Update on steroid recommendations for COPD exacerbations

Let’s start with a patient case.  An elderly patient is admitted through the emergency department with markedly worsening dyspnea and purulent sputum production over the last three days.  When reviewing his history, you find that he has GOLD grade 4 (very severe) COPD and experiences roughly one exacerbation per year that requires hospitalization.  His home medications for COPD include tiotropium (Spiriva) 18 mcg/inhalation once daily, albuterol MDI (Proventil HFA, ProAir HFA, or Ventolin HFA) 90 mcg/inhalation 2 inhalations every 4-6 hours as needed for dyspnea, and fluticasone/salmeterol (Advair Diskus) 250/50 mcg inhaled twice daily.  You are now deciding what steroid regimen should be initiated to manage this exacerbation.

Risk factors for stress ulcers and stress ulcer prophylaxis

Stress ulcer prophylaxis is a topic that comes up frequently on the internal medicine service but is not frequently given more than a moment of consideration.  Numerous studies have identified how acid-suppressive therapies (eg. namely proton pump inhibitors and histamine-2 receptor antagonists) are widely prescribed and often lacking an indication.  Studies of various designs have revealed that 46-73% of patients who receive acid-suppressive therapy while hospitalized do not have an indication.^1-3 

The most robust guideline to date for the use of acid-suppressive therapy for stress ulcer prophylaxis was published in 1999 and was comprised of data almost entirely from patients in the intensive care unit (ICU).⁴  At that time, there was only one randomized control trial addressing stress ulcer prophylaxis in the non-ICU setting.  These guidelines identified and determined the weight of various risk factors for the development of stress ulcers and these values are continued to be used today.  The presence or absence or risk factors should be used to determine the need for stress ulcer prophylaxis, not just admission to the ICU.  The summary of recommendations follows below.

Statins in liver disease?

A middle-aged patient arrives to his regularly scheduled clinic appointment looking for refills of his medication. His PMH includes HTN, hyperlipidemia, diabetes mellitus, obesity, and cirrhosis secondary to nonalcoholic fatty liver disease. His medications include antihypertensive and antihyperglycemic drugs in addition to atorvastatin 80 mg by mouth daily. At this time, you recall that statins have a risk for hepatotoxicity and are concerned whether it should be refilled at this time. What are the considerations for continuing statin therapy in this patient with known liver disease?

Elevation of liver enzymes is a well-known risk of statin therapy. Since the first statin was approved by the FDA in 1987, regular monitoring of liver enzymes to screen for elevations was routine practice. However, in 2012, the FDA revised the prescribing information for all statins to recommend serum aminotransferases be measured at baseline and then only thereafter if clinically indicated. There were primarily two reasons for this change:

“Sulfa” allergy cross-reactivity

Let’s start with a patient scenario.  A patient presents to the emergency room experiencing a heart failure exacerbation.  When entering the order for intravenous diuretics, you note that a cross-reactivity warning has popped up for a “sulfa” allergy.  What evidence is there for cross-reactivity between Loop diuretics and “sulfa” allergy and how should this affect your decision?

Vancomycin dosing and monitoring in hemodialysis

Let's start with a patient case.  A patient on hemodialysis (M/W/F) is admitted to the hospital with cellulitis who also meets sepsis criteria.  He has a history of an MRSA infection during a previous admission so you want to initiate vancomycin at this time.  The patient is 76 kg and still makes some urine.  What dosing strategy should you choose and when/should vancomycin concentrations be monitored?

Drug interaction between warfarin and acetaminophen?

The management of anticoagulant therapy is an important component of the treatment of various disease states. Maintaining the narrow therapeutic range required for the safe and effective use of warfarin is essential to avoid suboptimal dosing and adverse events. Numerous drug interactions with warfarin are present due to alterations in absorption, distribution, and metabolism.  The severity of interactions with warfarin varies greatly and dictates very different recommendations for management and monitoring. In the most insignificant interactions, no change in dosage or monitoring is necessary, whereas some interactions require a significant empiric reduction in warfarin dosage and close monitoring of INR.