The effect of a thoracic spinal block on fos expression in the lumbar spinal cord of the rat induced by a noxious electrical stimulus at the hindpaw.

BACKGROUND: Fos expression in the lumbar spinal cord, resulting from a noxious electrical stimulus at the hindpaw, is hypothesized to originate from three sources: direct sensory input of the noxious stimulus, local interactions in the spinal cord, and input of modulating signals from supraspinal regions. Our aim in this study was to discriminate among these sources by eliminating the supraspinal input. METHODS: Therefore, a spinal block was administered in male Wistar rats by administering a local anesthetic (bupivacaine) through an intrathecal catheter at the mid-thoracic level. This thoracic spinal block completely suppressed the noxious stimulation-induced withdrawal reflex that is normally elicited by electrical stimulus. Fos immunoreactivity (Fos-IR) was quantified in all laminae of the L4 segment of the spinal cord. RESULTS: Noxious stimulation resulted in a general and strong increase in Fos-IR in the ipsilateral dorsal horn, mainly in Laminae I, II, and V. Thoracic spinal block caused a remarkable increase in the amount of Fos-IR in Lamina V, but had no significant effect on the Fos-IR in Laminae I and II. CONCLUSIONS: The increase in Fos-IR in Lamina V may have resulted from the interruption of a pain-modulating descending mechanism from the brain. A known modulating descending mechanism is the serotonergic system, controlled by the periaqueductal gray. This system inhibits the neurons in the superficial laminae. Another nonserotonergic system originates in the anterior pretectal nucleus. The latter facilitates neurons in the superficial laminae, while neurons in Lamina V are inhibited. We conclude that both systems are probably involved in the observed effects of the peripheral noxious stimulation given in the present model.

A simplified approach to vertical infraclavicular brachial plexus blockade using hand-held Doppler.

In this observational study, we used Doppler ultrasound during the performance of vertical infraclavicular brachial plexus blockade. The success rate at inserting the needle at the point where the sound of the subclavian artery via Doppler reached its maximum audibility was compared with that of the classical insertion point. In 89 of the 100 patients, the medial or posterior cord was found at first needle pass. Using the Doppler point for insertion resulted in a significantly more lateral entry point compared with the classical point (P < 0.001) and was associated with a high success rate of infraclavicular block.

Continuous positive airway pressure breathing increases cranial spread of sensory blockade after cervicothoracic epidural injection of lidocaine.

BACKGROUND: Continuous positive airway pressure (CPAP) increases the caudad spread of sensory blockade after low-thoracic epidural injection of lidocaine. We hypothesized that CPAP would increase cephalad spread of blockade after cervicothoracic epidural injection. METHODS: Twenty patients with an epidural catheter at the C6-7 or C7-T1 interspace received an epidural dose of lidocaine while breathing at ambient pressure (control group), or while breathing with 7.5 cm H2O CPAP. After injection, we evaluated the spread of sensory blockade. Spirometry variables before and after epidural injection were also measured. RESULTS: Data are presented as median (interquartile range) values. Sensory block ranged from C7 (C4-7) to T4 (T4-6) in the control group and from C2 (C2-4) to T4 (T2-5) in the CPAP group (P = 0.003 for the cranial border). The total number of segments blocked was 7.5 (6.8-9.8) in the control group and 10 (8-12) in the CPAP group (P = 0.13). The number of segments blocked cranial to the injection site was one (0.8-3.5) in the control group and five (3.5-7) in the CPAP group (P = 0.006). The number of patients with a maximal cranial block (up to C2) was one in the control group and seven in the CPAP group (P = 0.02). In both groups, there was a small but significant decrease from baseline in spirometry values, with no differences between groups. CONCLUSION: Applying CPAP during cervicothoracic epidural injection of lidocaine resulted in a more cranial extension of sensory blockade when compared with breathing at ambient pressure.

Anesthesia-related morbidity and mortality after surgery for muscle biopsy in children with mitochondrial defects.

BACKGROUND: Children with mitochondrial defects (MD) may have an increased risk for cardiorespiratory and neurological complications from anesthesia. The aim of this study was to determine the incidence of perioperative complications and adverse events in children with MD. METHODS: We performed a retrospective review of the anesthesia, surgical and medical records of 155 children up to 10 years who underwent a diagnostic surgical muscle biopsy for suspected mitochondrial and muscle disorders between 1999 and 2003. The data of the 122 patients where a definite MD diagnosis was found were analyzed. Anesthesia was conducted according to the discretion of the attending staff. In children with MD the activity of the different complexes of the oxidative phosphorylation system was measured. RESULTS: From the preoperative assessment, signs of encephalopathy were most frequent (n = 93), followed by muscle weakness (n = 32), lactic acidosis (n = 15), cardiomyopathy and/or conduction defects (n = 10) and chronic respiratory problems (n = 7). The mean age of the children with MD was 32.4 months (SD = 26.9). The mean duration of anesthesia was 36.0 min (SD = 12.6) and the mean length of stay in the recovery room was 33.0 min (SD = 24.0). There were no major changes in heart rate or blood pressure which required pharmacological intervention during anesthesia or postanesthesia care unit (PACU) stay. A short episode of SpO2 <80% with airway obstruction occurred once in the PACU. Biochemical analysis in the children with a MD showed an isolated deficiency of one of the five protein complexes of oxidative phosphorylation in 42 children, a combination of complex deficiencies in 41 and no definite localization in 39 children. CONCLUSION: With standard preoperative assessment, monitoring and anesthesia management, there were no major peroperative and postoperative anesthesia-related complications in children undergoing surgical muscle biopsy with a MD diagnosis.

A comparison of epidural pressures and incidence of true subatmospheric epidural pressure between the mid-thoracic and low-thoracic epidural space.

BACKGROUND: Differences in epidural pressure (EP) may influence the spread of blockade in thoracic epidural anesthesia. We evaluated if EP and the incidence of subatmospheric EP differ between the mid- and low-thoracic epidural space. METHODS: Patients received an epidural catheter at the T3-5 (MID group, n = 20) or T7-10 (LOW group, n = 20) intervertebral space, respectively. The epidural space was identified using a Tuohy needle connected to a pressure transducer, after which EP was measured. RESULTS: The epidural space could not be identified in three patients who were excluded from the study. EP data are presented as median value (interquartile range). Median EP was 1 mm Hg (-1 to 4.5) in the MID group, and 4 mm Hg (2-7.8) in the LOW group (P = 0.04). The incidence of an EP

Continuous positive airway pressure breathing increases the spread of sensory blockade after low-thoracic epidural injection of lidocaine.

Factors affecting the distribution of sensory blockade after epidural injection of local anesthetics remain incompletely clarified. To evaluate if increasing intrathoracic pressure affects the spread of thoracic epidural anesthesia, we randomized 20 patients who received an epidural catheter at the T7-8 or T8-9 intervertebral space into 2 groups. The control group (n = 10) received an epidural test dose of 4 mL lidocaine 2% during spontaneous breathing at ambient pressure. The continuous positive airway pressure (n = 10) group received the same epidural test dose but during spontaneous respiration with 7.5 cm H2O continuous positive airway pressure. The groups were comparable with respect to demographic variables. Fifteen minutes after the conclusion of the epidural injection, the sensory block ranged from from T4 [median, interquartile range 2.75 segments] to T11 (interquartile range 3.5 segments) in the control group and from T5 (interquartile range 2.25 segments) to L2 (IQR 2.25 segments) in the continuous positive airway pressure group (P = 0.005 for the caudal border). The total number of segments blocked was 7 (median, interquartile range 2.25) in the control group and 11 (interquartile range 3.5) in the continuous positive airway pressure group (P = 0.004). The number of segments blocked caudad to the injection site was 3 (median, interquartile range 3.5) in the control group and 6 (interquartile range 2.25) in the continuous positive airway pressure group (P = 0.005). We conclude that continuous positive airway pressure increases the spread of sensory blockade in thoracic epidural anesthesia, primarily by a more caudad extension of sensory blockade.

Silent brain infarcts in patients with manifest vascular disease.

BACKGROUND AND PURPOSE: Silent infarcts are frequently found on MRIs of brains of healthy elderly persons (aged >60 years). The purpose of this study was to investigate the prevalence and determinants of silent infarcts in a population of patients with clinically manifest vascular disease. METHODS: To detect silent infarcts, MR images were made in 308 participants of the Second Manifestations of ARTerial disease (SMART) study (mean age, 58 years) without prior stroke or transient ischemic attack. These are patients referred to the University Medical Center Utrecht because of atherosclerotic vascular disease. Risk factors were assessed by questionnaire and by physical, ultrasonographic, and laboratory examinations. RESULTS: Silent infarcts were found in 51 patients (17%). Most infarcts (62%) were located in white matter, 20% in basal ganglia, 14% in brain stem and cerebellum, and 4% in cortical area. Categorical determinants for presence of silent infarct(s) that remained (borderline) significant after adjustment for age were hypertension (odds ratio [OR]=2.2; 95% CI, 1.2 to 4.2), abdominal aortic aneurysm (OR=2.4; 95% CI, 0.9 to 6.4), severe renal failure (OR=7.3; 95% CI, 2.1 to 25.2), and hyperhomocysteinemia (OR=2.6; 95% CI, 1.1 to 5.9). CONCLUSIONS: Patients with manifest vascular disease are at risk for silent infarcts at a younger age. In particular, patients with the aforementioned risk factors should be considered for treatment or (secondary) prevention.