multiple organ dysfunction syndrome2009
DESCRIPTION
modsTRANSCRIPT
Multiple Organ Multiple Organ Dysfunction SyndromeDysfunction Syndrome
Tianjin Medical University General Tianjin Medical University General Hospital Emergency CenterHospital Emergency Center
Denomination variationDenomination variation• 1973 secondary system function failure--- Tilney Summary data of 18 cases ARF patients after abdominal a
ortic aneurysm operation,and 17 patients died from organ failure during dialysis .
• 1975 - 1977 MOFS , multiple organ failure syndrome-----Baue , 1975 ( Yet the treatment did not save the lives.) MOF , multiple organ failure----- Eiseman , 1977• 1980‘s MSOF , multiple system organ failure----- Fry38/533 point out the relationship between MSOF and severe infe
ction• 1990‘s ※MODS,multiple organ dysfunction syndrome※
• In 1991,ACCP/SCCM proposed system inflammatory response syndrome(SIRS), sepsis,infection and MODS
• From then on ,MODS was widely used in clinical.• It can reflect the dynamic process of organ
dysfunction.• SIRS, Sepsis and MODS are different stages of a
same pathological course. MODS is the last stage.
OverviewOverview
• It has got great advance in etiology, pathophysiology, risk factor and prevention.
• It is also a leading cause of mortality in ICU.
• Failure of three or more organs is associated with a 90%~95% mortality
SIRS and MODSSIRS and MODS
• The advances in medicine in the last several years have increased survival rates.
• The increased survival rates have lead to the development of SIRS and MODS.
• SIRS is a generalized systemic inflammation in organs remote from an initial insult.
• 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.
• 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 12.0×109/L,less than 4.0 ×109/L,or with greater than 10%immature forms or bands.
• Sepsis the systemic response to infection,manifested by SIRS + the presence of viable bacteria in the blood.
Male 26yPost-subtotal excision of colonIleocolonic stoma leakageMultiple intestinal fistula
Abdominal abscess
Long-term application
of high caloria parente
ral nutrition ( fat emul
sion)
liver tumefaction
liver dysfunction
SGPT 36 SGOT 144 TB 167.9 DB 102.8
Positive blood cultivation
HR 150
RR 45
PaCO2 23.8
WBC 18700
septic shock
Renal function BUN 20.5 Cr 337 need inhalation of oxygen with mask continuous hemofiltration tracheotomy ventilator application
DefinitionDefinition
• 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.
• The etiology is an acute factor
• The failure of the organs is progressive and reversible.
• It is a syndrome
• It happens within 24 hours after trauma or episode.
• The final phase of chronic disease not belong to this syndrome.
High Risk Patients High Risk Patients
• Trauma patients
• Shock episode associated with a rupture aneurysm, acute pancreatitis, sepsis, burns, or surgical complications.
• Patients > 65 years of age because of their decreased organ reserve and the presence of co-morbidities.
• Severe trauma,multiple injury,massive blood loss,hypovolemia shock and infection
• Trauma and infection are the main factors
• Others:operation,massive blood transfusion and so on.
PathogenesisPathogenesis
1970s : injury→infection→sepsis →MOF
1990s : injury→stress reaction→SIRS →MODS→ MOF
Present : injury→stress reaction→ SIRS/CARS disequilibrium→MODS → MOF
• Bacteria infection
• SIRS
• Enteral barrier dysfunction
• Hypermetabolism
Systemic Inflammatory Systemic Inflammatory Response Syndrome (SIRS)Response Syndrome (SIRS)
SIRS with a presumed or confirmed infectious confirmed infectious process
sepsissepsisSIRSSIRSInfectionInfection Severe sepsiSevere sepsiss
Bacteremia
Severe sepsisSevere 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
ShockShock
SIRS,CARS and MODS SIRS,CARS and MODS
CARS compensate anti-inflammation reaction syndrome.1996 Bone raised .
MODS is determined by the balance of these anti-inflammatory and proinflammatory mediators .
TNF,IL, AA metabolites,and so on.
• SIRS,CARS imbalance will lead to MODS.
SIRS
CARS
CARS
MODS
MODS
SIRS
CARS
SIRS
CARS
MODS
MODS
SIRS
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
SIRS CARS
SIRSSIRS
SIRS CARS
CARSCARS
SIRS CARS
MARSMARS
29
Heat Redness Swelling Pain Loss Of FuncHeat Redness Swelling Pain Loss Of Func..
Enteral barrier dysfunctionEnteral barrier dysfunction
• Gastrointestinal tract plays an important role in MODS.
• bacteria translocation(paralytic ileus, drugs, TPN)
• An undrainage abscess cavity
HypermetabolismHypermetabolism
• Early period during Infection ,burn
• Catabolism is high,energy failure
DiagnosisDiagnosis
• Risk factors
• SIRS manifested
• Multiple organs dysfunction
Organ Specific ManifestationsOrgan Specific Manifestations
• GI dysfunction
• Hepatobiliary dysfunction
• Pulmonary dysfunction
• Renal dysfunction
• Cardiovascular dysfunction
• Coagulation system dysfunction
• others
Gastrointestinal DysfunctionGastrointestinal 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
Hepatobiliary DysfunctionHepatobiliary 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
Pulmonary DysfunctionPulmonary Dysfunction
• The lungs are usually the first organ affected in secondary MODS.
• Pulmonary dysfunction manifest as ARDS.
• ARDS generally presents 24-48 hours after the initial injury.
Renal DysfunctionRenal Dysfunction
Hypoperfusion
And
Renal toxic drugs
Ischemia of the Kidney
Azotemia
Creatinine clearance
Fluid and electrolyte imbalances
Fluid volume overload
Renal Function
Cardiovascular DysfunctionCardiovascular Dysfunction
Initial response• Myocardial depression• Right atrial pressure• SVR• Venous capacitance
• VO2
• CO• HR
Late response• Ventricular dilatation• Diastolic compliance• contractile function• CO• Ability to maintain BP
without vasopressors
Disseminated Intravascular Disseminated Intravascular Coagulation (DIC)Coagulation (DIC)
• Failure of the coagulation system is manifested as DIC.
• Results in simultaneous microvascular clotting and hemorrhage in organ systems because of the depletion of clotting factors.
Central Nervous SystemCentral Nervous System
Clinical Lab
Altered level of consciousness
Impaired mentation
Confusion
Delirium
Psychosis
Bispectral EEG monitoring
Metabolic/NutritionalMetabolic/NutritionalClinical Lab
Decreased lean body mass
Muscle wasting
Severe weight loss
Negative nitrogen balance
Hyperglycemia
Hypertriglyceridemia
Increased serum lactate
Decreased serum albumin,serum transferrin,prealbumin
Decreased retinol-binding protein
ImmuneImmune
Clinical Lab
Nosocomial Infection
Pyrexia
Decreased lymphocyte
anergy
TachycardiaHypotension
CVP PAWP
Enzyme Albumin
PT
Irritability Alteration confusion SomnolenceComa
TachypneaPaO2 <70 mm Hg
SaO2 <90%PaO2/FiO2 300
OliguriaAnuria
Creatin
Platelet PT/APTT Protein C D-dimer
PreventionPrevention
The best management is prevention
The principle are decrease the severity of the risk factor Lessen the inflammation Appropriate resuscitation and control of
infection Avoid unsuitable operation and use of
antibiotic Treat the dysfunction organ and malnutrition
PrognosisPrognosis
Marshall assessment Marshall assessment systemsystem (( 19951995 ))
organ
score
0 1 2 3 4
PaO2/FiO2 ≥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 21~6061~12
0121~2
40>240
HR ,次 /min ≤10.0 10.1~15.0
15.1~20.0
20.1~30.0
>30.0
BPC , ×109/L >12081~12
051~80 21~50 ≤20
GCS 15 13~14 10~12 7~9 ≤6
Significance in clinicalSignificance in clinical
• Each organ score is 4,altogether is 24
• The score is positive relation to mortality in ICU and the length stay in ICU.
• The score of GCS is the most important
The relationship between MODS score and the mortality of
patients in ICUMODS score
mortality(%)
0 0
9~12 25
13~16 50
17~20 75
>20 100
TreatmentTreatment
PrinciplePrinciple
• Control of infection
• Maintenance of tissue oxygenation
• Nutritional /Metabolic support
• Specific treatment
Stepwise approach to Stepwise approach to sepsis and septic shocksepsis and septic shock
• Step A = Airway: ensure that the airway is protected; if not intubate the patient.
• Step B = Breathing: address oxygenation and ventilation, administer oxygen and, if intubated, commence mechanical ventilation.
• Step C = Circulation: restore circulating volume with fluid resuscitation, invasive monitoring and vasopressors if necessary:.
Stepwise approach to sepsis Stepwise approach to sepsis and septic shock(cont.)and septic shock(cont.)
• Step D = Diagnosis / Detective work: obtain a history, examine the patient and make a “best guess” as to the source.
• Step E = Empiric therapy: start empiric antimicrobials, and activated Protein C if indicated.
• Step F = Find and control the source of infection
• Step G = Gut: feed it to prevent villus atrophy and bacterial translocation
Stepwise approach to sepsis Stepwise approach to sepsis and septic shock(cont.)and septic shock(cont.)
• Step H = Hemodynamics: assess adequacy of resuscitation and prevention of organ failure.
• 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.
• Step J = Justify your therapeutic plan and reassess
Stepwise approach to sepsiStepwise approach to sepsis and septic shock(cont.)s and septic shock(cont.)
• Step KL = Keep Looking. Have we adequately controlle57d the source? Are there secondary sources of infection/inflammation.
• Step MN = Metabolic and Neuroendocrine control. Tight control of blood sugar. Address adrenal insufficiency. Think about early aggressive dialysis in renal failure.
Clinical applicationClinical application• A man 38 years old,well-nourished ,• who sustained abdominal injuries and a live laceration that re
quired surgical intervention(exploratory laparotomy,repair of liver laceration,splenectomy)
• past history:No chronic health problems.• Signs and symptoms: during the immediate postoperative pe
riod(days 1 and 2),he was extubated.His oriented and hemodynamically stable.He required low-flow nasal oxygen to maintain a PaO2 of 75mmHg.He was tachycardic(100bpm) and mildly tachypneic ,and core temperature was 37℃,abdomen was distended,with absent bowel sounds.
• A nasogastric tube was draining small amounts of darkgreen drainge.His surgical wound was well approximated,with no redness or drainage.
• Lab data revealed normochromic normocytic anemia,leukocytosis count(13000/mm3),and an elevated serum lactate level.ABG values indicated a primary respiratory alkalosis and metabolic acidosis.
1.You suspect he is experiencing systemic inflammatory response syndrome(SIRS).What signs and symptoms are evident to support your suspicions?
2.What are your priorities for him at this time?
• On days 6 and 7 he remained intubated and required 100% O2 to maintain a PaO2 70mmHg. Core temperature was 38.4℃ and WBC count 18000/mm3 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.
• 4.which of his organs are failing?list the signs and symptoms to support you answer
• 5.what treatments should you anticipate being initiated to support his failing organs
Thank youThank you