Question

Difficulty: MediumGeneral Internal Medicine

A 6666-year-old man is brought to the emergency department by his daughter due to a 33-day history of progressively worsening shortness of breath and a persistent cough. He notes his baseline morning cough has increased in frequency, and his sputum has changed from clear to thick and yellowish-green. His medical history is significant for severe chronic obstructive pulmonary disease (COPD), hypertension, and hypothyroidism (managed with levothyroxine). He has a 4545-pack-year smoking history. His temperature is 37.8∘C37.8^\circ\text{C} (100.0∘F100.0^\circ\text{F}), pulse is 114/min114/\text{min}, blood pressure is 145/88 mm Hg145/88\text{ mm Hg}, respiratory rate is 28/min28/\text{min}, and oxygen saturation is 86%86\% on room air.

Physical examination reveals a barrel-shaped chest with accessory muscle use. Pulmonary auscultation demonstrates a prolonged expiratory phase, diffuse expiratory wheezes, and scattered rhonchi, but no crackles are heard. The jugular venous pressure is elevated at 10 cm H2O10\text{ cm H}_2\text{O}. Abdominal examination shows a liver edge that is palpable 3 cm3\text{ cm} below the right costal margin and is mildly tender. Trace bilateral lower extremity pitting edema is present.

Laboratory studies show:
Leukocyte count: 11,500/mm311,500/\text{mm}^3
Serum sodium: 139 mEq/L139\text{ mEq/L}
Serum potassium: 4.1 mEq/L4.1\text{ mEq/L}
Serum bicarbonate: 31 mEq/L31\text{ mEq/L}
Blood urea nitrogen: 18 mg/dL18\text{ mg/dL}
Serum creatinine: 0.9 mg/dL0.9\text{ mg/dL}
Thyroid-stimulating hormone (TSH): 0.2 \muU/mL0.2\text{ \mu U/mL} (Normal: 0.4−4.0 \muU/mL0.4-4.0\text{ \mu U/mL})
Free T4: 1.2 ng/dL1.2\text{ ng/dL} (Normal: 0.9−1.7 ng/dL0.9-1.7\text{ ng/dL})

Arterial blood gas analysis on room air shows a pH of 7.317.31, PaCO2\text{PaCO}_2 of 62 mm Hg62\text{ mm Hg}, and PaO2\text{PaO}_2 of 54 mm Hg54\text{ mm Hg}.

Chest radiography reveals hyperinflated lung fields, flattened diaphragms, and an enlarged right descending pulmonary artery. There are no pleural effusions or focal alveolar opacities.

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

  1. Inhaled albuterol and ipratropium, systemic glucocorticoids, and oral azithromycinAnswer
  2. B
    Intravenous furosemide and noninvasive positive-pressure ventilation
  3. C
    Intravenous piperacillin-tazobactam and intravenous vancomycin
  4. D
    Intravenous sodium bicarbonate infusion
  5. E
    Discontinuation of current levothyroxine therapy

Answer

The most appropriate management is the administration of inhaled albuterol and ipratropium, systemic glucocorticoids, and a macrolide antibiotic such as oral azithromycin.
The correct approach targets the primary pathophysiology of an acute chronic obstructive pulmonary disease (COPD) exacerbation. This patient presents with all three cardinal symptoms (increased dyspnea, increased sputum volume, and increased sputum purulence) requiring the standard triad of therapy: short-acting bronchodilators (albuterol and ipratropium) to relieve bronchospasm, systemic glucocorticoids to reduce airway inflammation, and an antibiotic (such as a macrolide or respiratory fluoroquinolone) to treat the likely bacterial trigger. Although the patient has signs of fluid overload, these are due to cor pulmonale (right-sided heart failure secondary to chronic pulmonary hypertension) rather than left-sided heart failure, making aggressive diuresis incorrect and potentially harmful.

Step-by-Step Solution

1
Analyze the patient's acute respiratory presentation and history.
The patient has a history of COPD and presents with the classic triad of an acute exacerbation: increased dyspnea, increased sputum volume, and increased sputum purulence.
Identifying the primary acute pathology is required to guide immediate life-saving therapy.
2
Differentiate the cause of the fluid overload signs (elevated JVP, hepatomegaly).
The physical exam shows right-sided fluid overload but no left-sided fluid overload (lungs lack crackles, CXR lacks pulmonary edema). This indicates cor pulmonale due to chronic hypoxia, not acute decompensated left heart failure.
Distinguishing right heart failure from left heart failure ensures the correct pathology (lungs vs. left ventricle) is targeted.
3
Interpret the arterial blood gas (ABG) and endocrine labs in context.
The ABG shows acute-on-chronic respiratory acidosis, requiring bronchodilators to improve ventilation. The low TSH with normal Free T4 represents euthyroid sick syndrome, requiring no intervention.
Accurate interpretation of confounding laboratory abnormalities prevents the administration of inappropriate and potentially harmful treatments.

Key Concept

Management of acute COPD exacerbation complicated by cor pulmonale
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