Intracranial hemorrhage
Intracranial hemorrhage refers to any form of bleeding within the skull. It can result from trauma, vascular abnormalities, hypertension, or other medical conditions. ICH is broadly categorized into several subtypes based on the location of the bleed: intracerebral hemorrhage, subarachnoid hemorrhage, epidural hemorrhage, and subdural hematoma. Each subtype has distinct causes, clinical features, and treatment approaches.
Epidemiology
Acute, spontaneous intracranial hemorrhage 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 may be classified as either traumatic or non-traumatic. 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, 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, 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. 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 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 leaks.Despite its advantages, MRI 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. However, the use of MRI is limited by safety concerns regarding metallic foreign bodies, longer imaging times, and higher sensitivity to motion, reducing availability, and increased cost.
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. This category includes intraparenchymal hemorrhage, which involves bleeding directly into the brain tissue, and intraventricular hemorrhage, which involves bleeding into the brain’s ventricular system—commonly observed in premature infants. Intra-axial hemorrhages are generally associated with a poorer prognosis and are more challenging to manage than extra-axial hemorrhages. Traumatic forms of intra-axial hemorrhage include hemorrhagic parenchymal contusions and cerebral microhemorrhages.
Extra-axial hemorrhage occurs within the cranial vault but outside the brain tissue. It encompasses three main subtypes: epidural hematoma, subdural hematoma, and subarachnoid hemorrhage, each defined by the specific meningeal compartment in which the bleeding occurs.
Hemorrhagic parenchymal contusion
Hemorrhagic parenchymal contusions most commonly occur following significant head trauma, particularly in cases involving rapid head movement or direct impact. These injuries result from the disruption of small arterial or venous vessels, leading to hemorrhage within the brain parenchyma. On computed tomography, they appear as hyperdense lesions. Magnetic resonance imaging, particularly with gradient echo sequences, is more sensitive than CT in detecting small hemorrhagic contusions.Contusions are frequently observed in areas of the brain adjacent to the base of the skull, such as the inferior frontal lobess and temporal lobes, commonly resulting from coup-contrecoup injuries. Those with parenchymal contusion require frequent follow-up imaging because such contusions may grow large enough to become hemorrhage and exert a significant mass effect on the brain.
Cerebral microhemorrhage
Cerebral microhemorrhages are small-scale hemorrhagic lesions that can be considered a minor form of hemorrhagic parenchymal contusion. They are typically located within the cerebral white matter and are challenging to detect using CT imaging. However, they are more readily identified on MRI, particularly with gradient echo or susceptibility-weighted imaging, where they appear as hypointense foci due to susceptibility blooming artifacts. Such microhemorrhages are frequently associated with diffuse axonal injury and located near the grey–white matter junction.Epidural hemorrhage
Epidural hemorrhage refers to bleeding between the dura mater and the inner surface of the skull, typically resulting from traumatic head injury. This condition is characterized by its inability to cross cranial suture lines due to the tight adhesion of the dura to the skull at these points. However, in rare cases—especially in children where skull sutures are not fully fused—epidural hemorrhages may extend across sutures if a fracture involves them.On computed tomography, epidural hemorrhages typically appear as biconvex hyperdense lesions confined by sutural boundaries. The source of bleeding may be arterial or venous. Arterial injuries, such as to the middle meninges artery, commonly at the pterion, lead to rapidly expanding hematomas. Venous sources are usually slower-growing and may involve dural venous sinuses, including the falx cerebri, tentorium cerebelli, or the superior sagittal sinus.
Anterior temporal EDH is usually caused by sphenoparietal sinus. Such EDH is limited and does not require surgery because its extension is confined within the sphenosquamosal suture and the superior or inferior orbital fissures. In 20% to 50% of epidural hemorrhage cases, there is a lucid interval during which the patient regains temporary consciousness after an initial loss; this is then followed by deterioration of conscious state.
When the epidural hematoma is large enough, it will cause mass effect on contralateral brain which lead to midline, subfalcine, and trans-tentorial herniations. This phenomenon can cause the subject to lose consciousness and eventually death. Large EDH often requires emergent surgical clot evacuation. Embolisation of middle meningeal artery is performed if the hemorrhage is medium or small.
Subdural hemorrhage
Subdural hemorrhage results from tearing of the bridging veins in the subdural space between the dura and arachnoid mater. It can cross the suture lines, but not across dural reflections such as falx cerebri or tentorium cerebelli. Therefore, subdural hematoma are typically confined to one side of the cerebral hemisphere.Density of SDH reduces as it progresses from acute to chronic forms. However, areas with low density may not represent chronic SDH entirely as unclotted blood products that are due to active bleed can also give low density appearance on CT scans especially those with coagulopathy. Those with SDH that have same density with brain parenchyma may represent acute bleed such as those with anemia, arachnoid tear, and the mixing of hemorrhage and CSF. SDH usually have high or mixed densities during first two days of trauma, followed by isodensity at 11 days after trauma, and hypodensity after 14 days of trauma. Membranes with granulation tissue can rupture within SDH, and give high density appearance on CT scan. Over a prolonged period of time, calcifications can form. SDH can be treated with burr hole drainage, craniotomy or port system placement for blood clot evacuation, or middle meningeal artery embolisation.
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. Clinical features depend on the location and severity of the injury. Patients may have a history of loss of consciousness but they recover and do not relapse. Symptoms vary but may include loss of consciousness, seizures, or focal neurologic deficits, with an onset that can be delayed by hours to days after injury.