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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Common intracranial complications following head injury are meningitis, usually associated with a basilar skull fracture or open-depressed skull fracture; delayed hematoma; hydrocephalus; and vascular injuries. Prophylactic antibiotics are not recommended for the management of basilar skull fractures. The best means of preventing infection from open-depressed skull fractures is operative debridement and thorough irrigation, though recent evidence suggests that select cases can be safely managed without operation. Serial CT scans should be obtained in severely head-injured patients to identify delayed hematomas. CT and MRI scans obtained several weeks or months after severe head injury frequently reveal enlarged ventricles, though only a small percentage of these patients have clinical hydrocephalus. Those that do, often benefit from a shunt. Vascular injuries frequently are not detected until ischemic symptoms develop hours or days after the injury. Recommended treatment for intimal tears or dissection is full anticoagulation, but in those with cerebral contusions or other intracranial lesions, this may present an unacceptable risk for intracranial hemorrhage. Pulmonary infections frequently occur following head injury, and can be associated with admission to the ICU and intubation. A large percentage of these infections are caused by enteric gram-negative organisms, and aggressive treatment with appropriate antibiotics is necessary. Aspiration of gastric contents is common in head-injured patients and is frequently complicated by bacterial superinfection. The routine use of antacids and H2 blocking agents leads to bacterial colonization of the stomach with anaerobes and gram-negative aerobes. Thus, empiric therapy for aspiration pneumonia should include clindamycin. Sinusitis is a frequent cause of fever and leukocytosis in patients with nasotracheal or nasogastric tubes in place for several days and often subsides spontaneously with removal of the tubes. Pulmonary edema is often caused by excessive fluid administration during resuscitation of these patients, and can be avoided by monitoring central venous pressures. Pulmonary edema may also be caused by ARDS, excessive catecholamine release, or primary cardiac failure. Most of these patients will benefit from early intubation and PEEP. Pulmonary emboli most often originate from deep venous thrombi, and there is increasing evidence that prophylaxis with low-dose heparin and pulsating boots can significantly reduce the incidence of both complications. Erosive gastritis is found in the majority of severely head-injured patients and may be due to ischemia of the gastric mucosa as well as gastric hyperacidity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Complications of head injury and their therapy. 182 50

Radiologic assessment of the cause of pulmonary parenchymal consolidation in end-stage heart failure may be difficult. From August 1982 to May 1989, 22 patients being considered for orthotopic cardiac allografts had parenchymal consolidation on their chest radiographs, most commonly in the right lower lobe. Our purpose was to determine from standard radiologic studies whether this consolidation represented alveolar pulmonary edema in an atypical basal distribution, pneumonia, or pulmonary infarction. This differentiation is important because pneumonia is an absolute and infarction is a relative contraindication to surgery, whereas successful transplantation can be performed in a setting of pulmonary edema. The chest radiographs were reviewed retrospectively. When available, pulmonary angiograms, nuclear medicine ventilation/perfusion scans, and needle biopsy findings were also evaluated. The radiologic assessment was correlated with the results of surgical, autopsy, or clinical outcome. None of the conventional modalities was very accurate--the plain chest film was correct in only 63%, nuclear medicine studies in 50%. Angiography was the single most useful test, with an accuracy of 75%.
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PMID:Problems in assessment of pulmonary parenchymal consolidation in heart transplant candidates. 185 70

Seventy-nine patients with ischemic mitral regurgitation were followed up for a period of 20 +/- 8 months. The risk of death increased with age and cardiac failure at the time of inclusion. The risk of cardiac events increased with these factors and also with raised serum creatinine and decreased echocardiographic fractional shortening. The global 2 year survival was 72.8% and survival without a further cardiac event was 48.7%. Surgery and angioplasty increased global survival and freedom from cardiac events of patients with severe regurgitation (74.9% and 68.8% versus 59.4% and 46.1% for medical therapy alone). The functional improvement was also greater in patients undergoing surgery or angioplasty (80% of patients in NYHA Stage I versus 53.8% in the medical group). Angioplasty was only performed in cases of paroxysmal mitral regurgitation by reversible papillary muscle ischemia. Surgery (coronary bypass usually associated with mitral valve replacement) was associated with better results than medical therapy alone in permanent mitral regurgitation by papillary muscle dysfunction or rupture. Despite a high immediate mortality, this option should be considered rapidly in cases of severe ischemic mitral regurgitation with pulmonary oedema.
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PMID:[Prognosis of ischemic mitral valve insufficiency]. 192 8

This paper presents a case of Irukandji syndrome (envenomation by the jellyfish, Carukia barnesi) with pulmonary oedema and hypokinetic cardiac failure. This case highlights the need for victims (and operators of tours venturing into the waters of North Queensland) to treat even apparently innocuous stings with vinegar and to avoid freshwater bathing and rubbing of stings immediately after such incidents. It also reinforces the use of phentolamine to treat the symptoms of catecholamine release associated with the syndrome. This patient required inotropic support and further underlines the need for practitioners to be aware that the syndrome can have severe sequelae and that central venous monitoring and inotropic management should be available when treating Irukandji stings.
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PMID:Cardiac failure following Irukandji envenomation. 197 28

An obese woman with a one-year history of episodic nocturnal chest pain was admitted because of shock and pulmonary edema. A clinical diagnosis of acute myocardial infarction and cardiogenic shock was made. She was ventilated and successfully resuscitated. Subsequent investigations showed no evidence of cardiac dysfunction or coronary disease, but sleep study confirmed the diagnosis of obstructive sleep apnea syndrome (OSAS). We suggest that the nocturnal angina and heart failure in this patient might have resulted from extreme hypoxemia produced by OSAS. This case raised the possibility that the high cardiovascular mortality rate reported in OSAS might not necessarily relate to underlying coronary artery disease. Further investigations are required to delineate the true incidence of coronary disease in patients with OSAS.
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PMID:Obstructive sleep apnea presenting with nocturnal angina, heart failure, and near-miss sudden death. 200 55

The importance of recognizing symptomatic heart failure with preserved left ventricular (LV) systolic function has only recently been appreciated. To determine its frequency and identify clinical features that make the bedside diagnosis likely, 82 patients admitted for decompensated heart failure were classified into 2 groups based on their LV systolic performance, as defined by fractional shortening (FS): group I (n = 59), with impaired systolic function (fractional shortening less than 24%), and group II (n = 23) with preserved systolic function (fractional shortening greater than or equal to 24%). Mean fractional shortening was 15 +/- 5% and 39 +/- 1% for groups I and II, respectively. Female gender (p less than 0.05), obesity (p less than 0.01) and diastolic blood pressure greater than or equal to 105 mm Hg (p less than 0.05) predominated in group II. Jugular venous distention was identified more frequently in group I (p less than 0.05). No statistically significant difference between the 2 groups was noted among various demographic variables (age, duration of symptoms, history of hypertension, ischemic heart disease and heavy alcohol drinking) or physical findings (S3 gallop, edema, cardiomegaly, pulmonary congestion and pulmonary edema). Echocardiographic mean left ventricular dimension measured 6.6 +/- 1 versus 5.0 +/- 1 cm (p less than 0.01) and mean posterior wall thickness 1.1 +/- 0.3 versus 1.4 +/- 0.4 cm (p less than 0.01) in group I and II, respectively. The combination of diastolic blood pressure greater than or equal to 105 mm Hg and an absence of jugular venous distention had a high specificity and positive predictive value (100%) for identifying group II patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bedside diagnosis of preserved versus impaired left ventricular systolic function in heart failure. 173 66

46-year-old male patient was born in Niigata Prefecture and thereafter lived in Tokyo. In late January 1985, he noticed swelling of the bilateral inguinal lymph-nodes followed by fever and lumbago. In February, he consulted a local doctor and hepatosplenomegaly, marked leukocytosis and renal dysfunction were pointed out and he was referred to our hospital on February 22nd. The clinical laboratory data on admission were as follows; WBC 23,200/microliter, serum-Ca 18.4 mg/dl, BUN 85.3 mg/dl, creatinine 5.4 mg/dl, antibody to ATLV x160. ATL was diagnosed by biopsy of lymph nodes and examinations of peripheral blood and bone marrow hemogram. Remission was achieved in March by the treatment with adriacin. Renal failure and hypercalcemia also improved. However his respiratory dysfunction gradually worsened. The chest radiographies++ showed pulmonary edema, although there was no clinical evidence of heart failure. When his condition became stable, TBLB was performed and revealed extensive deposition of calcium along alveolar septae, suggesting that pulmonary edema was induced by the metastatic calcification of the lung. After the second treatment for ATL, he died of pneumonia. The autopsy showed calcium deposition not only in the lung but in pyramids of the kidney and in sub-serous layer of the small intestine. There was no tumor cell invasion into the bone or parathyroid gland. High urinary c-AMP together with normal levels of PTH suggested that the hypercalcemia in this case was induced by PTH-related protein. It was concluded that careful treatment for hypercalcemia is important as regards the occurrence of pulmonary edema.
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PMID:[An autopsy case of adult T-cell leukemia complicated with metastatic calcification of the lung]. 204 Dec 50

Since Shumway carried out the first successful heart-lung transplant (HLT) in Stanford in 1981, HLT has become a new therapeutic means for patients with end-stage pulmonary disease or arterial hypertension. However, it is still rarely carried out because of a lack of donors and the complexity of the surgery and postoperative course. This review described the criteria for proper donor and recipient selection, as well as the anaesthetic and postoperative management of HLT patients at Marie Lannelongue Hospital. The lack of suitable organ grafts results, at least in part, from improper donor management. Pulmonary oedema by fluid overloading and excessive haemodilution should be carefully prevented. Low doses of catecholamines and vasopressin maintain circulatory stability and convenient organ function. The indications for HLT (primary pulmonary hypertension, Eisenmenger's complex, and end-stage bronchopulmonary disease) are all characterized by severe pulmonary hypertension, hypoxaemia and cardiac failure. Careful anaesthetic induction is required to avoid circulatory collapse. Cardiopulmonary bypass (CPB) should be started early, so that mediastinal dissection may be carried out in satisfactory haemodynamic conditions. After unclamping the aorta, circulatory support with fluid and catecholamine infusion is often required. High inspired oxygen fraction and end-expiratory positive pressure may be required because of reperfusion pulmonary oedema. Blood transfusion is often needed as there are major blood losses due to dissection of the posterior mediastinum during CPB. Postoperative catecholamine administration is prolonged over several days. Negative fluid balance is often necessary to reduce pulmonary oedema. Improvement in surgical technique, early extubation, and late prescription of steroids have reduced the incidence of tracheal complications. Acute renal failure often occurs as a result of prolonged CPB, hypovolaemia, drug nephrotoxicity and sepsis. Bacterial complications (pneumonia, mediastinitis) are the main causes of early death. After the 15th postoperative day, opportunistic infections and allograft rejection are the main complications. Since 1981, major advances in HLT recipient management resulted in improved survival rates (70-80% at 1 year, and 60-70% at 2 years for the best teams). Despite the complexity of management, and the longterm threat of obliterative bronchiolitis, HLT is, at present time, the only possibility for these young patients to recover a normal quality of life.
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PMID:[Anesthesia and intensive care for heart-lung transplantation]. 205 32

Emergency aortic valvuloplasty was performed as a last resort in 34 patients with an average age of 76 years with critical aortic stenosis in the terminal stages with congestive cardiac failure or cardiogenic shock. Emergency aortic valve replacement was considered to be too risky in these cases. The valve was dilated in all patients, resulting in a fall in mean peak-to-peak pressure gradients from 59 mmHg to 21 mmHg and an increase in valve surface area from 0.42 cm2 to 0.85 cm2. Significant improvement in myocardial function was observed immediately after the procedure with an increase of the cardiac index from 1.77 l/min/m2 to 2.07 l/min/m2 and of the ejection fraction from 28% to 35%. Complications were rare. There were no deaths or cerebrovascular accidents during the valvuloplasty procedure. Two patients died in hospital (6%) after the dilatation and two other patients who had persistent pulmonary oedema, underwent surgery; one died and the other had a good surgical result. A clear cut clinical improvement was obtained in the other 30 patients. The patients were followed up for an average of 15 +/- 7 months during which 15 died (50%), 6 +/- 5 months after dilatation. The other 15 survivors have a significant and unhoped for functional improvement. Three young patients later underwent surgical valve replacement in good clinical conditions with the same operative risk as that of standard candidates for aortic valve surgery. One other patient was operated on successfully during another relapse of cardiac failure. These results show that aortic valvuloplasty may be undertaken with a low risk even in the most critical clinical situations and that the procedure rapidly relieves the invalidating symptoms. It may be used as a bridge to surgery in patients with an unacceptable operative risk. The indications should be very flexible in young patients in terminal cardiac failure with cardiogenic shock or refractory pulmonary oedema.
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PMID:[Percutaneous aortic valvuloplasty as a last resort in patients with critical aortic valve stenosis]. 212 88

Diastolic heart failure is characterized by increased resistance to diastolic filling of one or both cardiac ventricles. Although some degree of diastolic failure exists in most patients presenting clinically with heart failure, a substantial subset of patients have relatively pure diastolic heart failure with normal systolic function. Diastolic heart failure can be due to structural abnormalities that increase resistance to ventricular inflow, and these structural abnormalities can be extramyocardial (e.g., constrictive pericarditis and mitral stenosis) or intramyocardial (e.g., fibrosis and amyloidosis). In addition to structural abnormalities, physiological derangement of myocardial inactivation and relaxation can contribute importantly to diastolic dysfunction in patients with heart failure. There is mounting evidence that advanced myocardial hypertrophy is associated with increased resistance to ventricular diastolic inflow due to both structural alteration (increased wall thickness and altered collagen matrix) and impaired diastolic relaxation of the hypertrophied myocardium. Physiological mechanisms for impaired relaxation in advanced hypertrophy remain controversial but can include disordered function of myocardial sarcoplasmic reticulum, subendocardial ischemia, and altered adenylate cyclase function. Diastolic dysfunction can play an important role in the genesis of flash pulmonary edema seen in patients with ischemic heart disease because myocardial ischemia is associated with a decline in relaxation rate, increased resistance to early diastolic filling, and in some cases, a striking upward shift in the left ventricular diastolic pressure-volume relation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diastolic dysfunction and congestive heart failure. 213 51


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