Rhabdomyolysis Part 1 – Diagnosis and Treatment
Matthew DeLaney MD
Take Home Points
- There are two causes of rhabdomyolysis; exertional and non-exertional. Patients with non-exertional rhabdomyolysis are often sicker with a worse prognosis.
- The initial CK level does not predict a bad outcome. Patients with concomitant acute kidney injury are more likely to have a bad outcome.
- Rhabdomyolysis is treated with fluids but no particular fluid has been shown superior.
- Alkalinization of the urine and diuretics have not been shown to have meaningful improvement in patient outcome.
- Rhabdomyolysis is the dissolution of striated muscles. This is the common pathway. However, there are many different ways to get rhabdomyolysis. How and why you get it determines how you will do in the future.
- This is not a new disease. It was described in the Old Testament in the Book of Numbers due to consumption of quail that had eaten hemlock. Much of the current data comes from natural disasters. Crush syndrome was identified in England in 1940s. Patients who had been trapped in rubble for prolonged times were found to have extensive muscle necrosis on autopsy and brown pigment in the renal tubules. There is increasing awareness of rhabdomyolysis due to an association with intense athletic cross-training.
- What is the pathophysiology of rhabdomyolysis?
- There is some injury to the cell resulting in increased intracellular calcium. The two main methods of injury are direct trauma to the myocyte or some alteration in energy production. Increased intracellular calcium eventually leads to lysis of the cell and release of the contents such as potassium, calcium, phosphates, creatine kinase and myoglobin.
- This may result in hyperkalemia and hypercalcemia.
- Myoglobin is filtered by the kidneys and concentrated in the renal tubules. This is thought to be the primary nephrotoxic agent associated with rhabdomyolysis. In an acidic environment, the myoglobin will precipitate and cause kidney damage through several mechanisms. It can obstruct the renal tubules, cause oxidative damage and vasoconstriction. This leads to myoglobinuria.
- Acute kidney injury is the most common complication associated with rhabdomyolysis. About 10% of cases of acute kidney injury in the US have rhabdomyolysis as the precipitating event. About 46% of patients with rhabdomyolysis will develop acute kidney injury.
- Who is at risk of rhabdomyolysis? Rhabdomyolysis may occur from a variety of mechanisms and the outcomes are as variable as the causes. This can be from non-exertional and exertional causes.
- Non-exertional causes include alteration of the production of energy of the cell and direct trauma. Hypoxia, carbon monoxide exposure, cyanide, compartment syndrome, vascular compression, immobilization (for example, rhabdomyolysis may occur after bariatric surgery due to prolonged immobilization), sickle cell disease, vasculitis, etc. Causes of direct trauma to the muscle include crush injuries, electrocution, hypothermia or hyperthermia, neuroleptic malignant syndrome, etc.
- The most common cause of non-exertional rhabdomyolysis is a drug side-effect. Statins are a common cause. Approximately 10% of patients on statins (in particular, simvastatin, atorvastatin or lovastatin) will experience some muscle effects; soreness, swelling or rhabdomyolysis. However, less than 1% of these patients will have clinically significant rhabdomyolysis. Patients taking fibrates or other p450 inhibitors along with their statins have a greater risk of rhabdomyolysis.
- Illegal drugs such as cocaine and methamphetamines are also included as chemical causes of rhabdomyolysis. The reason is unclear. Increased physical activity may contribute. Vasoconstriction and ischemia may also contribute.
- Anyone is at risk for exertional rhabdomyolysis. There are reports of people developing rhabdomyolysis from playing video games too long or minimal physical exertion. Higher risk activities include doing exercise that you are unused to doing or eccentric training. Crossfit incorporates eccentric training.
- The diagnosis may be tricky. There is a classic triad of symptoms of weakness, myalgia, and tea-colored urine. However, only 10% of patients with rhabdomyolysis will have this triad of symptoms. Some studies show that over 50% of patients with rhabdomyolysis do not report muscle pain or weakness. Tea-colored urine is only present in about 3-4% of cases.
- Have a high index of suspicion. Consider it in higher risk patients; sickle cell patients, casted or immobilized joints, myopathies, statin use, etc.
- How do we identify muscle breakdown? Myoglobin and creatine kinase may indicate muscle breakdown. Myoglobin is cleared rapidly and is less sensitive. Most recommendations do not recommend checking myoglobin.
- Creatine kinase typically increases within the first twelve hours. It peaks within 3-5 days and returns to baseline by about 10 days.
- How do you interpret the creatine kinase level? A normal reference range is 100 units/L (1.67 µkat/L). Most textbooks advise concern for rhabdomyolysis with five or more times the upper limit of normal (500-1000 units/L or 8.4-16.7 µkat/L). This is probably overly conservative. Most of the data indicates that the risk of acute kidney injury doesn’t increase until the CK level goes over 5000 units/L (83.5 µkat/L). The FDA advises that rhabdomyolysis requires 50 times the upper limit of normal or 10000 units/L with organ damage. Other organizations differentiate between mild rhabdomyolysis (less than 10 times the upper limit of normal), moderate rhabdomyolysis (10-49 times the upper limit of normal) and significant rhabdomyolysis (greater than 50 times the upper limit of normal).
- This mostly applies to non-exertional causes. Patients with exertional rhabdomyolysis may have significantly elevated levels but benign outcomes.
- CK levels help us identify rhabdomyolysis but do not indicate the prognosis.
- Baeza-Trinidad, R et al. Creatinine as predictor value of mortality and acute kidney injury in rhabdomyolysis. Intern Med J. 2015 Nov’45(11):1173-8. PMID: 26010490
- They found no association between creatine kinase levels on presentation and the development of renal failure or mortality. However, the initial creatinine levels did correlate with these outcomes.
- McMahon, GM et al. A risk prediction score for kidney failure or mortality in rhabdomyolysis. JAMA Intern Med. 2013 Oct 28; 173(19):1821-8. PMID: 24000014
- A study looking at more than 2000 patients admitted with rhabdomyolysis found the rate of need for dialysis or death only increased when CK levels were greater than 40000 units/L (668 µkat/L initially).
- They found that kidney function at the time of presentation was more predictive of prognosis. In-hospital mortality was 22.5% in patients with acute rhabdomyolysis and kidney injury at the time of presentation compared to 7.1% without an acute kidney injury.
- In addition to checking CK levels and creatinine, you should check electrolytes. You are looking for hyperkalemia and hypercalcemia. In early rhabdomyolysis, you may see hypocalcemia due to entrance into the cell. As the cells lyse, the calcium will increase. Treat hyperkalemia similar to that resulting from any other disease process. Many recommendations do not advise treatment of hypocalcemia. However, if the patient has hyperkalemia, you can give calcium for EKG changes.
- The classic board question is a patient with a urine dipstick positive for blood but only a few red blood cells noted on microscopy. However, this isn’t seen in the majority of patients with rhabdomyolysis.
- The goal of treatment is to decrease the rate of renal failure.There isn’t good supporting literature on optimal treatment.
- These patients need fluids. The recommendations say that fluids should be started within 6 hours. You want to target a urine output of about 250-300 cc/hr. You are trying to increase the renal tubular flow, decrease the accumulation of myoglobin and toxic products, correct dehydration and acidosis. The amount of fluids necessary is unclear.
- A study comparing 15 ml/kg of fluid to 40 ml/kg of fluid in bariatric patients found no difference in outcomes.
- Wool, DB et al. Intraoperative fluid replacement and postoperative creatine phosphokinase levels in laparoscopic bariatric patients. Obes Surg. 2010 Jun;20(6):698-701. PMID: 20198451
- The type of fluid probably doesn’t matter. A small double-blinded randomized controlled trial comparing 400 cc/h of lactated Ringer’s solution to 0.9% saline found that the patients were similar clinically after 12 hours. The pH was higher in the blood and urine of patients receiving lactated Ringer’s but outcomes were similar between the two groups.
- Cho, YS et al. Comparison of lactated Ringer’s solution and 0.9% saline in the treatment of rhabdomyolysis induced by doxylamine intoxication. Emerg Med J. 2007 Apr;24(4):276-80.PMID: 17384382
- Another classic teaching is that urine should be alkalinized to prevent precipitation of myoglobin. A urine pH of greater than 6.5 is targeted. There are some animal and retrospective studies that have shown some potential benefit. However, larger retrospective studies have shown that administration of bicarbonate does not decrease the severity of kidney injury, need for dialysis or risk of death. Alkalinization of the urine may be difficult to do and can result in downstream effects. It has not been shown superior to giving the patient an adequate amount of fluid.
- Diuretics have been discussed. However, the data is messy. Mannitol has been discussed but has not been studied apart from bicarbonate. Loop diuretics also sound good in theory but there is no evidence demonstrating effectiveness.
- The type of fluid probably doesn’t matter. A small double-blinded randomized controlled trial comparing 400 cc/h of lactated Ringer’s solution to 0.9% saline found that the patients were similar clinically after 12 hours. The pH was higher in the blood and urine of patients receiving lactated Ringer’s but outcomes were similar between the two groups.
- Baeza-Trinidad, R et al. Creatinine as predictor value of mortality and acute kidney injury in rhabdomyolysis. Intern Med J. 2015 Nov’45(11):1173-8. PMID: 26010490
Rhabdomyolysis Part 2 – Disposition
Matthew DeLaney MD
Take Home Points
- Differentiating between physiologic and pathologic can be difficult in exertional rhabdomyolysis but most patients will do fine.
- Patients with mild exertional rhabdomyolysis may be candidates for discharge home.
- Disposition can be tricky.
- For non-exertional cases of rhabdomyolysis, there is decent data to say that if the CK is less than 5000 (83.5 µkat/L) with normal renal function, the patient has a low chance of developing renal failure or mortality. This is an opportunity to have shared decision making with the patient. You can advise the patient that the labs are abnormal and they will need follow-up testing to make sure they aren’t worsening and are resolving. The patients need fluid and need to urinate. For patients at low risk for complications, this doesn’t have to happen in the hospital.
- If the patient has a CK greater than 5000 or any kidney injury, it is more complicated. It is unclear exactly what degree of kidney injury is significant. Don’t be cavalier. If the creatinine is elevated or the patient has a significantly elevated CK level, it may be better to admit them for monitoring.
- Exertional rhabdomyolysis.There is increasing awareness of this due to the popularity of CrossFit. When you exercise, your CK levels are likely to increase. We don’t know the point where this becomes pathologic.
- A study in marathon runners found the mean CK elevation 24 hours after the marathon was more than 20 times the upper limit of normal.
- Siegel, AJ et al. Elevated creatine kinase MB isoenzyme levels in marathon runners. Normal myocardial scintigrams suggest noncardiac source. 1981 Nov 6;246(18):2049-51.PMID: 7288991
- A study in 499 healthy military recruits doing two weeks of basic military training found that almost everyone had an elevated CK at some point during their training. When the levels were checked at day 7, they found that approximately 27% had CK levels greater than five times the upper limit of normal. 11% had levels greater than 10 times the upper limit of normal. They found no correlation between the CK level, amount of exertion, environmental conditions or reports of myalgia or weakness.
- These authors proposed that if the CK level was less than 50 times the upper limit of normal in the absence of muscle swelling, weakness, myoglobinuria, acute renal failure or electrolyte imbalance, it should not be categorized as clinically significant rhabdomyolysis.
- Kenney, K et al. Serum creatine kinase after exercise: drawing the line between physiological response and exertional rhabdomyolysis. Muscl Nerve. 2012 Mar;45(3):356-62.PMID: 22334169
- A study in 203 healthy volunteers had them perform 50 maximal eccentric elbow flexor contractions. They found 55% had CK elevations greater than 2000 at 4 days after performing the exercises. 13% had levels greater than 20000. Despite this, none of these patients had any adverse outcomes.
- Clarkson, PM et al. Serum creatine kinase levels and renal function measures in exertional muscle damage. Med Sci Sports Exerc. 2006 Apr;38(4):623-7.PMID: 16679975
- One of the biggest risk factors for exertional rhabdomyolysis seems to be unaccustomed physical activity. This may happen in clusters; for example, when sports teams adopt a new athletic regimen.
- Exertional rhabdomyolysis is almost always a benign disease.
- Oh, RC et al. Exertional rhabdomyolysis: a case series of 30 hospitalized patients. Mil Med. 2015 Feb;180(2):201:7. PMID: 25643388
- They took 30 cases of previously healthy military patients who were admitted to the hospital for exertional rhabdomyolysis. Some of this was attributed to CrossFit training and some was due to unaccustomed physical activity. The CK levels ranged from 1500 to 410000. Everyone recovered without dialysis or lasting kidney injury.
- How do we disposition patients with exertional rhabdomyolysis?
- Scalco, RS et al. Exertional rhabdomyolysis: physiological response or manifestation of any underlying myopathy? BMJ Open Sport Exerc Med. 2016 Sep 7;2(1):e000151.PMCID: PMC5117086
- They recommend evaluating the patient and CK to determine disposition home.
- If the patient has mild symptoms such as myalgias, normal vital signs, a clear trigger such as unaccustomed exercise and no renal failure, myoglobinuria or electrolyte derangements, it is probably safe to discharge the patient home.
- They looked at a CK level less than 10,000.
- Features of exertional rhabdomyolysis that are more concerning include abnormal vital signs (hyperthermic or hypothermic), muscle weakness, concern for compartment syndrome or electrolyte derangement.
- Ask the patient if this is their first time experiencing rhabdomyolysis. There are certain genetic conditions and myopathies that can predispose patients to rhabdomyolysis with minimal exertion. You may be more likely to admit the patient if they have had previous episodes.
- We don’t have great literature to say when patients can return to exercise. Most of the guidelines recommend taking a few weeks off of exercise and waiting until the CK completely normalizes. This may take 10-14 days. Start with light activity. Even if patients ignore these guidelines, the rate of recurrence of rhabdomyolysis from exertion in the general population is low (about 0.8 per year). Most of these patients will be fine.
- A study in marathon runners found the mean CK elevation 24 hours after the marathon was more than 20 times the upper limit of normal.
Pathologic condition in which necrosis of skeletal muscle occurs secondary to injury causing leaking of constituents into plasma. Myoglobin, creatnine kinase (CK) are the primary constituents.
Causes
Can be divided into traumatic and atraumatic. Most common causes are ETOH abuse, compression, seizures, and drug abuse. Other causes are direct trauma, hypothermia, infection, metabolic abnormalities (dka, hypokalemia, hypophosphatemia), and gangrene. Many drugs have been linked to rhabdo, but the most important class is the statins. Genetic muscle metabolism abnormalities can also predispose to rhabdo.
Pressor agents can also cause mild rhabdomyolysis
Because substance abuse and compression injury are such common causes, inquire about drug use, alcohol use, binge drinking, and immobilization.
The final common pathway of these causes is a significant increase in intracellular free ionized calcium. Increased calcium results either from direct injury to the muscle cell membrane or from insufficient energy supply to the muscle.
CK at least 5 times normal, but since peak levels may not be seen immediately, the cut-off for diagnosis is usually 3x normal. (Mb should be less than 5% of it) Peak levels are reached in 24-36 hours and then fall by ~40% a day.
Myoglobin, on the other hand, is cleared from the plasma very rapidly (1/2 life of 1-3 hours). If myoglobinuria is present, fairly specific, but its absence is not helpful.
Hepatic dysfunction with liver enzyme increase, hyperbillirubinemia, and elevated PT.
DIC can also ensue.
Potassium, phosphorous, organic acids, and purines released from the muscle cells can cause hyperkalemia, hyperphosphatemia, metabolic acidosis, and hyperuricemia. Hypocalcemia can be seen secondary to the hyperphosphatemia. If the patient has acute renal failure as a result of the rhabdo, it will usually result in an increased creatnine without a proportional rise in BUN. This is b/c of direct release of creatnine from the damaged muscle cells.
Compartment syndrome can be a cause or a serious complication of rhabdo. Compartment syndrome that occurs late in the course is due to large fluid volume uptake by damaged tissue.
The most serious complication is acute renal failure. The nephrotoxicity of myoglobin is dependant on hypovolemia, dehydration, and aciduria.
In crush injuries, give 1 liter bolus of NS followed by 1/2 normal at 200-700 cc/hr to achieve urine flow rates of 200-300 cc/hr.
In non-traumatic causes, 250 cc/hr of NS for 1 liter then switch to 1/2 NS at the rates above.
Mannitol can be given with intermittent boluses of 12.5-25 grams or add 10 gm to each liter of IVF.
Lasix does not help.
Alkalinize the urine to at least 6.5
Give 100 meq bolus then add 1-2 amps to each subsequent liter of fluids.
Crappy retrospective article showed no benefit to Mannitol or Bicarb (J Trauma Volume 56(6) June 2004)
Prophylaxis of acute renal failure in patients with rhabdomyolysis. Ren Fail. 1997 Mar;19(2):283-8. Homsi E, Barreiro MF, Orlando JM, Higa EM. Patients that develop rhabdomyolysis of different causes are at high risk of acute renal failure. Efforts to minimize this risk include volume repletion, treatment with mannitol, and urinary alkalinization as soon as possible after muscle injury. This is a retrospective analysis (from January 1, 1992, to December 31, 1995) of therapeutic response to prophylactic treatment in patients with rhabdomyolysis admitted to an intensive care unit (ICU). The diagnosis of rhabdomyolysis was based on creatinine kinase (CK) level (> 500 Ui/L) and the criteria for prophylaxis were: time elapsed between muscle injury to ICU admission < 48 h and serum creatinine < 3 mg/dL. Fifteen patients were treated with the association of saline, mannitol, and sodium bicarbonate (S + M + B group) and 9 patients received only saline (S group). Serum creatinine at admission was similar in both groups: 1.6 +/- 0.6 mg/dL in the S + M + B group and 1.5 +/- 0.6 mg/dL in the S group (p > 0.05). Maximum serum CK measured was 3351 +/- 1693 IU/L in the S + M + B group and 1747 +/- 2345 IU/L in the S group (p < 0.05). However the measurement of CK was earlier in S + M + B patients (1.7 vs 2.7 days after rhabdomyolysis). APACHE II scores were 16.9 +/- 7.4 and 13.4 +/- 4.9 in the S + M + MB and S groups, respectively (p > 0.05). *Despite the treatment protocol the serum levels of creatinine had similar behavior and reached normal levels in all patients in 2 or 3 days. *The saline infusion during the first 60 h on the ICU was 206 mL/h in the S group and 204 mL/h in S + M + B (p > 0.05). Mannitol dose was 56 g/day, and bicarbonate 225 mEq/day during 4.7 days. *Our data show that progression to established renal failure can be totally avoided with prophylactic treatment, and that once appropriate saline expansion is provided, the association of mannitol and bicarbonate seems to be unnecessary. * or Preventing renal failure in patients with rhabdomyolysis: do bicarbonate and mannitol make a difference? *Brown CV, Rhee P, Chan L, Evans K, Demetriades D, Velmahos GC: ** *J Trauma. 2004 Jun;56(6):1191-6. CONCLUSION: Abnormal CK levels are common among critically injured patients, and a CK level greater than 5,000 U/L is associated with RF. Bicarbonate/Mannitol does not prevent RF, dialysis, or mortality in patients with creatine kinase levels greater than 5,000 U/L. T*he standard of administering Bicarbonate/Mannitol to patients with post-traumatic rhabdomyolysis should be reevaluated.*
Start CVVH when Myoglobin is > 10,000
50% with ck>5000 will develop ARF
increased ldh and ast as well
causes profound intravascular depletion
myoglobin binds tamm-horsfal protein, cast formation is enhanced in acidic environments
lipid peroxidation
renal vasoconstrictors
blockage of NO renal vasodilation
(intens care med 2001;27:803)
The American Journal of Emergency Medicine Volume 24, Issue 4 , July 2006, Pages 509-510 This Document SummaryPlus Full Text + Links ·Full Size Images PDF (70 K) External Links Actions Cited By Save as Citation Alert E-mail Article Export Citation doi:10.1016/j.ajem.2006.03.020 Copyright © 2006 Elsevier Inc. All rights reserved. Correspondence Where does troponin I derive from in rhabdomyolysis? Josef Finsterer MDa, and Claudia Stöllberger MDb aNeurological Department Krankenanstalt Rudolfstiftung, A-1030 Vienna, Austria b2nd Medical Department, Krankenanstalt Rudolfstiftung, A-1030 Vienna, Austria Available online 17 June 2006. Referred to by: Reply to the Letter from Finsterer and Stöllberger, The American Journal of Emergency Medicine, Volume 24, Issue 4, July 2006, Pages 510-511 Siu Fai Lia, Jennifer Zapataa and Elizabeth Tillema SummaryPlus | Full Text + Links | PDF (52 K) Article Outline References With interest we read the article by Li et al on 109 patients with rhabdomyolysis among whom 55 (50%) also had elevated cardiac troponin I (cTnI). Of the 55, 32 were assessed as true positives, 18 as false positives, and 5 as indeterminate. Cocaine abuse, renal insufficiency, and myoglobinuria were excluded as causes of false-positive cTnI [1]. The report raises the following questions and concerns. The definition of rhabdomyolysis solely as creatine kinase (CK) elevation of more than 1000 U/L is insufficient. A more comprehensive definition of rhabdomyolysis requires the presence of tetraparesis, CK elevation more than 10 times the upper reference limit, myoglobinuria, hyperkaliemia, and coagulopathy [2]. According to this definition, the number of patients with rhabdomyolysis is presumably less than indicated. It is also of interest to know the cause of CK elevation in the included patients. It is well known that normal values of CK are dependent on the total muscle mass. Thus, they are usually different between women and men in most laboratories. The reference values applied in the present investigation, however, were unisexual. Why? How long did the patients stay at the ED? How long was the average follow-up duration? How many patients died during hospitalization? How many of the patients with true-positive and false-positive cTnI elevation had a myocardial infarction? How many of these patients underwent coronary angiography? The present study relied on the assumption that cTnI is solely released during myocardial ischemia. However, cTnI may also increase during myocardial damage from inflammation, intoxication, malignancy, or degeneration. This is why in addition to segmental or global wall motion abnormalities, features such as left ventricular hypertrabeculation/noncompaction, abnormal myocardial texture, left ventricular wall thickening, or reduced fractional shortening, diastolic dysfunction, or dilated cardiac cavities should be assessed on echocardiography. On electrocardiography, abnormalities other than signs of myocardial ischemia, such as left ventricular hypertrophy, expressed as various QRS indices, should be included in the evaluation. Some of the included patients might have presented with transient left ventricular dysfunction, also known as Takotsubo phenomenon, which is accompanied by CK elevation and can be precipitated by rhabdomyolysis [3]. Rhabdomyolysis may cause stress and thus myocardial damage with cTnI elevation. Because cTnI is as sensitive as cTnT in detecting myocardial necrosis caused by ischemia [4], it would be interesting to know whether cTnT was also determined and whether the frequency of false positives was as high as for cTnI. Cardiac troponin I may also be positive in malignancy with cardiac amyloidosis [5], pheochromocytoma [6], carcinoid syndrome [7], generalized seizures [8], stroke, shock, or massive pulmonary embolism [9]. Why were the 55 patients with positive cTnI not evaluated for causes of false-positive cTnI other than cocaine abuse, renal insufficiency, or myoglobinuria? Interestingly, there is a strong preponderance of male patients in the study population (male/female ratio, 3:1). Is this because myocardial infarction is more prevalent in men than in women or because of the higher muscle mass in men than in women? Was the male preponderance also present in the subgroup of the false positives? The absent correlation between peak cTnI and CK is not surprising as it was calculated for all 55 patients with positive cTnI. Consequently, it includes also the false positives in whom elevated CK most likely derives from a tissue other than the myocardium. The lower part of Table 1 is misleading. It appears impossible that 61 patients had myoglobinuria in the truly positive group, which consisted of 32 patients. This also holds true for more than 18 patients with cocaine abuse, myoglobinuria, renal failure, electrocardiogram abnormalities, and abnormal echocardiography in the false-negative group. It would be interesting to investigate the false positives prospectively by a neurologist to find out whether these patients had a neuromuscular problem or not. Determination of urine myoglobin is not sufficient to rule out neuromuscular disorder as many patients with elevated CK and muscle disease may have normal urine myoglobin. Was myoglobinuria more prevalent among patients with renal insufficiency or with normal renal function? In addition to the limitations already raised by the authors, we want to emphasize that a more thorough search for causes of false-positive cTnI has to be carried out than just looking for myoglobinuria, renal insufficiency, or cocaine abuse. Particularly, neuromuscular disorder, malignancy, Takotsubo phenomenon, cardiac amyloidosis, carcinoid syndrome, pheochromocytoma, shock, stroke, pulmonary embolism, or epilepsy cannot be definitively ruled out as causes of elevated cTnI by the methods applied. References [1] S.F. Li, J. Zapata and E. Tillem, The prevalence of false-positive cardiac troponin I in ED patients with rhabdomyolysis, Am J Emerg Med 23 (2005), pp. 860863. SummaryPlus | Full Text + Links | PDF (98 K) | Abstract + References in Scopus | Cited By in Scopus [2] G. Melli, V. Chaudhry and D.R. Cornblath, Rhabdomyolysis: an evaluation of 475 hospitalized patients, Medicine (Baltimore) 84 (2005), pp. 377385. Abstract-MEDLINE | Abstract-Elsevier BIOBASE | Abstract-EMBASE | Full Text via CrossRef | Abstract + References in Scopus | Cited By in Scopus [3] M. Kawabata, I. Kubo, K. Suzuki, T. Terai, T. Iwama and M. Isobe, Tako-Tsubo cardiomyopathy associated with syndrome malin: reversible left ventricular dysfunction, Circ J 67 (2003), pp. 721724. Abstract-MEDLINE | Abstract-EMBASE | Abstract + References in Scopus | Cited By in Scopus [4] J.S. Alpert, K. Thygesen, E. Antman and J.P. Bassand, Myocardial infarction redefineda consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction, J Am Coll Cardiol 36 (2000), pp. 959969. Abstract-MEDLINE | Abstract-EMBASE | Abstract-Elsevier BIOBASE | Abstract + References in Scopus | Cited By in Scopus [5] A. Zabernigg, R. Schranzhofer, A. Kreczy and K. Gattringer, Continuously elevated cardiac troponin I in two patients with multiple myeloma and fatal cardiac amyloidosis, Ann Oncol 14 (2003), p. 1791. Abstract-MEDLINE | Abstract-Elsevier BIOBASE | Full Text via CrossRef | Abstract + References in Scopus | Cited By in Scopus [6] F. Casazza, A. Capozi, B. Conconi and E. Schiaffino, Acute myocardial damage from a pheochromocytoma, Ital Heart J 1 (2000) (Suppl 5), pp. 686689. Abstract-EMBASE | Abstract-MEDLINE | Abstract + References in Scopus | Cited By in Scopus [7] W.G. Meijer, J.C. Swaanenburg, D. van Veldhuisen, I.P. Kema, P.H. Willemse and E.G. de Vries, Troponin I, troponin T, and creatine kinaseMB mass in patients with the carcinoid syndrome with and without heart failure, Clin Chem 45 (1999), pp. 22962297. Abstract-MEDLINE | Abstract-EMBASE | Abstract-Elsevier BIOBASE | Abstract + References in Scopus | Cited By in Scopus [8] A. Brobbey and K. Ravakhah, Elevated serum cardiac troponin I level in a patient after a grand mal seizure and with no evidence of cardiac disease, Am J Med Sci 328 (2004), pp. 189191. Abstract-MEDLINE | Abstract-EMBASE | Full Text via CrossRef | Abstract + References in Scopus | Cited By in Scopus [9] A. Jeremias and C.M. Gibson, Narrative review: alternative causes for elevated cardiac troponin levels when acute coronary syndromes are excluded, Ann Intern Med 142 (2005), pp. 786791. Abstract-EMBASE | Abstract-MEDLINE | Abstract + References in Scopus | Cited By in Scopus
Rhabdomyolysis and “False Positive” Troponin Elevation Cardiac troponin I (cTnI) is considered the most specific marker of cardiac muscle injury (1). Emergency Physicians commonly encounter patients with acute rhabdomyolysis who demonstrate marked CPK elevations. In such patients it is not unusual to find elevations of cTnI and the question arises as to whether the troponin elevation is due to acute coronary damage or is a “false positive” resulting from the rhabdomyolysis. In fact numerous studies demonstrate that the range of false-positive cTnI elevation in the setting of rhabdomyolysis ranges from 11% to 35% (the range is a result of different study methodologies, different assays, and different upper reference limits for cTnI) (1-4). The false positives may represent minor cardiac injuries that are undetected by EKG and echocardiography, or they may represent an underlying problem with cTnI assays. Troponin assays are immunoassays, and like all antibody assays, cross-reactions may occur, particularly in patients with rhabdomyolysis in whom the skeletal forms of troponin I are elevated (1,10). Of note, the false-positive elevations in cTnI are not affected by cocaine use, impaired renal function, or myoglobinuria (1). References: (1) Li SF, et al. The prevalence of false-positive cardiac troponin I in ED patients with rhabdomyolysis Am J Emerg Med 2005;23: 860-3. (2) Lavoinne A, Hue G Serum cardiac troponins I and T in early posttraumatic rhabdomyolysis Clin Chem 1998;44:667Â668. (3) Punukollu G, et al. Elevated serum cardiac troponin I in rhabdomyolysis Int J Cardiol 2004;96:35Â40. (4) Lofberg M, et al. Cardiac troponins in severe rhabdomyolysis Clin Chem 1996;42:1120Â1121. (5) Simpson JA, et al. Differential detection of skeletal troponin I isoforms in serum of a patient with rhabdomyolysis: markers of muscle injury? Clin Chem 2002;48:1112Â1114.
Comparison of Ringers and NS (Emerg Med J 2007;24:276)
CVVH
High Permeability dialysis membrane allows effective removal of myoglobin (Crit Care Med 2011;38:184)
allows elimination of molecules up to 30 kDa
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