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Query: UMLS:C0034063 (pulmonary edema)
 10,665 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

In a 49 year old man with blast crisis and massive leukocytosis due to chronic myelogenous leukemia, severe hypoxic respiratory failure developed despite a normal chest film. Correction of hypoxemia was observed after reduction of the white blood cell count by hydroxy-urea therapy. A similar episode occurred prior to death, and necropsy examination revealed extensive plugging of the pulmonary vasculature by leukemic blast cells but no infection or pulmonary edema. An inverse linear correlation was demonstrated between the peripheral white blood cell count and the efficiency of oxygen transfer in the lung as determined by the arterial to alveolar oxygen tension ratio. We postulate that mechanical obstruction and/or leukocyte mediated capillary endothelial injury caused the severe leukocyte mediated capillary endothelial injury caused the severe hypoxemia. Abnormalities of pulmonary gas exchange may be common in leukemic patients with markedly increased leukocyte counts.
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PMID:Reversible respiratory failure due to intravascular leukostasis in chronic myelogenous leukemia. Relationship of oxygen transfer to leukocyte count. 29 38

Forty-three patients (mean age 62 +/- 1 years) were treated for ventricular septal defect (VSD) secondary to myocardial infarction. Whenever possible, operation was postponed until six weeks post-onset chest pain. However, hemodynamic instability, evidenced by cardiogenic shock, refractory pulmonary edema, or a rising blood urea nitrogen (BUN) forced operation in 21 patients within 21 days post-infarct (Group I). In seven patients operation was performed three to six weeks post-infarct (Group II). In only eight patients could operation be delayed beyond six weeks post-infarct (Group III). Clinical deterioration, once begun, progressed rapidly, and could be reversed only temporarily by intra-aortic balloon pumping, used in 26 patients for safe conduct of cardiac catheterization and for peri-operative hemodynamic support. Hospital survival was achieved in 24 of the 36 operated patients (66%). In Group I patients, ten of 21 survived. In Group II, six of seven survived. In Group III, eight of eight patients survived. There have been five late deaths with a mean follow-up of 41 months in survivors. Improved survival has been achieved recently by the greater use of prosthetic material to replace necrotic muscle and by a transinfarct incision regardless of infarct location. Operative mortality before 1973 was 47%; mortality after 1973 was only 18%, with a concomitant reduction of mortality (30%) even in Group I patients.
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PMID:Surgery for post-myocardial infarct ventricular septal defect. 30 10

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

The pulmonary absorption of 14C-labeled urea, mannitol, inulin, and dextran was measured in vivo in anesthetized rats with alpha-naphthylthiourea (ANTU)-induced (5 mg/kg, ip) lung edema. At 1 h after ANTU treatment, the absorption of mannitol was significantly increased; in 4-h ANTU-treated animals, the absorption of urea was unchanged, whereas the absorption of mannitol, inulin and dextran was increased markedly compared to controls. Although disappearance of each solute from control lungs could be described by a single, first-order rate, absorption time curves for mannitol and inulin showed at least two components in edematous lungs: a fast component(s) and a slower, first-order component; fast-component rates for the two saccharides appeared to be similar; the slow-component rate for each compound was not significantly different from its control rate. The results suggest that fast-component absorption in ANTU-treated rats represents a fraction of instilled solute which entered damaged areas of lung where the porosity of the absorbing membranes was markedly increased, whereas slow-component absorption occurred from normal areas of lung.
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PMID:Quantitative changes in permeability of rat lung epithelium in lung edema. 64 Sep 20

Intravenous injection of ethchlorvynol (Placidyl) causes noncardiogenic pulmonary edema in humans and laboratory animals. We studied the effects of intravenous ethchlorvynol (15 to 25 mg per kg of body weight) on pulmonary alveolar membrane permeability to various endogenous and exogenous solutes in the in vivo saline-filled dog lung model. Baseline and postethchlorvynol times in minutes for 50 per cent equilibration between the blood and saline-filled alveoli were, respectively, for urea, 37.3 +/- 12.4 and 12 +/- 6.3; for albumin 8,160 +/- 4,400 and 267 +/- 93; for dextrans of molecular weight 10,400 daltons, 1,150 +/- 80 and 185 +/- 160; for dextrans of molecular weight 250,000 daltons, 24,000 +/- 800 and 1,120 +/- 900; for dextrans of molecular weight 500,000 daltons, 24,500 +/- 150 and 1,020 +/- 590. All of these pairs of values were significantly different (P less than 0.01). In addition, lung liquid histamine (but not blood histamine) concentrations increased significantly (P less than 0.001) after ethchlorvynol injection. Intravenous ethchlorvynol causes marked increases in alveolar membrane permeability.
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PMID:The effects of ethchlorvynol on pulmonary alveolar membrane permeability. 92 Oct 65

We studied the effects of three different doses (15, 20, and 25 mg/kg) of Perilla ketone (PK) on the blood-perfused in situ sheep lung while obtaining external measurements of lung transvascular protein flux. Lymph flow and lymphatic protein clearance increased significantly after all doses of PK. Severe pulmonary edema was confirmed by high postmortem wet-to-dry lung weight ratios and increased extravascular lung water from multiple indicator-dilution studies. Urea permeability-surface area product and effective diffusivity from multiple indicator-dilution studies also increased after PK infusion. Because we observed no evidence of increased capillary pressure or increased microvascular surface area after PK, we conclude that PK significantly increased pulmonary microvascular permeability. Certain aspects of the in situ PK response appeared to be dose dependent. The lungs responded rather quickly to high doses of PK, but an apparent latency period was noted with low doses of PK. Postmortem wet-to-dry lung weight ratios were always high but did not suggest dose dependence. However, times of postmortem measurements were not the same for all doses of PK. The external scan technique appeared to be sensitive to changes that occurred in the lung after PK. Externally detected albumin interstitial-to-plasma mass (mass I/P) ratios were substantially higher after PK than during control in situ studies. In some experiments, final mass I/P ratios increased above 4 approximately 2.0 h after PK compared with control values of 0.2 and 0.4. A delay time between injection and change in mass I/P slope was also observed, which decreased with increasing dose of PK. PK causes a permeability injury in the in situ sheep lung and provides a useful model for studying the sensitivity of permeability measurement techniques such as the external gamma-ray detection method.
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PMID:Effects of Perilla ketone on the in situ sheep lung. 155 25

We retrospectively reviewed 443 patients who had cardiopulmonary resuscitation (CPR). The focus of the study was to discover what preexisting factors should be assessed to determine the probability of survival. There were 88 successes out of 340 cases (25.9%). The absence of a previous myocardial infarction (MI), shock, partial pressure of oxygen (PaO2) less than 60 mm Hg, blood urea nitrogen (BUN) level greater than 20 mg/dL, pneumonia, pulmonary edema, and oliguria were found to predict a successful outcome. Logistic regression was used to predict percentage of successes in the various groups of patients with various clinical characteristics. The observed and predicted numbers of successes were in close agreement in most cases. We also constructed a classification function to predict whether an individual subject would survive the event for which CPR was required. Sixty-seven of the 88 observed successes would have been predicted, for an estimated sensitivity of 76%, and 164 of the 252 failures would have been predicted, for an estimated specificity of 65%. A large percentage (24%) of cases in which the patient actually survived CPR would have been predicted to be failures. We conclude that preexisting factors before a cardiopulmonary arrest do not accurately predict survival after CPR.
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PMID:Inpatient cardiopulmonary resuscitation: is survival prediction possible? 163 5

A variant of hepatorenal syndrome occurring in patients with chronic congestive heart failure following an episode of cardiogenic pulmonary edema, and in the absence of hypotension, is described. This was observed in 13 patients during an eleven-year period. The clinical picture is characterized by hepatic injury and functional renal impairment. Increase of serum glutamic oxaloacetic transaminase levels as high as 2100 IU; prolongation of prothrombin time; elevation of serum bilirubin, creatinine, blood urea nitrogen, and potassium levels; decrease in urinary sodium excretion; and a normal urinary sediment are the salient laboratory abnormalities of this entity. Treated with conventional medication, the patients' course was fatal in 4 cases. When the splanchnic vasodilator dopamine was added to the patients' management, 5 of 9 patients recovered. Cardiogenic hepatorenal syndrome is a severe but potentially reversible complication of heart failure. The apparently beneficial effect of low-dose dopamine needs further evaluation.
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PMID:Cardiogenic hepatorenal syndrome. 224 92

Clinical feature and creatinine metabolism were studied in 86 diabetic patients who had newly initiated dialysis treatment. In 32.5% of the patients, serum creatinine was below 8.0 mg/dl at the initiation of dialysis treatment. Gastrointestinal symptoms, general malaise, pulmonary edema and uremic encephalopathy were the causes which required dialysis treatment in those patients, and the frequency of pulmonary edema was significantly higher than in patients whose serum creatinine was above 8.0 mg/dl at the initiation of dialysis (p less than 0.05). There were no significant differences in serum urea nitrogen, potassium, sodium, albumin levels and hematocrit between low serum creatinine group (3.0-7.9 mg/dl) and high serum creatinine group (8.0-11.9 mg/dl) at the initiation of dialysis. Serum creatinine levels were highly correlated with creatinine generation rate (r = 0.788, p greater than 0.01). There was a significant correlation between creatinine generation rate and muscle volume (r = 0.863, p less than 0.001). Muscle volume of diabetic dialyzed patients was 29.5 +/- 7.0 cm3/cm in males and 26.9 +/- 5.0 cm3/cm in females, and those values were lower than those of non-diabetic dialyzed patients (p greater than 0.005). Frequency of the patients whose creatinine generation rate was below 1500 mg/day was 81.3% in diabetic hemodialyzed patients and this was significantly higher than in non-diabetic hemodialyzed patients (p less than 0.005). In conclusion, in patients with diabetic nephropathy who have to initiate dialysis treatment, uremic symptoms have progressed though serum creatinine levels are relatively low. This low serum creatinine levels in patients with diabetic end-stage renal disease are resulted from their low muscle volume.
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PMID:[Characteristics of the patients with diabetic nephropathy with relatively low serum creatinine at the initiation of dialysis]. 226 24


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