An internal medicine team is evaluating a 67-year-old male who presented to the emergency … — USMLE Step 2 CK

An internal medicine team is evaluating a $67$ -year-old male who presented to the emergency department with a $5$ -day history of progressively worsening shortness of breath, orthopnea, and lower extremity swelling. His medical history includes seropositive rheumatoid arthritis, for which infliximab was added to his methotrexate regimen $4$ months ago due to refractory joint pain. He also has a $35$ -pack-year smoking history. On physical examination, his temperature is $37.1^\circ\text{C}$ ( $98.8^\circ\text{F}$ ), blood pressure is $112/74\text{ mm Hg}$ , heart rate is $110\text{ /min}$ , and respiratory rate is $24\text{ /min}$ . Pulse oximetry shows $91\%$ on ambient air. Jugular venous distention is prominent at $45$ degrees. Chest auscultation reveals bilateral basilar crackles and a prominent third heart sound (S3). There is $2+$ bilateral pitting edema extending to the knees. Joint examination shows no active synovitis, warmth, or effusions. Which of the following is the most appropriate next step in the pharmacologic management of this patient's current condition?

A
Administer nebulized albuterol and oral prednisone
B
Initiate intravenous vancomycin and piperacillin-tazobactam
Discontinue infliximab and administer intravenous furosemideAnswer
D
Discontinue methotrexate and administer leucovorin
E
Measure serum thyroid-stimulating hormone and free thyroxine levels

Answer

Discontinue infliximab and administer intravenous furosemide

The correct action is to discontinue the tumor necrosis factor-alpha (TNF-alpha) inhibitor and administer a loop diuretic. This patient presents with classic signs of acute decompensated heart failure, including orthopnea, jugular venous distention, an S3 gallop, pulmonary crackles, and peripheral edema. TNF-alpha inhibitors (e.g., infliximab, etanercept, adalimumab) are known to precipitate new-onset heart failure or exacerbate underlying cardiac dysfunction. They are strictly contraindicated in patients with moderate to severe heart failure. Therefore, the essential next step is to immediately stop the offending medication and administer intravenous furosemide to manage the severe volume overload.

Step-by-Step Solution

Identify the primary clinical syndrome based on the physical examination findings.

The patient exhibits jugular venous distention, an S3 gallop, bilateral basilar crackles, and pitting edema, which establish a diagnosis of acute decompensated heart failure (ADHF).

Differentiating between cardiac, pulmonary, and infectious causes of acute dyspnea is the critical first step in determining management.

Determine the most likely precipitating cause of the heart failure in this specific patient.

The recent initiation of infliximab is the most likely trigger, as tumor necrosis factor-alpha (TNF-alpha) inhibitors are a known cause of new-onset or worsening heart failure.

Identifying medication-induced complications is essential in patients on complex immunosuppressive regimens to prevent ongoing toxicity.

Select the appropriate pharmacologic management based on the diagnosis and precipitant.

Discontinuation of the offending agent (infliximab) and initiation of a loop diuretic (intravenous furosemide) for symptomatic relief of volume overload.

ADHF requires immediate volume offloading, and the precipitating cardiotoxic medication must be stopped immediately.

Key Concept

Tumor necrosis factor-alpha (TNF-alpha) inhibitors can precipitate or exacerbate heart failure and should be discontinued if a patient develops signs of acute decompensated heart failure.

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