Microcirculatory dysfunction has been well reported in clinical studies in septic shock. However, no clinical studies have investigated microcirculatory blood flow behavior in hemorrhagic shock. The main objective of this study was to assess the time course of sublingual microcirculation in traumatic hemorrhagic shock during the first 4 days after trauma.
Prospective observational study.
Eighteen traumatic hemorrhagic shock patients.
The sublingual microcirculation was estimated at the study inclusion after surgical or angiographic embolization to control bleeding (D1), and then three times at 24-hour intervals (D2, D3, and D4).
Sublingual microcirculation was impaired for 72 hours despite restoration of the macrovascular circulation after control of bleeding in traumatic hemorrhagic shock patients. Furthermore, we found significantly higher decreases in the microvascular flow index and proportion of perfused vessels in high Sequential Organ Failure Assessment score patients at D4 (Sequential Organ Failure Assessment score ≥ 6) compared to low Sequential Organ Failure Assessment score patients at D4 (Sequential Organ Failure Assessment score < 6) without any differences in global hemodynamics between these two groups. Finally, the initial proportion of perfused vessels at D1 appears to be a good predictor of high Sequential Organ Failure Assessment score at D4.
Alterations of microcirculation in traumatic hemorrhagic shock patients result from the interplay among hemorrhage-induced tissue hypoperfusion, trauma injuries, inflammatory response, and subsequent resuscitation interventions. Despite restoration of the macrocirculation, the sublingual microcirculation was impaired for at least 72 hours. The initial proportion of perfused vessels appears to be a good predictor of high Sequential Organ Failure Assessment score at D4. Further studies are required to firmly establish the link between microvascular alterations and organ dysfunction in traumatic hemorrhagic shock patients.
1AP-HP, Service d’Anesthésie-Réanimation, Hôpitaux Universitaires Paris-Sud, Université Paris-Sud, Hôpital de Bicêtre, Le Kremlin-Bicêtre, France.
2Microcirculation, Bioénergétique, Inflammation et Insuffisance Circulatoire Aiguë, Equipe Universitaire 3509, Paris VII-Paris XI-Paris XIII, Paris, France.
3Baker IDI Heart and Diabetes Institute, Melbourne, VIC, Australia.
4Hôpitaux Universitaires de Strasbourg, Service d’Anesthésie-Réanimation Chirurgicale, Hôpital de Hautepierre, Université de Strasbourg, Fédération de Médecine Translationnelle de Strasbourg (FMTS), Equipe d’accueil EA 3072 “Mitochondrie, stress oxydant et protection musculaire” Strasbourg, France.
* See also p. 1556.
Dr. Huet is employed by Baker IDI. Dr. Vicaut consulted for Pfizer, Lilly, Sanofi, LFB, Abbott, Fresenius, and Stallergene. He lectured for Merck and Pfizer and his institution received grant support from Boehringer. Dr. Duranteau consulted and lectured for the LFB company. His institution consulted for the LFB company. The remaining authors have disclosed that they do not have any potential conflicts of interest.
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