CHIEF EDITORS NOTE: This article is part of a series of continuing education activities in this Journal through which a total
of 36 AMA/PRA category 1 credit hours can be earned in 2005. Instructions for how CME credits can be earned appear on
the last page of the Table of Contents.
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poses treatment guidelines that may help accelerate wound healing in disrupted wounds.
BACKGROUND
Wound complications include wound separation
without infection, superficial wound infection, deep
wound infection, wound dehiscence, and rarely, necrotizing fasciitis (see Appendix 1 for Centers for
Disease Control and Prevention [CDC] definitions of
wound infection). The incidence of wound complications in the obstetric population varies in the literature, with rates ranging from 2.8% to 26.6% (2,4
14). Although wound disruptions are frequently
preceded by infection, Martens et al (8) found a
wound disruption rate of 1.7% without infection.
Fascial dehiscence occurs in 0.3% of all cesarean
deliveries. The incidence of necrotizing fasciitis is
slightly less, with one review establishing a rate of
1.8 women per 1000 cesarean deliveries (5).
PATHOGENS
Microorganisms originating from the patient
and/or the patients immediate environment are the
primary sources for postpartum wound infections.
The genital tract and skin are the most influential
reservoirs for bacterial contamination. In a study by
Martens et al (8), the most prevalent pathogens cultured from infected cesarean wounds are Staphylococcus epidermidis, Staphylococcus aureus, Escherichia coli, and Proteus mirabilis. In another study of
wound microbiology, Roberts et al (14) identified the
most prominent pathogens as cervicovaginal flora
such as Ureaplasma species and Mycoplasma species.
WOUND HEALING PHYSIOLOGY
Wound healing occurs as a complex interplay of
multiple biologic and cellular processes, which are
codependent. A review of these complexities will aid
in understanding how wound healing is disrupted and
thus, how best to support the physiology of healing.
Full-thickness wound healing is carried out in three
phases (Fig. 1): inflammation, proliferation, and remodeling. The inflammatory phase occurs in response to the initial injury and is manifested by the
signs and symptoms of erythema, edema, warmth,
and drainage. The purpose of this phase is to control
bleeding and establish a clean wound bed. Hemostasis is initiated by activating the intrinsic and extrinsic
coagulation pathways and platelet aggregation. After
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istics of the host (such as vascular or chronic disease), suboptimal perioperative conditions (hypothermia), and surgical technique that traumatizes
tissue can all impede the normal phases of wound
repair (19,20). Risk factors for postcesarean wound
complication will also impede wound healing. These
factors are described subsequently, and are summarized
with recommendations for prevention in Table 1.
Obesity
Obesity is a major risk factor for postcesarean
wound complications (7). The etiology of wound
complications in obese women is probably related to
the poor vascularity of subcutaneous fat, serous fluid
collection, and hematoma formation. The obese gravida is prone to more frequent wound complications
even with the use of prophylactic antibiotics (2).
Cetin and Cetin (10) found that the wound disruption
rate increased significantly with thickened subcutaneous tissue. Women with subcutaneous tissue
greater than 2 cm had a wound disruption rate of
27.2% compared with 18.7% of controls. Studies
have shown that using a subcutaneous suture in all
patients with greater than 2-cm subcutaneous depth
significantly reduces the risk of wound disruption
(4,5,10,2123). Specifically, closure of excess subcutaneous tissue eliminates dead space, thus reducing
the formation of seromas.
Diabetes
Impaired wound healing is frequently seen in patients with diabetes. Cruse and Foord (24) reviewed
infection rates in 23,649 patients and found that
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diabetics had 5 times the risk of infection of nondiabetics, even with clean incisions. Although increased
levels of HgA1c were not shown to be positively
correlated to surgical site infections in a study (25),
diabetes and postoperative hyperglycemia were independent risk factors for a surgical site infection.
Another study, by Zerr et al (26), compared infection
rates before and after implementation of stricter
blood glucose goals and found that the rate of infection before implementation was 2.4% and after implementation, the rate was 1.5%. Zerr demonstrated
that glucose levels above 200 mg/dL in the immediate postoperative period were associated with an
increased surgical site infection rate. Additionally,
blood glucose levels above 200 mg/dL at 48 hours
postsurgery were significantly associated with deep
wound infection.
The explanation for the difference in diabetic wound
healing is complex. The disparity starts with alterations
in the inflammatory response generated by injury or
incision. These differences in enzyme secretion and
growth factor affect all the aspects of normal wound
healing such as collagen synthesis and deposition, leukocyte function, and tissue perfusion. Although a growing body of research in experimental models of diabetes
exists to investigate the use of vitamin A, exogenous
growth factors, and nitric oxide supplementation to
increase wound repair in diabetic patients, there are no
specific recommendations other than meticulous avoidance of hyperglycemia and strict regulation of insulin to
assist in wound healing. Specific blood glucose target
levels have not been identified, although as previously
mentioned in the Zerr study, blood glucose over 200
mg/dL were shown to increase surgical site infections.
TABLE 1
Risk factors for cesarean section wound complication practice recommendations to reduce risk
Risk factor
Obesity
Diabetes
Intrapartum chorioamnionitis
Postoperative endometritis
Prolonged rupture of membranes
Severe anemia
Stressphysiological or psychologic
Smoking
Anticoagulation therapy
Perioperative hypothermia
Severe hypertension
Inadequate nutrition
Practice recommendations
Subcutaneous suture
Stringent glucose control, insulin therapy
Decrease number of vaginal examinations
Judicious use of internal fetal monitoring
Prophylactic antibiotics at cord clamping
Prophylactic antibiotics
Correct anemia
Appropriate pain control/stress reduction
Smoking cessation or nicotine patch
Consider placement of closed drain system to avoid hematoma or seroma
formation
Maintenance of normal body temperature in operating room and recovery
room (use electric warming blanket)
Correct hypertension
Adequate protein, vitamin A, C, and zinc
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Chorioamnionitis
Tissue infection and clinical circumstances that
predispose to infection comprise the other major
reasons for suboptimal wound healing. Specifically,
long labors, prolonged rupture of membranes, and
frequent vaginal examinations are all known risk
factors for increasing the rate of infection. Indeed,
the intrauterine environment during labor can tremendously impact postpartum healing. Tran et al (9)
showed that chorioamnionitis increases the risk for
wound infection by a factor of 10.
Corticosteroids
Patients on chronic corticosteroid therapy are especially at risk for poor wound healing. Corticosteroids increase the risk of infection by suppressing
inflammation, inhibiting leukocyte function, retarding wound contraction, decreasing collagen matrix
deposition, and delaying epithelialization. Several
studies support the assertion that vitamin A can counteract some of the effects of corticosteroids (27,28).
Specifically, vitamin A restores the inflammatory
response, promotes epithelialization and the synthesis of collagen, further promoting wound healing and
remodeling (27). Interestingly, vitamin A does not
restore the process of contraction in a healing wound.
The recommended dose of vitamin A has not been
specifically researched, although current recommendations for supplementation for those patients on
steroids are 10,000 to 15,000 IU per day orally (29).
Vitamin A may also be administered topically so as
not to reverse the systemic therapeutic effects of
steroids (28). According to Drugs in Pregnancy and
Lactation (30), it is estimated that topically applied
retinoic acid is not detected in breast milk in clinically significant amounts. Furthermore, vitamin A
naturally occurs in breast milk. The recommended
daily allowance (RDA) for oral intake of vitamin A
during lactation is 4000 IU; adverse affects to the
nursing infant are unknown.
Stress
Stress, both physiological and psychologic, has a
deleterious impact on wound healing. In a study by
Kiecolt-Glaser et al (31), wound healing was significantly longer in women who were caregivers for
relatives with dementia than controls. Broadbent et al
(32) studied wound fluid for levels of interleukin-1,
interleukin-6 and matrix metalloproteinase-9, cytokines, and enzymes that are required to attract phago-
cause ileus, which further worsens a patients nutritional status (15). Protein deficit has been directly
correlated with wound dehiscence (39). Serum prealbumin can be used as a guide to nutritional status.
It has a half-life of 2 days and can therefore be used
as a short-term guide to protein levels (normal values
1938 mg/dL, severe protein depletion 05 mg/dL,
moderate protein depletion 510 mg/dL, mild protein
depletion 1015 mg/dL) (42). Although serum prealbumin levels are routinely ascertained in the elderly
at risk for malnutrition, it may be an area for future
study in the obstetric population. For patients who
have been kept nothing by mouth during a protracted
course of labor, it may be useful to determine protein
status and if found deficient, treat with high protein
supplement postoperatively. Clear liquid protein supplements are now available for those patients who
require clear liquids.
Vitamin supplementation is another consideration
for those patients who are at risk for a wound complication. Vitamin C is necessary for collagen synthesis, capillary wall integrity, fibroblast function,
and immunologic function. Vitamin C deficiency can
delay wound healing, although there is no strong
evidence for supplementation in patients who do not
have scurvy. The RDA for vitamin C during pregnancy and lactation is 70 and 90 mg, respectively.
Supplemental doses of 1000 to 2000 mg per day are
suggested in the chronic wound literature (43).
Zinc supplementation for accelerating healing
wounds has been studied with conflicting results
(44). Low serum zinc levels have been associated
with impaired healing. Zinc aids collagen formation
and supports immune function. The RDA in preg-
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TABLE 2
Prevention of surgical site infections
When
Guideline
24 h preprocedure
Immediately before operation
In the operating room
Postoperative
Modified from the 1999 Centers for Disease Control and Prevention guidelines for prevention of surgical site infection (65).
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use of antibacterial wash needs to start before surgical preparation of the patient in the operating room.
In fact, Hayek (47) showed a reduction in postoperative infection rates when patients showered twice in
24 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 bar
soap group. Other studies have shown a decrease in
skin colonization after showering with chlorhexidine
(48). Additionally, the manner in which the skin is
prepared is also important. Specifically, avoidance of
shaving the skin is emphasized, because the use of a
razor increases the risk of skin breakage, which can
allow pathogens direct access to the bloodstream.
Fig. 2. Secondary closure technique.
WOUND MANAGEMENT
Despite prophylactic measures and good surgical
technique, a small percentage of patients will still
experience wound complications. Wound management should consider strategies that expedite healing,
minimize complications and cost. Furthermore, principles of wound management should provide treatment to decrease cofactors that impede healing. Hematomas and seromas are commonly observed
problems after a cesarean delivery. These types of
situations require manual opening of the wounds to
allow drainage. After infection has been treated and
all of the hematoma/seroma evacuated, an open
wound can be managed in 3 ways: secondary closure,
secondary intention with dressings, and secondary
intention using negative pressure wound therapy.
Secondary Closure
Secondary closure can be performed once a wound
is free of infection or necrotic tissue and has started
to granulate. This procedure, which may be performed at the bedside using local anesthesia and/or
sedation, is done within 1 to 4 days after disruption
or evacuation of hematoma or seroma. A wound
cleanser is first needed to prep the area, and then a
polypropylene mattress suture is used to close the
skin and subcutaneous tissue en bloc. An illustration
of secondary closure technique is shown in Figure 2.
The suture may be removed 7 days after reclosure.
The practice of using secondary closure to repair
superficial wound dehiscence is supported by several
studies. Walters et al (49) found secondary closure to
be successful in 85% of cases. The mean time to
complete healing was 15.8 days in successful cases.
Those patients randomized to healing by secondary
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TABLE 3
Wound care product descriptions
Product
Antifungal cream
Calcium alginate
Enzymatic dbrider
Film
Foam
Gauze
Hydrogel
Silver nitrate
Description
Topical cream used as treatment for superficial fungal infections of the periwound skin; contains 2%
miconazole nitrate
Spun fibers derived from brown seaweed composed of calcium salts of alginic acid; calcium alginate is a
solid that exchanges calcium ions for sodium ions when it contacts any substance containing sodium
such as wound fluid; the resulting sodium alginate is a gel; nonadhesive, nonocclusive, conformable to wound bed; indicated for moderately or highly draining wounds; not indicated for deep
tunnels as a result of difficulty in retrieval; do not moisten before use; needs cover dressing
Topical solution that breaks down necrotic tissue by directly digesting the components of slough or
by dissolving the collagen that holds the necrotic tissue to the underlying wound bed; applied 1 to
3 times daily with dressing changes; little data is available to help guide product selection
Thin, transparent polyurethane sheets coated on one side with acrylic, hypoallergenic adhesive; the
adhesive will not stick to moist surfaces; impermeable to fluids and bacteria but semipermeable to
oxygen and water vapor; indicated in superficial wounds with little or no exudate
Polyurethane sheets containing open cells capable of holding fluids and pulling them away from the
wound bed; foams provide absorbency while keeping the wound moist; manufacturers vary in the
formulation; some include wound cleansers, moisturizers, and absorbing agents; indicated in
moderately or highly draining wounds; may be cut to conform to wound beds; not indicated for
narrow tunnels
Woven or nonwoven cotton or synthetic blends; nonimpregnated or impregnated with normal saline
or other substances
Formulated in sheets or gels; glycerin, saline, or water-based to hydrate the wound; indicated in dry
or minimally draining wounds; not intended to fill wound spaces
Used to treat overgrown granulation tissue; apply stick to hypergranulation tissue
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Vacuum-Assisted Closure
Negative pressure wound therapy (NPWT), also
known as vacuum-assisted closure, received U.S.
Food and Drug Administration approval in 1995. It
uses controlled levels of negative pressure to assist
and accelerate wound healing by evacuating localized edema with negative pressure. Bacterial colonization is reduced along with the evacuation of wound
drainage (58). Intermittent negative pressure causes
in periodic release of cytokines and inflammatory
factors important to the previously mentioned phases
of wound healing (59). Negative pressure also increases localized blood flow and oxygenation,
thereby promoting a nutrient-rich environment that
stimulates granulation tissue growth (60). Such cellular proliferation encourages angioneogenesis, uniform wound size reduction, and reepithelialization
(58). This therapy has been used in chronic wounds
such as diabetic foot ulcers (61). NPWT accelerated
wound closure significantly over traditional gauze
dressings in a study by Eginton et al (62). Recent
research in gynecologic oncology has looked at
NPWT as a reliable and safe method to treat wound
failures (63,64). The results thus far have been encouraging.
The dressing used for negative pressure wound
therapy is polyurethane foam that is trimmed to fit
the entire surface of the wound. Once the foam is
placed, evacuation tubing is laid on top of the
foam. A clear, adhesive dressing is placed over the
TABLE 4
Wound care product source sheet
Product
category
3M
Antifungal cream
Film
Tegaderm
Calcium alginate Tegagen HG,
Tegagen HI
Foam
3M Foam
Hydrogel
Soft cloth tape
(hypoallergenic)
Wound cleansers
Tegagel
Midipore
J&J
Molnlycke
Ferris
Coloplast Corp
Care-Tech Labs
Baza cream
Bioclusive, Select
Nu-Derm Alginate
Mefilm
Melgisorb
Sof-Foam
Meplilex
Nu-Gel
Normigel
Mefix
Polymem,
Polywic
Hypafix
Saline spray
Technicare
Comfeel SeaCleans
Enzymatic
dbrider
Collagenase
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CONCLUSION
Fig. 3. Indications, contraindications, and precautions for negative pressure wound therapy.
Recent developments using evidence-based research can decrease postcesarean morbidity for
women. Modern wound care strategies and products
developed to support wound healing physiology can
minimize healing time if a wound complication occurs. The information provided here can be useful to
improve clinical outcomes in other surgical procedures as well.
APPENDIX 1
Criteria for Defining a Surgical Site Infection
Superficial Incisional Surgical Site Infection
Fig. 4. Negative pressure using a foam dressing and evacuation tubing increases localized blood flow and oxygenation.
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the incision, which was opened or manipulated during an operation and at least one of the following:
1. Purulent drainage from a drain that is placed
through a stab wound into the organ/space.
2. Organisms isolated from an aseptically obtained culture of fluid or tissue in the organ/space.
3. An abscess or other evidence of infection involving the organ/space that is found on direct
examination, during reoperation, or by histopathologic or radiologic examination.
4. Diagnosis of an organ/space SSI by a surgeon
or attending physician.
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