Acute Respiratory Distress Syndrome (ARDS) is an unstable lung condition ranging from mild to severe and life-threatening. It can be caused by direct or indirect injury to the lungs. Direct injury is pulmonary in origin and includes pneumonia, aspiration, inhalation injury, fat embolism, high pressure mechanical ventilation, pulmonary contusion, near drowning, and reperfusion pulmonary edema. Indirect causes are extrapulmonary and include sepsis, transfusion of blood products, shock, burns, drug overdose, cardiopulmonary bypass, acute pancreatitis, severe trauma, head injury, and disseminated intravascular coagulation. (8) These methods of injury lead to the initiation of an inflammatory immune response and therefore the release of cellular and chemical mediators. The result is an increase in permeability of the alveolar membrane leading to in an influx of fluid into the alveoli. Interstitial fluid and bronchial obstruction causes a narrowing of the airway. A decrease in lung compliance and an increase in airway resistance lead to laborious breathing and ultimately severe hypoxia. ARDS is characterized by hypoxemia with supplemental oxygen, a decrease pulmonary compliance, dyspnea, noncardiac associated pulmonary edema, and increasing bilateral infiltrates on chest x-ray (BOOK, HESI).
The patient with ARDS will present with what initially seems to be pulmonary edema. This includes dyspnea, cyanosis and hypoxemia that doesn't respond to supplemental oxygen, a chest x-ray with bilateral infiltrates that appears similar to cardiogenic pulmonary edema, and crackles on auscultation. Unlike pulmonary edema, however, an ARDS patient will also have noncompliant lungs that are difficult to ventilate and increased dead space in the alveoli that will have poor perfusion but adequate ventilation (BOOK). The Berlin definition of ARDS, created in 2012, classifies the syndrome according to mild, moderate, and severe according to the PaO2/FiO2 ratio with a PEEP of 5 cmH2O. In mild ARDS, the PaO2/FiO2 was 200-300 and mortality was 27%. In moderate ARDS, PaO2/FiO2 was 100-200 and mortality was 32%. Lastly, in severe ARDS, PaO2/FiO2 was less than 100 and mortality was 45% (7).
Treatment of ARDS is widely controversial and dependent upon the severity of illness. Ultimately the major cause of death in these patients is not respiratory in origin but rather, multiorgan dysfunction syndrome with sepsis (BOOK). Therapy for ARDS is aimed primarily at identifying the underlying condition and preventing further injury. Typical supportive therapy begins with mechanical ventilation via intubation (BOOK). Mechanical ventilation via intubation is not without its risks, however. Namely, the pressures of the ventilation can contribute, or even worsen, ARDS. Other supportive therapies can be used for ARDS patients. These treatments are under-recognized and may lead to a decreased intubation rate and a lower mortality rate. Such therapies include non-invasive ventilation via a helmet or high flow nasal cannula. In fact, the American Thoracic Society came out with new guidelines for mechanical ventilation settings in ARDS patients. Although mechanical ventilation via intubation is the most prevalent supportive therapy in patients with ARDS, various other non-invasive treatment modalities exist and decrease mortality and intubation rates although they do not necessarily indicate a better prognosis.
Mechanical ventilation via intubation has traditionally been seen as the cornerstone for ARDS therapy. Countless risk factors and complications associated with invasive ventilation has made intubation an increasingly riskier choice for treatment of ARDS. Such complications include barotrauma, ventilator associated pneumonia, tracheoesophageal fistulas, excessive sedation, delirium, and ICU acquired weakness (2+5). Nurses are able to see firsthand the negative effects of intubation for ARDS patients and therefore they are the first to suggest and implement other strategies that would decrease intubation rates. Various methods of noninvasive ventilation have been used with success in this patient population. Such methods include: high flow nasal cannula, face masks, and helmets. Although each of these carry their own risks, they are valid alternatives for intubation.
Article 1: Helmet
A randomized clinical trial was performed “to determine whether helmet NIV could reduce the rate of intubation and improve patient outcomes†(2). The study compared the helmet, a “transparent hood that covers the entire head of the patients and has a rubber collar neck seal,†to the face mask (2). In their study, Patel, Wolde, Pohlman, Hall, & Kress (2016), examined 83 patients with ARDS, all of whom required NIV via a face mask for 8 hours in the MICU. These patients were randomly divided into two groups: patients who would continue using the face mask or patients who would begin using the helmet. Ultimately, there were 44 patietns in the helmet group and 39 patients in the face mask group. Their primary outcome was the number of patients who required intubation. Their secondary outcomes included “28-day invasive ventilator-free days (ie, days alive without mechanical ventilation), duration of ICU and hospital length of stay, and hospital and 90-day mortality (2). Ultimately, the researchers found that for the face mask group, the rate of intubation was substantially greater than those in the helmet group (61.6% vs 18.2% respectively). The secondary outcomes also favored the helmet. The helmet gorup had more ventilator-free days at 28 days vs 12.5 in the face mask group. They also had a lower mortality rate at 90 days with 15 people deceased compared to 22 patients in the face mask group. Both groups experienced skin breakdown at relatively the same percent. 7.6% of the face mask group had nose ulcers and 6.8% of the helmet group had neck ulcers. Ultimately, the study concluded that NIV via a helmet was substantially more effective at decreasing rates of intubation when compared to the face mask and even improved patient outcomes.
Patel, Wolde, Pohlman, Hall, & Kress (2016), found that the countless disadvantages with the facemask make it ineffective at preventing intubation in ARDS patients. Although the face mask is extremely effective for patients with COPD and cardiogenic pulmonary edema, the evidence does not support its use in patients with ARDS. With the face mask, the PEEP needed to be increased in order to improve oxygenation. At a higher level of PEEP, however, “face mask intolerance and air leak can impede effective oxygenation†(2). Noninvasive ventilation, however, has countless benefits including allowing patients to remain conscious and alert while in the ICU as Intubated patients are often sedated to reduce agitation and allow them to improve oxygenation. The most common reason for intubation differed between the two groups as well. In the face mask group, respiratory failure was the main reason for intubation, whereas it was neurological failure in the helmet group. The helmet was designed to prevent an air leak while allowing increased titration of positive airway pressure. It is also not without its risks like CO2 rebreathing and patient-ventilator dyssynchrony.
Ultimately, innovative strategies are continually being developed to improve patient outcomes for ARDS. As more providers realize the unnecessary risks of intubation, new methods of oxygen delivery are being used. The helmet allowed patients to avoid invasive ventilation and reduce mortality. Nurses working with the multidisciplinary team can suggest these novel approaches to spare their patients from unnecessary intubation and sedation.
Article 2:
Frat, Thille, Mercat, Girault, & Ragot (2015), set out to shed light on the effectiveness of high flow oxygen through a nasal cannula (HFNC) in ARDS patients. 310 patients met the criteria set by the researchers. They were divided into three groups with each group using a different oxygen therapy. One group used the HFNC, the second has standard oxygen therapy, and the third group had NIV. The standard oxygen group received continuous oxygen through a nonrebreather mask at 10 L/min. Oxygen saturations were to be maintained about 92% and so the flow rate was adjusted accordingly. The high flow oxygen was delivered through a specific nasal cannula after it was heated and humidified. A rate of 50L/min and an FiO2 of 1.0 was applied initally. To maintian SpO2 above 92%, the FiO2 was titrated. Standard oxygen therapy could be initated on these pateints after the HFNC was on for two calander days. A face mask was the method of delivery for the NIV group. Pressre support was applied and adjusted through the ventilator with the inital goal of an expired tidal volume of 7-10 mL/kg with a PEEP between 2-10 cm. The PEEP and FiO2 were adjusted to maintain SpO2 above 92%. NIV was required to be used for 8 hrs/day for at least 2 calander days.Although it was only applied in sessions at 1 hour, it could be applied again if the respiratory rate was over 25 breaths per minute or if the SpO2 was less than 92%. In the time when NIV was not applied, the patients received HFNC.
Article 3:
A study performed by Sehgal, Chaudhuri, Dhooria, Agarwal, & Chaudry (2015), aimed to investigate if the complications associated with endotracheal intubation could be avoided by using non-invasive ventilation instead. The benefits of NIV, including improving oxygenation, reducing dyspnea, and unloading respiratory muscles, are compelling reasons to use therapy this as a firstline treatment. In their study, 41 participants were admitted with diagnoses of mild-moderate ARDS. The study included only patients with “mild to moderate ARDS, two or less organ system involvement, and absence of shock at presentation†(10). As this study was done in India, the most common causes of ARDS were tropical infections and abdominal sepsis. All 41 patients were started on NIV for 24 hours. Depending on how the patient responded to NIV, they were either weaned off of NIV or intubated.
The decision to wean patients off NIV was made if they could maintian an SpO2 over 92% on FiO2 of 30% and the respiratory rate was 30 breaths/min or less. If the patient met the criteria of NIV failure, however, they qualified for intubation. The parameters for NIV failure in this study were, “Worsening of dyspnea, worsening of or lack of improvement in hypoxemia, persistence of respiratory rate >35 breaths/min, appearance of respiratory acidosis, circulatory shock, or altered sensorium (10). The primary outcome for this study was the number of patietns who were not intubted. Secondary outcomes included the duration of NIV, ICU stay, hospital mortality and improvement in ABGs at 1 and 4 hours.
NIV was only successful in 18 of the 41 patients (44%), the other 23 participants were intubated. Most common causes for intubation were refractory hypoxemia, shock, altered mentation, and mixed metabolic and respiratory acidosis. The duration of ventilation was substantially longer for the patients requiring intubation compared to NIV. The length of stay in the ICU was the same in both groups. None of the patients in the NIV success group died, whereas 19 of the 23 participants in the NIV faiure group died.
It should be noted that unfortuantely, the method of NIV was not listed in the study. As was discoverd in the aformentioned studies, the method of delivery with NIV is crucial.*****CONT.