Case 9: Deep Vein Thrombosis

- L.J., 70 y/o retired bus driver admitted with Right DVT

- Has 48 pack year smoking history, quitted 2 years ago
- Has had pneumonia several times and frequent episodes of A-fib
- 2 previous episodes of DVT and was diagnosed with rheumoid arthritis 3 years ago
- HPI: 2 mos ago he began experiencing SOB on exertion and noticed swelling of his R foreleg that
became progressively worse until it involved his thigh to the groin
- SO: wife, who brought LJ to the hospital when he c/o increasingly severe pain in his leg
- Doppler study indicated a probable thrombus vein extending distally to the lower leg
- Admitted for bed rest and to initiate heparin therapy
- Lab values : PT 12.4, INR 1.11, PTT 25 sec, Hgb 13.3 g/dl Hct 38.9, cholesterol 206 mg/dl. BMP is
normal
Deep Vein Thrombosis
description
A blood clot (thrombus) that forms inside a deep vein. It may partially or completely block blood
flow, or it could break off and travel to the lung. Deep vein thrombosis often occurs in the lower
legs (calves). Less often it occurs in the arm or pelvis.
causes
Pooling of blood in the vein, which triggers blood-clotting mechanisms. The pooling may occur
after prolonged bed rest, following surgery, or from long-lasting illness, such as heart attack,
stroke, or bone fracture.
risk increases with
Persons over 60.
Obesity.
Smoking.
Surgery and surgery recovery.
Cancer, heart failure, stroke, and polycythemia.
Bed rest for an extended time, burns, or injuries.
Blood disorders that increase the risk of blood clots.
Signs and Symptoms
Oedema
Calf pain
Tenderness
Swelling
Increased skin temperature
Engorgement of superficial leg veins
Slight fever
Positive Homans sign (discomfort in calf muscles on forced dorsiflexion
Initial assessment by observation and examination

Observation
Observe and record skin colour. Compare with unaffected side.
Is the area swollen? Compare with unaffected side.
Is oedema present?
Is the area painful? Check for pain at rest or on movement.
Is the area reddened? Compare with unaffected side.
Are any wounds present? If so, how long have they been present? Have they been
treated? By whom?

Physical examination
Check and record presence of distal pulses on the affected limb and compare with the
unaffected side.
Check and record heart rate, respiratory rate and depth, blood pressure and
temperature.
Is the area hot? Compare with unaffected side.
Palpate the area for pain or tenderness. Compare with the unaffected side.
Check for range of movement of proximal and distal joints. Does this increase pain?
Can the patient walk normally on the affected limb(s)?
Information to be collected during history taking
Information to be collected verbally
History of present problem:
How long has it been present?
When did it start?
Is it constant or intermittent?
Is it worse today than usual?
Is there any previous history of same or similar problem?
Is there any recent history of injury to the affected area?
Has there been any recent long distance travel (>4 hours) in last 4 weeks?
Has there been any previous surgery especially orthopaedic, pelvic or abdominal?
Is the area painful? If so, does anything relieve the pain or make it worse?
Has any medication been taken to relieve the problem?

Immediate management and investigations
Patients with suspected DVT are nursed on a stretcher-trolley, in a bed or
in a chair. Elevate the affected leg with some flexion of the knee (to
encourage venous drainage) and support it on a pillow in the position most
comfortable for the patient. Take a history (Boxes 11.2 and 11.3), measure
vital signs, gain intravenous (IV) access and take bloods for full blood count
(FBC), urea, electrolytes and clotting screen. In addition, oxygen
saturation may be measured and oxygen given if required. Measurement
of calf circumferences to provide a baseline for further evaluation may be
carried out 10 cm below the tibial tuberosity. A swelling of 3 cm greater
than the asymptomatic side is a relative indicator of DVT but is not
definitive. Application of graded compression stockings can reduce postthrombotic
syndrome by up to 60% (Gorman et al 2000). Explain
procedures to the patient and assess their potential for early discharge.
The principle of managing patients with a DVT is early initiation of
effective anticoagulant therapy with the aim of preventing further progression of the
thrombosis to the proximal veins and, thereby,
pulmonary embolism. Given that diagnosis on the basis of clinical features
is often inconclusive, management of suspected DVT is based on the
results obtained from one or more objective diagnostic investigations. To
support this, clinical risk factors (Box 11.1) are also assessed and taken into
account, as confirmation rates of DVT rise with the number of factors
present. Identification of an underlying cause, if present, will also guide the
treatment and prevention of further episodes (Gorman et al 2000).
The standard radiographic investigation for DVT is contrast
venography (Gorman et al 2000) but the painful, invasive nature of this
procedure, its technical difficulty and the time taken for completion make
it inappropriate for use in acute settings. Technological advances in recent
years have led to the introduction of non-invasive ultrasonography as a
first-line investigation for DVTs. Known as pulsed Doppler ultrasound,
this technique measures the velocity of moving objects (such as red blood
cells) in comparison to other objects.
Rapid, effective anticoagulant therapy is important in the initial
management of DVT. Treatment usually starts with an intravenous dose
of heparin (5000 units) followed by subcutaneous low molecular weight
heparin (LMWH) for 5 days. LMWH has been shown to be at least as
effective as the traditionally used unfractionated heparin in preventing
recurrent venous thromboembolism. In addition, it significantly reduces
the occurrence of major haemorrhage during initial treatment and
reduces overall mortality at the end of the patients follow-up period (van
den Belt et al 2000). Oral warfarin is usually started on day 1 with the dose
determined by algorithm.

The Wells clinical prediction guide for DVT (Anand et al 1998)
Clinical feature Score
Active cancer (treatment ongoing or within 6 months or palliative) 1
Paralysis, paresis or plaster of Paris on lower leg 1
Recently bedridden >3 days or major surgery within 4 weeks 1
Localised tenderness along distribution of deep vein system 1
Calf diameter >3 cm larger than the asymptomatic leg* 1
Pitting oedema 1
Entire swollen leg 1
Collateral superficial veins (non-varicose) 1
Alternative diagnosis (as likely or greater than that of DVT) 2
Adding the scores with a total as follows indicates probability of DVT:
0 = low probability = 3% frequency of DVT
12 = medium probability = 17% frequency of DVT
3+ = high probability = 75% frequency of DVT
*Measured 10 cm below tibial tuberosity
Ongoing assessment and treatment
Gorman et al (2000) suggest that the patients activated partial
thromboplastin time (aPTT) is checked every 6 hours until the target of
1.52.5 is reached or according to a heparin algorithm. Once reached, this
should be checked daily to maintain this range. Platelet count should also
be measured at the start of treatment and on day 5 to rule out
thrombocytopenia. Duration of treatment for DVT varies from 3 to 12
months depending upon the risk of recurrence of thrombosis.
Many patients who are referred with DVT can be discharged once
initial investigations and treatment have been completed. Pout et al (1999)
give an example of how a nurse-led outpatient clinic has successfully been
introduced to treat patients with daily doses of LMWH. This approach has
been adopted in other centres with the aim of improving the service to
patients and relieving pressure on individual MAUs

COMPLICATION
Pulmonary Embolism
2. Symptoms: dyspnea (73%), pleuritic pain (66%), cough (37%), leg pain or swelling (27%), hemoptysis
(13%), lightheadedness, loss of consciousness.

3. Signs: tachypnea (~80%), tachycardia (~80%), rales (51%), S4, loud P2, elevated JVP, fever.

4. Work-up: Always think of PE in patients with new or unexplained dyspnea and/or hypoxemia. Studies
should include:
CXR: abnormal in 84% but non-specific: atelectasis, effusion, basilar opacity, elevated diaphragm,
Westermarks sign (focal decreased pulmonary vessel perfusion), Hamptons hump (peripheral wedge
shaped density).
ECG: sinus tachycardia, S1Q3T3, right axis-deviation, RBBB, T wave inversions of V1-4, a-fib/flutter.
ABG: mean PaO2 70mmHg, < 60 (25%), < 80 (74%). Normal ABG does not rule out PE if clinical
suspicion high.
D-Dimer: if ELISA test available, a low result has an extremely high negative predictive value.
Spiral CT, V/Q Scan, LE doppler ultrasound. Echo can be useful in massive PE.

Treatment
Unfractionated heparin:
Low molecular weight heparin (enoxaparin): preferred treatment for ease of use; dose at 1mg/kg q12h
SQ. Continue for ~5 days, until INR is therapeutic (2.0-3.0) on warfarin. Relative contraindication if CrCl <
30 ml/min or weight > 120 kg. Can follow anti-factor Xa levels if available.

Warfarin: start when patient is stable (which may be on admission).

Thrombolytics: consider in massive PE with hemodynamic compromise (call pulmonary consult). Stop
heparin and dose tPA at 100 mg IV over 2 hours. Can use up to 14 days after initial onset of PE. Obtain
consent, review exclusion criteria, monitor frequently for neuro changes, and know full tPA protocol if you
are going to proceed to thrombolysis.

IVC filter: in patients who develop PE while anticoagulated, or in patients in whom anticoagulation is
contraindicated (recent surgery, CVA). Not effective as long-term treatment.


Start hypercoagulability workup when appropriate (i.e., when common risk factors are absent).