Clotting Disease in Pregnancy PBL

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Clotting Disease in Pregnancy

Transcript of Clotting Disease in Pregnancy PBL

Page 1: Clotting Disease in Pregnancy PBL

Clotting Disease in Pregnancy

Page 2: Clotting Disease in Pregnancy PBL

What is D-Dimer? D-dimer is a fibrin degradation product (or FDP)

FDP: Small Protein fragments that result once clot is broken up (i.e. fragments of the fibrin mesh) D-dimer is so named due to it being a dimer of to D domains,

connected to an E domain of Fibrin

D-dimer concentration may be determined by a blood test to help diagnose thrombosis. Not normally in the blood, unless the coagulation

pathway is active High Levels indicate clotting disorder favoring

thrombosis Used as diagnostic criteria for: deep venous

thrombosis, pulmonary embolism or disseminated intravascular coagulation 

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Causes of  schistocytes (aka Helmet Cells)

Schistocytes are present in microangiopathic hemolytic anemia This is a form of anemia caused by damage to the

endothelial walls of small blood vessels Clotting and irregularity of the cell walls damage

the RBCs The fibrin mesh (loose fibrin that extends into the

vessel) damages the RBCs, causing their irregular shape Specifically, this damage arises from the fibrin sticking to

the RBCs, which are then pulled away by the blood pressure, causing some of the cells to tear

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Causes of microangiopathic hemolytic anemia during pregnancy

Pre-eclampsia/Eclampsia HELLP (hemolysis, elevated liver enzymes, low platelets)

syndrome, which is characterized by hemolysis, elevated liver enzymes, and low platelets.

Linked to pre-existing hypertension (due to rushing of cells through damaged/very small vessels), which also is present in pre-eclampsia/eclampsia

Has to be very high ( >220 Systolic or >130 dystolic at rest), known as malignant hypertension

Possible link to Gestational diabetes Glycosylation damages the endothelial walls, resulting in clotting

and formation of microangiopathic hemolytic anemia Not confirmed. Link exists in traditional diabetes that has gone

unmanaged but seems to mostly hypothetical in gestational diabetes

SLE (Lupus)- Will have appeared as a pre-existing condtion in most cases, and our patient lacks the rash or other associated symptoms

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Causes of microangiopathic hemolytic anemia during pregnancySo, what else could it be? Disseminated intravascular coagulation (DIC)

syndrome Thrombotic thrombocytopenic purpura (TTP)

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Disseminated intravascular coagulation (DIC) syndrome The DIC syndrome is the most

common cause of an abnormal hemorrhage tendency during pregnancy. Also common during child birth or

immediately following In pregnancy it is an indicator of

an underlying issue with the pregnancy: Placental Abruption Eclampsia Retention of a dead fetus Amniotic fluid embolism, Placental retention Bacterial sepsis

Caused by systemic activation of the coagulation cascade by circulating clotting factors, with secondary activation of the fibrinolytic (clot breaking) system.

Rapid clotting results in depletion of clotting factors, resulting in lack of normal clotting

Diagnosis of the DIC syndrome: reduced levels of fibrinogen and

platelets, prolongation of the thrombin,

prothrombin and partial thromboplastin times

The presence of fibrin/fibrinogen degradation products (FDP) in the serum.

Treatment: Prompt removal of the source of

pro-coagulant material Replacement of depleted clotting

factors in some cases, anti-coagulation

with heparin.

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Thrombotic thrombocytopenic purpura (TTP) TTP has two forms: Primary

and secondary Secondary is associated with

pregnancy Time during pregnancy with

greatest risk for development of TTP–hemolytic uremic syndrome is near term and during the postpartum period.

Rare: 1/25000 Pregnancies Cause is unknown for

secondary TTP, beyond that pregnancy can trigger it

Symptoms: Fatigue Fever Bleeding (from nose, gums) Diarrhea Chest pain Kidney failure (dark urine,

jaundice) Neurologic Symptoms

(confusion, headaches, visual changes)

Thrombocytopenia microangiopathic hemolytic

anemia Treatment: Plasmaphoresis

and Prednisone

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My hypothesis: Fetal death occurred at 30 weeks. However,

fetus was not expelled This triggered the patient to suffer DIC syndrome

Alternative cause: Placenta Abruption

Patient lacks any confusion or other symptoms of TTP, has no history or signs of lupus, and their blood pressure is relatively low Though the low blood pressure could be due to

blood loss.