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Review Question - QID 104316

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QID 104316 (Type "104316" in App Search)
A 60-year-old man presents to the hospital with increasing shortness of breath for several hours. He is a smoker with a 40-pack-year history and does not see his physician regularly. He denies any fevers, chills, sick contacts, or worsening cough. His temperature is 37.3 C, blood pressure 130/64 mmHg, heart rate 98/min, respiratory rate 22/min, and SpO2 87% on room air. The patient is shown in Figure A. On physical exam, lung auscultation reveals diffuse wheezing, but no crackles. Cardiac auscultation is within normal limits. There is mild hepatomegaly and bilateral pitting pedal edema. His chest radiograph is shown in Figure B. The patient is started on furosemide, ipratropium, albuterol nebulizers, and IV methylprednisolone. His lab studies at the time of admission and 4 days later are shown below:

At admission: pH 7.33, HCO3- 29 mEq/L, sodium 135 mEq/L, potassium 4.4 mEq/L, chloride 99 mEq/L, BUN 26 mg/dL, creatinine 1.2 mg/dL, glucose 105 mg/dL.

4 days later: pH 7.31, HCO3- 17 mEq/L, sodium 140 mEq/L, potassium 3.2 mEq/L, chloride 114 mEq/L, BUN 55 mg/dL, creatinine 2.4 mg/dL, glucose 150 mg/dL.

What is the most likely cause of the patient's elevated creatinine?
  • A
  • B

Diabetic ketoacidosis

4%

1/28

Glucocorticoid treatment

4%

1/28

Worsening respiratory failure

11%

3/28

Acute renal failure

32%

9/28

Volume contraction

46%

13/28

  • A
  • B

Select Answer to see Preferred Response

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In patients with COPD exacerbations and signs of right-sided heart failure or cor pulmonale, diuretics such as furosemide must be used carefully, as these patients can develop decreased cardiac output resulting in prerenal renal failure.

Loop diuretics are often administered to COPD patients with cor pulmonale in order to decrease right ventricular filling pressures and peripheral edema. However, these agents must be used carefully, as these patients are prone to developing reduced cardiac output. One must follow the BUN and creatinine levels to monitor renal function. On admission, these patients generally have chronic respiratory acidosis compensated by increased bicarbonate levels. Concomitant metabolic acidosis from uremia resulting from injudicious diuretic therapy will decrease the bicarbonate level. These patients' potassium levels may also drop due to furosemide treatment.

Evensen reviews the management of COPD exacerbations. The first step for outpatients is to increase the dose of inhaled short-acting bronchodilators. Oral corticosteroids may be beneficial, especially for patients with purulent sputum. Antibiotics are beneficial for moderately or severely ill patients and should be considered for those with purulent sputum or inadequate symptom relief with bronchodilators and corticosteroids. Hospitalized patients should receive short-acting bronchodilators, continuous supplemental oxygen, antibiotics, and systemic corticosteroids. Those with worsening acidosis or hypoxemia should receive ventilatory support.

Shah reviews the treatment of pulmonary hypertension (PH). Secondary causes of pulmonary artery systolic pressure (PASP) elevation, most commonly left heart disease, are far more prevalent than isolated pulmonary arterial hypertension (PAH). Treatment of PH due to left heart disease is challenging, and pulmonary vasodilator therapy may worsen symptoms. Therefore, treatment of PH requires an understanding of (1) the use of echocardiography in diagnosing PH and (2) invasive hemodynamic testing prior to starting pulmonary vasodilator therapy; (3) differentiating PAH from pulmonary venous hypertension due to left heart disease; and (4) understanding the treatment strategies for PH and resultant right heart failure.

Figure A shows a patient with right-sided heart failure. Note the jugular venous distention. Figure B shows the chest radiograph of a patient with COPD. Note the hyperinflated lungs, lack of focal infiltrates, and flattened diaphragms. Illustration A shows the various clinical signs of right-sided heart failure.

Incorrect answers:
Answer 1: Ketoacidosis is unlikely since the glucose level is only mildly elevated and the anion gap (140-(114+17)=9) is not elevated. Renal failure can cause metabolic acidosis with or without an anion gap.
Answer 2: Glucocorticoid therapy can cause hypokalemia and metabolic alkalosis - this patient has metabolic acidosis.
Answer 3: This patient is unlikely to have worsening respiratory failure, as he has managed to keep his pH roughly the same, even in the presence of a new metabolic acidosis, which shows the ability of his lungs to compensate for the reduction in bicarbonate by reducing pCO2.
Answer 5: This patient has metabolic acidosis, not alkalosis.

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