People with intracerebral bleeding have symptoms that correspond to the functions controlled by the area of the brain that is damaged by the bleed. Other symptoms include those that indicate a rise in intracranial pressure caused by a large mass putting pressure on the brain. Intracerebral bleeds are often misdiagnosed as subarachnoid hemorrhages due to the similarity in symptoms and signs. A severe headache followed by vomiting is one of the more common symptoms of intracerebral hemorrhage. Collapsing is another symptom. Some people may experience continuous bleeding from the ear. Some patients may also go into a coma before the bleed is noticed.
Causes
Intracerebral bleeds are the second most common cause of stroke, accounting for 10% of hospital admissions for stroke. High blood pressure raises the risks of spontaneous intracerebral hemorrhage by two to six times. More common in adults than in children, intraparenchymal bleeds are usually due to penetrating head trauma, but can also be due to depressed skull fractures. Acceleration-deceleration trauma, rupture of an aneurysm or arteriovenous malformation, and bleeding within a tumor are additional causes. Amyloid angiopathy is a not uncommon cause of intracerebral hemorrhage in patients over the age of 55. A very small proportion is due to cerebral venous sinus thrombosis. Risk factors for ICH include:
Cigarette smoking may be a risk factor but the association is weak. Traumautic intracerebral hematomas are divided into acute and delayed. Acute intracerebral hematomas occur at the time of the injury while delayed intracerebral hematomas have been reported from as early as 6 hours post injury to as long as several weeks.
When due to high blood pressure, intracerebral hemorrhages typically occur in the putamen or thalamus, cerebrum, cerebellum, pons, or elsewhere in the brainstem.
Treatment
Treatment depends substantially on the type of ICH. Rapid CT scan and other diagnostic measures are used to determine proper treatment, which may include both medication and surgery.
Tracheal intubation is indicated in people with decreased level of consciousness or other risk of airway obstruction.
IV fluids are given to maintain fluid balance, using isotonic rather than hypotonic fluids.
Medication
One review found that antihypertensive therapy to bring down the blood pressure in acute phases appears to improve outcomes. Other reviews found an unclear difference between intensive and less intensive blood pressure control. The American Heart Association and American Stroke Association guidelines in 2015 recommended decreasing the blood pressure to a SBP of 140 mmHg. However, the evidence finds tentative usefulness as of 2015.
Giving Factor VIIa within 4 hours limits the bleeding and formation of a hematoma. However, it also increases the risk of thromboembolism. It thus overall does not result in better outcomes in those without hemophilia.
Frozen plasma, vitamin K, protamine, or platelet transfusions may be given in case of a coagulopathy. Platelets however appear to worsen outcomes in those with spontaneous intracerebral bleeding on antiplatelet medication.
Fosphenytoin or other anticonvulsant is given in case of seizures or lobar hemorrhage.
H2 antagonists or proton pump inhibitors are commonly given for to try to prevent stress ulcers, a condition linked with ICH.
Corticosteroids, were thought to reduce swelling. However, in large controlled studies, corticosteroids have been found to increase mortality rates and are no longer recommended.
Surgery
Surgery is required if the hematoma is greater than, if there is a structural vascularlesion or lobar hemorrhage in a young patient.
A craniectomy may take place, where part of the skull is removed to allow a swelling brain room to expand without being squeezed.
Prognosis
The risk of death from an intraparenchymal bleed in traumatic brain injury is especially high when the injury occurs in the brain stem. Intraparenchymal bleeds within the medulla oblongata are almost always fatal, because they cause damage to cranial nerve X, the vagus nerve, which plays an important role in blood circulation and breathing. This kind of hemorrhage can also occur in the cortex or subcortical areas, usually in the frontal or temporal lobes when due to head injury, and sometimes in the cerebellum. For spontaneous ICH seen on CT scan, the death rate is 34–50% by 30 days after the insult, and half of the deaths occur in the first 2 days. Even though the majority of deaths occurs in the first days after ICH, survivors have a long term excess mortality of 27% compared to the general population.
Intracerebral hemorrhage was first distinguished from strokes due to insufficient blood flow, so called "leaks and plugs", in 1823.
Research
The inflammatory response triggered by stroke has been viewed as harmful in the early stage, focusing on blood-borne leukocytes, neutrophils and macrophages, and resident microglia and astrocytes. A human postmortem study shows that inflammation occurs early and persists for several days after ICH. Modulating microglial activation and polarization might mitigate intracerebral hemorrhage-induced brain injury and improve brain repair. A new area of interest is the role of mast cells in ICH.
