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

In ten patients with idiopathic adult respiratory distress syndrome (ARDS) who had histopathologically diffuse alveolar damage (DAD), and who did not have specific underlying diseases, we compared the histopathological findings with their radiographic images in order to study the detail analysis of radiographic images and the clinical courses. These patients were roughly classified as having the interstitial pneumonia dominant type (type IP) of idiopathic ARDS, in which alveolar septal thickening, alveolitis, or both were the predominant histological findings and images showed increasing attenuation of lung fields with small honeycomb lung, or the organizing pneumonia dominant type (type OP), in which organizing exudate predominantly filled the alveoli histologically and images showed consolidation shadows with some air. Hyaline membrane was seen very frequently in patients with a short clinical course, and in accordance with a longer clinical course, widespread fibrosis and honeycomb lung covered by organizing hyaline membrane was seen with both types. Patients with type OP in whom collapse of the normal pulmonary structure was less and for whom changes on radiographic images were larger seemed to respond relatively favorably to steroid treatment, as judged from pulmonary function and radiographic images.
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PMID:Diagnostic imaging of idiopathic adult respiratory distress syndrome (ARDS)/diffuse alveolar damage (DAD) histopathological correlation with radiological imaging. 884 1

Pulmonary contusion is the most common injury identified in blunt chest trauma. Despite improvements in diagnostic imaging and critical care, the associated mortality has not appreciably changed over the last three decades. Parenchymal injury ultimately manifests as alveolar collapse and lung consolidation. Early detection and intervention toward minimizing injury progression provides the greatest chance for survival. Avoiding fluid overload, oxygen therapy, and a low threshold for mechanical ventilation are useful therapeutic guidelines. Complications include pneumonia and adult respiratory distress syndrome, which may occur in up to one half of all cases. Pulmonary contusion is a serious injury that may complicate patient management as well as pose a vital threat.
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PMID:Pulmonary contusion: a collective review. 889 9

To explore the pathophysiology of respiratory failure in an experimental pneumonia, a Pasteurella haemolytica broth culture was injected intratracheally into 12 calves, which were then studied over a period of 10 h. Measurements were made of inspired minute ventilation (VE), ventilatory pattern [inspiratory time (TI), expiratory time (TE), respiratory rate (RR) and tidal volume (VT)], transdiaphragmatic pressure (Pdi), occlusion pressure at the airway opening 100 milliseconds after onset of inspiration (Pawo100ms), arterial blood gas tensions and pH and recorded diaphragmatic electromyogram (EMGdi) and rectal temperature (Tr). On and after the third hour after inoculation, the animals varied in respect of clinical signs, Tr, RR, VE, Pawo100ms/EMGdi, and arterial gases and pH. In benign cases, diminished alertness, laboured respiration and fall of arterial oxygen pressure (PaO2) worsened up to 7 h after inoculation, but then progressively improved, VE being maintained at approximately 150% baseline throughout the study (10 h). Neither arterial carbon dioxide pressure (PaCO2) nor pH was altered. Moderate cases resembled benign cases in respect of laboured respiration, VE, PaO2 and PaCO2; however, pH was at first maintained at preinoculation levels, but declined thereafter. In severe cases, the animals were drowsy between hours 3 and 7, and became comatose between hours 8 and 10; in contrast to both benign and moderate cases: (1) RR was reduced by hour 5, (2) there was no trend towards recovery of PaO2 and pH, (3) VE, Pdi, Pawo100ms and Pawo100ms/EMGdi were severely decreased, and (4) PaCO2 increased. These results suggest that pneumonia does not alter ventilatory neuromuscular pump function in calves, unless concomitant cardiovascular collapse occurs. It is not clear whether fatal ventilatory failure is caused mainly by deterioration in ventilatory muscle fibre processes or structures, altered central nervous system adjustment of ventilatory timing, or cardiovascular dysfunction. However, inspiratory pressures fall when excitation to the diaphragm is still growing, which suggests peripheral respiratory muscle fatigue.
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PMID:The relation of ventilatory failure to pulmonary, respiratory muscle and central nervous system disturbances in calves with an experimentally produced pneumonia. 892 32

We present a case of acute lethal poisoning by oil of "epazote" (oil of chenopodium), in a 2 y 9 m female. The volatile oil was administered according to the advice of a "curandera" (female healer), in a total quantity of 40 ml. Clinical features of the poisoning were: vomiting, deep coma, seizures, mydriasis, apnea, metabolic acidosis, neurogenic shock and death. The EEG suggested a diffuse encephalopathy, the CT scan with an image of severe brain edema and ventricular collapse. Relevant postmortem findings were brain edema and neuronal necrosis, pneumonia, enteritis, pericholangitis, mild pancreatitis and tubular necrosis. The phytochemical analysis of volatile oil identified ascaridol, the main active compound of the chenopodium herbs, in a quantity of 39 mg/ml (1,560 mg in the dose administered), and Chenopodium graveolens as the plant employed to prepare it. According to the age of the patient, 60 mg of ascaridol would be the recommended dose formerly used in the treatment of parasitic disease. Thus 1,560 mg was 26 times higher than the recommended dose, and exceeded by 56% the dose of 1,000 mg reported as lethal in humans.
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PMID:[Fatal poisoning caused by oil of epazote, Chenopodium graveolens]. 896 84

We present a comparative histopathological study of both acute and chronic human adenovirus pneumonia, with reference to the cellular and extracellular matrix components. Seventeen lungs from autopsied patients whose ages ranged from 2 to 60 months were studied. Adenovirus types 1, 2, 3, 5, and 7 were isolated from 15 patients with acute lung disease, and types 2 and 7 were isolated from the other two patients with chronic pulmonary illness. The results indicated the occurrence of two basic patterns of adenovirus interstitial pneumonia (1) classic pattern (acute), characterized by necrosis and degeneration and many type II pneumocytes with intranuclear inclusion bodies, which were positive for adenovirus DNA by in situ hybridization, and (2) proliferative or proliferative-productive pattern (chronic), which presented with diffuse pulmonary fibrosis and the interstitial proliferation of fibroblast-like cells, compatible with myofibroblasts (positive for vimentin and alpha smooth muscle actin), and increase in collagen types I and III, elastic fibers, and proteoglycans. Alveolar collapse appears to be an important pathogenetic mechanism in the development of this pattern.
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PMID:Acute and chronic human adenovirus pneumonia: cellular and extracellular matrix components. 902 50

The epidemic spread of tuberculosis after World War II and the deficiency of appropriate antituberculotic drugs led to a renaissance of surgical procedure such as plombage thoracoplasty, initiated in 1891 by Tuffier. Especially in Germany the insertion of paraffin and polyethylene was used in order to achieve an extrapleural pneumothorax in order to collapse the tuberculous cavities in the upper lobes. Due to a high rate of early complications and the assumed cancerogenicity, in a considerable number of cases the material was removed soon after its deployment. In some cases with the filling remaining in place, 30-40 years later infections and/or neoplasms occurred. From 1985 to 1996 in two centers of thoracic surgery 13 patients underwent procedures for removal of filling material. The patients suffered from infections (n = 11), malignant lymphoma associated with infection of the plombage (n = 1) and bronchial carcinoma (n = 1). Technically, we performed the thoracoplasty described by Schede (n = 9). Schede's thoracoplasty in combination with a muscle flap repair (n = 1) or partial resection of the thoracic wall (n = 1), an empyemectomy (n = 1), and an en-bloc pleuropneumonectomy (n = 1). All patients suffered from multiple underlying diseases (COPD, coronary heart disease, diabetes mellitus). However, apart from beside two procedure related deaths (pulmonary embolism n = 1, pneumonia complicated by multi-organ failure n = 1) no other major complications were observed. The plombage material in the case of malignant lymphoma is probably carcinogenic in relation to the time of exposure and should be removed in all cases.
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PMID:[Delayed complications after extrapleural pneumonolysis for lung tuberculosis]. 941 Jun 83

This report details the first experimental production of clinical disease, mortality, and pathology resembling that of field infections by using Ornithobacterium rhinotracheale alone. Twenty-two-week-old male turkeys were exposed to O. rhinotracheale or lung homogenate from O. rhinotracheale-infected turkeys. Within 24 hr after inoculation, turkeys given O. rhinotracheale or lung homogenate intratracheally were depressed and coughing and had decreased feed intake. By 48 hr, several birds were coughing blood and ultimately died. Grossly, the lungs were reddened, wet, and heavy, failed to collapse, and were covered by tenacious tan-to-white exudate. Microscopically, the parabronchi and air capillaries were filled with fibrin, heterophils, macrophages, and small numbers of gram-negative bacteria. The pleura was often covered by a thick layer of fibrin, heterophils, and macrophages. Turkeys that survived to day 7 postinoculation had severe, subacute pneumonia. Ornithobacterium rhinotracheale was recovered from the lungs of most birds with pneumonia and was also cultured from the air sacs, sinuses, tracheas, spleens, and livers. All turkeys inoculated with O. rhinotracheale developed antibodies to O. rhinotracheale detectable by the serum plate agglutination test.
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PMID:Ornithobacterium rhinotracheale infection in turkeys: experimental reproduction of the disease. 953 93

A 29-y-old male attempted suicide with 3000 mg clozapine, 150 mg zopiclone, alprazolam and unknown quantities of alcohol. He was admitted in a deep hypotonic coma with respiratory depression, inhalation pneumonia and vascular collapse. Symptomatic treatment involved mechanical ventilation, vascular filling and antibiotics. The patient was discharged from the Intensive Care Unit 72 h after the suicide attempt with no sequelae. To detect and quantify clozapine in plasma, high-pressure liquid chromatography showed a 4 h absorption phase and a peak serum concentration of 5200 ng/ml. Three successive elimination t1/2 values of 38, 24 and 13 h were calculated.
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PMID:Non-fatal clozapine (LEPONEX) intoxication with toxicokinetic evaluation. 994 79

Children and young adults rarely present to the emergency department (ED) in cardiac arrest. This review examines published series on nontraumatic, cardiac arrest for patients aged 1 to 45 years and discusses the differential diagnosis for cardiovascular collapse. Among the most common entities encountered are cardiac diseases (hypertrophic cardiomyopathy, myocarditis), airway diseases (pneumonia, epiglottitis, and asthma), epilepsy, hemorrhage (gastrointestinal bleeding, ectopic pregnancy), and drug toxicity (tricyclic antidepressants, cocaine). ED management of children and young adults in cardiac arrest requires an understanding of the heterogeneous pathophysiologic mechanisms and etiologies leading to cardiopulmonary dysfunction in these patients. The emergency physician should give particular focus to airway management for toddlers and preadolescents, because respiratory diseases predominate. When treating an adolescent or young adult, the resuscitation team should also consider toxic causes as well as occult hemorrhage. Management considerations unique to this patient population are discussed.
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PMID:The etiology of cardiac arrest in children and young adults: special considerations for ED management. 1033 87

Pulmonary surfactant is a complex and highly surface active material composed of lipids and proteins which is found in the fluid lining the alveolar surface of the lungs. Surfactant prevents alveolar collapse at low lung volume, and preserves bronchiolar patency during normal and forced respiration (biophysical functions). In addition, it is involved in the protection of the lungs from injuries and infections caused by inhaled particles and micro-organisms (immunological, non-biophysical functions). Pulmonary surfactant can only be harvested by lavage procedures, which may disrupt its pre-existing biophysical and biochemical micro-organization. These limitations must always be considered when interpreting ex vivo studies of pulmonary surfactant. A pathophysiological role for surfactant was first appreciated in premature infants with respiratory distress syndrome and hyaline membrane disease, a condition which is nowadays routinely treated with exogenous surfactant replacement. Biochemical surfactant abnormalities of varying degrees have been described in obstructive lung diseases (asthma, bronchiolitis, chronic obstructive pulmonary disease, and following lung transplantation), infectious and suppurative lung diseases (cystic fibrosis, pneumonia, and human immunodeficiency virus), adult respiratory distress syndrome, pulmonary oedema, other diseases specific to infants (chronic lung disease of prematurity, and surfactant protein-B deficiency), interstitial lung diseases (sarcoidosis, idiopathic pulmonary fibrosis, and hypersensitivity pneumonitis), pulmonary alveolar proteinosis, following cardiopulmonary bypass, and in smokers. For some pulmonary conditions surfactant replacement therapy is on the horizon, but for the majority much more needs to be learnt about the pathophysiological role the observed surfactant abnormalities may have.
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PMID:Pulmonary surfactant in health and human lung diseases: state of the art. 1044 27


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