Preventing Renal Failure in Patients with Rhabdomyolysis - Assignment Example

RHABDOMYOLYSIS Rhabdomyolysis is a cellular syndrome that occurs when the plasma membrane in striated muscle cells is disrupted resulting in the release of creatinine phosphokinase (CK) and myglobin into the circulation. Rhabdomyolysis has many causes, including cocaine abuse, trauma, strenuous exercise, infections, hyperthermia and other conditions that alter electrolyte balance or disrupt the integrity of the plasma cell membrane. The pathophysiology of rhabdomyolysis occurs as a result of the release of myoglobin and potassium as the contents of the lysed muscle cells spill into the circulation. The physiological consequences include myoglobin toxicity and elevated levels of creatine phosphokinase (CK), and lactate dehydrogenase (LDH). Some patients may present with mild generalized symptoms such as weakness and localized muscle pain that occur in conjunction with an elevation of muscle enzymes in the circulation. More serious cases may present with severe symptoms such as renal failure. The most common signs of rhabdomyolysis are tea colored urine with co-occurring localized muscle pain. The diagnostic indication of rhabdomyolysis involves the detection of elevated muscle enzymes, especially phosphocreatine kinase, in the blood. Immediate diagnosis of this syndrome is crucial to prevent the development of life-threatening complications. Among the clinical assessments required to evaluate patients with suspected rhabdomyolysis are urinalysis, muscle enzyme assessment, and an analysis of blood chemistry. Bun, creatinine and potassium levels as well as compartment pressure should be checked and monitored as necessary. Adequate fluid intake is necessary to prevent or reverse possible kidney injury and life threatening electrolyte imbalances. This paper reviews the incidence, pathophysiology, clinical characteristics, diagnostic methods, advanced practice methods and research implications of rhabdomyolysis. Introduction Rhabdomyolysis is a physiological condition associated with the destruction of striated muscle cells that is classified based on laboratory and clinical findings characterized by the release of intracellular constituents into the circulation (Walsh and Amato, 2005). Rhabdomyolysis can be caused by a variety of factors. The most common causes of Rhabdomyolysis include direct muscle injury, strenuous exercise, cocaine abuse, infections, seizures, hyperthermia and electrolyte abnormalities (Walsh & Amato, 2005). Rhabdomyolysis is a critical problem that requires prompt diagnosis and intervention to prevent serious physiological consequences. The causes, diagnosis and treatment of this disorder are areas of active clinical research. Incidence Some of the earliest documented cases of rhabdomyolysis occurred in World War II when skeletal muscle injuries were observed in soldiers injured from the collapse of bombed-out buildings (Sahjian & Frankes, 2007). Rhabdomyolysis quickly became known as the “crush injury” syndrome because it was linked to this type of war injury. In 1988 there were over 1000 cases of rhabdomyolysis reported that were the result of injuries sustained in the Armenian earthquake (Walsh & Amato, 2005). Despite the well known crushing injuries associated with rhabdomyolysis, the prevalence of this disorder is not known because often it is misdiagnosed due to its many underlying causes. Crushing injuries like earthquakes and car wrecks were initially believed to be the only cause; however, updated research has provided evidence that rhabdomyolysis has multiple causes (Melli, Chaudhry, & Cornblath, 2005). Among the more recently identified causes of rhabdomyolysis are excessive physical exertion as seen in marathon runners, drug abuse and exposure to temperature extremes. Rhabdomyolysis is very common in cocaine users because the drug induces extensive vasoconstriction which leads to muscle plasma membrane rupture, ischemia and cellular death (Criddle, 2008). Pathophysiology The name “Rhabdomyolysis” is descriptive of the nature of the disorder. “Rhabdo” means striated; “myo” means muscle and “lysis” refers to membrane rupture; thus, rhabdomyolysis results from the destruction of muscle cells (Criddle, 2008). The cell membrane plays an important role in separating intracellular and extracellular compartments within the body. It accomplishes this by physically containing intracellular particles that cannot pass through the lipid bilayer structure of the cell membrane. The plasma cell membrane also selects what goes into and what stays out the cell by a mechanism termed selective permeability. This important regulatory function provided by the cell membrane plays an essential role in maintaining homeostasis within the body (Walsh & Amato, 2005). Alterations of the integrity of the cell membrane disrupt the human cellular system allowing extracellular components to enter the cell and intracellular components to rush out into the extracellular space (Criddle, 2008). The intracellular composition contains higher levels of potassium, magnesium and phosphate than the extracellular compartment. The extracellular space has higher levels of sodium, chloride and bicarbonate than the cell’s interior. This biochemical compartmentalization is maintained by the plasma cell membrane. Rhabdomyolysis results in a disruption of the physical and biochemical integrity of the plasma cell membrane that causes intracellular ions such as potassium to leak into the extracellular space where they may to rise to lethal levels (Criddle, 2008). Abnormally high levels of potassium cause cardiovascular manifestations (Melli et al, 2005). Cardiovascular changes are the most severe result of hyperkalemia and are the most common cause of death in clients with hyperkalemia (Melli et al., 2005). Bradycardia, hypotension and tall peaked t waves are often seen in patients with hyperkalemia. (Criddle, 2008). Ventricular fibrillation, complete heart block and ventricular standstill are additional complications of severe hyperkalemia (Criddle, 2008). The law of diffusion states that the greater the difference in concentration of solutes across a diffusible membrane, the faster the rate of net diffusion. In rhabdomyolysis, diffusion causes sodium to rush inside the cell due to the absence of an intact cell membrane. When sodium rushes into the cell, osmosis causes water to follow sodium ions into the cell causing massive cellular edema, swelling and extracellular dehydration. Because this happens rapidly, the patient should be monitored for cerebral edema, seizures and possibly death (Criddle, 2008). Adenosine triphospate (ATP) also plays a major role in rhabdomyolysis because it is the energy source for the cell membrane sodium potassium pump that maintains appropriate levels of intracellular and extracellular sodium and potassium (Walsh & Amato, 2005). ATP will not work under anaerobic conditions; therefore, if the body is deprived of oxygen, such as in asystole, or as a consequence of near-drowning incidents or any condition resulting in hypoxia, ATP will not be produced. Under these conditions, the sodium potassium pump cannot maintain the body’s equilibrium. This represents a potential cause of rhabdomyolysis as the defective sodium potassium pump fails to maintain electrolyte balance (Criddle, 2008). When the body is deprived of oxygen, anaerobic metabolism becomes the primary source of ATP production, which results in the production of excess lactic acid. The excess lactic acid may accumulate, especially in muscle cells which require a great deal of energy to sustain movement. Lactic acid accumulation occurs normally during strenuous exercise, after which it is broken down by aerobic metabolism. Under these conditions, cells are forced to use glucose without sufficient oxygen (anaerobic metabolism). As a result, glucose is incompletely metabolized, resulting in the accumulation of lactic acid. Lactic acid is what sometimes gives marathon runners a burning sensation in the buttocks area or a heavy sensation in the legs, which resolves quickly once the body slows down and oxygen is able to reach the tissues in sufficient quantities to metabolize the accumulated lactic acid. The problem in rhabdomyolysis occurs when the available oxygen is unable to compensate for the body’s demand over time, and massive amounts of lactic acid increase which can eventually drive the body into lactic acidosis (Criddle, 2008). Clinical Characteristics Initial symptoms of rhabdomyolysis may be vague and varied; for this reason, the disorder may go undiagnosed unless the healthcare provider is familiar with the clinical symptoms of this disorder (Huerta et al, 2003). Trauma patients are at the highest risk of developing rhabdomyolysis due to the high risk of rupturing the plasma membrane of muscle tissues as a direct consequence of injury (Huerta-Alardin, Varon, & Marik, 2003). Compartment syndrome often initiates rhabdomyolysis in trauma patients due the massive fluid resuscitation. Under these conditions, the skin stretches to capacity, thereby compressing the nerve vessels and often rupturing the plasma membrane resulting in electrolyte imbalances and the break down of myoglobin (Huerta et al., 2003). Other at risk populations include burn patients as well as patients with ischemia and life threatening infections (Walsh & Amato, 2005). As hyperkalemia is the most serious life-threatening complication of rhabdomyolysis, it is essential that postassium levels are assessed in all patients suspected of having rhabdomyolysis. Other electrolyte imbalances also manifest in in rhabdomyolysis such as imbalances of calcium, phosphate, sodium and sulfate. Metabolic acidosis may also occur as a result of increased levels of lactic acid in the circulation (Melli et al., 2005). The determination of creatinine phosphokinase (CK) levels in the circulation is a very useful tool for clinical assessment in patients with in rhabdomyolysis because it serves as an indicator for muscle cell breakdown (Melli et al., 2005). Normal levels for CK are 45 to 260 U/L; however, in patients with rhabdomyolysis levels range from 10000 to 200000 U/L (Criddle, 2008). In some cases, CK levels may reach 3 million U/L. Rhabdomyoysis is the only documented clinical condition in which CK levels ever exceed this level (Criddle, 2008). Maximum CK levels are generally attained in patients with rhabdomyolysis within 24 hours after onset. Patients with rhabdomyolysis usually develop renal failure as a consequence of the release of excessive myoglobin into the circulation from ruptured muscle tissue (Siqueira et al., 2002). Myoglobin released into the circulation from damaged muscle tissue forms a brown cast that clogs the tubules in the kidneys which causes obstruction, increased intratubular pressure and systemic edema Fernandez et al, 2005). Oliguria or coca-cola colored urine from the brown cast are often seen in patients with rhabdomyolysis as a result of the high levels of circulating myoglobin. Myoglobin levels in the blood that are higher than 30 ug/l are diagnostic for myoglobin release associated with damaged muscle tissue (Siqueira et al., 2002). Acidic urine (pH less than 5.6) promotes cast formation in the renal tubules and contributes to the further breakdown of myoglobin into toxic components which generate free oxygen radicals that injure the kidney tissue (Siqueira et al., 2002). Diagnostic Methods A diagnosis of rhabdomyolysis may be suspected in those who have suffered trauma, crushing injuries such as car accidents or consistent immobility for 6 hour or longer during airplane rides (Mazokopakis, 2008). Diagnosis may also be made in an in-patient setting in the context of declining renal function accompanied by increasing creatinine and urea levels (Mazokopakis, 2008). Early recognition is crucial to prevent serious complications, including death; however, diagnosis is complicated by the non-specific nature of the clinical illness. The initial symptoms of rhabdomyolysis can range from subtle signs such as muscle weakness to life-threatening renal failure (Mazokopakis, 2008). Urinalysis in patients with rhabdomyolysis will show possible electrolyte wasting, brown cast and protein. Urine dipsticks are useful in detecting myoglobinurea; however, if the test is positive further tests are needed to confirm rhabdomyolysis (Marcucci et al., 2007). A negative reading on the urine dipstick indicates the absence of both hemoglobin and myoglobin. An affirmative urine dipstick with the absence of red blood cells confirms myoglobiurea (Siqueira et al., 2002). Myoglobin released from the lysis of muscle cells does not bind to any specific protein. Its levels increase within the first 6 hours, but it is quickly filtered and excreted unless renal failure develops. Under these conditions, excess myoglobin contributes to the abnormal color of urine which is usually cola colored to dark black (Fernandez et al, 2005). Myoglobin accumulation damages the kidneys in several ways, causing nephropathy and obstruction of the renal tubules resulting in a brown cast that clots the tubules and contributes to systemic edema (Fernandez et al, 2005). The disadvantage of the urine test is that the results may not be readily available in emergency settings. Moreover, myoglobin alone is not a reliable indicator of rhabdomyolysis because it is rapidly excreted from the kidneys and has a short half-life which, therefore, makes it a less reliable indicator in the later stages of rhabdomyolysis (Huerta et al., 2003). The hallmark of rhabdomyolysis is an elevation of serum muscle enzymes (Criddle, 2008). CK levels are the most sensitive sign of muscle injury. This enzyme is released by damaged muscles; CK levels rise within the first 12 hours and remain elevated for 1-3 days. The normal range for CK levels are 45 to 260 u/l, total ck levels in rhabdomyolysis are 10000 to 200000 u/l, (Criddle,2008). Levels this high are only seen in rhabdomyolysis. Other conditions such as chronic muscular disorders and very strenuous physical exercise in normal individuals may be associated with CK levels of several hundred; however, these levels do not compare to the extremely high levels of CK observed in patients with rhabdomyolysis. The peak in CK levels positively correlate with probability of acute renal failure; the higher the CK level more likely the possibility of renal failure (Criddle, 2008). Compartment syndrome is a condition which is usually caused by injury associated bone fractures (Chawla, Asmar, & Smith, 2008). Swelling within the compartment causes increased pressure which has no room to expand and may potentially cause nerve damage and muscle ischemia if not detected rapidly. Direct measurements of CK levels should be carried in patients with signs of compartment disorder associated with bone fractures, because often rhabdomyolysis is caused by compartment syndrome in which muscle cells are damaged and myoglobin and CK levels rise (Chawla et al., 2008). Severe compartment syndrome is indicated as any pressure above 30 which requires fasciotomies (surgical openings of the fascia) to allow proper expansion of the tissue and to restore blood flow (Criddle, 2008). Diagnostic imaging of muscle damage associated with rhabdomyolysis using magnetic resonance image MRI is preferred to computerized tomography CT scan or ultrasound, because MRI is a more sensitive tool for the detection of muscle involvement compared with the other devices (Sahjian & Frankes, 2007). Muscle biopsy can also assist the diagnosis of rhabdomyolysis. Positive indicators associated with rhabdomyolysis include histological findings of the loss of cell nucleus and the presence of inflammatory cells (Sequeira et al., 2002). Advanced practice management It is vital that rhabdomyolysis be recognized early to prevent further muscle break down, renal damage and cardiovascular effects (Rosenberg & Walsh, 2008). After rhabdomyolysis has been diagnosed, the next step involves efforts to stabilize electrolyte abnormalities (Marcucci et al., 2007). Potassium levels generally peak 12 to 36 hours after injury. Severe elevations of moderate to high potassium levels require continuous ecg monitoring. Peaked t waves are also indicative of hyperkalemia (Marrucci et al., 2007). Hyperkalemia may be treated with calcium gluconate, which is administered to protect the heart from developing dysrhythmias (Rosenberg & Walsh, 2008). Beta blockers can also be given to help prevent cardiac arrhymthias. Dextrose may be administered to prevent hypoglycemia that can be precipitated by insulin treatment (10-15 U of regular insulin) (Brown et al, 2004). Insulin is given to help transport potassium back into the cell; however, insulin can only be used temporarily to aid potassium uptake. Kayexalate is also used to restore potassium balance (Brown et al., 2004). Kayexalate works by facilitating the uptake of excess potassium into the bowel to be excreted into the feces for permanent elimination. General dosing levels prescribed are 20-30 fms po or per rectal as an enema using 50 gms in 200 cc of water with 50 gms of sorbitol (Huerta et al., 2003). The nurse practitioner should also consider systemic side effects of rhabdomyolysis such as muscle damage and renal failure (Fernandez, Hong, & Bruno, 2005). Renal failure can potentially be prevented if toxic intracellular contents are prevented from precipitating in the renal tubules. Because excess myoglobin causes an aciditic effect on the kidneys, treatment should be focused on correcting renal pH levels (Fernandez et al., 2005). To achieve this, bicarbonate drips are often started; however, the most critical intervention to prevent renal failure in rhabdomyolyis is to restore intravascular volume as this facilitates the movement of nephrotoxins out of the renal tubules (Sequeira et al., 2002). For this reason, high hourly urine output is an important goal for these patients to help kidneys maintain function. Hypertonic IV fluids should never be given because they contribute to further intravascular dehydration. One-half normal saline or a bicarbonate drip is usually the treatment of choice (Sequeira et al., 2002). Continuous renal replacement therapy (CRRT) is one of the most prominent interventions to help save a patient’s life. CRRT is a type of dialysis used to continuously clear toxins from the body 24 hours a day (Criddle, 2008). CRRT has been shown to have remarkable effects in patient outcomes; with CRRT the patient experiences normal kidney function despite the fact that the kidney function is impaired because CRRT acts as a big kidney machine to eliminate toxins from the body on a continuous basis so that they do not accumulate for long periods in the body between dialysis treatments. CRRT has been shown to correct acid base imbalances and to correct electrolyte abnormalities when the kidneys are not able to function properly (Criddle, 2008). The acute care nurse practitioner must make every effort to limit the extent of muscle damage due to rhabdomyolysis (Chawla et al., 2008). In patients with compartment syndrome, rhabdomyolysis can be caused by continuous pressure that eventually ruptures the cells’ plasma membrane releasing intracellular contents. In these cases, it is necessary to relieve the excess pressure in the damaged compartment to prevent muscle damage by fasciotomy. A fasciotomy involves the surgical cutting of the skin down to the fascia and is required in any compartment with unrelieved high compartment pressure (Sequeira et al., 2002). Fasciotomies cause defects in cosmetic appearance but may be necessary to save a limb by restoring blood flow to the tissues and decreasing the effects of cellular membrane rupture. (Sequeira et al., 2002). The nurse practitioner should also monitor CK levels every 6 to 12 hours. CK levels will usually peak in the first 6 to 12 hours and then decrease thereafter (Sahjian & Frankes, 2007). Serum electrolytes should also be routinely monitored, especially potassium, to prevent fatal cardiac dysrhythmias (Sahjian & Frankes, 2007). Hypercalcemia should not be treated in patients with rhabdomyolysis because during cellular disintegration calcium is stored in the muscle tissues, but with hydration calcium floats back into the extracellular space which could lead to hypocalcaemia (Sequeira et al., 2002). Arterial pH is also a frequently drawn lab to monitor increasing acidity or alkalinity resulting from too much bicarbonate or normal saline administration (Sequeira et al., 2002). Urine output should be assessed hourly to note the onset or progression of renal failure. It has been suggested that transfer to an intensive care unit may be best for these patients so that they can be more closely monitored (Siqueira et al., 2002). Research implications One area of controversy in the treatment of patients with rhabdomyolysis involves the use of mannitol to prevent myoglobin associated renal toxicity (Brown et al., 2004). The indication for the administration of mannitol to patients with rhabdomyolysis is designed to enchance the elimination of the myoglobin cast from the renal tubules through osmotic diuresis. The use of mannitol in standard practice remains controversial. Some research studies suggest that the byproducts of mannitol may actually increase urine acidity. Other studies suggest that mannitol simply does not work. Clinical research studies indicated that there was no difference in the incidence of renal failure or mortality between groups of patients who were given bicarbonate and mannitol and those who did not receive bicarbonate and mannitol (Brown et al., 2004). It is clear that further research is needed to develop appropriate recommendations for the practice of administering mannitol to patients with rhabdomyolysis. While some nurse practitioners may feel very strongly about administration of bicarbonate to reverse the acidity in the renal tubules, there remains some controversy regarding this practice as well (Brown et al., 2004). Further research will be needed to resolve this issue because there is currently no prevailing evidence to indicate that alkalinization is beneficial to the patient; moreover, research data suggest that alkanization may also precipitate hypocalcaemia (Marcucci et al., 2007). Summary Rhabdomyolysis is a syndrome that causes electrolye imbalances and leakage of myoglobin from damaged muscle tissue into the circulation, leading to severe dehydration. Despite its association with the well-known crushing injuries, the prevalence and causes of rhabdomyolysis are only incompletely understood at present. For this reason, the condition is often misdiagnosed due to a lack of knowledge about its underlying causes. Moreover, there are many diverse documented conditions that may be associated with rhabdomyolysis, including cocaine abuse, trauma, infection, temperature extremes and compartment syndrome. Nurse practitioners play a vital role in the treatment and recognition of rhabdomyolysis. Rhabdomyolysis should be rapidly identified as the earlier the disorder is recognized, the better the chances of preserving renal function and preventing other life-threatening complications. Clinical symptoms vary depending on the onset, stage, and duration of rhabdomyolysis Universal signs include hyperkalemia and elevated CK levels. Laboratory tests such as elevated serum CK levels and urine with cast are indicative of rhabdomyolysis. Fluid replacement is essential for adequate volume resuscitation; however, the use of mannitol and bicarbonate still remain controversial. References Brown, C., Rhee, P., & Chan, L. (2004). Preventing renal failure in patients with rhabdomyolysis: do bicarbonate and mannitol make a difference? The Journal of Trauma, 56(1), 191-1196. Chawla, S., Asmar, A., & Smith C. (2008). Rhabdomyolysis:a lesson on the perils of exercising and drinking. American Journal of Emergency Medicine, 26(4), 521. Criddle, L. (2008). Rhabdomyolysis: pathophysiology, recognition and management. Journal of Pediatric Emergency Care, 24(4), 262- 268. Fernande,z W., Hung, O., & Bruno G. (2005). Factors predictive of acute renal failure and need for hemodialysis among ED patients with rhabdomyolysis. Am J Emerg Med., 23,1-7. Huerta-Alardin, A., Varon, J., & Marik, P. (2003). Bench to bedside review: rhabdomyolysis- an overview for clinicians. Critical Care Nurse, 23(6), 14-30. Marcucci, L., Martinez, E., Haut, E., Slonim, A., & Suarez, J. (2007). Avoiding Common ICU Errors. New York: Lippincott and Williams. Mazokopakis, E. (2008). Unusual causes of rhabdomyolysis. Internal Medicine Journal, 38(5), 364-367. Melli, G., Chaudhry, V., Cornblath, D. (2005). Rhabdomyolysis: an evaluation of 475 hospitalized patients. Medicine, 84, 377-385. Rosenberg, J., Walsh, K. (2008). Physician perspective: exertional rhabdomyolysis: risk factors, presentation and management. Athletic Therapy Today, 13(3), 11-20. Sahjian, M., Frankes, M. (2007). Crush injuries: pathophysiology and current treatment. The American Journal of Primary Health Care, 32(9), 13-18. Siqueira, R., Bezerra da sliva, G., Liborio, A., and de Francesco daher, E. (2002). Acute renal injury due to rhabdomyolysis. Saudi Journal of Kidney Diseases and Transplantation, 19 (5), 721-729.   Walsh, R., Amato, A. (2005). Toxic myopathies. Journal of Neuromuscular Clinical Disease, 23:397-428. Read More