Getting ready for the long races made me think about this topic. Intersting read, bottom line watch the fluid intake, and balance it out with glycogen replenishment during long races. Any ?'s e-mail me at
Redleaf.fitness@yahoo.comThe paper I wrote below has been reviewed by a Licensed Physical Therapist and a PhD. who's research is in the area of renal and kidney function.
Running Head:
RhabdomyolysisRhabdomyolysis
Emile Smith
River Valley Community College
Abstract:
Rhabdomyolysis is a condition of muscle fiber breakdown leading to a myoglobin release into the circulatory system. Myoglobin is the byproduct from muscle fiber degradation that is released into the bloodstream. The result of myoglobin released into the bloodstream effects the kidneys leading to Acute Renal Failure (ARF) resulting from tubular necrosis. If not treated aggressively the condition can be fatal. The condition is an uncommon diagnosis but requires serious attention by health care professionals, sports coaches, and athletic trainers.
History:
The symptoms were first noticed from victims of the 1908 Messina earthquake and WWI. Renal failure was being reported with victims of traumatic crushing type injuries. These reports were followed by studies showing the presence of muscle proteins in the circulatory systems of four victims during the 1941 “Blitzkrieg” bombings of WWII. Myoglobin was detected in the urine of the victims by spectroscopy (Craig, 2008). The symptoms demonstrated that the kidneys of the victims resembled those of patients that had received an incorrect match for a blood transfusion. In this scenario the received blood is being destroyed by the immune system and hemoglobin accumulates in the kidney. During an experiment in 1944 it was demonstrated that kidney failure was proportionately due to myoglobin (Craig, 2008). Rhabdomyolysis is linked to several causes, early intervention and awareness appears to be the best treatment.
Common Causes:
The cause of rhabdomyolysis during its early observations appeared to be traumatic injuries involving crushing blows typical of blunt trauma. Recently the condition has been observed through the participation of prolonged physical exertion in hot environments and can be exasperated with the use of alcohol and drugs. Additional risk factors of the condition include (Craig, 2008), (Silberberg, 2007).
· Alcoholism
· Crushing injuries
· Heat intolerance
· Heat stroke
· Ischemia or necrosis of the muscles due to arterial occlusion or deep vein thrombosis
· Use or overdose of drugs, predominately cocaine
· Seizures
· Low phosphate levels
Pathology:
The condition proceeds through a series of metabolic events that ultimately lead to the release of muscular skeletal contents (myoglobin) into the bloodstream. It is this release of myoglobin that results in the deleterious effects on the renal system. The initial metabolic event is the depletion of ATP. The sodium potassium pumps that provide homeostasis during muscle activation and relaxation are dependent on a constant supply of ATP. Intensity and duration of physical activity effect energy requirements by skeletal muscle. Overheating increases energy requirements, combined with exercise, causing ATP stores to be quickly exhausted. The use of varies drugs can directly and indirectly affect the production of ATP by skeletal muscle as well. When ATP stores are depleted the ATP dependent sodium potassium pumps no longer function. This leads to decreased extracellular and intracellular sodium ion concentration ratios. The response to the sodium imbalance is an increase in intracellular calcium levels. The accumulation of myoplasmic calcium causes an enzymatic activation of phospholipases and proteases resulting in muscles cells to lyse. Hypercalcemia produces muscle cramps and is accompanied with tetany. Hypernatremia typically associated with dehydration creates cellular dehydration and the death of muscle cells (Criner, Applet, Coker, Conrad, Holiday, 2002).
As intracellular sodium levels increase intracellular proteolytic enzymes are activated. These enzymes breakdown the intracellular structures of the muscle fibers causing them to be released into the circulatory system. This leads to microvascular damage and causes capillaries to leak creating local bruising. With continued leaking of capillaries developing intracompartmental pressure increases. The necrosis of muscle tissue produces a build up of muscle proteins in surrounding tissue ultimately leading to a translocation of extracellular fluid to other body compartments referred to as compartment syndrome. This leads to increased intracompartmental pressure causing ischemia. Deficient oxygen to muscle tissue results in muscle necrosis, developing into exasperated muscle tissue degradation. Depletion of ATP affects the potassium pumps ability to function causing extracellular potassium levels to increase. Potassium acts as a vasodilator at normal levels, at high levels it vasoconstricts leading to ischemia and muscle necrosis. Extremely high blood levels of potassium may lead to cardiac arrhythmias and cardiac arrest. (Criner, Applet, Coker, Conrad, Holiday, 2002).
As muscle cells die the release of isoenzymes creatine kinase and lactate dehydrogenase make their way into systemic circulation. Creatine kinase notably plays an important role in the conversion of ADP back to ATP (Brown, 2004).
The myoglobin released into systemic circulation eventually reaches the kidneys. As the serum threshold of myoglobin is reached, myoglobin occupies the kidney tubules causing acute renal failure (Brown, 2004), (Criner, Applet, Coker, Conrad, Holiday, 2002).
Common Signs and Symptoms:
Common signs and symptoms include muscle pain, fever and symptoms comparable to a viral infection. Muscle pain will be the most common and typically the most often reported from patients experiencing rhabdomyolysis. Signs and symptoms involving the muscles can involve muscle weakness to flaccid paralysis of the extremities. Motor dysfunction may be observed along with sensitivity to temperature extremes. These symptoms coincide with the catabolism of the musculature. Nausea and vomiting are additional symptoms and can be confused for viral infections (Silberberg, 2007).
With the release of potassium from the injured muscle and release from third spacing fluids, cardiac arrhythmias and bradycardia may be observed. There are reported symptoms of absent P waves and or peaked T waves revealed from ECG’s. Urine analysis will reveal blood and very high levels of creatine kinase (Criner, Applet, Coker, Conrad, Holiday, 2002).
Complications will involve pain not in-line with the injury and is not remedied through standard pain management procedures. The pain typically increases with eccentric muscle action or general use and movement. Cardiac arrhythmias, renal failure as discussed earlier are additional complications that can lead to mortality (Brown, 2004).
Diagnosis:
Rhabdomyolysis is diagnosed through an examination of the afore mentioned signs and symptoms related to tender and painful skeletal muscles. Should the physical signs and symptoms align themselves with the additional criteria including environmental and or extraneous substance exposure, urine and serum analysis will follow. Lab analysis is the most dependable approach for the diagnosing of rhabdomyolysis. However these markers have intrinsic flaws (04 Brown). Currently the most dependable diagnostic indicator is a serum creatine kinase analysis. To date no standard level for diagnostic determination of the condition has been established. However, since patients typically present themselves for medical intervention 24-36 hours post injury, this time frame inadvertently coincides with the fact that creatine kinase levels typically peak within this definitive period of diagnosis. The medical community has not defined a standard level of serum creatine kinase levels for diagnosis, however most healthcare professionals consider levels five times those of normal levels or greater to be a determination for diagnosis (Brown, 2004), (Criner, Applet, Coker, Conrad, Holiday, 2002).
Treatment:
Treatment for rhabdomyolysis begins with fluid replacement. The intent of the initial treatment is to minimize the injury to the renal tubules with fluids and buffering. There after a blood test will dictate the course of treatment along with the severity of the condition. Analysis of blood levels pertaining to electrolytes, blood urea nitrogen, calcium, magnesium, phosphorus, creatine, and transaminases guide in the direction of treatment (Brown, 2004).
Depending on the blood analysis the following may be administered.
Saline infusion is administered to prevent acute renal complications. Large quantities may be required, the goal is to prevent injury to renal tubules, dilute toxic substances, facilitate excretion, and increase renal perfusion pressure (Criner, Applet, Coker, Conrad, Holiday, 2002).
Catheterization is needed in all instances so urine levels can be accurately monitored (Criner, Applet, Coker, Conrad, Holiday, 2002).
Buffering, a process in which alkalization of the urine is used to address the toxicity. Myoglobin and urate are toxic to the kidney tubules in an acid environment. Alkalization can be achieved by adding 2 ampules of bicarbonate per liter of saline. The intent is to maintain urine pH levels at 7.5 or higher (Brown, 2004).
Medicinal intervention may include the use of dantrolene. Dantrolene helps to reduce intracellular calcium levels that were elevated from the release of calcium by the sarcoplasmic reticulum. Dantrolene will be administered intravenously and prescribed based on body weight (Brown, 2004).
Role of Physical Therapy:
Patients with subacute conditions are typically treated in an outpatient setting. Ounce the patient is capable of passing urine without difficulty and the urinary sediment is clear along with a stable metabolic file physical therapy should follow. The interventions most often prescribed include the following (Brown, 2004):
· Range of motion exercises, these involve both active and passive ROM.
· Aerobic training.
· Gradual/graded resistance training.
· Patient education about rhabdomyolysis and its prevention.
Precautions and Contraindications:
The main contraindication and precaution inline with physical therapy is proceeding with intervention too soon. The patient must be cleared of any ongoing pathologic processes, this is determined through blood and urine analysis along with monitoring urinary output. The process for most patients is in a time frame of 4 weeks for the onset of the condition to be corrected before patients can start physical therapy. Ounce physical therapy starts attention to gradual progression with intervention is the major precaution. This includes educating the patient about the importance of a gradual progression regarding all aspects of the treatment (Brown, 2004), (Criner, Applet, Coker, Conrad, Holiday, 2002).
Prevention of Rhabdomyolysis:
Patient education is the best method of prevention. The physical therapist and occupational therapist will play a support role in educating the patient and provide continued feedback about the prevention process. Prevention of rhabdomyolysis involves proper hydration before, during, and after exercise or during any form of prolonged physical activity, especially in hot environments.
Athletic coaches, military personnel, and parents should be aware of the signs and symptoms, observation of signs and symptoms along with monitoring fluid intake will help to address the onset of the condition. In some instances slight cases can be avoided from becoming catastrophic provided the signs and symptoms are noticed early enough.
Monitoring body weight before and after physical activity will lend insight into fluid loss and amounts needed for re-hydration (Brown, 2004), (Criner, Applet, Coker, Conrad, Holiday, 2002).
References cited:
Brown, T.P. (2004). Exertional Rhabdomyolysis. Physician & Sportsmedicine, April 2004, volume 32 issue 4, article retrieved 10/17/2004
http://web.ebscohost.com/ehost/delivery?vid=6&hid+9&sid+95c8ca25-9800-4450-8849 Craig, S. (2008). Rhabdomyolysis. emedicine from Web MD. article retrieved 10/17/2008
http://www.emedicine.com/EMERG/topic508.htm Criner, J.A, Appelt, M., Coker, C., Conrad, S., Holliday, J. (2002) Rhabdomyolysis: The Hidden Killer, Medsurg Nursing, Jannetti Publications, Inc. June 2002, volume 11/number 3. article retrieved 10/17/2008 <
Silberberg, C. (2007) Rhabdomyolysis. Medline Plus, Medical Encyclopedia. article retrieved 10/17/2008
http://www.nlm.nih.gov/medlineplus/print/ency/article/000473.htm
