Citations

Abstract Assuring clinical competence throughout the career of a neurosurgeon is of paramount importance for patient safety. We present the first comprehensive survey of all neurosurgeons board certified through the American Board of Neurological Surgery (ABNS) to evaluate perceptions of Maintenance of Certification (MOC). We administered a validated, online, confidential survey to 4899 neurosurgeons (2435 ABNS diplomates participating in MOC, 1440 diplomates certified prior to 1999 [time-unlimited certificates], and 1024 retired diplomates). We received 1449 responses overall (30% response rate). Our study found that most respondents believe that neurosurgeons should be required to participate in continuing professional improvement following initial board certification (75%). Most believe that specialty boards, working in conjunction with specialty societies, should require diplomates to participate in programs meant to promote continuous professional development (73%). The majority of respondents (76%) believed that self-assessment tests constituted a meaningful professional development activity, in addition to periodic case log reviews (33%) or quality improvement projects (32.6%). A plurality of respondents (44%) do not feel that the MOC process as currently structured provides them with value. There were no differences between those who were “grandfathered” and those who actively participate in MOC and no differences between those in private practice versus those in academics. The ABNS is cognizant of diplomate concerns and is actively developing new MOC paradigms to ensure that the process achieves both the goals of meeting the public interest and assuring that the quality of American neurosurgery remains exemplary.

OBJECTIVEPatient-reported outcomes have been increasingly mandated by regulators and payers to evaluate hospital and physician performance. The purpose of this study is to delineate the differences in patient-reported experience of hospital care for cranial and spinal operations.METHODSThe authors selected all patients who underwent inpatient, elective cranial or spinal procedures and completed the Hospital Consumer Assessment of Healthcare Providers and Systems (HCAHPS) survey at a single, high-volume, tertiary care institution between October 2012 and September 2015. The association of the surgical procedure and diagnosis with various HCAHPS composite measures, calculated across 9 domains using standard top-box methodology, was investigated. Multivariable logistic regression models were fitted for outcomes that were significant with procedure type and diagnosis group on univariate analysis, adjusting for age, sex, case complexity, overall health rating, and education level.RESULTSA total of 1484 patients met criteria and returned an HCAHPS survey. Overall, patients undergoing a cranial procedure gave top-box (most favorable) scores more often in pain management measure (66.3% vs 59.6%, p = 0.01) compared with those undergoing spine surgery. Furthermore, despite better discharge scores (93.1% vs 87.1%, p < 0.001), spinal patients were less likely to report excellent health (7.4% vs 12.7%). Lastly, patients with a primary diagnosis of brain or spinal tumor compared with those with degenerative spinal disease and those with other neurosurgical diagnoses provided top-box scores more often regarding communication with doctors (82.7% vs 76.4% vs 75.2%, p = 0.04), pain management (71.8% vs 60.9% vs 59.1%, p = 0.002), and global rating (90.4% vs 84.0% vs 87.3%, p = 0.02). On multivariable analysis, spinal patients had significantly lower odds of reporting top-box scores in pain management (OR 0.67, 95% CI 0.52–0.85; p = 0.001), staff responsiveness (OR 0.68, 95% CI 0.53–0.87; p = 0.002), and global rating (OR 0.59, 95% CI 0.42–0.82; p = 0.002), and significantly higher odds of top-box scoring in discharge information (OR 2.15, 95% CI 1.45–3.18; p < 0.001) than cranial patients. Similarly, brain tumor cases were associated with significantly higher odds of top-box scoring in communication with doctors (OR 1.46, 95% CI 1.01–2.12; p = 0.04), pain management (OR 1.81, 95% CI 1.29–2.55; p < 0.001), staff responsiveness (OR 1.88, 95% CI 1.33–2.66; p < 0.001), and global rating (OR 2.00, 95% CI 1.26–3.17; p = 0.003) compared with degenerative spine cases.CONCLUSIONSSignificant differences in patient-reported experience with hospital care exist across different cranial and spine surgery patient populations. Overall, spinal patients, particularly those with degenerative spine disease, rated their health and their hospital experience lower relative to cranial patients. Identifying weaker areas of hospital performance in target populations can stimulate quality initiatives that aim to increase the overall hospital score.

Background Pediatric pituitary adenoma is a rare skull base neoplasm, accounting for 3% of all intracranial neoplasms in children and 5% of pituitary adenomas. Compared with pituitary tumors in adults, secreting tumors predominate and longer disease trajectories are expected due to the patient age resulting in a natural history and treatment paradigm that is complex and controversial. Objectives The aims of this study were to describe a large, single-institution series of pediatric pituitary adenomas with extensive long-term follow-up and to conduct a systematic review examining outcomes after pituitary adenoma surgery in the pediatric population. Methods The study cohort was compiled by searching institutional pathology and operative reports using diagnosis and site codes for pituitary and sellar pathology, from 1956 to 2016. Systematic review of the English language literature since 1970 was conducted using PubMed, MEDLINE, Embase, and Google Scholar. Results Thirty-nine surgically managed pediatric pituitary adenomas were identified, including 15 prolactinomas, 14 corticotrophs, 7 somatotrophs, and 4 non-secreting adenomas. All patients underwent transsphenoidal resection (TSR) as the initial surgical treatment. Surgical cure was achieved in 18 (46%); 21 experienced recurrent/persistent disease, with secondary treatments including repeat surgery in 10, radiation in 14, adjuvant pharmacotherapy in 11, and bilateral adrenalectomy in 3. At the last follow-up (median 87 months, range 3–581), nine remained with recurrent/persistent disease (23%).Thirty-seven publications reporting surgical series of pediatric pituitary adenomas were included, containing 1,284 patients. Adrenocorticotropic hormone (ACTH)-secreting tumors were most prevalent (43%), followed by prolactin (PRL)-secreting (37%), growth hormone (GH)-secreting (12%), and nonsecreting (7%). Surgical cure was reported in 65%. Complications included pituitary insufficiency (23%), permanent visual dysfunction (6%), chronic diabetes insipidus (DI) (3%), and postoperative cerebrospinal fluid (CSF) leak (4%). Mean follow-up was 63 months (range 0–240), with recurrent/persistent disease reported in 18% at the time of last follow-up. Conclusion Pediatric pituitary adenomas are diverse and challenging tumors with complexities far beyond those encountered in the management of routine adult pituitary disease, including nuanced decision-making, a technically demanding operative environment, high propensity for recurrence, and the potentially serious consequences of hypopituitarism with respect to fertility and growth potential in a pediatric population. Optimal treatment requires a high degree of individualization, and patients are most likely to benefit from consolidated, multidisciplinary care in highly experienced centers.

The Okamoto spontaneously hypertensive rat (SHR) has been reported to have altered phosphate metabolism. Hypophosphaturia in the presence of increased serum parathyroid hormone (PTH) levels has been reported in the SHR. Therefore it has been postulated that the SHR may be hyporesponsive to the phosphaturic effect of endogenous PTH. In addition, the SHR exhibits enhanced renal sympathetic nerve activity. Recent studies demonstrated that stimulation of the renal adrenoreceptors decreases the phosphaturic response to PTH infusion. Thus a hyporesponsiveness to PTH in the SHR may be due in part to higher renal sympathetic tone. The present study determined the phosphaturic effect of a pharmacological dose of PTH (33 U/kg bolus and 1 U.kg-1.min-1 infusion) in the thyroparathyroidectomized SHR compared with its normotensive control, the Wistar Kyoto (WKY) rat. Three groups of clearance experiments were performed on male 10- to 14-wk-old SHR and WKY rats. In the first group of rats, the fractional excretion of phosphate (FEPi) in response to PTH infusion was 35.4 +/- 4.2% in the SHR (n = 6) and 26.2 +/- 3.0% in the WKY rat (n = 6), NS. In the second group, all animals underwent acute unilateral renal denervation (DNX). The FEPi in response to PTH was 35.3 +/- 1.5% in the innervated (INN) kidney of the SHR (n = 10) compared with 27.9 +/- 2.5% in the INN kidney of the WKY rat (n = 11), and 39.1 +/- 1.9% in the DNX kidney of the SHR compared with 30.5 +/- 2.0% in the DNX kidney of the WKY rat.(ABSTRACT TRUNCATED AT 250 WORDS)

his study was designed to characterize left ventricular (LV) function and mass in a modified cardiomyopathy model in the dog in which right ventricular pacing rates are gradually increased throughout 38 days. On the last day of the pacing protocol, ejection fraction was reduced (25 +/- 3 vs. 60 +/- 1%) and LV end-diastolic diameter index (a ratio of LV end-diastolic diameter to body weight, 2.09 +/- 0.02 vs. 1.79 +/- 0.08 mm/kg) and LV mass index (a ratio of LV mass to body weight, 5.2 +/- 0.3 vs. 4.3 +/- 0.2 g/kg) were greater than in the normal dogs (P < 0.05, respectively). Cardiac filling pressures increased, and LV diastolic function and coronary blood flow were impaired. After 4 wk of recovery from the progressive pacing protocol, LV end-diastolic diameter index (2.12 +/- 0.06 mm/kg) and LV mass index (5.6 +/- 0.2 g/kg) remained increased. Ejection fraction was improved (38 +/- 4%) but still depressed. LV diastolic function, coronary blood flow, and cardiac filling pressures returned to levels seen in the normal dogs. This modified cardiomyopathy model associated with LV hypertrophy complements the conventional tachycardia-induced cardiomyopathy model without LV hypertrophy.

The objective of this study was to examine the effect of NG-monomethyl-L-arginine (L-NMMA) on phosphate excretion in the presence and absence of parathyroid hormone (PTH). Renal clearances were obtained before and during infusion of L-NMMA (15 mg/kg bolus and 500 micrograms.kg-1.min-1 infusion) in Sprague-Dawley rats with intact parathyroid glands (n = 6), in thyroparathyroidectomized (TPTX) rats receiving a constant infusion of PTH-(1-34) (0.01-0.03 U.kg-1.min-1) (n = 11) throughout the experiment, or in TPTX rats, that received an acute infusion of PTH-(1-34) (33 U/kg bolus and 1 U.kg-1.min-1 infusion) after L-NMMA infusion alone (n = 7). In rats with intact parathyroid glands, L-NMMA increased the fractional excretions of phosphate (FEPi) and sodium (FENa) and mean arterial pressure (MAP) (delta 8.6 +/- 1.5%, delta 0.62 +/- 0.1%, and delta 26.7 +/- 4.9 mmHg, respectively; P < 0.05). In TPTX rats receiving a constant infusion of PTH, L-NMMA again increased FEPi, FENa, and MAP (delta 9.5 +/- 3.6%, delta 1.1 +/- 0.4%, and delta 28.4 +/- 4.5 mmHg, respectively; P < 0.05). However, in TPTX rats, L-NMMA alone did not increase FEPi (delta 0.9 +/- 0.3%), whereas the subsequent infusion of PTH with L-NMMA increased FEPi (delta 15.6 +/- 3.1%; P < 0.05). In an additional group of intact and TPTX rats, the fractional excretion of lithium (FELi) was measured as an index of proximal reabsorption. L-NMMA increased FELi in intact rats (delta 13.2 +/- 2.6%; P < 0.05), but not in TPTX rats (delta 4.2 +/- 3.3%). In conclusion, L-NMMA increases phosphate excretion in association with increases in MAP and FENa, and this phosphaturic effect is dependent on the presence of PTH.

In vivo panoramic imaging of regional cortical blood flow and intracellular brain pH with umbelliferone fluorescence was performed in fasted New Zealand White rabbits (n = 30) subjected to constant or stepwise increases in arterial PCO2 (PaCO2) up to 160 mmHg under 1.0% halothane anesthesia. At a PaCO2 of 40 mmHg, baseline brain pHi measured 7.03 +/- 0.04, while regional cortical blood flow was 47.0 +/- 4.3 ml.100 g-1.min-1. With an immediate but constant exposure to a PaCO2 of 60, 80, or 120 mmHg, at 15 min pHi fell to 6.94 +/- 0.03, 6.89 +/- 0.03, and 6.90 +/- 0.03 and recovered over 20, 80, and 120 min, respectively. At 160 mmHg PaCO2, pHi fell to 6.68 +/- 0.04 and remained acidotic. With stepwise increases in PaCO2 up to 80 mmHg, brain pHi decreased from 7.01 +/- 0.02 to 6.99 +/- 0.02, not significantly different despite a severe systemic acidosis of 7.022 +/- 0.034. At a PaCO2 of 120 and 160 mmHg, pHi dropped to 6.97 +/- 0.02 and 6.93 +/- 0.02, respectively. The difference in brain pHi between an immediate and stepwise exposure to a PaCO2 of 160 mmHg was significant (P < 0.005). These results demonstrate that brain pHi is tightly regulated across the cortical surface and resistant to profound changes in extracellular pH. The difference in pHi between the constant and incremental increases in PaCO2 suggests that there is upregulation of pH homeostatic mechanisms.

β-Adrenergic hyporesponsiveness in congestive heart failure (CHF) is mediated, in part, by nitric oxide (NO). NO and brain natriuretic peptide (BNP) share cGMP as a second messenger. Left ventricular (LV) function and inotropic response to intravenous dobutamine (Dob) were assessed during sequential intracoronary infusion of saline, HS-142-1 (a BNP receptor antagonist), and HS-142-1 + NG-monomethyl-l-arginine (l-NMMA) in anesthetized dogs with CHF due to rapid pacing and in normal dogs during intracoronary infusion of saline, exogenous BNP, and sodium nitroprusside (SNP). In CHF dogs, intracoronary HS-142-1 did not alter the inotropic response to Dob [percent change in first derivative of LV pressure (%ΔdP/d t) 47 ± 4% saline vs. 54 ± 7% HS-142-1, P = not significant]. Addition of intracoronary l-NMMA to HS-142-1 enhanced the response to Dob (%ΔdP/d t 73 ± 8% l-NMMA + HS-142-1, P < 0.05 vs. H142-1). In normal dogs, intracoronary SNP blunted the inotropic response to Dob (%ΔdP/d t 93 ± 6% saline vs. 71 ± 5% SNP, P < 0.05), whereas intracoronary BNP had no effect. In CHF dogs, the time constant of LV pressure decay during isovolumic relaxation increased with intracoronary HS-142-1 (48 ± 4 ms saline vs. 58 ± 5 ms HS-142-1, P < 0.05) and further increased with intracoronary l-NMMA (56 ± 6 ms HS-142-1 vs. 66 ± 7 ms l-NMMA + HS-142-1, P < 0.05). Endogenous BNP and NO preserve diastolic function in CHF, whereas NO but not BNP inhibits β-adrenergic responsiveness.

The effects on myocardial function and loading conditions of clinically relevant doses of the natriuretic peptides (NP) have not been established. The actions of single doses (100 ng ⋅ kg−1⋅ min−1iv over 30 min) of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) were studied in conscious normal dogs and in dogs with pacing-induced heart failure. All three NP reduced end-diastolic pressure in normal dogs, and ANP and BNP reduced end-diastolic volume. In heart failure ANP and BNP reduced EDP, and ANP reduced EDV. Arterial elastance was unchanged in normal dogs and in dogs with heart failure. ANP increased end-systolic elastance ( Ees) in normal dogs, whereas BNP tended to increase Ees( P = 0.06). In dogs with heart failure, no inotropic effect was seen. In normal dogs, all NP reduced the time constant of isovolumic relaxation (τ), and ANP and BNP reduced τ in dogs with heart failure. Increases in plasma cGMP in dogs with heart failure were blunted. The NP reduced preload and enhanced systolic and diastolic function in normal dogs. Effects of ANP and BNP on preload and diastolic function were maintained in heart failure. Lack of negative inotropic effects in heart failure supports the validity of the NP as therapeutic agents.

Myocardial actions of the vasodilator peptide adrenomedullin (ADM) in the intact animal are unknown. Negative and positive inotropic actions have been reported in ex vivo experiments. Myocardial and load-altering actions of ADM in dogs before and after development of heart failure were studied. With controlled heart rate (atrial pacing) and after β-blockade, ADM was administered to five normal dogs in doses of 20 ng · kg−1 · min−1iv, 100 ng · kg−1 · min−1iv, and 200 ng · kg−1 · min−1into the left ventricle (LV). LV peak systolic pressure and end-systolic volume decreased with each dose of ADM. End-systolic pressure decreased with the two higher doses. At the highest dose, arterial elastance and the time constant of LV isovolumic relaxation (τ) decreased, and LV end-systolic elastance ( Ees) increased. LV end-diastolic pressure and volume were unchanged. In five additional normal dogs receiving only the highest dose of ADM (200 ng · kg−1 · min−1intra-LV), to control for increased heart rate and sympathetic activation observed with the cumulative infusion, ADM produced arterial vasodilation but no change in Eesor τ. In four dogs with pacing-induced heart failure, ADM (200 ng · kg−1 · min−1intra-LV) was without effect on τ, Ees, and systolic or diastolic pressure and volume. In vivo, ADM appears to be a selective arterial dilator without inotropic or lusitropic effects. The vasodilatory actions are attenuated in heart failure.