[Perioperative anemia]. / Perioperative Anämie.

Anemia is a frequent finding, particularly in the elderly population, and usually indicative of a serious disease. The main causes of preoperative anemia are acute or chronic hemorrhage, iron deficiency, renal insufficiency, inflammatory and neoplastic diseases. A preexisting mild anemia may be enhanced or unmasked by surgically induced bleeding or repeated diagnostic phlebotomies, and by a postoperative erythropoietic dysfunction caused by the surgical trauma, irrespective of any hemorrhage. Low hemoglobin values are associated with a distinct increase of mortality and morbidity, both in the normal population and perioperatively and in the critically ill patients. The anemia-associated risk is exacerbated by preexisting cardiovascular disease, important intraoperative blood loss and advanced age. In contradiction to established therapeutical concepts, the administration of allogeneic blood beyond hemoglobin levels of 8-10 g/dl has not been found to decrease perioperative or intensive care morbidity or mortality. Rather, in addition to the inherent long-term risks of transfusions, a liberal transfusion strategy seems to increase the incidence of postoperative complications. Thus, current transfusion guidelines tend to be interpreted in an increasingly restrictive manner. Depending on the urgency of the clinical situation, the primary goal should be to diagnose and treat the underlying disease, rather than to focus on the symptom anemia. Time permitting, the patient's cardiovascular and pulmonary status should be optimized preoperatively. Furthermore, iron should be substituted to treat and prevent deficiency. Recombinant human erythropoietin has successfully been used to treat anemia of chronic renal failure and chronic disease, as well as in the perioperative and intensive care setting, and to support the efficiency of autologous programs.

Multiple agents potentiate alpha1-adrenoceptor-induced conduction depression in canine cardiac purkinje fibers.

BACKGROUND: Halothane more so than isoflurane potentiates an alpha1-adrenoceptor (alpha1-AR)-mediated action of epinephrine that abnormally slows conduction in Purkinje fibers and may facilitate reentrant arrhythmias. This adverse drug interaction was further evaluated by examining conduction responses to epinephrine in combination with thiopental and propofol, which "sensitize" or reduce the dose of epinephrine required to induce arrhythmias in the heart, and with etomidate, which does not, and responses to epinephrine with verapamil, lidocaine, and l-palmitoyl carnitine, a potential ischemic metabolite. METHODS: Action potentials and conduction times were measured in vitro using two microelectrodes in groups of canine Purkinje fibers stimulated at 150 pulses/min. Conduction was evaluated each minute after exposure to 5 microm epinephrine (or phenylephrine) alone or with the test drugs. Changes in the rate of phase 0 depolarization (Vmax) and the electrotonic spread of intracellular current were measured during exposure to epinephrine with octanol to evaluate the role of inhibition of active and passive (intercellular coupling) membrane properties in the transient depression of conduction velocity. RESULTS: Lidocaine (20 microm) and octanol (0.2 mm) potentiated alpha1-AR-induced conduction depression like halothane (0.4 mm), with maximum depression at 3-5 min of agonist exposure, no decrease of Vmax, and little accentuation at a rapid (250 vs. 150 pulses/min) stimulation rate. Thiopental (95 microm), propofol (50 microm), and verapamil (2 microm) similarly potentiated epinephrine responses, whereas etomidate (10 microm) did not. Between groups, the decrease of velocity induced by epinephrine in the presence of (10 microm) l-palmitoyl carnitine (-18%) was significantly greater than that resulting from epinephrine alone (-6%; 0.05

The influence of positioning on spectroscopic measurements of brain oxygenation.

This study was designed to evaluate the influence of body position during neurosurgical and cerebrovascular operations on regional cerebral oxygen saturation (rSO2). Awake volunteers (group I; n = 14), anesthetized patients (group II; n = 48) undergoing lumbar discectomy, and 12 patients undergoing carotid endarterectomy (group III) with internal carotid artery (ICA) stenosis were studied. Anesthesia in the patient groups was performed with sevoflurane (1.1 Vol% insp.) in N2O2/O2 mixture (FiO2 0.4) rSO2 was monitored with a INVOS 4100 cerebral oxymeter (Somanetics Corporation, Troy, MI). Measurements were done in all groups in supine position with head turned to the right and left side. Furthermore, in groups I and II, rSO2 was measured in right lateral, left lateral, prone, or sitting position. In each position the parameters were registered at three times (1, 3, and 5 min after taking up the position). In the healthy volunteers, the mean rSO2 values of both hemispheres were 71.3 +/- 5.0%. No significant changes of rSO2 were found interhemispherical and upon turning the head to both sides or positioning to the prone and both lateral positions. After assuming the sitting position, the decrease of rSO2 was not significant. In group II, rSO2 decreased significantly in the sitting position. In group III, baseline readings for rSO2 obtained from the side of ICA stenosis were significantly lower, compared to the contralateral side. After turning the head to the ipsilateral side, this difference diminished. In contrast, turning the head toward the contralateral side, the rSO2 difference remained nearly constant, both values decreasing constantly throughout the observation period. In conclusion, after different positioning maneuvers awake and under anesthesia, alterations of rSO2 can be registrated by near-infrared spectroscopy (NIRS).

The effects of the new antiarrhythmic E 047/1 on postoperative ischemia-induced arrhythmias in dogs.

UNLABELLED: Perioperative malignant ventricular tachyarrhythmias pose an imminent clinical danger by potentially precipitating myocardial ischemia and severely compromising hemodynamics. Thus, immediate and effective therapy is required, which is not always provided by currently recommended IV drug regimens, indicating a need for more effective drugs. We examined antiarrhythmic effects of the new benzofurane compound E 047/1 on spontaneous ventricular tachyarrhythmia in a conscious dog model. One day after experimental myocardial infarction, 40 dogs exhibiting tachyarrhythmia randomly received (bolus plus 1-h infusion) E 047/1 6 mg/kg plus 6 mg x kg(-1) x h(-1), lidocaine 1 mg/kg plus 4.8 mg x kg(-1) x h(-1), flecainide 1 mg/kg plus 0.05 mg x kg(-1) x h(-1), amiodarone 10 mg/kg plus 1.8 mg x kg(-1) x h(-1), or bretylium 10 mg/kg plus 20 mg x kg(-1) x h(-1). Electrocardiogram was evaluated for number of premature ventricular contractions (PVC), normally conducted beats originating from the sinoatrial node, and episodes of ventricular tachycardia. Immediately after the bolus, E 047/1 reduced PVCs by 46% and increased sinoatrial beats from 4 to 61 bpm. The ratio of PVCs to total beats decreased from 98% to 58%. Amiodarone and flecainide exhibited antiarrhythmic effects with delayed onset. Lidocaine did not suppress PVCs significantly, and bretylium was proarrhythmic. The antiarrhythmic E 047/1 has desirable features, suppressing ischemia-induced ventricular tachyarrhythmia quickly and efficiently, and may be a useful addition to current therapeutic regimens. IMPLICATIONS: Life-threatening arrhythmias of the heart after myocardial infarction or ischemia may be treated quickly and efficiently by the new drug E 047/1.

Effects of desflurane, sevoflurane and halothane on postinfarction spontaneous dysrhythmias in dogs.

BACKGROUND: Although desflurane (DES) and sevoflurane (SEV) have desirable features for use in patients with coronary artery disease, their effects on ventricular dysrhythmias following infarction are less known. We therefore examined the effects of DES and SEV upon spontaneous postinfarction ventricular dysrhythmias in dogs, and compared those effects to the well-established antidysrhythmic effects of halothane (HAL) in this model. METHODS: After institutional approval, the left anterior descending coronary artery was ligated in 16 adult mongrel dogs during isoflurane anesthesia. All dogs developed acute myocardial infarction and severe ventricular tachydysrhythmias. Twenty-two hours after infarction, dogs were anesthetized at 1.5 MAC with desflurane (10.8%) followed by sevoflurane (3.5%) in the treatment group (n = 10), or halothane (1.3%) in the other group (n = 6). Anesthetic gases were allowed to equilibrate for at least 20 min at each end-tidal concentration. At this time, the ECG was recorded for 9 min and evaluated for the number of ventricular ectopic and sinoatrial beats and summed duration of ventricular tachycardia. RESULTS: DES and SEV reduced the average rate of total ventricular ectopic beats by 40 +/- 4% and 42 +/- 4%, respectively. HAL decreased total ventricular ectopic rate by 59 +/- 6% and 62 +/- 5% after durations of anesthesia comparable to DES and SEV, respectively. Decreases in dysrhythmia in the presence of DES and SEV were significantly smaller than those produced by HAL after a comparable total duration of anesthesia. CONCLUSION: DES and SEV inhibit spontaneous postinfarction ventricular dysrhythmias, although attenuation of dysrhythmias was smaller than the inhibition during comparable doses of HAL.

Effect of thoracic epidural anesthesia on spontaneous postinfarction ventricular dysrhythmia in awake dogs.

BACKGROUND AND OBJECTIVES: Sympathetic neural activity contributes to the genesis of ventricular ectopic activity, particularly in the setting of myocardial ischemia and infarction, so thoracic epidural anesthesia should diminish ventricular ectopy by blocking sympathetic innervation of the heart. However, the possible antidysrhythmic effect of epidural anesthesia has been studied only in the presence of general anesthesia. We therefore examined changes in spontaneous postinfarction ventricular dysrhythmia during thoracic epidural anesthesia in awake dogs. METHODS: A survivable myocardial infarction was created by two-stage ligation of the left anterior descending coronary artery. The following day, multifocal idioventricular tachycardia was the predominant cardiac rhythm. Lidocaine was administered either by thoracic epidural catheter to achieve block of at least the first five thoracic segments or intravenously as a control for direct effects, without concurrent general anesthesia or sedation. Electrocardiographic recordings were analyzed for the number of ventricular ectopic and sinoatrial depolarizations. RESULTS: Epidural and intravenous administration both produced plasma lidocaine concentrations of about 2 mg/mL. There was no change in rhythm following intravenous lidocaine. During epidural anesthesia, total ectopic beats per minute decreased from 167 +/- 8 to 135 +/- 14 (mean +/- SE, P < .05), and the dysrhythmic ratio (ventricular beats/total beats) decreased from 0.93 +/- 0.03 to 0.81 +/- 0.08 (P < .05). However, ventricular tachydysrhythmia remained the predominant rhythm. CONCLUSIONS: Epidural block modestly reduces spontaneous ventricular dysrhythmia in a perioperative setting in dogs following a large myocardial infarction. These findings do not support the choice of thoracic epidural anesthesia for the purpose of preventing or decreasing severe ventricular dysrhythmia.

The response of anesthetic agent monitors to trifluoromethane warns of the presence of carbon monoxide from anesthetic breakdown.

OBJECTIVE: Trifluoromethane and CO are produced simultaneously during the breakdown of isoflurane and desflurane by dry CO2 absorbents. Trifluoromethane interferes with anesthetic agent monitoring, and the interference can be used as a marker to indicate anesthetic breakdown with CO production. This study tests representative types of gas monitors to determine their ability to provide a clinically useful warning of CO production in circle breathing systems. METHODS: Isoflurane and desflurane were reacted with dry Baralyme at 45 degrees C. Standardized samples of breakdown products were created from mixtures of reacted and unreacted gases to simulate the partial degrees of reaction which might result during clinical episodes of anesthetic breakdown using 1% or 2% isoflurane and 6% or 12% desflurane. These mixtures were measured by the monitors tested, and the indication of the wrong agent or a mixture of agents due to the presence of trifluoromethane was recorded and related to the CO concentration in the gas mixtures. RESULTS: When presented with trifluoromethane from anesthetic breakdown, monochromatic infrared monitors displayed inappropriately large amounts of isoflurane or desflurane. Agent identifying infrared and Raman scattering monitors varied in their sensitivity to trifluoromethane. Mass spectrometers measuring enflurane at mass to charge = 69 were most sensitive to trifluoromethane. CONCLUSION: Monochromatic infrared monitors were unable to indicate anesthetic breakdown via interference by trifluoromethane, but did indicate falsely elevated anesthetic concentrations. Agent identifying infrared and Raman monitors provided warning of desflurane breakdown via the interference of trifluoromethane by displaying the wrong agent or mixed agents, but may not be sensitive enough to warn of isoflurane breakdown Some mass spectrometers provided the most sensitive warnings to anesthetic breakdown via trifluoromethane, but additional data processing by some patients monitor units reduced their overall effectiveness.

Sympathetic and mesenteric venous responses to baroreceptor or chemoreceptor stimulation during epidural anesthesia in rabbits.

BACKGROUND: Baroreceptor and chemoreceptor reflexes maintain homeostasis through mechanisms that involve sympathetic activation. Because sympathetic control of the mesenteric veins plays a central role in hemodynamic responses to stress, the effects of epidural blockade on reflex responses to hypoxia and bilateral carotid occlusion (BCO) were examined by monitoring direct measures of splanchnic sympathetic neural traffic and mesenteric venous capacitance. METHODS: Rabbits were studied during alpha-chloralose anesthesia and mechanical ventilation. Sympathetic efferent nerve activity to the mesenteric vessels was measured by surgically placed electrodes, and mesenteric venous diameter was measured by videomicroscopy. Heart rate and mean arterial pressure were monitored by intraarterial cannulation. Intraluminal venous pressure was monitored by a servo-null micropressure technique. Responses were recorded during repeated administration of three different stresses, F1O2 = 0% for 40 s, F1O2 = 11% for 2.5 min, and BCO for 60 s. Animals received either thoracolumbar epidural blockade (0.4 ml/kg lidocaine 1.5%; n = 7) or 15 mg/kg intramuscular lidocaine (n = 7). RESULTS: Hypoxia and BCO produced sympathetic stimulation and active constriction of mesenteric veins. Epidural anesthesia accentuated the mean arterial pressure decrease from F1O2 of 0%, caused the 11% response to F1O2 to become depressor instead of pressor, and decreased the pressor effect BCO. Sympathetic efferent nerve activity and venous diameter responses to hypoxia and BCO were attenuated or eliminated. CONCLUSIONS: The hemodynamic effects of hypoxia result from a combination of direct depression and reflex activation. Thoracolumbar epidural anesthesia in rabbits impairs compensatory reflexes invoked by chemoreceptor stimulation and eliminates response to baroreceptor stimulation. Loss of splanchnic control of mesenteric capacitance contributes to the inhibition of the hemodynamic response to hypoxia or BCO during epidural anesthesia in rabbits.

Epinephrine dysrhythmogenicity is not enhanced by subtoxic bupivacaine in dogs.

Since bupivacaine and epinephrine may both precipitate dysrhythmias, circulating bupivacaine during regional anesthesia could potentiate dysrhythmogenic effects of epinephrine. We therefore examined whether bupivacaine alters the dysrhythmogenicity of subsequent administration of epinephrine in conscious, healthy dogs and in anesthetized dogs with myocardial infarction. Forty-one conscious dogs received 10 micrograms.kg-1.min-1 epinephrine. Seventeen animals responded with ventricular tachycardia (VT) within 3 min. After 3 h, these responders randomly received 1 or 2 mg/kg bupivacaine or saline over 5 min, followed by 10 micrograms.kg-1.min-1 epinephrine. In the bupivacaine groups, epinephrine caused fewer prodysrhythmic effects than without bupivacaine. VT appeared in fewer dogs and at a later time, and there were more sinoatrial beats and less ectopies. Epinephrine shortened QT less after bupivacaine than in control animals. One day after experimental myocardial infarction, six additional halothane-anesthetized dogs received 4 micrograms.kg-1.min-1 epinephrine until VT appeared. After 45 min, 1 mg/kg bupivacaine was injected over 5 min, again followed by 4 micrograms.kg-1.min-1 epinephrine. In these dogs, the prodysrhythmic response to epinephrine was also mitigated by preceding bupivacaine. Bupivacaine antagonizes epinephrine dysrhythmogenicity in conscious dogs susceptible to VT and in anesthetized dogs with spontaneous postinfarct dysrhythmias. There is no evidence that systemic subtoxic bupivacaine administration enhances the dysrhythmogenicity of subsequent epinephrine.

Magnetic resonance imaging of cerebrospinal fluid volume and the influence of body habitus and abdominal pressure.

BACKGROUND: Although the cerebrospinal fluid (CSF) is the pathway of anesthetic delivery and the diluent for neuraxially administered drugs, little is known about its volume, including variability among individuals, longitudinal distribution, or influence of body habitus. Models made to investigate subarachnoid anesthetic distribution lack valid dimensions. CSF volume was measured in volunteers, and the effect of obesity and abdominal compression on CSF volume was evaluated using magnetic resonance imaging. METHODS: Low thoracic and lumbosacral axial magnetic resonance images of 25 healthy volunteers were obtained at 8-mm intervals by fast spin-echo sequence, which highlights CSF. A repeat image series was performed in 15 subjects during external abdominal compression. In two subjects, images were obtained without compression for the entire vertebral column. Dural sac and spinal cord areas were determined in a blinded fashion for each image using video/digital analysis. Area of the sac minus area of the cord constituted area of CSF and roots ("CSF/root"); this area multiplied by 8 mm resulted in CSF/root volume per section. RESULTS: There is great interindividual variability in CSF/root volume. From the T11-T12 disc to the sacral terminus of the dural sac, the mean volume for all subjects is 49.9 +/- 12.1 ml (mean +/- SD; range 28.0-81.1 ml). This volume was significantly less in relatively obese subjects (42.9 +/- 9.5 ml) than in nonobese subjects (53.5 +/- 12.9 ml). Abdominal compression decreased CSF/root volume by 3.6 +/- 3.2 ml. Sections through intervertebral foramina showed the biggest decrease with abdominal compression, with a lesser change in sections with veins and no change in the absence of these anatomic features. Total vertebral CSF/root volume in two subjects was 94.84 and 120.01 ml, respectively. CONCLUSIONS: CSF volume is widely variable between individuals. The decreased CSF volume that results from increased abdominal pressure, such as with obesity or pregnancy, may produce more extensive neuraxial blockade through diminished dilution of anesthetic. The mechanism by which increased abdominal pressure decreases CSF volume is probably inward movement of soft tissue in the intervertebral foramen, which displaces CSF.

Mass spectrometry provides warning of carbon monoxide exposure via trifluoromethane.

BACKGROUND: The chemical breakdown of isoflurane, enflurane, or desflurane in dried carbon dioxide absorbents may produce carbon monoxide. Some mass spectrometers can give false indications of enflurane during anesthetic breakdown. METHODS: During clinical anesthesia with isoflurane or desflurane, the presence of carbon monoxide in respiratory gas was confirmed when enflurane was inappropriately indicated by a clinical mass spectrometer that identified enflurane at mass to charge ratio = 69. In vitro, isoflurane, enflurane, or desflurane in oxygen was passed through dried carbon dioxide absorbents at 35, 45, and 55 degrees C. Gases were analyzed by gas chromatography and by mass spectrometry. RESULTS: Mass spectrometry identified several clinical incidents in which 30-410 ppm carbon monoxide was measured in respiratory gas. Trifluoromethane was produced during in vitro breakdown of isoflurane or desflurane. Although these inappropriately indicated quantities of "enflurane" correlated (r2 > 0.95) to carbon monoxide concentrations under a variety of conditions, this ratio varied with temperature, anesthetic agent, absorbent type, and water content. CONCLUSIONS: Trifluoromethane causes the inappropriate indication of enflurane by mass spectrometry, and indicates isoflurane and desflurane breakdown. Because the ratio of carbon monoxide to trifluoromethane varies with conditions, this technique cannot be used to quantitatively determine the amount of carbon monoxide to which a patient is exposed. If any warning of anesthetic breakdown results from this technique then remedial steps should be taken immediately to stop patient exposure to carbon monoxide. No warning can be provided for the breakdown of enflurane by this technique.

[Reduction in the use of donated blood in surgical medicine]. / Reduktion des Fremdblutverbrauchs in der operativen Medizin.

After rapid changes in transfusion practice over the past few years, blood conservation techniques have become standard in modern perioperative management. As a result, the amount of homologous blood products transfused has been markedly reduced in some types of surgical procedures. Provided that skillful surgical technique is applied and the use of blood products is restricted, autologous transfusion techniques (predonation of autologous blood, preoperative plasmapheresis, acute normovolaemic haemodilution, and intra- and postoperative blood salvage) can be performed with an acceptable risk for patients. In addition, stimulation of erythropoiesis with recombinant human erythropoietin, supplemental iron therapy, and improving haemostasis by aprotinin may further reduce homologous blood requirements. All patients undergoing elective surgery have to be informed about the side effects of transfusion of homologous blood products and the possibility of blood-saving methods. An individual blood conservation plan, based on the patient's status and surgery, the equipment available, and personal experience should be worked out by the responsible anaesthesiologist, whereby a combination of different methods may be most effective. If storage is necessary, autologous blood products should be preparated like homologous products. The feasibility of predonation and retransfusion of autologous blood in patients with infectious diseases like hepatitis or acquired immune deficiency syndrome and the amount of labaratomy testing are still under discussion. Although blood conservation programs are time-consuming and more expensive, they reduce the various risks of using homologous blood products.

Erythropoietin in patients undergoing coronary artery bypass graft surgery.

Recombinant human erythropoietin (rHuEPO) has proved to be a useful drug that can aid in protecting patients from possible hazards of homologous blood. Use of rHuEPO for patients scheduled for coronary artery bypass graft (CABG) surgery can enhance the benefit of a preoperative autologous blood donation program while simultaneously minimizing its risks. The main objective are to decrease homologous transfusion requirements by increasing the amount of collected autologous blood and to maximize safety by ameliorating a pre- or postoperative anemia. The goal of this review is to assess the possible benefits of perioperative use of rHuEPO during CABG surgery. Furthermore, we evaluate its ability to augment the quality of collected blood and to lower the risk of autologous blood donation. Side effects, dosages, manner of administration, concomitant iron therapy and suggestions for special patient groups will be discussed.

[30 degree trunk elevation of the patient and quality of lumbar epidural anesthesia. Effects of elevation in operations on the lower extremities]. / 30 grad Rumpfhochlagerung des Patienten und Qualität der lumbalen Epiduralanästhesie. Auswirkungen der Lagerung bei Operationen an der unteren Extremität.

The spread and intensity of lumbar epidural anaesthesia are unpredictable. Moreover, segments L5 and S1 are frequently missed. In this study the effect of 30 degrees trunk elevation on the spread and intensity of lumbar epidural sensory and motor blockade and on the cardiovascular system were studied. METHODS. After oral premedication with 7.5 mg midazolam, 30 patients 20 to 40 years of age, ASA 1-2, were randomly allocated to one of two groups according to their body position during injection of 20 ml 2% lidocaine (3 + 8 + 9 ml) into a lumbar epidural catheter (L2/3 or L3/4) and during the following 30 min: supine horizontal position or supine 30 degrees trunk elevation with 30 degrees leg elevation (hammock position). The patients received 500 ml Ringer solution before the epidural injection, followed by more Ringer solution. Systolic and diastolic blood pressures and heart rate were monitored noninvasively every 5 min; 30 min after the epidural injection the spread of analgesia (dullness of pinprick) and anaesthesia (no sensation of pinprick) as well as motor block according to Bromage were tested. A spread of anaesthetic segments including T12 to L3 was considered adequate for hip surgery, L3 to L5 for knee surgery, and L3 to S2 for foot surgery. Student's t-test, ANOVA, chi-square (Wilcoxon), and Mann-Whitney tests were used for statistical analysis. P < 0.05 was considered statistically significant. RESULTS. The median cephalad level of analgesia was lower in patients with the hammock position than those with the horizontal position (L1 vs T10; P < 0.05). There was no significant difference in the cranial level of anaesthesia (L2 vs L1) (Table 2). No significant difference was seen in the number of patients having adequate anaesthesia for hip surgery. Anaesthesia in the segments L5 and S1 was seen in 2/15 patients in the horizontal position and 8/15 patients in the hammock position (P < 0.05). The hammock position resulted in a higher percentage of patients having adequate anaesthesia for knee surgery (60% vs 13%; P < 0.05) and foot surgery (53% vs 13%; P < 0.05) (Table 3). Motor block was more profound in patients in the hammock position (Table 4). Blood pressure and heart rate did not change significantly in patients in the horizontal position (Fig. 1); there was a decrease in both systolic (7 mmHg) and diastolic (5 mmHg) blood pressures in patients in the hammock position. Heart rate did not change significantly (Fig. 2). No patient needed vasopressor support; the body position could be maintained in all patients during the observation period. One or two epidural reinjections according to the spread of anaesthesia 30 min after the first injection and to the scheduled operation resulted in adequate anaesthesia in every patient. DISCUSSION. More patients in the hammock position developed adequate anaesthesia in the relevant segments for knee and foot operations than patients in the horizontal position. These included the frequently missed segments L5 and S1. Patients in the hammock position had a clinically insignificant drop in systolic and diastolic blood pressure. In contrast to the young and healthy patients in this study, more severe cardiovascular changes might result in geriatric and/or ill patients subjected to a hammock position. For this reason, use of the technique in geriatric and/or ill patients requires special attention.

Subcutaneous recombinant human erythropoietin and autologous blood donation before coronary artery bypass surgery.

Conventional therapies with recombinant human erythropoietin (rHuEPO) to sustain preoperative autologous blood collection entail high doses of the drug at short intervals. To evaluate the efficacy of a single weekly dose of rHuEPO for autologous blood collection, we randomly assigned 24 male patients scheduled for coronary artery bypass surgery to receive 400 IU/kg rHuEPO subcutaneously once a week or iron only. Patients were examined weekly and a total of up to 4 units of autologous blood were obtained if the hemoglobin level exceeded 12 g/dL. Patients receiving rHuEPO had consistently higher hemoglobin values than those receiving iron only (P < 0.001). Consequently, more autologous red cells were obtained from this group (776 +/- 49 mL vs 682 +/- 91 mL; P < 0.05). One patient receiving rHuEPO and eight in the control group required homologous blood at surgery (P < 0.01). These results suggest that 400 IU/kg rHuEPO administered subcutaneously once a week efficiently stimulates erythropoiesis and compensates the hemoglobin decrease after autologous blood donation.

[Hemofiltration in acute kidney failure. Experiences of a surgical intensive care station]. / Hämofiltration bei akutem Nierenversagen. Erfahrungen einer operativen Intensivstation.

Until recently acute renal failure (ARF) in critically ill patients has been known to have a very poor prognosis, particularly when associated with multiple organ failure (MOF). Mortality rates for ARF in combination with at least two other failing organ systems have ranged over 90%. Despite the use of intermittent hemodialysis no better outcome was possible until continuous arteriovenous hemofiltration (CAVH) was introduced by Kramer in 1977. From several extracorporeal clearance methods we chose to evaluate the pump-driven intermittent venovenous hemofiltration (HF) system in the ICU and its effect on mortality in MOF. PATIENTS and METHODS. Over a period of 39 months we evaluated 63 patients, 58 of them with MOF undergoing altogether 532 sessions of HF. The reason for the development of ARF was prerenal in 47% (circulatory shock, hypovolemia), renal in 43% (septic) and other problems in 10% (ARDS, cardiac failure). After special optimizing therapy for patients with ARF (10), HF was required for treatment as defined by a serum creatinine greater than 3 mg/dl (BUN greater than 150 mg/dl), oliguria of less than 30 ml/h or a creatinine clearance of less than 20 ml/min. Vascular access was obtained by a double lumen venous cannula inserted into the subclavian vein. HF was performed by a machine equipped with 3 roller pumps and an electronic fluid equilibration system using a hollow fiber filter running for 6-8 h. The average flow of ultrafiltrate was 74 ml/min. RESULTS. The average decrease per hemofiltration of creatinine levels was 1.97 +/- 0.77 mg/dl, of BUN 73.5 +/- 28.3 mg/dl. Moreover, we noticed decreasing platelet counts, fibrinogen and osmolarity levels, as well as a slight increase in pH values. Mortality was 37%. DISCUSSION. When comparing HF with other clearance methods such as hemodialysis there are some remarkable advantages: easier handling of the fluid and electrolyte balance; the possibility of total i.v. alimentation in septic, hypercatabolic patients, safe and precise administration of antibiotics, glycosides and sedatives because of their highly predictable and steady elimination rates throughout HF; last but not least, the removal of renal and vasoactive toxins. There was practically no impairment of the cardiovascular system during HF. Our experiences in the ICU show that HF has been successfully used with decreasing mortality. This kind of treatment improved the fate of the critically ill patient with ARF alone or combined with MOF to the extent that the patient's prognosis was excellent if the main surgical problems could be solved.