Management of Wound

CHIEF EDITOR’S NOTE: This article is part of a series of continuing education activities in this Journal through which a totalof 36 AMA/PRA category 1 credit hours can be earned in 2005. Instructions for how CME credits can be earned appear onthe last page of the Table of Contents.

Management of Wound ComplicationsFrom Cesarean Delivery

Sue Ellen Sarsam, CNM,* John P. Elliott,† and Garrett K. Lam, MD‡*Nurse Practitioner, Phoenix Perinatal Associates, an Affiliate of Obstetrix Medical Group of Phoenix, PC,

Phoenix, Arizona; †Associate Director of Perinatal Services, Phoenix Perinatal Associates, an Affiliate ofObstetrix Medical Group of Phoenix, PC, Phoenix, Arizona and Clinical Professor, University of Arizona

School of Medicine, Tucson, Arizona; and ‡Associate Director of Perinatal Services, Phoenix PerinatalAssociates, an Affiliate of Obstetrix Medical Group of Phoenix, PC, Phoenix, Arizona and Clinical Assistant

Professor, University of Arizona School of Medicine, Tucson, Arizona

Multiple factors account for the increasing number of cesarean delivery wound complications inthe United States; among them are an increase in cesarean delivery and an increase in thenumber of overweight and obese patients. This article reviews the pathophysiology of acutewound healing. Risk factors for cesarean delivery wound complications are identified anddescribed. Clinical practices that can reduce the risk of developing wound complications,including Centers for Disease Control and Prevention guidelines, are considered. Treatmentguidelines to accelerate wound healing such as secondary closure and negative pressurewound therapy in disrupted wounds are proposed. Older guidelines for management of woundsusing secondary intention are critiqued. Historical methods of wound care such as the practiceof using certain cleansers and the practice of wet to dry dressings are outdated. Modern woundhealing products are described.

Target Audience: Obstetricians & Gynecologists, Family PhysiciansLearning Objectives: After completion of this article, the reader should be able to describe the effects

of obesity on cesarean delivery wound healing, to improve methods of wound healing in the obese patient,and to explain why wet to dry dressing changes are not effective wound management.

Wound complications from cesarean delivery are asignificant emotional and economic burden in obstetriccare. The postpartum period is a challenging time forwomen, as a result of stressors such as fluctuations inhormone levels, caring for a newborn baby, and recov-ery from the actual delivery process. A postoperativewound complication further intensifies an already dif-

ficult period of adjustment. The economic burden isdifficult to quantify but is likely significant.

A recent review of obstetric practice in theUnited States revealed that cesarean delivery ac-counted for 26.1% of all births in 2002 (1). Con-currently, the number of overweight and obesepatients (an independent risk factor for woundcomplications (2)) is increasing rapidly. The Na-tional Health and Nutrition Examination Surveycalculate that, as of 2000, 64% of American adultswere either overweight or obese (3). These factorscan potentially lead to an increase in cesareandelivery wound complications. This article identi-fies clinical practices that may reduce the risk ofcesarean delivery wound complications and pro-

The authors have disclosed that they have no financial relation-ships with or interests in any commercial companies pertaining tothis educational activity.

Wolters Kluwer Health has identified and resolved all facultyconflicts of interest regarding this educational activity.

Reprint requests to: Garrett K. Lam, MD, Phoenix PerinatalAssociates, an affiliate of Obstetric Medical Group of Phoenix, PC,1331 N. 7th Street, Suite 275, Phoenix, AZ 85006. E-mail:[email protected].

CME REVIEWARTICLE Volume 60, Number 7OBSTETRICAL AND GYNECOLOGICAL SURVEY

Copyright © 2005by Lippincott Williams & Wilkins19

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poses treatment guidelines that may help acceler-ate wound healing in disrupted wounds.

BACKGROUND

Wound complications include wound separationwithout infection, superficial wound infection, deepwound infection, wound dehiscence, and rarely, ne-crotizing fasciitis (see Appendix 1 for Centers forDisease Control and Prevention [CDC] definitions ofwound infection). The incidence of wound compli-cations in the obstetric population varies in the liter-ature, with rates ranging from 2.8% to 26.6% (2,4–14). Although wound disruptions are frequentlypreceded by infection, Martens et al (8) found awound disruption rate of 1.7% without infection.Fascial dehiscence occurs in 0.3% of all cesareandeliveries. The incidence of necrotizing fasciitis isslightly less, with one review establishing a rate of1.8 women per 1000 cesarean deliveries (5).

PATHOGENS

Microorganisms originating from the patientand/or the patient’s immediate environment are theprimary sources for postpartum wound infections.The genital tract and skin are the most influentialreservoirs for bacterial contamination. In a study byMartens et al (8), the most prevalent pathogens cul-tured from infected cesarean wounds are Staphylo-coccus epidermidis, Staphylococcus aureus, Esche-richia coli, and Proteus mirabilis. In another study ofwound microbiology, Roberts et al (14) identified themost prominent pathogens as cervicovaginal florasuch as Ureaplasma species and Mycoplasma spe-cies.

WOUND HEALING PHYSIOLOGY

Wound healing occurs as a complex interplay ofmultiple biologic and cellular processes, which arecodependent. A review of these complexities will aidin understanding how wound healing is disrupted andthus, how best to support the physiology of healing.

Full-thickness wound healing is carried out in threephases (Fig. 1): inflammation, proliferation, and re-modeling. The inflammatory phase occurs in re-sponse to the initial injury and is manifested by thesigns and symptoms of erythema, edema, warmth,and drainage. The purpose of this phase is to controlbleeding and establish a clean wound bed. Hemosta-sis is initiated by activating the intrinsic and extrinsiccoagulation pathways and platelet aggregation. After

hemostasis is established, the platelets break down,releasing cytokines and growth factors such as plate-let-derived growth factors, transforming growth fac-tors B1 and B2, platelet-derived epidermal growthfactor, platelet-activating factor, insulin-like growthfactor-1, fibronectin, and serotonin. These cytokinesand growth factors then attract inflammatory cellssuch as neutrophils and monocytes to the wound site,which prevent infection by phagocytizing microor-ganisms. These white blood cells also release growthfactors such as fibroblast growth factor, epidermalgrowth factor, vascular endothelial growth factor,tumor necrosis factor, interleukin-1, and interferon-gamma, which trigger the activation of fibroblastsand keratinocytes to aid in healing. In a clean wound,the inflammatory phase lasts approximately 3 days.Many factors, however, can disrupt this cascade ofcellular events, including infection, diabetes, hyper-tension, and immunosuppression, thus causing a de-lay in wound healing.

The proliferative phase occurs next and consists of3 components: angiogenesis, collagen synthesis, andepithelialization. The purpose of angiogenesis is tocreate new vasculature to supply blood to the dam-aged area to aid healing. Collagen synthesis fills theopen wound with new connective tissue, depositing amatrix material to serve as the basis for wound clo-sure and scar formation. These processes occur si-multaneously and are codependent.

When wounds heal by primary intention, like insutured incisions, the rate of collagen formationreaches a peak around the fifth postoperative day. Itis possible to feel a ridge under the suture line, calledthe “healing ridge,” which is produced by the newlyformed collagen. If this ridge is not palpable, im-paired healing is likely, therefore placing the woundat risk for disruption (15).

The amount of collagen necessary to fill the woundis related to the volume of the defect to be filled.Wounds that are closed by approximating the inci-sion with suture only need a small amount of colla-gen. Wounds healed by secondary intention needgreater amounts of collagen and require a prolongedproliferative phase. Collagen production continuesfor weeks or months and is dependent on specificoxygen and nutritional requirements. If the host’snutritional or vascular status is compromised, woundhealing is delayed. This aspect of healing is ad-dressed in another section of this article.

Initially, the bed of a healing wound is filled withred, vascular granulation tissue. Over time, the heal-ing wound experiences a contraction of the woundbed with the opposing edges slowly pulling together.

Management of Wound Complications From Cesarean Delivery Y CME Review Article 463

There are several theories as to how this is mediated.One theory proposes that wound contraction is trig-gered by myofibroblasts (modified fibroblasts) thatrelease factors that cause contraction of the skin andtissue around the defect. Another theory suggests thatfibroblast cells are actually moving among the col-lagen matrix, causing a reorganization of the matrix,producing the wound bed contraction (16).

Epithelialization is the third component in the pro-liferative phase. Epithelial cells migrate, proliferate,and differentiate to resurface the wound defect, andcan only work over a moist, vascular wound surface.This fact was addressed in the work of Winter (17)and then Hinman (18), forming the basis for theconcept of moist wound healing. Dry or necroticwound surfaces thus impede epithelialization. In su-tured wounds, epithelialization occurs concurrentlywith collagen synthesis, whereas in open wounds,epithelialization takes place after granulation tissue isformed.

The final phase of wound healing is remodeling,which can continue for over 1 year. In this phase, theentire scar is reinforced through a process of collagenmaturation. Collagen fibers in nonwounded skinhave a basketweave pattern. In wounded and scarredtissue, the collagen produced is biochemically dis-tinct from that in nonwounded tissue and is laid downin a pattern parallel to the skin. The repaired scarrequires time to strengthen. Studies have shown thatafter 1 week, the strength of the scar is only 3% ofnormal skin, after 3 weeks the strength is 20%, andafter 3 months 80%. Thus, scar tissue is never asstrong as nonwounded tissue (16).

RISK FACTORS FOR POSTCESAREANWOUND COMPLICATIONS

Wound healing is distinctly shorter, more efficient,and organized when done through the process ofprimary intention. Infection, inhospitable character-

Fig. 1. Normal healing response in full-thickness wounds.

464 Obstetrical and Gynecological Survey

istics of the host (such as vascular or chronic dis-ease), suboptimal perioperative conditions (hypo-thermia), and surgical technique that traumatizestissue can all impede the normal phases of woundrepair (19,20). Risk factors for postcesarean woundcomplication will also impede wound healing. Thesefactors are described subsequently, and are summarizedwith recommendations for prevention in Table 1.

Obesity

Obesity is a major risk factor for postcesareanwound complications (7). The etiology of woundcomplications in obese women is probably related tothe poor vascularity of subcutaneous fat, serous fluidcollection, and hematoma formation. The obese grav-ida is prone to more frequent wound complicationseven with the use of prophylactic antibiotics (2).Cetin and Cetin (10) found that the wound disruptionrate increased significantly with thickened subcuta-neous tissue. Women with subcutaneous tissuegreater than 2 cm had a wound disruption rate of27.2% compared with 18.7% of controls. Studieshave shown that using a subcutaneous suture in allpatients with greater than 2-cm subcutaneous depthsignificantly reduces the risk of wound disruption(4,5,10,21–23). Specifically, closure of excess sub-cutaneous tissue eliminates dead space, thus reducingthe formation of seromas.

Diabetes

Impaired wound healing is frequently seen in pa-tients with diabetes. Cruse and Foord (24) reviewedinfection rates in 23,649 patients and found that

diabetics had 5 times the risk of infection of nondia-betics, even with clean incisions. Although increasedlevels of HgA1c were not shown to be positivelycorrelated to surgical site infections in a study (25),diabetes and postoperative hyperglycemia were inde-pendent risk factors for a surgical site infection.Another study, by Zerr et al (26), compared infectionrates before and after implementation of stricterblood glucose goals and found that the rate of infec-tion before implementation was 2.4% and after im-plementation, the rate was 1.5%. Zerr demonstratedthat glucose levels above 200 mg/dL in the immedi-ate postoperative period were associated with anincreased surgical site infection rate. Additionally,blood glucose levels above 200 mg/dL at 48 hourspostsurgery were significantly associated with deepwound infection.

The explanation for the difference in diabetic woundhealing is complex. The disparity starts with alterationsin the inflammatory response generated by injury orincision. These differences in enzyme secretion andgrowth factor affect all the aspects of normal woundhealing such as collagen synthesis and deposition, leu-kocyte function, and tissue perfusion. Although a grow-ing body of research in experimental models of diabetesexists to investigate the use of vitamin A, exogenousgrowth factors, and nitric oxide supplementation toincrease wound repair in diabetic patients, there are nospecific recommendations other than meticulous avoid-ance of hyperglycemia and strict regulation of insulin toassist in wound healing. Specific blood glucose targetlevels have not been identified, although as previouslymentioned in the Zerr study, blood glucose over 200mg/dL were shown to increase surgical site infections.

TABLE 1Risk factors for cesarean section wound complication practice recommendations to reduce risk

Risk factor Practice recommendations

Obesity Subcutaneous sutureDiabetes Stringent glucose control, insulin therapyIntrapartum chorioamnionitis Decrease number of vaginal examinations

Judicious use of internal fetal monitoringPostoperative endometritis Prophylactic antibiotics at cord clampingProlonged rupture of membranes Prophylactic antibioticsSevere anemia Correct anemiaStress–physiological or psychologic Appropriate pain control/stress reductionSmoking Smoking cessation or nicotine patchAnticoagulation therapy Consider placement of closed drain system to avoid hematoma or seroma

formationPerioperative hypothermia Maintenance of normal body temperature in operating room and recovery

room (use electric warming blanket)Severe hypertension Correct hypertensionInadequate nutrition Adequate protein, vitamin A, C, and zinc


Chorioamnionitis

Tissue infection and clinical circumstances thatpredispose to infection comprise the other majorreasons for suboptimal wound healing. Specifically,long labors, prolonged rupture of membranes, andfrequent vaginal examinations are all known riskfactors for increasing the rate of infection. Indeed,the intrauterine environment during labor can tre-mendously impact postpartum healing. Tran et al (9)showed that chorioamnionitis increases the risk forwound infection by a factor of 10.

Corticosteroids

Patients on chronic corticosteroid therapy are es-pecially at risk for poor wound healing. Corticoste-roids increase the risk of infection by suppressinginflammation, inhibiting leukocyte function, retard-ing wound contraction, decreasing collagen matrixdeposition, and delaying epithelialization. Severalstudies support the assertion that vitamin A can coun-teract some of the effects of corticosteroids (27,28).Specifically, vitamin A restores the inflammatoryresponse, promotes epithelialization and the synthe-sis of collagen, further promoting wound healing andremodeling (27). Interestingly, vitamin A does notrestore the process of contraction in a healing wound.The recommended dose of vitamin A has not beenspecifically researched, although current recommen-dations for supplementation for those patients onsteroids are 10,000 to 15,000 IU per day orally (29).Vitamin A may also be administered topically so asnot to reverse the systemic therapeutic effects ofsteroids (28). According to Drugs in Pregnancy andLactation (30), it is estimated that topically appliedretinoic acid is not detected in breast milk in clini-cally significant amounts. Furthermore, vitamin Anaturally occurs in breast milk. The recommendeddaily allowance (RDA) for oral intake of vitamin Aduring lactation is 4000 IU; adverse affects to thenursing infant are unknown.

Stress

Stress, both physiological and psychologic, has adeleterious impact on wound healing. In a study byKiecolt-Glaser et al (31), wound healing was signif-icantly longer in women who were caregivers forrelatives with dementia than controls. Broadbent et al(32) studied wound fluid for levels of interleukin-1,interleukin-6 and matrix metalloproteinase-9, cyto-kines, and enzymes that are required to attract phago-

cytes and regulate collagen matrix production forwound healing. Patients reporting higher stress hadsignificantly lower levels of interleukin-1, interleu-kin-6, and matrix metalloproteinase-9. Stress alsocauses endogenous hypercortisolemia from the sym-pathetic stimulation of adrenal glands to release theirglucocorticoid steroid reserves, which blunts the in-flammatory phase of wound healing. There is someevidence that psychoeducational therapy, stress re-duction techniques, hypnosis, music therapy, andacupuncture could reduce stress and reduce the riskof wound complications (33–35).

In animal and human models, postoperative painhas been shown to have a negative influence onimmune function and wound healing (36); however,the impact on wound healing using postoperativepain relief in humans is mixed. The stress responseproduced by surgery includes changes in the pituitaryand adrenal systems as well as metabolic changes,which suppresses the immune system (37). It is in-teresting to note that regional anesthesia (rather thangeneral anesthesia) has the most support in the liter-ature to decrease the stress response from surgicalprocedures. Specifically, in a study by Koltun (38),there was a significantly larger level of cortisol mea-sured in the urine for 24 hours postoperatively inpatients who had received general anesthesia overthat of patients who received epidural anesthesia.Another finding showed natural killer cell cytotoxic-ity to be significantly depressed in the general anes-thesia group over the epidural anesthesia group. Epi-dural anesthesia may block the afferent pain stimulisuppressing the stress response, whereas general an-esthesia may not.

Nutrition

Nutrition and nutritional supplementation to im-prove wound healing has been written about exten-sively, especially in the area of chronic wounds.Many recommendations have been made particularlywith regard to vitamin C, A, and zinc. The problemis that few human studies are available that identifyoptimal levels of nutrients for wound healing andwhether nutritional supplementation has any impactat all on the rate of healing. Adequate nutrition doesseem essential to proper wound healing (39,40). Thisfact is frequently overlooked but should be a priorityof postoperative management. Protein requirementsduring pregnancy are approximately 60 to 80 gramsper day (41). Lactation increases those requirementsby 5 grams per day. Surgical procedures increaseprotein requirements above these levels, yet also


cause ileus, which further worsens a patient’s nutri-tional status (15). Protein deficit has been directlycorrelated with wound dehiscence (39). Serum pre-albumin can be used as a guide to nutritional status.It has a half-life of 2 days and can therefore be usedas a short-term guide to protein levels (normal values19–38 mg/dL, severe protein depletion 0–5 mg/dL,moderate protein depletion 5–10 mg/dL, mild proteindepletion 10–15 mg/dL) (42). Although serum pre-albumin levels are routinely ascertained in the elderlyat risk for malnutrition, it may be an area for futurestudy in the obstetric population. For patients whohave been kept nothing by mouth during a protractedcourse of labor, it may be useful to determine proteinstatus and if found deficient, treat with high proteinsupplement postoperatively. Clear liquid protein sup-plements are now available for those patients whorequire clear liquids.

Vitamin supplementation is another considerationfor those patients who are at risk for a wound com-plication. Vitamin C is necessary for collagen syn-thesis, capillary wall integrity, fibroblast function,and immunologic function. Vitamin C deficiency candelay wound healing, although there is no strongevidence for supplementation in patients who do nothave scurvy. The RDA for vitamin C during preg-nancy and lactation is 70 and 90 mg, respectively.Supplemental doses of 1000 to 2000 mg per day aresuggested in the chronic wound literature (43).

Zinc supplementation for accelerating healingwounds has been studied with conflicting results(44). Low serum zinc levels have been associatedwith impaired healing. Zinc aids collagen formationand supports immune function. The RDA in preg-

nancy and lactation for zinc is 15 and 19 mg per day,respectively. There are no evidenced-based recom-mendations at this time for zinc supplementation.

Vitamin A is also frequently cited as necessary forwound healing. Vitamin A is necessary for a normalinflammatory response, increasing the number ofmonocytes and macrophages as well as stabilizingthe intracellular lysosomes of the white blood cells(29). Vitamin A has also been shown to acceleratecollagen production in animals (40). Doses and lac-tation implications have been discussed previously.

Hypothermia

It has been hypothesized that mild perioperativehypothermia (defined as 2°C below the normal corebody temperature of 36.5°C) can promote postoper-ative wound infection by causing vasoconstrictionand impaired immune function. There is some con-troversy in the literature as to the validity of thistheory (19,45,46). Recent research, on balance, doesshow a relationship between mild perioperative hy-pothermia and wound infection. Although an evi-denced-based recommendation cannot be made atthis time, active perioperative warming with a forcedair blanket seems theoretically warranted.

PREVENTION OF WOUNDCOMPLICATIONS

The first step in prevention of wound infectionstarts with the preparation of the operative site. Table2 presents the guidelines (modified from those pro-posed by the CDC) for prevention of wound infec-tion. Important to these suggestions is the fact that

TABLE 2Prevention of surgical site infections

When Guideline

�24 h preprocedure Shower 2� within 24 h using chlorhexidineImmediately before operation If hair removal necessary, use clippersIn the operating room Prepare patient skin using:

Alcohol (most rapid action, best against Gram-positive and Gram-negative bacteria) or,Iodine/iodophors (intermediate rapidity of action, best against Gram-positive bacteria)Antimicrobial prophylaxis

Asepsis and surgical technique:HemostasisGentle handling of tissuesRemove devitalized tissuesEradicate dead spaceMonofilament suturesClosed suction drains removed no longer than 24 h after procedureMaintain normothermia

Postoperative Incision careCover with sterile dressing for 24 to 48 h

Modified from the 1999 Centers for Disease Control and Prevention guidelines for prevention of surgical site infection (65).


use of antibacterial wash needs to start before surgi-cal preparation of the patient in the operating room.In fact, Hayek (47) showed a reduction in postoper-ative infection rates when patients showered twice in24 hours before surgery with chlorhexidine wash.The rate of Staphylococcus aureus-infected wounds(attributable to skin contamination) dropped by 50%in the chlorhexidine group compared with the barsoap group. Other studies have shown a decrease inskin colonization after showering with chlorhexidine(48). Additionally, the manner in which the skin isprepared is also important. Specifically, avoidance ofshaving the skin is emphasized, because the use of arazor increases the risk of skin breakage, which canallow pathogens direct access to the bloodstream.

WOUND MANAGEMENT

Despite prophylactic measures and good surgicaltechnique, a small percentage of patients will stillexperience wound complications. Wound manage-ment should consider strategies that expedite healing,minimize complications and cost. Furthermore, prin-ciples of wound management should provide treat-ment to decrease cofactors that impede healing. He-matomas and seromas are commonly observedproblems after a cesarean delivery. These types ofsituations require manual opening of the wounds toallow drainage. After infection has been treated andall of the hematoma/seroma evacuated, an openwound can be managed in 3 ways: secondary closure,secondary intention with dressings, and secondaryintention using negative pressure wound therapy.

Secondary Closure

Secondary closure can be performed once a woundis free of infection or necrotic tissue and has startedto granulate. This procedure, which may be per-formed at the bedside using local anesthesia and/orsedation, is done within 1 to 4 days after disruptionor evacuation of hematoma or seroma. A woundcleanser is first needed to prep the area, and then apolypropylene mattress suture is used to close theskin and subcutaneous tissue en bloc. An illustrationof secondary closure technique is shown in Figure 2.The suture may be removed 7 days after reclosure.The practice of using secondary closure to repairsuperficial wound dehiscence is supported by severalstudies. Walters et al (49) found secondary closure tobe successful in 85% of cases. The mean time tocomplete healing was 15.8 days in successful cases.Those patients randomized to healing by secondary

intention required a mean of 71 days of wound careto heal. In a study by Dodson et al (50), patients whowere treated with secondary closure required a meanof 17 days to heal, whereas those patients who wereallowed to heal by secondary intention took 61 daysto complete wound healing. The results of thesestudies are striking. Wounds healed on average 7weeks sooner in the secondary closure group.

Healing by Secondary Intention Using Dressings

Healing through secondary intention has histori-cally been the most common way to manage wounddisruption. The rise in the incidence of chronicwounds has encouraged the development of newwound care strategies and products to improve on theold “wet to dry” dressings.

MISCONCEPTIONS OF WOUND HEALING

It is important to describe several historical tenetsof wound care that are outdated before proceeding ina discussion of healing by secondary intention. Manystudies have documented that the use of productssuch as povidone iodine (51), Daikens solution (52)iodophor gauze, and hydrogen peroxide (53) are cy-totoxic to white blood cells and other vital woundhealing components. The use of these products candelay wound healing. Irrigation with normal saline orcommercial wound-cleansing solutions, which do notcontain any of the aforementioned components, willadequately remove surface bacteria without disrupt-ing the beneficial physiological process.

Another myth is that moist wounds are more prone todelayed healing because they are more likely to becomeinfected or break down and that keeping a wound dry

Fig. 2. Secondary closure technique.


promotes healing. Research, in the early 1960s (17,18),proved that in fact, wounds that are kept moist at alltimes are significantly quicker to heal than dry wounds.Moist wounds promote autolytic debridement, supportepithelial cell migration, and make dressing removaleasier, causing less trauma to viable tissue (54). In “wetto dry” dressings, saline-soaked gauze is allowed to dryand then removed. This causes new tissue, which hadadhered to the gauze, to be pulled away, consequentlydestroying healthy tissue. This technique is more ap-propriate for necrotic tissue debridement, and its valid-ity is debated by wound care experts who state that itshould be used on very necrotic tissue and stoppedwhen there is viable tissue (55).

MODERN WOUND CARE

Historically, dressing changes have been describedas frequently as 4 times daily. Frequent dressingchanges will slow wound healing by reducing woundtemperature, disrupting cellular function and chemi-cal reactions necessary for tissue repair. A study byThomas (56) has shown that it takes a wound 40minutes after dressing change to return to optimaltemperature. Additionally, mitosis and leukocyte ac-tivities can be slowed for up to 3 hours after woundcleansing. Temperature in humans must be kept be-tween 97.5o to 99oF (36.4o to 37.2oC) for cellularprocesses to be optimal. Understanding wound heal-

ing physiology and wound products allows woundcare to be chosen appropriately for each wound.Dressing changes can then be reduced to once dailyor even every other day, which enables the wound tomaintain a physiological environment.

Modern wound care dressing selection considers fac-tors such as the phase of healing, the volume of exudate,and the presence of necrotic tissue to determine the typeof dressing that will be most supportive of woundhealing. Dressing selection should optimize the woundbed by decreasing the risk of infection, removing ne-crotic tissue, managing exudate, eliminating deadspace, and maintaining wound temperature.

The risk of infection can be reduced by using anontoxic solution to cleanse the wound. Necrotictissue can be removed by sharp debridement or dailyapplications of enzymatic debriders that act on ne-crotic tissue but have no effect on healthy tissue.Drainage can be managed by using highly absorbentdressing material. Calcium alginate and foam areexamples of 2 newer materials used in wound carethat are highly absorbent and have been shown to beless painful during dressing changes than gauze. Ac-cording to the Cochrane Database (57), existing re-search is inadequate to show whether foam or cal-cium alginate accelerates wound healing time.Wound care products are described in Table 3. Asource guide is provided in Table 4.

TABLE 3Wound care product descriptions

Product Description

Antifungal cream Topical cream used as treatment for superficial fungal infections of the periwound skin; contains 2%miconazole nitrate

Calcium alginate Spun fibers derived from brown seaweed composed of calcium salts of alginic acid; calcium alginate is asolid that exchanges calcium ions for sodium ions when it contacts any substance containing sodiumsuch as wound fluid; the resulting sodium alginate is a gel; nonadhesive, nonocclusive, conform-able to wound bed; indicated for moderately or highly draining wounds; not indicated for deeptunnels as a result of difficulty in retrieval; do not moisten before use; needs cover dressing

Enzymatic débrider Topical solution that breaks down necrotic tissue by directly digesting the components of slough orby dissolving the collagen that holds the necrotic tissue to the underlying wound bed; applied 1 to3 times daily with dressing changes; little data is available to help guide product selection

Film Thin, transparent polyurethane sheets coated on one side with acrylic, hypoallergenic adhesive; theadhesive will not stick to moist surfaces; impermeable to fluids and bacteria but semipermeable tooxygen and water vapor; indicated in superficial wounds with little or no exudate

Foam Polyurethane sheets containing open cells capable of holding fluids and pulling them away from thewound bed; foams provide absorbency while keeping the wound moist; manufacturers vary in theformulation; some include wound cleansers, moisturizers, and absorbing agents; indicated inmoderately or highly draining wounds; may be cut to conform to wound beds; not indicated fornarrow tunnels

Gauze Woven or nonwoven cotton or synthetic blends; nonimpregnated or impregnated with normal salineor other substances

Hydrogel Formulated in sheets or gels; glycerin, saline, or water-based to hydrate the wound; indicated in dryor minimally draining wounds; not intended to fill wound spaces

Silver nitrate Used to treat overgrown granulation tissue; apply stick to hypergranulation tissue


Vacuum-Assisted Closure

Negative pressure wound therapy (NPWT), alsoknown as vacuum-assisted closure, received U.S.Food and Drug Administration approval in 1995. Ituses controlled levels of negative pressure to assistand accelerate wound healing by evacuating local-ized edema with negative pressure. Bacterial coloni-zation is reduced along with the evacuation of wounddrainage (58). Intermittent negative pressure causesin periodic release of cytokines and inflammatoryfactors important to the previously mentioned phasesof wound healing (59). Negative pressure also in-creases localized blood flow and oxygenation,thereby promoting a nutrient-rich environment thatstimulates granulation tissue growth (60). Such cel-lular proliferation encourages angioneogenesis, uni-form wound size reduction, and reepithelialization(58). This therapy has been used in chronic woundssuch as diabetic foot ulcers (61). NPWT acceleratedwound closure significantly over traditional gauzedressings in a study by Eginton et al (62). Recentresearch in gynecologic oncology has looked atNPWT as a reliable and safe method to treat woundfailures (63,64). The results thus far have been en-couraging.

The dressing used for negative pressure woundtherapy is polyurethane foam that is trimmed to fitthe entire surface of the wound. Once the foam isplaced, evacuation tubing is laid on top of thefoam. A clear, adhesive dressing is placed over the

foam and tubing to secure the unit to the woundsite. The evacuation tubing has slits cut into theproximal end, which will evacuate the wound fluidinto a collection chamber located on the com-puterized vacuum pump. The collection canistercan be emptied as needed. Controlled negativepressure is then applied by the vacuum-assistedclosure device, which is a small computerizedpump (4 inches by 2 inches, weighing 2 pounds)with a rechargeable battery. The tubing can beclamped and disconnected for short periods of time(no more than 2 hours at a time for a maximum of6 hours per day). Dressing changes are neededevery 48 hours. Indications, contraindications, andprecautions are noted in Figure 3. Illustrations ofthe NPWT dressing and the wound vacuum areseen in Figures 4 and 5.

Although negative pressure wound therapy isconsiderably more costly (approximately $100 perday) than gauze dressings, the time to completehealing is significantly reduced (62). Home healthnursing visits can be reduced to 3 times weeklyinstead of everyday for gauze-dressing changes.Our practice has seen significantly improved heal-ing for patients who have used the wound vacuum,particularly in obese patients. Closure of wounddehiscence by secondary intention in such womencan take months. Their deep subcutaneous layeralso makes secondary closure technically difficultto perform. NPWT ensures that the subcutaneous

TABLE 4Wound care product source sheet

Productcategory 3M J&J Molnlycke Ferris Coloplast Corp Care-Tech Labs Smith & Nephew

Antifungal cream Baza creamFilm Tegaderm Bioclusive, Select MefilmCalcium alginate Tegagen HG,

Tegagen HINu-Derm Alginate Melgisorb

Foam 3M Foam Sof-Foam Meplilex Polymem,Polywic

Hydrogel Tegagel Nu-Gel NormigelSoft cloth tape

(hypoaller-genic)

Midipore Mefix Hypafix

Wound cleans-ers

Saline spray Technicare

Comfeel Sea-Cleans

Clinical Care spray

Enzymaticdébrider

Collagenase

3M, 3M Center, St. Paul, MN 55144–1000Coloplast Corp, Holtedam 1, RK-3050 Humlebaek, DenmarkJohnson & Johnson, One Johnson & Johnson Plaza, New Brunswick, NJ 08933Care Tech Labs, 3224 S. Kingshighway Blvd, St. Louis, MO 63139Molnlycke, Gotenborg, SwedenSmith & Nephew Inc, 11775 Starkey Rd, Largo, FL 33779–1970Ferris Mfg Corp, 16W300 83rd St, Burr Ridge, IL 60527–5848


wound environment remains free from seroma andhematoma formation, thus assisting in maintainingan environment in which healing is optimized.

CONCLUSION

Recent developments using evidence-based re-search can decrease postcesarean morbidity forwomen. Modern wound care strategies and productsdeveloped to support wound healing physiology canminimize healing time if a wound complication oc-curs. The information provided here can be useful toimprove clinical outcomes in other surgical proce-dures as well.

APPENDIX 1

Criteria for Defining a Surgical Site Infection

Superficial Incisional Surgical Site Infection

Infection occurs within 30 days after the operationand infection involves only skin or subcutaneoustissue of the incision and at least one of the following(65):

1. Purulent drainage, with or without laboratoryconfirmation, from the superficial incision.2. Organisms isolated from an aseptically ob-tained culture of fluid or tissue from the superficialincision.3. At least one of the following signs or symptomsof infection: pain or tenderness, localized swelling,redness, or heat and superficial incision is delib-erately opened by surgeon, unless the incision isculture-negative.4. Diagnosis of superficial incisional surgical site

Fig. 3. Indications, contraindications, and precautions for neg-ative pressure wound therapy.

Fig. 4. Negative pressure using a foam dressing and evacua-tion tubing increases localized blood flow and oxygenation.

Fig. 5. Dressing application. A clear adhesive dressing isplaced over the foam to secure the unit to the wound site.


infection (SSI) by the surgeon or attending physi-cian.Do not report the following conditions as SSI:l. Stitch abscess (minimal inflammation and dis-charge confined to the points of suture penetration).2. Infection of an episiotomy or newborn circum-cision site.3. Infected burn wound.4. Incisional SSI that extends into the fascial andmuscle layers (see deep incisional SSI).Note: Specific criteria are used for identifying in-

fected episiotomy and circumcision sites and burnwounds.

Deep Incisional Surgical Site Infection

Infection occurs within 30 days after the operationif no implant is left in place or within 1 year ifimplant is in place and the infection appears to berelated to the operation and infection involves deepsoft tissues (eg, fascial and muscle layers) of theincision and at least one of the following:

1. Purulent drainage from the deep incision butnot from the organ/space component of the surgi-cal site.2. A deep incision spontaneously dehisces or isdeliberately opened by a surgeon when the patienthas at least one of the following signs or symp-toms: fever (�38°C), localized pain or tenderness,unless the site is culture-negative.3. An abscess or other evidence of infection in-volving the deep incision is found on direct exam-ination, during reoperation, or by histopathologicor radiologic examination.4. Diagnosis of a deep incisional SSI by a surgeonor attending physician.

Notes1. Report infection that involves both superficialand deep incision sites as deep incisional SSI.2. Report an organ/space SSI that drains throughthe incision as a deep incisional SSI.

Organ/Space Surgical Site Infection

Infection occurs within 30 days after the operationif no implant is left in place or within I year ifimplant is in place and the infection appears to berelated to the operation and infection involves anypart of the anatomy (eg, organs or spaces), other than

the incision, which was opened or manipulated dur-ing an operation and at least one of the following:

1. Purulent drainage from a drain that is placedthrough a stab wound into the organ/space.2. Organisms isolated from an aseptically ob-tained culture of fluid or tissue in the organ/space.3. An abscess or other evidence of infection in-volving the organ/space that is found on directexamination, during reoperation, or by histopatho-logic or radiologic examination.4. Diagnosis of an organ/space SSI by a surgeonor attending physician.

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Management of Wound

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