Imaging
Those who care for patients with pulmonary, critical care or sleep disorders rely heavily on chest radiology and pathology to determine diagnoses. The Southwest Journal of Pulmonary, Critical Care & Sleep publishes case-based articles with characteristic chest imaging and related pathology.
The editor of this section will oversee and coordinate the publication of a core of the most important chest imaging topics. In doing so, they encourage the submission of unsolicited manuscripts. It cannot be overemphasized that both radiologic and pathologic images must be of excellent quality. As a rule, 600 DPI is sufficient for radiographic and pathologic images. Taking pictures of plain chest radiographs and CT scans with a digital camera is strongly discouraged. The figures should be cited in the text and numbered consecutively. The stain used for pathology specimens and magnification should be mentioned in the figure legend. Those who care for patients with pulmonary, critical care or sleep disorders rely heavily on chest radiology and pathology to determine diagnoses. The Southwest Journal of Pulmonary, Critical Care & Sleep publishes case-based articles with characteristic chest imaging and related pathology. The editor of this section will oversee and coordinate the publication of a core of the most important chest imaging topics. In doing so, they encourage the submission of unsolicited manuscripts. It cannot be overemphasized that both radiologic and pathologic images must be of excellent quality. As a rule, 600 DPI is sufficient for radiographic and pathologic images. Taking pictures of plain chest radiographs and CT scans with a digital camera is strongly discouraged. The figures should be cited in the text and numbered consecutively. The stain used for pathology specimens and magnification should be mentioned in the figure legend.
Medical Image of the Month: Idiopathic Right Lower Lobe Pulmonary Vein Thrombus
Figure 1. CT angiogram chest sagittal view: showing low density filling defect consistent with pulmonary vein thrombus (yellow arrow).
Figure 2. A: CT angiogram chest axial view showing right lower lobe pulmonary vein thrombus. B: the vein (red arrow) is well differentiated by his lower contrast than the adjacent artery (blue arrows).
A 62-year-old man with a medical history notable only for a seasonal allergy, presented to the emergency department with complaints of shortness of breath with productive cough for 2 months which were worsening for the last 2 weeks. CTA chest revealed low density filling defect in the RLL vein consistent with RLL vein thrombus (Figures 1 and 2). After a comprehensive work up to rule out malignancy and hypercoagulable disorders, a diagnosis of idiopathic pulmonary vein thrombosis was made. The patient received heparin and was discharged with rivaroxaban.
Pulmonary vein thrombosis is a rare disease but can be fatal, usually patient presents with non-specific symptoms such as cough and shortness of breath (1). The etiology in most of cases is hypercoagulable disorders, malignancies, atrial fibrillation, post lung operations such as lobectomy and lung transplantation, or could be idiopathic as in our patient.
Timothy Jon Rolle MD1 and Mohammad Abdelaziz Mahmoud MD, DO2
1Department of Radiology and the 2Internal Medicine Residency
Midwestern University Arizona College of Osteopathic Medicine
Canyon Vista Medical Center
Tucson, AZ USA
Reference
- Chaaya G, Vishnubhotla P. Pulmonary vein thrombosis: a recent systematic review. Cureus. 2017 Jan 23;9(1):e993. [CrossRef] [PubMed]
Cite as: Rolle TJ, Mahmoud MA. Medical image of the month: idiopathic right lower lobe pulmonary vein thrombus. Southwest J Pulm Crit Care. 2020;20(1):7-8. doi: https://doi.org/10.13175/swjpcc048-19 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:
- Interpret and identify clinical practices supported by the highest quality available evidence.
- Establish the optimal evaluation leading to a correct diagnosis for patients with pulmonary, critical care and sleep disorders.
- Translate the most current clinical information into the delivery of high quality care for patients.
- 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)
- The chest radiograph appears normal
- The chest radiograph shows bilateral, symmetric lower lobe reticulation suggesting fibrotic disease
- The chest radiograph shows left upper lobe collapse
- The chest radiograph shows linear right lower lobe opacity suggesting scarring
- 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
Medical Image of the Week: Type A Aortic Dissection Extending Into Main Coronary Artery
Figure 1. Electrocardiogram at presentation showing ST segment elevation in anterior leads (arrows).
Figure 2. Coronary angiogram showing RAO caudal view of left main coronary artery after contrast injection with the smooth proximal linear irregularity suspicious for dissection flap into the left anterior descending artery (arrow).
Figure 3. Panel A: Computed tomography angiogram transverse view showing true lumen and false lumen of both ascending and descending aorta (arrow). Panel B: Computed tomography angiogram sagittal view showing dissection from root into abdominal aorta.
A 58-year-old woman with no significant past medical history, presented to the emergency department with complains of sudden onset, severe , non-radiating epigastric pain associated with nausea and vomiting. An electrocardiogram (EKG) done in emergency department showed ST segment elevation in the anterior leads (Figure 1). Blood pressure at presentation was 141/79, and she had symmetrical bilateral pulses of the upper extremities, no diastolic murmur, and no neurologic deficit. The patient was taken to catherization laboratory, for ST segment elevated myocardial infarction (STEMI). She was found have aortic dissection extending to the left main coronary artery (Figure 2). Cardiothoracic surgery was called immediately. Computed tomography angiogram (CTA) of the thoracic and abdominal aorta revealed Debakey type 1 aortic dissection. (Figure 3). The patient was taken to the operating room. Unfortunately, the patient suffered pulseless electrical activity (PEA) arrest during anesthesia induction from which she could not be revived.
Aortic dissection is a critical compromise in the lining of the main arterial outflow from the heart (1). Two theories have been proposed to explain the pathogenesis. A tear in the tunica intima, of the aorta, leads to blood from the aortic lumen surging into the tunica media (2). In contrast, the second theory holds that the vasa vasorum in the more outer portions of the tunica media hemorrhage first and then cause the rupture of the tunica intima (2). The pressure of the pulsatile blood flow extends the dissection, typically in an anterograde fashion (2). Anatomically aortic dissection is classified as Debakey 1,2, and 3 and Stanford A and B (1). Rarely aortic dissections can also extend in a retrograde fashion to reach the coronary ostia (3). Signs of myocardial ischemia including ST segment changes, adversely affect survival outcomes in patients with type A aortic dissection extending to the coronary arteries (4).
Ali Osama Malik MD1, Oliver Abela MD2, Chowdhury Ahsan MD2, and Jimmy Diep MD2
1Department of Internal Medicine
2Department of Cardiovascular Medicine
University of Nevada School of Medicine
Las Vegas, NV USA
References
- Golledge J, Eagle KA. Acute aortic dissection. Lancet. 2008 Jul 5;372(9632):55-66. [CrossRef] [PubMed]
- Patel AY, Eagle KA, Vaishnava P. Acute type B aortic dissection: insights from the International Registry of Acute Aortic Dissection. Ann Cardiothorac Surg. 2014 Jul;3(4):368-74. [CrossRef] [PubMed]
- Neri E, Toscano T, Papalia U, Frati G, Massetti M, Capannini G, et al. Proximal aortic dissection with coronary malperfusion: presentation, management, and outcome. J Thorac Cardiovasc Surg. 2001 Mar;121(3):552-60. [CrossRef] [PubMed]
- Imoto K, Uchida K, Karube N, Yasutsune T, Cho T, Kimura K, et al. Risk analysis and improvement of strategies in patients who have acute type A aortic dissection with coronary artery dissection. Eur J Cardiothorac Surg. Sep;44(3):419-24; discussion 24-5. [CrossRef] [PubMed]
Cite as: Malik AO, Abela O, Ahsan C, Diep J. Medical image of the week: type A aortic dissection extending into main coronary artery. Southwest J Pulm Crit Care. 2017;14(5):238-9. doi: https://doi.org/10.13175/swjpcc044-17 PDF
Medical Image of the Week: Massive Abdominal Aortic Aneurysm
Figure 1. Non-contrast CT A) axial, B) sagittal, and C) coronal views demonstrate a massive abdominal aortic aneurysm measuring 12.5 cm wide at maximal diameter.
Figure 2. Representative images from a CT-angiogram shows A) upper and B) lower abdominal axial sections showing renal artery involvement (red arrow) and substantial intramural thrombus (light blue brace). C) Coronal view demonstrates fusiform dilation of the iliacs (green arrow) and D) sagittal view demonstrates involvement of the thoracoabdominal aorta (pink arrow) and all major arterial branches of the abdominal aorta (celiac trunk, superior and inferior mesenteric arteries; dark blue arrows).
An 88 year-old presented to the emergency department with left flank and lower back pain as well as lower abdominal fullness. The fullness had started 2 days prior, but the left flank pain acutely started in the early morning before presenting. He had a history of unmedicated hypertension, hyperlipidemia, and mild vertigo. His review of systems was positive for chills and difficulty urinating but no hematuria. He was a non-smoker, and had undergone orthopedic surgeries but had otherwise avoided emergent hospitalizations.
On exam, vitals were unremarkable; there was no flank nor costovertebral angle tenderness; however, a midline pulsatile mass was present. An initial non-contrast CT abdomen/pelvis revealed a massive abdominal aortic aneurysm (AAA, Figure 1). Follow-up CT angiogram of the AAA can be seen in Figure 2. Upon further questioning, he had undergone a research study some 30 years earlier involving ultrasound to screen for AAA and was told he did not have one at the time.
AAA’s occur in 4-9% of the population (1-3) because of the diminished elastin in the infrarenal aorta. Inciting or etiologic factors include inflammatory, genetic and biochemical mediators, with positive risk factors including white race, atherosclerosis, smoking, male gender, hypertension, personal history of other arterial aneurysms, family history of AAA’s, and advancing age. Screening all men aged 65-79 has been shown to reduce mortality (2) despite the non-trivial mortality associated with elective AAA repair (3). Only 1% of 65 year-old men with a negative ultrasound will go on to develop an AAA (2).
The feared and fatal complication of AAA is rupture, and occurs in 10,500 ± 1,500 patients yearly in the U.S.A., with larger AAA’s posing higher annual risk of rupture (1-3). Emergent surgical repair mortality in the 30-50% that survive a rupture long enough to go to the operating room is roughly 50%.
The extensive nature of this patient’s aneurysm would have made for a nearly-impossible surgery, with operative mortality estimates between 15% using the British Aneurysm Repair Score (3) to 50% based on clinical opinion. This dissuaded the patient, his family, and vascular surgery team from pursuing elective repair. The patient desired discharge with pain medications and stricter blood pressure control with outpatient follow-up.
Michael Larson, M.D., Ph.D.
Tucson Hospitals Medical Education Program
Tucson, AZ, USA
References
- Lederle FA. Ultrasonographic screening for abdominal aortic aneurysms. Ann Intern Med. 2003 Sep 16;139(6):516-22. [CrossRef] [PubMed]
- Cosford PA, Leng GC. Screening for abdominal aortic aneurysm. Cochrane Database Syst Rev. 2007 Apr 18;(2):CD002945. [CrossRef] [PubMed]
- Grant SW, Hickey GL, Grayson AD, Mitchell DC, McCollum CN. National risk prediction model for elective abdominal aortic aneurysm repair. Br J Surg. 2013 Apr;100(5):645-53. [CrossRef] [PubMed]
Cite as: Larson M. Medical image of the week: massive abdominal aortic aneurysm. Southwest J Pulm Crit Care. 2016:13(1):30-1. doi: http://dx.doi.org/10.13175/swjpcc052-16 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
- 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]
- 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]
- 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
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
- 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]
- Rose PS, Punjabi NM, Pearse DB. Treatment of right heart pulmonary emboli. Chest. 2002;121(3):806-14. [CrossRef] [PubMed]
- 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