Acute Respiratory Distress Syndrome (ARDS)

Definition

Acute Respiratory Distress Syndrome (ARDS) [Chest X-ray R]

• Is a life-threatening serious illness characterized by hypoxic pulmonary infiltrates and acute onset.
• At the microscopic level, the disease is associated with capillary endothelial damage and diffuse alveolar damage.
• It has a high mortality rate and there are few effective treatment modalities to combat the condition.
• Once ARDS occurs, patients usually experience varying degrees of pulmonary artery vasoconstriction, which may subsequently develop pulmonary hypertension.

ARDS definition

• An acute illness, beginning within 7 days of the irritant event, characterized by bilateral lung infiltrates and severe progressive hypoxemia without any evidence of cardiogenic pulmonary edema.
• Defined as the ratio of oxygen in a patient’s arterial blood (PaO2) to oxygen in inspired air (FiO2). These patients have PaO2/FiO2 ratios below 300. The definition of ARDS was updated in 2012 as the Berlin definition [1].

Etiology

ARDS has many risk factors.

• Lung infections such as ARDS and COVID-19 infection vary between 17% and 41% [2]
• Pulmonary aspiration
• Extrapulmonary sources include sepsis, trauma, massive transfusion, drowning, drug overdose, fat embolism, toxic fume inhalation, and pancreatitis (these extrathoracic diseases and/or injuries trigger an inflammatory cascade that ultimately leads to lung injury) [1].

Some risk factors for ARDS include:

• Advanced age
• Female gender
• Smoking
• Alcohol use
• Aortic vascular surgery
• Cardiovascular surgery
• Traumatic brain injury

Epidemiology

• The estimated incidence of ARDS in the United States ranges from 64.2 to 78.9 cases per 100,000 person-years.
• 25% of ARDS cases are initially classified as mild (1/3 will progress to severe or moderate), and 75% of cases are moderate or severe.
• A review of the literature showed that the death rate fell by 1.1% per year between 1994 and 2006.
• The mortality rate of ARDS depends on the severity of the disease, with mortality rates of 27%, 32% and 45% for mild-moderate and severe disease, respectively [1].
• The prevalence of ARDS patients varies widely between geographic regions. Although the reason for the discrepancy is unclear, some have speculated that it may stem from differences in healthcare systems [3]. The ability to diagnose and differentiate secondary disease is Patients need to be properly documented and treated.

Pathological Process

ARDS represents stereotyped responses to various etiologies.

It progresses through different phases

1. Stage 1 – Damage to the alveolar-capillary barrier leading to pulmonary edema. Pulmonary epithelial and endothelial injury is characterized by inflammatory cell apoptosis and increased alveolar capillary permeability, leading to the development of alveolar edema and alveolar edema. Proteinosis. There is bidirectional leakage of fluid and protein into the alveoli, and bidirectional leakage of surfactant proteins and alveolar cytokines into plasma. The epithelial barrier is disrupted as type 2 alveolar cells proliferate, leading to surfactant dysfunction. alveolar edema This in turn reduces gas exchange leading to hypoxemia.
2. Proliferative phase – characterized by improved lung function and healing
3. Final fibrotic stage – marks the end of the acute disease process. Surfactant turnover was markedly increased, and intraepithelial fluid also highlighted fibrotic alveolitis early in the lung injury process.

• A hallmark of the damage pattern seen in ARDS is that it is heterogeneous. Lung segments may be more severely affected, resulting in reduced local lung compliance, which usually involves the base more than the apex.
• This difference in intrapulmonary pathology results in different responses to oxygenation strategies. While increasing positive end-expiratory pressure (PEEP) may improve oxygen diffusion in affected alveoli, it may cause deleterious volutrauma and atelectasis of adjacent unaffected alveoli. [1]

This 100 second video is a great introduction to ARDS

Cellular Involvement in ARDS:

• Neutrophils: Most abundant in epithelial lining and alveolar histology specimens. Although the chemotaxis of neutrophils across the epithelium does not cause damage, their proinflammatory nature releases reactive oxygen cytokines and many inflammatory mediators lead to damage to the basement membrane.
• Alveolar Macrophages: These are the most common cell type, and interstitial macrophages play an important role in defense. In patients with ARDS, the number of alveolar macrophages gradually increases.
• Epithelial cells: Contained within the alveolar epithelium are the highly metabolically active type 2 alveolar cells. Damaged epithelium leads to dysfunctional surfactants

Clinical Presentation and Assessment

The syndrome is characterized by :

• Dyspnea and hypoxemia develop gradually over hours to days, often requiring mechanical ventilation and intensive care unit-level care.
• The medical history aims to determine the underlying cause of the disease.
• When interviewing patients who were able to communicate frequently, they initially complained of mild dyspnea, but within 12-24 hours the respiratory distress escalated to severe requiring mechanical ventilation to prevent hypoxia.
• In the case of COVID 19 pneumonia or sepsis, the etiology may be obvious. In other situations, however, asking patients or relatives about recent exposures may be paramount for identifying pathogens.

The Physical Assessment may find

• Acute inflammatory phase: lasts 3-10 days, leading to hypoxemia and multiorgan failure. Patients typically present with progressive dyspnea, tachypnea, cyanosis, hypoxia, confusion, and pulmonary crackling.
• Systemic symptoms (depending on severity of disease), such as central or peripheral cyanosis due to hypoxemia, tachycardia, and altered mental status.
• Despite having 100% oxygen, the patient’s oxygen saturation remains low. Auscultation of the chest usually reveals rales, especially bibasal rales, but usually the entire chest is auscultated. [1]
• Healing proliferative phase: During this phase, lung scarring and pneumothorax are common

Note that secondary systemic and chest infections can occur during both stages.

Diagnostic Procedures

Diagnosis will be made by reviewing your medical history, physical examination and test results, according to the National Heart, Lung, and Blood Institute [4].

Medical History

• History of heart failure
• Does the patient have any direct or indirect clinical risk factors for ARDS?

Physical Examination

• Add breath sounds (such as crackling) to auscultation
• Heart auscultation
• Cyanosis

Test Results

• Arterial blood gases
• Chest x-ray
• Blood Tests
• Sputum Culture
• CT Scan
• Heart Failure Examination

Management / Interventions

Unfortunately, no medicines have been shown to be effective in preventing or managing ARDS.

The main treatment strategy is supportive care, focusing on

1. Reducing shunt fraction,
2. Increasing oxygen delivery
3. Decreasing oxygen consumption,
4. Avoiding further injury.

Patients are mechanically ventilated with diuretics to prevent fluid overload and given nutritional support until signs of improvement are observed.

The pattern of patient ventilation has an effect on lung recovery. There is evidence that certain ventilation strategies exacerbate alveolar damage and perpetuate lung damage in the setting of ARDS.

• Take care to prevent volutrauma (exposure to large tidal volumes), barotrauma (exposure to high plateau pressure), and atelectasis (exposure to atelectasis). [1]

Possible Interventions for ARDS

Carefully consider the risks and rewards of intervention, especially when the lungs are fragile

• Suctioning (Open / Closed)
• Ventilator Hyperinflation (VHI)  
• Positioning (see below).

Ventilator Hyperinflation (VHI)

A systematic review by Anderson et al (2015) [5] found that manual and ventilator hyperinflation had similar effects on secretion-clearing lung compliance, improving atelectasis and oxygenation without adverse cardiovascular effects Stability creates adverse risks. However, a manometer should be used Particular attention was paid to contraindications throughout the intervention.

Since high levels of PEEP are required to maintain lung recruitment in ARDS patients, hyperinflation delivered with a ventilator is ideal. In addition, the VHI allows continuous monitoring and monitoring of airway pressure, thereby titrating the delivered volume accordingly.

Prone Positioning

Prone positioning of patients with ARDS results in a significant increase in PaO2 in approximately 70% of patients. Dorsal lung recruitment can be improved by placing the patient in the prone position, resulting in a more even distribution of perfusion and improved V/Q match.

Evidence suggests that prone positioning is particularly beneficial in severely hypoxemic/severe ARDS patients, reducing ICU mortality without increasing airway complications.

• Explain and reassure patients that they will be safe and obtain consent if they are able to communicate.
• Close eyes and protect with gel or pad.
• Place the patient’s palms on the thighs, thumbs up, elbows straight, shoulders neutral.
• Use the sliding sheet to slide the patient over the edge.
• Roll the patient onto their side using the underlying sheet.
• Roll patient into prone.
• “Swimmer’s position” – the elbow with the head half-rotated should be bent no more than 90° to avoid pulling on the ulnar nerve and inward rotation of the other arm.
• Make sure there is no pressure on women’s breasts or men’s genitals.
• Place two pillows under each lower leg to prevent stretching of the peroneal nerve, placing them in a position to avoid the pressure of the mattress on the knees and toes.

Mechanical Ventilation

Mechanical ventilation is commonplace due to acute episodes of hypoxic respiratory failure and increased work of breathing. The pathophysiology of ARDS, particularly the fibrotic aspect, means that the approach and provision of support needs to be carefully considered to ensure Ventilator-induced lung injury (VLII) does not occur [6]

In ARDS patients, PEEP and tidal volume must be reduced to reflect the available fraction of the lungs available for ventilation. Otherwise, due to reduced lung compliance, this can lead to hyperstretching of the lungs, known as volutrauma. Repeated opening and closing of alveoli during Tidal swelling can also cause damage to lung tissue, known as pulmonary trauma. If the patient is not mechanically supported, both pulmonary trauma and volutrauma increase cytokines within the lung tissue, which may then enter the systemic circulation and potentially lead to a variety of diseases Organ failure [6]

Although the diagram below may be oversimplified, it attempts to highlight the optimal areas for ventilation in ARDS patients. The lower inflection point (LIP) is considered the pressure at which lung tissue is recruited. Upper Inflection Point (UIP) is the approximate pressure at which The alveoli become overinflated, which can cause damage. Therefore, the optimal ventilation location will be between the two steepest and most complex inflection points of the curve [7].

Moloney and Griffiths (2004)

Inverse Ratio Ventilation (IRV)

This mode of ventilation requires changing the normal inspiratory/expiratory ratio from 1:2 to 1:1 or 2:1. Although this mode of ventilation is intended to increase ventilation and collateral ventilation of poorly compliant lungs, the reduced expiratory time may lead to increased PCO2. However, if the hypercapnic acidosis occurs slowly, the intracellular acidosis will be well compensated, but any form of hypercapnia should be avoided in such cases or in persons at risk for increased intracranial pressure. This is called permissive hypercapnia.

A recent small study by Kotani et al (2016) [8] demonstrated that IRV provided acceptable gas exchange in 13 ARDS patients without complications.

Airway Pressure Release Ventilation (APRV)

This form of mechanical ventilation involves delivering CPAP in intermittent release phases. Long-term delivery of CPAP is thought to maintain adequate lung volume and alveolar recruitment, release designed to help remove CO2. Inspiration starts with more Beneficial pressure-volume relationship, thus facilitating oxygenation [9].

High Frequency Oscillation (HFO)

When using HFO, a continuous distending pressure (CDP) is set and an oscillating pump is used to deliver small tidal volumes at high frequency. As others have described before, this is another form of lung-protective ventilation with sustained lung recruitment. A systematic review by Sud et al. (2010) [11] found that HFO may improve survival and is less likely to cause harm, analyzing only 8 studies with fewer patients and wide confidence intervals. There are also no reports of blinding outcome assessors placing trials at risk of bias [11].

Extracorporeal Membrane Oxygenation (ECMO)

ECMO can be used in those patients with severe respiratory failure and when conventional treatments cannot maintain adequate oxygenation. ECMO can completely replace the function of the lungs, but due to various complications, risks and benefits need to be considered.

ECMO consists of an extracorporeal blood circuit through an oxygenator and a pump. Two vascular accesses are established, one for removal of venous blood and one for infusion of oxygenated blood. After blood is drawn from a large vein, it is pumped through a circuit containing an oxygenator Oxygenates blood and removes carbon dioxide. The blood is then returned through another cannula [12].

Inhaled Nitric Oxide

Nitric oxide is not only an endothelium-derived smooth muscle relaxant, it also contributes to neurotransmitter host defense against platelet aggregation and bronchodilation. Inhaled nitric oxide can be delivered continuously or injected using intermittent inhalation, a 20% increase in PaO2 is considered Respond positively. Nitric oxide inhalation improves oxygenation in 40% – 70% of ARDS patients, and it is usually used only as a temporary rescue in severely hypoxemic patients. [6]

Role of the Physiotherapist

Input from physical therapy is usually limited and minimal due to the high PEEP and high oxygen demand required. Since it is an interstitial lesion, discharge is generally not a problem. Treatment may consist only of positioning, such as lying prone to optimize gas exchange. need to be cautious Use a hands-on technique as you want to make sure you don’t lose the splinting effect of the ventilator’s PEEP on the lung unit. If discharge becomes a problem, ensure adequate humidification and other techniques to improve mucus clearance. Take minimal aspiration through the ETT. state-of-the-art review It is recommended to avoid repeated airway clearance in infants and children with acute lung disease [13].

Conclusions

• Although many risk factors for ARDS are known, ARDS cannot be prevented.
• Careful fluid management in high-risk patients may be helpful.
• Measures should be taken to prevent aspiration by elevating the head of the bed before feeding.
• Lung-protective mechanical ventilation strategies in high-risk non-ARDS patients can help prevent ARDS [1].

Resources

• Cochrane Review: Recruitment strategies for mechanically ventilated adults with acute respiratory distress syndrome
• Cochrane Review: Pressure-controlled versus volume-controlled ventilation in acute respiratory failure due to acute lung injury (ALI) or acute respiratory distress syndrome (ARDS)
• Cochrane commentary: High versus low positive end-expiratory pressure (PEEP) levels in mechanically ventilated adults with acute lung injury and acute respiratory distress syndrome
• Cochrane Review: Extracorporeal membrane oxygenation in critically ill adults
• Acute Respiratory Distress Syndrome. berlin definition
• ARDSNet: Summary of Mechanical Ventilation Protocols