Mechanisms of intracerebral hemorrhage after carotid endarterectomy

2001 ◽  
Vol 95 (6) ◽  
pp. 964-969 ◽  
Author(s):  
Robert D. Henderson ◽  
Thanh G. Phan ◽  
David G. Piepgras ◽  
Eelco F. M. Wijdicks
Keyword(s):  
Intracerebral Hemorrhage ◽  
Carotid Endarterectomy ◽  
Anticoagulation Therapy ◽  
High Rate ◽  
Control Group ◽  
Unusual Complication ◽  
Ischemic Event ◽  
Content Type ◽  
Cerebral Ischemic ◽  
Fine Print

Object. Intracerebral hemorrhage (ICH) is an uncommon complication of carotid endarterectomy (CEA), and carries a high rate of mortality and morbidity. Traditionally, attention has been focused on the cerebral hyperperfusion syndrome (HPS) as the leading cause of ICH after CEA. Other mechanisms, such as a perioperative cerebral ischemic event, cerebral infarction, and use of postoperative anticoagulation therapy, may also be important. Methods. The authors performed a retrospective case control study to identify factors leading to ICH after CEA. Records of CEAs performed over the past 10 years at the Mayo Clinic were searched for occurrences of ICH within 30 days of the procedure. The relationship of ICH to known cerebrovascular risk factors, perioperative electroencephalographic studies, and 133Xe cerebral blood flow (CBF) studies was compared with that in a control group. Hyperperfusion was defined as hypertension with symptoms of either severe headache, seizures, or confusion, or a doubling of intraoperative CBF values. The clinical history and imaging of ischemic events and the ICH were carefully reviewed to determine the possible underlying mechanism(s). Twelve (0.4%) of 2747 patients who underwent CEAs suffered a postoperative ICH. A doubling of CBF values was found in five of eight cases in which CBF studies were performed, and occurred more commonly in the patients with ICH than in controls. Clinical symptoms of the HPS were less common (three cases). A perioperative cerebral ischemic event (four cases) and anticoagulation therapy (six cases) were other contributors to a subsequent ICH. Seven of the 12 patients with ICHs died and five achieved a moderate outcome. Conclusions. An ICH following CEA is an unusual complication that occurs in the setting of hyperperfusion, perioperative cerebral ischemia, anticoagulation therapy, or multiple mechanisms. Identification of CBF doubling at surgery may assist in identifying patients at risk for ICH following CEA.

Risk of late stroke and survival following carotid endarterectomy procedures for symptomatic patients

1990 ◽  
Vol 73 (2) ◽  
pp. 193-200 ◽  
Author(s):  
Dennis A. Turner ◽  
Jay Tracy ◽  
Stephen J. Haines
Keyword(s):  
Carotid Endarterectomy ◽  
Life Table ◽  
Stroke Risk ◽  
Neurological Symptoms ◽  
Treatment Modalities ◽  
Control Group ◽  
Content Type ◽  
Postoperative Stroke ◽  
Fine Print

✓ The long-term outcome following carotid endarterectomy for neurological symptoms was analyzed using a retrospective life-table approach in 212 patients who had undergone 243 endarterectomy procedures. The postoperative follow-up period averaged 38.9 ± 2.1 months (mean ± standard error of the mean). The endpoints of stroke and death were evaluated in these patients. Patient groups with the preoperative symptoms of amaurosis fugax, transient ischemic attack, and prior recovered stroke were similar in terms of life-table outcome over the follow-up period. Sixty-two percent of symptomatic patients were alive and free of stroke at 5 years. The late risk of stroke (after 30 days postoperatively) averaged 1.7% per year based on a linear approximation to the hazard at each life-table interval (1.3% per year for ipsilateral stroke). The trend of late stroke risk was clearly downward, however, and could be fitted more accurately by an exponential decay function with a half-life of 33 months. Thus, the risk of stroke following carotid endarterectomy for neurological symptoms was highest in the perioperative period, slowly declined with time, and occurred predominantly ipsilateral to the procedure. The definition of a prospective medical control group remains crucial for a critical analysis of treatment modalities following the onset of premonitory neurological symptoms. In the absence of an adequate control group for this series, the calculated perioperative and postoperative stroke risk from this study was compared to data obtained from the literature on stroke risk in medically treated symptomatic patients. This uncontrolled comparison of treatment modalities suggests the combined perioperative and postoperative stroke risk associated with carotid endarterectomy to be modestly improved over medical treatment alone.

Postendarterectomy heparin-induced thrombocytopenia

1988 ◽  
Vol 69 (4) ◽  
pp. 632-634 ◽  
Author(s):  
Larry A. Rogers
Keyword(s):  
Platelet Count ◽  
Vascular Surgery ◽  
Carotid Endarterectomy ◽  
Potential Problem ◽  
Anticoagulation Therapy ◽  
Massive Bleeding ◽  
Drug Induced ◽  
Heparin Induced Thrombocytopenia ◽  
Content Type ◽  
Fine Print

✓ Two episodes of massive bleeding from a sutured arteriotomy were observed within 30 hours after carotid endarterectomy. The patient had received anticoagulation therapy with heparin for 72 hours prior to surgery. A platelet count of 93,000/cu mm was demonstrated following the second hemorrhage. The potential problem of drug-induced thrombocytopenia following vascular surgery is discussed.

Evaluation of the risks of anticoagulation therapy following experimental craniotomy in the rat

1985 ◽  
Vol 63 (6) ◽  
pp. 959-962 ◽  
Author(s):  
Keith L. Schaible ◽  
Lawrence J. Smith ◽  
Richard G. Fessler ◽  
Jacob R. Rachlin ◽  
Frederick D. Brown ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Anticoagulation Therapy ◽  
Early Postoperative Period ◽  
Activated Partial Thromboplastin Time ◽  
Content Type ◽  
Intracranial Surgery ◽  
Heparin Administration ◽  
Postoperative Interval ◽  
Potential Use ◽  
Fine Print

✓ The risk of hemorrhagic complications with anticoagulation therapy in patients following intracranial surgery has prevented investigation of the potential use of heparin in the early postoperative period. The authors have evaluated the safety of anticoagulation therapy following experimental craniotomy in male Holtzman rats. The dose and schedule of heparin administration, which elevated and maintained the activated partial thromboplastin time (APTT) within the therapeutic range of 15 to 3 × control APTT, was alternating doses of 400 and 500 IU/kg injected subcutaneously every 6 hours. This schedule was initiated 2, 4, 7, 10, and 14 days after craniotomy and was continued for 72 hours thereafter. The results demonstrated that the incidence of intracerebral hemorrhage declined as the postoperative interval prior to initiation of anticoagulation increased. If anticoagulation therapy was initiated during the first 7 postoperative days, the risk of intracerebral hemorrhage was high (mean 14.7%); however, if an additional 3 to 7 days elapsed prior to initiation of anticoagulation, the incidence of intracerebral hemorrhage dropped significantly (mean 0%) (p < 0.05). These results suggest that anticoagulation therapy can be safely initiated 10 to 14 days after craniotomy.

Early versus delayed heparin reversal after carotid endarterectomy in the dog

1983 ◽  
Vol 58 (5) ◽  
pp. 708-713 ◽  
Author(s):  
Mark S. Ercius ◽  
William F. Chandler ◽  
John W. Ford ◽  
William E. Burkel
Keyword(s):  
Blood Flow ◽  
Carotid Endarterectomy ◽  
Thrombus Formation ◽  
Early Period ◽  
Arterial Injury ◽  
Control Group ◽  
Content Type ◽  
Systemic Heparinization ◽  
Group 5 ◽  
Fine Print

✓ The present study investigates the hematological reaction to arterial injury during the first 10 minutes after endarterectomy in dogs to determine if heparin reversal during this early period predisposes to thrombus formation. Known platelet physiology would predict that heparinization during this early period would be useful to allow a fibrin-free platelet monolayer to form. After systemic heparinization (145 µ/kg) of the experimental animals, 42 endarterectomies were performed. Blood flow was then resumed for specific periods of time, and the vessels were prepared for scanning electron microscopy. Group 1 vessels (from the unheparinized control group) revealed mural thrombus formation after 10 minutes of blood flow. Group 2 vessels revealed the progressive formation of a fibrin-free platelet monolayer after 2, 5, or 10 minutes of blood flow resumption under systemic heparinization. Group 3 arteries, harvested at 10 minutes, underwent immediate (within 1 to 2 minutes after resumption of flow) heparin reversal with protamine sulfate, and demonstrated numerous patches of fibrin covering the platelet monolayer. Group 4 arteries, studied after 3 hours of blood flow, also underwent immediate heparin reversal. Two of these seven specimens had clumps of fibrin overlying the platelet monolayer. The Group 5 vessels had heparin reversal at 10 minutes, and demonstrated no fibrin overlying the platelet monolayer after 3 hours of blood flow. This study demonstrates the formation of a fibrin-free platelet monolayer over the endarterectomized vessel wall within 10 minutes of resumption of flow under systemic heparinization. These findings suggest that heparin may safely be reversed following a carotid endarterectomy if one awaits the initial critical 10 minutes of blood flow.

Evaluation of endorphin content in the CSF of patients with trigeminal neuralgia before and after Gasserian ganglion thermocoagulation

1981 ◽  
Vol 55 (6) ◽  
pp. 935-937 ◽  
Author(s):  
Giuseppe Salar ◽  
Salvatore Mingrino ◽  
Marco Trabucchi ◽  
Angelo Bosio ◽  
Carlo Semenza
Keyword(s):  
Cerebrospinal Fluid ◽  
Trigeminal Neuralgia ◽  
Control Group ◽  
Gasserian Ganglion ◽  
Content Type ◽  
Group Of Seven ◽  
Idiopathic Trigeminal Neuralgia ◽  
Significant Difference ◽  
Before And After ◽  
Fine Print

✓ The β-endorphin content in cerebrospinal fluid (CSF) was evaluated in 10 patients with idiopathic trigeminal neuralgia during medical treatment (with or without carbamazepine) and after selective thermocoagulation of the Gasserian ganglion. These values were compared with those obtained in a control group of seven patients without pain problems. No statistically significant difference was found between patients suffering from trigeminal neuralgia and those without pain. Furthermore, neither pharmacological treatment nor surgery changed CSF endorphin values. It is concluded that there is no pathogenetic relationship between trigeminal neuralgia and endorphins.

Matrix metalloproteinase—9 concentration after spontaneous intracerebral hemorrhage

2003 ◽  
Vol 99 (1) ◽  
pp. 65-70 ◽  
Author(s):  
Sònia Abilleira ◽  
Joan Montaner ◽  
Carlos A. Molina ◽  
Jasone Monasterio ◽  
José Castillo ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Neurological Diseases ◽  
Neurological Status ◽  
Acute Stage ◽  
Ct Scans ◽  
Enzyme Linked Immunosorbent Assay ◽  
Content Type ◽  
Blood Brain Barrier Disruption ◽  
Brain Barrier Disruption ◽  
Fine Print

Object. Matrix metalloproteinases (MMPs) are overexpressed in the presence of some neurological diseases in which blood—brain barrier disruption exists. The authors investigated the MMP-9 concentration in patients after acute intracerebral hemorrhage (ICH) and its relation to perihematomal edema (PHE). Methods. Concentrations of MMP-9 and related proteins were determined in plasma by performing an enzyme-linked immunosorbent assay of samples drawn after hospital admission (< 24 hours after stroke) from 57 patients with ICH. The diagnosis of ICH was made on the basis of findings on computerized tomography (CT) scans. The volumes of ICH and PHE were measured on baseline and follow-up CT scans at the same time that the patient's neurological status was assessed using the Canadian Stroke Scale and the Glasgow Coma Scale. Increased expression of MMP-9 was found among patients with ICH. In cases of deep ICH, MMP-9 was significantly associated with PHE volume (r = 0.53; p = 0.01) and neurological worsening (237.4 compared with 111.3 ng/ml MMP-9; p = 0.04). A logistic regression model focusing on the study of absolute PHE volume showed ICH volume as an independent predictor (odds ratio [OR] 3.37; 95% confidence interval [CI] 1.1–10.3; p = 0.03). A second analysis of relative PHE volume (absolute PHE volume/ICH volume) in patients with deep ICH demonstrated that the only factor related to it was MMP-9 concentration (OR 11.6; 95% CI 1.5–89.1; p = 0.018). Conclusions. Expression of MMP-9 is raised after acute spontaneous ICH. Among patients with deep ICH this increase is associated with PHE and the development of neurological worsening within the acute stage.

The use of intraarterial papaverine in the management of vasospasm complicating arteriovenous malformation resection

1995 ◽  
Vol 82 (2) ◽  
pp. 296-299 ◽  
Author(s):  
Michael K. Morgan ◽  
Maurice J. Day ◽  
Nicholas Little ◽  
Verity Grinnell ◽  
William Sorby
Keyword(s):  
Arteriovenous Malformation ◽  
Perfusion Pressure ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Venous Occlusion ◽  
Neurological Deterioration ◽  
Unusual Complication ◽  
Content Type ◽  
First Case ◽  
Normal Perfusion Pressure Breakthrough ◽  
Fine Print

✓ The authors report two cases of treatment by intraarterial papaverine of cerebral vasospasm complicating the resection of an arteriovenous malformation (AVM). Both cases had successful reversal of vasospasm documented on angiography. In the first case sustained neurological improvement occurred, resulting in a normal outcome by the time of discharge. In the second case, neurological deterioration occurred with the development of cerebral edema. This complication was thought to be due to normal perfusion pressure breakthrough, on the basis of angiographic arterial vasodilation and increased cerebral blood flow. These two cases illustrate an unusual complication of surgery for AVMs and demonstrate that vasospasm (along with intracranial hemorrhage, venous occlusion, and normal perfusion pressure breakthrough) should be considered in the differential diagnosis of delayed neurological deterioration following resection of these lesions. Although intraarterial papaverine may be successful in dilating spastic arteries, it may also result in pathologically high flows following AVM resection. However, this complication has not been seen in our experience of treating aneurysmal subarachnoid hemorrhage by this technique.

scholarly journals Direct evidence for a key role of protein kinase C in the development of vasospasm after subarachnoid hemorrhage

1992 ◽  
Vol 76 (4) ◽  
pp. 635-639 ◽  
Author(s):  
Shigeru Nishizawa ◽  
Nobukazu Nezu ◽  
Kenichi Uemura
Keyword(s):  
Signal Transduction ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Direct Evidence ◽  
Control Group ◽  
Content Type ◽  
Kinase C ◽  
Protein Kinase C Activity ◽  
Fine Print

✓ Vascular contraction is induced by the activation of intracellular contractile proteins mediated through signal transduction from the outside to the inside of cells. Protein kinase C plays a crucial role in this signal transduction. It is hypothesized that protein kinase C plays a causative part in the development of vasospasm after subarachnoid hemorrhage (SAH). To verify this directly, the authors measured protein kinase C activity in canine basilar arteries in an SAH model with (γ-32P)adenosine triphosphate and the data were compared to those in a control group. Protein kinase C is translocated to the membrane from the cytosol when it is activated, and the translocation is an index of the activation; thus, protein kinase C activity was measured both in the cytosol and in the membrane fractions. Protein kinase C activity in the membrane in the SAH model was remarkably enhanced compared to that in the control group. The percentage of membrane activity to the total was also significantly greater in the SAH vessels than in the control group, and the percentage of cytosol activity in the SAH group was decreased compared to that in the control arteries. The results indicate that protein kinase C in the vascular smooth muscle was translocated to the membrane from the cytosol and was activated when SAH occurred. It is concluded that this is direct evidence for a key role of protein kinase C in the development of vasospasm.

Early metabolic alterations in edematous perihematomal brain regions following experimental intracerebral hemorrhage

1998 ◽  
Vol 88 (6) ◽  
pp. 1058-1065 ◽  
Author(s):  
Kenneth R. Wagner ◽  
Guohua Xi ◽  
Ya Hua ◽  
Marla Kleinholz ◽  
Gabrielle M. de Courten-Myers ◽  
...  
Keyword(s):  
White Matter ◽  
Intracerebral Hemorrhage ◽  
Gray Matter ◽  
High Energy ◽  
Brain Regions ◽  
Large Animal ◽  
High Energy Phosphate ◽  
Content Type ◽  
Water Contents ◽  
Fine Print

Object. The authors previously demonstrated, in a large-animal intracerebral hemorrhage (ICH) model, that markedly edematous (“translucent”) white matter regions (> 10% increases in water contents) containing high levels of clotderived plasma proteins rapidly develop adjacent to hematomas. The goal of the present study was to determine the concentrations of high-energy phosphate, carbohydrate substrate, and lactate in these and other perihematomal white and gray matter regions during the early hours following experimental ICH. Methods. The authors infused autologous blood (1.7 ml) into frontal lobe white matter in a physiologically controlled model in pigs (weighing approximately 7 kg each) and froze their brains in situ at 1, 3, 5, or 8 hours postinfusion. Adenosine triphosphate (ATP), phosphocreatine (PCr), glycogen, glucose, lactate, and water contents were then measured in white and gray matter located ipsi- and contralateral to the hematomas, and metabolite concentrations in edematous brain regions were corrected for dilution. In markedly edematous white matter, glycogen and glucose concentrations increased two- to fivefold compared with control during 8 hours postinfusion. Similarly, PCr levels increased several-fold by 5 hours, whereas, except for a moderate decrease at 1 hour, ATP remained unchanged. Lactate was markedly increased (approximately 20 µmol/g) at all times. In gyral gray matter overlying the hematoma, water contents and glycogen levels were significantly increased at 5 and 8 hours, whereas lactate levels were increased two- to fourfold at all times. Conclusions. These results, which demonstrate normal to increased high-energy phosphate and carbohydrate substrate concentrations in edematous perihematomal regions during the early hours following ICH, are qualitatively similar to findings in other brain injury models in which a reduction in metabolic rate develops. Because an energy deficit is not present, lactate accumulation in edematous white matter is not caused by stimulated anaerobic glycolysis. Instead, because glutamate concentrations in the blood entering the brain's extracellular space during ICH are several-fold higher than normal levels, the authors speculate, on the basis of work reported by Pellerin and Magistretti, that glutamate uptake by astrocytes leads to enhanced aerobic glycolysis and lactate is generated at a rate that exceeds utilization.

Effect of sympathectomy on spinal blood flow autoregulation and posttraumatic ischemia

1982 ◽  
Vol 56 (5) ◽  
pp. 706-710 ◽  
Author(s):  
Wise Young ◽  
Vincent DeCrescito ◽  
John J. Tomasula
Keyword(s):  
Blood Flow ◽  
Spinal Injury ◽  
Sympathetic Ganglia ◽  
Control Group ◽  
Content Type ◽  
Systemic Pressure ◽  
Sympathetic Regulation ◽  
Mean Systemic Pressure ◽  
Paravertebral Sympathetic Ganglia ◽  
Fine Print

✓ The hypothesis that the paravertebral sympathetic ganglia play a role in spinal blood flow regulation was tested in cats. Five cats were subjected to paravertebral sympathectomy, two to combined sympathectomy-adrenalectomy, three to adrenalectomy alone, and five controls received no treatment. Laminectomy was carried out to expose the T4–10 cord, and autoregulation was tested by measuring blood flow from the lateral columns with the hydrogen clearance technique during manipulation of systemic pressure with intravenous saline infusion and nitroprusside administration. The cord was then contused at T-7 with a 400 gm-cm impact injury. Posttraumatic blood flow was recorded, and neurophysiological function was assessed with somatosensory evoked potential (SEP) monitoring. Before injury, blood flow in the untreated (control) group had no consistent relationship with mean systemic pressure over the range 80 to 160 mm Hg. In contrast, in all cats with paravertebral sympathectomy, whether accompanied by adrenalectomy or not, blood flows increased with systemic pressure (correlation coefficient 0.86, p < 0.01). After injury, the control and adrenalectomized cats showed blood flow decreases of > 60% to 4 to 6 ml/100 gm/min (p < 0.01) by 2 to 3 hours. However, cats with paravertebral sympathectomy maintained blood flow above 9 ml/100 gm/min for up to 3 hours after injury. All the sympathectomized cats recovered their SEP by the 3rd hour after injury, compared with none of the controls. Thus, in the absence of the paravertebral sympathetic ganglia, spinal blood flow autoregulation was impaired and the typical posttraumatic loss in blood flow did not occur. The sympathectomy also protected the spinal cords from the neurophysiological loss usually seen in 400 gm-cm injury. The data suggest the need for caution in using acetylcholine blocking agents to paralyze animals in experimental spinal injury, since these agents alter sympathetic activity and may influence the injury process. The spinal cord is an excellent model in which to investigate sympathetic regulation of central nervous system blood flow.

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