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

Smoke inhalation injury is a complex of disease processes best understood and treated when defined in terms of the time period after injury. The early phase (0 to 36 hrs) is characterized by diagnosis and treatment of carbon monoxide and cyanide toxicity and by management of early airways edema, bronchorrhea, and bronchoconstriction with aggressive pulmonary toilet. Between 1 and 5 days, the major characteristic is airways mucosal slough, tracheobronchitis, and increasing lung water and impaired gas exchange. Pulmonary toilet and infection control, as well as close management of fluid shifts, is the major treatment. With onset of the inflammation-infection phase, the risk of nosocomial pneumonia increases markedly, as does the impairment in lung function as a result of marked increase in oxygen consumption and CO2 production. Nutrition, stress modification, avoidance of muscle fatigue, and control of infection are the key treatment modalities.
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PMID:Smoke inhalation injury. 792 21

A 22-year-old woman was hospitalized because of fever of 39 degrees C and increasing dyspnoea. The chest radiograph demonstrated coarse confluent opacities bilaterally. Despite antibiotic treatment the condition deteriorated acutely after 2 days. All efforts to find an infectious agent, including immunological tests, were unsuccessful. Artificial ventilation became necessary because of increasing respiratory failure with an arterial oxygen partial pressure of 56 mm Hg, CO2 of 41 mm Hg and a respiratory rate of 60/min. Histological examination of a transthoracic lung biopsy revealed bronchiolitis obliterans organizing pneumonia, which was treated with prednisolone. The initial dose was 500 mg/d, gradually reduced to 12.5 mg/d over 2 weeks. The clinical and radiological findings improved markedly after 2 days and the patient discharged herself after 3 weeks and there was no follow-up.
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PMID:[Bronchiolitis obliterans organizing pneumonia with acute respiratory insufficiency]. 792 29

Amyotrophic lateral sclerosis is a rapidly progressive disease of unknown etiology resulting in tetraparalysis, dysarthria, dysphagia, and ultimately death from respiratory insufficiency. In the course of the disease, recurrent episodes of aspiration, pneumonia, dehydration, and malnutrition may necessitate nasoenteral tube placement, an inconvenient and unattractive arrangement in patients with dribbling and impaired swallowing. A percutaneous endoscopic gastrostomy seemed a better, though potentially hazardous, alternative in view of the often severely restricted pulmonary function of these patients. Therefore, we prospectively investigated the use of percutaneous endoscopic gastrostomy in 68 consecutive patients with amyotrophic lateral sclerosis. Minimum required pulmonary function was defined as forced vital capacity (FVC) of 1 L or more and CO2 gas exchange capability as pCO2 of 45 mm Hg or less. The methodology of insertion was adapted to facilitate the early removal of gastric air. Fifty-five patients (median FVC, 1.7 L; pCO2, 40 mm Hg) were eligible for the gastrostomy procedure, and 13 patients (median FVC, 0.8 L; pCO2, 47 mm Hg) were not. Despite the fact that modification of the method of insertion rendered the procedure more difficult, the success rate was 89% (49/55); it was 96% (49/51) when failures related to distorted anatomy were excluded. The procedure-related mortality rate was 1.8% and the 24-hour in-hospital mortality rate was 3.6%, mainly related to respiratory insufficiency. The 30-day out-of-hospital mortality rate was 11.5%. Major complications (3.6%) consisted of a spontaneously draining cutaneous abscess in 2 cases. Peristomal redness was present in 6 cases, and 5 patients required analgesics for wound pain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Percutaneous endoscopic gastrostomy in patients with amyotrophic lateral sclerosis and impaired pulmonary function. 792 37

The LPS patterns of 231 H.p. strains were studied by using SDS-PAGE. The strains were isolated from the nasal mucous membrane of clinical healthy animals, from animals with GK and from animals with pneumonia without any symptoms of GK. The LPS patterns of H.p. strains consists of 2 to 4 bands of high electrophoretical mobility. In all it was possible to distinguish seven different LPS electrophoretic profiles. The distribution of the H.p. isolates from clinically healthy animals and animals with GK or pneumonia to the 7 LPS electrophoretic profiles shows a similar picture. Variation in the growth conditions showed a process of a standardization of the LPS structure as a result of an increased CO2 atmosphere or lack of O2 respectively.
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PMID:[The lipopolysaccharide structure of Haemophilus parasuis strains in SDS-PAGE]. 799 42

We review current concepts about the clinical manifestations, diagnosis and treatment of patients with bronchiolitis obliterans (BO) with emphasis on clinical/pathological correlations and recent developments. BO is a relatively rare disease, but its incidence is probably higher than generally believed and is continuously rising, partly because of better recognition, but also because of increased exposure to industrial fumes, and its occurrence in lung transplantation. BO is characterized histologically by varying degrees of obliteration of the lumen of the respiratory bronchioles by organizing connective tissue often extending into the alveoli ('proliferative' BO with organizing pneumonia--BOOP) or by more extensive fibrosis and scarring of the more proximal, conductive bronchioles ('constrictive' BO). Diverse clinical conditions have been associated with the development of BO, notably viral and mycoplasma infection, toxic fume exposure and immune reactions in the setting of a collagen vascular disease, drug reaction or organ transplantation. The clinical course and features of BO may vary considerably according to the aetiology, histological pattern and stage of the disease. The most common presentation is that of a progressive dry cough and dyspnea, associated with diffuse patchy interstitial lung infiltrates on chest X-ray. In the more advanced cases, lung function tests show either restrictive or obstructive defects, depending on the extent of alveolar involvement, and hypoxemia without CO2 retention. The diagnosis is often possible on clinical grounds, however, in a seriously ill patient uncertainty should be resolved by tissue diagnosis, preferably by open lung biopsy. Treatment is based on symptomatic therapy. The use of corticosteroids is controversial, but common. Patients with BOOP are exceptional, in that there may be no underlying condition ('idiopathic' BOOP or cryptogenic organizing pneumonia--COP), a restrictive ventilatory defect is usual and the response to corticosteroids often remarkable.
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PMID:Bronchiolitis obliterans--current concepts. 814 Feb 11

The principal function of the lung is to facilitate the exchange of the respiratory gases, oxygen (O2) and carbon dioxide (CO2). When the lung fails as a gas exchanger respiratory failure ensues. Clinically, it is generally accepted that an arterial oxygen tension (PaO2) of less than 60 mmHg or a PaCO2 of greater than 50 mmHg, or both, whilst breathing room air are values consistent with the concept of respiratory failure. This article will deal, firstly, with some basic aspects of the physiology of pulmonary gas exchange and more specifically on the measurement of ventilation-perfusion (VA/Q) relationships, the most influential factor determining hypoxaemia. The second part highlights the most important findings on pulmonary gas exchange in the adult respiratory distress syndrome (ARDS) and other common acute respiratory failure conditions, such as pneumonia, acute exacerbation of chronic obstructive pulmonary disease (COPD) and status asthmaticus, based on the data obtained by means of the multiple inert gas elimination approach, a technique which gives a detailed picture of VA/Q ratio distributions.
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PMID:Pulmonary gas exchange in acute respiratory failure. 814 14

Malnutrition is a serious threat to patients with neuromuscular disease and marginally-compensated respiratory muscle weakness. It causes atrophy of inspiratory muscles, further weakening them. It reduces respiratory drive, potentially aggravating respiratory failure, either directly or indirectly, by promoting atelectasis and pneumonia, and it contributes strongly to such patients' risk of infection, their most common cause of death. In treating such patients, it must be remembered that abrupt increases in nutritional support, particularly with high percentages of carbohydrates, will increase CO2 production, potentially worsening ventilatory failure. Certain selected neuromuscular disease patients benefit from specific nutritional treatments (carnitine for carnitine deficient patients, high-calorie diets for muscular dystrophy and acid-maltase deficiency). Finally, the amino acid, fat, and nucleic acid content of the diet affects the immune response in beneficial or harmful ways, that are just now being elucidate. The potential for useful nutritional interventions in patients with neuromuscular diseases has never looked better, but is not yet fully realized. The challenges for the future will be to work out the beneficial and harmful effects of the various nutrients in the various diseases, to find ways to rapidly identify patients who will benefit, and to determine the safest, least uncomfortable, and most effective methods of delivery of the required nutrients.
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PMID:Nutritional factors in the pathogenesis and therapy of respiratory insufficiency in neuromuscular diseases. 825 75

A 32-year-old woman in the 26th week of pregnancy became ill, 6 days after returning from a trip to Indonesia, with a fever up to 42 degrees C, haemolytic anaemia (haemoglobin 7.6 g/dl) and thrombocytopenia (7,000/microliters). She had not been on any malaria prophylaxis. Chloroquine, quinine and pyrimethamine, administered after macrogametocytes of Plasmodium falciparum had been found in the blood smear, eliminated the parasites from the peripheral blood, but respiratory failure and treatment-resistant pneumonia occurred, leading to the adult respiratory distress syndrome (Morel stage 4). Because of threatened intrauterine death (resulting from premature placental separation during artificial ventilation) the child was delivered by an emergency section. Despite extensive conventional therapeutic measures the mother's respiratory state progressively deteriorated so that extracorporeal membrane CO2 elimination was instituted on the 17th day. First signs of improvement in respiratory functions were noted after six days. The extracorporeal CO2 elimination was discontinued after twelve days, because artificial ventilation could now be adequately controlled. The woman was gradually weaned from the ventilator and discharged home without symptoms after a total of 11 weeks in hospital. Her child has not shown any neurological symptoms.
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PMID:[Acute respiratory failure in tropical malaria during pregnancy. Successful treatment using extracorporeal CO2 elimination]. 818 19

The intravascular oxygenator (IVOX) is a new device which is implanted in the vena cava sup. and inf. where it oxygenates the blood and removes CO2. We report on its successful use in a young patient with severe pneumonia. This 21-year-old female was admitted to hospital with acute respiratory distress due to pneumococcal pneumonia and sepsis following chickenpox. Considering the rapidly progressive course with severe hypoxia and shock, PaO2/PaCO2 values of 6.5/6.4 kPa on mechanical ventilation with an FiO2 of 1.0 and a PEEP of 13 mbar, we decided to implant an intravascular oxygenator. Besides rapid improvement of oxygenation, we observed remarkable recovery of cardiovascular function such as an increase in mean arterial pressure and mixed-venous saturation, while the dose of vasopressors could be decreased. The intravascular oxygenator was removed without problems after 29 days of continuous use, when pulmonary function allowed an FiO2 of 0.45. The patient was discharged from the intensive care unit after 99 days in a good neurological and stable cardiovascular state.
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PMID:[Hemodynamic improvement during therapy using the intravascular oxygenator (IVOX)]. 847 57

Myxedema coma is characterized by severe lack of thyroid hormones, unconsciousness and serious restriction of vital functions. The mortality rate still ranges between 50 and 80%. In patients with inapparent hypothyroidism myxedema coma occasionally follows surgery, anesthesia or severe infection. A case of myxedema coma following surgery is reported. CASE REPORT. A 46-year-old woman was anesthesized for hip replacement. The intraoperative cardiovascular situation was characterized by hypotension and tachycardia. On the first postoperative day, unexpectedly a cardiac arrest occurred. Resuscitation with high doses of epinephrine was successful. There was no evidence of myocardial infarction, hypoxia and pulmonary embolism as causative factors for cardiac arrest. A pulmonary artery catheter was inserted and showed low cardiac output. Catecholamines and intravascular fluids were administered without hemodynamic improvement. In the next 5 days pneumonia was followed by ARDS and acute renal failure. After successful treatment of these complications the patient remained in deep coma. An intracerebral disease could be excluded by computerized tomography. Evaluation showed low thyroid hormones (T3; T4) and elevated TSH. The diagnosis of a myxedema coma was assumed. After failure of oral therapy with L-thyroxine (0.025-0.05 mg/day) for 10 days, intravenous therapy with 0.5 mg L-thyroxine was performed. Thirty-six hours later the patient regained consciousness, without cardiac complications. The patient progressed uneventfully under oral therapy with 0.1 mg L-thyroxine and was discharged from the hospital 6 weeks later. DISCUSSION. Pathophysiology and symptomatology of a case of postoperative myxedema coma are described (Tables 1-4). In this patient, the following symptoms occurred: low thyroid hormones (T3; T4), elevated TSH, deep coma, decreased ventilatory response to CO2, diminished myocardial contractility under catecholamine stimulation, impaired renal water excretion. After failure of oral substitution of L-thyroxine, intravenous therapy had to be performed in spite of the high risk of further cardiac complications in this patient. This led to complete recovery with normal neuropsychological and cardiopulmonary parameters. CONCLUSION. Myxedema coma is a rare complication in postoperative care, but in cases of inexplicable unconsciousness thyroid failure should be excluded. If myxedema coma is evident, intravenous therapy with L-thyroxine should be performed under the conditions of extended monitoring.
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PMID:[Myxedema coma as a rare postoperative complication]. 848 Sep 6


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