Venous Thromboembolism

Take home messages

• VTE causes around 60 000 deaths per year
• Up to 25% of inpatients develop a DVT
• Formal VTE assessment is mandated by NICE

Meet the Father of modern pathology

Behold - Rudolf Virchow - physician, anthropologist, pathologist, prehistorian, biologist, writer, editor, and politician, who you'll probably recognise from his eponymous node and triad fame.

Hey, it was the 1800s, when the entirety of medicine was a glorified pamphlet.

I can't decide what's cooler - the glasses, the beard, or the fact that his colleagues referred to him as the Pope of Medicine.

He was first to figure out the pathophysiology of pulmonary thromboembolism, nonchalantly coining both embolism and thrombosis in the process.

Contrary to popular belief, Ol' Rudy didn't actually devise the triad himself, it was named in his honour much later in the 1950s (we think) long after he had died.

The triad

These are the three things you need to be able to regurgitate in the exam, to show you understand the fundamentals of why blood clots when it shouldn't.

Blood, being in a constant state of clotting and unclotting, doesn't need much of a deleterious change in its environment to tip it too far in the wrong direction.

• If blood isn't flowing smoothly, it clots
• If blood is exposed to the collagen beneath the endothelium, it clots
• If there is another pathophysiological process going on that makes blood intrinsically more clotty, then guess what - it clots

We only really started paying proper attention to post op DVT risk in the 1930s, whereupon we started getting patients moving as soon as possible after surgery.

Then in the 1950s, along came heparin, followed by low molecular weight heparin in the 80s, which transformed VTE prophylaxis as one might imagine.

Then in the 1990s we started to see proper risk stratification with the Caprini and Padua prediction scores.

Then the GOATs of VTE, the DOACs joined the show properly in the 2010s.

Who gets it?

Anyone can get a DVT at any time, such is the nature of life and the inherent risk of pumping viscous living fluid thorough a squidgy human body.

That being said, there are specific risk factors that make thrombus formation much more likely.

How to prevent it

An injection a day keeps Virchow away.

It's not especially complicated - pick a component of the triad and see if you can modify it.

• Stasis - get blood moving
• Endothelial injury - minimise unnecessary trauma/indwelling lines
• Hypercoagulability - treat the causative issue and artificially thin the blood

Easy.

Mechanical options

We underestimate just how important the soleus muscle pump is for generating venous return from the legs and feet.

Working together with the valves, this muscle pump squidges blood back up the legs against gravity.

For a 6ft man with a leg measurement of 32 inches, that's nearly 60mmHg when standing upright, just to get the blood up to the pelvis.

It's easy to see, therefore, how quickly stasis can develop when we put patients in bed and leave them there for a few days.

To combat this we have a couple of options to mimic the soleic pumpage effect:

• Stockings that provide constant pressure
• Intermittent compression devices that mimic muscle contraction more closely
• Foot impulse devices that stimulate the plantar venous plexus

Which one you use will depend on the patient, the procedure and the protocols of your local institution, just remember there are some patients for whom mechanical thromboprophylaxis is contraindicated:

• Severe peripheral vascular disease
• Local skin infection, graft or necrosis
• Stroke
• Severe peripheral neuropathy

Pharmacological options

There are a number of agents available for your use to prevent unwanted internal clottage.

How you choose which one to use will depend on:

• The patient and their renal function and HIT risk
• The surgery and its bleeding risk profile
• The hospital and how much money it has

Regional anaesthesia

This is a double-edged sword. You can reduce the risk of venous thromboembolism with regional anaesthesia (and avoiding a GA), however if you're doing a spinal you need to be cautious about timings with regards to pharmacological prophylaxis

• Regional anaesthesia causes a temporary sympathectomy
• This causes vasodilatation and reduced peripheral vascular resistance
• This improves peripheral blood flow and reduces venous stasis

Education

We're always advised to try and ensure our patients are as informed as possible about their healthcare and treatments.

• Patients should be given written and verbal information before and after surgery
• In particular they should be alerted to the signs and symptoms to watch out for
• They also need to be educated on how to administer thromboprophylaxis at home

Tell me about caval filters

"Hello dearest patient, you seem to be having trouble keeping your blood flowing smoothly."

"I'd recommend we pop a titanium spider in your biggest vein, to catch all the flying clots and nom them all up."

The theory here is very simple. If you have a load of clot flying from the peripheral circulation towards the heart, it's better to catch them with a net in the IVC than let them block the pulmonary artery or saunter through a PFO and cause a massive stroke.

However

I attended a 'bleeding and clotting' conference a couple of years ago, at which one of the keynote speakers - a wisened haematologist - astutely remarked:

• "If you put a lump of metal in the IVC, it's going to generate a load of clot"
• "If we'd found a metal that didn't, we'd be making heart valves out of it and doing away with blood thinners"
• "IVC filters are essentially pointless"

This made a lot of sense at the time, and they are associated with a greater increase of recurrent DVTs, however there are still specific occasions when IVC filters are used for the management of thromboembolism.

Indications

• Known large proximal DVT and
• Embolism within last month and
• Can't have anticoagulation

Makes sense I guess.

Useful Tweets and Resources

References and Further Reading

Primary FRCA Toolkit

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