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)

We report the case of a 24-year-old white female in need of tocolysis during the 25th week of pregnancy with i.v. hexoprenaline, while suffering from a discrete influenza-like syndrome with nasal discharge and sinusitis. A few hours later fulminant acute adult respiratory distress syndrome (ARDS) developed. ARDS is a rare (0.5-5%) but feared complication of tocolysis with beta-2 mimetic agents and magnesium sulfate. Its physiopathology is obscure, but iatrogenic hyperhydration and lesions of the alveolar-capillary membrane are suspected. In this case both factors were involved, but lesions of the alveolar-capillary membrane were predominant. A direct toxic effect of beta-2 mimetic agents on the alveolar-capillary membrane has not been demonstrated and other factors favoring pulmonary edema during tocolysis with beta-2 mimetic agents, especially infections, are discussed.
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PMID:[Lesional pulmonary edema associated with tocolysis by hexoprenaline sulfate]. 153 26

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

Case 1: A 38-year-old female with a history of tonsillitis and sinusitis was admitted to our hospital because of lung edema. On admission, her serum creatinine increased to 5.57 mg/dL. Hypocomplementemia was not found. ASO and MPO-ANCA were 24 U/mL and 12 EU, respectively. She underwent emergency hemodialysis. Renal biopsy showed global sclerosis and fibrocellular crescentic formation, and marked angionecrosis was noted by light microscopy. Granular deposition of C3, IgG and IgM was seen along the capillary walls on immunofluorescence study. Glomerular intramembranous deposits were scattered on electron microscopy. She was treated with intravenous methylprednisolone pulse therapy, and following oral prednisolone administration was decreased gradually. No therapeutic effects were observed, and intermittent hemodialysis was continued and became maintenance hemodialysis therapy. Case 2: A 28-year-old female suffering from both pharyngitis and acute renal failure with systemic edema was admitted to our hospital. On admission, her serum creatinine and ASO were 4.31 mg/dL and 239 U/mL, respectively. MPO-ANCA was negative and CH50 was normal. Hemodialysis was initiated on the 6th hospital day. In renal biopsy, most glomeruli showed cellular crescentic formation, and marked angionecrosis was noted by light microscopy. Global sclerosis was not found in this case. Granular deposition of C3 resembling a starry sky pattern was seen along the capillary walls on immunofluorescence study. Electron microscopy revealed scattered glomerular subepithelial deposits. She was treated with intravenous methylprednisolone pulse therapy and then oral prednisolone administration. Because of the gradual improvement in renal function, hemodialysis was terminated after 53 sessions, however, the patient's chronic renal failure has persisted to date. In these two cases, the pathological findings supported the diagnosis of severe acute post-infectious glomerulonephritis with the characteristic crescentic and necrotizing glomerulonephritis with C3 deposition.
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PMID:[Crescentic and necrotizing glomerulonephritis with C3 deposition]. 1831 44