Bedside Snapshot

Normal (Adult)
Men ≤72 ng/mL, women ≤58 ng/mL (≤72 and ≤58 µg/L)
Urine <1 mg/L
Assay-specific; use your lab’s range
Critical Values
No universal critical value: interpret by trend and clinical context. Urine >15 mg/L, or serum above about 10,000 ng/mL (consensus threshold for considering hemoadsorption): high AKI risk
High Suggests
  • Rhabdomyolysis: crush, long lie, seizures, heat illness, stimulants
  • MI or other heart injury (troponin decides)
  • Exercise, viral myositis
  • Kidney failure (slow clearance)
Low Suggests
Rarely clinically significant: a normal value does not exclude rhabdomyolysis or MI if drawn late, because myoglobin clears within hours
Act Now If
Crush or long lie, dark urine, or high myoglobin or CK: monitor, 12-lead, check K⁺, start isotonic fluid; IV calcium for hyperkalemic ECG changes; notify receiving/medical control
Watch Out For
A normal myoglobin rules out nothing: it clears in hours. Use troponin for MI and CK, K⁺ and creatinine for rhabdomyolysis

Reference & Critical Ranges

Lab-specific ranges: Every lab sets its own interval, based on its analyzer and its population. Use the range printed on your report. The values below are typical.

Reference ranges

PopulationConventionalSINotes
Adult men (serum or plasma)
≤72 ng/mL
≤72 µg/L
Electrochemiluminescent immunoassay (ECLIA) at a US reference laboratory
Adult women (serum or plasma)
≤58 ng/mL
≤58 µg/L
Lower limit than men; use the sex-specific value
Urine (random)
<1 mg/L
<1 mg/L
Separate test; specimen must be refrigerated and alkalinized
Children and pregnancy
Use the adult range
—
Reference laboratories publish no age- or pregnancy-specific interval; confirm with your lab

Severity & critical values

LevelConventionalSIWhat it means / typical findings
Normal
Serum men ≤72, women ≤58 ng/mL; urine <1 mg/L
Same numbers in µg/L; urine mg/L
No significant ongoing muscle injury at the time of the draw (it clears within hours)
Mild elevation
Urine 1–15 mg/L (approximate band)
1–15 mg/L
Vigorous exercise, myocardial infarction, mild muscle injury and other conditions
Rising AKI risk
Serum about 370–8,000 ng/mL (cut-offs vary by study)
370–8,000 µg/L
Published thresholds for acute kidney injury (AKI) differ by assay and population; higher peaks carry more risk
Critical
Urine >15 mg/L, or serum >10,000 ng/mL
>15 mg/L; >10,000 µg/L
Heavy myoglobin load: high risk of pigment AKI. One consensus suggests considering hemoadsorption above 10,000 ng/mL
Critical values: There is no universal critical value. Urine myoglobin >15 mg/L or serum myoglobin >10,000 ng/mL? Treat that as high risk for kidney injury. Check potassium (K⁺), creatinine and the ECG now. A normal result on a late draw does not rule out rhabdomyolysis.

Conversion: 1 ng/mL = 1 µg/L (same number); urine 1 mg/L = 1,000 ng/mL

Causes of Abnormal Results

Rhabdomyolysis is usually defined by creatine kinase (CK). The cutoff is CK above 5 times the upper reference limit (URL), or above 1,000 U/L, with muscle symptoms. Some studies call CK above 5,000 U/L severe. Myoglobin rises from the same injuries. It just clears much faster.

High (myoglobin above the URL)

MechanismCommon causesBedside clue
Compression and trauma
Crush injury, compartment syndrome, long lie after a fall, vascular injury with reperfusion, mangled extremity, electrical burns or lightning strikes, recent intramuscular injection (minor, transient rise)
Entrapment time; tense, painful limb; pain on passive stretch; weak distal pulses; entry and exit wounds or a history of electrical contact
Exertional and hyperkinetic
Status epilepticus, extreme or unaccustomed exercise, severe dystonia
Recent seizure; unaccustomed workout; muscle pain and dark urine
Temperature extremes
Exertional heat stroke, malignant hyperthermia (MH), neuroleptic malignant syndrome (NMS), serotonin syndrome
High core temperature; rigidity; MH: rising end-tidal CO₂ (EtCO₂) after an anesthetic trigger
Drugs and toxins
Alcohol, cocaine, heroin, phencyclidine, statins (especially with kidney or liver disease), envenomation
Toxidrome, intoxication with immobility, new statin or interacting drug
Infection
Influenza (influenza B in children), other viral myositis, sepsis, Streptococcus pyogenes, Staphylococcus aureus
Child with calf pain who refuses to walk after a viral illness; fever and myalgia
Inherited and metabolic
Glycogen and fatty acid metabolism disorders, mitochondrial disease, muscular dystrophy, inflammatory myopathies (polymyositis, dermatomyositis), severe electrolyte disturbance, diabetic ketoacidosis
Recurrent episodes with exercise, fasting or illness; family history; subacute proximal weakness suggests an inflammatory myopathy
Heart muscle injury
Acute myocardial infarction (MI); after percutaneous coronary intervention (PCI); myocarditis; cardiac surgery; defibrillation or cardioversion
Ischemic symptoms and ECG; troponin, not myoglobin, makes the diagnosis
Reduced clearance
Acute or chronic kidney failure
Mild, steady elevation with normal CK
The classic triad is uncommon: Muscle pain, weakness and tea-colored urine show up together in fewer than 10% of patients. So go by the mechanism: crush, long lie, seizure, heat or stimulants. Suspect rhabdomyolysis even when the patient feels well.
Specimen cup of dark brown, tea-colored urine from a patient with rhabdomyolysis (myoglobinuria)
Figure 1: Dark, tea-colored urine from a patient with rhabdomyolysis (myoglobinuria). Source: Wikimedia Commons, James Heilman, MD, CC BY-SA 3.0

Low (below the reference interval)

Rarely clinically significant. A low or normal myoglobin tells you nothing on its own. Myoglobin clears within hours, so a late draw can miss real muscle injury.

Interpretation & Bedside Approach

Step-by-step approach

  1. Is it real? Grossly hemolyzed blood gets rejected. Urine myoglobin reads falsely low if the sample sat warm or acidic. Assays are not standardized, so compare results from the same lab.
  2. How sick is the patient? Get a 12-lead ECG and K⁺ first. Hyperkalemia is the early killer. Check urine output, temperature, mental status and every compartment of the injured limbs.
  3. Where is it on the timeline? Myoglobin peaks within hours. Its serum half-life is 1–3 h. CK peaks at 24–72 h. Normal myoglobin a day out with a high CK? That still means rhabdomyolysis.
  4. Pair it: CK, K⁺, creatinine, calcium, phosphate, bicarbonate, lactate, urinalysis with microscopy, and troponin if the heart is in question.
  5. Classify: CK above 5 times the URL (or above 1,000 U/L) with muscle symptoms is rhabdomyolysis. For chest pain, the 2021 AHA/ACC chest pain guideline rates CK-MB and myoglobin as not useful (Class 3: No Benefit). Use high-sensitivity troponin.
  6. Estimate risk and escalate: A McMahon score of 6 or more at admission flags high risk of kidney replacement therapy (KRT) or death. Hyperkalemia, rising creatinine, low urine output or compartment syndrome all need ICU-level care.

Pattern recognition

PatternSuggests
High myoglobin, high CK, dark urine, dipstick blood positive with few or no red cells
Rhabdomyolysis with myoglobinuria
High myoglobin, CK normal or only slightly raised, within hours of injury
Early muscle injury; CK has not peaked yet, so repeat CK
Normal myoglobin, very high CK
Late presentation: myoglobin has already cleared; risk still follows CK, K⁺ and creatinine
High myoglobin, rising and falling troponin, ischemic ECG
Acute MI (diagnosed on troponin)
Mild steady elevation, normal CK, kidney disease
Reduced renal clearance rather than new muscle injury

McMahon score (rhabdomyolysis, at admission)

VariablePoints
Age
>50 to ≤70 y: 1.5; >70 to ≤80 y: 2.5; >80 y: 3
Female sex
1
Initial creatinine
1.4–2.2 mg/dL: 1.5; >2.2 mg/dL: 3
Initial calcium <7.5 mg/dL
2
Initial CK >40,000 U/L
2
Cause not seizure, syncope, exercise, statin or myositis
3
Initial phosphate
4.0–5.4 mg/dL: 1.5; >5.4 mg/dL: 3
Initial bicarbonate <19 mEq/L
2

Sensitivity for needing KRT at a score of 6 or more was 86%, and specificity was 68%. The score uses CK, not myoglobin. It helps set expectations. It does not choose treatment.

Do not use myoglobin for chest pain: It is not heart-specific, and it adds nothing to troponin. A high myoglobin after a fall, seizure or shock tells you nothing about the heart. A normal one does not rule out MI.

Management Priorities

Emergency: Rhabdomyolysis or crush injury (myoglobinuria, hyperkalemia or rising creatinine)

  1. Monitor and assess: Put on the cardiac monitor and get a 12-lead ECG, IV access, K⁺ and a blood gas. Track urine output (catheter in severe cases), the compartments and core temperature.
  2. Stabilize the myocardium: Give IV calcium for hyperkalemic ECG changes, and repeat it if the changes persist. In crush injury, watch the ECG before release, during it and right after.
  3. Volume early: Start isotonic crystalloid as soon as possible, before a trapped limb is released. Titrate it to urine output, and stop at signs of fluid overload.
  4. Shift K⁺: Give insulin with dextrose, plus nebulized albuterol (dose on the albuterol page). The full algorithm lives on the potassium page.
  5. Stop the cause: Cool exertional heat stroke, stop seizures, use dantrolene for MH, and remove the trigger drug. Get an urgent surgical consult for compartment syndrome.

Medications

DrugAdult dosePediatric dose (max)Onset / key notes
Isotonic crystalloid: normal saline or lactated Ringer’s (rhabdomyolysis)
Start about 400 mL/hr IV (range 200–1,000 mL/hr); titrate fluid to a urine output goal set by protocol (commonly 1–3 mL/kg/hr). The urine output goal is not a fluid-rate cap
Shock: 10–20 mL/kg IV/IO bolus, reassess. Then 1.5–2 times maintenance, titrated to a protocol-dependent urine output goal. No fixed max
Titrate to urine output: no fixed max; stop for crackles, falling SpO₂ or edema. Anuria despite fluid: plan KRT
Normal saline (EMS crush injury)
Pre-release bolus and post-extrication rate per local protocol and medical direction
Per local protocol and medical direction
NASEMSO 2022 prefers saline because LR contains K⁺; titrate to urine output, no fixed max
Calcium chloride 10% (hyperkalemia with ECG changes)
1 g (10 mL) IV/IO over 5–10 min; repeat if ECG changes persist
20 mg/kg (0.2 mL/kg) IV/IO, max 1 g
Onset within minutes; central line or IO preferred. Not for asymptomatic hypocalcemia
Calcium gluconate 10% (hyperkalemia with ECG changes)
3 g (30 mL) IV over 5–10 min; repeat if ECG changes persist
60 mg/kg (0.6 mL/kg) IV, max 3 g
Does not lower K⁺: start a shift at once
Regular insulin with dextrose (hyperkalemia)
Insulin 10 units IV with dextrose 25 g. Protocols often use 5 units in AKI, low eGFR or low baseline glucose (protocol-dependent). Dextrose may be omitted only when glucose is above about 250 mg/dL
Per pediatric protocol: insulin 0.1 units/kg IV (max 10 units) with dextrose 0.5 g/kg (D10 5 mL/kg)
High-alert Check glucose often for several hours
Sodium bicarbonate 8.4% (not routine)
Crush (NASEMSO, per protocol): 1 mEq/kg IV over 5 min (max 50 mEq). Severe acidosis or hyperkalemia: per protocol
1 mEq/kg IV/IO slowly (max 50 mEq/dose). Infants and small children: dilute 1:1 to 4.2% and give slowly. Do not use undiluted 8.4% in neonates
EAST 2022 and AAST 2022 advise against routine use; lowers ionized calcium and adds sodium
Insulin is high-alert: Use an independent double-check and a measured dose. Check glucose before the dose and repeatedly after it. AKI prolongs insulin action, so the low can arrive late. Check glucose hourly for at least 4–6 h.

What not to give

  • Mannitol and loop diuretics: Not recommended to prevent AKI (EAST 2022, AAST 2022). Save a diuretic for fluid overload.
  • Calcium for an asymptomatic low calcium: Avoid it. Calcium can deposit in injured muscle, and it often rebounds high during recovery. Treat only symptomatic hypocalcemia or hyperkalemia.
  • Nephrotoxins: Stop NSAIDs and other avoidable nephrotoxic drugs.

Definitive care & disposition

  • Kidney replacement therapy: Used for the usual AKI indications: refractory hyperkalemia, acidosis or fluid overload, and oliguric AKI. It is not there to clear myoglobin or to prevent AKI. See hemodialysis and CRRT.
  • Hemoadsorption: A 2024 consensus statement suggests considering it when serum myoglobin exceeds about 10,000 ng/mL. The evidence is low-certainty. Some consensus authors are industry-linked. This is a specialist ICU decision.
  • Compartment syndrome: Get an urgent surgical consult for fasciotomy. A delay of more than 6 h can cost irreversible muscle.
  • Admit to ICU: hyperkalemia, AKI, McMahon score 6 or more, ongoing muscle injury or large fluid needs. Follow CK until it reliably falls.
  • Follow-up: Recurrent or exertional episodes need a workup for an inherited metabolic myopathy.

For pediatric fluid and drug math, go to weight-based dosing.

Doses are typical references. Follow local protocols, medical direction and institutional policy.

Field & Transport Considerations

Point-of-care testing

Many hospitals send myoglobin out, and the answer can take 1–4 days. Point-of-care devices for it exist, yet none is validated for AKI risk. Out in the field, you work from the mechanism, the urine color, a urine dipstick (blood positive), the ECG and, if your service has one, a point-of-care K⁺ from a cartridge blood-gas analyzer.

Before and during interfacility transport

SettingConsideration
EMS: crush or long lie
Start fluid before release; monitor the ECG before, during and after release; document entrapment time and total fluid
Before transfer
Send the latest CK, myoglobin, K⁺, creatinine and calcium with draw times, the ECG, hourly urine output and fluid totals
En route
Continuous ECG; hourly urine output by catheter; recheck K⁺ (blood gas) on long transports or after new ECG changes
Redirect or escalate
Hyperkalemia, anuria or compartment syndrome: go to a center with dialysis and surgical capability

Timing & Kinetics

ParameterValueClinical implication
Release
Within hours of muscle injury
The earliest of the muscle markers to rise and to peak
Peak after MI
Approximately 6 h after symptom onset in reperfused STEMI (one 2023 cohort: median about 5.75 h; about 3 h after PCI; approximate)
Too nonspecific to use for MI diagnosis
Serum half-life
1–3 h (general figure)
Falls fast once release stops; a late draw can be normal
Apparent decline after STEMI
Approximately 7.6 h from peak in the same STEMI cohort (approximate)
Slower than the general half-life because release continues
Clearance
Freely filtered by the kidney
Kidney failure keeps levels high; filtered myoglobin injures tubules
CK for comparison
Rises within 12 h, peaks 24–72 h, normal in about 5 days
CK is the marker to trend; repeat until it reliably falls
When to repeat labs
K⁺, creatinine and electrolytes every 8–12 h, more often if severe
Hyperkalemia and AKI can appear after a normal first set
Different clocks: Myoglobin runs on a short clock and reflects the last few hours. CK runs on a longer one and reflects the last few days. Lean on myoglobin early, then follow CK for the trend.

Special Populations

PopulationWhat changesClinical implication
Neonates & infants
No published age-specific interval; few data
Use the lab range and CK; seek pediatric specialist input early
Children & adolescents
Viral myositis (often influenza B, ages 5–9) is the leading cause under 12; trauma and exertion in adolescents
Viral myositis is usually benign with low AKI risk; recurrent episodes suggest a metabolic myopathy
Pregnancy
No pregnancy-specific interval
Interpret against the adult female range; manage rhabdomyolysis the same way with obstetric input
Older adults
Long lie after a fall; age above 55 increases trauma rhabdomyolysis risk
Age adds McMahon points; lower threshold for monitoring and careful fluid titration
CKD / dialysis
Reduced renal clearance raises baseline myoglobin
Compare with baseline and CK; anuric patients cannot clear a fluid load
Other: athletes, sex
Vigorous exercise raises myoglobin; women have a lower upper limit
Interpret after recent exertion with CK and symptoms; use the sex-specific limit

For pediatric fluid targets and dosing, see Management Priorities and the weight-based dosing page.

Interfering Factors & Pitfalls

Collection & handling

FactorEffectWhyAvoid / fix
Gross hemolysis
Rejected
Reference labs reject grossly hemolyzed specimens
Clean draw; redraw if hemolyzed
Delayed separation
Unreliable
Reference labs require serum or plasma off the cells within 2 h
Spin and separate promptly
Urine left warm or acidic
False −
Urine myoglobin is unstable; labs require refrigeration and alkalinization
Refrigerate; use the lab’s alkaline transport tube; deliver promptly

Physiologic / biologic

FactorEffectWhyAvoid / fix
Kidney failure
↑
Myoglobin is cleared by glomerular filtration
Compare with baseline and CK
Recent vigorous exercise
↑
Normal muscle stress releases myoglobin
Correlate with CK and symptoms; repeat
Late draw
False −
Half-life 1–3 h
Use CK, K⁺ and creatinine to judge severity

Assay & device-specific

FactorEffectWhyAvoid / fix
Different immunoassays
Values not interchangeable
Myoglobin assays are not standardized; published cut-offs are assay-specific
Trend on one lab and one assay
Urine dipstick “blood”
False + for hematuria
Myoglobin and hemoglobin are heme proteins that react on the pad
Microscopy: few or no red cells points to myoglobin or hemoglobin

Common misinterpretations

  • “Normal myoglobin, so no rhabdomyolysis”: Wrong after the first day. Follow CK.
  • “High myoglobin means a heart attack”: Skeletal muscle is the usual source. Troponin decides.
  • “Dark urine with a positive dipstick is hematuria”: Check microscopy for red cells.
  • “One number predicts AKI”: Cut-offs vary 20-fold between studies. Combine the result with CK, creatinine, K⁺ and urine output.

Physiology & Test Basics

What it measures

Myoglobin is a small, oxygen-binding heme protein. It sits in the cytoplasm of skeletal and cardiac muscle. Serum myoglobin tells you about muscle injury from any source. It cannot separate heart from skeletal muscle. Urine myoglobin is a different test, one that shows what the kidney is filtering.

Physiology & regulation

  • Size: About 17 kDa, smaller than troponin (29–37 kDa). That is why it leaks out early and clears fast.
  • Release: Membrane injury or ATP depletion lets calcium flood the cell. Myoglobin, K⁺, phosphate and CK spill out with it.
  • Clearance: The glomerulus filters it freely. It leaves in the urine, turning it dark.
  • Kidney injury: Myoglobin casts block the tubules. Heme drives oxidant injury. Renal vasoconstriction follows. Hypovolemia and acidic urine make it worse.

How it is measured

  • Blood: serum (red top or serum separator tube); lithium heparin (green) or EDTA (lavender or pink) plasma also accepted. Separate within 2 h.
  • Method: immunoassay, often electrochemiluminescent; many hospitals send it to a reference lab.
  • Urine: random or 24-h sample, refrigerated during collection and alkalinized for transport.
  • Timing: no fasting; record the draw time relative to the injury.

Why it matters

Myoglobin no longer has a role in diagnosing MI. Its value is in rhabdomyolysis. An early, high myoglobin signals heavy muscle injury and higher risk of pigment AKI. Meanwhile, the hyperkalemia from that same injury can kill first.

Clinical Pearls

Think mechanism, not lab value: Crush, long lie, prolonged seizure or heat illness? Assume rhabdomyolysis until you prove otherwise. Start fluid and watch the ECG before a myoglobin result ever shows up.
Release can kill: Free a crushed limb and it can flood the circulation with K⁺ and acid. Before release, have fluid running, the monitor on and calcium at hand.
Tea-colored urine, no red cells: Dipstick blood strongly positive, yet few or no red cells on microscopy? Think myoglobin or hemoglobin. Not bleeding.
Nursing: urine output is the dial: Titrate fluid to the urine output target every hour. Report output that persists low despite fluid, new crackles or falling SpO₂ right away.
Leave the calcium alone: Early hypocalcemia is common in rhabdomyolysis. Resist the urge to treat the number. Give calcium only for hyperkalemic ECG changes or symptoms. It often rebounds high during recovery.
Check every compartment: Pain out of proportion, pain on passive stretch, tense swelling: call surgery now. Past 6 h of delay, you lose muscle.
Ignore it for chest pain: If a legacy cardiac panel shows myoglobin, the MI call rests on serial high-sensitivity troponin and the ECG. Myoglobin does not get a vote.

References

  1. Gulati, M., Levy, P. D., Mukherjee, D., et al. (2021). 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR guideline for the evaluation and diagnosis of chest pain: A report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation, 144(22), e368–e454. https://doi.org/10.1161/CIR.0000000000001029
  2. Kodadek, L., Carmichael, S. P., Seshadri, A., et al. (2022). Rhabdomyolysis: An American Association for the Surgery of Trauma Critical Care Committee clinical consensus document. Trauma Surgery & Acute Care Open, 7(1), e000836. https://doi.org/10.1136/tsaco-2021-000836
  3. Sawhney, J. S., Kasotakis, G., Goldenberg, A., et al. (2022). Management of rhabdomyolysis: A practice management guideline from the Eastern Association for the Surgery of Trauma. American Journal of Surgery, 224(1 Pt A), 196–204. https://doi.org/10.1016/j.amjsurg.2021.11.022
  4. Lim, A. K. H. (2025). Predicting acute kidney injury in acute rhabdomyolysis. Journal of Clinical Medicine, 14(19), 6892. https://doi.org/10.3390/jcm14196892
  5. Kuok, M. C. I., & Chan, W. K. Y. (2025). Rhabdomyolysis in children: A state-of-the-art review. Children, 12(4), 492. https://doi.org/10.3390/children12040492
  6. Henrik Kristensen, J., Amalie Wistisen Koczulab, C., Anton Frandsen, E., et al. (2023). Kinetics of cardiac troponin and other biomarkers in patients with ST elevation myocardial infarction. IJC Heart & Vasculature, 48, 101250. https://doi.org/10.1016/j.ijcha.2023.101250
  7. Forni, L., Aucella, F., Bottari, G., et al. (2024). Hemoadsorption therapy for myoglobin removal in rhabdomyolysis: Consensus of the hemoadsorption in rhabdomyolysis task force. BMC Nephrology, 25, 247. https://doi.org/10.1186/s12882-024-03679-8
  8. National Association of State EMS Officials. (2022). National model EMS clinical guidelines (Version 3.0): Crush injury/crush syndrome. NASEMSO. https://nasemso.org/wp-content/uploads/National-Model-EMS-Clinical-Guidelines_2022.pdf

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