All wounds incurred on the battlefield are grossly contaminated with bacteria. Most will become infected unless appropriate treatment is initiated quickly.
The battlefield environment is conducive to wound infection due to
Diagnosis of a Wound Infection
Common Microorganisms Causing Battlefield Infections
Gram-positive cocci: staphylococci, streptococci, and enterococci.
Gram-negative rods: Escherichia Coli, Proteus, and Klebsiella.
Pseudomonas, Enterobacter, Acinetobacter, and Serratia are common nosocomial pathogens usually expected among casualties who have been hospitalized for an extended period, not those fresh off the battlefield.
Salmonella, Shigella, and Vibrio should be suspected in cases of bacterial dysentery.
Anaerobic Gram-positive and Gram-negative rods: Clostridia, Bacteroides, and Prevotella species.
Fungal species: Candida species should be suspected in casualties hospitalized for prolonged periods, those malnourished or immunosuppressed, or those who have received broad spectrum antibiotics, adrenocortical steroids, or parenteral nutrition. Empiric therapy should be considered in appropriate patients with presumptive evidence of fungal infection.
The greatest threat of infection to the wounded battlefield casualty is the development of clostridial myonecrosis (gas gangrene), commonly due to Clostridium perfringens.
Common Patterns of Infection
Skin, soft tissue, muscle, and bone: Primarily due to staphylococcal, streptococcal, and clostridial species. These infections include wound abscess, cellulitis, septic arthritis, osteomyelitis, necrotizing fasciitis, and gas gangrene.
Clostridium perfringens. can enter through any wound—even minor burns and corneal abrasions. Prophylaxis is required to prevent tetanus toxemia.
Intracranial: Meningitis, encephalitis, and abscess, commonly due to staphylococci and Gram-negative rods, which are difficult to treat due to the impervious nature of the meninges to common antibiotics.
A similar inflammatory response without infection can be caused by a focus of retained necrotic tissue, or the mere act of sustaining severe trauma.
Culprit microorganisms will not be recovered in all cases of sepsis syndrome.
Although typically associated with Gram-negative organisms, any bacterial or fungal agent can cause sepsis.
Prompt surgical debridement is the cornerstone of prophylaxis/treatment of war wound infections.
Excessive irrigation, especially under pressure, should be avoided, because this can dilute the body’s natural immune cellular defenses and contribute to bacteremia.
The skin is left open, and a lightly moistened sterile gauze dressing is applied.
Antibiotics should be started ASAP after wounding, then continued for 24 hours, depending on the size, extent of destruction, and degree of contamination of the wound.
If time from wounding to initiation of antibiotics is > 6 hours, or time from wounding to surgery is > 12 hours, give antibiotics using regimen for established infection.
The choice of empiric antibiotic is dependent on the part of the body injured (Table 10-1).
Once a battlefield wound has become infected, treatment is two-fold—surgical and medical.
Surgical strategy remains the same: Open the wound, remove infected and necrotic tissue, and inspect for foreign material.
Drainage is generally employed in abscess cavities to prevent premature closure and reformation.
Empiric broad-spectrum antibiotic therapy is initiated against likely pathogens and continued for 7 to 10 days.
Ideally, obtain cultures and tailor therapy to cover the actual pathogens recovered on Gram stain and culture. Routine bacteriology is often not available in forward medical facilities.
Because Bacteroides and Clostridia are difficult to culture, tailor antibiotic therapy to cover these organisms.
If the debrided wound still has possibly ischemic tissue or retained foreign material, the patient is returned to the OR every 1 to 2 days for redebridement, until absolute assurance of healthy, clean tissue is achieved.
Battlefield wounds are “tetanus-prone” due to high levels of contamination with Clostridium tetani.
Bacteria grow anaerobically and release a CNS toxin that results in muscle spasm, trismus, neck rigidity, and back arching.
Table 10-1. Empiric Antibiotic Coverage for War Injuries.
In addition to surgical debridement of war wounds, additional prophylactic measures for tetanus-prone wounds include
Administration of 0.5ml IM of tetanus toxoid if prior tetanus immunization is uncertain, less than three doses, or more than five years since last dose.
Administration of 250–500 units IM of tetanus immune globulin in a separate syringe and at a separate site from the toxoid if prior tetanus immunization is uncertain or less than three doses.
Treatment for established tetanus includes
IV antibiotics (penicillin G, 24 million U/d; or doxycycline, 100 mg bid; or metronidazole, 500 mg q6h for 7 days).
Tetanus immune globulin.
Wound debridement as needed.
IV diazepam to ameliorate the muscle spasm.
Place patient in a dark, quiet room free of extraneous stimulation.
May warrant endotracheal intubation, mechanical ventilation, and neuromuscular blockade.
Cellulitis is manifested by localized skin erythema, heat, tenderness, and swelling or induration.
Treatment: IV antibiotics against streptococcal and staphylococcal species (IV nafcillin, cefazolin or, in the penicillin-allergic patient, clindamycin or vancomycin).
Post-operative wound infections become evident by wound pain, redness, swelling, warmth, and/or foul or purulent discharge, with fever and/or leukocytosis.
Treatment: Open the wound, drain the infected fluid, and debride any necrotic tissue present.
The wound is left open and allowed to close via secondary intention.
Necrotizing soft tissue infections are the most dreaded infections resulting from battlefield wounding. These include clostridial myonecrosis (gas gangrene) and polymicrobial infections caused by Streptococcus, Staphylococcus, Enterococcus, Enterobacteriaceae, Bacteroides, and Clostridia.
The organisms create a rapidly advancing infection within the subcutaneous tissues and/or muscle by producing exotoxins that lead to bacteremia, toxemia, and septic shock.
All layers of soft tissue can be involved, including skin (blistering and necrosis), subcutaneous tissue (panniculitis), fascia (fasciitis), and muscle.
Clinical manifestations begin locally with severe pain, crepitus, and with clostridia, a thin, brown, foul-smelling discharge.
The skin may be tense and shiny, showing pallor or a bronze color.
Systemic signs include fever, leukocytosis, mental obtundation, hemolytic anemia, and hypotension, progressing rapidly to multiple organ failure and death in untreated or under-treated cases.
The diagnosis is made by history of severe unexpected wound pain combined with palpable or radiographic soft tissue gas (air in subcutaneous tissue and/or muscle).
Absence of soft-tissue gas does not exclude diagnosis of necrotizing infection.
Treatment is surgical, including early, comprehensive, and repeated (every 24–48 hours) debridement of all dead and infected tissue, combined with antibiotics.
Excision of affected tissue must be as radical as necessary (including amputation or disarticulation) to remove all muscle that is discolored, noncontractile, nonbleeding, or suspicious.
Identification of causative organisms often problematic: Treatment must be aimed at all possible organisms.
IV antibiotic therapy.
Clindamycin, 900 mg q8h; plus penicillin G, 4 million U q4; plus gentamicin, 5–7 mg/kg qd.
As a substitute for clindamycin: metronidazole, 500 mg q6h.
As a substitute for penicillin: ceftriaxone, 2.0 g q12h, or erythromycin 1.0 g q6h.
As a substitute for gentamicin: ciprofloxacin, 400 mg q12h.
Alternative regimen: penicillin G, 4 million U q4h plus imipenem, 500 mg q6h.
Regimens (start ASAP, continue x 24 hours post-op).
Single agent: cefotetan 1.0 g q12h, or ampicillin/sulbactam, 3 g q6h, or cefoxitin, 1.0 g q8h.
Triple agent: ampicillin 2 g q6h; plus anaerobic coverage (metronidazole, 500 mg q6h; or clindamycin, 900 mg q8h); plus gentamicin 5–7 mg/kg qd.
Established intraabdominal infection (peritonitis or abscess).
Same regimen as above, except continue for 7 to 10 days.
Drain all abscesses.
Empyema (generally Streptococcal) following penetrating thoracic trauma is typically due to contamination from the projectile, chest tubes, or thoracotomy.
Diagnosis: Loculations, air/fluid levels on radiograph, pleural aspirate.
Chest tube initially, and thoracotomy if unsuccessful.
Cefotaxime, or ceftriaxone, or cefoxitin, or imipenem.
Pneumonia is most frequently due to aspiration (eg, patients with head injury) and prolonged mechanical ventilation.
The diagnosis is made through radiograph finding of a new pulmonary infiltrate that does not clear with chest physiotherapy, combined with
Fever or leukocytosis.
Sputum analysis showing copious bacteria and leukocytes.
Empiric therapy is directed toward likely pathogens.
Aspiration: Streptococcal pneumonia, coliforms, and oral anaerobes are likely. IV antibiotics such as ampicillin/sulbactam, clindamycin, or cefoxitin have proven effective.
Ventilator-associated pneumonia: staphylococcus, Pseudomonas, and other nosocomial Enterobacteriaceae. Broad coverage is best with such agents as imipenem, ciprofloxacin, vancomycin, and/or ceftazidime, plus an aminoglycoside.
Sepsis can be defined as infection combined with a prolonged systemic inflammatory response that includes two or more of the following conditions.
Progression to septic shock is manifest by systemic hypoperfusion: profound hypotension, mental obtundation, or lactic acidosis. Treatment is a three-pronged approach:
It is often difficult to identify the source of sepsis, but it is the most important factor in determining the outcome. Potential sources of occult infection include
Intensive care support for sepsis involves vigorous resuscitation to restore perfusion to prevent multiple organ dysfunction. This requires optimization of hemodynamic parameters (pulmonary artery occlusion pressure, cardiac output, and oxygen delivery) to reverse anaerobic metabolism and lactic acidosis. Endpoints of resuscitation, such as urine output, base deficit, and blood lactate levels guide successful treatment. Until the source for sepsis is identified and actual pathogens isolated, empiric therapy with broad-spectrum intravenous antibiotics is warranted. Suitable regimens might include
Imipenem, 500 mg q6h.
Piperacillin and tazobactam (Zosyn), 3.375 g q6h; or ceftazidime, 2.0 g q8h; or cefepime, 2.0 g q12h; PLUS gentamicin, 5–7 mg/kg qd (based on once-daily dosing strategy and no renal impairment); or ciprofloxacin, 400 mg q12h.
Addition of vancomycin, 1.0 g q12h if methicillin-resistant Staphylococcus aureus is a likely pathogen.
Addition of linezolid, 600 mg q12h if vancomycin-resistant enterococcus (VRE) is a likely pathogen.
Battlefield casualties are at high risk for infection. In particular, war wounds are predisposed to infection due to environmental conditions on the battlefield, devitalized tissue, and foreign bodies in the wound. The key to avoiding wound infection is prompt and adequate wound exploration, removal of all foreign material, and excision of all dead tissue. All battlefield wounds and incisions should have the skin left open. Antibiotics play an adjunctive role in the prophylaxis of wound and other infections in the battlefield MTF. Knowledge of likely pathogens for particular infections and sites, as well as optimal antibiotics to eradicate those pathogens (Table 10-2), will aid the battlefield clinician in averting and treating infections.
Table 10-2. Spectrum and Dosage of Selected Antibiotic Agents.