INTRODUCTION — Skull fractures have plagued humankind throughout history . They occur when forces striking the head exceed the mechanical integrity of the calvarium. Significant skull fractures are often accompanied by moderate or severe intracranial injury and extracranial injuries associated with high-energy trauma, such as cervical and other spine fractures and thoracoabdominal injuries [2-9].
The epidemiology, mechanisms, clinical presentation, associated complications, and initial management of skull fractures in adults are reviewed here. Skull fractures in children and intracranial injuries are discussed separately. (See "Skull fractures in children: Clinical manifestations, diagnosis, and management" and "Intracranial epidural hematoma in adults" and "Subdural hematoma in adults: Etiology, clinical features, and diagnosis" and "Nonaneurysmal subarachnoid hemorrhage" and "Acute mild traumatic brain injury (concussion) in adults".)
EPIDEMIOLOGY — The incidence of skull fractures among head injured adults who present to emergency departments (ED) is unknown. The parietal bone is most frequently fractured, followed by the temporal, occipital, and frontal bones . Linear fractures are the most common, followed by depressed and basilar skull fractures. (See 'Definition and presentation of skull fracture types' below.)
Much of the data on skull fractures in adults come from studies of traumatic brain injury (TBI). Each year, approximately 2.8 million people sustain head injuries in the United States alone, resulting in approximately 2.5 million emergency evaluations, 300,000 hospital admissions, and 60,000 deaths .
According to one retrospective study of 207 head-injured patients, 37 percent of those with associated intracranial pathology sustained a linear skull fracture . According to another retrospective study of 2254 cases of head trauma from assault, approximately one-third sustained a skull fracture .
The most common causes of head injury in adults include:
●Motor vehicle collisions
Although skull fractures themselves may or may not indicate the presence of significant TBI, certain skull fracture types, such as depressed skull fractures, basilar skull fractures with associated cerebral spinal fluid (CSF) leak, and fractures of the temporal-parietal bone that traverse the middle meningeal artery and vein, are associated with significant morbidity and mortality [2-5,8,14,15].
ANATOMY AND MECHANISM OF INJURY — The skull is made up of the frontal, ethmoid, sphenoid, and occipital bones, two parietal bones, and two temporal bones (figure 1 and figure 2 and figure 3). The unique layered architecture of these bones enhances the skull's strength. Each bone consists of solid inner and outer layers, separated by a layer of cancellous bone (the diploë). In adults, the bones of the skull average between 2 and 6 mm in thickness; the bones in the temporal region are usually the thinnest and therefore at the greatest risk of fracture [16,17].
Patients who sustain a fracture of the temporal bone are at high risk for extra-axial hematoma (ie, bleeding beneath the skull but outside the brain parenchyma). This is due to the temporal bone's relative weakness and the proximity of the middle meningeal artery and vein. (See "Intracranial epidural hematoma in adults" and "Subdural hematoma in adults: Etiology, clinical features, and diagnosis".)
Fractures involving the frontal sinus are also considered high risk; they are frequently associated with contusions to the anterior portion of the frontal lobes and with dural tears. The thin cribriform plate is often shattered. Other high risk fractures include those over the transverse or sagittal sinus, due to the increased risk of major bleeding, and basilar skull fractures resulting in cerebral spinal fluid (CSF) otorrhea or rhinorrhea. (See 'Basilar skull fracture' below.)
Skull fractures occur from direct trauma to the head . The amount and dispersion of the kinetic energy involved primarily determine whether a skull fracture is linear or depressed. The smaller the area receiving the blow and the greater the energy delivered, the more likely that a depressed fracture will result.
PREHOSPITAL MANAGEMENT — The priorities of prehospital trauma management remain unchanged in patients with skull fractures. Prehospital personnel should assume a skull fracture exists in any patient who has sustained a significant head injury or other major trauma. High kinetic energy is needed to cause a skull fracture. Therefore, maintaining immobilization of the cervical and thoracic spine is of great importance.
Open or closed skull fractures can be associated with large scalp lacerations with profuse bleeding that can be difficult to control. Initial management consists of steady direct pressure at the source of bleeding. A dressing held in place by a circumferential head bandage is often NOT sufficient.
INITIAL EVALUATION — The initial assessment of any trauma patient is focused on the rapid identification and stabilization of life-threatening injuries. Patients with major head trauma may require airway protection. Bleeding from wounds associated with skull fractures can be profuse. Direct pressure (for approximately 15 minutes) is the initial treatment. Occasionally, large scalp lacerations require the placement of Raney Clips, which compress the small blood vessels feeding the lacerated portion of the scalp, thereby preventing bleeding (picture 1). Alternatively, large sutures may be placed in the scalp to control bleeding. Commercial hemostatic agents are becoming more widely available (see "Fibrin sealants"). The assessment and management of scalp lacerations is discussed in greater detail separately. (See "Assessment and management of scalp lacerations".)
After the primary trauma survey is performed and life-threatening issues are addressed, the emergency physician or trauma surgeon performs a secondary survey that may reveal findings suggestive of a skull fracture or intracranial injury. Such findings may include depressed mental status, focal cranial nerve or other neurologic deficits, scalp lacerations or contusions, bony step-off of the skull, or periorbital or retroauricular ecchymosis. Scalp wounds should NOT be probed. When examining potential skull fracture sites, the clinician should take care to avoid injury from bone edges or fragments. (See 'Definition and presentation of skull fracture types' below.)
The blunt force required to cause a skull fracture is substantial. Therefore, it is essential to rule out underlying traumatic brain injury. The emergency department work-up of patients with suspected skull fractures, or deemed to be at significant risk for intracranial injury based upon clinical assessment, is primarily radiographic. Clinical assessment of the patient with a minor head injury, including decision rules for imaging, is discussed separately. (See "Acute mild traumatic brain injury (concussion) in adults".)
DIAGNOSTIC IMAGING — Noncontrast computed tomography (CT) scan (including bone windows) is the imaging modality of choice for patients with a suspected skull fracture (image 1). Although research on the subject is scant, multidetector computed tomography (MDCT) using thin slices and three dimensional reconstructions appears to enable identification of virtually all clinically significant skull fractures. Tissue windows simultaneously allow for the identification of parenchymal injury (eg, cerebral contusion) as well as other forms of intracranial hemorrhage (eg, subdural hematoma).
Little evidence exists to guide the use of CT angiography or other types of angiography in the setting of skull fracture. If MDCT reveals findings suggestive of a basilar skull fracture involving the petrous portion of the temporal bone, it is reasonable to obtain CT angiography to assess for vascular injury . In one observational study, 13 of 71 patients with a basilar skull fracture sustained a cerebrovascular injury identified by angiography . Improvements in CT angiography have increased detection of vascular injury among patients with basilar skull fracture . It is generally best to discuss the need for angiography with a radiologist to determine the best approach.
Magnetic resonance imaging (MRI) is useful when vascular or ligamentous injury is suspected, but should be considered an ancillary study to CT.
Neuroimaging is required to establish the diagnosis of a cranial cerebrospinal fluid (CSF) leak for patients presenting with rhinorrhea or otorrhea when CSF is not identified on initial testing and for all patients who present with isolated neurologic symptoms suggestive of a cranial CSF leak, and is discussed in detail separately. (See "Cranial cerebrospinal fluid leaks", section on 'Neuroimaging'.)
Skull radiographs are of no benefit if a CT scan is to be performed. If CT is unavailable, skull radiographs using two views should be performed (image 2). However, fractures, especially depressed skull fractures, may be difficult to see on plain radiographs. Tangential views of the skull may improve detection. A CT should be obtained if plain radiographs reveal a skull fracture, in order to determine the presence of an intracranial hemorrhage. Although negative plain radiographs in a low risk clinical setting (eg, minor mechanism, normal neurologic examination) are reassuring, they cannot rule out intracranial injury.
Between 5 to 15 percent of patients with skull fractures also sustain cervical spine fractures [5,22]. A careful assessment for spinal and other concurrent injuries is essential. The circumstances of the injury and the patient's history and clinical presentation provide the basis for further diagnostic work-up. A toxicologic screen may be useful to assist in the assessment of a patient with altered mental status. (See "Cervical spinal column injuries in adults: Evaluation and initial management".)
DEFINITION AND PRESENTATION OF SKULL FRACTURE TYPES — Skull fractures can be categorized as linear, depressed, or basilar. In open skull fractures, lacerations of the scalp allow direct contact between the environment and the brain parenchyma, thereby increasing the risk of infection. In closed skull fractures, intact scalp tissue provides an effective barrier between the environment and the skull and brain tissue.
Linear skull fracture — A linear skull fracture is a single fracture that most often extends through the entire thickness of the calvarium (image 1). They occur most often in the temporoparietal, frontal, and occipital regions.
The great majority of linear skull fractures have minimal or no clinical significance. However, fractures that cross the middle meningeal groove in the temporal bone or major venous dural sinuses may disturb these vascular structures causing significant extra axial bleeding (ie, bleeding beneath the skull but outside the brain parenchyma). Separation (ie, diastasis) of skull sutures can occur following trauma and most often involves the coronal or lambdoid sutures.
Adults with simple, closed linear skull fractures usually present without neurologic symptoms. On examination, they may have swelling overlying the fracture site. The minority of patients who develop significant intracranial hemorrhage can present with depressed mental status, headache, vomiting, cranial nerve deficits, or other findings.
Depressed skull fracture — Depressed skull fractures occur when trauma of significant force drives a segment of the skull below the level of the adjacent skull (image 3 and image 4). These fractures often involve injury to the brain parenchyma and place patients at significant risk for central nervous system infection, seizures, and death if not identified early and managed appropriately [23-27]. Mortality appears to be high among patients with depressed fractures who present with a significant decline in mental status . No large prospective epidemiological studies exist to determine the incidence of depressed skull fractures. Of 1075 patients evaluated for head trauma at one major trauma center, 63 were noted to have a depressed skull fracture sustained through a nonpenetrating mechanism .
Depressed skull fractures may be closed or open. Closed (or simple) depressed fractures exist when no scalp laceration is present over or adjacent to the fracture. Open (or compound) depressed skull fractures exist when a scalp laceration lies over or adjacent to the fracture site. The majority of depressed skull fractures are open, and clinicians should assume that any depressed skull fracture is open until it is proven otherwise [23,24].
The degree of underlying brain injury determines the clinical presentation of patients with depressed skull fractures. About 25 percent of patients sustain at least a brief loss of consciousness . Wounds that may be associated with a depressed skull fracture should be inspected, and the external region around such wounds may be carefully palpated (although the usefulness of palpation is often limited due to swelling). However, the wound itself should NOT be blindly probed.
The force necessary to create a depressed skull fracture is significant and results from direct trauma from an object, such as a bat or club onto a small area [10,26,27,31,32]. Such mechanisms of injury can dislodge bone fragments or result in a portion of the skull becoming lodged beneath another segment. Bone fragments and the edges of depressed skull segments can easily lacerate the adjacent dura mater, creating a portal of entry into the cerebral spinal fluid (CSF), thereby increasing the risk of central nervous system (CNS) infection.
Basilar skull fracture — Basilar skull fractures involve at least one of the five bones that comprise the base of the skull: cribriform plate of the ethmoid bone, orbital plate of the frontal bone, petrous and squamous portion of the temporal bone, and the sphenoid and occipital bones . Basilar skull fractures occur most commonly through the temporal bone and thus, are at high risk for extra-axial hematomas, particularly epidural hematomas (image 5 and image 6). This is due to the temporal bone's relative weakness and the proximity of the middle meningeal artery and vein.
Clinical signs can often be used to diagnose basilar skull fractures and include the following:
●"Raccoon eyes" is a common term for periorbital ecchymosis, which suggests a basilar skull fracture or anterior or middle fossa facial trauma (picture 3). Like Battle sign, raccoon eyes are typically not present during the examination immediately following the injury but appear one to three days later.
●Clear rhinorrhea or otorrhea is found in up to 20 percent of temporal bone fractures. Such leaks may be detected within hours or up to several days after trauma.
●Hemotympanum is blood behind the tympanic membrane. It is a common finding in basilar skull fractures that involve the petrous ridge of the temporal bone and generally appears within hours of injury . Hemotympanum is detected by otoscopy, which reveals the blue to purple hue taken on by the tympanic membrane (picture 4).
The degree of underlying brain tissue and cranial nerve injury determines the neurologic presentation. Patients often develop nausea and vomiting due to the proximity of the brainstem centers involved in stimulating nausea and managing vestibular function. Oculomotor deficits from injuries to cranial nerves III, IV, or VI can occur, as may facial nerve palsies or hearing loss from injury to cranial nerves VII and VIII, respectively.
According to research performed to validate the Canadian Head CT rule, the signs of basilar skull fracture (ie, Battle sign, raccoon eyes, hemotympanum, otorrhea/rhinorrhea) are collectively highly predictive of a clinically important head injury . Smaller observational studies confirm the high predictive value of these findings [35,36].
Basilar skull fractures can cause a dural tear, creating a communication between the subarachnoid space, the paranasal sinuses, and the middle ear. CSF leaks develop in approximately 11 to 45 percent of basilar skull fractures according to retrospective studies [32,37,38]. These leaks can develop within one or up to several days following injury and may manifest as otorrhea or rhinorrhea, which are considered pathognomonic for a basilar skull fracture. Most traumatic CSF leaks resolve spontaneously within seven days, but in rare instances, they can persist for as long as several months. (See "Cranial cerebrospinal fluid leaks", section on 'Craniofacial trauma'.)
There are reports of tympanic membrane perforation in association with temporal and basilar skull fractures . Direct bleeding from the ear may occur in this situation. Any patient who is assessed to be at high risk for a temporal bone or basilar skull fracture and has bleeding from his ear should undergo a computed tomography (CT) scan of the head with thin cuts in the region of the temporal and basilar skull.
A rare but significant complication of a basilar skull fracture is traumatic carotid cavernous fistula (TCCF). According to a retrospective review, the overall incidence of TCCF in basilar skull fractures is 3.8 percent, with middle fossa basilar skull fractures having the highest association . Other examples of uncommon injuries sustained by the carotid artery that may occur following basilar skull fractures, particularly those involving the carotid canal, include thrombosis and dissection [41,42].
Elevated skull fracture — An elevated skull fracture is present when the fracture fragment is elevated above the underlying calvarium . These uncommon fractures most often affect the frontal skull and involve an impact that is tangential rather than perpendicular. Elevated skull fractures are often associated with significant intracranial injury, although the literature is limited.
Penetrating skull fracture — Penetrating injuries of the skull occur as a result of gunshot wounds, stab wounds, and blast injuries. They generally involve significant brain injury and intracranial hemorrhage. Emergency neurosurgical consultation is needed to determine management.
Tangential skull fractures warrant special mention. They are caused by an impact that occurs at an oblique angle to the skull. In one study, 24 percent of patients with tangential gunshot wounds (GSW) to the head sustained intracranial hemorrhage, while 16 percent had skull fractures . Any patient with a tangential GSW to the scalp should undergo CT scanning of the head because of this high association with intracranial injuries.
MANAGEMENT OF SPECIFIC INJURIES
Linear fractures — No specific intervention is necessary for linear skull fractures if a noncontrast computed tomography (CT) scan reveals no underlying brain injury or depressed fractures. Emergency neurosurgical consultation is obtained for patients with intracranial hemorrhage (ICH) associated with a linear skull fracture.
Patients are admitted for observation if there is any suspicion or clinical evidence of brain injury. The goal of observation is to detect any worsening of neurologic function as a delayed complication of ICH. Such findings usually appear within 24 hours of injury. Patients with linear skull fractures and evidence of ICH on CT should be observed in facilities with neurosurgery.
Patients with linear skull fractures but no evidence on CT of ICH should be observed in the emergency department (ED) for four to six hours prior to discharge to detect delayed complications of trauma . If the patient is neurologically intact and there are no significant extracranial injuries, the patient may then be discharged, provided there is adequate supervision at home for the subsequent 24 hours. Clear discharge instructions must be provided, including instructions to return to the ED immediately should symptoms suggestive of intracranial injury (eg, headache, vomiting, lethargy) develop.
Adult patients with simple linear skull fractures do not require long term follow-up unless they also demonstrate concussive symptoms or other evidence of mild traumatic brain injury. (See "Acute mild traumatic brain injury (concussion) in adults".)
Depressed fractures — Patients with depressed skull fractures are at increased risk of infection and seizures, and prophylactic measures are recommended :
●Tetanus status should be determined if possible and prophylaxis given as appropriate. (See "Tetanus-diphtheria toxoid vaccination in adults", section on 'Immunization for patients with injuries'.)
●We suggest that prophylactic antibiotics be given for five to seven days to prevent the risk of subsequent central nervous system (CNS) infection, although data supporting this approach is scant . Suggested antibiotics are identical to those for penetrating head trauma. (See 'Penetrating injuries' below.)
●Anticonvulsants are often given to reduce the risk of seizures, despite a dearth of supporting evidence [10,30]. The initiation of such therapy and drug selection should be performed in consultation with a neurosurgeon or neurologist. (See "Posttraumatic seizures and epilepsy".)
Patients with depressed skull fractures are admitted to neurosurgery, and this service should be consulted as soon as the injury is recognized.
The Brain Trauma Foundation suggests that open skull fractures depressed more than the thickness of the cranium be treated with elevation in the operating room; many neurosurgeons elect to elevate any fracture depressed greater than 5 mm below the adjacent inner table . Emergency elevation is generally recommended if there is a dural tear, pneumocephalus, an underlying hematoma, or a grossly contaminated wound . Most skull fractures that are depressed more than 1 cm are managed with early surgery to reduce the risk of infection .
Nevertheless, open, depressed skull fractures without evidence of dural penetration or significant complications (eg, intracranial hematoma, severe wound contamination, frontal sinus involvement) on CT may be managed nonoperatively . Uncomplicated, closed, depressed skull fractures may also be managed nonoperatively.
Basilar fractures — Intracranial hemorrhage caused by a basilar skull fracture frequently represents a surgical emergency and requires immediate neurosurgical consultation. All patients with basilar skull fractures require admission for observation, regardless of the need for surgical intervention. Clinicians should be suspicious of an epidural hematoma in patients with a temporal bone basilar skull fracture, and close neurologic monitoring is required. An emergency non-contrast CT scan of the head should be obtained for any noticeable change in mental status.
Basilar skull fractures can produce a dural tear, which can cause a cerebral spinal fluid (CSF) leak. Clinically, this is suggested by the presence of clear or blood-tinged rhinorrhea or otorrhea in a head-injured patient. (See "Cranial cerebrospinal fluid leaks", section on 'Clinical presentation'.)
CSF can be distinguished from local nasal secretions more accurately by the presence of CSF-specific proteins (eg, beta-trace protein, beta-2 transferrin). For patients with rhinorrhea or otorrhea, a CSF leak may be diagnosed when CSF proteins are found by analysis of a collected sample of watery discharge, but these laboratory techniques may be limited in many hospitals . Assessing rhinorrhea or otorrhea for the presence of CSF is discussed in detail separately. (See "Cranial cerebrospinal fluid leaks", section on 'Assess for presence of CSF in patients with rhinorrhea or otorrhea'.)
If the fluid is blood tinged, the "halo" sign (also called the "ring" or "target" sign) may be useful to determine the presence of CSF. To perform the test, a drop of the fluid is placed on a tissue or filter paper. A rapidly expanding ring of clear fluid around red blood defines a positive test. Of note, the halo test does not differentiate among CSF, saline, saliva, and other clear fluids; and is discussed in detail separately. (See "Cranial cerebrospinal fluid leaks", section on 'Patients with bloody discharge'.)
The majority of CSF leaks resolve spontaneously within one week of injury and without CNS complications [49,50]. We generally do not give prophylactic antibiotics initially for basilar skull fractures. In some cases, prophylaxis may be indicated, but this is best determined in consultation with the neurosurgeon and infectious disease specialist. The evidence against routine prophylactic antibiotic use is presented separately. (See "Cranial cerebrospinal fluid leaks", section on 'Initial conservative measures for other patients'.)
The incidence of bacterial meningitis rises substantially if a leak persists past seven days [50-52]. In such cases, we suggest immediate consultation with neurosurgery to determine the need for expedited repair of the leak. Further, consultation with infectious disease is prudent to determine whether treatment with antibiotics is warranted. When necessary, antibiotic selection is identical to that for penetrating head trauma. Patients with a CSF leak may also require pneumococcal vaccination . (See 'Penetrating injuries' below and "Cranial cerebrospinal fluid leaks", section on 'Meningitis' and "Pneumococcal vaccination in adults".)
Cranial nerve palsies are a delayed complication of basilar skull fractures. They generally present two to three days following injury and are due to nerve compression or contusion [53,54]. These palsies may respond to treatment with glucocorticoids, although no large clinical trials have been performed to support this approach. Common treatment regimens are similar to those used for nontraumatic palsies (eg, Bell's palsy). We suggest starting such treatment in consultation with otolaryngology or neurosurgery. (See "Bell's palsy: Pathogenesis, clinical features, and diagnosis in adults".)
Facial nerve palsies that appear acutely in association with basilar skull fractures are due to nerve transections. These injuries do NOT respond to glucocorticoid therapy and carry a poor prognosis for recovery of nerve function .
Elevated skull fractures — Elevated skull fractures may be associated with significant intracranial injuries . Often, the fragment must be freed from the surrounding tissue and repositioned. Grossly contaminated fragments should be removed, intravenous antibiotics given, and surgical consultation obtained.
Anticoagulated patients — Observational studies of patients taking anticoagulants (eg, warfarin, clopidogrel) who sustain minor head trauma without a skull fracture suggest such patients are at high risk of intracranial hemorrhage (ICH) and that signs of neurologic deterioration may not appear for up to six hours following injury [55-57]. Therefore, patients taking anticoagulants and who sustain head trauma of sufficient force to cause a skull fracture, particularly a basilar skull fracture, are at even greater risk for ICH. Such risk may be greatest among elderly patients [58-60]. (See "Risks and prevention of bleeding with oral anticoagulants".)
We suggest that all patients who are anticoagulated and have sustained a skull fracture be admitted to a facility with neurosurgery for a minimum of 24 hours of observation. Patients should be admitted to a hospital unit capable of performing hourly neurologic reassessments for a minimum of six hours. Thereafter, neurologic reassessment can be performed every two to four hours for the remainder of the observation period. An emergency head CT should be obtained if any sign of neurologic deterioration develops [61,62]. Reversal of excess anticoagulation from warfarin or newer anticoagulants (direct oral anticoagulants) is discussed separately. (See "Management of warfarin-associated bleeding or supratherapeutic INR" and "Management of bleeding in patients receiving direct oral anticoagulants".)
Patients at greater risk of bleeding from causes other than anticoagulants also require extreme caution and are managed in a similar fashion. The management of patients with hemophilia who have sustained head trauma is discussed separately. (See "Treatment of bleeding and perioperative management in hemophilia A and B", section on 'Serious, life-threatening bleeding and head trauma'.)
Penetrating injuries — Skull fractures sustained from penetrating trauma are considered open and patients are treated with intravenous antibiotics. Recommended antibiotics vary by the clinical setting and patient characteristics; they are summarized in the accompanying table (table 1 and table 2) and discussed in greater detail separately. (See "Treatment of bacterial meningitis caused by specific pathogens in adults".)
Immediate neurosurgical consultation is needed for all patients with potentially survivable injuries.
OUTCOMES — No large randomized trials looking at the management of isolated skull fractures have been performed. Outcome generally depends upon the severity of the underlying brain injury. (See "Intracranial epidural hematoma in adults" and "Subdural hematoma in adults: Etiology, clinical features, and diagnosis" and "Nonaneurysmal subarachnoid hemorrhage" and "Acute mild traumatic brain injury (concussion) in adults".)
ADDITIONAL INFORMATION — Several UpToDate topics provide additional information about fractures, including the physiology of fracture healing, how to describe radiographs of fractures to consultants, acute and definitive fracture care (including how to make a cast), and the complications associated with fractures. These topics can be accessed using the links below:
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: General issues of trauma management in adults" and "Society guideline links: Fractures of the skull, face, and upper extremity in adults".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: Skull fractures (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Clinical presentation – Clinical findings suggestive of a skull fracture or intracranial injury following trauma include: depressed mental status, focal cranial nerve or other neurologic deficits, scalp lacerations or contusions, bony step-off of the skull, periorbital or retroauricular ecchymosis, headache, and nausea and vomiting. Scalp wounds should NOT be probed. (See 'Initial evaluation' above.)
●Diagnostic imaging – The blunt force required to cause a skull fracture is substantial. Therefore, it is essential to rule out underlying traumatic brain injury. Multidetector computed tomography (MDCT) using thin slices and three dimensional reconstructions enables identification of clinically significant skull fractures and intracranial hemorrhage. (See 'Diagnostic imaging' above.)
●Linear fracture – The great majority of isolated linear skull fractures have no clinical significance. Fractures that cross the middle meningeal groove in the temporal bone or major venous dural sinuses may cause significant extra-axial bleeding. Adults with simple, closed linear skull fractures usually present without neurologic symptoms. (See 'Linear skull fracture' above.)
No specific intervention is necessary for linear skull fractures if a noncontrast computed tomography (CT) scan reveals no underlying brain injury. Such patients can be discharged after four to six hours of observation, assuming the absence of neurologic findings and significant non-cranial injuries, if they are not taking anticoagulants. Emergency neurosurgical consultation is obtained for patients with intracranial hemorrhage (ICH) associated with a linear skull fracture. Patients are admitted for observation if there is any suspicion or clinical evidence of brain injury.
●Depressed fracture – Depressed skull fractures occur when trauma of significant force drives a segment of the skull below the level of the adjacent skull. These fractures often involve injury to the brain parenchyma and place patients at significant risk for central nervous system infection, seizures, and death. The majority of depressed skull fractures are open. (See 'Depressed skull fracture' above.)
Patients with depressed skull fractures are admitted to a neurosurgery service. They should receive tetanus prophylaxis as appropriate. We suggest they also be treated with prophylactic antibiotics for five to seven days (Grade 2C). Suggested antibiotics are identical to those used for penetrating head trauma (see 'Penetrating injuries' above). Anticonvulsants are sometimes given; treatment should be initiated in consultation with neurosurgery.
●Basilar fracture – Basilar skull fractures occur most commonly through the temporal bone and patients with such fractures are at high risk for ICH. Clinical signs commonly used to diagnose basilar skull fractures include retroauricular or mastoid ecchymosis, periorbital ecchymosis, cerebrospinal fluid (CSF) rhinorrhea or otorrhea, and hemotympanum. (See 'Basilar skull fracture' above.)
Emergency neurosurgical consultation should be obtained for any ICH associated with a basilar skull fracture. All patients with basilar skull fractures require admission for observation. Complications may include CSF leak and cranial nerve injury.
●Anticoagulated patients – All patients who are taking anticoagulants and have sustained a skull fracture are at high risk for ICH and should be admitted for observation to a facility with neurosurgery, regardless of the absence of hemorrhage on initial CT imaging. Patients should be admitted to a hospital unit capable of performing hourly neurologic reassessments. (See 'Anticoagulated patients' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Michelle H Biros, MD, who contributed to an earlier version of this topic review.
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