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Acromegaly is a condition caused by an excessive secretion of growth hormones [1]. Hypertrophy in the face and extremities can cause enlarged lower jaws, macroglossia, and thickened pharyngeal and laryngeal soft tissues [2]. Hypertrophy in the vocal cord can lead to changes in the upper airway, making airway management difficult during trachea intubation [3,4]. For 50% of acromegalic patients, collateral circulation of radial artery and ulnar artery is not clearly visible in one hand or both hands [5]. Therefore, catheter should be carefully inserted into the radial artery in the wrist to continuously measure the blood pressure. We report a case of successful general anesthesia for an acromegalic patient. A 63 year-old male patient diagnosed with ossification of yellow ligament T11-12 and spinal stenosis L1-5 was hospitalized for an operation of posterolateral fusion T11-12 and decompression L1-5. Two years ago, a macroadenoma of 17 × 27 mm was observed in the patient by sella magnetic resonance imaging at another hospital. The height of the patient was 200 cm. His weight was 94 kg. Based on results of laboratory examination and chest x-ray performed before surgery, nospecific abnormal finding was observed. Electrocardiogram (ECG) revealed signs of AV block type I. Physical examination found clinical signs of Mallampati class III, jaw malocclusion, and macroglossia. After performing Allen's test, flushing did not occur in the left handeven in 15 seconds. Flushing in the right hand was delayed for 9 seconds. In the following upper extremity computed tomography angiography (CTA), collateral blood flow of radial and ulnar artery was not clearly visible (Fig. 1A). Fig. 1 Upper Extremity Computed Tomography Angiography (CTA). The collateral blood flow between radial and ulnar artery in both hands was not clearly visible (A). View of vocal cord by the Bullard laryngoscope showing a narrowed glottis due to hypertrophy in ... No premedication was carried out. After the patient arrived in the operation room, routine monitoring tests such as non invasive blood pressure, ECG, and pulse oximetry were performed. His vital signs were stable, with blood pressure (BP) at 135/70 mmHg, heart rate (HR) at 65 beats/min, and SpO2 at 99%. After preoxygenation with 100% oxygen (O2), 0.2 mg of glycopyrrolate was intravenously injected followed by 180 mg of 1% propofol. When his unconsciousness was confirmed, 80 mg of rocuronium was intravenously injected. After performing mask ventilation using oral airway, his vocal cord was observed using Bullard laryngoscope. His glottis became narrow (Fig. 1B). An armored tube with a diameter of 7.5 mm was intubated into the trachea. To continuously measure his BP, an invasive arterial catheterization was inserted into his dorsalis pedis artery in the left foot. His central venous pressure (CVP) was monitored using internal jugular vein catheterization. The operation lasted about 8 hours. Anesthesia was maintained with isoflurane at 1-1.5 vol% and remifentanil at 0.05 µg/kg/min in an O2-N2O mixture at a 1 : 1 ratio. During surgery, his systolic BP was maintained at 105-135 mmHg, with diastolic BP maintained at 55-75 mmHg. His HR was 60-90 beats/min, with SpO2 at 99% and CVP at 6-7 cmH2O. After the surgery, the patient fully recovered spontaneous breathing and consciousness. Extubation was performed. The patient was in a stable condition after the surgery. He was later transferred to the surgical intensive care unit. Upper airway changes often occur in acromegalic patients [2]. Due to changes in the upper airway, intubation can be difficult [3,4]. Preoperative examinations, such as head and neck movement, Mallampati classification, and thyromental distance, can predict the difficulty of intubation [3]. Our patient showed a good result of head and neck movement before surgery. However, he had Mallampati classification class III, 10 cm thyromental distance, macroglossia, and jaw malocclusion. Based on these findings, we predicted that intubation would be difficult. Therefore, we planned intubation using the Bullard laryngoscope. During intubation, it was confirmed that glottis was narrowed. An armored tube of 7.5 mm in diameter which was small for the patient's body size was inserted into the trachea. Since the intubation into the trachea of acromegalic patients is difficult, it is recommended to use Mackintosh Curve-shaped No. 5 blade or use other methods such as an intubating laryngeal airway mask and a light wand. Intubation into the trachea using fibroptic bronchoscope under consciousness is considered the safest way [4]. Radial artery, an invasive cannulation route in the wrist, is commonly used for continuous measurement of blood pressure. To make use of that route, the ulnar artery circulation to a hand should be checked for impairment first. If the radial artery cannulation is implemented without checking the ulnar artery circulation to a hand, it can cause ischemic damage to the hand. Allen's test can be used to detect impaired ulnar artery circulation to the hand. Acromegalic patients often have carpal ligament hypertrophy which leads to compression to the ulnar artery. Because of this, they can develop impaired ulnar artery circulation. Approximately 50% of acromegalic patients have impaired ulnar artery circulation in one or both of their hands, with 30% of those who have impaired ulnar artery circulation can develop carpal tunnel syndrome [5]. However, our patient did not exhibit any signs of carpal tunnel syndrome. Allent's test, which was performed before surgery, showed that flushing did not occur in the left hand even in 15 seconds, while the right hand exhibited a delayed response of 9 seconds. The upper extremity CTA did not clearly show the collateral blood flow of radial and ulnar artery in both hands. Therefore, it is necessary to secure a cannulation route into the dorsalis pedis artery for continuous monitoring of blood pressure. The intubation into the trachea of an acromegalic patient can be difficult due to anatomical changes. Radial artery cannulation may require extra attention and care due to impaired ulnar artery collateral circulation. Therefore, an accurate medical history checkup of related symptoms as well as strict evaluations and necessary tests must be performed before surgery. An adequate anesthesia plan must be set up and implemented.

The development of pulmonary thromboembolism (PTE) in high risk patients during surgery is not uncommon. Although it is difficult to make a prompt diagnosis due to its nonspecific symptoms, it is imperative to make an early diagnosis and provide proper treatment for a good prognosis. In our case, PTE developed in a high risk patient even after preventive measures of venous thromboembolism (VTE) during total hip replacement (THR) under spinal anesthesia. An 86-year-old male patient, weighing 79 kg, with a height of 165 cm was admitted for the treatment of subluxation of the right hip for which he had undergone revision THR 5 years ago. He was on hypertensive medication. After reduction and 12 days of absolute bed rest, we decided to carry out re-revision THR of the right hip because the pain did not subside. Considering the patient's old age, the 11 days of immobilization after the reduction, and the several risk factors for VTE (obesity, THR, etc.) that were present, graduated compression stockings were applied 4 days prior to the surgery and 40 mg of enoxaparin was administered 12 hours before the operation. Preoperative laboratory findings and examinations were normal except for mild aortic regurgitation on echocardiography and mild fatty liver on abdominal ultrasonography. Before initiating spinal anesthesia, the initial blood pressure (BP) was 160/90 mmHg, heart rate (HR) at 70 beats/min, and pulse oxygen saturation (SpO2) was 99% with an O2 2 L/min via nasal prongs. After achieving adequate spinal anesthesia, major surgical procedures were carried out without significant events and the estimated blood loss was 900 ml, and 2 pints of packed red blood cells were transfused. During skin closure, the BP decreased to 60/40 mmHg and the HR increased to 120 beats/min. The SpO2 abruptly decreased from 99 to 78%. The patient was tachypneic and complained of chest pain. Soon after, his mental status quickly deteriorated. Ten L/min of 100% oxygen via facial mask was applied and fluid resuscitation was initiated. The patient's position was changed to supine as soon as the skin closure was completed. Meanwhile, ephedrine (total of 25 mg) and phenylephrine (100 ug) were injected and invasive arterial BP measurement was started through the radial artery. The BP increased to 80/50 mmHg and HR was 110 beats/min. Arterial blood gas analysis (ABGA) results were pH 7.29, PaCO2 69.8 mmHg, PaO2 61 mmHg, and SaO2 81%. After intubating the patient, dopamine (15 µg/kg/min) and epinephrine (0.1 µg/kg/min) infusions were initiated. BP, HR, and end-tidal CO2 (ETCO2) were checked 15 minutes after intubation and they were 140/90 mmHg, 120 beats/min and 28 mmHg, respectively. ABGA results were pH 7.36, PaCO2 41 mmHg, PaO2 138.6 mmHg, and SaO2 98.2%. Under suspicion of PTE, trans-esophageal echocardiography (TEE) was carried out and emboli in the right atrium with bulging of the right atrial wall intothe left atrium were noted. After transferring the patient to the intensive care unit (ICU), the ventilator was set to the following: FiO2 1.0, synchronized intermittent mandatory ventilation mode 12 breaths/min, and tidal volume 600 ml. ABGA done at the ICU did not improve; pH was 7.26, PaCO2 58 mmHg, PaO2 68 mmHg, and SaO2 86.2%. Thus, heparin therapy was initiated 2 hours after the operation (5000 IU bolus injection followed by 800 IU/hr to maintain 1.5-2 times the normal activated partial thromboplastin time level). This resulted in an improvement of the ABGA results: pH was 7.37, PaCO2 46 mmHg, PaO2 110 mmHg, and SaO2 97%. 5 days later, the endotracheal tube was removed and 5 L/min oxygen via a face mask was initiated. Fourteen days later, no thrombosis was found on spiral computer tomography (CT) and the heparin infusion was stopped. Seventeen days later, the patient's vital signs were stable and thus, he was transferred to the general ward. PTE is a relatively common cardiovascular emergency. VTE is a broad concept which includes PTE and deep vein thrombosis (DVT). One investigation done in the US claims that 5 million cases of DVT develop every year and 10% of these cases causes PTE and 10% of the patients die from it [1]. VTE prevention can be divided into non-pharmacologic (stockings and pneumatic compression devices) and pharmacologic treatment (low-dose subcutaneous unfractionated heparin,low molecular weight heparin, and fondaparinux). Clinical findings of PTE include dyspnea, chest pain, cough, syncope, hemoptysis, high fever, tachycardia, hypotension, and tachypnea. ABGA results may show respiratory alkalosis, hypoxemia, increased arterial to ETCO2 gradient, etc. Righini et al. [2] reported that only 20% of clinically suspected patients are finally diagnosed as having PTE. When PTE is clinically suspected and the patient is hemodynamically stable, with anincreased D-dimer, the diagnosis can be made through multidetector CT scanning or ventilation-perfusion scanning. If the patient is hemodynamically unstable, immediate multidetector CT scanning is performed for the PTE diagnosis. Multidetector CT has 97% sensitivity in finding main pulmonary artery emboli [3]. As in our case, if the CT is not a viable option due to the patient's condition, bedside TEE can be used to make the diagnosis. Pruszczyk et al. [4] reported that diagnosing PTE with TEE compared to diagnosis with angiography results in 100% sensitivity and 80% specificity, and compared to CT, results in 90% sensitivity and 100% specificity. If a patient is hemodynamically unstable and has clinical and laboratory findings that are suspicious for PTE, appropriate and timely management must be performed even if emboli are not found and only indirect signs such as wall dysfunction, tricuspid valve regurgitation, and right to left interseptal bowing are noted. When PTE develops, it causes acute RV failure which may result in death due to systemic output loss. Thus, hemodynamic and respiratory support in a PTE patient is very important. The mainstay of PTE treatment includes anticoagulation, pharmacological thrombolysis, and mechanical thrombolysis. In hemodynamically unstable patients, aggressive treatment such as pharmacologic or mechanical thrombolysis must be performed. Intracranial disease, uncontrolled hypertension, recent major surgery (within 3 weeks) and trauma are contraindications of thrombolytic therapy. Since the early diagnosis and treatment of PTE is essential for a good prognosis, we must always take into consideration the possibility of PTE when non-specific clinical symptoms (dyspnea, hypotension, chest pain, etc) develop, and adequate diagnostic tools must be utilized, followed by proper and prompt management.

It is not easy to identify the exact pain-producing structures in degenerative spinal diseases. Intervertebral disc, facet joint and sacroiliac joint have been widely known as major causes of chronic low back pain (LBP) and referred pain. The afferent sympathetic fibers that pass through the L2 spinal nerve root are the cardinal pathway of sensation from the above three structures. Here, we discuss the effectiveness of L2 nerve root block for patients who are suffering from LBP and referred pain with compound causes.

Refractory status epilepticus is defined as seizure activity that continues after treatment with conventional anticonvulsants. An 8-month-old male had an operation for repair of small bowel perforation, and he suffered a febrile seizure that developed into refractory status epilepticus. Febrile seizure is the most common etiology for children with status epilepticus. We report here on a case of a patient with refractory status epilepticus, and he was managed with sevoflurane, an inhalational anesthetic. The patient was given an inspired concentration of 0.6－2 vol% sevoflurane for 15 days. After stopping of sevoflurane inhalation, he continued to experience intermittent convulsive status epilepticus that was successfully managed with using conventional anticonvulsants.

Background: Epidural PCA (patient controlled analgesia) is a well known postoperative pain control method. However its side effects are not well understood. This study will look into the frequency and progress of the side effects of the epidural PCA using bupivacaine and fentanyl mixture after gynecological surgery. Methods: About 100 female patients undergoing lower abdominal gynecologic surgery under the general anesthesia were studied regarding the side effects such as failure of pain control, nausea, vomit, sedation, pruritus, motor block and hypotension. Visual analogue scale (VAS) was used for the measurement of pain at rest and cough. The frequency and the progress of the side effects were also recorded at 2, 6, 12, 24, 36 and 48 hours after the surgery. The relationship between the insertion site of epidural PCA catheter and motor block, hypotension and the use of rescue drug were also analyzed. Results: VAS scores at cough were 12 to 21 point higher than at rest. Nausea and motor block were more severe than other side effects. The group having epidural PCA catheter inserted in the upper lumbar epidural space showed more severe motor block than the group having it inserted in the lower thoracic epidural space. Conclusions: The frequency of nausea and motor block were relatively higher than other side effects. So it is necessary to take a careful observation and an immediate treatment for these side effects in postoperative pain management using epidural PCA. Also the severity of motor block depends on the insertion site of epidural PCA catheter. Lower thoracic epidural space is considered to be a better insertion site than upper lumbar epidural space in reducing the motor block side effect.

Background: Antidepressants are being used as supplemental therapy in neuropathic and inflammatory pain. The mechanism of their inhibitory effect on experimental animal inflammation is not clear. Studies during the past few years clearly indicate an important role for nitric oxide (NO) in the inflammation and pain-processing system. We evaluated the effects of amitriptyline, desipramine and paroxetine on NO production in primary Schwann cell cultures. Methods: Primary cultures of the Schwarm cell were prepared from dorsal root ganglia of 1- to 3-day old Spraque-Dawley rats. Schwarm cells were cultured in the presence or absence of interferon- (500 ng/ml) plus tumor necrosis factor- (500 ng/ml), amitriptyline, desipramine or paroxetine. Production of NO was determined in the supernatant of the culture media. Results: Amitriptyline (10 ,/ml), desipramine (10,/ml) and paroxetine (10,/ml) inhibited NO release by 29.8%, 51.4%, and 66.8%, respectively. No drug had a toxic effect on cultured cells, which was determined by an LDH assay. Conclusions: Inhibition of NO production by Schwarm cells may be a mechanism by which some antidepressant medications affect inflammatory and neuropathic pain.

Background: The radial artery pressure is known to differ from central arterial pressure in normal patients (distal pulse amplification) and in the early postcardiopulmonary bypass period. We assumed that there may be a change in the normal relationship between central and peripheral arterial pressure in patients with hepatic failure due to an arterio-venous shunt caused by vasodilation and a complex surgical procedure with major vessel clamping. This study was done to examine the adequacy of the radial artery as a site for blood pressure monitoring in liver transplantation (TPL). Methods: We investigated when the pressure gradient developed and what mechanism could be responsible by comparing femoral to radial artery pressure in 11 patients undergoing liver transplantation. Radial and femoral artery pressures, systemic vascular resistance, cardiac output and temperature were compared during surgery in all 11 patients. Additionally measurements included pH, /kg, /kg, central venous pressure, puhnonary artery pressure and mixed venous oxygen saturation. Results: The femoral artery systolic pressure was higher than the corresponding radial artery pressures during the operation. Although not statistically significant, the radial mean and diastolic artery pressures were lower than corresponding the femoral artery pressure. Conclusions: Radial artery systolic pressures underestimate the femoral artery pressure when undergoing a liver TPL. Failure to recognize these effects on pressure recordings can lead to inappropriate patient management decisions.