Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mrs AB was admitted in the 34th week of pregnancy with eclampsia. Prompt parenteral (intravenous and intramuscular) administration of magnesium sulfate arrested the convulsions and prevented additional seizures. Because of a dangerously elevated blood pressure, intravenous hydralazine was administered to reduce the blood pressure. Unfortunately, the hydralazine was given more frequently than recommended, and the blood pressure was decreased rapidly and too far. This resulted in the development of a serious fetal bradycardia secondary to reduced uteroplacental perfusion. Fortunately, the blood pressure spontaneously recovered as did the fetus. Three hours after admission, Mrs AB was awake and alert. Her fetus had also recovered from the effects of the convulsions and the treatment with hydralazine. Mrs AB's laboratory values had all been reported by this time, and her intravenous intake and urinary output were well regulated. Importantly, because of the presence of significant hemoconcentration (hematocrit at 32 weeks' was 36 and at 34 weeks', 44), a careful search for pulmonary edema was made. Additionally, fluid administration was conservative in order not to produce pulmonary edema. At this point, an induction of labor was commenced. The induction of labor was rapidly successful, and Mrs AB delivered a small but vigorous male infant who subsequently did well. Mrs AB was monitored hourly for the first 12 hours postpartum to ensure adequate blood pressure control and to prevent pulmonary edema. Her subsequent puerperal course was without adverse incident. She diuresed massively, and her blood pressure rapidly returned to normal.
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PMID:Management of eclampsia. 806 75

Beginning in 1981, Prapokklao Regional Hospital in Chantaburi, Thailand, admitted all pregnant women with malaria to the obstetrics unit so midwives and obstetricians could learn how to better detect early signs or symptoms of malaria. Prior to 1981, they treated these women with quinine hydrochloride in a 500 ml 5% dextrose drip for 8 hours. They failed to detect hypoglycemia and pulmonary edema, however, resulting in many deaths. After 1981, they used 20 mg/kg quinine hydrochloride in a 250 ml 5% dextrose drip in 4 hours then 10 mg/kg quinine hydrochloride in a 250 ml 5% dextrose drip at the same rate at 8 hour intervals. Once the patient could take the drug orally, they administered 600 mg quinine sulfate at 8 hourly intervals for 7 days. They measured blood bilirubin levels and performed renal function tests on admission and on days 2 and 5. They monitored blood sugar levels on admission, at hourly intervals during intravenous quinine treatment, and every 4 hours during oral quinine treatment. Clinicians encouraged women who could drink to drink glucose syrup during quinine treatment. If, during treatment, a patient experienced unconsciousness or convulsions or blood sugar levels fell below 60 mg/dl, they would administer 100 ml of 50% glucose. If bilirubin levels remained high or a patient became jaundiced on day 2, clinicians monitored bilirubin on days 3 and 4. If levels increased, they reduced the dose 33% until the situation improved. They recorded urinary output hourly and measured central venous pressure. If the patient had normal pressure, but urinary output was less than 30 ml/hour, clinicians prescribed a diuretic. They kept patients in a propped-up position to reduced the likelihood of pulmonary edema. They monitored fluid intake and output and, in severe cases, central venous pressure. They allowed just enough fluid intake to maintain the pressure at 10-12 mm H20 and urine output at no less than 30 ml/hour. These efforts reduced maternal deaths in the unit from 341 to 54/100,000 live births (1981 - 8 deaths; 1986 - no deaths).
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PMID:Malaria in pregnant women: action for survival. 818 99

A 24-year-old woman was infected with falciparum malaria during travel to Kenya, complicated by intravascular coagulation and pulmonary edema. She was successfully treated with anti-malarial drugs including chloroquine, quinine sulfate and pyrimethamine, with a combined regimen of heparin, antithrombin III and nafamostat mesilate for disseminated intravascular coagulation, and with methylprednisolone pulse therapy for pulmonary edema. The present case emphasizes the importance of early diagnosis and appropriate treatment in terms of falciparum malaria. This case, in particular, is believed to be worth reporting as overseas travel is increasing and yet anti-malarial drugs are not readily available to most physicians in Japan.
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PMID:Falciparum malaria in an overseas traveler complicated by disseminated intravascular coagulation and pulmonary edema. 840 May 1

Fourteen body packers carrying 2-112 heroin packages are reported. Nine people swallowed the packets, and five inserted them rectally. The ingested packages were large and radio-opaque; they consisted of hard lumps of concentrated heroin usually covered with glove latex, white adhesive tape, and a toy balloon. There were two complications in the 14 patients. One patient developed a bowel obstruction; at laparotomy 8 packages were found in the stomach and 27 at the ileo-cecal valve. Another patient, with heroin wrapped only with black electrician's tape and no latex inner or outer wrappings, developed heroin intoxication, noncardiogenic pulmonary edema, and a bowel obstruction. Eighteen packages were surgically removed from his stomach and 26 from his bowel. We recommend bisacodyl suppositories, activated charcoal mixed with a 3% sodium sulfate cathartic, and phosphosoda enemas for package removal; close observation for heroin toxicity or bowel obstruction; and surgical intervention for continuing toxicity, retention of packages in the stomach, or bowel obstruction.
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PMID:Heroin body packers. 844 84

An unusual case diagnosed as connective tissue-type mast cell leukemia with marked mastocyte infiltration into visceral organs in a seven-year-old female Curly-Coated retriever is presented. Acute circulatory collapse, emesis, diarrhea, abdominal enlargement, icterus, cyanosis, dyspnea, pulmonary edema, hepatomegary, ascites, and right ventricular enlargement were observed. Hematologic and biochemical examinations revealed mast cell leukemia, mature neutrophilia, monocytosis, thrombocytopenia, hemolytic hyperbilirubinemia, hyperhistaminemia, renal and hepatic injuries. Mast cells were distributed systemically, but predominantly in the diaphragm and liver with a large mass among the serosa of ileum, cecum and colon. Mast cells were stained intensely by both safranin and berberine sulfate.
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PMID:Connective tissue-type mast cell leukemia in a dog. 1072 Jan 89

Patients with acute cardiogenic pulmonary edema require rapid assessment and therapy to prevent progression to respiratory failure and cardiovascular collapse. The goal of therapy is to decrease the pulmonary capillary wedge pressure by decreasing intravascular volume and shifting the blood volume into peripheral vascular beds. Mainstays of therapy include morphine sulfate (a venodilator and an anxiolytic), furosemide (a venodilator and diuretic), nitroglycerin preparations (venodilators), and, in some cases, aminophylline, nitroprusside, and beta-adrenergic agents or milrinone. Patients who do not respond to more conservative measures may require interventional procedures, including Swan-Ganz catheterization or arterial pressure monitoring, continuous positive airway pressure or mechanical ventilation, intra- aortic balloon counterpulsation, and mechanical removal of fluid. Because the prognosis for patients with acute cardiogenic pulmonary edema depends on identification and correction of the underlying disease process, it is essential to define the cause of the edema during and after stabilization of the patient. Evaluation should include Doppler echocardiography, cardiac catheterization, and coronary angiography.
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PMID:Acute Pulmonary Edema. 1109 92

A 55-year-old male Caucasian truck driver was dead at the scene after breathing hydrogen sulfide (H(2)S) produced by an accidental transfer of sodium hydrogen sulfide (NaHS) from a tanker truck to a tank containing 4% sulfuric acid (H(2)SO(4)) and iron(II) sulfate (FeSO(4)). Autopsy of the decedent's body revealed pulmonary edema and passive congestion in lungs, spleen, kidneys, and adrenal glands. Postmortem biological samples were analyzed for carbon monoxide, cyanide, ethanol, and drugs. Since a potential exposure to H(2)S was involved, blood was also analyzed for sulfide (S(2-)). The analysis entailed isolating S(2-) from blood as H(2)S using 0.5M H(3)PO(4), trapping the gas in 0.1M NaOH, and determining the electromotive force using a sulfide ion specific electrode. Acetaminophen at a concentration of 14.3 microg/ml was found in blood, and metoprolol was detected in the blood, liver, and kidney samples. The blood S(2-) level was determined to be 1.68 microg/ml. It is concluded that the cause of death was H(2)S poisoning associated with a hazardous material accident in an industrial situation.
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PMID:A fatality caused by accidental production of hydrogen sulfide. 1172 49

Initiated by numerous factors, acute lung injury is marked by epithelial and endothelial cell perturbation and inflammatory cell influx that leads to surfactant disruption, pulmonary edema, and atelectasis. This syndrome has been associated with a myriad of mediators including cytokines, oxidants, and growth factors. To better understand gene-environmental interactions controlling this complex process, the sensitivity of inbred mouse strains was investigated following acute lung injury that was induced by fine nickel sulfate aerosol. Measuring survival time, protein and neutrophil concentrations in BAL fluid, lung wet-to-dry weight ratio, and histology, we found that these responses varied between inbred mouse strains and that susceptibility is heritable. To assess the progression of acute lung injury, the temporal expression of genes and expressed sequence tags was assessed by complementary DNA microarray analysis. Enhanced expression was noted in genes that were associated with oxidative stress, antiprotease function, and extracellular matrix repair. In contrast, expression levels of surfactant proteins (SPs) and Clara cell secretory protein (ie, transcripts that are constitutively expressed in the lung) decreased markedly. Genome-wide analysis was performed with offspring derived from a sensitive and resistant strain (C57BL/6xA F(1) backcrossed with susceptible A strain). Significant linkage was identified for a locus on chromosome 6 (proposed as Aliq4), a region that we had identified previously following ozone-induced acute lung injury. Two suggestive linkages were identified on chromosomes 1 and 12. Using haplotype analysis to estimate the combined effect of these regions (along with putative modifying loci on chromosomes 9 and 16), we found that five loci interact to account for the differences in survival time of the parental strains. Candidate genes contained in Aliq4 include SP-B, aquaporin 1, and transforming growth factor-alpha. Thus, the functional genomic approaches of large gene set expression (complementary DNA microarray) and genome-wide analyses continue to provide novel insights into the genetic susceptibility of lung injury.
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PMID:Acute lung injury: functional genomics and genetic susceptibility. 1189 92

Immediate removal of the femoral artery sheath after coronary angioplasty may allow rapid mobilization and reduces the number of in-hospital days. We studied the early and 1-month clinical and angiographic follow-up of patients having heparin reversed with protamine after implantation of phosphorylcholine-coated metal (Divysio) stents, followed by removal of the femoral artery sheath. Fifty patients (37 men, mean age 59 +/- 10 years) with stable angina pectoris and a single totally occluded artery (1 unprotected left main stem, 15 left anterior descending, 11 left circumflex, 23 right) underwent coronary angioplasty. Antithrombotic medication was salicylic acid 75 to 160 mg before, heparin bolus 7,500 IU during, and protamine sulfate 25 mg and oral ticlopidine 250 mg after the procedure. Angiography was performed after 30 minutes and at 1 month. The mean number of stents was 1.4 +/- 0.6/lesion, with a mean final diameter of 2.69 +/- 0.40 mm. One stent thrombus was detected after 30 minutes and was treated with balloon dilatation. One patient underwent emergency bypass surgery for non-stent-related problems. Forty-six patients were mobile after 5 hours, and 2 after >5 hours. At 1 month there had been no major coronary end points, rehospitalizations, groin bleeding, or more thrombi. One episode of transient pulmonary edema occurred after protamine injection. Thirty-eight patients (79%) had no angina at 1 month, maximal bicycle exercise capacity increased from 128 +/- 42 to 160 +/- 45 W (p <0.05), and left ventricular ejection fraction increased from 63% to 68% (p <0.05). Thus, reversal of heparin with protamine sulfate after implantation of a phosphorylcholine-coated stent enables early mobilization. This approach seems safe in patients with 1 -vessel total occlusions and angioplasty could be performed as an outpatient procedure.
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PMID:Early mobilization after protamine reversal of heparin following implantation of phosphorylcholine-coated stents in totally occluded coronary arteries. 1200 42

Quinine sulfate, which has been available for many years, has not been implicated definitively in the development of pulmonary toxicity. A variety of adverse effects, however, have been reported with quinine administration. A 45-year-old woman with longstanding rheumatoid arthritis experienced wheezing, severe anxiety, breathlessness, cough, orthopnea, mild fever, chills, and pleuritic chest discomfort after taking a single dose of quinine for nocturnal leg cramps. Radiographic imaging demonstrated diffuse, bilateral pulmonary infiltrates suggestive of pulmonary edema. No cause other than acute quinine ingestion could be identified despite thorough cardiac and infectious disease evaluations. Clinicians should be aware of a possible association between quinine sulfate and pulmonary toxicity.
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PMID:Transient pulmonary infiltrates possibly induced by quinine sulfate. 1206 69


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