Bülent Serhan Yurtlu

Evaluation of the effectiveness of sugammadex for verapamil intoxication.

Previous studies have shown that medications from the cyclodextrin family bind to verapamil. The aim of our study was to determine whether sugammadex could bind to verapamil and prevent the cardiovascular toxicity of that drug. Twenty‐eight sedated Wistar rats were infused with verapamil at 37.5 mg/kg/h. Five minutes after the start of infusion, the animals were treated with a bolus of either 16 mg/kg, 100 mg/kg or 1000 mg/kg sugammadex. The control group was treated with an infusion without sugammadex. The heart rate and respiratory rate were monitored, and an electrocardiogram was recorded. The primary end‐point was the time to asystole. The verapamil infusion continued until the animals arrested. The asystole time for the S16 group was significantly longer compared to those for the control and S1000 groups (p < 0.05). The asystole time for the S1000 group was significantly shorter than those for all of the other groups (p < 0.05). Reflecting these data, there was a near doubling of the mean lethal dose of verapamil from 13.57 mg/kg (S.D. ±8.1) in the saline‐treated rats to 22.42 mg/kg (S.D. ±9.9) in the sugammadex 16 group (p < 0.05). However, for the sugammadex 1000 group, the mean lethal dose was found to be 6.28 ± 1.11 mg/kg. This dose is significantly lower than those for all of the other groups (p < 0.05). We found that treatment with 16 mg/kg sugammadex delayed verapamil cardiotoxicity in rats. However, 1000 mg/kg sugammadex accelerated verapamil cardiotoxicity in rats. Further studies must be conducted to investigate the interaction between verapamil and sugammadex.

Intravenous lipid infusion restores consciousness associated with olanzapine overdose.

To the Editor Originally described for the treatment of local anesthetic toxicity, lipid emulsion therapy has been described in cases of cardiac arrest and central nervous system depression after an overdose of antidepressants and hypnotic anesthetics. The following describes the return of consciousness after olanzepine ingestion. A written approval regarding publication of this report has been obtained from the patient. Three hours after ingesting 100 mg olanzapine, a 39-year-old woman with a previous diagnosis of schizophrenia was seen in our emergency department after gastric lavage and active charcoal treatment had been initiated in a referring hospital. Her arterial blood pressure and heart rate on arrival were 110/70 mm Hg and 90 beats per minute; she responded verbally to questioning and opened her eyes in response to painful stimuli; and her pupils were 5 mm in diameter and reactive to light. Her Glasgow Coma Scale (GCS) score was 10, with no additional positive neurological findings. All laboratory data were within normal limits except for mild leukocytosis. Electrocardiogram revealed normal sinus rhythm with no prolongation of QT interval. She was transferred to the intensive care unit (ICU), where her GCS gradually decreased to 7 at the eighth hour of the ICU stay. She had no response to verbal stimuli and only a flexion response to pain. Arterial blood pressure and heart rate were 120/75 mm Hg and 75 beats per minute and respiratory rate was 24 per minute. One hundred milliliters of 20% lipid emulsion was infused over 15 minutes, during which the respiratory rate gradually decreased from 24 to 12 to 14 during the infusion and the blood pressure and heart rate were not changed. At the end of the infusion, lightly touching her eyelids was associated with arousal and a GCS of 15 and mild agitation, which resolved spontaneously within a few hours. At the 18th hour of her ICU stay, her GCS again decreased to 11, 100 mL 20% lipid emulsion was infused over 30 minutes, and her GCS increased to 15. Agitation was not observed at this time. During the next 24 hours her level of consciousness did not change, and she was discharged from hospital after psychiatric review. Olanzepine is an antipsychotic drug used in the treatment of schizophrenia and delusional disorders with side effects after overdose, including somnolence, mydriasis, blurred vision, respiratory depression, hypotension, and extrapyramidal and anticholinergic effects. Intoxication with large doses may lead to central nervous system depression, tachycardia, and even death. Bioavailability of olanzepine after an oral dose is 65%, and maximum plasma concentrations are reached after 3 to 8 hours of ingestion. Palenzona et al. stated that acute olanzepine overdose causes fluctuations in mental status beginning from ingestion of as small a dose as 30 mg in mild cases, to often fatal, severe cases up to 840 mg ingestion. The relatively small dose of olanzepine in this report may account in part for the rapid return of consciousness. Although the role of lipid emulsion therapy in the treatment of local anesthetic toxicity is well defined, a mechanism of action is not yet clear. It is hypothesized that intravascular lipid creates a “lipid sink,” which may remove drug from tissue, eliminating the signs of intoxication, and in theory a similar mechanism of action may eliminate signs of intoxication with other lipid-soluble drugs. Antipsychotic drugs are lipid soluble, and olanzapine has a high affinity for lipid material. Current recommendations for treating local anesthetic toxicity is a dose 1.5 mL/kg 20% lipid bolus followed by a 0.25 mL/kg/min infusion. In our case, we did not follow the bolus with an infusion because she was hemodynamically stable and had recovered consciousness. However, recurrence of the decreased GCS prompted a second bolus of the lipid emulsion. This clinical picture was consistent with the long (27 to 31 hours) elimination half-life of olanzepine determined earlier. The rapid recovery of consciousness without significant side effects (other than transient mild agitation) suggests this therapy for intoxication after other similar drugs.

Precipitation in Gallipoli: sugammadex / amiodarone & sugammadex / dobutamine & sugammadex / protamine.

ISSN

Intravenous lipid emulsion prolongs survival in rats intoxicated with digoxin.

BACKGROUND Intravenous lipid emulsion eliminates the toxicity-related symptoms of several drugs. We hypothesized that intravenous lipid emulsion prolongs the survival time in digoxin-intoxicated rats. METHODS Electrocardiograms of 14 anesthesized Wistar rats were monitored. All of the rats received digoxin infusion at a rate of 12 mL/h (0.25 mg/mL). Five minutes after the start of digoxin infusion, animals were treated either with 12.4 mL/kg intravenous lipid emulsion (group L) or saline (group C). The primary outcome variable was time elapsed until asystole development. Cumulative dose of digoxin required to induce asystole was also recorded. RESULTS Mean time until asystole development in groups C and L were 21.28 ± 8.61 and 32.00 ± 5.41 minutes, respectively (P< .05). The mean lethal doses of digoxin in the groups C and L were 3.97 ± 1.54 and 6.09 ± 0.96 mg/kg, respectively (P< .05). CONCLUSION Intravenous lipid emulsion prolonged the time until asystole development and increased cumulative lethal dose in rats intoxicated with digoxin.

Anesthesia methods used by anesthetic specialists for circumcision cases. National survey study for Turkey

Objectives: To examine the anesthesiologist’s choice for anesthesia techniques and drugs in circumcision and determine the preoperative examination, intraoperative monitoring techniques, postoperative analgesia methods, and common complications among anesthesiologists working in Turkey. Methods: This cross-sectional study was conducted at Bulent Ecevit University Hospital, Zonguldak, Turkey, between May and July 2012. Survey data were obtained via survey forms through electronic data over the web. The questionnaire consists of 20 questions. These questions included demographic data, methods of anesthesia for circumcision, postoperative analgesia methods, and monitoring methods. Results: The data were obtained from 206 anesthesiologists who agreed to participate in the survey. Circumcision was performed most frequently in the age group of 3-6 years old. It was found that 47% of routine preoperative laboratory tests were coagulation parameters and complete blood count tests. The most common method of anesthesia was laryngeal mask. The frequency of administration of regional anesthesia was 37.4%, and caudal block was more preferable. Bupivacaine as a local anesthetic in regional anesthesia and midazolam and ketamine were the most preferred agents in sedoanalgesia. During regional anesthesia, ultrasound was most often used by anesthesiologists (31.6%). Conclusion: Ambulatory anesthesia protocols, which are also needed in circumcision, can be improved with international recommendation, and these protocols could be conformed as sociocultural structure in societies. This study should be regarded as a preliminary study to attract attention on anesthesia techniques in circumcision.

Pseudocholinesterase levels in patients under electroconvulsive therapy

Objectives: In this study, we aimed to retrospectively assess the correlation of pseudocholinesterase (PChE) levels with age, gender, body weight and diagnosed psychiatric diseases in electroconvulsive therapy (ECT) cases. Methods: This retrospective study was conducted at Bülent Ecevit University Hospital, Zonguldak, Turkey, between 2007 and 2011. In the study, 193 ECT case files were retrospectively scanned to evaluate PChE values before ECT and other file information. Results: There was no difference between gender in terms of PChE levels. Correlation analysis determined a weakly positive correlation between age (p=0.013; correlation coefficient [cc]: 0.178) and body weight (p<0.001; cc: 0.273) and PChE levels. No correlation was found between age, gender, weight or psychiatric diagnosis, and PChE levels. Conclusion: Neuromuscular blockage is a significant factor that increases patient safety, while increasing the efficacy of ECT. In choosing muscle relaxant agents, both patient factors and the pharmacological properties of the neuromuscular blocker should be considered. We think that in situations with delayed recovery of ECT cases without identified PChE levels, low PChE levels must be considered.

Anesthesia for the Pregnant Patient with Intrathoracic Tumor

Cancer in pregnancy is a rare occasion affecting less than 0.1% of all pregnancies. Either primary or secondary metastatic thoracic tumors during pregnancy account even a small portion of them. However, any lung tumor of a term pregnant has devastating potential influence during the anesthesia for childbirth. Due to extreme scarcity of these cases, there are no well-established anesthesia methods to overcome the problems encountered in this particular patient population. Data and information in this field are derived mainly from occasional case reports and mini reviews. The aim of this chapter is to give a structured information and to discuss the possible challenges that the anesthesiologist may come across.

Non-invasive mechanical ventilation and epidural anesthesia for an emergency open cholecystectomy

Non-invasive ventilation is an accepted treatment modality in both acute exacerbations of respiratory diseases and chronic obstructive lung disease. It is commonly utilized in the intensive care units, or for postoperative respiratory support in post-anesthesia care units. This report describes intraoperative support in non-invasive ventilation to neuroaxial anesthesia for an emergency upper abdominal surgery.

Avaliação dos efeitos de sugamadex e dexmedetomidina intra‐arterial: estudo experimental

BACKGROUND Intra-arterial injection of medications may cause acute and severe ischemia and result in morbidity and mortality. There is no information in the literature evaluating the arterial endothelial effects of sugammadex and dexmedetomidine. The hypothesis of our study is that sugammadex and dexmedetomidine will cause histological changes in arterial endothelial structure when administered intra-arterially. METHODS Rabbits were randomly divided into 4 groups. Group Control (n=7); no intervention performed. Group Catheter (n=7); a cannula inserted in the central artery of the ear, no medication was administered. Group Sugammadex (n=7); rabbits were given 4mg/kg sugammadex into the central artery of the ear, and Group Dexmedetomidine (n=7); rabbits were given 1μg/kg dexmedetomidine into the central artery of the ear. After 72h, the ears were amputated and histologically investigated. RESULTS There was no significant difference found between the control and catheter groups in histological scores. The endothelial damage, elastic membrane and elastic fiber damage, smooth muscle hypertrophy and connective tissue increase scores in the dexmedetomidine and sugammadex groups were significantly higher than both the control and the catheter groups (p<0.05). There was no significant difference found between the dexmedetomidine and sugammadex groups in histological scores. CONCLUSION Administration of sugammadex and dexmedetomidine to rabbits by intra-arterial routes caused histological arterial damage. To understand the histological changes caused by sugammadex and dexmedetomidine more clearly, more experimental research is needed.

Evaluation of the effects of intra-arterial sugammadex and dexmedetomidine: an experimental study

BACKGROUND Intra-arterial injection of medications may cause acute and severe ischemia and result in morbidity and mortality. There is no information in the literature evaluating the arterial endothelial effects of sugammadex and dexmedetomidine. The hypothesis of our study is that sugammadex and dexmedetomidine will cause histological changes in arterial endothelial structure when administered intra-arterially. METHODS Rabbits were randomly divided into 4 groups. Group Control (n=7); no intervention performed. Group Catheter (n=7); a cannula inserted in the central artery of the ear, no medication was administered. Group Sugammadex (n=7); rabbits were given 4mg/kg sugammadex into the central artery of the ear, and Group Dexmedetomidine (n=7); rabbits were given 1μg/kg dexmedetomidine into the central artery of the ear. After 72h, the ears were amputated and histologically investigated. RESULTS There was no significant difference found between the control and catheter groups in histological scores. The endothelial damage, elastic membrane and elastic fiber damage, smooth muscle hypertrophy and connective tissue increase scores in the dexmedetomidine and sugammadex groups were significantly higher than both the control and the catheter groups (p<0.05). There was no significant difference found between the dexmedetomidine and sugammadex groups in histological scores. CONCLUSION Administration of sugammadex and dexmedetomidine to rabbits by intra-arterial routes caused histological arterial damage. To understand the histological changes caused by sugammadex and dexmedetomidine more clearly, more experimental research is needed.