׫дҽѧӢÎÄÂÛÎÄÓÐÄÄЩ¸ñʽҪÇó¼°·½·¨

ʱ¼ä£º2020-10-19 14:02:19 ÂÛÎĸñʽ ÎÒҪͶ¸å

׫дҽѧӢÎÄÂÛÎÄÓÐÄÄЩ¸ñʽҪÇó¼°·½·¨

¡¡¡¡Ò½Ñ§Ó¢ÓïÂÛÎÄÊÇҽѧÆÚ¿¯µÄ³£¼ûµÄÎÄÌå¡£ÏÂÃæYJBYSС±àËÑË÷ÕûÀíÁ˹ØÓÚ׫дҽѧӢÎÄÂÛÎĵĸñʽҪÇó¼°·½·¨£¬¹©´ó¼Ò²Î¿¼ÔĶÁ£¬Ï£ÍûÄúϲ»¶!

׫дҽѧӢÎÄÂÛÎÄÓÐÄÄЩ¸ñʽҪÇó¼°·½·¨

¡¡¡¡¸ù¾ÝÓ¢¹úTheLancetÔÓÖ¾ºÍÏã¸ÛHong Kong Medical JournalÉÏËùµÇÔصÄÂÛÎÄÒÔ¼°¹úÍâÆäËüÆÚ¿¯Ëù¿¯µÇµÄÎÄÕÂÀ´·ÖÎö,´óÌå°üÀ¨ÒÔϼ¸¸ö·½ÃæÄÚÈÝ:±êÌâ¡¢ÕªÒª¡¢ÒýÑÔ¡¢·½·¨¡¢½á¹û¡¢ÌÖÂÛ¡¢ÖÂл¡¢²Î¿¼ÎÄÏס£¹ØÓÚÓ¢Óï±êÌâºÍÕªÒªµÄд×÷¸ñʽÔÚ±¾¿¯2003ÄêµÚ4ÆÚÉÏÒѾ­ÂÛÊö¡£ÏÖ¾ÍÂÛÎĵÄÒýÑÔ¡¢·½·¨¡¢½á¹û¡¢ÌÖÂÛ¡¢ÖÂлºÍ²Î¿¼ÎÄÏ××öÒ»ÏêϸÂÛÊö,ÒÔ÷϶ÁÕß¡£

¡¡¡¡1¡¡ÒýÑÔ(Introduction)

¡¡¡¡ÒýÑÔ¼´ÊÇÂÛÎĵĿª³¡°×¡£ÔÚÂÛÎĵÄÒýÑÔÖÐ,×÷ÕßÖ÷Òª½éÉÜÑо¿µÄ±³¾°ºÍÀíÓÉ,¾ßÌå˵Ã÷Ñо¿µÄÄÚÈÝ¡¢Ä¿µÄ¡¢ÌصãºÍÒâÒå¡£ÂÛÎĵı³¾°ºÍÀíÓÉÖ÷ÒªÖ¸Ñо¿Ö÷ÌâµÄÀúÊ·,ÏÖ×´,½øÕ¹ÒÔ¼°ÈÔÈ»´æÔÚµÄÎÊÌâ¡£ÒýÑÔ¿ÉÒÔ¶ÔÇ°ÈËÑо¿µÄ½á¹û,ÎÄÏ×ÕªÓýøÐÐÆÀÊö,²¢ÇÒÐðÊö×÷Õß×ÅÊÖÑо¿µÄÔ­Òò¼°Ñо¿µÄз¢Õ¹µÈ¡£

¡¡¡¡¸Ã²¿·ÖÄÚÈÝÔÚʱ̬Éϳ£ÔËÓÃÒ»°ã¹ýȥʱ,Ò»°ãÏÖÔÚʱ¼°ÏÖÔÚÍê³Éʱ¡£¾ÙÀý:

¡¡¡¡Introduction

¡¡¡¡The feasibility of ultrasonography for diagnosis of fetal cardiacabnormality was recognised in the early 1980s,and cardiac scanningis gradually being incorporated into fetal screening protocols.Theeffect of the screening process on the incidence and types ofcongenital heartdisease atterm has been difficultto ascertain becausemany pregnant women and infants travel great distances to specialistcentres which are farfrom their health authority.For a single centre,the geographical area from which its fetal referrals arrive is generallynot the same as the area attracting postnatal referrals,and the numberof births that each serves is impossible to define.The BritishPaediatric Cardiac Association(BPCA)undertook a nationalcollaborative study of fetal cardiac screening.The aim was to assessthe effect of fetal diagnosis of congenital heart disease on the patternof serious congenital heart disease at term.

¡¡¡¡2¡¡·½·¨(Methods)

¡¡¡¡¸Ã²¿·Ö¿ÉÒÀ¾ÝËùÑо¿µÄ¶ÔÏó»òʹÓõIJÄÁϺͲÉÓõķ½·¨,Ò²¿É·Ö±ð³Æ֮Ϊ:¶ÔÏóÓë·½·¨(Subjects and methods or Patients and methods),²ÄÁÏÓë·½·¨(Materials and methods)¡£·½·¨²¿·Öʵ¼ÊÉÏÊÇÂÛÎĵÄÖ÷Ìå,ËüÊǶÔÂÛÎĵÄÄÚÈݺͲÉÓõķ½·¨×÷³öÏêϸµÄÂÛÊö¡£¾ßÌåµÄ˳ÐòΪ:Ê×ÏÈÊÇËùʹÓõIJÄÁÏ»òÑо¿µÄ¶ÔÏó,Æä´ÎÊdzÌÐò°²ÅÅ,×îºóÊǽá¹û¼ÆËã»òͳ¼Æ·½·¨¡£·½·¨²¿·ÖÒ»°ãΪ»Ø¹ËÐÔÐðÊö,ÔÚʱ̬É϶à²ÉÓÃÒ»°ã¹ýȥʱ,ż¶ûÒ²ÓÐÓùýÈ¥Íê³Éʱ¡£²»¹ý,¼ÙÈôÐðÊöµÄÊǶ¨Òå,ÀíÂÛ,ͼ±íÄÚÈݼ°ÊýÖµ,ÊôÓڿ͹ÛÏÖÏó,¹Ê¿É²ÉÓÃÒ»°ãÏÖÔÚʱ¡£¾ÙÀý:

¡¡¡¡Patients and methods

¡¡¡¡The Information and Statistics Department of the Scottish Homeand Health Department collected data on the demographics andlaboratory results of all possible outbreak cases.We collected clinicaldata by reviewing the case notes of all cases admitted to hospital inthe Lanarkshire area.

¡¡¡¡All confirmed or probable cases ofEscherilchia coli(E coli)0157 infection,identified in the Lanarkshire area during the outbreakperiod,were included in the assessment and analysis.Confirmedcaseswere those in whom the outbreak strain ofE coliO157 wasisolated from stool samples.If stool cultureswere negative atthe locallaboratories,specimens were sent to Scotland'sE colireferencelaboratory in Aberdeen,for the more sensitive isolation method ofimmunomagnetic separation.Probable cases were those with bloodydiarrhoea or haemolytic uraemic syndrome(HUS)/thromboticthrombocytopenic purpura(TTP),an association with food sourcesimplicated in the outbreak,noE coliO157 isolated,and no otherorganism isolated.Adults were defined as patients 15 years of age orolder.

¡¡¡¡To allow standardisation of diagnosis in the face of a hugeclinical workload,a case definition for HUS and TTP was developedat the beginning of the outbreak.HUS was defined as evidence ofred-cell haemolysis(red-cell fragmentation on blood film and lactatedehydrogenase>1.5 times the upper limitof normal[our laboratory 0¡«480 IU/L])plus thrombocytopenia(platelets<150×109/L)with rising urea and creatinine concentrations.All three criteria hadto be met before the diagnosis could be made,but not necessarily onthe same blood sample.A diagnosis of TTPwas given to patientswhomet these laboratory criteria and developed new neurologicalsymptoms and signs.One patient was included as having developedHUS despite a minimum platelet count of 228×109/L(on death).

¡¡¡¡He had bloody diarrhoea,an association with an implicated foodsource,acute renal failure,the criteria for red-cell haemolysis,and afalling platelet count.

¡¡¡¡In the assessment of premorbid illness,medical historiesincluded as relevant were ischaemic heart disease,cardiac failure,hypertention,cerebrovascular disease,renal disease,diabetes,andimmunosuppression.Pulmonary oedemawas diagnosed on clinical andradiological evidence.

¡¡¡¡TPE was performed at three centres with three Cobe SpectraApheresis Systems(Cobe Laboratories Ltd,Gloucester,UK)and aBaxter Fenwal CS-3000 Plus Cell Separator(Baxter Healthcare,Newberry,UK).Plasma was exchanged with 2.0¡«2.4 Lfresh frozenplasma or cryosupernatant in refractory patients.The anticoagulantused was ACD-A.A combination of central and peripheral venousaccess was used.Intravenous hydrocortisone was given with eachexchange.Intravenous prostacyclin was also given to cases receivingTPE,at doses between 40 mg/h and 200 mg/h,where tolerated.Datawere analysed by means of SPSS(version 7.5).

¡¡¡¡3¡¡½á¹û(Results)¡£

¡¡¡¡½á¹û²¿·ÖÊÇÖ¸×÷ÕßÔÚʵÑé¹ý³ÌÖжÔʵÑéËù»ñµÃµÄ½á¹û½øÐп͹۵ÄÆÀÊö,Ò²¿ÉÒÔ˵ÊǶÔʵÑé½á¹û×÷³ö¹éÄÉ¡£¶øÇÒ½á¹û²¿·ÖÖ»ÊÇϵͳµØ½éÉÜÓëÖ÷ÌâÑо¿½ôÃÜÏà¹ØµÄÊý¾Ý,ÀýÈç,ÏÔ×ŵÄ`²îÒìÐÔ,PÖµµÈ,Æä½á¹û²¿·ÖÊǶԹýÈ¥µÄʵÑé×÷³ö¹éÄɸÅÊö,ÔÚʱ̬ÉÏͨ³£ÔËÓÃÒ»°ã¹ýȥʱ¡£¾ÙÀý:

¡¡¡¡Results

¡¡¡¡There were 262 cases ofE coliO157 infection in theLanarkshire area:200 confirmed cases and 62 probable cases.Themedian age of all affected was 53 years,but there were highernumbers at the extremes of age.47%(124/262)of infectedindividualswere over 55 years of age.13(5%)people died.In 10cases death was associated with the systemic complications ofE coliO157 infection.

¡¡¡¡28(11%)of the Lanarkshire cases ofE coliO157 met thediagnostic criteria forHUS/TTP.Casesmet the criteria forHUS/TTPa median of 7 days(range 4¡«15)after the onset of gastrointestinalsymptoms.A further eight cases had evidence of thromboticmicroangiopathy but did not meet the criteria for HUS/TTP and werenot eligible for TPE.22(79%)cases with HUS/TTP were adultsand six(21%)were children.The median age of adults whodeveloped HUS/TTP was 71 years and the median age of children 6years.The demographics,clinical features,treatment,laboratoryresults,and outcome of the adult cases with HUS/TTP are shown intable 1.Blood results are taken from the day that the diagnosticcriteria for HUS/TTP were met,before TPE in cases so treated.

¡¡¡¡The mortality rate in adults with HUS/TTP was 45%(ten of22).Seven of 12 cases aged over 70 years and three of ten aged 70years or less died.There were no deaths in children.Necropsiesweredone for all cases who died.Causes of death in patients with HUS/TTPwere acute renal failure secondary to HUS(two cases),cardiacarrest(two cases),intracerebral haemorrhage,cerebral infarction,acute myocardial infarction,multiple organ failure,hepatorenalsyndrome secondary to macronodular cirrhosis and septic shock.