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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Surgical management of the thoracoabdominal aortic aneurysm is a formidable undertaking. Presently two fairly distinct operative methods are available. The conventional technique, pioneered by Etheredge, involves replacement of the aneurysm with a synthetic graft and then, step by step, revascularization of the abdominal organs with prosthetic side limbs taken from the primary graft. Individual organ ischemic time is limited to that time required for the performance of each distal side limb anastomosis. The second operative method, first described by Crawford, consists of proximal and distal control of the aneurysm, followed by its incision to simultaneously expose the origin of all four major intra-abdominal arteries. Replacement is then rapidly performed with a tubular Dacron graft including anastomosis of these major intra-abdominal arteries to four elliptical graft incisions, from within the aneurysm. Total operating time is reduced at the expense of prolonged organ ischemia. The conventional method allows for step-by-step intraoperative planning and action, and this technique is accordingly recommended to most surgeons, who have had little experience with this unusual lesion. Our recent successful experience with two cases of extensive thoracoabdominal aortic aneurysms is described as well as a discussion of additional measures which may become useful in certain cases to favor a successful outcome. Finally the problem of potential resultant paraplegia is discussed.
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PMID:Thoracoabdominal aortic aneurysms. A review and current status. 15 75

The anatomy and physiology of the blood supply to the central nervous system from the aorta is outlined. Pertinent cases are reported, to illustrate the effect of impairment of this blood supply in producing ischemia of the brain, spinal cord, and peripheral nerves. In patients with such neurologic disease, especially if sudden in onset, a search for a circulatory basis in lesions of the aorta or its branches may be rewarding and crucial. With regard to reconstructive surgery of the aorta, certain precautions may be taken: maintenance of normotension, gentle dissection, preservation of segmental arteries when possible, bypass shunting, avoidance of prolonged aortic clamping and perhaps heparinization. Unfortunately, depending upon deficiencies in collateral circulation to the spinal cord, occasional cases of postoperative paraplegia will still occur, which are both unavoidable and unpredictable.
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PMID:Neurological complications of extraspinal. 18 47

The incidence, etiology, and clinical manifestations of spinal cord damage after abdominal aortic operations and abdominal aortography are defined on grounds of the authors' experience and of a survey of the pertinent literature. In the authors' experience the incidence of cord damage was 0.25% (three of 3,164) after abdominal aortic operations and 0.01% (two of 17,494) after abdominal aortography. As regards postoperative cord complications in the authors' series, they occurred only in cases of aneurysm, were 10 times more common in ruptured than in unruptured aneurysms, and the neurological loss usually was complete flaccid paraplegia (five of eight or 62%) with high mortality (three of eight or 38%), and rare partial (two of eight or 25%) or complete (one of eight or 13%) recovery. Recovery was more likely the lesser than neurological loss. The cause of postoperative spinal cord damage was ischemia resulting from the interruption of a critical radicular artery at the lower thoracic or high lumbar vertebral levels in the presence of anomalously located greater radicular or infrarenal radicular arteries. High aortic clamping and hypotension increased the probability of this occurrence, which essentially was unpredictable and, therefore, unavoidable. In postartographic cases the cord damage is more variable in its extent, and its cause is a chemical insult brought about by flooding the anterior spinal artery with contrast medium to which the patient probably is hypersensitive. In both groups treatment of the established clinical picture (paraplegia) is confined to support and rehabilitation.
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PMID:Spinal cord damage in surgery of the abdominal aorta. 61 71

Microperfusion of the spinal cords in cats was studied using a colloidal carbon perfusion technique following compression injury at 1/2 hour, 2 hours, 4 hours, 8 hours, 24 hours, and 51 days. Quantitative estimates of vascular filling were determined at these post-compression intervals. Microperfusion diminished in both the gray and white matter at 1/2 hour following injury and severe lack of perfusion was evident at 8 and 24 hours. Diminished filling of the vessels of gray and white matter seemed to parallel the degree of hemorrhagic necrosis of the gray matter. An increased number of vessels were evident in the spinal cords of long term survivals. The observation that microperfusion in the white matter of the spinal cord was diminished at 24 hours is at variance with some previous investigations. The hypoperfusion of the white matter found in this study suggests that ischemia plays a role in paraplegia resulting from experimental compression injury of the spinal cord.
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PMID:Microvascular perfusion experimental spinal cord injury. 67 93

Spinal cord blood flow (SCBF) was measured in 24 rhesus monkeys after injury to the cord produced by the inflatable circumferential extradural cuff technique. Measurement of regional blood flow in the white and gray matter of the cord in areas of 0.1 sq mm was achieved with the 14C-antipyrine autoradiographic technique and a scanning microscope photometer. After moderate cord injury (400 mm Hg pressure in the cuff maintained for 5 minutes), which produced paraplegia in 50% of animals and moderate to severe paresis in the other 50%, mean white matter SCBF was significantly decreased for up to 1 hour. White matter blood flow then rose to normal levels by 6 hours posttrauma and was significantly increased by 24 hours posttrauma. Gray matter SCBF was significantly decreased for the entire 24-hour period posttrauma. After severe cord injury (150 mm Hg pressure in the cuff maintained for 3 hours), which produced total paraplegia in almost all animals; SCBF in white and hours), which prodced total paraplegia in almost all animals, SCBF in white and gray matter was reduced to extremely low levels for 24 hours posttrauma. In addition, focal decreases in SCBF were seen in white and gray matter for considerable distances proximal and distal to the injury site. It is concluded that acute compression injury of the spinal cord is associated with long-lasting ischemia in the cord that increases in severity with the degree of injury.
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PMID:Effect of acute spinal cord compression injury on regional spinal cord blood flow in primates. 82 18

The clinical syndrome of paraplegia following acute occlusion of the infrarenal aorta may be caused by either ischemic spinal cord damage or ischemia of the cauda equina and sacral nerve roots and ganglia. The neurologic manifestations are similar and therefore specific anatomic diagnosis is difficult. From October 1972 to February 1975 a total of 31 patients with infrarenal aortic occlusion were treated at the Medizinische Hochschule in Hannover. In nine cases the occlusion up to the renal arteries was acute. Three of these patients presented beside acute ischemic manifestations on both legs and the lower abdominal wall, neurologic symptoms of paraplegia. The anatomic and hemodynamic aspects of ischemic spinal cord damage and those of ischemic lesions of the cauda equina and peripheral nerves are discussed. There appear to be three main mechanisms responsible for vascular paraplegia following acute infrarenal occlusion of the aorta: 1. it may be caused by thrombotic occlusion of a major radicular artery which arises below the level of occlusion. 2. it may be produced by thrombosis of a lumbar collateral acting as major supply to the cord when arteriosclerotic narrowing of the major radicular artery is present. Especially in states of severe hypotension critical interference of blood supply to the spinal cord will result. 3. Paraplegia by ischemia of the cauda and peripheral nervous tissue may also follow prolonged interruption of circulation to this area supplying spinal vessels from low lumbar and sacral arteries.
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PMID:[Paraplegia following acute infrarenal aortic occlusion (author's transl)]. 108 29

Serious spinal cord ischemia may follow infrarenal abdominal aortic surgery. Five cases are summarized and added to the 23 previously published cases in order to identify this syndrome, emphasize its importance, and draw attention to the possibility of spontaneous recovery which may occur. The multifactorial complex which comprises each patient's clinical picture clouds a precise and specific cause for paraplegia in these cases. However, neither hypotension, steal phenomena nor emboli are necessary for completion of the syndrome. The relevant spinal cord arterial anatomy indicates that the common anomalies which occur favor development of spinal cord ischemia in the arteriosclerotic population which requires aortic surgery. No means of prevention is possible at this time.
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PMID:Spinal ischemia following abdominal aortic surgery. 113 Aug 46

A traumatic transection of the upper descending thoracic aorta, undiagnosed, was complicated on the tenth day by an acute obstruction of the descending thoracic aorta. The upper body hypertension resulted in generalised convulsions and cardiac failure with pulmonary oedema. The lower body ischemia resulted in paraplegia, acute ischemia of the lower limbs, liver failure and anuria. An emergency revascularisation of the lower body was achieved by axillary-bifemoral bypass. The improvement of the clinical status allowed complete repair of the aortic transection two days after the extra-anatomic revascularisation. This case emphasizes the severity of the cases with impaired blood flow to the lower body and the benefit of the extra-anatomic bypass in pathology of the upper descending thoracic aorta when complete repair of the aortic transection is associated with an extremely high risk.
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PMID:[Traumatic rupture of the aortic isthmus revealed by acute obstruction of the descending thoracic aorta]. 128 8

Paraplegia from spinal cord ischemia during thoracoabdominal aneurysm repair remains an unpredictable and unpreventable complication. In an effort to prevent spinal cord ischemia during aortic cross-clamping, preoperative angiographic localization of the blood supply to the spinal cord was performed in dogs. Sixteen animals underwent 60 minutes of thoracoabdominal aortic cross-clamping either without (control, n = 8) or with (shunted, n = 8) a selective shunt. Shunting was performed from the aortic arch to that isolated aortic segment angiographically shown to supply the thoracolumbar anterior spinal artery. Spinal cord blood flow was measured with microspheres just prior to cross-clamping, at 5 and 60 minutes after cross-clamping and at 5 minutes after restoration of aortic blood flow. Functional neurologic outcome was evaluated in animals at 24 hours postoperatively. Shunting did not decrease spinal cord injury. Seven of the 8 animals in the control group and 7 of the 8 in the shunted group developed paraplegia or paraparesis. Thoracic, but not lumbar spinal cord blood flow, was significantly increased in shunted animals. Spinal cord blood supply in dogs may be more segmental than previously believed. Technical problems in angiographic localization, spinal artery spasm, loss of spinal cord autoregulation or poor collateral circulation from the distal thoracic to the lumbar cord may also account for these results. Although shunting to aortic segments supplying the anterior spinal artery during thoracoabdominal aortic clamping may be attractive in humans, no benefit could be shown in this experimental model.
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PMID:Failure of selective shunting to intercostal arteries to prevent spinal cord ischemia during experimental thoracoabdominal aortic occlusion. 129 34

Spinal cord evoked potentials elicited by direct stimulation of the spinal cord were monitored in 21 patients during thoracic or thoraco-abdominal aortic aneurysm surgery. Flexible catheter-type electrodes were used for both stimulating and recording. The basic pattern of the spinal cord evoked potential consisted of an initial spike and a subsequent polyphasic component. The earliest and most frequent alterations after cross-clamping of the aorta were changes in the configuration or amplitude of the polyphasic component. In 13 patients who exhibited no change except minor alterations of the polyphasic component during the initial test clamping for 15 or 20 min, subsequent graft replacements were safely performed without reimplantation of intercostal vessels. In 2 patients who had sudden cardiac arrests, the evoked potential completely disappeared. The polyphasic component disappeared first, followed by the initial spike. Another patient developed acute loss of the potential after the aneurysm was incised, presumably due to distal aortic hypoperfusion. In this case, prolonged distal hypotension resulted in flaccid paraplegia. Intraoperative monitoring of the spinal cord evoked potential is a useful method for the early detection of spinal cord ischemia during surgery requiring aortic occlusion.
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PMID:Intraoperative spinal cord monitoring during surgery for aortic aneurysm: application of spinal cord evoked potential. 137


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