IntroductionThe objective of this study was to investigate regional organ perfusion acutely following uncontrolled hemorrhage in an animal model that simulates a penetrating vascular injury and accounts for prehospital times in urban trauma. We set forth to determine if hypotensive resuscitation (permissive hypotension) would result in equivalent organ perfusion compared to normotensive resuscitation.MethodsTwenty four (n=24) male rats randomized to 4 groups: Sham, No Fluid (NF), Permissive Hypotension (PH) (60% of baseline mean arterial pressure - MAP), Normotensive Resuscitation (NBP). Uncontrolled hemorrhage caused by a standardised injury to the abdominal aorta; MAP was monitored continuously and lactated Ringer’s was infused. Fluorimeter readings of regional blood flow of the brain, heart, lung, kidney, liver, and bowel were obtained at baseline and 85 minutes after hemorrhage, as well as, cardiac output, lactic acid, and laboratory tests; intra-abdominal blood loss was assessed. Analysis of variance was used for comparison.ResultsIntra-abdominal blood loss was higher in NBP group, as well as, lower hematocrit and hemoglobin levels. No statistical differences in perfusion of any organ between PH and NBP groups. No statistical difference in cardiac output between PH and NBP groups, as well as, in lactic acid levels between PH and NBP. NF group had significantly higher lactic acidosis and had significantly lower organ perfusion.ConclusionsHypotensive resuscitation causes less intra-abdominal bleeding than normotensive resuscitation and concurrently maintains equivalent organ perfusion. No fluid resuscitation reduces intra-abdominal bleeding but also significantly reduces organ perfusion.

The purpose of the study was to assess the haemodynamic (blood pressure and heart rate) changes and stress responses (serum cortisol and serum amyloid A [SAA] concentrations) to surgery in piglets during total intravenous anaesthesia (TIVA) with propofol and fentanyl. After preanaesthetic medication with intramuscular midazolam (0.5 mg/kg body mass), ketamine (10 mg/kg) and butorphanol (0.5 mg/kg) anaesthesia was induced in five piglets, with intravenous propofol (1 mg/kg) followed by tracheal intubation and mechanical lung ventilation. Soft tissue surgery was performed in the jugular and inguinal regions during TIVA with propofol (8 mg/kg/h) and fentanyl (35 mg/kg/h). Anaesthesia was maintained for 300 min after surgery as the piglets were the control group of a project involving extracorporeal membrane oxygenation. Mean plasma cortisol concentration decreased significantly (P , 0.05) from 59 + 39.9 nmol/L (mean + 1 SD) before surgery to 7.5 + 2.5 nmol/L 300 min after end of surgical procedure. The mean SAA concentrations increased over the same period from 1.6 + 2.3 mg/mL to 4.2 + 5.6 mg/mL without statistical significance. The baseline ( presurgery) mean arterial pressure (MAP) was 72 + 9 mmHg compared with 72 + 11 mmHg 300 min after end of surgery. Neither heart rate nor lactate concentrations changed significantly over the same time points: heart rate was 104 + 11 and 103 + 15 beats/min whereas mean lactate concentrations were reduced from 1.14 + 0.45 mmol/L to 0.90 + 0.22 mmol/L. Haemodynamic stability, a decrease in serum cortisol and a non-statistically significant rise in mean SAA concentrations suggest that the anaesthetic described suppresses the stress response of piglets to surgery without adverse cardiovascular effects. Therefore, it may prove useful in cardiovascular research.

Background: Bacterial translocation (BT) from the gut can develop and persist after short periods of hemorrhagic shock secondary to traumatic injuries. Erythroopoietin (EPO) exerts hemodynamic and anti-inflammatory effects in addition to its erythropoietic effect. We tested the hypothesis that EPO given at the time of acute resuscitation with normal saline (NS), Ringer's lactate (RL) or 7.5% hypertonic saline (7.5%HTS) will limit shock-induced mucosal injury and BT. Methods: Rats were hemorrhaged 30 mL/kg over 10 minutes via arterial catheter for 50 minutes, then randomized to 1 of 6 resuscitation groups (n = 5/group): NS, NS+EPO, RL, RL+EPO, 7.5%HTS and 7.5%HTS+EPO. Intravenous EPO (1000 U/kg) was given at the start of NS or RL (3 times the volume of shed blood) and 4 mL/kg of 7.5%HTS+1 volume of RL resuscitation. Postresuscitation gut function was evaluated using agar cultures of mesenteric lymph nodes and portal vein plasma lipopolysaccharide, IL-6 and TNF-α levels. Three of 5 rats per group underwent light microscopic examination using semi-thin plastic sections of the distal ileum and fluorescein isothiocyanate dextran 4000 used to assess the distal ileum mucosal permeability to macromolecules. Results: Two hours postshock and resuscitation, BT to mesenteric lymph nodes decreased in the NS+EPO versus the NS group (299 ± 104 v. 1050 ± 105 CFU/gm, p < 0.05); the addition of EPO to the RL or 7.5%HTS had no effect. Comparing different solutions, there was a significant increase in BT in the NS group versus the RL+EPO, 7.5%HTS+EPO and 7.5%HTS groups (1050 ± 105 v. 357 ± 134, 462 ± 129, 428 ± 106 CFU/gm, respectively; p < 0.05). There were no significant differences in terminal ileum permeability between groups, but there was a noticeable trend in decreasing terminal ileum permeability in the EPO-treated groups: NS versus NS+EPO (18.0 ± 9.5 v. 12.9 ± 6.3 µg/mL, p = 0.84), RL versus RL+EPO (17.7 ± 5.9 v. 8.4 ± 2.7 µg/mL, p = 0.22) and 7.5%HTS versus 7.5%HTS+EPO (11.4 ± 6.4 v. 6.5 ± 2.9 µg/mL, p = 0.69). There was no significant morphological evidence of mucosal injuries and no cytokine differences between groups and within groups. Conclusion: Preliminary data from an uncontrolled mean arterial pressure hemorrhagic shock rat model revealed that BT is an early event occurring within 2 hours of injury and resuscitation before any evidence of histological injury. Erythroopoietin with NS significantly decreased BT to the portal vein as compared with NS alone, but not with RL and 7.5%HTS.Analgesia in the management of pediatric trauma in the resuscitative phase: the role of the trauma centre.

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