• Radiation Oncology Journal
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• v.32 no.4
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• pp.256-261
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• 2014

Purpose: We performed invasive thermometry to verify the elevation of local temperature in the liver during hyperthermia. Materials and Methods: Three 40-kg pigs were used for the experiments. Under general anesthesia with ultrasonography guidance, two glass fiber-optic sensors were placed in the liver, and one was placed in the peritoneal cavity in front of the liver. Another sensor was placed on the skin surface to assess superficial cooling. Six sessions of hyperthermia were delivered using the Celsius TCS electro-hyperthermia system. The energy delivered was increased from 240 kJ to 507 kJ during the 60-minute sessions. The inter-session cooling periods were at least 30 minutes. The temperature was recorded every 5 minutes by the four sensors during hyperthermia, and the increased temperatures recorded during the consecutive sessions were analyzed. Results: As the animals were anesthetized, the baseline temperature at the start of each session decreased by $1.3^{\circ}C$ to $2.8^{\circ}C$ (median, $2.1^{\circ}C$). The mean increases in temperature measured by the intrahepatic sensors were $2.42^{\circ}C$ (95% confidence interval [CI], 1.70-3.13) and $2.67^{\circ}C$ (95% CI, 2.05-3.28) during the fifth and sixth sessions, respectively. The corresponding values for the intraperitoneal sensor were $2.10^{\circ}C$ (95% CI, 0.71-3.49) and $2.87^{\circ}C$ (1.13-4.43), respectively. Conversely, the skin temperature was not increased but rather decreased according to application of the cooling system. Conclusion: We observed mean $2.67^{\circ}C$ and $2.87^{\circ}C$ increases in temperature at the liver and peritoneal cavity, respectively, during hyperthermia. In vivo real-time thermometry is useful for directly measuring internal temperature during hyperthermia.

• The Korean Journal of Pain
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• v.12 no.1
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• pp.36-42
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• 1999

Background: The current maximal recommended doses of lidocaine are 7 mg/kg with $5\;{\mu}g/ml$ of epinephrine. But in clinical practice, sometimes more doses of lidocaine are required to produce adequate regional anesthesia. Method: Twenty-two healthy women patients were divided into two groups and pretreated with valium 5 mg p.o., morphine 5 mg i.m., and midazolam 2 mg i.v. before operation. Of these, 7 mg/kg of 2% lidocaine with $5\;{\mu}g/ml$ of epinephrine were given to 11 patients epidurally. Initial 3 ml of epinephrine mixed lidocaine was given as a test dose and remaining doses were given 5 ml/30 sec with 3 min intervals. Radial arterial blood were drawn at 5, 10, 15, 20, 30, 45, 60, 90, 120 min to measure plasma lidocaine concentrations. After confirming all of the peak plasma concentrations of 7 mg/kg lidocaine were absolutely under $5\;{\mu}g/ml$, the other 11 patients were given 10 mg/kg of 2% lidocaine with $5\;{\mu}g/ml$ of epinephrine epidurally and blood samplings were taken according to the same method of 7 mg/kg group. The peak plasma concentration ($C_{max}$), time to reach to $C_{max}$ ($T_{max}$), time to reach to $T_4$, maximal sensory block level, systemic toxicity, and vital sign changes were investigated. Result: $C_{max}$ was significantly higher in 10 mg/kg group ($5.1{\pm}1.3\;{\mu}g/ml$) than 7 mg/kg group($3.3{\pm}0.5\;{\mu}g/ml$), but $T_{max}$ ($10.5{\pm}2.7$ min vs $10.9{\pm}3.1$ min) was not different. Time to reach $T_4$ was significantly shorter in 10 mg/kg group ($9.5{\pm}2.7$ min) than 7 mg/kg group ($12.7{\pm}3.2$ min) but maximal sensory block level ($T_{3.7{\pm}0.7}$ vs $T_{2.7{\pm}1.0}$) was not different. In four patients of 10 mg/kg group, peak plasma concentrations exceeded $5\;{\mu}g/ml$, but no systemic toxicities appeared. No significant vital sign changes were observed. Conclusion: The current maximal recommended doses of lidocaine, merely based on body weight are not always appropriate. Further studies are needed to determine more precise guideline of maximal doses that include various pharmacokinetic components.

• Archives of Reconstructive Microsurgery
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• v.19 no.2
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• pp.97-100
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• 2010

Purpose: Epidermolysis bullosa is a rare genetic disease, characterized by the presence of extremely fragile skin and formation of recurrent blister resulting from even a minor mechanical injury. Squamous cell carcinoma (SCC) is recognized as a complication of the chronic scarring associated with dystrophic epidermolysis bullosa (DEB). When a soft tissue defect happens in a patient with epidermolysis bullosa, it is difficult to cover it with a skin graft or a flap. We describe the successful use of a pedicled deep inferior epigastric perforator flap for the reconstruction of SCC associated with DEB in the groin. Methods: A 29-year-old man diagnosed with DEB at birth sustained an ulcer increasing in the right groin for the last 7 months. Under general anesthesia, the mass lesion and lymph nodes were removed and the resulting defect was covered with a pedicled deep inferior epigastric perforator flap. Results: The flap survived completely and his postoperative course was uneventful. Histopathological examination revealed a SCC in the right groin and malignant tumor cells in the removed lymph nodes as well. Additional positron emission tomogram showed a malignant lesion in the ileocecal area with regional lymph node metastasis. The patient was referred to an oncologist for chemotheraphy, but the patient refused to take it. During a 4-month follow-up period, there was no recurrence in the right groin. Conclusion: We suggest that perforator flaps can be considered as a reliable alternative for the reconstruction of soft tissue defects in a patient with DEB.

• Radiation Oncology Journal
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• v.21 no.4
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• pp.261-268
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• 2003

Purpose: To report the results of curative treatment for patients with tonsil cancer by retrospective analysis. Materials and Methods: From Jan. 1995 till Dec. 2000, 27 patients with squamous cell carcinoma of the tonsil received curative treatment at Samsung Medical Center. Therapeutic decision was made through multidisciplinary conference, and curative radiation therapy was favored when, (1) the patient's condition was not fit for general anesthesia and surgery, (2) the patient refused surgery, (3) complete resection was presumed impossible, or (4) too severe disability was expected after surgery. Surgery was the main local modality in 17 patients (S$\pm$RT group), and radiation therapy in 10 (RT$\pm$CT group). The median follow-up period was 41 months. Results: AJCC stages were I/II in four, III in two, and IV in 21 patients. The 5-year disease-free survival rate was 73.3$\%$ in all patients, 70.6$\%$ in the S$\pm$RT group, and 77.8$\%$ in the RT$\pm$CT group. Treatment failure occurred in seven patients, all with stage III/IV, and all the failures occurred within 24 months of the start of treatment. Five patients among the S$\pm$CT group developed treatment failures; 2 local, 2 regional, and 1 distant (crude rate=29.4$\%$). Two patients among the RT$\pm$CT group developed failures; 1 synchronous local and regional, and 1 distant (crude rate=20.0$\%$). The 5-year overall survival rate was 77.0$\%$ in all patients, 80.9$\%$ in the S$\pm$RT group, and 70.0$\%$ in the RT$\pm$CT group. Conclusion: We could achieve favorable results that were comparable to previously reported data with respect to both the rates of local control and of survival by applying S$\pm$RT and RT$\pm$CT. RT$\pm$CT is judged to be an alternative option that can avoid the functional disability after surgical resection.

• Applied Microscopy
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• v.24 no.4
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• pp.61-77
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• 1994

The calcium-binding proteins (CaBP), parvalbumin (PV) and calbindin-D 28K (calbindin) are particularly abundant and specific in their distribution, and present in different subsets of neurons in many brain regions. Although their physiological roles in the neurons have not been elucidated, they are valuable markers of neuronal subpopulations for anatomical and developmental studies. This study is designed to characterize dorsal lateral geniculate nucleus (dLGN) neurons and axon terminals in terms of differential expression of immunoreactivity (IR) for two well-known CaBPs, PV and calbindin. The experiments were carried out on 6 adult monkeys. Monkeys were perfused under deep Nembutal anesthesia with 2% paraformaldehyde and 0.2% glutaraldehyde in 0.1M phosphate buffer. After removal, the brains were postfixed for 6-8 hr in 2% paraformaldehyde at $4^{\circ}C$ and infiltrated with 30% sucrose at $4^{\circ}C$. Thereafter, they were frozen in dry ice. Serial sections of the thalamus, at $20{\mu}m$, were made in the frontal plane with a sliding microtome. The sections were stained for PV and calbindin with indirect immunocytochemical methods. For electron microscopy, after infiltration with 30% sucrose the blocks of thalamus were serially sectioned at $50{\mu}m$ with a Vibratome in the coronal plane and stained immediately by indirect ABC methods without Triton X-100 in incubation medium. Stained sections were postfixed in 0.2% osmium tetroxide, dehydrated and flat-embedded in Spurr resin. The block was then trimmed to contain only a selected lamina or interlaminar space. The dLGN proper showed strong PV IR in fibers in all laminae and interlaminar zones. Particularly dense staining was noted in layers 1 and 2 that contain many stained fibers from optic tract. Neuronal cell body stained with PV was concentrated only in the laminae. In these laminae staining was moderate in cell bodies of all large and medium-sized neurons, and was strong in cell bodies of some small neurons together with their processes. Calbindin IR was marked in the neuronal cell body and neuropil in the S layers and interlaminar zones whereas moderate in the neuropil throughout the nucleus. Regional difference in distribution of PV and calbindin IR cell is distinct; the former is only in the laminae and the latter in both the S layer and interlaminar space. The CaBP-IR elements were confined to about $10{\mu}m$ in depth of Vibratome section. The IR product for CaBP was mainly associated with synaptic vesicle, pre- and post-synaptic membrane, and outer mitochondrial membrane and along microtubule. PV-IR was noted in various neuronal elements such as neuronal soma, dendrite, RLP, F, PSD and some myelinated or unmyelinated axons, and was not seen in the RSD and glial cells. Only a few neuronal components in dLGN was IR for calbindin and its reaction product was less dense than that of PV, and scattered throughout cytoplasm of soma of some relay neurons, and was also persent in some dendrite, myelinated axons and RLP. The RSD, F, PSD and glial elements were always non-IR for calbindin. Calbindin labelled RLP were presynaptic to unlabeled dendrite or dendritic spine and PSD. Calbindin-labeled dendrite of various sizes were always postsynaptic to unlabeled RSD, RLP or F. From this study it is suggested that dLGN cells of different functional systems and their differential projection to the visual cortex can be distinguished by differential expression of PV and calbindin.

• Journal of Yeungnam Medical Science
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• v.10 no.2
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• pp.451-474
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• 1993

Lidocaline if frequently administered as a component of an anesthetic : for local or regional nerve blocks, to mitigate the autonomic response to laryngoscopy and tracheal intubation, to suppress the cough reflex, and for antiarrythmic therapy. Diazepam dectease the potential central nervous system (CNS) toxicity of local anesthetic agents but may modify the sitmulant action of lidocaine in addition to their own cardiovascular depressant. The potential cardiovascular toxicity of local anesthetics may be enhanced by the concomitant administration of diazepam. This study was designed to investigate the effects of lidocaine dose and pretreated diazepam to cardiovascular system and plasma concentration of lidocaine. Lidocaine in 100 mcg/kg/min, 200 mcg/kg/min, and 300 mcg/kg/min was given by sequential infusion to dogs anesthetized with halothane-nitrous oxide (Group I). And in group II, after diazepam pretreatment, lidocaine was infused by same way when lidocaine was administered in 100 mcg/kg/min, the low plasma levels ($3.97{\pm}0.22-4.48{\pm}0.36$ mcg/ml) caused a little reduction in cardiovascular hemodynamics. As administered in 200 mcg/kg/min, 300 mcg/kg/min, the higher plasma levels ($7.50{\pm}0.66-11.83{\pm}0.59$ mcg/ml) reduced mean arterial pressure (MAP), cardiac index (CI), stroke index (SI), left ventricular stroke work index (LVSWI), and right ventricular stroke work index (PVSWI) and increased pulmonary artery wedge pressure (PAWP), central venous pressure (CVP), systemic vascular resistance index (SVRI), but was associated with little changes of heart rate (HR), mean pulmonary artery pressure (MPAP), and pulmonary vascular resistance index (PVRI). When lidocaine with pretreated diazepam was administered in 100 mcg/kg/min, the low plasma level, the lower level than when only lidocaine administered, reduced MAP, but was not changed other cardiovascular hemodynamics. While lidocaine was infused in 200 mcg/kg/min, 300 mcg/kg/min in dogs pretreated diazepam, the higher plasma level ($7.64{\pm}0.79-13.79{\pm}0.82$ mcg/ml) was maintained and was associated with reduced CI, SI, LVSWI and incresed PAWP, CVP, SVRI but was a little changes of HR, MPAP, PVRI. After $CaCl_2$ administeration, CI, SI, SVRI, LVSWI was recovered but PAWP, CVP was rather increased than recovered. The foregoing results demonstrate that pretreated diazepam imposes no additional burden on cardiovascular system when a infusion of large dose of lidocaine is given to dogs anesthetized with halothanenitrous oxide. But caution may be advised if the addition of lidocaine is indicated in subjects who have impared autonomic nervous system and who are in hypercarbic, hypoxic, or acidotic states.