JDSA Abstracts

doi:10.2344/0003-3006-58.2.94

. 2011 Summer;58(2):94–105. doi: 10.2344/0003-3006-58.2.94

JDSA Abstracts

PMCID: PMC3198133

Anesth Prog. 2011 Summer;58(2):94-97. doi: 10.2344/0003-3006-58.2.94

Pharmacokinetics of ³H-Ropivacaine and ¹⁴C-Lidocaine after Maxillary Infiltration Anesthesia in Rats

Hiromi Kimi ^*, Mikiko Yamashiro ^*, Asako Serada ^*, Shuichi Hashimoto ^*,^*, Katsuhisa Sunada ^*

2010;38(3):262–271.

Ropivacaine is a long acting, amide-type local anesthetic with a structure similar to that of bupivacaine. Unlike bupivacaine, ropivacaine is exclusively a S-(–)-enantiomer and shows less central nervous and cardiovascular toxicity than bupivacaine does. Ropivacaine is widely used for epidural anesthesia, peripheral nerve block, local infiltration anesthesia and postoperative pain control. Pharmacokinetics of ropivacaine administered intravenously or epidurally have been reported, however, no report on pharmacokinetics of locally infiltrated ropivacaine is found.

With the objective of investigating the pharmacokinetics of ropivacaine following local infiltration anesthesia, we injected ³H-ropivacaine or ¹⁴C-lidocaine to the palatal mucosa of rats, measured distributions of radioactivity in the body, and compared the pharmacokinetics of these agents.

Approval from the Institutional Animal Care Committee was obtained before the commencement of this study, and all experiments were conducted in accordance with the rules and guidelines concerning the care and use for laboratory animal experiments.

Twenty µl of 0.5% ³H-ropivacaine or 2% ¹⁴C-lidocaine was injected to the palatal mucosa proximal to the right molar in rats. We studied distributions of these agents in brain, liver, and kidney 0.5, 2, 5, 10, 20, 30, and 60 minutes after injection, and for 48 hours in serum and urine by measuring radioactivity, and compared their pharmacokinetics (n = 8). The highest anesthetic level in the tissue observed at the time points of observation was regarded as the maximum value. Radioactive substances existed in liver, serum and urine 1 and 24 hours after injection were analyzed thin layer chromatography.

Ropivacaine reached the maximum levels 5 minutes after injection in the liver and kidney (1.4 ± 0.1 ng/mg and 2.3 ± 0.2 ng/mg, respectively), and after 2 minutes in the brain (0.7 ± 0.2 ng/mg). The levels at 10 minutes decreased to almost to 50% of the maximum levels. Amounts of ropivacaine in each tissue after 20, 30 and 60 minutes were much the same (Fig. 2A). On the other hand, lidocaine in the brain reached the maximum level (2.3 ± 0.3 ng/mg) after 5 minutes, and gradually decreased by length of time. Lidocaine levels in the liver and kidney markedly increased after 2 minutes. Nearly the same level was kept until after 60 minutes in the liver, the amount of lidocaine in the kidney tended to decrease after 30 minutes (Fig. 2B). In serum, the amount of radioactivity derived from ³H-ropivacaine reached the maximum after 0.5 minutes and rapidly decreased by 12 hours after injection (Fig. 3A). The radioactivity amount from ¹⁴C-lidocaine in serum reached the maximum after 2 hours and rapidly decreased by 6 hours later. No radioactivity was detected after 48 hours (Fig. 3B), whereas 8.2% of the maximum amount of radioactivity was detected in ropivacaine group. The amount of radioactivity in serum and urine demonstrated that ropivacaine and its metabolites remained longer than lidocaine and its metabolites (Fig. 5, 6).

Figure 2. — Concentrations of (A) ropivacaine or (B) lidocaine in the brain, liver, and kidney.

After 0.5% ³H-ropivacaine or 2% ¹⁴C-lidocaine was infiltrated into the right palatal mucosa proximal to the first molar of rats, each radioactivity in the brain (□), liver (•), or kidney (▵) was measured with a liquid scintillation counter (LSC-6100, Aloka). The concentration (ng/mg wet weight) of ropivacaine or lidocaine was included the metabolites, and was calculated by these specific radioactivity.

(A) The maximum values of ropivacaine were 0.7 ± 0.2 ng/mg in the brain (2 min), 1.4 ± 0.1 ng/mg in the liver (5 min), and 2.3 ± 0.2 ng/mg in the kidney (5 min). Data are mean ± SD (n = 8). The degree of significance of difference was measured with the 10 min value to the maximum value. Brain; 10 min vs 2 min, liver and kidney; 10 min vs 5 min: p<0.01. (B) The lidocaine concentration in the brain reached the maximum (2.3 ± 0.3 ng/mg) 5 min after the injection (5 min vs 2 min: p<0.01). The lidocaine concentration in the liver and kidney markedly increased 2 min later (2 min vs 0.5 min: p<0.01).

Figure 3. — Concentrations of radioactivity derived from (A) ³H-ropivacaine or (B) ¹⁴C-lidocaine in the serum.

After 0.5% ³H-ropivacaine or 2% ¹⁴C-lidocaine was infiltrated into the right palatal mucosa proximal to the first molar, the radioactive concentration (dpm/ml) in the serum was measured with the liquid scintillation counter.

(A) The serum concentration of radioactivity derived from ³H-ropivacaine reached the maximum (11,610 dpm/ml) 0.5 min after injection, and rapidly decreased until 12 hr later (12 hr vs 0.5 min: p<0.01). (B) The radioactivity concentration originated from ¹⁴C-lidocaine reached the maximum (938 dpm/ml) 2 hr after the injection, and sharply decreased by 6 hr later (6 hr vs 2 hr: p<0.01). No radioactivity was detected 48 hr after the injection.

Data are mean ± SD (n = 8).

Figure 5. — Chromatogram of radioactive metabolites derived from ³H-ropivacaine in the (A) liver, (B) serum, and (C) urine.

Radioactive substances which were extracted from the liver, serum, and urine at 1 hr (□) or 24 hr (▪) after injection with 0.5% ³H-ropivacaine into the right palatal mucosa proximal to the first molar, were separated by thin layer chromatography (TLC). The TLC plate was Silicagel 60F₂₅₄® (Merck, Germany). The area from the lower end of the plate to the solvent front was divided into 1 to 9 zones. A spot of ropivacaine on the plate was confirmed with UV lamp (253.7 nm). Authentic ropivacaine was detected in zone No. 5. Ropivacaine or the metabolite in each silica gel zone was scratched from the plate and ³H-radioactivity in the zone was measured with the liquid scintillation counter. The radioactivity in each zone as a percentage of the total radioactivity on the TLC plate was calculated.

Amounts of ³H-radioactivity measured in zone No. 5 after 1 hr were 23.0%, and more radioactivity was detected in zones No. 3 and No. 4 in the liver (No. 3 vs No. 5: p<0.01, No. 4 vs No. 5: p<0.01), 67.3% in the serum (No. 5 vs No. 6: p<0.01) and 63.0% in the urine (No. 5 vs No. 6: p<0.01). After 24 hr, more than 80% of the total radioactivity was detected in zones except zone No. 5.

Data are mean ± SD (n = 4).

Figure 6. — Chromatogram of radioactive metabolites derived from ¹⁴C-lidocaine in the (A) liver, (B) serum, and (C) urine.

Radioactive substances which were extracted from the liver, serum, and urine at 1 hr (□) or 24 hr (▪) after injection with 2% ¹⁴C-lidocaine into the right palatal mucosa proximal to the first molar were separated by TLC. Authentic lidocaine was detected in zone No. 4 on the TLC plate. Lidocaine or the metabolite in each silica gel zone was scratched from the plate and ¹⁴C-radioactivity in the zone was measured with the liquid scintillation counter. Amounts of ¹⁴C-radioactivity in zone No. 4 1 hr after the injection were 67.5% in the liver, 75.0% in the serum and 56.6% in the urine (Liver, serum and urine; No. 4 vs No. 3: p<0.01). After 24 hr, radioactivity was not detected in the TLC samples extracted from the liver and serum except from the urine.

Data are mean ± SD (n = 4).

Figure 1. — Chemical formulae of (A) 3H-ropivacaine and (B) 14C-lidocaine.

(A) Ropivacaine hydrochloridemonohydrate [dimethylphenyl-3H(N)].

(B) Lidocaine hydrochloride [carbonyl-14C].

*Asterisks indicate radioisotope labelled positions.

Figure 4. — Concentrations of radioactivity derived from (A) ³H-ropivacaine or (B) ¹⁴C-lidocaine in the urine.

After 0.5% ³H-ropivacaine or 2% ¹⁴C-lidocaine was infiltrated into the right palatal mucosa proximal to the first molar, the radioactive concentration (dpm/ml) in the urine was measured with the liquid scintillation counter.

(A) The concentration of radioactivity reached the maximum (489,367 dpm/ml) after 2 hr and hardly changed until 4 hr after injection. The concentration thereafter gradually decreased, and was 15.7% of the maximum after 24 hr (24 hr vs 2 hr: p<0.01). (B) The maximum concentration (56,180 dpm/ml) was observed after 1 hr. The concentration after 3 hr rapidly decreased to 4.7% of the maximum at 24 hr after injection 24 hr vs 1 hr: p<0.01).

Data are mean ± SD (n = 8).

The pharmaco-activities of the major metabolites of ropivacaine are not defined, however, the possibility of problems due to increase of serum concentration of these compounds caused by large or additional doses was suggested.

Department of Anesthesiology, The Nippon Dental University, School of Life Dentistry at Tokyo

*Research Center for Odontology, Section of Radioisotope Research, The Nippon Dental University, School of Life Dentistry at Tokyo

Anesth Prog. 2011 Summer;58(2):97-99. doi: 10.2344/0003-3006-58.2.94

Factors Affecting Rectal Temperature during Anesthesia for Dental Treatment in Mentally Disabled Patients

Akiko Shiki ¹, Yukio Ishikura ¹, Katsuya Ogata ¹

2010;38(3):272–278.

We have often observed that when anesthesia is induced in mentally disabled patients who refuse anesthesia, the rectal temperature is above 37°C and sometimes even above 37.5°C short after anesthesia induction. In this study, we analyzed the factors affecting rectal temperature during anesthesia in mentally disabled patients using multiple regression analysis.

We studied 181 cases (aged 6 and above) who underwent general anesthesia for dental treatment (Table 1). The patients were all mentally disabled, but they were not physically disabled. The room temperature was set to 25°C, with a variation of 2°C. In all cases, anesthesia was induced with nitrous oxide/oxygen/sevoflurane (5%) and was maintained with nitrous oxide/oxygen/sevoflurane (0.6–1.0%)/propofol (4–10 mg/kg, which was gradually reduced to 2 mg/kg/h). The thermoprobe was inserted into the rectum as soon as the patient fell asleep, and the rectal temperature was recorded every 15 minutes starting at 15 min after induction till the end of the operation. The body of the patient was covered with a bath towel and an electric blanket (50kW) after intubation. The electric blanket was heated only when the rectal temperature was below 36.9°C, and it was removed when it was 37.5°C or above.

Table 1.

Patient characteristics

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In the multiple regression analysis, the dependentvariables were rectal temperature at 15 and 120 min after induction of anesthesia. The analysis was performed at these 2 time points and stepwise with the following independent variables: autism, age, gender, preoperative refusal behavior grade, and climate (Table 2).

Table 2.

Classification codes for the independent variables

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Results: The values of partial correlation coefficients between independent variables were all lower than 0.4 (Table 3). At the 15 min time point after the induction, multiple R (R²) and the highest contribution with regard to refusal behavior were 0.2902 and 0.2053, respectively (Table 4). With regard to behavior, the comparison of mean values is presented in Table 5, and the graph showing changes in rectal temperature at the measuring time points is presented in Figure 1. At the 120 min time point after the induction, multiple R (R²) and the highest contribution with regard to climate were 0.4965 and 0.3349, respectively (Table 6). With regard to climate, the comparison of mean values and the graph showing changes in rectal temperature change are presented in Table 7 and Figure 2, respectively.

Table 3.

Matrix of partial correlation coefficients of independent variables

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Table 4.

Coefficients of determination at the 15 min time point after anesthesia induction

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Table 5.

Mean rectal temperature at the 15 min time point after anesthesia induction in each preoperative behavior group

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Table 6.

Coefficients of determination at the 120 min time point after anesthesia induction

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Table 7.

Mean rectal temperature at the 120 min time point after anesthesia induction in each group according to season

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Conclusions: Soon after induction of anesthesia, anxiety or fear was found to have the most potent effect on rectal temperature and caused it to increase to above normal levels. The increased rectal temperature gradually decreased and became stable within 60 min. At 120 min after induction, the environmental factor had the most potent effect; Therefore, it is suggested that attention should be paid to keep the body warm during anesthesia, especially during the cold season, since the mean rectal temperature may decrease to below 36°C during this season.

Ogata Dental Clinic

Anesth Prog. 2011 Summer;58(2):99-100. doi: 10.2344/0003-3006-58.2.94

Postoperative Sedation with a Combination of Dexmedetomidine Hydrochloride and Propofol with Patient-Controlled Sedation in Patients Undergoing Oral and Maxillofacial Surgery

Minako Ishii ^*, Hitoshi Higuchi ^*,^*, Ayako Jinzenjii ^*, Tomoko Hayashi ^*, Mai Sakaguchi ^*, Yukiko Arai ^*,^*, Yoshihisa Watanabe ^*, Yumiko Tomoyasu ^*,^*, Keita Yoshida ^*,^*, Shigeru Maeda ^*,^*, Takuya Miyawaki ^*

2010;38(3):279–283.

We studied the postoperative sedation with the combination of dexmedetomidine hydrochloride (DEX) and propofol using patient-controlled sedation (PCS) in patients undergoing oral and maxillofacial surgery whose tracheal tube was kept in place for their postoperative care. The study was conducted at the Okayama University Hospital between November 2005 and May 2007. The patients were divided into 2 groups: (1) DEX alone (DEX group: 20 patients), and (2) the combination of DEX and propofol with PCS (DEX + PCS group: 10 patients). Sedation was given to the patients at the sedation level of a Ramsay Score 3 or 4 in both groups. We retrospectively investigated the age, gender, and weight of the patients, as well as the type of surgery, sedative dose, and side effects in each group. Postoperative patients discomfort and amnesia were obtained from the answers to the questionnaire given a week after surgery, and the data were analyzed statistically with the Fisher's exact test or the Mann-Whitney test.

There were no significant differences in the demographic data (Table 1). The dose of DEX was 0.59 ± 0.20 µg/kg/h in the DEX group, and 0.42 ± 0.07 µg/kg/h in the DEX + PCS group. Significantly higher doses of DEX was needed in the DEX group, compared with the DEX + PCS group (p = 0.021) (Table 2). The rate of patients who felt uncomfortable during postoperative sedation was 80.0% in the DEX group, and 40.0% in the DEX + PCS group. The rate of patients who felt uncomfortable during postoperative sedation was significantly lower in the DEX + PCS group than in the DEX group (p = 0.045) (Fig. 1). The rate of patients who had amnesia was 10.0% in the DEX group and 20.0% in the DEX + PCS group. There were no significant differences in the rate of patients having amnesia between the two groups (Fig. 1).

Table 1.

Patient demographics

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Table 2.

Infusion rates of DEX and propofol

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In conclusion, the results suggest that postoperative sedation with the combination of DEX and propofol PCS effectively reduced the postoperative discomfort of patients undergoing oral and maxillofacial surgery while keeping the tracheal tube in place for their postoperative care.

Anesth Prog. 2011 Summer;58(2):100-101. doi: 10.2344/0003-3006-58.2.94

Perioperative Management of an Infant with Severe Growth Hormone Deficiency

Naoka Hamada ¹, Yoshinari Morimoto ¹, Nobuko Uno ¹, Hiroharu Maegawa ¹, Chizuko Yokoe ¹, Aya Masawaki ¹, Hitoshi Niwa ¹

2010;38(3):284–288.

Hypoglycemia can cause irreversible damage to the central nervous system. We provided anesthesia management to an infant diagnosed with severe growth hormone (GH) deficiency who manifested severe hypoglycemia in response to preoperative fasting.

The patient was a 10-month-old girl who was scheduled to undergo palatoplasty (1st stage). Immediately after birth, the patient showed apnea attacks and convulsion, as well as patent foramen ovale and hypoplasia of the corpus callosum. Mild hypoplasia of the mid-face was also shown. When cheiloplasty was performed in our hospital at 3 months of age, there were no symptoms of hypoglycemia.

Prior to this operation, there were no abnormalities detected on screening laboratory data or X-ray findings (Table 1). After 5 hours of pre-operative fasting, the patient developed convulsions and the blood glucose concentration was <20 mg/dl. The scheduled procedure was postponed, and the patient underwent general examination by the pediatrician. However, there were no apparent abnormalities in the hypothalamic-pituitary system. The pediatrician suggested that perioperative hypoglycemia could be prevented by infusion of glucose solution for a short-period fasting and palatoplasty was re-scheduled.

Table 1.

Endocrine laboratory data

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Formula was given to the patient 4 hours before surgery, and fruit juice was given 3 hours before surgery. When the patient was brought to the operating room, the blood glucose concentration was 52 mg/dl, and 2.6% glucose solution was initiated at 140 ml/h (485 mg/kg/h as glucose, up to 200 ml), following 4.3% glucose solution. The serum glucose concentration rose to 156 mg/dl after one hour, and 206 mg/dl at the end of anesthesia.

The 4.3% glucose solution was continued by 30 ml/h (172 mg/kg/h as glucose) postoperatively, which stabilized the blood glucose concentration at 77–96 mg/dl immediate after the operation. Thereafter, however, the patient showed persistent hypoglycemia (<20 mg/dl); which prompted us to investigate its cause. Upon blood testing, low values for GH and somatomedin C were observed, and the peak value of GH over 120 minutes on stimulation test using three hormones/drugs (arginine, thyroid stimulating hormone and gonadotropin-releasing hormone) and using clonidine, were 1.9 ng/ml and 1.54 ng/ml, respectively (Table 2). In addition, hypoplasia of the pituitary gland was observed on the MRI. Based on these findings, the patient was diagnosed with a severe type of GH deficiency and now undergoes GH replacement therapy as well as frequent formula feeding to avoid hypoglycemia. Seven months after the first stage operation, the patient underwent palatoplasty (2nd stage). The optimal control of blood glucose concentration was obtained using the same perioperative management.

Table 2.

Secretion stimulation test for growth hormone

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Because GH is a hormone released from the anterior lobe of the pituitary gland to maintain the blood glucose concentration, hypoglycemia occurs when the secretion of GH decreases. In this case, hypoglycemia was induced by prolonged preoperative fasting (5 hours) as well as GH deficiency. When a low serum concentration of GH is detected by blood testing, careful perioperative management strategies should be established. Adequate endocrine evaluation and glucose administration should be employed in infants when endocrine abnormalities are suggested.

Anesth Prog. 2011 Summer;58(2):101-102. doi: 10.2344/0003-3006-58.2.94

Anesthetic Management during Glossectomy in a Patient with a History of Living-Donor Lobar Lung Transplantation

Chizuko Yokoe ¹, Yoshinari Morimoto ¹, Naoka Hamada ¹, Machiko Fujimoto ¹, Mitsutaka Sugimura ¹, Hitoshi Niwa ¹

2010;38(3):289–294.

The number of patients undergoing lung transplantation is increasing and the survival rate has also improved significantly. However, there are few reports concerning the anesthetic management of patients who have undergone lung transplantation. We report the anesthetic management during glossectomy in a patient with lung transplantation.

A 22-year-old female (157.3 cm tall and 35.4 kg weight) had undergone living-donor lobar lung transplantation 9 months before the first visit to our hospital; the right and left lower lobes from her parents were transplanted. The transplanted lungs were surgically connected to the bilateral main bronchi. The patient was receiving immunosuppressive therapy with cyclosporine A (CYA; 160 mg/day), myco-phenolate mofetil (750 mg/day) and prednisolone (7.5 mg/day or 2.5 mg/day; every other day). Preoperative pulmonary function demonstrated a normal range except for a decreased vital capacity (1.04l, 33.8% predicted) resulting from the impaired capacity of the transplanted lung lobes. The patient was estimated to be grade II or III according to the Hugh-Jones classification. X-ray findings and arterial blood gas analysis appeared normal (Fig. 1).

On the day of surgery, 80 mg of CYA was orally administered 2 hours before anesthesia. 100 mg of hydrocortisone was intravenously administered just before induction and at the end of surgery, respectively. Anesthesia was induced with propofol (40 mg) and remifentanil (0.25 µg/kg/min), and nasotracheal intubation was performed following muscle relaxation with rocuronium bromide (20 mg). The tracheal tube was placed so that its cuff proceeded 1 cm through the vocal cords, to avoid traumatizing the bronchial anastomosis. Anesthesia was maintained with sevoflurane (1%) and remifentanil (0.1–0.2 µg/kg/min) in oxygen/air (Fio₂ 0.33).

During anesthesia, ventilation was maintained manually with a tidal volume of 300 ml, respiratory rate of 15–17 breaths/min, and peak airway pressure of 13 cmH₂O, which maintained good ventilation (Table 2). Because a reduced volume of urine was shown, acetate Ringer's solution with 5% glucose was infused at 150 ml/h.

Table 2.

Blood gas analyses during anesthesia

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Table 1.

Laboratory data on the previous day of operation

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Table 3.

Postoperative laboratory data

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After surgery was completed, intra-tracheal suction was performed while maintaining adequate anesthesia level to avoid bucking. The patient was awakened followed by ventilation with 100% oxygen, and the tracheal tube was removed. Appropriate immunosuppressive therapy was administered in the postoperative period.

During the anesthetic management for the patient with lung transplantation, there are some problems to be considered. (a) Ventilation should be maintained at a lower tidal volume due to the restricted capacity of the transplanted lobes. (b) Denervation of the transplanted lung results in a failure of the cough reflex distal to the bronchial anastomosis, and impaired mucocilliary function is likely to promote pneumonia. In addition, immunosuppressive therapy may promote infection. In the present case, we administered an antibiotic prophylactically and suctioned the trachea adequately under aseptic procedures.

Since dissection of the lymphatic vessels can increase the risk of pulmonary edema, fluid overload and hemodynamic changes were avoided. The volume of infusion was restricted despite the reduced urine output, and infusion was maintained postoperatively for a day to correct dehydration.

In the perioperative period, appropriate immunosuppressive therapy was administered; in particular, CYA administration was based on daily measurement of the serum concentration. Consequently, the patient was well controlled by these approaches to perioperative management.

Anesth Prog. 2011 Summer;58(2):102-104. doi: 10.2344/0003-3006-58.2.94

Multiple Episodes of Vasovagal Syncope during Dental Treatments with Intravenous Conscious Sedation: A Case Report

Erina Daigo ¹, Yasushi Sakuma ¹, Kazuhiro Kaneda ¹, Motoko Hirokane ¹, Yoshitaka Inamura ¹, Naotaka Kishimoto ¹, Naoe Komi ¹, Junichiro Kotani ¹

2010;38(3):295–300.

We experienced a case in which 3 episodes of loss of consciousness and asystole were observed on the electrocardiogram (ECG) during the five occasions of intravenous conscious sedation. The patient was a 39-year-old male (weight 64 kg, height 170 cm). He had experienced loss of consciousness twice in the past. We planned to give him dental treatment under intravenous sedation because he had phobia of dental treatment and a gag reflex. At first, we suspected that he might have had neurogenic shock, so we were especially careful about needle insertion during local anesthesia. The first episode of loss of consciousness occurred after the patient was medicated with flumazenil. So, it was believed that the abnormal reaction was caused by flumazenil. At that time, we could not confirm asystole because the ECG monitor was not used. The second episode of loss of consciousness occurred after midazolam (2 mg) was administered; wherein asystole was seen for approximately 20 seconds on the ECG. This was probably caused by anxiety due to inadequate depth of sedation. The third episode of loss of consciousness probably occurred due to anxiety triggered by a failure of venipuncture. The asystole was seen for approximately 20 seconds on the ECG (Fig. 1). In subsequent treatments, at the third and fourth intravenous sedation management, we were able to successfully prevent loss of consciousness by a well-maintained sedation level and prophylactic administration of intravenous atropine. In this case, causing a loss of consciousness may have been due to a vasovagal syncope (Fig. 2). Although we did not administer a psychological test, such a test may have been helpful to better understand the patient's state of mind. It is suggested that avoiding anxiety by providing adequate level of sedation and a prophylactic use of atropine may be useful.

Anesth Prog. 2011 Summer;58(2):104-105. doi: 10.2344/0003-3006-58.2.94

Tracheal Intubation Device with a CMOS Camera: An Improvement of the Device with a CCD Camera

Hiroshi Sehata ¹

Tracheal Intubation Device with a CMOS Camera: An Improvement of the Device with a CCD Camera

Hiroshi Sehata 2010;38(3):301–304.

We previously developed a device with a CCD camera for performing difficult tracheal intubations. The device consisted of a CCD camera, a tube for passing an introducer, small lights, and an introducer. A summary of the protocol for using the device is described below. The top of the device, containing the CCD camera is inserted into the oropharyngeal cavity. The camera enables the oropharynx, glottis and epiglottis to be observed on a TV monitor. While viewing the monitor, the introducer is inserted into the trachea through the vocal cords and the device is then withdrawn, leaving the introducer in the trachea. The intubation is then performed using the introducer.

The device has been useful for performing difficult intubations, but some intubations have been unsuccessful. Consequently, the device was improved in four ways.

The CCD camera was replaced with a CMOS camera. CCD stands for charge-coupled device, while CMOS stands for complementary metal oxide silicon. This replacement enabled the length of the device to be reduced from 4 cm to 2 cm. The CMOS is used as a CMOS sensor. The CMOS sensor consists of photodiodes and some transistors. The image of subjects passed through some transistors in the CMOS sensor creates an image on a liquid crystal display. The low cost, small size, and low power consumption are considered advantages of the CMOS sensor.
The top of the device can be turned toward the glottis. The top of the device can be tied with a wire which, when pulled, enables the top of the device to be turned within the glottis by a maximum of 30 degrees.
We notched a curve in the tube to allow it to bend in the correct direction.
We cut a groove in the entrance of the tube and fixed the wire in place.

This device has the advantage of being inexpensive, easy to use, and having a simple structure. The device can be made by an anesthesiologist for use in cases when intubation is expected to be difficult. The drawback for this device is that it is not useful in case of trismus; furthermore the device needs to be taken apart and cleaned after each use.

The improvements described above have been useful. Note that this device is not commercially available, and its usage requires a special informed consent of patients.