Head Trauma Ct Evaluation


Published on

Radiology Presentation

Published in: Education, Health & Medicine

Head Trauma Ct Evaluation

  1. 1. CT EVALUATION OF HEAD TRAUMA Dr.A.K.M.Salauddin Consultant ,Radiology & Imaging Bangladesh
  2. 2.  leading cause of death in children and young adults.  Peak age – 15 -24 yrs  Secondary peak > 50 years of age.  Twice as often among males compared to females.  Generaly caused by motor vehicle accidents, fall, assaults, violence and sports & recreation HEAD TRAUMAHEAD TRAUMA
  3. 3.  COMPUTED TOMOGRAPHY:-  C.T is the most important step in evaluation for head and contiguous spine injuries.  In a typical head injury windows and window level are used:- 1) Brain window 2) Intermediate window : to assess the subdural or epidural hematoma. 3) Bone window : to determine the presence or absence of a bony fracture. HEAD TRAUMAHEAD TRAUMA
  4. 4. MRI  sometimes valuable for following reasons:-  Show small extra-axial blood collection in sub-dural and epidural spaces.  Show non-haemorrhagic paranchymal lesions diffuse axonal injury,contusion.  Higher sensitivity in the sub-acute and chronic stages of head trauma.  MR is useful to show long term effects of head injury.  ( MR sometimes fail to demonstrate the sub-arachnoid haemorrhage, better seen in C.T )  MRI is generally following C.T, when C.T does not resolve the nature of brain injury. HEAD TRAUMAHEAD TRAUMA
  5. 5. (A) PRIMARY TRAUMATIC LESION. (a) skull fracture, scalp hematoma/ laceration (b)primary neuronal injury – 1.diffuse axonal injury. 2.contusions-  cortical contusions  subcortical gray matter/deep cerebral injury  primary brain stem injury. (c)primary hemorrhages- 1.Extra-axial haemorrhage  Epidural hematoma  Subdural hematoma  Subarachnoid haemorrhage. 2.Intracerebral haemorrhage  Intracerebral hemorage  Intraventri cular haemorrhage HEAD TRAUMAHEAD TRAUMA
  6. 6. (A) PRIMARY TRAUMATIC LESION (d) Primary vascular injuries- Traumatic arterio – venous fistulae-common carotid Cavernous fistula. Arterial pseudo-aneurysm – Location: branches of ACA+MCA Cavernous portion of ICA. Arterial dissection/laceration/transaction/occlusion. Dural sinus laceration/thrombosis/.occlusion. Cortical vein rupture/thrombosis. (e) Traumatic pia – arachnoid injury - post traumatic arachnoid cyst Subdural hygroma (f) other --- cranial nerve injury. HEAD TRAUMAHEAD TRAUMA
  7. 7. (B) SECONDARY TRAUMATIC LESION 1) Cerrebral herniation 2) Traumatic ischemia , infartion 3) Diffuse cerebral oedema 4) Diffuse hypoxic injury 5) Secondary “delayed’’ hemorrhage 6) Secondary brain stem injury or haemorrhage . 7) Others --e.g. fatty embolism , infection HEAD TRAUMA
  8. 8.  SCALP LESION  Scalp laceration  Scalp hematoma / subgaleal soft tissue swelling  Subgaleal extrusion of macerated brain through comminuted skull fracture .  Atreiovenous fistula or pseudo-aneurysm; usually involve superficial temporal or occipital arteries.  SKULL FRACTURES:  could be linear,depressed or diastatic and may involve cranial vault or skull base.  Skull radiographs and C.T are effective to demonstrate fractures..  SUTURAL DIASTASIS/ DIASTATIC FRACTURE:  Width of the suture more than 3 mm is recognized as sutural diastasis. (normally sutures are no wider than 2 mm.)  In adult diastasis of lambdoid suture is most common,could be bilateral. HEAD TRAUMA
  9. 9.  FRACTURE OF SKULL BASE: • Basilar skull fracture should be sought when blood behind tympanic membrane, otorrhoea, rinorrhoea, echymosis surrounds the orbits without direct orbital trauma,intracranial air,air fluid level in PNS or mastoid air cells. • High- resolution cranial C.T with thin section is best modalities to detect basilar fracture. • Basilar fracture cause compression or entrapment of cranial nertves. • petrous bone fracture causes- ossicular chain dislocation. • fracture of optic canal cause loss of vision. • Sphenoidal fractures can also be associated with disruption of intra- cavernous internal carotid artery, leading to pseudo- aneurysm or a carotid cavernous fistula. HEAD TRAUMA
  12. 12.  EPIDURAL HEAMATOMA: • Usually occurs within first 24 or 48 hours, delayed development or enlargement seen In 10 to 30%. • Etiology - due to damage of middle meningeal artery. - laceration of diploic veins. - dural sinus • located between the skull and dura with a focal biconvex configuration. EDH may cross dural attachments but not sutures. • Most common site temporo-parietal area. Posterior fossa EDH are relatively uncommon. • On C.T scan, uncommonly EDH may be bilentricular crescentic or irregular. • Brain adjacent to most EDHS is severely flattened or displaced. Secondary herniation are very common. HEAD TRAUMA
  13. 13.  EPIDURAL HEAMATOMA:. * C.T findings Acute, Sub-acute and Chronic.  Acute epidural haematoma- 2/3 uniformly high density 1/3 homogenous in attenuation  Isodene area due to serum  Hypodense area within indicate active bleeding  Sub-acute EDH- Homogenously hyperdense – consists of solid blood clot.  Chronic EDH – Hetrogenous or decreased attenuation as well as enhancing membrane peripheral enhancecment represent dura or membrane formation. * Imaging criteria whether a epidural haematoma may be treated conservatively are- (1) Diameter less than 1.5 cm (2) A minimal mid line shift of less than 2 mm (3) The patient must be intact neurologically without focal deficit. HEAD TRAUMA
  15. 15. SUBDURAL HEMATOMA: • SDHS are interposed between the dura and arachnoid. . Post traumatic subdural collection may be filled with CSF when there is tear in the arachnoid then called CSF hygroma. • Tpypically cresent shaped with concave medial and convex lateral border, which may extends diffusely. • May cross suture lines but not dural attachments. HEAD TRAUMA
  16. 16.  SUBDURAL HEMATOMA: • COMMON SITES: - over the fronto-parital convexities. - middle cranial fossa - para- falcial area. - inter- hemispheric fissure  Adjacent to the tentorium – may simulate intra- axial lesion. • Supra tentorial SDHS located adjacent to the tentorium shows well-defined medial margin corresponding to the edge of tentorium and sheet like area of increased density that slopes laterally • Infra tentorial SDHS located below the tentorium shows a sharp lateral margin corresponding to the edge of tentorium and increased density that slopes later laterally • Posterior fossa SDHS are rare. HEAD TRAUMA
  17. 17.  SUBDURAL HEMATOMA: • C.T Shows as crescent shaped extra- axial collection with a convex lateral and concave medial border. Occasionally may be biconcave shape. • ACUTE SDHS- Homogenously hyperdense - Up to 40%- mixed hyper/ hypodense - due to unclotted blood - serum extruded during clot retraction - C.S.F - Rarely isodense- in patients with – coagulopathies & severe anemia HEAD TRAUMA
  18. 18.  SUBACUTE SDHS:- • Isodense within a few day to a few weeks.Difficult to diagnosis clues -  Effacement of cortical sulci over cerebral convexity  Mid line shift  Delayed enhancement C.T scan performed after 4 to 6 hours.  CHRONIC SDHS :- Typically low attenuation in uncomplicated SDHS.  Mixed density in 5% cases- due to recurrent haemorrage  Enhancement following contrast  Shows calcification in 0.3 to 2.7% cases  SUBDURAL HYGROMA:-  Hypodense collection equal to CSF density.  More crescentic & bilateral  At surgery show clear fluid and lack of a membrane. HEAD TRAUMA
  21. 21. SUBARACHNOID HAEMORRAGE:- • Due to damage to blood vessels on the pia- arachnoid. • Intra- parenchymal haematoma rupture into the ventricular system may gain ascess to Subarachnoid space via the foramina of magendie and luschka. • Complication show communicating hydrocephalus due to fibroblasti • C.T is the modality of choice in the evaluation of SAH. SAH typically appear as an area of hypendensity in the basal cisterns, the sulci overlying cerebral convexities,the sylvian fissure and inter- hemispheric fissure. HEAD TRAUMA
  22. 22.  SUBARACHNOID HAEMORRAGE: • Normal calcified or ossified flex may be mistaken for parafalcine in older adolescents. • “ Pseudo sub- arachnoid haemorrhage” is seen incase of sever diffuse cerebral oedema • Posterior parafalcine or inter-hemispheric SAH can mimic the “Empty delta sign’’ of superior sagittal Sinus thrombosis. • SAH is rapidly cleared from the subarachnoid space. The majority of C.T scans performed within 1Week will appear normal. HEAD TRAUMA
  24. 24. INTRA - VENTRICULAR HAEMORRHAGEINTRA - VENTRICULAR HAEMORRHAGE  IVH are associated with other manifestations ofIVH are associated with other manifestations of primary intra-axial brain trauma . Such as DAIprimary intra-axial brain trauma . Such as DAI ,deep cerebral gray matter and brain stem,deep cerebral gray matter and brain stem lesions .lesions .  C.T shows high density intraventricular bloodC.T shows high density intraventricular blood with or without a fluid level.with or without a fluid level.  Occasionally focal choroid plexux haematomaOccasionally focal choroid plexux haematoma noted.noted. HEAD TRAUMA
  26. 26. INTRACEREBRAl HEMATOMA:  Bilateral or multiple.  Frequently associated with SAH & SDHS  Most frequently noted at the time of injury . may be delayed with 48 hours. .  Differentiated from hemorrhagic contusion by sharply marginated margin, perifocal hypodensity and mass effect. HEAD TRAUMA
  27. 27. INTRACEREBRAl HEMATOMA: ACUTE HEMATOMA - < 3 DAYS  C.T :-  Homogenous high density lesion (50 -70 HU) with irregular well - efined margins.  Usually surrounded by low attenuation (oedema, contusion ) with mass effect. SUBCUTE HEMATOMA ( 3 – 14 DAYS )  NCCT : Gradual decrease in density from periphery inward and becomes isodeme to brain Parenchya (1-2 HU per day during 2nd & 3rd week).  CECT : Peripheral rim enhancement at inner border of perilesional lucency. HEAD TRAUMA
  28. 28. INTRACEREBRA HEMATOMA:  CHRONIC HEMATOMA : > 14 DAYS C.T findings  Gradual Decreased / hypodensity .  Later show lucent hematoma (cephalomalacia due to proteolysis and phagocytosis +surrounding atrophy) with adjacent sulcal enlargement and ventricular dilation with ring blush ( DDX : tumor ) HEAD TRAUMA
  30. 30. DIFFUSE AXONAL INJURY:- Most common type of primary traumatic injury .  PATHOGENESIS  Cortex and deep structures move all different speed resulting in shearing strain along the course of white matter tracts especially all gray- white matter junction with axonal tears followed by Wallerion degeneration . Disruption of accompanying blood vessels show numerous small hemorrhage foci .  Diffuse & Bilateral HEAD TRAUMA
  31. 31. DIFFUSE AXONAL INJURY:-  Locations ( according to severity of trauma ) a) lobar white matter at cortico-medullary junction more common para sagital region of frontal lobe + periventricular region of temporal lobe, occasionally in parietal and occipital lobes. b) Internal + external capsule, corona radiate, cerebral peduncles . c) Corpus callosum d) Brain stem – postero lateral quadrants of mid brain + upper pons. HEAD TRAUMA
  32. 32. DIFFUSE AXONAL INJURY:-  C.T – Findings - Early imaging may be subtle or normal . - Foci of decreased density. - May show some degrees of cerebral swelling. - May show small focal hemorrhage or small petechial haemorrhage particularly at gray-white junction and corpus callosum. - May show extensive injury. HEAD TRAUMA
  34. 34. CONTUSION:-  Common type of primary intra-axial lesion . In 21% of head trauma patients.  PATH :- Tissue necrosis, capillary disruption, petechial hemorrhage followed by liquefaction + oedema after 4 to 7 days .contusion may be hemorrhagic or non- hemorrhagic.  MECHANISM :- Linear acceleration – deceleration forces / penetrating trauma / direct impaction. HEAD TRAUMA
  35. 35. CONTUSION:- 1. COUP :- Direct impact to stationary brain. Injury at the site of impaction. 2. COUNTER COUP :- Impact of moving brain on stationary clavarium opposite to the site of the coup and produced injury.  Contusions are typically superficial foci of punctate or linear hemorrhages that occur along gyral crests.  Location - Multiple bilateral lesion , temporal lobes most frequently involved. - Bneath an acute subdural hematoma. HEAD TRAUMA
  36. 36. CONTUSION:-  C.T - Initial findings may be subtle or absent. - Early findings focal / multiple poorly defined areas of low attenuation with irregular contour intermixed with a few tiny areas of increased density ( petechial hemorrhage) - Diffuse oedema and mass effect in immediate post-traumatic period,then gradually diminish over time. - Some degree of contrast enhancement. - Isodense to brain after 2 – 3 weeks. HEAD TRAUMA
  37. 37. CONTUSION
  38. 38. DEEP CEREBRAL AND BRAIN STEM INJURY  Less common than DAI and cortical contusions.  Represent 5% to 10% of primary traumatic brain injuries.  Most are induced by shearing forces,  Most patients have profound neurologic deficits and a poor prognosis..  C.T. Scan - often normal initially. - Petechial hemorrhages can sometimes be seen in lateral brain stem, periaquedctal region region and deep gray matter nuclei.  M.R shows brain stem lesions nicely. HEAD TRAUMA
  40. 40. PRIMARY VASCULAR INJURIES 1.Traumatic arterio – venous fistulae-common carotid Cavernous fistula. 2. Arterial pseudo-aneurysm – Location: branches of ACA+MCA Cavernous portion of ICA. 3. Arterial dissection/laceration/ transaction/occlusion. 4. Dural sinus laceration/ thrombosis / occlusion. 5. Cortical vein rupture / thrombosis.   HEAD TRAUMA
  41. 41. SECONDARY TRAUMATIC LESION 1) Cerrebral herniation 2) Traumatic ischemia , infartion 3) Diffuse cerebral oedema 4) Diffuse hypoxic injury 5) Secondary “delayed’’ hemorrhage 6) Secondary brain stem injury or haemorrhage . 7) Others --e.g. fatty embolism , infection HEAD TRAUMA
  42. 42. CEREBRAL HERNIATIONS  subfalcine  transtentorial – desending ascending  translar ( trans sphenoidal ) - desending ascending  tonsilar  miscellaneous - ( e.g – trans dural / trans cranial ) ( Most common subfalcine & transtentorial herniation) HEAD TRAUMA
  44. 44. SECONDARY TRAUMATIC LESION  Infraction - ipsilateral ACA compressed against flax.  Extra cranial herniation
  45. 45. HEAD TRAUMA SEQUELAE OF TRAUMA 1) Encephlomalacia and atrophy. 2) Pneumocephalus, Pneumatocele formation. 3) CSF Leaks and Fistulae. 4) Acquired Encephalocele or leptomeningeal cyst. 5) Cranial nerve injuries. 6) Diabetes incipidus. 7) Hydrocephalus. 8) Atrophy. 9) Subdural Hygroma. 10) Post traumatic abscess.
  46. 46. CONCLUSION :- • C.T is important modality for evaluation of an emergency patient with cranio-cerebral trauma. • Early & accurate ct evaluation cause better patients outcomes with a decrease morbidity & mortality statics. & Decrease in trauma related medical costs. HEAD TRAUMA
  47. 47. THANK YOU