Higher postoperative pain and increased morphine consumption follow pre- rather than post-incisional single dose epidural morphine.

BACKGROUND: Neuraxial administration of morphine is an effective way of controlling postoperative pain and reducing analgesic consumption. Some animal models have demonstrated that preemptive administration of neuraxial narcotics reduces pain, while others have revealed the contrary. In addition, there have been no consistent results in clinical settings. This double-blind, randomized study compared the effects of pre- vs. post-incisional administration of neuraxial morphine on postoperative pain perception and analgesic requirements over 48 hours following laparotomy for open colectomy under standardized general anesthesia. METHODS: Twenty patients received epidural morphine (3 mg) before the incision and saline after wound closure (MO1 group), and twenty patients received epidural saline before the incision and morphine after wound closure (MO2 group). Postoperatively, all patients received morphine boluses (1.5 mg) via intravenous patient-controlled analgesia (IV-PCA) and rescue doses of intramuscular diclofenac (75 mg) every 6 hours, as needed. RESULTS: MO1 patients used significantly (P<0.05) more morphine than the MO2 group during the first 24 postoperative hours and activated the PCA device more frequently throughout the 48-hour study period. The MO1 group was characterized by significantly (P<0.05) higher self-rated pain scores than the MO2 group throughout the study. The self-rated levels of sedation and satisfaction of the MO2 patients were also consistently better (P<0.05) than those of the MO1 patients, especially during the second postoperative day. CONCLUSION: Pre-incisional epidural morphine in patients undergoing open colonic surgery under general anesthesia was associated with more postoperative pain, a greater need for analgesics, and poorer patient satisfaction compared to post-incisional morphine administration.

Predictors of adverse outcome from candidal infection in a tertiary care hospital.

OBJECTIVES: To retrospectively delineate predictors of adverse outcome by looking at the demographic features, therapy and outcome of systemic candida infection in a large tertiary care university-affiliated medical center. METHODS: We reviewed the clinical data on 186 inpatients with candidemia over a 6-year period. The major reason for their hospital admission was an underlying malignancy or an infection other than candidemia. RESULTS: Candida albicans, tropicalis, parapsilosis, glabrata and krusei caused 54, 22, 13, 8 and 3% of the candidemia episodes, respectively. The overall mortality was 42% and it was highest in patients suffering from candidemia of the glabrata species (73%). Forty-eight (63%) of the 76 patients who received no anti-fungal treatment died compared to 38 (34%) of 110 patients who were treated (P < 0.05). Predictors of adverse outcome were intensive care unit stay, renal failure, thrombocytopenia and the need for mechanical ventilation or inotropic support. CONCLUSIONS: We identified four predictors of mortality from candidemia infection. Their validity should be further assessed and the specific candida strains and their susceptibility need to be methodically identified. Our data support immediate initiation of therapy at first identification of infection.

Cysteine-induced hypoglycemic brain damage: an alternative mechanism to excitotoxicity.

Central neural damage caused by L-cysteine (L-Cys) was first reported more than 30 years ago. Nevertheless, the exact mechanisms of L-Cys-mediated neurotoxicity are still unclear. Preliminary study in mice demonstrated that, following L-Cys injection, animals developed tachypnea, tremor, convulsions, and death in conjunction with documented hypoglycemia. The aim of the present study was to further investigate the mechanism of L-Cys-mediated hypoglycemic effect and neural damage. Neonatal ICR mice (n=6) were injected with L-Cys (0.5-1.5 mg/g body weight [BW]), and their blood glucose and insulin levels were determined up to 90 min following the injection. Experiments were repeated in chemically (streptozotocin [STZ]) pancreatectomized animals. Brain histology was assessed. Mice injected with L-Cys exhibited dose-dependent neurotoxicity and higher mortality as compared with controls. L-Cys (1.2-1.5 mg/g BW) caused severe hypoglycemia (glucose<42 mg/dl) ( P<0.001). In STZ-treated (diabetic) animals, L-Cys (1.5 mg/g BW) increased plasma insulin levels 2.3-fold and decreased serum glucose levels by 50% ( P<0.01). Brain histology revealed destruction of as much as 51% of hippocampal neurons in the L-Cys-treated mice but not in the glucose-resuscitated animals. These findings suggest that L-Cys injection can cause pronounced hypoglycemia and central neural damage which is glucose reversible. Since L-Cys is chemically different from the other excitatory amino acids (glutamate and aspartate), L-Cys-mediated neurotoxicity may be connected to its hypoglycemic effect.

Invasive group A streptococcal infections in a large tertiary center: epidemiology, characteristics and outcome.

BACKGROUND: Invasive group A streptococcal (GAS) infections are increasing alarmingly worldwide. PATIENTS AND METHODS: To determine the clinical and epidemiologic characteristics of invasive GAS in a large tertiary medical center, we retrospectively surveyed microbiology and medical records of patients with invasive GAS infections (isolation of Group A Streptococcus from a normally sterile site) treated in our hospital from January 1995 to December 1997. RESULTS: 70 patients with a median age of 48 years (range 2 months-88 years) were identified. Of the 70 identified, 53 (76%) were adults (age > or = 19 years). The most common co-morbid diseases for invasive GAS in adults were diabetes mellitus, congestive heart failure (CHF), malignancy and immunosuppression. A probable port of entry was identified in 31 (44%) of the cases. In children, varicella lesions were the major port of entry. Overall mortality rate was 17%: The difference in mortality between pediatric and adult cases was significant (0/17 vs 12/53, respectively; p = 0.03). Toxic shock syndrome (TSS) and necrotizing fasciitis were identified in 8.6% and 5.7% of the cases, respectively, with mortalities of 83.3% and 25%. Hyponatremia and hypocalcemia were more frequently observed among the severely ill. CONCLUSION: Invasive GAS infections tend to have an unexpected course and a broad clinical spectrum, ranging from local skin or pharyngeal involvement to deeply invasive fasciitis with TSS and high mortality. The elderly and those with underLying medical conditions are at utmost rsk for invasive GAS. Clear-cut guidelines for early therapeutic strategy, i.e. antibiotic administration and preemptive hospital admission are needed for community-based physicians.

Religious sensitivity pitted against the need to know: autopsy of Jewish children in Israel.

BACKGROUND: The aim of the study was to compare autopsy findings with antemortem findings in children who died in a pediatric intensive care unit. MATERIAL/METHODS: Consecutive series of patients who died in the pediatric intensive care unit during 2-year period were used. The study was conducted as a retrospective chart review at community, regional-referral, university-affiliated tertiary medical center of 1200 bed in Israel. RESULTS: Permission was given to perform autopsies on only 10 children (23.8%, mean age 85.7 months) out of the 42 who died during the study period. The mean length of stay in the pediatric intensive care unit prior to death was 13.3 days. Cardiac or hemato-oncologic diseases comprised the major pre-admission diagnoses. The autopsy revealed a major finding that, if known before death, would have altered clinical management in 50% of the patients: pneumonia, pneumonitis as well as intestinal perforation or necrosis. No correlation was found between patient length of stay in the intensive care unit and the autopsy disclosed information. CONCLUSIONS: Our findings support the importance of autopsy assessment in the pediatric intensive care setup. We believe that postmortem examination is also essential for improving the quality of pediatric patient care.

Circulating leptin levels after cardiopulmonary bypass in children.

OBJECTIVE: To characterize the dynamics of circulating leptin in children after cardiac surgery with cardiopulmonary bypass (CPB), which is known to induce a systemic inflammatory response. DESIGN: Investigative study. SETTING: University-affiliated tertiary care hospital. PARTICIPANTS: Eight children (age range, 3 months to 13 years) undergoing CPB to correct congenital heart disease. INTERVENTIONS: The time courses of leptin and cortisol levels were determined. Serial blood samples were collected from the arterial catheter or from the CPB circuit preoperatively; on termination of CPB; and at 2, 4, 8, 12, 18, and 24 hours postoperatively. Plasma was recovered immediately, divided into aliquots, and frozen at -70 degrees C until use. Leptin was measured by a human leptin radioimmunoassay kit. MEASUREMENTS AND MAIN RESULTS: Leptin levels during CPB decreased to 50% of pre-CPB levels (p < 0.01). After termination of CPB, levels increased gradually and peaked at 12 hours postoperatively (10 P.M. to 1 A.M.). Cortisol levels were inversely correlated to leptin levels (p = 0.016). CONCLUSION: CPB is associated with acute changes in circulating leptin levels. These changes parallel those in cortisol, showing an inverse relationship between leptin and cortisol, suggesting a relationship between the neurobiology of these systems that could be important for the neuroendocrine response to CPB. A prognostic role of leptin and its relationship to cortisol after CPB warrant further study.

Dextromethorphan and dexmedetomidine: new agents for the control of perioperative pain.

Most traditional opioids and non-steroidal anti-inflammatory drugs that are used to control perioperative pain have substantial side effects. The number of choices in clinical use was recently increased by two promising groups of drugs: N-methyl-D-aspartate receptor antagonists and central alpha2 agonists. One N-methyl-D-aspartate antagonist, dextromethorphan, blocks the generation of central pain sensation that arise from peripheral nociceptive stimuli by moderating the activity of N-methyl-D-aspartate. It pre-empts the sensation of acute pain at doses of 30-90 mg without serious side effects, while reducing the amount of analgesics required perioperatively by 50%. It is available in oral form and has a confirmed lack of effect on haemodynamics and respiration. Dexmedetomidine is a relatively new, highly selective central alpha2 agonist. Its sedative, pro-anaesthetic and pro-analgesic effects at 0.5-2 microg/kg given intravenously stem mainly from its ability to blunt the central sympathetic response by as yet unknown mechanism(s) of action. It also minimises opioid-induced muscle rigidity, lessens postoperative shivering, causes minimal respiratory depression, and has haemodynamic stabilising effects.

Wrist actigraphy in anesthesia.

STUDY OBJECTIVES: To examine the use of wrist actigraphy during and following anesthesia or monitored sedation and its ability to objectively assess sleep-related events. DESIGN: Uncontrolled study. SETTING: 1100-bed tertiary care municipal, university-affiliated medical center. PATIENTS AND INTERVENTIONS: 18 patients who underwent minor to medium lower-body surgical procedures with spinal or epidural anesthesia with sedation by propofol, midazolam, or isoflurane-based general anesthesia. MEASUREMENTS AND MAIN RESULTS: Wrist actigraphy was measured and evaluated. The actigraphic recordings accurately indicated the presence and time of occurrence of all relevant perioperative events including those related to anesthesia. Actigraphic data were more precise than equivalent attending anesthesiologist's subjective observations. The anesthesiologist detected changes in the patient's activity with a delay of minutes after they had been picked up by the actigraph. The integrated areas of recorded phases of midazolam-induced sedation and the occurrence and reversal of paradoxical reactions were distinctly discernible as such, unlike the less specifically defined description of the anesthesiologist. CONCLUSIONS: Real time actigraphic monitoring can provide clear-cut and objective indications of changes in the depth of anesthesia or sedation and its associated events during surgery and recovery.

Acute respiratory distress syndrome in children with malignancy--can we predict outcome?

PURPOSE: The purpose of this study was to delineate early respiratory predictors of mortality in children with hemato-oncology malignancy who developed acute respiratory distress syndrome (ARDS). MATERIALS AND METHODS: We conducted a retrospective chart review of children with malignant and ARDS who needed mechanical ventilation and were admitted to a pediatric intensive care unit from January 1987 to January 1997. RESULTS: Seventeen children with ARDS and malignancy aged 10.5 +/- 5.1 years were identified. Six of the 17 children (35.3%) survived. Sepsis syndrome was present in 70.6% of all the children. Peak inspiratory pressure, positive end-expiratory pressure (PEEP), and ventilation index values could distinguish outcome by day 3. A significant relationship between respiratory data and outcome related to efficiency of oxygenation, as determined by PaO(2)/FIO(2) and P(A-a)O(2), was present from day 8 after onset of mechanical ventilation. CONCLUSIONS: Peak inspiratory pressure, PEEP, and ventilation index values could distinguish survivors from nonsurvivors by day 3. This may assist in early application of supportive nonconventional therapies in children with malignancy and ARDS.

Combined pre-incisional oral dextromethorphan and epidural lidocaine for postoperative pain reduction and morphine sparing: a randomised double-blind study on day-surgery patients.

The reduction in acute pain perception following dextromethorphan has previously been investigated in patients undergoing general anaesthesia. This random and double-blind study examined the effects of pre-incisional oral dextromethorphan on postoperative pain and intravenous patient-controlled morphine demand in 60 day-surgery patients undergoing lower body surgery under lidocaine (1.6%-16 ml) epidural anaesthesia after receiving placebo, 60 or 90 mg dextromethorphan, 90 min pre-operatively. Postoperative pain was scored on a visual analogue scale from 1 to 10. In-hospital observation continued for 6 h and for 3 days at home; diclofenac was available throughout. Dextromethorphan-treated patients reported significantly (p < 0.05) less pain and sedation, and felt better. Patients who received dextromethorphan 90 mg had significantly (p < 0.05) lower heart and respiratory rates than those who received 60 mg. Medicated patients required half the morphine and diclofenac of placebo patients: 38% of patients who received 90 mg and 21% who received dextromethorphan 60 mg used no morphine or diclofenac whatsoever, a previously unreported finding.

Antagonization of TNF attenuates systemic hemodynamic manifestations of envenomation in a rat model of Vipera aspis snakebite.

OBJECTIVES: Tumor necrosis factor (TNF) has been reported as a mediator of local tissue injury following snake envenomation in an intact rat model. We investigated whether systemic release of TNF occurs following Vipera aspis envenomation. We further analyzed the possible connection between envenomation-related hemodynamic depression and TNF antagonization (TNF antibodies or soluble TNF receptor). DESIGN: A prospective, randomized, controlled experimental study using a rat model for snake envenomation. SETTINGS: A medical university hospital research laboratory. INTERVENTION: Eighty rats (300-400 g) were divided into four groups (n = 20): control and three experimental groups. Intramuscular injection of V. asis 500 microg/kg was administered to the three experimental groups: venom only (group 1), venom and 40 microg anti-TNF antibodies (group 2), venom and 250 microg soluble TNF receptor (p55-R; group 3). Hemodynamic parameters were monitored up to 4 h following venom injection. MEASUREMENTS AND RESULTS: A significant hemodynamic deterioration (reduction in heart rate and blood pressure) occurred 30 min following venom injection in group 1 compared to groups 2 and 3, where hemodynamic parameters remained stable throughout the 4 h observation period. Serum levels of TNF were detected 15 min after venom injection and peaked after 2 h at 485+/-12 pg/ml. CONCLUSIONS: The hemodynamic consequences of intramuscular injection of V. aspis venom can be blunted in a rat by systemic antagonization of TNF activity prior to venom injection. The poisonous hemodynamic effects of the V. aspis venom might be caused by systemic release of TNF.

Soluble P-selectin and the postoperative course following cardiopulmonary bypass in children.

BACKGROUND: Cytokine-inducible leucocyte-endothelial adhesion molecules were shown to affect the postoperative inflammatory response following cardiopulmonary bypass (CPB). Soluble P-selectin (sP-selectin) is one of these molecules. We investigated the correlation between plasma sP-selectin levels and the intra- and postoperative course in children undergoing CPB. METHODS: Serial blood samples of 13 patients were collected preoperatively upon initiation of CPB and seven times postoperatively. Plasma was recovered immediately and frozen at - 70 degrees C until use. Circulating soluble selectin molecules were measured with a sandwich enzyme-linked immunoabsorbent assay technique. RESULTS: The significant post-CPB changes in sP-selectins plasma levels were associated with patient characteristics, operative variables and postoperative course. sP-selectin levels correlated significantly with surgery time, aortic cross-clamping time and inotropic support, as well as with the postoperative Pediatric Risk of Mortality score, hypotension and tachycardia. CONCLUSIONS: A relation between CPB-induced mediators and both early and late clinical effects is suggested. The up-regulation and expression of sP-selectin indicate neutrophil activation as a possible mechanism for the increase, and inhibiting it may reduce the inflammatory response associated with CPB.

Beta-chemokine secretion patterns in relation to clinical course and outcome in children after cardiopulmonary bypass: continuing the search to abrogate systemic inflammatory response.

BACKGROUND: Surgery involving cardiopulmonary bypass (CPB) is frequently accompanied by a systemic inflammatory response partly triggered by neutrophils and monocyte-macrophages. Certain cytokines that are powerful leukocyte-chemotactic factors have recently been characterized and shown to be important in evoking inflammatory responses: monocyte chemoattractant protein-1 (MCP-1) has monocyte-macrophage chemotactic activity, and regulated-upon-activation normal T-cell expressed and secreted (RANTES) has a potent chemoattractant activity for mononuclear phagocytes. This prospective cohort study investigated possible roles of these chemokines in the inflammatory response to CPB and relationships between the changes in chemokine levels and the clinical course and outcome. METHODS: Systemic blood of 16 children undergoing CPB was collected after induction of anesthesia (base line); at 15 minutes after bypass onset; at CPB cessation; and at 1, 2, 4, 8, 12, and 24 hours afterward to measure MCP-1 and RANTES. RESULTS: The significant changes of plasma beta chemokine levels following CPB were associated with patient characteristics, operative variables, and postoperative course. Cardiopulmonary bypass of more than 2 hours, longer surgical times, inotropic support, and reoperation were associated with higher MCP-1 levels and lower RANTES levels. CONCLUSIONS: Our results suggest a relation between CPB-induced mediators and clinical effects, implying pathogenic roles for chemokines following CPB. These molecules should be considered as possible targets for therapeutic intervention.

Lung preconditioning with N-acetyl-L-cysteine prevents reperfusion injury after liver no flow-reflow: a dose-response study.

BACKGROUND: Circulating xanthine oxidase activity and the generated oxidants have been linked to lung reperfusion injury from no flow-reflow conditions in other organs after organ transplantation or surgery. N-acetyl-1-cysteine (NAC), an oxidant scavenger, promotes glutathione in its reduced form (GSH) that is depleted during ischemia. We have recently demonstrated its efficacy in protecting lungs from reperfusion injury if administered during reperfusion of postischemic liver. We now investigated whether preconditioning of lungs with NAC could attenuate lung respiratory or vascular derangement after no flow-reflow (ischemia-reperfusion, IR) and if this depends on lung GSH levels. METHODS: Rat isolated livers were stabilized and perfused with modified Krebs-Henseleit solution (KH) (control, n=12) or made ischemic (no flow, IR-0, n=12) for 2 hr. Meanwhile, lungs were isolated, ventilated, and stabilized (KH+bovine albumin 5%). Serial perfusion (15 min) of liver+lung pairs took place followed by lung only recirculation (45 min) with the accumulated solution. Another three controls and three ischemic groups included lungs treated during stabilization with NAC at 100 mg x kg(-1), 150 or 225 mg x kg(-1) (in 2.5, 3.7 or 5.5 mmol solutions, respectively). Results. Ischemic liver damage, expressed by circulating hepatocellular constituents, was associated with pulmonary artery and ventilatory pressure increases by 70-100% of baseline, abnormal wet-to-dry weight ratio, and abnormal bronchoalveolar lavage volume and content in the IR-0 (nontreated) and the IR-100 and IR-225 pretreated lungs. NAC-150 pretreatment afforded preservation for most parameters. GSH content in the IR-150 lung tissue was only 11% higher than that of IR-225, but 2-fold that in IR-0 and IR-100 GSH lungs. CONCLUSION: Lung preconditioning with NAC prevents reperfusion injury but not in a dose-related manner. Although enhanced GSH tissue content explains lung protection, GSH-independent NAC activity is another possibility.

Xanthine oxidase and tumor necrosis factor alpha: possible mediators of remote tissue injury after viper envenomation.

BACKGROUND: Tumor necrosis factor is associated with various local and systemic inflammatory sequelae following snakebite. Xanthine oxidase is a principal mediator of remote tissue injury (e.g., lungs, heart, liver). OBJECTIVE: To investigate in a snakebite-like animal model the as yet unexplored role of TNF and XO in mediating organ damage following snakebite. METHODS: Sprague-Dawley rats were injected intramuscularly with a non-lethal 500 micrograms/kg dose of Vipera aspis venom (n = 10) or saline (n = 10). Blood pressure and heart rate were continuously monitored, TNF-alpha was measured in the blood, and total XO + xanthine dehydrogenase activity was assessed in various tissues. Lung histology and permeability indices were analyzed. RESULTS: Venom injection caused a significant (P < 0.05) reduction in both heart rate and invasive arterial pressure. The blood circulating TNF levels were significantly higher in the intoxicated group (P < 0.05 vs. saline group), with changes seen at 30 minutes from intoxication in both groups. Total XO + XDH activity in the kidney, lung and liver of the venom-injected group was significantly (P < 0.05) higher than in the saline group, while the activity in the heart was similar. CONCLUSIONS: The mediation of remote organ and hemodynamic changes following intramuscular injection of a non-lethal dose of Vipera aspis venom can be attributed partly to TNF and partly to XO. More research is needed to better understand the role of either compound and the time frame of their activity before specific antagonists can be introduced for snakebite management.

Anesthesia for victims of nerve agents undergoing surgery: establishment of a management protocol.

Awareness of the effects of nerve agents still being stocked around the world has led to the establishment of protocols for rapid evacuation and decontamination of large civilian areas. Perioperative care protocol and procedures for the administration of anesthesia in lifesaving surgical intervention for combined multiple trauma and intoxicated casualties have not been established. There are also no guidelines for anesthetizing those casualties who had already been medicated on site. The only exception to anecdotal reports and isolated communications on these issues is the organophosphate poisoning database of substances which act similarly to the nerve agents or their antagonists. We gathered the few reports existing on the subjects in the literature and extrapolated the knowledge of the nature and action of various anesthetic drugs. We applied it to biological and physiological conditions that exist in combined chemical and multiple trauma casualties and consolidated the data into two charts that may serve as guidelines for preventing the avoidable hazardous outcomes.

N-acetyl-L-cysteine for preventing lung reperfusion injury after liver ischemia-reperfusion: a possible dual protective mechanism in a dose-response study.

BACKGROUND: Acute lung reperfusion injury (ALI) frequently follows an ischemic event in another organ, such as organ transplantation. We recently demonstrated that lung priming with N-acetyl-L-cysteine (NAC) prevented liver ischemia-reperfusion (IR)-induced ALI pending on reduced glutathione (GSH) amount of replenishment. We now assessed the therapeutic effect of NAC-in preventing ALI caused by liver IR-if administered to the lung during liver reperfusion. PROCEDURES: Rat isolated livers were stabilized (30 min) and then perfused with modified Krebs-Henseleit solution (control, n=20) or made globally ischemic (IR, n=20) for 2 hr. Rat lungs were isolated separately, ventilated, and stabilized (30 min) with Krebs plus 5% bovine albumin. Pairs of liver and lung were then reperfused together for 15 min, followed by only lung recirculation with the liver effluent for another 45 min. Three more controls (n=20 each) and three ischemic groups (n=20 each) included lungs which were treated with 100, 150 or 225 mg x kg(-1) NAC (0.5, 0.74, or 1.1 mmol, respectively) during the 15-min liver and lung reperfusion period. RESULTS: Pulmonary artery and ventilatory pressures and vascular resistance increased by 60-80% of baseline, compliance decreased, and bronchoalveolar lavage volume and content were abnormally high in the IR-nontreated and the IR-100 lungs. Most parameters in IR-150 and IR-225 lungs remained almost similar to controls. Postinsult GSH content in IR-100, -150, and -225 lungs was at 20%, 110%, and 90% above the IR-nontreated lungs, respectively. CONCLUSIONS: Lung treatment with NAC during its reperfusion with IR liver effluent prevented ALI. Lung GSH replenishment accounted for lung protection, but its content did not correlate directly with grade of protection; NAC itself seemingly afforded lung protection as well.

Acute respiratory distress syndrome in children: a 10 year experience.

BACKGROUND: Acute respiratory distress syndrome is a well-recognized condition resulting in high permeability pulmonary edema associated with a high morbidity. OBJECTIVES: To examine a 10 year experience of predisposing factors, describe the clinical course, and assess predictors of mortality in children with this syndrome. METHODS: The medical records of all admissions to the pediatric intensive care unit over a 10 year period were evaluated to identify children with ARDS. Patients were considered to have ARDS if they met all of the following criteria: acute onset of diffuse bilateral pulmonary infiltrates of non-cardiac origin and severe hypoxemia defined by < 200 partial pressure of oxygen during > or = 6 cm H2O positive end-expiratory pressure for a minimum of 24 hours. The medical records were reviewed for demographic, clinical, and physiologic information including PaO2/forced expiratory O2, alveolar-arterial O2 difference, and ventilation index. RESULTS: We identified 39 children with the adult respiratory distress syndrome. Mean age was 7.4 years (range 50 days to 16 years) and the male:female ratio was 24:15. Predisposing insults included sepsis, pneumonias, malignancy, major trauma, shock, aspiration, near drowning, burns, and envenomation. The mortality rate was 61.5%. Predictors of death included the PaO2/FIO2, ventilation index and A-aDO2 on the second day after diagnosis. Nonsurvivors had significantly lower PaO2/FIO2 (116 +/- 12 vs. 175 +/- 8.3, P < 0.001), and higher A-aDO2 (368 +/- 28.9 vs. 228.0 +/- 15.5, P < 0.001) and ventilation index (43.3 +/- 2.9 vs. 53.1 +/- 18.0, P < 0.001) than survivors. CONCLUSIONS: Local mortality outcome for ARDS is comparable to those in tertiary referral institutions in the United States and Western Europe. The PaO2/FIO2, A-aDO2 and ventilation index are valuable for predicting outcome in ARDS by the second day of conventional therapy. The development of a local risk profile may allow early application of innovative therapies in this population.

[Propofol anesthesia for craniotomy in patients who are awake].

During craniotomy, the patient's cooperation is needed during procedures in which continuous neurological examination and mapping of crucial regions close to the area to be resected area are required. We report our experience in 9 patients who underwent such procedures under intravenous propofol as the main sedating agent. This short-acting hypnotic was administered prior to and during the painful stages of the procedure. Patients were fully asleep when the skull was opened and the dural flap raised or excised. During the rest of the operation patients were lightly sedated but remained responsive and cooperative. This enabled precise intra-operative mapping of the brain and surgery-related neurological deficits were avoided. Respiratory depression or hemodynamic compromise were not encountered. All patients were comfortable during the operation and there were no additional neurological deficits after operation. We believe that propofol should be the main sedating agent used for these procedures.