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)

A 63 year old female, who was admitted to a psychiatric hospital for schizophrenia, was referred to our emergency room because of sudden loss of consciousness and convulsions. On arrival, she was drowsy and hypoxemic. Her chest X-ray showed cardiomegaly with pulmonary edema. ECG showed marked ST depression in precordial leads and serum chemistry revealed marked elevation of CPK, GOT and LDH along with hyponatremia and hypochloremia. She was immediately admitted to CCU on suspicion of acute non-transmural myocardial infarction complicated with congestive heart failure. After fluid restriction and intravenous infusion of dopamine she passed large amount of urine, and her consciousness level, electrolyte imbalance and ECG change, improved gradually. Although serum CPK level increased as high as 32,307 IU/ml, there were no signs of left ventricular asynergy on UCG and CPK isozyme analysis performed later revealed more than 99% of serum cCPK was MM-type. We concluded that water intoxication was the cause of the ECG change and the elevated serum CPK, GOT and LDH levels. There are few reports on elevated CPK level in association with water intoxication, in which rhabdomyolysis is speculated as the cause of CPK elevation. But there is no report on ECG change complicated with water intoxication. In our case, electrolyte imbalance caused by water intoxication seemed to play a major role in ST depression and QT prolongation. Although water intoxication is a rare disorder in the general population, it is not infrequent among patients with psychiatric diseases. Care must be taken when such patients present ECG change and serum enzyme elevation mimicking ischemic heart disease.
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PMID:[A water intoxication patient who showed remarkable ST depression and suspected ischemic heart disease]. 152 80

Fifty-two cases of acute phase subarachnoid hemorrhage were studied by brain CT scanning to determine the presence and incidence of ischemic myocardial disorder, the relationship between ischemic change and severity, disease prognosis, and the relationship between acute phase circulatory dynamics and so-called neurogenic pulmonary edema. In all cases, ECGs were carried out and CPK-MB determined. Some of the patients underwent Tl myocardial scintigraphy, echocardiography, cardiac catheterization, as well as circulatory dynamic investigation (by Swan-Ganz catheter) and arterial blood gas analysis. In 31 of the 52 cases (59.6%), 3-day ECG series revealed ischemic changes. These findings were backed up by other cardiac function tests, thus suggesting that myocardial ischemia was present. Results in cases undergoing cardiac catheterization revealed that the myocardial ischemic changes were not due to organic constriction of the coronary artery. Included in those cases in which ECG markedly changed and CPK-MB rose substantially were many patients for whom the prognosis was poor. Evaluation of respiratory function and circulatory dynamics in cases of so-called neurogenic pulmonary edema seemed to indicate decline in cardiac function owing to myocardial ischemic change. This could account for onset of symptoms. These findings support the need for adequate circulatory management in cases of acute subarachnoid hemorrhage with pulmonary edema and/or changes on ECG. In such cases, concurrent catheterization and cerebral angiography (cerebro-cardiac catheterization: CCC) proved effective for evaluating cardiac function and determining whether heart disease was also present.
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PMID:[Ischemic myocardial disorder in acute phase subarachnoid hemorrhage: clinical study of 52 patients]. 204 49

One hundred-thirty patients with acute subarachnoid hemorrhages were investigated to examine the relationship of neurogenic pulmonary edema to cardiac lesions. Abnormal electrocardiograms were observed in 99 of these patients. Left ventricular asynergy was detected in nine of the 99 patients by two-dimensional (2D) echocardiography. In addition to 2D echocardiography, chest radiography, electrocardiography, serum CPK measurements and cardiac catheterization were performed for these nine patients in the acute stages of their subarachnoid hemorrhages. Abnormal electrocardiographic findings included prolongation of QT intervals and marked ST-T changes, which were observed in all nine patients. Pulmonary edema associated with increased pulmonary arterial wedge pressures were noted in seven, and increases in CPK and MB-CPK in all patients, suggesting the occurrence of myocardial necrosis. An increase in serum catecholamine was observed in all patients. Coronary angiography was performed in two patients and revealed normal coronary arteries in both. Biopsy findings were available in three and demonstrated severe fragmentation at the sites of left ventricular asynergy. Pulmonary edema, electrocardiographic abnormalities and left ventricular asynergy improved markedly during the courses of hospitalization. We concluded that left ventricular asynergy and myocardial necrosis may occur during the acute stage of subarachnoid hemorrhage and could produce neurogenic pulmonary edema rather than or in addition to permeability edema.
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PMID:[Left ventricular asynergy and myocardial necrosis accompanied by subarachnoid hemorrhage: contribution of neurogenic pulmonary edema]. 210 11

One of the most common problems in emergency anesthesia for cerebral aneurysm surgery is clinically significant ECG abnormalities. We had a 58 year old patient with severe subarachnoid hemorrhage and diffuse lung edema leading to fatal outcome probably due to catecholamine myocardial injury. During the operative intervention with enflurane and oxygen anesthesia, ST elevation on ECG suddenly appeared and heart failure developed in this patient. Intraoperative ECG suggested the development of acute myocardial infarction of the anterior and inferior wall, but echocardiography revealed a discrepant result; the wall motion abnormality was confirmed in the apex only. The serum CPK in this patient increased a little over the normal limit perioperatively. Overall results suggested that a cause of this patient's death was myocardial injury due to the excessive release of catecholamine. Therefore, we urge the need of through cardiac examinations as well as the administration of preventive drugs for catecholamine myocardial injury in the perioperative management of patients with severe subarachnoid hemorrhage.
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PMID:[Anesthetic management of a patient with severe subarachnoid hemorrhage and diffuse lung edema]. 281 Jul 5

Methods of clinico-instrumental investigation and biochemical monitoring (CPK and its membranous fraction) were employed for examination of 432 patients with acute myocardial infarction (AMI). Among them there were patients with an uncomplicated course of disease (19.4%), recurrences (13.7%) and AMI spreading (9%). Lung edema, a cardiogenic shock, ventricular fibrillation and complicated cardiac rhythm disorders were not detected on the 1st day of disease. Clinico-anamnestic data provided no opportunity for defining factors promoting AMI recurrences whereas AMI spreading frequently developed in patients with repeated AMI, suffering from essential hypertension, obesity and heart failure. Higher diastolic pressure in the pulmonary artery, an increase in the cardiac volume, a decrease in the ejection fraction and left ventricular stroke work--changes which were most pronounced in AMI spreading, were noted in patients with AMI lingering forms. Signs of disseminated intravascular blood coagulation were noted in the venous and arterial blood of patients with lingering AMI forms. A high blood enzyme level was shown to be accompanied by a low level of antibodies to LDH and CPK.
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PMID:[Clinico-pathogenetic variants of protracted forms of acute myocardial infarct]. 361 39

A case of subarachnoid hemorrhage complicated by neurogenic pulmonary edema and neurogenic myocardial damage is reported. A 50-year-old woman was admitted following the sudden onset of headache and disturbance of consciousness due to a ruptured internal carotid posterior communicating artery aneurysm on the right side. She showed respiratory failure due to pulmonary edema, which subsequently improved with the mechanical ventilation. After that, she manifested chest distress and hypotensive episode then occurred. An ECG showed QS wave and ST elevation which suggested the presence of inferolateral myocardial damage. Subsequent rises in serum GOT, GPT, LDH and CPK were noticed. CPK-MB and LDH I and V isozyme levels rose. An echo cardiogram showed hypokinesis of the apical half of the left ventricular septum. The patient died on 5th hospital day due to rerupture of the cerebral aneurysm. Autopsy revealed diffuse myocytolysis with coagulation necrosis of the heart muscle without occlusion of coronary arteries. A small hemorrhagic lesion was found in the hypothalamus. We suggested that a hypothalamic lesion due to subarachnoid hemorrhage stimulated the sympathetic nervous system which in turn discharged endogenic catecholamine. This was probably accompanied by vasospasm of the coronary arteries and systemic peripheral arterioles. Furthermore, myocardial oxygen consumption could have been increased by the increase in catecholamine. Finally, it gave rise to neurogenic pulmonary edema and extensive diffuse myocytolysis of the heart occurred.
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PMID:[Myocardial damage (myocytolysis) caused by subarachnoid hemorrhage]. 409 85

A bolus of 1000 mg of 5-FU intravenously was given to a 54-year-old patient with adenocarcinoma of colon, a month after hemicolectomy. He had not received irradiation therapy. Five hours later he complained of severe chest pain; after 24 hours ecg. changes of pericarditis were seen and on heart auscultation a pericardial friction rub was heard. After 6 day the ecg. returned to the pattern of that on day of admission to the ICCU. Two further injections of 1000 mg of 5-FU were also followed by severe precordial pain and the same ecg. pattern. The pulmonary edema 14 hours after the second injection and the slight elevation of CPK value after the third injection strongly suggest myocardial cell damage. For the strictly temporal relationship between the clinical and electrocardiographic pattern with 5-FU administration intravenously, we are of the opinion that the perimyocarditis was due to the direct toxic action of 5-FU on pericardium and myocardium.
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PMID:[Early cardiotoxicity of 5-fluorouracil]. 734 80

Neuroleptic Malignant Syndrome (NMS) is a rare and life threatening complication of treatment with Neuroleptic medication. Phenothiazine and butyrophenones are most frequently implicated in this syndrome even though there are case reports with other drugs. In this paper we describe the classical presentation of this syndrome in eight cases who had been on either a butyrophenone, a phenothiazine or a combination of these drugs. In addition some of our patients were also on either Lithium and/or Amitrytiline for control of depressive symptoms. Fever, muscule rigidity and elevated CPK are the important criteria for diagnosis and they were noted in all our patients. In addition four of our patients fulfilled five of the six minor criteria laid down by Levenson. Both Sinemet and Bromocriptine were found to be effective in the treatment of seven of the eight cases. However treatment with Dantroline sodium was associated with severe muscle wasting in one of our cases and the drug had to be discontinued. Two of our patients developed suspected myoglobinuria with dark coloured urine and progressive renal failure. One patient died after development of renal failure, pulmonary edema and hyperkalemia as a consequence of this disorders.
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PMID:Management of neuroleptic malignant syndrome--a series of eight cases. 800 46

Toxicological effects of fenvalerate on rat lungs by bronchoalveolar lavage (BAL) and biochemical changes in 20 workers exposed to fenvalerate were studied. The results showed that the levels of CPK, albumin, TP, AKP, ACP, alpha 1-AT, MDH, LDH, glucose, and lactic acid in BAL fluid increased significantly, with a CPK level the most sensitive one. most of the above parameters in BAL fluid changed four hours after exposure and returned basically to normal on the fourth day after exposure. Only the levels of ACP, alpha 1-AT and albumin were found increased in their blood. It showed a good linear relationship between blood and BAL levels of alpha 1-AT and ACP. Changes in some biochemical parameters were also found in workers exposed to fenvalerate, which correlated to the length of their employment. The results suggested inhalation of fenvalerate may cause alveolitis, pulmonary edema, and damage to lung cells.
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PMID:[Biochemical and toxicological studies of fenvalerate on the lung]. 813 61

To clarify the optimal management and delineate the characteristics of patients with severe left main disease and cardiogenic shock as a result of an acute anterolateral myocardial infarction (left main shock syndrome), we analyzed the course of 13 such patients from September 1989 to June 1997. Of the 13 patients, 7 (53.8%) were managed with emergency coronary angioplasty (group A), 3 (23.1%) were treated with emergency coronary angioplsty following coronary bypass graft surgery (group B) and 3 (23.1%) underwent emergency coronary bypass graft surgery alone (group C). The interval from the beginning of myocardial ischemia to revascularization was 266 +/- 303 min. The degree of diameter stenosis found in the left main coronary artery was 98.1 +/- 1.8%. Overall in-hospital mortality for the 13 patient with left main shock syndrome was 76.9% (group A: 7/7; group B: 1/3; group C: 2/3, NS) and operative mortality was 61.5% (group A: 6/7; group B: 0/3; group C: 2/3, p = 0.03). When all 13 patients were examined together, the presence of ventricular tachycardia (VT) x ventricular fibrillation (Vf) was found to be the most powerful univariate predictor of operative death (p = 0.03). This is, 7 (87.5%) of the 8 patients with VT x Vf at presentation died within 30 postoperative days, and only 1 (20%) of the 5 patients without VT x Vf died (p = 0.03). Age, percent stenosis of the left main or right coronary arteries, the interval from the beginning of myocardial ischemia to revascularization, intubation, systolic pressure, fractional shortning, pulmonary artery pressure, pulmonary capillary wedge pressure, coronary risk factors, pulmonary edema, mitral regurgitation and percutaneous cardiopulmonary support failed to attain univariate significance at the P = .1 level. The postoperative peak CPK level was 15665 +/- 6710 IU/1 in operative death compared to 4733 +/- 2749 IU/1 in operative survival (p = 0.01). In conclusion, emergency coronary angioplasty following coronary bypass graft surgery for left main shock syndrome has been a very successful therapeutic option. Finally, for the entire group of 13 patients with left main shock syndrome, VT x Vf significantly decreased short-term survival.
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PMID:[Prognosis and management in patients with left main shock syndrome--emergency PTCA following CABG]. 1003 32


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