Cath Lab Digest

Contrary to what you might believe it is vital for wound care companies to have a completely unbiased view of the published scientific literature relating to their industry. Here I share my recent thinking as we enter a period of quickening development into the science behind the clinical effects of NPWT (Negative Pressure wound Therapy). It doesn’t pretend to be a comprehensive review but sets out the critical components for understanding the mechanisms.

NPWT might justifiably be said to have entered the mainstream of the clinical and scientific community with the publication of back-to-back papers in the same issue of the peer reviewed journal Annals of Plastic Surgery in 1997.1,2 In the first paper Morykwas et al describe experiments in pigs designed to explore and demonstrate the scientific mode of action of NPWT using open cell polyurethane (PU) foam as the filler which many will know simply as “black foam”. In the second paper Argenta et al describe a case series of some 300 patients treated with NPWT using open cell PU foam on a range of acute, sub-acute and chronic wounds. Since much of the literature on the scientific understanding of the mechanism of action (MOA) stems from the first Morykwas paper, it is appropriate to review that paper in a little detail.

The Morykwas paper reported four experiments. In the first experiment full thickness wounds were created on the backs of pigs. A laser Doppler probe was inserted into the healthy peri-wound skin to record any changes in blood flow. NPWT using PU foam was applied to the wounds at a range of pressures (-50, -75, -100 mm Hg etc) and the effects on blood flow were recorded. Increases in the Doppler signal were recorded. The effects last for 5-10 minutes. The greatest response was seen at -125 mm Hg. This pressure was then selected for further experiments. It is important to realize this is the only published evidence for recommending -125 mm Hg as the optimal pressure for NPWT.

In the second experiment full thickness wounds were again created on the backs of pigs; some wounds were connected to NPWT at -125 mm Hg and some were left as controls. Each day the animals were anesthetized and the volume remaining in the wound was measured by filling it with dental impression material, which was allowed to set and then removed to measure its volume. Note that on the backs of these pigs there was very little sideways wound contraction and these wounds filled entirely by granulation from the base. There was a statistically significant increase in granulation compared to the control wounds of some 60% after 10 days. (There were also some experiments where NPWT was applied intermittently and the granulation tissue grew even faster in those wounds. We will not review the implications for MOA and intermittent therapy in the interests of space, but this certainly a subject for future investigation.)

In the third experiment full thickness wounds were deliberately infected with bacteria (Staphylococcus aureus) so that the level of bacteria per g of tissue was above 105 (the threshold above which clinically wounds will not heal without some specific intervention). NPWT was applied to some wounds and others were left as controls. The level of bacteria in the wounds treated with NPWT was reduced more than 100 fold from over 105 to 103 per gram tissue.

The fourth experiment is rarely discussed but is perhaps the most remarkable of them all. On the flanks of anesthetized pigs rectangular random pattern skin flaps were created were the blood supply to the flap came from the single remaining upper edge. The flaps were deliberately created so that there was insufficient blood flow from the intact (proximal) edge and over 4-5 days the flaps suffered necrosis from the distal end to about 50% of their length. When NPWT was applied to the flaps after they had been created, they survived to about 65% of their length. Remarkably, when NPWT was applied to the intact skin for a 4-day period before the flaps were created, the flaps also survived to about 65% of their length when the flaps were raised from the previously treated skin. When NPWT was used both before and after creating the flaps, the effects were additive and the flaps survived to more than 0% of their length. This fascinating experiment is not well explained by our current theories although some kind of ischemic pre-conditioning mechanism would be a likely candidate.

They say that there is “nothing new under the sun” and this is particularly true for NPWT. Some eight years before the Morykwas and Argenta papers Mark Chariker a plastic surgeon working with nurse Katherine Jeter published an article describing how they used vacuum (at -60 to -80 mm Hg) applied to wounds filled with gauze under film dressings to manage entero-cutaneous fistula wounds.3 Their article described how this NPWT technique was able to facilitate healing and closure. The journal in which the Chariker-Jeter technique was published was a not prestigious peer reviewed journal like Annals of Plastic Surgery used by Morykwas & Argenta (you won’t find Chariker-Jeter it in a PubMed search) and although the Chariker-Jeter technique was used locally it was largely unnoticed until more recent times.

So how do foam and gauze operate under NPWT? Initially porcine model experiments at the University of Lund, Sweden showed a 1:1 relationship between the negative pressure applied and the negative pressure transmitted to the wound bed whether the wound is filled with foam or gauze.4 When the clinical effectiveness of NPWT applied with gauze at -80 mm Hg was reviewed in retrospective data from 30 patients wounds reduced on average by 15% per week. This is similar to the published rates of wound volume reduction from NPWT applied using foam at -125 mm Hg.5