Pathologist workforce in the United States: I. Development of a predictive model to examine factors influencing supply.

CONTEXT: Results of prior pathology workforce surveys have varied between a state of equilibrium and predictions of shortage. OBJECTIVE: To assess the current and future supply of pathologists, and apply a dynamic modeling tool for assessing the effects of changing market forces and emerging technologies on the supply of pathologists' services through 2030. DESIGN: Data came from various sources, including the literature, College of American Pathologists' internal data, and primary research through custom-developed surveys for the membership and for pathology practice managers RESULTS: Through 2010, there were approximately 18 000 actively practicing pathologists in the United States (5.7 per 100 000 population), approximately 93% of whom were board certified. Our model projects that the absolute and per capita numbers of practicing pathologists will decrease to approximately 14 000 full-time equivalent (FTE) pathologists or 3.7 per 100 000 in the coming 2 decades. This projection reflects that beginning in 2015, the numbers of pathologists retiring will increase precipitously, and is anticipated to peak by 2021. Including all types of separation, the net pathologist strength will begin falling by year 2015. Unless workforce entry or exit rates change, this trend will continue at least through 2030. These changes reflect the closure of many training programs 2 to 4 decades ago and the substantially decreased number of graduating residents. CONCLUSIONS: This comprehensive analysis predicts that pathologist numbers will decline steadily beginning in 2015. Anticipated population growth in general and increases in disease incidence owing to the aging population, to be presented in a companion article on demand, will lead to a net deficit in excess of more than 5700 FTE pathologists. To reach the projected need in pathologist numbers of nearly 20 000 FTE by 2030 will require an increase from today of approximately 8.1% more residency positions. We believe a pathologist shortage will negatively impact both patient access to laboratory services and health care providers' abilities to deliver more effective health care to their patient populations.

Elective appendectomy at the time of cesarean delivery: a randomized controlled trial.

OBJECTIVE: The purpose of this study was to compare postoperative morbidity in patients who underwent cesarean delivery with and without elective appendectomy. STUDY DESIGN: Subjects who underwent cesarean delivery were assigned randomly by computer-generated randomization to either standard cesarean delivery or cesarean delivery with appendectomy. Primary variables that were measured were operative times and markers of morbidity. Secondary outcome was appendiceal pathologic condition. RESULTS: Ninety-three subjects whose condition required cesarean delivery from July 2002 to May 2006 were enrolled (control subjects, 48; active subjects, 45). Operative time in the study group was increased by 8.8 minutes (P < or = .028). Postoperative morbidity findings were similar. Pathologic evaluation revealed 9 abnormalities that included acute appendicitis in 2 patients. CONCLUSION: Elective appendectomy at the time of cesarean delivery does not increase inpatient morbidity. Consideration can be given safely to elective appendectomy at the time of cesarean delivery in selected cases, such as women with palpable fecaliths and/or an abnormal appearing appendix, a history of pelvic pain, endometriosis, or anticipated intraabdominal adhesions.

Delta creatine kinase-MB outperforms myoglobin at two hours during the emergency department identification and exclusion of troponin positive non-ST-segment elevation acute coronary syndromes.

STUDY OBJECTIVE: Limited information is available about the diagnostic performance of creatine kinase (CK)-MB and myoglobin levels during the early evaluation of chest pain patients using cardiac troponins as the criterion standard for diagnosing acute myocardial infarction. In this study, we compare the sensitivity and specificity of the baseline, 2-hour absolute, and 2-hour delta values of myoglobin and CK-MB mass assay for detection of acute myocardial infarction using cardiac troponin I (troponin) as the sole marker of myocardial necrosis. METHODS: A prospective observational study was conducted of 975 chest pain patients with a baseline troponin level of 1.0 ng/mL or less (Abbott Axsym Assay) and an initial ECG nondiagnostic for injury. CK-MB, myoglobin, and troponin levels were all measured on the Abbott Axsym immunoassay. Acute myocardial infarction was diagnosed if there was at least 20 minutes of chest pain and any one of the following criteria within 24 hours of ED presentation: a serial increase in troponin to more than 1.0 ng/mL, new Q-wave formation in 2 contiguous leads, or patient death by cardiac or unknown cause. The optimal values of CK-MB and myoglobin were chosen at the most accurate value on the receiver operating characteristic (ROC) curve (ie, value with lowest false-negative and false-positive rate) of the 2-hour absolute and 2-hour delta value for predicting acute myocardial infarction. RESULTS: Acute myocardial infarction was diagnosed in 44 (4.5%) of the 975 study patients. ROC curve analysis revealed no statistically significant differences in areas for myoglobin and CK-MB values at baseline and 2 hours for determination of acute myocardial infarction. However, the ROC curve area of the delta CK-MB level significantly outperformed the ROC curve area of the delta myoglobin level for early identification of acute myocardial infarction (0.97 versus 0.81; 95% confidence interval [CI] for difference between areas 0.09 to 0.24). At the most accurate cutoff value, a 2-hour delta CK-MB level more than 0.7 ng/mL had a sensitivity of 93.2% (95% CI 81.3% to 98.5%), a specificity of 94.4% (95% CI 92.7% to 95.8%), a positive likelihood ratio of 16.7, and a negative likelihood ratio of 0.07. CONCLUSION: A 2-hour delta CK-MB level outperforms myoglobin level in the early identification and exclusion of acute myocardial infarction in non-ST-segment elevation chest pain patients. This finding suggests that myoglobin may no longer be the optimal early marker of acute myocardial infarction when troponins are used as the criterion standard.

The Erlanger chest pain evaluation protocol: a one-year experience with serial 12-lead ECG monitoring, two-hour delta serum marker measurements, and selective nuclear stress testing to identify and exclude acute coronary syndromes.

STUDY OBJECTIVE: We determine the overall use of a 6-step accelerated chest pain protocol to identify and exclude acute coronary syndrome (ACS) and to confirm previous findings of the use of serial 12-lead ECG monitoring (SECG) in conjunction with 2-hour delta serum marker measurements to identify and exclude acute myocardial infarction (AMI). METHODS: A prospective observational study was conducted over a 1-year period from January 1, 1999, through December 31, 1999, in 2,074 consecutive patients with chest pain who underwent our accelerated evaluation protocol, which includes 2-hour delta serum marker determinations in conjunction with automated SECG for the early identification and exclusion of AMI and selective nuclear stress testing for identification and exclusion of ACS. In patients not undergoing emergency reperfusion therapy, physician judgment was used to determine patient disposition at the completion of the 2-hour evaluation period: admit for ACS, discharge or admit for non-ACS condition, or immediate emergency department nuclear stress scan for possible ACS. A positive protocol was defined as a positive result in 1 or more of the 6 incremental steps in our chest pain evaluation protocol: (1) initial ECG diagnostic of acute injury or reciprocal injury; (2) baseline creatine kinase (CK)-MB level of 10 ng/mL or greater and index of 5% or greater or cardiac troponin I level of 2 ng/mL or greater; (3) new/evolving injury or new/evolving ischemia on SECG; (4) increase in CK-MB level of +1.5 ng/mL or greater or cardiac troponin I level of +0.2 ng/mL or greater in 2 hours; (5) clinical diagnosis of ACS despite a negative 2-hour evaluation; and (6) reversible perfusion defect on stress scan compared with on resting scan. All patients were followed up for 30-day ACS, which was defined as myocardial infarction (MI), percutaneous coronary intervention/coronary artery bypass grafting, coronary arteriography revealing stenosis of major coronary artery of 70% or greater not amenable to percutaneous coronary intervention/coronary artery bypass grafting, life-threatening complication, or cardiac death within 30 days of ED presentation. RESULTS: Discharge diagnosis in the 2,074 study patients consisted of 179 (8.6%) patients with AMI, 26 (1.3%) patients with recent AMI (decreasing curve of CK-MB), and 327 (15.8%) patients with 30-day ACS. At 2 hours, sensitivity and specificity for MI (AMI or recent AMI) of SECG plus delta serum marker measurements was 93.2% and 93.9%, respectively (positive likelihood ratio 15.3; negative likelihood ratio 0.07). At the completion of the full ED evaluation protocol (positive result in >or=1 of the 6 incremental steps), sensitivity and specificity for 30-day ACS was 99.1% and 87.4%, respectively (positive likelihood ratio 7.9; negative likelihood ratio 0.01). CONCLUSION: An accelerated chest pain evaluation strategy consisting of SECG, 2-hour delta serum marker measurements, and selective nuclear stress testing in conjunction with physician judgment identifies and excludes MI and 30-day ACS during the initial evaluation of patients with chest pain.