Disseminated Intravascular Coagulation Transcript
Disseminated Intravascular Coagulation (DIC)
This is Dr. Cal Shipley with a review of Disseminated Intravascular Coagulation in association with placental abruption.
Disseminated Intravascular Coagulation, also known as DIC or consumption coagulopathy, is a potentially fatal disorder. DIC can present as an acute life-threatening emergency, or as a chronic subclinical process. Whether DIC manifests itself in an acute or chronic fashion is dependent on the severity and rapidity of the underlying triggering mechanism.
Causes of DIC
Common causes of DIC in North America include infection, malignancy, trauma, and obstetrical complications. For the purposes of this presentation, I’m going to use acute placental abruption with hemorrhage as the underlying cause of DIC. Let’s start by looking at a term fetus, that is, one which has a gestational age of about 40 weeks. The cervix serves as the outlet for the uterus, and protrudes into the vagina.
The placenta is a plate-like structure which is attached to the wall of the uterus, and in conjunction with the umbilical cord, it acts as a conduit to transfer nutrients and oxygen from mother to baby, and carbon dioxide and waste products from baby to mother. You can see a more in-depth review of placental and umbilical cord physiology in the Obstetrics section under the Placenta directory at CalShipleyMD.com.
The placenta receives a rich blood supply from the mother via the uterine artery. The spaces between the villi of the placenta are filled with circulating blood participating in the exchange of nutrients and waste products. Typically in a term pregnancy, the placenta lies against the sidewall of the uterus, well clear of the cervical outlet. Earlier in the gestation period, however, in this example at 30 weeks, the placenta may actually lie over the cervical outlet, a condition known as placenta previa.
A placenta previa which persists until term can be a very serious condition, as the placenta will be physically obstructing the birth canal, and therefore the progress of labor, and may result in placental abruption with severe hemorrhage. The good news is that 90% of placenta previas occurring in the earlier stages of gestation will resolve spontaneously by term. As the uterus grows, the placenta is pulled up and away leaving the uterine outlet unobstructed.
The presence of a placenta previa at 30 weeks gestation carries with it an increased risk of placental abruption, particularly in mothers with a past history of abruption in previous pregnancies. In such circumstances, even relatively minor trauma, such as during a vaginal examination or forceful intercourse, may cause the placenta to abrupt, resulting in hemorrhage.
Placental Abruption and Disseminated Intravascular Coagulation
Placental abruption occurs when the placenta separates from the uterine wall, with rupture of the placental arterial attachments. Immediate and heavy hemorrhage may occur. As blood flows through the cervix and into the vagina, the first symptom noted by the mother is often heavy vaginal bleeding. Within minutes, a significant percentage of the mother’s blood volume may be lost, resulting in a drop in blood pressure and an increase in pulse rate.
The placental bleeding triggers the body’s clot forming mechanism. Damage to the walls of uterine arteries, that occurs in the abruption process, results in the secretion of activated tissue factor, a glycoprotein. Tissue factor facilitates the production and activation of multiple clotting factors, such as thrombin and factor VII. Clot formation begins. If the initial clot formation is not able to stop the hemorrhage, further tissue factor is secreted, and more clot formation is stimulated.
As this process continues, large quantities of clotting factors are consumed in the formation of clot, and the overall volume of clotting factors in the body begins to drop. This is the beginning of disseminated intravascular coagulation. Placental abruption results in the rupture of attached veins as well as arteries. As bleeding persists, tissue factor continues to be secreted, and eventually enters the vascular system via uterine veins.
From the uterine veins, the tissue factor spreads throughout the circulatory system. In the arterial system, small arteries known as arterioles give rise to capillaries, which carry oxygen-bearing red blood cells to all tissues of the body. Tissue factor is carried into the arterioles, where it stimulates the formation of small clots known as microthrombi. The formation of these small clots may occur throughout the body, and this is the hallmark of disseminated intravascular coagulation.
The microthrombi enter capillaries, where they obstruct the flow of red blood cells, cutting off critical oxygen supply to organs and tissues. Obstruction to red blood cell flow through capillaries may lead to dysfunction or outright failure of any organ in the body, and particularly affects those organs with high blood flow demand, such as the brain, kidneys, and the adrenal glands. In this example, based on an actual case, microthrombi caused extensive tissue death, also known as infarction, in the large and small intestines.
If the process of tissue factor-related clot formation is not interrupted, clotting factors are consumed, and may reach critically low levels in the bloodstream. This severe depletion in clotting factors may then result in uncontrolled hemorrhaging throughout the body. In the example I have presented today, hemorrhage was the underlying cause which triggered the secretion of high levels of tissue factor. In the case of other causes of DIC such as infection, trauma, and malignancy, high circulating levels of tissue factor occur as a by-product of abnormal biochemical processes associated with a specific disease state.
Cal Shipley, M.D. copyright 2020