多脏器功能障碍综合征及监护课件

多脏器功能障碍综合征及监护多脏器功能障碍综合征及监护MODS and intensive careMODS and intensive care1多脏器功能障碍综合征及监护MODS and intensiDenomination variationn1973 1973 secondary system function failuresecondary system function failure-TilneyTilney Summary data of 18 cases ARF patients after abdominal aortic aneurysm operation,and Summary data of 18 cases ARF patients after abdominal aortic aneurysm operation,and 17 patients died from organ failure during dialysis.17 patients died from organ failure during dialysis.n1975197519771977 MOFSMOFS，multiple organ failure syndromemultiple organ failure syndrome-BaueBaue，19751975 （Yet the treatment did not save the lives.)Yet the treatment did not save the lives.)MOF MOF，multiple organ failuremultiple organ failure-EisemanEiseman，19771977n 1980s 1980s MSOFMSOF，multiple system organ failuremultiple system organ failure-Fry38/533Fry38/533 point out the relationship between MSOF and severe infectionpoint out the relationship between MSOF and severe infectionn 1990s 1990s MODS,multiple organ dysfunction syndromeMODS,multiple organ dysfunction syndrome2Denomination variation1973 sCase 1Case 1Male 26yMale 26yPost-subtotal excision of colonPost-subtotal excision of colonIleocolonic stoma leakageIleocolonic stoma leakageMultiple intestinal fistulaMultiple intestinal fistula3Case 13Abdominal abscess4Abdominal 4Long-term application of high caloria parenteral nutrition(fat emulsion)liver tumefaction liver dysfunction SGPT 36 SGPT 36 SGOT 144 SGOT 144 TB 167.9 TB 167.9 DB 102.8DB 102.8 5Long-term application of5HR 170 HR 170 RR 55RR 55PaCOPaCO2 2 23.823.8WBC 18700WBC 18700Positive blood cultivation Positive blood cultivation 6HR 170 Positive blood cultivJan 16thJan 16th septic shockseptic shockJan 17th Jan 17th Renal functionRenal function BUN 20.5 BUN 20.5 Cr 337 Cr 337 need inhalation of need inhalation of oxygen with mask oxygen with mask continuous continuous hemofiltration hemofiltration Jan 19thJan 19th tracheotomytracheotomy ventilator application ventilator application 7Jan 16th7Case 2 male 59yExtensive anterior wall Myocardial infarction 20 days after onset(2002/3/6)continuous ventricular tachycardiaventricular fibrillation electric defibrillation 5 times antiarrhythmic drugs counter shock drugs ventilator application8Case 2 male 59y8HR 120 HR 120 RR 28RR 28PaCOPaCO2 2 26.826.8WBC 12600WBC 126009HR 120 9nRepeatedly ventricular tachycardia and fibrillation，totally 21 times electric defibrillationnContinuous hyperpyrexia、high WBC、HR90、RR22nCultivation negative,antibiotics no effectivenessnOrgan dysfunction came in crowdsnshocknRespiratory dysfunctionnDeterioration of liver functionnCast in urine routine test BUN、Cr oliguria、anurianCoagulation abnormalityndeath10Repeatedly ventricular tachycaAcute onsetManifestatin of excessive inflammationDeteriotation of pts conditions despite active therapyMultiple organ dysfunctionDifferent pts,Same progressCase 1:infectiousCase 2:noninfectious11Acute onsetDifferent pts,Sameqclinical behaviorclinical behaviorvAccumulativeAccumulativevSubstanceSubstancevirreversibleirreversibleqMultiple organ low functionMultiple organ low functionvcaused by interaction between organscaused by interaction between organsChronic disease Chronic disease Multiple organ low function Multiple organ low function 12clinical behaviorChronic diseaMODS followed by primary emergency MODS followed by primary emergency disease in 24 hoursdisease in 24 hoursqClinical manifestationClinical manifestationvburst outburst outvSimultaneousSimultaneousvdie quicklydie quicklyqprimary MODS primary MODS vIschemiaIschemiavischemia and reperfusionischemia and reperfusionvphysical and chemical injury factorphysical and chemical injury factor13MODS followed by primary emergSequential organ dysfunction Sequential organ dysfunction after emergency disease,MODSafter emergency disease,MODSqClinical behaviorClinical behaviorvDelayedDelayedvSequentialSequentialvReversibleReversibleqMODSMODSvExcessive inflammatory mediatorsExcessive inflammatory mediators14Sequential organ dysfunction a1.Direct injury of ischemia1.Direct injury of ischemiaOxygen&nutrient insufficiencyIntegrity of cell membrane organelle insultATP Extracellular fluid in-flowHydrolase activationNatrium in-flowcalcium in-flow 151.Direct injury of ischemiaOxy1.Direct injury of ischemia1.Direct injury of ischemiaqHypersensibitity in heart and brainqSelective ischemiaqEndothelial cell injury leads to high vascular permeability and low volume161.Direct injury of ischemiaHyppermeability of cell membraneNaNa+CaCa+H H2 2O OADPADPAMPAMPIMPIMPadenosinexanthinehypoxanthinehypoxanthine ribosideUric Acidoxygen-derived free radidicalsxanthine oxidasexanthine oxidaseXanthine dehydrogenaseIntracellular acidosisIntracellular acidosisLower protein synthesisLower protein synthesisInjury of ischemia and reperfusion17permeability of cell membraneVessel permeabilityVessel permeability WBC WBC chemotaxis monocyte/macrophage neutrophil elastinase PLA2 PLA2 ODFR TNF ILTNF IL8 et 8 et alal ILIL1 1 IL IL6 6 liverliver：acutephase reaction Remote organ injuryRemote organ injuryTissue damage Tissue damage etiological factor neutrophilAdherent molecule2.Excessive inflammation 2.Excessive inflammation SIRS MODS SIRS MODS Vascular endothelial cellSIRSMODS18Vessel permeability WBC chemClinical progressClinical progressuncontrolled uncontrolled stressstressSIRSSIRSCapillary leakage syndromeCapillary leakage syndromeMODSMODSMSOFMSOF19Clinical progressuncontrolled Important molecule in MODSImportant molecule in MODS Pro-inflammatory cytokines:TNF-,IL-1、2、6 etcqStimulate synthesis and release of other cytokinesqActivate neutrophiles,eosinophils and monocytes;activate T and B cell;chemotaxisqIncrease the expression of adherent molecule qActivate complement and coagulation systemqIncrease permeability of vessels,decrease BPqCause fever and catabolism of muscle20Important molecule in MODS PrImportant molecule in MODSImportant molecule in MODSAnti-inflammatory cytokines:IL-4、10 etcqMaintain and enhance the function of activated NK cells,monocytes,B and T cells，qInhibit proliferation of T,B cellqInhibit pro-inflammatory cytokines production,receptor expression and cytotoxicity of monocytesqInhibit adherent molecule expression of vascular endothelial cells(VECs)qInhibit H2O2、NO production of macrophageqInhibit antigen presentation and other assistant functions of monocytes and macrophage21Important molecule in MODS AnImportant cells in MODSImportant cells in MODSqPolymorphonuclear leucocyte（PMN）：Effector cell of inflammatory response.Could release several protein enzymes and ODFR to destroy VECs and stromaqVECs：When 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 MODSPolymorImportant organ in MODSImportant organ in MODSIntestinesqBecause 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 MODSIntestiuncontrolled stresscarbohydrate metabolism dysfunction,carbohydrate metabolism dysfunction,Insulin tolerance,without KetonemiaInsulin tolerance,without Ketonemiahyperkinetic circulatory state,hyperkinetic circulatory state,Hyperpyrexia,High Stroke volume,High Hyperpyrexia,High Stroke volume,High oxygen consumptionoxygen consumptionProtein metabolism dysfunction,high Protein metabolism dysfunction,high katabolism,acute phase proteinkatabolism,acute phase protein24uncontrolled stresscarbohydratnT T 38or 38or 3636nHRHR90 beat/min90 beat/minnRRRR2020/min or PaCOmin or PaCO2 232mmHg32mmHgnWBCWBC12000mm12000mm3 3 or or 4000mm4000mm3 3 or premature cells or premature cells 1010SepsisSepsisSystemic InflammatorySystemic InflammatoryResponse Syndrome(SIRS)Response Syndrome(SIRS)(SIR+Positive Culture)SIR+Positive Culture)(SIR without infection)SIR without infection)Systemic Inflammatory Response syndromeSystemic Inflammatory Response syndrome SIRSSIRS25T 38or 36SepsisSystemic InChaotic internal milieu during acute Chaotic internal milieu during acute phasephaseqDisturbance of electrolytes and acid-base balanceqFeverqCatabolism:emaciated,anemiaqAcute disseminated intravascular coagulationqArrhythmiaqHyperglycemia,no ketonemia26Chaotic internal milieu duringSecondary aldosteronism -high density urine without Proteinuria,oliguria -prerenal azotemia -swollenPlasma protein leakage -Interstitial edema -Hypoproteinemia -blood inspissasion -HypovolemiaCapillary leakage syndrome,CLS27Secondary aldosteronismPlasma Diagnosis of CLSqPositive body fluid balanceqBlood volume deficiencyqHypoproteinemiaqOrgan and total body Interstitial edemavlung Interstitial edemavcerebral Interstitial edema28Diagnosis of CLSPositive body Organs dysfunction or failureOrgan or systemdysfunctionfailurelungLiverkidneyintestineBloodHypoxemia,respirator at list 3-5daysARDS,PEEP10cmH2O,FiO20.5Bilirubin2-3mg/dL,Liver function2 normal valueBilirubin2-3mg/dL,icterusoliguriadialysisUntolerance of enteral nutrition5daysCurlingls ulcer needs blood transfusion,Acalculous cholecystitisPT or PTT elongation,platelet95%95%nKidney ARFKidney ARF only a fewonly a few31Influenced organLung ARDS31Acute Respiratory Distress Acute Respiratory Distress Syndrome,Syndrome,ARDSARDSqPathology of lungvHigh capillary permeabilityInterstitial edemavVasoconstriction,micro thrombosis communicating branch openingvAlveolar and small bronchusAtelectasisvDecreased alveolar surfactantvEdemavI type epithelial cells instead by II type cellqSymptomvTachypnea,respiratory distress can not be eased by oxygen inhalationvNo ralesvNo lung x-ray abnormality1.The early stage32Acute Respiratory Distress SynqPathologyPathologyvDeteriorated lung Interstitial Deteriorated lung Interstitial inflammation,usually complicated with SEPSISinflammation,usually complicated with SEPSISqSymptomSymptomvObviously dyspnoea and cyanosisneeds Obviously dyspnoea and cyanosisneeds ventilatorventilatorvIncreased respiratory tract secretion,ralesIncreased respiratory tract secretion,ralesvLung x-rayinfiltratesLung x-rayinfiltratesvDisturbance of consciousnessDisturbance of consciousnessvFebrile or high leucocyte Febrile or high leucocyte 2.The second stage33Pathology.The second stage333.Telophase qPathologyPathologyvLung parenchyma fibrosisLung parenchyma fibrosisvMicrovascular occlusionMicrovascular occlusionvIncreased preload,hypoxiaIncreased preload,hypoxiaqSymptomSymptomvDeep comaDeep comavArrhythmiabradycardiacardiac arrestArrhythmiabradycardiacardiac arrest343.Telophase Pathology34Diagnosis35Diagnosis35Acute Renal Failure,ARFAcute Renal Failure,ARFqEtiology vPrerenal3Hemorrhage,shock,fluid losing without appropriate fluid resuscitationvpost renal3both side ureter or urinary flow blockedvrenal3kidney ischemia(hematorrhea,sepsis,allergic reaction)3intoxication(aminoglycoside antibiotic,biotic toxin,chemical)36Acute Renal Failure,ARFEtiolo1.History and physical examinationvEtiologyvprerenal pathogenvpostrenal pathogenDiagnosis of ARF 371.History and physical examina2.Differentiation Diagnosis with prerenal ARF382.Differentiation Diagnosis wi3.Differentiation Diagnosis with Postrenal ARFqB type ultrasound(renal enlargement,ureter)qAbdominal x-rays(calcification,calculus or Obstruction)393.Differentiation Diagnosis wi4.4.Laboratory Urine testLaboratory Urine testqUrinary catheter to record urine volumeUrinary catheter to record urine volumeqUrine acidity/density(1.010-1.014)Urine acidity/density(1.010-1.014)qUrine microscopic examinationUrine microscopic examinationvRBC and renal tubule epithelia(renal cortex and RBC and renal tubule epithelia(renal cortex and renal medulla necrosis)renal medulla necrosis)vLarge Brown casts(renal failure casts)Large Brown casts(renal failure casts)vEosinophil(interstitial nephritis)Eosinophil(interstitial nephritis)vRed cell cast(glomerulonephritis)Red cell cast(glomerulonephritis)vNormal(prerenal or postrenal failure earlier Normal(prerenal or postrenal failure earlier period)period)404.Laboratory Urine testUrinar5.5.renal function renal function examinationexaminationnUrine urea nitrogen(175mmol/24h)nFractional excretion of filtrated sodium1 FENa（%）=（UNa/PNa）（PCr/UCr）100nosmotic pressure of urine *ARF-400 mOsm/LnBUN (more than 3.89.4mmol/L per day),Cr nUrine/Plasma Cr-1-ARF *1-prerenal415.renal function examinationUIntensive careqOrgan and system function Monitoring and supportvObject1.ameliorate oxygen metabolism2.ameliorate nutrien stateqTherapy aimed at stress and inflammatory MediatorsqTreatment of capillary leakageqTreatment of primary disease42Intensive careOrgan and systemOxygen metabolism MonitoringqCritical DO2qAssay of plasma lactic acid/pyruvic acid43Oxygen metabolism MonitoringCrOxygen associated indexqDODO2 2 Oxygen Delivery-Oxygen Delivery-Oxygen offered to the body in a certain period by circulatory system DO DO2 2COCO（1.38SaO1.38SaO2 2+0.003PaO+0.003PaO2 2）qVOVO2 2 Oxygen Consumption-Oxygen Consumption-Oxygen consumpted by all cells in a certain period.VO VO2 2Ca-vDOCa-vDO2 2CO10CO1044Oxygen associated indexDO2 OxyCritical DOCritical DO2 2VOVO2 2DODO2 2SepsisARDSMODSNormalCritical delivery oxygenCritical delivery oxygen45Critical DO2VO2DO2SepsisNormaLactic Acid and cells hypoxiaqLactic Acid-latent cells hypoxia lactic acidosis-tissue perfusion deficiency and cells hypoxia Lactic Acid normal value-0.5-1.5 mmol/L0.5-1.5 mmol/L 4-5 mmol/LSB and PH lactic acidosis qL/P rate -cells hypoxia L/P rate normal value-10:146Lactic Acid and cells hypoxiaLStrategy of ameliorate oxygen metabolismStrategy of ameliorate oxygen metabolism qImprovement of oxygen deliveryvrespiratory support-to improve arterial blood oxygen contentphigher inhalated oxygen concentration,ventilatorvincrease cardiac output pHeart rate,cardiac rhythm,cardiac contractility,preload/after loadvBlood systemprise hemoglobin concentration47Strategy of ameliorate oxygen Strategy of ameliorate oxygen metabolismStrategy of ameliorate oxygen metabolismqIncrease oxygen extraction ratiovAmeliorate interstitial edemavReduce blood capilary permeabilityvAmeliorate oxygen extraction of cells48Strategy of ameliorate oxygen Treatmen of CLSTreatmen of CLSqLimitation of water-intakeLimitation of water-intakevpremise:never get CO downpremise:never get CO downvInfusion volume decided by urine volume per Infusion volume decided by urine volume per hour when lung and brain interstitial edema hour when lung and brain interstitial edema happen.happen.qRise colloid osmotic pressureRise colloid osmotic pressureqUse powerful diureticUse powerful diureticqUse glucocorticoidUse glucocorticoid49Treatmen of CLSLimitation of wNutritional supportNutritional supportqMetabolism supportMetabolism supportvOffer nutritional substrate but never Offer nutritional substrate but never increase organ loading.increase organ loading.qMetabolism modulationMetabolism modulationvInhibition of catabolism hormonesInhibition of catabolism hormonesvPromote protein synthesis,ease negative Promote protein synthesis,ease negative nitrogen balancenitrogen balance50Nutritional supportMetabolism Nutritional supportNutritional supportqAdd accessoriesAdd accessoriesvPromote protein synthesis and cell growthPromote protein synthesis and cell growthvModulate immunologic responseModulate immunologic response qEnteral nutritionEnteral nutritionvProtect bowel blood-mucosa barrier Protect bowel blood-mucosa barrier(prevent from infection(prevent from infection)51Nutritional supportAdd accessoDiscussion of therapy for stress and Discussion of therapy for stress and inflammatory mediatorsinflammatory mediatorsqAntagonism and clearanceAntagonism and clearancevAim at excessive cytokinesAim at excessive cytokines -post-translation levelspost-translation levelsqReduction of synthesisReduction of synthesis vkeep the balance between pro-and anti-keep the balance between pro-and anti-cytokinescytokines -in -in transcription levelstranscription levels -in translation levelin translation level52Discussion of therapy for strCytokines modulationCytokines modulationqIn transcription levelIn transcription levelvAnti-mRNA expression Anti-mRNA expression (NF-B is in charge of many kinds of cytokine(NF-B is in charge of many kinds of cytokine expression.)expression.)qTranslation levelTranslation levelvReduce cytokines synthesisReduce cytokines synthesisqPost translation levelPost translation levelv Anti-cytokines(antibody or soluble Anti-cytokines(antibody or soluble receptor)receptor)vBlock receptor of cytokinesBlock receptor of cytokinesvClearance of Clearance of cytokines(plasmapheresiscytokines(plasmapheresis)53Cytokines modulationIn transcrTreatmen of ARDSTreatmen of ARDS3Correct hypoxemia quicklyCorrect hypoxemia quickly;use vuse ventilator as soon as entilator as soon as possiblepossible;appropriate PEEPappropriate PEEP（regain regain alveolar function and alveolar function and functional residual functional residual capacity)capacity)54Treatmen of ARDSCorrect hypoxeTreatmen of ARDSTreatmen of ARDS3Maintain Circulation and lung Maintain Circulation and lung interstitial edemainterstitial edema;Proper crystal/colloid rateProper crystal/colloid rate;DiureticDiuretic;Negative water balance Negative water balance(according to(according to CVP/PAWP,urine output and lung auscultation)CVP/PAWP,urine output and lung auscultation)55Treatmen of ARDSMaintain CircuTreatmen of ARDSTreatmen of ARDS3Prevent and treat infectionPrevent and treat infection3Block SIRSBlock SIRS;corticoid in the initial stagecorticoid in the initial stage;mediators inhibitor(Ibuprofen,mediators inhibitor(Ibuprofen,Dentoxifylline,TNF antibody)Dentoxifylline,TNF antibody)56Treatmen of ARDSPrevent and trTreatment of ARFTreatment of ARFOliguria or anuria stageOliguria or anuria stage (7-10days,average 5-6 and max.more than 1 month)(7-10days,average 5-6 and max.more than 1 month)1.1.confine water intakeconfine water intakeqEqual water intake and outputEqual water intake and output fluid intake per day=(dominant water losing)+fluid intake per day=(dominant water losing)+(non dominant water losing)-(endogeneous(non dominant water losing)-(endogeneous water)or 0.5kgwater)or 0.5kg2.2.nutrient nutrient qLow protein,high calorie,high VitaminLow protein,high calorie,high Vitaminqprotein synthesis hormonesprotein synthesis hormones57Treatment of ARFOliguria or anTreatment of ARFTreatment of ARF3.3.correct electrolytes imbalacorrect electrolytes imbalavHyperkalemiaHyperkalemiavHyponatremiaHyponatremiavHypocalcemiaHypocalcemiavAcidosisAcidosis4.4.Counterinfection Counterinfection 5.5.blood purification blood purification(CHF)(CHF)58Treatment of ARFcorrect electr1.1.Proper fluid intake to prevent excessive Proper fluid intake to prevent excessive losing of extracellular fluid:aboutlosing of extracellular fluid:about 1/31/31/2 water lose1/2 water lose2.2.Correct electrolyte imbalanceCorrect electrolyte imbalancevElectrolytes test everydayElectrolytes test everyday3.3.Increase protein intakeIncrease protein intake4.4.CounterinfectionCounterinfectionDiuresis stageDiuresis stage59Proper fluid intake to preventSummarySummary(1)(1)Differences between MODS and multiple Differences between MODS and multiple organ low functionorgan low functionLow functionLow functionMODSMODSprimary illness Chronic primary illness Chronic acuteacutePathogenesis interaction among organs hypoxia and Pathogenesis interaction among organs hypoxia and MediatorsMediatorsPathology NO capillary dysfunction Pathology NO capillary dysfunction capillary dysfunction capillary dysfunction Organ lesion accumulative Organ lesion accumulative subclinicalsubclinicalsubstantial su