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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Drugs are known to be a cause of pulmonary eosinophilia and several case reports of acute eosinophilic pneumonia associated with the use of cocaine have been reported. The changing pattern of heroin use, with a shift from intravenous use to smoking/inhalation of the substance, may lead to increased prevalence of heroin-induced pulmonary eosinophilia. We report on a case of a patient who had been inhaling heroin for about ten years. He presented with fever, cough, dyspnea and pleuritic chest pain. Chest radiograph showed unilateral pleural effusion with segmental atelectasis. Examination of pleuritic fluid aspirate and bronchoalveolar lavage fluid revealed significant eosinophilia. He was diagnosed with acute eosinophilic pneumonia. Rapid remission was achieved after heroin abstinence and initiation of corticosteroid treatment.
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PMID:Eosinophilic pneumonia associated with heroin inhalation: a case report. 1836 58

Coccidioidomycosis is endemic in the southwestern United States, resulting in 100,000 infections annually. The majority of these infections are asymptomatic or manifest as community-acquired pneumonia. In rare cases, patients can present with a mononuclear-cell predominant pyopneumothorax. The presence of spherules in tissue specimens is pathognomonic of this condition. A 72-year-old man born in Arizona with a heavy smoking history, presented with a 1-month history of weakness, night sweats, exertional dyspnea, and left pleuritic chest pain. The physical examination was remarkable for decreased breath sounds and dullness to percussion at the left lung base. His initial laboratory examination showed leukocytosis, eosinophilia, and elevated C-reactive protein. Computed tomography of the chest revealed a left lower lobe infiltrate, a cavity with air-crescent sign and hydropneumothorax. The pleural fluid was sampled and revealed an eosinophilic exudate with normal pH. Bacterial and fungal cultures of the pleural fluid were negative. Biopsy of the cavity wall showed chronic inflammation, fungal hyphae, and rare spherule-like structures. The surgical specimen culture grew Coccidioides immitis. Complement fixation for coccidioidomycosis performed on a serum sample was positive at a titer of 1:2 but a latex agglutinin test was negative. The patient was diagnosed with chronic fibrocavitary pneumonia with pyopneumothorax secondary to C. immitis infection and discharged on itraconazole for 1 year. Coccidioidomycosis can present in a variety of forms and should be part of the differential diagnosis in patients presenting with cavitation, air-crescent sign, eosinophilic pleural effusion, and hyphae and spherules on the tissue specimen. Chronic fibrocavitary pneumonia should be especially considered in patients who lived in endemic areas and have risk factors such as diabetes mellitus or pulmonary fibrosis related to smoking.
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PMID:Spherules, hyphae, and air-crescent sign. 1855 86

Pulmonary embolism (PE) is often evoked in patients with new-onset or worsening dyspnea, especially when it is associated with pleuritic chest pain. However, the prevalence of PE in patients with a clinical suspicion ranges from 20 % to as low as 5 %. Unfortunately, what exactly constitutes a clinical suspicion of PE in a patient with dyspnea can not be accurately standardized. The presence of risk factors for venous thromboembolism should prompt the search for PE. However, their absence does not rule out PE as the cause of the patient's symptoms, since around 30 % of patients with a first episode of PE have no risk or precipitating factors. Once PE is suspected, the diagnostic workup can be standardized and based on a large body of evidence, combining clinical assessment by a prediction rule, D-dimer measurement and CT angiography in patients with an elevated D-dimer level or a high clinical probability of PE. Patients with obvious alternative diagnoses such as acute left heart failure, pneumonia or acute coronary syndrome should not be investigated for PE.
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PMID:From dyspnea to pulmonary embolism. 1972 8

Pleural effusion is an uncommon manifestation of amiodarone toxicity and is usually associated with amiodarone-induced interstitial pneumonitis. We describe a 70-year-old woman who came to the emergency department with bilateral pleuritic chest pain and malaise 4 weeks after her amiodarone dose was increased from 200 mg/day to 600 mg/day. She had bilateral exudative pleural effusions without associated pneumonitis. She was diagnosed with amiodarone-induced pleural effusions after a thorough workup during her hospitalization excluded other causes for the effusions. Due to intractable arrhythmias, the patient's amiodarone was not discontinued, and she was discharged home. Four days later at a follow-up visit at the pulmonary clinic, the patient complained of worsening chest pain as well as dyspnea and cough. A computed tomography scan showed left-sided pleural effusion with multiple loculations. She underwent a pulmonary vein isolation procedure, and amiodarone was discontinued. She was treated with prednisone 40 mg/day, tapered over the next 2 weeks. Three weeks after the amiodarone was stopped, the patient was asymptomatic, and a chest radiograph showed complete resolution of the effusions. Review of the patient's medical records revealed that she had experienced similar symptoms and exudative pleural effusions 2 years earlier after a similar dose escalation of amiodarone; the symptoms and pleural effusions resolved after the amiodarone dosage was reduced. Use of the Naranjo adverse drug reaction probability scale indicated that the association between the pleural effusions and amiodarone was highly probable (score of 9). This case report emphasizes that amiodarone should be considered in the differential diagnosis of patients with exudative effusions after a thorough workup has excluded other causes. Amiodarone should be replaced with alternative antiarrhythmic therapy if clinically feasible, and corticosteroids may be beneficial.
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PMID:Amiodarone-induced loculated pleural effusion: case report and review of the literature. 2009 96

Infections due to Aspergillus species cause significant morbidity and mortality. Most are attributed to Aspergillus fumigatus, followed by Aspergillus flavus and Aspergillus terreus. Aspergillus niger is a mould that is rarely reported as a cause of pneumonia. A 72-year-old female with chronic obstructive pulmonary disease and temporal arteritis being treated with steroids long term presented with haemoptysis and pleuritic chest pain. Chest radiography revealed areas of heterogeneous consolidation with cavitation in the right upper lobe of the lung. Induced bacterial sputum cultures, and acid-fast smears and cultures were negative. Fungal sputum cultures grew A. niger. The patient clinically improved on a combination therapy of empiric antibacterials and voriconazole, followed by voriconazole monotherapy. After 4 weeks of voriconazole therapy, however, repeat chest computed tomography scanning showed a significant progression of the infection and near-complete necrosis of the right upper lobe of the lung. Serum voriconazole levels were low-normal (1.0 microg ml(-1), normal range for the assay 0.5-6.0 microg ml(-1)). A. niger was again recovered from bronchoalveolar lavage specimens. A right upper lobectomy was performed, and lung tissue cultures grew A. niger. Furthermore, the lung histopathology showed acute and organizing pneumonia, fungal hyphae and oxalate crystallosis, confirming the diagnosis of invasive A. niger infection. A. niger, unlike A. fumigatus and A. flavus, is less commonly considered a cause of invasive aspergillosis (IA). The finding of calcium oxalate crystals in histopathology specimens is classic for A. niger infection and can be helpful in making a diagnosis even in the absence of conidia. Therapeutic drug monitoring may be useful in optimizing the treatment of IA given the wide variations in the oral bioavailability of voriconazole.
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PMID:Aspergillus niger: an unusual cause of invasive pulmonary aspergillosis. 2029 3

The aim of our study was to obtain comprehensive insight into the bacteriological and clinical profile of community-acquired pneumonia requiring hospitalization. The patient population consisted of 100 patients admitted with the diagnosis of community-acquired pneumonia (CAP), as defined by British Thoracic society, from December 1998 to Dec 2000, at the Sher- i-Kashmir institute of Medical Sciences Soura, Srinagar, India. Gram negative organisms were the commonest cause (19/29), followed by gram positive (10/29). In 71 cases no etiological cause was obtained. Pseudomonas aeruginosa was the commonest pathogen (10/29), followed by Staphylococcus aureus (7/29), Escherichia coli (6/29), Klebsiella spp. (3/29), Streptococcus pyogenes (1/29), Streptococcus pneumoniae (1/29) and Acinetobacter spp. (1/29). Sputum was the most common etiological source of organism isolation (26) followed by blood (6), pleural fluid (3), and pus culture (1). Maximum number of patients presented with cough (99%), fever (95%), tachycardia (92%), pleuritic chest pain (75%), sputum production (65%) and leucocytosis (43%). The commonest predisposing factors were smoking (65%), COPD (57%), structural lung disease (21%), diabetes mellitus (13%), and decreased level of consciousness following seizure (eight per cent) and chronic alcoholism (one per cent). Fourteen patients, of whom, nine were males and five females, died. Staphylococcus aureus was the causative organism in four, Pseudomonas in two, Klebsiella in one, and no organism was isolated in seven cases. The factors predicting mortality at admission were - age over 62 years, history of COPD or smoking, hypotension, altered sensorium, respiratory failure, leucocytosis, and staphylococcus pneumonia and undetermined etiology. The overall rate of identification of microbial etiology of community-acquired pneumonia was 29%, which is very low, and if serological tests for legionella, mycoplasma and viruses are performed the diagnostic yield would definitely be better. This emphasizes the need for further studies (including the serological tests for Legionella, mycoplasma and viruses) to identify the microbial etiology of CAP.
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PMID:Bacteriological and clinical profile of Community acquired pneumonia in hospitalized patients. 2061 35

Despite prevention programs, tuberculosis is still endemic in developing countries. Extrapulmonary tuberculosis is increasing globally in the face of recent emergence of Human Immunodeficiency Virus (HIV) infection. Pleural tuberculosis is a common problem in daily clinical practice. We assessed 26 cases of tuberculous pleural effusion admitted in Bangabandhu Sheikh Mujib Medical University from 2002 to 2007. The diagnosis was based upon clinical examination, tuberculin reaction, imaging, pleural fluid analysis and response to antitubercular chemotherapy a surrogate clinical determinant. Apparently promising newer biochemical pleural fluid measurements were not utilized due to a number of limitations. The presenting symptoms found in this prospective analysis are fever (100%), nonproductive cough (73%), pleuritic chest pain (38%), loss of weight (38%) and shortness of breath (38%). A high index of suspicion after confident exclusion of malignancy and pneumonia is a clue to diagnosis. Out of 80 cases of extrapulmonary tuberculosis admitted during the study period, tuberculous pleural effusion constitutes 32.50%.
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PMID:Tuberculous pleural effusion. 2124 Jan 65

Community-acquired pneumonia is diagnosed by clinical features (e.g., cough, fever, pleuritic chest pain) and by lung imaging, usually an infiltrate seen on chest radiography. Initial evaluation should determine the need for hospitalization versus outpatient management using validated mortality or severity prediction scores. Selected diagnostic laboratory testing, such as sputum and blood cultures, is indicated for inpatients with severe illness but is rarely useful for outpatients. Initial outpatient therapy should include a macrolide or doxycycline. For outpatients with comorbidities or who have used antibiotics within the previous three months, a respiratory fluoroquinolone (levofloxacin, gemifloxacin, or moxifloxacin), or an oral beta-lactam antibiotic plus a macrolide should be used. Inpatients not admitted to an intensive care unit should receive a respiratory fluoroquinolone, or a beta-lactam antibiotic plus a macrolide. Patients with severe community-acquired pneumonia or who are admitted to the intensive care unit should be treated with a beta-lactam antibiotic, plus azithromycin or a respiratory fluoroquinolone. Those with risk factors for Pseudomonas should be treated with a beta-lactam antibiotic (piperacillin/tazobactam, imipenem/cilastatin, meropenem, doripenem, or cefepime), plus an aminoglycoside and azithromycin or an antipseudomonal fluoroquinolone (levofloxacin or ciprofloxacin). Those with risk factors for methicillin-resistant Staphylococcus aureus should be given vancomycin or linezolid. Hospitalized patients may be switched from intravenous to oral antibiotics after they have clinical improvement and are able to tolerate oral medications, typically in the first three days. Adherence to the Infectious Diseases Society of America/American Thoracic Society guidelines for the management of community-acquired pneumonia has been shown to improve patient outcomes. Physicians should promote pneumococcal and influenza vaccination as a means to prevent community-acquired pneumonia and pneumococcal bacteremia.
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PMID:Diagnosis and management of community-acquired pneumonia in adults. 2166 12

Bariatric surgery is a rapidly expanding surgical speciality. A patient developed new onset shortness of breath and pleuritic chest pain post-laparoscopic gastric bypass surgery. Investigations were consistent with type 1 respiratory failure. Such patients are at high risk of venous thromboembolism. A clinical diagnosis of a pulmonary embolus was made. Treatment was initiated with therapeutic dose low-molecular weight heparin (LMWH)-enoxaparin. Subsequently she developed bleeding from the anastomotic sites. Subsequent investigations, including a CT pulmonary angiogram, diagnosed hospital-acquired pneumonia to which she has responded to antibiotic treatment. There is little in the published literature as to the successful treatment of pulmonary embolus in bariatric patients, and little about the potentially devastating bleeding from the anastomotic sites by treatment with LMWH.
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PMID:Diagnostic difficulty of pulmonary embolus in a bariatric patient and complication of therapeutic dose low-molecular weight heparin to the surgical anastomosis. 2168 6

Spontaneous bacterial empyema (SBEM) is infection of a preexisting pleural effusion without evidence of pneumonia. It has been reported mostly in patients with hepatic hydrothorax. Only 1 case of SBEM in a noncirrhotic patient has been reported. We present an unusual case of bilateral SBEM from Streptococcus pneumoniae bacteremia in a noncirrhotic patient. A 52-year-old man presented with bilateral pleuritic chest pain and dyspnea for 2 days. His medical history included congestive heart failure, hemodialysis-dependent renal failure and known bilateral pleural effusions. No ascites or hepatosplenomegaly was noticed. Bilateral pleural effusions were again present on physical examination and confirmed by a chest computed tomography scan. Cardiac medical treatment and hemodialysis failed to improve his condition. Bilateral thoracentesis revealed purulent pleural fluid that was culture-positive for Streptococcus pneumonia as were blood cultures. There was no clinical or radiographic evidence of pneumonia. The detailed clinical course, treatment and highlighted points are described.
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PMID:Spontaneous bacterial empyema in a noncirrhotic patient: an unusual scenario. 2182 62


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