Cerebral Hemorrhage

Last updated date: 05-May-2023

Originally Written in English

Cerebral Hemorrhage


Cerebrovascular accident (CVA), sometimes known as a stroke, is the third largest cause of morbidity and mortality in many developed countries. Strokes can be either ischemic or hemorrhagic. When blood supply to a portion of the brain is cut off, an ischemic stroke develops. It's a rather common type of stroke. Cerebral Hemorrhage, often known as a stroke, is a deadly condition in which a hematoma occurs inside the brain parenchyma, with or without blood extension into the ventricles.

Management of Cerebral Hemorrhage ranges from medication to open surgery to actively drain the hematoma, with research underway to develop less intrusive ways to improve prognosis. Complications from a brain bleed are common. The bleeding prevents nerve cells from communicating with the rest of the body and resuming normal function.


What is Cerebral Hemorrhage?

hemorrhagic stroke

A hemorrhagic stroke happens when a blood artery ruptures, resulting in brain hemorrhage. Intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH) are two types of hemorrhagic stroke (SAH). SAH occurs when blood leaks into the subarachnoid space, whereas ICH occurs when blood leaks into the brain parenchyma.

Cerebral bleeding has been associated to considerable morbidity and mortality. The advancement of a hemorrhagic stroke is associated with worse results. Early discovery and treatment are crucial because to the characteristic rapid increase of bleeding, which causes rapid deterioration of awareness and neurological impairment.



The global incidence of stroke, both ischemic and hemorrhagic, was over 33 million in 2010, with hemorrhagic strokes accounting for more than a third of cases and more than half of all deaths. Despite the fact that the global prevalence of ICH is around 20 cases per 100,000 people per year, the occurrence of ICH in low/middle-income countries is double that of more economically developed nations.

Thankfully, the global fatality rate from such strokes has decreased. The higher risk in developing countries might be linked to a lack of basic preventative knowledge and restricted access to medical treatment.

Stroke, both ischemic and hemorrhagic, is the fourth leading cause of death in the United States, accounting for just under 20% of all cerebrovascular events.

ICH is more frequent in the elderly (above 55 years of age) and in men, with an African and Asian predilection. The frequency of ICH in the Japanese population has risen to 55 cases per 100,000 people, according to research, and this is attributed to an increase in the prevalence of alcohol intake and hypertension.


What causes a cerebral hemorrhage?

intracerebral hemorrhages

Non-traumatic Primary and secondary intracerebral hemorrhages account for 85 percent of all ICH and are linked to hypertension and amyloid angiopathy. Secondary hemorrhage is hypothesized to be induced by a variety of factors, including but not limited to bleeding diathesis (iatrogenic, congenital, or acquired), vascular anomalies, neoplasms, hemorrhagic conversion of an ischemic stroke, and drug abuse.

Primary or spontaneous ICH accounts for more than 85% of hemorrhagic strokes. When no other clinical or structural cause is found, a major ICH diagnosis is typically one of exclusion, and it is supported by a history of chronic hypertension, increasing age, and clot placement. Lipohyalinosis and degenerative changes in penetrating arterioles are thought to be the causes of Charcot-Bouchard aneurysms in small arterial arteries supplying deep brain areas in individuals with chronic arterial hypertension.

Hypertension causes more than 60% of primary bleeding, with hematomas most commonly detected in the posterior fossa, pons, basal ganglia, and thalamus. Lobar hemorrhages are typically the characteristic feature of amyloid angiopathy in the elderly. This is a degenerative disorder thought to be caused by apolipoprotein E gene variations that allow for increased amyloid buildup inside vessel walls.

In contrast, secondary ICH is caused by an underlying structural problem, such as vascular abnormalities or malignant tissue. Arteriovenous malformations, cavernous angiomas, cerebral aneurysms, and aorto-venous fistulae are commonly the cause of ICH in otherwise healthy young persons.

Cerebral hematomas can also be induced by a primary or metastatic lesion, or by hemorrhagic conversion of a recent ischemic stroke. Furthermore, congenial and acquired bleeding diathesis is a common cause of ICHs, which is becoming more common as a result of the large population of adults using anticoagulant (warfarin) and antiplatelet (aspirin) medicine.

The presence of cerebral amyloid angiopathy on imaging increases the chances of both lobar and recurrent ICH. Uncontrolled or untreated hypertension is a manageable risk factor in the elderly population that increases the risk of ICH by a factor of two. Other modifiable risk factors include alcohol, nicotine, and cocaine addiction. 



Pathophysiology of Cerebral Hemorrhage

Hemorrhages inside the cerebral parenchyma are commonly characterized as primary injury, which refers to the immediate tissue damage produced by the hematoma, and secondary injury, which refers to the subsequent pathological change caused by the hemorrhage. Although ICH was previously thought to be a single-event disease, it is now recognized as a dynamic disorder with multiple stages, which are as follows:

  1. The initial extravasation of blood into the parenchyma
  2. Subsequent bleeding around the clot causing expansion
  3. Swelling or edema around the hematoma

Acute ICH causes a fast increase in mass inside the brain's parenchyma, causing compression and disruption of the surrounding neuronal tissue, potentially affecting adjoining cell signaling pathways and resulting in localized neurological dysfunction. Blood evaporates within white matter, leaving small patches of intact brain tissue in and around the hematoma that may be recovered.

The initial indication of a hematoma in the brainstem may be loss of consciousness, followed by cardiorespiratory discomfort or possibly cardiac arrest. The initial hematoma's expansion, as measured by a volume increase of 33 to 50% on repeat CT scanning, is an important determinant in determining patients' prognosis and functional outcome. Clot enlargement of this size is seen in less than 40% of people and is related with increased morbidity and worse outcomes.

Over 70% of ICHs have been proven to grow during the first 24 hours due to chronic or recurrent bleeding. Both untreated hypertension and bleeding diathesis increase the chance of hematoma formation. The blood-brain barrier is thought to break, and the clot's mass impact causes a fast rise in intracranial pressure (ICP), causing distortion of the local tissue architecture and interrupting venous outflow, culminating in vascular engorgement.

The local mass effect on the tissues may cause stretching and microscopic rupture of the surrounding vasculature (venules and arterioles), allowing for tiny bleeding foci around the ICH's borders. Increased ICP causes tissue displacement or mass effect, which can result in herniation syndromes, as well as decreased cerebral perfusion pressures (CPP), which can result in secondary brain injury.


Cerebral Hemorrhage symptoms 

Cerebral Hemorrhage symptoms

As with other acute presentations, a succinct but complete history is crucial for forming a diagnosis. The length of symptoms and the period of ictus are critical details in the ICH history. The majority of vascular episodes are unanticipated and are induced by high-energy activities like exercise or heavy lifting, as well as the use of stimulants like cocaine and alcohol. A long smoking history has ramifications in vascular illness, such as hypertension and vasculitis, both of which are risk factors for ICH.

The most common sign of ICH is a rapid onset localized neurological impairment produced by the bleeding site and subsequent edema. This is typically accompanied with a decrease in the patients' conscious state, as measured by the Glasgow coma scale (GCS)

Other common symptoms and signs include headache, nausea/vomiting, seizures (both convulsive and non-convulsive), and a high diastolic blood pressure (>110 mmHg). The clot's spread into the ventricles can cause obstructive hydrocephalus, which is characterized by signs and symptoms of elevated intracranial pressure, such as postural headaches (worse while laying flat), papilledema, nausea, vomiting, diplopia, disorientation, and a lowered conscious level.

The first examination of the patient should include a check for airway patency and normal breathing. To sustain brain perfusion, first assess circulation and offer broad bore venous access while aiming for systolic blood pressure targets of 120 to 140 mmHg. A very low consciousness level (GCS8) requires immediate attention, and establishing an airway in a patient with a low conscious level is a high priority. The patient must next have a comprehensive peripheral inspection and examination, including evaluation of the pupils, because dilatation and inactivity of the pupils is an indicator of cerebral herniation and must be treated as soon as possible.

Once the patient is medically stable, confirm a clear history of anticoagulant/antiplatelet therapy or coagulation problems, as well as assess the patient's clotting function and other routine blood testing. Any coagulation abnormalities should be evaluated by a hematologist and treated as appropriate. 


Cerebral Hemorrhage Diagnosis

Cerebral Hemorrhage Diagnosis

A non-contrast CT scan remains the gold-standard imaging modality in the first diagnosis of ICH since it is widely available and rapid. A CT head can differentiate between many kinds of cerebral illness, including subarachnoid hemorrhage, ischemic stroke, and ICH. It can also suggest the hemorrhage's magnitude, surrounding edema, mass effect, intraventricular clot extension, and high intracranial pressure. Although it takes longer and is less generally available, MRI is an effective imaging tool for detecting ICH and can assist find old clots.

Acute ICH is shown on CT of the head as an area of hyperdensity within the parenchyma with surrounding hypodensity, indicating perivascular edema. Approximate clot volumes may be calculated by multiplying the clot's maximum depth, height, and length in centimeters by two.

Cerebral Hemorrhage Diagnosis

The detection of a vascular anomaly can also be helpful prior to clot evacuation in the emergency context, as surgeons frequently prefer to treat vascular malformations in a more elective/planned environment. 



Management of Cerebral Hemorrhage

The majority of care in the prehospital situation is airway, breathing, and circulatory support, with the goal of getting the patient to the nearest emergency room. A comprehensive narrative from any witnesses or family/caregivers at the scene of the occurrence is always valuable since it may reveal significant information about trauma, medical history, and drug history.

Early aggressive medical care in an acute hospital environment has been proven to have a direct influence on morbidity and death after a brain hemorrhage. Following a diagnosis, the immediate goal is to reduce the risk of rebleeding and hematoma growth within the first 24 to 72 hours. With the guidance of hematologists, any and all coagulation irregularities must first be rectified, including therapy of known factor deficits and reversal of any anticoagulation drugs the patient is known to be on.

Rising blood pressure is present in the majority of Intracerebral Hemorrhage (ICP) presentations for a variety of physiological causes, including discomfort, stress, a history of elevated blood pressure, and raised ICP. Because hematoma growth is a probable result of consistently increased systolic blood pressure, early medical care must include treatment of excessive blood pressure. However, blood pressure lowering should take the patients' normal blood pressure into account, since a hypertensive patient may be unable to sustain cerebral perfusion at a much lower SBP.

In people with SBP ranging from 150 to 220 mmHg, American stroke guidelines recommend lowering blood pressure to 140 mmHg. In the group of ICH patients with SBP > 220 mmHg, it is still important to reduce their blood pressure, but in a more controlled manner utilizing an infusion with continuous monitoring.

Strict blood glucose monitoring has been shown to improve the prognosis of ICH; nevertheless, additional research has found an increase in mortality in patients with cerebral hypoglycemia. As a result, guidelines recommend aiming for normoglycemia while strictly avoiding hypoglycemia. Patients with seizures who present to hospitals should be treated with antiseizure medicines such as phenytoin or levetiracetam. However, there is no indication that preventive anti-seizure medicine reduces the risk of ICH-related seizures.

Urgent consequences of ICH include intraventricular extension and hydrocephalus; the latter occurred more rapidly in posterior fossa hemorrhages due to the fourth ventricle's physical closeness and, as a result, its tendency to become occluded. In these circumstances, CSF diversion is the primary therapy, and an external ventricular drain (EVD) can be implanted, most typically into the right lateral ventricle. This results in a decrease in ICP and herniation.

Surgical evacuation of a clot inside the posterior fossa improves results in favorable surgical candidates if the clot is larger than 3 cm and causing brainstem compression, reduced level of awareness, and/or hydrocephalus. Patients with a higher GCS and a lower amount of blood at the time of operation had a better prognosis after surgery.




To reduce the mass effect induced by a supratentorial, big ICH, some surgeons may contemplate a decompressive craniectomy (with or without clot evacuation) for chosen patients who demonstrate no progress with medicinal treatment. A systematic study of decompressive craniectomy in the setting of supratentorial ICH found that survival rates increased, although morbidity remained high.

Recently, ICH therapy employing minimally invasive procedures has been developed and used globally, with the benefit of less parenchymal brain harm and shorter surgery time. Current approaches utilize stereotactic guidance and the insertion of a catheter that can administer thrombolysis into the clot while also allowing for aspiration if necessary.


Differential Diagnosis

Many illnesses can manifest acutely with symptoms and indications comparable to acute ICH. Other intracranial hemorrhages, such as a subarachnoid hemorrhage (SAH) and a subdural hemorrhage (both acute and chronic), neoplasms (primary and secondary), and infection, are frequently associated with the common symptoms of headache and nausea, as well as clinical manifestations of decreased consciousness, confusion, seizures, and focal neurological deficit.

The pathognomonic quick onset, intense headache 'like being smacked in the back of the head' is the major symptom of a SAH. Aside from this characteristic, which may not always be conveyed as eloquently, individuals may present in a manner similar to those with acute ICH. An unenhanced CT Head in a SAH would show blood in the subarachnoid space and ventricular cisterns rather than the parenchyma, as in an ICH.

Symptoms of an acute subdural hematoma may be similar. The important distinguishing characteristic, however, is a history of recent trauma before the appearance. Chronic subdural hemorrhages are most frequent among the elderly, especially those on blood-thinning medication, with a history of repeated falls followed by a longer period of headaches, disorientation, and/or localized neurological deficiency. Acute and chronic subdural hematomas can be distinguished on a plain CT head by the presence of a crescentic extra-axial collection that is hypodense in the chronic situation and hyperdense in the acute setting.

Brain cancers typically manifest themselves insidiously. Most patients can compensate due to their gradual growth until the intracranial pressure is high enough to cause symptoms such as headache, nausea, vomiting, seizures, and decreased GCS. When the history is examined more closely, there is typically evidence of a mild progressive history, and contrasted CT imaging is frequently necessary to make a diagnosis.

In certain cases, patients with neoplastic lesions may present with hemorrhages into a main or secondary brain tumor. This can lead to diagnostic ambiguity, which frequently necessitates delayed imaging, such as MR, to provide a more accurate diagnosis of underlying disease.



Cerebral Hemorrhage prognosis

Acute ICH can be fatal, with death mostly predicted by hematoma size, location, and the patients' GCS at the time of admission. At 30 days, the mortality rate can be as high as 50%, with the majority of these fatalities happening within 24 hours after the first shock, with intraventricular blood and hydrocephalus frequently playing a significant role in the patient's decline.

Patients who arrive at the hospital with a GCS of 9 and a clot size of 60 ml or more have a nearly 90% death rate. Because of the proclivity for the development of obstructive hydrocephalus and loss of life-sustaining function, posterior fossa and brainstem hemorrhages have a worse prognosis. At 6 months after the acute hemorrhage, less than 20% of individuals who survive are deemed to be autonomous. Furthermore, variables such as the patients' age and comorbidities influence outcomes after ICH.



An extension of the clot into the ventricles is found in around 30% to 50% of individuals with ICH. Because of the physical relationship to the third ventricle and the natural inclination for blood to travel medially, it is considered to be more frequent in thalamic hemorrhages. Patients with intraventricular hemorrhage (IVH) have lower functional results, which may be due to periventricular tissue compression and damage, inflammatory mediator reaction to blood products inside the ventricular system, and obstructive hydrocephalus and associated sequelae.

Obstructive hydrocephalus is a consequence of IVH that can result in potentially fatal complications due to elevated ICP. It is more common in persons who have a bigger blood volume within the ventricular channels. Pacchioni granulations within the arachnoid villi may become partially blocked by intraventricular blood products, resulting in communicating hydrocephalus, which can cause severe morbidity once again.

Seizures are frequently associated with the initial symptoms of ICH, although they can also be a later consequence in rare patients (two hours post hemorrhage). Approximately 70% of seizures occur within 24 hours after the first ictus, and the great majority (90%) occur within 72 hours. Early seizures (those that occur within two hours after the first ICH) are caused by alterations in the architecture of neuronal tissues as well as metabolic failure, whereas delayed seizures are more likely caused by gliosis and tissue scarring.

Venous thromboembolism (VTE), also known as deep vein thrombosis (DVT) and pulmonary embolism (PE), is a frequent complication encountered in most hospitalized patients, although it occurs at a rate of between 3% to 7% in individuals with ICH. Symptomatic DVTs are less prevalent, while asymptomatic DVTs can occur at an incidence of up to 17%. The high risk of VTE is most likely due to the immobility of patients with ICH, since many will have hemiplegia/hemiparesis.

As part of the body's normal stress reaction, approximately 60% of patients with ICH develop temporary hyperglycemia in the acute setting, lasting up to 72 hours. According to studies, there is a significant association between blood glucose levels and hematoma size, hematoma growth, and surrounding edema, making elevated blood glucose an independent predictor of poor functional results.

Despite having no such history before to admission, approximately 70% of patients are found to be hypertensive (BP higher than or equal to 140/90 mmHg) during the acute period following an ICH. The reasons for this phenomena are unknown, although one hypothesis is that as part of the stress response to elevated ICP, there may be activation of neuroendocrine pathways (sympathetic nervous system, renin-angiotensin axis) and higher cardiac output.



Intracerebral hemorrhage

Intracerebral hemorrhage, which occurs as a result of blood artery rupture in the brain, is a major public health issue that causes a high risk of mortality and disability in adults. Brain trauma, aneurysms, arteriovenous malformations, and brain cancers are all possible causes.

Treatment is heavily influenced by the kind of ICH. To establish optimal therapy, a rapid CT scan and other diagnostic techniques are employed. If the hematoma is more than 3 cm, there is a structural vascular lesion, or there is lobar bleeding in a young child, surgery is indicated. When a traumatic brain injury occurs in the brain stem, the risk of mortality from an intraparenchymal hemorrhage is very significant.