Rosen & Barkin's 5-Minute Emergency Medicine Consult (486 page)

• 969.1 Poisoning by phenothiazine-based tranquilizers
  
• 969.2 Poisoning by butyrophenone-based tranquilizers
  
• 969.3 Poisoning by other antipsychotics, neuroleptics, and major tranquilizers
  

BASICS

• Noncardiogenic pulmonary edema (NCPE) occurs secondary to accumulation of excess fluid and protein into the alveoli from factors other than increased pulmonary capillary pressure >18 mm Hg
  
• Permeability pulmonary edema:
  
  • Functional disruption of the capillary–alveolar membrane allows protein and fluid to move freely from the intravascular space into the alveolar space
    
• Pulmonary parenchymal changes are similar to CHF
  
• Concomitant CHF may occur in up to 20% of patients with acute respiratory distress syndrome (ARDS)
  
• Distinction between NCPE and CHF:
  
  • Pulmonary capillary pressure ≤18 mm Hg
    
  • Often apparent from the clinical circumstances
    
  • The concentration of protein in the alveolar fluid is identical to that of the intravascular space in patients with NCPE
    
  • Cephalad redistribution of blood flow, pulmonary effusions, and cardiomegaly are usually not present
    
• Adult respiratory distress syndrome:
  
  • Clinical presentation caused by permeability pulmonary edema
    
  • Associated with severe physiologic impairment
    
• Typically, onset of the edema is within 1–2 hr of the noxious insult.
  
• ∼250,000 cases occur each year in US
  

• ARDS is the #1 cause:
  
  • Caused by:
    
    • Sepsis
      
    • Pneumonia
      
    • Nonthoracic trauma
      
    • Inhaled toxins
      
    • Disseminated intravascular coagulation (DIC)
      
    • Radiation pneumonitis
      
• High-altitude pulmonary edema (HAPE) neurogenic pulmonary edema
  
• Narcotic overdose
  
• Pulmonary embolus
  
• Eclampsia
  
• Transfusion-related acute lung injury (TRALI)
  
• Re-expansion of a collapsed lung in patient with a pneumothorax
  
• Salicylate intoxication
  
• Inhaled cocaine use
  
• Near drowning
  
• HCTZ
  
• Uremia
  
• S/p cardiopulmonary bypass; especially if patient taking amiodarone
  

DIAGNOSIS

• Shortness of breath
  
• Fatigue
  
• Weakness
  
• Cough
  
• Malaise
  

• Scattered rhonchi and rales
  
• Hypoxia
  
• Dyspnea
  
• Tachypnea
  
• Accessory muscle use
  
• Tachycardia
  
• Pink, frothy sputum
  
• You will
  not
  see the stigmata of left- and right-sided heart failure
  
  • Lower-extremity swelling
    
  • Cardiomegaly
    

• History and physical is usually enough to distinguish between cardiogenic and NCPE
  
• The CXR is essential in confirming the diagnosis and in assessing severity.
  

General lab abnormalities are not specific to NCPE.

CXR:

• Initially can be normal
  
• Classic butterfly pattern of pulmonary edema
  
• Lack of cardiomegaly
  

Pulmonary artery catheter:

• Pulmonary capillary wedge pressures normal or near-normal in contrast to elevated pressures with cardiogenic pulmonary edema
  

• Cardiogenic pulmonary edema
  
• Diffuse alveolar hemorrhage
  
• Diffuse dissemination of cancer such as with lymphoma or leukemia
  
• Chronic obstructive pulmonary disease exacerbation
  
• Pulmonary embolus
  
• Restrictive lung disease
  
• Pneumonia
  

TREATMENT

• Patent airway
  
• Adequate oxygenation
  
• Cautions:
  
  • Patients will typically not respond to usual measures to treat CHF.
    

• Supplemental oxygen (nasal cannula or nonrebreather)
  
• IV catheter
  
• Continuous cardiac monitor
  
• Continuous pulse oximetry
  

• The treatment of NCPE is to treat underlying cause and give supportive care.
  
• Diuretics are
  not
  used.
  
• Noninvasive ventilatory support (BiPAP, CPAP) may be used if available and patient not in respiratory distress:
  
  • If oxygenation or ventilation not improving with noninvasive, intubation is required
    
• Endotracheal intubation is often necessary:
  
  • Improves oxygenation and ventilation
    
  • Decreases work of breathing
    
  • Use low tidal volumes of 6–8mL/kg to reduce barotrauma to the lungs
    
  • Initially place on 100% O
    _2:
    
    • Measure PO
      ₂
      and decrease FIO
      ₂
      accordingly.
      
  • Positive end-expiratory pressure (PEEP) of 5–10 cm H
    ₂
    O
    
• Steroids and cyclooxygenase inhibitors have not been proven effective.
  
• If at high altitude and concerned for HAPE, have the patient descend in elevation or put them in a hyperbaric chamber.
  
  • Nifedipine is adjunctive therapy to O
    ₂
    and descent.
    

FOLLOW-UP

All symptomatic patients should be admitted to ICU:

• Symptoms may worsen at any point for up to 3 days after noxious insult.
  

Asymptomatic patients (especially narcotic overdose, HAPE, or aspiration):

• Observe in ED for 6–12 hr and then discharge with close follow-up scheduled if no evidence of pulmonary edema is present and adequate oxygenation is demonstrated.
  

Patients, when discharged from the hospital, should seek medical follow-up within 48 hr.

• Utilizing diuretics in the acute setting may worsen patient condition.
  
• Failure to distinguish between cardiogenic and noncardiogenic etiologies is a pitfall as treatment is different.
  

• Fagenholz PJ, Gutman JA, Murray AF, et al. Treatment of high altitude pulmonary edema at 4240 m in Nepal.
  High Alt Med Biol
  . 2007;8(2):139–146.
  
• Putensen C, Theuerkauf N, Zinserling J, et al. Meta-analysis: Ventilation strategies and outcomes of the acute respiratory distress syndrome and acute lung injury.
  Ann Intern Med
  . 2009;151:566–576.
  
• Sigillito RJ, DeBlieux PM. Respiratory failure. In: Wolfson AB, Hendey GW, Ling LJ, et al., eds.
  Harwood-Nuss’ Clinical Practice of Emergency Medicine
  . 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005.
  
• Ware LB, Matthay MA. Clinical practice. Acute pulmonary edema.
  N Engl J Med.
  2005;353:2788–2796.
  

CODES

• 506.4 Chronic respiratory conditions due to fumes and vapors
  
• 508.1 Chronic and other pulmonary manifestations due to radiation
  
• 508.9 Respiratory conditions due to unspecified external agent