imaging in sah

Download Imaging  in  SAH

Post on 22-Nov-2014

133 views

Category:

Health & Medicine

0 download

Embed Size (px)

DESCRIPTION

Imaging In Sub Arachnoid Hemorrhage (SAH)

TRANSCRIPT

  • 1. IMAGING IN SAHDR.SARATHMENON.R, MD(Med),DNB(Med),MNAMSDM ResidentDept.of .NeurosciencesAmrita Institute of Medical Sciences,Kochi

2. INTRODUCTION Definition Epidemology Grading system Imaging modalities Differentials 3. IMAGING MODALITIES NCCT/CTA MRI /MRA Angiography Nuclear imaging Neurosonography 4. SAHWhat is it? Bleeding into the subarachnoid space (space betweenthe pia & arachnoid meningeal layers) where bloodvessels lie & CSF flowsWhere does the blood come from? An aneursym on a blood vessel in the subarachnoidspace has ruptured (~70%) Unknown (~15%) AVM (~10%) Rare causes (e.g. tumour) (~5%)Where does the blood go? Anywhere where CSF goes, may get hydrocephalus ifinto ventricle & causes obstruction of CSF circulation 5. SAH Incidence = 1/7000 people Higher chance if: Female 3rd trimester of pregnancy Middle-aged Abuse of stimulant drugs Connective tissue disorder Family history PCKD 6. SAH THE PROBLEM 80% in 40-65 year olds 15% in 20-40 year olds It can kill quickly 25% die within 24 hours 50% will be dead at 6 months It causes significant disability Cognitive impairment Neurological disability depending on size of bleed &complications encountered 7. GRADING OF SAH WFNS Grading : Grade GCS Motor Deficit I 15 Absent II 13-14 Absent III 13-14 Present IV 7-12 +/- V 3-6 +/- 8. MODIFIED H & H GRADINGGrade Description Mortality (%)Grade 0 Unruptured aneurysm --Grade I Asymptomatic or minimal headache with normalneurologic examination2Grade II Moderate to severe headache, nuchal rigidity, noneurologic deficit other than cranial nerve palsy5Grade III Lethargy, confusion, or mild focal deficit 15 20Grade IV Stupor, moderate to severe hemiparesis,possible early decerebrate rigidity, vegetativedisturbances30 40Grade V Deep coma, decerebrate rigidity, moribundappearance50 80 9. CT GRADING SYSTEM OF FISHER1 No subarachnoid blood detected2 Diffuse or vertical layers < 1 mm thick3 Localized clot and/or vertical layer > 1 mm4 Intracerebral or intraventricular clot with diffuse orno SAH 10. INVESTIGATIONS CT scan without contrast Lumbar puncture CTA Cerebral angiogram MRI/MRA98% sensitive @ 12 hours80% at day 350% at day 7Also good to see ifany associated ICHor hydrocephalus.May help localise thelocation of theaneurysm if there ismore than 1 & mayalso see AVM 11. CT SCAN- NCCT Evident in the largest subarachnoid spaces- suprasellar cisternand Sylvian fissures. most conspicuous within 2-3 days of onset Acute SAH is typically 50-60 Hounsfield units (HU). The protein content of the hemoglobin molecule is predominantlyresponsible for the attenuating effect of blood; absolutemeasurement in HU varies with the hematocrit value localizing the source of bleeding-- interhemispheric fissure,frontal lobe- Aco A- Sylvian fissure- I/L MCA- Posterior fossa- post.circulation aneurysmNCCT- Sensitivity-93-100% in first 24 hrs 12. Scrutinize these areas systematically for SAH Perimesencephalic cisterns Sylvian fissures Dilation of temporal horns suggestive ofhydrocephalus, which raises a possibility of SAH CTA: Multislice CTA 90-95% + for aneurysm ~ 2 mm 13. CORTICAL SAH 14. SAH-CISTERNAL 15. A nonenhanced computed tomography scan of thebrain that demonstrates an extensive SAH filling thebasilar cisterns in a patient with a rupturedintracranial aneurysm 16. SAH & LP CT & LP are critical to diagnosing SAH No need for LP if obvious blood in subarachnoid spaceon CT If NCCT ve, LP needed. Blood may not be evident on CT, especially if it isperformed > few days after bleed LP should only be performed after 12 hours of headacheonset If NCCT,LP VE, CTA to r/o saccular aneurysm 17. SAH & LP When blood enters the CSF (e.g. from SAH or during LP) thered cells are broken down & oxyhaemoglobin is released It then takes 12 hours for the oxyhaemoglobin to be convertedinto bilirubin conversion is via an enzyme found in the brain. Bilirubin in the CSF, therefore, tells us that blood must havebeen in the subarachnoid space for at least 12 hours Blood which entered the CSF during the LP would notencounter the enzyme & could not produce bilirubin The CSF will look xanthochromic (yellowish discolouration) ifbilirubin is present which they will look for with spectroscopy inthe lab 18. CTAsubarachnoid hemorrhage and contrastmedium filling the right sylvian fissure,the interhemispheric fissure, and thelateral and third ventricles 19. CTA SPOT SIGN 20. MRI/MRA (FLAIR) is the most sensitive for the detection of SAH FLAIR images, SAH appears as high signal-intensity(white) in normally low signal-intensity (black) CSFspaces. In acute SAH, FLAIR and CT scanning have similarfindings. T2- and T2*- low signal-intensity in normally high signal-intensitysubarachnoid spaces. T1-weighted - intermediate-intensity or high-intensitysignal in the subarachnoid space 21. MRA may be useful for evaluating aneurysms > 5mmand other vascular lesions that cause SAH 22. LEVEL OF CONFIDENCE FLAIR MRI is as sensitive as or more sensitive thanCT scanning in the evaluation of acute SAH compared with LP, FLAIR MRI cannot exclude SAH. MRI -valuable in the subacute phase of SAH, in whichthe density of hemorrhage on CT scans decreases. Magnetic field inhomogeneity - artifactual increase insignal intensity in sulci over the cerebral convexities onFLAIR images, which can mimic SAH. Hyperintensity in the subarachnoid space on FLAIRimages seen in meningitis or leptomeningealcarcinomatosis 23. SAH appears hyperintense on the T2-weighted and fluid-attenuated inversionrecovery (FLAIR) images and isointense to hypointense on the T1-weighted(T1W) image. Marked blooming is observed on the gradient-echo (GRE) image.Findings in the right parietal region extend into cortical sulci and suggesthyperacute or acute hemorrhage. 24. Sagittal T1-weighted image shows a right SDH (fig a). Axial fluidattenuated inversion recovery image demonstrates SAH (arrows)in the right parietal region (fig b). 25. NUCLEAR IMAGING not useful in the initial diagnosis of subarachnoidhemorrhage (SAH), role in the diagnosis of relatedvasospasm (SPECT) scanning with the radiopharmaceuticaltechnetium-99m (99m Tc) hexamethylpropyleneamineoxime (HMPAO). semiquantitative and qualitative in that the cerebellum isgenerally considered as a control value for normalperfusion Space-occupying lesions such as cerebral hematomacan cause perfusion defects on SPECT perfusionimaging 26. ANGIOGRAPHY standard imaging -intracranial aneurysms, arteriovenousmalformations (AVMs), and fistulae (AP), lateral, and one or more oblique views of bothcarotid and vertebral artery contrast injection studies submentovertical - the neck of a middle cerebral arterybifurcation aneurysm or anterior communicating arteryaneurysm aneurysm location, shape, neck size, and neck-to-maximaldiameter ratio - the aneurysm is better treated with opencraniotomy or with an endovascular technique. 27. LEVEL OF CONFIDENCE high degree of accuracy false-negative rate in the range of 1-2% A repeat cerebral arteriogram at 10-14 - initial angiogramnegative B/l selective external and internal carotid arteryangiograms - exclude a dural arteriovenous fistula B/l vertebral arteriograms of the neck ( selectivethyrocervical trunk and/or careful injections of the rightsuperior intercostal artery) demonstrate the arterial andvenous circulation of the cervical spinal cord If thorough arteriographic studies do not demonstrate aspecific cause for an SAH, a presumptive diagnosis ofidiopathic perimesencephalic hemorrhage is sometimesmade 28. An angiogram showing a bilobed aneurysm of aposteroinferior cerebellar artery immediately beforerupturing 29. onset of an aneurysmal rupture, withextravasation of contrast material into thesubarachnoid space from theanterosuperior aspect of a bilobedaneurysm in a posteroinferior cerebellarartery 30. later-phase angiogram of a rupturing bilobedaneurysm of a posteroinferior cerebellarartery shows progressive opacification of thesubarachnoid space in the posterior fossa 31. late angiogram demonstrating contrastmedium filling the posterior fossasubarachnoid spaces, including theambient, prepontine, and perimedullarycisterns 32. NEUROSONOGRAPHY Echoencephalography is useful for diagnosing germinalmatrix and intraventricular hemorrhage in the newborn transcranial Doppler USG - diagnosis and management ofvasospasm in patients with SAH. Serial transcranial Doppler USG - presence of vasospasm andallow for the maximization of medical therapy for vasospasmbefore the patient becomes symptomatic Flow measured in the middle cerebral arteries, which havehave flow velocities normally in the 30-80 cm/s range.Elevation to 120 cm/s indicates moderate vasospasm, andelevation to 200 cm/s indicates severe vasospasm sensitivity of transcranial Doppler ultrasonographic imaging forthe detection of vasospasm has been reported to be 85-90% 33. SAH: DIFFERENTIAL DIAGNOSIS Aneurysmal Nonaneurysmal Pseudo-SAH Reversible cerebral vasoconstriction syndrome(RCVS) 34. ANEURYSMAL SAH SAH caused by ruptured aneurysm Worst headache of life 40-60 years, M:F = 1:2 50% mortality, 20% rebleed within 1st 2 weeks Outcome inversely proportional to Hunt and Hess(H&H) grade and WFNS grade Severity of vasospasm/ischemia correlates withFisher CT grading (amount) 1 = no SAH visible 2 = diffuse, thin layer (< 1 mm) 3 = localized clot or thick layer (> 1 mm) 4 = intraventricular blood 35. ANEURYSMAL SAH NCCT: May show culprit aneurysm as filling defect withinhyperdense SAH Effaced cistern, hydrocephalus, +/- IPH CTA: 90-95% positive if > 2 mm MRA TOF: 85-95% sensitive for aneurysm > 3 mm DSA: current gold standard Highest amount of blood near site of rupture ACoA aneurysm anterior interhemispheric fissureMCA aneurysm Sylvian Basilar tip, SCA, PICA, VA prepontine cistern, foramenmagnum, 4th ventricle 36. Subarachnoid hemorrhag