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Noncardiogenic pulmonary edema

Monitor for evidence of cerebral edema, noncardiogenic (permeability) pulmonary edema, acute respiratory distress syndrome, hyperchloremic metabolic acidosis, and vascular thrombosis... [Pg.105]

Hypertonic intrathecal saline / -Adrenergic agonists Noncardiogenic pulmonary edema R 1... [Pg.981]

Management depends on therapeutic measures used for deep lung irritation and noncardiogenic pulmonary edema (see Nitrogen Oxides, above). [Pg.1216]

Upper and lower airway inflammation, pneumonitis Upper and lower airway inflammation, pneumonitis, noncardiogenic pulmonary edema Ocular and upper airway inflammation, lower airway and parenchymal injury with masssive exposure Ocular and upper airway inflammation, lower airway injury with massive exposure... [Pg.249]

Pneumonitis, noncardiogenic pulmonary edema Ocular and respiratory tract inflammation, pneumonitis central nervous system (CNS), kidney, and systemic effects Upper and lower airway injury, pneumonitis, CNS depression, seizures... [Pg.250]

Ocular and upper airway inflammation, noncardiogenic pulmonary edema, delayed onset bronchiohtis Ocular, upper, and lower airway inflammation pneumonitis... [Pg.250]

Patients who have had a severe exposure may develop noncardiogenic pulmonary edema. [Pg.494]

Humbert VH Jr, Munn NJ, Hawkins RF. Noncardiogenic pulmonary edema complicating massive dUtiazem overdose. Chest 1991 99(l) 258-9. [Pg.608]

Brass BJ, Winchester-Penny S, Lipper BL. Massive verapamil overdose complicated by noncardiogenic pulmonary edema. Am J Emerg Med 1996 14(5) 459-61. [Pg.608]

EUingson TL, Aboulafia DM. Dextran syndrome. Acute hypotension, noncardiogenic pulmonary edema, anemia, and coagulopathy following hysteroscopic surgery using 32% dextran 70. Chest 1997 111(2) 513-18. [Pg.1088]

Shustack A, Noseworthy TW, Johnston RG, Anderson BJ, Johnston D, Bailey RJ. Noncardiogenic pulmonary edema during intrabiliary infusion of mono-octanoin. Crit Care Med 1986 14(7) 659-60. [Pg.2314]

The victim should be removed to fresh air and monitored for respiratory distress. Early intravenous administration of corticosteroids is recommended to prevent or treat noncardiogenic pulmonary edema. Inhalation of sympathomimetic agents is used to treat bronchospasm and wheezing. Absorption can be prevented by dilution with 4-8 oz ( 118-237 ml) of milk or water. Absorption can also be prevented by gastric lavage in patients who are comatose or at the risk of convulsing. Charcoal, saline, or other cathartics can also be used. Cathartics should be avoided in patients with ileus or impaired renal function. [Pg.107]

Chemotherapy drugs can directly or indirectly cause acute pneumonitis (bleomycin, carmustine, gemcita-bine, methotrexate, mitomycin, procarbazine, and vinca alkaloids) pulmonary fibrosis (bleomycin, carmustine, cyclophosphamide, methotrexate, and mitomycin) hypersensitivity pneumonitis (bleomycin, methotrexate, and procarbazine) noncardiogeneic pulmonary edema (cytarabine, cyclophosphamide, methotrexate, mitomycin, and teniposide). Docet-axel is associated with fluid retention, which may result in pulmonary edema or pleural effusion. Some of these conditions respond to corticosteroid therapy but some cases of pulmonary fibrosis are fatal. [Pg.394]

Basic life-support measures should be instituted as necessary. Intensive support therapy may be required to correct respiratory failure and shock. Patients with mild to moderate toxicity may present with lethargy, miosis, decreased blood pressure, heart rate, temperature, and skeletal muscle tone. In patients experiencing severe toxicity, coma, respiratory depression, noncardiogenic pulmonary edema, apnea,... [Pg.1322]

Klein MD (1987) Noncardiogenic pulmonary edema following hydrochlorothiazide ingestion. Annals of Emergency Medicine 16 113-115. [Pg.2563]

Noncardiogenic pulmonary edema is most often due to heroin intoxication and may occur within minutes... [Pg.360]

Acute respiratory distress syndrome (ARDS) is a syndrome presenting with bilateral pulmonary infiltrates, high oxygen requirements (Pao2/Fi02 <200 mm Hg), and noncardiogenic pulmonary edema. [Pg.557]

Pulmonary edema may result from the failure of any of a number of homeostatic mechanisms. The most common cause of pulmonary edema is an increase in capillary hydrostatic pressure because of left ventricular failure. Excessive fluid administration in compensated and decompensated heart failure patients is the most frequent cause of iatrogenic pulmonary edema. Besides hydrostatic forces, other homeostatic mechanisms that may be disrupted include the osmotic and oncotic pressures in the vasculature, the integrity of the alveolar epithelium, interstitial pulmonary pressure, and the interstitial lymph flow. The edema fluid in cardiogenic pulmonary edema contains a low amount of protein, whereas noncardiogenic pulmonary edema fluid has a high protein concentration. This indicates that noncardiogenic pulmonary edema results primarily from disruption of the alveolar epithehum. The reader is referred to Chap. 28 for a detailed discussion of this topic. [Pg.582]

The most common drug-induced noncardiogenic pulmonary edema is ... [Pg.582]


See other pages where Noncardiogenic pulmonary edema is mentioned: [Pg.3]    [Pg.3]    [Pg.154]    [Pg.31]    [Pg.48]    [Pg.96]    [Pg.97]    [Pg.541]    [Pg.547]    [Pg.578]    [Pg.165]    [Pg.1215]    [Pg.1233]    [Pg.1235]    [Pg.1368]    [Pg.1369]    [Pg.1385]    [Pg.1387]    [Pg.215]    [Pg.249]    [Pg.493]    [Pg.723]    [Pg.712]    [Pg.1613]    [Pg.1743]    [Pg.146]    [Pg.688]    [Pg.703]    [Pg.582]    [Pg.582]   
See also in sourсe #XX -- [ Pg.582 , Pg.582 ]

See also in sourсe #XX -- [ Pg.361 , Pg.362 ]




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