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Case Study
Current Insights On The Multidisciplinary Treatment Of Necrotizing Fasciitis
July 2014
This author presents a multidisciplinary approach to diagnosing and treating a 54-year-old patient with diabetes who presented with intense pain and a toe that was turning black.
Necrotizing soft tissue infections are rare but potentially fatal. They are generally divided into three categories based upon anatomical involvement: crepitant cellulitis, necrotizing fasciitis and myonecrosis.
Crepitant cellulitis is characterized by infection limited to the skin. Typically, this infection involves ample soft tissue crepitus, limited pain and minimal systemic symptoms. Necrotizing fasciitis extends beyond the skin into the subcutaneous tissue and fascia. Usually, there is less air present in the soft tissue but pain is more pronounced and systemic symptoms are prominent. Myonecrosis includes muscle involvement, pronounced pain, systemic symptoms and further risk for loss of limb.
Despite these distinctions, one should note there is often significant overlap between these entities, depending upon the amount of tissue involved and the pathogens present.
Necrotizing soft tissue infections are characterized by rapidly developing tissue destruction due to the presence of bacterial enzymes and toxins. Vascular ischemia and tissue necrosis result from the combination of virulent factors present in the tissue. Typically, these infections are polymicrobial. There is usually the presence of an anaerobic organism (Bacteroides fragilis, Clostridium species, Peptostreptococcus species) with one or several members of the Enterobacteriaceae family (E. coli, Proteus species, Klebsiella species). Beta hemolytic streptococci such as Streptococcus pyogenes (Group A strep) may be present with either an anaerobe or an Enterobacteriaceae. Clostridium species can act alone to create a rapidly progressive illness, especially in cases of myonecrosis.
Necrotizing soft tissue infection is typically more severe in patients with an underlying immunodeficiency. Examples include poorly controlled diabetes mellitus, organ transplant recipients, chronic steroid use and the use of immune modulators, alcohol abuse with liver disease, and patients undergoing chemotherapy for malignancies.
In most cases, the anaerobic bacteria proliferate in an environment of local tissue hypoxia. Due to lower oxidation reduction potential, these bacteria produce gases such as hydrogen, nitrogen, hydrogen sulfide and methane, which accumulate in the soft tissue spaces because of reduced solubility in water.
Establishing the diagnosis can be challenging. Clinical findings may include swelling, pain, erythema, induration, crepitation, sloughing off of the skin, or a blistering and purulent collection. Initially, the diagnosis is a clinical one, which one can supplement with imaging (X-ray, magnetic resonance imaging, computed tomography, etc.). Physicians need to ensure immediate and aggressive treatment as necrotizing fasciitis causes rapid tissue destruction.
His past medical history included diabetes mellitus, hypertension and hyperlipidemia. The patient’s medications prior to hospital admission included Aleve, Centrum, Humalog insulin (Eli Lilly), gabapentin (Neurontin, Pfizer), Quinapril (Accupril, Pfizer), citalopram (Celexa, Forest Laboratories) and hydrocodone/acetaminophen as needed.
In the ER, the patient appeared mildly toxic. His temperature was 36.8ºC, pulse was 96 and respiratory rate was 12. There was significant edema throughout the foot and the right great toe was black in color (figure 1). The patient’s pain was at a level of 10 and palpation for pulses was impossible due to this pain level.
The diagnostic data included a white blood cell count of 24.5, an erythrocyte sedimentation rate of 97, a high sensitivity C-reactive protein of 287.02 and glucose of 57. X-rays revealed small collections of air surrounding the great toe extending into the midfoot (figure 2).
The patient went directly to the operating room where I amputated the great toe and first metatarsal head, debrided the first interspace and expressed all purulent material. I packed the surgical area and left it open. I admitted the patient to the hospital on intravenous piperacillin/tazobactam (Zosyn, Pfizer) and vancomycin.
The patient’s symptoms responded rapidly to surgery. His pain level dropped to a 5 of 10 within 24 hours and all signs of sepsis resolved. Two days after surgery, I removed the packing and he started negative pressure wound therapy (NPWT) with instillation using Dakin’s solution. Instillation therapy delivers and removes topical solutions to an infected wound at controlled times and also provides standard negative pressure (figure 3).
The NPWT with instillation therapy continued for one week. The patient then went back to the OR for further debridement and partial closure of the amputation site (figure 4). He was discharged to home on IV ceftriaxone and traditional Vacuum Assisted Closure (VAC therapy, KCI) therapy. The patient followed an uneventful postoperative course. I discontinued VAC therapy after two weeks (figure 5) and proceeded with traditional wound care and subsequent applications of Apilgraf (Organogenesis) (figure 6).
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A Closer Look At The Patient
A 54-year-old male patient with insulin-dependent diabetes presented to the emergency room after his wife found him slumped in his car. He reported that he had generalized weakness and shortness of breath for the past week. The patient recently noticed his great toe was turning black. In addition, during his first hour in the emergency room, erythema spread across the dorsum of the foot and his pain increased to a level of 10 of 10.![](https://s3.amazonaws.com/HMP/hmp_ln/imported/imagefield_thumbs/PT0714Davidson4.png)
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