Ultrasound guidance for upper and lower limb blocks.

BACKGROUND: Peripheral nerve blocks can be performed using ultrasound guidance. It is not yet clear whether this method of nerve location has benefits over other existing methods. This review was originally published in 2009 and was updated in 2014. OBJECTIVES: The objective of this review was to assess whether the use of ultrasound to guide peripheral nerve blockade has any advantages over other methods of peripheral nerve location. Specifically, we have asked whether the use of ultrasound guidance:1. improves success rates and effectiveness of regional anaesthetic blocks, by increasing the number of blocks that are assessed as adequate2. reduces the complications, such as cardiorespiratory arrest, pneumothorax or vascular puncture, associated with the performance of regional anaesthetic blocks SEARCH METHODS: In the 2014 update we searched the Cochrane Central Register of Controlled Trials (CENTRAL; 2014, Issue 8); MEDLINE (July 2008 to August 2014); EMBASE (July 2008 to August 2014); ISI Web of Science (2008 to April 2013); CINAHL (July 2014); and LILACS (July 2008 to August 2014). We completed forward and backward citation and clinical trials register searches.The original search was to July 2008. We reran the search in May 2015. We have added 11 potential new studies of interest to the list of 'Studies awaiting classification' and will incorporate them into the formal review findings during future review updates. SELECTION CRITERIA: We included randomized controlled trials (RCTs) comparing ultrasound-guided peripheral nerve block of the upper and lower limbs, alone or combined, with at least one other method of nerve location. In the 2014 update, we excluded studies that had given general anaesthetic, spinal, epidural or other nerve blocks to all participants, as well as those measuring the minimum effective dose of anaesthetic drug. This resulted in the exclusion of five studies from the original review. DATA COLLECTION AND ANALYSIS: Two authors independently assessed trial quality and extracted data. We used standard Cochrane methodological procedures, including an assessment of risk of bias and degree of practitioner experience for all studies. MAIN RESULTS: We included 32 RCTs with 2844 adult participants. Twenty-six assessed upper-limb and six assessed lower-limb blocks. Seventeen compared ultrasound with peripheral nerve stimulation (PNS), and nine compared ultrasound combined with nerve stimulation (US + NS) against PNS alone. Two studies compared ultrasound with anatomical landmark technique, one with a transarterial approach, and three were three-arm designs that included US, US + PNS and PNS.There were variations in the quality of evidence, with a lack of detail in many of the studies to judge whether randomization, allocation concealment and blinding of outcome assessors was sufficient. It was not possible to blind practitioners and there was therefore a high risk of performance bias across all studies, leading us to downgrade the evidence for study limitations using GRADE. There was insufficient detail on the experience and expertise of practitioners and whether experience was equivalent between intervention and control.We performed meta-analysis for our main outcomes. We found that ultrasound guidance produces superior peripheral nerve block success rates, with more blocks being assessed as sufficient for surgery following sensory or motor testing (Mantel-Haenszel (M-H) odds ratio (OR), fixed-effect 2.94 (95% confidence interval (CI) 2.14 to 4.04); 1346 participants), and fewer blocks requiring supplementation or conversion to general anaesthetic (M-H OR, fixed-effect 0.28 (95% CI 0.20 to 0.39); 1807 participants) compared with the use of PNS, anatomical landmark techniques or a transarterial approach. We were not concerned by risks of indirectness, imprecision or inconsistency for these outcomes and used GRADE to assess these outcomes as being of moderate quality. Results were similarly advantageous for studies comparing US + PNS with NS alone for the above outcomes (M-H OR, fixed-effect 3.33 (95% CI 2.13 to 5.20); 719 participants, and M-H OR, fixed-effect 0.34 (95% CI 0.21 to 0.56); 712 participants respectively). There were lower incidences of paraesthesia in both the ultrasound comparison groups (M-H OR, fixed-effect 0.42 (95% CI 0.23 to 0.76); 471 participants, and M-H OR, fixed-effect 0.97 (95% CI 0.30 to 3.12); 178 participants respectively) and lower incidences of vascular puncture in both groups (M-H OR, fixed-effect 0.19 (95% CI 0.07 to 0.57); 387 participants, and M-H OR, fixed-effect 0.22 (95% CI 0.05 to 0.90); 143 participants). There were fewer studies for these outcomes and we therefore downgraded both for imprecision and paraesthesia for potential publication bias. This gave an overall GRADE assessment of very low and low for these two outcomes respectively. Our analysis showed that it took less time to perform nerve blocks in the ultrasound group (mean difference (MD), IV, fixed-effect -1.06 (95% CI -1.41 to -0.72); 690 participants) but more time to perform the block when ultrasound was combined with a PNS technique (MD, IV, fixed-effect 0.76 (95% CI 0.55 to 0.98); 587 participants). With high levels of unexplained statistical heterogeneity, we graded this outcome as very low quality. We did not combine data for other outcomes as study results had been reported using differing scales or with a combination of mean and median data, but our interpretation of individual study data favoured ultrasound for a reduction in other minor complications and reduction in onset time of block and number of attempts to perform block. AUTHORS' CONCLUSIONS: There is evidence that peripheral nerve blocks performed by ultrasound guidance alone, or in combination with PNS, are superior in terms of improved sensory and motor block, reduced need for supplementation and fewer minor complications reported. Using ultrasound alone shortens performance time when compared with nerve stimulation, but when used in combination with PNS it increases performance time.We were unable to determine whether these findings reflect the use of ultrasound in experienced hands and it was beyond the scope of this review to consider the learning curve associated with peripheral nerve blocks by ultrasound technique compared with other methods.

Ultrasound guidance for peripheral nerve blockade.

BACKGROUND: Peripheral nerve blocks can be performed using ultrasound guidance. It is not yet clear whether this method of nerve location has benefits over other existing methods. OBJECTIVES: To assess whether the use of ultrasound to guide peripheral nerve blockade has any advantages over other methods of peripheral nerve location. SEARCH STRATEGY: We searched the following databases for relevant published trials: the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library 2008, Issue 3); MEDLINE (1966 to July 2008); EMBASE (1974 to July 2008); ISI Web of Science (1945 to 2008 ); CINAHL (1982 to July 2008); and LILACS (1980 to July 2008). We also handsearched meeting supplements. SELECTION CRITERIA: We included all identified randomized controlled trials (RCTs) comparing ultrasound-guided peripheral nerve block with at least one other method of nerve location. DATA COLLECTION AND ANALYSIS: Two authors independently assessed trial quality and extracted data. We attempted to contact study authors for additional information, where necessary. MAIN RESULTS: We included 18 trials containing data from 1344 patients. Ten trials assessed upper limb blocks and eight assessed lower limb blocks. Most compared ultrasound with peripheral nerve stimulation. All trials were assessed as having a moderate risk of bias due to inability to blind the practitioner. Meta-analysis was not performed because of the variety of blocks, techniques, and outcomes, and the review was based on the authors' assessment of the trials. Ultrasound guidance produced similar success rates in providing surgical anaesthesia (72% to 98.8%) when compared with peripheral nerve stimulation (58% to 93.1%). Major complication rates were low in all studies; however, the use of ultrasound appeared to reduce the incidence of vascular puncture or haematoma formation. Differences in study methodology made it difficult to compare block characteristics, however ultrasound improved quality of sensory block in six studies and motor block in four studies. Block onset time was found to be improved in six out of the 10 studies where this was assessed. Two studies assessed volume of local anaesthetic required and both found a significant reduction was possible when ultrasound was used. Ten studies assessed block performance time and five found a significant reduction with ultrasound, the mean difference in time taken was 1.5 to 4.8 minutes. AUTHORS' CONCLUSIONS: In experienced hands, ultrasound provides at least as good success rates as other methods of peripheral nerve location. Individual studies have demonstrated that ultrasound may reduce complication rates and improve quality, performance time, and time to onset of blocks. Due to wide variations in study outcomes we chose not to combine the studies in our analysis.

Dynamic cerebral autoregulation and baroreflex sensitivity during modest and severe step changes in arterial PCO2.

Changes in the partial pressure of arterial CO2 (PaCO2) regulates cerebrovascular tone and dynamic cerebral autoregulation (CA). Elevations in PaCO2 also increases autonomic neural activity and may alter the arterial baroreflex. We hypothesized that hypercapnia would impair, and hypocapnia would improve, dynamic CA and that these changes would occur independently of any change in baroreflex sensitivity (BRS). In 10 healthy male subjects, incremental hypercapnia was achieved through 4-min administrations of 4% and 8% CO2. Incremental hypocapnia involved two 4-min steps of hyperventilation to change end-tidal PCO2, in an equal and opposite direction, to that incurred during hypercapnia. End-tidal, arterial and internal jugular vein PCO2 were sampled simultaneously at baseline and during each CO2 step. Dynamic CA and BRS was assessed at baseline and during each step change in PaCO2 using spectral and transfer-function analysis of beat-by-beat changes in mean arterial blood pressure (MAP), heart rate and flow velocity in the middle cerebral arterial (MCAv). Critical closing pressure (CCP), an estimate of cerebrovascular tone, was estimated from extrapolation of the MAP-MCAv waveforms. Hypercapnia caused a progressive increase in PaCO2 and MCAv whereas hypocapnia caused the opposite effect. Despite marked changes in CPP, there were no evident change in transfer-function gain, coherence, MAP variability or BRS; however, both MCAv variability and phase in the very-low frequency range was reduced during the most severe level of hyper- and hypocapnia (P < 0.05), and were related to elevations in ventilation (R2 = 0.42-0.52, respectively; P < 0.001). It seems that hyperventilation, rather than PaCO2, has an important influence on dynamic CA.

Human cerebral arteriovenous vasoactive exchange during alterations in arterial blood gases.

Cerebral blood flow (CBF) is highly regulated by changes in arterial Pco(2) and arterial Po(2). Evidence from animal studies indicates that various vasoactive factors, including release of norepinephrine, endothelin, adrenomedullin, C-natriuretic peptide (CNP), and nitric oxide (NO), may play a role in arterial blood gas-induced alterations in CBF. For the first time, we directly quantified exchange of these vasoactive factors across the human brain. Using the Fick principle and transcranial Doppler ultrasonography, we measured CBF in 12 healthy humans at rest and during hypercapnia (4 and 8% CO(2)), hypocapnia (voluntary hyperventilation), and hypoxia (12 and 10% O(2)). At each level, blood was sampled simultaneously from the internal jugular vein and radial artery. With the exception of CNP and NO, the simultaneous quantification of norepinephrine, endothelin, or adrenomedullin showed no cerebral uptake or release during changes in arterial blood gases. Hypercapnia, but not hypocapnia, increased CBF and caused a net cerebral release of nitrite (a marker of NO), which was reflected by an increase in the venous-arterial difference for nitrite: 57 +/- 18 and 150 +/- 36 micromol/l at 4% and 8% CO(2), respectively (both P < 0.05). Release of cerebral CNP was also observed during changes in CO(2) (hypercapnia vs. hypocapnia, P < 0.05). During hypoxia, there was a net cerebral uptake of nitrite, which was reflected by a decreased venous-arterial difference for nitrite: -96 +/- 14 micromol/l at 10% O(2) (P < 0.05). These data indicate that there is a differential exchange of NO across the brain during hypercapnia and hypoxia and that CNP may play a complementary role in CO(2)-induced CBF changes.

Differential effects of acute hypoxia and high altitude on cerebral blood flow velocity and dynamic cerebral autoregulation: alterations with hyperoxia.

We hypothesized that 1) acute severe hypoxia, but not hyperoxia, at sea level would impair dynamic cerebral autoregulation (CA); 2) impairment in CA at high altitude (HA) would be partly restored with hyperoxia; and 3) hyperoxia at HA and would have more influence on blood pressure (BP) and less influence on middle cerebral artery blood flow velocity (MCAv). In healthy volunteers, BP and MCAv were measured continuously during normoxia and in acute hypoxia (inspired O2 fraction = 0.12 and 0.10, respectively; n = 10) or hyperoxia (inspired O2 fraction, 1.0; n = 12). Dynamic CA was assessed using transfer-function gain, phase, and coherence between mean BP and MCAv. Arterial blood gases were also obtained. In matched volunteers, the same variables were measured during air breathing and hyperoxia at low altitude (LA; 1,400 m) and after 1-2 days after arrival at HA ( approximately 5,400 m, n = 10). In acute hypoxia and hyperoxia, BP was unchanged whereas it was decreased during hyperoxia at HA (-11 +/- 4%; P < 0.05 vs. LA). MCAv was unchanged during acute hypoxia and at HA; however, acute hyperoxia caused MCAv to fall to a greater extent than at HA (-12 +/- 3 vs. -5 +/- 4%, respectively; P < 0.05). Whereas CA was unchanged in hyperoxia, gain in the low-frequency range was reduced during acute hypoxia, indicating improvement in CA. In contrast, HA was associated with elevations in transfer-function gain in the very low- and low-frequency range, indicating CA impairment; hyperoxia lowered these elevations by approximately 50% (P < 0.05). Findings indicate that hyperoxia at HA can partially improve CA and lower BP, with little effect on MCAv.

Human cerebrovascular and ventilatory CO2 reactivity to end-tidal, arterial and internal jugular vein PCO2.

This study examined cerebrovascular reactivity and ventilation during step changes in CO(2) in humans. We hypothesized that: (1) end-tidal P(CO(2)) (P(ET,CO(2))) would overestimate arterial P(CO(2)) (P(a,CO(2))) during step variations in P(ET,CO(2)) and thus underestimate cerebrovascular CO(2) reactivity; and (2) since P(CO(2)) from the internal jugular vein (P(jv,CO(2))) better represents brain tissue P(CO(2)), cerebrovascular CO(2) reactivity would be higher when expressed against P(jv,CO(2)) than with P(a,CO(2)), and would be related to the degree of ventilatory change during hypercapnia. Incremental hypercapnia was achieved through 4 min administrations of 4% and 8% CO(2). Incremental hypocapnia involved two 4 min steps of hyperventilation to change P(ET,CO(2)), in an equal and opposite direction, to that incurred during hypercapnia. Arterial and internal jugular venous blood was sampled simultaneously at baseline and during each CO(2) step. Cerebrovascular reactivity to CO(2) was expressed as the percentage change in blood flow velocity in the middle cerebral artery (MCAv) per mmHg change in P(a,CO(2)) and P(jv,CO(2)). During hypercapnia, but not hypocapnia, P(ET,CO(2)) overestimated P(a,CO(2)) by +2.4 +/- 3.4 mmHg and underestimated MCAv-CO(2) reactivity (P < 0.05). The hypercapnic and hypocapnic MCAv-CO(2) reactivity was higher ( approximately 97% and approximately 24%, respectively) when expressed with P(jv,CO(2)) than P(a,CO(2)) (P < 0.05). The hypercapnic MCAv-P(jv,CO(2)) reactivity was inversely related to the increase in ventilatory change (R(2) = 0.43; P < 0.05), indicating that a reduced reactivity results in less central CO(2) washout and greater ventilatory stimulus. Differences in the P(ET,CO(2)), P(a,CO(2)) and P(jv,CO(2))-MCAv relationships have implications for the true representation and physiological interpretation of cerebrovascular CO(2) reactivity.