Pulmonary Embolism — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mrs Anjali Patel, 74 years old. [1]

Presenting complaint: Acute onset of right-sided pleuritic chest pain and breathlessness that woke her from sleep, followed by a brief presyncopal episode on standing. She called an ambulance. In the emergency department she is breathless at rest but is maintaining her blood pressure. [1]

Past history:

• Stage 3 chronic kidney disease (baseline eGFR 45) of presumed hypertensive origin
• Hypertension (15 years)
• Osteoarthritis (knees)
• No prior thrombosis, no malignancy, no recent surgery, no hormone use
• Non-smoker, occasional alcohol [1]

Current medications:

• Perindopril 5 mg daily
• Amlodipine 10 mg daily
• Paracetamol 1 g three times daily as needed [1]

Examination findings (trainee elicits):

• Respiratory rate 26, SpO2 90 percent on room air (96 percent on 4 L nasal specs)
• Heart rate 110, blood pressure 128/76
• Raised JVP at 4 cm; loud pulmonary component of the second heart sound; right ventricular heave at the lower left sternal edge
• Chest clear; calves symmetrical, no tenderness
• Afebrile [1]

Investigations:

• Wells score 6 (PE likely)
• CTPA: large right lower lobe pulmonary embolus with right ventricular dilation
• Bedside echo: RV dilation with septal flattening, estimated RVSP 42 mmHg, preserved LV function
• Troponin 0.05 micrograms/L (ULN 0.04) — mildly elevated
• NT-proBNP 850 ng/L (mildly elevated)
• Haemoglobin 128 g/L, platelets 240, eGFR 42, D-dimer 2400 micrograms/L FEU
• ECG: sinus tachycardia, T-wave inversion in V1 to V3 [1]

Candidate's structured presentation (model)

Opening statement: [1]

"Mrs Patel is a 74-year-old retired teacher who presents with an unprovoked pulmonary embolism, confirmed on CT pulmonary angiography, with echocardiographic and biochemical evidence of right ventricular strain. She has stage 3 chronic kidney disease and hypertension. [1]

Her main problems are:

1. Unprovoked pulmonary embolism, intermediate-high risk (RV dysfunction on echo plus positive troponin), on anticoagulation
2. Right ventricular strain requiring monitoring for decompensation
3. Chronic kidney disease (eGFR 42) — relevant to drug choice
4. An unprovoked event in a 74-year-old — needs malignancy screening and a decision on long-term anticoagulation duration" [1]

Investigation summary: [1]

"Her CTPA confirmed a large right lower lobe pulmonary embolus. The Wells score of 6 placed her in the PE-likely category, so a D-dimer was not used to exclude the diagnosis — she went straight to imaging, which is the correct pathway. Her bedside echo shows right ventricular dilation with septal flattening, and her troponin is mildly elevated, which together classify her as intermediate-HIGH risk by the ESC framework. Her sPESI is 2 — pulse 110 and saturation under 95 percent — confirming she is not low-risk and requires inpatient admission. Her ECG shows T-wave inversion in the anterior leads, a recognised pattern of right heart strain. Her renal function is mildly impaired at eGFR 42, which is relevant to her anticoagulation choice." [1]

Management plan: [1]

1. Immediate:

   • Therapeutic anticoagulation with apixaban 10 mg twice daily for 7 days, then 5 mg twice daily (the AMPLIFY regimen). Apixaban is preferred here because it does not require a parenteral lead-in, is non-inferior to warfarin with less major bleeding, and remains valid at eGFR 42 without dose reduction. The 2.5 mg twice-daily reduction does not apply — she does not meet two of age at least 80, weight at most 60 kg, or creatinine at least 133 micromol/L.
   • Continuous cardiac monitoring, high-flow oxygen to keep saturations 94 to 98 percent, IV access.
   • A rescue-thrombolysis plan ready: alteplase 100 mg over 2 hours to activate immediately if she becomes hypotensive or shocked. [1]

2. Risk stratification and monitoring:

   • She is intermediate-high risk. Standard care is anticoagulation plus close monitoring. She should NOT receive prophylactic systemic thrombolysis — the PEITHO trial showed that lysis in intermediate-risk PE reduces death or decompensation but at the cost of significantly increased major bleeding and an intracranial haemorrhage rate of around 2 percent, with no net mortality benefit.
   • Serial troponin and BNP, repeat echo at 48 to 72 hours, hourly observations, and a clear escalation plan if her blood pressure falls. [1]

3. Renal considerations:

   • Monitor renal function daily during admission. If eGFR falls below 30, switch to an unfractionated heparin infusion (rapidly reversible, dialysis-filterable). Avoid dabigatran and use rivaroxaban only with caution in this range. [1]

4. Duration — this is an unprovoked PE:

   • After a first unprovoked PE with low bleeding risk, the recommendation is indefinite anticoagulation with periodic reassessment. The annual recurrence off anticoagulation is around 10 percent, and recurrent PE is often fatal.
   • Before committing, complete a focused malignancy screen (history, examination, age-appropriate colonoscopy and mammography review, basic bloods) and consider selective thrombophilia testing — though the yield in a 74-year-old is low.
   • Discuss the trade-off with her and review annually. [1]

5. Follow-up and surveillance:

   • Thrombosis clinic at 2 to 4 weeks to review tolerance and renal function.
   • Review at 3 and 6 months.
   • If she develops persistent or new dyspnoea at 3 to 6 months, screen for CTEPH with a V/Q scan — the incidence after a symptomatic PE is around 0.4 to 4 percent over two years. [1]

Examiner discussion questions

Q: "Her blood pressure drops to 84/50 an hour after admission. What do you do?" [1]

"This converts her to high-risk (massive) PE. I would give alteplase 100 mg intravenously over 2 hours immediately, alongside haemodynamic support — cautious 250 mL fluid boluses (no more, because volume overload worsens right ventricular failure), noradrenaline for vasoplegia, and dobutamine if cardiac output is low. I would hold the apixaban during the lytic infusion and resume anticoagulation once any bleeding is excluded, typically with heparin. If thrombolysis was absolutely contraindicated — recent intracranial surgery or haemorrhagic stroke — I would arrange surgical pulmonary embolectomy or catheter-directed thrombectomy in a centre with that capability. The mortality of untreated massive PE is over 50 percent; reperfusion is life-saving." [1]

Q: "Would you test her for factor V Leiden?" [1]

"Not routinely. Thrombophilia testing is selective — it is reserved for unprovoked VTE in a patient under 50, recurrent VTE, VTE in unusual sites (portal, mesenteric, cerebral), a strong family history, or recurrent fetal loss. Mrs Patel is 74 with a first unprovoked event; the yield of inherited thrombophilia testing is low and the result would not change my plan to anticoagulate her indefinitely. I WOULD test for antiphospholipid syndrome if she had a history of thrombosis or pregnancy loss, because finding it changes the duration and the drug choice — warfarin is preferred over DOACs in antiphospholipid syndrome after the TRAPS trial. I would also remember that antithrombin, protein C, and protein S levels are unreliable during the acute event and on anticoagulation, so testing must wait until at least two weeks after stopping therapy if it is done at all." [1]

Q: "She wants to know if her family should be tested." [1]

"Only if she is found to have a significant inherited thrombophilia — for example, homozygous factor V Leiden, antithrombin deficiency, or a compound defect — AND she has a first-degree relative with a confirmed venous thromboembolism. In that setting, screening first-degree relatives allows them to take prophylaxis during high-risk periods (surgery, immobilisation, pregnancy). In the absence of an identifiable defect, routine family testing is not recommended, because the absolute risk in relatives of a patient without a defined thrombophilia is modest and does not warrant lifelong prophylaxis." [1]

Q: "She is on perindopril. Does it interact with apixaban?" [1]

"No. There is no clinically significant interaction between an ACE inhibitor and apixaban. The main interactions with the direct oral anticoagulants are with strong inhibitors or inducers of P-glycoprotein and CYP3A4 — for example, ketoconazole, ritonavir, clarithromycin (raise levels), and rifampicin, phenytoin, carbamazepine, St John's wort (lower levels). I would review her full medication list for these. I would continue the perindopril and amlodipine for her hypertension, monitor her renal function closely, and ensure her blood pressure is not so aggressively treated that it impairs renal perfusion during her acute illness." [1]

Q: "What counselling would you give her before discharge?" [1]

"I would explain that pulmonary embolism is a blood clot in the lung, that the apixaban stops it growing and allows her body to dissolve it, and that she must take it reliably — missed doses meaningfully increase recurrence risk. I would counsel her on the signs of bleeding to watch for — black tarry stools, blood in the urine, prolonged nose or gum bleeding, large unexplained bruises, and any neurological symptoms (severe headache, weakness, visual change) that could indicate intracranial haemorrhage. I would advise her to seek urgent review if her breathlessness returns or worsens. I would tell her to avoid long-haul flights for at least two weeks, to stay well hydrated, and to use graduated compression stockings. I would give her a written action plan and arrange thrombosis clinic follow-up at two to four weeks." [1]

DCE Short Case — Cardiovascular Examination after PE

Instruction

"Examine this patient's cardiovascular system. You have 7 minutes for examination and 8 minutes for discussion." [1]

Key signs the patient demonstrates

• Raised jugular venous pressure at 4 cm with a normal waveform (right heart involvement)
• Right ventricular heave at the lower left sternal edge (parasternal)
• Accentuated pulmonary component of the second heart sound (P2) — the single most important sign of pulmonary hypertension
• Soft pansystolic murmur at the lower left sternal edge, louder on inspiration (functional tricuspid regurgitation from RV dilation)
• T-wave inversion on the ECG in V1 to V3 (right heart strain pattern)
• Clear lung fields — a discriminator from left heart failure [1]

Presentation template

"I examined Mrs Patel's cardiovascular system. She is comfortable at rest on 2 litres of nasal specs with a respiratory rate of 18. She is not clubbed. The pulse is 96 and regular. The blood pressure is 130/80. The JVP is elevated 4 cm. [1]

On palpation there is a right ventricular heave at the lower left sternal edge. The pulmonary component of the second heart sound is accentuated. There is a soft pansystolic murmur at the lower left sternal edge that is louder on inspiration, consistent with tricuspid regurgitation. The chest is clear to auscultation. There is no peripheral oedema, hepatomegaly, or ascites. The calves are symmetrical. [1]

In summary, these findings are consistent with a recent pulmonary embolism with persistent right ventricular strain and early pulmonary hypertension, without established right heart failure." [1]

Discussion template

1. Summarise findings → "recent PE with RV strain and early pulmonary hypertension."
2. Differential of the loud P2 → pulmonary hypertension from any cause — chronic thromboembolic disease, idiopathic pulmonary arterial hypertension, left heart disease, chronic lung disease with hypoxia, sleep apnoea. In her case the context is a recent PE.
3. Investigation pathway → echocardiography to estimate RVSP and assess RV function; V/Q scan to screen for chronic thromboembolic disease; right heart catheterisation for definitive haemodynamics if pulmonary hypertension is confirmed; pulmonary function tests to exclude parenchymal lung disease.
4. Management → anticoagulation for the index event; treat any underlying cause; if CTEPH is confirmed, refer for pulmonary endarterectomy (potentially curative) or balloon pulmonary angioplasty; riociguat for inoperable or residual disease; lifelong anticoagulation.
5. Prognosis → depends on right ventricular recovery and whether CTEPH develops; serial echocardiography and V/Q at three to six months; around 0.4 to 4 percent of PE survivors develop CTEPH. [1]