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NI FEATURE: FACING ADVERSITY…TOMORROW IS ANOTHER DAY! - LETTERS TO EDITOR
Year : 2019  |  Volume : 67  |  Issue : 2  |  Page : 534-536

Intracranial migrating bone dust: Innocuous or evil?


1 Department of Neurosurgery, Sree Chitra Tirunal Institute of Medical Sciences and Technology, Trivandrum, Kerala, India
2 Department of Pathology, Sree Chitra Tirunal Institute of Medical Sciences and Technology, Trivandrum, Kerala, India

Date of Web Publication13-May-2019

Correspondence Address:
Dr. George C Vilanilam
Department of Neurosurgery, SCTIMST, Trivandrum - 695 011, Kerala
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.258041

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How to cite this article:
Jaiswal PA, Vilanilam GC, Rajalakshmi P, Kumar KK, Abraham M. Intracranial migrating bone dust: Innocuous or evil?. Neurol India 2019;67:534-6

How to cite this URL:
Jaiswal PA, Vilanilam GC, Rajalakshmi P, Kumar KK, Abraham M. Intracranial migrating bone dust: Innocuous or evil?. Neurol India [serial online] 2019 [cited 2019 May 20];67:534-6. Available from: http://www.neurologyindia.com/text.asp?2019/67/2/534/258041




Sir,

Infective complications negatively influence the postoperative course of around 4–6% of elective cranial surgical procedures. Deep surgical site infections (SSIs), intracranial purulent collections/abscesses, and meningitis could alarmingly complicate seemingly innocuous and meticulously performed surgical procedures. Besides the risks of morbidity and mortality, these increase the cost of care and prolong the in-hospital stay. The cornerstone of effective management of infective complications remains prompt recognition and aggressive management, which often includes reexploration and surgical debridement besides antibiotics. Bone flap infection, subdural empyema, and cerebral abscess warrant feisty surgical management. Wound infections following “clean” neurosurgical procedures occur due to various procedural and systemic comorbid factors. Devitalized bone is an important nidus that contributes to SSI. The craniotomy bone flap itself is the postulated “foreign body” in several such infections. Rarely has free bone dust, used to fill the burr-hole defect (for early fusion and better cosmesis), been implicated for the same.[1],[2],[3],[4],[5],[6] We report an unusual case of bone dust migrating into the operative cavity following a standard craniotomy, leading to deep surgical site intracranial infection, effectively managed with a timely reexploratory effort.

A 43-year old male patient, without any known comorbidity, presented with habitual seizures of frontal semiology that had been occurring for more than four decades, with a seizure frequency of 10–15/month. He was diagnosed to have a right frontal focal cortical dysplasia with good electro-clinicoradiological concordance on a presurgical workup. Right frontal craniotomy and extended lesionectomy guided by intra-operative neuronavigation were performed. All standard aseptic precautions were taken during surgery and appropriate prophylactic antibiotics were administered. After the lesionectomy, the operative cavity was irrigated with saline and the dura was closed with a pericranial graft. The postoperative CT scan showed a good resection with no operative site hematoma [Figure 1]. The postoperative period was uneventful and he was discharged on postoperative day (POD) 5. However, he was readmitted on POD 13 in view of continuous low-grade fever of 3 days duration. The surgical wound appeared healthy, and there were no clinical signs of meningitis or foci of systemic infection. There was elevation of erythrocytic sedimentation rate [ESR] (104 mm in the first hour) and total leukocyte counts (15,100 cells/cm3 with neutrophil predominance) and the procalcitonin value was <0.05. The CT scan of the head showed a multiloculated collection in the postoperative cavity with multiple heterogeneous amorphous calcifications (average Hounsfield unit being175). The overlying craniotomy bone flap appeared elevated and there was mild adjacent cerebral edema. A small epidural collection was seen extending into the subcutaneous space along the bone flap. Lumbar puncture was not suggestive of meningitis. The wound swab showed gram-positive cocci in pairs but the culture did not grow any organism. Emergency reexploration and wound debridement were performed. Seropurulent fluid under pressure was encountered beneath the galea with multiple pus flakes over the bone, dura, and over the parenchyma. Multiple calcified grey-white bits of tissue (bone dust) with surrounding pus flakes, walled off from the parenchyma by congested granulation tissue, were removed piecemeal [Figure 2]. The bone flap was not replaced. The subsequent CT scan showed complete removal of the lesions and the cultures were negative. Histopathology of the contents showed exudates and remnants of “surgicel” material adherent to the neural parenchyma with interposed granulation tissue. The exudate was predominantly composed of degenerated neutrophils and macrophages with a few small fragments of mature bone containing osteoblasts. The neutrophilic infiltration was sparse and predominantly confined around the bone fragments. There was no evidence of granulomas or giant cells and Grams, Zeihl Neelsen, Gomori methanamine silver, and Periodic Schiff stains did not reveal any organism. The patient recovered remarkably well and continues to remain so at a 1-year follow-up.
Figure 1: (a and b) Preoperative MRI with T1 weighted imaging (WI) coronal and FLAIR axial cuts shows cortical thickening and blurring of grey-white junction with abnormal architecture of the subcortical layer. There is FLAIR hyperintensity in the right frontal white matter. (c) Axial postoperative non-contrast CT scan [NCCT] (24 h postoperative) following the resective surgery showing excision of the focal lesion without any hyperdensities. (d and e) Axial image of the follow-up NCCT (2 weeks postoperative) showing an irregular hyperdense foci with average Hounsfield units (HU) of 175. (f) Axial cut of NCCT following reexploration showing complete removal of the focal hyperdense lesions

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Figure 2: Postoperative changes in the cerebral parenchyma-reexplored granulation tissue (a, lower half) with exudate containing bone fragments (b and c). The exudate is composed of degenerated cells and few neutrophils around osteocyte-bearing bone fragments (hematoxylin and eosin, a: ×100, b: ×40, c: ×250)

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SSI is a dreaded common complication encountered in neurosurgical practice. Rarely, these could complicate further into deep surgical space and parenchymal infections, greatly increasing the associated morbidity. “Foreign bodies” are common culprits in these infections and could range from an endogenous bone to exogenous material like surgicel, bone wax, and cranial fixation screws. Surgical infections not only increase the burden on the health care in terms of hospital readmission, intensive care unit admission, and lengthening the hospital stay but also contribute to morbidity and mortality.[7] Various factors like age, diabetic status, type of surgery, placement of foreign bodies, and intracranial pressure (ICP) monitoring are substantial risk factors for postoperative SSIs.[8]

Devitalized free bone in the form of a craniotomy bone flap or free bone dust subserves as a “foreign body” and thus could be an infective nidus. One of the rare causes for SSI and meningitis is the migration of bone dust into the operative cavity. Thirty-three cases have been reported in the literature related to this phenomenon and and all of them were associated with a burr-hole procedure [Table 1], this being the first reported case of bone dust migration after a craniotomy. Alorainy proposed that small pieces of bone or bone dust from the calvarium after drilling for the external ventricular drain get lodged into the brain parenchyma or ventricles during insertion of the drainage tube.[1] Bone dust could contain viable osteoblasts that, when implanted into the vascular tissue, are capable of dividing and laying down new bone. This property is used to seal burr holes and encourage fusion in routine neurosurgical practice and is often considered an innocuous necessity. A similar phenomenon was reported by Thomson et al., in three cases of intracranial hypertrophic calcification in the frontal and occipital horns of the lateral or third ventricle walls following sealing of the third ventriculostomy burr holes with bone dust.[2] Enlargement of the migrating bone dust was noted by Choi et al., following brain parenchymal catheterization,[3] thus suggesting that it could be a nidus for further dystrophic calcification and osteogenesis.[9]
Table 1: Summary of previously reported cases of intracranial migrated bone dust

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Our patient is the first reported case in whom the spontaneous intracranial migration of bone dust occurred following an elective craniotomy, further precipitating an operative site parenchymal infection. The intracranial bone dust, a nidus for inflammatory reaction, was noted within 2 weeks of surgery. The interval for the recognition of calcification following surgery in the literature ranges from <1 day to as long as 1 year. Due to the fact that the calcific foci in the present case were detected within 14 days surgery, dystrophic calcification of the blood clot or necrotic brain tissues seem unlikely. Kafadar et al., have reported the migration of bone dust used for plugging a burr hole made for endoscopy surgery, following a lumbar puncture. This was attributed to the negative pressure gradient generated by the lumbar puncture and its possible transmission through the cerebrospinal fluid (CSF) pathway.[5] Abandoning the usage of bone dust for sealing burr holes and cleaning the burr-hole area before the insertion of drain tube have been recommended to avoid this complication.[4],[5],[6] Also, in certain locations like the ventricles, removal of the bone dust before neovascularization is established is an option as it can otherwise lead to CSF outflow obstruction.

We propose that the most likely etiology of calcific changes and the subsequent infection in our case was the migrating bone dust. The powdered bone produced by electric/pneumatic drills replaced back to plug the bone defects could have migrated into the brain parenchyma or operative cavity, aided further by CSF fluxes and dural defects. Hence, we advocate a rethinking of the routine practice of bone dust replacement after craniotomies, especially in situ ations vulnerable to infection.

Intracranial migration of the endogenous bone dust used to plug burr holes and bone defects after an elective craniotomy is a scarcely reported complication. This bone dust acts as a “foreign body” that could compound a SSI further into a deep-seated parenchymal infection. Aggressive reexploration and debridement is the key to effective treatment. Nevertheless, prevention of the complication by avoiding bone dust replacement or judiciously using it in vulnerable patients is advocated.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
 » References Top

1.
Alorainy IA. Introduction of skull bone fragments into the brain during external ventricular drain placement. Eur J Radiol 2001;40:218-23.  Back to cited text no. 1
    
2.
Thomson S, Tyagi AK, Chumas PD. Intracranial hypertrophic calcification complicating neuroendoscopy. Report of three cases. J Neurosurg 2003;98:186-9.  Back to cited text no. 2
    
3.
Choi TM, Cho KY, Lim BC, Lim JS, Lee RS. Multiple intracranial high density foci after brain parenchymal catheterization. Korean J Neurotrauma 2016;12:118-22.  Back to cited text no. 3
    
4.
Ji C, Ahn JG. Multiple intracranial calcifications as a complication of external ventricular drain placement. J Korean Neurosurg Soc 2010;47:158-60.  Back to cited text no. 4
    
5.
Kafadar A, Abuzayed B, Kucukyuruk B, Cetin E, Gazioglu N. Intracranial migration of bone dust after intraventricular neuroendoscopy complicating acute hydrocephalus and removal of bone dust: Case report. Neurosurgery 2010;67:E503-4.  Back to cited text no. 5
    
6.
Turhan T, Ersahin Y. Intraventricular migration of the bone dust. Is a second operation for removal necessary? Case report and review of the literature. Childs Nerv Syst 2011;27:719-22.  Back to cited text no. 6
    
7.
Anderson DJ. Surgical site infections. Infect Dis Clin North Am 2011;25:135-53.  Back to cited text no. 7
    
8.
Erman T, Demirhindi H, Göçer AI, Tuna M, Ildan F, Boyar B, et al. Risk factors for surgical site infections in neurosurgery patients with antibiotic prophylaxis. Surg Neurol 2005;63:107-12.  Back to cited text no. 8
    
9.
Kapila A. Calcification in cerebral infarction. Radiology 1984;153:685-7.  Back to cited text no. 9
    


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