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

Fibrinogen content was determined for each of 50 units of citrate-dextrose-phosphate (CPD)-preserved whole blood, packed red blood cells reconstituted with 250 ml. of saline, and packed red cells reconstituted with 250 ml. of purified plasma protein fraction (PPF). The total protein and albumin were measured, by electrophoresis, on each of 10 units of the three varieties of blood. The fibrinogen content of the two types of reconstituted cells was significantly lower than that of whole blood. Although the total protein/albumin content of whole blood and PPF-reconstituted red cells was similar, saline-reconstituted cells were markedly deficient in both total protein and albumin. Low fibrinogen and platelet levels subsequent to transfusion with reconstituted packed red cells can lead to an erroneous diagnosis of disseminated intravascular coagulation. Administration of large quantities of saline-reconstituted packed cells could be an etiologic factor in postoperative interstitial pulmonary edema.
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PMID:Fibrinogen and albumin deficiencies associated with packed red blood cell transfusions. 109 Feb 9

Hyskon (32 per cent dextran 70 in 10 per cent dextrose in water), a useful distension medium for hysteroscopic surgery, has significant side effects. A case of pulmonary edema following transcervical myoma resection is presented. Additional known side effects of Hyskon discussed include coagulation defects, spurious laboratory results, and anaphylaxis. Prevention and management of complications are described.
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PMID:Hyskon complications in hysteroscopic surgery. 170 73

Hysteroscopy using 32% Dextran-70 in 10% dextrose (Hyskon) is a common outpatient procedure. We report a case of pulmonary edema and coagulopathy in a 38-year-old, 48 kg female who had hysteroscopy and removal of an endocervical polyp using 700 ml of Hyskon over a 2-hour period. Low percutaneous oxygen saturation (SpO2) and vaginal bleeding developed postoperatively. A vaginal hysterectomy was performed. The coagulation profile showed coagulopathy, which was treated with transfusions of fresh frozen plasma and platelets. The patient developed overt pulmonary edema following the hysterectomy and was treated with positive pressure ventilation. The pathophysiology for the development of pulmonary edema and coagulopathy is discussed. Recommended limits for Hyskon volumes and instillation times are emphasized, as is careful recording of these parameters.
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PMID:Pulmonary edema and coagulopathy following intrauterine instillation of 32% dextran-70 (Hyskon). 171 31

Recently introduced chloroquine resistant malaria has altered the clinical picture and complicated the overall management of malaria. 113 adults with proved malaria admitted at Harare Central Hospital, Zimbabwe, were evaluated to determine the incidence, nature, relationship to morbidity and mortality and response to treatment of the complications due to malaria. 47.7 pc (52 of 109) patients had relatively chloroquine resistant malaria. 87.4 pc (99 of 113) had complications whose percentage frequency of occurrence were: Anaemia 51.2 pc, diarrhoea and/or vomiting 42.2 pc, cerebral malaria +/- fits 39.2 pc, renal insufficiency +/- hyperkalaemia 26.4 pc, hypoglycaemia 15.6 pc, jaundice 15.2 pc, neuro-psychiatric 15.0 pc, shock 10.6 pc, concurrent sepsis 8.9 pc, pulmonary oedema 3.5 pc and hyperpyrexia 1.7 pc. Multiple complications in the same patient were common. The combination of cerebral malaria and renal insufficiency had the worst mortality (p less than 0.001). All patients dialysed, however, survived. Non-iron deficiency anaemia, 91.7 pc (51 of 55) and diarrhoea and/or vomiting, were common, worsened morbidity but not mortality (p = 0.555). A seriously-ill patient with malaria should be suspected of having complications and chloroquine resistance and should be referred promptly to a centre with facilities for dialysis. Anti-malaria drugs should be mixed in a dextrose solution and iron supplements should not be given routinely.
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PMID:Complications of seasonal adult malaria at a central hospital. 209 79

Human recombinant interleukin-2 (rIL-2), with or without lymphokine-activated killer cells, has been shown to mediate tumor regressions in animals and in humans. A well-recognized adverse effect of rIL-2 is the development of a generalized vascular leak syndrome that involves the pulmonary microvasculature. We present a rabbit model for the study of rIL-2 pulmonary toxicity that closely reflects the human situation. Rabbits were treated with rIL-2 (Cetus) by two dose/schedule schemata. Separate control groups received rIL-2 excipient (Cetus) or 5% dextrose in water (D5W). In a short-term model, animals were treated with 10(6) Cetus units of rIL-2 in five bolus injections of 200,000 Cetus units each. In a long-term model, rabbits were treated with 3 (x) 10(6) Cetus units/kg of rIL-2 daily in three divided doses every 8 h for 9-11 doses (a schedule analogous to one used in human trials). Following treatment, animals were killed and examined for evidence of pulmonary toxicity. Among the treatment and control groups, there was no evidence of pulmonary leukostasis as determined by mean alveolar septal wall granulocytes per high power field or mean lung myeloperoxidase activity per gram of tissue. While there were no differences among the three treatment groups with regard to pulmonary edema formation (wet/dry weights), there was a tendency toward statistically significant differences between the rIL-2 and control groups. Pulmonary vascular permeability was assessed using i.v.-administered [125I]rabbit serum albumin (RSA) and expressed as mean bronchoalveolar lavage fluid/plasma [125I]RSA ratios. The rIL-2-treated animals had significantly increased pulmonary extravasation of [125I]RSA compared to controls, but there were no differences between the excipient- and D5W-treated controls. Lungs from rIL-2-treated (but not controls) animals displayed marked ultrastructural changes by electron microscopy in the arteriolar segment to include intracellular and subcellular blebs throughout the arteriole with separation of endothelial cells from basement membrane, interstitial edema, endothelial adhesion, and transmigration of lymphocytes into interstitium. Immunoperoxidase stains using an antirabbit T-cell monoclonal antibody demonstrated significant T-cell infiltration into the pulmonary interstitium of rIL-2-treated animals compared to controls. The long-term treatment model described appears to be highly suited for studies of rIL-2-induced pulmonary toxicity.
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PMID:Human recombinant interleukin-2 provokes acute pulmonary vascular endothelial injury in rabbits. 216 May 20

Abdominal aortic aneurysmectomy (AAA) results in thromboxane (Tx)A2 generation, a rise in mean pulmonary artery pressure (MPAP), leukopenia, and noncardiogenic pulmonary edema. This study tests whether mannitol, a hydroxyl radical scavenger, modifies these events. Patients received mannitol 0.2 g/kg (n = 14) or saline (n = 12) intravenously before infrarenal aortic clamping. With saline, 30 minutes after clamping, plasma TxB2 levels rose from 124 to 290 pg/mL (p less than 0.01), and MPAP rose from 19 to 27 mmHg (p less than 0.01). Aortic clamp release led to further increases in plasma TxB2 to 378 pg/mL (p less than 0.01) and MPAP to 34 mmHg (p less than 0.01). The white blood count (WBC) fell from 9800 to 4400/mm3 (p less than 0.01). Four to eight hours after surgery, physiologic shunting (Q[sc]S[xsc]/Q[sc]T[xsc]) rose from 9% to 20% (p less than 0.01) and peak inspiratory pressure (PIP) increased from 22 to 32 cmH2O (p less than 0.01). Chest radiography demonstrated pulmonary edema while the pulmonary wedge pressure was 12 mmHg, excluding left ventricular failure. By 24 hours pulmonary edema resolved and the PIP and PaO2 returned to baseline. Mannitol treatment relative to saline, during and after aortic clamping reduced plasma TxB2 levels to 155 and 198 pg/mL, respectively (p less than 0.01); MPAP to 21 and 26 mmHg (p less than 0.01); minimized the decline in WBC to 5850/mm3 (p less than 0.01), and the postoperative rise in Q[sc]S[xsc]/Q[sc]T[xsc] to 12%, and PIP to 28 cmH2O (both p less than 0.01). Chest radiography showed no pulmonary edema. Finally in vitro studies documented that mannitol 1 to 10(-4)M, but not dextrose, in a dose-dependent manner inhibited Tx synthesis by ADP-activated platelets. These data indicate that mannitol maintains pulmonary function after AAA by limiting ischemia-induced thromboxane synthesis.
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PMID:Pulmonary edema after aneurysm surgery is modified by mannitol. 1257 26

Hypernatremia is a potentially life-threatening electrolyte abnormality. This problem develops most often because of loss of water from the animal, but in rare cases hypernatremia results from gain of sodium chloride. Important conditions predisposing to hypernatremia include diarrhea, vomiting, heat stroke, fever, limited access to water, excessive diuretic use, renal diseases, and pituitary diabetes insipidus. This condition rarely develops if animals have adequate access to water. Clinical signs relate to central nervous system derangements and can progress to seizures and coma. Diagnosis is based on the serum sodium concentration; treatment should be instituted if it is greater than 170 mEq per L. Treatment is based on knowledge of the volume status of the patient and the probable cause for the hypernatremia. In general, 5 per cent dextrose in water or other hypotonic fluids are given slowly intravenously. The rate of administration should be adjusted so the water deficit is replaced over 48 to 72 h. Too rapid correction of hypernatremia can lead to cerebral edema and worsening of the animal. In cases of salt intoxication, diuretics must be given in addition to slow water replacement to avoid the development of pulmonary edema.
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PMID:Hypernatremia. 264 64

We investigated the effect of IL-2 in the isolated guinea pig lung perfused with phosphate-buffered Ringer's solution (containing 0.5 g/100 ml albumin and 5.5 mM dextrose) to determine the mechanism of IL-2-induced pulmonary edema. IL-2 (0 to 10,000 U/ml) was added to the perfusate following a 10 min baseline steady-state period. Pulmonary arterial pressure (Ppa), pulmonary capillary pressure (Ppc), and change in lung weight (as a measure of developing pulmonary edema) were recorded at 0, 10, 30, 40, and 60 min. The capillary filtration coefficient (Kf.c), an index of vascular permeability to water, was measured at 30 and 60 min. Infusion of IL-2 increased Ppc (from 3.9 +/- 0.1 cm H2O at baseline to 8.8 +/- 1.1 cm H2O at 60 min for IL-2 at 2000 U/ml, p less than 0.01; and from 3.8 +/- 0.1 cm H2O at baseline to 8.9 +/- 0.6 cm H2O at 60 min for IL-2 at 10,000 U/ml, p less than 0.01. The lung weight also increased (32% at IL-2 concentration of 2000 U/ml, and 26% at IL-2 concentration of 10,000 U/ml) The capillary filtration coefficient did not change with IL-2 infusion. The IL-2 response was prevented using the pulmonary vasodilator, papaverine. The infusion of IL-2 was associated with the generation of thromboxane A2(TxA2) in the effluent perfusate. Inhibition of TxA2 synthetase using Dazoxiben prevented the pulmonary vasoconstriction and edema response to IL-2. In addition, IL-2 had no effect on the transendothelial clearance of 125I-albumin. The results indicate that IL-2 causes pulmonary edema secondary to an increase in Ppc. The response is mediated by IL-2 stimulation of TxA2 generation from the lung.
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PMID:IL-2 induces pulmonary edema and vasoconstriction independent of circulating lymphocytes. 278 41

Nisoldipine, a calcium entry blocker, was given to 10 patients with congestive heart failure. During a 2 month follow-up period, 7 of the 10 patients were readmitted with pulmonary edema; daily furosemide doses were increased (128 +/- 87 to 192 +/- 135 mg/day, p less than 0.01), and plasma creatinine increased (1.5 +/- 0.5 to 1.8 +/- 0.6 mg/dl, p less than 0.05) (all values mean +/- SD). Despite this unfavorable clinical course, nisoldipine caused some beneficial chronic (1 month) hemodynamic effects. It decreased systemic vascular resistance (from 1,781 +/- 229 to 1,306 +/- 345 dynes X s X cm-5, p less than 0.01), decreased mean arterial pressure (from 88 +/- 0 to 74 +/- 4 mm Hg, p less than 0.001) and increased stroke volume index (from 27 +/- 6 to 33 +/- 9 ml/min per m2, p less than 0.02). Heart rate, pulmonary capillary wedge pressure and stroke work index did not change. However, nisoldipine's chronic renal and neurohumoral effects were not as favorable. These were assessed during a 5 hour water load (15 ml/kg body weight of 5% dextrose in water) and compared with the effects of a water load before therapy. Nisoldipine did not change creatinine clearance or sodium excretion, but decreased water excretion (from 58 +/- 35 to 46 +/- 40% of water load in 5 hours). Over this 5 hour study, mean plasma vasopressin was also higher with nisoldipine (1.9 +/- 2.3 versus 2.7 +/- 3.2 pg/ml, p less than 0.05), but mean plasma aldosterone was lower (67 +/- 31 to 47 +/- 27 mg/dl, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic renal and neurohumoral effects of the calcium entry blocker nisoldipine in patients with congestive heart failure. 288 Aug 84

En bloc transplantation of the heart and lungs was performed in 15 chacma baboons; the donor organs were stored between 4 and 6 hours before transplantation. The hearts were perfused in the donor animals with 15 ml/kg Wicomb's cardioplegic solution at 4 degrees C, the lungs with either 20 ml/kg 4 degrees C Collins' solution with an added 2.5% dextrose and 12 mEq magnesium sulfate (Collins' solution, group 1, n = 8), Collins' solution plus superoxide dismutase (40,000 U/L superoxide dismutase, group 2, n = 4), or Collins' solution plus superoxide dismutase plus peroxidase (5000 U/L peroxidase plus mannitol, group 3, n = 3). The pulmonary artery perfusion pressure was not allowed to exceed 50 cm water; the lungs were maintained at 30% to 50% inflation, and external cooling was applied. After explantation the thoracic organs were stored in 0.9% saline solution at 4 degrees C. In groups 1 (Collins' solution) and 2 (Collins' plus superoxide dismutase) all surviving baboons revealed normal blood gas values and normal light and electron microscopic histology at 24 hours. Three animals had further biopsies at intervals between 1 and 9 days, at which time the histology of the lungs proved normal and well preserved. All three baboons in group 3 (Collins' plus superoxide dismutase plus peroxidase) had grossly abnormal blood gas values from the time of operation, and all died within 9 hours; light microscopy of the lungs showed early lung infarctlike lesions and in one case pulmonary edema. These preclinical findings proved that storage of the lungs in Collins' solution with or without superoxide dismutase is possible for up to 5 hours; the addition of peroxidase had a detrimental effect.
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PMID:Successful orthotopic heart-lung transplantation in the baboon after five hours of cold ischemia with cardioplegia and Collins' solution. 311 42


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