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PubMed1998

Hypertonic saline resuscitation diminishes lung injury by suppressing neutrophil activation after hemorrhagic shock.

UNLABELLED: Hypertonic saline (HS) resuscitation after hemorrhage and sepsis has been shown to markedly reduce the development of lung injury in animals, compared with traditional resuscitation with lactated Ringer's (LR). These experiments examined the effect of HS on lung injury after hemorrhage without sepsis. The effects of HS and LR resuscitation on neutrophil trafficking, neutrophil adhesion, and neutrophil oxidative burst were studied. METHODS: BALB/c mice were hemorrhaged to a mean arterial pressure of 40 torr for 1 h. Animals were resuscitated with shed blood and either 4 mL/kg of 7.5% HS or LR in twice the volume of the shed blood. Lung histology was examined 24 h after hemorrhage. Lung myeloperoxidase content and bronchoalveolar lavage fluid neutrophil counts were obtained. Peripheral blood smears were obtained to determine the neutrophil percentage. Peripheral blood neutrophil CD11b expression and neutrophil H2O2 production were assayed by flow cytometry. RESULTS: HS animals had less lung injury than LR animals. The mean myeloperoxidase activity in HS versus LR animals was 1.79+/-1.33 U/100 mg versus 3.0+/-1.33 U/100 mg, respectively. The percentage of neutrophils in the bronchoalveolar lavage fluid of HS animals (3.8%+/-.8) was significantly less than that of LR animals (10.8%+/-2.1). This corresponded to a significantly higher peripheral blood neutrophil count in HS animals compared with LR animals, 41% vs. 20%, respectively. There was no difference in neutrophil expression of the CD11b integrin between the HS and LR groups. The neutrophils of LR animals had basal H2O2 production that was 107% greater than that of controls; HS suppressed this hemorrhage-induced activation by > 60%. HS resuscitation after hemorrhagic shock protects against the development of lung injury. This protection is due, in part, to suppression of the hemorrhage-induced neutrophil oxidative burst. HS resuscitation offers immunomodulatory potential after hemorrhagic shock.

Animals↗
PubMed1999

Inhibition of poly(ADP-ribose) synthetase improves vascular contractile responses following trauma-hemorrhage and resuscitation.

Hyporeactivity of vessels to constrictor agents is thought to contribute to cardiovascular decompensation following trauma-hemorrhage and resuscitation. In this study, we determined if inhibition of poly(ADP-ribose) synthetase (PARS) activity prevented the development of vascular hyporeactivity in rats following trauma-hemorrhage and resuscitation. Trauma consisted of a laparotomy that was closed and rats were hemorrhaged into a reservoir containing citrate to 40 mm Hg for 90 min. Resuscitation included 2/3 of the shed blood plus 2 1/3 of the shed volume as Ringer's lactate. Sham animals received the laparotomy and were time-matched. Induction of iNOS was assessed by reverse transcription-polymerase chain reaction (RT-PCR). Aortic rings isolated 6 h after the initiation of hemorrhage (4.5 h after resuscitation) showed decreased responsiveness to norepinephrine (peak developed tension 0.31+/-0.01 g/mg tissue) compared with sham rings (0.43+/-0.02 g/mg tissue), but no change in EC50 for this response (approximately 5x10(-8) M). Addition of the PARS inhibitor, 3-aminobenzamide, at the onset of resuscitation prevented the decrease in response of aortic rings. The addition of the structural analogue, 3-aminobenzoic acid, which does not inhibit PARS, did not prevent the decrease in vascular reactivity. These agents did not alter vascular responses to norepinephrine in sham animals. iNOS induction was not associated with depressed contractile function. These results indicate that decreased vascular reactivity was prevented by inhibition of PARS and that PARS activation was independent of iNOS induction following trauma-hemorrhage and resuscitation.

Animals↗
PubMed2002

Resuscitation from severe hemorrhagic shock after traumatic brain injury using saline, shed blood, or a blood substitute.

The original purpose of this study was to compare initial resuscitation of hemorrhagic hypotension after traumatic brain injury (TBI) with saline and shed blood. Based on those results, the protocol was modified and saline was compared to a blood substitute, diaspirin cross-linked hemoglobin (DCLHb). Two series of experiments were performed in anesthetized and mechanically ventilated (FiO2 = 0.4) pigs (35-45 kg). In Series 1, fluid percussion TBI (6-8 ATM) was followed by a 30% hemorrhage. At 120 min post-TBI, initial resuscitation consisted of either shed blood (n = 7) or a bolus of 3x shed blood volume as saline (n = 13). Saline supplements were then administered to all pigs to maintain a systolic arterial blood pressure (SAP) of >100 mmHg and a heart rate (HR) of <110 beats/min. In Series 2, TBI (4-5 ATM) was followed by a 35% hemorrhage. At 60 min post-TBI, initial resuscitation consisted of either 500 mL of DCLHb (n = 6) or 500 mL of saline (n = 5). This was followed by saline supplements to all pigs to maintain a SAP of >100 mmHg and a HR of <110 beats/min. In Series 1, most systemic markers of resuscitation (e.g., SAP, HR, cardiac output, filling pressures, lactate, etc.) were normalized, but there were 0/7 vs. 5/13 deaths within 5 h (P = 0.058) with blood vs. saline. At constant arterial O2 saturation (SaO2), mixed venous O2 saturation (SvO2), cerebral perfusion pressure (CPP), and cerebral venous O2 saturation (ScvO2) were all higher, intracranial pressure (ICP) was lower, and CO2 reactivity was preserved with blood vs. saline (all P < 0.05). In Series 2, SAP, ICP, CPP, and lactate were higher with DCLHb vs. saline (all P< 0.05). Cardiac output was lower even though filling pressure was markedly elevated with DCLHb vs. saline (both P< 0.05). Neither SvO2 nor cerebrovascular CO2 reactivity were improved, and ScvO2 was lower with DCLHb vs. saline (P < 0.05). All survived at least 72 h with neuropathologic changes that included sub-arachnoid hemorrhage, midline cerebellar necrosis, and diffuse axonal injury. These changes were similar with DCLHb vs. saline. Thus, whole blood was more effective than saline for resuscitation of TBI, whereas DCLHb was no more, and according to many variables, less effective than saline resuscitation. These experimental results are comparable to those in a recent multicenter trial using DCLHb for the treatment of severe traumatic shock. Further investigations in similar experimental models might provide some plausible explanations why DCLHb unexpectedly increased mortality in patients.

Animals↗
PubMed2003

Enalaprilat improves systemic and mesenteric blood flow during resuscitation from hemorrhagic shock in dogs.

We investigated the systemic and mesenteric cardiovascular effects of administering enalaprilat during resuscitation from hemorrhage. Dogs were hemorrhaged (mean arterial pressure [MAP] 40-45 mmHg for 30 min, then 30-35 mmHg for 30 min) and were then resuscitated with intermittent lactated Ringer's solution (200 mL/kg/h during first 40 min, and 60 mL/kg/h during the following 130 min, MAP 75-80 mmHg). A constant-rate infusion of saline with or without enalaprilat (0.02 mg/kg/h) was initiated after 40 min of resuscitation. Blood flows declined with hemorrhage, increased with resuscitation, and then declined during the initial 40 min of resuscitation. Enalaprilat administration resulted in blood flow increases not seen in the controls (ending values for cardiac index: 2.8 +/- 0.4 L/min/m2 vs. 1.6 +/- 0.3 L/min/m2; celiac arterial flow 314 +/- 66 L/min/m2 vs. 139 +/- 13 mL/min/m2; and portal venous flow 596 +/- 172 L/min/m2 vs. 414 +/- 81 mL/min/m2 for enalaprilat versus controls, respectively). The greater flows with enalaprilat appeared to be due to prevention of the increases in afterload noted in the controls (ending arterial elastance values 3.73 +/- 0.97 mmHg/m2/mL vs. 7.74 +/- 1.80 mmHg/m2/mL for enalaprilat versus controls, respectively). We conclude that administration of a constant-rate infusion of enalaprilat during resuscitation can be used to improve systemic and mesenteric blood flow.

Animals↗
PubMed2003

Ethanol intoxication and lactated Ringer's resuscitation prolong hemorrhage-induced lactic acidosis.

Ethanol (EtOH) blunts the respiratory and metabolic compensation during hemorrhage, resulting in a more severe lactic acidemia. We hypothesized that lactated Ringer's (LR) resuscitation may exacerbate this lactic acidemia. Male guinea pigs were implanted with arterial and venous catheters. Two days after catheter placement, conscious animals were injected intraperitoneally with 1 g/kg EtOH, 0.3 g/kg EtOH, or an equal volume of water 30 min before hemorrhage (60% of estimated blood volume). After 30 min of hemorrhagic shock, animals were resuscitated with isotonic saline (S) or LR at 1 mL/min (three times shed blood volume). Mean arterial blood pressure (MABP) was not affected by pretreatment with either dose of EtOH, but was significantly decreased by hemorrhage in all groups. Both S and LR resuscitation slightly increased MABP, but neither restored it to prehemorrhage values. Blood lactate levels increased in all groups during hemorrhage and remained elevated for 3 h in animals pretreated with 1 g/kg EtOH. In the group pretreated with 0.3 g/kg EtOH, pH decreased during shock but returned to prehemorrhage levels during the resuscitation period. Resuscitation with S returned pH to prehemorrhage values in animals pretreated with 1.0 g/kg EtOH. Resuscitation with LR did not exacerbate, but did prolong, the lactic acidemia after shock in animals pretreated with 1.0 g/kg EtOH. Administration of additional lactate during intoxication and hypovolemia for hemodynamic stabilization before blood transfusion may exacerbate a metabolic stress.

Acidosis↗
PubMed2000

Does witnessed cardiopulmonary resuscitation alter perceived stress in accident and emergency staff?

The aim of this study was to ascertain if the presence of patients' relatives during cardiopulmonary resuscitation altered perceived symptoms of stress in accident and emergency personnel participating in resuscitation attempts. An anonymous structured questionnaire survey of all accident and emergency staff participating in non-traumatic adult cardiopulmonary resuscitation was designed to elicit symptoms of an acute stress reaction within 24 hours based on ICD-10 diagnostic criteria. One hundred and fourteen staff replies were received, a reply rate of 89%. Twenty-five replies had two or more symptoms of an acute stress reaction. The grade or role of the staff member had no influence on the presence of stress symptoms. There was no difference in rates of reporting between staff resuscitating in the presence or absence of relatives. It is concluded that the presence of relatives witnessing resuscitation attempts does not affect self-reported stress symptoms in staff participating in resuscitation attempts.

Acute Disease↗
PubMed2001

Low-volume fluid resuscitation for presumed hemorrhagic shock: helpful or harmful?

For the past 4 decades, the standard approach to the trauma victim who is hypotensive from presumed hemorrhage has been to infuse large volumes of fluids as early and as rapidly as possible. The goals of this treatment strategy are rapid restoration of intravascular volume and vital signs towards normal, and maintenance of vital organ perfusion. The most recent laboratory studies and the only clinical trial evaluating the efficacy of these guidelines however, suggest that in the setting of uncontrolled hemorrhage, today's practice of aggressive fluid resuscitation may be harmful, resulting in increased hemorrhage volume and subsequently greater mortality. This has been demonstrated in animal models representative of penetrating trauma as well as those representative of blunt trauma. The data strongly suggest that limited or hypotensive resuscitation may be preferable for the trauma victim with the potential for ongoing uncontrolled hemorrhage. Limited resuscitation provides a mechanism of avoiding the detrimental effects associated with early aggressive resuscitation, while maintaining a level of tissue perfusion that although decreased from the normal physiologic range is adequate for short periods. Large randomized clinical trials are necessary to confirm this new laboratory data. Future research should focus on developing resuscitation methods that may actually enhance tissue perfusion during limited resuscitation and therefore offset its potential detrimental effects.

Animals↗
PubMed2003

Cardiopulmonary Resuscitation Guidelines 2000 update: what's happened since?

PURPOSE OF REVIEW: To examine the literature for new resuscitation science since the publication of the Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiac Care. RECENT FINDINGS: The two and a half years since the publication of the Guidelines 2000 have seen the advent of a number of new and important resuscitation studies. Such studies highlight the importance of simplification of cardiopulmonary resuscitation techniques and guidelines, including the elimination of the layperson pulse check and the need for a simple form of basic life support cardiopulmonary resuscitation that decreases interruptions of chest compressions. Automatic external defibrillators, even in the hands of nontraditional first responders, are effective and safe. A second prospective, randomized clinical trial of amiodarone for refractory ventricular fibrillation has again shown positive results in improving survival to hospital admission. Finally, mild hypothermia appears to be the first effective therapy at decreasing central nervous system injury when administered after resuscitation. SUMMARY: In this report, we review these new studies and discuss how they corroborate or alter the published 2000 guidelines.

Amiodarone↗
PubMedDate not supplied

A prospective study on the implications of a base deficit during fluid resuscitation.

An excessive base deficit (BD) and elevated serum lactate are increasingly recognized as important markers of a malperfusion state during the resuscitation of thermally injured patients. In a previous retrospective study, we found that patients with a BD less than -6 mmol/l during fluid resuscitation developed more severe systemic inflammatory response syndrome (SIRS), more frequent acute respiratory distress syndrome (ARDS), and more severe multiple organ dysfunction syndrome (MODS). The object of this study was to reexamine prospectively the relationship between the BD during fluid resuscitation and the subsequent development of SIRS, ARDS, and MODS by undertaking a prospective observational study of a cohort of consecutive burn patients. Analysis was completed on 38 patients with a mean age of 39 +/- 17 years and a mean %TBSA burn of 36 +/- 15%. The mean BD in the first 24 hours was less than -6 mmol/l in five patients (BD24 < -6 group), and was greater than -6 mmol/L in 33 patients (BD24 > -6 group). Patients in both groups were resuscitated to nearly identical endpoints of urinary output (1.2 ml/kg/hr in the BD24 < -6 group vs 1.3 ml/kg/hr in the BD24 > -6 group). Patients in the BD24 < -6 group had a trend toward a greater number of SIRS signs on the first postburn day, had a significantly higher incidence of ARDS (P =.02), and had significantly more severe MODS (P <.001) than patients in the BD24 > -6 group. The results concur with those of our previous retrospective study. Despite resuscitation to an acceptable urinary output, some burn patients develop a more extreme BD and go on to experience more severe organ dysfunction than do patients who do not generate a BD. The effect of specific correction of the BD during fluid resuscitation is not known at this time.

Adult↗
PubMed2004

Wide variation in cardiopulmonary resuscitation interruption intervals among commercially available automated external defibrillators may affect survival despite high defibrillation efficacy.

OBJECTIVE: Recent studies have associated interruptions of cardiopulmonary resuscitation imposed by automated external defibrillators (AEDs) with poor resuscitation outcome. In particular, the "hands-off" interval between precordial compressions and subsequent defibrillation shock has been implicated. We sought to determine the range of variation among current-generation AEDs with respect to this characteristic. MEASUREMENTS: Seven AEDs from six manufacturers were characterized via stopwatch and arrhythmia simulator with respect to the imposed hands-off interval. All AEDs were equipped with new batteries, and measurements were repeated five times for each AED. MAIN RESULTS: A wide variation in the hands-off interval between precordial compressions and shock delivery was observed, ranging from 5.2 to 28.4 secs, with only one AED achieving an interruption of <10 secs. Laboratory and clinical data suggest that this range of variation could be responsible for a more than two-fold variation in patient resuscitation success, an effect that far exceeds any defibrillation efficacy differences that may hypothetically exist. CONCLUSIONS: In addition to defibrillation waveform and dose, researchers should consider the hands-off cardiopulmonary resuscitation interruption interval between cardiopulmonary resuscitation and subsequent defibrillation shock to be an important covariate of outcome in resuscitation studies. Defibrillator design should minimize this interval to avoid potential adverse consequences on patient survival.

Cardiopulmonary Resuscitation↗
PubMed2006

A paradigm for inpatient resuscitation research with an exception from informed consent.

OBJECTIVE: Resuscitation research with an exception from informed consent (EFIC) has not been reported in the inpatient or pediatric setting, and little practical information exists to guide application of EFIC regulations to inpatient or pediatric research. The objective of this study was to assess the feasibility of conducting inpatient pediatric resuscitation research with EFIC using handouts to communicate with parents of potential participants and to determine how many parents would likely allow their child to participate in such research. DESIGN: Verbal questionnaire. SETTING: Pediatric intensive care units. PARTICIPANTS: Parents of pediatric intensive care unit patients. INTERVENTIONS: Three one-page handouts described proposed studies; version 1 described a trial of a new medication given during cardiac arrest, and versions 2a and 2b described of a trial of induced hypothermia, with version 2a in paragraph format and version 2b in bullet format. We asked parents of pediatric intensive care unit patients to review the handouts, and then we administered a verbal questionnaire to assess parental reactions to the handouts and to determine how many parents would allow their child to participate. MEASUREMENTS AND MAIN RESULTS: One or both parents of 91 patients were asked to participate; 100% agreed. Sixty-three percent said they would likely allow their child to participate in resuscitation research with EFIC if they were given a prospective opportunity to opt out. Parents who reviewed version 2b (bullet format) were more likely than parents who reviewed version 2a (paragraph format) to say that they would let their child participate. Parents were more supportive of a trial of induced hypothermia than of a trial of a new medication given during cardiopulmonary resuscitation. Parents endorsed conducting the community consultation process for inpatient resuscitation research with families and healthcare providers of critically ill patients. CONCLUSIONS: Inpatient pediatric resuscitation research is feasible using handouts to inform parents of a study and provide a prospective opportunity to opt out. Succinct, bullet-format handouts will yield higher participation rates than paragraph-format handouts.

Adolescent↗
PubMed2003

Complement activation during hemorrhagic shock and resuscitation in swine.

Activation of the complement (C) cascade is known to play a key role in the adverse immune consequences of hemorrhagic trauma with subsequent shock and resuscitation. However, it is not clear whether hypovolemia per se, without trauma and resuscitation, can also lead to C activation. To address this question, we studied the presence, kinetics, and cause of C activation in a porcine model of hemorrhagic shock and resuscitation in the absence of trauma. Pigs were bled to and kept at 35 mmHg for 90 min, followed by hypotensive resuscitation with different fluids and, finally, with shed blood. The animals developed severe lactic acidosis between 30 and 90 min, which was accompanied by a trend for initial rise and subsequent 40% drop of CH50/mL, indicating massive C activation even before resuscitation, i.e., before reperfusion damage could have occurred. Resuscitation with plasma expanders caused 20% additional C consumption, whereas whole blood raised CH50/mL. Plasma C5a decreased initially and then significantly increased at 60 and 180 min, whereas thromboxane B2 showed a 3-fold increase at 30 and 60 min. Plasma LPS was also increased above baseline at 90 and 180 min. In in vitro studies with pig blood, spontaneous C5a formation, as well as zymosan-induced C consumption, was significantly enhanced under the conditions of lactic acidosis. Our data suggest that lactic acidosis, endotoxemia, and possibly other ischemia-related tissue alterations act in a vicious cycle in inducing C activation and, hence, aggravation of shock. The biphasic course of CH50/mL and C5a changes may reflect yet unrecognized physiological responses to hemorrhage-related C activation.

Acidosis, Lactic↗
PubMed2006

Immune effects of resuscitation with HBOC-201, a hemoglobin-based oxygen carrier, in swine with moderately severe hemorrhagic shock from controlled hemorrhage.

HBOC-201, a hemoglobin-based oxygen carrier, improved physiologic parameters and survival in hemorrhagic shock (HS) animal models. However, resuscitation from HS and the properties of different fluids influence immune responses. The aim of this study was to determine if HBOC-201 significantly alters immune function in traumatic HS. Anesthetized pigs underwent soft tissue injury, controlled hemorrhage of 40% of blood volume, and resuscitation with HBOC-201 or Hextend, or no resuscitation. Sequential whole-blood samples were collected for analyses of leukocyte differential (hematology analyzer), T-lymphocyte subsets (CD3, CD4, and CD8) (FACS), lymphocyte adhesion marker CD49d (alpha4-integrin) expression (FACS), plasma cytokines-tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and IL-10-(ELISA), and lymphocyte apoptosis (annexin-V/propidium iodide staining) (FACS). Statistical analyses were performed by the mixed procedure. Total WBC counts decreased posthemorrhage in both resuscitation groups. Lymphocyte percentages decreased and PMN percentages increased around 4 h posthemorrhage in all groups. CD3 cells decreased in all groups, but CD4 and CD8 cells decreased only in the resuscitation groups. TNF-alpha levels were not detectable in any groups. IL-6 levels were similar across treatment groups (P > 0.05); however, IL-10 levels were higher in the HBOC group, as early as 1 h posthemorrhage (P = 0.04). Increases in lymphocytic CD49d expression levels and apoptosis occurred only in nonresuscitation and Hextend groups, respectively (P < or = 0.01). In comparison with Hextend, HBOC-201 had no significant adverse or beneficial effects on immune function in this model of moderately severe HS in swine, suggesting that it may be safe as a resuscitation fluid in HS patients.

Animals↗
PubMed2006

The cellular, metabolic, and systemic consequences of aggressive fluid resuscitation strategies.

Increasing evidence has demonstrated that aggressive crystalloid-based resuscitation strategies are associated with cardiac and pulmonary complications, gastrointestinal dysmotility, coagulation disturbances, and immunological and inflammatory mediator dysfunction. As large volumes of fluids are administered, imbalances in intracellular and extracellular osmolarity occur. Disturbances in cell volume disrupt numerous regulatory mechanisms responsible for keeping the inflammatory cascade under control. Several authors have demonstrated the detrimental effects of large, crystalloid-based resuscitation strategies on pulmonary complications in specific surgical populations. Additionally, fluid-restrictive strategies have been associated with a decreased frequency of and shorter time to recovery from acute respiratory distress syndrome and trends toward shorter lengths of stay and lower mortality. Early resuscitation of hemorrhagic shock with predominately saline-based regimens has been associated with cardiac dysfunction and lower cardiac output, as well as higher mortality. Numerous investigators have evaluated potential risk factors for developing abdominal compartment syndrome and have universally noted the excessive use of crystalloids as the primary determinant. Resuscitation regimens that cause early increases in blood flow and pressure may result in greater hemorrhage and mortality than those regimens that yield comparable flow and pressure increases late in resuscitation. Future resuscitation research is likely to focus on improvements in fluid composition and adjuncts to administration of large volume of fluid.

Abdominal Cavity↗
PubMed2006

Bovine polymerized hemoglobin versus Hextend resuscitation in a swine model of severe controlled hemorrhagic shock with delay to definitive care.

To compare the efficacy of low-volume resuscitation with bovine polymerized hemoglobin (HBOC-201) versus hetastarch (HEX) in an intermediate severity combat-relevant hemorrhagic shock swine model with a simulated delay to hospital care. Twenty-four anesthetized pigs were hemorrhaged 55% estimated blood volume in conjunction with a 5-min rectus abdominus crush. At 20 min, pigs were resuscitated with 10 mL/kg of HBOC-201 or HEX or nothing (NON); resuscitated pigs received additional infusions (5 mL/kg) at 30, 60, 120, or 180 min if hypotension or tachycardia persisted. Pigs were monitored for a 4-h "prehospital" period. At 4-h, hospital arrival was simulated: surgical sites were repaired, blood, or saline provided, and pigs were recovered from anesthesia. Pigs were monitored for 72 h and then killed for histological evaluation. One hundred percent (8/8) of HBOC-201-, 75% (6/8) of HEX-, and 25% (2/8) of NON-resuscitated pigs survived to 72 h (P = 0.007 overall, HBOC vs. HEX P > 0.05). Mean arterial pressure and mean pulmonary arterial pressure were highest in the HBOC-201 group (P < 0.001), and HR was lowest (P < 0.001). HBOC-201- and HEX-resuscitated pigs had comparable cardiac index and prehospital fluid requirements. HBOC-201 pigs had higher transcutaneous tissue oxygen tension, P < 0.001) and lower urine output (P < 0.001). At simulated hospital arrival, no HBOC-201 pigs required additional fluids or blood transfusion. In contrast, 100% of HEX pigs required blood transfusions (P < 0.01). In this swine model of controlled hemorrhage with low-volume resuscitation and delayed definitive care, HBOC-201 pigs had improved hemodynamics, transcutaneous tissue oxygen tension, and transfusion avoidance compared with HEX.

Animals↗
PubMed2003

A review of studies on the effects of hemorrhagic shock and resuscitation on the coagulation profile.

BACKGROUND: This study reports on the results of hemorrhagic shock (HS) plus resuscitation on the coagulation profile in severely injured patients and on the role of fresh frozen plasma (FFP) supplementation in a canine HS model. CLINICAL STUDIES: Primary hemostasis (platelet plug), secondary hemostasis (fibrin clot), and fibrinolysis were assayed in 22 injured patients who received an average of 21 units of packed red blood cells (PRBCs), 16.5 L crystalloid solution, and 1.25 L FFP during operation for control of bleeding. Measurements were obtained during operation and postoperatively at 5, 15, 36, and 84 hours and at 26 days. The platelet count during operation was 113,000/mm3, decreased to a nadir of 76,000/mm3 at 48 hours, and then increased to 563,000/mm2 by convalescence. Platelets were not given with resuscitation. The bleeding times and aggregation studies mirrored platelet levels until convalescence. HS led to significant reductions in fibrinogen (factor I), factor V, and factor VIII that normalized by day 1. The fibrinogen increased to supranormal levels by day 4 through day 26. Clotting times mirrored fibrinogen, factor V, and factor VIII levels. Fibrin split products were normal during operation and increased postoperatively through day 26. The increase in fibrin split products paralleled the increase in fibrinogen. EXPERIMENTAL STUDIES: The role of FFP supplementation in HS resuscitation was tested in two separate studies. After HS, the animals were resuscitated with shed blood and crystalloid; half the animals also received FFP. FFP did not improve the coagulation factors, fibrinogen and factors II, V, VII, and VIII. Thus, routine FFP supplementation for HS in humans was abandoned. This led to unexpected postoperative bleeding that in one instance caused death. Therefore, a second controlled study was used in which the FFP was given not only during blood volume restoration but also for an additional hour during continued ongoing controlled hemorrhage without shock. The second study demonstrated that the FFP prevented the reduction in coagulation factors compared with animals not receiving FFP. Clotting times paralleled coagulation protein levels. FFP is now used to supplement HS resuscitation in humans. CONCLUSION: Resuscitation from hemorrhagic shock can be successfully implemented by restoration of blood loss with blood, crystalloid, and FFP added to maintain coagulation proteins.

Animals↗
PubMed2003

Small-volume fluid resuscitation for the far-forward combat environment: current concepts.

Hemorrhage remains the primary cause of death on the battlefield in conventional warfare. With modern combat operations leading to the likelihood of significant time delays in air evacuation of casualties and long transport times, the immediate goals of the Army's Science and Technology Objectives in Resuscitation are to develop limited- or small-volume fluid resuscitation strategies, including permissive hypotension, for the treatment of severe hemorrhage to improve battlefield survival and prevent early and late deleterious sequelae. As an example, the U.S. Army has invested much effort in the evaluation of hypertonic saline dextran (HSD) as a plasma volume expander, at one tenth to one twelfth the volume of conventional crystalloids, in numerous animal models of hemorrhage. These studies have identified HSD as a potentially useful field resuscitation fluid. In addition, preliminary studies have used HSD under hypotensive resuscitation conditions, and it has been administered through intraosseous infusion devices for vascular access. This research suggests that many of the difficulties and concerns associated with fluid resuscitation for treating significant hemorrhage in the field can be overcome. For the military, such observations have important implications toward the development of optimal fluid resuscitation strategies under austere battlefield conditions for stabilization of the combat casualty.

Dose-Response Relationship, Drug↗
PubMed2004

Bladder mucosa pH and Pco2 as a minimally invasive monitor of hemorrhagic shock and resuscitation.

BACKGROUND: Continuous monitoring of pH, Pco2, and Po2 using fiberoptic sensor technology has been proposed recently as a clinical monitor of the severity of shock and impaired tissue perfusion. Surrogates of gut tissue perfusion such as gastric tonometry, although cumbersome, have been used to indirectly quantify the degree of gut ischemia. The purpose of this study was to demonstrate the feasibility of monitoring bladder mucosa (BM) and to compare urinary bladder mucosa and proximal jejunum mucosa interstitial pH and Pco2 during hemorrhagic shock and resuscitation. METHODS: Eleven male miniature swine (25-35 kg) (control, n = 4; shock, n = 7) underwent jejunal tonometry and cystostomy. A multisensor probe was placed adjacent to the BM. Urine was diverted. Normocarbia was maintained. Animals were hemorrhaged and kept at a mean arterial pressure of 40 mm Hg. When a constant infusion was required to maintain the mean arterial pressure at 40 mm Hg (decompensation), animals were resuscitated with shed blood plus two times the shed volume in lactated Ringer's solution (20 minutes) and observed for 2 hours. RESULTS: During decompensation, BM pH values decreased significantly from 7.33 +/- 0.08 to 7.01 +/- 0.2 (p < 0.01) and recovered to 7.11 +/- 0.19 at 120 minutes after completion of resuscitation. During decompensation, BM Pco2 values increased significantly compared with baseline (from 49 +/- 6 mm Hg to 71 +/- 19 mm Hg, p < 0.05) and returned to baseline with resuscitation. Jejunum mucosa and BM interstitial Pco2 correlated throughout shock and resuscitation (r = 0.49). Bland-Altman analysis demonstrated significant differences between jejunum mucosa (intramucosal pH) and BM interstitial pH. CONCLUSION: Shock-induced changes in the Pco2 of the BM are comparable to tonometric changes in the gut. These data suggest that continuous fiberoptic multisensor probe monitoring of the BM could potentially provide a minimally invasive method for the assessment of impaired tissue perfusion of the splanchnic circulation during shock and resuscitation.

Analysis of Variance↗