Intracranial hemorrhage

Intracranial hemorrhage (ICH), also known as intracranial bleed, is

Intracerebral bleeding affects 2.5 per 10,000 people each year.[1]

Signs and symptoms

Intracranial hemorrhage is a serious medical emergency because the buildup of blood within the skull can lead to increases in intracranial pressure, which can crush delicate brain tissue or limit its blood supply. Severe increases in intracranial pressure (ICP) can cause brain herniation, in which parts of the brain are squeezed past structures in the skull.^{[citation needed]}

Symptoms include severe headache, nausea/vomiting, seizures, dizziness or lightheadedness or vertigo, one-sided facial drooping, one-sided numbness, weakness, tingling, or paralysis, speech problems, blindness, deafness, memory issues, attention problems, balance problems, coordination problems and decreasing level of consciousness or complete loss of consciousness.

Brain stem hemorrhage may cause additional symptoms such as shortness of breath, dysphagia (difficulty swallowing), chewing problems, abnormal heart rate, and irregular heartbeat. Brain stem hemorrhage can cause cardiac arrest.

Causes

Trauma is the most common cause of intracranial hemorrhage. It can cause epidural hemorrhage, subdural hemorrhage, and subarachnoid hemorrhage. Other condition such as hemorrhagic parenchymal contusion and cerebral microhemorrhages can also be caused by trauma.^[3]

Non-traumatic causes of hemorrhage includes:

CT scan (

Swirl sign on CT scan (areas of low densities with surrounding areas of high densities) is indicative of active intracranial bleeding, high chance of death within one month, and poor subject's function in three months if the subject is still alive.[4]

When ICP is increased the heart rate may be decreased.

Traumatic

Types of intracranial hemorrhage are roughly grouped into intra-axial and extra-axial. Intra-axial hemorrhage is bleeding within the brain itself, or

Extra-axial hemorrhage, bleeding that occurs within the skull but outside of the brain tissue, falls into three subtypes: epidural hematoma, subdural hematoma, and subarachnoid hemorrhage.[3]

Hemorrhagic parenchymal contusion

This condition most commonly occurred in those with significant head movement or head impact. It is caused by injuries of small arterial or venous vessels, causing hemorrhage within the brain parenchyma, and give rise to hyperdense lesion on CT scan. MRI is more sensitive than CT scan in detecting such small hemorrhagic contusions, with the use of gradient echo sequence.^[3] Contusions are more commonly seen in the brain parenchyma near base of the skull such as inferior frontal lobes and temporal lobes as a result of Coup contrecoup injury. Those with parenchymal contusion would require frequent follow-up imaging because such contusions may grow large enough to become hemorrhage and exerts significant mass effect on the brain.^[3]

Cerebral microhemorrhages is a smaller form of hemorrhagic parenchymal contusion and are typically found in white matter. Such microhemorrhages are difficult to be detected on CT scan, but easily detected on gradient echo and susceptibility weighted imaging on MRI scan as hypointense susceptibility blooming. Such microhemorrhages are frequently associated with diffuse axonal injury and located near the grey-white matter junction.^[3]

Epidural hemorrhage

Subdural hematoma maybe less acute than epidural hematoma due to slower blood accumulation, but it still has the potential to cause brain herniation that may require surgical evacuation.[3] Clinical features depend on the site of injury and severity of injury. Patients may have a history of loss of consciousness but they recover and do not relapse. Clinical onset occurs over hours. Complications include focal neurologic deficits depending on the site of hematoma and brain injury, increased intracranial pressure leading to herniation of brain and ischemia due to reduced blood supply and seizures.^{[citation needed]}

Subarachnoid hemorrhage

A subarachnoid hemorrhage (SAH) is

Intracranial bleed in hypertensive subjects usually occurs at 50 to 60 years of life with 30 to 50% chance of death. Such hemorrhages are typically located in the

Cerebral amyloid angiopathy (CAA) is the deposition of Amyloid beta peptide protein within the brain. Accumulation of such peptide proteins within the walls of the arteries can cause weakening of the walls and causes microhemorrhages, SAH within the cerebral sulci or large cerebral intraparenchymal bleed. SAH in CAA can be differentiated from vasculitis by its presentations. SAH in CAA usually occurs in those who age more than 60 years, temporary motor and sensory deficits, and intracranial bleed in white matter adjacent to cerebral cortex. Basal ganglia, posterior fossa, and brainstem are spared. Boston criteria is used to determine the likelihood of a cerebral hemorrhage due to CAA. Definitive diagnosis of CAA is by performing brain biopsy^[3]

CT scan may show hyperdense intra-axial hemorrhage in the subcortical region. Diffuse white matter hypodensities in both cerebral hemispheres may represents microangiopathic changes. On MRI these lesions will be presented as blooming artifact on gradient echo and susceptibility weighted imaging.^[3]

Hemorrhagic conversion of ischemic infarction

43% of those with infarcted brain tissue will develop hemorrhagic conversion. Risk of hemorrhagic is further increased with recanalisation of veins or arteries. Several types of hemorrhages can occur such as petechial hemorrhages around the infarcted margin (HI1), confluent petechial hemorrhages within the infarcted tissue (HI2), hematoma occupying less than 30% of the infarcted tissue (PH1), hematoma involving greater than 30% of infarcted tissue with small mass effect (PH2), and hematoma involving greater than 30% of the infarcted tissue with significant mass effect. However, only PH2 is clinically significant.^[3] Those who has infarction should be monitored frequently with CT brains to access hemorrhagic conversions or worsening vasogenic oedema that may require neurosurgical decompression.^[3] Dual energy CT scan maybe useful to differentiate the high densities caused by reperfusion hemorrhage (bleeding after endovascular stroke treatment) and high density due to iodinated contrast administered during cerebral angiography.^[3]

Cerebral aneurysm

Besides from head injury, it may occur spontaneously, usually from a ruptured

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.^[10]

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.^[3]

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.^[3] 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.^[3]

Cortical venous/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.^[3] 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.^[3]

Vasculitis/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.^[3]

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.^[3]

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.^[11]

From limited observational data, it may be relatively safe to restart

^[1]

Further reading