Multiple Organ Dysfunction Syndrome2009


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  • Multiple Organ Dysfunction Syndrome2009

    1. 1. Multiple Organ Dysfunction Syndrome Tianjin Medical University General Hospital Emergency Center
    2. 2. Denomination variation <ul><li>1973 secondary system function failure --- Tilney </li></ul><ul><li>Summary data of 18 cases ARF patients after abdominal aortic aneurysm operation,and 17 patients died from organ failure during dialysis . </li></ul><ul><li>1975 - 1977 </li></ul><ul><li>MOFS , multiple organ failure syndrome -----Baue , 1975 </li></ul><ul><li>( Yet the treatment did not save the lives.) </li></ul><ul><li>MOF , multiple organ failure ----- Eiseman , 1977 </li></ul><ul><li>1980‘s </li></ul><ul><li>MSOF , multiple system organ failure ----- Fry38/533 </li></ul><ul><li>point out the relationship between MSOF and severe infection </li></ul><ul><li>1990‘s ※MODS,multiple organ dysfunction syndrome※ </li></ul>
    3. 3. <ul><li>In 1991,ACCP/SCCM proposed system inflammatory response syndrome( SIRS ), sepsis ,infection and MODS </li></ul><ul><li>From then on , MODS was widely used in clinical. </li></ul><ul><li>It can reflect the dynamic process of organ dysfunction. </li></ul><ul><li>SIRS, Sepsis and MODS are different stages of a same pathological course. </li></ul><ul><li>MODS is the last stage. </li></ul>
    4. 4. Overview <ul><li>It has got great advance in etiology, pathophysiology, risk factor and prevention. </li></ul><ul><li>It is also a leading cause of mortality in ICU. </li></ul><ul><li>Failure of three or more organs is associated with a 90%~95% mortality </li></ul>
    5. 5. SIRS and MODS <ul><li>The advances in medicine in the last several years have increased survival rates. </li></ul><ul><li>The increased survival rates have lead to the development of SIRS and MODS . </li></ul><ul><li>SIRS is a generalized systemic inflammation in organs remote from an initial insult. </li></ul><ul><li>MODS results from SIRS and is the failure of several interdependent organ systems. MODS is the major cause of death of patients in the critical care units. </li></ul>
    6. 6. <ul><li>SIRS 1991 ACCP/SCCM conference defined it as the presence of two or more of the following features (1) :temperature greater than 38℃ or less than 36℃; (2) heart rate faster than 90 beats per minute; (3) respiratory rate faster than 20 breaths per minute;and (4) white blood cell count greater than 12.0×10 9 /L,less than 4.0 ×10 9 /L,or with greater than 10%immature forms or bands. </li></ul>
    7. 7. <ul><li>Sepsis the systemic response to infection,manifested by SIRS + the presence of viable bacteria in the blood. </li></ul>
    8. 8. Male 26y Post-subtotal excision of colon Ileocolonic stoma leakage Multiple intestinal fistula
    9. 9. Abdominal abscess
    10. 10. Long-term application of high caloria parenteral nutrition ( fat emulsion) liver tumefaction liver dysfunction SGPT 36 SGOT 144 TB 167.9 DB 102.8
    11. 11. <ul><li>Positive blood cultivation </li></ul>HR 150 RR 45 PaCO 2 23.8 WBC 18700
    12. 12. septic shock Renal function BUN 20.5 Cr 337 need inhalation of oxygen with mask continuous hemofiltration tracheotomy ventilator application
    13. 13. Definition
    14. 14. <ul><li>MODS results from progressive physiologic failure of two or more separate organ systems.It is defined as the presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention. </li></ul>
    15. 15. <ul><li>The etiology is an acute factor </li></ul><ul><li>The failure of the organs is progressive and reversible . </li></ul><ul><li>It is a syndrome </li></ul><ul><li>It happens within 24 hours after trauma or episode. </li></ul><ul><li>The final phase of chronic disease not belong to this syndrome. </li></ul>
    16. 16. High Risk Patients <ul><li>Trauma patients </li></ul><ul><li>Shock episode associated with a rupture aneurysm, acute pancreatitis, sepsis, burns, or surgical complications. </li></ul><ul><li>Patients > 65 years of age because of their decreased organ reserve and the presence of co-morbidities. </li></ul>
    17. 17. <ul><li>Severe trauma, multiple injury,massive blood loss,hypovolemia shock and infection </li></ul><ul><li>Trauma and infection are the main factors </li></ul><ul><li>Others:operation,massive blood transfusion and so on. </li></ul>
    18. 18. Pathogenesis
    19. 19. <ul><li>1970s : injury->infection->sepsis ->MOF </li></ul><ul><li>1990s : injury->stress reaction->SIRS ->MODS-> MOF </li></ul><ul><li>Present : injury->stress reaction-> SIRS/CARS disequilibrium->MODS -> MOF </li></ul>
    20. 20. <ul><li>Bacteria infection </li></ul><ul><li>SIRS </li></ul><ul><li>Enteral barrier dysfunction </li></ul><ul><li>Hypermetabolism </li></ul>
    21. 21. Systemic Inflammatory Response Syndrome (SIRS)
    22. 22. SIRS with a presumed or confirmed infectious confirmed infectious process sepsis SIRS Infection Severe sepsis Bacteremia
    23. 23. Severe sepsis MODS The presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention Death Sepsis with  1 sign of organ failure Cardiovascular (refractory hypotension) Renal Respiratory Hepatic Hematologic CNS Metabolic acidosis Shock
    24. 24. SIRS,CARS and MODS
    25. 25. <ul><li>CARS compensate anti-inflammation reaction syndrome.1996 Bone raised . </li></ul>
    26. 26. <ul><li>MODS is determined by the balance of these anti-inflammatory and proinflammatory mediators . </li></ul><ul><li>TNF,IL, AA metabolites,and so on. </li></ul><ul><li>SIRS,CARS imbalance will lead to MODS . </li></ul>
    28. 28. Initial insult Bacteria. Viral trauma Local Pro-inflammatory response Local Anti-inflammatory response Systemic spillover of pro-inflammatory mediators Systemic spillover of anti-inflammatory mediators Systemic Reaction SIRS (pro-inflammatory ) CARS(anti-inflammatory ) Homeostasis SIRS & CARS balanced Cardiovascular compromise ( shock ) SIRS predominates Apoptosis (cell death) SIRS predominates Organ dysfunction SIRS predominates Suppression of the immune system CARS predominates
    30. 30. Heat Redness Swelling Pain Loss Of Func .
    31. 31. Enteral barrier dysfunction <ul><li>Gastrointestinal tract plays an important role in MODS. </li></ul><ul><li>bacteria translocation(paralytic ileus, drugs, TPN) </li></ul><ul><li>An undrainage abscess cavity </li></ul>
    32. 32. Hypermetabolism <ul><li>Early period during Infection ,burn </li></ul><ul><li>Catabolism is high,energy failure </li></ul>
    33. 33. Diagnosis
    34. 34. <ul><li>Risk factors </li></ul><ul><li>SIRS manifested </li></ul><ul><li>Multiple organs dysfunction </li></ul>
    35. 35. Organ Specific Manifestations <ul><li>GI dysfunction </li></ul><ul><li>Hepatobiliary dysfunction </li></ul><ul><li>Pulmonary dysfunction </li></ul><ul><li>Renal dysfunction </li></ul><ul><li>Cardiovascular dysfunction </li></ul><ul><li>Coagulation system dysfunction </li></ul><ul><li>others </li></ul>
    36. 36. Gastrointestinal Dysfunction Hypoperfusion Ischemia of the gut Decreased integrity of the gut lining Decreased peristalsis Translocation of normal GI bacteria into systemic circulation Colonization of normal GI flora up into the orpharynx Systemic infection and SIRS Aspiration of bacteria and initiation of a inflammatory response in the lung
    37. 37. Hepatobiliary Dysfunction Hypoperfusion Ischemia of the liver and gallbladder ischemic hepatitis acalculous cholecystitis Jaundice serum transaminase serum bilirubin Right upper pain and tenderness Abdominal distention Unexplained fever Loss of bowel sounds
    38. 38. Pulmonary Dysfunction <ul><li>The lungs are usually the first organ affected in secondary MODS. </li></ul><ul><li>Pulmonary dysfunction manifest as ARDS. </li></ul><ul><li>ARDS generally presents 24-48 hours after the initial injury. </li></ul>
    39. 39. Renal Dysfunction Hypoperfusion And Renal toxic drugs Ischemia of the Kidney Azotemia Creatinine clearance Fluid and electrolyte imbalances Fluid volume overload Renal Function
    40. 40. Cardiovascular Dysfunction <ul><li>Initial response </li></ul><ul><li>Myocardial depression </li></ul><ul><li>Right atrial pressure </li></ul><ul><li>SVR </li></ul><ul><li>Venous capacitance </li></ul><ul><li>VO 2 </li></ul><ul><li>CO </li></ul><ul><li>HR </li></ul><ul><li>Late response </li></ul><ul><li>Ventricular dilatation </li></ul><ul><li>Diastolic compliance </li></ul><ul><li>contractile function </li></ul><ul><li>CO </li></ul><ul><li>Ability to maintain BP without vasopressors </li></ul>
    41. 41. Disseminated Intravascular Coagulation (DIC) <ul><li>Failure of the coagulation system is manifested as DIC. </li></ul><ul><li>Results in simultaneous microvascular clotting and hemorrhage in organ systems because of the depletion of clotting factors. </li></ul>
    42. 42. Central Nervous System Bispectral EEG monitoring Altered level of consciousness Impaired mentation Confusion Delirium Psychosis Lab Clinical
    43. 43. Metabolic/Nutritional Negative nitrogen balance Hyperglycemia Hypertriglyceridemia Increased serum lactate Decreased serum albumin,serum transferrin,prealbumin Decreased retinol-binding protein Decreased lean body mass Muscle wasting Severe weight loss Lab Clinical
    44. 44. Immune Decreased lymphocyte anergy Nosocomial Infection Pyrexia Lab Clinical
    45. 45. Tachycardia Hypotension  CVP  PAWP  Enzyme  Albumin  PT Irritability Alteration confusion Somnolence Coma Tachypnea PaO 2 <70 mm Hg SaO 2 <90% PaO 2 /FiO 2  300 Oliguria Anuria  Creatin  Platelet  PT/APTT  Protein C  D-dimer
    46. 46. Prevention
    47. 47. <ul><li>The best management is prevention </li></ul><ul><li>The principle are </li></ul><ul><li>decrease the severity of the risk factor </li></ul><ul><li>Lessen the inflammation </li></ul><ul><li>Appropriate resuscitation and control of infection </li></ul><ul><li>Avoid unsuitable operation and use of antibiotic </li></ul><ul><li>Treat the dysfunction organ and malnutrition </li></ul>
    48. 48. Prognosis
    49. 49. Marshall assessment system ( 1995 ) organ score 0 1 2 3 4 PaO 2 /FiO 2 ≥ 40.0 30.1~40.0 20.1~30.0 10.1~20.0 ≤ 10.0 CRE , μmol/L ≤ 100 101~200 201~350 351~500 >500 BIL , μmol/L ≤ 20 21~60 61~120 121~240 >240 HR ,次 /min ≤ 10.0 10.1~15.0 15.1~20.0 20.1~30.0 >30.0 BPC , ×10 9 /L >120 81~120 51~80 21~50 ≤ 20 GCS 15 13~14 10~12 7~9 ≤ 6
    50. 50. Significance in clinical <ul><li>Each organ score is 4,altogether is 24 </li></ul><ul><li>The score is positive relation to mortality in ICU and the length stay in ICU. </li></ul><ul><li>The score of GCS is the most important </li></ul>
    51. 51. The relationship between MODS score and the mortality of patients in ICU MODS score mortality(%) 0 0 9~12 25 13~16 50 17~20 75 >20 100
    52. 52. Treatment
    53. 53. Principle <ul><li>Control of infection </li></ul><ul><li>Maintenance of tissue oxygenation </li></ul><ul><li>Nutritional /Metabolic support </li></ul><ul><li>Specific treatment </li></ul>
    54. 54. Stepwise approach to sepsis and septic shock <ul><li>Step A   = Airway :   ensure that the airway is protected; if not intubate the patient. </li></ul><ul><li>Step B = Breathing: address oxygenation and ventilation, administer oxygen and, if intubated, commence mechanical ventilation. </li></ul><ul><li>Step C = Circulation : restore circulating volume with  fluid resuscitation, invasive monitoring and vasopressors if necessary:. </li></ul>
    55. 55. Stepwise approach to sepsis and septic shock(cont.) <ul><li>Step D = Diagnosis / Detective work : obtain a history, examine the patient and make a “best guess” as to the source. </li></ul><ul><li>Step E = Empiric therapy : start empiric antimicrobials, and activated Protein C if indicated. </li></ul><ul><li>Step F = Find and control the source of infection </li></ul><ul><li>Step G = Gut: feed it to prevent villus atrophy and bacterial translocation </li></ul>
    56. 56. Stepwise approach to sepsis and septic shock(cont.) <ul><li>Step H = Hemodynamics: assess adequacy of resuscitation and prevention of organ failure. </li></ul><ul><li>Step I =  Iatrogenic: avoid hospital acquired injuries (DVT, line sepsis, pressure sores) and address other supportive issues – analgesia, sedation and psychospiritual welfare, control blood sugar and think about adrenal insufficiency. </li></ul><ul><li>Step J = Justify your therapeutic plan and reassess </li></ul>
    57. 57. Stepwise approach to sepsis and septic shock(cont.) <ul><li>Step KL = Keep Looking . Have we adequately controlle d the source? Are there secondary sources of infection/inflammation. </li></ul><ul><li>Step MN = Metabolic and Neuroendocrine control. Tight control of blood sugar. Address adrenal insufficiency. Think about early aggressive dialysis in renal failure. </li></ul>
    58. 59. Clinical application <ul><li>A man 38 years old,well-nourished , </li></ul><ul><li>who sustained abdominal injuries and a live laceration that required surgical intervention(exploratory laparotomy,repair of liver laceration,splenectomy) </li></ul><ul><li>past history :No chronic health problems. </li></ul><ul><li>Signs and symptoms: during the immediate postoperative period(days 1 and 2),he was extubated.His oriented and hemodynamically stable.He required low-flow nasal oxygen to maintain a PaO 2 of 75mmHg.He was tachycardic(100bpm) and mildly tachypneic ,and core temperature was 37℃,abdomen was distended,with absent bowel sounds. </li></ul><ul><li>A nasogastric tube was draining small amounts of darkgreen drainge.His surgical wound was well approximated,with no redness or drainage. </li></ul>
    59. 60. <ul><li>Lab data revealed normochromic normocytic anemia,leukocytosis count(13000/mm 3 ),and an elevated serum lactate level.ABG values indicated a primary respiratory alkalosis and metabolic acidosis . </li></ul><ul><li>1.You suspect he is experiencing systemic inflammatory response syndrome(SIRS).What signs and symptoms are evident to support your suspicions? </li></ul><ul><li>2.What are your priorities for him at this time? </li></ul>
    60. 61. <ul><li>On days 6 and 7 he remained intubated and required 100% O 2 to maintain a PaO 2 70mmHg. Core temperature was 38.4℃ and WBC count 18000/mm 3 with a shift to the left.However,blood, urine,and wound cultures were negative.Serum creatinine and blood urea nitrogen levels were approaching the need for hemodialysis.Hepatic function was altered as evidenced by elevated serum bilirubin,AST,ALT,and LDH;clinical jaundice was evident.Cardiovascular function was dependent on vasoactive drugs to maintain a subnormal cardiac output. </li></ul>
    61. 62. <ul><li>4.which of his organs are failing?list the signs and symptoms to support you answer </li></ul><ul><li>5.what treatments should you anticipate being initiated to support his failing organs </li></ul>
    62. 63. Thank you