Stephanie Phillips

An ipsilateral comparison of acceleromyography and electromyography during recovery from nondepolarizing neuromuscular block under general anesthesia in humans.

BACKGROUND: Residual neuromuscular block is defined as a mechanomyography (MMG) or electromyography (EMG) train-of-four (TOF) ratio <0.90, and is common in patients receiving neuromuscular blocking drugs. Objective neuromuscular monitoring is the only reliable way to detect and exclude residual neuromuscular block. Acceleromyography (AMG) is commercially available and easy to use in the clinical setting. However, AMG is not interchangeable with MMG or EMG. Currently, it is unclear what value must be reached by AMG TOF ratio to reliably exclude residual neuromuscular block. METHODS: During spontaneous recovery from neuromuscular block, we monitored TOF ratio on the same arm using AMG at the adductor pollicis and EMG at the first dorsal interosseus. AMG and EMG TOF ratios were compared by the Bland–Altman analysis for repeated measurements. The precision of each device was assessed by the repeatability coefficient. A small repeatability coefficient indicates high precision of the device. The agreement between the devices was assessed by the bias and the 95% limits of agreement. Small bias and narrow limits of agreement indicate strong agreement. We defined clinically acceptable agreement between AMG and EMG as a bias <0.025 and limits of agreement within −0.050 to 0.050, provided that the control comparison between EMG and itself can fulfill these criteria. RESULTS: In 26 patients, 261 comparisons between AMG and EMG were made. The repeatability coefficient of AMG and EMG were 0.094 (95% confidence interval [CI], 0.088–0.100) and 0.051 (95% CI, 0.048–0.055), respectively. The bias between AMG and EMG TOF ratio was 0.176 (95% CI, 0.162–0.190), with limits of agreement −0.045 to 0.396 (95% CI, −0.067 to 0.419). CONCLUSIONS: AMG is less precise than EMG and overestimates EMG TOF ratio by at least 0.15. The lack of agreement cannot be attributed to instrumental imprecision or the baseline difference between successive measurements during spontaneous recovery of neuromuscular function. Residual neuromuscular block cannot be excluded on reaching an AMG TOF ratio of 1.00.

Sugammadex reversal of rocuronium-induced neuromuscular blockade in two types of neuromuscular disorders: Myotonic dystrophy and spinal muscular atrophy.

Neuromuscular disorders like myotonic dystrophy (dystrophia myotonica or Steinerts disease) and spinal muscular atrophy are associated with perioperative complications related to muscle weakness. These patients have an increased sensitivity to non-depolarising neuromuscular blocking agents, which can lead to postoperative residual curarization (PORC) and its associated respiratory complications. Adequate reversal of neuromuscular blockade is essential to prevent this. Sugammadex is the first selective relaxant binding agent and it reverses rocuronium- and vecuronium-induced neuromuscular block. Two cases are reported in which the patients received sugammadex to reverse a rocuronium-induced neuromuscular block. Reversal of the rocuronium-induced neuromuscular block (NMB) in both cases was fast, effective and without recurarization, and no safety concerns were observed.

The Impact of Residual Neuromuscular Blockade, Oversedation, and Hypothermia on Adverse Respiratory Events in a Postanesthetic Care Unit: A Prospective Study of Prevalence, Predictors, and Outcomes.

BACKGROUND:Residual neuromuscular blockade (RNMB) has been linked to adverse respiratory events (AREs) in the postanesthetic care unit (PACU). However, these events are often not attributed to RNMB by anesthesiologists because they may also be precipitated by other factors including obstructive sleep apnea, opioids, or hypnotic agents. Many anesthesiologists believe RNMB occurs infrequently and is rarely associated with adverse outcomes. This study evaluated the prevalence and predictors of RNMB and AREs. METHODS:This prospective cohort study included 599 adult patients undergoing general anesthesia who received neuromuscular blocking agents. Baseline demographic, surgical, and anesthetic variables were collected. RNMB was defined as a train-of-four ratio below 0.90 measured by electromyography on admission to the PACU. AREs were defined based on the modified Murphy’s criteria. RESULTS:RNMB was present in 186 patients (31% [95% confidence interval (CI), 27%–35%]) on admission to the PACU. One or more AREs were experienced by 97 patients (16% [95% CI 13–19]). AREs were more frequent in patients with RNMB (21% vs 14%, P = .033). RNMB was significantly associated with age (adjusted relative risk [RR], 1.17 [95% CI, 1.06–1.29] per 10-year increase), type of operation (adjusted RR, 0.59 [95% CI, 0.34–0.99] for laparoscopic surgery compared with open abdominal surgery), and duration of operation (adjusted RR, 0.59 [95% CI, 0.39–0.86] for ≥90 minutes compared with <90 minutes). Using multivariate logistic regression, AREs were found to be independently associated with decreased level of consciousness (adjusted RR, 4.76 [95% CI, 1.49–6.76] for unrousable/unconscious compared with alert/awake) and lower core temperature (adjusted RR, 1.43 [95% CI, 1.04–1.92] per 1°C decrease). Although univariate analysis found a significant association between AREs and RNMB, the significance became borderline after adjusting for other covariates (adjusted RR, 1.46 [95% CI, 0.99–2.08]). CONCLUSIONS:The prevalence of RNMB in the PACU was >30%. Older age, open abdominal surgery, and duration of operation <90 minutes were associated with increased risk of RNMB in our patients. Our RR estimate for AREs was highest for depressed level of consciousness. When AREs occur in the PACU, potentially preventable causes including RNMB, hypothermia, and reduced level of consciousness should be readily identified and treated appropriately. Delaying extubation until the patient is awake and responsive may reduce AREs.

Therapeutic doses of neostigmine, depolarising neuromuscular blockade and muscle weakness in awake volunteers: a double-blind, placebo-controlled, randomised volunteer study

Neostigmine reverses non‐depolarising neuromuscular blockade, but may cause muscle weakness when administered after full recovery of neuromuscular function. We hypothesised that neostigmine in therapeutic doses impairs muscle strength and respiratory function in awake healthy volunteers. Twenty‐one volunteers were randomised to receive two doses of either intravenous (i.v.) neostigmine 2.5 mg with glycopyrrolate 450 μg (neostigmine group, n = 14) or normal saline 0.9% (placebo group, n = 7). The first dose was administered immediately after obtaining baseline measurements, and the second dose was administered 15 min later. All 14 volunteers in the neostigmine group received the first dose, mean (SD) 35 (5.8) μg.kg−1, but only nine of these volunteers agreed to receive the second dose, 34 (3.5) ?g.kg‐1. The primary outcome was hand grip strength. Secondary outcomes were train‐of‐four ratio, single twitch height, forced expiratory volume in 1 s, forced vital capacity, forced expiratory volume in 1 s/forced vital capacity ratio, oxygen saturation, heart rate and mean arterial pressure. The first dose of intravenous neostigmine with glycopyrrolate resulted in reduced grip strength compared with placebo, −20 (20) % vs. +4.3 (9.9) %, p = 0.0016; depolarising neuromuscular blockade with decreased single twitch height, −14 (11) % vs. −3.8 (5.6) %, p = 0.0077; a restrictive spirometry pattern with decreased predicted forced expiratory volume in 1 s, −15 (12) % vs. −0.47 (3.4) %, p = 0.0011; and predicted forced vital capacity, −20 (12) % vs. −0.59 (3.2) %, p < 0.0001 at 5 min after administration. The second dose of neostigmine with glycopyrrolate further decreased grip strength mean (SD) −41 (23) % vs. +1.0 (15) %, p = 0.0004; single twitch height −25 (15) % vs. −2.5 (6.6) %, p = 0.0030; predicted forced expiratory volume in 1 s −23 (24) % vs. −0.7 (4.4) %, p = 0.0063; and predicted forced vital capacity, −27.1 (22.0) % vs. −0.66 (3.9) %, p = 0.0010. Train‐of‐four ratio remained unchanged (p = 0.22). In healthy volunteers, therapeutic doses of neostigmine induced significant and dose‐dependent muscle weakness, demonstrated by a decrease in maximum voluntary hand grip strength and a restrictive spirometry pattern secondary to depolarising neuromuscular blockade.

The analgesic efficacy of intravenous lidocaine infusion after laparoscopic fundoplication: a prospective, randomized, double-blind, placebo-controlled trial

This study aimed to determine if intravenous lidocaine infusion reduces postoperative pain intensity following laparoscopic fundoplication surgery and to also validate the safety of intravenous lidocaine at the dose tested. This was an equally randomized, double-blind, placebo-controlled, parallel-group, single center trial. Adult patients undergoing laparoscopic fundoplication were recruited. The intervention group received 1 mg/kg intravenous lidocaine bolus prior to induction of anesthesia, then an intravenous infusion at 2 mg/kg/h for 24 hours. The primary outcome was pain, measured using a numeric rating scale for 30 hours postoperatively. Secondary outcomes were nausea and vomiting, opioid requirements, adverse events, serum lidocaine concentration, and length of hospital stay. The study was terminated after an interim analysis of 24 patients showed evidence of futility. There was no difference in postoperative pain scores (lidocaine versus control, mean ± standard deviation) at rest (2.0 ± 2.7 vs 2.1 ± 2.4, P=0.286) or with movement (2.0 ± 2.6 vs 2.6 ± 2.7, P=0.487). Three adverse events occurred in the lidocaine group (25% of patients). Intravenous lidocaine did not provide clinically significant analgesia to patients undergoing laparoscopic fundoplication. The serum lidocaine concentration of patients who experienced adverse events were within the therapeutic range. This trial cannot confirm the safety of intravenous lidocaine at the dose tested.

iPhone accelerometry for monitoring quantitative neuromuscular function

tional objective quantitative monitoring using mechanomyography and electromyography not being transferable to the operating theatre. These devices require immobilisation of the measured muscle and device calibration, and are subject to significant interference. In contrast, techniques using acceleromyography are suitable for clinical practice. Issues around calibration, drift and ‘normalisation’ have been debated [3], but a systematic review concluded that ‘(acceleromyography) improves detection of postoperative residual paralysis and that recovery of TOF ratio to unity indicates, with a high predictive value, recovery of pulmonary and upper airway function from residual neuromuscular blockade’ [4]. Movement of the stimulated limb will affect calibration of the device for twitch height measurement. However, although the twitch height may differ from the original value with limb movement, the train-offour ratio remains correct [5]. Acceleromyography reduces the incidence of recovery room muscle weakness and adverse respiratory events and enhances the quality of recovery [6, 7]. Baillard’s survey demonstrated the value of the type of strategy we support, involving clinical education, more widespread reversal of neuromuscular blockade and greater availability of quantitative nerve stimulators [8]. Over nine years, the incidence of residual neuromuscular blockade in their institution fell from 62% to 3%, with use of acceleromyography increasing from 2% to 60%. Existing monitors are not perfect, requiring familiarisation and set-up time, and are prone to interference. However, by encouraging manufacturers to produce equipment that is robust, reliable and easy to use, clinicians have a role to play in developing and using these monitors. This process should be lent a degree of urgency due to the publication of the updated AAGBI Recommendations for Standards of Monitoring [9], which recommend the mandatory use of quantitative peripheral nerve stimulators for patients receiving neuromuscular blocking drugs.

Paravertebral Catheter Placement, Under Direct Vision, for Postthoracotomy Analgesia.

Postthoracotomy pain can be severe and effective analgesia reduces postoperative pulmonary complications.1 Although the gold standard for postthoracotomy pain management has been epidural analgesia2 there is a trend toward paravertebral blockade (PVB) due to its simplicity and safety. PVB analgesia is comparable with epidural analgesia,3 but has a lower failure rate, a lower incidence of vomiting and urinary retention,4 and greater hemodynamic stability.5,6 We describe an intraoperative technique of PVB catheter placement for use with continuous infusion, which in our esophagectomy patient cohort, has proved quick, safe, and effective. A 2-mm skin incision is made 2 intercostal spaces below and medial to the thoracotomy incision and lateral to the spinous processes. The paraspinal fascia is penetrated with a Crile forceps and the depth to pleura noted. The catheter is introduced using an 11-G, 30.48-cm, ON-Q* Tunneler (ON-Q Kimberley Clark N.V., Da Vincilaan 1, Zaventem, Belguim) and peel apart sheath, which is bent to 30 degrees about 5 to 7 cm from the tip (this distance corresponding to the thickness of the chest wall noted on previous insertion of the Crile forceps). The introducer passes through the skin incision and muscle layers until the tip is palpable or visible deep to the parietal pleura. To maximize effectiveness of analgesia, care must be taken to not puncture the pleura at this point.7 A plane between chest wall and parietal pleura is developed in the paravertebral sulcus, the full length of the introducer (15 cm). The bend in the introducer will need to be progressively increased to maintain its subpleural position (Fig. 1). Dissection is facilitated by small oscillations of the introducer, so that the tip moves across the chest wall beneath the pleura in an arc like manner, forming an elliptical space between the 2 layers. The process can be further facilitated by injection of saline or local anesthetic solution through the introducer, lifting the pleura from its muscular attachments. Once the tip of the introducer is positioned 2 intercostal spaces cephalad to the incision, the stylette is removed and a primed ON-Q* Catheter is advanced the full length of the sheath, held in place externally with forceps, and the pull apart sheath removed (Fig. 2). The catheter is sutured in place and connected to an elastomeric pump, loaded with 550mL of 0.2% ropivacaine, with a fixed rate of 5mL/h or other infusion according to local practice. FIGURE 1. On-Q Tunneler dissecting between the parietal pleura from the muscular layer.

Laparoscopic image(s) of pneumothorax in repair of massive hiatus hernia

Laparoscopic repair of a massive hiatus hernia (LMHH), usually defined as greater than 50% of the stomach in the mediastinum, has been reported to be associated with a risk of pneumothorax of up to 22%. 1 A pneumothorax occurs when the parietal pleura is breached during the dissection of the herniated intra-thoracic stomach and the usually adherent hernia sac in the posterior mediastinum. Figure 1 is a labelled laparoscopic image of the posterior mediastinum that displays the right pleura in relation to the dissection of the thoraco-abdominal structures. Figure 2showsaleftpleuraldefect.Itcanbeseenthatthereduction and LMMH involves extensive mediastinal dissection of the peritoneum, crura, thoracic oesophagus, aorta and mediastinal hernia sac. A pneumothorax that occurs during a LMHH does not occur due to lung trauma.Abreach in the parietal pleura leads to insufflation of the pleural space with carbon dioxide (CO2) and the creation of a pressure-limited tension pneumothorax ‐ a ‘capnothorax’. 2 In a proportion of patients, we see a varying degree of ventilatory and haemodynamic compromise caused by reduced venous return and cardiac compression. The surgeon often identifies the breach in the pleura as soon as it occurs during thoracic dissection and its effects become apparent quickly.Thereisadropinarterialbloodpressure,unilateraldecreased breath sounds, hyper-resonance on chest percussion, possible tracheal deviation, paradoxical movement of the inferior diaphragmatic surfacewhenviewedlaparoscopicallybythesurgicalteamandforthe anaesthetist to report subcutaneous emphysema in the neck. Treatment is proportional to haemodynamic and respiratory compromise. Little compromise is treated by CO2 aspiration from thoracic and abdominal cavities at completion. More significant compromise is treated by immediate aspiration of CO2 and levelling of the patient position. Rapid recovery invariably occurs, and the operation is continued at lower abdominal insufflation pressures, and increased respiratory inspiratory pressures. Recurrent evidence of tension in the pleural cavity may require the pleural defect to be closed by a laparoscopic loop ligature. In our experience, it has not been necessary to convert to laparotomy, and the operation has been completed in all cases of pneumothorax. It has not been necessary to insert a pleural drain, and all patients have been discharged from hospital with no pneumothorax-related sequelae.