A 52-year-old man presented for exploratory laparotomy. He complained of fever, severe abdominal pain, and vomiting for 3 days. Past medical history was significant for Crohn’s disease, hypertension, and multiple bowel resections, the last of which was done 1 week ago. He weighed 176 pounds (80 kg) and stood 5 feet 9 inches (175 cm) tall. Clinically significant vital signs included heart rate, 123 beats per minute, blood pressure, 90/65 mm Hg, and respiratory rate, 29 breaths per minute. Laboratory findings included hematocrit of 46% and white blood cell count of 23,000/mm 3 . Sodium and creatinine were mildly elevated. Intraoperatively, the patient was hemodynamically unstable. Postoperatively, he remained intubated and ventilated in the intensive care unit. Overnight he became more difficult to ventilate with elevated peak airway pressures and increasing fraction of inspired oxygen (FiO 2 ) requirements.
Define acute respiratory distress syndrome.
Acute respiratory distress syndrome (ARDS) is characterized by inflammation of the lung parenchyma leading to impaired gas exchange, hypoxemia, and nonhydrostatic pulmonary edema. The incidence of ARDS in the intensive care unit (ICU) ranges from 4%–9%, with a mortality rate of approximating 40%–45%. ARDS was first described in 1967 by Ashbaugh et al. in 12 patients, who had cyanosis refractory to oxygen therapy, decreased lung compliance, and diffuse infiltrates on chest radiograph. By 1994, a new definition was established by the American-European Consensus Conference Committee (AECC) as follows:
Bilateral infiltrates on chest radiograph
Pulmonary capillary wedge pressure (PCWP) ≤18 mm Hg or absence of clinical evidence of left atrial hypertension
Acute lung injury considered to be present if PaO 2 /FiO 2 ratio ≤300
Acute respiratory distress considered to be present if PaO 2 /FiO 2 ratio ≤200
There has been some criticism regarding the AECC oxygenation criteria because they do not account for variations in the PaO 2 /FiO 2 ratio in response to varying levels of positive end expiratory pressure (PEEP). With the current definition, a patient with a PaO 2 /FiO 2 ratio <200 on a PEEP of 12 cm H 2 O is considered equivalent to a patient with a similar PaO 2 /FiO 2 ratio on a PEEP of 5 cm H 2 O. Investigators have advocated that a standardized PEEP/FiO 2 assessment is necessary to classify ARDS severity accurately. The PaO 2 /FiO 2 ratio has failed to predict ARDS outcomes consistently in epidemiologic studies. This failing is likely due to ignoring PEEP in their evaluation.
In a study from Spain by et al. (2012), one third of patients who died with a clinical diagnosis of ARDS did not have histologic evidence of diffuse alveolar damage on autopsy. This finding questions the current clinical criteria used for diagnosis of ARDS. With regard to the AECC chest radiograph definition of ARDS, there is some controversy regarding the lack of acknowledgment of the severity or distribution of infiltrates. Furthermore, the distribution of infiltrates seen on chest radiographs and computed tomography (CT) scans often disagree, questioning the use of chest radiograph rather than CT scan findings to diagnose ARDS. Finally, the criteria requiring PCWP <18 mm Hg is not easy to assess noninvasively and is flawed by interobserver measurement variability. Some authors have argued for the use of echocardiography; however, it is also dependent on interpretation and availability.
What are the common causes of acute respiratory distress syndrome?
ARDS is most often part of a systemic inflammatory process. Sepsis is associated with the highest risk of progression to ARDS. Various precipitating events can either directly or indirectly result in lung injury and eventually ARDS ( Table 86-1 ).
|Direct Lung Injury||Indirect Lung Injury|
Multiple blood transfusions
|Less common||Inhalational injury |
|Acute pancreatitis |
The inciting cause can be used to predict progression and prognosis of ARDS. For example, ARDS associated with trauma has a better prognosis compared with non–trauma-related injury. In terms of disease progression, pulmonary infections are associated with a higher risk of ARDS progression compared with nonpulmonary infections.
Explain the pathophysiology of acute respiratory distress syndrome.
ARDS develops when inflammatory cytokines injure the epithelium and endothelium of the lungs. In early phases, alveolar macrophages release proinflammatory cytokines such as tumor necrosis factors (TNF) and interleukin (IL)-1, IL-6, and IL-8. These cytokines attract neutrophils to the lungs, where they release a wide variety of substances (e.g., reactive oxygen species, proteases). These substrates injure alveolar epithelium and endothelium, leading to increased capillary permeability, which is the hallmark of ARDS. This results in leakage of protein-rich edema into the interstitium and air spaces. Protein-rich edema fluid in the alveolus inactivates surfactant and creates diffuse alveolar damage. ARDS may resolve completely in some patients, after the acute phase. In others, the disease progresses to persistent reduced lung compliance with increased alveolar dead space and interstitial fibrosis. For most patients who survive, pulmonary function returns to normal within 6–12 months. Most deaths are due to sepsis or multiorgan failure and not hypoxia.
Describe the ventilatory strategies for acute respiratory distress syndrome.
ARDS is treated with mechanical ventilation to correct hypoxemia and hypercapnia ( Box 86-1 ). The goals are to maintain acceptable gas exchange, minimize ventilator-induced lung injury, and treat underlying causes of illness. Although mechanical ventilation is the modality keeping these patients alive, it can also extend inflammation in response to cyclic tidal alveolar hyperinflation. Cyclic overdistention produced by excessive transpulmonary pressure is a determinant of ventilator-induced lung injury (VILI). et al. (1988) studied rat lungs to determine whether VILI resulted from a pressure-mediated or lung volume (stretch)–mediated injury. These investigators subjected rats to incremental peak inspiratory pressure, and the tidal volume was restricted in one group using a thoracoabdominal binder to limit chest wall excursion. High tidal volume ventilation, independent of airway pressure, produced severe lung injury, otherwise known as volutrauma. The investigators also found PEEP to be protective, preventing pulmonary epithelial damage and alveolar edema. The ARDS Clinical Network (ARDSnet) completed a landmark trial in 2000 with 861 patients with ARDS ( , 2000). Improved mortality was seen when a tidal volume of 6 mL/kg based on predicted body weight (PBW) was used compared with the traditional value of 12 mL/kg based on PBW. The group with tidal volume 6 mL/kg was restricted to a plateau pressure ≤30 cm H 2 O, and the group with tidal volume 12 mL/kg was restricted to a much higher plateau pressure of ≤50 cm H 2 O (Table 86-2). The low tidal volume group was found to have reduced levels of inflammatory mediators, which reflect less severe lung injury.