【医学课件大全】多脏器功能障碍综合征及监护（瑞金医学sicu）

多脏器功能障碍综合征及监护,上海第二医科大学附属瑞金医院SICU Surgical ICU of Ruijin Hospital Shanghai Second Medical University,MODS and intensive care,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 1980s MSOF，multiple system organ failure- Fry38/533 point out the relationship between MSOF and severe infection 1990s MODS,multiple organ dysfunction syndrome,3,Case 1 Male 26y Post-subtotal excision of colon Ileocolonic stoma leakage Multiple intestinal fistula,4,Abdominal abscess,5,Long-term application of high caloria parenteral nutrition ( fat emulsion) liver tumefaction liver dysfunction SGPT 36 SGOT 144 TB 167.9 DB 102.8,6,HR 170 RR 55 PaCO2 23.8 WBC 18700,Positive blood cultivation,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,8,Case 2 male 59y 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,9,HR 120 RR 28 PaCO2 26.8 WBC 12600,10,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,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,12,clinical behavior Accumulative Substance irreversible Multiple organ low function caused by interaction between organs,Chronic disease Multiple organ low function,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,14,Sequential organ dysfunction after emergency disease,MODS,Clinical behavior Delayed Sequential Reversible MODS Excessive inflammatory mediators,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,16,1.Direct injury of ischemia,Hypersensibitity in heart and brain Selective ischemia Endothelial cell injury leads to high vascular permeability and low volume,17,permeability of cell membrane,Intracellular acidosis,Lower protein synthesis,Injury of ischemia and reperfusion,18,Vessel permeability WBC chemotaxis,monocyte/macrophage,neutrophil,elastinase PLA2 ODFR,TNF IL8 et al IL1 IL6,liver：acute phase reaction,Remote organ injury,Tissue damage,etiological factor,neutrophil,Adherent molecule,2.Excessive inflammation SIRS MODS,Vascular endothelial cell,SIRS,MODS,19,Clinical progress,uncontrolled stress,SIRS,Capillary leakage syndrome,MODS,MSOF,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,21,Important molecule in MODS,Anti-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 H2O2、NO production of macrophage Inhibit antigen presentation and other assistant functions of monocytes and macrophage,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 VECs：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.,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.,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,25,T 38or 36 HR90 beat/min RR20/min or PaCO232mmHg WBC12000mm3 or 4000mm3 or premature cells 10,Sepsis,Systemic Inflammatory Response Syndrome (SIRS),(SIR+Positive Culture),(SIR without infection),Systemic Inflammatory Response syndrome SIRS,26,Chaotic internal milieu during acute phase,Disturbance of electrolytes and acid-base balance Fever Catabolism: emaciated,anemia Acute disseminated intravascular coagulation Arrhythmia Hyperglycemia, no ketonemia,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,28,Diagnosis of CLS,Positive body fluid balance Blood volume deficiency Hypoproteinemia Organ and total body Interstitial edema lung Interstitial edema cerebral Interstitial edema,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, platelet50-80thousand, Hypercoagulable state,DIC,central nervous system,cardiovascular system,Insanity,light orientation disorder,Progressive deepen coma,Ejection Fraction , capillary leakage,Irresponsivity to muscle strength drugs,30,Glasgow Score,31,Influenced organ,Lung ARDS 95% Kidney ARF only a few,32,Acute Respiratory Distress Syndrome, ARDS,Pathology of lung High capillary permeabilityInterstitial edema Vasoconstriction,micro thrombosis communicating branch opening Alveolar and small bronchusAtelectasis 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,33,Pathology Deteriorated lung Interstitial inflammation,usually complicated with SEPSIS Symptom Obviously dyspnoea and cyanosisneeds ventilator Increased respiratory tract secretion, rales Lung x-rayinfiltrates Disturbance of consciousness Febrile or high leucocyte,.The second stage,34,3. Telophase,Pathology Lung parenchyma fibrosis Microvascular occlusion Increased preload, hypoxia Symptom Deep coma Arrhythmiabradycardiacardiac arrest,35,Diagnosis,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),37,1.History and physical examination Etiology prerenal pathogen postrenal pathogen,Diagnosis of ARF,38,2.Differentiation Diagnosis with prerenal ARF,39,3.Differentiation Diagnosis with Postrenal ARF,B type ultrasound(renal enlargement, ureter) Abdominal x-rays(calcification, calculus or Obstruction),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),41,5. renal function examination,Urine urea nitrogen ( 175mmol/24h) Fractional excretion of filtrated sodium1 FENa（%）=（UNa/PNa）（PCr/UCr ）100 osmotic pressure of urine *ARF- 400 mOsm/L BUN (more than 3.89.4mmol/L per day) ,Cr Urine/Plasma Cr-1-ARF *1-prerenal,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,43,Oxygen metabolism Monitoring,Critical DO2 Assay of plasma lactic acid/pyruvic acid,44,Oxygen associated index,DO2 Oxygen Delivery-Oxygen offered to the body in a certain period by circulatory system DO2CO（1.38SaO2 + 0.003PaO2） VO2 Oxygen Consumption- Oxygen consumpted by all cells in a certain period. VO2Ca-vDO2CO10,45,Critical DO2,VO2,DO2,Sepsis ARDS MODS,Normal,Critical delivery oxygen,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- 10:1,47,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,48,Strategy of ameliorate oxygen metabolism,Increase oxygen extraction ratio Ameliorate interstitial edema Reduce blood capilary permeability Ameliorate oxygen extraction of cells,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,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,51,Nutritional support,Add accessories Promote protein synthesis and cell growth Modulate immunologic response Enteral nutrition Protect bowel blood-mucosa barrier (prevent from infection ),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,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),54,Treatmen of ARDS,Correct hypoxemia quickly use ventilator as soon as possible appropriate PEEP（regain alveolar function and functional residual capacity),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),56,Treatmen of ARDS,Prevent and treat infection Block SIRS corticoid in the initial stage mediators inhibitor (Ibuprofen, Dentoxifylline,TNF antibody),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 hor