Massive Rhabdomyolysis Research Articles

CONTINUOUS VENO-VENOUS HEMODIAFILTRATION IN MULTIPLE TRAUMA WITH ACUTE RENAL FAILURE

Abstract. Acute kidney injury (AKI) develops in 20 % of multiple trauma victims in intensive care units. In 10 % – 28 % of cases, these victims require renal replacement therapy. The aim of our study was to study the effect of continuous veno-venous hemodiafiltration (CVVHDF) on indicators of kidney function, hemodynamics, homeostasis and inflammation in victims of multiple trauma, complicated by rhabdomyolysis and AKI. Materials and methods. 71 victims with multiple trauma complicated by massive rhabdomyolysis and AKI were examined. The levels of total creatine kinase and myoglobin, indicators of kidney function, frequency of vasopressor support, indicators of general blood count, liver complex, coagulogram, and blood gas were studied. The study was conducted at admission, before and after each CVVHDF session and on the last day of treatment. The results. Multiple trauma with massive rhabdomyolysis resulted in AKI with oliguria, hyperazotemia, and hyperkalemia, as well as cardiovascular failure, anemia, hepatic dysfunction, and an inflammatory response. In the case of progressing renal failure despite conservative therapy, CVVHDF was started on day 2.7±0.5. After 1 session of CVVHDF, hyperazotemia was significantly reduced, and potassium levels were normalized. Indicators of the blood count and liver complex did not change. Due to the use of heparin in the circuit, there was a significant prolongation of activated partial thromboplastin time, which did not exceed the target values. 1 session of CVVHDF was sufficient for 71.8 % of victims. Among the survivors, restoration of diuresis was observed in 63.9 %. The mortality rate was 42.3 %. However, there was no significant difference in azotemia levels between survivors and non-survivors, but non-survivors had higher potassium levels, more severe thrombocytopenia, cardiovascular and hepatic failure, and hypocoagulation. In addition, the ISS score in non-survivors was 37.8 % (p=0.001) higher than in the survivors. Conclusions. Multiple trauma, complicated by massive rhabdomyolysis, causes the development of multiple organ failure, primarily renal. CVVHDF allows to effectively reduce the levels of azotemia and normalize the level of potassium after the first session, while avoiding abrupt fluctuations in the indicators of the function of other organs and systems. A single session of CVVHDF is sufficient to restore renal function in most patients. Mortality remains high and depends directly on the severity of anatomical injuries and the addition of insufficiency of other organs and systems.

Epidemiology and outcome of an acute kidney injuries in the polytrauma victims admitted at the apex trauma center in Dubai.

Polytrauma from road accidents is a common cause of hospital admissions and deaths, frequently leading to acute kidney injury (AKI) and impacting patient outcomes. This retrospective, single-center study included polytrauma victims with an Injury Severity Score (ISS) >25 at a tertiary healthcare center in Dubai. The incidence of AKI in polytrauma victims is 30.5%, associated with higher Carlson comorbidity index (P=0.021) and ISS (P=0.001). Logistic regression shows a significant relationship between ISS and AKI (odds ratio [OR], 1.191; 95% confidence interval [CI], 1.150-1.233; P<0.05). The main causes of trauma-induced AKI are hemorrhagic shock (P=0.001), need for massive transfusion (P<0.001), rhabdomyolysis (P=0.001), and abdominal compartment syndrome (ACS; P<0.001). On multivariate logistic regression AKI can be predicated by higher ISS (OR, 1.08; 95% CI, 1.00-1.17; P=0.05) and low mixed venous oxygen saturation (OR, 1.13; 95% CI, 1.05-1.22; P<0.001). The development of AKI after polytrauma increases length of stay (LOS)-hospital (P=0.006), LOS-intensive care unit (ICU; P=0.003), need for mechanical ventilation (MV) (P<0.001), ventilator days (P=0.001), and mortality (P<0.001). After polytrauma, the occurrence of AKI leads to prolonged hospital and ICU stays, increased need for mechanical ventilation, more ventilator days, and a higher mortality rate. AKI could significantly impact their prognosis.

Safety monitoring of drug-induced muscle injury and rhabdomyolysis: a biomarker-guided approach for clinical practice and drug trials.

Skeletal muscle tissue (SKM) may be damaged due to mechanical, metabolic, and exertional causes. However, drug-induced myopathy is among the most frequent causes of muscle disease. The clinical picture of drug-induced myopathies may be highly variable. It may present as asymptomatic or mild myalgias, with or without muscle weakness, which are likely underreported. However, it may also appear as chronic myopathy with severe weakness and, rarely, even as massive rhabdomyolysis with acute kidney injury (AKI). Unfortunately, the available biomarkers for SKM injury do not fully meet the needs for satisfactory detection of drug-induced damage, both in clinical and research settings, mainly due to their low sensitivity and specificity. Therefore, the present study proposes a strategy for drug safety monitoring using the available biomarkers of SKM injury. Moreover, we will discuss mechanisms of drug-induced SKM injury, traditional laboratory testing for SKM injury, and novel skeletal myocyte biomarkers under investigation. This can be incredibly useful in both clinical practice and for de-challenge/re-challenge investigational trials where the risk of drug-induced SKM injury is present.

Rhabdomyolysis Associated with Recent SARS-COV-2 Infection in a Patient with Carnitine Palmitoyltransferase II Deficiency.

Carnitine palmitoyltransferase II deficiency (CPT II) is an autosomal recessive inherited disorder of long-chain fatty acid oxidation in the mitochondrial matrix, resulting in an inability to utilize fat for energy in cells. The most frequent myopathic form occurs in young adults and is associated with recurrent episodes of exercise-induced rhabdomyolysis. The myopathic form is caused by the Ser113Leu mutation of the CPT II gene. Rarely, massive rhabdomyolysis could be complicated by acute kidney injury (AKI), cardiomyopathy, and respiratory insufficiency. We present a case of an 18-year old male with myalgia, muscular weakness, and dark-colored urine after prolonged exercise and a recent mildSARS-CoV-2infection. Massive rhabdomyolysis was diagnosed with markedly increased serum concentrations of myoglobin and creatine kinase, with normal kidney function. The patient experienced two similar episodes in the years 2017 and 2018, with rhabdomyolysis and AKI treated with hemodialysis. After excluding autoimmune and infectious diseases as causes of recurrent rhabdomyolysis, the patient was genetically tested and Ser113Leu mutation of the CPT II gene was confirmed. When a patient presents with myalgia and dark-colored urine triggered by minor physical activities, genetic testing for possible CPT II deficiency should be initiated. TheSARS-CoV-2infection could be a factor that triggers the occurrence of rhabdomyolysis and aggravates the severity of the attack in patients with CPT II deficiency.

Peroxisome Proliferator-Activated Receptor Delta Agonist (PPAR- δ) and Selective Androgen Receptor Modulator (SARM) Abuse: Clinical, Analytical and Biological Data in a Case Involving a Poisonous Combination of GW1516 (Cardarine) and MK2866 (Ostarine)

A 43-year-old male, sport coach, presented him-self at the Emergency unit of a local hospital for epigastric pain, myalgia pain and severe headache. He claimed having used for some days a combination of GW1516 (cardarine), a peroxisome proliferator-activated receptor delta agonist (PPAR- δ) and MK2866 (ostarine), a selective androgen receptor modulator (SARM) to gain skeletal muscles. Cytolysis with marked increase of alanine aminotransferase or ALT (up to 922 UI/L) and aspartate aminotransferase or AST (up to 2558 UI/L) and massive rhabdomyolysis with elevated creatine phosphokinase or CPK (up to 86435 UI/L) were the main unusual biochemistry parameters. Using a specific liquid chromatography coupled to tandem mass spectrometry method, cardarine and ostarine tested positive in blood at 403 and 1 ng/mL, respectively. In urine, due to extensive metabolism, the parent GW1516 was not identified, while ostarine was at 88 ng/mL. Finally, both drugs were identified in hair (2 cm in length, brown in colour), at 146 and 1105 pg/mg for cardarine and ostarine, respectively. This clearly demonstrates repetitive abuse over the last 2 months. Asthenia was persistent for 2 weeks and 6 weeks after the admission, the subject fully recovered.

Loss of membrane integrity drives myofiber death in lipin1-deficient skeletal muscle.

Mutations in lipin1 are suggested to be a common cause of massive rhabdomyolysis episodes in children; however, the molecular mechanisms involved in the regulation of myofiber death caused by the absence of lipin1 are not fully understood. Loss of membrane integrity is considered as an effective inducer of cell death in muscular dystrophy. In this study, we utilized a mouse line with selective homozygous lipin1 deficiency in the skeletal muscle (Lipin1Myf5cKO) to determine the role of compromised membrane integrity in the myofiber death in lipin1‐deficient muscles. We found that Lipin1Myf5cKO muscles had significantly elevated proapoptotic factors (Bax, Bak, and cleaved caspase‐9) and necroptotic proteins such as RIPK1, RIPK3, and MLKL compared with WT mice. Moreover, Lipin1Myf5cKO muscle had significantly higher membrane disruptions, as evidenced by increased IgG staining and elevated uptake of Evans Blue Dye (EBD) and increased serum creatine kinase activity in Lipin1Myf5cKO muscle fibers. EBD‐positive fibers were strongly colocalized with apoptotic or necroptotic myofibers, suggesting an association between compromised plasma membrane integrity and cell death pathways. We further show that the absence of lipin1 leads to a significant decrease in the absolute and specific muscle force (normalized to muscle mass). Our work indicates that apoptosis and necroptosis are associated with a loss of membrane integrity in Lipin1Myf5cKO muscle and that myofiber death and dysfunction may cause a decrease in contractile force.

Full recovery after massive rhabdomyolysis following exercise at 8000 feet

Full recovery after massive rhabdomyolysis following exercise at 8000 feet

Metabolic Acidosis Due To Pyroglutamic Acid.

Metabolic acidosis is a common clinical disturbance due to increased plasma acidity caused by a primary decrease in serum HCO3- concentration. It is classified as normal or high anion gap metabolic acidosis. High anion gap metabolic acidosis can result from either a decrease in unmeasured cations (K+, Ca2+, Mg2+) or an increase in unmeasured anions (PO43−, albumin). However, other anions such as lactic acid or keto acids may cause this acid-base disorder. It can also result from renal failure and intoxication (salicylate, methanol, ethylene glycol), or more rarely, from massive rhabdomyolysis and pyroglutamic (5-oxoproline) acidemia. Acidemia due to pyroglutamic acid should be considered when no other aetiology is found. High anion gap metabolic acidosis is diagnosed in children with inherited defects in enzymes of the γ-glutamyl cycle. In adults, this disorder from pyroglutamic acid has been described in association with chronic acetaminophen misuse. We report a case of pyroglutamic acidosis in a woman with acute misuse of acetaminophen concurrent with chronic use.LEARNING POINTParacetamol is an easily available drug with potentially harmful consequences.Accumulation of pyroglutamic acid (5-oxoproline) may be a cause of high anion gap metabolic acidosis.Reporting cases of 5-oxoprolinemia acidosis contributes to better understanding of the condition.

Clinical, virological, and biological parameters associated with outcomes of Ebola virus infection in Macenta, Guinea.

BACKGROUND. The pathogenesis of Ebola virus (EBOV) disease (EVD) is poorly characterized. The establishment of well-equipped diagnostic laboratories close to Ebola treatment centers (ETCs) has made it possible to obtain relevant virological and biological data during the course of EVD and to assess their association with the clinical course and different outcomes of the disease. METHODS. We were responsible for diagnosing EBOV infection in patients admitted to two ETCs in forested areas of Guinea. The pattern of clinical signs was recorded, and an etiological diagnosis was established by RT-PCR for EBOV infection or a rapid test for malaria and typhoid fever. Biochemical analyses were also performed. RESULTS. We handled samples from 168 patients between November 29, 2014, and January 31, 2015; 97 patients were found to be infected with EBOV, with Plasmodium falciparum coinfection in 18%. Overall mortality for EVD cases was 58%, rising to 86% if P. falciparum was also present. Viral load was higher in fatal cases of EVD than in survivors, and fatal cases were associated with higher aspartate aminotransferase (AST) and alanine aminotransferase (ALT), C-reactive protein (CRP), and IL-6 levels. Furthermore, regardless of outcome, EVD was characterized by higher creatine kinase (CPK), amylase, and creatinine levels than in febrile patients without EVD, with higher blood urea nitrogen (BUN) levels in fatal cases of EVD only. CONCLUSION. These findings suggest that a high viral load at admission is a marker of poor EVD prognosis. In addition, high AST, ALT, CRP, and IL-6 levels are associated with a fatal outcome of EVD. Damage to the liver and other tissues, with massive rhabdomyolysis and, probably, acute pancreatitis, is associated with EVD and correlated with disease severity. Finally, biochemical analyses provide substantial added value at ETCs, making it possible to improve supportive rehydration and symptomatic care for patients. FUNDING. The French Ministry of Foreign Affairs, the Agence Française de Développement, and Institut Pasteur.

Hypothermia and hypokalemia in a patient with diabetic ketoacidosis.

We present the case of a 36-year-old man with type-1 diabetes who was hospitalized with diabetic ketoacidosis (DKA). On admission, he had hypothermia, hypokalemia and combined metabolic and respiratory alkalosis, in addition to hyperglycemia. Hypothermia, hypokalemia and metabolic alkalosis, with a concurrent respiratory alkalosis, are not commonly seen in DKA. After admission, intravenous infusion of 0.45% saline was administered, which resulted in the development of pure metabolic acidosis. After starting insulin infusion, hypokalemia and hypophosphatemia became evident and finally resulted in massive rhabdomyolysis. Hyperkalemia accompanying oliguric acute kidney injury (AKI) warranted initiation of hemodialysis (HD) on Day-five. On the 45th hospital day, his urine output started to increase and a total of 22 HD sessions were required. We believe that in this case severe dehydration, hypothermia and hypokalemia might have contributed to the initial symptoms of DKA as well as the prolongation of AKI.

Rhabdomyolysis and Cardiomyopathy in a 20-Year-Old Patient with CPT II Deficiency

Aim. To raise the awareness of adult-onset carnitite palmitoyltransferase II deficiency (CPT II) by describing clinical, biochemical, and genetic features of the disease occurring in early adulthood. Method. Review of the case characteristics and literature review. Results. We report on a 20-year-old man presenting with dyspnea, fatigue, fever, and myoglobinuria. This was the second episode with such symptoms (the previous one being three years earlier). The symptoms occurred after intense physical work, followed by a viral infection resulting in fever treated with NSAIDs. Massive rhabdomyolysis was diagnosed, resulting in acute renal failure necessitating plasmapheresis and hemodialysis, acute hepatic lesion, and respiratory insufficiency. Additionally, our patient had cardiomyopathy with volume overload. After a detailed workup, CPT II deficiency was suspected. We did a sequencing analysis for exons 1, 3, and 4 of the CPT II gene and found that the patient was homozygote for Ser 113 Leu mutation in exon 3 of the CPT II gene. The patient recovery was complete except for the cardiomiopathy with mildly impaired systolic function. Conclusion. Whenever a patient suffers recurrent episodes of myalgia, followed by myoglobinuria due to rhabdomyolysis, we should always consider the possibility of this rare condition. The definitive diagnose of this condition is achieved by genetic testing.

Acute Kidney Injury

Acute Kidney Injury

Acute Kidney Injury

1. David T. Selewski, MD* 2. Jordan M. Symons, MD† 1. *Department of Pediatrics and Communicable Diseases, Division of Nephrology, C.S. Mott Children’s Hospital, University of Michigan, Ann Arbor, MI. 2. †Department of Pediatrics, Division of Nephrology, University of Washington School of Medicine, Seattle, WA. * Abbreviations: ACE: : angiotensin-converting enzyme AKI: : acute kidney injury AKIN: : Acute Kidney Injury Network ANCA: : antineutrophil cytoplasmic antibody ATN: : acute tubular necrosis ECG: : electrocardiogram FEurea: : fractional excretion of urea FENa: : fractional excretion of sodium KDIGO: : Kidney Disease: Improving Global Outcomes NSAID: : nonsteroidal anti-inflammatory drug RIFLE: : Risk, Injury, Failure, Loss, and End-stage The term acute kidney injury has replaced acute renal failure and represents a spectrum of clinically meaningful kidney damage. After completing this article, readers should be able to: 1. Recognize and define the spectrum of acute kidney injury (AKI). 2. Understand the diagnostic approach and be able to differentiate the main causes of AKI. 3. Understand the complications of AKI and the treatment of a child with AKI. Acute kidney injury (AKI), formerly called acute renal failure, is characterized by multiple abnormalities, including increases in serum creatinine and blood urea nitrogen, electrolyte abnormalities, acidosis, and difficulties with fluid management. We have come to realize that what was previously thought to be relatively minor damage to the kidney can have significant short-term effects on morbidity and mortality and potential long-term implications for the development of chronic kidney disease. Thus, the term acute kidney injury has replaced acute renal failure , suggesting the spectrum of kidney damage that can occur. ### Definition AKI is classically defined as an acute decrease in glomerular filtration rate, which results in an increase in serum creatinine. It is important to recognize the limitations of creatinine as a marker of AKI because an increase in creatinine can be delayed by as much as 48 hours after damage to the kidney has occurred. Despite this limitation, change in creatinine remains the gold standard for the diagnosis of AKI. An evolution in the definition of AKI to better understand, characterize, and study the disease spectrum, has occurred, which has sought to capture the clinical importance of even small variations in kidney function. In addition, previous definitions used in the literature were widely disparate; this …

Rhabdomyolyse massive : une complication rare de la maladie des emboles de cholestérol

A 79-year-old man with atherosclerosis presented blue toes and livedo reticularis. The patient had eroded aortic atheromatous plaques, and cholesterol embolization syndrome was suspected. An endovascular technique to exclude sources of cholesterol emboli was however performed. The patient immediately presented with severe muscle pain and total functional disability of lower limbs, new ischemic lesions of toes, anal and genital necrosis, and a livedo extended up to the abdomen. A massive rhabdomyolysis occurred associated with acute kidney injury and hyperkaliemia treated by continuous renal replacement therapy with regional citrate anticoagulation. Steroids have been introduced and renal function improved. Cholesterol crystals were also found on a skin biopsy, performed before endovascular procedure.

Combination of lipid metabolism alterations and their sensitivity to inflammatory cytokines in human lipin-1-deficient myoblasts

Lipin-1 deficiency is associated with massive rhabdomyolysis episodes in humans, precipitated by febrile illnesses. Despite well-known roles of lipin-1 in lipid biosynthesis and transcriptional regulation, the pathogenic mechanisms leading to rhabdomyolysis remain unknown. Here we show that primary myoblasts from lipin-1-deficient patients exhibit a dramatic decrease in LPIN1 expression and phosphatidic acid phosphatase 1 activity, and a significant accumulation of lipid droplets (LD). The expression levels of LPIN1-target genes [peroxisome proliferator-activated receptors delta and alpha (PPARδ, PPARα), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), acyl-coenzyme A dehydrogenase, very long (ACADVL), carnitine palmitoyltransferase IB and 2 (CPT1B and CPT2)] were not affected while lipin-2 protein level, a closely related member of the family, was increased. Microarray analysis of patients' myotubes identified 19 down-regulated and 51 up-regulated genes, indicating pleiotropic effects of lipin-1 deficiency. Special attention was paid to the up-regulated ACACB (acetyl-CoA carboxylase beta), a key enzyme in the fatty acid synthesis/oxidation balance. We demonstrated that overexpression of ACACB was associated with free fatty acid accumulation in patients' myoblasts whereas malonyl-carnitine (as a measure of malonyl-CoA) and CPT1 activity were in the normal range in basal conditions accordingly to the normal daily activity reported by the patients. Remarkably ACACB invalidation in patients' myoblasts decreased LD number and size while LPIN1 invalidation in controls induced LD accumulation. Further, pro-inflammatory treatments tumor necrosis factor alpha+Interleukin-1beta(TNF1α+IL-1ß) designed to mimic febrile illness, resulted in increased malonyl-carnitine levels, reduced CPT1 activity and enhanced LD accumulation, a phenomenon reversed by dexamethasone and TNFα or IL-1ß inhibitors. Our data suggest that the pathogenic mechanism of rhabdomyolysis in lipin-1-deficient patients combines the predisposing constitutive impairment of lipid metabolism and its exacerbation by pro-inflammatory cytokines.

A Case of Cocaine-Induced Myopathy

A Case of Cocaine-Induced Myopathy

Continuous Veno-Venous Hemofiltration for Massive Rhabdomyolysis After Malignant Hyperthermia: Report of 2 Cases

We present 2 cases of fulminant malignant hyperthermia (MH), complicated with massive rhabdomyolysis. The patients were successfully treated in the intensive care unit of our university teaching hospital, despite the lack of availability of dantrolene in our country, by early application of continuous veno-venous hemofiltration (CVVH). Both male patients developed fulminant malignant hyperthermia during anesthesia for oromaxillofacial surgery. CVVH was employed when the values of creatine phosphokinase (CPK), myoglobin (Mb), and lactate dehydrogenase (LDH) increased significantly. After emergency treatment and CVVH therapy, the values of CPK, Mb, and LDH in the blood plasma of the patients decreased significantly. The complications, including acute renal failure, disseminated intravascular coagulation, and acute respiratory distress syndrome were also treated without any obvious organ damage. Early detection and management are the keys to treat MH successfully. CVVH is a valuable therapeutic application in the initial/critical management of severe rhabdomyolysis. If these complications occur even with initial treatment with dantrolene, our experiences may be useful adjunctive treatments to consider.

Vibrio vulnificus septicemia in Thailand: A 12-year case series and report of two fatal massive rhabdomyolysis cases

Background: Vibrio vulnificus infection is prevalent among tropical coastal regions and septicemia due to this bacterium is often rapidly fatal. Our review of V. vulnificus cases in Thailand included microbiological and clinical analyses which have rarely been documented. They included a rare complication of rhabdomyolysis which has never been reported in this country. Objective: We reported a case series of V. vulnificus septicemia at a university hospital in Thailand during a 12-year period including two fatal cases with rhabdomylysis due to V. vulnificus infection. Methods: Our case series of patients with V. vulnificus septicemia was retrospectively reviewed to determine clinical presentations, risk factors, microbiologic data, hospital courses, treatment, and outcomes. Results: Twenty-nine patients, predominantly male, were identified. Most patients had underlying cirrhosis or related chronic liver diseases and 20 cases (69%) died rapidly. Cellulitis and necrotizing fasciitis were common presenting symptoms. Consumption of undercooked shellfish may be a local risk factor. Inadequate surgical intervention may be related to a high mortality rate. Two fatal cases with autopsy-proven acute massive rhabdomyolysis were described, which emphasized urgent appropriate management. Conclusion: This 29-case series identified that V. vulnificus septicemia had a high mortality rate. Chronic liver diseases are known underlying factors. Acute massive rhabdomyolysis is very rare as a fatal complication of V. vulnificus infection. Keywords: Cellulitis, cirrhosis, necrotizing fasciitis, rhabdomyolysis, septicemia, Vibrio vulnificus

Vibrio vulnificus septicemia in Thailand: A 12-year case series and report of two fatal massive rhabdomyolysis cases

Background: Vibrio vulnificus infection is prevalent among tropical coastal regions and septicemia due to this bacterium is often rapidly fatal. Our review of V. vulnificus cases in Thailand included microbiological and clinical analyses which have rarely been documented. They included a rare complication of rhabdomyolysis which has never been reported in this country. Objective: We reported a case series of V. vulnificus septicemia at a university hospital in Thailand during a 12-year period including two fatal cases with rhabdomylysis due to V. vulnificus infection. Methods: Our case series of patients with V. vulnificus septicemia was retrospectively reviewed to determine clinical presentations, risk factors, microbiologic data, hospital courses, treatment, and outcomes. Results: Twenty-nine patients, predominantly male, were identified. Most patients had underlying cirrhosis or related chronic liver diseases and 20 cases (69%) died rapidly. Cellulitis and necrotizing fasciitis were common presenting symptoms. Consumption of undercooked shellfish may be a local risk factor. Inadequate surgical intervention may be related to a high mortality rate. Two fatal cases with autopsy-proven acute massive rhabdomyolysis were described, which emphasized urgent appropriate management. Conclusion: This 29-case series identified that V. vulnificus septicemia had a high mortality rate. Chronic liver diseases are known underlying factors. Acute massive rhabdomyolysis is very rare as a fatal complication of V. vulnificus infection. Keywords: Cellulitis, cirrhosis, necrotizing fasciitis, rhabdomyolysis, septicemia, Vibrio vulnificus

Clinical experience with daptomycin for the treatment of patients with knee and hip periprosthetic joint infections

To investigate the clinical efficacy and safety of daptomycin in the treatment of hip and knee periprosthetic joint infections (PJIs). We completed a retrospective review of all patients in our institution (n=20) who were treated with daptomycin for hip or knee PJI, over the 36 month period from January 2008 until December 2010. Infection types included eight cases with acute infections, nine cases of chronic infection and three cases of positive intraoperative cultures. Methicillin-resistant coagulase-negative Staphylococcus was the most frequent microorganism found in surgical cultures (40%). Our patients, on average, received daptomycin as salvage therapy at a dose of 6.6 mg/kg/day for 44.9 days. The overall success rate was 78.6% after a median follow-up period of 20 months. In the subgroup of patients with acute PJIs, treatment with daptomycin, debridement and implant retention was successful in all cases. We found two cases of severe side effects (one case of acute renal failure due to massive rhabdomyolysis and one of eosinophilic pneumonia) and two cases of asymptomatic transient creatine phosphokinase (CPK) level elevation. The combination of high daptomycin doses with an adequate surgical approach could be a viable alternative in cases of difficult-to-treat Gram-positive PJIs. Due to the risk of potentially serious adverse events, serum CPK level should be closely monitored.