Differentiating necrotizing soft tissue infections from cellulitis by soft tissue infectious fluid analysis: a pilot study

Abstract

Background We conducted this study to evaluate the characteristics of the infectious fluid in soft tissue infection and investigate the utility of the biochemical tests and Gram stain smear of the infectious fluid in distinguishing necrotizing soft tissue infection (NSTI) from cellulitis. Methods This retrospective cohort study was conducted in a tertiary care hospital in Taiwan. From April 2019 to October 2020, patients who were clinically suspected of NSTI with infectious fluid accumulation along the deep fascia and received successful ultrasound-guided aspiration were enrolled. Based on the final discharge diagnosis, the patients were divided into NSTI group, which was supported by the surgical pathology report, or cellulitis group. The t test method and Fisher’s exact test were used to compare the difference between two groups. The receiver–operator characteristic (ROC) curves and area under the ROC curve (AUC) were used to evaluate the discriminating ability. Results Total twenty-five patients were enrolled, with 13 patients in NSTI group and 12 patients in cellulitis group. The statistical analysis showed lactate in fluid (AUC = 0.937) and LDH in fluid (AUC = 0.929) had outstanding discrimination. The optimal cut-off value of fluid in lactate was 69.6 mg/dL with corresponding sensitivity of 100% and specificity of 76.9%. The optimal cut-off value of fluid in LDH was 566 U/L with corresponding sensitivity of 83.3% and a specificity of 92.3%. In addition, albumin in fluid (AUC = 0.821), TP in fluid (AUC = 0.878) and pH in fluid (AUC = 0.858) also had excellent diagnostic accuracy for NSTI. The Gram stain smear revealed 50% bacteria present in NSTI group and all the following infectious fluid culture showed bacteria growth. Conclusions The analysis of infectious fluid along the deep fascia might provide high diagnostic accuracy to differentiate NSTI from cellulitis.

In-hospital mortality associated with necrotizing soft tissue infection due to Vibrio vulnificus: a matched-pair cohort study

“…There were studies considered liver cirrhosis as risk factor with increased mortality among NSTI patients [ 9 , 26 – 29 ]. Previous study had demonstrated that hyperlactatemia is significantly associated with in-hospital mortality in NSTI patients, even after adjusting for acidosis [ 30 , 31 ]. The result was similar in the present study, even in V. vulnificus infection.…”

Contemporary strategies for diagnosis and management of necrotizing soft tissue infections: Α review

“…NSTI encompass a group of destructive soft tissue bacterial necrotic disease processes, which can involve skin, subcutaneous fat, fascia(s) and/or muscle(s), associated with rapid spread along tissue planes, systemic toxicity and potentiality for high mortality [11,12,[16][17][18][19][20][21][22].Although NSTIs have some common clinical features, various entities have been recognized, such as streptococcal gangrene, gas gangrene (clostridial myonecrosis), synergistic necrotizing cellulitis and progressive bacterial synergistic gangrene [5]. Subtle differences may distinguish one entity from another, but the clinical approach to diagnosis and treatment is similar.…”

“…injure, scrape), where the organisms enter the soft tissue causing local infection, or (ii) occurring when a non-penetrating tissue injury (i.e. hematoma, muscle sprain) is infected by transient bacteremia, usually originating from the gastrointestinal or genitourinary tract [5,17,20,22,23]. A secondary infection by the host's own indigenous aerobic or anaerobic microflora usually leads to polymicrobial infection [4][5][6]14,16].…”

“…Once the pathogenic organisms reach the soft tissue, bacteria proliferate and release into the systemic circulation particularly destructive endotoxins causing acute inflammatory reactions(systemic inflammatory response syndrome, SIRS), that include increased permeability of the micro-vasculature (capillary leak syndrome), emigration of the leucocytes, and cytokine production by leukocytes [1,5,20]. The initiation of the cytokine cascade is directly associated with the vascular endothelial damage (toxin-induced platelet and leukocyte aggregation ,dermal capillary occlusion) and the development of fascial ischaemic necrosis [5,14,20]. The coagulation cascade of thromboplastin is activated resulting in disseminated microthrombosis of the feeding fascial vessels.…”

“…The coagulation cascade of thromboplastin is activated resulting in disseminated microthrombosis of the feeding fascial vessels. High-protein fluid exudates out of the blood vessels into the soft tissue and accumulates along the deep fascia [1,20]. Hypoxia and ischaemic destruction of the subcutaneous tissue and the deep fascia ensues as the process progresses, resulting in extensive necrosis and liquefaction of the fascias and the surrounding tissues [1,14,20].The most prominent affected skin areas might be in discrepancy with the position of the fascial necrosis [3].Typically, the disease is characterized by sudden onset, spreads along existing fascial planes, and deteriorates rapidly [22,23].…”