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Resuscitation from hemorrhagic shock with Ringer's ethyl pyruvate solution improves survival and ameliorates intestinal mucosal hyperpermeability in rats.

We previously showed that pretreatment with a solution of ethyl pyruvate in a calcium-containing balanced salt solution, Ringer's ethyl pyruvate solution (REPS), ameliorates gut mucosal damage in rats subjected to mesenteric ischemia/reperfusion. Herein, we sought to test the hypothesis that REPS would be beneficial as a post-treatment (i.e., resuscitation fluid) for hemorrhagic shock. Anesthetized Sprague-Dawley rats were bled to a mean arterial pressure (MAP) of 40 mmHg until 40% of shed blood was returned. The animals then were resuscitated over 60 min with the remaining shed blood plus twice the shed blood volume as either Ringer's lactate solution (RLS) or REPS. In Experiment 1, RLS or REPS was then infused for 3 h more (or until death) at 3 mL/kg/h. Read-outs were post-resuscitation ileal mucosal permeability to fluorescein-labeled Dextran with an average molecular mass of 4000 Da (FD4) and survival. Permeability, determined just before death (MAP < 40 mmHg) or after 4 h of resuscitation, was assessed using an ex vivo everted gut sac technique and is expressed as a clearance (nL/cm/min). In Experiment 2, the read-outs were ileal FD4 permeability measured at 60 min after starting resuscitation and gut and liver malondialdehyde (MDA) formation. FD4 clearance data were logarithmically transformed prior to performing statistical analyses. In Experiment 1, 4/8 (50%) of RLS-treated rats survived 4 h after resuscitation whereas 7/7 (100%) of REPS-treated rats survived (P< 0.05). Ileal FD4 clearances were 105 +/- 30*, 85 +/- 34*, and 38 +/- 7 for all rats treated with RLS, surviving rats treated with RLS, and rats treated with REPS, respectively (the asterisk indicates P < 0.05 vs. REPS). In Experiment 2, ileal FD4 clearances were 71 +/- 13* and 34 +/- 8 for rats treated with RLS and REPS (n = 5 each), respectively. Post-resuscitation levels of MDA in the ileum and liver were significantly lower in rats treated with REPS as compared with RLS. Resuscitation with REPS, a stable and nontoxic antioxidant solution, improves survival and ameliorates ileal mucosal permeability in a rat model of severe hemorrhagic shock.

Animals↗

Targeted resuscitation strategies after injury.

PURPOSE OF REVIEW: The management of the traumatically injured patient has evolved during the past half century despite continually high morbidity and mortality rates. The management of the trauma victim requires timely intervention and damage control in an attempt to maintain normal hemodynamic parameters and adequate systemic perfusion. There is a fine balance between oxygen delivery and consumption, and when this is perturbed, oxygen debt may ensue. The presence of ongoing oxygen debt is rather deleterious, resulting in an inflammatory cascade that can lead to multisystem organ dysfunction. The rapid identification and restoration of oxygen debt are central to the resuscitation of the critically ill patient, be it the result of sepsis or trauma. RECENT FINDINGS: Resuscitation end points have evolved that allow the physician to more rapidly identify a perturbation between oxygen delivery and consumption. Moreover, end points allow uniformity in gauging the adequacy of resuscitation: preventing under- and overresuscitation and serving as a basis to compare outcome measures in resuscitation trials. Recent technologic advances have allowed a greater wealth of clinical data that can be obtained via less invasive means. Examples of this include esophageal Doppler monitoring, sublingual capnography, orthogonal polarization spectral imaging, and lithium dilution cardiac output determinations. These devices can be used in concert with more traditional resuscitation end points (ie, lactate and base deficit) to maximize oxygen delivery and correct tissue dysoxia. In addition, the management of hemorrhagic shock is continuing to evolve and challenge the dogmatic practices of normotensive resuscitation. SUMMARY: This review addresses (1) resuscitation end points to optimize cardiac function, (2) resuscitation end points to assess the microcirculation, (3) recent developments in the management of hypotensive hemorrhagic shock, and (4) the translation of early goal-directed therapy from septic shock to use in trauma. Past findings are reflected on and direction for future investigation and clinical practice based on recent clinical advances is provided.

Acidosis↗

Update on pediatric resuscitation drugs: high dose, low dose, or no dose at all.

PURPOSE OF REVIEW: Pediatric resuscitation has been a topic of discussion for years. It is difficult to keep abreast of changing recommendations, especially for busy pediatricians who do not regularly use these skills. This review will focus on the most recent guidelines for resuscitation drugs. RECENT FINDINGS: Three specific questions will be discussed: standard dose versus high-dose epinephrine, amiodarone use, and the future of vasopressin in pediatric resuscitation. The issue of using high-dose epinephrine for cardiopulmonary resuscitation refractory to standard dose epinephrine has been a topic of debate for many years. Recently, a prospective, double-blinded study was performed to help settle the debate. These results will be reviewed and compared with previous studies. Amiodarone is a medication that was added to the pediatric resuscitation algorithms with the most recent recommendations from the American Heart Association in 2000. Its use and safety will also be discussed. Another topic that is resurfacing in resuscitation is the use of vasopressin. Its mechanism and comparisons to other agents will be highlighted, although its use in the pediatric patient has not been thoroughly studied. SUMMARY: Pediatric resuscitation is a constantly evolving subject that is on the mind of anyone taking care of sick children. Clinicians are continually searching for the most effective methods to resuscitate children in terms of short- and long-term outcomes. It is important to be familiar with not only the agents being used but also the optimal way to use them.

Adrenergic Agonists↗

Hypertonic saline resuscitation reduces apoptosis and tissue damage of the small intestine in a mouse model of hemorrhagic shock.

The effect of hypertonic saline resuscitation on intestinal damage and the incidence of apoptosis after hemorrhagic shock were investigated. After anesthesia, male BALB/c mice weighing 24-34 g were hemorrhaged to the mean arterial pressure of 40 +/- 5 mmHg for 90 min. Animals were randomly assigned to four groups: 1) resuscitation with 4 mL/kg of 7.5% NaCl (hypertonic saline; HS) + shed blood (SB); 2) resuscitation with two times the volume of shed blood of lactated Ringer's solution (2LR) + SB; 3) sham (catheter only); or 4) control (no treatment). Intestinal damage was graded based on the extent of the vacuolation at the basal area of the intestinal villi. Apoptosis of the small intestines was examined with the terminal deoxynucleotidyl transferase-mediated deoxyuridine 5-triphosphate nick-end labeling method and with DNA laddering. Caspase-3 activation, heat shock protein (HSP) 70, and HSP40 were assessed by western blotting. Apoptosis of the small intestine and intestinal damage were significantly lower (P < 0.01) in the HS+SB group compared with the 2LR+SB group 2 h and 6 h after hemorrhagic shock and resuscitation, respectively. This corresponded with more DNA fragmentation in the small intestine of the 2LR+SB group compared with the HS+SB group 2 h after hemorrhage and resuscitation. In addition, we observed less caspase-3 activation in the small intestine of the HS+SB group compared with the 2LR+SB group at 2 h after resuscitation. The content of HSP40 and HSP70 in the HS+SB group was similar to that in controls, but slightly decreased in the 2LR+SB group. HS resuscitation reduced intestinal damage and apoptosis after hemorrhagic shock, suggesting that HS resuscitation may improve the outcome after hemorrhagic shock by reducing apoptosis and damage to the small intestine.

Animals↗

Resuscitation with lactated ringer's does not increase inflammatory response in a Swine model of uncontrolled hemorrhagic shock.

Lactated Ringer's (LR) and normal saline (NS) are widely and interchangeably used for resuscitation of trauma victims. Studies show LR to be superior to NS in the physiologic response to resuscitation. Recent in vitro studies demonstrate equivalent effects of LR and NS on leukocytes. We aimed to determine whether LR resuscitation would produce an equivalent inflammatory response compared with normal saline (NS) resuscitation in a clinically relevant swine model of uncontrolled hemorrhagic shock. Thirty-two swine were randomized. Control animals (n = 6) were sacrificed following induction of anesthesia for baseline data. Sham animals (n = 6) underwent laparotomy and 2 h of anesthesia. Uncontrolled hemorrhagic shock animals (n = 10/group) underwent laparotomy, grade V liver injury, and blinded resuscitation with LR or NS to maintain baseline blood pressure for 1.5 h before sacrifice. Lung was harvested, and tissue mRNA levels of interleukin-6 (IL-6), granulocyte colony-stimulating factor (G-CSF), and tumor necrosis factor-alpha (TNF-alpha) were determined using quantitative reverse transcriptase polymerase chain reaction (Q-RT-PCR). Sections of lung were processed and examined for neutrophils sequestered within the alveolar walls. Cytokine analysis showed no difference in IL-6 gene transcription in any group (P = 0.99). Resuscitated swine had elevated G-CSF and TNF-alpha gene transcription, but LR and NS groups were not different from each other (P= 0.96 and 0.10, respectively). Both resuscitation groups had significantly more alveolar neutrophils present than controls (P < 0.01) and shams (P < 0.05) but were not different from one another (P= 0.83). LR and NS resuscitation have equivalent effects on indices of inflammation in the lungs in our model of uncontrolled hemorrhagic shock.

Animals↗

Early difference in tissue pH and microvascular hemodynamics in hemorrhagic shock resuscitation using polyethylene glycol-albumin- and hydroxyethyl starch-based plasma expanders.

The hamster chamber window model was subjected to hemorrhagic shock by the withdrawal of 50% of blood volume (BV). BV was restored 1 h after hemorrhage with a single volume infusion (resuscitation) of 25% BV with polyethylene glycol (PEG)-conjugated bovine serum albumin (Alb) and hydroxyethyl starch (HES). Hemorrhage, shock, and resuscitation were monitored continuously in terms of mean arterial pressure (MAP), microvascular blood flow, capillary perfusion, and tissue pH. Blood samples for laboratory parameters were taken at baseline, shock, and resuscitation. Intravascular and tissue pO2 were assessed after resuscitation, and microvascular oxygen supply and extraction were calculated and corrected for pH effect on hemoglobin saturation. Resuscitation with PEG-Alb restored systemic and microvascular parameters up to the end of the observation period (90 min). HES was identical to PEG-Alb resuscitation during the initial 10 to 15 min, but was not sustained subsequently. The trend of recovery in MAP for HES persisted beyond the time when both function capillary density and tissue pH decreased, thus MAP was not indicative of early microvascular dysfunction. Hemoglobin oxygen saturation estimation showed a significant pH dependence. However, oxygen-dependant parameters corrected for pH varied less than 10% from uncorrected data. Early differences found at the microvascular levels suggest that decisions to amend end-result of resuscitation may be short and on the order of minutes. Furthermore, PEG-Alb appears to provide early and long-term sustained systemic and microvascular recovery when used to restitute perfusion and metabolic conditions after resuscitation from hemorrhagic shock.

Animals↗

Monitoring skeletal muscle and subcutaneous tissue acid-base status and oxygenation during hemorrhagic shock and resuscitation.

Gastric tonometry correlates with the severity of blood loss during shock. However, tonometry is cumbersome, has a slow response time, and is not practical to apply in the acute resuscitation setting. We hypothesized that subcutaneous tissue (SC) and skeletal muscle (SM) pH, pCO2, and pO2 changes are comparable with changes seen in bowel tonometry during shock and resuscitation. Thirteen male mini-swine (25-35 kg; n = 4 control, n = 9 shock) underwent laparotomy and jejunal tonometry. A multisensor probe (Diametrics Medical, Roseville, MN) was placed in the carotid artery, the chest SC, and the adductor muscle of the leg (SM). PaCO2 was maintained between 40 and 45 mmHg. Shocked animals were hemorrhaged and kept at mean arterial pressure of 40 mmHg. Animals were bled until a reinfusion of >10% of the total shed blood was needed to maintain the mean arterial pressure at 40 mmHg. Animals were resuscitated with shed blood plus 2x shed volume in lactated Ringer's solution (20 min) and were observed for 3 h. The average blood loss was 47.2% +/- 8.7% of calculated blood volume. During the hemorrhagic phase, SM and SC displayed tissue acidosis (r2 = 0.951), tissue hypercapnea (r2 = 0.931), and tissue hypoxia (r2 = 0.748). Overall, pH displayed the best correlation between SM and SC during shock and resuscitation. PCO2 in the jejunum (tonometry), SM, and SC increased during decompensation. However, during resuscitation as tonometric pCO2 normalized, only SC pCO2 decreased to its baseline value, whereas the SM pCO2 decrease tended to lag behind. Bland-Altman analyses demonstrated that the variability of the tissue pH changes in SM and SC are predictable according to the phases of hemorrhage and resuscitation. Changes in tissue pH correlated during bleeding and during resuscitation among SC and SM, and these changes followed the trends in gut tonometry as well. Continuous pCO2 and pO2 monitoring in the SM and SC tissues had significant correlations during the induction of shock only. SM and SC continuous pH and pCO2 monitoring reflect bowel pCO2 values during hemorrhagic shock. The response of these indicators as potential surrogates of impaired tissue metabolism varies among tissues and according to the phases of hemorrhage or resuscitation.

Animals↗

Effects of hemorrhage and lactated Ringer's resuscitation on coagulation and fibrinogen metabolism in swine.

Hemorrhagic coagulopathy is a significant complication after traumatic injury, and much of the underlying mechanism remains unclear. We investigated the changes in fibrinogen metabolism and coagulation after a moderate hemorrhage and resuscitation. Pigs of either sex (weight, 40.9+/-0.8 kg) were anesthetized and instrumented with arterial and venous catheters and a thermodilution cardiac output catheter. Pigs were randomized into control (C; n=6), hemorrhage (H; n=6), and hemorrhage and resuscitation (H-LR; n=6) groups. Hemorrhage was induced by bleeding 35% of total blood volume for 30 min in H and H-LR groups. Resuscitation in H-LR group was performed using lactated Ringer's solution (LR) at 3 times the bled volume for 30 min. Fibrinogen metabolism was quantified using a primed constant infusion of 1-13C-phenylalanine (6 h) and d5-phenylalanine (4 h) and subsequent analysis by gas chromatograph-mass spectrometry, together with measurements of hemodynamics (hourly) and coagulation by thromboelastography (at baseline and 4 h after hemorrhage and resuscitation). Hemorrhage caused decreases in arterial pH and base excess, and an increase in arterial lactate content. Fluid resuscitation corrected these changes toward normal levels. Fibrinogen level was unchanged in C and decreased to 76%+/-4% in H and to 73%+/-3% in H-LR (both P<0.05, compared with baseline) after hemorrhage and resuscitation. Fibrinogen breakdown was increased from 3.0+/-0.4 mg kg-1 h-1 in C to 5.4+/-0.6 mg kg-1 h-1 in H and to 5.6+/-0.5 mg kg-1 h-1 in H-LR (both P<0.05, compared with control), but synthesis was unchanged. The clotting reaction time was unchanged in C and shortened to 93%+/-3% in H and to 91%+/-1% in H-LR (both P<0.05, compared with baseline). We conclude that hemorrhagic shock caused accelerated fibrinogen breakdown and coagulation. The LR resuscitation reduced tissue hypoxia indexes but did not affect the changes in fibrinogen metabolism and coagulation from hemorrhage. Thus, effective treatment of hemorrhage should include combining standard-of-care resuscitation with interventions to correct alterations in coagulation.

Animals↗

Near-infrared spectroscopy-guided closed-loop resuscitation of hemorrhage.

BACKGROUND: Endpoint resuscitation has been suggested as a better means to resuscitate penetrating injury. We performed computer-controlled closed-loop resuscitation using invasive cardiac output (CO) or noninvasive skeletal muscle oxygen saturation (SkMusSO(2)) via near infrared spectroscopy (NIRS). METHODS: Conscious sheep received a 4.0-mm aortotomy and uncontrolled hemorrhage at t = 0 min (T0) while resuscitation started at T20 using lactated Ringer's solution. RESULTS: The aortotomy rapidly decreased the mean arterial pressure (MAP) to approximately 30 mm Hg and CO to 20% to 30% of baseline. The SkMusSO(2) endpoint group required only half as much fluid through 4 hours of resuscitation as the CO endpoint group (34.9 +/- 8.4 mL/kg vs. 63.1 +/- 9.4 mL/kg). CO and MAP were lower in the SkMusSO(2) group after T60. Mean infusion volumes were 180% and 100% of the bled volume collected at autopsy in the CO and SkMusSO(2) groups. Brain and muscle oxygenation and base excess were as high or higher in the CO endpoint group. CONCLUSION: Closed-loop resuscitation with either CO or SkMusSO(2) endpoints effectively performs fluid resuscitation of severe uncontrolled hemorrhagic shock. Limited resuscitation may achieve favorable clinical results with volumes less than recommended by Advanced Trauma Life Support guidelines.

Animals↗

Low-volume resuscitation with a polymerized bovine hemoglobin-based oxygen-carrying solution (HBOC-201) provides adequate tissue oxygenation for survival in a porcine model of controlled hemorrhage.

BACKGROUND: We have shown in a previous work that HBOC-201 is able to reverse anaerobic metabolism at low volumes in a porcine model of controlled hemorrhage. On the basis of these results, we hypothesize that low-volume resuscitation with HBOC-201 in a porcine model of controlled hemorrhage provides adequate tissue oxygenation to limit end-organ damage and allow for survival of the animal. METHODS: Twenty-four Yorkshire swine (55-65 kg) were rapidly hemorrhaged to a mean arterial pressure (MAP) of 30 mm Hg, maintained hypotensive for 45 minutes, and then divided into four groups. The first group, Shed Blood (BL), was resuscitated with shed blood to baseline MAP. A second group, Shed Blood (60), underwent resuscitation for four hours at an MAP of 60 mm Hg with shed blood. The third group, LR + Blood, was resuscitated with lactated Ringer's (maximum, 40 mL/kg) followed by shed blood to baseline MAP. The final group, HBOC (60), underwent resuscitation for 4 hours at an MAP of 60 mm Hg with HBOC-201. Hemodynamic variables, urine output, blood gas analyses, lactate levels, and jejunal oximetry were followed throughout the experiment. Animals were allowed to survive and underwent necropsy on postinjury day 3. Histologic comparisons were made. Data were analyzed using analysis of variance/Duncan's multiple range test. RESULTS: All animals survived the hemorrhage/resuscitation. One animal in the LR + Blood group died on postinjury day 1. Heart rate, MAP, and arterial pH were similar between groups. Cardiac output was significantly lower throughout resuscitation in the HBOC (60) group. Jejunal oximetry was similar throughout the experiment in all groups, revealing a decline in Po2 during hemorrhage and return to baseline or near baseline during resuscitation. There was no evidence of renal dysfunction. Histologically, one animal in the LR + Blood group and four of six animals in the HBOC (60) group demonstrated mild hepatocellular damage. All other tissues examined were found to have no significant abnormalities. Elevations in serum aspartate aminotransferase levels were noted when comparing the HBOC (60) group to the Shed Blood (BL) and Shed Blood (60) groups on day 2. Significant decreases in hemoglobin levels were noted in the HBOC (60) group compared with all other groups beginning on day 2. CONCLUSION: Low-volume resuscitation with HBOC-201 provides adequate tissue oxygenation for survival in a porcine model of controlled hemorrhagic shock with no long-term organ dysfunction identified. Although some animals did show mild hepatocellular damage with elevations of aspartate aminotransferase at day 2, these findings did not appear to have clinical relevance, and the enzyme elevations were trending toward normal by the third postoperative day. Decreases in hemoglobin levels at the later time points were expected, given the half-life of the product.

Analysis of Variance↗

The role of transesophageal echocardiography in optimizing resuscitation in acutely injured patients.

BACKGROUND: The goal of resuscitation is to correct the mismatch between oxygen delivery and that of cellular demands. The pulmonary artery catheter (PAC) is frequently used to gauge the adequacy of resuscitation and guide therapy based on ventricular filling pressures. Transesophageal echocardiography (TEE) has emerged as a potential tool in assessing adequacy of acute hemodynamic resuscitation. The purpose of this study was to evaluate the role of TEE in assessing preload during ongoing volume resuscitation in trauma patients. METHODS: A retrospective review was conducted of acutely injured patients undergoing TEE during resuscitation from hemorrhagic shock from January 2002 to 2004 at a Level I trauma center. The indication for TEE was persistent hemodynamic instability in the absence of ongoing surgical hemorrhage. Variables included hemodynamic and PAC parameters, pre-TEE resuscitation volume, and vasopressor requirements. The impact of TEE findings on therapeutic decisions was evaluated. RESULTS: Twenty-five patients underwent TEE, 18 (72%) had an indwelling PAC with a mean pulmonary artery occlusion pressure of 19.3 mm Hg (range, 12-29 mm Hg) and mean cardiac index of 2.9 L/min/m2 (range, 1.6-4.6 L/min/m2). Twelve patients (48%) were receiving inotropes and/or vasopressors for hypotension at the time of TEE. Resuscitation volume within 6 hours before TEE included a mean of 6.5 L of crystalloid and 12.2 units of blood products (packed red blood cells, fresh frozen plasma, and platelets). TEE revealed left ventricular hypovolemia in 13 patients (52%) and altered therapy in 16 patients (64%), including additional volume (n = 13), addition of an inotrope (n = 4), and addition of a vasodilator (n = 1) in one patient with ventricular overdistention. Comparison of the abnormal and normal TEE groups revealed that only cardiac index was significantly different (2.6 L/min/m2 in the abnormal group vs. 3.9 L/min/m2 in the normal group; p = 0.005). Significant mitral valve regurgitation leading to valve replacement was identified in one patient. No clinically relevant pericardial effusion was identified. CONCLUSION: TEE altered resuscitation management in almost two thirds of patients. Many patients with "acceptable" pulmonary artery occlusion pressure parameters may in fact have inadequate left ventricular filling. In addition, TEE offers the advantage of direct assessment of cardiac valve competency, myocardial wall contractility, and pericardial fluid.

Adolescent↗

Small volume resuscitation with hypertonic saline is more effective in ameliorating trauma-hemorrhagic shock-induced lung injury, neutrophil activation and red blood cell dysfunction than pancreatitic protease inhibition.

BACKGROUND: Recognition of the limitations of standard crystalloid resuscitation has led to the search for alternative resuscitation strategies that might better limit the development of trauma-hemorrhage-induced organ dysfunction and systemic inflammation. Thus, the goal of this study was to compare the effects of two resuscitation strategies alone, and in combination, with those of standard resuscitation with Ringers lactate (RL). The two strategies were small volume resuscitation with hypertonic saline (HTS) and intraluminal inhibition of pancreatic proteases with the serine protease inhibitor nafamostat. METHODS: Male rats were subjected to trauma-hemorrhagic shock (T/HS) or trauma sham-shock (T/SS) and resuscitated with RL, HTS, nafamostat, or the combination of HTS and nafamostat. The T/HS model consisted of a laparotomy plus 90 minutes of shock (MAP 30 mm Hg). Three hours after the end of the shock or sham-shock period, lung permeability, pulmonary neutrophil sequestration, neutrophil activation, red blood cell deformability, and gut injury were assessed. RESULTS: Both HTS and nafamostat reduced T/HS-induced pulmonary permeability and neutrophil sequestration, as well as neutrophil activation as compared with resuscitation with RL. However, HTS was more effective than nafamostat in reducing T/HS-induced acute lung injury and neutrophil activation. Additionally, HTS, but not nafamostat, reduced T/HS-induced RBC rigidification. Lastly, gut injury after T/HS was reduced to the greatest extent by the combination of HTS plus nafamostat. CONCLUSION: Small volume resuscitation with HTS is more effective than RL and nafamostat in limiting T/HS-induced acute lung injury, neutrophil activation and red blood cell injury.

Animals↗

Measurement of acid-base resuscitation endpoints: lactate, base deficit, bicarbonate or what?

PURPOSE OF REVIEW: Inadequate oxygen delivery to the tissues frequently results in significant metabolic acidosis. The resultant cellular and organ dysfunction can increase morbidity, mortality and hospital stay. Early diagnosis of shock can lead to early resuscitation efforts that can prevent ongoing tissue injury. This review focuses on the metabolic, hemodynamic and regional perfusion endpoints utilized in the diagnosis of metabolic acidosis resulting from shock. Resuscitation strategies aimed at supranormal oxygen delivery will be discussed. RECENT FINDINGS: Serum pH, lactate, base deficit and bicarbonate have all been extensively studied as clinical markers of metabolic acidosis in shock. While their trend helps guide resuscitation, no single marker or specific value can be utilized to guide resuscitation for all patients. Hemodynamic parameters and regional tissue endpoints are designed to identify compensated shock before it progresses to uncompensated shock. Resuscitation strategies initiated in the early phases of shock can reduce complications and death. Efforts to resuscitate patients to supranormal oxygen delivery endpoints have demonstrated mixed success, with several notable complications. SUMMARY: Despite the large number of endpoints available to the clinician, none are universally applicable and none have independently demonstrated improved survival when guiding resuscitation. Patients who respond well to initial resuscitation efforts demonstrate a survival advantage over nonresponders.

Acidosis↗

'Do not attempt resuscitation' decision-making: a study exploring the attitudes and experiences of nurses.

At the time of the research being undertaken, a policy regarding resuscitation decisions did not exist at a local hospital. However, it was proposed that a new 'do not attempt resuscitation' policy should be implemented. Nurses' attitudes to, and experiences of, the communication involved in 'do not attempt resuscitation' decision-making were explored and compared with five variables (nurses' age, nurses' grade, years of nursing, area of nursing practice and length of nursing experience on current ward). Seventy-eight qualified nurses, who made up a convenience sample, participated in the study. An adapted questionnaire was used to explore nurses' attitudes to, and experiences of, 'do not attempt resuscitation' decision-making. The findings suggested that nurses' attitudes did generally concur with the guidelines outlined in the new policy. However, in practice, there were many disparities between nurses' experiences of current 'do not attempt resuscitation' decision-making and the policy's guidelines. There were no significant differences between nurses' attitudes to current 'do not attempt resuscitation' decision-making and the five variables. However, there was one significant difference identified between nurses' experiences and the area of nursing practice (p=0.008). To adhere to the principles of the forthcoming 'do not attempt resuscitation' policy at the local hospital, the research findings have suggested that changes need to occur to both nurses' attitudes to and nurses' experiences of current 'do not attempt resuscitation' decision-making.

Adult↗

Antenatal counselling, resuscitation practices and attitudes among Australian neonatologists towards life support in extreme prematurity.

A questionnaire survey of Australian neonatologists was conducted to ascertain their antenatal counselling and resuscitation practices, and attitudes towards life support in the extremely preterm infant. This study showed that in antenatal parental counselling, whether a paediatrician was given the opportunity to participate depends on the gestation at the time of the threatened preterm delivery The counselling employed almost invariably covered mortality and morbidity. The obstetrician's opinion was considered to be of utmost importance. Both financial and moral obligations were found to be of little importance in counselling and resuscitation. Only one-third of institutions had guidelines for limiting resuscitation. The onus remained on the neonatologists concerning which infant to resuscitate, and the level of the resuscitation to be conducted. In Australia, resuscitation at birth was restricted to infants of 23 weeks' gestation or above, and neonatologists did not believe the legal system has a role to play in limiting or mandating resuscitation of extremely preterm infants. Neither were they concerned with the threat of litigation when they decide to limit resuscitation. The majority of neonatologists agreed with their institution's approach to life support in extremely preterm infants. One grey area was the question of withholding assisted feeding in an infant for which the decision to withdraw life support has been made. Australia lacked a current consensus policy on selective non-treatment. The establishment of national guidelines would be helpful to aid Australian obstetricians and neonatologists in their clinical practice.

Adult↗

Physicians' neonatal resuscitation of extremely low-birth-weight preterm infants.

PURPOSE: To examine the perceptions of physicians who make delivery room decisions to resuscitate extremely low-birth-weight (ELBW) neonates at marginal viability. Nurses, parents, economists, and ethicists have questioned resuscitation of ELBW neonates, many of whom experience high levels of morbidity and mortality. Yet no systematic studies were found that addressed physicians' perceptions and delivery room decisions. DESIGN: Descriptive, using naturalistic inquiry. A national U.S. convenience sample was obtained in 1996-1997 of 54 physicians in five perinatal subspecialties who resuscitated ELBW neonates. METHODS: Tape-recorded and transcribed interviews were analyzed using NUD*IST software and line-by-line constant comparison. FINDINGS: Despite awareness of the high morbidity and mortality, 96% of the physicians offered resuscitation to all ELBW neonates in the delivery room. The main factors affecting their decisions were "the role of physician;" having been "trained to save lives;" the belief that "if called, I resuscitate;" the inability to determine gestational age; requests from parents to "do everything;" and the need to move from a "chaotic" delivery room to a controlled neonatal intensive care unit. Six major themes were: role expectation, uncertainty, awareness, internal and external forces, burden, and continuing quandaries. Physicians were burdened by the devastated and dying babies, by their inability to predict which neonates had a chance for intact survival, and by conflicts with colleagues about viability. Statistical probability of survival, legal constraints, and cost of care did not appear to affect greatly their decisions. Physicians asked that society and national policy makers set parameters for resuscitation. CONCLUSIONS: The American Academy of Pediatrics' Neonatal Resuscitation Protocol needs revision to delineate the ethical criteria for resuscitation. Early prenatal education for families which clearly teaches the margins of viability and outcomes of early deliveries is also recommended. Physicians must be supported in changing the recessitation paradigm.

Decision Making↗

Resuscitation of severe uncontrolled hemorrhage: 7.5% sodium chloride/6% dextran 70 vs 0.9% sodium chloride.

OBJECTIVES: Resuscitation studies of hypertonic saline using controlled and uncontrolled hemorrhage models yield conflicting results with regard to efficacy. These disparate results reflect the use of models and resuscitation regimens that are not comparable between studies. This study evaluated the effects of comparable and clinically relevant resuscitation regimens of 7.5% sodium chloride/6% dextran 70 (HSD) and 0.9% sodium chloride (NS) in a near-fatal uncontrolled hemorrhage model. METHODS: Thirty-six swine (14.2 to 21.4 kg) with 4-mm aortic tears were bled to a pulse pressure of 5 mm Hg (40-45 mL/kg). The animals were resuscitated with either NS or HSD administered in volumes that provided equivalent sodium loads at similar rates. Group II (n = 12) was resuscitated with 80 mL/kg of NS at a rate of 4 mL/kg/min. Group III (n = 12) received 9.6 mL/kg of HSD at a rate of 0.48 mL/kg/min. In both groups, crystalloid resuscitation was followed by shed blood infusion (30 mL/kg) at a rate of 2 mL/kg/min. Group I (controls; n = 12) were not resuscitated. RESULTS: One-hour mortality was significantly greater in group I (92%) as compared with group II (33%) and group III (33%) (Fisher's exact test; p = 0.004). Intraperitoneal hemorrhage was significantly greater in group II (34 +/- 20 mL/kg) and group III (31 +/- 13 mL/ kg) as compared with group I (5 +/- 2 mL/kg) (ANOVA; p < 0.05). There was no significant difference in hemodynamic parameters between groups II and III. CONCLUSION: In this model of severe uncontrolled hemorrhage, resuscitation with HSD or NS, administered in volumes that provided equivalent sodium loads at similar rates, had similar effects on mortality, hemodynamic parameters, and hemorrhage from the injury site.

Animals↗

Effects of delaying fluid resuscitation on an injury to the systemic arterial vasculature.

OBJECTIVES: To determine the effects of delaying fluid on the rate of hemorrhage and hemodynamic parameters in an injury involving the arterial system. METHODS: Twenty-one adult, anesthetized sheep underwent left anterior thoracotomy and transection of the left internal mammary artery. A chest tube was inserted into the thoracic cavity to provide a continuous measurement of blood loss. The animals were randomly assigned to one of three resuscitation protocols: 1) no fluid resuscitation (NR), 2) standard fluid resuscitation (SR) begun 15 minutes after injury, or 3) delayed fluid resuscitation (DR) begun 30 minutes after injury. All of the animals in the two resuscitation groups received 60 mL/kg of lactated Ringer's solution over 30 minutes. Blood loss and hemodynamic parameters were measured throughout the experiment. RESULTS: Total hemorrhage volume (mean +/- SD) at the end of the experiment was significantly lower (p = 0.006) in the NR group (1,499 +/- 311 mL) than in the SR group (3,435 +/- 721 mL) or the DR group (2,839 +/- 1549 mL). Rate of hemorrhage followed changes in mean arterial pressure in all groups. Hemorrhage spontaneously ceased significantly sooner (p = 0.007) in the NR group (21 +/- 14 minutes) and the DR group (20 +/- 15 minutes) than in the SR group (54 +/- 4 minutes). In the DR group, after initial cessation of hemorrhage, hemorrhage recurred in five of six animals (83%) with initiation of fluid resuscitation. Maximum oxygen (O2) delivery in each group after injury was as follows: 101 +/- 34 mL O2/kg/min at 45 minutes in the DR group, 51 +/- 20 mL O2/kg/min at 30 minutes in the SR group, and 35 +/- 8 mL O2/kg/min at 60 minutes in the NR group. CONCLUSIONS: Rates of hemorrhage from an arterial injury are related to changes in mean arterial pressure. In this animal model, early aggressive fluid resuscitation in penetrating thoracic trauma exacerbates total hemorrhage volume. Despite resumption of hemorrhage from the site of injury, delaying fluid resuscitation results in the best hemodynamic parameters.

Animals↗