CK: Difference between revisions
Ostermayer (talk | contribs) (Created page with "Creatine kinase (CK, also called CPK) is an enzyme found predominantly in skeletal muscle, cardiac muscle, and brain. When these tissues are damaged, CK leaks into the bloodstream. In the ED, CK is most commonly used in the evaluation of rhabdomyolysis and as an adjunct in certain cardiac and neuromuscular presentations.<ref name="StatPearls">Creatine Phosphokinase. ''StatPearls''. NCBI Bookshelf. Updated 2024.</ref> ==Background== *CK catalyzes the conversion of cr...") |
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Creatine kinase (CK, also called CPK) is an enzyme found predominantly in skeletal muscle, cardiac muscle, and brain. When these tissues are damaged, CK leaks into the bloodstream. In the ED, CK is most commonly used in the evaluation of [[rhabdomyolysis]] and as an adjunct in certain cardiac and neuromuscular presentations.<ref name="StatPearls">Creatine Phosphokinase. ''StatPearls''. NCBI Bookshelf. Updated 2024.</ref> | ==Background== | ||
*Creatine kinase (CK, also called CPK) is an enzyme found predominantly in skeletal muscle, cardiac muscle, and brain. | |||
*When these tissues are damaged, CK leaks into the bloodstream. | |||
*In the ED, CK is most commonly used in the evaluation of [[rhabdomyolysis]] and as an adjunct in certain cardiac and neuromuscular presentations.<ref name="StatPearls">Creatine Phosphokinase. ''StatPearls''. | |||
*NCBI Bookshelf. | |||
*Updated 2024.</ref> | |||
*CK catalyzes the conversion of creatine + ATP → phosphocreatine + ADP, providing energy to tissues with high metabolic demand<ref name="StatPearls"/> | *CK catalyzes the conversion of creatine + ATP → phosphocreatine + ADP, providing energy to tissues with high metabolic demand<ref name="StatPearls"/> | ||
*Three isoenzymes based on tissue of origin: | *Three isoenzymes based on tissue of origin: | ||
** | **CK-MM: Skeletal muscle (~98% of skeletal muscle CK) — the predominant source of elevated total CK in the ED | ||
** | **CK-MB: Cardiac muscle (~20–30% of cardiac CK) — largely supplanted by [[troponin]] for MI diagnosis | ||
** | **CK-BB: Brain — rarely measured clinically | ||
* | *Kinetics: CK rises within 2–12 hours of muscle injury, peaks at 24–36 hours, and declines at ~30–40% per day (half-life ~36 hours). Levels typically normalize within 3–5 days if injury resolves<ref name="Medscape">Rhabdomyolysis Workup. ''Medscape''. Accessed 2025.</ref> | ||
*Normal range: ~22–198 U/L (varies by lab, sex, race, and muscle mass; higher in males, African Americans, and those with greater muscle mass)<ref name="StatPearls"/> | *Normal range: ~22–198 U/L (varies by lab, sex, race, and muscle mass; higher in males, African Americans, and those with greater muscle mass)<ref name="StatPearls"/> | ||
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CK is ordered as an adjunct to clinical evaluation. Consider checking CK in the following ED presentations: | CK is ordered as an adjunct to clinical evaluation. Consider checking CK in the following ED presentations: | ||
* | *Muscle pain, weakness, or dark urine — [[rhabdomyolysis]] evaluation | ||
* | *Prolonged immobilization, found down, crush injury — occult rhabdomyolysis | ||
* | *Drug/toxin ingestion — cocaine, amphetamines, MDMA, ethanol, heroin, [[neuroleptic malignant syndrome|NMS]], [[serotonin syndrome]], statins | ||
* | *Seizures, agitation, physical restraint — rhabdomyolysis screening | ||
* | *Exertional heat illness — [[heat stroke]] workup | ||
* | *Chest pain — CK-MB historically used for MI; now supplanted by [[troponin]] (CK-MB may still add value in detecting reinfarction or periprocedural MI) | ||
* | *Suspected [[compartment syndrome]] — CK elevation supports diagnosis but does not replace pressure measurement | ||
==Differential Diagnosis== | ==Differential Diagnosis== | ||
===Causes of Elevated CK=== | ===Causes of Elevated CK=== | ||
* | *Rhabdomyolysis (most common ED-relevant cause): Trauma/crush injury, prolonged immobilization ("found down"), cocaine/amphetamines/MDMA, seizures, extreme exertion, [[heat stroke]], [[neuroleptic malignant syndrome]], [[serotonin syndrome]], [[malignant hyperthermia]], statins + fibrates, hypokalemia, hypothyroidism | ||
* | *Cardiac: [[Acute coronary syndrome]] (CK-MB fraction), myocarditis, cardiac surgery | ||
* | *Inflammatory myopathy: Polymyositis, dermatomyositis | ||
* | *Muscular dystrophy: Duchenne, Becker (can be markedly elevated) | ||
* | *Other: [[Hypothyroidism]], [[sickle cell disease]], intramuscular injections, recent surgery, intense exercise (benign exertional), statin myopathy, viral myositis, [[compartment syndrome]] | ||
* | *Mild elevations (2–10× normal): Common after vigorous exercise, IM injections, minor trauma — often clinically insignificant | ||
===Causes of Low CK=== | ===Causes of Low CK=== | ||
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==Evaluation== | ==Evaluation== | ||
===Workup=== | ===Workup=== | ||
* | *Total CK is the primary test ordered in the ED | ||
*When evaluating for '''rhabdomyolysis''', also order: | *When evaluating for '''rhabdomyolysis''', also order: | ||
**BMP/CMP (creatinine, potassium, calcium, phosphorus, bicarbonate) | **BMP/CMP (creatinine, potassium, calcium, phosphorus, bicarbonate) | ||
** | **Urinalysis — heme-positive on dipstick with few/no RBCs on microscopy suggests myoglobinuria | ||
**LDH, AST (both elevated in rhabdomyolysis; AST from muscle, not necessarily liver) | **LDH, AST (both elevated in rhabdomyolysis; AST from muscle, not necessarily liver) | ||
**Uric acid (often elevated) | **Uric acid (often elevated) | ||
**Coagulation studies if DIC concern | **Coagulation studies if DIC concern | ||
*Consider checking '''urine myoglobin''' if available, though it has a very short half-life (~2–4 hours) and may be negative by the time CK peaks | *Consider checking '''urine myoglobin''' if available, though it has a very short half-life (~2–4 hours) and may be negative by the time CK peaks | ||
* | *Serial CK every 6–12 hours to establish peak and trend — failure to decline suggests ongoing injury (consider [[compartment syndrome]] or persistent cause)<ref name="Medscape"/> | ||
*CK-MB and CK-MB index are '''rarely needed''' in the troponin era but may help distinguish cardiac vs. skeletal muscle source if total CK is very high and troponin is borderline | *CK-MB and CK-MB index are '''rarely needed''' in the troponin era but may help distinguish cardiac vs. skeletal muscle source if total CK is very high and troponin is borderline | ||
===Diagnosis=== | ===Diagnosis=== | ||
* | *Rhabdomyolysis: CK >5× upper limit of normal (~1,000 U/L) is the consensus threshold; CK ≥5,000 U/L increases risk of [[acute kidney injury]]; CK >15,000 U/L is a significant predictor of renal failure<ref name="Medscape"/><ref name="EMCrit">Rhabdomyolysis. ''EMCrit IBCC''. Updated 2024.</ref> | ||
* | *Mild CK elevation (200–1,000 U/L): Common after exercise, IM injections, seizures, minor trauma — usually clinically insignificant without symptoms or renal dysfunction | ||
* | *Dipstick heme-positive urine without RBCs = myoglobinuria until proven otherwise — assume rhabdomyolysis | ||
* | *Elevated AST out of proportion to ALT with elevated CK suggests muscle (not liver) as the source of the transaminase elevation — do not reflexively attribute elevated AST to hepatic injury in rhabdomyolysis | ||
==Management== | ==Management== | ||
*Management is directed at the underlying cause and prevention of [[acute kidney injury]] | *Management is directed at the underlying cause and prevention of [[acute kidney injury]] | ||
* | *[[Rhabdomyolysis]] with CK >5,000 U/L or AKI: | ||
**Aggressive IV crystalloid resuscitation (target urine output 200–300 mL/hr in adults) | **Aggressive IV crystalloid resuscitation (target urine output 200–300 mL/hr in adults) | ||
**Monitor and correct '''[[hyperkalemia]]''' (immediate life threat), hypocalcemia, hyperphosphatemia | **Monitor and correct '''[[hyperkalemia]]''' (immediate life threat), hypocalcemia, hyperphosphatemia | ||
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**Avoid nephrotoxins (NSAIDs, contrast if possible) | **Avoid nephrotoxins (NSAIDs, contrast if possible) | ||
**Bicarbonate for urine alkalinization is controversial and not routinely recommended | **Bicarbonate for urine alkalinization is controversial and not routinely recommended | ||
* | *Mild CK elevation without symptoms or renal dysfunction: Oral hydration, outpatient follow-up, repeat CK if persistent concern | ||
* | *Statin-associated myopathy: Hold statin; discuss with PCP regarding rechallenge vs. alternative agent | ||
==Disposition== | ==Disposition== | ||
* | *Admit if: CK >5,000 U/L with rising trend, AKI, [[hyperkalemia]], significant electrolyte derangements, ongoing muscle injury (e.g., [[compartment syndrome]]), or unable to maintain adequate oral hydration | ||
* | *Consider admission or observation for: CK 1,000–5,000 U/L with renal risk factors (dehydration, CKD, diabetes, NSAID use, cocaine use, multiple etiologies) | ||
* | *Discharge with follow-up if: Mild CK elevation (<1,000 U/L), normal renal function, no electrolyte abnormalities, able to hydrate orally, and clear benign etiology (e.g., post-exercise) | ||
* | *McMahon score may help risk-stratify patients with rhabdomyolysis for AKI and need for dialysis (validated score using age, sex, initial CK, creatinine, calcium, phosphate, bicarbonate, and etiology)<ref name="EMCrit"/> | ||
==See Also== | ==See Also== | ||
Revision as of 15:52, 19 March 2026
Background
- Creatine kinase (CK, also called CPK) is an enzyme found predominantly in skeletal muscle, cardiac muscle, and brain.
- When these tissues are damaged, CK leaks into the bloodstream.
- In the ED, CK is most commonly used in the evaluation of rhabdomyolysis and as an adjunct in certain cardiac and neuromuscular presentations.[1]
- CK catalyzes the conversion of creatine + ATP → phosphocreatine + ADP, providing energy to tissues with high metabolic demand[1]
- Three isoenzymes based on tissue of origin:
- CK-MM: Skeletal muscle (~98% of skeletal muscle CK) — the predominant source of elevated total CK in the ED
- CK-MB: Cardiac muscle (~20–30% of cardiac CK) — largely supplanted by troponin for MI diagnosis
- CK-BB: Brain — rarely measured clinically
- Kinetics: CK rises within 2–12 hours of muscle injury, peaks at 24–36 hours, and declines at ~30–40% per day (half-life ~36 hours). Levels typically normalize within 3–5 days if injury resolves[2]
- Normal range: ~22–198 U/L (varies by lab, sex, race, and muscle mass; higher in males, African Americans, and those with greater muscle mass)[1]
Clinical Features
CK is ordered as an adjunct to clinical evaluation. Consider checking CK in the following ED presentations:
- Muscle pain, weakness, or dark urine — rhabdomyolysis evaluation
- Prolonged immobilization, found down, crush injury — occult rhabdomyolysis
- Drug/toxin ingestion — cocaine, amphetamines, MDMA, ethanol, heroin, NMS, serotonin syndrome, statins
- Seizures, agitation, physical restraint — rhabdomyolysis screening
- Exertional heat illness — heat stroke workup
- Chest pain — CK-MB historically used for MI; now supplanted by troponin (CK-MB may still add value in detecting reinfarction or periprocedural MI)
- Suspected compartment syndrome — CK elevation supports diagnosis but does not replace pressure measurement
Differential Diagnosis
Causes of Elevated CK
- Rhabdomyolysis (most common ED-relevant cause): Trauma/crush injury, prolonged immobilization ("found down"), cocaine/amphetamines/MDMA, seizures, extreme exertion, heat stroke, neuroleptic malignant syndrome, serotonin syndrome, malignant hyperthermia, statins + fibrates, hypokalemia, hypothyroidism
- Cardiac: Acute coronary syndrome (CK-MB fraction), myocarditis, cardiac surgery
- Inflammatory myopathy: Polymyositis, dermatomyositis
- Muscular dystrophy: Duchenne, Becker (can be markedly elevated)
- Other: Hypothyroidism, sickle cell disease, intramuscular injections, recent surgery, intense exercise (benign exertional), statin myopathy, viral myositis, compartment syndrome
- Mild elevations (2–10× normal): Common after vigorous exercise, IM injections, minor trauma — often clinically insignificant
Causes of Low CK
- Low muscle mass (cachexia, elderly, sedentary)
- Connective tissue disease (e.g., rheumatoid arthritis — some patients)
- Liver disease, alcoholism
Evaluation
Workup
- Total CK is the primary test ordered in the ED
- When evaluating for rhabdomyolysis, also order:
- BMP/CMP (creatinine, potassium, calcium, phosphorus, bicarbonate)
- Urinalysis — heme-positive on dipstick with few/no RBCs on microscopy suggests myoglobinuria
- LDH, AST (both elevated in rhabdomyolysis; AST from muscle, not necessarily liver)
- Uric acid (often elevated)
- Coagulation studies if DIC concern
- Consider checking urine myoglobin if available, though it has a very short half-life (~2–4 hours) and may be negative by the time CK peaks
- Serial CK every 6–12 hours to establish peak and trend — failure to decline suggests ongoing injury (consider compartment syndrome or persistent cause)[2]
- CK-MB and CK-MB index are rarely needed in the troponin era but may help distinguish cardiac vs. skeletal muscle source if total CK is very high and troponin is borderline
Diagnosis
- Rhabdomyolysis: CK >5× upper limit of normal (~1,000 U/L) is the consensus threshold; CK ≥5,000 U/L increases risk of acute kidney injury; CK >15,000 U/L is a significant predictor of renal failure[2][3]
- Mild CK elevation (200–1,000 U/L): Common after exercise, IM injections, seizures, minor trauma — usually clinically insignificant without symptoms or renal dysfunction
- Dipstick heme-positive urine without RBCs = myoglobinuria until proven otherwise — assume rhabdomyolysis
- Elevated AST out of proportion to ALT with elevated CK suggests muscle (not liver) as the source of the transaminase elevation — do not reflexively attribute elevated AST to hepatic injury in rhabdomyolysis
Management
- Management is directed at the underlying cause and prevention of acute kidney injury
- Rhabdomyolysis with CK >5,000 U/L or AKI:
- Aggressive IV crystalloid resuscitation (target urine output 200–300 mL/hr in adults)
- Monitor and correct hyperkalemia (immediate life threat), hypocalcemia, hyperphosphatemia
- Serial CK, BMP, and urine output monitoring
- Avoid nephrotoxins (NSAIDs, contrast if possible)
- Bicarbonate for urine alkalinization is controversial and not routinely recommended
- Mild CK elevation without symptoms or renal dysfunction: Oral hydration, outpatient follow-up, repeat CK if persistent concern
- Statin-associated myopathy: Hold statin; discuss with PCP regarding rechallenge vs. alternative agent
Disposition
- Admit if: CK >5,000 U/L with rising trend, AKI, hyperkalemia, significant electrolyte derangements, ongoing muscle injury (e.g., compartment syndrome), or unable to maintain adequate oral hydration
- Consider admission or observation for: CK 1,000–5,000 U/L with renal risk factors (dehydration, CKD, diabetes, NSAID use, cocaine use, multiple etiologies)
- Discharge with follow-up if: Mild CK elevation (<1,000 U/L), normal renal function, no electrolyte abnormalities, able to hydrate orally, and clear benign etiology (e.g., post-exercise)
- McMahon score may help risk-stratify patients with rhabdomyolysis for AKI and need for dialysis (validated score using age, sex, initial CK, creatinine, calcium, phosphate, bicarbonate, and etiology)[3]
See Also
- Rhabdomyolysis
- Acute kidney injury
- Hyperkalemia
- Compartment syndrome
- Neuroleptic malignant syndrome
- Heat stroke
- Crush injury