A kliewer case_1doc
Upcoming SlideShare
Loading in...5

A kliewer case_1doc






Total Views
Views on SlideShare
Embed Views



2 Embeds 38

http://allisonkliewer.yolasite.com 20
http://sitebuilder.yola.com 18


Upload Details

Uploaded via as Microsoft Word

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
Post Comment
Edit your comment

A kliewer case_1doc A kliewer case_1doc Document Transcript

  • Allison KliewerCase: Exertional Rhabdomyolysis after Soccer TournamentDecember 19, 2012BHS Dietetic Internship
  • Case: Rhabdomyolysis Kliewer 2IntroductionExertional rhabdomyolysis is muscle injury usually resulting from eccentric muscleactions that result in lysis of skeletal muscle cells and the release of myoglobin and othercellular components into the circulation (Kulko et al, 2000). The breakdown of musculartissue can cause mild symptoms such as muscle soreness or can lead to acute renal failure(ARF) and possibly death. Epidemiologically rhabdomyolysis is often underreported (Stellaand Shariff, 2012). Boutaud and Robert reported that rhabdomyolysis affects one in 10,000people in the US per year (2010).Personal Data and Chief ComplaintOn September the third during a 3 day, 7 game soccer tournament, a 28 year oldAfrican American male soccer player in good health with no personal or family history ofrhabdomyolysis was presented with heat exhaustion and cramps. The pt had no significantfamily history, only that his mother had been told she was prediabetic. The medical historyprovided no indication of sickle cell testing before participation, so the patient’s sickle celltrait status is unknown. He is a nonsmoker, was not ingesting and medication orsupplements, and had not consumed alcohol. Patient denies any drug use even duringtournaments and denies taking any mediation the days leading up to the admittance. Pt hadexperienced mild leg cramps the day before during the tournament, and had to ask thecoach to seat him and let him drink water and stretch out his legs. Pt denied any recentweight gain or weight loss, difficulty swallowing or chewing, and any abnormal bowels. Thepatient was in good physical shape having been involved in soccer for over 23 years of hislife. Pt reports he has always been active and in general good health. Environmentalconditions for the first three days of the tournament were as follows: an average lowtemperature of 77 ˚F and an average high of 98.6 ˚F, with 60 % average humidity, and an
  • Case: Rhabdomyolysis Kliewer 3average wind speed of 9.6 mph (wunderground.com). The soccer tournament was held atthe Labor Day weekend at the outdoor Star Complex. The patient completed 5 games withthree lasting 60 minutes, and two lasting 90 minutes. In a regular game (60 minutes) thepatient usually plays around 30-45 minutes in the right back position. The patient’s legs andlower back began to cramp during the 6thgame. He then asked his coach to come out of thegame. On the sidelines patient reports everything began to cramp and within ten minutes ofbeing out of the game, EMS was called due to severe cramping of the major muscles of thelegs, back arms and patient reports that his hands were also cramping.Physical Examination and HistoryUpon admission the patient complained of continued cramping and muscularfatigue. The physical examination indicated an alert and oriented patient who was not incardio respiratory distress. The cardiovascular examination was normal with no tendernessor evident edema. Initial laboratory test indicated: high glucose at 125 mg/dl, high creatineat 2.16 mg/dl, low sodium at 130 mEq/L, low potassium at 3.1 mEq/L, low chloride at 90mEq/L, low carbon dioxide at 21 mEq/L, high calcium at 10.7 mg/dl, high total protein at 9.2gm/dl, high albumin at 5.8 gm/dl, high alanine aminotransferase at 47 IU/L, high aspartateaminotransferase at 68 IU/L, high bilirubin at 2.8 mg/dl, low glomerlular filtration rate at 43ml/min/1.73m2, high MCHC 36.9 g/dl, and a high creatine phosphokinase at 2817 IU/L.Urinary pH was normal and no myoglobinuria was present. The patient was then diagnosedwith rhabdomyolysis.Two years prior to accident, pt had an episode of severe dehydration during a soccertournament and had to be given intravenous fluid (IV) to rehydrate. Since then he hasalways stayed hydrated during soccer competition and training by drinking 2- 3, 32 ounce View slide
  • Case: Rhabdomyolysis Kliewer 4water bottles daily. He keeps a refillable water bottle at work so that he can keep track ofhis daily water intake. Pt has been an Air Force Civil Servant for 4 and half years. His title is aSystems Engineer. Patient’s home is Florida where he is currently living with a roommate. Ptis single. Patient was admit 9/03/12 and discharged ten days later on 9/13/12. The patientdenies any drug use and denies taking medication the days leading up to the event.Course of TreatmentOn day of admit patient was diagnosed with rhabdomyolysis and started on normalsaline (NS) at 200 IV fluid per hour. Zofran was given for nausea and vomiting and morphinewas given for pain. Soon after Baptist Health System potassium replacement protocol wasgiven along with magnesium sulfate protocol. The IV fluids were changed to NS with 20 mEqpotassium chloride at 150 ml/hr. Clinical diagnosis changed to rhabdomyolysis,hypokalemia, acute kidney injury (AKI), hypercalcemia, and transaminitis. On the second dayof stay rhabdomyolysis was worsening although patient did not ask for any painmedications. The IV fluids were changed back to 200 ml NS per hour. The hypokalemia andAKI was recorded as resolved while the hypercalemia and transaminitis worsened orcontinued. On the third day of stay strict urine output was ordered, and although there wasa decrease in muscle cramps and neuromuscular pain, acute renal failure was added to thediagnoses with a greatly elevated creatine phosphokinase (CPK). Aggressive hydration wascontinued and bicarbonate was added to treatment. The fourth day was remarkable fordecreased leg pain and aches, while rhabdomyolysis, hypokalemia, and ARF continued. Bythe fifth day of stay pt reported decreased muscle pain and CPK was trending down. Fluidswere to be decreased as tolerated. On the sixth day IF fluids were changed to NS withbicarbonate at 150 ml per hour. The pt reported feeling better with decreased muscle View slide
  • Case: Rhabdomyolysis Kliewer 5soreness. The rhabdomyolysis and ARF persisted while CPK continued to trend down withthe aggressive hydration. A goal was to keep urine pH to around 6.5 to prevent depositionon tubules. On the seventh day, the pt had no new complaints or problems. The ARF wasreported to be resolved and CPK continued to trend down. Fluids were decreased as pt wasclinically improving. On the eighth day of stay the patient continued to clinically improveand IV fluids were changed to NS with 20 mEq KCL plus bicarbonate at 100 ml per hour, andlater that day decreased to 75 ml per hour. The patient had no complaints of muscle pain ofaches on the ninth day of stay, and renal function was recorded as stable. The tenth day ofstay was remarkable for a normalizing CPK, stable renal function, no complaints of muscleaches or pain, and patient was weaned from all IF fluid and oral hydration was pushed astolerated. The tenth day of stay was the first day for high blood pressure to be diagnosed. Ptwas then discharged the following day with orders to continue hydration by drinking aminimum of 2 liters of fluid per day. No medications were ordered for discharge. Afollow-up appointment was made with the primary care physician in Florida within one totwo weeks. The patient discharge diagnoses were rhabdomyolysis, ARF, elevated bloodpressure, hypokalemia, transaminitis, and hypercalcemia.DiagnosisHeat Exhaustion (Two years prior)Athletes who compete or train in tropical conditions are at higher risk ofhyperthermia. Hyperthermia is caused by the inability to adequately dissipate body heatthat leads to a steady increase in body temperature with the consequence of heat relatedillness. Heat illness can begin with muscle cramps then lead to the more severe heat stroke,and if untreated, death. It takes an average of 14 days to become acclimated to tropicaltraining conditions. Acclimation is characterized by a heightened sweat response, reduced
  • Case: Rhabdomyolysis Kliewer 6sodium concentration released in sweat, and greater stability in cardiovascular functionduring exercise. Sweating will begin earlier during the exercise at a lower body temperatureand less sodium will be lost in the sweat due to the increased secretion of aldosterone(Stipanuk, 2006). However, even athletes who are acclimated to hot and humid conditionscan suffer from heat stroke. Heat cramps less severe than heat stroke, and are morecommon in athletes. Heat cramps often occur in people who are already acclimatized toperform in hot climates, but who consume large amounts of water without accompanyingsalt, to replace fluid loss (Stipanuk, 2006). Even with acclimation, the loss of sodium in sweatcan be considerable as the rate of sweat increases. This condition can be prevented withadequate salt and fluid intake during exercise. The patient in the present case experiencedheat exhaustion two years prior to the current event, and because of it has a goal remainhydrated by drinking two to three, 32 ounce water bottles per day.Hyponatremia in Positive Water BalanceExcess water intake results in diluted bodily fluid and both intracellular andextracellular compartments increase and their osmolarities decrease (Stipanuk, 2006). Theexcess water then distributes throughout the body to the intra and extracellularcompartments. In normal conditions the antidiuretic hormone is inhibited and excess wateris excreted.Hyponatremia is the dilution of serum sodium to levels below 130 mEq/L that can becaused by excessive fluid intake, excessive sodium loss through sweat, or both (Coulstonand Boushey, 2008). Symptoms of hyponatremia are almost identical to those ofdehydration, heat exhaustion and heat stroke, and can include nausea, vomiting, impairedcoordination, muscle cramps, and muscle weakness (Coulston and Boushey, 2008).Symptoms can include headache, confusion, nausea, cramps, seizure, coma, pulmonary
  • Case: Rhabdomyolysis Kliewer 7edema, and death (Kazen, 2012).HyperkalemiaHyperkalemia occurs when potassium concentration is over 5.5 mmol/L usuallywhen the kidneys are not functioning properly (Stipanuk, 2006). Metabolic acidosis fromtissue damage can cause a shift of intracellular potassium into to the plasma to causehyperkalemia (Stipaunk, 2006).Acute Renal FailureAcute Renal Failure is characterized by a sudden reduction in glumerlular filtrationrate (GFR) and typically occurs in previously healthy kidneys (Wilkens and Funeja, 2008).ARF can be caused by inadequate renal perfusion such that characterized by severedehydration.RhabdomyolysisRhabdomyolysis refers to a breakdown of skeletal muscle resulting in the release ofintracellular contents into the circulatory system (Khan, 2009). Cell contents includecreatine kinase (CK), glutamic oxalacetic transaminase, lactate dehydrogenase, aldolase,myoglobin, potassium, phosphates and purines (Khan, 2009). The leakage of these contentsinto the circulation can become severe and life threatening.Disease BackgroundHistoryRhabdomyolysis has a long history going back to the times of Moses in the Bible(Numbers 11:31-35) when God sends the Jews quail to eat when they complain about themanna God has provided for them. The Jews then develop rhabdomyolysis presumablycaused by the hemlock herbs consumed by the birds during migration that is linked to
  • Case: Rhabdomyolysis Kliewer 8myolysis (Elsayed and Reilly, 2010). The next record in literature was during Napoleon’s reinin 1812, when a surgeon recorded rhabdomyolysis in members of the army (Elsayed andReilly, 2010). The earliest and most extensive research was conducted after the Blitz ofLondon in 1941 during WWII, when crush syndrome was recorded and studied due to theinjuries caused by bombings and explosions (Elsayed and Reilly, 2010).EtiologyThe most common causes of rhabdomyolysis are illicit drug use, alcohol abuse,medical drug abuse, muscle disease, trauma, neuroleptic malignant syndrome, seizures, andimmobility. Sporadic strenuous exercise has also been known to cause rhabdomyolysis(Khan, 2009). Excess heat increases risk due to excess sweat loss that can causehypokalemia, and extreme heat and humidity can cause pre exertion fatigue (Khan, 2009).Excess heat alone can cause muscle damage because cellular destruction occurs faster athigh environmental temperatures (khan, 2009). Internal body temperature of at 107.6 ˚ F isthe point at which cells can no longer endure the heat can become damaged (Khan, 2009).Hyponatremia, hypernatremia, hypokalemia, and hypophosphataemia may lead torhabdomyolysis. Some foods have been found to cause rhabdomyolysis such as licorice, theingestion of magic mushrooms, and quail. Other causes are toxicities caused by rattlesnakevenom, hornets, brown recluse, and spider bites (Elsayed and Reilly, 2010).PhysiologyWithin the myocyte or muscle cell is the sarcolemma. The sarcolemma is a thinmembrane that encloses striated muscle fibers and pumps that regulate cellularelectrochemical gradients (Khan, 2009). Sodium-potassium-adenosine-triphosphate-pump(NA/K-ATPase pump) is located in the sarcolemma and maintains the intercellular Na to 10mEq/L by actively transporting Na in and out of the cell (Khan, 2009). Compared to the
  • Case: Rhabdomyolysis Kliewer 9exterior, the interior of the cell is negatively charged because positive charges aretransported across the membrane (Khan, 2009). The negative charge or negative gradientinside the cell pulls Na to the interior with an exchange for Ca by a separate ion exchangechannel (Khan, 2009). Therefore, the inside of the cell is low in calcium due to theCa-ATPase pump that promotes Ca into the sarcoplasmic reticulum and mitochondria (Khan,2009). Low Ca at rest in the sarcoplasm allows for an increase for the actin-myosin bindingmuscle contraction (Bosch, 2009). Every electrochemical pump requires and depends onATP for energy. If there is depletion in ATP, there is a dysfunction in the Na/K- ATPase pumpand the Ca-ATPase pump, which is the end result in most rhabdomyolysis cases (Khan,2009).Pathophysiology/PathogenesisRhabdomyolysis is destruction of myocytes resulting in a release of musclecomponents into the circulation. Within the myocyte of a muscle cell, there is thesarcolemma membrane that encloses the striated muscle fibers. The sacrolemma containspumps that regulate cellular electrochemical gradients by the use of adenosine triphosphate(ATP). An alteration of the function of ATP occurs during rhabdomyolysis. This ATP-pasedysfunction increases cellular permeability to sodium (Na) due to a reduced cellularproduction of ATP or a plasma membrane disruption, or both. The result is an accumulationof Na in the cytoplasm witch increases cellular calcium (Ca) concentration. An increase incalcium increases the activity of intracellular proteolytic enzymes that degrade the musclecell. A persistent increase in sarcoplasmic Ca leads to a persistent contraction and thereforeenergy depletion. When ATP or the energy is depleted within the cell, Ca dependent neutralproteases and phospholipases are activated and eventually cause a destruction ofmyofibrillar cytoskeleton membrane proteins. After activation, lysosomal digestion of the
  • Case: Rhabdomyolysis Kliewer 10muscle fiber contents occurs which result in the breakdown of the myofribrillar network andthe disintegration of the myocyte (Bosch, 2009). When the muscle cell breaks down itreleases potassium, aldolase, phosphorus, myoglobin, CK, lactate dehydrogenase, urate, andaspertate dehydrogenase into circulation. When more than 100 g of muscle cell breaksdown, the myoglobin released into circulation exceeds the protein binding capacity of theplasma and can precipitate in the glumerlular filtration rate (GFR). If myoglobin levelsremain increased in circulation, they can lead to renal tubular obstruction, directnephrotoxicity, and acute renal failure (ARF). Less severe cases involve chronic orintermittent muscle destruction with few symptoms and no renal failure (Bosch, 2009).LocationSwelling might not occur until after rehydration of fluids. Rhabdomyolysis mostfrequently involves the thighs, calves and lower back.SymptomsSerum creatine kinase (CK) is the most sensitive indicator of muscle damage and cancontinue to increase from two to 12 hours after the injury with peak values at 24-72 hours(Khan, 2009). A CK five times the normal value is accepted for diagnosis of rhabdomyolysis.Myoglobin may become visible in the urine due to excess levels in the plasma that exceedthe protein binding capacity. Not all cases of rhabdomyolysis have myoglobinuria. ElevatedAST without elevated ALT can be a clue to rhabdomyolysis.ComplicationsHypovolaemia can complicate rhabdomyolysis by increasing the fluid into necroticmuscle and accumulating in the affected limbs; as much as 12 L has been recorded (Bosch,2009). Compartment syndrome is characterized by ischemia and swelling. The increased
  • Case: Rhabdomyolysis Kliewer 11intracompartmental pressure leads to continued ischemia and additional damage andnecrosis. Prolonged ischemia and infarction of muscle tissue with persistent CK at 48-72hours can lead to inelastic fibrous tissue replacement of normal tissue and can cause severecontractures (Khan, 2009). Hepatic dysfunction occurs in an estimated 25% of patients withrhabdomyolysis. The proteases released from the injured muscle may inflame the hepatictissue (Khan, 2009). Increased release of sulfur containing proteins can overwhelm the renalexcretory mechanism and cause lactic acidosis from ischemia and acidosis of uremia (Khan,2009). Acute renal failure occurs about 33% of patients with rhabdomyolysis and is the mostserious compilation (Bosch, 2009). Factors included in ARF are hypovolaemia, acidosis,aciduria, tubular obstruction and nephrotoxic effects of myoglobin (Khan, 2009). ARF resultsdue to reduced plasma volume which potentiates renal hypoperfusion by renalvasoconstriction. The increased myoglobin and uric acid form obstructured casts, andlowered pH potentiate acute tubular necrosis (Khan, 2009). Therefore, ARF becomes aproblem when CK, potassium, Ca, creatine, and the urine myoglobin levels are irregulated.PrognosisThe prognosis of rhabdomyolysis patients heavily depends on the underlying causeof the condition and associated comorbidities. Based on the available evidence form casestudies and small retrospective studies, when treated early and aggressively,rhabdomyolysis has an good prognosis (Khan, 2009). Majority of patients withrhabdomyolysis induced acute kidney injury recover full renal function and have 80%long-term survival (Bosch, 2009). Boutaud and Roberts report that five percent of pts withrhabdomyolysis result in death that is around 1500 people in the US per year (2010).
  • Case: Rhabdomyolysis Kliewer 12Uniqueness of the CaseThe patient’s previous history of heat exhaustion requiring IV fluids had an impact onthe patient’s hydration pattern. Since that event, two years prior, patient has been drinkingover 12 cups of water per day. His hydration increased to over 24 cups of water ontournament days when he was competing. The patient was a good historian concerning hiswater intake and used reusable water bottles as references. During the tournament thepatient reports that he drank over one gallon and a half of water. At patient bedside wasthe one gallon reusable water bottle he used for tournaments. The pt states that he neveruses any sport drink because they make him sick to his stomach. He has only tried sportdrinks a few times, and he has not tried in years. The patient has never tried diluting thesports drinks.As previously discussed, hyponatremia is a risk factor for rhabdomyolysis. Normalserum sodium range is between 136 and 149 mEq/L. If serum sodium is under the level of135 mEq/L, as the patient was at 130 mEq/L upon admittance, hyponatremia is consideredas a diagnosis. Na is important because it facilitates rehydration, sustains thirst drive,promotes retention of fluids, and rapidly restores lost plasma volume during rehydration. Inthe case presented, hyponatremia can be assumed based on the serum sodiumconcentration at time of admit, and based on patients hydration records.The usual diet recall revealed inadequate energy intake related to poor food choiceas evidence by intake record. The patients has never tried or followed a diet. The patienthas abnormal diet during tournaments because the team pays for meals and the entireteam eats together, encouraging the patient to eat. The patient could recall eating anomelet for breakfast, Jason’s Deli sandwich for lunch and BBQ for dinner while in SanAntonio for the tournament. The patient’s usual diet is much different in that he very rarely
  • Case: Rhabdomyolysis Kliewer 13eats breakfast. The pt usually drinks water at work until lunch time when he goes to hisfavorite fast food chain Zaxby’s and orders a five piece fried chicken strips with a MinuteMaid Lite lemonade. The patient states that he does not order the full meal, or eat morethan that because he does not want to be full, or have a stomach ache during his two tothree hour afternoon soccer practice. After practice, the patient returns to his apartmentand usually does not cook dinner because he is too fatigued from the long practice playedon an outdoor soccer field. He only eats dinner four or five times a week, usually only whenhis roommate cooks a frozen pizza that he will only have two slices of. Pt states that hemight have a serving of either fruits or vegetables two or three times a week, on a goodweek. Based on the reported daily intake of the patient, he is consuming an estimated 1,210calories, 2,988 milligrams of sodium, 61 grams of fat, 77 grams of protein, and 76 grams ofcarbohydrates daily. The estimated daily needs of an athlete his size is 2,560 to 2,985calories per day based on 30 to 35 kilocalories per kilogram body weight, 102 to 136 gramsof protein based on 1.2 to 1.6 grams per kilogram body weight, and 385 to 682 grams ofcarbohydrates per day based on 4.5 to 8 grams per kilogram body weight. The patient statesthat his current diet has been the norm for over two years. Based on the patient’sstatements and daily intake records, the patient is most likely in a chronic state of negativeenergy balance.Chronic energy balance has many detrimental effects on sport performance and theathletes overall health. Athletes who train with a negative energy balance tend to have ahigher body fat percentage (Deutz et al, 2000). This is common among all athletesregardless of sport. Sprinters, gymnasts, runners, weight bearing sports all report higherbody fat percentages in those who are at a negative energy balance. Those athletes will alsoexperience a higher rate of muscle breakdown or protein catabolism (Maughan, 2002).
  • Case: Rhabdomyolysis Kliewer 14Decreased immune function is also reported in athletes who do not have adequate energybalance (Deutz et al, 2000 and Maughan, 2002).Most all energy used during exercise is from fat and carbohydrate oxidation.Carbohydrates are most important for athletes because they cannot be stored in adequateamounts compared to what a training regimen requires. That is why the goal of athletesshould be to maintain adequate dietary carbohydrate intake before and during exercise tocombat fatigue and to minimize stress hormones that have negative effect on immunity(Maughan, 2002). If glycogen stores that become depleted during exercise do not getreplenished, there are decrements in the training response (Maughan, 2002). The athletewill not be able to recover as fast, and will not be able to train as hard during the nexttraining session. Athletes who consume low carbohydrate diets tend to have difficulty insport performance compared to a high carbohydrate diet (Maughan, 2002). Lowcarbohydrate diets also increase the risk of injury and susceptibility to minor infections(Maughan, 2002).Athletes who have regimens of continued intense training have increased risk ofopportunistic infections (Maughan, 2002). Intense training also leads to an increase indamaged tissue due to the increase of free radicals released after intense exercise, resultingin incomplete recovery (Maughan, 2002).The effects of intense athletic training coupled with chronic negative energy balancecould have played an integrative role in the development of rhabdomyolysis in the presentcase.Nutrition Care ProcessPatient was seen on the eighth day of stay (9/11/12) following length-of-stayprotocol. Patient is 71 inches tall with a current weight of 85.28 kg at time of visit. Patient
  • Case: Rhabdomyolysis Kliewer 15was considered overweight with a body mass index of 26. Pt was on a normal diet with closeto 100% consumption at each meal. Patient did not have any complaints of difficultychewing or swallowing, nausea, vomiting, constipation, or diarrhea. Patient dined anyprevious weight gain or weight loss and states he has had his current diet/physical routinefor over 3 years. Pt was in good spirits at time of visit and was looking forward to goinghome to Florida. Lab values showed high CPK at 2352 UI/L and low blood urea nitrogen(BUN) at 7 mg/dl. The intake over output ratio was recorded at 1,693 over 2,476 forhydration. Estimated needs for weight maintenance was 2558 to 2984 at 30 to 35kilocalories per kilogram body weight, 68 to 85 grams protein at 0.8 to 1.0 grams perkilogram body weight, and fluid needs were based on 1 milliliter per kilocalorie per kilogrambody weight (1,693 to 2,476 ml/fl). Nutrition status was set as normal according to theBaptist Health System nutritional compromise parameters. Nutritional parameters werewithin normal limits as evidence by BMI, laboratory values, and percent intake. Therefore,no nutritional interventions were needed at time of visit.Patient UnderstandingWhen the patient was asked if he understood his condition, the patient appearedconfused and did not have a response. The patient stated that he thought he had a heatstroke. The patient also stated that in his more than 23 years as a soccer player, nutritionwas never a concern or of demonstrated importance by coaching staff or teammates. Whenasked, the patient stated nutritional expectations were never made clear to him. Theimportance of nutrition has never been made clear to him.Nutrition InterventionThe initial nutrition screen was unremarkable as the patients nutrition status wasnot impaired by any means. However, upon further interview with the patient, the dietary
  • Case: Rhabdomyolysis Kliewer 16patters were seen as inadequate.PESInadequate carbohydrate intake related to food and nutrition knowledge deficit andincreased energy needs due to physical activity as evidence by estimated carbohydrateintake less than recommended amounts and verbalized report of incomplete knowledgeInterventionBasic sport specific diet education was given to patient. Patient had no learningbarriers and was eager to learn about nutrition/diet and how it relates to sport. Theeducation began with identifying the importance of all the food groups and explaining theirrole in sport performance and recovery. Timing of meals was addressed along with theimportance of not skipping meals, as that was one of the patient’s problems. Carbohydrateswere discussed in more detail because of their important role on performance and thepatient’s previous lack of carbohydrate intake. Electrolyte replacement during activity wasfully discussed with strategies to accomplish this as a goal. The patient appeared to fullyunderstand the role nutrition plays in health and sport. The patient stated that he will havemany changes to make, but to avoid the hospital and play/perform better he will try todevelop a well rounded diet that meets his needs as an athlete. The patient’s response tothe education was excitement, and good compliance is anticipated.Personal ImpressionsI am very grateful that I had the opportunity to further research and conduct a casestudy on the presented condition. As I have had my own experience with rhabdomyolysis asa swim coach, I was somewhat familiar with the subject. I enjoyed giving an education andworking with an athlete, as that is my career goal. This case proved to me that I, or sports
  • Case: Rhabdomyolysis Kliewer 17nutritionists, are needed in the sports field. It is insulting to know that a soccer player, whohas been playing for over 23 years, has never once received any kind of nutritionaleducation. Or that an Air Force Civil Servant has never received nutritional education. Thewide-eyed excitement on the patients face when he finally learned about nutrition and howit relates to sport was a great experience. I hope to have the opportunity to experience thatevery day as I work towards becoming a registered dietitian.
  • Case: Rhabdomyolysis Kliewer 18ReferencesAnderson, R. & Barry, D. (2004). Clinical and laboratory diagnosis of acute renalfailure. Best Practice & Research Clinical Anesthesiology. 18(1): 1-20.Bosch, X., Poch, E., & Grau, J. (2009). Rhabdomyolysis and acute kidney injury. TheNew England Journal of Medicine. 361(1): 62-74.Bruso, J., Hoffman, M., Rogers, I., Lee, L., Towle, G., & Hew-Butler, T. (2010).Rhabdomyolysis and hyponatremia: A cluster of five cases at the 161-km 2009Western States Endurance Run. Wilderness & Environmental Medicine. 21:303-308.Capacchione, J., & Muldoon, S. (2009). The relationship between exertional heatillness, exertional rhabdomyolysis, and malignant hyperthermia. AnesthesiaResearch Society. 109(4): 1065-1069.Casares, P. & Marull, J. (2008). Over a million creatine kinase due to a heavywork-out: A case report. Cases Journal. 1(173): 1-4.Deutz, R., Benardot, D., Martin, D., & Cody, M. (2000). Relationship between energydeficits and body composition in elite female gymnast and runners. Medicineand Science in Sports and Exercise. 659-678.Falvo, M. & Bloomer, R. (2006). Review of exercise-induced muscle injury: Relevancefor athletic populations. Research in Sports Medicine. 14: 65-82.Hannah-Shmouni, F., McLeod, K., & Sirrs, S. (2012). Recurrent exercise-inducedrhabdomyolysis. Canadian Medical Associations Journal. 184(4): 426-430.Huerta-Alardin, A., Varon, J., & Marik, P. (2005). Bench –to-bedisde review:Rhabdomyolysis- an overview for clinicians. Critical Care. 9: 158-169.Kahanov, L., Eberman, l., Wasik, M., & Alvey, T. (2012). Exertional rhabdomyolysis ina collegiate American football player after preventive cold water immersion: Acase report. Journal of Athletic Training. 47(2): 228-232.Khan, F. (2009). Review: Rhabdomyolysis: A review of the literature. The NetherlandsJournal of Medicine. 67(9).Kulko, T., Tis, J., Moores, L., & Schaefer, R. (2000). The American Journal of SportsMedicine. 28(1): 117.Maughan, R. (2002). Plenary lecture: The athlete’s diet: Nutritional goals and dietarystrategies. The Nutritional Society. 61:87-96Parmar, S., Chauhan, B., DuBose, J., & Blake, L. (2012). Rhabdomyolysis after spinclas? The Journal of Family Practice. 61(10): 584-586.Skenderi, K., Kavouras, S., Anastasiou, C., Yiannakouris, N., & Matalas, A. (2006).
  • Case: Rhabdomyolysis Kliewer 19Exertional rhabdomyolysis during a 246-km continuous running race. AmericnCollege of Sports Medicine. 1054-1056.Thoenes, M. (2010). Rhabdomyolysis: When exercising becomes a risk. Journal ofPediatric Health Care. 24: 189-193.