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Pulmonary Edema [keywords]
- Hemoptysis: A Red Flag for Pseudoaneurysm After Pulmonary Artery Catheterization. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):99A.
Cardiovascular Student/Resident Case Report Posters IISESSION TYPE: Medical Student/Resident Case ReportPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: Pulmonary artery catheters (PAC) are routinely used in the diagnosis and management of pulmonary hypertension with minimal risks. Pulmonary artery pseudoaneurysm or rupture is a rare and potentially fatal complication of PA catheterization. We present a case of pulmonary artery catheter-induced pseudoaneurysm promptly diagnosed and treated by coil embolization.CASE PRESENTATION: A 69 year old woman with history of diabetes and hypertension was evaluated for three months history of lower extremity edema, abdominal distension and orthopnea. Transthoracic echocardiogram at that time was notable for diastolic dysfunction and right ventricular systolic pressure of ~55mmHg. Right and left heart catheterizations were performed to further investigate her heart failure. Left heart catheterization was notable for single vessel disease in Obtuse Marginal 2 and left ventricular end diastolic pressure of 27mmHg. Right heart catheterization was then performed under fluoroscopic guidance and showed pulmonary artery pressure of 56/33 mmHg and wedge pressure of 21mmHg. Unexpectedly, during removal of the pulmonary arterial catheter, the patient developed massive hemoptysis (~300ml). Cessation of the hemoptysis allowed for chest computed tomography (CT) to be performed as the patient remained hemodynamically stable. Chest CT revealed a right middle lobe pulmonary artery pseudoaneursym. Pulmonary angiography confirmed these findings as the source of hemoptysis. Two coils were successfully deployed: one in the pseudoaneurysm and the second coil in the feeding branch. She subsequently required a transfusion for a four gram decrease in her hemoglobin level. She did not have any further hemoptysis during her hospitalization and was discharged home.DISCUSSION: Pulmonary artery pseudoaneurysm or rupture, while rare, is the most serious and life-threatening complication from PAC insertions. Hemoptysis is the initial presenting symptom suggestive of PA injury in more than 80% of cases. Left untreated, risk of re-bleeding from the pseudoaneurysm is 30-40% with mortality rate of 40-70%. Our case illustrates the importance of prompt diagnosis and management of right middle lobe pseudoaneursym from pulmonary artery catheterizationCONCLUSIONS: Hemoptysis in patients who have undergone PAC should raise suspicion for pseudoaneurysm formation and receive prompt evaluation with CT scan or pulmonary angiogram. Timely recognition and treatment with surgery or coil embolization are necessary to prevent morbidity and mortality.Reference #1: Pulmonary artery pseudoaneurysm after Swan-Ganz catherization: a case presentation and review of literature. Nellaiyappan M, et al. European Heart Journal: Acute Cardiovascular Care 2014; Published online January 27, 2014. Reference #2: Catheter-induced pulmonary artery pseudoaneurysm formation: Three case reports and a review of the literature. Poplausky M, et al. Chest 2001; 120:2105-2111.DISCLOSURE: The following authors have nothing to disclose: Min Qi, Keriann Van Nostrand, William Carlos, Farzad LoghmaniNo Product/Research Disclosure Information.
- Pulmonary Venoocclusive Disease: A Case Report. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):890A.
Pulmonary Vascular Disease Student/Resident Case Report Posters IISESSION TYPE: Medical Student/Resident Case ReportPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: PVOD is a poorly understood syndrome characterized by progressive dyspnea and hypoxemia from PH due to extensive occlusion of the pulmonary venous circulation by fibrous tissue and thrombi.CASE PRESENTATION: A 58 year-old female presents for evaluation of worsening dyspnea and hypoxemia. Symptoms began 3 years ago after a presumed respiratory infection. Over the next 2 years she had multiple evaluations for dyspnea-all felt secondary to pneumonia and pleurisy. Last year she was diagnosed with a right upper lobe pulmonary embolism and completed 6 months of rivaroxaban. Past history revealed incidental identification of an enlarged axillary lymph node (LN) on mammogram at age 48. LN excision showed benign lymphatic tissue with non-caseating granulomas. Present evaluation revealed the following: normal spirometry with a significantly decreased DLCO (52%); six minute walk test of 700 feet with nadir oximetry of 79%; echocardiogram with mildly dilated right ventricle with reduced function, normal left ventricular function, and estimated pulmonary systolic pressure of 69mmHg; no evidence of mismatches on V/Q study; and computed tomography revealed diffuse mosaic attenuation pattern consistent with ground glass opacities with interlobular septal thickening and pulmonary venous obstruction with thrombi. Right heart catheterization revealed normal wedge pressure and pulmonary hypertension (PH) (55/20; mean 35mmHg). In addition to oxygen, warfarin and prednisone were initiated. The latter treatment was trialed given her remote history of non-caseating granulomas on a LN biopsy-raising the question of sarcoidosis as a unifying diagnosis where granulomata are responsible for venous obstruction. We referred our patient for lung transplantation as a therapeutic option.DISCUSSION: The diagnosis of PVOD is strongly suggested by PH with normal wedge pressures and radiographic findings of pulmonary edema. Estimated annual incidence is 1-2 cases per 10 million persons. The etiology is incompletely understood but may include hypercoagulability, genetic predisposition, prior respiratory infection, antineoplastic agents, and autoimmune disorders. Oxygen therapy is indicated in all hypoxemic PVOD patients and anticoagulation is recommended based on data from Group 1 PH patients. There is no convincing role for vasodilator therapy and a theoretical risk of precipitating life-threatening pulmonary edema exists. Immunosuppressives have been used anecdotally in patients with features of autoimmune diseases.CONCLUSIONS: Lung transplantation is the only treatment option that may confer survival advantage to date.Reference #1: Montani D et al. Pulmonary veno-occlusive disease. Medicine 2008;87:220Reference #2: Montani D et al. Pulmonary veno-occlusive disease. Respir Med 2010; 104 Suppl1:S23DISCLOSURE: The following authors have nothing to disclose: Ana Bonetti, Chirag Shah, Nataly Vasquez EncaladaNo Product/Research Disclosure Information.
- Pulmonary Tumor Thrombotic Microangiopathy in a Patient With Gastric Adenocarcinoma. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):887A.
Pulmonary Vascular Disease Student/Resident Case Report Posters ISESSION TYPE: Medical Student/Resident Case ReportPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: Pulmonary tumor thrombotic microangiopathy (PTTM) is a clinicopathologic entity with pulmonary tumor emboli and fibrocellular intimal proliferation that leads to acute pulmonary hypertension and sudden cardiovascular collapse in individuals with adenocarcinoma, usually of gastric origin. We report a case of PTTM diagnosed postmortem in a young Hispanic male with gastric carcinoma.CASE PRESENTATION: A 42 year old Hispanic male presented with 2 weeks of progressive dyspnea, non-productive cough, subjective fevers, and a 10 lb weight loss. Physical examination revealed tachypnea, hypoxemia with room air arterial oxygen saturation of 86%, and fine bibasilar rales. Chest X-ray suggested pulmonary edema (Panel A). CT pulmonary angiogram did not show evidence of pulmonary emboli, however, was notable for diffuse interlobular septal thickening, centrilobular micronodules and ground-glass opacities, and mediastinal, hilar, and upper abdominal lymphadenopathy (Panel B & C). An echocardiogram revealed severe right ventricular dilatation with estimated PA systolic pressure of 75 mmHg. A CT guided biopsy of a paraaortic lymph node revealed poorly differentiated adenocarcinoma likely of foregut origin. The patient's clinical course rapidly progressed to severe right heart failure, and was further complicated by respiratory failure requiring mechanical ventilation, acute renal failure requiring hemodialysis, and disseminated intravascular coagulation (DIC). Despite all efforts, the patient expired within 2 weeks of admission. Autopsy showed extensive tumour microemboli associated with proliferation of intimal fibromuscular cells and the formation of fibrin thrombi in the small pulmonary arteries and arterioles (Panel D - F) and poorly differentiated gastric adenocarcinoma with signet cells.DISCUSSION: PTTM is an extremely rare and fatal form of pulmonary arterial tumor embolism. The pathogenesis starts with formation of microscopic tumor cell emboli which induce local activation of coagulation and fibrocellular intimal proliferation. This leads to stenosis of pulmonary arterioles resulting in an increase in pulmonary vascular resistance causing pulmonary hypertension, hemolytic anemia, and DIC. Affected patients present with progressive dyspnea, cough, and signs of hypoxia and pulmonary hypertension. PTTM is very difficult to diagnose and most diagnoses are made post-mortem. The diagnosis may be established by pulmonary microvascular cytology, obtained through a wedged pulmonary artery catheter. No treatment has thus far been found to be of benefit. The disease progresses rapidly and is often fatal within a week or two of presentation.CONCLUSIONS: PTTM should be suspected in cancer patients with acute respiratory insufficiency and severe pulmonary hypertension in the absence of embolism in major pulmonary arteries.Reference #1: von Herbay A, Illes A, Waldherr R, Otto HF. Pulmonary tumor thrombotic microangiopathy with pulmonary hypertension. Cancer 1990; 66:587-592.DISCLOSURE: The following authors have nothing to disclose: Rohit Godbole, Abhijeet Ghatol, Jamie Betancourt, Nader KamangarNo Product/Research Disclosure Information.
- Suspected Idiopathic Pulmonary Vein Thrombosis. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):886A.
Pulmonary Vascular Disease Student/Resident Case Report Posters ISESSION TYPE: Medical Student/Resident Case ReportPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: Pulmonary vein thrombosis (PVT) is a rare disease entity usually associated with lung malignancy, radiofrequency ablation of atrial fibrillation, lung surgery or transplantation. We discuss an extremely rare case of idiopathic PVT.CASE PRESENTATION: A 70-year-old African American male, with history of tobacco abuse, COPD, and hypertension, presented with worsening dyspnea, atypical chest pain, and productive cough for 2 days. He had no fever, hemoptysis or recent immobilization. Physical examination was unremarkable except for mild bilateral wheezing. Chest X-ray showed lung hyperinflation with no evidence of pneumonia. CT of the chest revealed emphysematous changes and left lower PVT without pulmonary infarction, masses, or pulmonary embolism. Transesophageal echo (TEE) revealed decreased blood flow in left lower pulmonary vein with no evidence of anatomic stenosis, but due to the limited study thrombus was not identified. Patient had age-appropriate cancer screening with negative colonoscopy 3 months prior to admission. Hypercoagulability work up was negative. Patient was started on anticoagulation with warfarin and enoxaparin, in addition to bronchodilators and a short course of steroids.DISCUSSION: Only 5 cases of idiopathic PVT have been previously reported. PVT can present with cough, hemoptysis, dyspnea, and pleuritic chest pain or as progressive or recurrent pulmonary edema and pulmonary fibrosis. Rare complications of PVT, such as pulmonary gangrene and peripheral embolization, have been reported. A combination of diagnostic modalities can aid in diagnosis, including transthoracic echocardiography, TEE, pulmonary angiography, MRI, and CT. The appropriate management of PVT remains unclear, and frequently is dependent on the underlying etiology. Long-term anticoagulation can help prevent thrombus progression and peripheral embolization.CONCLUSIONS: Though initial management was targeted towards COPD exacerbation in our patient, further investigation was warranted as symptoms persisted. We believe our patient presented as a case of PVT mimicking a COPD exacerbation. One may argue that the TEE finding of decreased flow is suggestive of but not conclusive of PVT. As we were convinced with the CT finding of PVT, anticoagulation was started and patient was scheduled for follow up MRI. In our opinion, it is necessary to perform age appropriate cancer screening and a hypercoagulability profile to rule out secondary causes of PVT, as 2 cases of idiopathic PVT had associated abnormal thrombophilia profiles.Reference #1: Wu, J. P., et al. "Idiopathic pulmonary vein thrombosis extending to left atrium: a case report with a literature review." Chinese medical journal 125.6 (2012): 1197Reference #2: Selvidge SD, Gavant ML. Idiopathic pulmonary vein thrombosis: detection by CT and MR imaging. AJR Am J Roentgenol 1999; 172: 1639-1641Reference #3: Alexander GR, Reddi A, Reddy D. Idiopathic pulmonary vein thrombosis: a rare cause of massive hemoptysis. Ann Thorac Surg 2009; 88: 281-283DISCLOSURE: The following authors have nothing to disclose: Bashar Amr, Nang Kham, Viral Doshi, Tareq ZazaNo Product/Research Disclosure Information.
- Pulmonary Capillary Hemangiomatosis Masquerading as Asbestosis. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):885A.
Pulmonary Vascular Disease Student/Resident Case Report Posters ISESSION TYPE: Medical Student/Resident Case ReportPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: The accurate etiology of pulmonary arterial hypertension (PAH) can be challenging and misleading on the basis of clinical grounds alone. Here we present a unique case of severe PAH with unexpected findings on autopsy.CASE PRESENTATION: A 73 year-old man known to have history of heavy exposure to asbestos. He had been followed for interstitial lung disease (ILD), asbestosis with plaques and pulmonary hypertension. Patient was admitted with progressive worsening dyspnea (NYHA functional Class IV). His past medical history included coronary artery disease, hypertension, atrial fibrillation on warfarin and sleep apnea (OSA). His exam was consistent with ILD and right sided heart failure. Patient has systolic murmur which increases during inspiration, bibasilar inspiratory crackles and lower extremity edema. His chest x-ray showed bilateral interstitial infiltrates with evidence of pleural plaques. Recent right heart catheterization showed severe pulmonary arterial hypertension (table 1). Pulmonary function test was consistent with a restrictive pattern. His DLCO declined from 56% in 2010 to 36% in 2013. Patient had recent 6 minute walk test and was only able to walk 22% of his predicted distance. Limited autopsy of the heart and lungs ruled out pulmonary embolism, acute myocardial infarction or significant asbestosis, however, it showed profound pulmonary capillary hemangiomatosis (Figure 1).Pulmonary capillary hemangiomatosis (PCH) is rare cause of pulmonary arterial hypertension was first reported by Wagenvoort et al in 1978 . Less than 100 cases are reported to date. In this case, the interstitial lung disease is secondary to the proliferating capillary hemangiomatosis with hemosiderosis and fibrosis from chronic recurrent bleeding. The asbestosis contribution was minimal based on the trichrome staining which showed only mild interstitial fibrosis.PCH can present at any age. When pulmonary arterial hypertension is out of proportion to the mild restrictive pathophysiology, we should consider etiologies other than ILD or OSA. The precise diagnosis of PCH is very important because the treatment with pulmonary vasodilators such as prostacyclin can cause fatal pulmonary edema . Reference #1: Wagenvoort CA, Beetstra A, Spijker J. Capillary haemangiomatosis of the lungs. Histopathology. 1978; 2:401Y406.Reference #2: Dufour B, Maitre S, Humbert M, et al. High-resolution CT of the chest in four patients with pulmonary capillary hemangiomatosis or pulmonary venoocclusive disease. AJR Am J Roentgenol. 1998; 171:1321Y1324.DISCLOSURE: The following authors have nothing to disclose: Abdulmonam Ali, Sri krishna Chaitanya Arudra, Sarthi Shah, Vasuki Anandan, Ragheb AssalyNo Product/Research Disclosure Information.
- A Pragmatic Dilemma: A Case of Lung Adenocarcinoma Presenting as Upper and Lower Extremity Venous Thromboembolism and Protein C and S Deficiency. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):878A.
Pulmonary Vascular Disease Global Case ReportsSESSION TYPE: Global Case ReportPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: Cancer continues to be one of the major causes of venous thromboembolism (VTE) worlwide, and as such, a global health burden. In the Philippines, the incidence of cancer with VTE is yet to be established, although malignancy itself is the third leading cause of morbidity and mortality. Among the malignancy types, that of the lung ranks first. And although rare, patients with lung cancer, especially the adenocarcinoma type, are at an increased risk of VTE.CASE PRESENTATION: A 63 year-old obese female was admitted due to a 3-day history of swelling of the left leg associated with upper back pain. She is a non-smoker. Of note however is a history of spontaneous abortion and intake of oral contraceptive pills. On examination, she had mid-thigh and calf asymmetry with pitting edema and localized tenderness from left foot to the middle 3rd of the left thigh. Venous doppler study of the left lower extremity showed totally occlusive acute to subacute deep venous thrombosis of the venous segments. In view of the upper back pain and chest xray finding of miliary-form nodules in both lungs, a computerized tomography (C.T.) of the chest with intravenous contrast confirmed left lower lobe, left paraaortic and right prevascular masses. CT scan guided biopsy of the left lower lobe mass was consistent with lung adenocarcinoma. CT Venogram of the neck revealed upper extremity vein thrombosis. Subsequent hypercoagulability study showed Protein C and S deficiency. In view of the these findings, adequate anticoagulation and palliative chemotherapy were initiated.DISCUSSION: Venous thromboembolism has an incidence 1-3 in 1000 per year. The patient's age, obesity, intake of OCPs and diagnosis of lung cancer were identified risk factors for VTE. Of these risk factors, cancer is the most important and well-established. J.W. Blom et al pointed out that patients with adenocarcinoma have a higher risk of developing venous thromboembolism as compared to patients with squamous cell carcinoma. This was attributed to the interaction of circulating carcinoma mucins with leukocyte L-selectin and platelet P-selectin without requiring accompanying thrombin generation thereby generating microthrombi. The development of another focal thrombus on the upper extremity points out to other possible risk factors other than lung malignancy. Glaring in the patient's profile is the history of spontaneous abortion, thus, a hypercoagulability workup was done and showed Protein C and S deficiency. However, the patient had a prior intake of warfarin and heparin which can give a false positive result. Repeat testing for protein C and S is recommeneded at least 3 to 6 weeks from the discontinuation of anticoagulant treatment (B. Lipe et al, 2011). But because of the potential risks of VTE and its lifethreathening sequelae, repeat testing was forgone.Venous thromboembolism arising from two or more different areas warrants a thorough investigation in order to rule in and out an inherited or acquired cause. In this case, the dilemma exists between lung malignancy or thrombophilia as a cause of thrombosis. In either case, prudent and judicious treatment of the primary lung malignancy and adequate anticoagulant therapy could prevent future occurrence of thrombosis, and thus abating its potentially lifethreathening consequences.Reference #1: Blom JW, Osanto S, Rosendaal FR. The risk of a venous thrombotic event in lung cancer patients: higher risk for adenocarcinoma than squamous cell carcinoma. J Thromb Haemost 2004; 2: 1760-5Reference #2: S.M. Bates, R.Jaeschke, S.M.Stevens, S.Goodacre, P.S.Wells, M.D.Stevenson et al. Antithrombotic Therapy and Prevention of Thrombosis, 9th ed. American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. CHEST 2012; 141(2)(Suppl):e351S-e418S.Reference #3: B. Lipe, D. Ornstein. Deficiencies of natural anticoagulants, Protein C, Protein S and Antithrombin. Circulation 2011; 124:e365-e368.DISCLOSURE: The following authors have nothing to disclose: Edgardo TiglaoNo Product/Research Disclosure Information.
- Hemodialysis Catheter-Induced SVC Syndrome and Pulmonary Embolism. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):877A.
Pulmonary Vascular Disease Global Case ReportsSESSION TYPE: Global Case ReportPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: Superior vena cava (SVC) syndrome results from obstruction of blood flow through the SVC, usually due to compression from an adjacent intra-thoracic malignancy. Thrombosis is another much less frequent cause of SVC syndrome, despite the relatively common occurrence of thrombosis from central venous and hemodialysis (HD) catheters and pacemaker electrodes. To our knowledge, pulmonary embolism (PE) in the setting of catheter-related SVC syndrome and thrombosis has rarely been reported in living patients, and occasionally in patients observed at autopsy.A 28 year old female nonsmoking hairstylist with end-stage renal disease secondary to IgA nephropathy presented to an outside hospital with a few days of facial swelling, nausea, dizziness and pain with bending forward. She had initiated hemodialysis via right internal jugular (IJ) tunneled HD catheter 8 weeks prior. Her substance use, social and family history was unremarkable. Contrast-enhanced chest computed tomography (CT) was performed, demonstrating SVC obstruction with a large thrombus surrounding the HD catheter. A heparin drip was initiated, along with vancomycin after the patient developed Staphylococcus epidermidis bacteremia. Since the thrombus was situated proximal to the catheter lumen, HD was unaffected and was therefore continued. The patient was transferred to the Johns Hopkins Hospital for further management. On presentation, her temperature was 38.3, heart rate 96, blood pressure 134/61, oxygen saturation 99% on room air. Her physical exam was pertinent only for facial swelling and neck fullness. An SVC thrombus was confirmed with a repeat contrast-enhanced chest CT, which again showed an adherent, non-occlusive thrombus from the junction of the right IJ and subclavian vein, through the SVC to the level of the cavoatrial junction. Hypercoaguable workup was negative. The catheter was removed uneventfully, and a new catheter placed in the right internal jugular vein. On the ninth day of admission, she developed right-sided pleuritic chest pain with high-grade fevers and was found to have large emboli in the right main, middle, and lower pulmonary arteries. Echocardiogram was unremarkable, unchanged since admission. Three days later, she again developed similar chest pain with blood-tinged sputum. A non-contrast CT chest showed right middle and lower lobe infarction. The patient was treated with IV heparin and analgesics, and discharged on a 6-month course of warfarin. Nine months later, she underwent successful renal transplant.We present a case of HD catheter-related thrombosis leading to SVC syndrome and subsequent pulmonary embolism with pulmonary infarction. While SVC thrombosis arising from a HD catheter is rare, and a PE in this setting is even rarer, physicians should consider this potential complication in any patient with a HD catheter who develops shortness of breath, head fullness, facial edema, and/or neck vein distension. Once SVC syndrome is suspected, workup should include contrast-enhanced chest CT and consideration for empiric anticoagulation and line removal.Pulmonary embolism is a potential consequence of hemodialysis catheter-related thrombosis. Given the frequent use of central venous and HD catheters, future investigations are warranted to clarify the prevalence, pathophysiology, and risk factors for this potentially life-threatening complication.Reference #1: Goldstein MF, Nestico P, Olshan AR, Schwartz AB. Superior vena cava thrombosis and pulmonary embolus: association with right atrial mural thrombus. Arch Int Med. 1982;142(9):1726-1728. Reference #2: Madan AK, Almon JC, Harding M, Cheng SS, Slakey DP. Dialysis access-induced superior vena cava syndrome. Am Surgeon. 2002;68(10):904-906.Reference #3: Otten TR, Stein PD, Patel KC, Mustafa S, Silbergleit A. Thromboembolic Disease Involving the Superior Vena Cava and Brachiocephalic Veins. Chest. 2003;123(3):809-812.The following authors have nothing to disclose: Sritika Thapa, Biren Kamdar, Peter TerryNo Product/Research Disclosure Information.
- A Case of Acute Pulmonary Embolism Treated With Ultrasound-Assisted Catheter-Directed Thrombolysis. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):868A.
Pulmonary Vascular Case Report PostersSESSION TYPE: Affiliate Case Report PosterPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: Ultrasound-assisted catheter-directed thrombolysis (USAT) is a promising treatment for acute pulmonary embolism (PE). We present a case of acute PE in which this technology was successfully utilized.A 65 year old man presented with dyspnea following tibial fracture repair. Examination revealed a room air oxygen saturation of 77%, with normal hemodynamics. Breath sounds were normal bilaterally but there was right sided lower extremity edema. Laboratory studies were unremarkable aside from a troponin I of 0.62. A computer tomography scan with angiography demonstrated large bilateral pulmonary emboli originating within both main pulmonary arteries. A two-dimensional echocardiogram demonstrated new right ventricular strain. The patient was admitted to the intensive care unit and treated with unfractionated heparin and non invasive positive pressure ventilation (NIPPV) which he required for adequate oxygenation. Interventional radiology was consulted and the patient was treated with USAT for 24 hours without complication. A repeat pulmonary angiogram demonstrated significant reduction of clot burden and corresponded with clinical improvement in oxygenation and eventual discharge on room air.DISCUSSION: Patients with acute pulmonary embolism (PE) can be stratified into low, intermediate and high risk groups for short term mortality to help dictate management. An area of controversy involves the best therapeutic option for patients with intermediate risk acute PE. USAT is a novel treatment option in conjunction with anticoagulation for the treatment of acute PE. This modality allows for local delivery of TPA and endovascular ultrasound directly to the site of thrombus. An initial randomized controlled trial has shown this treatment to be effective in reducing right ventricular to left ventricular ratio at 24 hours without increased risk of bleeding. While improvement in mortality or clinical endpoints at ninety days have yet to be demonstrated, our case does provide an encouraging example of the potential benefit of this therapy.Ultrasound-assisted catheter-directed thrombolysis provides an additional treatment option for patients with intermediate risk acute PE, particularly in the setting of refractory hypoxemia or in patients with contraindications to systemic thrombolysis. Reference #1: Kucher N, Boekstegers P, et al. Randomized, controlled trial of ultrasound-assisted catheter-directed thrombolysis for acute intermediate-risk pulmonary embolism. Circulation 2014; 129:479.The following authors have nothing to disclose: Michael Colancecco, Rajesh Zacharias, Scott Kopec, Gisela BanauchNo Product/Research Disclosure Information.
- It's Not All Air! [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):866A.
Pulmonary Vascular Case Report PostersSESSION TYPE: Affiliate Case Report PosterPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: Venous air embolism(VAE) is a potentially life threatening condition that may be seen in situations other than high risk procedures.We present an interesting case initially diagnosed as VAE but subsequently also found to have saddle pulmonary embolism.A 68 year old female presented with one day history of chest pain and diaphoresis two weeks after laparoscopic hernia repair.She was hypotensive but had an otherwise normal physical examination.Her BP improved with fluids.EKG and troponin levels were normal.Non contrasted CT chest showed air throughout the venous system in the upper chest extending into right ventricle .Patient was admitted to the ICU for hemodynamic monitoring and was treated with hyperbaric oxygen.Her echocardiogram showed right heart strain and McConnell sign. Chest CT pulmonary angiogram(CTPA) revealed a saddle pulmonary embolism extending into all pulmonary vessels.Patient was started on IV heparin with resolution of symptoms.She was discharged on oral warfarin.CTPA after 6 months showed complete resolution of the pulmonary and air emboli.Venous air embolism(VAE) is the entrainment of air from the operative field into the venous or arterial vasculature,producing systemic effects.Mortality is related directly to volume of air entrained and rate of accumulation.Though most cases manifest acutely with cardiopulmonary symptoms many remain subclinical and get diagnosed during routine radiological assessment.VAE has been reported in procedures as benign as lumbar puncture,contrast CT chest and laproscopic surgery.The positive pressure inflation of gas used during laparoscopy is a significant embolism hazard.Air embolism may result not only in a catastrophic event like cardiogenic arrest but also pulmonary hypertension,edema and platelet aggregation.This case presented with delayed recognition of venous air embolism two weeks after laparoscopic hernia repair and concomitant pulmonary thromboembolism.Clinicians should be aware of this silent but dangerous entity that can occur during many seemingly routine operative procedures.Air embolism should be considered in the differential diagnosis of respiratory symptoms in patients who had a recent laparoscopic surgery.Acute pulmonary embolism may present concomitantly.Reference #1: Diagnosis and Treatment of Vascular air embolism; A Mirski et al; Anesthesiology 2007;106;164-77Reference #2: Richter et al.Air in the insufflation tube may cause fatal embolizations in laparoscopic surgery:Surg Endosc2013 May;27(5):1791-7.The following authors have nothing to disclose: Hammad Arshad, Mohammad Bilal, Marvin BalaanNo Product/Research Disclosure Information.
- PIIINP Is Associated With Worse Health Related Quality of Life in Pulmonary Arterial Hypertension. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):855A.
Pulmonary Hypertension (Poster Discussion)SESSION TYPE: Original Investigation PosterPRESENTED ON: Wednesday, October 29, 2014 at 01:30 PM - 02:30 PMPURPOSE: The goal of this study was to investigate the relationship between peripherally measurable collagen metabolism biomarkers and health related quality of life (HRQoL) in PAH patients.We prospectively enrolled 68 stable idiopathic, anorexigen-associated, and hereditary PAH subjects and 37 healthy controls with similar distributions of age and gender. Serum samples were analyzed for N-terminal propeptide of type III procollagen (PIIINP), c-terminal telopeptide of collagen type I (CITP), matrix metalloproteinase 9 (MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1). The Minnesota Living with Heart Failure (MLWHF), EQ-5D-3L (EQ-5D) and Short Form (SF-36) general health survey were administered at the time of blood draw. Univariate and multivariable linear regression models were used to assess associations between variables.Mean age of PAH patients and controls were similar (45±15 and 49±14 years respectively, mean±SD, p=0.18). The six-minute walk distance, Borg dyspnea score, WHO functional class, presence of edema, brain naturiectic peptide were all significantly different between controls and PAH patients (p<0.01 for all). CITP, PIIINP, MMP9, and TIMP1 levels, and all HRQoL domains were significantly different between controls and PAH patients (p<0.001 for each). PIIINP levels in particular were significantly associated with MLWHF physical (coef=1.63, and p=0.02), SF-36 physical (coef=-2.62, p=0.007), and EQ-5D aggregate (coef=0.21, p=0.03) scores also correlated well with PIIINP. An ROC curve analysis was conducted with moderate and severe versus mild PAH, using PIIINP as the predictor variable. Our result show that for each unit (1 µg/ml) increase in PIIINP, the odds increased by 1.62 (95% CI=1.06, 2.48 and p=0.025) and PIIINP cutoff value that gave the highest sensitivity and specificity is 4.64 µg/ml, with a sensitivity of 59.6% and a specificity of 60.0%.HRQoL is an important part of the patient health assessment. Lower PIIINP levels were associated with better quality of life domains, in particular those specific to PAH, suggesting that PIIINP levels may be a useful tool in clinical assessment of PAH patients.PIIINP levels may be a useful tool in clinical assessment of PAH patients.DISCLOSURE: The following authors have nothing to disclose: Emilio Tameez, Zeenat Safdar, Danielle Guffey, Charles Minard, Mark EntmanNo Product/Research Disclosure Information.