Can sepsis cause hyperkalemia and how is it managed?

Can Sepsis Cause Hyperkalemia?

Yes, sepsis can cause hyperkalemia primarily through the development of acute kidney injury (AKI), which impairs potassium excretion and leads to electrolyte disturbances including both hyperkalemia and hypokalemia. 1

Mechanisms of Sepsis-Induced Hyperkalemia

Primary Pathway: Acute Kidney Injury

• Sepsis causes AKI in over 50% of cases, with mortality rates up to 40%, making it the most common pathway to hyperkalemia in septic patients 2
• AKI develops through multiple mechanisms including volume depletion (hypovolemia), haemodynamic changes, direct viral/bacterial tubular injury, thrombotic vascular processes, glomerular pathology, and rhabdomyolysis 1
• Reduced potassium excretion from impaired renal function is the dominant mechanism causing hyperkalemia in sepsis 1

Secondary Contributing Factors

• Tissue breakdown and cellular injury during sepsis releases intracellular potassium (which contains 98% of total body potassium at 50-75 mEq/L/kg) into the extracellular space 1
• Metabolic acidosis commonly present in sepsis causes transcellular potassium shifts from intracellular to extracellular compartments 1
• Hemodynamic instability and microcirculatory dysfunction lead to renal medullary hypoxia, further impairing potassium handling 2

Iatrogenic Causes in Septic Patients

• Medications used in sepsis management frequently contribute to hyperkalemia, including beta-blockers, NSAIDs, heparin, and stored blood products 1
• Succinylcholine used for intubation can cause severe hyperkalemia in patients immobilized >3 days or with neuromuscular diseases 1

Clinical Significance in Sepsis

Prognostic Impact

• In patients with AKI combined with sepsis, admission potassium levels ≥4.5 mmol/L are associated with 22% increased risk of ICU 30-day mortality (adjusted HR 1.22,95% CI: 1.08-1.38) 3
• Each 1 mmol/L increase in potassium is associated with 13% increased mortality risk in this population 3
• Hyperkalemia in sepsis is associated with abnormal serum electrolyte levels and increased risk of dying 1

ECG Manifestations

• Hyperkalemia in septic shock can cause ST-segment elevation mimicking acute myocardial infarction (pseudo-MI), which resolves with potassium correction 4
• Life-threatening ECG changes include peaked T waves, widened QRS complexes, loss of P waves, and potentially asystole 5, 4

Management Algorithm for Sepsis-Associated Hyperkalemia

Step 1: Assessment and Monitoring

• Measure serum potassium, urea, creatinine, and electrolytes on admission and monitor closely 1
• Obtain 12-lead ECG immediately; ECG changes indicate urgent treatment regardless of potassium level 6
• Exclude pseudo-hyperkalemia from hemolysis or improper sampling before aggressive treatment 6
• Use bedside blood gas analyzers for rapid potassium determination 4

Step 2: Immediate Treatment (for K+ >6.0 mEq/L or ECG changes)

Cardiac Membrane Stabilization (onset: 1-3 minutes):

• Calcium chloride 10%: 5-10 mL IV over 2-5 minutes (preferred) 6
• OR calcium gluconate 10%: 15-30 mL IV over 2-5 minutes 6
• Effect lasts 30-60 minutes; does not lower potassium but prevents arrhythmias 6

Shift Potassium Intracellularly (onset: 15-30 minutes, duration: 4-6 hours):

• Regular insulin 10 units IV with 25g glucose (50 mL D50W) over 15-30 minutes 6
• Nebulized albuterol 10-20 mg over 15 minutes 6
• Sodium bicarbonate 50 mEq IV over 5 minutes only if metabolic acidosis present 1, 6

Eliminate Potassium from Body:

• Furosemide 40-80 mg IV only if hypervolemia, hyperkalemia, and/or renal acidosis present AND patient is non-oliguric 1
• Patiromer or sodium zirconium cyclosilicate for acute life-threatening hyperkalemia (NICE-approved) 1
• Hemodialysis for resistant hyperkalemia, especially in oliguric patients or ESRD 1, 6

Step 3: Address Underlying Causes

• Optimize fluid status (euvolemia) to reduce AKI incidence, though this is challenging in sepsis 1
• Correct volume depletion with intravenous fluids; fever and increased respiratory rate increase insensible losses 1
• Review and discontinue potassium-elevating medications when possible 1
• Do NOT use dopamine to improve renal function; it does not prevent renal failure and may cause harm 1

Step 4: Monitoring and Reassessment

• Recheck potassium within 1 hour after initial treatment, then frequently to assess response and monitor for rebound hyperkalemia 1, 5
• Temporary measures (insulin/glucose, albuterol) provide only transient effects (1-4 hours); rebound can occur after 2 hours 6
• Continuous ECG monitoring for moderate-severe hyperkalemia 7

Critical Pitfalls to Avoid

• Never use furosemide to "improve kidney function"—treat the patient, not the urine output 1
• Do not use high-dose steroids (hydrocortisone ≥300 mg/day) as they increase infection risk without mortality benefit 1
• Avoid sodium bicarbonate unless metabolic acidosis is documented; effectiveness is uncertain and acidosis may have protective effects 1, 6
• Do not use succinylcholine for intubation in patients immobilized >3 days due to risk of treatment-resistant hyperkalemia 1
• Recognize that patients with CKD, diabetes, or heart failure often tolerate potassium up to 6 mEq/L without arrhythmias 1

Referral Criteria

• Refer for specialist advice if AKI is worsening despite initial management or has not resolved after 48 hours 1
• Refer if there is diagnostic uncertainty, abnormal urinalysis suggesting intrinsic renal disease, or complex fluid management needs 1
• Consider hemodialysis consultation for usual indications for renal replacement therapy, particularly with no urine output 1