Introduction
Background
The skull is formed by the fusion of several flat bones held together by the cranial sutures. Each of the flat bones consists of a thick outer table, the spongy diploe and a thinner inner table. The inner table is lined by a thick, fibrous, adherent dura mater. A shallow subdural space lies between the inner surface of the dura and the thin arachnoid mater that covers the surface of the brain (see Image 1).
A skull fracture is a break in the skull bone and generally occurs as a result of direct impact. The skull is deformed by localized impact, which may damage the cranial contents even when the skull does not fracture. If the force and deformation is excessive, the skull fractures at or near the site of impact. Uncomplicated skull fractures themselves rarely produce neurologic deficit, but the associated intracranial injury may have serious neurologic sequelae. A fracture indicates that substantial force has been applied to the head and is likely to have damaged the cranial contents.
Skull fractures may occur with no associated neurologic damage, and conversely, fatal injury to membranes, blood vessels, and brain may occur without overlying fracture.
Four major types of skull fractures may occur: (1) linear, (2) depressed, (3) diastatic, and (4) basilar. Linear fractures, the most common, involve a break in the bone but no displacement, and generally no intervention is required. A depressed fracture results when bone fragments are driven inward, with or without a breach in the scalp. Depressed fractures may require surgery to correct the deformity. Diastatic fractures occur along the suture lines and usually affect newborns and infants in whom suture fusion has not yet happened. In this type of fracture, the normal suture lines are widened. Basilar fractures are the most serious and involve a break in the bone at the base of the skull. CSF rhinorrhea and otorrhea are known complications. Patients with a CSF leak may present with a discharge of clear fluid from their nose or ears due to a tear in the dura. These patients usually require close observation in the hospital.
Pathophysiology
Topics discussed in this section are forces and anatomic protection, types of skull fractures, injuries related to skull fractures, and intracranial hemorrhages related to skull fractures.
Forces and anatomic protection
The skull is vulnerable to external trauma. The force required to cause a skull fracture is variable and depends on several factors: the velocity, force, and weight of the instrument of impact; the direction of impact; the thickness of the hair, scalp and skull; and the part of the skull that is struck.
Skull fracture can result from merely walking into a fixed obstruction (which creates a force of 73 N, or 5 ft-lb), striking one's head on a hard surface (which creates a force of 510 N from a 4.5-kg adult head falling 1 m), falling from a standing position (873 N), running into an obstruction (1020 N), or being hit on the temple with an object such as a stone or golf ball.
The consequences of skull fractures may be severe because of intracranial axonal damage. The head is particularly susceptible to acceleration/deceleration and rotational forces because it is heavy in relation to its size; because of its mobility in 3 dimensions; and because it occupies a relatively unstable position, being secured only by the neck muscles and ligaments. The CSF and meningeal coverings surrounding the brain provide some protection against axonal brain injury due to skull fractures. The fascia and muscles of the scalp provide additional cushioning for the brain.
Cantu has shown that 10 times more force is required to fracture a cadaveric skull with overlying scalp than to fracture one without a scalp cover.1 Although these layers play a protective role, meningeal attachments to the interior of the skull may limit the movement of the brain, transmitting shearing forces on the brain. For instance, CSF plays a major role in coup injury (injury directly under the impact) and contrecoup injury (injury to the opposite side of the impact) to the brain. A blow to a stationary but movable head causes acceleration, and the brain floating in CSF lags behind, sustaining a coup injury. When a moving head hits a stationary object such as the floor, sudden deceleration results in a contrecoup injury to the brain.
Types of skull fractures
Types of skull fractures include linear skull fractures, depressed skull fractures, basilar skull fractures, ping-pong skull fractures, birth fractures, and growing skull fractures.
Linear skull fractures
Linear skull fractures are usually the result of low-energy transfer due to blunt trauma over a wide surface area of the skull. The fracture involves the entire thickness of the skull. Generally, these fractures are of little clinical significance unless they involve a vascular channel, a venous sinus groove, or a suture. Thus, complications include epidural hematoma, venous sinus thrombosis, and suture diastasis.
Depressed skull fractures
A high-energy transfer, such as a blow from a baseball bat, may cause a depressed skull fracture. This fracture is usually comminuted, with the bone fragments starting from the point of maximum impact and spreading peripherally. Most depressed fractures involve the frontoparietal region, because the bones in this area are relatively thin and because this part of the head is particularly prone to an assailant's attack.
A fracture is clinically significant and requires elevation when a fragment of bone is depressed deeper than the adjacent inner table. Depressed fractures may be closed or compound (open). Compound fractures may be exposed when they are associated with a skin laceration or when the fracture extends into the paranasal sinuses and the middle-ear structures.
Basilar skull fractures
A basilar fracture is a linear fracture involving the thick base of the skull. This fracture is often associated with dural tears. Most basilar fractures occur at 2 specific anatomic locations — namely, the temporal region and the occipital condylar region.
Temporal fractures are divided into 3 subtypes: longitudinal, transverse, and mixed.2 The longitudinal fracture is the most common subtype (70-90%) and involves the squamous part of the temporal bone, the superior wall of the external auditory canal, and the tegmen tympani. The fracture may run either anterior or posterior to the cochlea and labyrinthine capsule, ending in the middle cranial fossa near the foramen spinosum or in the mastoid air cells. Transverse fractures (5-30%) originate at the foramen magnum and extend through the cochlea and labyrinth, ending in the middle cranial fossa. As the name suggests, mixed fractures have components of both longitudinal and transverse fractures.
Occipital condylar fractures are generally the result of high-energy transfer from blunt trauma with axial compression, lateral bending, or rotational injury to the alar ligament. These fractures can be subdivided into 3 types based on the morphology and mechanism of injury,3 or alternatively, into stable and displaced fractures depending on the presence or absence of ligamentous injury.4 A type I fracture is due to axial compression injury, which results in a comminuted fracture of the occipital condyle. This fracture is stable. A type II fracture is caused by a direct blow, and though it is an extensive fracture of the basioccipital region, it is regarded as a stable injury because of the preserved alar ligament and tectorial membrane. A type III fracture is potentially unstable and regarded as an avulsion injury due to forced rotation and lateral bending.
Ping-pong skull fractures
A ping-pong skull fracture is akin to a greenstick fracture of the long bones in children. It occurs in the first few months of life and is usually caused by a fall when the skull hits the edge of a hard blunt object, such as a table. The skull appears deformed, with a shallow trench on the surface of the skull. The ping-pong skull fracture was first described in a newborn whose head was impinging against the mother's sacral promontory during uterine contractions. The use of forceps also may cause this injury to the skull, but this mechanism is rare.
Birth fractures
Caput succedaneum commonly occurs after vaginal delivery. It is related to a serosanguineous effusion, which appears as a soft-tissue swelling over the presenting part of the skull. Caput succedaneum is a benign process that generally resolves within 2 weeks and usually does not require any form of imaging.
A cephalohematoma may develop after an instrumental delivery and represents a subperiosteal hematoma. In contrast to a caput succedaneum, a cephalohematoma is limited by suture lines. A cephalohematoma may be visible on a plain radiograph as a subperiosteal elevation. Skull fractures may occur as a complication of forceps or vacuum extraction. Most are simple parietal linear fractures, but occasionally, they are more complex or depressed. In some cases, associated extradural hematoma, subdural hematoma, or axonal injury is observed.
Growing skull fractures
In children, most skull fractures heal rapidly, with no long-term sequelae. However, in a small minority of children, a fracture may remain un-united and enlarge to form a growing skull fracture (GSF). In 1816, John Hopkins described an infant with GSF after a head injury. Since then, cases of GSF continue to appear in the literature, with various names such as a leptomeningeal cyst, traumatic meningocele, cerebrocranial erosion, cephalhydrocele, meningocele, and spuria.
GSF is rare and affects 1.2-1.6% of patients with severe head injury, with a vast majority occurring in children younger than 3 years. However, patients of other ages may also be affected, and cases have been described in the perinatal period and in patients in their 60s. Most cases occur after falls, motor vehicle accidents, and child abuse. Cases related to difficult vacuum extraction and corrective surgery for craniosynostosis have also been described.
Most GSFs are located in the calvarium, but rare sites are the basiocciput and the orbital roof. The exact pathophysiology of the GSF remains elusive. Some factors are head injury associated with a large fracture, a dural tear that allows CSF into the fracture (as CSF flow is pulsatile), parenchymal injury beneath the skull with a dural defect, and injury during the period of maximum brain growth. Patients with GSF usually present with a gradually enlarging subgaleal mass, seizures, headache, or focal neurologic deficit. The diagnosis is based on clinical and imaging findings.
Serial conventional radiographs of the skull show evolution of the initial diastatic fracture into a larger defect. Although plain radiographs are sufficient for diagnosis, brain CT better defines the exact pathology. On CT, 3 types of GSFs are described: types I, II, and III. Type I is a GSF with a leptomeningeal cyst, which may be seen herniating through the skull defect into the subgaleal space. Type II is characterized by a damaged lesion or gliotic brain. In type III, a porencephalic cyst can be seen. MRI is preferred to CT for depicting dural tears early after the head injury and allows timely surgical intervention and prevention of growth of the fracture. Cranial Doppler studies have also been used to achieve an early diagnosis.
GSFs are treated surgically to reduce the herniated cerebral tissue and repair the dural laceration or to perform cranioplasty. Occasionally, shunt surgery is performed to decompress the cyst and treat localized dilatation of the ventricles. Early recognition of GSF is crucial to prevent long-term neurologic sequelae. Hence, radiologic and clinical follow-up is essential in cases of head trauma.
Injuries related to skull fractures
Injuries related to skull fractures include scalp injures, axonal injury, general penetrating injuries, missile wounds, stab wounds, and nonaccidental trauma.
Scalp injuries
The scalp is made up of several tissue layers: hairy skin; subcutaneous fat and connective tissue; the galea, which is a thin fibrous layer to which the flat epicranial muscles are attached; a thin layer of connective tissue; and the innermost layer, the periosteum of the bony skull.
The scalp may be injured with or without a breach in its surface. Lacerations are particularly common, as the scalp is readily crushed and split against the underlying bone. Most scalp lacerations are linear because of the convexity of the skull. When injured, the scalp often becomes markedly edematous, and hematoma formation is common above or below the galeal layer.
Axonal injury
Minor jarring of the intracranial contents may cause concussion and a clinical state of transient loss of consciousness due to temporary neuronal dysfunction. Retrograde amnesia is common. With more severe injury, a cerebral contusion may occur; this is classified into 2 types: coup and contrecoup.
Coup-type contusion or laceration of the brain surface often occurs at the site of a fracture, especially if it is depressed. A blow to the head when it is free to move accelerates the head and causes cerebral contusion at the point of impact. At the primary point of impact, a bruise, abrasion, or laceration of the scalp is often present.
Contrecoup-type brain contusions occur when the head strikes a stationary object (eg, when the falling head strikes the ground). The head decelerates abruptly while the intracranial contents continue moving forward to the point of impact. The result is a severe contusion in a region opposite the point of impact. This contrecoup contusion is more severe than the coup contusion. A severe contrecoup force may also cause a laceration on the brain surface. Therefore, a backward fall causes contrecoup contusions at the frontal and temporal poles of the brain, whereas a fall on the side of the head causes contrecoup contusions at the opposite temporal lobe. Generally, a forward fall does not cause contrecoup contusions on the back of the brain because the interior surface of the skull is smooth at this point.
After head trauma head, an underlying scalp injury and a skull fracture are not necessary for intracranial hemorrhage or brain contusion to occur. A rotation and acceleration/deceleration injury causes the brain tissues to glide over each other like a pack of cards and appears to cause axonal injury more widespread than that of a direct impact against the fixed, immobile head. This is the mechanism of extensive but subtle microscopic, diffuse axonal injury that is so common in motor vehicle accidents. Such diffuse axonal microscopic damage is not amenable to surgery. Diffuse axonal injury may be difficult to detect on autopsy, as the surface of the brain or brain sections may not reveal obvious findings.
Diagnosis usually requires expert neuropathologic examination by using special stains to demonstrate the subtle microscopic damage to nerve fibers. Diffuse axonal injury is often associated with edema. Shearing injury is also the cause of arteriolar rupture deep within the white matter of the brain, which in turn causes numerous, small, deep hemorrhages.
General penetrating injuries
The clinical and pathologic consequences of penetrating skull injuries depend on the mechanism and cause of the injury, as well as on the properties of the weapon or missile used, the energy of the impact, and the location and characteristics of the intracranial trajectory. Most primary penetrating injuries are complicated by a secondary neurologic insult. The injury initiates a biochemical cascade, which begins with disruption of the normal cell integrity caused by a mechanical force, producing the release of numerous enzymes, phospholipids, excitatory neurotransmitters, calcium, and free oxygen radicals that propagate further cell damage.
Missile wounds
Missiles can be subdivided into (1) low-velocity bullets, such as those used in air rifles, nail guns, stun guns (used for animal slaughter), handguns, shotguns, and shrapnel, and (2) high-velocity bullets, such as metal-jacket bullets fired from military weapons.
Missiles produce brain injury by causing laceration and crushing, cavitation, and shock waves. The injuries to the skull range from a graze to an entry wound and sometimes an exit hole (penetrating) or a depressed fracture, with results ranging from focal hemorrhage to extensive neuronal damage. Differentiating between penetrating and perforating skull wounds is important because of their different prognostic implications. A poor postsurgical outcome occurs in 50% of patients treated for perforating wounds, as compared with 20% of those with penetrating wounds.
Stab wounds
Penetrating skull stab wounds are uncommon. Stab wounds are caused by knives, nails, spikes, forks, scissors, and other sharp objects. Skull penetration most commonly occurs in the thinnest parts of the skull, such as the orbital surfaces and the squamous portion of the temporal bone. Injury to the brain usually occurs in the path of the penetrating stab wound. Unlike missile injuries, stab wounds have no concentric zone of coagulative necrosis caused by dissipated energy, and unlike motor vehicle accidents, stab wounds cause no diffuse, shearing brain injury.
Stab wounds may cause an intracranial hematoma or infarct. Cerebral damage caused by stabbing is largely restricted to the wound tract. Stab wounds occasionally produce a narrow, elongated defect (a slot fracture); this injury is diagnostic when identified. However, in some cases in which skull penetration is proven, no radiologic abnormality is identified. A stab wound to the temporal fossa is most likely to cause major neurologic injury because of the thinness of the squamous temporal bone and because of the short distance to the brainstem and blood vessels.
The type of skull fracture sustained and the underlying brain injury depends on the variation in skull thickness and on the strength and angle of the impact. A stab wound nearly perpendicular to the skull may cause bone fragments to travel along the same trajectory as that of the penetrating object, it may shatter the skull in an irregular pattern, or it may produce linear fractures that radiate away from the entry site. Tangential stab wounds result in complex single defects, with both internal and external beveling of the skull and varying degrees of neurologic injury.
Nonaccidental trauma
Most fractures in children are a result of falls and bicycle accidents, but skull fractures in infants may originate from neglect, falls, or abuse. Nonaccidental injury or shaken baby syndrome is a major cause of skull fractures and head injury in infants. The classic syndrome is an infant with a mean age of about 6 months who has retinal hemorrhages, subdural hematomas, and absent or minimal signs of external trauma. Because the parents seldom volunteer a history of nonaccidental injury or shaken baby syndrome, this condition is difficult to document and diagnose.
About 25% of all patients with shaken baby syndrome die. Usually, the child is grasped around the chest by using 2 hands and repeatedly shaken with its head moving forward and backward, causing rotational acceleration/deceleration injury. The chief complaints are usually vague and similar to those of many infectious processes. Injuries most often observed in inflicted head trauma are subgaleal hematomas, skull fractures, subarachnoid hemorrhages (SAHs), subdural hematomas, and parenchymal brain injuries.
In an infant, anything but a non-widely spaced simple linear fracture of the parietal bone should be viewed with suspicion and regarded as a nonaccidental injury until proven otherwise. Such fractures include depressed, stellate, comminuted, or other complex skull fractures. Some researchers believe that falls less than 3 ft rarely produce any kind of skull fracture and that skull fractures occur only with extremely violent forces. However, Plunkett demonstrated that simple and complex skull fractures can occur with short falls.5
Greenes and Schutzman showed that skull fractures may be asymptomatic and yet be associated with underlying dural or brain injury.6 Young infants (<6 mo) may have major cranial deformation due to an impact but no skull fracture because their skulls are malleable and elastic, whereas older children have more rigid adultlike ossified skulls and are more vulnerable to skull fractures.
Margulies and Thibault have shown that the fracture threshold for an infant is approximately 10% that of a child or adult.7 A special pattern of bilateral skull fractures can occur when crushing forces are applied against the infant skull. Skull fractures cannot occur without impact of the head against a rigid object. They cannot occur with shaking.
Hobbs retrospectively examined 89 children younger than 2 years with skull fractures: 29 with definite nonaccidental injury serially recorded and 60 who were consecutively admitted to hospital with skull fractures after accidents.8 Twenty deaths occurred, 19 of which were in abused children. Multiple injuries and an inadequate history assisted in diagnosing abuse. Fracture characteristics found considerably more often in the abused children were a multiple or complex configuration; depressed, wide, and GSFs; involvement of more than 1 cranial bone; nonparietal fracture; and associated intracranial injury, including subdural hematoma. No fractures >5.0 mm on presentation were found after accidents, but 6 GSFs were found in abused children.
Accidents usually resulted in single, narrow, linear fractures, most commonly in the parietal bone, with no associated intracranial injury. The results suggest that in young children with skull fracture in whom a minor fall is alleged, it is possible to recognize abuse by considering the fracture alone.
Intracranial hemorrhages related to skull fractures
Fractures may be associated with intracranial hemorrhage and/or axonal injury. The dural and arachnoid membranes and their associated blood vessels are readily torn by the impact and fractured bone fragments. The result can be hemorrhage and accumulation of hematoma acting as an intracranial space-occupying lesion.
Four types of intracranial hemorrhage are described: extradural hemorrhage (EDH), subdural hemorrhage (SDH), SAH, and intracerebral hemorrhage.
Extradural hemorrhage
The temporal bone is usually the thinnest part of the skull. A fracture at this site may tear the middle meningeal artery as it passes upward within a groove between the inner skull table and the dura. A blow to the temporal bone may result in a tear of the temporal artery without a fracture (15%). An arterial bleed from a middle meningeal artery accumulates, forming a hematoma between the inner skull table and stripped dura; this is called an EDH, which acts as a space-occupying lesion. This accumulation can be immediate or delayed.
EDH is easily overlooked, as mild concussion is followed by a lucid interval before neurologic symptoms and coma develop many hours later, when the enlarging hematoma begins to exert pressure on the brain. EDH is amenable to surgical decompression when diagnosed early.
Subdural hemorrhage
SDH is more common than an EDH. SDH is especially common in the elderly, children, and individuals with alcoholism. SDH is not usually associated with skull fractures. SDH may occur after sudden jarring or rotation of the head, a blow to the head, or a fall. Trauma to the head may be trivial. Movement of the brain relative to the dura, often associated with widened CSF spaces, causes shears and tears of the small veins that bridge the gap between the dura and the cortical surface of the brain. Blood from torn vessels accumulates over several hours and usually tracks extensively as a thin film over the surface of the brain. A small, self-limiting SDH may remain asymptomatic and be an incidental finding.
Subarachnoid hemorrhage
SAH hemorrhage may occur as a result of a ruptured intracranial arterial aneurysm or trauma. Traumatic SAH is usually associated with brain contusion or laceration. In rare cases, SAH is due to a direct blow to the side of the neck, which ruptures the vertebral artery as it enters the cranial cavity. This phenomenon is called traumatic basal SAH and is most often due to a blow to the side of the chin or jaw in an alcohol-induced fistfight. The degree of traumatic force required to cause a basal SAH is less than reasonably expected.
Intracerebral hemorrhage
Intracerebral hemorrhage may occur as a result of a ruptured atheromatous intracerebral arteriole, vasculitis, ruptured intracranial arterial aneurysm, or trauma. Traumatic intracerebral hemorrhage is usually due to extension of hemorrhage from surface contusions deep into the substance of the brain. Traumatic intracerebral hemorrhage may also be the result of rupture of small blood vessels deep within the brain due to shearing stress.
Frequency
United States
More than 60% of skull fractures are simple linear fractures, which are the most common variety, especially in children younger than 5 years. The temporal bone of the skull is fractured in 15-48% of all skull fractures, and basilar skull fractures represent 19-21%. Depressed fractures are frontoparietal (75%), temporal (10%), occipital (5%), or in other areas (10%). Most depressed fractures are open fractures (75-90%). The incidence of skull fractures is approximately 1 (0.02%) in 6413 population, or 42,409 people annually.
International
Data from England show that 28,948 (0.227%) of hospital consultant episodes were for fractures of the skull and facial bones in 2002-2003. Of these episodes, 95% required hospital admission.9
Mortality/Morbidity
Mortality from skull fractures is closely linked to the underlying brain injury. The immediate mortality from temporal bone fractures is due to associated brain injury and/or abdominal and thoracic trauma, most commonly blunt trauma. However, mortality may result from delayed complications of fracture, such as meningitis, though this is rare.
- Temporal bone fractures cause significant morbidity from complications, such as facial nerve paralysis, hearing loss, and vertigo. The incidence of facial nerve injury with a transverse fracture is twice that of a longitudinal fracture. Longitudinal fractures are more prevalent than transverse fractures. Facial nerve injury associated with longitudinal fractures is commonly incomplete, may be delayed, and may be the result of displaced fragments. When facial nerve paralysis is due to transverse fracture, paralysis may be immediate and complete.
- Both conductive and sensory hearing loss may be complications of temporal bone fractures. Conductive hearing loss is usually seen with longitudinal fracture and ossicular disruption. Sensory hearing loss is typically seen with transverse fracture and fracture of the vestibulocochlear apparatus.
- Vertigo after temporal bone trauma is often related to injury to the membranous labyrinth and vestibule. This injury may be either direct, with a fracture extending into the vestibular apparatus, or indirect, with the development of a perilymphatic fistula.
- Skull fractures may be associated with intracranial hemorrhage, which may create an intracranial space-occupying lesion.
- Cerebral edema associated with skull fractures is a common and frequently fatal complication of head injury and may develop within minutes or hours of injury. Cerebral edema may accompany diffuse axonal injury or a space-occupying lesion, such as an intracranial hematoma. In children, brain swelling may be the only identifiable feature of head injury. Severe brain edema or a large intracranial hemorrhage may cause downward brain displacement and coning, which is usually fatal.
- Infection from an open fracture may extend deeply, causing meningitis and a brain abscess.
- Posttraumatic epilepsy is a known complication of skull fractures and results from fibrosis of the meninges or gliosis of the underlying brain tissue.
- Evaluating a series of stab wounds, de Villiers reported a mortality rate of 17%, which was mostly related to vascular injury and massive intracerebral hematomas. With stab wounds to the skull, patients in whom a penetrating object is left in place have a mortality rate significantly lower than that of patients in whom the objects are removed (11% vs 26%).
Race
No racial predilection is reported.
Sex
- Men are approximately twice as likely as women to have a head injury. However, with advancing age, the incidence of falls increases and the risk of head injury and skull fractures in men and women equalizes.
- The male-to-female mortality ratio for head injuries is 3.4:1. However, the cause-specific ratio for firearm-related injuries is 6:1, whereas that for injuries related to road traffic accidents is 2.4:1.
Age
In individuals younger than 45 years, head injury is the leading cause of death. The risk of head injury peaks at 15-30 years of age. The risk is highest for individuals aged 15-24 years. Twenty percent of head injuries occur in children.
- Peak ages are similar for males and females.
- The highest mortality rate (32.8 deaths per 100,000 people) is found in those aged 15-24 years. In the United States, the mortality rate in patients 65 years or older is approximately 31.4 deaths per 100,000.
- Head trauma is the most common cause of mortality and morbidity related to physical abuse in infants. Head trauma is associated with intracranial injury in 60% of inflicted-injury deaths. More than one half of all brain injuries in children younger than 1 year are inflicted.
Anatomy
Skull thickness is not uniform, and therefore, the impact of forces required to cause a fracture depends on the site of the impact. The skull is thick at the glabella, the external occipital protuberance, the mastoid processes, and the external angular process. The skull vault is comparatively thinner than the base of the skull. The skull vault is composed of cancellous bone, the diploë, which is sandwiched between the inner and outer tables and consists of the lamina externa (1.5 mm) and the lamina interna (0.5 mm). The diploë does not form where the skull is covered with muscles, leaving the vault thin and prone to fracture.
Skull fractures are more easily sustained at the thin squamous temporal and parietal bones, the sphenoid sinus, the foramen magnum, the petrous temporal ridge, and the inner parts of the sphenoid wings at the skull base. The middle cranial fossa forms the thinnest part of the skull and thus represents the weakest part, which is further weakened by the presence of multiple foramina. Other sites at risk for fracture are the cribriform plate, the roof of orbits in the anterior cranial fossa, and the areas between the mastoid and dural sinuses in the posterior cranial fossa.
Presentation
The patient may be asymptomatic with just a bump on the head. Swelling may occur at the site of impact, and the skin may or may not be breached. Most patients with linear skull fractures are asymptomatic and present without loss of consciousness.
Signs and symptoms of skull fractures
Signs and symptoms of skull fractures include the following:
- Localized tenderness at the fracture site
- Headache
- Bleeding from the wound, ears, and/or nose
- Loss of consciousness
- Confusion
- Convulsions
- Restlessness, irritability
- Drowsiness
- Slurred speech
- Difficulties with balance
- Visual disturbances
- Nausea and vomiting
- Changes in pupil size
- Neck stiffness
Presentations of patients with skull fracture
Longitudinal temporal bone fractures result in ossicular chain disruption and conductive deafness of greater than 30 dB that lasts longer than 6-7 weeks. Temporary deafness generally resolves within 3 weeks and is caused by bleeding and edema in the middle ear. Injury to cranial nerves (CNs) VII, VI, and V cause facial palsy, nystagmus, and facial numbness, respectively. Transverse fractures to the temporal bone involve CN VIII and the labyrinth, resulting in nystagmus, ataxia, and permanent neural hearing loss.
Patients with fractures of the petrous temporal bone present with CSF otorrhea and bruising over the mastoids (ie, Battle sign). Anterior fossa fractures may be associated with CSF rhinorrhea and bruising around the eyes (ie, raccoon eyes).
Occipital condylar fracture is a rare but severe injury. Most patients with occipital condylar fracture, especially a type III fracture, are comatose, and they often have associated cervical spine injuries.
Vernet syndrome (jugular foramen syndrome) is involvement of CNs IX, X, and XI with the fracture. Patients present with difficulty in phonation and aspiration and with ipsilateral motor paralysis of the vocal cord, soft palate (curtain sign), superior pharyngeal constrictor, sternocleidomastoid, and trapezius. Sicard syndrome is occipital condylar fracture with involvement of CNs IX, X, XI, and XII.
Approximately 25% of patients with a depressed skull fracture do not report loss of consciousness, and another 25% lose consciousness for less than an hour. Symptoms depend on the extent of intracranial injury such as epidural hematoma, dural tears, and seizures.
The severity of head injury is assessed by using the Glasgow Coma Scale (GCS). The GCS was developed in 1974 as an assessment tool for patients with altered levels of consciousness. It is easy to use and reproducible when emergency technicians use it in the field. The GCS can also be used to follow-up patients in the hospital for signs of progressive deterioration. Patients who open their eyes spontaneously, obey commands, and are oriented have the maximum score of 15 points. Patients who are flaccid and who do not open their eyes or talk have the minimal score of 3 points. A GCS score of 8 or less is the accepted definition of a comatose patient. Therefore, a GCS score of 8 or less indicates severe head injury; 9-12, moderate head injury; and 13-15, mild head injury. This scale can be adapted for use in infants and young children, forming the basis of the Pediatric Coma Scale.
Bleeding from the ear or nose may obscure CSF leaks. When tapped on a tissue paper, CSF shows a clear ring of wet tissue beyond the bloodstain; this is called the halo, or ring, sign. CSF also can be detected by estimating the patient's glucose level and by measuring the tau-transferrin value.
Preferred Examination
Imaging plays a vital role in the diagnosis and characterization of head injuries. CT is an essential imaging modality in detecting intracranial lesions that require urgent surgical intervention, such as an acute subdural hematoma. Skull fractures are detected on plain radiographs in 5% of patients with mild head injuries, but the detection of a skull fracture on a radiograph is regarded as an indication for CT. Therefore, obtaining a radiograph can only delay the diagnosis of an associated intracranial injury. Because cervical spine trauma may accompany a head injury, radiographs of the cervical spine are indicated for many patients with head injury who have signs, symptoms, or a mechanism of injury that might result in spinal injury, as well as for those patients who are neurologically impaired.
Masters et al developed and prospectively tested a management strategy for the selection of patients who may benefit from skull radiography after head trauma.10 They offered recommendations for selection of patients who should receive CT following head injury. The effect of this study was to shift the focus of imaging of head injury away from skull radiography and toward the recognition of intracranial pathology, as demonstrated by CT.
Skull radiography is useful for imaging of calvarial fractures, penetrating injuries, and radiopaque foreign bodies.
CT is increasingly being used to identify minimal and minor head injury in patients who may benefit from observation; clinical criteria have not proven to be consistently reliable for the identification of those with significant intracranial injury. MRI depicts nonsurgical pathology not visible on CT. In the assessment of complications, CT may be appropriate; however, MRI is useful in identifying vestibular hemorrhage and delayed complications of head injury.
Ultrasonography is a noninvasive technique that may be useful for evaluating GSFs and associated intracranial hemorrhage in infants. In adults, the orbit can also be assessed for soft-tissue injury by using sonograms.
Cerebral angiography may be indicated if a vascular injury is suspected and if the patient is stable, though CT angiography (CTA) or magnetic resonance angiography (MRA) can be used to obtain similar information. CTA can be used for the evaluation of both intracranial and extracranial vessels. The American College of Radiology (ACR) has issued Appropriateness Criteria for imaging in cases of head injury (see Table).
Isotopic bone scans may be useful in children with suspected nonaccidental injury, as the scans may show fractures elsewhere in the body in various stages of healing. CSF rhinorrhea and otorrhea can be detected and localized by using overpressure cisternography with technetium-99m diethylenetriaminepentaacetic acid (DTPA).
Single-photon emission CT (SPECT), positron emission tomography (PET), and transcranial Doppler sonography have complementary roles in the assessment of brain injury.
Head trauma: ACR Appropriateness Criteria Scales*Open table in new window
Table
| Criterion | Skull Radiography | Cervical Spine Radiography | CT | MRI | MR Angiography | Cerebral Angiography |
|---|---|---|---|---|---|---|
| Minor and mild acute closed head injury (GCS score ³ 13, no neurologic deficit | 2 | 2 | 7 | NA | NA | NA |
| Minor or mild acute closed head injury, focal neurology | 2 | No consensus | 9 | 6 | 4 | NA |
| Moderate or severe acute closed head injury, stable | 4 | 8 | 9 | 6 | NA | NA |
| Mild or moderate acute closed head injury, child <2 y | 4 | 6 | 9 | 6 | NA | NA |
| Subacute or chronic head injury, normal CT scans, stable with cognitive and/or neurologic deficit | NA | NA | NA | 8 | 4 | NA |
| Chronic injury, neurologic dysfunction | NA | NA | 6 | 8 | 4 | NA |
| Subacute head injury, late neurologic deterioration | NA | NA | 8 | 8 | NA | NA |
| Chronic head injury, neurologic dysfunction | NA | NA | 6 | 8 | 4 | NA |
| Closed head injury, rule out carotid or vertebral artery dissection | NA | 5 | 4 | 8 (5 for Gd †) | 8 | 6 |
| Penetrating injury, stable, neurologically intact | 8 | 8 | 8 | 6 | 3 | 6 |
| Penetrating injury, with likelihood of injury to vessel | 8 | 8 | 8 | 6 | 8 | 8 |
| Head injury with depressed skull fracture | 8 | 6 | 9 | 6 | NA | NA |
| Penetrating injury: skull-base fracture | 6 | 6 | 9 | 6 | 6 | 4 |
| Head injury with calvarial fracture | 8 | 6 | 9 | 5 | NA | NA |
| Criterion | Skull Radiography | Cervical Spine Radiography | CT | MRI | MR Angiography | Cerebral Angiography |
|---|---|---|---|---|---|---|
| Minor and mild acute closed head injury (GCS score ³ 13, no neurologic deficit | 2 | 2 | 7 | NA | NA | NA |
| Minor or mild acute closed head injury, focal neurology | 2 | No consensus | 9 | 6 | 4 | NA |
| Moderate or severe acute closed head injury, stable | 4 | 8 | 9 | 6 | NA | NA |
| Mild or moderate acute closed head injury, child <2 y | 4 | 6 | 9 | 6 | NA | NA |
| Subacute or chronic head injury, normal CT scans, stable with cognitive and/or neurologic deficit | NA | NA | NA | 8 | 4 | NA |
| Chronic injury, neurologic dysfunction | NA | NA | 6 | 8 | 4 | NA |
| Subacute head injury, late neurologic deterioration | NA | NA | 8 | 8 | NA | NA |
| Chronic head injury, neurologic dysfunction | NA | NA | 6 | 8 | 4 | NA |
| Closed head injury, rule out carotid or vertebral artery dissection | NA | 5 | 4 | 8 (5 for Gd †) | 8 | 6 |
| Penetrating injury, stable, neurologically intact | 8 | 8 | 8 | 6 | 3 | 6 |
| Penetrating injury, with likelihood of injury to vessel | 8 | 8 | 8 | 6 | 8 | 8 |
| Head injury with depressed skull fracture | 8 | 6 | 9 | 6 | NA | NA |
| Penetrating injury: skull-base fracture | 6 | 6 | 9 | 6 | 6 | 4 |
| Head injury with calvarial fracture | 8 | 6 | 9 | 5 | NA | NA |
*Scales are designated 1-9, where 1 = least appropriate and 9 = most appropriate. Scales 1 and 2 have been omitted. NA = not applicable.
† Gd = gadolinium-enhanced MRI.
Limitations of Techniques
Conventional radiographs do not help in assessing intracranial complications associated with skull fractures. In addition, temporal bone fractures may be easily missed.
Temporal bone CT requires additional imaging time and patient cooperation, neither of which may be possible in the immediate posttraumatic period. CT cannot be used to distinguish between CSF and hemorrhage in the middle ear. CT does involve exposure to x-ray radiation, but the benefit of an accurate diagnosis far outweighs the risk. The effective radiation dose from this procedure is about 2 mSv, which is about the same as that which the average person receives from background radiation in 8 months. This dose is equal to the radiation dose of 100 posteroanterior (PA) chest radiographs.
MRI has limited availability in the acute trauma setting, long imaging times, sensitivity to patient motion, incompatibility with various medical and life-support devices, and relative insensitivity to SAH. Other disadvantages include the need for MRI-specific monitoring equipment and ventilators and the risk associated with imaging patients with certain indwelling devices or foreign bodies. Some of these limitations can be overcome by placing the MRI unit close to emergency care areas, with appropriate design and equipment for the management of acutely injured patients. The development of wide-bore magnets, fast imaging protocols, and MRI-compatible resuscitation equipment promise a greater role for MRI in the evaluation of closed head injuries.
Cisternography with99m Tc DTPA may not be immediately available, as this study is expensive and cumbersome. Cerebral angiography is an invasive procedure and generally performed only in patients in stable condition.
Differential Diagnoses
Other Problems to Be Considered
Sutures
Winding, serpiginous lines
Less than 2 mm in width, with same width throughout
Do not run in a straight line
Well-corticated sclerotic margins are symmetrical, with standard anatomic locations
Vascular markings
Engrave the inner table of the skull only
Less translucent than fractures
Ill-defined margins
Meningeal grooves taper as they run peripherally
Symmetrical branching pattern
Diploic venous markings are wide
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Further Reading
Keywords
basilar skull fracture, depressed skull fracture, linear skull fracture, diastatic skull fracture, radiating skull fracture, spider web skull fracture, hinge skull fracture, ring fracture, contrecoup skull fracture, ping pong fracture, growing skull fracture
