Necrotizing Fasciitis

Etiology

Necrotizing fasciitis is typically an acute process that occurs rapidly over several days. In approximately 80% of cases, it is a direct sequela of bacterial infection introduced through a break in the skin’s integrity. Gram-positive cocci, specifically strains of Staphylococcus aureus and Streptococci are responsible for most of these single-site source infections. Polymicrobial infections also occur because of a combination of gram-negative and anaerobic involvement.[4][5] The majority of patients have diabetes and a history of alcoholism. Patients with liver cirrhosis are also prone to necrotizing fasciitis.

Epidemiology

Necrotizing fasciitis affects about 0.4 per 100,000 people annually in the United States. It is as common in some areas as 1 in every 100,000 people.[6][7]

Pathophysiology

The infection rapidly transits the muscle fascia. After several days, the overlying skin, which initially appears unaffected, will transition to an erythematous, reddish-purple to bluish-gray hue. The skin's texture will become indurated, swollen, shiny, and warm in temperature. At this stage, the skin is exquisitely tender to palpation and can also be painful and out of proportion to presenting symptoms. Skin breakdown will begin in 3 to 5 days and is accompanied by bullae and cutaneous gangrene. Pain is reduced in the affected area secondary to thrombosed small vessels and the destruction of the subcutaneous tissues' superficial nerves. Advanced stages of the infection are characterized by systemic symptoms such as fever, tachycardia, and sepsis.[8] Anaerobic bacteria mixed with aerobic organisms are commonly found in most soft tissue infections. Aerobic bacteria include Clostridium, Bacteroides, coliforms, proteus, klebsiella, peptostreptococcus, and Pseudomonas. These organisms rapidly spread along with the subcutaneous tissues and deep fascial planes, causing vascular occlusion, tissue necrosis, and ischemia.

Histopathology

After debridement, tissue obtained from the operating room will usually show extensive superficial fascial necrosis. The majority of small and medium-sized blood vessels will be thrombosed. Aggregates of neutrophils will be observed in the fascia and subcutaneous tissues. Small vessel vasculitis and extensive fat necrosis will also be evident. All the glands in the dermis and subcutaneous tissues will also be necrotic. Gram stain will show clusters of various types of microorganisms.

History and Physical

Necrotizing infections are more commonly present with excruciating pain out of proportion to presenting symptoms and systemic septic signs than non-necrotizing infections. Physical findings of necrotizing soft tissue infections may include tenderness to palpation beyond the erythematous border, crepitus, and cellulitis. The presence of bullae, ecchymotic changes to the skin, and dysesthesia or paresthesia should also be treated as a necrotizing infection. Subcutaneous emphysema and crepitus are almost always present. Anesthesia may also be present in some areas due to injury to the nerve fibers. The infection can spread rapidly within hours; hence, suspicion should be high for necrotizing fasciitis in intense pain.

Evaluation

Any rapidly progressing skin or soft tissue infection should be managed aggressively due to the difficulty in differentiating non-necrotizing from necrotizing skin and soft tissue infections.[9][10][11] The Laboratory Risk Indicator for Necrotizing Infection Score was developed in a 2004 report to distinguish necrotizing soft tissue infections (NSTIs) from other severe soft tissue infections. The scoring system is hinged on abnormalities in 6 independent variables:

C-reactive protein, mg/L

• Less than 150 (0)
• More than 150 (4)

Total white cell count (WBC), cells/mm

•  Less than 15 (0)
•  15 to 25 (1)
•  More than 25 (2)

Hemoglobin, g/dl

•  More than 13.5 (0)
•  11 to 13.5 (1)
•  Less than 11 (2)

Sodium, mmol/L

• 135 or greater  (0)
• Less than 135 (2)

Creatinine, mg/dL

• 1.6 or less (0)
• More than 1.6 (2)

Glucose, mg/dL

• 180 or less (0)
• More than 180 (1)

A score of 6 has a positive predictive value of 92% and a negative predictive value of 96%. A score of 8 or greater represents a 75% risk of necrotizing infection. The diagnosis of NSTIs is still primarily clinical. Imaging may be useful in providing data when the diagnosis is uncertain. The most common plain film finding is similar to cellulitis with increased soft tissue thickness and opacity. Computed tomography has greater sensitivity than plain film in identifying necrotizing soft tissue infections. Plain X-rays have no value in the diagnosis. Sometimes, under local anesthesia, one may probe the area with a finger for signs of necrotizing tissue. In most cases, the necrotic tissue can be penetrated with little resistance. Aspiration and gram stain can also be done. B-mode color Doppler ultrasound can help in the early diagnosis of necrotizing fasciitis at the bedside. It should be understood that no lab or imaging test should delay surgical intervention.

Treatment / Management

These extremely ill patients should be transferred immediately to the intensive care unit. The sepsis causes refractory hypotension and diffuse capillary leak. Thus, the patient will need aggressive resuscitation with fluids and the use of inotropes to maintain blood pressure. The patient must be kept NPO (nothing by mouth) until seen by the surgeon. Nutrition is vital, but only after surgery has been completed. Enteral feedings should be started as soon as the patient is hemodynamically stable. The enteral feedings may help offset the massive negative protein balance due to catabolism.[5][12][13](B2)

Key concepts for treatment/management of skin and soft-tissue infections are:

Early diagnosis and differentiation between necrotizing and non-necrotizing skin and soft tissue infections

1. The early launch of appropriate empiric antibacterial coverage (wide-spectrum)
2. Adequate control of infection sources, such as aggressive surgical intervention for abscess drainage and debridement of NSTIs
3. Identification of infection-causing pathogens and applicable adjustment of antimicrobial coverage.

Antimicrobial therapy for necrotizing fasciitis is as follows:

1. Imipenem 1 g every 6 to 8 hours, daptomycin 6 mg/kg QD, and clindamycin 600 mg to 900 mg 4 times daily.
2. Piperacillin/tazobactam 3.375 g every 6 hours or 4.5 g every 8 hours, daptomycin 6 mg/kg QD, and clindamycin 600 mg to 900 mg 4 times daily.
3. Meropenem 1 g IV every 8 hours, vancomycin 15 to 20 mg/kg/dose every 8 to 12 hours, and clindamycin 600 mg to 900 mg 4 times daily.

Surgery 

The treatment of necrotizing fasciitis is surgery, and no time should be wasted calling for a surgical consult. The earlier the surgery is undertaken, the better the outcome. The surgery requires extensive, wide debridement of all necrotic tissues. In some cases, a second-look surgery may also be required. Early surgery may help minimize tissue loss and eliminate the need for amputation of a gangrenous extremity. With wide debridement, the wounds must be left open and packed with wet gauze. Daily dressing changes are mandatory. The patient's recovery is faster as long as the necrotic tissue is removed. A great deal of surgical judgment is required when faced with normal-appearing tissue that is not necrotic. In most cases, the tissues should be removed if there is any doubt about viability. Hemodynamic stability is often restored once the necrotic tissue and pus are removed. The patient should be kept intubated and monitored in a critical care unit. In some patients, daily surgical debridement may be required. During the surgery, meticulous attention should be paid to hemostasis. Some patients may require repeat visits to the operating room to remove necrotic tissue.

Soft-tissue Reconstruction

The plastic surgeon should be consulted once all the necrotic tissue is removed and there is evidence of granulation tissue. In most cases, primary closure is not possible, and hence the plastic surgeon may be required to reconstruct the soft tissues and close the wound with a muscle flap. If there is no adequate natural skin available for a skin graft, then one may need to use artificial skin. Another method of treatment includes the use of hyperbaric oxygenation. While the literature does suggest this modality can be used, most of these patients are in the intensive care unit attached to a variety of medical equipment, thus making the journey to the hyperbaric oxygen therapy facility difficult. Hyperbaric oxygen therapy may be effective for small wounds, but there is no evidence that this therapy improves healing or prolongs life for large wounds. Finally, it should be noted that hyperbaric oxygen therapy is an adjunctive treatment and not a substitute for surgical debridement. Hyperbaric oxygen treatment may be useful when the patient is stable. Some data show that this treatment can help reduce mortality. Hyperbaric oxygen is not a substitute for surgery but a complementary treatment.

Differential Diagnosis

The differential diagnosis for necrotizing fasciitis includes:

• Cellulitis
• Epididymitis
• Gas gangrene
• Orchitis
• Testicular torsion
• Toxic shock syndrome

Prognosis

Necrotizing fasciitis is a serious life-threatening infection with mortality rates ranging from 20 to 80%. Poor prognosis has been linked to certain streptococcal strains, advanced age, uncontrolled diabetes, state of immunosuppression, and delayed surgery. Even people who survive have a prolonged recovery with significant functional deficits.

Complications

The complications that can manifest with necrotizing fasciitis are as follows:

• Multiorgan failure
• Septic shock
• Loss of extremity
• Severe scarring
• Toxic shock
• Death