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Donat R Spahn

Publications and source records attributed to Donat R Spahn.

At least 37 records · Page 2Linked to original sources
PubMed2004

Blood management in intensive care medicine: CRIT and ABC--what can we learn?

In 284 US intensive care units the CRIT study (Anemia and blood transfusion in the critically ill--Current clinical practice in the United States) assessed allogeneic red blood cell (RBC) transfusion and outcome in 4892 patients. As in the former European ABC study (Anemia and blood transfusion in the critically ill), the mean pretransfusion hemoglobin was approximately 8.5 g/dl and RBC transfusions were independently associated with an increased mortality. These studies were purely observational and, therefore, despite the finest statistical models indicating that RBC transfusions were independently associated with a higher mortality, it remains possible that this adverse outcome is not due to a harmful effect of RBC transfusion in itself, but merely reflects the fact that transfused patients were sicker to start with. The definitive call is still out, but one mechanism by which RBC transfusion might be harmful now appears less likely; namely, storage lesion. In the CRIT study, mortality was not increased in patients receiving 'old' RBCs (>14 days stored) versus 'fresh' RBCs. The effect of leukoreduction could not be assessed since mainly nonleukoreduced RBCs were transfused. The evidence is mounting, however, that RBC transfusions are efficacious only when oxygen delivery is compromised. What can be done to diminish the use of RBC transfusions, its costs and side effects in intensive care medicine? There are two important options available today: decreasing blood loss for diagnostic purposes using pediatric sampling tubes, and establishing restrictive multidisciplinary transfusion guidelines and implementing them in daily clinical practice.

Anemia↗
PubMed2004

Strategies for transfusion therapy.

Transfusion of allogeneic red blood cells (RBCs), fresh frozen plasma (FFP) and platelets is associated with risks, and outcome studies comparing liberal and restrictive transfusion regimens are lacking in surgical patients. Therefore, guidelines have been established. They recommend first maintaining normovolaemia by the use of crystalloids and colloids. RBC transfusions are recommended for haemoglobin levels < 6 g/dl and for physiological signs of inadequate oxygenation such as haemodynamic instability, oxygen extraction > 50% and myocardial ischaemia (new ST-segment depressions > 0.1 mV, new ST-segment elevations > 0.2 mV or new wall motion abnormalities in transoesophageal echocardiography). FFP transfusions are recommended for urgent reversal of anticoagulation, known coagulation factor deficiencies, microvascular bleeding in the presence of elevated (> 1.5 times normal) prothrombin time (PT) or partial thromboplastin time (PTT) and microvascular bleeding after the replacement of more than one blood volume when PT or PTT cannot be obtained. Platelet transfusions are recommended prior to major operations in patients with platelet counts < 50,000/microl, intraoperatively with microvascular bleeding at platelet counts < 50,000/microl and in the range of 50,000-100,0000/microl following cardiopulmonary bypass and in patients undergoing surgery where already minimal bleeding may cause major damage such as in neurosurgery.

Adult↗
PubMed2004

Transfusion in the cardiac patient.

Transfusion guidelines in patients with coexisting cardiac diseases are similar to the ones in patients without such comorbidity, in that allogeneic blood transfusions most often are indicated at hemoglobin levels of less than 6.0 g/dL and hardly ever at hemoglobin levels greater than 10 g/dL. In the hemoglobin range of 6 to 10 g/dL, signs of impaired oxygenation should serve as transfusion indications, and such signs may be reached at higher hemoglobin values than in healthy patients. An inadequate oxygenation may become manifest globally in the form of a general hemodynamic instability with a tendency to hypotension and tachycardia despite normovolemia or an oxygen extraction of greater than 50%. An inadequate oxygenation in the form of myocardial ischemia may be manifested by new ST-segment depressions of greater than 0.1 mV, new ST-segment elevations greater than 0.2 mV, or new wall motion abnormalities in transesophageal echocardiography. Institutional guidelines also should consider local logistic characteristics such as the level of knowledge of physician and nurse staff caring for patients and the level of surveillance possible justifying eventually higher hemoglobin transfusion triggers, particularly in the postoperative period.

Critical Care↗
PubMed2004

Prevention of atelectasis formation during the induction of general anesthesia in morbidly obese patients.

UNLABELLED: Atelectasis caused by general anesthesia is increased in morbidly obese patients. We have shown that application of positive end-expiratory pressure (PEEP) during the induction of anesthesia prevents atelectasis formation in nonobese patients. We therefore studied the efficacy of PEEP in morbidly obese patients to prevent atelectasis. Twenty-three adult morbidly obese patients (body mass index >35 kg/m(2)) were randomly assigned to one of two groups. In the PEEP group, patients breathed 100% oxygen (5 min) with a continuous positive airway pressure of 10 cm H(2)O and, after the induction, mechanical ventilation via a face mask with a PEEP of 10 cm H(2)O. In the control group, the same induction was applied but without continuous positive airway pressure or PEEP. Atelectasis, determined by computed tomography, and blood gas analysis were measured twice: before the induction and directly after intubation. After endotracheal intubation, patients of the control group showed an increase in the amount of atelectasis, which was much larger than in the PEEP group (10.4% +/- 4.8% in control group versus 1.7% +/- 1.3% in PEEP group; P < 0.001). After intubation with a fraction of inspired oxygen of 1.0, PaO(2) was significantly higher in the PEEP group compared with the control group (457 +/- 130 mm Hg versus 315 +/- 100 mm Hg, respectively; P = 0.035) We conclude that in morbidly obese patients, atelectasis formation is largely prevented by PEEP applied during the anesthetic induction and is associated with a better oxygenation. IMPLICATIONS: Application of positive end-expiratory pressure during induction of general anesthesia in morbidly obese patients prevents atelectasis formation and improves oxygenation. Therefore, this technique should be considered for anesthesia induction in morbidly obese patients.

Adult↗
PubMed2003

Preconditioning by sevoflurane decreases biochemical markers for myocardial and renal dysfunction in coronary artery bypass graft surgery: a double-blinded, placebo-controlled, multicenter study.

BACKGROUND: Preconditioning by volatile anesthetics is a promising therapeutic strategy to render myocardial tissue resistant to perioperative ischemia. It was hypothesized that sevoflurane preconditioning would decrease postoperative release of brain natriuretic peptide, a biochemical marker for myocardial dysfunction. In addition, several variables associated with the protective effects of preconditioning were evaluated. METHODS: Seventy-two patients scheduled for coronary artery bypass graft surgery under cardioplegic arrest were randomly assigned to preconditioning during the first 10 min of complete cardiopulmonary bypass with either placebo (oxygen-air mixture only) or sevoflurane 4 vol% (2 minimum alveolar concentration). No other volatile anesthetics were administered at any time during the study. Treatment was strictly blinded to anesthesiologists, perfusionists, and surgeons. Biochemical markers of myocardial dysfunction and injury (brain natriuretic peptide, creatine kinase-MB activity, and cardiac troponin T), and renal dysfunction (cystatin C) were determined. Results of Holter electrocardiography were recorded perioperatively. Translocation of protein kinase C was assessed by immunohistochemical analysis of atrial samples. RESULTS: Sevoflurane preconditioning significantly decreased postoperative release of brain natriuretic peptide, a sensitive biochemical marker of myocardial contractile dysfunction. Pronounced protein kinase C delta and epsilon translocation was observed in sevoflurane-preconditioned myocardium. In addition, postoperative plasma cystatin C concentrations increased significantly less in sevoflurane-preconditioned patients. No differences between groups were found for perioperative ST-segment changes, arrhythmias, or creatine kinase-MB and cardiac troponin T release. CONCLUSIONS: Sevoflurane preconditioning preserves myocardial and renal function as assessed by biochemical markers in patients undergoing coronary artery bypass graft surgery under cardioplegic arrest. This study demonstrated for the first time translocation of protein kinase C isoforms delta and epsilon in human myocardium in response to sevoflurane.

Adult↗
PubMed2003

Perflubron emulsion in prolonged hemorrhagic shock: influence on hepatocellular energy metabolism and oxygen-dependent gene expression.

BACKGROUND: Liver dysfunction as a result of impaired oxygen availability frequently occurs following hemorrhage and contributes to delayed mortality. Artificial oxygen carriers may improve oxygen supply to vital organs while avoiding the need for allogeneic transfusion. METHODS: Rats were subjected to hemorrhagic hypotension (mean arterial pressure = 35-40 mmHg for 120 min) and were subsequently resuscitated with (1) stored whole rat blood, (2) pentastarch, or (3) pentastarch combined with perflubron emulsion (PFE; 2.7 or 5.4 g/kg body weight), a second-generation artificial oxygen carrier. Recovery of liver adenosine triphosphate, hepatocellular injury, and expression of glutamine synthetase 1, a gene that is induced by exposure of hepatocytes to low partial pressure of oxygen, were studied at 4 h of resuscitation. RESULTS: Stored whole blood or pentastarch failed to restore liver adenosine triphosphate concentrations after prolonged shock as compared to sham controls and resulted in increased gene expression of glutamine synthetase 1. Addition of 2.7 g PFE/kg restored liver adenosine triphosphate to control, whereas 5.4 g PFE/kg resulted in adenosine triphosphate concentrations significantly above control. Improved hepatocellular oxygen supply was also confirmed by restoration of the physiologic expression pattern of glutamine synthetase 1. Serum enzyme concentrations were highest after resuscitation with stored blood, whereas addition of PFE failed to further decrease enzyme concentrations as compared to pentastarch alone. CONCLUSIONS: Resuscitation with PFE is superior to stored blood or asanguineous resuscitation with respect to restoration of hepatocellular energy metabolism. The improved hepatocellular oxygen availability is reflected in normalization of oxygen-dependent gene expression. However, improved oxygen availability failed to affect early hepatocellular injury.

Acid-Base Equilibrium↗
PubMed2003

Development of neuropathic pain in the rat spared nerve injury model is not prevented by a peripheral nerve block.

BACKGROUND: The mechanisms responsible for initiation of persistent neuropathic pain after peripheral nerve injury are unclear. One hypothesis is that injury discharge and early ectopic discharges in injured nerves produce activity-dependent irreversible changes in the central nervous system. The aim of this study was to determine whether blockade of peripheral discharge by blocking nerve conduction before and 1 week after nerve injury could prevent the development and persistence of neuropathic pain-like behavior in the spared nerve injury model. METHODS: Bupivacaine-loaded biodegradable microspheres embedded in fibrin glue were placed in a silicone tube around the sciatic nerve to produce a conduction block. After sensory-motor testing of block efficacy, a spared nerve injury procedure was performed. Development of neuropathic pain behavior was assessed for 4 weeks by withdrawal responses to stimulation (i.e., von Frey filaments, acetone, pinprick, radiant heat) in bupivacaine microspheres-treated animals (n = 12) and in controls (n = 11). RESULTS: Bupivacaine microspheres treatment produced conduction blockade with a complete lack of sensory responsiveness in the sural territory for 6 to 10 days. Once the block wore off, the degree of hypersensitivity to stimuli was similar in both groups. CONCLUSIONS: Peripheral long-term nerve blockade has no detectable effect on the development of allodynia or hyperalgesia in the spared nerve injury model. It is unlikely that injury discharge at the time of nerve damage or the early onset of ectopic discharges arising from the injury site contributes significantly to the persistence of stimulus-evoked neuropathic pain in this model.

Animals↗
PubMed2003

Repetitive large-dose infusion of the novel hydroxyethyl starch 130/0.4 in patients with severe head injury.

UNLABELLED: In this prospective, controlled, randomized, single-center study, we investigated the safety of repetitive large-dose infusion of a novel hydroxyethyl starch solution (6% HES 130/0.4) in cranio-cerebral trauma patients. Patients were randomized to receive either HES 130/0.4 (n = 16) at repetitive doses of up to 70 mL x kg(-1) x d(-1) (which is the largest HES dose reported in the literature) or the control HES 200/0.5 (n = 15) up to its approved dose limit of 33 mL x kg(-1) x d(-1) followed by human albumin up to a total dose (HES 200/0.5 + albumin) of 70 mL x kg(-1) x d(-1). We found no differences between groups in mortality, renal function, bleeding complications, and use of blood products. There were also no major differences in coagulation variables. However, at some time points, factor VIII, von Willebrand factor, and ristocetin cofactor were higher in the HES 130/0.4 group despite the large HES doses administered. We conclude that HES 130/0.4 can safely be used in critically ill head trauma patients over several days at doses of up to 70 mL x kg(-1) x d(-1). IMPLICATIONS: There are concerns that infusion of certain hydroxyethyl starch (HES) types for plasma volume expansion may influence coagulation and renal function. We investigated the safety of the novel HES 130/0.4 in patients with severe cranio-cerebral trauma. The repetitive HES doses administered in this study are the largest reported in the literature.

Adolescent↗
PubMed2003

Prevention of atelectasis formation during induction of general anesthesia.

UNLABELLED: General anesthesia promotes atelectasis formation, which is augmented by administration of large oxygen concentrations. We studied the efficacy of positive end-expiratory pressure (PEEP) application during the induction of general anesthesia (fraction of inspired oxygen [FIO(2)] 1.0) to prevent atelectasis. Sixteen adult patients were randomly assigned to one of two groups. Both groups breathed 100% O(2) for 5 min and, after a general anesthesia induction, mechanical ventilation via a face mask with a FIO(2) of 1.0 for another 5 min before endotracheal intubation. Patients in the first group (PEEP group) had continuous positive airway pressure (CPAP) (6 cm H(2)O) and mechanical ventilation via a face mask with a PEEP of 6 cm H(2)O. No CPAP or PEEP was applied in the control group. Atelectasis, determined by computed radiograph tomography, and analysis of blood gases were measured twice: before the beginning of anesthesia and directly after the intubation. There was no difference between groups before the anesthesia induction. After endotracheal intubation, patients in the control group showed an increase of the mean area of atelectasis from 0.8% +/- 0.9% to 4.1% +/- 2.0% (P = 0.0002), whereas the patients of the PEEP group showed no change (0.5% +/- 0.6% versus 0.4% +/- 0.7%). After the intubation with a FIO(2) of 1.0, PaO(2) was significantly higher in the PEEP group than in the control (591 +/- 54 mm Hg versus 457 +/- 99 mm Hg; P = 0.005). Atelectasis formation is prevented by application of PEEP during the anesthesia induction despite the use of large oxygen concentrations, resulting in improved oxygenation. IMPLICATIONS: Application of positive end-expiratory pressure during the induction of general anesthesia prevents atelectasis formation. Furthermore, it improves oxygenation and probably increases the margin of safety before intubation. Therefore, this technique should be considered for all anesthesia induction, at least in patients at risk of difficult airway management during the anesthesia induction.

Adolescent↗
PubMed2002

The effect of increased FIO(2) before tracheal extubation on postoperative atelectasis.

UNLABELLED: General anesthesia promotes pulmonary atelectasis, which can be eliminated by a vital capacity (VC) maneuver (inflation of the lungs to 40 cm H(2)O for 15 s). High-inspired oxygen concentration favors recurrence of atelectasis. Therefore, 100% oxygen before tracheal extubation may contribute to atelectasis. To evaluate whether the use of 100% oxygen before extubation increases the amount of postoperative atelectasis, we studied 30 adults scheduled for elective surgery of the extremities. Ten minutes before the presumed end of surgery, patients were randomly assigned to (a) a fraction of inspired oxygen (FIO(2)) = 1.0 (n = 10), (b) VC maneuver + FIO(2) = 1.0 (n = 10), or (c) VC maneuver + FIO(2) = 0.4 (n = 10). The amount of atelectasis was measured by computed tomography scan, and oxygenation was studied by arterial blood gas analysis. Data were analyzed by one-way analysis of variance with Bonferroni correction. Results are presented as mean +/- SD; P < 0.05 was considered significant. In the VC maneuver + FIO(2) = 0.4 group, postoperative atelectasis was smaller (2.6% +/- 1.1% of total lung surface, P < 0.05) than in the FIO(2) = 1.0 group (8.3% +/- 6.2%) and in the VC maneuver + FIO(2) = 1.0 group (6.8% +/- 3.4%). Oxygen 100% at the end of general anesthesia promotes postoperative atelectasis. A safety margin in terms of oxygenation during tracheal extubation is essential, and further studies should therefore evaluate whether atelectasis formation could be prevented despite the use of 100% oxygen. IMPLICATIONS: For safety reasons, it is common to ventilate patients with 100% oxygen before tracheal extubation. This study demonstrates that this practice favors postoperative atelectasis.

Adolescent↗
PubMed2002

Volatile anesthetics mimic cardiac preconditioning by priming the activation of mitochondrial K(ATP) channels via multiple signaling pathways.

BACKGROUND: Volatile anesthetics induce pharmacological preconditioning in cardiac tissue. The purpose of this study was to test whether volatile anesthetics mediate this effect by activation of the mitochondrial adenosine triphosphate-sensitive potassium (mitoK(ATP)) or sarcolemmal K(ATP) (sarcK(ATP)) channel in rat ventricular myocytes and to evaluate the signaling pathways involved. METHODS: A cellular model of ischemia with subsequent hypoosmolar trypan blue staining served to determine the effects of 5-hydroxydecanoate, a selective mitoK(ATP) channel blocker, HMR-1098, a selective sarcK(ATP) channel blocker, diazoxide, a preconditioning mimicking agent, and various modulators of putative signaling pathways on cardioprotection elicited by sevoflurane and isoflurane. Microscopy was used to visualize and measure autofluorescence of flavoproteins, a direct index of mitoK(ATP) channel activity. RESULTS: Volatile anesthetics significantly enhanced diazoxide-mediated activation of mitoK(ATP) channels as assessed by autofluorescence of myocytes. Conversely, volatile anesthetics alone did not alter mitoK(ATP) channel activity, implying a priming effect of volatile anesthetics on mitoK(ATP) channels. Administration of the protein kinase C inhibitor chelerythrine completely blocked this effect. Also, pretreatment with volatile anesthetics potentiated diazoxide-mediated protection against ischemia, as indicated by a reduction in trypan blue-positive myocytes. Importantly, cardioprotection afforded by volatile anesthetics was unaffected by the sarcK(ATP) channel blocker HMR-1098 but sensitive to modulations of nitric oxide and adenosine-G(i) signaling pathways. CONCLUSIONS: Using autofluorescence in live cell imaging microscopy and a simulated model of ischemia, the authors present evidence that volatile anesthetics mediate their protection in cardiomyocytes by selectively priming mitoK(ATP) channels through multiple triggering protein kinase C-coupled signaling pathways. These observations provide important new insight into the mechanisms of anesthetic-induced preconditioning.

Adenosine Triphosphate↗
PubMed2002

Differential effects of anesthetics on mitochondrial K(ATP) channel activity and cardiomyocyte protection.

BACKGROUND: Mitochondrial adenosine triphosphate-sensitive potassium (mitoK(ATP)) channels play a pivotal role in mediating cardiac preconditioning. The effects of intravenous anesthetics on this protective channel have not been investigated so far, but would be of importance with respect to experimental as well as clinical medicine. METHODS: Live cell microscopy was used to visualize and measure autofluorescence of flavoproteins, a direct reporter of mitoK(ATP) channel activity, in response to the direct and highly selective mitoK(ATP) channel opener diazoxide, or to diazoxide following exposure to various anesthetics commonly used in experimental and clinical medicine. A cellular model of ischemia with subsequent hypoosmolar trypan blue staining served to substantiate the effects of the anesthetics on mitoK(ATP) channels with respect to myocyte viability. RESULTS: Diazoxide-induced mitoK(ATP) channel opening was significantly inhibited by the anesthetics R-ketamine, and the barbiturates thiopental and pentobarbital. Conversely, urethane, 2,2,2-trichloroethanol (main metabolite of alpha-chloralose and chloral hydrate), and the opioid fentanyl potentiated the channel-opening effect of diazoxide, which was abrogated by coadministration of chelerythrine, a specific protein kinase C inhibitor. S-ketamine, propofol, xylazine, midazolam, and etomidate did not affect mitoK(ATP) channel activity. The significance of these modulatory effects of the anesthetics on mitoK(ATP) channel activity was substantiated in a cellular model of simulated ischemia, where diazoxide-induced cell protection was mitigated by R-ketamine and the barbiturates, while urethane, 2,2,2-trichloroethanol, and fentanyl potentiated myocyte protection. CONCLUSIONS: These results suggest distinctive actions of individual anesthetics on mitoK(ATP) channels and provide evidence that the choice of background anesthesia may play a role in cardiac protection in both experimental and clinical medicine.

Adenosine Triphosphate↗
PubMed2002

Esmolol improves left ventricular function via enhanced beta-adrenergic receptor signaling in a canine model of coronary revascularization.

BACKGROUND: Recent American Heart Association guidelines highlight the paucity of data on effectiveness and/or mechanisms underlying use of beta-adrenergic receptor (beta AR) antagonists after acute coronary syndromes in patients subsequently undergoing revascularization. It is important to assess whether beta AR antagonists might protect the heart and improve ventricular function in this scenario. The authors therefore used esmolol (an ultra-short-acting beta AR antagonist) to determine whether beta AR antagonist treatment improves left ventricular function in a canine model of acute reversible coronary ischemia followed by coronary reperfusion during cardiopulmonary bypass (CPB). The authors also tested whether the mechanism includes preserved beta AR signaling. METHODS: Dogs were randomized to either esmolol or saline infusions administered during CPB (n = 29). Pre-CPB and end-CPB transmyocardial left ventricular biopsies were obtained; plasma catecholamine concentrations, myocardial beta AR density, and adenylyl cyclase activity were measured. In addition, left ventricular systolic shortening and postsystolic shortening were determined immediately prior to each biopsy. RESULTS: While beta AR density remained unchanged in each group, isoproterenol-stimulated adenylyl cyclase activity decreased 26 +/- 6% in the control group but increased 38 +/- 10% in the esmolol group (pre-CPB to end-CPB, mean +/- SD, P = 0.0001). Left ventricular systolic shortening improved in both groups after release of coronary (LAD) ligature; however, the esmolol group increased to 72 +/- 23% of pre-CPB values compared to 48 +/- 12% for the control group (P = 0.0008). CONCLUSIONS: These data provide prospective evidence that esmolol administration results in improved myocardial function. Furthermore, the mechanism appears to involve enhanced myocardial beta AR signaling.

Adenylyl Cyclases↗
PubMed2002

Use of perflubron emulsion to decrease allogeneic blood transfusion in high-blood-loss non-cardiac surgery: results of a European phase 3 study.

BACKGROUND: This single-blind randomized study in general surgery evaluated the efficacy of perflubron emulsion (PFC) as an artificial oxygen carrier being used to augment preoperative acute normovolemic hemodilution to reduce and avoid transfusion of both allogeneic erythrocytes and erythrocytes from preoperative autologous donation compared with standard of care. METHODS: Subjects (N = 492) with hemoglobin concentrations of 12-15 g/dl undergoing noncardiac surgical procedures with 20 ml/kg or greater expected blood loss were randomized into two groups. Control patients were transfused intraoperatively at a hemoglobin concentration less than 8.0 +/- 0.5 g/dl or at protocol-defined, physiologic triggers. PFC-treated patients first underwent acute normovolemic hemodilution to hemoglobin of 8.0 +/- 0.5 g/dl, followed by dosing with perflubron emulsion (1.8 g/kg). When hemoglobin reached less than 6.5 +/- 0.5 g/dl, an additional 0.9-g/kg dose was given. PFC patients were transfused at hemoglobin less than 5.5 +/- 0.5 g/dl or at predefined physiologic triggers. After surgery, hemoglobin was maintained at 8.5 +/- 0.5 g/dl or greater in all patients until discharge. Efficacy endpoints included the number of allogeneic and preoperative autologous donation units transfused and the percentage of subjects avoiding transfusion. RESULTS: Both groups had similar hemoglobin concentrations at screening (13.5 +/- 1.0 g/dl) and at discharge: 10.8 +/- 1.2 g/dl (PFC) and 11.1 +/- 1.3 g/dl (control). At 24 h, more patients in the PFC group avoided allogeneic and preoperative autologous donation erythrocyte transfusions (53% vs. 43%, < 0.05), and fewer erythrocytes were transfused (1.5 +/- 4.8 vs. 2.1 +/- 3.9 units; median, 0 vs. 1 unit; P = 0.013). By day of discharge, these differences were not significant in the intent-to-treat population, but overall there were less allogeneic and preoperative autologous donation erythrocyte transfusions in the PFC group (696 vs. 846 units). In the protocol-defined target population (n = 330 subjects with blood loss > or = 20 ml/kg), significantly greater avoidance of any erythrocyte transfusion was maintained through day of hospital discharge (26% vs. 16% in the PFC and control groups, respectively; P < 0.05), and there was also a significant reduction in the number of erythrocyte units transfused (3.4 +/- 2.9 vs. 4.9 +/- 2.4 units; median 2 vs. 4 units; P < 0.001). Adverse events rates were similar in the PFC (86%) and control (81%) groups; however, more serious adverse events were reported in the PFC group (32%) than in controls (21%; P < 0.05). Overall mortality was 3%, and the difference between groups (PFC, 4% vs. controls, 2%) was not statistically significant. CONCLUSIONS: Augmented acute normovolemic hemodilution with PFC reduces transfusion needs in patients undergoing noncardiac surgical procedures with blood loss 20 ml/kg or greater.

Adult↗