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      Group B streptococcal necrotizing fasciitis from a decubitus ulcer

      brief-report
      , ,
      International Journal of Emergency Medicine
      Springer-Verlag

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          Abstract

          A 29-year-old man with paraplegia secondary to a gunshot wound presented to the emergency department (ED) with worsening abdominal pain over the past 2 weeks with associated fever, dysuria, nausea, and vomiting. He had been diagnosed with a urinary tract infection (UTI) 2 days earlier and was started on antibiotics without improvement. On examination he was afebrile, tachycardic up to 140, tachypneic, and diaphoretic. His abdomen was rigid and diffusely tender to palpation with hypoactive bowel sounds. He had a mildly tender 3 × 3 cm decubitus ulcer on his buttocks. His WBC was elevated at 18, with an absolute neutrophil count of 11.09 and 3.17 bands. The creatine kinase was elevated at 1,001 and a serum lactate level was 8.7. Abdominal computed tomography (CT) showed free air dissecting into the retroperitoneal and peritoneal fascial planes consistent with necrotizing fasciitis (Fig. 1, Fig. 2, Fig. 3, and Fig. 4). Fig. 1 Chest X-ray showing subdiaphragmatic free air Fig. 2 CT scan through the abdomen showing free air Fig. 3 CT scan through the pelvis showing free air Fig. 4 CT scan through the lower pelvis showing air tracking The patient was taken for emergent exploratory laparotomy and extensive debridement. Throughout his hospital course he returned to the operating room (OR) a total of 11 times for further debridement and repair of complications, which included a perforated cecum and a colocutaneous fistula. Cultures from the wound grew Prevotella bivia and group B streptococci, while cultures of the peritoneal tissue grew only group B streptococci. Neither blood nor urine cultures grew any bacteria. In addition to his numerous surgeries he was treated with IV clindamycin and piperacillin/tazobactam. After 10 weeks of hospitalization he was transferred to a rehab facility. Necrotizing fasciitis, more commonly known as the “flesh-eating disease,” is an aggressive and highly destructive infection of fascia and muscle with a high morbidity and mortality. Necrotizing fasciitis from decubitus ulcers is rare, with only a few reported cases [1, 2]. The diagnosis can be difficult, as symptoms are nonspecific and the initial skin lesions are often benign compared to the underlying tissue destruction [3]. A high index of suspicion should be present when abdominal radiographs demonstrate subcutaneous emphysema in a patient with skin lesions [4]. On CT, free air with evidence of soft tissue invasion is consistent with the diagnosis [2]. This case is unique because the decubitus ulcer and peritoneal samplings both grew and isolated group B streptococci as the causative agents; necrotizing fasciitis is typically caused by group A streptococci, Staphylococcus aureus, Vibrio vulnificus, Clostridium perfringens, Bacteroides fragilis, or mixed flora.

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          Most cited references4

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          Molecular pathogenesis of necrotizing fasciitis.

          Necrotizing fasciitis, also known as the flesh-eating disease, is a severe invasive infection associated with very high rates of human morbidity and mortality. It is most commonly caused by group A Streptococcus(GAS), a versatile human pathogen that causes diseases ranging in severity from uncomplicated pharyngitis (or strep throat) to life-threatening infections such as necrotizing fasciitis. Herein, we review recent discoveries bearing on the molecular pathogenesis of GAS necrotizing fasciitis. Importantly, the integration of new technologies and the development of human-relevant animal models have markedly expanded our understanding of the key pathogen-host interactions underlying GAS necrotizing fasciitis. For example, we now know that GAS organisms secrete a variety of proteases that disrupt host tissue and that these proteolytic enzymes are regulated by multiple transcriptional and posttranslational processes. This pathogenesis knowledge will be crucial to supporting downstream efforts that seek to develop novel vaccines and therapeutic agents for this serious human infection.
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            Necrotizing soft tissue infection from decubitus ulcer after spinal cord injury.

            A case of necrotizing soft tissue infection in a patient with spinal cord injury with extension of infection into the spinal canal and spinal cord is presented. To review the history, risk factors, pathophysiology, diagnosis, treatment, and morbidity and mortality regarding necrotizing soft tissue infection as they relate to spinal cord injury. Necrotizing soft tissue infection related to decubitus ulcers is rare. To our knowledge, this is the first report of this disease related to a sacral decubitus ulcer with extension of the necrotizing infection into the spinal canal. The clinical, radiographic, and pathologic features associated with necrotizing soft tissue infection are presented. The patient presented with a late-stage necrotizing soft tissue infection requiring extensive de-bridement of necrotic tissue, which the patient underwent on admission. The patent died of refractory septic shock and multiple-organ failure after surgery. Necrotizing soft tissue infections from decubitus ulcers are rare and unpredictable, and ultimately have a progressively aggressive course. The case reported herein is the first report of necrotizing soft tissue infection from a decubitus ulcer in a patient with spinal cord injury with extension into the spinal canal and spinal cord.
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              Necrotizing fasciitis: an uncommon consequence of pressure ulceration.

              Pressure ulcers may occur in patients with chronic illnesses, especially in those who are bed-bound or chair-bound. Local measures usually suffice to allow primary ulcer healing and support skin grafting or tissue transfer reconstruction. On rare occasions, however, pressure ulcers may progress to invasive infection and necrosis of adjacent soft tissues, possibly leading to necrotizing fasciitis. Early recognition and aggressive medical and surgical therapy are required to halt disease progression and prevent patient mortality. Two cases are presented to describe the severity of this soft-tissue infection.
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                Author and article information

                Contributors
                +1-201-3175014 , klossb@upstate.edu
                brotonc@upstate.edu
                rodrigue@upstate.edu
                Journal
                Int J Emerg Med
                International Journal of Emergency Medicine
                Springer-Verlag (London )
                1865-1372
                1865-1380
                3 November 2010
                3 November 2010
                December 2010
                : 3
                : 4
                : 519-520
                Affiliations
                Department of Emergency Medicine, Upstate Medical University, 550 East Genesee Street, Syracuse, NY 13202 USA
                Article
                243
                10.1007/s12245-010-0243-3
                3047834
                21373352
                386efbb3-ea5c-49f4-b029-53e5721198fd
                © © The Author(s). This article is published with open access at Springerlink.com 2010
                History
                : 8 June 2010
                : 6 September 2010
                Categories
                Clinical Images
                Custom metadata
                © Springer-Verlag London Ltd 2010

                Emergency medicine & Trauma
                Emergency medicine & Trauma

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