Complicaciones pulmonares de la neumonía química: A propósito de un caso / Pulmonary complications of chemical pneumonía; a case report

La aspiración de hidrocarburos puede causar un daño significativo a los pulmones al inducir una respuesta inflamatoria, alveolitis exudativa hemorrágica y pérdida de la función del tensioactivo pulmonar. El efecto secundario más grave de la aspiración de hidrocarburos es la neumonía por aspiración. Anteriormente se han notificado casos de neumotórax, neumatocele, síndrome de dificultad respiratoria aguda (SDRA), absceso pulmonar, fístula broncopleural, derrame pleural bilateral hemorrágico y pioneumotórax. En este artículo presentamos el caso de un paciente hospitalizado debido a neumonía por aspiración que desarrolló pleuritis y neumotórax después de ingerir disolvente para pintura. Se presenta este caso ya que raramente se ha informado en niños como causa de complicaciones pulmonares diferentes. Es necesario evaluar integralmente a los pacientes con complicaciones asociadas a la intoxicación por hidrocarburos. Debe evitarse el alta hospitalaria temprana de los pacientes, quienes deben ser controlados durante, al menos, 48 horas, aunque no tengan síntomas respiratorios. Debe considerarse que los pacientes con neumonía química pueden tener complicaciones pulmonares graves.

Hydrocarbon aspiration (HA) can cause significant lung disease by inducing an inflammatory response, hemorrhagic exudative alveolitis, and loss of surfactant function. The most serious side effect of HA is aspiration pneumonia. Pneumothorax, pneumatocele, acute respiratory distress syndrome (ARDS), pulmonary abscess, bronchopleural fistula, bilateral hemorrhagic pleural effusion and pyopneumothorax were previously reported. Hereby we report a patient hospitalized due to aspiration pneumonia who developed pleurisy and pneumothorax after drinking paint thinner. It is presented as it was seldom reported in children to cause distinct pulmonary complications. Patients with complaints associated withhydrocarbon poisoning must be fully evaluated. They must not be discharged from the hospital early and must be followed for at least 48 hours even if they don't have respiratory symptoms. It should be kept in mind that severe pulmonary complications can develop in patients with chemical pneumonia.

Utility of adenosine deaminase (ADA), PCR & thoracoscopy in differentiating tuberculous & non-tuberculous pleural effusion complicating chronic kidney disease.

Background & objectives: Pleural effusion is a common occurrence in patients with late-stage chronic kidney disease (CKD). In developing countries, many effusions remain undiagnosed after pleural fluid analysis (PFA) and patients are empirically treated with antitubercular therapy. The aim of this study was to evaluate the role of adenosine deaminase (ADA), nucleic acid amplification tests (NAAT) and medical thoracoscopy in distinguishing tubercular and non-tubercular aetiologies in exudative pleural effusions complicating CKD. Methods: Consecutive stage 4 and 5 CKD patients with pleural effusions underwent PFA including ADA and PCR [65 kDa gene; multiplex (IS6110, protein antigen b, MPB64)]. Patients with exudative pleural effusion undiagnosed after PFA underwent medical thoracoscopy. Results: All 107 patients underwent thoracocentesis with 45 and 62 patients diagnosed as transudative and exudative pleural effusions, respectively. Twenty six of the 62 patients underwent medical thoracoscopy. Tuberculous pleurisy was diagnosed in six while uraemic pleuritis was diagnosed in 20 subjects. The sensitivity and specificity of pleural fluid ADA, 65 kDa gene PCR, and multiplex PCR were 66.7 and 90 per cent, 100 and 50 per cent, and 100 and 100 per cent, respectively. Thoracoscopy was associated with five complications in three patients. Interpretation & conclusions: Uraemia remains the most common cause of pleural effusion in CKD even in high TB prevalence country. Multiplex PCR and thoracoscopy are useful investigations in the diagnostic work-up of pleural effusions complicating CKD while the sensitivity and/or specificity of ADA and 65 kDa gene PCR is poor.

Familial Infestation of Paragonimus westermani with Peritonitis and Pleurisy / 대한소화기학회지

Human paragonimiasis was endemic in Korea until the 1960's, and nowadays, the prevalence is decreasing. However, it is still one of the important helminthic diseases. Though it is essentially a pulmonary disorder, it may involve brain, muscle, mesentery, genital tract, pleura, peritoneum, spinal cord, spleen, and liver. We experienced two cases of paragonimiasis in a family who had ingested raw crabs together for 7 months. A 57-year-old female patient was admitted due to abdominal pain, diarrhea and tenesmus for 6 months. And, her 35-year-old son complained of cough, chest discomfort and dyspnea. The definite diagnosis for paragonimiasis could be made by the detection of the egg and adult worm from stool, sputum and involved lesion. Neither an egg or worm was detected. However, they were diagnosed based on the food history, laboratory data including serum eosinophilia, ELISA for specific IgG, pleural and peritoneal fluid examination, radiological findings, and intradermal tests. They were treated with praziquantel and their symptoms improved rapidly over 2 days. Both patients were asympromatic at a follow-up visit 2 months later.

Disseminated paracoccidioidomycosis with peripleuritis in an AIDS patient

La paracoccidioidomicosis es una de las micosis sistémicas endémicas más frecuentes de Latinoamérica, causada por un hongo dimorfo. En los pacientes con SIDA se presenta como una enfermedad grave y diseminada, con un amplio espectro de manifestaciones clínicas. Los niveles de linfocitos T CD4 + son habitualmente < de 200 cél/&181;L. Presentamos un caso de paracoccidioidomicosis diseminada con peripleuritis y abscesos subcutáneos sobre la pared torácica como manifestación inicial del SIDA. En países endémicos, la paracoccidioidomicosis debe incluirse como una complicación oportunista de los pacientes con SIDA.