Intracerebral hemorrhage

People with intracerebral bleeding have symptoms that correspond to the functions controlled by the area of the brain that is damaged by the bleed.[7] These localizing signs and symptoms can include hemiplegia (or weakness localized to one side of the body) and paresthesia (loss of sensation) including hemisensory loss (if localized to one side of the body).[8] These symptoms are usually rapid in onset, sometimes occurring in minutes, but not as rapid as the symptom onset in ischemic stroke.[8] Other symptoms include those that indicate a rise in intracranial pressure caused by a large mass (due to hematoma expansion) putting pressure on the brain.[7] These symptoms include headaches, nausea, vomiting, a depressed level of consciousness, stupor and death.[8] Continued elevation in the intracranial pressure and the accompanying mass effect may eventually cause brain herniation (when different parts of the brain are displaced or shifted to new areas in relation to the skull and surrounding dura mater supporting structures). Brain herniation is associated with hyperventilation, extensor rigidity, pupillary asymmetry, pyramidal signs, coma and death.[9]

Hemorrhage into the basal ganglia or thalamus causes contralateral hemiplegia due to damage to the internal capsule.[8] Other possible symptoms include gaze palsies or hemisensory loss.[8] Intracerebral hemorrhage into the cerebellum may cause ataxia, vertigo, incoordination of limbs and vomiting.[8] Some cases of cerebellar hemorrhage lead to blockage of the fourth ventricle with subsequent impairment of drainage of cerebrospinal fluid from the brain.[8] The ensuing hydrocephalus, or fluid buildup in the ventricles of the brain leads to a decreased level of consciousness and coma.[8] Brainstem hemorrhage most commonly occurs in the pons and is associated with cranial nerve palsies, pinpoint (but reactive) pupils, gaze palsies, facial weakness, and coma (if there is damage to the reticular activating system).[8]

Axial CT scan showing hemorrhage in the posterior fossa[10]

Intracerebral bleeds are the second most common cause of stroke, accounting for 10% of hospital admissions for stroke.[11] High blood pressure raises the risks of spontaneous intracerebral hemorrhage by two to six times.[10] 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,[12][13][14] rupture of an aneurysm or arteriovenous malformation (AVM), and bleeding within a tumor are additional causes. Amyloid angiopathy is not an 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:[15]

• Hypertension (high blood pressure)
• Diabetes mellitus
• Menopause
• Excessive alcohol consumption
• Severe migraine

Hypertension is the strongest risk factor associated with intracerebral hemorrhage and long term control of elevated blood pressure has been shown to reduce the incidence of hemorrhage.[8] Cerebral amyloid angiopathy, a disease characterized by deposition of amyloid beta peptides in the walls of the small blood vessels of the brain, leading to weakened blood vessel walls and an increased risk of bleeding; is also an important risk factor for the development of intracerebral hemorrhage. Other risk factors include advancing age (usually with a concomitant increase of cerebral amyloid angiopathy risk in the elderly), use of anticoagulants or antiplatelet medications, the presence of cerebral microbleeds, chronic kidney disease, and low low density lipoprotein (LDL) levels (usually below 70).[16][17] The direct oral anticoagulants (DOACs) such as the factor Xa inhibitors or direct thrombin inhibitors are thought to have a lower risk of intracerebral hemorrhage as compared to the vitamin K antagonists such as warfarin.[8]

Cigarette smoking may be a risk factor but the association is weak.[18]

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.

Spontaneous ICH with hydrocephalus on CT scan[10]

Both computed tomography angiography (CTA) and magnetic resonance angiography (MRA) have been proved to be effective in diagnosing intracranial vascular malformations after ICH.[19] So frequently, a CT angiogram will be performed in order to exclude a secondary cause of hemorrhage[20] or to detect a "spot sign".

Intraparenchymal hemorrhage can be recognized on CT scans because blood appears brighter than other tissue and is separated from the inner table of the skull by brain tissue. The tissue surrounding a bleed is often less dense than the rest of the brain because of edema, and therefore shows up darker on the CT scan.[20]

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.[23]
• IV fluids are given to maintain fluid balance, using isotonic rather than hypotonic fluids.[23]

The risk of death from an intraparenchymal bleed in traumatic brain injury is especially high when the injury occurs in the brain stem.[32] 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.[12] 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.[12][33] Larger volumes of hematoma at hospital admission as well as greater expansion of the hematoma on subsequent evaluation (usually occurring within 6 hours of symptom onset) are associated with a worse prognosis.[8][34] Perihematomal edema, or secondary edema surrounding the hematoma, is associated with secondary brain injury, worsening neurological function and is associated with poor outcomes.[8] Intraventricular hemorrhage, or bleeding into the ventricles of the brain, which may occur in 30-50% of patients, is also associated with long term disability and a poor prognosis.[8] Brain herniation is associated with poor prognoses.[8]

For spontaneous intracerebral hemorrhage seen on CT scan, the death rate (mortality) is 34–50% by 30 days after the injury,[10] and half of the deaths occur in the first 2 days.[35] 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.[36] Of those who survive an intracerebral hemorrhage; 12-39% are independent with regards to self care, others are disabled to varying degrees and require supportive care.[37]

The incidence of intracerebral hemorrhage is estimated at 24.6 cases per 100,000 person years with the incidence rate being similar in men and women.[8][37] The incidence is much higher in the elderly, especially those who are 85 or older, who are 9.6 times more likely to have an intracerebral hemorrhage as compared to those of middle age.[37] It accounts for 20% of all cases of cerebrovascular disease in the United States, behind cerebral thrombosis (40%) and cerebral embolism (30%).[38]

Intracerebral hemorrhage was first distinguished from strokes due to insufficient blood flow, so called "leaks and plugs", in 1823.[6] Franklin D. Roosevelt, the 32nd President of the United States, died from a cerebral hemorrhage in 1945 and so did Soviet dictator Joseph Stalin in 1953.

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.[39][40] A human postmortem study shows that inflammation occurs early and persists for several days after ICH.[41] Modulating microglial activation and polarization might mitigate intracerebral hemorrhage-induced brain injury and improve brain repair.[42] A new area of interest is the role of mast cells in ICH.[40][43]

• Hemphill JC, 3rd; Greenberg, SM; Anderson, CS; Becker, K; Bendok, BR; Cushman, M; Fung, GL; Goldstein, JN; Macdonald, RL; Mitchell, PH; Scott, PA; Selim, MH; Woo, D (28 May 2015). "Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association". Stroke: A Journal of Cerebral Circulation. 46 (7): 2032–60. doi:10.1161/STR.0000000000000069. PMID 26022637.