Updated: Feb 1, 2008
The brain is surrounded by cerebrospinal fluid (CSF), enclosed in meningeal covering, and protected inside the skull. Furthermore, the fascia and muscles of the scalp provide additional cushioning to the brain. Test results have shown that 10 times more force is required to fracture a cadaveric skull with overlaying scalp than the one without.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.
CSF plays a major role in coup and countercoup injuries to the brain. A blow to a stationary but moveable head causes acceleration, and the brain floating in CSF lags behind, sustaining an injury directly underneath the point of impact (coup injury). When a moving head hits the floor, sudden deceleration results in an injury to the brain on the opposite side (countercoup injury).
Anatomy of fracture
The causative forces and fracture pattern, type, extent, and position are important in assessing the sustained injury. The skull is thickened at the glabella, external occipital protuberance, mastoid processes, and external angular process and is joined by 3 arches on either side. The skull vault is composed of cancellous bone (diploë) sandwiched between 2 tablets, 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.
The skull is prone to fracture at certain anatomic sites that include the thin squamous temporal and parietal bones over the temples and 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 is the weakest, with thin bones and multiple foramina. Other places prone to fracture include the cribriform plate and the roof of orbits in the anterior cranial fossa and the areas between the mastoid and dural sinuses in the posterior cranial fossa.
Skull fracture is described in Edwin Smith's papyrus, the oldest known surgical paper.2 The papyrus describes a conservative and expectant approach to skull trauma, with better results compared with a more aggressive and less favorable approach described in Hippocratic medicine.3
Charles Bell first described occipital condylar fracture in 1817 based on an autopsy finding.4 The same fracture was described for the first time as an x-ray finding in 1962 and by computed tomography (CT) in 1983.5,6
Fractures of the skull can be classified as linear or depressed. Linear fractures are either vault fractures or skull base fractures. Vault fractures and depressed fractures can be either closed or open (clean or dirty/contaminated), as is depicted in Image 1.
Linear fracture results from low-energy blunt trauma over a wide surface area of the skull. It runs through the entire thickness of the bone and, by itself, is of little significance except when it runs through a vascular channel, venous sinus groove, or a suture. In these situations, it may cause epidural hematoma, venous sinus thrombosis and occlusion, and sutural diastasis, respectively. Differences between sutures and fractures are summarized in Table 1.
Table 1. Differences Between Skull Fractures and Sutures
| Fractures | Sutures |
|---|---|
|
|
In essence, a basilar fracture is a linear fracture at the base of the skull. It is usually associated with a dural tear and is found at specific points on the skull base.
Temporal fracture
Temporal bone fracture is encountered in 75% of all skull base fractures. The 3 subtypes of temporal fractures are longitudinal, transverse, and mixed.7 See Images 2 and 3.
Longitudinal fracture occurs in the temporoparietal region and involves the squamous portion of the temporal bone, the superior wall of the external auditory canal, and the tegmen tympani. These fractures 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, respectively. Longitudinal fracture is the most common of the 3 subtypes (70-90%)
Transverse fractures begin at the foramen magnum and extend through the cochlea and labyrinth, ending in the middle cranial fossa (5-30%).
Mixed fractures have elements of both longitudinal and transverse fractures.
Yet another classification system of temporal bone fractures has been proposed. This system divides temporal bone fractures into petrous and nonpetrous fractures; the latter includes fractures that involve mastoid air cells. These fractures do not present with cranial nerve deficits.8
Occipital condylar fracture
Occipital condylar fracture results from a high-energy blunt trauma with axial compression, lateral bending, or rotational injury to the alar ligament. These fractures are subdivided into 3 types based on the morphology and mechanism of injury.9 An alternative classification divides these fractures into displaced and stable, ie, with and without ligamentous injury.10
Type I fracture is secondary to axial compression resulting in comminution of the occipital condyle. This is a stable injury.
Type II fracture results from a direct blow, and, despite being a more extensive basioccipital fracture, type II fracture is classified as stable because of the preserved alar ligament and tectorial membrane.
Type III fracture is an avulsion injury as a result of forced rotation and lateral bending. This is potentially an unstable fracture.
Clivus fractures
Fractures of the clivus are described as a result of high-energy impact sustained in motor vehicle accidents. Longitudinal, transverse, and oblique types have been described in the literature. A longitudinal fracture carries the worst prognosis, especially when it involves the vertebrobasilar system. Cranial nerves VI and VII deficits are usually coined with this fracture type.11
Depressed skull fractures result from a high-energy direct blow to a small surface area of the skull with a blunt object such as a baseball bat. Comminution of fragments starts from the point of maximum impact and spreads centrifugally. Most of the depressed fractures are over the frontoparietal region because the bone is thin and the specific location is prone to an assailant's attack. A free piece of bone should be depressed greater than the adjacent inner table of the skull to be of clinical significance and requiring elevation (see Image 4).
A depressed fracture may be open or closed. Open fractures, by definition, have either a skin laceration over the fracture or the fracture runs through the paranasal sinuses and the middle ear structures, resulting in communication between the external environment and the cranial cavity. Open fractures may be clean or contaminated/dirty.
Simple linear fracture is by far the most common type of fracture, especially in children younger than 5 years. Temporal bone fractures represent 15-48% of all skull fractures. Basilar skull fractures represent 19-21% of all skull fractures. Depressed fractures are frontoparietal (75%), temporal (10%), occipital (5%), and other (10%). Most of the depressed fractures are open fractures (75-90%).
In newborns, "ping-pong" depressed fractures are secondary to the baby's head impinging against the mother's sacral promontory during uterine contractions.12 The use of forceps also may cause injury to the skull, but this is rare.
Skull fractures in infants originate from neglect, fall, or abuse. Most of the fractures seen in children are a result of falls and bicycle accidents. In adults, fractures typically occur from motor vehicle accidents or violence.
Linear skull fracture
Most patients with linear skull fractures are asymptomatic and present without loss of consciousness. Swelling occurs at the site of impact, and the skin may or may not be breached.
Basilar skull fracture
Patients with fractures of the petrous temporal bone present with CSF otorrhea and bruising over the mastoids, ie, Battle sign. Presentation with anterior cranial fossa fractures is with CSF rhinorrhea and bruising around the eyes, ie, "raccoon eyes." Loss of consciousness and Glasgow Coma Score may vary depending on an associated intracranial pathologic condition.
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 that resolves in less than 3 weeks is due to hemotympanum and mucosal edema in the middle ear fossa. Facial palsy, nystagmus, and facial numbness are secondary to involvement of the VII, VI, and V cranial nerves, respectively. Transverse temporal bone fractures involve the VIII cranial nerve and the labyrinth, resulting in nystagmus, ataxia, and permanent neural hearing loss.
Occipital condylar fracture is a very rare and serious injury.13 Most of the patients with occipital condylar fracture, especially with type III, are in a coma and have other associated cervical spinal injuries. These patients also may present with other lower cranial nerve injuries and hemiplegia or quadriplegia
Vernet syndrome or jugular foramen syndrome is involvement of the IX, X, and XI cranial nerves with the fracture. Patients present with difficulty in phonation and aspiration and ipsilateral motor paralysis of the vocal cord, soft palate (curtain sign), superior pharyngeal constrictor, sternocleidomastoid, and trapezius.
Collet-Sicard syndrome is occipital condylar fracture with IX, X, XI, and XII cranial nerve involvement.14,15,16
Depressed skull fracture
Approximately 25% of patients with depressed skull fracture do not report loss of consciousness, and another 25% loose consciousness for less than an hour. The presentation may vary depending on other associated intracranial injuries such as epidural hematoma, dural tears, and seizures.
Adults with simple linear fractures who are neurologically intact do not require any intervention and may even be discharged home safely and asked to return if symptomatic. Infants with simple linear fractures should be admitted for overnight observation regardless of neurological status. Neurologically intact patients with linear basilar fractures also are treated conservatively, without antibiotics. Temporal bone fractures are managed conservatively, at least initially, because tympanic membrane rupture usually heals on its own.
Simple depressed fractures in neurologically intact infants are treated expectantly. These depressed fractures heal well and smooth out with time, without elevation. Seizure medications are recommended if the chance of developing seizures is higher than 20%. Open fractures, if contaminated, may require antibiotics in addition to tetanus toxoid. Sulfisoxazole is a common recommendation.
Types I and II occipital condylar fractures are treated conservatively with neck stabilization, which is achieved with a hard (Philadelphia) collar or halo traction.
The role of surgery is limited in the management of skull fractures. Infants and children with open depressed fractures require surgical intervention. Most surgeons prefer to elevate depressed skull fractures if the depressed segment is more than 5 mm below the inner table of adjacent bone. Indications for immediate elevation are gross contamination, dural tear with pneumocephalus, and an underlying hematoma. At times, craniectomy is performed if the underlying brain is damaged and swollen. In these instances, cranioplasty is required at a later date. Another indication for early surgical intervention is an unstable occipital condylar fracture (type III) that requires atlantoaxial arthrodesis. This can be achieved with inside-outside fixation.17
Delayed surgical intervention is required in ossicular incongruencies resulting from a longitudinal skull base fracture of the temporal bone. Ossiculoplasty may be needed if hearing loss persists for longer than 3 months or if the tympanic membrane has not healed on its own. Another indication is persistent CSF leak after a skull base fracture. This requires precise detection of the site of leak before any surgical intervention is instituted.
Blind probing of skull wounds should be avoided. Patients are prepared for surgery, and exploration is performed in the operating suite under direct vision to prevent loose pieces of bone from damaging the underlying brain. Patients with open contaminated wounds are treated with tetanus toxoid and broad-spectrum antibiotics, especially in a delayed presentation.
Overview
To maintain intracranial pressure, mannitol (1 g/kg) may be given at the beginning, and the PaO2 should be kept at 30-35 mm Hg during the surgery. Patients should be secured firmly to the table, allowing Trendelenburg or reverse Trendelenburg positioning if required. A lazy "S" or a horseshoe-shaped incision is made over the depression. A bicoronal incision is preferred for forehead depressions.
Bony fragments are elevated, and the dura is inspected for any tears. If a dural tear is found, it should be repaired. Special attention is given to hemostasis to prevent postoperative epidural collection. Bony fragments are soaked in antibiotic/isotonic sodium chloride solution and are reassembled. Larger pieces may be wired together. Alternatively, titanium mesh also may be used to cover the defect. Methyl methacrylate can be used instead of the bone pieces, but this should be avoided in children. Indeed, absorbable bone plates and screws are recommended for use in children.
Venous sinus tears
Depressed fracture over a venous sinus poses a unique situation requiring special attention. The decision to operate is based on the neurological status of the patient, the exact location of the sinus involved, and the degree of venous flow compromise. A preoperative angiogram with venous flow phase or magnetic resonance angiography is recommended whenever a depressed fracture is thought to be over a venous sinus. Useful data regarding the position and extent of occlusion and transverse sinus dominance is obtained that can affect decisions regarding surgery.
A neurologically stable patient with a closed depressed fracture over a venous sinus should be observed. A patient with an open depressed fracture over a patent venous sinus who is neurologically stable should undergo skin debridement without elevation of the fracture, but if the patient is neurologically unstable, urgent elevation of the depressed fragment is required. On the other hand, if the patient is neurologically stable and the sinus is thrombosed, it can be assumed that ligation of the sinus can be tolerated.
Usually, the anterior one third of the superior sagittal sinus can be ligated without any consequences; however, tears in the posterior two thirds need repair, either primarily or with a galea or pericranium patch. Alternatively, a piece of muscle or Gelfoam may be sutured over the sinus.
Special surgical techniques are used when a skull fracture communicates with mastoid or frontal air sinuses. The communication of the intracranial space with the outside world needs to be eliminated.18
Other than the usual immediate postoperative care, the risk of intracranial hematoma and venous sinus thrombosis should be kept in mind in contaminated depressed fractures.
Adults with simple linear fractures of the vault, without any loss of consciousness at the time of initial presentation and with no other complications, do not require long-term follow-up. On the other hand, infants with similar fractures with dural tears need to be monitored more closely because of the possibility of the skull fracture expanding.
Patients with contaminated open depressed skull fractures treated surgically should be monitored with repeat CT scans a few times over the next 2-3 months to check for abscess formation. Follow-up also is dictated by the complications associated with skull fractures, for example, seizures, infections, and removal of bone pieces at the time of initial debridement.
Failure to recognize skull fracture has more consequences than the complications resulting from treatment. The chance of a concomitant cervical spine injury is 15%, and this should be kept in mind when assessing a patient with skull fracture.
Linear skull fracture
In infants and children, a simple linear fracture, if associated with a dural tear, can lead to subepicranial hygroma or a growing skull fracture (leptomeningeal cyst). This may take up to 6 months to develop, resulting from the brain pulsating against a dural defect that is larger than the bone defect. Repair of such a defect is performed using a split-thickness bone graft.
A fracture line crossing over a vascular groove, such as the middle meningeal artery, may form an epidural hematoma.19 Similarly, a fracture line that crosses over a suture may cause sutural diastasis.
Basilar skull fracture
The risk of infection is not high, even without routine antibiotics, especially with CSF rhinorrhea. Facial palsy and ossicular chain disruption associated with basilar fractures are discussed in Clinical. However, notably, facial palsy that starts with a 2- to 3-day delay is secondary to neurapraxia of the VII cranial nerve and is responsive to steroids, with a good prognosis. A complete and sudden onset of facial palsy at the time of fracture usually is secondary to nerve transection, with a poor prognosis.
Other cranial nerves also may be involved in basilar fractures. Fracture of the tip of the petrous temporal bone may involve the gasserian ganglion. An isolated VI cranial nerve injury is not a direct result of fracture, but it may be affected secondarily because of tension on the nerve. Lower cranial nerves (IX, X, XI, and XII) may be involved in occipital condylar fractures, as described earlier in Vernet and Collet-Sicard syndromes (vide supra). Sphenoid bone fracture may affect the III, IV, and VI cranial nerves and also may disrupt the internal carotid artery and potentially result in pseudoaneurysm formation and caroticocavernous fistula (if it involves venous structures). Carotid injury is suspected in cases in which the fracture runs through the carotid canal; in these instances, CT-angiography is recommended.
Depressed skull fracture
In addition to the risk of infection in contaminated depressed skull fractures, a risk of developing seizures also exists. The overall risk of seizures is low but is higher if the patient loses consciousness for longer than 2 hours, if an associated dural tear is present, and if the seizures start in the first week of injury.
Although skull fractures carry a significant potential risk of cranial nerve and vascular injuries and direct brain injury, most skull fractures are linear vault fractures in children and are not associated with epidural hematoma. Most skull fractures, including depressed skull fractures, do not require surgery. Hence, all of the potential complications listed are associated with a graver prognosis if the primary fracture is missed during the diagnostic workup.
20 Controversy exists in the use of antibiotics for fractures and the need to elevate a depressed skull fracture. The use of antibiotics generally is not required unless the open fracture is obviously contaminated. Similarly, whether to elevate a depressed skull fracture is mostly the surgeon's choice, dictated by the need for cosmesis.
The use of resorbable bone plates cross-linked with Bone matrix protein-2 (BMP-2) is touted as a novel method of delivery and may enhance fracture healing.21 Another delivery system with scaffolds that deliver plasmid DNA encoding for bone morphogenetic protein-4 (BMP-4) has been tested in rodents and has shown promise.
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Huang YC, Simmons C, Kaigler D, Rice KG, Mooney DJ. Bone regeneration in a rat cranial defect with delivery of PEI-condensed plasmid DNA encoding for bone morphogenetic protein-4 (BMP-4). Gene Ther. Mar 2005;12(5):418-26. [Medline].
Shibuya TY, Wadhwa A, Nguyen KH, Panossian AM, Kim S, Wong H. Linking of bone morphogenetic protein-2 to resorbable fracture plates for enhancing bone healing. Laryngoscope. Dec 2005;115(12):2232-7. [Medline].
skull fractures, linear skull fractures, basilar skull fractures, temporal fractures, depressed skull fractures, skull trauma, occipital condylar fractures, linear fractures, depressed fractures, vault fractures, transverse temporal bone fractures, longitudinal temporal bone fractures, occipital condylar fractures, clivus fractures, skull wounds, coup injury, countercoup injury
Nazer H Qureshi, MD, Staff Physician, Department of Neurosurgery, University of Arkansas for Medical Sciences
Nazer H Qureshi, MD is a member of the following medical societies: American Association of Neurological Surgeons, Congress of Neurological Surgeons, and World Society for Stereotactic and Functional Neurosurgery
Disclosure: Nothing to disclose.
Griffith Harsh IV, MD, Director of Neurosurgical Oncology, Professor, Department of Neurosurgery, Stanford Medical Center, Stanford University School of Medicine
Griffith Harsh IV, MD is a member of the following medical societies: American Association of Neurological Surgeons, American College of Surgeons, American Medical Association, California Medical Association, Neurosurgical Society of America, North American Skull Base Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.
Michael G Nosko, MD, PhD, Chief, Division of Neurosurgery, Director of Neurovascular Surgery, Medical Director of Neuroscience Unit, Associate Professor, Department of Surgery, University of Medicine and Dentistry at New Jersey
Michael G Nosko, MD, PhD is a member of the following medical societies: Academy of Medicine of New Jersey, Alpha Omega Alpha, American Association of Neurological Surgeons, American College of Surgeons, American Heart Association, American Medical Association, New York Academy of Sciences, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Allen R Wyler, MD, Medical Director, Northstar Neuroscience, Inc
Allen R Wyler, MD is a member of the following medical societies: American Academy of Neurological and Orthopaedic Surgeons, American Association of Neurological Surgeons, and Society of Neurological Surgeons
Disclosure: Nothing to disclose.
Herbert H Engelhard III, MD, PhD, Director, UIC Neuro-Oncology Program, Chief, Division of Neuro-Oncology, Associate Professor, Department of Neurosurgery, University of Illinois at Chicago
Herbert H Engelhard III, MD, PhD is a member of the following medical societies: American Association for Cancer Research, American Association of Neurological Surgeons, American College of Surgeons, American Medical Association, American Society for Cell Biology, American Society of Clinical Oncology, Chicago Medical Society, Congress of Neurological Surgeons, Illinois State Medical Society, Society for Neuro-Oncology, and Society for Neuroscience
Disclosure: Nothing to disclose.
Allen R Wyler, MD, Medical Director, Northstar Neuroscience, Inc
Allen R Wyler, MD is a member of the following medical societies: American Academy of Neurological and Orthopaedic Surgeons, American Association of Neurological Surgeons, and Society of Neurological Surgeons
Disclosure: Nothing to disclose.
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