Splanchnic perfusion during delayed, hypotensive, or aggressive fluid resuscitation from uncontrolled hemorrhage.
The purpose of this study was to determine the effect of three different fluid resuscitation strategies on splanchnic perfusion in a clinically relevant model of uncontrolled hemorrhage after liver trauma. Anesthetized swine were instrumented with a gastric near-infrared spectroscopy probe (GStO2), a jejunal tonometer (PrCO2), a portal vein catheter (SpvO2, lactate), and an ultrasonic blood flow probe on the superior mesenteric artery. The liver was lacerated to produce uncontrolled hemorrhage and a shock state characterized by a 40-60% decrease in cardiac output and a decrease in mean arterial pressure (MAP) to 42 +/- 1 mmHg. Animals were randomly assigned to either delayed resuscitation (n = 6); hypotensive resuscitation with lactated Ringer's infusion to MAP = 60 mmHg (n = 6); or aggressive resuscitation with LR to MAP >/= 75 mmHg (n = 6). For the remainder of the protocol, the treatment was identical. The data showed that blood loss (47 +/- 7 and 45 +/- 10 mL/kg) and total fluid requirements (118 +/- 73 and 171 +/- 85 mL/kg) were similar with either hypotensive or aggressive resuscitation. In contrast, with delayed resuscitation, both values were lower (27 +/- 2 mL/kg and 87 +/- 33 mL/kg, both P < 0.05). Despite aggressive resuscitation, SpvO2 and GstO2 were about 10% lower (both P < 0.05 within group) and PrCO2 was about 20 mmHg higher (P < 0.05 within group) than the corresponding values in the other two groups. Thus, delayed resuscitation minimized the blood loss but did not restore tissue oxygenation, whereas aggressive resuscitation was associated with maximal blood loss and splanchnic hypoperfusion. For this reason, it is reasonable to conclude that hypotensive resuscitation might be an effective strategy to maintain splanchnic perfusion after blunt abdominal trauma and uncontrolled hemorrhage.
Varela
J Esteban
JE
Daughty Family Department of Surgery, Division of Trauma, Ryder Trauma Center, University of Miami School of Medicine, Florida 33136, USA.
Cohn
Stephen M
SM
Diaz
I
I
Giannotti
Giovanni D
GD
Proctor
Kenneth G
KG
D000136:Acid-Base Equilibrium / Q000187:drug effects / Q000502:physiology; D000818:Animals; D001783:Blood Flow Velocity / Q000187:drug effects / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002245:Carbon Dioxide / Q000097:blood; D002302:Cardiac Output / Q000502:physiology; D005440:Fluid Therapy; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006470:Hemorrhage / Q000209:etiology / Q000628:therapy*; D007552:Isotonic Solutions / Q000494:pharmacology; D019344:Lactic Acid / Q000097:blood; D008099:Liver / Q000293:injuries*; D008297:Male; D017538:Mesenteric Artery, Superior / Q000502:physiology; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D011169:Portal Vein / Q000502:physiology; D019106:Postoperative Hemorrhage; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D015424:Reperfusion / Q000379:methods*; D012151:Resuscitation / Q000379:methods*; D000077325:Ringer's Lactate; D013152:Splanchnic Circulation / Q000502:physiology*; D013552:Swine
D007552:Isotonic Solutions; D000077325:Ringer's Lactate; D002245:Carbon Dioxide; D019344:Lactic Acid; D010100:Oxygen