Normal perfusion pressure breakthrough: the role of capillaries

1997 ◽  
Vol 86 (3) ◽  
pp. 519-524 ◽  
Author(s):  
Lali H. S. Sekhon ◽  
Michael K. Morgan ◽  
Ian Spence
Keyword(s):  
Brain Tissue ◽  
Perfusion Pressure ◽  
Brain Parenchyma ◽  
Cerebral Hypoperfusion ◽  
Cell Region ◽  
Complete Excision ◽  
Content Type ◽  
Normal Perfusion Pressure Breakthrough ◽  
Fine Print ◽  
Adjacent Brain

✓ Excision of human cerebral arteriovenous malformations (AVMs) can be complicated by postoperative edema and hemorrhage in adjacent brain tissue, despite the complete excision of the malformation. Various theories have purported to explain the hemodynamic basis for this predisposition, including disordered autoregulation causing “normal perfusion pressure breakthrough” and obstruction of venous drainage leading to “occlusive hyperemia.” This study did not evaluate the arterial or venous circulations in this scenario, but rather examined the capillaries in adjacent brain parenchyma for any structural deficiencies that would predispose the brain to the postoperative formation of edema and hemorrhage. Arteriovenous fistulas (AVFs) were created surgically in the necks of 10 male Sprague—Dawley rats, which caused chronic cerebral hypoperfusion with a reduction in cerebral blood flow of between 25% and 50%. Ten age-matched animals were used as controls. Twenty-six weeks after AVF formation the animals were killed and perfusion fixed. Their brain tissue was prepared for light microscopic studies by staining for glial fibrillary acidic protein or for transmission electron microscopy. In the CA1 pyramidal cell region of the hippocampus, it was found that in the animals with AVFs there was increased capillary density and absent astrocytic foot processes in some of these vessels. It was concluded that these vessels had developed as a result of neovascularization in response to chronic cerebral ischemia and that their anatomical configuration made them prone to mechanical weakness and instability following the increase in perfusion pressure that occurs in adjacent brain parenchyma after AVM excision. The authors believe that this study pinpoints a structural accompaniment to the hemodynamic changes that occur in brain tissue in the vicinity of cerebral AVMs that predispose these areas to the formation of edema and hemorrhage after AVM excision.

Surgical management of large AVM's by staged embolization and operative excision

1987 ◽  
Vol 67 (1) ◽  
pp. 17-28 ◽  
Author(s):  
Robert F. Spetzler ◽  
Neil A. Martin ◽  
L. Philip Carter ◽  
Richard A. Flom ◽  
Peter A. Raudzens ◽  
...  
Keyword(s):  
Perfusion Pressure ◽  
Complete Excision ◽  
Content Type ◽  
Stable Xenon ◽  
Staged Approach ◽  
Cortical Cerebral Blood Flow ◽  
Normal Perfusion Pressure Breakthrough ◽  
Operative Excision ◽  
Cortical Perfusion ◽  
Fine Print

✓ A series of 20 patients with giant arteriovenous malformations (AVM's) managed with staged embolization and surgical resection is presented. Complete excision was accomplished in 18 of these patients. There were no deaths and only three complications, of which one was disabling. Further evidence for the presence of low perfusion surrounding the AVM, emphasizing the risk of normal perfusion pressure breakthrough, is provided by cortical perfusion pressure, cortical cerebral blood flow (CBF), and stable xenon computerized tomography CBF measurements. The staged approach to giant AVM management is a proposed method to render AVM's that were previously considered inoperable or marginally operable into totally excisable lesions, while maintaining an acceptable level of morbidity and mortality.

A new rat model of chronic cerebral hypoperfusion associated with arteriovenous malformations

2002 ◽  
Vol 97 (5) ◽  
pp. 1198-1202 ◽  
Author(s):  
Jian Hai ◽  
Meixiu Ding ◽  
Zhilin Guo ◽  
Bingyu Wang
Keyword(s):  
Electron Microscopy ◽  
Animal Model ◽  
Arteriovenous Malformations ◽  
Perfusion Pressure ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Model Group ◽  
Content Type ◽  
The Right ◽  
Fine Print

Object. A new experimental model of chronic cerebral hypoperfusion was developed to study the effects of systemic arterial shunting and obstruction of the primary vessel that drains intracranial venous blood on cerebral perfusion pressure (CPP), as well as cerebral pathological changes during restoration of normal perfusion pressure. Methods. Twenty-four Sprague—Dawley rats were randomly assigned to either a sham-operated group, an arteriovenous fistula (AVF) group, or a model group (eight rats each). The animal model was readied by creating a fistula through an end-to-side anastomosis between the right distal external jugular vein (EJV) and the ispilateral common carotid artery (CCA), followed by ligation of the left vein draining the transverse sinus and bilateral external carotid arteries. Systemic mean arterial pressure (MAP), draining vein pressure (DVP), and CPP were monitored and compared among the three groups preoperatively, immediately postoperatively, and again 90 days later. Following occlusion of the fistula after a 90-day interval, blood—brain barrier (BBB) disruption and water content in the right cortical tissues of the middle cerebral artery territory were confirmed and also quantified with transmission electron microscopy. Formation of a fistula resulted in significant decreases in MAP and CPP, and a significant increase in DVP in the AVF and model groups. Ninety days later, there were still significant increases in DVP and decreases in CPP in the model group compared with the other groups (p < 0.05). Damage to the BBB and brain edema were noted in animals in the model group during restoration of normal perfusion pressure by occlusion of the fistula. Electron microscopy studies revealed cerebral vasogenic edema and/or hemorrhage in various amounts, which correlated with absent astrocytic foot processes surrounding some cerebral capillaries. Conclusions. The results demonstrated that an end-to-side anastomosis between the distal EJV and CCA can induce a decrease in CPP, whereas a further chronic state of cerebral hypoperfusion may be caused by venous outflow restriction, which is associated with perfusion pressure breakthrough. This animal model conforms to the basic hemodynamic characteristics of human cerebral arteriovenous malformations.

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.

Pathology of arteriovenous malformations embolized with isobutyl-2-cyanoacrylate (bucrylate)

1981 ◽  
Vol 55 (5) ◽  
pp. 819-825 ◽  
Author(s):  
Harry V. Vinters ◽  
Gérard Debrun ◽  
John C. E. Kaufmann ◽  
Charles G. Drake
Keyword(s):  
Arteriovenous Malformations ◽  
Therapeutic Embolization ◽  
Brain Parenchyma ◽  
Pathological Examination ◽  
Foreign Body Giant Cell ◽  
Cell Reaction ◽  
Cerebral Arteriovenous Malformations ◽  
Content Type ◽  
Fine Print ◽  
Adjacent Brain

✓ There is controversy as to the possible toxic effects of isobutyl-2-cyanoacrylate (bucrylate) when this substance is used for purposes of therapeutic embolization. Two cases are presented in which cerebral arteriovenous malformations were resected, one 42 days and the other a year after bucrylate embolization. In both, pathological examination revealed a brisk intimal foreign-body giant-cell reaction wherever bucrylate was present in a vessel, along with chronic inflammation in the vessel walls and adjacent brain parenchyma. The findings are discussed in the light of other observations on the histotoxicity of bucrylate.

Is stagnating flow in former feeding arteries an indication of cerebral hypoperfusion after resection of arteriovenous malformations?

2001 ◽  
Vol 95 (1) ◽  
pp. 36-43 ◽  
Author(s):  
Bernhard Meyer ◽  
Horst Urbach ◽  
Carlo Schaller ◽  
Johannes Schramm
Keyword(s):  
Brain Tissue ◽  
Arteriovenous Malformations ◽  
Cerebral Hypoperfusion ◽  
Clear Trend ◽  
Content Type ◽  
Before And After ◽  
Group A ◽  
Cortical Ischemia ◽  
Group B ◽  
Fine Print

Object. The authors' goal in this study was to challenge the proposed mechanism of the occlusive hyperemia theory, in which it is asserted that stagnating flow in the former feeding arteries of cerebral arteriovenous malformations (AVMs) leads to parenchymal hypoperfusion or ischemia, from which postoperative edema and hemorrhage originate. Methods. Cortical oxygen saturation (SaO2) was measured in 52 patients by using microspectrophotometry in areas adjacent to AVMs before and after resection. The appearance of the former feeding arteries was categorized as normal (Group A); moderately stagnating (Group B); and excessively stagnating (Group C) on postoperative angiographic fast-film series. Patients and SaO2 values were pooled accordingly and compared using analysis of variance and Duncan tests (p < 0.05). Angiographic stagnation times in former feeding arteries were correlated in a linear regression/correlation analysis with SaO2 data (p < 0.05). All values are given as the mean ± standard deviation. The average median postoperative SaO2 in Group C (15 patients) was significantly higher than in Groups B (17 patients) and A (20 patients) (Group C, 75.2 ± 8.5; Group B, 67.5 ± 10.8; Group A, 67.1 ± 12 %SaO2), as was the average postoperative increase in SaO2 (Group C, 25.9 ± 14.9; Group B, 14.6 ± 14; Group A, 11.1 ± 14 %SaO2). Angiographically confirmed stagnation times were also significantly longer in Group C than in Group B (Group C, 5.6 ± 2.5; Group B, 1.3 ± 0.6 seconds). A significant correlation/regression analysis showed a clear trend toward higher postoperative SaO2 levels with increasing stagnation time. Conclusions. Stagnating flow in former feeding arteries does not cause cortical ischemia, but its presence on angiographic studies is usually indicative of hyperperfusion in the surrounding brain tissue after AVM resection. In the context of the pathophysiology of AVMs extrapolations made from angiographically visible shunt flow to blood flow in the surrounding brain tissue must be regarded with caution.

Microvascular pathological features of immediate perinidal parenchyma in cerebral arteriovenous malformations: giant bed capillaries

2003 ◽  
Vol 98 (4) ◽  
pp. 823-827 ◽  
Author(s):  
Walid Attia ◽  
Tsuyoshi Tada ◽  
Kazuhiro Hongo ◽  
Hisashi Nagashima ◽  
Toshiki Takemae ◽  
...  
Keyword(s):  
Brain Tissue ◽  
Arteriovenous Malformations ◽  
Brain Parenchyma ◽  
Pathological Features ◽  
Hemodynamic Changes ◽  
Content Type ◽  
Pericapillary Space ◽  
Hematoxylin And Eosin ◽  
The Brain ◽  
Fine Print

Object. The behavior of brain tissue in cases of arteriovenous malformations (AVMs) is a matter of debate. The authors believe that the local microvascular environment in the AVM bed shares the hemodynamic changes influencing that behavior in one way or another. The purpose of this study was to investigate the microvascular pathological features in the immediate perinidal brain tissue. Methods. This retrospective study was conducted using excised AVM specimens obtained in 35 patients, from which the authors selected 20 specimens that fulfilled the criteria for sufficient brain tissue around the excised nidus. Specimens were stained with hematoxylin and eosin, and the immediate perinidal microvascular environment was examined using light microscopy. Conclusions. Eighty-five percent of the AVMs studied showed the presence of huge, dilated capillaries, and 65% showed severe congestion of these capillaries. The authors have named these capillaries “giant bed capillaries.” In this study capillary bleeding was shown in AVMs, and a pericapillary space was seen around some vessels. The brain parenchyma containing AVMs with these findings proved to be significantly ischemic.

Complications of surgery for arteriovenous malformations of the brain

1993 ◽  
Vol 78 (2) ◽  
pp. 176-182 ◽  
Author(s):  
Michael K. Morgan ◽  
Ian H. Johnston ◽  
John M. Hallinan ◽  
Neville C. Weber
Keyword(s):  
Arteriovenous Malformations ◽  
Perfusion Pressure ◽  
Morbidity Rate ◽  
Separate Analysis ◽  
Content Type ◽  
Complete Surgical Resection ◽  
Complications Of Surgery ◽  
Normal Perfusion Pressure Breakthrough ◽  
The Brain ◽  
Fine Print

✓ A series of 112 patients undergoing complete surgical resection of arteriovenous malformations (AVM's) of the brain between 1974 and 1990 were analyzed for complications and 12-month outcomes. The cohort consisted of 44 patients with small AVM's (< 2 cm in diameter), 43 patients with medium-sized AVM's (2 to 4 cm in diameter), and 25 patients with large AVM's (> 4 cm in diameter). There was a 3.6% series mortality rate and an 18% morbidity rate. One of the four deaths was caused by normal perfusion pressure breakthrough. Analysis of logistic regression found that the most important factor influencing the occurrence of complications in this series was AVM size (p = 0.005) and that the occurrence of complications (p < 0.001) and the neurological grade at the time of surgery (p < 0.004) both significantly contributed to the outcome at 12 months. This study stresses the importance of defining complications in terms of rigid criteria when analyzing AVM series in order to allow for a correct evaluation of the risk:benefit ratio of surgery. Furthermore, it emphasizes the need for a separate analysis of the importance of complications upon outcome.

Enlarged perivascular spaces mimicking multicystic brain tumors

2005 ◽  
Vol 102 (6) ◽  
pp. 1142-1146 ◽  
Author(s):  
Jochen Rohlfs ◽  
Thomas Riegel ◽  
Munzir Khalil ◽  
Joanna Iwinska-Zelder ◽  
Hans-Dieter Mennel ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Brain Tumors ◽  
Obstructive Hydrocephalus ◽  
Brain Parenchyma ◽  
Perivascular Spaces ◽  
Cystic Lesions ◽  
Content Type ◽  
Surgical Option ◽  
Fine Print ◽  
Adjacent Brain

✓ The authors present two cases in which enlarged Virchow—Robin spaces were located in the basal ganglia and the thalamomesencephalic region. The incidence of such huge cystic lesions is extremely rare. The expanding nature of these lesions, demonstrated by the patients' progressive symptoms due to compression of the adjacent brain parenchyma and obstructive hydrocephalus, mimicked that of brain tumors. The two patients were successfully treated by neuroendoscopic cystocisternostomy or ventriculocystostomy. To the authors' knowledge there have been only two published reports on expanding Virchow—Robin spaces that produced a compressive effect or consequent hydrocephalus and were directly fenestrated using neuroendoscopic techniques. Neuroendoscopy appears to offer an effective surgical option in the treatment of symptomatic Virchow—Robin spaces.

Experimental rat model of chronic cerebral hypoperfusion–reperfusion mimicking normal perfusion pressure breakthrough phenomenon

Neurocirugía ◽  
2020 ◽  
Vol 31 (5) ◽  
pp. 209-215
Author(s):  
Juan Manuel Revuelta ◽  
Álvaro Zamarrón ◽  
José Fortes ◽  
Gregorio Rodríguez-Boto ◽  
Jesús Vaquero ◽  
...  
Keyword(s):  
Rat Model ◽  
Perfusion Pressure ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Experimental Rat Model ◽  
Normal Perfusion Pressure Breakthrough

Cerebral oxygen and microdialysis monitoring during aneurysm surgery: effects of blood pressure, cerebrospinal fluid drainage, and temporary clipping on infarction

2002 ◽  
Vol 96 (6) ◽  
pp. 1013-1019 ◽  
Author(s):  
Rupert Kett-White ◽  
Peter J. Hutchinson ◽  
Pippa G. Al-Rawi ◽  
Marek Czosnyka ◽  
Arun K. Gupta ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cerebrospinal Fluid ◽  
Brain Tissue ◽  
Total Duration ◽  
Wilcoxon Test ◽  
Fisher Exact Test ◽  
Content Type ◽  
The Impact ◽  
Temporary Clipping ◽  
Fine Print

Object. The aim of this study was to investigate potential episodes of cerebral ischemia during surgery for large and complicated aneurysms, by examining the effects of arterial temporary clipping and the impact of confounding variables such as blood pressure and cerebrospinal fluid (CSF) drainage. Methods. Brain tissue PO2, PCO2, and pH, as well as temperature and extracellular glucose, lactate, pyruvate, and glutamate were monitored in 46 patients by using multiparameter sensors and microdialysis. Baseline data showed that brain tissue PO2 decreased significantly, below a mean arterial pressure (MAP) threshold of 70 mm Hg. Further evidence of its relationship with cerebral perfusion pressure was shown by an increase in mean brain tissue PO2 after drainage of CSF from the basal cisterns (Wilcoxon test, p < 0.01). Temporary clipping was required in 31 patients, with a mean total duration of 14 minutes (range 3–52 minutes), causing brain tissue PO2 to decrease and brain tissue PCO2 to increase (Wilcoxon test, p < 0.01). In patients in whom no subsequent infarction developed in the monitored region, brain tissue PO2 fell to 11 mm Hg (95% confidence interval 8–14 mm Hg). A brain tissue PO2 level below 8 mm Hg for 30 minutes was associated with infarction in any region (p < 0.05 according to the Fisher exact test); other parameters were not predictive of infarction. Intermittent occlusions of less than 30 minutes in total had little effect on extracellular chemistry. Large glutamate increases were only seen in two patients, in both of whom brain tissue PO2 during occlusion was continuously lower than 8 mm Hg for longer than 38 minutes. Conclusions. The brain tissue PO2 decreases with hypotension, and, when it is below 8 mm Hg for longer than 30 minutes during temporary clipping, it is associated with increasing extracellular glutamate levels and cerebral infarction.

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