Radiology resident competency in detecting basilar artery occlusion: a simulation-based assessment.

PURPOSE: Basilar artery strokes are rare but can have characteristic imaging findings that can often be overlooked. This retrospective study aims to assess radiology residents' ability to identify CT imaging findings of basilar artery occlusion in a simulated call environment. METHODS: The Wisdom in Diagnostic Imaging Emergent/Critical Care Radiology Simulation (WIDI SIM)-a tested and reliable computer-aided emergency imaging simulation-was employed to assess resident readiness for independent radiology call. The simulations include 65 cases of varying complexity, including normal studies, with one case specifically assessing basilar artery stroke. Residents were presented with a single, unique case of basilar artery occlusion in two separate years of testing and were only provided with non-contrast CT images. Residents' free text responses were manually scored by faculty members using a standardized grading rubric, with errors subsequently classified by type. RESULTS: A total of 454 radiology residents were tested in two separate years on the imaging findings of basilar artery occlusion using the Wisdom in Diagnostic Imaging simulation web-based testing platform. Basilar artery occlusion was consistently underdiagnosed by radiology residents being tested for call readiness irrespective of the numbers of years in training. On average, only 14% of radiology residents were able to correctly identify basilar artery occlusion on non-contrast CT. CONCLUSIONS: Our findings underscore a potential gap in radiology residency training related to the detection of basilar artery occlusion, highlighting the potential need for increased educational efforts in this area.

Rhabdomyolysis in McArdle disease caused by scuba diving.

McArdle disease is a glycogen storage disease that results in rhabdomyolysis during intense exercise. A number of different triggers have been described. We evaluated a patient with McArdle disease who presented with rhabdomyolysis after recreational scuba diving. There was no concern for barotrauma or decompression sickness. His symptoms resolved with standard-of-care management for non-diving-related rhabdomyolysis. Features of his experience provoked questions about the diving-related factors contributing to his presentation. We present the case and explore possible mechanisms of diving-related injury in patients with McArdle disease, including the possible effects of hyperoxia, hyperbaria, hypothermia and strenuous activity.

Impact of a focused review course in cardiovascular and thoracic surgery on test performance.

Background: The Core Curriculum Review Course in Cardiovascular and Thoracic Surgery is a 4-day educational program consisting of 77 didactic lectures that provide a comprehensive review of the material required for surgeons preparing for the American Board of Thoracic Surgery competency written examination. The lectures are supplemented with a written syllabus and interactive audience participation system. We sought to determine whether participation in this course could improve participants' performance on a cardiothoracic subject-based test. Methods: Sixty-five participants attended the 2018 course. Before beginning the course lectures, a multiple-choice pretest consisting of 77 questions was administered via mobile application to gauge the participants' baseline knowledge. A second multiple-choice posttest was made available beginning 7 weeks after the course, also by mobile application. Results: Twenty-nine participants completed both the pretest and the posttest. The median pretest score was 47% (36 of 77 correct answers). The median posttest score was 61% (47 of 77 correct answers), representing an increase of 14%. The Wilcoxon signed-rank test indicated a significant difference between the pretest and posttest scores (z = -4.36; P = .00). Overall, 25 participants (86%) improved their posttest score. Conclusions: The core curriculum review course was successful in improving participants' performance on the course tests, indicating that the participants' fund of knowledge was likely increased by attendance at the program. Additional strategies should be considered to address particular areas of study both for individual participants and for residents currently in training.

Alveolar inflation during generation of a quasi-static pressure/volume curve in the acutely injured lung.

OBJECTIVE: Lower and upper inflection points on the quasi-static curve representing a composite of pressure/volume from the whole lung are hypothesized to represent initial alveolar recruitment and overdistension, respectively, and are currently utilized to adjust mechanical ventilation in patients with acute respiratory distress syndrome. However, alveoli have never been directly observed during the generation of a pressure/volume curve to confirm this hypothesis. In this study, we visualized the inflation of individual alveoli during the generation of a pressure/volume curve by direct visualization using in vivo microscopy in a surfactant deactivation model of lung injury in pigs. DESIGN: Prospective, observational, controlled study. SETTING: University research laboratory. SUBJECTS: Eight adult pigs. INTERVENTIONS: Pigs were anesthetized and administered mechanical ventilation, underwent a left thoracotomy, and were separated into two groups: control pigs (n = 3) were subjected to surgical intervention, and Tween lavage pigs (n = 5) were subjected to surgical intervention plus surfactant deactivation by Tween lavage (1.5 mL/kg 5% solution of Tween in saline). The microscope was then attached to the lung, and the size of each was alveolus quantified by measuring the alveolar area by computer image analysis. Each alveolus in the microscopic field was assigned to one of three types, based on alveolar mechanics: type I, no visible change in alveolar size during ventilation; type II, alveoli visibly change size during ventilation but do not totally collapse at end expiration; and type III, alveoli visibly change size during tidal ventilation and completely collapse at end expiration. After alveolar classification, the animals were disconnected from the ventilator and attached to a super syringe filled with 100% oxygen. The lung was inflated from 0 to 220 mL in 20-mL increments with a 10-sec pause between increments for airway pressure and alveolar confirmation to stabilize. These data were utilized to generate both quasi-static pressure/volume curves and individual alveolar pressure/area curves. MEASUREMENTS AND MAIN RESULTS: The normal lung quasi-static pressure/volume curve has a single lower inflection point, whereas the curve after Tween has an inflection point at 8 mm Hg and a second at 24 mm Hg. Normal alveoli in the control group are all type I and do not change size appreciably during generation of the quasi-static pressure/volume curve. Surfactant deactivation causes a heterogenous injury, with all three alveolar types present in the same microscopic field. The inflation pattern of each alveolar type after surfactant deactivation by Tween was notably different. Type I alveoli in either the control or Tween group demonstrated minimal change in alveolar area with lung inflation. Type I alveolar area was significantly (p <.05) larger in the control as compared with the Tween group. In the Tween group, type II alveoli increased significantly in area, with lung inflation from 0 mL (9666 +/- 1340 microm2) to 40 mL (12,935 +/- 1725 microm2) but did not increase further (220 mL, 14,058 +/- 1740 microm2) with lung inflation. Type III alveoli initially recruited with a relatively small area (20 mL lung volume, 798 +/- 797 microm2) and progressively increased in area throughout lung inflation (120 mL, 7302 +/- 1405 microm2; 220 mL, 11,460 +/- 1078 microm2) CONCLUSION: The normal lung does not increase in volume by simple isotropic (balloon-like) expansion of alveoli, as evidenced by the horizontal (no change in alveolar area with increases in airway pressure) pressure/area curve. After surfactant deactivation, the alveolar inflation pattern becomes very complex, with each alveolar type (I, II, and III) displaying a distinct pattern. None of the alveolar pressure/area curves directly parallel the quasi-static lung pressure/volume curve. Of the 16, only one type III atelectatic alveolus recruited at the first inflection point and only five recruited concomitant with the second inflation point, suggesting that neither inflection point was due to inflection point was due to massive alveolar recruitment. Thus, the components responsible for the shape of the pressure/volume curve include all of the individual alveolar pressure/area curves, plus changes in alveolar duct and airway size, and the elastic forces in the pulmonary parenchyma and the chest wall.

Tidal volume increases do not affect alveolar mechanics in normal lung but cause alveolar overdistension and exacerbate alveolar instability after surfactant deactivation.

OBJECTIVE: We utilized microscopy to measure the impact of increasing tidal volume on individual alveolar mechanics (i.e., the dynamic change in alveolar size during tidal ventilation) in the living porcine lung. DESIGN: In three anesthetized, mechanically ventilated pigs, we observed normal alveoli (n = 27) and alveoli after surfactant deactivation by Tween 20 lavage (n = 26) at three different tidal volumes (6, 12, and 15 mL/kg). Alveolar area was measured at peak inspiration (I) and at end expiration (E) by image analysis and I minus E was calculated as an index of alveolar stability (I-Edelta). MEASUREMENTS AND MAIN RESULTS: In normal alveoli, increasing tidal volume did not change alveolar area at I (6 mL/kg = 9726 +/- 848 microm; 15 mL/kg = 9,637 +/- 884 microm ), E (6 mL/kg = 9747 +/- 800 microm; 15 mL/kg = 9742 +/- 853 microm ), or I-Edelta (6 mL/kg = -21 +/- 240 microm; 15 mL/kg = -105 +/- 229 microm ). In contrast, with surfactant deactivation, increasing tidal volume significantly increased alveolar area at I (6 mL/kg = 11,413 +/- 1032 microm; 15 mL/kg = 13,917 +/- 1214 microm ), at E (6 mL/kg = 10,462 +/- 906 microm; 15 mL/kg = 12,000 +/- 1066 microm ), and I-Edelta (6 mL/kg = 825 +/- 276 microm; 15 mL/kg = 1917 +/- 363 microm ). Moreover, alveolar instability (increased I-Edelta) was significantly increased at all tidal volumes with altered surface tension when compared with normal alveoli. CONCLUSIONS: We conclude that high tidal volume ventilation does not alter alveolar mechanics in the normal lung; however, in the surfactant-deactivated lung, it causes alveolar overdistension and exacerbates alveolar instability.

Alveolar mechanics alter hypoxic pulmonary vasoconstriction.

OBJECTIVES: Hypoxic pulmonary vasoconstriction is the primary physiologic mechanism that maintains a proper ventilation/perfusion match, but it fails in diffuse lung injuries such as acute respiratory distress syndrome. Acute respiratory distress syndrome is associated with pulmonary surfactant loss that alters alveolar mechanics (i.e., dynamic change in alveolar size and shape during ventilation), converting normal stable alveoli into unstable alveoli. We hypothesized that alveolar instability stents open pulmonary microvessels and is the mechanism of hypoxic pulmonary vasoconstriction failure associated with acute respiratory distress syndrome. DESIGN: Prospective, randomized, controlled study. SETTING: University research laboratory. SUBJECTS: Ten adult pigs. INTERVENTIONS: Anesthetized ventilated pigs were prepared surgically for hemodynamic monitoring and were subjected to a right thoracotomy. An in vivo microscope was attached to the right lung, and the microvascular response to hypoxia (F(IO(2)), 15%) was measured in a lung with normal stable alveoli and in a lung with unstable alveoli caused by surfactant deactivation (Tween lavage). MEASUREMENTS AND MAIN RESULTS: Alveolar instability, defined as the difference between alveolar area at peak inspiration and end expiration and assessed as a percentage change (I-E Delta%), was significantly increased after Tween (23.9 +/- 3.0, I-E Delta%) compared with baseline (2.4 +/- 1.0, I-E Delta%). Alveolar instability was associated with the following microvascular changes: a) increased vasoconstriction (Tween, 14.9 +/- 1.0%) in response to hypoxia compared with baseline (10.8 +/- 1.2%, p <.05); and b) increased mean vascular diameter (Tween, 41.2 +/- 1.5 microm) compared with the mean diameter at baseline (24.6 +/- 1.0 microm, p <.05). CONCLUSION: Unstable alveoli stent open pulmonary vessels, which may explain the failure of hypoxic pulmonary vasoconstriction in acute respiratory distress syndrome.