Clinical Significance of Long-Term Follow-Up of Children with Posttraumatic Skull Base Fracture

Original Article

Clinical Significance of Long-Term Follow-Up of Children with Posttraumatic Skull Base Fracture Sharon Leibu1, Guy Rosenthal2, Yigal Shoshan2, Mony Benifla1,2

OBJECTIVE: To assess the incidence of cerebrospinal fluid (CSF) leak and meningitis, and the need for prophylactic antibiotics, antipneumococcal vaccination, and surgical interventions, in children with a skull base fracture.

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a policy of not administering prophylactic antibiotics or pneumococcal vaccine. Long-term follow up is important to identify delayed complications.

METHODS: We reviewed the records of children with a skull base fracture who were admitted to our tertiary care center between 2009 and 2014.

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RESULTS: A total of 196 children (153 males), age 1 month to 18 years (mean age, 6
4 years), were hospitalized with skull base fracture. Causes of injury were falls (n [ 143), motor vehicle accidents (n [ 34), and other (n [ 19). Fracture locations were the middle skull base in 112 patients, frontal base in 62, and occipital base in 13. Fifty-four children (28%) had a CSF leak. In 34 of these children (63%), spontaneous resolution occurred within 3 days. Three children underwent surgery on admission owing to a CSF leak from an open wound, 3 underwent CSF diversion by spinal drainage, and 4 (2%) required surgery to repair a dural tear after failure of continuous spinal drainage and acetazolamide treatment. Twenty-eight children (14%) received prophylactic antibiotic therapy, usually due to other injuries, and 11 received pneumococcal vaccination. Two children developed meningitis, and 3 children died. Long-term follow up in 124 children revealed 12 children with delayed hearing loss and 3 with delayed facial paralysis.

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CONCLUSIONS: This is the largest pediatric series of skull base fractures reporting rates of morbidity and longterm outcomes published to date. The rate of meningitis following skull base fracture in children is low, supporting

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Key words Meningitis - Prophylactic antibiotics - Skull base fracture - Traumatic brain injury - Vaccination -

Abbreviations and Acronyms CSF: Cerebrospinal fluid CT: Computed tomography GCS: Glasgow Coma Scale GOS: Glasgow Outcome Score

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INTRODUCTION

T

raumatic brain injury is a leading cause of death in children. Skull fractures are relatively common following head trauma in children, with 4%e20% of such fractures occurring at the base of the skull. Main causes of head trauma in children include motor vehicle accidents, falls from heights, and blunt trauma. Skull base fractures are less common in the pediatric population than in adults; thus, the management and treatment of these fractures in children have been less well studied and are based mainly on currently accepted treatment protocols for adults.1-5 In the pediatric population, skull base fractures are not always apparent on routine computed tomography (CT) scans performed in the emergency department; thus, clinical examination is the most important first step in diagnosis.6 Delay in diagnosis can lead to severe complications, including meningitis, cerebrospinal fluid (CSF) leak, cranial nerve injury, and even death.4,7-10 Nonetheless, previous studies have shown that children with a normal neurologic examination and no brain injury on CT are at low risk for complications and can be managed as outpatients.6 CSF leak, a known complication of skull base fractures, can present as rhinorrhea or otorrhea. This complication, which occurs in 10%e30% of cases, results from tearing of the dura in the area of the fracture. The leak usually occurs (55%e80%) within the first 48 hours after injury.5,6,10,11 Because most leaks stop

From the 1Neurosurgical Pediatric Unit and 2Neurosurgery Department, Hadassah Ein Kerem Medical Center, Jerusalem, Israel To whom correspondence should be addressed: Mony Benifla, M.D. [E-mail: [email protected]] Citation: World Neurosurg. (2017) 103:315-321. http://dx.doi.org/10.1016/j.wneu.2017.04.068 Journal homepage: www.WORLDNEUROSURGERY.org Available online: www.sciencedirect.com 1878-8750/$ - see front matter ª 2017 Elsevier Inc. All rights reserved.

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spontaneously, initial treatment is conservative; continued leakage under conservative treatment often indicates the need for surgical intervention.5,7,11 Among adults, the risk of CSF leak leading to meningitis increases with the duration of the leak, at an incremental rate of 10%e50%.7,10,12 In this study, we characterized the clinical course and overall outcomes of children who sustained skull base fractures and assessed the incidence of CSF leak and meningitis, the need for surgical intervention, and the risk of subsequent neurologic deficits. Our findings provide information regarding the need for prophylactic antibiotics and antipneumococcal vaccination.

We reviewed the charts of patients age <18 years presenting at Hadassah Medical Center between January 2009 and December 2014 with a skull base fracture following an isolated traumatic brain injury. Children with multiple traumatic injuries were excluded from this study. We recorded demographic data, mechanism of injury, neurologic status, and findings of neuroimaging studies (e.g., brain CT) on presentation. As is routine in our department, patients were monitored for the development of CSF leak and meningitis during the course of hospitalization, and the neurologic outcome at the day of discharge was evaluated using the Glasgow Outcome Scale (GOS). The GOS is a 5-point scale that rates a patient’s postinjury level of function (1, dead; 5, normal activity with minor motor or mental disabilities). The rate of rehospitalization in a neurology or neurosurgery department and the duration of hospitalization were evaluated as well. Subgroups of patients were compared using the Pearson c2 and Fisher exact tests. Further statistical analyses were performed on the following clinical variables: age, location of fracture, Glasgow Coma Scale (GCS) score at presentation, mechanism of injury, intracranial bleeding status, and duration of hospitalization. Each of these variables was entered into a univariate logistic regression analysis model. The dependent variable was the experience (yes/no) of a CSF leak. The level of statistical significance was set at P < 0.01. RESULTS Between January 2009 and December 2014, 196 children (153 males [78%], mean age, 6.4
4.3 years; median age, 5 years [range, 1 month to 18 years]) were hospitalized in our pediatric neurosurgical unit with skull base fracture. The duration of hospitalization ranged from 1 to 38 days (median, 4 days; mean, 5.4
4.8 days). Table 1 summarizes the demographic and clinical characteristics of the cohort. Blunt trauma was the mechanism of injury in 98% of cases, whereas 2% suffered penetrating injury. The main cause was a fall from height, occurring in 143 children (73%), followed by motor vehicle accident (n ¼ 34; 17%) and other means (e.g., falling heavy object, physical violence; n¼ 19; 10%). The most common fracture location was the middle of the skull base (n ¼ 112; 57%), followed by the frontal base (n ¼ 62; 32%), and occiput (n ¼ 13; 7%). Among children with minor head trauma (GCS 14e15), the most common fracture site was the middle of the skull base; in those with moderate head trauma, frontal fractures were most common. The rate of multiple skull base fractures was higher in children

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Number (%)

Characteristic

Sex Male Female

153 (78.1) 43 (21.9)

Cause of trauma MVA Fall

PATIENTS AND METHODS

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Table 1. Demographic and Clinical Characteristics of Children with Skull Base Fracture

Other

34 (17.3) 143 (73) 19 (9.7)

Mechanism of injury Blunt Penetrating

193 (98) 3 (2)

Skull base fracture location Anterior

62 (31.6)

Middle

112 (57.1)

Posterior

13 (6.6)

Multiple

9 (4.6)

GCS at admission 3e8

18 (9.2)

9e13

8 (4.1)

14e15

170 (86.7)

Clinical presentation None

36 (18.4)

Vomiting

36 (18.4)

Loss of consciousness

27 (13.8)

Seizure

3 (1.5)

Otorrhagia

34 (17.3)

Rhinorrhagia

11 (5.6)

Mixed

49 (25)

Intracranial CT findings None

86 (43.9)

Bleeding (e.g., EDH, SDH)

60 (30.6)

Pneumocephalus

37 (18.9)

Edema

1 (0.5)

Mixed

32 (16.3)

CSF leak No

142 (72.4)

Yes

54 (27.6)

Type of CSF leak Otorrhea

36 (67.9)

Rhinorrhea

12 (22.6) Continues

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Table 1. Continued

3 children who presented with direct leaks from the wound had open depressed fractures and underwent surgery, including dural closure, on admission. Another 3 children required continued spinal drainage, and 4 children needed surgery to correct the fracture and the tear in the dura mater. One child underwent surgery for frontal sinus encephalocele, 1 child underwent surgery 1 year after an anterior skull base fracture with persistent leak, and 2 children underwent surgery for middle fossa fracture and continuous otorrhea; 1 of these children experienced meningitis and seizures (Figure 1). All 4 children who underwent surgery had failed acetazolamide treatment and continuous spinal drainage. Severe head trauma was found to be a significant risk factor for the development of CSF leak (odds ratio, 6.7; 95% confidence interval, 2.4e19). In addition, associations were found between CSF leak and the cause of trauma, clinical presentation on admission, anatomic location of the fracture (Figure 2), and the development of neurologic deficits (Table 2). According to the univariate logistic regression model applied, sustaining a motor vehicle accident increased the risk of CSF leak by 3-fold relative to trauma from a fall (P < 0.01), and the presence of otorrhagia and rhinorrhagia on presentation increased the risk of CSF leak by 16-fold and 3-fold, respectively (P < 0.001). Two children developed pneumococcal meningitis, at 10 days and 30 days after the injury. Both were treated with antibiotics without neurologic sequelae or further CSF leak. Twenty-eight children (14.3%) received preventive antibiotic treatment, some after surgery for other reasons (e.g., orthopedics, mouth and jaw) or injury to the middle ear or the orbit. Eleven children (5.6%) received antipneumococcal vaccination. Only 6 children (3%) were discharged from the hospital with a GOS of 2e3, and 3 children (1.5%) died. The remaining 187 children (95%) were discharged in generally good condition, with a GOS of 4e5. From a neurologic perspective, the majority of children (86.7%) were discharged without severe deficits, 5 children had hemiparesis, and 9 had facial nerve paralysis of varying degrees. Follow-up data after discharge were available for 124 children (63%); the follow-up period ranged from 2 weeks to 4 years, with an average of 4 months (Table 3). Neurologic deficits present at discharge and on long-term follow-up are summarized in Table 3. Of the 124 children who had long-term follow-up, 17 (7.2%) developed late-onset signs and symptoms that were not evident at hospital discharge, 8 complained of new headaches, 5 had reported behavioral changes, and 3 developed facial nerve paralysis of varying degrees following minor head injury. One patient who had sustained a severe head injury developed late-onset oculomotor paralysis due to a pseudoaneurysm. Hearing deficit was diagnosed during hospitalization in 8 of the 112 children (7%) with a middle skull base fracture. In another 12 children (11%), hearing loss was diagnosed by routine audiography performed at 2e4 weeks after discharge; thus, a total of 20 children (18%) experienced a hearing deficit.

Number (%)

Characteristic

Mixed

3 (3.8)

From wound

3 (5.7)

Time from trauma to CSF leak At presentation

42 (77.8)

After 24 hours

7 (13)

After 2 weeks or longer

5 (9.3)

Duration of CSF leak Up to 3 days

34 (63)

3e7 days

16 (29.6)

One week or longer

4 (7.4)

Treatment of CSF leak Conservative

47 (88.9)

CD

3 (5.6)

CD þ operation

4 (5.6)

GOS at discharge 1e3

9 (4.6)

4e5

187 (95.4)

Neurologic deficit at discharge None Hemiparesis CN deficit Other

170 (86.7) 5 (2.6) 9 (4.6) 12 (6.1)

MVA, motor vehicle accident; GCS, Glasgow Coma Scale; CT, computed tomography; EDH, epidural hematoma; SDH, subdural hematoma; CSF, cerebrospinal fluid; CD, continuous drainage; GOS, Glasgow Outcome Scale; CN, cranial nerves.

with severe head injuries (22%) compared with those without such injuries. Thirty-six children (18.4%) presented at the emergency room without any clinical findings, 36 (18.4%) reported vomiting or vomited in the emergency room, 34 (17.3%) presented with otorrhagia, and 11 (5.6%) presented with rhinorrhagia. Twenty-seven children (13.8%) experienced loss of consciousness, and 3 (1.5%) had seizures. Most of the children (n ¼ 170; 87%) were completely conscious on presentation to the emergency room, with a GCS of 14e15. Eighteen children presented with severe head trauma, with a GCS of 3e8; 10 children arrived with a GCS of 9e13. CSF leak occurred in 54 children (28%), including 36 (68%) with otorrhea, 12 (23%) with rhinorrhea, 3 with both rhinorrhea and otorrhea, and 3 with a direct leak from an open wound. In 42 children (78%), the leak was diagnosed on admission; in 7 (13%), the leak started 24 hours or more after reception, and in 5 (9.3%), the leak appeared at least 2 weeks after the traumatic event. In the majority of children (63%), the leak stopped spontaneously, within 3 days. Four children had chronic leak persisting for 1 week or longer. In most cases (89%), the leak stopped spontaneously. The

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DISCUSSION We report a low rate of meningitis among 196 children with skull base fractures who presented at our hospital over a 6-year period. Our findings support a recently published study that reported normal GCS, neurologic examination, and CT imaging findings in

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Figure 1. Computed tomography scans of an 11-year-old boy with a middle fossa skull base fracture. At 2 years after the injury, he presented with cerebrospinal fluid (CSF) leak, pneumococcal

most children with basilar skull fractures admitted to the emergency department after blunt head trauma. Taken together, these findings suggest that children with skull base fractures are usually at low risk for complications and can be discharged from the emergency department.6 Despite the significant biological, biomechanical, and anatomic differences between children and adults, some of which should influence decisions about diagnosis and treatment,4,13-17 owing to a lack of knowledge, the management of skull base fractures in children remains based on experience in adults. Fracture Location In our cohort, 57% of the children presented with a temporal bone fracture. This finding concurs with previous studies of children reporting that fractures occur most often in the middle skull base, in the temporal bone,1,4,14 and contrasts with a recent study of adults reporting that the majority of fractures occur at the anterior skull base.10 This difference apparently stems from anatomic differences in the facial structures of children and

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meningitis, and seizures, and subsequently underwent skull base reconstruction. At 5 years after the surgery, the child had no CSF leak or neurologic deficits. Arrow indicates fracture location.

adults. First, in childhood, the ratio of skull to facial volume is roughly 1:8; with maturation, this ratio decreases to 1:2.5. Thus, with age, the frequency of fractures in the facial bones that compose the frontal skull base rises and the frequency of temporal fractures decreases.17 Second, in small children, the frontal and maxillary sinuses are not fully developed, and thus the transfer of energy from an impact differs from that in adults, and the fracture line appears in a different anatomic area. In this context, Devin Coon et al15 reported anterior skull base fractures to be more common on the orbital roof. Such fractures occur more frequently in children age <7 years because the frontal sinuses are still undeveloped, and thus trauma to the upper part of the skull is transferred directly to the orbit. Generally, treatment of orbital roof fractures is conservative, but it is important to discount damage to the eyeball, disruption of eyeball movement, and changes in eyeball pressure. Follow-up is also important, because fractures in facial bones can incur damage during development and cause deformation.

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Table 3. Long-Term Neurologic Deficits Neurologic Deficit

CSF Leakage In this study, the rate of CSF leak was similar to previously reported rates. Fifty-four of the 196 children (28%) developed CSF leak. Among these children, 68% had otorrhea due to temporal bone fracture and 32% suffered rhinorrhea following anterior skull Table 2. Comparison of Patients with and without CSF Leak Characteristic

without CSF Leak (%)

with CSF Leak (%)

P Value

Male

76.8

81.5

0.47

Female

23.2

18.5

Sex

Mechanism of injury MVA

14.1

25.9

Fall

81

51.9

Other

4.9

22.2

Anterior

36.6

18.5

Middle

54.2

64.8

<0.001

Fracture location

Posterior

7

Multiple

2.1

0.008

5.6 11.1

Any neurologic deficit at discharge No

93

70.4

Yes

7

29.6

CSF, cerebrospinal fluid; MVA, motor vehicle accident.

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On Follow-Up, Number (%)

Hearing loss

8 (4)

20 (16)

Cranial nerve deficit

8 (4)

11 (9)

Headache

8 (4)

10 (8)

Behavioral changes

4 (2)

8 (6)

Hemiparesis

5 (2.5)

1 (1)

Other

2 (1)

5 (4)

196

124

Number of patients

Figure 2. Locations of skull base fractures.

On Discharge, Number (%)

base fracture. In the majority of cases, the leak resolved within 3 days. Four children who presented with late CSF leak required surgical intervention to close the fistula, in addition to the 3 children who underwent surgery soon after the injury for depressed skull fracture and transcutaneous CSF leakage. In the study by Perheentupa et al.,4 7 children (11%) were diagnosed with CSF leak, including 2 children with frontal fractures who were treated surgically. Kitchens et al.18 reported an 8% rate of CSF leak following basilar skull fracture, with no patients requiring surgery. Kadish and Schunk19 reported an 19% incidence of CSF leak following skull base fracture; none of their patients needed surgery, and only 1 patient developed meningitis. Observation alone is the first step in managing a posttraumatic CSF leak. In 80%e95% of adult patients, the leak stops spontaneously,12,20 although Friedman et al.21 reported spontaneous leak cessation in only 53% of their cases. Patients with a persistent leak may be treated with a pharmacologic agent that inhibits CSF production, such as acetazolamide, and may be fitted with an external CSF drainage device. Surgical intervention is indicated in patients with a persistent CSF leak lasting 10e14 days, and in those with complications associated with the leak, such as enlarging pneumocephalus or uncontrolled meningitis; in previous studies, 5%e45% of adult patients required surgical fistula closure.21-25 Following our policy of observation for 4e7 days, then administration of acetazolamide and CSF drainage for 5 more days, CSF leak ceased in all of our children with early CSF leak. Interestingly, 5 children (2.6%) developed late-onset CSF leak (occurring 2 weeks or longer after the injury). Only 1 of these children had early-onset rhinorrhea, which ceased spontaneously during hospitalization and resumed during outpatient follow-up. Therefore, early leakage is not predictive of late leakage. Accordingly, caregivers and family physicians need guidance on the possibility and signs of late CSF leak. Of the 5 children with late CSF leak in our cohort, 1 was treated successfully by continuous drainage, and the other 4 needed surgical intervention for persistent CSF fistula. Even though many pediatric neurosurgical services treat children with late-onset CSF leak, this condition remains underreported.

<0.001

Prophylactic Antibiotics and Immunization A significant complication of CSF leak is the development of meningitis, the risk of which increases as the leak persists. The

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risk in adults reaches 10%e50% at 1 week after leak onset.11,26-29 Mortality is as high as 10% in patients with meningitis, yet prophylactic antibiotic treatment for skull base fractures and CSF leak remains widely debated in the literature. The results of a meta-analysis that included 3 pediatric reports28 did not demonstrate a benefit of antibiotic prophylaxis in patients with skull base fractures (with or without CSF leak) without clinical evidence of meningitis.28 That meta-analysis included 12 studies with 2 arms: a control arm treated conservatively without prophylactic antibiotics and a study arm treated with prophylactic antibiotics. Only 3 of the 12 studies concluded that administration of prophylactic antibiotics to all patients with CSF leak, regardless of the presence or absence of clinical evidence of meningitis, ensures a better prognosis. In another meta-analysis, Kerman et al.27 reviewed 5 reports that compared the use of prophylactic antibiotics with conservative treatment alone in patients with skull base fractures, and found no significant differences between the 2 groups. Our policy is to reserve the use of prophylactic antibiotics for patients with CSF leak in whom meningitis is suspected or clinically evident. Only 2 of the 54 children with CSF leaks in our cohort developed pneumococcal meningitis. Both children were treated with antibiotics, and both experienced full recovery. Neither received antibiotics during presentation (prophylactically or for another reason). Owing to the small number of patients with meningitis, the identification of risk factors was not possible. Nonetheless, this low incidence suggests that preventive antibiotic treatment is not needed for children with CSF leak after skull base fracture. The administration of pneumococcal vaccines in patients with CSF leak is recommended in several European countries,30 mainly for children, but has not been thoroughly investigated, and its benefit is unclear. The main rationale for administering this vaccine is to prevent the development of meningitis in the late phase of a CSF leak31; however, in our cohort, only 2 children (1%) developed meningitis in the 10e30 days after the injury, and none developed delayed meningitis. Thus, our data do not support the administration of preventive antipneumococcal vaccine. A double-blind randomized prospective study is needed to determine the benefit of both prophylactic antibiotics and

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pneumococcal vaccination for patients who experience CSF leak as a result of skull base fracture. Long-Term Complications Among the 124 children followed in our clinic, 3 developed delayed facial nerve palsy and 1 sustained delayed oculomotor palsy. Interestingly, 11% experienced delayed headache and behavioral problems, which also may develop in children with head injuries unrelated to skull base fractures. Although follow-up was recorded for only 124 children, it is likely that all children with complications related to head injuries were referred to our neurosurgical service, which is the sole such service in our region. The relatively high rate of delayed complications highlights the need for long-term follow-up of children with skull base fracture. Of relevance, a recent study concluded that because complications such as meningitis and CNS fistula may take weeks to develop, patients discharged from the emergency department on the same day should be closely followed by their primary physician, with particular attention given to neurologic examination findings.6 Owing to this study’s retrospective design, clinical signs and symptoms, as well as discharge criteria, were not universal. The possibility of treatment bias should be considered as well, given that patients were managed by various doctors in the emergency room and in the department, and the identification and documentation of anamnesis, clinical, and imaging findings may differ among physicians. Based on this retrospective analysis, we intend to create guidelines for a prospective observational study. CONCLUSION In summary, the rate of meningitis following traumatic brain injury with skull base fracture is very low. This low rate indicates that prophylactic antibiotics and antipneumococcal vaccines are not necessary, even in the presence of CSF leak. Early and delayed CSF leak can be managed conservatively in the vast majority of cases. Surgery to repair CSF fistula is reserved for patients who fail CSF diversion and acetazolamide therapy. We found relatively high rates of delayed symptoms and signs, including facial and oculomotor nerve palsy. Close long-term follow-up of children with skull base fracture is important.

5. Ziu M, Savage JG, Jimenez DF. Diagnosis and treatment of cerebrospinal fluid rhinorrhea following accidental traumatic anterior skull base fractures. Neurosurg Focus. 2012;32:E3. 6. Tunik MG, Powell EC, Mahajan P, Schunk JE, Jacobs E, Miskin M, et al. Clinical presentations and outcomes of children with basilar skull fractures after blunt head trauma. Ann Emerg Med. 2016;68:431-440.e1. 7. Katzen JT, Jarrahy R, Eby JB, Mathiasen RA, Margulies DR, Shahinian HK. Craniofacial and skull base trauma. J Trauma. 2003;54:1026-1034. 8. Sarkar K, Keachie K, Nguyen U, Muizelaar JP, Zwienenberg-Lee M, Shahlaie K. Computed tomography characteristics in pediatric versus adult traumatic brain injury. J Neurosurg Pediatr. 2014;13: 307-314.

9. Scholsem M, Scholtes F, Collignon F, Robe P, Dubuisson A, Kaschten B, et al. Surgical management of anterior cranial base fractures with cerebrospinal fluid fistulae: a single-institution experience. Neurosurgery. 2008;62:463-469 [discussion: 469-471]. 10. Yellinek S, Cohen A, Merkin V, Shelef I, Benifla M. Clinical significance of skull base fracture in patients after traumatic brain injury. J Clin Neurosci. 2016;25:111-115. 11. Yilmazlar S, Arslan E, Kocaeli H, Dogan S, Aksoy K, Korfali E, et al. Cerebrospinal fluid leakage complicating skull base fractures: analysis of 81 cases. Neurosurg Rev. 2006;29:64-71. 12. Brodie HA. Prophylactic antibiotics for posttraumatic cerebrospinal fluid fistulae. A metaanalysis. Arch Otolaryngol Head Neck Surg. 1997;123: 749-752.

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13. Bonfield CM, Naran S, Adetayo OA, Pollack IF, Losee JE. Pediatric skull fractures: the need for surgical intervention, characteristics, complications, and outcomes. J Neurosurg Pediatr. 2014;14: 205-211. 14. Clauser L, Dallera V, Sarti E, Tieghi R. Frontobasilar fractures in children. Childs Nerv Syst. 2004; 20:168-175. 15. Coon D, Yuan N, Jones D, Howell LK, Grant MP, Redett RJ. Defining pediatric orbital roof fractures: patterns, sequelae, and indications for operation. Plast Reconstr Surg. 2014;134:442e-448e. 16. McCutcheon BA, Orosco RK, Chang DC, Salazar FR, Talamini MA, Maturo S, et al. Outcomes of isolated basilar skull fracture: readmission, meningitis, and cerebrospinal fluid leak. Otolaryngol Head Neck Surg. 2013;149:931-939. 17. Sirichai P, Anderson PJ. Orbital fractures in children: 10 years’ experience from a tertiary centre. Br J Oral Maxillofac Surg. 2015;53:938-942. 18. Kitchens JL, Groff DB, Nagaraj HS, Fallat ME. Basilar skull fractures in childhood with cranial nerve involvement. J Pediatr Surg. 1991;26:992-994. 19. Kadish HA, Schunk JE. Pediatric basilar skull fracture: do children with normal neurologic findings and no intracranial injury require hospitalization? Ann Emerg Med. 1995;26:37-41.

20. McGuirt WF Jr, Stool SE. Cerebrospinal fluid fistula: the identification and management in pediatric temporal bone fractures. Laryngoscope. 1995; 105(4 Pt 1):359-364. 21. Friedman JA, Ebersold MJ, Quast LM. Persistent posttraumatic cerebrospinal fluid leakage. Neurosurg Focus. 2000;9:e1. 22. Abuabara A. Cerebrospinal fluid rhinorrhoea: diagnosis and management. Med Oral Patol Oral Cir Bucal. 2007;12:E397-E400. 23. Baltas I, Tsoulfa S, Sakellariou P, Vogas V, Fylaktakis M, Kondodimou A. Posttraumatic meningitis: bacteriology, hydrocephalus, and outcome. Neurosurgery. 1994;35:422-426 [discussion: 426-427]. 24. Dalgic A, Okay HO, Gezici AR, Daglioglu E, Akdag R, Ergungor MF. An effective and less invasive treatment of post-traumatic cerebrospinal fluid fistula: closed lumbar drainage system. Minim Invasive Neurosurg. 2008;51:154-157. 25. Tas¸demiroglu E, Patchell RA. Classification and management of skull base fractures. Neurosurg Q. 2002;12:42-62. 26. Brodie HA, Thompson TC. Management of complications from 820 temporal bone fractures. Am J Otol. 1997;18:188-197. 27. Kerman M, Cirak B, Dagtekin A. Management of skull base fractures. Neurosurg Q. 2002;12:23-41.

28. Villalobos T, Arango C, Kubilis P, Rathore M. Antibiotic prophylaxis after basilar skull fractures: a meta-analysis. Clin Infect Dis. 1998;27:364-369. 29. Iacob G, Iacob S, Cojocaru I. Prophylactic antibiotics in neurosurgery. Rev Med Chir Soc Med Nat Iasi. 2007;111:643-648 [in Romanian]. 30. Pebody RG, Leino T, Nohynek H, Hellenbrand W, Salmaso S, Ruutu P. Pneumococcal vaccination policy in Europe. Euro Surveill. 2005;10:174-178. 31. Glarner H, Meuli M, Hof E, Gallati V, Nadal D, Fisch U, et al. Management of petrous bone fractures in children: analysis of 127 cases. J Trauma. 1994;36:198-201.

Conflict of interest statement: The authors declare that the article content was composed in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Received 5 March 2017; accepted 10 April 2017 Citation: World Neurosurg. (2017) 103:315-321. http://dx.doi.org/10.1016/j.wneu.2017.04.068 Journal homepage: www.WORLDNEUROSURGERY.org Available online: www.sciencedirect.com 1878-8750/$ - see front matter ª 2017 Elsevier Inc. All rights reserved.

Contact the Editorial Office Edward C. Benzel, M.D. Editor-in-Chief, WORLD NEUROSURGERY Chairman, Department of Neurosurgery, Cleveland Clinic 9500 Euclid Avenue / S-40 Cleveland, OH 44195 Tel: 216-444-7381 Fax: 216-445-9908 E-mail: [email protected] Website: www.WORLDNEUROSURGERY.org

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