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