Basic Knowledge and Film Practices: Head Trauma

Name: Basic Knowledge and Film Practices: Head Trauma
Uploaded: 2017-06-28T20:11:11+00:00
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Description: Basic Knowledge and Film Practices: Head Trauma

Basic Knowledge and Film Practices: Head Trauma
Nuttha Sanghan, M.D. Radiology Department Prince of Songkla University

Head Trauma Imaging modalities Primary traumatic lesions
Secondary effects

Imaging Modalities Skull radiography Calvarial fractures
Penetrating injuries Radiopaque foreign bodies Shift away from skull radiography toward CT scan AJNR 2007: 28;

Imaging Modalities CT Scan MRI Faster Wide availablility
Lack contraindication High accuracy Treatable lesions MRI Longer time Lesser availability Difficult monitoring More sensitive Parenchyma Extraparenchyma Lower accuracy Skull fracture AJNR 2007: 28;

Primary Traumatic Lesions
Skull and scalp lesions Extraaxial hemorrhage Epidural hematoma (EDH) Subdural hematoma (SDH) Subarachnoid hemorrhage (SAH) Intraaxial lesions Diffuse axonal injury (DAI) Cortical contusion Deep gray matter/brainstem injury

Skull and Scalp Lesions
Skull fractures Linear fracture Comminuted fracture Depressed fracture Compound fracture Diastatic fracture

S : skin C : connective tissue A : [galea] aponeurosis L : loose connective tissue P : periosteum Traumatic Lesions A cephalohematoma is a traumatic subperiosteal accumulation of blood confined by the cranial sutures, as opposed to caput succedaneum, which is a hemorrhage within the skin that crosses suture lines and is usually located at the vertex. A cephalohematoma also differs from a subgaleal hematoma, which is a hemorrhage subjacent to the aponeurosis covering the scalp beneath the occipitofrontalis muscle and is also not confined by the cranial sutures (Fig 23). The prevalence of cephalohematomas is close to 1%–2% in spontaneous vaginal deliveries and 3%–4% in forcepsor vacuum-assisted deliveries (71). In cases of prolonged resorption, cephalohematomas begin to calcify (72) and have a characteristic clinical and radiologic appearance. They tend to increase in size after birth and manifest as a tense and firm mass, occasionally with an underlying skull fracture. Resolution usually occurs without treatment by a few weeks to 3–4 months of age. Although cephalohematomas are not usually of clinical significance, they may present a challenge for the clinician because they occasionally become infected, requiring drainage and antibiotic therapy (72,73). At CT and MR imaging, acute cephalohematomas appear as crescent-shaped lesions adjacent to the outer table of the skull (Fig 24). Chronic cephalohematomas may calcify and appear hyperattenuating at CT (Fig 25) (71,72). During the evolution of a cephalohematoma, a mixed picture of erosive changes and periosteal reaction can be worrisome, especially in the absence of a good clinical history. At MR imaging, signal intensity typically follows that of subacute hemorrhage (ie, hyperintensity on T1- and T2- weighted images) but may vary depending on the stage of the hemorrhage. ************************ caput succedaneum : subcutaneous haematoma, most commonly secondary to vacuum assisted delivery subgaleal haematoma : haematoma within the potential space between the galea aponeurosis and the skull periosteum cephalohaematoma : subperiosteal and therefore bound by the suture line

Bilateral subgaleal hematoma

Acute and chronic cephalohematoma; a crescent-shaped soft-tissue mass in the periosteum of the left parietal and a partially calcified mass in the periosteum of the left parietal bone. The mass originated from a cephalohematoma. Radiographics 2004; 24:1655–1674

Extraaxial hemorrhage Epidural hematoma (EDH) Subdural hematoma (SDH) Subarachnoid hemorrhage (SAH)

Epidural Hematoma (EDH)
1-4% craniocerebral trauma Lucid interval 50% Delay 10-30% 24-48 hours

Imaging Displaced dura matter Certain diagnosis Focal biconvex/lentiform configuration Not cross suture Cross dural attachments Falx cerebri Tentorium cerebelli

Arterial origin Laceration: fracture 85-90% Stretching Temporal/temporoparietal region: MMA Venous origin Lacerated dural sinus Posterior cranial fossa

Classic arterial epidural hematoma; a lentiform, high attenuation collection adjacent to the right temporal lobe, caused by skull fracture with middle meningeal artery injury. Neurotherapeutics 2011; 8:

Venous epidural hematoma; scalp soft tissue swelling with lentiform EDH and pneumocephalus indicated an associated skull fracture. CT venogram was obtained as the fracture line extended over the expected location of the right transverse sinus. The opacified transverse sinuses are patent with compression and displacement from the inner table by the EDH caused by injury to the transverse sinus. Neurotherapeutics 2011; 8:

Size variable 2/3 hyperdense 1/3 mixed hyper/hypodense Swirl sign Low density: active bleeding Osborn

Coronal reconstructions Vertex EDH

Small EDH Not always differentiation SDH Classic shape Fracture

Mortality 5% Poor outcome Delayed diagnosis Posterior cranial fossa

Subdural Hematoma (SDH)
10-20% craniocerebral trauma 30% fatal injuries Lack trauma Stretching & tearing of bridging veins Asymptomatic-unconsciousness Superior cerebral(bridging) veins drain into the superior saggital sinus

Imaging Crescent shape Cross suture Not cross dural attachment

Supratentorial convexity Posterior cranial fossa Falx-tentorium Nonaccidental trauma 2.Intracranial bleeding 2.1 Subdural hemorrhage (SDH) มักพบว่า มีมากกว่าหนึ่งตำแหน่ง ,Mixed density และอาจพบ Chronic subdural hemorrhage ร่วมด้วย โดยเฉพาะอย่างยิ่งการเกิด Interhemispheric SDH (มักเป็นด้าน posterior) ค่อนข้างเป็นตัวบ่งถึง Inflicted head injury ส่วนในกลุ่มที่เกิดจากอุบัติเหตุ มักไม่ค่อยพบ SDH หรือถ้าพบก็มักมีขนาดเล็ก และอยู่ในด้านที่ถูกกระแทก และสัมพันธ์กับกลไกการเกิดอุบัติเหตุที่รุนแรงมาก 2.2 Epidural hemorrhage (EDH) อาจเกิดจาก เด็กตกลงมาหัวกระแทกพื้น แต่พบว่า สัมพันธ์กับ abuse น้อยกว่า SDH 2.3 Subarachnoid hemorrhage (SAH) มักพบร่วมกับ SDH Parenchymal injury ซึ่งขึ้นอยู่กับกลไก และความรุนแรง ของการเกิดการบาดเจ็บ โดยถ้าพบว่า มี lesion ชนิด subacute หรือ chronic (infarction , atrophy , encephalomalacia with ventriculomegaly) มักอยู่ในกลุ่ม abuse มากกว่าชนิด acute parenchymal injury 2.4 Skull fracture กลุ่มนี้มักสัมพันธ์กับการเกิดอุบัติเหตุมากกว่า และมักเป็น linear fracture บริเวณ parietal bone รอยแยกมักห่างมากกว่า 2 มิลลิเมตร สิ่งที่พึงระลึกในผู้ป่วย abuse คือ ประวัติของการบาดเจ็บ ไม่สัมพันธ์กับลักษณะบาดแผลและรอยแตก 2.5 Skeletal fracture 20-50% ของ inflicted head injury มีการบาดเจ็บนอกศีรษะ ซึ่งรูปแบบของการบาดเจ็บ มักได้แก่ Metaphyseal avulsion lesions ของ long bone,Rib fracture, Acromion fracture หรือการหักแบบ Spiral fracture

Acute (a few days) Hyperdense 60% Mixed 40% Nearly isodense Coagulopathy Severe anemia

Subacute (a few weeks) Isodense Displaced GW interface Sulci-inner table Contrast administration Cortical vessels Neomembrane

Chronic (months) Hypodense Neomembrane Capillary-rich Rebleeding 10-40% Mixed density Fluid-fluid levels Septate-loculation Calcification 1-2%

AJR 2011: 196;

Differentiation Epidural hematoma Fracture 85-95% Arterial/venous
Biconvex Not cross suture Cross dura Subdural hematoma Stretching/tearing Bridging cortical veins Crescent Cross suture Not cross dura

Subarachnoid Hemorrhage (SAH)
Moderate to severe head trauma Superficial sulci CSF cisterns

Common causes Head trauma Intracranial aneurysm Perimesencephalic hemorrhage Less frequent etiologies Arteriovenous malformation Arterial dissection Extension from intracerebral hemorrhage Perimesencephalic nonaneurysmal hemorrhage is AKA pretruncal nonaneurysmal hemorrhage Perimesencephalic nonaneurysmal hemorrhage is a benign form of subarachnoid hemorrhage (SAH). Angiographic changes of vasospasm are uncommon in patients with this type of hemorrhage (like because of the small amount of hemorrhage in this condition).

Pseudo-subarachnoid hemorrhage Severe diffuse brain edema Relatively hyperdense vasculatures A pseudo-SAH finding is a CT pseudolesion that shows SAH-like findings, in which the cisterns and cerebral sulci appear hyperattenuated relative to the brain parenchyma. This is a synergistic result of distention of the superficial vessels arising from elevated intracranial pressure and severe brain edema manifesting as hypoattenuated parenchyma A 34-year-old man with cardiac arrest. A, On the first day, no abnormal finding is seen. B, On the 8th day, the brain shows diffuse low attenuation with obliteration of cisterns-sulci and narrowed ventricles. High-attenuation areas along sylvian fissures and tentorium cerebelli. C, On the 129th day, brain edema becomes more severe with more prominent high attenuation areas.

Pseudo-empty delta sign: SSS thrombosis Posterior parafalcine/interhemispheric SDH SAH around sinus Note pseudo empty delta sign (arrow, A). Empty delta sign of cerebral venous thrombosis is applicable only on contrast-enhanced CT A pseudodelta sign can also be seen in patients with hyperattenuating acute subarachnoid hemorrhage around the sinus or subdural empyema or in patients with a posterior parafalcine interhemispheric hematoma. In these cases, administration of contrast material should opacify the sinus, obliterating the lucent center of the pseudodelta. AJR 2007; 189:

Intraaxial lesions Diffuse axonal injury (DAI) Cortical contusion Deep gray matter/brainstem injury

Diffuse Axonal Injury (DAI)
Shear-strain deformation Acceleration/deceleration Rotational force Diffuse, bilateral

Locations GW interface Corpus callosum Posterior body Splenium Dorsolateral upper brainstem Sequentially deeper with increasing severity

Imaging Initial normal/subtle Nonhemorrhagic 80% Hypodense foci Site of shearing Petechial hemorrhages 20-50% Tip of the iceberg Delayed scans with new lesions

Diffuse axonal injury in a patient who was on anticoagulants: CT scan on day1 and day 2

Diffuse axonal injury: small hemorrhagic foci in the right parasagittal posterior frontal lobe and in the splenium of the corpus callosum Neurotherapeutics 2011; 8:

Cortical Contusions Second primary intraaxial lesions
Less initial loss of consciousness Gray matter More vascularity Likely hemorrhage Variable size

Cortical Contusions Locations Temporal lobe Frontal lobe Petrous part
Greater sphenoid wing Frontal lobe Cribiform plate-orbit Planum sphenoidale Lesser sphenoid wing

Cortical Contusions Locations Cerebellum 10% Gliding contusion
Superior vermis Tonsils Inferior hemisphere Gliding contusion Parasagittal region emedicine.medscape.com

Cortical Contusions

A typical coup-contrecoup pattern of injury with an extracranial/skull injury at the point of direct impact and a more pronounced area of intracranial contusions at the directly opposite side of the head.

Cortical Contusions Evolve with time Early 24-48 hours
Ill-defined low density Small petechial hemorrhage 24-48 hours More lesions 20% delayed hemorrhage

Cortical Contusions Blossoming of hemorrhagic contusions.
(a)Multiple intracranial hemorrhages including a subtle left temporal hemorrhagic contusion, SDH along the right tentorium and SAH in the basilar cisterns and Sylvian fissure. (b) CT scan 6 hours later demonstrates expansion of the left temporal contusion. Neurotherapeutics 2011; 8:

Intraventricular Hemorrhage (IVH)
1-5% close head injury Other primary intraaxial lesions Etiology Disrupted subependymal veins Ruptured intracranial hemorrhage Focal choroid plexus hematoma Isolated IVH better outcome

Deep Gray Matter/Brainstem Injury
5-10% primary brain injury Direct trauma Shearing force Disrupted perforating blood vessels Petechial hemorrhage Locations Dorsolateral brainstem Diffuse axonal injury Duret hemorrhage Periaqueductal region Deep gray matter

9-year-old boy with motor vehicle accident.
Initial CT showed subcortical hemorrhagic foci in left fronal lobe. Due to persistent reduced vigilance, MRI was ordered Diffuse axonal injuries in classic locations: Gray/white matter interface (predominantly in frontal and temporal lobes), the corpus callosum (especially the splenium) and the dorsolateral midbrain

Secondary Effects Diffuse brain swelling Cerebral herniations
Secondary hemorrhage Traumatic ischemia/infarct

Diffuse Brain Swelling
Cerebral hyperemia Increased blood volume Cerebral edema Vasogenic: disrupted BBB Cytotoxic: failured cell membrane pumps

Diffuse cerebral swelling in this 32-year-old patient who sustained head trauma: diffuse sulcal effacement but relative preservation of gray-white differentiation. Neurotherapeutics 2011; 8:

Twofold higher in children More prone to dysautoregulation Vasodilatation and hyperemia Cerebral swelling

Cerebral Herniations Increased intracranial pressure
Herniaed brain to another compartment Bony ridges Dural folds

Cerebral Herniations Subfalcine Uncal Transtentorial Tonsillar Central
Descending Ascending Tonsillar Central Transcalvarial This diagram illustrates the main types of brain herniation. In this case it is due to a mass lesion (a subdural hematoma) that is also causing secondary edema to the adjacent brain. Subfalcine Herniation: (1)The cingulate gyrus is pushed laterally away from the expanding mass and herniates beneath the falx cerebri. Transtentorial (Uncal) Herniation: (3) Due to the cerebral edema, the uncus of the temporal lobe (medial temporal lobe) herniates downward into the posterior fossa. Central herniation (2) occurs when there is downward pressure centrally and can result in bilateral uncal herniation. Tonsillar Herniation: (4)If there is also edema or hemorrhage causing swelling in the cerebellum, the tonsil (or tonsils) of the cerebellum herniates downward into the foramen magnum.

Neurotherapeutics 2011; 8: 39-53.
Subfalcine herniation (cingulate herniation): A unilateral supratentorial mass or hemorrhage results in a midline shift. If the pressure pushing the brain to one side is great enough, one of the hemispheres is pushed under the falx (subfalcine). This may compress the anterior cerebral artery. There is ipsilateral lateral ventricle compression and contralateral lateral ventricle dilation (due to obstruction of the foramen of Monroe). Large left holohemispheric and parafalcine subdural hematoma results in midline shift and subfalcine herniation. Neurotherapeutics 2011; 8:

The left and center images show the suprasellar cistern
The left and center images show the suprasellar cistern. Its anterior borders are formed by the frontal lobes (F). Its lateral borders are formed by the uncus (U) of the temporal lobes. The left image shows the 5-pointed star appearance of the suprasellar cistern where the posterior border is formed by the pons (Po). The black arrow points to the fourth ventricle. The center image shows a higher cut where the suprasellar cistern has a 6-pointed star appearance since the posterior border is formed by the cerebral peduncles (P) which have a central cleft. When ICP increases, the suprasellar cistern space is compressed. The space may still be visible; however, with severe intracranial hypertension, the cistern is obliterated due to encroachment of brain tissue that normally forms the borders of the suprasellar cistern. Depending on the cause of the intracranial hypertension, the suprasellar cistern may be totally obliterated in global or severe ICP increase. In focal lesions, brain tissue may encroach into only one part of the suprasellar cistern. In early unilateral uncal herniation, the uncus of the temporal lobe (lateral border of the suprasellar cistern) will protrude into the suprasellar cistern. The right image shows the quadrigeminal cistern (black arrow). Note the "baby's bottom" appearance of its anterior border. When ICP is increased, the quadrigeminal cistern space is compressed or obliterated.

Uncus protrudes into suprasellar cistern.

Subacute subdural hematoma producing extensive midline shift with subfalcine and right uncal herniation. There is trapping of the ventricles with acute ependymal cerebrospinal fluid seepage, predominantly in the left periatrial and occipital regions.

Descending transtentorial herniation due to massive subdural hematoma
Cerebral Herniations Descending transtentorial herniation due to massive subdural hematoma radiologyimages.blogspot.com

Descending transtentorial herniation

Cerebral Herniations

Cerebral Herniations Tonsillar herniation Rare Foramen magnum
Compressing medulla Upper cervical spinal cord Early Difficult on axial view Best on sagittal MRI

Secondary Hemorrhage

Neurotherapeutics 2011; 8: 39-53.
Secondary Hemorrhage Large left holohemispheric and parafalcine subdural hematoma results in midline shift and uncal herniation. Downward brainstem herniation has led to classic Duret hemorrhage. Neurotherapeutics 2011; 8:

Secondary Hemorrhage Extensive cerebral edema with descending transtentorial herniation and a relatively large hemorrhage in brainstem. Because there is brain herniation, this hemorrhage is most likely Duret hemorrhage.

Secondary Hemorrhage Thin chronic subdural hematoma with abnormal signal in the contralateral crus cerebri; Kernohan’s notch phenomenon.

Traumatic Ischemia/Infarction
2% traumatic brain injuries Mechanical compression PCA-transtentorial herniation ACA-subfalcine herniation Perforating branches

Right-sided holohemispheric subdural hematoma results in subfalcine and uncal herniation with subsequently developed infarcts in ACA and PCA distributions with infarction of the posterior limb of the right internal capsule due to compression of the anterior choroidal artery with uncal herniation. Neurotherapeutics 2011; 8:

Primary vascular injuries Vasospasm Dissection Laceration Occlusion Pseudoaneurysm

CT screening-basal skull fracture Carotid canal Sphenoid bone Petrous temporal bone Occipital bone Implement CT angiography Conventional angiography

Referrence AJNR 2007: 28; Gentry LR, Knopp EA. Head Trauma. In: Atlas SW, editor. Magnetic resonance imaging of the brain and spine. 4th ed. Philadelphia: Lippincott Williams & Wilkins;

Referrence Neurotherapeutics 2011; 8: 39-53.
Yousem DM, Grossman RI. Head Trauma. In: Neuroradiology. 3rd ed. Philadelphia: Mosby; p กนกพร โอฬารรัตนชัย. ภาพรังสีกะโหลกศีรษะ. ใน: จันทิมา เอื้อตรง-จิตต์, สนาน สิมารักษ์, บรรณาธิการ. รังสีวิทยาพื้นฐาน. พิมพ์ครั้งที่ 1. เชียงใหม่: ธนุชพริ้นติ้ง; หน้า

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