{"id":404,"date":"2020-08-13T20:25:25","date_gmt":"2020-08-13T20:25:25","guid":{"rendered":"https:\/\/brooksidepress.org\/basic_obgyn\/?page_id=404"},"modified":"2020-10-20T17:02:24","modified_gmt":"2020-10-20T17:02:24","slug":"postpartum-hemorrhage","status":"publish","type":"page","link":"https:\/\/brooksidepress.org\/basic_obgyn\/advanced-training\/postpartum-hemorrhage\/","title":{"rendered":"Postpartum Hemorrhage"},"content":{"rendered":"<p><iframe loading=\"lazy\" src=\"https:\/\/www.youtube.com\/embed\/Ny3V045oqP0\" width=\"560\" height=\"315\" frameborder=\"0\" allowfullscreen=\"allowfullscreen\"><span data-mce-type=\"bookmark\" style=\"display: inline-block; width: 0px; overflow: hidden; line-height: 0;\" class=\"mce_SELRES_start\">\ufeff<\/span><\/iframe><\/p>\n<p>Duration 9:41<\/p>\n<input type='hidden' bg_collapse_expand='69e9c851746fa3092217533' value='69e9c851746fa3092217533'><input type='hidden' id='bg-show-more-text-69e9c851746fa3092217533' value='Show Transcript'><input type='hidden' id='bg-show-less-text-69e9c851746fa3092217533' value='Hide Transcript'><button id='bg-showmore-action-69e9c851746fa3092217533' class='bg-showmore-plg-button bg-blue-button  '   style=\" color:#fcf7f7;\">Show Transcript<\/button><div id='bg-showmore-hidden-69e9c851746fa3092217533' ><\/p>\n<p>00:00<br \/>\naapko basic science topic hemorrhage in<br \/>\n00:02<br \/>\nobstetrics postpartum hemorrhage is<br \/>\n00:04<br \/>\ncommon the w-h-o reports post-prom<br \/>\n00:06<br \/>\nhemorrhage is the leading cause of<br \/>\n00:08<br \/>\nmaternal mortality accounting for 35% of<br \/>\n00:11<br \/>\nall maternal deaths in severe cases of<br \/>\n00:13<br \/>\nhemorrhage is important to consider the<br \/>\n00:15<br \/>\ndiagnosis of disseminated intravascular<br \/>\n00:16<br \/>\ncoagulation in this video we will review<br \/>\n00:20<br \/>\nthe basic principles of normal<br \/>\n00:21<br \/>\nhemostasis review the physiologic<br \/>\n00:24<br \/>\nchanges associated with coagulation<br \/>\n00:25<br \/>\nduring pregnancy and review the<br \/>\n00:27<br \/>\npathophysiology and management of di C<br \/>\n00:30<br \/>\nplease meet our patient miss Hayne she<br \/>\n00:33<br \/>\nis a 35 year old gravity&#8217; 3 para 2 at 36<br \/>\n00:36<br \/>\nweeks gestational age with chronic<br \/>\n00:37<br \/>\nhypertension she presents with vaginal<br \/>\n00:39<br \/>\nbleeding and abdominal pain to labor and<br \/>\n00:41<br \/>\ndelivery on exam vital signs are notable<br \/>\n00:44<br \/>\nfor blood pressure 100 over 60 pulse of<br \/>\n00:46<br \/>\n98 abdomen is tender to palpation in M<br \/>\n00:50<br \/>\npelvic exam there&#8217;s significant clot in<br \/>\n00:52<br \/>\nthe vagina with active bleeding from the<br \/>\n00:53<br \/>\ncervix to commentary demonstrates<br \/>\n00:56<br \/>\nuterine tachy systole labs demonstrated<br \/>\n00:58<br \/>\nhemoglobin of 8.5 platelet count of<br \/>\n01:01<br \/>\n240,000 per thrombin teen of 12.8<br \/>\n01:04<br \/>\nactivated partial thromboplastin time of<br \/>\n01:06<br \/>\n27 and fibrinogen of 450 her symptoms<br \/>\n01:10<br \/>\nare concerning for placental abruption<br \/>\n01:11<br \/>\nand she is presenting with abdominal<br \/>\n01:13<br \/>\npain and bleeding let&#8217;s look more<br \/>\n01:15<br \/>\nclosely at her labs what specifically do<br \/>\n01:18<br \/>\nPT PTT and fibrinogen measure these labs<br \/>\n01:21<br \/>\nare useful to assess clotting function<br \/>\n01:23<br \/>\nand patients pta measures the extrinsic<br \/>\n01:25<br \/>\npathway of the coagulation cascade and<br \/>\n01:27<br \/>\nincludes factors 7 10 5 and thrombin<br \/>\n01:30<br \/>\nwhich is also known as factor 2 PTT<br \/>\n01:33<br \/>\nmeasures an intrinsic pathway an easy<br \/>\n01:36<br \/>\nway to remember this is that includes<br \/>\n01:37<br \/>\nall factors except for 7 including<br \/>\n01:39<br \/>\nfactors 12 11 9 8 10 5 and 2 both<br \/>\n01:45<br \/>\npathways converge to form thrombin and<br \/>\n01:47<br \/>\nsubsequently fiber tension which is<br \/>\n01:48<br \/>\ncleaved to form fibrin necessary for<br \/>\n01:50<br \/>\nKlat formation let&#8217;s take a look at<br \/>\n01:52<br \/>\nnormal hemostasis to truly understand<br \/>\n01:54<br \/>\nthe role clotting factors play in clot<br \/>\n01:56<br \/>\nformation and why coagulation labs are<br \/>\n01:58<br \/>\nhelpful in determining if coagulopathy<br \/>\n01:59<br \/>\nis present in our patients in normal<br \/>\n02:03<br \/>\nhemostasis a platelet plug first occurs<br \/>\n02:05<br \/>\nat the site of injury this is a blood<br \/>\n02:07<br \/>\nvessel with epithelial cells<br \/>\n02:09<br \/>\nwhen injury occurs platelets adhere to<br \/>\n02:11<br \/>\nthe site of injury with the help of von<br \/>\n02:12<br \/>\nwillebrand factor at the same set of<br \/>\n02:15<br \/>\ninjury tissue factors released<br \/>\n02:17<br \/>\ninteraction of tissue factor with factor<br \/>\n02:19<br \/>\n7 initiates clotting and is considered<br \/>\n02:22<br \/>\nthe primary event of the Cascade the<br \/>\n02:24<br \/>\nsubsequently activates factors 10 and 9<br \/>\n02:27<br \/>\nactivated factor 9 combines with<br \/>\n02:29<br \/>\nactivated factor 8 to activate factor 10<br \/>\n02:32<br \/>\nactivated factor 10 with activated<br \/>\n02:34<br \/>\nfactor 5 generates a small and minor<br \/>\n02:36<br \/>\nthrombin the small amount of thrombin<br \/>\n02:39<br \/>\nactivates platelets as well as factors 5<br \/>\n02:41<br \/>\n8 and 11 which leads to the application<br \/>\n02:43<br \/>\nof thrombin generation the so called<br \/>\n02:46<br \/>\nthrombin burst this propagation accounts<br \/>\n02:48<br \/>\nfor the majority of thrombin generated<br \/>\n02:50<br \/>\nin addition activated factor 12<br \/>\n02:52<br \/>\nactivates 11 on the surface of activated<br \/>\n02:54<br \/>\nplatelets which provides an alternative<br \/>\n02:57<br \/>\nroute for generation of thrombin let&#8217;s<br \/>\n02:59<br \/>\ntake a moment to review how clotting<br \/>\n03:00<br \/>\nfactors relate to PT and PTT I&#8217;m<br \/>\n03:03<br \/>\ncircling was considered the extrinsic<br \/>\n03:05<br \/>\npathway which again is measured by PT<br \/>\n03:07<br \/>\nand this is the intrinsic pathway<br \/>\n03:09<br \/>\nmeasured by PTT<br \/>\n03:11<br \/>\nlet&#8217;s pause read and apply patients with<br \/>\n03:15<br \/>\nhemophilia a have factor 8 deficiency<br \/>\n03:18<br \/>\nwhat lab findings would you expect for<br \/>\n03:20<br \/>\nPT and PTT in the patient with this<br \/>\n03:22<br \/>\ndisorder since factor a is part of the<br \/>\n03:25<br \/>\nintrinsic pathway and not the extrinsic<br \/>\n03:27<br \/>\npathway we expect an increased PTT and<br \/>\n03:31<br \/>\nnormal PT let&#8217;s continue with the<br \/>\n03:34<br \/>\nCascade thrombin then converts<br \/>\n03:36<br \/>\nfibrinogen into fibrin fibrin monomers<br \/>\n03:39<br \/>\nare then cross-linked by factor 13 to<br \/>\n03:41<br \/>\nform a clot what keeps the clot from<br \/>\n03:44<br \/>\npropagating indefinitely termination of<br \/>\n03:46<br \/>\nclotting is an important step in normal<br \/>\n03:48<br \/>\nhemostasis and also prevents clotting<br \/>\n03:50<br \/>\nwhen it is not required thrombin<br \/>\n03:52<br \/>\nstimulates the activation of<br \/>\n03:53<br \/>\nantithrombin through negative feedback<br \/>\n03:56<br \/>\nthrombin and 10a are inhibited similarly<br \/>\n03:58<br \/>\ntissue factor pathway inhibitor and<br \/>\n04:00<br \/>\nhabits tissue factor protein C is also<br \/>\n04:03<br \/>\nactivated with the assistance of protein<br \/>\n04:05<br \/>\ns activated protein C then inhibits<br \/>\n04:08<br \/>\nfactor 5 finally the clot is removed<br \/>\n04:11<br \/>\nwith the activation of plasma plasma<br \/>\n04:13<br \/>\nningen binds fibrin and tissue<br \/>\n04:15<br \/>\nplasminogen activator which converts<br \/>\n04:17<br \/>\nplasminogen to proteolytic plasma<br \/>\n04:19<br \/>\nplasmon cleaves fibrin releasing fibrin<br \/>\n04:22<br \/>\ndegradation products and d-dimer&#8217;s let&#8217;s<br \/>\n04:26<br \/>\nremember our patient now that we know<br \/>\n04:28<br \/>\nwhat the labs are measuring what is<br \/>\n04:30<br \/>\nnormal for pregnancy during pregnancy<br \/>\n04:33<br \/>\nthere&#8217;s an increase in some coagulation<br \/>\n04:34<br \/>\nfactors and decrease in some anti<br \/>\n04:36<br \/>\ncoagulation factors to decrease<br \/>\n04:38<br \/>\nexcessive bleeding postpartum the<br \/>\n04:40<br \/>\nchanges create a relative<br \/>\n04:41<br \/>\nhypercoagulable state procoagulant<br \/>\n04:43<br \/>\nfactors fibrinogen factors 2 7 8 9 10 12<br \/>\n04:49<br \/>\nand 13 increased by 20 to 200 percent in<br \/>\n04:52<br \/>\naddition there&#8217;s a decrease in<br \/>\n04:54<br \/>\nanticoagulant protein s in antithrombin<br \/>\n04:57<br \/>\nother proteins such as c 5 and 11 remain<br \/>\n05:00<br \/>\nrelatively unchanged in pregnancy the<br \/>\n05:03<br \/>\nplacental bed plays a role deciduous<br \/>\n05:06<br \/>\ncells that line the placental bed<br \/>\n05:07<br \/>\nstrongly expressed tissue factor when<br \/>\n05:10<br \/>\nthis is released at sites of decidua<br \/>\n05:11<br \/>\nYama initiation of the coagulation<br \/>\n05:13<br \/>\ncascade occurs these factors along with<br \/>\n05:16<br \/>\nmy own material contraction all<br \/>\n05:17<br \/>\ncontribute to decreasing the risk for<br \/>\n05:19<br \/>\nexcessive bleeding at the time of<br \/>\n05:20<br \/>\ndelivery factors typically return to<br \/>\n05:23<br \/>\nnormal levels six to twelve weeks<br \/>\n05:24<br \/>\npostpartum and how does this affect labs<br \/>\n05:28<br \/>\nin pregnancy PT again measuring the<br \/>\n05:31<br \/>\nextrinsic pathway generally stays the<br \/>\n05:33<br \/>\nsame with no market changes PTT<br \/>\n05:35<br \/>\nmeasuring the intrinsic pathway is<br \/>\n05:37<br \/>\nusually shortened by up to four seconds<br \/>\n05:39<br \/>\nin the third trimester<br \/>\n05:40<br \/>\nin addition fibrinogen is markedly<br \/>\n05:43<br \/>\nelevated with normal levels ranging from<br \/>\n05:45<br \/>\n350 to over 600 milligrams per deciliter<br \/>\n05:48<br \/>\nlet&#8217;s go back to our patient she<br \/>\n05:51<br \/>\ncontinues to have heavy vaginal bleeding<br \/>\n05:53<br \/>\nin addition repeat vital signs<br \/>\n05:55<br \/>\ndemonstrated blood pressure of 80 over<br \/>\n05:57<br \/>\n40<br \/>\n05:57<br \/>\npulse of 120 labs are also redrawn her<br \/>\n06:01<br \/>\nhemoglobin is now seven platelets are<br \/>\n06:04<br \/>\n70,000 PT is 15.5 PTT is 39 and<br \/>\n06:08<br \/>\nfibrinogen is 250 what is happening to<br \/>\n06:12<br \/>\nour patient she is hypotensive and<br \/>\n06:15<br \/>\ntachycardic her labs are consistent with<br \/>\n06:17<br \/>\nanemia and thrombocytopenia she has<br \/>\n06:20<br \/>\nevidence of coagulopathy as PT and PTT<br \/>\n06:22<br \/>\nare elevated and fibrinogen is low in<br \/>\n06:25<br \/>\nsevere cases of hemorrhage is important<br \/>\n06:28<br \/>\nto consider the diagnosis of di c in d<br \/>\n06:30<br \/>\nIC the processes of coagulation and<br \/>\n06:33<br \/>\nBrunell Isis become abnormally activated<br \/>\n06:35<br \/>\nwithin the vasculature but what is the<br \/>\n06:38<br \/>\nunderlying pathophysiology of di see the<br \/>\n06:41<br \/>\ntypical sequence of events is as follows<br \/>\n06:43<br \/>\nendothelial damage may cause release of<br \/>\n06:46<br \/>\nprocoagulant enzymes or phospholipids<br \/>\n06:48<br \/>\nactivation of the coagulation cascade<br \/>\n06:49<br \/>\nleads to production of thrombi in the<br \/>\n06:51<br \/>\nmicro vascular and\/or larger vessels<br \/>\n06:54<br \/>\nextensive formation of thrombi in turn<br \/>\n06:56<br \/>\nleads to consumption of platelets<br \/>\n06:58<br \/>\ncoagulant and anticoagulant factors<br \/>\n07:00<br \/>\nrapid consumption of factors outpaces<br \/>\n07:03<br \/>\ntheir production creating a consumptive<br \/>\n07:04<br \/>\ncoagulopathy with impaired coagulation<br \/>\n07:08<br \/>\nfibrinolysis is activated at sites the<br \/>\n07:10<br \/>\nthrombus formation with generation of<br \/>\n07:12<br \/>\nfibrin degradation products such as<br \/>\n07:13<br \/>\nd-dimer large amounts of degradation<br \/>\n07:15<br \/>\nproducts interfere with both fibrin clot<br \/>\n07:18<br \/>\nformation and platelet aggregation<br \/>\n07:19<br \/>\ncausing impaired coagulation tissue or<br \/>\n07:22<br \/>\norgan damage may result from reduced<br \/>\n07:23<br \/>\nperfusion thrombosis and or bleeding<br \/>\n07:26<br \/>\nlabs demonstrated thrombocytopenia hypo<br \/>\n07:29<br \/>\nfibrinogen amia increased d-dimer&#8217;s and<br \/>\n07:31<br \/>\nprolonged PT and PTT it is important to<br \/>\n07:35<br \/>\nnote that obstetric complications are<br \/>\n07:36<br \/>\ncommon causes of di see including<br \/>\n07:39<br \/>\nabruption and fetal demise amniotic<br \/>\n07:41<br \/>\nfluid embolism preeclampsia and help<br \/>\n07:43<br \/>\nsyndrome and postpartum hemorrhage let&#8217;s<br \/>\n07:45<br \/>\nreview the underlying pathophysiology in<br \/>\n07:47<br \/>\nplacental abruption and fetal demise<br \/>\n07:49<br \/>\nthere&#8217;s significant injury and necrosis<br \/>\n07:51<br \/>\nof fetal placental tissue increasing the<br \/>\n07:53<br \/>\nrelease of pro coagulants in amniotic<br \/>\n07:56<br \/>\nfluid embolism amniotic fluid rich in<br \/>\n07:58<br \/>\nprocoagulant in anticoagulants is<br \/>\n08:00<br \/>\nreleased into the circulation<br \/>\n08:02<br \/>\npreeclampsia and help contributes to<br \/>\n08:04<br \/>\nendothelial cell damage which activates<br \/>\n08:06<br \/>\ncoagulation hemorrhage can lead to shock<br \/>\n08:09<br \/>\nresulting in severe tissue hypoxia<br \/>\n08:11<br \/>\nresulting a release of tissue factor<br \/>\n08:12<br \/>\nfrom damaged cells the treatment of di C<br \/>\n08:15<br \/>\nis focused on correcting the underlying<br \/>\n08:17<br \/>\ncause maintenance of volume status and<br \/>\n08:19<br \/>\nsupportive measures and replacement of<br \/>\n08:21<br \/>\nblood products replacement of products<br \/>\n08:23<br \/>\nis justified in patients who have<br \/>\n08:24<br \/>\nserious bleeding or at high risk for<br \/>\n08:26<br \/>\nbleeding red blood cell transfusion is<br \/>\n08:28<br \/>\nnecessary for severe bleeding platelet<br \/>\n08:30<br \/>\ntransfusions should be given if<br \/>\n08:32<br \/>\nplatelets are less than 15,000 with<br \/>\n08:33<br \/>\nserious bleeding<br \/>\n08:34<br \/>\ncoagulation factor replacement should be<br \/>\n08:36<br \/>\ngiven to patients with severe bleeding<br \/>\n08:38<br \/>\nwho exhibits signs of coagulopathy let&#8217;s<br \/>\n08:40<br \/>\ngo back to the clan cascade to see our<br \/>\n08:42<br \/>\nreplacement products correct<br \/>\n08:43<br \/>\ncoagulopathy fresh frozen plasma<br \/>\n08:45<br \/>\ncontains fibrinogen and<br \/>\n08:47<br \/>\ncoagulation factors cryoprecipitate on<br \/>\n08:49<br \/>\nthe other hand has a smaller volume and<br \/>\n08:51<br \/>\nis rich and fibrinogen factors 8 and 13<br \/>\n08:53<br \/>\nas well as von Willebrand factor if I&#8217;m<br \/>\n08:56<br \/>\nWillebrand factor helps platelets adhere<br \/>\n08:57<br \/>\nto the site of injury let&#8217;s pause read<br \/>\n09:01<br \/>\nand apply if you suspect di see in a<br \/>\n09:05<br \/>\npatient what lab studies would support<br \/>\n09:07<br \/>\nthis diagnosis labs consistent with di C<br \/>\n09:10<br \/>\ninclude increased PT and PTT and<br \/>\n09:13<br \/>\ndecrease fibrinogen and platelets this<br \/>\n09:16<br \/>\nconcludes the fqo basic science video on<br \/>\n09:18<br \/>\nhemorrhage in this video we covered<br \/>\n09:20<br \/>\nnormal hemostasis physiologic changes<br \/>\n09:23<br \/>\nassociated with coagulation during<br \/>\n09:25<br \/>\npregnancy in the pathophysiology and<br \/>\n09:27<br \/>\nmanagement of di sea<br \/>\n09:29<br \/>\n[Music]<\/p>\n<p><\/div>\n<hr \/>\n<p><iframe loading=\"lazy\" src=\"https:\/\/www.youtube.com\/embed\/6P9ETqav1DQ\" width=\"560\" height=\"315\" frameborder=\"0\" allowfullscreen=\"allowfullscreen\"><\/iframe><\/p>\n<p>Duration 11:41<\/p>\n<input type='hidden' bg_collapse_expand='69e9c8517539a6039157103' value='69e9c8517539a6039157103'><input type='hidden' id='bg-show-more-text-69e9c8517539a6039157103' value='Show Transcript'><input type='hidden' id='bg-show-less-text-69e9c8517539a6039157103' value='Hide Transcript'><button id='bg-showmore-action-69e9c8517539a6039157103' class='bg-showmore-plg-button bg-blue-button  '   style=\" color:#fcf7f7;\">Show Transcript<\/button><div id='bg-showmore-hidden-69e9c8517539a6039157103' ><\/p>\n<p>00:01<br \/>\nhello and welcome to this aapko basic<br \/>\n00:04<br \/>\nscience objective video about uterine<br \/>\n00:06<br \/>\natony the objectives of this video are<br \/>\n00:08<br \/>\nto understand the mechanism of uterine<br \/>\n00:10<br \/>\nmuscle architecture and contractility<br \/>\n00:12<br \/>\ndescribe how risk factors for uterine<br \/>\n00:14<br \/>\natony interfere with myometrium<br \/>\n00:16<br \/>\ncontraction appreciate the mechanism of<br \/>\n00:19<br \/>\naction and pharmacology of uterotonic<br \/>\n00:21<br \/>\nagents and describe the physiologic<br \/>\n00:24<br \/>\nmechanism by which mechanical therapy<br \/>\n00:26<br \/>\nimproves uterine tone this is miss ghana<br \/>\n00:29<br \/>\nbleat alotta or miss gb and she is<br \/>\n00:32<br \/>\npregnant with twins miss gb is in labor<br \/>\n00:34<br \/>\nand her uterus is working hard let&#8217;s<br \/>\n00:36<br \/>\nquickly review the basics before she<br \/>\n00:38<br \/>\ndelivers the layers of the uterine myoma<br \/>\n00:41<br \/>\ntrium are made up of millions of smooth<br \/>\n00:43<br \/>\nmuscle cells they are organized in<br \/>\n00:45<br \/>\nlayers which run in multiple directions<br \/>\n00:47<br \/>\nuterine smooth muscle is made up of<br \/>\n00:49<br \/>\nbundles of myocytes which are organized<br \/>\n00:51<br \/>\nto form a continuous layer and give the<br \/>\n00:53<br \/>\nuterus its contractile function there<br \/>\n00:56<br \/>\nare three layers of fibres stratum some<br \/>\n00:58<br \/>\nvascular a stratum vascular II and<br \/>\n01:00<br \/>\nstratum supra vascular II that runs<br \/>\n01:03<br \/>\nsukham French lis Lajja &#8211; de lis and<br \/>\n01:05<br \/>\nobliquely throughout the myometrium<br \/>\n01:08<br \/>\nlet&#8217;s pause think and apply why is a<br \/>\n01:11<br \/>\npatient with her placenta located in the<br \/>\n01:13<br \/>\nlower uterine segment an increased risk<br \/>\n01:15<br \/>\nfor uterine atony the lower uterine<br \/>\n01:18<br \/>\nsegment has fewer layers of smooth<br \/>\n01:20<br \/>\nmuscle to contract a slow bleeding from<br \/>\n01:21<br \/>\nthe spiral arterioles following delivery<br \/>\n01:23<br \/>\nof the placenta nor is the lower uterine<br \/>\n01:25<br \/>\nsegment able to generate enough force to<br \/>\n01:27<br \/>\nexpel clots that have formed when blood<br \/>\n01:30<br \/>\ncollects in the lower uterine segment<br \/>\n01:32<br \/>\nfurther distension decreases the ability<br \/>\n01:34<br \/>\nof the available actin and myosin<br \/>\n01:35<br \/>\nmyofibrils<br \/>\n01:36<br \/>\nto attach and contract on a cellular<br \/>\n01:40<br \/>\nlevel smooth muscle contraction is<br \/>\n01:42<br \/>\nmediated by an increase in intracellular<br \/>\n01:43<br \/>\ncytoplasmic calcium this activates<br \/>\n01:46<br \/>\nmyosin light-chain kinase which<br \/>\n01:48<br \/>\ncatalyzes the phosphorylation of light<br \/>\n01:50<br \/>\nchain myosin phosphorylated myosin<br \/>\n01:53<br \/>\ninteracts with actin and activase ATPase<br \/>\n01:56<br \/>\nATP hydrolysis and ATPase generates<br \/>\n01:59<br \/>\nforce and the muscle contracts smooth<br \/>\n02:02<br \/>\nmuscle relaxation begins with the<br \/>\n02:04<br \/>\nsequestration of calcium in the<br \/>\n02:06<br \/>\nsarcoplasmic reticulum with a<br \/>\n02:08<br \/>\ndephosphorylation of myosin light-chain<br \/>\n02:10<br \/>\nbye phosphatase and inactivation of &#8211;<br \/>\n02:13<br \/>\nlight chain kinase recall that the<br \/>\n02:16<br \/>\nspiral arterioles are located within the<br \/>\n02:18<br \/>\nwall of the myometrium and act to<br \/>\n02:20<br \/>\nprovide circulation to the pregnant<br \/>\n02:21<br \/>\nuterus and it&#8217;s placental bed there are<br \/>\n02:24<br \/>\non average 120 of these arterioles which<br \/>\n02:27<br \/>\nlack a muscular layer do-do and no<br \/>\n02:28<br \/>\ntrophoblastic remodeling when the<br \/>\n02:31<br \/>\nplacenta separates these vessels are<br \/>\n02:32<br \/>\navulsed at the WA central site<br \/>\n02:35<br \/>\nhemostasis is achieved when the<br \/>\n02:37<br \/>\nmyometrium contracts and compresses<br \/>\n02:38<br \/>\nthese vessels eventually leading to<br \/>\n02:40<br \/>\nclotting and obliteration of their lumen<br \/>\n02:43<br \/>\nms gb is slowly progressing in labor<br \/>\n02:46<br \/>\nafter her pitocin was started 18 hours<br \/>\n02:48<br \/>\nago although she has started on<br \/>\n02:50<br \/>\nantibiotics for chorioamnionitis the<br \/>\n02:53<br \/>\nbabies look great and her labor course<br \/>\n02:55<br \/>\ncontinues right after miss GB delivers<br \/>\n02:58<br \/>\nshe quickly begins hemorrhaging the<br \/>\n03:00<br \/>\ncause of the postpartum bleeding is<br \/>\n03:02<br \/>\ndetermined to be uterine atony but why<br \/>\n03:05<br \/>\never did this happen MS GP was so<br \/>\n03:08<br \/>\nhealthy there are three main mechanisms<br \/>\n03:11<br \/>\nthat lead to uterine atony<br \/>\n03:13<br \/>\nlet&#8217;s take each one in turn the first<br \/>\n03:16<br \/>\nmechanism is over distension of the<br \/>\n03:18<br \/>\nuterus this can occur with fetal<br \/>\n03:20<br \/>\nmacrosomia multiple fetuses<br \/>\n03:22<br \/>\npolyhydramnios and distension with blood<br \/>\n03:25<br \/>\nclots over distension pulls apart actin<br \/>\n03:29<br \/>\nand myosin so they cannot overlap to<br \/>\n03:31<br \/>\nconnect and bind which limits the<br \/>\n03:32<br \/>\ncontractile ability of the smooth muscle<br \/>\n03:35<br \/>\nthe second mechanism is anaesthesia such<br \/>\n03:38<br \/>\nas halogenated agents and conduction<br \/>\n03:40<br \/>\nanesthesia that can lead to hypotension<br \/>\n03:43<br \/>\nthe hypotension causes a decrease in<br \/>\n03:46<br \/>\ncirculating oxytocin which decreases<br \/>\n03:48<br \/>\nuterine contraction the third mechanism<br \/>\n03:51<br \/>\nis the result of an exhausted myometrium<br \/>\n03:53<br \/>\nthis can happen in the setting of a very<br \/>\n03:56<br \/>\nfast labor prolonged labor with oxytocin<br \/>\n03:58<br \/>\nstimulation and chorioamnionitis<br \/>\n04:01<br \/>\nrepeated exposure to oxytocin leads to<br \/>\n04:04<br \/>\noxytocin receptors desensitization and a<br \/>\n04:06<br \/>\nloss in capacity to respond the<br \/>\n04:09<br \/>\npathophysiology of chorioamnionitis<br \/>\n04:11<br \/>\nleading to uterine atony is not well<br \/>\n04:14<br \/>\nunderstood likely that inflammation<br \/>\n04:17<br \/>\nleads to dysfunctional myometrium<br \/>\n04:18<br \/>\ncontractility<br \/>\n04:20<br \/>\nit is hypothesized that the inflammatory<br \/>\n04:22<br \/>\nprocess consumes energy that would<br \/>\n04:24<br \/>\notherwise be readily available for<br \/>\n04:26<br \/>\nuterine smooth muscle contraction<br \/>\n04:28<br \/>\nanother hypothesis is that cytokine<br \/>\n04:30<br \/>\ninduced nitric acid production inhibits<br \/>\n04:33<br \/>\nmitochondrial energy production and<br \/>\n04:35<br \/>\nimpairs contractile function in myocytes<br \/>\n04:37<br \/>\nlet&#8217;s pause think and apply why does<br \/>\n04:41<br \/>\nprolonged use of magnesium increase the<br \/>\n04:43<br \/>\nrisk of uterine atony magnesium competes<br \/>\n04:46<br \/>\nfor and blocks the calcium channels<br \/>\n04:48<br \/>\nthrough which calcium enters the<br \/>\n04:49<br \/>\nintracellular cytoplasm without an<br \/>\n04:52<br \/>\nincrease in intracellular calcium to<br \/>\n04:54<br \/>\nactivate light-chain kinase the<br \/>\n04:56<br \/>\nmechanism by which smooth muscle fibers<br \/>\n04:57<br \/>\ncontract is inhibited thankfully<br \/>\n05:00<br \/>\nalthough Miss GB had many risk factors<br \/>\n05:02<br \/>\nsuch as over uterine distension with<br \/>\n05:04<br \/>\ntwins and myometrium exhaustion with a<br \/>\n05:06<br \/>\nprolonged labor and chorioamnionitis<br \/>\n05:08<br \/>\nthere are many medications and<br \/>\n05:10<br \/>\nprocedures to help stop her bleeding<br \/>\n05:13<br \/>\noxytocin or pitocin is used for both<br \/>\n05:15<br \/>\nprevention and treatment of postpartum<br \/>\n05:17<br \/>\nhemorrhage oxytocin is a non peptide<br \/>\n05:20<br \/>\nproduced in the paraventricular nucleus<br \/>\n05:21<br \/>\nof the hypothalamus and released by the<br \/>\n05:24<br \/>\nposterior pituitary gland it can be<br \/>\n05:26<br \/>\ngiven intravenously or intramuscularly<br \/>\n05:29<br \/>\nhowever in spite of it being a first<br \/>\n05:31<br \/>\nline of therapy there is no standardized<br \/>\n05:33<br \/>\nrate or optimal dose oxytocin works by<br \/>\n05:36<br \/>\nstimulating myometrium contractility by<br \/>\n05:38<br \/>\nan increase in intracellular calcium the<br \/>\n05:41<br \/>\nrate limiting step is the number of<br \/>\n05:43<br \/>\noxytocin receptors on the myometrium the<br \/>\n05:46<br \/>\nhighest concentration is at the fundus<br \/>\n05:47<br \/>\nand the receptor concentration decreases<br \/>\n05:49<br \/>\nas you move to the lower uterine segment<br \/>\n05:51<br \/>\nand cervix IV onset is almost immediate<br \/>\n05:55<br \/>\nwhile IM is about three to seven minutes<br \/>\n05:57<br \/>\nthe half-life is between 10 to 12<br \/>\n06:00<br \/>\nminutes and there is no difference in<br \/>\n06:01<br \/>\nthe efficacy between IV and IM usually<br \/>\n06:05<br \/>\npatients do not have any side effects<br \/>\n06:07<br \/>\nfrom oxytocin due to its structural<br \/>\n06:10<br \/>\nsimilarity to vasopressin exceedingly<br \/>\n06:13<br \/>\nhigh doses could lead to water<br \/>\n06:14<br \/>\nintoxication hyponatremia and coma now<br \/>\n06:18<br \/>\nlet&#8217;s pause think and apply in a patient<br \/>\n06:21<br \/>\nhaving an 18-week DNA who encounters<br \/>\n06:24<br \/>\npost abortive uterine atony why might<br \/>\n06:26<br \/>\noxytocin not be as effective in treating<br \/>\n06:28<br \/>\nuterine atony<br \/>\n06:29<br \/>\nas it is at term<br \/>\n06:31<br \/>\nrecruitment of oxytocin receptors and<br \/>\n06:34<br \/>\nthe effective hypertrophy on smooth<br \/>\n06:36<br \/>\nmuscle cells is sub-optimal at this<br \/>\n06:38<br \/>\ngestational age methyl ergo no vein or<br \/>\n06:41<br \/>\nmother giant is another uterotonic<br \/>\n06:43<br \/>\ncommonly used for uterine atony it is a<br \/>\n06:46<br \/>\nsemi-synthetic amide<br \/>\n06:48<br \/>\nergo derivative and the usual dose is<br \/>\n06:51<br \/>\n0.2 milligrams<br \/>\n06:52<br \/>\nintramuscularly every two to four hours<br \/>\n06:54<br \/>\nit can also be given orally methyl<br \/>\n06:57<br \/>\naergon ovine works by creating a<br \/>\n06:59<br \/>\nsustained contraction by acting as an<br \/>\n07:02<br \/>\nagonist on the 5-ht ii receptor found in<br \/>\n07:05<br \/>\nuterine smooth muscle onset of action is<br \/>\n07:08<br \/>\nusually two to five minutes for<br \/>\n07:09<br \/>\nintramuscular and five to ten for oral<br \/>\n07:11<br \/>\nadministration this is a very highly<br \/>\n07:14<br \/>\neffective uterotonic a common<br \/>\n07:16<br \/>\nsecond-line agent systemic<br \/>\n07:18<br \/>\nvasoconstriction can lead to<br \/>\n07:20<br \/>\nhypertensive urgency especially in those<br \/>\n07:22<br \/>\nwith elevated blood pressure due to<br \/>\n07:23<br \/>\nchronic HTN or preeclampsia and should<br \/>\n07:26<br \/>\nnot be used in these patients similar<br \/>\n07:29<br \/>\nHTN urgency can also be seen in patients<br \/>\n07:31<br \/>\nusing protease inhibitors for HIV<br \/>\n07:33<br \/>\ntreatment karma Proust or Hema Bay is a<br \/>\n07:36<br \/>\nthird highly effective uterotonic that<br \/>\n07:38<br \/>\nis often used if methyl Erica nouvion is<br \/>\n07:40<br \/>\ncontraindicated karma Prost is an<br \/>\n07:43<br \/>\nanalogue of 15 methyl prostaglandin F 2<br \/>\n07:45<br \/>\nalpha the 250 microgram dose is<br \/>\n07:47<br \/>\nadministered intramuscularly and can be<br \/>\n07:50<br \/>\nrepeated every 15 to 90 minutes with a<br \/>\n07:52<br \/>\nmaximum of eight doses biomaterial<br \/>\n07:55<br \/>\nintracellular free calcium is increased<br \/>\n07:58<br \/>\nby prusik Landon&#8217;s and this increased<br \/>\n07:59<br \/>\navailability of calcium leads to<br \/>\n08:01<br \/>\nincreased myosin light-chain kinase<br \/>\n08:03<br \/>\nactivity augmenting contractile response<br \/>\n08:05<br \/>\nof the uterus to most common side<br \/>\n08:08<br \/>\neffects include diarrhea due to smooth<br \/>\n08:10<br \/>\nmuscle relaxation in the<br \/>\n08:11<br \/>\ngastrointestinal system and bronchospasm<br \/>\n08:13<br \/>\nmaking it contraindicated in asthmatic<br \/>\n08:15<br \/>\npatients misoprostol or site attack is a<br \/>\n08:19<br \/>\nsynthetic analogue of prostaglandin e1<br \/>\n08:21<br \/>\nit is a low-cost easily stored<br \/>\n08:24<br \/>\nmedication that can be administered by<br \/>\n08:25<br \/>\nin many routes although not part of an<br \/>\n08:28<br \/>\ninitial treatment for acne misoprostol<br \/>\n08:30<br \/>\nhas a role in management especially if<br \/>\n08:32<br \/>\nother agents are not available or<br \/>\n08:34<br \/>\ncontraindicated misoprostol is given in<br \/>\n08:37<br \/>\ndoses of six hundred to a thousand<br \/>\n08:39<br \/>\nmicrograms and almost any mucous<br \/>\n08:41<br \/>\nmembrane oral buccal SLE badge<br \/>\n08:45<br \/>\nor rectal it stimulates uterine<br \/>\n08:47<br \/>\ncontractions similar to oxytocin the per<br \/>\n08:50<br \/>\noral and buccal roots have the fastest<br \/>\n08:52<br \/>\nonset of 3 to 5 minutes most side<br \/>\n08:54<br \/>\neffects are minimal such as GI upset or<br \/>\n08:57<br \/>\ntransient fever in some situations such<br \/>\n09:00<br \/>\nas for MS GB uterotonic are not able to<br \/>\n09:03<br \/>\ncontrol the uterine atony in this<br \/>\n09:05<br \/>\nscenario there are several procedures<br \/>\n09:07<br \/>\nthat can also be performed to decrease<br \/>\n09:09<br \/>\nand\/or stop the postpartum hemorrhage<br \/>\n09:11<br \/>\nthe most common procedure performed in<br \/>\n09:13<br \/>\nthe setting of uterine atony is uterine<br \/>\n09:15<br \/>\nmassage<br \/>\n09:16<br \/>\nthis helps to evacuate the uterus of any<br \/>\n09:19<br \/>\nclots as well as Rhea proximate<br \/>\n09:20<br \/>\nmyofilaments to promote contraction this<br \/>\n09:23<br \/>\ncan be done while utero tonics are being<br \/>\n09:25<br \/>\nadministered another option would be a<br \/>\n09:27<br \/>\nuterine artery ligation this would<br \/>\n09:30<br \/>\ndecrease the post pressure to the uterus<br \/>\n09:31<br \/>\nslow bleeding from the spiral arterioles<br \/>\n09:34<br \/>\nin the placental bed decreased blood and<br \/>\n09:36<br \/>\nclot collection in the uterus and<br \/>\n09:37<br \/>\ndecrease overall distension of the<br \/>\n09:39<br \/>\nuterus similar to uterine massage by<br \/>\n09:42<br \/>\ndecreasing over distension Mya filaments<br \/>\n09:44<br \/>\nare able to really tap remove muscle<br \/>\n09:47<br \/>\ncontraction a b-lynch stitch causes<br \/>\n09:50<br \/>\nmanual compression of the uterus which<br \/>\n09:52<br \/>\ncan also aid in riah proximities smooth<br \/>\n09:54<br \/>\nmuscle fibers the manual compression is<br \/>\n09:56<br \/>\ndone by using sutures which go over the<br \/>\n09:59<br \/>\nuterus like suspenders the only other<br \/>\n10:01<br \/>\noption to consider short of hysterectomy<br \/>\n10:04<br \/>\nis a bakery balloon it is<br \/>\n10:06<br \/>\ncounterintuitive to consider placing<br \/>\n10:08<br \/>\nsomething to further distend the uterine<br \/>\n10:10<br \/>\ncavity however the main role of the<br \/>\n10:12<br \/>\nballoon is to provide counter pressure<br \/>\n10:14<br \/>\nat the placental site and allow for<br \/>\n10:16<br \/>\ncompression of the spiral arterioles<br \/>\n10:18<br \/>\nwith eventual decrease in flow and<br \/>\n10:20<br \/>\nimprove clotting and eventual hemostasis<br \/>\n10:22<br \/>\nat the site this measure can also be<br \/>\n10:25<br \/>\nused to provide time for utero tonics to<br \/>\n10:28<br \/>\ntake effect thankfully from Miss GB she<br \/>\n10:31<br \/>\nhad a multidisciplinary team which had<br \/>\n10:33<br \/>\npracticed to handle her obstetric<br \/>\n10:35<br \/>\nemergency she responded well to euro<br \/>\n10:37<br \/>\ntonics and by manual massage and is now<br \/>\n10:40<br \/>\nenjoying time with her two newborns<br \/>\n10:42<br \/>\nthis concludes this aapko basic science<br \/>\n10:45<br \/>\nobjective video about uterine atony<br \/>\n10:47<br \/>\nyou should now be able to understand the<br \/>\n10:50<br \/>\nmechanism of uterine muscle architecture<br \/>\n10:52<br \/>\nand contractility describe how risk<br \/>\n10:54<br \/>\nfactors for uterine atony interfere with<br \/>\n10:57<br \/>\nmyometrium contraction<br \/>\n10:58<br \/>\nappreciate the mechanism of action and<br \/>\n11:00<br \/>\npharmacology of uterotonic agents and<br \/>\n11:03<br \/>\ndescribe the physiologic mechanism by<br \/>\n11:05<br \/>\nwhich mechanical therapy improves<br \/>\n11:07<br \/>\nuterine tone thanks for watching<br \/>\n11:10<br \/>\n[Music]<br \/>\n11:19<br \/>\n[Music]<br \/>\n11:25<br \/>\n[Music]<br \/>\n11:37<br \/>\nyou<\/p>\n<p><\/div>\n<hr \/>\n<p><iframe loading=\"lazy\" src=\"https:\/\/www.youtube.com\/embed\/SEQPKTceWp4\" width=\"560\" height=\"315\" frameborder=\"0\" allowfullscreen=\"allowfullscreen\"><\/iframe><\/p>\n<p>Duration: 7:09<\/p>\n<input type='hidden' bg_collapse_expand='69e9c851763d94025585649' value='69e9c851763d94025585649'><input type='hidden' id='bg-show-more-text-69e9c851763d94025585649' value='Show Transcript'><input type='hidden' id='bg-show-less-text-69e9c851763d94025585649' value='Hide Transcript'><button id='bg-showmore-action-69e9c851763d94025585649' class='bg-showmore-plg-button bg-blue-button  '   style=\" color:#fcfafa;\">Show Transcript<\/button><div id='bg-showmore-hidden-69e9c851763d94025585649' ><\/p>\n<p>00:04<br \/>\nPostpartum hemorrhage is a significant loss of blood after giving birth, and it\u2019s the<br \/>\n00:10<br \/>\nnumber one reason for maternal morbidity and maternal death around the world.<br \/>\n00:15<br \/>\nSpecifically it\u2019s defined as losing more than 500ml of blood after a vaginal delivery<br \/>\n00:20<br \/>\nor more than 1000ml after a cesarean section delivery.<br \/>\n00:26<br \/>\nOf course, deliveries can be messy and it\u2019s impossible to measure the precise amount of<br \/>\n00:29<br \/>\nblood that\u2019s lost.<br \/>\n00:30<br \/>\nIn addition, there\u2019s the possibility of internal bleeding.<br \/>\n00:33<br \/>\nSo additional criteria to consider for postpartum hemorrhage include a decrease of 10% or more<br \/>\n00:38<br \/>\nin hematocrit from baseline, and changes in a mother\u2019s heart rate, blood pressure, and<br \/>\n00:44<br \/>\noxygen saturations &#8211; all of which suggest a significant blood loss.<br \/>\n00:49<br \/>\nSignificant bleeding in the first 24 hours after delivery is called primary postpartum<br \/>\n00:53<br \/>\nhemorrhage, and after that it\u2019s called secondary, or late, postpartum hemorrhage.<br \/>\n00:59<br \/>\nThe most common causes of postpartum hemorrhage can be lumped into four groups which can easily<br \/>\n01:04<br \/>\nbe remembered as the \u201c4 Ts\u201d: Tone, Trauma, Tissue, and Thrombin.<br \/>\n01:12<br \/>\nTone refers to a lack of uterine tone or uterine atony \u2013 basically a soft, spongy, boggy<br \/>\n01:19<br \/>\nuterus, and this is the main cause of postpartum hemorrhage, generally resulting in a slow<br \/>\n01:24<br \/>\nand steady loss of blood.<br \/>\n01:27<br \/>\nThe uterus is a muscular organ wrapped by three layers of smooth muscle called the myometrium,<br \/>\n01:33<br \/>\nwhich contracts during labor to dilate and efface the cervix and ultimately push out<br \/>\n01:37<br \/>\nthe fetus and placenta.<br \/>\n01:40<br \/>\nAfter delivery, the myometrium continues to contract and this squeezes down on the placental<br \/>\n01:45<br \/>\narteries at the point where they are attached to the uterine wall, clamping them shut, thereby<br \/>\n01:51<br \/>\nreducing uterine bleeding.<br \/>\n01:53<br \/>\nThe contractions continue for a few weeks after the delivery.<br \/>\n01:57<br \/>\nWith uterine atony, though, the uterus fails to contract after birth, and those placental<br \/>\n02:02<br \/>\narteries don\u2019t clamp down, leading to excessive bleeding.<br \/>\n02:10<br \/>\nUterine atony can be caused by several things, repeated distention of the uterus as a result<br \/>\n02:14<br \/>\nof multiple pregnancies, overstretching from twins or triplets, or any condition that causes<br \/>\n02:19<br \/>\ntoo much uterine stretching can interfere with efficient uterine contractions and lead<br \/>\n02:24<br \/>\nto diminished tone and eventual uterine atony.<br \/>\n02:29<br \/>\nUterine atony can also occur when the uterine muscles fatigue during the delivery process<br \/>\n02:33<br \/>\nbecause of prolonged labor.<br \/>\n02:35<br \/>\nIt can also occur when a woman is unable to empty her bladder, since a full bladder can<br \/>\n02:40<br \/>\npush against the uterus and interfere with uterine contractions.<br \/>\n02:43<br \/>\nFinally, some commonly used obstetric medications such as anesthetics (especially halothane),<br \/>\n02:50<br \/>\nmagnesium sulfate, nifedipine, and terbutaline can all interfere with uterine contractions<br \/>\n02:57<br \/>\nand increase the risk of uterine atony.<br \/>\n03:01<br \/>\nUterine atony can be treated by fundal massage, massaging the fundus \u2013 the upper section<br \/>\n03:06<br \/>\nof the uterus which is typically near the umbilicus right after birth.<br \/>\n03:10<br \/>\nFundal massage causes the smooth muscle in the wall uterine wall to contract and harden.<br \/>\n03:15<br \/>\nIf a full bladder seems to be interfering with contractions, a woman can urinate or<br \/>\n03:20<br \/>\nhave a catheter placed if she\u2019s unable to void by herself.<br \/>\n03:24<br \/>\nMedications to help firm up the uterus can also be given, and if necessary, the bleeding<br \/>\n03:28<br \/>\nmay be stopped surgically.<br \/>\n03:30<br \/>\nAlright the next \u2018T\u2019, trauma, refers to damage to any of the genital structures &#8211; the<br \/>\n03:36<br \/>\nuterus, cervix, vagina, or perineum.<br \/>\n03:40<br \/>\nThis can include the incision from a cesarean delivery, incidental trauma from a baby coming<br \/>\n03:45<br \/>\nthrough the vaginal canal, or trauma from instruments used in the delivery.<br \/>\n03:50<br \/>\nFor example, the use of forceps, vacuum extraction, or an episiotomy, a small cut used to enlarge<br \/>\n03:56<br \/>\nthe vaginal opening, can all cause unintended bleeding.<br \/>\n04:01<br \/>\nSometimes the bleeding is in a concealed location and a hematoma can form and go unnoticed for<br \/>\n04:08<br \/>\nhours after delivery.<br \/>\n04:11<br \/>\nA key to recognizing a hematoma is severe pain and persistent bright red vaginal bleeding<br \/>\n04:16<br \/>\nin spite of a firmly contracted uterus.<br \/>\n04:20<br \/>\nIn general, any trauma-related bleeding is an emergency and the site of bleeding has<br \/>\n04:24<br \/>\nto be repaired right away &#8211; generally by applying pressure and stitching lacerations.<br \/>\n04:33<br \/>\nTissue refers to placental fragments retained in the uterine cavity.<br \/>\n04:36<br \/>\nThe entire placenta normally separates from the uterine wall in the third stage of labor,<br \/>\n04:42<br \/>\nbut occasionally a part of the placenta remains behind in the uterus.<br \/>\n04:46<br \/>\nIn placenta accreta, the placenta invades the myometrium so it doesn\u2019t easily separate<br \/>\n04:51<br \/>\nfrom the uterus.<br \/>\n04:54<br \/>\nPlacenta accreta or simply too much traction on the umbilical cord can both cause the placenta<br \/>\n04:58<br \/>\nto be retained.<br \/>\n05:00<br \/>\nThis in turn prevents effective uterine contractions, and leads to uterine atony.<br \/>\n05:08<br \/>\nThe goal here is to prevent this from happening in the first place by making sure that the<br \/>\n05:11<br \/>\nplacenta comes out completely intact, and removing any tissue that does get retained<br \/>\n05:16<br \/>\nas soon as possible.<br \/>\n05:19<br \/>\nThrombin, the final T, refers to the mother having some condition that prevents blood<br \/>\n05:25<br \/>\nclots from forming normally &#8211; for example, a genetic disorder like von Willebrand disease<br \/>\n05:30<br \/>\nor an obstetric condition like eclampsia and placental abruption which may result in a<br \/>\n05:35<br \/>\nclotting disorder, the most dangerous of which is disseminated intravascular coagulation<br \/>\n05:40<br \/>\nor DIC.<br \/>\n05:42<br \/>\nThese are conditions that prevent a clot from forming normally when there\u2019s a bleed, and<br \/>\n05:46<br \/>\nthis can make even a tiny bleed into a serious problem since it won\u2019t easily stop.<br \/>\n05:51<br \/>\nThe treatment for each of these is specific to the specific underlying cause.<br \/>\n05:58<br \/>\nPostpartum hemorrhage is an obstetric emergency and maintaining adequate circulating volume<br \/>\n06:03<br \/>\nis a key priority.<br \/>\n06:05<br \/>\nRegardless of the cause, intravenous fluids and blood products may be used to ensure that<br \/>\n06:09<br \/>\nthe vital organs are well perfused.<br \/>\n06:13<br \/>\nAs a quick recap, postpartum hemorrhage is the most common cause of maternal morbidity<br \/>\n06:17<br \/>\nand mortality around the world, and the causes are the 4 T\u2019s: Tone (atony), Trauma, Tissue,<br \/>\n06:24<br \/>\nand Thrombus (coagulopathy).<br \/>\n06:25<br \/>\nThe most common cause &#8211; uterine atony &#8211; can usually be managed with fundal massage and<br \/>\n06:31<br \/>\nmedications to help the uterus contract.<\/p>\n<p><\/div>\n<hr \/>\n<p><iframe loading=\"lazy\" src=\"https:\/\/www.youtube.com\/embed\/2d84AtDz2HY\" width=\"560\" height=\"315\" frameborder=\"0\" allowfullscreen=\"allowfullscreen\"><span data-mce-type=\"bookmark\" style=\"display: inline-block; width: 0px; overflow: hidden; line-height: 0;\" class=\"mce_SELRES_start\">\ufeff<\/span><\/iframe><\/p>\n<p>Duration 8:03<\/p>\n<input type='hidden' bg_collapse_expand='69e9c8517689f9018360021' value='69e9c8517689f9018360021'><input type='hidden' id='bg-show-more-text-69e9c8517689f9018360021' value='Show Transcript'><input type='hidden' id='bg-show-less-text-69e9c8517689f9018360021' value='Hide Transcript'><button id='bg-showmore-action-69e9c8517689f9018360021' class='bg-showmore-plg-button bg-blue-button  '   style=\" color:#fcfafa;\">Show Transcript<\/button><div id='bg-showmore-hidden-69e9c8517689f9018360021' ><\/p>\n<p>00:14<br \/>\nfollow an escalating sequence of actions<br \/>\n00:17<br \/>\nto control postpartum hemorrhage but<br \/>\n00:20<br \/>\nwhenever blood loss is significant call<br \/>\n00:22<br \/>\nfor additional personnel give IV fluid<br \/>\n00:25<br \/>\nresuscitation and test for coagulopathy<br \/>\n00:28<br \/>\nfirst give oxytocin and do uterine<br \/>\n00:30<br \/>\nmassage routine measures done after<br \/>\n00:33<br \/>\nplacental delivery to increase uterine<br \/>\n00:35<br \/>\ntone particularly a funeral tone is poor<br \/>\n00:38<br \/>\ngive a second drug to increase uterine<br \/>\n00:41<br \/>\ntone and check for and remove retained<br \/>\n00:43<br \/>\nproducts of conception particularly a<br \/>\n00:46<br \/>\nfew Turan tone is good look for and<br \/>\n00:49<br \/>\nrepair bleeding vaginal lacerations<br \/>\n00:51<br \/>\ncervical lacerations are both then if<br \/>\n00:55<br \/>\nneeded tamponade the uterus using a<br \/>\n00:57<br \/>\nballoon or gloss packing if bleeding<br \/>\n01:01<br \/>\npersists do a laparotomy to place<br \/>\n01:03<br \/>\nuterine compression sutures removed<br \/>\n01:06<br \/>\nretained products of conception or both<br \/>\n01:08<br \/>\nas a last resort do arterial<br \/>\n01:11<br \/>\nembolisation or ligation or hysterectomy<br \/>\n01:19<br \/>\nif postpartum hemorrhage is significant<br \/>\n01:23<br \/>\ncall for additional nursing assistance<br \/>\n01:25<br \/>\nand notify anesthesia due volume<br \/>\n01:28<br \/>\nresuscitation as for other causes of<br \/>\n01:30<br \/>\nhemorrhage as needed with significant<br \/>\n01:33<br \/>\nhemorrhage send labs considering<br \/>\n01:36<br \/>\ndisseminated intravascular coagulation<br \/>\n01:38<br \/>\nas well as inherited coagulopathy lay up<br \/>\n01:41<br \/>\ntests should include fibrinogen level as<br \/>\n01:44<br \/>\nwell as CBC with platelets PT and PTT<br \/>\n01:48<br \/>\nand type and screen for possible<br \/>\n01:50<br \/>\ntransfusion next address the source of<br \/>\n01:53<br \/>\nbleeding most commonly uterine atony<br \/>\n01:56<br \/>\nduring delivery of the placenta oxytocin<br \/>\n02:00<br \/>\nis given routinely ideally as an<br \/>\n02:02<br \/>\ninfusion using 20 units and 1 liter of<br \/>\n02:04<br \/>\nIV normal saline solution or another<br \/>\n02:07<br \/>\ncrystalloid solution beginning at 10<br \/>\n02:09<br \/>\nmilliliters per minute which is 600<br \/>\n02:11<br \/>\nmilliliters per hour<br \/>\n02:13<br \/>\nyou may increase the rate to give as<br \/>\n02:15<br \/>\nmuch as 500 milliliters over 10 minutes<br \/>\n02:18<br \/>\nuterine fungal massage is also done<br \/>\n02:20<br \/>\nroutinely after delivery of the placenta<br \/>\n02:22<br \/>\nif bleeding persists despite these<br \/>\n02:25<br \/>\nroutine measures due by manual uterine<br \/>\n02:28<br \/>\nmassage simultaneously rubbing the<br \/>\n02:30<br \/>\nuterine fundus and anterior vaginal<br \/>\n02:32<br \/>\nfornix use a sterile glove on your<br \/>\n02:34<br \/>\ninside hand give a second uterotonic<br \/>\n02:37<br \/>\ndrug two of the choices are<br \/>\n02:39<br \/>\nintramuscular injections intramuscular<br \/>\n02:42<br \/>\nchoices include methyl ergo Naveen 0.2<br \/>\n02:46<br \/>\nmilligrams or one milliliter unless the<br \/>\n02:50<br \/>\nwoman has hypertension and 16 methyl<br \/>\n02:53<br \/>\nprostaglandin F 2 alpha 250 micrograms<br \/>\n02:57<br \/>\nunless the woman has asthma an<br \/>\n02:59<br \/>\nalternative is rectal miss approach tall<br \/>\n03:01<br \/>\n800 to 1000 micrograms<br \/>\n03:04<br \/>\nkharbut Osen 100 micrograms IV is an<br \/>\n03:08<br \/>\nalternative prostaglandin that is more<br \/>\n03:10<br \/>\nheat stable than 16 methyl prostaglandin<br \/>\n03:14<br \/>\nf2 alpha but is not available in the<br \/>\n03:17<br \/>\nUnited States because Carbet Osen can be<br \/>\n03:20<br \/>\nused without having been refrigerated as<br \/>\n03:22<br \/>\ncan miss a pro stall these drugs can<br \/>\n03:25<br \/>\noften be given in resource-poor areas<br \/>\n03:28<br \/>\nconsider retained products of conception<br \/>\n03:30<br \/>\nas a cause if uterine atony<br \/>\n03:33<br \/>\npersists<br \/>\n03:35<br \/>\nif bleeding persists particularly if the<br \/>\n03:38<br \/>\nuterus is firm consider a vaginal or<br \/>\n03:41<br \/>\ncervical laceration so look for and<br \/>\n03:43<br \/>\nrepair these be sure to examine the<br \/>\n03:46<br \/>\npatient with proper positioning and<br \/>\n03:47<br \/>\nlighting have an assistant use<br \/>\n03:49<br \/>\nretractors if necessary also<br \/>\n03:52<br \/>\nparticularly if the uterus is not firm<br \/>\n03:55<br \/>\npalpate inside the uterus for retained<br \/>\n03:57<br \/>\nproducts of conception and remove them<br \/>\n03:59<br \/>\ndo ultrasound agree if you are unsure<br \/>\n04:01<br \/>\nwhether retained products are present if<br \/>\n04:04<br \/>\nmeasures thus far failed to slow<br \/>\n04:07<br \/>\nbleeding begin full bore volume<br \/>\n04:09<br \/>\nresuscitation has done for other causes<br \/>\n04:11<br \/>\nof hemorrhage replace intravascular<br \/>\n04:13<br \/>\nvolume first using crystalloid up to two<br \/>\n04:16<br \/>\nliters<br \/>\n04:16<br \/>\nif further volume is needed Francie&#8217;s<br \/>\n04:20<br \/>\npacked red blood cells also insert a<br \/>\n04:23<br \/>\nbladder catheter to monitor urine output<br \/>\n04:25<br \/>\nand closely monitor heart rate and blood<br \/>\n04:27<br \/>\npressure gather equipment to do uterine<br \/>\n04:30<br \/>\ntamponade to tamponade the uterus insert<br \/>\n04:34<br \/>\nan intrauterine balloon which must be<br \/>\n04:36<br \/>\nplaced and filled using ultrasonographic<br \/>\n04:39<br \/>\nguidance the balloon tip should be close<br \/>\n04:41<br \/>\nto the uterine fundus fill a balloon<br \/>\n04:44<br \/>\nwith saline until bleeding is controlled<br \/>\n04:45<br \/>\nor the capacity of the balloon is<br \/>\n04:47<br \/>\nreached this commercially available<br \/>\n04:49<br \/>\nBakri balloon can hold 300 to 500<br \/>\n04:53<br \/>\nmilliliters vaginal packing may be<br \/>\n04:55<br \/>\nneeded to hold the balloon in place<br \/>\n04:57<br \/>\nremove the balloon gradually and within<br \/>\n05:00<br \/>\n24 hours if a balloon cannot be used use<br \/>\n05:05<br \/>\nring forceps to pack the uterus with<br \/>\n05:07<br \/>\ngauze<br \/>\n05:09<br \/>\nif significant hemorrhage persists treat<br \/>\n05:12<br \/>\noperatively usually first trying<br \/>\n05:14<br \/>\ncompression sutures however before<br \/>\n05:17<br \/>\nplacement compressed the uterus manually<br \/>\n05:19<br \/>\nto ensure that the bleeding stops when<br \/>\n05:21<br \/>\nthe uterus is compressed<br \/>\n05:23<br \/>\nif retained products of conception or<br \/>\n05:26<br \/>\nintrauterine clots are possible do a<br \/>\n05:28<br \/>\nhistory Tommy and completely evacuate<br \/>\n05:30<br \/>\nthe uterus manually this uterus shows a<br \/>\n05:34<br \/>\nhistory Tommy incision use a rapidly<br \/>\n05:37<br \/>\nabsorbable suture such as 2o chromic on<br \/>\n05:40<br \/>\na large curved needle various<br \/>\n05:43<br \/>\ncompression sutures are effective some<br \/>\n05:46<br \/>\nare shown in this figure the most<br \/>\n05:48<br \/>\ncommonly used compression sutures are<br \/>\n05:50<br \/>\nthe B Lynch and as shown here the<br \/>\n05:52<br \/>\nmodified B Lynch sutures place the<br \/>\n05:56<br \/>\nneedle into the uterine cavity at the<br \/>\n05:57<br \/>\nlateral edge of the lower anterior<br \/>\n05:59<br \/>\nuterus and then out the other side do<br \/>\n06:02<br \/>\nthis below the histor atomy incision if<br \/>\n06:05<br \/>\nthere is one now put the needle in and<br \/>\n06:08<br \/>\nthen out of the top of the uterine<br \/>\n06:10<br \/>\nfundus<br \/>\n06:12<br \/>\nnext insert the needle and move it from<br \/>\n06:14<br \/>\none side to the other<br \/>\n06:15<br \/>\non the lower posterior uterus<br \/>\n06:22<br \/>\ntake another bite at the top of the<br \/>\n06:24<br \/>\nfundus<br \/>\n06:27<br \/>\nfinish the modified b-lynch suture by<br \/>\n06:30<br \/>\ntaking a bite similar to the first one<br \/>\n06:32<br \/>\nbut on the opposite lateral side<br \/>\n06:38<br \/>\ncut the needle from the suture tie the<br \/>\n06:42<br \/>\nsuture closed an assistant should<br \/>\n06:45<br \/>\nsimultaneously compress the uterus<br \/>\n06:49<br \/>\neither after or before doing the<br \/>\n06:51<br \/>\ncompression suture close the histor<br \/>\n06:53<br \/>\natomy incision begin with an anchor<br \/>\n06:56<br \/>\nsuture at one end of the histor otta me<br \/>\n07:05<br \/>\nyou<br \/>\n07:12<br \/>\ncomplete the closure using a running<br \/>\n07:14<br \/>\nlocked suture<br \/>\n07:21<br \/>\nyou<br \/>\n07:23<br \/>\nwhen finished cut and tie in the usual<br \/>\n07:26<br \/>\nfashion<br \/>\n07:32<br \/>\nyou<br \/>\n07:35<br \/>\nput the sutured compressed uterus back<br \/>\n07:37<br \/>\ninto the abdominal cavity if bleeding<br \/>\n07:40<br \/>\npersists despite all the described<br \/>\n07:42<br \/>\ninterventions options include uterine<br \/>\n07:45<br \/>\nartery ligation hypogastric artery<br \/>\n07:48<br \/>\nligation arterial embolisation by<br \/>\n07:51<br \/>\ninterventional radiology and ultimately<br \/>\n07:53<br \/>\nhysterectomy<\/p>\n<p><\/div>\n<hr \/>\n<p>&nbsp;<\/p>\n","protected":false},"excerpt":{"rendered":"<p>\ufeff Duration 9:41 Duration 11:41 Duration: 7:09 \ufeff Duration 8:03 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