Proper wound management begins with a pertinent patient history (Table 39-1).1,2 A variety of patient factors have adverse effects on wound healing and increase the rate of wound infection—extremes of age, diabetes mellitus, chronic renal failure, obesity, malnutrition, the use of immunosuppressive medications, the presence of connective tissue disorders, and protein and vitamin C deficiencies.1 Predictive factors for infection are the wound characteristics of location, age, depth, configuration, and contamination.7,8
TABLE 39-1Pertinent Medical History ||Download (.pdf) TABLE 39-1 Pertinent Medical History
Pain, swelling, paresthesias, muscle weakness
Type of force causing injury
Crush (blunt) or shear (sharp)
Bite or puncture
Elements of contamination
Time elapsed from injury until initial cleansing
Time elapsed from injury until presentation
Wound care performed prior to ED arrival
Object that caused injury (glass, wood, etc.)
Cleanliness of body and environment at time of injury and afterward
Factors resulting in injury
Intentional or unintentional
Occupation or nonoccupation related
Assault or self-inflicted
Foreign body potential
Did the object break or shatter?
Foreign body sensation
Removal of portion of object
Occupation and handedness
Anesthetics, analgesics, antibiotics, and latex
Chronic medical conditions that increase risk of infection
Chronic medical conditions that increase likelihood of poor wound healing
Previous scar formation (hypertrophic scars or keloids)
Ascertain the tendency of patients to form hypertrophic scars or keloids by both history and examination, as past experience may predict poor scar formation. Black and Asian patients are more prone to keloid formation than whites. Hypertrophic scars are due to tissue tension during wound healing, and these scars stay within the original wound boundaries and tend to undergo partial spontaneous regression within 1 to 2 years. Keloids are genetically linked variations in wound healing, resulting in the production of excess collagen beyond the original wound boundaries (Figure 39-1). Once they form, keloids rarely decrease in size.
A large keloid extending beyond the original wound margins. [Reproduced with permission from Sztajnkrycer MD, Trott AD: Wounds and soft tissue injuries, in Knoop KJ, Stack LB, Storrow AB (eds): Atlas of Emergency Medicine, 2nd ed. Figure 18-37. Copyright © 2002, 1997, by The McGraw-Hill Companies, Inc. All rights reserved.]
Obtain a detailed history of allergies or prior adverse reactions to anesthetic agents or antibiotics. Review any prior allergies to latex.9 Determine the status of prior tetanus immunization and the need for further tetanus vaccination (see chapter 156, Tetanus).
Review the mechanism of injury to identify the presence of potential wound contaminants and foreign bodies. Bite wounds are at high risk for infection and are generally managed differently than other lacerations (see chapter 46, Puncture Wounds and Bites). Foreign bodies are common in puncture wounds, wounds associated with broken glass, and motor vehicle collisions.10,11,12,13 Ask about the presence of a foreign body sensation. In adults, those reporting a foreign body sensation are more likely to have a retained foreign body than those who do not (positive likelihood ratio = 2.49 and negative likelihood ratio = 0.69).14 This question has little utility in children.15
Both foreign body retention and visible contamination increase the risk of infection.7,8 Organic and inorganic components of soil can cause infection even from very small doses of bacterial inoculum. Clay is the major inorganic soil component responsible for infection. Conversely, sand grains and black dirt from roadways are relatively inert.
The likelihood of wound infection varies according to the forces applied at the time of injury.7,8 The most common mechanism for traumatic wounds is blunt force. The skin is crushed against underlying bone and tears or splits from the subsequent tension. Sharp objects produce shear forces that cut skin cleanly. Crush injuries produce more tissue devitalization and are more susceptible to infection than wounds from shear forces.
Low-energy impact injuries may not result in lacerations, but instead may disrupt vessels, leading to ecchymosis or hematoma formation. Some hematomas spontaneously resorb. Those that become encapsulated may eventually require aspiration or incision and drainage.
Determine the time that the injury occurred. Although the growth of the bacterial inoculum is directly related to the time interval from injury to laceration repair,1,7 there is no clearly defined relationship of time to closure to clinical infection16,17,18 (Table 39-2). Therefore, time from injury until presentation is only one element to be considered, in addition to the wound etiology, location, degree of contamination, host risk factors, and the importance of cosmetic appearance, before determining whether or not to perform primary wound closure. Wounds that are not closed primarily because of a high risk of infection should be considered for delayed primary closure after 4 days. The clinical consensus of wound care experts is that after 4 days of open wound management, the risk of infection after closure substantially decreases, although this approach has not been subjected to randomized controlled trials.19
TABLE 39-2Risk of Wound Infection as Function of Time From Injury to Closure ||Download (.pdf) TABLE 39-2 Risk of Wound Infection as Function of Time From Injury to Closure
|Reference ||Comments ||Distinction Between Early and Late Closure (h) ||Infection Rate/Inadequate Healing With Early Closure ||Infection Rate/Inadequate Healing With Late Closure ||Percent age Difference (95% CI) |
|Morgan et al., 198016 ||Hand and forearm; all patients received IM penicillin and half received PO clindamycin ||4 ||10/148 (7%) ||14/69 (21%) ||13.5% (3.2% to 23.9%) |
|Baker and Lanuti, 199018 ||Children, 59% head and neck location ||6 ||32/2665 (1.2%) ||2/147 (1.3%) ||0.16% (–1.76% to 2.08%) |
|Berk et al., 198817 || |
Trunk and extremities
15.1% (5.4% to 24.8%)
–1.8% (–9.9% to 6.4%)
22.5% (8.6% to 36.4%)
Determine whether the wound was the result of an intentional, unintentional, or workplace event. Most states have regulations that require the reporting of intentional injuries, and patients with self-inflicted injuries may need psychiatric evaluation. Occupational injuries may require alternative follow-up arrangements.
The anatomic location of the injury helps predict the clinical outcome, both in terms of infection risk and cosmetic result7,8,15,20 (Table 39-3). The risk of infection is determined largely by the interplay between baseline bacterial colonization and vascular blood supply. With respect to bacterial colonization, the density of the bacterial population is low on the upper arms, legs, and torso. Conversely, moist areas of the body, such as the axilla, perineum, toe webs, and intertriginous areas, harbor millions of bacteria per square centimeter, including anaerobes. Obviously, any wounds with human or animal fecal contaminants run a high risk of infection, even with therapeutic intervention.
TABLE 39-3Risk of Wound Infection After ED Closure ||Download (.pdf) TABLE 39-3 Risk of Wound Infection After ED Closure
|Location ||Risk of Infection (%) |
|Head and neck ||1–2 |
|Upper extremity ||4 |
|Lower extremity ||7 |
Wounds located on highly vascular areas, such as the face or scalp, are less likely to be infected than wounds located in less vascular areas.7,8,15,17,20 The increased vascularity of the area more than offsets the high bacterial inoculum found in the scalp, and lacerations of the scalp and face have a very low infection rate regardless of the intensity of cleansing.21 While prophylactic oral antibiotics have traditionally been considered as warranted for intra-oral lacerations, there is inconclusive evidence to support their use.22