多脏器功能障碍综合征与监护课件

,单击此处编辑母版标题样式,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,*,单击此处编辑母版标题样式,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,*,单击此处编辑母版标题样式,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,多脏器功能障碍综合征及监护,MODS and intensive care,多脏器功能障碍综合征及监护MODS and intensi,2,Denomination variation,1973,secondary system function failure,-,Tilney,Summary data of 18 cases ARF patients after abdominal aortic aneurysm operation,and 17 patients died from organ failure during dialysis .,19751977,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 infection,1990,s,MODS,multiple organ dysfunction syndrome,2Denomination variation1973,3,Case 1,Male 26y,Post-subtotal excision of colon,Ileocolonic stoma leakage,Multiple intestinal fistula,3Case 1,4,Abdominal,abscess,4Abdominal,5,Long-term application of,high caloria parenteral,nutrition ( fat emulsion),liver tumefaction,liver dysfunction,SGPT 36,SGOT 144,TB 167.9,DB 102.8,5Long-term application of,6,HR 170,RR 55,PaCO,2,23.8,WBC 18700,Positive blood cultivation,6HR 170 Positive blood culti,7,Jan 16th,septic shock,Jan 17th,Renal function,BUN 20.5,Cr 337,need inhalation of oxygen with mask,continuous hemofiltration,Jan 19th,tracheotomy,ventilator application,7Jan 16th,8,Case 2 male,59,y,Extensive anterior wall,Myocardial infarction,20,days after onset,(2002/3/6),continuous ventricular tachycardia,ventricular fibrillation,electric defibrillation 5 times,antiarrhythmic drugs,counter shock drugs,ventilator application,8Case 2 male 59y,9,HR 120,RR 28,PaCO,2,26.8,WBC 12600,9HR 120,10,Repeatedly ventricular tachycardia and fibrillation,，,totally 21 times electric defibrillation,Continuous hyperpyrexia,、,high WBC,、,HR90、RR22,Cultivation negative, antibiotics no effectiveness,Organ dysfunction came in crowds,shock,Respiratory dysfunction,Deterioration of liver function,Cast in urine routine test,BUN、Cr,oliguria,、,anuria,Coagulation abnormality,death,10Repeatedly ventricular tachy,11,Acute onset,Manifestatin of excessive inflammation,Deteriotation of pts conditions despite active therapy,Multiple organ dysfunction,Different pts, Same progress,Case 1: infectious,Case 2:noninfectious,11Acute onsetDifferent pts, Sa,12,clinical behavior,Accumulative,Substance,irreversible,Multiple organ low function,caused by interaction between organs,Chronic disease,Multiple organ low function,12clinical behaviorChronic dis,13,MODS followed by primary emergency disease in 24 hours,Clinical manifestation,burst out,Simultaneous,die quickly,primary MODS,Ischemia,ischemia and reperfusion,physical and chemical injury factor,13MODS followed by primary eme,14,Sequential organ dysfunction after emergency disease,MODS,Clinical behavior,Delayed,Sequential,Reversible,MODS,Excessive inflammatory mediators,14Sequential organ dysfunction,15,1.Direct injury of ischemia,Oxygen & nutrient insufficiency,Integrity of cell membrane,organelle insult,ATP,Extracellular fluid in-flow,Hydrolase activation,Natrium in-flow,calcium in-flow,151.Direct injury of ischemiaO,16,1.Direct injury of ischemia,Hyper,sensibitity in heart and brain,Selective ischemia,Endothelial cell injury leads to high vascular permeability and low volume,161.Direct injury of ischemiaH,17,permeability of,cell membrane,Na,+,Ca,+,H,2,O,ADP,AMP,IMP,adenosine,xanthine,hypoxanthine,hypoxanthine riboside,Uric Acid,oxygen-derived free radidicals,xanthine oxidase,xanthine oxidase,Xanthine dehydrogenase,Intracellular acidosis,Lower protein synthesis,Injury of,ischemia and reperfusion,17permeability of cell membran,18,Vessel permeability WBC,chemotaxis,monocyte,/,macrophage,neutrophil,elastinase,PLA2,ODFR,TNF IL8 et al,IL1,IL6,liver：,acutephase reaction,Remote organ injury,Tissue damage,etiological factor,neutrophil,Adherent molecule,2.Excessive inflammation,SIRS MODS,Vascular,endothelial cell,SIRS,MODS,18Vessel permeability WBC ch,19,Clinical progress,uncontrolled stress,SIRS,Capillary leakage syndrome,MODS,MSOF,19Clinical progressuncontrolle,20,Important molecule in MODS,Pro-inflammatory cytokines:TNF-,IL-,1、2、6,etc,Stimulate synthesis and release of other cytokines,Activate neutrophiles,eosinophils and monocytes;activate T and B cell;chemotaxis,Increase the expression of adherent molecule,Activate complement and coagulation system,Increase permeability of vessels,decrease BP,Cause fever and catabolism of muscle,20Important molecule in MODS,21,Important molecule in MODS,A,nti-inflammatory cytokines: IL-,4、10,etc,Maintain and enhance the function of activated NK cells,monocytes,B and T cells,，,Inhibit proliferation of T,B cell,Inhibit pro-inflammatory cytokines production , receptor expression and cytotoxicity of monocytes,Inhibit adherent molecule expression of vascular endothelial cells(VECs),Inhibit H,2,O,2,、NO production of macrophage,Inhibit antigen presentation and other assistant functions of monocytes and macrophage,21Important molecule in MODS,22,Important cells in MODS,Polymorphonuclear leucocyte（PMN）：Effector cell of inflammatory response. Could release several protein enzymes and ODFR to destroy VECs and stroma,V,ECs,：,W,hen activated, VECs express higher adherence to PMN and higher clotting competence;also they produce pro-inflammatory cytokines and vasodilating agent to magnify inflammatory response; finally, capillary leakage syndrome comes if VECs were destroyed.,22Important cells in MODSPolym,23,Important organ in MODS,Intestines,Because of stress, fasting and catabolism,the blood-mucosa barrier of intestines could be destructed, the bacteria and toxin tranlocate to blood circulation and the latter could enhance inflammatory response to form vicious cycle. So intestines are called “motor” of inflammatory response,and are sources of late stage infectons of MODS pts,.,23Important organ in MODSIntes,24,uncontrolled stress,carbohydrate metabolism dysfunction, Insulin tolerance, without Ketonemia,hyperkinetic circulatory state, Hyperpyrexia, High Stroke volume,High oxygen consumption,Protein metabolism dysfunction , high katabolism, acute phase protein,24uncontrolled stresscarbohydr,25,T 38or,36,HR90 beat/min,RR20,/,min or PaCO,2,32mmHg,WBC12000mm,3,or 4000mm,3,or premature cells,10,Sepsis,Systemic Inflammatory,Response Syndrome (SIRS),(,SIR+Positive Culture),(,SIR without infection),Systemic Inflammatory Response syndrome,SIRS,25T 38or 36SepsisSystemic,26,Chaotic internal milieu during acute phase,Disturbance of electrolytes and acid-base balance,Fever,Catabolism: emaciated,anemia,A,cute disseminated intravascular coagulation,Arrhythmia,Hyperglycemia, no ketonemia,26Chaotic internal milieu duri,27,Secondary aldosteronism,-,high density urine without,Proteinuria, oliguria,-,prerenal azotemia,-,swollen,Plasma protein leakage,-,Interstitial edema,-,Hypoproteinemia,-,blood inspissasion,-,Hypovolemia,Capillary leakage syndrome,CLS,27Secondary aldosteronismPlasm,28,Diagnosis of CLS,Positive body fluid balance,Blood volume deficiency,Hypoproteinemia,Organ and total body Interstitial edema,lung Interstitial edema,cerebral Interstitial edema,28Diagnosis of CLSPositive bod,29,Organs dysfunction or failure,Organ or system,dysfunction,failure,lung,Liver,kidney,intestine,Blood,Hypoxemia, respirator at list 3-5days,ARDS,PEEP10cmH2O,FiO20.5,Bilirubin2-3mg/dL, Liver function2,normal value,Bilirubin2-3mg/dL,icterus,oliguria,dialysis,Untolerance of,enteral nutrition5days,Curlingls ulcer needs blood transfusion, Acalculous cholecystitis,PT or PTT elongation, platelet95%,Kidney,ARF,only a few,31Influenced organLung ARDS,32,Acute Respiratory Distress,Syndrome,ARDS,Pathology of lung,High capillary permeability,Interstitial edema,Vasoconstriction,micro thrombosis,communicating branch opening,Alveolar and small bronchus,Atelectasis,Decreased alveolar surfactant,Edema,I type epithelial cells instead by II type cell,Symptom,Tachypnea, respiratory distress can not be eased by oxygen inhalation,No rales,No lung x-ray abnormality,1.The early stage,32Acute Respiratory Distress S,33,Pathology,Deteriorated lung Interstitial inflammation,usually complicated with SEPSIS,Symptom,Obviously dyspnoea and cyanosis,needs ventilator,Increased respiratory tract secretion, rales,Lung x-ray,infiltrates,Disturbance of consciousness,Febrile or high leucocyte,.The second stage,33Pathology.The second stage,34,3.,T,elophase,Pathology,Lung parenchyma fibrosis,Microvascular occlusion,Increased preload, hypoxia,Symptom,Deep coma,Arrhythmia,bradycardia,cardiac arrest,343. Telophase Pathology,35,Diagnosis,35Diagnosis,36,Acute Renal Failure, ARF,Etiology,Prerenal,Hemorrhage, shock, fluid losing without appropriate fluid resuscitation,post renal,both side ureter or urinary flow blocked,renal,kidney,ischemia (hematorrhea,sepsis, allergic reaction),intoxication(aminoglycoside antibiotic, biotic toxin, chemical),36Acute Renal Failure, ARFEtio,37,1.History and physical examination,Etiology,prerenal pathogen,postrenal pathogen,Diagnosis of ARF,371.History and physical exami,38,2.Differentiation Diagnosis with prerenal ARF,382.Differentiation Diagnosis,39,3.Differentiation Diagnosis with Postrenal ARF,B type ultrasound,(renal enlargement, ureter),Abdominal x-rays,(calcification, calculus or Obstruction),393.Differentiation Diagnosis,40,4.,Laboratory Urine test,Urinary catheter to record urine volume,Urine acidity/density(1.010-1.014),Urine microscopic examination,RBC and renal tubule epithelia(renal cortex and renal medulla necrosis),Large Brown casts(renal failure casts),Eosinophil (interstitial nephritis),Red cell cast(glomerulonephritis),Normal(prerenal or postrenal failure earlier period),404. Laboratory Urine testUrin,41,5.,renal function examination,Urine urea nitrogen,(,175mmol/24h),Fractional excretion of filtrated sodium1,FE,Na,（%）=（U,Na,/P,Na,）（P,Cr,/U,Cr,）100,osmotic pressure of urine,*ARF-,400,mOsm/L,BUN (more than,3.89.4,mmol/L per day) ,Cr,Urine/Plasma Cr-1-ARF,*1-prerenal,415. renal function examinatio,42,Intensive care,Organ and system function Monitoring and support,Object,ameliorate oxygen metabolism,ameliorate nutrien state,Therapy aimed at stress and inflammatory Mediators,Treatment of capillary leakage,Treatment of primary disease,42Intensive careOrgan and syst,43,Oxygen metabolism Monitoring,Critical DO,2,Assay of plasma lactic acid/pyruvic acid,43Oxygen metabolism Monitoring,44,Oxygen associated index,DO,2,Oxygen Delivery-,Oxygen offered to the body in a certain period by circulatory system,DO,2,CO（1.38SaO,2,+ 0.003PaO,2,）,VO,2,Oxygen Consumption-,Oxygen consumpted by all cells in a certain period.,VO,2,Ca-vDO,2,CO10,44Oxygen associated indexDO2 O,45,Critical DO,2,VO,2,DO,2,Sepsis,ARDS,MODS,Normal,Critical delivery oxygen,45Critical DO2VO2DO2SepsisNor,46,Lactic Acid and cells hypoxia,Lactic Acid,-,latent cells hypoxia,lactic acidosis,-,tissue perfusion deficiency and cells hypoxia,Lactic Acid normal value-,0.5-1.5 mmol/L,4-5 mmol/LSB and PH,lactic acidosis,L/P rate,-,cells hypoxia,L/P rate,normal value- 10:1,46Lactic Acid and cells hypoxi,47,Strategy of ameliorate oxygen metabolism,Improvement of oxygen delivery,respiratory support-to improve arterial blood oxygen content,higher inhalated oxygen concentration,ventilator,increase cardiac output,Heart rate, cardiac rhythm, cardiac contractility, preload/after load,Blood system,rise hemoglobin concentration,47Strategy of ameliorate oxyge,48,Strategy of ameliorate oxygen metabolism,Increase,oxygen extraction ratio,Ameliorate interstitial edema,Reduce blood capilary permeability,Ameliorate oxygen extraction of cells,48Strategy of ameliorate oxyge,49,Treatmen of CLS,Limitation of water-intake,premise: never get CO down,Infusion volume decided by urine volume per hour when lung and brain interstitial edema happen.,Rise colloid osmotic pressure,Use powerful diuretic,Use glucocorticoid,49Treatmen of CLSLimitation of,50,Nutritional support,Metabolism support,Offer nutritional substrate but never increase organ loading.,Metabolism modulation,Inhibition of catabolism hormones,Promote protein synthesis ,ease negative nitrogen balance,50Nutritional supportMetabolis,51,Nutritional support,Add accessories,Promote protein synthesis and cell growth,Modulate immunologic response,Enteral nutrition,Protect bowel blood-mucosa barrier (prevent from infection,),51Nutritional supportAdd acces,52,Discussion of therapy for stress and inflammatory mediators,Antagonism and clearance,Aim at excessive cytokines,-,post-translation levels,Reduction of synthesis,keep the balance between pro- and anti- cytokines,- in,transcription levels,-,in translation level,52Discussion of therapy for s,53,Cytokines modulation,In transcription level,Anti-mRNA expression,(NF-B is in charge of many kinds of cytokine expression.),Translation level,Reduce cytokines synthesis,Post translation level,Anti-cytokines(antibody or soluble receptor),Block receptor of cytokines,Clearance of cytokines(plasmapheresis,),53Cytokines modulationIn trans,54,Treatmen of ARDS,Correct hypoxemia quickly,use v,entilator as soon as possible,appropriate PEEP,（,regain alveolar function and functional residual,capacity),54Treatmen of ARDSCorrect hypo,55,Treatmen of ARDS,Maintain Circulation and lung interstitial edema,Proper crystal/colloid rate,Diuretic,Negative water balance,(according to CVP/PAWP , urine output and lung auscultation),55Treatmen of ARDSMaintain Cir,56,Treatmen of ARDS,Prevent and treat infection,Block SIRS,corticoid in the initial stage,mediators inhibitor (Ibuprofen, Dentoxifylline,TNF antibody),56Treatmen of ARDSPrevent and,57,Treatment of ARF,Oliguria or anuria stage,(7-10days,average 5-6 and max. more than 1 month),confine water intake,Equal water intake and output,fluid intake per day=(dominant water losing )+ (non dominant water losing) - (endogeneous water)or 0.5kg,nutrient,Low protein, high calorie,high Vitamin,protein synthesis hormones,57Treatment of ARFOliguria or,58,Treatment of ARF,correct electrolytes imbala,Hyperkalemia,Hyponatremia,Hypocalcemia,Acidosis,Counterinfection,blood purification,(CHF),58Treatment of ARFcorrect elec,59,Proper fluid intake to prevent excessive losing of extracellular fluid: about,1/31/2 water lose,Correct electrolyte imbalance,Electrolytes test everyday,Increase protein intake,Counterinfection,Diuresis stage,59Proper fluid intake to preve,60,Summary,(1),Differences between MODS and multiple organ low function,Low function,MODS,primary illness Chronic acute,Pathogenesis interaction among organs hypoxia and Mediators,Pathology NO capillary dysfunction capillary dysfunction,Organ lesion accumulative subclinical,substantial functional,irreversible reversible,60Summary(1) Differences betwe,61,(2),Differences between MODS and primary MODS,The effect of ischemia , ischemia-reperfusion or other injury factor on cells,The first strikeprimary MODS,Organell injury,Cell edema and necrosis,Cell injury mediated by inflammatory mediators,T,he second strike secondary MODS,Cell membrane injury,Cell metabolism dysfunction, apoptosis,61(2) Differences between MODS,62,(3),Modern opinion of MODS development,Excessive inflammatory response runs through the course ,and is the main threaten to life.,Once SIRS triggers single organ dysfunction, the pathophysiological state will get worse progressively, and finally MODS come up.,SIRS ,sepsis and their complications construct a CONTINUM,and MOF is the most severe consequence.,62(3)Modern opinion of MODS de,知识回顾,Knowledge Review,知识回顾Knowledge Review,