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Ard spresentation

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Miguel Garcia
Miguel Garcia

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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Acute Respiratory Distress Syndrome ARDS
Overview Previously called 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)
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)
Pathophysiology Diffuse alveolar damage Increased permeability Damage to alveolar or capillary endothelium Inflammation (cytokines, leukotrienes, TNF) Increased neutrophils ? Reactive Severe pulmonary shunting hypoxemia Pulmonary hypertension
Causative Insults Sepsis Aspiration Trauma Drug overdose Fractures Near drowning Burns Cardiopulmonary Massive bypass transfusion Pancreatitis Pneumonia Fat embolism
Presentation Acute dyspnea and hypoxemia within hours to days of an inciting event Critically ill Dyspnea, rapidly progressing Tachypnea Agitation Increasing O2 demands Often multisystem organ failure
Physical Exam Unspecific Tachypnea Tachycardia Cyanosis Rales Sepsis Hypotension Peripheral vasoconstriction Manifestation of the underlying cause i.e abdominal finding pancreatitis
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
Workup ABG Hypoxemia Respiratory alkalosis initially Respiratory Acidosis ( late) BNP- exclude cardiogenic pulmonary edema CXR diffuse bilateral infiltrates Echocardiogram Possible CT
Treatment Treatment is supportive + underlying cause No effective drug for prevention nor management Xigris Nitric Oxide Liquid surfactant New hopes Simvastatin TNF and interleukin antibodies
Treatment Fluid management 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
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

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Ard spresentation

  • 2. Overview Previously called 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 Diffuse alveolar 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 Acute dyspnea 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 Treatment is supportive + underlying cause No effective drug for prevention nor management Xigris Nitric Oxide Liquid surfactant New hopes Simvastatin TNF and interleukin antibodies
  • 11. Treatment Fluid management 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