Subarachnoid hemorrhage

Etiology of subarachnoid hemorrhage In most cases, the cause of spontaneous subarachnoid hemorrhage is a ruptured intracranial aneurysm. Arterial aneurysms of the brain, like aneurysms of other localization, represent a limited or diffuse expansion of the lumen of an artery or a protrusion of its wall. Most aneurysms of the arteries of the brain have the characteristic appearance of a small thin-walled sac, in which the bottom, middle part and the so-called neck can usually be distinguished. Due to these anatomical features, such aneurysms are often called saccular aneurysms. Less commonly, the aneurysm looks like a large spherical formation or diffuse artery expansion over a considerable extent (the so-called S-shaped aneurysms). Most aneurysms are located on the arteries at the base of the brain. Their favorite localization is the sites of division and anastomosis of the arteries of the brain. Especially often, aneurysms are localized on the anterior communicating artery at the site of the origin of the posterior communicating artery from the internal carotid artery or in the region of the branches of the middle cerebral artery. A relatively small part of aneurysms is localized in the system of vertebral and basilar arteries. 

Aneurysms are more common in women than in men. The question of the origin of saccular aneurysms, which make up the overwhelming majority of aneurysms, remains largely open to this day. According to most authors, the formation of aneurysms is based on defects in the development of the vascular system of the brain; another (less numerous) group of researchers emphasizes the role of atherosclerosis and hypertension as one of the main causes of saccular aneurysms. The concept of traumatic genesis of cerebral aneurysms was proposed by MB Kopylov (1962), who believes that at the moment of injury, the pressure in the arteries of the brain increases sharply. Under the influence of such a hemohydraulic shock, damage to the arterial wall may occur with the subsequent development of an aneurysm. A small part of aneurysms develops due to the ingestion of infected emboli into the artery of the brain. These so-called mycotic aneurysms are predominantly located on the convexital surface of the brain. They most often develop in young people with lingering septic endocarditis. In the origin of large spherical and S-shaped aneurysms, atherosclerosis undoubtedly plays a leading role. Not all aneurysms cause clinical symptoms. Most of the aneurysms are accidental findings during postmortem examination. Aneurysms are found in people of various ages – from infancy to senile. Clinically, aneurysms manifest themselves as subarachnoid hemorrhages in the fourth and fifth decades of life. Other causes of subarachnoid hemorrhage include atherosclerotic and hypertensive changes in blood vessels, primary and metastatic brain tumors, inflammatory diseases, uremia, and blood diseases. Clinical presentation of subarachnoid hemorrhage Usually, subarachnoid hemorrhage develops suddenly, without any precursors. Only in a small part of patients before hemorrhage symptoms are observed due to the presence of an aneurysm – limited pain in the frontal-orbital region, paresis of the cranial nerves (more often the oculomotor nerve). 

A ruptured aneurysm can occur at a time of physical or emotional stress. The first symptom of subarachnoid hemorrhage is a sudden acute headache, which the patients themselves define as a “blow”, as a feeling of “spreading hot fluid in the head .” At the first moment of the disease, the pain may be local in nature (in the forehead, back of the head), then it becomes diffuse. In the future, the patient develops pain in the neck, back and legs. Almost simultaneously with the headache, nausea and multiple vomiting occur. Following an attack of headache, loss of consciousness occurs. In mild cases, the loss of consciousness is short-lived (10-20 minutes), in severe cases, the unconscious state lasts for many hours and even days. At the time of the rupture of the aneurysm or shortly thereafter, epileptic seizures may occur. For hemorrhages from arterial aneurysms, the rapid development of the meningeal symptom complex is especially characteristic. Examination of the patient reveals stiffness of the occipital muscles, Kernig’s and Brudzinsky’s symptoms, photophobia, general hyperesthesia. Only in the most severely patients with inhibition of reflex activity, meningeal symptoms may be absent. A common symptom that accompanies subarachnoid hemorrhage is a mental disorder. The degree of mental disorder can vary from mild confusion, disorientation to severe psychosis. Often, after hemorrhage, psychomotor agitation is observed or memory impairments develop, characteristic of the Korsakov syndrome. As a reaction to poured blood into the intrathecal space, as well as as a result of irritation of the hypothalamic region, in the acute period there is an increase in body temperature to 38-39 ° C, changes in the blood in the form of moderate leukocytosis and a shift in the leukocyte formula to the left. 

Along with this, in many patients who do not suffer from essential hypertension, an increase in blood pressure is observed. In severe cases, with massive hemorrhages, there are pronounced disorders of vital functions: cardiovascular activity and respiration. In the acute stage of subarachnoid hemorrhage, a number of symptoms are caused by a rapid increase in intracranial pressure (headache, vomiting). An increase in intracranial pressure and the resulting obstruction of venous outflow lead to the development of congestion in the fundus. In addition to varicose veins and swelling of the optic nipples, retinal hemorrhages can be found. In a large percentage of cases with subarachnoid hemorrhage, paresis of the cranial nerves and symptoms of focal brain damage are also observed. Cranial nerve lesions in patients with spontaneous subarachnoid hemorrhages are pathognomonic for rupture of basal arterial aneurysms. Most often, there is an isolated paresis of the oculomotor nerve that occurs at the time of rupture of the aneurysm or shortly after it. In the overwhelming majority of cases, an isolated unilateral lesion of the oculomotor nerve is observed with hemorrhage from an aneurysm located at the site of the origin of the posterior communicating artery from the internal carotid artery. Hemorrhages from aneurysms of the internal carotid and anterior communicating arteries near the optic nerves and chiasm are relatively often accompanied by visual impairment. Dysfunction of other cranial nerves is less common. 

There are two main causes of cranial nerve damage in patients with arterial aneurysms. Firstly, direct compression of the nerve by the aneurysm and, secondly, hemorrhage into the nerve and its sheaths at the moment of rupture of the aneurysm, followed by the formation of connective tissue perineural adhesions. Many patients develop symptoms of focal brain damage: paresis of the extremities, sensory disturbances, speech disorders, etc. The occurrence of these symptoms is most often due to concomitant cerebral hemorrhage or local cerebral ischemia caused by arterial spasm or ischemia due to thrombosis of the aneurysm. A lot of works are currently devoted to the study of the clinical manifestations of arterial spasm during rupture of arterial aneurysms, pathological changes in the brain caused by spasm. Judging by the angiographic data, the most pronounced spasm of the arteries is observed near the aneurysm, but in some cases spasm of the arteries located at a distance from it can also be found. The duration of spastic contraction of the arteries most often does not exceed 2-4 weeks. It has been suggested that acute brainstem ischemia developing as a result of spasm is the most likely cause of a number of severe symptoms accompanying ruptured aneurysm, such as loss of consciousness, respiratory and cardiac disorders. Of interest is the fact that arterial spasm can cause not only cerebral ischemia near a ruptured aneurysm, but also a distant hemispheric lesion. So, with aneurysms of the anterior communicating artery, it is often possible to detect local symptoms caused by impaired blood circulation in the basin of the anterior cerebral arteries – paresis of the legs, mental changes, and praxis defects. Spasm of the middle cerebral artery leads to paresis of the opposite limbs, impaired sensitivity in them and aphatic phenomena. The causes of arterial spasm during rupture of arterial aneurysms have not been studied enough. It is suggested that factors such as damage to the artery wall and its segmental nervous apparatus by toxic products of the decay of blood cells are of great importance. 

Course and prognosis of subarachnoid hemorrhages The prognosis of intracranial hemorrhages caused by rupture of arterial aneurysms is unfavorable. In most cases, the case is not limited to a single hemorrhage. Repeated hemorrhages from aneurysms are especially difficult. With them, paresis, paralysis are more often observed, and the mortality rate is approximately twice as high as with primary hemorrhages. Observation of patients who underwent subarachnoid hemorrhage made it possible to establish that the main part of relapses occurs 2-4 weeks after the first hemorrhage. 2 months after the rupture of the aneurysm, repeated hemorrhages occur relatively rarely. During the first 4-6 weeks, up to 60% of patients with hemorrhages from arterial aneurysms die. Diagnosis of subarachnoid hemorrhage The clinic of subarachnoid hemorrhage can be considered well understood, and in typical cases the diagnosis does not cause serious difficulties. However, in some cases at the onset of the disease, when the meningeal symptom complex has not yet fully developed and symptoms such as vomiting, headache, fever come to the fore, a diagnosis of acute intoxication and food poisoning may be mistakenly made. In other cases, with a relatively mild gradual development of the syndrome of subarachnoid hemorrhage, there is a suspicion of cerebrospinal meningitis. Diagnostic difficulties in most cases can be easily eliminated with a lumbar puncture. The diagnosis of subarachnoid hemorrhage is confirmed when there is blood in the cerebrospinal fluid. The fluid must be examined quickly to avoid (incorrect therapeutic measures. In the first days after subarachnoid hemorrhage, the cerebrospinal fluid is more or less intensely colored with blood. However, macroscopic analysis of the bloody fluid is not sufficient to confirm the diagnosis. It is recommended to centrifuge the fluid taken. In the fluid obtained after centrifugation, when subarachnoid hemorrhage is determined by xanthochromia. In addition, the diagnosis of subarachnoid hemorrhage in the first hours of the disease can be confirmed by the presence of leached erythrocytes during microscopic examination of the cerebrospinal fluid.

A day or more after subarachnoid hemorrhage, macrophages and lymphocytic cytosis of the brain appear in it. precise localization, shape and size are possible only with the help of angiography.Even the most thorough neurological examination in most cases allows it is only more or less likely to assume aneurysm of the cerebral arteries, and accurate topical diagnosis of aneurysms, especially multiple aneurysms, is practically impossible. The dangers associated with transporting a patient to specialized neurosurgical hospitals are in many cases exaggerated. Difficulties for the differential diagnosis often arise with subarachnoid hemorrhages from brain tumors that had previously been asymptomatic. However, an increase in focal symptoms of damage to the brain substance, as well as neutrophilic cytosis in the cerebrospinal fluid, observed during the entire period of the disease with brain tumors, allow a correct diagnosis to be made. Treatment of subarachnoid hemorrhage Treatment of subarachnoid hemorrhage includes conservative and surgical methods, depending on the etiology that caused the intrathecal hemorrhage. Strict bed rest must be observed for 6 weeks. The duration of this period is due to the fact that the vast majority of repeated hemorrhages from aneurysms occur within 1-11 / 2 months after the first. In addition, a significant period is required for the formation of strong connective tissue adhesions near the ruptured aneurysm. In the acute stage of hemorrhage, in order to create conditions for thrombosis of the aneurysm, drugs are shown that increase blood coagulability (vicasol, calcium chloride), as well as drugs aimed at inhibiting the fibrinolytic activity of the blood. For this purpose, aminocaproic acid is used 10-15 g daily during the first 3-6 weeks, which are dangerous for repeated hemorrhage. Since even slight tension or excitement can cause an increase in blood pressure and provoke repeated hemorrhage, sedation is necessary. The appointment of these drugs in the acute period of hemorrhage is all the more shown that many patients who have suffered hemorrhage from aneurysms are agitated. 

With strong excitement, the use of drugs such as diazepam (seduxen), chlorpromazine, etc. is required. It is important to control the bowel function. The rupture of the aneurysm is often accompanied by an increase in blood pressure, therefore, it becomes necessary to prescribe drugs that reduce the level of blood pressure. In cases where the rupture of the aneurysm is accompanied by widespread and persistent spasm of the cerebral arteries, it becomes necessary to use drugs that eliminate the spastic contraction of the arteries and improve collateral circulation. Unfortunately, existing vasodilators are ineffective for arterial spasm caused by ruptured aneurysm. Also indicated is therapy aimed at combating cerebral edema and intracranial hypertension. For this purpose, repeated lumbar punctures, saluretics, glycerol and parenteral barbiturates are used. Surgical is a radical method of treating arterial aneurysms. Surgical intervention until recently was considered an indication for the prevention of recurrent hemorrhage, which usually develops within 2-6 weeks after the rupture of the aneurysm. However, in recent years, this issue has been revised, since, according to a number of observations, conservative therapy aimed at inhibiting fibrinolysis and carried out during a period dangerous for the development of relapse reliably prevents repeated subarachnoid hemorrhages. With subarachnoid hemorrhage (SAH), blood flows into the space between the arachnoid membrane and the brain substance itself. The main reasons for this condition are rupture of the aneurysm (all of them are located subarachnoid) and head trauma, also the reasons include the dissection of the arterial vessel wall. Risk factors for spontaneous SAH: hypertension, significant daily fluctuations in blood pressure, taking oral contraceptives (in women), use of cocaine, amphetamine and other sympathomimetics, alcohol use, amyloid angiopathy, anticoagulant or thrombolytic therapy, vascular malformations, intracranial venous thrombosis. Diagnosis of subarachnoid hemorrhage: CT is the method of choice. In case of subarachnoid hemorrhage, it is computed tomography that allows it to be visualized most fully and reliably. Here there is a direct dependence of the reliability of visualization on the time elapsed after the moment of hemorrhage (if less than 12 hours have passed after the moment of the onset of SAH, the reliability will be very high, if 12-24 hours have passed, the reliability will be lower, since the blood can be partially lysed during this time and it will be difficult for the interpreter to decide on the conclusion).

local_offerevent_note November 30, 2020

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