What level of cpk is dangerous

URL of this page: https://medlineplus.gov/lab-tests/creatine-kinase/

Índice Show

Alternative Names
How the Test is Performed
How to Prepare for the Test
How the Test will Feel
Why the Test is Performed
Normal Results
What Abnormal Results Mean
Considerations

This test measures the amount of creatine kinase (CK) in the blood. CK is a type of protein, known as an enzyme. It is mostly found in your skeletal muscles and heart, with lesser amounts in the brain. Skeletal muscles are the muscles attached to your skeleton. They work with your bones to help you move and give your body power and strength. Heart muscles pump blood in and out of the heart.

There are three types of CK enzymes:

CK-MM, found mostly in skeletal muscles
CK-MB, found mostly in the heart muscle
CK-BB, found mostly in brain tissue

A small amount of CK in the blood is normal. Higher amounts can mean a health problem. Depending on the type and level of CK found, it can mean you have damage or disease of the skeletal muscles, heart, or brain.

Other names: CK, total CK, creatine phosphokinase, CPK

A CK test is most often used to diagnose and monitor muscular injuries and diseases. These diseases include:

Muscular dystrophy, a rare inherited disease that causes weakness, breakdown, and loss of function of skeletal muscles. It mostly occurs in males.
Rhabdomyolis, a rapid breakdown of muscle tissue. It can be caused by a serious injury, muscle disease, or other disorder.

The test can be used to help diagnose a heart attack, though not very often. CK testing used to be a common test for heart attacks. But another test, called troponin, has been found to be better at detecting heart damage.

You may need a CK test if you have symptoms of a muscular disorder. These include:

You may also need this test if you had a muscle injury or stroke. CK levels may not peak until up to two days after certain injuries, so you may need to be tested a few times. This test can help show if you have damage to your heart or other muscles.

A health care professional will take a blood sample from a vein in your arm, using a small needle. After the needle is inserted, a small amount of blood will be collected into a test tube or vial. You may feel a little sting when the needle goes in or out. This usually takes less than five minutes.

You don't need any special preparations for a CK test.

There is very little risk to having a blood test. You may have slight pain or bruising at the spot where the needle was put in, but most symptoms go away quickly.

If your results show you have a higher than normal level of CK, it may mean you have an injury or disease of the muscles, heart, or brain. To get more information, your provider may order tests to check the levels of specific CK enzymes:

If you have higher than normal CK-MM enzymes, it may mean you have a muscle injury or disease, such as muscular dystrophy or rhabdomyolis.
If you have higher than normal CK-MB enzymes, it may mean you have an inflammation of the heart muscle or are having or recently had a heart attack.
If you have higher than normal CK-BB enzymes, it may mean you have had a stroke or brain injury.

Other conditions that can cause higher than normal CK levels include:

If you have questions about your results, talk to your health care provider.

Learn more about laboratory tests, reference ranges, and understanding results.

Other blood tests, such as an electrolyte panel and kidney function tests, may be ordered along with a CK test.

Learn how to cite this page

Creatine phosphokinase (CPK) is an enzyme in the body. It is found mainly in the heart, brain, and skeletal muscle. This article discusses the test to measure the amount of CPK in the blood.

Alternative Names

CPK test

How the Test is Performed

A blood sample is needed. This may be taken from a vein. The procedure is called a venipuncture.

This test may be repeated over 2 or 3 days if you are a patient in the hospital.

How to Prepare for the Test

No special preparation is needed most of the time.

Tell your health care provider about any medicines you are taking. Drugs that can increase CPK measurements include amphotericin B, certain anesthetics, statins, fibrates, dexamethasone, alcohol, and cocaine.

How the Test will Feel

You may feel slight pain when the needle is inserted to draw blood. Some people feel only a prick or stinging sensation. Afterward, there may be some throbbing.

Why the Test is Performed

When the total CPK level is very high, it most often means there has been injury or stress to muscle tissue, the heart, or the brain.

Muscle tissue injury is most likely. When a muscle is damaged, CPK leaks into the bloodstream. Finding which specific form of CPK is high helps determine which tissue has been damaged.

This test may be used to:

Diagnose heart attack
Evaluate cause of chest pain
Determine if or how badly a muscle is damaged
Detect dermatomyositis, polymyositis, and other muscle diseases
Tell the difference between malignant hyperthermia and postoperative infection

The pattern and timing of a rise or fall in CPK levels can be significant in making a diagnosis. This is particularly true if a heart attack is suspected.

In most cases other tests are used instead of or with this test to diagnose a heart attack.

Normal Results

Total CPK normal values:

10 to 120 micrograms per liter (mcg/L)

Normal value ranges may vary slightly among different laboratories. Some labs use different measurements or test different samples. Talk to your provider about the meaning of your specific test results.

What Abnormal Results Mean

High CPK levels may be seen in people who have:

Brain injury or stroke
Convulsions
Delirium tremens
Dermatomyositis or polymyositis
Electric shock
Heart attack
Inflammation of the heart muscle (myocarditis)
Lung tissue death (pulmonary infarction)
Muscular dystrophies
Myopathy
Rhabdomyolysis

Other conditions that may give positive test results include:

Hypothyroidism
Hyperthyroidism
Pericarditis following a heart attack

Risks

Risks associated with having blood drawn are slight but may include:

Excessive bleeding
Fainting or feeling lightheaded
Hematoma (blood accumulating under the skin)
Infection (a slight risk any time the skin is broken)

Considerations

Other tests should be done to find the exact location of muscle damage.

Factors that may affect test results include cardiac catheterization, intramuscular injections, trauma to muscles, recent surgery, and heavy exercise.

References

Anderson JL. St segment elevation acute myocardial infarction and complications of myocardial infarction. In: Goldman L, Schafer AI, eds. Goldman-Cecil Medicine. 25th ed. Philadelphia, PA: Elsevier Saunders; 2016:chap 73.

Carty RP, Pincus MR, Sarafraz-Yazdi E. Clinical enzymology. In: McPherson RA, Pincus MR, eds. Henry's Clinical Diagnosis and Management by Laboratory Methods. 23rd ed. Philadelphia, PA: Elsevier; 2017:chap 20.

Mccullough PA. Interface between renal disease and cardiovascular illness. In: Zipes DP, Libby P, Bonow RO, Mann DL, Tomaselli GF, Braunwald E, eds. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 11th ed. Philadelphia, PA: Elsevier; 2019:chap 98.

Nagaraju K, Gladue HS, Lundberg IE. Inflammatory diseases of muscle and other myopathies. In: Firestein GS, Budd RC, Gabriel SE, McInnes IB, O'Dell JR, eds. Kelley and Firestein's Textbook of Rheumatology. 10th ed. Philadelphia, PA: Elsevier Saunders; 2017:chap 85.

Review Date: 01/28/2019

Received 2017 Apr 28; Accepted 2017 Jun 12.

This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)

Patient: Male, 36

Final Diagnosis: Rhabdomyolysis induced acute renal failure

Symptoms: Diarrhea • generalized weakness

Medication: —

Clinical Procedure: Hemodialysis • intubation

Specialty: Critical Care Medicine

Unusual setting of medical care

Rhabdomyolysis is a syndrome caused by muscle breakdown. It can be caused by traumatic as well as non-traumatic factors such as drugs, toxins, and infections. Although it has been initially associated with only traumatic causes, non-traumatic causes now appear to be at least 5 times more frequent. In rhabdomyolysis, the CK levels can range anywhere from 10 000 to 200 000 or even higher. The higher the CK levels, the greater will be the renal damage and associated complications.

We present the case of a patient with exceptionally massive rhabdomyolysis with unusually high CK levels (nearly 1 million) caused by combined etiologic factors and complicated with acute renal failure.

A 36-year-old African American male patient with no significant past medical history and a social history of cocaine and alcohol abuse presented with diarrhea and generalized weakness of 2 days’ duration. He was found to be febrile, tachycardic, tachypneic, and hypoxic. The patient was subsequently intubated and admitted to the medical ICU. Laboratory work-up showed acute renal failure with deranged liver functions test results, and elevated creatine kinase of 701,400 U/L. CK levels were subsequently too high for the lab to quantify. Urine legionella testing was positive for L. pneumophilia serogroup 1 antigen and urine toxicology was positive for cocaine. The patient had a protracted course in the ICU. He was initially started on CVVH, and later received intermittent hemodialysis for about 1 month.

In the presence of multiple etiologic factors, rhabdomyolysis can be massive with resultant significant morbidity. Clinicians should have a high index of suspicion for rhabdomyolysis in the presence of multiple factors, as early recognition of this diseases is very important in the prevention and active management of life-threatening conditions.

MeSH Keywords: Acute Kidney Injury, Cocaine, Creatine Kinase, Legionnaires’ Disease, Rhabdomyolysis

Rhabdomyolysis is a clinical syndrome characterized by elevated serum creatine kinase (CK) and other serum muscle enzymes. It can be a life-threatening condition due to associated conditions such as acute renal failure, severe electrolyte abnormalities, and acid base disorders.

The hallmark of rhabdomyolysis is elevated CK levels [1]. The mean peak CK reported for each of a variety of different causes and for patients with both single and multiple causes ranged from approximately 10 000 to 25 000 in the largest case series [2]. Common causes are trauma, muscle compression, hyperthermia, drugs and toxins like cocaine. Among infectious causes, legionella is a known bacterial cause of rhabdomyolysis [3]. The exact underlying mechanism involved in alcohol-induced rhabdomyolysis is unknown. Prolonged immobility and coma in short-term alcohol intoxication, and electrolyte abnormalities and acid base imbalances in long-term alcohol abuse have been implicated in causing rhabdomyolysis [4,5]. It can also be due to the direct toxic effects of ethanol on the skeletal muscles [6]. Prolonged vasoconstriction with resultant muscular ischemia, prolonged immobility, and compression or muscular hyperactivity with resultant secondary muscle injury are believed to be the underlying causes in cocaine-induced rhabdomyolysis [7]. Legionella-induced rhabdomyolysis is thought to be due to endotoxins or exotoxins and direct bacterial invasion [8].

We report the case of a patient managed for massive rhabdomyolysis with unusually high CK levels of greater than 701,400 U/L, resulting in acute renal failure, severe electrolyte abnormalities, significant acid base disturbances, and a prolonged hospital stay. Alcohol, cocaine, and legionella infection were the causative factors for severe rhabdomyolysis in this critically ill patient. The purpose of this article is to highlight the combined effect of multiple causative factors in rhabdomyolysis and the associated morbidity.

A 36-year-old African American male patient with no significant past medical history presented with diarrhea and generalized weakness of 2 days’ duration. He reported drinking 4 pints of vodka daily and regular use of cocaine. His last alcohol drink was 3 days prior to hospital admission, at which time he also took an unspecified amount of cocaine. He reported no similar episodes in the past. He was not on any medications at home. On physical examinations, he was found to have a temperature of 102°F (38.9°C), blood pressure of 138/94, pulse of 125 bpm, respiratory rate of 20 breaths per minute, and oxygen saturation of 98% on room air. He was drowsy but easily arousable. He was tachypneic with normal bilateral vesicular breath sounds, tachycardic with regular rhythm, no JVD, and no pedal edema. His abdomen was soft, non-tender, and nondistended, with no organomegaly and neurologic examination was significant for reduced power (3/5) in all his extremities with normal sensations.

While in the Emergency Department, he became more tachypneic, tachycardic, and hypoxic and was intubated on the day of admission (7/12). He was started on fluids and broad-spectrum antibiotics as per sepsis protocol and admitted to the medical ICU, where he was noted to be oliguric with a urine output of only 100 ml of muddy brown urine after initial vigorous fluid resuscitation.

In the ICU, patient was being managed for acute hypoxic respiratory failure secondary to legionella pneumonia sepsis, acute renal failure, severe electrolyte abnormalities, and acid base disturbances secondary to massive rhabdomyolysis. Laboratory work-up results are shown in Table 1. Initial chest X-ray was normal but the repeat X-ray (Figure 1) on day 2 of hospital admission showed new right lower-lobe consolidation. Echocardiography showed both diastolic and systolic dysfunction with trace pericardial effusion, and EKG showed sinus tachycardia with right atrial enlargement.

CXR showing right lower-lobe pneumonia.

Laboratory Investigations.

Sodium	133 mmol/L (135–145)	Aspartate aminotransferase AST	2847 U/L (10–40)
Potassium	4.75 mmol/L (3.5–5.0)	Alanine aminotransferase ALT	550 U/L (7–56)
Urea nitrogen	33 mg/dl (7–20)	Alkaline phosphatase	63 iU/L (44–147)
Creatinine	4.8 mg/dl (0.6–1.2)	Bilirubin	0.6 mg/dL (0.3–1.0)
Phosphate	12.7 mg/dl (2.5–4.5)	Albumin	2.3 g/dL (3.5–5.5)
Bicarbonate	12 mmol/L (24–30)	Serum alcohol level	<3 mg/dl (£5)
Anion gap	19 mEq/L (3–11)	Arterial blood gases on room air
GFR*	6.8 ml/min (90–120)	pH	7.399 (7.35–7.45)
Calcium	5 mg/dL (8.5–10.2)	PaCo2	20.4 mmHg (38–42)
Creatine kinase	701,400 U/L (52–336 male)	PO2	91 mmHg (80–100)
Hemoglobin	19.4 g/dL (13.5–17.5)
Hematocrit	59.3% (38.8–50)
White cells	27.1×103 (3500–10 500 cell/mcL)
Platelets	216×103 (150 000–500 000/mcL)
Thrombin time	10.7 seconds (11–13.5)
PTT**	29.4 seconds (30–40)
Uric acid level	15.2 mg/dl (2.4–6.0)
Urine legionella antigen test: Positive for L. pneumophila serogroup 1 antigen. Urine toxicology: Positive for cocaine. Urine analysis (UA): Cloudy appearance with trace glucose, 3+ bilirubin, +1 ketones, specific gravity 1.025, 3+blood, ph: 7.0, 3+ protein, urobilinogen: 2.0, WBC 0–2, and RBC 0–2. Influenza and respiratory syncytial virus (RSV): Not detected. Clostridium difficile: Negative. Tracheal aspirate culture, blood cultures, urine culture results: No growth.

Patient was started on CVVH (Continuous Venovenous Hemofiltration) on day 2 of hospital stay (7/13) of hospital admission, with some improvement in renal function. He was extubated 4 days later (7/16). Despite Initial improvement, he continued to have persistent acute kidney injury with no significant renal recovery, large extracellular fluid volume, and remained oligo-anuric; therefore, a decision was made to start the patient on intermittent hemodialysis on day 7 (7/20). He remained in the ICU for a total of 8 days, after which was transferred to general medicine floor. Patient was discharged home after about a month, at which time he was clinically stable with stable renal panel and normal creatine kinase levels.

Rhabdomyolysis can be induced by many different causes, but it is usually the result of multiple contributing factors. Although it was initially associated almost exclusively with traumatic conditions, non-traumatic causes now appear to be at least 5 times more frequent [5].

Clinically, patients may be symptomatic or totally asymptomatic. When symptomatic, they can present with the classical triad of muscle pain, weakness, and brown urine or decreased urine, or with nonspecific symptoms like fatigue, nausea, vomiting, fever, or confusion [7]. Acute kidney injury (AKI) occurs in 33–50% of patients with rhabdomyolysis [9] and the most reliable laboratory parameter used for the diagnosis of this condition is the measurement of serum CK levels.

Our patient, an active alcohol and cocaine abuser, presented with generalized weakness and diarrhea, and was found to have legionella pneumonia with sepsis and acute renal failure with severe electrolyte abnormalities and acid base disturbances due to massive rhabdomyolysis. What is unique about this case is that the combination of these could be a reason for the exponential rise of creatine kinase, resulting in severe morbidity and protracted hospital course. The other important point to note in this case is that acute renal failure could have been easily attributed to other factors like sepsis, severe dehydration, shock, or medication, and rhabdomyolysis-induced acute renal failure could have been easily missed if CK levels were not checked. Such comorbid conditions increase the risk of death. It is therefore important that, in the presence of these risk factors, and in appropriate clinical settings, CK levels should be checked early to detect rhabdomyolysis.

Rhabdomyolysis caused by multiple factors is associated with exceptionally high CK levels. Higher CK levels are associated with greater burden on the kidneys, causing acute renal failure, severe electrolyte abnormalities, and acid base disturbances, resulting in significant morbidity. Early rhabdomyolysis assessment should not be missed in similar cases, particularly in a toxicological patient. Timely diagnosis and treatment of the disease can prevent such life-threatening conditions.

1. Miller ML. Uptodate Inc; c2017. Causes of rhabdomyolysis [Internet] [last updated: Oct 13, 2016 cited 2017, April 26 ]. Available from: http://www.uptodate.com/contents/causes-of-rhabdomyolysis. [Google Scholar]

2. Melli G, Chaudhry V, Cornblath DR. Rhabdomyolysis: An evaluation of 475 hospitalized patients. Medicine (Baltimore) 2005;84:377–85. [PubMed] [Google Scholar]

3. Blanco JR, Zabalza M, Salcedo J, et al. Rhabdomyolysis of infectious and noninfectious causes. South Med J. 2002;95(5):542–44. [PubMed] [Google Scholar]

4. Qiu LL, Nalin P, Huffman Q, et al. Nontraumatic rhabdomyolysis with long-term alcohol intoxication. Am Board Fam Med. 2004;17(1):54–58. [PubMed] [Google Scholar]

5. Efstratiadis G, Voulgaridou A, Nikiforou D, et al. Rhabdomyolysis updated. Hippokratia. 2007;11:129–37. [PMC free article] [PubMed] [Google Scholar]

6. Papadatos SS, Deligiannis G, Bazoukis G, et al. Nontraumatic rhabdomyolysis with short-term alcohol intoxication – a case report. Clin Case Rep. 2015;3(10):769–72. [PMC free article] [PubMed] [Google Scholar]

7. Nemiroff L, Cormier S, LeBlanc C, Murphy N. Don’t you forget about me: Considering acute rhabdomyolysis in ED patients with cocaine ingestion. Can Fam Physician. 2012;58(7):750–54. [PMC free article] [PubMed] [Google Scholar]

8. Koufakis T, Gabranis I, Chatzopoulou M, et al. Severe Legionnaires’ disease complicated by rhabdomyolysis and clinically resistant to moxifloxacin in a splenectomised patient: Too much of a coincidence? Case Rep Infect Dis. 2015;2015:793786. [PMC free article] [PubMed] [Google Scholar]

9. Lima RS, da Silva Junior GB, et al. Acute kidney injury due to rhabdomyolysis. Saudi J Kidney Dis Transpl. 2008;19(5):721–29. [PubMed] [Google Scholar]

Articles from The American Journal of Case Reports are provided here courtesy of International Scientific Information, Inc.