Acute Respiratory Distress Syndrome

Acute Respiratory Distress Syndrome

Acute Respiratory Distress Syndrome

On this page

PARDS Intro - Tiny Lungs, Big Trouble

  • Pediatric Acute Respiratory Distress Syndrome (PARDS): Acute, diffuse, inflammatory lung injury leading to respiratory failure.
  • Hallmarks: ↑ pulmonary vascular permeability, protein-rich alveolar edema, ↓ lung compliance, and severe hypoxemia.
  • Pathophysiology: Diffuse alveolar damage (DAD) → endothelial & epithelial injury, surfactant dysfunction, hyaline membrane formation. PARDS Pathophysiology: Alveolar Damage and Edema
  • PALICC 2015 Diagnostic Criteria:
    • Timing: Onset within 7 days of a known clinical insult.
    • Chest Imaging: New infiltrate(s) consistent with acute pulmonary parenchymal disease.
    • Origin of Edema: Respiratory failure not fully explained by cardiac failure or fluid overload.
    • Oxygenation Impairment (non-cyanotic children, invasive ventilation): Oxygenation Index (OI) $\geq$ 4 or Oxygen Saturation Index (OSI) $\geq$ 5 (if SpO₂ $\leq$ 97%).

    ⭐ A key feature of the PALICC definition is the use of Oxygenation Index (OI) or Oxygen Saturation Index (OSI) to objectively define and stratify PARDS severity, replacing the PaO₂/FiO₂ ratio used in adult ARDS definitions for younger children or when PaO₂ is unavailable.

PARDS Causes - The Usual Suspects

  • Direct Lung Injury (Pulmonary Origin):
    • Pneumonia (bacterial, viral, fungal)
    • Aspiration (gastric contents, meconium)
    • Inhalation injury (smoke, toxins)
    • Lung contusion (trauma)
    • Near-drowning
  • Indirect Lung Injury (Extrapulmonary Origin):
    • Sepsis
    • Severe trauma with shock
    • Major burns
    • Pancreatitis
    • Multiple transfusions (TRALI)
    • Drug overdose (e.g., salicylates)

⭐ Pneumonia is the most common direct cause, and sepsis is the most common indirect cause of PARDS.

PARDS Signs & Dx - Spotting the Storm

  • Signs: Rapid dyspnea, tachypnea, ↑ work of breathing, refractory hypoxemia, cyanosis.
  • Dx Criteria (PALICC 2015): 📌 T-I-O-O
    • Timing: Within 7 days of insult.
    • Imaging: New bilateral opacities (CXR/CT). CXR of pediatric ARDS with bilateral opacities
    • Origin: Edema not from cardiac failure/fluid overload.
    • Oxygenation: Impaired (see flowchart).

PARDS Severity (Invasive Ventilation):

  • Mild: OI 4 to <8; OSI 5 to <7.5
  • Moderate: OI 8 to <16; OSI 7.5 to <12.3
  • Severe: OI ≥16; OSI ≥12.3
  • OI = $MAP \times FiO_2 \times 100 / PaO_2$
  • OSI = $MAP \times FiO_2 \times 100 / SpO_2$

PARDS Management - Gentle Breaths, Big Support

  • Lung Protective Ventilation (LPV): Cornerstone strategy.
    • Tidal Volume (Vt): $4-8$ mL/kg PBW.
    • Plateau Pressure (Pplat): Target < $28-30 \text{ cm H}_2\text{O}$.
    • Driving Pressure ($\Delta P$ = Pplat - PEEP): Aim < $15 \text{ cm H}_2\text{O}$.
    • Permissive Hypercapnia: Tolerate $\uparrow P_aCO_2$; target pH > $7.20$.
    • PEEP: Titrate for SpO2 88-92% & lung mechanics.
  • Conservative Fluid Management: Maintain euvolemia, avoid overload.
  • Prone Positioning: Early for moderate-severe PARDS ($P_aO_2/F_iO_2 < 150$); 12-16 hrs/day.
  • Sedation & Analgesia: Optimize comfort, facilitate ventilator synchrony.
  • Neuromuscular Blockade (NMB): Short course for early, severe PARDS ($P_aO_2/F_iO_2 < 120$).
  • Rescue Therapies: HFOV, iNO, ECMO for refractory hypoxemia.

⭐ Target tidal volumes in LPV for PARDS: $4-8$ mL/kg PBW, aiming for pH > $7.20$ to minimize ventilator-induced lung injury (VILI).

PARDS Outcomes - The Aftermath

  • Mortality: Varies (18-30%), higher with comorbidities.
  • Short-term Complications:
    • Ventilator-associated pneumonia (VAP)
    • Barotrauma (pneumothorax, pneumomediastinum)
    • Nosocomial infections
    • Multiple organ dysfunction syndrome (MODS)
  • Long-term Sequelae (Survivors):
    • ↓ Lung function (months to years)
    • Neurocognitive impairment
    • Post-traumatic stress disorder (PTSD)
    • ↓ Quality of life

⭐ Common complications include ventilator-associated pneumonia (VAP) and barotrauma. Significant long-term sequelae in pediatric survivors can include impaired lung function and neurocognitive deficits persisting for months to years post-discharge, impacting their overall quality of life and development trajectory after critical illness from PARDS episodes requiring intensive care unit (ICU) admission and mechanical ventilation support strategies during their hospital stay for acute respiratory distress syndrome management protocols implemented by healthcare providers in pediatric intensive care units (PICU).

High‑Yield Points - ⚡ Biggest Takeaways

  • PARDS diagnosis uses PALICC criteria, adapted from adult Berlin definition.
  • Acute hypoxemia (PaO2/FiO2 ≤ 300) and new bilateral pulmonary opacities on imaging.
  • OI & OSI stratify severity (e.g., OI > 16 or OSI > 12.3 for severe PARDS).
  • Lung-protective ventilation (LPV): low tidal volumes (~6 mL/kg PBW), optimal PEEP.
  • Prone positioning & ECMO for severe, refractory hypoxemia.
  • Conservative fluid management crucial; avoid overload.
  • High mortality, especially with sepsis or immunocompromise.

Practice Questions: Acute Respiratory Distress Syndrome

Test your understanding with these related questions

Following tests are done for assessing fetal lung maturity. Which of the following test results does not indicate adequate fetal lung maturity?

1 of 5

Flashcards: Acute Respiratory Distress Syndrome

1/9

Treatment of Reye's syndrome involves infusion of 20% _____ and fresh frozen plasma

TAP TO REVEAL ANSWER

Treatment of Reye's syndrome involves infusion of 20% _____ and fresh frozen plasma

glucose

browseSpaceflip

Enjoying this lesson?

Get full access to all lessons, practice questions, and more.

Start Your Free Trial