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Neurogenic Pulmonary Edema

History. First reported in 1908 by Dr.Shanahan, 11 patients who had epileptic seizures.World War I and Vietnam WarA relatively rare form of pulmonary edema, develops within a few hours of well-defined neurologic insult. Clinical presentations. NPE characteristically presents within minutes to hour

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Neurogenic Pulmonary Edema

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    1. Neurogenic Pulmonary Edema ???:Ri ???

    2. History First reported in 1908 by Dr.Shanahan, 11 patients who had epileptic seizures. World War I and Vietnam War A relatively rare form of pulmonary edema, develops within a few hours of well-defined neurologic insult

    3. Clinical presentations NPE characteristically presents within minutes to hours of a severe CNS insult Sudden onset of dyspnea is the most common symptom; mild hemoptysis may occur as well Crackles, respiratory distress, normal jugular venous pressure and absence of cardiac gallop

    4. Causes Major causes: Epileptic seizure Cerebral hemorrhage Head injury

    5. Causes Minor causes: Multiple sclerosis with medullary involvement Non-hemorrhagic strokes Bulbar poliomyelitis Air embolism Brain tumors, Electroconvulsive therapy

    6. Frequency In USA, 1/3 of patients with status epilepticus have evidence of NPE 71% of fatal cases of SAH are complicated by NPE Incidence of NPE is significantly lower in children than in aldults

    7. Pathophysiology The exact cause of NPE is unknown Key etiologic factor:IICP Animal studies suggest the hypothalamus, medulla(A1,A5), nuclei of solitary tract, area postrema, IICP, activation of sympathetic system have potential roles

    8. Mechanism Changes in capillary hydrostatic pressure LA pressure? because of sympathetic tone?and venous return LV performance may deteriorate secondary to the direct effect of catecholamines Pulmonary vasoconstriction ? capillary hydrostatic pressure?

    9. Mechanism Changes in pulmonary capillary permeability Some direct nervous system control over the pulmonary capillary permeability Epinephrine, norepinephrine, secondary mediators may directly increase pulmonary vascular permeability

    10. Workup Lab studies:not helpful Imaging studies:CXR Procedures: Swan-Ganz catheter:systemic blood pressure, cardiac output and pumonary capillary wedge pressure are normal in the time NPE is diagnosed clinically.

    11. Differentials Pneumonia, Aspiration Pneumonia, Bacterial Pulmonary Edema, Cardiogenic

    12. Treatment Supportive and conservative treatment Focus treatment on the underlying disease NPE usually resolves within 48~72 hrs Oxygen is required in most patients

    13. Treatment Mechanical ventilation may be necessary, either face mask or ET GCS score = 8 should be intubated PEEP with hypocarbia may be required to ?ICP Tidal volumes set 5~8 ml/kg to avoid excessively high inflation pressure

    14. Treatment The peak inspiratory pressure should be kept below 30 cmH2O ICP monitor is probably appropriate if PEEP exceeds 10 cmH2O Sufficient cardiac output (cardiac index > 2.2 L/min/m2) and hemoglobin (>10 g/L) are required

    15. Treatment Pharmacological agent are not used routinely in treatment of NPE Alpha blocker can prevent NPE in experimental models, but no human have established the safety and efficacy of these agent

    16. Prognosis NPE usually is well tolerated by patient, and usually resolves within 48~72 hrs Prognosis is determined by the couse of underlying neurological problems Anesthesiology clinics of North America vol 19. number 2, June 2001 America Rev Respiratory Disease 1978 Oct ; 118(4): 738-6 e-Medicine Specialties, pulmonary edema, neurogenic

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