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Pulmonary reaction during intramedullary fracture management in traumatic shock: an experimental study.

Immediate nailing of shaft fractures in severely injured patients causes fat embolization. This method therefore is considered potentially dangerous, since fat intravasation in association with multiple trauma and subsequent endotoxemia might lead to pulmonary dysfunction. We therefore studied the pathophysiologic events of intramedullary nailing in the lungs of sheep with chronic instrumentation including lung lymph fistula. In the 7 animals in group I closed nailing of the intact tibia and femur was performed. Group II (n = 7) animals sustained hypovolemic shock and retransfusion prior to nailing, while group III (n = 11) animals were treated like those in group II and further challenged on the following two days with endotoxin. Group III was compared with group IV (n = 6), in which endotoxin was given only once without additional trauma. Nailing in group I led to a significant increase of the MPAP from 10.8 to 13.8 mm Hg postoperatively (p < 0.05), but no increase in lung permeability. Only additional hypovolemia, retransfusion and nailing as performed in groups II and III showed significant increase of the lymph flow (QI) from 4.4 mL/h to 12.4 mL/h and the protein clearance (Pclear) from 3 to 6.3. A significant difference of the pulmonary permeability between group I and II was only observed postoperatively. There was no difference in the lung response between group III and IV. This ovine study corroborates that although nailing causes a moderate increase in pulmonary pressure, it does not lead to increased lung permeability. Only additional hemorrhagic shock, even when adequately resuscitated, leads to lung disturbance postoperatively. The subsequent endotoxin challenge does not aggravate lung injury.

Animals↗

Tissue hemoglobin O2 saturation during resuscitation of traumatic shock monitored using near infrared spectrometry.

BACKGROUND: Near infrared (NIR) spectrometry offers a noninvasive monitor of tissue hemoglobin O2 saturation and has been developed to report a quantitative clinical variable, StO2 [= HbO2/(HbO2 + Hb)]. In this study, a prototype NIR oximeter was used to investigate the hypothesis that changes in systemic O2 delivery index (D(O2)I) would be reflected by changes in StO2 in skeletal muscle, subcutaneous tissue, or both, as reperfusion occurs during shock resuscitation. StO2 was also compared with other indices of severity of shock or adequacy of resuscitation, including arterial base deficit, lactate, gastric mucosal P(CO2) (PgCO2), and mixed venous hemoglobin O2 saturation (S(VO2)). METHODS: Skeletal muscle and subcutaneous tissue StO2 were monitored simultaneously in eight severely injured trauma patients (88% blunt mechanism; age, 42 +/- 6 years; Injury Severity Score, 27 +/- 3) during standardized shock resuscitation in the intensive care unit with the primary goal of D(O2)I > or = 600 mL O2/min/m2 for 24 hours, and for an additional 12 hours during transition from resuscitation to standard intensive care unit care. RESULTS: Skeletal muscle StO2 increased significantly from 15 +/- 2% (mean +/- SEM) at the start of resuscitation to 49 +/- 14% at 24 hours, and to approximately 55% from 25 to 36 hours. Subcutaneous tissue StO2 approximately 82% and was significantly greater than skeletal muscle StO2 throughout. D(O2)I increased significantly from 372 +/- 54 to 718 +/- 47 mL O2/min/m2 during resuscitation. Over 36 hours, mean D(O2)I and skeletal muscle StO2 were highly correlated (r = 0.95). Neither D(O2)I-PgCO2 nor D(O2)I-S(VO2) were significantly correlated; neither S(VO2) nor subcutaneous tissue StO2 changed significantly. CONCLUSION: Hemoglobin O2 saturation was monitored noninvasively and simultaneously in skeletal muscle and subcutaneous tissues as StO2 (%) by using a prototype NIR oximeter. Skeletal muscle StO2 tracked systemic O2 delivery during and after resuscitation. As a rapidly deployable, noninvasive monitor of peripheral tissue oxygenation and O2 delivery, skeletal muscle StO2 obtained using NIR spectrometry would be useful to guide resuscitation in the intensive care unit, to monitor resuscitation status in the operating room, and, potentially, in combination with indicators such as base deficit and lactate, to detect shock during initial assessment of the severe trauma patient in the emergency department.

Adult↗

Tissue oxygen saturation predicts the development of organ dysfunction during traumatic shock resuscitation.

BACKGROUND: Near-infrared spectroscopy (NIRS) can continuously and noninvasively monitor tissue oxygen saturation (StO2) in muscle and may be an indicator of shock severity. Our purpose was to evaluate how well StO2 predicted outcome in high-risk torso trauma patients presenting in shock. METHODS: The primary outcome in this prospective study was multiple organ dysfunction syndrome (MODS). StO2 data were obtained upon hospital arrival and for 24 hours along with other known predictors of hypoperfusion and clinical outcomes. Clinicians were blinded to StO2 measurements. RESULTS: Seven Level I trauma centers enrolled 383 patients, 50 of whom developed MODS. Minimum StO2 performed similarly to maximum base deficit (BD) in discrimination of MODS patients. The sensitivity for both measures (StO2 cutoff = 75%; BD cutoff = 6 mEq/L) was 78%, the specificity was 34% to 39%, the positive predictive value was 18% to 20% and the negative predictive value was 88% to 91%. StO2 and BD were also comparable in predicting death. CONCLUSIONS: NIRS-derived muscle StO2 measurements perform similarly to BD in identifying poor perfusion and predicting the development of MODS or death after severe torso trauma, yet have the additional advantages of being continuous and noninvasive.

Adolescent↗