DVT and pulmonary embolism

Virchow's triad

• Stasis: immobility (bedbound after trauma, after abdominal or orthopaedic surgery), long flights, paralysis, heart failure, pregnancy. Immobilisation is the commonest single cause.
• Endothelial injury: surgery, trauma, previous DVT, central lines.
• Hypercoagulability: cancer, pregnancy and the puerperium, oestrogens (combined pill, HRT), obesity, nephrotic syndrome, inflammatory bowel disease; inherited thrombophilia (factor V Leiden, the commonest; prothrombin G20210A; protein C, protein S and antithrombin deficiency) and acquired (antiphospholipid syndrome, HIT, myeloproliferative disease, PNH).
• Migratory superficial thrombophlebitis in different veins of arms and legs (Trousseau sign of malignancy) points to pancreatic carcinoma (and other mucin-secreting adenocarcinomas of lung and stomach). In a young male smoker think of Buerger disease.

Deep vein thrombosis

• Thrombi usually start in calf veins (valve pockets, soleal sinuses) and extend proximally; the popliteal is the commonest site found on scanning. Proximal thrombi in the femoral and iliac veins are the commonest source of pulmonary emboli; the embolus passes through the right heart and lodges in the pulmonary arteries.
• Features: unilateral swelling (calf difference over 3 cm), pain, tenderness, pitting oedema, dilated superficial veins; many are silent. Phlegmasia cerulea dolens: massive iliofemoral DVT with a blue, painful leg and risk of venous gangrene.
• Diagnosis: Wells score; if DVT is unlikely, D-dimer (sensitive but not specific: a negative result excludes, a positive one proves nothing); if likely or D-dimer positive, compression duplex ultrasound.
• May–Thurner syndrome: recurrent left iliofemoral DVT in a young woman because the right common iliac artery compresses the left common iliac vein against the fifth lumbar vertebra; anticoagulation alone often fails, and venous stenting may be needed.
• Treatment: DOAC (apixaban, rivaroxaban) or LMWH; 3 months for a provoked DVT; unprovoked or recurrent DVT, antiphospholipid syndrome and antithrombin deficiency often need long-term treatment. Duration depends mainly on whether the event was provoked; thrombophilia results rarely change it. Catheter-directed thrombolysis for selected iliofemoral DVT; IVC filter only when anticoagulation is impossible.
• Pregnancy: LMWH throughout (it does not cross the placenta). Warfarin is teratogenic (embryopathy with nasal hypoplasia and stippled epiphyses, worst at 6–12 weeks) and causes fetal bleeding near term; it is safe in breastfeeding after delivery.
• Warfarin skin necrosis: in the first days of warfarin, protein C (short half-life) falls before factors II, IX and X, causing a transient prothrombotic state; painful purple patches on fatty areas (thigh, breast) appear, especially in protein C deficiency. Prevent by overlapping with heparin until the INR is therapeutic.

Complications of DVT

• Pulmonary embolism: the most dangerous, early complication.
• Post-thrombotic syndrome: the commonest late complication (in up to half of proximal DVTs). The thrombus organises and recanalises, and the process destroys the vein valves; reflux plus residual obstruction cause venous hypertension: aching, swelling, pigmentation, eczema and gaiter ulcers years later.
• Recurrence.

Pulmonary embolism

• Symptoms: sudden breathlessness, pleuritic pain, haemoptysis, tachycardia, collapse with massive PE. ECG: sinus tachycardia (commonest), S1Q3T3, right heart strain, RBBB.
• Physiology: the blocked lung region is ventilated but not perfused, so it becomes alveolar dead space (V/Q infinite); in that region alveolar PO₂ rises towards inspired values and alveolar PCO₂ falls. Blood is diverted to the rest of the lung, causing V/Q mismatch, so arterial PO₂ falls; hyperventilation keeps arterial PCO₂ normal or low. Pleuritic pain and haemoptysis mean infarction, which is uncommon because the lung has a dual (bronchial) supply.
• A loud pulmonary component of the second heart sound (P2) is the most specific sign of pulmonary hypertension; a right ventricular heave and raised JVP support it.
• CT pulmonary angiography is the investigation of choice; V/Q scan in pregnancy, contrast allergy or renal impairment; bedside echo if unstable. Massive PE with hypotension: thrombolysis (alteplase) or embolectomy. Recurrent small emboli lead to chronic thromboembolic pulmonary hypertension.

Superficial thrombophlebitis

• A tender, red, cord-like superficial vein, often in varicose veins or at a cannula site. Irritant IV drugs (potassium chloride, amiodarone, erythromycin, diazepam, some chemotherapy) inflame veins; rotate cannulas and dilute infusions.
• Within 3 cm of the saphenofemoral junction it may extend into the deep veins: scan and anticoagulate.

Varicose veins

• Dilated, tortuous superficial veins from valve incompetence, mostly the great saphenous vein (saphenofemoral junction) and the small saphenous (saphenopopliteal junction).
• Anatomy for surgery: the saphenofemoral junction lies about 3–4 cm below and lateral to the pubic tubercle, where the great saphenous vein passes through the saphenous opening into the femoral vein, which lies medial to the femoral artery (the arterial pulse is at the mid-inguinal point). The great saphenous vein runs in front of the medial malleolus with the saphenous nerve below the knee; the small saphenous vein runs behind the lateral malleolus with the sural nerve.
• Primary varicose veins: familial wall and valve weakness, standing occupations, female sex, pregnancy, obesity, age. Secondary: post-thrombotic deep vein damage, pelvic masses, pregnancy, arteriovenous fistula, Klippel–Trénaunay.
• Symptoms: aching, heaviness, itching and swelling by evening; bleeding, thrombophlebitis, skin changes, ulcers.
• Examination: saphena varix (soft groin lump with a cough thrill that empties lying down), Trendelenburg and tourniquet tests (historical), Perthes test (deep vein patency). Duplex ultrasound is the investigation of choice (reflux over 0.5 seconds).
• CEAP clinical classes: C1 telangiectasia, C2 varicose veins, C3 oedema, C4 skin changes (pigmentation, eczema, lipodermatosclerosis, atrophie blanche), C5 healed ulcer, C6 active ulcer.
• Treatment: compression, elevation, weight loss; endovenous thermal ablation (laser or radiofrequency) is first line for truncal reflux; foam sclerotherapy, glue; open high ligation and stripping to the knee (stripping below the knee risks the saphenous nerve; small saphenous surgery risks the sural nerve).

Chronic venous insufficiency and venous ulcers

• Failed calf muscle pump and incompetent deep, superficial or perforator valves cause ambulatory venous hypertension. Capillaries leak fibrinogen and red cells: fibrin cuffs, trapped white cells, haemosiderin pigmentation, varicose eczema, lipodermatosclerosis (inverted champagne-bottle leg), atrophie blanche, then ulceration.
• Venous ulcers are the commonest leg ulcers (about 70%): in the gaiter area above the medial malleolus, shallow with sloping edges, granulating base, moderate pain eased by elevation, warm foot, pulses present.
• Check the ABPI before compression: above 0.8 allows full compression; arterial disease often coexists.
• Treatment: multilayer graduated compression (mainstay), elevation, exercise, wound care, antibiotics only for cellulitis, early ablation of superficial reflux (faster healing, fewer recurrences), grafting for large ulcers, lifelong stockings.
• A non-healing ulcer with a rolled or heaped edge needs biopsy for Marjolin ulcer (squamous carcinoma).

Lymphoedema

• Primary (Milroy congenital; praecox at puberty; tarda) or secondary (filariasis, the commonest cause worldwide; node dissection, radiotherapy, tumour, recurrent infection). Non-pitting later; Stemmer sign (cannot pinch the skin at the base of the second toe). Complex decongestive therapy, compression, skin care; treat cellulitis promptly. Chronic lymphoedema after mastectomy carries a small risk of lymphangiosarcoma.

Remember Valves fail, pressure rises, capillaries leak, skin breaks: every venous ulcer follows that chain.

Exam trap Check the ABPI before compression; arterial disease must be excluded first.

Exam trap Warfarin is avoided in pregnancy; use LMWH. Early warfarin can cause skin necrosis by lowering protein C first.

How FCPS asks about this

• Recurrent migratory superficial thrombophlebitis: look for pancreatic carcinoma (Trousseau).
• Saphenofemoral junction: 3–4 cm below and lateral to the pubic tubercle; femoral vein medial to the artery.
• Recurrent left iliofemoral DVT in a young woman: May–Thurner, right common iliac artery compressing the left vein.
• Post-thrombotic ulcer: recanalised thrombus destroys valves, causing venous hypertension.
• PE physiology: dead space with high alveolar PO₂ in the blocked area, low arterial PO₂, normal or low PCO₂; loud P2 for pulmonary hypertension.
• Source and sequence: femoral and iliac veins seed most emboli; D-dimer excludes, duplex confirms.
• Ulcers: venous at the medial malleolus, arterial punched out and distal, neuropathic painless at pressure points.