Heart failure with reduced ejection fraction (HFrEF)

A 68-year-old male with hypertension, type 2 diabetes mellitus, and coronary artery disease presents with progressive dyspnea for 2 weeks. He reports fatigue, orthopnea, paroxysmal nocturnal dyspnea, bilateral lower extremity edema, and recent weight gain. Examination reveals elevated jugular venous pressure, bilateral pitting edema, diffuse pulmonary crackles, a displaced apical impulse, and an S3 gallop. Chest X-ray shows cardiomegaly, pulmonary congestion, and bilateral pleural effusions. BNP and NT-proBNP are elevated, with worsening renal function and hyponatremia. Echocardiography demonstrates a dilated left ventricle, global hypokinesis, and LVEF 35%. Diagnosis?

Diagnosis is Decompensated heart failure with reduced ejection fraction (HFrEF), with pulmonary and systemic congestion.

Known coronary artery disease makes an ischemic etiology an important consideration, but global hypokinesis alone does not establish ischemic cardiomyopathy.

1. Definition

Heart failure is a clinical syndrome characterized by typical symptoms and signs associated with structural or functional cardiac abnormalities, supported by laboratory or imaging evidence of pulmonary or systemic congestion or abnormal cardiac output.

This patient has:

1.      Pulmonary congestion: dyspnea, orthopnea, PND, crackles, and pleural effusions

2.      Systemic congestion: elevated JVP, peripheral edema, and weight gain

3.      LV systolic dysfunction: LV dilation, global hypokinesis, and LVEF 35%

The diagnosis is based on the overall clinical syndrome, not on EF, BNP, or any single test alone.

2. Ejection Fraction Classification

EF terminology is evolving.

1.      2026 ESC guideline: HFrEF is defined as LVEF <50%

2.      2026 Second Universal Definition: emphasizes reduced, preserved, and improved EF phenotypes rather than a single rigid numerical cutoff

In this patient, LVEF 35% is unequivocally reduced.

The 2026 ESC guideline also uses the term decompensated heart failure because clinical deterioration may occur gradually or rapidly.

3. Etiology

Important causes of HFrEF include:

1.      Ischemic heart disease

2.      Chronic hypertension

3.      Dilated or genetic cardiomyopathy

4.      Valvular heart disease

5.      Tachyarrhythmia-mediated cardiomyopathy

6.      Myocarditis

7.      Alcohol, cocaine, or cardiotoxic drugs

8.      Infiltrative or storage disorders

In this patient, coronary artery disease and hypertension are the leading etiologic considerations.

Further ischemic evaluation should depend on symptoms, ECG and troponin findings, prior coronary anatomy, and whether revascularization would alter management.

4. Pathophysiology

Reduced LV contractility → reduced stroke volume and cardiac output → neurohormonal activation

Major compensatory mechanisms include:

1.      RAAS activation → vasoconstriction and sodium retention

2.      Sympathetic activation → increased vascular tone and cardiac workload

3.      ADH activation → water retention and possible dilutional hyponatremia

Elevated LV filling pressures produce pulmonary congestion, while systemic venous congestion causes elevated JVP, edema, and may contribute to renal dysfunction.

Persistent neurohormonal activation promotes LV dilation, fibrosis, adverse remodeling, and progressive systolic dysfunction.

5. Clinical and Diagnostic Assessment

This patient is clearly congested or "wet."

Perfusion status should also be assessed using:

1.      Blood pressure

2.      Mental status

3.      Extremity temperature

4.      Urine output

5.      Lactate when hypoperfusion is suspected

Natriuretic peptides

BNP and NT-proBNP support the diagnosis but are not diagnostic in isolation.

In patients with acute or decompensated dyspnea:

1.      BNP <100 pg/mL makes heart failure less likely

2.      NT-proBNP <300 pg/mL makes heart failure less likely

Elevated concentrations must be interpreted clinically because renal dysfunction, older age, and atrial fibrillation can increase natriuretic peptide levels, whereas obesity may lower them.

Other important investigations

1.      ECG

2.      Cardiac troponin

3.      CBC

4.      Electrolytes

5.      Creatinine and eGFR

6.      Liver function tests

7.      Glucose and HbA1c

8.      Iron studies

9.      Thyroid function when appropriate

Echocardiography should assess LVEF, LV and RV structure and function, wall motion, valvular disease, and pulmonary pressures.

Cardiac MRI or coronary evaluation may be appropriate when the underlying etiology requires clarification.

Right heart catheterization is not routine and is reserved for selected patients with uncertain hemodynamics, significant hypoperfusion or shock, or advanced heart failure evaluation.

6. Management of Decompensated HFrEF

The immediate goals are:

1.      Relieve congestion

2.      Maintain adequate perfusion

3.      Identify and treat the precipitating cause

4.      Initiate or optimize disease-modifying therapy once stable

6.1 IV Loop Diuretics

IV loop diuretics are first-line therapy for significant congestion.

Monitor:

1.      Urine output

2.      Daily weight

3.      Fluid balance

4.      Blood pressure

5.      Creatinine

6.      Sodium

7.      Potassium

8.      Magnesium

If response is inadequate:

1.      Increase the loop diuretic dose

2.      Consider sequential nephron blockade with a thiazide-type diuretic or acetazolamide in selected patients

A modest rise in creatinine during successful decongestion does not automatically require stopping diuresis. Volume status, perfusion, electrolytes, and overall response should guide treatment.

6.2 Oxygen and Ventilatory Support

Oxygen should not be administered routinely to nonhypoxemic patients.

Supplemental oxygen is appropriate when significant hypoxemia is present, particularly SpO2 <90%.

Noninvasive ventilation should be considered for acute pulmonary edema with significant respiratory distress or persistent hypoxemia.

6.3 Vasodilators

IV nitrates may be considered when:

1.      Blood pressure is adequate

2.      Significant hypertension or increased afterload is present

3.      Pulmonary congestion remains prominent

Avoid vasodilators in significant hypotension.

6.4 Inotropes and Vasopressors

Inotropes are not routine therapy for congestion.

They are reserved for:

1.      Cardiogenic shock

2.      Significant hypoperfusion

3.      Low-output states with threatened end-organ perfusion

If vasopressor support is required in cardiogenic shock, norepinephrine is generally preferred.

6.5 Identify the Precipitating Cause

Important precipitants include:

1.      Acute coronary syndrome or ischemia

2.      Arrhythmia

3.      Uncontrolled hypertension

4.      Infection

5.      Pulmonary embolism

6.      Acute valvular or mechanical complications

7.      Medication or dietary nonadherence

8.      NSAIDs or other sodium-retaining drugs

9.      Progressive renal dysfunction

7. Guideline-Directed Medical Therapy After Stabilization

Once clinically and hemodynamically stable, foundational HFrEF therapy should be initiated or optimized promptly.

The four major disease-modifying drug classes are:

1.      ARNI, preferably sacubitril/valsartan when appropriate, or ACE inhibitor or ARB when ARNI cannot be used

2.      Evidence-based beta blocker: carvedilol, metoprolol succinate, or bisoprolol

3.      Mineralocorticoid receptor antagonist: spironolactone or eplerenone

4.      SGLT2 inhibitor: dapagliflozin or empagliflozin

SGLT2 inhibitors provide benefit regardless of the presence of diabetes.

For steroidal MRA therapy, commonly used safety criteria include:

1.      eGFR >30 mL/min/1.73 m²

2.      Serum potassium <5.0 mEq/L

Renal function and potassium require close monitoring.

Beta blockers should be initiated or up-titrated after the patient is clinically stable and adequately decongested. Chronic beta-blocker therapy is generally continued during hospitalization unless shock, severe hemodynamic instability, or another contraindication develops.

Loop diuretics are continued as required to maintain euvolemia but are primarily symptom-relieving rather than disease-modifying therapy.

8. Selected Additional Therapy

Depending on the clinical setting:

1.      Ivabradine: selected symptomatic patients with LVEF ≤35%, sinus rhythm, HR ≥70 bpm despite maximally tolerated beta-blocker therapy

2.      Hydralazine plus isosorbide dinitrate: selected patients, particularly when renin-angiotensin system inhibition cannot be used or when otherwise guideline indicated

3.      Digoxin: may reduce HF hospitalization in selected symptomatic patients

4.      IV iron: for appropriate patients with iron deficiency

5.      Anticoagulation: only when another indication exists, such as atrial fibrillation, venous thromboembolism, or intracardiac thrombus

Routine anticoagulation is not indicated solely for HFrEF.

9. Device Therapy

Device decisions should generally follow optimization of medical therapy and reassessment of LV function.

ICD

Primary-prevention ICD evaluation is appropriate when LVEF remains ≤35% despite at least 3 months of optimized GDMT, with consideration of HF symptoms, ischemic versus nonischemic etiology, timing after myocardial infarction or revascularization, and expected meaningful survival.

Primary-prevention ICD implantation is not recommended within 40 days after myocardial infarction.

CRT

The strongest conventional indication is:

1.      LVEF ≤35%

2.      Persistent symptoms despite GDMT

3.      Sinus rhythm

4.      LBBB

5.      QRS ≥150 ms

Selected patients outside these criteria may also benefit depending on QRS morphology, QRS duration, rhythm, and pacing requirements.

10. Prognosis and Follow-Up

Adverse prognostic features include:

1.      Persistent congestion

2.      Renal dysfunction

3.      Hyponatremia

4.      Hypotension or hypoperfusion

5.      Recurrent HF hospitalization

6.      Persistently elevated natriuretic peptides

7.      Persistently reduced LVEF

After stabilization:

1.      Optimize disease-modifying therapy

2.      Monitor renal function, electrolytes, blood pressure, and volume status

3.      Reassess LVEF after adequate therapy optimization when it will influence ICD or CRT decisions

4.      Continue guideline-directed HF therapy even if LVEF subsequently improves, unless a contraindication develops

Key Clinical Insight

Orthopnea + PND + elevated JVP + pulmonary crackles + peripheral edema + S3 + radiographic pulmonary congestion + LVEF 35% strongly support decompensated HFrEF with pulmonary and systemic congestion.

Initial management centers on IV loop diuresis and treatment of the precipitating cause. Oxygen is reserved for hypoxemia, vasodilators are used selectively when blood pressure permits, and inotropes or vasopressors are reserved for hypoperfusion or cardiogenic shock.

After stabilization, establish foundational therapy with ARNI or ACE inhibitor or ARB, an evidence-based beta blocker, an MRA, and an SGLT2 inhibitor as tolerated.

References

1.      Køber L, Adamo M, et al. 2026 ESC Guidelines for the management of heart failure. Eur Heart J. 2026. doi:10.1093/eurheartj/ehag100.

2.      Walsh MN, Kober L, Sliwa K, et al. AHA/ACC/ESC/WHF Expert Consensus Document: Second Universal Definition of Heart Failure (2026). J Am Coll Cardiol. 2026. doi:10.1016/j.jacc.2026.05.036.

3.      Maddox TM, Januzzi JL Jr, Allen LA, et al. 2024 ACC Expert Consensus Decision Pathway for Treatment of Heart Failure With Reduced Ejection Fraction. J Am Coll Cardiol. 2024;83(15):1444-1488. doi:10.1016/j.jacc.2023.12.024.

4.      Hollenberg SM, Stevenson LW, Ahmad T, et al. 2024 ACC Expert Consensus Decision Pathway on Clinical Assessment, Management, and Trajectory of Patients Hospitalized With Heart Failure Focused Update. J Am Coll Cardiol. 2024;84(13):1241-1267. doi:10.1016/j.jacc.2024.06.002.

5.      Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. Circulation. 2022;145:e895-e1032. doi:10.1161/CIR.0000000000001063.

Acute Pericarditis

A 30-year-old male presents to the emergency department with central chest pain for the past few days. The pain is pleuritic and positional, worsening with inspiration and improving when sitting up and leaning forward. He reports fever, myalgia, and sore throat 2 weeks earlier. Examination reveals a pericardial friction rub over the left parasternal region. CRP and ESR are elevated, with normal or mildly elevated troponin. ECG demonstrates diffuse concave ST-segment elevation and PR-segment depression without a territorial pattern or significant reciprocal ST depression except in aVR. Diagnosis?

Diagnosis is Acute pericarditis, most likely idiopathic or presumed viral. If troponin is elevated above the assay upper reference limit with preserved LV systolic function, the diagnosis is myopericarditis.

1. Definition

Acute pericarditis is an inflammatory pericardial syndrome, with or without pericardial effusion, with symptoms lasting ≤4 weeks.

Typical features include:

1.      Sharp, pleuritic, positional chest pain

2.      Pericardial friction rub

3.      Widespread ST-segment elevation and PR-segment depression

4.      Evidence of systemic or pericardial inflammation

2. Etiology

Common causes include:

1.      Idiopathic or presumed viral

2.      Tuberculosis and other bacterial infections

3.      Autoimmune or autoinflammatory disease

4.      Post-cardiac injury syndromes

5.      Malignancy

6.      Uremia

7.      Drugs and radiation

A preceding viral syndrome supports a presumed viral or post-viral mechanism, but a specific viral cause should not be assumed without evidence.

3. Pathophysiology

Inflammation of the pericardium produces:

1.      Pleuritic, positional chest pain

2.      Pericardial friction rub

3.      Systemic inflammatory marker elevation

4.      Pericardial effusion in some patients

A rapidly accumulating significant effusion may cause cardiac tamponade.

Concomitant myocardial involvement may produce troponin elevation and, when more extensive, ventricular dysfunction.

4. Diagnosis

Under the 2025 ESC framework, a definite clinical diagnosis requires a compatible clinical presentation plus more than one additional criterion, including:

1.      Pericardial friction rub

2.      PR-segment depression or widespread ST-segment elevation

3.      Elevated CRP

4.      New or worsening pericardial effusion

5.      Pericardial edema or late gadolinium enhancement on cardiac MRI

This patient has typical pericardial chest pain, a friction rub, elevated inflammatory markers, and characteristic ECG abnormalities, strongly establishing the diagnosis.

5. Diagnostic Evaluation

5.1 ECG

Typical findings include:

1.      Widespread concave ST-segment elevation

2.      PR-segment depression

3.      Reciprocal PR elevation and ST depression in aVR

4.      Absence of a coronary territorial pattern

These findings strongly support pericarditis but do not independently exclude acute coronary syndrome when clinical suspicion for ACS remains.

5.2 Laboratory Findings

1.      CRP and ESR are commonly elevated

2.      Troponin is generally normal in isolated pericarditis

3.      Troponin elevation indicates myocardial injury

Definite pericarditis with elevated troponin but no new LV dysfunction is classified as myopericarditis.

Troponin elevation with new focal or global LV systolic dysfunction suggests predominant myocarditis with pericardial involvement, often termed perimyocarditis.

5.3 Imaging

Transthoracic echocardiography is the first-line imaging test and should assess:

1.      Pericardial effusion

2.      Cardiac tamponade

3.      LV and RV function

A normal echocardiogram does not exclude pericarditis.

Cardiac MRI is particularly useful when the diagnosis is uncertain, myocardial involvement is suspected, or disease is complicated, recurrent, or refractory.

6. Management

6.1 First-Line Therapy

For uncomplicated idiopathic or presumed viral pericarditis:

1.      Aspirin or an NSAID at full anti-inflammatory doses

2.      Colchicine for 3 months

3.      Proton pump inhibitor for gastroprotection

Aspirin or NSAID therapy is generally given for approximately 1 to 2 weeks, then tapered according to symptoms and inflammatory activity.

Colchicine reduces the risk of persistent or recurrent pericarditis.

6.2 Corticosteroids

Corticosteroids are not first-line therapy for uncomplicated idiopathic or presumed viral pericarditis.

Before corticosteroids are introduced because of an incomplete response, the patient should be reassessed for an alternative or specific cause, particularly infection.

Low to moderate dose corticosteroids may be considered when:

1.      Aspirin or NSAIDs are contraindicated

2.      Symptoms persist despite appropriate first-line treatment after reassessment

3.      A specific indication exists, such as autoimmune disease

When required, corticosteroids should generally be used with colchicine and tapered slowly. High doses and rapid tapering increase the risk of recurrence.

6.3 Physical Activity

Restrict strenuous physical activity during active disease.

Return to activity should be individualized and occur after clinical remission, including resolution of symptoms and normalization of inflammatory markers and other abnormal investigations.

For uncomplicated disease, this generally requires at least several weeks, often approximately 1 month.

7. High-Risk Features

Hospital admission and further etiologic evaluation are appropriate when high-risk features are present.

Major high-risk features include:

1.      Fever >38°C

2.      Subacute onset

3.      Large pericardial effusion >20 mm

4.      Cardiac tamponade

5.      Failure to respond to aspirin or NSAID therapy after at least 1 week

Additional risk features include:

1.      Myocardial involvement

2.      Immunosuppression

3.      Trauma

4.      Oral anticoagulant therapy

Patients without high-risk features can often be managed as outpatients with close follow-up.

8. Complications

Important complications include:

1.      Recurrent pericarditis

2.      Pericardial effusion

3.      Cardiac tamponade

4.      Myopericarditis

5.      Constrictive pericarditis, which is uncommon in idiopathic or presumed viral disease

Key Clinical Insight

Pleuritic positional chest pain relieved by sitting forward + pericardial friction rub + widespread ST-segment elevation and PR-segment depression strongly support acute pericarditis.

First-line treatment is aspirin or an NSAID plus colchicine for 3 months, with gastroprotection.

Troponin elevation indicates myocardial involvement. Pericarditis with elevated troponin and preserved LV function is myopericarditis, while new LV dysfunction suggests predominant myocarditis with pericardial involvement.

References

1.      Schulz-Menger J, Collini V, Gröschel J, et al. 2025 ESC Guidelines for the management of myocarditis and pericarditis. Eur Heart J. 2025;46(40):3952-4041. doi:10.1093/eurheartj/ehaf192.

2.      Wang TKM, Klein AL, Cremer PC, et al. 2025 Concise Clinical Guidance: An ACC Expert Consensus Statement on the Diagnosis and Management of Pericarditis. J Am Coll Cardiol. 2025;86(25):2691-2719. doi:10.1016/j.jacc.2025.05.023.

3.      Imazio M, Brucato A, Cemin R, et al. A randomized trial of colchicine for acute pericarditis. N Engl J Med. 2013;369(16):1522-1528. doi:10.1056/NEJMoa1208536.

4.      Chiabrando JG, Bonaventura A, Vecchié A, et al. Management of Acute and Recurrent Pericarditis: JACC State-of-the-Art Review. J Am Coll Cardiol. 2020;75(1):76-92. doi:10.1016/j.jacc.2019.11.021.

Deep Venous Thrombosis (DVT)

A 50-year-old male presents to the emergency department with right calf pain and swelling on the third postoperative day after open cholecystectomy. He has hypertension treated with amlodipine. Examination reveals right calf tenderness. Blood pressure is 120/80 mm Hg, pulse rate 88 beats/min, respiratory rate 18 breaths/min, oxygen saturation 92% on room air, and temperature 97.9°F. D-dimer is elevated. Duplex ultrasonography demonstrates a right lower-extremity venous thrombus with loss of normal venous compressibility. Diagnosis?

Diagnosis is Acute surgery-provoked right lower-extremity deep vein thrombosis (DVT).

Recent major surgery is a strong transient provoking factor. The ultrasound report should specify whether the DVT is proximal or isolated distal, because management differs.

The oxygen saturation of 92% is abnormal. If confirmed and not otherwise explained, the patient should also be assessed for concomitant pulmonary embolism.

1. Definition

Deep vein thrombosis is the formation of a thrombus within the deep venous system, most commonly in the lower extremities.

DVT and pulmonary embolism together constitute venous thromboembolism (VTE).

2. Etiology and Risk Factors

The pathogenesis is explained by Virchow's triad:

1.      Venous stasis

2.      Endothelial injury or activation

3.      Hypercoagulability

Important risk factors include:

1.      Recent surgery or hospitalization

2.      Immobility

3.      Previous VTE

4.      Active malignancy

5.      Pregnancy or estrogen exposure

6.      Obesity and increasing age

7.      Inherited or acquired thrombophilia

In this patient, recent major surgery and postoperative immobility are the principal provoking factors.

3. Pathophysiology

Venous stasis, vascular injury or activation, and hypercoagulability promote thrombus formation in the deep veins.

The thrombus produces:

1.      Venous obstruction

2.      Local inflammation

3.      Pain and swelling

The thrombus may propagate proximally or embolize to the pulmonary circulation, causing pulmonary embolism.

Proximal DVT carries a higher risk of clinically significant PE than isolated distal DVT.

4. Clinical Features

Typical findings include:

1.      Unilateral leg pain

2.      Unilateral swelling

3.      Tenderness along the deep venous system

4.      Pitting edema

5.      Warmth or erythema

Clinical findings alone cannot reliably confirm or exclude DVT.

Homans sign is unreliable and should not be used diagnostically.

Features that should raise concern for associated PE include:

1.      New dyspnea

2.      Pleuritic chest pain

3.      Tachycardia

4.      Syncope

5.      Unexplained hypoxemia

5. Diagnostic Evaluation

5.1 Clinical Probability

The 2-level DVT Wells score is commonly used before imaging:

1.      ≥2 points: DVT likely

2.      ≤1 point: DVT unlikely

Once diagnostic ultrasound confirms DVT, further clinical probability scoring is unnecessary.

5.2 D-dimer

D-dimer is highly sensitive but poorly specific.

It is most useful when DVT remains uncertain, particularly in patients with a low or unlikely pretest probability.

Recent surgery commonly elevates D-dimer, reducing its specificity. Therefore, the elevated D-dimer in this patient is nonspecific and adds no diagnostic value once ultrasound has confirmed DVT.

5.3 Compression Duplex Ultrasonography

Compression ultrasonography is the first-line imaging test for suspected lower-extremity DVT.

The key diagnostic finding is:

1.      Failure of the affected vein to compress

Other supportive findings include:

1.      Visualization of intraluminal thrombus

2.      Abnormal or absent venous Doppler flow

The thrombus should be classified as:

1.      Proximal DVT, involving the popliteal vein or more proximal veins

2.      Isolated distal DVT, confined to the calf veins

6. Management

6.1 Anticoagulation

Therapeutic anticoagulation is the cornerstone of treatment for acute proximal DVT unless contraindicated.

For eligible patients, direct oral anticoagulants such as apixaban or rivaroxaban are generally preferred for ongoing therapy.

Because this patient is only 3 days postoperative, first assess:

1.      Adequacy of surgical hemostasis

2.      Active bleeding

3.      Hemoglobin and platelet count

4.      Renal function

5.      Need for further invasive procedures

Anticoagulation should begin when postoperative hemostasis is considered adequate.

If rapid interruption or reversal may be required because of significant bleeding risk or possible reoperation, intravenous unfractionated heparin may be preferred initially. LMWH is another parenteral option when appropriate. Transition to a DOAC can be considered once postoperative bleeding risk is acceptable.

6.2 Duration

For a DVT provoked by a major transient risk factor such as surgery, the standard treatment duration is generally 3 months.

Extended or indefinite anticoagulation is usually unnecessary when the provoking factor has resolved and there are no other indications for prolonged therapy.

6.3 Isolated Distal DVT

If ultrasound demonstrates an isolated distal calf DVT:

1.      Anticoagulate for 3 months when significant symptoms or risk factors for thrombus extension are present

2.      In selected low-risk patients without severe symptoms or extension risk factors, serial ultrasonography once weekly for 2 weeks may be used instead of immediate anticoagulation

3.      Start anticoagulation if the thrombus extends, particularly if it reaches the proximal veins

6.4 Thrombus Removal

Routine thrombolysis or thrombectomy is not indicated for most DVTs.

Catheter-based thrombus removal may be considered for:

1.      Limb-threatening DVT, including phlegmasia cerulea dolens

2.      Selected patients with severe symptomatic iliofemoral or iliocaval DVT, particularly in experienced centers

Recent major surgery substantially increases bleeding risk and is an important limitation to thrombolytic therapy.

6.5 Inferior Vena Cava Filter

An IVC filter should not routinely be added to anticoagulation.

A retrievable IVC filter may be considered when acute proximal DVT or PE is present and therapeutic anticoagulation is contraindicated.

The filter should be removed when anticoagulation can safely be established.

7. Additional Management and Prevention

1.      Early ambulation is generally encouraged when clinically tolerated

2.      Routine bed rest is unnecessary once the patient is stable

3.      Graduated compression stockings are not routinely recommended solely to prevent post-thrombotic syndrome, although they may help selected patients with persistent symptoms

4.      Appropriate VTE prophylaxis should be used during future high-risk hospitalizations or surgical procedures

5.      Routine thrombophilia testing is not indicated for a clearly surgery-provoked DVT

8. Complications

Important complications include:

1.      Pulmonary embolism

2.      Post-thrombotic syndrome

3.      Recurrent VTE

4.      Phlegmasia cerulea dolens, a rare limb-threatening form of extensive DVT

Key Clinical Insight

Recent major surgery + unilateral calf pain and swelling + a noncompressible deep vein on ultrasound strongly establish acute surgery-provoked DVT.

D-dimer is nonspecific after recent surgery and is unnecessary once ultrasound confirms the diagnosis.

Proximal DVT requires therapeutic anticoagulation unless contraindicated. Surgery-provoked DVT is generally treated for 3 months.

Because oxygen saturation is 92% on room air, confirm the finding and assess for pulmonary embolism if the hypoxemia is otherwise unexplained.

References

1.      Stevens SM, Woller SC, Baumann Kreuziger L, et al. Antithrombotic Therapy for VTE Disease: Second Update of the CHEST Guideline and Expert Panel Report. Chest. 2021;160(6):e545-e608. doi:10.1016/j.chest.2021.07.055.

2.      Stevens SM, Woller SC, Baumann Kreuziger L, et al. Antithrombotic Therapy for VTE Disease: Compendium and Review of CHEST Guidelines 2012-2021. Chest. 2024;166(2):388-404. doi:10.1016/j.chest.2024.03.003.

3.      Ortel TL, Neumann I, Ageno W, et al. American Society of Hematology 2020 Guidelines for Management of Venous Thromboembolism: Treatment of Deep Vein Thrombosis and Pulmonary Embolism. Blood Adv. 2020;4(19):4693-4738. doi:10.1182/bloodadvances.2020001830.

4.      Schlager O, Campello E, Madaric J, et al. 2025 ESVM Guidelines on interventional treatment of venous thromboembolism. Vasa. 2025;54(6):365-381. doi:10.1024/0301-1526/a001211.

5.      National Institute for Health and Care Excellence. Venous thromboembolic diseases: diagnosis, management and thrombophilia testing. NICE Guideline NG158. Published March 26, 2020. Updated August 2, 2023. Reviewed May 1, 2026.