Coagulation Defects In

Obstetrics
BY
DR.EISSA MAHMOUD
 Normal coagulation (2processes(
1. Plug of platelets in response to
disruption of vascular endothelium
&exposure of collagen →platelet
adhesion & clamping
2. Formation of fibrin cap (coagulation
cascade)
 Coagulation cascade (intrinsic &extrinsic
pathways)
• Intrinsic pathway:
- Its components circulating in the blood stream
- Its function measured by PTT and primarily
affected by heparin therapy
• The extrinisic pathway :
- Initiated by tissue thromboplastin ( lll) + extrinsic
coenzyme (Vll) activate factor x (common
pathway )
- Measured by PT & inhibited by warfarin therapy
• Both pathways culminate in activation
factor X which initiates the common
pathway
 Coagulation cascade
Intrinsic pathway Extrinsic pathway

Xll Thromboplastin
lll
Xl

lX

Vlll Vll
X
 X
Common pathway
Phosphplipids + Xa + Va + Ca + platelet
surface factors
Prothrombin(ll)
Thrombin
Fbrinogen(l)
Fibrin
Fibrin degradation
 Antagonism of coagulation cascade

• Clot prevention :
- Antithrombin lll , alpha two macroglobulin and
alpha one antitrypsin inhibit factor
- Protein c & ltscofactor s → inactivate factor V
and Vlll
• Clot dissolution :
Plasminogen →plasmin Ẁ enhances fibrin
degradation
 Pathophysiology of DIC
• Tissue destruction →releasa thrombo plastin (lll)
into the circulation e.g abruption (extrinisic)→ the
main cause of DIC
- Endothelial injury → collagen & other tissue
factors are realsed in the circulation → activate
factor X e.g pre-eclampsia
- Certain endotoxins and exotoins activate factor X
- Proteases as present in mucin produced by
neopasms →direct activation of factor X
 Coagulation Defects In Obstetrics

• Defiency of coagulation factors with

tendency to bleeding results from
disseminated intravascular coagulation
( DIC ) , dilutional coagulopathy and
excessive infusion with Dextran solution .
Disseminated Intravascular
Coagulation
paradoxic situation in which both
thrombotic & fibrinolytic mechanism
are simultaneously activated
→coagulation &haemorrhagic
diseses are present at the same time
A) Disseminated Intravascular Coagulation
1. When DIC occurs there is consumption of blood
platelets, fibrinogen and clotting factors
2. This is accompanied by increased activity of the
fibrinolytic system to produce lysis of the fibrin thrombi
to maintain patency of the microcirculation
3. This results in increased fibrin degradation products
4. Bleeding occurs when plasma fibrinogen reaches
100mg% or less
5. During pregnancy the fibrinogen level is 400-600mg%
Aetiology
The causes of DIC and hypofibrinogenaemiain
obstetrics include:
1. Sever placental abruption . Commonest cause
and responsible for 60-70% of cases
2. Missed abortion. The degenerated placenta or
dead fetus liberates thrombopastin which enters
the maternal circulation causing intravascular
3. Intrauterine death (1∕3 cases > 5 wk )
4. Septic abortion , puerperal sepsis,
chorioamnionitis and pyelonephritis
The endotoxin of Gram-negative organisms as E
coli leads to:
(a)Damage of vascular endothelium (b) clump
of platelets (c) activates factor12

5. Amniotic fluid embolism , the amniotic fluid

contains thromboplastin
6. Sever pre-eclampsia and eclampsia due to
damage of capillary endothelial cells and
release ofthromboplastin from degenerated
placenta
7. Uterine rupture and any extensive tissue
damage . (a) trauma may cause release of
thromboplastin from damaged tissues in the
circulation .(b) formation of a large haematoma
may consume fibrinogen and other clotting
factors (c) uterine rupture may allow amniotic
fluid to enter maternal circlation

8. Incompatible blood transfusion red cell leads to

release of thromboplastin
9. Acute fatty liver of pregnancy it may present
like preeclampsia
• Diagnosis
A. Failure of the blood to coagulate may give to
petechiae epistaxis , haematuria , bleeding from
needle puncture sites and postpartum
hemorrhage
B. The clot observation test ( weiner test) . It is a
rapid bedside test . 5 ml of venous blood are
withdrawn in a test tube normally clot formed in
6-12 min . Failure of any clot to from within 10
minutes indicates that fibrinogen is less than 100
mg % . If clot incubated at 37c , dissolves after 30
minutes . It means excessive fibrinolytic activity
C . A coagulation profile is ordered which
will show :
1. Plasma fibrinogen is reduced (N: 200 -
300 mg% in pregnacy 400-600 mg% )
2 - Bleeding time : N :2 - 4 min , increase
in DIC due to decrease platelt
3 – Clotting time : N: 6 – 12 min
4- Platelet count is decreased ( ˂ 150,000
per cu.mm)
5- Prothrombin time (PT) is increased ( N:
10-15seconds
6 . Thrombin time ( T T) is increased ( N :
25 -35 seconds
7 . Partial thromboplastin time ( PT T)
isincreased ( N:25-35 seconds)
8 . Antithrombin III consumption is
increased so its level or activity is
decreased( N:22-39mg /dl or activity 84-
123% )
9 .D-Dimers. These products rise when
there is thrombosis and are
morespecific than fibrin degradation
products (above o.5 ug is abnormal)
. D-dimers result from lysis of fibfin
throbi by plasmin , so they only
increase when there is clot formation
10-Fibrin degradation (split )
products (N 10 ug%) are
increased (more than40
micrograms / ml)
Eibrin degradation products may
increase in absence of thrombosis as
in liver disease as they are cleared by
the liver
Treatment
1. Treatment of the cause , e.g, if DIC is due to infection ,
broad spectrum antibiotic are given
2. Fresh whole blood to replace the blood volume , red
cells and clotting factors . If whole blood is not
availabe , give packed red cells and fresh frozen
plasma( FFP ) or cryo-precipitate
3. Plateles are transfused if platelet count is below
50,000/cu.mm.
4. Administration of antithrombin III concentrate may
improve the condition
5. Recombinant activated factor 7 ( rf FVIIa )
6. Heparin . In case of a dead fetus and
when laboratory tests indicate DIC but
the patient is not bleeding . Heparin is
given to raise the fibrinogen level to
above 200mg %
7. The coagulation defect corrects itself
spontaneously within 24hours after
delivery or removal of the cause
Effect Shelf life Unit volume (ml) Content Blood component
Increases hematocrit 3% 35 days 500 RBC,WBC, Plt , Whole blood
unit clotting factors
Increases hematocrit 3% 35 days 250 RBC, minimal WBC Packed red cells
unit less risk for febrile and plt
reaction, which mainly
results from WBC content

Increases hematocrit 3% 24 hrs at -80⁰ 175 RBC , minimal WBC Frozen red cells
unit 72 hrs at 4 ⁰ c and plt

Increases the platelet count 5 dats at 22⁰c 50 Plt Platelet

by 5000-10000 /mm3 unit
gives a minimum of 6 units

Increases fibrinogen 10 1 year at – 18 ⁰c 250 Coagulation factors Fresh frozen plasma

mg/dl /unit give one unit 24 hrs at 4 ⁰ c including fibrinogen
after every 4 units of packed
RBCs

Increases fibrinogen 10 1 year at – 18⁰ c 40 Factor Vlll Von Cryo-precipitate

mg/dl/unit :give a minimum 4 hrs at 4 ⁰ c willebrands
of 10 units when there is fibrinogen
hypofibrinogenemia
B) Dilutional Coagulopathy
This can result if large amounts of intravenous fluids or
blood ( 5 units or more ) are given
This leads to dilution of coagulation factors and tendency
to bleeding
So a unit of FFP should be given for every 5 units of
transfused blood
D) Dextran infusion
Excessive infusion with dextran may cause coagulopathy
Dextran forms a fibrinogen – dextran complex leading to
Hypofibrinogenemia and prevents aggregation of
platelets
Notes
1. Fibrin degration products prevent formation offibrin
clots ,inhibit myomt. Contraction, cause toxic
myocarditis,so increase bleed. And shock
2. Cryoprecipitate . Obtained from fresh frozen plasma
bywarming to 4 c . It supplies fibrinogen factor VIII,
and von willebrand factor . Each unit of
cryoprecipitate raises thefibrinogen level about
10mg/ dl
3. One unit of platelets rasis the platelet count by
10,000/mm3
4. Causes of Hypofibrinogenemia include causes of DIC ,
dilutional coagulopathy and dextran infusion
5. Dextran innterferes with cross-
matching
6 . Platelet concentrate contains some
red blood cells and so needsto be
ABOandRhesus compatible
7 . Measurement of antithrombin IIIis the
most sensitive test to diagnose DIC
 Amniotic fluid embolism (AFE)
(Anaphylactoid syndrome of pregnancy)
• INCIDENCE
1in 8000 to 1 in 80,000 deliveries .
• AETIOLOGY
1. The exact cause is unknown
2. It may be due to sudden escape of a large volume of
amniotic fluid into the maternal venous circulation
after rupture of membranes during labour
3. The amniotic fluid emboli will block the pulmonary
arterioles and capillaries leading to pulmonary
hypertension and hypoxia
4. Hypoxia leads to left ventricular heart failure and death
5. The condition tends to occur in labours with strong
uterine contractions and when the uterus is excessively
stimulated by oxytocin infusion or prostaglandin.
6. It may also occur during (C.S) and after rupture of the
uterus
7. It is suggested that AFE is an immune response caused by
exposure of the mother to amniotic fluid leading to
anaphylatic reaction and shock
8. It usually occurs at the time of delivery , but has been
reporter after amniocentesis and therapeutic abortion
9. also uterine hyperstimulation is found in less than 10%of
patients
• Clinical picture
1. The patient develops sudden severe dyspnea
2. Cyanosis and cough with frothy and Blood stained
sputum
3. This is immediately followed by apnea and profound
shock
4. Chest pain is unusual
5. Death occurs in 25% of cases within one hour and the
majrity who survive will develop disseminated
intravascular coagulation (DIC) with bleeding from the
genital tract and from all sites of trauma
6. The amniotic fluid contains thromboplastin which leads
to intravascular coagulation
Diagnosis
-It is based on clinical picture and laboratory studies
which include :-Complete blood count , Arterial blood
gases , Coagulation profile and it often diagnosed by
exclusion
-Diagnosis in the past was confirmed by postmortem
examination to detect the presence of amniotic fluid
elements as – A- fetal squamous cells – B- lanugo
hair – C- vernix caseosa – D- meconium in pulmonary
arterioles and capillaries
However only 50-70% of patients dying from this
syndrome have this finding
Also amniotic fluid elements in the pulmonary circulation
are detected in normal pregnancy
• Differntial diagnosis
This includes
1. Pulmonary thromboembolism
2. Aspiration pneumonia
3. Myocardial infarction
4. Septic shock
5. Other causes of sudden postpartum collapse
• Treatment
1. Oxygen is supplied by an endotracheal tube and
mechanical ventilation
2. Treatment of shock:
a) Blood volume expansion by colloids , crystalloids, or
blood
b) Pressor agents such as dopamine or norepinephrine
3. Digitalis if there is left ventricular failure which is
common
4. Treatment of pulmonary oedema which is common
(70%) by diuretics as frusemide ( lasix)
5. Corticosteroids may help as the syndrome may be
immune mediated ( hydrocortisone 500mg IV every 6
hours until the patient recovers)
6. When DIC occurs it is treated properly
7. If maternal cardiac arrest occurs before delivery , the
fetus is delivered immediately by forceps or by CS if
conditions are not favourable for vaginal delivery .
Prognosis
8. Maternal mortality is about 60%
9. Many of the women ( 75%) who survive will suffer
neurlolgical damage secondary to hypoxia
10.Neonatal survival is about 75% with 50% of those
surviving will suffer neurological problems
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