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Query: UMLS:C0032290 (aspiration pneumonia)
 2,291 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Disodium edetate (ethylenediaminetetraacetic acid, disodium salt; disodic EDTA), 3 g, was given, via an intravenous normal saline drip of 30 min, to 25 patients in order to assess a benefit for anaesthesia practice. A significant reduction of both volume and acidity of the gastric secretion was found in all the 10 patients with peptic ulcer having received the drug. The peak of the change was 1 h after administration. In other 10 non-ulcer patients undergoing orthopaedic surgeries under epidural anaesthesia with lidocaine 2%, 5 mg kg-1, pH of the gastric juice unanimously rose, from 2.24 +/- 0.28 to 4.10 +/- 0.21 1 h after EDTA with a P derived from paired difference analysis of less than 0.001. A similar group of patients receiving only normal saline showed no important changes in pH (from 2.37 +/- 0.24 to 2.34 +/- 0.19). The pH of the fundic surface, measured directly under fiberscopic control in further 5 patients suffering from peptic ulcer, was found also to rise from 1.84 +/- 0.21 to 4.62 +/- 0.34 1 h after EDTA, P less than 0.001. Total and ionized calcium changed unsignificantly. Disodic EDTA in the dose and manner used in this study showed no clinical side-effects. The constant and obvious effect of inhibition of the gastric secretion as well as the dynamics of such an action recommend disodic EDTA to be tried in reducing the aspiration pneumonia morbidity.
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PMID:Inhibitory effect of disodium edetate on gastric secretion. 308 72

Omeprazole, a gastric acid pump inhibitor, dose-dependently controls gastric acid secretion: the drug has greater antisecretory activity than histamine H2-receptor antagonists. Omeprazole 20 to 40 mg/day is more effective than histamine H2-receptor antagonists in the short term treatment of duodenal ulcer, gastric ulcer and reflux oesophagitis. Available data suggest that omeprazole 10 to 40 mg/day is also more effective than ranitidine in the maintenance therapy of duodenal ulcer and reflux oesophagitis. The drug is also effective in patients with duodenal ulcer, gastric ulcer or reflux oesophagitis poorly responsive to histamine H2-receptor antagonists. The efficacy of omeprazole 20 mg/day appears to be similar to that of lansoprazole 30 mg/day in the short term treatment of duodenal ulcer, gastric ulcer and reflux oesophagitis. However, most available studies have been reported in abstract form only, and 2 of 3 studies in patients with duodenal ulcer have shown greater healing rates at 2 (but not 4) weeks with lansoprazole. Helicobacter pylori eradication decreases duodenal ulcer relapse rates and appears to be associated with improved duodenal ulcer healing rates. Evidence also suggests that H. pylori eradication is associated with reduced gastric ulcer relapse rates. Omeprazole monotherapy may suppress but does not eradicate H. pylori infection. Eradication rates with omeprazole 20 or 40 mg twice daily plus amoxicillin usually up to 2 g/day (3 g/day in a few studies) for 2 weeks appear to be similar to those of standard triple therapy (bismuth salt plus metronidazole, plus tetracycline or amoxicillin) or omeprazole plus clarithromycin, although eradication rates vary widely. Omeprazole plus amoxicillin appears to be better tolerated than triple therapy and represents a first-line treatment alternative in patients with H. pylori-associated peptic ulcer disease. Omeprazole plus amoxicillin plus metronidazole appears to be more effective than omeprazole plus amoxicillin in patients with metronidazole-sensitive H. pylori infection. Omeprazole remains a treatment of choice in patients with Zollinger-Ellison syndrome. The dosages should be adjusted according to individual response. However, relatively low dosages of 10 to 40 mg/day may be sufficient in some patients. The drug has also shown promise in the treatment of children with severe reflux oesophagitis, in patients with reflux oesophagitis and coexisting systemic sclerosis, and in the prevention of aspiration pneumonia. Evidence suggests that omeprazole is more effective than ranitidine in patients with nonsteroidal anti-inflammatory drug (NSAID)-induced gastric damage who continue to take NSAIDs, especially in patients with large gastric ulcers; however, completion of ongoing studies is required to verify this.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Omeprazole. An update of its pharmacology and therapeutic use in acid-related disorders. 752 98

Penicillin VK, a widely used antibiotic for treatment of gram-positive coccal infections, was nominated for study by the National Cancer Institute because rodent carcinogenicity studies for this drug had not been performed. The chemical (94% or 98% pure, USP grade) was administered orally (by gavage in corn oil) because oral administration is the primary route used to treat infections in humans. Fourteen-day, 13-week, and 2-year studies were conducted in F344/N rats and B6C3F1 mice. Additional studies were performed to evaluate the potential for genetic damage in bacteria and mammalian cells. Fourteen-Day and Thirteen-Week Studies: In the 14-day studies, penicillin VK was administered at doses of 150-2,400 mg/kg. No compound-related deaths or dose-related histopathologic lesions were seen in rats or mice. Final mean body weights of dosed male rats were 5%-17% lower than that of controls; weights of dosed and control female rats were comparable. Final mean body weights of dosed mice were 5%-9% lower than those of controls. Diarrhea was observed in all dosed groups of rats and mice. In the 13-week studies, male and female rats received doses of 180-3,000 mg/kg and male and female mice received doses of 250-3,000 mg/kg. No compound-related deaths were seen in rats or mice. Final mean body weights of rats that received 3,000 mg/kg were 11% lower than those of the vehicle controls for males and 6% lower for females. For mice, mean body weights were comparable. Diarrhea occurred in male rats at doses of 750 mg/kg and above and in female rats at doses of 1,500 and 3,000 mg/kg. Mucous cell metaplasia of the glandular stomach was observed in male and female rats receiving 1,500 and 3,000 mg/kg. Lesions of the glandular stomach (inflammation, mucous cell metaplasia, and eosinophilic cytoplasmic change) and the forestomach (papillary hyperplasia and hyperkeratosis) were seen in all groups of dosed mice. The severity of lesions at 1,000 mg/kg or below was considered minimal. Based on these results, doses selected for rats and mice in the 2-year studies were 0, 500, or 1,000 mg/kg. Body Weight and Survival in the Two-Year Studies: Mean body weights of dosed and vehicle control male and female rats and male mice were comparable. Mean body weights of dosed female mice were 4%-16% lower than those of the vehicle controls from week 28 to the end of the study. Diarrhea was observed for dosed male and female rats and for dosed male mice. Survival of low and high dose male rats and high dose female rats was reduced (male rats: vehicle control, 34/50; low dose, 19/50; high dose, 16/50;female rats: 29/50; 26/50; 16/50). Survival of male and female mice was comparable to that of the vehicle controls (male mice: 24/50; 36/50; 26/50; female mice: 36/50; 32/50; 32/50). Nonneoplastic and Neoplastic Effects in the Two-Year Studies: Nonneoplastic lesions occurred at low incidences in the nasal mucosa, lung, and forestomach of dosed male rats and in the nasal mucosa and lung of dosed female rats. Congestion and aspiration pneumonia occurring in dosed rats dying before week 104 was the principal cause of death in these animals. Nonneoplastic lesions of the gastric fundal gland (eosinophilic cytoplasmic change and dilatation) and glandular stomach (cyst, chronic focal inflammation, hyperplasia, fibrosis, and squamous metaplasia) were seen in dosed male and female mice, and lesions of the gallbladder (eosinophilic cytoplasmic change) were seen in male mice. Slight increases in the incidences of adenomas of the pituitary gland in high dose male rats and of fibroadenomas or adenomas (combined) of the mammary gland in low dose female rats were observed. These were not considered to be compound-related lesions. The incidence of hepatocellular adenomas was decreased in high dose male mice (14/50; 15/49; 4/49). No compound-related neoplasms were seen in female mice. Genetic Toxicology: Penicillin VK was not mutagenic in Salmonella typhimurium strains TA98, TA100, TA1535, or TA1537 with or without exogenous metabolic activation. The chemical was mutagenic onl exogenous metabolic activation. The chemical was mutagenic only with activation in the mouse lymphoma L5178Y/TK± forward mutation assay. Incubation of Chinese hamster ovary cells with penicillin VK resulted in increased frequencies of sister chromatid exchanges and chromosomal aberrations in the absence of metabolic activation under the conditions of delayed harvest to compensate for chemical-induced cell cycle delay, no effects from penicillin VK exposure were observed in these cells in the presence of S9. Audit: The data, documents, and pathology materials from the 2-year studies of penicillin VK were audited. The audit findings show that the conduct of the studies is documented and support the data and results given in this Technical Report. Conclusions: Under the conditions of these 2-year gavage studies, there was no evidence of carcinogenic activity of penicillin VK for F344/N rats or for B6C3F1 mice administered 500 or 1,000 mg/kg penicillin VK in corn oil gavage, 5 days per week for 2 years. Nonneoplastic lesions were seen in the glandular stomach of dosed mice. Decreased survival of low and high dose male rats and of high dose female rats reduced the sensitivity of the studies for determining the presence or absence of a carcinogenic response in this species. Synonyms: 4-thia-1-azabicyclo(3.2.0)heptane-2-carboxylic acid, 3,3-dimethyl-7-oxo-6-(2-phenoxy-acetamide)-, monopotassium salt; penicillin V potassium; penicillin V potassium salt; D-a-phenoxymethylpenicillinate K salt; phenoxymethylpenicillin potassium; PVK Trade Names: Antibiocin; Apsin VK; Aracil; Arcasin; Aspin VK; Beromycin; Beromycin 400; Betapen VK; Calciopen K; Cliacil; Compocillin VK; Distakaps V-K; Distaquaine V-K; Dowpen V-K; DQV-K; Fenoxypen; Icipen; Isocillin; Ispenoral; Ledercillin VK; Megacillin oral; Oracil-VK; Orapen; Ospeneff; Pedipen; Penagen; Pencompren; Pen-Vee K; Pen-V-K powder; Penvikal; Pfizerpen VK; Qidpen VK; Robicillin VK; Rocillin-VK; Roscopenin; SK-Penicillin VK; Stabilin VK Syrup 125; Stabilin VK Syrup 62.5; Sumapen VK; Suspen; Uticillin VK; V-Cil-K; V-Cillin K; Veetids; Vepen
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PMID:NTP Toxicology and Carcinogenesis Studies of Penicillin VK (CAS No. 132-98-9) in F344/N Rats and B6C3F1 Mice (Gavage Studies). 1273