Severe carbon monoxide poisoning during desflurane anesthesia.
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Biomedical subjects
Publications and source records attributed to D I Sessler.
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BACKGROUND: General anesthetics increase the sweating-to-vasoconstriction interthreshold range (temperatures not triggering thermoregulatory defenses), whereas fever is believed to only increase the setpoint (target core temperature). However, no data characterize thresholds (temperatures triggering thermoregulatory defenses) during combined anesthesia and fever. Most likely, the combination produces an expanded interthreshold range around an elevated setpoint. The authors therefore tested the hypothesis that thermoregulatory response thresholds during the combination of fever and anesthesia are simply the linear combination of the thresholds resulting from each intervention alone. METHODS: The authors studied eight healthy male volunteers. Fever was induced on the appropriate days by intravenous injection of 30 IU/g human recombinant interleukin 2 (IL-2), followed 2 h later by an additional 70 IU/g. General anesthesia consisted of desflurane 0.6 minimum alveolar concentration (MAC). The volunteers were randomly assigned to the following groups: (1) control (no desflurane, no IL-2); (2) IL-2 alone; (3) desflurane alone; and (4) desflurane plus IL-2. During the fever plateau, volunteers were warmed until sweating was observed and then cooled to vasoconstriction. Sweating was evaluated from a ventilated capsule and vasoconstriction was quantified by volume plethysmography. The tympanic membrane temperatures triggering significant sweating and vasoconstriction identified the respective response thresholds. Data are presented as the mean +/- SD; P < 0.05 was considered significant. RESULTS: The interthreshold range was near 0.40 degrees C on both the control day and during IL-2 administration alone. On the IL-2 alone day, however, the interthreshold range was shifted to higher temperatures. The interthreshold range increased significantly during desflurane anesthesia to 1.9+/-0.6 degrees C. The interthreshold range during the combination of desflurane and IL-2 was 1.2+/-0.6 degrees C, which was significantly greater than on the control and IL-2 alone days. However, it was also significantly less than during desflurane alone. CONCLUSION: The combination of desflurane and IL-2 caused less thermoregulatory inhibition than would be expected based on the effects of either treatment alone. Fever-induced activation of the sympathetic nervous system may contribute by compensating for a fraction of the anesthetic-induced thermoregulatory impairment.
BACKGROUND: Effective treatment and prevention of hyperthermia and shivering-like tremor during labor is hindered by a poor understanding of their causes. The authors sought to identify the incidence of nonthermoregulatory shivering-like tremor and the factors associated with this activity. METHODS: The authors studied women in spontaneous full-term labor who chose epidural analgesia (n = 21) or opioid sedation (n = 31). Shivering-like tremor and sweating were evaluated by observation. Core temperature was recorded in the external auditory canal using a compensated infrared thermometer. Arteriovenous shunt tone was evaluated with forearm minus fingertip skin temperature gradients; gradients less than 0 were considered evidence of vasodilation. Tremor was considered nonthermoregulatory when core temperature exceeded 37 degrees C and the arms were vasodilated. Pain was evaluated using a visual analog scale. RESULTS: Shivering-like tremor was observed in 18% of 290, 30-min data-acquisition epochs before delivery. The patients were both normothermic and vasodilated during 15% of these epochs. Shivering was observed in 16% of 116 postdelivery epochs and was nonthermoregulatory in 28%. Sweating was observed in 30% of predelivery epochs, and the patients were both hypothermic and vasoconstricted during 12%. The mean core temperature in patients given epidural analgesia was approximately 0.2 degrees C greater than in those given sedation. Hyperthermia was observed during 10 epochs (38.4+/-0.3 degrees C) during epidural analgesia and during 10 epochs (38.4+/-0.3 degrees C) with sedation. The patients were vasoconstricted in more than 50% of these epochs in each group. Multivariate mixed-effects modeling identified high pain scores and vasoconstriction as significant predictors of shivering. There were no predictors for shivering epochs in patients who were simultaneously normothermic and vasodilated. Significant predictors of sweating were time before delivery, high pain scores, hypothermia with vasoconstriction, high thermal comfort, and low mean skin temperature. There were no predictors for sweating epochs in patients who were simultaneously hypothermic and vasoconstricted. CONCLUSIONS: This study confirms the clinical impression that some peripartum shivering-like tremor is nonthermoregulatory. The authors also identified nonthermoregulatory sweating. These data indicate that shivering-like tremor and sweating in the peripartum period is multifactorial.
BACKGROUND: Previous studies indicate that anesthesia and surgery induce an inflammatory reaction in alveolar macro phages. However,they filed to independently evaluate the relative contributions of factors including mechanical ventilation, general anesthesia, and surgical stress. Therefore, the authors tested the hypothesis that inflammatory reactions at the cellular level in alveolar macrophages are induced within 2 h of inhalation of volatile anesthetics under mechanical ventilation. METHODS: After administration of pentobarbital, rats were allocated to the nonventilated control or spontaneous or mechanical ventilation (n = 15/group) for 2 h at a fraction of inspired oxygen (FI(O2)) of 0.21. In a separate series of experiments, rats were mechanically ventilated without volatile anesthesia, or during exposure to halothane, enflurane, isoflurane, or sevoflurane (n = 15/group). Pulmonary lavage was performed, and RNA was extracted from harvested cells. The mRNA for the proinflammatory cytokines interleukin (IL)-1alpha, IL-1beta, IL-6, macrophage inflammatory protein-2 (MIP-2), interferon gamma (IFN-gamma), and tumor necrosis factor alpha (TNF-alpha) were measured by semiquantitative reverse transcription-polymerase chain reaction using beta-actin as an internal standard. Pulmonary lavage concentrations of these cytokines were measured by enzyme-linked immunoassay. RESULTS: The lavage cell count and cytology were similar in each series of the experiment. Gene expression of MIP-2 and TNF-alpha was greater during mechanical than spontaneous ventilation and nonventilation control However, the concentrations of cytokines except MIP-2 and TNF-alpha were less than detection levels. During exposure to volatile anesthetics, gene expression for IL-1beta, MIP-2, IFN-gamma, and TNF-alpha all increased significantly compared with mechanical ventilation alone. Significant increases in lavage concentrations of MIP-2 and TNF-alpha were also observed. CONCLUSIONS: Gene expression of proinflammatory cytokines increase after inhalation of volatile anesthetics under mechanical ventilation. These data indicate that inhalation of volatile anesthetics under mechanical ventilation induces an inflammatory response at the transcriptional level within 2 h.
BACKGROUND: Thermoregulatory control is based on both skin and core temperatures. Skin temperature contributes approximately 20% to control of vasoconstriction and shivering in unanesthetized humans. However, this value has been used to arithmetically compensate for the cutaneous contribution to thermoregulatory control during anesthesia--although there was little basis for assuming that the relation was unchanged by anesthesia. It even remains unknown whether the relation between skin and core temperatures remains linear during anesthesia. We therefore tested the hypothesis that mean skin temperature contributes approximately 20% to control of vasoconstriction and shivering, and that the contribution is linear during general anesthesia. METHODS: Eight healthy male volunteers each participated on 3 separate days. On each day, they were anesthetized with 0.6 minimum alveolar concentrations of isoflurane. They then were assigned in random order to a mean skin temperature of 29, 31.5, or 34 degrees C. Their cores were subsequently cooled by central-venous administration of fluid at approximately 3 degrees C until vasoconstriction and shivering were detected. The relation between skin and core temperatures at the threshold for each response in each volunteer was determined by linear regression. The proportionality constant was then determined from the slope of this regression. These values were compared with those reported previously in similar but unanesthetized subjects. RESULTS: There was a linear relation between mean skin and core temperatures at the vasoconstriction and shivering thresholds in each volunteer: r2 = 0.98+/-0.02 for vasoconstriction, and 0.96+/-0.04 for shivering. The cutaneous contribution to thermoregulatory control, however, differed among the volunteers and was not necessarily the same for vasoconstriction and shivering in individual subjects. Overall, skin temperature contributed 21+/-8% to vasoconstriction, and 18+/-10% to shivering. These values did not differ significantly from those identified previously in unanesthetized volunteers: 20+/-6% and 19+/-8%, respectively. CONCLUSIONS: The results in anesthetized volunteers were virtually identical to those reported previously in unanesthetized subjects. In both cases, the cutaneous contribution to control of vasoconstriction and shivering was linear and near 20%. These data indicate that a proportionality constant of approximately 20% can be used to compensate for experimentally induced skin-temperature manipulations in anesthetized as well as unanesthetized subjects.
BACKGROUND: Nitrous oxide limits intraoperative hypothermia because the vasoconstriction threshold with nitrous oxide is higher than with equi-minimum alveolar concentrations of sevoflurane or isoflurane, presumably because of its stimulating actions on the sympathetic nervous system. Xenon, in contrast, does not cause sympathetic activation. Therefore, the authors tested the hypothesis that the vasoconstriction threshold during xenon-isoflurane anesthesia is less than during nitrous oxide-isoflurane anesthesia or isoflurane alone. METHODS: Fifteen patients each were randomly assigned to one of three 1-minimum alveolar concentration anesthetic regimens: (1) xenon, 43% (0.6 minimum alveolar concentration) and isoflurane, 0.5% (0.4 minimum alveolar concentration); (2) nitrous oxide, 63% (0.6 minimum alveolar concentration) and isoflurane 0.5%; or (3) isoflurane, 1.2%. Ambient temperature was maintained near 23 degrees C and the patients were not actively warmed. Thermoregulatory vasoconstriction was evaluated using forearm-minus-fingertip skin temperature gradients. A gradient exceeding 0 degrees C indicated significant vasoconstriction. The core-temperature threshold that would have been observed if skin had been maintained at 33 degrees C was calculated from mean skin and distal esophageal temperatures at the time of vasoconstriction. RESULTS: The patients' demographic variables, preinduction core temperatures, ambient operating room temperatures, and fluid balance were comparable among the three groups. Heart rates were significantly less during xenon anesthesia than with nitrous oxide. The calculated vasoconstriction threshold was lowest with xenon (34.6+/-0.8 degrees C, mean +/- SD), intermediate with isoflurane alone (35.1+/-0.6 degrees C), and highest with nitrous oxide (35.7+/-0.6 degrees C). Each of the thresholds differed significantly. CONCLUSIONS: Xenon inhibits thermoregulatory control more than isoflurane, whereas nitrous oxide is the least effective in this respect.
BACKGROUND: Spontaneous tremor is relatively common in normothermic patients after operation and has been attributed to many causes. The hypothesis that nonthermoregulatory shivering-like tremor is facilitated by postoperative pain was tested. In addition, the effects of intravenous lidocaine on nonthermoregulatory tremor were evaluated. METHODS: Patients undergoing knee surgery were anesthetized with 2 microg/kg intravenous fentanyl and 0.2 mg/kg etomidate. Anesthesia was maintained with 1.7 +/- 0.8% (mean +/- SD) isoflurane. Intraoperative forced-air heating maintained normothermia The initial 44 patients were randomly allocated to receive an intra-articular injection of 20 ml saline (n = 23) or lidocaine, 1.5% (n = 21). The subsequent 30 patients were randomly allocated to receive an intravenous bolus of 250 microg/kg lidocaine followed by an infusion of 13 microg x kg(-1) x h(-1) lidocaine or an equivalent volume of saline when shivering was observed. Patient-controlled analgesia was provided for all patients: 3.5 mg piritramide, with a lockout interval of 5 min, for an unlimited total dose. Shivering was graded by a blinded investigator using a four-point scale. Pain was assessed by a 100-mm visual analog scale (0 = no pain and 100 = worst pain). The arteriovenous shunt status was evaluated with forearm-minus-fingertip skin-temperature gradients. RESULTS: Morphometric characteristics and hemodynamic responses were similar in the four groups. Core and mean skin temperature remained constant or increased slightly compared with preoperative values, and postoperative skin-temperature gradients were negative (indicating vasodilation) in nearly all patients. After intra-articular injection of saline, pain scores for the first postoperative hour averaged 46 +/- 32 mm (mean +/- SD), and 10 of the 23 (43%) patients shivered. In contrast, the pain scores of patients who received intra-articular lidocaine were significantly reduced to 5 +/- 9 mm and shivering was absent in this group (P < 0.05). In the second portion of the study, neither intravenous lidocaine nor saline reduced the magnitude or duration of nonthermoregulatory tremor or the patients' pain scores. CONCLUSIONS: Intra-articular, but not intravenous, lidocaine reduced surgical pain and prevented nonthermoregulatory shivering. Therefore, these data indicate that postoperative pain facilitates nonthermoregulatory shivering.
BACKGROUND: High concentrations of inspired oxygen are associated with pulmonary atelectasis but also provide recognized advantages. Consequently, the appropriate inspired oxygen concentration for general surgical use remains controversial. The authors tested the hypothesis that atelectasis and pulmonary dysfunction on the first postoperative day are comparable in patients given 30% or 80% perioperative oxygen. METHODS: Thirty patients aged 18-65 yr were anesthetized with isoflurane and randomly assigned to 30% or 80% oxygen during and for 2 h after colon resection. Chest radiographs and pulmonary function tests (forced vital capacity and forced expiratory volume) were obtained preoperatively and on the first postoperative day. Arterial blood gas measurements were obtained intraoperatively, after 2 h of recovery, and on the first postoperative day. Computed tomography scans of the chest were also obtained on the first postoperative day. RESULTS: Postoperative pulmonary mechanical function was significantly reduced compared with preoperative values, but there was no difference between the groups at either time. Arterial gas partial pressures and the alveolar-arterial oxygen difference were also comparable in the two groups. All preoperative chest radiographs were normal. Postoperative radiographs showed atelectasis in 36% of the patients in the 30%-oxygen group and in 44% of those in the 80%-oxygen group. Relatively small amounts of pulmonary atelectasis (expressed as a percentage of total lung volume) were observed on the computed tomography scans, and the percentages (mean +/- SD) did not differ significantly in the patients given 30% oxygen (2.5% +/- 3.2%) or 80% oxygen (3.0% +/- 1.8%). These data provided a 99% chance of detecting a 2% difference in atelectasis volume at an alpha level of 0.05. CONCLUSIONS: Lung volumes, the incidence and severity of atelectasis, and alveolar gas exchange were comparable in patients given 30% and 80% perioperative oxygen. The authors conclude that administration of 80% oxygen in the perioperative period does not worsen lung function. Therefore, patients who may benefit from generous oxygen partial pressures should not be denied supplemental perioperative oxygen for fear of causing atelectasis.
BACKGROUND: Despite new anesthetic drugs and antiemetics, particularly 5-hydroxytryptamines, the incidence of postoperative nausea or vomiting remains between 20% and 70%. The authors tested the hypothesis that supplemental perioperative oxygen administration reduces the incidence of postoperative nausea or vomiting. METHODS: Patients undergoing colon resection were anesthetized with fentanyl and isoflurane. During and for 2 h after surgery they were randomly assigned to (1) 30% oxygen, balance nitrogen (n = 119); or (2) 80% oxygen, balance nitrogen (n = 112). The incidence of nausea or vomiting during the first 24 postoperative hours was evaluated by nurses blinded to group assignment and oxygen concentration. Data were analyzed with unpaired t or Mann-Whitney U tests. Results are presented as means +/- SD; P < 0.05 was considered significant. RESULTS: Factors known to influence nausea and vomiting were comparable in the two groups. Perioperative oxygen saturation was well within normal limits in each treatment group; saturations the first postoperative morning were comparable in each group. Supplemental oxygen reduced the incidence of postoperative nausea or vomiting from 30% in the patients given 30% oxygen to 17% in those given 80% oxygen (P = 0.027). CONCLUSIONS: Supplemental oxygen reduced the incidence of postoperative nausea or vomiting nearly twofold after colorectal surgery. The mechanism by which oxygen administration reduces the incidence of these postoperative sequelae remains unknown but may be related to subtle intestinal ischemia. Because oxygen is inexpensive and essentially risk-free, supplemental oxygen appears to be an effective method of reducing postoperative nausea and vomiting.
BACKGROUND: Smoking alters numerous alveolar macrophage functions and is an important risk factor for postoperative pulmonary complications. The authors therefore tested the hypothesis that smoke exposure impairs antimicrobial and proinflammatory responses in alveolar macrophages during halothane and isoflurane anesthesia with mechanical ventilation. METHODS: Thirty control rats and 30 rats exposed to cigarette smoke were mechanically ventilated with 1.5 minimum alveolar concentration halothane and isoflurane. Ten smoke-exposed and control animals were assigned to one of three different anesthetic durations (0, 2, and 6 h). The fraction of aggregated cells and cell distribution were determined. Opsonized and unopsonized phagocytosis was measured. Microbicidal activity was determined as the ability to kill Listeria monocytogenes. The expression of interleukin (IL)-1alpha, IL-1beta, IL-6, macrophage inflammatory protein-2, interferon-gamma, and tumor necrosis factor-alpha was measured by semiquantitative reverse-transcription polymerase chain reaction. Pulmonary lavage concentrations of these cytokines were measured by enzyme-linked immunosorbent assay. RESULTS: During both halothane and isoflurane anesthesia, the fraction of aggregated macrophages increased, whereas unopsonized and opsonized phagocytosis and microbicidal activity decreased significantly over time in both groups. Responses observed in smoke-exposed rats were almost twice as great as those observed in the control rats. Gene expression and production of all proinflammatory cytokines except IL-6 increased 2-20-fold during anesthesia. The increases in IL-1beta, interferon-gamma, and tumor necrosis factor-alpha in the control rats were 1.5-8 times greater than those in the smoke-exposed rats. CONCLUSION: Antimicrobial and proinflammatory responses of alveolar macrophages during anesthesia were markedly suppressed by smoke exposure. Our data suggest that smoke exposure reduces the efficacy of immune defenses during anesthesia.
UNLABELLED: Anesthesia and surgery induce macrophage aggregation and neutrophil influx, responses that characterize an inflammatory reaction in the distal airway. We thus evaluated the time-dependent expression of genes for proinflammatory cytokines during propofol and isoflurane anesthesia. We studied patients anesthetized with propofol (n = 20) or isoflurane (n = 20). Alveolar macrophages were harvested by bronchoalveolar lavage immediately, 2, 4, and 6 h after induction of anesthesia, and at the end of surgery. RNA was extracted from harvested cells and cDNA was synthesized by reverse transcription. Expression of interleukin-1beta (IL-1beta), IL-6, IL-8, interferon gamma, and tumor necrosis factor-alpha was measured by semiquantitative polymerase chain reaction using beta-actin as an internal standard. We observed two 10-fold increases in gene expression of all proinflammatory cytokines except IL-6. The increases in IL-8 and interferon gamma were 1.5-3 times greater during isoflurane than propofol anesthesia. Expression of the genes for IL-1beta and tumor necrosis factor-alpha was similar with each anesthetic. Our data thus indicate that the pulmonary inflammatory response accompanying anesthesia and surgery is accompanied by the expression of proinflammatory cytokines, and that this expression was in some cases greater during isoflurane than propofol anesthesia. IMPLICATIONS: Gene expression of proinflammatory cytokines in alveolar macrophages increased significantly over time. The increases were greater during isoflurane than propofol anesthesia, suggesting that inflammatory responses at transcriptional levels in alveolar macrophages are modulated by the type and duration of anesthesia.
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Thermoregulatory defenses are characterized by thresholds, the core temperatures triggering each response. Core body temperature is normally maintained within the interthreshold range, temperatures between the sweating and vasoconstriction thresholds that do not trigger autonomic defenses. This range usually spans only some 0.2 degrees C, but it remains unknown whether similar precision is maintained during the circadian core temperature cycle of about 0.8 degrees C. Accordingly, we evaluated the interthreshold range at four times of the day. We studied ten male volunteers, each at 3 a.m., 8 a.m., 3 p.m., and 8 p.m. At least 12 h elapsed between tests, and the order was randomly assigned. At each study time, volunteers were warmed peripherally until sweating was observed. Skin temperature was subsequently kept constant while core temperature was decreased by central-venous infusion of ice-cold fluid until peripheral vasoconstriction was detected. The volunteers were not permitted to sleep during threshold determinations, although sleep was not otherwise controlled. The core temperature triggering an evaporative water loss of 40 g.m-2.h-1 identified the sweating threshold. Similarly, the vasoconstriction threshold was defined by the core temperature triggering the initial decreases in plethysmographic finger tip blood flow. The interthreshold range at 3 a.m. was twice that observed at the other study times (P<0.05). Our data suggest that autonomic control of body temperature is reduced at 3 a.m., even when sleep is denied. This result contradicts the general perception that circadian variation alters the thermoregulatory target temperature, but not precision of body temperature control.
BACKGROUND: We evaluated a novel bandage that incorporates a thermostatically controlled radiant heater. We first determined optimal bandage temperature, based on increases in subcutaneous oxygen tension, a measure correlating well with resistance to infection and wound strength. We then tested the hypothesis that prolonged radiant heating would increase collagen deposition in experimental thigh wounds. METHODS: The experimental bandages were positioned on the anterior thigh of 8 volunteers, and heated for 2 hours at 38 degrees C, 42 degrees C, or 46 degrees C, in a random order. Subcutaneous oxygen tension under the bandage was recorded from an electrode positioned within a subcutaneous tonometer. We studied 10 volunteers in the second protocol. For 1 week, the experimental bandage was continuously applied to one thigh, and heated to 38 degrees C using a 2-hour on/off cycle. On the alternate week, a standard gauze bandage was applied to the contralateral thigh. Treatment order was randomly assigned. Wound collagen deposition under each bandage was evaluated with subcutaneous polytetrafluoroethylene tubes, which were removed and assayed for hydroxyproline on the eighth day. Data are presented as means +/- SDs. RESULTS: Skin temperature during heating ranged from 36 degrees C to 37.5 degrees C. Oxygen tension increased approximately 50% during heating, but the increase was comparable at the three tested temperatures. Even after heating was discontinued, subcutaneous oxygen tension remained elevated for the remaining 3 study hours. Collagen deposition after 1 week of active heating was 3.4 +/- 1.0 microg/ cm. After 1 week of control treatment, collagen deposition was 3.2 +/- 1.1 microg/cm (P = not significant). CONCLUSIONS: Our data suggest that radiant heating at 38 degrees C significantly increases subcutaneous oxygen tension, and presumably resistance to infection. However, prolonged heating at this temperature does not increase wound collagen deposition.
Poikilothermia syndrome is a rare cause of intrinsic thermoregulatory failure. Patients with this syndrome regulate body temperature poorly, if at all. Recently, a patient was referred to us who had clinical evidence of poikilothermia syndrome, as well as long-standing multiple sclerosis. Computerized tomography and magnetic resonance scanning failed to identify a hypothalamic lesion. The patient was gradually warmed to sweating, and then cooled to vasoconstriction and shivering. The core-temperature thresholds triggering each defence were calculated, after compensating for the changes in skin temperature. The calculated sweating threshold was 38.3 degrees C (normal: 37.0 +/- 0.3 degrees C). The vasoconstriction threshold was 34.4 degrees C (normal: 36.4 +/- 0.3 degrees C). The sweating-to-vasoconstriction interthreshold range was thus approximately 4 degrees C, which is between 10 and 20 times the normal value. The shivering threshold was 31.8 degrees C (normal: 35.6 +/- 0.3 degrees C). The vasoconstriction-to-shivering range was thus approximately 2.5 degrees C which is more than twice the normal value. The pattern of thermoregulatory failure in this patient resembled that resulting from general anaesthesia.
The accuracy of tracheal temperature as a measure of core temperature is relatively poor during high-flow ventilation (6 litre min-1 fresh-gas flow). It is unknown if accuracy improves when lower fresh-gas flow rates are used. We tested the hypothesis that tracheal temperature accuracy would improve with low-flow ventilation (1 litre min-1). We studied 20 ASA Physical Status I and II patients undergoing general anaesthesia for lower abdominal surgery. Deep body temperatures were measured at the middle of the sternum using a Coretemp "deep-tissue" thermometer. Tracheal temperatures were monitored from thermistors incorporated into the tracheal tube cuffs. Oesophageal temperatures were measured from thermocouples incorporated into stethoscopes positioned at the point of maximal heart sounds. Sternal temperature correlated reasonably well with distal oesophageal temperatures, both being within the 0.5 degree C cut-off for accuracy and precision. Tracheal temperatures were lower than oesophageal temperatures during both high- and low-flow ventilation. Tracheal temperatures were 0.7 degree C less during high-flow ventilation and 0.9 degree C less during low-flow ventilation. The precision in both cases was adequate. We conclude that tracheal temperatures were insufficiently accurate for routine clinical use, even when fresh- gas flow was restricted to 1 litre min-1. In contrast, the deep temperatures were sufficiently accurate and precise for routine clinical use.
UNLABELLED: Since 1993, we have progressively adopted three techniques to reduce transfusion requirements during major orthopedic surgery: red-cell scavenging, acute normovolemic hemodilution, and active patient warming. We retrospectively evaluated all 821 elective hip and knee arthroplasties performed in our institution beginning with July 1993. Target minimal hematocrits were guided by patient ages and cardiovascular status. The first approximately 500-mL blood loss was replaced with crystalloid at a ratio of 3 mL for each milliliter of blood loss. Additional blood loss was replaced with colloid, hemodilution blood (when available), and scavenged red cells (when available). Allogenic transfusions were then administered as necessary to maintain target hematocrits, which were prospectively defined based on the patient ages and cardiovascular health. Univariate analysis was applied initially. Significant predictors of transfusion requirement were subsequently entered into a stepwise multiple regression to account for confounding factors, including age, type of anesthesia (regional versus general) and type of surgery (primary versus hardware replacement). Postoperative hemoglobin concentrations were similar over the years of study and among the patients given each treatment. During the study period, allogenic blood requirements decreased from 1.3 +/- 1.7 U/patient to 0.6 +/- 1.4 U/patient (mean +/- SD). Both univariate and regression analyses indicated that each treatment significantly reduced transfusion requirements (P < 0.05). We conclude that red-cell scavenging, hemodilution, and active cutaneous warming each reduce allogenic blood requirements during hip and knee arthroplasties. IMPLICATIONS: We retrospectively evaluated three strategies to reduce overall blood loss: red-cell scavenging, acute normovolemic hemodilution, and active patient warming. During the study period, allogenic blood requirements decreased by a factor of 2. Each treatment contributed to this reduction. We therefore conclude that each treatment reduces allogenic blood requirements during hip and knee arthroplasties.