Pulmonary edema: Difference between revisions

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***Incr afterload > incr pulm edema
***Incr afterload > incr pulm edema
*Pts often intravascularly depleted; avoid diuretics!
*Pts often intravascularly depleted; avoid diuretics!
==Causes==
*[[Congestive heart failure|Cardiogenic]]
*Non-cardiogenic
**Hypertensive crisis.
*[[Negative pressure pulmonary edema]] (Upper airway obstruction)
*Neurogenic causes
**[[Seizures]]
**[[Blunt head trauma]]
**[[Strangulation]]
**[[Electrocution]]
*Other
**[[ARDS]]
**Inhalation of hot or toxic gases
**[[Pulmonary contusion]]
**Aspiration
**Reexpansion edema (post large volume thoracocentesis, resolution of pneumothorax, post decortication, removal of endobronchial obstruction, effectively a form of negative pressure pulmonary oedema.
Reperfusion injury, i.e. postpulmonary thromboendartectomy or lung transplantation
Immersion pulmonary edema[7][8]
Multiple blood transfusions
Severe infection or inflammation which may be local or systemic. This is the classical form of ALI-ARDS.
There are also a range of causes of pulmonary edema which are less well characterised and arguably represent specific instances of the broader classifications above.
Arteriovenous malformation
Hantavirus pulmonary syndrome
High altitude pulmonary edema (HAPE), probably a manifestation of neurogenic pulmonary edema[9][10]
Envenomation, such as with the venom of Atrax robustus[11]
Flash pulmonary edema
Swimming induced pulmonary edema


==Diagnosis==
==Diagnosis==
*Crackles
*Crackles
*Respiratory distress
*Respiratory distress
==Specific types==
*[[Negative pressure pulmonary edema]]
**Forced inspiration against obstructed airway causes large negative intrathoracic pressure, leading to pulmonary edema<ref>Bhaskar B, Fraser JF. Negative pressure pulmonary edema revisited: Pathophysiology and review of management. Saudi J Anaesth. 2011 Jul-Sep; 5(3): 308–313.</ref>
**Mostly due to postoperative laryngospasm, sudden drops in PEEP (high PEEP to manual BVM), trauma such as hanging, strangulation, foreign bodies, etc.
**Diagnosis
***Hypoxemia (may be sudden and large - beware "fake" or "not real" SpO2), stridor, retractions, accessory muscle use, crackles/wheezes
***CXR shows diffuse interstitial and alveolar infiltrates
***CT shows preferential central/nondependent distribution of edema (as opposed to other forms of pulmonary edema)
**Treatment
***Relieve airway obstruction
***Vent with generous PEEP and diuretics


==Differential Diagnosis==
==Differential Diagnosis==

Revision as of 20:42, 24 March 2015

Background

  • Cardiogenic vs Non-Cardiogenic (ARDS/Altitude/Neurogenic)
  • Mechanism of Cardiogenic
    • Failing heart > pulm edema > stress response > incr afterload
      • Incr afterload > incr pulm edema
  • Pts often intravascularly depleted; avoid diuretics!

Causes

Reperfusion injury, i.e. postpulmonary thromboendartectomy or lung transplantation Immersion pulmonary edema[7][8] Multiple blood transfusions Severe infection or inflammation which may be local or systemic. This is the classical form of ALI-ARDS. There are also a range of causes of pulmonary edema which are less well characterised and arguably represent specific instances of the broader classifications above.

Arteriovenous malformation Hantavirus pulmonary syndrome High altitude pulmonary edema (HAPE), probably a manifestation of neurogenic pulmonary edema[9][10] Envenomation, such as with the venom of Atrax robustus[11] Flash pulmonary edema Swimming induced pulmonary edema


Diagnosis

  • Crackles
  • Respiratory distress

Differential Diagnosis

Acute dyspnea

Emergent

Non-Emergent

Treatment

  1. CPAP/BiPAP with PEEP 6-8; titrate up to PEEP of 10-12
  2. Nitroglycerin
    1. Dosing Options
      1. Sublingual 0.4 mg q5min
      2. Nitropaste (better bioavailability than oral Nitroglycerin)
      3. Intravenous: 0.1mcg/kg/min - 5mcg/kg/min

Generally start IV Nitroglycerin 50mcg/min and titrate rapidly (150mcg/min or higher)to symptom relief

  • If NTG fails to reduce BP consider nitroprusside (reduces both preload and afterload) or ACE-inhibitiors (preload reducer)
  • After pt improves titrate down NTG as enaliprilat (0.625 - 1.25mg IV) or captopril are started
  • Morphine is no longer recommended do to increased morbidity

See Also

References

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