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PubMed2004

Noninvasive muscle oxygenation to guide fluid resuscitation after traumatic shock.

BACKGROUND: Three different protocols tested the hypothesis that hind limb muscle tissue O(2) saturation (StO(2)), measured noninvasively with near-infrared spectroscopy (NIRS), is as reliable as invasive systemic oxygenation indices to guide fluid resuscitation. METHODS: In series 1, swine (n=30) were hemorrhaged, then received either no fluid, a fixed volume of colloid (15 mL/kg), or shed blood plus lactated Ringer's (LR) titrated to MAP >60 mm Hg. In series 2, swine (n=16) received a penetrating femur injury, a 47% to 55% hemorrhage to determine a median lethal dose (LD(50)) then shed blood plus LR titrated to MAP >60 mm Hg. In series 3, swine (n=5) received the femur injury plus LD(50) hemorrhage, and were resuscitated with LR titrated to StO(2) >50%. RESULTS: In series 1, StO(2) tracked mixed venous O(2) saturation (SvO(2)), but discriminated between 3 survivor groups better than SvO(2), arterial lactate, or arterial base excess. In series 2, StO(2) tracked SvO(2) but discriminated between 2 survivor groups better than SvO(2), arterial lactate, or arterial base excess. In series 3, animals survived to extubation when resuscitated to an StO(2) target. CONCLUSIONS: Noninvasive muscle StO(2) determined by NIRS was more reliable than invasive oxygenation variables as an index of shock. Because muscle StO(2) can be easily monitored in emergency situations, it may represent an improved method to gauge the severity of shock or the adequacy of fluid resuscitation after trauma.

Animals↗
PubMed2002

Secondary abdominal compartment syndrome is an elusive early complication of traumatic shock resuscitation.

BACKGROUND: The term secondary abdominal compartment syndrome (ACS) has been applied to describe trauma patients who develop ACS but do not have abdominal injuries. The purpose of this study was to describe major trauma victims who developed secondary ACS during standardized shock resuscitation. METHODS: Our prospective database for standardized shock resuscitation was reviewed to obtain before and after abdominal decompression shock related data for secondary ACS patients. Focused chart review was done to confirm time-related outcomes. RESULTS: Over the 30 months period ending May 2001, 11 (9%) of 128 standardized shock resuscitation patients developed secondary ACS. All presented in severe shock (systolic blood pressure 85 +/- 5 mm Hg, base deficit 8.6 +/- 1.6 mEq/L), with severe injuries (injury severity score 28 +/- 3) and required aggressive shock resuscitation (26 +/- 2 units of blood, 38 +/- 3 L crystalloid within 24 hours). All cases of secondary ACS were recognized and decompressed within 24 hours of hospital admission. After decompression, the bladder pressure and the systemic vascular resistance decreased, while the mean arterial pressure, cardiac index, and static lung compliance increased. The mortality rate was 54%. Those who died failed to respond to decompression with increased cardiac index and did not maintain decreased bladder pressure. CONCLUSIONS: Secondary ACS is an early but, if appropriately monitored, recognizable complication in patients with major nonabdominal trauma who require aggressive resuscitation.

Abdominal Injuries↗
PubMed1996

Acadesine and lipopolysaccharide-evoked pulmonary dysfunction after resuscitation from traumatic shock.

BACKGROUND: We have reported that the purine precursor acadesine (AICAR) improved the microcirculation, repleted adenosine triphosphate, and attenuated local and lung neutrophil infiltration after intestinal reperfusion and that it quickly improved systemic hemodynamics after resuscitation from hemorrhagic shock. This study evaluated the therapeutic potential of AICAR after fluid resuscitated trauma. METHODS: Anesthetized (fentanyl) mongrel pigs were subjected to tissue injury plus hemorrhage and randomized to receive resuscitation fluids comprised of shed blood plus either lactated Ringer's solution (LR) or AICAR (1 or 10 mg/kg bolus + 0.5 mg/kg/min x 30 min). Thereafter either LR or AICAR (1 or 10 mg/kg) was administered at 12-hour intervals for 72 hours. In a smaller series (n = 7) a single bolus (0.5 mg/kg) of the adenosine deaminase inhibitor deoxycoformycin was administered at the time of resuscitation. After 72 hours, and endotoxin challenge (0.5 microgram/kg, lipopolysaccharide [LPS]) was administered. RESULTS: At 1 mg/kg (n = 9), AICAR had no obvious effect versus LR (n = 31). At 10 mg/kg AICAR (n = 11), the fluid required to stabilize hemodynamics after trauma was higher (66 +/- 5 versus 52 +/- 3 ml/kg/hr, p = 0.014), but there were fewer deaths 3 days after trauma versus LR (0 of 11 versus 4 of 31, p = 0.210), fewer deaths within 5 hours after LPS administration (3 of 11 versus 16 of 27, p = 0.074), and a longer survival time after LPS administration (4.5 +/- 0.3 versus 3.9 +/- 0.2 hr, p = 0.054). Deoxycoformycin had similar salutary effects on survival after LPS administration. LPS increased protein permeability of pulmonary capillaries, increased peak inspiratory pressures on constant tidal volume, increased dead space ventilation, and caused progressive arterial desaturation on 0.65 FiO2 (all p < 0.05). This pulmonary dysfunction was associated with a compensatory increase in cardiac output, decrease in systemic vascular resistance, increase in O2 consumption, and rise in plasma cortisol level (all p < 0.05). All these changes were blunted or eliminated with 10 mg/kg AICAR. Hematocrit and systemic pressures were maintained relatively constant after LPS administration with fluid resuscitation, but less was required with AICAR versus LR (40 +/- 8 versus 83 +/- 14 ml/kg/hr, p = 0.023). AICAR caused a concentration-related reduction in CD18 expression on LPS-stimulated neutrophils in vitro, but there was no effect versus LR on circulating leukocyte counts in vivo and no effect of AICAR on LPS-stimulated production of tumor necrosis factor in vitro or in vivo. CONCLUSIONS: 1. AICAR reduced the pulmonary dysfunction associated with posttrauma endotoxemia but had no effect on circulating leukocytes, so its mechanism could be related to an adenosine-mediated improvement in peripheral perfusion or O2 use. 2. AICAR is a generic compound that is safe and apparently efficacious in human beings, so AICAR prophylaxis could be cost-effectively administered to trauma patients.

Adenosine↗
PubMed1980

The use of mixed venous blood gas determinations in traumatic shock.

A series of 10 seriously injured patients requiring resuscitation and definitive operative control of hemorrhage was studied. Simultaneous arterial and mixed venous blood gases were measured sequentially throughout the resuscitative and operative periods. Improvement of the mixed venous oxygen saturation was associated with survival. In this study, mixed venous oxygen saturations were valuable predictors of survival and were a helpful parameter to monitor during the resuscitative, operative, and immediate postoperative periods.

Humans↗