neuroradiology head trauma
TRANSCRIPT
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By Dr Tariq Masood
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Cranial trauma is a major problem in accident and emergency departments and in one series provided 10% of the patients seen.
It is also responsible for 150 000 hospital admissions per year in the UK
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It is not necessary for every patient who suffers a head injury to undergo a CT scan. In the acute phase, the indications are deterioration of the patient's conscious level, with or without focal neurological signs..
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Sedation and/or general anesthesia should be employed without hesitation when indicated, since the recently traumatized patient may be very restless
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Accumulation of blood in the potential space between dura mater and bone
EDH is considered to be the most serious complication of head injury, requiring immediate diagnosis and surgical intervention (mortality rate associated with epidural hematoma has been estimated to be 5-50%)
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Usually results from a brief linear contact force to the calvaria that causes separation of the periosteal dura from bone and disruption of interposed vessels due to shearing stress
Skull fractures occur in 85-95% of adult cases
Extension of the hematoma usually is limited by suture lines owing to the tight attachment of the dura at these locations.
The temporoparietal region and the middle meningeal artery are involved most commonly (66%)
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Epidural hematoma complicates 2% of cases of head trauma (approximately 40,000 cases per year)
Alcohol and other forms of intoxication have been associated with a higher incidence of epidural hematoma
Sex◦ more frequent in men, with a male-to-female ratio of 4:1
Age ◦ rare in individuals younger than 2 years◦ rare in individuals older than 60 years because the dura
is tightly adherent to the calvaria
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Head trauma Lucid interval between the initial loss of
consciousness at the time of impact and a delayed decline in mental status (10-33% of cases)
Headache Nausea/vomiting Seizures Focal neurological deficits (eg, visual field
cuts, aphasia, weakness, numbness)
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Noncontrast CT scanning of the head (imaging study of choice for intracranial EDH) not only visualizes skull fractures, but also directly images an epidural hematoma
It appears as a hyperdense biconvex or lenticular-shaped mass situated between the brain and the skull, though regions of hypodensity may be seen with serum or fresh blood
MRI also demonstrates the evolution of an epidural hematoma, though this imaging modality may not be appropriate for patients in unstable condition
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Rapidly clotting blood collection below the inner layer of the dura but external to the brain and arachnoid membrane
Typically, low-pressure venous bleeding of bridging veins (between the cortex and venous sinuses) dissects the arachnoid away from the dura and layers out along the cerebral convexity
It conforms to the shape of the brain and the cranial vault, exhibiting concave inner margins and convex outer margins (crescent shape)
Frequency is related directly to the incidence of blunt head trauma
It’s the most common type of intracranial mass lesion, occurring in about a third of those with severe head injuries
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Mortality◦ Simple SDH (no parenchymal injury) is associated with a
mortality rate of about 20%◦ Complicated SDH (parenchymal injury) is associated with
a mortality rate of about 50% Age
◦ It’s associated with age factors related to the risk of blunt head trauma
◦ More common in people older than 60 years (bridging veins are more easily damaged/falls are more common)
◦ Bilateral SDHs are more common in infants since adhesions existing in the subdural space are absent at birth
◦ Interhemispheric SDHs are often associate with child abuse
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Usually involves moderately severe to severe blunt head trauma
Acute deceleration injury from a fall or motor vehicle accident, but rarely associated with skull fracture
Generally loss of consciousness Any degree or type of coagulopathy should
heighten suspicion of SDH Commonly seen in alcoholics because they’re
prone to thrombocytopenia, prolonged bleeding times, and blunt head trauma
Patients on anticoagulants can develop SDH with minimal trauma and warrant a lowered threshold for obtaining a head CT scan
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MRI is superior for demonstrating the size of an acute SDH and its effect on the brain, however noncontrast head CT is the primary means of making a diagnosis and suffice for immediate management purposes
Noncontrast head CT scan (imaging study of choice for acute SDH) ◦ The SDH appears as a hyperdense (white) crescentic mass
along the inner table of the skull, most commonly over the cerebral convexity in the parietal region. The second most common area is above the tentorium cerebelli
Contrast-enhanced CT or MRI is widely recommended for imaging 48-72 hours after head injury because the lesion becomes isodense in the subacute phase
In the chronic phase, the lesion becomes hypodense and is easy to appreciate on a noncontrast head CT scan
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Subdural hematoma - Axial CT scan though the level of the lateral ventricles shows right-sided subdural hematoma along the convexity (red arrow) and
falx (green arrow), with severe midline shift from right to left
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Isodense subdural. Note mass effect and effacement of sulci which suggest diagnosis prior to contrast medium.
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Post-enhancement scan of another isodense subdural. The lesion stands out against the enhanced surface of the brain
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Epidural Hematoma◦ Potential space between
the dura and the inner table of the skull
◦ Can’t cross sutures◦ Skull fractures in
temporoparietal region◦ Middle meningeal artery◦ Lenticular or biconvex
shape◦ Lucid interval◦ Common in alcoholics◦ Medical emergency◦ CT without contrast◦ Evacuate via burr holes
Subdural Hematoma
◦ Between the dura mater and the arachnoid mater
◦ Can cross sutures◦ Cortical bridging veins◦ Crescent shape◦ Loss of consciousness◦ Common in elderly◦ Common in alcoholics◦ Medical emergency◦ CT without contrast◦ Evacuate via burr holes
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Traumatic intracerebral haematomas It may be impossible to distinguish these
from spontaneous intracerebral haemorrhage.
The frontal and temporal lobes are classic sites, which are less commonly affected by spontaneous episodes.
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Both types are of high density, but traumatic bleeding is more frequently multifocal and in cases with a poor prognosis may be seen to involve the brainstem.
It is also more commonly associated with low-density areas and brain swelling, even in the acute stages.
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The blood may extend to the ventricles or the subarachnoid space.
Retrobulbar or subperiosteal orbital haematomas are readily diagnosed in the context of head trauma as high-density lesions within the orbits or applied to the bone
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NECT Brain showing hematoma in the left putamen
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NECT Brain showing right temporoparietal intracerebral hematoma with mass effect.
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Cerebral contusion and edema Two types of cerebral contusion may be
detected by CT scanning: hemorrhagic and non-hemorrhagic.
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Hemorrhagic contusion commonly seen in the frontal and temporal
lobes, although any part of the cerebrum, cerebellum or brainstem may be affected.
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It appears as a mass lesion of mixed high and low density not dissimilar to multifocal traumatic hemorrhage, but generally more diffuse-the area of swelling may be very extensive.
The hemorrhagic areas may not be evident in the very acute stage, occurring only 24 hours or more later.
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Non-haemorrhagic contusion cannot reliably be distinguished from
cerebral oedema, but tends to be more focal and space-occupying. Considerable enhancement may be seen with intravenous contrast medium; this does not occur with oedema.
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Multifocal haemorrhages andcontusions in both hemispheres.
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Cerebral trauma. Contusions in Rightt temporal lobe.
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Diffuse brain damage About 50% of patients who suffer
immediate prolonged unconsciousness following a head injury have no obvious mass or focal lesions.
this is true of about one-third of fatal cases.
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In these patients the lesions present have been classified into four types:
1. Multiple petechial haemorrhages 2. Diffuse axonal injury 3. Brain swelling 4. Hypoxic brain damage.
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Multiple petechial haemorrhages This type of injury is seen throughout the
white matter and brainstem and is rapidly fatal. It is therefore more likely to be seen at postmortem than in an imaging department.
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Diffuse axonal injury (white matter shearing)
This severe injury may show virtually no macroscopic change in the affected brain.
There is disruption of axons in the subcortical parasagittal white matter and in various other sites, including the internal and external capsules, fornix and cerebellum
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It is claimed to result from acute lateral acceleration or deceleration of the brain within the rigid cranium and can occur without anything actually striking the head. It occurs most commonly in automobile accidents.
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The patient is unconscious from the moment of impact and remains unconscious, vegetative or severely disabled until death.
Despite the severe brain damage and the very grave state of the patient there may be little or nothing shown at imaging
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Small focal haemorrhages have been described in the corpus callosum and in the posterolateral quadrant of the rostral brainstem and such lesions could theoretically be demonstrated, as can small subcortical haemorrhages.
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Brain swelling Diffuse swelling of the entire brain occurs
mainly in children and adolescents. The pathogenesis is debated and it is thought to be due to vasodilatation and increased cerebral blood volume in the first place.
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Diffuse swelling of the ipsilateral hemisphere can also occur with local and mass lesions , including acute subdural haematoma and extensive unilateral contusions. Focal oedema may also occur with haemorrhages and contusions.
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With diffuse bilateral swelling the ventricles are compressed and appear small, like slits, at imaging; the basal cisterns may be occluded and the sulci effaced. The white matter shows no reduction in density and appears normal at CT, although evidence of oedema may be seen in cases with prolonged coma
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1)Subcortical small haemorrhages associated with shearing injury, and a few large haemorrhages.
(2) Head injury in a child. There is cerebral
oedema mainly on the left, associated with compression of the ventricles and some shift to the right.
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Hypoxic damage This is due either to a prolonged drop in
systolic blood pressure, or to arterial spasm, or to both. Evidence of hypoxic damage is seen in the first place at major arterial boundary zones, and frank infarction may later ensue.
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Hypoxia and subsequent infarction may also result from brain swelling and tentorial herniation compromising the posterior cerebral circulation, or from trauma to major vessels. Imaging may show little in the early stages but later will demonstrate evidence of infarction.
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Skull fractures Fractures are, in most instances, best
diagnosed by a combination of clinical features and plain radiography.
However, basal fractures, which are often difficult to demonstrate or to assess fully by these means, may be shown very clearly by CT scanning.
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Depressed fractures can be clearly demonstrated and their relationship to the underlying brain better shown than by plain X-ray films.
However, the chief value of the CT scan is in the assessment of underlying brain damage and haematoma formation.
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(A) Depressed fracture in the left temporal region with underlying
Haemorrhagic contusions.
(B) Same case at higher level to show bone detail
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Intracranial air Whether subdural or subarachnoid, air is
well shown by CT and implies a dural tear communicating with a sinus or other air-containing cavity. Intracerebral air (aerocele) is also well shown and its site of origin can be identified prior to surgery.
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(C) Frontal aerocele. (D) Bone window filmshowing frontal fracture and connection with top of frontal sinus.
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Foreign bodies Intracranial foreign bodies may be
accurately localized by CT scanning. The value of the technique is in the demonstration of the position of the foreign body relative to, and its effects on, the intracranial structures, features which cannot be seen on plain radiographs.
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Good demonstration of the relationships of metallic objects may, however, be prevented by the resulting artifacts. Wooden fragments may appear less dense than brain.
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CT scan showing the wooden foreign body (13 x 2.7 x 2.5 cm)entering the right temporal bone and reaching the left parietal bone with blood along its path
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Ct scan showing metallic intracranial foreign body
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