Pediatric neurosurgery through the lens of time-driven activity-based costing: a pilot study.

OBJECTIVE: Time-driven activity-based costing (TDABC) is a method used in cost accounting that has gained traction in health economics to identify value optimization initiatives. It measures time, assigns value to time increments spent on a patient, and integrates the cost of material and human resources utilized in each episode of care. In this study, the authors report the first use of TDABC to evaluate costs in a pediatric neurosurgical practice. METHODS: A clinical pathway was developed with a multifunction team. A time survey among each care team member, including surgeons, medical assistants (MAs), and patient service representatives (PSRs), was carried out prospectively over a 10-week period at a pediatric neurosurgery clinic. Consecutive patient encounters for Chiari malformation (CM), hydrocephalus, or tethered cord syndrome (TCS) were included. Encounters were categorized as new or established. Relative annual personnel costs, using the salary of a PSR as a reference (i.e., 1.0-unit cost), were calculated for all members using departmental financial data after adjustments. The relative capacity cost rates (minute-1) for each personnel, a representation of per capita cost per minute, were then derived, and the relative costs per visit were calculated. RESULTS: A total of 110 visits (24 new, 86 established) were captured, including 40% CM, 41% hydrocephalus, and 19% TCS encounters. Surgeons had the highest relative capacity cost rate (118.4 × 10-6), more than 10-fold higher than that of an MA or PSR (10.65 × 10-6 and 9.259 × 10-6, respectively). Surgeons also logged more time with patients compared with the rest of the care team in nearly all visits (p ≤ 0.002); consequently, the total visit costs were primarily driven by the surgeon cost (p < 0.0001). Overall, surgeon cost constituted the vast majority of the total visit cost (92%-93%), regardless of whether the visits were new or established. Visit costs did not differ by diagnosis. On average, new visits took longer than established visits (p < 0.001). This difference was largely driven by new CM visits (44.3 ± 13.7 minutes), which were significantly longer than established CM visits (29.8 ± 9.2 minutes; p = 0.001). CONCLUSIONS: TDABC may reveal opportunities to maximize value by highlighting instances of variability and high cost in each module of care delivery. Physician leaders in pediatric neurosurgery may be able to use this information to allocate costs and streamline value care pathways.

TrkB-mediated sustained neuroprotection is sex-specific and Erα-dependent in adult mice following neonatal hypoxia ischemia.

BACKGROUND: Neonatal hypoxia ischemia (HI) related brain injury is one of the major causes of life-long neurological morbidities that result in learning and memory impairments. Evidence suggests that male neonates are more susceptible to the detrimental effects of HI, yet the mechanisms mediating these sex-specific responses to neural injury in neonates remain poorly understood. We previously tested the effects of treatment with a small molecule agonist of the tyrosine kinase B receptor (TrkB), 7,8-dihydroxyflavone (DHF) following neonatal HI and determined that females, but not males exhibit increased phosphorylation of TrkB and reduced apoptosis in their hippocampi. Moreover, these female-specific effects of the TrkB agonist were found to be dependent upon the expression of Erα. These findings demonstrated that TrkB activation in the presence of Erα comprises one pathway by which neuroprotection may be conferred in a female-specific manner. The goal of this study was to determine the role of Erα-dependent TrkB-mediated neuroprotection in memory and anxiety in young adult mice exposed to HI during the neonatal period. METHODS: In this study, we used a unilateral hypoxic ischemic (HI) mouse model. Erα+/+ or Erα-/- mice were subjected to HI on postnatal day (P) 9 and mice were treated with either vehicle control or the TrkB agonist, DHF, for 7 days following HI. When mice reached young adulthood, we used the novel object recognition, novel object location and open field tests to assess long-term memory and anxiety-like behavior. The brains were then assessed for tissue damage using immunohistochemistry. RESULTS: Neonatal DHF treatment prevented HI-induced decrements in recognition and location memory in adulthood in females, but not in males. This protective effect was absent in female mice lacking Erα. The female-specific improved recognition and location memory outcomes in adulthood conferred by DHF therapy after neonatal HI tended to be or were Erα-dependent, respectively. Interestingly, DHF triggered anxiety-like behavior in both sexes only in the mice that lacked Erα. When we assessed the severity of injury, we found that DHF therapy did not decrease the percent tissue loss in proportion to functional recovery. We additionally observed that the presence of Erα significantly reduced overall HI-associated mortality in both sexes. CONCLUSIONS: These observations provide evidence for a therapeutic role for DHF in which TrkB-mediated sustained recovery of recognition and location memories in females are Erα-associated and dependent, respectively. However, the beneficial effects of DHF therapy did not include reduction of gross tissue loss but may be derived from the enhanced functioning of residual tissues in a cell-specific manner.

Periods of low oxygen delivery and blood flow to the brains of newborns are known to cause life-long impairments to their cognitive ability as adults. Interestingly, male newborns are more susceptible to this injury than females. The mechanisms causing this sex difference are poorly understood. Here we test the role of the nerve growth factor receptor tyrosine kinase B (TrkB) in providing long-term neuroprotection following neonatal hypoxia­ischemia (HI) in mice. We have previously shown that when mice are treated with the TrkB agonist 7,8-dihydroxyflavone (DHF) in the days following neonatal HI, the result is short-term neuroprotection only in females and this protection is dependent on the presence of the estrogen receptor alpha receptor ([Formula: see text]). In this study, we extend these observations by subjecting mice either with or without [Formula: see text] to HI. Some of the mice were then treated with DHF immediately after HI. As adults, we performed tests to assess the mice's memory and anxiety-like behavior. At the end of these tests, we assessed the brains for tissue loss. Our results show that as adults the DHF treatment following HI in neonatal mice preserved memory only in females and this effect was dependent on the presence of [Formula: see text]. In addition, DHF therapy triggered anxiety-like behavior in mice lacking [Formula: see text]. We also show that this neuroprotection is not dependent on preservation of brain tissue following the injury. These results provide insight into the mechanisms behind the female resistance to hypoxic ischemic episodes as newborns.

A Novel Approach for Free, Affordable, and Sustainable Microsurgery Laboratory Training for Low- and Middle-Income Countries: University of Wisconsin-Madison Microneurosurgery Laboratory Experience.

BACKGROUND AND OBJECTIVES: In low- and middle-income countries (LMICs), approximately 5 million essential neurosurgical operations per year remain unaddressed. When compared with high-income countries, one of the reasons for this disparity is the lack of microsurgery training laboratories and neurosurgeons trained in microsurgical techniques. In 2020, we founded the Madison Microneurosurgery Initiative to provide no-cost, accessible, and sustainable microsurgery training opportunities to health care professionals from LMICs in their respective countries. METHODS: We initially focused on enhancing our expertise in microsurgery laboratory training requirements. Subsequently, we procured a wide range of stereo microscopes, light sources, and surgical instrument sets, aiming to develop affordable, high-quality, and long-lasting microsurgery training kits. We then donated those kits to neurosurgeons across LMICs. After successfully delivering the kits to designated locations in LMICs, we have planned to initiate microsurgery laboratory training in these centers by providing a combination of live-streamed, offline, and in-person training assistance in their institutions. RESULTS: We established basic microsurgery laboratory training centers in 28 institutions across 18 LMICs. This was made possible through donations of 57 microsurgery training kits, including 57 stereo microscopes, 2 surgical microscopes, and several advanced surgical instrument sets. Thereafter, we organized 10 live-streamed microanastomosis training sessions in 4 countries: Lebanon, Paraguay, Türkiye, and Bangladesh. Along with distributing the recordings from our live-streamed training sessions with these centers, we also granted them access to our microsurgery training resource library. We thus equipped these institutions with the necessary resources to enable continued learning and hands-on training. Moreover, we organized 7 in-person no-cost hands-on microanastomosis courses in different institutions across Türkiye, Georgia, Azerbaijan, and Paraguay. A total of 113 surgical specialists successfully completed these courses. CONCLUSION: Our novel approach of providing microsurgery training kits in combination with live-streamed, offline, and in-person training assistance enables sustainable microsurgery laboratory training in LMICs.