HYPOFIBRINOGENEMIA

Disseminated Intravascular Coagulation

(DIC) or Consumptive Coagulopathy.
 HYPOFIBRINOGENEMIA
 PHYSIOLOGICAL BACKGROUND
In late pregnancy, there is increased concentration of
coagulation factors I (fibrinogen: level is 350-650 mg/dL),
VII,VIII,IX and X. Other plasma factors and platelet count
(150 000-400 000/cmm) do not change remarkably.
 DEFINITION
A widespread hematological condition characterized by
accelerated fibrin formation and lyses. There is
consumption of platelets and coagulation factors in
variable quantities.
Signs of hypofibrinogenaemia develop when its level goes
below 100 mg/dL
 Etiology (Pregnancy related)
 Common causes
 Massive blood loss with inadequate replacement. Massive
crystalloid or colloid replacement
 Placental abruption.
 Severe pre-eclampsia/eclampsia or HELLP syndrome.
 Rare causes
 Sepsis.
 Retained dead fetus (for more than 3-4 weeks).
 Amniotic fluid embolism.
 Acute fatty liver of pregnancy.
 Adult RDS, acute hemolytic transfusion reactions,
autoimmune disease, hematological malignancies and solid
tumors.
 MECHANISM
 Pathologically accelerated coagulation: occurs via the extrinsic
pathway (thromboplastin from tissue destruction) or the intrinsic
pathway (collagen and other tissue components when endothelial
integrity is lost). Finally factor X (Prothrombinase) is activated. The
formed thrombin (activated factor II) changes fibrinogen (factor I) to
fibrin (monomers and polymers-clot-). Factor X can be activated
directly by proteases present in mucin of amniotic fluid or
neoplasms.

 Fibrinolysis: the fibrin monomers combine with tissue

plasminogen activator and plasminogen which release plasmin.
Plasmin lyses the fibrin mono and polymers to form a series of
fibrin degradation products (FDPs) including the D-dimer.
 CLINICAL PICTURE

 Postpartum or antepartum hemorrhage.

 Persistent bleeding from venipuncture sites or
after catheter insertion.
 Spontaneous bleeding from gums and nose.
 Generalized oozing in surgical fields.
 Purpuric areas at pressure sites
(thrombocytopenia and incoagulable blood).
 Investigations

Aiming to detect fibrinolysis.

 FDPs and fibrin D-dimer (normally absent).
 Prolonged PT and PTT(PTT may be normal).
 Low fibrinogen, falling antithrombin III & low platelet
count (CBC should be done).
 Weiner test (clot observation test): 5-10 cc of blood in a
test tube are incubated at 37ºC. A) Normally a clot forms
within 3-8 minutes. B) a clot forms after a longer time
and dissolves within one hour = hypofibrinogenemia. C)
No clot is formed = afibrinogenemia.
 TREATMENT
 It must be directed to the underlying cause to reverse
defibrination. Two wide-bore IV cannulas are inserted.
 If PT is > 1.5 times the control value, transfuse fresh
frozen plasma (FFP). The goal is to keep PT within 2-3
sec. of the control value.
 If fibrinogen level is < 100 mg/dL, transfuse
cryoprecipitate. Ten units of cryoprecipitate are usually
given after every 2 to 3 units of plasma. Each unit of
cryoprecipitate increases the fibrinogen by 10 mg/dL.
OR give Fibrinogen 4-10 g IV.
 TREATMENT
 Platelets should be transfused if the count is < 20 000/cmm or if
clinically significant bleeding occurs with a platelet count between
20 000 and 50 000/cmm. Each platelet unit increases count by
10,000/cmm. The usual rate of platelet transfusion is 1-3 U/ 10Kg/
day.
 Antifibrinolytics as Epsilon Amino Caproic Acid (EACA) 4-6 g IV
OR trasylol 2-4 ampules IV ( 5 ml ampoule contains 25 000 U), is
not recommended in most types of obstetric coagulopathy to avoid
organ ischemia and infarction unless all above mentioned
measures fail to control bleeding.
 Heparin infusion trying to stop coagulation is condemned when the
vascular system integrity is compromised.