Soft Tissue Infections


Necrotizing Soft Tissue Infections (NSTIs)

  1. Pathophysiology
    • bacteria gain entry into the subcutaneous tissues
    • subcutaneous tissues have a poor blood supply and relative tissue hypoxia, which can lead to a poor immune response to infection
    • bacteria can produce exotoxins, which causes direct necrosis as well as vasoconstriction and thrombosis
    • additional exotoxins can lead to sepsis and multiorgan dysfunction
    • involved tissues may include the epidermis, dermis, subcutaneous tissue, fascia, and muscle

  2. Microbiology
    1. Polymicrobial Infections (Type I)
      • 75% of NSTIs are polymicrobial, with an average of 4 organisms isolated
      • decubitus ulcers, diabetic foot infections, perineal infections are usually polymicrobial
      • most common gram-positive organisms are staph aureus, strep pyogenes, and enterococcus
      • E. coli is the most common gram-negative bacteria
      • Bacteroides and Peptostreptococcus are the most common anaerobes isolated
      • water-borne infections often contain Vibrio (salt water) and Aeromonas species (fresh water)

    2. Monomicrobial Infections (Type II)
      • tend to be more aggressive and lethal than polymicrobial infections

      1. Group A β-hemolytic Streptococcus
        • most common monomicrobial isolate
        • causes a rapidly progressive NSTI with systemic toxicity and high mortality rates
        • produces multiple proteolytic enzymes that cause extensive tissue destruction

      2. Clostridial Infections
        • anaerobic bacteria found in the soil
        • Clostridium perfringens is the most common isolate
        • produces multiple toxins that cause tissue necrosis, gas formation, microvascular thrombosis
        • α-toxin is most associated with tissue destruction, and has a toxic effect on neutrophils
        • traumatic wounds, puncture wounds, and wounds from IV drug use are at high risk for clostridial infection

      3. MRSA
        • community-acquired MRSA produces coagulases that can lead to direct tissue invasion and necrosis
        • high risk populations include contact sports team members, prisoners, military recruits, institutionalized patients, day care residents

  3. Clinical manifestations
    • NSTIs are rapidly virulent, and patients quickly develop signs and symptoms of sepsis with high fever, tachycardia, and systemic toxicity
    • most commonly involves the lower extremities, perineum (Fournier gangrene), or abdominal wall

    1. Physical Exam
      • early findings include warmth, erythema, tenderness, and may be mistaken for cellulitis
      • swelling, induration, edema, and exquisite tenderness may be present
      • skin may blister and slough, and exude foul-smelling drainage
      • crepitus is present only in a minority of patients, and cannot be used as the basis of diagnosis

  4. Diagnosis
    • early diagnosis is critical to reducing the morbidity and mortality of NSTIs, and relies on clinical judgement rather than diagnostic testing

    1. Lab Studies
      • nonspecific
      • leukocytosis with a high bandemia is usually present
      • acidosis, hyponatremia, thrombocytopenia, and coagulopathy indicate severe infection
      • elevated CK or AST suggests a deep infection involving the fascia or muscle

    2. Imaging
      • should not delay operative treatment
      • plain films may show unsuspected air in the soft tissues
      • CT or MRI may show only edema or fat-stranding, and this does not rule out a NSTI

      Late Stage Hidradenitis
    3. Surgical Exploration
      • only way to make the diagnosis of necrotizing infection
      • a suspicion of an NSTI is all that is required for surgical exploration
      • fascia will appear swollen and dull-gray in appearance
      • a thin exudate without pus may be present
      • tissue planes separate easily by blunt dissection
      • nonbleeding tissue, vascular thrombosis, and noncontractile muscle all indicate nonviable tissue

  5. Treatment
    1. Initial Measures
      • patients require aggressive fluid resuscitation
      • vasopressors and inotropes may be necessary
      • aggressive glycemic control is necessary in diabetics

    2. Antibiotics
      • broad-spectrum drugs should be started empirically on presentation
      • MRSA, streptococcus, clostridia should initially be covered, as well as gram-negative and anaerobic organisms
      • if vibrio infection is a possibility, antibiotics active against this organism should be started as well

    3. Surgery
      • survival is directly related to the rapidity of operative intervention
      • debridement 24 hours after hospital admission is associated with a ninefold increase in mortality
      • all devitalized skin and soft tissue must be excised, without consideration for future reconstruction
      • extremity NSTIs often will require a guillotine amputation one joint above the obvious infection
      • perineal wounds will usually require colonic diversion
      • multiple return trips to the OR for wound inspection and further debridement is expected
      • initial wound management should be with standard wet-to-dry dressing changes

    4. Adjunct Treatments
      • enteral or parenteral nutritional support should be initiated early since these patients are highly catabolic
      • negative pressure wound therapy maintains a moist wound environment, manages wound exudate, and stimulates the formation of granulation tissue
      • no evidence to suggest that hyperbaric oxygen treatment improves outcomes

    5. Reconstruction
      • should be started as soon as no further surgical debridement is required, and systemic toxicity has resolved
      • split-thickness skin grafts are used to cover most wounds
      • occasionally, complicated flap closure is required, usually under the direction of a plastic surgeon

Hidradenitis Suppurativa

  1. Clinical Manifestations
    • inflammatory disease of the skin characterized by painful subcutaneous nodules, abscesses, internetworking sinus tracts, and foul-smelling drainage
    • chronic disease can result in significant scarring
    • most commonly affected sites are the axillary, inguinal, perineal, mammary, and inframammary areas

  2. Pathophysiology
    • traditionally felt to occur as a result of apocrine gland occlusion from keratotic debris, resulting in bacterial proliferation, infection, and abscess formation
    • more recent evidence suggests that the underlying mechanism is hair follicle occlusion
    • staph and strep species are the most common organisms
    • obesity and smoking are risk factors
    • poor hygiene is thought to exacerbate the process rather than initiate it

  3. Management
    1. Early Stage Disease

      2. Early Stage Hidradenitis
      1. Antibiotics
        • topical or oral antibiotics are the main treatment
        • clindamycin is the first-line drug
        • tetracycline, minocycline, and rifampin are also used

      2. Lifestyle Modifications
        • weight loss and smoking cessation
        • warm baths

      3. Additional Measures
        • steroid injections have been successful in some cases
        • antiandrogens have an unclear role in treatment
        • laser hair ablation has shown short-term efficacy, but long-term results are unclear

    2. Chronic Disease

      3. Late Stage Hidradenitis
      1. Surgery
        • wide surgical excision of affected skin and subcutaneous tissues is the procedure of choice
        • primary wound closure is rarely feasible
        • large wounds will require split-thickness skin grafts or flaps for closure
        • smaller wounds may close by secondary intention
        • wound vacs may be used to speed up secondary closure or bolster skin grafts

Bites

  1. Mammalian Bites
    1. Epidemiology
      • dogs account for 80% - 90% all bites in the U.S., followed by cat bites and human bites
      • Pit bulls, Rottweilers, and German shepherds account for most of the serious bites

      Pit Bull Bite Wound
    2. Microbiology
      • wound infection is the main complication of animal bites
      • 3% - 18% of dog bites and 50% of cat bites become infected
      • Pasteurella is found in 50% of dog bites and 75% of cat bites
      • staphylococcus, streptococcus and Eikenella corrodens are the most common human isolates
      • human bites can also transmit HBV, HCV, and HIV

    3. Management
      1. Wound Care
        • tetanus prophylaxis as necessary
        • early wound cleaning is critical for minimizing infection
        • wounds with devitalized tissue will require debridement
        • the OR is often the best place to inspect, clean, and debride bite wounds

      2. Wound Closure
        • options include primary repair, delayed primary repair, or secondary closure
        • anatomic location of the bite, timing of the bite, and source of the bite determine the optimal closure method

        1. Low Risk Wounds
          • most lacerations located on the face, scalp, neck, and mouth can be closed primarily if they present with 24 hours of injury
          • clean lacerations located on the arms, legs, and trunk can be closed primarily if they present within 6 – 12 hours of injury

        2. High Risk Wounds
          • wounds located on the hand, wrist, foot, or over a major joint
          • puncture wounds (difficult to wash out)
          • through and through cheek bite
          • cat bites
          • human hand bites (clenched fist injury)
          • most high risk wounds are left open and undergo delayed primary repair in 3 – 5 days
          • bites on the hands and feet are usually left open to heal by secondary intention because of their high risk of infection
          • clenched fist wounds have a high risk of injury to the extensor tendon or joint capsule and can result in septic arthritis or osteomyelitis

          Clenched Fist Injury
          Clenched Fist Injury (Fight Bite)

      3. Antibiotics
        • prophylactic antibiotics are usually given for high risk bites
        • Augmentin covers most expected pathogens

  2. Brown Recluse Spider Bites
    1. Epidemiology
      • found throughout the U.S.
      • have a characteristic violin-shaped marking on the cephalothorax

      Brown Recluse Spider
    2. Toxicology
      • venom contains sphingomyelinase D, which causes skin necrosis, coagulation, and hemolysis

    3. Clinical Manifestations
      • patients are often completely unaware of the bite
      • in mild cases, pain, itching, swelling, and erythema may develop at the site
      • in more severe cases, a necrotic wound with eschar formation may develop over several days
      • necrosis is more severe in fatty areas such as the abdominal wall, buttock, and thigh

      Brown Recluse Bite Stages
    4. Management
      • tetanus prophylaxis as needed
      • debridement is indicated for obviously necrotic tissue or secondarily infected tissue
      • to avoid overly aggressive debridement, surgery can usually be delayed until the wound is well-demarcated
      • in the most severe cases, a skin graft may be necessary for wound coverage







References

  1. Sabiston, 20th ed., pgs 532 - 544
  2. Cameron, 13th ed., 862 – 866, 866 – 871
  3. Schwartz, 10th ed., pgs 473 - 485
  4. UpToDate. Necrotizing Soft Tissue Infections. Dennis L. Stevens, MD, PhD, Larry M. Baddour, MD, FIDSA, FAHA. Feb 28, 2020. Pgs 1 – 23
  5. UpToDate. Surgical Management of Necrotizing Soft Tissue Infections. Alan D. Rogers, MBChB, Shahriar Shahrokhi, MD, FRCSC, FACS. Aug 12, 2019. Pgs 1 – 32