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PubMed2005

Embolic stroke complicating Staphylococcus aureus endocarditis circumstantially linked to rectal trauma from foreign body: a first case report.

BACKGROUND: Diagnostic and therapeutic instrumentation of the lower gastrointestinal tract has been reported to result in bacteremia and endocarditis. No such case has been reported in persons with a history of rectal foreign body insertion despite its potential for greater trauma. CASE PRESENTATION: A 58-year-old male was admitted with confusion and inability to speak. His past history was notable for hospitalization to extract a retained plastic soda bottle from the rectosigmoid two years prior. On examination, he was febrile, tachycardic and hypotensive. There was an apical pansystolic murmur on cardiac examination. He had a mixed receptive and expressive aphasia, and a right hemiparesis. On rectal examination he had perianal erythema and diminished sphincter tone. Magnetic resonance imaging of the brain showed infarction of the occipital and frontal lobes. Transesophageal Echocardiography of the heart revealed vegetations on the mitral valve. All of his blood culture bottles grew methicillin sensitive Staphylococcus aureus. He was successfully treated for bacterial endocarditis with intravenous nafcillin and gentamicin. The rectum is frequently colonized by Staphylococcus aureus and trauma to its mucosa can lead to bacteremia and endocarditis with this organism. In the absence of corroborative evidence such as presented here, it is difficult to make a correlation between staphylococcal endocarditis and anorectal foreign body insertion due to patients being less than forthcoming CONCLUSION: There is a potential risk of staphylococcal bacteremia and endocarditis with rectal foreign body insertion. Further studies are needed to explore this finding. Detailed sexual history and patient counseling should be made a part of routine primary care.

Endocarditis, Bacterial↗
PubMed1994

Embolic stroke after unanticoagulated cardioversion despite prior exclusion of atrial thrombi by transoesophageal echocardiography.

Recent studies in patients with atrial fibrillation, not on anticoagulation, suggest that if transoesophageal echocardiography (TEE) excludes the presence of thrombi, early cardioversion can be performed safely without the need for anticoagulation before the procedure. Immediately after successful cardioversion, however, left atrium or left atrial appendage stunning may be present, potentially carrying a risk for de novo thrombus formation. Furthermore, the presence of spontaneous contrast is considered as a contraindication for unanticoagulated cardioversion since it has been associated with postcardioversion thromboembolism. We present a case in which stroke developed in relation to unanticoagulated cardioversion regardless of careful prior evaluation with TEE.

Aged↗
PubMed2001

Patency of cerebral microvessels after focal embolic stroke in the rat.

In patients with thrombotic stroke, the occluded artery often reopens over time. This results through a natural dissolution of the occluding material, and fragments of the material may move downstream to obstruct distal arteries. The current study was undertaken to investigate the patency of brain microvessels at varying time intervals after injection of a preformed clot into the right internal carotid artery of rats. Cerebral microvessels in brain sections were visualized using immunohistochemistry for fibronectin (detecting existing microvessels) and Evans blue (visualizing perfused microvessels). The percentage of patent microvessels was calculated as the number of Evans blue-positive microvessels divided by the number of fibronectin-positive microvessels. In normal control animals, results showed that 98% +/- 3% (mean +/- SD) of microvessels in the cortex and 94% +/- 14% in the striatum were patent. In the ischemic animals, immediately after clot injection, microvessels in the cortex and striatum were occluded, mainly in the territory irrigated by the middle cerebral artery. One hour after clot injection, microvessels had reopened in most of the cortex but remained occluded in some portions of the striatum, possibly as a result of downstream movement of fragments formed from the original clot. By 3 hours after clot injection, microvessels in the cortex were patent in all animals, whereas in the striatum microvessels were patent in 50% of the animals. In the other 50%, small striatal perfusion deficits persisted. At 24 hours after clot injection, microvessels were patent in both the cortex and striatum of all animals except one. These findings suggest that intracerebral clots dissolve spontaneously in a relatively short period of time, but that fragments formed from the clot may obstruct more distal blood vessels. It is likely that clot fragments lodge in arteries with lower blood flow and poor collateral perfusion, where they continue to cause ischemia for a longer duration. These results may in part explain the resistance of the striatum to neuroprotective strategies used for the treatment of focal cerebral ischemia.

Animals↗
PubMed1998

Reperfusion after thrombolytic therapy of embolic stroke in the rat: magnetic resonance and biochemical imaging.

The effect of thrombolytic therapy was studied in rats submitted to thromboembolic stroke by intracarotid injection of autologous blood clots. Thrombolysis was initiated after 15 minutes with an intracarotid infusion of recombinant tissue-type activator (10 mg/kg body weight). Reperfusion was monitored for 3 hours using serial perfusion- and diffusion magnetic resonance imaging, and the outcome of treatment was quantified by pictorial measurements of ATP, tissue pH, and blood flow. In untreated animals, clot embolism resulted in an immediate decrease in blood flow and a sharp decrease in the apparent diffusion coefficient (ADC) that persisted throughout the observation period. Thrombolysis successfully recanalized the embolized middle cerebral artery origin and led to gradual improvement of blood flow and a slowly progressing reversal of ADC changes in the periphery of the ischemic territory, but only to transient and partial improvement in the center. Three hours after initiation of thrombolysis, the tissue volume with ADC values less than 80% of control was 39 +/- 22% as compared to 61 +/- 20% of ipsilateral hemisphere in untreated animals (means +/- SD, P = .03) and the volume of ATP-depleted brain tissue was 25 +/- 31% as compared to 46 +/- 29% in untreated animals. Recovery of ischemic brain injury after thromboembolism is incomplete even when therapy is started as early as 15 minutes after clot embolism. Possible explanations for our findings include downstream displacement of clot material, microembolism of the vascular periphery, and events associated with reperfusion injury.

Adenosine Triphosphate↗
PubMed1987

Left atrial metastasis presenting as recurrent embolic strokes.

Tumour emboli from an endocardial metastasis of an endometrial stromal sarcoma caused recurrent and ultimately fatal strokes in a woman of 40. Endocardial metastases are rare. They are known to embolise to the pulmonary and systemic arteries but not to cause recurrent cerebral emboli.

Adult↗
PubMed1999

Three-dimensional measurement of cerebral microvascular plasma perfusion, glial fibrillary acidic protein and microtubule associated protein-2 immunoreactivity after embolic stroke in rats: a double fluorescent labeled laser-scanning confocal microscopic study.

Early astroglial response to post-ischemic microvascular hypoperfusion may contribute to progressive cerebral microcirculatory impairment and ischemic neuronal injury. Using laser-scanning confocal microscopy and three fluorescent probes, we measured in three-dimensions cerebral microvascular plasma perfusion, astrocytic reactivity, and neuronal injury assessed by fluorescein isothiocyanate (FITC)-dextran, GFAP immunoreactivity, and microtubule associated protein-2 (MAP2) immunoreactivity, respectively, in rats subjected to 2 h of middle cerebral artery occlusion. Three-dimensional quantitative analysis revealed that 2 h of embolic ischemia resulted in a significant (P<0.05) reduction of cerebral microvascular plasma perfusion in the ipsilateral cortex and subcortex. Tissue within the ipsilateral cortex and subcortex with low plasma perfusion exhibited a significant (P<0.05) increase in GFAP immunoreactivity compared with the homologous contralateral tissue. Three-dimensional re-constructed images showed that prominent GFAP immunoreactive astrocytes surrounded large vessels with decreased plasma perfusion in downstream capillaries in the ipsilateral MCA territory when compared to the vessels in the contralateral homologous tissue. Triple fluorescence probe-stained sections showed that tissue with decreased plasma perfusion and with increased GFAP immunoreactivity was accompanied by a reduction of MAP2 immunoreactivity. The present study demonstrates that an impairment of microvascular perfusion induces an early increase in GFAP immunoreactivity, and reactive astrocytes may contribute to a further reduction of cerebral microvascular plasma perfusion. The three-dimensional quantitative imaging analysis used in the present study provides a means to investigate parenchymal cellular responses to changes of cerebral microvascular plasma perfusion after MCA occlusion.

Animals↗
PubMed1992

Recombinant tissue plasminogen activator in acute thrombotic and embolic stroke.

An open angiography-based, dose rate escalation study on the effect of intravenous infusion of recombinant tissue plasminogen activator (rt-PA) on cerebral arterial recanalization in patients with acute focal cerebral ischemia was performed at 16 centers. Arterial occlusions consistent with acute ischemia in the carotid or vertebrobasilar territory in the absence of detectable intracerebral hemorrhage were prerequisites for treatment. After the 60-minute rt-PA infusion, arterial perfusion was assessed by repeat angiography and computed tomography scans were performed at 24 hours to assess hemorrhagic transformation. Of 139 patients with symptoms of focal ischemia, 80.6% (112) had complete occlusion of the primary vessel at a mean of 5.4 +/- 1.7 hours after symptom onset. No dose rate response of cerebral arterial recanalization was observed in 93 patients who completed the rt-PA infusion. Middle cerebral artery division (M2) and branch (M3) occlusions were more likely to undergo recanalization by 60 minutes than were internal carotid artery occlusions. Hemorrhagic infarction occurred in 20.2% and parenchymatous hematoma in 10.6% of patients over all dose rates, while neurological worsening accompanied hemorrhagic transformation (hemorrhagic infarction and parenchymatous hematoma) in 9.6% of patients. All findings were within prospective safety guidelines. No dose rate correlation with hemorrhagic infarction, parenchymatous hematoma, or both was seen. Hemorrhagic transformation occurred significantly more frequently in patients receiving treatment at least 6 hours after symptom onset. No relationship between hemorrhagic transformation and recanalization was observed. This study indicates that site of occlusion, time to recanalization, and time to treatment are important variables in acute stroke intervention with this agent.

Acute Disease↗
PubMed1988

Embolic stroke from cardiac papillary fibroelastomas.

We describe two patients with cerebral emboli originating from a cardiac papillary fibroelastoma and compared them with six patients reported in the literature. Surgical excision was curative in both of our patients. The surface topography of the tumor, as visualized by scanning electron microscopy, is described.

Adult↗
PubMed1991

Embolic stroke following carotid radiation angiopathy demonstrated with I-123 IMP brain SPECT.

Radiation angiopathy was developed by the process of accelerated atherosclerosis at the site of irradiation. The case of a 44-year-old man with right hemiparesis showing a high signal intensity in the left semioval center on MRI and a defect in the left temporo-parietal area with subsequent filling-in with I-123 IMP brain SPECT is reported. Digital subtraction angiography showed typical radiation angiopathy with ulceration in the left common carotid artery. Twenty-four years previously, he underwent curative irradiation of a neck mass that revealed Hodgkin's disease by biopsy. The emboli formed at the site of radiation-induced angiopathy and caused cerebral infarction. The perfusion abnormality in the territory of the embolic artery was detected by I-123 IMP SPECT. Long-term survivors of neck irradiation are at high risk for the development of carotid arterial disease and should be watched carefully.

Adult↗
PubMed1993

Thrombolytic intervention in acute thrombotic and embolic stroke.

Stroke is one of the leading causes of death in the industrial nations of the world. Up to now, there has been no therapeutic strategy available which has been proven by controlled clinical trials. In the majority of acute stroke patients acute thrombosis contributes to carotid and vertebrobasilar arterial occlusions. Therefore, significant interest has focused on the possible value of fibrinolytic therapy in acute stroke. The principal goal is the rapid lysis of occluding thrombus with a minimum risk of intracranial or systemic hemorrhage. Clinical investigations on thrombolysis in cerebrovascular ischemia included different plasminogen-activators such as urokinase, streptokinase, and tissue plasminogen activator, either given systemically or locally via an intraarterial catheter. The pivotal trials conducted so far have revealed a wide range of recanalization rates, an acceptable safety and, also, encouraging effects on neurologic outcome. Thrombolysis itself carries the risk of intracranial bleeding, a practical limitation of this approach in acute stroke. On the other hand, hemorrhagic infarction and parenchymatous hematoma are natural consequences of thromboembolic stroke, possibly as a result of persistent occlusion of an artery. Hemorrhage following thrombolysis seems to show the same features seen in untreated patients and with an incidence similar to that in untreated patients. Future developments in thrombolysis in acute stroke should include improved early recruitment of patients, evaluation of noninvasive techniques in the pretreatment assessment of patients, the evaluation of advanced invasive techniques for delivery of the thrombolytic agent and assessment of combined treatment strategies. Clinical studies evaluating these strategies are currently under way.

Cerebral Hemorrhage↗
PubMed1994

Enhancement of serotonergic immunoreactivity in sympathetic cerebrovascular nerve fibers after experimental embolic stroke.

We examined 5-hydroxytryptamine-like immunoreactive cerebrovascular nerve fibers in rats after experimental thromboembolic stroke. Although there were no visible 5-hydroxytryptamine-like immunoreactive nerve fibers in normal animals, we found many of these fibers near the clot emboli 30 min after the stroke, and the number of fibers increased slightly with time. In immunohistochemical double staining, these fibers corresponded to neuropeptide Y-like immunoreactive nerve fibers. And they were not observed in animals after superior cervical ganglionectomy. These findings suggest that the sympathetic nerves take up serotonin released from intraluminal aggregating platelets.

Animals↗
PubMedDate not supplied

Embolic stroke in a child with idiopathic dilated cardiomyopathy.

An eleven year old boy presented with sudden onset right-sided hemiplegia and ipsilateral lower facial weakness. Two-dimensional echo revealed the diagnosis of idiopathic dilated cardiomyopathy with multiple intracardiac clots. MRI scan of head showed infarctions in the area of caudate nuclei, putamen, brain stem and cerebellum. On anticoagulation therapy, all thrombi, except one, disappeared. The child died 2.5 months later due to resistant cardiac failure.

Anticoagulants↗
PubMed1996

Good clinical outcome in a patient with a large CT scan hypodensity treated with intra-arterial urokinase after an embolic stroke.

Hypodense regions demonstrated by CT within 6 hours of the onset of stroke may reflect irreversibly damaged tissue, and some have suggested that patients with such findings should be spared the risks of thrombolytic therapy since they are unable to benefit from it. We report here a patient with a low-density area demonstrated by CT less than 6 hours after onset of symptoms who improved dramatically after successful intra-arterial thrombolysis.

Cerebral Angiography↗
PubMed1979

Angiographically undetected ulceration of the carotid bifurcation as a cause of embolic stroke.

The accuracy of angiographic diagnosis of carotid artery ulceration was evaluated. Of those carotid bifurcations showing ulceration at surgery, 60% were diagnosed as having ulcers at angiography. Half of the remaining ulcers occurred in smooth, benign-appearing plaques and were too small to be seen at angiography. An incorrect angiographic diagnosis of ulceration was made in 17 of 50 carotid arteries; in most cases this was due to the presence of a subintimal hematoma in the wall of the artery.

Carotid Artery Diseases↗
PubMed1985

Nonseptic cardiogenic cerebral embolic stroke: clinical-CT correlations.

We studied 35 patients with nonseptic cardiogenic cerebral emboli. In 28 cases, there was sudden onset with maximal neurologic deficit within 1 hour; in 7 cases, there was progression in 24 hours. In six cases, neurologic abnormality worsened in the first week after an initial period of stabilization. CT showed evidence of a cerebral infarct in all cases; in nine cases, this was hemorrhagic. There was more than one lesion in six cases. In four of the six cases with delayed neurologic deterioration, later CT showed increased mass effect or recent hemorrhage within the infarct.

Adult↗
PubMed1987

Clot embolic stroke in the vertebrobasilar system of rabbits: a transfemoral angiographic technique.

Previous animal models of thromboembolic stroke have focused upon the carotid artery system. An alternative approach utilizing the vertebrobasilar system in rabbits is presented here. Left vertebral artery catheterization was accomplished relatively simply in this model using transfemoral angiographic techniques. Twenty-four-hour-old clot emboli with calculated volumes in the range of 0.007-0.11 cc were delivered by this route and found to lodge at the juncture of the basilar tip and the Circle of Willis in 11 of 13 rabbits. Intra-arterial infusion of streptokinase in one animal resulted in angiographically complete clearing of clot. Certain technical advantages in this particular approach are discussed.

Animals↗