Definition

Thromboembolism happens when a blood clot (thrombus) forms in a blood vessel or the heart, breaks free, and moves through the circulation until it blocks a distant vessel, resulting in reduced or interrupted blood flow and causing ischemia or infarction.

Description

In the U.S., venous thromboembolism (VTE) is the most commonly discussed subtype, including deep vein thrombosis (DVT) and pulmonary embolism (PE). Though less frequent, arterial thromboembolism plays a crucial role in causing ischemic stroke, myocardial infarction, and peripheral arterial occlusion.

Classification of Thromboembolism

• Based on the Involvement of the Circulatory System
  • Venous Thromboembolism (VTE):
  • Deep Vein Thrombosis (DVT): the formation of a blood clot in the deep veins, typically in the legs or pelvis.
  • Pulmonary Embolism (PE): an embolus moves to the pulmonary arteries, blocking blood flow to the lungs.
  • Arterial Thromboembolism:
  • Cerebral thromboembolism leads to ischemic stroke.
  • Coronary thromboembolism leads to myocardial infarction.
  • Peripheral arterial thromboembolism leads to acute limb ischemia.
• Derived from the Origin
  • Distant thromboembolism happens when a clot develops somewhere else, like in a leg vein, and then travels to the lungs.
• According to the Clinical Course
  • Acute thromboembolism: sudden onset, often life-threatening (e.g., PE, ischemic stroke)
  • Chronic/recurrent thromboembolism: persistent or recurrent events, often requiring long-term anticoagulation.
• Special Subtypes
  • Septic thromboembolism: a clot that contains infectious material, such as from endocarditis or IV drug use.

Epidemiology

Incidence/Prevalence

• Venous thromboembolism (VTE) affects about 1–2 in every 1,000 individuals each year, rendering it a common cardiovascular condition.
• The lifetime risk of VTE is approximately 5%, and there is a 20–30% chance of recurrence within 10 years.

Age

• The likelihood of VTE rises significantly with age, especially after 60 years.
• Pediatric VTE is uncommon but becoming more frequent in hospitalized children, particularly those with central venous catheters.

Gender

• Men experience a slightly higher incidence and recurrence of VTE after middle age.
• Women of reproductive age face higher risks from pregnancy, oral contraceptives, and hormone therapy.

Race

• The incidence of VTE is higher among African Americans than among Whites.
• Asian Americans and Hispanics show a lower incidence.

Risk factors

• General
  • Cancer (especially pancreatic, liver, lung).
  • Major surgery (orthopedic, pelvic, abdominal).
  • Trauma or fractures.
  • Prolonged immobility (bed rest, long travel).
  • Pregnancy and postpartum period.
  • Oral contraceptives or hormone therapy.
  • Obesity (BMI >30).
  • Smoking.
  • Central venous catheter use.
  • COVID-19 or other pro-inflammatory infections.
  • Chronic inflammatory diseases such as IBD and lupus.
  • Nephrotic syndrome.
  • Varicose veins.
  • Family history of VTE.
• Physiological
  • Hypercoagulability (Virchow’s triad component)
    • Inherited thrombophilias (e.g., Factor V Leiden, prothrombin mutation).
    • Elevated clotting factors (e.g., fibrinogen, Factor VIII).
    • Antiphospholipid antibody syndrome.
  • Venous stasis
    • Reduced venous return caused by immobility, heart failure, or paralysis
    • Compression from tumors or pregnancy.
  • Endothelial injury
    • Surgery, trauma, central lines.
    • Inflammation (e.g., sepsis, vasculitis).
  • Hormonal influences
    • Estrogen promotes the production of clotting factors.
    • Testosterone therapy (less common).
  • Hemodynamic changes
    • Dehydration leads to increased blood viscosity.
    • Hypoxia leads to endothelial dysfunction.
  • Blood composition changes
    • Elevated platelets (thrombocytosis).
    • Polycythemia vera.
    • Hyperhomocysteinemia.

Etiology

• Hypercoagulability (blood that is more prone to forming clots).
  • Inherited thrombophilias: Factor V Leiden mutation, Prothrombin G20210A mutation, Protein C and S deficiencies, Antithrombin III deficiency.
  • Acquired conditions include cancer, pregnancy, use of oral contraceptives, hormone replacement therapy, antiphospholipid antibody syndrome, obesity, and smoking.
  • Medical conditions include sepsis, nephrotic syndrome, inflammatory bowel disease, and COVID-19-associated coagulopathy.
• Endothelial Injury (damage to the vessel lining)
  • Trauma and fractures.
  • Surgery, particularly orthopedic and pelvic procedures.
  • Indwelling catheters or central lines.
  • Atherosclerosis or other vascular diseases.
• Venous Stasis (sluggish or reduced blood flow)
  • Prolonged periods of immobility, such as long flights, bed rest, hospitalization, or recovery after surgery.
  • Heart failure.
  • Paralysis or damage to the spinal cord.
  • Varicose veins or chronic venous insufficiency.
• Pathophysiology
  • Thrombus Formation
    • An imbalance between procoagulant and anticoagulant mechanisms initiates thrombus formation.
    • Venous thrombi are usually composed of fibrin with entrapped red blood cells, often called "red clots."
    • Arterial thrombi are primarily composed of platelets, often called “white clots,” resulting from high shear stress at the locations of atherosclerotic plaque rupture.
  • Embolization
    • A portion of the thrombus could break loose and move through the bloodstream.
    • Venous clots usually travel to the pulmonary arteries, leading to pulmonary embolism (PE).
    • Arterial thrombi or emboli can migrate to the brain (causing ischemic stroke), heart (leading to myocardial infarction), or limbs (resulting in acute limb ischemia).
  • Obstruction and Ischemia
    • An embolus gets stuck in a vessel that is too small for it to pass through.
    • This causes ischemia, hypoxia, and tissue infarction downstream of the blockage.
  • Systemic Effects
    • In PE: Increased pulmonary vascular resistance leads to right ventricular strain, hypoxemia, and hemodynamic collapse during massive PE.
    • In a stroke, focal neurological deficits arise from decreased blood flow to the brain. In MI: Myocardial necrosis caused by coronary blockage.

History

• Chief Complaint
  • DVT (Deep Vein Thrombosis):
    • Pain in the leg, along with swelling, redness, and warmth.
    • Usually affects one side, typically in the calf or thigh.
  • Pulmonary Embolism (PE):
    • Sudden onset of shortness of breath, pleuritic chest pain, cough (which may include hemoptysis), tachycardia, and syncope.
  • Arterial Thromboembolism (including Stroke, MI, and Limb Ischemia):
    • Sudden neurological symptoms such as weakness, facial droop, or aphasia.
    • Chest pain or pressure, radiating to the arm or jaw (MI).
    • Sudden limb pain, pallor, and pulselessness indicate acute limb ischemia.
• History of Present Illness (HPI)
  • Provoking factors include recent surgery, trauma, immobilization, pregnancy, and long flights.
  • Associated symptoms: DVT—heaviness and functional limitation; PE—dizziness, syncope, anxiety; Stroke—visual disturbances and confusion.
• Past Medical History
  • History of previous VTE, stroke, or MI.
  • Known thrombophilia conditions include Factor V Leiden, prothrombin mutation, and antiphospholipid syndrome.
  • Active cancer is a significant risk factor for malignancy.
  • Recent surgery, hospitalization, trauma, or fractures.
  • Chronic conditions include heart failure, COPD, inflammatory bowel disease, and obesity.
• Medication History
  • Use of oral contraceptives, hormone replacement therapy, or tamoxifen.
  • Anticoagulant or antiplatelet therapy (including adherence and recent discontinuation).
  • Chemotherapy or immunotherapy for cancer.

Physical findings on examination

• Unilateral leg swelling (most common).
• Calf tenderness or pain, especially when pressed on (palpation).
• Increased warmth in the affected limb.
• Erythema or dusky discoloration.
• Pitting edema (localized).
• Palpable cord (thrombosed vein).
• Dilated superficial collateral veins.
• Cyanosis (in extensive DVT).
• Low-grade fever (subfebrile, nonspecific).
• Tachypnea (most consistent finding).
• Tachycardia.
• Hypoxia (SpO₂ < 90%).
• Pleuritic chest pain.
• Hemoptysis (in infarction).
• Accentuated P2 (pulmonary valve closure).
• Jugular venous distension in massive PE.
• Hypotension or shock in massive or submassive PE.
• RV heave or gallop (suggests strain).

Laboratory Tests

• D-Dimer
  • Elevated during active clot formation and breakdown.
  • High sensitivity, low specificity.
  • Useful for ruling out VTE in low-risk patients.
  • Age-adjusted cutoff: Age (years) × 10 µg/L (for patients >50).
• CBC with Platelets
  • Baseline for anticoagulation safety.
  • Detects thrombocytopenia (e.g., HIT risk).
• PT/INR
  • Required for warfarin monitoring.
  • Target INR: 2.0–3.0 for most VTE cases.
• aPTT
  • Used to monitor unfractionated heparin.
  • Not required for LMWH or DOACs.
• Creatinine & eGFR
  • Assess renal function before initiating DOAC or LMWH.
  • Dose adjustment required in renal impairment.
• Liver Function Tests (LFTs)
  • Baseline for DOAC safety (e.g., apixaban, rivaroxaban).
• Troponin & BNP (in PE)
  • Elevated in submassive/massive PE.
  • Indicates RV strain and poorer prognosis.
• Anti-Xa Level (select cases)
  • Used in LMWH monitoring for obesity, pregnancy, or renal dysfunction.
  • Not routinely recommended.
• Thrombophilia Panel (select cases)
  • Factor V Leiden, Protein C/S deficiency, Antithrombin III.
  • Indicated in cases of unprovoked or recurrent VTE, young patients, or those with a family history.
• Lupus Anticoagulant & Antiphospholipid Antibodies
  • For autoimmune-related thrombosis.
  • Consider recurrent miscarriage or arterial events.

Diagnostic Tests

• Diagnostic Imaging tests
  • Compression duplex ultrasonography used for DVT diagnosi.
  • CT pulmonary angiography (CTPA) used for PE diagnosis.
  • V/Q scan used for PE when CTPA contraindicated.
  • Venography/MR venography (less common).

Differential Diagnosis

• For Deep Vein Thrombosis (DVT):
  • Cellulitis – redness, warmth, and systemic symptoms.
  • Baker’s cyst – posterior knee swelling, ultrasound helps differentiate.
  • Muscle strain or tear – localized pain without venous involvement.
  • Venous insufficiency – chronic edema, skin changes.
  • Lymphedema – non-pitting, bilateral, painless swelling.
  • Superficial thrombophlebitis – palpable cord and localized tenderness.
  • Compartment syndrome – sudden pain and neurovascular issues.
  • Popliteal vein aneurysm – rare, mimics DVT.
• For Pulmonary Embolism (PE):
  • Acute coronary syndrome – chest pain, ECG changes, elevated troponin.
  • Pneumonia – fever, cough, infiltrates on imaging.
  • COPD exacerbation – wheezing, hyperinflation, and known history.
  • Pericarditis – positional chest pain, friction rub.
  • Aortic dissection – tearing pain, pulse deficit.
  • Pneumothorax – sudden shortness of breath, absent breath sounds.
  • Anxiety or panic attack – hyperventilation, routine imaging.
  • Heart failure – bilateral crackles, elevated BNP.
• For Cerebral Embolism (Stroke):
  • Hypoglycemia – altered mental status, reversible with glucose.
  • Seizure or post-ictal state – temporary deficits and EEG findings.
  • Migraine with aura – visual or sensory symptoms, gradual onset.
  • Bell’s palsy – isolated facial weakness, no limb involvement.
  • Brain tumor – progressive symptoms confirmed by imaging.
  • TIA – transient symptoms <24 hours, no infarct on imaging.

General treatment items

• Unfractionated Heparin (UFH) – IV; rapid onset and reversible.
• Low Molecular Weight Heparin (LMWH) – e.g., enoxaparin; subcutaneous.
• Direct Oral Anticoagulants (DOACs) – apixaban, rivaroxaban, dabigatran, edoxaban.
• Warfarin – requires INR monitoring; used for long-term therapy or in special populations.

Surgical Interventions

• Surgical thrombectomy – for large proximal clots.
• Catheter-based clot retrieval – in select PE cases.
• Venous interruption procedures – seldom performed.

Adjunctive Therapies

• Oxygen therapy – for hypoxia in PE.
• IV fluids – for hypotension or shock.
• Analgesics – for pleuritic chest pain
• Compression stockings – to prevent post-thrombotic syndrome.
• IVC filter – when contraindicated for anticoagulation or in cases of recurrent PE.

Medications indicated with specific doses

Toxoids

• Not applicable

Immunoglobulins

• Not applicable

Vasodilators

• Vasodilators are used mainly for pulmonary embolism (PE) with pulmonary hypertension or right ventricular strain, and for chronic thromboembolic pulmonary hypertension (CTEPH). They don't treat clots, but lower pulmonary vascular resistance and relieve symptoms.
• Pulmonary Vasodilators Used in CTEPH Following PE.
• Riociguat (Adempas)
  • Class: Pulmonary vasodilator that stimulates soluble guanylate cyclase.
  • FDA-approved in the U.S. for CTEPH that is inoperable or persists after pulmonary endarterectomy.
  • Start with a dose of 1 mg taken orally three times a day, and increase by 0.5 mg every 2 weeks as needed, up to a maximum of 2.5 mg three times daily based on blood pressure tolerance.
• Sildenafil (Revatio, Viagra)
  • Class: PDE-5 inhibitor that induces pulmonary vasodilation.
  • Sometimes used off-label for pulmonary hypertension following thromboembolism.
  • Dose (for pulmonary arterial hypertension): 20 mg taken orally three times a day.
• Treprostinil (Remodulin, Tyvaso) / Epoprostenol (Flolan, Veletri)
  • Prostacyclin analogues are potent vasodilators for the pulmonary arteries.
  • Used in cases of advanced pulmonary hypertension, occasionally in CTEPH patients who cannot undergo surgery.
  • Inhaled dose of Treprostinil: Begin with 18 mcg (3 breaths) four times a day, and adjust as tolerated.
  • Epoprostenol IV infusion: Start at two ng/kg/min, and increase gradually as tolerated.

Thrombolytic agents

• Alteplase (tPA – Tissue Plasminogen Activator)
  • FDA-approved for: pulmonary embolism (massive or high-risk PE with hemodynamic instability), ischemic stroke, and ST-elevation myocardial infarction.
  • Dosage for Pulmonary Embolism:
    • Administer 100 mg IV over 2 hours (standard dose).
    • Some protocols recommend 0.6 mg/kg IV over 15 minutes (maximum 50 mg) for patients with a high bleeding risk.
  • Dose for Ischemic Stroke (administer within 3–4.5 hours of symptom onset):
    • 0.9 mg/kg IV (maximum 90 mg):
    • 10% administered as an IV bolus over one minute.
    • 90% administered as a continuous infusion over 60 minutes.
  • Dose for STEMI:
    • Administer a 15 mg IV bolus, followed by 0.75 mg/kg over 30 minutes (up to 50 mg), then 0.5 mg/kg over 60 minutes (up to 35 mg); totaling 100 mg within 90 minutes.
• Tenecteplase (TNK-tPA)
  • FDA-approved for: Acute MI.
  • Gaining more attention for use in stroke and PE (not yet FDA-approved in the U.S., but off-label use occurs in some centers).
  • Dose for STEMI (single IV bolus over 5 sec):
  • <60 kg → 30 mg
  • 60–69 kg → 35 mg
  • 70–79 kg → 40 mg
  • 80–89 kg → 45 mg
  • ≥90 kg → 50 mg
• Reteplase (rPA)
  • FDA-approved for: Acute MI.
  • Not usually used for PE in U.S. clinical practice.
  • Dose for STEMI:
  • Administer 10 units IV as a bolus, then repeat with another 10 units IV bolus after 30 minutes, each over 2 minutes.

Dietary or Activity restrictions

• Vitamin K Intake:
  • Avoid significant fluctuations in foods high in vitamin K, such as spinach, kale, and broccoli.
  • Maintain consistent intake if on warfarin to stabilize INR.
• Hydration:
  • Encourage sufficient fluid intake to prevent hemoconcentration and clot formation.
• Supplements:
  • Avoid high-dose vitamin E, fish oil, or herbal supplements (e.g., ginkgo, garlic, ginger) without provider approval—they may increase bleeding risk.
• During Acute Phase (DVT/PE diagnosis):
  • Avoid strenuous activity until stabilized.
  • Elevate the affected limb (for DVT) to reduce swelling.
• Post-Stabilization:
  • Encourage early walking to boost venous blood flow.
  • Avoid prolonged sitting or immobility (e.g., >2 hours without movement)
  • Resume moderate aerobic activity (e.g., walking, swimming) once cleared
  • Avoid contact sports or high-risk activities while on anticoagulants.
• Travel Precautions:
  • For flights >4 hours: walk periodically, stay hydrated, consider compression stockings.
• Compression Therapy:
  • Graduated compression stockings may be used for symptom relief in selected patients to aid DVT recovery and prevent PTS.

Disposition

Admission Criteria

• Hemodynamic Instability
  • Systolic BP < 100 mmHg or signs of shock
  • Tachycardia > 110 bpm with hypoxia (SpO₂ < 90%)
• Respiratory Compromise
  • Dyspnea at rest or exertion.
  • Respiratory rate > 30/min.
  • Need for supplemental oxygen.
• Comorbidities Requiring Inpatient Care
  • Active malignancy with complications.
  • Renal or hepatic failure.
  • Recent surgery or trauma.
  • Pregnancy or postpartum state.
• Bleeding Risk or Anticoagulation Contraindication
  • Active bleeding or high HAS-BLED score.
  • Platelet count < 50,000/µL.
• Social or Logistical Barriers
  • Inadequate home support or follow-up.
  • Cognitive impairment or poor medication adherence.
  • No access to outpatient anticoagulation services.
• Special Populations
  • VTE with suspected HIT (Heparin-Induced Thrombocytopenia).
  • Recurrent VTE despite anticoagulation.

Discharge criteria

• Clinical Stability
  • Hemodynamically stable (SBP ≥ 100 mmHg, HR < 110 bpm).
  • Oxygen saturation ≥ 90% on room air.
  • No signs of active bleeding or new thrombus detected.
• Adequate Anticoagulation Plan
  • Anticoagulant initiated and tolerated (e.g., DOAC, LMWH, warfarin).
  • INR in therapeutic range if on warfarin.
  • No contraindications for outpatient anticoagulation.
• Low Risk of Complications
  • PESI score class I–II or Hestia criteria met.
  • No RV strain or significant clot burden seen on imaging.
  • No high-risk comorbidities requiring inpatient care.
• Follow-Up Arranged
  • PCP or anticoagulation clinic appointment within 7 to 14 days.
  • Lab monitoring plan (e.g., INR, renal function).
  • Imaging follow-up if indicated (e.g., repeat ultrasound or echo).

Monitoring

• Clinical Monitoring:
  • Vital signs: BP, HR, RR, O2 saturation (especially in PE).
  • Signs of bleeding: bruising, hematuria, melena, and neurological changes.
  • Limb circumference and tenderness (for DVT).
  • Dyspnea, chest pain, syncope (for PE recurrence).
• Laboratory Monitoring:
  • CBC with platelets – baseline and periodic testing (bleeding risk).
  • PT/INR – for warfarin (target INR 2.0–3.0).
  • Anti-Xa levels are not usually recommended but might be considered for obesity, pregnancy, renal impairment, or extreme body weight.
  • Creatinine – assess renal clearance for DOAC/LMWH dosing.
• Imaging Follow-up:
  • Use compression ultrasound only if symptoms persist or worsen.
  • CT pulmonary angiography – for suspected recurrent PE.
  • Echocardiography – assess RV strain in submassive and massive PE.
• Anticoagulation Monitoring:
  • DOACs – do not require routine lab monitoring; check adherence and renal function.
  • Warfarin – home INR testing is optional for stable patients.
• Duration & Follow-up:
  • Initial VTE: 3–6 months anticoagulation
  • Unprovoked or chronic risk: consider indefinite therapy.
  • Reassess bleeding risk and recurrence risk every 3 to 6 months.

Patient Education

• Goals: Understand what a blood clot (thromboembolism) is and how it impacts health.
• Prevent recurrence by recognizing and reducing risk factors for new clots.
• Ensure medication safety: Assist the patient in using prescribed anticoagulants correctly.
• General education: Promote early detection by teaching how to recognize warning signs of clotting or bleeding complications.
• Encourage a safe and active recovery along with lifestyle adjustments.
• Assist in keeping a regular dosing schedule.
• Action Plan for Patients and Families:
• Schedule consistent follow-up visits with your healthcare provider.
• Inquire about early mobilization and the utilization of compression devices.
• Comprehend the use of prophylactic anticoagulants before discharge.

Complications

• Pulmonary Embolism (PE)
  • Acute respiratory failure.
  • Right ventricular strain or failure.
  • Hypoxia-caused organ damage.
  • Sudden death (especially massive PE).
• Post-Thrombotic Syndrome (PTS)
  • Chronic limb pain, swelling, and heaviness.
  • Skin discoloration, venous eczema.
  • Venous ulcers (severe cases).
  • Occurs in ~20–50% of DVT cases.
• Chronic Thromboembolic Pulmonary Hypertension (CTEPH)
  • Progressive shortness of breath, fatigue, and right ventricular dysfunction.
  • Occurs in ~4% of PE survivors.
• Recurrent VTE
  • ~30% recurrence risk after initial episode.
  • Higher in malignancy, thrombophilia, or unprovoked VTE.
• Bleeding (from anticoagulation)
  • GI, intracranial, or retroperitoneal hemorrhage.
  • Risk increases with age, renal impairment, and polypharmacy.
• Embolic Stroke
  • If the thrombus travels to the cerebral circulation.
  • May cause permanent neurological deficits.
• Pregnancy Complications
  • Maternal morbidity/mortality.
  • Fetal loss (in untreated or massive PE).
• Disability & Reduced Quality of Life
  • Chronic pain, fatigue, reduced mobility.
  • Psychological distress (anxiety, fear of recurrence).

Prevention

• Pharmacologic Prophylaxis:
  • Low molecular weight heparin (LMWH) – preferred for cancer, pregnancy, and post-surgery.
  • Unfractionated heparin (UFH) – alternative in renal impairment.
  • DOACs (e.g., apixaban, rivaroxaban) – used for VTE prophylaxis and treatment in selected patients; use with caution in active cancer with high bleeding risk.
  • Aspirin – limited role; may reduce recurrence in select low-risk patients.
• Mechanical Prophylaxis:
  • Intermittent pneumatic compression (IPC) devices.
  • Graduated compression stockings (GCS).
• Lifestyle & Behavioral Measures:
  • Early ambulation post-surgery or hospitalization.
  • Hydration and mobility during long travel.
  • Smoking cessation, weight loss, and physical activity.
  • Avoid using estrogen-containing medications in high-risk individuals.
• Risk-Based Protocols:
  • Use validated risk assessment tools (Padua or Caprini scores) to guide prophylaxis decisions.
  • Reevaluate VTE risk and bleeding risk every 24–48 hours in hospital settings.
  • Tailor prophylaxis based on individual risk factors (e.g., cancer, pregnancy, surgery).

Prognosis

• Overall mortality: ~10–30% for untreated PE; <5% with prompt anticoagulation.
• Recurrence risk: ~10% at 1 year; ~25–30% at 5 years without long-term prophylaxis.
• Cancer-associated VTE: 2nd leading cause of death in malignancy; poorer prognosis.
• Post-thrombotic syndrome (PTS): Happens in about 20–50% of DVT cases; causes chronic pain and edema.
• Chronic thromboembolic pulmonary hypertension (CTEPH): ~4% of PE survivors.
• Pregnancy-related VTE: High maternal morbidity; prognosis improves with LMWH treatment.
• Long-term anticoagulation: Decreases recurrence but raises bleeding risk; needs risk-benefit assessment.

Associated conditions

• Malignancy (e.g., pancreatic, lung, gastrointestinal, hematologic).
• Recent surgery or trauma, primarily orthopedic or abdominal.
• Prolonged immobilization (e.g., hospitalization, long flights).
• Pregnancy and postpartum state.
• Hormonal therapy (e.g., oral contraceptives, HRT).
• Obesity and metabolic syndrome.
• Heart failure and atrial fibrillation.
• COVID-19 and other systemic infections.
• Autoimmune disorders (e.g., antiphospholipid syndrome, lupus).
• Inherited thrombophilias (e.g., Factor V Leiden, Protein C/S deficiency).
• Nephrotic syndrome.
• Inflammatory bowel disease (Crohn’s disease, ulcerative colitis).
• Chronic kidney disease.
• Smoking and a sedentary lifestyle.

Synonyms

• Embolic occlusion
• Thrombotic embolism
• Venous thromboembolism (VTE)
• VTE (Venous thromboembolism)

ICD-10-CM

• I26.99 - Other pulmonary embolism without acute cor pulmonale.
• I74.8 - Embolism and thrombosis of other arteries.
• I82.90 - Acute embolism and thrombosis of unspecified vein.
• I63.4 - Cerebral embolism (cerebral infarction due to embolism).

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