Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Complications are the major causes of illness and death after burning and most of them stem from the burn wound. Their origin and importance are reviewed with emphasis on problems and growing points in knowledge. Fluid leakage from the circulation into the burn is the cause of hypovolemic shock, but the underlying permeability changes in the burn are only partly understood. Other nonbacterial complications include acute cardiac failure, acute anemia, hemolytic jaundice, renal failure, encephalopathy, complex hypermetabolic effects including pseudodiabetes, gastric and duodenal ulceration, deep vein thrombosis and pulmonary embolism, pulmonary and glomerular microthrombosis, hepatic jaundice, and arterial thrombosis. Involvement of the airway in conflagrations carries special hazards like glottic edema and inhalation of irritant fumes. Nowadays, bacterial causes are dominant and these remain the main challenge. Bacterial infection and invasion of the burn are usually responsible for septicemia, bronchopneumonia, and pyelonephritis although other sources also contribute. Indirect manifestations of septicemia include paralytic ileus, acute gastric dilatation, toxic myocarditis, and some cases of renal failure. Therapeutic complications like agranulocytosis, thrombocytopenia, and colitis occur at times. High concentrations of oxygen given therapeutically can produce fatal aseptic hypoxic pneumonitis.
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PMID:A review of the complications of burns, their origin and importance for illness and death. 44 73

This is a prospective study on 24 patients with chronic renal failure. Thirteen of them had evidence of acute uraemic encephalopathy. Of those 9 patients were found to have dilutional hyponatraemia, two patients severe salt and water depletion and one patient septicaemia. Hyponatraemia was associated with pulmonary oedema in 3 patients. Correction of salt and water disturbances and treatment of heart failure improved cerebral functions in 10 (77%) patients. It is therefore concluded that dilutional hyponatraemia probably leading to cerebral oedema is a reversibe major factor in the development of acute uraemic encephalopathy. This, if left uncorrected, may prove fatal especially in tropical countries.
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PMID:Acute uraemic encephalopathy in tropical countries. 70 18

Severe arterial hypertension in children constitutes a high-risk situation requiring rapid and effective therapy. We have assessed the clinical value of sodium nitroprusside as a rapidly acting antihypertensive agent. Twenty children admitted with hypertensive crises of renal origin were treated with intravenous infusion of sodium nitroprusside at an average rate of 1.4 mug/kg/min. Desired levels of blood pressure were reached in all patients within one to 20 minutes. Rapid improvement of cardiac failure was observed in all patients, and neurologic signs of distress disappeared in 16 of the 20 children within 24 to 48 hours of treatment, permitting substitution of oral medication. One patient died of cerebral hemorrhage without improvement of encephalopathy. There were no undesirable effects of therapy or deterioration of renal function in any patient.
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PMID:Sodium nitroprusside treatment of severe arterial hypertension in children. 118 53

A girl of 10-5/12 years is described, who had diabetes mellitus from the age of 5 years on and who developed bilateral ptosis, pigment degeneration of the retina and bilateral impairment of hearing at the age of nine years. A few weeks before death she suffered from an acute gastrointestinal infection which was successfully treated by a hydroxyquinoline derivative. In the days following a severe encephalopathy and signs of cardiac involvement appeared. A month later the girl died of bulbar paralysis and acute heart failure. Histology showed remnants of a granulomatous inflammation in the heart, the kidneys, the pancreas and the skeletal muscles. Furthermore there was a widespread spongiosis in the white substance of the brain, with large astrocytes, and partly also in the basal ganglia, the brain stem and the cerebellum. Foci of sudanophilic tissue necrosis resembling Wernicke's Encephalopathy were found in the medulla oblongata and the spinal cord. The peripheral nerves appeared partially demyelinated and showed axonal lesions. This case is classified as a Juvenile Type of so-called Canavan's Disease. It shows some resemblence to the "Progressive Chronic Ophthalmoplegia with Spongiform Encephalopathy described by Daroff, Kearn and Sayre. The possible neurotoxical effects of the hydroxyquinoline therapy are discussed.
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PMID:[Juvenile spongy dystrophy of CNS with necrosis of the medulla. A. complication of hydroxyquinoline therapy (author's transl)]. 124 13

The measurement of red cell deformability index (RCDI) was made in 29 patients with cor pulmonale and 31 persons of normal controls, at the same time blood gas values and plasma osmolarity were also measured. The results were as follows: (1) The RCDI of patients with acute respiratory and cardiac failure especially with respiratory encephalopathy was significantly lower than that of patient in stable conditions and normal controls. There was no significant difference in RCDI between patients in stable conditions and controls. (2) The PaO2 and pH (in a range of 7.31-7.39) were positively correlated with RCDI. There was no significant difference in RCDI between patients with normal plasma osmolarity and those with abnormal one. We suggested that this might contribute to the increase in pulmonary arterial pressure; and that the hypoxemia and acidosis might play an important role in decrease of RCDI.
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PMID:[Observation on red cell deformability in patients with cor pulmonale]. 130 10

The classical form of thiamine deficiency in children is comprised of peripheral neuropathy, encephalopathy and high-output cardiac failure, predominantly right-sided. "Shoshin beriberi" cardiac failure has a different presentation, with vasoconstriction, hypotension and severe metabolic acidosis. A three-month breast-fed infant developed these features (biochemical tests confirmed the diagnosis). His mother, although non-symptomatic, had biochemical evidence of thiamine deficiency.
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PMID:Shoshin beriberi in an infant of a thiamine-deficient mother. 142 19

An 83-day-old male infant had convulsions, hypertrophic cardiomyopathy, and lactic acidosis. Cranial computed tomography revealed low-density areas in both parieto-occipital lobes and in the left temporal lobe. Muscle biopsy did not reveal ragged-red fibers, but abnormal mitochondria were found in the capillary endothelial cells as well as in the muscle fibers. At 5 months of age, the patient developed purpura on the soles and palms. Skin biopsy showed degeneration of the endothelial cells with abnormal mitochondria in the arterioles and capillaries. Myelinated nerves in the skin had vacuolated axons with swollen mitochondria, and their myelin sheaths showed vacuolation. At 9 months of age, he died of heart failure, and autopsy revealed abnormal mitochondria in the myocardium but not in the coronary vessels. Our findings indicate that the symptoms of the mitochondrial encephalopathy, myopathy, lactic acidosis, and strokelike episodes (MELAS) syndrome cannot be fully explained by the mitochondrial angiopathy alone.
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PMID:MELAS of infantile onset: mitochondrial angiopathy or cytopathy? 186 30

Protein energy malnutrition and infection are largely responsible for the very high postneonatal and toddler mortality ratios of developing countries. Availability of food is just one environmental factor in the aetiology of protein energy malnutrition--many others such as size at birth, infection and culture play a role. Diet needs as careful prescription as any other form of therapy, but in the severely malnourished child it is only one aspect of management; care is necessary to avoid or detect 6 complications: hypothermia, hypoglycaemia, encephalopathy, intractable diarrhoea, cardiac failure, and infection. Prevention should be incorporated within the child health services as a whole and delivered with them; however central government, and the food industry from farming to retailing, play an at least as important role as health care professionals.
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PMID:Protein energy malnutrition: problems and priorities. 195 28

Six cases of cocaine-related deaths of infants have covered the spectrum of potentially devastating effects. They include an intrauterine death of a 35-week-old fetus following acute maternal cocaine abuse; anoxic encephalopathy at birth with 3 months' vegetative survival from a similar episode; traumatic compression asphyxia in a 4-month-old; infectious cardiomyopathy with heart failure in a twin at age 21 months following maternal cocaine abuse at birth; malnutrition and dehydration in a 7-week-old during continuing cocaine abuse by the parents; and a teenage sibling's cocaine lacing of a baby milk bottle ingested by his 6-week-old brother. All the cases had positive toxicological screening for cocaine or metabolites or both in the mother at delivery or in the infant at birth, or both. There were no instances of sudden infant death syndrome (SIDS, or "crib death"). Pathologic and toxicologic, as well as birth, developmental, and social data are presented. An integrated medical, public health, law enforcement, and educational policy to prevent or at least ameliorate these tragic cases, now approaching epidemic proportions, has yet to be developed. A careful obstetrical history and examination of the mother, indication on the birth certificate of maternal drug abuse, and notification of health authorities (by birth certificate checking, among other ways) may send an early warning message to providers for intercession. Active ingestion/injection and passive inhalation by older children and teenagers require more intensive monitoring and aggressive interaction by pediatricians, social workers, school authorities, and employers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cocaine babies: the scourge of the '90s. 200 78

Regular drug treatment in mild hypertension (diastolic blood pressure 90-104 mm Hg) reduces death from stroke, and other non-coronary vascular events. The optimum strategy remains sequential monotherapy with the lowest effective dose, with drug combinations as an option. A beta-adrenoceptor blocker or low-dose thiazide is good value treatment for many patients. beta-Blockers are good for young (under 50 years), anxious non-smoking men, men after myocardial infarction, and renal failure patients. Older persons over about 65 years, women, smokers, stroke victims, and liver disease patients should generally take a thiazide or calcium ion-channel blocker. Pregnant women and untreated gouty patients should avoid diuretics. Calcium blockers and angiotensin-converting enzyme inhibitors are preferable in severe or insulin-dependent diabetes and renal failure, and angiotensin manipulators or thiazides in heart failure or peripheral vessel disease. Hyperlipidaemia should not generally exclude thiazides or beta-blockers. Some hypertensive stroke patients without encephalopathy may not need antihypertensive drug treatment for the first 24-48 hours. Drug treatment should be tailored to individuals according to their general condition, physiological age, and any concurrent disease or medication. Unwanted drug reactions should not deter patients from fulfilling social and economic goals. The desired treatment end-point is a diastolic pressure of 85-89 mm Hg, but a compromise is usual in poorly motivated young men, and the elderly.
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PMID:Optimising drug management of individuals with cryptogenic hypertension. 202 55


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