What are the potential causes of hyperkalemia in a patient with a left shoulder infection, hyponatremia (low sodium), and hyperglycemia (elevated glucose)?

Causes of Hyperkalemia in a 44-Year-Old with Left Shoulder Infection, Hyponatremia, and Hyperglycemia

In this clinical scenario, the most likely causes of hyperkalemia are acute kidney injury from infection/sepsis, hyperglycemia-induced transcellular potassium shifts, and potentially medications (NSAIDs, antibiotics) used to treat the shoulder infection. 1, 2

Primary Mechanisms to Consider

1. Infection-Related Causes

• Acute kidney injury (AKI) from sepsis/infection is the most critical concern, as all cases of hyperkalemia-induced cardiac arrest in one retrospective study had acute kidney injury present 3
• Shoulder infections, particularly if severe or associated with bacteremia, can precipitate AKI through sepsis-induced renal hypoperfusion and acute tubular necrosis 4
• Extensive tissue injury or burns from the infection can release intracellular potassium into the bloodstream 5

2. Hyperglycemia-Induced Potassium Shifts

• Hyperglycemia (glucose 198 mg/dL) causes transcellular potassium shifts from intracellular to extracellular space due to hyperosmolarity and insulin deficiency 2, 4
• The hyperosmolar state creates an osmotic gradient that pulls water and potassium out of cells 5
• This mechanism is particularly important in diabetic patients or those with stress hyperglycemia from acute infection 3, 2

3. Medication-Induced Hyperkalemia

• NSAIDs commonly used for shoulder pain/infection can cause hyperkalemia by reducing renal potassium excretion 3, 4
• Trimethoprim-sulfamethoxazole (if used for infection coverage) blocks epithelial sodium channels in the distal nephron, reducing potassium excretion 6
• Other antibiotics and pain medications should be reviewed systematically 7

Secondary Contributing Factors

Hyponatremia Connection

• The concurrent hyponatremia (sodium 131 mEq/L) suggests possible SIADH from infection/sepsis, which can coexist with hyperkalemia in critically ill patients 5
• Hyponatremia may indicate volume depletion or renal dysfunction, both of which impair potassium excretion 3

Metabolic Acidosis

• Infection/sepsis commonly causes metabolic acidosis, which shifts potassium from intracellular to extracellular space 3, 2
• The chloride level of 97 mEq/L (low-normal) may suggest a metabolic alkalosis or mixed acid-base disorder requiring arterial blood gas analysis 7

Critical Diagnostic Steps

Immediate Assessment Required

• Obtain ECG immediately to assess for peaked T waves, widened QRS, or other cardiotoxic changes regardless of potassium level 1, 4
• Verify true hyperkalemia by repeating measurement with proper technique to exclude pseudohyperkalemia from hemolysis 6, 8
• Measure serum creatinine and calculate eGFR to assess renal function, as kidney disease is the most common cause of severe hyperkalemia 3, 6

Medication Review

• Systematically review all medications including:
  • NSAIDs for pain management 3, 4
  • Antibiotics (especially trimethoprim-containing) 6
  • Any RAAS inhibitors (ACE inhibitors, ARBs) if patient has comorbid conditions 3, 1
  • Potassium-sparing diuretics 6

Laboratory Evaluation

• Arterial blood gas to assess for metabolic acidosis from sepsis 3, 7
• Complete metabolic panel to evaluate renal function and concurrent electrolyte abnormalities 6
• Blood glucose monitoring to confirm hyperglycemia and assess for diabetic ketoacidosis 5, 2
• Urinalysis and urine electrolytes to assess renal potassium handling 8

Common Clinical Pitfalls to Avoid

• Do not assume normal ECG excludes dangerous hyperkalemia - ECG changes can be absent or atypical even with severe hyperkalemia 7, 4
• Do not overlook transcellular shifts - patients with hyperglycemia and infection are at high risk for rebound hyperkalemia after initial treatment 1, 8
• Do not delay treatment while awaiting repeat potassium levels if ECG changes are present 1, 7
• Do not miss occult renal dysfunction - even mild elevations in creatinine can significantly impair potassium excretion 3, 6

Risk Stratification

High-Risk Features in This Patient

• Acute infection increases risk of AKI and tissue breakdown 3, 4
• Hyperglycemia suggests either diabetes (chronic risk factor) or stress response (acute illness severity) 3, 2
• Hyponatremia may indicate SIADH or volume depletion, both suggesting significant systemic illness 5
• Age 44 years with multiple metabolic derangements suggests underlying comorbidity (diabetes, kidney disease) 3, 4