This site or third-party tools used by this make use of cookies necessary for the operation and useful for the purposes described in the cookie policy. By clicking on "I accept" you consent to the use of cookies.

Subarachnoid hemorrhages (ESA)

  1. Gastroepato
  2. Neurology
  3. Hemorrhagic stroke
  4. Subarachnoid hemorrhages
  5. Occlusive pathology of cerebral arteries
  6. Metabolic coma
  7. The brain decay

Subarachnoid hemorrhages (ESA)

They represent, together with massive hypertensive hemorrhages, one of the two main causes of intracranial hemorrhage. However, we are not talking about intracerebral hemorrhage but of hemorrhages occurring in the subarachnoid space.

Subarachnoid haemorrhage (also called ESA) means a bleeding that takes place in the area between the arachnoid and the pia mater, two membranes that surround the brain. Sometimes it can occur spontaneously, usually due to the rupture of a brain aneurysm, or it can be a consequence of a head injury. ESA is a form of stroke and includes 1-7% of all strokes. It is a medical emergency and can lead to death or serious disability, especially if it is not recognized and treated at an early stage. Approximately half of all ESA cases are fatal, including 10-15% of them before the patient is able to reach a hospital.

Etiology

In 80% to 90% of cases, ESAs are caused by the rupture of an intracranial aneurysm. Other possible causes are cavernous angioma, trauma, leukemia, hemorrhagic diathesis and haemorrhages due to brain metastases. In reality, aneurysms do not exclusively cause subarachnoid hemorrhages. This is true in most cases of congenital aneurysms, which are free within subarachnoid cisterns. The other rarer aneurysms cause more often cerebral hemorrhages (for example aneurysms of the anterior communicating artery or of the basilar) or, in cases where the aneurysm invades the arachnoid, of the subdural hematomas.
Frequent vascular lesions of the brain are arteriovenous malformations and aneurysms. A congenital "Berry" or saccular endocranial aneurysm is the cause in about 85% of patients. Bleeding may cease spontaneously. Aneurysm hemorrhage can occur in every age group, but is more common between the ages of 40 and 65. Less common causes are mycotic aneurysms, arteriovenous malformations and haemorrhagic diseases.

Arteriovenous malformations

Encephalic arteriovenous malformations are characterized by dilated and entangled blood vessels, in which the arteries meet directly with the veins. Arteriovenous malformations occur most often at the junction of the cerebral arteries, usually in the parenchyma of the fronto-parietal region, of the frontal lobe, of the lateral portion of the cerebellum or of the overlying occipital lobe. Arteriovenous malformations can also occur within the dura mater. Arteriovenous malformations can directly bleed or compress the brain tissue; it may result in epileptic seizures or ischemia.
• localization of the aneurysm
• dimensions and morphology
• shape, margins, collar width, ratio (body / collar ratio)

Sites of cerebral aneurysms

• 30% front communicant
• Rear communicant 25%
• Average cerebral 20%
• Internal carotid 10%
• Basic 5%
• Another 10%
• 20% multiple

Clinic

Subarachnoid hemorrhages almost always occur in the absence of premonitory signs. Only in 10% of cases are preceded by headache or non-specific symptoms, resulting from the expansion of the aneurysm. They manifest themselves with:
• intense, unbearable headache, frequently localized at the occipital level, without apparent cause. There may be irradiation towards the back and the lower extremities;
• vegetative symptoms such as fever, nausea, vomiting, episodes of sweating, tachyarrhythmias;
• alterations of consciousness, in about half of the cases. In a third of the cases, these are slight alterations (confusion, disorientation), in another third they are evident (with a reaction preserved to pain stimuli) and in the remaining third only the reflexes are present, without any reaction to pain stimuli:
• meningism, ie pain caused by distension of the meninges, with the corresponding stretching reactions;
• focal symptoms due to hematoma compression. You can observe paralysis, disturbances of the word or sensitivity, spasms, alterations of the visus;
• generalized or focal epileptic seizures.

Hunt and Hess classification

According to the Hunt and Hess classification the following stages are recognized:
• stage I: mild headache, normal neurological examination, conserved state of consciousness;
• stage II: headache and meningism, disorders of the cranial nerves, but without other focal signs;
• stage III: obnubilation and disorientation, with or without other deficits;
• stage IV: alterations of consciousness with reaction to preserved pain, usually associated with hemipa-rendered and vegetative alterations;
• stage V: deep coma, possibly stiffness due to decerebration.

Isolated dilatation of a pupil and loss of pupillary reflex to light may be a sign of a brain hernia following an increase in intracranial pressure. As a result of hemorrhaging, the body produces large amounts of adrenaline and similar hormones. This leads to a sharp increase in blood pressure, the heart is noticeably under stress and pulmonary edema (fluid accumulation in the lungs) may occur, cardiac arrhythmias (irregularity in heartbeat and rhythm), changes in the electrocardiogram occur in 27% of cases up to cardiac arrest in 3% of cases

Diagnosis

During the physical examination, particular attention must be paid to detecting alterations in consciousness, paralysis of the cranial nerves, focal neurological signs, hemiparesis, asymmetry of reflexes and meningism. Finally, the signs of Kernig and Brudzinski can be searched for.
In the vast majority of cases, the CT allows the diagnosis of hemorrhage to be made on the first day. Faced with a typical clinical picture and a negative CT, lumbar puncture is indicated. The possible results are:
• in the acute ESAs, in the three tubes blood is collected without differences between one tube and the other;
• in the case of traumatic puncture, a progressive clearing of the liquid is observed proceeding from the first to the last tube;
• if the bleeding goes back to a period between four hours and two weeks before, the liquid obtained will be yellowish. By means of digital angiography for image subtraction performed before surgery, it is possible to accurately locate the re-sponsible aneurysm of hemorrhage. In these cases the aneurysm is masked by the presence of blood at the peri-vascular level or by the spasm of the vessel.

Neurological diagnostic procedures

The lumbar puncture is contraindicated if increased intracranial pressure is suspected, as the sudden reduction in cerebrospinal fluid pressure may weaken the bruising of the broken aneurysm by a clot, causing further bleeding.
The liquor findings suggesting subarachnoid hemorrhage include high GR numbers, xanthochromy and increased blood pressure. The presence of GR in the cerebrospinal fluid can also be caused by trauma during lumbar puncture. A traumatic lumbar puncture is suspected if the GR counts decrease in samples of cerebrospinal fluid collected sequentially during the same lumbar puncture. Moreover, about 6 h or more after a subarachnoid hemorrhage, the GRs become crenate and undergo lysis, determining xantochromia of the supernatant of the cerebrospinal fluid, with the presence of GR crenates (visible on microscopic examination of the cerebrospinal fluid); these findings usually indicate that subarachnoid haemorrhage preceded lumbar puncture. If the doubt persists, the diagnosis of hemorrhage must be presumed or the lumbar puncture must be repeated after 8-12 hours.
In patients with subarachnoid hemorrhage, a conventional brain angiography should be performed as soon as possible after the initial bleeding episode; alternatives include angio-MR and angio-CT. In all 4 arteries (2 carotid and 2 vertebral arteries) the contrast medium should be injected since up to 20% of patients (especially women) have multiple aneurysms.
On the ECG, subarachnoid haemorrhage may cause elevation or sub-segmentation of the ST segment. This can cause a syncope, mimicking a myocardial infarction. Other possible ECG alterations include QRS or QT prolongation and symmetrically inverted, sharp or deep T waves.

Prognosis

Approximately 35% of patients die after the first aneurysmal subarachnoid hemorrhage; another 15% die within a few weeks for a subsequent break. After 6 months, a second break occurs with a frequency of about 3% / year. In general, the prognosis is severe in the case of aneurysm, better in the case of arteriovenous malformation and optimal in the case in which there are no lesions with the angiography of the 4 vessels, presumably because the source of the bleeding is in this case small and collapsed or thrombosed. Among the survivors, neurological outcomes are frequent, even when the treatment is optimal.

Neurology