Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032290 (aspiration pneumonia)
 2,291 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some elderly patients with chronic illness such as stroke, or Parkinsonism cannot take food orally because of dysphagia. In such cases, tube feeding can be used as a supplement to oral intake when malnutrition is present. This route allows for easier nursing care and decreases the frequency of aspiration pneumonia. Complications of tube feeding include nutrient deficiency states, pulmonary aspiration, gastrointestinal and metabolic disorders. We report two cases with complications of acute gastric ulcer which was thought to be induced with long-term tube feeding. Case 1 was a 61-year-old male patient with Parkinson's disease for ten years. L-DOPA had been administered with good control of his condition. However, his ability to swallow has deteriorated gradually. As he often suffered from aspiration pneumonia, nasogastric tube feeding was performed. After three years of tube feeding, he suddenly vomited much bloody material. He died from massive bleeding with acute gastric dilatation. Autopsy showed giant acute gastric ulcer covered with coagulated blood. UL3, 50 mm in maximum diameter, was observed in the middle portion of the greater curvature, where the top of tube probably came in contact with the gastric wall. Case 2 was an 83-year-old female patient with stroke and chronic heart failure. She had been hospitalized for about one year because of the intermittent deterioration of her cardiac condition. Furthermore, her inability to swallow increased during her hospitalization. She also suffered from aspiration pneumonia. Nasogastric tube feeding was performed to prevent aspiration pneumonia and malnutrition. She died of acute heart failure after twelve months. Autopsy revealed heart dilatation, old myocardial infarction and stroke. In addition, two acute gastric ulcers (UL3.10 and 30 mm in diameter) were recognized; one was in the upper portion of the greater curvature, the other in the lower portion of the greater curvature. The location of these gastric ulcers was unusual. Moreover, they coincided with location of top of the nasogastric tube. From these two cases, we conclude that in long-term tube feeding the tip of the tube often comes in contact with the gastric wall, and gastric ulcer could be produced by repeated mechanical stimulus of the wall. Reports of acute gastric ulcer induced by tube feeding have not been published previously. Therefore, we should pay much attention to this complication in the care of the elderly people with long-term tube feeding.
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PMID:[Long-term nasogastric feeding and complications of acute gastric ulcer in two elderly patients]. 143 62

Gastroesophageal reflux (GER) has been known to occur in infants but was thought to be normal. As a result of increased recognition of GER and a clear documentation of GER with extended (18 to 24 hour) esophageal pH monitoring, several severe complications of GER in children have become apparent. An immature cardiorespiratory system is susceptible to some complications of GER such as apnea, choking, recurrent cough or wheezing, and recurrent aspiration pneumonia. Noncardiorespiratory complications include weight loss, esophagitis, anemia, irritability, posturing, malnutrition, and developmental delays. Nursing assessment contributes to a complete clinical picture and the subsequent treatment choice of the physician. To form an accurate assessment of the child with suspected GER, the nurse must be aware of the symptoms and complications of this condition and must precisely execute diagnostic studies, particularly extended esophageal pH monitoring. Nursing responsibilities also include providing a safe yet stimulating environment for the child, teaching parents to participate in the child's care, supporting parents through hospitalization, and preparing both the parents and child for discharge and follow-up care at home.
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PMID:Nursing responsibility in the diagnosis, care, and treatment of the child with gastroesophageal reflux. 176 48

The prevalence of dysphagia in the elderly ("presbyphagia") is probably still underestimated, though this disorder represents a major geriatric problem; special attention is necessary to prevent malnutrition, dehydration and aspiration pneumonia. Primary presbyphagia due to physiological, age-related changes of the swallowing mechanism must be differentiated from secondary presbyphagia attributable to diseases which are more frequent in the elderly. Transnasal pharyngo-laryngo-fiberendoscopy, videofluoroscopy and the "modified barium swallow" are of particular value in the diagnostic approach to presbyphagia. The possibilities of treatment are limited. They are aimed at dietary adjustments, compensatory mechanisms based on the properties of the volume and consistency of the food, proper feeding position and help by other persons. Individual swallowing exercises by a speech therapist are particularly valuable. Surgical procedures for the treatment of underlying organic disorders are less often indicated in presbyphagia.
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PMID:[Dysphagia in the elderly]. 176 68

Gastroesophageal reflux (GER) has been known to occur in infants but was thought to be normal. As a result of increased recognition of GER and a clear documentation of GER with extended (18 to 24 hour) esophageal pH monitoring, several severe complications of GER in children have become apparent. An immature cardiorespiratory system is susceptible to some complications of GER such as apnea, choking, recurrent cough or wheezing, and recurrent aspiration pneumonia. Noncardiorespiratory complications include weight loss, esophagitis, anemia, irritability, posturing, malnutrition, and developmental delays. Nursing assessment contributes to a complete clinical picture and the subsequent treatment choice of the physician. To form an accurate assessment of the child with suspected GER, the nurse must be aware of the symptoms and complications of this condition and must precisely execute diagnostic studies, particularly extended esophageal pH monitoring. Nursing responsibilities also include providing a safe yet stimulating environment for the child, teaching parents to participate in the child's care, supporting parents through hospitalization, and preparing both the parents and child for discharge and follow-up care at home.
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PMID:Nursing responsibility in the diagnosis, care, and treatment of the child with gastroesophageal reflux. 154 68

The indications, methods, and complications of nutritional support of 90 patients admitted with a primary complaint of dysphagia were reviewed. Patients were divided into two groups based on etiology of dysphagia (central neurologic vs local mechanical dysfunction). All patients on admission exhibited marked malnutrition with an average weight loss of 12 +/- 9.8% body weight, serum transferrin 165 +/- 60.1 mg/dl, and albumin 3.2 +/- 0.85 mg/dl. All patients were placed on either enteral (63%) or parenteral (37%) nutrition. Twenty-seven percent of all patients suffered a complication of nutritional therapy. Patients with nasoenteric tubes had a 10% complication incidence (aspiration or endotracheal placement of tube) resulting in a 30% mortality rate; significantly higher (p less than 0.05) than seen with other modalities. Any form of upper enteric feeding (nasoenteric or gastrostomy) was associated with significantly increased (p less than 0.01) risk of aspiration pneumonia. It is concluded that patients admitted to hospital with dysphagia as the major complaint suffer from severe malnutrition, and that upper gastrointestinal intubation should not be employed for feeding until the dysphagia has resolved.
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PMID:Nutritional support of the dysphagic patient: methods, risks, and complications of therapy. 210 17

A case of oculopharyngeal muscular dystrophy in an elderly woman of French-Canadian background presenting with dysphagia is discussed. Typical features of the clinical presentation include bilateral ptosis and dysphagia with significant potential for morbid outcomes of aspiration pneumonia and malnutrition. Although relatively uncommon, this diagnosis should be considered in an elderly person with dysphagia, a history of ptosis, and the proper family background. Surgical treatment appears to improve the signs and symptoms of this disease.
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PMID:Oculopharyngeal muscular dystrophy as a cause of dysphagia in the elderly. 394 5

Nasoenteral alimentation is less hazardous, cheaper and more physiological than parenteral nutrition. Serious complications of tube feeding such as bleeding from esophageal lesions or aspiration pneumonia have become rare since soft silicone-rubber or polyurethane tubes are used and the diets are delivered into the jejunum rather than into the stomach. The costs of full enteral alimentation are 25 to 50% of that caused by total parenteral nutrition. For intraduodenal or intrajejunal feeding continuous infusion of an elemental or oligopeptide diet is necessary. At the beginning of the feeding program infusion rate must be slowly increased over four to five days to avoid diarrhea, abdominal cramping and vomiting. The caloric requirements depend on the extent of protein energy malnutrition and hypercatabolism of the individual patient. Although follow-up of the patient's nutritional status and water- and electrolyte balance in the hospital must be extremely close at the beginning, tube feeding can be continued--if necessary--by home enteral nutrition later on.
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PMID:[Enteral tube feeding--an alternative to parenteral infusion therapy]. 642 4

Many patients with chronic diseases develop malnutrition. Force feeding with either enteral tube of parenteral infusions often succeeds in ameliorating this problem in hospitalized patients. However, after discharge many patients are incapable of sustaining adequate dietary intake. As a consequence, malnutrition may persist or recur. The authors' previous experience using nocturnal enteral tube feedings in patients with glycogen storage disease suggested that malnourished patients also might benefit from enteral tube feedings at home. Fourteen undernourished patients selected for domestic enteral tube feedings clearly demonstrated a tolerance, which included adequate gastric emptying, to the infusions during their hospitalization. They ranged in age from 2 months to 68 yr. Infusion pumps delivered the feedings continuously. At home, 12 patients experienced substantial weight gains. Two maintained their weight while they received intensive chemotherapy for malignancies. Except for the two patients with short bowel syndrome, all patients were weaned successfully to oral feedings after 1 to 3 months. The only apparent complication was possible aspiration pneumonia in a patient with neurological dysfunction. This further experience with domestic enteral tube alimentation indicates that selected patients can be managed effectively, safely and economically with nasogastric nutritional support on an outpatient basis.
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PMID:Nasogastric tube feeding at home: a method for adjunctive nutritional support of malnourished patients. 678 77

Deficiency of liver arginase (AI) is characterized clinically by hyperargininemia, progressive mental impairment, growth retardation, spasticity, and periodic episodes of hyperammonemia. The rarest of the inborn errors of urea cycle enzymes, it has been considered the least life-threatening, by virtue of the typical absence of catastrophic neonatal hyperammonemia and its compatibility with a longer life span. This has been attributed to the persistence of some ureagenesis in these patients through the activity of a second isozyme of arginase (AII) located predominantly in the kidney. We have treated a number of arginase-deficient patients into young adulthood. While they are severely retarded and wheelchair-bound, their general medical care has been quite tractable. Recently, however, two of the oldest (M.U., age 20, and M.O., age 22) underwent rapid deterioration, ending in hyperammonemic coma and death, precipitated by relatively minor viral respiratory illnesses inducing a catabolic state with increased endogenous nitrogen load. In both cases, postmortem examination revealed severe global cerebral edema and aspiration pneumonia. Enzyme assays confirmed the absence of AI activity in the livers of both patients. In contrast, AII activity (identified by its different cation cofactor requirements and lack of precipitation with anti-AI antibody) was markedly elevated in kidney tissues, 20-fold in M.O. and 34-fold in M.U. Terminal plasma arginine (1500 mumols/l) and ammonia (1693 mmol/l) levels of M.U. were substantially higher than those of M.O. (348 mumols/l and 259 mumols/l, respectively). By Northern blot analysis, AI mRNA was detected in M.O.'s liver but not in M.U.'s; similarly, anti-AI crossreacting material was observed by Western blot in M.O. only. These findings indicate that, despite their more long-lived course, patients with arginase deficiency remain vulnerable to the same catastrophic events of hyperammonemia that patients with other urea cycle disorders typically suffer in infancy. Further, unlike those other disorders, an attempt is made to compensate for the primary enzyme deficiency by induction of another isozyme in a different tissue. Such substrate-stimulated induction of an enzyme may be unique in a medical genetics setting and raises novel options for eventual gene therapy of this disorder.
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PMID:Arginase deficiency manifesting delayed clinical sequelae and induction of a kidney arginase isozyme. 845 80

White muscle disease (nutritional myodegeneration) of foals is a peracute to subacute myodegenerative disease affecting skeletal and cardiac muscle. It is caused by a dietary deficiency of selenium and vitamin E, usually in association with predisposing factors such as a high intake of dietary unsaturated fats or unaccustomed exercise. White muscle disease has been observed in foals from birth to 1 year of age, particularly those foals born to dams fed selenium-deficient diets, during gestation. The disease in foals may present as an acute, fulminant syndrome, which is rapidly fatal, or a subacute syndrome characterized by profound muscular weakness. Failure of passive transfer, aspiration pneumonia, and stunting are frequent complications. Markedly increased muscle enzyme and low glutathione peroxidase activities are common findings in affected foals. Foals with the subacute form of the disease may survive if they are supplemented early with selenium; however, mortality rates ranging from 30% to 45% have been reported, even for this form of the disease.
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PMID:White muscle disease of foals. 910 50


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