Basics of Brain hemorrhage

Dr.R.Rengarajan

• Intracranial haemorrhage is a collective term encompassing many different conditions characterised by the extravascular accumulation of blood within different intracranial spaces.

• Extra-axial hemorrhage– extradural haemorrhage (EDH)– subdural haemorrhage (SDH)– subarachnoid haemorrhage (SAH)

• Intra-axial hemorrhage– intracerebral haemorrhage - basal ganglia, lobar,

pontine and cerebellar– intraventricular haemorrhage (IVH)

• CT scan is almost always the first imaging modality used to assess patients with suspected intracranial haemorrhage.

• Acute blood is markedly hyperdense compared to brain parenchyma.

• CT angiography is increasingly used to assess for a vascular underlying cause, where location/appearance of bleed make a primary haemorrhage less likely.

• CT venogram can be used to reliably assess for patency of the dural venous sinuses.

• MRI is typically requested when an underlying abnormality is being sought, particularly when an underlying tumour is suspected.

• MRI of haemorrhage can pose some challenges in that the appearance of blood changes depending on the sequence and the time since the haemorrhage and the size and location of the bleed.

• Cerebral angiography is usually performed when a vascular abnormality is suspected and the CT angiogram is either normal (and index of suspicion is high) or equivocal.

Extra-axial hemorrhage

Lining layers

• Dura is a thick tough membrane.

• The inner surface of dura is lined by a transparent flimsy membrane called the arachnoid membrane.

• The third layer is the pia mater which tightly hugs the brain going into every sulcus and gyrus on the brain surface.

Spaces

• Extradural or epidural – between the skull and the dura

• Subdural – potential space between the dura and arachnoid membrane

• Subarachnoid space – relatively large space which is filled with CSF

• Blood clots within the pia mater are called as intraaxial

Characteristics

Characteristics

• Site• Size• Side• Shifts

• Symptoms and signs

Site

Size

Side

Shifts

• The mass effect may produce compression of the ventricles and shift of the 3rd ventricle and septum pellucidum to the opposite side.

• Such displacement can produce severe brain or vascular damage.

• These displacements are called herniations. Patients with sufficient mass effect are at risk for transtentorial and subfalcine brain herniation and death.

TYPES OF BRAIN HERNIATION

Subfalcine herniationThe supratentorial brain, along with the lateral ventricle

and septum pellucidum, herniates beneath the falx and shifts across the midline toward the opposite side.

Transtentorial herniationUsually, the cerebral hemispheres are displaced

downward through the incisura beneath the tentorium compressing the ipsilateral temporal horn and causing dilatation of the contralateral temporal horn.

Foramen magnum/tonsillar herniation Infratentorial brain is displaced downward through the foramen

magnum.

Sphenoid herniationSupratentorial brain slides over the sphenoid bone either anteriorly

(in the case of the temporal lobe) or posteriorly (for the frontal lobe).

Extracranial herniationDisplacement of brain through a defect in the cranium.

Epidural hemorrhage

• Epidural haematomas do not normally cross suture lines as the dura insertion is tough thereby restricting the enlarging clot to the confines of the sutures of that particular bone.

• Hence they compress the brain and appear biconvex.

• Typically extradural hematomas are seen in young patients who have sustained head trauma, usually with an associated skull fracture.

• The source of bleeding is typically from a torn meningeal artery, usually the middle meningeal artery.

• An associated skull fracture is present in about 80% of cases.

Subdural hemorrhage

• Subdural hematomas are crescent shaped in comparison to extradural hematomas.

• Subdural haemorrhages are believed to be due to stretching and tearing of bridging cortical veins as they cross the subdural space to drain into an adjacent dural sinus.

• These veins rupture due of shearing forces when there is a

sudden change in the velocity of the head.

• They are usually more extensive than extradural hematomas.

• In contrast to extradural haemorrhage, SDH is not limited by sutures, but are limited by dural reflections, such as the falx cerebri, tentorium, and falx cerebelli.

• Overall 85% of subdural haematomas are unilateral.

• Common sites for subdural hematomas are fronto-parietal convexities and the middle cranial fossa.

• Isolated inter-hemispheric/ parafalcine subdural hematomas are seen more frequently in children, and are common in cases of non-accidental trauma.

• In the vast majority of cases, CT scans are sufficient

to make the diagnosis and manage these patients.

• Hyper-acuteRelatively iso-dense to the adjacent cortex, with a swirled appearance do

to mixture of clot, serum and ongoing unclotted blood.

• AcuteHomogeneously hyperdense extra-axial collection that spreads diffusely

over the affected hemisphere.

• SubacuteIso-dense to the adjacent cortex.

• ChronicHypodense and can be iso-dense to CSF, and mimic subdural hygromas.

• Acute on chronicHypodense collection with a haematocrit level (located posteriorly).

Chronic subdural hematoma

Acute on chronic sub-dural haematoma

Acute on chronic SDH

Indirect signs of SDH

• CSF filled sulci do not reach the skull but rather fade out into the subdural

• Mass effect including sulcal distortion and midline shift

• Apparent thickening of the cortex

Huge isodense subdural haematoma causing gross compression to the left hemisphere including subfalcine herniation of the cingulate gyrus

Subarachnoid hemorrhage

• The distinction between SAH and intracerebral hemorrhage is important because spontaneous subarachnoid haemorrhage is most frequently caused by aneurysm rupture, which is fatal in one third of cases.

• The majority of aneurysms occur around the circle of Willis, hence aneurysmal subarachnoid haemorrhage tends to appear mainly in the basal cisterns and sylvian fissure on CT scan.

• The main blood vessels in the brain travel in the subarachnoid space, hence when an aneurysm ruptures, it bleeds into the subarachnoid space where there is very little to tamponade the bleed.

Usual locations

• The Interhemispheric FissureThe interhemispheric fissure is the home of the anterior communicating

artery and anterior cerebral artery aneurysms, the commonest site of aneurysms. Subarachnoid haemorrhage here is characterized by interhemispheric blood or haematoma and not infrequently it ruptures into the ventricle.

• The Sylvian FissuresThe sylvian fissures are home to middle cerebral artery aneurysms. It is

important to note that the sylvian fissures communicate freely with the central sulcus and other sulci that run to the convexity of the brain.

• The Ambient Cisterns

The ambient cisterns surround the midbrain and communicate with the interpeduncular fossa where the circle of Willis is located.

Bleeding into this space could come from several places and is easily recognized by the ‘loss’ of the dark CSF density around the midbrain.

So that even if they (the ambient cisterns which are normally hypodense) were to appear isodense with brain, then a focused scrutiny is required to look for other evidence of SAH.

• Prepontine Cisterns

The prepontine cistern is a very important location to scrutinize for SAH because basilar tip aneurysms make their home here and hyperdense blood from SAH could be easily obscured by the surrounding bone, which forms the anterior boundary of this space.

Associated features

• Hydrocephalus• Infarction• Giant aneurysm• Hematoma

Hydrocephalus

• Hydrocephalus (often transient) is a frequent accompaniment of SAH.

• The brain CT scan may show only early hydrocephalus characterized by dilatation of the temporal horns of the lateral ventricles.

• This should be taken as a strong clue of recent SAH because in the normal brain scan the temporal horns are usually not visible or barely seen.

Infarction

• Low densities in the brain parenchyma associated with a recent (≥3–10 days) history of SAH when present implies established or imminent infarction or oedema of the brain.

• The hypodensities in SAH tend to cross vascular boundaries and be more pronounced in the watershed areas.

• This complication which represents vasospasm with ischemia usually occurs after the third day.

Giant aneurysms

• Giant or large aneurysms may be visible on brain CT scan.

• They exert a lot of mass effect and may precipitate hydrocephalus.

• Aneurysms generally have a more smooth and rounded outline compared to tumours and are often located in the areas where aneurysms are usually found – the suprasellar cistern and the sylvian fissures.

• In addition, SAH associated with tumours like gliomas, meningioma or pituitary tumors for example, is a very rare occurrence.

Hematoma

• Subarachnoid haemorrhage associated with intracerebral haematoma also signifies large volume of haemorrhage and the location is often in the temporal lobe (middle cerebral artery aneurysm) or the frontal lobes – interhemispheric haematoma from anterior communicating artery aneurysm.

• The typical appearance consists of subarachnoid haemorrhage in the usual locations associated with a large hyperdense clot inside the brain proper.

• The important differential diagnosis here is hypertensive intracerebral haemorrhage, which can be distinguished from aneurysmal haemorrhage with haematoma by the classic basal ganglia location of the former as well as the lack of a significant SAH.

SAH epilogue

Intra-axial hemorrhage

Intracerebral hematoma

• Intracerebral haematomas are clots located entirely within the substance of the brain or the larger part of it is in the substance of the brain

• But they may track into the ventricles or into the subdural space.

• Contusions are small intracerebral haemorrhages that often occur in areas where the brain comes in contact with the very rough floor of the skull like the floor of the frontal lobe and the temporal lobe.

• They also occur in deeper brain structures from shear injury and larger contusions form intracerebral haematomas.

• The principal concern in intracerebral haematoma is the mass effect and functional damage.

• Spontaneous intracerebral haematoma is often the result of uncontrolled hypertension or amyloid angiopathy.

• The lenticulostriate vessels arise from the middle cerebral artery bringing relatively high hydrostatic pressure from the carotid to the internal capsule, basal ganglia and thalamus.

• These areas are therefore prone to hypertensive haemorrhage and are the usual locations although a large haemorrhage could rupture into the ventricles.

Basal ganglial haemorrhage

• A basal ganglial haemorrhage is a common form of intracerebral haemorrhage.

• Usually as a result of poorly controlled long standing hypertension, and the stigmata of chronic hypertensive encephalopathy are often present.

• Other sites of hypertensive haemorrhages are the pons, and the cerebellum.

Lobar haemorrhage

• Primary lobar haemorrhages (usually due to cerebral amyloid angiopathy) are typically seen in elderly.

• Younger patients may also develop lobar haemorrhages, but in such cases they usually have an underlying lesion (e.g. cerebral AVM).

• CT is usually the modality first obtained, and demonstrates hypderdense collection of blood, located superficially within the lobes of the brain

• Extension into the subdural or subarachnoid and even intraventricular space (the later is far more common in basal ganglia haemorrhages) may be seen.

Pontine haemorrhage

• Most commonly due to long standing poorly controlled chronic hypertension.

• Primary pontine haemorrhages account for approximately 10% of all intracranial haemorrhages.

• Typically patients are elderly with a long history of poorly controlled hypertension.

• Pontine hemorrhages can also be due to vascular malformations, tumours, downward herniation (duret haemorrhages) and supratentorial surgery (remote haemorrhage).

Cerebellar haemorrhage

• Most frequently seen in the setting of poorly controlled hypertension.

• Although the can of course also be secondary to an underlying lesion (e.g. tumour or vascular malformation) or due to supratentorial surgery .

• Larger bleeds can impair consciousness and obstruct the fourth ventricle resulting in obstructive hydrocephalus.

Intraventricular haemorrhage

• Intraventricular haemorrhage (IVH) merely denotes the present of blood within the ventricular system of the brain, and is responsible for significant morbidity due to the development of obstructive hydrocephalus in many of these patients.

Some of the more common causes of primary intraventricular haemorrhage in adults include :

• intraventricular tumours• vascular malformations

Secondary causes of intraventricular haemorrhage include: • intracerebral haemorrhage hypertensive haemorrhage,

especially basal ganglia haemorrhage (common)• subarachnoid haemorrhage

Role of MRI in bleeds

• Neuroradiological semeiology is based on the time elapsed since the onset of the intraaxial bleeding.

• The temporal evolution of the MR characteristics of blood is caused both by alterations of the erythrocytes as well as the haemoglobin present under several differing conditions.

• Haemoglobin alterations are influenced by various factors, including: pH, conditions of osmolarity, temperature, partial oxgen pressure (pO2) and the metabolic microenvironment along with the concentration of the oxidizable sublayers.

• In the hyperacute phase (in the first 12 hours from onset )

• Intraparenchymal haemorrhagic foci are composed of intact red blood cells with high oxygen saturation and therefore containing oxyhaemoglobin.

• The MR relaxation times are longer than those of the surrounding tissue due to the local alteration in free water content and protein concentration.

• isointensity on the T1-weighted images, • minor hyperintensity on PD-weighted images, and• isointensity on the T2-weighted images

• In the oxygen-dependent acute phase (12 hours - 2 days),

• The pO2 within the extravasated blood starts to drop fairly quickly, and consequently there is a reduction in the haemoglobin’s oxygen saturation, with the eventual formation of deoxyhaemoglobin.

• The presence of deoxyhaemoglobin in the haemorrhagic lesion translates into

• relative hypo-isointensity on T1-weighted images, • iso-hypointensity on PD-weighted images and • rather marked hypointensity on T2- weighted images.

• The subacute, glucose-dependent phase (2- 14 days) is characterized by two events that occur in parallel but slightly out of phase with one another, partly sharing the same pathogenic mechanisms: – the formation of metahaemoglobin (methaemoglobin: 2-7 days)

and – erythrocyte lysis (7-14 days).

• Methaemoglobin causes a reduction in T1 relaxation due to the dipole-dipole interaction between the external shell electrons of the methaemoglobin and water protons.

• relative hyperintensity on T1-weighted images, • hyperintensity on PD-weighted images and• hypointensity on T2-weighted images.

• Once erythrocyte lysis has taken place, a loss of T2 relaxation enhancement occurs, as methaemoglobin assumes a homogeneous distribution, which translates into hyperintensity of the MR signal on T2-weighted images.

• relative hyperintensity on T1- weighted images, • hyperintensity on PD-dependent images and• hyperintensity on T2- weighted images.

• The chronic phase of haematoma evolution is characterized by the phagocytosis of erythrocyte lysis products by microphages around periphery of the haemorrhagic collection.

• Within the macrophages heme iron accumulates primarily within lysosome vacuoles in the form of haemosiderin.

• The presence of haemosiderin causes increased T2 relaxation and therefore hypointensity on T2-weighted images within the peripheral rim of the haemorrhagic lesion that persists indefinitely.

• In the meantime, methaemoglobin within the haemorrhagic collection continues to cause MR signal hyperintensity on the T1- and T2- weighted images.

• Subsequently, as months pass, methaemoglobin breaks down into derivatives that do not have T1 relaxation effects.

• MRI can also sometimes provide information that indicates the underlying cause of the bleeding.

• Apart from arterial hypertension, and excluding trauma, intracerebral bleeding typically is caused by vascular malformations or richly vascularized intracerebral neoplasias.

Site

• Nucleo-capsular haemorrhages (between the basal ganglia nuclei and the internal capsule: 50%) - capsulo-lenticular, capsulo-thalamic and capsulocaudate.

• Lobar haemorrhages (35%)

• Infratentorial haemorrhages (10%)

• Intraventricular haemorrhages (5%)

Morphology and structure

• Intraaxial haematomas can be round or oval, with well-defined margins, or alternatively irregular with dendritic margins or even with completely irregular boundaries having a somewhat map-like appearance.

• Haematoma morphology can be linked to either a vascular malformation/ aneurysm or a spontaneous aetiology, however, haematomas with irregular margins are more commonly encountered in patients with blood dyscrasias.

Number

• Intraaxial blood collections tend to be single in number.

• The finding of multiple haemorrhagic foci, usually in a superficial lobar position (excluding those of traumatic origin), point in the direction of a diagnosis of a – blood disorder (including iatrogenic anticoagulation),– multiple haemorrhagic neoplastic metastases (including

melanoma) or – dural venous sinus thrombosis with venous

infarcts/haemorrhages.

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