids)

↓ Hepatic blood flow → Hepatic atrophy

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6
Q

Congenital PSS?

A

CONGENITAL PSS

75% of PSS cases (more common)

Caused by abnormal embryonal blood vessels; Associated with portal hypertension; May be intra-hepatic or extra-hepatic

Young > Old

Intrahepatic PSS

Always solitary

§ Persistent embryonal ductus venosus

§ Left, central & right division: Left division morphology is

consistent with failure of ductus venosus closure

Predisposed: Large dogs > Small dogs

Irish wolfhound; Golden retriever; Irish setter; Labrador; Old English

sheepdog; German Shepherd

Extrahepatic PSS

Always solitary

Anatomically abnormal communication between the portal system

and v. cava caudalis or v. azygous

Predisposed: Small & toy dogs > Large dogs; Cats

Yorkie; Cairn terrier; Shih Tzu; Maltese terrier; Pug; Mini

Schnauzer; Poodle

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7
Q

Acquired Pss?

A

ACQUIRED PSS

Multiplex, collateral vessels; Narrow & twisting

Protective compensatory response to portal hypertension; See also

arterioportal fistula (APF) later

Predisposed: Old animals > Young animals

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8
Q

Hepatic microvascular dysplasia?

A

Other Vascular Diseases

HEPATIC MICROVASCULAR DYSPLASIA (HMD)

Special form of congenital hypoplasia to the portal vein

Ø Portal hypertension

Formation of intralobular microvascular shunts form

Predisposed: Small breeds > Large breeds

Cairn terrier; Yorkshire terrier

CSx: Ø CSx or may be mild

Dx

§ Lab. D: ↑ BA

§ US: Trans-colonic portal scintigraphy normal; Ø

Macroscopic shunt

§ Biopsy

Tx: Diet; Lactulose

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9
Q

Arterioportal fistula?

A

ARTERIOPORTAL FISTULA (APF)

Connection forms between A. hepatica & V. portae

Congenital

Leads to:

§ Portal hypertension

§ Ascites

§ Acquires PSS

§ GI oedema

CSx: Continuous murmur (fremitus) (turbulent flow over the affected

liver lobe); GI oedema; Ascites

Dx: US: Hepatic AV fistula: Distended, twisting, echo-loose portal

branch within a liver lobe; Hepatofugal blood flow* above the liver

lobe

*Hepatofugal blood flow is abnormal flow of blood is from:

Periphery of the liver → Porta → Backwards along v. portae

Tx: Lobectomy; Treatment of portal hypertension

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10
Q

Hepatic venous outflow obstruction?

A

HEPATIC VENOUS OUTFLOW OBSTRUCTION

Budd-Chiari-like syndrome

Young dogs > Older dogs

Abnormal development of vessels before differentiation into veins &

arteries

↑ Arterial pressure → Dilation of portal branch + hepatofugal flow

Frequently with arterioportal fistula & primary hypoplasia of the

portal vein (PHPV)

Diagnosis

§ Colour doppler US; Celiac arteriography; Laparotomy

§ Biopsy: Thick-walled arterial vessel; Dilated venous

vessels; Fistula

§ Lab. D: Mild anaemia; Leucocytosis; Hypoproteinaemia;

Normal liver enzymes; ↑ BA

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11
Q

Hepatic encephalopathy?

A

Hepatic encephalopathy

Metabolic dysfunction of the brain due to liver dysfunction

Can occur when 70% of hepatic function is lost

May be caused by any hepatic disease, but more commonly PSS or

hepatic toxicosis

Younger animals: Caused mostly by shunts

Older animals: Caused mostly by neoplasia or cirrhosis

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12
Q

Acute hepatic Encephalopathy?

A

ACUTE HEPATIC ENCEPHAOPATHY

Rare (<10% of cases); Acute liver failure

Pathophysiology

Cause: Liver necrosis (diffuse; severe; 70-80% of the liver) (this

could be caused by toxins, infection, drugs or ischaemia)

Severe brain oedema then leads to ↑ intracranial pressure

Clinical signs

See CSx associated with Grade 3 & 4 HE later

§ Seizures

§ Semi-coma; Coma

Diagnosis

§ Lab. D: ↑ NH3!

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13
Q

Chronic Hepatic encephalopathy?

A

CHRONIC HEPATIC ENCEPHALOPATHY

More common (90% of cases)

Portosystemic shunt + ↓ Liver function

Pathophysiology

Portosystemic hepatic encephalopathy (PSE) → Chronic Hepatic encephalopathy → Portosystemic vascular anastomosis (allowing the

diversion of portal blood into the systemic circulation) → HE

Dog: High reserve capacity (preventing HE from developing in most

cases); In rare cases, there may be a congenital urea cycle enzyme

deficiency

Cat: Lower reserve capacity; Congenital enzyme deficiency means

that arginine isn’t synthesised in the liver ∴ inadequate NH3

detoxification

Anorexia → ↓ Arginine → Hepatic lipidosis → ↑NH3

Finally: Leads to deranged neurotransmitter systems

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14
Q

Clinical signs of hepatic encephalopathy?

A

CLINICAL SIGNS OF HEPATIC ENCEPHALOPATHY

Episodic intensity & severity

CNS signs are attributed to the deranged neurotransmitter systems,

brain oedema and hypoglycaemia. These clinical signs are expressed

as differing grades of hepatic encephalopathy. These are shown in the

table below.

Grade of HE Clinical signs

1 Lethargy; Apathy; Depression; Personality

changes; PU; Anorexia

2

Ataxia; Disorientation; Compulsive pacing;

Circling; Head pressing; Apparent blindness;

Personality changes; Salivation; PU

3 Stupor; Severe salivation (cats); Seizures

4 Coma; Non-responsive

Other clinical signs

§ Anorexia § Vomiting

§ Weight loss § Ptyalism

§ Diarrhoea § PU/PD

§ Urolithiasis § Cystitis

§ Stranguria § Dysuria

§ Haematuria § Pollakiuria

§ Crystalluria

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15
Q

Lab D of hepatic encephalopathy?

A

LAB. D OF HEPATIC ENCEPHALOPATHY

Haematology: Non-regenerative microcytic anaemia; Acanthocytes;

Poikilocytosis

Biochemistry

Hepatocellular dysfunction

§ Normal or ↑↑ ALP; ↑↑ALT; ↑↑AST; ↑↑GGT; ↑↑Br

§ ↑ BA; ↑ NH3

§ Signs of liver dysfunction: ↓ BUN; ↓ Urea; ↓ Chol;

↓ Albumin; ↓ Blood glucose; Coagulopathy

Urinalysis

§ ↓USG: Isosthenuria; Hyposthenuria (PU/PD)

§ Ammonium-biurate crystals

§ Urolithiasis: Haematuria; Proteinuria; Pyuria

Liver function tests

↑ NH3; ↑ BA

§ Ammonia tolerance test (ATT)

§ Post prandial ammonia tolerance test (APTT)

↑ BA

§ Fasting BA

§ Post prandial BA

↓↓ Protein C

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16
Q

Imaging of hepatic encephalopathy?

A

IMAGING OF HEPATIC ENCEPHALOPATHY

Ultrasound

Colour Doppler

§ Smaller liver; ↓ Size & number of intrahepatic veins;

Shunting vessels; Blood flow direction

§ Enlarged kidneys

CT

Contrast portography & angiography

§ Used to locate the anatomical location of PSS

§ Surgical catheterisation of mesenteric/splenoportography

Artery

Trans-colonic scintigraphy

17
Q

Treatment of Acute HE?

A

TREATMENT OF ACUTE HE

§ Treatment of seizures (propofol is preferred over BZDs);

Start the patient on Levetiracetam medication

§ Treatment of brain oedema: Mannitol

§ Fluids; Electrolytes; Acid-base correction

§ ↓ NH3 & toxins

Rectal enema

Therapeutic/retention enema: Neomycin; Lactulose

Non-absorbable disaccharide: Lactulose

§ PO antibiotics: Rifaximin; Metronidazole; Amoxiclav

§ Gastro-protectants

§ Treatment of coagulopathy

18
Q

Treatment of Chronic HE?

A

TREATMENT OF CHRONIC HE

§ Treat any underlying disease and ↓ NH3 production first (by

using lactulose)

§ Antibiotics

§ Diet: Remember we want to ↓ NH3 production but HE is

caused by endogenous protein degradation, so therefore we

wont alter the dietary protein intake.

§ High carbohydrate

§ Moderate fibre intake

§ Regular small meals