Intracerebral hemorrhage

Source: Wikipedia, the free encyclopedia.
Intracerebral hemorrhage
Other namesCerebral haemorrhage, cerebral hemorrhage, intra-axial hemorrhage, cerebral hematoma, cerebral bleed, brain bleed, hemorrhagic stroke
ventricular drain[1]
Prognosis20% good outcome[2]
Frequency2.5 per 10,000 people a year[2]
Deaths44% die within one month[2]

Intracerebral hemorrhage (ICH), also known as hemorrhagic stroke, is a sudden bleeding into

decreased level of consciousness or total loss of consciousness, neck stiffness, and fever.[2][1]

Hemorrhagic stroke may occur on the background of alterations to the blood vessels in the brain, such as cerebral

brain tumors and an intracranial aneurysm, which can cause intraparenchymal or subarachnoid hemorrhage.[1]

The biggest risk factors for spontaneous bleeding are

blood thinners, and cocaine use.[2] Diagnosis is typically by CT scan.[1]

Treatment should typically be carried out in an

corticosteroids is frequently avoided.[1] Sometimes surgery to directly remove the blood can be therapeutic.[1]

Cerebral bleeding affects about 2.5 per 10,000 people each year.[2] It occurs more often in males and older people.[2] About 44% of those affected die within a month.[2] A good outcome occurs in about 20% of those affected.[2] Intracerebral hemorrhage, a type of hemorrhagic stroke, was first distinguished from ischemic strokes due to insufficient blood flow, so called "leaks and plugs", in 1823.[6]

Epidemiology

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.

cerebral embolism (30%).[9]

Types

Intraparenchymal hemorrhage

herniation syndromes
.

Intraventricular hemorrhage

physical trauma or from hemorrhagic stroke
.

30% of intraventricular hemorrhage (IVH) are primary, confined to the ventricular system and typically caused by intraventricular trauma, aneurysm, vascular malformations, or tumors, particularly of the choroid plexus.

traumatic brain injuries.[12] Thus the hemorrhage usually does not occur without extensive associated damage, and so the outcome is rarely good.[13][14]

Signs and symptoms

People with intracerebral bleeding have symptoms that correspond to the functions controlled by the area of the brain that is damaged by the bleed.

ischemic stroke.[7] While the duration of onset not be as rapid, it is important that patients go to the emergency department as soon as they notice any symptoms as early detection and management of stroke may lead to better outcomes post-stroke than delayed identification.[16]

A mnemonic to remember the warning signs of stroke is

Cincinnati Prehospital Stroke Scale (CPSS).[19] Use of these scales is recommended by professional guidelines.[20] FAST is less reliable in the recognition of posterior circulation stroke.[21]

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.[15] These symptoms include headaches, nausea, vomiting, a depressed level of consciousness, stupor and death.[7] 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.[10]

Hemorrhage into the

persistent vegetative state (if there is damage to the reticular activating system).[7]

Causes

Axial CT scan showing hemorrhage in the posterior fossa[22]

Intracerebral bleeds are the second most common cause of

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.[citation needed
]

Risk factors for ICH include:[11]

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.

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.[7]

Cigarette smoking may be a risk factor but the association is weak.[29]

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.[citation needed]

Diagnosis

Spontaneous ICH with hydrocephalus on CT scan[22]

Both computed tomography angiography (CTA) and magnetic resonance angiography (MRA) have been proved to be effective in diagnosing intracranial vascular malformations after ICH.[12] So frequently, a CT angiogram will be performed in order to exclude a secondary cause of hemorrhage[30] 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.[30] The oedema surrounding the haemorrhage would rapidly increase in size in the first 48 hours, and reached its maximum extent at day 14. The bigger the size of the haematoma, the larger its surrounding oedema.[31] Brain oedema formation is due to the breakdown of red blood cells, where haemoglobin and other contents of red blood cells are released. The release of these red blood cells contents causes toxic effect on the brain and causes brain oedema. Besides, the breaking down of blood-brain barrier also contributes to the odema formation.[13]

Apart from CT scans, haematoma progression of intracerebral haemorrhage can be monitored using transcranial ultrasound. Ultrasound probe can be placed at the temporal lobe to estimate the volume of haematoma within the brain, thus identifying those with active bleeding for further intervention to stop the bleeding. Using ultrasound can also reduces radiation risk to the subject from CT scans.[14]

Location

When due to high blood pressure, intracerebral hemorrhages typically occur in the putamen (50%) or thalamus (15%), cerebrum (10–20%), cerebellum (10–13%), pons (7–15%), or elsewhere in the brainstem (1–6%).[32][33]

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.

Medications

Rapid lowering of the blood pressure using

American Stroke Association guidelines in 2015 recommended decreasing the blood pressure to a SBP of 140 mmHg.[1] However, later reviews found unclear difference between intensive and less intensive blood pressure control.[38][39]

Giving

Factor VIIa within 4 hours limits the bleeding and formation of a hematoma. However, it also increases the risk of thromboembolism.[34] It thus overall does not result in better outcomes in those without hemophilia.[40]

Frozen plasma, vitamin K, protamine, or platelet transfusions may be given in case of a coagulopathy.[34] Platelets however appear to worsen outcomes in those with spontaneous intracerebral bleeding on antiplatelet medication.[41]

The specific reversal agents idarucizumab and andexanet alfa may be used to stop continued intracerebral hemorrhage in people taking directly oral acting anticoagulants (such as factor Xa inhibitors or direct thrombin inhibitors).[7] However, if these specialized medications are not available, prothrombin complex concentrate may also be used.[7]

Only 7% of those with ICH are presented with clinical features of seizures while up to 25% of those have subclinical seizures. Seizures are not associated with an increased risk of death or disability. Meanwhile, anticonvulsant administration can increase the risk of death. Therefore, anticonvulsants are only reserved for those that have shown obvious clinical features of seizures or seizure activity on electroencephalography (EEG).[42]

H2 antagonists or proton pump inhibitors are commonly given to try to prevent stress ulcers, a condition linked with ICH.[34]

Corticosteroids were thought to reduce swelling. However, in large controlled studies, corticosteroids have been found to increase mortality rates and are no longer recommended.[43][44]

Surgery

Surgery is required if the

vascular lesion or lobar hemorrhage in a young patient.[34]

A

vasculature to close off or dilate blood vessels, avoiding invasive surgical procedures.[45]

Aspiration by

endoscopic drainage may be used in basal ganglia hemorrhages, although successful reports are limited.[34]

A craniectomy holds promise of reduced mortality, but the effects of long‐term neurological outcome remain controversial.[46]

Prognosis

About 8 to 33% of those with intracranial haemorrhage have neurological deterioration within the first 24 hours of hospital admission, where a large proportion of them happens within 6 to 12 hours. Rate of haematoma expansion, perihaematoma odema volume and the presence of fever can affect the chances of getting neurological complications.[47]

The risk of death from an intraparenchymal bleed in traumatic brain injury is especially high when the injury occurs in the

blood circulation and breathing.[24] 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.[24][49] 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.[7][50] Perihematomal edema, or secondary edema surrounding the hematoma, is associated with secondary brain injury, worsening neurological function and is associated with poor outcomes.[7] 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.[7] Brain herniation is associated with poor prognoses.[7]

For spontaneous intracerebral hemorrhage seen on CT scan, the death rate (mortality) is 34–50% by 30 days after the injury,[22] and half of the deaths occur in the first 2 days.[51] Even though the majority of deaths occur in the first few days after ICH, survivors have a long-term excess mortality rate of 27% compared to the general population.[52] Of those who survive an intracerebral hemorrhage, 12–39% are independent with regard to self-care; others are disabled to varying degrees and require supportive care.[8]

References

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