Intracranial hemorrhage

Acute, spontaneous intracranial hemorrhage (ICH) is the second most common form of stroke, affecting approximately 2 million people worldwide each year. In the United States, intracranial hemorrhage accounts for about 20% of all cerebrovascular accidents, with an incidence of approximately 20 cases per 100,000 people annually. Intracranial hemorrhages is diagnosed more frequently in men and individuals over the age of 55, with incidence increasing with age. In low-income countries, the risk is higher, potentially due to reduced access to healthcare and limited education about primary prevention. == Risk factors and causes ==

Intracranial hemorrhage (ICH) may be classified as either traumatic or non-traumatic (spontaneous). Traumatic causes include head trauma resulting from falls, vehicular accidents, or physical assault. Non-traumatic causes are more varied and often related to underlying conditions. Chronic hypertension is the most common non-traumatic cause, particularly in deep brain structures such as the basal ganglia, thalamus, pons, and posterior fossa. Other spontaneous causes include cerebral amyloid angiopathy, especially among the elderly, as well as bleeding disorders such as hemophilia and thrombocytopenia, vascular malformations like arteriovenous malformation (AVMs), and brain tumors. The use of anticoagulant or antiplatelet medications, such as warfarin and aspirin, has been associated with increased hematoma volume and expansion. Illicit drug use, particularly cocaine and methamphetamine, can cause abrupt spikes in blood pressure leading to vessel rupture and subsequent hemorrhage. Additional risk factors that increase the likelihood of intracranial hemorrhage include smoking, heavy alcohol consumption, advanced age, a family history of stroke, diabetes, hyperlipidemia, obesity, and sedentary lifestyle. Hypertension remains the most prevalent and well-established risk factor, contributing to over 60% of primary bleeds. == Signs and symptoms ==

Intracranial hemorrhage is a dynamic and potentially life-threatening process that begins with blood extravasation into the brain parenchyma. This can be followed by bleeding extension, cerebral edema formation, and increased intracranial pressure (ICP), all of which can lead to neural tissue compression. Common signs and symptoms include a sudden onset of focal neurological deficits, which vary depending on the location of the hemorrhage. Decreased levels of consciousness are frequently observed and are assessed using the Glasgow Coma Scale (GCS). Other manifestations include headache, nausea, vomiting, and seizures. Patients may also present with speech disturbances, unilateral weakness or paralysis, sensory deficits, visual impairments, and problems with coordination or balance. Raised diastolic blood pressure is a common clinical finding. Seizures occur in up to 70% of causes, usually within the first 24 to 72 hours following hemorrhage onset. If bleeding extends into the ventricles, hydrocephalus may develop. Brainstem hemorrhages are especially dangerous and can result in cardiorespiratory instability, decreased consciousness, and even cardiac arrest. Long-term complications of intracranial hemorrhages may include post-stroke epilepsy and vascular cognitive impairment. ==Diagnosis==

A non-contrast CT scan (computed tomography) of the brain is commonly used as the initial imaging modality in suspected cases of intracranial hemorrhage. CT is preferred in emergency settings due to its speed, availability, and high sensitivity for detecting acute brain injuries, enabling rapid triage and surgical decision-making. Examples of brain diseases that require urgent intervention are: large-volume hemorrhage, brain herniation, and cerebral infarction. Additional advantages of CT imaging include its effectiveness in detecting bony fractures, vascular injuries, and cerebrospinal fluid (CSF) leaks. Despite its advantages, MRI (magnetic resonance imaging) has higher sensitivity than CT scan for the detection of epidural hemorrhage, subdural hemorrhage, subarachnoid hemorrhage, non hemorrhagic contusions in the cortex, hemorrhagic parenchymal contusions, brainstem injuries, and white matter axonal injuries. MRI is typically used when a patient continues to display neurological symptoms despite a normal CT scan. A swirl sign on CT imaging— representing areas of low density with surrounding areas of high density— suggest active intracranial bleeding. The presence of this sign is associated with an increase in risk of death within one month and a poor functional prognosis at three months among survivors. ==Traumatic==

). Intracranial hemorrhages are broadly classified into intra-axial and extra-axial types, based on the location of the bleeding relative to the brain tissue. Intra-axial hemorrhage refers to bleeding that occurs within the brain parenchyma or ventricular system. These injuries result from the disruption of small arterial or venous vessels, leading to hemorrhage within the brain parenchyma. Such microhemorrhages are frequently associated with diffuse axonal injury and located near the grey–white matter junction. When the epidural hematoma is large enough, it will cause mass effect on contralateral brain which lead to midline, subfalcine (below the falx cerebri), and trans-tentorial (crossing tentorium cerebelli) herniations. This phenomenon can cause the subject to lose consciousness and eventually death. On CT imaging, traumatic SAH is usually localized to the cerebral sulci near the vertex of the head and typically spares the basal cisterns. Severe trauma can cause SAH in all regions of the brain. When the SAH volume is large, rarely it can cause cerebral infarction a few days after trauma due to arterial vasospasm. Although CT scans are more frequently used for initial evaluation, MRI is more sensitive than CT in detecting SAH. Findings may include hyperintense signal of fluid-attenuated inversion recovery (FLAIR) sequence and blooming artifact on susceptibility weighted imaging (SWI). Further vascular imaging, such as CT angiography (CTA) or MR angiography (MRA), is recommended in certain situations—particularly when a skull fracture involves the carotid canal, due to the risk of post-traumatic vasospasm impairing cerebral perfusion. These imaging techniques are also used when the hemorrhage pattern is atypical for trauma, as in isolated SAH located in the basal cisterns, Sylvian fissure, or anterior interhemispheric fissure. Such patterns may suggest ruptured intracranial aneurysms, and warrant further investigation. ==Non-traumatic==

Hypertensive bleed Hypertensive intracerebral hemorrhage (ICH) typically occurs in individuals between 50 and 60 years of age and is associated with high mortality, with case fatality rates ranging from 30% to 50%. CT scan has 100% sensitivity of detecting SAH at 6 to 24 hours after symptoms onset. The diagnosis is generally confirmed with a CT scan of the head. If CT scan is normal but SAH is still strongly suspected, lumbar puncture can be done at six to twelfth hours after the onset of headache. This is to determine the presence of blood within the cerebrospinal fluid (CSF). Those with SAH will have blood and bilirubin within their CSF because of the degradation of their red blood cells. Meanwhile, those who has blood within CSF due to traumatic lumbar puncture will not have bilirubin within CSF. SAH is generally located within basal cisterns, extends diffusely to all subarachnoid spaces (cerebral sulci) or into the ventricular system, or brain parenchyma. Modified Fisher scale is used to describe the volume and distribution of SAH, just predicting the probability of cerebral artery vasospasm after SAH. Treatment is by prompt neurosurgery or radiologically-guided interventions with medications and other treatments to help prevent recurrence of the bleeding and complications. Since the 1990s, many aneurysms are treated by a minimal invasive procedure known as endovascular coiling, which is carried out by instrumentation through large blood vessels. However, this procedure has higher recurrence rates than the more invasive craniotomy with clipping. Cerebral ateriovenous malformation Cerebral ateriovenous malformation (Cerebral AVM) is characterised by abnormal shunting between cerebral arteries and veins without going through capillaries. Instead the blood goes through a collection of small vessels from arteries to veins. These collection of abnormal small vessels is termed as "nidus". This condition happens in 0.1% of the population has a risk of 2 to 4% per year for intracranial bleeding. Once ruptured, it results in intraparenchymal hemorrhage, intraventricular hemorrhage and SAH. Rupture of cerebral AVM often occurs in young people and children. Cerebral AVM can be diagnosed by computed tomography angiography (CTA) brain, magnetic resonance angiography (MRA) brain, or digital subtraction angiography (DSA). DSA is important to determine whether there is nidal or perinidal aneurysm. Dural arteriovenous fistulae Dural arteriovenous fistulae (DAVF) is the direct connection between dural or cerebral arteries with dural venous sinuses or cortical veins. It accounts for 10 to 15% of intracranial arteriovenous shunts. DAVF lacks a nidus. Signs and symptoms of DAVF are: headache, tinnitus, neurological deficits involving cranial nerves, and increased intracranial pressure. DAVF once ruptured, will produce intraparenchymal hemorrhage or SAH. Increase in number of vessels near dural venous sinuses as seen on CTA is suggestive of DVAF. 4DCT may increase the sensitivity of detecting DAVF. In MRI scans, susceptibility weighted imaging (SWI) and arterial spin labelling sequences (labelling protons in blood without the use of contrast media to determine blood flow) are useful in evaluating DAVF. The patterns of draining veins from the fistula determines the risk of DAVF rupture. Increased pressure within the dural venous sinuses causes backpressure into the cortical veins, thus making cortical veins more prone to rupture. The risk of hemorrhage is graded by Cognard and Borden grading systems. These grading systems are based upon the DSA. Cortical venous and cerebral venous sinus thrombosis Dural venous sinus thrombosis (DVST) and cortical venous thrombosis (CVT) commonly presents with headache, increased intracranial pressure, or seizures. DVST is more common than CVT. DVST are frequently caused by infections in the skull base, dehydration, thrombophilia, meningioma, and other dural tumours. On CT scans, brain parenchymal hemorrhage that does not confined to specific arterial territory along with hyperdense appearance on dural venous sinuses raises the suspicion of DVST. Further evaluation with CT venography, MR venography, and post gadolinium MRI provides accurate diagnosis of venous thrombosis and follow-up after treatment. These studies demonstrate thrombus as filling defect or lack of signal. Vasculitis and vasculopathy Those with vasculitis may be presented with headache, behavioural changes, neurological deficits, or intracranial bleeding. Sulcal SAH is the most common form of intracranial bleed caused by vasculitis. On CT scans, sulcal SAH is seen as hyperdensity within the cerebral sulcus, while on MRI, it is seen as hyperintensity on FLAIR sequence, and hypointensity on GRE/SWI sequence. DSA is important in making the diagnosis of vasculitis or vasculopathy. Mycotic aneurysm It is arterial outpouchings arise from distal cerebral arteries. These are pseudoaneurysm, caused by thrombus clogging the distal arteries, which results in inflammation and small tears at the site of occlusion. These inflammation and thrombis can caused by infective endocarditis, artificial heart valve or other heart problems. Similar to vasculitis, rupture of mycotic aneurysm also causes SAH in cerebral sulci, mostly located in the vertex. If mycotic aneurysm is located more proximally, it will produce diffuse SAH pattern. CTA or MRA would produce focal outpouching or increase in diameter of the vessel. Meanwhile, GRE/SWI MRI sequence would produce focal hypointensity. Small mycotic aneurysms are difficult to be seen on CT or MRI. Thus, DSA is useful in identifying these lesions. ==Management==

For those who is already on blood thinners such as aspirin or clopidogrel for prevention of myocardial infarction or stroke, traumatic intracranial hemorrhage should prompt the use of platelet function assays (PFA-100) to assess the effect of these antiplalelet agents. After that, plateletpheresis can be started to increase the aggregation of platelets, thus stopping the intracranial bleed. In those with impaired kidney functions, desmopressin or cryoprecipitate can be used instead. From limited observational data, it may be relatively safe to restart blood thinners after an ICH as it is associated with reduced thromboembolic complications with similar risk of recurrent hemorrhage when compared to those did not start blood thinners after an ICH. ==Comparison==