Rhabdomyolysis related to acute recreational drug toxicity—A Euro-DEN study

Abstract

Background This study was conducted to retrospectively assess the relationships between: rhabdomyolysis (quantified by creatine kinase (CK) activity) and kidney injury (quantified by serum creatinine concentration), sex, age, body temperature on admission, presence of seizures, and agitation or aggression in patients presenting to the Emergency Department with acute recreational drug toxicity. We also investigated the association with the substances ingested. Methods All presentations to the 16 sentinel Euro-DEN centres in 10 European countries with acute recreational drug toxicity during the first year of the Euro-DEN study (October 2013 to September 2014) were considered. Cases that had abnormal CK activity recorded as part of routine clinical care were divided into 3 cohorts depending on peak CK activity. Cases with normal CK activity were included as a control group (4th cohort). Results Only 1,015 (18.4%) of the 5,529 Euro-DEN presentations had CK activity concentration recorded. Of this group 353 (34.8%) had also creatinine concentration measured. There were 375 (36.9%) with minor rhabdomyolysis, 69 (6.8%) with moderate rhabdomyolysis, and 24 (2.4%) with severe rhabdomyolysis; 547 (53.9%) were included in the control group. There was a positive correlation between CK activity and creatinine concentration (correlation coefficient r = 0.71, p<0.0001). There was no correlation between CK activity and body temperature at the time of presentation to the ED (correlation coefficient r = 0.07, p = 0.03). There was a positive correlation between CK activity and length of stay in the hospital (r = 0.31, p<0.001). There was no association between CK activity and the presence of seizures (p = 0.33) or agitation/aggression (p = 0.45), patients age (p = 0.4) or sex (p = 0.25). The 5 most common agents amongst patients presenting with rhabdomyolysis were: cocaine (n = 107; 22.9% presentations), amphetamine (76; 16.2%), cannabis (74; 15.8%), GHB/GBL (72; 15.4%) and heroin (67; 14.3%). The distribution of rhabdomyolysis in 5 most common drugs was (drug; patients with rhabdomyolysis, patients without rhabdomyolysis): cocaine (107, 122), cannabis (74, 117), GHB/GBL (72, 81), amphetamine (76, 66), heroin (67, 70). Conclusions Abnormal values of CK activity occurred in almost half (46.1%) of presentations to the Emergency Department with acute recreational drug toxicity in whom CK activity was measured; however, severe rhabdomyolysis is seen in only a small minority (2.4%). Those with rhabdomyolysis are at significantly higher risk of kidney injury and have a longer length of hospital stay.

Atraumatic Bilateral Acute Compartment Syndrome of the Lower Legs: A Review of the Literature

“…Multiple cases in our review highlight the association between intoxication from both alcohol and drug use, resulting in a prolonged state of immobilisation, and the subsequent presentation of compartment syndrome complicated by rhabdomyolysis. Acute alcohol intoxication with prolonged immobilisation is one of the most common causes of rhabdomyolysis [ 46 ], and abnormal CK levels are present in almost half of those who attend the emergency department following recreational drug use [ 47 ].…”

Rhabdomyolysis after the Intake of Illicit Drugs as a Cause of Acute Renal Failure

“…Rhabdomyolysis (RM) is striate muscle-cell damage with the release of intracellular substances to the circulation-myoglobin, muscular enzymes, potassium, etc., with or without the development of acute renal injury [1]. The major laboratory markers of RM are: increased levels of myoglobin in the plasma/serum and urine and plasma/serum levels of creatin kinase, lactate dehydrogenase and amino transferase, high potassium, uric acid and phosphate plasma/serum levels, metabolic acidosis, hypercoagulation and changes in calcium levels (both hypoand hypercalcemia) can be observed [1] [2] [3] [4].…”

“…Rhabdomyolysis (RM) is striate muscle-cell damage with the release of intracellular substances to the circulation-myoglobin, muscular enzymes, potassium, etc., with or without the development of acute renal injury [1]. The major laboratory markers of RM are: increased levels of myoglobin in the plasma/serum and urine and plasma/serum levels of creatin kinase, lactate dehydrogenase and amino transferase, high potassium, uric acid and phosphate plasma/serum levels, metabolic acidosis, hypercoagulation and changes in calcium levels (both hypoand hypercalcemia) can be observed [1] [2] [3] [4]. RM can be caused by a wide spectrum of metabolic, traumatic and infectious agents and can be classified as traumatic (after muscle physical trauma, electrocution, muscular compression/immobilization) and non-traumatic (after physical exercise, thermal trauma, muscle hypoperfusion, in infections, intoxications, use of certain prescription or illicit drugs, electrolyte and endocrinological disturbances, autoimmune and genetic diseases of the muscles and metabolism, or idiopathic) […”

“…The intake of illicit drugs (e.g., cocaine, amphetamine, 3,4-mthyl enedioxy methamphetamine [MDMA, ecstasy], cannabis, and heroin) is becoming one of the most common causes of RM in adolescents and adults, especially in combination with alcohol and energy drinks and after strenuous physical efforts (dancing and/or training) [1] [3] [4] [5]. The underlying mechanisms of RM in illicit drug intake include: changes in vascular tone and muscle hypoperfusion, muscular trauma (in drug-induces changes of consciousness with long-term muscular compression), changes in body temperature (hypo-or hyperthermia), hypoglycemia and/or acidosis, dehydration, striate muscle-cell energy depletion, direct toxicity.…”

Rhabdomyolysis Occurring After Use of Cocaine Contaminated With Fentanyl Causing Bilateral Brachial Plexopathy

“…Substances indicated as precipitating factors include alcohol, opioids, cocaine, and amphetamines. 3,4 As rhabdomyolysis progresses, swelling and edema can compress surrounding structures. Therefore, in cases of rhabdomyolysis involving the muscles of the neck and shoulder girdle, external compression of the brachial plexus can potentially cause brachial plexopathy.…”