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Difficulty: MediumRheumatology and Immunology

A 64-year-old woman with a 10-year history of severe, erosive rheumatoid arthritis comes to the emergency department due to a 2-week history of worsening shortness of breath, orthopnea, and a persistent dry cough. Four months ago, her rheumatologist added a new biologic disease-modifying antirheumatic drug (DMARD) to her regimen of methotrexate and folic acid due to inadequate joint symptom control. She also has a history of mild asthma and diet-controlled type 2 diabetes mellitus.

Vital signs are temperature 37.1°C (98.8°F), blood pressure 110/70 mm Hg, pulse 108/min, and respirations 22/min. Oxygen saturation is 92% on room air.

Physical examination reveals jugular venous distention to 10 cm H2O. Pulmonary auscultation reveals bibasilar crackles without wheezing. Cardiac examination shows a regular tachycardia with a prominent S3 gallop. There is 2+ pitting edema in the bilateral lower extremities.

Laboratory StudyResultReference Range
Sodium135 mEq/L136–145 mEq/L
Potassium4.2 mEq/L3.5–5.0 mEq/L
Chloride101 mEq/L95–105 mEq/L
Bicarbonate18 mEq/L22–28 mEq/L
Blood urea nitrogen32 mg/dL7–18 mg/dL
Creatinine1.6 mg/dL0.6–1.2 mg/dL
Thyroid-stimulating hormone (TSH)5.8 µU/mL0.4–4.0 µU/mL
Free thyroxine (T4)1.1 ng/dL0.9–1.7 ng/dL
Arterial Blood Gas (Room Air)ResultReference Range
pH7.347.35–7.45
PaO268 mm Hg75–105 mm Hg
PaCO235 mm Hg33–45 mm Hg

Chest radiograph reveals bilateral interstitial markings, prominent pulmonary vasculature, and cardiomegaly.

Which of the following is the most appropriate next step in the management of this patient?

  1. Discontinue the recently added biologic agent and administer intravenous furosemideAnswer
  2. B
    Administer nebulized bronchodilators and oral prednisone
  3. C
    Administer intravenous sodium bicarbonate
  4. D
    Initiate oral levothyroxine therapy
  5. E
    Start empiric intravenous piperacillin-tazobactam

Answer

Discontinue the recently added biologic agent and administer intravenous furosemide
This patient is presenting with classic signs of acute decompensated heart failure (ADHF), including orthopnea, jugular venous distention, an S3 gallop, and pulmonary edema (crackles, bilateral interstitial markings). In a patient with severe rheumatoid arthritis whose regimen was recently stepped up to include a biologic DMARD, the most likely culprit is a tumor necrosis factor (TNF)-alpha inhibitor (e.g., etanercept, adalimumab, infliximab). TNF-alpha inhibitors carry a black-box warning for causing new-onset heart failure or exacerbating existing cardiac disease. The most appropriate next step in management is to immediately discontinue the offending biologic agent and treat the fluid overload with an intravenous loop diuretic such as furosemide.

Step-by-Step Solution

1
Identify the primary clinical syndrome based on the patient's presentation and examination.
The combination of orthopnea, jugular venous distention, an S3 gallop, pulmonary crackles, and peripheral edema strongly indicates acute decompensated heart failure (ADHF).
Accurate diagnosis of the acute cardiopulmonary crisis is required before identifying the underlying trigger.
2
Connect the new-onset ADHF to the patient's recent medical history, specifically the medication changes.
The patient was recently started on a new biologic DMARD for rheumatoid arthritis. Tumor necrosis factor (TNF)-alpha inhibitors (e.g., etanercept, infliximab, adalimumab) are common biologic DMARDs that are known to cause or worsen heart failure.
Identifying the iatrogenic cause of the patient's deterioration is essential for proper management.
3
Determine the most appropriate immediate management for the acute condition and the offending agent.
The offending TNF-alpha inhibitor must be discontinued immediately, and standard ADHF therapy (intravenous loop diuretics like furosemide) should be initiated to offload volume.
Continuing the offending agent will worsen the heart failure, and immediate symptom relief requires diuresis.

Key Concept

Tumor necrosis factor (TNF)-alpha inhibitors can cause new-onset heart failure or exacerbate underlying cardiac dysfunction. In affected patients, the offending biologic must be discontinued and standard heart failure therapy initiated.
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Topics

Rheumatology and Immunology

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