|Year : 2014 | Volume
| Issue : 2 | Page : 68-70
Disseminated tuberculosis presenting as acute lung injury
Mary Grace, VK Shameer, Renjith Bharathan, Kavitha Chandrikakumari
Department of Medicine, Government Medical College, Thrissur, Kerala, India
|Date of Web Publication||23-Jun-2014|
Department of Medicine, Government Medical College, Thrissur, Kerala
Source of Support: None, Conflict of Interest: None
Tuberculosis presenting as acute lung injury is distinctly uncommon, even in India where tuberculosis an endemic disease. Simultaneously, acute lung injury is a highly fatal complication of tuberculosis. A high index of suspicion is needed to diagnose tuberculosis in such cases. Failure to initiate early treatment can have disastrous consequences as exemplified in this case report. This case attempts to highlight the need to consider tuberculosis as one of the likely causative factors for acute lung injury and the importance of starting empirical antituberculous therapy in suspected cases early.
Keywords: Acute lung injury, disseminated tuberculosis, tuberculosis
|How to cite this article:|
Grace M, Shameer V K, Bharathan R, Chandrikakumari K. Disseminated tuberculosis presenting as acute lung injury. J Assoc Chest Physicians 2014;2:68-70
|How to cite this URL:|
Grace M, Shameer V K, Bharathan R, Chandrikakumari K. Disseminated tuberculosis presenting as acute lung injury. J Assoc Chest Physicians [serial online] 2014 [cited 2019 May 20];2:68-70. Available from: http://www.jacpjournal.org/text.asp?2014/2/2/68/135115
| Introduction|| |
Acute lung injury is an uncommon manifestation of tuberculosis even in India where tuberculosis is an endemic disease.  Disseminated tuberculosis can have varied clinical presentations because it can affect multiple organs. The protean and nonspecific clinical features and the difficulty in establishing Mycobacterium tuberculosis as the etiological agent contributes to the delay in the diagnosis which in turn leads to the delay in the initiation of specific treatment and consequently increased mortality. We are highlighting a case of disseminated tuberculosis which presented as acute lung injury, the etiologic diagnosis of which could only be established postmortem.
| Case report|| |
A 40-year-old previously asymptomatic female presented with fever of nearly 1 month duration. The fever was intermittent, high grade fever with chills and rigor at the time of presentation she also complained of abdominal pain constipation and cough with sputum production associated with exertional breathlessness of about 2-3 days duration. She did not give a history of taking treatment for tuberculosis in the past. She was not hypertensive or diabetic.
On examination, she was severely dyspneic with respiratory rate of 60/min SpO 2 on room air was 46%, blood pressure was 120/84 mm of Hg, pulse rate was 126/min. Auscultation of the chest revealed bilateral crepitations other systems examination was unremarkable.
Investigations hemoglobin 11.5 g%, total count 6700/mm 3 , polymorphs 73%, lymphocyres 23%, erythrocyte sedimentation rate 60 mm in the 1 st h, platelet count 2.5 lakhs/mm 3 , random blood sugar 67 mg%, serum creatinine 1.2 mg%, serum bilirubin total 1.4 mg%, serum total protein 4.5 g%, serum albumin 2.4 g%, serum alanine aminotransferase 144 U/L, serum aspartate aminotransferase 77 U/L, serum alkaline phosphatase 391 U/L C-reactive protein 32 mg% antinuclear antibodies negative. Ultrasound scan of abdomen, echocardiogram did not reveal any abnormality. Leptospira and dengue antibody screen was negative. Widal human immunodeficiency virus, hepatitis B surface antigen, anti-hepatitis C virus were negative. Sputum acid fast bacilli (AFB) stain and cultures was negative X-ray chest showed bilateral lower zone nodular opacities [Figure 1], X-ray chest]. Arterial blood gas analysis PaO 2 74 mm Hg PaCO 2 32 mm of Hg, pH 7.432 HCO 3 32 mmol/L.
Her SpO 2 improved to 93% on giving O 2 inhalation via mask. She was started on pulse steroids, antiviral drugs and broad spectrum antibiotics considering the possibility of viral pneumonia/interstitial lung disease. Computed tomography (CT) scan of the chest and abdomen showed bilateral extensive ground glass opacities, mild hepatosplenomegaly and mildly enlarged paraaortic lymph nodes [Figure 2], CT chest]. The pulse steroid was followed-up with oral steroids. After 2 days, she improved and was sent home on steroids. She was lost to follow-up. After nearly 2 months, she returned in a state of acute respiratory failure. She was put on mechanical ventilator, but she succumbed after 48 h.
|Figure 2: Computed tomography chest showing bilateral ground glass opacities|
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Postmortem needle biopsy was taken from lung and liver. Sections of lung tissue showed granulomatous inflammation composed of epitheloid cells a few lymphocytes and caseous necrosis. Sections form liver showed caseating granulomas composed of epitheloid cells, Langerhans giant cells. AFB staining was positive.
| Discussion|| |
Disseminated tuberculosis is caused by widespread hematogenous dissemination of tubercle bacilli from an active caseous focus. This can occur during the course of primary infection with M. tuberculosis or as late generalized tuberculosis. The necrotic caseous material released into the blood causes embolization of the capillaries of various organs with a predilection for the organs with the richest blood supply namely liver, spleen lungs, bone marrow, and brain. Lipoarabinomannan, which is a component of cell wall of M. tuberculosis is postulated to cause activation of macrophages with the release of tumor necrosis factor-alpha and interleukin-1 beta, which in turn causes endothelial injury and thereby lead to acute lung injury.  While clinically miliary tuberculosis constitutes <2% of all cases of tuberculosis in autopsy studies military tuberculosis accounts for approximately 40% of all cases of tuberculosis. Traditionally miliary tuberculosis was a disease of infants and children. Now it is found to affect young adults  and elderly people. Another new change being noticed now is the female preponderance. The age and the gender of the patient in this case report conform to this observation. Clinical features of disseminated tuberculosis are nonspecific constitutional symptoms such as fever, weight loss, evening rise of temperature, dyspnea, dry cough, or cough with scanty sputum may be present. The duration of symptoms prior to onset of respiratory failure is a clue to tuberculosis because a shorter duration of symptoms is to be expected in viral pneumonia, which can be differential diagnosis of such a presentation. Presence of choroidal tubercles is pathognomonic of disseminated tuberculosis.  This can serve as a useful clinical sign in such confusing situations. Rarer manifestations of tuberculosis include acute lung injury, glomerulonephriits, thyrotoxicosis, mycotic aneurysm of the aorta. The onset of acute respiratory distress syndrome (ARDS) may be acute or subacute the clinical signs include tachypnea bilateral crepitations in lung fields hepatomegaly, splenomegaly. Establishing an etiological diagnosis of tuberculosis even when there is clinical suspicion is a challenge. AFB positivity in sputum is about 30% while in bronchoalveolar lavage it varies between 27% and 100%, respectively. AFB positive granulomas in the liver approaches 88-100%, bone marrow approximately 80% and transbroncial biopsy 70-100% and lymph node nearly 100%. In this patient also sputum AFB staining and culture were negative but the granulomas in the liver and lung and lung stained positive for AFB. Unlike cavitary tuberculosis the granulomas of miliary tuberculosis are more frequently smear negative and noncaseating. In such cases polymerase chain reaction amplification of formalin fixed tissue with subsequent DNA probe hybridization may provide accurate diagnosis. Tuberculin anergy is more common in miliary tuberculosis than in other forms of tuberculosis. The characteristic finding in chest X-ray is bilateral nodular opacities 1-3 mm in diameter (seen in 90% of patients). Less common findings n chest X-ray are consolidation, cavities, calcification, granulomas and pleural effusion. Our patient also had bilateral nodular lesions in the lower zones bilaterally. The differential diagnosis of this X-ray findings include sarcoidosis, pneumoconiosis, hypersensitivity pneumonitis, and metastasis.  High resolution CT (HRCT) is more specific than chest X-ray. HRCT may show findings in cases where X-ray chest is noncontributory. The imaging findings include miliary nodules (which is the most common finding),  ground glass opacities (second most common finding), interlobar septal thickening. The HRCT finding of ground glass opacities made us think of interstial lung disease and the response to steroids was also in favor of this possibility. The mortality rate in disseminates tuberculosis ranges between 25% and 30%, while miliary tuberculosis presenting with ARDS has mortality rate is nearly 60%. Delay in initiation of treatment is associated with worse outcome. Complications like acute lung injury, acute kidney injury, disseminated intravascular coagulation septic shock and multiorgan failure are also poor prognostic factors.  This case highlights the need to consider tuberculosis as one of the likely causative factors for acute lung injury and the importance of starting empirical antituberculous therapy in suspected cases early.
| References|| |
|1.||Mohan A, Sharma SK, Pande JN. Acute respiratory distress syndrome (ARDS) in miliary tuberculosis: A twelve year experience. Indian J Chest Dis Allied Sci 1996;38:157-62. |
|2.||Bhalla A, Mahapatra M, Singh R, D'Cruz S. Acute lung injury in miliary tuberculosis. Indian J Tuberc 2002;49:125. |
|3.||Sharma SK, Mohan A, Sharma A. Challenges in the diagnosis and amp; treatment of miliary tuberculosis. Indian J Med Res 2012;135:703-30. |
|4.||Abi-Fadel F, Gupta K. Acute respiratory distress syndrome with miliary tuberculosis: A fatal combination. J Thorac Dis 2013;5:E1-4. |
|5.||Zhang J, Handorf C. Miliary tuberculosis presenting as acute respiratory distress syndrome, septic shock, DIC, and multiorgan failure. Tenn Med 2004;97:164-6. |
[Figure 1], [Figure 2]