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CT imaging of Brain in Clinical Practice by Dr. Vaibhav Yawalkar

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CT imaging of Brain in Clinical Practice by Dr. Vaibhav Yawalkar

  1. 1. CT Imaging (Brain) in Clinical Practice Dr Vaibhav Yawalkar MD
  2. 2. Imaging in ER  Cranial computed tomography (CT) is an extremely useful diagnostic tool used routinely in the care of ER patients.  The attending physician needs to be able to accurately interpret and act upon certain CT findings without specialist (e.g., radiologist) assistance, because many disease processes are time dependent and require immediate action.  It has been shown that even a brief educational intervention can significantly improve the physician’s ability to interpret cranial CT scans.
  3. 3. PRINCIPLE  Collimated X-rays are passed through the patient and information is obtained with a detector on the other side.  The X-ray source and the detector are interconnected and rotated around the patient during scanning period.  Digital computers then assemble the data that is obtained and integrate it to provide a cross sectional image (tomogram)
  4. 4.  A 2D image is obtained at each level by 360 degree rotation of Xray source and detectors around the patient, which gives information about inside of tissue.  Sequential 2D images can be combined to obtain full 3D image.
  5. 5.  X-rays are absorbed to different degrees by different tissues. Dense tissues such as bone absorb the most x- rays, and hence allow the fewest passing through the body part being studied to reach the film or detector.  This ability to block x-rays as they pass through a substance is known as attenuation.  In CT, these attenuation coefficients are mapped to an arbitrary scale between −1000 hounsfield units [HU] (air) and +1000 HU (bone)
  6. 6.  Imagine a CT film to be bright grey(silver coloured) to start with and the xrays falling on it makes that particular area darker.  More the exposure to xrays darker will be the area.
  7. 7. DIFFERENT SHADES OF GREY  The reference density for comparison is the brain, being the largest component inside the skull. Anything of the same density as the brain is called ISODENSE.  Anything of higher density (whiter) than the brain is called HYPERDENSE, and the skull is the best example of a hyperdense.  Similarly, anything of lower density (darker tone) than brain is described as HYPODENSE. The cerebrospinal fluid (CSF) is the typical example of a hypodense structure in the brain CT scan. Air is also hypodense and surrounds the regular outline of the skull in CT.
  8. 8. DESCRIPTION Approx. HU DENSITY Calcium > 1000 Hyperdense Acute blood 60-80 Hyperdense Grey matter 38 (32-42) Hyperdense White matter 30 (22-32) Isodense CSF 0-10 HYPODENSE Fat -30 to - 100 Hypodense Air - 1000 Hypodense
  9. 9. INDICATIONS  To diagnose CNS infections and their complications  Stroke: to distinguish infarct from hemorrhage  Acute changes in mental status  Focal neurologic findings  Trauma  Suspected SAH  CNS tumors or ICSOLs  Ct angiography before thrombolysis  Ct venogram for cerebral venous thrombosis(cvt)
  10. 10. CT  Advantages –  Easy availability / Low cost  Fast  Better for bone and acute haemorrage, lesions of skull base and calvarium  Calcification  Less limited by patient factors  Disadvantages-  High radiation  Poor visualisation of posterior fossa lesions
  11. 11. Viewing Planes  Axial  Coronal  Sagittal
  12. 12. INTERPRETATION OF CT BRAIN  1-GENERAL INFORMATION  2-EXTRACRANIAL TISSUE  3-CRANIAL BONE  4-BLOOD  5-CSF FLOW  A-VENTRICULAR SYSTEM  B-CISTERNS  6-BRAIN TISSUE  A-MASS LESIONS  B-SULCI & GYRI  C-GRY & WHITE DIFFERENTIATION
  13. 13. A C B D E F G
  14. 14. A C B D E F G
  15. 15. A C B D E F
  16. 16. A C B D E F G I H
  17. 17. A C B D E F G
  18. 18. A C B D E F G
  19. 19. A C B D
  20. 20. IDENTIFYING CNS PATHOLOGY ON CRANIAL CT SCANS  First step is to simply compare one half of the scan against the other half. If there are significant differences (for instance if the right and left halves are not the same), then the scan is abnormal. SYMMETRY–MIRROR IMAGE
  21. 21. IDENTIFYING CNS PATHOLOGY ON CRANIAL CT SCANS  Radiologists use a “center-out” technique, in which the examiner starts from the middle of the brain and works outward.  Clinicians advocate a problem-oriented approach, in which the clinical history directs the examiner to a particular portion of the scan.  A preferred method, one that has been demonstrated to work in the ER is to use the mnemonic “blood can be very bad”.  In this mnemonic, the first letter of each word prompts the clinician to search a certain portion of the cranial CT scan for pathology.  The clinician is urged to use the entire mnemonic when examining a cranial CT scan because the presence of one pathologic state does not rule out the presence of other.
  22. 22. What to look for: “ Blood Can Be Very Bad”  Blood  Cisterns  Brain  Ventricles  Bone
  23. 23. Blood  Blood is the most common hyperdense abnormality found on a brain CT scan. So if a hyperdense appearance is not in the right location for bone then it must be blood, until proven otherwise.  So the rule of thumb is that ‘anything white in the CT scan is either blood or bone’.
  24. 24. Exceptions:  There are two common exceptions to this rule.  The Pineal gland is a little Calcified speck in the middle of the CT scans of most adults.  The second exception is the calcified choroid plexus, which is located in the body of each lateral ventricle
  25. 25. Calcified Pineal gland Calcified Choroid plexus
  26. 26. Physiologic calcifications  Choroid plexus- rare before 10yrs  Basal ganglia- rare before 40ys  Pineal gland- common after 30 year  Falx  Dentate nuclei
  27. 27.  Blood—Acute hemorrhage appears hyperdense (bright white) on CT. This is due to the fact that the globin molecule is relatively dense and hence effectively absorbs x-ray beams.  As the blood becomes older and the globin breaks down, it loses this hyperdense appearance, beginning at the periphery and moving towards centre.  Localization of the blood is as important as identifying its presence.
  28. 28.  On the CT scan, blood will become isodense with the brain at 1 to 2 weeks, depending on clot size, and will become hypodense with the brain at approximately 2 to 3 weeks.
  29. 29. Peidural hematoma Convex shape Subdural hematoma Cresent shape
  30. 30. Intra parenchymal hemorrhage in putamen Sub arachnoid hemorrhage ( hyperdensities in sylvian fissure, basal cysterns)
  31. 31. Intraparenchymal haemorrhage with intraventricular extension
  32. 32. Infarcts  Infarctions can be seen as early as 2 to 3 hours following the event, but most will not begin to be clearly evident on the CT scan for 12 to 24 hours. Infact immediate CT scans may be completely normal in these cases.  The earliest change seen in areas of ischemia is loss of gray-white differentiation, due to influx of water into the metabolically active gray matter.  The release of osmotically active substances (arachidonic acid, electrolytes, lactic acid) from the necrotic brain tissue causes cerebral edema. This is aggravated by vascular injury and leakage of proteins in the interstitial space. By 3-4 days, interstitial fluid accumulates in the infarct and around it.
  33. 33.  The key principle behind successful use of the CT scan in dealing with ischemic stroke is KNOWING WHERE TO LOOK, AND WHAT TO LOOK FOR! And WHEN TO LOOK!  The golden rule with stroke as with most of emergency neurosurgery or neurology is that, the clinical symptoms reign supreme. Infarcts
  34. 34. Non-contrast CT scan of a 61-year-old male with sudden onset right hemiplegia two and a half hours prior to the CT scan. He is diabetic and hypertensive. The CT findings are often only as important as the question it was intended to answer! What was the clinical question in requesting a CT scan Here?
  35. 35. Non-contrast CT scan of the same patient after 8 hours now showing the obvious left basal ganglia infarct Justifying the need of follow up scans.
  36. 36.  One specialized type of stroke frequently identified on CT imaging is a lacunar infarction, which are small, discrete nonhemorrhagic lesions usually secondary to hypertension and found in the basal ganglia region.  They frequently are clinically silent.
  37. 37. Lacunar infarct in Basal ganglia.
  38. 38. Infarcts Anterior cerebral artery infarct
  39. 39. Middle cerebral artery infarct Hyper dense MCA sign Internal cerebral artery infarct ACA+MCA
  40. 40. Posterior cerebral artery infarct
  41. 41. Cisterns  Cisterns are potential spaces formed where there is a collection of CSF surrounding the Brain.  There are four key cisterns that the physician needs to be familiar with in order to identify increased intracranial pressure as well as the presence of blood in the subarachnoid space.
  42. 42. Cisterns  Circummesencephalic: Hypodense CSF ring around the midbrain; most sensitive marker for increased intracranial pressure; will become effaced first with increased pressure and herniation syndromes.  Suprasellar: Star-shaped hypodense space above the sella and pituitary; location of the circle of Willis, hence an excellent location for identifying aneurysmal subarachnoid hemorrhage.  Quadrigeminal: W-shaped cistern at the top of the midbrain; can be a location for identifying traumatic subarachnoid hemorrhage, as well as an early marker of increased intracranial pressure.  Sylvian: Bilateral CSF space located between the temporal and frontal lobes of the brain; another good location to identify subarachnoid haemorrhage.
  43. 43. CT appearance of increased intracranial pressure: A: normal intracranial pressure B: elevated intracranial pressure. A B
  44. 44. Ventricles:  Pathologic processes can cause either dilation (hydrocephalus) or compression/shift of the ventricular system.  Hydrocephalus frequently is first evident in dilation of the temporal horns, which are normally small with a slit- like morphology.  It is likely that enlargement is the result of brain volume loss rather than the increased ventricle size, particularly in older ages.  Conversely, if the ventricles are large, but the brain appears “tight” with sulcal effacement and loss of sulcal space, then the likelihood of hydrocephalus is high.
  45. 45. Increasing degrees of temporal horn Dilatation in worsening hydrocephalus
  46. 46. Gross hydrocephalus, showing dilatation of frontal horns, body and occipital horns.
  47. 47. Effacement of sulci due to raised ICP
  48. 48. Evan’s Index for Hydrocephalus  Maximum transverse diameter of Frontal Horns divided by Maximum internal transverse diameter of cranium If Index is > 0.3 , suggests Hydrocephalus.
  49. 49. CNS infections  Meningitis: Radiological signs:  Meningeal enhancement  Cerebral edema  To look for fractures of skull base and other complications.
  50. 50.  In cases of suspected bacterial meningitis with clouded consciousness, an immediate cranial CT is recommended before lumbar puncture to rule out causes for swelling that might lead to herniation. CT findings are mostly normal. Contrast-enhanced CT may show beginning meningeal enhancement, which becomes more accentuated in later stages of disease. CT is important and sufficient to define pathology of the base of skull that may be causative and require rapid therapeutic intervention and surgical consultation.
  51. 51. Meningeal enhancement in case of meningitis
  52. 52. Space occupying lesions (SOL)  Brain Abscess  Primary Tumors  Metastases
  53. 53. Space occupying lesions  Such lesions will present with one or more of the following clinical problems:  Features of raised ICP  Convulsions  Headache  Focal neurological deficits  With/without altered level of consciousness.  Fever in brain abscesses.  Slow-growing tumours may give rise to a longer duration of symptoms.
  54. 54. Points to be considered to study ICSOLs  Mass effect  Enhancement on contrast  Appearance  Location
  55. 55. Mass effect  The side with a tumour or abscess is more likely to have the sulci squeezed (effaced) and often the lateral ventricle on that side is also compressed ,and in more severe cases there is midline shift towards the normal side.  This is often the first clue that there may be a lesion ,prompting the intravenous injection of contrast to see if the lesion takes up contrast and become brighter.  Most brain tumours will declare their presence by a significant mass effect from their size or by the severe oedema around them
  56. 56. Non-contrast CT scan showing alterations of the normal sulcal pattern as evidence of mass effect from an  A) isodense meningioma  B) a low-density glioma  C) hyperdense meningioma
  57. 57. Enhancement  “Enhancement simply means it is appearing clearer” that is higher density compared to the pre-contrast scan.  When injected intravenously the contrast material concentrate in vascular areas of the brain including tumours and abscess walls thereby making them appear hyperdense and hence easier to see.  Meningiomas and lymphomas tend to enhance uniformly and intensely whereas malignant gliomas and abscesses may show an intermediate degree of enhancement in which there is an outer enhancing ring surrounding a core of non-enhancing low density (necrotic centre), which fails to take up the contrast.  Abscesses typically show THIN UNIFORM enhancing wall surrounding the pus whereas the ring of enhancement in gliomas is thicker with more solid tumour in the wall
  58. 58.  In general abscesses have a thinner and smoother enhancing ring with no chunk of enhancing tumour along the wall.  Whereas the enhancing ring in malignant gliomas and metastatic tumours tends to be thicker and irregular and there may be an asymmetric large chunk of enhancing tumour as part of the wall.  Hypodensities in INFARCTIONS will have DIFFUSE margins as compared to SMOOTHER margins in above lesions.
  59. 59.  Tumours such as Meningiomas are obvious and call for little differential diagnosis. Pre- and post-contrast CT scans of a 22-year-old male that presented with seizures. Effect of contrast is obvious.
  60. 60. Contrast-enhanced CT scan showing a brain abscess in a patient on immunosuppression therapy for SLE. Lesions show smooth outline of the rings of enhancement. Brain Abscess
  61. 61. Contrast-enhanced brain CT scan illustrating a uniformly enhancing left parafalcine meningioma. It is solid and very Unlikely an abscess. It is benign and carries a good prognosis
  62. 62.  Malignant gliomas and metastatic tumours share the property of ring enhancement with abscesses and are therefore the subject of much clinical controversy.  A patchy irregular enhancement will suggest a partially solid and cystic tumour like a glioma, and a ring enhancing, circular lesion with central hypodensity will suggest an abscess with the important differential diagnosis of a metastasis.
  63. 63. Contrast CT scan showing a left frontal irregularly enhancing tumour with solid and cystic components. This is a typical appearance for a high-grade glioma usually glioblastoma.
  64. 64. Cystic, solid and partially calcified with Irregular enhancement Glioblastoma multiforme
  65. 65. Location  A uniformly enhancing tumour with a broad based attachment to the dura, it is a meningioma until proven otherwise.  A ring-enhancing lesion located deep in the white matter, is most likely  A Glioblastoma (if soild/cystic/ irregularly enhancing) or  An abscess (if thin ring enhancement and hollow core)  A metastasis (if multiple)
  66. 66. Thin Ring of Abscess Thick ring of glioma
  67. 67. Lesions mimicking abscess, but multiple lesions and clinical history if available favours METASTASIS
  68. 68. Metastasis
  69. 69. DDs for multiple ring enhancing lesions  Tuberculoma  Neurocysticerosis  CNS cryptococcosis  Metastasis  Abscess  Glioblastoma  Granulomas  Toxoplasmosis / Lymphoma (common in AIDS)  Neurosarcoidosis
  70. 70. Ring Enhancing Lesions with Perilesional Edema  TUBERCULOMA VS  NEUROCYSTICERCOSIS
  71. 71.  Cysticerci are usually round in shape, 20 mm or less in size with ring enhancement or visible scolex, and cerebral edema severe enough to produce midline shift and focal neurological deficit is not seen.  Tuberculomas are usually irregular, solid and greater than 20 mm in size. They are often associated with severe perifocal edema and focal neurological deficits.  A lesion greater than 20 mm is likely a Tuberculoma.  Visualization of an enhancing or a calcified eccentric dot which represented the scolex, could be considered a definite imaging feature of cysticercus etiology
  72. 72. Tuberculomas with perilesional Edema
  73. 73. Multiple NCC
  74. 74. Multiple NCC in Vesicular stage: scolex can be seen inside cysts
  75. 75. Contrast Nephropathy  Rise in serum creatinine level of at least 1 mg/dL within 48 hours of contrast administration.  Incidence more when used Ionic contrast material.  Mechanism of Injury:  Renal Tubular Obstruction  Endothelial cell damage  Immunological Reactions  There is favourable prognosis and creatinine levels return to normal in 1-2 weeks.
  76. 76. Risk Factors:  Age > 80 Years  Pre-existing renal disease [Creatinine > 2 mg/dL]  Solitary Kidney  DM / Dehydration / Paraproteinemia  Patients on Nephrotoxic Medications
  77. 77. Prevention Using non-ionic contrast Using low dose of contrast Prior Hydration Using bicarbonate and acetylcysteine
  78. 78. Allergic Reactions to contrast  Incidence 0.04 % with Non-ionic contrast.  History of Atopy, bronchial asthma or other allergies are at more risk.  If patient has history of prior contrast allergy and if contrast absolutely required: Premedicate with:  12 Hours before administration: Prednisolone 50 mg PO  2 Hours before: Prednisolone 50 mg + Cimetidine 300 mg  Just before administration : IV Diphenhydramine 50 mg

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