Rhabdomyolysis is a medical condition that results in rapid dissolution of skeletal muscles that are affected by the disease. The disruption in skeletal muscles affects the intracellular components like myoglobin and Creatine Kinase (CK) thus impairing their functionality. Rhabdomyolysis is thus exhibited when creatine kinase (CK) is elevated to levels that are life-threatening when there is an imbalance of the electrolytes, acute renal failure (ARF), and coagulation in the intervascular canals. Rhabdomyolysis’s development is often linked to different diseases, injuries, medications, and toxins. Various scholars have described and researched themes concerning rhabdomyolysis, and the existing literature offers insight into the causes, diagnosis, and preventions methods.
Epidemiology
Based on the historical analysis and research records, the evaluation of myopathy and rhabdomyolysis have been challenging as their definition was lacking. The release of Clinical Advisory on the use and safety of statins by the American College of Cardiology (ACC), American Heart Association (AHA) and the National Heart, Lung, and Blood Institute (NHLBI) illustrated an attempt at defining rhabdomyolysis and myopathy (Zutt, Van Der Kooi, Linthorst, Wanders, & De Visser, 2014) . As such, little knowledge exists on rhabdomyolysis, which calls for more research findings and evaluations in line with rhabdomyolysis treatment.
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Pathophysiology
Regardless of rhabdomyolysis’s causation agents being diverse, research asserts that the pathogenesis occurs in a straightforward manner that results in myocyte destruction coupled with component release into circulation (Keltz, Khan, Mann, 2015) . Normal myocyte has the sarcolemma that contains many pumps responsible for the regulation of cellular electrochemical gradients. The maintenance of intercellular sodium concentration remains at ten mEq/l often sustained by pumps laced with sodium-potassium adenosine triphosphate (Na/K-ATPase) in the sarcolemma (Torres, Helmstetter, Kaye, & Kaye, 2015) . The Na/K-ATPase is responsible for the active transport of sodium from the interior parts of the cell to the exterior. The process occurs with the gradient pulling sodium to the cell’s interior, which also pushes calcium through a different ion channel. The active calcium exchanger allows a low intracellular exchange. As such, calcium entry into the sarcoplasmic reticulum and mitochondria is achieved. In the end, anything that damages the ion channels in the form of injury to myocytes results in depletion of adenosine triphosphate (ATP), which ultimately leads to improper balance in the concentration of the electrolyte concentration in the cells
Muscle injury occurrence forces an influx of Na+ and Ca2+ in the cells. The increase in intracellular Na+ forces water into the cell, which disrupts the intracellular space. On the other hand, too much intake of Ca2+ results in the development of myofibrillar contractions that depletes the ATP. Additionally, lysis of cellular membrane occurs as a result of prolonged Ca2+ intake that activates proteases and phospholipases, which are dependent on Ca2+ (Torres, Helmstetter, Kaye, & Kaye, 2015) . Ultimately, the changes and effects of all mentioned elements result in a self-sustaining myolytic cascade, which eventually develops into muscle fiber necrosis.
Causes
In theory, muscle damage of any kind and by extension any action or entity that would result in muscle damage is capable of initiating rhabdomyolysis. The majority of rhabdomyolysis issues in adults arise as a result of drug and alcohol abuse, use of medical drugs, trauma, and immobility (Scalco et al., 2015) . According to data presented in pediatric populations, the skewness is towards diverse causes, which suggests that rhabdomyolysis seen in most patients is as a result of viral myositis, trauma, connective tissue disorder, exercises, and overdose (Torres, Helmstetter, Kaye, & Kaye, 2015) . The frequent causes of rhabdomyolysis include;
Statins
The therapeutic use of statins in the world arose due to their influence on patient’s mortality rate, especially those suffering from cardiovascular disease. However, the side effects of the drug are capable of inducing myopathy. To this end, the patients’ regimen needs to be analyzed. The US Food and Drug Administration (FDA) was among the first organization to point out the adverse effects of statins. Indeed, statins injure the liver, cause a decline in cognition, cause type 2 diabetes mellitus, and rhabdomyolysis (Torres, Helmstetter, Kaye, & Kaye, 2015) . The expansion of warning labels to include all the above risks was thus aimed at notifying the public of its effects.
Trauma
Both blunt (resulting from physical assault) and crush injuries cause trauma-induced rhabdomyolysis. In crush injuries such as those from collapsing buildings or bombings, rhabdomyolysis is seen only when the muscle compression is relieved (Torres, Helmstetter, Kaye, & Kaye, 2015) . The occurrence of rhabdomyolysis is only possible when there is acute muscle compression, which often results in the release of the necrotic muscle into the circulatory system.
Exertion
A core issue challenging the diagnosis of exertional rhabdomyolysis is the natural rise of CK serum levels after activities that are strenuous. In essence, the surge is different in every human being. In other words, a level that could be moderate to one person could cause exertion rhabdomyolysis to another (Torres, Helmstetter, Kaye, & Kaye, 2015) . Additionally, an increase in temperature and humidity during exertion or exercise could act as inducing factors.
Temperature
Heat stroke, Neuroleptic Malignant Syndrome (NMS) and Malignant Hyperthermia (MH) can cause rhabdomyolysis. The occurrence of heat stroke starts when the body’s temperature exceeds 40.5°C (Torres, Helmstetter, Kaye, & Kaye, 2015) . The longer the exposure, the dire the consequences. Prolonged exposure not only leads to rhabdomyolysis but also other associated issues including hypotension, lactic acidosis, and hypoglycemia. Ironically, exertion rhabdomyolysis rarely occurs among women. This has been attributed to the high estrogen levels in women with muscles. As such, women displaying rhabdomyolysis should receive check up on underlying muscle ailment.
Muscle Ischemia
Cell necrosis of the muscles could result in prolonged oxygen deprivation periods, thus forming a basis upon which rhabdomyolysis could occur. The causes of muscle ischemia include blood vessel compression, which can occur during surgery or other activities, thromboses, emboli, compartment syndrome, and sickle cell disease (Torres, Helmstetter, Kaye, & Kaye, 2015) . In rare occasions, hypothermia could result in rhabdomyolysis through reduced muscle perfusion.
Infection
Rhabdomyolysis is present in individuals’ having different infections often ranging from muscle infections to sepsis. Propositions for the infection center on hypoxia in the tissues or dehydration, the release of toxins into the body, fever, direct invasion of bacteria into the muscles, and tremors in the body. Legionella bacteria are at the forefront as causation elements of rhabdomyolysis. Influenza A and B are the major viruses that cause the condition to worsen (Torres, Helmstetter, Kaye, & Kaye, 2015) . Other viruses include herpes simplex, varicella zoster, and the West Nile virus, and unless treated or controlled, they could escalate into more complicated scenarios.
Symptoms
The classic symptoms of rhabdomyolysis include myalgia, weakness, and urine that is tea colored. These symptoms could have adverse effects on the patient. Systematic manifestations of rhabdomyolysis include tachycardia, the malaise that has a general impact, fever, nausea, and vomiting (Torres, Helmstetter, Kaye, & Kaye, 2015) . Clinical signs come in the form of intravascular coagulation and multiorgan failure.
Diagnosis
To accurately diagnose an individual with rhabdomyolysis, a physician should review the history of the patient as well as do a physical examination. Any patient who shows signs of trauma, sepsis, muscular disease, and immobilization should get tested for rhabdomyolysis (Adams, 2012). Indirect clues that can warrant tests include the presence of muscle injury coupled with an unexpected serum rise of either phosphate or aspartate transaminase. Important physical clues could be gathered by using a neuromuscular examination with a focus on the extremities (Torres, Helmstetter, Kaye, & Kaye, 2015). More information could be deduced from pulse sensation, muscle power, and size. However, plasma CK is the gold standard upon which laboratory diagnosis should focus. Regardless of a threshold being non-existent, five times the normal range is a cause for concern. Testing the urine myoglobin will also attest to the positivity of erythrocytes, which could be used to gauge the body’s health concerning rhabdomyolysis.
Management
If rhabdomyolysis is suspected, regardless of the underlying causes, a core aspect of the treatment goal is to ensure that acute kidney injury is avoided. Possible fluid accumulation in the compartments of the muscles is associated with hypovolemia, and as such, managing the fluids is core to preventing prerenal azotemia. Azotemia can be avoided by aggressive hydration rate. Alternatively, saline solutions alternated hourly with glucose solutions together with sodium bicarbonate could be used as a cure or remedy. However, before one uses urinary alkalization where sodium bicarbonate or sodium acetate are the core elements, they should be aware that the method is unproven (Torres, Helmstetter, Kaye, & Kaye, 2015) . Whichever option is taken by the patient, side effects should be analyzed to minimize the impact of the disease.
Conclusion
Rhabdomyolysis’s complexity is often associated with morbidity and mortality. Although direct traumatic experiences are the core causing conditions, research identifies other factors such as toxins, infections, and muscle ischemia. Importantly, genetic disorders, exertion and heat stroke should be considered during the implementation of prevention measures. The symptoms of rhabdomyolysis include myalgia, body weakness, and myoglobinuria where the CK is elevated to sensitive levels. Ultimately, all clinicians should be aware of the various causes, diagnostic patterns, and treatment options available to manage the condition.
References
Adams, J. G. (2012). Emergency Medicine E-Book: Clinical Essentials (Expert Consult -- Online) . Saunders.
Keltz, E., Khan, F. Y., & Mann, G. (2015). Exertional rhabdomyolysis. Sports Injuries: Prevention, Diagnosis, Treatment and Rehabilitation , 2211-2226.
Scalco, R. S., Gardiner, A. R., Pitceathly, R. D., Zanoteli, E., Becker, J., Holton, J. L., ... & Quinlivan, R. (2015). Rhabdomyolysis: a genetic perspective. Orphanet journal of rare diseases , 10 (1), 51.
Torres, P. A., Helmstetter, J. A., Kaye, A. M., & Kaye, A. D. (2015). Rhabdomyolysis: pathogenesis, diagnosis, and treatment. The Ochsner Journal , 15 (1), 58-69.
Zutt, R., Van Der Kooi, A. J., Linthorst, G. E., Wanders, R. J. A., & De Visser, M. (2014). Rhabdomyolysis: review of the literature. Neuromuscular Disorders , 24 (8), 651-659.
