In this two-part study we attempted to find a method for preventing lip laceration during tracheal intubation. First, we retrospectively investigated the frequency and location of lip lacerations that occurred during tracheal intubation. This survey revealed that 145 patients (4.9%) out of 2, 963 experienced some form of lip injury during intubation. Of these, lacerations occurred on the top lip in 127 cases (87.6%). These finding suggested that the application of a mouthpiece and a mouth gag could prevent the injury to the top lip.In the second part of the study, we recorded the incidence of lip laceration in 100 patients who wore a bite prevention apparatus during intubation and in 100 patients who underwent intubation without such a device. Lip laceration occurred in 12% of the group with the apparatus and 45% of the group without the protective lip device. This apparatus is effective in preventing lip laceration during tracheal intubation.

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Concerning the three nondepolarizing neuromuscular blocking drugs pancuronium, vecuronium and rocuronium, we calculated the time required for recovery from some muscle relaxation rates (e. g. 99%) to another rate (e. g. 50%) after maintaining a constant relaxation rate (e. g. 99%) by changing the administration rate using PID (proportional plus integral plus derivative) control and the combined pharmacokinetic-pharmacodynamic model, and we also calculated the contextsensitive half-times of these three drugs. For this analysis, we used known pharmacokinetic parameters3), 4) and the pharmacodynamic parameters which were calculated from our own date of the three nondepolarizing muscle relaxants under general anesthesia using an inhalation anesthetic (<1MAC). The neuromuscular effects of these three drugs were mechanically monitored by measuring the twitch tension of the adductor pollicis muscle with stimulation of the ulnar nerve at the wrist.
The context-sensitive half-time curve of rocuronium was shorter than that of vecuronium but the 99-50% recovery time curve of rocuronium was longer than that of vecuronium. Both of 99-50% recovery time curves of the three neuromuscular blocking drugs were cumulatively increasing at 360 minutes of continuous administration. The 90-50% and the 90-75% recovery time curves reached plateaus in vecuronium and rocuronium beyond 120 minutes of administration, but in pancuronium both of these time curves were rising untill 240 minutes. If "kss(E)" is the administration rate of a neuromuscular blocking agent in the steady state which maintains "E"% relaxation rate, then we obtained kss (99)/kss(90)=1.5 and kss(90)/kss (75)=1.2 in both pancuronium and vecuronium, and kss (99)/kss(90)=2.0 and kss(90)/kss (75)=1.4 in rocuronium. Consequently, rocuronium requires a greater change of infusion rate to profound relaxation rate from 75% or 90% to 99% than pancuronium or vecuronium.
The context-sensitive half-time of these three nondepolarizing neuromuscular blocking drugs were much different from their duration times due to their nonlinearities of pharmacodynamics.

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A 20-Year-old patient with Leber's hereditary optic atrophy, which did not respond to conventional ophthalmologic treatment including high doses of adrenocortical steroid, administration of vitamin B12, etc., but did respond to Stellate ganglion block (SGB), demonstrated an improved binocular visual acuity. His visual acuity was 0.07 (right, corrected), and 0.02 (left, corrected), and a large central scotoma was seen in the visual field before SGB. SGB was performed twice daily in the right eye for 7 months. As a result, the patient's visual acuity improved to 0.6 (right, corrected), and 0.2 (left, corrected), along with a reduction in the central scotoma and an improved central vision. Although the mechanism for the ophthalmologic effect of SGB on ophthalmopathy is still not completely understood, SGB is considered to be an effective choice for the treatment of this hereditary disease and no long-term side effects have been reported.

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We experienced two surgical cases with hemostatic disorder in the preoperative period. Prothrombin (PT) activity was decreased in both patients, while activated partial thromboplastin time, bleeding time, fibrinogen antigen and D-dimer were normal. There was no disorder in the intrinsic pathway, common pathway, platelets and fibrinolysis. It was suspected that these coagulopathies were caused by inhibition of the extrinsic pathway in the coagulation system. In order to check the extrinsic pathway, a hepaplastin test (HPT) was performed and showed a decreased value. These findings suggested that F VII which is vitamin K-dependent coagulation factor, should be decreased. Vitamin K1 (10mg) was intravenously administerd, PT activity and HPT increased to within the normal range during the preoperative period. And PIVKA-II has increased when Vitamin K1 was not yet given. Both patients, therefore were diagnosed as having vitamin K deficiency-induced coagulopathy. Vitamin K deficiency in patients are considered to be caused by cephem antibiotics containing N-methyl-thiotetrazole and no oral intake of food for a few days preoperatively. The patients did not develop postoperative bleeding at all. In the case of hemostatic disorder, the diagnosis of coagulopathy as well as control of the hemostasis is still important in preoperative anesthetic management.

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We experienced two surgical cases with hemostatic disorder in the preoperative period. Prothrombin (PT) activity was decreased in both patients, while activated partial thromboplastin time, bleeding time, fibrinogen antigen and D-dimer were normal. There was no disorder in the intrinsic pathway, common pathway, platelets and fibrinolysis. It was suspected that these coagulopathies were caused by inhibition of the extrinsic pathway in the coagulation system. In order to check the extrinsic pathway, a hepaplastin test (HPT) was performed and showed a decreased value. These findings suggested that F VII which is vitamin K-dependent coagulation factor, should be decreased. Vitamin K1 (10mg) was intravenously administerd, PT activity and HPT increased to within the normal range during the preoperative period. And PIVKA-II has increased when Vitamin K1 was not yet given. Both patients, therefore were diagnosed as having vitamin K deficiency-induced coagulopathy. Vitamin K deficiency in patients are considered to be caused by cephem antibiotics containing N-methyl-thiotetrazole and no oral intake of food for a few days preoperatively. The patients did not develop postoperative bleeding at all. In the case of hemostatic disorder, the diagnosis of coagulopathy as well as control of the hemostasis is still important in preoperative anesthetic management.

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A 59-year-old man was referred to our clinic for severe low back pain and phantom limb pain of the lower extremities which was caused by spinal cord injury due to metastatic backbone cancer. For relief of the pain, oral administrations of and subcutaneous injection of morphine were started. However, because this failed to control his pain, we started the patient on a trial of subcutaneous ketamine injections (100mg•d-1) after the ketamine test. The phantom limb pain disappeared quickly after the administration of ketamine. We changed administration method from subcutaneous to intravenous because of intractable redness and induration of the injection sites after 4 weeks. Thereafter, the pain was well-controlled until the patient died. This case shows that ketamine is a useful therapeutic for treating phantom limb pain caused by the invasion of cancer into the spinal cord.

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A 62-year-old male with cardiac amyloidosis underwent an emergent laparotomy. Cardiac failure had been treated with furosemide at does of up to 480mg•d-1. Upon admission, the patient was severely edematous, and echocardiography showed enhancement of myocardial granular sparkling and impaired diastolic function. Before surgery, deslanoside and furosemide were administered intravenously. Anesthesia was induced with thiopental, ketamine and vecuronium, and maintained with oxygen, nitrous oxide, ketamine and fentanyl. The patient was extubated in the operating room and was transferred to the intensive care unit and then to the ward. The patient was saved from congestive heart failure with deslanoside and furosemide. Two months later, however, he suddenly went into cardiac arrest and died. In a patient with cardiac amyloidosis, preoperative assessment of the cardiac function by echocardiography, and preparation for a cardiac emergency were considered to be especially important.

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We had a case of anesthetic management of a patient with Noonan syndrome and associated hypertrophic cardiomyopathy (HCM). A 5-month-old boy, who was diagnosed with Noonan syndrome and associated HCM, underwent the repair of pulmonary stenosis and the closure of an atrial septal defect. The HCM persisted after the cardiac surgery, and this caused simultaneous diastolic dysfunction and outlet stenosis of the left ventricle (LV).
Although HCM is one of the major causes of cardiac dysfunction, it is not an indication for surgical treatment. Under these conditions, evaluation of the LV preload was essential for perioperative management.

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