The vacuum-assisted closure (V.A.C®) system for surgical site infection with involved vascular grafts

Abstract

Background

In vascular surgery, surgical site infection is the most common postoperative morbidity, occurring in 5–10% of vascular patients. The optimal management of surgical site infection with involved lower limb vascular grafts remains controversial. We present our 6-year results of using the V.A.C.® system in surgical site infection with involved vascular grafts.

Methods

A retrospective 6-year review of patient who underwent a VAC® therapy for postoperative surgical site infection in lower limb with involved vascular grafts in our department between January 2006 and December 2011. V.A.C therapy was used in 40 patients. All patients underwent surgical wound revision with VAC® therapy and antibiotics.

Results

The mean time of use of the V.A.C. system was 14.2 days. After mean of 12 days in 34 of 40 patients, in whom the use of VAC® therapy resulted in delayed primary closure or healing by secondary intention. The mean postoperative follow-up time was 61.67 months, during which 3 patients died.

Conclusion

We showed that the V.A.C.® system is valuable for managing specifically surgical site infection with involved vascular grafts. Using the V.A.C.® system, reoperation rates are reduced; 85% of patients avoided graft replacement.

Keywords

SSI vascular graft infection VAC wound infection

Introduction

Surgical site infection (SSI) and vascular graft infection are serious complications in vascular surgery. SSI occurs in 5–10% of patients who undergo vascular surgery,^1,2 and the incidence of vascular graft infection varies from 1 to 6%.^3,4 The incidence of infrainguinal arterial prosthetic graft infection is 2.5%.⁵ Deep postoperative wound infection with involved vascular grafts increases mortality risk (6–75%) and limb loss (22–75%).^6–8 Postsurgical infections in vascular surgery are multifactorial, resulting from a complex interplay of patient, surgical, and environmental factors.

Infrainguinal open bypass procedures have the highest infection rates, especially when synthetic prosthetic material is used (10–30%). The reasons include the groin being a major reservoir of bacteria, infected lymph glands, surgical division of lymphatic channels, the proximity of the groin to the peritoneum, and the superficial location of vascular grafts in the groin. Abdominal aortic aneurysm repair and endovascular techniques are associated with the lowest rates of SSI (less than 1%).⁹

Some reports describe success with wound debridement and drainage and antibiotics and muscle flap surgery for eradication of infection.¹⁰ Alternative methods to preserve the graft were introduced to minimize surgical trauma, but have a failure rate of up to 35%.^11,12 However, in patients with exposed synthetic vascular grafts, removal and distal revascularisation with extraanatomic bypass with autogenous vein, cryopreserved homograft (biological), and prosthetic grafts has been reported as the safest approach.¹³

The VAC® system is a non-invasive method of promoting healing in difficult wounds that fail to respond to other treatment modalities. The V.A.C.® system is based on the application of negative pressure (50–150 mm Hg) by controlled suction to the wound surface. Blood perfusion and oxygenation are crucial to ensure proper healing; this system increases microcirculation in the wound and capillary blood flow at the wound edge as well as decreasing interstitial edema and stimulating granulation (reduction of wound size). The V.A.C.® system reduces bacterial colonization and protects the vascular graft by maintaining its integrity.

The optimal management of vascular graft infection in the lower limb remains controversial; no guidelines currently exist. We present our 6-year experience with the use of the V.A.C.® system in SSI with involved vascular grafts.

Methods

A retrospective study of patient records from January 2006 to December 2011 of all patients receiving V.A.C. therapy for SSI with involved vascular grafts was performed. Forty patients (34 males, 6 females, median age, 72.4 years (age range, 54–90) developed Szilagyi grade III infection in the Department of Cardiovascular Surgery, University Hospital of Geneva. Twenty-eight patients had groin incision-healing problems, and 12 patients at the proximal or distal popliteal incision, in combination with a fully exposed vascular graft.

At admission, 40 patients had pain at the surgical site. All wounds showed macroscopic signs of local wound infection, such as wound inflammation or leakage of fluid and were partially open for a length of at least 4 cm. Twenty-two patients had a palpable collection in area, a possible abscess. All 40 patients had an elevated CRP > 10 mg/l (mean 77.15 mg/l, range, 15–240), 16 patients showed WBC > 10 G/L (mean 13.37, range, 10.5–19.8), and 8 patients presented temperature > 37.5℃. All patients underwent CT scan, with 20 demonstrating per-graft fluid collections.

After wound cultures and laboratory examinations were obtained, primary broad-spectrum antibiotics were started. After identification of bacteria, treatment was adjusted. Operative wound revision (washout and debridement) was performed in all patients. Preoperatively, the vascular graft was visible in all cases. V.A.C.® therapy was started immediately postoperatively.

Intraoperatively, and during V.A.C.® dressing changes, cultures were obtained. Antibiotic treatment was adapted to culture results and was administered in parallel to V.A.C.® therapy in all patients. V.A.C.® dressing change was performed every 72 h.

Initial intervention, time to V.A.C.® placement, total V.A.C. treatment time, method of final closure, total length of hospital length, time to complete healing, and total follow-up time were recorded.

Patients

All 40 patients underwent surgery in our department. Primary indications for vascular intervention were peripheral arterial disease. Surgeries performed included femoro-popliteal bypass (n = 28), aorto-bifemoral bypass (n = 4), ilio-femoral bypass (n = 2), popliteal-tibial bypass (n = 3), femoro-tibial bypass (n = 2), and femoral-femoral bypass (n = 1). Graft used was polytetrafluorethylene (PTFE®, Intervascular, Ciotat, France) in 22 cases (Figure 1), polyethylenterephthalat (Dacron®, Intervascular, Ciotat, France) in 12 cases, V. Saphena Graft in 4 cases, and Homograft (cryopreserved biologic material) (Homograft Bank®, Brussels, Belgium) in 2 cases. Thirty-two cases were elective and 8 were emergency cases. Patients received 2 g of IV cefazolin (Cephazolin®, Labatec-Pharma, Switzerland) within 60 min of surgery and every 6 h thereafter for 24 h postoperatively.

Figure 1.

Infected groin wound with exposed prosthesis (Dacron®) in a 76-year-old patient. Debridement was performed and V.A.C.® therapy initiated.

The interval between the first surgery and appearance of wound infection symptoms was anywhere between 10 days and 7 years. There were 23 cases of early infection (less than 30 days) and 17 late infections (greater than 30 days) after graft implantation.

Wound and graft cultures demonstrated Staphylococcus aureus (n = 12), Pseudomonas aeruginosa (n = 6), MRSA (n = 4), Enterococcus faecalis (n = 4), Enterobacter cloacae (n = 1), and Steptococcus agalactiae (n = 1). In the remaining 12 cases, cultures contained two different organisms: S. aureus and E. faecalis (n = 3), S. aureus, and E. coli (n = 3), S. aureus and Proteus mirabilis (n = 4), and S. aureus and Citrobacter (n = 2) (Table 1). About 65% of patients had hyperlipidemia, 60% were current or previous smokers, 40% were diabetics, 47% had hypertension, 38% were obese, and 35% had ischemic heart disease.

Table 1.

Characteristics of the patients and findings.

SI. no.	Age (years)	Sex	Initial surgery/bypass	Graft type	Interval 1. OP- symptoms (weeks)	Szilagyi Grad III	Clinical symptoms	WBc (max. G/L)	CRP (max. mg/l)*	Microbiology wound cultures
1	90	M	Iliofemoral	PET	6 L	Groin	Pain, fever, open wound	9.2	65	Staphylococcus aureus
2	79	F	Femoropopliteal	PTFE	2 E	Groin	Pain, non-healed wound	11.5	77	Staphylococcuss aureus
2	79	F	Femoropopliteal	PTFE	2 E	Groin	Pain, non-healed wound	11.5	77	E. coli
3	60	M	Femoropopliteal	PTFE	8 L	Groin	Pain, wound leackage	8.3	93	Staphylococcuss aureus
3	60	M	Femoropopliteal	PTFE	8 L	Groin	Pain, wound leackage	8.3	93	Proteus mirabilis
4	75	M	Femoropopliteal	PTFE	6 L	Groin	Pain, open wound	13.6	87	Staphylococcus aureus
5	76	F	Femorotibial	PTFE	2 E	Lower limb	Pain, non-healed wound	13.5	104	Staphylococcus aureus
6	79	M	Femoropopliteal	PTFE	2 E	Groin	Pain, Pain, open wound	19.2	110	Staphylococcuss aureus
6	79	M	Femoropopliteal	PTFE	2 E	Groin	Pain, Pain, open wound	19.2	110	Citrobacter
7	76	M	Femoropopliteal	PTFE	5 L	Groin	Pain, open wound	6.5	65	Pseudomonas aeruginosa
8	78	M	Femoropopliteal	PET	7 L	Groin	Pain, non-healed wound	7.3	46	Staphylococcuss aureus
8	78	M	Femoropopliteal	PET	7 L	Groin	Pain, non-healed wound	7.3	46	Proteus mirabilis
9	63	M	Femoropopliteal	PET	2 E	Groin	Pain, fever, open wound	18.4	150	Pseudomonas aeruginosa
10	69	M	Femoropopliteal	PET	8 L	Groin	Pain, fever, open wound	13.2	143	MRSA
11	72	M	Femoropopliteal	PET	1 E	Groin	Pain, wound leackage	6.5	53	Enterococcus faecalis
12	49	M	Femoropopliteal	PET	3 E	Lower limb	Pain, non-healed wound	9.5	165	Staphylococcuss aureus
12	49	M	Femoropopliteal	PET	3 E	Lower limb	Pain, non-healed wound	9.5	165	Enterococcus faecalis
13	80	M	Femoropopliteal	PTFE	2 E	Groin	Pain, fever, open wound	6.2	73	Staphylococcus aureus
14	76	F	Femorotibial	V. Saphena	6 L	Lower limb	Pain, wound leackage	7.0	51	Staphylococcus aureus
15	74	M	Femoropopliteal	V. Saphena	5 L	Groin	Pain, non-healed wound	8.3	45	Enterococcus faecalis
16	74	M	Femoropopliteal	PTFE	12 L	Groin	Pain, wound leackage	7.0	56	Pseudomonas aeruginosa
17	54	M	Femoropopliteal	PTFE	3 E	Groin	Pain, wound leackage	9.8	85	MRSA
18	62	M	Aortobifemoral	PTFE	4 L	Groin	Pain, non-healed wound	7.9	69	Staphylococcuss aureus
18	62	M	Aortobifemoral	PTFE	4 L	Groin	Pain, non-healed wound	7.9	69	Enterococcus faecalis
19	82	M	Popliteotibial	V. saphena	3 E	Lower limb	Pain, wound leackage	9.4	105	Staphylococcus aureus
20	60	F	Femoropopliteal	PTFE	2 E	Lower limb	Pain, fever, open wound	14.5	120	Pseudomonas aeruginosa
21	52	M	Femoropopliteal	PTFE	2 E	Groin	Pain, open wound	11.6	59	Staphylococcuss aureus
21	52	M	Femoropopliteal	PTFE	2 E	Groin	Pain, open wound	11.6	59	E. coli
22	62	M	Femoropopliteal	PTFE	1 E	Groin	Pain, wound leackage	9.8	85	Staphylococcuss aureus
22	62	M	Femoropopliteal	PTFE	1 E	Groin	Pain, wound leackage	9.8	85	Proteus mirabilis
23	70	M	Femoropopliteal	PET	3 E	Lower limb	Pain, open wound	10.7	74	Staphylococcus aureus
24	87	F	Femoropopliteal	PET	2 E	Groin	Pain, open wound	11.2	89	Enterococcus faecalis
25	79	M	Femoropopliteal	PTFE	5 L	Groin	Pain, wound leackage	10.8	45	Staphylococcuss aureus
25	79	M	Femoropopliteal	PTFE	5 L	Groin	Pain, wound leackage	10.8	45	Citrobacter
26	59	M	Aortobifemoral	PTFE	2 E	Groin	Pain, wound leackage	8.3	94	Staphylococcuss aureus
26	59	M	Aortobifemoral	PTFE	2 E	Groin	Pain, wound leackage	8.3	94	Proteus mirabilis
27	82	M	Femoropopliteal	PET	4 L	Lower limb	Pain, wound leackage	7.6	55	Pseudomonas aeruginosa
28	81	M	Femoropopliteal	PET	3 E	Lower limb	Pain, non-healed wound	6.3	26	Staphylococcuss aureus
28	81	M	Femoropopliteal	PET	3 E	Lower limb	Pain, non-healed wound	6.3	26	E. coli
29	66	M	Aortobifemoral	PTFE	2 E	Groin	Pain, non-healed wound	8.9	86	Staphylococcus aureus
30	73	M	Femoro-femoral	PTFE	6 L	Groin	Pain, wound leackage	6.8	81	Staphylococcuss aureus
30	73	M	Femoro-femoral	PTFE	6 L	Groin	Pain, wound leackage	6.8	81	Enterococcus faecalis
31	79	W	Popliteotibial	V. Saphena	3 E	Lower limb	Pain, non-healed wound	10.8	45	Staphylococcus aureus
32	82	M	Femoropopliteal	PTFE	3 E	Lower limb	Pain, wound leackage	7.9	87	Pseudomonas aeruginosa
33	65	M	Femoropopliteal	PTFE	12 L	Lower limb	Pain, non-healed wound	13.6	66	MRSA
34	75	M	Femoropopliteal	PET	2 E	Groin	Pain, non-healed wound	9.8	23	Staphylococcus aureus
35	76	F	Popliteotibial	Homograft	2 E	Lower limb	Pain, non-healed wound	7.9	19	Staphylococcus aureus
36	79	M	Femoropopliteal	Homograft	1 E	Groin	Pain, fever, open wound	6.9	45	Enterococcus faecalis
37	76	M	Iliofemoral	PTFE	4 L	Groin	Pain, fever, open wound	10.5	39	Enterobacter cloacae
38	80	M	Femoropopliteal	PET	2 E	Groin	Pain, fever, open wound	11.0	51	Staphylococcus aureus
39	77	M	Femoropopliteal	PTFE	24 L	Groin	Pain, non-healed wound	6.1	15	Steptococcus agalactiae
40	71	M	Aortobifemoral	PTFE	364 L	Groin	Pain, non-healed wound	19.8	240	MRSA

E: early infection < 30 days after implantation; L: late infection > 30 days after implantation; MRSA: methicillin-resistant Staphylococcus aureus; PET: polyethylenterephthalat (Dacron); PTFE: polytetrafluorethylen.

Treatment policy of VAC® therapy

V.A.C. therapy was initiated at the time of surgical debridement, on the same day. The V.A.C. sponge (KCI®, San Antonio, TX) was cut to the size of the wound and placed within it. Visible graft material was covered by overlying fascia, tissue, or by a protective barrier with an non-adhesive silicon-based dressing (Mepitel®, Mölnlycke Health care AB, Götebourg, Sweden). The procedure using the VAC device involved fitting a cut piece of VAC GranuFoam® (KCI, San Antonio, TX) into the wound and fixing this with a special adhesive drape. A 4-cm hole was cut into the drape over which a turbing disc was applied, and the distal end of the turbing was connected to the V.A.C. canister. The negative pressure was adjusted between 75 and 125 mm Hg in a continuous mode, depending on patient support and pain. The V.A.C. GranuFoam® was changed every 2–4 days by a wound care nurse under clean, but not necessarily sterile conditions. Bacterial cultures were also taken during wound dressing changes; when the size and edema decreased and the wound was macroscopically and microscopically infection free (indicated by a negative culture), the wound surface completely granulated, and then primary or delayed primary closure was performed.

Results

The mean time of VAC® treatment was 14.2 days (range 12 to 20) days. Thirty-four of 40 patients (85%) reached sterility of the wound and improvement of the infection parameters (CRP, WBc) within 12 days of V.A.C.® and antibiotherapy. Among these, 27 wounds were surgically closed after completion of V.A.C.® therapy; six wounds were healed by secondary intention after the completion of V.A.C.®. One patient muscle flaps for primary surgical closure (Figure 2). The average hospital stay in this group was 18.5 (range, 14–22) days. The total antibiotic therapy mean was 27.7 (range, 23–34) days, and it was continued for 14 days after wound closure in all cases.

Figure 2.

After 14 days of V.A.C.® therapy, after which secondary wound closure with muscle flap was performed.

Six of 40 patients with synthetic vascular grafts (Dacron® or PTFE®) had persistent bacterial colonization after mean 14.8 days of V.A.C.® therapy (4 MRSA, 1 P. aeruginosa, 1 S. aureus + E. faecalis) in both the wound and on the graft itself (4 femoro-popliteal, 2 popliteo-tibial). In these patients, there were no signs of wound granulation and any improvement in the clinical signs of infection (e.g. CRP). Resection of the infected vascular prosthesis was indicated in 6 (15%) patients, who underwent aggressive debridement, complete graft excision, and replacement with homograft and direct surgical wound closure. Postoperative antibiotics were continued until clinical signs of infection decreased (10–15 days). Wound culture of the excised prosthetic grafts demonstrated high-bacterial colonization rates. The average length of hospital stay in this group was 25.1 (range, 23–30) days. There was no VAC-associated hemorrhage. There were no mortalities and no procedure-related morbidities at 3, 6, and 12 months in all patients. The mean postoperative follow-up time was 61.7 (range, 36–83) months. During follow-up, three patients died at the ages of 94, 83.6, and 84.8 years from unrelated causes, after a mean follow-up time of 53.7 (range, 48–58) months.

Discussion

The most serious complication of vascular surgery is SSI with graft infection. Gram-positive organisms are the most common pathogens, causing up to 80% of wound infections. S. aureus and coagulase negative staphylococci are the two most frequently encountered organisms. Approximately 20–25% of wound infections are attributable to Gram-negative bacteria, with Escherichia coli, Pseudomonas aeruginosa, Proteus, and Klebsiella pneumoniae, the most common. Increasingly, antibiotic-resistant organisms are responsible for SSI.^14,15 Manian et al.¹⁶ reported a 9% rate of MRSA in surgical site infection in 1995, climbing to 30% in 2000. Engemann et al.¹⁷ found that patients with a MRSA wound infection had a mortality rate of 20.7% and an additional $40,000 in healthcare costs compared with methicillin-sensitive S. aureus. A patient with SSI will require 17 days more hospitalization, will be twice as likely to die, is 60% more likely to require level III care, and will be five times more likely to require readmission.¹⁸

The classification system for SSI and extracavitary vascular graft infection was established in 1972 by Szilagyi. He described grade I infection, involving only the dermis, grade II, extending into the subcutaneous tissue but not invading the arterial graft, and grade III, which involves the arterial implant (vascular prosthesis) itself. Early infection correlates with a Szilagyi grade III wound infection. These infections are caused by virulent, hospital-acquired bacteria, and present with signs of sepsis such as fever, leukocytosis, bacteremia, and signs of an infected wound (inflamed tissues, pus). A late infection is a result of graft colonization by “low virulence” organisms such as Staphylococcus epidermidis or Candida. They are indolent and usually show no signs of sepsis and do not have positive cultures of the perigraft tissues.^6,19 These classifications are necessary to define the pathology and prognosis and quickly employ appropriate treatment. Alternative treatments to graft preservation and to limit surgical trauma have a failure rate of up to 35%.^10–12 However, the procedure of choice in patients with infected, exposed synthetic vascular grafts is graft excision and distal extraanatomic bypass with autogenous vein graft, cryopreserved homograft (biological), and prosthetic graft,¹³ which is associated with additional high costs, long hospital stay, and risk of complications.

This noninvasive wound closure system uses controlled, localized subatmospheric pressure (50–125 mm Hg). The mechanism stimulates microcirculation to the wound, decreases interstitial edema, promotes granulation, and reduces bacterial colonization in the wound.^20,21 It also helps to decrease the frequency of dressing changes and the time between debridement and definitive closure, lowering the costs of hospital stay.^22,23

The experience of V.A.C.® therapy in lower limb SSI with involved vascular grafts is limited.²⁴ Only four reports of Szilagyi grade III wound infection treated with V.A.C.® are published.^25,26 The largest study included 24 patients, which used a modified V.A.C.® system and suture wound closure, with a 100% success rate²⁷ and the longest mean follow-up time (29.5 months). Svensson et al.²⁶ used the V.A.C.® system in patients with Szilagyi grade III groin wound infections and reported a success rate of >70%. There have been few reports of V.A.C.®-associated bleeding.^25,26 We confirm the proposition of the manufacturer that extreme care must be taken to protect the vascular anastomosis. All exposed blood vessels must be protected by overlying fascia, tissue, or a protective barrier such as Mepitel® (Mölnlycke Health care AB, Götebourg, Sweden) prior to application of GranuFoam® (polyurethane Foam, KCI, San Antonio, TX) sponge and starting negative pressure.²⁸ In our experience, V.A.C.® therapy demonstrated graft preservation in 85% of SSIs with involved grafts, no morbidity or limb loss, and wound granulation that allowed for complete secondary or muscle flap closure.

Conclusion

We present our long-term experience with the safety and effectiveness of V.A.C.® therapy in the management of SSI with involved vascular grafts. V.A.C.® therapy reduces bacterial colonization of the wound and promotes wound healing in 85% of patients, avoiding the need for graft replacement. Vascular graft replacement is always associated with high mortality and mortality, increased length of hospital stay, and high-healthcare costs.

Footnotes

Funding

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

Conflict of interest

None declared.

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