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

Combustion toxicology is complex so, although victims exposed to combustion products are mainly treated symptomatically, it is important to identify those situations when specific therapeutic measures might be of importance. Victims presenting respiratory symptoms including severe cough, bronchoconstriction, hypoxia and respiratory distress should be given oxygen and ventilatory assistance or support. Furthermore, bronchoconstriction should be treated with bronchodilators (beta-2-adrenoreceptor agonists, theophylline). Corticosteroids should be considered both for inhalation and systemically due to the risk of developing toxic pulmonary oedema that may appear after a symptom-free interval that might last up to 48-72 h. Victims with impaired consciousness should be regarded as being exposed to carbon monoxide and cyanides. Apart from oxygen and optimal symptomatic treatment hyperbaric oxygen therapy should be considered in carbon monoxide poisoning. Certain cyanide antidotes, namely those with low intrinsic toxicity (as sodium thiosulphate, hydroxocobalamin) should be given liberally in these situations. Other specific therapeutic measures that might be considered when appropriate are administration of organophosphate antidotes (atropine, oximes), heavy metal chelators (e.g. dimercaptopropane sulfonate, dimercaptosuccinic acid) and methemoglobinemia antidotes (methylthionine, toluidine blue). Inhalation of hot fumes may cause upper respiratory tract oedema (e.g. laryngeal oedema) necessitating orotracheal intubation and ventilatory support.
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PMID:Hospital treatment of victims exposed to combustion products. 147 Nov 83

In December, 1984, in Bhopal, India, a massive leak of methyl isocyanate (MIC) resulted from operational and equipment malfunctions in a pesticide plant. Many thousands of residents of the city, most in proximity to the plant, suffered sublethal and lethal respiratory injuries, the expected consequences of high-level exposure to this type of potent irritant chemical vapour. Animal toxicologic information was limited prior to the accident, but has since confirmed that the lung is the major target of these lethal injuries, invariably with pulmonary oedema. Early concerns regarding acute cyanide intoxication were not supported by subsequent scientific inquiry. Superficial corneal erosions did not result in permanent eye injury. The primary medical (and, presumably, legal) issue which is unresolved, and perhaps unresolvable, is the incidence and determinants of long-term respiratory injury in the survivors. Available evidence, which is limited, suggests that chronic damage, when present, is, or resembles, fibrosing bronchiolitis obliterans, the expected consequence when permanent injury results from acute, high-level irritant gas exposure. Definition of the follow-up population is uncertain, and exposure information is lacking. Dose-response relationships are not likely to emerge from follow-up studies.
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PMID:Disaster at Bhopal: the accident, early findings and respiratory health outlook in those injured. 345 52

Pyridoxal 5'-phosphate (PLP), the active form of vitamin B6, readily forms complexes with a wide variety of potentially toxic substances, including cyanide (KCN), spermine (SPM), gentamicin (GM), and dopamine (DOP). The role of PLP as an antidote for these toxicants in vivo was studied. Rats were given intraperitoneal injections of the toxicant, followed by injections of either saline or PLP. For KCN, PLP increased the LD50 from 0.088 to 0.188 mmol/kg and extended the survival time at the highest dose employed from a median of 3 min to a median of 60 min. For SPM, PLP increased the LD50 from 0.162 to 0.262 mmol/kg and prevented death from renal failure at all doses employed except the highest. PLP protected against GM-induced neuromuscular paralysis and death. In the case of DOP, results were equivocal, but no deaths were seen in the PLP-treated rats. The combination of individually nontoxic doses of GM, DOP, and SPM caused death with renal tubular necrosis, pulmonary edema and hemorrhages, congestion of the viscera, and a diffuse coagulopathy. Because many seriously ill patients have elevated SPM levels and are given GM and/or DOP, we suggest that further investigation of the potential protective role of PLP in serious illness be undertaken.
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PMID:Pyridoxal 5'-phosphate as an antidote for cyanide, spermine, gentamicin, and dopamine toxicity: an in vivo rat study. 357 25

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

1. Action potentials have been recorded from single laryngeal motor fibres, with expiratory or inspiratory phases, in cats anaesthetized with pentobarbitone and breathing through a tracheal cannula.2. Pneumothorax increased the discharge of both inspiratory and expiratory units, the inspiratory response being greatly reduced by bilateral vagotomy below the origin of the recurrent laryngeal nerves.3. Addition of a ;viscous' resistance to breathing, or asphyxial rebreathing through an added dead space, increased the activity of inspiratory units and decreased that of expiratory units.4. Induction of pulmonary oedema decreased the discharge of inspiratory units and increased that of expiratory units. After vagotomy the response of inspiratory units was reversed.5. Intravenous injections of potassium cyanide increased the activity of both types of unit.6. Chemical irritation of the laryngeal mucosa decreased the discharge of inspiratory units and increased that of expiratory units, whether the vagi were intact or cut.7. It is concluded that expiratory unit discharge can be correlated with expiratory laryngeal resistance, but that inspiratory unit discharge does not correlate so well with inspiratory laryngeal resistance.8. The relationship between laryngeal motor-fibre activity and the contractions of the inspiratory and expiratory muscles of breathing is discussed.
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PMID:Reflex control of discharge in motor fibres to the larynx. 441 12

Eleven patients in hypertensive crisis were treated with iv sodium nitroprusside (SNP). In all cases, rapid clinical improvement was obtained. Nevertheless, 9 patients developed progressive resistance to the hypotensive effect of the drug. For the first 2 h, the mean infusion rate was 1.68 +/- 0.64 micrograms/kg . min. For the next 6 h, the mean infusion rate had to be increased to 3.1 +/- 1.14 micrograms/kg . min in order to maintain diastolic blood pressure below 110 mm Hg. Hemodynamic measurements demonstrated that this resistance was related to a marked rise in cardiac index without tachycardia. In the 6 patients with pulmonary edema who developed resistance to SNP, blood pressure control was obtained by fluid depletion. In the 3 patients without pulmonary edema who developed resistance to SNP, blood pressure control was obtained by iv acebutolol. The authors conclude that SNP rapidly improves critical hypertension. Progressive resistance to the hypotensive effect of the drug can occur in some cases and is related to a marked rise in cardiac index, which can be rapidly antagonized with fluid depletion or a beta-blocking agent to avoid SNP accumulation and cyanide toxicity.
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PMID:Resistance to sodium nitroprusside in hypertensive patients. 707 20

Sodium nitroprusside is a potent and ultrafast-acting antihypertensive agent. Limited clinical experience and uncertainty about toxicity have restricted its use in obstetrics. The authors have used nitroprusside concomitantly with hemodynamic monitoring in 4 obstetric patients with severe pregnancy-induced hypertension unresponsive to conventional therapy. The patients with acute congestive heart failure and pulmonary edema responded rapidly and dramatically to nitroprusside. No signs of fetal distress associated with lowering of the arterial pressure were observed, and significant cyanide levels were not detected in a fetal cord blood sample. Nitroprusside should be reserved for refractory hypertensive emergencies in pregnancy. Hemodynamic monitoring is required for adjusting nitroprusside administration and fluid balance. In short-term usage, the authors' experience suggests that maternal and fetal toxicity may not be serious concerns.
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PMID:Use of sodium nitroprusside in complications of gestational hypertension. 712 43

Because fetal rat lungs have lower baseline levels of both surfactant and antioxidant enzymes than full-term newborn rats, we questioned whether prematurely delivered rats might be more susceptible to O2 toxicity than those born at term. In the present studies, prematurely delivered rats (gestational d 21 of 22) and full-term rat pups were simultaneously put in > 95% O2 after birth. Surprisingly, we found that the preterm rats were not more susceptible to O2-induced lung damage and lethality than full-term newborns, but, in fact, the composite percentage of survival was even greater in the preterm pups from 7 to 9 d in hyperoxia and were similar thereafter up to 14 d in high O2. In addition, the preterm rats showed significantly decreased lung wet/dry weight ratios and consistently less severe pathologic evidence of pulmonary edema compared with term rats at 6 and 8 d of O2 exposure. The premature pups demonstrated the capability of inducing pulmonary antioxidant enzyme responses to hyperoxia by 3 d, and had significantly elevated copper-zinc superoxide dismutase, catalase, and glutathione peroxidase activities (and lung surfactant contents) at 6 d of O2 exposure compared with the term rats in O2. The rates of lung total O2 consumption and cyanide-resistant O2 consumption at d 6 in hyperoxia were not different for preterm versus term pups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparative responses of premature versus full-term newborn rats to prolonged hyperoxia. 816 59

The histotoxic effects of chronic cyanide insult on heart, lung and pancreatic tissues, and some corroborative enzyme and metabolite changes were studied in New Zealand White rabbits using colorimetric, enzymatic and histochemical methods. Two groups of rabbits were fed for 10 months on either pure growers mash or grower mash +702 ppm inorganic cyanide. There were no significant differences in time-course profiles of serum amylase and fasting blood glucose between the cyanide-fed group and control. Pancreatic islet and heart histologies showed no pathological changes, and there were no significant differences in both serum and heart aspartate transaminase activities between the two groups. However, there were significant decreases (P<0.01) in alkaline phosphatase activity in the lungs of the cyanide-fed group, with corresponding significant (P<0.05) increases in the serum activity of the enzyme. Histological examination of lung tissue of the cyanide-treated rabbits revealed focal areas of pulmonary oedema and necrosis. These results suggest the existence of variabilities in tissue susceptibilities to the toxic effect of chronic cyanide exposure. It would appear that chronic cyanide exposure may not predispose to diabetes in the presence of adequate protein intake.
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PMID:Differential effects of chronic cyanide intoxication on heart, lung and pancreatic tissues. 1082 6

A 55-year-old male Caucasian truck driver was dead at the scene after breathing hydrogen sulfide (H(2)S) produced by an accidental transfer of sodium hydrogen sulfide (NaHS) from a tanker truck to a tank containing 4% sulfuric acid (H(2)SO(4)) and iron(II) sulfate (FeSO(4)). Autopsy of the decedent's body revealed pulmonary edema and passive congestion in lungs, spleen, kidneys, and adrenal glands. Postmortem biological samples were analyzed for carbon monoxide, cyanide, ethanol, and drugs. Since a potential exposure to H(2)S was involved, blood was also analyzed for sulfide (S(2-)). The analysis entailed isolating S(2-) from blood as H(2)S using 0.5M H(3)PO(4), trapping the gas in 0.1M NaOH, and determining the electromotive force using a sulfide ion specific electrode. Acetaminophen at a concentration of 14.3 microg/ml was found in blood, and metoprolol was detected in the blood, liver, and kidney samples. The blood S(2-) level was determined to be 1.68 microg/ml. It is concluded that the cause of death was H(2)S poisoning associated with a hazardous material accident in an industrial situation.
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PMID:A fatality caused by accidental production of hydrogen sulfide. 1172 49


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