October 01, 2009
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Pedal deception: Can we trust what we see?

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A 54-year-old man presented to the ED with complaint of painful left foot with onset over the past three days and increasing discomfort. He denied any history of redness or swelling — just development of a large blister on the bottom of his foot with impaired, painful ambulation. He also noted loss of appetite along with night sweats but denied nausea, vomiting or fever. He also denied trauma or stepping on anything. However, in the days prior to onset, he recalled wearing boots that were wet from walking in the snow as well as an episode of running barefoot on the streets when his shoe slipped off two separate times while running.

His past medical history was positive for type 2 diabetes, peripheral neuropathy and prior left foot infection. His only medication was insulin. He had no known drug allergies and review of systems was unremarkable. Upon physical exam, the patient was alert and oriented with stable vital signs. He appeared a little weakened from loss of appetite but overall unimpressive with regard to lethargy.

Exam revealed painful left foot and large bulla with overlying hyperkeratotic tissue to the plantar forefoot with underlying dark, purplish discoloration. Proximally, there was noted evidence of serosanguinous discharge (figure A). Pedal pulses, both dorsalis pedis and posterior tibial, were faintly palpable. Neurologically, he exhibited complete loss of epicritic and protective sensation except to the affected area. Prior first ray amputation was evident. Erythema was unremarkable with no edema present. Radiographs revealed pockets of free air within the bulla as well as proximal extension to the sulcus of the third metatarsophalangeal joint area. Blood cultures were negative. His labs were unremarkable aside from a blood glucose of 421 mg/dL and a white blood cell count of 13.8 with no left shift.

Figure A. Man with diabetes presenting with large bulla
Figure A. Man with diabetes presenting with large bulla with overlying hyperkeratotic tissue and underlying violaceous discoloration. Note evidence of serosanguinous discharge proximally.
Figure B. After initial surgical incision and drainage
Figure B. After initial surgical incision and drainage. Note extensive necrotic tissue present exhibited as grayish discoloration.
Photos courtesy of:
Patris Toney, DPM, MPH

The patient was taken to the operating room for emergent surgical incision and drainage with debridement of all nonviable tissue. Upon initial incision, contents of the bulla were noted to be soft, caseous substance with admixture of serosanguinous and dishwater-tinged drainage with accompanying strong fetid malodor. The underlying tissue was grayish in discoloration. Undermining to the third toe proximal to the sulcus was also noted. Debridement of subcutaneous and proximal fascial tissues was performed to the level of healthy bleeding (figures B and C). A secondary debridement was performed three days later. Intraoperative wound cultures demonstrated group G streptococcus and Klebsiella oxytoca. The patient was antibiosed on IV metronidazole (Flagyl, GD Searle) and vancomycin. Upon discharge, his blood glucose was 221 mg/dL and his white blood cell count was 8.5. The resulting wound was healed using MediHoney during the initial first few weeks post-op followed by bioengineered skin substitute (Dermagraft, Advanced BioHealing) applications in addition to off-loading to reach complete epithelialization without incident (figures D and E).


Figure C. After surgical debridement
Figure C. After surgical debridement: viable, healthy bleeding tissue.
Figure D. Appearance on day of first bioengineered skin substitute application
Figure D. Appearance on day of first bioengineered skin substitute application.

Figure E. Six weeks later
Figure E. Six weeks later, complete epithelialization after six applications with adjunctive offloading.

What is your diagnosis?

A. Friction blister.

B. Necrotizing fasciitis.

C. Neuropathic diabetic foot ulcer.

D. Gas gangrene.

Case Discussion:

Answer: B

Necrotizing fasciitis is a destructive infection that attacks the subcutaneous and fascial tissues and even deeper. This infection has many names including suppurative fasciitis, hemolytic streptococcal gangrene and Fournier’s gangrene, to list a few. Necrotizing soft tissue infections are often divided into three categories: necrotizing fasciitis, necrotizing cellulitis and myonecrosis. Overall, this infection is dangerous and can prove life-threatening. Susceptible individuals include those with cancer, diabetes, HIV/AIDS, IV drug users and the vascularly impaired along with others who are immunocompromised. Additionally, trauma and foreign body have been incited as causes. Thus, individuals considered overall healthy can be affected.

Patients may present without concrete history of injury and typically describe a scenario of insidious onset of escalating pain and swelling to the affected area with changes in coloration ensuing. As time progresses and if left untreated, the area can become anesthetized and the patient may encounter sepsis, coma and potentially death. Initially, the typical presentations for the infectious process are often subtle if present at all, particularly in patients with diabetes who have altered immune response. Fever and sepsis may be encountered as time progresses. The pain, which is present, is often determined to be out of proportion to the physical presentation of the patients in regard to the objective physical exam. Furthermore, in neuropathic diabetes patients, the pain is either dismissed or regarded as diabetic neuropathy. In some cases, the patient may appear to be healthy without distress or signs of physical ailment. In other cases, the patient may demonstrate a contradictory septic presentation in comparison to the degree of the pathologic presentation. This could be attributed to the hidden destruction that ensues as the infection destroys the underlying subcutaneous and fascial tissues of the affected area with the true nature of the damage only exposed upon deeper exploration.

Physical exam findings may include dark purplish or dusky violaceous area of tissue discoloration associated with area of insult. The surrounding tissues may exhibit erythema of varying degrees without raised borders. Edema may or may not be present. Soft tissue crepitus with undermining of the peripheral tissue may also be encountered. Additionally, histopathological and lab findings often lag clinical diagnosis. Radiographs may demonstrate the presence of free air or gas pockets within the tissues. However, absence of gas on radiographs does not negate the presence of anaerobes.

Treatment varies along the continuum of care; however, fluid resuscitation, antibiosis and surgical intervention are of importance foundationally. When contemplating the antibiotic, keep in mind that in the diabetic patient, the wound may exhibit a polymicrobial presence with mixed flora of both aerobic and anaerobic bacteria. Causative microorganisms include Staphylococcus aureus, group A hemolytic streptococcus, Peptostreptococcus, Bacteroides, Clostridium, Klebsiella, Pseudomonas, Proteus and Enterobacteriaceae. Thus, initial antibiosis should entail coverage of the more common organism such as Staphylococcus and Streptococcus along with anaerobic coverage. Recently a series of community-associated methicillin-resistant S. aureus infections have been associated with necrotizing fasciitis infections.

Surgical intervention is aimed at eradication of all infected, necrotic and nonviable tissue. In severe cases, surgical intervention may include loss of a limb. Other adjuvant treatment modalities include hyperbaric oxygen, negative pressure therapy, skin grafting, use of bioengineered skin substitutes or use of other wound care biologics to help achieve healing. In diabetic patients, the path to healing involves a marriage of patience and time.

Necrotizing fasciitis is a deceptive and complicated infection. Early on, it is elusive, but with time, the patient may become quite ill. Thus, high clinical suspicion is warranted, and one should never ignore pain in an insensate, neuropathic patient with diabetes.

Patris Toney, DPM, MPH, is an Attending Staff Physician at Mount Sinai Hospital in Chicago and Past Fellow at the Center for Lower Extremity Ambulatory Research/National Center for Limb Preservation. James E. Fullwood, Jr. is a fourth-year podiatry student at the Dr. William M. Scholl College of Podiatric Medicine at Rosalind Franklin University of Medicine and Science in Chicago.