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)

Clinical studies were performed in 27 consecutive patients with high-altitude pulmonary edema who were transported from the mountains to Shinshu University Hospital, Matsumoto, Japan. The altitude of onset was 2,680 m to 3,190 m above sea level. Symptoms included marked dyspnea, cough, and stridor. Physical findings included cyanosis, tachycardia, and rales. Neurologic disturbances, which were seen in 17 patients, included headache, vomiting, memory disturbance, clouding of consciousness, or coma. Chest roentgenograms revealed patchy infiltrates throughout the pulmonary fields, often in an asymmetric pattern, and enlargement of the right ventricle. Hemodynamic studies by right cardiac catheterization showed that high-altitude pulmonary edema was noncardiogenic. Scintiscans of the lungs with technetium-99m-macroaggregated albumin (99mTc-MAA) performed in one patient showed decreased perfusion of 99mTc-MAA in the area of infiltrates. Pulmonary edema fluid collected through the endotracheal tube in two patients was rich in protein. Computerized tomograms of the brain showed small ventricles and cisterns, disappearance of sulci, and diffuse low density of the cerebrum, indicating cerebral edema in eight of nine cases. Retinal hemorrhage and papilledema were observed in five patients.
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PMID:Clinical features of patients with high-altitude pulmonary edema in Japan. 366 94

Two cases of fulminant fat embolism syndrome that were fatal are reported as complications of total hip replacement. The major clinical features were severe hypotension and cardiac arrest in one case and postoperative coma in the other case. Both patients had severe acute respiratory failure that resulted from pulmonary oedema.
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PMID:Fat embolism syndrome with total hip replacement. 377 11

Three patients with hyperosmolar coma were treated with intravenous isotonic saline, dextrose, and hypotonic saline solutions. The development of pulmonary edema and increasing hypernatremia precluded the further use of sodium solutions, and the presence of severe hyperglycemia made the further use of dextrose solutions undesirable. To provide further solute-free fluid, intravenous sterile water was administered through a central venous catheter. The hyperosmolar state improved, and all patients survived without biochemical evidence of hemolysis or clinical evidence of cerebral edema.
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PMID:Hyperosmolar coma treated with intravenous sterile water. A study of three cases. 396 86

The authors report five patients who developed transient arterial hypotension immediately after the rupture of cerebral aneurysms. They manifested deep coma (three cases), abnormal electrocardiogram (four cases), and remarkable pulmonary edema (two cases). The level of consciousness in all three patients who were in deep coma improved with the normalization of blood pressure. Although two patients died of recurrent hemorrhage, the other three patients were discharged in satisfactory condition. Serious clinical conditions that are not terminal and are caused by arterial hypotension immediately after the rupture of cerebral aneurysms are sometimes reversible with adequate treatment.
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PMID:Reversible arterial hypotension after acute aneurysmal subarachnoid hemorrhage. 396 9

Previous investigations have reported an 11 to 71% incidence of pulmonary edema following CNS injury, based on post-mortem examinations. No premortem assessment to date has been made of the frequency and severity of in vivo pulmonary fluid accumulation following acute head injury. The thermal green dye technique was used to objectively determine extravascular lung water (EVLW) in 18 comatose patients with severe acute intracranial injuries resulting from trauma or spontaneous subarachnoid hemorrhage. Patients with aspiration, lung contusion, or pneumonia were excluded from the study. Control values for EVLW were obtained on admission from a group of 13 traumatized patients without head injury or evidence of pulmonary disease or injury. Intracranial injury patients who had EVLW values greater than two standard deviations above the control group mean were considered to have pulmonary edema. The incidence of pulmonary edema in this series was 50% (9/18). Extravascular lung water was determined post mortem in five patients using the gravimetric method of Pearce. The results suggest that pulmonary edema is a distinct clinical event occurring frequently after acute intracranial injury. Edema appears to be mediated by increased pulmonary microvascular permeability, and is not primarily dependent on postinjury changes in intracranial pressure or pulmonary vascular pressures.
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PMID:Pulmonary extravascular fluid accumulation following intracranial injury. 635 1

285 patients affected by carbon monoxide poisoning were admitted in our intensive care unit over a period of two years (from july 1980 to july 1982). 18 patients had a pulmonary edema (P.E.). The occurrence of P.E. was more frequent when coma was grade 2, 3 or 4 (p less than 10(-3]. The acute physiologic score (weighting of physiologic measurements) as proposed by Knauss is higher in patients with P.E. (p less than 10(-2]. However death is never due to P.E.; about 54 patients with coma, 5 died; death is related to neurologic aggravation. Neurologic sequelae are not related to the occurrence of P.E. but to a delay in hyperbaric oxygen therapy. These date show that prognosis of carbon monoxide poisoning is related to neurological status and is not influenced by the occurrence of P.E. when correctly treated and when hyperbaric oxygen therapy is early realized.
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PMID:[Acute pulmonary edema in carbon monoxide poisoning. Prognostic effect]. 666 88

A collective nitrous fumes poisoning (five cases) is reported. Two patients (case 3 and case 4) were comatose, in severe respiratory distress. Shock and slate blue cyanosis were noted. Physical examination and chest X ray revealed acute pulmonary edema-Methemoglobin levels were 71,3% (case 3) and 58% (case 4). Despite treatment both of them died from severe hypoxia resulting in cardiorespiratory arrest. Post-mortem examination was performed upon these four men. On admission the last one (case 5) was conscious, and in good hemodynamic condition. Acute pulmonary edema and cyanosis were present. Methemoglobin level was 37,3%. This patient recovered appropriate therapy. For case 1 and 2 acute anoxia due to methemoglobinemia seems to be cause of death. For cases 3 and 4 death is due to hypoxemia associated with pulmonary edema.
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PMID:[Collective acute poisoning by nitrous gases]. 667 8

A brief survey of disseminated intravascular coagulation (DIC) is presented, with clinical, paraclinical and pathologoanatomical characteristic. The difficulties in making the diagnosis at the clinic are stressed upon, authors' observations on one male subject, admitted to the clinic with multiple extensive subcutaneous hemorrhages are reported, that were followed by successive pareses of the lower and upper limbed. The case had a lethal end with manifestations of pulmonary edema and cerebral coma on the base of the disseminated intravascular coagulation. The diagnosis was made, while still living, by skin biopsy and later at necropsy--confirmed thrombus in the lungs, heart, kidneys and brain.
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PMID:[Description of disseminated intravascular coagulation in a case diagnosed intravitally]. 667 87

A 44-year old man presented a postanoxic coma and acute pulmonary oedema after cardiopulmonary resuscitation in the acute phase of myocardial infarction. Early haemodynamic measurements revealed low right and left ventricular filling pressures and a low cardiac output. Haemodynamic and clinical improvement was obtained after volume expansion. The cause of low-pressure pulmonary oedema occasionally seen in patients with acute myocardial infarction is sometimes unclear. In the present case, a neurogenic mechanism may be involved. The early diagnosis of this oedema has important therapeutic implications.
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PMID:[Low-capillary-pressure pulmonary edema occurring in the acute phase of myocardial infarction]. 670 19

The authors report a case of severe hypertriglyceridemia (148.5 mmol/l) in a 27-year-old woman admitted for coma of unknown origin. Initial investigations revealed ketoacidosis, pancreatitis and noncardiogenic pulmonary edema. The diabetes was unknown. Ketoacidosis was rapidly controlled. The hypertriglyceridemia was corrected by one course of plasma exchange (4,400 ml) during which the patient returned to consciousness. The patient recovered without any sequelae. Only 2 similar cases, treated by plasma exchange, have been reported in the literature until now.
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PMID:Treatment by plasma exchange of a patient with hyperlipidemia and diabetic ketoacidosis with lesional pulmonary edema and acute pancreatitis. 681 94


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