Medical Image of the Week: Bilateral Vocal Cord Paralysis

Figure 1. Flow-volume curve demonstrating flattening of both the inspiratory and expiratory limbs consistent with extra-thoracic obstruction.

Figure 2. Video demonstrated the vocal cords essentially fixed in the adducted position during the inspiratory and expiratory cycle.

A 59-year-old morbidly obese woman with acute hypoxemic respiratory failure secondary to pulmonary emboli required emergency intubation. She was described by the anesthesiologist as having a difficult airway. The patient was liberated from the ventilator after two days. Following extubation she complained of hoarse voice and dyspnea. Physical exam revealed audible stridor. The upper airway was normal by CAT imaging. Flow-volume curve demonstrated marked flattening of both the inspiratory and expiratory limbs, consistent with a fixed extra-thoracic obstruction (Figure 1). Endoscopy revealed the vocal cords to be in the adducted position, with minimal movement throughout the respiratory cycle, consistent with bilateral vocal cord paralysis (Figure 2).

Traumatic intubation follows thyroid surgery as the most common cause of bilateral vocal cord paralysis (1). In a minority of patients spontaneous recovery may occur. Surgical treatment options include cordotomy or tracheostomy. Nocturnal BIPAP has been used in patients who decline surgery (2).

Charles J. Van Hook MD, Britt Warner PA-C, Angela Taylor MD,  and Jacquelynn Gould MD.

Longmont United Hospital

Longmont, CO USA

References

1. Brandwein M, Abramson AL, Shikowitz MJ. Bilateral vocal cord paralysis following endotracheal intubation. Arch Otolaryngol Head Neck Surg. 1986 Aug;112(8):877-82. [CrossRef] [PubMed]
2. Rosenthal LH, Benninger MS, Deeb RH. Vocal fold immobility: a longitudinal analysis of etiology over 20 years. Laryngoscope. 2007 Oct;117(10):1864-70.[CrossRef] [PubMed]

Cite as: Van Hook CJ, Warner B, Taylor A, Gould J. Medical image of the week: bilateral vocal cord paralysis. Southwest J Pulm Crit Care. 2017;15(2):82-3. doi: https://doi.org/10.13175/swjpcc099-17 PDF

Medical Image of the Week: Tortuosity of Thoracic Aorta Mimicking a Lung Mass

Figure 1. PA (A) and lateral (B) chest X-ray showing a 5x4 cm round mass with sharp margins in retrocardiac area.

Figure 2. A-C: Initial CT image showing thoracic aorta acutely angulated above the diaphragm and crossing to the right side of the chest. Then the aorta acutely angulates again and descends into the abdomen on the right. D: Follow-up CT image after 2 years showing saccular dilatation of transverse area of thoracic aorta.

An 83-year-old female presented with epigastric discomfort and nausea for 1 month. Her past medical history included hypertension and osteoarthritis. Her vital signs at were unremarkable. Her electrocardiogram revealed only atrial premature beats. Laboratory examination, including complete blood count, liver function test, blood urea nitrogen, creatinine, and electrolytes were normal.

Esophagogastroduodenoscopy revealed minimal changes of reflux esophagitis, erosive gastritis, and extrinsic compression of lower esophagus. Her chest x-ray (Figure 1) showed a 5x4 cm sized round retrocardiac mass with sharp margin. Chest CT was ordered to evaluate the lung mass and it revealed that acutely angulated lower thoracic aorta which crossed from left to right above the left diaphragm (Figure 2). After treatment with a proton pump inhibitor and a gastrointestinal pro-motility agent, her symptoms gradually decreased. Follow-up CT after 2 years shows saccular dilatation of the transverse area of thoracic aorta (Figure 2D), however, she has no specific symptoms.

Abnormal vascular structures like a severe tortuous thoracic aorta occasionally can be confused with a lung mass or neoplasm. The most common cause of aortic disease mimicking lung mass on CXR is an aortic aneurysm (1). Some cases have reported an intervention or even an operation being performed. The symptoms of tortuosity of thoracic aorta are varied from asymptomatic to dysphagia, gastroesophageal reflux, nausea and vomiting (2). Therefore, clinical symptom is not helpful to diagnose the underlying cause. As in this case, chest computed tomography (CT) can be beneficial for the differential diagnosis between vascular lesion and lung mass. Chest CT also gives additional information for communication of the aneurysm with the aorta, relationship of vascular structure to mediastinal organs. In children, Loeys-Dietz syndrome or arterial tortuosity syndrome should be considered (3). If aortic aneurysm or tortuosity of aorta is diagnosed as a cause in older age, close observation should be performed because of the possibility of progression to aortic aneurysm, dissection or compression of adjacent organs.

Jong Seol Park, MD and Yong Sung Kim, MD, PhD

Department of Internal Medicine

Wonkwang University Sanbon Hospital

Gunpo, Korea

References

1. Wixson D, Baltaxe HA, Sos TA. Pitfalls in the plain film evaluation of the thoracic aorta: the mimicry of aneurysms and adjacent masses and the value of aortography. Part I. Transverse aortic arch. Cardiovasc Radiol. 1979 Apr 27;2(2):69-76. [CrossRef] [PubMed]
2. Badila E, Bartos D, Balahura C, Daraban AM. A rare cause of Dysphagia - Dysphagia aortica - complicated with intravascular disseminated coagulopathy. Maedica (Buchar). 2014 Mar;9(1):83-7. [PubMed]
3. Na KJ, Park KH. Multiple aortic operations in loeys-dietz syndrome: report of 2 cases. Korean J Thorac Cardiovasc Surg. 2014 Dec;47(6):536-40. [CrossRef] [PubMed] 

Cite as: Park JS, Kim YS. Medical image of the week: tortuosity of thoracic aorta mimicking a lung mass. Southwest J Pulm Crit Care. 2017;15(2):80-1. doi: https://doi.org/10.13175/swjpcc086-17 PDF 

August 2017 Imaging Case of the Month

Brandon T. Larsen, MD, PhD¹

Michael B. Gotway, MD²

Departments of Pathology¹ and Radiology²

Mayo Clinic Arizona

Scottsdale, Arizona USA

Clinical History: A 67-year-old man with a 23 pack-year history of smoking, stopping 6 years earlier, presented with a year-long history of intermittent hemoptysis consisting of small specs of blood particularly in the morning after he awoke. No sputum discoloration was reported and the patient denied shortness of breath, fever, shortness of breath, and chills. The patient also denied rash, joint pain, and night sweats. His past surgical history was remarkable only for an appendectomy, tonsillectomy, and repair of an ankle fracture, all as a young man. The patient did report some asbestos exposure in the past. He takes a multivitamin and occasional over-the counter pain relievers, but was not taking prescription medications.

Physical examination: unremarkable and the patient’s oxygen saturation was 98% on room air.

Laboratory evaluation: largely unremarkable.  Quantiferon testing for Mycobacterium tuberculosis was negative. An outside otolaryngology examination was reported to show no abnormalities. Frontal 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 shows a mediastinal mass
2. The chest radiograph shows multifocal consolidation and pleural effusion
3. The chest radiograph shows multifocal smooth interlobular septal thickening
4. The chest radiograph shows a possible focal air space opacity
5. The chest radiograph shows small cavitary pulmonary nodules

Cite as: Larsen BT, Gotway MB. August 2017 imaging case of the month. Southwest J Pulm Crit Care. 2017;15(2):69-79. doi: https://doi.org/10.13175/swjpcc098-17 PDF

Medical Image of the Week: Portal Vein Thrombosis in a Patient with Polycythemia Vera

Figure 1 Panel A: CT of the abdomen demonstrating a thrombus within the portal vein (black arrow). Panel B: CT showing extension of the thrombus into the splenic vein (black arrow).

A 39-year-old man with no past medical history presented with acrocyanosis of his left second toe and right upper abdominal pain. Initial labs showed polycythemia, leukocytosis and thrombocytosis that were unchanged with intravenous fluid administration. A CT of the abdomen was obtained and showed portal vein thrombosis without evidence of cirrhosis (Figure 1). Subsequent studies revealed a positive JAK2 V617F mutation and low erythropoietin levels consistent with polycythemia vera (PV). The patient was placed on anticoagulation, low dose aspirin, and received phlebotomy.

PV is a chronic myeloproliferative neoplasm defined by an increase in red blood cell mass in the absence of a physiologic stimulus. The 2016 World Health Organization classification of myeloid neoplasms and acute leukemia has three major criteria and one minor criterion in the diagnosis of PV. Diagnosis requires either 3 major criteria or 2 major with 1 minor criterion (1).

Major Criteria for Polycythemia Vera

1. Increased hemoglobin level(>16.5 in men, >16 in women) or hematocrit(>49 in men, >48 in women)
2. Bone marrow biopsy showing hypercellularity for age with trilineage growth
3. JAK2 V617F or JAK2 exon 12 mutation

Minor Criterion for Polycythemia Vera

1. Serum erythropoietin level below the reference range of normal.

Due to the propensity of unusual thrombosis once a diagnosis is made therapy should be initiated without delay.  PV should be treated with phlebotomy followed by maintenance therapy with continued phlebotomy or hydroxyurea to maintain target hematocrit levels and with low dose aspirin (2,3). 

Hamayon Babary, MD and Muthena Maklad, MD

Department of Internal Medicine

University of Nevada School of Medicine: Las Vegas

Las Vegas, NV USA

References

1. Arber DA, Orazi A, Hasserjian R, Thiele J, Borowitz MJ, Le Beau MM, Bloomfield CD, Cazzola M, Vardiman JW. The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia. Blood. 2016 May 19;127(20):2391-405. [CrossRef] [PubMed]
2. Marchioli R, Finazzi F, Specchia G, et al. Cardiovascular events and intensity of treatment in polycythemia vera. N Engl J Med. 2013 Jan 3;368(1):22-33. [CrossRef] [PubMed]
3. Landolfi R, Marchioli R, Kutti J, Gisslinger H, Tognoni G, Patrono C, Barbui T; European Collaboration on Low-Dose Aspirin in Polycythemia Vera Investigators. Efficacy and safety of low-dose aspirin in polycythemia vera. N Engl J Med. 2004 Jan 8;350(2):114-24. [CrossRef] [PubMed] 

Cite as: Babary H, Maklad M. Medical image of the week: portal vein thrombosis in a patient with polycythemia vera. Southwest J Pulm Crit Care. 2017;15(2):67-8. doi: https://doi.org/10.13175/swjpcc073-17 PDF

Medical Image of the Week: Coral Reef Aorta

Figure 1. Coronal (A) and lateral (B) thoracic CT in soft tissue windows showing the coral reef calcification (arrows).

A 52-year-old woman with no past medical history presented to the emergency department with signs and symptoms concerning for pneumonia. Chest x-ray showed incidental findings of a calcified aortic mass. Subsequently, a follow up computed tomography scan (CT) was obtained which showed coral reef aorta (Figure 1). On physical examination, vital signs were only significant for mildly elevated blood pressure to 146/62 mmHg. She also had normal and equal pulses and pressures throughout all 4 extremities. In retrospect, patient had complaints of bilateral lower extremity claudication on strenuous exercise.

Coral reef aorta, a rare condition that was first described in 1984 by Qvarfordt et al. (1) is characterized by an eccentric, heavily calcified polypoid lesion and stenosis of the juxtarenal and suprarenal aorta. The rock-hard, irregular, gritty, whitish surface of the calcification strongly resembled a coral reef. The most common presentation is severe hypertension and intermittent claudication. Magnetic resonance angiogram (MRA) and CT have the ability to diagnose and appreciate the extent of this phenomenon (2).

Lance Eberson MS¹ and Sehem Ghazala MD²

¹College of Medicine and ²Department of Internal Medicine

University of Arizona

Tucson, Arizona, USA

References

1. Qvarfordt PG, Reilly LM, Sedwitz MM, Ehrenfeld WK, Stoney RJ. "Coral reef" atherosclerosis of the suprarenal aorta: a unique clinical entity. J Vasc Surg. 1984 Nov;1(6):903-9. [CrossRef] [PubMed]
2. Kopani K, Liao S, Shaffer K. The Coral Reef Aorta: Diagnosis and Treatment Following CT. Radiol Case Rep. 2016 Oct 4;4(1):209. eCollection 2009. [CrossRef] [PubMed] 

Cite as: Eberson L, Ghazala S. Medical image of the week: coral reef aorta. Southwest J Pulm Crit Care. 2017:15(1):49. doi: https://doi.org/10.13175/swjpcc080-17 PDF

Medical Image of the Week: Hematopneumatoceles from Pulmonary Lacerations

Figure 1. Chest x-ray showing irregular patchy regions of ill-defined consolidation in the left upper lobe and lingula, as well as suggestion of cystic changes (arrow).

Figure 2. Chest CT axial views, soft tissue and lung windows at the level of the aortic arch (A), right pulmonary artery (B) and the heart (C) showing mixed consolidative and nodular left lung opacities suggestive of pulmonary contusions, as well as contrecoup injury in the right lung, in addition to multiple cystic spaces containing air-fluid levels consistent with pulmonary lacerations.

Figure 3. Chest CT coronal views, soft tissue and lung windows showing consolidative and nodular lung opacities as well as fluid layering in cystic spaces (red arrows). A shattered spleen (yellow arrow) is also seen.

A 17-year-old man was brought to the emergency room after a fall from a 50-foot bridge. He was hypoxemic on presentation, requiring endotracheal intubation. Chest computed tomography (CT) revealed bilateral airspace opacities consistent with pulmonary contusions, and multiple air-fluid levels diagnostic of pulmonary lacerations (Figures 1-3).

Pulmonary lacerations are rare complications of blunt chest trauma (1). They can be contained within the lung parenchyma or may extend through the visceral pleura causing a pneumothorax. Due to its elastic recoil, the surrounding lung tissue pulls back from the laceration resulting in a round or oval cavity that may fill with air (pneumatocele), blood (hematocele) or both (hematopneumatocele). Lacerations are often obscured on chest x-ray as they are usually surrounded by contusion, requiring a CT for detection (2). They are classified into four types according to the mechanism of injury: Type 1 (compression rupture injury, most common type, usually centrally located), Type 2 (shearing against the thoracic spine, involving the paraspinal region of the lower lobes), Type 3 (rib penetration into the lung periphery, usually associated with a pneumothorax) and Type 4 (adhesion tear, in regions of pleuropulmonary adhesions) (3). Pulmonary lacerations heal more slowly than contusions and may last up to several months, over time becoming increasingly filled with blood, before regressing (2).

Our patient underwent an exploratory laparotomy with a splenectomy. The pulmonary lacerations were managed conservatively. He was successfully extubated on day#10 and discharged home on day#14 with a plan to follow his lacerations with monthly chest radiography.

Udit Chaddha MD¹, Darren Maehara MD¹, Ioan Puscas DO¹, Ashley Prosper MD², and Ramyar Mahdavi MD¹

¹Division of Pulmonary, Critical Care and Sleep Medicine and ²Department of Radiology

Keck School of Medicine of the University of Southern California

Los Angeles, CA USA

References

1. Nishiumi N, Maitani F, Tsurumi T, Kaga K, Iwasaki M, Inoue H. Blunt chest trauma with deep pulmonary laceration. Ann Thorac Surg. 2001;71(1):314-8. [CrossRef] [PubMed]
2. Kaewlai R, Avery LL, Asrani AV, Novelline RA. Multidetector CT of blunt thoracic trauma. Radiographics. 2008;28(6):1555-70. [CrossRef] [PubMed]
3. Wagner RB, Crawford WO, Schimpf PP. Classification of parenchymal injuries of the lung. Radiology. 1988;167(1):77-82. [CrossRef] [PubMed]

Cite as: Chaddha U, Maehara D, Puscas I, Prosper A, Mahdavi R. Medical image of the week: hematopneumatoceles from pulmonary lacerations. Southwest J Pulm Crit Care. 2017;15(1):46-8. doi: https://doi.org/10.13175/swjpcc078-17 PDF 

Medical Image of the Week: Idiopathic Subglottic Stenosis

Figure 1. Flow-loop demonstrating fixed large airway obstruction.

Figure 2. Subglottic stenosis.

A 40 year-old previously healthy woman presented with a three-month history of exercise-induced shortness of breath. Clinical exam revealed inspiratory stridor. Spirometry was remarkable for flattening of the inspiratory and expiratory limbs of the flow-volume loop (Figure 1). Fiberoptic bronchoscopy revealed subglottic tracheal stenosis (Figure 2). The patient subsequently underwent successful balloon dilation of the involved segment and has remained symptom free.

Tracheal stenosis may be related to previous airway trauma, collagen vascular disease, sarcoidosis, or vasculitis. The clinical presentation is characterized by exertional dyspnea with stridor.  The flow-volume loop classically demonstrates a pattern of fixed upper airway obstruction, with flattening of both the inspiratory and expiratory limbs of the curve. CAT scanning is usually supportive of the diagnosis, and bronchoscopy is confirmatory. In the absence of an identifiable etiology, the condition is termed idiopathic tracheal stenosis. Idiopathic subglottic stenosis is a subgroup of tracheal stenosis that occurs in young women, and that is limited to the first two rings of the proximal trachea (1). Bronchoscopic tools, including balloon dilation, laser, and electrocautery have all been used with safety and efficacy for the treatment of idiopathic subglottic stenosis (2).

Charles J. Van Hook MD and Britt Warner PA

Longmont United Hospital

Longmont, CO USA

References

1. Nussbaumer-Ochsner Y, Thurnheer R. Images in clinical medicine: subglottic stenosis. N Engl J Med. 2015 Jul 2;373(1):73. [CrossRef] [PubMed]
2. Solly WR, O'Connell RJ, Lee HJ, Sterman DH, Haas AR. Diagnosis of idiopathic tracheal stenosis and treatment with papillotome electrocautery and balloon bronchoplasty. Respir Care. 2011 Oct;56(10):1617-20. [CrossRef] [PubMed]

Cite as: Van Hook CJ, Warner B. Medical image of the week: idiopathic subglottic stenosis. Southwest J Pulm Crit Care. 2017;15(1):39-40. doi: https://doi.org/10.13175/swjpcc076-17 PDF 

July 2017 Imaging Case of the Month

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, Arizona USA

Clinical History: A 56-year-old man with no significant past medical history presented with complaints of cough, shortness of breath, and productive sputum. Frontal and lateral chest radiography (Figure 1) was performed.

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

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

1. The chest radiograph shows a diffuse linear, interstitial pattern
2. The chest radiograph shows a large pleural effusion
3. The chest radiograph shows a mediastinal mass
4. The chest radiograph shows numerous small nodules
5. The chest radiograph shows right lower lobe consolidation

Cite as: Gotway MB. July 2017 imaging case of the month. Southwest J Pulm Crit Care. 2017;15(1):17-27. doi: https://doi.org/10.13175/swjpcc090-17 PDF 

Medical Image of the Week: Zenker’s Diverticulum

Figure 1. Panel A: PA view chest x-ray shows possible cavitation with air-fluid level in the right upper lobe (arrow). Panel B: lateral view chest x-ray shows possible cavitation with air-fluid level in the right upper lobe (arrow).

Figure 2. Coronal section of the thoracic CT scan shows focal dilation of the upper thoracic esophagus which contains fluid (arrow).

Figure 3.  Endoscopic view of the upper esophagus showing the diverticulum with impacted food bolus.

A 71-year-old man with history of recurrent aspiration pneumonia and previous esophageal surgery presented to the Emergency Department with acute hypoxia and leukocytosis. Imaging, above, showed a consolidation in the RUL and on lateral view an air fluid level. This was suspicious for infection or malignancy. For the ongoing concern for possible esophageal pathology given previous surgery, GI was consulted and upper endoscopy performed.  He was found to have an esophageal dilation at repair site of a previous Zenker’s diverticulum filled with food.

Zenker’s Diverticulum is a defect in the muscular wall of the hypopharynx in an area known as Killian's triangle. This condition is male predominant mainly occurring in the 3^rd to 4^th decade and/or the 7^th to 8^th decade of life.  The out pouching created will accumulate food and eventually lead to high incidences of aspiration pneumonia. Treatment is usually surgical in nature and can cause vocal cord damage and even recurrence of the outpouching (1).  

Chandra Stockdall MD and Roberto Swazo MD

Department of Internal Medicine

Banner University Medical Center South Campus

Tucson, AZ USA

Reference

1. Mulder C, Van Delft F. Zenker’s diverticulum. UpToDate. May, 2017. Available at: http://www.uptodate.com/contents/zenkers-diverticulum (requires subscription, accessed 6/30/17).

Cite as: Stockdall C, Swazo R. Medical image of the week: Zenker's diverticulum. Southwest J Pulm Crit Care. 2017;15(1):15-6. doi: https://doi.org/10.13175/swjpcc075-17 PDF

Medical Image of the Week: Superior Sulcus Tumor with Neural Invasion

Figure 1. Computed tomography of the chest (axial image) shows a large left upper lobe cavitary mass (red arrow), consistent with known squamous cell carcinoma.

Figure 2. MRI of cervical and thoracic spine (sagittal image) reveals the mass abuts the spinal column with tumor invasion through the neural foramen at C7-T1 and T1-T2 (blue arrow).

Figure 3. A 22-guage needle is advanced with its tip anterior to the longus coli muscle at the level of C6 (yellow arrow). Ethanol solution was injected into this space.

A 78-year-old woman with left upper lobe squamous cell carcinoma presented with severe left arm and upper posterior chest pain. The pain was described as a severe burning sensation with “pins and needles”, and there was loss of motor function in the arm. This neuropathic pain was refractory to escalating doses of opioids and gabapentin. She was receiving chemotherapy with paclitaxel and carboplatin and completed five radiation treatments. On physical examination, there was atrophy of the left forearm and hand muscles. No evidence of Horner’s syndrome was noted.

A CT of the chest with contrast (Figure 1) showed a 5.8 cm apical segment left upper lobe cavitary mass consistent with a superior sulcus tumor and concomitant pulmonary embolism. An MRI of the cervical and thoracic spine (Figure 2) showed a large apical necrotic tumor abutting the upper thoracic spine with invasion of the neural foramina at C7-T1, T1-T2, and T2-T3, consistent with invasion into the brachial plexus.

In an attempt to improve her symptoms, the interventional radiologist performed a left stellate ganglion block with 1% lidocaine and 0.25% bupivacaine (Figure 3). There was minimal initial improvement so a repeat block was done three days later with notable reduction in arm pain. For a permanent block, a stellate ganglion block was performed with 2% lidocaine and 98% ethanol. The patient had significant palliation of the neuropathic pain in her left arm and shoulder.

Sue Cassidy ANP-BC ACHPN, Tina Skrepnik MD, Bree Johnston MD MPH, and Linda Snyder MD

University of Arizona College of Medicine

Departments of Internal Medicine and Radiation Oncology

Tucson, AZ USA

References

1. Kratz JR, Woodard G, Jablons DM. Management of lung cancer invading the superior sulcus. Thorac Surg Clin. 2017 May;27(2):149-157. [CrossRef] [PubMed]
2. De Leon-Casasola OA. Critical evaluation of chemical neurolysis of the sympathetic axis for cancer pain. Cancer Control. 2000 Mar-Apr;7(2):142-8. [PubMed]

Cite as: Cassidy S, Skrepnik T, Johnston B, Snyder L. Medical image of the week: superior sulcus tumor with neural invasion. Southwest J Pulm Crit Care. 2017;14(6):320-1. doi: https://doi.org/10.13175/swjpcc071-17 PDF

Medical Image of The Week: Urothelial Carcinoma with Pulmonary Metastases Presenting with Shoulder Pain

Figure 1. AP view of the left shoulder demonstrated multiple pulmonary nodules.

Figure 2. Coronal view of chest CT demonstrating innumerable pulmonary nodules with thick walled cavitations.

Figure 3. Axial view of chest CT demonstrating innumerable pulmonary nodules with thick walled cavitations.

A 68 year old man with a past medical history significant only for mild hyperlipidemia and distant cigar smoking presented to this primary physician’s office with a chief complaint of left sided shoulder pain for more than 6 months duration. His only other complaint was a hacking morning cough that was attributed to GERD after resolution with omperazole therapy. He was without any other complaints such as weight loss, fevers, chills, night sweats, shortness of breath, or dyspnea on exertion. His physical exam was without any abnormality. An initial radiograph of the rileft shoudler was obtained which was without any obvious bony abnormality but demonstrated numerous potential pulmonary nodules (Figure 1).  He was then referred to pulmonology for further assessment. A chest CT scan peformed with contrast again demonstrated numerous pulmonary nodules with thick walled central cavitations throughout the lung parenchyma bilaterally (Figures 2 & 3). Additional testing performed included Coccidioides serologies, c-ANCA, p-ANCA, Quantiferon Gold, PSA, and rheumatoid arthritis serology (RF/CCP) all of which were negative. He was taken for a CT guided lung biopsy of one of the nodules and the biopsy result demonstrated a poorly-differentiated carcinoma with focal squamous differential; nuclear “salt and pepper” features; along with immunostaining consistent with poorly differentiated urothelial cell carcinoma. The patient was referred to oncology but refused potential palliative chemotherapy.

The differential diagnoses for cystic and cavitary lung disease is very broad, therefore it is of utmost importance to differentiate between cystic and cavitary diseases. Typically, cystic lung diseases are round parenchymal lucencies with a thin wall, typically <2mm in thickness, whereas cavitary lung disease are round luciencies typically with a wall >4mm in thickness, but overlapp between cystic and cavitary lung disease does exist (1,2). Without evidence or symptomology to suggest malignancy, initial differential diagnosis must include infectious causes of cystic/cavitating lung disease. In regions such as the Southwestern United States where diseases such as Coccidioidomycosis is endemic, this must be included in the differential diagnosis, as does other potential infectious cystic/cavitating lung disease such as M. tuberculosis, Pneumocystis infection, or Klebsiella infection (2). Granulomatosis with polyangiitis (Wegener’s granulomatosis), as well as other rheumatologic conditions must also be included in the initial differential diagnosis. In this case, infectious and rheumatologic testing was negative. Biopsy was then necessary to determine etiology which was consistent with a metastatic urothelial carcinoma. A CT urogram was performed which was without evidence of primary tumor. Literature review suggests that approximately 65% of metastatic urothelial cancers metastasize to the lung, and often form nodules with central necrosing cavitations (3).

Benjamin Jarrett MD, MPH¹, Huthayfa Ateeli, MBBS², Harbhajan Singh, MD²

¹Department of Internal Medicine and ²Department of Pulmonary and Critical Care Medicine

University of Arizona College of Medicine and Southern Arizona VA Healthcare System

Tucson, Arizona USA

References

1. Raoof S, Bondalapati P, Vydyula R, et al. Cystic lung diseases: algorithmic approach. Chest. 2016 Oct;150(4):945-65. [CrossRef] [PubMed]
2. Gadkowski LB, Stout JE. Cavitary pulmonary disease. Clin Microbiol Rev. 2008 Apr;21(2):305-33. [CrossRef] [PubMed]
3. Shinagare AB, Fennessy FM, Ramaiya NH, Jagannathan JP, Taplin ME, Van den Abbeele AD. Urothelial cancers of the upper urinary tract: metastatic pattern and its correlation with tumor histopathology and location. J Comput Assist Tomogr. 2011 Mar-Apr;35(2):217-22. [CrossRef] [PubMed]

Cite as: Jarrett B, Ateeli H, Singh H. Medical image of the week: urothelial carcinoma with pulmonary metastases presenting with shoulder pain. Southwest J Pulm Crit Care. 2017;14(6):315-7. doi: https://doi.org/10.13175/swjpcc067-17 PDF 

Medical Image of the Week: Spontaneous Pneumothorax in End Stage Fibrotic Lung Disease

Figure 1. Chest x-ray showing moderate-sized right pneumothorax with a pigtail chest tube in place, diffuse reticular interstitial opacities.

Figure 2. Chest CT showing extensive centrilobular emphysema, moderate right pneumothorax with pigtail chest drain on the right, subpleural reticular opacities with peripheral and basilar preponderance suggesting interstitial fibrotic lung disease, and diffuse lung cysts - heterogenous in size.

A 61-year-old nonsmoking man with chronic obstructive lung disease, pulmonary hypertension, pulmonary fibrosis, hypertension, coronary artery disease with congestive heart failure, presented with recurrent pneumothorax, pneumomediastinum, extensive subcutaneous emphysema and bronchopleural fistula.

The patient reported ongoing symptoms of exertional dyspnea, fatigue, and coughing for years. His environmental exposures were notable for exposure to birds since early childhood. He had 6 cockatiels and 2 doves living inside his home and is directly responsible for their care. Former occupational exposures include painting and sandblasting. Family history was notable for early onset non specified lung disease in his father, and rheumatoid arthritis in his mother.

Lung function testing performed prior to the bronchopleural fistula revealed moderate obstructive ventilatory defect with severely limited DLCO. Chest x-ray (Figure 1) revealed a moderate-sized right pneumothorax with a pigtail chest tube in place and diffuse reticular interstitial opacities. His CT chest (figure 2) revealed extensive subcutaneous emphysema, diffuse lung cysts that are heterogenous in size, and subpleural reticular opacities with peripheral and basilar preponderance. Bronchoalveolar lavage revealed no infection, with predominant monocyte/ macrophages. Alpha-1 antitrypsin (A1AT) was normal, as were autoimmune panels. A hypersensitivity pneumonitis panel revealed positive IgG to Aureobasidium pullulans. A presumptive diagnosis of chronic hypersensitivity pneumonitis was made.

Spontaneous pneumothorax (SP), a potentially life-threatening complication, is defined by the accumulation of air in the pleural space with secondary lung collapse, and can be categorized as primary (without apparent lung disease) or secondary pneumothorax. While chronic obstructive pulmonary disease and Pneumocystitis jirovecii pneumonia are the most common causes of secondary spontaneous pneumothorax, other structural lung diseases such as fibrotic lung diseases have also been linked to SP. Interstitial lung diseases distort lung architecture and trigger formation of subpleural blebs that are susceptible to rupture leading to extra-alveolar air collection and air leakage in the pleural space. Presence of persistent air leak, as in our case, mandates surgical consideration to accelerate recovery and prevent recurrence of secondary SP.

Roula Altisheh MD and Tara Carr MD

Division of Pulmonary, Allergy, Critical Care and Sleep Medicine

Banner-University Medical Center

Tucson, AZ USA

References

1. Sahn S, Heffiner J. Spontaneous Pneumothorax. N Engl J Med 2000; 342:868-74 [CrossRef] [PubMed]
2. Onuki T, Ueda S, Yamaoka M, Sek iya Y, Yamada H, Kawakami N, Araki Y, Wakai Y, Saito K, Inagaki M, Matsumiya N. Primary and secondary spontaneous pneumothorax: prevalence, clinical features, and in-hospital mortality. Can Respir J. 2017: 6014967.  [CrossRef] [PubMed]
3. Koschel D, Handzhiev S, Cardoso C, Rolle A, Holotiuk O, Höffken G. Pneumomediastinum as a primary manifestation of chronic hypersensitivity pneumonitis. Med Sci Monit. 2011 Dec;17(12):CS152-5. [PubMed]
4. Ichinose J, Nagayama K, Hino H, et al. Results of surgical treatment for secondary spontaneous pneumothorax according to underlying diseases. Eur J Cardiothorac Surg. 2016;49(4):1132–6. [CrossRef] [PubMed]

Cite as: Altisheh R, Carr T. Medical image of the week: spontaneous pneumothorax in end stage fibrotic lung disease. Southwest J Pulm Crit Care. 2017;14(6):308-10. doi: https://doi.org/10.13175/swjpcc065-17 PDF 

Medical Image of the Week: Saber Sheath Trachea

Figure 1. A: Narrowing in the mid and lower parts of the trachea on the scout film (arrow). B: Cross sectional image from chest computed tomography (CT) showing coronal narrowing of the trachea (arrow).  C: Cross sectional images from chest computed tomography (CT) showing sagittal widening of the trachea (arrow).  No mass or external compression seen.

Figure 2. Bronchoscopy image that shows the coronal narrowing and sagittal widening of the (A) proximal trachea, (b) mid trachea and (C) distal trachea.

A 79-year-old man with chronic obstructive pulmonary disease (COPD) and an active smoker was transferred for evaluation of tracheal narrowing and concerns of malignant external compression versus tracheobronchomalacia for possible stenting.

The patient underwent both chest computed tomography (Figure 1) and bronchoscopy (Figure 2) that confirmed the diagnosis of saber-sheath trachea and ruled out external compression. The airway was still adequately patent during inspiration and expiration with no clear dynamic collapse.

Saber-sheath trachea is commonly described as intra-thoracic coronal narrowing and sagittal widening of the trachea (like a sword sheath). Repetitive cartilaginous injury from excessive coughing and elevated intra-thoracic pressure causes degeneration and calcification of the trachea cartilage, leading to remodeling and bending of the tracheal cartilage (1). Presence of saber-sheath trachea is highly associated with obstructive lung disease, which is present in our patient (2). There is no known specific treatment for saber-sheath trachea, however if patient with saber-sheath trachea were to require intubation, air leak can be a concern due to the rigid deformity of the trachea (3).

See-Wei Low, MD¹; Huthayfa Ateeli, MD²; James Knepler, MD²

¹ Department of Internal Medicine and ² Pulmonary, Allergy, Critical Care and Sleep Medicine

Banner University Medical Center Tucson

Tucson, AZ, USA

References

1. Ismail SA, Mehta AC. "Saber-sheath" trachea. J Bronchol Intervent Pulmonol 2003;10:296-7. [CrossRef]
2. Greene R. Saber-sheath trachea: relation to chronic obstructive pulmonary disease. AJR Am J Roentgenol. 1978;130:441-5. [CrossRef] [PubMed]
3. Wallace E, Chung F. General anesthesia in a patient with an enlarged saber-sheath trachea. Anesthesiology. 1998;88:527-9. [CrossRef] [PubMed] 

Cite as: Low S-W, Ateeli H, Knepler J. Medical image of the week: saber sheath trachea. Southwest J Pulm Crit Care. 2017;14(6):283-4. doi: https://doi.org/10.13175/swjpcc056-17 PDF 

June 2017 Imaging Case of the Month

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, Arizona USA

Clinical History: A 30-year-old woman with no significant past medical history presented with complaints of chronic back pain, partially controlled with Ibuprofen. Recently she began to notice shortness of breath. Frontal and lateral chest radiography (Figure 1) was performed.

Figure 1. Frontal (A) and lateral (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 pages)

1. The chest radiograph shows a diffuse linear, interstitial pattern
2. The chest radiograph shows a large pleural effusion
3. The chest radiograph shows a mediastinal mass
4. The chest radiograph shows multifocal, bilateral consolidation
5. The chest radiograph shows numerous small nodules

Cite as: Gotway MB. June 2017 imaging case of the month. Southwest J Pulm Crit Care. 2017;14(6):269-78. doi: https://doi.org/10.13175/swjpcc068-17 PDF 

Medical Image of the Week: Coronary Artery Ectasia

Figure 1. Coronary angiogram demonstrating ectatic right coronary artery (black arrow) with minimal laminar flow of contrast dye. 100% occlusion of distal RCA noted (white arrow), as well as sternotomy wires from prior CABG.

Figure 2. Intravascular ultrasound (IVUS) demonstrating dilated, ectatic right coronary artery with maximum dimension 9-10 mm (white line).

A 70-year-old man with a history of coronary artery disease and previous 3 vessel coronary artery bypass grafting (CABG) was admitted to the coronary care unit with acute chest pain and EKG concerning for ST elevations in II, III, aVF with first degree AV block. Troponins were negative on admission, and peaked at 35 ng/ml. The patient was taken immediately to the cardiac catherization lab for acute inferior ST elevation myocardial infarction (STEMI), and was found to have coronary artery ectasia throughout with diffuse atherosclerotic disease. 100% occlusion was noted in the distal RCA, but the wire was not able to be passed through the blockage due to tortuous and dilated vessels vessels. Left circumflex and left anterior descending arteries showing similar ectatic findings without acute blockage. No stents were able to be engaged in the RCA given the large diameter from the ectasia. The RCA notably had a diameter of 7-10 mm in width with minimal laminar flow of contrast dye (Figure1), and was confirmed with Intravascular Ultrasound (IVUS, Figure 2). Echocardiogram showed an ejection fraction of 55% with normal left ventricular function. Since stents were not able to be placed, the patient was medically optimized with aspirin, ticagrelor, and a high intensity statin. The patient felt improved following medical optimization, and was discharged home in stable condition with cardiology follow up.

Coronary ectasia is a disease of the coronary arteries in which the vessel lumen is increased greater than 1.5 times in size (1). It is a very rare finding, with only 1.2-2% of coronary caths demonstrating ectasia. Clinical findings are believed to be due to increased wall stress and thinning of the arterial wall in the setting of atherosclerosis causing progressive dilation and remodeling (2). Ectasia is also commonly found in patients with connective tissue disease and vasculitis, classically Marfan syndrome and Kawasaki disease. Conventional stents are generally too small in diameter to be utilized. Treatment is largely devoted towards decreasing cardiac risk factors and avoiding medications that slow coronary blood flow such as nitrates (3).

Adam Berlinberg MD¹, Steven Stroud MD¹, Jaren Trost MD¹, Karl Kern MD²

¹Department of Internal Medicine and ²Department of Cardiology, Sarver Heart Center, Banner University Medical Center; Tucson, AZ

References

1. Lin CT, Chen CW, Lin TK, Lin CL. Coronary artery ectasia. Tzu Chi Med J 2008;20:270-4. [CrossRef]
2. Hsu PC, Su HM, Lee HC, Juo SH, Lin TH, Voon WC, Lai WT, Sheu SH. Coronary artery collateral circulation in patients of coronary ectasia with significant coronary artery disease. PLoS One. 2014;9(1): e87001. [CrossRef] [PubMed]
3. Eitan A, Roguin A. Coronary artery ectasia: new insights into pathophysiology, diagnosis, and treatment. Coron Artery Dis 2016;27(5):420-8. [CrossRef] [PubMed] 

Cite as: Berlinberg A, Stroud S, Trost J, Kern K. Medical image of the week: coronary artery ectasia. Southwest J Pulm Crit Care. 2017;14(5):253-4. doi: https://doi.org/10.13175/swjpcc049-17 PDF

Medical Image of the Week: Lymphangitic Carcinomatosis

Figure 1. Mass like consolidation and interlobular septal thickening (arrows). 

A 64-year-old woman, never-smoker, was evaluated for shortness of breath and left leg swelling. An abnormal initial chest X-Ray lead to computed tomography (CT) scan of the chest. She was also diagnosed with deep vein thrombosis (DVT) of her left leg.

CT of the chest with intravenous contrast showed a mass-like consolidation in the right upper lobe and thickening of the peripheral interlobular septa and of the bronchovascular bundles consistent with lymphangitic carcinomatosis (Figure 1). Endobronchial ultrasound (EBUS) guided transbronchial needle aspirations of the station 10 R Lymph node were positive for adenocarcinoma of lung origin.

Lymphangitic carcinomatosis occurs when cancer cells spread along the pulmonary lymphatic system and result in thickening of the bronchovascular bundle, the interlobular septa, or both (1). Histopathologically, specimens show interlobular and subpleural interstitial desmoplastic thickening and obstruction of lymphatic vessels by tumor cells. It carries a poor prognosis.

Mohammad R. Dalabih, MBBS¹ and Joshua Malo, MD²

¹Pulmonary Consultants LLC, Tacoma, WA USA

²Division of Pulmonary, Allergy, Critical Care. And Sleep, University of Arizona College of Medicine, Tucson, AZ USA

Reference

1. Munk PL, Müller NL, Miller RR, Ostrow DN. Pulmonary lymphangitic carcinomatosis: CT and pathologic findings. Radiology. 1988 Mar;166(3):705-9. [CrossRef] [PubMed]

Cite as: Dalabih MR, Malo J. Medical image of the week: lymphangitic cacinomatosis. Southwest J Pulm Crit Care. 2017;14(5):240. doi: https://doi.org/10.13175/swjpcc053-17 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

1. Golledge J, Eagle KA. Acute aortic dissection. Lancet. 2008 Jul 5;372(9632):55-66. [CrossRef] [PubMed]
2. 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]
3. 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]
4. 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 

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: Pulmonary Vein Thrombosis

Figure 1. Axial CT view shows the thrombus in the pulmonary vein (arrows) and collateral formation.

Figure 2. Coronal view of thoracic CT angiography  showing thrombus in the pulmonary vein (arrow).

A 71-year-old woman with chronic lymphocytic leukemia and remote left lower lobe pneumonectomy presented to the emergency department from an outpatient clinic with symptoms of cough, progressive shortness of breath, and fatigue for 2 weeks.  Pertinent physical examination findings included adequate oxygen saturation at room air, known II/VI systolic mitral murmur with radiation through the precordium, and a well-healed left lower lobe pneumonectomy scar.  Imaging was remarkable for acute pulmonary venous thrombosis (PVT) of the left inferior pulmonary vein with involvement of several tributary veins (Figures 1 and 2). Given the rarity of PVT, treatment guidelines have yet to be established (1); however, consensus appears to be systemic anticoagulation, thrombectomy, or resection (1-3).  Therefore, the patient was initially placed on a heparin drip upon admission and was discharged on an oral anticoagulant.

Pulmonary vein thrombosis (PVT) is a rare condition only described through case reports, that is potentially life threatening and presents with nonspecific symptoms. Common inciting events are lung transplantation, pneumonectomy (typically early after surgery and mainly left upper lobe pneumonectomy), radiofrequency ablation complication, malignancy (either lung or metastatic), idiopathic and atrial fibrillation (1-3). 

Close clinical follow up is necessary as life-threatening complications can occur, such as gangrene of the lung (which can occur if there is no collateral circulation from the intercostal veins) or embolic stroke (3). Current literature review suggests CT or MRI as imaging modality of choice for tracking regression or resolution of disease. TEE may also be used to assess for extension of thrombi into the left atrium (1,3).

Jessica Vondrak, MD and Bonnie Barbee, MD

Department of Internal Medicine

Banner University Medical Center

Tucson, AZ USA

References

1. Chaaya G, Vishnubhotia P. Pulmonary Vein Thrombosis: A Recent Systematic Review. Cureus. 2017 Jan 23;9(1):e993. [CrossRef] [PubMed]
2. Selvidge SD, Gavant ML. Idiopathic pulmonary vein thrombosis: detection by CT and MR imaging. AJR AM J Roentgenol. 1999 Jun;172(6):1639-41. [CrossRef] [PubMed]
3. Porres DV, Morenza OP, Pallisa E, Rogue A, Andreu J, Martinez M. Learning from the pulmonary veins. Radiograhpics. 2013 Jul-Aug;33(4):999-1022. [CrossRef] [PubMed]

Cite as: Vondrak J, Barbee B. Medical image of the week: pulmonary vein thrombosis. Southwest J Pulm Crit Care. 2017;14(5):228-9. doi: https://doi.org/10.13175/swjpcc048-17 PDF 

May 2017 Imaging Case of the Month

Prasad M. Panse, MD and Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, Arizona USA

Clinical History: Clinical History: A 32-year-old man presented for routine physical examination. His past medical history is unremarkable and the physical examination and basic laboratory data were within normal limits.

A frontal chest radiograph (Figure 1) was performed.

Figure 1: Frontal (A) and lateral (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 nine pages)

1. The frontal chest radiograph shows an abnormal mediastinal contour
2. The frontal chest radiograph shows basal predominant fibrotic abnormalities
3. The frontal chest radiograph shows large lung volumes with a cystic appearance
4. The frontal chest radiograph shows multifocal small pulmonary nodules
5. The frontal chest radiograph shows no abnormal findings

Cite as: Panse PM, Gotway MB. May 2017 imaging case of the month. Southwest J Pulm Crit Care. 2017;14(5):201-12. doi: https://doi.org/10.13175/swjpcc055-17 PDF