Citation

Burk AM, Martin M, Flierl MA, Rittirsch D, Helm M, Lampl L, Bruckner U, Stahl GL, Blom AM, Perl M, Gebhard F, Huber-Lang MS. Shock 2012; 37(4): 348-354.

Affiliation

1Dept. of Traumatology, Hand-, Plastic-, and Reconstructive Surgery, University Hospital Ulm, 89075 Ulm, Germany 2Dept. of Laboratory Medicine, Medical Protein Chemistry, SkÅne University Hospital, Lund University, MalmÖ, Sweden 3Dept. of Anaesthesiology, Military Hospital Ulm, 89081 Ulm, Germany 4Center for Experimental Therapeutics and Reperfusion Injury, Dept. of Anaestehesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.

Copyright

(Copyright © 2012, The Shock Society, Publisher Lippincott Williams and Wilkins)

DOI

10.1097/SHK.0b013e3182471795

PMID

22258234

PMCID

PMC3306539

Abstract

After severe tissue injury, innate immunity mounts a robust systemic inflammatory response. However, little is known about the immediate impact of multiple trauma on early complement function in humans. In the present study we hypothesized that multiple trauma results in immediate activation, consumption and dysfunction of the complement cascade and that the resulting severe "complementopathy" may be associated with morbidity and mortality.Therefore a prospective multicenter study with 25 healthy volunteers and 40 polytrauma patients (mean injury severity score [ISS] = 30.3 ± 2.9) was performed. After polytrauma serum was collected as early as possible at the scene, upon admission to the emergency room and 4, 12, 24, 120 and 240 hours post trauma and analysed for the complement profile. Complement hemolytic activity (CH-50) was massively reduced within the first 24 h after injury, recovered only 5 days after trauma and discriminated between lethal and non-lethal 28-day outcome. Serum levels of the complement activation products C3a and C5a were significantly elevated throughout the entire observation period and correlatedwith the severity of traumatic brain injury and survival. The soluble terminal complement complex SC5b-9 and mannose-binding lectin (MBL) showed a biphasic response after trauma. Key fluid phase inhibitors of complement, such as C4b-binding protein (C4BP) and factor I, were significantly diminished early after trauma.The present data indicate an almost synchronically rapid activation and dysfunction of complement suggesting a trauma-induced "complementopathy" early after injury. These events may participate to the impairment of the innate immune response observed after severe trauma.

Language: en