Diagnosing and Treating Necrotizing Fasciitis

Traditionally in school and training we learn that the hallmark of a diagnosis of necrotizing fasciitis is the presence of dishwater-colored pus. These patients are usually in septic shock, with a high mortality rate, and require emergent wide debridement and possibly major amputation. Occasionally these cases occur in healthy patients who unfortunately came into contact with a particularly aggressive strain of bacteria. This is a description of necrotizing fasciitis type II.

There is another version, however, that can manifest much more subtly from strains of bacteria not known to be very aggressive. These patients may not be septic or experience pain. This is necrotizing fasciitis type I.¹ These bacteria can colonize healthy hosts without causing problems, but if the host is immunocompromised enough (such as with diabetes and peripheral arterial disease), the colonization can become necrotizing fasciitis type I.

Difficulties With Diagnosing Necrotizing Fasciitis Type I

Necrotizing fasciitis type I is difficult to diagnose because clinical findings are subtle, and advanced imaging is not reliable. Magnetic resonance imaging (MRI) or computed tomography (CT) scans may show soft tissue edema in the fascia, but cannot definitively distinguish it as injury or necrosis.² Labs may not show leukocytosis and vital signs may be normal. The most telltale clinical sign of necrotizing fasciitis that differentiate it from simple cellulitis is bullae of the skin.³

Bullae, especially when hemorrhagic or associated with ecchymosis, are a sign of internal bleeding, typically seen with trauma and infection. Internal bleeding occurs through a cascade of events. Bacteria enter the skin through a tiny portal or via hematogenous spread, and settle into any area under the skin, which can sometimes be an area of previous musculoskeletal injury such as an ankle sprain or stress fracture. Bacteria releases exotoxins, which causes the coagulation system to clot, creating thrombosis. The microvascular and sometimes macrovascular circulation is disrupted, leading to bleeding internally. Ecchymoses and petechiae develop when the bleeding occurs in the subcutaneous tissue. Finally, hemorrhagic bullae occur when enough pressure builds up to bleed into epidermis.¹

Case 1: A Patient With MRSA and Gangrenous Skin

A 60-year-old patient with diabetes and a renal transplant presented to the emergency room 3 times over the course of a week for cellulitis and each time was sent home on oral antibiotics because he lacked signs of sepsis. On his fourth presentation to the emergency room, he was admitted for diabetic ketoacidosis and concern for cellulitis of the ankle. He remained without leukocytosis and with stable vital signs. I consulted on this case before completion of imaging.

On physical exam, there were a few patches of gangrenous skin, some with well-defined borders and a larger one with poorly defined borders (Figure 1). I noted extensive erythema and petechiae. Most concerning was the hemorrhagic bullae adjacent to a necrotic patch of skin. The erythema extended from his lateral malleolus to near the Achilles tendon. I did not identify any portal of entry or clear wound that seeded the infection. He had palpable pedal pulses, and an arterial duplex showed patent triphasic flow to all tibial vessels.

I immediately brought this patient to the operating room for a fasciotomy and debridement to bleeding margins. The pathology report was consistent with necrotizing fasciitis and cultures revealed methicillin-resistant Staphylococcus aureus (MRSA), which confirms the diagnosis of necrotizing fasciitis type I.

Case 2: Septic Shock Following an Infected Toe Fracture

A 30-year-old male presented to the emergency department in septic shock and newly diagnosed diabetes. He had sustained an open fifth toe fracture 2 weeks prior, which I feel likely seeded the infection. The CT scan identified subcutaneous edema with no soft tissue emphysema, suggesting cellulitis. On physical exam, he had necrotic bone exposed in the open fifth toe fracture with extensive ecchymosis and hemorrhagic blisters involving his toes, dorsal foot, and lateral leg (Figure 2). I obtained source control with an open transmetatarsal amputation, fasciotomies and wide debridement of his foot and leg. Cultures grew Streptococcus pyogenes, consistent with necrotizing fasciitis type II.

The patient underwent several subsequent operative debridements, including negative pressure wound therapy, scaffold grafting, and finally split-thickness skin grafting. His wounds went on to heal in 3 months.

Case 3: When Erythema Indicates Necrosis

This is a 70-year-old male with diabetes, peripheral arterial disease, and a right fourth toe with dry gangrene for 2 months. He underwent angioplasty and subsequent referral to our podiatry clinic. On physical exam, he had dry gangrene with well-defined borders on the dorsal aspect of the foot. However, on the plantar aspect, near the digital sulcus (Figure 4A), the gangrene had poorly defined borders with a very subtle cellulitis that extended towards the arch (Figure 4B). There was no soft tissue emphysema on plain films.

Gangrene is not always accompanied by soft tissue emphysema. When gangrene has poorly defined borders and erythema, the erythema indicates early stages of subcutaneous necrosis.¹ In time, the erythematous skin may become gangrenous. In patients with peripheral vascular disease and immunocompromise, the erythema can be even more subtle due to the patient’s inability to mount a significant response; thus the damage under the skin can be more devastating than expected. Another factor that makes this particular patient’s erythema much more subtle is the depth of the infection within the plantar foot. Dorsal foot infections are much more superficial, and thus the erythema is more obvious. Plantar foot infections may not have erythema as obvious as on dorsal skin. This patient’s presentation was concerning for necrotizing fasciitis type I.

He was admitted to the hospital for intravenous antibiotics and underwent a partial fourth ray amputation (Figure 4C). The soft tissue necrosis underlying the plantar foot erythema was advanced, and extended towards the master knot of Henry. Cultures grew Corynebacterium striatum, a commensal bacteria. Over the next few days, the wound continued to develop interval necrosis. He underwent an additional angioplasty, followed by open transmetatarsal amputation with staged closure, and multiple revision procedures. He eventually went on to heal 4.5 months later (Figure 4D).

In Conclusion

These case studies illustrate how clues in the physical exam can guide surgical decision making. These clues can give insight into determining the extent and severity of infection, unlike radiographs and advanced imaging which are not as reliable.² In summary, the biggest clue to differentiate a necrotizing type infection is bullae formation.³ A second clue that can help increase the level of suspicion that erythema is not a simple cellulitis but more likely necrotizing soft tissue infection, is to look for necrosis or gangrene in the entry point. Assuming the entry point to be the area of maximum infection, it may signal what the erythema is going to evolve into with time.

Dr. Chiu is a Fellow of the American College of Foot and Ankle Surgeons, and an Assistant Professor in the Department of Orthopaedics and Rehabilitation at the University of New Mexico School of Medicine in Albuquerque, NM. He is also in private practice in Albuquerque, NM.

References

1.     Stevens DL, Bryant AE. Necrotizing soft-tissue infections. N Engl J Med. 2017 Dec 7;377(23):2253-2265. doi: 10.1056/NEJMra1600673. PMID: 29211672.
2.     Ali SZ, Srinivasan S, Peh WC. MRI in necrotizing fasciitis of the extremities. Br J Radiol. 2014 Jan;87(1033):20130560. doi: 10.1259/bjr.20130560. Epub 2013 Nov 28. PMID: 24288403; PMCID: PMC3898976.
3.     Goh T, Goh LG, Ang CH, Wong CH. Early diagnosis of necrotizing fasciitis. Br J Surg. 2014 Jan;101(1):e119-25. doi: 10.1002/bjs.9371. Epub 2013 Nov 29. PMID: 24338771.