naloxone and Aortic-Dissection

Acute distal aortic dissection rarely causes spinal cord ischemia presenting with paraplegia or paraparesis. Spinal cord involvement has poor outcomes, and there is no established effective treatment for this disorder. In this report we describe the acute conservative treatment of two cases of paraplegia/paraparesis due to acute type B aortic dissection. Early reversal of lower-limb dysmobility was achieved.

Topics: Aged; Antihypertensive Agents; Aortic Aneurysm; Aortic Dissection; Cardiovascular Agents; Cerebrospinal Fluid; Drainage; Humans; Male; Naloxone; Paraparesis; Spinal Cord Injuries

Although naloxone has been used to prevent ischemic spinal cord injury (SCI), its effect on excitatory amino acids (EAAs) has not been understood. We investigated the clinical significance of naloxone by measuring EAAs in the cerebrospinal fluid (CSF) in patients undergoing thoracoabdominal aortic surgery.. Twenty-seven patients (15 men and 12 women; mean age, 66 +/- 12 years) undergoing prosthetic replacement of the thoracoabdominal aorta (n = 19) or the descending thoracic aorta (n = 8) from April 1997 to June 2003 under distal perfusion and mild hypothermia were enrolled in this cohort study with historical controls. Their etiology was 7 dissections and 20 nondissections. In 16 patients (naloxone group), intravenous infusion of naloxone (1 microg/kg/h) was continued until the patients became alert. In the remaining 11 patients (control group) naloxone was not given. CSF drainage was used in all patients. CSF levels of EAAs, glutamate, aspartate, and glycine were measured at 6 points in time until 72 hours postoperatively, using a high-performance liquid chromatography method.. In 5 patients with SCI (2 patients in control group, 3 in naloxone group), CSF levels of glutamate and glycine continued to increase even at 72 hours postoperatively, and were significantly more elevated than those in patients without SCI ( P < .0001, glutamate; P = .0006, glycine). Postoperative maximum levels of CSF glutamate and glycine were also significantly higher in patients with postoperative SCI than in patients without SCI (glutamate: 215.3% +/- 158.6% vs 32.9% +/- 37.3% increase from baseline, P < .0001; glycine: 309.1% +/- 218.2% vs 89.2% +/- 103.1% increase from baseline, P = .0036). CSF levels of glutamate and aspartate in naloxone group were significantly lower than those in control group ( P = .0161, glutamate; P < .0001, aspartate). Postoperative maximum level of CSF aspartate was also significantly lower in the naloxone group than in the control group (8.3% +/- 75.5% vs 119.7% +/- 120.6% increase from baseline, P = .0077). In multivariate logistic regression analysis, postoperative maximum CSF glutamate >100% from baseline ( P < .001) and postoperative maximum level of CSF glycine ( P = .005)were identified as the independent risk factors for SCI. Both SCI ( P < .001) and postoperative maximum level of CSF glycine ( P = .005) were the independent predictors for postoperative maximum level of CSF glutamate >100% from baseline.. CSF levels of EAAs are elevated in patients with SCI. CSF glutamate is the strongest independent predictor of SCI. Naloxone is effective in lowering CSF levels of EAAs.

Topics: Adult; Aged; Aorta, Abdominal; Aorta, Thoracic; Aortic Aneurysm; Aortic Dissection; Blood Vessel Prosthesis Implantation; Cohort Studies; Excitatory Amino Acids; Female; Humans; Male; Middle Aged; Naloxone; Narcotic Antagonists; Spinal Cord Injuries; Treatment Outcome

Forty-seven patients who were treated for thoracoabdominal or thoracic aneurysms over a 5 1/2-year period were analyzed for neurologic deficit risk. Patients were divided into two groups for analysis. Twenty-four patients, who were treated from January 1984 to December 1986, did not undergo spinal fluid drainage or naloxone administration (group A). Twenty-three patients, who were treated from January 1987 to August 1989, had spinal fluid drainage (group B); 12 patients in this group also received naloxone as an intravenous drip at 1 microgram/kg/hr for 48 hours after surgery. Permanent neurologic deficits occurred in seven (29%) group A patients but in only one (4%) group B patient, who did not receive naloxone (p less than 0.03). The first two group B patients to receive naloxone showed complete reversal of neurologic deficits on waking from anesthesia. This significant reduction in neurologic deficit was associated with an increased 1-year survival rate (72% in group A, 91% in group B). We conclude that the use of naloxone and spinal fluid drainage reduces the incidence of neurologic deficit that is associated with repair of thoracoabdominal and thoracic aortic aneurysms. This reduction in neurologic deficit is associated with improved survival in the long term. The observed reversal of postoperative neurologic deficits with naloxone implicates opiates as a major factor in the pathophysiology of spinal cord ischemia.

Topics: Adult; Aged; Aged, 80 and over; Aorta, Abdominal; Aorta, Thoracic; Aortic Aneurysm; Aortic Dissection; Drainage; Humans; Middle Aged; Naloxone; Nervous System Diseases; Postoperative Complications; Regression Analysis; Risk Factors; Survival Analysis