Dexamethasone treatment in chronic subdural haematoma.

INTRODUCTION: Neurosurgeons are familiar with chronic subdural haematoma (CSH), a well-known clinical entity, which is usually treated by some modality of trepanation. Despite the excellent outcomes obtained by surgery, complications may occur, some of which may be potentially severe or fatal. Furthermore, up to 25% recurrence rate is reported. The authors present a novel approach to the management of CSH based on the use of dexamethasone as the treatment of choice in the majority of cases. PATIENTS AND METHODS: Medical records of 122 CSH patients were retrospectively reviewed. At admission, symptomatic patients were classified according to the Markwalder Grading Score (MGS). Those scoring MGS 1-2 were assigned to the Dexamethasone protocol (4 mg every 8h, re-evaluation after 48-72 h, slow tapering), and those scoring MGS 3-4 were, in general, assigned to the Surgical protocol (single frontal twistdrill drainage to a closed system, without irrigation). Patients were followed in the Outpatient Office with neurological assessment and serial CT scans. RESULTS. Between March 2001 and May 2006, 122 consecutive CSH patients (69% male, median aged of 78, range 25-97) were treated. Seventy-three percent of the patients exhibited some kind of neurological defect (MGS 2-3-4). Asymptomatic patients (MGS 0) were left untreated. Initial treatment assignment was: 101 dexamethasone, 15 subdural drain, 4 craneotomy and 2 untreated. Twenty-two patients on dexamethasone ultimately required surgical drain (21.8%). Favourable outcome (MGS 0-1-2) was obtained in 96% and 93.9% of those treated with dexamethasone and surgical drain, respectively. Median hospital stay was 6 days (range 1- 41) for the dexamethasone group and the whole series, and 8 days (range 5-48) for the surgical group. Overall mortality rate was 0.8% and re-admissions related to the haematoma reached 14.7% (all maintained or improved their MGS). Medical complications occurred in 34 patients (27.8%), mainly mild hyperglycemic impairments. Median outpatient follow up was 25 weeks (range 8-90), and two patients were lost. DISCUSSION: The rationale for the use of dexamethasone in CSH lies in its anti-angiogenic properties over the subdural clot membrane, as it is derived from experimental studies and the very few clinical observations published. Surgical evacuation of CSH is known to achieve excellent results but no well-designed trials compare medical versus surgical therapies. The experience obtained from this series lets us formulate some clinical considerations: dexamethasone is a feasible treatment that positively compares to surgical drain (and avoided two thirds of operations); the natural history of CSH allows a 48-72 h dexamethasone trial without putting the patient at risk of irreversible deterioration; eliminates all morbidity related to surgery and recurrences; does not provoke significant morbidity itself; reduces hospital stay; does not preclude ulterior surgical procedures; it is well tolerated and understood by the patient and relatives and it probably reduces costs. The authors propose a protocol that does not intend to substitute surgery but to offer a safe and effective alternative. CONCLUSION: Data obtained from this large retrospective series suggests that dexamethasone is a feasible and safe option in the management of CSH. In the author's experience dexamethasone was able to cure or improve two thirds of the patients. This fact should be confirmed by others in the future. The true effectiveness of the therapy as compared to surgical treatment could be ideally tested in a prospective randomized trial.

Preservation of bone flap after craniotomy infection.

INTRODUCTION: The estimated incidence of craniotomy infection is 5%, ranging from 1-11% depending on the presence of certain risk factors, such as, prior radiation therapy, repeated surgery, CSF leak, duration of surgery over 4h, interventions involving nasal sinuses and emergency surgeries. The standard treatment for infected craniotomies is bone flap discarding and delayed cranioplasty. Adequate cosmetic results, unprotected brain and disfiguring deformity until cranioplasty are controversial features following bone removal. We present a limited series of five patients with craniotomy infection, that were successfully treated with wound debridement, in situ bone sterilization, reposition of the bone flap and antibiotic irrigation through a wash-in and wash-out draining system, all in the same surgical procedure. All infections cleared and every patient saved his/her bone flap. PATIENTS AND METHODS: We retrospectively reviewed the records of 5 patients with craniotomy infection that presented with wound swelling, purulent discharge and fever. The operative technique consisted on three manoeuvres: wound debridement, bone flap sterilization (either autoclaved or soaked in a sterilizing solution), and insertion of subgaleal/epidural drains for non-continuous antibiotic irrigation (vancomycin 50mg in 20cc of saline every 12h alternating with cephotaxime 100mg in 20cc of saline every 12h). Also, patients received equal systemic endovenous antibiotherapy and oral antibiotics after discharge, until complete resolution of infection and wound healing. RESULTS: Patients in the series (2 women and 3 men) ranged in age from 36 to 77. No patient had received prior radiation therapy and only one had undergone surgery involving nasal sinuses. The initial operations correspond to craniotomies performed for two intracranial tumours (meningiomas), one arteriovenous malformation and two decompressive craniotomies (haemorrhagic contusions and acute subdural haematoma). The duration of surgeries ranged from 1h30' to 5h30', only two operations extending over 4 hours. The interval between the initial surgery and the reintervention ranged from 11 to 227 days. Staphyloccocus spp were cultured in all patients. For bone sterilization povidone scrubbing was used in all patients, autoclave in two and soaking the flap in a sterilizing solution in three. All patients cleared infection and achieved complete wound healing in 2-3 weeks after the re-operation. Follow up ranged from 4 to 18 months. One patient died as a consequence of sepsis in the context of pneumonia some weeks after wound healing. DISCUSSION: Recent multivariate analyses have demonstrated that the presence of a CSF leak and the performance of repeated operations are the most important independent risk factors for craniotomy infection, with associated odds ratios for infection as high as 145 and 7, respectively. Regular antibiotic administration at anaesthesia induction seems to decrease the rate of craniotomy infection by half, both in the entire population and in low-risk subsets. Organisms involved in craniotomy infections are common pathogens usually contaminating neurosurgical procedures or normal skin flora germs. Auguste and McDermott have recently presented a case series of 12 patients in which successful salvage procedures for infected craniotomy bone flaps were performed using a continuous wash-in, wash-out indwelling antibiotic irrigation system, that needed close observation of the neurological status since obstruction of the outflow system could precipitate brain herniation. The method we present is as effective as theirs and avoids such complication since only small quantities of antibiotic solutions (20 cc) are instilled during each dose administration.

Large chondroma of the dural convexity in a patient with Noonan's syndrome. Case report and review of the literature.

INTRODUCTION: Intracranial chondromas are extremely rare intracranial tumours that usually arise from the skull base synchondrosis. Exceptionally, they may grow from cartilage rests within the dura mater of the convexity or the falx. They may be part of Ollier's multiple enchondromatosis or Maffuci's syndrome. We describe the case of a young male diagnosed of Noonan's syndrome that underwent resection of a large intracranial chondroma arising from the dural convexity. To our best knowledge this is the first report of such association. CASE REPORT: An 18-year-old male presented with a single generalized seizure. The patient was previously diagnosed of Noonan's syndrome on the basis of his special phenotype (Turner-like), low stature, cardiac malformation, retarded sexual and bone development and normal karyotype. He harboured mild psychomotor retardation. Physical and neurological examinations were unremarkable. Brain Magnetic Resonance image showed a large well-circumscribed intracranial mass in the dural convexity of the left frontal-parietal lobes, with heterogeneous contrast enhancement and no peritumoural oedema. The patient was initiated on valproic acid and underwent craniotomy and complete excision of the tumour. The tumour was firm, white-greyish, avascular and could be finely dissected away from the cortex. Postoperative seizures required additional anticonvulsant therapy. He was discharged uneventfully. The pathological study revealed a mature chondroma. Subsequent brain MRI studies have shown no evidence of recurrence after 33 months of follow up. DISCUSSION: Chondromas comprise less than 0.3% of intracranial tumours. Only twenty-five cases of intracranial dural convexity chondromas are reported in the literature. Several hystopathogenetic theories have been proposed: metaplasia of meningeal fibroblasts and perivascular meningeal tissue, traumatic or inflammatory cartilaginous activation of fibroblasts and growth of aberrant embryonal cartilaginous rests in the dura mater. Chondromas present clinical features similar to meningiomas. CT scan imaging shows a mass of variable density due to different degrees of calcification with minimum to moderate contrast enhancement. MRI studies show a well-circumscribed lesion without surrounding tissue oedema, that exhibit heterogeneous signal with intermediate to low intensity on T1-weighted images and mixed intensity on T2-weighted images with minimum enhancement. Angiogram is clue to differentiate from meningiomas since chondromas are completely avascular. Complete tumour resection including its dural attachment is the treatment of choice. Long-term prognosis is favourable. Radiation therapy is currently not recommended for residual tumours or inoperable patients due to risk of malignization. Noonan's syndrome (also known as pseudo-Turner syndrome) is a complex familial genetic disorder with a phenotype that resembles that of Turner's syndrome but exhibits no chromosomal defect. No predisposition of Noonan's syndrome for tumoural development is reported in the literature. Association of a dural convexity chondroma with Noonan's syndrome is unique as far as the literature is concerned.

Large chondroma of the dural convexity in a patient with Noonan’s syndrome. Case report and review of the literature

Introducción. Los condromas intracraneales sontumores extremadamente raros que suelen surgir dela sincondrosis de la base craneal. Excepcionalmente,puede crecer a partir de restos cartilaginosos en laduramadre de la convexidad o en la hoz. Se han relacionado con la encondromatosis múltiple de Ollier y con el síndrome de Maffuci. Describimos el caso de unvarón joven diagnosticado de síndrome de Noonan enel que se resecó un condroma gigante de la convexidad.Esta asociación no está descrita en la literatura hasta el momento. Caso clínico. Varón de 18 años de edad que presenta una única crisis comicial generalizada comodebut clínico. Estaba previamente diagnosticado desíndrome de Noonan basándose en su fenotipo especial(Turner-like), baja estatura, presencia de malformacióncardíaca, retraso en la maduración ósea y sexual, ycariotipo normal. No presentaba alteraciones significativas en la exploración física y neurológica salvo un leve retraso mental. El estudio de resonancia magnética cerebral mostró una masa intracraneal de gran tamaño, bien circunscrita, dependiente de la convexidad dural frontoparietal izquierda, con captación heterogéneade contraste y sin edema perilesional. Comenzó tratamiento con ácido valproico y se realizó una resección completa de la lesión. El tumor era de consistencia dura, blanco-grisáceo, avascular y pudo disecarse por completo de la corteza. Presentó crisis comiciales postoperatorias que precisaron tratamiento combinado con un segundo anticomicial. Anatomía patológica: condroma maduro. Las RM de control han mostrado ausencia de recidiva tras 33 meses de seguimiento. Discusión. Los condromas comprenden menos del 0,3% de los tumores intracraneales. Hasta la fecha, sólo se han descrito veinticinco casos de condromas de convexidad dural en la literatura. Se han propuesto diversas teorías histopatogénicas: metaplasia de fibroblastos meníngeos y tejido meníngeo perivascular, activación traumática o inflamatoria de fibroblastos hacia cartílago, y crecimiento de restos cartilaginosos embrionarios aberrantes en la duramadre. Los condromas presentan características clínicas similares a los meningiomas. La imagen de TAC muestra una masa de densidad variable debido a los diferentes grados de calcificación con mínima a moderada captación de contraste. Los estudios de RM evidencian una masa bien circunscrita sin edema perilesional, de señal heterogénea, hipointensa en T1 y de intensidad mixta en T2, y con captación mínima de contraste. La angiografía los diferencia perfectamente de los meningiomas pues aquéllos son totalmente avasculares. El tratamiento de elección es la resección completa incluyendo la duramadre adyacente. El pronóstico a largo plazo es excelente. El tratamiento con radioterapia no se recomienda ni en los restos tumorales ni en los pacientes inoperables, debido al riesgo de malignización. El síndrome de Noonan (tambiénconocido como pseudo-Turner) es una enfermedadgenética familiar compleja cuyo fenotipo se asemejaal del síndrome de Turner pero no presenta defectocromosómico. Hasta la fecha, no se ha descrito en laliteratura una predisposición al desarrollo de tumoresen los pacientes con Noonan ni tampoco la asociaciónde este síndrome con un condroma de convexidad cerebral

Introduction. Intracranial chondromas are extremelyrare intracranial tumours that usually arise fromthe skull base synchondrosis. Exceptionally, they maygrow from cartilage rests within the dura mater of theconvexity or the falx. They may be part of Ollier's multiple enchondromatosis or Maffuci's syndrome. We describe the case of a young male diagnosed of Noonan'ssyndrome that underwent resection of a large intracranialchondroma arising from the dural convexity. To our best knowledge this is the first report of such association.Case report. An 18-year-old male presented with asingle generalized seizure. The patient was previouslydiagnosed of Noonan's syndrome on the basis of hisspecial phenotype (Turner-like), low stature, cardiacmalformation, retarded sexual and bone developmentand normal karyotype. He harboured mild psychomotorretardation. Physical and neurological examinationswere unremarkable. Brain Magnetic Resonance imageshowed a large well-circumscribed intracranial massin the dural convexity of the left frontal-parietal lobes, with heterogeneous contrast enhancement and no peritumoural oedema. The patient was initiated on valproic acid and underwent craniotomy and complete excision of the tumour. The tumour was firm, white-greyish, avascular and could be finely dissected away from the cortex. Postoperative seizures required additional anticonvulsant therapy. He was discharged uneventfully. The pathological study revealed a mature chondroma. Subsequent brain MRI studies have shown no evidence of recurrence after 33 months of follow up.Discussión. Chondromas comprise less than 0.3% ofintracranial tumours. Only twenty-five cases of intracranial dural convexity chondromas are reported inthe literature. Several hystopathogenetic theories havebeen proposed: metaplasia of meningeal fibroblasts andperivascular meningeal tissue, traumatic or inflammatorycartilaginous activation of fibroblasts and growthof aberrant embryonal cartilaginous rests in the duramater. Chondromas present clinical features similar tomeningiomas. CT scan imaging shows a mass of variabledensity due to different degrees of calcification withminimum to moderate contrast enhancement. MRI studiesshow a well-circumscribed lesion without surroundingtissue oedema, that exhibit heterogeneous signalwith intermediate to low intensity on T1-weightedimages and mixed intensity on T2-weighted images withminimum enhancement. Angiogram is clue to differentiatefrom meningiomas since chondromas are completelyavascular. Complete tumour resection including itsdural attachment is the treatment of choice. Long-termprognosis is favourable. Radiation therapy is currentlynot recommended for residual tumours or inoperablepatients due to risk of malignization. Noonan's syndrome(also known as pseudo-Turner syndrome) is a complex familial genetic disorder with a phenotype that resembles that of Turner's syndrome but exhibitsno chromosomal defect. No predisposition of Noonan'ssyndrome for tumoural development is reported in theliterature. Association of a dural convexity chondromawith Noonan's syndrome is unique as far as the literatureis concerned