nsti Flashcards
(18 cards)
Necrotizing soft tissue infection (NSTI) is the term used to describe a subset of soft tissue infections involving?
skin, subcutaneous tissue, muscle, and fascia that cause vascular occlusion, ischemia, and necrosis.
NSTIs are associated with virulent bacterial and fungal organisms and encompass syndromes including?
Fournier gangrene, Ludwig angina, flesh-eating disease, hemolytic streptococcal gangrene, necrotizing fasciitis (NF), and myonecrosis.
Toxic shock syndrome (TSS) is an?
acute, severe, systemic inflammatory response initiated by a microbial infection at a normally sterile site, usually exotoxin-releasing Staphylococcus or Streptococcus spp. TSS manifests as an acute, early occurrence of circulatory shock and multiorgan dysfunction that can include renal and/or hepatic dysfunction, coagulopathy, acute respiratory distress syndrome, and/or an erythematous rash.
A report of 47 dogs with NSTI found a mortlity rate of?.
53% mortality rate, but the majority of deaths were due to euthanasia, so this outcome is difficult to interpret
Risk factors identified in human medicine include?
age more than 50 years, atherosclerosis or peripheral vascular disease, obesity, trauma, hypoalbuminemia, diabetes mellitus, and glucocorticoid usage
NSTI can be stratified into four categories based on type of infection (Box 97.1).
Type I NSTI is polymicrobial, type II NSTI is monomicrobial, type III NSTI is associated with Gram-negative, often marine-related organisms, and type IV NSTI is associated with fungal infection.
Most of the veterinary cases reported could be categorized as type?
II NSTI3 associated with a history of minor trauma and inoculation with virulent bacteria. Infection can spread rapidly, and seemingly limited infections can cause limb-threatening and life-threatening systemic sequelae.
Type I infections: Polymicrobial
type 2?
Type III infections:
Type IV infections
Type I infections: Polymicrobial
* Mixed anaerobes and aerobes * Usually isolate four or more organisms Type II infections: Monomicrobial * Commonly β-hemolytic Streptococcus
Type III infections: Gram-negative monomicrobials
* Clostridia infections * Includes marine organisms Type IV infections: Fungal * Such as Candida infections
Enhanced toxicity of virulent streptococci through the release of?
exotoxin superantigens, cell envelope proteinases, hyaluronidase, complement inhibitor, M-protein, protein F, and streptolysins amplifies cytokine release and induction of a systemic inflammatory response and septic shock.
Clostridial toxins can cause? 1
hemolysis, platelet aggregation, leukocyte destruction, and histamine release, in addition to damage to the vascular endothelium, collagen, and hyaluronic acid.
Occlusion of nutrient vessels can lead to extensive undermining of apparently normal-appearing skin, followed by gangrene of the subcutaneous fat, dermis, and epidermis, evolving into ischemic necrosis.
what is is a key pathologic process of NSTI.
Microbial invasion associated with localized thrombosis leading to liquefactive necrosis of the superficial fascia and soft tissueOcclusion of nutrient vessels can lead to extensive undermining of apparently normal-appearing skin, followed by gangrene of the subcutaneous fat, dermis, and epidermis, evolving into ischemic necrosis.
what are hallmark signs of NSTI?
Rapid progression (extension within a few hours) and disproportionate localized pain
A diagnostic scoring system called the laboratory risk indicator for necrotizing fasciitis (LRINEC) score is based on?
the measurement of C-reactive protein, white blood cell count, hemoglobin, sodium, creatinine, and glucose and has been used in human patients to predict NF, although it has failed to detect some cases, and its role is under debate.29,30
An unvalidated NSTI assessment score incorporates mean arterial pressure into the LRINEC score, which may increase the diagnostic accuracy for identifying NF in people.31
A variety of imaging findings are associated with NSTI.
Subcutaneous air seen on plain film radiographs is rare but characteristic of necrotizing lesions with gas-producing organisms (Fig. 97.3). Ultrasound evidence of fluid accumulation along the deep fascia and fluid accumulation at a depth of >2 mm support the diagnosis of NSTI in people with clinical signs of NF (Fig. 97.4).32 Computed tomography features suggestive of NSTI include asymmetric fascial thickening, hypodermal fat inflammation, and gas in the soft tissue planes.33,34 Magnetic resonance imaging (MRI) may prove helpful in determining the extent of deep tissue infections not readily identified from the skin surface because of its soft tissue and multiplanar imaging capabilities. Thickened fascia with high signal intensity in T2 images is commonly seen on MRI.34 Absence of deep fascial involvement can exclude NF. However, MRI cannot differentiate NSTI from nonnecrotizing problems, and the time involved in obtaining MRI results may delay surgery.35 Advanced diagnostic imaging should never delay time to surgical intervention.
Definitive diagnosis of TSS requires?
positive streptococcal or staphylococcal culture findings and evidence of septic shock.
Definitive diagnosis of NSTI is based on?
the histopathologic findings, including fascial necrosis and myonecrosis. Pathologic descriptions also include deep angiothrombotic microbial invasion and liquefactive necrosis.36,37 Frozen section biopsy can provide a rapid diagnosis at the time of surgical exposure.38 Because of the rapid progression of disease and the time in obtaining results, rapid treatment and immediate surgical evaluation are necessary when there is a clinical suspicion of a NSTI.
Rapid administration of appropriate antimicrobial therapy is an essential part of treatment.
Penicillin G, aminopenicillins (ampicillin, amoxicillin), and cephalosporins target Gram-positive and many Gram-negative organisms and should be part of the initial antimicrobial therapy plan. However, high tissue concentrations of Group A streptococcal organisms can put them in a stationary phase, causing penicillins to become ineffective.39 Clindamycin remains effective during the stationary phase and turns off exotoxin synthesis, inhibits streptococcal M-protein synthesis (which facilitates mononuclear phagocytosis), and suppresses lipopolysaccharide-induced monocyte synthesis of tumor necrosis factor.40 It also provides coverage for anaerobic organisms. Aminoglycosides and third-generation cephalosporins may increase Gram-negative organism coverage. Gentamicin has a synergistic effect with penicillin against streptococci. For broad-spectrum coverage in the compromised patient, the authors would recommend clindamycin in combination with an aminoglycoside or third-generation cephalosporin.
Fluoroquinolone administration, specifically enrofloxacin, is not recommended why?
because it may have limited activity against streptococcal infection and may cause bacteriophage-induced lysis of S. canis, enhancing its pathogenicity
