VTE: DVT and PE

Dr Kelda Sheridan Dr Sophie Bennett

Aims and Objectives

Explore underlying mechanisms of VTE Recognise and assess common presentations of DVT/PE Discuss principles of diagnosis and management Explore complications and outcome Apply in a relevant clinical context

Introduction and Background

Venous thromboembolism (VTE) clot formation in veins Spectrum: DVT PE

Multifactorial prothrombotic state

Virchows Triad
- Changes in vessel wall (trauma) - Changes in blood flow (haemostasis) - Changes in blood constituents (hypercoagulability)

WARFARIN

Clot Formation
Tissue factor pathway

HEPARIN
Contact Pathway

International normalised ratio (INR)

Activated partial thromboplastin time (APTT)

Final common pathway

Prothrombin time (PT)

Taken and adapted from www.biosbcc.net, 2013.

Prothrombotic Risk Factors

Taken from Fenner & Oliver, 2012(backgroundJ)

Continued
Major Risk Factors Recent surgery Immobility Malignancy Pregnancy Fracture/Varicose Veins History of PE/DVT Obesity Minor Risk Factors CVP catheter OCP/HRT Obesity Long distance travel Thrombophilia
- Deficiencies in antithrombin, protein C, protein S, factor V Leiden - Excess of factors II, VIII, IX, XI, fibrinogen(basicsci)

Important Because
Fatal if untreated - cardiac arrest (PE) or post-thrombotic syndrome (DVT) 25,000 deaths annually A leading cause of morbidity and mortality in hospital patients Often difficult to diagnose Progression: 90% of PEs due to limb DVTs Risk of recurrence

Presenting Features
SYMPTOMS
Asymptomatic Pain Features of PE Iliofemoral region:
Fewer features Severe pain Occasional swelling of thigh Ankle oedema

SIGNS
Tenderness Erythema Swollen calf Engorged superficial veins Homans sign: Phlegmasia ceulea dolens (rare!):
Cyanotic discolouration Severe oedema Venous gangrene

Homans sign
Pain in calf on dorsiflexion of foot Often present with lower limb DVT Not diagnostic of DVT Homan sign will be positive with all calf lesion

Anatomy
Majority of DVT occur in the calf Distal DVTs are often asymptomatic & thought to resolve spontaneously Proximal DVTs are often symptomatic

DVT facts
50% of untreated symptomatic patients with DVT will develop PE within 3 months Without thromboprophylaxis 50% of patients following prostatectomy develop DVT 50% of patients following cerebral vascular event develop DVT without thromboprophylaxis 10% patients with MI have a clinically detectable DVT

Diagnosis
Clinical diagnosis is unreliable Conditions mimicking DVT:
Ruptured Bakers cyst Haematoma Venous insufficiency Cellulitis Compartment syndrome

Modified Wells score

Modified Wells score

Low probability score (<2) D-dimer Clinical symptoms & D-dimer have a combined sensitivity of 80% High Wells score (>2) Ultrasound + D-dimer Ultrasound >95% sensitivity & specificity for proximal DVT Ultrasound sensitivity 11100% and specificity 60-100% for distal symptomatic DVT

D-dimer

Management of DVT
Main aim to prevent PE

Treatment dose LMWH

eGRF>30? Yes No
Enoxaparin 1.5mg/kg

:
Tinzaparin 175 units/kg

Warfarin: 1st DVT: 3/6 months for below/above knee 2nd/recurrent DVT: lifelong

Presenting Features
SYMPTOMS
SOB Pleuritic chest pain +/- Haemoptysis Cough Syncopy Dizziness Leg pain

SIGNS
Tachycardia Hypotension Cyanosis Increased JVP Pleural rub/effusion RV heave Use of accessory muscles Signs of DVT

Approach
History
A ?patent, stridor/wheeze
- concerned crash call

B - assess RR, pattern, symmetry

- Sit up, 15L 02 via non-rebreathe mask, ABG

C tachycardia, hypotensive, syncopy

- IV access, bloods, fluids, ?catheterise

D GCS, glucose, urine dip (?DKA) E Hx, examine, look at notes, other info

Get Senior Help early!!!

Investigations
Bloods (FBC, U+E, Troponin) ABG (T1RF:P0210.6kPa, /normal C02 ) ECG (Evidence of Right Ventricular Strain) CXR (effusion/normal)

Echocardiography
Two-level Wells Score

 Tachycardia RBBB V1 and V6

Right Axis Deviation I and III T-wave inversion V1-V4

S1Q3T3 (10% of PEs poor outcome)

Taken from www.sccm.org

Suspected PE Two-level PE Wells Score

Clinical feature Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) An alternative diagnosis is less likely than PE Heart rate > 100 beats per minute Immobilisation for more than 3 days or surgery in the previous 4 weeks Previous DVT/PE Haemoptysis Malignancy (on treatment, treated in the last 6 months, or palliative) Clinical probability simplified scores PE likely PE unlikely
Taken from NICE Clinical Guideline 144, 2012

Points 3 3 1.5 1.5 1.5 1 1

Patient score

More than 4 points 4 points or less

Diagnosis
PE Likely (4)
Positive

PE Unlikely (4)

Immediate CTPA* or VQ Scan (if CTPA

CI (renal failure - eGFR 30ml/min/1.73m2) or allergy) *If not available immediately start treatment (parenteral anticoagulant) then CTPA

D-Dimer test
Negative

No further action
(unless DVT suspected)

Taken from acutemed.co.uk, 2013

Taken from Sheare,2011

Management
Assess haemodynamic stability
Stable
Therapeutic anticoagulant LMWH, fondaparinux or unfractionated heparin (UFH) (start immediately) LMWH 1.5mg/kg (175units/kg) Start warfarin (5-10mg od) Continue LMWH for 5 days until INR therapeutic (2.0-3.0) Alteplase 10mg IV over 12mins (then 90mg IV infusion over 2hrs) or 50mg bolus

Unstable
Consider thrombolysis in massive PE/impending cardiac arrest Recombinant human tissue plasminogen activator fibrinolysis

Treatment
LMWH
Enoxaparin (clexane), tinzaparin (LTHT) or daltaparin Lower risk of heparin induced thrombocytopenia (HIT) Fondaparinux (synthetic pentsaccharide) and LMWH promote factor Xa inhibition

Unfractionated heparin (UFH)

- Quicker onset, preferred in renal failure and bleeding as can be reversed quickly with protamine - IV Bolus followed by infusion ( short half-life)

Medical or surgical embolectomy

- When thrombolysis/anticoagulation CI/not effective

Inferior vena cava filter

- Following embolectomy - Recurrent PEs - When anticoag CI

Heparin Infusion Chart

Warfarin
Vitamin K antagonist Initial dosage based upon baseline PT Usually 5-10mg INR measured every 24-48 hours and dosage adjusted Tx for 3-6 months for isolated PE and lifelong if recurrent/significant risk factors Other oral anticoagulants dabigatran etexilate (direct thrombin inhibitor) and rivaroxaban (activated Factor X inhibitor)

On Discharge..
Yellow book Warfarin Clinic Appointment

Consider thrombophilia testing (if no cause identified)

?underlying malignancy CT thorax/abdo/pelvis

Cases
FY1 on call bleeped by nurse Hi Dr...Mr Red Leg has come from A+E with a diagnosis of cellulitis and is complaining of painful leg A patent, talking in full sentences B RR 16, SATS 96%, Chest clear C - BP 120/90, HR 100 regular, catheterised D- GCS 15, glucose 5 E/Hx- On IV flucloxacillin for R leg cellulitis, swollen, tender +++ R calf, erythematous Medical notes unclear if Ix for DVT photocopied A+E notes with pages missing Modified Wells score - 4 D-dimer + USS R leg confirms DVT Treatment: tinzaparin 175mg/kg & start warfarin. Stop flucloxacillin.

Cases
FY1 in A+E informed by triage nurse that Mr Unhelpful, 62yrs, is c/o SOB and feeling rubbish A patent, speaking intermittently B RR 32, SATS 92% on 2L 02 via nc , reduced air entry bibasally, ABG p02 8 (otherwise N) 15L non-rebreathe mask C- BP 110/75, HR 115 regular, peripheries cool but cap refill normal D- GCS 15, glucose 6 E- Left calf tender, swollen and red, when asked he recalls its been sore for a while analgesia Hx long distance lorry driver, heavy smoker, HTN and IBD Ix Bloods, CXR, ECG NAD SPEAK TO SENIORS Two-level PE Wells Score (4.5 signs of DVT and tachycardic) CTPA immediately and therapeutic tinzaparin (1.5mg/kg) commenced Warfarin started when diagnosis of PE confirmed

Cases
FY1 in respiratory medicine on your normal ward round when you notice Mrs Badlungs (76yrs) slumped over in bed. A patent but making wheezing noises, venturi mask on her head sit pt up and re-site mask (noises disappear) B RR 40, SATS 82% on 28% venturi, crackles in R base, ABG pH 7.4, p027, C02 10, HC03- 32 (chronic T2RF) 15L initially then highest venturi C- BP 90/60, HR 120 regular, catheterised (30ml in last 2hrs), D- GCS 14 (E3, V5 M6), glucose 4.5 E- varicose veins, on co-amoxiclav and clarithromycin for CURB 4 CAP Hx known COPD, IHD, stage 3 CKD, you look on drug chart no prophylactic anticoagulant prescribed Ix Bloods, CXR (R basal consolidation), ECG RBBB and T-wave inversion (V1-3) Two-level PE Wells Score (3 tachycardic, 3 days of inactivity) D-dimer + D/W seniors re CTPA and starting heparin

Cases
Surgical FY1 on call bleeped by nurse Hi Dr...Mrs Clot (42yrs) in bed 1 has just desaturated to 85%, can you come and r/v? A patent but struggling to talk sit up,15L 02 non-rebreathe mask B RR 40, SATS 85%, Chest clear, ABG p02 8 C - BP 85/50, HR 140 regular, catheterised (15ml in last 4hrs) fluid challenge/fluid resus D- GCS 15, glucose 5 E/Hx- day 3 post-op for R hemicolectomy for malignancy, on OCP GET HELP QUICKLY PATIENT HAEMODYNAMICALLY UNSTABLE Ix Bloods, CXR, ECG S1Q3T3 Two-level PE Wells Score (7 tachycardic, malignancy, surgery and other diagnoses unlikely) D/W seniors re thrombolysis

VTE Prophylaxis
Most important patient safety measure All medical and surgical patients (unless CI) Trust specific LTHT
-

Tinzaparin 3500-4500 units od (medium-high risk) Enoxaparin 20-40mg SC od (if renal impairment or 75yrs) If 40kg or 100kg tinzaparin 50units/kg SC od

TEDs/Flowtrons

Thank you!!

References
National Institute for Health and Clinical Excellence. Clinical guideline 144. Venous thromboembolic diseases: the management of venous thromboembolic diseases and the role of thrombophilia testing. London: National Institute for Health and Clinical Excellence; 2012. British Thoracic Society Standards of Care Committee Pulmonary Embolism Guideline Development Group. British Thoracic Society guidelines for the management of suspected acute pulmonary embolism. Thorax 2003; 58:470484. Goldharber S. Advanced treatment strategies for acute pulmonary embolism, including thrombolysis and embolectomy. J Throm Haemost 2009; 7(1): 3227. Pulmonary Embolism. http://bestpractice.bmj.com/best-practice/monograph/116.html Oxford Handbook for The Foundation Programme. 3rd Edition. 2011. Fenner L, Oliver C. Prevention of deep vein thrombosis and pulmonary embolus. Anaesthesia and Intensive Care. 2012; 13(12):609-12. Shen et al. Copy number variations of the F8 gene are associated with venous thromboembolism. Blood Cells, Molecules and Diseases 50. 2013:259262. Patel et al. Burden of Illness in venous ThromboEmbolism in Critical care: a multicenter observational study. Journal of Critical Care. 2005; 20:341 347 Ho, Wai Khoon, Deep vein thrombosis:risks and diagnosis, Focus Clots,Australian Family Physician, Vol 39, No 7, July 2010 Kumar & Clark, Clinical Medicine, 6th Edition, pp870-871