LALE KARABIYIK

In the development of neurological complications due to central venous cannulation, the properties of the anatomical region and the experience of the practitioner are important. In this case report, an inadvertent brachial plexus anesthesia after repeated local anesthetic infiltrations during failed attempts of internal jugular venous cannulation by an inexperienced practitioner in cardiovascular intensive care unit is described. The neurological complications due to central venous cannulation are reviewed in the light of actual literature data.

Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV 2). This novel virus is originally described in Wuhan region of China and rapidly spread mainly through respiratory droplets and close contact all over the World. World Health Organisation (WHO) has declared this virus as a pandemic. Intensive care units are required to prepare for the challenges associated with intensive care unit admission, organization, infection prevention, follow-up and management of critically ill patients with COVID-19. In this review, we summarized the crucial considerations and recommendations on critical care management of COVID-19 patients.

SIR—Osteogenesis imperfecta (OI) is a rare autosomal inherited disease of the connective tissue, with an incidence of approximately 1 in 30 000 live births. The primary bone lesion is the lack of normal ossification of the endochondral bone, resulting in very fragile bones. The main anaesthetic problems are airway control and intubation, and the risk of anaesthetic agents triggering hyperthermia (1). The possibility of a relationship between OI and malignant or nonmalignant hyperthermia has been previously discussed in the literature and patients with OI have been described with symptoms and signs similar to those of malignant hyperthermia during general anaesthesia (2–4). In this letter, we describe two different anaesthetic approaches for two paediatric cases with OI undergoing orthopaedic surgery. Case 1: A 16-month-old boy weighing 12 kg was anaesthetized by inhalation of sevoflurane and nitrous oxide at induction and maintenance of anaesthesia. Case 2: A 12-year-old girl weighing 12 kg was anaesthetized by total intravenous anaesthesia with propofol and remifentanil. In both cases, dantrolene sodium, sodium bicarbonate and cold intravenous solutions were available before both procedures. Preoperative routine screens were within the normal range. Electrocardiogram, pulse oximeter, intraarterial blood pressure, FiO2, PECO2, rectal temperature and depth of anaesthesia were monitored continuously. Because of the parents’ reluctance, regional anaesthetic techniques were not performed. Malignant hyperthermia triggering agents such as halothane, enflurane and succinylcholine were avoided. Anticholinergics were also avoided because of possible exacerbations of hyperthermia. Postoperative analgesia was provided by paracetamol. As inhalational anaesthesia is the most common technique in paediatric anaesthesia worldwide, we used sevoflurane for the first case. There were no abnormal physical findings except blue sclerae and short neck. He was premedicated with midazolam 0.1 mgÆkg rectally. After inhalational induction with sevoflurane and nitrous oxide in oxygen, a size 2 LMA (LMA) was inserted. Anaesthesia was maintained with sevoflurane 1–3% and nitrous oxide 50% in oxygen and remifentanil infusion (0.25 lgÆkgÆmin). Arterial blood gas analysis revealed a slight metabolic acidosis without hypoxaemia (pH: 7.32, BE: )5.3 mmolÆl, PO2 : 12.6 kPa (97 mmHg), HCO 3 : 19.3 mmolÆl) after induction. We were not able to find any specific reason for this. Although the first 30 min of anaesthesia were uneventful, the heart rate increased from 115 to 130 bÆmin later. Slight metabolic acidosis without hypoxaemia continued. The rectal temperature was 36.5 C. Arterial PO2, PCO2, pH and blood pressure were normal at that time. Heart rate remained at 130 bÆmin for 10 min then increased to 160 bÆmin (40% above the baseline) until the end of the surgery. The duration of anaesthesia was 1 h. Heart rate was 160 bÆmin and temperature rose to 38.3 C at 20 min postoperatively. Arterial blood gas analysis still revealed a slight metabolic acidosis without hypoxaemia. Tachycardia persisted even in sleep. There was neither a volume deficit nor a diagnosed infection. During the following 6 h his temperature continued to rise to a maximum of 39.2 C. He received O2 via a mask, active cooling and paracetamol for analgesia and antipyrexia. Temperature eventually fell to 36.7 C and arterial blood gas values and heart rate returned to normal. At no time postoperatively were hypoxaemia or hyperkalaemia observed. The patient was discharged on the second postoperative day. The second case was kyphoscoliotic and had deformities of the upper and lower extremities. She had experienced several fractures and two previous operations. Hyperpyrexia had occurred during these procedures when isoflurane had been used for maintenance of anaesthesia. She had a short neck with a modified Mallampati score of 3. She was premedicated with midazolam 0.07 mg kg intravenously. After anaesthesia was induced with propofol 2 mgÆkg and remifentanil 1 lgÆkg, a size 3 intubating laryngeal mask was inserted with the head and neck in the neutral cervical position. Anaesthesia was maintained with a propofol infusion (initial rate 10 mgÆkgÆh followed by 4 mgÆkgÆh) and remifentanil infusion (0.25 lgÆkgÆmin). The patient was spontaneously breathing and ventilation was continued with a mixture of oxygen in air in a closed circuit. Arterial blood gas analysis was normal throughout the procedure and temperature did not increase. Oxygen saturation remained above 95%, heart rate and blood pressure were within ±10% of preoperative limits. No rigidity was observed. Recovery was uneventful and she was discharged on the second postoperative day. In our previous report, we described the safety of TIVA in an adult patient with OI (5). We also found that TIVA was safe in this presented paediatric case. Two paediatric cases are described with OI in which the LMA was used, one with inhalational…

To assess the effect of esmolol added to propofol-remifentanil combination for hypotensive anesthesia on hemodynamic conditions, consumption of anesthetic drugs, and recovery, during elective septorhinoplasty. This prospective, randomized study was carried out at Gazi University, Faculty of Medicine, Ankara, Turkey in 2005. Following Institutional Ethical Committee approval, 40 American Society of Anesthesiologists (ASA) I patients were divided into 2 equal groups group remifentanil infusion RP and group esmolol infusion (RP-E). After anesthesia induction with propofol (2-2.5 mg/kg), the mean arterial pressure was aimed to be between 50 mm Hg and 65 mm Hg for controlled hypotensive anesthesia in both groups. In group RP, a remifentanil infusion of 0.1-0.5 microg/kg/min was titrated, following a bolus of 1 microg/kg; for group RP-E, an esmolol infusion of 100-300 mg/kg/min was titrated, following a bolus of 500 microg/kg; to achieve a target blood pressure. In addition, propofol was infused according to depth of anesthesia to maintain anesthesia in both groups. Electrocardiography, heart rate, blood pressure, cardiac output, and consumption of anesthetic drugs were recorded. Postoperatively, recovery times, visual analog pain scores, and side effects were observed. The decrease in the intraoperative heart rate was more significant in group RP-E than in group RP. The remifentanil consumption was much lower in group RP-E. The recovery times were similar in both groups. Addition of esmolol to propofol-remifentanil combination leads to a decrease in remifentanil consumption, without a decrease in cardiac output during hypotensive anesthesia.

Dystrophic epidermolysis bullosa is a rare genetically mechanobullous disorder, characterized by an excessive susceptibility of the skin and mucosa to separate from the underlying tissues after mechanical trauma. Avoiding mechanical stimulation of the skin and mucous membranes is essential in the anesthetic management. These case reports describes bilateral nerve block in two patients with an anticipated airway difficulty due to epidermolysis bullosa. We report the successful applications of intraoperative indirect electrocardiogram monitoring without electrodes and bilateral axillary and midhumeral nerve block using levobupivacaine in combination with lidocaine in patients who had previously undergone repeated general anesthesia. We conclude that regional anesthesia should be preferred in patients with dystrophic epidermolysis bullosa, especially those who had previously undergone repeated general anesthetic procedures.

We have investigated the effect of nitrous oxide on the middle ear pressure, comparing inhalational anaesthesia with nitrous oxide and halothane and total intravenous anaesthesia with propofol-alfentanil. Fifty patients with normal healthy ears were divided into two groups. In one group (n = 25), anaesthesia was induced with thiopentone 6 mg kg-1, and maintained with halothane 1% and nitrous oxide 66% in oxygen. In the other group (n = 25), anaesthesia was induced with alfentanil 25 micrograms kg-1 and propofol 2 mg kg-1, and maintained with an infusion of alfentanil 10 micrograms kg-1 min-1 for the first 10 min and then with 0.5 microgram kg-1 min-1 and with propofol 10 mg kg-1 h-1 for the first 10 min, 8 mg kg-1 h-1 for the following 10 min and 6 mg kg-1 h-1 thereafter. Patients were ventilated with an oxygen-air mixture (F1O2 = 0.33). Middle ear pressures were measured during the pre-, intra- and post-anaesthetic period in both ears. A progressive rise was observed (P < 0.05) in the first group, whereas values were within the normal limits clinically and there was no statistically significant change in those receiving total intravenous anaesthesia during the intra-anaesthetic period. The time to reach peak pressure with inhalational anaesthesia was 60 min (181.5 mmH2O) and to return to normal was 30 min (49.5 mmH2O) after cessation of nitrous oxide administration. The incidence of nausea and vomiting was less in the patients not receiving nitrous oxide.

To assess the effect of esmolol added to propofol-remifentanil combination for hypotensive anesthesia on hemodynamic conditions, consumption of anesthetic drugs, and recovery, during elective septorhinoplasty. This prospective, randomized study was carried out at Gazi University, Faculty of Medicine, Ankara, Turkey in 2005. Following Institutional Ethical Committee approval, 40 American Society of Anesthesiologists (ASA) I patients were divided into 2 equal groups group remifentanil infusion RP and group esmolol infusion (RP-E). After anesthesia induction with propofol (2-2.5 mg/kg), the mean arterial pressure was aimed to be between 50 mm Hg and 65 mm Hg for controlled hypotensive anesthesia in both groups. In group RP, a remifentanil infusion of 0.1-0.5 microg/kg/min was titrated, following a bolus of 1 microg/kg; for group RP-E, an esmolol infusion of 100-300 mg/kg/min was titrated, following a bolus of 500 microg/kg; to achieve a target blood pressure. In addition, propofol was ...

During insertion of the double lumen tube in patients with ankylosing spondylitis, cervical neutral position should be maintained to avoid vertebral and spinal injuries. Although flexible fiberoptic bronchoscopic intubation is the gold standard, available FOB size is not compatible with that of the endobronchial lumen of the double lumen tube. This problem should be solved according to institutional capabilities. In this report we present a case of insertion of double lumen tube in neutral position using flexible fiberoptic bronchoscope and airway exchanger catheter in a thoracotomy patient with extremely limited neck mobility due to ankylosing spondylitis.

Our objective was to examine the clinical properties of two anesthetic regimens, propofol target-controlled infusion (TCI), or desflurane using remifentanil TCI under bispectral index (BIS) guidance during ear, nose, and throat (ENT) procedures. FORTY CONSENTING PATIENTS WHO SCHEDULED FOR ENT PROCEDURES WERE PROSPECTIVELY STUDIED AND WERE INCLUDED IN ONE OF THE TWO GROUPS: TCI group or desflurane (DES) group. General anesthesia was induced with 3 ng mL(-1) and 4 μg mL(-1) effect site concentrations (Ce) of remifentanil and propofol, respectively, with TCI system. After intubation, while propofol infusion was continued in the TCI group, it was ceased in the DES group and desflurane with an initial delivered fraction of 6% was administered. The Ce of propofol infusion and inspired fraction of desflurane was adjusted in order to keep BIS as 50 ± 10. General mean values of mean arterial pressure (MAP) and heart rate (HR) for the TCI group was significantly higher than DES group (89.3 mmHg and 72.4 bpm vs. 77.1 mmHg and 69.5 bpm). Early emergence from anesthesia did not significantly differ between the groups. The rate of patients' Aldrete score (ARS) to reach 10 was found to be 100% at the 15(th) min in both groups. Bispectral index guided combinations of remifentanil TCI either with propofol TCI or desflurane anesthetic regimens are both suitable for patients undergoing ENT surgery. The lower blood pressure in the remifentanil TCI with desflurane anesthetic regimens may be a significant advantage.

SIR—Osteogenesis imperfecta (OI) is a rare autosomal inherited disease of the connective tissue, with an incidence of approximately 1 in 30 000 live births. The primary bone lesion is the lack of normal ossification of the endochondral bone, resulting in very fragile bones. The main anaesthetic problems are airway control and intubation, and the risk of anaesthetic agents triggering hyperthermia (1). The possibility of a relationship between OI and malignant or nonmalignant hyperthermia has been previously discussed in the literature and patients with OI have been described with symptoms and signs similar to those of malignant hyperthermia during general anaesthesia (2–4). In this letter, we describe two different anaesthetic approaches for two paediatric cases with OI undergoing orthopaedic surgery. Case 1: A 16-month-old boy weighing 12 kg was anaesthetized by inhalation of sevoflurane and nitrous oxide at induction and maintenance of anaesthesia. Case 2: A 12-year-old girl weighing 12 kg was anaesthetized by total intravenous anaesthesia with propofol and remifentanil. In both cases, dantrolene sodium, sodium bicarbonate and cold intravenous solutions were available before both procedures. Preoperative routine screens were within the normal range. Electrocardiogram, pulse oximeter, intraarterial blood pressure, FiO2, PECO2, rectal temperature and depth of anaesthesia were monitored continuously. Because of the parents’ reluctance, regional anaesthetic techniques were not performed. Malignant hyperthermia triggering agents such as halothane, enflurane and succinylcholine were avoided. Anticholinergics were also avoided because of possible exacerbations of hyperthermia. Postoperative analgesia was provided by paracetamol. As inhalational anaesthesia is the most common technique in paediatric anaesthesia worldwide, we used sevoflurane for the first case. There were no abnormal physical findings except blue sclerae and short neck. He was premedicated with midazolam 0.1 mgÆkg rectally. After inhalational induction with sevoflurane and nitrous oxide in oxygen, a size 2 LMA (LMA) was inserted. Anaesthesia was maintained with sevoflurane 1–3% and nitrous oxide 50% in oxygen and remifentanil infusion (0.25 lgÆkgÆmin). Arterial blood gas analysis revealed a slight metabolic acidosis without hypoxaemia (pH: 7.32, BE: )5.3 mmolÆl, PO2 : 12.6 kPa (97 mmHg), HCO 3 : 19.3 mmolÆl) after induction. We were not able to find any specific reason for this. Although the first 30 min of anaesthesia were uneventful, the heart rate increased from 115 to 130 bÆmin later. Slight metabolic acidosis without hypoxaemia continued. The rectal temperature was 36.5 C. Arterial PO2, PCO2, pH and blood pressure were normal at that time. Heart rate remained at 130 bÆmin for 10 min then increased to 160 bÆmin (40% above the baseline) until the end of the surgery. The duration of anaesthesia was 1 h. Heart rate was 160 bÆmin and temperature rose to 38.3 C at 20 min postoperatively. Arterial blood gas analysis still revealed a slight metabolic acidosis without hypoxaemia. Tachycardia persisted even in sleep. There was neither a volume deficit nor a diagnosed infection. During the following 6 h his temperature continued to rise to a maximum of 39.2 C. He received O2 via a mask, active cooling and paracetamol for analgesia and antipyrexia. Temperature eventually fell to 36.7 C and arterial blood gas values and heart rate returned to normal. At no time postoperatively were hypoxaemia or hyperkalaemia observed. The patient was discharged on the second postoperative day. The second case was kyphoscoliotic and had deformities of the upper and lower extremities. She had experienced several fractures and two previous operations. Hyperpyrexia had occurred during these procedures when isoflurane had been used for maintenance of anaesthesia. She had a short neck with a modified Mallampati score of 3. She was premedicated with midazolam 0.07 mg kg intravenously. After anaesthesia was induced with propofol 2 mgÆkg and remifentanil 1 lgÆkg, a size 3 intubating laryngeal mask was inserted with the head and neck in the neutral cervical position. Anaesthesia was maintained with a propofol infusion (initial rate 10 mgÆkgÆh followed by 4 mgÆkgÆh) and remifentanil infusion (0.25 lgÆkgÆmin). The patient was spontaneously breathing and ventilation was continued with a mixture of oxygen in air in a closed circuit. Arterial blood gas analysis was normal throughout the procedure and temperature did not increase. Oxygen saturation remained above 95%, heart rate and blood pressure were within ±10% of preoperative limits. No rigidity was observed. Recovery was uneventful and she was discharged on the second postoperative day. In our previous report, we described the safety of TIVA in an adult patient with OI (5). We also found that TIVA was safe in this presented paediatric case. Two paediatric cases are described with OI in which the LMA was used, one with inhalational…

The aim of this study was to determine the role of sevoflurane and/or nitrous oxide on bacterial growth under conditions in vitro similar to those of clinical practice. We assessed these effects on Pseudomonas aeruginosa, Acinetobacter lwoffii, and Staphylococcus aureus growth. Bacterial inoculums were prepared from reference strains in nutritive broth. Airtight chambers were filled with bacterial suspensions. Each strain was studied with and without exposure to sevoflurane and/or nitrous oxide at baseline, after 1 and 3 h. Serial dilutions and agar plates were made and the colonies were counted. P. aeruginosa were grown after exposure to the nitrous oxide alone (2.8 x 10(3) colony-forming units/ml; CFU ml(-1)) after 3 h according to the control (P < 0.05). A. lwoffii were grown after exposure to the nitrous oxide and sevoflurane with nitrous oxide (8.7 x 10(3) and 8.0 x 10(3) CFU ml(-1)) (P < 0.05), respectively. There were no changes in S. aureus growth in controls and anesthesia groups. We conclude that the effects of anesthetic agents on bacterial growth may change owing to the type of anesthetic and microorganism.