Journal - Rhabdomyolysis - Article Example

Running Title: The Seemingly Infinite Causes of Rhabdomyolysis and Resultant Diagnosis Problems Name of Student: University: Subject Code: Course Instructor: Date Assignment is due: The Seemingly Infinite Causes of Rhabdomyolysis and Resultant Diagnosis Problems: Complexity in the Pathophysiology Leading to Rhabdomyolysis Rhabdomyolysis (Journal Article) Abstract This article explores the underlying problem in diagnosing and treating Rhabdomyolysis consequent to there being numerous causative conditions that usually point health care providers to misleading directions. The paper establishes that there is only one cause of Rhabdomyolysis namely, damaged muscle skeletal muscles released into the central circulatory system. However, there are seemingly infinite causes that trigger such muscle damage/breakdown. The article categorizes numerous causative conditions that lead to muscle damage and which can all be classified as risk factors for Rhabdomyolysis. The gigantic number of all these causes is itself astounding as the paper argues. This means that even though the prognosis of Rhabdomyolysis is as an easily treatable medical condition, the immense number of causes makes it very complicated to diagnose. Again, the prognosis itself relies heavily on the identification of the cause of muscle destruction since treatment always begins with the discontinuation of such muscle destroying agents. Without identifying the cause of muscle destruction, Rhabdomyolysis can never be barred from reaching such complication levels as of renal and kidney failure. It is these numerous causative conditions therefore, that complicate diagnosis and treatment. The paper concludes that while being an easy to diagnose and treat condition, the reason why Rhabdomyolysis continues to be a great problem in health care provision circles is its seemingly limitless causative conditions that make diagnosis overly complicated. Introduction This article constitutes a research on Rhabdomyolysis with a particular interest on the numerous causes and risk factors for the condition and how these seemingly infinite causes and risk factors complicate diagnosis in health care provision. The article begins with an introduction of Rhabdomyolysis as a medical condition before going into details into what the condition constitutes from a clinical perspective. After the introduction, the article undertakes a detailed discussion of the many causes and risk factors of Rhabdomyolysis, categorizing in a simplified and analyzable manner. The thesis of the article is to establish how these many causes become a problem in diagnosing a Rhabdomyolysis patient. As such, the next section of the paper will evaluate the complexity in the Pathophysiology that leads to and results from Rhabdomyolysis. Further, the article will also review the problems in diagnosing and treating the condition from a secondary health care environment, before terminating with a tenable conclusion of the issues raised throughout the paper. Rhabdomyolysis is not a newly discovered condition. The available literature however points to its pioneer description in any medical discourse at around 1940 in London after some crush injury victims consequent to the World War II (Nabil, 2010). Even the bible has several accounts of medical condition that resonate with the traits of Rhabdomyolysis. For instance, in the eleventh chapter of Numbers, verses 31 to 33, the Pentateuch narrates about the Jews demanding wholesome food as they were traveling from Egypt to Israel, but still within the desert. God thus sent multitudes of quail as a response to their complaints and the Jews ate quail meat with a vengeance. The plague that broke out as a consequence killed multitudes and its description is exactly as the known symptoms of Rhabdomyolysis. While not called Rhabdomyolysis as it is now, the medical condition existed even then (Allison and Bedsole, 2003). According to Vanholder, et al (2000), the name Rhabdomyolysis, originates from two Greek roots namely rhabdo for striated and myo for muscle. When lysis for breakdown is added to the roots, the term Rhabdomyolysis gains the meaning of breakdown of striated skeletal muscles (Bywaters & Beall, 1998). The clinical understanding of Rhabdomyolysis is not complicated as will be discussed hereafter, but what complicates the condition to most health care providers is diagnosing and determining the cause of Rhabdomyolysis in most cases. Understanding Rhabdomyolysis The medical condition referred to as Rhabdomyolysis results when skeletal muscle fibers and muscle fiber contents (myoglobin) are broken down and released into a person’s bloodstream. Sauret, Marinides and Wang (2002) say that, since these contents are not naturally expected to be part of the blood constitution, they end up harming other vital organs and jeopardizing many body operations, especially the kidneys, which are responsible in cleansing the blood (Bosch, Poch & Grau, 2009). In most cases, the contents build up malfunctions in the kidney until there is acute kidney damage (Nabil, 2010). When the cells of skeletal muscle break down, they release myoglobin, which are the oxygen-carrying pigmentation of muscles; and the myoglobin combines with electrolytes and enzymes all from inside skeletal muscle cells. This combination, with the active agent being myoglobin is highly toxic to a kidney (Bosch, Poch & Grau, 2009). To understand this phenomenon in its real context, one needs to review the human anatomy at brief. The human body has three different muscle types namely, the skeletal muscles, the heart muscle and the smooth muscle. Skeletal muscles are primarily used for body movement such as in moving the body skeleton at the numerous joints (Nabil, 2010). It is the skeletal muscle framework that is mainly affected at the onset of Rhabdomyolysis (Nabil, 2010). The common prognosis of Rhabdomyolysis is that it can be treated largely and most of its symptoms reversed. If diagnosed early; and most importantly the cause identified and corrected, Rhabdomyolysis has a very high rate of recovery (Craig, 2010). Here in lies the problem. Identifying the cause of Rhabdomyolysis makes all the difference in determining the prognosis of an individual patient. Like no other disease known to man, Rhabdomyolysis enjoys the sole repute of having a prognosis totally dependent on its underlying cause for each patient and whether complications accrue encourse treatment (Craig, 2010). According to Vanholder, et al (2000), research statistics indicate that Rhabdomyolysis patients with acute renal and kidney failure have a mortality rate of not less than as 20% globally (Nabil, 2010). The only way to stop Rhabdomyolysis from getting as complicated as, is to diagnose which muscles are breaking down, why and how to stop them and thus protect these vital organs from further endangerment by the cellular components of the broken down muscles (Craig, 2010). This underscores, yet again, the importance of identifying the cause of Rhabdomyolysis for each individual patient (Craig, 2010). Causes of Rhabdomyolysis Most literature on the area and even this article so far, always speak of the causes of Rhabdomyolysis being many. Incidentally, Rhabdomyolysis has only one cause. Rhabdomyolysis can only be caused by muscle damage/breakdown since that is the only way that the cellular protein, the myoglobin pigment, can be released into the circulatory system to be filtered out by kidneys (Bosch, Poch & Grau, 2009). That is the only known cause of Rhabdomyolysis. Now the problem arises when one seeks to identify what cause the muscle damage (Goldman & Ausiello, 2007). There are a hundred and one causes of muscle breakdown, all of which can then trigger Rhabdomyolysis. In essence therefore, while there is only one cause for Rhabdomyolysis, there are seemingly infinite risk factors that cause the cause of Rhabdomyolysis. As already noted, the disorder is triggered by damaged skeletal muscles such that any condition that damages or results to damage of skeletal muscles is a potential cause of Rhabdomyolysis. Sauret, Marinides and Wang (2002) say that, trauma is the single greatest risk factor in Rhabdomyolysis. However, the Rhabdomyolysis etiologies fall under several subcategories namely traumatic causes, exercise-induced causes, toxicological causes, environmental causes, metabolic causes, infection causes, immunologic causes and even inherited causes (Nabil, 2010). In traumatic causes, several occurrences have been documented as causes of a Rhabdomyolysis onset. These include any significant blunt trauma including crush injury that damages skeletal muscles (Bywaters and Beall, 1998). A High-voltage electrical shock injury has also been know to destroy skeletal muscles and thus predispose Rhabdomyolysis. The trauma can also be caused by extensive burns which destroy muscle cells (Craig, 2010). Interestingly, some literature have also included near drowning as a cause of the muscle damage that predisposes Rhabdomyolysis as well as prolonged immobilization such as results after excessive alcohol and drug consumption (Parks, Reed and Knochel, 1989; Richards, 2000), or an incapacitating stroke after prolonged surgical procedures (Craig, 2010). The second risk factor that may trigger skeletal muscles damage and thus predispose Rhabdomyolysis are those resultant fro exercises and exercising. In exercises, sometimes people induce excessive muscular activity until muscle breakdown accrues. Such instances include sporadic but strenuous exercises such as marathons, bodybuilding squats, weight lifting push-ups and aerobic sit-ups exercises. These will lead to damaged muscles and thus Rhabdomyolysis, especially when done regularly and excessively. Other exercise-induced muscle damages with a Rhabdomyolysis risk include status epilepticus, severe dystonia, excessive use of the computer keyboard or prolonged computer gaming as well as acute psychosis. The third cause of severe muscle damage with a risk factor for Rhabdomyolysis is the toxin-mediated muscle damage such as results from chemical substance abuse (Richards, 2000). Notable in this area are such substances as ethanol, heroin, methanol, cocaine, ethylene glycol, amphetamine, isopropanol, methadone, barbiturates, phencyclidine, MDMA ecstasy (so called 3,4-methylenedioxymethamphetamine) or LSD (lysergic acid diethylamide) (Richards, 2000). According to Vanholder, et al (2000), researchers have also confirmed variously that it is not just the drug substances that can cause toxic-mediated muscle damage in Rhabdomyolysis. Even prescription and or non-prescription medications can induce toxic-mediated muscle breakdown (Richards, 2000). Most notable medications in this respect include antihistamines, caffeine, salicylates, Quinine, fibric acid derivatives such as fenofibrate and bezafibrate, gemfibrozil, clofibrate and fenofibrate, neuroleptics (antipsychotics), anesthetics, paralytic agents such as the malignant hyperthermia syndrome, corticosteroids, amphotericin B, statins such as 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors or even protease inhibitors. Other known medications that are Rhabdomyolysis risk factors due to their ability to induce muscle damage include theophylline, selective serotonin reuptake inhibitors (known for serotonin syndrome), cyclic antidepressants, aminocaproic acid, phenylpropanolamine, propofol and several more (Craig, 2010). The other risk factors for Rhabdomyolysis due to muscle breakdown are those induced by other toxins such as carbon monoxide, Hypophosphatemia, toluene, hyperthermia, hemlock herbs coming from quail (frequent in Rhabdomyolysis cases in the Mediterranean regions), venom from snakes and spiders (most notably the cobra and the black widow spider) as well as serious envenomations by Africanized honeybees. The known environmental triggers of muscle damage that could cause Rhabdomyolysis are hyperthermia and hypothermia. The known metabolic triggers of muscle damage in Rhabdomyolysis cases include the same, hyponatremia and hypernatremia, as well as hypokalemia, diabetic ketoacidosis, hypothyroidism, hyperthyroidism and nonketotic hyperosmolar diabetic coma (Craig, 2010). The viral disease infectious agents that trigger muscle damage in known Rhabdomyolysis instances include HIV/Aids, influenza A and B, coxsackievirus, adenovirus, ebstein-barr virus, echovirus, herpes simplex virus, cytomegalovirus, parainfluenza virus, west Nile virus and varicella-zoster virus (Craig, 2010). The bacterial disease infectious agents that may cause Rhabdomyolysis cases include francisella tularensis, group B streptococci, plasmodium species, streptococcus pneumonia, streptococcus pyogenes, bacillus species, escherichia coli, staphylococcus epidermidis, vibrio species, borrelia burgdorferi, salmonella species, clostridium perfringens and clostridium tetani among others (Mazokopakis, 2007). In fungal diseases infectious agents for known Rhabdomyolysis cases include the candida species and the aspergillus species (Craig, 2010). There are some causative diseases that attack the connective tissue and ultimately end up as Rhabdomyolysis such as polymyositis and dermatomyositis (Craig, 2010). Similarly, there are some inherited disorders that could trigger muscle damage leading to Rhabdomyolysis such as enzyme deficiency in lipids, carbohydrate and amino acids as well as myopathies. Some literature have pointed out that Rhabdomyolysis sometimes occur sickle cell anemia patients and can easily be mistaken for a pain crisis (Goldman & Ausiello, 2007). Complexity of the Pathophysiology Leading to Rhabdomyolysis and resulkatant problems in Diagnosis and treatment With all these possible causes and many other unmentioned above, it is hard to point out precisely the proper diagnosis of a Rhabdomyolysis case. According to Vanholder, et al (2000), it can be suspected in almost anyone who has had a trauma, crush, prolonged immobilization or numerous infections. In the initial stages of Rhabdomyolysis, the only symptoms detectable are those of the cause and not of Rhabdomyolysis since the body changes induced by the condition itself are always slow to show (Nabil, 2010). In most cases therefore, Rhabdomyolysis is only diagnosed in its late stages when deteriorating kidney function points clinicians to seek for the cause of the kidney malfunctions (Bosch, Poch & Grau, 2009). At such times, the clinicians will be able to point out the abnormal increases of urea and creatinine in urine and the urine output itself decreasing (Nabil, 2010). The condition of Rhabdomyolysis accrues from a rapid destruction and decomposition of skeletal muscles. The broken down muscle cells are then leakage into the circulatory system, filtered by the kidneys and then passed on to urine (Bosch, Poch and Grau, 2009). As noted in the introduction, the process would otherwise not be not as serious if it were not for the muscle protein known as myoglobin which is highly toxic to kidneys (Goldman and Ausiello, 2007). As such, when the kidneys are struggling to filter the muscle cells from the blood, myoglobin slowly kills the kidney tissues until they fail (Bosch, Poch & Grau, 2009). The structure of skeletal muscles features a particular type of protein component known as myoglobin. Myoglobin can easily dissolve in blood and that is exactly what happens when the muscle cells they are part of break down at the onset of Rhabdomyolysis. That is why, in diagnosing Rhabdomyolysis, one of the most reliable tests is to test for myoglobin in urine samples (Bywaters & Beall, 1998). It is not only the myoglobin that leaks into the circulatory system. Many other cellular contents such as enzymes also find their way into the systemic circulation, thus further compounding the problem. Besides the chemical components of muscles, the dead muscle tissues themselves can cause large amounts of blood fluids to be accumulated in the muscles thus reducing the circulating volume in the systemic circulation leading to reduced blood flow and supply to the kidneys (Bosch, Poch & Grau, 2009). Again, it is not only the kidneys that get affected by the leak, but all the other organs of the circulatory system one the potentially toxic muscle cell contents leak into the bloodstream. A common and late-stage pathway of Rhabdomyolysis is usually a disturbance of the myocyte calcium homeostasis. Sauret, Marinides and Wang (2002) say that, this disturbance cause nephrotoxic effects consequent to liberated myocyte contents resulting to acute renal failure. Notably, Rhabdomyolysis can cause muscle injuries, muscle pain and general body weakness thereby throwing diagnosis into a totally different target than the condition itself (Mazokopakis, 2007). Chances of the wrong diagnosis increase when Rhabdomyolysis take up such symptoms that are clearly attributable to other conditions. As can be seen in the following picture, the complications can affect even the legs consequent to failing kidneys. Source: (Bosch, Poch & Grau, 2009) According to Vanholder, et al (2000), this often leads to late diagnosis of the condition as well as o wrong primary diagnosis. It is only after considerable hospitalization in some instances that clinicians will eventually arrive at a Rhabdomyolysis diagnosis (Goldman & Ausiello, 2007). Once diagnosed however, the treatment of the condition always starts with the discontinuation of the cause of muscle breakdown or the underlying skeletal muscles’ disease. Only serious cases with such complications as kidney and renal failure require such therapy as hydration (Nabil, 2010). Conclusion This article has helped express the underlying problem in diagnosing and treating Rhabdomyolysis consequent to there being numerous causative conditions that usually point health care providers to misleading directions. As the paper has established, there is only one cause of Rhabdomyolysis – which is damaged muscle skeletal muscles released into the central circulatory system, but seemingly infinite causes that trigger such muscle damages. According to the argument herein, the prognosis of Rhabdomyolysis relies heavily on the identification of the cause of muscle destruction since treatment always begins with the discontinuation of such muscle destroying agents. Without identifying the cause of muscle destruction, Rhabdomyolysis can never be barred from reaching complication levels such as of renal and kidney failure. The article has categorized many causative conditions of muscle damage that can be classified as risk factors for Rhabdomyolysis and the discussed how these numerous causative conditions complicate diagnosis and treatment. Conclusively therefore, while being an easy to diagnose and treat condition, the reason why Rhabdomyolysis continues to be a great problem in health care provision circles is because its seemingly limitless causative conditions make such diagnosis overly complicated. References Allison, R. and Bedsole, L. (2003). The Other Medical Causes of Rhabdomyolysis. American Journal of the Medical Sciences. Vol. 326 (2). pp. 79-88. Byard, R. Gilbert, J and Lokan, R. (1998). Amphetamine Derivative Fatalities in South Australia-Is "Ecstasy" the Culprit? American Journal of Forensic Medicine & Pathology. Vol. 19 (3). pp 261-265. Bosch, X., Poch, E. & Grau, J. (2009). Rhabdomyolysis and acute kidney injury. New England Journal of Medicine. Vol. 361 (1). pp. 62–72. Bywaters, E. &Beall, D. (1998). Crush injuries with impairment of renal function. Journal of American Society of Nephrolology. Vol. 9 (2). pp. 322–332. Craig, S. (2010). Rhabdomyolysis. Medscape. Viewed on 29 July 2010. From http://emedicine.medscape.com/article/827738-overview Goldman, L. & Ausiello, D. (eds). (2007). Cecil Medicine. 23 edition. Philadelphia, Pa: Saunders Elsevier. Nabil, S. (2010). Rhabdomyolysis. MedicineNet, Inc. Viewed on 29 July 2010. From http://www.medicinenet.com/rhabdomyolysis/article.htm Mazokopakis, E. (2007). Unusual causes of Rhabdomyolysis. Internal Medicine Journal. Vol. 38 (5). pp. 364 – 367 Parks, J., Reed, G. and Knochel, J. (1989). Cocaine-Associated Rhabdomyolysis . episodes of acute rhabdomyolysis associated with documented evidence. American Journal of the Medical Sciences.Vol. 297(5). pp. 334-336. Richards, J. (2000). Rhabdomyolysis and drugs of abuse. Journal of Emerging Medicine. Vol. 19 (1). pp. 51–56. Sauret, J., Marinides, G. & Wang, G. (2002). Rhabdomyolysis. American Family Physician. Vol. 65 (5). pp. 907–912. Vanholder, R., Sever, M., Erek, E. & Lameire, N. (2000). Rhabdomyolysis. Journal of American Society of Nephrolology. Vol. 11 (8). pp 1553–1561. Read More