PubMed Health⌕ Search

Biomedical subjects

U M Illievich

Publications and source records attributed to U M Illievich.

At least 19 recordsLinked to original sources
PubMed2006

Laparoscopic versus open myomectomy: a double-blind study to evaluate postoperative pain.

The advantages of laparoscopic over open surgery have been documented in nonblinded settings. Our prospective, double-blind setting evaluated pain scores 72 h after surgery by comparing patients who underwent laparoscopic myomectomy or with laparotomy. Forty women referred for conservative myomectomy were included in the study. After stratification (myoma size, number of myomas, and surgeon), patients were randomized to either laparoscopy (n = 19) or laparotomy (n = 21) and received a standardized anesthesia and patient-controlled analgesia for 24 h after surgery. Identical wound dressings were applied to blind the patient and the observer to the surgical approach. The postoperative pain scores were documented on a visual analog scale (VAS; 0 = no and 10 = unbearable pain) at 24, 48, and 72 h after surgery. As the primary outcome variable, we calculated the mean overall VAS-score at these time points. P < 0.05 (t-test and analysis of covariance) was considered statistically significant. There were no differences in patient characteristics among the groups. The mean overall VAS score at 24, 48, and 72 h was statistically significantly lower in the laparoscopic group compared with the laparotomy group (2.28 +/- 1.38 versus 4.03 +/- 1.63; P < 0.01). Our data demonstrate, for the first time in a double-blind setting, that laparoscopic myomectomy reduces postoperative pain for 72 h after surgery compared with laparotomy.

Adult↗
PubMed2003

A comparison of propofol and sevoflurane anaesthesia: effects on aortic blood flow velocity and middle cerebral artery blood flow velocity.

We compared systemic (aortic) blood flow and cerebral blood flow velocity in 30 patients randomly allocated to receive either propofol or sevoflurane anaesthesia. Cerebral blood flow velocity (CBFv) was measured in the middle cerebral artery using transcranial Doppler. Systemic blood flow velocity (SBFv) was measured in the aorta using transthoracic Doppler sonography at the level of the aortic valve. Bispectral index (BIS) was used to measure the depth of anaesthesia. Measurements were made in the awake patient and repeated during propofol or sevoflurane anaesthesia, with BIS measurements of 40-50. The effects of SBFv on CBFv were estimated by calculating the cerebral/systemic blood flow velocity-index (CsvI). A CsvI value of 100 indicating a 1 : 1 relationship between CBFv and SBFv. The results demonstrated that propofol anaesthesia produced a significantly greater reduction in CsvI than did sevoflurane anaesthesia [propofol: 60 (19); sevoflurane: 83 (16), p = 0.009, t-test]. This suggests a direct reduction in CBFv independent of SBFv during propofol anaesthesia. The greater reduction of CBFv occurring during propofol anaesthesia may be due to lower cerebral metabolic demand compared with sevoflurane anaesthesia at comparable depths of anaesthesia.

Adult↗
PubMed2003

The effect of graded hypothermia (36 degrees C-32 degrees C) on hemostasis in anesthetized patients without surgical trauma.

UNLABELLED: The isolated effects of hypothermia on hemostasis have not been investigated in healthy humans. We cooled 16 anesthetized patients scheduled for elective intracranial surgery to 32 degrees C body core temperature and assessed prothrombin time (PT), activated partial thromboplastin time, thrombelastogram (TEG), closure time, and platelet count at 36 degrees C, 34 degrees C, and 32 degrees C body core temperature after the induction of anesthesia but before surgical intervention. Activated partial thromboplastin time, hematocrit, and closure time did not change, whereas PT and platelet count decreased during cooling. Platelet count decreased without a decrease in hematocrit; hence, a dilution by administered fluids seemed unlikely. The small decrease of platelet count is probably clinically irrelevant in patients with normal platelet count and function. The small decrease in PT indicates an alteration of the extrinsic pathway of coagulation. TEG measurements showed a delay of clot formation in temperature-adjusted measurements but showed no change if the test temperature was 37 degrees C. This indicates that hypothermia reduces plasmatic coagulation and platelet reactivity. However, the clot strength is not altered by hypothermia. All coagulation variables remained within the normal ranges. Our results may indicate that moderate short-term (4-h) hypothermia has only minor adverse effects in healthy humans. We can make no statement about the effects of hypothermia of longer duration. IMPLICATIONS: This study investigated the isolated effects of hypothermia in healthy anesthetized humans. We found only minor effects of body temperature reduction to 32 degrees C on assessed coagulation variables, indicating only minor effects in otherwise healthy humans.

Adult↗
PubMed2001

Influence of aortic blood flow velocity on changes of middle cerebral artery blood flow velocity during isoflurane and sevoflurane anaesthesia.

BACKGROUND AND OBJECTIVE: We studied the influence of systemic (aortic) blood flow velocity on changes of cerebral blood flow velocity under isoflurane or sevoflurane anaesthesia. METHODS: Forty patients (age: isoflurane 24-62 years; sevoflurane 24-61 years; ASA I-III) requiring general anaesthesia undergoing routine spinal surgery were randomly assigned to either group. Cerebral blood flow velocity was measured in the middle cerebral artery by transcranial Doppler sonography (depth: 50-60 mm). Systemic blood flow velocity was determined by transthoracic Doppler sonography at the aortic valve. Heart rate, arterial pressure, arterial oxygen saturation and body temperature were monitored. After standardized anaesthesia induction (propofol, remifentanil, vecuronium) sevoflurane or isoflurane were used as single agent anaesthetics. Cerebral blood flow velocity and systemic blood flow velocity were measured in the awake patient (baseline) and repeated 5 min after reaching a steady state of inspiratory and end-expiratory concentrations of 0.75, 1.00, and 1.25 mean alveolar concentrations of either anaesthetic. To calculate the influence of systemic blood flow velocity on cerebral blood flow velocity, we defined the cerebral-systemic blood flow velocity index (CSvI). CSvI of 100% indicates a 1:1 relationship of changes of cerebral blood flow velocity and systemic blood flow velocity. RESULTS: Isoflurane and sevoflurane reduced both cerebral blood flow velocity and systemic blood flow velocity. The CSvI decreased significantly at all three concentrations vs. 100% (isoflurane/sevoflurane: 0.75 MAC: 85 +/- 25%/81 +/- 23%, 1.0 MAC: 79 +/- 19%/74 +/- 16%, 1.25 MAC: 71 +/- 16%/79 +/- 21%; [mean +/- SD] P = 0.0001). CONCLUSIONS: The reduction of the CSvI vs. 100% indicates a direct reduction of cerebral blood flow velocity caused by isoflurane/sevoflurane, independently of systemic blood flow velocity.

Adult↗
PubMed1999

Extracerebral organ dysfunction and neurologic outcome after aneurysmal subarachnoid hemorrhage.

OBJECTIVE: To analyze the influence of extracerebral organ system dysfunction after aneurysmal subarachnoid hemorrhage (SAH) on mortality and neurologic outcome. DESIGN: Observational study with retrospective data extraction. SETTING: Neurosurgical intensive care unit (NICU) at a primary level university hospital, supervised and staffed by both members of the Clinic of Neurosurgery and the Clinic of Anesthesiology and General Intensive Care. PATIENTS: Two hundred forty-two patients treated for intracranial aneurysm rupture within 7 days of the most recent SAH. INTERVENTIONS: Routine neurosurgical interventions for obliteration of the ruptured aneurysm (microsurgery, Guglielmi Detachable Coils embolization) and for treatment of posthemorrhagic hydrocephalus (ventriculostomy, cerebrospinal fluid shunt implantation). MEASUREMENTS AND MAIN RESULTS: Respiratory, renal, hepatic, cardiovascular, and hematologic organ system functions were evaluated both individually and in aggregate by using a modified version of the Multiple Organ Dysfunction (mMOD) score. Of 1,452 organ system functions assessed in 242 patients during their NICU stay, 714 organ system functions were intact (cerebral: 0, extracerebral: 714), 556 organ systems had mild-to-moderate dysfunctions (mMOD scoremax 1-2 for the affected organ system; cerebral: 153, extracerebral: 403), and 182 organ systems failed (mMOD scoremax 3 for the affected organ system; cerebral: 89, extracerebral: 93). Severity of extracerebral organ system dysfunctions correlated with the degree of neurologic impairment (Hunt and Hess [H&H] score) in a graded fashion. Similarly, the chance to develop systemic inflammatory response syndrome (SIRS) during the NICU stay increased with increasing admission H&H grade. The incidence of SIRS and septic shock was 29% and 10.3%, respectively. The mortality rate was 40.2% in patients with SIRS and 80% for patients suffering septic shock. Seventy-seven percent of extracerebral organ system failures (OSFs) occurred in conjunction with SIRS: 51% of respiratory OSFs, 97% of renal OSFs, 100% of hepatic OSFs, 96% of cardiovascular OSFs, and 73% of hematopoietic OSFs. Both CNS dysfunction and extracerebral organ system dysfunctions were significantly related to neurologic outcome. The probability of unfavorable neurologic outcome significantly increased with both decreasing cerebral perfusion pressure (CPP) and increasing severity of extracerebral organ dysfunction. CONCLUSION: Aneurysmal SAH and its neurologic sequelae accounted for the principal morbidity and mortality in the current series. Development of extracerebral organ system dysfunction was associated with a higher probability of unfavorable neurologic outcome. Systemic inflammation (SIRS) and secondary organ dysfunction were the principal non-neurologic causes of death.

Adult↗
PubMed1998

The arterial to end-tidal carbon dioxide gradient increases with uncorrected but not with temperature-corrected PaCO2 determination during mild to moderate hypothermia.

UNLABELLED: End-tidal carbon dioxide (PETCO2) monitoring is recommended as a basic standard of care and is helpful in adjusting mechanical ventilation. Gas solubility changes with temperature, which might affect the PaCO2 and thereby the gradient between PaCO2 and PETCO2 (PA-ETCO2) under hypothermic conditions. We investigated whether the PA-ETCO2 changes during mild to moderate hypothermia (36 degrees C-32 degrees C) using PaCO2 measured at 37 degrees C (uncorrected PaCO2) and PaCO2 corrected to actual body temperature. We preoperatively investigated 19 patients. After anesthesia had been induced, controlled ventilation was established to maintain normocarbia using constant uncorrected PaCO2 to adjust ventilation (alpha-stat acid-base regimen). Body core temperature was reduced without surgical intervention to 32 degrees C by surface cooling. Continuous PETCO2 was monitored with a mainstream PETCO2 module. The PA-ETCO2 was calculated using the uncorrected and corrected PaCO2 values. During body temperature reduction from 36 degrees C to 32 degrees C, the gradient between PETCO2 and uncorrected PaCO2 increased 2.5-fold, from 4.1 +/- 3.7 to 10.4 +/- 3.8 mm Hg (P < 0.002). The PA-ETCO2 remained unchanged when the corrected PaCO2 was used for the calculation. We conclude that when the alpha-stat acid-base regimen is used to adjust ventilation, the PA-ETCO2 calculated with the uncorrected PaCO2 increases and should be added to the differential diagnosis of widened PA-ETCO2. In contrast, when the corrected PaCO2 is used for the calculation of the PA-ETCO2, the PA-ETCO2 remains unaltered during hypothermia. IMPLICATIONS: We investigated the impact of induced hypothermia (36 degrees C-32 degrees C) on the gradient between PaCO2 and PETCO2 (PA-ETCO2). The PA-ETCO2 increased 2.5-fold when CO2 determinations were not temperature-corrected. Hypothermia should be added to the differential diagnosis of an increased PA-ETCO2 when the alpha-stat acid-base regimen is used.

Adult↗
PubMed1998

Pulmonary function and radiographic abnormalities related to neurological outcome after aneurysmal subarachnoid hemorrhage.

OBJECT: This observational study is based on a consecutive series of 207 patients with aneurysmal subarachnoid hemorrhage who were treated within 7 days of their most recent bleed. The purpose of the study was to evaluate the effect of respiratory failure on neurological outcome. METHODS: Pulmonary function was assessed by determination of parameters describing pulmonary oxygen transport and exchange, by using composite scores for quantification of lung injury (lung injury score [LIS]) and mechanical ventilator settings (PIF score). Pulmonary function was related to the Hunt and Hess (H & H) grade assigned to the patient at hospital admission (p < 0.001). The pattern and time course of lung injury differed significantly between patients with H & H Grade I or II, Grade III, and Grade IV or V. Hunt and Hess grade, Fisher computerized tomography grade, intracranial pressure, cerebral perfusion pressure, LIS, ratio of PaO2 to the fraction of inspired oxygen (FiO2), and the ratio of the alveolar-minus-arterial oxygen tension difference (AaDO2) to FiO2 were related to neurological outcome (p < 0.001). The LIS on the day of maximum lung injury remained an independent predictor of outcome (p = 0.01) in a stepwise logistic regression analysis. The probability of poor neurological outcome significantly increased with both decreasing cerebral perfusion pressure and increasing severity of lung injury. CONCLUSIONS: The overall mortality rate was 22.2% (46 of 207 patients). Subarachnoid hemorrhage and its neurological sequelae accounted for the principal mortality in this series. Medical (nonneurological and nontreatment-related) complications accounted for 37% of all deaths. Systemic inflammatory response syndrome with associated multiple organ dysfunction syndrome was the leading cause of death from medical complications. The authors conclude that respiratory failure is related to neurological outcome, although it is not commonly the primary cause of death from medical complications.

Adult↗
PubMed1997

Changes in oxygenation variables during progressive hypothermia in anesthetized patients.

Because deliberate hypothermia is becoming commonly used during neurosurgery, this study was performed to investigate the effects of a progressive reduction of body core temperature (T) on whole body oxygenation variables in patients undergoing elective intracranial surgery. In 13 patients (Hypothermic Group), T was reduced to 32.0 degrees C using convective-based surface cooling. In six patients (Control Group), T was maintained at 35.5 degrees C during the entire study period. The cardiac index (CI) was determined with a pulmonary artery catheter by thermodilution. Whole body oxygen delivery (DO2) was calculated from CI and arterial oxygen content. Whole body oxygen consumption (VO2), carbon dioxide production (VCO2), and energy expenditure (EE) were determined by ventilation gas analysis (indirect calorimetry). Mixed venous oxygen tension at 50% saturated hemoglobin (P50), and whole body oxygen extraction ratio (O2ER) were calculated. Repeated-measures analysis of variance and the Mann-Whitney test were used for statistical analysis. Data are expressed as means +/- SD. VO2 (from 100 +/- 13 to 77 +/- 11 ml.min-1.m-2), VCO2 (from 75 +/- 7 to 57 +/- 7 ml.min-1. m-2), EE (from 667 +/- 67 to 509 +/- 66 kcal.d-1.m-2), P50 (from 23.8 +/- 1.7 to 20 +/- 0.9 mm Hg), and O2ER (from 0.29 +/- 0.05 to 0.22 +/- 0.03%) decreased significantly in the Hypothermic Group between 35.5 and 32.0 degrees C (p < 0.05). None of these variables changed in the Control Group and at 32.0 degrees C VO2, VCO2, EE, P50, and O2ER were significantly lower in the Hypothermic Group than in the Control Group. DO2 remained unchanged in both groups. We conclude that progressive hypothermia in anesthetized patients reduces metabolic rate but does not change DO2. The significant decrease in O2ER may partly be related to a leftward shift of the oxyhemoglobin dissociation curve, as evidenced by the decrease in P50.

Aged↗
PubMed1995

Thermoregulatory vasoconstriction impairs active core cooling.

BACKGROUND: Many clinicians now consider hypothermia indicated during neurosurgery. Active cooling often will be required to reach target temperatures < 34 degrees C sufficiently rapidly and nearly always will be required if the target temperature is 32 degrees C. However, the efficacy even of active cooling might be impaired by thermoregulatory vasoconstriction, which reduces cutaneous heat loss and constrains metabolic heat to the core thermal compartment. The authors therefore tested the hypothesis that the efficacy of active cooling is reduced by thermoregulatory vasoconstriction. METHODS: Patients undergoing neurosurgical procedures with hypothermia were anesthetized with either isoflurane/nitrous oxide (n = 13) or propofol/fentanyl (n = 13) anesthesia. All were cooled using a prototype forced-air cooling device until core temperature reached 32 degrees C. Core temperature was measured in the distal esophagus. Vasoconstriction was evaluated using forearm minus fingertip skin-temperature gradients. The core temperature triggering a gradient of 0 degree C identified the vasoconstriction threshold. RESULTS: In 6 of the 13 patients given isoflurane, vasoconstriction (skin-temperature gradient = 0 degrees C) occurred at a core temperature of 34.4 +/- 0.9 degree C, 1.7 +/- 0.58 h after induction of anesthesia. Similarly, in 7 of the 13 patients given propofol, vasoconstriction occurred at a core temperature of 34.5 +/- 0.9 degree C, 1.6 +/- 0.6 h after induction of anesthesia. In the remaining patients, vasodilation continued even at core temperatures of 32 degrees C. Core cooling rates were comparable in each anesthetic group. However, patients in whom vasodilation was maintained cooled fastest. Patients in whom vasoconstriction occurred required nearly an hour longer to reach core temperatures of 33 degrees C and 32 degrees C than did those in whom vasodilation was maintained (P < 0.01). CONCLUSIONS: Vasoconstriction did not produce a full core temperature "plateau," because of the extreme microenvironment provided by forced-air cooling. However, it markedly decreased the rate at which hypothermia developed. The approximately 1-h delay in reaching core temperatures of 33 degrees C and 32 degrees C could be clinically important, depending on the target temperature and the time required to reach critical portions of the operation.

Adult↗
PubMed1994

Effect of hyperglycemia on peri-ischemic neurotransmitter levels in the rabbit hippocampus.

This study examined the effect of preexisting hyperglycemia on the extracellular concentrations of glutamate and glycine in the rabbit hippocampus using in vivo microdialysis during brief episodes of transient global ischemia. Hyperglycemia has repeatedly been shown to exacerbate the neurologic injury produced by episodes of global cerebral ischemia. Under hypoxic conditions, glucose may be metabolized to glutamate, a known neurotoxin which has been implicated as a mediator of ischemic neuronal cell death. In this study, microdialysis probes were stereotactically inserted into the dorsal hippocampus of anesthetized rabbits. Animals were randomized to receive an i.v. infusion of either saline or dextrose. Global cerebral ischemia was then produced by the combination of neck tourniquet inflation and the induction of systemic hypotension. Administration of dextrose had no effect on these basal levels of glutamate or glycine. During ischemia, glutamate and glycine concentrations increased several-fold when compared with baseline. However, hippocampal glutamate concentrations were lower in the dextrose-treated groups during the peri-ischemic period (P = 0.02). Glycine concentrations were higher during the reperfusion period in the dextrose-treated animals when compared with saline controls (P = 0.03). The increased concentration of extracellular glycine which was observed in the dextrose-treated animals may contribute to the neurologic injury which occurs during episodes of global ischemia. The results of this study suggest that hyperglycemia does not exert its detrimental effects by increasing the extracellular concentration of glutamate.

Animals↗