Ventilation-perfusion Scan Research Articles

12199 Uncontrolled Graves Disease Leading To The Development Of Pulmonary Hypertension

Abstract Disclosure: A. Agrawal: None. N. Shaykh: None. C. Marsalisi: None. L. Lam: None. C. Harrison: None. G.Y. Gandhi: None. Introduction: Graves’ disease can cause cardiorespiratory complications by increasing cardiac output, inducing endothelial dysfunction, and increasing the metabolism of intrinsic pulmonary vasodilating substances. Case: A 26-year-old female with a one-year history of Graves’ disease presented with chest pressure, shortness of breath, worsening orthopnea, a 40-pound weight loss, and subjective fevers. Her home methimazole dose was 10 mg daily, which she had missed for four days before admission. Her BP was 153/90 mmHg, heart rate 117 bpm, and temperature 100.7° F. She had mild bilateral proptosis and an enlarged but non-tender thyroid, which caused her difficulty swallowing. TSH was undetectable less than 0.005 mIU/L (0.27-4.2 mIU/L), and thyroid hormone levels were significantly elevated free T4 greater than 7.77 ng/dL (0.8-1.7 ng/dL) and free T3 29.1 pg/mL (2-4.4 pg/mL). TSI was high at 5.66 IU/L (0-0.55 IU/L) as was BNP at 1,642 pg/mL (0-125 pg/mL). Cardiac troponin was 105 ng/dL (less than 14 ng/dL) with a peak of 106 ng/dL. A Burch-Warsofsky score of 50 was highly suggestive of thyroid storm. She initially received 1 mg of IV propranolol, 1,000 mg of PTU, and 4 mg of dexamethasone followed by hydrocortisone 100 mg, methimazole 20, propanol 20 mg, and two doses of SSKI. A transthoracic echocardiogram was remarkable for severe right atrial and ventricular enlargement, and pulmonary artery pressure measured 55 mmHg (normal 20-30 mmHg). Autoimmune testing, including ANA, c-ANCA, p-ANCA, rheumatoid factor, anti-CCP, anti-SS-A, anti-SS-B antibodies, ultrasound for deep vein thrombosis, and ventilation-perfusion scan were negative. There was no history of congenital heart defects or valvulopathy. The patient reached a euthyroid state and was discharged home on methimazole 20 mg daily. Discussion: Although frequently underappreciated, pulmonary hypertension is present in 30 to 65% of Graves’ disease patients when systematically ascertained. Elevated thyroid hormones can increase heart rate, contractility, venous return, and cardiac output. An imbalance between vasoconstriction and vasodilation, along with endothelial dysfunction, can cause pulmonary vascular effects of hyperreactivity, remodeling, and thrombosis. An autoimmune mechanism is plausible due to an association between antithyroid antibodies and pulmonary hypertension. Right heart catheterization remains the gold standard for diagnosis, though in this case, it was not pursued in the acute setting. This case reinforces the importance of screening for pulmonary hypertension in patients with Graves’ disease and possibly normalizing pulmonary hypertension, thereby avoiding irreversible complications. Clinicians should consider reassessing for pulmonary hypertension even after long-term control of the thyrotoxic state, as about 30% of these patients have persistent pulmonary hypertension. Presentation: 6/3/2024

12199 Uncontrolled Graves Disease Leading To The Development Of Pulmonary Hypertension

Abstract Disclosure: A. Agrawal: None. N. Shaykh: None. C. Marsalisi: None. L. Lam: None. C. Harrison: None. G.Y. Gandhi: None. Introduction: Graves’ disease can cause cardiorespiratory complications by increasing cardiac output, inducing endothelial dysfunction, and increasing the metabolism of intrinsic pulmonary vasodilating substances. Case: A 26-year-old female with a one-year history of Graves’ disease presented with chest pressure, shortness of breath, worsening orthopnea, a 40-pound weight loss, and subjective fevers. Her home methimazole dose was 10 mg daily, which she had missed for four days before admission. Her BP was 153/90 mmHg, heart rate 117 bpm, and temperature 100.7° F. She had mild bilateral proptosis and an enlarged but non-tender thyroid, which caused her difficulty swallowing. TSH was undetectable less than 0.005 mIU/L (0.27-4.2 mIU/L), and thyroid hormone levels were significantly elevated free T4 greater than 7.77 ng/dL (0.8-1.7 ng/dL) and free T3 29.1 pg/mL (2-4.4 pg/mL). TSI was high at 5.66 IU/L (0-0.55 IU/L) as was BNP at 1,642 pg/mL (0-125 pg/mL). Cardiac troponin was 105 ng/dL (less than 14 ng/dL) with a peak of 106 ng/dL. A Burch-Warsofsky score of 50 was highly suggestive of thyroid storm. She initially received 1 mg of IV propranolol, 1,000 mg of PTU, and 4 mg of dexamethasone followed by hydrocortisone 100 mg, methimazole 20, propanol 20 mg, and two doses of SSKI. A transthoracic echocardiogram was remarkable for severe right atrial and ventricular enlargement, and pulmonary artery pressure measured 55 mmHg (normal 20-30 mmHg). Autoimmune testing, including ANA, c-ANCA, p-ANCA, rheumatoid factor, anti-CCP, anti-SS-A, anti-SS-B antibodies, ultrasound for deep vein thrombosis, and ventilation-perfusion scan were negative. There was no history of congenital heart defects or valvulopathy. The patient reached a euthyroid state and was discharged home on methimazole 20 mg daily. Discussion: Although frequently underappreciated, pulmonary hypertension is present in 30 to 65% of Graves’ disease patients when systematically ascertained. Elevated thyroid hormones can increase heart rate, contractility, venous return, and cardiac output. An imbalance between vasoconstriction and vasodilation, along with endothelial dysfunction, can cause pulmonary vascular effects of hyperreactivity, remodeling, and thrombosis. An autoimmune mechanism is plausible due to an association between antithyroid antibodies and pulmonary hypertension. Right heart catheterization remains the gold standard for diagnosis, though in this case, it was not pursued in the acute setting. This case reinforces the importance of screening for pulmonary hypertension in patients with Graves’ disease and possibly normalizing pulmonary hypertension, thereby avoiding irreversible complications. Clinicians should consider reassessing for pulmonary hypertension even after long-term control of the thyrotoxic state, as about 30% of these patients have persistent pulmonary hypertension. Presentation: 6/3/2024

Management and Outcomes of Pulmonary Embolism in the Oldest-Old.

Treatment for pulmonary embolism has expanded to include Direct Oral Anticoagulants (DOACs). The incidence of pulmonary-embolism (PE) in "oldest-old" age group (≥85 years) is rapidly increasing, but there is limited research on its management and clinical outcomes. To examine the differences in management and outcomes in those aged ≥85 years compared to other age groups. We performed a retrospective cohort-study of 373 consecutive patients with pulmonary embolism confirmed on imaging by Computed Tomography Pulmonary Angiogram (CTPA) or Ventilation Perfusion (VQ) Scan at a principal referral hospital in Sydney, Australia. Data collected include clinical and demographic data, Charlson comorbidity index, treatment type and outcomes including complications, recurrent venous thromboembolism, and mortality. Across the age groups, DOACS were prescribed to 53.4% (n=199) of patients. In oldest-old patients with PE, LMWH bridging to warfarin was the most frequently prescribed treatment, used in 46.2% (n=18, 95% CI: 30.8%-61.5%, p=0.003) of these patients. The mortality rate for patients on LMWH was 13.9% (n=5, 95% CI: 4.2%-37.5%, p=0.553). Overall, major bleeding incidents were rare, occurring in just 1.7% (n=4, 95% CI: 0.4%-3.3%) of patients, with no significant differences in outcomes across age groups. DOACs are increasingly used as the treatment modality of choice in atrial fibrillation but are less well studied in pulmonary embolism, particularly in oldest-old patients. We found that the safety and efficacy profile of DOACs in pulmonary embolism treatment is similar across the age groups. Our study does not support any change in treatment protocols of PE in the oldest old, but further studies are required to confirm our findings.

Unilateral hyperlucent lung: Swyer James Macleod Syndrome

Swyer James Macleod Syndrome, also known as unilateral hyperlucent lung syndrome, is a rare lung condition characterized by the underdevelopment of one lung. This syndrome typically occurs in childhood and is often discovered incidentally during imaging studies for unrelated conditions.Individuals with Swyer James Macleod Syndrome may experience symptoms such as recurrent respiratory infections, shortness of breath, and decreased exercise tolerance. Diagnosis is typically made through imaging studies such as chest X-rays,computed tomography or ventilation-perfusion scans.

Diagnostic management of acute pulmonary embolism

Straightforward, accurate diagnostic management in patients presenting with clinically suspected pulmonary embolism (PE) is essential, since starting anticoagulant treatment may give important adverse effects of bleeding, while false exclusion of the disease may lead to recurrent VTE, with associated morbidity and mortality. In the past three decades, considerable improvement in the diagnostic management of PE has been made. Computed tomography pulmonary angiography (CTPA) has largely replaced conventional pulmonary angiography and ventilation-perfusion lung scanning as the imaging methods of choice. Several diagnostic algorithms, all able to minimize the need for radiological imaging have been developed and validated. Lastly, within the diagnostic algorithms, varying d-dimer cut-off levels have successfully been introduced to further downsize the need for radiological imaging.

Chronic Thromboembolic Pulmonary Hypertension

: While the majority of patients have complete resolution of their acute pulmonary embolism (PE) after an adequate course of anticoagulation, some patients remain symptomatic with evidence of chronic PE. Chronic Thromboembolic Pulmonary Hypertension (CTEPH) and Chronic Thromboembolic Pulmonary Disease (CTEPD) are terms that describe symptomatic patients with chronic thromboembolic occlusions of the pulmonary arteries with or without pulmonary hypertension, respectively. Here, we review the definitions, epidemiology, pathobiology, diagnosis and management of CTEPH. The chronic PE in CTEPH is essentially a scar in the pulmonary vasculature and is accompanied by a pulmonary arteriolar vasculopathy. Ventilation-perfusion scanning is the most sensitive screening test for CTEPH, and diagnosis must be confirmed by right heart catheterization (RHC). Treatment decisions require a multidisciplinary team and guidance from additional imaging, usually CT or pulmonary angiography. While pulmonary endarterectomy (PEA) to remove the chronic PE surgically is still the first-line treatment for appropriate candidates, there is an expanding role for balloon pulmonary angioplasty (BPA) and medical treatment, as well as multimodality treatment approaches that incorporate all of those options. New imaging modalities and treatment strategies hold the promise to improve our care and management of CTEPH patients in the future.

Impact of COVID-19 on Ventilation-Perfusion (V/Q) Scans: A Comparative Analysis of Pre-COVID-19 Era V/Q Scans and Post-COVID-19 Era Perfusion Scans.

Introduction The COVID-19 pandemic has profoundly impacted medical practices, including nuclear medicine. To minimize aerosol transmission risks, lung perfusion scintigraphy was preferred over traditional ventilation-perfusion (V/Q) scintigraphy during the pandemic. This study compares lung perfusion scans performed during COVID-19 with V/Q scans from the pre-COVID era. After reviewing this study, the reader will learn about V/Q scintigraphy and lung perfusion. Methods This retrospective observational study, conducted from December 2018 to July 2021, involved 868 patients - 511 in the pre-COVID era and 357 in the post-COVID era - at a single tertiary care center. The pretest probability of pulmonary embolism (PE) was determined using Wells' criteria, and data including demographics, clinical findings, and diagnostic test results (V/Q or lung perfusionscintigraphy) were collected. Results A 30% decline in lung scans was observed during the pandemic. In the pre-COVID era, 68.3% of scans had low, 27.8% had intermediate, and 3.9% had high probability for PE. During the pandemic, perfusion-only scans showed 57.3% low, 32.9% indeterminate, and 9.8% high probability for PE. Among COVID-19-positive patients, 48.9% had intermediate, and 11.1% had high probability scans. The rise in indeterminate and high-probability scans during the pandemic is attributed to COVID-19-related lung changes and hypercoagulability. Conclusion The perfusion component of lung scans is typically sufficient for evaluating acute PE. Omitting the ventilation part of the V/Q scan had minimal impact, with only a 5.1% increase in indeterminate/non-diagnostic scans using perfusion-only modified Prospective Investigation of Pulmonary Embolism Diagnosis II (PIOPED II) criteria during the post-COVID-19 era, likely due to underlying lung parenchymal involvement in COVID-19 patients. Additionally, there was a 5.9% rise in high-probability scans, attributed to the hypercoagulability and vascular complications associated with COVID-19.

One year follow-up and literature review of three young-age cases with high risk pulmonary thromboembolism

High-risk pulmonary thromboembolism (PTE) is an emergency clinical condition with high mortality. High-risk pulmonary thromboembolism is generally seen in immobile patients, elderly, have malignancies, and have a long-term travel history. Our aim here is to emphasize that high-risk pulmonary thromboembolism may also occur in young patients. Considering the symptoms and risk factors such as oral contraceptive use, obesity, and operation history, PTE can be detected with Pulmonary Computed Tomography-Angiography (CTPA) or Ventilation Perfusion Scintigraphy (V/Q) when necessary. It should be verified that it is not. Genetic mutation, obesity, oral contraceptive use, and previous operation history were accepted as risk factors in the young patients we treated and followed up with high-risk Pulmonary Thromboembolism presented here. After the diagnosis of pulmonary thromboembolism was made at the first stage in our patients who applied to the emergency department, the risk group was determined by taking into account the current guidelines. Three patients considered to be at high risk were evaluated for thrombolytic therapy. Two patients without contraindications were given a full dose, and one patient was given a half dose of thrombolytic. After being monitored in intensive care for the first 24 hours, they were taken to the service. Due to their young age (<45 years), their thrombophilia panel was checked. Anticoagulant treatments were started and follow-ups were planned at 3 months, 6 months, and 1 year after discharge. During the follow-up visits, CTPA, echocardiography (ECHO), and lower extremity Doppler ultrasound imaging were performed.

Anomalous bronchial artery origin - canary in the coal mine - for diagnosing chronic thromboembolic pulmonary hypertension

Anomalous bronchial artery origins may have clinical implications beyond their anatomical curiosity. In this case, the identification of such an anomaly led to the diagnosis of chronic thromboembolic pulmonary hypertension (CTEPH). A 49-year-old male with a history of recurrent deep vein thrombosis (DVT) and pulmonary embolism (PE) on anticoagulation presented with chest pain and shortness of breath. Laboratory analysis was remarkable for a troponin peak of 14.74 ng/ml, a brain natriuretic peptide level of 602 pg/ml and a D-dimer level of 0.62 µg/ml. Electrocardiogram showed non-specific ST elevation in the anterolateral and inferior leads. Computed tomography angiography (CTA) of the chest was positive for PE involving the right lower lobe pulmonary arterial tree. Echocardiogram showed reduced left ventricular function (ejection fraction 38%) and akinesis of the antero-apical and infero-apical segments. Cardiac catheterization revealed non-obstructive coronary arteries, and an anomalous origin of a right bronchial artery from the right coronary artery. The right bronchial hypertrophied as it supplied collateral flow to the occluded right pulmonary artery. This anomaly and the patient’s history of multiple DVT/PEs while on therapeutic levels of warfarin with near normal D-dimer levels raised suspicion for a false positive PE. Pulmonary angiogram revealed chronic occlusion in branches of the right pulmonary artery, mean pulmonary artery pressure of 36 mmHg and no acute thrombus. Ventilation-perfusion scan confirmed the diagnosis of CTEPH. The patient underwent successful pulmonary thromboendarterectomy and subsequently had normalization of mean pulmonary artery pressure. This case underscores the importance of a comprehensive diagnostic approach, and consideration of alternative explanations for imaging findings, that unveiled the diagnosis of a complex and life-threatening condition such as CTEPH.

Chronic thromboembolic pulmonary hypertension in acute pulmonary embolism: a risk factor evaluation study

Aims: Pulmonary thromboembolism (PTE) is a highly mortal disease, defined by presence of thrombus partially or completely obstructing pulmonary arteries and/or veins, commonly originated from deep venous system. Chronic thrombroembolic pulmonary hypertension (CTEPH) is a rare complication of PTE with high mortality if not treated properly. In recent studies, incidence of CTEPH was found between %0,4-9,1. Due to clinically silent PTE in roughly %50 of patients, it is difficult to pinpoint the exact incidence of CTEPH. In this study, we aim to investigate PTE patients during their long-term follow up to observe CTEPH presence and evaluate CTEPH risk factors. Methods: Patients who had been evaluated in emergency service and/or admitted to pulmonary medicine ward between January 2014 and January 2017 with PTE diagnosis confirmed by computed tomography pulmonary angiogram (CTPA) were accepted retrospectively into the study. Their echocardiography, CTPA and lower extremity venous Doppler ultrasonography at 3., 6. and 12. months follow up were also included. In the patient group with pulmonary arterial pressure (PAP ) above 50 mmHg and residual thrombosis at CTPA, ventilation-perfusion scintigraphy had been performed and was added to the study. Among those suitable for CTEPH, right cardiac catheterization had been done to confirm the diagnosis and accepted as CTEPH. In addition to this group, patients who were not found suitable for right cardiac catheterization but wereclinically suitable for CTEPH are also included in the CTEPH group. Results: Average age of patients included into the study was 62(±16, 5), with 71 (%39) being male and 111 (%61) female. As for risk factors, 130 (%71,4) had acquired, 16 (%8,8) had genetic and the rest 36 (%19,8) did not have any prominent risk factors. At time of diagnosis, 10 patients were accepted as massive, 26 as sub massive and the rest 139 were considered non-massive PTE. Due to hemodynamic instability, 7 (%3,8) patients were given thrombolytic therapy. During 1 year follow-up, 5 (%2,7) patients were diagnosed with CTPH. When further investigation was performed on these 5 patients, atrial fibrillation (AF), persistent thrombosis at 12. month follow up CTPA and PAP above 55 mmHg upon time of diagnosis were found significant risk factors (p being 0,001/0,023/0,009 respectively). In multivariate analysis, no independent predictive factors were found in regards to CTEPH diagnosis. Conclusion: CTEPH is a preventable complication of PTE with severe mortality and morbidity if not properly treated. It might prove useful to utilize echocardiography and CTPA together, especially in those in high risk groups, for diagnosis of patients in early stage of CTEPH with no evident signs or symptoms.

Comparison of three diagnostic strategies for suspicion of pulmonary embolism: planar ventilation-perfusion scan (V/Q), CT pulmonary angiography (CTPA) and single photon emission CT ventilation-perfusion scan (SPECT V/Q): a protocol of a randomised controlled trial

IntroductionPulmonary embolism (PE) is a challenge to diagnose and when missed, exposes patients to potentially fatal recurrent events. Beyond CT pulmonary angiography (CTPA) and planar ventilation/perfusion (V/Q) scan, single photon...

Implementation, Clinical Benefit and Safety of a D-Dimer-Focused Pulmonary Embolism Testing Pathway in the Emergency Department

Computed tomography pulmonary angiogram (CTPA) is overused during pulmonary embolism (PE) testing in the emergency department (ED), whereas prediction rules and D-dimer are underused. We report the adherence, clinical benefit, and safety of a D-dimer-only strategy to guide need for PE imaging in the ED. This was a prospective multicenter implementation study in 2 EDs with historical and external controls. Patients with suspected PE underwent D-dimer testing and imaging (CTPA or ventilation-perfusion scan) when D-dimer levels were 500 ng/mL or more. PE was ruled out if D-dimer was less than 500 ng/mL or with negative imaging. The primary implementation outcome was the proportion of patients tested for PE in adherence with the pathway. The primary clinical benefit outcome was the proportion of patients tested for PE who received pulmonary imaging. The primary safety outcome was diagnosis of PE in the 30 days following negative PE testing postimplementation. Between January 2018 and June 2021, 16,155 patients were tested for PE, including 33.4% postimplementation, 30.7% preimplementation, and 35.9% in an external control site. Adherence with the D-dimer-only pathway was 97.6% (adjusted odds ratio (aOR) post- versus preimplementation 5.26 (95% confidence interval 1.70 to 16.26). There was no effect on the proportion undergoing PE imaging. Imaging yield increased aOR 4.89 (1.17 to 20.53). Two cases of PE (0.04%; 0.01% to 0.16%) were diagnosed within 30 days. In this Canadian ED study, the uptake of a D-dimer-only PE testing strategy was high. Implementation was associated with higher imaging yield and a D-dimer level of less than 500 ng/mL safely excluded PE.

Post-Pulmonary Embolism Syndrome: An Update Based on the Revised AWMF-S2k Guideline.

In survivors of acute pulmonary embolism (PE), the post-PE syndrome (PPES) may occur. In PPES, patients typically present with persisting or progressive dyspnea on exertion despite 3 months of therapeutic anticoagulation. Therefore, a structured follow-up is warranted to identify patients with chronic thromboembolic pulmonary disease (CTEPD) with normal pulmonary pressure or chronic thromboembolic pulmonary hypertension (CTEPH). Both are currently understood as a dual vasculopathy, that is, secondary arterio- and arteriolopathy, affecting the large and medium-sized pulmonary arteries as well as the peripheral vessels (diameter < 50 µm). The follow-up algorithm after acute PE commences with identification of clinical symptoms and risk factors for CTEPH. If indicated, a stepwise performance of echocardiography, ventilation-perfusion scan (or alternative imaging), N-terminal prohormone of brain natriuretic peptide (NT-proBNP) level, cardiopulmonary exercise testing, and pulmonary artery catheterization with angiography should follow. CTEPH patients should be treated in a multidisciplinary center with adequate experience in the complex therapeutic options, comprising pulmonary endarterectomy, balloon pulmonary angioplasty, and pharmacological interventions.

Subsegmental Pulmonary Embolism Post Cesarean Section: A Case Report

Diagnosing pulmonary embolism during pregnancy and the postpartum period can indeed be challenging due to overlapping symptoms with normal pregnancy changes. It's important for healthcare providers to maintain a high index of suspicion and use appropriate diagnostic tools, such as imaging studies like CT pulmonary angiography or ventilation-perfusion scans, while considering the maternal and fetal risks involved in the diagnostic process. We report a case of postpartum subsegmental pulmonary embolism.

Contemporary approaches to pulmonary embolism diagnosis: a clinical review.

The optimal diagnosis strategy for pulmonary embolism (PE) in the emergency department (ED) remains complex. This review summarizes PE diagnosis with clinical presentation, decision rules and investigations for acute PE. This review was performed using studies published between January 1, 2010, and September 1, 2023. PE should be considered in ED in patients with chest pain, shortness of breath, syncope or signs of deep veinous thrombosis. Definitive diagnosis of PE relies on thoracic imaging, with the use of chest tomographic pulmonary angiogram or ventilation-perfusion lung scintigraphy. To limit the continuous increased use of chest imaging, the clinical probability should be the first step for PE workup. The pulmonary embolism rule-out criteria (PERC) can rule out PE at this stage. If not, for low or intermediate probability, several clinical decision rules have been validated, either by ruling out PE on clinical signs, or by raising D-dimer thresholds (YEARS or PEGeD [Pulmonary Embolism Graduated D-Dimer] criteria) or by combination of these different rules. It is recommended that patients with a high clinical probability of PE should undergo chest imaging without the need for D-dimer testing. The PE diagnostic approach can be tailored in specific populations such as pregnant, younger, COVID-19, or cancer patients. PE diagnosis workup illustrates the complexity of modern probabilistic-based approaches of decision-making in medicine. It is recommended to use a Bayesian approach with the evaluation of clinical probability, then order D-dimer if the PERC rule is positive, then adapt the D-dimer threshold for ordering chest imaging using clinical decision rules.

Optimizing emergency department imaging utilization for pulmonary emboli: A study on the effects of IV contrast rationing

PurposeTo study the impact of a contrast mitigation protocol on imaging utilization for pulmonary embolism (PE) in the emergency department (ED). Material and methodsMedical records of ED patients with suspected PE who underwent CT pulmonary angiography (CTPA) or ventilation-perfusion (VQ) scans were analyzed in control (3/15/22–4/15/22) and test (5/15/22–6/15/22) periods. The test period included a contrast mitigation protocol due to a global iodinated contrast shortage (05/2022–06/2022). Out of 610 scans, 28 were excluded for non-PE indications. Patient demographics, time metrics, and imaging reports were recorded. ResultsAmong 11,019 ED visits, there were 582 imaging events for suspected PE. The test period exhibited a significantly lower imaging rate of 4.16 % compared to 6.54 % in the control period (p < 0.001). CTPA usage decreased by 47.73 %, while VQ scan usage increased by 775.00 % during the test period. Test period positivity rate was 0.82 %, with CTPA at 0.58 % (1/173) and VQ scan at 1.43 % (1/70). In the control period, the positivity rate was 0.29 %, with CTPA at 0.30 % (1/331) and VQ scan at 0.00 % (0/8). Previous hospitalization history was significantly higher in the test period (70/243 vs. 39/339, p < 0.001). The positivity rates between the two periods showed no significant difference (p = 0.57). There were no significant differences in ED length of stay and image acquisition times. ConclusionThe contrast mitigation protocol reduced CTPA use, increased VQ scans, and maintained positivity rates and image acquisition times. However, concerns persist about unnecessary imaging and low positivity rates, necessitating further research to optimize PE diagnostic algorithms.

Ventilation-perfusion scan for diagnosing pulmonary embolism: do chest x-rays matter?

Ventilation-perfusion (V/Q) scan coupled with single photon emission computed tomography (SPECT) is commonly used for the diagnosis of pulmonary embolism (PE). An abnormal chest x-ray (CXR) is deemed to hinder the interpretation of V/Q scan and therefore a normal CXR is recommended prior to V/Q scan. To determine if an abnormal CXR impacted on V/Q scan interpretation and subsequent management. A retrospective cohort analysis of all patients who underwent a V/Q scan for diagnosis of suspected acute PE between March 2016 and 2022 was performed. CXR reports were reviewed and classified as normal or abnormal. Low-dose computerised tomography was routinely performed in patients above the age of 70. Data regarding V/Q scan results and subsequent management including initiation of anticoagulation for PE or further diagnostic investigations were collected. A total of 340 cases were evaluated. Of the positive V/Q scans (92/340), 98.3% of the normal CXR were anticoagulated compared to 100% of the abnormal CXR group. Of the negative V/Q scans (239/340), no cases were started on anticoagulation and no further investigations were performed across both normal and abnormal CXR groups. Indeterminate results occurred in only 9 cases with no significant difference in management between normal and abnormal CXR groups. An abnormal CXR does not affect the reliability of V/Q scan interpretation in the diagnosis of PE when coupled with SPECT. Unless clinically indicated, the mandate by clinical society guidelines for a normal CXR prior to V/Q should be revisited.

Abstract 17520: Dynamic Intrapulmonary Shunting in the Setting of Amphetamine Use

Description of Case: A 35-year-old female non-smoker with ADHD on amphetamine for the past 3 months and family history of hereditary hemorrhagic telangiectasia (HHT) presented with significant exertional dyspnea for 1 week. She was hypoxic to 82% while walking, with normal oxygen saturation at rest. Transthoracic echocardiogram with agitated saline revealed extracardiac right-to-left shunting with exercise and Valsalva. This was confirmed by dobutamine stress echocardiogram with agitated saline (Figure 1A). Transesophageal echocardiogram with agitated saline (Figure 1B) revealed no shunt through the foramen ovale, but it demonstrated bubbles entering from the left upper pulmonary vein, suggestive of an extracardiac shunt from a pulmonary arteriovenous malformation (AVM). Right heart catheterization and pulmonary angiogram revealed normal pressures, and no pulmonary abnormalities with normal pulmonary venous return. Supine right heart catheterization with exercise revealed normal pressures, although the initial pulmonary artery (PA) saturation was 28%; repeat PA saturation one minute later was 48%. Arterial saturation was 95%. Pulmonary function testing, ventilation perfusion scan, high-resolution CT chest, and coronary CT angiogram were unremarkable. The patient was instructed to avoid all stimulants, and to take a non-hormonal contraceptive. At her 3-month follow-up, she reported significant improvement in her symptoms. She underwent a 6-minute walk test, and her lowest oxygen saturation was 88%. Discussion: This patient presented with exertional hypoxia, normal saturations at rest, evidence of an extracardiac shunt only with exertion and absence of clear sources of the shunt on imaging. With her family history of HHT, this is suggestive of a small pulmonary AVM that opened by elevated PA pressures, likely triggered by amphetamine use, and its discontinuation led to symptom resolution.

Analysis of predictive factors in children with high suspicion of pulmonary embolism.

Since there is a limited number of predictive models designed for pediatric patients with pulmonary embolism (PE), healthcare providers have resorted to utilizing the Wells criteria and PE Rule-out Criteria (PERC) that have been validated for use in adults. The objective of the study is to identify the predictive factors for PE and assess the effectiveness of the PERC, Wells, and pediatric-specific PE (PPE) criteria. The study included individuals between the ages of 0-18 years who underwent pulmonary CT angiography and/or ventilation-perfusion scintigraphy with suspicion of PE. Demographic characteristics, symptoms, physical examination findings, risk factors, and laboratory and imaging results were retrospectively analyzed, and PERC, Wells, and PPE criteria were applied to the study population. Of the 110 patients included in the study, 27 (24.5%) had PE. Saturation, albumin, cough, calf swelling, central catheter, and malignancy were found to significantly contribute to the model. The total weighted risk score, which represents the sum of all predictive scores, ranged from 0 to 16 with a mean of 5.41 ± 4.02. When the cut-off >6.5, the model had good discrimination power for positive PE (AUC 0.79, 77% sensitivity, and 70% specificity). In our study, the Wells criteria showed a sensitivity of 96% and a specificity of 24%. The PERCexhibited a sensitivity of 96% and a specificity of 21%, while the PPE demonstrated a sensitivity of 74% and a specificity of 30%. While the sensitivity of Wells, PERC, and PPE models was higher than our developed model, their specificities were considerably lower than our model.

Survival Outcomes in Patients with Intermediate and High-Risk Pulmonary Embolism Treated with Low Molecular Weight or Unfractionated Heparin: Time to Start of Anticoagulant Therapy

Introduction Venous Thromboembolism (VTE), including pulmonary embolism (PE), is the third most common cause of vascular disease related death in the United States. If left untreated, the mortality of PE is as high as 30%. The main-stay of treatment for PE involves anticoagulant therapy (AT), commonly with low molecular weight heparin (LMWH), or unfractionated heparin (UFH). Prior data has demonstrated a reduction in mortality with anticoagulant timing. In one study, 30-day all-cause mortality was lower in patients who achieved therapeutic AT, as defined by activated partial thromboplastin time (aPTT), within 24 hours of ER presentation. However, recent data demonstrated low numbers of patients with therapeutic range aPTT at 24 hours (&amp;lt; 30%). Thus, we aimed to assess the association between time to anticoagulant therapy from emergency room (ER) presentation and 30-day PE-associated mortality. Methods We performed a retrospective cohort study of patients at Barnes Jewish Hospital between January 2021 and April 2023 for which the Pulmonary Embolism Response Team (PERT) was activated. Patients with intermediate-low, intermediate-high, or massive (high-risk) PE who presented to the emergency department or urgent care facility with signs/symptoms concerning for PE were included. PE was objectively confirmed on imaging studies (CT or VQ Scan). Only patients initiated on UFH or LMWH were included. Patient demographic and hemodynamic data were collected on presentation. Those with low-risk PE, those started on an AT other than UFH/LMWH, and those who died prior to the start of AT were excluded. Time from ER presentation (as estimated by triage vital signs) to start of AT was calculated based on review of the Electronic Medical Record. The primary outcome was PE-associated mortality within 30 days. PE-associated mortality was defined as: deaths directly caused by PE, deaths caused by the treatment of PE, and multifactorial deaths with PE as a contributing illness. Using logistic regression, we calculated the association between each doubling of the time until AT was given and PE-associated mortality. Results A total of 184 patients met inclusion criteria, 138 patients with intermediate-risk PE and 46 with massive PE. 81% of patients received UFH (n = 149) and 19% received LMWH (n = 35). PE-associated mortality occurred in 5.1% (n = 7) of patients in the intermediate-risk group and 32.6% (n = 15) in the high-risk group. The average time from ER triage to start of AT was 5 hours in intermediate-risk patients who survived versus 8.1 hours in those who died. The average time from ER triage to start of AT was 5.3 hours in massive PE patients who survived versus 5.4 hours in those who died. After adjusting for massive PE classification and sPESI score, each doubling of time in delay of AT from ER presentation was associated with 1.27 increased odds of PE-associated death (odds ratio (OR) 1.27, 95% confidence interval (CI) 0.85, 1.89) (Table 1). The discrimination of the model was very good with a c-statistic of 0.83 for prediction of PE-associated 30-day mortality. When only analyzing patients with intermediate-risk PE, each doubling of time in delay of AT from ER presentation was associated with 2.72 increased odds of PE-associated death (OR 2.72, 95% CI 1.11, 6.78) (Table 1). Conclusions In patients with intermediate-risk or massive PE, each doubling of the time from patient presentation to the ER to start of anticoagulant therapy was associated with 1.27 increased odds in the risk of PE-associated 30-day mortality. This association was more pronounced in patients with intermediate-risk PE. Future efforts should be aimed at decreasing time from ER presentation to start of anticoagulant therapy in patients with PE such as through quality improvement projects and/or triage protocolization.