The gentlebirth.org website is provided courtesy of
Ronnie Falcao, LM MS, a homebirth midwife in Mountain View, CA
This brief but well-referenced post analyzes cesarean rates relative to differences in maternal diagnoses or pregnancy complexity. On average, the likelihood of cesarean delivery for an individual woman varied between 19 and 48 percent across hospitals.”
Birth attendants often claim that their high cesarean rate is due to their clientele - that they provide care for a lot of high-risk clients. This analysis shows that:
Among lower risk women, likelihood of cesarean delivery varied between 8 and 32 percent across hospitals.
Among higher risk women, likelihood of cesarean delivery varied between 56 and 92 percent across hospitals.
Hospital variability did not decrease after adjusting for patient diagnoses, socio-demographics, and hospital characteristics.
This shows that practice variation in cesarean rates is real, substantive, and not just a reflection of the mother’s risk level.
Tips for Choosing a Care Provider - great overview! from Henci Goer
The following conditions are possible precursors to DIC:
DIC is a situation of inappropriate coagulation within the blood vessels which leads to the consumption of clotting factors, thus resulting in the failure of the clotting mechanism at the site of bleeding. DIC begins with an event (possibly one of the above) that triggers widespread clotting with the formation of microthrombi throughout the circulation. The clotting factors are then used up. The DIC triggers fibrinolysis ( the breakdown of fibrin occurring as a response to the presence of clotted blood) and FDP production (Fibrin Degradation Products, the products of fibrinolysis). The FDPs reduce the efficiency of normal clotting. (Myles Textbook for Midwives, Bennett and Browne)
So, we have two things happening at once here. First the widespread clotting within vessels in the body (possibly due to the above conditions), then fibrinolysis, the bodies' response to this abnormal clotting by attempting to break up the unneeded clots, which leads to the production of FDPs that further reduce the efficiency of an already gone awry clotting process. (my comments)
If DIC occurs during or after delivery, the reduced level of clotting factors and the presence of FDPs prevent normal hemostasis (arrest of bleeding) at the placental site. FDPs inhibit myometrial action and prevent the uterine muscle from constricting the blood vessels in a normal way. Torrential hemorrhage may be the outcome, and even if clotting does occur, the clot is unstable (due to both Fibrinolysis and FDPs). Microthrombi in the bloodstream may cause circulatory obstruction in the small blood vessels and lead to cyanosis of fingers and toes to CVAs, or organ failure. (Myles Textbook for Midwives, Bennett and Brown)
So, DIC is not just a pregnancy related condition (DIC can occur in non-pregnant men, women and children), but it can become even worse due to the placental site being an open bleeding wound, and that the FDPs are interfering with the normal ligation of the vessels in the site. Also because the placental site is like an open window to the circulation, microthrombi can easily pass into maternal circulatory system, and result in stroke (CVA), organ death, brain death, coma, and death as basically, the vessels are blocked off, and no 02 can get through, or simply due to severe blood loss with shock and then death occurring. (my comments)
Possible explanations for predisposing events to DIC: (my condensation of Myles)
Placental abruption causes damaged tissue at placental site and large quantities of thromboplastins ( released by damaged tissues and 1st step in blood clotting) are released into the circulation, resulting in large scale clotting throughout system, not just placental site. The faster the placenta is delivered postabruption, the lesser the chance of DIC.
Intra-uterine fetal death with retained fetus of more than 3 or 4 weeks causes thromboplastins to be released from the fetal tissue, into the maternal circulation, causing the onset of clotting problems as above.
Amniotic fluid embolism (the process of amniotic fluid entering the maternal circulation, and usually causing pulmonary embolism) causes thromboplastins from the amniotic fluid to be released into maternal circulation.
Intra uterine infection causes endotoxins to be released into the maternal circulation and these damage the blood vessels causing the release of thromboplastins.
Pre-eclampsia and eclampsia are unknown, and unclear precursors to DIC. They do know that pre and eclampsia patients have higher amounts of FDPs in the blood and urine than others.
So that leaves retained placenta, possibly due to the mechanical, or physical attempts at removal forcing thromboplastins into system. Transfusion reaction, I could find nothing on why this may lead to DIC. (my comments)
Signs or symptoms of possibly evolving DIC include: Major bruising, bleeding from venipuncture sites and skin sutures, gastrointestinal and genitourinary bleeding. (In other words, bleeding from all orifices, and any puncture sites) (Human Labor and Birth, Oxorn and Foote)
Medical treatment depends on the cause of the DIC and whether it is
occurring intrapartally or not. Basically it involves removing the cause
(i.e. delivery of placenta if it is retained, abrupted, etc....delivery
of fetus if retained, quick delivery if severe eclampsia and so on, hysterectomy
if bleeding cannot be controlled from placental site) then and/or con-currently
treat DIC, (similar to treatment of hemorrhage) blood and plasma transfusions
with appropriate support measures. Sometimes Cryoprecipitate, Heparin,
or Epsilon Aminocaproic acid are used to attempt to correct clotting deficiencies
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