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)

Acute pulmonary oedema usually has a fatal outcome. In this clinical report, we present rare cases of pulmonary oedema that were associated with Japanese B encephalitis, lymphangitis in breast carcinoma, fat embolism due to long-bone fracture, and the rupture of cerebral mycotic aneurysms. A total of 18 patients in the four disease categories were collected in two teaching hospitals in Taipei and Hualien. Upon admission, routine and specific examinations were taken and all patients showed clear lungs by chest X-ray; however, signs of acute pulmonary oedema occurred within 7 days. After resuscitation, all patients died of acute pulmonary oedema. In patients with fat embolism, the levels of non-esterified plasma fatty acids, cGMP, 5-hydroxytryptamine (serotonin) and nitrates/nitrites were increased during pulmonary oedema. Immunohistochemical staining revealed virus infection and neuronal death, predominantly in the medial, ventral and caudal medulla in cases of Japanese B encephalitis. The pulmonary oedema due to central sympathetic activation in Japanese B encephalitis may be related to destruction of depressor mechanisms in the medulla. The rupture of mycotic aneurysms is known to cause cerebral compression that results in acute pulmonary oedema. Blockade of lymphatics, capillaries and venules in breast carcinoma with lymphangitis causes the development of rapid lung oedema. The pathogenesis of pulmonary oedema is much more complicated in fat embolism. Mediators such as cGMP, 5-hydroxytryptamine, nitric oxide and presumably other chemical substances may also be involved.
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PMID:Acute pulmonary oedema: rare causes and possible mechanisms. 1260 84

Acute respiratory distress syndrome (ARDS) can be associated with various disorders. Among these, coronavirus infection may cause life-threatening severe acute respiratory syndrome (SARS). In this review, we present animal models and techniques for the study of ARDS, and discuss the roles and possible mechanisms of various chemical factors, including nitric oxide (NO). Our early work revealed that cerebral compression elicits severe hemorrhagic pulmonary edema (PE), leading to central sympathetic activation that results in systemic vasoconstriction. The consequence of systemic vasoconstriction is volume and pressure loading in the pulmonary circulation. Vasodilators, but not oxidant radical scavengers, are effective in the prevention of centrogenic PE. In isolated perfused lung, exogenous and endogenous NO enhances lung injury following air embolism and ischemia/reperfusion. In contrast, NO synthase (NOS) inhibitors reverse such lung injury. Although NO is important in maintaining vasodilator tone, hypoxia-induced pulmonary vasoconstriction is accompanied by an increase instead of a decrease in NO release. In animal and isolated lung studies, endotoxin produces acute lung injury that is associated with increases in cytokines and inducible NOS mRNA expression, suggesting that NO is toxic to the lung in endotoxin shock. Recently, we reported several rare cases that indicate that ARDS in patients with Japanese B encephalitis, lymphangitis with breast cancer and fat embolism is caused by different mechanisms. Our early and recent studies on ARDS and PE may provide information for clinical practice and the understanding of the pathogenesis of SARS.
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PMID:Acute respiratory distress syndrome. 1457 60

Japanese encephalitis (JE) is numerically the most important global cause of encephalitis and so far confirmed to have caused major epidemics in India. Most of the reported studies have been in children. This largest study involving only adults, belonging to four epidemics, is being reported from Gorakhpur. The aim of this study is to detail the acute clinical profile (not viral) outcome and to classify the sequelae at discharge. This prospective study involved 1,282 adult patients initially diagnosed as JE admitted during the epidemics of 1978, 1980, 1988, and 1989, on identical clinical presentation and CSF examination. In the meantime, the diagnosis of JE was confirmed by serological and/or virological studies in only a representative number of samples (649 of 1,282 cases). Eighty-three left against medical advice (LAMA) at various stages, so 1,199 of 1,282 were available for the study. Peak incidence of [1,061 of 1,282 (83%)] of clinically suspected cases was from September 15 to November 2. Serum IgM and IgG were positive in high titers in 50.87% (330 of 649) and IgM positive in CSF in 88.75% (109 of 123) of the cases. JE virus could be isolated from CSF and brain tissue in 5 of 5 and 4 of 5 samples, respectively. Altered sensorium (AS) in (96%), convulsions (86%), and headache (85%) were the main symptoms for hospitalization by the third day of the onset. Other neurological features included hyperkinetic movements in 593 of 1,282 (46%)-choreoathetoid in 490 (83%) and bizarre, ill-defined in 103 (17%). The features of brain stem involvement consisted of opsoclonus (20%), gaze palsies (16%), and pupillary changes (48%) with waxing and waning character. Cerebellar signs were distinctly absent. Dystonia and decerebrate rigidity was observed in 43 and 6%, respectively, paralytic features in 17% and seizures in 30%. Many non-neurological features of prognostic importance included abnormal breathing patterns (ABP) (45%), pulmonary edema (PO) (33%), and upper gastrointestinal hemorrhage (UGIH) (16%). Injection dexamethasone was used in 1978 in all 208 cases, including 21 of PO. Patients were later randomized alternately in dexa and non-dexa groups. Forty-six cases of PO from the non-dexa group were transferred to the dexa group as an ultimate life-saving measure. Thus, it was administered in 737 of 1,199 patients including 529 patients from the later epidemics in doses of 4 mg IV every 8 h for 7 days. Of 1,199, 462 did not receive it. There was no significant difference in mortality (p > 0.05) between the dexa (42.47%) and the non-dexa group (42.86%). All PO cases expired; so after the exclusion of the PO cases from dexa group, the difference of 6.14% (42.86 and 36.72) became significant (p < 0.01) (511 of 1,199 (43%) expired, [320 of 511 (63%) died within 3 days of hospitalization]). Out of a total of 1,199 patients treated, 688 (57%) were discharged; 23 of 688 (3%) without any sequelae and 665 of 688 (97%) with neuropsychiatric deficits classified into nine groups. During the four epidemics, the diagnosis of JE was basically on identical clinical presentation of acute encephalitic syndrome (AES) consisting of (1) abrupt onset of fever, headache, and AS, (2) dystonias and various movement disorders, (3) opsoclonus and gaze palsies, (4) CSF findings, and (5) the presence of residual neuropsychiatric and neurological features in the survivors.
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PMID:Japanese encephalitis (JE). Part I: clinical profile of 1,282 adult acute cases of four epidemics. 2167 23