SLIDE SUMMARY:  Necrotizing fasciitis is characterized by pannicular and fascial necrosis.  However, it can be caused by a variety of infectious agents, and each syndrome has some distinctive pathological and therapeutic features.  If not otherwise specified, “necrotizing fasciitis” tends to imply that due to streptococcus.  Surgical treatment by complete excision and drainage is mandatory.  Later reconstruction depends on principles related to large wounds of any cause.
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	Numerous papers and book chapters exist to educate you on the basic biology and clinical science behind these infections.  This presentation will focus on the clinical arts of managing these problems for good results: for acute life-saving treatment and for long term function-restoring management.
	Necrotizing fasciitis can mean any of several forms of severe, rapidly progressive and lethal (if untreated) infections.  Much of the drama and public attention to “necrotizing fasciitis” goes to classic Group A streptococcal panniculitis.  The terminology is not important.  Understanding the behavior of these infections, is important: the generic implications for life and death and urgent thorough treatment, but also the relative differences and nuances of care that arise from the types of organisms that are responsible.
	All necrotizing fasciitides have in common that the infection causes infarction and destruction of tissue, far in excess of the normal injury that occurs from reactive inflammation.  As with most inflammatory soft tissue pathologies, the primary target or susceptible tissues are the subcutaneous adipose fascias.  Rapid extension of the disease, tangentially through the fascias, is the norm.  Skin necrosis is typically a secondary event, due to loss of the trans-pannicular perforators which provide blood supply to the skin, or due to toxic chemical injury from the organism (depending on the type of infection).  Muscular fascias are likewise more resistant, and muscles underneath, or viscera, can be involved by extension (or they can be a primary target for Clostridia).
	When the disease is active and rapidly spreading, gross pathology can be divided into several zones which have implications for surgical treatment (see Slide 7).
	General classes of rapidly progressive infectious panniculitis, or toxic necrotizing fasciitis include these:
	Synergistic gangrene:  This is the most common type in daily medical practice.  It is usually due to a mixed flora of pyogenic enteric organisms, typically aerobes and anaerobes, which create synergistic microenvironments which facilitate each others growth and metabolism.  Being due to enteric flora, these infections are most prevalent in abdominal and pelvic related problems, including bowel perforations, complicated genitourinary infections, enteric contamination of skin and musculoskeletal laceration or ulceration, perianal or perirectal abscesses, and so on - including the classic Fournier’s gangrene.  Pathologically, there is progressive suppuration and abscess formation in the adipose panniculus, working its way into various fascial planes, and sometimes killing muscle.  Patients can be extremely ill from general inflammatory effects and from endotoxins and others toxins.  These patients can be gravely ill, and prompt drainage and debridement are mandatory.  However, the biology of these infections are distinctly different than the “necrotizing fasciitis” of streptococcal infamy.  These infections are due to organisms which are individually fairly benign, the stuff of everyday GI and GU infections.  It is in the synergy of mixed flora that they become more destructive.  There is a bit of latitude in the surgical treatment:  there is no lesser sense of urgency, and delays in care ARE NOT excusable, and thorough debridement remains the goal - BUT - if the exigencies of the illness and logistics of a trip to the OR are hampered in any way, these patients have a bit more leeway for a simpler drainage and debridement.  For example, if the problem occurred in the groin after a vascular procedure, and the patient is on potent anti-platelet drugs, these abscesses can be effectively managed by gross debridement of loose necrosis and pus, and wide opening of the wound, but without incurring the bleeding of a formal sharp excision through still viable but highly inflamed and hyperemic tissues.  This will generally arrest progress of the infection, while maintaining a good risk-benefit balance for the patient.  Broad spectrum antibiotics are obviously mandatory.
	Clostridial myofasciitis - Aka “gas gangrene”, is often the result of ranch and soil injuries, or enteric injuries.  This is a serious fulminant disease which requires a serious expedited surgical response.  Muscles as well as fascias are targets.  Exotoxins have lytic necrotizing effects on the infected tissues, but they also have disseminated intercurrent toxicities for other organs.  No delays in management can be tolerated.
	Streptococcal fasciitis.  This is what people really mean when they talk about the classic N.F.  Strep species other than in Group A, and staphylococcal species can all cause the same syndrome.  Incidental other organisms can cause the same thing, including unexpected oddballs such as salmonella.  However, it is the exotoxins in Group A strep which are particularly pernicious and prone to rapid spreading and “streptococcal toxic shock syndrome” (STSS) with intercurrent organ failure.  It can start off a bit more insidiously than some of the other types of fasciitis, but when the diagnosis is made, the imperative for rapid surgery is the same as for gas gangrene.  These types of fasciitis can have distinctive findings, including:   non-odorous (as opposed to synergistic or enteric gangrene); fascial necrosis and suppuration are often not lytic and cavitary (as is the case for enteric abscesses); severe watery edema, which is a survival and proliferative advantage for the organisms;  scarlet color.  Complete thorough excision is required.  See Slide 7 for more details.
	Atypical infections.  These are due to fungus, mycobacteria, actinomycetes, and such atypical non-bacterial pathogens.  They tend to be “slow” infections - think TB versus pneumonia or a post-pneumonic abscess - but once vessels start to occlude and tissues infarct, the destruction can seem to occur quickly.  Typically, a relatively slow granulomatous inflammation was cooking in the fascias prior to severe skin involvement.  Mucormycosis is distinctive in that vascular occlusion rather than inflammation or exotoxicity is the cause of problems.  These patients typically have a more insidious and seemingly less urgent onset, but the implications for curative surgery and reconstruction are the same.
	As discussed in later slides, surgical excision is mandatory, and the sooner the better, with Clostridial and Streptococcal N.F. having the most immediacy for surgery.  However, the nature of the required surgery is the same for all such patients with any of these diseases.  Surgery is required for three components of the problem:
	1 - GET RID OF THE DISEASE, by as thorough and complete wound excision or debridement as possible.
	2 - PATCH UP THE RESULTING WOUNDS, by the the usual arts of plastic surgery, whenever wound conditions and patient conditions permit.
	3 - RECONSTRUCT LATE SEQUELAE such as scar contractures, or amputation management, etc.
	The surgery is analogous to the surgery needed for burns, deglovings, and any large or acute wound.  Burns and trauma do not have the same type of illness, and acute and critical patient management are different than N.F. in many ways.  But, the surgery of cleaning up the mess, preparing the wounds for closure, then patching them up, then restoring function - that is what core plastic surgery is all about.  Large wounds, small wounds - it doesn’t make a difference - the surgical principles and methods arte the same for all of these conditions.
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	TOP - A young derelict paraplegic patient with long standing pressure sores.  Synergistic fasciitis - Fournier’s gangrene - is a very infrequent complication of ordinary ischial pressure ulcers, and in fact, it was not the problem here.  Rather the patient developed pressure necrosis of the anus, leading to ischiorectal infection, which then spread rapidly, involving tissues throughout the buttock, pelvis, and thigh, including other pressure bursas.  The image here is a couple of weeks after debridement and wound care, ready to begin closure.
	CENTER - A patient with severe rheumatoid and multi-drug immunosuppression developed fairly rapid skin necrosis, leg ulceration, and febrile toxicity.  While rheumatoid panniculitis notoriously causes extensive ulceration of the leg, that process is relatively slow and indolent, and does not involve the muscular proximal leg.  Biopsies and cultures showed aspergillus.
	BOTTOM - This is a 19 year old man who developed fevers and malaise after a minor skin scrape.  This was followed by rapid erythroderma, edema, pain, and progressive toxicity.  This is the quintessential Group A Strep N.F.