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Query: UMLS:C0032285 (pneumonia)
 54,520 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

The clinical presentation, complications and sensitivity pattern was studied in 30 cases of enteric fever. Fever was the main presenting feature in all. Other associated predominant presenting feature were vomiting in 15 (50%), Loose motion 9 (30%), Cough 6 (20%), headache 4 (13.33%) and altered sensorium in 2 (6.66%). The various complications observed during hospital stay were myocarditis 5 (6.16%), Paralytic ileus 2 (6.66%), Pneumonia 1 (3.33%) and Joint effusion in 2 (6.66%) cases respectively. In laboratory parameters-mild elevation of blood urea and SGOT/SGPT were detected in 1st week, which returned to normal in 2-3 weeks time. In vitro sensitivity of organism isolated (24 cases) were as follow--Chloramphenicol 7 (29.16%), Ampicillin 8 (33.33%), Gentamicin 22 (91.66%), Amikacin 24 (100%), Cefotaxime 22 (91.66%), Ciprofloxacin 24 (100%), and Ofloxacin 24 (100%). Clinical response to Ofloxacin and Ciprofloxacin was 100%, and fever subsided in 3-5 days.
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PMID:Changing profile of enteric fever--in summer-91. 130 27

Kawasaki disease (KD) often presents as an acute multisystem febrile illness which is most often self-limiting. During an 11-year period, 39 patients with KD, aged 11 weeks to 15 years (mean 2.5 years), were admitted to the Queen Elizabeth Hospital, Barbados. Eighty-seven per cent of children were less than 4 years of age. There were 26 males (67%) and 13 females (33%) with a sex ratio of 2:1. A peak occurrence was observed in 1985 and the mean hospital stay of cases was 12.7 days. Treatment regimens included antibiotics in 36 patients (93%), aspirin in 32 (82%) and steroids in 3 (7%). Major complications were observed in 11 patients (26%), with these being gastrointestinal bleeding in 1, broncho-pneumonia in 3 and cardiac abnormalities in 7 (18%). Among the latter were abnormal proximal coronary arteries in 5 patients (2 with dilatation and 3 with aneurysms) and carditis in 2. Other complications included croup (1), hydrops of the gallbladder (2), paralytic ileus (1), and abnormal focal neurological signs in two patients. There were no deaths. Follow-up ranged between one month and four years. Although KD often presents as a benign self-limiting illness, it is extremely important to make a diagnosis early in the course of the illness, institute appropriate therapy and be on the alert for possible fatal complications.
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PMID:Outcome of Kawasaki disease in Barbados. 152 36

Nutrition in acute spinal cord injury is complicated. Not every aspect of nutrition as it relates to the acutely injured spinal cord patient is known. The stress response to injury, fever, infection, sepsis, and surgery alter nutritional needs, as does the spinal cord injury itself. The sequelae of spinal cord injury, including denervation atrophy and paralysis, glucose intolerance, skin and wound breakdown, poikilothermy, anemia, respiratory paralysis, pneumonia, paralytic ileus, gastrointestinal ulcers and hemorrhage, neurogenic bowel and bladder, and depression, all affect the nutritional needs of the patient. Orthopedic appliances, pharmacologic agents, and other injuries can also alter nutritional requirements. Nutritional assessment in acute spinal cord injury is also complex. It should include medical and diet history, physical examination, intake and output measurements, prediction of energy expenditure and protein requirements, or--even better--measurements of energy expenditure with indirect methodology, using the metabolic cart or pulmonary artery catheter. Application of computerized tomography and radioisotope studies may prove valuable in the future. Finally, the direct relationship between nutrition and physiologic alterations of acute spinal cord injury necessitates that the critical care nurse incorporate nutrition-focused thinking into many aspects of the acute spinal cord--injured patient's care.
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PMID:Nutrition in acute spinal cord injury. 226 60

Splenectomy for massive splenomegaly and hypersplenism carries a significant morbidity and mortality. We have used partial splenic embolization (PSE) as an effective alternative to splenectomy. Ten PSE procedures were performed on nine patients without mortality and with minimal morbidity. The age of the patients ranged from 8 months to 32 years (mean 14 years). The causes of splenomegaly and hypersplenism included cystic fibrosis with cirrhosis (2), tyrosinemia and cirrhosis (1); thalassemia (1), hemophilia with Human Immune Deficiency Virus infection (2), chronic hepatitis with portal hypertension (1), malignant histiocytosis (1), and Wiskott-Aldrich Syndrome (1). All procedures were performed under local anesthesia with sedation. A percutaneous femoral artery approach to the splenic artery was used to deliver Ivalon sponge particles (280-800 microns) into the spleen. Splenic infarction was assessed by postembolization angiograms. All of the patients except one demonstrated improvement of hematologic parameters. In one patient, however, cytopenia improved only after a second embolization. In the total series, there was an early mean rise of 8,600/mm3 in the leukocyte count (range 2,900-14,900) and 212,000/mm3 in the platelet count (range 30,000-718,000). Follow-up ranged from 4 months to 7 years. Improvement of the blood picture has been persistent in seven of the eight patients who showed initial improvement. Transient procedural complications included fever (5), pleural effusion (2), pneumonia (1), and splenic abscess (1). One patient had paralytic ileus lasting for 10 days and one patient developed a streptococcal peritonitis 3 weeks after embolization. No patient developed pancreatitis or vascular compromise of other abdominal viscera.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Partial splenic embolization. An effective alternative to splenectomy for hypersplenism. 226 5

Pneumonia and cardiac arrhythmias represent the most common life-threatening complications during delirium tremens. Electrolyte abnormalities are common underlying conditions in chronic alcoholics and they may further complicate the management of patients with alcohol-withdrawal syndrome or with delirium tremens. The authors present two cases in which the clinical picture of severe paralytic ileus complicating delirium tremens was closely associated with electrolyte status and postulate that the two were cause-effect related. A careful electrolyte supplement therapy guided by a strict monitoring of electrolyte balance and renal function proved to be particularly useful in successful management.
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PMID:Severe electrolyte abnormalities and paralytic ileus complicating delirium tremens. 271 18

Chronic intestinal pseudo-obstruction is a rare disorder characterized by ineffective intestinal propulsion in the absence of mechanical factors. It depends on isolated or associated disturbances of intrinsic and extrinsic innervation of the smooth muscle, neurotransmitters and hormones. In children the most common causes are postoperative paralytic ileus, pneumonia or pancreatitis, occurring usually in the first year of life. There is also hereditary transmission, comprising the familial visceral myopathy (hollow visceral myopathy) and the familial visceral neuropathy. The pseudo-obstruction may be associated with congenital anomalies (digestive or not) in 10 to 30% of the cases, mainly malrotation, pyloric stenosis and bladder atony. Diagnostic difficulties may lead to exploratory laparotomy. A precise diagnosis requires judicious interpretation of radiologic, manometric, radioisotopic and hystologic findings. Medical treatment includes drugs acting on gastrointestinal motility as well as hydroelectric and nutritional support, besides treatment or prevention of infections. It is possible that in the future these patients may be treated by surgical implantation of electrodes promoting gastrointestinal myoelectrical stimulation.
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PMID:Diagnosis and management of chronic intestinal pseudo-obstruction syndromes in infancy and childhood. 307 60

Calorie and protein supplementation improves nutritional status. This support may improve outcome and decrease morbidity and mortality in acutely brain-injured patients. Investigators have observed a poor tolerance to enteral feedings after brain injury and have noted that this persists for approximately 14 days postinjury. This delay has been attributed to increased gastric residuals, prolonged paralytic ileus, abdominal distention, aspiration pneumonitis, and diarrhea. In the present investigation, 23 brain-injured patients with an admission 24-hour peak Glasgow Coma Scale (GCS) score between 4 and 10 were studied for 18 days from hospital admission. The mean duration from injury to initiation of full-strength, full-rate enteral feeding was 11.5 days. Seven of the 23 patients tolerated enteral feedings within the first 7 days following hospital admission (mean 4.3 days), four patients tolerated feedings between 7 and 10 days postadmission (mean 9 days), and 12 patients did not tolerate feedings until after 10 days postinjury (mean 15.9 days). There was a marginally significant relationship between low GCS scores on admission and length of days to enteral feeding tolerance (p = 0.07). A significant inverse relationship was observed between daily peak intracranial pressure (ICP) and time to tolerance of feedings (p = 0.02). There was no significant relationship between feeding tolerance and days to return of bowel sounds (p = 0.12). Serum albumin levels decreased during the investigation (mean +/- standard error to the mean: 3.2 +/- 0.12 gm/dl on Day 1; 2.7 +/- 0.23 gm/dl on Day 16; normal = 3.5 to 5.0 gm/dl), whereas the percentage of patients tolerating feedings increased over the course of the study. The authors conclude that patients with acute severe brain injury do not adequately tolerate feedings via the enteral route in the early postinjury period. Tolerance of enteral feeding is inversely related to increased ICP and severity of brain injury. It is suggested that parenteral nutritional support is required following brain injury until enteral nutrition can be tolerated.
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PMID:Intolerance to enteral feeding in the brain-injured patient. 312 7

Of 582 patients who underwent percutaneous nephrolithotomy, 4% had complications. The most common complications were fever (23%) and bleeding necessitating transfusion (12%). Extravasation was seen in 7% of patients and transient ureteral obstruction in 6%. Other complications included pneumothorax or hydrothorax, pneumonia/atelectasis, paralytic ileus, nephrostomy-tube dislodgment or urine drainage from the flank lasting more than 1 week, significant infection, urinoma formation, renal pelvic laceration, ureteral avulsion, ureteropelvic or ureteral stricture, bowel injury, or escape of stone fragments into the retroperitoneum. Seven patients (1%) required immediate surgery: four to repair renal pelvic lacerations, one to repair a ureteral avulsion, and two to control bleeding after nephrostomy-tube removal when embolization failed. Four patients required delayed surgery for ureteral or ureteropelvic junction strictures, which may have been caused by a tissue reaction to the stones rather than by the procedure itself. There were two deaths--one from respiratory failure in a patient with severe interstitial pulmonary fibrosis and chronic renal failure and the other from myocardial infarction in an obese diabetic patient with hypertension.
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PMID:Complications of percutaneous nephrolithotomy. 349 9

Strongyloidiasis is a human intestinal parasitosis caused by the nematode Strongyloides stercoralis. In most cases the infection is subclinical, but rarely, disseminated strongyloidiasis may occur in debilitated or immunocompromised patients, and in those who receive immunosuppressive agents. In this report, we describe an unusual case of severe disseminated strongyloidiasis, with intestinal, pulmonary and neurological manifestations, in a previously healthy male. The onset of the disease was acute with headache and neck stiffness, due to subarachnoid-ventricular haemorrhage. During a protracted clinical course the patient developed diarrhoea, abdominal pain, recurrent paralytic ileus, pneumonitis and respiratory distress, malabsorption and weight loss, diagnosis was delayed due to the complicated course and rarity of the disease. The diagnosis finally established during evaluation for malabsorption by demonstrating larvae of S. stercoralis in the jejunal mucosal biopsy and faeces. Response to mebendazole treatment was prompt with complete recovery and resolution of all systemic manifestations. Early diagnosis and treatment of strongyloidiasis in the intestinal phase is critical in the prevention of dissemination, which may prove lethal due to life-threatening complications.
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PMID:Disseminated strongyloidiasis with uncommon manifestations in Greece. 378 11


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