Thromboembolic diseases include thrombophlebitis,
phlebothrombosis, septic pelvic thrombophlebitis and pulmonary
embolism. They are a major cause of morbidity and mortality in
DVT and PE are distinct but related aspects of vascular venous
Incidence of thromboembolism is 0.2% in ante-natal period
and 0.6% in postpartum. The incidence rises to 1-2% post
caesarian section. Pulmonary embolism has a mortality rate
of 15% in 50% of patients with DVT. Unfortunately only 5-
10% are symptomatic.
Pregnancy increases risk x 5-10 fold
0.71/1000 (DVT) : 0.15/1000 (PE)
Ileo-femoral more common than calf vein (72% versus
Increased with age, caesarian section, bed rest and prior
history of DVT/PE)
Disorder of blood vessel wall
Disordered blood flow (stasis)
Abnormality of blood constituents
××Recap the clot forming physiological cascade
and the fibrinolysis cascade
Venous stasis – changes in tone and
Vascular damage at time of delivery
APTT, PS (free and total), APCr
FVIII:C, VWF, Fibrinogen
PAI-1 and PAI-2
A. Patient factors:
Age>40 risk increase exponentially with age
Obesity (BMI > 30kg/m2
Varicose veins or venous thrombophlebitis
Oral contraceptives & HRT; estrogen is responsible
Pregnancy: due to
(i) Hormonal changes
(ii) Pressure on veins by fetus
Highest incidence in puerperium especially just after
Dehydration: increase blood viscosity
Immobility: Stasis of blood
Long distance travel: due to
Due to these factors blood becomes more sticky specially if
journey is for more than 5 hours
B. Surgical conditions:
Especially includes surgery for more than half an hour
Abdominal, pelvis, orthopedic surgery to lower limb
Increased use of central venous line has caused more
involvement of upper limbs in D.V.T.
C. Medical Conditions
Inflammatory bowel disease
Malignancy or its treatment
E. Anti-Coagulant Deficiences:
Antithrombin III: such patients are also
relatively resistant to heparin Therapy
Factor II Leiden: Genetic polymorphism of
Factor V Leiden: Mutation leading to APC
Heparin cofactor II
Prothrombin G20210 A mutation
F. Increased Clotting factors:
XI and VIII
G. Antiphospholipid Antibodies:
D.V.T. of iliac, femoral or popliteal vein
leg swelling, warmth, erythema, increased tissue turgor, distention
of superficial veins and appearance of prominent venous
collaterals. In some patients deoxyhemoglobin in straight veins
gives it a cyanotic hue called as ‘Phlegmasia cerulea dolens’.
In markedly edematous legs, interstitial tissue pressure may
exceed capillary perfusion pressure causing pallor – ‘Phlegmasia
Tenderness is present along individual vein and a cord may be
D.V.T. of calf vein: commonest complaint calf pain especially when
standing or walking
There may be tenderness or warmth, increased tissue turgor or
modest swelling. Homan’s Signs: positive
50% of clients are asymptomatic
Clinical Diagnosis unreliable due to
differential diagnosis but serial limb
measurements are suggestive of diagnosis
and treatment follow-up
Screening investigations – impedance
Definitive diagnosis – Doppler ultrasound, CT
PE – ventilation perfusions scan
*** venograms and pulmonary angiograms not
done in pregnancy
◦ Bed rest with elevation of the affected limb
◦ Avoid Deep Palpation
◦ Compression stocking
Acute phase heparin administration – it acts
indirectly by activating plasma Antithrombin III.
Dose: i.v. bolus 7500-10,000 IU followed by
continuous infusion so that 1000-1500 IU/Hr is
Deep S.C. injection of 10,000-20,000 U every 8-12
hrs can also be given.
This treatment is maintained for at least 5-7 days vis
a vis clinical symptoms
Test used to monitor heparin therapy include
coagulation time, activated partial
thromboplastin time, thrombin clotting time,
and heparin assay. Heparin should not be
given if the platelet count is below 50,000/µL.
The partial thromboplastin time should be 1.5-
2 times the control value during heparin
Heparin if administered in the first trimester of
pregnancy as WARFARIN causes
S/E of heparin include:
• osteoporosis and
• fatty necrosis
Antidote of heparin, protamine sulphate 1mg
per 100 units
Heparin must be stopped at least one day prior to
Low molecular weight heparin is equally effective used in
fixed OD or BD doses for 6-14 days.
ADVANTAGES of low molecular weight heparin includes:
i. Increased binding of plasma proteins or endothelium in turn leading to
a. Increased bioavailability
b. Predictable anticoagulant response
ii. Affinity for macrophages resulting in increase half life
iii. Affinity for plts and platelet factor 4 binding to osteoblasts
iv. No monitoring required
v. No hospitalization require
vi. Convenient O.D. doses
vii. Decreased incidence of thrombocytopenia
viii. Osteopenia Unknown
Oral anticoagulant, acts by indirectly interfering with the synthesis of
Vit. K dependent clotting factors in liver, 5-15 mg is started during first
week of heparin therapy as early as the first day if APTT is in
therapeutic range. Dose adjusted accordingly to P.T. INR should be
maintained 1.5-2.5 times control. Heparin can then be withdrawn
* Embryopathy includes: nasal hypoplasia, skeletal abnormalities, and
multiple central nervous system abnormalities.
Antidote vitamin K 5mg I.V.
Warfarin must be avoided in the first trimester and after 36 weeks
◦ Extend use of warfarin throughout puerperium
◦ Introduction of anticoagulant therapy in the next
pregnancy 2 weeks prior to symptoms of
◦ Use of LMWH in clients with cardiac prosthesis
and on bed rest during pregnancy
◦ Avoid use of estrogen containing contraceptives
Partial thromboplastin time (PTT) and activated partial thromboplastin time (aPTT)
Activated protein C resistance (APCR) describes a hemostatic disorder characterized by a poor anticoagulant response to activated protein C (APC). This results in an increased risk of venous thrombosis, including deep vein thrombosis and pulmonary embolism.
von Willebrand factor (VWF) is a blood glycoprotein involved in hemostasis.
Thrombophlebitis (throm-boe-fluh-BY-tis) is an inflammatory process that causes a blood clot to form and block one or more veins, usually in your legs. The affected vein might be near the surface of your skin (superficial thrombophlebitis) or deep within a muscle (deep vein thrombosis, or DVT)
Hormone replacement therapy(HRT)
Nephrotic syndrome is a kidney disorder that causes your body to pass too much protein in your urine. Nephrotic syndrome is usually caused by damage to the clusters of small blood vessels in your kidneys that filter waste and excess water from your blood.
Behcet's syndrome, is a rare disorder that causes blood vessel inflammation throughout your body.
Homocysteinemia, a separate but related entity, is defined as elevation of the homocysteine level in blood. This condition has also been referred to as homocyst(e)inemia to reflect metabolites that may accumulate.
In fact, a high level of homocysteine is a risk factor for heart disease.
Polycythemia refers to an increase in the number of red blood cells in the body. The extra cells cause the blood to be thicker, and this, in turn, increases the risk of other health issues, such as blood clots.
Thrombocythemia is a disease in which your bone marrow makes too many platelets. Platelets are blood cell fragments that help with blood clotting. Having too many platelets makes it hard for your blood to clot normally. This can cause too much clotting, or not enough clotting.
Paroxysmal nocturnal hemoglobinuria (PNH) is a rare acquired, life-threatening disease of the blood. The disease is characterized by destruction of red blood cells (hemolytic anemia), blood clots (thrombosis), and impaired bone marrow function (not making enough of the three blood components).
Resistance to activated protein C (APC resistance) is a term used to describe abnormal resistance of human plasma to the anticoagulant effects of human APC. APC resistance is characterized by a reduced anticoagulant response of patient plasma after adding a standard amount of APC.
Thrombocytopenia is a condition characterized by abnormally low levels of platelets
Osteopenia is a condition that begins as you lose bone mass and your bones get weaker.