COMPILATION ON

PUERPERAL VENOUS
THROMBOSIS AND
PULMONARY EMBOLISM

BY
SHAMBHULING HEBBALLI
III rd BAMS.
A.M.V. HUBLI.

DEPT. OF PRASOOTI & STREEROGA,

A.M.V. HUBLI.

UNDER GUIDANCE OF
DR. J. MUMMIGATTI.
BSc,BSAM,BAMS

HOD,DEPT. OF PRASOOTI &

STREEROGA,

A.M.V. HUBLI

DR.C.P. DIXIT.
BSAM,BAMS.

PROFESSOR.

DR.ANITA MARIBASHETTI.
MD(AYU)

LECTURER.

PUERPERAL VENOUS THROMBOSIS AND

PULMANARY EMBOLISM
INDEX
1. Introduction
2. Etiopathogenesis
3. Deep vein thrombosis
a) Dignosis
b) Symptoms
c) Investigation.
4. Pelvic thrombo Phlebitis
5. Clinical feature
6. Poeventive measure
7. Management
Pulmonary embolism
a) Introduction
b) Sligns & Symptoms
c) Diagnosis
d) Management

PUERPERAL VENOUS THROMBOSIS AND PULMNARY

EMBOLISM
Introduction
The thrombosis of log vein and pelvic is one of the common
and important complication in perpurium especially in the western
the prevalence is however low in Asian and African countries.
Venous thrombo embolic disease include
- Deep vein thrombosis cileombosis cileofemoral.
- Thrombophlebitis superficial and deep veins.
- Septic pelvic thrombophlebitis.
- Pulmonary embolus.
Etiopathogenesis:
1) In normal pregnancy there is rise in concentration of
coagulation factors I, II, III, IV, V, VI, VII, VIII, IX, X, XII
plasma fibrinolytic inhibitors are produced by the placenta and
the level of protein sis markedly decreased..
2) Alteration in blood constitutuents increased number of young
platelets at their adhesiveness.
3) Venous stasis is increased due to compression of gravid uterus
to the inferior vena cava and iliac vein this stasis causes
damage to endothelial cells.
4) Thrambophilias are hypercoaguable states in pregnancy that
increases risk of venous thrombosis it may be inherited or
acquired. Inherited thrombophilias all the genetic condition
associated with the deficiency of anti thrmoboin III protein C
protein S others are factor V leiden mutation and hyper

homocysteinemia. Aquired thrombophilias are due to presence

of lupus anticoagulanter and antipospolipid antibodies.
5) Other acquired risk factors for thrombosis are
a. Advanced age and perity.
b. Operative delivery.
c. Obesity
d. Anamia
e. Heart diseases
f. Infection pelvic cellulities.
g. Trauma to venous wall
Deep vein thrombosis:
Diagnosis: Clinical diagnosis unreliable in majority it remains
asymptomatic.
Symptom include: Pain in calf muscle and rise in remprature
odema of legs on examination a symmefric leg. Odema (diffrance in
circumference) between affected and normal leg more than 2cm is
significant a positive Homans sign pain in caff on dorsiflexion of
foot may be present.
Investigation:
The following biophysical tests are employed to confirm the
diagnosis. Doppler ultrasound to detect the changes the velocity of
blood flow in the femoral vein by nothing the alteration of
charecterstic whoosh sound which is audible from patent vein partial
occtusion or presence of big collateral circulation may give rise false
+ve result. It is non invasive method and can be performed even
with the portable unite with puplex Doppler ultrasound and DVT

real time ultrasoundgraphy, can defect intramural thrombus and is

helpful to study the blood flow through the veins diagnostic cirtaria
of DVT with ultrasound all (a) soft tissue mass within the venous
lumen. (b) non compressibility of vein.
Venography By injuctin non ionic water soluble radio
opaque dye to note the filling defect in venous lumen is realiable
method if carefully interpreted venagram is restricted in pregnancy
and if needed performed using and abdominal shield, with lead
aprons.
Fibrinogen scanning I251 fibrinogen scaning is not
recommended.for DVT diagnosis in pregnancy due to the risk iof
radiation exposure to the fetus cabauf 2 racls radio labeled iodine
crosses the placenta it is taken by the fetus thyroid gland it is also
secreted in the breast milk.
Pelvic thromboplebities:
Postpartum thromboplebitis is originates n the thrombosed
vein at the placental site by organism such as anacrobic styeptocoai
or bacteroids fragili. When localized in the pelvis it is called pelvic
thromboplebitis. There is no specific clinical features of pelvic
thrombophlebitis but it should be suspected in a case where the
pyrexia continues for more than a week inspite antibiotic therapy.
Extra pelvic speed
1) Through right ovarian vein into inferior venacava, and thence
to the lungs.
2) Through the left ovarian vein to the left renal vein and thence
to the left kidney.

3) Retrograde extension toilio femoral veins to produce the

clinical pathological entity of phlegmasia alba dolen;s or white
leg plegmasia alba dolens (syn white leg). It is the
clinicopathological condition usually caused by retrograde
extension of pelvic thrombophlebit

to involve iliofemoral

vein. The femoral vein may be directly effected from accident

cellulites the condition seledom met now adays.
Clinical features:
1) It usually develop second week of perpurium.
2) Mild pyrexia is common prior to the dramatic local
manifestations. At times the fever may by high with cells and
rigor.
3) Evidences of constitatinal distrabances such as head ache
malasia and rising pulse rate or features of toxaemia may be
present..
4) The effected leg is swollen painfull white cold the pain is due
to arterial spasm asaresulted irritation from the near by
thrombosed vein.
5) Blood count shows polymorphonecleum leucocytesis.
The diagnosis may be made by ultrasound may be made by
ultrasound computed tomography (CT) scan or by magnetic
resonance imaging (MRI) atrial of heparine therapy may be
considered when the symptom improve with heaparine therapy
diagnosis is confirmed.

Prophylaxis for venous thromboembalism (VIE) in pregnancy

and perpeurium:
Preventive measure include:
- Prevention of trauma sepsis anaemia in pregnancy and
labour dehydration during delivery should be avoided.
- Use of elastic compression stocking and intermittent
phecmatic compression during surgery.
- Leg exercise early ambulation are encouraged following
operative delivery.
Women at risk of venous thromboembolism during pregnancy
have been grauped in to different catogories depending on presence
of risk factors. Thrombo prophylaxis to such a women depends on
specific risk factors and the category.
1) The low risk women has no personal and family history of
VTE and are heterozygous for factor V leidenm meutation
such a women need no thrmboprophylaxis.
2) High risk women is one who has preveous VTE or VTE in
present pregnancy or anti thrombin III deficiency such a
women need low moleaulary it heparine prophylaxis
throught pregnancy and post partum 6 weeks women with
antitrombine III deficiency can be treated with antithrombin
III concentrate prophylactically.

Management:
1) The patient is put to bed rest with the foot end rised in
effected level of heart.
2) Pain in effected area can be releved by analgesics.

3) Appropriate antibiotics are to be administered.

4) Anticoagulants.

(a)

Heaparine

15000

units

are

administererd intravenously followed by 10000 units 4 to 6

hourly for four to 6 injection when the blood coagulation is
likely to be depressed to the therapeutic level. Heaparien is
continued for at keast 7-10 days or even longer if
thromboplastine time (APTT) to 1.5-2.5 times indicates
effectiove and safe anticoagulant low molecular lit
heaparine (LMWH) can be used safly in pregnancy.
Enoxaparine 40mg daily is given. It does not crose the
placenta. (b) A drug of coamarin series warferine is
commonly used orally with an ovarlapp of at least 3 days
with heparine the initial daily does of 7mg for 2 days is
adequate for induction subsequent mainteanance does
depend upon international normalized ratio (INR) which
should be within the range of 2-3 daily maintenance dose of
wartarin is sually 5 to 9mg to be taken at the same time
each day the anticoagulant therapy should be continued till
all evedabce of disease have disappeared which generally
takes 3-6 months neighter anticoagulant should prevent the
mother from breast feeding.
5) As soon as pain subsides gentie movements is allowed on
bed by the end of first week high quality elastic stocking
are fitted on the effected leg before metabolism.
6) Vena cava filters are used for patient where anticoagulant
therapy is contraindicated vena cava may be completely
ligated by Teflon clips.

7) Fibrinolutic agents like streptokinase produce rapid

resultion of pulmonary emboli.
8) Venous thrombotomy is needed for massive pulmonary
emboli.
Pulmonary Embolism:
Pulmonary embolism is leading cause internal dath in many
centres specially in the developed countries after the sharp decline of
maternal mortality due to hemorrhage hypertension or in the pelvis
is most likely the cause of pulmonary embolism but in about 8090%, it occurs without any previous clinical manifestation of deep
vein thrombosis. The predisposing factors are those already
mentioned in venous thrombosis the clinical features depend on size
of embolus and on the preceding health status of the patient. The
classic symptom of massive pulmonary embolism are sudden
collapse with acute chest pain and air hunger death usually occurs
within short time from shock and vaginal inhibition.

Signs and symptoms of Pulmonary embolism:

Tachypnoea dyspnoea pleurite chest pain cough tachycardia
haemoptysis and rise in temperature > 37C.
Diagnosis X-ray of the chest shows diminished vascular
marking in area of infraction elvation of done of diaphragm and
often effusion. It is useful to rule out pneamenia and atelectasis.
ECG tachycardia right axis shift.
Arterial blood gas:
Po2 35mm Hg on room air is reassuring < 95% on room air
needs further investigation.
Dopher ultrasound:
Can identify a DVT when the test is Tve for DVT
anticoagulant therapy should be started.
Lung scan: (ventilation / perfusion scan)
Perfusion scan will detect are of diminished blood flow
whrease aredaction in perfusion with mentaince of ventilation
indicates pulmonary embolism MRI can be used in pregnancy as the
risk of ionizing radiation is absent.