case rhabdomyolysis

Allison Kliewer

Case: Exertional Rhabdomyolysis after Soccer Tournament

December 19, 2012

BHS Dietetic Internship

Case: Rhabdomyolysis Kliewer 2

Introduction

Exertional rhabdomyolysis is muscle injury usually resulting from eccentric muscle

actions that result in lysis of skeletal muscle cells and the release of myoglobin and other

cellular components into the circulation (Kulko et al, 2000). The breakdown of muscular

tissue can cause mild symptoms such as muscle soreness or can lead to acute renal failure

(ARF) and possibly death. Epidemiologically rhabdomyolysis is often underreported (Stella

and Shariff, 2012). Boutaud and Robert reported that rhabdomyolysis affects one in 10,000

people in the US per year (2010).

Personal Data and Chief Complaint

On September the third during a 3 day, 7 game soccer tournament, a 28 year old

African American male soccer player in good health with no personal or family history of

rhabdomyolysis was presented with heat exhaustion and cramps. The pt had no significant

family history, only that his mother had been told she was prediabetic. The medical history

provided no indication of sickle cell testing before participation, so the patient’s sickle cell

trait status is unknown. He is a nonsmoker, was not ingesting and medication or

supplements, and had not consumed alcohol. Patient denies any drug use even during

tournaments and denies taking any mediation the days leading up to the admittance. Pt had

experienced mild leg cramps the day before during the tournament, and had to ask the

coach to seat him and let him drink water and stretch out his legs. Pt denied any recent

weight gain or weight loss, difficulty swallowing or chewing, and any abnormal bowels. The

patient was in good physical shape having been involved in soccer for over 23 years of his

life. Pt reports he has always been active and in general good health. Environmental

conditions for the first three days of the tournament were as follows: an average low

temperature of 77 ˚F and an average high of 98.6 ˚F, with 60 % average humidity, and an


average wind speed of 9.6 mph (wunderground.com). The soccer tournament was held at

the Labor Day weekend at the outdoor Star Complex. The patient completed 5 games with

three lasting 60 minutes, and two lasting 90 minutes. In a regular game (60 minutes) the

patient usually plays around 30-45 minutes in the right back position. The patient’s legs and

lower back began to cramp during the 6th game. He then asked his coach to come out of the

game. On the sidelines patient reports everything began to cramp and within ten minutes of

being out of the game, EMS was called due to severe cramping of the major muscles of the

legs, back arms and patient reports that his hands were also cramping.

Physical Examination and History

Upon admission the patient complained of continued cramping and muscular

fatigue. The physical examination indicated an alert and oriented patient who was not in

cardio respiratory distress. The cardiovascular examination was normal with no tenderness

or evident edema. Initial laboratory test indicated: high glucose at 125 mg/dl, high creatine

at 2.16 mg/dl, low sodium at 130 mEq/L, low potassium at 3.1 mEq/L, low chloride at 90

mEq/L, low carbon dioxide at 21 mEq/L, high calcium at 10.7 mg/dl, high total protein at 9.2

gm/dl, high albumin at 5.8 gm/dl, high alanine aminotransferase at 47 IU/L, high aspartate

aminotransferase at 68 IU/L, high bilirubin at 2.8 mg/dl, low glomerlular filtration rate at 43

ml/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 diagnosed

with rhabdomyolysis.

Two years prior to accident, pt had an episode of severe dehydration during a soccer

tournament and had to be given intravenous fluid (IV) to rehydrate. Since then he has

always stayed hydrated during soccer competition and training by drinking 2- 3, 32 ounce


water bottles daily. He keeps a refillable water bottle at work so that he can keep track of

his daily water intake. Pt has been an Air Force Civil Servant for 4 and half years. His title is a

Systems Engineer. Patient’s home is Florida where he is currently living with a roommate. Pt

is single. Patient was admit 9/03/12 and discharged ten days later on 9/13/12. The patient

denies any drug use and denies taking medication the days leading up to the event.

Course of Treatment

On day of admit patient was diagnosed with rhabdomyolysis and started on normal

saline (NS) at 200 IV fluid per hour. Zofran was given for nausea and vomiting and morphine

was given for pain. Soon after Baptist Health System potassium replacement protocol was

given along with magnesium sulfate protocol. The IV fluids were changed to NS with 20 mEq

potassium chloride at 150 ml/hr. Clinical diagnosis changed to rhabdomyolysis,

hypokalemia, acute kidney injury (AKI), hypercalcemia, and transaminitis. On the second day

of stay rhabdomyolysis was worsening although patient did not ask for any pain

medications. The IV fluids were changed back to 200 ml NS per hour. The hypokalemia and

AKI was recorded as resolved while the hypercalemia and transaminitis worsened or

continued. On the third day of stay strict urine output was ordered, and although there was

a decrease in muscle cramps and neuromuscular pain, acute renal failure was added to the

diagnoses with a greatly elevated creatine phosphokinase (CPK). Aggressive hydration was

continued and bicarbonate was added to treatment. The fourth day was remarkable for

decreased leg pain and aches, while rhabdomyolysis, hypokalemia, and ARF continued. By

the fifth day of stay pt reported decreased muscle pain and CPK was trending down. Fluids

were to be decreased as tolerated. On the sixth day IF fluids were changed to NS with

bicarbonate at 150 ml per hour. The pt reported feeling better with decreased muscle


soreness. The rhabdomyolysis and ARF persisted while CPK continued to trend down with

the aggressive hydration. A goal was to keep urine pH to around 6.5 to prevent deposition

on tubules. On the seventh day, the pt had no new complaints or problems. The ARF was

reported to be resolved and CPK continued to trend down. Fluids were decreased as pt was

clinically improving. On the eighth day of stay the patient continued to clinically improve

and IV fluids were changed to NS with 20 mEq KCL plus bicarbonate at 100 ml per hour, and

later that day decreased to 75 ml per hour. The patient had no complaints of muscle pain of

aches on the ninth day of stay, and renal function was recorded as stable. The tenth day of

stay was remarkable for a normalizing CPK, stable renal function, no complaints of muscle

aches or pain, and patient was weaned from all IF fluid and oral hydration was pushed as

tolerated. The tenth day of stay was the first day for high blood pressure to be diagnosed. Pt

was then discharged the following day with orders to continue hydration by drinking a

minimum of 2 liters of fluid per day. No medications were ordered for discharge. A follow-

up appointment was made with the primary care physician in Florida within one to two

weeks. The patient discharge diagnoses were rhabdomyolysis, ARF, elevated blood pressure,

hypokalemia, transaminitis, and hypercalcemia.

Diagnosis

Heat Exhaustion (Two years prior)

Athletes who compete or train in tropical conditions are at higher risk of

hyperthermia. Hyperthermia is caused by the inability to adequately dissipate body heat

that leads to a steady increase in body temperature with the consequence of heat related

illness. 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 tropical

training conditions. Acclimation is characterized by a heightened sweat response, reduced


sodium concentration released in sweat, and greater stability in cardiovascular function

during exercise. Sweating will begin earlier during the exercise at a lower body temperature

and 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 conditions

can suffer from heat stroke. Heat cramps less severe than heat stroke, and are more

common in athletes. Heat cramps often occur in people who are already acclimatized to

perform in hot climates, but who consume large amounts of water without accompanying

salt, to replace fluid loss (Stipanuk, 2006). Even with acclimation, the loss of sodium in sweat

can be considerable as the rate of sweat increases. This condition can be prevented with

adequate salt and fluid intake during exercise. The patient in the present case experienced

heat exhaustion two years prior to the current event, and because of it has a goal remain

hydrated by drinking two to three, 32 ounce water bottles per day.

Hyponatremia in Positive Water Balance

Excess water intake results in diluted bodily fluid and both intracellular and

extracellular compartments increase and their osmolarities decrease (Stipanuk, 2006). The

excess water then distributes throughout the body to the intra and extracellular

compartments. In normal conditions the antidiuretic hormone is inhibited and excess water

is excreted.

Hyponatremia is the dilution of serum sodium to levels below 130 mEq/L that can be

caused by excessive fluid intake, excessive sodium loss through sweat, or both (Coulston

and Boushey, 2008). Symptoms of hyponatremia are almost identical to those of

dehydration, heat exhaustion and heat stroke, and can include nausea, vomiting, impaired

coordination, muscle cramps, and muscle weakness (Coulston and Boushey, 2008).

Symptoms can include headache, confusion, nausea, cramps, seizure, coma, pulmonary


edema, and death (Kazen, 2012).

Hyperkalemia

Hyperkalemia occurs when potassium concentration is over 5.5 mmol/L usually

when the kidneys are not functioning properly (Stipanuk, 2006). Metabolic acidosis from

tissue damage can cause a shift of intracellular potassium into to the plasma to cause

hyperkalemia (Stipaunk, 2006).

Acute Renal Failure

Acute Renal Failure is characterized by a sudden reduction in glumerlular filtration

rate (GFR) and typically occurs in previously healthy kidneys (Wilkens and Funeja, 2008).

ARF can be caused by inadequate renal perfusion such that characterized by severe

dehydration.

Rhabdomyolysis

Rhabdomyolysis refers to a breakdown of skeletal muscle resulting in the release of

intracellular contents into the circulatory system (Khan, 2009). Cell contents include creatine

kinase (CK), glutamic oxalacetic transaminase, lactate dehydrogenase, aldolase, myoglobin,

potassium, phosphates and purines (Khan, 2009). The leakage of these contents into the

circulation can become severe and life threatening.

Disease Background

History

Rhabdomyolysis 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 the

manna God has provided for them. The Jews then develop rhabdomyolysis presumably

caused by the hemlock herbs consumed by the birds during migration that is linked to


myolysis (Elsayed and Reilly, 2010). The next record in literature was during Napoleon’s rein

in 1812, when a surgeon recorded rhabdomyolysis in members of the army (Elsayed and

Reilly, 2010). The earliest and most extensive research was conducted after the Blitz of

London in 1941 during WWII, when crush syndrome was recorded and studied due to the

injuries caused by bombings and explosions (Elsayed and Reilly, 2010).

Etiology

The most common causes of rhabdomyolysis are illicit drug use, alcohol abuse,

medical drug abuse, muscle disease, trauma, neuroleptic malignant syndrome, seizures, and

immobility. Sporadic strenuous exercise has also been known to cause rhabdomyolysis

(Khan, 2009). Excess heat increases risk due to excess sweat loss that can cause

hypokalemia, and extreme heat and humidity can cause pre exertion fatigue (Khan, 2009).

Excess heat alone can cause muscle damage because cellular destruction occurs faster at

high environmental temperatures (khan, 2009). Internal body temperature of at 107.6 ˚ F is

the point at which cells can no longer endure the heat can become damaged (Khan, 2009).

Hyponatremia, hypernatremia, hypokalemia, and hypophosphataemia may lead to

rhabdomyolysis. Some foods have been found to cause rhabdomyolysis such as licorice, the

ingestion of magic mushrooms, and quail. Other causes are toxicities caused by rattlesnake

venom, hornets, brown recluse, and spider bites (Elsayed and Reilly, 2010).

Physiology

Within the myocyte or muscle cell is the sarcolemma. The sarcolemma is a thin

membrane that encloses striated muscle fibers and pumps that regulate cellular

electrochemical gradients (Khan, 2009). Sodium-potassium-adenosine-triphosphate-pump

(NA/K-ATPase pump) is located in the sarcolemma and maintains the intercellular Na to 10

mEq/L by actively transporting Na in and out of the cell (Khan, 2009). Compared to the


exterior, the interior of the cell is negatively charged because positive charges are

transported across the membrane (Khan, 2009). The negative charge or negative gradient

inside the cell pulls Na to the interior with an exchange for Ca by a separate ion exchange

channel (Khan, 2009). Therefore, the inside of the cell is low in calcium due to the Ca-

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 binding

muscle contraction (Bosch, 2009). Every electrochemical pump requires and depends on

ATP for energy. If there is depletion in ATP, there is a dysfunction in the Na/K- ATPase pump

and the Ca-ATPase pump, which is the end result in most rhabdomyolysis cases (Khan,

2009).

Pathophysiology/Pathogenesis

Rhabdomyolysis is destruction of myocytes resulting in a release of muscle

components into the circulation. Within the myocyte of a muscle cell, there is the

sarcolemma membrane that encloses the striated muscle fibers. The sacrolemma contains

pumps that regulate cellular electrochemical gradients by the use of adenosine triphosphate

(ATP). An alteration of the function of ATP occurs during rhabdomyolysis. This ATP-pase

dysfunction increases cellular permeability to sodium (Na) due to a reduced cellular

production of ATP or a plasma membrane disruption, or both. The result is an accumulation

of Na in the cytoplasm witch increases cellular calcium (Ca) concentration. An increase in

calcium increases the activity of intracellular proteolytic enzymes that degrade the muscle

cell. A persistent increase in sarcoplasmic Ca leads to a persistent contraction and therefore

energy depletion. When ATP or the energy is depleted within the cell, Ca dependent neutral

proteases and phospholipases are activated and eventually cause a destruction of

myofibrillar cytoskeleton membrane proteins. After activation, lysosomal digestion of the


muscle fiber contents occurs which result in the breakdown of the myofribrillar network and

the disintegration of the myocyte (Bosch, 2009). When the muscle cell breaks down it

releases potassium, aldolase, phosphorus, myoglobin, CK, lactate dehydrogenase, urate, and

aspertate dehydrogenase into circulation. When more than 100 g of muscle cell breaks

down, the myoglobin released into circulation exceeds the protein binding capacity of the

plasma and can precipitate in the glumerlular filtration rate (GFR). If myoglobin levels

remain increased in circulation, they can lead to renal tubular obstruction, direct

nephrotoxicity, and acute renal failure (ARF). Less severe cases involve chronic or

intermittent muscle destruction with few symptoms and no renal failure (Bosch, 2009).

Location

Swelling might not occur until after rehydration of fluids. Rhabdomyolysis most

frequently involves the thighs, calves and lower back.

Symptoms

Serum creatine kinase (CK) is the most sensitive indicator of muscle damage and can

continue 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 exceed

the protein binding capacity. Not all cases of rhabdomyolysis have myoglobinuria. Elevated

AST without elevated ALT can be a clue to rhabdomyolysis.

Complications

Hypovolaemia can complicate rhabdomyolysis by increasing the fluid into necrotic

muscle 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


intracompartmental pressure leads to continued ischemia and additional damage and

necrosis. Prolonged ischemia and infarction of muscle tissue with persistent CK at 48-72

hours can lead to inelastic fibrous tissue replacement of normal tissue and can cause severe

contractures (Khan, 2009). Hepatic dysfunction occurs in an estimated 25% of patients with

rhabdomyolysis. The proteases released from the injured muscle may inflame the hepatic

tissue (Khan, 2009). Increased release of sulfur containing proteins can overwhelm the renal

excretory 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 most

serious compilation (Bosch, 2009). Factors included in ARF are hypovolaemia, acidosis,

aciduria, tubular obstruction and nephrotoxic effects of myoglobin (Khan, 2009). ARF results

due to reduced plasma volume which potentiates renal hypoperfusion by renal

vasoconstriction. The increased myoglobin and uric acid form obstructured casts, and

lowered pH potentiate acute tubular necrosis (Khan, 2009). Therefore, ARF becomes a

problem when CK, potassium, Ca, creatine, and the urine myoglobin levels are irregulated.

Prognosis

The prognosis of rhabdomyolysis patients heavily depends on the underlying cause

of the condition and associated comorbidities. Based on the available evidence form case

studies and small retrospective studies, when treated early and aggressively,

rhabdomyolysis has an good prognosis (Khan, 2009). Majority of patients with

rhabdomyolysis 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 with

rhabdomyolysis result in death that is around 1500 people in the US per year (2010).


Uniqueness of the Case

The patient’s previous history of heat exhaustion requiring IV fluids had an impact on

the patient’s hydration pattern. Since that event, two years prior, patient has been drinking

over 12 cups of water per day. His hydration increased to over 24 cups of water on

tournament days when he was competing. The patient was a good historian concerning his

water intake and used reusable water bottles as references. During the tournament the

patient reports that he drank over one gallon and a half of water. At patient bedside was the

one gallon reusable water bottle he used for tournaments. The pt states that he never uses

any sport drink because they make him sick to his stomach. He has only tried sport drinks a

few times, and he has not tried in years. The patient has never tried diluting the sports

drinks.

As previously discussed, hyponatremia is a risk factor for rhabdomyolysis. Normal

serum sodium range is between 136 and 149 mEq/L. If serum sodium is under the level of

135 mEq/L, as the patient was at 130 mEq/L upon admittance, hyponatremia is considered

as a diagnosis. Na is important because it facilitates rehydration, sustains thirst drive,

promotes retention of fluids, and rapidly restores lost plasma volume during rehydration. In

the case presented, hyponatremia can be assumed based on the serum sodium

concentration at time of admit, and based on patients hydration records.

The usual diet recall revealed inadequate energy intake related to poor food choice

as evidence by intake record. The patients has never tried or followed a diet. The patient has

abnormal diet during tournaments because the team pays for meals and the entire team

eats together, encouraging the patient to eat. The patient could recall eating an omelet for

breakfast, Jason’s Deli sandwich for lunch and BBQ for dinner while in San Antonio for the

tournament. The patient’s usual diet is much different in that he very rarely eats breakfast.


The pt usually drinks water at work until lunch time when he goes to his favorite fast food

chain Zaxby’s and orders a five piece fried chicken strips with a Minute Maid Lite lemonade.

The patient states that he does not order the full meal, or eat more than that because he

does not want to be full, or have a stomach ache during his two to three hour afternoon

soccer practice. After practice, the patient returns to his apartment and usually does not

cook dinner because he is too fatigued from the long practice played on an outdoor soccer

field. He only eats dinner four or five times a week, usually only when his roommate cooks a

frozen pizza that he will only have two slices of. Pt states that he might have a serving of

either fruits or vegetables two or three times a week, on a good week. Based on the

reported daily intake of the patient, he is consuming an estimated 1,210 calories, 2,988

milligrams of sodium, 61 grams of fat, 77 grams of protein, and 76 grams of carbohydrates

daily. The estimated daily needs of an athlete his size is 2,560 to 2,985 calories per day

based on 30 to 35 kilocalories per kilogram body weight, 102 to 136 grams of protein based

on 1.2 to 1.6 grams per kilogram body weight, and 385 to 682 grams of carbohydrates per

day based on 4.5 to 8 grams per kilogram body weight. The patient states that his current

diet has been the norm for over two years. Based on the patient’s statements and daily

intake records, the patient is most likely in a chronic state of negative energy balance.

Chronic energy balance has many detrimental effects on sport performance and the

athletes overall health. Athletes who train with a negative energy balance tend to have a

higher body fat percentage (Deutz et al, 2000). This is common among all athletes

regardless of sport. Sprinters, gymnasts, runners, weight bearing sports all report higher

body fat percentages in those who are at a negative energy balance. Those athletes will also

experience a higher rate of muscle breakdown or protein catabolism (Maughan, 2002).

Decreased immune function is also reported in athletes who do not have adequate energy


balance (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 adequate

amounts compared to what a training regimen requires. That is why the goal of athletes

should be to maintain adequate dietary carbohydrate intake before and during exercise to

combat fatigue and to minimize stress hormones that have negative effect on immunity

(Maughan, 2002). If glycogen stores that become depleted during exercise do not get

replenished, there are decrements in the training response (Maughan, 2002). The athlete

will not be able to recover as fast, and will not be able to train as hard during the next

training session. Athletes who consume low carbohydrate diets tend to have difficulty in

sport performance compared to a high carbohydrate diet (Maughan, 2002). Low

carbohydrate 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 of

opportunistic infections (Maughan, 2002). Intense training also leads to an increase in

damaged tissue due to the increase of free radicals released after intense exercise, resulting

in incomplete recovery (Maughan, 2002).

The effects of intense athletic training coupled with chronic negative energy balance

could have played an integrative role in the development of rhabdomyolysis in the present

case.

Nutrition Care Process

Patient was seen on the eighth day of stay (9/11/12) following length-of-stay

protocol. Patient is 71 inches tall with a current weight of 85.28 kg at time of visit. Patient

was considered overweight with a body mass index of 26. Pt was on a normal diet with close


to 100% consumption at each meal. Patient did not have any complaints of difficulty

chewing or swallowing, nausea, vomiting, constipation, or diarrhea. Patient dined any

previous weight gain or weight loss and states he has had his current diet/physical routine

for over 3 years. Pt was in good spirits at time of visit and was looking forward to going

home 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 for

hydration. Estimated needs for weight maintenance was 2558 to 2984 at 30 to 35

kilocalories per kilogram body weight, 68 to 85 grams protein at 0.8 to 1.0 grams per

kilogram body weight, and fluid needs were based on 1 milliliter per kilocalorie per kilogram

body weight (1,693 to 2,476 ml/fl). Nutrition status was set as normal according to the

Baptist Health System nutritional compromise parameters. Nutritional parameters were

within normal limits as evidence by BMI, laboratory values, and percent intake. Therefore,

no nutritional interventions were needed at time of visit.

Patient Understanding

When the patient was asked if he understood his condition, the patient appeared

confused and did not have a response. The patient stated that he thought he had a heat

stroke. The patient also stated that in his more than 23 years as a soccer player, nutrition

was never a concern or of demonstrated importance by coaching staff or teammates. When

asked, the patient stated nutritional expectations were never made clear to him. The

importance of nutrition has never been made clear to him.

Nutrition Intervention

The initial nutrition screen was unremarkable as the patients nutrition status was not

impaired by any means. However, upon further interview with the patient, the dietary

patters were seen as inadequate.


PES

Inadequate carbohydrate intake related to food and nutrition knowledge deficit and

increased energy needs due to physical activity as evidence by estimated carbohydrate

intake less than recommended amounts and verbalized report of incomplete knowledge

Intervention

Basic sport specific diet education was given to patient. Patient had no learning

barriers and was eager to learn about nutrition/diet and how it relates to sport. The

education began with identifying the importance of all the food groups and explaining their

role in sport performance and recovery. Timing of meals was addressed along with the

importance of not skipping meals, as that was one of the patient’s problems. Carbohydrates

were discussed in more detail because of their important role on performance and the

patient’s previous lack of carbohydrate intake. Electrolyte replacement during activity was

fully discussed with strategies to accomplish this as a goal. The patient appeared to fully

understand the role nutrition plays in health and sport. The patient stated that he will have

many changes to make, but to avoid the hospital and play/perform better he will try to

develop a well rounded diet that meets his needs as an athlete. The patient’s response to

the education was excitement, and good compliance is anticipated.

Personal Impressions

I am very grateful that I had the opportunity to further research and conduct a case

study on the presented condition. As I have had my own experience with rhabdomyolysis as

a swim coach, I was somewhat familiar with the subject. I enjoyed giving an education and

working with an athlete, as that is my career goal. This case proved to me that I, or sports

nutritionists, are needed in the sports field. It is insulting to know that a soccer player, who


has been playing for over 23 years, has never once received any kind of nutritional

education. Or that an Air Force Civil Servant has never received nutritional education. The

wide-eyed excitement on the patients face when he finally learned about nutrition and how

it relates to sport was a great experience. I hope to have the opportunity to experience that

every day as I work towards becoming a registered dietitian.

References


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