Learning Outcome
Acute respiratory distress syndrome (ARDS) is a life-threatening condition of seriously ill patients, characterized by poor oxygenation, pulmonary infiltrates, and acuity of onset. On a microscopic level, the disorder is associated with capillary endothelial injury and diffuse alveolar damage. ARDS is defined as an acute disorder characterized by bilateral lung infiltrates and severe progressive hypoxemia in the absence of any evidence of cardiogenic pulmonary edema. ARDS is defined by the patient's oxygen in arterial blood (PaO2) to the fraction of the oxygen in the inspired air (FiO2). These patients usually have a PaO2/FiO2 ratio of less than 200. Once ARDS develops, patients usually have varying degrees of pulmonary artery vasoconstriction and may subsequently develop pulmonary hypertension. ARDS carries a high mortality, and few effective therapeutic modalities exist to combat this condition.[1][2] Nursing Diagnosis
ARDS has many risk factors. Besides pulmonary infection or aspiration, extra-pulmonary sources include sepsis, trauma, massive transfusion, drowning, drug overdose, fat embolism, inhalation of toxic fumes, and pancreatitis. These extra-thoracic illnesses and/or injuries trigger an inflammatory cascade culminating in pulmonary injury.[3] Estimates of ARDS incidence in the United States range from 64.2 to 78.9 cases/100,000 person-years. Twenty-five percent of ARDS cases are initially classified as mild and 75% as moderate or severe. However, a third of the mild cases go on to progress to moderate or severe disease.[1] A literature review revealed a mortality decrease of 1.1% per year for the period 1994 through 2006. However, the overall pooled mortality rate for all the studies evaluated was 43%.[2] Risk factors for ARDS include:
The syndrome is characterized by the development of dyspnea and hypoxemia, which progressively worsens within hours to days, frequently requiring mechanical ventilation and intensive care unit-level care. The history is directed at identifying the underlying cause which has precipitated the disease. When interviewing patients that can communicate, they often start to complain of mild dyspnea initially, but within 12 to 24 hours, the respiratory distress escalates, becoming severe and requiring mechanical ventilation to prevent hypoxia. The etiology may be obvious in the case of pneumonia or sepsis. However, in other cases, questioning the patient or relatives on recent exposures may also be paramount in identifying the causative agent. The physical examination will include findings associated with the respiratory system, such as tachypnea and increased effort to breathe. Systemic signs may also be evident depending on the severity of illness, such as central or peripheral cyanosis resulting from hypoxemia, tachycardia, and altered mental status. Despite 100% oxygen, patients have low oxygen saturation. Chest auscultation usually reveals rales, especially bibasilar, but are often auscultated throughout the chest. The diagnosis of ARDS is made based on the following criteria: acute onset, bilateral lung infiltrates on chest radiography of a non-cardiac origin, and a PaO/FiO ratio of less than 300 mmHg. It is further sub-classified into mild (PaO2/FiO2 200 to 300 mmHg), moderate (PaO2/FiO2 100 to 200 mmHg), and severe (PaO2/FiO2 less than 100 mmHg) subtypes. Mortality and ventilator-free days increase with severity. A CT scan of the chest may be required in pneumothorax cases, pleural effusions, mediastinal lymphadenopathy, or barotrauma to properly identify infiltrates as pulmonic in location. Assessment of left ventricular function may be required to differentiate from or quantify the contribution of congestive heart failure to the overall clinical picture. This assessment can be achieved via invasive methods such as pulmonary artery catheter measurements or non-invasively, such as cardiac echocardiography or thoracic bioimpedance, or pulse contour analysis. However, the use of pulmonary artery catheters is controversial and should be avoided if clinically possible, and noninvasive measures for assessment should be exhausted first. Bronchoscopy may be required to assess pulmonary infections and obtain material for culture. Other laboratory and/or radiographic tests will be guided by the underlying disease process, which has triggered the inflammatory process that has led to the development of ARDS. Also, laboratory tests will be needed as patients with ARDS are highly likely to develop or be affected by associated multi-organ failure, including but not limited to renal, hepatic, and hematopoietic failures. Regularly obtaining complete blood count with differential, comprehensive metabolic panel, serum magnesium, serum ionized calcium, phosphorus levels, blood lactate level, coagulation panel, troponin, cardiac enzymes, and CKMB are recommended if clinically indicated.[3][4][5] Unfortunately, no drug has been proven to be effective in preventing or managing ARDS. The chief treatment strategy is supportive care, along with adequate nutrition. Patients are mechanically ventilated, guarded against fluid overload with diuretics, and given nutritional support until evidence of improvement is observed. Interestingly, the mode in which a patient is ventilated affects lung recovery. Evidence suggests that some ventilatory strategies can exacerbate alveolar damage and perpetuate lung injury in the context of ARDS. Care is placed in preventing volutrauma (exposure to large tidal volumes), barotrauma (exposure to high plateau pressures), and atelectrauma (exposure to atelectasis).[1][6] A lung-protective ventilatory strategy is advocated to reduce lung injury. The NIH-NHLBI ARDS Clinical Network Mechanical Ventilation Protocol (ARDSnet) sets the following goals: Tidal volume (V) from 4 to 8 mL/kg of ideal body weight (IBW), respiratory rate (RR) up to 35 bpm, SpO2 88% to 95%, plateau pressure (P) less than 30 cm H2O, pH goal 7.30 to 7.45, and inspiratory-to-expiratory time ratio less than 1. To maintain oxygenation, ARDSnet recognizes the benefit of PEEP. The protocol allows for a low or a high PEEP strategy relative to FiO2. Either strategy tolerates a PEEP of up to 24 cm HO in patients requiring 100% FiO2. The inspiratory-to-expiratory time ratio goal may need to be sacrificed and an inverse inspiratory-to-expiratory time ratio strategy instituted to improve oxygenation in a certain clinical situation. Novel invasive ventilation strategies have been developed to improve oxygenation. These include airway pressure release ventilation and high-frequency oscillation ventilation. These open-lung ventilation strategies can be supplemented with recruitment maneuvers. Patients with mild and some with moderate ARDS may benefit from non-invasive ventilation to avoid endotracheal intubation and invasive mechanical ventilation. These modalities include continuous positive airway pressure (CPAP), bi-level airway pressure (BiPAP), proportional-assist ventilation, and high flow nasal cannula. A plateau pressure of less than 30 cm HO can be achieved using several strategies. Again, this is to reduce the risk of barotrauma. One strategy is to maintain as low a V and PEEP as possible. Also, increasing the rise and/or inspiration times can also help maintain the P goal. Finally, the flow rate can be decreased as an adjunct to decreasing the P. High P is also a product of decreased lung compliance from non-cardiogenic pulmonary edema, a salient feature of ARDS pathophysiology. Improving lung compliance will improve P and oxygenation goal attainment. Neuromuscular blockade has been used in this endeavor. Neuromuscular blockers instituted during the first 48 hours of ARDS improved 90-day survival and increased time off the ventilator.[12] Other causes of decreased lung compliance should be sought and addressed. These include, but are not limited to, pneumothorax, hemothorax, thoracic compartment syndrome, and intraabdominal hypertension. Prone position has shown benefits in about 50% to 70% of patients. The improvement in oxygenation is rapid and allows a reduction in FiO2 and PEEP. The prone position is safe, but there is a risk of dislodgement of lines and tubes. It is believed that in the prone position, there is the recruitment of dependent lung zones, improved diaphragmatic excursion, and increased functional residual capacity. To derive the benefits, the patient needs to be maintained in the prone position for at least 8 hours a day. Non-ventilatory strategies have included prone positioning and conservative fluid management once resuscitation has been achieved.[14][7][8] Extracorporeal membrane oxygenation (ECMO) has recently been advocated as salvage therapy in refractory hypoxemic ARDS.[9] Nutritional support via enteral feeding is recommended. A high-fat, low-carbohydrate diet containing gamma-linolenic acid and eicosapentaenoic acid has been shown in some studies to improve oxygenation. Care must also be taken to prevent pressure sores; thus, frequent patient repositioning or turning is recommended when feasible. Skin checks per nursing routine are also advised. Physical therapy should be involved in exercising the patient when they are liberated from mechanical ventilation and stable to participate in therapy. Nursing Management
When To Seek Help
The outcomes for most patients with ARDS are guarded. Even those who recover have a prolonged recovery, marked by muscle wasting, polyneuropathy, and weakness. ICU care with continuous monitoring. ARDS is a serious disorder of the lung which has the potential to cause death. Patients with ARDS may require mechanical ventilation because of hypoxia.[10] The management is usually in the ICU with an interprofessional healthcare team. ARDS has effects beyond the lung. Prolonged mechanical ventilation often leads to bedsores, deep venous thrombosis, multi-organ failure, weight loss, and poor overall functioning. It is important to have an integrated approach to ARDS management because it usually affects many organs in the body. These patients need nutritional support, chest physiotherapy, treatment for sepsis if present, and potentially hemodialysis. Many of these patients remain in the hospital for months and even those who survive face severe challenges due to a loss of muscle mass and cognitive changes (due to hypoxia). There is ample evidence showing that an interprofessional team approach leads to better outcomes as it facilitates communication and ensures timely intervention.[11] The team and responsibilities should consist of the following:
Outcomes Despite advances in critical care, ARDS still has high morbidity and mortality. Even those who survive can have a poorer quality of life. While many risk factors are known for ARDS, there is no way to prevent the condition. Besides the restriction of fluids in high-risk patients, close monitoring for hypoxia by the team is vital. The earlier the hypoxia is identified, the better the outcome. Those who survive have a long recovery period to regain functional status. Many continue to have dyspnea even with mild exertion and thus are dependent on care from others. Even though many risk factors for ARDS are known, there is no way of preventing ARDS. However, careful management of fluid in high-risk patients can be helpful. Steps should be taken to prevent aspiration by keeping the head of the bed elevated before feeding. Discharge planning should include medication reconciliation, detailed home care planning (whether by family members or in-home/visiting nursing), and plans for follow-up visits and evaluations. Patients and caregivers must be counseled on signs of when to contact the clinician in the event of exacerbation or deterioration of the patient's condition. Review Questions Acute Respiratory Distress Syndrome. Image courtesy S Bhimji MD 1. Gajic O, Dabbagh O, Park PK, Adesanya A, Chang SY, Hou P, Anderson H, Hoth JJ, Mikkelsen ME, Gentile NT, Gong MN, Talmor D, Bajwa E, Watkins TR, Festic E, Yilmaz M, Iscimen R, Kaufman DA, Esper AM, Sadikot R, Douglas I, Sevransky J, Malinchoc M., U.S. Critical Illness and Injury Trials Group: Lung Injury Prevention Study Investigators (USCIITG-LIPS). Early identification of patients at risk of acute lung injury: evaluation of lung injury prediction score in a multicenter cohort study. Am J Respir Crit Care Med. 2011 Feb 15;183(4):462-70. [PMC free article: PMC3056224] [PubMed: 20802164] 2.Wang Y, Zhang L, Xi X, Zhou JX., China Critical Care Sepsis Trial (CCCST) Workgroup. The Association Between Etiologies and Mortality in Acute Respiratory Distress Syndrome: A Multicenter Observational Cohort Study. Front Med (Lausanne). 2021;8:739596. [PMC free article: PMC8558376] [PubMed: 34733862] 3.Zambon M, Vincent JL. Mortality rates for patients with acute lung injury/ARDS have decreased over time. Chest. 2008 May;133(5):1120-7. [PubMed: 18263687] 4.Shrestha GS, Khanal S, Sharma S, Nepal G. COVID-19: Current Understanding of Pathophysiology. J Nepal Health Res Counc. 2020 Nov 13;18(3):351-359. [PubMed: 33210623] Sedhai YR, Yuan M, Ketcham SW, Co I, Claar DD, McSparron JI, Prescott HC, Sjoding MW. Validating Measures of Disease Severity in Acute Respiratory Distress Syndrome. Ann Am Thorac Soc. 2021 Jul;18(7):1211-1218. [PMC free article: PMC8328371] [PubMed: 33347379] 6.Sharma NS, Lal CV, Li JD, Lou XY, Viera L, Abdallah T, King RW, Sethi J, Kanagarajah P, Restrepo-Jaramillo R, Sales-Conniff A, Wei S, Jackson PL, Blalock JE, Gaggar A, Xu X. The neutrophil chemoattractant peptide proline-glycine-proline is associated with acute respiratory distress syndrome. Am J Physiol Lung Cell Mol Physiol. 2018 Nov 01;315(5):L653-L661. [PMC free article: PMC6295514] [PubMed: 30091378] 7.Huang D, Ma H, Xiao Z, Blaivas M, Chen Y, Wen J, Guo W, Liang J, Liao X, Wang Z, Li H, Li J, Chao Y, Wang XT, Wu Y, Qin T, Su K, Wang S, Tan N. Diagnostic value of cardiopulmonary ultrasound in elderly patients with acute respiratory distress syndrome. BMC Pulm Med. 2018 Aug 13;18(1):136. [PMC free article: PMC6090678] [PubMed: 30103730] 8.Chen WL, Lin WT, Kung SC, Lai CC, Chao CM. The Value of Oxygenation Saturation Index in Predicting the Outcomes of Patients with Acute Respiratory Distress Syndrome. J Clin Med. 2018 Aug 08;7(8) [PMC free article: PMC6111712] [PubMed: 30096809] 9.Rawal G, Yadav S, Kumar R. Acute Respiratory Distress Syndrome: An Update and Review. J Transl Int Med. 2018 Jun;6(2):74-77. [PMC free article: PMC6032183] [PubMed: 29984201] 10.Cherian SV, Kumar A, Akasapu K, Ashton RW, Aparnath M, Malhotra A. Salvage therapies for refractory hypoxemia in ARDS. Respir Med. 2018 Aug;141:150-158. [PMC free article: PMC6186150] [PubMed: 30053961] 11.Guérin C, Reignier J, Richard JC, Beuret P, Gacouin A, Boulain T, Mercier E, Badet M, Mercat A, Baudin O, Clavel M, Chatellier D, Jaber S, Rosselli S, Mancebo J, Sirodot M, Hilbert G, Bengler C, Richecoeur J, Gainnier M, Bayle F, Bourdin G, Leray V, Girard R, Baboi L, Ayzac L., PROSEVA Study Group. Prone positioning in severe acute respiratory distress syndrome. N Engl J Med. 2013 Jun 06;368(23):2159-68. [PubMed: 23688302] 12.National Heart, Lung, and Blood Institute PETAL Clinical Trials Network. Moss M, Huang DT, Brower RG, Ferguson ND, Ginde AA, Gong MN, Grissom CK, Gundel S, Hayden D, Hite RD, Hou PC, Hough CL, Iwashyna TJ, Khan A, Liu KD, Talmor D, Thompson BT, Ulysse CA, Yealy DM, Angus DC. Early Neuromuscular Blockade in the Acute Respiratory Distress Syndrome. N Engl J Med. 2019 May 23;380(21):1997-2008. [PMC free article: PMC6741345] [PubMed: 31112383] 13.National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network. Wiedemann HP, Wheeler AP, Bernard GR, Thompson BT, Hayden D, deBoisblanc B, Connors AF, Hite RD, Harabin AL. Comparison of two fluid-management strategies in acute lung injury. N Engl J Med. 2006 Jun 15;354(24):2564-75. [PubMed: 16714767] 14.Brodie D, Bacchetta M. Extracorporeal membrane oxygenation for ARDS in adults. N Engl J Med. 2011 Nov 17;365(20):1905-14. [PubMed: 22087681] 15.Combes A, Hajage D, Capellier G, Demoule A, Lavoué S, Guervilly C, Da Silva D, Zafrani L, Tirot P, Veber B, Maury E, Levy B, Cohen Y, Richard C, Kalfon P, Bouadma L, Mehdaoui H, Beduneau G, Lebreton G, Brochard L, Ferguson ND, Fan E, Slutsky AS, Brodie D, Mercat A., EOLIA Trial Group, REVA, and ECMONet. Extracorporeal Membrane Oxygenation for Severe Acute Respiratory Distress Syndrome. N Engl J Med. 2018 May 24;378(21):1965-1975. [PubMed: 29791822] 16.Yang P, Formanek P, Scaglione S, Afshar M. Risk factors and outcomes of acute respiratory distress syndrome in critically ill patients with cirrhosis. Hepatol Res. 2019 Mar;49(3):335-343. [PMC free article: PMC6560637] [PubMed: 30084205] 17.Gadre SK, Duggal A, Mireles-Cabodevila E, Krishnan S, Wang XF, Zell K, Guzman J. Acute respiratory failure requiring mechanical ventilation in severe chronic obstructive pulmonary disease (COPD). Medicine (Baltimore). 2018 Apr;97(17):e0487. [PMC free article: PMC5944543] [PubMed: 29703009] 18.Chiumello D, Coppola S, Froio S, Gotti M. What's Next After ARDS: Long-Term Outcomes. Respir Care. 2016 May;61(5):689-99. [PubMed: 27121623] 19.Villar J, Schultz MJ, Kacmarek RM. The LUNG SAFE: a biased presentation of the prevalence of ARDS! Crit Care. 2016 Apr 25;20(1):108. [PMC free article: PMC4843206] [PubMed: 27109238] 20.Bos LD, Cremer OL, Ong DS, Caser EB, Barbas CS, Villar J, Kacmarek RM, Schultz MJ., MARS consortium. External validation confirms the legitimacy of a new clinical classification of ARDS for predicting outcome. Intensive Care Med. 2015 Nov;41(11):2004-5. [PubMed: 26202043] |
What important independent nursing interventions should be used in caring for a child with respiratory dysfunction?
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