Infections

Michael A. West and Daniel Dante Yeh

INTRODUCTION

Death after traumatic injury has been described in terms of a trimodal distribution. Immediate and acute (<24 hours) deaths usually result from uncontrolled hemorrhage, but infections and multiple organ dysfunction syndrome, which often arise from infection, are responsible for a significant proportion of late deaths. Indeed, infection is responsible for most deaths in patients who survive longer than 48 hours after trauma.¹ Trauma-related infections are generally divided into those that result directly from the injury (e.g., due to contamination that occurs in conjunction with the traumatic injury) and nosocomial infections that arise in the health care setting, secondary to treatment of the injury. The pathogens involved can be exogenous or endogenous bacteria, depending on the mechanism of injury and/or the iatrogenic cause. Most post-traumatic infections are polymicrobial and involve a mixture of aerobic and anaerobic organisms.² In one series, 37–45% of all trauma patients experienced infectious complications during their initial hospitalization. Furthermore, in the same study, 80% of trauma patients staying at least 7 days in the intensive care unit met systemic inflammatory response syndrome (SIRS) criteria.³ Therefore, it is important that all caregivers understand the principles of surgical infections in the context of trauma patients. This chapter discusses the following: factors that normally prevent infection, how trauma disrupts or overwhelms normal host defenses, how to recognize and treat the most common infectious complications after traumatic injury, principles that can be employed to prevent infection, and how those principles can be applied chronologically during the treatment of trauma patients.

PATHOGENESIS OF INFECTION

Humans have evolved mechanisms to avoid infection despite the ubiquitous presence of bacteria in our environment and throughout our bodies. Under normal circumstances there is a balance between bacteria, intact environmental barriers, and host defenses (see Fig. 18-1). With surgery in general, and trauma in particular, there is a disruption in this balance that significantly increases the probability of developing an infection (Fig. 18-2). Bacteria are abundant on the surface of the skin, within the oral cavity, and present in increasing numbers down the length of the gastrointestinal tract. Bacterial numbers differ at various locations, and the pathogenic species and their respective numbers at different anatomic sites are summarized in Table 18-1. Trauma disrupts the environmental barriers that prevent bacteria from gaining access to normally sterile regions of the body. When inoculation of bacteria into normally sterile sites occurs, infection will ensue if bacteria can proliferate faster than the host defense mechanisms can eradicate them. Furthermore, there is potential for much greater disruption of normal barriers with trauma than occurs with elective surgery as there is often concomitant hypoperfusion (shock), devitalized tissue, and retained foreign bodies.

FIGURE 18-1 Under normal circumstances the determinants of infection, microbial factors, environmental factors, and host defenses interact such that there is no infection. (Adapted with permission from Meakins JL, et al. Host defenses. In: Howard RJ, Simmons RL, eds. Surgical Infectious Diseases. 2nd ed. Norwalk, CT: Appleton & Lange; 1988. Copyright © The McGraw-Hill Companies, Inc.)

FIGURE 18-2 (A) Under circumstances in which there is excessive microbial contamination, (B) serious disruption of environmental barrier, (C) impaired host defenses, or (D) all factors that ensure there will be an increased likelihood of developing infection (shaded intersection of determinants of infection).

TABLE 18-1 Pathogenic Microorganisms Present at Various Anatomic Sites

Environmental Barriers

Normally, entry of microbes is limited by the integrity of environmental barriers. These environmental barriers include intact skin, respiratory, gastrointestinal, and genitourinary tracts.⁴ The importance of intact skin is clearly evident when one considers the potential for microbial infection seen in burn patients or in patients with toxic epidermal necrolysis.² Many traumatic injuries are associated with an alteration in the integrity of the skin. Even minor lacerations and abrasions have the potential to disrupt crucial environmental barriers. Interventions that are made in the process of caring for trauma patients, such as insertion of intravenous or urinary catheters, tube thoracostomy, etc., disrupt the integument and may provide skin bacteria access to sterile sites. Furthermore, the quantitative number of microbes required to produce clinical infection is significantly decreased in the presence of foreign bodies, blood, or devitalized tissue.²

Microbial Factors

The bacteria that are responsible for clinical infections in surgery or trauma patients constitute a minority of the skin or gastrointestinal flora and they generally possess one or more virulence factors that facilitate infection and increase their pathogenicity. In contrast, the vast majority of endogenous and environmental bacteria are relatively nonpathogenic. For example, more than 99% of the colonic flora is nonpathogenic anaerobes that never cause clinical infections. Similarly, most skin bacteria are lactobacilli, which do not cause clinical infection either. In contrast, Staphylococcus aureus, the most common pathogen associated with surgical site infections (SSI), has numerous virulence factors that facilitate invasion and thwart host defenses. In the abdominal cavity, Escherichia coli and Bacteroides fragilis are the prototypical organisms associated with intra-abdominal infection, yet they account for only 0.01% and 1% of colonic bacteria, respectively. Indeed, to some extent the normal presence of overwhelming numbers of nonpathogenic bacteria constitutes a defense against infection. That is, infection is proportionately less likely if 99% of the inoculum is incapable of producing infection. This concept of adherent resident bacteria preventing invasion has been termed colonization resistance.⁴ This is an important point as skin and gastrointestinal flora changes considerably when trauma patients are hospitalized, both in terms of number and proportion of virulent bacteria and in terms of susceptibility to antibiotics, should an infection develop.

Skin flora is relatively homogeneous, although bacterial numbers are higher in the axilla and groin areas. The endogenous skin bacteria are predominately gram-positive aerobic Staphylococcus and Streptococcus species, along with Corynebacterium and Propionibacterium.⁴ As noted above, S. aureus is the most common pathogen present on the skin. Most recently an increasing number of S. aureus isolates from trauma patients and other community-acquired infections have been methicillin resistant (MRSA).^5,6 This fact, along with knowledge of the local incidence of MRSA, needs to be taken into account in terms of appropriate empiric or prophylactic antibiotic selection for these patients.⁶ The oral and nasopharynx harbor large numbers of bacteria, with streptococcal species being most frequently present. Much smaller numbers of bacteria, typically 10²–10³ CFU/mL, are present in the normal stomach, because the normally acid pH of the stomach inhibits bacterial growth. Gastric bacterial numbers increase in the absence of gastric acid as in patients on proton pump inhibitors. Bacterial numbers are much higher in the small intestine, and the density of bacteria increases further as chyme progresses from the duodenum to the terminal ileum. Bacterial counts in the proximal gastrointestinal tract are in the range of 10⁴–10⁵ CFU/mL, whereas numbers in the terminal ileum are close to colonic densities (10⁸–10¹⁰ CFU/mL). Bacterial numbers in the colon are even higher, with approximately 10¹¹–10¹² CFU/mL of stool, although many of these colonic bacteria are nonpathogenic. These large numbers are also associated with very low oxygen tension, and 99.9% of bacteria present are anaerobes. The urogenital, biliary, pancreatic ductal, and distal respiratory tracts do not possess resident microflora in healthy individuals.⁴

Host Defense Mechanisms

Host defense refers to endogenous factors that counteract microbial invasion. In addition to the environmental factors and colonization resistance described above, humoral and cellular host defense mechanisms that are crucial to eliminate bacteria within a sterile space exist. Initially, several primitive and relatively nonspecific host defenses including proteins such as lactoferrin, fibrinogen, and complement begin to act against invading microbes. Lactoferrin sequesters the critical microbial growth factor iron, thereby limiting microbial growth. Fibrinogen within the inflammatory fluid has the ability to trap large numbers of microbes during the process in which it polymerizes into fibrin.⁴ Complement is activated on contact with bacteria and viruses, from tissue damage, or when IgG/IgM antibodies recognize microbial agents. Activation of complement releases C3a and C5a, which are potent chemotaxins that result in recruitment of neutrophils and macrophages. These components enhance endothelial adhesiveness and increase vascular permeability. Complement activation can directly destroy microbial agents via formation of a membrane attack complex (composed of complement proteins C5–C9) and enhance microbial phagocytosis by way of C1q and C3bi subunits. In vitro studies have shown that 50–70% of a moderate inoculum is eliminated prior to the influx of phagocytic host cells.

Many different tissues also contain resident innate immune cells. These include macrophages, dendritic cells, Kupffer cells, glial cells, mesangial cells, and alveolar macrophages.⁷ These innate immune cells express a wide variety of pathogen-associated molecular pattern (PAMP) receptors on their surface.^8–10 The best known examples of PAMPs are the toll-like receptors (TLRs) of which there are now more than 10 well-described receptor molecules.¹⁰ TLRs bind to ligands on bacteria (or damaged host tissue), and TLR binding results in activation of these cells. Activated macrophages secrete a wide array of substances in response leading to amplification and regulation of the acute proinflammatory response (Fig. 18-3). Sequential release of protein cytokines, including tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), IL-6, IL-8, and interferon-gamma (INF-γ), follows. These mediators produce the signs and symptoms (fever, tachycardia, tachypnea, leukocytosis, etc.) that we associate with infection. IL-8 is a very potent chemoattractant for neutrophils, which are primarily responsible for ongoing microbial phagocytosis and intracellular microbial killing. Unfortunately, the same process that recruits neutrophils and stimulates phagocytosis and oxidative killing may also be responsible for damage to host tissues. Simultaneous with the innate immune proinflammatory response there is production of anti-inflammatory mediators, such as IL-10, also.¹¹ Some of these mediators may contribute to the immune hyporesponsiveness of trauma over the ensuing days (Table 18-2).

TABLE 18-2 Immunologic Defects Associated with Traumatic Injuries

FIGURE 18-3 Schematic depiction of how acute injury simultaneously initiates the proinflammatory systemic inflammatory response syndrome (SIRS) and the anti-inflammatory compensatory anti-inflammatory response syndrome (CARS). Under normal circumstances there is a defined temporal period in which these initial responses surge and resolve. When a second or subsequent insult (“hit”) is imposed on this response, it may lead to multiple organ dysfunction syndrome (MODS) and death in a significant subset of patients. (Reproduced with permission from Ni Choileain N, Redmond HP: Cell response to surgery. Arch Surg. 2006;141(11):1132–1140. Copyright © 2006 American Medical Association. All rights reserved.)

Particular anatomic locations have additional unique factors that defend against infection.¹³ For example, the peritoneal cavity has lymphatic channels on the undersurface of the diaphragm that facilitate removal of bacteria.¹⁴ The subdiaphragmatic surface is a lower-pressure area, due to the effect of respiratory excursion, and this serves to move free fluid within the peritoneal cavity to this location. Movement of the diaphragm “pumps” this fluid into the thoracic duct and from there it gains rapid access to the systemic circulation. Experimental studies show that labeled bacteria inoculated into the peritoneal cavity appear in the thoracic duct within 6 minutes and in the bloodstream within 12 minutes.¹³ The respiratory tract has unique host defenses that help to ensure the sterility of the lung parenchyma as well. Goblet cells within the respiratory mucosa secrete mucin that helps to traps bacteria. Ciliated respiratory epithelial cells move the mucus centrally where it, and the bacteria trapped within it, can be expectorated by coughing. The presence of endotracheal tubes, smoking, inhaled toxins, and some anesthetic agents interfere with mucociliary clearance mechanisms, and this may predispose to pneumonia. Bacteria or other microbes that gain access to the alveoli are normally phagocytosed by alveolar macrophages, although the macrophage activation that may accompany this process has been proposed as one possible pathogenetic mechanism for acute lung injury (ALI) or adult respiratory distress syndrome (ARDS).^15–17

MICROBIOLOGY

To a very large extent the microbial agents responsible for infections or infectious complications after trauma are the same agents that cause most other surgical or ICU-associated infections. Table 18-1 shows the most common infectious agents that cause trauma-associated infections at various anatomic sites. Generally, Staphylococcus spp. and Streptococcus spp. are the most common pathogens responsible for infections in which the traumatic injury or operative intervention needed to treat the injury did not transgress a mucosal surface. For traumatic injuries that involve the aerodigestive tract the most common isolates are E. coli (43.4%), S. aureus (18.9%), Klebsiella pneumoniae (14.4%), and Entercoccus faecalis (5.6%).¹ Hospitalized trauma patients develop nosocomial bacterial infections from the usual ICU-associated pathogens (Table 18-3). There are a few important infectious agents that can be associated with trauma, that are seldom encountered in other settings including rabies virus, Clostridium tetani, and Vibrio spp.

TABLE 18-3 ICU Pathogens Isolated from Patients with Ventilator-Associated Pneumonia

Rabies

Rabies is a rare, but potentially fatal, clinical disease caused by the rabies virus. It is an RNA virus that is present in the saliva of mammals and transmission to humans generally occurs following a bite from a rabid animal. Prior to the development of a vaccine by Louis Pasteur, bites from a rabid animal were uniformly fatal. In North America, raccoons, skunks, bats, foxes, coyotes, and bobcats are the primary reservoirs. Most human rabies cases have no documented exposure to a rabid animal and the majority of these cases are associated with bat bites. Many victims underestimate the importance of a bat bite and a substantial portion do not even recall being bitten. Bats (Carnivora and Chiroptera) represent the ultimate zoonotic reservoir for the virus, as well. The rabies virus is highly labile and can be inactivated readily by ultraviolet radiation, heat, desiccation, and other environmental factors.

The word “rabies” derives from the Latin rabere meaning “to rage” and refers to the clinical manifestations of the disease that include hyperactivity, disorientation, hallucinations, and bizarre behavior. The rabies virus is neurotropic and causes an acute encephalitis. Other hallmarks of the disease include hydrophobia and aerophobia, as these stimuli tend to cause intense laryngeal and pharyngeal spasm. Once the patient begins manifesting symptoms, death is nearly certain. With increased vaccination and postexposure prophylaxis (PEP) over the past 50 years, the clinical disease is becoming increasingly uncommon, with only 32 cases of human rabies reported in the United States between 1980 and 1998. That said, it is important for the practitioner of emergency medicine/surgery to be knowledgeable about rabies since animal bites are encountered frequently in clinical practice.

Humans are not routinely vaccinated against rabies. Rather, domestic animals receive routine rabies vaccinations. If a human is bitten by a rabid animal, rabies can be prevented by PEP before the virus enters the central nervous system during the incubation period. The diagnosis of rabies can be made rapidly by identification of rabies virus in the brain of a potentially infected animal. This procedure can be performed in a timely manner, but requires euthanizing the suspected animal. The incidence of positive rabies tests ranges from as high as 6–10% in wild animals down to levels of ˜1% in domestic pets. If the rabies test is negative, then no postexposure vaccination or prophylaxis is needed. An acceptable alternative approach, if the suspected source is a domestic pet (dog, cat, ferret, etc.), is that the offending animal be quarantined and observed for 10 days. If the animal exhibits signs of rabies, the exposed person should begin PEP immediately and the animal should be euthanized and its brain tissue tested for rabies. If the animal is confirmed to have rabies, PEP should be completed. When the test results are negative, PEP can cease.

Immediate measures that should be taken to decrease the risk of rabies transmission include thorough washing of bite and scratch wounds with soap and water, followed by application of povidone–iodine or alcohol. Human rabies immune globulin (HRIG) and rabies vaccine should be given in all cases except in persons who have been immunized previously.¹⁹ Immune globulin should never be delivered in the same syringe as the vaccine, as this will cause precipitation. The Advisory Committee on Immunization Practices (ACIP) of the Centers for Disease Control and Prevention (CDC) and the American Academy of Pediatrics recommend a single dose (20 IU/kg) of HRIG be given to provide protection for the first 2 weeks until the vaccine elicits an antibody response. Detailed and up-to-date information for rabies exposure is available on the CDC’s Web site (http://www.cdc.gov/RABIES/), and this site should be consulted for the latest information. The ACIP recommends a regimen of human diploid cell vaccine (Imovax^®) for PEP on days 0, 3, 7, 14, and 28 along with a single dose of HRIG on day 0. Once initiated, rabies prophylaxis should not be interrupted or discontinued because of local or mild systemic reactions to the vaccine.

Tetanus

Tetanus is a rare, life-threatening condition that is caused by toxins produced by C. tetani, a spore-forming, gram-positive bacillus.²⁰ Clostridial spores can survive indefinitely, and they are ubiquitous in soil and feces. Under anaerobic conditions the spores can germinate into mature bacilli, which elaborate the neurotoxins tetanospasmin and tetanolysin. Tetanospasmin is the toxin that produces most clinical symptoms by interfering with motor neuron release of the inhibitory neurotransmitters gamma-aminobutyric acid (GABA) and glycine. This loss of inhibition results in muscle spasm (usually spasm of the masseter muscle) and severe autonomic overactivity manifested by high fever, tachycardia, and hypertension. Historically, tetanus was highly fatal, but intensive medical therapy with neuromuscular blockade, mechanical ventilation, and ICU monitoring has lowered the case fatality rate to 11–28%. Since the mid-1970s there have been <100 tetanus cases reported annually in the United States. Even so, clinicians and trauma surgeons must remain alert for the potential of clostridial contamination and provide tetanus prophylaxis.²⁰

The diagnosis of tetanus is made on clinical grounds alone, as there are no laboratory tests that can diagnose the condition or rule it out. Tetanus immunization is accomplished as a component of standard early childhood immunizations (diphtheria–pertussis–tetanus [DPT]), with administration of tetanus toxoid (TT) every 5–10 years to maintain immune memory. There have been no deaths reported in individuals who have been fully immunized. The CDC recommendations for tetanus prophylaxis depend on the wound characteristics and the prior immunization status of the patient. A wound with extensive contamination, one that is poorly vascularized, or with extensive soft tissue trauma is considered to be a tetanus-prone wound. A tetanus booster should be administered to patients who have received primary immunization, but who have not received TT during the past 10 years, or the past 5 years for tetanus-prone wounds.¹⁹ In patients who have never undergone primary immunization, human tetanus immune globulin (HTIG) should be administered along with TT at a different site. Antitetanus antibody binds to exotoxins and neutralizes their toxicity. High-risk groups such as the elderly, human immunodeficiency virus (HIV)–infected individuals, and intravenous drug users (IVDU) who had received primary vaccination may not have tetanus antibodies and more liberal use of HTIG should be considered in these groups.¹⁹

Infections Associated with Marine Trauma

Vibrio vulnificus is a gram-negative rod present in seawater that can result in atypical, necrotizing soft tissue infections when traumatic injuries occur in the ocean.^21–23 V. vulnificus is common in warm seawater and thrives in water temperatures greater than 68°F (20°C). The organism is not associated with pollution or fecal waste. Approximately 25% of V. vulnificus infections are caused by direct exposure of an open wound to warm seawater containing the organism. Exposure typically occurs when the patient is participating in water activities such as boating, fishing, or swimming. Infections are occasionally attributed to contact with raw seafood or marine wildlife. The risk of developing Vibrio infection is much higher in immunocompromised patients or patients with preexisting hepatic disease or diabetes mellitus.²² Established infection with V. vulnificus can be highly invasive with mortality rates of 30–40% and a mortality greater than 50% in immunocompromised patients. A recent published report documented a 37% mortality rate even after implementation of a specific treatment guideline for necrotizing Vibrio infections.²¹

Patients with wound infections caused by V. vulnificus develop painful cellulitis that progresses rapidly.^22–24 Physical examination will often reveal marked swelling and painful, hemorrhagic bullae surrounding traumatic wounds. In some cases, there can be rapid progression and associated systemic symptoms. Marked local tissue swelling with hemorrhagic bullae is characteristic. Systemic symptoms include fever and chills, and bacteria are present in the bloodstream in more than 50% of patients. Hypotension or septic shock may be an early symptom and alterations in mental status occur in approximately one third of patients. Table 18-4 summarizes clinical symptoms present in patients with Vibrio infection. It is important for trauma surgeons to be aware of the potential for Vibrio infections in the appropriate clinical setting, because antibiotic treatment is distinctly different from the agents typically employed for trauma patients. Aggressive surgical debridement, incision and drainage of purulent collections, and even amputation may be crucial adjuncts for management of occasionally severe soft tissue infections.²² A recent experience in 30 patients found that fasciotomy was needed in all patients, and 17% required amputation.²¹ Recommended antibiotics include doxycycline (100 mg iv/po bid), ceftazidime (2 g q 8 hours), cefotaxime (2 g q 8 hours), or ciprofloxacin (750 mg po bid or 400 mg iv q 12 hours).^22,25

TABLE 18-4 Clinical Characteristics Associated with Vibrio vulnificus Wound Infections

Traumatic injuries that occur in freshwater conditions may develop infections from Aeromonas hydrophila.²⁴ A. hydrophila is a gram-negative anaerobic rod that is a common pathogen of fish and amphibians. Cutaneous inoculation of the organism can result in cellulitis, abscesses, and, occasionally, necrotizing soft tissue infections. Like the situation with Vibrio infections, patients with hepatic disease and immunocompromised patients have a greater risk of developing generalized disease. A. hydrophila can be recovered from the bloodstream in a significant proportion of patients and this fact, along with a history of injury in fresh water, will aid in alerting clinicians to the correct diagnosis. Antibiotic agents active against A. hydrophila include third-generation cephalosporins, fluoroquinolones, doxycycline, or trimethoprim–sulfamethoxazole.²⁴

PREVENTION OF INFECTIONS

General Principles

As in all other aspects of surgical care, it is preferable to try to prevent infections wherever possible. A number of interventions and practices have been demonstrated to be highly effective in preventing infections after elective operations, and many of those techniques have specific application in the care of injured patients. In this section, the current evidence-based interventions to prevent infection that are applicable to trauma patients are discussed.

Prophylactic Antibiotics

Prophylactic antibiotics are intended to prevent development of infection. The concept of prophylaxis presupposes that infection is not present at the time. The decision to use prophylactic antibiotics and the choice of agents are based on the risk of developing SSI. There are very good data regarding SSI rates for elective surgery and the incidence of SSI by wound class for elective operations is shown in Table 18-5. Traditionally, Class I or clean wounds are those that do not violate the respiratory, alimentary, or genitourinary tracts. The wound infection rate is approximately 2%. Class II, or clean-contaminated wounds, refers to elective operations on potentially contaminated organs, such as the gastrointestinal tract, genitourinary tract, and respiratory tree (the procedure will violate a mucosal surface, which can never be completely sterile). The usual incidence of infection for these types of wounds is 5–10%. Contaminated wounds (Class III) differ from Class II wounds by the degree of spillage, with an incidence of infection of 15–30%. Finally, Class IV or dirty-infected wounds are characterized by frank pus or extensive and prolonged contamination. These wounds are characterized by an infection rate of >30% if primary closure is attempted.²⁷ Emergent operative interventions increase the wound class by one step, so it is clear that higher wound infection rates will be encountered in dealing with patients who have acute traumatic injuries that require operative intervention.

TABLE 18-5 Classification of Surgical Wounds^a

In trauma surgery, the majority of wounds encountered will be Class III or IV, and the luxury of a preinoculation dose of antibiotics, as recommended by the Surgical Care Improvement Project (SCIP), is usually unavailable.²⁸ With this in mind, it is prudent to administer a single dose of an agent with activity against community-acquired aerobic and anaerobic pathogens as soon as possible for all patients requiring operation in the thorax or abdomen. Evidence-based guidelines for antibiotic prophylaxis of other surgical interventions or different anatomic sites are summarized in Table 18-6.

TABLE 18-6 Evidence-Based Recommendations for Antibiotic Prophylaxis for Specific Interventions or Injuries

The issue of postoperative continuation of prophylactic antibiotics in penetrating abdominal trauma has been investigated extensively. The Eastern Association for the Surgery of Trauma (EAST) has published guidelines derived from an evidence-based review.⁴⁰ A single preoperative dose of prophylactic antibiotics with broad-spectrum aerobic and anaerobic coverage is recommended for trauma patients sustaining penetrating abdominal wounds. Absence of a hollow viscus injury requires no further administration. If, however, a hollow viscus injury is present, there are sufficient Class I and Class II data to recommend continuation of prophylactic antibiotics for only 24 hours. Timely discontinuation of prophylactic antibiotics is important because the practice of prolonged administration of a prophylactic antibiotic has been linked to increased rates of subsequent nosocomial infections with resistant organisms.⁴¹ To maintain adequate tissue and serum levels of antibiotics in the face of ongoing hemorrhage and vasoconstriction, the administered dose may be increased 2- or 3-fold and repeated after every 10th unit of blood product transfusion, although there is not strong evidence to support this practice.

Surgical Scrub

Until recently, povidone–iodine scrub has been the standard disinfectant used for surgical prep and scrub. This supremacy has been challenged by several well-designed studies performed in elective surgery showing significantly lower SSI rates with the use of chlorhexidine–alcohol compared with iodine (9.5% vs. 16.1%).⁴² The fact that chlorhexidine–alcohol begins bacterial killing immediately on contact and does not require drying for antimicrobial effectiveness makes it potentially attractive for use in emergent surgery. One caveat regarding use of alcohol-based disinfectants is that it is imperative that the solutions be dry if electrocautery is used during surgical procedures to avoid intraoperative fires.

Double Gloving

Glove perforation is an underappreciated phenomenon that may adversely impact the sterility of an operative procedure. Microperforation rates as high as 16% have been reported.⁴³ When two pairs of gloves are used, inner glove perforation rate is substantially lower. In addition to patient outcome, the surgeon must consider personal safety. Epidemiologic studies report that the prevalence of HIV or hepatitis C is as high as 20–65% and 10–45%, respectively, in an urban university hospital population for patients undergoing lymph node biopsy or drainage of a soft tissue infection.⁴⁴ More recently, Brady et al.⁴⁵ reported that the seroprevalence of undiagnosed hepatitis C virus (HCV) infection was 7.9% with another 7.8% of the population having preexisting HCV infection.

Temperature Control

Hypothermia has been shown to be a strong prognostic indicator of poor outcome when considered in the context of the “triad of death” (hypothermia, acidosis, coagulopathy).⁴⁶ In addition to inducing an acquired coagulopathy, hypothermia has profound adverse effects on SSI rates. In elective colorectal surgery a prospective, randomized study compared a group in whom intraoperative normothermia (36.6^°C) was maintained to a control group with mild hypothermia (34.7°C). The normothermic group had a significantly lower rate of SSI (6% vs. 19%) and a 20% shorter hospital stay.⁴⁷ The precise mechanism for the beneficial effects of normothermia remains unclear, but may relate to tissue perfusion and improved host defense. Therefore, every reasonable effort should be made to maintain normothermia.

Supplemental Oxygen

The role of oxygen in development of SSI was examined in another prospective randomized study in patients undergoing elective colorectal operations. The authors observed a significantly lower SSI rate when 80% versus 30% inspired oxygen was delivered during the operation.⁴⁸ It is noteworthy that other studies have failed to replicate these results⁴⁹ and that this intervention has never been studied in a trauma population; however, an alternative interpretation of this study in elective patients is that it is best to avoid lower intraoperative F_iO₂.

Suture Material

There has recently been an extensive marketing effort advocating the use of antibiotic-coated sutures to decrease SSI. Several anecdotal reports describe impressive decreases in the incidence of wound infections (4.9% down from 10.8%) when the authors switched to antibiotic-coated suture.⁵⁰ Sutures decrease the inoculum of bacteria needed to establish infection and can serve as a foreign body within potentially infected wounds. So while it is clear that studies to specifically compare the efficacy of antibiotic-coated sutures with regular sutures are needed before strong recommendations can be made, there is a sound physiologic basis for a potential benefit. An additional consideration, however, is whether this intervention, like many others, is cost-effective.

Blood Transfusion

Autologous blood transfusion can be lifesaving for an exsanguinating patient, but numerous authors have reported worse infectious complications with increased blood utilization both in the immediate resuscitation^51–54 and when used in a delayed fashion.^55–57 Transfusion results in a multitude of immunosuppressive effects, including: (1) decreased CD3+, CD4+ and CD8+ cells; (2) overall reduced T-cell proliferation to mitogenic stimuli; (3) decreased natural killer cell activity; (4) defective antigen presentation; and (5) impaired cell-mediated immunity.⁵⁸ The increased risk of infection associated with blood transfusion appears to be dose dependent^57,59 and logistic regression analyses report that the risk of infection increases 13% per unit transfused.⁶⁰ Taylor et al.⁶¹ report that for each unit of packed red blood cells (PRBCs) transfused, the odds of developing a nosocomial infection were increased by a factor of 1.5. The age of the transfused blood is an additional risk factor for infectious complications.^62–64 As blood ages in the blood bank, it undergoes predictable changes that affect its ability to deliver oxygen. This “storage lesion” includes the following: (1) an increased affinity of hemoglobin for oxygen and reduced oxygen release to tissues; (2) depletion of 2,3-diphosphoglyerate (2,3-DPG) with resultant inadequacy of oxygen transport by red blood cells; (3) reduction in deformability, altered adhesiveness, and aggregability; and (4) accumulation of bioactive compounds with proinflammatory effects. In trauma patients, Offner and coworkers⁶⁴ estimated that each transfused unit of RBC older than 14 days increased the risk of major infection by 13%.

To minimize infectious risk, one should limit blood transfusion in nonbleeding patients. A large multicenter randomized study reported the safety of a restrictive transfusion strategy (trigger of 7.0 g/dL hemoglobin) compared to a liberal strategy with a trigger of 10.0 g/dL. In fact, patients who were younger and less sick had over double mortality rates when liberally transfused. When the subgroup of trauma patients was reviewed in a secondary analysis, McIntyre et al.⁶⁵ confirmed the safety of the restrictive strategy. Additionally, practices to be avoided include transfusing multiple units of blood in stable nonbleeding patients, using blood as a volume expander, and transfusing blood preemptively in anticipation of future operative blood loss. Advanced age should not be used as a sole criterion to transfuse a patient. Several recent guidelines describe transfusion of autologous RBCs in trauma patients in the postresuscitation period.^66,67

Nutritional Support

The timing, adequacy, and route of administration of nutrition to trauma patients have definite implications for infectious complications. Adequate nutrition is essential for patient recovery and healing of traumatic wounds. This is because trauma causes increased metabolism and protein turnover, and this results in a catabolic state characterized by skeletal muscle breakdown, impaired healing, and immunosuppression. After resuscitation is complete nutritional support should be instituted and the enteral route is preferred. Numerous trials have compared enteral nutrition (EN) with parenteral nutrition (PN). Advantages of the enteral route include lower cost, maintenance of function of the gut mucosal barrier, and more physiologic delivery of nutrients while the advantages of PN are primarily related to the consistency of adequate calorie provision. Based on the available high-quality studies, the evidence strongly favors the use of EN over PN in regards to infectious complications.^68–70 Traditional markers of nutrition (albumin, transferrin, and retinal-binding protein) are restored better using EN.⁶⁹ An additional factor that has been implicated in infectious complications is the issue of glycemic control. Current recommendations relating to glycemic control⁷¹ are in flux, but it appears clear that results are improved when high levels of glucose are avoided. Enthusiasm for “very tight” glucose control has waned after several studies showed no benefit and increased complications with attempts to maintain blood glucose <110 mg/dL.^72–74

Tracheostomy

Although several studies comparing early and late tracheostomy have been performed, there is still no consensus regarding whether earlier tracheostomy impacts development of ventilator-associated pneumonia (VAP).^75–77 The current EAST recommendations (Level 3) are that early tracheostomy be considered in trauma patients anticipated to require mechanical ventilation of >7 days.⁷⁸ The decision to perform tracheostomy is often institution and surgeon specific. A recent meta-analysis identified high-risk groups that were likely to benefit from early (≤72 hours) tracheostomy.⁷⁵

TRAUMA-RELATED INFECTIONS

Diagnosis of Infection

Almost by definition, infectious problems are never the presenting complaint of a patient who has sustained an acute traumatic injury; however, recognition of an infection in a patient recovering from traumatic injuries is a common, and sometimes challenging, clinical problem. Several of the signs and symptoms that we commonly associate with infections are frequently present in trauma patients. The immediate physiologic and immunologic response to tissue injury is initiation of the inflammatory response. Acute traumatic injuries cause the cardinal signs of inflammation including pain (dolor), edema (turgor), heat (calor), redness (rubor), and loss of function (functio laesa). Furthermore, trauma victims will often have several of the SIRS criteria (e.g., tachycardia, elevated temperature, elevated WBC) in the setting of a clinical context in which they are at increased risk for infection.⁷⁹

Diagnosis of infection requires a high clinical suspicion, tempered by knowledge of the most likely infectious complications at various time points after injury. Finally, this is filtered by experience with caring for patients with similar injuries. As discussed in the earlier section on “Prevention of Infections,” the preferred management of infections is to prevent their occurrence. When prevention measures have been ineffective, the diagnosis of infection is based on clinical, laboratory, and radiologic methods. Most trauma patients, especially those requiring operative interventions, those with open fractures, or those who have sustained penetrating trauma, will be treated with a course of empiric antibiotics (Table 18-7). The choice of specific antimicrobial agents is determined by the endogenous pathogens or likely exogenous contamination (e.g., exposure to Vibrio spp. with marine trauma, exposure to Clostridium sp. with farm injury) that would be present at the anatomic site of injury.

TABLE 18-7 Recommendations for Antibiotic Choice and Duration for Different Anatomic Regions and Mechanisms of Injury

Hospitalized patients are at risk for development of nosocomial infections and diagnosis is made on the basis of a high suspicion with laboratory and/or radiologic confirmation. In most cases, bacterial culture constitutes the “gold standard” for diagnosis of infection, although at times it can be impractical or impossible to obtain adequate samples. The most specific culture information, if available, is obtained with quantitative or semiquantitative methods (e.g., burn wound biopsy, bronchoscopic alveolar lavage [BAL], or non-BAL). In cases where cultures cannot be obtained, empiric treatment is initiated based on the most likely pathogenic organisms and adjusted based on clinical response. Evidence-based recommendations have been developed for diagnosis and antimicrobial treatment of most hospital-acquired infections,^81–86 albeit not specifically addressing trauma patients. The trauma glue grant (www.gluegrant.org) has proposed a standard operating procedure (SOP) to go about identifying the source of infection in critically ill trauma patients (Fig. 18-4).⁸⁸

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