Multiple Causes of Vascular Occlusion and Necrosis

Beyond the Obvious: Understanding the Multiple Causes of Vascular Occlusion and Necrosis

Every injector needs to understand what causes vascular occlusion and how to avoid necrosis, but it’s much more nuanced than you might think. While many clinicians believe that putting filler into an artery instantly blocks it and stops blood flow causing a necrotic injury, the reality is far more complex. In fact, there are multiple theories about what can cause vascular compromise – and some of them may surprise you.

The Problem with Traditional Thinking

You might think, like many clinicians, that if you put filler into an artery, you will instantly block it and stop blood flow, causing a necrotic injury. But there’s a problem with this theory. Many surgeons, including Dr. Subbio, have explained that in surgery they often remove whole sections of arteries or tie them off and never untie them – and it doesn’t cause a necrotic injury.

This raises an important question: if complete arterial blockage doesn’t always cause necrosis in surgery, what else is happening when we see tissue death after filler injections?

The answer lies in understanding that necrosis isn’t just about complete blockage of main vessels. Many cases of necrosis where you actually get tissue breakdown have only a delayed capillary refill, not a completely absent capillary refill. This creates a rather confusing situation about what is actually causing the issue.

The reality is probably quite a gray area – significant compromise in blood flow through partial blockage of the main vessel and blockage of some of the smaller vessels, but not complete blockage, can still lead to necrosis. And there are several other mechanisms at play that we need to understand.

Mechanism 1: Pressure on the Capillaries

We know from general medicine that pressure sores occur simply when you put mechanical pressure on the outside of a group of capillaries or vessels. You get these on pressure points around the body – if you leave a patient in bed without moving for long enough, their skin will necrose.

The same thing happens in certain areas of the face, particularly in the midline for some reason. The chin, nose, and glabella all have a particular propensity to necrose in a different way.

What This Looks Like Clinically

When you see a patient with pressure-induced necrosis, it appears as an area of necrosis that tends to be round and is associated with high-pressure tissues.

• In the chin: The dermis can feel quite thick in some patients. A circular lesion around the surface of the chin underneath a pressure point is sometimes caused by high volume, high pressure, high G Prime dermal filler products.
• In the glabella: You might see patients treating lines in the glabella who get a distinct black line that doesn’t track the supratrochlear artery. It’s just over the section they injected, resulting in superficial necrosis. This fits with pressure from the filler on the capillaries rather than the artery itself – otherwise, you’d expect more of the area to be affected.
• The nose tip – the best example: The tip of the nose has no major arteries in it – it’s essentially a capillary bed. With the Tinkerbell nose tip lift, there are a large number of patients who either have a red nose that persists for several weeks, sometimes with pain. A small subsection of those patients will actually get some mild tissue breakdown – pustules forming, some peeling of the skin.

This tends to be less severe but can become quite severe if the pressure is high enough and left for long enough that none of the dermis gets any blood supply. These cases are unlikely to be caused by intravascular injection – they’re more likely the result of high G Prime products pushing on capillaries.

Mechanism 2: External Compression of Arteries

The next situation is where filler compresses around the outside of the artery. There are some interesting insights from general medicine where occasionally compression of a vessel causes vasoconstriction. When vessels are traumatized either with filler around them on the outside or filler partially inside them, you may trigger an inflammatory process and vascular constriction or spasm that could potentially cause necrosis.

What’s really happening here is the vessel is tightening up due to either mechanical pressure of the filler or a combination of mechanical pressure plus vasoconstriction.

A Revealing Case Study

One particularly memorable case involved a patient who had modeling across an entire face – the whole face looked like it had blood flow restriction after just two nasolabial fold filler injections. On ultrasound, the filler was sitting underneath a vessel, and there was a vessel pumping. The only explanation was that there had been vasoconstriction caused by trauma to the vessel.

Coincidentally – or maybe not coincidentally – the patient also had Raynaud’s syndrome, a phenomenon well known to cause vasoconstriction in the digits. Treatment with Nifedipine led to full recovery.

This case demonstrated that vasoconstriction can clearly cause significant vascular compromise clinically. While the body would likely have eventually kicked in and caused some vasodilation, the combination of vasoconstriction with mechanical pressure could potentially cause necrosis.

Mechanism 3: Venous Occlusion – The Rare but Real Risk

Thankfully, most of our face is a network, which means if you block a particular vein in one area, there are many other ways blood can drain from the area. But you can imagine if drainage is significantly impaired, there wouldn’t be enough of an exit route for new blood to come in, and you could cause some form of necrotic injury from decreased outflow.

The Eye: A Special Case

The easiest place to understand this would probably be in the eye, which is more of a closed system, though it’s quite hard to hit those veins.

A very interesting case from Dr. Patrick Treacy involved a patient injected with Volbella in the nose. This was linked with a venous sinus thrombosis that occurred a few days later, causing blindness. Venous sinus thrombosis is a known cause of blindness in medicine generally, but could it be triggered by a low molecular weight dermal filler that causes blood clotting? This is yet another way that patients may suffer from a type of vascular occlusion – purely about the venous system being affected by intravascular injection.

In other parts of the face, patients might get:

• A kind of bogginess
• Swelling
• Ruddiness (due to decreased oxygen blood flow)

But actual necrosis is less likely with venous occlusion because there are multiple ways out. The eyes, or if the occlusion is large enough, are a different story.

Understanding the Venous Anatomy Risk

Looking at the anatomy helps understand how venous occlusion could potentially affect drainage and cause blindness. The veins that run within the orbit connect quite closely to where the nose is. If you injected enough filler into these veins, an occlusion or blood clot in the basal plexus could potentially cause decreased venous drainage from both eyes.

This would be the worst-case scenario: the inability for blood to leave the eye means new fresh blood cannot enter either, and the vessels that supply the retina cannot replenish blood flow to the eye.

A blockage or clot in the basal plexus causes:

1. Decreased drainage from the eye
2. Inability for fresh blood to enter
3. Loss of blood supply to the retina
4. Resulting in blindness

This could be caused by either a low viscosity or high viscosity product injected in the nose, passing into the basal plexus, causing inflammation, clotting, and potentially even infection.

How to Differentiate: Bruise vs. Impending Necrosis

One of the problems clinicians face almost daily is how to tell the difference between a bruise and impending necrosis. Understanding these different mechanisms helps with diagnosis:

Pressure Necrosis Signs:

• Round, localized area of concern
• In thick dermis areas (chin, nose tip, glabella)
• Associated with high volumes or firm products
• May present with persistent redness before progressing

Vascular Compression/Spasm:

• Broader area of mottling
• May affect entire regions of the face
• Patient may have history of vascular conditions (like Raynaud’s)
• Can respond to vasodilators

Venous Occlusion:

• Bogginess and swelling
• Decreased capillary refill but not absent
• Ruddiness or duskiness to the skin
• May progress more slowly than arterial occlusion

Prevention Strategies Based on Mechanism

Understanding these different mechanisms allows for targeted prevention:

For Pressure Necrosis:

• Check tissue compressibility before injecting (especially nose tip and chin)
• If you squeeze the tissue and there’s minimal space between cartilage/bone and skin, be cautious
• Use softer products in low volumes
• Avoid high G Prime products in tight spaces
• Check product contraindications (many fillers say “contraindicated in the glabella”)

For Vascular Compression:

• Ask about vascular conditions like Raynaud’s
• Use gentle injection pressure
• Avoid overcorrection that could exceed intravascular pressure
• Consider smaller volumes over multiple sessions

For Venous Occlusion:

• Be especially careful in the nose area
• Understand the connection between nasal vessels and the basal plexus
• Consider using products less likely to cause clotting

Treatment Implications

These different mechanisms also mean different treatment approaches might be needed:

• Pressure necrosis: May require immediate decompression, massage, and potentially removal of product
• Vascular spasm: Could benefit from vasodilators like Nifedipine
• Venous occlusion: May need aggressive anticoagulation in addition to standard treatments

The Bottom Line: It’s More Complex Than We Thought

Many of these mechanisms are theoretical because they’re very hard to prove in real cases about what’s causing the disruption in blood flow. But understanding that vascular compromise isn’t just about “filler in artery = blockage” is crucial for modern aesthetic practice.

The key takeaway is that necrosis can occur through multiple pathways:

1. Direct arterial occlusion (the traditional understanding)
2. Pressure on capillary beds
3. External compression causing vasospasm
4. Venous occlusion affecting drainage
5. Combinations of the above

Each mechanism has different risk factors, presentations, and optimal treatments. As aesthetic injectors, we need to think beyond the simple model of arterial blockage and consider all these potential causes when preventing, diagnosing, and treating vascular complications.

Moving Forward with Better Understanding

This more nuanced understanding of vascular occlusion should make us better, safer injectors. By recognizing that different areas of the face have different vulnerabilities – the midline’s susceptibility to pressure necrosis, the potential for vasospasm in susceptible patients, the unique venous drainage risks around the eyes – we can tailor our techniques and product choices accordingly.

Remember: the goal isn’t to make you fearful of complications, but to arm you with knowledge that will help guide decisions that reduce risk. Understanding these multiple mechanisms is what separates practitioners who simply follow protocols from those who truly understand the why behind their clinical decisions.

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