Spinal cord stimulation in diabetic lower limb critical ischaemia: transcutaneous oxygen measurement as predictor for treatment success.
(9/205)
OBJECTIVES: to evaluate whether transcutaneous oxygen tension (TcpO(2)) measurements could be used as a specific prognostic parameter in selecting diabetic patients for permanent device implantation. METHODS: sixty consecutive diabetic patients (28 with autonomic neuropathy), classified as Fontaine stage III or IV, underwent spinal cord stimulation (SCS) for ischaemic pain, after failed conservative or surgical treatment. Pedal TcpO(2)on the dorsum of the foot and ankle-pressure Doppler measurements were performed before, and 2 and 4 weeks after implantation. RESULTS: limb salvage and good pain relief were achieved in 35 patients, while in 12 partial pain relief and limb salvage for at least 6 months were obtained. In 13 patients the method failed and the ischaemic limbs were amputated. Only 3 of the 28 patients with neuropathy had any long-term benefit. Limb salvage was achieved in those patients with a significant increase in TcpO(2)within 2 weeks of stimulation. The stage of the neuropathy was inversely related to the success of SCS therapy. The ankle-brachial pressure index (ABPI) did not change after stimulation. CONCLUSIONS: diabetic patients with significant increase of TcpO(2)and pain relief during a 2-week test period may be successfully treated by long-term SCS unless they have advanced autonomic neuropathy. (+info)
Near infrared spectroscopy (NIRS) distinguishes seizure types.
(10/205)
Near infrared spectroscopy (NIRS) is a noninvasive method for bedside measurement of cerebral oxygenation (SaO(2)). The purpose of this study was to establish differences in SaO(2)for complex partial seizures (CPS) and rapidly secondarily generalized CPS (RCPS). We studied eight adults with medically refractory epilepsy undergoing evaluation for temporal lobectomy. We continually measured cerebral SaO(2)via a Somanetic Invos 3100a cerebral oximeter, pre-ictal (5 minutes), ictal, immediate (30 seconds) post-ictal, and late post-ictal (5 minutes after ictus). Seventeen seizures (12 CPS, four RCPS and one subclinical) were recorded in eight patients. The percentage change in cerebral SaO(2)from pre-ictal to ictal periods was derived. Cerebral SaO(2)increased (percentage change, mean: 16.6, SD: 13.9) for CPS and decreased (percentage change, mean: 51.1, SD: 18.1) for RCPS. No change in cerebral oximetry was recorded for the subclinical seizure. Post-ictal (immediate and late) increase in cerebral SaO(2)was seen for 11 of the 17 seizures (nine CPS and two RCPS). Peripheral SaO(2)rose greater than 93% for all CPS and the subclinical seizure, but decreased between 78 and 84% during RCPS. These results suggest NIRS distinguishes cerebral SaO(2)patterns between CPS and RCPS. The decrease in peripheral SaO(2), however, may account for the decrease in cerebral SaO(2)seen in generalized seizures. (+info)
Effect of P-glycoprotein modulation on the clinical pharmacokinetics and adverse effects of morphine.
(11/205)
AIMS: To investigate the effect of acute P-glycoprotein inhibition by the multidrug-resistance (MDR) modulator valspodar (SDZ PSC 833; PSC) on the pharmacokinetics, and potentially adverse pharmacodynamic effects of morphine, and its principal pharmacologically active metabolites, morphine-3-glucuronide (M3G) and morphine-6-glucuronide (M6G). METHODS: In a double-blind, three-way crossover study, the pharmacokinetic and potentially adverse pharmacodynamic effects (reaction time, transcutaneous PCO2, blood pressure) of morphine were compared with and without acute inhibition of P-glycoprotein by PSC. The effects of PSC alone were also evaluated. The study was performed in 18 healthy male volunteers and pharmacodynamic effects analysed by measuring the area under the effect (AUE) curve. 150 mg PSC (or its placebo) was given as an i.v. infusion over 2 h. With the expected inhibition of Pgp 1 h after starting PSC infusion, 7.5 morphine HCl (or its placebo) was infused over 2 h. RESULTS: The infusion of PSC resulted in blood concentrations expected to inhibit Pgp mediated transport. While the pharmacokinetics of plasma morphine and M6G. were unaffected there was a small but statistically significant increase in the AUC and Cmax of M3G (11.8 and 8.3%, respectively). The t(1/2) and tmax were unaffected. The pharmacokinetic parameters of PSC were not affected by coadministration with morphine. PSC did not significantly affect the adverse events of morphine, as assessed by spontaneous reporting. Compared with PSC alone, morphine elicited an increase in reaction time (Emax 48 ms, compared with the predose absolute reaction time of 644 ms), which was not detected by the alertness-drowsiness score, indicating only slight sedation. There was a significant decrease in systolic blood pressure (Emin -9 mm Hg), and a trend for a fall in diastolic blood pressure (Emin -14.5 mm Hg) and respiratory rate (Emin -1.8 breath x min(-1)). For all these parameters, the effects of PSC/morphine were similar to that of PSC alone, suggesting some attenuation of morphine's effect. In contrast, morphine caused a significant increase in PCO2 (Emax 0.69 kPa) compared to PSC alone, indicating slight respiratory depression. This increase was similar to that of the PSC/morphine combination. CONCLUSIONS: Acute inhibition of P-glycoprotein by PSC in this setting does not affect the pharmacokinetic or safety-related pharmacodynamic profile of morphine in a clinically significant manner. (+info)
Safety of patient-maintained propofol sedation using a target-controlled system in healthy volunteers.
(12/205)
We investigated the safety of a patient-maintained system that allows individuals to operate a target-controlled infusion of propofol to achieve sedation. Ten healthy volunteers were recruited and instructed to try to anaesthetize themselves with the system. A target-controlled infusion of propofol was set to deliver a target propofol concentration of 1 microgram ml-1, and the subjects allowed to increase the target in increments of 0.2 microgram ml-1 by pressing a control button twice in 1 s. There was a lockout time of 2 min and a maximum permitted target concentration of 3 micrograms ml-1. Heart rate and pulse oximetry oxygen saturation (SpO2) were monitored continuously, and non-invasive arterial pressure, ventilatory frequencies and sedation scores were measured every 5 min. Sedation was continued until the subject stopped pressing the button. A keyword was then read for the individual to remember and sedation discontinued. There were no instances of significant decrease of SpO2 or loss of airway control. Maximum target blood concentration of propofol recorded ranged from 1.4 to 3 micrograms ml-1. Two subjects became oversedated, one of whom was unrousable with loss of eyelash reflex. No subject could recall the keyword, although one recognized it from a list of 10 words. We conclude that the patient-maintained sedation system described could not be guaranteed to produce only conscious sedation in all patients, and that close clinical supervision by an anaesthetist would still be required for safe operation. (+info)
Asynchronous breathing during sleep.
(13/205)
BACKGROUND: Children rarely complain of symptoms associated with sleep disordered breathing (SDB). Paradoxical inward rib cage movement (PIRCM) during sleep might prove useful for detecting SDB. AIMS: (1) To determine the correlation between the degree of PIRCM and other measures of disordered breathing during sleep. PIRCM occurs physiologically throughout rapid eye movement sleep in neonates, while no PIRCM has been reported during sleep in adolescents. (2) To determine the chronological changes in the degree of PIRCM. METHODS: PIRCM was quantified by means of the laboured breathing index (LBI). LBI was determined by respiratory inductive plethysmography; PIRCM accompanies a high LBI. Sleep recordings obtained for 101 subjects for various reasons (aged from 3.5 months to 19 years) were analysed. RESULTS: In 22 records, the minimum SaO2 value was 90% or more and no obstructive apnoea of more than 10 seconds was observed. In these 22 records, LBI during rapid eye movement sleep decreased significantly with age, reaching the mature low level at 3.3 years of age. In the other 79 records, LBI correlated well with measures of obstructed breathing during sleep. CONCLUSIONS: By paying more attention to PIRCM, more obstructed breathing during sleep might be found among children aged 3 years or more. (+info)
Tourniquet-induced wound hypoxia after total knee replacement.
(14/205)
We have investigated whether the thigh tourniquet used during total knee replacement (TKR) influenced the development of postoperative wound hypoxia and was a cause of delayed wound healing. We allocated randomly 31 patients (31 TKRs) to one of three groups: 1) no tourniquet; 2) tourniquet inflated at low pressure (about 225 mmHg); and 3) tourniquet inflated to high pressure of about 350 mmHg. Wound oxygenation was measured using transcutaneous oxygen electrodes. In the first week after surgery, patients with a tourniquet inflated to a high pressure had greater wound hypoxia than those with a low pressure. Those without a tourniquet also had wound hypoxia, but the degree and duration were less pronounced than in either of the groups with a tourniquet. Use of a tourniquet during TKR can increase postoperative wound hypoxia, especially when inflated to high pressures. Our findings may be relevant to wound healing and the development of wound infection. (+info)
Interobserver and intraobserver reproducibility of peripheral blood and oxygen pressure measurements in the assessment of lower extremity arterial disease.
(15/205)
INTRODUCTION: Peripheral blood pressure measurements play a prominent role in the diagnosis and follow-up of patients with peripheral vascular diseases. Toe pressure of the hallux (TP1) and second toe (TP2) and transcutaneous oxygen pressure (TCPO2) measurements are becoming more important. The ankle/brachial pressure index (ABPI) is known to be a reliable parameter, but the toe pressure and TCPO2 are evaluated less thoroughly. Therefore, we evaluated the reproducibility of TP1, TP2, TCPO2, ABPI, ankle pressure (AP), and brachial pressure (BP). PATIENTS AND METHODS: In 54 patients with various stages of peripheral vascular disease, the intraobserver and interobserver reproducibility of BP, AP, ABPI, TP1, TP2, and TCPO2 was investigated by calculating the repeatability coefficient (RC) and the intraclass correlation coefficient (ICC) and by using Bland-Altman plots. RESULTS: The intraobserver and interobserver reproducibility at 1 day and after 1 week of BP, AP, ABPI, and TP1 was substantial and comparable (ICC range, 0.80-0.99), except for the BP after 1 week. The TP2 and TCPO2 were less reproducible (ICC range, 0.62-0.98). The interobserver RC of BP was 31 mm Hg; of AP, 44 mm Hg; of ABPI, 27%; of TP1, 41 mm Hg; of TP2, 67 mm Hg; and of TCPO2; 30 mm Hg. The difference plot showed that the observer variability was equally distributed across the range of pressure in all measurements. CONCLUSION: The BP, AP, ABPI, and TP1 have a substantial intraobserver and interobserver reproducibility, whereas TP2 and TCPO2 show worse reproducibility. Especially when low values (or values around a cutoff value) are measured, the RC should be taken into account, and repetition of the measurement is advocated. (+info)
Establishing predictive indicators for the status of loaded soft tissues.
(16/205)
Two complementary techniques were employed to assess the soft tissue response to applied pressure. The noninvasive methods involve the simultaneous measurement of the local tensions of oxygen and carbon dioxide (tcPO2 and tcPCO2) and the collection and subsequent analysis of sweat collected from the sacrum, a common site for the development of pressure sores. All tests were performed on able-bodied subjects. Results have indicated that oxygen levels (tcPO2) were lowered in soft tissues subjected to applied pressures of between 40 (5.3 kPa) and 120 mmHg (16.0 kPa). At the higher pressures, this decrease was generally associated with an increase in carbon dioxide levels (tcPCO2) well above the normal basal levels of 45 mmHg (6 kPa). There were also considerable increases, in some cases up to twofold, in the concentrations of both sweat lactate and urea at the loaded site compared with the unloaded control. By comparing selected parameters, a threshold value for loaded tcPO2 was identified, representing a reduction of ~60% from unloaded values. Above this threshold, there was a significant relationship between this parameter and the loaded/unloaded concentration ratios for both sweat metabolites. These parameters may prove useful in identifying those subjects whose soft tissue may be compromised during periods of pressure ischemia. (+info)