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DIC in OBSTETRICS( Disseminated IntravascularCoagulation)


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Definiton

-also known as consumptive coagulopathy

- a pathological activation ofcoagulation (blood clotting)mechanisms that happens in response to a variety ofdiseases which leads to the formation of thrombi in the

microvasculature of the body.

a complex systemic thrombohemorrhagic disorderinvolving the generation of intravascular fibrin and theconsumption of procoagulants and platelets, and also

because of systemic circulation of thrombin and plasminthat result to intravascular coagulation and hemorrhage.


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OverviewDIC is a pathophysiological process and not a disease. It is

when the body's natural ability to regulate blood clotting doesnot function properly because of excessive consumption of

clotting factors and platelets within circulation.

This causes the blood's clotting cells (platelets) to clump

together and clog small blood vessels throughout the body.

This excessive clotting damages organs, destroys blood cells,

and depletes the supply of platelets and other clotting factors

so that the blood is no longer able to clot normally. This often

causes widespread bleeding, both internally and externally.
http://www.webmd.com/hw-popup/platelethttp://www.webmd.com/hw-popup/platelet


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Pathophysiology

Pregnancy Hypercoagulability

Pregnancy normally induces:

concentrations of coagulation factors I

(fibrinogen), VII, VIII, IX, X.

plasminogen levels

Plasma factors and platelets do not change

so remarkably.Plasmin is normally decreased.


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Pathological activation of coagulation

I. Coagulation maybe activated via:

a. extrinsic pathway by thromboplastin from tissuedestruction

b. intrinsic pathway by collagen and other tissue

components when there is loss of endothelial

integrity.

II. Tissue factor is released and complexes with

factor VII, which in turn activates tenase (factor IX)

and prothrombinase (factor X) complexes.


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Common inciting factors of DIC:

Thromboplastin, endotoxin and exotoxins

from placental abruption

Direct activation of factor X by proteases

Amniotic fluid contains abundant mucin

from fetal squames which causes rapiddefibrination with amniotic fluid embolism.


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- Consumptive coagulopathy is almostalways seen as a complication of an

identifiable, underlying pathologicalprocess against which treatment must bedirected to reverse defibrination.

- With pathological activation of

procoagulants that trigger consumptivecoagulopathy, there is consumption ofplatelets and coagulation factors in variablequantities.

- As a consequence, fibrin may be depositedin small vessels of virtually every organssystem.


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- Small vessels are protected becausecoagulation release fibrin monomers

that contain with tissue plasminogenactivator and plasminogen wichreleases plasmin.

- Plasmin lyses fibrinogen, fibrinmonomers, and fibrin polymers toform a series of fibrinogen-fibrinderivatives.

- Measured by immunoassay, theseare known as fibrin degradtionproducts as split products.


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Conditions associated with DIC in

obstetrics

Abruptio placenta

Amniotic fluid embolism

Pre-eclampsia and eclampsiaabortion


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Abruptio Placenta

Etiology:

the placenta breaks away, or abrupts, from the wall ofthe uterus too early, before the baby is born.

(http://www.webmd.com/baby/tc/placenta-abruptio-topic-overview)

The hypertensive states of pregnancy are associated

with 2.5 17.9% incidence of placental separation.
http://www.webmd.com/baby/tc/placenta-abruptio-topic-overviewhttp://www.webmd.com/baby/tc/placenta-abruptio-topic-overview


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Predisposing factors:

maternal age,

multiparty,

uterine distention (multiple gestation, hydramnios),

vascular disease (DM, SLE),

thrombophilias,uterine anomalies or tumors (leiomyoma),

cigarette smoking,

alcohol consumption (>14 drinks/day),

coccaine use,

possibly maternal type O blood


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Amniotic fluid Embolism

a rare obstetric emergency in which it is postulated thatamniotic fluid, fetal cells, hair, or other debris enter thematernal circulation, causing cardiorespiratory collapse.

(http://emedicine.medscape.com/article/253068-overview)

The etiology of coagulopathy associated with amnioticfluid embolism is incompletely understood, but it isknown that amniotic fluid has a potent totalthromboplastin and antifibrinolytic activity. Both of which

increase with advancing gestational age.

The response to amniotic fluid embolus in humans maybe biphasic, initially resulting in intense vasospasm,severe pulmonary hypertension, and hypoxia


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Pre-eclampsia and Eclampsia

Preeclampsia usually occurs with first pregnancies.

May be seen:

with twins (or multiple pregnancies)

in women older than 35 years,

in women with high blood pressure before pregnancy,

in women with diabetes

in women with other medical problems (such as

connective tissue disease and kidney disease).


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Preeclampsia is also associated with:

problems with the placenta (such as too much

placenta, too little placenta)

how the placenta attaches to the wall of the uterus.

hydatidiform mole pregnancies


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Abortion

- Serious disruption of the coagulation mechanism as theconsequence of abortion may develop in the folowing:

Prolonged retention of a dead fetus

Sepsis syndrome Medical induction with prostaglandin During instrumental termination of the pregnancy Intrauterine instillation of hypertonic saline or urea

solutions

thromboplastin is released from the placenta, fetus anddecidua because of the necrobiotic effect of the hypertonicsolutions, which then initiates coagulation within thematernal circulation.


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Clinical features presentation in pregnancy may be more

sudden and unexpected causing:> Generalized bleeding> Localized hemorrhage> Purpura> Petechiae

> Fever> Hypertension> Proteinuria> Hypoxia

Widespread fibrin deposition may affect lungs,brain, kidney, liver Chronic DIC may have minimal or absentclinical signs and symptoms


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Prognosis

- The likelihood of life threatening hemorrhages in

obstetrical situations complicated by consumptive

coagulopathy depends not only on the extent of

coagulation defects but on whether the

vasculature is intact or ruptured

- With gross derrangement of blood coagulation,

there maybe fatal hemorrhage when vascular

integrity is disrupted yet no hemorrhage as long as

all blood vessels remain intact.


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Diagnostic Procedures

D-dimer test. This blood test helps determine whether a person's blood

is clotting normally by measuring a substance (fibrin)

Prothrombin time (PT/INR). This blood test measures how long it takes

blood to clot.

Fibrinogen. This blood test measures how much fibrinogen is in the

blood. Fibrinogen is a protein that plays a part in blood clotting.Complete blood count (CBC). counting the number of red blood cells

and white blood cells. CBC results cannot diagnose DIC, but they

provide information to help the doctor make a diagnosis.

Blood smear. The number, size, and shape of red blood cells, white

blood cells, and platelets are recorded. Blood cells often look damaged

and abnormal in people with DIC.


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Practical markers of disseminated intravascular coagulation

MJ 2003;327:974-977 (25 October), doi:10.1136/bmj.327.7421.974)


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Therapeutic Management

Control of the underlying disease: because prolongation of

exposure to the triggering factors worsens DIC, it is

important to eliminate the etiologic factors as rapidly as

possible. Elimination of the cause of DIC can be easily

performed in obstetrics, for example, by cesarean section.

(Bruchim, Y. et al. Disseminated Intravascular Coagulation

(2008)COMPENDIUM Vol. 30,No. 10)

***If not achieved, attempts of using anticoagulation


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Management

Prophylactic transfusion of platelets at delivery does not

reduce the incidence of postpartum hemorrhage or

hasten normalization of the platelet count.15 Patients with

DIC should be given fresh frozen plasma and packed red

blood cells.(Padden, M.HELPP Syndrome: Recognition and Perinatal Management

(2008) Compendium Vol30, No10)

Antithrombin Therapy

AT is considered to be the primary inhibitor of circulatingthrombin, and AT levels are considerably reduced in DIC.


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Management

ThrombomodulinTherapy may be beneficial in DIC as a sole treatment with no APC transfusion.119

Thrombomodulin had a beneficial effect on coagulation in humans and animals

and appeared to reduce pulmonary vascular injury and leukocyte

accumulation.94,120 These effects were not dependent on thrombomodulins

thrombin-binding properties but were probably mediated through an increase in

APC.94,119

Interleukin-10 and AntiTumor Necrosis Factor Antibodies

Administration of recombinant interleukin-10, an antiinflammatory cytokine, has

been shown to completely nullify the endotoxin-induced effects on coagulation.

(Bruchim, Y. et al. Disseminated Intravascular Coagulation

(2008)COMPENDIUM Vol. 30,No. 10)


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Management

Synthetic serine protease inhibitors: continuous infusion of gabexate

mesilate (FOY) or nafamostat mesilate (FUT) is effective for DIC. Controlled

multicenter trials showed a significant improvement not only in clinical

response but also in platelet counts and prothrombin time (PT) in the AT

group compared with the FOY group.

Activated protein C (APC): can inhibit thrombin generation and accelerate

fibrinolytic activity. APC (5,000 to 10,000 units) is administered for 2 days in

patients with placental abruption complicated by DIC. APC is a very safe,

effective, and useful agent for the treatment of DIC.

(Thachil J, Toh CH. Disseminated intravascular coagulation in obstetricdisorders and its acute haematological management. (2001)


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Members:Santos, Criselda

Shih, Chun I

Silla, Earica

Sim, Samantha C

Siquijor, Michel Analie V

Solleza, Earl John

Tamayo, James

Tan, Irene CarmelleTauro, Charlene Gayle

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