Non traumatic haemorrhage
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PRESENTATION ON NON TRAUMATIC HAEMORRHAGE
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Non traumatic haemorrhage
- 2. IMAGING RECOMMENDATIONS APPROACH TO HAEMORRHAGE SOME COMMON HAEMORRHAGES
- 3. ICH ?? Intracranial haemorrhage is a collective term encompassing many different conditions characterised by the extravascular accumulation of blood within different intracranial spaces. Spontaneous (i.e., nontraumatic) intracranial hemorrhage (ICH) and vascular brain disorders are second only to trauma as neurologic causes of death and disability.
- 4. IMAGING RECOMMENDATIONS NCCT- In pt with sudden FND , haemorrhage is suspected until proved otherwise. CTA-in young -in pt with sudden clinical deterioration and mixed density haematoma. MRI-follow up- benign in ordered fashion -bizarre in tumoral ich
- 5. APPROACH TO ICH Localization of hemorrhage Intraaxial vs. extraaxial Single vs. multiple compartments Age of hemorrhage Etiology
- 7. 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.
- 9. 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
- 11. Intra-axial hemorrhage ◦ intracerebral haemorrhage - basal ganglia, lobar, pontine and cerebellar ◦ intraventricular haemorrhage (IVH) Extra-axial hemorrhage ◦ extradural haemorrhage (EDH) ◦ subdural haemorrhage (SDH) ◦ subarachnoid haemorrhage (SAH)
- 12. Intra-axial haemorrhage 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. The principal concern in intracerebral haematoma is the mass effect and functional damage.
- 13. Intraparenchymal Hemorrhage Basal ganglia ◦ Elderly - HTN ◦ Young - Drug abuse Lobar ◦ Elderly - Amyloid, HTN, neoplasm, SVT ◦ Young – AVM, coagulopathy, SVT Gray-white interface ◦ Metastases, septic emboli, fungal infection • Multifocal haemorrhage in white matter - AHLE Common causes by Location
- 14. EXTRA-AXIAL HG non traumatic SAH ◦ Aneurysmalconvexalperimesencephalic EDH ◦ Bleeding disorders ◦ Craniofacial inf ◦ Bone infarction ◦ Dural sinus thrombosis ◦ Vascular lesions of calvaria
- 15. SDH ◦ Intracranial hypotension-2 to LP, myelography, spinal anaesthesia, or cranial sx ◦ Bleeding disorders ◦ Dural sinus thrombosis ◦ Hyponatremic dehydration ◦ Meningitis ◦ Vasculopathy or avm ◦ Dural haemangiomas ◦ Ruptured cortical artery aneurysm
- 16. EVOLUTION OF ICH
- 18. on CT Scan Acute hemorrhage Physiology: depends on electron density, shows linear relationship between •attenuation and •hematocrit, Hb concentration and protein content. Typically On CT : acute hemorrhages are usually hyperdense as compared to normal brain. Atypically On CT : acute hematomas appear isodense if • hematocrit is very low(as in extreme anemia when Hb conc drops to 8-10g/dl) •In coagulation disorders • Failure of clot retraction
- 19. SubAcute hemorrhage Physiology: with time attenuation of ICH decreases. Resolving clots first liquefy and then reabsorb starting at periphery and progressing centrally. Typically On CT : between 1 to 6wks subacute hemorrhages becomes isodense with adjacent brain parenchyma. Sometimes they show peripheral enhancement on contrast administration because there is blood brain barrier breakdown in vascularized capsule.
- 20. Chronic hemorrhage These are hypodense compared to adjacent brain , unless rebleeding has occurred. High attenuation within them is usually secondary to rebleed resulting in “target sign” on postcontrast CT scans.
- 22. MR CHANGES the two most important biophysical properties in the generation of MR signal intensity patterns ◦ changing oxygenation states of hemoglobin ◦ and the integrity of red blood cell (RBC) membranes
- 25. HYPERACUTE HAEMATOMA •Extravasated blood- fully oxygenated •Oxy blood- diamagnetic. •Signal due to water content •Iso-hypo on T1 & hyper on T2 •At periphery on T2-thin, irregular rim of marked hypointensity RBC MEMBR INTACT No dipole-dipole interactions •diffusion MR-restricted diffusion
- 27. ACUTE HAEMATOMA Deoxyhemoglobin -paramagnetic (χ > 0). NO dipole–dipole interactions
- 28. SUBACUTE HAEMATOMA ENERGY OF RBCS DECLINE FE2+-FE3+ HB-METHB-HIGH SI ON T1 PERIPHERAL – CENTER
- 29. LATE SUBACUTE After cell lysis- high intensity on T2-weighted images T1WI shows an almost uniformly hyperintense late subacute hematoma with a central hypointensity T2WI shows uniformly hyperintense fluid surrounded by a hypointense hemosiderin rim .
- 30. T2* GRE scan shows “blooming” around the rim of the clot while the center is heterogeneously hyperintense. DWI shows no diffusion restriction; hyperintensity in the inferior portion of the clot is T2 “shine-through.
- 31. CHRONIC HAEMATOMA Chronic hematoma. Left ganglionic hyperintense lesion with surrounding rim of markedly hypointense hemosiderin indicates residua of chronic hematoma on T2 (A). Note some of the signal of the fluid-filled residual cavity is suppressed on fluid-attenuated inversion recovery (B).
- 32. On mri imaging ICH appearance depends mainly on Sequential degradation of Hb Stage Blood products Unpaired electron Magnetic prop. T1WI T2WI Hyperacute OxyHb 0(ferrous form) Diamagnetic Iso Iso / Hi Acute DeoxyHb 4 (ferrous) Paramag. Iso Low Early subacute Met-Hb (in cells) 5(ferric) Paramag. Hi Low Late subacute Met-Hb (in sol.) 5(ferric) Paramag. Hi Hi Chronic hemosiderin ferric Low/ iso Low
- 33. ETIOLOGY OF ICH
- 34. HYPERTENSIVE HG Most common cause is Hypertension •Significantly in elderly patient. •Mainly in areas supplied by MCA branches and basilar arteries. •Most common site is basal ganglia .(poor prognosis esp. with IVH). •Less common manifestation of hypertension is hypertensive encephalopathy(HE).
- 36. Hypertensive intracerebral haemorrhage Locations: In order of frequency: 1.Basal ganglia haemorrhage 2.Thalamic haemorrhage 3.Pontine haemorrhage 4.Cerebellar haemorrhage
- 37. Chronic Hypertensive encephalopathy •In patients with raised B.P.(failure of autoregulatory mechanism) •Characterized by multiple microbleeds In basal ganglia and cerebellum White matter hyperintensities on T2FLAIR T2* showing multifocal microbleeds
- 38. Hypertensive hemorrhage Deep gray matter and brainstem Small remote hemorrhages without any correlative clinical events
- 39. Amyloid angiopathy Peripheral distribution, often parietooccipital Spare basal ganglia Multiple hemorrhages, differing ages
- 41. Amyloid angiopathy Most common cause of recurrent ICH in elderly normotensive patients . Three form of amyloid deposits occur in CNS: 1.Amyloid core of senile plaque 2. Cortical and leptomeningeal vessel wall deposits 3. Extension from small vessels into the surrounding brain parenchyma. Later two together called as Amyloid Angiopathy. Location Multiple haemorrhage at corticomedullary junction, sparing basal ganglia and brain stem.
- 42. CT showing areas are in the outer part of the brain that is characteristic for CAA-related strokes. Thus CT and MRI shows multiple peripherically located hemorrhages of different age.
- 43. Cavernous angioma- Clusters of hyperintensity on T1- weighted images with peripheral circumferential rims of hypointensity on T2-weighted images Abut pial or ventricular surface; also pons is favored location May have associated venous angioma, seen best after intravenous contrast
- 44. Arterial infarction Hemorrhage localized to cortex Nonhemorrhagic component of lesion is within arterial vascular distribution
- 45. Venous infarction Hematoma in white matter or at gray–white junction Often temporal lobe; can be bithalamic • Associated with major dural sinus occlusion.
- 46. Hemorrhagic neoplasm Oncology associated ICH due to Malignancy induced Coagulopathy • Leukemia • Patient on chemotherapy Intra tumoral hematoma • Primary CNS tumor • Metastatic tumors
- 47. Primary Brain Tumors Increased tumour vascularization with dilated, thin-walled vessels and tumour necrosis are the most important mechanisms of haemorrhage.,includes- •glioblastoma multiforme •pituitary adenoma •ependymoma •central neurocytoma •choroid plexus carcinoma •ganglioglioma •pilocytic astrocytoma •haemangiopericytoma •oligodendroglioma •pineocytoma •CNS germinoma •chordoma •schwannoma •cavernous haemangioma •atypical teratoid/rhabdoid tumour
- 48. Glioblastoma multiforme common cause of ICH in -normotensive -nondemented elderly patient Pilocytic Astrocytoma seen in younger group rarely hemorrhage.
- 49. Oligodendrogliomas commonly show hemorrhagic foci Ependymomas bleeds repeatedly(esp of spinal cord) thus cause intraventricular obstructive hydrocephalus
- 50. Pituitary Adenoma m.c. nongial hemorrhagic primary tumor. Primary CNS Lymphoma rarely necrotic or hemorrhagic, but hemorrhage common in HIV infected patients.
- 51. Haemorrhagic intracranial metastases Melanoma Renal cell carcinoma Choriocarcinoma Thyroid carcinoma: m.c. papillary Lung carcinoma Breast carcinoma Hepatocellular carcinoma On MRI mets show marked heterogenecity due to different age of blood degradation products
- 52. Melanoma metastasis Small cell lung cancer metastases Breast cancer metastasis
- 53. Hemorrhagic neoplasm Multiple stages of hematoma in same lesion Debris–fluid levels Persistent deoxyhemoglobin, absent hemosiderin Identification of nonneoplastic tissue Inappropriate enhancement with acute hematoma Perihematoma “edema” and mass effect in late hemorrhage
- 55. Features Benign ICH Neoplastic ICH Hemosiderin rim Complete Irregular or absent Nonhemorrhagic tumor foci (enhances on CECT) Absent present Hemorrhage evolution Ordered on sequential scans Disordered / delayed Edema / mass effect Resolves with time Persist Benign v/s Neoplastic ICH
- 56. ICH due to Blood dyscrasias and Coagulopathy Iatrogenic Non iatrogenic •Vit k deficiency •Hepatocellular disease •Dic •Heparin •Warfarin •Thrombolytic •Antiplatelets etc. Most common site – supratentorial intraparenchymal
- 57. Infectious •– Necrotizing Encephalitis (Herpes Simplex) •– Angioinvasive Organism (aspergillus, mucor) •– Mycotic Aneurysm HSV encephalitis
- 58. SOLITARY SPONTANEOUS pICH Newborns and Infants Common o Germinal matrix hemorrhage (< 34 gestational weeks) o Dural venous sinus thrombosis (≥ 34 gestational weeks) Children Common o Vascular malformations (˜ 50%) Less common o Hematologic disorder o Vasculopathy o Venous infarct Young Adults Common o Vascular malformation o Drug abuse Less common o Venous occlusion o PRES (eclampsia, preeclampsia) Middle-aged and Elderly Adults Common o Hypertension o Amyloid angiopathy o Neoplasm (primary, metastatic) Less common o Venous infarct o Coagulopathy
- 59. MULTIPLE SPONTANEOUS ICHs Children and Young Adults Multiple cavernous malformations Hematologic disorder/malignancy Middle-aged and Older Adults Common o Chronic hypertension o Amyloid angiopathy Less common o Hemorrhagic metastases o Coagulopathy, anticoagulation All Ages Common o Dural sinus thrombosis o Cortical vein occlusion Less common o PRES o Vasculitis o Septic emboli Rare but important o Thrombotic microangiopathy o Acute hemorrhagic leukoencephalopathy
- 60. 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
- 61. NON TRAUMATIC SAH ANEURYSMAL SAH PERIMESENCEPHALIC SAH CONVEXAL SAH
- 62. ANEURYSMS •Most common cause of non traumatic SAH •Most common presentation is SAH. CT •IOC for SAH. •High attenuation is seen in subarachnoid space. •Most aneurysm arise from the circle of Willis (berry aneurysms) and on rupture fills basal cistern and sylvian fissure. •Subacute and chronic are difficult to detect on CTscans
- 63. MRI •o “Dirty” CSF on T1WI •o Hyperintense cisterns, sulci on FLAIR •Sensitive as able to visualise it well in the first 12 hours typically as a hyperintensity in the subarachnoid space on FLAIR . •Better modality for subacute and chronic SAH than CT. T1 T2
- 64. Angiography o CTA positive in 95% if aneurysm ≥ 2 mm o DSA reserved for complex aneurysm, CTA negative
- 65. Usual locations The Interhemispheric Fissure-ACOA aneurysm The Sylvian Fissures- MCA bifurcation
- 67. Prepontine Cisterns-BASILAR TIP aneurysm
- 68. PERIMESENCEPHALIC SAH benign subarachnoid hemorrhage subtype that is anatomically confined to the perimesencephalic and prepontine cisterns (6-9). Etiology-UNKNOWN-??VENOUS pnSAH is the most common cause of nontraumatic, nonaneurysmal SAH. Mild-moderate headache peak age of presentation -between 40 and 60 years Imaging NECT scans show focal accumulation of subarachnoid blood around the midbrain (in the interpeduncular and perimesencephalic cisterns) and in front of the pons Highresolution CTA is a reliable noninvasive alternative to catheter angiography in ruling out underlying aneurysm or dissection in such cases. Differential Diagnosis aneurysmal SAH. Traumatic SAH (tSAH) Convexal SAH
- 70. CONVEXAL SAH Isolated spontaneous nontraumatic SAH that involves the sulci over the brain vertex is called convexal or convexity subarachnoid hemorrhage (cSAH). restricted to the hemispheric convexities, sparing the basal and perimesencephalic cisterns (6-12). Etiology dural sinus and cortical vein thrombosis (CoVT), arteriovenous malformations, dural AV fistulas, arterial dissection/stenosis/occlusion, mycotic aneurysm, vasculitides, amyloid angiopathy, coagulopathies, Reversible cerebral vasoconstriction syndrome (RCVS), and PRES.
- 71. cSAH have nonspecific headache CT FINDINGS. Most cases of cSAH are unilateral, involving one or several dorsolateral convexity sulci basal cisterns are typically spared. MR FINDINGS. Focal sulcal hyperintensity on FLAIR is typical in cSAH. T2* (GRE, SWI) shows “blooming” in the affected sulci . ANGIOGRAPHY. CTA, MRA, or DSA can be helpful in evaluating patients with convexal SAH secondary to vasculitis, dural sinus and/or cortical vein occlusion, and RCVS.
Editor's Notes
- Evolution of intraparenchymal hemorrhage on magnetic resonance. In the earliest stage of acute hematomas, blood is still oxygenated within intact red blood cells (RBCs). Separate plasma water with clot retraction and a small amount of edema may be seen at this early time point. Rapid deoxygenation, first at the periphery and then throughout the hematoma, occurs, whereas RBCs remain intact. Note the slight increase in edema. As the lesion undergoes oxidation, the peripheral hemoglobin within intact RBCs forms methemoglobin. Although this oxidation process and conversion to methemoglobin occur throughout the hematoma, RBCs lyse. As free methemoglobin is formed, hemosiderin and other iron storage forms are deposited within macrophages in the adjacent brain. Eventually, the lesion contains no intact RBCs, and methemoglobin is resorbed or metabolized, leaving only a collapsed cleft lined by hemosiderin and ferritin without any notable central constituents.
- Freshly extravasated erythrocytes of arterial blood contain, for the purposes of practical discussion, fully oxygenated hemoglobin ), oxygenated blood is diamagnetic (χ < 0).
- Hyperacute hematoma. The bulk of the lesion is isointense on the T1-weighted image (A) and slightly hyperintense on the proton density–weighted (B) and T2-weighted (C) images. Note the peripheral rim of marked hypointensity, best seen on gradient recalled echo (D). In addition, serum from clot retraction (open arrow) is identifiable adjacent to the hematoma and external to the rim of hypointensity, indicating that the hypointense rim is part of the clot and not the brain.
- Acute hematoma. The lesion near the fourth ventricle is isointense on T1-weighted image (A) and becomes hypointense on proton density– (B) and T2-weighted (C) images. Minimal hyperintensity is already present on the periphery of the hematoma on T1-weighted image, indicating conversion to intracellular methemoglobin. A cerebral hematoma causes compression of surrounding tissue, reducing perfusion and therefore oxygen delivery from fresh blood to these regions. Deoxygenation of the extravasated blood occurs due to several factors. The underperfused surrounding tissue lowers the tissue partial pressure of oxygen, thereby promoting oxygen dissociation. The erythrocytes are not aerobic but convert glucose to lactate anaerobically. The resultant lower pH also promotes oxygen dissociation through the Bohr effect. The accumulation of CO2 similarly promotes this effect. , when deoxyhemoglobin is packaged within erythrocytes, the magnetic susceptibility of the interior of the RBC is different from the suspending diamagnetic environment (extracellular plasma), resulting in susceptibility variations within the hematoma. These susceptibility inhomogeneities result in T2* relaxation enhancement In acute hematomas, there is no evidence of high intensity on T1-weighted images within the bulk of the hematomas. In fact, the acute hematoma is isointense or minimally hypointense to brain on T1-weighted images. The lack of hyperintensity of intracellular deoxyhemoglobin is attributed to the quaternary structure of the deoxyhemoglobin molecule, which precludes water protons from attaining the requisite proximity to the unpaired electrons of the paramagnetic deoxyhemoglobin molecule (Fig. 13.6). The result of the relatively large distance between water protons and the unpaired electrons of deoxyhemoglobin results in a lack of the dipole–dipole interaction between these substances. Therefore, no T1 shortening is observed on T1-weighted images. In practice, it is common to see a very thin peripheral conversion to methemoglobin at the initial time point of imaging on T1-weighted images, even though most of the lesion is isointense (Figs. 13.19 and 13.20). Note that the hypointensity of acute hematomas on T1-weighted images is mainly a reflection of T2 shortening, in that the signal has already decayed, due to the extremely short T2 of deoxyhemoglobin, even at the relatively short TE used on T1-weighted images. Therefore, the hypointensity on what is called a T1-weighted image is actually a T2 effect.
- As the energy status of the erythrocytes declines, the reductase enzyme systems of the RBC (NADH-cytochrome b5 reductase, NADPH-flavin reductase) (73) used to maintain the heme iron in the ferrous oxidation state become nonfunctional. Hemoglobin is oxidized to methemoglobin, in which the iron, still bound to the heme moiety within the globin protein, is in the ferric state with five d electrons. As such, the iron is paramagnetic (χ > 0). high intensity is present on T1-weighted images whenever methemoglobin exists. . This high signal intensity of early subacute hematomas typically begins at the periphery of the hematoma and converges radially inward (44) (Fig. 13.21). With the initial appearance of peripheral intracellular methemoglobin, the center of the hematoma is unchanged (compartmentalized intracellular deoxyhemoglobin remains). Early subacute hematoma with intracellular methemoglobin. Hyperdense hematoma in the left frontal lobe on computed tomography (A) is high intensity on T1-weighted image (B) and markedly hypointense on T2-weighted (C) and fluid-attenuated inversion recovery (FLAIR) (D) images, consistent with intracellular methemoglobin. Hyperintense edema surrounding the lesion is especially well seen on FLAIR (D).
- The decline in energy status of the RBC causes loss of membrane integrity. Because the loss of RBC integrity removes the paramagnetic aggregation responsible for the susceptibility-induced T2 relaxation process, the effective T2 shortening now disappears. This phenomenon has been documented to occur on lysis of red cells containing deoxyhemoglobin in in vitro experiments (38). These changes occur along with the further formation of methemoglobin from deoxyhemoglobin. Hemolysis results in the accumulation of extracellular methemoglobin within the hematoma cavity. The extracellular methemoglobin further enhances T1 relaxation (38) and is manifested as high intensity on the T1-weighted images (Figs. 13.20 and 13.22). Concurrent with these changes, high signal intensity also appears on the T2-weighted images. As already stated, most subacute hematomas in clinical practice are already seen as high intensity on both T1-weighted and T2-weighted images.