Tadayuki Honda

Beneficial effect of a prone position for patients with hypoxemia after transthoracic esophagectomy.

ObjectiveAlthough the prone position has been reported to improve arterial oxygenation in patients with acute respiratory distress syndrome, there have been no reports on its efficacy in patients with hypoxemia after transthoracic esophagectomy with three-field lymphadenectomy. This study was undertaken to assess the efficacy of the prone position on hypoxemia after three-field lymphadenectomy for thoracic esophageal carcinoma. DesignProspective randomized clinical study. SettingGeneral intensive care unit at a university hospital. Interventions and MeasurementsSixteen patients who underwent three-field lymphadenectomy and showed hypoxemia (Pao2/Fio2 ratios of <200 under positive end-expiratory pressure of >5 cm H2O) on the fifth postoperative day were randomly assigned to prone (eight patients) and nonprone (eight patients) groups. Prone position for 6 hrs was carried out for four consecutive days. The Pao2/Fio2 ratio, the duration of ventilatory support, and length of stay, were measured. ResultsOxygenation: The Pao2/Fio2 ratio markedly increased by 32% ± 22% in seven of eight patients (p < .05) when the patients were moved from the supine to the prone position. The Pao2/Fio2 ratio after the fourth prone position (238 ± 55, p < .05) was significantly higher than that before the first trial of prone position (166 ± 25) in these seven patients. Duration of ventilatory support and intensive care unit length of stay: Both the ventilation period (11.6 ± 2.2 vs. 14.0 ± 1.6 days, p = .0029) and the length of stay in the intensive care unit (12.8 ± 4.4 vs. 17.2 ± 3.4 days, p = .0032) were significantly shorter in the prone group compared with the nonprone group. The Pao2/Fio2 ratio at the time of cessation of prone positioning was significantly higher than the corresponding value in the nonprone group. ConclusionIn hypoxemic patients after three-field lymphadenectomy, the prone position improved arterial oxygenation without any deleterious effects. The beneficial effect of the prone position is possibly attributable to opening of the bronchi obstructed by secretions.

Clinical and cardiac features of patients with subarachnoid haemorrhage presenting with out-of-hospital cardiac arrest

BACKGROUND Subarachnoid haemorrhage (SAH) is known as one of the aetiologies of out-of-hospital cardiac arrest (OHCA). However, the mechanisms of circulatory collapse in these patients have remained unclear. METHODS AND RESULTS We examined 244 consecutive OHCA patients transferred to our emergency department. Head computed tomography was performed on all patients and revealed the existence of SAH in 14 patients (5.9%, 10 females). Among these, sudden collapse was witnessed in 7 patients (50%). On their initial cardiac rhythm, all 14 patients showed asystole or pulseless electrical activity, but no ventricular fibrillation (VF). Return of spontaneous circulation (ROSC) was obtained in 10 of the 14 patients (14.9% of all ROSC patients) although all resuscitated patients died later. The ROSC rate in patients with SAH (71%) was significantly higher than that of patients with either other types of intracranial haemorrhage (25%, n=2/8) or presumed cardiovascular aetiologies (22%, n=23/101) (p<0.01). On electrocardiograms, ST-T abnormalities and/or QT prolongation were found in all 10 resuscitated patients. Despite their electrocardiographic abnormalities, only 3 patients showed echocardiographic abnormalities. CONCLUSIONS The frequency of SAH in patients with all causes of OHCA was about 6%, and in resuscitated patients was about 15%. The initial cardiac rhythm revealed no VF even though half had a witnessed arrest. A high ROSC rate was observed in patients with SAH, although none survived to hospital discharge.

The Influence of Nicardipine-, Nitroglycerin-, and Prostaglandin E 1 -Induced Hypotension on Cerebral Pressure Autoregulation in Adult Patients During Propofol-Fentanyl Anesthesia

UNLABELLED We investigated the influence of drug-induced hypotension at a mean arterial pressure (MAP) of 60-70 mm Hg on cerebral pressure autoregulation in 45 adult patients during propofol-fentanyl anesthesia. Time-averaged mean blood flow velocity in the right middle cerebral artery (Vmca) was continuously measured at a PaCO(2) of 39-40 mm Hg by using transcranial Doppler ultrasonography. Hypotension was induced and maintained with a continuous infusion of nicardipine, nitroglycerin, or prostaglandin E(1). Cerebral autoregulation was tested by a slow continuous infusion of phenylephrine to induce an increase in MAP of 20-30 mm Hg. From the simultaneously recorded data of Vmca and MAP, cerebral vascular resistance (CVR) was calculated as MAP/Vmca. Furthermore, the index of autoregulation (IOR) was calculated as DeltaCVR/DeltaMAP, where DeltaCVR = change in CVR and DeltaMAP = change in MAP. The test was performed twice for each condition on each patient: baseline and hypotension. The IOR during baseline was similar among the groups. During nitroglycerin- and prostaglandin E(1)-induced hypotension, IOR was not different from baseline. In contrast, during nicardipine-induced hypotension, IOR significantly decreased compared with baseline (0.37 +/- 0.08 versus 0.83 +/- 0.07, P < 0.01). In conclusion, nicardipine, but not nitroglycerin or prostaglandin E(1), significantly attenuates cerebral pressure autoregulation during propofol-fentanyl anesthesia. IMPLICATIONS Vasodilators may influence cerebral autoregulation by changing cerebral vascular tone. Nicardipine, but not nitroglycerin or prostaglandin E(1), attenuated cerebral pressure autoregulation in normal adult patients during propofol-fentanyl anesthesia.

Cerebral air embolism complicating percutaneous thin-needle biopsy of the lung: complete neurological recovery after hyperbaric oxygen therapy

Percutaneous thin-needle biopsy of the lung is a wellestablished method for obtaining pulmonary tissue for histological examination because of its minimal invasiveness and excellent diagnostic accuracy [1,2]. It is generally safe, but some complications have been recognized. The most frequent complication is pneumothorax [3]. Systemic arterial air embolism is a very rare but sometimes fatal complication. Here we report a case of cerebral air embolism after percutaneous thin-needle biopsy in a patient who showed complete neurological recovery after hyperbaric oxygen therapy.

Effects of nicardipine-, nitroglycerin-, and prostaglandin E1-induced hypotension on human cerebrovascular carbon dioxide reactivity during propofol-fentanyl anesthesia

STUDY OBJECTIVE To investigate the effects of nicardipine-, nitroglycerin-, and prostaglandine E1-induced hypotension on cerebrovascular carbon dioxide (CO2) reactivity over a wide range of arterial CO2 tension (PaCO2) (PaCO2; range 25 to 50 mmHg). DESIGN Prospective, randomized study. SETTING Operating room of a university-affiliated hospital. PATIENTS 36 ASA physical status I and II patients without cerebrovascular disease, hypertension, or diabetes mellitus, undergoing an elective abdominal surgery. INTERVENTIONS Patients were randomly allocated to one of three groups (nicardipine-, nitroglycerin-, or prostaglandin E1-induced hypotension group; 12 in each group). Anesthesia was induced and maintained with a bolus dose, followed by a continuous infusion of propofol (6.7 +/- 1.5 mg/kg/hr) and fentanyl (1.68 +/- 0.4 micrograms/kg/hr). Deliberate hypotension of mean arterial pressure 55 to 60 mmHg was induced and maintained with a bolus dose, followed by a continuous infusion of nicardipine (6.80 +/- 0.75 micrograms/kg/min), nitroglycerin (3.20 +/- 1.10 micrograms/kg/min), or prostaglandin E1 (0.103 +/- 0.052 microgram/kg/min). MEASUREMENTS AND MAIN RESULTS Time-averaged mean red blood cell velocity in the right middle cerebral artery (Vmca) at PaCO2 ranging from 25 to 50 mmHg was measured with transcranial Doppler ultrasonography. A minimum of six simultaneous measurements of Vmca and PaCO2 were obtained during baseline and deliberate hypotension in each patient. Absolute slope between Vmca and PaCO2 during baseline and deliberate hypotension was determined individually by linear regression analysis. Absolute slope was treated as the variable, because it yielded a significant close correlation coefficient (r > 0.95; p < 0.05). Comparisons between baseline and deliberate hypotension were made by analysis of variance for repeated measures. Mean absolute slope was significantly reduced from 1.88 +/- 0.57 cm/sec/mmHg (mean +/- SD) to 1.21 +/- 0.46 in the nicardipine group (p < 0.05), from 1.75 +/- 0.69 to 1.35 +/- 0.47 in the nitroglycerin group (p < 0.05), and from 1.95 +/- 0.89 to 1.33 +/- 0.70 (p < 0.05) in the prostaglandin E1 group, respectively. CONCLUSION Nicardipine-, nitroglycerin-, and prostaglandin E1-induced hypotension attenuate the human cerebrovascular CO2 reactivity during propofol-fentanyl anesthesia.

The effects of nicardipine on dynamic cerebral autoregulation in patients anesthetized with propofol and fentanyl.

UNLABELLED We investigated the effects of nicardipine on dynamic cerebral pressure autoregulation in 13 normal adult patients undergoing gynecologic or orthopedic surgery. Anesthesia was induced and maintained with propofol and fentanyl. Hypotension to a mean arterial pressure of 60-65 mm Hg was induced and maintained with a continuous infusion of nicardipine. Time-averaged mean blood flow velocity in the right middle cerebral artery was measured continuously by using transcranial Doppler ultrasonography. The cerebral autoregulatory responses were activated by releasing thigh cuffs. The actual blood flow velocity in the right middle cerebral artery response to acute change in mean arterial pressure was fitted to 1 of 10 computer-generated curves to determine the dynamic rate of cerebral autoregulation (dRoR), and the best fitting curve was used. The autoregulation test was repeated until two values of dRoR were obtained at baseline and during induced hypotension. Nicardipine significantly reduced dRoR values of 13.1% +/- 3.6%/s at baseline to 8.3% +/- 2.6%/s during hypotension (P: < 0.01). During deliberate hypotension induced by nicardipine, the cerebral dynamic autoregulatory response is impaired in normal adult patients. IMPLICATIONS During deliberate hypotension induced by nicardipine, the cerebral dynamic autoregulatory response is impaired in normal adult patients.

Naloxone improves arterial blood pressure and hypoxic ventilatory depression, but not survival, of rats during acute hypoxia.

ObjectiveTo investigate the effects of naloxone and morphine during acute hypoxia. DesignProspective, randomized animal study. SettingUniversity laboratory. SubjectsTwenty-eight adult male Sprague Dawley rats, weighing 300–350 g. InterventionsThe rats were implanted with a femoral catheter and subcutaneous electrodes for electrocardiogram recording and were randomly assigned to receive morphine (5 mg/kg), naloxone (5 mg and 10 mg/kg), or normal saline (control) (n = 7 in each). Fifteen minutes after intraperitoneal injection of the drug, each rat was exposed to hypoxic gas (5% oxygen, 95% N2) for 70 mins. Hypoxic survival time was measured. Mean arterial pressure (MAP), arterial pH, Paco2, Pao2, and base excess were measured before injection (baseline), 14 mins after injection (H0), and 6 mins (H1), 33 mins (H2), and 48 mins (H3) after exposure to hypoxia. Measurements and Main Results Hypoxic survival was similar between the naloxone 5 mg/kg and control groups (p = .183), significantly lower in the naloxone 10 mg/kg group (p < .01), and significantly higher in the morphine 5 mg/kg group (p < .05) compared with controls. MAP significantly decreased in all groups. However, at H2–H3, MAP was better preserved in both naloxone groups and was lower in the morphine group compared with controls. Paco2 was maintained higher at H0–H3 in the morphine group and lower at H2–H3 in both naloxone groups compared with controls. ConclusionDuring acute hypoxia, naloxone preserves arterial blood pressure and attenuates hypoxic ventilatory depression by antagonizing endogenous opiates, but it does not improve hypoxic survival. In contrast, morphine, which enhances the action of endogenous opiates, does improve hypoxic survival. The acute hypoxic tolerance of morphine may be partly attributable to a depression of oxygen consumption, increased cerebral blood flow secondary to high Paco2, and protective actions mediated by &dgr;-opioid receptors.

Aortic aneurysm in a four-year-old child with tuberous sclerosis.

We present a case of aortic aneurysm in a four‐year‐old child complicated with tuberous sclerosis. We used the same general principles as for adult patients and successfully managed our patient. Our methods included the use of isoflurane plus epidural anaesthesia, dopamine to maintain blood pressure, and induced mild hypothermia to reduce brain metabolism and to prevent spinal cord damage during aortic cross‐clamping. Intensive monitoring including EEG was beneficial to the anaesthetic management.

A patient with severe hypercalcemia in multiple organ dysfunction syndrome: Role of elevated circulating 1α,25(OH)2vitamin D levels

A 54‐year‐old man was transferred to our ICU because of systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS). He died after 38 days of intensive care. During treatment, his serum calcium (Ca) levels continued to increase and reached 3.95 mmol/L, while the ionized Ca levels reached 2.30 mmol/L before his death. He presented with severe kidney injury, pancreatitis, and hemorrhagic gastric erosion that worsened his prognosis; these were possibly associated with the hypercalcemia. His circulating 1α,25‐dihydroxyvitamin D [1,25(OH)2D] level was elevated (75.7 to 204 pg/mL), whereas the levels of 25‐hydroxyvitamin D, parathyroid hormone, and parathyroid hormone–related peptide were not. Liver histology revealed immunoreactivity for 25‐hydroxyvitamin D 1α‐hydroxylase (CYP27B1) in some of the hepatocytes, in which the localization pattern was similar to that of lysozyme‐positive hepatocytes. Our ICU has previously encountered 22 similar MODS patients who presented with hypercalcemia over the last 8 years. SIRS with severe kidney and liver injuries are common clinical findings in hypercalcemic patients with MODS. Of the 23 hypercalcemic MODS patients, including the present patient, 17 had circulating 1,25(OH)2D levels exceeding 70 pg/mL despite severe kidney injury. Extrarenal activation of CYP27B1 seems to play a role in the development of hypercalcemia in this disease condition. Clinicians need to be aware that severe hypercalcemia may occur in MODS patients.

Prior mechanical injury inhibits rise in intracellular Ca2+ concentration by oxygen-glucose deprivation in mouse hippocampal slices

Prior mechanical brain microinjury has been found to have a preventive effect on brain ischemia. To investigate the mechanism responsible for this, the effect of mechanical brain injury on changes in intracellular free Ca2+ concentration ([Ca2+]i) in response to ischemic insult was studied in mouse hippocampal slices. The mechanical injury was made by inserting a 25G hypodermic needle into the CA1 region of the hippocampus in mice anesthetized with pentobarbital. Sagittal slices of the hippocampus were prepared two hours, and 1, 3, 7, and 14 days after the brain injury. Changes in [Ca2+]i in the slices by oxygen-glucose deprivation were analyzed from fluorescence images, using fura-2. Increases in [Ca2+]i induced by oxygen-glucose deprivation were inhibited in the vicinity of the injury 1 and 3 days after injury. [Ca2+]i levels were lower in the posterior side from the injury than in the anterior side 1 and 3 days after injury. No significant regional differences in [Ca2+]i responses were found 2 h or 7 and 14 days after the injury. Membrane potential and membrane resistance of CA1 neurons in the vicinity of the injury measured 1 day after the injury were not significantly altered in comparison with non-injured slices. These results indicate that mechanical brain injury inhibits ischemic [Ca2+]i increase. This inhibition may be induced not only by damage of the presynaptic fibers projecting to the CA1 neurons but also by the other certain factor(s) that prevent [Ca2+]i increase, and it appears to be related to the protective effect of prior mechanical injury against ischemic neuronal damage.