Base deficit after major trauma directly relates to neutrophil CD11b expression: a proposed mechanism of shock-induced organ injury

Intensive Care Med. 1997 May;23(5):504-9. doi: 10.1007/s001340050365.


Objective: To determine whether expression of neutrophil integrin receptors is related to the degree of post-traumatic shock.

Design: Data were collected prospectively on patients with major trauma admitted to the surgical intensive care unit.

Setting: Denver General Hospital, Colorado.

Patients and participants: 17 severely injured adults.

Measurements and results: The mean fluorescence intensity and per cent positive of neutrophil integrin receptors CD11 b, CD18 and CD11 a, and systolic blood pressure, blood transfusion, lactate and base deficit as indices of shock. CD11 b expression on circulating neutrophils was increased 6 and 12 h after trauma. After correcting for the other shock indices, base deficit predicted CD11 b expression at 12 h. CD11 b expression was negatively correlated with the circulating neutrophil count.

Conclusions: The degree of metabolic acidosis after trauma correlates directly with CD11 b receptor expression on circulating neutrophils. This relation may be the mechanism whereby post-traumatic shock results in neutrophil sequestration and neutrophil-mediated organ injury and failure.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Acidosis / complications*
  • Adolescent
  • Adult
  • Analysis of Variance
  • CD18 Antigens / metabolism
  • Humans
  • Lymphocyte Function-Associated Antigen-1 / metabolism
  • Macrophage-1 Antigen / adverse effects
  • Macrophage-1 Antigen / metabolism*
  • Middle Aged
  • Multiple Organ Failure / etiology*
  • Neutrophils / physiology*
  • Prospective Studies
  • Regression Analysis
  • Shock, Traumatic / complications
  • Shock, Traumatic / metabolism*
  • Shock, Traumatic / physiopathology
  • Time Factors
  • Up-Regulation / physiology


  • CD18 Antigens
  • Lymphocyte Function-Associated Antigen-1
  • Macrophage-1 Antigen