Here's a letter I wrote for a school assignment directed to an Admin. at the Center for Medicare & Medicaid. Seems they have left out some information on a service they offer. Also the notion of meds. we have got to get it through the heads of the Docs and big industry that we need to get people off the meds and off the couch and start eating food that does not come in a box, a can, or a bag. If it did not come from the earth don't eat it.
Mr. Berwick,
In response to your post published on the healthcare.gov web-site. I would like to take this opportunity to acknowledge the benefits of prevention and discuss steps and goals to consider with the progression of prevention through healthcare.
It is important to identify that preventative measures such as bone scans, colon-rectal screens, and mammograms are all important aspects of preventative healthcare. The fact that the services are available at no cost to the beneficiary will have the potential to create a positive impact on the future utilization of health services and costs in the future. As you remarked “you can pay know or pay later” can be viewed from two perspectives in my opinion. The first is the actual utilization of the preventative services in an effort to reduce the need of more expansive interventions designed to treat the illness the preventative screen is intended to detect. The other aspect helps transition to the idea of “time invested” with preventative measures. The notion of investing time spent at moments before a health complication presents vs. spending the time addressing the health issue once it develops. Which cost’s more? Is the cost of personal time more valuable than monetary cost’s?
One of the preventative benefits offered through Medicare at no cost to the beneficiary is an “annual wellness visit” with a participating doctor. As a young healthy adult planning for my future I believe this service to be an important aspect of health prevention. In my effort to plan for my future health I made efforts to research what is offered from this service and the potential benefits that may develop from its utilization. However, upon researching the link to the official US Medicare hand book provided in your post I was unable to learn of the intent of this benefit. It was not presented, I only learned of the “one time welcome to healthcare physical exam’. This leaves me bewildered in the sense that while proactive services such as education for nutritional modification and smoking cessation are offered, no where did I learn of any health and wellness approaches or guidance for physical activity.
In addition I am curious as to what proactive steps will be taken to reduce the number of medications people need to take. Would not encouraging people to eat properly and acquire the appropriate types of exercise help reduce and potentially curtail the need and associated costs of medications? Your presentation highlighted the fact that June is “National Prevention and Wellness Month”. My confusion lies with the fact that many of the preventative measures offered are at still some cost to the public in order for them to be implemented. While all of theses preventative measures carry merit, I am disappointed to see an absence of an approach to education with regards to proactive approaches that beneficiaries can act on for themselves through the guidance of the “annual wellness visit”.
In closing I am optimistic from your post that we are on the right track for health prevention through proactive measures. I encourage this direction but we need to continue moving away from the “biomedical model” for health prevention and move more towards the “biopsychosocial”. Having an “annual wellness visit” to encourage the investment of efforts through time to encourage health while still healthy has the potential to create decreased future costs as the result of complications from unhealthy behaviors.
Thank you for taking the time to present this information on the healthcare.gov blog.
Sincerely,
Emile Smith, PTA, CPT
Thursday, June 23, 2011
Sunday, March 13, 2011
Pain
Endless thoughts of nerve endings twitching in pain. Thoughts of lactic acid rushing and surging through my body fosters excitement for whats to come. Good times bring it on. To ride mono-cog, ya gotta love the hurt, the burn, the sting. That sting, that very lasting surge of effort that questions your motives to climb, to cross the line.
Monday, August 24, 2009
Dark Horse 40 Race Recap
USA cycling appears to acknowledge Marathon events as 63 miles in length. So I can’t classify the Dark Horse 40 as a marathon but coupled with the heat, and the fact that the Cat 1 Single Speed field started with 27 racers and 15 crossed the finish line has something to say about that day. It was already 80+ degrees by 8:00am. Racing at “12 Hours of Great Glen” seven days earlier, I was accepting of my 10th place finish at the Dark Horse 40. The Bethel Cycle Dirt Squad was there so my motivation was to race with my distant friends and support the Club at the race. Frank Dailey of Bethel Cycle had a great performance with a 12th place finish. Frank has just recently started racing Single Speed and moving up to Cat 1. Great job Frank!!! Also from Bethel Cycle Johan Koserius placed 3rd in the Cat 1 40-49 class. I saw Johan at the end of the race and noticed his rear wheel was missing a tire. I'll leave the explanation to him, that's commitment. Tony Muffatti placed 2nd in his Cat 1 age category, super performance in extremely HOT conditions. Sean Cavanaugh raced and finished strong as well. Sean has been busy balancing two new additions to his family and keeping the busy shop running smoothly not providing him the time in the saddle he prefers. A big thank you to Scott and Connor for the water bottle hand-offs. I have to admit I was sweating bullets just getting things together in the parking lot before the race. After pedaling down and back to the registration tent I decided to lighten my gear selection. The day before Greg was ribbing us Single Speeders about our gear selections and the “Geek Talk” that accompanies such discussions. No equation can make up for the fact that my legs had not recovered from Great Glen the week before. 34/20 was the right gear for me and my legs for the Dark Horse 40 on that day, but it wasn't tall enough to keep up with the top guy’s running 34/17. Flatting on the last lap ate up a few minutes and forced me to fight back for the 10th position. Doug Jenne from Bare Knuckle Brigade made me work for that 10th place and pushed me to clear the climbs that many racers were forced to walk. It was good to see Doug, he put out a great performance as well.
Monday, August 10, 2009
12 Hours of Great Glen with Great Friends!!
Redemption from the 909.A solo 2nd place finish at 12 Hours of Great Glen.
SS full rigid 34/20 against the gearies.
Chris Gagnon from MTB MIND took 1st, to tie laps with Chris and lose to time completed on a SS is OK with me. Congrats to Chris!! 
Love and Thanx to my crew Ross Bonacci and my wife Lisa. Without them the results would have been different.
Rob Stine and Tom Parsons were great to watch as they flew by me doin laps on their 4 man teams, those boy's were flying. 
Shout out to Todd "Cha-Ching", Jay from Claremont Cycle Depot, and Robin nice job also you guy's.
Friday, July 24, 2009
Rain, The Tour, 12 Hour Races and Achie Wrists
It's been an un-eventfull season.
Two flats at the Stupid 50 in PA. after sitting pretty with the top riders. The flats proceeded in putting me in the back of the pack. Fun race though worth doing next year.
Broken Niner Frame (things that make you go HMM?) after a podium finesh at Putney, Ouch 33/19 in wet conditions was the wrong gear.
Attempted a 12 hour race on absolutely no rest/sleep with a rigid fork using a 34/20 gear only to back out after 7 hours unable to hold the handle bars. Seems that 50 miles or 6.5 hours of riding is my max with a rigid.
Hats off to James Harmon, with an impressive performance at the 12 hour race, as well as Rob Stine pulling a 3rd at 6hours of Pat's Peak.
Watching Lance in the tour has inspired me not to think too much about my age (;-/)
Keep'm turn'n over!
E'
Wednesday, March 11, 2009
Stay Hydrated
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.com
The 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: Rhabdomyolysis
Rhabdomyolysis
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
The 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: Rhabdomyolysis
Rhabdomyolysis
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
Monday, March 9, 2009
Health Scare: T.B.
Hi to everyone, sorry for no new updates. After dealing with a recent "positive TB test" I was unfortunately distracted from getting any new posts up.
In a means to offer a preview for some up coming topics, I'll be posting some exercises to help get the shoulders ready for the season. I will also show and discuss some basic yet essential core exercises to get us ready to roll this season.
Quick shout-out to Rob, James and congrats to Sean on the multiple additions to his family.
Peace,
E'
In a means to offer a preview for some up coming topics, I'll be posting some exercises to help get the shoulders ready for the season. I will also show and discuss some basic yet essential core exercises to get us ready to roll this season.
Quick shout-out to Rob, James and congrats to Sean on the multiple additions to his family.
Peace,
E'
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