Case of postoperative increased anesthesia level with spinal anesthesia

A patient, 35 weeks and 2 days gestation with twins, was scheduled for cesarean section. Spinal anesthesia was induced with the patient in lateral decubitus position using 2.2 ml hyperbaric bupivacaine 0.5% at the L3-4 interspace. The patient was placed immediately in supine position. After 5 min, sensory block level was confirmed T5. Operation was performed with no complications. Patient left the operating room 60 min after the induction. In the ward, the patient complained of respiratory distress and inability to move hands. Sensory block level reached C4 2 hours after spinal anesthesia induction. Four hours after induction, patient's sensory and motor paralysis recovered completely. In our operating room, patient enters and leaves with moving slide hatch machine. So patient's body moves to right and left side. We think that the increased anesthesia level was caused by this rolling of the body. We must be cautious about the increased anesthesia level when spinal anesthesia is induced.     

The effect of cyclooxygenase-2 inhibition on analgesia and spinal fusion

BACKGROUND: Cyclooxygenase (COX)-2-specific inhibitors demonstrate analgesic efficacy comparable with that of conventional nonsteroidal anti-inflammatory drugs but are associated with reduced gastrointestinal side effects and an absence of antiplatelet activity. Thus, they can be administered to patients undergoing spinal fusion surgery without an added risk of bleeding. However, concerns regarding a possible deleterious effect on bone-healing have limited their routine use. Celecoxib, a COX-2 inhibitor, recently was approved for the treatment of acute pain. The goals of the present study were to examine the analgesic efficacy of celecoxib and to determine the incidence of nonunion at one year following spinal fusion surgery. METHODS: Eighty patients who were scheduled to undergo spinal fusion received either celecoxib or placebo one hour before the induction of anesthesia and every twelve hours after surgery for the first five postoperative days. Pain scores and morphine use were recorded one hour after arrival in the post-anesthesia care unit and at four, eight, twelve, sixteen, twenty, and twenty-four hours later. Intraoperative blood loss was recorded. The status of the fusion was determined radiographically at the time of the one-year follow-up. RESULTS: There were no differences in demographic data or blood loss between the two groups. Pain scores were lower in the celecoxib group at one, four, eight, sixteen, and twenty hours postoperatively. There were no differences between the two groups with regard to the pain scores at twelve and twenty-four hours postoperatively. Morphine use was lower in the celecoxib group at all postoperative time-intervals. There was no difference between the celecoxib group and the placebo group with regard to the incidence of nonunion at the time of the one-year follow-up (7.5% [three of forty] compared with 10% [four of forty]). CONCLUSIONS: The perioperative administration of celecoxib resulted in a significant reduction in postoperative pain and opioid use following spinal fusion surgery. In addition, the short-term administration of this COX-2-specific non-steroidal anti-inflammatory drug had no apparent effect on the rate of nonunion at the time of the one-year follow-up.     

Ventilatory responses to hypercapnia during tetracaine spinal anesthesia

The effect of spinal anesthesia with hyperbaric tetracaine with epinephrine on resting ventilation and on ventilatory responsiveness to CO2 rebreathing was studied in 10 unpremedicated patients. Resting end-tidal PCO2 (PETCO2) decreased from 37 +/- 3 mmHg (mean +/- SD) to 34 +/- 2 mmHg after induction of spinal anesthesia (p less than 0.05). Minute ventilation (VE) and occlusion pressure (P0.1) at PETCO2 = 55 mmHg increased during spinal anesthesia from 32.0 +/- 12.9 to 40.2 +/- 17.0 l/min and from 5.0 +/- 1.8 to 8.6 +/- 4.7 cmH2O, respectively. The magnitude of the increase in VE during spinal anesthesia correlated inversely with age. Spinal anesthesia was not associated with significant changes in vital capacity, maximal inspiratory pressure, or the slopes of the lines relating VE or P0.1 to PCO2. These results show increased ventilatory responsiveness to CO2 (a parallel leftward shift of the CO2 response curve) with tetracaine spinal anesthesia.     

Histologic characterization of acute spinal cord injury treated with intravenous methylprednisolone

OBJECTIVE: Many substances have been investigated for attenuation of spinal cord injury after acute trauma; however, pharmacologically only steroid administration has shown clinical benefits. This study attempts to characterize local spinal cord histologic response to human dose equivalent (HDE) intravenous methylprednisolone (MP) administration in a rodent model of acute spinal cord injury. DESIGN: Forty-eight Sprague-Dawley rats were divided equally into control and experimental groups. Each group was subdivided into eight sets of three animals each, according to postinjury intervals. Paraplegia after lower thoracic laminectomy was achieved using a standardized weight drop technique. INTERVENTION: Within one hour, experimental animals were treated with HDE MP followed by 23-hour continuous infusion of HDE MP. Spinal cords were harvested at variable intervals postinjury and prepared for histologic/immunohistochemistry examination. MAIN OUTCOME MEASUREMENTS: Edema, necrosis, and glial fibrillary acidic protein (GFAP) positivity in the specimens from treated/control groups were graded by microscopy and immunohistochemistry staining and compared in a blinded manner by a qualified neuropathologist and senior authors. RESULTS: Minimal differences were observed between control and MP-treated animals at zero and four hours. At eight hours, increased white matter and medullary edema was evident in control versus MP-treated rats. This trend continued through twelve, sixteen, twenty-four, forty-eight, and seventy-two hours. No difference was observed in the astrocytic response to injury by GFAP immunohistochemistry between the groups. CONCLUSIONS: Histologically, MP reduces the development of severe edema and preserves spinal cord architecture adjacent to the site of injury. In contrast, MP does not alter the development of spinal cord necrosis or astrocytic response at the zone of injury.     

Respiratory effects of spinal anaesthesia for Caesarean section

We report the changes observed in a number of pulmonary function tests performed on 36 patients undergoing Caesarean section under spinal anaesthesia. The tests comprised peak expiratory flow, forced expiratory volume in one second, forced vital capacity, forced expiratory volume in one second to forced vital capacity ratio and the maximal mid-expiratory flow. Significant changes occurred that are consistent with a restrictive ventilatory defect. These changes persisted for four hours after the induction of spinal anaesthesia. Administration of 35% oxygen by facemask failed to change significantly fetal umbilical vein pH or partial pressure of oxygen.     

Transient neurological syndrome after spinal hyperbaric bupivacaine: a new case

A 47-year-old woman underwent hysteroscopy and removal of an endometrial polyp because of irregular, acyclic bleeding of 6 months' duration. The procedure was carried out under spinal anesthesia. No adverse events occurred during puncture or surgery, or in the immediate postoperative recovery period. Recovery from the sensory and motor block was normal. Twenty-four hours after surgery gluteal and lower limb pain and paresthesia developed, with no sensory or motor deficit. The symptoms suggested transient neurological syndrome. This syndrome has been defined by pain in the lower limbs, buttocks, thighs and calves after uncomplicated spinal anesthesia and full recovery from the sensorimotor block during the immediate postoperative period (first 24 hours). The condition is self-limiting and does not leave permanent neurological sequelae. Recent studies have demonstrated biochemical and anatomical changes that provide a structural basis for this clinical entity. According to this literature, transient neurological syndrome might be a mild expression of local anesthetic toxicity. Recent findings show that the initial injury to the nerve cell membrane, induced by high concentrations of local anesthetic could lead to permanent neuronal damage.     

Respiratory effects of spinal anesthesia: resting ventilation and single-breath CO2 response

The effects of spinal anesthesia with bupivacaine or lidocaine on resting pulmonary ventilation and on the response to the single-breath carbon dioxide test were studied in 11 unpremedicated patients. Resting end-tidal PCO2 decreased from 34.8 +/- 4.5 (mean +/- SD) to 31.6 +/- 4.6 mm Hg after induction of spinal anesthesia (P = 0.002). The decrease in end-tidal PCO2 correlated negatively with patient age (r = -0.67, P = 0.02) and positively with spinal analgesic level (r = 0.58, P = 0.06). Breath-to-breath variability of ventilation increased during spinal anesthesia. Spinal anesthesia was not associated with statistically significant changes in tidal volume, respiratory rate, minute ventilation, mean inspiratory flow rate, inspiratory duty cycle duration, or the response to the single-breath CO2 test.     

Systemic and regional blood-flow changes during spinal anesthesia in the rhesus monkey.

The radioactive microsphere technique was used to determine the distribution of cardiac output and regional blood flow in rhesus monkeys before and 10,20,40, and 80 minutes after induction of spinal anesthesia. Five monkeys were studied during low spinal anesthesia (sensory level T10) and five other monkeys were studied during high spinal anesthesia (sensory level T1). Each monkey served as its own control. There was no significant change in regional blood flow during T10 spinal anesthesia. During T1 spinal anesthesia, blood flow (per 100 g of tissue) to kidneys was significantly reduced at 20, 40, and 80 minutes, blood flows to liver and carcass were significantly reduced at 20 and 40 minutes and blood flows to miscellaneous organs (lymph nodes, salivary glands, etc.) were significantly reduced throughout anesthesia. Blood flows to heart, brain, and lower extremity during T1 spinal anesthesia showed only non-significant changes. Vascular resistance in the lower extremity was significantly reduced during both levels of spinal anesthesia, indicating arteriolar dilatation. Also, during both levels of anesthesia, the lungs received an increased proportion of the radioactive microspheres, suggesting increased peripheral arteriovenous shunting of microspheres due to the arteriolar dilatation.     

Ventilatory responses to hypercapnia during bupivacaine spinal anesthesia

The effect of spinal anesthesia with isobaric 0.5% bupivacaine on ventilatory responsiveness to CO2 rebreathing was studied in ten unpremedicated patients. Minute ventilation (VE) at end-tidal PCO2 = 55 mm Hg increased from 18.7 +/- 6.7 L/min (mean +/- SD) to 22.3 +/- 10.1 L/min after induction of spinal anesthesia (P less than 0.05). Occlusion pressure (P0.1) at PCO2 = 55 mm Hg also increased, from 3.8 +/- 1.5 to 5.0 +/- 1.7 cm H2O (P less than 0.05). Spinal anesthesia was not associated with significant changes in vital capacity, maximal inspiratory pressure, resting end-tidal PCO2, or the slopes or intercepts of the lines relating VE or P0.1 to PCO2. These results show an increased ventilatory responsiveness to CO2 with bupivacaine spinal anesthesia.     

10000例氯普鲁卡因腰麻或腰-硬联合麻醉经验

目的：探讨国产氯普鲁卡因膜麻或腰-硬联合麻醉的效果和安全性。方法：回顾分析10000例下腹部以下手术患者按产科、妇科．营外科．骨科和泌尿外科分为五组,均采用西产氯普鲁卡西冻干粉用生理盐水稀释成2．5％或3％溶液用于膜麻或腰-硬联合麻醉（L2-3）。监测患者BP、HR、SpO2,观察麻醉起效与消失过程。以及下胶运动阻滞程度与麻醉并发症。结果：腰麻平均起效和平面固定时间五组相似,分别为24s和7.7min,最高阴滞平面平均为T5（C1-T10）。取得下肢运动阻滞3级者五组均超过94%。腰麻效果满意率平均99.8%,硬膜外辅助后麻醉满意率提升到99.9%,单次腰麻完全消失平均72min,其中产科组长于其他组（P〈0.05）。腰麻后所有患者BP都下降。五组低血压发生率分别为34%,7%,9%,15%和10%。恶性呕吐发生率分别为43%,11%,14%,14%和9%,在产科和妇科分别因腰麻有16例和9例发生呼吸抑制。这些情况经麻黄碱,阿托品和人工辅助通气处理好转,未发生硬膜外用药误入蛛网膜下腔现象,未见明显神经系统并发症和其他不良反应。结论：国产氯普鲁卡因冻干粉溶解后腰麻或腰-硬联合麻醉有效、安全。     

Comparative spinal neurotoxicity of prilocaine and lidocaine

BACKGROUND: Reports of major and minor sequelae following lidocaine spinal anesthesia have generated interest in an alternative short-acting intrathecal agent. Of the available anesthetics suitable for short-duration spinal anesthesia, prilocaine is perhaps the most promising agent. However, data comparing the neurotoxicity of these agents are lacking. Accordingly, the present experiments investigate whether prilocaine and lidocaine differ with respect to sensory impairment and histologic damage when administered intrathecally in the rat. METHODS: Ninety rats were divided into three groups to receive an intrathecal infusion of 2.5% prilocaine in saline, 2.5% lidocaine in saline, or normal saline. The animals were assessed for persistent sensory impairment 4 days after anesthetic administration using the tail-flick test. Three days later, the animals were killed, and specimens of the spinal cord and nerve roots were obtained for histopathologic examination. RESULTS: Prilocaine and lidocaine produced equivalent elevations in tail-flick latency that differed significantly from saline. Histologic injury scores with prilocaine were greater than with lidocaine, but this difference did not reach statistical significance. CONCLUSIONS: The propensity for persistent functional impairment or morphologic damage with intrathecal prilocaine is at least as great as with lidocaine. Although the substitution of prilocaine for lidocaine may reduce the incidence of transient neurologic symptoms, it is unlikely to reduce the risk of actual neural injury. This discrepancy may indicate that transient neurologic symptoms and neurologic deficits after spinal anesthesia are not mediated by the same mechanism.     

Increased functional vulnerability to acute compression injury of a spinal cord segment under barbiturate anesthesia

Posttraumatic changes in polysynaptic reflex activity and axonal long-tract conduction were measured after transient compression of the L-7 spinal cord segment of cats, either made high spinal and unanesthetized or left intact under pentobarbital anesthesia. The severity of acute post-injury changes increased significantly in the anesthetized animals. Partial recovery and stabilization of functional deficits were observed in the spinal cat, but not in the anesthetized one. These findings suggest that, at least in the acute postinjury stage, pentobarbital anesthesia may enhance functional damages after experimental spinal cord compression.     

Heart rate responses to body tilt during spinal anesthesia

To evaluate whether low-pressure baroreceptors located in the right atrium could affect the heart rate (HR) during spinal anesthesia, the authors determined the effects of right atrial pressure changes associated with body tilt on HR in 40 unpremedicated patients. Ten-degree head-up body tilt produced significant increases in HR of 6 +/- 1 and 6 +/- 1 beats/min (mean +/- SE, P less than 0.01) and significant decreases in systolic arterial pressure of 2.8 +/- 0.9 and 6.6 +/- 1.7 mm Hg (P less than 0.01) during low (T-10 +/- 0.2, n = 20) and high (T-4 +/- 0.2, n = 20) analgesic levels of tetracaine spinal anesthesia, respectively. Ten-degree head-down body tilt caused significant decreases in HR without significant changes in systolic arterial pressure during spinal anesthesia. The reflex HR responses to body tilt were similar between low and high levels of spinal anesthesia and were preserved after administration of sedatives. The magnitudes of changes in right atrial pressure associated with body tilt were similar during spinal anesthesia and after sedation. These findings suggest that HR responses to head-up body tilt are mediated mainly by arterial baroreceptors even in the face of decreased venous return during low or high levels of spinal anesthesia and that light sedation does not impair this reflex HR response.     

Ischemic preconditioning reduces neurologic injury in a rat model of spinal cord ischemia.

BACKGROUND: Ischemic preconditioning (IPC) is an endogenous cellular protective mechanism whereby brief, noninjurious periods of ischemia render a tissue more resistant to a subsequent, more prolonged ischemic insult. We hypothesized that IPC of the spinal cord would reduce neurologic injury after experimental aortic occlusion in rats and that this improved neurologic benefit could be induced acutely after a short reperfusion interval separating the IPC and the ischemic insult. METHODS: Forty male Sprague-Dawley rats under general anesthesia were randomly assigned to one of two groups. The IPC group (n = 20) had 3 minutes of aortic occlusion to induce spinal cord ischemia 30 minutes of reperfusion, and 12 minutes of ischemia, whereas the controls (n = 20) had only 12 minutes of ischemia. Neurologic function was evaluated 24 and 48 hours later. Some animals from these groups were perfusion-fixed for hematoxylin and eosin staining of the spinal cord for histologic evaluation. RESULTS: Survival was significantly better at 48 hours in the IPC group. Sensory and motor neurologic function were significantly different between groups at 24 and 48 hours. Histologic evaluation at 48 hours showed severe neurologic damage in rats with poor neurologic test scores. CONCLUSIONS: Ischemic preconditioning reduces neurologic injury and improves survival in a rat model of spinal cord ischemia. The protective benefit of IPC is acutely invoked after a 30-minute reperfusion interval between the preconditioning and the ischemic event.     

Spinocath导管连续蛛网膜下隙阻滞的临床应用

目的 应用Spinocath导管行连续蛛网膜下隙阻滞，观察麻醉效果，血液动力学变化及术后可能的并发症。方法 择期行下腹部及下肢手术病人20例，选L2-3或L3-4间隙行连续蛛网膜下隙阻滞，首量0.5%的重比重布比卡因1-2ml，术中每隔60-90分钟追加0.5-1ml，术后随访72小时。结果 Spinocath导管连续蛛网膜下隙阻滞可以在手术的过程中连续提供满意的镇痛和肌松，对循环和呼吸的影响小。结论 Spinocath导管连续蛛网膜下隙阻滞血液动力学稳定，并发症少，可应用于脐以下部位手术的麻醉。     

The effects of lactated Ringer's solution infusion on cardiac output changes after spinal anesthesia

We evaluated the effects of an infusion of lactated Ringer's (LR) solution on changes in cardiac output (CO) after spinal anesthesia. Seventy-five patients scheduled for lower extremity surgery under spinal anesthesia were studied. We measured CO (impedance cardiography method) and blood pressure for 25 min before and 30 min after spinal anesthesia. Patients were randomly assigned to three groups. In the No Infusion group, no LR solution was given during the period of measurements. The LR Before group received 12 mL/kg of LR solution within 20 min before spinal anesthesia. The LR After group received 12 mL/kg of LR solution within 20 min starting immediately after spinal anesthesia. After spinal anesthesia, CO decreased by 13.9% in the No Infusion group. In the LR Before group, CO increased after the infusion by 20% and returned to baseline value 30 min after spinal anesthesia. In the LR After group, CO increased after spinal anesthesia, and 30 min after spinal anesthesia, CO was 11.3% above baseline. We conclude that the decrease in CO after spinal anesthesia can be prevented by the infusion of an LR solution, with CO reaching the highest value while the infusion is running. IMPLICATIONS: We studied the effects of lactated Ringer's solution infusion on cardiac output changes after spinal anesthesia. If the patients received no infusion, cardiac output decreased after spinal anesthesia. However, if the patients received lactated Ringer's solution infusion, cardiac output was maintained.     

A no-laminectomy spinal cord compression injury model in mice

The purpose of this study was to develop a minimally invasive recovery model of spinal cord injury in the C57Bl/6J mouse. Without laminectomy, the epidural space was exposed by disruption of the T10-T11 interspinous ligament. Perpendicular to the rostral-caudal axis of the spine, a 1.5-mm silicone tube (O.D. 0.047 in.) was placed in the T11 epidural space. Prior to placement, a suture was passed through the tube allowing withdrawal of the tube after discontinuation of anesthesia. After 1, 30, 60, or 120 min (n = 5-8) of spinal cord compression (SCC), the tube was withdrawn. Neurological function was measured at 1, 3, 7, and 14 days after injury followed by histologic analysis. BBB locomotor score, rotarod latency, and screen grasping were worsened in a SCC duration-dependent manner (p < 0.0001). With increasing SCC duration, the number of histologically normal neurons in the ventral horns decreased (p < 0.0001) while the cross-sectional area of spinal cord with pancellular necrosis increased (p < 0.0001). Increased duration of SCC caused progressive rostral-caudal spread of histologic damage. The results indicate that this is a simple, reliable model with neurologic and histologic injury highly dependent on SCC duration. This model may be useful for study of spinal cord injury in genetically modified mice in the absence of anesthetic confounds while leaving the vertebral column intact.     

Temperature effects on feline cortical and spinal evoked potentials

To evaluate the effects of hypothermia on the somatosensory evoked potentials, baseline cortical and spinal evoked responses were obtained following induction of anesthesia at normal body temperature in five cats. The body temperature was lowered between 5 degrees and 6 degrees C and repeat cortical and spinal evoked responses were obtained. The cats were warmed to their original normal temperatures and the cortical and spinal evoked responses were repeated. After cooling the spinal evoked responses showed an average 40% increase in the latency (range 29-51%). Three of the animals showed a change in the normal waveform with the development of two distinct peaks instead of a single waveform. This was thought to be due to the varied vulnerability of the different cortical tracts to the lower temperature. Upon rewarming, the average latency returned to within 2.7% of the initial value, and the double waveform reunited to form a single wave. With cooling, the cortical evoked responses showed a similar consistent increase in latency. However, there was a much larger variability in the appearance of the waveforms. There was a range from an almost nonexistent wave in two cats to various waveform changes in the other cats. After rewarming there was a much slower return to normal latency in waveform than was found with the spinal evoked potentials. These experimental findings revealed an apparent deleterious, although reversible, effect on the somatosensory evoked potentials. Until the physiologic effects of cooling on the spinal cord are better understood, it is recommended that the temperature of patients undergoing spinal instrumentation be kept as close to normal as possible.     

Asymptomatic spinal cord neoplasm detected during induction of spinal anesthesia

We report a case of an asymptomatic spinal cord neoplasm detected during the placement of a 25-gauge Whitacre spinal needle for spinal anesthesia before elective cesarean delivery. Subarachnoid blood was repeatedly aspirated during otherwise uncomplicated induction of spinal anesthesia. Magnetic resonance imaging revealed a spinal cord ependymoma in the lumbar spine. Asymptomatic spinal cord neoplasms and ependymomas are reviewed. Central nervous system pathology should be considered in the presence of persistent subarachnoid blood.     

Laparoscopic ventral hernia repair under spinal anesthesia: a feasibility study

BACKGROUND: Regional anesthesia has not been used as the sole anesthetic procedure in laparoscopic ventral hernia repair due to the fear of potential adverse effects of the pneumoperitoneum. However, there are recent reports on the feasibility of performing laparoscopic procedures, such as cholecystectomy, in fit patients, under spinal anesthesia alone. The current study aimed to detect the feasibility of performing laparoscopic ventral hernia repair under spinal anesthesia. METHODS: Twenty-five American Society of Anesthesiologists (ASA) I or II patients underwent laparoscopic ventral hernia repair with low-pressure CO2 pneumoperitoneum under spinal anesthesia. In 9 cases the hernia was umbilical/para-umbilical, in 5 cases epigastric, and in 11 cases incisional. Intraoperative incidents, complications, postoperative pain, and recovery in general, as well as patient satisfaction at follow-up examination, were prospectively recorded. RESULTS: All operations were completed laparoscopically and conversion from spinal to general anesthesia was not required in any of the cases. Median pain score at 4 hours postoperatively was .5 (range 0-5), at 8 hours 1.5 (range 0-6), and at 24 hours 1.5 (range 0-4). Most patients were discharged 24 hours after the operation; the median hospital stay was 1 day (range 1-3 days). At 2-weeks follow-up, no late complications were detected and all patients reported being satisfied with the anesthetic procedure. CONCLUSION: Laparoscopic ventral hernia repair with low-pressure CO2 pneumoperitoneum can be successfully and safely performed under spinal anesthesia. Furthermore, it seems that spinal anesthesia is associated with minimal postoperative pain and smooth recovery.