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

Bradykinin metabolism by peptidases of the pulmonary endothelium has been investigated in the previously uninjured, ventilated, and asanguinously perfused rat lung. The influence of short-duration (up to 20 min) abnormal ventilation and perfusion conditions on bradykinin metabolism was assessed. Neither variation of the oxygen concentration (0 to 45%) nor omission of carbon dioxide in the ventilatory gas altered bradykinin metabolism significantly. Tidal volume variation did not alter bradykinin metabolism, and exclusion of one lung from the perfusion circuit reduced the capacity to degrade bradykinin proportionately. Acidification of the perfusion medium to pH 5 did not alter bradykinin metabolism. Acetylsalicylic acid in the perfusate protected the lung from an otherwise irreversible pressure increase associated with high-dose bradykinin perfusion. Endotoxin and hydrogen peroxide in the perfusate did not alter bradykinin metabolism. However, ammonia in the ventilatory gas caused immediate pulmonary edema, diminished lung capacity to metabolize bradykinin and altered the pattern of bradykinin metabolic products. The pulmonary endothelium itself, in the absence of blood, maintains its capacity to metabolize bradykinin under an extraordinary range of conditions.
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PMID:Kinin metabolism in the perfused ventilated rat lung. II: Influence of ventilation, perfusion, and perfusate composition variation on bradykinin metabolism in uninjured lung. 144 86

The clinical signs and lesions of Nubian goats and Desert sheep orally dosed with fresh and dry leaves and stems of Ipomoea carnea at 2.5, 5 and 10 g/kg/day were studied. The signs of Ipomoea poisoning were inappetence, depression, weakness of the hind limbs, dyspnea, staggering, and pallor of the visible mucous membranes. The main lesions were focal necrosis and fatty vacuolation of centrilobular hepatocytes, accumulation of fibroblasts in hepatic portal tracts, degeneration or necrosis of the cells of the renal proximal convoluted tubules, hemorrhage in renal cortices, in renal medullas and in cardiac muscle fibers, focal pulmonary edema, and emphysema and straw-colored fluid in serous cavities. Increased serum aspartate amino transferase and ammonia concentrations, and decreased concentrations of total protein, calcium and magnesium in the serum of Ipomoea-poisoned animals were detected. Hematological changes indicated the development of normocytic normochromic anaemia.
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PMID:The effects of Ipomoea carnea on goats and sheep. 362 12

This study was undertaken to determine the site of initial pulmonary injury in smoke inhalation. A hotel fire in Houston, Texas, resulted in the on-site deaths of 10 white people (2 to 62 years of age). All underwent autopsy examinations which included measurement of carbon monoxide (CO) and cyanide (CN) levels, as well as electron microscopy of lung samples. Average CO levels of 40% and CN levels of 0.6 ppm were obtained. In all cases, the lungs were heavy, hyperemic, and edematous with soot staining the tracheobronchial mucosa. Light microscopy showed soot, pulmonary congestion, and edema. Electron microscopy confirmed the presence of interstitial and intraalveolar congestion and edema. Carbon particles were also present, and occasionally were seen undergoing phagocytosis by alveolar macrophages. Intracellular edema with focal bleb and vesicle formation was prominent within Type I pneumocytes in 9 of 10 cases. Endothelial cells showed similar but much less severe changes, lacking the distinct blebs seen in the Type I cells. This investigation reveals that smoke, like ammonia inhalation and nitric acid instillation, appears to cause pulmonary edema by initial injury to the Type I pneumocyte.
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PMID:Smoke inhalation: an ultrastructural study of reaction to injury in the human alveolar wall. 378 Jun 43

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

A flock of goats received a diet with 1% urea for at least 1 y. A new batch of concentrate was offered increasing the level of urea to 4.2%. Eighteen of 54 goats showed acute signs of ammonia toxicosis. Ten goats died within 60 min; 4 goats and a buck with convulsions recovered when treated by administration of vinegar and infusion of saline solution, diuretics, and atropine. Three goats with mild signs recovered within 1 h without treatment. The mean ammonia concentration and rumen pH content were 820 mg/L and 7.7, respectively. Generalized congestion, intense pulmonary edema, and slight tubular nephrosis were found in 3 goats on necropsy. The outbreak was self-limiting and no more cases occurred when the diet was removed.
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PMID:Ammonia toxicity from urea in a Brazilian dairy goat flock. 1075 Jan 72

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

Three hundred sixty-seven male Wistar rats were used to compare the efficiency of urea cycle amino acids (arginine, citrulline and ornithine; Group O), furosemide (Group F), and fluid therapy (saline solution; Group FT) to treat ammonia toxicity. Rats were injected ip initially with an ammonium acetate solution at 99.9% of the lethal dose. Three min later the rats were allocated randomly to Group C (control, received 1.2 mL distilled water). Group O (amino acids listed earlier, 2 mmol/kg bw), Group F (furosemide, 2 mg/kg bw), Group FT (7mL saline), or Groups O+F, O+FT, F+FT, or O+F+FT. All treatments were given ip except for Group F given im injections. Plasma ammonia, urea and creatinine, and hematocrit and pulmonary dry matter were determined. The highest survival rates were obtained with O+FT (57%) and O+F+FT (62.5%); only 6% of the controls survived. Plasma ammonia levels were ten-fold lower in rats treated with O+FT and O+F+FT (p<0.0001). Fatally-poisoned rats had higher plasma ammonia, creatinine and hematocrit and exhibited pulmonary edema. Surviving rats had lower plasma urea. Animals given treatments with O, FT and F had (p<0.005) higher urea, lower creatinine and less severe pulmonary edema, respectively, than those untreated.
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PMID:Treatment of ammonia intoxication in rats with urea cycle amino acids, furosemide and fluids. 1267 88

The authors encountered a case of portal-systemic venous shunt newly diagnosed after initiation of hemodialysis. A 68-year-old Japanese woman began hemodialysis because of symptoms of uremia including loss of appetite and pulmonary edema. Loss of consciousness occurred suddenly after her ninth session of hemodialysis. No hepatic functional abnormality was found other than hyperammonemia (314 microg/dL [184 micromol/L]). Loss of consciousness subsequently occurred often after hemodialysis. Color Doppler ultrasonography and magnetic resonance angiography depicted a large shunt between the left gastric vein and left renal vein resulting in portal flow entering the systemic circulation via the renal vein. Because the shunt was large, ligation of it was performed surgically. Results of histologic examination of a liver biopsy specimen obtained intraoperatively were normal. The patient became well postoperatively. This patient's encephalopathy appeared to be caused by the flow of ammonia-rich portal venous blood into the systemic circulation via the large shunt owing to a decrease in intravenous pressure after rapid hemodialysis. Portal-systemic shunt encephalopathy should be recognized as a "new" neuropsychiatric disorder characteristic of patients undergoing hemodialysis.
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PMID:Hemodialysis-related portal-systemic encephalopathy. 1533 38

We herein describe the clinical course of a consecutive series of fulminant hepatic failure patients treated with a molecular adsorbent recirculating system (MARS), a cell-free albumin dialysis technique. From November 2000 to September 2002, seven adult patients ages 22-61 (median, 41), one male (14.2%) and six females (85.7%), affected by fulminant hepatic failure underwent seven courses (one to five sessions each, 6 hr in duration) of extracorporeal support using the MARS technique. Pre- and posttreatment blood glucose, liver function tests, ammonia, arterial lactate, electrolytes, hemodynamic parameters, arterial blood gases, liver histology, Glasgow Coma Scale, and coagulation studies were reviewed. No adverse side effects such as generalized bleeding on noncardiogenic pulmonary edema, often seen during MARS treatment, occurred in the patients included in this study. Six patients (85.7%) are currently alive and well, and one (14.2%) died. Four patients (57%) were successfully bridged (two patients in 1 day and two other patients in 4 days) to liver transplantation, while two (5%) recovered fully without transplantation. All the measured variables stabilized after commencement of the MARS. No differences were noted between the pre- and the post-MARS histology. We conclude that the MARS is a safe, temporary life support mechanism for patients awaiting liver transplantation or recovering from fulminant hepatic failure.
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PMID:Fulminant hepatic failure bridged to liver transplantation with a molecular adsorbent recirculating system: a single-center experience. 1641 11

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


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