重庆医科大学儿科学教案讲课题目：Neonatal Septicemia 新生儿败血症教师：余加林授课题目TEACHINGTOPICNeonatalSepticemia新生儿败血症第几次课TIMES3rd教学方法METHODSClass teaching教学对象OBJECTIVESeven years students学时:TIME40x1minutes教学目标PURPOSEmaster the definitionand clinical manifestationsofneonatal septicemialearn principle of antibiotics selection教学重点和难点.clinical manifestationsPURPOSE/DIFFICULTIES2. key points of treatmentlaborratorytests4. principle of antibiotics selection教学内容的深化与拓宽1.Septicemia isthechiefcauseofneonatal death indevelopingcountries.The developmentsFurther study: the new conception of septicemia, and therelationshipandfndsepticem教学要求的英语单词SisspmiaPathgnacteriastaphylcci&oliGrouEnglish requirementsStreptococcus, GBS, Infectious gateway, Descending infection, Ascendinginn,iacboobranbr,pall,thay,judfhypothermia,temperature instability,poorhandling,hypoglycemiahyperglycemia, blood gas derangements, increased respiratory rate, apneagrunting, cyanosis实践性教学安排One teaching hourofclinical workshopClinical study 教材及参考资料沈晓明，王卫平。儿科学北京：人民卫生出版社,2008USED/2.TEXTBOOK杨锡强，易著文．儿科学。北京：人民卫生出版社,2008REFERENCESTaeusch HW, Ballard RA, Gleason CA. Elsevier Saunders: Avery'sdiseases of the newborn,8th edition,2005教具 TEACHING AIDSop教学程序Procedures详细见讲稿主要内容及安排（教学内容详细安排、教学方法的运用、师生活动设计、及时间分配）：
重庆医科大学儿科学教案 讲课题目：Neonatal Septicemia 新生儿败血症 教师： 余加林 授课题目 TEACHING TOPIC Neonatal Septicemia 新生儿败血症 第几次课 TIMES 3 rd 教学方法 METHODS Class teaching 教学对象 OBJECTIVE Seven years students 学时: TIME 40×1 minutes 教学目标 PURPOSE 1. master the definition and clinical manifestations of neonatal septicemia 2. learn principle of antibiotics selection 教学重点和难点 PURPOSE/ DIFFICULTIES 1．clinical manifestations 2．key points of treatment 3．laboratory tests 4．principle of antibiotics selection 教学内容的深化与拓宽 The developments 1．Septicemia is the chief cause of neonatal death in developing countries. 2．Further study: the new conception of septicemia, and the relationship and differences between sepsis and septicemia. 教学要求的英语单词 English requirements Sepsis, septicemia, Pathogenic Bacteria, staphylococci & E coli, Group B Streptococcus, GBS, Infectious gateway, Descending infection, Ascending infection, iatrogenic, blood-brain barrier, pallor, lethargy, jaundice, fever, hypothermia, temperature instability, poor handling, hypoglycemia / hyperglycemia, blood gas derangements, increased respiratory rate, apnea, grunting, cyanosis 实践性教学安排 Clinical study One teaching hour of clinical workshop. 教材及参考资料 TEXT BOOK USED/ REFERENCES 1. 沈晓明，王卫平. 儿科学. 北京: 人民卫生出版社, 2008 2. 杨锡强，易著文. 儿科学. 北京: 人民卫生出版社, 2008 3. Taeusch HW, Ballard RA, Gleason CA. Elsevier Saunders: Avery’s diseases of the newborn, 8th edition, 2005 教具 TEACHING AIDS ppt 教学程序 Procedures （教学内容详细安排、教学方法的运用、师生活动设计、及时间分配）： 详细见讲稿主要内容及安排
讲稿主要内容及安排备注（授时间安排课形式）（分钟）题目Neonatal Septicemia 新生儿败血症[定义]ClassDefinition5'teachingSystemic disease associated with the presence and persistence of pathogenicmicroorganisms or their toxins in the blood.(Dorland, 27th ed)Incidence:1-4Newborns/1000LB/YearMeningitis:5-25%Case fatality:25% (2 - 60%)[病原菌] Pathogenic Bacteriadominative strains dfferent in different region and diferent eraIn China:staphylococci葡萄球菌&Ecoli 大肠杆菌Class5opportunist pathogen 机会致病菌：S.e表皮葡萄球菌、P.a绿脓杆菌、克teaching雷伯杆菌、entericbacilli肠杆菌、Clostridium perfringens产气英膜梭菌、Cjejuni空肠弯曲菌、H.p 幽门螺杆菌Inwest: GBS、Listerella[感染途经 Infectiousgateway() antepartum infection Class5--from blood circulation, eg Listerella, Campylobacterfetusteaching+ pregnancy maternal infectiondcavatro
讲稿主要内容及安排 备注（授 课形式） 时间安排 （分钟） 题目 Neonatal Septicemia 新生儿败血症 Class teaching 5’ [定义] Definition Systemic disease associated with the presence and persistence of pathogenic microorganisms or their toxins in the blood. (Dorland, 27th ed) Incidence: 1- 4 Newborns /1000 LB / Year Meningitis: 5 - 25 % Case fatality: ~ 25 % (2 - 60%) [病原菌] Pathogenic Bacteria Class teaching 5‘ dominative strains different in different region and different era In China: staphylococci 葡萄球菌 & E coli 大肠杆菌 opportunist pathogen 机会致病菌：S.e 表皮葡萄球菌、P.a 绿脓杆菌、克 雷伯杆菌、enteric bacilli 肠杆菌、Clostridium perfringens 产气荚膜梭菌、 C.jejuni 空肠弯曲菌、H.p 幽门螺杆菌 In west: GBS、Listerella [感染途经] Infectious gateway Class teaching 5‘ (1) antepartum infection - from blood circulation, eg. Listerella, Campylobacter fetus → pregnancy maternal infection - iatrogenic eg, puncture on amniotic fluid cavity, intrauterine transfusion
(2) intrapnfectio-- Ascending infection*premature rupture of membrane (PROM) for 6-12h could haveopportunity,50%incidencefor24h.Usually>18hasriskfactors* prolonged labor-- inhalation, ingestioniatrogenic* take blood sample from scalp* put electrodes* put obstetric forceps(3) postpartum infection (most common)Staphylococcus areus* needle mouth*pressbreasordmanagemenlatrogen* UVC,UAC* Ventilation, eg. S. epidermidis, P. aeruginosa[发病机制]Non-specific immunity defectionpoor barrier functiondefective development of lymph nodes+low level of C3, C5,opsonin et alneutrophil produce andreserve000low function of cytokinesBarrier function not integrity , umbilical stump , deficiency of blood-brainClassbarrier,5teachingSpecific immunity defection+ Ig G : the more ltle gastational age , the lower IgG, and more easyinfections*IgM、IgA Not able to cross placenta, so low content in body and easytoG- bacterial infections+ Tcells : Be primary state and poor produce cytokine[临床表现] Clinical manifestationClass10teachingClinical manifestation is non- specificity
(2) intrapartum infection - Ascending infection *premature rupture of membrane (PROM) for 6-12h could have opportunity , 50% incidence for 24h. Usually >18h as risk factors * prolonged labor - inhalation, ingestion - iatrogenic * take blood sample from scalp * put electrodes * put obstetric forceps (3) postpartum infection (most common) - Staphylococcus areus * needle mouth * press breast * unclean cord management - iatrogenic * UVC, UAC * Ventilation, eg. S. epidermidis, P. aeruginosa [发病机制] Class teaching 5’ Non-specific immunity defection ❖ poor barrier function ❖ defective development of lymph nodes ❖ low level of C3, C5 , opsonin et al ❖ poor neutrophil produce and reserve ❖ low function of cytokines Barrier function not integrity，umbilical stump，deficiency of blood-brain barrier， Specific immunity defection ❖ Ig G：the more little gastational age ，the lower IgG, and more easy infections ❖ IgM、IgA：Not able to cross placenta, so low content in body and easy to G－bacterial infections ❖ T cells：Be primary state and poor produce cytokine [临床表现] Clinical manifestation Class teaching 10’ Clinical manifestation is non- specificity
General featurespallor, lethargy jaundicefever, hypothermia, temperature instability (note 1/3 of confirmed sepsiscases are normothermic)poor handlinghypoglycaemia /hyperglycaemiablood gas derangements(including acidosis and lactate accumulation)Respiratory : increased respiratory rate, apnoea , grunting , cyanosisCVS : tachycardia , bradycardic episodes , poor perfusion, hypotensionCutaneous : petechiae , bruising , bleeding from puncture sitesGIT : poor feeding , vomiting , abdominal distension , feed intolerance ,bilious aspirates /vomits , loose stoolsCNS : lethargy, irritability , seizures[实验室检查]InvestigationsI. bacteriology study1.Blood culture (mandatory)Classtake sample underaseptic techniquebeforeadministration of antibiotics10'as soon as possibleteaching- anaerobic culture p.r.n if GI perforation-L-type bacterial culture p.rn if penicillins or cephalosporins exposuresamplefromgastric juice&external auditorycanal for smear orculturewithin 1 hour of life if antepartum infection suspected- samples for culture include CSE, serous cavityfluid,catherter engBlood culture , CSF culture from Lumber puncture , supper pubicaspiation,SPA,Swab fromextemalauditory canals2. special antigen & DNA-forGBS andKantigen ofE colicounter immunoelectrophoresislatex agglutination test, ELISA- polymerase chain reaction(PCR) →16S rRNADNAprobe
General features： pallor, lethargy, jaundice fever, hypothermia, temperature instability (note 1/3 of confirmed sepsis cases are normothermic) poor handling hypoglycaemia / hyperglycaemia blood gas derangements(including acidosis and lactate accumulation) Respiratory：increased respiratory rate，apnoea ，grunting，cyanosis CVS：tachycardia ，bradycardic episodes，poor perfusion，hypotension Cutaneous：petechiae ，bruising，bleeding from puncture sites GIT：poor feeding，vomiting，abdominal distension，feed intolerance， bilious aspirates /vomits，loose stools CNS：lethargy，irritability，seizures [实验室检查] Investigations Class teaching 10’ Ⅰ. bacteriology study 1. Blood culture (mandatory) - take sample under aseptic technique before administration of antibiotics as soon as possible - anaerobic culture p.r.n if GI perforation - L-type bacterial culture p.r.n if penicillins or cephalosporins exposure - sample from gastric juice & external auditory canal for smear or culture within 1 hour of life if antepartum infection suspected - samples for culture include CSF, serous cavity fluid, catherter end Blood culture ， CSF culture from Lumber puncture ， supper pubic aspiration, SPA，Swab from external auditory canals 2. special antigen & DNA - for GBS and K1 antigen of E coli →counter immunoelectrophoresis, latex agglutination test, ELISA - polymerase chain reaction(PCR) →16S rRNA - DNA probe
II. Non-specific markers1.Full Blood Examination(FBE)→ The Polymorphonucleocyte (PMN) count2. immature / total neutrophils ratio (1/1)≥0.163. platelet count4. C-reactive protein (CRP), CRP rises approximately 12 hours after onsetof sepsis and returns to normal within 2 to 7 days of successful treatment[诊断] diagnosisDefinitive diagnosisClinical manifestation plus positive cultureClass2'Clinical diagnosisteachingClinical manifestation plus one of follows:Non-specific markers positive ≥2Pathogenic bacterium antigen(+) or DNA(+)[治疗] TreatmentAntibacterials therapyPrinciple of medicationBactericide selected accord ing to pathogenic bacteria2. Intravenously3. Combination4. Enough dose and course of treatmentAim directly at causative organismsG+ (eg. Staphylococci)penicillinase-fast penicillin,First generationClass8'cephalosporin,vancomycinteachingG- -→Ampicillin, aminoglycosides, third generation cephalosporinCombination : antibacterial spectrum comprising G+, G-for unknowetiological agent Usage: <7d q12h, >7d q8h; treatment course: 7-14d usually21dayformeningitisSpecial antibacterials :Amikacin : broad spectrum , side effect : ototoxicitydisadvantage: low concentration in CSF
Ⅱ. Non-specific markers 1.Full Blood Examination(FBE) → The Polymorphonucleocyte (PMN) count 2. immature / total neutrophils ratio (I/T)≥0.16 3. platelet count 4. C-reactive protein (CRP), CRP rises approximately 12 hours after onset of sepsis and returns to normal within 2 to 7 days of successful treatment [诊断] diagnosis Class teaching 2’ Definitive diagnosis Clinical manifestation plus positive culture Clinical diagnosis Clinical manifestation plus one of follows: 1. Non-specific markers positive ≥2 2. Pathogenic bacterium antigen(+) or DNA(+) [治疗] Treatment Class teaching 8’ Antibacterials therapy Principle of medication: 1. Bactericide selected according to pathogenic bacteria 2. Intravenously 3. Combination 4. Enough dose and course of treatment Aim directly at causative organisms G+ (eg. Staphylococci)→penicillinase-fast penicillin，First generation cephalosporin，vancomycin G- → Ampicillin, aminoglycosides, third generation cephalosporin Combination : antibacterial spectrum comprising G+, G- for unknow etiological agent Usage: <7d q12h, >7d q8h; treatment course: 7-14d usually 21 day for meningitis Special antibacterials： Amikacin：broad spectrum，side effect：ototoxicity disadvantage: low concentration in CSF