‘A PC DVT’

By Laura Fosang

Claire Blandford

Tania Rahman

Daniel Freedman

MR P.C. 41yr male 30th may

PC: pain & swelling of R leg

HPC: Pain & swelling for 4 days

getting worse and now unable to walk

Site: R calf

Onset: Gradual

Character: sharp & shooting

Radiation: upper thigh

Associated: ?S.O.B

Relieved by: rest

Exacebated by: movement

PMH: 1999 DVT R leg

2001?DVT R leg

FH: Nil

DH: no medication

NKDA

Alcohol: 6-12 cans of skulls super/day for 20 yrs

7/7 of dependence criteria

Smokes 25 ciagrettes/day for 20 yrs = 25pack yr

Smokes cannabis /crack cocaine when available

SH: Has been homeless for 10 days after split with partner

unemployed for 20 yrs

long history of trouble with police and prison.

SE: Resp: S.O.B.O.E cough

GI: Distended abdomen, diarrhoea due to poor diet

CNS: Dizziness after alcohol

On examination:

Appearance: dishevelled, agitated, poor dentition

CVS: Heart rate: 110bpm BP: 140/86

Heart sounds: I+II+0

RESP: RR 15

End Expiratory wheeze throughout both lungs

ABDO: Distended with 2cm liver edge no tenderness

LEG: Red, Swollen (> 6cm than L leg) and painful R calf, pain in R popliteal fossa.

Differential Diagnosis:

•DVT

•Ruptured Bakers Cyst

•Cellulitis

Plan: Admit & Investigate

Investigations

Blood results: Hb 17.2 WBC 10 Platelet

283 MCV96 RBC

5.52 Hct0.5 MCH31.2 MCHC34.5

Coagulation: INR 1.0 APTT

1.29 TT56

Investigations 2

U+Es Na132

K 4.6 Cl 100 HCO3 23 urea 3.1 creat.

89

glucose 5.9

LFTs BR25 ALT64 ALP86 Alb38 GGT276

D-dimers0.44

Deep Vein Thrombosis (DVT)

Definition Epidemiology Risk factors Pathogenesis Clinical features Assessment Management Prophylaxis

Definition

Thrombus: solid mass formed in circulation from constituents of blood

Deep Vein Thrombosis: formation of a thrombus within a deep vein of the leg particularly in the calf

partial or complete occlusion of lumen

Epidemiology

Incidence: 5 per 10 000 general pop ~ 30% surgical patients 1/4 patients after MI 1/2 patients after ischaemic stroke 10-20% extend proximally further 1-5% develop PE

Risk factors

Patient factors: age obesity

immobilitypregnancy previous DVT/PE FH recent trauma smoking

Surgery: especially to pelvis, hip and lower limbs

Drugs: high doses of oestrogens

Risk factors 2

Medical:malignancycardiac failure recent MI CVA

infection nephrotic

syndrome IBD varicose veins SLE

Haematological: polycythaemia thrombocytosis thrombophilia

Pathogenesis

Virchow’s triad: development of a thrombus depends on 1) altered blood constituents 2) altered blood flow 3) endothelial damage

DVT - hypercoaguability and stasis

Pathogenesis 2

1) Altered blood constituents: hypercoagulability

blood clots more readily activated coagulation proteins

risk of platelet aggregation in antithrombotic proteins

Pathogenesis 3

2) Altered blood flow: stasis platelet contact with endothelium flow fresh blood containing clotting

factor inhibitors

no clearance of blood containing activated coagulation factors

Clinical features

asymptomatic present with features of PE calf/thigh pain + tenderness leg swelling, redness + warmth engorged superficial veins

Clinical features 2

ankle oedema Homan’s sign: resistance to forced

foot dorsiflexion often with pain in calf cyanotic discolouration of limb with

severe oedema (complete occlusion) mild fever

Initial Assessment1. Clinical Assessment of Patient

what is the probability of them having a DVT ?

2. Use of D-Dimer • fibrin breakdown products

• raised if > 0.4mg/L

Has a sensitivity of 93% but specificity of just 25%

Useful to exclude DVT if the result is negative (NPV = 99.5%)(NPV = 99.5%)

D-dimer results need to be interpreted with caution in:

a) concurrent anticoagulant use c) age >70

b) co-morbid cancer d) post-surgery

Wells Clinical Prediction Guide (1997)

Clinical Parameter: Score Active Cancer (treatment ongoing/ or within 1

6mths/ or palliative) Paralysis or recent plaster immobilisation 1 Recently bed-ridden for >3days, or 1

major surgery <4wks Localised tenderness along distribution of deep veins 1 Entire leg swelling 1 Calf swelling >3cm compared to assymptomatic leg 1 Pitting oedema (> in sx leg) 1 Collateral superficial veins (non-varicose) 1 Alternative diagnosis (as likely or > that of DVT) -2

Interpretation

Total the score:-

From Anand SS et al. JAMA. 1998; 279 [14]; 1094

HIGH probability

MODERATE probability

LOW probability

75% DVT freq.

17% DVT freq.

3% DVT freq.

Score >/ 3

Score 1or 2

Score \< 0

Management Flow ChartApply Clinical Model

Low PTP High PTPModerate PTP

Rules out DVT

US normal US abnormal

Venography

Normal Abnormal

Rules out DVT

DVT Anticoag. Therapy

Repeat US in 7days

US normal US abnormal

DVT Anticoag. Therapy

Normal Abnormal

Rules out DVT

DVT Anticoag. Therapy

US abnormal US normal

DVT Anticoag. Therapy

Venography

Normal Abnormal

Rules out DVT

DVT Anticoag. Therapy

Investigation Options Duplex Ultrasound

Non-invasive technique. Combines US with Doppler flow studies. Sensitivity and Specificity rates 98%. Criteria US: failure to compress the vessel lumen(due to occluding thrombus) Doppler: absence of normal doppler signals.

-ves: non-occulding thrombi hard to detect, diff. to differentiate // old and new clots.

Contrast VenographyContrast medium injected distal to suspected DVT. X-ray imaging demonstrates site & size of thrombus. Invasive technique, painful, risk of contrast reaction.

MRIUseful in IVC or iliac vein thrombosis. In 2nd/ 3rd trimester is better than doppler as the gravid uterus alters flow patterns.

Treatment Aims; prevent PE, morbidity, minimise risk of

developing post-phelebitic syndrome. AnticoagulationAim for INR >2.

Give: Start Warfarin 5mg daily +

S/cut LMWH Dalteparin (dose adjusted for body wght)

Continue dalteparin for 5d or until INR is controlled.Heparin has no intrinsic thrombolytic activity, however, will prevent clot extension, incidence of PE, chance of recurrent thrombosis.

Need to overlap Heparin with Warfarin as warfarin takes 3-5 days to have full effect

Treatment 2

Duration of anti-coagulation therapy• Above Knee DVT at least 6 months

• Trifurcation of Popliteal 3 months

• Below Trifurcation not required. But r/v in 7 days to check no progression.

• If recurrent DVT may continue therapy indefinately

Caution in patients with risk of bleeding:• liver disease • peptic ulcer

• alcohol abuse* • hypertension

• heart failure • drugs enhancing warfarin’s effect

e.g: TCA’s, metronidazole, allopurinol, cimetidine

Outpatient .vs. Inpatient Many patients with a proximal DVT are safe to

be managed as out-pts.

Exclusion criteria for out-pt management:-1) Suspected/ Proven PE

2) Complicated DVT (e.g- bilateral)

3) Patients with cancer

4) Conditions which risk of bleeding (recent surgery, PUD, Malignant HT, recent CVA, co-existing coagulopathy)

5) Conditions with risk recurrent thrombosis (extensive proximal DVT, recurrent DVT, Pregnancy, inherited/acq hypercoag state)

6) Poor compliance

7) Inadequate support

Other Treatment Options Thrombolytic Therapy

Streptokinase or tPA. Destroys the fibrin mesh of clot. Reserved for: I) pts with new LARGE clots, those with risk long term Cx due to a clotting disorder or other predisposing condition.

Filter Insertionsmall metal filter inserted into IVC to prevent PE’s. Consider use in patients who can’t tolerate anti-coagulation or hx of PE’s despite adequate anti-coagulation

Surgery Thrombectomy or Embolectomy

Removal of clot via surgery or catheter. Consider in pt’s who can’t be anti-coagulated or who have massive ileofemoral vein thrombosis where the limb is at risk.

Prophylaxis Mobilisation Hydration Blood flow stimulation -

• TED stockings

• Ripple matresses

Prophylactic Anticoagulation -• Heparin 5000u s/c, 12hrly.

• Warfarin

• Aspirin

Fate of ThrombiThrombosed Vein

Resolution

Organisation & incorporation into wall

Organisation & Recanalisation

Propagation towards heart

Embolisation

Complications of DVT

Acute Pulmonary Embolism (PE) in 33-46% (may be asymptomatic)

Haemorrhagic complications of anticoagulant Rx Systemic paradoxical embolisation

– (e.g. CVA if patient has a patent foramen ovale)

Chronic venous insufficiency Postphlebitic syndrome Complete venous occlusion

– leading to cyanotic limb discoloration, severe oedema, pain and even venous gangrene

Pulmonary Embolus - PE

Commonest Cause: leg or pelvic thrombus embolised through the venous system and right heart before lodging in the lungs.

Rarer causes include: – RV thrombus post MI; – septic emboli (from right heart endocarditis); – fat, air or amniotic fluid embolism; – neoplastic cells;– parasites.

PE - Clinical Features

Depend on number, size and distribution of emboli

Symptoms include:– acute shortness of breath– pleuritic chest pain– haemoptysis– dizziness– syncope

Signs include:– pyrexia– cyanosis– tachypnoea– hypotension JVP– pleural rub– pleural effusion

– loud P2

– RV heave– cyanosis– AF

PE - Investigations

Chest X-Ray (CXR)– may be normal– may show signs of:

• oligaemia• dilated pulmonary art.• Linear atelectasis• small pleural effusion• wedge-shaped

opacities• (rarely) cavitations

Electrocardiogram (ECG)– may be normal– may show:

• tachycardia• RBBB• RV strain• (rarely) “classical”

SIQIIITIII pattern

PE - Investigations 2

D-Dimer if thrombus present• if undetectable then

excludes diagnosis of PE

Arterial Blood Gases (ABG)– may show:

PaO2

PaCO2

Other Imaging– CT Pulmonary

Angiography• can show clots to the

5th order of pulmonary arteries

– V/Q Scan– Spiral CT

PE - Treatment

Anticoagulation– Low Molecular Weight (LMW) Heparin until INR

>2.0– Warfarin treatment for a minimum of 3 months

Vena Caval Filter– when anticoagulation either dangerous or

ineffective in preventing emboli