[Kinking of the endotracheal tube in a prone patient associated with the inadequate withdrawal maneuver of the Pentax-AWS Airway Scope].

We report a case of intraoperative kinking of an endotracheal tube (ETT) in a prone patient during spine surgery. We postulate that one of the risk factors involved with kinking was the inadequate withdrawal maneuver of Pentax-AWS Airway Scope (AWS). Patient was a 69-year-old woman with hypertension, diabetes mellitus, and rheumatoid arthritis, undergoing C4-6 laminoplasty under general anesthesia in the prone position. A 7.0-mm polyvinyl endotracheal tube (Paker Flex-Tip Tube) was placed to 21 cm at the right angle of the mouse without difficulty using the AWS. Both peak inspiratory pressure (PIP) and partial pressure of end-tidal carbon dioxide began to rise gradually from 24 to 28 cmH2O and 38 to 44 mmHg, respectively. Although over 30 cmH2O in PIP repeatedly appeared after that, we did not find any remarkable change of ventilation except for weak breath sound. Thereafter, when we checked the tube with a flexible fiberoptic bronchoscope, it could not pass through the tube. At first, we asked the surgeon to release neck flexion as much as possible. This procedure could not correct the kink completely but allowed the passage of bronchoscope in the ETT. Then, we tried to reposition the ETT by inserting the bronchoscope beyond the point of kinking for maintaining luminal patency and adequate ventilation. The subsequent anesthetic course was uneventful. Kinking of the ETT in the oral cavity is an uncommon problem but we must keep in mind as one of the differential diagnoses. When using the AWS for endotracheal intubation, we recommend the confirmation of the position of the ETT to be normal in the oral cavity by direct laryngoscopy.

[A case of late drug-eluting stent thrombosis during postoperative period after 5 years of stent implantation].

Stent thrombosis during perioperative period is a critical complication for patients treated with drug-eluting stent (DES). We experienced a case of late DES thrombosis 5 years after initial implantation. A 48-year-old man with familial hyperlipidemia, angina pectoris and chronic pulmonary emphysema, was diagnosed with esophageal carcinoma, and scheduled for esophagectomy. He was first treated with DES 5 years ago, and he underwent repeated revascularization for re-stenosis. He had received anti-platelet therapy up to 1 week prior to the current operation, which was replaced by heparin administration. The surgical procedure was uneventful, and he tolerated it well. Immediately after his admission to ICU, sporadic premature ventricular contraction and ST-elevation occurred, leading to ventricular fibrillation. Emergent coronary angiography revealed re-stenosis of the right coronary artery treated with DES 5 years ago. At present, there was no definite guideline, on the management of DES during perioperative period. It is important for us to decide continuing antiplatelet therapy balancing the risk of stent thrombosis with surgical bleeding in each patient.

[A case of transient postoperative median nerve palsy due to the use of the wrist holder to stabilize an intra-arterial catheter].

We experienced a case of right median nerve palsy at the distal forearm following abdominal surgery. We postulate that the cause of the median nerve palsy is overextension of the wrist by the inappropriate fixation with a holder. The patient was a 46-year-old man with habit of smoking receiving low-anterior resection of the rectum under general and epidural anesthesia in lithotomy position. During surgery his upper limbs were placed on padded arm board abducted about 80 degrees and affixed with soft cotton. His forearms were slightly supinated, whereas his elbows were not over-extended. A 22 G cannula was inserted in the right radial artery and the right wrist was fixed with plastic-holder with soft pad. This position was maintained throughout the operation approximetly for 250 minutes. During anesthesia any special events regarding hemodynamic variables were not observed. He complained of numbness in the palmar side of the digits 1-3 on his right hand without motor disturbance 4 hours after the operation. Examination by the anesthesiologist revealed median nerve palsy. Fortunately, this symptom gradually but completely resolved over the next few days. The possible causes of this neuropathy include the overextension of the wrist or the unexpected extension of the elbow beyond the acceptable range by the supination of forearm, which was induced by the attachment used to stabilize an intra-arterial catheter. Therefore, in the current case we should have returned the wrists promptly to the neutral position following arterial catheter placement to prevent the median nerve palsy. This case suggests the importance of holding the proper position of the arm during surgery.

Onset of pulmonary ventilation in fetal sheep produces pial arteriolar constriction dependent on cytochrome p450 omega-hydroxylase activity.

With the onset of ventilation at birth, cerebral blood flow decreases as oxygenation increases, but the mechanism of cerebral vasoconstriction is unknown. Cytochrome P-450 omega-hydroxylase activity metabolizes arachidonic acid to 20-HETE, a potent vasoconstrictor, in a physiologically relevant O(2)-dependent manner. We tested the hypothesis that the omega-hydroxylase inhibitor, 17-octadecynoic acid (17-ODYA), reduces cerebral vasoconstriction during in utero ventilation with O(2) in fetal sheep. In anesthetized pregnant sheep near term, the fetal head was exposed with the rest of the body remaining in utero. Pial arteriolar diameter was measured by intravital microscopy through a closed cranial window superfused with vehicle or 17-ODYA. Mechanical ventilation of the fetal lungs with a high O(2) mixture to increase arterial Po(2) from approximately 20 to approximately 90 Torr markedly decreased pial arteriolar diameter by 24 + or - 3% (+ or - SE) without a change in arterial pressure. In contrast, superfusion of 17-ODYA completely blocked the decrease in diameter (2 + or - 3%) with increased oxygenation. Vasoconstriction to hypocapnia was intact after returning to the baseline intrauterine oxygenation state, thereby indicating that the effect of 17-ODYA was selective for increased oxygenation. In cerebral arteries isolated from fetal sheep, increasing oxygenation increased 20-HETE production. We conclude that cytochrome P-450 omega-hydroxylase activity makes an important contribution to cerebral vasoconstriction associated with the onset of ventilation at birth.

[Postoperative epidural hematoma remote from the site of craniotomy for STA-MCA anastomosis].

We experienced a case in which the cause of acute brain swelling following resection of dura matter could not be recognized until the postoperative CT scan. A 30-year-old woman presented with a 4-year history of Moyamoya disease. Right hemiplegia developed a month before operation, so that the anti-platelet therapy was continued. At the end of dural resection the brain started to bulge and the brain swelling increased progressively. The patient was immediately placed on a head up position and received a rapid administration of mannitol for the treatment. The operator performed the echo examination for clarifying the cause of the brain swelling, but they could not find it. As the brain swelling slightly improved by the treatment, the surgery was performed continuously At the end of the operation the patient was moved for a CT scan and it showed mass effect caused by epidural hematoma over the left temporal region distant from the site of craniotomy. Evacuation of the hematoma was carried out urgently. At discharge, she was conscious and had no focal neurological deficits. The occurrence of the epidural hematoma is one of the reasons for unknown brain swelling during surgery. We strongly recommend that any sudden deterioration during the operation should be treated with emergency CT scan.

[Use of high-dose dexmedetomidine infusion for anesthesia and sedation in a patient for microlaryngeal surgery maintained with spontaneous breathing].

We experienced the anesthetic management using high-dose dexmedetomidine for microlaryngeal surgery maintaining spontaneous breathing. The anesthesia was maintained with dexmedetomidine infusion (initial dose 6 microg x kg(-1) x hr(-1) over 10 min followed by continuous infusion of 0.5 microg x kg(-1) x hr(-1)), intermittent small doses of fentanyl and topical application of lidocaine on the tongue, pharynx and larynx. The infusion of dexmedetomidine was increased over 30 min to 3 microg x kg(-1) x hr(-1) to reach the adequate sedation level and maintained at this rate for a further 15 min during the operation. During the whole perioperative period, there was no respiratory depression as measured by arterial blood gas analysis that recorded normal PaCO2 in the patient breathing supplemental oxygen. Hypotension (systemic arterial blood pressure less than 100 mmHg) occurred twice during dexmedetomidine administration, but was normolized by ephedrine administration. The preservation of respiratory drive offers the possibility that this anesthetic technique may be another method for providing anesthesia for the patient with a difficult airway. Moreover, there is one consensus on the importance of the basic principle that adequate topical or intravenous anesthesia is also essential during high-dose dexmedetomidine infusion.

Role of nitric oxide in cerebrovascular reactivity to NMDA and hypercapnia during prenatal development in sheep.

Cerebral vasodilatory responses evoked by activation of NMDA receptors and by hypercapnia are important factors in the integrated vascular response to perinatal cerebral ischemia. Cerebral vasodilation to NMDA is mediated by nitric oxide in adult and newborn animals, whereas vasodilation to hypercapnia is thought to become modulated by nitric oxide, at least in swine, after the newborn period. The developmental role of nitric oxide in the cerebral blood flow response to NMDA and hypercapnia was investigated at mid- and late gestation in fetal sheep. Superfusion of 300microM NMDA over the cerebral cortex through a closed cranial window on the exteriorized head of an anesthetized fetus increased laser-Doppler flow by 41+/-7% (+/-S.E.) at 0.65 gestation. The increase was reduced by superfusion of a nitric oxide synthase inhibitor (18+/-8%). At 0.9 gestation, the response to NMDA was augmented (85+/-24%) compared to that at 0.65 gestation and was reduced by a nitric oxide synthase inhibitor (32+/-6%). In unanesthetized fetal sheep, hypercapnic reactivity of microsphere-determined cerebral blood flow was not significantly attenuated by nitric oxide synthase inhibition at 0.65 gestation (4.6+/-0.7 to 3.7+/-1.0% change/mmHg pCO2) or at 0.9 gestation (4.0+/-0.7 to 3.5+/-0.9% change/mmHg pCO2). Therefore, nitric oxide-dependent cerebrovascular dilation to NMDA-receptor activation is present as early as 0.65 gestation in fetal sheep and increases further during the last trimester, whereas vasodilation to hypercapnia remains unchanged and independent of nitric oxide during the last trimester. Hence, cerebrovascular reactivities to different stimuli do not mature concurrently.

Effects of dexmedetomidine on cerebral circulation and systemic hemodynamics after cardiopulmonary resuscitation in dogs.

PURPOSE: Our purpose was to examine the effect of dexmedetomidine, when used with phenylephrine during cardiopulmonary resuscitation (CPR), on the cerebral and systemic circulations. METHODS: In pentobarbital-anesthetized, mechanically ventilated dogs, we evaluated pial vessel diameters, cerebral oxygen extraction, and systemic hemodynamics before and after cardiac arrest (5 min) and resuscitation, in the presence or absence of dexmedetomidine (n = 7 each; dexmedetomidine or control group). RESULTS: In both groups: (a) pial arterioles were dilated at 5 and 15 min after CPR, and had returned to baseline diameters at 30 min; (b) sagittal sinus pressure was significantly raised at 5 and 15 min after CPR; and (c) cerebral oxygen extraction was decreased at 5, 15, and 30 min after CPR, and had returned to baseline level at 60 min after CPR. We could find no differences between the two groups in the cerebral circulation after CPR. However, the number of defibrillation electric shocks required to restore spontaneous circulation (5.5 vs 3.6; P < 0.05), the dose of phenylephrine used for CPR (1193 microg vs 409 microg; P < 0.01), and the number of postresuscitation ventricular ectopic beats observed during the first 120 min after successful resuscitation (1606 vs 348; P < 0.05) were all significantly lower in the dexmedetomidine group. CONCLUSION: Although intravenous dexmedetomidine, as used for CPR, does not have a beneficial effect on either cerebral vessels or cerebral oxygen extraction, it may reduce the number of defibrillation shocks needed and the number of postresuscitation ventricular ectopic beats, and help to bring about stable systemic circulation after CPR.

Contribution of adenosine A2A and A2B receptors and heme oxygenase to AMPA-induced dilation of pial arterioles in rats.

Nitric oxide (NO) has been implicated in mediation of cerebral vasodilation during neuronal activation and, specifically, in pharmacological activation of N-methyl-d-aspartate (NMDA) and kainate receptors. Possible mediators of cerebral vasodilation to alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) have not been well studied in mature brain, although heme oxygenase (HO) activity has been implicated in newborn pigs. In anesthetized rats, 5 min of topical superfusion of 30 and 100 microM AMPA on the cortical surface through a closed cranial window resulted in increases in pial arteriolar diameter. The dilatory response to AMPA was not inhibited by superfusion of an NO synthase inhibitor, a cyclooxygenase-2 inhibitor, or a cytochrome P-450 epoxygenase inhibitor, all of which have been shown to inhibit the cortical blood flow response to sensory activation. However, the 48 +/- 13% dilation to 100 microM AMPA was attenuated 56-71% by superfusion of the adenosine A(2A) receptor antagonist ZM-241385, the A(2B) receptor antagonist alloxazine, and the HO inhibitor chromium mesoporphyrin. Combination of the latter three inhibitors did not attenuate the dilator response more than the individual inhibitors, whereas an AMPA receptor antagonist fully blocked the vasodilation to AMPA. These results indicate that cortical pial arteriolar dilation to AMPA does not require activation of NO synthase, cyclooxygenase-2, or cytochrome P-450 epoxygenase but does depend on activation of adenosine A(2A) and A(2B) receptors. In addition, CO derived from HO appears to play a role in the vascular response to AMPA receptor activation in mature brain by a mechanism that is not additive with that of adenosine receptor activation.

[Bilateral recurrent laryngeal nerve paralysis in a child following a neurosurgical operation].

We experienced a case of 7-year-old boy who developed bilateral recurrent laryngeal nerve paralysis following an elective neurosurgical operation under oxygen-nitrous oxide-isoflurane anesthesia. He underwent a removal of brain tumor in the supratentorial region on supine position. After the removal of the endotracheal tube in the intensive care unit, he developed marked respiratory effort and inspiratory stridor. A diagnosis of bilateral recurrent laryngeal nerve paralysis was made by a direct diagnostic laryngoscopy. The patient needed continuous care for his airway patency with tracheotomy tube in place, and his normal vocal cord mobility recovered on the 23 rd postoperative day. Common cause of recurrent nerve injury following general anesthesia is either the procedure of endotracheal intubation itself or trauma due to surgical manipulation. In the present case, an endotracheal tube, a transesophageal stethoscope and a nasogastric tube inserted into the narrow laryngeal space might have been a cause of this complication. Moreover, accidental extreme flexion of his neck which occurred during the surgery might also be an additional cause. This case suggests that recurrent laryngeal nerve paralysis due to anesthetic instruments around the larynx is a possible cause of complications during general anesthesia in pediatric patients.

[Overdose of vecuronium during general anesthesia to an infant].

We experienced an accidental case in which 5 mg of vecuronium was administered to a 5 kg infant boy, aged 2 months, incrementally for 55 minutes during general anesthesia. He received general anesthesia at the hospital where there is no anesthesiologist. After surgery the surgeon felt an unusual situation during emergence period from general anesthesia and then noticed overdose of vecuronium. They got in touch with our department immediately and requested us to follow him up. When we reached at the bedside, we could not observe voluntary movement by him. By using neuromuscular monitoring, we could determine that a paralysis was still maintained. After a while, he started to move and breathe himself. Extubation was performed safely 4 and half hours after the final administration of vecuronium. Finally, he could recover with no adverse effect. To predict the optimal dose of a non-depolarizing muscle relaxant to a pediatric patient, routine monitoring of neuromuscular block is effective and essential.

Automated cardiac output measurement by transesophageal color Doppler echocardiography.

UNLABELLED: Automated cardiac output measurement (ACOM), which integrates digital color Doppler velocities in space and in time, has been validated using transthoracic echocardiography but has not been tested using transesophageal echocardiography (TEE). Therefore, we determined the feasibility of the ACOM method by TEE in 36 patients undergoing cardiovascular surgery. Regions of interest for ACOM were placed within a color sector across the main pulmonary artery (PA), the mitral annulus, and the left ventricular outflow tract. Cardiac output was determined from the PA flow, the mitral flow, and the left ventricular ejection flow at each view using the ACOM method. We compared measurements of cardiac output derived from the ACOM method with measurements simultaneously obtained by thermodilution (TD). In the mitral flow analysis, the values derived from ACOM correlated well with those from TD (R(2) = 0.85; mean difference = 0.01 +/- 0.58 L/min in the 2-chamber view; R(2) = 0.78; mean difference = -0.10 +/- 0.68 L/min in the 4-chamber view). In the PA flow analysis, the values derived from ACOM did not correlate with those from TD (R(2) = 0.30). In the left ventricular outflow tract analysis, it was very difficult to obtain the optimal view (44%) in which color Doppler flow signals adequately appeared. Using the ACOM method, we obtained good correlation and agreement for cardiac output measurements in the mitral flow analysis compared with TD. The ACOM method is a practical and rapid method to measure cardiac output by TEE analysis of mitral flow. IMPLICATIONS: Automated cardiac output measurement by transesophageal color Doppler echocardiography is a practical and rapid method to measure cardiac output. This technique is a promising new approach to echocardiographic quantification in the intraoperative setting.

Hypothermia attenuates the vasodilator effects of dexmedetomidine on pial vessels in rabbits in vivo.

UNLABELLED: Studies have indicated that mild to moderate hypothermia or dexmedetomidine may have neuroprotective properties in animal models. In this study, we investigated the effects of hypothermia on dexmedetomidine-induced responses in cerebral vessels in anesthetized rabbits by using the cranial-window preparation. After instrumentation under pentobarbital anesthesia, 12 rabbits were assigned to 1 of 2 equal groups: normothermic (nasopharyngeal and intrawindow temperature, 38.5 degrees C-39.5 degrees C) or hypothermic (33.0 degrees C-34.0 degrees C). Each rabbit received three different concentrations (10(-7), 10(-5), and 10(-3) M) of dexmedetomidine under the window, and cerebral pial vessel diameters were measured in a sequential manner. In the normothermic group, dexmedetomidine induced a significant concentration-dependent dilation in both large and small arterioles. In the hypothermia group, dexmedetomidine produced a U-shaped dose-response in both large and small cerebral arterioles (concentration-related vasoconstriction at 10(-7) and 10(-5) M, but vasodilation at 10(-3) M). In cerebral venules, a similar pattern of results was obtained, but changes were generally smaller than in arterioles. In conclusion, topically applied dexmedetomidine induces concentration-dependent dilation in cerebral arterioles in normothermic rabbits anesthetized with pentobarbital, but mild to moderate hypothermia attenuates these responses, with smaller dexmedetomidine concentrations causing vasoconstriction. IMPLICATIONS: In normothermic rabbits anesthetized with pentobarbital, topically applied dexmedetomidine induces a concentration-dependent dilation in both large and small cerebral arterioles, but mild to moderate hypothermia attenuates these responses.