Israel Medical Association Journal

Background: Modern medicine has improved survival rates in burn care. However, this progress has led to a new challenge of sepsis, which has become the leading cause of death in burn patients, accounting for over 50% of mortality. The diagnosis and treatment of sepsis in the burn care unit pose significant challenges due to the hypermetabolic state of the patient, which can mask septic signs and symptoms. This situation underscores the urgent need for improved strategies in sepsis management in burn patients.

Objectives: To assess the predictors of morbidity and mortality among severe burn patients.

Methods: Rambam Health Care Campus is the referral center for burn patients in northern Israel. We reviewed 5 years of patient records, noting information regarding sepsis, laboratory results, infections, and overall morbidity and mortality. In addition, a comparative cohort of burn patient records without sepsis was compared.

Results: Thirty patients had recorded sepsis. Total and direct bilirubin were associated with higher mortality (P < 0.05). Elevated white blood cell count and platelet count at admission were also associated with mortality (P < 0.05). The most prominent burn areas were the arms, head, and legs. The leading cause of injury was fire, followed by an explosion. Burns of total body surface area ≥ 40% was associated with sepsis.

Conclusions: Sepsis is a complex challenge when diagnosing and treating burned patients. Identifying specific traits and prognostic factors is crucial to adequately treat these patients. Research in burn care and sepsis management is essential.

Background: Cell-mediated immunity is impaired in uremia. Cell-matrix interactions of immune cells such as CD4+T lymphocytes with extracellular matrix are an important requirement for an intact immune response. The adherence of CD4+T cells of healthy subjects (normal T cells) to ECM components is inhibited in the presence of uremic serum. Such decreased adhesive capacity is also found in T cells of dialysis patients. Various chemokines and cytokines affect the attachment of CD4+T cells to ECM.

Objective: To evaluate chemokine (MIP-1β and RANTES) and tumor necrosis factor α-induced adhesion of CD4+T cells to ECM in a uremic milieu.

Methods: We examined adhesion of normal CD4+T cells (resting and activated) to intact ECM in response to soluble or bound chemokines (MIP-1β and RANTES) and to TNF-α following incubation in uremic versus normal serum. Thereafter, we evaluated the adhesion of resting CD4+T cells from dialysis patients in a similar fashion and compared it to that obtained from a healthy control group.

Results: Addition of uremic serum diminished soluble and anchored chemokine-induced attachment of normal resting and activated CD4+T cells to ECM compared to a normal milieu (a peak response of 10–11% vs. 24–29% for soluble chemokines, P<0.001; 12–13% vs. 37–39% for bound chemokines on resting cells, P<0.01; and 18–20% vs. 45–47% for bound chemokines on activated cells, P<0.02). The same pattern of response was noted following stimulation with immobilized TNF-α (7 vs. 12% for resting cells, P<0.05; 17 vs. 51% for activated cells, P<0.01).  Adherence of dialysis patients’ cells to ECM following stimulation with both bound chemokines was reduced compared to control T cells (15–17% vs. 25–32%, P<0.0000). In contrast, adherence following stimulation by TNF-α was of equal magnitude.

Conclusions: Abnormal adhesive capacity of T lymphocytes to ECM in uremia may, in part, be related to a diminished response to MIP-1β, RANTES and TNF-α. However, whereas reduced adhesion to chemokines was present in both normal CD4+T cells in a uremic environment and in dialysis patients’ T cells, TNF-α-induced adhesion was found to be inhibited only in normal cells in a uremic milieu.

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ECM = extracellular matrix

TNF-α = tumor necrosis factor-a