Administration Of Succinylcholine Research Articles

Massive Intraoperative Pulmonary Embolism Coincident with the Administration of Succinylcholine

Massive Intraoperative Pulmonary Embolism Coincident with the Administration of Succinylcholine

Human Malignant Hyperthermia Associated with Desflurane Anesthesia

Human Malignant Hyperthermia Associated with Desflurane Anesthesia

Glycogen depletion and lactate accumulation in human intercostal muscles after administration of succinylcholine

I.m. glycogen content, lactate concentration and staining intensity for glycogen in slow- (ST) and fast-twitch (FTa and FTb) fibres were determined in the external and internal intercostal muscles after thoracotomy. Thirteen patients received a precurarizing dose of a non-depolarizing neuromuscular blocking agent followed by the depolarizing agent, succinylcholine, to facilitate intubation of the trachea (succinylcholine group). Nine patients received pancuronium or gallamine (control group). There were no significant differences in ventilatory functional capacity between the two groups. In the external intercostal muscles, lower i.m. glycogen content was observed in the succinylcholine compared with the control group (P < 0.05). I.m. glycogen was depleted from the FT fibres and in particular from FTb fibres, while little depletion was noted in ST fibres. In both the external and internal intercostal muscles, a higher lactate concentration was observed in the succinylcholine than in the control group (P < 0.05). The results indicate that the use of succinylcholine for tracheal intubation stimulated breakdown of i.m. glycogen, particularly in fast-twitch muscle fibres, and caused accumulation of lactate in intercostal muscles.

Generalized Muscle Rigidity and Hypercarbia with Halothane and Isoflurane

Generalized Muscle Rigidity and Hypercarbia with Halothane and Isoflurane

The Evaluation of Postoperative Myalgia after Administration of Succinylcholine and the Effect of Pancuronium Pretreatment

The Evaluation of Postoperative Myalgia after Administration of Succinylcholine and the Effect of Pancuronium Pretreatment

Hyperkalemia Following Succinylcholine Administration in Elderly Patient with Chronic Hypokalemia: A case report

Hyperkalemia Following Succinylcholine Administration in Elderly Patient with Chronic Hypokalemia: A case report

Decreased serum choline concentrations in humans after surgery, childbirth, and traumatic head injury.

The serum levels of choline decreased by approximately 50% in patients having a surgery under general as well as epidural anesthesia. The decrease is lasts for two days after surgery. Intravenous administration of succinylcholine, either by a single bolus injection or by a slow continuous infusion, increased the serum choline levels several folds during surgery. In these patients, a significant decrease in the serum choline levels was observed one and two days after surgery. In 16 pregnant women at the term, serum choline levels were higher than the value observed in 19 nonpregnant women. The serum choline levels decreased by about 40% or 60% after having a childbirth either by vaginal delivery or caesarean section, respectively. Serum choline levels in blood obtained from 9 patients with traumatic head injury were significantly lower than the observed levels in blood samples obtained from healthy volunteers. These observations show that serum choline levels increase during pregnancy and decrease during stressful situations in humans.

Bilateral Vocal Cord Paralysis After Radical Cystectomy in a Patient with a History of Bulbar Polio

Bilateral Vocal Cord Paralysis After Radical Cystectomy in a Patient with a History of Bulbar Polio

Rapid sequence intubation in adults with elevated intracranial pressure: A survey of emergency medicine residency programs

A questionnaire entitled “Survey of Protocols for Rapid Sequence Intubation in Previously Healthy Adults with Elevated Intracranial Pressure” was distributed to the program directors of all 100 emergency medicine residency programs listed in the Directory of Graduate Medical Education Programs in February 1995. The medical literature on rapid sequence intubation in patients with suspected intracranial pressure elevations was reviewed. The findings of the review were compared with the survey responses. Sixty-seven program directors responded to the survey. Sixty-five programs performed rapid sequence intubation in their institution. Five programs performed 0 to 10 procedures annually. Six performed 10 to 30 annually, 19 performed 30 to 50, 17 performed 50 to 100, and 18 performed more than 100. Succinylcholine and vecuronium were the most frequently used neuromuscular blockers. Midazolam and thiopental were the most frequently used sedative induction agents. Most programs use a defasciculating agent prior to succinylcholine administration. The majority of programs do not use a priming agent before the use of a nondepolarizing neuromuscular blocking agent. Intravenous lidocaine was routinely administered prior to neuromuscular blockade. Fentanyl was the most frequently used other pretreatment medication. Rapid sequence intubation is used to facilitate definitive, emergent airway management in patients with suspected intracranial pressure elevations in almost all of the emergency medicine residency programs that responded to the survey. Most of these programs follow the guidelines recommended in the medical literature. The majority of these guidelines, however, are based on statistical data performed in the laboratory or nonemergency environments. Further clinical studies in an emergency medicine environment must be performed to determine the optimal drug regimen for rapid sequence intubation in patients with elevated intracranial pressure.

A Multicenter Study of Bispectral Electroencephalogram Analysis for Monitoring Anesthetic Effect

Bispectral analysis (BIS) of the electroencephalogram (EEG) has been shown in retrospective studies to predict whether patients will move in response to skin incision. This prospective multicenter study was designed to evaluate the real-time utility of BIS in predicting movement response to skin incision using a variety of general anesthetic techniques. Three hundred patients from seven study sites received an anesthetic regimen expected to give an approximately 50% movement response at skin incision. EEG was continuously recorded via an Aspect B-500 monitor and BIS was calculated in real time from bilateral frontocentral channels displayed on the monitor. Half of the patients were randomized to a treatment group in which anesthetic drug doses were increased to produce a lower BIS. In the control group, BIS was recorded, but no action taken on the data displayed. A determination of movement in response to skin incision was made in the 2 min succeeding incision. Retrospective pharmacodynamic modeling was performed using STANPUMP to estimate effect-site concentrations of intravenously administered anesthetics. BIS values were significantly higher in the control group (66 +/- 19) versus the BIS-guided group, in which additional anesthesia was administered to produce a lower BIS (51 +/- 19). The movement response rate was significantly higher in the control group at 43% compared with 13% in the BIS-guided group, but response rates were low at sites which used larger doses of opioids. Logistic regression analysis showed that BIS, estimated opioid effect-site concentrations, and heart rate (in that order) were the best predictors of movement at skin incision. This study demonstrates that dosing anesthetic drugs to lower BIS values achieves a lower probability of movement in response to surgical stimulation. BIS is a significant predictor of patient response to incision, but the utility of the BIS depends on the anesthetic technique being used. When drugs such as propofol or isoflurane are used as the primary anesthetic, changes in BIS correlate with the probability of response to skin incision. When opioid analgesics are used, the correlation to patient movement becomes much less significant, so that patients with apparently "light" EEG profiles may not move or otherwise respond to incision. Therefore, the adjunctive use of opioid analgesics confounds the use of BIS as a measure of anesthetic adequacy when movement response to skin incision is used as the primary end point.

Laryngeal mask airway in severe cervical ankylosis

We present a case of the successful use of a laryngeal airway (LMA) to ventilate the lungs of a patient with severe ankylosing spondylitis for surgery requiring intense muscular relaxation. The use of an LMA in such circumstances is controversial. The patient was a 61-yr-old man with severe emphysema, a cervical spine fixed in marked anterior flexion, and reduced mouth opening (35 mm). The patient refused an awake tracheal intubation because of a previous distressing experience with a fibreoptic awake nasal intubation and an 11 day SICU stay with controlled ventilation via an endotracheal tube. Attempts at spinal blocks had failed in the past. After administration of thiopentone and succinylcholine a #4 LMA was inserted and the lungs were safely ventilated for a 10 min reduction of a dislocated femoral head. The present view that severe ankylosing spondylitis is a contraindication to the use of an LMA may need revision in view of this and other reports of successful airway management in patients with that disease.

P158 Bilateral phrenic and peripheral axonal neuropathy secondary to the administration of succinylcholine

P158 Bilateral phrenic and peripheral axonal neuropathy secondary to the administration of succinylcholine

Induction of Dystrophin-Associated Proteins Together with Nicotinic Acetylcholine Receptors by Denervation in the Absence of Dystrophin in Skeletal Muscles ofmdxMice

We purified the nicotinic acetylcholine receptor from digitonin-solubilized rabbit skeletal muscle by affinity chromatography and detected many proteins linked to AChR, including dystrophin, adhalin, β-dystroglycan, utrophin, rapsyn, and actin. To determine whether or not AChR links to dystrophin-associated proteins (DAPs) without dystrophin, we studied the effects of denervation on AChR and DAPs in the skeletal muscle of amdxmouse. Following surgical denervation, the levels of adhalin and β-dystroglycan dramatically increased at the extrajunctional sarcolemma with AChR, suggesting that their association is independent of dystrophin. Furthermore, the diffuse extrajunctional appearance of adhalin, β-dystroglycan, and AChR was observed after pharmacological denervation through the subcutaneous administration of succinylcholine. Since the depletion of DAPs and the subsequent disruption of sarcolemmal linkage are believed to be a primary cause of muscle cell necrosis in dystrophinopathies, pharmacological denervation may have some beneficial effect on these diseases.

Delayed Bronchial Stenosis After Blunt Chest Trauma

Delayed Bronchial Stenosis After Blunt Chest Trauma

The effect of succinylcholine on energy metabolism studied by 31P-NMR spectroscopy in rat denervated skeletal muscle.

The goals of this study were: (1) to demonstrate the differences of metabolic changes induced by succinylcholine (SCh) administration between normal and denervated muscle by 31P-NMR spectroscopy: (2) to determine whether three kinds of drugs (vecuronium, midazolam and magnesium sulfate) could prevent these metabolic changes. Following unilateral sciatic nerve section, 20 male Wistar rats were studied at three-week intervals. After SCh 1 mg.kg-1 was administered intravenously, the changes of the inorganic phosphate/phosphocreatine (Pi/PCr) ratio, the beta ATP/(PCr+Pi) ratio, and intracellular pH were measured by 31P-NMR both in normal and denervated hind limb muscles of 5 rats. The other 15 rats were allocated to the pretreatment groups by the following drugs: vecuronium 0.02 mg.kg-1, midazolam 0.1 mg.kg-1 and magnesium sulfate 60 mg.kg-1. After pretreatment 3 min before SCh administration, we measured the same parameters by 31P-NMR. SCh administration did not change the Pi/PCr ratio in normal muscle, but significantly increased that in denervated muscle (P < 0.05). This increase of the Pi/PCr ratio was also observed in all pretreated groups but was minimal as compared with that in non-pretreatment denervated muscle. These data suggested that SCh administration decreased the level of "energy reserve" in denervated muscle, and that this metabolic change was not totally inhibited by vecuronium, midazolam, or magnesium sulfate.

Prior hypothermia attenuates malignant hyperthermia in susceptible swine.

This study was designed to determine the extent by which mild or moderate hyperthermia attenuates the triggering of malignant hypothermia (MH) induced by the combined administration of halothane and succinylcholine. Sixteen susceptible swine were initially anesthetized with nontriggering drugs and then either kept normothermic (approximately equal to 38 degrees C, n = 6) or cooled to induce mild (approximately equal to 35 degrees C, n = 6), or moderate (approximately equal to 33 degrees C, n = 4) hypothermia. Next, after a 30-min control period, the normothermic and mildly hypothermic animals were administered 1 minimum alveolar anesthetic concentration (MAC) halothane followed by a bolus dose of succinylcholine (2 mg/kg). Within 10 min all normothermic animals developed fulminant MH, whereas the onset of MH was slowed or was absent in the mildly hypothermic group. To test whether moderate hypothermia could more effectively minimize the signs of a MH episode, this group of animals was exposed to 1.5 MAC halothane followed 10 min later by a 3-mg/kg bolus of succinylcholine. MH was not induced and anesthesia was then changed to nontriggering drugs (ketamine and pancuronium). The animals were then aggressively rewarmed to 38 degrees C: a slight increase in the ETCO2 was detected, but MH episodes did not spontaneously occur. Subsequently, the readministration of halothane and succinylcholine rapidly provoked fulminant MH. We concluded that the induction of mild hypothermia impairs triggering and reduces the progression of MH induced by the combined administration of halothane and succinylcholine, whereas moderate hypothermia was completely protective and thus could be considered for prophylaxis.

Pharmacodynamics of Rocuronium With and Without Prior Administration of Succinylcholine

Comment Carefully controlled clinical trials are needed to establish the pharmacokinetic and pharmacodynamic behavior of new drugs to define dosing guidelines for routine use and to permit comparisons with other drugs, thereby enabling clinicians to properly “place” the new agent in their arsenal. This investigation appears to be a straightforward characterization of the kinetics of onset and offset of neuromuscular blockade with a single dose of rocuronium and in comparison with a single dose of succinylcholine. Succinylcholine clearly had a faster onset, and rocuronium had onset times typical of nondepo-larizing blockers, but the times for both drugs provided adequate intubating conditions. Importantly, the duration of rocuronium blockade was not increased by prior succinylcholine administration, and there was no evidence of cumulation. More careful reading of this paper, however, reveals a paradox: intubating times were unrelated to the onset of neuromuscular blockade. Ulnar nerve stimulation and thumb adduction force monitoring were used. The investigator/intubator was blinded and not in the operating room at the time of drug administration. When the first twitch of the train-of-four reached 80% depression (T180) the investigator was called to the operating room to perform the intubation. Times to T180 were 41 ± 15 and 70 ± 24 sec for succinylcholine and rocuronium, respectively. Times to completion of intubation were 76 ± 29 and 85 ± 23 sec for succinylcholine and rocuronium, respectively. We are faced with major questions. Why, despite significantly longer T180 times for rocuronium, was the time for completion of intubation the same? Why did it take the intubator an average of 35 sec to intubate after succinylcholine but only an average of 15 sec after rocuronium? The investigators offer some possible explanations. They state that “most succinylcholine patients felt ”tighter“ during laryngoscopy.” However, this is not supported by the data on intubation scores, which were the same in

Succinylcholine-induced intraocular hypertension reflects muscular contracture. An experimental study in pigs

The increase in intraocular pressure (IOP) following administration of succinylcholine (SCH) was believed to result from an increase in extraocular muscle tone, stimulation of orbital smooth muscle and choroidal vasodilation [1]. Recently, a different mechanism, based on SCH induced cycloplegia and increased resistance to aqueous humour outflow was postulated, and any significant contribution from extraocular muscle tone was denied [2]. We have assessed the muscular contribution to ΔIOP in an experimental setting. With approval from the regional ethics committee, we have investigated the mechanism of SCH induced IOP increase in six acutely instrumented, anaesthetized pigs (9±1 weeks, 25-28 kg piritramide + N2O), using a previously described model [3]. IOP was measured continuously manometrically in the anterior chambers of both eyes. All extraocular muscles of one eye were removed surgically, the other eye served as control. After haemodynamic variables had stabilised, 1.5 mg kg−1 SCH were given. When IOP had peaked and reached a plateau, dantrolene was administered (5 mg kg−1 by rapid infusion). After IOP had returned to baseline, a second dose of SCH was given. Pressure in the intact eyes increased significantly with the first dose of SCH; this effect was not significant in the eyes that had had the extraocular muscles removed nor in either eye after the second dose, following dantrolene. SCH produces a contracture of multiple innervated extraocular muscle fibres, which is abolished by dantrolene [4]. We believe that, in our study, the transient, pronounced increase in IOP in the intact eyes may be ascribed to such contracture; the minor increase in IOP observed in the operated eyes and also after (intracellular) muscle relaxation with dantrolene possibly reflects choroidal vascular engorgement or other phenomena. An increase in resistance to aqueous humour outflow resulting from SCH induced cycloplegia [2] is unlikely to account for an IOP increase as rapid as that seen with the administration of SCH. Although the origin of SCH induced intraocular pressure rise is probably multifactorial, the largest proportion of this effect is due to extraocular muscle tone.

Unexplained Transient Postoperative Myocardial Dysfunction in a Previously Healthy Child

Unexplained Transient Postoperative Myocardial Dysfunction in a Previously Healthy Child

Prolonged d-tubocurarine infusion and/or immobilization cause upregulation of acetylcholine receptors and hyperkalemia to succinylcholine in rats.

Hyperkalemic cardiac arrest after the administration of succinylcholine (SCh) to critically ill intensive care patients has been attributed to changes in the acetylcholine receptors (AChRs) at the muscle membrane. The current study attempts to characterize the contributory roles of chronic administration of nondepolarizing muscle relaxants typified by d-tubocurarine (dTC) and/or of immobilization on AChR upregulation and the relationship of these AChR changes to SCh-induced hyperkalemia. Rats received chronic subparalytic infusion of saline or dTC for 28 days via subcutaneous osmotic pumps inserted while they were under anesthesia. Approximately half of the saline- or dTC-treated rats underwent bilateral hind-limb immobilization with plaster casts for the same duration as the infusion. After 4 weeks, the osmotic pumps were removed, and 24-48 h later, the blood potassium concentrations were measured at baseline and at 1, 3, 5, 7, and 10 min after SCh (3 mg/kg). At the end of this period, the gastrocnemius muscle was excised for quantitation of AChR number using (125)I-alpha-bungarotoxin. At 28 days, the weight gain in mobile animals receiving saline or dTC infusion did not differ, nor did that in immobilized animals receiving saline or dTC infusion, confirming that infusion of dTC did not unduly affect the ability of the animals to feed. The maximal potassium change after SCh occurred at 5 min. Potassium responses to SCh changed (mean +/- SE): (1) from 3.9 +/- 0.04 to 4.5 +/- 0.1 mEq/1 in the mobile saline- treated control group, where the AChR concentration was 18.4 +/- 2 fmol/mg protein; (2) from 3.9 +/- 0.03 to 5.1 +/- 0.1 in the mobile dTC-infused group (AChRs = 48.6 +/- 7); (3) from 3.8 +/- 0.1 to 5.5 +/- 0.3 in the immobilized saline- treated group (AChRs = 107.4 +/- 14); and (4) from 3.8 +/- 0.1 to 6.3 +/- 0.2 in the immobilized-dTC-treated group (AChRs = 183.5 +/- 23). There was a significant positive correlation between maximal change in blood potassium concentration and the respective AChR concentration in the gastrocnemius of the same animal (r = 0.81, P<0.01). Subtherapeutic (subparalytic) doses of chronic infusion of dTC (with no immobilization) or immobilization alone (with no dTC) independently increased number of AChRs. The infusion of dTC with immobilization caused the greatest upregulation of AChRs. The magnitude of the increase in blood potassium to SCh was directly dependent on AChR number. This study shows direct evidence and confirms previous speculation that AChR number plays an important role in the magnitude of the hyperkalemic response to SCh. Presuming this represents an appropriate model for patients who are immobilized and/or receiving nondepolarizing muscle relaxants for prolonged periods, exaggerated blood potassium responses to SCh are possible when either or both of these perturbations are present in patients.