ACUTE RESPIRATORY DISTRESS SYNDROME

ARDS
a clinical syndrome of severe dyspnea of rapid onset, hypoxemia, and diffuse pulmonary infiltrates leading to respiratory failure Annual incidence: 60/100,000 10% of ICU admissions
~20% meet ARDS criteria

Diagnostic Criteria for ARDS

Oxygenation Onset Chest Radiograph Absence of Left Atrial Hypertension PaO2/FiO2 200 Acute Bilateral alveolar or interstitial infiltrates PCWP 18 mmHg or no clinical evidence of increased left atrial pressure

ETIOLOGY
caused by diffuse lung injury from many underlying medical and surgical disorder
may be direct or indirect

Risk of developing ARDS are increased in patients suffering from more than one predisposing medical or surgical condition Other Clinical Variables: older age, chronic alcohol abuse, metabolic acidosis, and severity of critical illness

Clinical Disorders Commonly Associated with ARDS

DIRECT LUNG INJURY Pneumonia Aspiration of gastric contents Pulmonary contusion Near-drowning Toxic inhalation injury INDIRECT LUNG INJURY Sepsis Severe trauma -Multiple bone fractures -Flail chest -Head trauma -Burns Multiple transfusions Drug overdose Pancreatitis Postcardiopulmonary bypass

Clinical Course and Pathophysiology

The natural history of ARDS is marked by three phasesexudative, proliferative, and fibroticeach with characteristic clinical and pathologic features

 Exudative: First 7 days-early alveolar edema and neutrophil-rich leukocytic infiltration of the lungs with subsequent formation of hyaline membranes from diffuse alveolar damage Proliferative: 7 to 21-interstitial inflammation and early fibrotic changes Fibrotic: 3wks- substantial fibrosis and bullae formation

EXUDATIVE PHASE
alveolar capillary endothelial cells and type I pneumocytes (alveolar epithelial cells) are injured loss of the normally tight alveolar barrier Edema fluid accumulates in the interstitial and alveolar spaces
Edemaaeration and atelectasis (collapse) lung complianceintrapulmonary shunting and hypoxemiawork of breathingDYSPNEA with rapid shallow breathing and TACHYPNEA Respi fatigue Respi Failure

EXUDATIVE PHASE
Significant concentrations of cytokines (interleukin 1 and 8, TNF) and lipid mediators ( leukotriene B4) are present Response: leukocytes (especially neutrophils) traffic into the pulmonary interstitium and alveoli INFLAMMATION Pulmonary vascular injury also occurs early with vascular obliteration by microthrombi and fibrocellular proliferation
microvascular occlusion pulmonary arterial blood flow to ventilated portions of the lungdead space PULMONARY HTN, SEVERE HYPOXEMIA, HYPERCAPNIA

PROLIFERATIVE PHASE
YAYYY!!! First signs of resolution: initiation of lung repair, organization of alveolar exudates, and a shift from a neutrophil- to a lymphocytepredominant pulmonary infiltrate proliferation of type II pneumocytes along alveolar basement membranes
specialized epithelial cells that synthesize new pulmonary surfactant and differentiate into type I pneumocytes

OH NOOO!!! presence of alveolar type III procollagen peptide, a marker of pulmonary fibrosis

FIBROTIC PHASE
the alveolar edema and inflammatory exudates of earlier phases are now converted to extensive alveolar duct and interstitial fibrosis
Intimal fibroproliferation in the pulmonary microcirculation leads to progressive vascular occlusion and pulmonary hypertension

Acinar architecture is markedly disrupted, leading to emphysema-like changes with large bullae PHYSIOLOGIC CONSEQUENCES: an increased risk of pneumothorax, reductions in lung compliance, and increased pulmonary dead space require long-term support on mechanical ventilators and/or supplemental oxygen

MECHANICAL VENTILATOR
Noninvasive (ex.face mask) or Conventional GOAL in ARDS: maintain oxygenation while avoiding oxygen toxicity and complications maintain oxygen saturation in the range of 85-90%, with the aim of reducing the fraction of inspired oxygen (FIO2) to less than 65% within the first 24-48 hours a tidal volume of 6 mL/kg predicted body weight is recommended, with adjustment of the tidal volume to as low as 4 mL/kg if needed to limit the inspiratory plateau pressure to 30 cm water or less almost always necessitates the use of moderate-tohigh levels of positive end-expiratory pressure (PEEP)

COMPLICATIONS
Barotrauma
Due to repeated alveolar overdistention and recurrent alveolar collapse

Nosocomial pneumonia Oxygen toxicity Tracheal stenosis Ventilator-associated pneumonia (VAP)

a result of aspiration from the upper airways through small leaks around the endotracheal tube cuff most common organisms: Pseudomonas aeruginosa, enteric gram-negative rods, and Staphylococcus aureus

SUPPORTIVE TREATMENT
Fluid management (Diuretics/Dialysis)
To maintain a normal or low left atrial filling pressure to minimize pulmonary edema and prevent further decrements in arterial oxygenation and lung compliance

Glucocorticoids

MUST TREAT UNDERLYING CAUSE!!!!

PROGNOSIS
Mortality: 26-44% ->80% due to sepsis and nonpulmonary organ failure Major risk factors are nonpulmonary
Patients >75 yo (~60%mortality) compared to those <45yo (~20%) patients >60yo with ARDS and sepsis have a threefold higher mortality compared to those <60 Preexisting organ dysfunction (chronic liver disease, cirrhosis, chronic alcohol abuse, chronic immunosuppression, sepsis, chronic renal disease)

RECOVERY: Patients usually recover their maximum lung function within 6 months **Indices of oxygenation and ventilation, including the PaO2/FIO2 ratio, do not predict the outcome or risk of death.