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Acute respiratory distress syndrome with many complication

Acute respiratory distress syndrome with many complication. SC ：張家豪，許崇善 Supervisor ： CR 康庭瑞. Patient ’ s Profile. Name ：翁 XX Age: 40 y/o Gender: Female Admission date: 2005/12/08~ Chief complain Sudden onset of headache and conscious loss on the morning of 12/08. Brief History.

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Acute respiratory distress syndrome with many complication

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  1. Acute respiratory distress syndrome with many complication SC：張家豪，許崇善 Supervisor：CR康庭瑞

  2. Patient’s Profile • Name：翁XX • Age: 40 y/o • Gender: Female • Admission date: 2005/12/08~ • Chief complain Sudden onset of headache and conscious loss on the morning of 12/08

  3. Brief History • Present Illness This 40 y/o female patient has suffered from migrane for many years. Severe headache and concious when she is shopping in the market about 10 a.m this morning. She was brought to 永和耕莘hospital for help. SAH was suspected and referred to our ER. Angiography showed a aneurysm over right distal ICA. After angiography performed, short of breath, desaturation 70%, SBP drop to 80mmHg were noted.Strider and wheezing also noted. Contrast medium allergy was suspected.Intubation was performed and steroid was administered.

  4. Brief history • Past history 1. Hyperthyroidism post operation 2. Drug and food allergy: contrast • Physical examination Consciousness: E3V4M6 at ER T/P/R: 38.1/110/12 BP: 150/90 mmHg

  5. Progress Note 12/9 (2:00 am) • Desaturation to 80%, PH:7.26, PO2:45.9 HCO3:45.3, BE:-10, CVP: 13 • CXR: Lung edema r/o fluid overload or anaphylaxis of contrast medium • BP : 88/60 mmHg • Adjust PEEP :14 FiO2:100%  PH 7.38 PO2 48.7, PCO2 32.6, HCO3 19.3, BE – 4.4

  6. 12/10 T/P/R: 36.9/120/19 BP: 99/71 mmHg SpO2: 96% FiO2: 90% PEEP: 14 12/11 T/P/R: 37/140/12 BP: 135/95 mmHg PaO2: 60 mmHg FiO2:60% PEEP:12 CVP:15 Progress note

  7. Progress note 12/12 • T/P/R: 37.1/138/23 • BP: 111/99mmHg • SpO2: 92% • FiO2: 80% PEEP:14 • Neurogenic lung edema

  8. Progress note 12/12 • On CVP (8:00 am) R’t IJV failure L’t IJV • Desaturation to 72% (8.50 pm) • R’t lung breathig sound decreased • Pneumothorax

  9. Chest tube • 100cc bloody fluid drainged • SaO2: 100%

  10. Progress note 12/13 • T/P/R:37.7/122/16 • BP:101/71 mmHg • SpO2: 96% • PEEP:14 FiO2: 100%

  11. Progress note 12/14 (1:30 am) On ECMO • on R’t IJV and R’t FV • due to severe hypoxia despite maximum MV support

  12. Progress note 12/14 (7:45 pm) • Facial and bilateral upper extremities swelling • R/o SVC syndrome • Change Venous catheter from R’t IJV L’t femoral V

  13. Progress note 12/19 • Hypotension • Asymmetric chest wall movement • Needle aspiration: a few blood • Explored previous chest tube wound by finger: blood 300~500 ml • Reon chest tube

  14. Progression note • 12/20 (07:40) • Hypotension • Low tidal volume and compliance • Chest tube: 1100 ml blood drained • Consult CS

  15. Progress note (12/20) • Massive transfusion in 12hours (pre-op) PRBC 10U FFP 24U PLT 36U Cryoprecipitate 12U

  16. Discussion

  17. Hemothorax Etiology • Traumatic Blunt trauma Penetrating trauma (including iatrogenic) • Nontraumatic or spontaneous Neoplasia (primary or metastatic) Complications of anticoagulation Pulmonary embolism with infarction infections Miscellaneous

  18. Pathophysiology • Large hemothoraces are usually related to injury of vascular structures. • Hemodynamic manifestations associated with massive hemothorax are those of hemorrhagic shock. • Related respiratory manifestations include tachypnea and, in some cases, hypoxemia.

  19. Treatment • Chest tube • Surgical 1. Greater than 1000 mL of blood is evacuated immediately after tube thoracostomy. 2. Bleeding from the chest continues, defined as 150-200 mL/h for 2-4 hours. 3. Persistent blood transfusion is required to maintain hemodynamic stability.

  20. ECMO

  21. Complication of ECMO Mechanical complication • Clots in the circuit are the most common mechanical complication (19%). • Cannula placement can cause damage to the internal jugular vein • Air in the circuit can range from a few bubbles to a complete venous air lock • Oxygenator failure,pump, Heat exchanger

  22. Neurologic Hemorhagic Cardiac Pulmonay Renal GI Infection Metabolic Complication of ECMO

  23. Acute respiratory distress syndrome The Acute respiratory distress syndrome NEJM, May.4 2000, SC：張家豪，許崇善 Supervisor：CR康庭瑞

  24. What’s in today’s presentation • Introduction • Definitions • Pathogenesis • Clinical presentation • Cause and predisposing conditions • In our patient • Treatment

  25. Epidemiology • Common, devastating clinical syndrome. • 75 per 100.000 population to 12.6-18 per 100.000 population depending on definition. • Mortality rate of 40 to 60 % attributable to sepsis or MOD rather than primary cause • Mortality of this disease may be decreasing. -- 53-68%(1983) to 36%(1993) (in Seattle) -- 66%(1990-1993) to 34%(1994-1997) (UK) • Improvement in supportive care and mechanical ventilation.

  26. Latest Definition in 1994

  27. Clinical presentation • Initially tachypnea, dyspnea, and normal auscultatory findings in the chest. • Alter mental status may occur in elderly P’t. • Tachycardia with mild cyanosis and coarse rales occur later. • Disease progress is not correlated to the clinical finding --- Arterial blood gas is required.

  28. Most common 40% Cause and predisposing conditions • Massive transfusion (more than 50 percent of a patient's blood volume in 12 to 24 hours) Chronic alcohol abuse, Chronic lung disease, Low serum pH

  29. Etiology • Sepsis • Aspiration of gastric contents • Infectious pneumonia (VAP) • Severe trauma and surface burns • Massive Blood transfusion • Transfusion related acute lung injury (TRALI) • Following relief of upper airway obstruction • Lung and bone marrow transplantation • Drugs – Contrast allergy • Others – Neurogenic pulmonary edema

  30. Sepsis and Massive Transfusion • Sepsis is the most common cause of ARDS. • Unexplained ARDS with new fever, hypotension or a clinical predisposition to serious infections – Sepsis should keep in mind. • Alcoholism – decrease glutathione, increase inappropriate leukocyte adhesion to endothelium. • Transfusion of more than 15 units of blood is an important risk factor for ARDS. • Massive transfusion induced SIRS mimic reaction in our bodies.

  31. Transfusion related acute lung injury (TRALI) Introduction • Also named pulmonary leukoagglutinin reactions • TRALI is defined as noncardiogenic pulmonary edema related to transfusion therapy. • TRALI can progress to ARDS. • TRALI is a life-threatening adverse effect. (Third common transfusion related death) • Mortality rate is 5 -8%, lower than ARDS(30-50%)

  32. Transfusion related acute lung injury Clinical presentation & Diagnosis • Occured with plasma containing blood product -- Whole blood, PRBCS, FFP, Platelets. • Dyspnea, cough, fever (Very often) • Systemic hypotension or hypertension • Common occur after 1-2 h transfusion (< 6h) • Resolution <4 days (81%) • Edema fluid/plasma protein >0.75 more likely. • TRALI is almost always combined with leukopenia

  33. Transfusion related acute lung injury Double hit hypothesis • First hit：Underlying condition of the patient -- Adherence of neutrophils to lung endothelium -- Surgery, sepsis, trauma,massive trsansfusion • Second hit：Transfusion of injurious blood -- Activates these primed neutrophils -- Release reactive oxygen species -- Capillary leak and pulmonary edema

  34. Transfusion related acute lung injury Prevention • Excluding multiparous donor from donor pool. • Multiparous donor are often motivated donor • Avoid old blood component.

  35. Ventilator Associated PneumoniaIntroduction • Hospital-acquired pneumonia (HAP) -- Any case of pneumonia starts >48 hours after admission • Ventilator associated pneumonia (VAP) -- HAP happen after >48 hours intubation with no clinical evidence suggesting the presence or likely development of pneumonia at the time of initial intubation • Second common nosocomial infections in medical ICUs

  36. Ventilator Associated PneumoniaRisk factor

  37. Ventilator Associated PneumoniaDiagnosis & Pathogen • Often, a presumptive diagnosis of pneumonia is made when fever, leukocytosis, purulent secretions, a new infiltrate on chest radiography • >103 colony-forming units (CFU)/mL of bacteria grew from the protected specimen brush sample or > 104 CFU/mL of bacteria grew from the bronchoalveolar lavage fluid. • Pseudomonas aeruginosa, Enterobacter species, Klebsiella pneumoniae, Acinetobacter species,and MRSA

  38. Neurogenic Pulmonary EdemaIntroduction • NPE usually developing after acute central nervous system injury. • NPE is classified as ARDS, but the pathophysiology and prognosis are different • NPE is a serious and common complication after SAH that contribute to pool survival and neurological deficits • Post-mortem lung edema -- 46-52 % • Survival after SAH lung edema -- 23 %, 6% threaten to life

  39. Neurogenic Pulmonary EdemaClinical presentation • Dyspnea and mild hemoptysis present within minutes to hours of CNS insult. • Tachypnea, tachycardia, basilar rales. • Will resolve within hours to several days.

  40. Neurogenic Pulmonary EdemaEtiology & Pathogenesis • Epileptic seizure • Head injury (After CNS surgery) • Cerebral hemorrhage (SAH) • Increase of capillary hydrostatic pressure. (Initially) -- Sympathetic activation -- Pulmonary vasoconstriction -- Increase starling force (Hydrostatic pressure ) • Increase pulmonary capillary permeability. (Late) -- Massive epinephrine, Norepinephrine induce

  41. Contrast media induce lung edema • The pulmonary adverse effects after contrast media injection including bronchospasm, pulmonary edema and increase in the pulmonary arterial blood pressure • Induced pulmonary edema can be secondary to endothelial injury causing an increase in the permeability of the microcirculation • Mechanism is not well-established

  42. In our patient, ARDS • 12/9 – Desaturation to 80%, hypotension (88/60mmHg). • CXR– Bilateral lung edema. • Fi02—100% PaO2=45.9, pH=7.26 • CVP=13cmH20 • Acute lung edema or ARDS? -- Fluid overload? -- Previous pneumonia? -- Contrast anaphylatic shock induce? -- Other cause?

  43. In our patient, ARDS Etiology • Sepsis, Infection -- No fever (36.8), Leukocytosis (15.51K/μL), Seg(95.2) -- CRP=0.12 -- Sepsis is not likely • Aspiration of gastric contents -- No history and no witness of aspiration but coma, NG? -- Temporary rule out • Severe trauma and surface burns -- No history -- Not likely

  44. In our patient, ARDS Etiology • Infectious pneumonia (VAP) -- After 48 hours using ventilator -- No fever (36.9), Leukocytosis (22.53K/μL), Seg(93.3) -- CRP=3.38, VAP is highly suspected

  45. In our patient, ARDS Etiology • Transfusion related acute lung injury (TRALI) -- During OP 4U PRBCs, 6U FFP -- Noncardiogenic pulmonary edema onset before 6 hours -- Leukocytosis (15.51K/μL) -- No resolution, TRALI can not be ruled out • Massive Blood transfusion -- During OP 4U PRBCs, 6U FFP -- 12/19-12/20 PRBC10U, FFP 24U, PLT 36U, Cryo 12U -- Blood volume = 50x70=3500ml -- Must be a risk factor of ARDS

  46. In our patient, ARDS Etiology • Contrast allergy -- After angiogram, short of breath, desaturation 70% SBP drop to 80 mmHg, Strider and wheezing. -- No case report of contrast induce ARDS was found -- Cause of pulmonary edema can’t be ruled out • Neurogenic lung edema -- SAH S/P CNS surgery -- Mild resolution from hours or several days -- Our patient no resolution may due to complex disease (Hemothorax, Massive transfusion, Contrast) -- Highly suspected

  47. In our patient, ARDS Etiology • Neurogenic lung edema combine and massive transfusion . • Contrast media allergy and TRALI can not be rule out.

  48. Treatment of ARDS • Remove of underlying cause of risk factor • Prone position • Mechanical ventilation • Fluid and hemodynamic management • Surfactant therapy • Inhaled nitric oxide and other vasodilators • Glucocorticoid and other antiinflammatory agents

  49. Ventilator induce lung injury (VILI) • High volume and pressures can increase permeability pulmonary edema in uninjured lung and enhanced edema in the injured lung. • Alveolar over distension and cyclic opening and closing of atelectatic alveoli -- Initiated proinflammatory cytokines cascade • Traditional mechanical ventilation (10-15ml/kg) may promote further lung injury,( resolution)

  50. Mechanical ventilation • Fi02 titrated to 0.6 if the SaO2>90% • Higher PEEP (>12mm Hg) will decrease cardiac output – monitor CO, SaO2 is needed • Low tidal volume (<6ml/Kg) is rocommanded. • Permissive hypercapnia (PaCO2 =50-77 mmHg, pH=7.2-7.3) can be will tolerated • Limiting airway pressure take priority over FiO2 • ECMO alone has shown no advantage, but combine with other strategy will have a role. (Fetal bleeding) • Combine strategies better than single strategy

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