Negative Pressure Wound Therapy Achieved by Vacuum-Assisted Closure: Evaluating the Assumptions

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Ostomy Wound Manage. 2007;53(1):52-57.
G. Stephen Morris, PT, PhD; Kevin E. Brueilly, MPT; and Heather Hanzelka, MPT


  Managing and treating complex wounds always have been difficult. The aging of the population and the survival of individuals with multiple comorbidities and more complex pathologies have increased wound care challenges. In 1997, Argenta and Morykwas1 published a prospective cohort study describing a new wound management method that involved the continuous and/or intermittent application of subatmospheric pressure to human wounds for extended periods of time.

The authors identified 300 wound patients who presented with chronic wounds (eg, pressure ulcers, stasis ulcers), subacute wounds (wounds that had been open <7 days), and acute wounds (wounds that had been open <12 hours). All patients were treated with negative pressure until the wounds were completely healed, progressed to a point where they could be closed by a surgical procedure (skin graft or muscle flap), or the patient refused further treatment or died. Using these endpoints, 296 of 300 wounds had a positive response to negative pressure wound therapy (NPWT). {C} wound vac

  Negative pressure technology subsequently became known by several pseudonyms, including vacuum-assisted closure (VAC), topical negative pressure (TNP), vacuum sealing technique (VST), and sealed surface wound suction (SSS); it is informally referred to as the wound vac. While its novelty and origins are controversial,2 this technology has been patented and cleared for marketing by the US Food and Drug Administration (a regulatory mechanism that does not require submission of data from controlled efficacy trials). Currently, the wound vac is in widespread use throughout North America and Europe3; however, its relative effectiveness (enhanced ability to bring about wound closure as compared to other, more standard methods of wound therapies) and efficacy (singular capacity to bring about wound closure) remain in question. The utility of a new therapy also must be examined in terms of its cost effectiveness – ie, whether the technology produces similar or better outcomes at equal or lower costs – should be considered. The purpose of this paper is to describe the device, discuss the mechanisms by which it is thought to effect wound healing, and examine its relative efficacy. Information about the cost effectiveness of this technology remains to be published.

Literature Review

  The device. Wound vac technology involves the use of a medical grade, reticulated polyurethane ether foam dressing that is attached to a non-collapsible evacuation tube which, in turn, is attached to a vacuum source. Side ports in the tube allow for communication between the tube and the reticulated foam dressing. The reticulated foam dressing is cut to closely conform to the geometry of the wound bed and is placed in the wound defect so the tube lies parallel to the skin. The reticulated foam dressing serves both to absorb wound exudate and to evenly distribute the negative pressure over the entire wound. An adhesive drape consisting of a transparent film is placed over the foam dressing and the tube, extending 3 to 5 cm beyond the edges of the wound, and is affixed to intact periwound skin, creating an airtight compartment over the wound bed. Distally, the evacuation tube is connected to a collection vessel that is connected to an adjustable vacuum pump. When the device is in operation, the pump creates a negative pressure that pulls effluent from the wound into a collection vessel. Typically, the vacuum pump can be programmed to provide various amounts of negative pressure on an intermittent or continuous basis depending on the wound type. The general architecture, foam types, drapes, and regulation of the vacuum pump can be modified according to the characteristics of each wound.1,4,5 Presenting specific guidelines for the use of negative pressure devices is beyond the scope of this review; the reader is referred elsewhere for such information.5-7

  Suggested mechanisms of action.
  Altered blood flow. In wounds where the edges are not opposed, healing generally is thought to occur by secondary intention, a process that requires the creation of a matrix of small blood vessels and connective tissue across the wound defect. Once created, this matrix forms a passageway over which the keratinocytes migrate, covering and re-epithelializing the wound defect.8 Vacuum-assisted closure may assist in this process by increasing blood flow to the wound margins, which not only increases the delivery of oxygen and other nutrients, but also assists in the removal of waste products.3,4 Using a laser Doppler to monitor blood flow, Morykwas et al9 observed that a vacuum system increased blood flow in the margins of experimental wounds in anesthetized swine by approximately four-fold. This increase in blood flow lasted only 5 to 7 minutes with continuous application of the vacuum, while intermittent application of a vacuum (5 minutes on, 2 minutes off) resulted in continuous elevation in blood flow above basal levels to the wound edges. Granulation tissue also appeared at a greater rate in wounds treated with the wound vac, leading to the suggestion that increased blood flow was responsible for the accelerated formation of granulation tissue and subsequent wound healing.9 Chen et al10 also observed an increase in blood flow to wounds experimentally created in the ears of white rabbits and subsequently treated with vacuum-assisted technology. Microscopic examination and image pattern analysis revealed that increased blood flow was the result of increased vascular diameter, blood flow velocity, and blood volume, as well as increased angiogenesis and endothelial proliferation.

  Wackenfors et al11,12 employed a swine model to further study the impact of the wound vac on blood flow in the immediate and adjacent vicinity of an acute wound. They observed that the wound vac decreased blood flow (hypoperfusion) in the immediate proximity of wounds created in anesthetized swine but increased blood flow (hyperperfusion) in areas 1.5 to 3.0 cm away from the wound. The changes in blood flow were directly linked to the amount of negative pressure imposed on the wound. Interestingly, blood flow in the area of hypoperfusion increased by approximately 50% over basal levels when the negative pressure was “off,” suggesting that a reactive hyperemia response occurred during the “off” part of the intermittent vacuum cycle.11 The authors suggest that periodically removing the negative pressure creates a period of hyperperfusion and resulting “hyperoxygenation” of the tissue; thus, preventing chronic ischemia. Because of the contrasting regional effects on blood flow, these investigators argue that the beneficial impact of negative pressure is related to its ability to reduce wound edema and to tamponade superficial bleeding instead of its ability to increase blood flow.11,12

  Mechanical deformation. One can imagine that a pressure gradient across soft tissue might lead to the mechanical deformation of cells. Mechanically stretching isolated cells from several organs is known to stimulate cell mitosis, cell proliferation, and angiogenesis.13,14 Specific signaling molecules and genes that lead to cellular changes in response to this type of cell deformation have been identified.13,14 It has been suggested that the application of negative pressure hastens wound healing in a similar manner.3,15 The presumption is that the application of negative pressure disrupts the balance between the extracellular matrix and the intracellular cytoskeleton, resulting in the release of various intracellular second messengers, including some that upregulate cell growth.15 Computer modeling based on histologic studies suggests that the pressures used in the wound vac create tissue strain sufficient to deform cells by as much as 20%, a change known to induce cell proliferation in vitro.15 Although these cellular changes have not been demonstrated in vivo, it is quite likely that negative pressures create such changes in a wound.15,16 Venturi et al16 suggested that intermittent negative pressure is more effective than continuous negative pressure in stimulating wound healing because continuous pressure causes less cell deformation.

   Pressure gradient. Negative pressure may directly stimulate wound healing by simply creating a pressure gradient that “pulls” materials or cells from the wound bed or from the surrounding tissues into the wound bed and then into the foam dressing of the wound vac. Several mechanisms have been proposed to explain the benefits of this phenomenon. The ongoing inflammatory response around a wound results in local tissue edema and swelling, a condition that adversely affects diffusion of needed nutrients and oxygen from the vascular bed to the wound.16 Lambert et al3 and Venturi et al16 suggest that a wound vac might “pull” this extra fluid out of the interstitial spaces, reducing edema and improving nutrient delivery to the wound. It has been demonstrated that the wound vac reduces edema in and around acute experimental burns in swine17 but it remains to be demonstrated if these effects occur in humans.

  All types of wounds are known to contain cytotoxic compounds including proteases, cytokines, metalloprotease, and oxygen-free radicals, all of which are produced largely by neutrophils.18-21 These compounds break down the extracellular matrix and granulation tissue found in wounds (proteases, metalloprotease, and oxygen-free radicals) and it has been suggested that they inhibit the migration of needed repair cells (cytokines) into the wound, thus delaying wound closure.19,21 These compounds have been found in the effluent obtained from wound vac-treated human wounds, suggesting that the removal of cytotoxic compounds might be a viable mechanism by which the wound vac enhances wound healing.20

  Human wounds typically are colonized by bacteria and may become infected if their numbers exceed 105. If the bacterial population in human wounds can be kept below 105 organisms per gram of tissue, wound healing can progress, but excessive wound colonization by bacteria increases the amount of cytotoxic compounds and diverts available resources away from wound closure.22-24 Application of the wound vac has been shown to decrease the bacterial count within experimentally induced abdominal midline wounds in swine whose wounds had been inoculated with Staphylococcus aureus or S. epidermidis.9 In contrast, a retrospective review of 25 patient charts found that a wound vac failed to reduce the bacterial colonization of acute wounds.25 The latter findings may suggest that the effectiveness of vacuum-assisted closure may not be associated with a reduction in the bioburden of the wound. Because these two studies differ in the frequency of dressing changes (daily versus every 3 to 5 days), the frequency of dressing change rather than negative pressure may be the most important issue.

  It also has been suggested that the pressure gradient may act by simply pulling or drawing greater numbers of keratinocytes into and across the wound; thereby, increasing the population of cells necessary for wound healing.3 Negative pressure gradients also may favor the approximation of soft tissue and reduce the likelihood of soft tissue retraction.26 Also, the simple action of bringing and holding the wound edges closer together would promote wound healing. Again, no evidence is available to support the notion that a wound vac enhances wound healing by either of these mechanisms.

  Efficacy. Vacuum-assisted closure has been available for approximately a decade. A Medline/PubMed search of materials published between 1996 and May 2006 yielded 188 articles written in English that describe wound vac technique and outcomes. Of these publications, 11 (5.8%) were animal studies, seven (3.7%) were categorized as randomized controlled trials, and 22 (11.8%) were categorized as reviews. The remaining were case studies and case series. Negative pressure has been used to treat a broad range of non-healing wounds ranging from chronic wounds (pressure ulcers, diabetic foot ulcers, and venous stasis ulcers) to traumatic wounds to burns and surgical wounds. With few exceptions, the published results suggest that the wound vac is useful in generating wound closure. Few adverse effects related to wound vac use (eg, dehydration, bleeding, pain, and infection) have been reported.3,4,27 Although the available evidence collected from case studies strongly suggests that wound vac use is effective in promoting wound healing, it remains largely undetermined whether the device is more effective than current standard care in reducing wound healing times, costs, or pain or in improving quality of life.

  In an effort to determine if the wound vac is more effective than more conventional treatments in the management of chronic wounds, Evans and Land4 published a Cochrane review of available randomized controlled clinical studies comparing the wound vac with other wound dressing methods. All studies involving vacuum-assisted closure devices were reviewed. As no consensus for successful outcome measures for wound healing were available at the time of their review, the authors selected the time required for complete wound healing, rates of change in wound area and volume, and proportion of wounds completely healed within the trial period. Eight prospective randomized control studies were identified. Of these, three were excluded because they were animal studies and three were excluded because they examined acute rather than chronic human wounds. The two randomized controlled trials that met inclusion criteria for this review involved a total of 34 patients. Compared to normal saline wet-to-moist gauze dressings, the wound vac was reported to expedite a reduction in wound volume and reduce the number of days required for satisfactory healing to occur. Important methodological weaknesses were identified in both studies, including inappropriate randomization, type of data presented (mean or median), and lack of statistical analysis of data. Evans and Land4 concluded that these two small studies provided “weak evidence” to suggest that the wound vac “may be superior to saline gauze dressings in healing chronic human wounds.” These authors also called for multicenter, well designed, adequately powered, randomized controlled studies to evaluate the relative effectiveness of the wound vac

.   The issue of the relative effectiveness of the wound vac was revisited by Samson et al27 in 2004 when available data were reviewed by the Agency for Healthcare Research and Quality (AHRQ). This review was undertaken in an attempt to determine 1) if the wound vac provides better outcomes than conventional care and 2) if the wound vac used as an adjunct to traditional therapy provides better outcomes than conventional care alone. Only randomized control trials were included in this analysis and only those studies that compared 1) the outcomes of other wound healing interventions with those of the wound vac, 2) the outcomes of standard wound care with those of the wound vac, or 3) the outcomes achieved with the wound vac with those of a placebo trial. Six of the 467 studies involving 135 patients met the selection criteria and were reviewed. Five of the six studies compared the wound vac to standard care (usually moist dressings changed at least once daily). All six studies included in the review were rated poor in quality because of 1) inadequate randomization, 2) inconsistent baseline variables (age, wound duration, and wound size) across groups in the same study, 3) small sample sizes, generating concern over adequate power, and 4) lack of adjustment for confounders. Reported outcomes included both complete healing and “satisfactory healing”; hence, comparisons were difficult. Four of the six studies suggested that the wound vac was more effective in reducing wound area than standard care; three of the six studies reported the wound vac decreased wound dimensions. The observed differences were statistically significant in only two of the six studies. The authors of this review concluded, “This body of evidence is insufficient to support definitive conclusions about the effectiveness of vacuum-assisted closure in the treatment of wounds.”27 Furthermore, it was observed that the small number of patients in these wound vac trials may have rendered the studies insufficiently powered to successfully detect differences.

  Recently, Armstrong and Lavery28 reported on the use of the wound vac in healing diabetic foot ulcers in a randomized control trial involving 162 patients with diabetic foot wounds. Patients were treated with the wound vac or moist wound therapy until the wound closed or for a maximum of 112 days of treatment. All patients received preventative or therapeutic offloading pressure relief as indicated. Statistical analysis was by intention to treat. Compared to the control group, a greater number of wounds in the wound vac-treated group closed and a faster rate of granulation tissue formation and fewer amputations were reported. Although generally positive, concerns about the results of this study remain, including potential conflict of interest bias (the study was funded by the manufacture of the device), reported wound differences in both groups, confusion over actual endpoints, low power, and poor descriptions of adverse events.29-31


  Wound vac use is widespread and apparently effective. Several plausible and testable hypotheses by which the device might bring about these changes have been offered but scant objective data have been collected to support or refute any of these hypotheses in either humans or animal models. Focused inspection of the available data (Evans and Land4 and the AHRQ27) conscientiously note that data available to support the use of the wound vac over current standard care of wounds are limited. Furthermore, wound vac treatment has primarily been compared to moist saline gauze dressing, a wound covering that may not provide optimal healing, and many study designs have excluded comparisons with many newer and potentially more beneficial wound dressings.32 Finally, cost-effectiveness studies need to be conducted because resultant data will impact reimbursement and subsequently the use of this technology.

  These conclusions do not discount the wound vac’s usefulness in the treatment of non-healing or slow healing wounds. They simply suggest that more carefully controlled studies with greater numbers of subjects must be conducted before stronger, more definitive conclusions can be reached. As the AHRQ report27 observed, such studies are currently underway and once completed should provide greater insight into the efficacy of using negative pressure in the treatment of wounds. Successfully conducting such studies will be difficult for a number of reasons but the results will provide much-needed guidance into clinical and financial decision making regarding optimal wound care.33


1. Argenta LC, Morykwas MJ. Vacuum-assisted closure: a new method for wound control and treatment: clinical experience. Ann Plast Surg. 1997;38(6):563-577.

2. Greer SE. Whither subatmospheric pressure dressing? Ann Plast Surg. 2000;45(3):332-334.

3. Lambert K, Hayes P, McCarthy M. Vacuum assisted closure: a review of development and current applications. Eur J Vasc Endovasc Surg. 2005;29(3):219-226.

4. Evans D, Land L. Topical negative pressure for treating chronic wounds. Brit J Plast Surg. 2001;54(3):238-242.

5. Mendez-Eastman S. Guidelines for using negative pressure wound therapy. Adv Skin Wound Care. 2001;14(6):314-321.

6. Wound Ostomy Continence Nursing Society. Guideline for Management of Wounds in Patients with Lower-Extremity Neuropathic Disease. Glenview, Ill: Wound Ostomy Continence Nursing Society;2004.

7. Armstrong DG, Attinger C, Boulton AJM, et al. Guidelines regarding negative pressure wound therapy in the diabetic foot: results of the Tucson expert consensus conference. Ostomy Wound Manage. 2004;50(4 suppl B):3S-27S.

8. Dealy C. The Care of Wounds – A Guide for Nurses. Oxford, UK: Blackwell Scientific Publications;1999.

9. Morykwas MJ, Argenta LC, Shelton-Brown EI, McGuirt W. Vacuum-assisted closure: a new method for wound control and treatment: animal studies and basic foundation. Ann Plast Surg. 1997;38(6):553-562.

10. Chen SZ, Li J, Li XY, Xu LS. Effects of vacuum-assisted closure on wound microcirculation: an experimental study. Asian J Surg. 2005;28(3):211-217.

11. Wackenfors A, Sjogren J, Gustafsson R, et al. Effects of vacuum-assisted closure therapy on inguinal wound edge microvascular blood flow. Wound Rep Regen. 2004;12(6):600-606.

12. Wackenfors A, Gustafsson R, Sjogren J, et al. Blood flow responses in the peristernal thoracic wall during vacuum-assisted closure therapy. Ann Thorac Surg. 2005;79(5):1724-1730.

13. Iwasaki H, Eguchi S, Ueno H, Marumo F, Hirata Y. Mechanical stretch stimulates growth of vascular smooth muscle cells via epidermal growth factor receptor. Am J Physiol: Heart, Circ Physiol. 2000;278(2):H521-H529.

14. Sanchez-Esteban J, Wang Y, Gruppuso PA, Rubin LP. Mechanical stretch induces fetal type II cell differentiation via an epidermal growth factor receptor-extracellular-regulated protein kinase signaling pathway. Am J Respir Cell Mol Biol. 2004;30(1):76-83.

15. Saxena V, Hwang CW, Huang S, et al. Vacuum-assisted closure: microdeformations of wounds and cell proliferation. Plast Reconstr Surg. 2004;114(5):1086-1096.

16. Venturi ML, Attinger CE, Mesbahi AN, Hess CL, Graw KS. Mechanisms and clinical applications of the vacuum-assisted closure (VAC) device. Am J Clin Dermatol. 2005;6(3):185-194.

17. Morykwas MJ, David LR, Schneider AM, et al. Use of subatmospheric pressure to prevent progression of partial-thickness burns in a swine model. J Burn Care Rehabil. 1999;20(1):15-21.

18. Yager DR, Nwomeh BC. The proteolytic environment of chronic wounds. Wound Repair Regen. 1999;7(6):433-441.

19. Mustoe T. Understanding chronic wounds: a unifying hypothesis on their pathogenesis and implications for therapy. Am J Surg. 2004;187(5A):65S-70S.

20. Yager Dorne R, Zhang LY , Liang HX, et al. Wound fluids from human pressure ulcers contain elevated matrix metalloproteinase levels and activity compared to surgical wound fluids. J Invest Derm. 1996;107(5):743-748.

21. Henry G, Garner WL. Inflammatory mediators in wound healing. Surg Clin North Am. 2003;83(3):483-507.

22. Krizek TK, Robson MC, Kho E. Bacterial growth and skin graft survival. Surg Forum. 1967;18:518-519.

23. Robson MC, Heggers JP. Bacterial quantification of open wounds. Mil Med. 1969;134(1):19-24.

24. Robson MC. Wound infection: a failure of wound healing caused by an imbalance of bacteria. Surg Clin North Am. 1997;77(3):637-650.

25. Weed T, Ratliff C, Drake DB. Quantifying bacterial bioburden during negative pressure wound therapy. Ann Plast Surg. 2004;52(3):276-280.

26. Fenn CH, Butler PE. Abdominoplasty wound-healing complications: assisted closure using foam suction dressing. Br J Plast Surg. 2001;54(4):348-351.

27. Samson DJ, Lefevre F, Aronson N. Wound-Healing Technologies: Low-Level Laser and Vacuum-Assisted Closure. Evidence Report/Technology Assessment No. 111. (Prepared by the Blue Cross and Blue Shield Association Technology Evaluation Center Evidence-based Practice Center, under Contract No. 290-02-0026.) AHRQ Publication No. 05-E005-2. Rockville, Md: Agency for Healthcare Research and Quality; 2004:December.

28. Armstrong DG, Lavery LA, the Foot Study Consortium. Negative pressure wound therapy after partial diabetic foot amputation: a multicentre, randomized controlled trial. Lancet. 2005;366(9498):1704-1710.

29. Chantelav E. Negative pressure therapy in diabetic foot wounds. Lancet. 2006;367(9512):726-727.

30. Maegele M, Gregor S, Peinemann F, Sauerland S. Negative pressure therapy in diabetic foot wounds. Lancet. 2006;367(9512):725-726.

31. Williams DT. Negative pressure therapy in diabetic foot wounds. Lancet. 2006;367(9512):725.

32. Jones V, Grey JE, Harding KG. Wound dressings. Brit Med J. 2006;332(7544):777-778.

33. Chan YC, Nichol I, Evans GH, Stansby G. Managing the diabetic foot with the use of vacuum assisted closure: a call for more studies. Int J Clin Pract. 2006;60(3):256-257.


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