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Case Management: Acute Respiratory Failure

Case Management: Acute Respiratory Failure. Santos, Jennifer Joy Santos, Ma. Socorro Tiongson , Denver. Y.d. 57 year old Female Widow Born Again Christian Right-handed from Baclaran , Paranaque. Patient Profile. Chief Complaint : Dyspnea

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Case Management: Acute Respiratory Failure

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  1. Case Management:Acute Respiratory Failure Santos, Jennifer Joy Santos, Ma. Socorro Tiongson, Denver

  2. Y.d. • 57 year old • Female • Widow • Born Again Christian • Right-handed • from Baclaran, Paranaque

  3. Patient Profile • Chief Complaint : Dyspnea • Non-hypertensive, non-diabetic, non-asthmatic • No history of PTB • With a finding of an intracranial mass (temporal lobe) in CT scan c/o PGH (2005)

  4. History of present illness

  5. History of present illness

  6. History of present illness

  7. History of present illness

  8. History of present illness

  9. History of present illness

  10. paST MEDICAL HISTORY

  11. Family history • (+) HPN- mother • (+) CVD- siblings • (+) MI- brother • (-) known Cancer of any type • (-) PTB, DM

  12. Personal /social history • Non-smoker • Non alcoholic beverages • Denies illicit drug use • Works in buy and sell business • Church worship leader • High school graduate • Lives with youngest daughter aged 16 y/o in their old house, while the other 2 daughters are now living with their respective families

  13. Course at the emergency room

  14. PBS: normocytic, hypochromic (++), (+) toxic granulation in PMNs. Reticulocytes adequate.

  15. abG

  16. PTB extensive disease with possible cavitation Pneumonia with consolidation Subsegmentalatelectasis, L • WAT IS OUR aditional READING of this XRAY? • Elevated Right diaphragm can mean pulmonary contraction • - cardiac reading?

  17. Course at the emergency room

  18. Course at the emergency room

  19. Course at the emergency room

  20. Other pertinent laboratory results 3/11 • ETA GS: 0-2 gram (-) bacilli; 0-2 yeast cells • KAYA KAYA NATING MAHANAP YUNG CULTURE STUDIES NYA PARA MALAMAN UNG ETIOLOGIC AGENT? =)

  21. Physical examination on admission • Awake, conscious, responsive, intubated @ET 7.5 L18, NICRD • BP= 120/80 HR=120 RR=40s T=37.6 • HEENT: pale palpebral conjunctivae, anictericsclerae, pupils 2mm EBRTL, (+) NVE, (+) Anterior neck mass 3x4 cm firm, nodular, movable. (-) CLAD • Chest: Equal chest expansion, harsh breath sounds, (+) crackles bilateral LF mid to base, (-) wheezes. • Heart: DHS, tachycardic, regular rhythm, apex beat at 5th ICS anterior axillary line. (-) murmurs. • Abdomen: soft, flabby, normoactive bowel sounds, (-) masses/tenderness • Extremities: pink nailbeds, full and equal pulses, CRT<2 sec. (-) edema/cyanosis, (+) grade I sacral ulcer, Right

  22. management

  23. Course at the ward

  24. Labs

  25. Other pertinent laboratory findings 3/12 • CKMB 23.5 • CK total 42 Rules out ACS

  26. Course at the ward

  27. 3/11/2010, 9 AM Course in the ward • noted BP 70/50 • A> ARDS 2’ CAP HR • Sepsis secondary to CAP HR • PTB cat I • Intracranial mass, R lobe • DTG in storm, s/p RAI • IFG • Dyslipidemia • Anemia prob secondary to chronic disease. • Dopamine drip started

  28. Course in the ward : 3/12/2010

  29. Labs

  30. 3/12 : 12-L ECG: MFAT, normal axis, non-specific ST-T wave changes

  31. Course in the ward

  32. Sinus tachycardia, normal axis, low voltage complexes, NSSTTWC

  33. Discussion

  34. Acute Respiratory Distress Syndrome (ARDS)

  35. ARDS • Severe dyspnea of acute onset (< 2 weeks) • Hypoxemia • Diffuse bilateral pulmonary infiltrate on CXR • PaO2/FiO2 < 200 mmHg • No elevated left atrial pressure (PCWP <18 mm Hg) • Respiratory • Failure

  36. Causes

  37. Three Phases Recovery Exudative Proliferative Fibrotic 0 7 14 21 6 mos

  38. Diffuse alveolar and endothelial damage Increase pulmonary vascular permeability Atelectasis and increase work of breathing: Dyspnea Tachypnea Hypoxemia Microvascular occlusion, pulmonary hypertension, increase in dead space: Hypercapnia Alveolar edema PMN infiltration of lungs Hyaline membrane formation Inactivation of surfactant due to exudates Accumulation in dependent portions Atelectasis

  39. Proliferative Phase • Time of Lung repair • Layering of exudates • Lymphocytic infiltration • Type II pneumocytes reproduce surfactant

  40. Fibrotic Phase • Fibrosis • Emphysema like changes (bullae) • Vascular occlusion • Complications: • Pulmonary Hypertension • Pneumothorax • Increase in dead space

  41. Mechanical Ventilation • Augments the increase in work of breathing • But can aggravate lung injury via repeated Alveolar Overdistention and Recurrent Alveolar Collapse • Set MV at lower tidal volumes • 6 ml/kgBW( vs standard 12ml/kgBW) • Optimal PEEP for alveolar recruitment : • 12-15 cmHg • Target RR < 35 • ARDS net protocol: Low volume, High frequency ventilation

  42. Management • Manage Respiratory Acidosis • Fluid restriction and diuretic • to reduce left atrial filling pressure • Dry Lungs are Happy Lungs! • Steroids • anti-inflammatory  No role!

  43. Mortality • 41-65% • Mostly from non-pulmonary causes (Sepsis, organ failure) • Recovery of lung function within 6 months

  44. Acute Respiratory Failure

  45. Inability of the lung to meet the metabolic demands of the body • Dysfunction in lung’s main function: • Oxygenation • Carbon Dioxide elimination • PaO2 <60 mmHg • PaCO2 >50 mmHg • Develops 4-48 hours

  46. Signs • Tachypnea • Exaggerated use of accessory muscles • Intercostal, supraclavicular and subcostal retractions • Neuromuscular disease: signs of respiratory distress may not be obvious • CNS disease: bradypnea + shallow breathing

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