Etiology and key risk factors
The development of intracerebral hemorrhage is caused by the rupture of pathologically altered vessels. The main cause, accounting for about 60% of all episodes, is arterial hypertension. Hypertensive hemorrhages have a specific tropism for the basins of the perforating arteries of the brain.
Other important etiological factors include:
- Amyloid angiopathy. This is a fairly common cause of hemorrhages in senile age. It is based on the deposition of a specific amyloid protein in the middle layer (tunica media) and adventitia (tunica adventitia) of small cortical arteries and arterioles, which makes their walls fragile.
- Vascular anomalies. Arteriovenous malformations (AVMs) and aneurysms of intracranial vessels.
- Blood coagulation disorders. Leukemia, hemophilia, thrombocytopenia, and various hemorrhagic diatheses.
- Toxic factors. Substance abuse (cocaine, amphetamine, methamphetamine).
- Alcohol abuse. This factor acts indirectly: toxic liver damage leads to impaired synthesis of coagulation factors and subsequent hypocoagulability.
- Other pathologies. Cerebral arteritis, arterial dissection, and intracranial venous thrombosis.
Role of pharmacotherapy in hemorrhage development
Hemorrhagic stroke can act as a severe iatrogenic complication in the treatment of other cardiovascular diseases, primarily ischemic lesions and transient ischemic attacks (TIAs). The risk of brain hemorrhage increases while taking medications that reduce blood clotting:
- Thrombolytics. For example, recombinant tissue plasminogen activator (rt-PA), used to dissolve blood clots in vascular occlusion (such as the basilar or middle cerebral artery).
- Oral anticoagulants. Warfarin (especially when exceeding the target INR value of 2.0–3.0) and novel oral anticoagulants (dabigatran, rivaroxaban, apixaban) prescribed for cardioembolic strokes.
- Antiplatelet agents. Acetylsalicylic acid (aspirin), clopidogrel, dipyridamole.
Typical localization
In arterial hypertension, the rupture of perforating arteries leads to the formation of hematomas in strictly defined areas of the brain.
| Anatomical structure | Share of all hypertensive hemorrhages |
|---|---|
| Basal ganglia (nuclei basales) and internal capsule | 50% |
| Thalamus (thalamus) | 15% |
| Pons (pons) | 10% |
| Cerebellum (cerebellum) | 10% |
Pathogenesis and developmental variants
The formation of the lesion in hemorrhagic stroke can proceed via two main types: the formation of a massive hematoma or in the form of hemorrhagic infiltration of brain tissues.
The mechanism of brain tissue damage is complex. First, primary cell death of nervous tissue occurs directly in the zone of blood effusion. Then, secondary injury rapidly joins. It is associated with physical compression of brain tissue by the formed hematoma, a sharp decrease in perfusion and the development of ischemia around the hemorrhage focus, as well as a critical increase in intracranial pressure (ICP).
Blood effused into the parenchyma can spread beyond the primary focus. Blood breakthrough into the subarachnoid space (forming parenchymal-subarachnoid hemorrhage) or into the ventricular system of the brain (parenchymal-ventricular hemorrhage) is possible.
Complications and outcomes
Massive hemorrhages are characterized by an extremely severe course due to a pronounced mass effect. A large volume of effused blood causes displacement (shift) of brain structures. The most fatal complication is compression of the brainstem — in particular, transtentorial herniation (entrapment of the midbrain in the tentorial notch). In the vast majority of cases, this condition leads to a fatal outcome.
In situations of non-fatal outcome, when the hematoma volume does not cause critical displacement, gradual regression of ischemia and brain tissue edema begins only 1–2 weeks after the vascular catastrophe.
Briefly: answers to topical questions
What are the characteristic clinical symptoms and signs of hemorrhagic stroke upon admission?
The characteristic clinical manifestations of hemorrhagic stroke are the rapid development of combined focal and general cerebral symptoms.
- General cerebral symptoms — headache and impaired consciousness, which often prevail over focal syndromes.
- Focal symptoms — depend on the localization (for example, severe contralateral hemiparesis in lesions of the basal ganglia or brainstem symptoms in brainstem lesions).
- Meningeal symptoms — detected immediately or within a few hours after the hemorrhage.
In 10% of cases, generalized epileptic seizures may develop.
Which instrumental diagnostic method is the gold standard for the emergency detection of hemorrhagic stroke?
The leading instrumental examination method and the method of choice for detecting hemorrhagic stroke is X-ray computed tomography (CT) of the brain. CT allows determining the localization and volume of the hematoma, identifying the displacement of brain structures, hydrocephalus, and the penetration of blood into the ventricular system, as well as ruling out cerebral infarction. It is impossible to reliably distinguish hemorrhagic stroke from ischemic stroke based solely on the clinical picture, so neuroimaging is required.
What types of displacement and brain herniation syndromes exist in massive hemorrhage?
In massive hemorrhage, two main types of brain herniation (displacement) are distinguished, leading to compression of the brainstem and disruption of vital functions:
- Upward herniation — transtentorial displacement of the mediobasal part of the temporal lobe medially and downward under the cerebellar tentorium, which causes compression of the upper parts of the brainstem (midbrain entrapment).
- Downward herniation — tonsillar displacement of the cerebellar tonsils downward through the foramen magnum into the spinal canal, leading to compression of the caudal part of the brainstem.
Transverse displacement of the brain is also distinguished, the progression of which is an indication for surgical decompression.
What are the main indications for emergency surgical removal of an intracerebral hematoma?
Indications for surgical treatment of an intracerebral hematoma are determined taking into account the patient's age, localization, and size of the hematoma. For large hematomas with a volume of more than 20 cm³, surgical removal is advisable and justified by clinical studies. Removal of small hematomas is not recommended; in deeply located hematomas, it is fraught with damage to healthy brain tissue. With very large hemorrhages with a volume of more than 60 cm³, the prognosis for recovery is poor even after neurosurgical intervention. With increasing edema and transverse displacement of the brain, delayed secondary decompressive craniectomy is recommended.
What is the basic medical tactic for blood pressure control and discontinuation of anticoagulants in hemorrhagic stroke?
The basic tactic includes blood pressure monitoring with the correction of identified disorders (general measures are similar to those for ischemic stroke). If a stroke develops against the background of taking oral anticoagulants, their intake must be temporarily interrupted. To stop life-threatening bleeding, the following are used:
- Specific antidotes — for example, idarucizumab (active only against dabigatran etexilate).
- Prothrombin complex concentrate — blood coagulation factors II, VII, IX, and X in combination, allowing the stabilization of the hematoma.
- Nonspecific hemostasis agents.
Class and exam questions
Why is alcohol abuse considered a risk factor for hemorrhagic stroke?
Alcohol acts indirectly: its toxic effect leads to impaired liver function, which in turn causes hypocoagulation (reduced blood clotting) and increases the risk of spontaneous hemorrhage.
What is the essence of amyloid angiopathy?
This is a pathology of senile age, in which a specific amyloid protein is deposited in the middle and outer layers of small cortical arteries and arterioles, leading to their fragility and ruptures.
What medications can trigger intracerebral hemorrhage?
Hemorrhage can be a complication of pharmacotherapy with thrombolytics (rtPA), anticoagulants (warfarin, DOACs), or antiplatelet agents (aspirin, clopidogrel).
Where is hemorrhage most commonly localized in arterial hypertension?
In half of the cases, the basal ganglia and internal capsule are affected. The thalamus (15%), pons, and cerebellum (10% each) are also frequently involved.
What else to study on this topic
- Secondary prevention of ischemic stroke and TIA
- Use of anticoagulants: warfarin and INR monitoring
- Carotid endarterectomy and stenting
- Clinical presentation of ischemia in the internal carotid artery territory
- Intra-arterial thrombolysis for basilar artery occlusion
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