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

Forty-nine patients who sustained acute traumatic rupture of the aorta at the level of the isthmus were treated in our hospital between 1976 and 1990. Four patients died before surgery and 45 patients were operated upon using a pump oxygenator partial bypass in all but 2 cases (1 clamp and sew and 1 shunt). The tear was circumferential in 33 and partial in 12 cases. Direct suture was used in the 12 partial and in 21 of the circumferential tears. A dacron tube was used in 12 patients. Hospital mortality was 3 resulting from brain damage, prolonged shock before surgery and necrosis of the colon 4 weeks after operation. No paraplegia was observed. There were 2 cases of neurological disturbance (2 spinal cord dysfunction 5 and 8 days, respectively, after surgery). These complications were transient. Among the 42 survivors, 1 was lost to follow-up. The clinical aortic status of the remaining 41 was excellent. Aortic reconstitution as assessed by digital aortic angiography was excellent in the 33 cases examined with 2 exceptions (graft stenosis, false aneurysm). Our experience and review of a large series indicate: the use of a partial bypass with pump oxygenator decreases the probability of medullary ischemia, but the risk of spinal cord ischemia is not eliminated. When intra-abdominal lesions are life-threatening, laparotomy must preceed thoracotomy. Clinical results assessed in long-term survivors are excellent, especially after direct repair.
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PMID:Acute traumatic isthmic aortic rupture. Long-term results in 49 patients. 138 50

The efficacy of pharmacologic agents for prevention and control of oxygen-derived free radical damage in ischemia-reperfusion injury of the spinal cord was assessed in a swine model of thoracic and thoracoabdominal aortic crossclamping. Animals were exposed to 30 minutes of ischemia that induced lethal, irreversible injury and paraplegia. The experimental groups were as follows: group A (n = 7), control group, receiving no pharmacologic intervention; group B (n = 7), deferoxamine 50 mg/kg/day administered intravenously over 3 to 4 hours before ischemia; group C (n = 7), allopurinol pretreatment 50 mg/kg/day for 3 days; and group D (n = 7), superoxide dismutase 60,000 units administered with 50,000 units before removal of the aortic crossclamp and 10,000 units over 10 minutes of reperfusion. Proximal hypertension was controlled with sodium nitroprusside and volume depletion. The methods of assessment were neurologic by a modified Tarlov criteria and blood flow by radiolabeled microspheres. Results of blood flow assessment confirmed a true ischemic episode of 30 minutes for all animals in all groups. The blood flow fell significantly during ischemia (p less than 0.01) and a hyperemic response was evident in the early reperfusion period. All animals in control group A were paraplegic. The group B (deferoxamine) results were superior; 85% had grade III function on a modified Tarlov scale, with animals in the group standing and even walking with difficulty. Only one animal in this group had good movements of hind limbs but was unable to stand or walk. Neurologic recovery was limited in the allopurinol group (group C), with 85% showing slight neurologic recovery with limited movement of the hind limbs. The animals in the superoxide dismutase group (group D) all had good recovery, with strong motor response of hind limbs, but were not able to stand. In summary, the results of this experimental protocol confirmed the possible role of oxygen-derived free radicals in the pathophysiology of spinal cord injury, induced by aortic crossclamping. Moreover, it proved that ischemia-reperfusion injury could be altered by pharmacologic interventions.
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PMID:Pharmacologic interventions for prevention of spinal cord injury caused by aortic crossclamping. 149 87

The prevalence of morbidity is a major deterrent to the success of aortic aneurysm replacement operations. We have developed a model of spinal cord ischemia, based on the amplitude reduction of the motor-evoked potential, which produces approximately a 90% prevalence of paraplegia. Regional blood flow was studied with the use of radioactive microspheres, and results showed that there was a significant decrease in flow to the lumbar cord (85% reduction) during aortic occlusion, followed by a twofold to threefold hyperemia that persisted for 24 hours. Histopathologic examination of the cord revealed that the greater portion of microgliosis, spongiosis, and neuronal damage was confined to the gray matter of the cord, and its severity increased as one progressed caudally. The somatosensory-evoked potential disappeared before the motor-evoked potential L-2 signal in all dogs, with a mean disappearance time of 10.9 +/- 5.6 minutes, compared with 21 +/- 6.6 minutes for the motor-evoked potential. Both the sensory-evoked potential and the motor-evoked potential cord signal were present 24 hours later in all dogs tested. The peripheral nerve motor-evoked potential disappeared within 1 minute of cord ischemia, was not present 24 hours later, and hence appears to be too sensitive to use as an indicator of spinal cord damage. Plotting spinal cord motor-evoked potential amplitude reduction versus both histopathologic damage and regional blood flow revealed a positive correlation between motor-evoked potential amplitude reduction, decreased cord perfusion, and increased histopathologic damage. In addition, it may be possible to make inferences about the neurologic status of a subject based on the magnitude and time-course of the motor-evoked potential's amplitude reduction and wave morphology.
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PMID:Correlation of motor-evoked potential response to ischemic spinal cord damage. 149 88

Postoperative paraplegia is a relatively rare complication in reconstructive surgery for coarctation of the aorta and the operative treatment is usually performed without any adjuncts. A 59-year-old male patient underwent replacement of descending thoracic aorta with vascular prosthesis under the monitoring of SEP and spinal cord perfusion pressure (SCPP) [pressure difference between mean distal aortic pressure (MDAP) and the cerebrospinal fluid pressure (CSFP)]. During cross-clamping of the aorta, MDAP decreased from 61 to 40 mmHg and CSFP increased from 6 to 15 mmHg, SCPP was 25 mmHg, and the amplitude of the SEP waves rapidly decreased. As the ischemic changes of spinal cord were suspected, the aortic cross-clamping was released. The amplitude of SEP recovered to the preoperative level immediately after de-clamping. In order to prevent spinal cord ischemia, the partial cardio-pulmonary bypass was employed, and SCPP was maintained above 60 mmHg, so that SEP did not show any ischemic changes during cross-clamping of the aorta. The patient did not develop any neurological deficit postoperatively. The monitoring of SEP and SCPP appears to be useful for prevention of postoperative paraplegia in the surgical treatment for coarctation of the aorta.
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PMID:[Reconstructive surgery in 59-year-old patient with coarctation of aorta under the monitoring of somatosensory evoked potential and spinal cord perfusion pressure]. 156 47

Between May 1966 and June 1991, 129 patients underwent surgical repair of thoracoabdominal aneurysms, with an overall 30-day mortality rate of 35%. In 75 operations (58%) performed electively, 11 deaths (15%) occurred, and in 54 cases (42%) of either symptomatic or ruptured aneurysms 34 deaths (63%; p less than 0.001) occurred. No one survived among six patients with preoperative hypotension (less than 90 mm Hg) or cardiac arrest. In 16 patients (12%) the etiology of aneurysms was a result of chronic aortic dissection, and the mortality rate in this subgroup was 44%. In the remaining 113 patients (88%) where the etiology was atherosclerosis, 38 deaths occurred (34%; p = 0.433). Spinal cord ischemia occurred in 25 cases (21%) among 116 patients who survived operation. Partial ischemia occurred in six cases (25%), and complete paraplegia occurred in the remainder. Complete and partial paraplegia occurred in 16 of 42 cases (38%) when all of the thoracic aorta was replaced (Crawford groups I, II) and in 9 of 74 cases (12%) when only the abdominal or lower thoracic aorta was replaced (Crawford groups III, IV; p = 0.016). Other complications included myocardial infarction (14 cases, 11%), respiratory failure (46 cases, 36%), and renal failure (33 cases, 27%). The major prospect for improved early survival of patients with thoracoabdominal aneurysms seems to be early detection and elective repair before the occurrence of symptoms.
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PMID:Thoracoabdominal aneurysm repair: a representative experience. 157 33

Infrarenal circumaortic occlusion devices were operatively placed in 74 New Zealand white rabbits. Two days after operation the animals were randomly assigned to one of seven treatment groups: I, control, n = 23; II, halothane, n = 8; III, thiopental, n = 12; IV, ketamine (30 mg/kg intravenously), n = 6; V, halothane+hypothermia, n = 8; VI, thiopental+hypothermia, n = 12; VII, ketamine+hypothermia, n = 5. In each group, the infrarenal aorta was occluded for 21 minutes. Final neurologic recovery after restitution of blood flow was graded as acute paraplegia, delayed paraplegia (neurologic deficit developing after initial recovery), or normal. Halothane alone was of no benefit. Hypothermia with any anesthetic was completely protective and reduced neurologic deficits to 0% compared with 91% in controls (p less than 0.05). Thiopental and ketamine treatment each reduced acute paraplegia to 17% (as compared with 61% in controls) and increased delayed paraplegia from 30% in controls to 75% and 50%, respectively (p less than 0.05 for thiopental, p = 0.10 for ketamine). The authors interpret the increase in delayed deficits and decrease in acute deficits as being the result of partial spinal cord protection. These findings document that this model of spinal cord ischemia is sufficiently sensitive to identify interventional treatments that protect the ischemic spinal cord.
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PMID:Protecting the ischemic spinal cord during aortic clamping. The influence of anesthetics and hypothermia. 161 78

A case of acute aortic dissection (AAD) presenting as sudden, transient paraplegia and severe back pain is reported. The patient was a 66-year-old male with a 10-year-history of hypertension. The pain characteristically migrated from the back to the neck and then returned to the back. He showed complete transverse myelopathy at the level of the 9th thoracic cord. Computed tomography disclosed internal displacement of aortic intimal calcifications, without abnormalities in the spinal canal, and myelography showed no spinal canal block or stenosis. Electrocardiography and chest x-ray indicated nonspecific changes of high amplitudes and mild cardiomegaly, respectively. Together, these findings suggested acute aortic dissection with spinal cord ischemia. The initial systolic blood pressure of 220 mmHg was lowered with medication, and the pain was controlled with morphine. He recovered fully and was discharged 80 days after the onset of symptoms, with no neurological deficits. AAD carries a very poor prognosis unless treated immediately. Therefore, it is very important to promptly differentiate this disorder from spinal vascular conditions that also produce back pain and paraparesis.
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PMID:Transient paraplegia caused by acute aortic dissection--case report. 169 75

The Nauta impregnation method was used to map the neuronal changes in the canine lumbosacral segments following ischemia and reperfusion. The early perikaryal changes ensuing during the first phase after 30 min of thoracic aorta cross-clamping alone or followed by 30 min of reperfusion were mapped. During the second phase (one to six postischemic reperfusion days) the dendritic, preterminal and synaptic degeneration developed. The influence of 30 min cross-clamping immediately followed by perfusion fixation is characterized by the occurrence of flocculent argyrophilic clusters in the cytoplasm of middle-sized and large neurons of L3-S1 segments. Declamping of the thoracic aorta followed by 30 min of reperfusion basically modifies the susceptibility of lumbosacral neurons to Nauta impregnation promoting somatic and dendritic argyrophilia mainly of small (less than 15 microns) neurons, localized mostly in the fifth, sixth and seventh layers, respectively. This early appearing somatic and dendritic argyrophilia is not abolished by a pretreatment of sections with acetone in which cholesterol and its esters are highly soluble, or chloroform-methanol which extracts total lipid. After 24 h of reperfusion the somatic and dendritic argyrophilia is lost but the first signs of drop-like degeneration are detected in all but three superficial dorsal horn layers. At the end of the third reperfusion day, an atypical form of bouton degeneration was found, consisting of massive occurrence of enlarged (greater than 4 microns) boutons encircled by a clear halo. Laminar distribution of enlarged degenerating boutons coincides with laminar quantitative distribution of small argyrophilic neurons detected 30 min after reperfusion. The basic orientation of the many terminal fibres attached to enlarged boutons suggests that they belong to the axons localized mainly in the lateral and anterior columns. Despite a dense argyrophilic network pervading the gray matter of lumbosacral segments only pale shadows of middle-sized and large neurons were found at the end of the sixth reperfusion day and neither somatic nor vessel wall argyrophilia could be detected. All animals surviving one, three and six days postoperatively suffered from fully developed paraplegia.
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PMID:Mapping of the canine lumbosacral spinal cord neurons by Nauta method at the end of the early phase of paraplegia induced by ischemia and reperfusion. 172 92

We tested, in the dog, the hypothesis that selective deep hypothermia (19 degrees to 12 degrees C) of the spinal cord protects it from the ischemia that follows double aortic cross-clamping. The extracorporal perfusion system consisted of heat exchanger and a pump, infusing saline solution at 5 degrees C into the subarachnoid space (L-6) and draining it through the cisterna magna. After 30 minutes this system cools a normally perfused spinal cord to a stable temperature gradient of 13 degrees C (inflow) to 18 degrees C (outflow). Proximal and distal intrathecal, proximal and distal aortic, and central venous pressures were continuously recorded. Rectal temperature was maintained between 36.5 degrees C and 38.5 degrees C. Eight control dogs had cross-clamping of the aorta below the left subclavian artery and above the diaphragm without cord hypothermia. Nine experimental dogs had cord hypothermia initiated 50 minutes before systemic heparinization (100 U/kg) and double cross-clamping of the aorta. Cross-clamping was maintained for 45 minutes. The aorta was then unclamped, heparin was reversed, cord cooling was discontinued, and the dura was closed. Hindlimb function of animals was graded by use of Tarlov's scale at recovery and 24 hours later. The dogs were then killed, and the cords were removed and fixed for microscopy. All control animals were paraplegic and had histologic confirmation of spinal cord infarction. All experimental animals had intact hindlimb function and normal appearing cords on histologic examination. A two-tailed Fisher's exact test (chi square) shows this difference to be significant to p = 0.00004. In the dog selective deep hypothermia of the cord avoids the ischemic injury induced by aortic cross-clamping that results in paraplegia. The implications of these findings in thoracoabdominal aortic clamping in humans is discussed.
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PMID:Selective deep hypothermia of the spinal cord prevents paraplegia after aortic cross-clamping in the dog model. 172 92

Improvements in the operative management of acute traumatic thoracic aortic aneurysm have resulted in safe and expeditious repair. Nonetheless, multisystem injuries continue to inflict significant numbers of deaths. From 1970 to 1990, 108 patients with acute traumatic thoracic aortic aneurysm were evaluated. Mean injury severity score, excluding aortic injury, was 17.5. Ninety-three patients (86%) survived beyond initial resuscitation and came to operation. Median interval from injury to aortic repair was 8 hours (range, 2 hours to 19 days); there were five operative deaths. Lethal nonaortic injuries included 18 closed head injuries, four myocardial contusions, two intraabdominal vascular injuries, and one pulmonary contusion. The overall mortality rate was 39% of total admissions (42 of 108), and 29% of survivors of resuscitation (27 of 93). It is significant that only 11 of the 42 deaths (26%) were directly attributable to thoracic aortic aneurysm. Adjuncts to prevent spinal cord ischemia (shunt/bypass) were used in 76 patients, whereas 12 underwent clamp/repair. Postoperative paraplegia developed in 5 of 79 patients (6.8%, including 4 of 68 (5.9%) repaired with shunt/bypass and 1 of 11 (9.1%) repaired with clamp/repair (p = NS). Among those who developed paraplegia, the injury severity score was 27.0, and the median interval from injury to repair was 4.9 hours (range, 2 to 6.5). Intraoperative hypotension occurred in three of five patients with paraplegia. Death in patients with thoracic aortic aneurysm is due primarily to associated injuries and has remained relatively constant over the 20-year period of review. Overall injury severity, intraoperative hypotension, and extensive aortic tissue destruction may correlate with the development of postoperative paraplegia; however, a larger population sample is required to confirm this conclusion. A plea is made for standardized reporting of all patients with thoracic aortic aneurysm.
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PMID:Acute traumatic aortic aneurysm: the Duke experience from 1970 to 1990. 173 94


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