Fluid Resuscitation Of Hemorrhagic Shock Research Articles

Is restrictive fluid resuscitation beneficial not only for hemorrhagic shock but also for septic shock?: A meta-analysis.

Background:Whether to use limited fluid resuscitation (LFR) in patients with hemorrhagic shock or septic shock remains controversial. This research was aimed to assess the pros and cons of utilizing LFR in hemorrhagic shock or septic shock patients.Methods:PubMed, Cochrane Library, Embase, Web of science, CNKI, VIP, and Wan Fang database searches included for articles published before December 15, 2020. Randomized controlled trials of LFR or adequate fluid resuscitation in hemorrhagic shock or septic shock patients were selected.Result:This meta-analysis including 28 randomized controlled trials (RCTs) and registered 3288 patients. The 7 of 27 RCTs were the patients with septic shock. Others were traumatic hemorrhagic shock patients. Comparing LFR or adequate fluid resuscitation in hemorrhagic shock or septic shock patients, the summary odds ratio (OR) was 0.50 (95% confidence interval [CI] 0.42–0.60, P < .00001) for mortality, 0.46 (95% CI 0.31–0.70, P = .0002) for multiple organ dysfunction syndrome (MODS), 0.35 (95% CI 0.25–0.47) for acute respiratory distress syndrome (ARDS), and 0.33 (95% CI 0.20–0.56) for disseminated intravascular coagulation (DIC).Conclusion:Limited fluid resuscitation is the benefit of both traumatic hemorrhagic shock patients and septic shock patients.

Effects of different types of fluid resuscitation for hemorrhagic shock on splanchnic organ microcirculation and renal reactive oxygen species formation.

IntroductionFluid resuscitation is an indispensable procedure in the acute management of hemorrhagic shock for restoring tissue perfusion, particularly microcirculation in splanchnic organs. Resuscitation fluids include crystalloids, hypertonic saline (HTS), and synthetic colloids, and their selection affects the recovery of microcirculatory blood flow and reactive oxygen species (ROS) formation, which is often evident in the kidney, following reperfusion. In this study, the effects of acute resuscitation with 0.9 % saline (NS), 3 % HTS, 4 % succinylated gelatin (GEL), and 6 % hydroxyethyl starch (HES) 130/0.4 were compared in a hemorrhagic shock rat model to analyze restoration of microcirculation among various splanchnic organs and the gracilis muscle and reperfusion-induced renal ROS formation.MethodsA total of 96 male Wistar rats were subjected to sham operation (sham group), hemorrhagic shock (control group), and resuscitation with NS, HTS, GEL and HES. Two hours after resuscitation, changes in the mean arterial pressure (MAP), serum lactate level and the microcirculatory blood flow among various splanchnic organs, namely the liver, kidney, and intestine (mucosa, serosal muscular layer, and Peyer’s patch), and the gracilis muscle, were compared using laser speckle contrast imaging. Renal ROS formation after reperfusion was investigated using an enhanced in vivo chemiluminescence (CL) method.ResultsMicrocirculatory blood flow was less severely affected by hemorrhaging in the liver and gracilis muscle. Impairment of microcirculation in the kidney was restored in all resuscitation groups. Resuscitation in the NS group failed to restore intestinal microcirculation. Resuscitation in the HTS, GEL, and HES groups restored intestinal microcirculatory blood flow. By comparison, fluid resuscitation restored hemorrhagic shock-induced hypotension and decreased lactatemia in all resuscitation groups. Reperfusion-induced in vivo renal ROS formation was significantly higher in the GEL and HES groups than in the other groups.ConclusionAlthough fluid resuscitation with NS restored the MAP and decreased lactatemia following hemorrhagic shock, intestinal microcirculation was restored only by other volume expanders, namely 3 % HTS, GEL, and HES. However, reperfusion-induced renal ROS formation was significantly higher when synthetic colloids were used.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-015-1135-y) contains supplementary material, which is available to authorized users.

0921. Effect of norepinephrine on intestinal oxygenation during fluid resuscitation of hemorrhagic shock in mice

Hemorrhagic shock resuscitation aims at maintaining tissue perfusion while waiting for hemorrhage control. Fluid resuscitation remains the first line therapy to improve tissue perfusion but a vasoconstrictor (most often norepinephrine) may be associated to stabilize the mean arterial pressure (MAP) level and avoid hemodilution while waiting for transfusion. However, the arteriolar vasoconstriction induced by norepinephrine could have deleterious effects on tissue perfusion during hypovolemia due to hemorrhage.

Impact of fluid resuscitation with hypertonic-hydroxyethyl starch versus lactated ringer on hemorheology and microcirculation in hemorrhagic shock

The choice of volume expander for fluid resuscitation in hemorrhagic shock is still debated. Changes in plasma viscosity (PV) are barely investigated while PV modulates functional capillary density, microcirculation and organ function. The present study evaluated the impact of 2 strategies of fluid resuscitation in hemorrhagic shock in pigs. Ten pigs were subjected to hemorrhagic shock and randomly assigned to a low viscosity fluid regimen (Lactated Ringer's, LR) group or a high viscosity regimen (hypertonic-hydroxyethyl starch, HES) for volume resuscitation. Sublingual microcirculatory flow and tissue oxygen tension were assessed together with macro- and microcirculatory, biochemical and rheological variables at baseline, 30 minutes after hemorrhagic shock, immediately after reaching resuscitation endpoints (R-0), and 60 minutes after resuscitation (R-60). PV decreased similarly in both groups following resuscitation (from 1.36 [1.32-1.38] to 1.21 [1.21-1.23] for LR, and from 1.32 [1.31-1.32] to 1.20 [1.17-1.21] mPa.s for HES). No differences were found between the groups for other rheological variables, microcirculatory flow or tissue oxygen tension at R-0 and R-60. Despite a 6-fold difference in the volumes required to achieve blood flow endpoints, commercially available volume expanders had similar effects on rheological and microcirculatory variables, irrespective of their viscosity. Our findings are consistent with the absence of clinically relevant differences between crystalloid and colloid resuscitation of hemorrhagic shock.

Fluid Resuscitation for Hemorrhagic Shock in Tactical Combat Casualty Care: TCCC Guidelines Change 14-01--2 June 2014.

This report reviews the recent literature on fluid resuscitation from hemorrhagic shock and considers the applicability of this evidence for use in resuscitation of combat casualties in the prehospital Tactical Combat Casualty Care (TCCC) environment. A number of changes to the TCCC Guidelines are incorporated: (1) dried plasma (DP) is added as an option when other blood components or whole blood are not available; (2) the wording is clarified to emphasize that Hextend is a less desirable option than whole blood, blood components, or DP and should be used only when these preferred options are not available; (3) the use of blood products in certain Tactical Field Care (TFC) settings where this option might be feasible (ships, mounted patrols) is discussed; (4) 1:1:1 damage control resuscitation (DCR) is preferred to 1:1 DCR when platelets are available as well as plasma and red cells; and (5) the 30-minute wait between increments of resuscitation fluid administered to achieve clinical improvement or target blood pressure (BP) has been eliminated. Also included is an order of precedence for resuscitation fluid options. Maintained as recommendations are an emphasis on hypotensive resuscitation in order to minimize (1) interference with the body's hemostatic response and (2) the risk of complications of overresuscitation. Hextend is retained as the preferred option over crystalloids when blood products are not available because of its smaller volume and the potential for long evacuations in the military setting.

Attenuation of ischemia-reperfusion injury in swine resuscitated for hemorrhagic shock by low-dose inhaled nitrite or carbon monoxide

Fluid resuscitation of hemorrhagic shock is frequently associated with reperfusion injury and secondary organ damage. Studies suggest that low doses of both nitrite and carbon monoxide may protect tissues and organs from this reperfusion injury by limiting mitochondrial free radical production. We explored the effects of very small doses of nitrite and carbon monoxide on tissue injury in a porcine model of hemorrhagic shock.

Optimization of Oxygen Delivery in Fluid Resuscitation for Hemorrhagic Shock: A Computer Simulation Study

The main objective of fluid resuscitation in hemorrhage induced hypovolemia is to increase oxygen delivery to vital organs and to restore other hemodynamic variables to acceptable physiological range. Since replacement of blood with fluid causes both increase in cardiac output and decrease in the plasma oxygen carrying unit concentration, there is an overall opposing effect on total oxygen delivery rate to tissue. Thus, optimal fluid infusion rate and volume may be expected. The purpose of this study was to study the temporal dynamics of oxygen delivery rate during fluid replacement in a controlled hemorrhage scenario and seek these optimal values. A hemodynamic model of the human adult cardiovascular system was developed to simulate and evaluate arterial oxygen delivery at normal and at hemorrhagic conditions in different fluid resuscitation regimes. The results demonstrated the existence of a unique optimal fluid replacement regimen for maximal oxygen delivery rate at different controlled bleeding scenarios. The maintenance of high oxygen delivery rate was better with lower fluid infusion rates. The model results indicate that hematocrit and mean arterial pressure can be used to determine the optimal infusion rate and fluid infusion endpoint in fluid resuscitation.

Ringer’s Malate Solution Protects Against the Multiple Organ Injury and Dysfunction Caused by Hemorrhagic Shock in Rats

Malic acid, in the form of its anion malate, is a key intermediate in the major biochemical energy-producing cycle known as the citric acid or Krebs cycle. In this study, the authors investigated the protective effect of a novel crystalloid solution of Ringer's malate following fluid resuscitation of hemorrhagic shock using a rat model. Under general anesthesia, Sprague-Dawley male rats were subjected to 60 min of hemorrhagic shock (40 mmHg for 60 min) followed by crystalloid resuscitation. Groups were as follows: (1) sham shock, (2) normal saline, (3) Ringer's lactate, and (4) Ringer's malate. The experiment was terminated at 4 h after resuscitation. Mean arterial blood pressure (MAP) and blood biophysical parameters were monitored during the experiment. The alanine aminotransferase, aspartate aminotransferase, urea, creatinine, superoxide dismutase, and malondialdehyde levels in plasma were detected. The intestine, liver, lung, and renal histopathology were measured. It was found that Ringer's malate could increase MAP immediately and maintain MAP for a long time. Ringer's malate could reduce the level of alanine aminotransferase, aspartate aminotransferase, urea, and creatinine. At the same time, the activity of superoxide dismutase was increased, and the level of malondialdehyde was decreased. Histopathology indicated that Ringer's malate can protect against the multiple organ injury caused by hemorrhagic shock in rats. Ringer's malate prevented circulatory failure and alleviated multiple organ dysfunction syndrome in animals with hemorrhagic shock. The study suggests that Ringer's malate solution could be a potential novel therapeutic agent for fluid resuscitation.

Fluid Resuscitation of Hemorrhagic Shock with Hemoglobin Vesicles in Beagle Dogs: Pilot Study

Resuscitation of hemorrhagic shock requires volume replacement and restoration of oxygen metabolism. Artificial oxygen carriers that can both expand blood volume and deliver oxygen have been developed as resuscitation fluids. We employed hemoglobin vesicles (HbV), a cellular-type artificial oxygen carrier, in a Beagle dog hemorrhagic shock model to prove the efficacy of HbV. Hemorrhagic shock was introduced in splenectomized Beagle dogs by withdrawing 50% of circulating blood from the femoral artery. Shock was maintained for 60 minutes before isovolemic resuscitation with HbV dispersed in 5% albumin in saline (HbV), lactated Ringer's solution (LR), 5% human serum albumin in saline (HSA), or autologous shed blood (ASB). One animal in the LR group died 150 min after resuscitation. All other animals survived 4 h of the experiment. The mean arterial pressure remained significantly lower in the LR group than in the HbV group but did not differ significantly among the HbV, Alb, and ASB groups. Immediately after resuscitation, the HbV group showed a significantly higher mean pulmonary arterial pressure, which decreased within 10 minutes to the baseline level. The cardiac output was significantly higher in the Alb group than in the others, indicating compensation for low oxygen delivery per unit blood. The post-resuscitation hematocrit was 36% in the ASB group and decreased in the other groups (20-22%). Serum chemistry data from the HbV group were unremarkable. HbV contributed 32% of the post-resuscitation oxygen delivery. Collectively, HbV is comparable to ASB and HSA as a resuscitation fluid and is an effective oxygen carrier.

Fluid resuscitation in multiple trauma patients

Fluid resuscitation in trauma patients with hemorrhagic shock is controversially discussed in the literature. The coincidence of brain injury complicates management of these patients. This article summarizes the current knowledge on nonblood component fluid resuscitation and choice of fluids in patients with multiple trauma. Whereas current evidence suggests the efficacy of fluid therapy in hemorrhagic shock without active bleeding, experimental and clinical data demonstrate that aggressive volume challenge may be futile or even deleterious in the setting of uncontrolled hemorrhage. Large amounts of isotonic crystalloids may be associated with hypothermia, acidosis and inflammation. In patients with traumatic brain injury hypertonic solutions may positively influence inflammation and intracranial pressure without affecting neurologic outcome or mortality. To date no large-scale clinical studies exist to either support or refute the use of nonblood component fluid resuscitation of hemorrhagic shock in trauma patients. The optimal choice of fluid remains to be determined, but existing evidence suggests avoiding crystalloids in favor of hypertonic solutions. The role of modern, iso-oncotic colloids in the treatment of hemorrhagic shock has not yet been sufficiently defined. In patients with concomitant brain injury, arterial hypotension must be avoided and infusion of hypotonic solutions is obsolete, whereas administration of hypertonic solutions may exert beneficial effects beyond hemodynamic stabilization.

Nitroglycerin attenuates vasoconstriction of HBOC-201 during hemorrhagic shock resuscitation

Background Vasoconstriction, an inherent property of Hemoglobin Based Oxygen Carriers (HBOC) potentially due to nitric oxide (NO) scavenging, may increase cardiovascular complications in HBOC resuscitated trauma patients. The purpose of this study was to determine if co-administration of a weak NO donor, intravenous nitroglycerin (NTG), with HBOC-201 during resuscitation from hemorrhagic shock could safely attenuate HBOC-201 vasoconstriction. Methods and results Hemorrhagic shock was induced in 44 swine randomized to receive fluid resuscitation with HBOC, HBOC + NTG10 mcg/kg/min, HBOC + NTG20 mcg/kg/min, HBOC + NTG40 mcg/kg/min, Hetastarch (HES), HES + NTG20 mcg/kg/min, NTG20 mcg/kg/min and Lactated Ringers (LR). HBOC resuscitation from hemorrhagic shock increased mean arterial pressure (MAP = 94 ± 33 mmHg), mean pulmonary artery pressure (MPAP = 29 ± 11 mmHg) and systemic vascular resistance (SVR = 2684 ± 871 dyn s/cm 5) in comparison to HES. Co-administration of NTG during HBOC resuscitation attenuated vasoconstriction with HBOC + 40 mcg/kg/min demonstrating the most robust reduction in vasoconstriction (MAP = 59 ± 23 mmHg, MPAP = 18 ± 7 mmHg, and SVR = 1827 ± 511 dyn s/cm 5), although the effects were transient. Co-administration of NTG with HBOC did not alter base deficit, lactate, methemoglobin levels, nor cause profound hypotension during resuscitation. Conclusion Nitroglycerin attenuates vasoconstrictive properties of HBOC when co-administered during resuscitation in this swine model of hemorrhagic shock. Translational survival studies are required to determine if this strategy of attenuation of the vasoconstriction of HBOC-201 reduces cardiovascular complications and improves outcome with HBOC fluid resuscitation for hemorrhagic shock.

Effect of fluid resuscitation for hemorrhagic shock on oxygenation of subjects in early period of first visit of high altitude area, an experimentation on dogs

To investigate the effect of fluid resuscitation on oxygenation of subjects with hemorrhagic shock in early period of first visit to area of high altitude, an experiment in dogs was performed. A model of serious hemorrhagic shock was reproduced by exsanguination resulting in a lowering of mean arterial pressure to (35+/-5) mm Hg (1 mm Hg=0.133 kPa) maintain for 1 hour. Thirteen mongrel dogs were carried to an area of 3,780 metres above sea level from an area of 1,510 metres, and they were randomly divided into three groups, namely lactated Ringer's (LR) group, 6% hydroxyethyl starch (HES) group, and control group. The dogs in LR group were infused intravenously LR in 1.5 times the volume of blood loss; those in 6% HES group were given HES in equal volume. No fluid infusion was given in the control group. After 1 hour of resuscitation, LR was intravenously given at 5 ml.kg(-1).h(-1) in all groups as maintenance dose. The changes in oxygenation were observed. All animals in control group were dead after 2 hours. One hour after establishment of shock, the oxygen consumption (VO(2)), oxygen delivery (DO(2)), oxygen extraction ratio (O(2)ER), arterial oxygen saturation (SaO(2)) in two resuscitation groups were significantly lower than those before shock, but venous oxygen saturation (Sv(2)) and alveolar-arterial oxygen difference (A-aDO(2)) were significantly higher (all P<0.05). In LR group, the oxygenation parameters including VO(2), DO(2), O(2)ER, SaO(2) after 2 hours of resuscitation were significantly higher than those 1 hour after shock, while A-aDO(2) was significantly lower (all P<0.05); and in HES group, VO(2), DO(2), O(2)ER were significantly higher than those 1 hour after shock, while SvO(2) was significantly lower (all P<0.05). All dogs with serious hemorrhagic shock would die of hemorrhagic shock in the early period of entering a high altitude area if fluid resuscitation is denied. Two hours after infusion of LR in 1.5 times of quantity of blood loss, oxygenation can be restored to expected normal values. Infusion of 6% HES with an equal volume of blood loss, oxygenation dose not reach expected level 2 hours after resuscitation.

Effects of Different Fluid Resuscitation Speeds on Blood Glucose and Interleukin-1 Beta in Hemorrhagic Shock

Fluid resuscitation is an important treatment for hemorrhagic shock. However, evidence of guidelines for fluid resuscitation is limited. The expressions of blood glucose and proinflammatory cytokines under different resuscitation rates are still unknown. In this study, the status of blood glucose and interleukin-1beta (IL-1beta) between rapid and slow fluid resuscitation for hemorrhagic shock were compared. Twenty-four male Wistar-Kyoto rats were used in the study. The volume of blood withdrawal was 40% of the total blood volume of a rat and fluid resuscitation was given immediately after blood withdrawal. Rats were randomly divided into control group, 10 minutes rapid group, and 12 hours slow group. Our findings show that a 10 minutes rapid infusion may provide the blood pressure and heart rate stability at early phase of hemorrhage. Moreover, rapid infusion decreases blood glucose and IL-1beta at 1, 3, 6, 9, 12, 18, and 48 hours after fluid resuscitation. However, the levels of glucose and IL-1beta were not different between control and the slow group. Rapid fluid resuscitation ameliorates hyperglycemia and inflammatory response after hemorrhagic shock. Knowledge of advanced treatment will facilitate optimal care delivery for patients with hemorrhagic shock.

Effect of electro-acupuncture at Zusanli points on gastric emptying and plasma contents of NO and MTL during oral fluid resuscitation of hemorrhagic shock in rats with blood volume loss

Effect of electro-acupuncture at Zusanli points on gastric emptying and plasma contents of NO and MTL during oral fluid resuscitation of hemorrhagic shock in rats with blood volume loss

Influencing factors for gastric emptying rate during oral fluid resuscitation of hemorrhagic shock in rats with 40% blood volume loss

Influencing factors for gastric emptying rate during oral fluid resuscitation of hemorrhagic shock in rats with 40% blood volume loss

Response to “Delayed Fluid Resuscitation in Hemorrhagic Shock Induces Proinflammatory Cytokine Response”

Response to “Delayed Fluid Resuscitation in Hemorrhagic Shock Induces Proinflammatory Cytokine Response”

HYPERTONIC 15% SODIUM PYRUVATE OFFERS NO INITIAL RESUSCITATION ADVANTAGE COMPARED WITH 8% HYPERTONIC NACL IN SHEEP WITH MULTIPLE HEMORRHAGES

Initial fluid resuscitation of hemorrhagic shock might be enhanced by the infusion of monocarboxylate-energy substrates. We evaluated hemodynamics, metabolism, and fluid dynamics for initial resuscitation of hemorrhage using small volume 15% sodium pyruvate solution (HPY) compared with osmotically matched 8% hypertonic saline (HS). Instrumented conscious sheep were hemorrhaged 25 mL/kg at time zero through 15 min (T0-T15) and 5 mL/kg for 5 min at T50 to T55 and T70 to T75. Fluid resuscitation from T30 to T180 was performed by a computer-controlled closed-loop system, which titrated infusion rate to a mean arterial pressure of 90 mmHg. Initial infusion was 4 mL/kg of either HPY or HS, followed by the administration of lactated Ringer. Both HPY and HS restored cardiac index similarly. The lactate/pyruvate ratio was used to assess metabolic debt and was significantly higher (T180), whereas oxygen delivery was significantly lower (T120) with HPY versus HS. Total fluid administered was similar, with 43.7 +/- 6.2 mL/kg for HPY and 39.4 +/- 6.8 mL/kg for HS. Plasma volume was similarly increased and approached baseline values for both groups. Initial resuscitation with small volume HPY offered no hemodynamic or metabolic advantage compared with small volume HS when the fluids were infused to an end point pressure.

Delayed Fluid Resuscitation in Hemorrhagic Shock Induces Proinflammatory Cytokine Response

This study is designed to determine the effects of delayed fluid resuscitation on the hemodynamic changes and cytokine responses in a rat model of hemorrhagic shock. Wistar male rats (n=40; 8/group) were subjected to a volume-controlled hemorrhagic shock for 30 minutes and received lactated Ringer's solution resuscitation as follows: (1) immediate resuscitation, (2) delayed resuscitation begun 30 minutes after hemorrhage (delayed resuscitation 30), (3) delayed resuscitation begun 45 minutes after hemorrhage (delayed resuscitation 45), (4) delayed resuscitation begun 60 minutes after hemorrhage (delayed resuscitation 60), or (5) unresuscitated group, induction of hemorrhagic shock without resuscitation. Hemodynamic parameters were recorded and blood samples were collected at 0 minutes and at 30, 90, 150, 210, 270, and 330 minutes after hemorrhage for plasma levels of interleukin (IL) 6, IL-10 and tumor necrosis factor alpha (TNF-alpha). Repeated-measurement analysis of variance was used for within- and between-groups comparisons. Final mean blood pressure, serum levels of lactate, and hematocrit levels after immediate resuscitation were not different from those in the delayed resuscitation groups. Comparing with the unresuscitated group, TNF-alpha and IL-6 concentrations were significantly higher, whereas IL-10 concentrations were significantly lower in the 4 resuscitation groups. Circulating concentrations of IL-6 were significantly higher in the delayed resuscitation 45 (P<.001) and delayed resuscitation 60 (P<.001) groups. Circulating concentrations of TNF-alpha and IL-10 in the 4 resuscitation groups were comparable throughout the experimental period. Delayed fluid resuscitation in hemorrhagic shock induces increased production of proinflammatory cytokines, and the release of cytokine was correlated with the time delayed for resuscitation.

Effects of arginine vasopressin during resuscitation from hemorrhagic hypotension after traumatic brain injury*

Two series of experiments were designed to evaluate whether early arginine vasopressin improves acute outcome following resuscitation from traumatic brain injury and severe hemorrhagic hypotension. Prospective randomized, blinded animal study. University laboratory. Thirty-three swine. In series 1 (n = 19), after traumatic brain injury with hemorrhage and 12 mins of shock (mean arterial pressure approximately 20 mm Hg), survivors (n = 16) were initially resuscitated with 10 mL/kg crystalloid. After 30 mins, crystalloid and blood with either 0.1 unit x kg(-1) x hr(-1) arginine vasopressin or placebo was titrated to a mean arterial pressure target >or=60 mm Hg. After 90 mins, all received mannitol and the target was cerebral perfusion pressure >or=60 mm Hg. To test cerebrovascular function, 7.5% inhaled CO2 was administered periodically. In series 2 (n = 14), the identical protocol was followed except the shock period was 20 mins and survivors (n = 10) received a bolus of either arginine vasopressin (0.2 units/kg) or placebo during the initial fluid resuscitation. In series 1, by 300 mins after traumatic brain injury with arginine vasopressin (n = 8) vs. placebo (n = 8), the fluid and transfusion requirements were reduced (both p < .01), intracranial pressure was improved (11 +/- 1 vs. 23 +/- 2 mmHg; p < .0001), and the CO2-evoked intracranial pressure elevation was reduced (7 +/- 2 vs. 26 +/- 3 mm Hg, p < .001), suggesting improved compliance. In series 2, with arginine vasopressin vs. placebo, cerebral perfusion pressure was more rapidly corrected (p < .05). With arginine vasopressin, five of five animals survived 300 mins, whereas three of five placebo animals died. The survival time with placebo was 54 +/- 4 mins (p < .05 vs. arginine vasopressin). Early supplemental arginine vasopressin rapidly corrected cerebral perfusion pressure, improved cerebrovascular compliance, and prevented circulatory collapse during fluid resuscitation of hemorrhagic shock after traumatic brain injury.

Endpoints for fluid resuscitation in hemorrhagic shock.

Vigorous intravenous fluid resuscitation has become widely accepted as the optimum management of hemorrhagic shock in trauma. There is now, however, sufficient evidence for this position to be reviewed. Hypotensive or delayed resuscitation has been postulated as a means by which the mortality associated with treatment can be reduced. It has been suggested that overresuscitation with intravenous fluids may worsen hemorrhage. This article discusses the possible adverse effects of "conventional" resuscitation and examines the evidence to support alternative treatment modalities.