2.Change of inspired oxygen concentration in low flow anesthesia
Jiwook KIM ; Donghee KANG ; Hochul LEE ; Sungwon RYU ; Siejeong RYU ; Doosik KIM
Anesthesia and Pain Medicine 2020;15(4):434-440
Background:
There are several advantages of low flow anesthesia including safety, economics, and eco-friendliness. However, oxygen concentration of fresh gas flow and inspired gas are large different in low flow anesthesia. This is a hurdle to access to low flow anesthesia. In this study, we aimed to investigate the change in inhaled oxygen concentration in low flow anesthesia using oxygen and medical air.
Methods:
A total of 60 patients scheduled for elective surgery with an American Society of Anesthesiologist physical status I or II were enrolled and randomly allocated into two groups. Group H: Fresh gas flow rate (FGF) 4 L/min (FiO₂ 0.5). Group L: FGF 1 L/min (FiO₂ 0.5). FGF was applied 4 L/min in initial phase (10 min) after intubation. After initial phase FGF was adjusted according to groups. FGF continued at the end of surgery. Oxygen and inhalation anesthetic gas concentration were recorded for 180 min at 15 min interval.
Results:
The inspired oxygen concentration decreased by 5.5% during the first 15 min in the group L. Inspired oxygen decreased by 1.5% during next 15 min. Inspired oxygen decreased by 1.4% for 30 to 60 min. The inspired oxygen of group L is 35.4 ± 4.0% in 180 min. The group H had little difference in inspired oxygen concentration over time and decreased by 1.8% for 180 min.
Conclusions
The inspired oxygen concentration is maintained at 30% or more for 180 min in patients under 90 kg. Despite some technical difficulties, low flow anesthesia may be considered.
3.Diagnosis of Palpable Breast Masses by the Modified Triple Test Score: A prospective study.
Bin Soo KIM ; Jin Kwon KIM ; Sung Il CHO ; Donghee RYU ; Hyo Young YUN ; Young Jin SONG
Journal of Korean Breast Cancer Society 2002;5(1):46-51
PURPOSE: The modified triple test (MTT; physical examination, ultrasonography, and fine-needle aspiration cytology) for palpable breast masses yielded 100% diagnostic accuracy when all 3 components were concordant (all benign or all malignant) in our previous study. However, about 30% of cases were discordant and required open or core needle biopsy. This study is designed to evaluate the modified triple test by scoring system, based on our experience, and to develop a method to further limit the need for surgical biopsy of discordant cases. METHODS: The MTT was performed in 175 palpable breast masses of 166 female patients between August 1998 and June 2001 at the Outpatient Clinic, Department of Surgery, Chungbuk National University Hospital. Each component of the MTT was assigned 1, 2, or 3 points for a benign, suspicious, or malignant result, respectively, yielding a total modified triple test score (MTTS) from 3 to 9 points, and 25 cases with 3 points of MTTS were clinically followed up without histological confirmation. RESULTS: Among 175 cases, concordant cases were 120 (68.6%); benign cases was 66 (37.7%), and malignant cases were 54 (30.8%). Concordant cases had 100% of diagnostic accuracy, sensitivity, and specificity. Among the 25 cases of benign concordant (MTTS 3 points), no case was proved to be malignant through clinical follow-up observation. Total discordant cases were 55 (31.4%); 15 cases of 4 points (8.6%), 11 cases of 5 points (6.3%), 4 cases of 6 points (2.3%), 18 cases of 7 points (10.3%), 7 cases of 8 points (4.0%). In each discordant group, 0 cases of 4 points (0%), 2 cases of 5 points (18.2%), 3 cases of 6 points (75%), 15 cases of 7 points (83.8%), and 7 cases of 8 points (100%) were proved to be malignant by histologic confirmation. Aspiration cytology has the highest specificity and positive predictive value of the 3 MTT components. CONCLUSION: Palpable breast masses that score 3 or 4 points by MTTS are benign and could be clinically followed up, and masses that score 8 or 9 points are malignant and should undergo defiitive therapy. Confirmatory biopsy might be applied on only 20% of the masses the reserve MMTTS of 5, 6, and 7 points.
Ambulatory Care Facilities
;
Biopsy
;
Biopsy, Fine-Needle
;
Biopsy, Large-Core Needle
;
Breast*
;
Chungcheongbuk-do
;
Diagnosis*
;
Female
;
Follow-Up Studies
;
Humans
;
Physical Examination
;
Prospective Studies*
;
Sensitivity and Specificity
;
Ultrasonography
4.Antiproliferative Effect of Phenylbutyrate in AsPC-1 Pancreatic Cancer Cell Line.
Chang JIN ; Jin Woo PARK ; Jae Woon CHOI ; Hoon KANG ; Guang Bi JIN ; Su Mun CHOI ; Sung Su PARK ; Donghee RYU ; Lee Chan JANG
Korean Journal of Hepato-Biliary-Pancreatic Surgery 2006;10(1):1-9
PURPOSE: Phenylbutyrate is an effective redifferentiating agent in several human cancers. Recently phenylbutyrate has been reported to inhibit histone deacetylase activity. We investigated the effects of sodium 4-henylbutyrate (Na-4-PB) on cell proliferation in a human pancreatic cancer cell line. METHODS: A human pancreatic cancer cell line, Aspc-1 was purchased from Korean Cell Line Bank. Antiproliferative effects of sodium 4-phenylbutyrate were measured by MTT assay and their mechanisms were evaluated by apoptosis assay and cell cycle analysis. RESULTS: After 3 days of treatment with Na-4-PB at the concentration of 2.5, 5, 7.5, and 10 mM, relative growth inhibition compared to control was 21.3+/-8.3% (mean+/-SD), 37.8+/-2.3%, 46.7+/-0.5%, and 56.7+/-1.7% respectively (p < 0.05). Antiproliferative effect of Na-4-PB was also time-dependent. Combination treatment with Na-4-PB and troglitazone, a PPARg agonist, increased antiproliferative effects but was not synergistic. After 48 hour treatment with Na-4-PB, early apoptotic cell population in control, 2.5, and 5 mM of Na-4-PB was 29.6%, 44.2%, and 65.9%, respectively. After 24 hour treatment with Na-4- PB, G0/G1 phase population in control, 2.5, and 5 mM of Na-4-PB was 55.0%, 67.4%, and 65.8%, respectively. CONCLUSION: Na-4-PB inhibited pancreatic cancer cell proliferation by inducing apoptosis and cell cycle arrest at G0/G1 phase in time- and dose-dependent manner. Combination treatment with Na-4-PB and other chemotherapeutic agents such as troglitazone, a PPARg agonist, can enhance antiproliferative effects. Na-4-PB might be a promising potential therapeutic agent for patients with pancreatic cancer.
Apoptosis
;
Cell Cycle
;
Cell Cycle Checkpoints
;
Cell Line*
;
Cell Proliferation
;
Histone Deacetylases
;
Humans
;
Pancreatic Neoplasms*
;
Sodium
5.Characterization of Acinetobacter baumannii Co-producing Carbapenemases OXA-23 and OXA-66, and armA 16S Ribosomal RNA Methylase at a University Hospital in South Korea.
Hye Won JEONG ; Bo Ra SON ; Dong Ick SHIN ; Donghee RYU ; Seung Bok HONG ; Kyudong HAN ; Kyeong Seob SHIN
Korean Journal of Clinical Microbiology 2011;14(2):67-73
BACKGROUND: In the present study, the resistance mechanisms against carbapenems and aminoglycosides for 23 strains of multi-drug-resistant Acinetobacter baumannii isolated at a university hospital were investigated. METHODS: The minimal inhibitory concentrations (MICs) were determined via broth microdilution or Etest. The genes encoding OXA-type carbapenemases and 16S rRNA methylase were identified using multiplex PCR, and the amplified products were sequenced. Conjugation experiments were conducted, and an epidemiologic study was performed using enterobacterial repetitive intergenic consensus (ERIC)-PCR. RESULTS: In the isolates, the MICs of the tested aminoglycosides, including arbekacin, were >1024 microg/mL; the MICs of aztreonam, cefepime, ceftazidime, and ciprofloxacin ranged from 64 to 128 microg/mL; and the MICs of carbapenem ranged from 32 to 64 microg/mL, as determined through the broth microdilution test. According to the E-test, the MICs of ampicillin/sulbactam and colistin were 8 and 0.25 to 0.38 microg/mL, respectively. Sequence analysis confirmed that all of the isolates expressed carbapenemases OXA-23 and OXA-66, as well as armA 16S rRNA methylase. In addition, ISAba1 was identified upstream of the gene encoding OXA-23. OXA-23 and armA were not transferred to Escherichia coli J53 cells in the transconjugation experiments. ERIC-PCR molecular fingerprinting produced a single pattern in all cases. CONCLUSION: The co-production of OXA-23 and armA 16S rRNA methylase may be attributed to the multidrug resistance of the A. baumannii isolates in the present study. Stricter surveillance and more rapid detection are necessary to prevent the spread of this type of resistance in the future.
Acinetobacter
;
Acinetobacter baumannii
;
Aminoglycosides
;
Aztreonam
;
Carbapenems
;
Ceftazidime
;
Cephalosporins
;
Ciprofloxacin
;
Colistin
;
Consensus
;
Dermatoglyphics
;
Dibekacin
;
Drug Resistance, Multiple
;
Epidemiologic Studies
;
Escherichia coli
;
Methyltransferases
;
Multiplex Polymerase Chain Reaction
;
Republic of Korea
;
RNA, Ribosomal, 16S
;
Sequence Analysis
6.The correlation of heart rate between natural sleep and dexmedetomidine sedation
Donghee KANG ; Changwoo LIM ; Dong jin SHIM ; Huiyoung KIM ; Ji wook KIM ; Hyung joo CHUNG ; Yusom SHIN ; Joo Duck KIM ; Sie Jeong RYU
Korean Journal of Anesthesiology 2019;72(2):164-168
BACKGROUND: Sedation by dexmedetomidine, like natural sleep, often causes bradycardia. We explored the nature of heart rate (HR) changes as they occur during natural sleep versus those occurring during dexmedetomidine sedation. METHODS: The present study included 30 patients who were scheduled to undergo elective surgery with spinal anesthesia. To assess HR and sedation, a pulse oximeter and bispectral index (BIS) monitor were attached to the patient in the ward and the operating room. After measuring HR and BIS at baseline, as the patients slept and once their BIS was below 70, HR and BIS were measured at 5-minute intervals during sleep. Baseline HR and BIS were also recorded before spinal anesthesia measured at 5-minute intervals after dexmedetomidine injection. RESULTS: During natural sleep, HR changes ranged from 2 to 19 beats/min (13.4 ± 4.4 beats/min), while in dexmedetomidine sedation, HR ranged from 9 to 40 beats/min (25.4 ± 8.5 beats/min). Decrease in HR was significantly correlated between natural sleep and dexmedetomidine sedation (R2 = 0.41, P < 0.001). The lowest HR was reached in 66 min during natural sleep (59 beats/min) and in 13 min with dexmedetomidine sedation (55 beats/min). The time to reach minimum HR was significantly different (P < 0.001), but there was no difference in the lowest HR obtained (P = 0.09). CONCLUSIONS: There was a correlation between the change in HR during natural sleep and dexmedetomidine sedation. The bradycardia that occurs when using dexmedetomidine may be a normal physiologic change, that can be monitored rather than corrected.
Anesthesia, Spinal
;
Bradycardia
;
Dexmedetomidine
;
Heart Rate
;
Heart
;
Humans
;
Hypnotics and Sedatives
;
Operating Rooms
7.The correlation of heart rate between natural sleep and dexmedetomidine sedation
Donghee KANG ; Changwoo LIM ; Dong jin SHIM ; Huiyoung KIM ; Ji wook KIM ; Hyung joo CHUNG ; Yusom SHIN ; Joo Duck KIM ; Sie Jeong RYU
Korean Journal of Anesthesiology 2019;72(2):164-168
BACKGROUND:
Sedation by dexmedetomidine, like natural sleep, often causes bradycardia. We explored the nature of heart rate (HR) changes as they occur during natural sleep versus those occurring during dexmedetomidine sedation.
METHODS:
The present study included 30 patients who were scheduled to undergo elective surgery with spinal anesthesia. To assess HR and sedation, a pulse oximeter and bispectral index (BIS) monitor were attached to the patient in the ward and the operating room. After measuring HR and BIS at baseline, as the patients slept and once their BIS was below 70, HR and BIS were measured at 5-minute intervals during sleep. Baseline HR and BIS were also recorded before spinal anesthesia measured at 5-minute intervals after dexmedetomidine injection.
RESULTS:
During natural sleep, HR changes ranged from 2 to 19 beats/min (13.4 ± 4.4 beats/min), while in dexmedetomidine sedation, HR ranged from 9 to 40 beats/min (25.4 ± 8.5 beats/min). Decrease in HR was significantly correlated between natural sleep and dexmedetomidine sedation (R2 = 0.41, P < 0.001). The lowest HR was reached in 66 min during natural sleep (59 beats/min) and in 13 min with dexmedetomidine sedation (55 beats/min). The time to reach minimum HR was significantly different (P < 0.001), but there was no difference in the lowest HR obtained (P = 0.09).
CONCLUSIONS
There was a correlation between the change in HR during natural sleep and dexmedetomidine sedation. The bradycardia that occurs when using dexmedetomidine may be a normal physiologic change, that can be monitored rather than corrected.