Venous Thromboembolism

[1]

Meet the patient

A 67-year-old man, day 5 after a total hip replacement, sits up to use the bedpan and is stopped by a sharp, stabbing pain in the right side of his chest every time he breathes in. He is tachycardic at 112, oxygen saturations 92 percent on room air, and his right calf is 4 cm bigger than the left, warm and tender along the deep veins.[1]

The two questions that will decide his next hour are the two that decide every VTE: is this an embolus from that calf? and is the right ventricle beginning to fail? Hold those two questions and the whole topic slots into place — the swollen calf is the source, the pleuritic pain is the embolus, and the hunt for right-ventricular strain is what separates a patient you anticoagulate from one you lyse.[1][3]

DVT and PE are one disease on one continuum

DVT and PE are not two diseases; they are one thrombus read along its length. A clot forms in the deep veins of the leg, most often at a valve cusp in the calf, and may stay put, propagate proximally, or break off and travel through the right heart into the pulmonary arterial tree. Where you catch it along that journey is what you call it — DVT in the leg, PE in the lung — but the biology, the prevention, and the anticoagulation are identical, which is why the 2019 ESC guideline treats them as a single entity.[1][3]

VTE is the third commonest cardiovascular disease after acute MI and stroke, with an annual incidence of 1 to 2 per 1000 adults, rising to 5 to 7 per 1000 past the age of 70 and 10 to 15 per 1000 past 80. The headline that earns marks: it is the commonest preventable cause of in-hospital death, roughly half of all events are hospital-associated, and up to 60 percent of those are preventable with thromboprophylaxis — the single biggest argument for the admission VTE risk assessment.[1]

[1] [11]

Virchow's triad — the three axes every risk factor sits on

Every VTE risk factor, and every treatment, maps onto one of three axes. Name them in order at every viva and the rest of the topic organises itself:[1][3]

[1]

Etymology for viva gold: Rudolf Virchow published the triad in 1856, not as a list of causes but as the conditions under which a thrombus forms — stasis, injury, and "changes in the constitution of the blood". A century and a half later it still frames every teaching round because no risk factor escapes it.[1]

The mnemonic the exam rewards — HITS for provoked VTE:[1]

[1]

Classification — the splits that drive the decision

VTE is sorted by anatomy, by severity, and by provocation — and each split drives a different decision: anatomy and severity drive the acute plan; provocation drives the duration. The splits every final-prof candidate must reproduce:[1][2]

[1]

The classification that sets the acute decision is PE severity (massive / intermediate / low), integrating haemodynamics with right-ventricular status on imaging and biomarkers. The classification that sets the duration of anticoagulation is provoked versus unprovoked versus recurrent versus cancer-associated — keep them separate in your head and you will not confuse the two questions examiners ask.[1][2]

Pathophysiology — a red clot at a valve cusp that breaks a thin-walled ventricle

A venous thrombus is a red clot, not a white one — fibrin and red cells dominate, platelets are minor players. That single fact explains why we anticoagulate (block fibrin) rather than antiplatelet, and why the arterial ACS toolkit is the wrong tool here. The clot grows in layered bands (lines of Zahn), anchored at a valve cusp and propagating in the direction of flow.[1]

The journey from calf to catastrophically failing right ventricle runs in four steps:[1][3]

• Form — stasis behind a calf valve cusp lets activated factors escape hepatic clearance; a fibrin-rich red clot anchors at the cusp.
• Propagate — the clot grows proximally, layer by layer, into the popliteal, femoral, then iliac veins.
• Embolise — the free-floating tail breaks off, transits the right heart, and lodges in the pulmonary arterial tree; a large embolus may straddle the bifurcation as a saddle embolus.
• Fail the RV — the right ventricle, which cannot generate a systolic pressure above about 50 mmHg, dilates and fails when acute obstruction raises pulmonary pressure past that ceiling.[1][3]

Why the right ventricle fails is the most examinable mechanism in the topic. A normal RV cannot generate a systolic pressure above about 50 mmHg. Acute obstruction of more than about half the pulmonary arterial bed pushes pulmonary pressure past that ceiling; RV afterload rises, stroke volume falls, and the thin-walled RV dilates. The interventricular septum bows into the LV, preload drops, cardiac output falls, and the patient arrests in an obstructive, not a pump, failure. The same pathophysiology produces the RV strain pattern on echo (dilatation, hypokinesis, septal flattening — the "D-sign", McConnell's sign) and the RV/LV ratio over 1.0 on CT.[1][3]

Clinical presentation — the DVT pentad and the PE syndrome

At least half of calf-vein DVTs are clinically silent, and many PEs announce themselves only as unexplained dyspnoea. The classical patterns are taught because they are specific, not because they are sensitive — the absence of the pattern does not exclude VTE, which is why probability scoring precedes imaging.[1]

The DVT pentad (asymmetric, unilateral, along the deep venous system):[1]

• Swelling — the most sensitive sign; an asymmetry over 3 cm in calf circumference (measured 10 cm below the tibial tuberosity) is a Wells item.
• Pain — deep, dull, calf pain that may worsen on dorsiflexion (Homan's sign — historical, non-specific; do not rely on it).
• Erythema and warmth — overlying the thrombus; cyanosis or duskiness in iliofemoral DVT.
• Tenderness — along the line of the deep veins; a palpable cord suggests superficial thrombophlebitis, a different condition.
• Prominent superficial collateral veins — a sign of chronic deep venous obstruction, not an acute clot.[1]

The PE syndrome — dyspnoea is the commonest symptom (70 to 80 percent in PIOPED), pleuritic chest pain reflects pulmonary infarction, and sinus tachycardia is the commonest sign:[1]

• Dyspnoea and tachypnoea — the commonest symptom; new, unexplained, out of proportion to the chest X-ray.
• Pleuritic chest pain — sharp, worse on inspiration; reflects pulmonary infarction or pleural irritation.
• Tachycardia — sinus tachycardia over 100/min; over 110/min and the SBP under 100 feed the sPESI.
• Cough and haemoptysis — classically a feature of pulmonary infarction; haemoptysis is a Wells item.
• Syncope or pre-syncope — the most distinctive symptom of massive PE; signals acute right-ventricular failure and low output.
• Hypotension and shock — the definition of massive PE; bedside shows cool peripheries, oliguria, raised JVP, clear lungs.[1]

Everyone forgets the atypical presentations, and that is where PE is missed. In the elderly, a fall, unexplained tachycardia, or "another admission with pneumonia" may be the only clue; in pregnancy, pleuritic pain and mild hypoxia are too easily written off as dyspnoea of pregnancy; in the post-operative patient, an unexplained tachycardia and hypoxia on day 3 to 5 is PE until excluded; and in anyone with prior VTE, new leg swelling or pleuritic pain is recurrence until proven otherwise.[1][3]

The killer mimics — exclude the dissection, the pneumonia, the cellulitis

Before you anticoagulate, exclude the mimics — because anticoagulation and thrombolysis are not benign, and several mimics are killed by them. The single most dangerous mimic of PE is acute aortic dissection, which anticoagulation can convert into a fatal rupture. Run both face-offs at every bedside.[1]

[1] [1]

The single differential to exclude before you anticoagulate is aortic dissection — tearing pain to the back, a pulse or blood-pressure differential between the arms, a new aortic regurgitation murmur, a widened mediastinum on chest X-ray. Anticoagulating a dissection mistaken for PE is the preventable death that ends careers; the bedside question takes ten seconds and must precede every first dose.[1]

Bedside probability — Wells, PERC, and PESI before any scan

The bedside score is a probability tool, not a diagnostic one — and D-dimer rules out, it never rules in. Score first, then decide whether D-dimer is even worth drawing. The scores below are reproduced verbatim; convert every threshold to "over" and "under" so they survive the viva.[1]

Wells score for DVT — the most widely validated clinical probability score:[1]

• Active cancer (treatment within 6 months or palliative) — 1
• Paralysis, paresis, or recent plaster immobilisation of the lower extremity — 1
• Bedridden for 3 days or more, or major surgery within 12 weeks — 1
• Localised tenderness along the distribution of the deep venous system — 1
• Entire leg swollen — 1
• Calf swelling 3 cm or more compared with the asymptomatic side (measured 10 cm below the tibial tuberosity) — 1
• Pitting oedema confined to the symptomatic leg — 1
• Collateral superficial veins (non-varicose) — 1
• Previously documented DVT — 1
• Alternative diagnosis at least as likely as DVT — minus 2 (subtracts points)[1]

Interpretation: a Wells DVT of 3 or more is high probability (about 75 percent DVT prevalence), 1 to 2 is moderate, and 0 or less is low (about 5 percent). High probability goes straight to Doppler ultrasound; moderate and low go to D-dimer first, imaging only if D-dimer is positive — and a low Wells plus a D-dimer below the age-adjusted cutoff excludes DVT.[1]

Wells score for PE — the parallel score for the lung:[1]

• Clinical signs and symptoms of DVT (leg swelling, pain with palpation of the deep veins) — 3
• PE is the most likely diagnosis (or equally likely) — 3
• Heart rate over 100/min — 1.5
• Immobilisation (bed rest over 3 days) or surgery in the previous 4 weeks — 1.5
• Previous, objectively diagnosed DVT or PE — 1.5
• Haemoptysis — 1
• Active cancer (treatment within 6 months or palliative) — 1[1]

Interpretation: a Wells PE over 6 is high probability (about 60 percent PE prevalence), 2 to 6 is moderate, and under 2 is low. Many emergency departments use the dichotomised version — "PE likely" (over 4) versus "PE unlikely" (4 or less), which simply combines moderate and high for the imaging decision.[1]

The PERC rule lets you skip even the D-dimer in a low-probability patient. A patient is PERC-negative only when all eight are absent:[1]

• Age under 50
• Pulse under 100/min
• Oxygen saturation at least 95 percent on room air
• No unilateral leg swelling
• No haemoptysis
• No surgery or trauma within 4 weeks
• No prior DVT or PE
• No oestrogen use[1]

PERC-negative AND low clinical probability excludes PE without a D-dimer — saving a test and a wait in roughly a fifth of patients who present with possible PE. The classic trap is reaching for D-dimer in everyone; PERC exists precisely to spare the low-risk patient the false-positive cascade that ends in an unnecessary CTPA.[1]

PESI and the simplified sPESI stratify diagnosed PE for prognosis and disposition — sPESI scores one point each for age over 80, active cancer, chronic cardiopulmonary disease, heart rate over 110, SBP under 100, and oxygen saturation under 90 percent. An sPESI of 0 marks a 30-day mortality of about 1 percent, the patient who may be managed as an outpatient.[1][2]

Investigations — D-dimer rules out, imaging rules in

The test ladder depends on the anatomical target and the pre-test probability. Score first, then D-dimer, then image — in that order — and you will neither over-investigate nor miss.[1][2]

• D-dimer — highly sensitive (about 98 percent) but poorly specific; a normal D-dimer in a low- or moderate-probability patient rules out VTE (negative likelihood ratio under 0.05). A raised D-dimer is not diagnostic — it is elevated in cancer, infection, pregnancy, the post-operative state, and with age. The age-adjusted cutoff (age times 10 ng/mL for the over-50s) improves specificity in the elderly without losing sensitivity.
• Compression Doppler ultrasound — the imaging standard for DVT; non-compressibility of the vein under probe pressure is the diagnostic criterion. Sensitivity for proximal DVT is over 95 percent; distal DVT is harder to image but lower-risk, and can be serially rescanned at one week if isolated.
• CT pulmonary angiography (CTPA) — the gold standard for PE; identifies a filling defect down to the subsegmental level, quantifies RV strain (RV/LV ratio), and gives an alternative diagnosis (pneumonia, effusion, dissection). Risks are iodinated contrast (allergy, AKI) and radiation.
• V/Q scintigraphy — the functional alternative, preferred in pregnancy (lower foetal radiation in some protocols) and in contrast allergy or renal failure; a normal V/Q excludes PE, a high-probability scan diagnoses it, and SPECT V/Q is preferred in pregnancy.
• Bedside echocardiography — immediately actionable in suspected massive PE; RV dilatation, hypokinesis, septal flattening, McConnell's sign. A normal echo in experienced hands essentially excludes massive PE.[1][3]

[1]

Adjunct tests serve risk-stratification and the differential: troponin and BNP/NT-proBNIN (RV micro-infarction and stretch — prognostic in submassive and massive PE), ABG (hypoxaemia with hypocapnia from hyperventilation; a normal A-a gradient is unusual and questions the diagnosis), and ECG (excludes ACS; may show sinus tachycardia, S1Q3T3 in about 10 to 15 percent of massive PE, right-bundle-branch block, T inversion in V1 to V3). Thrombophilia screening is reserved for selected patients — young (under 50) unprovoked VTE, recurrent VTE, unusual sites (cerebral venous sinus, mesenteric), family history — and is best drawn at least 4 weeks off anticoagulation, because acute-phase changes confound factor VIII, antithrombin, and protein S.[1]

Management — anticoagulation first, a DOAC by default

The definitive treatment of VTE is prompt anticoagulation, risk-stratified duration, and prevention of complications. The escalation ladder climbs cleanly with severity: anticoagulation alone for low-risk PE, anticoagulation plus monitoring for intermediate-low, rescue catheter-directed therapy or an IVC filter for intermediate-high, and systemic thrombolysis or surgical embolectomy for massive PE.[1][2]

The 2019 ESC and 2018 ASH guidelines converge on a DOAC first-line for the majority of patients without cancer or pregnancy. The DOAC dose ladder is a named cluster rule — learn the loading doses, because the step-down date is fixed:[1][2]

[1] [4] [6] [7] [8]

The classic trap — DOACs in renal failure. Dabigatran is avoided when CrCl is under 30 mL/min; rivaroxaban and edoxaban are avoided under 15. Apixaban is usable in mild-to-moderate renal impairment but reduced to 2.5 mg BD when two of three hold: age over 80, weight under 60 kg, creatinine over 1.5 mg/dL (AMPLIFY criteria). In end-stage renal disease on dialysis, prefer warfarin or UFH.[1]

LMWH — when the DOAC steps aside

LMWH remains first-line in pregnancy and, with modern caveats, in cancer-associated VTE. Enoxaparin 1 mg/kg subcutaneously twice daily (dalteparin 200 IU/kg daily, tinzaparin 175 IU/kg daily) does not cross the placenta and needs no INR monitoring — the two properties that keep it indispensable.[1]

• Pregnancy and lactation — DOACs are contraindicated (teratogenic in animal studies); dalteparin, enoxaparin, and tinzaparin are safe throughout. Warfarin is teratogenic (warfarin embryopathy at 6 to 12 weeks) and reserved postpartum; LMWH and warfarin are breastfeeding-safe.
• Cancer-associated VTE — LMWH was the traditional first-line (CLOT, 2003), but apixaban is now non-inferior to dalteparin (Caravaggio), with a higher rate of major GI bleeding in GI/GU cancers. Current ASH and ASCO guidance: LMWH or apixaban or rivaroxaban are acceptable, with LMWH still preferred in GI/GU cancer, thrombocytopenia, or very high bleeding risk.
• Severe renal impairment (CrCl under 30) — LMWH accumulates; switch to unfractionated heparin (UFH) infusion, 18 IU/kg/h titrated to an aPTT 1.5 to 2.5 times control, when rapid reversibility is needed.
• Thrombocytopenia or HIT — switch to argatroban, bivalirudin, or fondaparinux; never LMWH.[1][9]

Warfarin, heparin, and the 5-day overlap rule

Warfarin is no longer first-line for VTE, but it retains a role in mechanical heart valves (DOACs contraindicated), severe CKD (eGFR under 15), antiphospholipid syndrome with arterial events (DOACs are inferior — TRAPS), and patient preference or availability.[2]

The regimen that earns marks is the overlap, and the reason for the overlap is a named trap. Start warfarin 5 mg daily (lower in the elderly, frail, or liver disease), start LMWH on day 1 alongside it, and continue LMWH for at least 5 days AND until the INR is 2.0 to 3.0 on two consecutive measurements. Target INR 2.0 to 3.0 (aim 2.5).[1]

The named trap — warfarin-induced skin necrosis. Warfarin knocks out the vitamin-K-dependent factors in sequence: protein C (an anticoagulant) falls first, ahead of factors II, IX, and X, producing a transient procoagulant window 3 to 10 days in. In protein C or S deficiency this precipitates cutaneous microvascular thrombosis — necrosis of the breasts, thighs, and buttocks. The prophylaxis is the overlap: never start warfarin without concomitant heparin, and never load high (use 5 mg, not 10 mg, in known deficiency).[2]

Unfractionated heparin (UFH) — IV infusion, 18 IU/kg/h (70 IU/kg bolus in acute PE), titrated to aPTT 1.5 to 2.5 times control or anti-Xa 0.3 to 0.7 IU/mL. Use it when you need rapid reversibility (protamine), renal failure (no accumulation), high bleeding risk, or imminent thrombolysis — and avoid it entirely in patients with a history of HIT.[1]

Massive PE — thrombolysis first, do not wait for the scan

Massive (high-risk) PE is a resuscitation emergency, not a diagnostic puzzle. The patient is dying of acute right-ventricular failure, and the only intervention proven to cut mortality is immediate systemic thrombolysis. If the patient is in shock with unequivocal RV strain on echo and the bedside mimics (tamponade, tension pneumothorax, acute MI) are excluded, treat on haemodynamics alone — do not send an unstable patient to the scanner.[1][3][10]

Resuscitation around the lytic is calibrated to a failing right ventricle. Oxygen to target SpO2 94 to 98 percent (intubate only if tiring — positive pressure drops preload and PE patients can arrest on induction); a cautious 250 mL crystalloid bolus over 15 minutes (excess fluid worsens RV overload); and noradrenaline as first-line vasopressor to support RV coronary perfusion, with dobutamine 5 to 15 mcg/kg/min added for low output. Avoid pure systemic vasodilators (GTN, nitroprusside) — they collapse RV coronary perfusion.[1]

Catheter-directed thrombolysis, IVC filter, and embolectomy — the rescue ladder

When systemic thrombolysis is absolutely contraindicated or has failed, the rescue ladder has three rungs, each with a defined indication.[1][3]

• Catheter-directed thrombolysis (CDT) and mechanical thrombectomy — for high-risk PE when systemic lysis is absolutely contraindicated, and for selected intermediate-high-risk PE where bleeding risk is judged high or expertise is available; also the consideration in iliofemoral DVT and phlegmasia cerulea dolens.
• Surgical embolectomy — bilateral pulmonary artery thrombectomy on cardiopulmonary bypass, by an experienced cardiac surgeon; salvage in arrest or failed lysis.
• Retrievable IVC filter — when anticoagulation is absolutely contraindicated (active major bleed) or in recurrent PE despite adequate anticoagulation; it does not prevent DVT progression and is removed once anticoagulation can resume (typically 3 to 6 months).
• VA-ECMO — bridging to recovery or surgery in refractory obstructive shock in experienced centres.[1][2]

The intermediate-risk (submassive) question is what PEITHO settled. Routine systemic thrombolysis in normotensive intermediate-risk PE reduced haemodynamic decompensation but at the cost of major bleeding including stroke, with no net mortality benefit — so thrombolysis is not routinely first-line in this group. The modern approach is anticoagulation plus close monitoring, with CDT reserved for the deteriorating selected patient.[10]

How long? — provoked three months, unprovoked and cancer indefinite

The duration of anticoagulation is set by provocation, not by anatomy. Get this single decision right and you have answered the question examiners ask at follow-up.[1][2]

• Provoked by a transient reversible factor (surgery, trauma, immobility, pregnancy, oestrogen) — 3 months, then stop; recurrence is about 5 percent per year afterwards, and neither a cancer screen nor a thrombophilia screen is routine.
• First unprovoked VTE — at least 3 to 6 months, but most patients extend to indefinite with annual reassessment, because recurrence is about 10 percent per year off anticoagulation (20 to 25 percent at 5 years). An age-appropriate cancer screen at presentation is cost-effective.
• Cancer-associated VTE — at least 6 months, then continued as long as the cancer is active or on treatment.
• Recurrent unprovoked VTE — indefinite; extended apixaban 2.5 mg BD is the lowest-bleeding option (AMPLIFY-EXT).[2][5]

Special populations — cancer, pregnancy, renal failure

Cancer-associated VTE. About 15 to 20 percent of all VTE, commonest in pancreatic, gastric, brain, ovarian, and lung cancers. LMWH, apixaban, or rivaroxaban are all acceptable first-line (ASH, ASCO); apixaban is non-inferior to dalteparin (Caravaggio) but carries higher major-GI bleeding in GI/GU cancers, where LMWH remains preferred. Treat at least 6 months, then indefinitely while the cancer is active; for recurrence despite anticoagulation, switch to higher-dose LMWH, add an IVC filter, and reconsider the regimen.[1][9]

Pregnancy and the postpartum. A 5-fold VTE risk, highest in the first 6 weeks postpartum. DOACs are contraindicated; LMWH throughout pregnancy (enoxaparin 1 mg/kg BD or dalteparin weight-based), stopped 24 hours before planned delivery and restarted 4 to 6 hours postpartum; continue for at least 6 weeks postpartum and at least 12 weeks total. Diagnose suspected DVT with Doppler ultrasound first; for suspected PE use CTPA or V/Q SPECT under a low-radiation protocol — do not withhold the indicated scan for fear of pregnancy. LMWH and warfarin are breastfeeding-safe.[1]

Renal failure. Calculate CrCl (Cockcroft-Gault) before choosing the agent. At CrCl 30 to 50, dose-adjust (rivaroxaban to 15 mg daily); under 30, avoid dabigatran; under 15, avoid rivaroxaban and edoxaban, and prefer warfarin or UFH. For CTPA in CKD, pre-hydrate with isotonic crystalloid, minimise contrast, or choose V/Q. The age-adjusted D-dimer and PERC are especially useful in the elderly, where D-dimer specificity collapses.[1]

When PE kills you later — chronic thromboembolic pulmonary hypertension

CTEPH is the late complication, and it is curable. Organised fibrotic thrombus in the pulmonary arterial tree produces a progressive pulmonary hypertension that presents months to years after a PE as insidious dyspnoea and exercise intolerance with signs of right-heart failure. The incidence is 2 to 4 percent after PE (Pengo, NEJM 2004 — 1 percent at 6 months, 3.1 percent at 1 year, 3.8 percent at 2 years).[11]

The V/Q scan is the screening test of choice — segmental unmatched perfusion defects — confirmed by pulmonary angiography. The only curative treatment is pulmonary endarterectomy (curative in 70 to 80 percent); for the inoperable or those with residual disease, balloon pulmonary angioplasty and riociguat are the alternatives. Lifelong anticoagulation follows either way. The teaching point: unexplained dyspnoea after a PE earns a V/Q scan — not another chest X-ray.[3][11]

Complications — post-thrombotic syndrome, bleeding, HIT, warfarin necrosis

The complications come from both the disease and the treatment, and the two named traps are exam favourites.[1][2]

• Post-thrombotic syndrome — chronic venous hypertension after proximal DVT affects about 50 percent (5 to 10 percent severe, with ulceration); early anticoagulation and good compression stockings reduce it.
• Anticoagulant bleeding — major bleeding runs 1 to 2 percent per year on a DOAC, slightly higher on warfarin. Idarucizumab (5 g IV) specifically reverses dabigatran; andexanet alfa reverses the factor Xa inhibitors (apixaban, rivaroxaban, edoxaban); four-factor PCC is the non-specific option.
• HIT — the named trap. Heparin-induced thrombocytopenia presents 5 to 14 days after heparin exposure (sooner if previously sensitised) with a platelet fall over 50 percent, new thrombosis, or skin necrosis at injection sites. Stop all heparin — LMWH, flushes, lines — and start argatroban, bivalirudin, or fondaparinux; never start warfarin alone (venous limb gangrene).
• Warfarin-induced skin necrosis — 3 to 10 days after starting warfarin in protein C/S deficiency; prophylaxis is the LMWH overlap for at least 5 days and until the INR is therapeutic.[1][2]

The trials that changed practice

The 2019 ESC guideline unified VTE into one risk-stratified algorithm with DOACs first-line, and is the document examiners quote. The landmark trials every candidate must cite, and what each changed:[1]

[7] [8] [4] [5] [6] [9] [10]

How VTE patients come to harm — the preventable list

• Death from an unrecognised aortic dissection that was anticoagulated or lysed as "PE" — the preventable death. Exclude dissection clinically before any antithrombotic.[1]
• A missed massive PE — syncope with clear lungs and a raised JVP treated as "vasovagal", dying in the scanner queue instead of receiving alteplase.[1][3]
• An unnecessary CTPA in a PERC-negative patient, chasing a false-positive D-dimer into a contrast load and an overdiagnosed subsegmental PE.[1]
• A DOAC given in severe renal failure — dabigatran under CrCl 30 accumulating and bleeding.[1]
• LMWH continued in HIT — the platelet count collapses and new thrombosis appears; stop all heparin, start argatroban.[1]
• Warfarin started without a heparin bridge in protein C deficiency — warfarin-induced skin necrosis of the breasts and thighs.[2]
• A provoked VTE treated indefinitely, or an unprovoked VTE stopped at 3 months — bleeding in the first, recurrence in the second.[2][5]
• Anticoagulation of an aortic dissection mistaken for PE — the one harm that is always preventable and always lethal.[1]

The mantra, and the mnemonic

The mantra: Virchow first, Wells next, D-dimer to rule out, DOAC to treat — and never anticoagulate a dissection.[1]

[1]

And the PE syndrome in one line: sudden dyspnoea, pleuritic pain, sinus tachycardia, and hypoxia out of proportion to the chest X-ray — and in the massive form, syncope with clear lungs and a raised JVP.[1][3]

Ward-round test — three stems, thirty seconds each

Stem 1 — the man from the top of the topic (answer)

The 67-year-old, day 5 after a hip replacement, with pleuritic chest pain, tachycardia at 112, saturations 92 percent, and a swollen right calf. He is haemodynamically stable. What is your next step, and your first drug? Model: This is provoked PE from a proximal DVT until proven otherwise. He is haemodynamically stable, so no thrombolysis. Score him (Wells PE is high — clinical signs of DVT and PE the likely diagnosis), exclude the bedside mimics (no tearing back pain, no pulse differential, ECG to exclude STEMI), then CTPA. While imaging is arranged, start anticoagulation — apixaban 10 mg BD (or LMWH if you prefer a parenteral lead-in) provided there is no bleeding contraindication. Image the leg with Doppler ultrasound as well; the swollen calf is the source.[1]

Stem 2 — the syncope with clear lungs (answer)

A 72-year-old collapses at home, brought in hypotensive at 78/50, oxygen saturations 88 percent, JVP raised, lung fields clear, ECG showing sinus tachycardia with T inversion in V1 to V3. Bedside echo shows a dilated RV with septal flattening. What do you do in the next 15 minutes? Model: This is massive (high-risk) PE — hypotension, raised JVP, clear lungs, RV strain on echo. Do not send her to CT in this state. Give alteplase 100 mg IV over 2 hours (or 0.6 mg/kg over 15 minutes if she arrests) on the echo-and-clinical diagnosis, after excluding contraindication; support with noradrenaline, cautious fluids, and oxygen. Confirm with CTPA only once she is stabilised. The single intervention that cuts her mortality from ~30 percent to ~6 to 8 percent is the lytic — the trap is waiting for the scan.[1][3][10]

Stem 3 — the platelet count that falls on heparin (answer)

A patient on day 9 of enoxaparin for a proximal DVT has a platelet count that has fallen from 280 to 110 (a 60 percent drop) and a new swollen, painful contralateral leg. What happened, and what is the next move? Model: This is heparin-induced thrombocytopenia (HIT) — platelet fall over 50 percent with new thrombosis, 5 to 14 days after heparin exposure. Stop all heparin immediately — LMWH, flushes, and lines — and start argatroban, bivalirudin, or fondaparinux. Do not start warfarin alone (venous limb gangrene). Send a HIT antibody (PF4) test to confirm, but treat on clinical suspicion without waiting. The trap is continuing LMWH because "it is not really heparin" — it is, and it kills.[1]

References

1. [1]Konstantinides SV, Meyer G The 2019 ESC Guidelines on the Diagnosis and Management of Acute Pulmonary Embolism Eur Heart J, 2019.PMID 31697840
2. [2]Witt DM, Nieuwlaat R, Clark NP, et al. American Society of Hematology 2018 guidelines for management of venous thromboembolism: optimal management of anticoagulation therapy Blood Adv, 2018.PMID 30482765
3. [3]Jaff MR, McMurtry MS, Archer SL, et al. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association Circulation, 2011.PMID 21422387
4. [4]Agnelli G, Buller HR, Cohen A, et al. Oral apixaban for the treatment of acute venous thromboembolism N Engl J Med, 2013.PMID 23808982
5. [5]Agnelli G, Buller HR, Cohen A, et al. Apixaban for extended treatment of venous thromboembolism N Engl J Med, 2013.PMID 23216615
6. [6]Schulman S, Kearon C, Kakkar AK, et al. Dabigatran versus warfarin in the treatment of acute venous thromboembolism N Engl J Med, 2009.PMID 19966341
7. [7]Bauersachs R, Berkowitz SD, Brenner B, et al. Oral rivaroxaban for symptomatic venous thromboembolism N Engl J Med, 2010.PMID 21128814
8. [8]Büller HR, Prins MH, Lensin AW, et al. Oral rivaroxaban for the treatment of symptomatic pulmonary embolism N Engl J Med, 2012.PMID 22449293
9. [9]Agnelli G, Becattini C, Meyer G, et al. Apixaban for the Treatment of Venous Thromboembolism Associated with Cancer N Engl J Med, 2020.PMID 32223112
10. [10]Meyer G, Vicaut E, Danays T, et al. Fibrinolysis for patients with intermediate-risk pulmonary embolism N Engl J Med, 2014.PMID 24716681
11. [11]Pengo V, Lensing AWA, Prins MH, et al. Incidence of chronic thromboembolic pulmonary hypertension after pulmonary embolism N Engl J Med, 2004.PMID 15163775