Portosystemic shunts (PSS), also known as liver shunts, are abnormal vascular connections between the portal and systemic venous circulation that allow blood to bypass the liver.
Overview and Clinical Importance
Portosystemic shunts (PSS), also known as liver shunts, are abnormal vascular connections between the portal and systemic venous circulation that allow blood to bypass the liver. In cats, this condition causes hepatic encephalopathy, stunted growth, and urinary tract abnormalities due to the accumulation of toxins that would normally be metabolized by the liver. While relatively uncommon in cats (reported incidence of 2.5 per 10,000 cats), PSS represents a critical topic for NAVLE examination due to its distinct clinical presentation and management challenges.
Understanding the pathophysiology, clinical signs, diagnostic approach, and treatment options for feline portosystemic shunts is essential for board success and clinical practice.
| Classification |
Characteristics |
Key Points for Cats |
| Congenital |
Present at birth; usually single vessel; failure of embryonic vessels to close |
80% of feline PSS; typically diagnosed less than 2 years of age |
| Acquired |
Multiple vessels; develop secondary to portal hypertension from chronic liver disease |
Older cats; CANNOT be surgically ligated; medical management only |
| Extrahepatic (EHPSS) |
Shunt vessel outside liver parenchyma; connects portal vein tributaries to systemic veins |
Greater than 95% of feline congenital PSS; left gastric vein most common origin |
| Intrahepatic (IHPSS) |
Shunt within liver parenchyma; often patent ductus venosus |
Rare in cats; when present, usually left divisional |
Pathophysiology
Normal Hepatic Circulation
In normal physiology, the portal vein carries nutrient-rich but toxin-laden blood from the gastrointestinal tract, spleen, and pancreas to the liver. The liver receives approximately 80% of its blood supply from the portal vein and 20% from the hepatic artery. This portal blood undergoes first-pass metabolism in hepatocytes, where ammonia is converted to urea via the urea cycle, and other toxins are detoxified or eliminated.
Pathophysiology of Shunting
When a portosystemic shunt is present, portal blood bypasses the liver and enters the systemic circulation directly. This results in several pathological consequences:
- Hepatic atrophy: Loss of hepatotrophic factors (insulin, glucagon) leads to reduced liver size (microhepatia)
- Hepatic encephalopathy (HE): Accumulation of ammonia, mercaptans, false neurotransmitters, and GABA causes neurological dysfunction
- Impaired urea cycle: Decreased BUN due to reduced ammonia conversion to urea
- Ammonium biurate crystalluria: Increased urinary excretion of ammonia and uric acid leads to crystal and urolith formation
- Impaired drug metabolism: Prolonged recovery from sedation/anesthesia due to decreased hepatic clearance
High-YieldOn the NAVLE, remember that ammonia is the KEY toxin causing hepatic encephalopathy. Ammonia crosses the blood-brain barrier, is converted to glutamine in astrocytes, causing osmotic swelling and neurological dysfunction. Clinical signs often worsen after eating (protein meals increase ammonia production).
| System |
Clinical Signs |
| Neurological (HE) |
Depression, lethargy, disorientation, head pressing, circling, ataxia, seizures, apparent blindness, behavioral changes, stupor, coma
UNIQUE TO CATS: Ptyalism (hypersalivation) - seen in 73% of cats |
| Gastrointestinal |
Vomiting (24-71%), diarrhea, inappetence, weight loss, pica |
| Urinary |
Dysuria, hematuria, stranguria (8-39% of cats); ammonium urate urolithiasis; FLUTD signs |
| General/Constitutional |
Stunted growth, failure to thrive, poor body condition, polyuria/polydipsia (less common than dogs) |
| Unique Feline Signs |
Copper-colored irises (38% of cats) - inappropriate for breed; prolonged anesthetic/sedative recovery |
Classification of Portosystemic Shunts
NAVLE TipCats almost always have EXTRAHEPATIC shunts (greater than 95%), unlike dogs where intrahepatic shunts are common in large breeds. The left gastric vein is the most common vessel of origin in cats. Remember: Small breeds and cats = extrahepatic; Large breed dogs = often intrahepatic.
| Grade |
Clinical Signs |
| Grade 1 |
Listlessness, depression, mental dullness, personality changes, excessive urination |
| Grade 2 |
Incoordination, disorientation, compulsive pacing/circling, head pressing, apparent blindness, ptyalism |
| Grade 3 |
Stupor, severe salivation, seizures (uncommon but possible) |
| Grade 4 |
Coma - unresponsive to stimuli |
Signalment and Breed Predispositions
Epidemiology
- Age at presentation: Median 8 months; range from weeks to several years (some cats remain undiagnosed until adulthood)
- Sex predisposition: Male cats more commonly affected; 25% of affected males have concurrent cryptorchidism
- Incidence: Approximately 2.5 per 10,000 cats in referral practice
Breed Predispositions
- Domestic Shorthair (most commonly diagnosed due to population prevalence)
- Persian and Himalayan - genetic component suspected
- Siamese
- British Shorthair
- Ragdoll
- Birman and Tonkinese
| Test |
Expected Finding |
Clinical Significance |
| BUN |
Decreased |
Reduced conversion of ammonia to urea due to bypassed liver |
| Albumin |
Normal to slightly decreased |
Cats with PSS often have NORMAL albumin (unlike dogs) |
| Glucose |
Normal to decreased |
Decreased glycogen storage and gluconeogenesis |
| Cholesterol |
Normal in cats (decreased in dogs) |
Species difference - cats maintain normal cholesterol |
| ALT/ALP |
Mild to moderate elevation |
ALP increase partly due to bone turnover in young animals |
| MCV |
Microcytosis (15% of cats) |
Microcytic normochromic anemia; altered iron metabolism |
Clinical Signs
Clinical signs in cats with PSS are often variable, intermittent, and may wax and wane. Signs typically worsen after eating due to increased protein absorption and ammonia production.
Hepatic Encephalopathy Grading
High-YieldPTYALISM (hypersalivation) is a HIGHLY characteristic sign in cats with PSS - present in up to 73% of affected cats. This is rarely seen in dogs with PSS. When you see a young cat with intermittent neurological signs AND drooling that worsens after eating, think PSS!
| Test |
Expected Result |
Important Notes |
| Fasting Ammonia |
Elevated (greater than 100 microg/dL suggests PSS) |
Sample must be kept on ice and analyzed immediately; sensitivity 83%, specificity 86% |
| Fasting Bile Acids |
Elevated (normal less than 10 micromol/L) |
Sensitivity 58-100%; stable in serum |
| Postprandial Bile Acids |
Markedly elevated (often greater than 50-100 micromol/L) |
100% sensitivity for PSS detection; MOST RELIABLE TEST |
Diagnosis
Laboratory Findings
Liver Function Tests - Essential for Diagnosis
NAVLE TipThe BILE ACID STIMULATION TEST is the most reliable screening test for PSS in cats. Always obtain BOTH fasting and 2-hour postprandial samples. Postprandial bile acids have 100% sensitivity for detecting portosystemic shunting. Ammonia is less stable and can give false negatives if not handled properly.
Urinalysis Findings
- Low urine specific gravity: Due to poor medullary concentration gradient from decreased urea production
- Ammonium biurate crystalluria: Present in 20-43% of cats; golden-brown crystals with characteristic 'thorn apple' shape at 400x magnification
- Ammonium urate urolithiasis: Present in approximately 12% of cats with PSS; radiolucent (require contrast studies or ultrasound)
Diagnostic Imaging
Radiography
- Microhepatia - small liver with cranially displaced stomach
- Renomegaly - enlarged kidneys (mechanism unclear)
- Cannot visualize the shunt vessel itself (plain radiographs have limited value)
Abdominal Ultrasound
- Microhepatia, reduced visibility of portal vasculature
- Anomalous vessel connecting portal vein to systemic circulation
- Portal vein diameter less than caudal vena cava diameter
- Operator-dependent; sensitivity 68-74% for extrahepatic shunts in experienced hands
CT Angiography (CTA) - Gold Standard
- GOLD STANDARD for PSS diagnosis and surgical planning
- Sensitivity 96%, specificity 89% - significantly higher than ultrasound
- Provides precise shunt morphology, origin, and insertion
- Allows 3D reconstruction for surgical planning
- Requires general anesthesia - use caution due to prolonged recovery risk
Nuclear Scintigraphy
Trans-splenic or per-rectal portal scintigraphy using Technetium-99m pertechnetate can quantify shunt fraction but does not provide morphologic detail. Less commonly used now that CT angiography is widely available.
| Treatment |
Dosage |
Mechanism/Notes |
| Lactulose |
0.5 mL/kg PO q8-12h; titrate to soft stool |
Acidifies colonic contents, traps ammonia as ammonium (NH4+), prevents absorption; osmotic laxative effect |
| Metronidazole |
7.5 mg/kg PO q12h |
Reduces urease-producing bacteria; REDUCE DOSE due to hepatic metabolism; watch for neurotoxicity |
| Ampicillin |
22 mg/kg PO q8h |
Alternative antibiotic for ammonia-producing bacteria |
| Dietary Management |
Moderate protein restriction |
Highly digestible protein diet; Hill's l/d or Royal Canin Hepatic; small frequent meals; CATS NEED ADEQUATE PROTEIN - do not over-restrict |
| Hepatoprotectants |
SAMe, Ursodiol, Vitamin E |
Support remaining hepatic function; antioxidant protection |
Medical Management
Medical management is indicated for pre-surgical stabilization (minimum 2 weeks recommended before surgery), patients not suitable for surgery, and long-term management of acquired shunts.
High-YieldLACTULOSE is the cornerstone of medical management for hepatic encephalopathy. It works by: (1) Acidifying colonic contents to trap ammonia as NH4+, (2) Osmotic catharsis to reduce ammonia absorption time, (3) Promoting bacterial metabolism of ammonia. Titrate dose to achieve 2-3 soft stools per day.
Emergency Management of Hepatic Encephalopathy Crisis
- IV Fluid Therapy: 0.45% NaCl + 2.5% dextrose; avoid lactated Ringer's (lactate requires hepatic conversion)
- Warm Water Enema with Lactulose: Diluted lactulose enema to reduce colonic ammonia
- Correct Hypoglycemia: Dextrose supplementation as needed
- Seizure Control: Use with CAUTION - benzodiazepines and barbiturates have prolonged half-life; levetiracetam may be safer
- NPO: Withhold food until stable, then reintroduce highly digestible protein
| Technique |
Description |
Feline Survival |
| Ameroid Constrictor |
Casein ring in steel collar placed around shunt; absorbs fluid and slowly occludes vessel over 2-5 weeks |
33-75% survival; 75% good outcome if survive |
| Cellophane (Thin Film) Banding |
Cellophane strip wrapped around shunt; induces fibrosis and gradual occlusion; may provide partial immediate attenuation |
82% mid-term survival; 66-100% reported |
| Suture Ligation |
Partial or complete acute ligation with suture; portal pressure monitoring required; complete ligation only if tolerated |
66-75% if tolerate complete ligation |
| Transvenous Coil Embolization |
Minimally invasive; coils placed in shunt via jugular access; primarily for intrahepatic shunts |
Limited feline data; used more in dogs |
Surgical Treatment
Surgical attenuation is the treatment of choice for congenital portosystemic shunts. The goal is to gradually redirect portal blood flow through the liver while avoiding acute portal hypertension.
Postoperative Complications in Cats
CRITICAL: Postoperative neurological complications are MORE COMMON in cats than dogs. Close monitoring is essential for the first 5 days post-surgery.
- Seizures: 8-22% of cats; most common serious complication; occur days 1-5 post-op
- Central blindness: Up to 44% of cats; may be transient or permanent
- Portal hypertension: Can occur with too-rapid shunt occlusion; causes ascites, GI signs
- Multiple acquired shunts (MAPSS): Develop in 5-18% if portal hypertension occurs
- Persistent shunting: Incomplete shunt occlusion; may require continued medical management
NAVLE TipCats have a HIGHER complication rate after PSS surgery than dogs, particularly neurological complications. Seizures are the most common cause of perioperative mortality. Treatment includes phenobarbital or levetiracetam, with propofol CRI if refractory. Prophylactic anticonvulsants (levetiracetam) may be considered, though evidence in cats is limited.
| Management Type |
Expected Outcome |
| Surgical - Complete Attenuation |
Best long-term outcome; 66-82% survival to discharge; majority have good to excellent quality of life |
| Surgical - Partial Attenuation |
Less favorable; may require ongoing medical management; some develop acquired shunts |
| Medical Management Alone |
Variable; some cats managed well long-term; others deteriorate; median survival shorter than surgical |
| Acquired (Multiple) Shunts |
Poor prognosis; medical management only; underlying liver disease dictates outcome |
Prognosis
Exam Focus: Prognosis after surgical attenuation of congenital PSS is 'FAIR' for cats (compared to 'FAVORABLE' for dogs). This reflects the higher complication rate in cats. However, cats that survive the perioperative period and achieve complete shunt occlusion generally have good long-term outcomes.