Chryssoula Staikou

Impact of anaesthetic drugs and adjuvants on ECG markers of torsadogenicity

Drug-induced prolongation of cardiac repolarization may trigger malignant ventricular arrhythmias, such as torsade de pointes. The duration of QT interval, QT corrected for heart rate (QTc), JT interval, QT dispersion (QTd), QT variability index, and transmular dispersion of repolarization (TDR) are ECG markers of torsadogenicity. All volatiles, especially isoflurane and desflurane, have been found to prolong QTc and QTcd, while sevoflurane has probably no effects on TDR. Among i.v. anaesthetics, propofol seems superior due to its minimal effects on QTc and TDR; moreover, a decrease in QTc and QTcd has been demonstrated in many studies. Regarding opioids, fentanyl, alfentanil, and remifentanil produce no effects on QTc, while sufentanil, at high doses, may induce QT prolongation. Succinylcholine, but not the non-depolarizing neuromuscular blockers, produces QTc prolongation which can be attenuated by opioids and β-blockers. Reversal of neuromuscular block with anticholinesterase-anticholinergic combinations has been associated with significant QTc prolongation, while such an effect has not been demonstrated for sugammadex, even at high doses. Local anaesthetics have probably no intrinsic action on duration of repolarization; nevertheless, an extensive subarachnoid sympathetic block may increase the duration of QTc. On the contrary, thoracic epidural anaesthesia has been associated with a decrease in both QTc and TDR. Among adjuvants, midazolam seems to have no effect on QTc and TDR, while commonly used antiemetics, such as droperidol, domperidone, and most 5-HT3 antagonists, produce significant QT prolongation. The effects of anaesthetic drugs and techniques on electrocardiographic torsadogenic markers should be considered in the perioperative management of patients with preexisting repolarization abnormalities.

Perioperative management of hereditary arrhythmogenic syndromes

Patients with inherited cardiac channel disorders are at high risk of perioperative lethal arrhythmias. Preoperative control of symptoms and a multidisciplinary approach are required for a well-planned management. Good haemodynamic monitoring, adequate anaesthesia and analgesia, perioperative maintenance of normocarbia, normothermia, and normovolaemia are important. In congenital long QT syndrome, torsades de pointes should be prevented with magnesium sulphate infusion and avoidance of drugs such as droperidol, succinylcholine, ketamine, and ondansetron. Propofol and epidural anaesthesia represent safe choices, while caution is needed with volatile agents. In Brugada syndrome, β-blockers, α-agonists, and cholinergic drugs should be avoided, while isoproterenol reverses the ECG changes. Propofol, thiopental, and volatiles have been used uneventfully. In congenital sick sinus syndrome, severe bradycardia resistant to atropine may require isoproterenol or epinephrine. Anaesthetics with vagolytic properties are preferable, while propofol and vecuronium should be given with caution due to risk of inducing bradyarrhythmias. Neuraxial anaesthesia should produce the least autonomic imbalance. Arrhythmogenic right ventricular dysplasia/cardiomyopathy induces ventricular tachyarrhythmias, which should be treated with β-blockers. Generally, β-adrenergic stimulation and catecholamine release should be avoided. Halothane and pancuronium are contraindicated, while large doses of local anaesthetics and epinephrine should be avoided in neuraxial blocks. In catecholaminergic polymorphic ventricular tachycardia, β-blocker treatment should be continued perioperatively. Catecholamine release and β-agonists, such as isoproterenol, should be avoided. Propofol and remifentanil are probably safe, while halothane and pancuronium are contraindicated. Regional anaesthesia, without epinephrine, is relatively safe. In suspicious cardiac deaths, postmortem examination and familial screening are recommended.

Impact of Graded Hypothermia on Coagulation and Fibrinolysis

BACKGROUND Hypothermia has a detrimental effect on hemostatic mechanism. The purpose of this experimental study was to investigate the effect of graded hypothermia on markers of the anticoagulant system (antithrombin III and protein C) and fibrinolytic system (plasminogen, α(2)-antiplasmin), and on vascular wall and other tissue specimens. MATERIALS AND METHODS Ten New Zealand rabbits were subjected to mild and then moderate core hypothermia of 32 °C for 60 min. Blood samples were obtained at normothermic (T(1)), mild (T(2)), and moderate (T(3)) hypothermic conditions. Chromogenic assay methods were used to determine quantitatively (%) the activity of antithrombin III, protein C, plasminogen, and α(2)-antiplasmin. Hypothermic values were compared with the normothermic values. Tissue and vessel wall specimens were examined under light microscope. RESULTS Reduction of activity (%) from normothermia (T(1)) to mild (T(2)) and moderate (T(3)) hypothermia was found for antithrombin III (103.40 ± 12.54, 87.40 ± 13.50, and 82.70 ± 20.78, respectively, with statistically significant difference between T(1)-T(3): P = 0.03), for protein C (70.1 ± 7.51, 56.30 ± 8.34, and 53.1 ± 7.34, with statistically significant difference between T(1)-T(2) and T(1)-T(3): P = 0.015 for both comparisons) and α(2)-antiplasmin (97 ± 9.63, 80.60 ± 11.73, and 83.70 ± 13.94, with statistically significant difference between T(1)-T(2): P = 0.006). Plasminogen activity was increased (14.50 ± 0.52, 16.30 ± 1.63, and 17.30 ± 2.45, with statistically significant difference between T(1)-T(2) and T(1)-T(3): P = 0.033 for both comparisons). Histologic examination revealed no significant lesions on tissue and vessel wall specimens. CONCLUSIONS The results of our study suggest that even though the hypothermia period was relatively short, the processes of coagulation and fibrinolysis were altered with simultaneous changes.

General versus neuraxial anaesthesia for caesarean section: Impact on the duration of hospital stay

Summary We investigated retrospectively the duration of hospital stay of 1,619 women who received general (GA) (n = 582) or neuraxial anaesthesia (combined spinal-epidural [CSEA] (n = 614), epidural [EA] (n = 423)) for caesarean delivery over the years 2002–2005. Hospital stay was also analysed for the different obstetricians involved. Overall duration of hospital stay differed between 2002 and 2005 (p < 0.0001) but not between CSEA and EA (p = 0.460). Overall duration of hospital stay differed between neuraxial and GA group (p < 0.001). Duration of hospital stay of the GA group showed a progressive decrease between 2002 and 2005 (p = 0.002). Duration of hospital stay after neuraxial anaesthesia differed between 2002 and 2005 (p = 0.013) and among different surgeons (p < 0.001). Discharge rates from the hospital were shorter after neuraxial anaesthesia versus GA for the 3rd and 4th postoperative days (p < 0.001 and p < 0.001, respectively). Neuraxial anaesthesia for caesarean section seems to be associated with shorter duration of hospital stay than GA.

Airway injury caused by a Portex single-use bougie

To the Editor: The tracheal tube introducer (bougie) is widely used to facilitate difficult intubation. However, single-use introducers, compared to reusable ones, appear to be more traumatic [1-3]. A 61-year-old woman with esophageal reflux and no predictive signs of difficult intubation received rapidsequence induction with application of cricoid pressure. Direct laryngoscopy revealed a Cormack-Lehane grade 3 view. An unlubricated Single Use Tracheal Tube Introducer (SIMS Portex, Hythe, Kent, UK) was advanced into the trachea without any resistance. Correct placement was indicated by the tracheal “clicks” sensation. The tracheal tube was advanced easily over the bougie and through the larynx, without 90° anticlockwise rotation. However, when attempting to remove the bougie, it was stuck inside the tracheal tube. We succeeded in removing it by withdrawing it gradually, as gently as possible. After the endotracheal tube was connected to the breathing system, we noticed blood coming out of the tube. Mild endotracheal suction was performed repeatedly and bleeding gradually ceased. Hypoxia did not occur at any time. When the surgery was completed, the patient recovered uneventfully and her postoperative course was uncomplicated. The Portex single-use bougie was introduced in 1997, due to concerns about microbial contamination via multiple use. It has a different design from the multiple-use introducer [4]. The Portex Venn Reusable Tracheal Tube Introducers are made with a braided polyester base with a resin coating, while the single-use Portex introducer is a hollow tube, coated with plastic. The difference in material may explain the increased resistance we felt between the introducer and tube, and the difficulty in withdrawing the unlubricated bougie from the tube. Zwaal and Gupta also described an inability to advance a tracheal tube over an unlubricated single-use Portex bougie [5]. The manufacturer recommends that tracheal introducers be lubricated before use. The airway trauma may not have been related to the difficulty in removing the introducer, as it may have occurred when the bougie was advanced into the trachea. Another possible mechanism is tissue blockage between the angled distal end of the introducer and the tracheal tube when the bougie was withdrawn. The multiple-use introducer has an angled (40°) tip with rounded end, while the single-use bougie has an angled, less flexible tip with a more flattened end. The peak force exerted by the single-use bougie on tissue is greater, especially when it is held close to the tip [1-3]. These characteristics render the single-use bougie more likely to cause tissue injury than the multiple-use device [6]. In light of our experience, the anesthesiologists in our department agreed not to use single-use introducers in their practice any longer. It should be stressed that the 1997 version of the Portex single-use introducer is no longer produced. Although many departments still use the “old” version, a new version is available. The quality of single-use equipment should be improved, in order to be safe and effective when used.

Gabapentin for acute and chronic post-surgical pain

Pain after surgery remains a significant clinical problem as it impairs recovery adversely and may lead to the transition to chronic pain. Opioid medications are far from ideal agents in suppressing postoperative pain. Gabapentin –an anticonvul-sant with antihyperalgesic properties- originally efficacious against neuropathic pain seems to be very promising for the management of pain after surgery as well. Gabapentin, by decreasing noxious stimulus-induced excitatory neurotransmitter release at the spinal cord, may attenuate central sensitization, and eventually decrease postoperative late pain. Furthermore, different sites of action may be pertinent to a synergistic effect with opioids. Both actions (antihyperalgesic effect and syn-ergy with opioid analgesia) may manifest as analgesia and/or opioid-sparing effect after surgery. This has been confirmed by a variety of clinical studies, in a variety of settings. Most of these studies have shown that either single preoperative or repeated doses of gabapentin, continued for up to a few days after surgery, decrease acute postoperative pain and/or need for postoperative opioids. This has been shown for procedures such as abdominal and vaginal hysterectomy, breast surgery for cancer (mastectomy or lumpectomy), lumbar discectomy and spinal fusion, laparoscopic cholecystectomy and other, such as ENT surgery. Finally, a few studies indicate that perioperative gabapentin may as well decrease chronic pain several weeks after surgery.

Anaesthetic management and perioperative monitoring of a patient with narcolepsy.

thought to be the responsible mechanism [5], but, after phenytoin-dependent antiplatelet antibodies were demonstrated, an immune-mediated destructive process was deemed more likely [4]. It has been postulated that the epoxide metabolite of phenytoin covalently binds to platelet walls, inducing antiplatelet antibodies against the hapten created, leading to destruction of circulating platelets [6]. The necessary metabolism of phenytoin to phenytoin epoxide, platelet binding and subsequent immune response would account for the delay in onset of thrombocytopaenia. Low concentrations of epoxide hydrolase, the enzyme responsible for the breakdown of phenytoin epoxide, would potentially predispose patients to phenytoin-induced thrombocytopaenia, on top of those unknown factors that contribute to idiosyncratic reactions. Interestingly, it has been demonstrated that dexamethasone can induce certain hepatic cytochrome p450 enzymes, but inhibits epoxide hydrolase production, conceivably resulting in an increased concentration of phenytoin epoxide [7]. Other agents that potentially increase the concentration of phenytoin epoxide, and have therefore been implicated as a contributory factor in phenytoin-induced thrombocytopaenia, include histamine-2-receptor antagonists [6]. The treatment of phenytoin-induced thrombocytopaenia is discontinuation of phenytoin and, if the patient has associated life-threatening haemorrhage, platelet transfusion. Giving 1 g kg of intravenous immunoglobulin has been associated with a rapid increase in the platelet count, and should be considered [3]. Although an uncommon complication of treatment, this case highlights that phenytoin-induced thrombocytopaenia can be potentially fatal in neurosurgical patients if undetected before surgery. We recommend that a repeat platelet count be performed on all patients that are started on phenytoin before surgery, especially if it has been prescribed in combination with dexamethasone.

Intravenous lidocaine does not affect the anesthetic depth during rapid sequence induction and intubation as assessed by Bispectral Index monitoring: a randomized double blind study.

Introduction We investigated the impact of intravenous lidocaine on anesthetic depth, as assessed by Bispectral Index score (BIS), and hemodynamic responses to rapid sequence induction/intubation. Material and methods Eighty-four surgical patients with risk factors for regurgitation/aspiration were randomized to receive either lidocaine 1.5 mg/kg or normal saline in a double-blind fashion. Propofol 2 mg/kg, lidocaine or normal saline, followed by rocuronium 1 mg/kg were administered intravenously and trachea was intubated under cricoid pressure application. The BIS scores were recorded before induction of anesthesia, immediately after, at 30 s and 1 min after rocuronium injection and every 30 s after intubation, for 10 min. Systolic/diastolic blood pressure and heart rate were measured before induction, immediately after and at 1 min following rocuronium administration, and every minute for 10 min after intubation. Results Data from 78 patients were analyzed. Demograpic characteristics did not differ between the study groups. A total of 24 BIS scores were recorded for each patient. No difference was found in BIS values between lidocaine and control groups at any time point (F = 2.936, p = 0.91). Also no difference was detected in heart rate, systolic and diastolic blood pressure at any time point of the study period between the two groups (F = 0.063, p = 0.80, F = 0.007, p = 0.93, F = 0.435, p = 0.51 respectively). No episodes of significant bradycardia occurred and none of the patients reported awareness/recall of the procedure. Conclusions Lidocaine 1.5 mg/kg given intravenously during rapid sequence induction does not affect BIS values, or blunt the hemodymanic response to laryngoscopy and intubation.

Changes in Total Serum Glycosaminoglycan Levels in Patients Undergoing Renal Transplantation: Preliminary Data

PurposeTo study the involvement of glycosaminoglycans (GAGs) in the immunological process of renal disease. They are related to cytokines, which are known to play an important role in acute graft rejection after renal transplantation.MethodsWe studied 40 patients on maintenance hemodialysis for chronic renal failure, who underwent renal transplantation from a live donor. We measured serum GAGs preoperatively, intraoperatively, and on postoperative days (PODs) 2 and 10. The clinical outcome and other biochemical markers, such as blood urea nitrogen and serum creatinine, were also recorded.ResultsThe total serum GAG levels decreased after renal transplantation in patients with normal graft function (group N). However, in patients with acute graft rejection post-transplantation (group R), the GAG levels remained significantly elevated.ConclusionsTotal serum GAGs fluctuate in renal transplantation and their association with graft rejection should be investigated further.

Postoperative pain after major abdominal surgery: is it gender related? An observational prospective study.

Gender may be associated with postoperative pain. This study aimed to assess pain intensity and postoperative analgesic requirements in female and male patients scheduled for major abdominal surgery.