Necrotizing fasciitis: case series and review of the literature on clinical and medico-legal diagnostic challenges

Abstract

Necrotizing fasciitis (NF) is a life-threatening infection of soft tissues spreading along the fasciae to the surrounding musculature, subcutaneous fat and overlying skin areas that can rapidly lead to septic shock and death. Due to the pandemic increase of medical malpractice lawsuits, above all in Western countries, the forensic pathologist is frequently asked to investigate post-mortem cases of NF in order to determine the cause of death and to identify any related negligence and/or medical error. Herein, we review the medical literature dealing with cases of NF in a post-mortem setting, present a case series of seven NF fatalities and discuss the main ante-mortem and post-mortem diagnostic challenges of both clinical and forensic interests. In particular, we address the following issues: (1) origin of soft tissue infections, (2) micro-organisms involved, (3) time of progression of the infection to NF, (4) clinical and histological staging of NF and (5) pros and cons of clinical and laboratory scores, specific forensic issues related to the reconstruction of the ideal medical conduct and the evaluation of the causal value/link of any eventual medical error.

The LRINEC Score—An Indicator for the Course and Prognosis of Necrotizing Fasciitis?

“…The diagnosis of NF poses great challenges to physicians, as the soft tissue infection first spreads to deeper layers, making the impression of the extent of the infection deceptive and the initial nonspecific symptoms easily confusing [16][17][18]. Especially in severely ill patients, it is of enormous importance to identify high-risk patients at an early stage and to be able to use an objective parameter to assess the severity of the disease in addition to the clinical assessment.…”

Manejo exitoso de fascitis necrotizante con un sistema de presión negativa artesanal

“…However, the evidence of massive fascial necrosis, with the absence of bleeding during surgical debridement is the most objective point for the confirmation of the diagnosis 6 . The process by which the patient reaches this clinical state begins with harm in the superficial fascia, minor trauma or localized infection, showing erythema and induration of the skin 7 , regardless of its origin, factors like the proliferation of bacteria and release of inflammatory toxins allow the extension of the process horizontally 2 . Most of the bibliographic reports agree that the complex interactions between the host and the factors specific virulence are the conditioning factors for tissue damage through proinflammatory cytokines 3 , presenting signs of clinical toxicity, such as fever, confusion, dizziness, weakness and malaise, appearance of rashes, purulent and hemorrhagic flicten, inflammation with increased disproportionate pain, and subcutaneous emphysema with focused gas in certain areas.…”

“…Most of the bibliographic reports agree that the complex interactions between the host and the factors specific virulence are the conditioning factors for tissue damage through proinflammatory cytokines 3 , presenting signs of clinical toxicity, such as fever, confusion, dizziness, weakness and malaise, appearance of rashes, purulent and hemorrhagic flicten, inflammation with increased disproportionate pain, and subcutaneous emphysema with focused gas in certain areas. The worst-case scenario involves shock and multiorgan failure, acidosis, coagulopathy, changes in mental status 7 , coupled by the thrombosis of microvessels that perpetuate the lesion of the tissues affecting the deep planes and the superficial dermis 2 . The differential diagnoses that should be considered are anaerobic streptococcal myositis, pyomyositis, necrotizing synergistic cellulitis (Meleney's syndrome), Clostridium myonecrosis, or gas gangrene 1 .…”

Tender Nonhealing Lesion on the Leg

“…Infection can spread along fascial planes for several days without affecting the overlying skin, leading to delayed diagnosis. 11 The first signs to appear are disproportionate pain and a change in skin color to reddish-purple or bluish-gray. Next, the skin will become indurated, swollen, shiny, and more painful.…”

“…Next, the skin will become indurated, swollen, shiny, and more painful. 11 Skin breakdown will begin in 3 to 5 days and is accompanied by bullae and cutaneous gangrene. The involved area becomes painless due to thrombosis of the small vessels that supply the superficial nerves.…”