Diabetes insipidus (DI) after endoscopic transsphenoidal surgery (ETSS) can lead to increased morbidity, longer hospital stays, and increased medication requirements. Predicting which patients are at high risk for developing DI can help direct services to ensure adequate care and follow-up. The objective of this study was to review our institution's experience with ETSS and determine which clinical/laboratory variables are associated with DI in this patient population. The authors wanted to see if there was an easily determined single value that would help predict which patients develop DI. This represents the largest North American series of this type. We retrospectively reviewed the charts of patients who had undergone ETSS for resection of sellar and parasellar pathology between 2006 and 2011. We examined patient and tumor characteristics and their relationship to postoperative DI. Out of 172 endoscopic transsphenoidal surgeries, there were 15 cases of transient DI (8.7%) and 14 cases of permanent DI (8.1%). Statistically significant predictors of postoperative DI (p < 0.05) included tumor volume and histopathology (Rathke's cleft cyst and craniopharyngioma). Significant indicators of development of DI were postoperative serum sodium, preoperative to postoperative change in sodium level, and urine output prior to administration of 1-deamino-8-D-arginine vasopressin. An increase in serum sodium of ≥2.5 mmol/L is a positive marker of development of DI with 80% specificity, and a postoperative serum sodium of ≥145 mmol/L is a positive indicator with 98% specificity. Identifying perioperative risk factors and objective indicators of DI after ETSS will help physicians care for patients postoperatively. In this large series, we demonstrated that there were multiple perioperative risk factors for the development of DI. These findings, which are consistent with other reports from microscopic surgical series, will help identify patients at risk for diabetes insipidus, aid in planning treatment algorithms, and increase vigilance in high risk patients.
Spinal hematomas are a rare but serious complication of spinal epidural anesthesia and are typically seen in the epidural space; however, they have been documented in the subdural space. Spinal subdural hematomas likely exist within a traumatically induced space within the dural border cell layer, rather than an anatomical subdural space. Spinal subdural hematomas present a dangerous clinical situation as they have the potential to cause significant compression of neural elements and can be easily mistaken for spinal epidural hematomas. Ultrasound can be an effective modality to diagnose subdural hematoma when no epidural blood is visualized. We have reviewed the literature and present a full literature review and a case presentation of an 82-year-old male who developed a thoracolumbar spinal subdural hematoma after spinal epidural anesthesia. Anticoagulant therapy is an important predisposing risk factor for spinal epidural hematomas and likely also predispose to spinal subdural hematomas. It is important to consider spinal subdural hematomas in addition to spinal epidural hematomas in patients who develop weakness after spinal epidural anesthesia, especially in patients who have received anticoagulation.
This case report discusses the rare issue of an atrophic cervical pedicle at the C6 level in a patient found unconscious with a jumped facet and an unknown mechanism of injury. A means to discern between traumatic jumped facets versus congenital anomalies is addressed, including missing pedicles, which is encountered at the C6 level in this case. A literature review revealed that the most common level where this occurs is at the C6 level. The structural anatomic pathologies and the variants relative to congenital facet atrophy are identified, including the location and the surrounding vasculature; more specifically, the vertebral arteries. This information is helpful to assist clinicians when discerning between a traumatic subluxation injury that requires instrumentation and reduction versus a congenital anomaly that can usually be managed conservatively.
Background: Intracranial migration of odontoid screws is a rare but serious complication of anterior odontoid screw fixation not often reported in literature by neurosurgeons. Here, we describe the second case in literature of intracranial migration of an odontoid screw. Case Description: A 64-year-old neurologically intact patient with a type II odontoid fracture secondary to trauma underwent anterior odontoid screw fixation without any intraoperative complications. He tolerated the procedure well, and postoperative imaging demonstrated near anatomic correction of the fracture with satisfactory placement of the lag screw. Unfortunately, the patient was subsequently lost to follow up and he presented 7 months later for a routine outpatient computed tomography (CT) of the cervical spine, which demonstrated upward migration of the screw into the intracranial cavity abutting the medulla, with CT angiography of the neck also confirming the screw lying between the two vertebral arteries. Magnetic resonance imaging of the cervical spine also demonstrated the odontoid screw lying within close proximity to the ventral cervicomedullary junction, marginating the left vertebral artery. Subsequently, the patient was managed with removal of the odontoid screw and posterior cervical arthrodesis and instrumented fusion. Conclusion: Our case demonstrates the rare but serious complication of intracranial odontoid screw migration, which we bring to the attention of the neurosurgical community. The recognition of risk factors for this complication and optimized management of this rare occurrence is important for surgeons to recognize.
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