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Organic foreign bodies of the skull base are an uncommon problem with the potential for serious morbidity that present complicated treatment dilemmas best managed by a multidisciplinary approach. A 58-year-old male presented to the emergency department with fevers and mental status changes and was found to have bacterial meningitis. Computed tomography of the sinuses revealed two adjacent defects of the ethmoid roof with associated soft tissue density concerning for an encephalocele. He had a remote history of a penetrating left maxilla injury with a stick 13 years earlier. An attempted endoscopic repair of the defects revealed a pulsating splinter of wood emanating from the ethmoid roof defect. Neurosurgery and infectious disease were consulted and several wood fragments were removed endoscopically from the intracranial space. The skull base defects were closed using a septal cartilage underlay and free mucosal overlay graft. The patient has done well in follow-up with no evidence of cerebrospinal fluid leak. Organic foreign bodies from skull base trauma can have a delayed presentation and require a multidisciplinary team approach. In the appropriate setting endoscopic removal is a minimally morbid option.
Traumatic injury to the skull base can present unique diagnostic and therapeutic challenges. The emergence of advanced endoscopic techniques has expanded the otolaryngologist's role in treating lesions of the skull base. The endoscopic repair of skull base defects and cerebrospinal fluid (CSF) leaks has been demonstrated to have superior efficacy and decreased morbidity in comparison to open craniotomy approaches.1 The traditional approach for removal of an intracranial foreign body is through an open craniotomy, but in select cases both endoscopic transcranial2 and endonasal endoscopic approaches have been described.3,4,5 We present an interesting case of a man with meningitis in the setting of a remote history of maxillofacial and skull base trauma who was found to have two defects of the ethmoid roof and an intracranial foreign body. A discussion of the multidisciplinary evaluation and endoscopic approach to this problem is provided.
A 57-year-old man who had recently emigrated from El Salvador presented to the emergency department with fever to 103°F, severe headache, nausea and vomiting, and mental status changes in the setting of a sinus infection that was diagnosed 2 days earlier. On initial evaluation, he was unresponsive to verbal stimulation but withdrew all extremities to painful stimuli. His white blood cell (WBC) count was 14,500 with a left shift. Lumbar puncture revealed an opening pressure of 38 cm H2O and purulent fluid. The CSF had 1070 WBCs, glucose 34 mg/dL (normal 50 to 75) and total protein 254 mg/dL (normal 5 to 55). Computed tomography (CT) of the head and sinuses revealed two left-sided ethmoid roof defects with bulging soft tissue from the anterior cranial fossa (Figs. 1 and 2). The largest defect measured 1.5×1.2 cm in diameter and magnetic resonance imaging revealed findings consistent with an encephalocele. The patient was administered intravenous vancomycin, ceftriaxone, acyclovir, and clindamycin and admitted to the intensive care unit (ICU). CSF cultures grew Streptococcus pneumoniae and antibiotic coverage was narrowed to ceftriaxone. He rapidly improved. He was discharged to a rehabilitation hospital to complete 2 weeks of intravenous ceftriaxone. He was readmitted 2 weeks after completion of antibiotics for surgical repair of the skull base defect.
The patient's past medical history was notable for left-sided penetrating maxillofacial trauma sustained in a fall from a tree with resultant impalement by a stick 13 years earlier. This resulted in an extended hospital stay requiring prolonged antibiotic therapy. No history of CSF leak or skull base repair was elicited. He had no other significant past medical history.
The patient went to the operating room for an endoscopic repair of the skull base defect. While elevating the mucosa around the defect of the encephalocele, a cavity was entered that contained cloudy fluid and a foreign body with the appearance of wood extending through the defect and into cerebral parenchyma. The foreign body was pulsating and there was concern that it could be intimately associated with a major vascular structure. In addition, further fragments could not be ruled out, and if present the skull base repair would in effect wall off an infected nidus. After consultation with neurosurgery, the decision was made to leave the foreign body in place, abort the repair to avoid a potentially severe intracranial bleed, and perform additional imaging to rule out close approximation to major intracranial vessels and/or the presence of additional foreign bodies. Cultures from the ethmoid sinus grew few methicillin-resistant Staphylococcus aureus, coagulase-negative staphylococci, and diphtheroids. The patient had received intravenous ceftriaxone on call to the procedure, and was maintained on intravenous vancomycin, metronidazole, and ceftazidime postoperatively for several weeks. A CT angiogram was completed revealing no large vessels adjacent to the skull base defect and no foreign bodies were apparent on imaging. In conjunction with neurosurgery, the patient was taken back to the operating room for endoscopic foreign body removal and repair of the skull base defects 9 days later. A sliver of wood was removed and moderate bleeding was encountered. This was controlled with bipolar cautery and Surgicell (Johnson and Johnson, Langhorne, PA). The posterior skull base defect was repaired with an underlay of Durepair (Medtronic, Goleta, CA) and septal cartilage followed by an overlay of free mucosa, and the anterior defect adjacent to the crista galea was repaired with a Durepair underlay and an overlay of free mucosa. There was no CSF leak at the completion of the case. A postoperative CT scan revealed a left inferior frontal intraparenchymal hemorrhage. The patient had no focal neurologic signs. He was admitted to the ICU for monitoring and a follow-up CT scan showed no interval increase in the hemorrhage. He was discharged home on the sixth postoperative day, and completed a 3-week postoperative course of intravenous vancomycin, ceftazidime, and oral metronidazole. After 6 weeks follow-up, the patient was feeling well with no evidence of CSF leak. The pathology revealed foreign body material consistent with plant tissue (Fig. 3).
Patients who develop late complications from traumatic skull base injury may go unrecognized for years secondary to spontaneous healing of the CSF leak or an incorrect diagnosis of some more benign condition like allergic rhinitis. In cases of spontaneous healing the dura does not regenerate and the intracranial space is separated and protected from the nasal cavity by a thin layer of nasal mucosa and scar tissue. This can be an inadequate barrier to the spread of sinonasal infection and bacterial meningitis may occur years after skull base injuries.6 This potential complication of skull base defects may lead to long-term neurologic sequelae and can result in death. In this case the patient presented with meningitis 13 years after his initial injury. A retrospective review of patients with posttraumatic CSF leaks who were treated conservatively (bed rest with or without lumbar drainage) found that 29% (5/17) developed meningitis. This finding suggests that there is a significant risk of ascending bacterial meningitis with a history of skull base trauma.7 A retrospective analysis by Bernal-Sprekelsen et al attempted to specifically address the impact of surgical repair of skull base defects (in the presence or absence of a CSF leak) on the prevention of meningitis.8 In this series of 39 patients who underwent repair only 1 patient developed a recurrent CSF fistula and meningitis. Of the 15 patients who developed meningitis prior to repair there were no further episodes of meningitis at a mean follow-up of 65 months. The results of a retrospective case series can be difficult to apply prospectively, but this was the first series to suggest that repair of skull base defects may prevent ascending meningitis.
Intracranial foreign bodies pose a significant risk for the development of meningitis and brain abscess. Traumatic injury with objects such as pencils and chopsticks often present with innocuous wounds or minor epistaxis. Nishio et al presented a case report of an intracranial abscess presenting 7 years following a chopstick injury in which the upper eyelid was penetrated and a piece of wood was left in the frontal lobe.9 In reviewing the literature they found 23 cases of transorbital penetration of the dura with wooden objects and in 11 of these 23 cases the patients were asymptomatic at presentation. Bursick et al presented a case report and review of intracranial pencil injuries.10 Two patients in this review had transnasal penetrating trauma through the cribriform plate that presented with meningitis 4 and 5 years after the initial injury. Traumatic injury resulting in intracranial wooden foreign bodies occurred primarily in children who fell while carrying sharp objects such as pencils or chopsticks. Miller et al presented the largest series of cases of intracranial wooden foreign bodies.11 In this series of 42 patients that spanned both the pre- and postantibiotic era, 48% of the patients developed a brain abscess. Among patients in the postantibiotic era, infection complicated 64% of the cases and there was a 25% mortality. There are numerous qualities to wood that make it particularly prone to infection, including its porous quality and predisposition to fragmentation. The most common organisms found in this series were Staphylococcus aureus, β-hemolytic streptococci, and Streptococcus pneumoniae. Our patient developed S. pneumoniae meningitis 13 years following his original injury. The most common organism to cause community-acquired meningitis in the setting of a CSF leak is S. pneumoniae, while Neisseria meningitidis and Haemophilus influenza are other common pathogens.12,13,14 As is evident from the review of Miller et al that spans the pre- and postantibiotic era, the use of antibiotics is essential to treatment and avoidance of further intracranial complications. The typical antibiotic course for a brain abscess is 6 weeks of intravenous antibiotics that have good CSF penetration. Following removal of a foreign body from the brain, intravenous antibiotics that achieve good CSF levels should be given for 3 to 6 weeks if a brain abscess is present surrounding the foreign body. A careful history and high index of suspicion is necessary to establish the diagnosis of a retained intracranial foreign body. In cases where there are no neural or vascular injuries and there is no active CSF leak, the relative absence of significant presenting symptoms can give patients and practitioners a false sense of security.
Wooden materials pose a significant diagnostic challenge because of variable appearance on imaging. The density of wood depends on both the type and on the degree of water absorption. It can change with the duration of the foreign body. When wood is dry it can be difficult to differentiate from fat tissue and air in the sinuses. Specht et al describe a case of a wooden golf tee that passed through the optic canal into the interpeduncular fossa.15 The foreign body was not located on the CT scan, but was appreciated as a low-intensity object on MRI. In general, the use of wide window widths on CT scans is helpful in delineating wooden foreign bodies.16 The wooden foreign body in our case had been present for 13 years and it was not visible on CT or MRI. The utility of imaging in diagnosing an intracranial wooden foreign body depends upon the size of the object and the duration of its presence.
There have been at least three prior reports of transnasal endoscopic removal of foreign bodies in the acute setting.3,4,5 In contrast, our patient presented 13 years following the trauma that resulted in the intracranial foreign body. There was substantial scar tissue and an encephalocele present at the ethmoid roof that demanded careful dissection. There was no radiographic evidence of a foreign body and we cannot be certain that every fragment was removed, but an endoscopic approach was chosen to decrease morbidity hoping that no further fragments were present. The use of CT image guidance facilitated a safe dissection of the scarred and recently infected skull base. Dodson et al similarly reported using CT image guidance to define the skull base defect and find two metallic pen nibs located above the ethmoid roof.3 While CT image guidance is not necessary for uncomplicated sinus surgery it can serve as a useful adjunct in more complicated cases involving the skull base. We found it to be particularly useful in our case given the distorted anatomy from the patient's history of trauma and infection as it allowed careful dissection of both skull base defects. If this patient were to develop any further episodes of meningitis or a brain abscess an open approach would be indicated.
The delayed clinical presentation of intracranial foreign bodies is an uncommon clinical problem requiring a multidisciplinary approach to care. In the appropriate setting an endonasal endoscopic approach is a less invasive and minimally morbid option to foreign body removal and repair of the skull base defect. Consultation with neurosurgery and infectious disease is an essential component to the comprehensive care of such patients. Given the difficulty in identifying small foreign bodies with conventional imaging modalities, the surgeon needs to be prepared for possible complications related to removal. The potential for severe vascular injury when contemplating removal of an unexpected intracranial foreign body should prompt a conservative progression. In this case we elected to abort the initial procedure to obtain further imaging and also allowed for preparation for the potential need of a craniotomy approach. Endoscopic techniques applied in the appropriate setting can safely be used to manage intracranial pathology including foreign body removal.