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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nitrogen idoxide (NO2) is both edematogenic and cytotoxic to the lung. Preexposure to NO2 protects against mortality from formation of excessive pulmonary edema (tolerance) and, depending on the preexposure schedule, may or may not protect against the cytotoxic effects of NO2 in the lung. Measurement of DNA synthesis in hamster lung was used to study the question of whether the more subtle cytological injury induced by NO2 is mediated by a system which also exhibits tolerance. It was found that when hamsters are preexposured daily to 10 ppm NO2, they develop tolerance against normally lethal concentrations of NO2; are protected against further cytological injury from 10 ppmNO2; but are not protected from the cytotoxic effects of NO2 greater than 10 ppm. Animals exposed weekly to 10 ppm NO2 are not protected from further cytotological injury induced byweekly exposures to 10 ppm NO2, but do develop tolerance against lethal concentrations of NO2. Thus the data indicate that induction of tolerance to NO2 does not necessarily protect the cell populations of the lung from the cytotoxic effects of NO2.
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PMID:Stimulation of DNA synthesis in lungs of hamsters tolerant to nitrogen dioxide. 42 33

The harmful effect of iron excess was studied in an experiment using fifteen adult sheep. The animals were divided into three groups of 5 each. The sheep of the group I were kept as controls, those of the group II and III were supplemented with iron in doses of 80 and 40 mg/kg body weight (BW)/24 h respectively. The animals of group II died after a period of 3-7 weeks showing anorexia, loss of weight, diarrhoea, depression and symptoms of circulatory and respiratory failure. From the animals of group III one died after 13 weeks, with symptoms of pulmonary oedema, while the other 4 survived for 22 weeks, together with the animals of the control group. The iron-supplemented animals presented increased values of Serum Iron (SI), Total Iron Binding Capacity (TIBC), percent Transferring Saturation (% SAT), Alanino aminotransferase (ALT), serum Alkalin Phosphatase (SAP), Serum Urea Nitrogen (SUN) Creatinine, Phosphorus and decreased values of serum Copper concentration. These parameters were greater in group II. The iron concentration in the liver, spleen, myocardium and kidneys was also much higher than in the controls. The histological examination revealed degeneration of the liver, spleen, myocardium and kidneys in both groups, while cells overloaded with hemosiderin were seen in the third group only. In conclusion, it was shown that chronic intoxication may occur in sheep overdosed with iron. The toxic dose of iron ranged between 40 and 80 (mg/Kg body weight) per day and was close to 40 mg, when iron was administered in the soluble from FeCl3.6H2O.
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PMID:Iron toxicity in sheep. 253 32

Wet nappies at night could cause infants at risk to die. Tyler first suspected this ten years ago when his head was jerked back from his infant son's cot by the pungent odour of ammonia gas. This theory is consistent with the full epidemiology of cot-death. Ammonia is an insidious poison which has a wide and varied range of effects on the respiratory and nervous systems according to concentration and length of exposure. At its mildest it irritates the tissues. In larger doses ammonia can cause pulmonary oedema and pneumonitis. It can also cause stenosis of affected organs. Its chief danger lies in its potential to disrupt oxygenation at every level throughout the body. Acute and chronic poisoning profiles indicate the possibility that numbers of infants reported as dying from gastro-intestinal or respiratory disease could have been ammonia poisoning victims. Predisposing factors, such as smoking during pregnancy, are shown to contribute to the vulnerability of the infant to ammonia poisoning. The theory provides the framework for the development of an effective programme of infant death prevention.
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PMID:Cot-death: the ammonia factor. 399 99

The fibroproliferative reaction to acute lung injury may limit restoration of normal lung function and increase mortality in patients with acute lung injury. A biologic marker of collagen synthesis in the lung may be useful for studying the pathogenesis of acute lung injury and for identifying patients with acute lung injury who are at high risk for death and might benefit from new therapeutic modalities. Using an immunoassay, type III procollagen NH2 terminal peptide was measured in the pulmonary edema fluid of 44 patients with either acute lung injury or hydrostatic pulmonary edema (control group) within the first 24 h after endotracheal intubation for acute respiratory failure. Patients with acute lung injury (n = 33) or hydrostatic edema (n = 11) had the same degree of lung dysfunction as measured by the severity of oxygenation defect, the level of positive end-expiratory pressure, the decrease in static lung compliance, and the extent of infiltrates on the chest radiograph. However, the median procollagen III level was 5-fold higher in the pulmonary edema fluid of patients with acute lung injury than in the patients with hydrostatic pulmonary edema (p = 0.0001). Of the 33 patients with acute lung injury, 21 patients died and 12 lived. Nonsurvivors had significantly higher procollagen III levels than did survivors (p = 0.05). The positive and negative predictive values for nonsurvival for a procollagen III level > or = 1.75 U/ml were 74 and 83%, respectively. The relative risk of dying in the presence of a procollagen III value > or = 1.75 U/ml was 4.5 (95% CI, 0.7 to 27). Collagen synthesis in the lung, as reflected by elevated levels of procollagen III in pulmonary edema fluid, begins within the first 24 h of acute lung injury concurrent with the acute phase of increased endothelial and epithelial permeability to protein. This evidence suggests that fibrosing alveolitis begins much earlier in the course of clinical acute lung injury than has previously been appreciated. In addition, the presence of an elevated level of procollagen III is an early predictor of poor outcome. Thus, elevation of procollagen III in pulmonary edema fluid may have both pathogenetic and prognostic significance in patients with acute lung injury.
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PMID:Early detection of type III procollagen peptide in acute lung injury. Pathogenetic and prognostic significance. 931 2

Chemical burns are associated with significant morbidity, especially anhydrous ammonia burns. Anhydrous ammonia is a colorless, pungent gas that is stored and transported under pressure in liquid form. A 28 year-old patient suffered 45% total body surface area of second and third degree burns as well as inhalational injury from an anhydrous ammonia explosion. Along with fluid resuscitation, the patient's body was scrubbed every 6 h with sterile water for the first 48 h to decrease the skin pH from 10 to 6-8. He subsequently underwent a total of seven wound debridements; initially with allograft and then autograft. On post burn day 45, he was discharged. The injuries associated with anhydrous ammonia burns are specific to the effects of ammonium hydroxide. Severity of symptoms and tissue damage produced is directly related to the concentration of hydroxyl ions. Liquefactive necrosis results in superficial to full-thickness tissue loss. The affinity of anhydrous ammonia and its byproducts for mucous membranes can result in hemoptysis, pharyngitis, pulmonary edema, and bronchiectasis. Ocular sequelae include iritis, glaucoma, cataracts, and retinal atrophy. The desirability of treating anhydrous ammonia burns immediately cannot be overemphasized. Clothing must be removed quickly, and irrigation with water initiated at the scene and continued for the first 24 h. Resuscitative measures should be started as well as early debridement of nonviable skin. Patients with significant facial or pharyngeal burns should be intubated, and the eyes irrigated until a conjunctivae sac pH below 8.5 is achieved. Although health care professionals need to be prepared to treat chemical burns, educating the public, especially those workers in the agricultural and industrial setting, should be the first line of prevention.
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PMID:Anhydrous ammonia burns case report and review of the literature. 1081 76

Ammonia is a common household and industrial chemical. In the medical literature and the electronic press there are many descriptions of accidental spills of anhydrous ammonia, but apart from the Chechen war, there is no evidence of its intentional use by a terrorist to date. When considering its characteristics, ammonia tankers may pose an imminent threat for a civilian population nearby. This short review attempts to highlight the main health issues and basic principles of medical management after exposure to ammonia. Ammonia can directly cause damage due to its irritating as well as alkaline properties. The management of toxic exposure to ammonia is largely supportive and there is no specific antidote. Emergency medical response on site includes rapid evacuation, life-saving procedures and decontamination if necessary and if possible. Major clinical manifestations include respiratory symptoms, such as hypoxia, bronchospasm and pulmonary edema, as well as hypovolemia and burns to the skin and eyes. The immediate medical management consists of life-saving procedures and supportive care, while broad-range antibiotics and systemic corticosteroids may have a role in preventing late onset complications.
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PMID:Ammonia--when something smells wrong. 1875 37

Nitrogen oxides are representative chemicals of occupational and environmental exposure, which can lead to fatal pulmonary injury. These oxides are also known to cause delayed occurrence of bronchiolitis obliterans (BO). Herein, we report a case of nitrogen oxide-induced lung injury. A 50-year-old man developed pulmonary edema after nitric acid exposure. Hypoxemia and respiratory failure were immediately improved after introduction of corticosteroid pulse therapy with supplemental oxygen. This was followed by administration of oral prednisolone, and delayed BO did not develop. This case supports the therapeutic efficacy of corticosteroids against pulmonary injury and late-onset BO after nitrogen oxide exposure.
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PMID:Successful treatment of pulmonary injury after nitrogen oxide exposure with corticosteroid therapy: A case report and review of the literature. 2813 25

Nitric acid (HNO3) is a strong acid and oxidizing agent used for various applications including production of ammonium nitrate in the fertilizer industry. Nitrogen oxides formed when nitric acid interacts with the environment have been implicated in inhalation injuries. This describes a case of a 49-year-old male who presented to the emergency department complaining of an acute onset of shortness of breath approximately 12 hours after being exposed to nitric acid fumes. He presented with a room air oxygen saturation of 80 percent with moderate to severe respiratory distress. His plain film chest radiograph showed bilateral pulmonary infiltrates and pulmonary edema. Over a seven-day hospital course, he had an improvement in his clinical status and chest X-ray with normal pulmonary function tests one month after discharge. Although exposure to the fumes of nitric acid is known to cause delayed pulmonary edema, it is rarely reported in the medical literature. This case serves as a reminder to consider exposure to fumes of nitric acid in a patient presenting with pulmonary edema and highlights the importance of obtaining a work history.
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PMID:Pulmonary Edema Occurring after Nitric Acid Exposure. 3077 39