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3)    ADULT RESPIRATORY DISTRESS SYNDROME (LOW PRESSURE PULMONARY EDEMA)


ARDS is the name given to the clinical manifestation of a number of indirect lung injury states characterized by dyspnea, severe hypoxemia, and decreased lung compliance with radiographic evidence of diffuse bilateral pulmonary infiltrates. Alveolar consolidation with fluid, protein, and inflammatory cells in the presence of a normal capillary or wedge pressure is also a characteristic finding, i.e., low pressure pulmonary edema. The altered permeability results in a rapid movement of fluid from plasma to interstitial space with even a normal capillary (wedge) pressure. The causes and differential diagnosis of ARDS are presented.


Adult Respiratory Distress Syndrome

Causes

Differential

  • Tissue inflammation
  • Infection-sepsis
  • Non-lung trauma
  • High pressure edema
  • Inhalation injury
  • Pneumonia
  • Focal atelectasis

 

Pathophysiology and Diagnosis

The lung damage is the result of a systemic process initiated by burn tissue, infection or inflammation rather than a direct lung injury. However, the term "ARDS" is commonly but inappropriately used to describe direct lung injury processes, such as an inhalation injury. There are probably several distinct ARDS state, each with a different cause. Although the pathophysiology may be extremely complex and the etiologic agents varied, the presenting signs and symptoms for the ARDS states are nearly identical. The hypoxemia produced is characteristically refractory to an increase in fractional inspired oxygen, indicating increased shunting. In addition, the degree of shunt is not directly correlated with the degree of increased water content, as is the case with cardiogenic edema.

Diagnosis

  • Progressive hypoxemia, shunt
  • Decreased lung compliance
  • Bilateral diffuse lung infiltrate

 

Typical histologic findings with ARDS which includes alveolar inflammation, thickened septal from protein leak (pink), congestion and decreased alveolar volume


There is definitely a significant ventilatory impairment or airways component to the disease process not related to water. There is a decrease in dynamic compliance and functional residual capacity resulting in increased ventilation to perfusion mismatch, probably due to mediator-induced broncho constriction.

ARDS Treatment Summary

  • Initial Onset

Administer oxygen: maintain oxygen saturation more than 90%
Determine and delete source of lung response
Maintain perfusion but avoid volume overload

  • Phase 2 (2-7 days post-onset)

Administer oxygen; maintain oxygen saturation more than 90%
May need positive airway pressure (PEEP, CPAP)
Avoid volume overload (consider pulmonary artery catheter)

  • Phase 3 (10 days plus)

Requires positive pressure ventilation; add PEEP
Needs pulmonary artery catheter
Adjust PEEP, tidal volume to improve static compliance and arterial oxygen tension but not impair oxygen delivery
Maintain wedge pressure below 15mmHg, preferably 10 to 12 mmHg.
Maintain blood volume and hemoglobin

 

Typical patterns of ARDS with diffuse internal infiltrates

Positive end-expiratory pressure
Advantages

    - Increases functional residual capacity
    - Recruits additional lung units improving compliance
    - Reduces pulmonary shunt fraction
    - Allows for a decrease in FIO2
    - Can decrease preload in congestive heart failure

Disadvantages

    - Increase mean airway pressure leading to reduced venous return
    - Can increase VD/VT by impairing perfusion to hyper expanded 
       lung
    - Can increase pulmonary vascular resistance and right-heart 
      dsyfunction
    - Altered renal blood flo with increase in ADH release
    - Barotrauma caused by increased pressure

Primary Indications

    - Treat hypoxemia when patient already receiving an FIO2 of less 
    than or equal to 0.5 and with bilateral diffuse pulmonary infiltrates
    - Treat a shunt of less than or equal to 20% in patient with diffuse 
    disease
    - To maintain FRC after airway injury such as smoke inhalation

VD/VT, physiologic deadspace ratio; ADH, antidiuretic hormone; FRC, functional residual capacity.

 


Common Pitfalls

Underestimation of Risks for Pneumonia:

Once resuscitation is completed and the patient has become stabilized and is beginning to be more active, there is a tendency to be lulled into complacency regarding pulmonary support. The patient remains at high risk for pneumonia for several weeks.

Underestimation of Increased Ventilatory Requirements in

Perioperative Period:

Maintenance of a "normal" minute ventilation in the perioperative period is not adequate in a patient generating up to twice the normal amount of carbon dioxide. Hypercapnia in the intraoperative or early postoperative period with its resultant massive catecholamine release can almost always be avoided by maintaining preoperative ventilatory needs in the intra- and postoperative period.

Underestimation of the Workload of Breathing During the

Hypermetabolic State:

A two- to threefold increase in minute ventilation is a substantial work load. Ventilatory assist may be needed and should be initiated before respiratory deterioration.

Underutilization of the Tracheostomy:

Although a tracheostomy is usually not indicated in the first several days and is contraindicated through burn tissue, its use for chronic respiratory support is very advantageous. A tracheostomy through a non-burn or excised and grafted skin can improve pulmonary toilet, improve rehabilitation efforts by physical therapy, and will improve comfort.

 

THIS CONCLUDES THE END OF PULMONARY PROBLEMS

 


 

 


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