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)

Over a period of 10 months, we conducted a prospective randomized controlled trial of endoscopic injection for the arrest of peptic ulcer hemorrhage in 84 patients. We injected pure alcohol (PA, 99.8%), 50% glucose in water (G/W), 3% NaCl solution, and normal saline solution (N/S, controls) to stop bleeding. The ultimate success rates in the four groups were: 81% (17/21) in the PA group, 80% (16/20) in the 50% G/W group, 65.2% (15/23) in the 3% NaCl group, and 80% (16/20) in the N/S group (p greater than 0.05). The volume of blood transfusion (mean +/- s. e. m.) for each patient was 1,200 ml +/- 433 ml in the PA group, 1,130 +/- 356 ml in the 50% G/W group, 1,704 +/- 330 ml in the 3% NaCl group, 1,400 +/- 548 ml in the N/S group (p greater than 0.05). The duration of hospitalization (mean +/- s. e. m.) was 5.7 +/- 1.5 days in the PA group, 3 +/- 1.3 days in the 50% G/W group, 6.1 +/- 1.1 days in the 3% NaCl group, and 5 +/- 1.1 days in the N/S group (p greater than 0.05). No complication of perforation or aspiration pneumonia was observed during hospitalization. We suggest that endoscopic injection with the above solutions be used as the first line of therapeutic endoscopy for arrest of peptic ulcer hemorrhage.
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PMID:Endoscopic injection to arrest peptic ulcer hemorrhage: a prospective, randomized controlled trial; preliminary results. 193 73

We assessed the possibility of improvements in the management of the potentially fatal acute hyperglycaemic complications of diabetes by a review of all deaths in patients who presented to the Alfred Hospital, Melbourne, with diabetic ketoacidosis or hyperosmolar coma during the 16 years, 1973-1988. All late deaths of patients during hospitalization were included in the mortality data. In the 610 episodes of diabetic ketoacidosis (pH, 7.30 or lower) or hyperosmolar coma (osmolality, 350 mOsmol/kg or greater), only one death occurred as a result of the acute metabolic disturbance--in a patient who had suffered a cardiac arrest before admission to hospital. The over-all mortality rate was 6.2% (38 deaths). The mortality rate was 4.9% (26 deaths) for 528 episodes of diabetic ketoacidosis and 14.6% (12 deaths) for 82 episodes of hyperosmolar coma. Patients with diabetic ketoacidosis who died were older than were those who survived (64 +/- 13 years compared with 40 +/- 21 years, respectively; P less than 0.001). Mortality in patients with hyperosmolar coma did not relate to age, initial blood-glucose level or osmolality. Twelve deaths resulted from bacterial pneumonia and two deaths resulted from aspiration pneumonia. Other major causes of death were mesenteric and iliac thromboses (six cases), myocardial infarction (eight cases) and cerebral haemorrhage (two cases). Of the 26 deaths that were associated with diabetic ketoacidosis, only two deaths--as a result of aspiration pneumonia and bowel infarction, respectively--were assessed as potentially avoidable after the patient's admission to hospital. Eight of the 12 hyperosmolar-coma-associated deaths occurred in newly recognized diabetic patients in whom there were avoidable delays in diagnosis. We conclude that further improvements in outcome will be difficult to achieve, but that efforts should be directed towards the earlier diagnosis of diabetes and the earlier recognition and treatment of associated acute pulmonary and vascular complications.
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PMID:Deaths associated with diabetic ketoacidosis and hyperosmolar coma. 1973-1988. 210 75

In oil-producing states, the proximity of livestock to drilling operations and production sites often results in poisoning of animals from ingestion of crude oil, condensate, salt water, heavy metals, and caustic chemicals. The heavy metals encountered most frequently are lead from pipe joint compound and arsenicals and chromates used as corrosion inhibitors. Numerous toxic and caustic chemicals are used in drilling muds and fluids. Crude oil and salt water spills are common occurrences around production sites. Pipeline breaks may result in exposure of livestock to crude oil or refined petroleum hydrocarbons. Ingestion of petroleum hydrocarbons may result in sudden death from peracute bloat. The most common cause of illness or death following exposure to petroleum hydrocarbons is aspiration pneumonia, which may cause a chronic progressive deterioration of health, with death after several days or weeks. Cases in which livestock are exposed to oil, salt water, or caustic chemicals, but do not die acutely or from aspiration pneumonia are more frustrating to diagnose. In these cases, parasitism, poor nutrition, and other debilitating diseases must be considered. Anorexia, weight loss, and decreased rumen motility may be caused by a disruption of normal rumen function. Petroleum hydrocarbons, salt water, and caustic chemicals have the potential of altering rumen flora and enzymatic processes as well as damaging the ruminal and gastrointestinal epithelium. The toxicity of petroleum hydrocarbons appears to be related more closely to the volatility and viscosity of the product than to other factors. The more volatile straight chain and aromatic petroleum hydrocarbons have a greater potential for aspiration pneumonia and may produce an anesthetic-like action if absorbed systemically. The more volatile petroleum hydrocarbons also are more irritating to skin and mucous membranes and appear to be more damaging to rumen flora. Treatment of petroleum hydrocarbon ingestion is aimed at preventing aspiration pneumonia and the animal's absorption of highly volatile components. Activated charcoal slurries and, in some instances, vegetable oil may be used to absorb the ingested petroleum or alter its viscosity to minimize absorption and aspiration. These procedures should be followed by the administration of rumenatories or saline cathartics to hasten the evacuation of the gastrointestinal tract. Chronic poor performance animals with anorexia and rumen dysfunction may respond to fresh rumen inoculant, intravenous glucose, and B-complex vitamins. Prognosis primarily hinges on whether or not aspiration pneumonia has occurred. Treatment of aspiration pneumonia rarely is effe
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PMID:Toxicology of oil field wastes. Hazards to livestock associated with the petroleum industry. 266 11

Glucose disposal was studied in six very low birth weight infants (birth weight 1093 +/- 67 g (M +/- SEM), gestational age 29.8 +/- 0.6 weeks, postnatal age 5.2 +/- 0.9 days) by constant infusion steady state technique. All babies required artificial ventilation because of respiratory distress syndrome (four) or aspiration pneumonia (two). Nine healthy prematures of comparable birth weight, gestational age, and postnatal age formed the control group. During a constant glucose infusion at a rate of 8 mg/kg/min (7.7 +/- 0.2) mean blood glucose levels of the sick infants were higher than the corresponding control values. All sick babies had glycosuria (glucose excretion 34 +/- 19 mg/kg/hr compared to none of the controls 0.8 +/- 0.2, p less than 0.01). Glucose disposal in the sick prematures was significantly decreased in comparison to the healthy infants [92.6% (78.7 to 99.3%) of input rate vs. 99.8% (99.7 to 99.9%), p less than 0.01]. It is concluded that sick very low birth weight infants tend to develop hyperglycemia, glucosuria, impaired glucose disposal, and renal caloric wasting when exogenous glucose is supplied at a rate of 8 mg/kg/min, which is usually well tolerated by healthy prematures.
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PMID:[Glucose disposal in very low birth weight infants ]. 712 56

There are no satisfactory animal models for the study of anaerobic lung abscess. Aspiration of food, gastric mucin, or hydrochloric acid, or any combination of these, along with oropharyngeal bacteria, is commonly believed to cause aspiration pneumonia and lung abscess. In the animal model described, none of the adjuvants was effective in producing anaerobic lung abscesses. Anaerobic bacteria derived from dental scrapings of a healthy adult (Peptococcus morbillorum, Fusobacterium nucleatum, Eubacterium lentum, and Bacteroides fragilis), when inoculated transtracheally without any adjuvants into New Zealand male white rabbits, consistently produced lung abscesses. Neither B fragilis by itself nor a mixture of P. morbillorum, F. nucleatum, and E. lentum without the addition of B. fragilis produced lung abscesses. The bacterial isolates used in this study were stored in prereduced chopped-meat-glucose medium and subcultured several times and were found effective in reproducing anaerobic lung abscesses repeatedly. This animal model is suitable for the study of pathogenesis, diagnosis, and treatment of B. fragilis-associated anaerobic lung abscess.
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PMID:Animal model for anaerobic lung abscess. 721 63

We report a 49-year-old man who presented progressive dysarthria, dysphagia, and left hemiparesis. The patient was well until June 28th of 1993 when he noted 'weakness' in his both legs; despite his weakness, he could play golf on that day. In the beginning of July, he noted difficulty in swallowing solid foods. He was admitted to the neurosurgery service of our hospital on July 15th of 1993 and a neurologic consultation was asked on July 17th. Neurologic examination at that time revealed an alert but somewhat childish man who appeared to have some difficulty in paying attention to questions. He was disoriented to time and showed difficulty in recent memory and calculation. Higher cerebral functions were intact. The optic fundi were normal; pupils were isocoric and reacted to light promptly; ocular movements were intact, however, he showed difficulty in convergence. Facial sensation and facial muscles were intact. He had no deafness. He showed slurred speech and difficulty in swallowing solid foods. The remaining cranial nerves were intact. Motor-wise, he was able to walk normally and no weakness or atrophy was noted. Mild ataxia was noted in the finger-to-nose and the heel-to-knee test on the left. Muscle stretch reflexes were normal and symmetric, however, the plantar response was extensor bilaterally. Sensation was intact and no meningeal signs were noted. General routine laboratory findings were unremarkable. CSF was under a normal pressure containing 1 cell/microliter, 68 mg/dl of protein, and 54 mg/dl of glucose. Cranial CT scan showed low density areas involving the pons, midbrain, left thalamus, and the left parietal cortex. In MRI, these areas presented low signal intensity in T1-weighted images and high signal intensity in T2-weighted in images. The brain stem appeared swollen. Gadolinium enhancement was negative. He was given a course of steroid pulse with 1 g/day of DIV methylprednisolone for three days followed by oral steroid. He showed only temporary improvement in swallowing. In the subsequent course, he showed progressive deterioration in dysarthria and dysphagia. A biopsy was performed on the left parietal lobe lesion. After biopsy, he was treated with steroid and glycerol without improvement. A course of chemotherapy with procarbazine, MCNU, and vincristine was given; he did not respond to chemotherapy. His left hemiparesis deteriorated. He developed aspiration pneumonia from dysphagia and expired on October 22, 1993. The patient was discussed in a neurologic CPC, and the chief discussant arrived at the conclusion that the patient had astrocytoma grade III involving the pons, midbrain, thalamus, and the parietal cortex.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 49-year-old man with progressive dysarthria, dysphagia, and left hemiparesis]. 749 19

Human status epilepticus (SE) is consistently associated with cognitive problems, and with widespread neuronal necrosis in hippocampus and other brain regions. In animal models, convulsive SE causes extensive neuronal necrosis. Nonconvulsive SE in adult animals also leads to widespread neuronal necrosis in vulnerable regions, although lesions develop more slowly than they would in the presence of convulsions or anoxia. In very young rats, nonconvulsive normoxic SE spares hippocampal pyramidal cells, but other types of neurons may not show the same resistance, and inhibition of brain growth, DNA and protein synthesis, and of myelin formation and of synaptogenesis may lead to altered brain development. Lesions induced by SE may be epileptogenic by leading to misdirected regeneration. In SE, glutamate, aspartate, and acetylcholine play major roles as excitatory neurotransmitters, and GABA is the dominant inhibitory neurotransmitter. GABA metabolism in substantia nigra (SN) plays a key role in seizure arrest. When seizures stop, a major increase in GABA synthesis is seen in SN postictally. GABA synthesis in SN may fail in SE. Extrasynaptic factors may also play an important role in seizure spread and in maintaining SE. Glial immaturity, increased electronic coupling, and SN immaturity facilitate SE development in the immature brain. Major increases in cerebral blood flow (CBF) protect the brain in early SE, but CBF falls in late SE as blood pressure falters. At the same time, large increases in cerebral metabolic rate for glucose and oxygen continue throughout SE. Adenosine triphosphate (ATP) depletion and lactate accumulation are associated with hypermetabolic neuronal necrosis. Excitotoxic mechanisms mediated by both N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors open ionic channels permeable to calcium and play a major role in neuronal injury from SE. Hypoxia, systemic lactic acidosis, CO2 narcosis, hyperkalemia, hypoglycemia, shock, cardiac arrhythmias, pulmonary edema, acute renal tubular necrosis, high output failure, aspiration pneumonia, hyperpyrexia, blood leukocytosis and CSF pleocytosis are common and potentially serious complications of SE. Our improved understanding of the pathophysiology of brain damage in SE should lead to further improvement in treatment and outcome.
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PMID:Pathophysiological mechanisms of brain damage from status epilepticus. 838 2

All stroke patients ideally should be admitted to a stroke unit in which personnel are familiar with strategies for taking care of stroke patients. Prevention of worsening cerebral ischemia by appropriate blood pressure and serum glucose management, fever control, and supplemental oxygen for hypoxemic patients is recommended. Recognition of common complications, such as aspiration pneumonia and deep venous thrombosis, highlights the need for swallowing evaluation and the use of pneumatic compression devices or subcutaneous heparin. Patients should be monitored closely for deterioration in their neurologic status and should have complications appropriately addressed. After evaluation of stroke etiology, appropriate secondary stroke prophylaxis should be selected and initiated before hospital discharge.
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PMID:Post-emergency department management of stroke. 1237 68

Adding pectin to an elemental formula increases its viscosity through gelatinization, thus presumably preventing gastro-oesophageal reflux and aspiration pneumonia. We investigated the influence of the viscosity of an elemental formula on gastric emptying. Eleven healthy volunteers underwent three tests at intervals of >1 week. After fasting for >8 h, each subject received a test meal (enteral nutrition solution, enteral solution plus pectin, or water). Then gastric emptying (continuous (13)C breath test), gastro-oesophageal intraluminal pressures, oesophageal pH, and blood levels of glucose, insulin and gastrin were all measured simultaneously. The gastric emptying coefficient was significantly increased by adding pectin to enteral nutrition (3.01 +/- 0.10 vs 2.78 +/- 0.10, mean +/- SE, P < 0.05). The antral motility index was also significantly higher with pectin than without at 45-60 min and 60-75 min after the test meal (526 +/- 237 vs 6.5 +/- 4.6 mmHg s(-1) and 448 +/- 173 vs 2.3 +/- 2.3 mmHg s(-1) respectively; P < 0.05). Plasma glucose was significantly higher with pectin than without it at 60 min after ingestion (141.5 +/- 6.03 vs 125.8 +/- 4.69 microM mL(-1), P < 0.05). In healthy individuals, pectin increased the viscosity of enteral nutrition and accelerated gastric emptying.
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PMID:High-viscosity liquid meal accelerates gastric emptying. 1797 39

ABSTRACT Body packers are people who illegally carry drugs, mostly cocaine as well as opium and/or heroin, concealed within their bodies. The packets are inserted in the mouth, rectum, or vagina in order to get across borders without being detected. In this presentation we report a case of an opium body packer and review the available scientific literature by focusing on mechanisms of toxicity and treatment approach. The patient was a 35-year-old man who had lethargy, respiratory depression, tachycardia, normal blood pressure, hyperthermia, and pinpoint pupils on presentation. No past medical history was obtained and the only positive history was his travel from Afghanistan 2 days earlier, which he had given to emergency personnel before arriving at our hospital. Complete blood cells and kidney and liver tests were all in normal range. In the emergency department, the patient was treated with oxygen, naloxone, and hypertonic glucose. One dose of activated charcoal (1 g/kg) was administered orally. After intravenous injection of naloxone (4 mg), the lethargy, respiratory depression, and miosis were resolved. The patient was admitted to the intensive care unit and 90 min after admission, the patient redeveloped respiratory distress and lost consciousness. He was intubated and mechanically ventilated due to the suspicious of body packing. Plain abdominal x-ray showed multiple packets throughout the gastrointestinal tract; 81 packets were removed by surgery and three of them were left due to leaking. After removing the packets, the patient was treated conservatively. He suffered a pulmonary infection (aspiration pneumonia) and he regained consciousness after 4 days. Upon recovery the patient was seen by a psychiatrist prior to going to prison. Surgery is recommended for body packers who have significant signs or symptoms.
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PMID:A case report of opium body packer; review of the treatment protocols and mechanisms of poisoning. 2002 Sep 70


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