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Ard spresentation
Acute Respiratory Distress Syndrome (ARDS) is a severe lung condition characterized by diffuse alveolar damage and severe hypoxemia. It is defined by acute onset, bilateral lung infiltrates seen on x-ray, and low oxygen levels with no cardiac cause. ARDS has many potential causes including sepsis, trauma, pneumonia, and near drowning. Treatment focuses on supportive care of the lungs and underlying condition. Mortality was historically high but is now around 30-40% with improved critical care, though long term outcomes are often impaired.
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Ard spresentation
- 1. Acute Respiratory DistressSyndrome ARDS
- 2. Overview • Previouslycalled Adult Respiratory Distress Syndrome • Defined in 1994 American-European Consensus Conference on ARDS: • Most sever Acute Lung Injury • Diffuse alveolar damage • Severe hypoxemia (PaO2/FIO2 < 200) • Bilateral pulmonary infiltrates • Absence of cardiogenic pulmonary edema (PCWP <18 mmHg)
- 3. Epidemiology •75 cases/ 100,000 population • Can occur at any age • Risks • advanced age • No sex preference • female sex (only in trauma) • cigarette smoking • alcohol use. • High APACHE score (any underlying cause)
- 4. Pathophysiology • Diffusealveolar damage • Increased permeability • Damage to alveolar or capillary endothelium • Inflammation (cytokines, leukotrienes, TNF) • Increased neutrophils ? Reactive • Severe pulmonary shunting hypoxemia • Pulmonary hypertension
- 5. Causative Insults • Sepsis • Aspiration • Trauma • Drug overdose • Fractures • Near drowning • Burns • Cardiopulmonary • Massive bypass transfusion • Pancreatitis • Pneumonia • Fat embolism
- 6. Presentation • Acutedyspnea and hypoxemia • within hours to days of an inciting event • Critically ill • Dyspnea, rapidly progressing • Tachypnea • Agitation • Increasing O2 demands • Often multisystem organ failure
- 7. Physical Exam •Unspecific • Tachypnea • Tachycardia • Cyanosis • Rales • Sepsis • Hypotension • Peripheral vasoconstriction • Manifestation of the underlying cause • i.e abdominal finding pancreatitis
- 8. Differential Diagnosis • Pulmonary hemorrhage • Transfusion-related • Near drowning acute lung injury (TRALI) • Drug reaction • Acute eosinophilic • Noncardiogenic pneumonia pulmonary edema • Reperfusion injury • Hamman-Rich • Leukemic infiltration syndrome • Fat embolism syndrome • Retinoic acid syndrome • Acute hypersensitivity pneumonitis
- 9. Workup • ABG • Hypoxemia • Respiratory alkalosis initially • Respiratory Acidosis ( late) • BNP- exclude cardiogenic pulmonary edema • CXR diffuse bilateral infiltrates • Echocardiogram • Possible CT
- 10. Treatment • Treatmentis supportive + underlying cause • No effective drug for prevention nor management • Xigris • Nitric Oxide • Liquid surfactant • New hopes • Simvastatin • TNF and interleukin antibodies
- 11. Treatment • Fluidmanagement • Resuscitation vs. maintenance • Negative fluid balance “dry side of normal” • Ventilation • Lung protective • High PEEP ( , low TV ( 6 mL/kg) • Neuromuscular block- improved 90 day survival • ECMO- no improved survival • Proning- no improve survival • Nutrition • Enteral, antioxidants, eicosapentaenoic acid, and gamma-linoleic acid
- 12. Prognosis • Mortality • Before 1990 , 40-70% • Recent 30-40% • Better understanding and treatment of sepsis. • Increased in older patients • Morbidity • VAP • Weight loss/muscle weakness • Only 49% survivors return to work