Resistance towards nondepolarising muscle relaxants: prolonged onset time: A systematic review.

BACKGROUND: Nondepolarising muscle relaxants (NDMRs) provide optimal conditions for tracheal intubation and improve surgical conditions. Several clinical conditions, diseases and pharmacological interactions have been suggested to cause resistance towards NDMRs that may translate into difficult intubation or inadequate operating conditions during surgery. OBJECTIVE: The aim of this study was to evaluate the current evidence of patient groups with resistance towards NDMRs. A prolonged onset time was defined as a difference that exceeded 25% compared with controls. DESIGN: A systematic review of randomised controlled trials and cohort studies. DATA SOURCES: A comprehensive search was performed in 2016 in PubMed and EMBASE. ELIGIBILITY CRITERIA: Patients with conditions or diseases, or patients taking medication, which lead to resistance towards current NDMRs (rocuronium, vecuronium, cisatracurium, atracurium, mivacurium and pancuronium). Included outcomes were onset time defined as the time between administration of NDMR to maximal (90, 95 or 100%) depression of baseline twitch height of the first twitch in a train-of-four. RESULTS: Twenty-five studies were included. Strong evidence supports a prolonged onset time of rocuronium in patients with thermal injury and Duchenne muscular dystrophy. Moderate evidence supports a prolonged onset time of NDMRs during hypothermia and in patients with infection, oculopharyngeal muscular dystrophy, liver cirrhosis treated with ulinastatin, when remifentanil is administered prior to administration of an NDMR, in fasting patients being rehydrated intravenously prior to administration of NDMR, in children with end-stage renal failure and in patients with atrial or ventricular septal defects. CONCLUSION: A prolonged onset time should be suspected in patients with thermal injury and Duchenne's muscular dystrophy. Further, evidence supports a prolonged onset time in patients with infection, oculopharyngeal muscular dystrophy, congenital heart defects, kidney failure, liver cirrhosis treated with ulinastatin along with remifentanil or intravenous fluids administered prior to NDMR.

Migraine and risk of perioperative ischemic stroke and hospital readmission: hospital based registry study.

OBJECTIVE:  To evaluate whether patients with migraine are at increased risk of perioperative ischemic stroke and whether this may lead to an increased hospital readmission rate. DESIGN:  Prospective hospital registry study. SETTING:  Massachusetts General Hospital and two satellite campuses between January 2007 and August 2014. PARTICIPANTS:  124 558 surgical patients (mean age 52.6 years; 54.5% women). MAIN OUTCOME MEASURES:  The primary outcome was perioperative ischemic stroke occurring within 30 days after surgery in patients with and without migraine and migraine aura. The secondary outcome was hospital readmission within 30 days of surgery. Exploratory outcomes included post-discharge stroke and strata of neuroanatomical stroke location. RESULTS:  10 179 (8.2%) patients had any migraine diagnosis, of whom 1278 (12.6%) had migraine with aura and 8901 (87.4%) had migraine without aura. 771 (0.6%) perioperative ischemic strokes occurred within 30 days of surgery. Patients with migraine were at increased risk of perioperative ischemic stroke (adjusted odds ratio 1.75, 95% confidence interval 1.39 to 2.21) compared with patients without migraine. The risk was higher in patients with migraine with aura (adjusted odds ratio 2.61, 1.59 to 4.29) than in those with migraine without aura (1.62, 1.26 to 2.09). The predicted absolute risk is 2.4 (2.1 to 2.8) perioperative ischemic strokes for every 1000 surgical patients. This increases to 4.3 (3.2 to 5.3) for every 1000 patients with any migraine diagnosis, 3.9 (2.9 to 5.0) for migraine without aura, and 6.3 (3.2 to 9.5) for migraine with aura. : Patients with migraine had a higher rate of readmission to hospital within 30 days of discharge (adjusted odds ratio 1.31, 1.22 to 1.41). CONCLUSIONS:  Surgical patients with a history of migraine are at increased risk of perioperative ischemic stroke and have an increased 30 day hospital readmission rate. Migraine should be considered in the risk assessment for perioperative ischemic stroke.

Effects of Depth of Propofol and Sevoflurane Anesthesia on Upper Airway Collapsibility, Respiratory Genioglossus Activation, and Breathing in Healthy Volunteers.

BACKGROUND: Volatile anesthetics and propofol impair upper airway stability and possibly respiratory upper airway dilator muscle activity. The magnitudes of these effects have not been compared at equivalent anesthetic doses. We hypothesized that upper airway closing pressure is less negative and genioglossus activity is lower during deep compared with shallow anesthesia. METHODS: In a randomized controlled crossover study of 12 volunteers, anesthesia with propofol or sevoflurane was titrated using a pain stimulus to identify the threshold for suppression of motor response to electrical stimulation. Measurements included bispectral index, genioglossus electromyography, ventilation, hypopharyngeal pressure, upper airway closing pressure, and change in end-expiratory lung volume during mask pressure drops. RESULTS: A total of 393 attempted breaths during occlusion maneuvers were analyzed. Upper airway closing pressure was significantly less negative at deep versus shallow anesthesia (-10.8 ± 4.5 vs. -11.3 ± 4.4 cm H2O, respectively [mean ± SD]) and correlated with the bispectral index (P < 0.001), indicating a more collapsible airway at deep anesthesia. Respiratory genioglossus activity during airway occlusion was significantly lower at deep compared with light anesthesia (26 ± 21 vs. 35 ± 24% of maximal genioglossus activation, respectively; P < 0.001) and correlated with bispectral index (P < 0.001). Upper airway closing pressure and genioglossus activity during airway occlusion did not differ between sevoflurane and propofol anesthesia. CONCLUSIONS: Propofol and sevoflurane anesthesia increased upper airway collapsibility in a dose-dependent fashion with no difference at equivalent anesthetic concentrations. These effects can in part be explained by a dose-dependent inhibiting effect of anesthetics on respiratory genioglossus activity.