procedures, trauma and delivery. Clinical
manifestations of dysfibrinogenemia are very
heterogeneous, ranging from absence of clinically
relevant symptoms to major bleeding, and even
thrombosis.
The evidence of thromboembolic
complications in patients with fibrinogen
deficiency (in around 30% of the subjects 5 ) is
difficult to explain, given the pro-coagulant
properties of fibrinogen. The main interpretation
is that the low levels of fibrinogen may promote
a weak clot, more susceptible to the lytic effects
of plasmin. This could result in a partial or
total clot breakdown, with embolisation of
clot parts.
More common are the acquired conditions,
which may derive from liver disease,
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HHE 2018 | hospitalhealthcare.com
disseminated intravascular coagulation (DIC),
thrombolytic therapy, haemodilution or
consumption. Basically, acquired
hypofibrinogenemia results from a reduced
synthesis (liver disease), excessive activation of
the haemostatic system with consumption of the
substrates (disseminated intravascular
coagulation), severe haemodilution (heart surgery
with cardiopulmonary bypass especially in
newborns and infants; resuscitation of trauma
patients), or excessive fibrinogen breakdown
(hyperfibrinolysis).
Low levels of fibrinogen may lead to an
increased risk of bleeding. The clinical scenarios
where this condition is more common include
sepsis with DIC, cardiac surgery with
cardiopulmonary bypass, trauma, post-partum