Is it true that arterial occlusive disease is an absolute contraindication for intermittent pneumatic compression (IPC)?

The Answer

Not at all!

Unfortunately, many medical professionals are under the impression that applying even a small external pressure to an ischemic limb with reduced distal arterial pressures may serve to reduce or completely stop the already-compromised blood flow. This article presents strong evidence that, contrary to popular belief, IPC can bring life-changing benefits to those who cannot undergo revascularization.

History

Part of the reason this dogma exists is because, for many who consider it, applying IPC to ischemic limbs seems counterintuitive and likely dangerous. Also contributing to this myth are the literature reviews written by investigators as far back as 1934 who showed a poor understanding of the physiological mechanisms. Though these measured acute effects of compression on increased blood flow in ischemic limbs and relief of symptoms, the assessments made about IPC therapy were muddled due to the use of a great variety of compression schemes and devices. This lack of clarity resulted in literature that only served to feed misgivings about IPC as a treatment modality.

Physiological & Optimization Studies | ACI Medical

To demystify the true value of IPC, our goal was to determine the physiological mechanisms of action, to optimize IPC design for maximal acute effect, and to determine if there is a clinical benefit to patients with lower extremity ischemic disease.

We started with physiological studies¹ with compression applied to the dependent limb, which showed these acute mechanisms:

• Increased arterial-venous pressure gradient
• Reduced peripheral resistance
• Abolition of the veno-arteriolar reflex

Further studies² concerned optimization:

• Pressure:  at least 120 mmHg
  This high pressure is required to empty the veins in the dependent limb, which temporarily reduces venous pressure to near zero and increases the arterial-to-venous pressure gradient and therefore, flow. Reducing venous pressure also serves to temporarily abolish the veno-arteriolar reflex, which allows for arteriolar dilation.
• Timing:  3 second pulses followed by 17 seconds of low pressure
  An essential requirement for an arterial pump is the ability to quickly reach inflation and deflation pressures with rise times of 0.25 to 0.30 seconds and fall times under 0.5 seconds.  This rapid squeeze and release creates blood velocities that apply shear stress to the endothelium which releases nitric oxide and further supports the large acute vasodilatory effect in the arterioles.
• Compressed tissues:  foot, ankle and calf regions
  In order to maximize blood flow through the major arteries and to the toes where ischemic disease often presents, we found that a circumferential foot bladder including the ankle should be compressed first, followed one second later by compression of the calf with a relatively large asymmetrical bladder.

Randomized Controlled Trials | ACI Medical

Intermittent Claudication

Once the arterial IPC device was optimized, three randomized controlled trials³ were performed on patients with intermittent claudication. Not only did these trials yield significantly increased walking distances of two to three times, but also sustained “permanent” improvements begged the question, “What long term mechanisms might be at work?”

Limb Salvage due to Arteriogenesis

Further studies⁴ showed that arteriogenesis (the opening of collaterals) was responsible for improved ABI’s, PVR’s, toe pressures and popliteal flow. A recently published study from 2010⁵ reported a 94% limb salvage rate at 3.5 years in patients who were unable to undergo revascularization procedures.

Arterial Assist Device, NOT Lymphedema Pump

ArtAssist®…The Arterial Assist Device®

Today, it is widely-known that IPC devices are designed for prophylaxis against deep vein thrombosis (DVT) and for treatment of lymphedema. However, the understanding behind these devices does not coincide with our exploration of IPC to treat severe forms of arterial disease. Lymphedema and DVT devices do not apply enough pressure to the dependent limb to adequately empty the veins, nor do they apply and release pressure rapidly enough to stimulate release of nitric oxide (NO). While such devices will not significantly improve blood flow in the ischemic limb, it is difficult to say whether they would be harmful without further study.

References in this Publication

1. Effect of intermittent pneumatic foot compression on popliteal artery haemodynamics. Delis, K.T.; Labropoulos, N.; Nicolaides, A.N.; Glenville, B.; and Stansby, G. Imperial College School of Medicine, Academic Vascular Surgery, St. Mary’s Hospital, London, UK. Eur J Vasc Surg, p. 270-277, vol. 19, no. 3, March 2000.
2. Optimum intermittent pneumatic compression stimulus for lower-limb venous emptying. Delis, K.T.; Azizi, A.A.; Stevens, R.J.G.; Wolfe, J.H.N. and Nicolaides, A.N. Irvine Lab for Cardiovascular Investigation and Research Academic Vascular Surgery, Imperial College School of Medicine, St. Mary’s Hospital, London, UK. Eur J Vasc Endovasc Surg 19, 261-269 (2000).
3. Improvement in walking ability, ankle pressure indices and quality of life in vascular claudication using intermittent pneumatic foot and calf compression:  a randomized controlled trial. Delis, K.T.; Nicolaides, A.N.; Cheshire, N.J.W.; Wolfe, J.H.N. St. Mary’s Hospital, London, UK. British Journal of Surgery December 2002; Volume 88, Issue 4:605-606.
4. Angiographic improvement after rapid intermittent compression treatment (ArtAssist®) for small vessel obstruction. Van Bemmelen, P.; Char, D.; Giron, F.; and Ricotta, J.J. Dept. of Surgery, Div. of Vascular Surgery, State University of New York at Stony Brook, NY. Ann Vasc Surg 2003; 17:224-228.
5. Sequential compression biomechanical device in patients with critical limb ischemia and nonreconstructable peripheral vascular disease. Sultan, S.; Hamada, N.; Soylu, E.; Fahy, A.; Hynes, N. and Tawfick, W. Department of Vascular and Endovascular Surgery, University College Hospital, Galway, Journal of Vascular Surgery 2011; 54:440-447.