Acuterespiratory distress syndrome
Acuterespiratory distress syndrome: Excerpt from Handbook of Diseases
A form of pulmonary edema that causes acute respiratory failure, acute respiratory distress syndrome (ARDS, shock lung, stiff lung) results from increased permeability of the alveolocapillary membrane. Fluid accumulates in the lung interstitium, alveolar spaces, and small airways, causing the lung to stiffen. Effective ventilation is thus impaired, prohibiting adequate oxygenation of pulmonary capillary blood. Severe ARDS can cause intractable and fatal hypoxemia; however, patients who recover may have little or no permanent lung damage.
Causes
ARDS can result from any one of several respiratory and nonrespiratory causes:
aspiration of gastric contents
sepsis (primarily gram-negative), trauma (lung contusion, head injury, long bone fracture with fat emboli), or oxygen toxicity
viral, bacterial, or fungal pneumonia or microemboli (fat or air emboli or disseminated intravascular coagulation)
drug overdose (barbiturates, glutethimide, narcotics) or blood transfusion
smoke or chemical inhalation (nitrous oxide, chlorine, ammonia)
pancreatitis, hypertransfusion, cardiopulmonary bypass
near drowning.
Altered permeability of the alveolocapillary membranes causes fluid to accumulate in the interstitial space. If the pulmonary lymphatics can’t remove this fluid, interstitial edema develops. The fluid collects in the peribronchial and peribronchiolar spaces, producing bronchiolar narrowing.
Hypoxemia occurs as a result of fluid accumulation in alveoli and subsequent alveolar collapse, causing the shunting of blood through nonventilated lung regions. In addition, regional differences in compliance and airway narrowing cause regions of low ventilation and inadequate perfusion, which also contribute to hypoxemia.
Signs and symptoms
ARDS initially produces rapid, shallow breathing and dyspnea within hours to days of the initial injury (sometimes after the patient’s condition appears stable). Hypoxemia develops, causing an increased drive for ventilation. Because of the effort required to expand the stiff lung, intercostal and suprasternal retractions result. Fluid accumulation may produce crackles and rhonchi, and worsening hypoxemia causes restlessness, apprehension, mental sluggishness, motor dysfunction, and tachycardia (possibly with transient increased arterial blood pressure).
Severe ARDS causes overwhelming hypoxemia, which, if uncorrected, results in hypotension, decreasing urine output, respiratory and metabolic acidosis and, eventually, ventricular fibrillation or standstill.
Diagnosis
On room air, arterial blood gas (ABG) analysis initially shows a decreased partial pressure of arterial oxygen (Pao2) — less than 60 mm Hg — and a decreased partial pressure of arterial carbon dioxide (Paco2) — less than 35 mm Hg. The resulting pH usually reflects respiratory alkalosis. As ARDS becomes more severe, ABG levels indicate respiratory acidosis (a Paco2 greater than 45 mm Hg) and metabolic acidosis (a bicarbonate level less than 22 mEq/L) as well as a decreasing Pao2, despite oxygen therapy.
Pulmonary artery (PA) catheterization helps identify the cause of pulmonary edema: It allows evaluation of pulmonary artery wedge pressure (PAWP); collection of PA blood, which shows decreased oxygen saturation, indicating tissue hypoxia; measurement of PA pressure; and measurement of cardiac output via thermodilution.
Serial chest X-rays initially show bilateral infiltrates; in later stages, the X-rays show ground-glass appearance and, eventually (as hypoxemia becomes irreversible), “whiteouts” of both lung fields. This is seen more clearly by the use of computed tomography of the chest.
A differential diagnosis must rule out cardiogenic pulmonary edema, pulmonary vasculitis, and diffuse pulmonary hemorrhage. To establish the cause of ARDS, laboratory work should include a sputum Gram stain, culture and sensitivity tests, and blood cultures to detect infections; a toxicology screen for drug ingestion; and, when pancreatitis is a consideration, a serum amylase determination.
Treatment
When possible, treatment is designed to correct the underlying cause of ARDS and to prevent progression and potentially fatal complications of hypoxemia and respiratory acidosis. Supportive medical care involves administering humidified oxygen through a tight-fitting mask, which allows for the use of continuous positive airway pressure. Hypoxemia that doesn’t respond adequately to these measures requires ventilatory support with intubation, volume ventilation, positive end-expiratory pressure (PEEP), and increased ratio ventilation. Other supportive measures include fluid restriction, diuretics, and the correction of electrolyte and acid-base abnormalities.
UNDER STUDY: Experimental treatments are in progress using whole lung lavage with fluorocarbons. Initial therapies in select cases have been promising.
CLINICAL TIP: When ARDS requires mechanical ventilation, a sedative, narcotic, or neuromuscular blocker may be prescribed to minimize restlessness — and thereby oxygen consumption and carbon dioxide production — as well as to facilitate ventilation.
If ARDS results from fat emboli or chemical injury to the lungs, a short course of high-dose steroids may help if given early. Treatment to reverse severe metabolic acidosis with sodium bicarbonate may be necessary, and the use of fluids and a vasopressor may be required to maintain blood pressure. Treatable infections require an antimicrobial.
Special considerations
Frequently assess the patient’s respiratory status. Be alert for retractions on inspiration. Note rate, rhythm, and depth of respirations, and watch for dyspnea and the use of accessory muscles of respiration. On auscultation, listen for adventitious or diminished breath sounds. Check for clear, frothy sputum that may indicate pulmonary edema.
If the patient is hypoxemic, observe and document his neurologic status, including level of consciousness and mental sluggishness.
Maintain a patent airway by suctioning, using sterile, nontraumatic technique. Ensure adequate humidification to help liquefy tenacious secretions.
Closely monitor heart rate and blood pressure. Watch for arrhythmias that may result from hypoxemia, acid-base disturbances, or electrolyte imbalance.
With PA catheterization, know the desired PAWP level. Check readings often, and watch for decreasing mixed venous oxygen saturation.
Monitor serum electrolyte levels, and correct any imbalances. Measure intake and output, and weigh the patient daily.
Check ventilator settings frequently, and empty condensate from tubing promptly to ensure maximum oxygen delivery. Monitor ABG levels; check for metabolic and respiratory acidosis and Pao2 changes.
If the patient has severe hypoxemia, he may need controlled mechanical ventilation with PEEP and increased ratio ventilation. Give sedatives, as needed, to reduce restlessness and paralytics to ensure compliance with ventilator settings.
Because PEEP may decrease cardiac output, check for hypotension, tachycardia, and decreased urine output. Suction only as needed so that PEEP is maintained, or use an in-line suctioning apparatus.
Reposition the patient often, and note any increase in secretions, temperature, or hypotension, which may indicate a deteriorating condition.
Accurately record caloric intake. Give tube feedings and parenteral nutrition, if required.
Perform passive range-of-motion exercises, or help the patient perform active exercises, if possible. Provide meticulous skin care. Allow periods of uninterrupted sleep.
Provide the patient with emotional support.
CLINICAL TIP: If the patient has suffered an injury that may adversely affect the lungs, watch for respiratory changes, especially during the 2- to 3-day period after the injury, when he may appear to be improving.
Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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