DIC in OBSTETRICS

( Disseminated Intravascular
Coagulation)
Definiton
-also known as consumptive coagulopathy

- a pathological activation of coagulation (blood clotting)

mechanisms that happens in response to a variety of
diseases which leads to the formation of thrombi in the
microvasculature of the body.

a complex systemic thrombohemorrhagic disorder

involving the generation of intravascular fibrin and the
consumption of procoagulants and platelets, and also
because of systemic circulation of thrombin and plasmin
that result to intravascular coagulation and hemorrhage.
Overview
DIC is a pathophysiological process and not a disease. It is
when the body's natural ability to regulate blood clotting does
not 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.
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.
 Pathological activation of coagulation
I. Coagulation maybe activated via:
a. extrinsic pathway by thromboplastin from tissue
destruction
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.
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 rapid
defibrination with amniotic fluid embolism.
- Consumptive coagulopathy is almost
always seen as a complication of an
identifiable, underlying pathological
process against which treatment must be
directed to reverse defibrination.
- With pathological activation of
procoagulants that trigger consumptive
coagulopathy, there is consumption of
platelets and coagulation factors in variable
quantities.
- As a consequence, fibrin may be deposited
in small vessels of virtually every organs
system.
- Small vessels are protected because
coagulation release fibrin monomers
that contain with tissue plasminogen
activator and plasminogen wich
releases plasmin.
- Plasmin lyses fibrinogen, fibrin
monomers, and fibrin polymers to
form a series of fibrinogen-fibrin
derivatives.
- Measured by immunoassay, these
are known as fibrin degradtion
products as split products.
Conditions associated with DIC in
obstetrics

Abruptio placenta
Amniotic fluid embolism
Pre-eclampsia and eclampsia
abortion
Abruptio Placenta
Etiology:

the placenta breaks away, or abrupts, from the wall of

the 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.
 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
Amniotic fluid Embolism
a rare obstetric emergency in which it is postulated that
amniotic fluid, fetal cells, hair, or other debris enter the
maternal circulation, causing cardiorespiratory collapse.

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

The etiology of coagulopathy associated with amniotic

fluid embolism is incompletely understood, but it is
known that amniotic fluid has a potent total
thromboplastin and antifibrinolytic activity. Both of which
increase with advancing gestational age.

The response to amniotic fluid embolus in humans may

be biphasic, initially resulting in intense vasospasm,
severe pulmonary hypertension, and hypoxia
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).
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

Abortion

- Serious disruption of the coagulation mechanism as the

consequence 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 and
decidua because of the necrobiotic effect of the hypertonic
solutions, which then initiates coagulation within the
maternal circulation.
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 absent
clinical signs and symptoms
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.
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.
 Practical markers of disseminated intravascular coagulation

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

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 circulating
thrombin, and AT levels are considerably reduced in DIC.
Management
Thrombomodulin
Therapy 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 thrombomodulin’s
thrombin-binding properties but were probably mediated through an increase in
APC.94,119

Interleukin-10 and Anti–Tumor 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)
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 obstetric

disorders and its acute haematological management. (2001)
Members:
Santos, Criselda
Shih, Chun I
Silla, Earica
Sim, Samantha C
Siquijor, Michel Analie V
Solleza, Earl John
Tamayo, James
Tan, Irene Carmelle
Tauro, Charlene Gayle