EC-IC bypass 10 years later: is it valuable?
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Biomedical subjects
Publications and source records attributed to D G Piepgras.
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OBJECTIVE: Reducing surgical risks to the minimum in carotid endarterectomy has become crucial, especially with the results of recent clinical trials extending indications to asymptomatic patients. The use of the saphenous vein patch graft (SVPG) has been suggested to reduce early postoperative thrombosis and cerebral infarct as well as late recurrent stenosis. However, the exact risks and complications involved in this technique are not known. METHODS: During a 23-year period (1972-1994), 2888 carotid endarterectomies with SVPG for primary carotid stenosis were performed by the Neurosurgical Cerebrovascular Service at the Mayo Clinic. The data from all patients were retrospectively analyzed, emphasizing postoperative complications related to SVPG. RESULTS: There were five postoperative vein ruptures (0.17%), four cases of aneurysm formation, and three cases of deep infection necessitating surgical intervention. The vein patch ruptured in one male patient and four female patients (mean age, 69 yr). All ruptures occurred within 4 days of the primary operation, including two during the first 24 hours. All patients with rupture underwent emergency surgery and were found to have intact suture lines and tears in the middle of the grafts. Two patients recovered without deficits, one suffered major disability, and the other two died. Aneurysm of the patch developed in two male patients and two female patients (mean age, 71 yr). All of the patients developed painless pulsatile neck masses 1 to 9 years after the initial surgery; two also had recurrent ischemic symptoms. All of the patients with aneurysms underwent surgical correction without consequences. CONCLUSION: Although the benefit of routine use of SVPG in carotid endarterectomy is still the focus of debate, this analysis showed that its use adds a small but definite risk of serious complications related to inherent weakness of the venous tissue. If a surgeon chooses to use a patch graft, our recommendation is for use of a synthetic material rather than vein.
OBJECTIVE: The number of patients with congenital heart disease who survive to adolescence and adulthood continues to increase. We review our experience with noninfectious intracranial aneurysms and cervicocephalic arterial dissections in patients with congenital heart disease, expanding the clinical spectrum of the cerebrovascular abnormalities that may be encountered in this group of patients. METHODS: All patients with congenital heart disease and intracranial aneurysms of cervicocephalic arterial dissections, who were evaluated at the Mayo Clinic between 1969 and 1992, were identified. RESULTS: Congenital heart disease was diagnosed in 3 (8%) of 36 children with intracranial aneurysms, in 5 (0.3%) of 1994 adults with intracranial aneurysms, in 1 (4%) of 25 children with cervicocephalic arterial dissections, and in 5 (2%) of 250 adults with cervicocephalic arterial dissections. The mean age of the 14 patients was 32 years (range, 13-58 yr). The congenital heart disorders consisted of complex cardiac anomalies in three patients (truncus arteriosus, transposition of the great arteries, and tricuspid atresia in one patient each), pulmonic valve or arterial stenosis in two patients, aortic coarctation in four patients, and bicuspid aortic valve in five patients. Only one patient had an intracranial aneurysm and coarctation of the aorta. CONCLUSION: Individuals with a variety of congenital heart disorders may be at an increased risk of intracranial aneurysm development and cervicocephalic arterial dissection, particularly in adolescence. The muscular arteries of the head and neck are derived from neural crest cells and the neural crest is also of major importance in early cardiac development, suggesting that an abnormality of the neural crest may be the common pathogenetic factor explaining this association.
BACKGROUND AND PURPOSE: Among patients with spontaneous cervical artery dissections, the risk of recurrent arterial dissection is relatively low at 1% per year, but this risk may be higher for patients with a family history of arterial dissections. We compared the risk of a recurrent arterial dissection in patients with familial versus non familial disease. METHODS: Long-term follow-up was established in 200 patients (104 women and 96 men with a mean age of 44.9 years) with spontaneous cervical artery dissections evaluated at a single institution between 1970 and 1990. RESULTS: Among the 200 patients, 10 (5%) were identified who had a family history of spontaneous arterial dissections. In a multivariate analysis, family history was the only significant variable associated with the risk of recurrent dissection (X2=15.51; P=.0001). A recurrent arterial dissection was identified in 5 (50%) of the 10 patients with familial disease compared with 11 (5.8%) of the 190 patients with nonfamilial disease, with an estimated relative risk of 6.3 (95% confidence interval, 2.2 to 18.3; P=.0007). CONCLUSIONS: Among patients with spontaneous cervical artery dissections, a family history of arterial dissection is an important risk factor for the development of a recurrent arterial dissection.
Cranial nerve palsy was present in 23 of 190 consecutive adult patients (12%) with spontaneous dissection of the extracranial internal carotid artery. Ten patients (5.2%) had a syndrome of lower cranial nerve palsies (with invariable involvement of cranial nerve XII with or without additional involvement of cranial nerves XI, X, and IX), seven (3.7%) had palsy of cranial nerve V, and five (2.6%) had a syndrome of ocular motor palsies. Palsy of cranial nerve VIII and ischemic optic neuropathy occurred in one patient each. Three patients had dysgeusia without other cranial nerve involvement, presumably due to involvement of the chorda tympani nerve. Headache or face pain (often unilateral) was present in 83% of patients. Other associated manifestations were cerebral ischemic symptoms, bruits, or oculosympathetic palsy. In one patient, cranial nerve palsy was the only manifestation of internal carotid artery dissection, and in another patient, the disease presented only as a palsy of cranial nerve XII and oculosympathetic palsy. In six patients, a syndrome of hemicrania and ipsilateral cranial nerve palsy was the sole manifestation of internal carotid artery dissection. Cranial nerve palsy is not rare in internal carotid artery dissection. Compression or stretching of the nerve by the expanded artery may explain some but not all of the palsies. An alternative mechanism is likely interruption of the nutrient vessels supplying the nerve.
A deficiency of alpha 1-antitrypsin has been implicated in the development of arterial aneurysms, including intracranial aneurysms. The authors determined the prevalence of alpha 1-antitrypsin deficiency of different phenotypes in 100 consecutive patients with intracranial aneurysms and compared the distribution of alpha 1-antitrypsin phenotypes to that in the general population (904 people). The study population consisted of 44 men and 56 women with a mean age of 52 years (range 15-81 years). The heterozygous alpha 1-antitrypsin deficiency states (PiMS and PiMZ) were more common in patients (16%) than in the general population (7%), providing an odds ratio of 2.56 (95% confidence interval (CI) 1.32-4.75; p = 0.005). In addition, one patient (1%) was homozygous for the deficient allele (PiZZ) compared to an expected number of 0.015, providing an odds ratio of 67.0 (95% CI 2.0-363.3; p = 0.015). These findings lead the authors to suggest that the heterozygous and homozygous alpha 1-antitrypsin deficiency states are genetic risk factors for the development of intracranial aneurysms.
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This investigation summarizes and evaluates the results of a clinical protocol that we designed to care for patients with acute liver failure (ALF). Adult patients with ALF were enrolled in the protocol. Grade II portal-systemic encephalopathy prompted admission to the intensive care unit (ICU). Patients who met the clinical criterion were activated for liver transplantation. Intracranial pressure (ICP) was monitored in patients with grade III encephalopathy. An increase in ICP was treated with hyperventilation, diuretics, barbiturates, or a combination thereof. Survival was considered to have occurred if the patient left the hospital alive. Our series included 25 patients. Orthotopic liver transplantation (OLT) was performed on 19 patients, 12 of whom survived. Only 2 of 6 patients who did not undergo transplantation survived. Ten of 11 patients who underwent transplantation before reaching grade IV encephalopathy survived. Only 2 of 8 patients who underwent transplantation after reaching grade IV survived (P = .006). The causes of death included cerebral edema (3 patients), disseminated aspergillosis (3 patients), and other (5 patients). ICP was monitored in 11 patients. Increased pressure was documented by seven of the monitors placed. There was one focal hemorrhage secondary to a subdural monitor. Outcome is improved if transplantation occurs before grade IV encephalopathy. ICP monitoring can be accomplished without significant risk of hemorrhage. In our series, infection with aspergillus occurred frequently and with fatal outcome.
Intracranial hypotension is a cause of diffuse enhancement of the pachymeninx with gadolinium, which often is associated with subdural fluid collections. We reviewed the results of meningeal biopsy in six patients with intracranial hypotension and diffuse pachymeningeal enhancement to correlate the MRI findings with histopathologic observations and to explain the abnormalities seen on MRI. Grossly, the dura mater was unremarkable in all patients, as were the leptomeninges, except for one patient with prolonged (18 months) intracranial hypotension in whom the arachnoid was thickened and opaque. Microscopically, the dura mater was entirely normal on its epidural aspect; however, a fairly thin zone of fibroblasts and thin-walled small blood vessels in an amorphous matrix was noted on the subdural aspect. In the patient with longstanding symptoms, diffuse benign arachnoidal cell proliferation was also noted, probably a reaction triggered by longstanding changes in the subdural area, as noted in the five other patients. There was no evidence of inflammation, infection, or metastatic neoplasia. These findings suggest that in intracranial hypotension, the dural-meningeal abnormalities probably represent reactive secondary phenomena, likely related to hydrostatic changes in the CSF, and not a primary meningeal process.
Some patients with aneurysmal subarachnoid hemorrhage (SAH) never reach the hospital alive ("sudden death") and, although their numbers are significant, they are not included in most studies of SAH. To clarify the clinical profile of sudden death from aneurysmal SAH, we reviewed the epidemiology and clinicopathologic features of patients with aneurysmal SAH who never reached medical attention. Using the medical record linkage system employed for epidemiologic studies for the population of Rochester, Minnesota, we identified all patients who were diagnosed with aneurysmal SAH between 1960 and 1989. There were 80 women and 33 men with a mean age of 55 years. Of these 113 patients, 13 (12%) died without reaching medical attention. The proportion of those with sudden death remained stable during the study period. In comparing patients with sudden death with those who reached medical attention, the only significant variable was the frequency of posterior circulation aneurysms that was found in 38%, compared with 14% in those who received medical attention (p = 0.042). At autopsy, intraventricular hemorrhage was present in 12 patients (92%) with sudden death, and intracerebral hemorrhage was present in two (15%). Twelve patients (92%) had acute pulmonary edema. In our community, the frequency of sudden death from aneurysmal SAH has not changed during the last three decades in spite of the advances in medical care. The typical clinical profile of sudden death in SAH includes intraventricular hemorrhage, pulmonary edema, and a ruptured posterior circulation aneurysm. Intracerebral hemorrhage is uncommonly associated with sudden death from aneurysmal SAH.
An elevated serum carcinoembryonic antigen (CEA) without evidence of neoplasia was noted in an 84-year-old woman. She subsequently developed a lytic skull lesion, which at surgery proved to be an atypical meningioma. Immunohistochemical analysis demonstrated that this tumor was producing CEA. This aggressive meningioma required two further resections and adjuvant radiotherapy in the following 18 months. Serum elevation of CEA has been reported only twice in association with meningiomas; both of those tumors were of the secretory subtype.
The first 48 hours after aneurysmal subarachnoid hemorrhage are critical in determining final outcome. However, most patients who die during this initial period are not included in hospital-based studies. We investigated the occurrence of subarachnoid hemorrhage in a population-based study to evaluate possible predictors of poor outcome. All patients diagnosed with aneurysmal subarachnoid hemorrhage between 1955 and 1984 were selected for analysis of mortality in the first 30 days using the medical record-linkage system employed for epidemiological studies in Rochester, Minnesota. One hundred and thirty-six patients were identified. The mean age of these 99 women and 37 men was 55 years. Rates for survival to 48 hours were 32% for the 19 patients with posterior circulation aneurysms, 77% for the 87 patients with anterior circulation aneurysms, and 70% for the 30 patients with a presumed aneurysm (p < 0.0001). Rates for survival to 30 days were 11%, 57%, and 53%, respectively, in these three patient groups (p < 0.0001). Clinical grade on admission to the hospital, the main variable predictive of death within 48 hours, was significantly worse in patients with posterior circulation aneurysms than in others (p < 0.0001). The prognosis of ruptured posterior circulation aneurysms is poor. The high early mortality explains why posterior circulation aneurysms are uncommon in most clinical series of patients with subarachnoid hemorrhage. The management of incidentally discovered intact posterior circulation aneurysms may be influenced by these findings.
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The familial occurrence of intracranial aneurysms has been well described. However, intracranial aneurysms are not rare and the great majority of reported families consist of only two affected members. Therefore, the familial aggregation of intracranial aneurysms could be fortuitous. The authors investigated the familial occurrence of aneurysmal subarachnoid hemorrhage (SAH) in their community to determine whether family members of patients with a ruptured aneurysm are at an increased risk of developing an SAH. All 81 patients from Rochester, Minnesota, who suffered an SAH between 1970 and 1989 from a proven aneurysmal rupture were identified, and they or their families were contacted and a family history was obtained. The number of expected SAHs among first-degree relatives was calculated using previously established age- and sex-specific incidence rates in the community of Rochester. Of the 81 index patients, 76 had complete follow up for family history. Fifteen (20%) of these 76 patients had a first- or second-degree relative with aneurysmal SAH. The number of observed first-degree relatives with aneurysmal SAH was 11, compared to an expected number of 2.66, giving a relative risk of 4.14 (95% confidence interval 2.06-7.40; p < 0.001). In the authors' community, aneurysmal SAH was familial in one of five patients, and this familial aggregation was not fortuitous. The increase in familial risk of aneurysmal SAH is approximately fourfold among first-degree relatives.
The authors report a case of a 45-year-old woman with pulsatile tinnitus who was found to have an unusual spontaneous fistula between the petrous internal carotid artery and internal jugular vein. The fistula resolved spontaneously, possibly related to daily manual compression of the ipsilateral common carotid artery. The patient also had a contralateral carotid artery dissection, multiple intracranial arachnoid cysts, and hemifacial atrophy. Her medical history was significant for easy bruisibility, abnormal scarring, and mitral valve prolapse. This association appears unique and may represent a previously underscribed generalized connective tissue disorder.
A case of repeated vertebrobasilar ischemic attacks related to head rotation (bow hunter's stroke) is reported. With head rotation of 45 degrees or more to the right, the patient would become lightheaded and feel as if she were going to lose consciousness. Angiography performed when head rotation was to the right revealed mechanical compression of the left vertebral artery at the foramen transversarium of the axis and an occluded right vertebral artery. Untethering of the vertebral artery as it passed through the foramen transversarium of the atlas in this case completely relieved the patient's symptoms. The authors conclude that contralateral vertebral artery occlusion predisposed this patient to symptomatic vertebrobasilar insufficiency secondary to ipsilateral vertebral artery mechanical stenosis induced by head turning.
To evaluate the late results and the natural history of long saphenous vein bypass grafts (SVGs) between the extracranial and intracranial circulation, the authors retrospectively analyzed 202 consecutive SVGs performed at the Mayo Clinic from 1979 to 1992. The distal anastomosis was to the vertebrobasilar system in 98 patients and to the carotid artery system in 103 patients. Surgical indications were advanced cerebroocclusive disease in 63% (127 cases), giant aneurysm in 37% (74 cases), and neoplasm in one patient. In 125 patent SVGs follow-up information was obtained for longer than 1 year and in 23 patent SVGs it was over 10 years (maximum 13 years, median 6.5 years). Most of the graft failures (76%) occurred during the 1st year after surgery, with 42% of all graft failures found during the first 24 hours after operation. Late graft attrition occurred in only 10 patients (8%). Cumulative patency at 1 year was 86% +/- 3%, at 5 years 82% +/- 4%, and at 13 years 73% +/- 19%. Neurological worsening at the time of occlusion developed in 72% of patients with early occlusion, whereas 80% of patients with late graft occlusion had no new neurological symptoms. Long-term patency of SVGs for cerebral revascularization appears to be excellent, with an average failure rate of 1% to 1.5% per year following the 1st year after surgery. To minimize early graft thrombosis, meticulous attention must be paid to technical detail.
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