Common causes of pediatric respiratory distress
Practice EssentialsAcute respiratory distress syndrome (ARDS) continues to contribute significantly to the disease burden in today’s arena of pediatric critical care medicine. It is an acute, diffuse, inflammatory lung injury caused by diverse pulmonary and non-pulmonary etiologies. Pathophysiology is characterized by increased vascular permeability, increased lung weight and loss of aerated tissue within the 7 days of insult. Hypoxemia, bilateral opacities on the chest x-ray, decreased lung compliance and increased physiological dead space are telltale clinical signs. Diffuse alveolar damage characterized by edema, inflammation, hyaline membrane formation or pulmonary hemorrhage are the pathological hallmark. [1] Show Here are the most recent practice essentials from a critical care stand point. The Berlin definition eliminated the taxonomy of Acute Lung Injury (ALI) and classified ARDS in to mild, moderate and severe categories based on severity of oxygenation compromise. Minimum PEEP requirement was included for the assessment of oxygen requirement. It also eliminated necessity of pulmonary artery wedge pressure criteria for pulmonary edema. They instead suggested utilization of clinical criteria, in case of presence of risk factors of ARDS. They recommended echocardiogram and the other objective assessment, if the risk factors for ARDS are not present. [1] A panel of 27 pediatric experts, the Pediatric Acute Lung Injury Consensus Conference (PALICC) Group, subsequently developed nomenclature pertinent for pediatric patients. They included oxygenation index (OI), oxygen saturation index (OSI) and the pulse oximetric saturation to fraction of inspired oxygen ratio - S/F (SPO2/FiO2). The committee recommended utilization of low tidal volume (5-8 mL/kg of predicted body weight), positive end expiratory pressure (PEEP) in the range of 5-15 cm H2O, limiting plateau pressure to 28-32 cm H2O, permissive hypercapnia strategy and acceptance of low SPO2 in the range of 88-92% if PEEP is as high as 10 cm H2O. Routine use of steroids, prone positioning, surfactant and liquid ventilation is not recommended. PEEP higher than 15 might be needed for severe cases of pediatric ARDS, but requires close monitoring of ventilator induced lung injury. Utilization of High Frequency Oscillatory Ventilation (HFOV) can be considered in cases with plateau airway pressure higher than 28. Although PALICC had a weak agreement on this recommendation. Meticulous consideration of inhaled nitric oxide therapy in severe ARDS cases and in cases bridging to extra corporeal life support (ECLS). [2]  BackgroundThe discussion of ARDS is incomplete without appreciating historic work by Ashbaugh and colleagues, who were first to describe the concept of ARDS in 1967. They presented eleven adults and one pediatric patient who suffered from acute onset of tachypnea and hypoxemia refractory to supplemental oxygen. The authors also discussed the benefits of positive end expiratory pressure (PEEP) for the management of atelectasis and a plausible role of corticosteroids in certain cases. The loss of lung compliance was noted clinically and pulmonary inflammation, edema and hyaline membrane formation were seen on autopsy. These observations were significant and remain indispensable even after 48 years. [3] ARDS was referred as adult respiratory distress syndrome in some of the studies. [4] But now it is consistently known as acute respiratory distress syndrome (ARDS), because it is a well-known entity in pediatric population since the first description in 1967. [3] In the last 5 decades, our knowledge and experience has grown substantially and the definition continues to evolve. The American-European Consensus Conference (AECC) definition of ARDS was published in 1994 [5, 6] and had certain limitations which were addressed 17 years later by Berlin definition in 2012. [1] The Pediatric Acute Lung Injury Consensus Conference Group made recommendations relevant to the pediatric population afterwards. [2] See the image below. See Acute Respiratory Distress Syndrome: A Complex Clinical Condition, a Critical Images slideshow, for more information on this life-threatening condition characterized by acute respiratory failure, hypoxemia, and pulmonary edema. DefinitionBerlin definition requires all of the following criteria to diagnose ARDS. [1]
Mild: PaO2/FiO2 ratio > 200 to < 300 mm Hg with PEEP or CPAP > 5 cm H2O (could be derived from noninvasive ventilation in mild ARDS) Moderate: PaO2/FiO2 ratio > 100 to < 200 mm Hg, PEEP > 5 cm H2O Severe: PaO2/FiO2 ratio < 100 mm Hg, PEEP > 5 cm H2O This PaO2/FiO2 ratio is applicable at the altitude < 1000 m. For altitudes > 1000 m, following correction factor should be applied: PaO2/FiO2 X (barometric pressure/760) The Berlin definition eliminated the taxonomy of Acute Lung Injury (ALI) and created three 3 exclusive subgroups of ARDS as described above. A minimum PEEP level was also added across the subgroups along with the requirement of FiO2. They also removed the requirement of Pulmonary Artery Wedge Pressure (PAWP) to exclude cardiac origin of pulmonary edema. Instead, they suggest utilization of noninvasive tests like echocardiography to exclude hydrostatic edema, if the risk factors for ARDS are not present. Pediatric ARDS is distinct from adult ARDS in various aspects. Hence a panel of 27 experts met over the period of 2 years from March, 2012 to March 2014 to identify distinguishing features of pediatric ARDS, to define nomenclature and provide recommendation pertinent to the pediatric population with ARDS. The committee made 132 recommendations with strong agreement and 19 recommendations with weak agreement.48 The relevant recommendations are discussed throughout this article. Below are the two definitions (pediatric ARDS and at risk of pediatric ARDS) recommended by The Pediatric Acute Lung Injury Consensus Conference Group. (PALICC) [2] Pediatric ARDS (PARDS) definition has incorporated Berlin definition criteria for onset of disease, chest imaging and origin of edema. The panel also included specific criteria for age, utilization of oxygen saturations (SPO2), OI (oxygenation index) and OSI (oxygen saturation index) as mentioned below. The purpose of utilizing SPO2 and OSI was to avoid invasive monitoring needed for obtaining PaO2. Age: The panel recommended excluding patients with peri-natal lung diseases, otherwise no age specific criteria. Oxygenation: Presence of hypoxemia is essential to the diagnosis of ARDS. Utilization of OI or SF ratio instead of P/F ratio was recommended. Non-invasive mechanical ventilation, no stratification of severity Full face mask bi-level ventilation or CPAP > 5 cm of H2O, PF ratio < 300 or SF ratio < 264 Invasive mechanical ventilation, with stratification of severity Mild: OI 4-< 8, OSI 5-< 7.5; Moderate: OI 8-< 16, OSI 7.5-< 12.3, Severe: OI>16, OSI > 12.3 Special population (chronic lung disease, left ventricular dysfunction, cyanotic heart disease): Presence of standard criteria for age, onset, origin of edema, new infiltrates on chest imaging, and acute onset hypoxemia from baseline which meet the criteria of oxygenation as discussed above. All of these cannot be explained by underlying disease. The panel also developed definition of “At risk of PARDS”. The definition had same criteria as PARDS for age, onset, chest imaging and origin of edema. The criteria for oxygenation were different as mentioned below. Oxygenation:
Nasal mask CPAP or BiPAP, FiO2 > 40 to maintain oxygen saturations (SPO2) 88-97% Oxygen via mask, nasal canula or high flow: SPO2 88-97 with age specific flow; 2L/min for age < 1 year, 4L/min for age 1-5 years, 6L/min for age 5-10 years and 8L/min for age > 10 years.
Oxygen supplementation to maintain SPO2 from > 88%, OI < 4 or OSI < 5 The equations can be derived as below.
For example, a patient receiving mechanical ventilation with a mean airway pressure of 20 cm H2O, FiO2 of 0.6 has SPO2 of 98% and PaO2 of 85 mm Hg. OI = (0.6 X 20 x 100)/85 = 14.11 OSI = (0.6 X 20 x 100)/98 = 12.24 P/F ratio = 85/0.6 = 141.66 This patient has moderate ARDS. Go to Acute Respiratory Distress Syndrome and Barotrauma and Mechanical Ventilation for complete information on these topics. PathophysiologyARDS follows cascade of events after direct pulmonary or systemic insult resulting into the disruption of alveolar-capillary unit. The pathophysiology of ARDS is complex and multifaceted involving 3 distinct components: (1) nature of the stimulus (2) host response to the stimulus, and (3) the role of iatrogenic factors. To understand this complex process, it is important to understand the physiology and functional anatomy. Physiology and functional anatomy Human lung development begins with 50 million alveoli in the neonatal lung and completes with 500 million alveoli and approximately 50 m2 of surface area in an adult lung. Substantial part of the alveolarization occurs during first 2 years of life. The normal alveolar epithelium is comprised of two distinct types of cells. Type I alveolar cells are flat, account for 90% of the alveolar surface area and are covered with a thin layer of alveolar lining fluid. They participate in the gas exchange and are exposed to very high oxygen concentration. So they are vulnerable to oxidative injury, but recent literature suggests that type I cells may have an active system against the oxidative stress. They are end cells because they are incapable of proliferation and differentiation. They actually arise from type II cells. Type II alveolar cells are cuboidal or rounded cells that account for the remaining 10% of alveolar surface area and are resistant to injury. They do not participate in the gas exchange but are involved in surfactant production, ion transport and other pulmonary defense mechanisms. [7, 8, 9, 10, 11, 12] Alveolar epithelium and pulmonary microvascular endothelium create a two-layered alveolar-capillary barrier. This barrier serves the function of gas exchange, maintains the integrity of pulmonary morphology and protection from external injury. Disruption of this barrier results in increased permeability, influx of protein rich edema fluid into the alveolar sacs, dysfunction of surfactant production, and defective ion transport leading to impaired fluid clearance from alveolar cells. These changes are the hallmark of ARDS pathophysiology and are accompanied by dysregulated inflammation from dysfunctional leukocytes and influx of pro-inflammatory cytokines like interleukins and tumor-necrosis factor. The role of neutrophils in this mechanism is controversial. Animal models have favored both neutrophil dependent and neutrophil independent lung injury. It is also unclear if neutrophilic inflammation is the cause or the result of lung injury. Dysfunction of platelets and coagulation cascade results in microvascular thrombosis and capillary occlusion. [7, 8, 9, 10, 11, 12] This course of ARDS pathophysiology was previously described into 3 histopathologic stages including exudative, proliferative and fibrotic phase. The timing of these stages is variable and in fact, recent evidence is suggestive of beginning of resolution and fibrotic phase early in the course of ARDS. [10] At the clinical level, respiratory distress occurs secondary to surfactant depletion, alveolar edema, cellular debris within the alveoli, and increased airway resistance. Surfactant loss leads to alveolar collapse because of increased surface tension, which is analogous to the situation observed in premature infants with infant RDS (IRDS). As alveoli collapse, closing lung volume capacity rises above the patient’s functional residual capacity (FRC), further increasing atelectasis and the work of breathing. This is reflected as reduced lung. In addition, the remaining viable lung may be conceptualized as being smaller rather than stiff. Although the total lung compliance is reduced, a small portion of the lung may be participating in the gas exchange. Those remaining intact lung regions have better compliance and are thus subject to overdistention and potential air leak complications (eg, pneumothorax) when exposed to excessive inflating pressures. The net effect is impairment in oxygenation. A widened interstitial space between the alveolus and the vascular endothelium decreases oxygen-diffusing capacity. Hypoxia arises as a result of the change described above. Collapsed alveoli result in either low ventilation-perfusion (V/Q) units or a right-to-left pulmonary shunt. The end result is marked venous admixture, the process whereby deoxygenated blood passing through the lungs does not absorb sufficient oxygen and causes a relative desaturation of arterial blood when it mixes with blood that is already oxygenated. Pulmonary hypertension may also ensue from ARDS. Hypoxemia, hypercarbia, and small-vessel thrombosis together can elevate pulmonary arterial pressures. Persistent pulmonary hypertension can result in increased right ventricular work, right ventricular dilatation, and, ultimately, left ventricular outflow tract obstruction secondary to intraventricular septum shifting toward the left ventricle. These changes, in turn, may decrease cardiac output and further reduce oxygen delivery to vital organs. Iatrogenic factors may further complicate the clinical picture. Oxygen toxicity, volutrauma, barotraumas, fluid overload can further aggravate the lung injury and worsening lung compliance and oxygenation. Resolution of ARDS is again very complex and active process. Alveolar edema resolves by active transport mechanism, where water follows sodium and chloride ions. Termination of inflammation involves anti-inflammatory mediators like IL-10, tissue growth factor (TGF) β and pre resolution mediators like polyunsaturated fatty acids including lipoxins, resolvins, and protectins. Animal models have shown the role of platelets in repair of vascular endothelium, whereas epithelial repair is carried out by alveolar progenitor cells including type II alveolar cells, Clara cells and integrin α6β4 alveolar epithelial cells. [11] If the injury is severe, disorganized and insufficient, epithelial repair may result into fibrosis and loss of lung function. The description of ARDS pathophysiology comes from adults and mature animal studies. Future research has been encouraged in pediatric population and juvenile animals. [11] EtiologyARDS occurs as consequences of diverse pulmonary and non-pulmonary etiologies. Most common conditions associated with ARDS are sepsis and infectious pneumonia (bacterial and viral). [8] [13, 14, 15, 16, 17] Sepsis related ARDS cases may carry poor prognosis, if they are associated with shock and thrombocytopenia. [15] Other more common etiologies include bronchiolitis, aspiration pneumonia, aspiration of gastric contents, major trauma, pulmonary contusion, burns, inhalational injury, massive transfusions or transfusion-related acute lung injury (TRALI). [8, 13, 14, 15, 16, 17] Transfusion of all type of blood products including packed red blood cells, fresh frozen plasma and platelets has been associated with development of ARDS. [18, 19] Other causes include acute pancreatitis, fat embolism, envenomation, drowning or submersion injuries, drug reaction, malignancy and lung transplantation. [8, 13, 14, 15, 16, 17] Ventilator induced lung injury (VILI) has also been documented as one of the etiologies for development of ARDS. [20] Noninfectious lung injury can occur after stem cell transplantation. However, a separate entity of idiopathic pulmonary syndrome has been described as well in this context. [21, 22, 23] EpidemiologyThe incidence of ARDS is certainly lower in pediatric population as compared to the adults. The adult studies have reported very wide range of incidence; from 17.9-86.2 per 100,000 person-years. [24, 25, 26, 27] For the population 15 years and older, age adjusted incidence was 86.2 per 100,000 person-years, 38.5% hospital mortality; accounting for estimated 190,600 cases of acute lung injury, 74,500 deaths and 3.6 million hospital days each year in the United States. [27] The incidence in the pediatric population is reported between 2.2 to 12.8 per 100,000 person-years. From the critical care perspective, ALI/ARDS accounts for 2.2% to 2.6% of pediatric intensive care unit (PICU) admissions, [13, 28] 8.3% of those receiving mechanical ventilation for more than 24 hours [29] and the PICU and the hospital mortality ranging between 18% to 32.8%. [13, 30, 29, 31, 28] The Pediatric Respiratory Distress Incidence and Epidemiology (PARDIE) study, which involved 27 countries, found that pediatric ARDS occurs in about 3% of patients in PICUs and in about 6% of those who are receiving mechanical ventilation. In addition, among mechanically ventilated patients, the greatest number of new cases of pediatric ARDS occurred in North America, in high-income countries, and during non-summer months. [32] The age related statistics of ARDS can be obtained by comparing the results of two different studies from King County, Washington, USA that were conducted around the same time between 1999 and 2000. [27, 31] Table. (Open Table in a new window)
Incidence and severity of ARDS is somewhat similar at different geographical location. The study from Australia and New Zealand reported incidence of 2.95 per 100,000 person-years, 2.2% of PICU admissions and 30% of PICU mortality. [13] A Dutch study reported incidence of 2.2 per 100,000 person-years and 20.4% mortality. [30] Investigators in Spain found the incidence of 3.9 per 100,000 patients-years and the PICU mortality of 26%. [29] German study showed incidence of 3.2 per 100,000 person-years. [33] The incidence in the US based study was a little higher of 12.8 per 100,000 person-years, however the mortality was slightly lower 18%. [31] Chinese literature revealed 2.6% of PICU admission for ARDS with a mortality of 32.8%. [28] Of note, the above reported epidemiological data is from the studies prior to the Berlin definition, a study which eliminated the category of ALI and classified ARDS in to mild, moderate and severe. So the epidemiology of both ALI and ARDS has been included here. Environmental and genetic influence ARDS develops after the insult from diverse etiologies discussed above. However the heterogeneity of susceptibility and the outcome is intriguing. This could partially be explained by environmental and genetic influences. However, the research is still growing in this area. From the environmental stand point, literature from adult population has shown increased risk of ARDS with alcohol abuse [34, 35] and smoking (active and passive) after blunt trauma. [36] The association of passive smoking could be implied to the pediatric population. From genetic stand point, a total of 34 genes have been reported to impact the ARDS susceptibility. [37] Majority of them are linked to the currently described pathophysiological pathways of ARDS. These include inflammation, epithelial cell function, endothelial cell function, coagulation, oxidative injuries, apoptosis and platelet cellular process. [37, 38, 39] [40, 41] The other reported genetic mutations associated with ARDS were linked to surfactant dysfunction [37] and to the epidermal growth factor gene polymorphism in males. [42] There is not enough literature suggesting ethnic differences for ARDS incidence and outcomes. Vast majority of initial genetic studies were in European population. The literature is scant for the other ethnic backgrounds. Thus far approximately nine genes in African population and three genes in Asian population have been reported to be linked with ARDS. [37] Studies have reported poor outcomes in African American with ARDS as compared to the patients of the other ethnicity. [43, 44, 45] Although in one study higher mortality was associated with higher severity of illness on presentation in patients with Black race. Higher mortality in Hispanic patients was not explainable by severity of illness on presentation in the same study. [44] Some of the epidemiological studies have reported slightly higher incidence of ARDS among male children (54% to 63%) [13, 29, 31] ; however, the mortality (31% in male children) was not significantly different. [13] One adult study reported higher mortality among males. [45] There is also not enough literature in the area of genetics pertinent to the pediatric ARDS in the context of growing lung and developing immunity. [2] PrognosisComplicationsSeveral complications are associated with ARDS, though many of these are due to the precipitating conditions that lead to ARDS. Acute complications include air-leak syndromes, ventilator-induced lung infection (VILI), and multiple organ dysfunction syndrome (MODS), although definitive evidence linking this syndrome to ARDS or ventilator use remains controversial. Numerous pulmonary complications may result from ARDS. The most common are the air-leak syndromes, particularly pneumothorax but also pneumomediastinum, pneumopericardium, pneumoperitoneum, and subcutaneous emphysema. Features of a pneumothorax include decreased air entry on the side of the air leak, an increased percussion note on the same side, and tracheal deviation away from the affected side in a tension pneumothorax. Heart sounds may be muffled, and signs of decreased cardiac output may be observed with a tension pneumothorax. Clinicians must also maintain a high index of suspicion for tension pneumothoraces as a cause for acute onset of decreased cardiac output. VILI is an entity receiving attention with the publication of landmark trials suggesting that a “kinder, gentler” form of mechanical ventilation improves outcomes in ARDS. VILI most likely has several causes, including excessive lung stretching due to high tidal volumes, repetitive opening and closing of alveoli leading to shear stress, oxygen toxicity, and cytokine release. ARDS patients may also be compromised from a cardiovascular standpoint. Patients with sepsis, trauma, or other multisystem insults may lose their ability to tolerate higher airway pressures often required to maintain adequate oxygenation. Higher airway pressures lead to a higher net intrathoracic pressure, which results in decreased preload and cardiac output. Moreover, hypoxia, hypercarbia, and acidosis may elevate pulmonary artery pressures, increasing right ventricular afterload and leading to increased right ventricular work. Right ventricular dilatation can develop and then result in leftward movement of the intraventricular septum and cause left ventricular outflow tract obstruction. Gastrointestinal complications commonly observed in the critically ill population include stress ulcers, liver failure, pancreatitis, and pancreatic insufficiency, leading to glucose intolerance. Renal failure may result from the primary illness or may occur secondarily as a result of poor cardiac output, acute tubular necrosis, and MODS. Secondary or nosocomial pneumonia is not uncommon in critically ill children. In addition to Staphylococcus aureus, other organisms more typically isolated include Pseudomonas species, Acinetobacter baumannii, Stenotrophomonas maltophilia, Escherichia coli, and Candida species. Bacteremia from indwelling vascular catheters and skin ulcerations may also occur. Risk of urinary tract infection increases with prolonged indwelling Foley catheters. Critical illness polyneuropathy and myopathy (CIPNM) is seen in a subset of patients of unclear etiology. Many factors have been identified to have an increased association with CIPNM, such as sepsis, systemic inflammatory response syndrome, MODS, and prolonged mechanical ventilation. Use of muscle relaxants, especially in conjunction with steroids, appears to have a particularly high association with CIPNM. Initial reports describe CIPNM with concomitant use of nondepolarizing muscle relaxants and corticosteroids. However, case reports of weakness with cisatracurium and corticosteroids have also been described. Clinically, patients develop profound or flaccid weakness that is often prolonged. This may complicate the mechanical ventilator weaning process and may also require inpatient rehabilitation care upon discharge from the hospital. [46, 47]
Author Prashant Purohit, MD Pediatric Intensivist, Kapi’olani Medical Center for Women and Children Disclosure: Nothing to disclose. Coauthor(s) Dale W Steele, MD, MS Professor of Emergency Medicine, Pediatrics, and Health Services, Policy, and Practice, Warren Alpert Medical School of Brown University; Attending Physician, Department of Pediatric Emergency Medicine, Rhode Island Hospital Dale W Steele, MD, MS is a member of the following medical societies: American Academy of Pediatrics, American Statistical Association, Society for Medical Decision Making Disclosure: Nothing to disclose. G Patricia Cantwell, MD, FCCM Professor of Clinical Pediatrics, Chief, Division of Pediatric Critical Care Medicine, University of Miami Leonard M Miller School of Medicine/ Holtz Children's Hospital, Jackson Memorial Medical Center; Medical Director, Palliative Care Team, Holtz Children's Hospital; Medical Manager, FEMA, South Florida Urban Search and Rescue, Task Force 2 G Patricia Cantwell, MD, FCCM is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, Wilderness Medical Society Disclosure: Nothing to disclose. Lennox H Huang, MD, FAAP Chief Medical Officer, The Hospital for Sick Children; Associate Professor of Pediatrics, University of Toronto Faculty of Medicine; Associate Clinical Professor of Pediatrics, McMaster University School of Medicine, Canada Lennox H Huang, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American Association for Physician Leadership, Canadian Medical Association, Ontario Medical Association, Society of Critical Care Medicine Disclosure: Nothing to disclose. Specialty Editor Board Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Nothing to disclose. Chief Editor Timothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, Wisconsin Medical Society Disclosure: Nothing to disclose. Additional Contributors Garry Wilkes, MBBS, FACEM Associate Director, Emergency Medicine, Goulburn Valley Health, Victoria, Australia; Clinical Associate Professor, University of Western Australia; Adjunct Associate Professor, Edith Cowan University, Western Australia Disclosure: Nothing to disclose. Andrew K Feng, MD Attending Physician, Division of Pediatric Critical Care, Kapiolani Medical Center for Women and Children Andrew K Feng, MD is a member of the following medical societies: Society of Critical Care Medicine Disclosure: Nothing to disclose. What are the causes of respiratory distress in children?There can be many causes of respiratory distress in children. Usually it is caused by infections, chronic illness or a blocked airway. A child who was premature at birth or has been in the hospital for respiratory problems may be at greater risk.
What are 5 causes of respiratory distress?What causes ARDS?. pneumonia or severe flu.. sepsis.. a severe chest injury.. accidentally inhaling vomit, smoke or toxic chemicals.. near drowning.. acute pancreatitis – a serious condition where the pancreas becomes inflamed over a short time.. an adverse reaction to a blood transfusion.. What are common respiratory issues with pediatrics?Sinusitis (in the sinuses) Bronchitis (in the larger airways that lead into the lungs) Bronchiolitis (in the smaller airways in the lungs) Pneumonia (in the air sacs inside the lungs)
What is the most common cause of respiratory distress?However, only a few common causes account for most cases of ARDS; in the medical intensive care unit population, the most common causes include pneumonia, sepsis, and aspiration. Factors that may predispose a patient to develop ARDS have also been identified.
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