Embolism and Thrombosis: DVT, PE Emergency Care

Table of Contents

EMBOLISM AND THROMBOSIS: DVT, PULMONARY EMBOLISM, ARTERIAL EMBOLISM, DIAGNOSIS, EMERGENCY MANAGEMENT AND NURSING CARE

Deep vein thrombosis and pulmonary embolism pathway illustration

Add a suitable educational image showing venous thrombosis, clot migration and pulmonary or arterial embolism here.

Why this topic matters: Thrombosis and embolism are time-critical problems. A clot may obstruct venous return, travel to the lungs as a pulmonary embolus, occlude a brain or limb artery, or produce organ ischaemia before obvious signs develop. Emergency-care students must recognise risk, assess the patient without dislodging a clot, start safe escalation, distinguish DVT from life-threatening PE, and monitor anticoagulation and bleeding.

Learning objectives

Define thrombosis, embolism, thromboembolism, venous thromboembolism and arterial embolism.
Explain Virchow’s triad and connect stasis, endothelial injury and hypercoagulability with clot formation.
Recognise risk factors and clinical features of DVT, PE, acute limb ischaemia, embolic stroke, mesenteric ischaemia and other embolic emergencies.
Perform a structured ABCDE, focused history, six-P limb assessment and time-critical triage.
Describe the roles of Wells assessment, D-dimer, compression ultrasound, CT pulmonary angiography, V/Q scanning, ECG, echocardiography and arterial imaging.
Outline first aid, pre-hospital transfer, anticoagulation, reperfusion, thrombolysis, embolectomy and supportive care according to severity and local protocol.
Administer and monitor anticoagulants and thrombolytics safely, including renal, pregnancy, cancer and bleeding considerations.
Plan nursing surveillance, prevention, patient education, discharge safety-netting and prevention of recurrence.

1. Key definitions and concepts

Thrombosis is formation of a blood clot within a blood vessel or heart chamber. A thrombus can remain attached to the vessel wall, enlarge, obstruct flow or fragment. Embolism occurs when travelling material—most often a clot—moves through the circulation and lodges in a vessel too small for it to pass. Thromboembolism combines clot formation and migration.

Term	Meaning	Emergency relevance
Deep-vein thrombosis (DVT)	Clot in a deep vein, commonly the calf, femoral or iliac veins.	May obstruct venous return, extend proximally or embolise to the lungs.
Pulmonary embolism (PE)	Embolic material obstructing a pulmonary artery or its branches.	May cause hypoxaemia, right-ventricular failure, shock or sudden death.
Arterial embolism	Material travelling in the arterial circulation and blocking tissue perfusion.	Can cause acute limb ischaemia, stroke, myocardial or mesenteric infarction.
In-situ arterial thrombosis	Clot forms within a diseased artery, often over atherosclerotic plaque.	Produces acute-on-chronic ischaemia and may require urgent revascularisation.
Paradoxical embolism	Venous embolus crosses a right-to-left shunt, such as a patent foramen ovale, and enters systemic arteries.	Can cause an otherwise unexplained stroke or limb ischaemia.
Septic embolus	Infected material travels from endocarditis or another focus.	Causes infarction plus infection; requires cultures, antibiotics and source control.
Fat, air, amniotic or foreign-body embolus	Non-thrombotic material enters the circulation.	May follow long-bone fracture, vascular procedures, childbirth or injection injury.

Safety principle: Treat sudden breathlessness, syncope, unexplained pleuritic chest pain, new unilateral limb swelling, a cold pulseless limb or a focal neurological deficit as a potential embolic emergency. Do not massage a suspected DVT and do not delay monitored transfer for routine tests.

2. Virchow’s triad and normal clot control

Haemostasis normally seals vessel injury through vasoconstriction, platelet adhesion and activation, coagulation-fibrin formation and later fibrinolysis. Thrombosis occurs when clot formation exceeds protective anticoagulant and fibrinolytic mechanisms. Virchow’s triad organises the three major contributors:

Venous stasis: immobility, paralysis, long travel, heart failure, dehydration, casts and venous compression slow flow and allow activated clotting factors to accumulate.
Endothelial or vessel-wall injury: surgery, trauma, fractures, central venous catheters, inflammation, atherosclerotic plaque, smoking and infection expose thrombogenic surfaces.
Hypercoagulability: cancer, pregnancy, oestrogen, inherited thrombophilia, antiphospholipid syndrome, severe infection, nephrotic syndrome and dehydration increase clotting tendency.

Clinical reasoning: A patient may have more than one component—for example, a postoperative patient with tissue injury, immobility and dehydration. Risk assessment must therefore be repeated after admission, surgery, deterioration and changes in mobility.

3. Causes and risk factors

Risk factor or setting	Mechanism or example	Questions and nursing action
Recent surgery, trauma or fracture	Endothelial injury, inflammation and reduced mobility.	Record procedure, date, bleeding risk, mobility and prescribed prophylaxis.
Hospitalisation and immobility	Venous stasis from bed rest, paralysis, sedation, plaster or long-distance travel.	Document mobility, encourage safe movement and apply mechanical prophylaxis when ordered.
Previous VTE or family history	Suggests persistent or inherited thrombotic tendency.	Ask about DVT/PE, age at event and anticoagulant history; communicate prominently.
Malignancy and cancer treatment	Tumour procoagulants, inflammation, chemotherapy and venous devices.	Assess weight loss, treatment, line sites, bleeding and medicine interactions.
Pregnancy and postpartum period	Physiological hypercoagulability, venous compression and reduced mobility.	Ask gestation/postpartum status; use pregnancy-safe imaging and anticoagulant advice.
Oestrogen exposure	Combined hormonal contraception or hormone therapy can increase risk.	Document preparation, duration, smoking and other risk factors; refer for review.
Heart failure, atrial fibrillation or recent MI	Stasis in chambers or poor circulation; atrial thrombi can embolise systemically.	Check rhythm, anticoagulant adherence, stroke symptoms and cardiac history.
Inflammation and infection	Sepsis, COVID-19 and inflammatory disease activate coagulation.	Trend fever, perfusion, oxygenation and laboratory results; escalate deterioration.
Obesity, smoking, dehydration and age	Inflammation, viscosity, endothelial dysfunction and reduced mobility.	Use non-judgemental prevention counselling and individualise safe activity.
Central venous catheter or dialysis access	Local vessel trauma and altered flow cause upper-limb or catheter thrombosis.	Inspect limb and line, compare pulses, swelling, pain and catheter function.
Inherited or acquired thrombophilia	Factor V Leiden, prothrombin mutation, protein C/S or antithrombin deficiency, antiphospholipid syndrome.	Ask about recurrent or unprovoked events; testing is specialist-led and timing-sensitive.

4. Types and patterns of embolism

4.1 Venous thromboembolism

Distal DVT: calf-vein clot; may remain local or extend proximally.
Proximal DVT: popliteal, femoral or iliac clot with greater embolic risk.
PE: clot in pulmonary arteries; severity ranges from small stable embolus to obstructive shock.
Chronic thromboembolic disease: persistent obstruction may produce exercise limitation and pulmonary hypertension.

4.2 Systemic arterial embolism

Cardioembolic: atrial fibrillation, left-ventricular thrombus after MI, dilated cardiomyopathy, prosthetic valves or endocarditis.
Paradoxical: venous clot crosses a cardiac or pulmonary shunt.
Atheroembolic: cholesterol or plaque debris travels after vascular manipulation.
Peripheral embolism: acute arm or leg ischaemia with sudden pain, pallor, pulselessness, paraesthesia, paralysis and poikilothermia.
Cerebral embolism: sudden focal deficit, aphasia, facial droop or visual loss.
Mesenteric embolism: severe abdominal pain out of proportion to early examination, especially with atrial fibrillation.
Coronary embolism: acute myocardial ischaemia or infarction without a typical plaque event.

4.3 Non-thrombotic embolism

Fat embolism syndrome after long-bone or pelvic fracture: respiratory distress, neurological change and petechiae, usually after a delay.
Air or gas embolism after vascular access, diving, surgery or injection: sudden dyspnoea, chest pain, confusion, seizure or collapse.
Amniotic-fluid embolism around labour or postpartum: sudden hypoxia, hypotension, coagulopathy and cardiovascular collapse.
Septic emboli from infective endocarditis: fever, murmur and infarcts or abscesses in brain, spleen, kidney or limbs.

5. Pathophysiology: from clot to tissue injury

Stasis or injury activates platelets, tissue factor and the coagulation cascade.
Thrombin converts fibrinogen to fibrin; the mesh traps cells and enlarges the thrombus.
A venous clot may extend toward the iliac veins. A fragment detaches and travels through the inferior vena cava, right atrium and right ventricle.
The embolus lodges in a pulmonary artery. Obstruction increases pulmonary vascular resistance and right-ventricular afterload.
Right-ventricular dilatation reduces left-ventricular filling and cardiac output; hypoxaemia, hypotension and shock may follow.
An arterial embolus blocks oxygen delivery beyond the obstruction. Anaerobic metabolism, acidosis, nerve dysfunction and muscle necrosis develop as ischaemia persists.
Reperfusion of a severely ischaemic limb can release potassium, acid and myoglobin, causing arrhythmia, renal injury and compartment syndrome.

Time matters: PE with shock and acute limb ischaemia are immediately life-threatening. Stroke, mesenteric ischaemia and myocardial embolism also require rapid specialist activation; a normal early examination does not exclude evolving infarction.

6. Clinical presentation

6.1 Deep-vein thrombosis

New unilateral swelling, usually of the calf, thigh or whole limb.
Deep pain or tenderness, often worse with standing or walking; do not rely on Homan’s sign.
Warmth, erythema or dusky discoloration; superficial collateral veins may become prominent.
Calf or thigh circumference difference compared with the opposite side.
DVT can be silent. Do not wait for leg findings if the patient has unexplained PE symptoms.

6.2 Pulmonary embolism

Sudden unexplained dyspnoea, tachypnoea, pleuritic chest pain, cough or haemoptysis.
Tachycardia, anxiety, hypoxaemia, dizziness, syncope or a sense of impending death.
Hypotension, raised JVP, cool skin, altered consciousness and oliguria indicate high-risk obstructive shock.
Low-grade fever, unilateral DVT signs or new oxygen requirement may be present.
PE may occur without symptoms of DVT and may mimic pneumonia, asthma, ACS, sepsis or panic.

6.3 Acute arterial embolism or thrombosis: the six Ps

Six-P finding	What to assess	Meaning and action
Pain	Sudden severe pain, onset and progression.	Ischaemic pain requires immediate vascular escalation and analgesia without masking reassessment.
Pallor	Compare colour with the opposite limb and dependent position.	Pale or mottled skin indicates poor arterial flow.
Pulselessness	Palpate and Doppler proximal and distal pulses; document both limbs.	Absent pulse is a late sign but is a vascular emergency.
Paraesthesia	Numbness, pins and needles, two-point discrimination and sensation.	Progressive sensory loss threatens limb viability.
Paralysis	Active movement, ankle/toe or wrist/finger power.	Weakness or paralysis suggests advanced ischaemia and possible irreversible injury.
Poikilothermia	Coldness compared with the other limb.	Temperature loss plus the other Ps demands urgent revascularisation review.

6.4 Other embolic emergencies

Embolic stroke: sudden face or arm weakness, speech difficulty, visual loss, ataxia or neglect. Use FAST and activate the stroke pathway.
Mesenteric ischaemia: abrupt severe abdominal pain, vomiting, diarrhoea or bloody stool; pain may be disproportionate to palpation findings.
Fat embolism: fracture history followed by hypoxaemia, confusion, agitation or petechial rash.
Septic embolism: fever, rigors, murmur, focal neurological or limb signs and positive-culture risk.

7. Focused history: OPQRST-SAMPLE

Question	Ask specifically	Why it matters
Onset and time	Exact time, sudden or gradual, at rest or after surgery/travel, last known well for stroke.	Determines tissue-threat and eligibility for time-dependent therapy.
Provocation/palliation	Walking, breathing, position, limb elevation, rest, analgesia or oxygen.	Helps distinguish musculoskeletal, pleuritic, venous and arterial patterns but cannot exclude VTE.
Quality and region	Pressure, pleuritic pain, calf ache, tearing limb pain, abdominal pain or neurological deficit.	Maps the vascular territory and dangerous differentials.
Severity and course	Pain score, dyspnoea grade, progression, syncope, weakness, coldness or colour change.	Deterioration suggests extension, embolisation or shock.
Associated features	Cough, haemoptysis, fever, palpitations, bleeding, pregnancy, trauma, neurological signs or oliguria.	Identifies PE, infection, cardioembolic source, contraindications and complications.
Risk history	Recent operation, fracture, admission, immobility, travel, cancer, pregnancy, oestrogen, previous VTE, thrombophilia and family history.	Builds pre-test probability and guides prophylaxis.
Medicine and bleeding	Anticoagulant/antiplatelet name, last dose, adherence, allergies, kidney disease, previous haemorrhage or stroke.	Prevents unsafe anticoagulation or thrombolysis.
Cardiac and infection history	Atrial fibrillation, MI, valve, endocarditis, fever, intravenous drug use or indwelling lines.	Suggests systemic or septic embolic sources.

8. Immediate assessment and emergency triage

Safety and help: call the emergency, vascular, respiratory, stroke or surgical team according to presentation. Bring monitoring, oxygen, suction and resuscitation equipment.
Airway: assess voice, patency and protection. Prepare airway support for reduced consciousness or shock.
Breathing: respiratory rate, work, chest movement, oxygen saturation, cyanosis and auscultation. Give titrated oxygen for hypoxaemia or respiratory distress according to local targets.
Circulation: pulse, BP, rhythm, skin, capillary refill, temperature, IV access and shock. Obtain bloods without delaying life-saving transfer.
Disability: consciousness, glucose, pupils, FAST screen, limb sensation and power. Record the last known well time for suspected stroke.
Exposure: inspect both limbs, circumference, colour, warmth, swelling, pulses, wounds, catheter sites and bleeding while maintaining dignity and warmth.
Do not massage or repeatedly manipulate a suspected DVT. Keep the patient at rest until PE and arterial compromise are assessed; use a monitored transfer for instability.
Record the clock: symptom onset, first contact, ECG, imaging request, anticoagulant or thrombolysis time, referral and response to treatment.

Red flags requiring immediate escalation: syncope or hypotension, severe hypoxaemia, cardiac arrest, rapidly worsening breathlessness, new focal neurological deficit, pulseless/cold/paralysed limb, severe abdominal pain out of proportion, active major bleeding or suspected aortic dissection.

9. Diagnostic assessment

9.1 DVT and PE probability

Use a validated clinical probability tool such as the two-level Wells DVT or PE score. It supports, but does not replace, examination and senior judgement.
In a low-probability pathway, a D-dimer may help rule out VTE when the assay and protocol are appropriate. D-dimer rises with age, pregnancy, infection, cancer, surgery and inflammation, so a positive result is not diagnostic.
In likely VTE, proceed directly to imaging and use interim therapeutic anticoagulation if imaging is delayed and bleeding risk is acceptable under local protocol.

9.2 Tests and nursing considerations

Investigation	What it contributes	Nursing considerations
Compression duplex ultrasound	Non-compressible vein, absent flow or clot extension in suspected DVT.	Explain procedure, compare sides, avoid vigorous massage and report severe pain or deterioration.
CT pulmonary angiography (CTPA)	Directly visualises pulmonary arterial filling defects and alternative chest pathology.	Check pregnancy, contrast allergy, renal function, IV access and ability to lie flat; monitor after contrast.
Ventilation–perfusion scan	Assesses mismatch when CTPA is unsuitable or unavailable.	Explain breath-hold/tracer steps and recognise nondiagnostic results.
ECG and cardiac biomarkers	May show sinus tachycardia, right-heart strain, arrhythmia or myocardial injury; does not exclude PE.	Obtain urgently in unstable patients and repeat after deterioration.
ABG and lactate	Quantifies hypoxaemia, ventilation, acidosis and tissue hypoperfusion.	Do not delay imaging or treatment in a crashing patient; monitor puncture site.
Bedside echocardiography	Right-ventricular dilatation/dysfunction, pressure overload, thrombus or alternative shock causes.	Useful in unstable PE when CT transfer is unsafe; escalate new RV failure.
Full blood count, PT/INR, aPTT, renal/liver function	Baseline haemoglobin, platelets, clotting and medicine clearance.	Report thrombocytopenia, severe anaemia, coagulopathy or renal impairment before therapy.
Arterial Doppler/CT angiography	Localises arterial occlusion and collateral flow in acute limb ischaemia.	Continue six-P and pulse checks; do not delay vascular consultation for routine imaging if limb is threatened.
Brain CT/MRI and vascular imaging	Distinguishes haemorrhage, infarction and large-vessel occlusion in embolic stroke.	Record last-known-well time, glucose and anticoagulant use; activate stroke team.

10. First aid and pre-hospital management

Recognise the emergency, call emergency transport and state suspected PE, stroke, acute limb ischaemia or DVT with risk factors.
Keep the patient resting; position semi-sitting for breathlessness unless shock or another condition dictates otherwise. Avoid unnecessary walking in suspected PE or acute limb ischaemia.
Assess ABCDE, attach pulse oximetry and cardiac monitoring, obtain BP and glucose, and establish IV access if trained and authorised.
Give oxygen only when hypoxaemic or in significant respiratory distress; titrate to the local target rather than giving unmonitored high-flow oxygen.
Do not massage a swollen limb, apply tight compression to an acutely ischaemic limb, or give oral food/drink when invasive treatment may be required.
For cardiac arrest, begin high-quality CPR and follow ALS. For suspected stroke, keep nil by mouth, check glucose and activate the stroke pathway.
Bring the medicine chart, anticoagulant history, allergies, last-known-well or onset time, ECG, observations and imaging results with the patient.

11. Management of DVT

11.1 Immediate priorities

Confirm probability and arrange compression ultrasound. If imaging is delayed in likely DVT, therapeutic anticoagulation may be started after checking bleeding risk and local protocol.
Assess for PE symptoms at every contact: dyspnoea, chest pain, syncope, hypoxaemia, tachycardia or hypotension require immediate PE management.
Start prescribed anticoagulation unless active major bleeding, severe thrombocytopenia, recent intracranial haemorrhage or another contraindication is present.
Elevate and mobilise gradually as advised; avoid vigorous massage. Compression hosiery is individualised and should not be applied before arterial flow and skin status are assessed.

11.2 Anticoagulant options

Direct oral anticoagulants may be used for many adults after clinician assessment, but renal function, drug interactions, pregnancy, breastfeeding, extremes of weight and cancer site affect selection.
Low-molecular-weight heparin or unfractionated heparin may be used when rapid onset, pregnancy, renal failure, procedures or instability require a parenteral option.
Vitamin K antagonist therapy requires overlap and INR monitoring when selected. Teach adherence and interactions rather than stopping treatment when bruising occurs without advice.
Duration is individualised according to provoked or unprovoked VTE, recurrence risk, cancer, bleeding risk and patient preference.

12. Management of pulmonary embolism

12.1 Risk stratification

Risk group	Clinical picture	Priority management
High-risk (massive PE)	Cardiac arrest, obstructive shock or persistent hypotension; may have severe RV dysfunction.	Resuscitation, oxygen/ventilatory support, urgent anticoagulation and specialist reperfusion evaluation. Systemic thrombolysis, catheter therapy or surgical embolectomy may be considered.
Intermediate-risk	Normotensive but RV dysfunction and/or positive cardiac biomarkers.	Admit to monitored care, anticoagulate and observe closely; rescue reperfusion is reserved for deterioration in most protocols.
Low-risk	Stable haemodynamics, low clinical severity and no major comorbidity.	Anticoagulation, education and selected outpatient or short-stay care only when a validated pathway and follow-up are available.

12.2 Hospital management sequence

Call senior emergency/respiratory/cardiology support, provide monitored oxygenation and repeat ABCDE.
Start therapeutic anticoagulation when PE is likely and bleeding risk is acceptable; do not delay for every laboratory result if the patient is unstable.
Use cautious fluids for hypotension; excessive fluid can worsen right-ventricular failure. Vasopressor support and advanced ventilation follow critical-care protocol.
For high-risk PE, assess systemic thrombolysis contraindications. If thrombolysis is contraindicated or fails, refer for catheter-directed therapy or surgical embolectomy where available.
Continue ECG, BP, oxygen saturation, mental status, urine output and peripheral perfusion monitoring. Reassess after every intervention.
Investigate provoking factors, malignancy, pregnancy, thrombophilia and right-heart recovery during follow-up rather than delaying acute stabilisation.

12.3 Inferior vena cava filters

An IVC filter is not routine treatment. It may be considered when acute VTE exists and therapeutic anticoagulation is absolutely contraindicated, or when embolism recurs despite appropriate treatment after specialist review. Document indication, retrieval plan and follow-up.

13. Management of acute arterial embolism and limb ischaemia

Recognise the six Ps and document onset, motor/sensory status, skin temperature, colour and Doppler/palpable pulses in both limbs.
Call vascular surgery immediately for a threatened or immediately threatened limb. Do not delay referral while waiting for imaging.
Keep the limb dependent and warm with loose coverings; do not elevate a critically ischaemic limb or apply heat directly.
Give prescribed analgesia, establish IV access, keep nil by mouth for possible intervention and administer urgent anticoagulation if ordered and not contraindicated.
Prepare for catheter thrombolysis, surgical embolectomy, thrombectomy, bypass or angioplasty according to anatomy and viability.
After reperfusion, monitor for compartment syndrome, reperfusion hyperkalaemia, acidosis, myoglobinuria, renal injury, bleeding and recurrent loss of pulses.
Search for the source—atrial fibrillation, ventricular thrombus, valve disease, endocarditis, aneurysm or aortic plaque—and prevent recurrence.

14. Embolic stroke, mesenteric and special emergencies

Stroke: use FAST, record last-known-well, check glucose, keep nil by mouth, activate stroke imaging and do not give aspirin or anticoagulant until haemorrhage and eligibility have been assessed.
Mesenteric ischaemia: severe abdominal pain with atrial fibrillation or vascular disease is an emergency; keep nil by mouth, resuscitate, provide analgesia, obtain lactate/imaging and call surgery.
Fat embolism syndrome: stabilise airway and oxygenation, immobilise fractures, monitor neurological status and seek orthopaedic/critical-care advice.
Air embolism: stop the source, call resuscitation support, give high-concentration oxygen when indicated, position and manage according to specialist protocol.
Septic embolus: obtain cultures where this does not delay treatment, begin prescribed antibiotics, assess for endocarditis and involve infectious-disease/cardiology teams.
Pregnancy/postpartum: use a multidisciplinary team; select imaging and anticoagulant strategies that protect mother and fetus, and never dismiss PE because dyspnoea is common in pregnancy.
Cancer-associated thrombosis: balance recurrence and bleeding, consider tumour site, platelet count, renal function and drug interactions; coordinate oncology care.

15. Anticoagulants, thrombolytics and safety monitoring

Medicine or group	Purpose	Safety checks and nursing care
Unfractionated heparin	Rapid anticoagulation with short half-life; useful around procedures or severe renal impairment.	Check weight, aPTT/anti-Xa protocol, platelets, bleeding, infusion pump and reversal plan.
Low-molecular-weight heparin	Predictable anticoagulation for VTE, pregnancy and selected cancer patients.	Check renal function, weight, injection technique, platelet trend and bruising; do not rub injection site.
Direct oral anticoagulants	Oral factor Xa or thrombin inhibition for selected DVT/PE.	Check indication, renal/liver function, interactions, adherence, missed-dose advice and bleeding signs.
Warfarin or another vitamin K antagonist	Long-term anticoagulation when selected, including some mechanical valves.	INR monitoring, consistent vitamin-K intake, interaction and pregnancy counselling; bridge as prescribed.
Systemic thrombolytic	Rapid clot lysis for selected high-risk PE, stroke or limb-threatening cases.	Screen for intracranial haemorrhage, recent surgery/trauma, uncontrolled BP, bleeding and aortic dissection; monitor neurological and access-site bleeding.
Antiplatelet therapy	Important in arterial thrombosis and atherosclerotic embolic disease.	Assess allergy, gastrointestinal or intracranial bleeding, platelet count and concurrent anticoagulants.
Protamine, vitamin K, PCC or specific antidotes	Reverse selected anticoagulants during life-threatening bleeding or urgent procedures.	Use only under senior protocol; document agent, dose, response and repeat coagulation tests.

Bleeding safety: Check gums, urine, stool, vomit, skin, puncture sites, headache, back pain, weakness and falling BP. Report suspected intracranial or internal bleeding immediately. Never stop anticoagulation independently; obtain urgent clinician review.

16. Nursing management and monitoring

16.1 Priority assessment

Trend airway, respiratory effort, oxygen saturation, respiratory rate, pulse, rhythm, BP, temperature, consciousness and urine output.
For DVT, measure and compare limb circumference, swelling, warmth, colour, pain, sensation and distal pulses.
For PE, assess chest pain, dyspnoea, haemoptysis, syncope, JVP, signs of RV failure and response to oxygen.
For arterial ischaemia, repeat the six Ps and Doppler pulses at prescribed intervals; report any loss of movement or sensation.
Review anticoagulant dose, last administration, renal function, haemoglobin, platelets, coagulation results, allergies and interactions.

16.2 Interventions and rationales

Intervention	Rationale and practical action
Maintain monitored rest during instability	Reduces oxygen demand and detects PE shock, arrhythmia or worsening ischaemia early; mobilise only when safe.
Administer medicines using the rights of administration	Verify patient, medicine, dose, route, time, indication, allergies, renal function, contraindications and response.
Prevent pressure injury and venous stasis	Reposition, hydrate appropriately, encourage prescribed movement and use mechanical prophylaxis correctly.
Protect a threatened limb	Keep dependent and warm, avoid tight dressings or direct heat, preserve skin and prepare for vascular intervention.
Watch for bleeding	Inspect access sites and body fluids, minimise unnecessary punctures, apply prolonged pressure and escalate early.
Communicate deterioration with SBAR	State onset, six-P/ABCDE findings, observations, anticoagulant history, test results and the response required.
Support psychological needs	Explain why monitoring and anticoagulation are necessary, address fear of death or bleeding, and use teach-back.
Prepare safe transfer	Send ECG, imaging, laboratory values, medicine chart, allergies, onset time, oxygen requirement and escalation contacts.

17. Prevention of thrombosis and recurrence

Complete a VTE risk and bleeding assessment on admission and after surgery, delivery, trauma, transfer or clinical deterioration.
Use early mobilisation, leg exercises, hydration appropriate to condition and avoidance of prolonged uninterrupted sitting.
Apply prescribed intermittent pneumatic compression or graduated stockings only after checking arterial circulation, skin integrity and fit.
Administer pharmacological prophylaxis on time unless contraindicated; document omitted doses and escalate.
Teach travel measures: move calves, walk when safe, hydrate and seek advice for previous VTE or major risk factors.
Address smoking, obesity, uncontrolled diabetes, hypertension, cancer care, contraception and adherence to anticoagulation.
Plan follow-up for recurrent symptoms, post-PE breathlessness, pulmonary hypertension, post-thrombotic syndrome, renal function and duration of therapy.

18. Complications

Complication	Clues	Priority response
Obstructive shock or cardiac arrest from PE	Hypotension, syncope, severe hypoxaemia, pulselessness or PEA.	Resuscitation, oxygen/ventilation, urgent senior help and reperfusion evaluation.
Recurrent or progressive VTE	New dyspnoea, chest pain, swelling or rising oxygen need.	Repeat ABCDE, imaging and adherence/medicine review.
Major anticoagulant bleeding	Haematemesis, melaena, haematuria, severe headache, fall in BP or falling haemoglobin.	Stop further doses only under emergency protocol, resuscitate, reverse when indicated and locate source.
Post-thrombotic syndrome	Chronic swelling, heaviness, skin changes or venous ulcer after DVT.	Compression and vascular review after arterial assessment; skin and mobility care.
Chronic thromboembolic pulmonary hypertension	Persistent exertional dyspnoea, fatigue, reduced exercise tolerance months after PE.	Follow-up echocardiography and specialist pulmonary vascular referral.
Acute limb necrosis, compartment syndrome or renal injury	Persistent pain, paralysis, tense swelling, dark urine, oliguria, hyperkalaemia or acidosis after ischaemia/reperfusion.	Emergency vascular/critical-care review, pressure assessment and renal/electrolyte management.
Embolic stroke or organ infarction	Focal neurological deficit, abdominal pain, renal infarct or splenic pain.	Activate the relevant stroke, surgical or medical emergency pathway.

19. Discharge, education and safety-netting

Explain whether the event was provoked, unprovoked, venous or arterial and how long therapy is planned.
Use teach-back for dose, timing, missed-dose instructions, interactions, pregnancy advice, travel and follow-up blood tests.
Give written warning signs: sudden breathlessness, chest pain, coughing blood, fainting, new limb swelling/coldness/weakness, severe headache, black stool, blood in urine or uncontrolled bleeding.
Tell the patient to carry an anticoagulant card or medicine list and inform clinicians before procedures, dental work or new medicines.
Encourage safe mobility and hydration; avoid contact injury and over-the-counter NSAIDs unless approved.
Arrange review for anticoagulant monitoring, malignancy or thrombophilia assessment when appropriate, and persistent breathlessness or post-thrombotic symptoms.

20. Worked clinical scenarios

Scenario 1: Postoperative DVT with possible PE

A 58-year-old becomes breathless and tachycardic three days after hip surgery. One calf is swollen. The nurse stops mobilisation, performs ABCDE, gives titrated oxygen for hypoxaemia, attaches ECG monitoring, obtains IV access, calls the emergency team and reports the operation, prophylaxis doses and onset. The patient is transferred for urgent imaging; the nurse does not massage the calf.

Scenario 2: High-risk PE

A patient with cancer has sudden dyspnoea, syncope, BP 78/45 mmHg and cool skin. The team recognises obstructive shock, calls critical care, supports oxygenation, obtains bedside echo and prepares anticoagulation and reperfusion assessment. Repeated large unmonitored fluid boluses are avoided because RV failure may worsen.

Scenario 3: Acute limb ischaemia

A patient with atrial fibrillation develops abrupt severe left-leg pain, pallor, coldness, numb toes and absent pedal pulses. The nurse documents the six Ps and onset, keeps the limb dependent and warm, keeps the patient nil by mouth, gives prescribed analgesia, establishes IV access and calls vascular surgery immediately. Imaging does not delay limb-saving review.

Scenario 4: Anticoagulant bleeding

A patient taking anticoagulation reports severe headache and becomes confused after a fall. The nurse treats this as possible intracranial bleeding, performs ABCDE and glucose assessment, calls emergency support, avoids further unapproved doses, checks the medicine and last-dose time, and prepares urgent neuroimaging and reversal according to protocol.

CLOT-PE
C – Check circulation, six Ps and chest symptoms · L – Look for risk factors and last-known-well/onset · O – Oxygen and ABCDE, not routine high-flow oxygen · T – Tests: Wells, D-dimer, ultrasound, CTPA and ECG · P – Protect from bleeding and mobilise safely · E – Escalate early for shock, stroke or threatened limb.

21. Examination and revision questions

Define thrombosis, embolism, thromboembolism, DVT and PE.
Explain Virchow’s triad with one clinical example for each component.
List at least eight risk factors for VTE and identify which are modifiable.
Describe typical and atypical features of DVT and PE.
What are the six Ps of acute limb ischaemia, and why is motor loss especially urgent?
Explain how a DVT travels to become a PE and causes right-ventricular failure.
Compare the roles and limitations of Wells score, D-dimer, compression ultrasound and CTPA.
Outline first aid and ABCDE for a patient with suspected PE.
Compare management of low-risk, intermediate-risk and high-risk PE.
State the nursing checks before and after heparin, DOACs and thrombolysis.
Describe the immediate nursing actions for acute limb ischaemia.
List major bleeding and recurrent VTE warning signs for discharge teaching.

Key takeaways

VTE includes DVT and PE; PE can occur without leg symptoms and can rapidly cause obstructive shock.
Virchow’s triad—stasis, vessel injury and hypercoagulability—guides prevention and risk assessment.
Sudden dyspnoea, syncope, hypotension, a cold pulseless limb or focal neurological deficit demands immediate escalation.
Use validated probability tools and imaging; D-dimer is a rule-out aid in selected low-probability patients, not a stand-alone diagnosis.
Anticoagulants prevent extension and recurrence; thrombolysis or embolectomy is reserved for selected life-threatening or limb-threatening events.
Safe nursing care combines ABCDE, serial observations, six-P assessment, medicine and bleeding surveillance, communication and prevention.

Suggested references

National Institute for Health and Care Excellence (NICE). Venous thromboembolic diseases: diagnosis, management and thrombophilia testing (NG158).
European Society of Cardiology/European Respiratory Society. 2019 Guidelines on acute pulmonary embolism: diagnosis and management.
Centers for Disease Control and Prevention. About venous thromboembolism and blood-clot symptoms.
CDC Yellow Book. Deep vein thrombosis and pulmonary embolism: clinical presentation and prevention.
World Health Organization. Cardiovascular diseases, including DVT and pulmonary embolism.
Use current Uganda Ministry of Health, ambulance, emergency-department, stroke, vascular and anticoagulation protocols for local referral, medicine availability and treatment targets.