Necrotizing Soft Tissue Infections - Clinical Manifestations

Clinical Findings

               A wide range of signs and symptoms can be seen in patients with necrotizing soft tissue infections. In general these can be grouped into local and systemic findings and their presence usually depends on the time of diagnosis within a continuum in the progression and extent of the infection. Most patients report a precipitating event like trauma, injection, chronic wound/boil, etc, although up to 20% can have idiopathic etiology with no identifiable cause. Initial findings include erythema, swelling (a), warmth and pain, often associated with tachycardia. As the infection spreads tense edema and pain out of proportion to appearance ensue and are relatively sensitive in predicting necrotizing soft tissue infections (b). At this point the skin compartment is usually spared but systemic symptoms are typically present including fever and tachycardia. When the infection progresses further, thrombosis of nutrient skin vessels occurs leading to blue discoloration that resembles ecchymoses (c), followed by bullae, and finally, necrosis of the skin (d). At this time, nerve damage also occurs and physical exam may reveal areas of hyperesthesia combined with anesthetetic portions of the skin. Systemic signs include hypotension and associated findings consistent with severe sepsis/septic shock including mental obtundation, cardiovascular and/or pulmonary collapse among other organ system failures. Hard signs of necrotizing soft tissue infections include tense edema beyond the obvious area of inflammation, pain out of proportion to appearance, crepitus, skin blisters/bullae, skin discoloration and necrosis, usually associated with symptoms representing severe sepsis or septic shock (Table 2). If these are present, the diagnosis of necrotizing soft tissue infections is highly likely. However, most large series report the presence of 1 or more of these signs in only 10-40% of patients, and swelling, erythema and pain (typical finding for all soft tissue infections regardless of the severity) are the most common signs, present in 70-90% of the cases. The presence of subcutaneous gas diagnosed either by physical exam or by radiological studies is also an ominous sign of necrotizing soft tissue infections and can be associated with virtually any bacteria as opposed to the common perception of its unique association with clostridial infections. Most bacteria, especially facultative Gram negative rods such as Escherichia coli, make insoluble gases whenever they are forced to use anaerobic metabolism. Thus the presence of gas in a soft tissue infection implies anaerobic metabolism. Since human tissue cannot survive in an anaerobic environment, gas associated with infection implies dead tissue and therefore the presence of a surgical infection (e).

a).  82 year diabetic with necrotizing fasciitis diagnosed sugically. XR revealed gas within the soft tissue and examination revealed marked crepitance to palpation.		(a).  78 year old with chronic diabetic foot ulcer who developed a necrotizing Group B Streptococcal infection.
(b). Tense Edema Beyond Area of Inflammation in a Patient with Necrotizing Soft.		(e). Subcutaneous Gas in a Plane X-ray of a Patient with Necrotizing Soft Tissue Infection.
(c).  45 year old cirrhotic male presented with pain, lymphangitis and eccymosis of leg following minor trauma and was diagnosed with necrotizing fasciitis. Patient had blood and wound cultures positive for Streptococcus pyogenes.
(d). 45 year old cirrhotic male with necrotizing fasciitis 5 days after presentation. He was not a surgical candidate due to coagulopathy. Blood and wound cultures were positive for Streptococcus pyogenes.			(d). Skin Discoloration/Ecchymosis in a Patient with Necrotizing Soft Tissue.

 

Table 2. Clinical Hard Signs of Necrotizing Soft Tissue Infections

Hard signs of NSTI

Tense edema beyond areas of inflammation Pain out of proportion to appearance Crepitus Skin discoloration / ecchymosis Blisters/bullae Skin necrosis Subcutaneous gas +/- Systemic compromise as severe sepsis/shock

 

Anatomic Location

               Necrotizing soft tissue infections can occur in virtually any anatomic location. Most series show a predilection in the incidence of extremity infection (60-80%) followed by perineal (Fournier’s gangrene, 12-16%) and trunk infections (10-12%), but this can vary according to the specific patient population studied. Fournier’s gangrene was first described by a French dermatologist in 1883 (Jean-Alfred Fournier) and referred as to necrotizing soft tissue infections of the male genitalia in young healthy patients (f). The term has been expanded to include necrotizing soft tissue infections of the perineal area in both male and female patients. It is usually secondary to skin infections, colorectal sources and urologic infections in descending order of frequency and is characteristically polymicrobial in nature. It is associated with a lower mortality when compared to other types of necrotizing soft tissue infections (16% in a recent review including 1,726 cases), although its management is associated with complications derived from complex wound care and testicular, urethral, vaginal and/or rectal involvement (g).

 

 

Progression of Infectious Process

               The progression of necrotizing soft tissue infections from its precipitating cause to the florid manifestations of local and systemic derangements usually occurs over a series of days. However, occasionally patients can present with a chronic infection that slowly progresses to cause necrotizing changes over weeks with a more subacute course. It is important to assess these patients with the same approach rather than incorrectly accept the perception of non-necrotizing processes as the cause for their infection. Finally, patients with history of intravenous drug use as well as those with infections caused by Mucormycosis, Vibrio species, GAS and Clostridial species often present with rapidly progressive and aggressive infections that require immediate surgical treatment to minimize the risk of mortality that can occur within 24 hours of onset of the infection.