Subarachnoid hemorrhage is a condition caused by cerebral bleeding, in which blood accumulates in the subarachnoid space of the cerebral membranes. It is characterized by intense and sharp headache, short-term loss of consciousness and confusion in combination with hyperthermia and meningeal symptom complex. It is diagnosed according to CT and angiography of the brain; if they are unavailable, by the presence of blood in the cerebrospinal fluid. The basis of treatment is basic therapy, relief of angiospasm and surgical shutdown of cerebral aneurysm from the bloodstream.
ICD 10
I60 Subarachnoid hemorrhage
General information
Subarachnoid hemorrhage (SAH) is a separate type of hemorrhagic stroke, in which blood is poured into the subarachnoid (subarachnoid) space. The latter is located between the arachnoid (arachnoid) and soft cerebral membranes, contains cerebrospinal fluid. Blood spilled into the subarachnoid space increases the volume of fluid in it, which leads to an increase in intracranial pressure. Irritation of the soft cerebral membrane occurs with the development of aseptic meningitis.
Vascular spasm that occurs in response to bleeding can cause ischemia of certain areas of the brain with the occurrence of ischemic stroke or TIA. Subarachnoid hemorrhage accounts for about 10% of all ACVA. The frequency of its occurrence per year varies from 6 to 20 cases per 100 thousand population. As a rule, SAH is diagnosed in people over 20 years of age, most often (up to 80% of cases) in the age range from 40 to 65 years.
Causes
Most often, subarachnoid bleeding is a complication of cerebrovascular diseases and head injuries.
- Rupture of a vascular aneurysm. It is the cause of subarachnoid hemorrhage in 70-85% of cases. In the presence of a cerebral aneurysm, the probability of its rupture ranges from 1% to 5% per year and from 10% to 30% throughout life. Diseases often accompanied by the presence of a cerebral aneurysm include: Ehlers —Danlos syndrome, phacomatosis, Marfan syndrome, Willis circle anomalies, aortic coarctation, congenital hemorrhagic telangiectasia, polycystic kidney disease, etc. congenital diseases. Cerebral AVMs usually lead to hemorrhage into the ventricles of the brain or parenchymal-subarachnoid bleeding and are rarely an etiofactor of isolated SAH.
- Head injuries. Subarachnoid hemorrhage of traumatic genesis occurs during TBI and is caused by vascular injury with a skull fracture, brain contusion or compression. An example of such a SAH is a subarachnoid hemorrhage caused by a birth trauma of a newborn. Risk factors for a newborn’s SAH are a narrow pelvis in a woman in labor, rapid childbirth, delayed pregnancy, intrauterine infections, large fetus, fetal abnormalities, prematurity.
- Pathology of the extracranial arteries. Subarachnoid hemorrhage may occur due to dissection of the vertebral or carotid artery. In the vast majority of cases, we are talking about the stratification of the extracranial sections of the vertebral arteries, extending into its intradural section.
- Rare factors. In some cases, the cause of SAH is myxoma of the heart, cerebral tumor, vasculitis, angiopathy with amyloidosis, sickle cell anemia, various coagulopathies, anticoagulant treatment.
Risk factors
Along with the immediate causes of SAH, there are contributing factors: arterial hypertension, alcoholism, atherosclerosis and hypercholesterolemia, smoking. In 15-20% of SAH, it is not possible to determine the cause of hemorrhage. In such cases, they talk about the cryptogenic nature of the SAH. Such variants include non-aneurysmic perimesencephalic benign subarachnoid hemorrhage, in which bleeding occurs in the cisterns surrounding the midbrain.
Classification
According to the etiofactor, subarachnoid hemorrhage is classified into post-traumatic and spontaneous. Traumatologists often face the first option, and specialists in the field of neurology often face the second. Depending on the area of hemorrhage, isolated and combined SAH are distinguished. The latter, in turn, is divided into subarachnoid-ventricular, subarachnoid-parenchymal and subarachnoid-parenchymal-ventricular.
In world medicine, Fischer’s classification is widely used, based on the prevalence of SAH according to the results of CT scans of the brain. In accordance with it, they distinguish:
- Class 1 — there is no blood
- Class 2 — SAH with a thickness of less than 1mm without clots
- Class 3 — SAH with a thickness of more than 1 mm or with the presence of clots
- Class 4 — predominantly parenchymal or ventricular hemorrhage.
Subarachnoid hemorrhage symptoms
Pre – hemorrhagic period
Precursors of SAH are observed in 10-15% of patients. They are caused by the presence of an aneurysm with thinned walls through which the liquid part of the blood seeps. The time of occurrence of harbingers varies from a day to 2 weeks before the SAH. Some authors distinguish it as a pre-hemorrhagic period. At this time, patients note transient cephalgia, dizziness, nausea, transient focal symptoms (trigeminal nerve damage, oculomotor disorders, paresis, visual disturbances, aphasia, etc.). In the presence of a giant aneurysm, the clinic of the pre-hemorrhagic period has a tumor-like character in the form of progressive cerebral and focal symptoms.
Acute period
Subarachnoid hemorrhage manifests itself with acute intense headache and disorders of consciousness. With aneurysmal SAH, an unusually strong, lightning-fast increasing cephalgia is observed. When the arteries are dissected, the headache is of a two-phase nature. Short-term loss of consciousness and confusion persisting up to 5-10 days is typical. Psychomotor agitation is possible. Prolonged loss of consciousness and the development of its severe disorders (coma) indicate in favor of severe bleeding with blood pouring into the cerebral ventricles.
The pathognomonic sign of SAH is the meningeal symptom complex: vomiting, rigidity of the muscles of the occiput, hyperesthesia, photophobia, the shell symptoms of Kernig and Brudzinsky. It appears and progresses on the first day of hemorrhage, may have different severity and persist from several days to a month. The addition of focal neurological symptoms on the first day speaks in favor of combined parenchymal-subarachnoid hemorrhage. The later appearance of focal symptoms may be a consequence of secondary ischemic damage to brain tissues, which is observed in 25% of SAH.
Usually, subarachnoid hemorrhage occurs with a rise in temperature to febrility and viscero-vegetative disorders: bradycardia, arterial hypertension, in severe cases — respiratory and cardiac disorders. Hyperthermia may be delayed in nature and occurs as a consequence of the chemical action of blood breakdown products on the cerebral membranes and the thermoregulatory center. In 10% of cases, epiprimes occur.
Atypical forms
In one third of patients, subarachnoid hemorrhage has an atypical course masquerading as migraine paroxysm, acute psychosis, meningitis, hypertensive crisis, cervical radiculitis.
- Migraine form. It proceeds with the sudden appearance of cephalgia without loss of consciousness. The meningeal symptom complex manifests itself after 3-7 days against the background of deterioration of the patient’s condition.
- False hypertonic form. It is often regarded as a hypertensive crisis. Because it is manifested by cephalgia against the background of high blood pressure figures. Subarachnoid hemorrhage is diagnosed at a follow-up examination of the patient with deterioration or repeated bleeding.
- The false-inflammatory form mimics meningitis. There is cephalgia, febrility, pronounced meningeal symptoms.
- The false psychotic form is characterized by the predominance of psychosymptomatics: disorientation, delirium, pronounced psychomotor agitation. It is observed when the aneurysm of the anterior cerebral artery, which supplies blood to the frontal lobes, ruptures.
Complications
Analysis of the results of transcranial Dopplerography showed that subarachnoid hemorrhage is almost always complicated by cerebral vascular spasm. However, clinically significant spasm is noted, according to various data, in 30-60% of patients. Cerebral angiospasm usually develops on 3-5 days. SAH and reaches a maximum on 7-14 days. Its degree directly correlates with the volume of blood spilled. In 20% of cases, primary subarachnoid hemorrhage is complicated by ischemic stroke. With repeated SAH, the frequency of cerebral infarction is 2 times higher. Complications of SAH also include concomitant hemorrhage in the parenchyma of the brain, a breakthrough of blood into the ventricles.
In about 18% of cases, subarachnoid hemorrhage is complicated by acute hydrocephalus, which occurs when the outflow of cerebrospinal fluid is blocked by formed blood clots. In turn, hydrocephalus can lead to swelling of the brain and dislocation of its structures. Among the somatic complications, dehydration, hyponatremia, neurogenic pulmonary edema, aspiration or congestive pneumonia, arrhythmia, myocardial infarction, decompensation of existing heart failure, PE, cystitis, pyelonephritis, stress ulcer, LCD bleeding are possible.
Diagnostics
A typical clinical picture allows a neurologist to suspect a subarachnoid hemorrhage. In the case of atypical forms, early diagnosis of SAH is very difficult. All patients with suspected subarachnoid hemorrhage are shown a CT scan of the brain. The method makes it possible to reliably establish a diagnosis in 95% of SAH; to identify hydrocephalus, bleeding into the ventricles, foci of cerebral ischemia, brain edema.
- Visualization techniques. The detection of blood under the spider web is an indication for cerebral angiography in order to determine the source of bleeding. Modern noninvasive CT or MRI angiography is performed. In patients with the most severe degree of SAH, angiography is performed after stabilization of their condition. If the source of bleeding cannot be determined, then repeated angiography is recommended after 3-4 weeks.
- Lumbar puncture. If a subarachnoid hemorrhage is suspected, it is performed in the absence of CT and in cases when, in the presence of a classical SAH clinic, it is not diagnosed during CT. Detection of blood or xanthochromia in the cerebrospinal fluid is an indication for angiography. In the absence of such changes in the cerebrospinal fluid, another cause of the patient’s condition should be sought.
- Ultrasound. Transcranial ultrasound and cerebral vascular ultrasound make it possible to detect angiospasm in the early stages of SAH and monitor the state of cerebral circulation in dynamics.
- During diagnosis, subarachnoid hemorrhage should be differentiated from other forms of ACVA (hemorrhagic stroke, TIA), meningitis, meningoencephalitis, occlusive hydrocephalus, traumatic brain injury, migraine paroxysm, pheochromocytoma.
Treatment
Basic and specific therapy
Basic therapy of SAH is an action to normalize cardiovascular and respiratory functions, correction of basic biochemical constants. In order to reduce hydrocephalus with its increase and relief of cerebral edema, diuretic therapy (glycerol or mannitol) is prescribed. With the ineffectiveness of conservative therapy and the progression of cerebral edema with the threat of dislocation syndrome, decompressive trepanation of the skull, external ventricular drainage is indicated.
The basic therapy also includes symptomatic treatment. If subarachnoid hemorrhage is accompanied by convulsions, anticonvulsants (lorazepam, diazepam, valproic acid) are included; with psychomotor agitation – sedatives (diazepam, droperidol, sodium thiopental); with repeated vomiting — metoclopramide, domperidone, perfenazine. In parallel, therapy and prevention of somatic complications are carried out.
So far, subarachnoid hemorrhage does not have effective conservative methods of specific treatment that allow to stop bleeding or limit the amount of blood spilled. In accordance with the pathogenesis, specific therapy of SAH is aimed at minimizing angiospasm, preventing and treating cerebral ischemia. The standard of therapy is the use of nimodipine and ZN therapy. The latter makes it possible to maintain hypervolemia, controlled hypertension and hemodilution, as a result of which the rheological properties of blood and microcirculation are optimized.
Surgical treatment
Surgical treatment of SAH is optimal in the first 72 hours. It is performed by a neurosurgeon and is aimed at excluding a ruptured aneurysm from the bloodstream. The operation may consist in clipping the aneurysm neck or endovascular insertion of a balloon catheter filling its cavity. Endovascular occlusion is preferable in case of unstable condition of the patient, high risk of complications of open surgery, early angiospasm. With decompensation of cerebral angiospasm, stenting or angioplasty of the spasmed vessel is possible.
Prognosis and prevention
In 15%, subarachnoid hemorrhage ends in death even before medical care is provided. Lethality in the first month in patients with SAH reaches 30%. With coma, mortality is about 80%, with repeated SAH — 70%. Surviving patients often have residual neurological deficits. The prognosis is most favorable in cases when angiography fails to identify the source of bleeding. Apparently, in such cases, there is an independent closure of the vascular defect due to its small size.
The probability of repeated hemorrhage every day of the first month is kept at the level of 1-2%. Subarachnoid hemorrhage of aneurysmal genesis is repeated in 17-26% of cases, with AVM — in 5% of cases, with SAH of other etiology — much less often. Prevention of SAH involves the therapy of cerebrovascular pathologies, TBI and the elimination of risk factors.