Skull fractures, that are fractures of the cranial vault and base of skull, excluding facial fractures, are the results of significant force to the head and are classified according to the integrity of the overlying skin, the site, the shape of the fracture and the final position of the bony fragments.  As a result of the force applied there is often associated brain injury. 

Skull fractures in all but the neonate are caused by significant impact force to the cranium and may be associated with a variety of other injuries, both intracranial and extracranial. The cranial vault develops form membranous bone, with ossification of the bones commencing at six weeks gestation and the syndesmotic sutures fusing by the fifth decade.  Growth of the skull vault is driven by the growth of the underlying brain, with maximum rate of growth in the first twelve months during which time the brain doubles its weight.  Growth of the skull is complete by ten to twelve years.  This development of the skull is important as different types of fractures occur in the different age groups. 

Incidence:

Simple linear fractures constitutes about 50% of all, and the compound fractures about 25%. Simple depressed fractures make up about 6 %.

Mechanisms of injury:

The biomechanics of skull fractures depend on a direct force being applied to the skull, however there are the following variables,   surface area of the force,  velocity of the force, point impact, and the age of the patient. 

Experimental evidence has shown that a force of 400 to 700Kg must he applied to the skull for less than 0.001 of a second to cause a fracture.  If the force is applied over a longer time it will result in acceleration of the head. Bone in the adult and older child, has great resistance to compression but little resistance to tensile strain, and thus when direct force is applied to the skull, the skull is deformed instantaneously with the weaker tensile strength resulting in the inner table fracturing initially  and if the force is of sufficient strength then the outer table will also fracture.  These findings are not true for young children where the bone still has elastic properties and can therefore be deformed without fracturing.  The propagation of the fracture depends on the force applied and the local anatomy, namely, the thickness of the bone and the presence of bony ridges.

Sutural diastasis can occur in young patients without significant force, but in the adult patient with fused sutures it is a sign of significant trauma and may well be associated with intracranial complications.

Remote effects of forces applied to the skull can result in fractures at a site distant to that of the impact, due to the transmission of energy through the facial bones or with the development of a release fracture. With the application of a force to the skull, the shortening of a skull diameter in line with the force of lengthening of the diameter at right angles to the force causes a reversal of the energy forms, with the compressive strain on the inner table and the tensile strain on the outer table.

Diagnosis:  

Simple linear fractures may only present with a boggy scalp swelling, with a range of neurological signs and varying levels of consciousness. Compound fractures may well have associated evidence of a dural laceration with CSF leak or brain herniating through the wound.  

Radiology: 

Skull X-rays have been the standard radiological investigation in head injuries, and still have their place, even with the introduction of CT scans. The advantages of skull x-rays are, the majority of linear fractures are revealed, air fluid levels are well shown within the para-nasal sinuses and cranium, the cranio-cervical junction is well delineated on skull x-rays, the majority of adult patients have a calcified pineal gland and therefore in departments with no access to CT scans, a skull x-ray may reveal midline shift due to a mass lesion, management plans can be made on the result of a skull x-ray. The diagnosis of a base of skull fracture remains clinical and may not be shown on skull x-rays but the associated radiological signs of pneumocephaly and air-fluid level in the frontal or sphenoid sinuses suggest the presence of such a fracture.

Linear fracture-plain X-ray

Patients who require a CT scan do not require a skull x-ray.  

CT Scanning has revolutionized the management of trauma, in particularly head injuries, with good resolution of the cranial vault on axial bone windows’ and the intracranial contents on ‘soft tissue windows’, but there are limitations with imaging the posterior fossa and for base of skull imaging  coronal scans must be done.  Two dimensional CT scanning in trauma patients is sufficient in the radiological assessment of skull fractures, with no further information gained from three dimensional scanning. 

Magnetic resonance imaging is not superior to CT scanning in the acute assessment of head injured patients, due to the length of time taken for each scan, the use of non ferro-magnetic anesthetic equipment and the poor resolution of the bone.

CLASSIFICATION:

Fractures of the cranial vault and base of skull are the results of significant force to the head and are classified according to the integrity of the overlying skin, the site, the shape of the fracture and the final position of the bony fragments.  As a result of the force applied there is often associated brain injury.  The classification is important as it highlights the various complications, as well as the different approaches to their management.   

There are many systems to classify skull fractures, as listed below; however the most practical system is a combination of all three:

·         Linear, or displaced (slot, comminuted, depressed or elevated)  skull fractures.  

·         Simple or compound (related externally to the integrity of the overlying scalp and/or internally involving the paranasal air sinuses, or mastoid air cells)  

·         Anatomically, base of skull or vault fractures.

Linear fractures:   These fractures are significant if the fracture line crosses a meningeal artery or one of its branches (may lead to extradural hemorrhage), a dural venous sinus (may result in venous thrombosis, headache, and seizures), and extends into the paranasal sinuses. In the base it usually skirts the foramina because of the strong buttresses of bone around the foramina. Compound fractures carries the risk of infection and cortical thrombophlebitis and require thorough debridement and prophylactic antibiotics. In children, these fractures are often widely separated (usually lambdoid sutural diastasis) and usually heal by union within few months unlike in adults.

Growing fracture (Cranio-cerebral erosion):

Linear fracture-CT scan

In children, some linear fractures are associated with torn dura due to dense attachment of the dura to the bone in this age group. A rare complication, which occurs in 0.6% of linear skull fractures in pediatric patients: 90% occur before the age of three. The fracture is associated with a dural tear, preventing primary dural healing and resulting in progressive enlargement and eversion of the fracture line. The arachnoid sac may contain CSF and herniated brain with or without porencephaly.   The treatment for the two forms is different, as the former requires a duro-cranioplasty (debridement of the damaged brain and dural repair)  whilst the latter a shunt, in order to prevent progressive neurological deterioration.  

Displaced fracture:

Simple depressed fracture are more common in children. Birth injuries, and fall from a height are the common causes. Any depression more than 5 mm is likely to have injured the dura. In a pond fracture, the inner table and the dura are intact. 

Surgical elevation is recommended by many. Others argue that the damage occurs at the time of injury and elevation do not help. No reliable data is available to support surgery except for cosmetic purposes. Elevation over a sinus area may be hazardous. 

Depressed fracture-CT	Depressed fracture-3D CT	Pond fracture	Elevated fracture

Compound depressed fracture is an emergency to prevent infective sequelae.

Surgery for these patients is initial local wound closure after thorough cleaning and removal of  foreign bodies, to achieve hemostasis and prevent infection. If there is no dural laceration this will be the definitive treatment.

Definitive surgery must be performed as soon as possible, if there is a suspected dural laceration or intracranial hematoma or moderate to severe wound contamination. Dural laceration should be suspected if there is CSF in the wound, brain herniation, pneumocephaly in the absence of a base of skull fracture or on imaging there is intracranial air, the outer table of the skull is depressed below the inner table(or any depression above 5 mm), or a spicule of bone within the cranium  

The surgical principles are:

·         Thorough cleaning of the wound with great attention to removal of all foreign bodies and debridement of devitalized scalp.

·         Removal of the bone around the fracture with a craniotomy or craniectomy to reveal a margin of normal dura and then removing the depressed fragment without causing further cortical laceration.

·         Define the dural edges and extend the opening to inspect the underlying brain, evacuate intradural hematoma, foreign bodies and achieve hemostasis.

·         Dural closure, with primary suturing if there is no significant dural loss; however if there is a large dural defect, a duraplasty must be performed, using pericranium, fascia lata or an appropriate xenograft.

·         Bone fragments can be replaced if the wound is thoroughly cleaned, there is no clinical evidence of wound infection,  the surgery is performed within 24 hours of injury and the patient is treated with the appropriate antibiotics .

·         Frontal depressed fractures with associated facial fractures should be treated acutely as a combined procedure, as patients who have a high Glasgow Coma Score, no evidence of raised ICP or displacement of midline structures, do not appear to have an increase in operative morbidity . Earlier approaches to the management were with two or three operations, the initial neurosurgical procedure followed 7 to 10 days later by maxillo-facial reconstruction; however acute surgery is possible with improvements in neuroanesthesia, neurointensive care and the new plating sets for reducing and fixing these fractures.

·         Scalp wound must be closed primarily or if there is a large skin defect the scalp can be ‘expanded’ by making parallel release incisions in the galea parallel to the wound or using a rotation flap to cover the fracture, with skin grafting the donor site.

Compound elevated fractures are caused by tangential injuries which slice off a portion of the scalp, skull and the underlying dura. 

Slot fractures are always contaminated and are due to penetrating trauma caused by a blade, axe or machete, and therefore usually associated with a dural laceration. Principles of treatment are the same as in compound depressed fractures.

Basal fractures:   The local anatomy of the skull base, with the paranasal sinuses and mastoid air cells in close proximity to the dura, usually renders these fractures compound.    There has been no adequate controlled study to assess the benefit of prophylactic antibiotics in the prevention of post-traumatic meningitis in patients with base of skull fractures. The working party of the British Society for Antimicrobial Chemotherapy recommends close monitoring of patients to diagnose meningitis early and treat appropriately.   Base of skull fractures can be sub-divided anatomically into the fossae  namely, anterior, middle and posterior  fossa fractures.   Anterior Fossa Fractures may be presumed with  scalp emphysema,peri- orbital hematomas/panda or raccoon eyes where there is subconjuntival hemorrhage with no posterior limit, epistaxis, anosmia, CSF rhinorrhoea, or blindness, suggest an anterior fossa fracture.   Epistaxis is usually managed with adequate nasal packing. The olfactory nerve filaments are fine and delicate and can get injured in cribriform plate fractures. Anosmia may be missed in acute stages. An associated dural tear may result in CSF rhinorrhoea; it usually stops in 3-4 days. Persistent cases require a repair.   Optic foramen region fractures may result in optic nerve injuries and warrant immediate attention.    Pneumocephalus, due to entry of air from the sinuses, is an emergency. The patient develops a tension pneumocephalus due to a dural flap valve or with the use of positive airway pressure with an anaesthetic mask. A twist drill  to let out the air may be life saving.   Middle fossa fractures often extend to anterior fossa and posteriorly to petrous pyramid. Blood in the external auditory meatus, deafness, facial palsy, or delayed appearance of subgaleal altered blood over the mastoid ( Battle sign) may point to a middle fossa fracture.    The fracture may also injure the cavernous sinus, and may result in carotico-cavernous fistula.

Contrast cisternography-CSF leak thru' ant cranial fossa fracture Fracture cribriform plate with CSF rhinorrhoea Traumatic penumocephalus

The 3rd, the 4th, and the 6th nerves are at risk. The 3rd nerve paresis in patients with a normal level of consciousness are due to traction injuries, however if a sign of transtentorial herniation, the third nerve palsy will be preceded by a decrease in the patient’s level of consciousness. The 4th nerve has the long subarachnoid course and may sustain traction injury. The 5th nerve lies in the lateral wall of the cavernous sinus with the three divisions exiting through the middle fossa, where fractures can injury the nerve directly. The 6th nerve is tethered by the posterior cerebral and superior cerebellar arteries as it exits the brain stem and as it enters the cavernous sinus through Dorello’s canal, therefore any shift in the brain stem relative to the base of skull can cause traction on this nerve.  

 

Longitudinal fracture due to a lateral blow is common, and may result in facial nerve injury. The less common transverse fracture as a result of occipital blows involve the 7th and 8th nerves along with disruption of vestibular and cochlear components of the labyrinth. The facial nerve is susceptible to injury within the petrous bone from middle fossa fractures.  Facial nerve palsy immediately after the injury suggests traction, torsion or tearing of the nerve, whilst those that are of delayed onset are due to nerve swelling or a compressive haematoma in the facial canal and both groups of patients may be treated conservatively as the recovery of facial nerve function is 91.7% in the former and 94.1% in the later. Some surgeons recommend large doses of steroids to prevent a delayed facial palsy. Surgical decompression/ repair  via transmastoid translabyrinthine approach is being tried in facial nerve injuries with varying reports.

Deafness from a middle fossa fracture, if associated with a facial palsy, suggests a neural injury.  If not, ossicular dislocation must be excluded as this is a treatable form of deafness.  Therefore all patients with a middle fossa base of skull fracture must have full hearing assessment within two weeks of injury.  

CSF otorrhoea is rare and subsides spontaneously almost invariably.    CSF  rhinorrhoea (with an intact tympanic membrane) may require surgical intervention. Pituitary failure is rare complication, but should be suspected if the patient has bilaterally dilated pupils and refractory hypertension.  The majority of these patients has a disrupted optic chiasm as well as disrupted pituitary stalk    Post. fossa fractures are rare. associated cervical spine injuries must be ruled out.. The 6th to12th nerves may be injured.

Posterior fossa fracture-CT scan

CONCLUSION: 

Skull fractures, per se may be of no clinical significance, however when associated with decreased level of consciousness, or a focal neurological deficit, it may be an indicator of an intracranial hematoma or cortical contusion. A force severe enough to fracture the skull may produce brain damage as well.

The risk of intracranial hematomas in adults and pediatric patients with head injuries depends on two important clinical findings, namely, a skull fracture and the patient’s level of consciousness. The risks of intracranial hemorrhage (extradural, subdural, intracerebral) following a skull fracture depend on the age and the level of consciousness of the patient. 1 in 12 of children and 1 in 4 of adults with decreased GCS and fracture, have an ICH. 

Infection results from delayed treatment or inadequate treatment of the compound fractures, ranging from superficial wound infection to the more severe intracranial complications of meningitis, subdural empyema or brain abscess.

Hence a skull fracture should alert the neurosurgeon when patients, with a history of head injury, present with a neurological problem.