Hiroshi Endoh

Headache after attempted epidural block: the role of intrathecal air.

Background Postmeningeal puncture headache (PMPH) is typically attributed to the loss of cerebrospinal fluid (CSF). However, when it occurs after an attempted epidural puncture, it may be due to either CSF loss or, potentially, to the subarachnoid injection of air used as a part of “loss‐of‐resistance” testing. This study was performed to examine the relation between intrathecal air and PMPH. Methods Using a loss‐of‐resistance test with an air‐filled (n = 1,812; air group) or saline‐filled (n = 1,918; saline group) syringe, epidural block was performed in patients with acute or chronic pain. The dura was judged to be perforated not only when backflow of CSF was recognized in the needle but also when signs and symptoms solely attributable to meningeal perforation were seen, such as high spinal blockade or severe motor blockade. The incidence, onset time, and duration of PMPH in the air and saline groups were compared. In all patients with signs of meningeal perforation, brain computed tomography was examined. Results The incidence of PMPH in the air group (32 cases) was significantly higher than that in the saline group (5 cases), although the occurrences of meningeal perforation between the air (48 cases) and saline (51 cases) groups did not differ significantly. Intrathecal air bubbles were detected on brain computed tomography in both the deep supraspinal structures such as the ventricles, Silvian fissures and cisterns, and the superficial subarachnoid space in 30 of 32 patients with PMPH in the air group, whereas no intrathecal air bubbles were seen in the saline group. PMPH was significantly more rapid in onset and shorter in duration in the air group than that in the saline group. Conclusions The use of air for loss‐of‐resistance testing during epidural block was associated with a higher incidence of PMPH, which might be attributable to subarachnoid air injection and CSF leakage.

Management of intractable pain with percutaneous epidural spinal cord stimulation : differences in pain-relieving effects among diseases and sites of pain

This study is a survey of the overall clinical results achieved with our pain treatment method, percutaneous epidural low-frequency (1.6-8.0 Hz) spinal cord stimulation. It examines the relationship between the effectiveness of epidural spinal cord stimulation (ESCS) and diseases or sites of pain. Continuous indwelling of the catheter electrodes in the posterior epidural space ranged from 3 to 67 days, and the duration of percutaneous ESCS varied from less than 1 wk to more than 1 yr. Complete pain relief (100%) was achieved during stimulation in 11.5% of the patients (52 of 454). Complete (100%) to partial (more than 30%) pain relief occurred in 71.1% of the patients. In six (1.3%) patients pain was aggravated by stimulation. Analgesics and/or sedatives were discontinued completely after treatment in 52 patients (11.5%) and reduced in 263 patients (57.9%). The number of patients who rated pain relief better than 50% was significantly more in carcinoma/sarcoma and causalgia (P < 0.001), and significantly less in postherpetic neuralgia and thromboangitis obliterans/arterial sclerosis obliterans (P < 0.001) than the average in all diseases. There was a significantly high responsiveness to ESCS in female patients in comparison to male patients (P < 0.05). Pain in the head/face, neck/upper extremities, and trunk responded more to ESCS than pain in the lower extremities. Alleviation of pain by ESCS was lower when the verbal pain score was high. There were no major complications in percutaneous ESCS. Thus, we have demonstrated that pain-alleviating effects of ESCS varies significantly by disease and site of pain, and that this simple percutaneous method can be used for a relatively long period.

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.

Does central venous pressure or pulmonary capillary wedge pressure reflect the status of circulating blood volume in patients after extended transthoracic esophagectomy

PurposeWe investigated whether central venous pressure (CVP) or pulmonary capillary wedge pressure (PCWP) can accurately reflect the status of circulating blood volume (CBV) during the perioperative period in adult patients after extended transthoracic esophagectomy.MethodsIn 16 adult patients undergoing esophagectomy, simultaneous measurements of CVP, PCWP, and CBV were made at the following seven points: baseline (before surgery) and at 0, 12, 24, 36, 48, and 60 h after admission to the intensive care unit (ICU). CBV was estimated at the bedside with a pulse-dye densitometry method using indocyanine green. The relationship between CBV and these filling pressures was analyzed by linear regression.ResultsA total of 122 paired observations were made. The mean value of CBV decreased by approximately −20% at admission to the ICU and increased by approximately 24% of baseline at 48 h after surgery. The time course of CVP and PCWP was similar to that of CBV: both decreased at admission to the ICU, then gradually increased, and peaked at 48 h after surgery. However, both pressures remained within normal ranges, and the actual changes from baseline were small. There was no significant relationship between CBV and CVP (r = 0.17, P = 0.07), and between CBV and PCWP (r = 0.03, P = 0.78).ConclusionNeither CVP nor PCWP accurately reflected the status of CBV in adult patients after extended transthoracic esophagectomy.

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 pentobarbital and ketamine on brain injury-induced anti-ischemic activity

Survival rates following incomplete brain ischemia induced during pentobarbital anesthesia were significantly higher in mice with a minor brain injury, inflicted one week before, than in those given a sham operation. Improvement of the survival rates in mice with brain injury, however, became insignificant when brain ischemia was imposed during ketamine anesthesia, suggesting that the actions of certain factors or protective mechanisms against brain ischemia, developed by brain injury, are antagonized by ketamine and/or potentiated by barbiturate anesthesia.

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.