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The impact of the reserve military neurosurgeon: practice, community, and service

Richard Menger, Benjamin F. Mundell, J. Will Robbins, Peter Letarte, Randy Bell, and in conjunction with Council of State Neurosurgical Societies and AANS/CNS Joint Committee of Military Neurosurgeons

OBJECTIVE

Papers from 2002 to 2017 have highlighted consistent unique socioeconomic challenges and opportunities facing military neurosurgeons. Here, the authors focus on the reserve military neurosurgeon who carries the dual mission of both civilian and military responsibilities.

METHODS

Survey solicitation of current active duty and reserve military neurosurgeons was performed in conjunction with the AANS/CNS Joint Committee of Military Neurosurgeons and the Council of State Neurosurgical Societies. Demographic, qualitative, and quantitative data points were compared between reserve and active duty military neurosurgeons. Civilian neurosurgical provider data were taken from the 2016 NERVES (Neurosurgery Executives Resource Value and Education Society) Socio-Economic Survey. Economic modeling was done to forecast the impact of deployment or mobilization on the reserve neurosurgeon, neurosurgery practice, and the community.

RESULTS

Seventy-five percent (12/16) of current reserve neurosurgeons reported that they are satisfied with their military service. Reserve neurosurgeons make significant contributions to the military’s neurosurgical capabilities, with 75% (12/16) having been deployed during their career. No statistically significant demographic differences were found between those serving on active duty and those in the reserve service. However, those who served in the reserves were more likely to desire opportunities for improvement in the military workflow requirements compared with their active duty counterparts (p = 0.04); 92.9% (13/14) of current reserve neurosurgeons desired more flexible military drill programs specific to the needs of practicing physicians. The risk of reserve deployment is also borne by the practices, hospitals, and communities in which the neurosurgeon serves in civilian practice. This can result in fewer new patient encounters, decreased collections, decreased work relative value unit generation, increased operating costs per neurosurgeon, and intangible limitations on practice development. However, through modeling, the authors have illustrated that reserve physicians joining a larger group practice can significantly mitigate this risk. What remains astonishing is that 91.7% of those reserve neurosurgeons who were deployed noted the experience to be rewarding despite seeing a 20% reduction in income, on average, during the fiscal year of a 6-month deployment.

CONCLUSIONS

Reserve neurosurgeons are satisfied with their military service while making substantial contributions to the military’s neurosurgical capabilities, with the overwhelming majority of current military reservists having been deployed or mobilized during their reserve commitments. Through the authors’ modeling, the impact of deployment on the military neurosurgeon, neurosurgeon’s practice, and the local community can be significantly mitigated by a larger practice environment.

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Hemin: levels in experimental subarachnoid hematoma and effects on dissociated vascular smooth-muscle cells

Peter B. Letarte, Kristine Lieberman, Kazuhiko Nagatani, Robert A. Haworth, Gerard B. Odell, and Thomas A. Duff

✓ Although hemin is known to exert toxic effects on a variety of cell types, its possible participation in the genesis of cerebral vasospasm has received little attention. The authors measured the concentration of hemin in experimental subarachnoid clot and studied its effects on the morphology and 45Ca++ uptake of vascular smooth-muscle cells dissociated from canine carotid artery.

Craniectomies were performed in five dogs under general anesthesia, and 3 to 5 ml of autologous whole blood was deposited in the supraclinoid subarachnoid compartment. The concentration of hemin recovered by Folch extraction from clotted material removed 7 days after surgery was 390 ± 247 µM (mean ± standard error of the mean). Mean vascular smooth-muscle cell length after 40 minutes of exposure to 50 µM hemin was 37.3 ± 1.2 µm (control 51.6 ± 1.6 µm) (p < 0.01). The mean percent permeation of 45Ca++, measured by a dual label technique, of cells exposed to hemin was 200.9% ± 23% (control 102.9% ± 4.3%) (p < 0.01).

These findings indicate that hemin accrues in subarachnoid hematoma, that it exerts a constrictive effect on vascular smooth-muscle cells, and that this effect is associated with an increased uptake of Ca++. This study demonstrates that hemin should be included in the list of potential agents that participate in the development of cerebral vasospasm.

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The effect of hemoglobin and its metabolites on energy metabolism in cultured cerebrovascular smooth-muscle cells

Kazuhiko Nagatani, Jeffery E. Masciopinto, Peter B. Letarte, Robert A. Haworth, and Thomas A. Duff

✓ Cerebral arteries in spasm have been found to contain low levels of adenosine triphosphate (ATP), and it has been postulated that this change in levels results from hypoxia produced by arterial encasement in clotted material. This study was undertaken to determine whether any of four blood-derived agents, ferrous hemoglobin, methemoglobin, hemin, or bilirubin, is capable of reducing energy levels in cerebral artery smooth-muscle cells.

Twenty-four-hour exposure of cultured canine basilar artery cells to ferrous hemoglobin and bilirubin led to a significant decline in ATP levels (to 8.9 nmol/mg protein and 2.8 nmol/mg protein, respectively) versus control (16.6 nmol/mg protein); methemoglobin and hemin showed no effect. Bilirubin but not hemoglobin was found to interfere with electron transport and with creatine phosphokinase activity in intact cells; however, bilirubin showed no inhibitory effect on this enzyme in cell-free conditions. The findings indicate that hemoglobin and bilirubin may be responsible for diminished energy levels in cerebral arteries. These observations also suggest that bilirubin may exert its effect on ATP by impairing mitochondrial function.