Prevention of spinal cord ischemia after thoracic aortic occlusion

Paraplegia has been a devastating and unpredictable complication following surgical procedures necessitating temporary occlusion of the thoracic aorta. This study was undertaken to investigate the effect of the pressure gradient between the aortic pressure distal to the occlusion and cerebrospinal fluid pressure (CSFP), defined as "Relative spinal cord perfusion pressure" (RSPP) on the development of ischemia to the spinal cord by using somatosensory evoked potentials (SEP). In 30 mongrel dogs, the thoracic aorta just distal to the left subclavian artery was occluded for either 30 or 120 minutes until SEP disappeared. RSPP was maintained at 20, 30 or 40 mmHg in each dog by adjusting the degree of occlusion of th aorta and/or changing CSFP by withdrawal of cerebrospinal fluid or injection of normal saline into the subarachnoid space. SEP were recorded as a cortical response to the electrical stimulation of bilateral peroneal nerves. SEP did not disappear for 30 or 120 minutes when RSPP was 40 mmHg. It would be concluded that 40 mmHg or higher of RSPP is necessary in order to prevent the spinal cord ischemia due to the temporary occlusion of the thoracic aorta.     

Brown-Séquard syndrome following removal of a cerebrospinal fluid drainage catheter after thoracic aortic surgery

Neurological deficit remains a devastating complication of thoracic aortic surgery despite advances in methods to protect the spinal cord from ischemia. Various techniques have been used, including the combination of cerebrospinal fluid (CSF) drainage and distal aortic perfusion to decrease the incidence of postoperative neurological deficit. These deficits are usually bilateral and result in paraplegia. In this case report we present a patient with Type B aortic dissection and thoracoabdominal aortic aneurysm repair with insertion of a lumbar CSF drainage catheter. Postoperatively, the patient developed unilateral neurological features consistent with Brown-Séquard syndrome after removal of the CSF catheter. The lumbar cerebrospinal fluid catheter was reinserted and the CSF was drained. Medullary T6-7 signal abnormalities were seen on spinal cord magnetic resonance imaging, and we suggest that the spinal cord suffered a direct injury during catheter removal. The patient had an uneventful recovery. IMPLICATIONS: We describe a patient who developed unilateral neurologic features suggestive of Brown-Sequard syndrome following removal of a cerebrospinal fluid catheter after thoracic aortic surgery. We suggest that the spinal cord was injured during catheter removal. The catheter was reinserted and the patient had a full neurologic recovery.     

Winner of the ESVS prize 1989. Microcirculation of the spinal cord during proximal aortic cross-clamping

The relationship between the cerebrospinal fluid pressure (CSFP) and the microcirculation of the spinal cord was studied during cross-clamping (XC) of the thoracic aorta in pigs. CSFP was recorded via an intrathecal catheter. The microcirculation was measured by the laser Doppler technique using a needle probe inserted percutaneously into the spinal cord. A left thoracotomy was performed, and the thoracic aorta was cross-clamped for 30 minutes distal to the left subclavian artery. Prior to XC a pulsatile flux recording from the spinal cord (SCF) was observed. Following cross-clamping of the aorta SCF was dramatically reduced (P less than 0.001), then stabilised at 40% of base-line values. During XC, variations in CSFP were observed but these changes were not statistically significant. CSFP gradually increased to pre cross-clamp levels following release of XC (P less than 0.05). SCF increased 51% following removal of 1 ml of cerebrospinal fluid (P less than 0.05). By injection of 0.9% saline at body temperature SCF was totally inhibited at CSFP above 15 mmHg. Occlusion of the azygos vein increased CSFP 1.3 mmHg (P less than 0.05) whereby SCF decreased 58% (P less than 0.01). Following release of XC of a hyperaemic period of the SCF was demonstrated in ten out of 13 animals. In conclusion, SCF was significantly influenced by changes in CSFP during XC of the thoracic aorta. The findings support the theory that removal of spinal fluid during XC of the thoracic aorta may increase the perfusion pressure to the spinal cord, thereby improving its blood supply.     

Prolonged loss of leg myogenic motor evoked potentials during thoracoabdominal aortic aneurysm repair, without postoperative paraplegia

No postoperative paraplegia occurred in a patient whose leg myogenic motor evoked potentials (mMEPs) disappeared during thoracoabdominal aortic aneurysm repair. A 69-year-old man underwent resection and repair of a type III (Crawford classification) thoracoabdominal aneurysm. An epidural catheter was placed into the epidural space for epidural cooling, and a Swan-Ganz catheter was placed into the subarachnoid space for cerebrospinal fluid (CSF) drainage. Continuous CSF pressure and temperature measurement was carried out the day before surgery. The mMEPs gradually disappeared 10 min after proximal double aortic clamping and complete aortic transection. Selective perfusion of intercostal arteries was started about 20 min after the loss of the mMEPs, but the mMEPs were not restored. Possibly, spinal cord hyperemia, induced by selective perfusion of the intercostal vessels, narrowed the subarachnoid space so that CSF could not be satisfactorily drained during surgery. The spinal cord hyperemia may have decreased spinal function and suppressed the leg mMEPs. The persistence of the loss of mMEPs was undeniably due to the influence of the anesthetic agent or a perfusion disorder in the lower-extremity muscles. Of note, moderate spinal cord hypothermia and postoperative CSF drainage probably resulted in improved lower-limb motor function.     

Stimulating thoracic epidural placement via a lumbar approach causes significant spinal cord damage in a porcine model

Background

Continuous thoracic epidural analgesia is a valuable and common technique for analgesia but involves risk to the spinal cord. There is significant pediatric experience safely placing thoracic epidurals via a caudal approach. The use of a stimulating catheter offers the advantage of real-time confirmation of appropriate catheter placement. We hypothesize that the tip of a stimulating epidural catheter can be reliably advanced to the thoracic epidural space with lumbar insertion in a porcine model.

Methods

This prospective experimental porcine study evaluated the feasibility of placing the tip of a stimulating epidural catheter to a predefined thoracic epidural location after percutaneous lumbar epidural access in six live pigs. After the lumbar epidural space was accessed, a stimulating epidural catheter was advanced until the targeted thoracic myotome was stimulated. The final position of the catheter in relation to the targeted location was determined by fluoroscopy. All animals were euthanized at the end of the experiment, necropsy and spinal cord histology were then performed to assess the extent of spinal cord damage.

Results

In all animals the epidural catheter tip could be accurately advanced to the targeted thoracic myotome. Gross subdural bleeding occurred in three of the six animals and deep spinal damage was observed in two of the six animals. In one animal, the catheter was placed in the subarachnoid space.

Conclusions

Accurate access to the thoracic epidural space is possible via a lumbar approach using a stimulating epidural catheter. Based on gross and histopathological examination, this technique resulted in frequent complications, including subdural hemorrhage, deep spinal cord damage, and subarachnoid catheter placement.     

Ventriculostomy-related infections: a critical review of the literature

OBJECTIVE: To provide a critical evaluation of the published literature describing risk factors for ventriculostomy-related infections (VRIs) and the efficacy of prophylactic catheter exchange. METHODS: A MEDLINE literature search was performed, and data were extracted from studies published from 1941 through 2001. RESULTS: Published criteria for diagnosing VRIs are highly variable. Intraventricular hemorrhage, subarachnoid hemorrhage, cranial fracture with cerebrospinal fluid leak, craniotomy, systemic infections, and catheter irrigation all predispose patients to the development of VRIs. Extended duration of catheterization is correlated with an increasing risk of cerebrospinal fluid infections during the first 10 days of catheterization. Prophylactic catheter exchange does not modify the risk of developing later VRIs in retrospective studies. CONCLUSION: Categorizing suspected cerebrospinal fluid infections as contaminants, colonization, suspected or confirmed VRIs, or ventriculitis more accurately describes the patient's clinical condition and may indicate different management strategies. A prospective, randomized clinical trial is required to further evaluate the efficacy of prophylactic catheter exchange in limiting the incidence of VRIs during prolonged catheterization. Although prophylactic catheter exchange remains a practice option, the available data suggest that this procedure is not currently justified.     

Cerebrospinal fluid drainage and deep systemic hypothermia with total absence of circulation for spinal cord protection during surgery on the thoracic aorta

A 53-yearold man with a dissecting aneurysm of Stanford's type-B or Crawford's type I measuring 8.5 cm in diameter underwent replacement of the distal descending aorta and the thoracic aorta using techniques for spinal cord protection involving deep hypothermia at 17 degrees C and lasting 38 minutes with total absence of circulation. A subarachnoid catheter was inserted at the lumbar level to monitor spinal fluid pressure as well as to provide drainage if pressure exceeded 10 mm Hg. During surgery 60 ml was drained, followed by 95 ml after surgery on the same day and 325, 262 and 169 ml on the following three days.No signs of neurological deficit were observed during the postoperative period. Clinical course was good until hypovolemic shock developed 27 days after the operation due to upper digestive tract bleeding caused by two duodenal ulcers that perforated the gastroduodenal artery. Emergency antrectomy and vagotomy were performed. The patient died from multiple organ failure.Spinal cord injury continues to be one of the most feared complications after excision of thoracic and thoracoabdominal aorta aneurysm. Currently, various ways of protecting the spinal cord are practiced, including drainage of cerebrospinal fluid, partial bypass of the femoral artery, intercostal artery reimplantation, drug therapy and local spinal and/or systemic hypothermia. These methods, together with shorter clamping time have achieved a reduction in the incidence of spinal cord injuries.     

Clinical features and pathomechanisms of syringomyelia associated with spinal arachnoiditis

BACKGROUND: Syringomyelia is a common intramedullary lesion associated with spinal arachnoiditis and obstruction of the foramen magnum such as in Chiari's malformation. Disturbance of cerebrospinal fluid flow around the spinal cord has an important role in the development of syringomyelia due to spinal arachnoiditis; however, the exact mechanisms have not been clarified. The purpose of this retrospective study is to understand the clinical features and pathomechanisms of syringomyelia secondary to spinal arachnoiditis and to provide the current choice of surgical treatment in this difficult clinical entity. METHODS: Clinical and radiological findings in 15 patients with syringomyelia associated with spinal arachnoiditis who underwent surgical treatment in our institutes between 1982 and 2000 were reviewed. All patients presented with paraparesis or tetraparesis on admission. RESULTS: Magnetic resonance imaging (MRI) or computed tomography-myelography revealed that the syrinx predominantly existed at the thoracic levels. Five patients showed complete block of the thoracic subarachnoid space by conventional myelography. T2-weighted MRI showed diffuse intramedullary hyperintensity at the level of arachnoiditis. As the first surgical treatment, 10 patients underwent syringo-peritoneal shunt placement. Three patients were treated with a syringo-subarachnoid shunt, and 2 patients were treated with a ventriculoperitoneal shunt. Eight patients required further shunting operations for syringomyelia 2 months to 12 years after the first surgery. Neurologic improvement was obtained in 9 patients (60%) with decreased size of the syrinx. One patient remained stable; 5 patients showed gradual deterioration. CONCLUSIONS: The syrinx originated from the thoracic levels where severe adhesion of the subarachnoid space was present. The mechanisms of syrinx formation may be based on the increased interstitial fluid in the spinal cord. Shunting procedures were effective in some population of the patients. Decompression procedures of the spinal subarachnoid space may be an alternative primary surgical treatment except for patients with longitudinally extensive arachnoiditis.     

Intrathecal Adenosine following Spinal Nerve Ligation in Rat: Short Residence Time in Cerebrospinal Fluid and No Change in A1 Receptor Binding

Background: Intrathecal adenosine produces a remarkably prolonged effect to relieve mechanical hypersensitivity after peripheral nerve injury in animals. The purpose of the current study was to investigate whether this reflected an alteration in kinetics of adenosine in cerebrospinal fluid or in the number of spinal A1 adenosine receptors after nerve injury.

Methods: Male rats were anesthetized, and the left L5 and L6 spinal nerves were ligated. Two weeks later, a lumbar intrathecal catheter and intrathecal space microdialysis catheter were inserted. Adenosine, 20 [mu]g, was injected intrathecally in these and in normal rats, and microdialysates of the intrathecal space were obtained. Radioligand binding studies of adenosine A1 receptors were determined in spinal cord tissue from other normal and spinal nerve-ligated rats.

Results: Adenosine disappeared from rat cerebrospinal fluid within 30 min after intrathecal injection, with no difference between normal and spinal nerve-ligated animals. A1 adenosine receptor binding sites in the spinal cord were increased after spinal nerve ligation. This increase disappeared when adenosine deaminase was added to the membrane homogenates, suggestive of decreased endogenous adenosine in the membranes of nerve-ligated animals.     

Prevention of spinal cord injury after cross-clamping of the thoracic aorta

Paraplegia has been a devastating and unpredictable complication following cross-clamping of the thoracic aorta. In this study, the effect of the pressure gradient between the aortic pressure distal to occlusion and cerebrospinal fluid pressure (CSFP), defined as relative spinal cord perfusion pressure (RSPP), on the development of spinal cord injury was investigated. In 32 mongrel dogs, the thoracic aorta just distal to the left subclavian artery was cross-clamped. After a complete loss of somatosensory evoked potentials (SEP) had been confirmed, the dogs were divided into six groups by an additional cross-clamp interval and RSPP as follows: Group I (n = 6): 0 mmHg for 10 minutes; Group II (n = 8): 0 mmHg for 20 minutes; Group III (n = 3): 7.5 mmHg for 20 minutes; Group IV (n = 3): 7.5 mmHg for 40 minutes; Group V (n = 6): 15 mmHg for 40 minutes and Group VI (n = 6): 15 mmHg for 60 minutes. RSPP was adjusted by either withdrawal of cerebrospinal fluid or injection of normal saline solution into the subarachnoid space. SEP were generated by the stimulation of bilateral peroneal nerves. The incidence of postoperative paraplegia was 0% in Groups I and V, 33% in Group III, 50% in Group VI and 100% in Groups II and IV. This study showed that RSPP plays an important role in the development of spinal cord injury during cross-clamping of the thoracic aorta. Therefore, RSPP should be maintained at as high a level as possible in order to prevent spinal cord injury even if SEP disappear during aortic occlusion.     

Monitoring of intrathecal oxygen tension during experimental aortic occlusion predicts ultrastructural changes in the spinal cord

OBJECTIVE: To study the correlation between intrathecal PO2 and ultrastructural changes in the spinal cord during thoracic aortic occlusion in pigs. MATERIAL AND METHODS: In 18 pigs, online intrathecal oxygenation was monitored by a multiparameter Paratrend catheter (Biomedical Sensors, High Wycombe, United Kingdom) during 60 minutes' clamping of the proximal and distal descending thoracic aorta. The animals were randomly divided into 2 groups (A and B) depending on the level of distal aortic clamping. Distal aortic perfusion was restored through an aorto-iliac shunt, which also maintained low thoracic segmental perfusion of the spinal cord in group B. Perfusion-fixation technique was used before harvesting the spinal cord specimens, which later were evaluated with light and electron microscopy by an independent observer. Intrathecal parameters were interpreted as normal if PO2 was more than 0.8 kPa and PCO2 was less than 12 kPa, as intermediate ischemia if PO2 was 0.8 or less or PCO (2) was more than 12 kPa, and as absolute ischemia if PO2 was 0.8 or less and PCO2 was more than 12 kPa. RESULTS: Among 6 animals with ultrastructural changes of absolute spinal cord ischemia-reperfusion injury, 5 also had absolute ischemia according to variables derived by the Paratrend catheter. The 2 methods were in agreement in 3 of 5 animals with intermediate ischemia-reperfusion changes and in 5 of 6 animals with normal findings. The accuracy of cerebrospinal fluid PO2 and PCO2 to predict electron microscopy-verified intermediate or absolute ischemia-reperfusion injury was 94%. CONCLUSIONS: Monitoring of intrathecal PO2 after clamping of the descending aorta correlated with ultrastructural changes in the spinal cord in this pig model.     

Unraveling the riddle of syringomyelia

The pathophysiology of syringomyelia development is not fully understood. Current prevailing theories suggest that increased pulse pressure in the subarachnoid space forces cerebrospinal fluid (CSF) through the spinal cord into the syrinx. It is generally accepted that the syrinx consists of CSF. The here-proposed intramedullary pulse pressure theory instead suggests that syringomyelia is caused by increased pulse pressure in the spinal cord and that the syrinx consists of extracellular fluid. A new principle is introduced implying that the distending force in the production of syringomyelia is a relative increase in pulse pressure in the spinal cord compared to that in the nearby subarachnoid space. The formation of a syrinx then occurs by the accumulation of extracellular fluid in the distended cord. A previously unrecognized mechanism for syrinx formation, the Bernoulli theorem, is also described. The Bernoulli theorem or the Venturi effect states that the regional increase in fluid velocity in a narrowed flow channel decreases fluid pressure. In Chiari I malformations, the systolic CSF pulse pressure and downward motion of the cerebellar tonsils are significantly increased. This leads to increased spinal CSF velocities and, as a consequence of the Bernoulli theorem, decreased fluid pressure in narrow regions of the spinal CSF pathways. The resulting relatively low CSF pressure in the narrowed CSF pathway causes a suction effect on the spinal cord that distends the cord during each systole. Syringomyelia develops by the accumulation of extracellular fluid in the distended cord. In posttraumatic syringomyelia, the downwards directed systolic CSF pulse pressure is transmitted and reflected into the spinal cord below and above the traumatic subarachnoid blockage, respectively. The ensuing increase in intramedullary pulse pressure distends the spinal cord and causes syringomyelia on both sides of the blockage. The here-proposed concept has the potential to unravel the riddle of syringomyelia and affords explanations to previously unanswered clinical and theoretical problems with syringomyelia. It also explains why syringomyelia associated with Chiari I malformations may develop in any part of the spinal cord including the medullary conus. Syringomyelia thus preferentially develops where the systolic CSF flow causes a suction effect on the spinal cord, i.e., at or immediately caudal to physiological or pathological encroachments of the spinal subarachnoid space.     

Disturbances of cerebrospinal fluid flow attributable to arachnoid scarring cause interstitial edema of the cat spinal cord

OBJECTIVE: Spinal arachnoid scarring may be caused by trauma, inflammation, surgery, spinal instability, degenerative diseases, or malformations and may lead to progressive neurological deficits and syringomyelia. We wanted to investigate the effects of focal arachnoid scarring in the cervical spinal canal of cats on pressures in the subarachnoid space and spinal cord tissue, as well as on spinal cord histological features. METHODS: Twenty-nine adult cats were used for this study. Nine animals served as control animals, whereas 20 animals received a focal arachnoid scar at C1-C2, which was produced by placement of a kaolin-soaked fibrin sponge on the posterior surface of the spinal cord. After 4 months, pressure recordings above and below the scar, in the subarachnoid space and spinal cord, were performed. Elasticity measurements were performed with small bolus injections. Morphometric analyses of brain and ventricle volumes, sizes of the central canal, and sizes of the perivascular spaces in gray and white matter were also performed. RESULTS: No animal developed clinical or neurophysiological evidence of neurological symptoms at any time. In the kaolin-treated group, pressure recordings revealed a significant increase in the subarachnoid pressure at C1, because of the cerebrospinal fluid flow obstruction. Pressure gradients tended to increase at all measuring points. A significant difference was detected between the spinal cord and subarachnoid space at C2, where the intramedullary pressure exceeded the subarachnoid pressure. Elasticity was significantly increased in the spinal cord at C2. Intracranially, no evidence of hydrocephalus was observed. In the spinal cord, perivascular spaces were significantly enlarged in the posterior white matter above the arachnoid scar and in the central gray matter below the area of scarring in the cervical cord. CONCLUSION: Arachnoid scarring at C1-C2 produces an interstitial type of edema in the central gray matter below the area of scarring in the cat cervical cord, because of altered cerebrospinal fluid and extracellular fluid flow dynamics. These changes may be interpreted as the initial stage in the development of syringomyelic cavities.     

Management of a spinal catheter that became in tr avas cular

The management of a misplaced spinal catheter in an 83-year-old women undergoing elective knee surgery, in whom clear cerebrospinal fluid and blood were alternately aspirated through the catheter during the surgical procedure, is described. In the face of catheter misplacement, before administering general anesthesia, the authors recommend using a small "test dose" of local anesthetic to confirm subarachnoid location of catheter despite lack of frank reflux of cerebrospinal fluid.     

Intrathecal adenosine following spinal nerve ligation in rat: short residence time in cerebrospinal fluid and no change in A(1) receptor binding.

BACKGROUND: Intrathecal adenosine produces a remarkably prolonged effect to relieve mechanical hypersensitivity after peripheral nerve injury in animals. The purpose of the current study was to investigate whether this reflected an alteration in kinetics of adenosine in cerebrospinal fluid or in the number of spinal A1 adenosine receptors after nerve injury. METHODS: Male rats were anesthetized, and the left L5 and L6 spinal nerves were ligated. Two weeks later, a lumbar intrathecal catheter and intrathecal space microdialysis catheter were inserted. Adenosine, 20 microg, was injected intrathecally in these and in normal rats, and microdialysates of the intrathecal space were obtained. Radioligand binding studies of adenosine A1 receptors were determined in spinal cord tissue from other normal and spinal nerve-ligated rats. RESULTS: Adenosine disappeared from rat cerebrospinal fluid within 30 min after intrathecal injection, with no difference between normal and spinal nerve-ligated animals. A1 adenosine receptor binding sites in the spinal cord were increased after spinal nerve ligation. This increase disappeared when adenosine deaminase was added to the membrane homogenates, suggestive of decreased endogenous adenosine in the membranes of nerve-ligated animals. CONCLUSION: These data show that prolonged alleviation of hypersensitivity observed with intrathecal adenosine in this animal model of neuropathic pain is not due to prolonged residence in cerebrospinal fluid, although pharmacokinetics in tissues are unknown. Similarly, there is no evidence for up-regulation in spinal A1 adenosine receptors after spinal nerve ligation, and the adenosine deaminase experiment is consistent with a depletion of adenosine in spinal cord tissue after spinal nerve ligation.     

Prevention of spinal cord injury after cross-clamping of the thoracic aorta

Paraplegia has been a devastating and unpredictable complication following surgical procedures involving temporary occlusion of the thoracic aorta. This study was undertaken to determine the effect of the pressure gradient between the aortic pressure distal to the occluding aortic clamp and cerebrospinal fluid pressure, defined as “Relative spinal cord perfusion pressure” (RSPP) on the development of the ischemic spinal cord injury. In twelve mongrel dogs, the thoracic aorta just distal to the left subclavian artery was cross-clamped. Somatosensory evoked potentials (SEP) were generated by peripheral stimulation of the bilateral peroneal nerves. After complete loss of SEP was evident, six dogs, Group 1, were subjected to occlusion of the descending thoracic aorta for a period of 20 minutes with maintenance of 0 mmHg of RSPP, by an injection of normal saline into the subarachnoid space. Six other dogs, Group 2, likewise underwent 40 minutes of aortic occlusion, keeping the RSPP at 15 mmHg by withdrawal ofcerebrospinal fluid. All the dogs in Group 1 developed paraplegia, whereas all the dogs in Group 2 demonstrated complete postoperative recovery without any neurological sequelae. Thus, RSPP is a most important factor in the development of the ischemic spinal cord injury during the temporary thoracic aortic occlusion.     

Experimental syringohydromyelia induced by adhesive arachnoiditis in the rabbit: changes in the blood-spinal cord barrier, neuroinflammatory foci, and syrinx formation

There are many histological examinations of syringohydromyelia in the literature. However, there has been very little experimental work on blood permeability in the spinal cord vessels and ultrastructural changes. We prepared an animal model of spinal adhesive arachnoiditis by injecting kaolin into the subarachnoid space at the eighth thoracic vertebra of rabbits. The animals were evaluated 4 months later. Of the 30 rabbits given kaolin injection into the cerebrospinal fluid, 23 showed complete circumferential obstruction. In the 7 animals with partial obstruction of the subarachnoid space, intramedullary changes were not observed. However, among the 23 animals showing complete obstruction of the subarachnoid space, dilatation of the central canal (hydromyelia) occurred in 21, and intramedullary syrinx (syringomyelia) was observed in 11. In animals with complete obstruction, fluorescence microscopy revealed intramedullary edema around the central canal, extending to the posterior columns. Electron microscopy of hydromyelia revealed a marked reduction of villi on the ependymal cells, separation of the ependymal cells, and cavitation of the subependymal layer. The dilated perivascular spaces indicate alterations of fluid exchange between the subarachnoid and extracellular spaces. Syringomyelia revealed that nerve fibers and nerve cells were exposed on the surface of the syrinx, and necrotic tissue was removed by macrophages to leave a syrinx. Both pathologies differ in their mechanism of development: hydromyelia is attributed to disturbed reflux of cerebrospinal fluid, while tissue necrosis due to disturbed intramedullary blood flow is considered to be involved in formation of the syrinx in syringomyelia.     

腰大池置管持续引流治疗胸椎黄韧带骨化术后脑脊液漏

目的探讨腰大池置管持续引流治疗胸椎黄韧带骨化术后脑脊液漏的效果。方法2003年3月～2011年3月对15例胸椎黄韧带骨化术后脑脊液漏应用一次性颅脑外引流器从L3-4椎间隙行硬膜外穿刺,置管于蛛网膜下腔引流脑脊液。结果切口引流时间2～8d,平均4d;腰大池置管时间3～10d,平均6d。15例术后随访6个月,无一例出现脑脊液复发、切口感染和颅内感染并发症。结论腰大池置管持续引流治疗胸椎黄韧带骨化术后脑脊液漏安全、有效。     

Spinal cord injury in experimental thoracic aortic occlusion: investigation of combined methods of protection.

The efficacy of combined methods of spinal cord protection during thoracoabdominal aortic reconstruction was evaluated because a recent clinical study failed to substantiate the value of cerebrospinal fluid drainage when used alone in the prevention of paraplegia. The effect of cerebrospinal fluid drainage and aortofemoral shunting were analyzed with regard to neurologic outcome and spinal cord blood flow in a model of thoracic aortic occlusion. In addition, we studied the use of motor-evoked potentials as compared with somatosensory-evoked potentials in monitoring cord perfusion. Thirty-two dogs underwent proximal and distal thoracic aortic occlusion for 60 minutes. The control group (n = 8) underwent thoracic aortic cross-clamping only. Spinal cord protection was used in three groups: cerebrospinal fluid drainage alone (n = 8), aortofemoral shunting alone (n = 8), and cerebrospinal fluid drainage and aortofemoral shunting (n = 8). Neurologic outcome improved in all treatment groups as compared with controls (p less than 0.001). The addition of cerebrospinal fluid drainage to aortofemoral shunting did not further improve neurologic outcome. Spinal cord blood flow measured with microspheres in the lumbar gray matter was significantly higher in the dogs with aortofemoral shunting (+/- cerebrospinal fluid drainage) as compared with those with cerebrospinal fluid drainage alone (p less than 0.05) or the controls (p less than 0.001). Aortofemoral shunting also prevented the development of acidosis and hyperglycemia. Loss or changes in amplitude and latency of motor-evoked potentials did not distinguish between the groups. Loss of somatosensory-evoked potentials had a high sensitivity (92%) but lower specificity (68%) in predicting neurologic injury, whereas loss of motor-evoked potentials had a high specificity (100%) but a very low sensitivity (16%). We conclude that cerebrospinal fluid drainage or aortofemoral shunting significantly improve spinal cord blood flow and neurologic outcome. The greatest increase in spinal cord blood flow was seen with aortofemoral shunting, which also prevented metabolic disturbances of reperfusion. Although the addition of cerebrospinal fluid drainage to aortofemoral shunting was the only group in which no neurologic injury occurred, this group did not have a significant improvement in outcome when compared with aortofemoral shunting alone. Spinal cord ischemia was more accurately detected with somatosensory-evoked potentials when aortofemoral shunting was used, whereas motor-evoked potentials recorded from the spinal cord were not sensitive enough to predict neurologic injury.     

The effect of fentanyl anesthesia and intrathecal naloxone on neurologic outcome following spinal cord injury in the rat

Whereas opiate receptor agonists have resulted in spinal cord damage; opiate receptor antagonists have demonstrated protection against spinal cord injury. Because opioids are used in clinical anesthesia, the effect of an opiate antagonist was evaluated on neurologic outcome in a rat model of spinal cord injury occurring during opioid anesthesia. One day prior to spinal cord injury, a catheter was inserted into the spinal subarachnoid space with the tip at T8. On the day of spinal cord injury a balloon tipped catheter was inserted in the epidural space with the tip at the thoracolumbar junction. Spinal cord injury was produced by balloon inflation during one of the following states: 1) group 1 (A/S), injury was produced in awake rats and saline was administered in the subarachnoid space immediately following injury; 2) group 2 (F/S), injury was produced during a fentanyl/nitrous oxide (N2O) anesthetic, and subarachnoid saline administered; and 3) group 3 (F/Nx), injury was produced during a fentanyl/N2O anesthetic, and subarachnoid naloxone (1 mg/kg) was administered immediately following injury. Dose-response curves describing the relationship between the duration of balloon inflation and the percentage of animals with a persistent neurologic deficit were constructed and compared for differences by use of a group t test. The duration of balloon inflation required to produce a neurologic deficit was greater in both the F/S and F/Nx groups than in the A/S group (P less than 0.05). There was no difference between the F/S and F/Nx groups. In summary, in rats receiving a fentanyl/N2O anesthetic, neurologic outcome was improved compared with the awake state.(ABSTRACT TRUNCATED AT 250 WORDS)