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

Complex physiologic responses occur as nonacclimatized lowland dwellers ascend above 10,000 feet, with a resulting partial pressure of arterial oxygen of less than 60 mm Hg. There are marked hemodynamic changes and shifts in body fluids that may result in organ dysfunction. The suspected pathogenesis of these acute hypobaric hypoxic-induced illnesses is discussed. Cerebral dysfunction may present as acute mountain sickness or high-altitude cerebral edema. Usually asymptomatic high-altitude retinal hemorrhage and noncardiogenic high-altitude pulmonary edema also are described. All of these illnesses apparently represent a spectrum of pathologic states initiated by an exaggerated vascular response to hypoxia. With the exception of retinopathy, high-altitude illness can be prevented by slow ascent. Early recognition of cerebral or pulmonary edema and immediate descent will prevent serious consequences of nonacclimatized persons who are acutely exposed to hypobaric environments.
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PMID:The pathophysiology of acute high-altitude illness. 675 Oct 81

We have studied electrocardiograms, chest radiographs, and digitised apex echocardiograms in 16 patients with malignant hypertension before and after up to six months of antihypertensive treatment and compared them with those of eight patients with severe benign hypertension. Adequate blood pressure reduction was obtained in 14 with resolution of retinopathy, but one patient died and another had poor blood pressure control. Nine had electrocardiographic criteria of left ventricular hypertrophy which did not change with treatment and 10 had lateral ischaemia which resolved in seven. The malignant hypertensives were divided into seven with and nine without a previous hypertensive history. Both groups had normal echocardiographic cavity dimensions, but the former group tended to have hypertrophy (similar to that in benign hypertensives) and the latter did not. After adequate reduction of blood pressure, no change in wall and septal thickness occurred (except in one patient with poor blood pressure control). At entry, malignant hypertensives showed delayed mitral valve opening with significant cavity dimension increase during prolonged isovolumic relaxation, reduced peak rate, and prolonged duration of cavity dimension increase and cavity shape change (inward wall motion) during the upstroke of the apexcardiogram which showed a tall "a" wave. After reduction of blood pressure, though the delay in mitral valve opening persisted, the timing of A2 returned towards normal and the dimension change during the upstroke of the apexcardiogram and the relative height of the "a" wave were reduced but remained significantly different from normal. Some patients without a previous hypertensive history may develop a malignant phase without left ventricular hypertrophy on the electrocardiogram or echocardiogram. They maintain their pump function even with radiological pulmonary oedema, have incoordinate relaxation and contraction, and have abnormal filling. Similar functional abnormalities were found in malignant hypertensives with hypertrophy. Treatment to reduce blood pressure reduces incoordinate contraction, but impaired diastolic function persists as in benign hypertension, suggesting that these abnormalities are the result of altered myocardial properties that may occur without hypertrophy.
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PMID:Malignant hypertension: cardiac structure and function at presentation and during therapy. 683 34

Oxygen therapy is administered to decrease tissue hypoxia and to relieve arterial hypoxemia. High concentrations of oxygen are often used in patients with adult respiratory distress syndrome. Supplying oxygen to animals has been known to produce tissue damage, with toxicity increasing with the increase of oxygen concentrations and exposure pressures. End-organ damage from hyperoxia depends on both the concentration of oxygen administered and the oxygen pressure during exposure. Prolonged exposure to hyperbaric oxygen causes central nervous system and pulmonary toxicity, which results in atelectasis, pulmonary edema, and seizures. Lung damage may occur as a result of normobaric hyperoxia. A severe retinopathy (retrolental fibroplasia) occurs in neonates during oxygen exposures. For all of these reasons, the lowest possible concentration of oxygen that relieves tissue hypoxia is recommended in patients with adult respiratory distress syndrome.
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PMID:Oxygen toxicity. 808 71

Patent ductus arteriosus (PDA) in preterm newborns prior to 28 weeks of gestation has led to many challenges regarding the type and timing of treatment regimens. A PDA results in increased pulmonary blood flow and redistribution of flow to other organs. Several co-morbidities (i.e., necrotizing enterocolitis, intracranial hemorrhage, pulmonary edema/hemorrhage, bronchopulmonary dysplasia, and retinopathy) are associated with the presence of a PDA, but whether or not a PDA is responsible for their development is still unclear. The prostaglandin inhibitor, indomethacin, is effective in the treatment of PDA. Questions regarding the optimal timing of the intervention--early prophylaxis or treatment, once signs and symptoms become evident--have challenged physicians for decades. Both evidence and experience are explored in this article. Comparative physiology between the full-term and preterm newborn and the barriers preventing the necessary cascade of events leading to permanent constriction of the PDA are reviewed.
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PMID:Patent ductus arteriosus: pathophysiology and management. 1662 16

A patent ductus arteriosus (PDA) results in increased pulmonary blood flow and redistribution of flow to other organs. Several co-morbidities (i.e., necrotizing enterocolitis, intracranial hemorrhage, pulmonary edema/hemorrhage, bronchopulmonary dysplasia, and retinopathy) are associated with the presence of a PDA, but whether or not a PDA is responsible for their development is still unclear. In this review, comparative physiology between the full term and preterm newborn and the barriers preventing the necessary cascade of events leading to permanent constriction of the PDA are reviewed.
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PMID:Mechanisms regulating the ductus arteriosus. 1677 73

Hypertensive emergencies must be distinguished from severe blood pressure elevations without acute target organ damage. Clinical examination (chest pain, dyspnoea, neurological disorders, ECG, retinal examination) and laboratory tests (blood and urine tests, cerebral imaging in case of neurological disorders) have to be immediately performed. Immediate referral to an intensive care unit is indicated, and an intravenous antihypertensive therapy has to be implemented. Blood pressure objectives depend on the associated acute pathology (myocardial infarction, pulmonary oedema, aortic dissection, severe pre-eclampsia and eclampsia of pregnancy, hypertensive encephalopathy, retinopathy, subarachnoid hemorrhage, cerebral hemorrhage, ischemic stroke treated or not with thrombolysis).
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PMID:[Hypertensive emergencies in adults: a practical review]. 2054 34

High-altitude retinopathy is one of altitude-related illnesses. Its signs include high-altitude retinal hemorrhages, dilated vessels and peripapillary hyperemia. Increased intracranial pressure seems to be the main cause of all high-altitude diseases including high-altitude retinopathy, cerebral oedema and high-altitude pulmonary oedema. We present the case of high-altitude retinopathy in a 35-year-old woman who reported decreased vision in her right eye, scotomas and high-altitude retinopathy after ascending to more than 7000 meters above sea level. The associated optical coherence tomography findings, fundus photography and literature review are presented. High-altitude retinopathy is an important multifactorial condition of unknown mechanism and etiology, which significantly impacts human vision. Climbing high mountains can cause retinopathy in otherwise healthy people and may lead to permanent sequelae such as retinal nerve fiber layer and optic nerve defects. These symptoms, however, may resolve without causing any permanent damage to the retina. Conservative treatment may help to relieve them. With increasing popularity of mountaineering, ophthalmologists should be prepared to diagnose and treat high-altitude retinopathy.
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PMID:High-altitude retinopathy--case report. 2579 81

Malaria is the most important parasitic diseases of humans and one of the leading causes of morbidity and mortality in tropical countries. Earlier Plasmodium vivax was considered as a benign infection, but now it is recognized as a cause of severe malarial disease. It causes severe malarial disease similar to those as Plasmodium falciparum including cerebral malaria, severe anaemia, severe thrombocytopenia, hepatic dysfunction, shock, acute respiratory distress syndrome (ARDS), acute renal failure, and pulmonary oedema. Malarial retinopathy includes retinal whitening, vessel changes, retinal hemorrhages and papilledema. However, retinal hemorrhages are very rare in Plasmodium vivax infestation. Hereby, we report a case of 30-year-old man, who presented with fever with chills and diminution of vision. He was found to have Plasmodium vivax infection with retinal hemorrhages. He was treated successfully with artisunate, primaquine and doxycycline, completely recovered after one month.
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PMID:Retinal Hemorrhages in Severe Non-cerebral Plasmodium vivax Malaria in an Adult. 2626 50

Juvenile dermatomyositis (JDM) is a multisystem vasculopathy that infrequently presents with acute complications (1). We report here the case of a 12-year-old girl with JDM who developed Thrombotic Thrombocytopenic purpura (TTP) and Purtscher's retinopathy. This is the second pediatric case of JDM with TTP and Purtscher's retinopathy in the literature. The diagnosis of JDM was based on her clinical presentation (fever, myalgia, proximal muscle weakness, characteristic skin rash and elevated muscle enzymes) (2). Despite improvement of rash, fever and weakness with corticosteroids and intravenous Immunoglobulins (IVIG), the patient developed retinopathy, thrombocytopenia, hemolytic anemia, renal failure, and pulmonary edema within 1 week of initial treatment. A clinical diagnosis of TTP and Purtscher's retinopathy was made and her ADAMTS13 activity was found to be low. Regardless of aggressive treatment with pulse steroid therapy, IVIG, plasmapheresis along with multiple infusions of Fresh Frozen plasma (FFP), her condition deteriorated. In view of her worsening condition, she received one dose of Rituximab and within 48 h, her hematological and retinal involvements improved. Rituximab was given at the same dose once weekly thereafter for 4 total doses. Her disease process was halted, and retinopathy improved significantly in 48 h and continued to gradually improve over 3 weeks of maintenance therapy with cyclosporine, methotrexate, and IVIG and then stabilized. This report documents the association of TTP and Purtscher's retinopathy with JDM, emphasizing that early recognition and prompt treatment with rituximab along with the current standard of care treatment i.e., Vincristine, corticosteroids and plasmapheresis could be of potential benefit in controlling disease activity.
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PMID:Juvenile Dermatomyositis (JDM) Complicated by Thrombotic Thrombocytopenic Purpura (TTP) and Purtscher's Retinopathy Responsive to Rituximab: Case Report and Literature Review. 3285 May 49