Efficiency of spinal anesthesia versus general anesthesia for lumbar spinal surgery: a retrospective analysis of 544 patients.

BACKGROUND: Previous studies have shown varying results in selected outcomes when directly comparing spinal anesthesia to general in lumbar surgery. Some studies have shown reduced surgical time, postoperative pain, time in the postanesthesia care unit (PACU), incidence of urinary retention, postoperative nausea, and more favorable cost-effectiveness with spinal anesthesia. Despite these results, the current literature has also shown contradictory results in between-group comparisons. MATERIALS AND METHODS: A retrospective analysis was performed by querying the electronic medical record database for surgeries performed by a single surgeon between 2007 and 2011 using procedural codes 63030 for diskectomy and 63047 for laminectomy: 544 lumbar laminectomy and diskectomy surgeries were identified, with 183 undergoing general anesthesia and 361 undergoing spinal anesthesia (SA). Linear and multivariate regression analyses were performed to identify differences in blood loss, operative time, time from entering the operating room (OR) until incision, time from bandage placement to exiting the OR, total anesthesia time, PACU time, and total hospital stay. Secondary outcomes of interest included incidence of postoperative spinal hematoma and death, incidence of paraparesis, plegia, post-dural puncture headache, and paresthesia, among the SA patients. RESULTS: SA was associated with significantly lower operative time, blood loss, total anesthesia time, time from entering the OR until incision, time from bandage placement until exiting the OR, and total duration of hospital stay, but a longer stay in the PACU. The SA group experienced one spinal hematoma, which was evacuated without any long-term neurological deficits, and neither group experienced a death. The SA group had no episodes of paraparesis or plegia, post-dural puncture headaches, or episodes of persistent postoperative paresthesia or weakness. CONCLUSION: SA is effective for use in patients undergoing elective lumbar laminectomy and/or diskectomy spinal surgery, and was shown to be the more expedient anesthetic choice in the perioperative setting

Noninvasive continuous optical monitoring of absolute cerebral blood flow in critically ill adults

We investigate a scheme for noninvasive continuous monitoring of absolute cerebral blood flow (CBF) in adult human patients based on a combination of time-resolved dynamic contrast-enhanced near-infrared spectroscopy (DCE-NIRS) and diffuse correlation spectroscopy (DCS) with semi-infinite head model of photon propogation. Continuous CBF is obtained via calibration of the DCS blood flow index (BFI) with absolute CBF obtained by intermittent intravenous injections of the optical contrast agent indocyanine green. A calibration coefficient (gamma) for the CBF is thus determined, permitting conversion of DCS BFI to absolute blood flow units at all other times. A study of patients with acute brain injury (N = 7) is carried out to ascertain the stability of gamma. The patient-averaged DCS calibration coefficient across multiple monitoring days and multiple patients was determined, and good agreement between the two calibration coefficients measured at different times during single monitoring days was found. The patient-averaged calibration coefficient of 1.24 x 10(9) (mL/100 g/min)/(cm(2)/s) was applied to previously measured DCS BFI from similar brain-injured patients||in this case, absolute CBF was underestimated compared with XeCT, an effect we show is primarily due to use of semi-infinite homogeneous models of the head.54115Agências de fomento estrangeiras apoiaram essa pesquisa, mais informações acesse artig

Quantification of cerebral blood flow in adults by contrast-enhanced near-infrared spectroscopy: Validation against MRI

The purpose of this study was to assess the accuracy of absolute cerebral blood flow (CBF) measurements obtained by dynamic contrast-enhanced (DCE) near-infrared spectroscopy (NIRS) using indocyanine green as a perfusion contrast agent. For validation, CBF was measured independently using the MRI perfusion method arterial spin labeling (ASL). Data were acquired at two sites and under two flow conditions (normocapnia and hypercapnia). Depth sensitivity was enhanced using time-resolved detection, which was demonstrated in a separate set of experiments using a tourniquet to temporally impede scalp blood flow. A strong correlation between CBF measurements from ASL and DCE-NIRS was observed (slope = 0.99 ± 0.08, y-intercept = −1.7 ± 7.4 mL/100 g/min, and R2 = 0.88). Mean difference between the two techniques was 1.9 mL/100 g/min (95% confidence interval ranged from −15 to 19 mL/100g/min and the mean ASL CBF was 75.4 mL/100 g/min). Error analysis showed that structural information and baseline absorption coefficient were needed for optimal CBF reconstruction with DCE-NIRS. This study demonstrated that DCE-NIRS is sensitive to blood flow in the adult brain and can provide accurate CBF measurements with the appropriate modeling techniques

Defining a Taxonomy of Intracranial Hypertension Is ICP More Than Just a Number?

Intracranial pressure (ICP) monitoring and control is a cornerstone of neuroanesthesia and neurocritical care. However, because elevated ICP can be due to multiple pathophysiological processes, its interpretation is not straightforward. We propose a formal taxonomy of intracranial hypertension, which defines ICP elevations into 3 major pathophysiological subsets: increased cerebral blood volume, masses and edema, and hydrocephalus. (1) Increased cerebral blood volume increases ICP and arises secondary to arterial or venous hypervolemia. Arterial hypervolemia is produced by autoregulated or dysregulated vasodilation, both of which are importantly and disparately affected by systemic blood pressure. Dysregulated vasodilation tends to be worsened by arterial hypertension. In contrast, autoregulated vasodilation contributes to intracranial hypertension during decreases in cerebral perfusion pressure that occur within the normal range of cerebral autoregulation. Venous hypervolemia is produced by Starling resistor outflow obstruction, venous occlusion, and very high extracranial venous pressure. Starling resistor outflow obstruction tends to arise when cerebrospinal fluid pressure causes venous compression to thus increase tissue pressure and worsen tissue edema (and ICP elevation), producing a positive feedback ICP cycle. (2) Masses and edema are conditions that increase brain tissue volume and ICP, causing both vascular compression and decrease in cerebral perfusion pressure leading to oligemia. Brain edema is either vasogenic or cytotoxic, each with disparate causes and often linked to cerebral blood flow or blood volume abnormalities. Masses may arise from hematoma or neoplasia. (3) Hydrocephalus can also increase ICP, and is either communicating or noncommunicating. Further research is warranted to ascertain whether ICP therapy should be tailored to these physiological subsets of intracranial hypertension

Patient Transport and Brain Oxygen in Comatose Patients

Abstract OBJECTIVE Transport of critically ill intensive care unit patients may be hazardous. We examined whether brain oxygen (brain tissue oxygen partial pressure [PbtO2]) is influenced by transport to and from a follow-up head computed tomography (transport head computed tomography [tHCT]) scan. METHODS Forty-five patients (24 men, 21 women; Glasgow Coma Scale score ≤8; mean age, 47.3 ± 19.0 years) who had a traumatic brain injury (n = 26) or subarachnoid hemorrhage (n = 19) were retrospectively identified from a prospective observational cohort of PbtO2 monitoring in a neurosurgical intensive care unit at a university-based level I trauma center. PbtO2, intracranial pressure, and cerebral perfusion pressure were monitored continuously and compared during the 3 hours before and after 100 tHCT scans. RESULTS The mean PbtO2 before and after the tHCT scans for all 100 scans was 37.9 ± 19.8 mm Hg and 33.9 ± 17.2 mm Hg, respectively (P = .0001). A decrease in PbtO2 (>5%) occurred after 54 tHCTs (54%) and in 36 patients (80%). In instances in which a decrease occurred, the average decrease in mean, minimum, and maximum PbtO2 was 23.6%, 29%, and 18.1%, respectively. This decrease was greater when PbtO2 was compromised (<25 mm Hg) before tHCT. An episode of brain hypoxia (<15 mm Hg) was identified in the 3 hours before tHCT in 9 and after tHCT in 19 instances. On average, an episode of brain hypoxia was 46.6 ± 16.0 (standard error) minutes longer after tHCT than before tHCT (P = .008). Multivariate analysis suggests that changes in lung function (PaO2/fraction of inspired oxygen [FiO2] ratio) may account for the reduced PbtO2 after tHCT (parameter estimate 0.45, 95% confidence interval: 0.024–0.871; P = .04). CONCLUSION These data suggest that transport to and from the intensive care unit may adversely affect PbtO2. This deleterious effect is greater when PbtO2 is already compromised and may be associated with lung function

Does the melatonin receptor 1B gene polymorphism have a role in postoperative delirium?

INTRODUCTION:Patients undergoing cardiac surgery are at high risk for postoperative delirium, which is associated with longer hospital and intensive care lengths of stays, increased morbidity and mortality. Because sleep disturbances are common in delirium, melatonin has been an area of interest in the treatment of delirium. The rs10830963 single nucleotide polymorphism of the melatonin receptor 1B gene can cause pathological dysfunction of this receptor and is associated with delayed morning offset of melatonin. We hypothesized patients undergoing aortic cardiac surgery who have the risk genotype of a melatonin receptor 1B polymorphism would have a higher incidence of postoperative delirium. METHODS:Ninety-eight patients undergoing aortic root or valve surgery underwent analysis for melatonin receptor 1B single nucleotide polymorphism, rs10830963. Using a validated method, CHART-DEL, all charts were retrospectively reviewed and scored for the presence of delirium while blinded to the results of the melatonin receptor 1B gene polymorphism. RESULTS:Genotyping for melatonin receptor 1B polymorphism was acceptable in 76 subjects of European descent of which 18 (23.7%) had delirium. Four of seven subjects with the risk genotype had delirium versus only 20.3% of subjects without the risk genotype. This carried an odds ratio of 5.2 (1.0, 26.1), p = 0.050. CONCLUSION:This observation suggests a role of the risk genotype of a melatonin receptor 1B polymorphism in the development of postoperative delirium. These hypotheses generating results warrant further prospective studies in a larger cohort group with delirium, circadian rhythm and melatonin assessments

Phenylephrine Infusion Prevents Impairment of ATP- and Calcium-Sensitive Potassium Channel-Mediated Cerebrovasodilation after Brain Injury in Female, but Aggravates Impairment in Male, Piglets through Modulation of ERK MAPK Upregulation

Traumatic brain injury (TBI) contributes to morbidity in children and boys, and hypotension worsens outcome. Extracellular signal-related kinase (ERK) mitogen-activated protein kinase (MAPK) is upregulated more in males and reduces cerebral blood flow (CBF) after fluid percussion injury (FPI). Increased cerebral perfusion pressure (CPP) via phenylephrine (Phe) sex-dependently improves impairment of the cerebral autoregulation seen after FPI through modulation of ERK MAPK upregulation, which is aggravated in males, but is blocked in females. Activation of ATP- and calcium-sensitive (Katp and Kca) channels produces cerebrovasodilation and contributes to autoregulation, both of which are impaired after FPI. Using piglets equipped with a closed cranial window, we hypothesized that potassium channel functional impairment after FPI is prevented by Phe in a sex-dependent manner through modulation of ERK MAPK upregulation. The Katp and Kca agonists cromakalim and NS 1619 produced vasodilation that was impaired after FPI more in males than in females. Phe prevented reductions in cerebrovasodilation after cromakalim and NS 1619 in females, but reduced dilation after these potassium channel agonists were given to males after FPI. Co-administration of U 0126, an ERK antagonist, and Phe fully restored dilation to cromakalim, calcitonin gene-related peptide (CGRP), and NS 1619, in males after FPI. These data indicate that Phe sex-dependently prevents impairment of Katp and Kca channel-mediated cerebrovasodilation after FPI in females, but aggravates impairment in males, through modulation of ERK MAPK upregulation. Since autoregulation of CBF is dependent on intact functioning of potassium channels, these data suggest a role for sex-dependent mechanisms in the treatment of cerebral autoregulation impairment after pediatric TBI