•Central diabetes insipidus (CDI) is a well-known complication following pituitary surgery, brain trauma or subarachnoid hemorrhage.•Surgical resection of non-sellar tumors does not commonly result ...in CDI.•Irritation of the pituitary stalk due to air entrapment in the sellar region may lead to CDI.•Careful clinical and biological postoperative monitoring remains essential to correctly diagnose and manage CDI following neurosurgery.
Neuroendocrine dysfunction is a common complication of several neurosurgical conditions. In particular, central diabetes insipidus (CDI) can occur subsequent to traumatic brain injury, subarachnoid hemorrhage, cerebral tumors or as a result of a complication following pituitary neurosurgery. In contrast, surgical resection of non-sellar tumors does not commonly result in CDI, with only a few cases reported in the literature.
We report the case of a 40-year-old man who presented a transient CDI following surgical resection of a pineal papillary tumor via an occipital interhemispheric trans-tentorial approach. The underlying pathogenesis of CDI occurring post resection of tumors arising at a distance from the sella is not yet clearly understood, especially since there is no evidence of direct compression of the pituitary stalk. With regards to our case, we hypothesize that restauration of the initial obstructive hydrocephalus might induce a rapid intracranial pressure variation leading to hemodynamics changes of the portal hypophyseal vascular system. Postoperative air entrapment in the sellar region might also lead to irritation of the pituitary stalk.
This case highlights that CDI may happen as a consequence of pineal tumor resection and advocates for a careful postoperative monitoring.
Fibrous cap thickness (FCT) is an important determinant of atheroma stability. We evaluated the feasibility and potential clinical implications of measuring the FCT of internal carotid artery plaques ...with a new ultrasound system based on boundary detection by dynamic programming.
We assessed agreement between ultrasound-obtained FCT values and those measured histologically in 20 patients (symptomatic S=9, asymptomatic AS=11) who underwent carotid endarterectomy for stenosing (>70%) carotid atheromas. We subsequently measured in vivo the FCT of 58 stenosing internal carotid artery plaques (S=22, AS=36) in 54 patients. The accuracy in discriminating symptomatic from asymptomatic plaques was assessed by receiver operating characteristic curves for the minimal, mean, and maximal FCT. Decision FCT thresholds that provided the best correct classification rates were identified. Agreement between ultrasound and histology was excellent, and interobserver variability was small. Ultrasound showed that symptomatic atheromas had thinner fibrous caps (S versus AS, median 95% CI: minimal FCT=0.42 0.34 to 0.48 versus 0.50 0.44 to 0.53 mm, P=0.024; mean FCT=0.58 0.52 to 0.63 versus 0.79 0.69 to 0.85 mm, P<0.0001; maximal FCT=0.73 0.66 to 0.92 versus 1.04 0.94 to 1.20 mm, P<0.0001). Mean FCT measurement demonstrated the best discriminatory accuracy (area under the curve 95% CI: minimal 0.74 0.61 to 0.87; mean 0.88 0.79 to 0.97; maximal 0.82 0.71 to 0.93). The decision threshold of 0.65 mm (mean FTC) demonstrated the best correct classification rate (82.8%; positive predictive value 75%, negative predictive value 88.2%).
FCT measurement of carotid atheroma with ultrasound is feasible. Discrimination of symptomatic from asymptomatic plaques with mean FCT values is good. Prospective studies should determine whether this ultrasound marker is reliable.