2019-05-03 from uptodate
Creatine kinase — Serum CK levels at presentation are usually at least five times the upper limit of normal, but range from approximately 1500 to over 100,000 international units/L. 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 series [8]; exceptions were the three patients with malignant hyperthermia, whose values averaged almost 60,000.
The CK is generally entirely or almost entirely of the MM or skeletal muscle fraction; a small proportion of the total CK may be from the MB or myocardial fraction. The presence of MB reflects the small amount found in skeletal muscle rather than the presence of myocardial disease. Elevations in serum aminotransferases are common and can cause confusion if attributed to liver disease. In one study, aspartate aminotransferase (AST) was elevated in 93.1 percent and alanine aminotransferase (ALT) in 75 percent of rhabdomyolysis cases in which the CK was greater than or equal to 1000 units/L [9]. In only one instance was the ALT greater than the AST, although the AST declines faster than the ALT as the rhabdomyolysis resolves, such that the two may equalize after a few days [10]. (See "Muscle enzymes in the evaluation of neuromuscular diseases".)
The serum CK begins to rise within 2 to 12 hours following the onset of muscle injury and reaches its maximum within 24 to 72 hours. A decline is usually seen within three to five days of cessation of muscle injury. CK has a serum half-life of about 1.5 days and declines at a relatively constant rate of about 40 to 50 percent of the previous day's value [5,6,11]. In patients whose CK does not decline as expected, continued muscle injury or the development of a compartment syndrome may be present.
CK 院內參考數值 380. 超過五倍或超過 1000 可診斷.
Laboratory Tests
Useful laboratory tests that should be ordered include the following:
Useful laboratory tests that should be ordered include the following:
Complete blood count (CBC), including hemoglobin, hematocrit, and platelets
Serum chemistries, including blood urea nitrogen (BUN), creatinine, glucose, calcium, potassium, phosphate, uric acid, and liver function tests (LFTs)
Prothrombin time (PT)
Activated partial thromboplastin time (aPTT) – Thromboplastin released from injured myocytes can cause disseminated intravascular coagulation (DIC)
Serum aldolase
Lactate dehydrogenase (LDH)
Hyperkalemia, an immediate threat to life in the hours immediately after injury, occurs in 10-40% of cases. Liberated potassium can cause life-threatening dysrhythmias and death. Hyperphosphatemia does not require specific therapy. Hypocalcemia occurs early in the course of rhabdomyolysis. Supplemental calcium is not recommended. Increased purine metabolism causes hyperuricemia. Specific therapy with uricosuric agents or allopurinol is not indicated.
一項研究發現, 追蹤 97位急診病患, 第一次肌酸酐 1.7 以下. 沒有病患發生急性腎衰竭.
The BUN-creatinine ratio may be decreased because of the conversion of liberated muscle creatine to creatinine. In an emergency department (ED)-based study of 97 adults with rhabdomyolysis, no patient presenting in an ED setting with an initial creatinine level of less than 1.7 mg/dL developed ARF. [66]
One series of 109 ED patients with rhabdomyolysis found that 50% had anelevated cardiac troponin I level. Of these, 58% were ultimately found (on the basis of electrocardiography [ECG] and echocardiography) to be true positives, 33% were false positives, and 9% were indeterminate. [67]
A study analyzed the specific features and mortality of patients with rhabdomyolysis and the relation between creatinine, creatine kinase and mortality. The study concluded that despite being a diagnostic marker for rhabdomyolysis, initials creatine kinase levels do not predict mortality. However, the authors added that creatinine initial levels are related to progression to acute renal injury and mortality at 30 days. [68]
Creatine kinase
CK 通常在肌肉受傷之後 12 小時內上升, 24-36 小時到達顛峰, 之後每天下降 30-40%. CK的血中半衰期約 36 小時, 通常肌肉受傷緩解後 3-5 天會下降. 如果無法下降, 要考慮持續性肌肉損傷或出現腔室症候群. 如果超過 15000 要考慮腎衰竭.
The diagnosis of rhabdomyolysis can be confirmed using certain laboratory studies.[14] The most reliable and sensitive indicator of muscle injury is creatine kinase (CK). Assessing CK levels is most useful because of its ease of detection in serum and its presence in serum immediately after muscle injury.
CK levels rise within 12 hours of muscle injury, peak in 24-36 hours, and decrease at a rate of 30-40% per day. [69] The serum half-life of CK is approximately 36 hours. CK levels decline 3-5 days after resolution of muscle injury [14] ; failure of CK levels to decrease suggests ongoing muscle injury or development of a compartment syndrome. The peak CK level, especially when it is higher than 15,000 U/L, may be predictive of renal failure. [70]
CK 超過正常上限五倍可診斷橫紋肌溶解, 但經常超過 一百倍, 疾病早期可能只有上升達正常值 2-3 倍. 建議全套血液檢查. 每 6-12 小時抽血檢驗.
Total CK elevation is a sensitive but nonspecific marker for rhabdomyolysis. CK levels 5 times the reference range suggest rhabdomyolysis, though CK levels in rhabdomyolysis are frequently as high as 100 times the reference range or even higher. Suspect early rhabdomyolysis in patients with serum CK levels in excess of 2-3 times the reference range and risk factors for rhabdomyolysis; initiate a full laboratory workup. Because the total CK may increase from the initial values, draw repeat total CK levels every 6-12 hours until a peak level is established.
General investigations
The most reliable test in the diagnosis of rhabdomyolysis is the level of creatine kinase (CK) in the blood. This enzyme is released by damaged muscle, and levels above 5 times the upper limit of normal (ULN) indicate rhabdomyolysis. Depending on the extent of the rhabdomyolysis, concentrations up to 100,000 U/l are not unusual.[5] CK concentrations rise steadily for 12 hours after the original muscle injury, remain elevated for 1–3 days and then fall gradually.[3] Initial and peak CK levels have a linear relationship with the risk of acute kidney failure: the higher the CK, the more likely it is that kidney damage will occur.[14] There is no specific concentration of CK above which kidney impairment definitely occurs; concentrations below 20,000 U/l are unlikely to be associated with a risk of kidney impairment, unless there are other contributing risk factors. Mild rises without kidney impairment are referred to as "hyperCKemia".[4][13] Myoglobin has a short half-life, and is therefore less useful as a diagnostic test in the later stages.[3] Its detection in blood or urine is associated with a higher risk of kidney impairment.[14] Despite this, use of urine myoglobin measurement is not supported by evidence as it lacks specificity and the research studying its utility is of poor quality.[15]
血中 LDH 可能上升
其他肌肉損傷指數：aldolase, troponin,. carbonic anhydrase type 3, fatty acid binding protein 通常用在慢性肌肉疾病
GOT/GPT 也會上升，有 25％橫紋肌溶解症病患會同時合併實際的肝臟損傷
橫紋肌溶解症可能合併高血鉀
初期可能低血鈣
Elevated concentrations of the enzyme lactate dehydrogenase (LDH) may be detected.[8][14] Other markers of muscle damage, such as aldolase, troponin, carbonic anhydrase type 3 andfatty acid-binding protein (FABP), are mainly used in chronic muscle diseases.[14] The transaminases, enzymes abundant in both liver and muscle tissue, are also usually increased; this can lead to the condition being confused with acute liver injury, at least in the early stages. The incidence of actual acute liver injury is 25% in people with non-traumatic rhabdomyolysis; the mechanism for this is uncertain.[3]
High potassium levels tend to be a feature of severe rhabdomyolysis.[3] Electrocardiography (ECG) may show whether the elevated potassium levels are affecting the conduction system of the heart, as suggested by the presence of T wave changes or broadening of the QRS complex.[16] Low calcium levels may be present in the initial stage due to binding of free calcium to damaged muscle cells.[3]
尿液試紙可能出現血液陽性反應 但顯微鏡之下不一定會看見紅血球，跟溶血反應類似
發生腎損傷時，尿液可以看見 cast （pigmented and granular）
Urinalysis by urine test strip may reveal a positive result for "blood", even though no red blood cells can be identified on microscopy of the urine; this occurs because the reagent on the test strip reacts with myoglobin.[5] The same phenomenon may happen in conditions that lead to hemolysis, the destruction of red blood cells; in hemolysis the blood serum is also visibly discolored, while in rhabdomyolysis it is normal.[8][13] If kidney damage has occurred, microscopy of the urine also reveals urinary casts that appear pigmented and granular.[4]
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http://emedicine.medscape.com/article/1007814-overview
肌酸激酶 Creatine kinase
The diagnosis of rhabdomyolysis can be confirmed using certain laboratory studies.[14] The most reliable and sensitive indicator of muscle injury is creatine kinase (CK). Assessing CK levels is most useful because of its ease of detection in serum and its presence in serum immediately after muscle injury.
CK levels rise within 12 hours of muscle injury, peak in 24-36 hours, and decrease at a rate of 30-40% per day.[66] The serum half-life of CK is approximately 36 hours. CK levels decline 3-5 days after resolution of muscle injury[14] ; failure of CK levels to decrease suggests ongoing muscle injury or development of a compartment syndrome. The peak CK level, especially when it is higher than 15,000 U/L, may be predictive of renal failure.[67]
Total CK elevation is a sensitive but nonspecific marker for rhabdomyolysis. CK levels 5 times the reference range suggest rhabdomyolysis, though CK levels in rhabdomyolysis are frequently as high as 100 times the reference range or even higher. Suspect early rhabdomyolysis in patients with serum CK levels in excess of 2-3 times the reference range and risk factors for rhabdomyolysis; initiate a full laboratory workup. Because the total CK may increase from the initial values, draw repeat total CK levels every 6-12 hours until a peak level is established.
治療 輸液
Fluid Resuscitation
Expansion of extracellular volume is the cornerstone of treatment and must be initiated as soon as possible. No randomized trials of fluid repletion regimens in any age group have been done.[3] Retrospective studies of patients with severe crush injuries resulting in rhabdomyolysis suggest that the prognosis is better when prehospital personnel provide fluid resuscitation.[72] Support of intravascular volume increases the glomerular filtration rate (GFR) and oxygen delivery and dilutes myoglobin and other renal tubular toxins.
Expansion of extracellular volume is the cornerstone of treatment and must be initiated as soon as possible. No randomized trials of fluid repletion regimens in any age group have been done.[3] Retrospective studies of patients with severe crush injuries resulting in rhabdomyolysis suggest that the prognosis is better when prehospital personnel provide fluid resuscitation.[72] Support of intravascular volume increases the glomerular filtration rate (GFR) and oxygen delivery and dilutes myoglobin and other renal tubular toxins.
Patients with a CK elevation in excess of 2-3 times the reference range, appropriate clinical history, and risk factors should be suspected of having rhabdomyolysis. Obtain intravenous (IV) access with a large-bore catheter. For adults, administer isotonic fluids at a rate of approximately 400 mL/h (may be up to 1000 mL/h based on type of condition and severity) and then titrate to maintain a urine output of at least 200 mL/h.[3]
Because injured myocytes can sequester large volumes of extracellular fluid, crystalloid requirements may be surprisingly large. In patients with CK levels of 15,000 IU/L or greater, higher volumes of fluid, on the order of at least 6 L in adults, are required.[73] (Consider central venous pressure measurement or Swan-Ganz catheterization in patients with cardiac or renal disease. These invasive studies can assist in the assessment of the intravascular volume.) Repeat the CK assay every 6-12 hours to determine the peak CK level.
Aggressive and early hydration with isotonic sodium chloride solution is important for the prevention of pigment-associated renal failure. The composition of repletion fluid is controversial and may also include sodium bicarbonate. Initial fluid use in young children has been recommended to be 20 mL/kg; in adolescents, 1-2 L/h has been recommended. Subsequent hydration at a level 2-3 times maintenance may be sufficient.[11, 74] Few studies of fluid repletion regimens in children are available.[11]
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