Mediator-dependent secondary injury after unilateral blunt thoracic trauma

Sherry M. Melton, Kimberly A. Davis, Charles B. Moomey, Timothy C. Fabian, Kenneth G. Proctor

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

The pathophysiologic sequence leading to respiratory failure after chest trauma can be an inevitable consequence of the primary injury or a secondary, mediator-driven inflammatory process. To distinguish between these alternatives, a simple cross-transfusion experiment was performed. A captive bolt gun injured the chest of anesthetized pigs that were mechanically ventilated with Fio2 = .21, .50, or .50 plus indomethacin (5 mg/kg intravenous; 15 min before injury). Tube thoracostomy immediately followed. After 30 min, blood from these injured donors was transfused into three matched groups of naive recipients (n = 8, 6, and 4, respectively) for a 33% exchange transfusion. Two control groups received blood from uninjured donors with tube thoracostomies only (Fio2 = .21, n = 7; Fio2= .50, n = 10). Within 15-30 min after transfusion, in recipients from injured donors versus controls, lung compliance was decreased 20%, stroke volume and cardiac output were decreased 50%, and pulmonary vascular resistance was increased >300% (all p < .05). These changes recovered to baseline within 60-90 min. The stable metabolite of thromboxane A2, thromboxane B2, increased >500% in plasma within 15 min and remained elevated for >120 min. All responses were similar at 21% or 50% O2, which suggests that hypoxia per se is not a cause of mediator production. All responses were eliminated by indomethacin. By 24 h, histologic changes included atelectasis in 3/3 recipients from injured donors versus 0/3 recipients from uninjured donors. We conclude that 1) blunt chest trauma releases blood borne mediators, including prostanoids; 2) these mediators can cause secondary cardiopulmonary changes in naive recipients similar to those produced by chest trauma; 3) the progression to trauma-induced respiratory failure is multifactorial; 4) early pharmacologic intervention, rather than supportive care alone, may benefit some victims of severe chest trauma.

Original languageEnglish (US)
Pages (from-to)396-402
Number of pages7
JournalShock
Volume11
Issue number6
StatePublished - Jun 1999

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Thorax
Wounds and Injuries
Thoracostomy
Tissue Donors
Blood Donors
Indomethacin
Respiratory Insufficiency
Lung Compliance
Pulmonary Atelectasis
Firearms
Cardiac Output
Vascular Resistance
Stroke Volume
Prostaglandins
Research Design
Swine
Control Groups

All Science Journal Classification (ASJC) codes

  • Critical Care and Intensive Care Medicine
  • Physiology

Cite this

Melton, S. M., Davis, K. A., Moomey, C. B., Fabian, T. C., & Proctor, K. G. (1999). Mediator-dependent secondary injury after unilateral blunt thoracic trauma. Shock, 11(6), 396-402.

Mediator-dependent secondary injury after unilateral blunt thoracic trauma. / Melton, Sherry M.; Davis, Kimberly A.; Moomey, Charles B.; Fabian, Timothy C.; Proctor, Kenneth G.

In: Shock, Vol. 11, No. 6, 06.1999, p. 396-402.

Research output: Contribution to journalArticle

Melton, SM, Davis, KA, Moomey, CB, Fabian, TC & Proctor, KG 1999, 'Mediator-dependent secondary injury after unilateral blunt thoracic trauma', Shock, vol. 11, no. 6, pp. 396-402.
Melton SM, Davis KA, Moomey CB, Fabian TC, Proctor KG. Mediator-dependent secondary injury after unilateral blunt thoracic trauma. Shock. 1999 Jun;11(6):396-402.
Melton, Sherry M. ; Davis, Kimberly A. ; Moomey, Charles B. ; Fabian, Timothy C. ; Proctor, Kenneth G. / Mediator-dependent secondary injury after unilateral blunt thoracic trauma. In: Shock. 1999 ; Vol. 11, No. 6. pp. 396-402.
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abstract = "The pathophysiologic sequence leading to respiratory failure after chest trauma can be an inevitable consequence of the primary injury or a secondary, mediator-driven inflammatory process. To distinguish between these alternatives, a simple cross-transfusion experiment was performed. A captive bolt gun injured the chest of anesthetized pigs that were mechanically ventilated with Fio2 = .21, .50, or .50 plus indomethacin (5 mg/kg intravenous; 15 min before injury). Tube thoracostomy immediately followed. After 30 min, blood from these injured donors was transfused into three matched groups of naive recipients (n = 8, 6, and 4, respectively) for a 33{\%} exchange transfusion. Two control groups received blood from uninjured donors with tube thoracostomies only (Fio2 = .21, n = 7; Fio2= .50, n = 10). Within 15-30 min after transfusion, in recipients from injured donors versus controls, lung compliance was decreased 20{\%}, stroke volume and cardiac output were decreased 50{\%}, and pulmonary vascular resistance was increased >300{\%} (all p < .05). These changes recovered to baseline within 60-90 min. The stable metabolite of thromboxane A2, thromboxane B2, increased >500{\%} in plasma within 15 min and remained elevated for >120 min. All responses were similar at 21{\%} or 50{\%} O2, which suggests that hypoxia per se is not a cause of mediator production. All responses were eliminated by indomethacin. By 24 h, histologic changes included atelectasis in 3/3 recipients from injured donors versus 0/3 recipients from uninjured donors. We conclude that 1) blunt chest trauma releases blood borne mediators, including prostanoids; 2) these mediators can cause secondary cardiopulmonary changes in naive recipients similar to those produced by chest trauma; 3) the progression to trauma-induced respiratory failure is multifactorial; 4) early pharmacologic intervention, rather than supportive care alone, may benefit some victims of severe chest trauma.",
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