DVT + PE Flashcards
DEEP VEIN THROMBOSIS
• Thrombus which forms in deep veins typically of the Lower Limbs; Occurs commonly after
periods of immobilisation
• Asymptomatic, or can present as Calf Pain (Often with Swelling, Redness and Engorged
Superficial Veins); Affected side warmer and may have Ankle Oedema; Homan’s Sign (Pain in
calf on Dorsiflexion) is non-specific
• Complete occlusion, particularly of large veins, may lead to cyanotic discolouration and
Severe Oedema, which may progress to Venous Gangrene
Destruction of Deep Vein Valves leads to Post-Thrombotic Limb – Pain, swelling which
worsens on standing ± Venous Eczema; TED stockings for life
Pulmonary Embolism
can occur as sequelae, but more frequent with Iliofemoral thrombosis
and is rare with thrombosis below level of knee; 20-30% of patients have spread that occurs
proximally without clinical evidence, so Ultrasound monitoring is important
Management of Deep Vein Thrombosis
• Clinical Diagnosis unreliable; D-Dimers have sensitivity of 80%;
Confirmation of Iliofemoral Thrombosis by B Mode Venous
Compression, Ultrasound or Doppler Ultrasound with
Sensitivity/Specificity over 90%
• Below knee only detected reliably with Non-invasive Venography,
Ultrasound, Fibrinogen Scan; Invasive Venogram detects all thrombi
• Anticoagulation for Below-Knee Thrombi recommended for 6 weeks to prevent extension;
Bed rest until fully anti-coagulated; Mobilised with TED stockings
o Anticoagulation either using Warfarin (Bridged with LMWH) or DOACs depending on
local policy (E.g. Rivaroxaban)
• Permanent Anticoagulation for recurrent DVT; Thrombolysis occasionally for patients with
large Iliofemoral Thrombosis
Prevention of Deep Vein Thrombosis
• All patients assessed on admission (and 24 hours alter or if change occurs in clinical condition)
• Medical patients at risk if reduced mobility >3 days, or if mobility reduced + >1 risk factor
• Surgical patients at risk if prolonged surgery (>90 mins or 60 minus for Pelvis/LL), acute
inflammatory/intraabdominal condition, significantly reduced mobility or >1 risk factor
Risk Factors for Deep Vein Thrombosis
- Age >60yrs, Family/PMHx, Significant Comorbidities, Obesity (>30BMI),
- Pregnancy/Childbirth, COCP/Oestrogen, Malignancy
- Critical Care Admission, Known Thrombophilia, Dehydration
Post-Thrombotic Limb Syndrome
• =Post-Phlebitis Syndrome; Long term complications of Venous Thrombosis
• Pain, Heaviness, Itching, Tingling, Oedema and Swelling, Varicosities and Venous Insufficiency,
Discolouration and Haemosiderin Deposition, Ulceration
• Occurs due to damage to venous valves – Valvular incompetency compounded with
persistent venous obstruction leads to Venous and Capillary Hypertension
o Rupture of superficial veins, Subcutaneous haemorrhage, Increased inflammatory
response and Tissue Permeability
• Elevation, Compression, Exercise, Weight Management, Analgesia, Wound care for ulcers
o Vascular Surgery following failure of conservative management –
o Psychological treatment for anxiety and depression associated with chronicity
PULMONARY EMBOLISM
• Thrombus from Systemic Veins or Right Heart (<10% of cases) might dislodge and embolise
into Pulmonary Arterial System; 10% of Clinical Pulmonary Emboli are fatal
• Most come from Pelvic or Abdominal veins; Occasionally Femoral or Axillary; After Pulmonary
Embolism, Lung tissue is inflated but not perfused leading to an Intrapulmonary Dead Space
resulting in Impaired Gas Exchange; Non-perfused lung eventually does not produce
surfactant resulting in Alveolar collapse exacerbating Hypoxaemia
• Reduction of cross-sectional area of Pulmonary Artery leads to elevation of Pulmonary
Arterial Pressure and reduction in Cardiac Output; Non-perfused zone might infarct although
not common due to Bronchial Circulation and Airways providing oxygenation
Presentations of Pulmonary Embolism
• Pleuritic Chest Pain and Haemoptysis present only when Infarction has occurred
o Small/Medium PE – Impaction in Terminal Pulmonary Vessel; Pleuritic Chest Pain and
SOB; Haemoptysis in 30% often >3 days after event; Tachypnoea, Pleural Rub and
Coarse Crackles over area involved; Blood stained Pleural Effusion might develop
o Massive PE – Sudden collapse due to acute obstruction of RV outflow; Severe Central
Chest Pain (Cardiac Ischaemia) with Shock, Pallor and Sweatiness
▪ Syncope if CO is transiently but dramatically reduced
▪ Tachypnoea, Tachycardia, Hypotension (<90mmHg) and Peripheral Shutdown
▪ Raised JVP (Prominent ‘a’ wave), RV Heave, Gallop Rhythm and Widely Split
S2 (Pulmonary Hypertension)
o Multiple Recurrent PE – Increased SOB over weeks/months; Weakness, Exertional
Syncope, Angina; Pulmonary Hypertension due to multiple occlusions of Pulmonary
Vasculature; RV Overload and Heave with Loud P2
Small/Medium Pulmonary Embolism
• CXR might be normal – Linear Atelectasis or Blunting of
Costophrenic Angle is not uncommon; Wedge shaped
pulmonary infarct, Abrupt cut-off of Pulmonary Artery or
Translucency of underperfused distal zone might be seen
• ECG usually normal except with Sinus Tachycardia; Sometimes AF or Tachyarrhythmia; Might
have evidence of RV strain
• Infarction will cause Leucocytosis, ↑ESR and LDH; If D-Dimer
negative PE is ruled out
• V/Q Scanning – Pulmonary 99mTc Scintigraphy demonstrates
underperfused areas which, if unaccompanied by ventilation
defect (Inhalation of radioactive Xenon), suggestive of
Pulmonary Embolism; Matched defect might also occur in
Infarction or Emphysematous Bullae; Is reported as a probability
and needs clinical correlation
• Ultrasound Scanning for Pelvic/Iliofemoral Veins
• CTPA; MRA – Similar results, used if CTPA is contraindicated (e.g. Pregnancy)
Massive Pulmonary Embolism
• CXR shows Pulmonary Oligaemia (Hypovolaemia) sometimes with Dilatation of Pulmonary
Arteries in Hila; Often no changes
• ECG – RA Dilation (P Pulmonale) in II; RV Stain and Dilatation leads to RAD, RBBB and TWI in
Right Precordial (V1-V2); Rarely, the S1Q3T3 (S wave in I, Q and TWI in III)
• ABG – Arterial Hypoxaemia with low CO2 (T1RF)
• Echo – Vigorously contracting LV with dilated RV and Clot in RVOT
• CTPA and MRA are important radiological tools for diagnosis
Multiple Recurrent Pulmonary Embolism
CXR might be normal; Enlarged Pulmonary Arterioles; ECG might be normal or PHTN; Leg
Ultrasound might show Thrombi, V/Q might show defect and HRC shows small emboli
Diagnosis of Pulmonary Embolism
• Assessed by Wells Score; High probability
patients proceed to HRCT with contrast
(CTPA); If CTPA negative – D-dimers;
• V/Q Scanning if unable to tolerate contrast
(E.g. Pregnancy)
• Low/Intermediate Risk should have D-
dimers; Negative D-dimer rules out PE;
Positive requires CTPA investigation
• Patients haemodynamically unstable (Shock, SBP <90mmHg, drop of more than 40mmHg
require urgent CTPA or Echo for RV dysfunction
o Normal RV suggests alternative Diagnosis
Treatment of Pulmonary Embolism
• High Flow O2 (60-100%) unless Significant Chronic Lung Disease; Patients with Pulmonary
Infarcts require Bed rest and Analgesia
• Initial Anticoagulation with SC LMWH (or IV UFH) followed by Warfarin; Alternative regimens
with DOACs e.g. Rivaroxaban
• IV fluids or Inotropic agents sometimes required for Massive PE; Step up to ICU
• Fibrinolysis – Thrombolytics (E.g. Alteplase) has been shown to clear PE more rapidly and
confer survival benefit for massive PE; For unstable patients or if RV dysfunction is present
• Surgical Embolectomy rarely necessary, last resort in severe haemodynamic compromise
• Prevention – Physical methods added as recurrent emboli can still occur despite
anticoagulation (e.g. IVC filter above level of Renal Veins)
Thrombolysis and Thrombectomy For Massive PE
• Thrombolysis is typically first line – 10% risk of Major Haemorrhage, 1.7% Intracranial bleed
• Thrombectomy typically for patients if CI to Thrombolysis (Prev Haem Stroke, Major Surgery,
Trauma, GI Bleeding, CNS tumour, Bleeding Diathesis etc)
o NB: Exceptions exist – Can still consider thrombectomy as CI are relative if life-
threatening, high risk PE (Based on ESC guidelines)
• Measurement of RV Dysfunction might be helpful to guide escalation of treatment
