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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