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ARDS Acute Respiratory Syndrome

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ARDS, Acute Respiratory Syndrome, Wet Lung, Stiff Lung, patient, Cebu, CDUH, Evardone

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ARDS Acute Respiratory Syndrome

  1. 1. JOSE SOCRATES “DEE” EVARDONE PULMO ROTATOR SEPT 2015 IM LEVEL 2 C D U H
  2. 2. ACTUAL CASE
  3. 3. Patient profile V.I. Filipino male, 48 years old, Married (-) DM (-) HPN NON-smoker Occasional alcohol drinker Prev hosp- 6/2015- acid related peptic disease,
  4. 4. CHIEF COMPLAINT Abdominal Pain
  5. 5. HISTORY OF PRESENT ILLNESS • 10 years PTA, onset of intermittent abdominal pain, epigastric area mixed with burning and colicky • Admitted 4x due to this condition • no UTZ nor UGIE was done, managed as Acid related disease, takes Buscopan as his reliever • 1 day PTA, recurrence of the abdominal pain, peri- umbilical, epigastric and substernal in location, VAS of 9/10 • Px consulted a physician and was immediately referred here • (-) weight loss • (-) melena • (-) vomiting • (-) diarrhea • (-) fever
  6. 6. PE in the ER Conscious, coherent, NIRD Warm, good turgor and mobility, CRT <2 seconds, No rashes, Anicteric sclerae, pink palpebral conjunctivae Equal chest expansion, clear breath sounds Distinct heart sounds, normal rate, regular rhythm Flat, no scars/lesion, Hypoactive bowel sounds, soft, (+) tenderness on all quadrants, direct and indirect, no organomegaly, Strong peripheral pulses, no edema, Neurologic: Unremarkable BP: 110/80mmHg, HR: 73 bpm, RR: 20c Temp: 37.2°C GUT: (-) KPS
  7. 7. on admission IMPRESSION -Acute Abdomen probably 2 to Bleeding PUD DIAGNOSTICS 1. CBC, UA, CXR, Xray of the Abdomen, amylase, lipase, sgpt, TBDB THERAPEUTICS 1. Hydration with PNSS 2. PPI 3. NPO Differential -Cholelithiases -Cholecystitis -Acute Pancreatitis
  8. 8. CBC Adm Hgb 18.0 Hct 55 WBC Seg Bas Eos Lymph Mono 19,000 80 0 0 12 8 Platelet 120 MCV MCH MCHC 87.8 28.7 32.1 CHEM Amylase 2,450 Lipase 17,420 Creatinine 2.28 CrClear 33 ml/min LDH 4360 AST 237 ALT 55 Alk Phos 35 BUN 28 Potassium 5.1 Sodium 133 BUN/Crea 12.28 CHEM TB 1.2 DB 0.6 IB 0.6 Albumin 3.2 Globulin 2.7
  9. 9. FIRST HOSPITAL DAY
  10. 10. 3rd HOSPITAL DAY
  11. 11. 4th HOSPITAL DAY
  12. 12. SOURCES
  13. 13. INTRODUCTION
  14. 14. • distinct type of hypoxemic respiratory failure • acute abnormality of both lungs • First recognized in the 1960s • Military clinicians in Vietnam called it Shock Lung • Civilian clinicians called it ADULT respiratory distress syndrome • Clinical hallmarks of ARDS are: – hypoxemia and – bilateral radiographic opacities • Pathological hallmark is diffuse alveolar damage • ARDS is an acute, diffuse, inflammatory lung injury that leads to: – increased pulmonary vascular permeability, – increased lung weight, and – a loss of aerated tissue
  15. 15. • 60 cases /100,1000 population • 10% of all ICU admissions involve acute respiratory failure, 20% of these meet ARDS criteria (2% in all ICU px)
  16. 16. RESPIRATORY PHYSIOLOGY
  17. 17. Respiratory Membrane
  18. 18. Respiratory Membrane
  19. 19. Respiratory Membrane
  20. 20. Respiratory Membrane
  21. 21. DEFINITION
  22. 22. Acute Respiratory Distress Syndrome ARDS (clinical syndrome) severe dyspnea of rapid onset hypoxemia diffuse pulmonary infiltrates RESPIRATORY FAILURE Acute respiratory distress syndrome (ARDS) is a clinical syndrome of severe dyspnea of rapid onset, hypoxemia, and diffuse pulmonary infiltrates leading to respiratory failure.
  23. 23. ETIOLOGY
  24. 24. DIAGNOSTIC EVALUATION
  25. 25. DIAGNOSTICS • Excluding cardiogenic pulmonary edema a. Brain natriuretic peptide (BNP) b. Echocardiography c. Right heart catheterization • Excluding other causes of hypoxemic respiratory failure a. Noninvasive respiratory sampling i. tracheobronchial aspiration or ii. mini-bronchoalveolar lavage (mini-BAL) b. Flexible bronchoscopy c. Lung biopsy a. The results of the biopsy resulted in the addition of specific therapy in 60 percent of patients b. withdrawal of unnecessary therapy in 37 percent
  26. 26. CLINICAL COURSE AND PATHOPHYSIOLOGY
  27. 27. Acute Respiratory Distress Syndrome
  28. 28. Acute Respiratory Distress Syndrome Exudative Phase
  29. 29. A R D S
  30. 30. Acute Respiratory Distress Syndrome Exudative Phase plasma proteins aggregate hyaline membrane whorls Alveolar edema collapse intrapulmonary shunting and hypoxemia DYSPNEA Pulmonary Hypertension Hypercapnia within 12–36 h after the initial insult can be delayed by 5–7 days
  31. 31. Exudative Phase
  32. 32. Proliferative Phase • usually lasts from day 7 to day 21 • Most patients recover rapidly and are liberated from mechanical ventilation during this phase • Some patients develop progressive lung injury and early changes of pulmonary fibrosis • Histologically: 1. the initiation of lung repair, 2. the organization of alveolar exudates, and 3. a shift from a neutrophil- to a lymphocyte-predominant pulmonary infiltrate 4. type II pneumocytes proliferate along alveolar basement membranes • synthesize new pulmonary surfactant and • differentiate into type I pneumocytes
  33. 33. Fibrotic Phase • many patients with ARDS recover lung function 3–4 weeks • require long-term support on mechanical ventilators and/or supplemental oxygen • extensive alveolar-duct and interstitial fibrosis • emphysema-like changes, with large bullae • The physiologic consequences include – an increased risk of pneumothorax, – reductions in lung compliance, and – increased pulmonary dead space • substantial burden of excess morbidity • associated with increased mortality risk
  34. 34. Fibrotic Phase
  35. 35. TREATMENT
  36. 36. • Recent reductions in ARDS mortality rates are largely the result of general advances in the care of critically ill patients caringforthesepatients requirescloseattentionto the recognition and treatment of underlying medical and surgical disorders the minimization of procedures and their complications prophylaxis against venous thromboembolism, gastrointestinal bleeding, aspiration, excessive sedation, and central venous catheter infections prompt recognition of nosocomial infections provision of adequate nutrition
  37. 37. 1.MANAGEMENT OF MECHANICAL VENTILATION 2.FLUID MANAGEMENT 3.NEUROMUSCULAR BLOCKADE 4.GLUCOCORTICOIDS 5.OTHER THERAPIES
  38. 38. 1.MANAGEMENT OF MECHANICAL VENTILATION Ventilator-Induced Lung Injury • mechanical ventilation can aggravate lung injury • require two processes: 1. repeated alveolar overdistention 2. recurrent alveolar collapse • (6 mL/kg of predicted body weight) VS (12 mL/kg predicted body weight) • Mortality rate 31% vs 40% This improvement in survival represents the most substantial ARDS-mortality benefit that has been demonstrated for any therapeutic intervention to date
  39. 39. 1. MANAGEMENT OF MECHANICAL VENTILATION Prevention of Alveolar Collapse • the presence of alveolar and interstitial fluid and the loss of surfactant can lead to a marked reduction of lung compliance • Without an increase in end-expiratory pressure, significant alveolar collapse can occur at end-expiration • 12–15 mmHg in ARDS, is a theoretical “optimal PEEP” for alveolar recruitment • Keep the lung open • Three large randomized trials have investigated the utility of PEEP-based strategies to keep the lung open, improvement in lung function was evident but overall mortality rates were not altered significantly
  40. 40. A R D S
  41. 41. 1. MANAGEMENT OF MECHANICAL VENTILATION Prevention of Alveolar Collapse • Until more data become available on the clinical utility of high PEEP, it is advisable to set PEEP to minimize Fio2 and optimize Pao2 • inverse-ratio ventilation (I:E >1:1) –can improve oxygenation and –can help reduce Fio2 to ≤0.60 –no benefit in ARDS mortality risk PRONE POSITIONING: • improved arterial oxygenation • hazardous
  42. 42. A R D S
  43. 43. Permissive Hypercapnia and Tracheal Gas Insufflation • The use of lower VTs (to avoid VILI) often results in respiratory acidemia, an effect that has been termed “permissive hypercapnia” • The theoretical detrimental effects of hypercapnia include: – myocardial depression, – increased pulmonary vascular resistance, and – decreased renal blood flow • most clinically important adverse effect of hypercapnia is elevated intracranial pressure from increased cerebral blood flow • data suggesting that hypercapnia has protective effects, including attenuation of free radical–mediated lung injury and pulmonary inflammation • TGI is a technique whereby a gas flow is introduced via a small catheter placed in the endotracheal tube, with its tip near the carina. • TGI has been proposed as an adjunct to permissive hypercapnia, as the insufflated gas improves CO2 clearance from the anatomic dead space and ventilator tubing. A R D S
  44. 44. PRONE POSITIONING A R D S
  45. 45. PRONE POSITIONING A R D S
  46. 46. 2. FLUID MANAGEMENT • Increased pulmonary vascular permeability leading to interstitial and alveolar edema fluid rich in protein Low left atrial filling pressure: 1. minimizes pulmonary edema and prevents further decrements in arterial oxygenation and lung compliance; 2. improves pulmonary mechanics; shortens ICU stay and the duration of mechanical ventilation; and 3. is associated with a lower mortality rate in both medical and surgical ICU patients • aggressive attempts to reduce left atrial filling pressures with fluid restriction and diuretics
  47. 47. 3. NEUROMUSCULAR BLOCKADE •In severe ARDS, sedation alone can be inadequate for the patient ventilator synchrony •Cisatracurium besylate for 48h •blockade increased the rate of survival and ventilator-free days without increasing ICU- acquired paresis •however, these results must be replicated prior to their widespread application in clinical practice
  48. 48. 4. GLUCOCORTICOIDS •Few studies have shown any benefit. •Current evidence does not support the use of high-dose glucocorticoids in the care of ARDS patients.
  49. 49. •ANTIOXIDANTS •GRANULOCYTE-MONOCYTE COLONY STIMULATING FACTOR •INHALED VASODILATORS –Nitric oxide –Prostacyclin •ANTI-INFLAMMATORY THERAPIES –Glucocorticoids –Macrolide antibiotics •BETA AGONISTS •MESENCHYMAL STEM CELLS Novel therapies
  50. 50. 1. N-acetylcysteine 2. Procysteine (L-2-oxothiazolidine-4-carboxylate) 3. Glutamine 4. Antioxidant preparations (selenium, beta carotene, zinc, vitamin E and C) 5. Lisophylline 6. Intravenous prostaglandin E1 7. Neutrophil elastase inhibitors 8. Ibuprofen 9. Activated protein C 10. Ketoconazole 11. Statins 12. Surfactant INEFFECTIVE OR HARMFUL THERAPIES
  51. 51. PROGNOSIS & OUTCOMES
  52. 52. • Recent mortality estimates for ARDS range from 26% to 44% • mortality in ARDS is largely attributable to nonpulmonary causes, with sepsis and nonpulmonary organ failure accounting for >80% of deaths • The major risk factors for ARDS mortality are nonpulmonary – Age – Preexisting organ dysfunction from chronic medical illness 1. chronic liver disease, 2. cirrhosis, 3. chronic alcohol abuse, 4. chronic immunosuppression, 5. sepsis, 6. chronic renal disease, 7. failure of any nonpulmonary organ, and 8. increased APACHE III scores MORTALITY
  53. 53. • direct lung injury – nearly twice as likely to die vs indirect • Predicted mortality risks: 1. An early (within 24 h of presentation) elevation in pulmonary dead space (>0.60) 2. Severe arterial hypoxemia (Pao2/Fio2, <100 mmHg) • little additional value in predicting ARDS mortality rom other measures of the severity of lung injury: a. the level of PEEP (≥10 cm H2O), b. respiratory system compliance (≤40 mL/cm H2O), c. the extent of alveolar infiltrates on chest radiography, and d. the corrected expired volume per minute (≥10 L/min) MORTALITY
  54. 54. • majority of patients recover nearly normal lung function • usually recover maximal lung function within 6 months • One year after endotracheal extubation, >1/3 will have a normal Spirometry values and diffusion capacity • Unlike mortality risk, recovery of lung function is strongly associated with the extent of lung injury in early ARDS • Associated with less recovery of pulmonary function: 1. Low static respiratory compliance, 2. high levels of required PEEP, 3. longer durations of mechanical ventilation, and 4. high lung injury scores Physical function after 5 years – despite normal lung function 1. Exercise limitation 2. Decreased physical quality of life Functional Recovery in ARDS Survivors
  55. 55. KEYPOINTS defined by acute hypoxemia, bilateral infiltrates on chest radiograph, and the absence of left atrial hypertension Direct and Indirect Lung injury The pathogenesis of ARDS is not clear, but increased permeability of the alveolar-capillary membrane due to neutrophilic infiltration of the lungs is thought to be an important factor ARDS is a syndrome, not a specific diagnosis; clinicians must, therefore, look for the cause in order to institute specific therapy The mortality rate for ARDS has fallen since the 1980s and is now about 40%. Mechanical ventilation is lifesaving but, when inappropriately applied, can induce or aggravate lung injury Most deaths in patients with ARDS are from multiorgan failure rather than hypoxia per se. No pharmacologic therapies have been shown to improve survival in ARDS; Many survivors of ARDS suffer from a reduced quality of life and cognitive impairment
  56. 56. 4th HOSPITAL DAY
  57. 57. 6th HOSPITAL DAY
  58. 58. THANK YOU

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