review article neurogenic pulmonary edema n.
Download
Skip this Video
Loading SlideShow in 5 Seconds..
Review Article Neurogenic pulmonary edema PowerPoint Presentation
Download Presentation
Review Article Neurogenic pulmonary edema

Loading in 2 Seconds...

play fullscreen
1 / 15

Review Article Neurogenic pulmonary edema - PowerPoint PPT Presentation


  • 802 Views
  • Uploaded on

Review Article Neurogenic pulmonary edema. Acta Anaesthesiol Scand 2007; 51: 447-445 R4 이동현. Neurogenic pulmonary edema(NPE) Defined as acute pulmonary edema occurring shortly after a central neurologic insult

loader
I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
capcha
Download Presentation

PowerPoint Slideshow about 'Review Article Neurogenic pulmonary edema' - dacey


Download Now An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
review article neurogenic pulmonary edema

Review ArticleNeurogenic pulmonary edema

ActaAnaesthesiol Scand 2007; 51: 447-445

R4 이동현

slide2

Neurogenic pulmonary edema(NPE)

      • Defined as acute pulmonary edema occurring shortly after a central neurologic insult
      • Often present without pre-existing cardiovascular or pulmonary pathology that could explain the edema
      • But, dose not exclude a coexisting effect of neurologic insult on myocardial function
        • Cause of confusion in reported incidence of NPE
e pidemiology
Epidemiology
  • Cases reported in
    • Subarachnoid hemorrhage(SAH)
    • Traumatic brain injuries
    • Cervical medulla injuries
    • Cerebral thrombosis
    • Cerebral gas embolism
    • Intracerebral hemorrhage
    • Intracranial tumors
    • Epilepsy
    • Postoperative intracranial surgery
    • Enterovirus encephalitis(hand, foot, mouse disease)
    • Meningitis
    • Multiple sclesosis
  • Brambrink and Dick
    • Cerebral hemorrhage(71%), seizure activity(2%), cerebral trauma(1%)
epidemiology
Epidemiology
  • SAH
    • Main cause of NPE
    • Pulmonary edema after SAH : 23%
    • Friedman et al : NPE in 2% of 305 SAH pts
    • Between D1 and D7 after SAH
    • Most important risk factors
      • Clinical and radiological severity of SAH
      • Vertebral artery origin
    • Positive correlation
      • Age
      • Delay to surgery
      • Intentional hypervolemia
    • Early detection and treatment of NPE minimize mortality associated with SAH.
epidemiology1
Epidemiology
  • Head injury
    • Up to 20% of severe head injury
    • In autopsy database
      • Incidence of NPE : 32%
      • 50% in victims dying within 96 hrs.
  • Status epilepticus
    • 1/3 of status epilepticus patients
    • Major cause of NPE in children
    • Occurs mainly during post-ictal period
    • Can be recurrent
p athophysiology
Pathophysiology
  • Hemodynamic mechanism
      • Adrenergic response to cerebral insult
      • Intense pulmonary vasoconstriction
      • Increase in pulmonary hydrostatic pressure
      • Increase in permeability of pulmonary capillaries
  • Inflammatory mechanism
      • Also induce an increase in permeability of pulmonary capillaries
  • NPE trigger zones
      • Hypothalamus
      • Medulla oblongata
pathophysiology
Pathophysiology
  • Hemodynamic mechanism
    • Sudden increase in ICP induce
      • α-adrenergic response
      • Increase in pulmonary and systemic vasoconstriction
      • Subsequent fluid shift into pulmonary alveoli and and interstitial space
    • Pulmonary vasoconstriction increase cardiac workload
      • Severe myocardial depression
      • Even stunned myocardium
      • Cf) patients with hypertensive cardiomyopathy
        • Less sensitive to catecholamine
        • Some protection against this acute effect
pathophysiology1
Pathophysiology
  • Norepinephrine and neuropeptide Y
    • Located in sympathetic nerve ending
    • Play important role in NPE
      • Vasoconstrictive action
      • Increasing pulmonary vascular permeability
  • Endothelin-1
    • One of the most potent vasoconstrictor
    • Time dependent increase in rats with NPE
    • Intrathecal injection in rats 22-fold increase in pulmonary vascular permeability
      • Activation of medullaryendothelin receptors
      • Stimulate norepinephrine release
  • Nitric oxide
    • Endothelial-mediated vasodilatation
    • In rats with cerebral trauma, injection of nitric oxide synthase inhibitor increase mortality
pathophysiology2
Pathophysiology
  • Inflammatory mechanism
    • Cerebral insult cause local inflammatory reaction
    • Brain cytokines and chemokines
      • Produced by astrocytes and microglial cell
      • TNF-α, IL-1β, IL-6
      • Diffuse into systemic circulation after BBB disruption
      • Cause peripheral organ inflammation
      • Cause expression of substance P, neurokinin A
        • Bronchoconstriction
        • Edema of bronchial mucosa
        • Increase of pulmonary capillary permeability
        • Increase leukocyte activation
d iagnosis
Diagnosis
  • Clinical presentation
    • No specific clinical presentation
      • Signs of acute pulmonary edema
      • Usually lack of signs of LV failure
      • Tachypnea, tachycardia, basal pulmonary crackles, respiratory failure and lack of cardiac gallop
    • Unilateral NPE seems to be possible
  • Complementary investigations
    • CXR : bilateral pulmonary infiltrates
    • Echocardiogram, TE Doppler, CVP : normal
    • ECG : unchanged
    • No specific biologic marker
      • Troponin Ic, brain natriuretic peptide(BNP) elevation
      • Blood C-reactive protein, IL-6 level can be increased
d ifferential diagnosis
Differential diagnosis
  • Aspiration pneumonia and ventilator-associated pneumonia
    • Complications associated with impairment of consciousness
    • Blood level of pro-calcitonin : evidence of invasive bacterial infection
  • Ventilation-induced lung injury
    • Decreased tolerance to alveolar stretching
    • Over-inflation injury
    • Increased susceptibility to reperfusion injury
t reatment management
Treatment/management
    • May resolve in 48-72 h with appropriate Mx
    • Prognosis is dependent on neurologic injury.
  • Acute neurologic insult
      • Control of triggering CNS insult
        • Decrease ICP, evacuate hematoma, treat convulsion
      • Classical pulmonary edema therapy
    • Ventilation
      • Patients with serious NPE : must be intubated early, sedated and ventilated with PEEP
      • PEEP < 15 cmH2O : not impede cerebral perfusion pr.
      • Permissive hypercapnia and prone position
      • Direct tracheal insufflation
      • Nitric oxide inhalation
treatment management
Treatment/management
  • Hemodynamic function
    • Reduce preload and afterload
    • Increase myocardial contractility
    • Hypotensive agent without cerebral vasodilatory effects : urapidil, clonidine
    • Dobutamine
    • Epinephrine and norepinephrine
    • Diuretics
  • Neurologic care
    • Decreasing high ICP
    • Optimizing cerebral perfusion pressure
    • Mannitol or hypertonic saline
treatment management1
Treatment/management
  • Brain death
    • Permissive hypercapnia, nitric oxide inhalation
      • Optimize V/Q ratio
      • Decrease pulmonary vascular pressure
    • Vasoactive drugs
      • Maintain peripheral organ hypoperfusion
      • Prevent multiorgan failure
c onclusion
Conclusion
  • NPE should be considered when patients with central neurologic injury suddenly become dyspneic or present with decreased PaO2/FiO2 ratio.
  • Associated mortality is high.
  • Recovery is usually rapid with appropriate management.
  • Early treatment of underlying neurologic cause is cornerstone of NPE Mx.
  • Most patients should be intubated, sedated, ventilated with PEEP and maintained with normal hemodynamic stability.
  • NPE in brain death is major cause of graft dysfunction and even of transplantation failure.