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 Table of Contents  
CASE REPORT
Year : 2017  |  Volume : 5  |  Issue : 2  |  Page : 83-86

Pneumothorax in a case of community-acquired pneumonia due to Acinetobacter


Department of Respiratory Medicine, J.N. Medical College, Wardha, Maharashtra, India

Date of Web Publication4-Jul-2017

Correspondence Address:
Babaji Ghewade
Department of Respiratory Medicine, J.N. Medical College, Sawangi Meghe, Wardha - 442 001, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2320-8775.177510

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  Abstract 

Acinetobacter baumannii is an uncommon but important cause of severe community-acquired pneumonia (CAP), especially in tropical/subtropical regions and in patients with underlying lung disease. Here, we present a case of acute fulminant CAP in a young female patient with underlying cystic lung disease which presented with secondary spontaneous pneumothorax. The patient went into acute respiratory failure and recovered completely with treatment.

Keywords: Acinetobacter baumannii, community-acquired pneumonia, cystic lung disease, spontaneous pneumothorax


How to cite this article:
Ghewade B, Abrahm EA, Chaudhari S, Agrawal B. Pneumothorax in a case of community-acquired pneumonia due to Acinetobacter. J Assoc Chest Physicians 2017;5:83-6

How to cite this URL:
Ghewade B, Abrahm EA, Chaudhari S, Agrawal B. Pneumothorax in a case of community-acquired pneumonia due to Acinetobacter. J Assoc Chest Physicians [serial online] 2017 [cited 2019 Oct 20];5:83-6. Available from: http://www.jacpjournal.org/text.asp?2017/5/2/83/177510


  Introduction Top


Acinetobacter baumannii, an aerobic Gram-negative coccobacillus, is a well-recognized pathogen causing nosocomial pneumonia, predominantly in patients with endotracheal intubation, prolonged mechanical ventilation, underlying lung diseases, or who are being treated in an Intensive Care Unit (ICU).[1] However, it is an uncommon cause of severe community-acquired pneumonia (CAP), especially in tropical/subtropical regions and other places with warm and humid seasons.[2] Here, we report a case of a young female having underlying cystic lung disease who was misdiagnosed to have tuberculosis, developed bilateral pneumonia, and presented with secondary spontaneous pneumothorax.


  Case Report Top


An 18-year-old female patient presented to our institute with fever, increased breathlessness (Grade I → Grade III MMRC), productive cough for 15 days, and chest pain on the right side for 2 days. Two months before, she had a history of dry cough, breathlessness, and had been to a Peripheral Health Centre. She was diagnosed to have smear-negative pulmonary tuberculosis on the basis of history and chest X-ray showing few cystic lesions in both upper zones and was put on category I directly observed treatment short (DOTS) treatment which she was taking for 2 months. She also had complaints of irregular menses for 6 months. Past history and personal history were not significant.

On examination, the patient was thinly built with body mass index of 17.7 kg/m 2 and febrile with temperature at 99.6°F. She had a normal jugular venous pulse with no pallor, icterus, clubbing, cyanosis, lymphadenopathy, and pedal edema. Her pulse was 110/min, regular, normovolemic, and peripheral pulses were felt bilaterally. Respiratory rate was 34/min, thoracoabdominal blood pressure was 90/64 mm Hg in right arm in the supine position, and oxygen saturation was 84% on room air.

Upper respiratory tract examination was normal except deviated nasal septum to the right side. In the lower respiratory tract, trachea was shifted to the left side, respiratory movements and breath sounds were diminished on the right side, and there was hyperresonant note all over the right side. On left side, there was impaired percussion note in lower lung fields with tubular bronchial breathing, increase in vocal resonance, whispering pectoriloquy, and mild crackles over lower lobe areas. Provisional diagnosis of pneumothorax on the right side with left lower lobe consolidation was made, and the patient was given supplemental oxygen and subjected to investigations.

Chest X-ray posteroanterior (PA) view confirmed the right-sided pneumothorax with left lower lobe consolidation and there was also haziness in the visualized parts of collapsed right lung. International Classification of Diseases (ICD) tube was inserted in the right 4th intercostal space in mid-axillary line immediately. After ICD insertion, breath sounds were bilaterally equal, but signs of consolidation were found over right lower lobe area. Post ICD chest X-ray confirmed the clinical findings [Figure 1]a. Injection amoxicillin with clavulanic acid and amikacin were started intravenously.
Figure 1: (a) Post International Classification of Diseases chest X-ray posteroanterior view showing bilateral lower zone consolidation with International Classification of Diseases in situ on the right side. (b) High-resolution computed tomography thorax showing bilateral multiple cystic lesions in upper zones and bilateral ground glass opacities in lower zones with right pneumothorax and International Classification of Diseases in situ

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Her laboratory investigations showed hemoglobin 10 g%, leukocytosis with 84% neutrophils, normal platelet counts and erythrocyte sedimentation rate 18 mm at the end of 1 h. Liver and kidney function tests were normal along with normal blood sugar, and ELISA test for HIV was nonreactive. Arterial blood gas (ABG) was suggestive of Type I respiratory failure (pH –7.4, PO2 –41.6%, PCO2 –33%, HCO3 –24.8%, and SaO2 –80%).

The patient's condition deteriorated in the next 2 days in spite of antibiotics, and supplemental oxygen was unable to maintain oxygen saturation and needed noninvasive positive pressure ventilation support. The pleural fluid collected from the ICD was sent for investigations, showed pH –7.2, proteins –3.6 g%, lactate dehydrogenase (LDH) –1780 IU, sugar –70 mg%, and total leukocyte count (TLC) –2200 with the presence of mixed population of polymorphs and lymphocytes along with reactive mesothelial cells and morphology suggestive of acute mixed leukocytic exudation, adenosine deaminase 32 IU, triglycerides 31 mg/dl, and no growth on culture. Her sputum smear was negative for acid-fast Bacilli (AFB). Ultrasonography (USG) abdomen and pelvis showed multiple porta-peripancreatic lymphadenopathy with mild ascites and omental thickening and USG-guided fine needle aspiration cytology of lymphnode showed no cellularity.

High-resolution computed tomography (HRCT) thorax [Figure 1]b showed bilateral ground glass opacities with air bronchogram and reticular thickening in interstitium with right-sided pneumothorax and ICD in situ. Multiple

well-defined cysts in both lung fields, more in the upper lobes, were a remarkable finding and possibilities of pulmonary lymphangioleomyomatosis, cystic sarcoidosis, and histiocytosis X was considered. Cause of bilateral pneumonitis still remains unresolved.

Further investigations showed serum LDH 1135 IU/L (200–400), serum ANA –10.2 (<20 μ/l), Mantoux test – nonreactive, and serum calcium –7.9 mg/dL. ABG analysis showed pH –7.4, PO2 –41 mm Hg, PCO2 – 33 mm Hg, HCO3 –24.8 mmol/L, and SaO2 –68.2%. Serum angiotensin converting enzyme – negative, 24 h urinary protein –0.5 g. Fasting lipid profile showed serum cholesterol –216 mg%, high-density lipoprotein –216, low-density lipoprotein –123, very low-density lipoprotein –39, and triglyceride –194. Widal test, paracheck for MP, and HbsAg tests were negative.

Fiber optic bronchoscopy was performed under topical anesthesia, showed minimally inflammed endobronchial mucosa. BAL and bronchial brush were negative for AFB, TLC was 480 cells with 90% polymorphs and 10% lymphocytes, and cytology showed benign epithelial cells in inflammatory and hemorrhagic background. Growth of A. baumannii species was seen on BAL culture and was sensitive to imipenem and resistant to amikacin.

Antibiotics were changed according to the BAL culture sensitivity reports. Injection piperacillin - tazobactam and tablet faropenem were administered for the next 2 weeks along with methyl prednisolone and supportive treatment. The patient started responding to the treatment and before removal of ICD, repeat bronchoscopy with transbronchial lung biopsy was performed, which was suggestive of Type II pneumocyte proliferation and hemorrhage indicative of resolving adult respiratory distress syndrome. Smooth muscle proliferation of the airways was also seen. BAL culture yielded no growth. ICD was removed after confirming no air leak. Final diagnosis of acute fulminant community-acquired pneumonia by A. baumannii leading to ARDS with underlying cystic lung disease - pulmonary lymphangioleiomyomatis presenting with secondary spontaneous pneumothorax was made.

The patient improved with treatment and follow-up chest X-ray PA view [Figure 2]a and HRCT thorax [Figure 2]b showed significant improvement, but the underlying cystic lesions remained persistent. The patient maintained SaO2 of 97% on room air and was discharged on tablet faropenem 200 mg TDS and tablet progesterone 10 mg/day × 14 days. Further follow-up X-ray after 1 month [Figure 3] showed complete resolution of lower lobe lesions, but the persistence of upper lobe cystic lesions.
Figure 2: (a) Follow-up X-ray after 1 month showing significant resolution of bilateral consolidation. (b) Follow-up high-resolution computed tomography after 1 month showing near complete resolution of the lower lobe consolidation, but persistent cystic lesions in upper lobes

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Figure 3: Follow-up X-ray chest after 2 months - complete regression of lower lobe consolidations

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  Discussion Top


A. baumannii is an uncommon but important cause of severe CAP, especially in tropical/subtropical regions and other places with warm and humid seasons. It is an aerobic Gram-negative coccobacillus, present abundantly in fresh water and soil. It is a well-recognized pathogen causing nosocomial pneumonia, predominantly in patients with endotracheal intubation, prolonged mechanical ventilation, underlying lung diseases, or who are being treated in an ICU. CAP due to A. baumannii is uncommon.[2],[3],[4] Our patient had asymptomatic underlying lung disease for an unknown duration which when became symptomatic was misdiagnosed as tuberculosis. She had no improvement in spite of taking DOTS treatment regularly and developed bilateral CAP, which presented with secondary spontaneous pneumothorax.

Pulmonary lymphangioleiomyomatosis (LAM) is a rare, idiopathic, diffuse, and progressive interstitial lung disease that afflicts young women of childbearing age. It occurs as a sporadic disease or with tuberous sclerosis complex, which can be inherited as an autosomal dominant disorder. Most patients (70%) are 20–40 years of age at the time of onset of symptoms or diagnosis.[5] Sporadic LAM is an uncommon disease occurring in approximately 4.9/1000,000 women.[6] Spontaneous pneumothorax is common and occurs in almost two-third of cases. Grossly and microscopically, the normal architecture of lung is distorted by multiple small cysts. The predominant pathology is proliferation of atypical smooth muscle, occurs around the bronchovascular structures. HRCT chest often confirms the diagnosis, and tissue confirmation may not be necessary.[7] The natural history of this disorder is thought to be progressive with a median survival of 8–10 years after diagnosis. Oophorectomy, progesterone (10 mg/day), tamoxifen (20 mg/day), and luteinizing hormone-releasing hormone analogs have all been used with supportive evidence.


  Conclusion Top


Many Gram-positive and Gram-negative organisms are known causes of severe CAP. In patients with underlying lung diseases, Acinetobacter species should be considered as one of the potential causes for such severe CAP.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Salas Coronas J, Cabezas Fernández T, Alvarez-Ossorio García de Soria R, Díez García F. Community-acquired Acinetobacter baumannii pneumonia. Rev Clin Esp 2003;203:284-6.  Back to cited text no. 1
    
2.
Oh YJ, Song SH, Baik SH, Lee HH, Han IM, Oh DH. A case of fulminant community-acquired Acinetobacter baumannii pneumonia in Korea. Korean J Intern Med 2013;28:486-90.  Back to cited text no. 2
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3.
Dexter C, Murray GL, Paulsen IT, Peleg AY. Community-acquired Acinetobacter baumannii: Clinical characteristics, epidemiology and pathogenesis. Expert Rev Anti Infect Ther 2015;13:567-73.  Back to cited text no. 3
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4.
Davis JS, McMillan M, Swaminathan A, Kelly JA, Piera KE, Baird RW, et al. A 16-year prospective study of community-onset bacteremic Acinetobacter pneumonia: Low mortality with appropriate initial empirical antibiotic protocols. Chest 2014;146:1038-45.  Back to cited text no. 4
[PUBMED]    
5.
Cohen MM, Pollock-BarZiv S, Johnson SR. Emerging clinical picture of lymphangioleiomyomatosis. Thorax 2005;60:875-9.  Back to cited text no. 5
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6.
Harknett EC, Chang WY, Byrnes S, Johnson J, Lazor R, Cohen MM, et al. Use of variability in national and regional data to estimate the prevalence of lymphangioleiomyomatosis. QJM 2011;104:971-9.  Back to cited text no. 6
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7.
Tobino K, Johkoh T, Fujimoto K, Sakai F, Arakawa H, Kurihara M, et al. Computed tomographic features of lymphangioleiomyomatosis: Evaluation in 138 patients. Eur J Radiol 2015;84:534-41.  Back to cited text no. 7
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