To cite this article: Kline JA, Mitchell AM, Kabrhel C, Richman PB, Courtney DM. Clinical criteria to prevent unnecessary diagnostic testing in emergency department patients with suspected pulmonary embolism. J Thromb Haemost 2004; 2: 1247-55.See also Le Gal G, Bounameaux H. Diagnosing pulmonary embolism: running after the decreasing prevalence of cases among suspected patients.This issue, pp 1244-6; Linkins L.-A., Bates SM, Ginsberg JS, Kearon C. Use of different D-dimer levels to exclude venous thromboembolism depending on clinical pretest probability. This issue, pp 1256-60.Summary. Overuse of the D-dimer to screen for possible pulmonary embolism (PE) can have negative consequences. This study derives and tests clinical criteria to justify not ordering a D-dimer. The test threshold was estimated at 1.8% using the method of Pauker and Kassirer. The PE rule-out criteria were derived from logistic regression analysis with stepwise backward elimination of 21 variables collected on 3148 emergency department patients evaluated for PE at 10 US hospitals. Eight variables were included in a block rule: Age < 50 years, pulse < 100 bpm, SaO 2 > 94%, no unilateral leg swelling, no hemoptysis, no recent trauma or surgery, no prior PE or DVT, no hormone use. The rule was then prospectively tested in a low-risk group (1427 patients from two hospitals initially tested for PE with a D-dimer) and a very lowrisk group (convenience sample of 382 patients with chief complaint of dyspnea, PE not suspected). The prevalence of PE was 8% (95% confidence interval: 7-9%) in the low-risk group and 2% (1-4%) in the very low-risk group on longitudinal follow-up. Application of the rule in the low-risk and very lowrisk populations yielded sensitivities of 96% and 100% and specificities of 27% and 15%, respectively. The prevalence of PE in those who met the rule criteria was 1.4% (0.5-3.0%) and 0% (0-6.2%), respectively. The derived eight-factor block rule reduced the pretest probability below the test threshold for D-dimer in two validation populations, but the rule's utility was limited by low specificity.
Background and objectives: No prospective study has reported the incidence of contrast-induced nephropathy (CIN) or the associated morbidity and mortality after contrast-enhanced computed tomography (CECT) in the outpatient setting.Design, setting, participants, & measurements: We enrolled and followed a prospective, consecutive cohort (June 2007 through January 2009) of patients who received intravenous contrast for CECT in the emergency department of a large, academic, tertiary care center. Outcomes measured were as follows (1) CIN: An increase in serum creatinine >0.5 mg/dl or >25% 2 to 7 d after contrast administration; (2) severe renal failure: An increase in serum creatinine to >3.0 mg/dl or the need for dialysis at 45 d; and (3) renal failure as a contributing cause of death (consensus of three independent physicians) at 45 d.Results: The incidence of CIN was 11% (70 of 633) among the 633 patients enrolled. Fifteen (2%) patients died within 45 d, including six deaths after study-defined CIN. Seven (1%) patients developed severe renal failure, six of whom had studydefined CIN. Of the six patients with CIN and severe renal failure, four died, and adjudicators determined that renal failure significantly contributed to all four deaths. Thus, CIN was associated with an increased risk for severe renal failure and death from renal failure.Conclusions: CIN occurs in >10% of patients who undergo CECT in the outpatient setting and is associated with a significant risk for severe renal failure and death.
Objectives
Contrast-enhanced computed tomography of the pulmonary arteries (CTPA) has become the mainstay to evaluate patients with suspected pulmonary embolism (PE), and is one of the most common contrast-enhanced CT imaging studies performed in the emergency department (ED). While contrast-induced nephropathy (CIN) is a known complication, this risk is not well-defined in the ED or other ambulatory setting. The aim of this study was to define the risk of CIN following CTPA.
Methods
The authors enrolled and followed a prospective, consecutive cohort (June 2007 through January 2009) of patients who received intravenous contrast for CTPA in the ED of a large, academic tertiary care center. Study outcomes included 1) CIN defined an increase in serum creatinine ≥0.5 mg/dL or ≥25%, 2 to 7 days following contrast administration; and 2) severe renal failure defined as an increase in serum creatinine to ≥3.0 mg/dL, or the need for dialysis within 45 days and/or renal failure as a contributing cause of death at 45 days, determined by the consensus of three independent physicians.
Results
One hundred seventy-four patients underwent CTPA, which demonstrated acute PE in 12 (7%, 95% CI = 3% to 12%). Twenty-five patients developed CIN (14%, 95% CI = 10% to 20%) including one with acute PE. The development of CIN after CTPA significantly increased the risk of the composite outcome of severe renal failure or death from renal failure within 45 days (relative risk = 36, 95% CI = 3 to 384). No severe adverse outcomes were directly attributable to complications of venous thromboembolism (VTE) or its treatment.
Conclusions
In this population, CIN was at least as common as the diagnosis of PE after CTPA; the development of CIN was associated with an increased risk of severe renal failure and death within the subsequent 45 days. Clinicians should consider the risk of CIN associated with CTPA and discuss this risk with patients.
Summary. Objective: To estimate the frequency of contrast nephropathy after computed tomography angiography (CTA) to rule out pulmonary embolism (PE) in the emergency department (ED) setting. Methods: We prospectively followed patients undergoing CTA for PE, while in the ED, for 45 days. Patients who refused follow-up or were receiving hemodialysis were excluded. Severe renal failure was defined as an increase in creatinine ‡ 3.0 mg dL )1 or a need for hemodialysis within the follow-up period. Patients were also followed for laboratorydefined contrast nephropathy, defined as an increase in creatinine of > 0.5 mg dL )1 or > 25%, within seven days following CTA. Results: A total of 1224 patients were followed, and 354 [29%, 95% confidence interval (CI): 26-32%] patients had paired (preCTA and post-CTA) creatinine measurements. None developed renal failure (0/1224; 0%, CI: 0-0.3%). 44 patients developed laboratory-defined contrast nephropathy, corresponding to an overall frequency of 4% (44/1224; CI: 3-5%) and 12% (44/354; 95% CI: 9-16%) among those with paired creatinine measurements. Conclusions: Following CTA for PE, the incidence of severe renal failure was very low, but the incidence of laboratory-defined contrast nephropathy (4% overall and 12% of those with paired measurements) was higher than expected.
The threshold for frequent PED use was more than 5 visits per patient within the first 36 months of life. Further study is needed to better define this population and develop targeted interventions to ensure care provision occurs in the ideal setting.
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