Neurogenic pulmonary edema

Cardiac arrhythmias are common in the first few days but seldom need treatment (Andreoli et al. 1987 Brouwers et al. 1989), although electrocardiographic monitoring is advisable. Neurogenic pulmonary edema is rare but can occur very early, causing... 

The authors assumed that she had developed neurogenic pulmonary edema, probably worsened by the co-existing myocardial disease. 

Adult respiratory distress syndrome Pulmonary hypertension-associated edema (cardiogenic) Congestive heart failure Mitral stenosis Hypoalbuminemia Veno-occlusive disease Lymphatic dysfunction Unknown mechanisms High-altitude pulmonary edema Neurogenic pulmonary edema Narcotic-induced pulmonary edema... 

Neurogenic pulmonary edema. Neurogenic pulmonary edema develops rapidly (within minutes) after a severe injury to the brain or spinal cord such... 

Narcotic-induced pulmonary edema. Pulmonary edema is a common sequel to narcotic overdose (morphine, heroin, methadone, and propoxyphene) and is associated with a significant mortality rate. The exact mechanism has not been delineated, but two reasonable hypotheses have been suggested. First, narcotic-induced pulmonary edema may be a form of neurogenic pulmonary edema because both syndromes have complications of cerebral edema and hypothalamic dysfunction (Jaffe, 1970). Second, narcotics are known to release histamine, which may alter alveolar capillary membrane permeability (Brashear et al, 1974). Early treatment with narcotic antagonists produces immediate reversal of respiratory depression and miosis, while the pulmonary edema resolves more slowly. 

In reaction to a report of pulmonary edema and hypoglycemia (SEDA-24, 488) it has been noted that in many cases, one or more seizures precede pulmonary edema (acute respiratory distress syndrome), suggesting a neurogenic mechanism (65). 

There is some evidence that the pulmonary edema and vascular coUapse may be of neurogenic origin also. The symptoms in animals systemicaUy poisoned by the y-isomer alone are essentially similar to those caused by mixtures, although the onset may be earlier. Workers acutely exposed to high air concentrations of lindane and its decomposition products show headache, nausea, and irritation of eyes, nose, and throat. 

In conclusion, the clinical and experimental observations on pulmonary edema suggest that its pathogenesis is rather complex and may involve humoral, hemodynamic, and neurogenic factors (see Table 9-4). How these factors interact remains to be established. 

The biological actions of capsaicin are primarily attributable to release of the neuropeptide substance P, calcitonin gene-related peptide (CGRP), and neurokinin A from sensory neurons. These transmitters from primary sensory neurons communicate witir other cell types. They produce alterations in the airway mucosa and neurogenic inflammation of the respiratory epithelium, airway blood vessels, glands, and smooth muscle. Alterations in multiple effector organs lead to bronchoconstriction, increased vascular permeability, edema of the tracheobronchial mucosa, elevated mucosal secretion, and neutrophil chemotaxis (Tominack and Spyker, 1987). Capsaicin-induced effects of bronchoconstriction, vasodilation, and plasma protein extravasation are mediated by substance P. In addition, substance P can cause bronchoconstriction through stimulation of c-fibers in pulmonary and bronchial circulation. 

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