Page 42 - FOCUS December 2017

PHARMACY SERVICES
Medication induced hyperkalemia
Matthew Shearman, PharmD Candidate and Katie Gulick, PharmD, BCPS
Hyperkalemia is a common yet severe electrolyte abnormality that
is seen in the hospital setting. Its incidence has been measured between 1.3% and 10% of hospitalized patients, and has a mortality rate of 1 in 1,000 patients. It is characterized by a potassium concen- tration greater than 5.0mEq/L, and can lead to a variety of symptoms such as muscle paralysis, paresthesias, dyspnea, palpitations, chest pain, and nausea and vomiting. Once concentrations exceed 8.5 mEq/L, fatal side effects such as respiratory paralysis and cardiac arrest can occur. Given the severity of this condition, it is essential that providers are aware of the common etiologies behind hyperka-
lemia. One of the most common is drug-induced hyperkalemia. It is estimated that between 35% - 75% of cases are due to the effects of medications. There are numerous drugs that can affect potassium levels in hospitalized patients. By understanding the drugs and their mechanisms, providers can be on the lookout for patients who might be at an increased risk of developing hyperkalemia, gain insight or
to determine the cause of a patient’s hyperkalemia. Potassium can be increased when a patient ingests too much salt, when excretion is inhibited, or when stores are shifted from the intracellular space to the extracellular space. | CONTINUED
MECHANISM CAUSING HYPERKALEMIA
MEDICATION CLASS AND EXAMPLES
POTASSIUM-CONTAINING AGENTS
• Aggressive potassium Repletion
• Metabolic demands change
• Drug containing a potassium salt not for repletion
• Potassium Chloride, Penicillin G, Packed Red Blood Cells
DRUGS THAT INHIBIT EXCRETION THROUGH THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM (RAAS) PATHWAY leads to reduced aldosterone signaling through the mineralocorticoid receptor which prevents the activation
of the Na+/K+-ATPase in the distal tubule and collecting ducts
• Directly Inhibit one of the enzymes or receptors of the RAAS pathway
• ACE inhibitors (e.g., lisinopril), ARBs (e.g., valsartan), direct renin inhibitors (e.g., aliskiren), and aldosterone antagonists (e.g., spironolactone)
• Indirect inhibition of RAAS via inhibition of prostaglandin I2, preventing the release of renin
• NSAIDs: (e.g., Ketorolac [case reports]6, Celecoxib, Indomethacin)5
• Inhibit aldosterone production by reducing the number and affinity of angiotensin II receptors
• Unfractionated heparin and low molecular weight heparin (e.g., enoxaparin)
DRUGS THAT INHIBIT EXCRETION
• Inhibits luminal sodium channels
• Potassium sparing diuretics: (e.g., Triamterene, Amiloride) Antibiotics: (e.g., Trimethoprim, Pentamidine)
• Unknown mechanism, possible induction of hypoaldosteronism
• Calcineurin inhibitors: Cyclosporin, Tacrolimus
POTASSIUM SHIFTS
• Decrease activity of Na+/K+-ATPase transporters
• Digoxin and blockers (e.g., Propranolol)
• Hyperosmolarity leading to acidosis
• Mannitol and Contrast agents
• Depolarization
• Succinylcholine
42 • FOCUS DECEMBER 2017
THERAPEUTIC NOTES