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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twelve cases of severe altitude illness are reported in which the neurological signs and symptoms dominated the clinical picture. Pulmonary oedema, retinal haemorrhage, thrombophlebitis and pulmonary embolism, bronchopneumonia, and coronary-artery disease were also present in several of the patients but the primary problem seems to have been cerebral oedema. Other published cases support this impression. Patients who were returned to low altitude early in the disease fared well; two patients died, and in both cases evacuation had been delayed. The most effective prevention lies in slow ascent, though in one case reported here the rate of climb was well within the recommended limit. Recommended management is rapid descent to low altitude at earliest indication of cerebral or pulmonary oedema, intravenous dexamethasone or betamethasone in large doses, hydration, diuresis (frusemide has been most used), and perhaps other intravenous therapy with hyperosmolar materials such as mannitol, urea, 50% saline, or 50% sucrose. Prognosis is good if descent and treatment are started early, but permanent damage may be anticipated if the patient is unconscious for any prolonged period before descent.
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PMID:Cerebral form of high-altitude illness. 5 82

The authors report 6 cases of acute respiratory failure complicating chronic bronchial and lung disease admitted to hospital with the diagnosis of: heart disease, 3 cases, pulmonary oedema, pulmonary embolism, atrial flutter; status asthmaticus : one case; neuro-psychiatric disease : 2 cases (toxic coma and agitation). The authors emphasize the frequency of chronic bronchial disease and recall the signs of acute decompensation discussing the possible difficulties in diagnosis and the therapeutic implications.
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PMID:[Deceptive and revealing clinical forms of acute respiratory insufficience in chronic bronchopneumopathies]. 19 94

We have recently described a new method for measuring distributions of ventilation-perfusion ratios (VA/Q) based on inert gas elimination. Here we report the initial application of the method in normal dogs and in dogs with pulmonary embolism, pulmonary edema, and pneumonia. Characteristic distributions appropriate to the known effects of each lesion were observed. Comparison with traditional indices of gas exchange revealed that the arterial PO2 calculated from the distributions agreed well with measured values, as did the shunts indicated by the method and by the arterial PO2 while breathing 100 per cent 02. Also the Bohr dead space closely matched the dispersion of ventilation in realtion to VA/Q. Assumptions made in the method were critically evaluated and appear justified. These include the existence of a steady state of gas exchange, an alveolar-end-capillary diffusion equilibration, and the fact that all of the observered VA/Q inequality occurs between gas exchange units in parallel. However, theoretical analysis suggests that the method can detect failure of diffusion equilbration across the blood-gas barrier should it exist. These results suggest that the method is well-suited to clinical investigation of patients with pulmonary disease.
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PMID:Distribution of ventilation-perfusion ratios in dogs with normal and abnormal lungs. 23 70

The spectrum of pulmonary complications in 28 of 66 burn victims is analyzed according to time of onset and resultant radiographic features. Immediately recognizable pulmonary abnormalities are usually due to chemical pulmonary edema and inhalation pneumonitis. Complications manifested 2-5 days after injury include pulmonary microembolism, adult respiratory distress syndrome, and atelectasis. Delayed complications are major pulmonary embolism, pneumonia, and adult respiratory distress syndrome. In this series, 25 patients (89%) developing pulmonary complications died. The critical role of serial chest radiographs in the evaluation and management of burn victims is emphasized.
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PMID:The radiographic spectrum of pulmonary complications in burn victims. 40 38

The effects of acute pulmonary hypertension on the fraction of cardiac output shunted through pulmonary arteriovenous communications have been studied in dogs as a possible cause of hypoxia following pulmonary embolization. Pulmonary artery pressure was increased twofold and then fourfold above control values by embolization of the pulmonary vascular bed with polystyrene microspheres. Quantitative measurements of arteriovenous shunt were determined from the fraction of 50 mu radioactively labeled microspheres injected into the inferior vena cava which passed through the pulmonary circulation into systemic vascular beds. There was no increase in the fraction of pulmonary blood flow passing through pulmonary arteriovenous connections, 50 mu in diameter or greater, with pulmonary microembolism when FIo2 was 1. There was a small increase in arteriovenous shunt fraction when pulmonary artery pressure was increased with an FIo2 of 0.21. Physiological shunt measured by the oxygen technique did not increase with pulmonary embolism, but total venous admixture rose significantly. Postmortem gravimetric measurements of lung water indicated pulmonary edema. We conclude that anatomic arteriovenous shunt channels have little physiological significance after pulmonary microembolism in the dog lung. The major cause of hypoxia immediately after pulmonary microembolism is ventilation/perfusion imbalance, probably caused by pulmonary edema.
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PMID:Effect of pulmonary microembolism on arteriovenous shunt flow. 70 53

In a retrospective study, the P-terminal force in Lead V1 (PTF-V1) was measured in three groups, each of 35 patients, with the respective diagnoses of acute myocardial infarction without pulmonary edema, acute pulmonary embolism, and acute pulmonary edema. In all but one of the patients with acute pulmonary edema, a highly negative PTF-V1 value was obtained, whereas by contrast, all the patients with pulmonary embolism had normal PTF-V1 values. Four of the patients with acute myocardial infarction had abnormal PTF-V1 values, although at the time there was no clinical or radiologic evidence of pulmonary edema. However, one of these patients did develop acute pulmonary edema a few hours later. Measurement of the PTF-V1 is a simple noninvasive test that may, therefore, be useful in separating patients with acute pulmonary embolism from those with acute or impending pulmonary edema.
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PMID:P-wave analysis in myocardial infarction, pulmonary edema, and embolism. 111 59

A young, pregnant woman with angiographically proved pulmonary emboli developed pulmonary edema and wheezing without evidence of left ventricular failure. This cast study points out the unusual association of pulmonary embolism with pulmonary edema, wheezing, and hyper-reactive airways in a patient with a positive family history of allergy, but no antecedent history of bronchospasm. Mechanisms for the occurrence of noncardiogenic pulmonary edema and wheezing after pulmonary embolism are reviewed.
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PMID:Pulmonary edema and wheezing after pulmonary embolism. 116 36

In this neuropathologic study of 41 cases diagnosed as status epilepticus (SE) over a 10-year period at the University College Hospital, Ibadan (UCH), we found that the commonest cause was infection of the central nervous system (17 cases). The other aetiologic factors were: metabolic derrangement/toxic (14 cases) and cerebrovascular disease which was the most frequent cause in subjects above 12 years of age. It was encountered in 6 cases. Space occupying lesions which involved the frontal lobes were found in 4 cases. The conditions associated with the disease at death were: cerebral oedema, pulmonary oedema; pulmonary consolidation and pulmonary embolism. Our findings highlight the importance of looking for treatable conditions in patients presenting with this grave condition in this environment.
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PMID:Aetiology of status epilepticus in Ibadan: a neuropathologic study. 130 89

Several respiratory complications have been described in patients with ulcerative colitis (UC), and are the subject of this review. Involvement of the bronchial tree is the most frequent of them. Chronic bronchitis (16 patients) and bilateral bronchiectasis (16 patients) are responsible for chronic disabling bronchial suppuration. Symptoms related to the bronchial disease most often develop in patients in whom the diagnosis of ulcerative colitis is already established (88% of cases). Occurrence before the diagnosis of UC is possible, but unusual. Bronchial involvement can develop in patients whose UC is in complete remission, or who have undergone coloproctectomy up to several years earlier. Impressive improvement of cough and sputum production commonly occur following inhaled steroids. This is of great diagnostic and therapeutic significance. Other complications include subacute asphyxiating tracheal obstruction due to intralumenal inflammatory overgrowth (1 patient), small airways disease and panbronchiolitis (2 patients), BOOP (4 patients), pulmonary angiitis (6 patients), desquamative interstitial pneumonitis and granulomatosis (2 and 3 patients respectively), biapical pulmonary infiltrates (2 patients) and serositis. In addition, UC patients can develop less specific pulmonary problems such as pulmonary edema, pulmonary embolism and sulfasalazopyridine-induced pneumonitis and fibrosis.
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PMID:[Respiratory manifestations of hemorrhagic rectocolitis]. 176 14

Common intracranial complications following head injury are meningitis, usually associated with a basilar skull fracture or open-depressed skull fracture; delayed hematoma; hydrocephalus; and vascular injuries. Prophylactic antibiotics are not recommended for the management of basilar skull fractures. The best means of preventing infection from open-depressed skull fractures is operative debridement and thorough irrigation, though recent evidence suggests that select cases can be safely managed without operation. Serial CT scans should be obtained in severely head-injured patients to identify delayed hematomas. CT and MRI scans obtained several weeks or months after severe head injury frequently reveal enlarged ventricles, though only a small percentage of these patients have clinical hydrocephalus. Those that do, often benefit from a shunt. Vascular injuries frequently are not detected until ischemic symptoms develop hours or days after the injury. Recommended treatment for intimal tears or dissection is full anticoagulation, but in those with cerebral contusions or other intracranial lesions, this may present an unacceptable risk for intracranial hemorrhage. Pulmonary infections frequently occur following head injury, and can be associated with admission to the ICU and intubation. A large percentage of these infections are caused by enteric gram-negative organisms, and aggressive treatment with appropriate antibiotics is necessary. Aspiration of gastric contents is common in head-injured patients and is frequently complicated by bacterial superinfection. The routine use of antacids and H2 blocking agents leads to bacterial colonization of the stomach with anaerobes and gram-negative aerobes. Thus, empiric therapy for aspiration pneumonia should include clindamycin. Sinusitis is a frequent cause of fever and leukocytosis in patients with nasotracheal or nasogastric tubes in place for several days and often subsides spontaneously with removal of the tubes. Pulmonary edema is often caused by excessive fluid administration during resuscitation of these patients, and can be avoided by monitoring central venous pressures. Pulmonary edema may also be caused by ARDS, excessive catecholamine release, or primary cardiac failure. Most of these patients will benefit from early intubation and PEEP. Pulmonary emboli most often originate from deep venous thrombi, and there is increasing evidence that prophylaxis with low-dose heparin and pulsating boots can significantly reduce the incidence of both complications. Erosive gastritis is found in the majority of severely head-injured patients and may be due to ischemia of the gastric mucosa as well as gastric hyperacidity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Complications of head injury and their therapy. 182 50


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