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Ann Thorac Surg 2003;76:1190-1197
© 2003 The Society of Thoracic Surgeons
a Department of Anesthesiology, University of Pennsylvania, Philadelphia, PA, USA
b Department of Surgery, University of Pennsylvania, Philadelphia, USA
c Department of Surgery, Pennsylvania Hospital, Philadelphia, Pennsylvania, USA
* Address reprint requests to Dr Cheung, University of Pennsylvania, 3400 Spruce St, Ravdin 4 Courtyard, Philadelphia, PA 19104-4283, USA.
e-mail: cheungal{at}mail.med.upenn.edu
Presented at the Thirty-ninth Annual Meeting of The Society of Thoracic Surgeons, San Diego, CA, Jan 31–Feb 2, 2003.
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Abstract |
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METHODS: Four hundred thirty-two patients had descending thoracic or thoracoabdominal aortic repair between 1993 and 2002. One hundred sixty-two of those patients (age range, 67 ± 13 years) had repairs performed with ECC, systemic anticoagulation, and lumbar CSF drainage. Repairs performed without CSF drainage, without ECC, or by stent graft (n = 53) were excluded. The CSF catheters were inserted at L3 to L5. Cerebrospinal fluid was drained to maintain pressures of 10 to 12 mm Hg. In the absence of neurologic deficit or coagulopathy, the catheters were capped at 24 hours and removed at 48 hours. Cerebrospinal fluid drainage was continued beyond 24 hours for delayed onset paraparesis.
RESULTS: Cerebrospinal fluid drains were used in 135 thoracoabdominal aortic aneurysms (extent I, n = 63; extent II, n = 25; extent III, n = 39; extent IV, n = 8) and 27 descending thoracic aortic repairs (aneurysm, n = 24; traumatic aortic injury, n = 2; aortic coarctation, n = 1). Partial left heart bypass was used in 132 patients, full cardiopulmonary bypass without deep hypothermic circulatory arrest in 5, and cardiopulmonary bypass with adjunctive deep hypothermic circulatory arrest in 25. Time between catheter insertion and anticoagulation was 153 ± 60 minutes. Heparin achieved an average maximum activated clotting time of 528 ± 192 seconds. Average ECC time was 114 ± 77 minutes. Average deep hypothermic circulatory arrest time was 40 ± 12 minutes. Mortality was 14.1% (23 of 162), and permanent paraplegia was 4.9% (8 of 162). No epidural or spinal hematoma was observed. Six (3.7%) patients had catheter-related complications (temporary abducens nerve palsy [n = 1]; retained catheter fragments [n = 2]; retained catheter fragment and meningitis [n = 1]; isolated meningitis [n = 1]; and spinal headache [n = 1]).
CONCLUSIONS: The CSF drainage in thoracic aortic surgery using ECC with full anticoagulation did not result in hemorrhagic complications. The permanent paraplegia rate in this complex patient population consisting of combined distal arch, thoracoabdominal aortic procedures were low, and lumbar CSF catheter-related complications had no permanent sequelae.
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Introduction |
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Increased use of both ECC and lumbar CSF drainage in an effort to decrease the risk of postoperative paraplegia has been an evolving practice in the surgical and anesthetic management of patients with thoracic aortic and TAAA disease at the University of Pennsylvania. To better define the risks associated with lumbar CSF drainage in this patient population, the thoracic aortic surgical database was analyzed to identify patients undergoing thoracic aortic reconstruction with ECC who suffered complications associated with lumbar CSF drainage.
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Material and methods |
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All patients were exposed through a posterolateral thoracotomy. The incision was extended past the costal cartilages and retroperitoneal lateral to the rectus muscle for TAAA. Circulation management consisted of either partial left heart bypass (LHB) with moderate core cooling to 32°C LHB or a hypothermic technique utilizing full CPB through the left chest with an open proximal anastomosis. Systemic heparin dose for ECC was determined using the heparin response test (Rx/Dx Hemachron [International Technidyne, Inc, Edison, NJ]), targeting an activated clotting time (ACT) greater than or equal to 350 seconds for LHB and ACT greater than or equal to 400 seconds for CPB. Left heart bypass was used in most patients with a staged segmental reconstruction of the aorta. Left heart bypass flow rates averaged 2.5 L per minute adjusted to achieve a target distal aortic perfusion pressure of at least 60 mm Hg, while maintaining a proximal aortic pressure of at least 90 mm Hg. During the mesenteric anastomosis, perfusion cannulas to the renal arteries and superior mesenteric artery were utilized off the cardioplegia line from the CPB circuit. Intercostal arteries were not selectively perfused during LHB. The hypothermic technique was used if a concomitant distal arch aneurysm needed resection, if a proximal aortic cross clamp could not be applied, or if LHB could not be performed. Circulation management during an open proximal anastomosis at the distal aortic arch consisted of DHCA at a mean lowest nasopharyngeal temperature of 14.5°C, together with total body retrograde cerebral perfusion through the superior vena cava at 12°C, in a slight Trendelenberg position with a target central venous pressure of approximately 15 mm Hg [5]. This usually translated into a retrograde cerebral perfusion flow of 300 to 500 mL per minute. The total dose of heparin, maximum ACT, duration of ECC, duration of DHCA, and minimum nasopharyngeal temperature during deliberate hypothermia were recorded from perfusion records. After completion of the open proximal anastomosis, the proximal arterial circulation was reinitiated by the Dacron graft, and rewarming was started while distal perfusion was maintained through the femoral artery or its equivalent. Mannitol (25 g), methylprednisolone (1 gm), magnesium (2 g), and lidocaine (200 mg) were administered upon initiation of LHB or CPB. Intercostal arteries were reimplanted in all patients with dissecting aortic aneurysms and selectively in patients with atherosclerotic aneurysms if a large patch of intercostal arteries were identified between the T7 and L1 vertebral levels. Neurophysiologic monitoring with electroencephalography and lower extremity somatosensory evoked potentials was performed during the operation in the majority of patients.
Patients were admitted to a surgical intensive care unit after operation. Vital signs, core temperature, cardiac output, arterial pressure, central venous pressure, pulmonary artery pressures, and the lumbar CSF pressure were recorded at 15-minute to 60-minute intervals. The mean arterial pressure was maintained in a range of 75 mm Hg to 85 mm Hg using vasopressors or vasodilators (nicardipine) depending on the perceived strength of the arterial anastomosis and the risk of bleeding. Lumbar CSF was drained in 10 mL aliquots per hour to maintain a lumbar CSF pressure of less than or equal to 12 mm Hg. In the absence of a neurologic deficit, lumbar CSF drainage was discontinued 24 hours after the operation, and the catheter was removed at 48 hours after the operation. The platelet count, prothrombin time, international normalized ratio, and partial thromboplastin time were assessed and the coagulopathy was corrected before lumbar CSF catheter removal. No patients were treated with systemic anticoagulant therapy or low-molecular-weight heparin thromboprophylaxis before lumbar CSF catheter removal.
Immediate onset paraplegia detected after emergence from general anesthesia was classified as permanent if there was no neurologic recovery or classified as reversible if there was partial or complete recovery of neurologic function. Delayed-onset postoperative paraplegia or paraparesis was treated by CSF drainage for a lumbar CSF pressure greater than or equal to 10 mm Hg and by vasopressors to increase the mean arterial pressure to at least 95 mm Hg [3]. Delayed-onset postoperative paraplegia was also classified as permanent if there was no recovery of neurologic function or classified as reversible if there was partial or complete recovery of neurologic function. All neurologic examinations were performed by a neurologist. Early death was defined as death occurring during or after an operation, before neurologic assessment could be performed. Late postoperative death was defined as death after an operation before hospital discharge. As part of an ongoing quality assessment procedure, all complications related to lumbar CSF drainage were identified and reviewed prospectively. In addition, the medical records of all patients in the study were retrospectively reviewed to verify the use of lumbar CSF drainage together with ECC and to search for any additional complications that could be related to lumbar CSF drainage.
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Results |
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The average elapsed time (mean ± standard deviation) between catheter insertion and heparin administration was 153 ± 60 minutes (Table 2). The average total dose of heparin administered intravenously for ECC was 15,427 ± 8,070 United States Pharmacopeia units, which achieved an average maximum ACT of 528 ± 191 seconds. The average total duration of ECC was 114 ± 77 minutes. In the 25 patients undergoing DHCA, the average duration of DHCA was 40 ± 12 minutes. The average minimum nasopharyngeal temperature was 29.8 ± 7.6°C for ECC without DHCA and 14.2 ± 2.1°C for CPB with DHCA. Aprotinin was administered to 12 patients operated on using DHCA and 37 patients operated on using LHB. Aminocaproic acid was administered to 5 patients operated on using DHCA and 21 patients operated on using LHB.
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Patient 2
Patient 2 is a 73-year-old woman with a past medical history of degenerative joint disease of the lumbosacral spine who underwent repair of a 6.5 cm thoracic aorta using LHB. A lumbar CSF drain was inserted before operation, but only minimal CSF drained from the catheter during and after operation. The lumbar CSF catheter was removed on POD 2, and inspection of the catheter revealed that the distal 1.7 cm tip had fractured off within the patient (Fig 1).
No attempt was made to retrieve the catheter fragment because the patient was asymptomatic and had no evidence of CSF leakage or infection. The patient was discharged on POD 10.
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Patient 4
Patient 4 was a 21-year-old woman who underwent repair of a thoracic aortic pseudoaneurysm as a consequence of traumatic aortic transection from a motor vehicle accident 10 days earlier. The operation was performed using LHB. The lumbar CSF drain that was inserted before the operation was fractured under the skin during an attempted removal on POD 2. A computed tomographic scan of the lumbar spine demonstrated a retained catheter fragment extending from the paraspinal soft tissue at the level of L4 into the subarachnoid space to the level of L1. On POD 2 the patient underwent a lumbar exploration and the retained catheter fragment was removed after it was identified exiting the lateral para-spinous musculature between the L3 and L4 hemi-lamina. The patient recovered without sequelae and was discharged on POD 11.
Patient 5
Patient 5 was a 41-year-old woman with Marfan's syndrome with a previous Stanford type B aortic dissection who underwent repair of an extent II TAAA using LHB. A lumbar CSF drain was inserted before the operation. The initial postoperative course was complicated by bleeding and coagulopathy that required blood transfusion. On POD 1 the patient complained of a headache and diplopia, and examination revealed right abducens nerve palsy. Computed tomographic scan of the head revealed herniation of the cerebellar tonsils and a decreased amount of CSF surrounding the pons and medulla consistent with intracranial hypotension from excessive CSF drainage. Cerebrospinal fluid drainage was discontinued and the lumbar CSF drain was removed on POD 3. The abducens nerve palsy resolved after several days, and the patient was eventually discharged on POD 22.
Patient 6
Patient 6 was a 78-year-old man who underwent repair of an 8-cm extent II TAAA with LHB. The lumbar CSF drain that was inserted before the operation fractured in the lumbar soft tissue during an attempted removal on the evening of POD 1. Computed tomographic scan of the lumbar spine showed the retained catheter tip within the paravertebral soft tissue at the level of L2 to L3. Based on a neurosurgical consultation, it was decided not to remove the retained catheter tip. The subsequent hospital course was complicated by the onset of new left occipital and cerebellar infarcts and respiratory insufficiency requiring tracheostomy. On POD 12, a diagnostic lumbar puncture was performed for persistent fever and decreased level of consciousness. The CSF revealed an 84 white blood cell count per mm3 with 55% segmented neutrophils and a protein concentration of 94 mg/dL. The patient was treated for presumed bacterial meningitis with vancomycin and cefepime. The CSF culture did not grow bacteria, but CSF obtained from a second lumbar puncture after 10 days of antibiotic therapy demonstrated resolution of pleocytosis with an 8 white blood cell count per mm3 with 26% segmented neutrophils and a protein concentration of 40 mg/dL. The patient was eventually discharged to a rehabilitation unit on POD 62.
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Comment |
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The rate of catheter-associated meningitis was 1.2%. This observed rate was considerably less than the 4.2% rate of meningitis reported when lumbar CSF drainage was used for the treatment of communicating hydrocephalus or traumatic cranial CSF leakage [6]. The presenting signs of meningitis in both patients were persistent fever and altered mental status. Lumbar puncture demonstrating CSF pleocytosis and elevated protein concentration was diagnostic for meningitis. Both patients who had meningitis develop had risk factors for infection. One patient had a previous ventriculostomy for head trauma and the second patient had a retained lumbar CSF catheter fragment. Early diagnosis and antibiotic therapy was effective for the treatment of meningitis associated with lumbar CSF drainage.
Temporary abducens nerve palsy caused by herniation of the cerebellar tonsils as a consequence of excessive lumbar CSF drainage was a complication early in the case series. Transient abducens nerve palsy has been a recognized complication of lumbar puncture, spinal anesthesia, myelography, and ventricular shunting presumed to be caused by nerve traction as a consequence of intracranial hypotension. Intracranial subdural hematoma from excessive lumbar CSF drainage caused by stretching and tearing of dural veins has also been reported in patients after TAAA repair [7–8]. In one reported series, the incidence of subdural hematoma was 3.5% (8 of 230 patients) with an associated mortality of 50% [8]. In that series, 7 of 8 of the patients with subdural hematoma had CSF drained through a "pop-off" valve to a pressure of 5 cm H2O (3.7 mm Hg) and drained an average of 690 mL of CSF per patient [8]. To decrease the risk of intracranial hypotension from excessive CSF drainage, a policy was instituted in our program to continuously monitor the lumbar CSF pressure with a pressure transducer during and after operation. In the study by Coselli and colleagues [2], CSF was drained when lumbar CSF pressure exceeded 10 mm Hg. In contrast, our standard postoperative protocol permitted intermittent CSF drainage in 10 mL aliquots per hour for a lumbar CSF pressure of greater than or equal to 12 mm Hg, unless specified by a physician [3]. In the event of delayed postoperative paraplegia, CSF was drained for lumbar CSF pressures of greater than or equal to 10 mm Hg [3–4]. Surprisingly, only 1 patient in our series had a postlumbar puncture headache that resolved with conservative treatment.
Despite systemic anticoagulation with an average ACT of more than 400 seconds, no hemorrhagic complications from lumbar CSF drainage were detected. In contrast, a reported series found a 3.2% incidence of intra-spinal hematoma complicating lumbar CSF drainage for TAAA repair [9]; it is possible that asymptomatic epidural or spinal hematomas or hemorrhagic complications were missed in the 4 patients with early deaths. With epidural anesthesia experiences, case reports suggest that the greatest risk of epidural or spinal hematoma have occurred during epidural catheter removal, particularly in patients treated with low-molecular-weight heparin for thromboprophylaxis [10–12]. Our standard policy to check for laboratory evidence of coagulation defects before removing the lumbar CSF drain at an average of 48 hours after operation may have been an important factor in decreasing the risk of epidural hematoma. The average elapsed time of 153 minutes between lumbar CSF catheter insertion and administration of heparin may have also reduced the risk of hemorrhagic complications. Securing the lumbar CSF catheter to prevent catheter movement during operation while the patient was anticoagulated for ECC may have been another factor in decreasing the risk of hemorrhagic complications. The data could not establish a relationship between heparin dose or target ACT and the risk of hemorrhagic complications from CSF drainage. In the series reported by Cosselli and colleagues [2], no lumbar CSF catheter hemorrhagic complications were reported with a heparin dose (1 mg/kg) for partial left heart bypass. Although heparin doses tended to be less in our early experience, our current protocol targeted a dose of heparin to achieve an ACT of greater than 400 seconds for ECC based on the belief that the risk of incomplete anticoagulation during ECC is greater than the risk of hemorrhagic complications. There was not enough data in this experience to dictate the management of patients who had evidence of trauma related to the insertion or attempted insertion of the lumbar CSF catheter immediately before the operation. In addition, there was insufficient evidence to suggest that patients with blood appearing in the CSF drain should be management differently.
The relatively low incidence of complications associated with lumbar CSF drainage for thoracic aortic reconstruction performed using ECC justified the continued use of this technique for the prevention and treatment of postoperative paraplegia. Lumbar CSF drainage used in combination with vasopressor therapy contributed to full or partial neurologic recovery in 11 of 15 patients (73%) who developed delayed-onset postoperative paraplegia. The overall permanent paraplegia rate in this series of patients with perioperative lumbar CSF drainage for thoracic aortic operations was 4.9% with an immediate postoperative permanent paraplegia rate of only 2.4%. These permanent paraplegia rates were comparable with those reported in other large series suggesting a potential benefit of the routine use of ECC and lumbar CSF drainage for repair of thoracic aortic aneurysms [1–2].
This study only analyzed patients who underwent successful insertion of a lumbar CSF catheter before operation. Reasons for not performing lumbar CSF drainage in individual patients included emergent operations associated with hemodynamic instability, severe scoliosis of the lumbosacral spine, prior lumbar spine surgery, technically difficult or unsuccessful catheter insertion, coagulopathy at the time of operation, or operations that had a low anticipated risk of postoperative paraplegia. Analysis of the complications associated with lumbar CSF drainage suggested that the majority of complications were potentially avoidable with the use of continuous CSF pressure transduction, intermittent CSF drainage, supervised catheter removal, and early detection and treatment of catheter-related meningitis. Based on this experience, there has been a trend toward increased use of lumbar CSF drainage for descending thoracic or thoracoabdominal aortic operations performed using ECC in patients at risk for postoperative paraplegia. Although a much larger clinical series would be necessary to establish the exact risk of complications that occur infrequently, reversible spinal cord ischemia was the predominant cause of delayed-onset postoperative paraplegia. Lumbar CSF drainage and arterial pressure augmentation for the emergency treatment of spinal cord ischemia should not be delayed in order to obtain imaging studies to evaluate the cause of lower extremity weakness or to rule out epidural or spinal hematoma. In conclusion, lumbar CSF drainage was performed safely in a large number of patients undergoing thoracic aortic reconstruction using ECC with systemic anticoagulation.
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Discussion |
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TopAbstractIntroductionMaterial and methodsResultsCommentDiscussionReferences |
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With the apparent trend toward an increased use of cerebrospinal fluid (CSF) drainage in the surgical management of pathology of the descending and thoracoabdominal aorta, your group is to be congratulated for contributing to the evaluation of the safety of such drainage. In addition, you have pointed out to us many of the challenges in the management and treatment of such patients, including the morbidity and mortality encountered. For example, your hospital mortality was 14.1% (4 early and 19 late), a paraplegia rate ultimately of 4.9% and a mortality rate for those patients with permanent paraplegia (5 of 8, or 63%).
In our own work, we have excluded patients requiring full cardiopulmonary bypass and the required additional heparinization from CSF drainage due to a concern for hemorrhagic complications. I was encouraged by the lack of such complications in your patients, particularly in this cohort with cardiopulmonary bypass and full heparinization. However, this ultimately comprised only 30 patients (19% of the entire group), a relatively small sample size, precluding any strong conclusions.
You are also to be commended for your development and implementation of a standard protocol for CSF drainage, with particular note to your efforts toward correction of coagulopathy prior to drain removal at 48 hours. We have found this to be useful in our own patients, particularly those with high CSF outputs persisting beyond 24 to 48 hours and in patients with transient deficits that recovered after CSF drainage.
I recently reviewed the results of 326 patients that we treated over an 18-month period of time from January 2000 to mid-2002. All of these patients had left heart bypass or extracorporeal circulation, but none of them had deep hypothermic circulatory arrest. We encountered none of the catheter fractures that you have reported; we had no patients with meningitis and no epidural or spinal hematomas. We did, however, have 2 patients with intracranial hypotension, 6 with spinal headaches, and 9 with catheter malfunction. This latter group consisted primarily of patients in whom the drainage was not able to be adequately obtained through the catheter during the expected postoperative time period, and consequently these catheters were removed early. Certainly care should be taken to avoid the excessive drainage of CSF fluid perioperatively, as you have so wisely pointed out, and all patients should be monitored meticulously to avert severe complications such as intracerebral bleeding. We, too, have avoided the use of this "pop-off" concept, but rather have managed our patients with direct drainage under strict protocol.
I have a few questions. First, what were the causes of early death in your experience? I would be interested in knowing if any of these were secondary to cerebral complications and whether or not they might be secondarily related to CSF drainage.
Could the authors specifically address cerebral complications and how they assess them? Do they evaluate such complications identically in those patients undergoing deep hypothermic circulatory arrest as compared with other patients with descending thoracic and thoracoabdominal aortic aneurysms not having circulatory arrest? We have been inclined to obtain an immediate computed tomographic (CT) scan or magnetic resonance image (MRI) scan in any patient who exhibits any sign of stroke, headache, or encephalopathy to rule out the possibility of intracranial hemorrhage or other problems before proceeding with immediate neurosurgical intervention, if necessary.
Eleven of your 15 patients had delayed paraplegia; partial or full neurological recovery was elucidated in your presentation. But why were these patients excluded from the CSF drainage at their initial procedure, if they were indeed excluded? And with this, I would like you to clarify just a bit further, I know you have reported on this in the past, but what is your exact approach to delayed paraplegia? How do you manage this? What period of time elapses between the insertion of the CSF catheter and how much fluid is consequently drained in such patients?
Once again, I would like to congratulate you for a fine presentation and an excellent paper. Thank you.
DR CHEUNG: First of all, it is a privilege to have Dr Coselli comment on our paper because he has clearly set the standard for the surgical management of patients with thoracic aortic disease.
In reply to your first question, we had an early death rate of 2.5%. We defined early death as death during or immediately after operation before a neurologic evaluation could be performed. Most of those patients died from multiorgan dysfunction or massive bleeding and were unable to be resuscitated. Hence, we could not elucidate whether or not those patients had complications related to the lumbar CSF drain or paraplegia, but we do not believe the presence of a lumbar CSF drain complication would have made a difference in outcome in that group of patients.
We acknowledge that our experience with lumbar CSF drainage in patients with deep hypothermic circulatory arrest was small, as there were only 25 patients. However, the magnitude of anticoagulation in those patients was not that different in comparison with the other patients, and we think that supports, at least in this limited experience that this procedure can be safely performed.
In terms of using the CT or MRI scan to look for hemorrhagic complications, our approach as dictated by our protocol, was that when a patient had neurologic injury develop, specifically delayed onset paraplegia, the emphasis was on immediate treatment with CSF drainage and arterial blood pressure augmentation, because the most likely problem is spinal cord ischemia. Based on this experience and the experience that has been published, hemorrhagic complications are rare and unusual. The more likely problem is spinal cord ischemia, which has to be treated immediately in order to achieve a favorable outcome. Obtaining an imaging study should not be performed if it is going to delay the immediate institution of therapy. Certainly, if the lesion does not improve, an imaging study would be appropriate. In our limited experience, we have not found hemorrhagic complications in patients with permanent paraplegia who had imaging studies.
In the case of delayed onset paraplegia, we do not typically track the volume of CSF drained. Our pressure threshold for CSF drainage is set lower if there is a delayed onset paraplegia, so that CSF is drained when the lumbar CSF pressure exceeds 10 mm Hg. Our initial treatment also includes augmenting the arterial blood pressure to a mean arterial pressure of 95 mm Hg. If we do not observe a response, we continue to augment the mean arterial pressure an additional 5 mm Hg at a time until a response is observed or until we deem that the patient is not going to respond.
Let me also add that we routinely monitor most patients with somatosensory evoked potential monitoring during the operation, use mild deliberate hypothermia, and administer mannitol, methylprednisolone, lidocaine, and magnesium as pharmacologic neuroprotectants. However, we are not certain of the relative importance of these different interventions and whether they contribute to our ability to rescue patients with delayed onset paraplegia.
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