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I have completed bits of my EM training from India. Currently I am boarded with credentials from Christian Medical College, Vellore and also from the prestigious Royal College of Emergency Medicine, UK.  I am currently working in London as an A&E doctor, trying to appreciate the differences in the practise and culture of Emergency Medicine across different healthcare systems. I have always been an avid FOAMed supporter because FOAMed played an indispensable role during the days of my initial training. Through this blog, I aspire to disseminate knowledge and stay up to date with the EM literature. 

Monday, August 3, 2015

ARDS: Rapid Review

Introduction
  • ARDS is diffuse inflammatory injury of the lungs.
  • It causes refractory hypoxemia and diffuse infiltrates on CXR due to dense infiltration of the lungs with an inflammatory exudate.
  • AKA shock lung, stiff-lung syndrome, leaky capillary pulmonary edema, noncardiogenic pulmonary edema, acute lung injury, adult respiratory distress syndrome.

Etiology
Direct
Indirect
Pnemonia
Sepsis
Aspiration
Trauma
Inhalational Injury
Burns
Drowning
Pancreatitis
Fat emboli
Blood Transfusion
Pulmonary Contusion
Shock

Pathogenesis
  • Circulating neutrophils are activated that lead to their sequestration in the pulmonary microcirculation and entry into the lung parenchyma.
  • Neutrophils degranulate to release proteolytic enzymes and toxic oxygen metabolites causing damage of the capillaries leading to exudation of protein-rich fluid, erythrocytes, and platelets into the lungs.
  • The cellular and proteinaceous exudation eventually fills and obliterates the distal airspaces causing hypoxia.
  • Progressive inflammation results in fibrin accumulation, leads to structural remodeling and pulmonary fibrosis.

Clinical Features
  1.  Acute onset
  2.  Bilateral infiltrates on CXR
  3.  P/F ratio < 300mm Hg
  4.  No evidence of LVF or fluid overload
  5.  Presence of a predisposing condition
Caveat: CXR can be unrevealing in the first few hours after symptom onset.

Diagnostic Criteria:

In 1994, expert consensus gave a diagnostic criteria that included:
  • PaO2/FIO2 200 mm Hg for ARDS
  • PaO2/FIO2 300 mm Hg for ALI (Acute Lung Injury)\
  • Pulmonary artery wedge pressure (PAWP) 18 mm Hg (to rule out LVF)

In 2012, European task force revised the criteria (Berlin Criteria):
  • ALI was eliminated as a clinical entity, and the PaO2/FIO2 for ARDS was set at 300 mm Hg
  • PaO2/FIO2 determination should be conducted at a PEEP of 5 cm H2O
  • PCWP measurement was eliminated

Problems with these criteria:
  •       Non-specific
  •       Tendency for misdiagnosis
  •       PAWP is problematic because the wedge pressure is not a measure of capillary hydrostatic pressure. It is measured in the absence of blood flow and this can lead to over diagnosis of ARDS. In reality, only half of the patients with the premortem diagnosis of ARDS had postmortem evidence of ARDS.

Frequent imitators: Pneumonia and hydrostatic pulmonary edema

The classic radiographic appearance of ARDS as shown in the image below is not always seen. CXR often mimics cardiogenic pulmonary edema. So, CXR alone should not be used to exclude ARDS.
Classic ARDS. fine granular infiltrates with “ground glass” appearance, evenly distributed throughout both lungs, with relative sparing of the lung bases.

Atypical CXR for ARDS – Hilar infiltrates confined to the lower lung fields, obliteration of the left hemidiaphragm suggesting pleural effusion. These features could be mistaken for hydrostatic pulmonary edema

Bronchoalveolar Lavage (BAL)
  • Reliable method for distinguishing between ARDS and cardiogenic pulmonary edema.
  • BAL fluid is analyzed for the presence of neutrophils and protein.
  • Normal lavage fluid has < 5% neutrophils and in ARDS up to 80% neutrophils can be seen. A low neutrophil count in lung lavage fluid almost excludes the diagnosis of ARDS.

MANAGEMENT ARDS
The treatment of ARDS should begin by treating the inciting condition, follwed by:
1. Fluid Management
Try and maintain a neutral fluid balance without under and overhydrating them. Unwanted fluid accumulation in the lungs can aggravate the respiratory failure. Literature has shown that avoiding a positive fluid balance in patients with ARDS can reduce the time on mechanical ventilation and mortality.
2. Steroids
No consistent survival benefit. Some possible benefits are reduction in markers of inflammation, improved gas exchange, shorter duration of mechanical ventilation, and shorter length of stay in the ICU.
Recommended only in cases of early severe ARDS and unresolving ARDS.
Early Severe ARDS: PaO2/FIO<200 mm Hg with PEEP of 10 cm H2O.
Unresolving ARDS: In cases where ARDS does not begin to resolve after 7 days, but should begin no later than 14 days after the onset of illness. Steroids can also help to halt the progression to pulmonary fibrosis.
3. Ventilation strategies 
Mechanical ventilation can damage the lungs in ARDS as a result of overdistension of functional alveoli (volutrauma) and collapse of small airways (atelectrauma). Lung protective Ventilation (LPV) is a standard method of mechanical ventilation in ARDS.
  •       TV: 4-8ml/kg IBW
  •       Start with a PEEP of 5cm H2O and titrate
  •       Select lowest FIO2 to achieve a targets SpO2 of 88-95%
  •       Plateau Pressure < 30cm H2O
  •       Accept Permissive Hypercapnia

Lets look at some basic ventilator related terminologies before we go further:
Ventilator-induced lung injury (VILI): With large tidal volumes, distal airspaces may develop stress fractures in the alveolar capillary interface leading to infiltration of the lung parenchyma with an inflammatory exudate. This is a volume-related lung injury (volutrauma). Use low TV to prevent volutrauma.  
Biotrauma: During large-volume mechanical ventilation, proinflammatory cytokines  appear in the lungs and systemic circulation. This can cause biotrauma via further neutrophil activation and inflammatory infiltration in the lungs. 
Atelectrauma: Mechanical ventilation is associated with cyclic opening and closing of small airways, and this can be another source of lung injury called as atelectrauma that eventually damages the airway epithelium. Use PEEP to prevent atelectrauma.

ARDS lungs are baby lungs..
In the past, large tidal volume ventilation (12-15ml/kg) was a standard practice to reduce the tendency for atelectasis during mechanical ventilation. But in patients with ARDS, these large inflation volumes are delivered into lungs that have only a fraction of the normal functional lung volume (lung volumes markedly reduce in ARDS aka baby lungs), this may result in over distension and rupture of the distal airspaces.
Below is a CT image that reveals the usual areas of lungs affected by ARDS (posterior) and the functional portion of unaffected lungs (anterior).
CT (ARDS): Lung consolidation is confined to the posterior lung regions, which are the dependent regions in the supine position. The uninvolved lung in the anterior one-third of the thorax represents the functional portion of the lung.

Positive End-Expiratory Pressure (PEEP) – Prevent Atelectrauma
Use PEEP of at least 5 cm H2O to prevent the collapse of small airways at the end of expiration. The goal is to prevent the cyclic opening and closing of small airways and reduce the risk of atelectrauma. Go further up on PEEP if there is a problem in maintaining pO2 and FIO2 > 50% is required.
Permissive Hypercapnia
One of the consequences of low tidal volume ventilation is a decrease in CO2 elimination in the lungs, which can result in hypercapnia and respiratory acidosis. To get the benefits of low volume ventilation, hypercapnia is allowed to persist as long as there is no evidence of harm (permissive hypercapnia). An arterial PCO 2 levels of 60–70 mm Hg and arterial pH levels up to 7.2–7.25 are acceptable.
ARDS Network: Lung protective ventilation is one of the few measures that has been shown to improve survival in ARDS. The largest trial was conducted by the ARDS Network has shown that ventilation with the lower tidal volume (6 mL/kg) was associated with a shorter duration of mechanical ventilation and reduced mortality.

Other therapies to improve arterial oxygenation for refractory hypoxemia:
  • High Frequency Oscillatory Ventilation: deliver small tidal volumes (1–2 mL/kg) using rapid pressure oscillations (300 cycles/min). This again limits the risk of volutrauma and atelectrauma. No survival benefit.
  • Inhaled Nitric Oxide: Selective pulmonary vasodilator that can improve arterial oxygenation in ARDS by increasing flow to areas of high dead space ventilation. No associated survival benefit. Watch for methemoglobinemia and renal dysfunction.
  • Prone Position: Can improve pulmonary gas exchange by diverting blood away from poorly aerated lung regions in the posterior thorax and increasing blood flow in aerated lung regions in the anterior thorax. Some improvement in mortality if combined with LPV. Issues:  labor intensive, problems with nursing care.
  • ECMO: Variable success in patients with refractory hypoxemia, last option.

Key Points:     
  • ARDS is not limited to lungs. It is a systemic inflammatory condition and majority of them succumb to MODS, not respiratory failure.
  • Diagnostic criteria for ARDS are non-specific.
  • A negative BAL almost excludes the diagnosis of ARDS.
  • Use lung protective ventilation in ARDS (TV: 4-8ml/kg IBW, PEEP of 5cm H2O,  SpO2 of 88-95%, Plateau Pressure < 30cm H2O, accept permissive hypercapnia)
     
       


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