Acute Respiratory Distress Syndrome (ARDS) is a severe form of acute lung injury characterized by sudden and progressive pulmonary edema, increasing bilateral infiltrates, hypoxemia unresponsive to oxygen supplementation, and the absence of an elevated left atrial pressure.
The occurrence of Acute Respiratory Distress Syndrome (ARDS) depends on several factors. Infectious diseases, which can result in ARDS, vary widely by geographic region. For example, malaria is the most frequent cause of ARDS in some parts of the world but does not exist in most of North America.
People at risk for Acute Respiratory Distress Syndrome (ARDS) are those with or at risk for the underlying diseases associated with the syndrome. The most common of these is sepsis, a severe infection that spreads throughout the body via the bloodstream. Victims of trauma and those who aspirate stomach contents into the lung are also at high risk for ARDS. A less common cause of direct injury is the inhalation of high concentrations of toxic gases, which can occur with severe smoke inhalation and in industrial accidents.
Direct & Indirect Injury
The cause of the acute lung injury can be either direct, with the injurious agent reaching the lung through the airways or by trauma to the chest, or indirect, with the injurious agent arriving at the lungs through the bloodstream. The affected areas in Acute Respiratory Distress Syndrome (ARDS) are the alveoli (air sacs), where oxygen enters the blood and carbon dioxide leaves it (gas exchange). The thin wall between the blood and air is made up of the blood capillary and the alveolar wall (alveolar-capillary membrane). The alveolar-capillary membrane is extremely delicate, less than 0.5 micrometers in width at its thinnest segment where gas exchange takes place. (For comparison, an average human hair is about 100 micrometers in width.) In ARDS, both the capillary and alveolar cells are injured, whether the initiating process is direct or indirect. Injury to this membrane allows fluid to spill into the lung, thus hindering or preventing gas exchange.
The aspiration of stomach contents into the lung or the inhalation of toxic gases are examples of direct injury causing Acute Respiratory Distress Syndrome (ARDS). Indirect lung injury, however, is a more common cause of ARDS and is usually associated with severe infections or severe trauma. Regardless of the initiating event, an inflammatory chain reaction is set off. Molecules released by infected or injured cells signal white cells from the blood to enter the affected area. The incoming white blood cells combine with resident cells to produce more chemicals (called cytokines and chemokines), which induce a variety of actions involved in the in inflammatory process. Inflammation is usually beneficial, in that it promotes killing and containment of infectious agents and clearing of the debris created by the infection or injury. Occasionally, however, exuberant inflammation can spread beyond the originally damaged organ via the bloodstream to injure other organs and tissues at distant sites. This systemic process is called sepsis when the initiating insult is an infection, but a similar, if not identical, process can occur when the original insult is traumatic injury.
Sepsis or sepsis-like syndromes can cause injury and failure of many organs. When they affect the lungs, they most commonly cause Acute Respiratory Distress Syndrome (ARDS). In patients with sepsis or sepsis-like syndromes, the lungs are often the first organ to be injured. They are often the most severely injured organ, and they frequently represent the only organ failure that is recognized clinically. This association may be because the lungs are the only organ to receive all the blood of the body. Although all the blood flows through the chambers of the heart, only a fraction of the blood supplies the heart tissues themselves. Thus the lungs receive the full brunt of the injurious cytokines and other molecules. The leakage of fluid through the alveolar-capillary membrane and flooding of alveoli interferes with oxygenation and causes shortness of breath and respiratory distress. The excess alveolar fluid mixes with the normal lung surfactant and can destabilize the alveoli, allowing them to collapse and thus not be available for breathing.
The microbes causing sepsis leading to Acute Respiratory Distress Syndrome (ARDS) vary widely in type and geographic distribution. In developed countries, bacterial infections are the most common, often with organisms partially or highly resistant to antibiotics that are common in hospital environments. Viruses that cause pneumonias can cause ARDS. In fact, most of the deaths in the severe acute respiratory syndrome (SARS) and H1N1 influenza epidemics were due to ARDS.
• Rapid onset of severe dyspnea, usually 12 to 48 hours after an initiating event
• Intercostal retractions and crackles may be present
• Arterial hypoxemia not responsive to oxygen supplementation
• Lung injury then progresses to fibrosing alveolitis with persistent, severe hypoxemia
• Increased alveolar dead space and decreased pulmonary compliance
Prevention of Acute Respiratory Distress Syndrome (ARDS) can be accomplished by preventing the infections and injuries that cause it. Even if trauma or infection cannot be prevented, early aggressive treatment may avert ARDS. Promptly hydrating persons in shock or administering antibiotics to persons with pneumonia may correct the underlying process enough to prevent ARDS from developing.
• Identify and treat the underlying condition; provide aggressive, supportive care (intubation and mechanical ventilation; circulatory support, adequate fluid volume, and nutritional support).
• Use supplemental oxygen as the patient begins the initial spiral of hypoxemia.
• Monitor ABG values, pulse oximetry, and pulmonary function testing.
• As disease progresses, use positive end-expiratory pressure (PEEP).
• Treat hypovolemia carefully; avoid overload (inotropic or vasopressor agents may be required).
• There is no specific pharmacologic treatment for ARDS except supportive care. Numerous pharmacologic treatments are under investigation to stop the cascade of events leading to ARDS (eg, surfactant replacement therapy, pulmonary antihypertensive agents, and antisepsis agents).
• Provide nutritional support (35 to 45 kcal/kg daily).
• Closely monitor the patient; frequently assess effectiveness of treatment (eg, oxygen administration, nebulizer therapy, chest physiotherapy, endotracheal intubation or tracheostomy, mechanical ventilation, suctioning, bronchoscopy).
• Consider other needs of the patient (eg, positioning, anxiety, rest).
• Identify any problems with ventilation that may cause an anxiety reaction: tube blockage, other acute respiratory problems (eg, pneumothorax, pain), a sudden decrease in the oxygen level, the level of dyspnea; or ventilator malfunction.
• Sedation may be required to decrease the patient’s oxygen consumption, allow the ventilator to provide full support of ventilation, and decrease the patient’s anxiety.
• If sedatives do not work, paralytic agents (used for the shortest time possible) may be administered (with adequate sedation and pain management); reassure the patient that paralysis is a result of the medication and is temporary; describe the purpose and effects of the paralytic agents to the patient’s family.
• Closely monitor patients on paralytic agents: ensure that the patient is not disconnected from ventilator and that all ventilator and patient alarms are on at all times, provide eye care, minimize complications related to neuromuscular blockade, anticipate the patient’s needs regarding pain and comfort.