Why is CPK (Creatine Phosphokinase) checked in patients after a seizure?

Why CPK is Checked in Seizure Patients

CPK (creatine phosphokinase) is checked after seizures primarily to detect rhabdomyolysis from intense muscle activity during generalized tonic-clonic seizures, which can lead to acute kidney injury requiring aggressive fluid resuscitation and monitoring.

Primary Diagnostic Purpose

• CPK elevation occurs specifically after generalized tonic-clonic seizures due to intense skeletal muscle contractions, with levels rising 8.0 to 19.2 times baseline in approximately 15% of cases 1
• The test helps differentiate true epileptic generalized tonic-clonic seizures from psychogenic seizures, as CPK does not elevate after psychogenic events despite vigorous muscular activity 1
• No CPK elevation occurs after complex partial, focal motor, absence, or tonic seizures, making it specific for generalized tonic-clonic activity 1

Detection and Prevention of Acute Kidney Injury

• Serial CPK monitoring is essential when levels exceed 5000 U/L, as this indicates significant rhabdomyolysis risk 2
• Patients with CPK >15,000 IU/L require aggressive fluid resuscitation exceeding 6L to prevent acute kidney injury and need for renal replacement therapy 3
• All patients with significantly elevated CPK after seizures demonstrate eGFR <90 mL/min/1.73m², necessitating close renal function monitoring 2

Clinical Algorithm for CPK Monitoring

When to check CPK:

• After any witnessed or suspected generalized tonic-clonic seizure 1, 4
• When patients present with electrolyte disorders post-seizure 2
• In alcohol-related seizures, which produce the greatest CPK elevations 4

What to monitor alongside CPK:

• Serial assessment of myoglobin, eGFR, and electrolytes should be performed concurrently 2
• Urine output and pH monitoring (maintain pH >6.5) through bladder catheterization when rhabdomyolysis is present 3

Treatment Thresholds Based on CPK Levels

• CPK >5000 U/L: Initiate fluid resuscitation, urine alkalization, and diuretic agents 2
• CPK >15,000 IU/L: Administer volumes >6L for severe rhabdomyolysis 3
• Continue monitoring until CPK trends downward, typically showing 10-fold decrease over 4 days with appropriate treatment 5

Important Clinical Pitfalls

• Peak CPK elevation occurs days after the seizure, not immediately—the highest recorded level of 39,300 U/L occurred on day 5 post-seizure 2
• Alcohol-related seizures produce disproportionately high CPK levels and should trigger more aggressive monitoring 4
• Antiepileptic drugs, particularly levetiracetam, can independently cause rhabdomyolysis, so unexplained rising CPK despite no further seizures warrants medication review 5
• The isoenzyme is skeletal muscle CK-MM, not cardiac, so elevated CPK does not indicate myocardial injury 4

Risk Stratification

Higher risk for significant CPK elevation:

• Patients with multiple or prolonged generalized tonic-clonic seizures 1
• Alcohol-related seizures 4
• Elderly patients or those with cardiovascular risk factors (though this relates more to troponin than CPK) 6

Lower risk (CPK checking not routinely indicated):

• Complex partial seizures 1
• Absence seizures 1
• Focal motor seizures without generalization 1
• Psychogenic non-epileptic events 1