April 2023 Medical Image of the Month: Atrial Myxoma in the setting of Raynaud’s Phenomenon: Early Echocardiography and Management of Thrombotic Disease

Figure 1. ECG demonstrating sinus bradycardia and T-wave inversion in lead III and aVF.

Figure 2.  Transthoracic echo apical four-chamber view (zoomed) demonstrating 2.3 x 2.6 cm echogenic mass of the left atrium. LV = left ventricle. RA = right atrium. LA = left atrium.

Figure 3.  Transesophageal echo, midesophageal long axis view demonstrating 2.5 x 1.71 cm echogenic left atrial mass attached to upper dome of the left atrium. LA = left atrium. LV = left ventricle.

A 43-year-old woman presents to the Emergency Department (ED) with right-sided weakness and numbness for several hours. Medical history is significant for Raynaud’s Phenomenon (RP), initially presenting six months prior to presentation, manifesting as intermittent episodes of painless discoloration of multiple fingers.  Cardiac exam was unremarkable with regular rhythm and no discernable murmur. Neurological exam demonstrated right arm pronator drift. Other examination findings were unremarkable. Labs demonstrated a troponin of 0.00 ng/mL, C-reactive protein of 2.28 mg/dL, and an erythrocyte sedimentation rate of 40 mm/hr. The electrocardiogram (ECG) demonstrated sinus bradycardia and notable for T-wave inversion in lead III and aVF, but without any ST-segment deviations (Figure 1).  Magnetic Resonance Imagining (MRI) of the brain demonstrated acute ischemic left frontal, left parietal, and right parietal infarcts along with mild subcortical left parietal infarct, concerning for venous or watershed distal embolic arterial infarct. MRI Angiogram of the brain showing diminutive bilateral, lateral transverse dural venous sinuses, consistent with thrombus. The patient’s neurological deficits resolved within five hours of ED arrival. Given the background diagnoses of RP and new thrombosis, a complete autoimmune and hypercoagulability workup was pursued and was otherwise negative.

As part of acute stroke work-up, the patient also underwent transthoracic echocardiogram (TTE) with a bubble study, which was significant for left atrial (LA) echogenic intracardiac structure attached to the superior part of the LA (Figure 2). Transesophageal Echocardiogram (TEE) was performed which demonstrated a large, 2.5 x 1.71 cm mass, consistent with an atrial myxoma, not appearing to involve the interatrial septum but instead thought to originate from the upper dome of the atrium immediately adjacent to the pulmonary veins (Figure 3). Patient was also evaluated by neurology and started on anticoagulation with parental continuous unfractionated heparin infusion given the dural venous sinus thrombosis and a possible hypercoagulable state due to the underlying myxoma. Patient underwent surgical resection of the atrial mass Histopathological examination of the resected mass was consistent with the diagnosis of atrial myxoma.

Although atrial myxomas are the most common primary cardiac tumor, clinical presentation ranges from incidental imaging findings to profound life-threading cardiovascular manifestations (1). This range of presentation is closely associated with size, mobility, and location (2). Pinede et al. studied 112 cases of atrial myxomas and reported that signs of cardiac obstruction were the primary manifestation of LA myxoma. Approximately, 67% of patients presented with signs of cardiac obstruction, such as heart failure, syncope, or myocardial infarction, while embolic signs were only present in 29% of patients. Systemic signs including fever and weight loss were only reported in 34% of patients with only 5% of patients having associated connective tissue disease (3). Rarely, RP has been described as the primary presenting symptom of atrial myxoma (4,5), underscoring the utility of maintaining a high degree of suspicion when symptomatology coexists.

RP is a vascular response to stress or cold temperature that appears as color changes in the digits (6). Although primary RP has no known underlying etiology, it is more commonly seen in female patients with a history of smoking, migraine headaches, and cardiovascular disease (6). This is in contrast to secondary RP, which presents in patient with an underlying autoimmune rheumatic disease including, but not limited, to Systemic Sclerosis, Mixed Connective Tissue Disease, Systemic Lupus Erythematosus, Sjogren’s Syndrome, and hematologic disorders such as Cryoglobulinemia, Cold Agglutinins Disease, and Paraproteinemia (7).

Atrial myxoma may rarely make its initial appearance under the guise of RP (4). This phenomenon is likely attributable to overproduction of IL-6 by the myxoma (9-11). Our patient presented with RP six months prior to her presentation to the ED with right-sided weakness and numbness and a complete autoimmune and hypercoagulability workup was negative; this may suggest that the underlying pathophysiology of her RP is the associated overproduction of IL-6 by the atrial myxoma.

TTE may be considered in the initial diagnostic evaluation of a patient presenting with RP without additional findings suggestive of secondary etiologies. Given that myxomas are typically localized within the atrial lumen, transthoracic echocardiography is a highly sensitive modality for diagnosis, whereas CT and MRI may also help in diagnostics in uncertain cases. Once suspicion of a cardiac myxoma has been supported by imaging modalities, surgical removal of the tumor should be performed as soon as possible due to the risk of myxoma associated embolic episodes (5).  Post intervention, long term prognosis is excellent with an approximated 5% rate of recurrence (3). Long-term follow-up with serial TTE are recommended, particularly in younger patients (3) but there is no specific guideline regarding the frequency of TTE surveillance post atrial myxoma resection.

Ali A. Mahdi MD, Chris Allahverdian MD, Vishal Patel MD, Serap Sobnosky MD

Dignity Health, St. Mary Medical Center, Department of Internal Medicine, Long Beach, CA

References

1. Roberts WC. Primary and secondary neoplasms of the heart. Am J Cardiol. 1997 Sep 1;80(5):671-82. [CrossRef] [PubMed]
2. Zaher MF, Bajaj S, Habib M, Doss E, Habib M, Bikkina M, Shamoon F, Hoyek WN. A giant left atrial myxoma. Case Rep Med. 2014;2014:819052. [CrossRef]
3. Pinede L, Duhaut P, Loire R. Clinical presentation of left atrial cardiac myxoma. A series of 112 consecutive cases. Medicine (Baltimore). 2001 May;80(3):159-72. [CrossRef] [PubMed]
4. Skanse B, Berg No, Westfelt L. Atrial myxoma with Raynaud's phenomenon as the initial symptom. Acta Med Scand. 1959 Jul 25;164:321-4. [CrossRef] [PubMed]
5. Reynen K. Frequency of primary tumors of the heart. Am J Cardiol. 1996 Jan 1;77(1):107. [CrossRef] [PubMed]
6. Abdulla, M. C., & Alungal, J. (2015). Atrial myxoma in a primigravida presenting as Raynaud’s phenomenon. Rheumatology Reports, 7(1). [CrossRef]
7. Prete M, Favoino E, Giacomelli R, et al. Evaluation of the influence of social, demographic, environmental, work-related factors and/or lifestyle habits on Raynaud's phenomenon: a case-control study. Clin Exp Med. 2020 Feb;20(1):31-37. [CrossRef] [PubMed]
8. Khouri C, Blaise S, Carpentier P, Villier C, Cracowski JL, Roustit M. Drug-induced Raynaud's phenomenon: beyond β-adrenoceptor blockers. Br J Clin Pharmacol. 2016 Jul;82(1):6-16. [CrossRef] [PubMed]
9. Jourdan M, Bataille R, Seguin J, Zhang XG, Chaptal PA, Klein B. Constitutive production of interleukin-6 and immunologic features in cardiac myxomas. Arthritis Rheum. 1990 Mar;33(3):398-402. [CrossRef] [PubMed]
10. Saji T, Yanagawa E, Matsuura H, Yamamoto S, Ishikita T, Matsuo N, Yoshirwara K, Takanashi Y. Increased serum interleukin-6 in cardiac myxoma. Am Heart J. 1991 Aug;122(2):579-80. [CrossRef] [PubMed]
11. Parissis JT, Mentzikof D, Georgopoulou M, Gikopoulos M, Kanapitsas A, Merkouris K, Kefalas C. Correlation of interleukin-6 gene expression to immunologic features in patients with cardiac myxomas. J Interferon Cytokine Res. 1996 Aug;16(8):589-93. [CrossRef] [PubMed]

Cite as: Mahdi AA, Allahverdian C, Patel V, Sobnosky S. April 2023 Medical Image of the Month: Atrial Myxoma in the setting of Raynaud’s Phenomenon: Early Echocardiography and Management of Thrombotic Disease. Southwest J Pulm Crit Care Sleep. 2023;26(4):56-58. doi:https://doi.org/10.13175/swjpccs006-23 PDF

April 2022 Medical Image of the Month: COVID Pericarditis

Figure 1. A: Pericardial enhancement on thoracic CT (red arrows). B: Thoracic CT in lung windows showing mosaic attenuation (black arrows) and bilateral pleural effusions (red arrows).

Figure 2. A: Static image of parasternal short axis on transthoracic echocardiogram showing moderate, generalized pericardial effusion with right ventricular diastolic collapse (red arrow). B. Static image of parasternal long axis on transthoracic echocardiogram again showing a moderate, generalized pericardial effusion (red arrow). Lower panel: video of echocardiogram in parasternal long axis view.

A 76-year-old patient presented with fatigue and shortness of breath after missing one session of dialysis. Past medical history included end stage renal disease on hemodialysis and atrial fibrillation on anticoagulation. Initial labs showed that she was COVID positive with mild elevation in troponin and a BNP 1200. While an inpatient, she had received a few sessions of dialysis and treatment for COVID (including dexamethasone and remdesivir). Initial echo showed an ejection fraction of 60-65% with a small generalized pericardial effusion, a thickened pericardium with calcification. A few days after admission patient was suddenly noted to be hypotensive with systolic blood pressure in the 70s and altered mental status. Repeated labs showed a D-Dimer of 17,232, leukocytosis, lactic acidosis, troponin 0.556 ng/ml and arterial blood gas with metabolic acidosis. With a worsening clinical picture, repeat imaging was obtained. CT angiography of the chest was negative for pulmonary embolism; however, it showed a large pericardial effusion with reduced size of the right ventricle more so than left, concerning for cardiac tamponade (Figure 1A). CT chest also showed moderate-to-large pleural effusions with scattered mosaic attenuation of the lung parenchyma (Figure 1B). Repeat transthoracic echocardiogram had a moderate generalized pericardial effusion with right ventricular diastolic collapse concerning for pericardial tamponade (Figure 2). Her airway was secured with endotracheal intubation and vasopressors added for hemodynamic support. Pericardiocentesis was indicated however, patient’s INR was severely elevated in the setting of anticoagulation use. Efforts were made to lower INR with FFP; however, patient had a PEA arrest the following day and expired.

COVID-19 has been classically known for its detrimental lung damage; however, it has shown to cause extrapulmonary effects as well. Cardiac injury is one phenomenon that has been seen with the fulminant inflammatory state that COVID is known to cause. With a few cases reported for COVID pericarditis, it is a possible culprit when all other causes have been ruled out. Pericardial involvement can be seen in about 20% of COVID 19 cases, with effusion found in about 5% of patients (1). Concomitant myocarditis can also be found in up to 17% of patients. Having isolated cardiac involvement with COVID is rare, with most cases presenting mainly as lung involvement in addition to other organs affected as well. Clinically, patients with pericarditis typically experience chest pain and in the setting of COVID infection, an increase in inflammatory markers. Characteristic findings of pericarditis include friction rub on auscultation, diffuse ST elevations on EKG and a potential progression to pericardial effusion on echo. When a pericardial effusion becomes large enough, it can progress to cardiac tamponade (2). Having a high clinical suspicion for tamponade is crucial in a patient who has developed respiratory distress and hypotension in the setting of recent viral pericarditis. It is a clinical diagnosis and requires rapid treatment with pericardiocentesis to prevent cardiac arrest.

Sarah Youkhana, MD¹ and Maged Tanios, MD²

St. Mary Medical Center, Long Beach, CA USA

¹Internal Medicine Resident, PGY-3

²Medical Director, Critical Care Services

References

1. Diaz-Arocutipa C, Saucedo-Chinchay J, Imazio M. Pericarditis in patients with COVID-19: a systematic review. J Cardiovasc Med (Hagerstown). 2021 Sep 1;22(9):693-700. [CrossRef] [PubMed]
2. Imazio M, Gaita F, LeWinter M. Evaluation and Treatment of Pericarditis: A Systematic Review. JAMA. 2015 Oct 13;314(14):1498-506. [CrossRef] [PubMed]

Cite as: Youkhana S, Tanios M. April 2022 Medical Image of the Month: COVID Pericarditis. Southwest J Pulm Crit Care Sleep 2022;24(4):62-3. doi: https://doi.org/10.13175/swjpccs006-22 PDF

Medical Image of the Month: Severe Left Ventricular Hypertrophy

Figure 1. An electrocardiogram demonstrates left ventricular hypertrophy by voltage and non-voltage criteria.

Figure 2. Parasternal long view of the heart demonstrates marked left ventricular hypertrophy with partial obstruction of the left ventricular outflow tract.

The patient is a 56-year-old man with a history of hypertension who was admitted to ICU after the administration of nitroglycerin for chest pain in the setting of hypertensive emergency resulted in a sudden drop in systolic BP drop from 220 to 106. The above images depict LVH on EKG (Figure 1) along with severe concentric LVH (End-diastolic-wall-thickness = 22mm) with significant apical and septal thickening resulting in partial obstruction of the left ventricle outflow tract concerning for HCM vs HHD (Figure 2).

Significant morphological overlap between HCM and HHD makes establishing a diagnosis difficult and often requires more advanced tissue characterization in the form of cardiac MR. In a patient with severe LVH, a diagnosis of HCM should be considered if ≥ 1 myocardial segment has a LV end-diastolic wall thickness (EDWT) ≥ 15mm on transthoracic echo¹. Additional features such as systolic anterior motion of the mitral valve (SAM) are also useful in establishing a diagnosis of HCM, especially in those with concomitant hypertension. A large majority of patients with HCM have elongated mitral valve leaflets which can protrude into the LV cavity. During systole, the mitral valve leaflet moves towards the interventricular septum which is thickened in patients with LVH. This creates a left ventricular outflow obstruction (LVOTO) that causes shortness of breath, chest pain, and syncope. This ultimately increases the risk of arrhythmias and sudden cardiac death.

Treatment of LVOT obstruction is indicated in all symptomatic patients. First line medical management functions to increase preload with negatively inotropic medications such as beta-blockers, disopyramide and verapamil. In patients who are persistently symptomatic despite optimal medical therapy, septal reduction therapy via alcohol septal ablation (ASA) or septal myomectomy (SM) are standard of care². Long-term data suggests there is no difference in cardiovascular mortality when comparing ASA and SM. However, those receiving ASA have lower periprocedural complications but more often require implantation of pacemakers or reintervention in the future.

April L. Olson MD MPH, Nicholas G. Blackstone MD, Benjamin J. Jarrett MD, and Janet M. Campion MD MPH

University of Arizona College of Medicine at South Campus

Tucson, AZ USA

References

1. Rodrigues JC, Rohan S, Ghosh Dastidar A, Harries I, Lawton CB, Ratcliffe LE, Burchell AE, Hart EC, Hamilton MC, Paton JF, Nightingale AK, Manghat NE. Hypertensive heart disease versus hypertrophic cardiomyopathy: multi-parametric cardiovascular magnetic resonance discriminators when end-diastolic wall thickness ≥ 15 mm. Eur Radiol. 2017 Mar;27(3):1125-1135. [CrossRef] [PubMed]
2. Osman M, Kheiri B, Osman K, Barbarawi M, Alhamoud H, Alqahtani F, Alkhouli M. Alcohol septal ablation vs myectomy for symptomatic hypertrophic obstructive cardiomyopathy: Systematic review and meta-analysis. Clin Cardiol. 2019 Jan;42(1):190-197. [CrossRef] [PubMed]

Cite as: Olson AL, Blackstone NG, Jarrett BJ, Campion JM. Medical Image of the Month: Severe Left Ventricular Hypertrophy. Southwest J Pulm Crit Care. 2020;21(4):80-1. doi: https://doi.org/10.13175/swjpcc052-20 PDF

August 2020 Imaging Case of the Month: Piecing Together a Cause for Multisystem Abnormalities

Prasad M. Panse MD

Clinton E. Jokerst MD

Michael B. Gotway MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale, AZ USA

Clinical History: A 65-year-old woman with chronic hoarseness and dyspnea now presents with complaints of diarrhea and bloating. The patient indicated her dyspnea had developed over the previous year, now occurring after one flight of stairs. The patient also complains of some substernal burning after waling 2-3 blocks. Her past medical history was largely unremarkable, and her past surgical history included only a cesarean section and carpal tunnel surgery. She has no allergies and her medications included thyroxine, fluoxetine, and a steroid inhaler. She was a previous smoker for 8 years, quitting 30 years ago. Upon directed questioning, the patient also complains of generalized weakness and 13-14 lbs. weight loss in the previous year.

Physical examination showed normal vital signs and was remarkable only for atrophy of the patient’s right calf muscles, which the patient claimed she knew about and had occurred over the previous year and a half. The neurologic examination was entirely normal. The examining physician noted that the patient’s tongue appeared somewhat enlarged and reddened, but was not coated and midline upon protrusion.

The patient’s complete blood count and serum chemistries showed all values within the normal range except for a serum albumin level of 2.9 gm/dL (normal, 3.5-5 gm/dL). Her erythrocyte sedimentation rate was mildly elevated at 55 mm/h (normal, 0-29 mm/hr). The patient was referred for chest radiography (Figure 1).

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 be directed to the second of nine pages)

1. The chest radiograph shows mediastinal and peribronchial lymph node enlargement
2. The chest radiograph shows multifocal basal consolidation
3. The chest radiograph shows normal findings
4. The chest radiograph shows numerous small nodules
5. The chest radiograph shows small bilateral pleural effusions

Cite as: Panse PM, Jokerst CE, Gotway MB. August 2020 imaging case of the month: piecing together a cause for multisystem abnormalities. Southwest J Pulm Crit Care. 2020;21(2):23-34. doi: https://doi.org/10.13175/swjpcc045-20 PDF 

Medical Image of the Month: Malignant Pleural and Pericardial Effusions

Figure 1. CTA chest axial view showing moderate pericardial effusion, bilateral pleural effusions and an anterior mediastinal mass.

Figure 2. Echocardiography subcostal four-chambered view showing a large pericardial effusion with right ventricular collapse during diastole.

A 67-year-old woman with a history of presumed thymoma presented to the emergency department with four weeks of progressive shortness of breath and wheezing. CT imaging of the chest on arrival demonstrated a 13.1 x 8.6 x 8.2 cm anterior mediastinal mass with compression of the SVC, pulmonary veins, and right pulmonary artery (Figure 1). A moderate pericardial effusion was also seen. A transthoracic echocardiogram was performed to further evaluate the pericardial effusion, which revealed diastolic collapse of the right ventricle consistent with cardiac tamponade (Figure 2). The patient was taken for urgent pericardiocentesis, which drained 450cc of sanguineous fluid. Percutaneous biopsy of the mass revealed poorly differentiated carcinoma suspicious for a primary breast malignancy. Cytology of the pericardial fluid did not demonstrate malignancy, however. Cytology of subsequent pleural effusion also was not positive for malignancy, although, both effusions are believed to be related to the malignancy even if no malignant cells were present on analysis.

Malignant pericardial effusions account for 18-23% of cases, and are one of the most common causes of hemorrhagic effusions. Multiple types of cancers can involve the pericardium; lung cancer is the most common but lymphoma, leukemia, melanoma, and breast cancer are other potentially causative malignancies. Presence of a symptomatic malignant effusion is a poor prognostic indicator with median survival on the order of 2-4 months after diagnosis, although certain malignancies (e.g. hematologic rather than solid) may have better results (1).

Nathan Coffman MD and Jessica Vondrak MD

Department of Internal Medicine

Banner University Medical Center

University of Arizona

Tucson, AZ USA

Reference

1. Dequanter D, Lothaire P, Berghmans T, Sculier JP. Severe pericardial effusion in patients with concurrent malignancy: a retrospective analysis of prognostic factors influencing survival. Ann Surg Oncol. 2008 Nov;15(11):3268-71. [CrossRef] [PubMed] 

Cite as: Coffman N, Vondrak J. Medical image of the month: Malignant pleural and pericardial effusions. Southwest J Pulm Crit Care. 2018;17(5): . doi: https://doi.org/10.13175/swjpcc107-18 PDF 

Medical Image of the Week: Cardiac Magnetic Resonance Imaging Findings of Severe RV Failure

  

Figure 1. Transthoracic echocardiography, short-axis view (1A) and four-chamber view (1B) demonstrating leftward deviation with flattening of interventricular septum (“D-sign”) due to increased right ventricular pressure and volume overload from severe pulmonary arterial hypertension (PAH). RV=right ventricle. RA=right atrium. LV=left ventricle.

Figure 2. Cardiac Magnetic Resonance Imaging, sagittal view (2A), and cross-sectional view (2B) show the same signs of massive right ventricular (RV) pressure and volume overload with severe RV dysfunction. RV ejection fraction of 13%. RV=right ventricle. RA=right atrium. LV=left ventricle. LA=left atrium.

A 56-year-old man with history a of alcohol abuse presents with progressive shortness of breath on exertion, bilateral lower extremity swelling and 12-pound weight gain over two weeks.

His transthoracic echocardiography (Figure 1) demonstrated severely increased global right ventricle (RV) size, severely dilated right atrium (RA), severe pulmonary artery (PA) dilation, moderate tricuspid regurgitation (TR) and right ventricular systolic pressure (RVSP) estimated at 85 + central venous pressure (CVP) in the context of severely reduced RV systolic function.  Right heart catheterization (RHC) showed PA pressure (systolic/diastolic, mean) of 94/28, 51 mmHg with a PA occlusion pressure of 12 mmHg. After extensive evaluation, our patient’s presentation of right heart failure seemed to be a manifestation of idiopathic pulmonary arterial hypertension.

Our patient subsequently had cardiac MRI (cMRI) with findings shown above (Figure 2). CMRI is a valuable, three-dimensional imaging modality that provides detailed morphology of the cardiac chambers along with accurate quantification of chamber volumes, myocardial mass and transvalvular flow (1). Cardiac MRI is an accurate tool to estimate the RV function at baseline and to follow up response to treatment. RV function at presentation and after treatment are very important determinants of prognosis independent of other hemodynamic indices (2).  

Kelly Wickstrom, DO¹, Huthayfa Ateeli, MBBS², Sachin Chaudhary, MD²

¹Internal Medicine Department and ²Pulmonary and Critical Care Division

Banner University Medical Center

Tucson, AZ USA

References

1. Grünig E, Peacock AJ. Imaging the heart in pulmonary hypertension: an update. Eur Respir Rev. 2015 Dec;24(138):653-64. [CrossRef] [PubMed]
2. Swift AJ, Wild JM, Nagle SK, et al. Quantitative magnetic resonance imaging of pulmonary hypertension: a practical approach to the current state of the art. J Thorac Imaging. 2014 Mar;29(2):68-79. [CrossRef] [PubMed]

Cite as: Wickstrom K, Ateeli H, Chaudhary S. Medical image of the week: cardiac magnetic resonance imaging findings of severe RV failure. Southwest J Pulm Crit Care. 2018;16(5):252-3. doi: https://doi.org/10.13175/swjpcc047-18 PDF

Medical Image of the Week: VA Shunt Remnant Fibrosing into Right Atrium

Figure 1. Transthoracic echocardiography demonstrating tubular echo density in the right atrium (arrow).

Figure 2: Transesophageal echocardiography demonstrating the VA shunt remnant fibrosed (vs. calcified) in SVC (arrow) extending into right atrium (RA).

A 71-year-old man with a history of ventriculo-atrial (VA) shunt, removed in 2004 due to infection, was admitted to the hospital complaining of syncopal symptoms for one day’s duration. On presentation he denied any symptoms of syncope or focal weakness. The patient was placed on telemetry monitoring, and overnight observation demonstrated multiple sinus pauses with frequent episodes of premature atrial contractions. Stat transthoracic echocardiography (TTE) on the night of admission demonstrated a right tubular echodensity in the right atrium crossing the tricuspid valve (Figure 1). Follow up transesophageal echocardiography (TEE) redemonstrated evidence of a tubular structure in the SVC extending into the right atrium with evidence of fibrosis (?calcification)(Figure 2). These studies demonstrate the importance of echocardiographical work up in any patient with risk of retained foreign body even after reported removal (1).

Richard Young, MD; Joshua Sifuentes, MD; Joao Paulo Ferreira, MD

Department of Internal Medicine

Banner University Medical Center

University of Arizona

Tucson, Arizona USA

Reference

1. Choi CH, Elahi MM, Konda S. Iatrogenic retained foreign body in the right atrium. Lessons to Learn. Int J Surg Case Rep. 2013;4(11):985-7. [CrossRef] [PubMed]

Cite as: Young R, Sifuentes J, Ferreira JP. Medical image of the week: VA shunt remnant fibrosing into right atrium. Southwest J Pulm Crit Care. 2017;14(3): 117-8. doi: https://doi.org/10.13175/swjpcc023-17 PDF

Medical Image of the Week: Catheter-Induced Right Atrial Thrombus

  

Figure 1. Panel A: Apical 4 chamber view showing intra cardiac mass (arrow) in the right atrium located above the closed tricuspid valve in systole (left). Panel B: The mass moves into the right ventricle through the open tricuspid valve in diastole.

Figure 2. Axial TRUFISP MRI images through the mediastinum demonstrate a central venous catheter (yellow arrow) within the distal superior vena cava (a-b) and proximal right atrium (c).  A hypointense lesion (red arrow) is seen extending from and in close approximation of the catheter tip (d-e).  Axial T1 post-contrast MRI image through the heart demonstrates no associated enhancement (f) in this lesion. These findings are most consistent with a catheter-related thrombus. 

A 71-year-old woman with a history of renal amyloidosis complicated by end stage renal disease on long term hemodialysis through a permacath presented with complaints of recurrent syncope during hemodialysis. When propped up at 45 degrees, her examination showed an early systolic murmur located over her right upper sternal border and a crescendo systolic murmur located over left axillary region. The murmurs were grade 2/6 in intensity but increased to 4/6 when propped up at 90 degrees. A transthoracic echocardiogram revealed a 2.5 x 2.7 cm echogenic mass arising from the right atrial side of AV groove and prolapsing through the open tricuspic valve into the right ventricle during diastole (Figure 1). On contrast enhanced cardiac magnetic resonance imaging, the mass was identified as a thrombus measuring 2.9 x 2.7 x 2.2 cm and connected to the distal tip of the dialysis catheter (Figure 2).

It is difficult to confidently determine the best catheter tip position to avoid thrombosis.  Although placement of the catheter tip in the right atrium may decrease thrombosis, this location is debatable and subject to controversy (1). The optimal treatment for catheter-induced right atrial thrombus is also an area of controversy (2).  

Anticoagulation therapy is preferred over surgery by most physicians. For our patient, we treated her with warfarin to a target INR (International Normalized Ratio) of 2 to 3.  We were concerned about the possibility of thrombus detachment and catastrophic embolism. We retained the internal jugular catheter in place and obtained a new femoral access site for future hemodialysis.

Manjinder Kaur DO, Hem Desai MBBS, Emily S Nia MD, and Imo Ebong MD

Department of Medicine

University of Arizona

Tucson, AZ USA

References

1. Vesely TM. Central venous catheter tip position: a continuing controversy. J Vasc Interv Radiol. 2003 May;14(5):527-34. [CrossRef] [PubMed]
2. Lalor PF, Sutter F. Surgical management of a hemodialysis catheter-induced right atrial thrombus. Curr Surg. 2006 May-Jun;63(3):186-9. [CrossRef] [PubMed] 

Cite as: Kaur M, Desai H, Nia ES, Ebong I. Medical image of the week: catheter-induced right atrial thrombus. Southwest J Pulm Crit Care. 2016;13(2):82-3. doi: http://dx.doi.org/10.13175/swjpcc062-16 PDF

Medical Image Of The Week: Tricuspid Valve Vegetation with Septic Pulmonary Emboli

Figure 1. Chest radiograph on presentation consistent with septic pulmonary embolic and cavitation.

Figure 2. Echocardiogram demonstrating a highly mobile echo-dense vegetation attached to the atrial side of the tricuspid valve.

A 28-year-old woman with a history of extensive intravenous heroin use presented to the hospital with generalized chest and abdominal pain. Vital signs were remarkable for hypotension, tachypnea, and tachycardia. Laboratory studies revealed leukocytosis, hyponatremia, acute kidney injury, and lactic acidosis. A radiograph of the chest demonstrated multiple airspace opacities throughout the bilateral lungs with associated cavitary lesions and a small right-sided pleural effusion (Figure 1). A transthoracic echocardiogram was obtained, which demonstrated a 3.6 cm x 2.0 cm tricuspid valve vegetation (Figure 2). Blood cultures identified methicillin-sensitive Staphylococcus aureus.

Infective endocarditis, valvular vegetation, and septic pulmonary emboli are common complications of intravenous drug use. Staphylococcus aureus is the most common bacterial cause of infective endocarditis among intravenous drug users (1). Like endocarditis, patients with septic pulmonary emboli often present with non-specific clinical manifestations such as fever (86%), dyspnea (48%), and chest pain (49%) (2). Management may be surgical or medical, and determining the best course is complicated by social and psychiatric factors affecting adherence to treatment. Cardiac valve surgery has been advocated early for large right-sided vegetations but carries high morbidity and expense, as well as risk of compromised recovery, in the setting of ongoing IV drug use. Even for patients with valvular vegetations ≥ 1cm, medical therapy alone may be a safe option under some circumstances in the absence of other surgical indications (3).

Sarah Harris BA¹, Kady Goldlist MD², Maria Tumanik DO², Cameron Hypes MD MPH^3,4

¹ University of Arizona College of Medicine

² Department of Internal Medicine, Banner University Medical Center – South Campus

³ Department of Medicine, Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine

 ⁴Department of Emergency Medicine

University of Arizona

Tucson, AZ USA

References

1. Ortiz-Bautista C, López J, García-Granja PE, et al. Current profile of infective endocarditis in intravenous drug users: The prognostic relevance of the valves involved. Int J Cardiol. 2015;187:472-4. [CrossRef] [PubMed]
2. Ye R, Zhao L, Wang C, Wu X, Yan H. Clinical characteristics of septic pulmonary embolism in adults: a systematic review. Respir Med. 2014 Jan;108(1):1-8. [CrossRef] [PubMed]
3. Otome O, Guy S, Tramontana A, Lane G, Karunajeewa H. A retrospective review: significance of vegetation size in injection drug users with right-sided infective endocarditis. Heart Lung Circ. 2016 May;25(5):466-70. [CrossRef] [PubMed] 

Cite as: Harris S, Goldlist K, Tumanik M, Hypes C. Medical image of the week: tricuspid valve vegetation with septic pulmonary emboli. Southwest J Pulm Crit Care. 2016:12(6):253-4. doi: http://dx.doi.org/10.13175/swjpcc042-16 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

Medical Image of the Week: Pericardial Effusion in a Setting of Bacterial Endocarditis

Figure 1. Single portable semi-upright chest radiograph with findings of an enlarged cardiomediastinal silhouette, and indistinctness of the perihilar vasculature.

Figure 2. Axial contrast enhanced computed tomography—soft tissue windows. A large concentric rim (fluid density) surrounds all four chambers of the heart, consistent with a pericardial effusion. Notice how the right ventricle is normal, which can be collapsed in cardiac tamponade.

A 25-year-old man with an extensive history of intravenous drug abuse presents to the hospital with worsening shortness of breath and fevers for two weeks. In the emergency department, he was initially provided breathing treatments including ipratropium/albuterol and methylprednisolone. As the patient still required supplemental oxygen, a chest radiograph was performed to evaluate for an underlying infectious etiology.

However, the chest radiograph portrayed an enlarged cardiomediastinal silhouette in a “water-bottle” appearance and obscuration of the hilar vessels (Figure 1). Given these findings, there was a high concern for a pericardial effusion, and the physicians opted for further cross-sectional imaging. The contrast enhanced computed tomography (CT) images confirmed the aforementioned diagnosis (Figure 2). As blood cultures eventually grew Staphylococcus aureus, and given the patient’s extensive history of intravenous drug abuse, there was a high suspicion for bacterial endocarditis. A subsequent echocardiogram verified several valvular vegetations in keeping with endocarditis. The patient’s vitals remained stable throughout the hospital course, and he was continued on long-term antibiotic therapy.

Chest radiographs are often unreliable in depicting pericardial effusions, as they require at least 200 mL of pericardial fluid to portray an enlarged cardiomediastinal silhouette (1).  As fluid continues to accumulate in the pericardial space, the increase in pericardial pressure on the chambers can eventually lead to cardiac tamponade—a form of cardiogenic shock (2). Cardiac tamponade will result in a decrease in stroke volume, decreased blood pressure, and ultimately a diminished cardiac output; all of which require immediate intervention (2). Echocardiography remains the imaging modality of choice given its portability and high sensitivity in diagnosing pericardial fluid (3).

Amrit Hansra, MD

Department of Medical Imaging

University of Arizona

Tucson, AZ

References

1. Restrepo CS, Lemos DF, Lemos JA, et al. Imaging findings in cardiac tamponade with emphasis on CT. Radiographics. 2007 Nov-Dec;27(6):1595-610. [CrossRef] [PubMed]
2. Spodick DH. Acute cardiac tamponade. N Engl J Med. 2003 Aug 14;349(7):684-90. [CrossRef] [PubMed]
3. Chong HH, Plotnick GD. Pericardial effusion and tamponade: evaluation, imaging modalities, and management. Compr Ther. 1995 Jul;21(7):378-85. [PubMed] 

Cite as: Hansra A. Medical image of the week: pericardial effusion in a setting of bacterial endocarditis. Southwest J Pulm Crit Care. 2016 Mar;12(3):110-1. doi: http://dx.doi.org/10.13175/swjpcc009-16 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: ECHO findings of Apical Ballooning Syndrome

  Figure 1. Panel A: Four chamber view of the heart at the end of diastole with a dilated left ventricle. Panel B: Same four chamber view of the heart at the end of systole with a dilation and akinesis of the apical portion (arrow) of the heart consistent with apical ballooning/stress cardiomyopathy

A 79 year old man with a history of lung cancer. bladder cancer, chronic obstructive pulmonary disease, and coronary artery disease with two previous myocardial infarctions, presented to the emergency department with respiratory failure secondary to pulmonary edema. Further evaluation was significant for non-ST segment elevation myocardial infarction. Cardiac catheterization was remarkable for a focal, eccentric 95% stenosis of the proximal to mid left anterior descending artery that failed stenting due to extensive calcifications. An echocardiogram (ECHO, Figure 1) revealed an ejection fraction of 47% with akinesis of the mid to distal anterior, lateral, inferior, septal and apical segments consistent with takotsubo cardiomyopathy.

Takotsubo cardiomyopathy, aka apical ballooning syndrome or stress induced cardiomyopathy, is a subtype of heart failure typically defined by proposed criteria from the Mayo Clinic that includes: 1. transient hypokinesis, akinesis, or dyskinesis in the left ventricular mid segments with or without apical involvement frequently occurring, but not always, in context to a stressful trigger; 2. the absence of angiographic evidence of obstructive coronary disease or plaque rupture; 3. new ECG abnormalities (ST-segment elevation and/or T-wave inversion) or modest elevation in cardiac troponin; and 4. the absence of pheochromocytoma and myocarditis (1). It predominantly occurs in post-menopausal women in relation to unexpected emotional or physical stress. Characteristic ECHO findings demonstrate a symmetrical regional wall motion abnormalities extending equally into the apical inferior and lateral wall with overall global hypokinesia (Figure 1) (2).

Sachin Kalarn MSIV; Sophie Galson MD; Kristina Skinner DO; Ryan Nahapetian MD, MPH

University of Arizona

Tucson, AZ

References

1. Akashi YJ, Goldstein DS, Barbaro G, Ueyama T. Takotsubo cardiomyopathy: a new form of acute, reversible heart failure. Circulation. 2008;118(25):2754-62. [CrossRef] [PubMed]
2. Chockalingam A, Xie GY, Dellsperger KC. Echocardiography in stress cardiomyopathy and acute LVOT obstruction. Int J Cardiovasc Imaging. 2010;26(5):527-35. [CrossRef] [PubMed]

Reference as: Kalarn S, Galson S, Skinner K, Nahapetian R. Medical image of the week: ECHO findings of aprical ballooning syndrome. Southwest J Pulm Crit Care. 2015;10(4):150-1. doi: http://dx.doi.org/10.13175/swjpcc024-15 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: Paradoxical Stroke

Figure 1. Vegetation seen on the tricuspid valve on the transthoracic echocardiogram (arrow). RA=right atrium, RV=right ventricle.

Figure 2. Patent foramen ovale (PFO) with right to left shunt of the agitated saline contrast on the trans-esophageal echocardiogram (arrow). RA=right atrium, LA=left atrium.

Figure 3. Acute left cerebellar stroke, hyper-dense lesion on T2 weighted MRI of the brain. (encircled).

A 23-year-old man with a history of intravenous drug abuse (IVDA) was admitted to the intensive care unit (ICU) secondary to sepsis. His blood cultures were positive for methicillin sensitive Staphylococcus aureus. Transthoracic echocardiogram showed vegetation on the tricuspid valve (Figure 1). He had multiple systemic emboli leading to suspicion for right to left shunt, which was confirmed by the agitated saline test during the echocardiogram (Figure 2). Cerebellar strokes likely secondary to posterior circulation embolic phenomenon was also seen (Figure 3). Overall, after a protracted ICU course complicated by multi-organ failure, he improved and is continuing treatment and rehabilitation at this time.

Right-sided infective endocarditis (IE) incidence is low, accounting for 5-10% of all cases of IE (1). IVDA is a well-known cause of tricuspid valve endocarditis. Usual features of tricuspid endocarditis are fever, bacteremia and pulmonary septic emboli. Patent foramen ovale (PFO) is estimated in up to 25% of the general population. Management of PFO for secondary stroke prevention remains controversial. Closure can be achieved surgically or percutaneously. The efficacy of closure of a PFO on the rate of recurrent stroke has not been established.

Laila Abu Zaid MD¹, Evbu Enakpene MD² and Bhupinder Natt MD³

¹Department of Internal Medicine

²Division of Cardiovascular Diseases

³Division of Pulmonary, Allergy, Critical Care and Sleep Medicine

University of Arizona Medical Center

Tucson, AZ.

Reference

1. Akinosoglou K, Apostolakis E, Marangos M, Pasvol G. Native valve right sided infective endocarditis. Eur J Intern Med. 2013;24(6):510-9. [CrossRef] [PubMed]

Reference as: Zaid LA, Enakpene E, Natt B. Medical image of the week: paradoxical stroke. Southwest J Pulm Crit Care. 2014;9(5):278-80. doi: http://dx.doi.org/10.13175/swjpcc135-14 PDF

Medical Image of the Week: Pulmonary Arteriovenous Malformations

Figure 1. Cardiac ultrasound showing right to left shunting.

Figure 2. Thoracic CT scan showing arteriovenous malformations (AVM's, arrows).

A 34 year old woman presented to the clinic with exertional dyspnea since childhood. Oxygen saturations in clinic were 92% on room air. On review of systems she admitted to recurrent epistaxis and her daughter also suffered from frequent epistaxis. Bubble contrast echocardiography showed severe right to left shunting without evidence of intracardiac shunt (Figure 1). Computed tomography angiogram of the chest revealed multiple bilateral arteriovenous malformations (AVM’s), the largest measuring 9mm on coronal images (Figure 2). MRI of the brain was negative for AVM’s. She was referred to interventional radiology for microcoil embolization. She met two of four Curaçao criteria for the diagnosis of hereditary hemorrhagic telangiectasia (HHT), giving her “possible HHT”. She was referred for genetic testing to confirm the diagnosis.

Chris Strawter MD and Laura Meinke MD

University of Arizona

Tucson, Arizona

References

1. Lacombe P, Lacout A, Marcy PY, et al. Diagnosis and treatment of pulmonary arteriovenous malformations in hereditary hemorrhagic telangiectasia: an overview. Diagn Interv Imaging. 2013;94:835-48. [CrossRef] [PubMed]
2. Gossage JR, Kanj G. Pulmonary arteriovenous malformations. A state of the art review. Am J Respir Crit Care Med. 1998;158:643-61. [CrossRef] [PubMed]
3. Faughnan ME, Palda VA, Garcia-Tsao G, et al. International guidelines for the diagnosis and management of hereditary haemorrhagic telangiectasia. J Med Genet. 2011;48:73-87. [CrossRef] [PubMed]

Reference as: Strawter C, Meinke L. Medical image of the week: pulmonary arteriovenous malformations. Southwest J Pulm Crit Care. 2014;9(4):238-9. doi: http://dx.doi.org/10.13175/swjpcc131-14 PDF 

Medical Image of the Week: Idiopathic Pulmonary Artery Hypertension

Figure 1. EKG showing sinus rhythm, right bundle branch block and peaked ('pulmonary') p waves (arrow).

Figure 2. Two view chest X-ray showing right ventricular hypertrophy (arrows, note filling of the retrosternal space by an enlarged right ventricle in the lateral view) and enlarged central pulmonary arteries (arrowhead).

 

  Figure 3. Axial CT angiogram of the chest below the carina showing dilated pulmonary artery (diameter of pulmonary artery greater than aorta, arrow).

 

Figure 4. Panel A: Parasternal short axis view shows septal bowing to the left, a severely dilated right ventricle and a D-shaped left ventricle. Panel B: Four chamber view shows right atrial and ventricular dilatation.

A 39-year-old woman presented to the clinic with a history of progressive shortness of breath of 6-month duration associated with bilateral lower extremity edema, fatigue, lightheadedness, palpitations and occasional substernal chest pain. Her past medical history was unremarkable other than mild anemia. On physical exam her respiratory rate was 20 breaths per minute and O2 saturation 94% on room air by pulse oximetry. There was jugular venous distention at 12 cm, 2+ bilateral lower extremity edema, a 5/6 systolic murmur over the left sternal border with a sternal heave. Labwork was unremarkable except for an elevated BNP 657 (normal value < 100 pg/mL).

EKG (Figure 1) showed sinus rhythm with right bundle branch block. A 2-view chest X-ray (Figure 2) showed an enlarged right ventricle as well as dilated pulmonary arteries with no parenchymal infiltrates. CT angiography confirmed CXR findings (Figure 3) and was negative for pulmonary embolism. A 2D echocardiogram revealed a preserved left ventricle ejection fraction with right ventricular pressure of 80 mmHg + CVP, severe tricuspid regurgitation, decreased right ventricular function (as assessed by a Tricuspid annular plane systolic excursion of 10 mm) and flattened septum, suggestive of right ventricular overload (Figure 4). A right heart catheterization was performed revealing pulmonary pressures of 105/45 mmHg with a mean of 63 mmHg, a wedge pressure of 11 mmHg, a pulmonary vascular resistance of 13.19 Wood units and a cardiac output of 3.94 L/min.

The patient was admitted to the intensive care unit to start treatment with intravenous treprostinil and was eventually discharged home with subcutaneous treprostrinil.

Pulmonary arterial hypertension (PAH) is a disease of the pulmonary circulation characterized by a progressive elevation in pulmonary vascular resistance that leads to right ventricular failure and premature death. It is defined as a mean pulmonary artery pressure at rest of 25 mmHg or higher (1). Idiopathic (group 1) PAH requires the exclusion of parenchymal pathology or venous thromboembolic disease as well as a mean wedge pressure less than 15 mmHg. The initial symptoms of PH are the result of an inability to adequately increase cardiac output during exercise which eventually will progress to signs and symptoms of right ventricular failure such as lower extremity edema, syncope/presyncope and chest pain (2,3). Early recognition is of paramount importance to institute adequate treatment.

Roberto J. Bernardo, MD and Carlos Tafich Rios, MD

Internal Medicine Residency, Department of Medicine

University of Arizona, Tucson, AZ

References 

1. McLaughlin VV, Archer SL, Badesch DB, et al. ACCF/AHA 2009 expert consensus document on pulmonary hypertension: a report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents and the American Heart Association: developed in collaboration with the American College. Circulation. 2009. 119:2250-94. [CrossRef] [PubMed] 
2. Runo JR, Loyd JE. Primary pulmonary hypertension. Lancet. 2003. 361:1533-44. [CrossRef] [PubMed]
3. Peacock AJ. Primary pulmonary hypertension. Thorax. 1999;54:1107-18. [CrossRef] [PubMed]

Reference as: Bernardo RJ, Rios CT. Medical image of the week: idiopathic pulmonary artery hypertension. Southwest J Pulm Crit Care. 2014;9(2):101-3. doi: http://dx.doi.org/10.13175/swjpcc101-14   PDF

Medical Image of the Week: Malignant Pericardial Effusion and Cardiac Tamponade

Figure 1. EKG showing sinus tachycardia, low QRS voltage and electric alternans, suggesting pericardial effusion.

Figure 2. Chest X-ray pre- and post-pericardiocentesis. Panel A: Cardiomegaly with water bottle shape shown before procedure. Panel B: resolution after drainage of 1.8 L of pericardial fluid.

Figure 3. Echocardiogram showing massive pericardial effusion (dashed line), floating heart, and collapsed right atrium and ventricle that are consistent with cardiac tamponade.

Figure 4. Intra-pericardial space pressure tracing with maximum pressure measured at 25 mmHg.

A 53 year old woman with history of metastatic breast cancer presented to the emergency department (ED) with worsening shortness of breath for 2 weeks. She was initially diagnosed with grade III breast intraductal carcinoma was estrogen receptor, progesterone receptor, and HER2 negative 5 years earlier. A lumpectomy was performed followed by 4 cycles of chemotherapy with cyclophosphamide and taxol as well as radiation therapy. However, follow-up CT and MRI and subsequent biopsy demonstrated metastatic disease in the left adrenal gland, right ovary, and mediastinal lymph nodes, for which additional chemotherapy was started a month prior to presentation. In the ED, the patient was tachycardic and tachypneic. Vital signs showed BP 112/94 mmHg, HR 118 /min, RR 28 /min, temperature 97.5 °F, and SpO₂ 97 % with room air. EKG showed sinus tachycardia, low QRS voltage with electric alternans (Figure 1), and chest x-ray demonstrated cardiomegaly with a water bottle shaped heart (Figure 2A), suggesting pericardial effusion. Over the hour at ED, patient developed sudden hypotension with BP of 78/44. 1 L of normal saline was administrated immediately, and patient was transferred to cardiac catherization laboratory for emergent pericardiocentesis. Echocardiogram before the procedure demonstrated massive pericardial effusion and a floating heart in the pericardial space (Figure 3). Intra-pericardial pressure was measured at 25 mmHg (Figure 4). A total of 1.8 L of sanguineous fluid was drained. Pericardial fluid cell count with differential and chemistry showed WBC 2444 /μL, RBC 1480000 /μL, lymphocytes 32 /μL , neutrophils 64 /μL, glucose 108 mg/dL, and protein 5.2 g/dL, and cytology analysis with fluid demonstrated adenocarcinoma, confirming the diagnosis of malignant pericardial effusion and cardiac tamponade. Chest x-ray after the procedure showing resolution of the water bottle-shaped heart (Figure 2B). Elective thoracotomy with pericardiectomy was performed the next day, and patient was eventually discharged in stable condition.

Pericardial effusion seen in cancer patients may results from several sources. Constrictive pericarditis with pericardial effusion can arise as a complication of radiation therapy. Uremia and certain medications can induce pericardial effusion as well. Metastatic cardiac involvement may causes pericardial effusion. A previous autopsy study showed 10.7 % of patients with underlying malignancy had metastatic disease in the heart (1). Adenocarcinoma is the most frequently found cell type, and lung cancer, malignant lymphoma and breast cancers are the most common primary tumors metastasizing to the heart. Symptoms of malignant pericardial effusion include shortness of breath, cough, chest pain, and edema. Vaitkus et al. (2) proposed three goals in the management of symptomatic malignant pericardial effusion:1) relief of immediate symptoms, 2) determination of cause, and 3) prevention of recurrence (2). No single modality has been proved to be superior since most patients with malignant pericardial effusion need more than one therapeutic modality. Pericardiocentesis is commonly used for acute symptomatic relief while other chemical or mechanical modalities such as systemic chemotherapy, radiation therapy, intrapericardial sclerosing agents, indwelling pericardial catheter, or thoracotomy with pericardiectomy are options to prevent relapse.

Seongseok Yun, MD PhD; Juhyung Sun, BS; Rorak Hooten, MD; Yasir Khan, MD;Craig Jenkins, MD

Department of Medicine, University of Arizona, Tucson, AZ 85724, USA

References

1. Klatt EC, Heitz DR. Cardiac metastases. Cancer. 1990;65(6):1456-9. [CrossRef]
2. Vaitkus PT, Herrmann HC, LeWinter MM. Treatment of malignant pericardial effusion. JAMA. 1994;272(1):59-64. [CrossRef] [PubMed] 

Reference as: Yun S, Sun J, Hooten R, Khan Y, Jenkins C. Medical image of the week: malignant pericardial effusion and cardiac tamponade. Southwest J Pulm Crit Care. 2014;8(6):343-6. doi: http://dx.doi.org/10.13175/swjpcc048-14 PDF

Medical Image of the Week: Infective Endocarditis in an IV Drug User

Figure 1. Transthoracic echocardiogram showing a large, irregular, mobile mass attached to the mitral valve annulus (arrows).

A 30 year old man presented with a one week history of fever, chills, body aches, and fatigue, as well as lower extremity and right wrist edema and pain. The patient also had a history of intravenous (IV) drug use. On exam, a previously undocumented 3/6 blowing crescendo murmur was heard at the fifth intercostal space in the midclavicular line. Transthoracic echocardiogram demonstrated a large, irregular, mobile mass, measuring 2.0 x 2.5 cm, attached to the posterior mitral annulus (Figure 1). Cardiothoracic surgery performed a primary repair of the mitral valve.

Abigail S. Hawke, MD

Department of Internal Medicine

University of Arizona

Tucson, Arizona

Arthia Satyanarayan, MS III

University of Arizona College of Medicine

Tucson, Arizona

Reference as: Hawke AS, Satyanarayan A. Medical image of the week: infective endocarditis in an IV drug user. Southwest J Pulm Crit Care. 2013;7(6):348. doi: http://dx.doi.org/10.13175/swjpcc156-13 PDF

Medical Image of the Week: Eisenmenger Syndrome and Hemoptysis

A 26 year-old female with Eisenmenger syndrome presented with hemoptysis. An echocardiogram showed an enlarged right ventricle and two large mid-muscular ventricular septal defects (VSD) with right to left shunting (Figures 1 and 2).

Figure 1. Apical four-chamber view of the heart as seen on a transthoracic echocardiogram demonstrating an enlarged right ventricle (RV) and two large mid muscular ventricular septal defects (*).  RA - right atrium, LA - left atrium, LV - left ventricle.

Figure 2.  Apical four-chamber view on a transthoracic echocardiogram.  Color Doppler jets (blue color) demonstrate right-to-left shunt through the two mid-muscular ventricular septal defects seen in Figure 1.

A contrast enhanced CT of the chest showed an enlarged pulmonary artery, no evidence of pulmonary embolism and the VSDs (Figure 3 and 4).

Figure 3. Contrast enhanced CT of chest demonstrating markedly enlarged main pulmonary artery (arrow), approximately twice the size of the ascending aorta (straight arrow).

Figure 4. Contrast enhanced CT of chest showing ventricular septal defects (arrows).

Eisenmenger syndrome is a condition in which increased pulmonary blood flow secondary to a left to right intracardiac shunt leads to irreversible pulmonary vascular obstructive disease.  The resultant high pulmonary vascular resistance causes reversal and right to left intracardiac shunt.  Hemoptysis is a common complication of Eisenmenger syndrome and has been reported as the cause of death in 11-29% of patients. It can be caused by pulmonary artery thrombosis, pulmonary embolism, rupture of aortopulmonary collaterals, pulmonary artery dissection and hemorrhage due to an aneurysm or thin-walled arterioles, infectious sources or a bleeding diathesis.  Treatment of hemoptysis in patients with Eisenmenger syndrome is challenging because they are at increased risk for bleeding and thrombotic complications. Hemoptysis in patients with Eisenmenger syndrome is often self-limited; however, it can be severe and life threatening. It is estimated that nearly 90% of patients with congenital heart disease survive into adulthood therefore adult pulmonologists may encounter this clinical scenario.  Our patient’s hemoptysis resolved spontaneously and she remains clinically stable.

Jamie Nicole Colombo DO*, Linda Snyder MD^¶, and Daniela Lax MD^§

Department of Pediatrics*, Division of Pediatric Cardiology^§

Division of Pulmonary, Critical Care, Allergy and Sleep Medicine^¶

University of Arizona

Reference as: Colombo JN, Snyder L, Lax D. Medical image of the week: Eisenmenger syndrome and hemoptysis. Southwest J Pulm Crit Care. 2013;6(5):231-3. PDF