August 2024 Imaging Case of the Month: An Unexplained Pleural Effusion

Matthew T. Stib MD

Michael B. Gotway MD

Department of Radiology

Mayo Clinic, Arizona

Scottsdale, AZ USA

Clinical History: A 65-year-old woman with presents with intermittent right-sided chest pain and shortness of breath / dyspnea on exertion for several months’ duration.

The patient’s past medical history includes a history of myocardial infarction with stent placement and atrial fibrillation. She has no prior surgical history aside from carpal tunnel release and tonsillectomy.

The patient is a lifelong non-smoker, she reports no allergies and she drinks alcohol only socially and denies illicit drug use. Her medications include Xarelto (rivaroxaban) for her atrial fibrillation, alendronate, atorvastatin, metoprolol, and pantoprazole in addition to a multivitamin.

On physical examination the patient was obese but not in acute distress, with normal blood pressure, pulse rate, and respiratory rate. Her pulmonary and cardiovascular examination was unremarkable aside for dullness to percussion over the right posterior and lateral thorax, and her musculoskeletal examination did not disclose any abnormalities. She was neurologically intact. Oxygen saturation at rest on room air  95%, 93% with exercise.

A complete blood count showed a normal white blood cell count at 6.5 x 10⁹/L (normal, 3.4 – 9.6 x 10⁹/L), with a normal absolute neutrophil count of 3.65 x 10⁹/L (normal, 1.4 – 6.6 x 10⁹/L); the percent distribution of lymphocytes, monocytes, and eosinophils was normal. Her hemoglobin and hematocrit values were 13 gm/dL (normal, 13.2 – 16.6 gm/dL) and 39.7% (normal, 34.9 – 44.5%). The platelet count was normal at 274 x 10⁹/L (normal, 149 – 375 x 10⁹/L). The patient’s serum chemistries and liver function studies were largely normal, including an albumin level at 4.3 gm/dL (normal, 3.5 – 5 gm/dL), with mildly elevated alanine aminotransferase at 59 U/L (normal, 7-45 U/L) and aspartate aminotransferase of 68 U/L (normal, 8-43 U/L); alkaline phosphatase levels, bilirubin, and coagulation studies were normal. SARS-CoV-2 PCR testing was negative. The erythrocyte sedimentation rate was normal at 8 mm/hr (normal, 0-29 mm/hr), as was her C-reactive protein at <2 mg/L (normal, <2 mg/L).  

Frontal chest radiography (Figure 1) was performed.

Figure 1. Frontal and lateral chest radiography. To view Figure 1 in a separate, enlarged window click here.

Which of the following statements regarding this chest radiograph is accurate? (Click on the correct answer to be directed to the second of seventeen pages)

1. Frontal chest radiography shows normal findings
2. Frontal chest radiography shows a moderate-to-large right pleural effusion
3. Frontal chest radiography shows mediastinal lymphadenopathy
4. Frontal chest radiography shows pneumothorax
5. Frontal chest radiography shows numerous small nodules

Cite as: Stib MT, Gotway MB. August 2024 Imaging Case of the Month: An Unexplained Pleural Effusion. Southwest J Pulm Crit Care Sleep. 2024;29(2):9-18. doi: https://doi.org/10.13175/swjpccs038-24 PDF

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

October 2022 Medical Image of the Month: Infected Dasatinib Induced Chylothorax-The First Reported Case

Figure 1. Upright PA chest radiograph (A) demonstrates a large left-sided pleural effusion with some lateral fluid suggesting loculation. Bedside ultrasound to guide thoracentesis (B) demonstrates multiple loculations within the effusion (arrowheads). Thoracentesis yielded 2 liters of milky white fluid (C).

Figure 2. Axial lung window (A) and soft tissue window (B) reconstructions from a chest CT with intravenous contrast performed following thoracentesis demonstrates a circumferential irregular left-sided pleural effusion with air space disease within the left lower lobe concerning for infection. A simple-appearing right-sided effusion is noted as well (*).

Case Report

A 45-year-old man with chronic myeloid leukaemia (CML) on dasatinib presented to the emergency department with a 2-week history of dry cough, worsening shortness of breath and left-sided chest pain that had worsened on the day of presentation. On examination, oxygen saturation was 98% on 2 L nasal cannula, respiratory rate 22 bpm, pulse 77 bpm, blood pressure 117/90 mmHg and his temperature was 37.9° C (100.2 F). Examination of the left chest showed no air entry and stony dull percussion note.

Laboratory results were significant for leucocytosis with a neutrophil count of 11.2, elevated CRP of 414, mildly elevated lactate of 1.1. Initial chest X-ray showed large left-sided pleural effusion and a small volume right effusion (Figure 1A). The patient was started on IV piperacillin /tazobactam, blood cultures were obtained and the dasatinib was held.

Ultrasound-guided left thoracentesis and drain placement was performed, on ultrasound the effusion demonstrated several loculations (Figure 1B). An 18Fr drain was inserted and 2L of white purulent/milky material fluid was drained (Figure 1C). Pleural fluid analysis showed abundant neutrophils, macrophages, lymphocytes and a few reactive mesothelial cells. Cytological analysis was negative for malignant cells. The fluid was exudative by Light’s criteria as total protein was 52.9 g/l and serum protein was 77 g/l with the ratio 0.68. Triglyceride level was 2.0 mmol/l and fluid cholesterol was 1.6 mmol/L indicative of chylothorax.

Over time, pleural cultures were positive for beta haemolytic Strep group C/G sensitive to penicillin G and erythromycin and both fungal and tuberculosis cultures were negative. Blood cultures were negative. Antimicrobial therapy was deescalated to Penicillin G. A subsequent chest CT (following intra-pleural fibrinolytic therapy) showed small left basal effusion with overlying consolidation and no occlusive lesion identified (Figure 2). After 9 days the pleural drain was removed, and the patient had no reaccumulation of their chylothorax. The patient remained clinically well and was discharged after a course of four weeks of antibiotics. At a 2 week follow up the patient was asymptomatic and had a normal physical exam. His inflammatory markers were back to normal CRP was 0.5 and WBC count was 6.5.

Discussion

Chylothorax is accumulation of chyle into the pleural space related to obstruction or disruption of the thoracic duct. It is a rare condition that may arise from diverse etiologies broadly categorized as traumatic or non-traumatic/spontaneous (1). Chylothorax is widely believed to be inherently bacteriostatic, with rare incidence of infected chylous effusions affecting a wide variety of patients with different causative organisms and a mostly benign course (2).

Dasatinib is a second-generation tyrosine kinase inhibitor that is recommended as the first-line therapy for newly diagnosed chronic myeloid leukaemia (CML) or acute lymphoblastic leukaemia (ALL) with positive Philadelphia chromosome (Ph+) or as an alternative for the failure of prior therapy for CML. Dasatinib is known to cause fluid retention which commonly presents as an exudative pleural effusion (3), chylothorax is rarely seen with 7 cases in total related to dasatinib use were published in the literature (4).

This is the first reported case of infected chylothorax among the population using dasatinib. Infected chylothorax in general is rare, affecting wide variety of patients with different organisms and mostly benign course (2). In this report the patient was stable on presentation and showed good response to antibiotics, chest drainage, holding of dasatinib and dietary fat restriction. Given the loculated appearance of the fluid the patient benefited from a dose of thrombolysis, which was reported as an option in such a scenario (5).

In patients with CML on dasatinib presenting with pleural effusion, the medication should be considered as one of the possible causes. Furthermore, infected chylothorax should be considered in the deferential diagnosis as a source of sepsis in patients presenting with a sepsis-like clinical picture and pleural effusion. The case also reflects the importance of bedside ultrasound in both clinically examining the patients and as a guide for thoracentesis and guidance for therapy.

Mortada Mohammed¹ MD MRCPI, Mohanad Abdelrahim² MD, Keshav Sharma³ MD MRCPI

¹Respiratory medicine registrar Wexford General Hospital, Wexford, Ireland

²Medical Senior House officer Wexford General Hospital, Wexford, Ireland

³Consultant Respiratory and General Medicine Physician, Wexford General Hospital, Wexford, Ireland

References

1. McGrath EE, Blades Z, Anderson PB. Chylothorax: aetiology, diagnosis and therapeutic options. Respir Med. 2010 Jan;104(1):1-8. [CrossRef] [PubMed]
2. Eubank L, Gabe L, Kraft M, Billheimer D. Infected chylothorax: a case report and review. Southwest J Pulm Crit Care. 2018 Aug 25;17(2):76–84. [CrossRef]
3. Keating GM. Dasatinib: A Review in Chronic Myeloid Leukaemia and Ph+ Acute Lymphoblastic Leukaemia. Drugs. 2017 Jan;77(1):85-96. [CrossRef] [PubMed]
4. Chen B, Wu Z, Wang Q, Li W, Cheng D. Dasatinib-induced chylothorax: report of a case and review of the literature. Invest New Drugs. 2020 Oct;38(5):1627-1632. [CrossRef] [PubMed]
5. Nair SK, Petko M, Hayward MP. Aetiology and management of chylothorax in adults. Eur J Cardiothorac Surg. 2007 Aug;32(2):362-9. [CrossRef] [PubMed]

Cite as: Mohammed M, Abdelrahim M, Sharma K. October 2022 Medical Image of the Month: Infected Dasatinib Induced Chylothorax-The First Reported Case. Southwest J Pulm Crit Care Sleep. 2022;25(4):47-9. doi: https://doi.org/10.13175/swjpccs036-22 PDF

August 2022 Imaging Case of the Month: It’s All About Location

Michael B. Gotway MD

Department of Radiology

Mayo Clinic, Arizona

5777 East Mayo Boulevard

Phoenix, Arizona 85054

A 78–year–old man with a history of hyperlipidemia, hypertension, paroxysmal atrial fibrillation, and transcatheter aortic valve replacement on anticoagulation presented to the Emergency Room with a 2-month history of cough and exertional shortness of breath. He denied fever, chills, nausea, and chest pain. The patient had undergone three COVID-19 vaccines, the most recent 3 months earlier. He had noted some recent bruising, but denied any recent trauma.

The patient’s past medical history also included a history of prostate carcinoma 10 years earlier treated with radiation therapy. The patient’s past surgical history was remarkable for remote vasectomy, endoscopic sinus surgery and percutaneous aortic valve replacement. He was a former smoker and reported no allergies or illicit drug use; alcohol use was at most moderate, consisting of an occasional beer. The patient’s medications included a statin, warfarin, and metoprolol.

The patient’s physical examination showed normal vital signs and was remarkable only for some decreased breath sounds over the left lower thorax. The patient was afebrile. Bruising was noted involving the right hand and right abdominal wall, but without limitations in range of motion or associated pain.

A complete blood count showed a hemoglobin and hematocrit value of 7.7 gm/dL (normal, 13.2-16.6 gm/dL) and 23.9% (normal, 38.3–48.6%) and a platelet count of <2 x x10⁹/L (normal, 135-317 x10⁹/L). The white blood cell count was minimally abnormal at 9.7 x10⁹/L (normal, 3.4-9.6 x10⁹/L), with a mild left shift with a neutrophil level of 7.11 x10⁹/L (normal, 1.56-6.45 x10⁹/L). The eosinophil count was normal, but reticulocytes were elevated at 4.06% (normal, 0.60-2.71%). The INR was elevated at 2.3, with a prolonged prothrombin time of 25.8 sec (normal, 9.4-12.5 sec). Fibrinogen was also mildly abnormally elevated. Serum chemistries were largely within normal limits, with a mild elevation in lactate dehydrogenase at 273 U/L (normal, 122–222 U/L). Serum iron values were low at 30 mg/dL (normal, 50-150 mg/dL), with the total iron binding capacity abnormally decreased also. An ECG was unremarkable. A serum NT-Pro BNP value was elevated at 1174 pg/mL (normal, ≤122 pg/mL). Liver and renal function were within normal limits.

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

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

Which of the following represents an appropriate interpretation of the frontal chest and lateral radiograph? (Click on the correct answer to be directed to the second of twelve pages)

1. Frontal chest radiography shows a large left pleural effusion
2. Frontal chest radiograph shows focal right lung opacity
3. Frontal chest radiography shows pleural calcification
4. Frontal chest radiography shows right peribronchial lymph node enlargement
5. More than one of the above

Cite as: Gotway MB. August 2022 Imaging Case of the Month: It’s All About Location. Southwest J Pulm Crit Care Sleep. 2022;25(2):15-22. doi: https://doi.org/10.13175/swjpccs034-22 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

Medical Image of the Month: Bilateral Atrial Enlargement

Figure 1. Portable chest radiograph showing elevation of the left mainstem bronchus (red arrow).

Figure 2. Thoracic CT scan showing right atrial enlargement (blue circle) and left atrium (red circle).

Figure 3. Upper Image: Static image from echocardiogram showing right atrial enlargement (white circle). Lower image: video of echocardiogram.

A 97-year-old woman was repeatedly admitted for dyspnea, hypoxemia and treated with antibiotics for presumed left lower lobe pneumonia. She has a past medical history of atrial fibrillation, congestive heart failure and sick sinus syndrome with placement of a cardiac pacemaker. Notably on physical examination, she had heart rate of 110 beats/minute, temperature of 98.8°F, blood pressure of 122/72 mm Hg, and a respiratory rate of 27 breaths/minute. She had a sternal heave, a grade 4/6 "blowing" holosystolic murmur, a loud S2, jugular venous distension and an enlarged liver. Chest x-ray showed obscuration of the left lower lobe - the left heart border cannot be seen, and the L mainstem bronchus is straightened and lifted superiorly (Figure 1). An image of the heart is shown from a CT abdomen obtained 6 months previously, showing cardiomegaly, particularly massive atrial enlargement (Figure 2). An ultrasound showed bilateral atrial enlargement with moderate mitral regurgitation and severe tricuspid regurgitation (Figure 3). The left ventricular ejection fraction was 55%, but with abnormal septal motion. She was treated with gentle diuresis to help relieve volume overload, and isosorbide dinitrate for preload and afterload reduction. Pulmonary hypertension was attributed to chronic mitral regurgitation. The cause was unclear - the patient remembered that her brother had rheumatic fever as a young recruit in WWII, but didn't know whether she had ever experienced it.

Atrial enlargement can be of prognostic significance. Left atrium size has been found to be a predictor of mortality due to both cardiovascular issues as well as all-cause mortality (1). Larger right atrium than left atrium has been associated with all-cause mortality in elderly patients with heart failure (2).

Robert A. Raschke, MD

University of Arizona College of Medicine-Phoenix

Phoenix, AZ USA

References

1. Patel DA, Lavie CJ, Milani RV, Shah S, Gilliland Y. Clinical implications of left atrial enlargement: a review. Ochsner J. 2009 Winter;9(4):191-6. [PubMed]
2. Almodares Q, Wallentin Guron C, Thurin A, Fu M, Kontogeorgos S, Thunstrom E, Johansson MC. Larger right atrium than left atrium is associated with all-cause mortality in elderly patients with heart failure. Echocardiography. 2017 May;34(5):662-7. [CrossRef] [PubMed]

Cite as: Raschke RA. Medical image of the month: bilateral atrial enlargement. Southwest J Pulm Crit Care. 2019;19(1):10-1. doi: https://doi.org/10.13175/swjpcc023-19 PDF

Medical Image of the Month: Massive Right Atrial Dilation After Mitral Valve Replacement

Figure 1. Chest radiograph demonstrating massive cardiomegaly with pulmonary congestion and markedly dilated right atrium.

Figure 2. Transthoracic echocardiogram demonstrating marked dilation of the right atrium to 9.6 cm in its greatest dimension.

A 92-year-old woman with a history of mechanical mitral valve replacement (+25 years prior to presentation), coronary artery bypass grafting, pacemaker placement and heart failure (EF 25%) presented from a nursing facility for dyspnea of 1 day’s duration. Recently, the patient had experienced a bowel perforation s/p surgical repair 3 weeks prior.

Admission chest radiograph was significant for massive cardiomegaly with pulmonary congestion and markedly dilated right atrium (Figure 1). Formal echocardiography was ordered, which re-demonstrated the patient’s known heart failure with reduced ejection fraction. Additionally, all 4 chambers of the heart were noted to be dilated, but the right atrium was revealed to be severely enlarged to >9 cm (Figure 2). On review of outside records, the patient’s cardiac history was notable for chronic dilation of the RA, RV and LA for several years with low, but stable, LV ejection fraction. Ultimately, the patient was noted to have worsening abdominal distension concerning for acute abdomen. However rather than pursue additional aggressive work up after her recent surgery, comfort measures were preferred.

This case illustrates some of the possible long-term effects of mitral valve replacement. In recent years mitral valve repair has become the preferred method over replacement for degenerative valve disease in western countries (1). While there are documented short term benefits to both mitral valve replacement and mitral valve repair long term data is less available (2). Long-term survival in most studies is reported in 5,10, and 15-year intervals. As was the case with our patient, patients with mitral valve replacement greater than 20 years in age have significantly less information associated with them. Although at this time longitudinal studies suggest benefits for both mitral valve replacement and repair, further investigation into long term complications is warranted (3). As our society continues to age, understanding the risks and complications associated with previous valve repair will help guide therapeutic interventions in the geriatric patient.

Richard Young, MD* and Alexander Ravajy, BS**

*University of Arizona Department of Internal Medicine

**University of Oklahoma Department of Microbiology

Banner University Medical Center

Tucson, AZ USA

References

1. Gammie JS, Sheng S, Griffith BP, Peterson ED, Rankin JS, O'Brien SM, Brown JM. Trends in mitral valve surgery in the United States: results from the Society of Thoracic Surgeons Adult Cardiac Surgery Database. Ann Thorac Surg. 2009 May;87(5):1431-7. [CrossRef] [PubMed]
2. McNeely CA, Vassileva CM. Long-term outcomes of mitral valve repair versus replacement for degenerative disease: a systematic review. Curr Cardiol Rev. 2015;11(2):157-62. [CrossRef] [PubMed]
3. Christina MV, Gregory M, Christian M, Theresa B, Stephen M, Steven S, Stephen H. Long term survival of patients undergoing mitral valve repair and replacement a longitudinal analysis of Medicare fee-for-service beneficiaries. Circulation. 2013;127(18):1870–6. [CrossRef] [PubMed]

Cite as: Young R, Ravajy A. Medical image of the month: Massive right atrial dilation after mitral valve replacement. Southwest J Pulm Crit Care. 2018;18(1):8-9. doi: https://doi.org/10.13175/swjpcc111-18 PDF 

Medical Image of the Week: Malposition of Central Venous Catheter

Figure 1. Portable anterior-posterior chest x-ray showing the tip of the catheter projecting on the left lung filed instead of crossing the midline.

Figure 2. Coronal images of computed tomography of head, neck, and upper chest. Yellow arrows showing the anatomical course of the left internal jugular catheter. Left upper image showing the catheter entering the internal jugular vein. Right lower image showing the tip of the catheter in the left inferior pulmonary vein.

A 66-year-old man a with history of systolic heart failure and end-stage renal disease on hemodialysis was admitted to the intensive care unit due to cardiogenic shock requiring inotropes. As left arm fistula was clotted, left internal jugular vein triple-lumen catheter (IJC) was placed to obtain a hemodialysis access. Central line placement was performed under ultrasound guidance with no complications. A confirmatory chest x-ray revealed central venous catheter malposition; the catheter tip did not cross the midline; instead, it projected over the left lung field which was concerning for arterial puncture of the carotid artery (Figure 1). Bedside ultrasonography showed an appropriate catheter placement in the left internal jugular vein, but the final catheter tip location was unclear. The transduced pressure was low; approximately 5mmHg. A blood gas sample from the catheter was compatible with arterial blood; pH 7.42, pCO2 34, and pO2 92. Computed tomography scan of the head and neck showed the IJC entering the left jugular vein, coursing within an anomalous left pulmonary vein, and terminating within the left inferior pulmonary vein (Figure 2). The catheter was not used and was withdrawn without complications.

One of the notable complications of central venous catheter (CVC) placement is malposition, with an approximate rate of 6,7 % (1). Catheter malposition indicates that the catheter tip lies outside the recommended position (within the mid lower part of the superior vein cava (SVC) above its junction with the right atrium and parallel to the vessel walls). Possible sites of central catheter malposition include the carotid artery, azygos vein, persistent left‑sided SVC, internal mammary vein, vertebral vein, pericardium, pleural space, thoracic duct and mediastinum (2). As artery puncture in the carotid artery can lead to serious complications, malposition of the catheter should be addressed in a stepwise approach. Initially bedside ultrasound should be performed to determine the anatomical catheter course and the position of the tip. A pressure transducer is also helpful in differentiating venous versus arterial waveform and measuring the transduced pressure, obtaining arterial blood gases and eventually confirming the catheter position with CT scan or CT angiography. Malposition of the jugular catheterization incidentally revealing partial anomalous of pulmonary venous return was described in a very few cases in literature, the catheter was used for seven days for continuous veno-venous hemofiltration in one of these cases (3). At this time there is insufficient literature to determine the safety of using CVC inserted in an anomalous pulmonary vein.

Mohamad Muhailan, MD and Muhamad Alhaj Moustafa, MD

Department of Internal Medicine

MedStar Washington Hospital Center

Washington, DC USA

References

1. Schummer W, Schummer C, Rose N, Niesen WD, Sakka SG. Mechanical complications and malposition of central venous cannulations by experienced operators. A prospective study of 1794 catheterizations in critically ill patients. Intensive Care Med. 2007 Jun;33(6):1055-9. [CrossRef] [PubMed]
2. Wang L, Liu ZS, Wang CA. Malposition of central venous catheter: Presentation and management. Chin Med J (Engl). 2016 Jan 20;129(2):227-34. [CrossRef] [PubMed]
3. Grillot N, Figueiredo S, Aubry A, Leblanc PE, Duranteau J. Unusual dialysis catheter position due to partial anomalous pulmonary venous return: Diagnosis and management. Anaesth Crit Care Pain Med. 2016 Jun;35(3):233-5. [CrossRef] [PubMed]

Cite as: Muhailan M, Moustafa MA. Medical image of the week: Malposition of central venous catheter. Southwest J Pulm Crit Care. 2018;17(1):30-1. doi: https://doi.org/10.13175/swjpcc084-18 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: 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: 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: Mediastinal Metastases Causing Right Ventricular Outflow Obstruction

Figure 1. Computed tomography (CT) of chest showed large right mediastinal mass (arrow) causing mass effect on the heart.

Figure 2.  Echocardiography showing large extra-cardiac mass (white arrow) compressing on right ventricle and its outflow tract (black arrow).

A 36-year-old man with a history of testicular choriocarcinoma with metastases to the lung presented with a 2-days history of hemoptysis. Initial diagnosis of the malignancy was made about 5 months earlier and he was treated with platinum based chemotherapy with a partial response.

He reported two days of significant hemoptysis, associated with shortness of breath and pleuritic chest pain and rapidly developed acute hypoxic respiratory failure requiring emergent intubation and mechanical ventilation. Computed tomography (CT) of chest showed large right mediastinal mass with diffuse reticular and nodular opacities predominantly in the left lung (Figure 1).

A pulmonary angiogram was performed that showed multiple active bleeding sites in the bronchial arterial system. These were treated with embolization. He developed shock and during investigations the echocardiogram showed a significant compression of the superior vena cava, right atrium and right ventricle by the malignant mass (Figure 2). Despite aggressive therapy and resuscitative therapies he continued to deteriorate and did not survive the hospital stay.

Mediastinal tumors are a rare cause of extrinsic right ventricular outflow tract (RVOT) obstruction. Echocardiography is an important tool in the assessment of hemodynamic effects caused due to such pathology including degree of compression and pressure gradients.

Kai Rou Tey MD¹, Bhupinder Natt MD²

¹Department of Internal Medicine, University of Arizona College of Medicine- South Campus, Tucson, AZ USA

²Division of Pulmonary, Critical Care, Allergy and Sleep, University of Arizona Medical Center, Tucson, AZ USA

Cite as: Tey KR, Natt B. Medical image of the week: mediastinal metastases causing right ventricular outflow obstruction. Southwest J Pulm Crit Care. 2016:12(1):22-3. doi: http://dx.doi.org/10.13175/swjpcc145-15 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: Septated Pleural Effusion

Figure 1. Thoracic ultrasound showing pleural effusion with multiple septations.

An 83 year old man with a history of metastatic malignant melanoma and atrial fibrillation on warfarin was admitted for shortness of breath. He underwent a diagnostic and therapeutic thoracentesis for a large right sided pleural effusion, suspected to be malignancy related. Three days later, he had transferred to the ICU for respiratory distress. An ultrasound of the thorax revealed a large loculated effusion with multiple septations (Figure 1). A large bore chest tube was placed and revealed a hemothorax, which may have been related to the previous thoracentesis.

In an observational study of ultrasound characteristics of pleural effusions, complex septations were more commonly seen in non-malignant effusions than malignant effusions (25.4% vs. 7.5%). In non-malignant effusions, the septated pattern was associated with infections, specifically tuberculosis and pneumonia (1).

While metastases in melanoma commonly involve the thoracic cavity, malignant pleural effusions are rare and are seen in about 2% of cases. In very rare instances, effusions from metastatic melanoma can be black in appearance (2). There has also been a case report of a massive hemothorax related to melanoma implants on the pleura (3).

Candy Wong, MD¹; Soyoung Park, MD²; Courtney Walker, DO²; and Laura Meinke, MD¹

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

²Department of Medicine

University of Arizona

Tucson, AZ

References

1. Bugalho A, Ferreira D, Dias SS, Schuhmann M, Branco JC, Marques Gomes MJ, Eberhardt R. The diagnostic value of transthoracic ultrasonographic features in predicting malignancy in undiagnosed pleural effusions: a prospective observational study. Respiration. 2014;87:270-8. [CrossRef] [PubMed]
2. Liao WC, Chen CH, Tu CY. Black pleural effusion in melanoma. CMAJ. 2010;182(8):E314. [CrossRef] [PubMed]
3. Gibbons JA, Devig PM. Massive hemothorax due to metastatic malignant melanoma. Chest. 1978;73(1):123. [CrossRef] [PubMed]

Cite as: Wong C, Park S, Walker C, Meinke L. Medical image of the week: septated pleural effusion. Southwest J Pulm Crit Care. 2015;11:110-1. doi: http://dx.doi.org/10.13175/swjpcc085-15 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: 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