scholarly journals Cerebral Vasospasm: Mechanisms, Pathomorphology, Diagnostics, Treatment

2021 ◽  
Author(s):  
Irina Alexandrovna Savvina ◽  
Yulia Mikhailovna Zabrodskaya ◽  
Anna Olegovna Petrova ◽  
Konstantin Alexandrovich Samochernykh
Keyword(s):  
Cerebral Aneurysms ◽  
Endothelial Damage ◽  
Cerebral Vessels ◽  
Secondary Complications ◽  
Subarachnoidal Hemorrhage ◽  
Paroxysmal Sympathetic Hyperactivity ◽  
Modern Methods ◽  
Mechanisms Of Formation ◽  
Causes Of Mortality ◽  
Vascular Spasm

Cerebral vessels constriction is one of the leading causes of mortality and disability in patients with acute cerebral circulatory disorders. The most dangerous type of acute cerebrovascular disease accompanied by high mortality is ruptured cerebral aneurysms with subarachnoidal hemorrhage (SAH). Following a constriction of the cerebral vessels on the background of SAH is the reason for brain ischemia. This chapter will focus on the mechanisms of formation of cerebral vascular spasm, pathomorphological aspects of the cerebral vessels constriction, and the stages of vascular spasm—the development of constrictive-stenotic arteriopathy, contractural degeneration of smooth muscle cells, and endothelial damage. We will cover classifications of cerebral vessels constriction by prevalence and severity, modern methods of clinical and instrumental diagnostics and treatment including paroxysmal sympathetic hyperactivity syndrome associated with the development of secondary complications, a longer stay of the patients in the ICU, higher disability and mortality.

Endovascular treatment of cerebral aneurysms with the use of stents in small cerebral vessels

2010 ◽  
Vol 32 (2) ◽  
pp. 119-122 ◽  
Author(s):  
Jingbo Zhang ◽  
Xianli Lv ◽  
Chuhan Jiang ◽  
Youxiang Li ◽  
Xinjian Yang ◽  
...  
Keyword(s):  
Endovascular Treatment ◽  
Cerebral Aneurysms ◽  
Cerebral Vessels

scholarly journals The role of nimodipine and magnesium sulfate in the prevention and treatment of vascular spasm in patients in the acute rupture of cerebral aneurysms

2020 ◽  
Vol 10 (4) ◽  
pp. 53-60
Author(s):  
Aleksandr A. Kalinkin ◽  
A. G. Vinokurov ◽  
O. N. Kalinkina ◽  
G. М. Yusubalieva ◽  
S. M. Chupalenkov
Keyword(s):  
Magnesium Sulfate ◽  
Cerebral Arteries ◽  
Cerebral Aneurysms ◽  
Drug Action ◽  
Adverse Outcomes ◽  
Action Mechanisms ◽  
Prevention And Treatment ◽  
Acute Rupture ◽  
Vascular Spasm

Vascular spasm in patients with hemorrhage from rupture of cerebral aneurysms is the main cause of adverse outcomes of the disease. One way to treat persistent contraction of cerebral arteries is to use nimodipine and magnesium sulfate. This literature review presents studies on the use of nimodipine and magnesium sulfate in the treatment of vascular spasm, and highlights the main links of pathogenesis and drug action mechanisms.

Paroxysmal Sympathetic Hyperactivity

2020 ◽  
Vol 40 (05) ◽  
pp. 485-491
Author(s):  
Rachael A. Scott ◽  
Alejandro A. Rabinstein
Keyword(s):  
Spinal Cord ◽  
Brain Diseases ◽  
Secondary Complications ◽  
Adequate Treatment ◽  
External Stimulation ◽  
Sympathetic Hyperactivity ◽  
Paroxysmal Sympathetic Hyperactivity ◽  
Inhibitory Modulation ◽  
Intravenous Morphine ◽  
Dystonic Posturing

AbstractParoxysmal sympathetic hyperactivity (PSH) is a relatively common, but often unrecognized, complication of acute diffuse or multifocal brain diseases, most frequently encountered in young comatose patients with severe traumatic brain injury. It is presumed to be caused by loss of cortical inhibitory modulation of diencephalic and brain stem centers and possible additional maladaptive changes in the spinal cord that combine to produce exaggerated sympathetic responses to stimulation. The syndrome consists of repeated sudden episodes of tachycardia, tachypnea, hypertension, sweating, and sometimes fever and dystonic posturing. The diagnosis is clinical. Treatment includes reducing any external stimulation that can trigger the episodes, and starting abortive (e.g., intravenous morphine) and preventive medications (e.g., gabapentin, propranolol, clonidine). Prompt and adequate treatment of PSH may reduce the likelihood of secondary complications, such as dehydration, weight loss and malnutrition, and muscle contractures.

Comaneci neck bridging device for the treatment of cerebral aneurysms

2015 ◽  
Vol 8 (2) ◽  
pp. 181-185 ◽  
Author(s):  
Rishi Gupta ◽  
Frank D Kolodgie ◽  
Renu Virmani ◽  
Ronen Eckhouse
Keyword(s):  
Light Microscopy ◽  
Cerebral Aneurysms ◽  
Chronic Phase ◽  
Endothelial Damage ◽  
Endothelial Injury ◽  
Adjunctive Treatment ◽  
New Zealand White Rabbits ◽  
The Right ◽  
Bare Platinum Coils ◽  
Platinum Coils

Background and purposeAdjunctive devices are commonly employed in the treatment of wide necked cerebral aneurysms. Balloon remodeling and permanent stent implantation may lead to thromboembolic complications or the need for antiplatelet use. A temporary stent that does not lead to complete flow arrest may be beneficial.MethodsWe studied 20 New Zealand white rabbits in whom aneurysms were created using elastase and ligation of the right common carotid artery. The aneurysms were then embolized with bare platinum coils along with adjunctive treatment using the Comaneci device or the Hyperglide balloon. Assessments were made for endothelial injury using scanning electron microscopy (SEM) and light microscopy.Results20 rabbits of mean±SD weight 3.1±0.2 kg were studied. Twelve rabbits were treated with the Comaneci device and eight with the Hyperglide balloon. There were no substantial differences on SEM or light microscopy in the subacute and chronic phase to suggest the Comaneci device caused endothelial injury.ConclusionsThe Comaneci device is a new adjuvant treatment for bridging of wide necked aneurysms with the advantage of averting flow arrest during deployment. There does not appear to be any evidence of significant endothelial damage during deployment in preclinical studies.

Brucella-related cerebral aneurysms/subarachnoidal hemorrhage: a short review featuring a case report

2008 ◽  
Vol 31 (3) ◽  
pp. 337-341 ◽  
Author(s):  
Serdar Kaya ◽  
Murat Velioglu ◽  
Ahmet Colak ◽  
Murat Kutlay ◽  
Mehmet Nusret Demircan ◽  
...  
Keyword(s):  
Case Report ◽  
Cerebral Aneurysms ◽  
Short Review ◽  
Subarachnoidal Hemorrhage

scholarly journals ANALYSIS OF THE CAUSES OF MORTALITY AFTER HIGH AMPUTATIONS OF THE LOWER EXTREMITIES FOR CRITICAL ISCHEMIA

2021 ◽  
pp. 68-73
Author(s):  
S.V. Fedorenko ◽  
Keyword(s):  
Atrial Fibrillation ◽  
Medical Records ◽  
Causes Of Death ◽  
Postoperative Mortality ◽  
Lower Extremities ◽  
Multiple Organ ◽  
Critical Ischemia ◽  
Risk Of Death ◽  
Modern Methods ◽  
Causes Of Mortality

Despite the development of modern methods of diagnosis and treatment of obliterating atherosclerosis of the lower extremities in 38-65% of patients, the disease progresses with the development of critical ischemia of the lower extremities. This often requires amputation at various levels. Postoperative mortality in this case reaches 20% or more. The aim of this work was to study the causes of death in patients after amputation of the lower extremities for critical ischemia. We studied 296 medical records and 52 autopsy reports of the deceased, which were used to amputate the lower extremities. It turned out that the mortality rate in women is 1.9 times higher than in men. The risk of death is increased by the presence of coronary heart disease in a patient with grade 2B circulatory failure and atrial fibrillation. The most common immediate cause of death after amputation is multiple organ failure.

Ultrastructure of pulmonary microvasculature in acute endotoxemia

1978 ◽  
Vol 36 (2) ◽  
pp. 470-471
Author(s):  
R. G. Gerrity ◽  
M. Richardson
Keyword(s):  
Polymorphonuclear Leukocytes ◽  
Alveolar Epithelium ◽  
Endothelial Damage ◽  
Capillary Endothelium ◽  
Type Ii Cells ◽  
Type Ii ◽  
Interstitial Edema ◽  
Pulmonary Capillaries ◽  
Lung Ultrastructure ◽  
Fibrin Thrombi

Dogs were injected intravenously with E_. coli endotoxin (2 mg/kg), and lung samples were taken at 15 min., 1 hr. and 24 hrs. At 15 min., occlusion of pulmonary capillaries by degranulating platelets and polymorphonuclear leukocytes (PML) was evident (Fig. 1). Capillary endothelium was intact but endothelial damage in small arteries and arterioles, accompanied by intraalveolar hemorrhage, was frequent (Fig. 2). Sloughing of the surfactant layer from alveolar epithelium was evident (Fig. 1). At 1 hr., platelet-PML plugs were no longer seen in capillaries, the endothelium of which was often vacuolated (Fig. 3). Interstitial edema and destruction of alveolar epithelium were seen, and type II cells had discharged their granules into the alveoli (Fig. 4). At 24 hr. phagocytic PML's were frequent in peripheral alveoli, while centrally, alveoli and vessels were packed with fibrin thrombi and PML's (Fig. 5). In similar dogs rendered thrombocytopenic with anti-platelet serum, lung ultrastructure was similar to that of controls, although PML's were more frequently seen in capillaries in the former (Fig. 6).

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