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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Their frequency is estimated with difficulty, although on autopsy pulmonary edema is found almost routinely. It is a major complication of overdoses (48 p. 100 of severe intoxications). Their formation can be suspected, when after the first phase of respiratory depressions, with coma, myosis, and a variable latent period, a second attack of respiratory insufficiency occurs with tachypnea, and cyanosis. The chest X-ray shows diffuse alveolar infiltration, sparing the apices. The heart being generally of normal size. Rapid disappearance of this infiltrate (24 to 48 hours) enables the elimination of two diagnoses: pneumonia due to inhalation of gastric fluid, an infectious pneumonia. Their pathogenesis remains very debatable: - in the majority of cases abrupt L.V.F. can be eliminated: -on the other hand it could be an allergic accident of the anaphylactic type, or local liberation of histamine, or a local toxic action on the pulmonary capillaries; - hypoxia, secondary to respiratory depression, could lead to pulmonary edema, by the same mechanism as at altitude; - finally, owing to the central neurological disorders a neurogenic theory can be put forward. Their treatment is essentially a combination of Nalorphine with oxygen therapy (by mask, or if necessary by assisted, controlled ventilation) with prevention of inhalation of gastric fluid (gastric emptying) or curative treatment of possible aspiration by antibiotics, and cortico-steroids. Diuretics can be useful, as well as cardiotonics.
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PMID:[Pulmonary edemas due to acute heroin poisoning]. 0 75

Mendelson's syndrome is discussed with a review of the literature and presentation of 27 personal cases studies. Accidental aspiration of gastric fluid occurs primarily during anesthesia, in cranial trauma victims, and in toxic coma patients. Tissue damage is proportional to the acidity and the quantity of aspirated fluid. The initial clinical manifestations are often serious, sometimes leading to acute respiratory distress syndrom with pulmonary edema. Frequent infectious complications, often with anaerobic microbes, are deciding factors in the prognosis. Artificial ventilation with positive pressure (sometimes continuous) is often necessary. Administration of corticosteroids at high doses is likely favorable. Prophylactic administration of antibiotics is initially directed against anaerobic agents. The prevention of this serious syndrome should be a primary concern of anesthesiologists and physicians treating comatous patients.
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PMID:[Mendelson's syndrome]. 2 27

The workforce of Alberta, a province rich in fossil fuel, faces an increasing risk of exposure to hydrogen sulfide (H2S). Basic knowledge of the population exposed during the years 1969 to 1973 inclusive was accumulated to identify the immediate medical and management problems. Data were recorded from three sources of records: the Workers' Compensation Board of Alberta, the Alberta Hospital Services Commission and the provincial coroner's office. There were 221 cases of exposure to H2S. The overall mortality was 6%; 5% of victims were dead on arrival at hospital. Admission to hospital was required for 65% of the victims arriving at a hospital emergency room (78% of the 221). Acute problems were coma, dysequilibrium and respiratory insufficiency with pulmonary edema. Increased attention to cardiopulmonary resuscitation at the exposure site and during transportation to hospital is necessary to reduce the mortality from H2S exposure. No long-term adverse effects were apparent in the survivors.
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PMID:Hydrogen sulfide poisoning: review of 5 years' experience. 14 53

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

Hypoxic pulmonary disorders and head injuries associated with increased intracranial pressure (ICP) frequently co-exist. Positive end-expiratory pressure (PEEP) improves hypoxemia but has been reported to impede cerebral venous return, potentially causing a further increase in ICP. This study examined the effects of PEEP on ICP at different levels of brain compliance. continuous ICP recordings were obtained after insertion of Scott cannulas to the lateral ventricles of seven comatose patients. Brain compliance was assessed by calculation of the pressure volume index. Patients were maintained in a 30 degrees head-up position. Maintenance of PEEP to levels of 40 cm H2O pressure for as long as 18 hours did not increase ICP in patients with either normal or low intracranial compliance, and did not increase ICP in the absence of pulmonary disease. Central venous pressure and pulmonary artery wedge pressure increased proportionately as PEEP was increased. No consistent changes were found in blood pressure recordings, nor were there any reductions in cardiac output found during the studies. Abrupt discontinuation of PEEP did not result in increased ICP except for a transient rise on two occasions when respiratory secretions became copious and the patients were inadequately ventilated. Improved oxygenation in two patients as a result of PEEP was concomitant with improved intracranial compliance and neurological status. In patients with brain injuries, PEEP improves arterial oxygenation without increasing ICP as previously supposed. Consequently, PEEP is a valuable form of therapy for the comatose patient with pulmonary disorders such as pneumonia or pulmonary edema.
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PMID:Effects of positive end-expiratory pressure on intracranial pressure and compliance in brain-injured patients. 32 31

A rhesus monkey (Macaca mulatta), accidentally exposed to vapors of methyl methacrylate for 22 hours was found in a comatose condition. Attempts to revive the animal were unsuccessful. Necropsy revealed a diffusely mottled liver, pulmonary edema, and atelectasis. The thoracic cavities each contained 30 ml of clear yellow fluid. Histopathologic review of the tissues showed central lobular liver necrosis, pulmonary edema, pulmonary emphysema, and atelectasis. Analysis of a blood sample obtained from the monkey 1.5 hours prior to death showed a normal hemogram, but elevated values for serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, lactate dehydrogenase, phosphohexose isomerase, blood urea nitrogen, and serum sodium. The pathologic findings, laboratory results, and clinical history suggested a diagnosis of methyl methacrylate poisoning.
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PMID:Accidental methyl methacrylate inhalation toxicity in a rhesus monkey (Macaca mulatta). 40 81

Accidental acute mercury vapor poisoning in three persons is reported. Three hours after exposure, symptomatology began by chills, vomiting, diarrhea and chest pain. Two patients, respectively 67 and 77 year old, presented severe pulmonary edema, then neurological symptoms with tremor and coma. This toxic pulmonary edema, which entailed artificial ventilation, was followed in both cases by an acute interstitial pulmonary fibrosis which led to death respectively after six and sixteen days. In the third case (a thirty eight year old patient) a skin rash, erythematous and pustuliform was observed. Analysis for total mercury by flameless atomic absorption showed very high mercury levels in blood and urine of the three patients. The effect of treatment by Dimercaptopropanol on renal excretion of mercury was studied. Optic and electron microscopy of the lung of the two patients who died showed the pulmonary changes of acute interstitial fibrosis.
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PMID:Accidental acute mercury vapor poisoning. 50 88

Acute hemodynamic changes during heroin overdose have not been frequently reported. We observed 2 male patients aged 24 and 21 years admitted in coma and shock and presenting severe mixed acidosis, with, respectively, pH 6.80, PaCO2 72 mm Hg, PaO2 70 mm Hg, BE -18 mEq/l, lactic acid 16.5 mmol/l, and pH 6.86, PaCO2 94 mm Hg, PaO2 46 mm Hg, BE -16 mEq/l, lactic acid 5.45 mmol/l. The hemodynamic data of the first patient showed a low output failure state associated with high filling pressures, suggesting biventricular heart failure. In the second case, clinically and radiologically marked pulmonary edema was associated with a hyperdynamic state and moderately elevated pulmonary artery pressure, but normal pulmonary capillary pressure. The possible pathophysiological mechanisms of those different, hemodynamic patterns are discussed.
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PMID:[Massive heroin intoxication. Hemodynamic studies]. 53 62

A patient with massive exposure to tetrachloroethylene fumes presented with coma and severe pulmonary edema. Sequential blood gases, chest x-rays, and clinical findings showed dramatic improvement with conventional but aggressive management and the patient recovered completely. There was no evidence of permanent renal, hepatic, or central nervous system damage.
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PMID:Pulmonary edema due to tetrachloroethylene. 61 50

At least four doses of quinine followed by a single dose of mefloquine or by a single dose of sulfadoxine-pyrimethamine are two highly effective regimens for chloroquine-resistant falciparum malaria. Mefloquine alone is valuable in ambulant patients. Chloroquine-sensitive falciparum malaria can be treated with a course of chloroquine. Vivax and all other types of malaria should be treated with sequential chloroquine and primaquine. Quinine, by intravenous infusion, is the most effective drug for severe falciparum malaria. The optimum intravenous dose varies between 5 mg/kg and 10 mg/kg administered over four hours. Intravenous or oral quinine should be administered about every 12 hours and the total daily dose of quinine should rarely exceed 20 mg/kg. Intravenous fluid input should be controlled in falciparum malaria to prevent pulmonary oedema. Established renal failure is best treated by dialysis. The value of adrenocortical steroids for falciparum coma has not been established. Fresh blood transfusion may be helpful in small doses for severe anaemia and to replace clotting factors. Anticoagulants, such as heparin, should not be used in falciparum malaria.
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PMID:The treatment of malaria. 76 37


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