9 - Secondary Immunodeficiency in Burns and after Surgical Trauma

Abstract

The trauma patient has a greatly increased risk of developing bacterial septicaemia because of alterations in host defence systems. The hypothesis presented in this paper is that severe injury initially triggers changes in crucial monocyte (MO) activities which are then reflected in inimical alterations in both the specific immune and the non-specific inflammatory host defence systems. We have attempted to identify those critical interactions of the inflammatory and immune pathways which are altered after both burns and multiple injuries. Assays are described to monitor post-trauma changes in the following MO functions: production of plasminogen activator (PA), generation of tissue procoagulant factor (TF), synthesis of prostaglandin E2 (PGE2), synthesis of complement components, and production of endogenous pyrogen (EP). We have correlated the patients’ altered MO functions to aberrations in their immune functions as measured by a decrease in mitogen responses, an increase in suppressor T cell activity, or an increase in inhibitory MO function. Seventeen patients who had undergone splenectomy for trauma and nineteen thermally injured patients with >30 per cent third-degree burns were studied. Eight out of seventeen of the asplenic trauma patients and nine out of nineteen of the burn patients experienced MO/PA and mitogen hyporesponsiveness. All of the thermally injured patients identified as having decreased host resistance experienced major septic complications, and seven of these patients succumbed to disseminated sepsis. Of the eight asplenic trauma patients who showed decreased MO and immune function, six developed septic complications. All eight of the asplenic patients who had decreased MO/PA production also showed abnormally elevated MO/TF production, and all of these patients also developed coagulation abnormalities. The altered responses in these asplenic patients occurred approximately six to ten days post injury. In contrast, the burn patients’ hyporesponsiveness occurred three to five days post injury and was not accompanied by a concomitant rise in MO/TF production. Instead, they appeared to have very early (one to three day) increases in MO/PGE2 production. These data suggest that the trauma-mediated mechanisms involved in depressing host resistance may differ between the asplenic and the thermally injured patient. Identification of the underlying mechanisms which cause loss of host resistance should aid the development of therapy designed to prevent or attenuate these changes.