Abstract
A review of the evidence base for the use of vacuum‐assisted closure (VAC) therapy is presented, analysing both experimental and clinical data.
Keywords: Vacuum‐assisted closure, VAC, Topical negative pressure, TNP, Wound, Evidence‐based medicine
Introduction
It is widely acknowledged that topical negative pressure (TNP) therapy (1) forms an important component of the wound care armamentarium (2) with a wide variety of documented indications for use 3, 4, 5, 6, 7, 8. While various techniques have been used to implement TNP 9, 10, 11, the gold standard method for delivery is using the vacuum‐assisted closure (VAC) system. Indeed, the evidence base for the clinical efficacy of TNP is virtually wholly founded on this commercially available system. One should therefore be careful not to extrapolate this evidence base to directly apply to other systems. While VAC therapy is widely accepted, its mode of action has, until recently, been poorly understood. It would therefore seem timely to present the recent evidence base for its mechanisms of action and the corresponding clinical benefits.
VAC therapy uses negative pressure to promote wound healing. It comprises an open pore foam conduit (cut to fit a wound), which is covered by a semi‐permeable adhesive drape, attached to a microprocessor‐controlled therapy unit. The unit applies negative pressure to the foam–wound interface through a specialised tube, which also transfers accumulated fluid to a canister. VAC can be applied using a variety of computerised protocols, which use a number of waveforms, allowing the user to select continuous or intermittent therapy. Delivery of negative pressure is rigorously maintained: the efficacy and consistency of this delivery have been experimentally confirmed (12). However, it has also been shown that the type of foam used (13) and any interface dressing (12) may alter the target pressure and blood flow response (12) and therefore affect optimal delivery of the therapy.
The potential mechanisms by which wound healing is promoted under these conditions were first put forward by Morykwas et al. in 1997 14, 15. Research over the past decade has further elucidated these benefits, both in physiological and in clinical terms. This review analyses the evidence base for the use of VAC therapy, linking experimental and clinical data. This evidence base is summarised in 1, 2.
Table 1.
Summary of evidence base promoting the use of vacuum‐assisted closure (VAC) in wound care management – mechanisms of action: experimental data
| Hypothesis | Paper | Main findings |
|---|---|---|
| Mechanical forces stimulate a biological response | Saxena et al. (22) | • Tissue strains (micro‐strains) of 5–20% can be obtained with standard VAC therapy |
| • Deformations predicted by computer model similar in morphology to surface undulations seen histologically in VAC‐treated wounds | ||
| Greene et al. (25) | • Microvessel density significantly higher in those areas of wound with foam contact compared with pre‐treatment and to those areas without foam contact | |
| Perfusion is increased | Morykwas et al. (14) | • In porcine model, blood flow levels increased fourfold when 125 mmHg negative pressure applied to wounds |
| • Random pattern flap survival significantly increased compared with controls | ||
| Timmers et al. (13) | • Fivefold increase in cutaneous blood flow under VAC dressings in intact human forearm skin (black foam) and nearly threefold (white foam) | |
| Wackenfors et al. (29) | 60‐minute VAC therapy led to: | |
| • Increased blood flow | ||
| • Increased partial pressures of oxygen and lactate | ||
| Kamolz et al. (27) | • Perfusion in severely burnt hand significantly higher compared with control (silver sulphadiazine‐treated hand) after 2 and 3 days of VAC therapy | |
| Exudate is removed and oedema reduced | Kamolz et al. (27) | In burnt hand wounds treated with VAC: |
| • Increased amount of fluid removed | ||
| • Oedema reduction | ||
| Wound fluid composition is altered | Shi et al. (39) | MMP‐1 and MMP‐13 messenger RNA levels decreased with VAC therapy |
| Greene et al. (25) | Reduced activities of MMP‐9/neutrophil gelatinase‐associated lipocalin, MMP‐9 and latent and active forms of MMP‐2 | |
| Stechmiller et al. (40) | Eight hospitalised patients with pressure ulcers treated with VAC therapy: | |
| • Significant decrease of TNF‐α at days 1, 2 and 7 after start of therapy | ||
| • Rapid improvement in MMP‐3 and MMP‐9 levels | ||
| • Decreased ratio of MMP‐3:TIMP‐1 | ||
| Granulation tissue formation is enhanced | Morykwas et al. 14, 41 | • Higher rates of granulation tissue in VAC‐treated porcine wounds compared with controls |
| • 125 mmHg negative pressure forms granulation tissue at significantly higher rate than 25 mmHg of 500 mmHg |
MMP, matrix metalloproteinase; TIMP‐1, tissue inhibitor of metalloproteinases‐1.
Table 2.
Summary of evidence base promoting the use of vacuum‐assisted closure (VAC) in wound care management – clinical benefits of VAC therapy: evidence levels I and II
| Wound volume/size is reduced | Ford et al. (44) | RCT comparing wound gel products with VAC therapy in stage III or IV pressure ulcers |
| • Non significant reduction in ulcer volume following VAC therapy | ||
| Joseph et al. (45) | RCT comparing 6 weeks VAC therapy to standard wet‐to‐moist dressings in leg ulcers: | |
| • 78% reduction in wound volume with VAC (30% with standard dressings; significant difference) | ||
| Eginton et al. (43) | Crossover RCT of VAC therapy and moist wound dressings | |
| • Significant reduction in wound volume using VAC compared with controls | ||
| Wound beds are more rapidly prepared | Armstrong et al. (46) | Large multicentre RCT of patients with complex diabetic foot amputation wounds comparing VAC therapy and moist wound therapy: |
| • Significant increased rate of formation of granulation tissue in VAC therapy patients (42 versus 84 days) | ||
| Vuerstaek et al. (47) | Prospective RCT of hospitalised patients with chronic leg ulcers, treated with VAC therapy or advanced wound care: | |
| • Patients ready to receive skin graft in significantly shorter time than controls (7 versus 17 days) | ||
| Wound healing is faster | Armstrong et al. (46) | Large multicentre RCT of patients with complex diabetic foot amputation wounds comparing VAC therapy and moist wound therapy: |
| • Significant reduction in time to median complete wound closure (56 versus 77 days) | ||
| • Significantly greater proportion of patients achieved complete wound closure in study period | ||
| Vuerstaek et al. (47) | Prospective RCT of hospitalised patients with chronic leg ulcers, treated with VAC therapy or advanced wound care: | |
| • Reduced median total healing time for VAC therapy (29 versus 45 days) | ||
| Graft take is enhanced | Moisidis et al. (48) | RCT comparing VAC therapy with standard bolster dressings in the same wounds: |
| • Trend towards higher rate of epithelialisation in VAC‐treated grafts | ||
| • Blinded independent assessment of quality of grafts suggested quality of grafts in VAC‐treated patients significantly better | ||
| Jeschke et al. (49) | RCT of dermal template used for reconstruction of large effects, either alone or in combination with fibrin glue and VAC therapy | |
| • Significant increased take rate in VAC‐treated group | ||
| • Significant reduction in time needed for skin grafting | ||
| • Quality of grafts assessed as significantly superior | ||
| Vuerstaek et al. (47) | Prospective RCT of hospitalised patients with chronic leg ulcers, treated with VAC therapy or advanced wound care: | |
| • Median percentage of successful skin grafts significantly different (P = 0·011) between VAC and control groups (83 versus 70%) | ||
| Drainage time is reduced for acute wounds | Stannard et al. (50) | RCT of traumatic haematomas; VAC therapy compared with pressure dressings: |
| • Time to drain wound significantly shortened (1·6 versus 3·1 days) | ||
| RCT of postoperative high‐impact fracture wounds, comparing VAC therapy with standard dressings: | ||
| • Significant reduction in drainage time (1·8 versus 4·8 days) | ||
| Complications are reduced | Ford et al. (44) | RCT comparing wound gel products with VAC therapy in stage III or IV pressure ulcers: |
| • Trend towards reduced white blood cell counts in VAC‐treated wounds | ||
| Stannard et al. (50) | RCT of traumatic haematomas; VAC therapy compared with pressure dressings: | |
| • Infection rate in VAC‐treated haematomas half that of controls | ||
| Joseph et al. (45) | RCT comparing 6 weeks VAC therapy to standard wet‐to‐moist dressings in leg ulcers: | |
| • Significantly lower complications in VAC‐treated group | ||
| Armstrong et al. (46) | Large multicentre RCT of patients with complex diabetic foot amputation wounds comparing VAC therapy and moist wound therapy: | |
| • Trend towards fewer re‐amputations for patients treated with VAC therapy | ||
| Schwien et al. (51) | Retrospective matched‐group analysis of patients with stage II or IV pressure ulcers, treated in the home care environment with either VAC or standard therapy: | |
| • Lower rates of hospitalisation and emergency care for wound problems in VAC‐treated patients | ||
| Response to first‐line treatment is enhanced | Sjögren et al. (52) | Retrospective controlled analysis of post‐sternotomy mediastinitis patients, comparing VAC therapy with standard treatment: |
| • Significant increase in response to first‐line treatment in VAC‐treated patients (100 versus 62·5%) | ||
| Increased patient survival | Sjögren et al. (52) | Retrospective controlled analysis of post‐sternotomy mediastinitis patients, comparing VAC therapy with standard treatment: |
| • 30‐day survival rate 100% with VAC treatment; 85% with conventional treatment | ||
| • 1‐ and 2‐year survival rates also significantly better for the VAC‐treated group | ||
| Sjögren et al. (53) | Large retrospective comparison between patients with mediastinitis treated with VAC therapy and those cardiac patients who did not have mediastinitis: | |
| • No significant difference in early or late survival between the groups | ||
| VAC therapy is cost effective | Moues et al. (55) | RCT of wounds requiring surgical closure: |
| • VAC therapy patients spent significantly less time in hospital than controls | ||
| • Nursing costs significantly reduced in VAC therapy group | ||
| Vuerstaek et al. (47) | Prospective RCT of hospitalised patients with chronic leg ulcers, treated with VAC therapy or advanced wound care: | |
| • Total wound care costs 25–30 lower for VAC than for standard wound care (P = 0·001) |
RCT, randomised controlled trial.
Review of the evidence
How VAC therapy supports wound healing – experimental data
VAC therapy is believed to work by:
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Promoting a moist wound environment
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Creating mechanical forces that stimulate a biological response
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Promoting perfusion
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Reducing oedema
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Altering wound fluid composition
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Assisting in granulation tissue formation
Experimental evidence to back up these claims will be addressed in turn.
A closed, moist wound environment
It is commonly accepted that a closed, moist wound environment facilitates healing by preventing tissue dehydration, accelerating angiogenesis, increasing breakdown of dead tissue and fibrin and potentiating the interaction of growth factors with their target cells 16, 17, 18, 19, 20, 21, In addition, pain and exposure to infection should be reduced. Applied correctly, these conditions should be met by VAC therapy because the VAC drape is designed to be occlusive, yet semi‐permeable.
Mechanical forces may stimulate a biological response
Several authors have reported that mechanical stimulation of cells leads to increased proliferation. Stress induced by the negative pressure applied through the foam dressing during VAC therapy is said to produce three‐dimensional stress within the cells (micro‐strain) as well as across the whole area of the wound (macro‐strain).
Wound edges are conceivably pulled inwards in a centripetal fashion by the negative pressure of VAC therapy, providing wound contracture, or macro‐strain (2). Evidence in support of this is presented in the clinical section of this review.
Cellular stretch (or micro‐strain) is said to occur when the negative pressure drags the tissue surface into the foam pores. Two studies in particular provide evidence for micro‐strain occurring during VAC therapy. Saxena et al. (22) created a computer model of a wound and simulated VAC application. At typical clinical settings, the authors were able to induce average tissue strains in the range of 5–20%, which is analogous to in vitro strain levels shown to promote cellular proliferation 23, 24. In addition, the deformation predicted by the model was similar in morphology to the surface undulations observed in histological sections of wounds treated with VAC therapy (22).
Microdeformations can, by definition, only occur in those areas with foam contact. Greene et al. (25) conducted an intra‐wound comparison of the chronic wounds of debilitated patients treated with VAC therapy, demonstrating a difference between those areas with and without foam contact. Microvessel density, as measured by immunohistochemistry, was significantly greater in those areas with foam contact, as compared with pre‐treatment and with those areas without foam contact, both at 1 and 2 weeks of therapy (P values all equal to or less than 0·05). This was interpreted as signifying increased proliferation and angiogenesis (Figure 1).
Figure 1.

Results from Greene et al. (25), demonstrating that microvessel density is significantly higher in those areas of wound with foam contact, compared with those areas without foam contact, both at 1 and 2 weeks of therapy. VAC, vacuum‐assisted closure.
Perfusion may be increased
Optimal blood perfusion is necessary to deliver nutrients, oxygen, cells and growth factors to a healing wound and to remove waste products, free radicals and carbon dioxide. In addition, in a patient treated systemically with antibiotics, improved perfusion leads to improved delivery of antibiotics to the wound (26).
Multiple studies have reported positive effects of VAC therapy on tissue perfusion 13, 14, 27, 28, 29. Morykwas et al. (14) presented a series of studies using wounds in a pig model that were subjected to VAC therapy. In this original paper, two observations were made that suggested that VAC therapy promoted perfusion. First, Doppler measured blood flow levels increased fourfold when 125 mmHg negative pressure was applied to the wounds. Second, random pattern flap survival significantly increased (P ≤ 0·05) by 21% compared with controls. The increase in survival seen with VAC therapy is comparable to that achieved using pharmacological modalities (30).
Timmers et al. (13) performed similar studies of cutaneous blood flow using VAC dressings over intact human forearm skin in healthy volunteers, recording over a fivefold increase with the black (polyurethane) foam and a nearly threefold increase with the white (polyvinyl alcohol) foam (Figure 2). Comparison of blood flow at baseline and at a negative pressure of 300 mmHg showed a statistically significant difference (P < 0·001).
Figure 2.

Graph [from Timmers et al. (13)] showing vacuum‐assisted closure therapy increases local blood perfusion in healthy subjects, recording over a fivefold increase with the black (polyurethane) foam and a nearly threefold increase with the white (polyvinyl alcohol) foam.
Wackenfors et al. (29) not only recorded an increase in blood flow with 60 minutes of VAC therapy in their porcine model but also measured enhanced wound fluid partial pressures of oxygen and lactate. This they attributed to the increase in microvascular blood flow, further adding that the combination of oxygen and lactate is known to promote wound healing 31, 32.
In addition to the immediate effect on local perfusion, VAC therapy has also been shown to stimulate perfusion at later time points during the healing process. In a clinical study of bilateral partial‐thickness hand burns, Kamolz et al. (27) applied VAC therapy to the more severely burnt hand, with silver sulphadiazine being applied to the other. Whereas perfusion was lower in the VAC‐treated hand before start of treatment, it was significantly higher when compared with perfusion in the silver sulphadiazine‐treated control hand after 2 and 3 days of VAC application (P = 0·001 and P = 0·006, respectively) (Figure 3). This may have particular relevance in preventing progression of a burn over days from partial thickness to full thickness via impaired perfusion through the zone of stasis.
Figure 3.

Difference in perfusion calculated by vacuum‐assisted closure (VAC)‐treated perfusion units minus control treated in bilateral partial‐thickness hand burns, from Kamolz et al. (27). NS, not significant.
Exudate is removed and oedema may be reduced
That the VAC therapy removes fluid from the wound is not disputed. It is also said to reduce oedema. In the aforementioned study by Kamolz et al., a ‘noteworthy’ amount of fluid was removed from the burn wound and a ‘clinically obvious’ oedema reduction was observed in comparison to the silver sulphadiazine‐treated hand (27).
Fluid composition may be altered
Increased levels of pro‐inflammatory cytokines, such as tumour necrosis factor‐α (TNF‐α), are correlated with chronic inflammation 33, 34, 35. It has also been shown that chronic wound fluid contains abnormally high proteases such as matrix metalloproteinases (MMPs), elastase, plasmin and thrombin 34, 36, 37. Excessive protease activity in chronic wounds results in abnormal degradation of the extracellular matrix, negatively impacting wound healing (38). Evidence is now accumulating that VAC therapy leads to the removal of such pro‐inflammatory cytokines and proteases.
Shi et al. (39) studied the changes in MMP‐1, MMP‐2 and MMP‐13 in chronic wounds after treatment with VAC by quantifying the expression of messenger RNA encoding these proteins. They reported that both MMP‐1 and MMP‐13 decreased, with the steepest decline demonstrable for MMP‐13. The previously mentioned study by Greene et al. (25), which recorded increased microvessel density in wounds where microdeformations were occurring, also measured MMP activity using zymography. Activities of MMP‐9/neutrophil gelatinase‐associated lipocalin, MMP‐9 and latent and active forms of MMP‐2 were reduced by 15–76% in VAC‐treated wounds.
Reduction of both MMPs and TNF‐α has been reported by Stechmiller et al. (40). Eight hospitalised patients with pressure ulcers showed a significant decrease of TNF‐α in wound fluids at day 1, day 3 and day 7 after the start of VAC therapy. In addition, a rapid improvement in MMP‐3 and MMP‐9 levels was seen, and a decrease in the ratio of MMP‐3 to tissue inhibitor of metalloproteinases‐1 (MMP‐3:TIMP‐1) relative to baseline was reported.
Enhancement of granulation tissue formation
Production of extracellular matrix is seen clinically as formation of granulation tissue. Granulation tissue forms as part of the proliferative stage of wound healing. Absence of granulation tissue is a feature of a non healing wound (22). Granulation tissue is a consistently reported finding resulting from treatment with VAC therapy.
Studies by Morykwas et al. 14, 41 have reported higher rates of granulation tissue formation upon application of VAC therapy to porcine wounds compared with controls and have showed that the recommended negative pressure of 125 mmHg forms granulation tissue at a significantly higher rate than wounds treated with low (25 mmHg) or high (500 mmHg) negative pressure (P < 0·0001) (Figure 4).
Figure 4.

Increase rate of granulation tissue formation with vacuum‐assisted closure (VAC) therapy in porcine wounds, demonstrating optimal granulation and wound volume reduction at negative pressures of 125 mmHg, from Morykwas et al. (41).
Clinical benefits of VAC therapy – randomised control and case control studies
How these experimentally derived observations translate into clinical advantage will now be reviewed. Since its introduction, VAC therapy has been used in an expanding variety of clinical situations. The clinical benefits of VAC therapy have been quoted as:
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Reduction of wound volume/size
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More rapid wound bed preparation
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Faster wound healing
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Enhancement of rate of graft take
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Decreased drainage time for acute wounds
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Reduction of complications
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Enhancement of response to first‐line treatment
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Increased patient survival
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Reduction of cost
Although there are over 300 peer‐reviewed journal articles describing VAC use, in the following review only the highest levels of evidence available (levels I and II) will be described [SIGN grading system (42)].
Reduction of wound volume/size
At least three randomised controlled trials (RCTs) have reported wound volume and/or size reduction following VAC therapy 43, 44, 45.
Ford et al. (44) randomised patients with stage III or IV pressure ulcers to either the ‘Healthpoint’ system of wound gel products or VAC therapy. A total of 22 patients (35 wounds) completed 6 weeks of treatment. There was a non significant reduction in ulcer volume favouring VAC therapy (42·1% reduction for wound gels and 51·8% for VAC).
Joseph et al. (45) compared VAC therapy with standard wet‐to‐moist dressings in the treatment of 24 patients with 36 recalcitrant leg ulcers. At the end of 6 weeks, the percent reduction in wound volume was 78% for VAC therapy compared with 30% for the control group (P = 0·038).
In a crossover RCT, Eginton et al. (43) compared VAC therapy with moist wound dressings in the treatment of diabetic foot wounds. Wounds were photographed weekly and wound dimensions calculated in a blinded fashion using spatial analysis software. Although the sample size was small (six patients completing treatment), VAC therapy significantly (P < 0·005) reduced wound volume by 59% (±9·7%) compared with moist dressings(−0·1 ± 1·7%).
A summary of the results from these three studies is showed graphically in Figure 5. While all these studies are small, their results do add weight to the clinical notion that VAC therapy helps reduce wound volume.
Figure 5.

Graph depicting results of three randomised controlled trials reporting on volume/size reduction with vacuum‐assisted closure (VAC) therapy 43, 44, 45.
More rapid wound bed preparation
As previously outlined, VAC therapy is likely to cause microdeformational forces and increases in perfusion. Granulation tissue formation has been documented under these favourable conditions. Granulation tissue forms the essential component in wound bed preparation. Two RCTs have evaluated granulation tissue formation in challenging chronic wounds treated with VAC therapy.
Granulation tissue formation was evaluated in a large multicentre RCT of 162 patients with complex diabetic foot amputation wounds. The control treatment consisted of advanced moist wound therapy (hydrogels, hydrocolloids, foams and alginates) according to consensus guidelines. Patients were treated until complete wound closure or up to 112 days. The proportion of patients who presented with 0–10% granulation at baseline and later achieved 76–100% was assessed. The authors reported that VAC therapy patients developed this level of granulation tissue in a mean of 42 days compared with 84 days in control patients (P = 0·002) (46).
In another prospective RCT (47), 60 hospitalised patients with chronic leg ulcers (of mixed origin) were evaluated. The wound beds of VAC therapy patients were ready to receive a skin graft in a significantly shorter time than control patients who were treated with advanced wound care (hydrogels, hydrocolloids, alginates and films). The median preparation time was 7 days [95% confidence interval (CI) = 5·7–8·3] in the VAC group versus 17 days in the control group (95% CI = 10–24) (P = 0·005).
Faster wound healing
The combination of new granulation tissue and drawing together of wound edges is essential for the healing of ulcers. The above evidence suggests that VAC therapy aids in both these processes. It is therefore perhaps not surprising that both RCTs mentioned in the preceding section reported that patients treated with VAC therapy achieved wound closure earlier than patients treated with other modalities.
The RCT reported by Armstrong et al. (46) documented that patients treated with VAC therapy achieved complete wound closure in a median time of 56 days compared with a median time of 77 days for control patients (P = 0·005). In addition, a significantly greater proportion of patients treated with VAC therapy versus control achieved complete wound closure in the 112‐day study period (56 versus 39%, respectively; P = 0·040). Vuerstaek et al. (47) reported a median total healing time of 29 days (95% CI = 25·5–32·5) for the VAC therapy‐treated patients compared with 45 days (95% CI = 36·2–53·8) for the controls (P = 0·0001).
Enhancement of graft take
VAC therapy has been documented to improve skin graft take in a number of non comparative studies. Three RCTs have examined the role of VAC therapy in graft take.
Vuerstaek et al. (47) evaluated success of graft take as a secondary endpoint of their RCT of their hospitalised patients with chronic leg ulcers. Both VAC‐treated and conventionally prepared wound beds received full‐thickness punch skin grafts. The median percentage of successful skin grafts differed significantly (P = 0·011) between the VAC and the control groups, with 83 ± 14% versus 70 ± 31% (Figure 6).
Figure 6.

Vacuum‐assisted closure (VAC) therapy showing a significantly better take of graft and of dermal template 47, 49.
Moisidis et al. (48) divided the wounds of their 20 patients in half at time of split‐thickness skin grafting, so that each patient served as their own control. Half of the wound was covered with a VAC dressing and half with standard bolster dressings, with an intervening bridge between the portions. They reported a non significant higher rate of epithelialisation in the grafts treated with VAC dressings. In addition, an independent physician, blinded to the therapy, subjectively assessed the quality of the grafts. For those areas treated with VAC therapy, the quality of the graft was found to be better in 50% and equivalent in 35% compared with controls (P < 0·05).
Another RCT reports on the use of a dermal template (integra) either alone or in combination with fibrin glue and VAC therapy for the reconstruction of large defects. The take rate was 78 ± 8% in the conventional treatment group and 98 ± 2% in the fibrin/VAC therapy group (P < 0·003) (Figure 6). There was also a significant reduction in the time needed for subsequent skin grafting (P < 0·002). In the same cohort of patients, the quality of grafts was also reported as superior (P < 0·05) to those of the control group (49).
Decreased drainage time for acute wounds
Because VAC therapy removes blood and excess serous fluid from wounds, the time period that wounds drain for should be lessened. One RCT has measured drainage time for wounds in the trauma setting, comparing VAC therapy with standard dressings. The first part of the study randomised 44 patients with draining haematomas after high‐speed impact to either pressure dressings or a VAC. Patients in the pressure dressing group drained for a mean of 3·1 days compared with 1·6 days for the VAC group (P = 0·03). The second part of the study randomised a further 44 patients with postoperative wounds over calcaneous, pilon or high‐energy tibial plateau fractures. Patients received either standard dressings over their surgical incision or a VAC dressing. Again, a significant difference (P = 0·02) was present when comparing drainage in the standard group (4·8 days) and the VAC group (1·8 days). The authors suggested that although their data are preliminary, surgical incisions may seal more rapidly after the application of a VAC over both haematomas and surgical incisions (50).
Reduction of complications
Local and systemic complications, such as infection, are often a challenge in complex wound care. VAC therapy, by virtue of its efficacy in removing fluid from the wound and promoting perfusion, may contribute to a reduction in the number of wound healing complications said to be experienced by VAC therapy patients.
The aforementioned RCT described by Ford et al. (44) in which VAC therapy was compared with the use of wound gel products in promoting ulcer healing reported the number of lymphocytes and neutrophils present in each group’s ulcers. A non significant decrease in the number of white blood cells was documented in the VAC group, with a trend towards an increased number in the standard care group.
The infection rate for the patients with haematomas treated with VAC therapy in Stannard’s study (50) was half that of the controls. In the RCT reported by Joseph et al. (45), the number of complications was significantly lower in the VAC‐treated compared with the wet‐to‐moist treated chronic wounds (P = 0·0028). Complications in this 6‐week study included osteomyelitis, wound infections and fistulas. In the large diabetic foot amputation wound RCT (46), a trend towards fewer re‐amputations for patients treated with VAC therapy compared with control treatment was seen (P = 0·06).
Extending these ideas further, Schwien et al. (51) performed a retrospective matched‐group analysis of 60 VAC therapy patients and 2288 non VAC therapy patients with stage III or IV pressure ulcers all treated in the home care environment. Those treated with VAC therapy experienced lower rates of hospitalisation and emergency care for wound problems.
Enhancement of response to first‐line treatment
VAC therapy may also simplify treatment, enhancing the numbers of patients who respond to first‐line treatment. Sjögren et al. compared outcomes for post‐sternotomy mediastinitis treated in conventional fashion with surgical revision, closed irrigation or reconstruction with omentum or pectoral muscle flaps or with VAC therapy followed by re‐wiring. The control group of 40 patients were treated between July 1994 and December 1998. The 61 VAC therapy patients were treated between January 1999 and December 2003. Follow‐up was performed in April 2004 and was 100% complete. All the VAC therapy patients responded well to first‐line treatment, while 37·5% of those in the control group failed to respond to treatment (P < 0·001) (52).
Increased patient survival
Two studies have looked at the mortality of cardiac patients who develop mediastinitis and suggest a survival advantage if VAC therapy is used. The first study from Sjögren et al. (52), described above, also showed that the 30‐day survival rate was 100% with VAC treatment but 85% with the conventional treatment group (Figure 7). Moreover, the 1‐year survival rate was 93% in the VAC therapy group but only 82% in the control group, with rates dropping to 83 and 59%, respectively, at 5 years.
Figure 7.

Increased survival for vacuum‐assisted closure (VAC) therapy‐treated patients. P < 0·01 for results at 30 days and P < 0·05 for results at 6 months, 1 and 5 years, from Sjögren et al. (52).
The same authors performed a further large retrospective study of coronary artery bypass patients treated between January 1999 and September 2004 (53). A total of 4781 patients without mediastinitis were compared with 46 patients who developed mediastinitis and were treated with VAC therapy (without additional muscle flaps). There was no significant difference in early or late survival between the groups. Thus, the patients treated with VAC therapy fared as well as the non infected cohort (Figure 8).
Figure 8.

No difference in survival for vacuum‐assisted closure (VAC) therapy‐treated patients with mediastinitis compared with patients without mediastinitis, from Sjögren et al. (53).
Reduction in cost
The material costs of VAC therapy are of course higher than most conventional treatment, such as moist gauze. However, these costs have been shown by several authors in economic evaluations to be compensated for 47, 54, 55. Compensations include reduced number or length of hospitalisation, reduced intensive therapy unit stay, fewer time‐consuming dressing changes, reduced wound surface area, better response to first‐line treatment and shorter duration until wounds are ready for surgical intervention.
Vuerstaek et al. (47) noted that the total wound care costs for hospitalised chronic leg ulcer patients were 25–30% lower for VAC than for standard wound care (P = 0·001).
Moues et al. (55) performed a RCT of 54 patients with full‐thickness wounds that required surgical closure. Patients were randomised to either VAC therapy or saline gauze treatment. The direct medical costs of the total number of resources needed to achieve a healthy granulated wound bed, ready for surgery, were calculated. VAC therapy patients spent less time in hospital than the control groups, with significant cost savings (P < 0·05) (Figure 9). Nursing costs were also reduced significantly (P < 0·0001) (Figure 10).
Figure 9.

Vacuum‐assisted closure (VAC) therapy patients spent less time in hospital than the control groups, with significant cost savings (P < 0·05), from Moues et al. (55).
Figure 10.

Nursing costs were also reduced significantly (P < 0·0001) for vacuum‐assisted closure (VAC)‐treated patients, from Moues et al. (55).
Conclusions
This review summarises recent research into the mechanisms believed to account for the efficacy of VAC therapy, which include promoting a moist wound environment, creating mechanical forces that stimulate a biological response, promoting perfusion, reducing oedema, altering wound fluid composition and assisting in granulation tissue formation. From these foundations, high‐quality clinical trials are outlined, which translate into clinical benefit for patients. These benefits include reduction of wound volume/size, more rapid wound bed preparation, faster wound healing, enhancement of rate of graft take, decreased drainage time for acute wounds, reduction of complications, enhancement of response to first‐line treatment, increased patient survival and reduction of cost.
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