Indications

• Patients with open (compound) cranial fractures depressed greater than the thickness of the cranium should undergo operative intervention to prevent infection.
• Patients with open (compound) depressed cranial fractures may be treated nonoperatively if there is no clinical or radiographic evidence of dural penetration, significant intracranial hematoma, depression greater than 1 cm, frontal sinus involvement, gross cosmetic deformity, wound infection, pneumocephalus, or gross wound contamination.
• Nonoperative management of closed (simple) depressed cranial fractures is a treatment option.

Timing

• Early operation is recommended to reduce the incidence of infection.

Methods

• Elevation and debridement is recommended as the surgical method of choice.
• Primary bone fragment replacement is a surgical option in the absence of wound infection at the time of surgery.
• All management strategies for open (compound) depressed fractures should include antibiotics.

The presence of a cranial fracture has consistently been shown to be associated with a higher incidence of intracranial lesions, neurological deficit, and poorer outcome4, 8, 12, 14. Indeed, Chan et al.4 found cranial fracture to be the only independent significant risk factor in predicting intracranial hematomas in a cohort of 1178 adolescents. Macpherson et al.12 found that 71% of 850 patients with a cranial fracture had an intracranial lesion (i.e., contusion or hematoma), compared with only 46% of 533 patients without a cranial fracture. Hung et al.8 determined that patients with both loss of consciousness and cranial fracture were at significantly greater risk of developing a "surgically significant intracranial hematoma" than those with one or neither condition. Servadei et al.14 showed the importance of cranial fracture in predicting the presence of intracranial lesions, even in minor head injuries (Glasgow Coma Scale score 14 or 15). These studies underscore the importance of cranial fractures as indicators of clinically significant injuries, as well as the importance of computed tomographic (CT) scans in evaluation of all patients with known or clinically suspected cranial fractures.

Depressed cranial fractures may complicate up to 6% of head injuries in some series7, and account for significant morbidity and mortality. Compound fractures account for up to 90% of these injuries3, 6, 17, and are associated with an infection rate of 1.9 to 10.6%9, 13, 16, 17, an average neurological morbidity of approximately 11%6, an incidence of late epilepsy of up to 15%10, and a mortality rate of 1.4 to 19%3, 5-7, 17. By convention, compound depressed cranial fractures are treated surgically, with debridement and elevation, primarily to attempt to decrease the incidence of infection. Closed ("simple") depressed cranial fractures undergo operative repair if the extent of depression is greater than the full thickness of the adjacent calvarium, with the theoretical benefits of better cosmesis, a diminution in late-onset posttraumatic epilepsy, and a reduction in the incidence of persistent neurological deficit. There is, however, very little literature to support these management strategies, despite their widespread, and theoretically sound, practice. There is Class III literature that addresses the efficacy of surgical management of these injuries, and it argues against automatic surgical treatment of all compound fractures7.

Most of the literature reviewed focuses predominantly on infectious complications, seizures, surgical technique (e.g., bone fragment replacement versus removal), or the predictive power of cranial fracture for the presence of other intracranial pathology. Several large studies of patients with cranial fracture shed light on the breadth of issues associated with such lesions and are discussed below, under Scientific Foundation. However, some of these studies were conducted before the CT-scan era, and thus, although important for our understanding of the injury itself, are not included for critical analysis.

A MEDLINE computer search using the following key words: "skull" and "fracture" and "depressed" between 1975 and 2001 was performed. A total of 224 documents were found. The search was narrowed to include the key words: "surgery" or "operation" or "elevation". A total of 122 articles were found, 5 of which met the criteria for critical analysis. In addition, the reference lists of all articles were reviewed, and additional articles were selected for background information. The results of this analysis were incorporated into the review presented here. Papers primarily addressing the following topics were not included: patients with associated medical illnesses, sinus fractures, cranial base fractures, isolated orbital or facial fractures, and pre-CT era reports. In general, papers with the following characteristics were also excluded: case series with less than 10 patients evaluated by CT scan and with incomplete outcome data (mortality or Glasgow outcome score), case reports, operative series with operations occurring longer than 14 days from injury. Several articles with case series of less than 10 patients were examined and reviewed because of the limited number of patient series evaluating the acute surgical management of depressed cranial fractures in the CT era. Selected articles were evaluated for design, prognostic significance, therapeutic efficacy, and overall outcome. In addition, several articles were reviewed for the purposes of historical perspective.

Closed, linear cranial fractures are considered nonoperative lesions unless associated with surgical intracranial masses. Controversy surrounds appropriate management of depressed cranial fractures. Compound depressed cranial fractures are depressed fractures with an overlying scalp laceration in continuity with the fracture site and with galeal disruption, and have conventionally been treated with debridement and surgical elevation3, 6, 9, 14. Simple depressed cranial fractures have no galeal disruption and are traditionally managed with surgical elevation only if the extent of depression equals or exceeds the thickness of adjacent, intact bone, or if there is an associated intracranial hematoma with mass effect that requires evacuation.

The rationale for aggressive treatment of depressed cranial fractures stems from their association with infection and late epilepsy. Cosmetic deformity also plays a role in surgical decision making. Such complications, and their potential sequelae, are well documented. In a series of 359 patients with compound cranial fractures, Jennett and Miller9 documented a 10.6% incidence of infection, which was associated with a significantly higher incidence of persistent neurological deficit, late epilepsy (defined as seizures longer than 1 wk from injury), and death. Operative debridement reduced the incidence of infection to 4.6% in their series. Operative delay greater than 48 hours from injury dramatically increased the incidence to 36.5%. There was no difference in infection rate between surgical cohorts who had bone fragments replaced versus removed - results supported by a series of 225 patients with depressed cranial fracture reported by Braakman3, and a treatment strategy reported as early as Macewan in 18889. In a separate report of 1000 patients with nonmissile depressed cranial fractures, Jennett et al.10 documented a 15% incidence of late epilepsy, which was significantly associated with posttraumatic amnesia longer than 24 hours, torn dura, the presence of focal neurological signs, and the presence of early epilepsy (i.e., within 1 wk of injury). In the closed-fracture patients in this series, there was no difference in incidence of epilepsy between the elevated and nonelevated cases. Additionally, there was a higher incidence of late epilepsy in patients with elevated compound fractures. The authors explain this finding by documenting a higher incidence of those factors independently associated with late epilepsy, such as dural tearing and long posttraumatic amnesia, in the elevated-fracture patient cohort. These series were reported before the CT era, however, they offer us a clear picture of both the range of complications associated with nonmissile depressed cranial fractures and the controversies surrounding management strategies.

The primary question facing the neurosurgeon regarding depressed cranial fracture is whether to operate. Heary et al.7 reported a group of patients with compound depressed cranial fractures in which nonsurgical therapy was used for a subgroup of 26 patients without clinical or radiographic evidence of dural violation or significant underlying brain injury. They concluded that patients with open (compound) depressed cranial fractures may be treated nonoperatively if there is no clinical or radiographic evidence of dural penetration, significant intracranial hematoma, depression greater than 1 cm, frontal sinus involvement, gross deformity, wound infection, pneumocephalus, or gross wound contamination. No infectious complications occurred. Similarly, van den Heever and van der Merwe16 reported an equally low incidence of infection in a group of nonoperatively treated patients that included 139 compound depressed fractures. Surgical indications in their series included clinical characteristics of the wound. CT scans were not routinely used unless a neurological deficit was present on admission.

Although these studies are retrospective and nonrandomized, and, thus, subject to inherent biases, they clearly demonstrate that at least a select group of patients with compound depressed cranial fractures will do well without surgery.

Another challenge to traditional thinking that has surfaced in the literature involves the proper surgical management of compound depressed cranial fractures with respect to the bone fragments. Conventional treatment involves operative debridement, elevation of the fracture, removal of bone fragments, and delayed cranioplasty. However, this subjects the patient to a second operation (i.e., cranioplasty), with its attendant risks and complications. Kriss et al.11, Jennett and Miller9, and Braakman3 showed that infectious complications are not increased by primary bone fragment replacement. Wylen et al.17 retrospectively reviewed a series of 32 patients who underwent elevation and repair of a compound depressed cranial fracture with primary replacement of bone fragments within 72 hours of injury. Patients treated longer than 72 hours after injury and patients who presented with existing infection were excluded from the study. There were no infectious complications. Blankenship et al.2 also demonstrated a 0% infection rate in 31 children with compound depressed cranial fractures treated with primary bone fragment replacement, regardless of the degree of contamination of the wound at the time of surgery. Thirty patients in this series were treated within 16 hours of injury. Likewise, Adeloye and Shokunbi1 report the success of immediate bone replacement, without infectious sequelae, in 12 patients with compound depressed fractures, 11 of whom were treated within 10 hours of injury. Four patients in their series were treated with freefragment removal secondary to the greater severity of parenchymal injury, suggesting benefit from the decompression that bone removal would provide. Despite the retrospective, uncontrolled, nonrandomized design of these observational studies, they clearly demonstrate the feasibility of immediate bone fragment replacement without a corresponding increase in infectious sequelae, thus, obviating the need for a second surgical procedure.

The majority of studies are case series. No controlled, prospective clinical trials of treatment using surgical versus nonsurgical management have been published. The majority of data support debridement and elevation of grossly contaminated compound depressed cranial fractures as soon as possible after injury. However, several retrospective studies demonstrate successful nonoperative management of some patients with less-severe compound depressed cranial fractures on the basis of CT and clinical criteria. In the absence of gross wound infection at the time of presentation, immediate replacement of bone fragments seems not to increase the incidence of infection if surgery is performed expeditiously, and this replacement eliminates the need for subsequent cranioplasty and its attendant risks and complications. No controlled data exist to support the timing of surgery or the use of one technique over another.

To improve the strength of recommendations above the option level, well-controlled trials of surgical technique are warranted, and should examine issues of bone fragment replacement versus removal, dural laceration repair, etc., and their respective relationship to outcome variables, such as incidence of infection, incidence of epilepsy, need for reoperation, surgical complications, and, most importantly, neurological and neuropsychological outcomes.