Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
169 Cards in this Set
- Front
- Back
|
Describe a subgaleal hematoma:
|
The subgaleal hematoma is the most common manifestation of scalp injury and can be recognized on CT or MR as focal soft tissue swelling of the scalp located beneath the subcutaneous fibrofatty tissue and above the temporalis muscle and calvarium.
|
|
|
What is the most common type of skull fracture?
|
Nondisplaced linear fractures of the calvarium are the most common type of skull fracture. They may be difficult to detect on CT scans, especially when the fracture plane is parallel to the plane of section.
|
|
|
How are skull fractures managed?
|
Isolated linear skull fractures do not require treatment. Surgical management is usually indicated for depressed and compound skull fractures.
|
|
|
What should you look for if you see a depressed skull fracture?
|
Depressed fractures are frequently associated with an underlying contusion.
|
|
|
When can pneumocephalus be seen in trauma?
|
Intracranial air (“pneumocephalus”) may be seen with compound skull fractures or fractures involving the paranasal sinuses.
|
|
|
What are some clinical signs of temporal bone fracture?
|
Patients with fractures of the temporal bone may present with deafness, facial nerve palsies, vertigo, dizziness, or nystagmus. Clinical symptoms are often masked in the presence of other serious injuries. Physical signs of temporal bone fracture include hemotympanum, CSF otorrhea, and ecchymosis over the mastoid process (“Battle's sign”).
|
|
|
What are some indirect signs of temporal bone fracture?
|
Findings such as opacification of the mastoid air cells, fluid in the middle ear cavity, pneumocephalus, or occasionally pneumolabyrinth, should raise the suspicion of a temporal bone fracture.
|
|
|
What are the two types of temporal bone fractures?
|
Fractures of the temporal bone can be classified as longitudinal or transverse depending on their orientation relative to the long axis of the petrous bone. If the fracture parallels the long axis of the petrous pyramid, it is termed a “longitudinal” fracture; fractures perpendicular to the long axis of the petrous bone are termed “transverse” fractures. “Mixed” fracture types also occur.
|
|
|
Which is more common, a longitudinal or a transverse fracture of the temporal bone?
|
The longitudinal temporal bone fracture represents 70% to 90% of temporal bone fractures.
|
|
|
Which is more severe, a longitudinal or a transverse fracture of the temporal bone? Describe the possible complications:
|
A transverse fracture has more severe complications including: sensorineural hearing loss, severe vertigo, nystagmus, and perilymphatic fistula. Facial palsy is seen in 30% to 50% of these cases and is often complete. Transverse fractures may also involve the carotid canal or jugular foramen, causing injury to the carotid artery or jugular vein.
|
|
|
What are the two general forms of head injury?
|
Traumatic head injury can be divided into primary and secondary forms. Primary lesions are those that occur as a direct result of a blow to the head. Secondary lesions occur as a consequence of primary lesions, usually as a result of mass effect or vascular compromise. Secondary lesions are often preventable, whereas primary injuries, by definition, have already occurred by the time the patient arrives in the emergency department.
|
|
|
What type of vessel is injured in an epidural hematoma?
|
Epidural hematomas are usually arterial in origin and often result from a skull fracture that disrupts the middle meningeal artery. Venous epidural hematomas are less common than arterial epidurals and tend to occur at the vertex, posterior fossa, or anterior aspect of the middle cranial fossa. Venous epidural hematomas usually occur as a result of disrupted dural venous sinuses.
|
|
|
Are all epidural hematomas associated with a skull fracture?
|
They may occur from stretching or tearing of meningeal arteries without an associated fracture, especially in children. Overall, skull fractures are seen in 85% to 95% of cases.
|
|
|
Describe the CT appearance of an epidural hematoma:
|
On CT, acute epidural hematomas appear as well-defined, high-attenuation lenticular or biconvex extra-axial collections. Associated mass effect with sulcal effacement and midline shift is frequently seen. Bone windows usually demonstrate an overlying linear skull fracture. Because epidural hematomas exist in the potential space between the dura and inner table of the skull, they usually will not cross cranial sutures, where the periosteal layer of the dura is firmly attached.
|
|
|
Which type of epidural hematoma can cross cranial suture lines?
|
Near the vertex, however, the periosteum forms the outer wall of the sagittal sinus and is less tightly adherent to the sagittal suture. Therefore, vertex epidurals, which are usually of venous origin from disruption of the sagittal sinus, can cross the midline.
|
|
|
What should you think of if an acute epidural hematoma appears heterogenous?
|
This finding may indicate active extravasation of fresh unclotted blood into the collection and warrants immediate surgical attention.
|
|
|
What type of vessel is injured in subdural hematomas?
|
Subdural hematomas are typically venous in origin, resulting from stretching or tearing of cortical veins that traverse the subdural space en route to the dural sinuses. They may also result from disruption of penetrating branches of superficial cerebral arteries.
|
|
|
Why are subdural hematomas usually bigger than epidural hematomas?
|
Because the inner dural layer and arachnoid are not as firmly attached as the structures that make up the epidural space, the subdural hematoma typically extends over a much larger area than the epidural hematoma.
|
|
|
What is the mechanism of injury that causes subdural hematomas? What are other associated injuries seen with subdurals?
|
Patients with a subdural hematoma commonly present after acute deceleration injury from a motor vehicle accident or fall. The same mechanism can cause cortical contusions and DAI, which are frequently seen in association with acute subdural hematomas.
|
|
|
Describe the CT appearance of a subdural hematoma:
|
On axial CT, acute subdural hematomas appear as crescent-shaped extra-axial collections of high attenuation. Most subdural hematomas are supratentorial, located along the convexity. They are also frequently seen along the falx and tentorium. Because dural reflections form the falx cerebri and tentorium, subdural collections will not cross these structures. Unlike epidural hematomas, subdural hematomas can cross sutural margins and, in fact, are frequently seen layering along the entire hemispheric convexity from the anterior falx to the posterior falx. Diffuse swelling of the underlying hemisphere is common with subdural hematomas.
|
|
|
What should you think of if you see an acute subdural hematoma that is isodense or hypodense to brain?
|
Occasionally, acute subdural blood may be isodense or hypodense in patients with severe anemia or active extravasation (“hyperacute” subdural hematoma).
|
|
|
When is a "hematocrit effect" seen in subdural hematomas?
|
A sediment level or “hematocrit effect” may be seen either from rebleeding or in patients with clotting disorders
|
|
|
What should you think of if you see a heterogenous subdural hematoma?
|
Rebleeding during evolution of a subdural hematoma causes a heterogeneous appearance from the mixture of fresh blood and partially liquefied hematoma.
|
|
|
What do chronic subdural hematomas look like on CT?
|
Chronic subdural hematomas have low attenuation values, similar to those of CSF. On noncontrast CT scans, it can be difficult to distinguish them from prominent subarachnoid space secondary to cerebral atrophy.
|
|
|
How can you tell chronic subdural hematomas apart from prominent subdural spaces related to brain atrophy?
|
Contrast enhancement can help by demonstrating an enhancing capsule or displaced cortical veins.
|
|
|
What clues can help you see a subacute subdural hematoma during its isodense phase?
|
Although the subdural hematoma itself is less conspicuous during this isodense phase, there are indirect signs on a noncontrast CT scan that should lead to the correct diagnosis. These include effacement of sulci, displacement of cortex with white matter “buckling,” and midline shift.
|
|
|
How long does it take for a subdural hematoma to appear isodense to brain?
|
During the transition from acute to chronic subdural hematomas, an isodense phase occurs, usually between several days and 3 weeks after the acute event.
|
|
|
What do subdural hematomas look like on MR?
|
The MR appearance of subdural hematomas depends on the biochemical state of hemoglobin, which varies with the age of the hematoma. Acute subdural hematomas are isointense to brain on T1WIs and hypointense on T2WIs. MR is particularly helpful during the subacute phase, when the subdural hematoma may be isodense or hypodense on CT scans. T1WIs will demonstrate high signal intensity caused by the presence of methemoglobin in the subdural collection. This high signal clearly distinguishes subdural hematomas from most nonhemorrhagic fluid collections.
|
|
|
What vessels are injured in traumatic subarachnoid hemorrhage?
|
It results from the disruption of small subarachnoid vessels or direct extension into the subarachnoid space by a contusion or hematoma.
|
|
|
What do subarachnoid hemorrhages look like on CT?
|
On CT, subarachnoid hemorrhage appears as linear areas of high attenuation within the cisterns and sulci.
|
|
|
How can you differentiate subarachnoid hemorrhage from subdural hematoma?
|
Subarachnoid collections along the convexity or tentorium can be differentiated from subdural hematomas by their extension into adjacent sulci.
|
|
|
What do subarachnoid hemorrhages look like on MR?
|
Hyperacute subarachnoid hemorrhage may be more difficult to detect on conventional MR than it is on CT scans, because it can be isointense to brain parenchyma on T1W and T2W images. Subacute subarachnoid hemorrhage may be better appreciated on MR because of its high signal intensity at a time when the blood is isointense to CSF on CT. Chronic hemorrhage on MR scans may show hemosiderin staining in the subarachnoid space, which appears as areas of markedly decreased signal intensity on T1- and T2-weighted sequences (“superficial hemosiderosis”).
|
|
|
Describe the different mechanisms by which intraventricular hemorrhage can occur:
|
-First, it can result from rotationally induced tearing of subependymal veins on the surface of the ventricles.
-Another mechanism is by direct extension of a parenchymal hematoma into the ventricular system. -Third, intraventricular blood can result from retrograde flow of subarachnoid hemorrhage into the ventricular system through the fourth ventricular outflow foramina. |
|
|
What complication are patients with intraventricular hemorrhage at risk for?
|
Patients with intraventricular hemorrhage are at risk for subsequent hydrocephalus by obstruction, at the level of either the aqueduct or the arachnoid villi.
|
|
|
What percent of DAI cases are visible on CT?
|
Only approximately 20% of lesions contain sufficient hemorrhage to be visible on CT scans, accounting for the low sensitivity of this modality.
|
|
|
What does DAI look like on CT?
|
Most common is the finding of small, petechial hemorrhages at the gray–white junction of the cerebral hemispheres or corpus callosum. Ill-defined areas of decreased attenuation on CT may occasionally be seen with nonhemorrhagic lesions.
|
|
|
What does DAI look like on MR?
|
On MR, nonhemorrhagic DAI lesions appear as small foci of increased signal on T2WIs (T2 prolongation) within the white matter. The lesions tend to be multiple, with as many as 15 to 20 lesions seen in patients with severe head injury. If seen on T1WIs, they appear as subtle areas of decreased intensity. Petechial hemorrhage causes a central hypointensity on T2WIs and hyperintensity on T1WIs within a few days as a result of intracellular methemoglobin. The conspicuity of DAI on MR diminishes over weeks to months as the damaged axons degenerate and the edema resolves. Residual findings might include nonspecific atrophy or hemosiderin staining, which can persist for years and is especially obvious on gradient-echo sequences.
|
|
|
Where are lesions of DAI usually found?
|
DAI is seen in characteristic locations that correlate with the severity of the trauma. Patients with the mildest forms of injury have lesions confined to the frontal and temporal white matter, near the gray–white junction. The lesions typically involve the parasagittal regions of the frontal lobes and periventricular regions of the temporal lobes. Patients with more severe trauma have DAI involving lobar white matter as well as the corpus callosum, especially the posterior body and splenium. The corpus callosum accounts for approximately 20% of all DAI lesions. DAI in the most severe cases involves the dorsolateral aspect of the midbrain and upper pons, in addition to the lobar white matter and corpus callosum.
|
|
|
What things distinguish DAI from brain contusions clinically?
|
-Patients with cortical contusions are much less likely to have loss of consciousness at the time of injury than are patients with DAI.
-Contusions are also associated with a better prognosis than DAI. |
|
|
Where do cortical contusions tend to occur?
|
Contusions characteristically occur near bony protuberances of the skull and skull base. They tend to be multiple and bilateral and are more commonly hemorrhagic than DAI. Common sites are the temporal lobes above the petrous bone or posterior to the greater sphenoid wing, and the frontal lobes above the cribriform plate, the planum sphenoidale, and the lesser sphenoid wing. Less than 10% of lesions involve the cerebellum. Contusions can also occur at the margins of depressed skull fractures.
|
|
|
What do cortical contusions look like on CT?
|
The CT appearance of cortical contusions characteristically varies with the age of the lesion. Many nonhemorrhagic lesions are initially poorly seen but become more obvious during the first week because of associated edema. Hemorrhagic lesions are seen as foci of high attenuation within superficial gray matter (Fig. 3.17b). These may be surrounded by larger areas of low attenuation secondary to surrounding edema. During the first week, the characteristic CT pattern of mixed areas of hypodensity and hyperdensity (“salt and pepper” pattern) becomes more apparent. Areas of prior contusion can often be recognized as foci of encephalomalacia within the same characteristic locations just described.
|
|
|
What do cortical contusions look like on MR?
|
On MR, contusions appear as poorly marginated areas of increased signal on proton density and T2-weighted sequences. They are recognized because of their characteristic distribution in the frontal and temporal lobes and often have a “gyral” morphology. Hemorrhage causes heterogeneous signal intensity that varies depending on the age of the lesion. Hemosiderin staining from hemorrhage of any cause leads to markedly decreased signal intensity on a T2WI, especially at higher field strengths. This signal loss can persist indefinitely as a marker of prior hemorrhage.
|
|
|
Define intraparenchymal hemorrhage:
|
Occasionally, intraparenchymal hemorrhage is seen that is not necessarily associated with cortical contusion but rather represents shear-induced hemorrhage from the rupture of small intraparenchymal blood vessels. This lesion is known simply as an intracerebral hematoma.
|
|
|
Where are intracerebral hematomas usually located?
|
Most intracerebral hematomas are located in the frontotemporal white matter, although they have also been described in the basal ganglia. They are often associated with skull fractures and other primary neuronal lesions, including contusions and DAI.
|
|
|
What do intracerebral hematomas look like clinically?
|
In the absence of other significant lesions, patients with intracerebral hematomas can remain lucid after their injury. When symptoms develop, they commonly result from the mass effect associated with an expanding hematoma. Intracerebral hematomas can also present late secondary to delayed hemorrhage, which is another cause of clinical deterioration during the first several days after head trauma.
|
|
|
What do intracerebral hematomas look like on imaging?
|
They look like intraparenchymal hemorrhage, but intracerebral hematomas tend to have less surrounding edema than cortical contusions because they represent bleeding into areas of relatively normal brain.
|
|
|
Describe subcortical gray matter injury:
|
Subcortical gray matter injury is an uncommon manifestation of primary intra-axial injury and is seen as multiple petechial hemorrhages primarily affecting the basal ganglia and thalamus. These represent microscopic perivascular collections of blood that may result from disruption of multiple small perforating vessels.
|
|
|
Which artery is most often injured? Where?
|
The internal carotid is the most often injured artery, especially at sites of fixation. These include its entrance to the carotid canal at the base of the petrous bone and its exit from the cavernous sinus below the anterior clinoid process.
|
|
|
What does vascular injury look like on MR?
|
MR findings of vascular injury include the presence of an intramural hematoma (best seen on a T1WI with fat suppression) or intimal flap with dissection, or the absence of normal vascular flow void with occlusion. An associated parenchymal infarction might also be seen.
|
|
|
Define carotid-cavernous fistula:
|
A carotid cavernous fistula (CCF) is a communication between the cavernous portion of the internal carotid artery and the surrounding venous plexus. The lesion typically follows a full-thickness arterial injury, resulting in venous engorgement of the cavernous sinus and its draining tributaries (e.g., the ipsilateral superior ophthalmic vein and inferior petrosal sinus). The CCF may also result from ruptured cavernous carotid aneurysms.
|
|
|
Which patients are at increased risk of cartodi-cavernous fistula?
|
A CCF most often results from severe head injury. Skull base fractures, especially those involving the sphenoid bone, indicate patients at increased risk for associated cavernous carotid injury.
|
|
|
What do carotid-cavernous fistulas look like on MR?
|
On MR, the CCF may manifest as an enlarged superior ophthalmic vein, a cavernous sinus, and petrosal sinus flow voids. There may be evidence of proptosis, swelling of the preseptal soft tissues, and enlargement of the extraocular musculature.
|
|
|
How are carotid-cavernous fistulae diagnosed?
|
Diagnosis usually requires selective carotid angiography with rapid filming to demonstrate the site of communication.
|
|
|
Describe dural fistulae:
|
Dural fistulas are also associated with trauma. For example, they may be caused by laceration of the middle meningeal artery with resultant formation of a fistula connecting the meningeal artery to the meningeal vein. Drainage via meningeal veins prevents formation of an epidural hematoma. Patients may be asymptomatic or present with nonspecific complaints, including tinnitus.
|
|
|
Which head injuries absolutely require direct impact to the head?
|
Only skull fractures and epidural hematomas require a physical blow to the head.
|
|
|
What causes diffuse cerebral swelling?
|
Diffuse cerebral swelling is a common manifestation of head trauma. It may occur either because of an increase in cerebral blood volume (hyperemia) or an increase in tissue fluid content (cerebral edema).
|
|
|
What causes cerebral swelling in kids and adolescents?
What does it look like on imaging? |
-Cerebral swelling from hyperemia is most commonly seen in children and adolescents.
-The pathogenesis is poorly understood but appears to be the result of loss of normal cerebral autoregulation. -Hyperemia is recognized on CT as ill-defined mass effect, effacement of sulci, and normal attenuation of brain. |
|
|
What does diffuse cerebral swelling look like?
|
Generalized mass effect, with effacement of sulci, suprasellar and quadrigeminal plate cisterns, and compression of the ventricular system. Effacement of the brainstem cisterns indicates severe mass effect and may herald impending transtentorial herniation. The cerebellum and brainstem are usually spared and may appear hyperdense relative to the cerebral hemispheres. Often, the falx and cerebral vessels appear dense, mimicking acute subarachnoid hemorrhage.
|
|
|
What does subfalcine herniation look like?
|
The cingulate gyrus is displaced across the midline under the falx cerebri. Compression of the adjacent lateral ventricle may be seen on CT scans, as well as enlargement of the contralateral ventricle from obstruction at the level of the foramen of Monro. Both anterior cerebral arteries (ACAs) may be displaced to the contralateral side.
|
|
|
What is the most common type of brain herniation?
|
Subfalcine
|
|
|
What are patients with subfalcine herniation at risk of?
|
These patients are at risk of ACA infarction in the distribution of the callosomarginal branch of the ACA, where it becomes trapped against the falx.
|
|
|
What does uncal herniation look like?
|
The medial aspect of the temporal lobe is displaced medially over the free margin of the tentorium. Uncal herniation causes focal effacement of the ambient cistern and the lateral aspect of the suprasellar cistern. Rarely, displacement of the brainstem causes compression of the contralateral cerebral peduncle against the tentorial margin, resulting in peduncular hemorrhage or infarction.
|
|
|
What is Kernohan's notch?
|
-Rarely in uncal herniation, displacement of the brainstem causes compression of the contralateral cerebral peduncle against the tentorial margin, resulting in peduncular hemorrhage or infarction.
-The focal impression on the cerebral peduncle is known as Kernohan's notch. |
|
|
In uncal herniation, what is the focal impression on the contralateral cerebral peduncle known as?
|
Kernohan's notch
|
|
|
What cranial nerve can be damaged by uncal herniation?
|
the third
|
|
|
What does descending transtentorial herniation look like?
|
Descending transtentorial herniation is recognized by effacement of the suprasellar and perimesencephalic cisterns. Pineal calcification, usually seen at about the same level as calcified choroid plexus in the trigones of the lateral ventricles, is displaced inferiorly.
|
|
|
What are the two types of transtentorial herniation?
|
ascending and descending
|
|
|
Which is more common, ascending or descending transtentorial herniation?
|
Descending
|
|
|
What does ascending transtentorial herniation look like?
|
Large posterior fossa hematomas can cause ascending transtentorial herniation, in which the vermis and portions of the cerebellar hemispheres can herniate through the tentorial incisura.
|
|
|
Define tonsillar herniation:
|
Posterior fossa hematomas can also cause herniation of the cerebellar tonsils downward through the foramen magnum.
|
|
|
Describe external herniation:
|
External herniation can occur in which swelling or mass effect causes the brain to herniate through a calvarial defect. This can be posttraumatic or occur at the time of craniotomy and prevent closure of the skull flap.
|
|
|
Give some reasons why head trauma patients would develop hydrocephalus:
|
Hydrocephalus can occur after subarachnoid or intraventricular hemorrhage as a result of either impaired CSF reabsorption at the level of the arachnoid granulations or obstruction at the level of the aqueduct or fourth ventricular outflow foramina. Mass effect from cerebral swelling or an adjacent hematoma can also cause hydrocephalus by compression of the aqueduct or outflow foramina of the fourth ventricle. Asymmetric lateral ventricular dilatation can be produced by compression of the foramen of Monro.
|
|
|
Give some reasions why head trauma patients would develop infarction/ischemia:
|
Posttraumatic ischemia or infarction can result from raised intracranial pressure, embolization from a vascular dissection, or direct mass effect on cerebral vasculature from brain herniation or an overlying extra-axial collection. In addition, patients may suffer diffuse ischemic damage from acute reduction in cerebral blood flow or from hypoxemia secondary to respiratory arrest or status epilepticus.
|
|
|
Uncal herniation places patients at risk of what?
|
posterior cerebral artery infarction
|
|
|
What vessel is at risk of infarction in uncal herniation?
|
posterior cerebral artery infarction
|
|
|
What vessel is at risk of infarction in subfalcial herniation?
|
anterior cerebral artery
|
|
|
What vessel is at risk of infarction in tonsillar herniation?
|
posterior inferior communicating artery
|
|
|
Tonsillar herniation places patients at risk for what?
|
Infarction of the posterior inferior communicating artery
|
|
|
What types of imaging would best show a CSF leak?
|
Radionuclide cisternography is highly sensitive for the presence of CSF extravasation; however, CT scanning with intrathecal contrast is required for detailed anatomic localization of the defect.
|
|
|
What has to present for there to be a CSF leak?
|
A dural tear
|
|
|
What has to be present for there to be CSF otorrhea?
|
CSF otorrhea occurs when a communication between the subarachnoid space and middle ear occurs in association with disruption of the tympanic membrane.
|
|
|
Describe a leptomeningeal cyst:
|
Leptomeningeal cyst or “growing fracture” is caused by a traumatic tear in the dura, which allows an outpouching of arachnoid to occur at the site of a suture or skull fracture. This leads to progressive, slow widening of the skull defect or suture, presumably as a result of CSF pulsations. The leptomeningeal cyst appears as a lytic skull defect on CT or plain skull films, which can enlarge over time.
|
|
|
What does encephalomalacia look like on CT and MR?
|
-CT demonstrates fairly well-defined areas of low attenuation, with volume loss.
-There may be dilation of adjacent portions of the ventricular system. -Encephalomalacia will follow CSF signal on MR sequences, except for gliosis, which appears as increased signal intensity on both proton-density and T2-weighted images. |
|
|
What would make you think that a particular case of encephalomalacia is secondary to trauma?
|
The appearance of encephalomalacia is not specific for posttraumatic injury, but the locations are characteristic: anteroinferior frontal and temporal lobes. Focal volume loss along the white matter tracts associated with cell death is known as wallerian degeneration and may be seen on CT and especially MR studies.
|
|
|
What is the most common brainstem injury?
|
The most common form of primary brainstem injury is DAI.
|
|
|
Where is brainstem DAI usually seen? What is it associated with?
|
It affects the dorsolateral aspect of the midbrain and upper pons. The superior cerebellar peduncles and the medial lemnisci are particularly vulnerable. Brainstem DAI is nearly always seen in association with lesions of the frontal or temporal white matter and corpus callosum.
|
|
|
What can brainstem DAI be confused with? How can you tell the difference?
|
A rare form of primary injury caused by direct impact of the free margin of the tentorium on the brainstem. Brainstem DAI is nearly always seen in association with lesions of the frontal or temporal white matter and corpus callosum. This distinguishes between the two.
|
|
|
Other than DAI, what other primary brainstem injury can be seen?
|
Primary brainstem injury may also occur in the form of multiple petechial hemorrhages in the periaqueductal regions of the rostral brainstem. This form of injury represents disruption of penetrating brainstem blood vessels by shear strain and carries a grim prognosis.
|
|
|
Describe pontomedullary separation:
|
An extremely rare form of indirect primary brainstem injury is the pontomedullary separation or rent. As the name implies, this represents a tear in the ventral surface of the brainstem at the junction of the pons and medulla. There is a spectrum of severity ranging from a small tear to complete avulsion of the brainstem. Pontomedullary separation can occur without associated diffuse cerebral injury. This lesion is usually fatal.
|
|
|
How is the brainstem affected by global hypoperfusion?
|
Brainstem infarction from hypotension-induced cerebral hypoperfusion is usually seen in conjunction with supratentorial ischemic injury. The brainstem may be relatively spared in hypoxic injury.
|
|
|
How can you tell primary brainstem lesions from secondary?
|
Brainstem lesions that occur as a result of downward herniation, hypoxia, or ischemia usually involve the ventral or ventrolateral aspect of the brainstem, in contrast to primary brainstem lesions, which are most common in the dorsolateral aspect of the brainstem.
|
|
|
What is a Duret hemorrhage?
|
This is a midline hematoma in the tegmentum of the rostral pons and midbrain seen in association with descending transtentorial herniation. It is believed to result from stretching or tearing of penetrating arteries as the brainstem is caudally displaced.
|
|
|
What is a midline hematoma in the pons area associated with descending transtentorial herniation called?
|
A Duret hemorrhage
|
|
|
Where do brainstem infarcts tend to occur?
|
The brainstem infarct is another type of secondary brainstem injury that typically occurs in the central tegmentum of the pons and midbrain.
|
|
|
Is wood hyper- or hypodense to brain?
|
Hypodense
|
|
|
What features of a cranial gunshot wound portend a poorer prognosis?
|
Gunshot wounds in which the bullet crosses the midline or in which small fragments are seen displaced from the main bullet are associated with a poorer prognosis.
|
|
|
What percent of pediatric head injuries are from nonaccidental trauma?
|
Nonaccidental trauma accounts for at least 80% of deaths from head trauma in children younger than 2 years of age. It is important to consider the possibility of child abuse and to recognize the characteristic features of these suspected cases.
|
|
|
What is the second most common skeletal injury in cases of child abuse?
|
Skull fractures represent the second most common skeletal injury in child abuse (the most common is long bone fracture).
|
|
|
What is the most common intracranial manifestation of child abuse?
|
Subdural hematomas are the most commonly recognized intracranial complication from child abuse. Epidural hematomas are not frequently seen in child abuse.
|
|
|
What do subdural hematomas from child abuse tend to look like on CT?
|
Subdural hematomas in child abuse often are found in the posterior interhemispheric fissure. These are seen on CT as hyperdense collections with a flat medial border along the falx and an irregular convex lateral border. Subdural hematomas may also be found along the convexity, over the tentorial surface, at the skull base, or in the posterior fossa.
|
|
|
Describe BESSI:
|
Occasionally, low-density extra-axial fluid collections are seen in infants without any clear precipitating trauma or infection. These most often represent dilated CSF spaces, known as “benign enlargement of the subarachnoid space of infancy,” but can mimic chronic subdural hematomas. They occur in neurologically intact infants 3 to 6 months of age who present with enlarging head circumference. In this setting, they require no treatment and usually regress by age 2.
|
|
|
What are low-density extra-axial fluid collections seen in infants without any clear precipitating trauma or infection called?
|
“benign enlargement of the subarachnoid space of infancy” or BESSI
|
|
|
Why do children tend to get diffuse cerebral swelling?
|
The initial swelling is believed to be caused by vasodilation associated with loss of autoregulation. At this stage, the injury may be reversible, despite dramatic findings on CT.
|
|
|
What does diffuse cerebral swelling from child abuse look like on CT?
|
CT scans show global effacement of the subarachnoid space and compressed ventricles. As the brain becomes edematous, the normal attenuation of gray and white matter may appear indistinguishable or even reversed. The cerebral hemispheres will demonstrate diffusely decreased attenuation. The brainstem, cerebellum, and possibly deep gray matter structures may be spared.
|
|
|
Why is it thought that children are lesss likely to get cortical contusions?
|
Cortical contusions occur but are considered less common, possibly because the inner surface of the skull is relatively smooth in children.
|
|
|
What is an intracranial injury specific to infants?
|
In infants, head trauma may lead to tears at the gray–white junction, especially in the frontal and temporal lobes.
|
|
|
What are some chronic sequelae of head injury in kids?
|
Chronic sequelae of head injury in children include chronic subdural collections (which may occasionally calcify), global cerebral atrophy, and encephalomalacia.
|
|
|
Why are facial bones hard to see on MR?
|
The facial bones are difficult to visualize on MR scanning because they and the adjacent aerated sinuses are relatively void of signal.
|
|
|
What is the best way to evaluate trauma to the temporomandibular joint?
|
MR
|
|
|
What does orbital emphysema suggest?
|
-Orbital emphysema is most commonly caused by fracture of the thin medial orbital wall.
-Orbital floor blowout fractures can also cause orbital emphysema. |
|
|
What is a plain film finding of intracranial midline shift?
|
Rarely, a shift of pineal calcification can be detected, indicating the presence of intracranial mass effect.
|
|
|
What is a potentially serious injury to the nasal bones? What are the possible complications?
|
One potentially serious injury that can be suggested on plain films or CT is a septal hematoma. Trauma to the septal cartilage may lead to hematoma formation between the perichondrium and cartilage, which can cause cartilage necrosis by disrupting the vascular supply. An organized hematoma can also cause difficulty in breathing and may predispose to septal abscess formation.
|
|
|
What is a "blow-in" fracture?
|
Rarely, fragments from an orbital floor fracture buckle upward into the orbit, an injury referred to as a “blow-in” fracture.
|
|
|
What bone is always involved in a LeFort fracture?
|
All involve the pterygoid plates
|
|
|
How do you deal with LeFort fractures that aren't bilaterally symmetric?
|
The three Le Fort fractures initially described are bilateral processes. Frequently, similar patterns of injury are seen on one side only and are known as “hemi–Le Forts.” Combinations also occur, such as a Le Fort I pattern on one side and a Le Fort II pattern on the other.
|
|
|
Describe a LeFort I fracture:
|
-Le Fort I or “floating palate” fracture is a horizontal fracture through the maxillary sinuses.
-It extends through the nasal septum and walls of the maxillary sinuses into the inferior aspect of the pterygoid plates. -The fracture plane is parallel to the plane of axial CT images but is recognized by the fracture of all walls of both maxillary sinuses. -The Le Fort I fracture is more often seen in the pure form than either the Le Fort II or Le Fort III fractures. |
|
|
Describe a LeFort II fracture:
What injuries are associated with a LeFort II fracture? |
Le Fort II or “pyramidal” fracture describes a fracture through the medial orbital and lateral maxillary walls. It begins at the bridge of the nose and extends in a pyramidal fashion through the nasal septum; frontal process of the maxilla; medial wall of the orbit; inferior orbital rim; superior, lateral, and posterior walls of the maxillary antrum; and midportion of the pterygoid plates. The zygomatic arch and lateral orbital walls are left intact. The Le Fort II is usually associated with posterior displacement of the facial bones, resulting in a “dish-face” deformity and malocclusion. The infraorbital nerve is frequently injured.
|
|
|
Describe a LeFort III fracture:
|
Le Fort III fracture, or “craniofacial dysjunction,” is a horizontally oriented fracture through the orbits. It begins near the nasofrontal suture and extends posteriorly to involve the nasal septum, medial and lateral orbital walls, zygomatic arch, and base (superior aspect) of the pterygoid plates. Patients with a Le Fort III fracture also have dish-face deformity and malocclusion. Injury to the infraorbital nerve is less commonly seen with Le Fort III than with Le Fort II fractures.
|
|
|
What is a feature of a LeFort III fracture seen on plain films?
|
A recognizable feature on plain films is the elongated appearance of the orbits on Waters and Caldwell views.
|
|
|
What is a nasoethmoidal complex injury?
|
Nasoethmoidal complex injuries describe the constellation of findings seen as a result of a blow to the midface between the eyes. This term encompasses a wide variety of different fracture complexes that are best described by listing the specific fractures seen on CT scans. These injuries may include fractures of the lamina papyracea; inferior, medial, and supraorbital rims; frontal or ethmoid sinuses; orbital roofs; nasal bone and frontal process of the maxilla; and sphenoid bone.
|
|
|
What is a feature of a nasoethmoidal complex injury seen on plain films?
|
Nasoethmoidal fractures can be suspected on plain films when the lateral view shows posterior displacement of nasion.
|
|
|
Describe simple and compound fractures of the mandible:
|
-Simple fractures are most common in the ramus and condyle and do not communicate externally or with the mouth.
-Compound fractures are those that communicate internally through a tooth socket or externally through a laceration. |
|
|
Which mandibular fractures tend to be compound?
|
Fractures of the body of the mandible are almost always compound fractures.
|
|
|
What is a plain film feature of a subcondylar mandibular fracture?
|
Subcondylar fractures may be recognized on plain films by the “cortical ring” sign, a well-corticated density seen above the condylar neck on lateral views because of the horizontal axis of the fragment.
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
|
|
?
|
