|Year : 2018 | Volume
| Issue : 2 | Page : 80-83
Diffuse Alveolar Hemorrhage: A Very Rare but Catastrophic Complication After Percutaneous Transluminal Coronary Angioplasty
Ravi A Dosi1, Siddhant Jain2, Arpit Jain1, Satish Motiwale1, Prakash Joshi1, Arun Chandelkar1
1 Department of Respiratory Diseases and Sri Aurobindo Institute of Medical College and PGI, Indore, Madhya Pradesh, India
2 Department of Cardiology, Sri Aurobindo Institute of Medical College and PGI, Indore, Madhya Pradesh, India
|Date of Web Publication||10-Jul-2018|
Ravi A Dosi
124, Tilak Nagar Main Road, Savindnagar, Tilak Nagar, Indore 452018, Madhya Pradesh
Source of Support: None, Conflict of Interest: None
In this write-up, we report a case of persistent hemoptysis after percutaneous transluminal coronary angioplasty (PTCA), which was diagnosed as diffuse alveolar hemorrhage (DAH). DAH is a life-threatening medical emergency that can be caused by numerous disorders and it, further, presents with hemoptysis, anemia, and diffuse alveolar infiltrates. Early diagnosis is usually required for this noninfectious cause in post PTCA patient, as it is very rare complication.
Keywords: diffuse alveolar hemorrhage, percutaneous transluminal coronary angioplasty, persistent hemoptysis
|How to cite this article:|
Dosi RA, Jain S, Jain A, Motiwale S, Joshi P, Chandelkar A. Diffuse Alveolar Hemorrhage: A Very Rare but Catastrophic Complication After Percutaneous Transluminal Coronary Angioplasty. J Assoc Chest Physicians 2018;6:80-3
|How to cite this URL:|
Dosi RA, Jain S, Jain A, Motiwale S, Joshi P, Chandelkar A. Diffuse Alveolar Hemorrhage: A Very Rare but Catastrophic Complication After Percutaneous Transluminal Coronary Angioplasty. J Assoc Chest Physicians [serial online] 2018 [cited 2019 Mar 24];6:80-3. Available from: http://www.jacpjournal.org/text.asp?2018/6/2/80/233809
| Introduction|| |
Diffuse alveolar hemorrhage (DAH) syndrome is caused by a disruption of the alveolar-capillary basement membrane, which results in bleeding into the alveolar spaces. There is a sudden flow of blood into multiple sites of alveoli and may culminate into an acute, life-threatening event. Infectious or toxic agents, systemic vasculitis, for example, Behcet’s syndrome, Henoch-Schoenlein purpura, and Wegener’s granulomatosis, connective tissue diseases, for example, Goodpasture’s syndrome, and systemic lupus erythematosis and drugs, for example, amiodarone and penicillamine are well-known etiologic factors. The diagnosis of DAH relies on clinical suspicion combined with laboratory, radiologic, and pathologic findings. Early recognition is crucial, because prompt diagnosis and treatment are necessary for survival. Corticosteroids (CS) and immunosuppressive agents remain the gold standard of treatment. This article aims to provide a general review on this rare complication of percutaneous transluminal coronary angioplasty (PTCA).
| Case Report|| |
We report a case of diffuse alveolar hemorrhage in a 55-year-old male after PTCA, even when no glycoprotein IIb/IIIa inhibitors were given.
This patient came with the complaints of shortness of breath and severe chest pain predominantly on the left side of the chest and radiating towards back and jaw. This patient had a history of myocardial infarction 10 years back, and then he was given medications for the same. He was chronic smoker with history of 40 pack years and a diagnosed case of chronic obstructive airway disease, for which metered-dose inhaler was prescribed to him, but he was not taking medications regularly. The electrocardiography (ECG) of the patient suggested inferior wall ST elevation MI, and two-dimensional echocardiography (2D-ECHO) suggested regional wall motion abnormalities in right coronary artery (RCA) territory and left ventricular ejection fraction 45–50%. Cardiac marker (troponin I) readings also were raised, hence, the diagnosis of acute inferior wall myocardial infarction (IWMI) was made, and he was thrombolysed with reteplase. After stabilization of patient, angiography was performed that showed double vessel disease, RCA 90% stenosis, and left anterior descending artery 80% stenosis. So PTCA and RCA stenting was performed, poststenting ballon dilatation was performed with 4 × 12MM NC SAPPHIRE BALLON used STENT used was REIVAS 4 × 18 mm and during procedure 9000 unit of heparin was given. Patient was completely stable, and good hemostatis is achieved after the procedure.
Patient complained of blood tinged sputum started first day post procedure there were no spike of fever, counts within normal limit, respiratory system examination suggestive of bilateral crackles at lung base left more than right, X-ray chest shows nonspecific patchy bilateral infiltrates [Figure 1]. On high suspicion of DAH, stands for contrast enhanced computed tomography (CECT) chest was performed, which gave the diagnosis of diffuse alveolar hemorrhage [[Figure 2] and [Figure 3]]. Antinuclear antibodies (ANA) profile came negative.
|Figure 2: (a) Patchy area of ground glass attenuation seen in apical, posterior segment of both upper lobe. Centriacinar emphysematous change in both upper lobe. (b) Patchy area of ground glass attenuation seen in both lower lobe|
Click here to view
This patient was treated on high dose steroid, that is, 500 mg methylprednisolone injection daily for 5 days, and the patient responded well and treated. X-ray chest was taken after 5 days of treatment. And it shows huge improvement.
| Discussion|| |
DAH is a rare and potentially life-threatening condition characterized by diffuse blood leakage from the pulmonary microcirculation into the alveolar spaces due to microvascular damage. It is mostly a clinicopathologic syndrome that may have numerous causes such as autoimmune disorders, left heart disease, infections, drug toxicities, coagulopathies, and malignancies.
DAH may present with the symptoms of dyspnea, hemoptysis, cough, and hypoxemic respiratory failure as well as the presence of diffuse alveolar infiltrations on chest radiography. A drop in hematocrit or hemoglobin can be present but are difficult to document. Even one third of patients do not have hemoptysis. The alveolar infiltrates are mostly bilateral but can be unilateral. Early bronchoscopy with bronchoalveolar lavage is usually required to confirm the diagnosis and to rule out infection. The diagnosis is confirmed by the observation of the accumulation of red blood cells, fibrin, or hemosiderin-laden macrophage in the alveolar space on pathologic biopsy. Histologically DAH can show pulmonary capillaritis, pulmonary hemorrhage, and diffuse alveolar damage. Pulmonary capillaritis is the most common underlying pathology of DAH and is often caused by systemic vasculitis. DAH may be presented in acute, sub acute, or repetitive patterns with variable severity.,,
The diagnosis of DAH is made clinically in an appropriate clinical context and may be supported by radiography, bronchoscopy, and pathologic examination. Occasionally, the diagnosis is made by exclusion. DAH may be mistaken clinically as acute pulmonary edema, which is a common complication of acute coronary syndrome. Therefore, a low threshold of clinical suspicion should be maintained to initiate proper management of this potentially fatal condition. In our case, bronchoscopy could not be performed, as patient had recent myocardial infarction.
CS and immunosuppressive agents remain the gold standard for most patients. Recombinant-activated human factor VII seems to be a promising new therapy, but further evaluation is needed. Immunosuppressive agents are the mainstay of therapy for DAH, especially if associated with systemic or pulmonary vasculitis. Most experts recommend intravenous methylprednisolone (Solu-Medrol) at up to 500 mg every 6 h, although lower doses seem to have similar efficacy, for 4 or 5 days, followed by a gradual taper to maintenance doses of oral steroids. Other immunosuppressive drugs such as cyclophosphamide, azathioprine, methotrexate, mycophenolate mofetil, and etanercept may be used in DAH, especially in severe cases refractory to first-line therapy with CS. Plasmapheresis is indicated for DAH associated with Goodpasture’s syndrome or other vasculitic processes, in which the titers of pathogenic immunoglobulins and immune complexes are very high. Before the institution of immunosuppressive therapy, patients with systemic vasculitis had a mortality rate of 75%. CS therapy alone improved mortality.
DAH has also been associated with the use of antiplatelet agents (aspirin, ticlopidine, ticagrelor), low molecular weight heparin, amiodarone and rivaroxaban and hyaluronic acid dermal fillers (cosmetic product), but none of the case reported after PTCA.
There have been limited data about risk factors for the development of DAH due to antithrombotic agent use. Literature suggests that history of acute myocardial infarction, older age, prolonged or complicated angioplasty, underlying chronic lung disease, pulmonary hypertension or elevated pulmonary capillary wedge pressure (PCWP) in patients treated with platelet Gp IIb/IIIa inhibitors may be associated with a higher risk of developing DAH.,, Our patient had an acute anterior wall ST-Elevation myocardial infarction (STEMI) with old coronary artery disease (CAD) and chronic lung disease and was treated with anticoagulant. DAH may be facilitated by alveolar permeability, which is increased in most smokers. A combination of these risk factors may have contributed to the development of DAH to a certain extent.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Collard HR, Schwarz MI. Diffuse alveolar hemorrhage. Clin Chest Med 2004;25:583-92.
Schnabel A, Holl-Ulrich K, Dalhoff K, Reuter M, Gross WL. Efficacy of transbronchial biopsy in pulmonary vaculitides. Eur Respir J 1997;10:2738-43.
Colby TV, Fukuoka J, Ewaskow SP, Helmers R, Leslie KO. Pathologic approach to pulmonary hemorrhage. Ann Diagn Pathol 2001;5:309-19.
Lara AR, Schwarz MI. Diffuse alveolar hemorrhage. Chest 2010;137:1164-71.
Ioachimescu OC, Stoller JK. Diffuse alveolar hemorrhage: Diagnosing it and finding the cause. Cleve Clin J Med 2008;75:258-80.
Henke D, Falk RJ, Gabriel DA. Successful treatment of diffuse alveolar hemorrhage with activated factor VII. Ann Intern Med 2004;140:493-4.
Klemmer PJ, Chalermskulrat W, Reif MS, Hogan SL, Henke DC, Falk RJ. Plasmapheresis therapy for diffuse alveolar hemorrhage in patients with small-vessel vasculitis. Am J Kidney Dis 2003;42:1149-53.
Yildirim F, Kara I, Okuyan H, Abacı A, Türkoğlu M, Aygencel G. Diffuse alveolar hemorrhage associated with low molecular weight heparin and dual anti-platelet therapy after percutaneous coronary intervention. Clin Respir J 2017;11:1071-3.
Hayashi S, Maruoka S, Nakagawa Y, Takahashi N, Hashimoto S. Diffuse alveolar hemorrhage associated with low molecular weight heparin. Respirol Case Rep 2013;1:2-4.
Iskandar SB, Abi-Saleh B, Keith RL, Byrd RP Jr, Roy TM. Amiodarone-induced alveolar hemorrhage. Southern Med J 2006;99:383-8.
Hammar SP. Fatal pulmonary hemorrhage after taking anticoagulation medication. Respir Med Case Rep 2015;15:66-70.
Guo J, Xu M, Xi Y. Tirofiban-induced diffuse alveolar hemorrhage: After primary angioplasty. Texas Heart Inst J 2012;39:99-103.
Khanlou H, Eiger G, Yazdanfar S. Abciximab and alveolar hemorrhage. New Engl J Med 1998;339:1861-3.
Aguirre FV, Topol EJ, Ferguson JJ, Anderson K, Blankenship JC, Heuser RR et al.
Bleeding complications with the chimeric antibody to platelet glycoprotein IIb/IIIa integrin in patients undergoing percutaneous coronary intervention. Circulation 1995;91:2882-90.
Travis WD, Koss MN. Pulmonary vasculitis. In: Dail DH, Hammar SP, editors. Pulmonary Pathology. 2nd
ed. Berlin: Springer-Verlag, Inc. 1994. p. 1027-95.
[Figure 1], [Figure 2], [Figure 3]