Medical Image of the Month: Hampton Hump and Palla Sign

Figure 1. A chest radiograph demonstrates a wedge-shaped opacity in the right lung base (red circle) and enlargement of the right descending pulmonary artery branch (blue arrow) consistent with a Hampton hump and Palla sign, respectively.

Figure 2. A computed tomography angiogram (CTA) of the chest in a lung window demonstrates a wedge-shaped opacity in the right middle lobe consistent with a Hampton hump (red circle).

Figure 3. A CTA of the chest demonstrates an embolus in the right main pulmonary artery which appears slightly dilated (red circle).

Figure 4. A CTA of the chest demonstrates extension of the pulmonary embolus into the right lower lobe pulmonary arterial branch (blue circle) along with a right middle lobe pulmonary infarction (red circle) which is better demonstrated in Figure 2.

A 51-year-old lady presented to emergency room with acute, severe, right-sided pleuritic chest pain, mild cough and dyspnea at rest. She underwent a lumbar spine laminotomy and foraminotomy twelve days prior to her presentation with limited mobility after her operation. On examination, she was tachypneic and tachycardic. Her blood pressure and oxygen saturations on room air were normal. Chest auscultation revealed a few crackles in the right lung base. There was no pedal edema or calf tenderness.

A chest radiograph demonstrated a right lower lobe wedge-shaped opacity along with right hilar prominence (Figure 1). She was initially diagnosed with a right lower lobe pneumonia and was admitted to step-down unit for further management. However, her history, clinical examination, and chest radiograph findings suggested the high likelihood a pulmonary embolism. A computed tomography angiogram (CTA) of the chest confirmed the diagnosis of a pulmonary embolism (Figures 2-4).

Based her clinical presentation and radiology results, the patient was diagnosed with a sub-massive pulmonary embolism (PE). She was treated with an intravenous heparin drip. She was hemodynamically stable throughout the hospital admission. Her echocardiogram showed no evidence of right ventricular strain. Eventually, she was transitioned to oral anticoagulation and was discharged home in good condition.

Discussion

The wedge-shaped right lower lobe opacity and right hilar prominence correspond to a Hampton hump and Palla sign, respectively. A Hampton hump represents a pulmonary infarction secondary to PE, and it was named by the radiologist Aubrey Hampton in 1940 (1). The Palla sign is an enlarged right descending pulmonary artery, an observation made in 1983 by a radiologist, Antonio Palla (2). Both signs can be seen on chest radiography and may aid in the diagnosis of a PE.

Although these radiologic findings of PE are rare, practicing physicians should be aware of these findings as they can be extremely helpful and expediate the diagnosis of a PE. On the other hand, misinterpretation of these findings can lead to a delay in the diagnosis of other significant chest pathologies.

Abdulmonam Ali MD and Naga S Sirikonda MD

SSM Health

Mount Vernon, IL USA

References

1. Hampton AO, Castleman B. Correlation of postmortem chest teleroentgenograms with autopsy findings with special reference to pulmonary embolism and infarction. Am J Roentgenol. 1940;43:305–26.
2. Palla A, Donnamaria V, Petruzzelli S, Rossi G, Riccetti G, Giuntini C. Enlargement of the right descending pulmonary artery in pulmonary embolism. AJR Am J Roentgenol. 1983;141:513-7. [CrossRef] [PubMed]

Cite as: Ali A, Sirikonda NS. Medical image of the month: Hampton hump and Palla sign. Southwest J Pulm Crit Care. 2019;19(5):144-5. doi: https://doi.org/10.13175/swjpcc041-19 PDF

November 2018 Imaging Case of the Month: Respiratory Failure in a 36-Year-Old Woman

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ USA

Clinical History: A 36–year old woman presented with complaints of shortness of breath and worsening dyspnea on exertion. She had a reported history of central nervous system vasculitis of uncertain etiology, treated with azathioprine and prednisone currently, and cyclophosphamide in the past. Her symptoms reportedly responded well to this regimen. Her diagnosis of central nervous system vasculitis was established 6 months earlier when the patient presented with upper extremity paresthesia, headache, left arm weakness, diplopia, and a right eye visual field deficit, evidently with brain imaging showing some pathologic changes, although those records were not available at her presentation. Reportedly she responded well to her immunosuppressive therapy and her steroid and azathioprine doses had been tapered accordingly. Her past medical history was otherwise remarkable for a history of migraine headaches, depression, childhood asthma, hemorrhagic cystitis due to cyclophosphamide (which prompted discounting this drug in favor of azathioprine for the purported central nervous system vasculitis) in the past, and endometriosis.

The patient is a former smoker for a total of 5 pack-years, quitting years previously. She is the mother of a 3-year-old child. The patient denied alcohol and drug use. A history of penicillin allergy was elicited. In addition to azathioprine and prednisone, her medications included inhaled budesonide, Bactrim, escitalopram, topiramate, and sumatriptan/naproxen sodium as well as a multivitamin. There was some history of fenfluramine/phentermine (“Fen-Fen”) use years earlier.

Her physical examination was largely unremarkable. The patient complained of head pain and was visibly mildly dyspneic, but her lungs were clear and no abnormal heart sounds were detected. Her extremities appeared normal- no ecchymosis, cyanosis, or clubbing was detected. She did have some prior history suggesting the presence of erythema nodosum, now presenting as an erythematous region on the right lower extremity, which underwent biopsy, although changes characteristic of erythema nodosum were not present at her current examination. Reportedly this region had been injured when she bumped the right lower extremity on a chair, and this injury evidently became infected, requiring drainage, yielding cultures positive for Staphylococcus aureus and, about 1 month later, Actinomyces israelii. Her vital signs should normal pulse rate and blood pressure, breathing at 26 breaths / minute. Her room air oxygen saturation was 93%.

Frontal and lateral chest radiography (Figure 1) was performed.

Figure 1. Frontal (A) and lateral (B) chest radiography.

Which of the following represents the most accurate assessment of the chest radiographic findings? (Click on the correct answer to be directed to the second of twelve pages)

1. Chest radiography shows basilar fibrotic opacities
2. Chest radiography shows bilateral pleural effusions
3. Chest radiography shows cavitary pulmonary lesions
4. Chest radiography shows marked cardiomegaly
5. Chest radiography shows numerous small nodular opacities

Cite as: Gotway MB. November 2018 imaging case of the month: Respiratory failure in a 36-year-old woman. Southwest J Pulm Crit Care. 2018;17(5):119-33. doi: https://doi.org/10.13175/swjpcc114-18 PDF

December 2017 Imaging Case of the Month

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ USA

Imaging Case of the Month CME Information  

Completion of an evaluation form is required to receive credit and a link is provided on the last panel of the activity.

0.25 AMA PRA Category 1 Credit(s)™

Estimated time to complete this activity: 0.25 hours

Lead Author(s): Michael B. Gotway, MD. All Faculty, CME Planning Committee Members, and the CME Office Reviewers have disclosed that they do not have any relevant financial relationships with commercial interests that would constitute a conflict of interest concerning this CME activity. 

Learning Objectives: As a result of completing this activity, participants will be better able to:

1. Interpret and identify clinical practices supported by the highest quality available evidence.
2. Establish the optimal evaluation leading to a correct diagnosis for patients with pulmonary, critical care and sleep disorders.
3. Translate the most current clinical information into the delivery of high quality care for patients.
4. Integrate new treatment options for patients with pulmonary, critical care and sleep related disorders.

Learning Format: Case-based, interactive online course, including mandatory assessment questions (number of questions varies by case). Please also read the Technical Requirements.

CME Sponsor: University of Arizona College of Medicine at the Arizona Health Sciences Center.

Current Approval Period: January 1, 2017-December 31, 2018

Clinical History: A 57-year-old woman with a past medical history remarkable only for hyperlipidemia undergoing statin therapy presented with a history of slowly progressive dyspnea on exertion for at least months, possibly longer. The patient denied cough, hemoptysis, and chest pain.

Physical examination was largely unremarkable and the patient’s oxygen saturation was 96% on room air while resting. The patient’s vital signs were within normal limits.

Laboratory evaluation was unremarkable. Quantiferon testing for Mycobacterium tuberculosis was negative, and testing for coccidioidomycosis was unrevealing.

Frontal and lateral chest radiography (Figure 1) was performed.

Figure 1. Frontal chest radiography.

Which of the following statements regarding the chest radiograph is most accurate? (Click on the correct answer to proceed to the second of nine pages)

1. The chest radiograph appears normal
2. The chest radiograph shows bilateral, symmetric lower lobe reticulation suggesting fibrotic disease
3. The chest radiograph shows left upper lobe collapse
4. The chest radiograph shows linear right lower lobe opacity suggesting scarring
5. The chest radiograph shows numerous small miliary nodules

Cite as: Gotway MB. December 2017 imaging case of the month. Southwest J Pulm Crit Care. 2017;15(6):2563-66. doi: https://doi.org/10.13175/swjpcc149-17 PDF

The “Hidden Attraction” of Cardiac Magnetic Resonance Imaging for Diagnosing Pulmonary Embolism

Ahmed A. Harhash MD¹

James Cassuto MD PhD²

Ryan J. Avery MD³

Phillip H. Kuo MD PhD³ 

¹Division of Cardiology, Department of Medicine, and the ³Department of Radiology University of Arizona, Tucson, Arizona USA

²Department of Radiology, Jackson Memorial Hospital, Miami, Florida USA

Abstract

While various modalities exist for the diagnosis of pulmonary embolism (PE), CT pulmonary angiography (CTPA) is the most widely used and can establish the diagnosis quickly and reliably. We report a patient who presented with syncope who developed pulseless electrical activity (PEA) arrest in the emergency department. Given the presence of acute renal injury, CTA was felt to be contraindicated. A ventilation-perfusion lung (VQ) scan demonstrated low probability for PE; however, echocardiography revealed evidence for right heart strain. Subsequent cardiac magnetic resonance imaging (CMR) unexpectedly revealed a saddle PE. This case highlights the potential role for MR for the diagnosis of PE when high clinical suspicion is discordant with results of conventional imaging.

Introduction

High-risk acute pulmonary embolism (PE) - generally defined as patients presenting with shock or hypotension- is associated with up to 22% 30-day mortality (1). The role of imaging for diagnosing PE is critical, with CT pulmonary angiography (CTPA) the most widely used and generally accepted as the test of choice. CTPA offers high sensitivity and specificity for PE, short acquisition time, and the ability to diagnose alternative diagnoses in patients presenting with symptoms suggesting acute PE but with negative CTPA results. In the setting of stable chronic renal insufficiency (GFR ≥30 mL/min/1.73m2) the risk of contrast-induced nephropathy from intravenous iodinated contrast media is low, and administration of iodinated intravenous contrast in this setting considered safe for most patients (2). However, few data regarding the safety of CTPA in the setting of worsening acute kidney injury are available. In these circumstances, an understanding of alternative imaging modalities for the assessment of suspected acute PE is critical. 

Case Presentation

A 61-year-old man with no past medical history presented unresponsive to the emergency department after collapsing while shopping. The patient was minimally arousable during initial assessment and reported sudden onset of shortness of breath prior to syncope. In the emergency room, the patient developed pulseless electrical activity- cardiac arrest. Return of spontaneous circulation was achieved after 2-cycles of CPR and endotracheal intubation. The patient then developed ventricular fibrillation with return of spontaneous circulation following defibrillation. The ECG demonstrated supraventricular arrhythmia with right bundle branch block. Emergent cardiac catheterization was performed for possible acute coronary syndrome but revealed no obstructive lesions. CT pulmonary angiography was then considered to evaluate for PE, however alternative examinations were pursued secondary to acute kidney injury (creatinine 2.3 mg/dL vs. baseline 1.1 mg/dL). Transthoracic echocardiography revealed right ventricular enlargement and hypokinesis (Figure 1).

Figure 1. Apical four chamber view (transthoracic echocardiogram after intravenous administration of DEFINITY® perflutren lipid microsphere) demonstrated septal flattening consistent with right ventricular pressure/volume overload (black arrows).

Immediate anticoagulation with intravenous heparin infusion was started as clinical suspicion for PE was high, particularly given the presence of right heart strain. The patient regained hemodynamic stability and was extubated by hospital day three. To assess for the presence of PE, a VQ scan was performed, which showed low probability for PE (Figure 2). 

Figure 2. Nuclear ventilation-perfusion scan was performed first with 50 millicuries of technetium-99m diethylenetriaminepentaacetic acid aerosol administered via inhalation with multi-view planar imaging of the lungs, followed by intravenous administration of 6 millicuries of technetium-99m macroaggregated albumin with repeat multi-view planar imaging. Matched ventilation-perfusion defects are seen involving the anterior and apical right upper lobe and basal posterior left lower lobe (black arrows), no segmental mismatched perfusion defects were detected. The final impression was low probability for acute pulmonary embolism.

As the RV dysfunction remained unexplained, cardiac magnetic resonance (CMR) was performed to evaluate right ventricular function and revealed no intrinsic RV disease, but did reveal a central, “saddle” PE (Figure 3).  

Figure 3. Axial black blood cardiac MRI sequence (free breathing HASTE, TR 700 ms, TE 46 ms, slice thickness 8mm, slice gap 2mm) was performed prior to intravenous contrast injection and revealed a non-obstructive saddle embolus at the bifurcation of the pulmonary trunk (white arrows).

Discussion

The incidence of symptomatic venous thromboembolism in adults is 1-2:1000, with one-third of patients presenting with PE. Early diagnosis is the cornerstone for improving outcomes due to acute PE - mortality decreases from 25% to 2-8% with prompt management (3). As the array of imaging modalities expands, the role and value of radiologists as consultants for guiding clinicians for the evaluation of PE also increases, particularly for complicated patients. This case highlights both a pitfall in the use of VQ scanning and a role for MR for evaluating PE. For PE patients with non-occlusive thrombus and balanced oligemia, as in the patient presented, lungs may show no mismatched defects. This situation may lead to a falsely low probability VQ scan result as the test relies upon the relative perfusion (or lack thereof) of lung segments compared to others. Prior to the VQ scan, the patient had been anticoagulated for three days with marked clinical improvement. Accordingly, the VQ scan might have been high probability had it been performed prior to anticoagulation. As reported in the PIOPED I study, which integrated both clinical and imaging findings, a low probability VQ scan in the context of high clinical suspicion was associated with 21% probability of PE at catheter pulmonary angiography (4).

This case demonstrates that CMR can incidentally diagnose central PE, although CMR protocols are optimized for cardiac evaluation and not for PE detection, and therefore should never be used in place of dedicated exams for PE.

Magnetic resonance pulmonary angiography offers several advantages for PE evaluation compared with CTPA, including utilization of non-ionizing radiation and not requiring the use of iodinated contrast agents. However, historically, pulmonary MR imaging has been hampered by long acquisition times, limited spatial resolution, and inadequate volumes of coverage compared with CTPA (5). The largest efficacy study of the use of MR pulmonary angiography for the diagnosis of acute PE was the PIOPED III study, in which 371 patients underwent contrast-enhanced pulmonary MRA for the assessment of suspected PE. Pulmonary MR examinations were compared with references standards to establish or exclude the diagnosis of PE. In the PIOPED III study, pulmonary MRA was found to be technically inadequate in 25% of patients, typically the result of poor pulmonary arterial opacification or motion artifacts, with the sensitivity of pulmonary MRA only 57% when including the patients with technically inadequate examinations (6). While specificity for PE diagnosis was high (99%), the sensitivity of pulmonary MRA only rose to 78% when technically limited examinations were excluded. The PIOPED III study has frequently been cited as a cautionary note regarding the use of pulmonary MR to diagnose PE, but it should be noted that this study only employed one technique for the evaluation of possible PE- pulmonary MRA- and the technical aspects of the MR acquisition are now over a decade old (5). Recent improvements in scanner technology, including shorter echo times, time-resolved imaging, improved receiver coils and gradients, more optimized bolus injection techniques, and the implementation of parallel imaging, have reduced acquisition times and decreased artifacts, allowing for more robust MR pulmonary imaging (5). Furthermore, a multiparametric approach to venous thromboembolism imaging using MR, including unenhanced imaging employing balanced steady state free precession sequences combined with enhanced imaging, first using time-resolved contrast-enhanced perfusion imaging, followed by pulmonary MRA using a rapid 3D spoiled gradient echo sequence (typically several vascular phase acquisitions are obtained to optimize pulmonary arterial enhancement), and completed with an additional post-contrast T1-weighted spoiled gradient recalled acquisition, provide complete pulmonary vascular assessment and offer multiple methods for PE detection should one particular sequence be suboptimal (5). A more recent single center study of 190 patients undergoing magnetic resonance pulmonary angiography using a multiparametric approach as the primary study to evaluate for PE showed the negative predictive value of the test to be 97% at 3-months and 96% at 12-months follow-up, similar to CTPA (7). Furthermore, while magnetic resonance pulmonary angiography may show somewhat reduced sensitivity for the detection of distal segmental and sub-segmental PE compared with CTPA, the clinical relevance of such small emboli remains in doubt and many patients with such small emboli may not require anticoagulation.         

Conclusion

We report the somewhat unusual finding of central, “saddle” PE diagnosed using cardiac MR in a patient with clinical suspicion for PE but a low probability VQ scan. Our study highlights the important and growing role of MR for the diagnosis of acute PE and serves as a reminder to evaluate all structures within the field of view, not just the heart, when interpreting CMR examinations. Even with the amazing advances in imaging, no imaging modality is perfect and clinical acumen should never be replaced or discounted, especially for a diagnosis as critical as PE.

References

1. Becattini C, Agnelli G, Lankeit M, et al. Acute pulmonary embolism: mortality prediction by the 2014 European Society of Cardiology risk stratification model. Eur Respir J. 2016 Sep;48(3):780-6. [CrossRef] [PubMed]
2. Davenport MS, Khalatbari S, Cohan RH, Dillman JR, Myles JD, Ellis JH. Contrast material-induced nephrotoxicity and intravenous low-osmolality iodinated contrast material: risk strati cation by using estimated glomerular ltration rate. Radiology. 2013;268(3):719-728. [CrossRef] [PubMed]
3. Lavorini F, Di Bello V, De Rimini ML, et al. Diagnosis and treatment of pulmonary embolism: a multidisciplinary approach. Multidiscip Respir Med. 2013 Dec 19;8(1):75. [CrossRef] [PubMed]
4. Worsley DF, Alavi A. Comprehensive analysis of the results of the PIOPED Study. Prospective Investigation of Pulmonary Embolism Diagnosis Study. J Nucl Med. 1995 Dec;36(12):2380-7. [PubMed]
5. Schiebler ML, Nagle SK, François CJ. Effectiveness of MR angiography for the primary diagnosis of acute pulmonary embolism: clinical outcomes at 3 months and 1 year. J Magn Reson Imaging. 2013 Oct;38(4):914-25. [CrossRef] [PubMed]
6. Stein PD, Chenevert TL, Fowler SE, Goodman LR, Gottschalk A, Hales CA, et al. Gadolinium-enhanced magnetic resonance angiography for pulmonary embolism: amulticenter prospective study (PIOPED III). Ann Intern Med 2010;152(7):434-43, . [CrossRef] [PubMed]
7. Schiebler ML, Nagle SK, François CJ. Effectiveness of MR angiography for the primary diagnosis of acute pulmonary embolism: clinical outcomes at 3 months and 1 year. J Magn Reson Imaging. 2013;38(4):914-25. [CrossRef] [PubMed]

Cite as: Harhash AA, Cassuto J, Avery RJ, Kuo PH. The “hidden attraction” of cardiac magnetic resonance imaging for diagnosing pulmonary embolism. Southwest J Pulm Crit Care. 2017;14(5):230-5. doi: https://doi.org/10.13175/swjpcc057-17 PDF 

Medical Image of the Week: Lynch Syndrome

Figure 1. Coronal CT of the chest showing bilateral filling defects in pulmonary arteries representing pulmonary emobolism.

Figure 2. Coronal CT of the abdomen/pelvis showing periaortic lymphadenopathy suggestive for metastatic disease.

Figure 3. Coronal CT of the abdomen/ pelvis showing a 13 x 13.6 cm solid and cystic mass above and to the right of the uterus concerning for right ovarian neoplasm.

A 43-year-old woman with a history of anemia, thrombocytopenia, and recent treatment for pyelonephritis was transferred to our hospital for increasing shortness of breath. Four months prior to admission, she developed unprovoked bilateral deep vein thrombosis (DVT) and pulmonary emboli (PE) and was started on rivaroxaban at that time. At presentation, she was complaining of worsening shortness of breath, heavy menstrual bleeding and pain in her calves. CT angiography of chest showed multiple pulmonary emboli to the lower lobes and left upper lobe (Figure 1) and lower extremity venous Doppler showed extensive, acute deep vein thrombosis involving the femoral, popliteal and calf veins bilaterally.

Rivaroxaban was held due to anemia and thrombocytopenia and there was concern for respiratory failure since she developed new DVT and PE. She was transfused with 1 unit of packed red blood cells and started on a heparin drip. She continued to have significant menorrhagia, the heparin drip was discontinued, and subsequently, an inferior vena cava filter was placed.

On further questioning, the patient reported a 26 pound weight loss over the past three weeks. This combined with her menorrhagia requiring blood transfusion prompted further imaging. CT of the abdomen and pelvis showed a 13 x 13.6 cm solid and cystic mass representing a right ovarian neoplasm that was contiguous with the uterus as well as periaortic adenopathy suggestive of metastasis (Figures 2 and 3). Further investigation into the patient’s family history identified significant history for breast and ovarian cancers on her maternal side. Genetic testing of the patient showed a germline mutation in the MSH2 gene, consistent with Lynch syndrome.

Lynch syndrome, also known as hereditary non-polyposis colorectal cancer, is a hereditary cancer syndrome characterized by mutations in DNA mismatch repair genes. The majority of affected individuals will develop colorectal or endometrial malignancies; however these individuals are also at increased risk for developing ovarian neoplasms. The lifetime risk of developing ovarian cancer in women with Lynch syndrome is 7% (3-14%) compared to 1.4% in the general population (1). However, there is no survival difference between women with Lynch syndrome and the general population (1). If ovarian malignancy is present at diagnosis of Lynch syndrome, prophylactic hysterectomy and bilateral salpingo-oophorectomy is recommended (2). Otherwise, management can include prophylactic surgery or screening with annual pelvic exams and transvaginal ultrasounds. Persons with lynch syndrome should also receive surveillance for other associated malignancies such as colorectal or endometrial cancer (1,2).

Abha Athale MS¹, Christopher Morrison MD², Robert Betancourt MD³ and Jennifer Segar MD³

¹ Midwestern University Arizona College of Osteopathic Medicine

² Tucson Hospitals Medical Education Program

³ Department of Internal Medicine, Banner University Medical Center-Tucson Medical Center, Tucson, AZ

References

1. Koornstra JJ, Mourits MJ, Sijmons RH, Leliveld AM, Hollema H, Kleibeuker JH. Management of extracolonic tumours in patients with Lynch syndrome. Lancet Oncol. 2009 Apr;10(4):400-8. [CrossRef] [PubMed]
2. Lindor NM, Petersen GM, Hadley DW, Kinney AY, Miesfeldt S, Lu KH, Lynch P, Burke W, Press N. Recommendations for the care of individuals with an inherited predisposition to Lynch syndrome: a systematic review. JAMA. 2006 Sep 27;296(12):1507-17. [CrossRef] [PubMed]

Cite as: Athale A, Morrison C, Betancourt R, Segar J. Medical image of the week: Lynch syndrome. Southwest J Pulm Crit Care. 2016;13(5):202-4. doi: http://dx.doi.org/10.13175/swjpcc087-16 PDF 

Medical Image of the Week: Saddle Pulmonary Embolism

Figure 1. Thoracic axial computed tomography angiogram (CTA) demonstrating saddle embolism within bilateral pulmonary arteries with extension into sub-segmental branches.

Figure 2. Coronal CTA.

A 66-year-old woman with recent history of left knee surgery and L2-L5 spinal fusion within the past month presented to the Emergency Department (ED) with pleuritic chest pain and shortness of breath for three days. On admission, reported crushing diffuse substernal chest pain worsened to 10/10 on the pain scale on the day of presentation. In the ED, physical examination was remarkable for tachycardia, tachypnea, diaphoresis and hypotension. Initial electrocardiogram was significant for sinus tachycardia with S1Q3T3 pattern. thoracic computed tomography angiogram (CTA) showed saddle pulmonary embolus (PE) with extension into segmental vasculature, right greater than left (Figures 1 and 2). A bedside echocardiogram demonstrated diastolic and systolic bowing of the intraventricular septum into the left ventricle. An emergent trans-thoracic echocardiogram confirmed flattened septum consistent with right ventricle pressure overload with right ventricular systolic pressure of 55 mmHg + central venous pressure (CVP) and reduced left ventricular ejection fraction of 38%. Her hemodynamic condition was stabilized by administering intravenous norepinephrine infusion. Interventional radiology was contacted for an emergent catheter directed thrombolysis. Ten milligrams of tissue plasminogen activator (tPA) was injected into the pulmonary artery with subsequent removable inferior vena cava filter placement. Vasoactive medications were titrated down and stopped four hours following tPA administration and anticoagulation with intravenous heparin was commenced. The patient was discharged from the hospital after initiation of rivaroxaban.

Saddle pulmonary embolism (SPE) is a form of large pulmonary thromboembolism that straddles the main pulmonary arterial branch at the bifurcation. The incidence of SPE is found in about 2.6% of the PE cases (1). The choice of diagnostic testing for PE is CTA based on multiple studies demonstrating CTA was both sensitive and specific for PE especially in moderate to high clinical probability PE (2,3). Suspicion for PE in our patient included sedentary status following knee replacement surgery, tachycardia, S1Q3T3 pattern on EKG, evidence for right ventricular strain on echocardiography, and no other diagnosis more likely thus lead to high clinical suspicion of pulmonary embolism with a Well’s score for PE of 6.

Faraz Jaffer, MD¹ See Wei Low, MD¹ and Sairam Parthasarathy, MD²

¹Department of Internal Medicine, Banner - University Medical Center

²Department of Allergy, Pulmonary, Critical Care and Sleep Medicine

Banner-University Medical Center

Tucson, AZ USA

References

1. Ryu JH, Pellikka PA, Froehling DA, Peters SG, Aughenbaugh GL. Saddle pulmonary embolism diagnosed by CT angiography: frequency, clinical features and outcome. Respir Med. 2007 Jul;101(7):1537-42. [CrossRef] [PubMed]
2. Van Belle A, Büller HR, Huisman MV, et al. Effectiveness of managing suspected pulmonary embolism using an algorithm combining clinical probability, D-dimer testing, and computed tomography. JAMA. 2006 Jan 11;295(2):172-9. [CrossRef] [PubMed]
3. Stein PD, Fowler SE, Goodman LR, et al. Multidetector computed tomography for acute pulmonary embolism. N Engl J Med. 2006 Jun 1;354(22):2317-27. [CrossRef] [PubMed] 

Cite as: Jaffer F, Low SW, Parthasarathy S. Medical image of the week: saddle pulmonary embolism. Southwest J Pulm Crit Care. 2016 May;12(5):192-3. doi: http://dx.doi.org/10.13175/swjpcc024-16 PDF

May 2016 Imaging Case of the Month

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ USA

Imaging Case of the Month CME Information  

Members of the Arizona, New Mexico, Colorado and California Thoracic Societies and the Mayo Clinic are able to receive  0.25 AMA PRA Category 1 Credits™. Completion of an evaluation form is required to receive credit and a link is provided on the last panel of the activity.

0.25 AMA PRA Category 1 Credit(s)™

Estimated time to complete this activity: 0.25 hours

Lead Author(s): Michael B. Gotway, MD. All Faculty, CME Planning Committee Members, and the CME Office Reviewers have disclosed that they do not have any relevant financial relationships with commercial interests that would constitute a conflict of interest concerning this CME activity. 

Learning Objectives:
As a result of this activity I will be better able to:    

1. Correctly interpret and identify clinical practices supported by the highest quality available evidence.
2. Will be better able to establsh the optimal evaluation leading to a correct diagnosis for patients with pulmonary, critical care and sleep disorders.
3. Will improve the translation of the most current clinical information into the delivery of high quality care for patients.
4. Will integrate new treatment options in discussing available treatment alternatives for patients with pulmonary, critical care and sleep related disorders.

Learning Format: Case-based, interactive online course, including mandatory assessment questions (number of questions varies by case). Please also read the Technical Requirements.

CME Sponsor: University of Arizona College of Medicine at the Arizona Health Sciences Center.

Current Approval Period: January 1, 2015-December 31, 2016

Financial Support Received: None.

Clinical History:  A 58-year-old man with hypertension presents for a routine health examination. As part of his routine evaluation, frontal and lateral chest radiography (Figure 1) was performed.  

Figure 1. Frontal (panel A) and lateral (panel B) chest radiography.

Which of the following statements regarding the chest radiograph is most accurate? (Click on the correct answer to proceed to the second of eight panels)

1. The frontal chest radiograph shows a small lung nodule
2. The frontal chest radiograph shows a small metallic focus just posterior to the inferior sternum
3. The frontal chest radiograph shows an unusual right-sided mediastinal contour
4. The frontal chest radiograph shows asymmetrically increased attenuation of the left thorax compared with the right
5.  The frontal chest radiograph shows normal findings

Cite as: Gotway MB. May 2016 imaging case of the month. Southwes J Pulm Crit Care. 2016 May;12(5):180-91. doi: http://dx.doi.org/10.13175/swjpcc040-16 PDF 

Medical Image of the Week: Pulmonary Thomboembolism Complicated by Free Floating Atrial Thrombus

Figure 1. Thoracic CT angiogram showing filling defects in the right pulmonary arterial system (arrows).

 

Figure 2. Thoracic CT angiogram showing filling defects in the left pulmonary arterial system (arrow).

 

Figure 3. Video of transthoracic echocardiogram showing thrombus in the right atrium.

An 82-year-old female presented to the emergency department four days after suffering a fall at home. She complained of left hip pain, weakness and shortness of breath. Physical exam demonstrated a blood pressure of 82/60 mm Hg, pulse of 120 bpm, and room air oxygen saturation measured by pulse oximetry of 81%. Exam was otherwise remarkable for pain on movement of the left hip. Laboratory exam was remarkable for troponin of 2.5 ng/ml and pro-beta natiuretic peptide of 31,350 pg/ml. Chest radiograph demonstrated elevation of the right hemidiaphragm. EKG demonstrated sinus tachycardia with a rightward axis and an interventricular conduction defect. Left hip film disclosed a non-displaced femoral neck fracture. CAT-angiography of the chest revealed pulmonary emboli involving all five lobes with significant bilateral proximal pulmonary arterial filling defects (Figures 1,2). Venous Doppler examination demonstrated left lower extremity deep vein thrombosis. Trans-thoracic echocardiogram demonstrated right ventricular enlargement and a large unattached, right atrial thrombus (Figure 3). The patient was treated with 100 mg of tissue plasminogen activator (tPA) administered over 2 hours, followed by intravenous unfractionated heparin, with subsequent improvement of both her hemodynamic and oxygenation status. A repeat echocardiogram 48 hours after the administration of tPA demonstrated complete resolution of the right atrial clot. The patient has continued to do well.

Discussion

Free floating right heart thrombi (FFRHT), also known as “emboli in transit”, are mobile, unattached masses, and may be present in up to 18% of patients with pulmonary emboli (1). Untreated, the mortality of FFRHT approaches 100%. Therapeutic options include anticoagulation (28.6% mortality), surgical embolectomy (23.8% mortality), and thrombolysis (11.3% mortality, survival benefit (p<0.05) )(2). There are case reports of percutaneous catheter directed therapies, with varying degrees of success described (1,3). Floating right heart thrombi represent a severe subset of pulmonary thromboembolic disease and warrant immediate intervention. Although therapy must be individualized, thrombolysis appears to offer improved survival when compared to anticoagulation or surgical embolectomy.

Charles J. VanHook, Douglas Tangel, James Jonas

Department of Intensive Care Medicine

Longmont United Hospital

Longmont, CO USA

References

1. Chartier L, Bera J, Delomez M, Asseman P, Beregi JP, Bauchart JJ, Waremburg H, Thery C. Free-floating thrombi in the right heart. Circulation. 1999;99:2779-83. [CrossRef] [PubMed]
2. Rose PS, Punjabi NM, Pearse DB. Treatment of right heart pulmonary emboli. Chest. 2002;121(3):806-14. [CrossRef] [PubMed]
3. Maron B, Goldhaber SZ, Sturzu AC, Rhee DK, Ali B, Pinak BS, Kirshenbaum JM. Cather-directed thomobolysis for giant right atrial thrombus. Circulation:Cardiovascular Imaging 2010;3:126-7. [CrossRef] [PubMed]

Cite as: VanHook CJ, Tangel D, Jonas J. Medical image of the week: pulmonary thromboembolism complicated by free floating atrial thrombus. Southwest J Pulm Crit Care. 2015;11(6):252-3. doi: http://dx.doi.org/10.13175/swjpcc119-15 PDF

Medical Image Of The Week: Westermark Sign

Figure 1. Chest x-ray showing decrease pulmonary vasculature on the right upper lobe (red circle, Westermark sign).

Figure 2. Coronal section of the CT angiogram showing occlusive thrombosis on the right pulmonary artery. 

A 71 year old man was evaluated in the Emergency Department for acute onset of dyspnea. On exam he was tachypneic, tachycardic and hypoxemic requiring 6 L/min of oxygen. He had recently underwent prostatectomy for prostate cancer. Past medical history was also significant for coronary artery disease treated with coronary bypass.

The chest x-ray (Figure 1) shows unilateral oligemia concerning for a pulmonary embolus and the CT angiogram of the chest (Figure 2) confirms the diagnosis.

While the chest radiograph is normal in the majority of pulmonary emboli, the ‘Westermark sign’ may be seen in up to 2% of the cases (1). It represents a focus of oligemia seen distal to a pulmonary embolism. The finding is a result of a combination of dilation of the pulmonary artery proximal to the thrombus and the collapse of the distal vasculature. 

Muna Omar MD¹, Tammer Elaini MD² and Bhupinder Natt MD¹

¹Division of Pulmonary, Allergy , Critical Care and Sleep Medicine

²Department of Internal Medicine

University of Arizona Medical Center

Tucson, AZ

Reference

1. Worsley DF, Alavi A, Aronchick JM, Chen JT, Greenspan RH, Ravin CE. Chest radiographic findings in patients with acute pulmonary embolism: observations from the PIOPED Study. Radiology. 1993;189(1):133-6. [CrossRef] [PubMed] 

Reference as: Omar M, Elaini T, Natt B. Medical image of the week: Westermark sign. Southwest J Pulm Crit Care. 2015;10(3):125-6. doi: http://dx.doi.org/10.13175/swjpcc015-15 PDF

Medical Image of the Week: Bilateral Atrial Appendage Thrombi

Figure 1. Panel A: Right atrial appendage (RAA) thrombus (red arrow) on chest computerized tomorgraphy angiogram (CTA). Panel B: Left atrial appendage (LAA) thrombus (yellow arrow) on chest CTA. Panel C: RAA thrombus (red arrow) on transesophageal echocardiography (TEE). Panel D: LAA thrombus (yellow arrow) on TEE.

A 63-year-old man with a past history significant for hypertension, low back pain and polysubstance abuse (tobacco and marijuana) presented with shortness of breath and hemoptysis for the last 8 days prior to admission. His initial exam showed elevated jugular venous pressure and bilateral basal crackles with reduced air entry on the right lower lung zone.

The patient was found to be in atrial fibrillation with a rapid ventricular response. His initial chest X-ray showed a moderate right-sided pleural effusion. Immediate bedside echo was concerning for bilateral ventricular dysfunction with concerns of right-sided heart pressure and volume overload. A chest CT angiogram was obtained and showed acute lower lobe pulmonary embolism, with possible distal infarct, moderate right sided pleural effusion, and filling defects in both atrial appendages concerning for thrombi (Figure 1, Panels A & B).

The patient was started on therapeutic anticoagulation and underwent therapeutic thoracentesis, gentle diuresis, and rate control for his atrial fibrillation. A few days later, a trans-esophageal echo confirmed the bilateral atrial thrombi (Figure 1, Panels C & D).

Huthayfa Ateeli MBBS¹, Andrew Kovoor MD¹, Hem Desai MBBS¹, Alana Stubbs MD², Tam Nguyen MD³

¹Department of Medicine, ²Radiology Department, and ³Cardiology Division

University of Arizona and Southern Arizona VA Health Care System

Tucson, AZ

References

1. Kim YY, Klein AL, Halliburton SS, Popovic ZB, Kuzmiak SA, Sola S, Garcia MJ, Schoenhagen P, Natale A, Desai MY. Left atrial appendage filling defects identified by multidetector computed tomography in patients undergoing radiofrequency pulmonary vein antral isolation: a comparison with transesophageal echocardiography. Am Heart J. 2007;154(6):1199-205. [CrossRef] [PubMed]
2. Shapiro MD, Neilan TG, Jassal DS, Samy B, Nasir K, Hoffmann U, Sarwar A, Butler J, Brady TJ, Cury RC. Multidetector computed tomography for the detection of left atrial appendage thrombus: a comparative study with transesophageal echocardiography. J Comput Assist Tomogr. 2007;31(6):905-9. [CrossRef] [PubMed] 

Reference as: Ateeli H, Kovoor A, Desai H, Stubbs A, Nguyen T. Medical image of the week: bilateral atrial appendange thrombi. Southwest J Pulm Crit Care. 2015;10(1):54-5. doi: http://dx.doi.org/10.13175/swjpcc006-15 PDF

Medical Image of the Week: ECG in PE

Figure 1. ECG on presentation demonstrating sinus tachycardia, anterior precordial T wave inversions and S1Q3T3, classic ECG findings of pulmonary embolism.

Figure 2. Panel A: CT angiogram demonstrating bilateral pulmonary embolism involving nearly every segmental and subsegmental pulmonary artery. Panel B: Echocardiogram, apical 4-chamber view, with dilated right ventricle and poor function. Panel C: Right leg ultrasound showing acute, non-occlusive thrombus; the right side of the image demonstrates incompressibility of the right femoral vein.

A 44-year-old male long distance truck driver with no known medical history presented with intermittent episodes of dyspnea for the past 24 hours, and an episode of exertional syncope just prior to hospitalization. The patient complained of sharp severe chest pain and reports several week history of right leg swelling. Initial Electrocardiogram (ECG, Figure 1) shows sinus tachycardia and signs of right ventricular strain with an associated troponin elevation. CT pulmonary angiography confirmed bilateral, extensive pulmonary emboli (PE) (Figure 2A, arrow at left pulmonary artery embolus). An echocardiogram showed severe right ventricular systolic dysfunction (Figure 2B, arrow indicated RV). Duplex ultrasound of the right leg showed extensive, acute, non-occlusive thrombus (Figure 2C, arrow indicates clot failing to compress). The patient received an IVC filter due to substantial clot burden. A hypercoagulability workup was negative.

The ECG is part of the typical evaluation for syncope, chest pain and shortness of breath. Multiple studies evaluating the utility of the ECG in the diagnosis of PE have been conducted (1-3). One study in patients with suspected PE undergoing diagnostic testing found that only tachycardia and incomplete right bundle branch block were significantly more prevalent in patients with PE than those without. Another study found a 39% rate of sinus tachycardia in those ultimately found to have PE compared to 24% in those who had negative studies. The S1Q3T3 phenomenon was present in 12% of those with PE vs 3% in those without. One or more traditional findings of right ventricular strain: S1Q3T3, right bundle branch block, or right axis deviation was present in only 13% of patients with PE who had RV dilation on echocardiography, however these findings were also present in 8.8% of patients with PE without evidence of RV dysfunction. Non-specific ECG findings such as sinus tachycardia and ST-T changes are the most commonly identified ECG abnormalities in patients with PE. Overall the ECG as a test for PE exhibits poor test characteristics and thus has little clinical utility for its diagnosis, despite the frequent emphasis on these findings in medical education.

Our patient’s ECG demonstrates several classic findings suggestive of PE including sinus tachycardia, S1Q3T3, and T-wave inversions in the anterior precordial leads. While certain ECG findings do correlate with the presence of PE they are frequently present in patients without PE and absent in those with the disease. ECG may have some utility in risk stratification by identifying signs of right heart strain, however echocardiography is the preferred modality.

Taylor Shekell MD², Cameron Hypes MD MPH^1,2, Yuval Raz MD¹

¹ Department of Medicine, Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine

² Department of Emergency Medicine

University of Arizona Medical Center

Tucson, AZ

References

1. Rodger M, Makropoulos D, Turek M, Quevillon J, Raymond F, Rasuli P, Wells PS. Diagnostic value of the electrocardiogram in suspected pulmonary embolism. Am J Cardiol. 2000;86:807-9. [CrossRef] [PubMed]
2. Sinha N, Yalamanchili K, Sukhija R, Aronow WS, Fleisher AG, Maguire GP, Lehrman SG. Role of the 12-lead electrocardiogram in diagnosing pulmonary embolism. Cardiol Rev. 2005;13:46-9. [PubMed]
3. Stein P, Matta F, Sabra M, et al. Relation of electrocardiographic changes in pulmonary embolism to right ventricular enlargement. Am J Cardiol. 2013;112:1958-61. [CrossRef] [PubMed] 

Reference as: Shekell T, Hypes C, Raz Y. Medical image of the week: ECG in PE. Southwest J Pulm Crit Care. 2015;10(1):44-6. doi: http://dx.doi.org/10.13175/swjpcc162-14 PDF

Medical Image of the Week: PE with Infarct and Pulmonary Cavitation

Figure 1. Panels A & B: thoracic CT scan showing multiple pulmonary emboli (arrows). Panel C: frontal chest radiograph showed extensive left lung opacification most dense in the left upper lobe. Panel D: frontal chest radiograph taken 3 weeks later showing mild volume loss of the left upper lobe with a large lucency suggestive of cavitation (arrow). Panel E: thoracic CT scan confirming the cavitation.

A 49 year old man with a history of COPD presented to the ER with the sudden onset of chest pain at 3:30 AM waking him from sleep. His pain was left sided, felt like broken ribs, and was worse with deep inspiration. He acknowledged some shortness of breath which was worse over baseline for the past couple days without cough or hemoptysis. The patient was tachycardic but comfortable with SpO2 saturation 98% on 2 liters. He had trace edema and pleurisy. Laboratory evaluation was unremarkable except for a WBC count 13,000 X 10⁶ cells/L. Chest x-ray was unremarkable but thoracic CT scan showed pulmonary emboli (PE) involving left upper and lower lobar arteries (Figure 1A and 1B, arrows). Anticoagulation was started and the patient experienced increasing shortness of breath, worsening oxygenation and fever to 102ºF. On Day 2, frontal chest radiograph showed extensive left lung opacification most dense in the left upper lobe (Figure 1C). Hemoglobin dropped from 12 to 9.8 g/dL suggesting alveolar hemorrhage. He improved over the next week but low grade fevers persisted and a chest x-ray taken 3 weeks later showed mild volume loss of the left upper lobe with a large lucency suggestive of cavitation (Figure 1D, Arrow). Thoracic CT confirmed a cavitary lesion in the left apex in the region of prior thrombus with adjacent consolidated atelectasis within a background of emphysema (Figure 1E).  The patient was lost to follow up after 6 months of anticoagulation.

Pulmonary infarction is relatively uncommon, occurring in less than 10% of PE, due to dual and collateral blood supply to the lung. Cavitary infarcts are even less common (4% in autopsy studies) and are more likely in those with pulmonary venous hypertension (1). Cavitary infarcts are more likely to occur when the infarct size in larger than 4 cm and most often occurs in the mid and upper lung zones. Despite alveolar hemorrhage, anticoagulation should be continued.

Kenneth S. Knox, MD and Veronica A. Arteaga, MD

Divisions of Pulmonary and Critical Care Medicine and Thoracic Imaging

University of Arizona

Tucson, AZ

Reference 

1. Libby LS, King TE, LaForce FM, Schwarz MI. Pulmonary cavitation following pulmonary infarction. Medicine (Baltimore). 1985;64(5):342-8. [CrossRef] [PubMed]

Reference as: Knox KS, Arteaga VA. Medical image of the week: PE with infarct and pulmonary cavitation. Southwest J Pulm Crit Care. 2014;9(6):333-4. doi: http://dx.doi.org/10.13175/swjpcc158-14 PDF