Acute Respiratory Distress Syndrome ARDS

• There is lung injury manifested as increased perme­ability of alveolar capillary membrane, diffuse alveo­lar damage, proteinaceous pulmonary edema.
• Age: ARDS or Acute Respiratory Distress Syndrome may occur in children or adults.
• Syndrome characterized by abrupt onset of diffuse lung injury with severe hypoxemia and bilateral pulmonary infiltrates
• Absence of left atrial hypertensiom (HTN)
• By consensus, PaO₂/FiO₂ <200
• Most severe form of acute lung injury
• System(s) affected: Pulmonary; Cardiovascular
• Synonym(s): Shock lung; Wet lung; Noncardiac pulmonary edema
• Acute respiratory distress syndrome (ARDS) develops rapidly and includes severe dyspnea and hypoxemia;
• it typically causes respiratory failure.
• Key diagnostic criteria for ARDS include  diffuse bilateral pulmonary infiltrates on chest x-ray (CXR);   Pa_O2 (arterial partial pressure of oxygen in mmHg)

Criteria of ARDS

• Severe hypoxemia
• Decreased pulmonary compliance
• Diffuse pulmonary infiltrates on chest X-ray.
• It is a form of noncardiogenic pulmonary edema. Acute Lung Injury (ALI) is a less severe form of ARDS.

All criteria

• Acute onset
• PaO2/FI0₂ < 300mg Hg
• Chest X-ray – Bilateral infiltrates.
• PAP –< 18 mmHg (Pulmonary artery pressure is less than 18mmHg).
• No clinical evidence of left atrial hypertension.

ARDS criteria

• Acute onset
• PaO2/FI0₂ < 200mg Hg
• Bilateral infiltrates.
• PCWP ~ 18 mmHg (Pulmonary capillary wedge pres­sure is less than 18mmHg).
• No clinical evidence of increased LA pressure.

 Predisposing factors

• Severe sepsis, trauma, aspiration of gastric contents. 40% of these will develop ARDS.
•  A H/O chronic alcohol abuse increases risk of ARDS.
• ARDS occurs within 5 days of the precipitating event.
•   50% develop within 1 day.

Risk Factorsfor Acute Respiratory Distress Syndrome (ARDS)

• Severe infection (localized or systemic ) most common
• Aspiration of gastric contents
• Shock
• Infection
• Lung contusion
• Nonthoracic trauma
• Toxic inhalation
• Near drowning
• Multiple blood transfusions

Clinical feature of ARDS

• There is : Increased respiratory rate
• Dyspnoea
• In sepsis there is increased ne.
• In pancreatitis, there is increased serum amylase level.

Physical Exam in ARDS

• Flat neck veins
• Hyperdynamic pulses
• Physiologic gallop
• Absence of edema
• Tachypnea and tachycardia during the 1st 12– 24 h; respiratory distress
• Lethargy, obtundation
• Moist, cyanotic skin: Manifestations of underlying disease

X-ray:

• diffuse infiltrates with heterogenous pattern – more in dependent lung.

Pathophysiology of Acute Respiratory Distress Syndrome (ARDS)

• 3 phases:
  • Acute exudative phase: Characterized by profound hypoxia and associated with inflammation with infiltration of inflammatory and proinflammatory mediators and diffuse alveolar damage
  • Fibrosing alveolitis phase: Coincides with recovery or after ~1–2 weeks; patients continue to be hypoxic and have increased dead space and decreased compliance.
  • Resolution may require 6–12 months.
• Heightened inflammatory response Initiation
• Acceleration
•   Injury.

Causes of Acute Respiratory Distress Syndrome (ARDS)

• Trauma
• Aspiration of gastric contents –
• Drowning
• Contusion to lungs
• Toxin inhalation
• Sepsis syndrome
• Non-thoracic trauma
• Pancreatitis
• CABG.
• There is mediator and cytokine-release like TNF alpha interleukin-
• 1. Neutrophils cause acceleration of rseponse
• Release of oxygen, metabolites and proteases causes injury leading to MODS (Multiple Organ Dysfunction, Syndrome).

• Pulmonary edema
• Bronchial wall edema
• Narrowing of bronchi leading to :
• Bronchospasm
• High pulmonary vascular resistance
• High pulmonary arteriolar pressure due to
• release of thromboxane A2 and leukotrines.
• There may be recovery or chronic pulmonary disease. Chronic changes in lung often leads to death.

Treatment of Acute Respiratory Distress Syndrome (ARDS)

• No single drug or combination of drugs prevents or treats full-blown ARDS. Treatment is supportive while addressing the underlying cause.
• Supplemental oxygen
• Ventilatory support most often requires endotracheal intubation with emphasis on lower tidal volumes per weight and optimization of positive end-expiratory pressure (PEEP).
• 02 inhalation is not effective.
• Mechanical ventilation should be instituted. Mechanical ventilation can lead to 02 toxicity, barotrauma, pneumothorax, pneumo-mediasti­num, SIC emphysema.
• Tidal volume of 10 ml/Kg can lead to barotrauma. Maximum inflation pressure < 35cm H₂0.
• Tidal volume should be <6 ml/kg.
• FI0₂ is kept < .6
• Pa0₂ maintained at 60 mmHg.
• PEEP added 5 cm H₂0 up to 20 cm H₂0. Restriction of fluids.
• Inotropic agents: Dobutamine to maintain adequate cardiac output after appropriate fluid resuscitation fails to restore perfusion
• Deep vein thrombosis (DVT) prophylaxis
• Ulcer prophylaxis
• Inhaled B₂ agonists may be helpful during the resolution phase.
• Maintain lowest possible intravascular hydrostatic pressure.
• Hypercapnia, respiratory acidosis occurs with mechanical ventilation called permissive hyper­capnia.
• Steroids may be given. Give surfactants, nitric oxide inhalation to reduce pulmonary arterial pressure.
• Mortality 50% to 70% Early mortality <3 days Late mortality >3 days