RESUMEN
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.
Asunto(s)
Diabetes Insípida/etiología , Neuroendoscopía/efectos adversos , Arginina Vasopresina/metabolismo , Desamino Arginina Vasopresina/metabolismo , Diabetes Insípida/metabolismo , Femenino , Humanos , Masculino , Neoplasias Hipofisarias/metabolismo , Neoplasias Hipofisarias/cirugía , Estudios RetrospectivosRESUMEN
OBJECTIVE: Intracranial hypertension (ICH) remains the single most difficult therapeutic challenge for the acute management of severe traumatic brain injury (TBI). We reviewed the published trials of therapeutic moderate hypothermia to determine its effect on ICH and compared its efficacy to other commonly used therapies for ICH. METHODS: A PubMed database search was done using various combinations of the search terms "brain injury," "therapeutic hypothermia," "intracranial hypertension," "barbiturates," "mannitol," "hypertonic saline," "hyperventilation," "decompressive craniectomy," and "CSF drainage." RESULTS: We identified 11 prospective randomized clinical TBI trials comparing hypothermia vs. normothermia treatment for which intracranial pressure (ICP) data was provided, and 6 prospective cohort studies that provided ICP data before and during hypothermia treatment. In addition, we identified 37 clinical TBI studies of lumbar CSF drainage, mannitol, hyperventilation, barbiturates, hypertonic saline, and decompressive craniectomy that provided pre- and posttreatment ICP data. Hypothermia was at least as effective as the traditional therapies for ICH (hyperventilation, mannitol, and barbiturates), but was less effective than hypertonic saline, lumbar CSF drainage, and decompressive craniectomy. Ultimately, however, therapeutic hypothermia does appear to have a favorable risk/benefit profile. CONCLUSION: Therapeutic moderate hypothermia is as effective, or more effective, than most other treatments for ICH. If used for 2-3 days or less there is no evidence that it causes clinically significant adverse events. The lack of consistent evidence that hypothermia improves long-term neurologic outcome should not preclude consideration of its use for the primary treatment of ICH since no other ICP therapy is held to this standard.
Asunto(s)
Lesiones Encefálicas/terapia , Cuidados Críticos/métodos , Hipotermia Inducida , Hipertensión Intracraneal/terapia , Lesiones Encefálicas/complicaciones , Humanos , Hipertensión Intracraneal/etiologíaRESUMEN
OBJECTIVE: The long-term behavioral effects of mild global ischemia have not been well described. We used short (5 min) asphyxic-cardiac arrest that resulted in no apparent gross neurological deficits to study the long-term effects of mild hypoxic ischemia on the neurobehavioral status of rats. METHODS: Fifteen adult, male Wistar rats were studied. One group was given asphyxic-cardiac arrest (CA) for 5 min (n=10) and the other group had Sham procedure (n=5). Neurobehavioral testing was performed before and 2 weeks after CA. The neurobehavioral evaluations were: neurological deficit score (NDS), Y Maze, open field, pre-pulse inhibition (PPI) of acoustic startle reflex (ASR), wire hanging, and inclined screen. RESULTS: At 24h post-CA, all of the rats regained normal neurological function as measured by NDS, an integral score for consciousness, brainstem reflexes, sensorimotor function and simple behavioral reflex tests. However, 1 week after CA, the rats exhibited significant activity reductions in the open field and in spontaneous alternation in the Y maze. The CA rats also showed a significant decrease in startle reaction amplitude and startle inhibition in the PPI tests. Two weeks after CA, the changes in motor activity and deficits in PPI remained significant, but the spontaneous alternation recovered. The muscle strength test of wire hanging and inclined screen tests did not exhibit significant change. CONCLUSION: We present a rodent model of mild CA that, despite apparent full recovery of global neurological function at 24h post-resuscitation, exhibited long-term cognitive injury lasting for at least 2 weeks after CA. This model may help understand better the injury associated with CA and develop management strategies for mild brain injury.
Asunto(s)
Trastornos del Conocimiento/etiología , Paro Cardíaco/complicaciones , Paro Cardíaco/psicología , Enfermedades del Sistema Nervioso/etiología , Animales , Asfixia/complicaciones , Asfixia/fisiopatología , Asfixia/psicología , Trastornos del Conocimiento/fisiopatología , Trastornos del Conocimiento/terapia , Modelos Animales de Enfermedad , Paro Cardíaco/terapia , Masculino , Enfermedades del Sistema Nervioso/fisiopatología , Enfermedades del Sistema Nervioso/terapia , Ratas , Ratas Wistar , Recuperación de la Función/fisiología , Resucitación , Factores de TiempoRESUMEN
Diabetes insipidus (DI) is a common complication following pituitary surgery and can be transient or permanent. Neurogenic DI occurs following injury to the magnocellular neurons in the hypothalamus that produce and transport arginine vasopressin (AVP) and form the hypothalamo-hypophyseal tract. DI is defined by a constellation of signs and symptoms resulting in dilute high-volume urine output and increasing serum osmolality. The body's inability to concentrate urine leaves the patient dehydrated and leads to metabolic abnormalities that can be life threatening if not recognized and treated in a timely manner with an exogenous AVP analog. The reported incidence of postsurgical central DI varies from 1 to 67%. This wide range likely reflects inconsistencies in the working definition of DI across the literature. Factors affecting the rate of DI include pituitary tumor size, adherence to surrounding structures, surgical approach, and histopathology of pituitary lesion. The likelihood of postoperative DI can be reduced by careful preservation of the neurovascular structures of the hypothalamus, infundibulum, and neurohypophysis. Vigilance and meticulous surgical technique are essential to minimize injury to these critical regions that can lead to postsurgical DI.
Asunto(s)
Diabetes Insípida Neurogénica/etiología , Procedimientos Neuroquirúrgicos/efectos adversos , Neoplasias Hipofisarias/cirugía , Complicaciones Posoperatorias/metabolismo , Desamino Arginina Vasopresina/uso terapéutico , Diabetes Insípida Neurogénica/metabolismo , Diabetes Insípida Neurogénica/prevención & control , Endoscopía , Humanos , Microcirugia , Hipófisis/anatomía & histología , Hipófisis/metabolismo , Complicaciones Posoperatorias/prevención & control , Vasopresinas/metabolismoRESUMEN
Lymphocytic hypophysitis is an uncommon autoimmune condition that often results in significant morbidity. Although most cases resolve spontaneously or after a short course of steroids, rarely, refractory cases can cause persistent neurological deficits despite aggressive medical and surgical management. A 41-year-old woman presented with progressive visual loss in the left eye and was found to have a sellar mass. She underwent transsphenoidal surgery because of lesion enlargement. Histopathology was consistent with adenohypophysitis with B-cell predominance. Despite steroid treatment, her neurological condition worsened and she experienced loss of vision in the right eye. Craniotomy with decompression of the right optic nerve was performed. Her condition improved initially, but she continued to have progressive visual compromise over the following months. She was therefore treated with rituximab, a monoclonal antibody against B cells. Her vision improved significantly within a few weeks. There was no clinical or radiographic exacerbation 2 years after starting immunotherapy. Rituximab, an anti-CD20 antibody that specifically depletes B lymphocytes, can be an effective treatment strategy for patients with steroid-refractory, B cell-predominant lymphocytic hypophysitis.
Asunto(s)
Anticuerpos Monoclonales de Origen Murino/uso terapéutico , Enfermedades Autoinmunes/tratamiento farmacológico , Factores Inmunológicos/uso terapéutico , Linfocitosis/tratamiento farmacológico , Enfermedades de la Hipófisis/tratamiento farmacológico , Adulto , Enfermedades Autoinmunes/diagnóstico , Enfermedades Autoinmunes/patología , Linfocitos B/efectos de los fármacos , Linfocitos B/patología , Biopsia , Femenino , Humanos , Linfocitosis/diagnóstico , Linfocitosis/patología , Enfermedades de la Hipófisis/diagnóstico , Enfermedades de la Hipófisis/patología , Recurrencia , Rituximab , Agudeza Visual/efectos de los fármacosRESUMEN
Transorbital penetrating injury (TPI), an uncommon subset of head trauma, requires prompt multidisciplinary surgical intervention. While numerous case reports appear in the literature, there is a lack of discrete recommendations for initial evaluation, surgical intervention, and postoperative care of patients with TPI. A retrospective review of 4 cases of TPI at the University of Michigan Health System was undertaken to assess for diagnosis, treatment, and follow-up. In addition, a PubMed search using the terms "penetrating orbital trauma," "penetrating orbital injury," "transorbital penetration," and "transorbital penetrating injury" were used to search for articles discussing the presentation and management of penetrating orbital trauma. All 4 of the patients at the University of Michigan underwent focused physical examination performed by a multidisciplinary trauma team followed by dedicated maxillofacial and head CT scanning. The patients' treatments varied, depending on the mechanism and extent of the injury. An analysis of the case series presented here as well as other published cases suggests an algorithm for diagnosis and treatment for patients with TPI, which includes focused evaluation, diagnostic imaging with maxillofacial CT scanning, and management of the injury that focuses on the path of penetration and the presence of the foreign body in situ at the time of presentation. Magnetic resonance imaging is indicated in patients who have indwelling wooden foreign bodies. Angiography should be performed in patients with suspected vascular injury. Treatment decisions should be made by a multidisciplinary team with input from neurosurgery, ophthalmology, otolaryngology, and maxillofacial surgery.