Sugammadex may be required or used in multiple emergency situations. Moderate and high doses of this compound can be used inside and outside the operating room setting. In this communication, recent developments in the use of sugammadex for the immediate reversal of rocuronium-induced neuromuscular blockade were assessed. In emergency surgery and other clinical situations necessitating rapid sequence intubation, the tendency to use rocuronium followed by sugammadex instead of succinylcholine has been increasing. In other emergency situations such as anaphylactic shock caused by rocuronium or if intubation or ventilation is not possible, priority should be given to resuming ventilation maintaining hemodynamic stability, in accordance with the traditional guidelines. If necessary for the purpose of resuming ventilation, reversal of neuromuscular blockade should be done in a timely fashion.

Cerebral Function and Muscle Afferent Activity Following Intravenous Succinylcholine in Dogs Anesthetized with Halothane: The Effects of Pretreatment with a Defasciculating Dose of Pancuronium. By WL Lanier, PA Iaizzo, and JH Milde. Anesthesiology 1989; 71:87-95. Reprinted with permission. By the mid-1980s, it was widely assumed that if the depolarizing muscle relaxant, succinylcholine, given IV, produced increases in intracranial pressure, it did so because fasciculations produced increases in intrathoracic and central venous pressures that were transferred to the brain; however, there was no direct evidence that this was true. In contrast, we explored the possibility that the succinylcholine effect on the brain was explained by the afferentation theory of cerebral arousal, which predicts that agents or maneuvers that stimulate muscle stretch receptors will tend to stimulate the brain. Our research in tracheally intubated, lightly anesthetized dogs discovered that IV succinylcholine (which does not cross the blood-brain barrier) produced a doubling of cerebral blood flow that lasted for 30 min and corresponded to activation of the electroencephalogram and increases in intracranial pressure. Later, in our Classic Paper, we were able to assess simultaneously cerebral physiology and afferent nerve traffic emanating from muscle stretch receptors (primarily muscle spindles). We affirmed that the cerebral arousal response to succinylcholine was indeed driven by muscle afferent traffic and was independent of fasciculations or increases in intrathoracic or central venous pressures. Later research in complementary models demonstrated that endogenous movement (e.g., coughing, hiccups) produced a cerebral response very similar to IV succinylcholine, apparently as a result of the same muscle afferent mechanisms, independent of intrathoracic and central venous pressures. Thus, the importance of afferentation theory as a driver of the cerebral state of arousal and cerebral physiology during anesthesia was affirmed.

Malignant hyperthermia (MH) is a rare but life-threatening genetic disorder of the skeletal muscles triggered by inhalation anesthetics or succinylcholine. A 49-year-old female developed symptoms of MH shortly after a lumbar surgery. Despite being insidious, MH was diagnosed based on the clinical grading scale. We incidentally discovered fine fasciculations in extremities while inserting an ultrasound-guided arterial catheter. On receiving dantrolene, her symptoms improved within 20 minutes; a subsequent ultrasound revealed no fasciculations. Although halothane contracture testing was not available, the fasciculations that resolved with dantrolene administration in a MH suspected patient opens up a new potential avenue of diagnostics.

First, we review the definitively severed myotendinous junction and recovery by the cytoprotective stable gastric pentadecapeptide BPC 157 therapy, its healing that might combine both transected and detached tendon and transected muscle, ligament and bone injuries, applied alone, as native peptide therapy, effective in rat injury, given intraperitoneally or in drinking water or topically, at the site of injury. As a follow up, we reviewed that with the BPC 157 therapy, its cytoprotective ability to organize simultaneous healing of different tissues of and full recovery of the myotendinous junction might represent the particular muscle therapy against distinctive etiopathology muscle disabilities and weakness. In this, BPC 157 therapy might recover many of muscle disabilities (i.e., succinylcholine, vascular occlusion, spinal cord compression, stroke, traumatic brain injury, severe electrolyte disturbances, neurotoxins, neuroleptics, alcohol, serotonin syndrome and NO-system blockade and tumor-cachexia). These might provide practical realization of the multimodal muscle-axis impact able to react depending on the condition and the given agent(s) and the symptoms distinctively related to the prime injurious cause symptoms in the wide healing concept, the concept of cytoprotection, in particular. Further, the BPC 157 therapy might be the recovery for the disabled heart functioning, and disabled smooth muscle functioning (various sphincters function recovery). Finally, BPC 157, native and stable in human gastric juice, might be a prototype of anti-ulcer cytoprotective peptide for the muscle therapy with high curing potential (very safe profile (lethal dose not achieved), with suited wide effective range (µg-ng regimens) and ways of application).

Myotonic dystrophy (dystrophia myotonica; DM) is an uncommon progressive hereditary muscle disorder that can present with variable severity at birth, in early childhood, or most commonly as an adult. Patients with DM, especially type 1 (DM1), are extremely sensitive to the respiratory depressant effects of sedative-hypnotics, anxiolytics, and opioid agonists. This case report describes a 37-year-old male patient with previously undiagnosed DM1 who received dental care under minimal sedation using intravenous midazolam. During the case, the patient experienced 2 brief episodes of hypoxemia, the second of which required emergency intubation after propofol and succinylcholine and resulted in extended hospital admission. A lipid emulsion (Liposyn II 20%) infusion was given approximately 2 hours after the last local anesthetic injection due to slight ST elevation and suspicion of local anesthetic toxicity (LAST). Months after treatment, the patient suffered a fall resulting in a fatal traumatic brain injury. Complications noted in this case report were primarily attributed to the unknown diagnosis of DM1, although additional precipitating factors were likely present. This report also provides a basic review of the literature and clinical guidelines for managing myotonic dystrophy patients for dental care with local anesthesia, sedation, or general anesthesia.

Calpainopathy is characterized by symmetric and progressive weakness of proximal limb-girdle muscles. The age at onset of muscle weakness ranges from two to 40 years. The phenotype shows intra- and interfamilial variability ranging from severe to mild. Three autosomal recessive calpainopathy phenotypes have been identified based on the distribution of muscle weakness and age at onset: Pelvifemoral limb-girdle muscular dystrophy (LGMD) (Leyden-Möbius LGMD) phenotype, the most frequently observed calpainopathy phenotype, in which muscle weakness is first evident in the pelvic girdle and later in the shoulder girdle, with onset that may occur as early as before age 12 years or as late as after age 30 years. Scapulohumeral LGMD (Erb LGMD) phenotype, usually a milder phenotype with infrequent early onset, in which muscle weakness is first evident in the shoulder girdle and later in the pelvic girdle. HyperCKemia, usually observed in children or young individuals, in which individuals are asymptomatic and have high serum creatine kinase (CK) concentrations. The autosomal dominant form of calpainopathy shows a variability of clinical phenotype, ranging from almost asymptomatic to wheelchair dependence after age 60 years in few cases with a generally milder phenotype than the recessive form. Clinical findings of calpainopathy include the tendency to walk on tiptoe, difficulty in running, scapular winging, waddling gait, and slight hyperlordosis. Other findings include symmetric weakness of proximal more than distal muscles in the limbs, trunk, and periscapular area; laxity of the abdominal muscles; Achilles tendon shortening; scoliosis; and joint contractures. Affected individuals typically do not have cardiac involvement or intellectual disability.

Tracheal extubation is a risky phase of anaesthesia. Most complications that occur when an endotracheal tube is removed are of minor nature, but those that require critical action can end in serious complications or even death. Patient - A 55-year-old woman was admitted for elective transabdominal hysterectomy and adnexal procedures. Anaesthesia - Standard monitoring. For induction, we used fentanyl, propofol, and rocuronium. The maintenance phase of anaesthesia was without complications. After extubation, the patient presented with severe trismus and mask ventilation was unsuccessful (cannot ventilate) - It was not until 200 mg of succinylcholine was administered that the masseter muscle spasm subsided. Extubation is a process that must always be planned. A routine approach and lack of a contingency plan is responsible for a number of complications related to the period of patient awakening and associated with the removal of the endotracheal tube. Trismus, in response to extubation, is a phenomenon not described in the literature in non-high risk patients.

Recent data indicated a high incidence of inappropriate management of neuromuscular block, with a high rate of residual paralysis and relaxant-associated postoperative complications. These data are alarming in that the available neuromuscular monitoring, as well as myorelaxants and their antagonists basically allow well tolerated management of neuromuscular blockade. In this first European Society of Anaesthesiology and Intensive Care (ESAIC) guideline on peri-operative management of neuromuscular block, we aim to present aggregated and evidence-based recommendations to assist clinicians provide best medical care and ensure patient safety. We identified three main clinical questions: Are myorelaxants necessary to facilitate tracheal intubation in adults? Does the intensity of neuromuscular blockade influence a patient's outcome in abdominal surgery? What are the strategies for the diagnosis and treatment of residual paralysis? On the basis of this, PICO (patient, intervention, comparator, outcome) questions were derived that guided a structured literature search. A stepwise approach was used to reduce the number of trials of the initial research (n = 24 000) to the finally relevant clinical studies (n = 88). GRADE methodology (Grading of Recommendations, Assessment, Development and Evaluation) was used for formulating the recommendations based on the findings of the included studies in conjunction with their methodological quality. A two-step Delphi process was used to determine the agreement of the panel members with the recommendations: R1 We recommend using a muscle relaxant to facilitate tracheal intubation (1A). R2 We recommend the use of muscle relaxants to reduce pharyngeal and/or laryngeal injury following endotracheal intubation (1C). R3 We recommend the use of a fast-acting muscle relaxant for rapid sequence induction intubation (RSII) such as succinylcholine 1 mg kg -1 or rocuronium 0.9 to 1.2 mg kg -1 (1B). R4 We recommend deepening neuromuscular blockade if surgical conditions need to be improved (1B). R5 There is insufficient evidence to recommend deep neuromuscular blockade in general to reduce postoperative pain or decrease the incidence of peri-operative complications. (2C). R6 We recommend the use of ulnar nerve stimulation and quantitative neuromuscular monitoring at the adductor pollicis muscle to exclude residual paralysis (1B). R7 We recommend using sugammadex to antagonise deep, moderate and shallow neuromuscular blockade induced by aminosteroidal agents (rocuronium, vecuronium) (1A). R8 We recommend advanced spontaneous recovery (i.e. TOF ratio >0.2) before starting neostigmine-based reversal and to continue quantitative monitoring of neuromuscular blockade until a TOF ratio of more than 0.9 has been attained. (1C).

Malignant Hyperthermia (MH) is a rare, hereditary, life-threatening disease triggered by volatile anesthetics and succinylcholine. Rarely, MH can occur after non-pharmacological triggers too. MH was detected more often in children and young adults, which makes this topic very important for every pediatric specialist, both anesthesiologists and intensivists. MH crisis is a life-threatening severe hypermetabolic whole-body reaction. Triggers of MH are used in pediatric intensive care unit (PICU) as well, volatile anesthetics in difficult sedation, status asthmaticus or epilepticus, and succinylcholine still sometimes in airway management. Recrudescence or delayed onset of MH crisis hours after anesthesia was previously described. MH can also be a cause of rhabdomyolysis and hyperpyrexia in the PICU. In addition, patients with neuromuscular diseases are often admitted to PICU and they might be at risk for MH. The most typical symptoms of MH are hypercapnia, tachycardia, hyperthermia, and muscle rigidity. Thinking of the MH as the possible cause of deterioration of a patient's clinical condition is the key to early diagnosis and treatment. The sooner the correct treatment is commenced, the better patient´s outcome. This narrative review article aims to summarize current knowledge and guidelines about recognition, treatment, and further management of MH in PICU.

Purpose: This study aimed to evaluate the frequency at which postintubation sedation is administered following use of long-acting paralytic agents compared to short-acting paralytic agents during rapid sequence intubation performed in the emergency department. Methods: This retrospective, single-center study of intubated patients in the emergency department analyzed the difference in time to administration of additional sedation following use of a short-acting paralytic (succinylcholine) compared to use of a long-acting paralytic (rocuronium or vecuronium). A total of 387 patients were available for analysis. The primary outcome was additional sedation given within 15 minutes following administration of a paralytic agent. The secondary outcome sought to evaluate the incidence of hyperkalemia due to paralytic agents by comparing potassium level before and after paralytic administration. Results: 46.9% of patients who received a short-acting paralytic agent received additional sedation within 15 minutes, compared to 40.9% of patients who received a long-acting paralytic agent. The Chi-square analysis comparing the short and long-acting paralytic groups showed no statistically significant difference (χ² [1, N = 387] = 1.24, P = .266) in the frequency of additional sedation administered. Excluding patients who did not receive any additional sedation, the mean time from paralytic administration to additional sedation in all patients was 20.03 ± 18 minutes. No statistically significant difference was detected between groups regarding changes in potassium level. Conclusion: The use of long-acting paralytic agents was not associated with increased time to administration of sedation compared to shortacting paralytic agents. There is an opportunity to reduce the time to sedation administration for intubated patients receiving both short- and long-acting paralytic agents.

A 21-year-old woman developed an acute myotonic reaction while undergoing anaesthesia using succinylcholine. Examination later showed she had shoulder, neck and calf hypertrophy, bilateral symmetrical ptosis and eyelid, handgrip and percussion myotonia. Peripheral neurophysiology studies identified significant, continuous myotonic discharges in both upper and lower limbs. Genetic analysis identified a c.3917G>A (p.Gly1306Glu) mutation in the SCN4A gene, confirming a diagnosis of sodium channel myotonia. Succinylcholine and other depolarising agents can precipitate life-threatening acute myotonic reactions when given to patients with myotonia. Patients with neuromuscular disorders are at an increased risk of perioperative anaesthetic complications. We report a woman who developed an acute myotonic reaction whilst undergoing anaesthesia, in the context of an unrecognised myotonic disorder. We then discuss an approach to the diagnosis of myotonic disorders.

Pseudocholinesterase is a serine hydrolase enzyme, primarily produced in the liver that catalyzes the hydrolysis of choline esters, most prominently succinylcholine and mivacurium.[1] It is imperative to differentiate this from “true” cholinesterase, also known as acetylcholinesterase, which occurs in higher concentrations within conducting tissues such as the central/peripheral nervous systems and neuromuscular junctions.[2] Due to multiple locations and theoretical functions within the human body, pseudocholinesterase often gets referred to through various enzymatic names, including plasma cholinesterase, serum cholinesterase, acetylcholine acetylhydrolase, and butyrylcholinesterase.[3] In addition to possessing multiple names, the enzyme exists in a multitude of pharmacogenetic variations, with butyrylcholinesterase (BuChE) operating as the major human cholinesterase form. When comparing concentrations within the human plasma, the ratio of pseudocholinesterase (BuChE) to true cholinesterase (AChE) overwhelmingly favors BuChE by a ratio of 1000 to 1.[3]

Neuromuscular blockade is frequently used in anesthesia to facilitate endotracheal intubation, optimize surgical conditions, and assist with mechanical ventilation in patients who have reduced lung compliance. Neuromuscular blocking agents (NMBAs) come in two forms: depolarizing neuromuscular blocking agents (e.g., succinylcholine) and nondepolarizing neuromuscular blocking agents (e.g., rocuronium, vecuronium, atracurium, cisatracurium, mivacurium). The class of NMBAs used for achieving neuromuscular blockade must be selected carefully based on patient factors, the type of procedure being performed, and clinical indication.

Malignant hyperthermia (MH) is an acute hypermetabolic crisis, triggered in susceptible patients by the administration of succinylcholine or a volatile anesthetic agent. When providing anesthetic care for MH-susceptible patients, a total intravenous anesthetic technique with propofol or other sedative hypnotic is frequently chosen. Remimazolam is a novel benzodiazepine which, like midazolam, has sedative, anxiolytic, and amnestic properties. Ester metabolism results in a half-life of 5-10 min and a limited context sensitive half-life. We present anecdotal experience with its use as an adjunct to propofol anesthesia in a patient with a suspected family history of MH. Previous reports of the use of remimazolam in MH-susceptible patients are reviewed and its potential role in such patients discussed.

Pseudocholinesterase deficiency, also known as butyrylcholinesterase deficiency, refers to a rare acquired or inherited defect in the pseudocholinesterase enzyme produced by the liver.[1] In clinical anesthesia practice, the muscle relaxants succinylcholine and mivacurium are drugs used to optimize intubating conditions and surgical exposure.[2] The drugs succinylcholine and mivacurium are both metabolized by the pseudocholinesterase enzyme.[3]  Patients with defective forms of pseudocholinesterase will have a reduced ability to metabolize these two muscle relaxants and will present with prolonged muscular paralysis from standard doses of succinylcholine and mivacurium.[3]