Prophylaxis and Treatment of Infections Associated with Penetrating Traumatic Injury

Kyle Petersen; Paige Waterman

Expert Rev Anti Infect Ther. 2011;9(1):81-96.

Abstract and Introduction

Abstract

Accidents or violence can result in penetrating trauma in the adult population. Contaminated penetrating foreign bodies introduced at the time of wounding cause infection, especially high velocity projectiles, which result in cavitation. Surgical debridement reduces potential infection; however, perioperative antibiotics are usually indicated owing to studies demonstrating high rates of sepsis in the pre-antibiotic era. Trauma-associated pathogens include Gram-positive, Gram-negative and anaerobic pathogens. Antibiotic resistance is increasing, and several recent panels have sought to develop guidelines for perioperative prevention and empiric treatment of infection to limit usage and reduce selective pressure for resistance. We review infections of the CNS, thorax, abdomen and extremities following penetrating trauma injury, as well as the data supporting a reasonable antimicrobial approach.

Introduction

Infection associated with penetrating trauma is generally a sequela of accidents or violence. As this subject has a broad scope, we have limited discussion to infections from traumatic injuries in adults. Penetrating traumas differ from blunt traumas, such as motor vehicle accidents, in that the skin is penetrated by the traumatic injury such as sharp objects and missiles. A critical aspect of penetrating trauma is the formula of kinetic energy, energy (E) = ½MV² , where M is mass and V velocity. Thus velocity of the penetrating object is a more important component of the injury than object size.^[1] Injuries can be divided into very low energy (VLE) such as knife or stab wounds, low energy (LE) such as handguns, and high energy (HE) such as military rifles.

A review of the infection epidemiology in VLE injury is unrevealing. A large study of almost 40,000 knife wounds from Canadian emergency rooms failed to describe infection rates.^[2] A recent review of 70 arrow injuries reported a 1.4% infection rate.^[3] Stab wounds to the spine 'rarely become infected'.^[4,5] Knife wounds of the abdomen are perhaps the exception; a recent paper where knife wounds comprised 19% of abdominal injuries described a 50% infection rate.^[6] Knife injuries have comprised two trials of antibiotic prophylaxis for intra-abdominal infection (IAI)^[7,8] but these are not designed to describe epidemiology. Otherwise, we found no further epidemiologic descriptions. Clearly, a well-designed trial to describe infection rates and pathogens encountered in VLE injuries is needed. The paucity of literature suggests that infections in these types of injuries are perhaps unlikely, with the exception of blunt objects with irregular tips such as screwdrivers, which can introduce foreign material.^[9] This is intuitive because the LE of the injury does not cause cavitation, allowing for all wound surfaces to re-approximate, creating a greater surface area in contact with the immune system, and preventing pathogen and foreign debris spread into surrounding tissue.^[9]

Penetrating missiles can be further differentiated into those from bullets, and those from fragmentation weapons such as grenades, antipersonnel mines or, as in recent asymmetrical warfare conflicts, the 'improvised explosive device' (IED).^[10] IEDs are homemade using a variety of materials intended to penetrate, blast and burn with unique and unpredictable injury patterns. This differentiation is important as the resulting wound from each weapon is unique. Bullets have an available kinetic energy of 1500–3000 joules (J) for military rifles, 300–500 J for handguns and 10–150 J for some fragmentation devices.^[11] This energy lacerates, contuses and displaces body tissues. In LE wounds, injury is confined to the track of the projectile where the tissue is crushed by the bullet or fragment.^[11] HE wounds produce a radial injury around the track of the projectile with a temporary cavity where contaminants can be widely dispersed.^[11] Fragmentation device impact velocities with high explosives such as IEDs vary by fragment size and proximity to the device detonation, but range from 100–1000 m/s.^[11] This results primarily in soft-tissue injury, sometimes with adjacent bony involvement. Furthermore, fragmentation devices create multiple wounds that are irregularly shaped and heavily contaminated with foreign bodies such as soil and clothing, with subsequent infection highly likely.^[11] Most bullets are pointed and thereby initially transfer little material at entry. However, if cavitation occurs, bullet material may be sucked into the exit site as the cavity collapses back down and become widely dispersed, increasing infection risk.^[11]

Bullets, despite being the product of an explosion that creates heat, were shown to be nonsterile in the 1960s.^[12] Contamination notwithstanding, over 50% of bullet fragments are left unextracted without developing secondary infection, probably because metallic foreign bodies do not readily serve as a nidus of infection and have a low inflammatory potential.^[13] Nonmetallic foreign bodies appear to be a greater cause of infection.^[13] War wounds have the highest infection potential, owing to their HE projectiles, a contaminated wounding environment and delay to definitive surgery compared with LE civilian injuries.^[14] A study of 17,726 combat wound casualties during the Vietnam war showed an infection incidence of 3.9% in the first 2 weeks after injury.^[15] In reality, the incidence was probably higher because data was collected at an in-theater hospital; many patients lost to follow-up after 15 days might have gone on to suffer late infection.

Although primarily young and without comorbidities, the penetrating trauma patient is often a diagnostic conundrum, and nowhere is this more apparent than in HE injuries. Owing to massive hemorrhage, tissues are ischemic with impaired leukocyte and antimicrobial delivery to affected tissues.^[16] Furthermore, multiple transfusions are required, in effect causing a complete exchange transfusion, removing the victims' circulating immunity.^[17] There may be accompanying traumatic brain injury, impairing autonomic regulatory mechanisms. Recent studies indicate that severe blast injury (so prevalent in the current conflict) overwhelms the immune system, thus sustained hyperinflammation ensues, which the host cannot physiologically regulate.^[18] This dysregulation can lead to systemic inflammatory response syndrome (fever, hypotension and leukocytosis, among others) that may mimic infection, making diagnosis difficult and leading to inappropriate antibiotic administration.^[19] Conversely, these factors can also increase infection susceptibility at the penetrating injury site requiring antibiotic treatment.^[20] Thus, the decision of when to administer antibiotics and what agent to select is an important and challenging one in penetrating trauma injury.

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Table 1. Strength of recommendation and quality of evidence.
Assessment	Type of evidence
*Strength of recommendation*
Grade A	Good evidence to support a recommendation for use
Grade B	Moderate evidence to support a recommendation for use
Grade C	Poor evidence to support a recommendation
*Quality of evidence*
Level I	Evidence from at least one properly designed, randomized controlled trial
Level II	Evidence from at least one well-designed clinical trial, without randomization; from cohort or case-controlled analytic studies (preferably from >one center); from multiple time series; or from dramatic results of uncontrolled experiments
Level III	Evidence from opinions of respected authorities, based on clinical experience, descriptive studies or reports of expert committees

Table 2. Epidemiology and recommended prophylaxis and empiric treatment for CNS infection following penetrating trauma.
Seminal papers (type)	Pathogens described	Prophylactic antibiotic of choice (level of evidence)	Duration of prophylaxis (level of evidence)	Empiric treatment of choice^† (level of evidence)	Duration of treatment (level of evidence)
No controlled trials of prophylaxis or therapy exist	Scalp wound: Coagulase-negative Staphylococcus Meningitis: Coagulase-negative Staphylococcus Staphylococcus aureus Gram-negative facultative aerobes Anaerobes^‡ Rapidly growing mycobacteria^§	Cefazolin 1 g iv. q 8 h or ceftriaxone 2 g q 24 h^¶ Penicillin allergic: Vancomycin 15 mg/kg divided q 6 h plus ciprofloxacin 400 mg iv. q 12 h (BIII)	5 days (BII)	Vancomycin 15 mg/kg divided q 6 h plus cefepime or ceftazidime or meropenem 2g q 8 h^# (BIII)	21 days (BIII)

^†Empiric antimicrobials should be 'de-escalated' to target susceptibility of pathogens isolated from culture as soon as possible.
^‡If oral injury or soil contamination occurs.
^§Rarely found.
^¶Consider adding gentamicin and penicillin prophylaxis if wound grossly contaminated.
^#Consider ciprofloxacin for β-lactam allergy.
iv.: Intravenously; q: Every.

Table 3. Epidemiology and recommended prophylaxis and empiric treatment for maxillofacial infection following penetrating trauma.
Seminal papers (type)	Pathogens described	Prophylactic antibiotic of choice(level of evidence)	Duration of prophylaxis (level of evidence)	Empiric treatment of choice^† (level of evidence)	Duration of treatment (level of evidence)	Ref.
Chole and Yee (prospective randomized trial) Andreasen et al. (meta-analysis)	Pseudomonas spp. Staphylococcus aureus Escherichia coli and Klebsiella spp. Candida spp. Proteus mirabilis Bacteroides fragilis Peptococcus Peptostreptococcus	Cefazolin 2 g iv. q 8 h Or Clindamycin 900 mg iv. q 8 h^‡ (BI)	24 h (AI)	Ampicillin/sulbactam 2 g iv. q 6 h Or Clindamycin 600 mg iv. q 8 h plus moxifloxacin 400 mg every day^‡ (BIII)	10–14 days or 2–3 days after wound closed 6 weeks for mandibular osteomyelitis (BIII)	[38] [39]

^†Empiric antimicrobials should be 'de-escalated' to target susceptibility of pathogens isolated from culture as soon as possible.
^‡Consider clindamycin regimen for β-lactam allergy.
iv.: Intraveniously; q: Every.

Table 4. Epidemiology and recommended prophylaxis and empiric treatment for thoracic infections following penetrating trauma.
Seminal papers (type)	Pathogens described	Prophylactic antibiotic of choice (level of evidence)	Duration of prophylaxis (level of evidence)	Empiric treatment of choice^† (level of evidence)	Duration of treatment (level of evidence)	Ref.
Maxwell et al. (prospective, randomized) Sanabria et al. (meta-analysis)	Empyema with tube thoracostomy: Coagulase-negative Staphylococcus Delayed onset (>48 h after admission): Coagulase-negative Staphylococcus MRSA Gram-negative facultative aerobes Anaerobes Abdominal contamination: Enterococcus spp. Candida spp.	Cefazolin 1 g iv. q 8 h (BII)^‡	24 h (BII)	Vancomycin 15 mg/kg divided q 6 h plus cefepime or ceftazidime or meropenem 2 g q 8 h^‡ (BIII)	21 days (BIII)^§	[60] [59]

^†Empiric antimicrobials should be 'de-escalated' to target susceptibility of pathogens isolated from culture as soon as possible.
^‡Aminoglycosides should be avoided.
^§Could be shortened if adequate drainage achieved earlier.
iv.: Intravenously; MRSA: Methicillin-resistant Staphylococcus aureus; q: Every.

Table 5. Epidemiology and recommended prophylaxis and empiric treatment for abdominal infection following penetrating trauma.
Seminal papers (type)	Pathogens described	Prophylactic antibiotic of choice (level of evidence)	Duration of prophylaxis (level of evidence)	Empiric treatment of choice^† (level of evidence)	Duration of treatment (level of evidence)	Ref.
Fullen et al. (retrospective cohort) Fabian et al. (prospective randomized) Griswold et al. (prospective randomized) Velmahos et al. (prospective observational) Brand et al. (Cochrane review)	Escherichia coli Enterobacter cloacae Klebsiella spp. Proteus mirabilis Bacteroides spp.	Cefoxitin 2 g iv. q 6 h Or Moxifloxacin 400 mg iv. daily or ciprofloxacin 400 mg iv. q 24 h Plus Metronidazole 500 mg q 8 h^‡ (AI)	24 h (AI)	Moderate injury: Ticarcillin/clavulanate 3.1 g q 4–6 h or cefoxitin 2 g iv. q 6 h or ertapenem 1 g iv. q 24 h or moxifloxacin 400 mg iv. q 24 h^‡ Severe injury:carbapenem or piperacillin/tazobactam 4.5 g iv. q 6 h (AII)	4–7 days (BIII)	[71] [73] [74] [76] [70]

^†Several other regimens possible [58].
^‡Empiric antimicrobials should be 'de-escalated' to target susceptibility of pathogens isolated from culture as soon as possible.
iv.: Intravenously; q: Every.

Table 6. Epidemiology and recommended prophylaxis and empiric treatment for extremity infections following penetrating trauma.
Seminal papers (type)	Pathogens described	Prophylactic antibiotic of choice (level of evidence)	Duration of prophylaxis (level of evidence)	Empiric treatment of choice^† (level of evidence)	Duration of treatment (level of evidence)	Ref.
Johnson et al. (retrospective review) Mody et al. (retrospective review) Ostermann et al. (retrospective cohort) Gosselin et al. (Cochrane review) Dellinger et al. (prospective randomized) Patzakis et al. (prospective, randomized)	Soft tissue: Coagulase-negative Staphylococcus Streptococcus spp. Acinetobacter spp.^‡ Escherichia coli ^‡ Pseudomonas aeruginosa ^‡ Osteomyelitis: Staphylococcus aureus (often MRSA) Orthopedic hardware: S. aureus (often MRSA) Acinetobacter spp.	Penicillin 2–4 mu q 4 h or cefazolin 1 g iv. q 8 h^§ β-lactam allergy: Clindamycin 900 mg iv. q 6 h (BII) Local: Consider cefazolin or tobramycin beads especially in Grade III fractures (BII)	1–5 days (AI)	Gram positive: Vancomycin 15 mg/kg divided q 6 h or Daptomycin 4–6 mg/kg iv. q 24 h or linezolid 600 mg q 24 h^¶# Gram negative: Cefepime 2 g q 8 h or ceftazidime 2 g q 12 h or carbapenem (BIII)	Soft tissue: 7–14 days (BII) Osteomyelitis: 4–6 weeks (BII) Hardware: 4–6 weeks (BII)^††	[96] [99] [111] [107] [110] [109]

Empiric antimicrobials should be de-escalated to target susceptibility of pathogens isolated from culture as soon as possible.
^†Seen after 5 days of initial injury.
^‡Metronidazole added when infections develop after 72 h.
^¶Linezolid toxicity limits utility when used for >2 weeks duration.
^#Rifampin (± quinolone) may improve outcomes.
^††Duration depends upon removal of hardware.
iv.: Intravenously; MRSA: Methicillin-resistant Staphylococcus aureus; mu: Million units; q: Every.

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