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)

Transient left ventricular apical ballooning syndrome (TLVAB), also known as Takotsubo cardiomyopathy, is a cardiac syndrome characterized by transient left ventricular dysfunction in the absence of obstructive atherosclerotic coronary artery disease. An episode of emotional and/or physiologic stress frequently precedes presentation of this syndrome. TLVAB may initially present as an acute coronary syndrome characterized by chest pain, pulmonary edema, electrocardiographic changes, elevated cardiac enzymes, and cardiogenic shock. This syndrome is still underestimated today and the potential appearance of TLVAB during the perioperative period can be a great challenge. Adequate beta-blockade is the mainstay in the treatment of patients with TLVAB during the acute phase and also for long-term management.
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PMID:Perioperative transient left ventricular apical ballooning syndrome: Takotsubo cardiomyopathy: a review. 2020 56

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

Traumatic injuries of the mitral valve are rare but life threatening complications of high speed motor vehicle accidents. The physician must recognize traumatic mitral valve injuries early and arrange for immediate surgical repair, because if the papillary muscle ruptures completely, florid congestive failure and pulmonary edema develop rapidly. The signs and symptoms of traumatic mitral valve injuries vary. In general, the patient complains of chest pain and is hypotensive, dyspneic and cyanosed. He may have a bruised anterior chest wall, fractured ribs, unstable sternum and a flail chest, but extensive and severe cardiac damage from blunt trauma can occur without external evidence of chest injury. Traumatic mitral valve injuries should be suspected in any patient who has a blunt chest injury when a previously undocumented systolic murmur is discovered along the lower left sternal border or apex of the heart. The patient's deterioration, and the development of symptoms and signs of congestive heart failure support the diagnosis.
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PMID:Traumatic rupture of a papillary muscle of the mitral valve due to blunt thoracic trauma. 2128 34

Neurogenic stunned myocardium (NSM) and Takotsubo cardiomyopathy (TCM) are two syndromes that coexist in the medical literature. They share many common features. We hypothesized that they, in fact, represent the same syndrome. We collected and analyzed case reports of transient left ventricular (LV) dysfunction in neurologic conditions. Cases were compared based on the diagnosis and then based on the pattern of wall motion abnormality. Of 112 cases, 61 were diagnosed as TCM and 37 as NSM, and in 14 cases, the authors used both terms. Overall, the patients with NSM were younger, and the severity of LV systolic dysfunction and timing of recovery was similar, as well as the prevalence of cardiac enzyme elevation. Pulmonary edema on presentation was more prevalent in patients with NSM while chest pain and ST-segment elevation was more common in patients with TCM. While only regional, predominantly apical, wall motion abnormality was described in TCM, some patients in the NSM group had global LV dysfunction. NSM and TCM likely share the same mechanism and pathologic substrate. Their natural course is almost identical. They both likely represent the same syndrome of stress-induced cardiomyopathy. Current definition of stress-induced cardiomyopathy includes only regional wall motion abnormalities. It should be expanded to include all varieties of wall motion abnormalities including global hypokinesis.
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PMID:Neurogenic stunned myocardium and takotsubo cardiomyopathy are the same syndrome: a pooled analysis. 2160 86

We report the case of a healthy 21-year-old woman who performed iterative breath-hold dives in relatively cold water, not exceeding depths of 5 meters but with "empty lungs." At the end of a dive, after experiencing an intense involuntary diaphragmatic contraction underwater, she presented hemoptysis followed by chest pain and cough. Chest radiography and computed tomography were performed 24 hours later, confirming the diagnosis of pneumomediastinum. The clinical course was benign: However, chest pain and effort dyspnea lasted for a few weeks. The pathophysiology of this accident may be explained by a combination of mechanisms involved in several clinical entities, namely pulmonary edema of immersion, pulmonary barotrauma and spontaneous pneumomediastinum.
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PMID:Hemoptysis and pneumomediastinum after breath-hold diving in shallow water: a case report. 2172 55

A 67-year-old woman presented to the emergency room with progressive claudication, chest pain, and flash-pulmonary edema. Her past medical history was significant for poorly controlled hypertension requiring multiple antihypertensive medications, renal insufficiency, and tobacco abuse. Diagnostic evaluation revealed an extensive exophytic plaque localized to the paravisceral aorta resulting in high-grade stenoses of the proximal aorta as well as the celiac, superior mesenteric, and left renal arteries. She underwent surgical revascularization through a retroperitoneal aortic exposure and trapdoor aortic endarterectomy, the technical conduct of which is described in this manuscript. The patient recovered uneventfully and experienced resolution of her claudication and pulmonary symptoms, improved blood pressure control, and normalization of her creatinine. Review of the medical literature pertaining to management of proximal occlusive disease of the abdominal aorta is discussed.
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PMID:Retroperitoneal trapdoor endarterectomy for paravisceral "coral-reef" aortic plaque. 2266 68

Leptospirosis is a neglected global disease with significant morbidity and mortality. Cardiac complications such as chest pain, arrhythmias, pulmonary oedema and refractory shock have been reported in patients with severe disease. However, the frequency and extent of cardiac involvement in leptospirosis, are under-reported and poorly understood. Multiple factors may contribute to clinical manifestations that suggest cardiac involvement, causing diagnostic confusion. A variety of electrocardiographic changes occur in leptospirosis, with atrial fibrillation, atrioventricular conduction blocks and non-specific ventricular repolarization abnormalities being the most common. Electrolyte abnormalities are likely to contribute to electrocardiographic changes; direct effects on Na(+)-K(+)-Cl(-) transporters in the renal tubules have been postulated. Echocardiographic evidence of myocardial dysfunction has not been adequately demonstrated. The diagnostic value of cardiac biomarkers is unknown. Histopathological changes in the myocardium have been clearly shown, with myocardial inflammation and vasculitis present in postmortem studies. Nonetheless, the pathophysiology of cardiac involvement in leptospirosis is poorly understood. Cardiac involvement, demonstrated electrocardiographically or clinically, tends to predict poor outcome. No specific therapies are available to prevent or treat cardiac involvement in leptospirosis; current management is based on correction of deranged homeostasis and supportive therapy. Evidence suggests that direct myocardial damage occurs in patients with severe leptospirosis, and further studies are recommended to elucidate its pathophysiology, clinical features and contribution to overall prognosis, and to identify appropriate diagnostic investigations and specific therapies.
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PMID:Cardiac involvement in leptospirosis. 2281 58

A 44-year-old female was presented to our department with a 4-day history of shortness of breath and chest pain. The chest X-ray showed pneumothorax with completely collapsed left lung. Thoracentesis was performed. She complained of dyspnea and the oxygen saturation decreased to 74% after thoracentesis. The 2nd chest X-ray and computed tomography demonstrated a left-sided pulmonary edema. A 67-year-old man came to our department complaining of persistent cough. The chest X-ray showed pneumothorax with collapsed right middle and lower lobes. Thoracentesis was performed. He complained of dyspnea and the oxygen saturation decreased to 87% after thoracentesis. The 2nd chest X-ray and computed tomography demonstrated an expanded right upper lobe, but also pulmonary edema in the right middle and lower lobes. Those patients were treated with supplemental oxygen without endotracheal intubation. Their oxygen saturation stabilized within 12 hours. They were successfully treated with the sole administration of oxygen.
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PMID:[Reexpansion pulmonary edema following thoracentesis]. 2391 48

Reexpansion pulmonary oedema is a rare but possibly lethal complication of thoracic drainage for pneumothorax. Morbidity and mortality of this complication remains high (up to 20% of lethal cases) and as such deserves our attention. We report a case of ipsilateral left-sided pulmonary oedema following chest tube insertion in a 42-year-old male patient with spontaneous pneumothorax. Pneumothorax can be expected to last for up to 3 weeks (from the first presentation of sudden dyspnoea and chest pain). The pathophysiology of this lung affection has not yet been completely elucidated; the crucial role is probably played by damage to the endothelium which is followed by increased endothelial permeability during ischemia-reperfusion injury in a rapidly reexpanding lung. The main risk factors for the development of RPE are young age (the younger the patient, the higher the risk), the female sex, the degree of lung collapse, a pneumothorax that lasts more than 24 hours, a reexpansion of the lung in less than ten minutes, the use of a suction system, and - in cases of a pleural effusion - an evacuation volume of more than 2000 ml. Although in patients with these risk factors the administration of initial negative pressure should be avoided, this procedure remains common practice in pneumothorax treatment in the Czech Republic. Thoracic surgeons are more likely to use the suction system than pulmonologists (70% versus 52%). RPE manifestation ranges from benign clinical course (patients are free of complaints with only pathological chest radiography findings) to potentially lethal rapid respiratory failure with circulatory shock. Most patients develop RPE within 1 hour of expansion and the ipsilateral lung is affected. Only rarely can pulmonary oedema be bilateral, or in the contra-lateral lung. Treatment of RPE is supportive and depends on the individual patients condition, ranging from mere monitoring to mechanical ventilation for serious cases. Positive pressure mechanical ventilation and the utilization of positive end-expiratory pressure (PEEP) remains the gold standard of treatment.
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PMID:[Reexpansion pulmonary oedema after drainage of a long-term spontaneous pneumothorax - a case report]. 2396 19

A 19-years old, previously healthy male, ingested the higher amount of rifampicin, isoniazyd, pyrazinamide, ketoprofene and alcohol. Within less than 20 hours he developed dyspnoe, pruritus, red man syndrome, and ECG changes suggesting acute coronary syndrome appeared - ST interval elevation. In the next few hours chest pain appeared and troponin I concentration was elevated (13.54 ng/ml). The performed echocardiography revealed global hypokinesis with the decreased left ventricular ejection fraction (approx. 30%). There was no significant pathological changes in coronarography, except for slowed blood flow. Further patient developed cardiogenic shock, pulmonary oedema and died within 32 hours from medication overdose.
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PMID:Fatal suicidal poisoning with antituberculosis agents with ST elevation and acute coronary syndrome symptoms--a case report. 2446 13


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