MODS标准教案正文.docx

1、MODS标准教案正文Chapter11 Multiple Organ Dysfunction Syndrome (MODS) MODS Course ObjectsBy the end of this hour, the students will be able to Understand the diagnostic criteria, pathogenesis , prevention and treatment of MODSMaster the clinic manifestation, diagnosis, prevention and treatment of Acute Res

2、piratory Distress Syndrome.Correctly understand and use of the following terms :SIRS CARS MODS MOF ALI ARDS1. Introduction 1.1 DefinitionMultiple Organ Dysfunction Syndrome has been characterized as progressive sequential dysfunction or failure of two or more organ systems -ARDS ARF DIC SU etc. from

3、 an refractory inflammatory response to Severe Injury Sepsis or Shock. Historical Perspective of MODS1.1Clinical Characteristics Function of organs is normal before MODS occurred & MODS be taken bad with stress response or SIRS Generally failure organ No primary injured organ Several days interval b

4、etween primary injury & removed organ dysfunction usually 24h The degree of organs dysfunction is inconsistent with pathologic damage degree of organs Acute onset , refractory with conventional treatment( anti-shock anti-infection) & high mortality MODS is reversible except terminal 400,000 $/pt.1.3

5、Risk Factors of MODS Major Causes -Injuries (Severe trauma Burn & Post-operation ) -Sepsis -Shock Post Cardiopulmonary Resucitation (CPR) Acute hemorrhagic necrosis pancreatitis Miscellaneous -include age (65), malnutrition, Immunologic disorders , blood transfusion and preexisting chronic disease s

6、uch as cancer or diabetes etc. 1.4 Pathophysiology of MODS Injury or endotoxin release Vascular endothelial damage Neuroendocrine response Release of inflammatory mediators Activation of complement, coagulation, kallikrein/kinin systems Vascular Changes Maldistribution of systemic and organ blood fl

7、ow Hypermetabolism Oxygen supply/demand imbalance Tissue hypoxia Organ dysfunction1.5 Pathogenesis of MODS Unbalance between SIRS systemic inflammatory response syndrome & CARS compenstory anti-inflammatory response syndrome. Gut bacterial translocation Ischemia-reperfusion injury Proinflammatory cy

8、tokines: TNF alpha IL - 1, IL 6, IL 8, IL 12 Interferon gamma Anti-inflammatory cytokines IL 4, IL 10, IL 13 Transforming growth factor (TGF) - beta1.6 MODS Determinants after onset Some patients recover without complications while others develop septic shock Cause Difference in the degree of inflam

9、matory response to the infection Tumor necrosis factor-alpha (TNF-) - principal mediator of septic shock Mortality and hemodynamic derangement closely correlated with the TNF- levelBacteria translocationOrgan Ischemia-reperfusion injury1.7 Specific Organ Responses of MODS Heart: - MID Cardiac Dysfun

10、ction or heart failure Lung: V/Q mismatch Hypoxemia Increased microvascular permeability Interstitial/alveolar edema ARDS Gastrointestinal/Hepatic: Impaired GI motility Bacterial translocation MODS Stress-ulcer GI bleeding Hepatic dysfunction Kidney: Altered renal function ATN/ acute renal failure I

11、ncreases mortality rate Neurologic: Encephalopathy Peripheral polyneuropathy 68% - 100% Hematologic: Leukocytosis/leukopenia Thrombocytopenia Coagulopathy DIC 15% - 20%MODS Clinical categories Primary MODS: early organ dysfunction Secondary MODS: later organ dysfunction Most common manifestations of

12、 severe MODS: ARDS, ARF, DIC, Stress Ulcer.1.8 MODS Diagnosis Principal diagnostic criterions of MODS: -History Severe Sepsis Trauma Shock Post great or complex operation Post CPR -Clinical manifestations of SIRS &CARS -Two or more organ systems dysfunctionSIRS Diagnosis Widespread inflammatory resp

13、onse in absence of documented infection Need 2 or more: Temp 380C (100.40F) or 90 bpm Respiratory rate 20 /min or PaCO2 12,000 cells/mm3, 10% immature (band) formMODS Early Diagnoses Early exactly judgement to SIRS & organ systemic dysfunction Acquaintance to Risk Factors of MODS Pathogenesis SIRS +

14、 organ dysfuction Clinical characteristics of MODS Think much of organ dysfunction than organ failure Pay attention to hepatic gasro-intestinal hematologic organ systemic dysfunction1.9 MODS Prevention &Treatment Current therapy of MODS is aimed at prevention and supportive care. Three general areas

15、 are: -source control -restoration and maintenance of oxygen transport -metabolic support. Functional state of organs especially circulation & respiration Prevent & control infection Early management of first outbreak organ dysfunction Improve general situation &maintenance internal environment stab

16、ilization Intensive Gastro-intestinal protect Monitor systems & organs immunotherapy Source control is a major emphasis, as persistence of a source guarantees a high mortality risk from MODS. Malnutrition is one of the primary manifestations of MODS. 2. Acute Respiratory Distress Syndrome ARDS2.1 AR

17、DS Historical PerspectivesOriginal Definition Acute respiratory distress Cyanosis refractory to oxygen therapy Decreased lung compliance Diffuse infiltrates on chest radiograph Difficulties: lacks specific criteria controversy over incidence and mortalityARDS 1994 Consensus Acute onset may follow ca

18、tastrophic event Bilateral infiltrates on chest radiograph PAWP 18 mm Hg no clinical evidence of left heart failure Two categories: Acute Lung Injury - PaO2/FiO2 ratio 300 ARDS - PaO2/FiO2 ratio 2002.2 Epidemiology Earlier numbers inadequate (vague definition) Using 1994 criteria: 17.9/100,000 for a

19、cute lung injury 13.5/100,000 for ARDS Current epidemiologic study underway In children: approximately 1% of all PICU admissions2.3 ARDS Inciting Factors Trauma Infections Shock & DIC ARF Acute hemorrhagic necrotic pancreatitis Blood transfusion Aspiration of gastric contents or Inhalation of toxic

20、gases and fumes Drugs and poisons2.3 ARDS Pathogenesis Inciting event Inflammatory mediators Damage to microvascular endothelium Damage to alveolar epithelium Increased alveolar permeability results in alveolar edema fluid accumulation Target organ injury from hosts inflammatory response and uncontr

21、olled liberation of inflammatory mediators Localized manifestation of SIRS Neutrophils and macrophages play major roles Complement activation Cytokines: TNF-a, IL-1b, IL-6 Platelet activation factor PAF Eicosanoids: prostacyclin, leukotrienes, thromboxane Free radicals Nitric oxide2.4 ARDS Stages2.4

22、.1 Acute, exudative phase rapid onset of respiratory failure after trigger diffuse alveolar damage with inflammatory cell infiltration hyaline membrane formation capillary injury protein-rich edema fluid in alveoli disruption of alveolar epithelium Basement membrane disruption Type I pneumocytes des

23、troyed Type II pneumocytes preserved Surfactant deficiency inhibited by fibrin decreased type II production Microatelectasis/alveolar collapse2.4.2 ARDS Proliferative Phase Proliferative Phase : persistent hypoxemia development of hypercarbia fibrosing alveolitis further decrease in pulmonary compli

24、ance pulmonary hypertension Type II pneumocyte proliferate differentiate into Type I cells reline alveolar walls Fibroblast proliferation interstitial/alveolar fibrosisNORMAL ALVEOLUS2.4.3 ARDS Fibrotic Phase Characterized by: local fibrosis vascular obliteration Repair process: resolution vs fibros

25、isARDS2.4.4 Recovery phase Recovery phase (Recuperative/Terminal Phase) gradual resolution of hypoxemia improved lung compliance resolution of radiographic abnormalities2.5 ARDS Clinical FeaturesAcute dyspnea/tachypnea rales/rhonchi/wheezingResistant hypoxemia PaO2/FIO2 150 200 mmHgCXR diffuse, bila

26、teral infiltratesNo evidence of LV failure (PAWP 18 mmHg)ARDSABNORMALITIES OF GAS EXCHANGE Hypoxemia: HALLMARK of ARDS Increased capillary permeability Interstitial and alveolar exudate Surfactant damage Decreased FRC Diffusion defect and right to left shunt early diffuse alveolar damage with hyalin

27、e membrane disease Medium power section (40x) lung parenchyma Extensive thickening of alveolar septum (wall) Congestion of lung capillaries; with endothelium leakage Alveolar edema Intensely eosinophilic noncellular hyaline membrane material in alveolar air spaceARDS late diffuse alveolar damage wit

28、h Type-2 pneumocyte migration (hi-mag) The blue arrows point to the type II pneumocytes which are very prominent; their nuclei protruding into the alveolar space. The arrows highlight the thickened septum (alveolar wall). The septum contains excess collagen, fibroblasts, and lymphocytes. Hyaline mem

29、branes are not present at this stage. 2.6 ARDS Differential Diagnosis CARDIOGENIC PULMONARY EDEMABronchopneumoniaHypersensitivity pneumonitis Pulmonary hemorrhage Acute interstitial pneumonia (Hamman-Rich Syndrome)ARDS Mortality 40-60% Deaths due to: multi-organ failure sepsis Mortality may be decre

30、asing in recent years better ventilatory strategies earlier diagnosis and treatment2.7 ARDS MANAGEMENT2.7.1 Monitoring: Respiratory Hemodynamic Metabolic Infections Shock Trauma sepesis (sources) Fluids/electrolytes2.7.2 ARDS Basic Principles in the Ventilatory Accomplish effective gas exchange Avoid complications reduced cardiac output barotrauma oxygen toxicity ventilator-induced lu