Can Alcohol Cause High Creatine Kinase Levels?

Can Alcohol Cause High Creatine Kinase Levels
Levels of CK can rise after a heart attack, skeletal muscle injury, or strenuous exercise. They can also go up after drinking too much alcohol or from taking certain medicines or supplements.

Can alcohol increase creatine kinase?

Abstract – Binge drinking of alcohol may lead to acute alcoholic myopathy with rhabdomyolysis, which is characterized by skeletal muscle damage, elevated serum creatine kinase (CK), and myoglobinuria. This study was undertaken to test whether alcohol acts directly on the skeletal muscles to enhance the leakage of CK, and to assess the influence of fiber-type composition and repetitive contractions of the muscle on the effect of alcohol.

After 4 hr of incubation in normal physiological solution at 37 degrees C, mean leakage of CK was 0.7 units/mg from isolated rat extensor digitorum longus (EDL), which has more fast-twitch glycolytic muscle fibers, and 1.2 units/mg from the soleus, which has more slow-twitch oxidative muscle fibers.

Ethanol at 0.1, 0.2, and 0.5% concentrations caused significantly greater increase in leakage of CK from soleus than from EDL. In normal physiological solution, electrical stimulation at 1 Hz for 4 hr increased the leakage of CK by about the same degree in both EDL and soleus.

  • In the presence of 0.1 and 0.2% ethanol, electrical stimulation markedly potentiated the alcohol-induced leakage of CK from both soleus and EDL.
  • These results indicate that alcohol increases the leakage of CK by acting directly on skeletal muscle fibers, especially of the slow-twitch oxidative type, and that repeated muscle contractions potentiate the alcohol effect.

These studies suggest that exercise may increase the chances of rhabdomyolysis in the alcoholics.

Does alcohol increase creatine levels?

Background Moderate alcohol consumption has been consistently associated with beneficial health effects on cardiovascular disease. In contrast, the association between alcohol consumption and renal dysfunction is less clear. Methods We conducted a prospective cohort study of 11 023 initially healthy men who provided blood samples 14 years after a baseline assessment of alcohol consumption. We categorized alcohol consumption into 1 or fewer, 2 to 4, 5 to 6, and 7 or more drinks per week. The main outcome measures were elevated creatinine levels (defined as ≥1.5 mg/dL ) and reduced estimated glomerular filtration rates (defined as ≤55 mL/min). We used logistic regression to calculate multivariable-adjusted odds ratios (ORs) and 95% confidence intervals (CIs). Results After 14 years, 473 men (4.3%) had elevated creatinine levels and 1296 (11.8%) had reduced glomerular filtration rates. Compared with men who consumed no more than 1 drink per week, men who consumed 2 to 4 drinks weekly had a multivariable-adjusted OR of 1.04 (95% CI, 0.81-1.32), men who consumed 5 to 6 drinks per week had an OR of 0.92 (95% CI, 0.68-1.25), and men who consumed at least 7 drinks weekly had an OR of 0.71 (95% CI, 0.55-0.92) ( P =,01 for trend across categories). Similar associations were observed between alcohol consumption and decreased glomerular filtration rates. Hypertension, diabetes mellitus, and cholesterol level did not attenuate these effects. Conclusions In this large cohort of apparently healthy men, alcohol consumption was not associated with an increased risk of renal dysfunction. Instead, these data suggest an inverse relationship between moderate alcohol consumption and the risk of renal dysfunction. The adverse health effects of long-term consumption of large amounts of alcohol and of acute alcohol intoxication are well established.1 During the past 20 years, however, numerous studies have found that moderate alcohol consumption is associated with health benefits, such as a reduced risk of coronary heart disease, 2 ischemic stroke, 3 and others.4, 5 The risk reduction is generally attributed to the beneficial effects of alcohol on lipids and hemostatic factors.6 – 9 The effect of alcohol consumption has also been investigated for a variety of renal disorders. Moderate alcohol consumption has been shown to be protective in the formation of kidney stones.10 With respect to renal cell carcinoma, higher levels of alcohol intake seemed to offer protection in women, whereas no association between alcohol intake and renal cell carcinoma was observed in men.11 One prospective study 12 found no association between alcohol consumption and the development of renal dysfunction, whereas 2 retrospective analyses found an increased risk of renal dysfunction 13 or end-stage renal disease.14 Because vascular diseases and chronic renal dysfunction are highly correlated, 15 and because the pathogenic principles of nephrosclerosis and coronary atherosclerosis are similar, it is possible that moderate consumption of alcohol may have a positive effect on the development of renal dysfunction.16 The Physicians’ Health Study (PHS) provided a unique opportunity to prospectively examine the association between alcohol consumption and renal dysfunction in a large cohort of more than 11 000 male US physicians during 14 years of follow-up. The study population consisted of participants in the PHS, a completed randomized trial of the use of aspirin and beta carotene in the primary prevention of cardiovascular disease (CVD) and cancer. The design and results of the PHS have been described in detail previously.17, 18 The Brigham and Women’s Hospital institutional review board approved the study. The trial population consisted of 22 071 apparently healthy male physicians without a history of CVD, cancer, current liver disease or renal dysfunction (defined as renal failure or insufficiency), or other major illnesses at baseline in 1982. Most of the participants (94.3%) were white; 2.8% were Asian, 0.7% were African American, and 2.2% were other ethnicity. Baseline information was self-reported and was collected using a mailed questionnaire that asked about many demographic, medical history, and lifestyle variables, including alcohol consumption. Every 6 months for the first year and annually thereafter, participants were sent follow-up questionnaires that asked about personal characteristics, medical history, and health behaviors during the study period. Blood collection and analysis The method of blood collection was published in detail previously.19, 20 Briefly, at baseline in 1982 and during follow-up in 1996, participants were invited to provide an EDTA blood sample. In 1996, a total of 11 360 blood samples were received. Creatinine could be analyzed in 11 104 of these samples; of those, 4497 physicians had remaining blood samples from the baseline blood collection for which creatinine could be evaluated. Creatinine was analyzed at the same time in all blood samples, using an automated Jaffe rate method on a SYNCHRON LX20 autoanalyzer (Beckman Coulter, Fullerton, Calif) for quantification of creatinine. Plasma creatinine is stable in chilled next-day whole blood samples preserved with EDTA.21 To assess quality control, masked duplicate split samples were submitted; the coefficient of variation for these masked split samples was 7.1%. The difference in mean (SD) between the study samples and the repeated quality control samples was 0.018 (0.67) mg/dL (2 μmol/L). Intrabatch coefficients of variation on internal quality control runs were 1.4% to 3.6%. Information on alcohol consumption Information about alcohol consumption was collected at baseline and on the 84-month questionnaire. Answer categories included “rarely/never,” “1 to 3 drinks per month,” “1 drink per week,” “2 to 4 drinks per week,” “5 to 6 drinks per week,” “daily,” and “2 or more drinks per day.” We a priori combined the 3 lowest categories and the 2 highest categories and categorized alcohol consumption into 4 groups (≤1 drink per week, 2-4 drinks per week, 5-6 drinks per week, and ≥7 drinks per week). Our primary outcome was elevated creatinine level, defined as 1.5 mg/dL or greater (≥133 μmol/L) at the time of follow-up blood sample collection in 1996. We also examined reduced glomerular filtration rate (GFR), estimated using the Cockcroft-Gault equation 22 GFR = /, A reduced GFR was defined as 55 mL/min or less. Because the best measure of renal function in large-scale epidemiologic studies has not been determined, 23 we also evaluated the change in creatinine concentration in participants for whom baseline and follow-up blood creatinine measurements were available (n = 4497). We evaluated several different cutoff values for increases in creatinine concentration (ranging from ≥0.3 to ≥0.6 mg/dL ). Information on alcohol intake at baseline was missing for 81 of the 11 104 physicians with creatinine measurements in 1996, leaving a sample of 11 023 participants for this analysis. We compared the characteristics of participants with respect to alcohol consumption category using general linear models (SAS version 8.2; SAS Institute Inc, Cary, NC) to compare continuous measurements adjusted for age. We used direct standardization to adjust categorical variables for age in 5-year age groups. We used logistic regression to analyze the association between alcohol intake and elevated creatinine levels, low GFRs, and change in creatinine concentration. We calculated age- and multivariable-adjusted odds ratios (ORs) and 95% confidence intervals (CIs). We made a distinction in the multivariable models between variables considered potential confounders and those considered potential intermediate markers, that is, variables known to be affected by alcohol consumption and suspected to contribute to renal dysfunction. However, because it was considered desirable to measure the contribution of alcohol to renal dysfunction separate from the intermediary variables, analyses were performed separately with and without controlling for these variables. In the first multivariable model (model 1), we controlled for age in 5-year increments (<45, 45-49, 50-54, 55-59, 60-64, 65-69, and ≥70 years), body mass index at baseline (quartiles), smoking (never, past, and current), physical activity (none, <5 times per week, and ≥5 times per week), history of diabetes mellitus at baseline, parental history of myocardial infarction before age 60 years, and randomized treatment assignment (aspirin and beta carotene). In the second model (model 2), we controlled for all the variables in the first model plus a self-reported history of hypertension at baseline (defined as a systolic blood pressure ≥140 mm Hg, a diastolic blood pressure ≥90 mm Hg, or antihypertensive medication use at baseline regardless of blood pressure); the development of hypertension, diabetes mellitus, or CVD (defined as myocardial infarction, stroke, angina, or coronary artery bypass graft) during follow-up; and a history of an elevated cholesterol level at baseline. Of the 11 023 study participants, 4259 (38.6%) reported alcohol consumption of 1 or fewer drinks per week, 2582 (23.4%) of 2 to 4 drinks per week, 1474 (13.4%) of 5 to 6 drinks per week, and 2708 (24.6%) of 7 or more drinks per week. The age-adjusted characteristics of the study participants according to alcohol consumption categories are summarized in Table 1, Men who consumed at least 7 drinks per week were older, were leaner, had higher systolic and diastolic blood pressures, were more likely to develop hypertension during follow-up, and smoked more frequently. On the other hand, they exercised less and were less likely to have developed CVD and diabetes mellitus during follow-up. After a mean of 14.2 years of follow-up, 473 men (4.3%) had elevated creatinine levels (≥1.5 mg/dL ). A total of 1296 men (11.8%) had decreased GFRs (≤55 mL/min) based on the Cockcroft-Gault estimation. The age- and multivariable-adjusted ORs of elevated creatinine levels for the categories of alcohol consumption are summarized in Table 2, The multivariable-adjusted OR of developing an elevated creatinine level of 1.5 mg/dL or greater declined with increasing alcohol intake. Compared with men who consumed no more than 1 drink per week, men who consumed 2 to 4 drinks per week had a multivariable-adjusted OR of 1.04 (95% CI, 0.81-1.32), men who consumed 5 to 6 drinks per week had an OR of 0.92 (95% CI, 0.68-1.25), and men who consumed 7 or more drinks per week had an OR of 0.71 (95% CI, 0.55-0.92). There was a significant inverse trend across increasing alcohol intake categories ( P =,01). Additional adjustments for potential intermediate variables (model 2) only slightly changed the ORs of the association between the highest alcohol consumption and creatinine levels. When we separated the highest alcohol intake group into categories of 7 drinks per week and 8 or more drinks per week, this trend continued ( P =,008) ( Figure ). The multivariable ORs for reduced GFRs demonstrated the same tendencies ( Table 3 ). There was a significant inverse trend across alcohol consumption categories with respect to decreased GFRs (≤55 mL/min). Men who consumed 7 or more drinks per week had a multivariable-adjusted OR of 0.76 (95% CI, 0.64-0.91) compared with men who consumed 1 or fewer drinks per week. There was also a significant trend across alcohol intake categories ( P =,002). Model 2 yielded similar results. Adjustments for categories of blood pressure did not appreciably change the effect estimate between alcohol intake and renal function. We also considered different ethnicities as a potential confounding variable, in particular African American. However, because most PHS participants were white (94.3%) and only a small proportion were African American (0.7%), inclusion of an indicator for African American or other ethnic categories did not yield materially different results for the association between alcohol consumption and risk of renal dysfunction. We did not find different effects of the association between alcohol consumption and risk of renal disease in stratified analyses based on tertiles of baseline GFR. The association between alcohol consumption and change in creatinine concentration depended on the chosen cutoff value. Of the 4497 participants for whom creatinine measurements were available in 1982 and 1996, no association was observed between alcohol consumption and a creatinine level increase of 0.3 mg/dL or greater (≥27 μmol/L). However, raising the cutoff value for increased creatinine level revealed an inverse association. With a cutoff value of 0.6 mg/dL or greater (≥53 μmol/L), men who consumed at least 7 drinks per week had an age-adjusted OR of 0.49 (95% CI, 0.25-0.96; P =,04 for trend) compared with those who never or rarely drank. Multivariable adjustments (model 1) increased the OR to 0.54 (95% CI, 0.27-1.07; P =,09 for trend). In addition, we evaluated the association between alcohol consumption as reported on the 84-month questionnaire and elevated creatinine level (≥1.5 mg/dL ) in 1996. Compared with men who consumed 1 or fewer drinks per week, men who consumed 2 to 4 drinks per week had a multivariable adjusted OR of 1.08 (95% CI, 0.85-1.38), men who consumed 5 to 6 drinks per week had an OR of 0.80 (95% CI, 0.59-1.09), and men who consumed at least 7 drinks per week had an OR of 0.66 (95% CI, 0.49-0.87). The trend test across alcohol intake categories after 84 months of follow-up was also significant ( P =,003). The inclusion of potential intermediate variables did not substantially change these estimates. The ORs for decreased GFRs were similar. The results of this large prospective cohort study do not indicate that alcohol consumption is associated with an increased risk of renal dysfunction in apparently healthy men. Instead, the data suggest an inverse relationship between moderate alcohol consumption and the subsequent risk of renal dysfunction in men. Men who consumed at least 7 drinks per week had an approximately 30% lower risk of increased creatinine levels (≥1.5 mg/dL ) in a 14-year period than men who consumed 1 or fewer drinks (OR, 0.71; 95% CI, 0.55-0.92). This inverse relationship persisted after adjustment for potential confounding variables and continued in the higher alcohol intake category. Similar results were observed for decreased GFRs of 55 mL/min or less. The association between alcohol consumption and change in creatinine level also supported these findings. We interpret the overall evidence from these analyses as an indication that alcohol might have a protective effect on renal function. Our study solely focuses on the association between alcohol consumption and risk of renal dysfunction, and we did not evaluate the potential harmful effects of alcohol consumption. Conclusions about the overall effects of alcohol intake cannot be drawn from our study. Moderate alcohol consumption has been observed to have a favorable effect on several diseases in numerous studies during the past 20 years. Individuals who consume small to moderate amounts of alcohol are at decreased risk for CVD, including myocardial infarction, 24 peripheral arterial disease, 25 angina pectoris, 26 and ischemic stroke, 3 and have a decreased risk of dying.5 Beneficial effects of moderate alcohol consumption on renal function are plausible; in recent years, traditional risk factors for CVD have been associated with an increased risk of developing renal dysfunction.15, 27 Furthermore, autopsy data 16 suggested potential beneficial effects of alcohol consumption on the hyalinization in renal arterioles. In a prediction model for new-onset renal disease, several traditional CVD risk factors showed significant associations.28 In this study, however, alcohol consumption was not considered. In addition, there is evidence that the consumption of light to moderate amounts of alcohol decreases the risk of type 2 diabetes mellitus 4 and has preventive effects on the development of arteriosclerosis in patients with type 2 diabetes mellitus.29 A recent prospective cohort study 12 found no statistically significant association between alcohol consumption and risk of decline in renal function among 1658 apparently healthy women. This study, however, suggested beneficial effects of moderate alcohol consumption on renal function, with an approximately 20% risk reduction. The sample size of this study might have been too small to detect any statistically significant association. Our finding stands in contrast to those of previously published retrospective studies. A population-based case-control study 14 reported an approximately 4-fold increase in the risk of end-stage renal disease among individuals who consumed more than 2 alcoholic drinks per day after adjustment for potential confounders. Another case-control study 13 also concluded that individuals who consumed 2 or fewer drinks per day had higher serum creatinine concentrations than matched controls who did not drink alcohol. This study, however, provided evidence that drinkers in higher alcohol intake categories had reduced creatinine levels compared with their nondrinking controls. These differences may be explained by the different study designs or by the fact that alcohol might have different effects on future renal function in healthy individuals than in those with preexisting renal disease. It has been argued that alcohol consumption may result in renal disease because of alcohol-induced hypertension.30 Indeed, in our study, the prevalence and incidence of hypertension was statistically significantly higher among participants who consumed 7 or more alcoholic drinks per week. However, this group had a decreased risk of renal dysfunction. Men with the highest amounts of alcohol intake also had the highest high-density lipoprotein (HDL) cholesterol levels compared with men who rarely or never consumed alcohol. This result is consistent with earlier experimental studies 6, 9 showing that moderate drinking increases several HDL cholesterol subfractions. Besides some antithrombotic properties, 31 an alcohol-induced increase in HDL cholesterol subfractions has been discussed to be the major mechanism for the cardiovascular benefit of moderate alcohol consumption. Because it has been shown that low HDL cholesterol levels (<40 mg/dL ) increases the risk of renal dysfunction, 27 it is plausible that an alcohol-related increase in HDL cholesterol may explain the potential beneficial effect seen in our analysis of renal dysfunction. The potential beneficial effect of alcohol intake on renal function observed in our study could also be mediated by the positive effect of moderate drinking on the incidence of diabetes mellitus 4, 32, 33 and the protective effect on atherosclerosis among patients with type 2 diabetes mellitus.29 Heavy alcohol consumption or intoxication has been linked to acute renal failure via rhabdomyolysis.34 This specific question, however, could not be studied in our cohort because heavy alcohol consumption was uncommon. The strengths of this study include its large size, its long follow-up of more than 14 years, its prospective method of data collection, and the relatively homogeneous nature of the cohort, which reduces confounding by several variables, including access to medical care, educational attainment, and socioeconomic status. Furthermore, we evaluated the association between alcohol consumption and risk of renal dysfunction using several different outcomes, including change in creatinine levels. This study has several limitations that should be considered. Men who participated in the PHS may differ in many ways from the general population. Thus, our results may not necessarily be extended to women or other populations. Regarding the specifics of our study, there is currently little biological basis to postulate that the mechanism by which alcohol may affect renal function would be materially different between PHS participants and other populations. Regarding ethnicity, recent studies 35, 36 provided evidence that the most striking difference between African Americans and whites was not the prevalence of moderate-to-severe chronic kidney disease but rather the more frequent progression to kidney failure among African Americans. Indeed, there is a higher prevalence of major risk factors for renal dysfunction among African Americans.37 However, inclusion of an indicator variable for African American in our multivariable models did not yield different results (data not shown). Because of the low numbers, we could not evaluate whether a different association between alcohol consumption and renal disease exists in African Americans. In support of generalizability, the association between alcohol consumption and CVD found in other PHS analyses 3 - 5, 25, 26 follows the findings of other population-based research.38 The GFR estimated using the Cockcroft-Gault equation has been criticized. However, when we repeated the analyses using the simplified version of the Modification of Diet in Renal Disease Study equation 39 to estimate GFR, the results were similar (data not shown). Another consideration in evaluating studies of alcohol and disease is that drinking habits can change with time. However, in a sensitivity analysis using information on alcohol consumption from the 84-month follow-up questionnaire, the results were similar. As in most other alcohol-oriented epidemiologic studies, we relied on self-reported levels of alcohol consumption. Other studies 40 of health professionals have demonstrated that this population provides reliable reports of alcohol use. In addition, the prospective method of exposure collection would lead to random misclassification and thus to a potential underestimation of the association between alcohol consumption and renal dysfunction. In addition, blood samples were available only for a subsample of the PHS cohort, and for only a smaller fraction were baseline and follow-up creatinine levels measured. Finally, confounding remains a possible alternative explanation for our finding; however, multiple covariate adjustments did not materially alter the results. In summary, this large prospective cohort study shows that moderate alcohol consumption is not associated with an increased risk of renal dysfunction in men. Instead, our data suggest an inverse relationship between moderate alcohol consumption and the risk of developing renal dysfunction. Correspondence: Tobias Kurth, MD, ScD, Division of Preventive Medicine, Brigham and Women's Hospital, 900 Commonwealth Ave E, Boston, MA 02215-1204 ( [email protected] ). Accepted for Publication: January 18, 2005. Financial Disclosure: None. Funding/Support: This work was supported by grants CA 34944, CA 40360, HL 26490, and HL 34595 from the National Institutes of Health, Bethesda, Md. Previous Presentation: The study was presented in part at the American Society of Nephrology meeting; November 14, 2003; San Diego, Calif. Acknowledgment: We thank the participants in the PHS for their outstanding commitment and cooperation and the entire PHS staff for their expert and unfailing assistance.1. National Institute on Alcohol Abuse and Alcoholism, 10th Special Report on the US Congress on Alcohol and Health. Rockville, Md US Dept of Health and Human Services2000; 2. Rimm EBWilliams PFosher KCriqui MStampfer MJ Moderate alcohol intake and lower risk of coronary heart disease: meta-analysis of effects on lipids and haemostatic factors. BMJ 1999;3191523- 1528 PubMed Google Scholar Crossref 3. Berger KAjani UAKase CS et al. Light-to-moderate alcohol consumption and risk of stroke among U.S. male physicians. 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Sarnak MJLevey AS Cardiovascular disease and chronic renal disease: a new paradigm. Am J Kidney Dis 2000;35 ((suppl 1)) S117- S131 PubMed Google Scholar Crossref 16. Burchfiel CMTracy REChyou PHStrong JP Cardiovascular risk factors and hyalinization of renal arterioles at autopsy: the Honolulu Heart Program. Arterioscler Thromb Vasc Biol 1997;17760- 768 PubMed Google Scholar Crossref 17. Steering Committee of the Physicians' Health Study Research Group, Final report on the aspirin component of the ongoing Physicians' Health Study. N Engl J Med 1989;321129- 135 PubMed Google Scholar Crossref 18. Hennekens CHBuring JEManson JE et al. Lack of effect of long-term supplementation with beta carotene on the incidence of malignant neoplasms and cardiovascular disease. N Engl J Med 1996;3341145- 1149 PubMed Google Scholar Crossref 20. Kurth TGlynn RJWalker AM et al. Analgesic use and change in kidney function in apparently healthy men. Am J Kidney Dis 2003;42234- 244 PubMed Google Scholar Crossref 21. Youngman LDLyon VCollins RPeto R Problems with mailed blood in large-scale epidemiologic studies and methods for correction, FASEB J 1993;7A66 Google Scholar 23. Hsu CYChertow GMCurhan GC Methodological issues in studying the epidemiology of mild to moderate chronic renal insufficiency. Kidney Int 2002;611567- 1576 PubMed Google Scholar Crossref 25. Camargo CA JrStampfer MJGlynn RJ et al. Prospective study of moderate alcohol consumption and risk of peripheral arterial disease in US male physicians. Circulation 1997;95577- 580 PubMed Google Scholar Crossref 26. Camargo CA JrStampfer MJGlynn RJ et al. Moderate alcohol consumption and risk for angina pectoris or myocardial infarction in U.S. male physicians. Ann Intern Med 1997;126372- 375 PubMed Google Scholar Crossref 27. Schaeffner ESKurth TCurhan GC et al. Cholesterol and the risk of renal dysfunction in apparently healthy men. J Am Soc Nephrol 2003;142084- 2091 PubMed Google Scholar 28. Fox CSLarson MGLeip EPCulleton BWilson PWLevy D Predictors of new-onset kidney disease in a community-based population. JAMA 2004;291844- 850 PubMed Google Scholar Crossref 29. Wakabayashi IKobaba-Wakabayashi RMasuda H Relation of drinking alcohol to atherosclerotic risk in type 2 diabetes. Diabetes Care 2002;251223- 1228 PubMed Google Scholar Crossref 30. Parekh RSKlag MJ Alcohol: role in the development of hypertension and end-stage renal disease. Curr Opin Nephrol Hypertens 2001;10385- 390 PubMed Google Scholar Crossref 31. Ridker PMVaughan DEStampfer MJGlynn RJHennekens CH Association of moderate alcohol consumption and plasma concentration of endogenous tissue-type plasminogen activator. JAMA 1994;272929- 933 PubMed Google Scholar Crossref 32. de Vegt FDekker JMGroeneveld WJ et al. Moderate alcohol consumption is associated with lower risk for incident diabetes and mortality: the Hoorn Study. Diabetes Res Clin Pract 2002;5753- 60 PubMed Google Scholar Crossref 33. Wannamethee SGShaper AGPerry IJAlberti KG Alcohol consumption and the incidence of type II diabetes. J Epidemiol Community Health 2002;56542- 548 PubMed Google Scholar Crossref 34. Muthukumar TJha VSud AWanchoo ABambery PSakhuja V Acute renal failure due to nontraumatic rhabdomyolysis following binge drinking. Ren Fail 1999;21545- 549 PubMed Google Scholar Crossref 35. Weiner DETighiouart HAmin MG et al. Chronic kidney disease as a risk factor for cardiovascular disease and all-cause mortality: a pooled analysis of community-based studies. J Am Soc Nephrol 2004;151307- 1315 PubMed Google Scholar Crossref 36. Hsu CYLin FVittinghoff EShlipak MG Racial differences in the progression from chronic renal insufficiency to end-stage renal disease in the United States. J Am Soc Nephrol 2003;142902- 2907 PubMed Google Scholar Crossref 37. Sharma SMalarcher AMGiles WHMyers G Racial, ethnic and socioeconomic disparities in the clustering of cardiovascular disease risk factors. Ethn Dis 2004;1443- 48 PubMed Google Scholar 38. Booyse FMParks DA Moderate wine and alcohol consumption: beneficial effects on cardiovascular disease. Thromb Haemost 2001;86517- 528 PubMed Google Scholar 39. Levey ASCoresh JBalk E et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Ann Intern Med 2003;139137- 147 PubMed Google Scholar Crossref 40. Giovannucci EColditz GStampfer MJ et al. The assessment of alcohol consumption by a simple self-administered questionnaire. Am J Epidemiol 1991;133810- 817 PubMed Google Scholar

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Should I worry about high CK levels?

What is a creatine kinase (CK) test? – 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.

  • 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

Can anxiety increase creatine kinase?

4.2.1. Psychological Stress – Psychiatric illness is characterized by diverse neural abnormalities, running the gamut from neuroendocrine and neurotransmission systems to neuroanatomical and neurotrophic factors, and these processes have significant energy requirements.

Psychological stress is associated with impairments in energy metabolism, which increase the susceptibility of neurons to the negative effects of reactive oxygen species (oxidative stress), including lipid peroxidation, protein carboxylation, DNA damage and apoptosis ( Seifried et al., 2007 ). In view of this evidence, chronic psychological stress is considered a precipitating factor in the onset of psychiatric disorders ( Caspi et al., 2003 ; Duman and Monteggia, 2006 ; Pittenger and Duman; 2008, Sapolsky, 2000 ).

For instance, in mice, chronic mild stress damaged mitochondrial structure and function in the hippocampus and prefrontal cortex and increased depression-like behavior ( Gong et al., 2011 ). Given that creatine metabolism depends on mitochondrial function, it is hypothesized that stress causes changes in creatine, phosphocreatine, or creatine kinase in brain areas linked with mental illness.

  • If this is the case, stress-related psychiatric disorders may benefit from creatine supplementation or other agents that stimulate creatine kinase to reverse the deleterious effects of stress on mitochondrial dysfunction.
  • Moreover, creatine supplementation may be beneficial in safeguarding the brain because it prevents oxidative damage from the formation of reactive oxygen species through direct antioxidant activity ( Sestili et al., 2006 ; Young et al., 2010 ).

The effects of psychological stress on brain creatine metabolism have not been directly studied in humans, but stress-induced impairments in brain metabolite concentrations have been investigated in animal models of stress. Using MRS neuroimaging and histological techniques, researchers have found that subordinate animals exposed repeatedly to experiences of psychosocial defeat by dominant animals exhibit significantly less total creatine (the sum of creatine + phosphocreatine), reduced hippocampal volume, and impaired neurogenesis ( Czéh et al., 2001 ; Fuchs et al., 2002 ; van der Hart et al., 2003).

  • Moreover, these studies showed that the effects of stress on total creatine concentrations and neuroplasticity were reversed after treatment with tianeptine (Stablon) and clomipramine (Anafranil), and a novel substance P antagonist (L-760,735).
  • Another study using MRS imaging ex vivo found that rats subjected to single prolonged stress showed reduced creatine concentrations in the medial prefrontal cortex compared to non-stress controls ( Knox et al., 2010 ).

On the basis of these findings, it is difficult to know whether the effects of stress on creatine occur upstream or downstream of mitochondria, but the creatine-phosphocreatine circuit may be an important mediator or target of drug action. One known study in animals has directly assessed the effects of creatine supplementation on stress-induced impairments.

Can drinking alcohol the night before a blood test affect liver enzymes?

HOW LONG DOES ALCOHOL STAY IN YOUR SYSTEM? – Alcohol has a noticeable effect on the body, even when consumed in small amounts. Our body continues to break down alcohol at a steady rate after drinking. Trace amounts of alcohol may remain in the blood several days also after its consumption.

Alcohol is metabolized at a relatively predictable rate. Most of the people can expect blood alcohol concentrations (BAC) to drop at a rate of 0.015 per hour. This means that following last alcoholic drink of the night, the alcohol present in the body is being metabolized and eliminated at a rate of 0.015.

On an average to flush the impact of alcohol, the human body needs anything between 7 to 10 hours. This is totally dependent on the quantity of alcohol consumed. The thumb rule is the more you drink, the longer you should expect it to take for alcohol to clear from your body.

  • CAN ALCOHOL AFFECT BLOOD TEST? Patients are advised to abstain from drinking alcohol before fasting blood test as it may affect the blood results, causing irregular enzyme levels.
  • Blood tests specifically prohibiting alcohol consumption prior to the administration include the triglyceride test and the gamma glutamyl transferase (GGT) test.

It will lead to an elevated level of LFT’s (Liver Function Tests). Those who have recently consumed alcohol prior to a blood test are advised to discuss the matter with their physician to determine if the test should be postponed. Each blood test is independent, so it is important to ask the doctor if you should fast before the test or take any other precaution (many tests require a patient to avoid a certain type of foods even 5-7 days before a test is conducted).

So, fasting may be important because what you eat and drink may change test results. (Also Read: Are my lab results affected by when and what I ate last night? ) Blood tests also can help find potential problems at an initial stage, when treatments or lifestyle changes may work best. Hence, if your doctor has advised you not to consume alcohol before the test, then the instructions should not be ignored.

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How high is too high for creatine kinase?

By Jon-Emile Kenny, MD Faculty Peer Reviewed A 37-year-old man, with no past medical history and taking finasteride for male pattern baldness, is admitted to Medicine with profound lower extremity weakness after a weekend of performing multiple quadriceps exercises. His measured creatine phosphokinase (CPK) is over 35,000 IU/liter. I wonder to myself, what is the risk to his kidneys and can I mitigate the damage? Rhabdomyolysis means destruction of striated muscle. Physical manifestations range from an asymptomatic illness with an elevation in the CPK level, to a life-threatening condition associated with extreme elevations in CPK, electrolyte imbalances, disseminated intravascular coagulation (DIC), and acute kidney injury (AKI). CPK elevations are frequently classified as mild, moderate, or severe. These classifications roughly correspond to less than 10 times the upper limit of normal (or 2,000 IU/L), 10 to 50 times the upper limit of normal (or 2,000 IU/L to 10,000 IU/L), and greater than 50 times the upper limit of normal (or greater than 10,000 IU/L), respectively (2). The risk of renal failure increases above 5,000 to 6,000 IU/L, Interestingly, one series found that only patients with a peak CK greater than 20,000 IU/L failed to respond to diuresis and required dialysis, No studies have found a normal range of CPK levels following exercise. However, the incidence of renal failure does not correlate with CPK levels alone. After triathalons, athletes may have CPK elevations of greater than 20,000 IU/L without any renal compromise, A review of 35 patients with exercise-induced rhabdomyolysis, with an average admission CPK level of 40,000 IU/L, revealed no cases of acute renal failure, The risk of renal failure increases with co-morbid conditions such as sepsis, dehydration, and acidosis, Hypovolemia and aciduria are felt to be key pathophysiological events leading to acute kidney injury in the setting of muscle breakdown. Damage to the kidneys is mediated by heme-proteins released from myoglobin, There are four converging pathways by which heme-proteins harm the kidneys: 1) renal vasoconstriction; 2) cytokine activation; 3) precipitation of Tamm-Horsfall protein at an acid pH with subsequent cast-nephropathy; and 4) acid-sensitive renal free-radical production, Due to the many liters of fluid sequestered in injured muscle, patients with rhabdomyolysis are profoundly volume depleted. Consequently, homeostatic mechanisms, such as the renin-angiotensin, aldosterone, and vasopressin systems, are activated, leading to renal vasoconstriction. Various cytokines induced in rhabdomyolysis have also been shown to have similar effects on renal perfusion, Because myoglobin becomes concentrated in the presence of aciduria, it precipitates with Tamm-Horsfall protein and also induces free radical production, Given the aforementioned mechanisms of acute kidney injury, evidence of CPK elevation should lead to attempts to protect the kidneys. Treatment should include reversal of fluid deficits with or without urinary alkalinization. Reversal of hypovolemia with copious amounts of intravenous (IV) normal saline, with individualized urine output goals, is the mainstay of therapy, While no prospective clinical trials have proven the efficacy of volume resuscitation, retrospective analyses support its use, In one study, investigators compared the clinical outcomes of two groups of patients who developed crush syndrome during building collapses. All seven patients in the group that had IV fluids delayed for more than six hours required dialysis, whereas none of the seven patients with similar injuries in the group that received IV fluids at the time of extrication developed acute renal failure, Despite the protective effects of urinary alkalinization on experimental models of heme-protein nephrotoxicity and similarly positive reports from various case series, evidence from randomized controlled trials is lacking. A retrospective study of 24 patients demonstrated that augmentation with mannitol and bicarbonate may have no benefit over and above aggressive fluid resuscitation with saline alone, Further, Brown and colleagues retrospectively identified patients with trauma-induced renal failure and CPK levels greater than 5,000 IU. Roughly 40% of these patients received mannitol and bicarbonate with fluid resuscitation, while the remainder received saline alone. No significant differences in the incidence of dialysis or in the mortality rate between the two groups were observed, Nevertheless, large volume saline repletion without alkalinization raises the risk of hyperchloremic acidosis and may perpetuate kidney injury. In a recent NEJM review, Bosch et al. especially recommend both normal saline and sodium bicarbonate in patients with metabolic acidosis, Important to note, studies comparing saline versus saline plus urinary alkalinization are complicated by variable definitions of renal failure (e.g. creatinine > 2.0 mg/dL versus need for dialysis), large variations in study design and patient selection, the number of patients studied, and inconsistent amounts of time between injury and treatment, In summary, renal injury with high serum CPK values becomes a true concern when levels of CPK reach 5,000 IU/L and the patient has serious co-morbid disease such as volume depletion, sepsis or acidosis. Otherwise, values of up to 20,000 IU/L may be tolerated without untoward event. The key pathophysiological events are volume depletion and aciduria, which should be corrected immediately and primarily with ample IV normal saline and secondarily with urinary alkalinization. As our patient was young and healthy, he was administered IV normal saline only, with a goal of 200 cc per hour of urine output, until his CPK levels trended below 6,000 IU/L. He was counseled on appropriate exercise routines and urged to stop his 5-alpha reductase inhibitor, as this class of drugs has been associated with rhabdomyolysis. He did not experience any renal injury and his weakness improved. He was discharged home 36 hours following his admission. Editorial comment: Studies have suggested that there is a limited time to prevent renal injury, perhaps as little as 6 hours after rhabdomyolysis occurs. Patients should always have their extracellular volume repleted after experiencing third-spacing of plasma volume into injured muscle, in part attributed to the osmotic effects of local proteolysis. However, if kidney injury is already established, continuing to force IV fluids into a patient with renal failure may lead to volume overload and pulmonary edema. This same limitation may explain why alkalinization is of unproven benefit: it’s difficult to get the bicarbonate into the urine if GFR is low. If urine pH fails to rise after volume repletion is achieved, the risk of continued sodium bicarbonate administration far outweighs the little chance of benefit at that late point. Of note, third-spacing into muscle may lead to compartment syndrome with compression of arteries and nerves; surgical consultation and measurement of compartment hydrostatic pressure is sometimes needed though the risks and benefits of fasciotomy are debated. Dr. Kenny is a chief resident in internal medicine at NYU Langone Medical Center Peer reviewed by David Goldfarb, MD, Professor of Medicine, Department of Medicine (Nephrology), NYU Langone Medical Center and Chief of Nephrology at the Department of Veterans Affairs New York Harbor. Image (model of finasteride) courtesy of Wikimedia Commons. References: (1) Huerta-Alardín et al. Bench-to-bedside review: Rhabdomyolysis – an overview for Clinicians. Critical Care April 2005 Vol 9 No 2.158 – 169. (2) Latham and Nichols. How Much can Exercise Raise the CK level – and does it matter? The Journal of Family Practice. Vol: 57 (8) 545-546. (3) Eneas et al. The effect of infusion of mannitol– sodium bicarbonate on the clinical course of myoglobinuria. Arch Intern Med 1979;139(7):801– 5. (4) Sinert et al. Exercise-induced rhabdomyolysis. Ann Emerg Med.1994 Jun;23(6):1301-6. (5) Ward MM. Factors predictive of acute renal failure in rhabdomyolysis. Arch Intern Med 1988;148:1553-7. (6) Bagely et al. Rhabdomyolysis. Intern Emerg Med.2007 Oct;2(3):210-8 (7) Zager R: Rhabdomyolysis and myohemoglobinuric acute renal failure. Kidney Int 1996, 49:314-326. (8) Ron et al. Prevention of acute renal failure in traumatic rhabdomyolysis. Arch Intern Med 144:277—280, 1984. (9) Salahudeen et al. Synergistic renal protection by combining alkaline-diuresis with lipid peroxidation inhibitors in rhabdomyolysis: possible interaction between oxidant and nonoxidant mechanisms. Nephrol Dial Transplant 1996; 11(4):635–42. (10) Mathes et al. Rhabdomyolysis and myonecrosis in a patient in the lateral decubitus position. Anesthesiology 1996;84(3):727– 9. (11) Homsi et al. Prophylaxis of acute renal failure in patients with rhabdomyolysis. Ren Fail 1997, 19:283-288. (12) Brown et al. Preventing renal failure in patients with rhabdomyolysis: do bicarbonate and mannitol make a difference? J Trauma 2004, 56:1191-1196. (13) Bosch et al. Rhabdomyolysis and acute kidney injury. N Engl J Med.2009 Jul 2;361(1):62-7 (14) Malinoski et al. Crush injury and rhabdomyolysis Critical Care Clinics – Volume 20, Issue 1 (January 2004).

What level of CK is concerning?

Normal Range – There is still no universally agreed upon range for creatine kinase. Different laboratories have different normal ranges, reported in U/L (units per liter) or ukat/L (microkatals per liter). People who have greater muscle mass have higher CK levels.

What happens if you have too much creatine kinase?

Exceptionally High Creatine Kinase (CK) Levels in Multicausal and Complicated Rhabdomyolysis: A Case Report Received 2017 Apr 28; Accepted 2017 Jun 12. © Am J Case Rep, 2017 This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International ()

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.

  1. The patient was subsequently intubated and admitted to the medical ICU.
  2. Laboratory work-up showed acute renal failure with deranged liver functions test results, and elevated creatine kinase of 701,400 U/L.
  3. CK levels were subsequently too high for the lab to quantify.
  4. Urine legionella testing was positive for L.
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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, 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,

Common causes are trauma, muscle compression, hyperthermia, drugs and toxins like cocaine. Among infectious causes, legionella is a known bacterial cause of rhabdomyolysis, 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,

It can also be due to the direct toxic effects of ethanol on the skeletal muscles, 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,

Legionella-induced rhabdomyolysis is thought to be due to endotoxins or exotoxins and direct bacterial invasion, 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.

  1. 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.
  2. Laboratory work-up results are shown in,
  3. Initial chest X-ray was normal but the repeat X-ray () 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)   PaCo 2 20.4 mmHg (38–42)
Creatine kinase 701,400 U/L (52–336 male)   PO 2 91 mmHg (80–100)
Hemoglobin 19.4 g/dL (13.5–17.5)
Hematocrit 59.3% (38.8–50)
White cells 27.1×10 3 (3500–10 500 cell/mcL)
Platelets 216×10 3 (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, 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,

  1. Acute kidney injury (AKI) occurs in 33–50% of patients with rhabdomyolysis and the most reliable laboratory parameter used for the diagnosis of this condition is the measurement of serum CK levels.
  2. 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.
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Blanco JR, Zabalza M, Salcedo J, et al. Rhabdomyolysis of infectious and noninfectious causes. South Med J.2002; 95 (5):542–44.4. Qiu LL, Nalin P, Huffman Q, et al. Nontraumatic rhabdomyolysis with long-term alcohol intoxication. Am Board Fam Med.2004; 17 (1):54–58.5.

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Don’t you forget about me: Considering acute rhabdomyolysis in ED patients with cocaine ingestion. Can Fam Physician.2012; 58 (7):750–54.8. 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 :793786.9.

Can CK be falsely elevated?

Abstract – Hemolysis can cause falsely elevated creatine kinase (CK) values when spectrophotometric methods of measurement are used. This apparent increase in CK is due to the red blood cell enzyme adenylate kinase. In an attempt to reduce this interference, most commercial CK kits employ adenosine monophosphate and/or diadenosine pentaphosphate as adenylate kinase inhibitors.

  • To determine whether hemolyzed specimens should be accepted for testing, we measured the CK values of 26 serum samples, each with six different concentrations of added hemolysate.
  • The results showed that hemolysis had an additive effect on CK, with an average increase in CK of approximately 10 U/L for every 1 g/L of hemoglobin.

In most settings, this increase is not clinically significant. In the case of massive hemolysis, the hemoglobin concentration of the serum can be measured to correct the apparent CK value. The exclusion of hemolyzed specimens is unnecessary.

How long does it take for CK levels to go down?

Serum CK (Creatine Kinase) – Serum CK concentration, mainly the CK-MM subtype, is the most sensitive indicator of damage to muscles. Serum CK begins to rise approximately 2 to 12 hours after the onset of muscle injury, peaks within 24 to 72 hours, and then declines gradually in 7–10 days.

  1. A persistently elevated CK level suggests continuing muscle injury, development of a compartment syndrome or continuing muscle stress (e.g.
  2. Prolonged exercise or infection) 2,
  3. Currently, there is not a clearly agreed level of serum CK that is evident for diagnosis of rhabdomyolysis.
  4. However, a CK level higher than 5 times of its normal value is accepted by many authors as diagnostic criteria.

Moreover, some studies establish the low specificity of serum CK levels. Kenney et al. found in their contingent of 499 young healthy recruits a CK elevation of 10 times that regarded as normal, none diagnosed as exertional rhabdomyolysis, and suggesting either coexisting myoglobinuria or CK level of 50 folds of normal as a diagnostic threshold 106,

How long do CK levels stay elevated?

PHYSICAL ACTIVITY RAISES CK – CK levels transiently rise after exercise or heavy manual labor. Serum CK levels may increase to as much as 30 times the upper limit of normal within 24 hours of strenuous physical activity, then slowly decline over the next 7 days.

Can coffee raise CK levels?

Also caffeine consumption and eccentric exercise has led to significant increase in CK levels only at 24 hours after exercise (37.18 percent).

Can drinking water lower creatinine?

Creatinine is a waste product that can build up in the blood due to kidney disease and other factors. Staying hydrated, taking dietary measures, and using supplements can help reduce creatinine levels in the body. Creatinine is a natural waste product that the muscles create.

  1. The kidneys remove it from the body, and it is present in the blood and urine.
  2. As well as kidney problems, excess creatinine can also result from a high intake of protein, intense exercise, and the use of certain medications or supplements.
  3. Doctors often use a creatinine test to determine how well the kidneys are functioning.

High levels of creatinine in the blood or urine can be a sign that the kidneys are not filtering the blood effectively. Having high levels of creatinine is not life threatening, but it may indicate a serious health issue, such as chronic kidney disease,

Can creatinine levels go back to normal?

– If the kidneys are not functioning as they should, creatinine levels can increase in the blood. Several factors can cause high creatinine levels. These factors range from diet and medications to underlying health conditions. Levels should return to normal following treatment of the underlying issue.

Does walking increase creatine kinase?

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As a library, NLM provides access to scientific literature. Inclusion in an NLM database does not imply endorsement of, or agreement with, the contents by NLM or the National Institutes of Health. Learn more about our disclaimer. Dtsch Arztebl Int.2016 May; 113(19): 344.

Physical exercise or strenuous sporting activities can increase blood creatine kinase (CK) levels—something to bear in mind in patients with suspected statin-associated muscle symptoms. In their article about CK increases under statin treatment, Laufs et al. have repeatedly highlighted this important aspect ( 1 ).

Nevertheless, some comments are necessary to supplement the information provided. Muscle exercise stress does not regularly “increase CK levels to 500–600 U/L” ( 1 ); in this respect, there is considerable interindividual variability. The majority of competitive athletes have raised CK level in the blood ( 2 ).

  • In individual cases, CK levels may occur that are clearly above 1000 U/L ( 3 ).
  • However, some athletes show only moderate or no response (non-responders) ( 4 ).
  • Regular preventative exercise with relatively constant muscular-mechanical stress is not often associated with CK increases.
  • On the other hand, CK levels respond to marked changes in the amount and intensity of exercise.

Thus, CK levels may increase significantly after unusual and eccentric types of exercise. This primarily applies to strength and speed-strength exercise stress ( 4 ). Therefore, taking a thorough exercise history is important to resolve issues with differential diagnosis.

  1. A cut-off CK concentration of more than 4x upper limit of normal (ULN) is of little diagnostic value.
  2. One can only agree with the authors that patients with suspected exercise-induced CK increases should observe a training break of one week.
  3. Unfortunately, competitive athletes often find it quite impossible to do this.

Marked increases in CK activity in the blood are often associated with an increase in aminotransferases; here, glutamic oxaloacetic transaminase (GOT)/aspartate aminotransferase (AST)—because of its higher muscular activity—shows a stronger response compared with glutamic pyruvate transaminase (GPT)/alanine aminotransferase (ALT).

What is the highest CK level recorded?

3 Guy’s and St. Thomas’ NHS Foundation Trust, UK Serum Creatinine Kinase (CK) is used as a diagnostic and prognostic marker in rhabdomyolysis. We present 32-year-old male with exertional rhabdomyolysis following a spin cycling class, with a peak serum CK level of 332,200 U/L. He was admitted for intravenous fluid therapy and then followed-up in the outpatient setting; renal function remained stable throughout. We review the literatures and explain why a combination of patient and environmental factors are important in the pathogenesis of exertional rhabdomyolysis. Despite a markedly elevated level of serum CK, and a correlation between serum CK and the risk of renal dysfunction being well-documented in the literature, normal renal function was noted in our case throughout. Although there is no clear consensus as to whether an elevated serum CK in the absence of renal failure warrants inpatient management, we propose that there could be a cohort of patients who could be managed in the outpatient setting with follow-up. Rhabdomyolysis, Exercise, Creatine kinase, Acute kidney injury, Exercise medicine Rhabdomyolysis occurs as a result of skeletal muscle damage. A disruption of the integrity of muscle fibres allows release of intracellular skeletal muscle components into the extracellular space and plasma, which can have harmful effects. These components include myoglobin, Creatine Kinase (CK), and electrolytes. High levels of myoglobin in the serum overwhelm the capacity of the myoglobin-binding protein haptoglobin, resulting in myoglobinuria, which can precipitate acute renal failure. Physical causes of rhabdomyolysis include trauma and exertion, of which strenuous exercise or seizure-related muscle contractions are common, Non-physical causes of rhabdomyolysis are more vast; these include a range of medications, toxins, infections, electrolyte abnormalities, endocrine disorders, as well as genetic conditions, Irrespective of cause, membrane ion channel dysfunction and intracellular Adenosine Triphosphate (ATP) depletion allows activation of a final common pathway and a cascade of muscle fibre damage, A triad of myalgia, muscle weakness, and myoglobinuria presenting as dark brown-coloured urine describes the typical features of rhabdomyolysis. However, only 10% of affected patients have all three symptoms, with dark-coloured urine being seen most often, In fact, rhabdomyolysis can range from an asymptomatic illness with only biochemical disturbance, to a life-threatening condition with electrolyte abnormalities and acute renal failure. A diagnosis of rhabdomyolysis is made following the detection of intracellular skeletal muscle enzymes in the serum. Myoglobin is rapidly metabolised and excreted, and hence is not suitable as a diagnostic marker. CK is a more sensitive biomarker of skeletal muscle injury. A serum CK level greater than 1,000 U/L in the presence of skeletal muscle injury is diagnostic for rhabdomyolysis. Serum CK is also a useful prognostic measure for the development of renal impairment, with levels of 5,000 U/L or greater being associated with increased risk of Acute Kidney Injury (AKI), The mainstay of treatment for rhabdomyolysis is supportivewith intravenous fluid resuscitation and correction of serum electrolytes. Intravenous sodium bicarbonate is used to correct systemic acidosis; there is no evidence to support sodium bicarbonate as a superior choice of fluid replacement when acidaemia is not present, Renal replacement therapy may be required. We present a case of exercise-induced rhabdomyolysis following a spin cycle class. Biochemical investigations revealed a serum CK level of more than 300,000 U/L, with preserved renal function. In the literature, there is only one case of exercise-induced rhabdomyolysis with a serum CK level greater than that reported in our case study, A 32-year-old male patient presented to the emergency department following a one-day history of passing dark brown-coloured urine. He completed a cycling spin class lasting 45-minutes three days prior to presentation. He also complained of a two-day history of bilateral quadricep muscle tenderness, worse on walking. He had no other medical problems of note and did not take any prescription or over-the-counter medications. He denied the use of illicit substances. The patient reported an active lifestyle consisting of regular light exercise, including completion of a cycling spin class some months previously. On initial assessment, the patient was haemodynamically stable and clinically euvolaemic. Initial examination was unremarkable other than mild quadricep muscle swelling bilaterally and bilateral quadriceps muscle tenderness. Neurological examination of the lower limbs was unremarkable, with normal power in all muscle groups bilaterally. Knee extension and flexion against resistance elicited mild discomfort. A urine dipstick on presentation revealed 3+ blood, 2+ protein, and was negative for nitrites, leukocytes, glucose and ketones. Blood tests, including a renal and liver profile and serum CK, were performed from the time of presentation up to the point of discharge (Table 1). Blood tests on presentation revealed normal renal function. Serum CK was markedly elevated at 332,200 U/L. A full blood count performed on presentation was unremarkable, with a haemoglobin of 152 mg/L (normal range 110-150 g/L) and white cell count 8.95 × 10 9 /L (normal range 3.5-11 × 10 9 /L). Table 1: Blood test results from day 0 (day of presentation) up to day 11 (day of discharge from outpatient setting): Na + (serum sodium; normal range 135-145 mmol/L), K+ (serum potassium; normal range 3.5-5 mmol/L), urea (normal range 1.8-7.1 mmol/L), serum creatinine (normal range 60-110 μmol/L), eGFR (estimated glomerular filtration rate; normal range < 90 ml/min/1.73 m 2 ), total bilirubin (normal range View Table 1 The patient was admitted to hospital under the medical team. Oral fluids were encouraged and supplemented with three litres of intravenous fluids in the first 24-hours.24-hours into the admission, repeat blood tests revealed a serum CK of 129,520 U/L with normal renal function. Oral fluids were supplemented with a further litre of intravenous fluids in the following 24-hour period. Serum CK on day 3 of the admission was 103,320 U/L, and the patient was discharged from the inpatient setting. Bloods tests were repeated two-days post-discharge (day 4 post-presentation) in the outpatient setting: serum CK was 22,046 U/L, renal function remained static. Bloods testswere repeated one week later (day 11 post-presentation). Renal function was again normal, and serum aminotransferase levels had drastically fallen. Serum CK was 485 U/L, and the patient was discharged from the outpatient setting. Exertional rhabdomyolysis refers to the breakdown of skeletal muscle following a period of strenuous activity. Strenuous exercise precipitates both membrane dysfunction as well as intracellular ATP depletion, which propagate a cascade of muscle fibre damage, A study of United States military personnel estimated the incidence of exertional rhabdomyolysis as 22.2 cases per 100,000 per year, Serum CK is used as both a diagnostic marker and prognostic marker in rhabdomyolysis. Hospitalisation is warranted for individuals with significantly raised CK levels or in the presence of complications. Marathon runners who complete a marathon in a shorter duration have a higher peak of serum CK compared to runners who take longer to complete the same distance, This reveals the importance of the intensity of the exercise, rather than just the length of exercise, for the development of exertional rhabdomyolysis. Environmental factors including temperature and humidity associated with a sauna have been proposed to increase the risk of exertional rhabdomyolysis, The patient in our case study had taken part in a spin class of similar intensity just months previously and experienced only mild muscle aches. This supports the importance of a combination of patient and environmental factors, and not just the length and duration of exercise alone, in the pathogenesis of exertional rhabdomyolysis. Markedly elevated serum CK levels in exertional rhabdomyolysis have been documented in the literature, for example a 37-year-old male with a peak serum CK level of 95,100 U/L following a period of high-intensity training, A case study of 30 patients in a military hospital with exertional rhabdomyolysis revealed that higher levels of serum CK were associated with a prolonged period of hospitalisation, The highest serum CK level measured in these patients was 233,180 U/L, There is only one case in the literature of exertional rhabdomyolysis with a serum CK level higher than that of our case, Renal dysfunction in rhabdomyolysis is owed to a combination of direct myoglobin toxicity, the production of intraluminal casts, and renal vasoconstriction. Although CK is not directly involved in the pathogenesis of renal dysfunction in rhabdomyolysis, serum CK levels of more than 5,000 U/L are associated with increased risk of AKI, The patient in our case had a serum creatinine at baseline despite a serum CK level of 332,200 U/L. Similarly, Casares and colleagues report normal renal function in their case of exertional rhabdomyolysis with an exceptionally high serum CK, Despite the serum CK level beingrelated to the degree of muscle damage, we propose that serum CK alone is not always a reliable predictor of renal dysfunction in exertional rhabdomyolysis. Features other than the degree of skeletal muscle injury, such as the presence of medical co-morbidities, are likely to play a key role. Our patient was admitted to hospital for intravenous fluid hydration because of an exceptionally high serum CK, despite there being no clear consensus as to whether an elevated serum CK in the absence of renal failure warrants inpatient management. Literature suggests to continue intravenous fluids until the serum CK falls below 1,000 U/L and myoglobinuria resolves, However, there are no clear guidelines to support this. In our patient, oral fluid intake was supplemented with intravenous fluids during the first 48-hours of the admission. Renal function remained stable throughout, and serum CK levels were observed to normalise in the outpatient setting over the following week. We propose that there could be a cohort of patients without medical co-morbidities or evidence of renal dysfunction at the time of presentation, who could be managed in the outpatient setting with follow-up. This case study should be combined with other literature when deciding on best management for these patients. There are no further acknowledgements. The authors declare no conflicts of interest. The authors declare no further sources of support. The authors all contributed to the above manuscript.

See also:  Does Alcohol Stain?

Bosch X, Poch E, Grau JM (2009) Rhabdomyolysis and acute kidney injury. N Engl J Med 361: 62-72. Torres PA, Helmstetter JA, Kaye AM, Kaye AD (2015) Rhabdomyolysis: Pathogenesis, Diagnosis, and Treatment. Ochsner J 15: 58-69. Cervellin G, Comelli I, Lippi G (2010) Rhabdomyolysis: Historical background, clinical, diagnostic and therapeutic features. Clin Chem Lab Med 48: 749-756. Safari S, Yousefifard M, Hashemi B, Baratloo A, Forouzanfar MM, et al. (2016) The value of serum creatine kinase in predicting the risk of rhabdomyolysis-induced acute kidney injury: A systematic review and meta-analysis. Clin Exp Nephrol 20: 153-161. Scharman EJ, Troutman WG (2013) Prevention of kidney injury following rhabdomyolysis: A systematic review. Ann Pharmacother 47: 90-105. Casares P, Marull J (2008) Over a millon Creatine Kinase due to a heavy work-out: A case report. Cases J 1: 173. Giannoglou GD, Chatzizisis YS, Misirli G (2007) The syndrome of rhabdomyolysis: Pathophysiology and diagnosis. Eur J Intern Med 18: 90-100. Alpers JP, Jones LK (2010) Natural history of exertional rhabdomyolysis: A population-based analysis. Muscle Nerve 42: 487-491. Honda S, Kawasaki T, Kamitani T, Kiyota K (2017) Rhabdomyolysis after High Intensity Resistance Training. Intern Med 56: 1175-1178. Oh RC, Arter JL, Tiglao SM, Larson SL (2015) Exertional rhabdomyolysis: A case series of 30 hospitalized patients. Mil Med 180: 201-207. Siegel AJ, Silverman LM, Lopez RE (1980) Creatine kinase elevations in marathon runners: Relationship to training and competition. Yale J Biol Med 53: 275-279. Schwaber MJ, Liss HP, Steiner I, Brezis M (1994) Hazard of sauna use after strenuous exercise. Ann Intern Med 120: 441-442. Sauret JM, Marinides G, Wang GK (2002) Rhabdomyolysis. Am Fam Physician 65: 907-912.

Kyriakides J, Khani A, Khamar R (2021) Exertional Rhabdomyolysis: A Case Report of an Exceptionally Elevated Serum Creatine Kinase (CK) Level. Int J Sports Exerc Med 7:203.

What enzymes are elevated in alcoholism?

DIAGNOSIS – Diagnosing ALD is a challenge. A history of heavy alcohol use along with certain physical signs and positive laboratory tests for liver disease are the best indicators of disease. Alcohol dependence is not necessarily a prerequisite for ALD, and ALD can be difficult to diagnose because patients often minimize or deny their alcohol abuse.

  • Even more confounding is the fact that physical exams and lab findings may not specifically point to ALD (9).
  • Diagnosis typically relies on laboratory tests of three liver enzymes: gamma–glutamyltransferase (GGT), aspartate aminotransferase (AST), and alanine aminotransferase (ALT).
  • Liver disease is the most likely diagnosis if the AST level is more than twice that of ALT (9), a ratio some studies have found in more than 80 percent of alcoholic liver disease patients.

An elevated level of the liver enzyme GGT is another gauge of heavy alcohol use and liver injury. Of the three enzymes, GGT is the best indicator of excessive alcohol consumption, but GGT is present in many organs and is increased by other drugs as well, so high GGT levels do not necessarily mean the patient is abusing alcohol.

What stimulates creatine kinase?

Stimulation of creatine kinase activity by calcium-regulating hormones in explants of human amnion, decidua, and placenta.

Is creatine kinase related to liver?

Relationship between creatine kinase and liver enzymes in war wounded with rhabdomyolysis , January 2022, Pages 166-170 Rhabdomyolysis is a frequent complication in war wounded. Its complex pathophysiology suggests that it not only affects kidneys but also other organs such as the liver. The aim of this study was to evaluate the relationship between creatine kinase (CK) and liver enzymes in war wounded with rhabdomyolysis. War wounded admitted to the intensive care unit of Percy Military Hospital between 2009 and 2017 with a rhabdomyolysis (CK peak >1,000 U/L) were included. They were divided in two groups: mild (CK peak <10,000 U/L) and severe rhabdomyolysis (CK peak ≥10,000 U/L). Demographic characteristics, peaks in transaminases, alkaline phosphatase (ALP), bilirubin, and CK were recorded. Mann Whitney-U test and, Fisher's exact test were used as appropriate. A Pearson's correlation test was used to determine the correlation between CK and liver enzymes after a log-normal transformation of the data. Fifty-one patients were included (31 in the mild and 20 in the severe rhabdomyolysis group). Patients in the severe rhabdomyolysis group were more likely victims of explosions (85% vs 39%, p = 0.003). The transaminases peak was significantly higher in the severe rhabdomyolysis group (median AST peak 398 (270–944) vs 91 (63–157) U/L, p <0.0001, and median ALT peak 106 (77–235) vs 45 (34–71) U/L, p <0.0001). Bilirubin and ALP were higher in the severe rhabdomyolysis group (39 (25–49) vs 14(11–23) U/L, p = 0.0031 and 84 (55–170) vs 52 (39–85) U/L, p = 0.0063, respectively). We found a significant positive linear correlation between CK and ALT ( r = 0.73, p <0.0001), AST ( r = 0.89, p <0.0001), ALP ( r = 0.41, p = 0.0035), and bilirubin ( r = 0.37, p = 0.0083). We found a statistically significant positive correlation between CK and liver enzymes in rhabdomyolysis war wounded, indicating that hepatic damage occurs when rhabdomyolysis is severe and associated with elevated bilirubin and ALP. Further studies are needed to confirm this phenomenon and elucidate the pathophysiological mechanism. Rhabdomyolysis refers to the lysis of skeletal muscle cells which causes the release of their intracellular contents into the circulation (aspartate amino transferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), creatine kinase (CK), myoglobin, and electrolytes). Rhabdomyolysis can have multiple causes including toxic, traumatic, genetic, or infectious, Acute kidney failure is a classic complication of rhabdomyolysis. The pathophysiology of renal impairment is complex. The most well-known cause is myoglobin intratubular precipitation at acidic urinary pH, Rhabdomyolysis is also responsible for intracellular water sequestration leading to hypovolemia, which is compensated by activation of the renin-angiotensin-aldosterone-system responsible for the vasoconstriction of the afferent renal artery and renal ischemia, Finally, the release of myoglobin into the circulation leads to an oxidative stress, an inflammatory cascade, and immune cell recruitment. The complexity of this pathophysiology along with the important role played by immune cells and inflammation suggests that aggression may not only affect kidneys but also other organs. Akmal et al. highlighted the risk of liver damage after non-traumatic rhabdomyolysis in a study involving 34 patients where hepatic dysfunction manifested itself through an increase in transaminases, bilirubin, LDH, and a decrease in prothrombin time, In military trauma patients, rhabdomyolysis is frequent and severe. It is responsible for an increase in mortality when associated with acute renal failure, Although initial mortality of war wounded, including death by exsanguination, has been decreasing for years, mostly due to improved care, training soldiers in combat rescue, and progress in forward resuscitation, death by exsanguination remains one of the leading causes of death in severe trauma patients, Teaching soldiers how to apply tactical tourniquets on wounded members with hemorrhage within minutes after trauma has reduced mortality by exsanguination, Despite these advances in battlefield resuscitation, deaths due to coagulopathy and multiple organ failure persist. Missions often last longer and take soldiers further afield (e.g., in the Sahel) leading to longer tourniquet times which in turn increases the risk of severe rhabdomyolysis. We believe, as Akmal et al. had observed in non-traumatic rhabdomyolysis, that severe post-traumatic rhabdomyolysis can lead to liver damage. We found no studies in the literature that assessed this relationship. The aim of this study was thus to evaluate the relationship between creatine kinase and liver enzymes in rhabdomyolysis war wounded. The study was performed in accordance with the Declaration of Helsinki and received approval from the institutional review board of the Percy Military Hospital, France (52–2020 HIA-CS). Written informed consent was waived. We included 51 patients, 31 of which in the mild and 20 in the severe rhabdomyolysis group (Fig.1). There were no significant differences between the two groups regarding age, sex, BMI, number of blood products transfused, ISS, or death (Table 1). Patients with severe rhabdomyolysis were more often victims of explosions (85% vs 39%, p = 0.003). Similarly, more battlefield tourniquets had been applied in the severe group (16 (80%) vs 10 (32%), p = 0.0002). Severe acute kidney injury (KDIGO stage In this study, we observed that patients in the severe rhabdomyolysis group had more frequently been victims of explosions (82.4% vs 36%, p = 0.01).y Unlike Stewart et al.,, we found no significant differences regarding KDIGO stage, possibly due to the small sample size; although patients with severe rhabdomyolysis appeared to have a higher KDIGO stage (40% in the severe rhabdomyolysis group had a KDIGO stage ≥ 2 vs 16% in the mild group). Unsurprisingly, patients in the severe group had Severe traumatic rhabdomyolysis appears to be associated with hepatic dysfunction in war wounded. If unrecognized, this association can lead to errors when interpreting anomalies in the hemostasis assessment, expose patients to the risk of overtransfusion, and delay administration of appropriate therapy. Bilirubin and ALP seem to be specific markers of rhabdomyolysis–related liver damage. Further studies are needed, however to confirm or disprove this hypothesis and elucidate the underlying We have no conflict of interest to declare. Editorial assistance, in the form of language editing and correction, was provided by XpertScientific Editing and Consulting Services This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

C. Karcher et al. F.A. Wagener et al. X. Bosch et al. R.A. Zager Z.Z. Liu et al. M. Akmal et al.

Mechanical ventilation of trauma patients is common, and many will require a higher than normal fraction of inspired oxygen (FiO 2 ) to avoid hypoxaemia. The primary objective of this study was to assess the association between FiO 2 and all-cause, one-year mortality in intubated trauma patients. Adult trauma patients intubated in the initial phase post-trauma between 2015 and 2017 were retrospectively identified. Information on FiO 2 during the first 24 hours of hospitalisation and mortality was registered. For each patient the number of hours of the first 24 hours exposed to an FiO 2 ≥ 80%, ≥ 60%, and ≥ 40%, respectively, were determined and categorised into exposure durations. The associations of these FiO 2 exposures with mortality were evaluated using Cox regression adjusting for age, sex, body mass index (BMI), Injury Severity Score (ISS), prehospital Glasgow Coma Scale (GCS) score, and presence of thoracic injuries. We included 218 intubated trauma patients. The median prehospital GCS score was 6 and the median ISS was 25. One-year mortality was significantly increased when patients had received an FiO 2 above 80% for 3-4 hours compared to <2 hours (hazard ratio (95% CI) 2.7 (1.3-6.0), p= 0.011). When an FiO 2 above 80% had been administered for more than 4 hours, there was a trend towards a higher mortality as well, but this was not statistically significant. There was a significant, time-dependent increase in mortality for patients who had received an FiO 2 ≥ 60%. There was no significant relationship observed between mortality and the duration of FiO 2 ≥ 40%. A fraction of inspired oxygen above 60% for more than 2 hours during the first 24 hours of admission was associated with increased mortality in intubated trauma patients in a duration-dependent manner. However, given the limitations of this retrospective study, the findings need to be confirmed in a larger, randomized set-up. Uncontrolled bleeding is the primary cause of death in complex liver trauma and perihepatic packing is regularly utilized for hemorrhage control. The purpose of this study was to investigate the effectiveness of a novel inflatable device (the airbag) for perihepatic packing using a validated liver injury damage control model in swine. The image of the human liver was digitally isolated within an abdominal computerized tomography scan to produce a silicone model of the liver to mold the airbag. Two medical grade polyurethane sheets were thermal bonded to the configuration of the liver avoiding compression of the hepatic pedicle, hepatic veins, and the suprahepatic vena cava after inflation. Yorkshire pigs ( n = 22) underwent controlled hemorrhagic shock (35% of the total blood volume), hypothermia, and fluid resuscitation to reproduce the indications for damage control surgery (coagulopathy, hypothermia, and acidosis) prior to a liver injury. A 3 × 10 cm rectangular segment of the left middle lobe of the liver was removed to create the injury. Subsequently, the animals were randomized into 4 groups for liver damage control (240 min), Sponge Pack ( n = 6), Pressurized Airbag ( n = 6), Vacuum Airbag ( n = 6), and Uncontrolled ( n = 4). Animals were monitored throughout the experiment and blood samples obtained. Perihepatic packing with the pressurized airbag led to significantly higher mean arterial pressure during the liver damage control phase compared to sponge pack and vacuum airbag 52 mmHg (SD 2.3), 44.9 mmHg (SD 2.1), and 32 mmHg (SD 2.3), respectively ( p < 0.0001), ejection fraction was also higher in that group. Hepatic hemorrhage was significantly lower in the pressurized airbag group compared to sponge pack, vacuum airbag, and uncontrolled groups; respectively 225 ml (SD 160), 611 ml (SD 123), 991 ml (SD 385), 1162 ml (SD 137) ( p < 0001). Rebleeding after perihepatic packing removal was also significantly lower in the pressurized airbag group; respectively 32 ml (SD 47), 630 ml (SD 185), 513 ml (SD 303), ( p = 0.0004). Intra-abdominal pressure remained similar to baseline, 1.9 mmHg (SD 1), ( p = 0.297). Histopathology showed less necrosis at the border of the liver injury site with the pressurized airbag. The pressurized airbag was significantly more effective at controlling hepatic hemorrhage and improving hemodynamics than the traditional sponge pack technique. Rebleeding after perihepatic packing removal was negligible with the pressurized airbag and it did not provoke hepatic injury. The diagnosis of penetrating isolated diaphragmatic injuries can be challenging because they are usually asymptomatic. Diagnosis by chest X-ray (CXR) is unreliable, while CT scan is reported to be more valuable. This study evaluated the diagnostic ability of CXR and CT in patients with proven DI. Single center retrospective study (2009–2019), including all patients with penetrating diaphragmatic injuries (pDI) documented at laparotomy or laparoscopy with preoperative CXR and/or CT evaluation. Imaging findings included hemo/pneumothorax, hemoperitoneum, pneumoperitoneum, elevated diaphragm, definitive DI, diaphragmatic hernia, and associated abdominal injuries.230 patients were included, 62 (27%) of which had isolated pDI, while 168 (73%) had associated abdominal or chest trauma. Of the 221 patients with proven DI and preoperative CXR, the CXR showed hemo/pneumothorax in 99 (45%), elevated diaphragm in 51 (23%), and diaphragmatic hernia in 4 (1.8%). In 86 (39%) patients, the CXR was normal. In 126 patients with pDI and preoperative CT, imaging showed hemo/pneumothorax in 95 (75%), hemoperitoneum in 66 (52%), pneumoperitoneum in 35 (28%), definitive DI in 56 (44%), suspected DI in 26 (21%), and no abnormality in 3 (2%). Of the 57 patients with isolated pDI the CXR showed a hemo/pneumothorax in 24 (42%), elevated diaphragm in 14 (25%) and was normal in 24 (42%). Radiologic diagnosis of DI is unreliable. CT scan is much more sensitive than CXR. Laparoscopic evaluation should be considered liberally, irrespective of radiological findings. The International Classification of diseases- based Injury Severity Score (ICISS) obtained by empirically derived diagnosis-specific survival probabilities (DSPs) is the best-known risk-adjustment measure to predict mortality. Recently, a new set of pooled DSPs has been proposed by the International Collaborative Effort on Injury Statistics but it remains to be externally validated in other cohorts. The aim of this study was to externally validate the ICISS using international DSPs and compare its prognostic performance with local DSPs derived from Greek adult trauma population. This retrospective single-center cohort study enrolled adult trauma patients (≥ 16 years) hospitalized between January 2015 and December 2019 and temporally divided into derivation ( n = 21,614) and validation cohorts ( n = 14,889). Two different ICISS values were calculated for each patient using two different sets of DSPs: international (ICISSint) and local (ICISSgr). The primary outcome was in-hospital mortality. Models' prediction was performed using discrimination and calibration statistics. ICISSint displayed good discrimination in derivation (AUC = 0.836 CI 95% 0.819–0.852) and validation cohort (AUC = 0.817 CI 95% 0.797–0.836). Calibration using visual analysis showed accurate prediction at patients with low mortality risk, especially below 30%. ICISSgr yielded better discrimination (AUC = 0.834 CI 95% 0.814–0.854 vs 0.817 CI 95% 0.797–0.836, p ˂,05) and marginally improved overall accuracy (Brier score = 0.0216 vs 0.0223) compared with the ICISSint in the validation cohort. Incorporation of age and sex in both models enhanced further their performance as reflected by superior discrimination ( p ˂,05) and closer calibration curve to the identity line in the validation cohort. This study supports the use of international DSPs for the ICISS to predict mortality in contemporary trauma patients and provides evidence regarding the potential benefit of applying local DSPs. Further research is warranted to confirm our findings and recommend the widespread use of ICISS as a valid measure that is easily obtained from administrative data based on ICD-10 codes. Routinely collected health data (RCHD) offers many opportunities for traumatic brain injury (TBI) research, in which injury severity is an important factor. The use of clinical injury severity indices in a context of RCHD is explored, as are alternative measures created for this specific purpose. To identify useful scales for full body injury severity and TBI severity this study focuses on their performance in predicting these currently used indices, while accounting for age and comorbidities. This study utilized an extensive population-based RCHD dataset consisting of all patients with TBI admitted to any Belgian hospital in 2016. Full body injury severity is scored based on the (New) Injury Severity Score ((N)ISS) and the ICD-based Injury Severity Score (ICISS). For TBI specifically, the Abbreviated Injury Scale (AIS) Head, Loss of Consciousness and the ICD-based Injury Severity Score for TBI injuries (ICISS) were used in the analysis. These scales were used to predict three outcome variables strongly related to injury severity: in-hospital death, admission to intensive care and length of hospital stay. For the prediction logistic regressions of the different injury severity scales and TBI severity indices were used, and error rates and the area under the receiver operating curve were evaluated visually. In general, the ICISS had the best predictive performance (error rate between 0.06 and 0.23; AUC between 0.82 and 0.86 ). A clearly increasing error rate can be noticed with advancing age and accumulating comorbidity. Both for full body injury severity and TBI severity, the ICISS tends to outperform other scales. It is therefore the preferred scale for use in research on TBI in the context of RCHD. In their current form, the severity scales are not suitable for use in older populations.

: Relationship between creatine kinase and liver enzymes in war wounded with rhabdomyolysis

Can caffeine increase creatine kinase?

Main content – Abstract : Background: The studies were shown that creatinekinasein may be increased and its occurs following vigorous eccentric exercises and delayed onset muscle soreness. Objective: The aim of this paper was survey The Effect of Caffeine Consumption on Creatine Kinase Levels Following Eccentric Exercise.

Results: The results show that, as a result of eccentric exercise, creatine kinase significantly increased only at 24 hours after exercise (68.80 percent). Also caffeine consumption and eccentric exercise has led to significant increase in CK levels only at 24 hours after exercise (37.18 percent). Conclusion: It appears that caffeine consumption increases the removal of waste and reduces DOMS.

Therefore, it is recommended that trainers or physiotherapists use coffee to quickly reduce serum creatine kinase and DOMS. Key words: creatinekinasein, vigorous eccentric exercises, muscle soreness Get Full Access Gale offers a variety of resources for education, lifelong learning, and academic research.