DVT IN

PREGNANCY/
PUERPERIUM
.
GROUP MEMBERS
Obadiah Kibiwott- H12/01786/18
Natasha Musimbi –H12/01753/18
Naisoi Kerorio – H12/01769/18
Kelly Ingabo – HP12/01475/17
Donald Kipkalya - H12/01741/18
Victor Onsongo - H12/01782/18
Mike Odhiambo – H12/01743/18
Daniel Kiiru – H12/01759/18
Alex theuri – H12/01687/18
Onyari Pauline- H12/03885/18
 Outline
Definition
Pathophysiology
History
Predisposing factors
Examination findings
Differentials
Investigations
Treatment
Complications
Prognosis
Prophylaxis
Conclusion
DEFINITION
It is the formation of a blood clot or clots within the venous vascular cavity.

Pregnancy is a hypercoagulable state

Thrombosis of the leg veins and pelvic veins is one of the common and important
complications in puerperium, especially in the Western countries
A pregnant woman has a fivefold risk of DVT compared to general population.
Caesarean section increases the incidence by 1-2%
Mortality
Death from DVT is attributable to massive pulmonary embolism.
Epidemiology
Pregnancy and puerperium are well-established risk factors for venous
thromboembolism (VTE)
The age-adjusted incidence ranges from 5 to 50 times higher in
pregnant versus non-pregnant women
Complicates 1 in 500-2000 pregnancies
More common post partum
Antepartum risk is equally distributed across trimesters
Twice as higher after a caesarean section than vaginal delivery
 Hemostasis
Formation of clots in the walls of damaged blood vessels
Prevention of blood loss
Maintaining blood in a fluid state within the vascular system
Components of hemostasis
◦ Vascular spasm
◦ Initiation and formation of platelet plug
◦ Propagation of coagulation cascade
◦ Termination of antithrombotic control mechanisms
◦ Removal of clot by fibrinolysis
Clotting cascade
Hemostasis
Control mechanisms and termination of clotting
◦ Antithrombin, heparin and glucosaminoglycan heparan sulfate
◦ Activated protein C and S
◦ Tissue factor pathway inhibitor
◦ Prostacyclin and thromboxane
◦ Nitric oxide
Clot elimination and
fibrinolysis
Anatomical changes in
pregnancy and peuperium
Venous Stasis
◦ Gravid uterus
◦ Low capacitance vessels
◦ Immobilisation

Endothelial injury
◦ vascular injury and changes at the uteroplacental surface during delivery
◦ instrumental, or surgical delivery
Coagulation changes in
pregnancy
Increase in levels of Fibrinogen by 50% (450mg/dl
cf. 300mg/dl)
Other factors increased: Factor VII, VIII, IX, X
Factor II (prothrombin) increased slightly
Factors XI, XII & protein S reduced
Resistance to activated protein C.
Decreased platelet per unit volume
Basic pathology for venous thrombosis are—
(i) Vascular stasis,
(ii) (ii) Hypercoagulability of blood (pregnancy), and
(iii) (iii) Vascular endothelial trauma (Virchow’s triad 1856). Other pregnancy-specific risk factors are as mentioned below:
(iv) Venous thromboembolic diseases include:
(v) (a) Deep vein thrombosis (iliofemoral) 
(vi) (b)Thrombophlebitis (superficial and deep veins)
(vii) (c)Pulmonary embolus

Pathophysiology:
(1) In a normal pregnancy there is rise in concentration of coagulation factors I, II, VII, VIII, IX, X, XII. Plasma
fibrinolytic inhibitors are produced by the placenta and the level of protein S is markedly (40%) decreased;
(2) Alteration in blood constituents—increased number of young platelets and their adhesiveness;
(3) Venous stasis is increased due to compression of gravid uterus to the inferior vena cava and iliac veins. This stasis
causes damage to endothelial cells;
(4) Thrombophilias are hypercoagulable states in pregnancy that increase the risk of venous thrombosis. It may be
inherited or acquired. Inherited thrombophilias are the genetic conditions associated with the deficiencies of
antithrombin III, protein C, protein S and prothrombin gene mutation. Others are factor V Leiden mutation and
hyperhomocysteinemia.
Acquired thrombophilias are due to the presence lupus anticoagulant and antiphospholipid antibodies
Inherited Thrombophilia and
their effects on the coagulation
cascade.
HISTORY
The symptoms and signs of Deep Venous thrombosis(DVT) are related to the
degree of obstruction to venous outflow and inflammation of the vessel wall.
Clinical diagnoses of DVT is neither specific or sensitive with the false positive
rate as high as 50%. Many patients are asymptomatic however the history
may include the classical features which are;-
oEdema/Leg swelling of affected site of the legs
oLeg pain (50% of patients) and pain on dorsiflexion of the leg(Homan’s sign)
oTenderness(75% of patients)
oLocal cyanosis
oFever
oWarmth and erythema of the skin can be present over area of thrombosis
Risk factors
Immobilization Prior use of oral contraceptives
Surgery Pregnancy or postpartum status
Obesity Stroke
Prior history of VTE Malignancy
Trauma
Thrombophilias
 PREDISPOSING FACTORS

Thrombophilia
Inherited thrombophilias are conditions that increase the risk of
thromboembolic disease.
During pregnancy, the thrombogenic potential of these disorders is enhanced
because of pregnancy-associated changes in several coagulation factors.
There are two types of thrombophlias:
Acquired thrombompilias.
Inherited thrombompilias
Acquired Thrombophilias (P.131)
Also called antiphospholipid syndrome.
Presence in the serum of at least one type of autoantibody known as an
antiphospholipid antibody (aPL).
Lupus anticoagulant antibodies
Anticardiolipin antibody antibodies
Their presence predispose to risk of thromboembolism and other
obstetric morbidities( recurrent abortions, preeclampsia, stillbirths)
Inherited Thrombophilias
Are genetic conditions that increase the risk of thromboembolic
disease. And other obstetric morbidities( abortions, Preeclamsia,
IUGR,stillbirths)
Factor V Leiden, the most common cause of activated protein C
resistance
Prothrombin gene mutation (PGM)
Antithrombin (AT) deficiency
Protein C deficiency
Protein S deficiency
Clinical presentation

DVT is more common in the left than the right leg.

WHY
 Reason

Increased venous stasis in the left leg due to compression of the left
iliac vein by the right iliac artery,
Compression of the inferior vena cava by the gravid uterus itself
EXAMINATION FINDINGS/SIGNS
1) Edema of affected limb usually unilateral.Commoner on the left as the left
common iliac vein is crossed by the right common iliac & left internal iliac
arteries thus increasing resistance to flow. A circumference of 2-3cm greater in
the affected limb than in the normal limb 10 cm from the tibial tuberosity and
20cm from ASIS(Anterior Superior Iliac Spine)
2) Pain and tenderness usually confined to the calf muscles or acting along the
course of the deep veins in the medial thigh.
3) Fever usually low grade.
4) Homan’s sign i.e. discomfort in the calf muscles on forced dorsiflexion of the foot
with the knee straight. (1/3 of patients with DVT)
5) Cyanosis of the affected limb
6) Warmth on the affected limb
DIFFERENTIAL DIAGNOSES
oCellulitis (may coexist)
oRuptured Baker's cyst (both may coexist) - especially in individuals with pre-existing rheumatoid disease
of the knee
oSpontaneous/post-traumatic calf haematoma
oOsteomyelitis
oPyomyositis
oPulmonary embolism
oThrombophlebitis superficial or septic
oLymphangitis
oVaricose veins
oLymphedema
oAchilles tendonitis
oArterial insufficiency
oAsymptomatic peripheral edema secondary to CHF, Liver failure, renal failure or nephrotic syndrome.
INVESTIGATIONS (p.131)

)DEEP VENOUS THROMBOSIS

Imaging Studies
a) Colour Doppler U/S - Gold standard
The flow of blood as detected by reflection of waves on rbcs is absent in DVT.
b) Impedance Plethysmography
Is based on recording changes in blood volume of an extremity, which are directly
related to venous outflow. Standardized graphs are used to discriminate normal IPG
study results from abnormal results.
c) IV contrast Venography
Is most definitive mtd of dx venous thrombosis bt 1-2% of patients develop phlebitis
following procedure
d) MRI
Reserved for specific occasions which ultra-sound findings are equivocal or negative
ultra-sound findings but strong clininical suspicion.
e) CT-SCAN
Requires contrast agents and ionizing radiation. DXT exposure to the foetus is
negligible unless pelvic veins are imaged
Lab Studies

D-dimer Blood test

Are fibrin degradation products (FDP)
D-dimer fibrin fragments are present in fresh fibrin clot and
in fibrin degradation products or cross-linked fibrin.
Monoclonal abs specific for the D-dimer fragment are used
to differentiate fibirn-specific clot form non-cross linked
fibrin and from fibrinogen. Thus has high sensitivity for
venous thromboembolism.
Low sensitivity
 B) PULMUNARY EMBOLISM
a) Ventilation–perfusion scanning and computed tomographic (CT)
angiography are associated with relatively low radiation exposure for the
fetus
-Maternal radiation exposure (particularly to the breast) is lower with
ventilation–perfusion scanning.
b)The American Thoracic Society and the Society of Thoracic Radiology
clinical practice guidelines for the evaluation of suspected PE in pregnancy
suggest that chest X Ray can be used in initial evaluation,
Then VQ scan if the chest X Ray is normal
CTPA if the chest X Ray is abnormal
Treatment
Rationale
◦ Prevent further clot extension
◦ Prevention of acute pulmonary Embolism(PE) cos association with high
mortality > 60%.
◦ Reducing the risk of recurrent thrombosis
◦ Limiting development of late complications e.g. postphlebitic syndrome,
chronic venous insufficiency.
TREATMENT
Consists of anti-coagulation, bed rest and analgesia.
1) Supportive management
Consists of elevating the affected limb(s), serial measurements, elastic stockings and analgesia. Thus will
alleviate the oedema and improve venous return & promote early ambulation.
2) Definitive management i.e. Anti-coagulation
a) Heparin
used in the Acute phase
Can use either Unfractionated Heparin(UFH) or Low molecular weight heparin(LMWT)
i)Using UFH, start with 10,000-15,000IU IV followed by continous IV infusion of 10,000IU/ 4-6hrly. Aim is
to make the APTT/KCCT 1.5-2X the control values
UFH can also be used s.c @ 10,000-15,000IU tds. Heparin cannot cross the placenta due to its high
molecular weight (16000-40000 daltons)
Pharmacodynamics
Anti-thrombin (an endogenous inhibitor of coagulation) inhibits clotting factor proteases by forming
equimolar stable complexes with them. Heparin catalyzes the anti-thrombin-protease reaction
without being consumed. Anti thrombin inhibits the intrinsic pathway {Factor IIa (Thrombin), Factor
IXa (Christmas factor), Factor Xa (Stuart-Prower factor)}
Heparin enhances Anti-Thrombin activity.
Pharmacokinetics of UFH
Onset of action - 30mins
T1/2 - 1.5hrs
Duration of action - 8hrs
Adverse effects
oThrombocytopenia- is immune mediated and develops 6-10 days presenting with artertial
thrombosis-White Clot syndrome. It results from irreversible aggregration of platelets
induced by heparin
oOsteoporosis-prolonged use
oHyper K+- inhibits aldosterone secretion
oHypersensitivity
oAlopecia (rare)
Antidote;
Protamine sulphate 1mg/100U heparin IVI given within 15mins; Max dose; 50mg (if
exceeded may itself have anticoagulant effect).
ii) LMWT heparin (enoxaparin (clexane®), dalteparin)
o Inhibit FXa but have less effect on anti-thrombin & on coagulation in general
o Convenient to use - SC OD/BD
o Longer duration of action
o Does not require monitoring
o Reduce dose in renal insufficiency
o Disadvantage is their high cost.
b) Oral anticoagulation
Warfarin- Coumarin derivative
Is started once the acute phase is over and the APTT/KCCT IS 1.5-2X the control. Warfarin is
continued for 3-4 days while on Heparin s.c. unitl the INR IS 2-3X the control then Heparin
can be discontinued.
Initial dose is 5mg od and is titrated to get an INR OF 2-3X the control
Pharmacodynamics
Blocks the γ-carboxylation of several glutamate residues in extrinsic pathway (Vitamin K
dependent) factors II, VII, IX, & X as well as the endogenous anticoagulant protein C & S.
The blockade results in incomplete molecules that are biologically inactive in coagulation.
 Warfarin use in pregnancy:
Controversial cos associated teratogenicity.
Use after first trimester, convert patient back to Heparin at 36 weeks in preparation for
labor to avoid bleeding- neonate and mother.
Instituted after delivery till end of puerperium.
oLifelong in recurrent DVT, proximal DVT
Pharmacokinetics
Onset of action - 48-72hrs
T1/2 - 36hrs
Adverse effects
oHypercoagulability within the first few days of administration due to the rapid
degradation of Protein C & S which have a short half life in plasma (2.5-3hrs)
thus heparin is administered together with Warfarin for first 3-4 days.
Warfarin Antidote
oStop the drug and administer large doses of vitamin K 1 (phytonadione) 10mg - takes 6-
8hrs to take effect (disadvantage) & FFP or factor IX concentrates or cryoprecipitates
oIn emergencies, use fresh frozen plasma(FFP) or fresh blood.
warfarin embryopathy
Warfarin crosses placenta and has teratogenic potential.
There is convincing evidence that warfarin administration between the
sixth and ninth weeks of gestation is potentially teratogenic
The most common developmental abnormalities affect bone and
cartilage; causing chondromalacia punctata, with stippled epiphyses
and nasal and limb hypoplasia
warfarin embryopathy
central nervous system (CNS) abnormalities (including optic atrophy,
microcephaly, mental retardation, spasticity, and hypotonia)
Fetal or neonatal hemorrhage is a concern when warfarin is
administered in the third trimesters.
So avoided in pregnancy when Heparin admnistration possible.
Avoid before week 14-16, convert to Heparin injection at 36 weeks as
you await labor.
c) Other treatment modalities are;
Venous thrombectomy still has a role in the management of patients with extensive
iliofemoral disease in which limb loss is imminent
IVC filters may be used in;
o Active bleeding
o When anti-coagulants fail
o To minimize risk of PE during venous thrombectomy

PROPHYLAXIS
oHeparin 5000IU s.c. bd
oJunior Aspirin 1 tablet od
oClaxane (LMWT Heparin) 40 mg od s.c.

PROGNOSIS
All patients with proximal vein DVT are at long term risk of chronic venous innsufficiency.
Approximately 20% of untreated proximal(above the calf) DVTs progress to pulmonary
emboli, and 10-20% of these are fatal. With anti-coagulation therapy the mortality is
decreased 5- to 10- fold.
COMPLICATIONS
oAcute Pulmonary embolism
oSystemic embolism
oChronic venous insufficiency
oPost- phlebitic syndrome( i.e. pain and edema in the affected limb without new clot
formation)
oSoft tissue ischaemia associated with massive clot and very high venous pressures
phlegmasia cerulea dolens
PREVENTION
oAvoid prolonged bed rest
oEarly ambulation following Surgery

CONCLUSION
DVT is a clinical condition which needs early diagnoses so as to reduce the incidence of
pulmonary embolism and death.
Subsequent Pregnancies
Prophylactic anticoagulation.
THANK YOU