Melanie M. Hogg
Carolinas Medical Center
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Featured researches published by Melanie M. Hogg.
Journal of Thrombosis and Haemostasis | 2012
Jeffrey A. Kline; Melanie M. Hogg; D. M. Courtney; Chadwick D. Miller; Alan E. Jones; Howard A. Smithline
Summary. Background: Increasing the threshold to define a positive D‐dimer could reduce unnecessary computed tomographic pulmonary angiography (CTPA) for a suspected pulmonary embolism (PE) but might increase rates of a missed PE and missed pneumonia, the most common non‐thromboembolic diagnosis seen on CTPA.
Journal of Thrombosis and Haemostasis | 2010
D. M. Courtney; Chadwick D. Miller; Howard A. Smithline; N. Klekowski; Melanie M. Hogg; Jeffrey A. Kline
Summary. Background: Emergency physicians rely on the interpretation of radiologists to diagnose and exclude pulmonary embolism (PE) on the basis of computerized tomographic pulmonary angiography (CTPA). Few data exist regarding the interobserver reliability of this endpoint. Objective: To quantify the degree of agreement in CTPA interpretation between four academic hospitals and an independent reference reading (IRR) laboratory. Methods: Hospitalized and emergency department patients who had one predefined symptom and sign of PE and underwent 64‐slice CTPA were enrolled from four academic hospitals. CTPA results as interpreted by board‐certified radiologists from the hospitals were compared against those from the IRR laboratory. CTPAs were read as indeterminate, PE− or PE+, and percentage obstruction was computed by the IRR laboratory, using a published method. Agreement was calculated with weighted Cohen’s kappa. Results: We enrolled 492 subjects (63% female, age 54 ± 1 years, and 16.7% PE+ at the site hospitals). Overall agreement was 429/492 (87.2%; 95% confidence interval 83.9–90.0). We observed 13 cases (2.6%) of complete discordance, where one reading was PE+ and the other reading was PE−. Weighted agreement was 92.3%, with kappa = 0.75. The median percentage obstruction for all patients was 9% (25th–75th percentile interquartile range: 5% to − 30%). For CTPAs interpreted at the site hospitals as PE− or indeterminate but read as PE+ by the IRR laboratory, the median of percentage obstruction was 6% (4–7%). Conclusion: We found in this sample a good level of agreement, with a weighted kappa of 0.75, but with 2.6% of patients having total discordance. Overall, a large proportion of clots were distal or minimally occlusive clots.
Journal of Thrombosis and Haemostasis | 2009
Jeffrey A. Kline; M. R. Marchick; Melanie M. Hogg
1 Douketis JD, Gu C, Piccioli A, Ghirarduzzi A, Pengo V, Prandoni P. The long-term risk of cancer in patients with a first episode of venous thromboembolism. J Thromb Haemost 2009; 7: 546–51. 2 Akl EA, vanDoormaal FF, BarbaM,KamathG,Kim SY,Kuipers S, Middeldorp S, Yosuico V, Dickinson HO, Schünemann HJ. Parenteral anticoagulation for prolonging survival in patients with cancer who have no other indication for anticoagulation. Cochrane Database Syst Rev 2007; CD006652. 3 Niers TMH, Brüggemann LW, Klerk CPW, Muller FMJ, Buckle T, Reitsma PH, Richel DJ, Spek CA, van Tellingen O, Van Noorden CJF. Differential effects of anticoagulants on tumor development of mouse cancer cell lines B16, K1735 and CT26 in lung. Clin Exp Metastasis 2009; 26: 171–8. 4 Feistritzer C, Riewald M. Endothelial barrier protection by activated protein C through PAR1-dependent sphingosine 1-phosphate receptor-1 cross-activation. Blood 2005; 105: 3178–84. 5 Klerk CPW, Niers TMH, Brüggeman LW, Smorenburg SM, Richel DJ, Spek CA, Van Noorden CJF. Prophylactic plasma levels of the low molecular weight heparin nadroparin do not affect colon cancer tumor development in mouse liver. Thromb Res 2009; doi:10.1016/j.thromres.2009.03.005. 6 Hu L, Lee M, Campbell W, Perez-Soler R, Karpatkin S. Role of endogenous thrombin in tumor implantation, seeding and spontaneous metastasis. Blood 2004; 104: 2746–51. 7 Amirkhosravi A, Mousa SA, Amaya M, Francis JL. Antimetastatic effect of tinzaparin, a low-molecular-weight heparin. J Thromb Haemost 2003; 1: 1972–6. 8 Stevenson JL, Choi SH, Varki A. Differential metastasis inhibition by clinically relevant levels of heparin – correlation with selectin inhibition, not antithrombotic activity. Clin Cancer Res 2005; 11: 7003–11. 9 Weitz JI. A novel approach to thrombin inhibition. Thromb Res 2003; 109 (Suppl. 1): S17–22. 10 Buller HR, Sohne M, Middeldorp S. Treatment of venous thromboembolism. J Thromb Haemost 2005; 3: 1554–60. 11 Nierodzik ML, Plotkin A, Kajumo F, Karpatkin S. Thrombin stimulates tumor–platelet adhesion in vitro and metastasis in vivo. J Clin Invest 1991; 87: 229–36. 12 Palumbo JS, Barney KA, Blevins EA, ShawMA,Mishra A, FlickMJ, Kombrinck KW, Talmage KE, Souri M, Ichinose A, Degen JL. Factor XIII transglutaminase supports hematogenous tumor cell metastasis through a mechanism dependent on natural killer cell function. J Thromb Haemost 2008; 6: 812–19. 13 Brüggemann LW, Versteeg HH, Niers TM, Reitsma PH, Spek CA. Experimental melanoma metastasis in lungs of mice with congenital coagulation disorders. J Cell Mol Med 2008; 12: 2622–7. 14 Sciumbata T, Caretto P, Pirovana P, Pozzi P, Cremonesi P, Galimberti G, Leoni F, Marcucci F. Treatment with modified heparins inhibits experimental metastasis formation and leads, in some animals, to longterm survival. Invasion Metastasis 1996; 16: 132–43. 15 Crissman JD, Hatfield J, Schaldenbrand M, Sloane BF, Honn KV. Arrest and extravasation of B16 amelanotic melanoma in murine lungs. A light and electron microscopic study. Lab Invest 1985; 53: 470–8.
Circulation-cardiovascular Imaging | 2014
Jeffrey A. Kline; Alan E. Jones; Nathan I. Shapiro; Jackeline Hernandez; Melanie M. Hogg; R. Darrel Nelson
Background—Use of pretest probability can reduce unnecessary testing. We hypothesize that quantitative pretest probability, linked to evidence-based management strategies, can reduce unnecessary radiation exposure and cost in low-risk patients with symptoms suggestive of acute coronary syndrome and pulmonary embolism. Methods and Results—This was a prospective, 4-center, randomized controlled trial of decision support effectiveness. Subjects were adults with chest pain and dyspnea, nondiagnostic ECGs, and no obvious diagnosis. The clinician provided data needed to compute pretest probabilities from a Web-based system. Clinicians randomized to the intervention group received the pretest probability estimates for both acute coronary syndrome and pulmonary embolism and suggested clinical actions designed to lower radiation exposure and cost. The control group received nothing. Patients were followed for 90 days. The primary outcome and sample size of 550 was predicated on a significant reduction in the proportion of healthy patients exposed to >5 mSv chest radiation. A total of 550 patients were randomized, and 541 had complete data. The proportion with >5 mSv to the chest and no significant cardiopulmonary diagnosis within 90 days was reduced from 33% to 25% (P=0.038). The intervention group had significantly lower median chest radiation exposure (0.06 versus 0.34 mSv; P=0.037, Mann–Whitney U test) and lower median costs (
Annals of Emergency Medicine | 2014
Jeffrey A. Kline; Nathan I. Shapiro; Alan E. Jones; Jackeline Hernandez; Melanie M. Hogg; R. Darrell Nelson
934 versus
Clinical Physiology and Functional Imaging | 2006
Jeffrey A. Kline; Melanie M. Hogg
1275; P=0.018) for medical care. Adverse events occurred in 16% of controls and 11% in the intervention group (P=0.06). Conclusions—Provision of pretest probability and prescriptive advice reduced radiation exposure and cost of care in low-risk ambulatory patients with symptoms of acute coronary syndrome and pulmonary embolism. Clinical Trial Registration—URL: http://www.clinicaltrials.gov. Unique identifier: NCT01059500.
American Journal of Respiratory and Critical Care Medicine | 2010
Jeffrey A. Kline; Melanie M. Hogg; D. Mark Courtney; Chadwick D. Miller; Alan E. Jones; Howard A. Smithline; Nicole Klekowski; Randy Lanier
STUDY OBJECTIVE Excessive radiation exposure remains a concern for patients with symptoms suggesting acute coronary syndrome and pulmonary embolism but must be judged in the perspective of pretest probability and outcomes. We quantify and qualify the pretest probability, outcomes, and radiation exposure of adults with both chest pain and dyspnea. METHODS This was a prospective, 4-center, outcomes study. Patients were adults with dyspnea and chest pain, nondiagnostic ECGs, and no obvious diagnosis. Pretest probability for both acute coronary syndrome and pulmonary embolism was assessed with a validated method; ultralow risk was defined as pretest probability less than 2.5% for both acute coronary syndrome and pulmonary embolism. Patients were followed for diagnosis and total medical radiation exposure for 90 days. RESULTS Eight hundred forty patients had complete data; 23 (3%) had acute coronary syndrome and 15 (2%) had pulmonary embolism. The cohort received an average of 4.9 mSv radiation to the chest, 48% from computed tomography pulmonary angiography. The pretest probability estimates for acute coronary syndrome and pulmonary embolism were less than 2.5% in 227 patients (27%), of whom 0 of 277 (0%; 95% confidence interval 0% to 1.7%) had acute coronary syndrome or pulmonary embolism and 7 of 227 (3%) had any significant cardiopulmonary diagnosis. The estimated chest radiation exposure per patient in this ultralow-risk group was 3.5 mSv, including 26 (3%) with greater than 5 mSv radiation to the chest and no significant cardiopulmonary diagnosis. CONCLUSION One quarter of patients with chest pain and dyspnea had ultralow risk and no acute coronary syndrome or pulmonary embolism but were exposed to an average of 3.5 mSv radiation to the chest. These data can be used in a clinical guideline to reduce radiation exposure.
Academic Emergency Medicine | 2012
Jeffrey A. Kline; Diane M. Corredor; Melanie M. Hogg; Jackeline Hernandez; Alan E. Jones
Background: The classical alveolar pCO2–pO2 relationship predicts that pulmonary embolism (PE) causes a low ratio of pCO2/pO2 at end expiration. Our purpose was to define a simple protocol to collect expired pCO2/pO2 to diagnose PE. Emergency department patients with suspected PE were enrolled. Clinical pretest probabilities for PE were estimated prior to diagnostic testing using the Canadian score and clinicians’ unstructured estimate. Patients provided three 30‐s periods of tidal breathing, separated by three deep exhalations. Expired pCO2, pO2 and breath volume were measured. All patients underwent standardized objective testing for PE including 90‐day follow‐up. Diagnosis (PE+) required anticoagulation for image‐proven PE within 90 days.
Emergency Medicine Australasia | 2013
Jeffrey A. Kline; Jackeline Hernandez; Melanie M. Hogg; Alan E. Jones; D. Mark Courtney; Christopher Kabrhel; Deborah B. Diercks; Matthew T. Rondina; James R. Klinger
RATIONALE Pulmonary embolism (PE) decreases the exhaled end-tidal ratio of carbon dioxide to oxygen (etCO(2)/O(2)). OBJECTIVES To test if the etCO(2)/O(2) can produce clinically important changes in the probability of segmental or larger PE on computerized tomography multidetector-row pulmonary angiography (MDCTPA) in a moderate-risk population with a positive D-dimer. METHODS Emergency department and hospitalized patients with one or more predefined symptoms or signs, one or more risk factors for PE, and 64-slice MDCTPA enrolled from four hospitals. D-dimer greater than 499 ng/ml was test(+), and D-dimer less than 500 ng/ml was test(-). The median etCO(2)/O(2) less than 0.28 from seven or more breaths was test(+) and etCO(2)/O(2) greater than 0.45 was test(-). MDCTPA images were read by two independent radiologists and the criterion standard was the interpretation of acute PE by either reader. PE size was then graded. MEASUREMENTS AND MAIN RESULTS We enrolled 495 patients, including 60 (12%) with segmental or larger, and 29 (6%) with subsegmental PE. A total of 367 (74%) patients were D-dimer(+), including all 60 with segmental or larger PE (posterior probability 16%). The combination of D-dimer(+) and etCO(2)/O(2)(+) increased the posterior probability of segmental or larger PE to 28% (95% confidence interval [CI] for difference of 12%, 3.0-22%). The combination of D-dimer(+) and etCO(2)/O(2)(-) was observed in 40 patients (8%; 95% CI, 6-11%), and none (0/40; 95% CI, 0-9%) had segmental or larger PE on MDCTPA. No strategy changed the prevalence of subsegmental PE. CONCLUSIONS In moderate-risk patients with a positive D-dimer, the et etCO(2)/O(2) less than 0.28 significantly increases the probability of segmental or larger PE and the etCO(2)/O(2) greater than 0.45 predicts the absence of segmental or larger PE on MDCTPA.
BMJ Open | 2016
Stacy Reynolds; Jonathan R. Studnek; Kathleen Bryant; Kelly L. Vanderhave; Eric Grossman; Charity G. Moore; James Young; Melanie M. Hogg; Michael S. Runyon
OBJECTIVES In a patient with symptoms of pulmonary embolism (PE), the presence of an elevated pulse, respiratory rate, shock index, or decreased pulse oximetry increases pretest probability of PE. The objective of this study was to evaluate if normalization of an initially abnormal vital sign can be used as evidence to lower the suspicion for PE. METHODS This was a prospective, noninterventional, single-center study of diagnostic accuracy conducted on adults presenting to an academic emergency department (ED), with at least one predefined symptom or sign of PE and one risk factor for PE. Clinical data, including the first four sets of vital signs, were recorded while the patient was in the ED. All patients underwent computed tomography pulmonary angiography (CTPA) and had 45-day follow-up as criterion standards. Diagnostic accuracy of each vital sign (pulse rate, respiratory rate, shock index, pulse oximetry) at each time was examined by the area under the receiver operating characteristic curve (AUC). RESULTS A total of 192 were enrolled, including 35 (18%) with PE. All patients had vital signs at triage, and 174 (91%), 135 (70%), and 106 (55%) had second to fourth sets of vital signs obtained, respectively. The initial pulse oximetry reading had the highest AUC (0.63, 95% confidence interval [CI] = 0.50 to 0.76) for predicting PE, and no other vital sign at any point had an AUC over 0.60. Among patients with an abnormal pulse rate, respiratory rate, shock index, or pulse oximetry at triage that subsequently normalized, the prevalences of PE were 18, 14, 19, and 33%, respectively. CONCLUSIONS Clinicians should not use the observation of normalized vital signs as a reason to forego objective testing for symptomatic patients with a risk factor for PE.