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Necrotizing Fasciitis - 10/8/2012

posted Oct 8, 2012, 7:35 AM by Rohit Das   [ updated Dec 27, 2012, 6:45 AM by Purnema Madahar ]

Skin infection, e.g. cellulitis most commonly, is a very prevalent issue, especially in the middle-aged and elderly population, occurring with an incidence of about 200 cases per 100,000 patient-years. It’s a fairly common admitting diagnosis that we encounter, often with a degree of disinterest. The goal of this daily is to remove that disinterest, and make you worry about something that kills 25-35% of the time, and leads to long-term morbidity 80-90% of the time – Necrotizing Fasciitis (NF).

·  What are the epidemiology and risk factors for development of NF? It’s pathogenesis?

·         How can we diagnose this deadly disease, as rapidly as possible?

·         What is the optimal management for NF? Prognosis?

What is the epidemiology and risk factors for development of NF? It’s pathogenesis?

·         It is generally agreed that NF is due to microbial invasion of the subcutaneous tissue, via trauma or direct spread from nearby organs. The central process seems to be mediated by both bacterial toxin production and our immune response, both ultimately leading to a common final pathway – tissue ischemia. Extensive cytokine release also leads to more systemic symptoms of SIRS/sepsis, which can ultimately culminate in shock and death.

·         In the U.S., NF is relatively uncommon, with 0.04 cases occurring per 1,000 person-years. NF is often differentiated by the microbial etiology – Type 1 is characterized by multimicrobial infection (combination of anaerobes, gram-positive cocci and gram-negative rods), while Type II is NF due to group A Strep, usually alone but sometimes in association with Staph/MRSA. Necrotizing infection by Vibrio vulnificus (remember…skin break…sea water…bad news) is classified as type III NF by some sources.

·         Type I infection is, by far, most common, accounting for 55-75% of cases. Prominent risk factors include DM, immunosuppression, and peripheral vascular disease. Other, less defined, risk factors include obesity, CKD, HIV, alcohol abuse and IV drug use…among many others. Type II infection is far less common, and occurs in healthy, young individuals.

·         Type I tends to occur in the perineum (Fournier’s Gangrene) and truncal areas, while Type II tends to occur on the extremities, though truncal involvement is reported.

How can we diagnose this deadly disease, as rapidly as possible?

·         The absolute key to NF is to always have it in the back of your mind, and diagnose it as fast as possible. Table 3 of the attached article provides a nice synopsis of symptoms/signs present at admission. Very importantly, pain/tenderness BEYOND the margins of erythema, is present in 70-90% of patients. This is reflective of the “stages” of NF, as nicely outlined in Figure 1. Since it requires thrombosis/loss of integrity of a large amount of the capillary bed to manifest erythema, skin changes reflective of the true degree of subcutaneous involvement do not occur until late in the illness. Common things we think of as typical for necrotizing infection occur in only a minority of patients at admission, like crepitus (10-30%) or bullae (20-40%). Later in the course, affected areas may become insensate due to extensive tissue ischemia and necrosis.

·         In 2000, Wall et. al. (study attached), via a retrospective analysis and a multiple regression model, developed a scoring system to diagnose NF (depicted on Table 5 of the review article). A score of >8 had a pretty good PPV (around 94%) and a score <6 had a good negative predictive value (95%). However, this model has not been validated in a prospective cohort, so it’s utility remains a bit in question…

·         Imaging has pretty good sensitivity for NF, with CT at around 80% and MR at around 90-100%. However, they are both not very specific diagnostic modalities (50-75%). Regardless, imaging takes too long to get around these parts…so definitely don’t depend on it for a diagnosis that emphasizes URGENCY.

What is the optimal management for NF? Prognosis?

·         The bottom line is that people with NF need surgical intervention, for delineation of the true extent of infection and COMPLETE debridement – ASAP. Studies have shown that a surgical delay of >24 hours from hospital admission leads to almost a nine-fold increase in mortality, and that the adequacy of initial debridement is the single most important predictor of mortality (RR of around 7.5).

·         Other prognostic factors, though less well-defined, include age, DM, renal failure, and WBC >20 and/or serum creatinine > 2…among several others.

·         Antibiotic coverage should be very broad, covering for the above organisms typical for Type I infections. Acceptable regimens include Clindamycin (for its antitoxin effects), a beta lactam/beta-lactamase inhibitor (like Pip/Tazo) and an agent for MRSA coverage. But again…SURGERY! IVIg and Hyperbaric Oxygen are other options, though data behind these therapeutics are very limited...

Yea…Necrotizing Fasciitis = BADNESS. Please read the attached review article, and hone in on your knowledge on when to suspect, and how to diagnose, this very deadly disease. If you miss it, as detailed above, the prognosis is horrendous.

Off to interviews Tuesday and Wednesday…so the Weiler side of the daily shall remain quiet. KEEP READING!!!

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