Sepsis Development After Burn Injury

sepsis development burns mrproadm

sepsis development burns pct
Figure 1. Time course of MR-proADM and PCT levels in the time period surrounding the occurrence of infection (Inf), ranging from 2 days prior to infections (T-2) and 4 days post infection (T+4). Symbols indicate statistical significance in concentrations (P < 0.05).

Approximately 180,000 deaths per year are caused by severe burns, with non-fatal burns a leading cause of morbidity and prolonged hospitalisation.

The leading causes of death are the onset and progression of sepsis and multiorgan failure Ref-1. Hence, the implementation and optimisation of early sepsis treatment strategies may help facilitate a decrease in mortality Ref-2. In addition, an early diagnosis of developing sepsis may also be crucial in helping to initiate more appropriate antimicrobial therapeutic strategies Ref-3.

Sepsis diagnosis following severe burns, however, can be complicated by the development and presence of a systemic inflammatory response syndrome (SIRS), and the non-specific nature of established indicators such as fever, white blood cell count (WBC), and C-reactive protein (CRP) Ref-4-8. Hence alternative and more accurate biomarkers or indicators of sepsis development are required.

In a study by Gille et al. (2017), severe burn patients with an average total burn surface area of 28.8% were enrolled. Inhalation injury was observed in 16.7% of patients. Sepsis onset occurred, on average, 6 days after initial burn injury, with the leading cause of sepsis being the burn wound itself, followed by pneumonia and abdominal infection. Both MR-proADM and PCT were significantly increased in the presence of sepsis, whereas no significant differences were found on septic and non-septic days for either WBC or maximum body temperature.

The time period surrounding sepsis diagnosis found differences between MR-proADM and PCT, with a significant increase in MR-proADM levels one day before sepsis diagnosis itself, peaking on the day of diagnosed infection. The first significant increase in PCT levels was observed on the day of sepsis diagnosis, peaking one day after infection.

Whilst MR-proADM may be more suitable for the early recognition of sepsis in a burn injury setting due to earlier concentration increases, PCT demonstrated marginally higher specificity and sensitivity for sepsis diagnosis, and may therefore be more suitable as a marker of therapeutic control. The combination of both biomarkers may help to diagnose and treat sepsis development more efficiently.

References Sepsis development after burn injury

Ref-1: Rowan MP, Cancio LC, Elster EA, et al. Burn wound healing and treatment: review and advancements. Crit Care. 2015;19:243.

Ref-2: Gille J, Ostermann H, Dragu A, Sablotzki A. MR-proADM: A New Biomarker for Early Diagnosis of Sepsis in Burned Patients. J Burn Care Res. 2017;38(5):290-298.

Ref-3: Kumar A, Roberts D, Wood KE, et al. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Crit Care Med. 2006;34(6):1589-1596.

Ref-4: Murray CK, Hoffmaster RM, Schmit DR, et al. Evaluation of white blood cell count, neutrophil percentage, and elevated temperature as predictors of bloodstream infection in burn patients. Arch Surg. 2007;142(7):639-642.

Ref-5: Lavrentieva A, Kontakiotis T, Lazaridis L, et al. Inflammatory markers in patients with severe burn injury. What is the best indicator of sepsis? Burns. 2007;33(2):189-194.

Ref-6: Sachse C, Machens HG, Felmerer G, Berger A, Henkel E. Procalcitonin as a marker for the early diagnosis of severe infection after thermal injury. J Burn Care Rehabil. 1999;20(5):354-360.

Ref-7: Barati M, Alinejad F, Bahar MA, et al. Comparison of WBC, ESR, CRP and PCT serum levels in septic and non-septic burn cases. Burns. 2008;34(6):770-774.

Ref-8: Jeschke MG, Finnerty CC, Kulp GA, Kraft R, Herndon DN. Can we use C-reactive protein levels to predict severe infection or sepsis in severely burned patients? Int J Burns Trauma. 2013;3(3):137-143.

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