08 | How to care for patients with portosystemic shunts

Portosystemic shunts were the first ‘big’ referral medical condition I really found out about - and really took an interest in.

It was when my own rescue kitten, who I adopted from work back in 2012, was diagnosed with one that I realised referral medicine was a thing.

I sat in a consulting room at a specialist centre about 2 hours away from home (with a medicine specialist who I now work with… funny how things come full circle) after Mavis had had another week-long bout of ataxia and some head-pressing and salivation episodes.

Fast-forward to a sedation and abdominal ultrasound, and she’s off home with some lactulose, amoxiclav and a hepatic diet - whilst I run some coagulation tests at work ahead of her scheduled shunt surgery.

 

It was then, when I was sitting there being told the risks of things like portal hypertension, and post-attenuation neurological syndrome, that I realised how much intensive nursing she was going to need after surgery.

We know that portosystemic shunts are challenging cases both at the time of diagnosis, under anaesthesia, and in the acute postop period - there are a lot of complications, and on top of this, we’re usually dealing with small patients, in poor body condition, with complications like hypoglycaemia.

So how can we best care for them, and what skills can we use in the process? Well, in order to start planning our nursing care, we need to understand what a portosystemic shunt is, and how they affect our patients.

What is a portosystemic shunt?

A portosystemic shunt is a vascular anomaly causing blood from the GI tract to bypass the liver and directly enter the systemic circulation.

In a normal patient, blood from the GI tract flows to the liver via the portal vein, so that nutrients can be appropriately delivered to the liver, and waste products can be eliminated.

When a patient has a PSS, some blood will bypass the portal vein, flowing around the liver rather than through the liver - resulting in things like poor delivery of nutrients (and therefore poor growth), and waste products accumulating in the body, since the liver can’t appropriately eliminate them.

One of these waste products is ammonia - which is a potent neurotoxin. As ammonia - amongst other waste products - accumulates in the body, we begin to see neurological signs. This is known as hepatic encephalopathy.

Portosystemic shunts can be either congenital or acquired, and they can be intrahepatic - where the anomalous vessel is within the liver itself - or extrahepatic - where the anomalous vessel is outside of the liver.

Congenital Portosystemic Shunts

As the name suggests, a congenital shunt is one which a patient is born with. They are seen more commonly in dogs than cats and tend to be single vessels, rather than multiple vessels.

Generally, cats and small dogs have congenital extrahepatic shunts, whereas large dogs have congenital intrahepatic shunts.

Acquired Portosystemic Shunts

Acquired shunts are defined as multiple, tortuous vessels. They represent recanalisation of pre-existing portosystemic collateral vessels, and form secondary to portal hypertension - where pressure within the portal vein becomes too high.

They commonly occur as a result of underlying liver diseases, portal vein thrombosis, and congenital atresia (narrowing) of the portal vein.

What signs do we see in PSS patients?

Clinical signs in the PSS patient are variable, and include things like:

  • Small body stature

  • Failure to thrive

  • Poor body condition

  • Neurological signs

  • Lethargy

  • Depression

  • Seizures

  • Headpressing

  • Blindness

  • Ptyalism - hypersalivation (particularly in cats)

  • PUPD

Signs of underlying liver disease will also be seen in patients with acquired shunts, and in some cases, we will see lower urinary tract signs in PSS patients.

These are commonly seen as the high circulating ammonia levels cause ammonium biurate uroliths to occur - meaning things like haematuria, pollakiuria and, in severe cases, urinary tract obstruction can be seen.

How is a PSS diagnosed?

Like many of our other liver diseases, we diagnose a PSS based on biochemistry and haematology findings, and imaging of the abdomen - to look for evidence of a shunting vessel (or vessels).

Biochemistry

Biochemistry can be completely normal, or can show changes associated with liver dysfunction - including a low BUN, low glucose, low cholesterol, low creatinine and low albumin.

In some cases, ALT and ALP can be elevated - but most of the time they are normal.

Looking at more specific biochemical tests of liver function, ammonia levels can be elevated in patients not currently receiving treatment for HE, and a bile acid stimulation test will be elevated, since flow of bile acids back to the liver will be impaired in these patients.

Haematology

Haematology commonly reveals a microcytosis, with a low MCV (mean corpuscular volume). PCV can also be slightly low in these patients.

We know PSS patients can have smaller red blood cells - the reason for this is not fully understood, but is suspected to be due to abnormalities in iron metabolism.

Imaging

Ultrasound or CT is generally used to diagnose a PSS. About 85% of congenital shunts are identified on ultrasound, so the absence of a visible shunting vessel doesn’t mean one isn’t present. If it’s very small, for example, contrast CT may be required for definitive diagnosis.

Ultrasound with colour flow doppler generally reveals a small liver with reduced portal flow, and a tortuous or anomalous vessel. If ammonium biurate uroliths are present, these can also be seen in the lower urinary tract.

CT with angiography is commonly used for diagnosis - this involves administering a bolus of iodinated contrast medium IV, and then following this with the scanner to identify the abnormal vessel. The team can watch the contrast flow through it, easily identifying the vessel and it’s connections to the portal and systemic circulation. This makes surgical planning much easier. 

Other imaging options include portovenography - which is typically performed during the time of surgery. This involves cannulating a mesenteric vessel, administering contrast through it, and using intraoperative fluoroscopy to watch the contrast flow through the abdominal vessels - highlighting the shunt.

What about treatment?

So now you’ve got a diagnosis, it’s time to talk treatment. We can break this down into 2 major sections - treating the hepatic encephalopathy, and surgical management of a congenital PSS.

Managing Hepatic Encephalopathy

Any acutely neurological patient requires urgent treatment to reduce their ammonia levels and restore normal mentation.

This is indicated in both congenital and acquired shunts - in acquired shunts, this treatment remains lifelong, alongside management of the underlying liver disease present.

In patients with congenital shunts, we treat them for HE prior to surgery, to stabilise them and improve their anaesthetic risk level. We then continue this medical management until the shunting vessel is completely closed, which can take weeks to months. Some patients will have incomplete shunt closure, and require ongoing medical management (like my cat, because… well, she’s a vet nurse cat).

We treat HE with a combination of:

  • Lactulose

  • Antibiotics

  • Antiseizure medications

  • Dietary adjustments

  • +/- Probiotics

To alter the levels of ammonia-producing bacteria in the gut, decrease absorption of ammonia, and adjust the amount of ammonia produced in response to protein breakdown.

Surgical Management

Surgery is indicated in congenital portosystemic shunts. It’s the treatment of choice where possible, as hepatic function will continue to decline whilst blood flow continues to be shunted away from the liver.

The goal of surgery is to close anomalous vessel and restore normal blood flow through the liver. This is either performed immediately, via full closure of the vessel with a ligature, or gradually, via attenuation of the vessel.

Usually gradual attenuation is performed, as the risks of portal hypertension are higher with complete closure, and many patients will not tolerate this. This gradual closure is achieved either with a cellophane band, or an ameroid constrictor.

And what about nursing care?

Nursing care requirements for the PSS patient are vast. There are many risks associated with surgery, including neurological signs, portal hypertension, and haemorrhage - and the nurse must be able to spot any changes in patient status rapidly, and troubleshoot as needed.

On top of this, we need to be thinking about nutrition - particularly the type and amount of protein in the patient’s diet, hydration, pain management, drug metabolism, anaesthesia monitoring and recovery care, and managing lines, catheters and indwelling devices.

So there you have it…

That’s it - a complete overview of portosystemic shunts in cats and dogs! To recap everything we’ve been chatting about in this episode, portosystemic shunts are anomalous blood vessels that cause the shunting of blood from the GI tract around the liver, rather than through it. They can be congenital or acquired, intrahepatic or extrahepatic, and the most common signs our patients will present with are neurological, alongside poor growth in young patients with congenital shunts.

Medical management initially aims to reduce ammonia levels and eliminate the signs of HE. This is required to stabilise congenital PSS patients prior to surgery, and is the long-term treatment in acquired shunt patients. Surgery is the only definitive cure for a PSS; this is achieved typically by gradually closing the vessel using a cellophane band or ameroid constrictor.

Postoperatively, the nursing care requirements are vast - including intensive monitoring and managing lines and indwelling devices, alongside maintaining normoglycaemia, analgesia, nutrition, supporting fluid balance and general nursing care.

Did you enjoy this episode? If so, I’d love to hear what you thought - screenshot it and tag me on instagram (@vetinternalmedicinenursing) so I can give you a shout out, and share it with a colleague who’d find it helpful!

Thanks for learning with me this week, and I’ll see you next time!

References and Resources

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07 | How to treat and care for cats with hepatic lipidosis