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Query: UMLS:C0476273 (respiratory distress)
 19,632 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The involvement of the pulmonary vessels by tumour emboli may lead to a clinical picture defined as 'subacute cor pulmonale'. Information about this syndrome has been limited to case reports and a few series. A study of 214 autopsied cancer patients was undertaken to investigate the clinical signs and symptoms of tumour involvement of the pulmonary vessels (TIPV). The lungs were removed as a block and 15 sections (3 from each lobe) were analyzed. Clinical data about right ventricular failure, dyspnoea, cough, pleuritic chest pain, cyanosis, engorgement of jugular veins, peripheral oedema, haemoptysis and haemoptoic sputum were obtained from the medical records of each patient. Tumour emboli were detected in 89 cases, and no respiratory symptoms were recorded in 39. The presence of dyspnoea and cyanosis were highly significant in the group with TIVP, and right ventricular failure and peripheral oedema showed slight significant differences between the patients with and without TIPV. The classical picture of subacute cor pulmonale was observed in 13 patients and TIPV was considered to be the main cause of death in 29 cases. Our results indicate that although the development of subacute cor pulmonale was rare in patients with cancer, TIPV may be suspected when the patient presents respiratory distress and should be included in the differential diagnosis of dyspnoea in cancer patients.
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PMID:Clinical aspects of tumour involvement of the pulmonary vessels. 141 97

The case of a 19-year-old white female who presented with marked respiratory distress and pleuritic chest pain following freebased cocaine smoking is presented. A ventilation-perfusion scan revealed radioactive aerosol trapping in the large airways with multiple ventilation defects of the small airways, a finding compatible with reactive airway disease of the large airways and concomitant mucous plugging of the small airways. Freebased cocaine, impurities of the freebasing process, or admixtures to the freebased cocaine provided prior to smoking, are proposed as possible etiologies in what appears to be a condition of environmentally induced reactive airway disease, a previously unreported effect of cocaine use.
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PMID:Freebased cocaine smoking and reactive airway disease. 266 70

Three cases of primary pulmonary rhabdomyosarcoma in adults are presented. The patients were all men between the ages of 57 and 78 yr (mean 67.5). All patients presented with symptoms referable to their tumors, including cough, shortness of breath, pleuritic chest pain, and weight loss. In one patient, a history of tobacco and alcohol abuse was obtained. Anatomically, two tumors were located in the left upper lobe and one in the left lower lobe. Grossly, the tumors ranged in size from 6 to 11.5 cm and were tan-gray, firm masses with areas of necrosis and hemorrhage. Histologically, the tumors were characterized by a spindle cell proliferation admixed with areas showing a pleomorphic cell population with numerous rhabdomyoblasts and areas of hemorrhage and necrosis. Immunohistochemically, all three tumors showed strong positivity with desmin and myoglobin antibodies and negative staining with antibodies against keratin, epithelial membrane antigen, and S-100 protein. All patients had a fatal outcome. Two patients died a few days after admission with respiratory distress; the third one died 2 years after diagnosis with widely metastatic disease. Autopsy findings in all cases disclosed disseminated metastases to multiple abdominal and thoracic organs. Primary pulmonary rhabdomyosarcoma should be considered in the differential diagnosis of poorly differentiated pulmonary neoplasms in adults and should be distinguished from other primary and metastatic sarcomas.
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PMID:Primary pulmonary rhabdomyosarcomas: a clinicopathologic and immunohistochemical study of three cases. 853 1

A 57-year-old man experienced sudden onset of pleuritic chest pain and respiratory distress 10 days after undergoing four-vessel coronary artery bypass grafting (CABG). The surgery was performed after cardiac catheterization had shown right coronary artery dominance and the presence of lesions occluding 40% of the mid right coronary artery, 20% of the left main coronary artery, and 99% of the lower left anterior descending artery and its first diagonal branch. The patient had initially presented with acute dyspnea following an episode of crushing, nonradiating pain in the left chest and was diagnosed as having a non-Q-wave myocardial infarction after cardiac enzyme testing. His hospital course before and immediately after CABG was uneventful. The first sign of difficulty was detected one week after surgery, on day 17. An echocardiogram showed a small pericardial effusion, moderate to severe concentric thickening of the left ventricle, a left ventricular ejection fraction of 0.60 (normal, 0.67 +/- 0.08), normal valves, and normal segmental wall motion. The pleural chest pains began two days later, on day 19.
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PMID:Complication after arterial bypass grafting. 979 41

Reported here is a case of Bacillus cereus pneumonia that occurred in a patient with acute lymphoblastic leukemia. The presentation was severe, essentially marked by respiratory distress and pleuritic chest pain. Classic empirical treatment initiated for febrile neutropenia did not cover this rare pathogen and appropriate therapy was therefore delayed. B. cereus is most often a culture contaminant, but it can also be responsible for self-limited gastrointestinal intoxication and, more rarely, severe systemic diseases. Virulence in the case of systemic disease is attributed to tissue necrosis mediated by toxin release. B. cereus pneumonia, as described in the English-language literature, mainly affects immunocompromised patients and most often has a fatal outcome. Thus, the identification of B. cereus in clinical specimens of severely ill immunocompromised patients should lead physicians to question its clinical significance.
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PMID:Bacillus cereus pneumonia in a patient with acute lymphoblastic leukemia. 1530 Apr 57

Rituximab, a humanized monoclonal antibody approved for malignant lymphoma, is being increasingly, effectively, and safely used for immune thrombocytopenic purpura (ITP) and other humoral autoimmune disorders. We report the case of a 43-year-old man with ITP refractory to steroids and intravenous immunoglobulin who developed acute respiratory distress syndrome (ARDS) after a single infusion of rituximab. Dyspnea, hypoxemia, and pleuritic chest pain occurred within 24 hours of rituximab administration, and there was no other apparent explanation. Progressive hypoxemia mandated endotracheal intubation 1 week after rituximab administration and led to death 4 weeks after admission. ARDS has been associated with the administration of other monoclonal antibodies, such as infliximab, gemtuzumab ozogamicin, and OKT3 and is believed to be directly mediated by release of proinflammatory cytokines. ARDS is rarely associated with rituximab infusion for lympho-proliferative disorders, but it should be considered by those administering rituximab, especially when a patient develops severe pulmonary symptoms soon after infusion.
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PMID:Acute respiratory distress syndrome after rituximab infusion. 1629 24

A previously healthy 29-year-old male presented to the emergency department with pleuritic chest pain, nonproductive cough, and dyspnea. He was treated empirically for community acquired pneumonia and discharged to home. Two days later, the patient presented with respiratory distress along with neutrophilia, thrombocytopenia, elevated liver function tests, and hemoconcentration. Radiographs of his chest showed bilateral lung infiltrates and pleural effusions. He was admitted to the hospital and developed cardiopulmonary failure and died the following day. Serologic tests for hantavirus pulmonary syndrome confirmed the diagnosis.
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PMID:Case report of hantavirus pulmonary syndrome and review. 1769 39

The objective of the present paper is to describe the clinical and computed tomography features of 'explosive pleuritis', an entity first named by Braman and Donat in 1986, and to propose a case definition. A case report of a previously healthy, 45-year-old man admitted to hospital with acute onset pleuritic chest pain is presented. The patient arrived at the emergency room at 15:00 in mild respiratory distress; the initial chest x-ray revealed a small right lower lobe effusion. The subsequent clinical course in hospital was dramatic. Within 18 h of admission, he developed severe respiratory distress with oxygen desaturation to 83% on room air and dullness of the right lung field. A repeat chest x-ray, taken the morning after admission, revealed complete opacification of the right hemithorax. A computed tomography scan of the thorax demonstrated a massive pleural effusion with compression of pulmonary tissue and mediastinal shift. Pleural fluid biochemical analysis revealed the following concentrations: glucose 3.5 mmol/L, lactate dehydrogenase 1550 U/L, protein 56.98 g/L, amylase 68 U/L and white blood cell count 600 cells/mL. The pleural fluid cultures demonstrated light growth of coagulase-negative staphylococcus and viridans streptococcus, and very light growth of Candida albicans. Cytology was negative for malignant cells. Thoracotomy was performed, which demonstrated a loculated parapneumonic effusion that required decortication. The patient responded favourably to the empirical administration of intravenous levofloxacin and ceftriaxone, and conservative surgical methods in the management of the empyema. This report also discusses the patient's rapidly progressing pleural effusion and offers a potential case definition for explosive pleuritis. Explosive pleuritis is a medical emergency defined by the rapid development of a pleural effusion involving more than 90% of the hemithorax over 24 h, which causes compression of pulmonary tissue and mediastinal shift to the contralateral side.
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PMID:Explosive pleuritis. 1815 25

An elderly gentleman presented with acute dyspnoea and right-sided pleuritic chest pain. Two-weeks previously an oesophageal stent had been inserted for dysphagia secondary to oesophageal carcinoma. With low PaO(2), a neutrophilic leucocytosis, raised inflammatory markers and a right-sided pleural effusion, antibiotics were prescribed for pneumonia. Computed tomographic pulmonary angiogram (CTPA) ruled out pulmonary embolus. The patient rallied transiently and his effusion improved. His respiratory distress returned 14 days later. A chest x-ray revealed a right-sided hydropneumothorax, and a chest drain-released stomach contents from the pleural cavity. A gastrografin swallow and endoscopy demonstrated malignant oesophageal rupture. An attempt to re-stent failed, and the patient returned to the ward for palliation. His initial presentation was likely that of an oesophageal leak, and not pneumonia. Oesophageal rupture is difficult to diagnose due to ambiguous signs, symptoms and radiological findings. Swift diagnosis significantly improves the outcome, therefore clinicians presented with similar cases should consider the diagnosis early.
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PMID:Oesophageal rupture: a tough diagnosis to swallow. 2329 21

A sinus of Valsalva aneurysm is a dilatation of the aortic wall caused by the lack of continuity between the middle layer of the aortic wall and the aortic valve. It has an incidence of <0.1%. The most common cause of a sinus of Valsalva aneurysms is congenital, although they may also be acquired. The most common complication is rupture into the right atrium or ventricle, with rupture into the left chambers occurring very rarely. We present a 40-year-old man admitted to the hospital with an acute onset of respiratory distress and pleuritic chest pain. Transthoracic echocardiography followed by transesophageal echocardiography showed rupture of a noncoronary aneurysm of Valsalva sinus into the left atrium. The jet from the fistula caused retrograde flow into the pulmonary veins.
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PMID:Rupture of a noncoronary sinus of Valsalva aneurysm into the left atrium: a rare cause of acute pulmonary edema. 2400 88


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