2. › Introduction
› Patient Profile
› Disease background
› Admission
› Nutrition Care Process
› Summary and Reflection
3. › Exertional rhabdomyolysis is a muscle
injury the results in the lysis of skeletal
muscle and the release of celllular
components into the circulation
› In severe cases can lead to death
› Rhabdomyolysis affects 1/10,000
people in the US per year
(Boutaud and Robert, 2010 and Stella and Shariff, 2012)
4. › 28 year old African American Male
› Admission: 9/03/12 Discharge: 9/13/12
› Initial DX: heat exhaustion and cramps
› Admit through ER from soccer
tournament
› PMH: heat exhaustion requiring IV fluids
2 at soccer tournament 2 years prior
› Family HX: insignificant
› Single, lives with roommate
5. › Native to Florida where he currently
lives
› Has been a Civil Servant for >4 years in
the Air Force as a Systems Engineer
› Currently completing his
undergraduate degree
› Position: Right back
› Been playing soccer for 23 years
6. › Ht: 71 in - 6’ 11”
› Wt: 91.17 kg – 200 lbs
› No previous wt gain/loss
› No difficulty swallowing/chewing or BM
› Denies any substance abuse
› Previously healthy individual
7. › Numbers 11: 31-35
› 1812 during Napoleon’s rein
› 1941 during WWII after the Blitz of
London referred to as “crush syndrome”
(Elsayed and Reilly, 2010)
8. › Breakdown of skeletal muscle resulting
in the release of intracellular contents
› Leakage of contents can become
severe and life threatening
(Khan, 2009)
9. › Illicit drug use, alcohol abuse, muscle
disease, trauma, seizures and immobility
› Sporadic strenuous exercise can cause
exertional rhabdomyolysis
› Excess heat increases risk
› Hypokalemia
› Hyponatremia
10. › Myocyte is muscle cell
› Sarcomlemma is a thin membrane that
encloses striated muscle fibers and
electrochemical gradients
› Intercellular Na is maintained at 10 mEq/L by
active transport
› Interior of cell is negatively charged and can
pull Na to interior for Ca exchange
(Khan, 2009)
11. › Low levels of intracellular Ca allows for
increased actin-myosin muscle
contraction
› Na/K-ATPase pump and Ca-ATPase
pump
› Every electrochemical pump requires
ATP
› ATP depletion = Pump dysfunction
resulting in rhabdomyolysis
12. › Destruction of myocytes
› Dysfunction of the electrochemical
pumps located in the sacrolemma
membrane
› Altered ATP = Na in cytoplasm =
intracellular Ca
› Proteases and phospholipases activate
= destruction of myofibrillar cytoskeletal
membrane proteins
(Bosch, 2009 and Khan 2009)
13. › Muscle cell breaks down, K, aldolase,
phosphorus, myoglobin, creatine
kinase, lactate dehydrogenase, urate,
apsertate dehydrogenase are released
into circulation
› >100 g of muscle breaks down -
myoglobin releases into the circulation
› myoglobin leads to renal tubular
obstruction, nephrotoxicity, and ARF
(Khan, 2009)
14. › Muscle damage can increase from 2-12
hrs after injury
› Peak values at 24-72 hrs
› Creatine Kinase (CK) 5 x normal value is
accepted for dx
› Myoglobin might become visible in the
urine
15. › Hypovolaemia: fluid into necrotic
muscle
› Compartment syndrome: ischemia and
swelling
› Hepatic dysfunction
› Lactic acidosis
› Acute Renal Failure ~ 33% of
rhabdomyolysis
16. › Depends on underlying cause
› If treated early and aggressively, good
prognosis
› 80% have recovered renal function
› 1,500 die of rhabdomyolysis per year
17. › Pt initial diagnosis was heat exhaustion
with cramps, then later the primary
diagnosis changed to Rhabdomyolysis
with Acute Renal Failure
› Pt was hospitalized for 10 days
› Pt expressed a lack of understanding
related to his condition
18. › Pt experienced exertional
rhabdomyolysis after playing a soccer
tournament
22. › Facilitates rehydration
› Sustains the thirst drive
› Promotes retention of fluids
› More rapidly restores lost plasma
volume during rehydration
23. › Water intoxication
› < 135 mEq/L of sodium in the blood
› Excessive water intake
› Osmotic imbalance
24. › Acute Renal Failure: abrupt decrease in
renal function sufficient enough to result
in retention of nitrogenous waste and
disrupt fluid and electrolyte homeostasis
(Anderson, 2009)
25. › Exercise Associated Hyponatremia (EAH)
› Facilitates rhabdomyolysis through
changes in intracellular K or Ca
concentration resulting in hypotonic cell
swelling
› Lysis from exertion and thermal strain =
spacing of fluids = AVP secretion and
facilitates EAH
(Bruso, 2010)
26. › Higher average energy deficit = higher
body fat percentage
› rate of protein catabolism
› ↓ immune function
(Deutz et al, 2000 and Maughan, 2002)
27. › Oxidation of fat and CHO for energy
› Body stores of CHO are relatively low
› Glycogen stores deplete during
strenuous exercise
› CHO not replenished = decrements in
training response
(Maughan, 2002)
28. › Low-CHO diet = difficulty in sport
performance compared to high-CHO
diet
› Low-CHO diet risk of injury and
susceptibility to minor infections
› High-CHO might be difficult to achieve
due to daily practicalities of most
athletes
(Maughan, 2002)
29. › risk of opportunistic infections
› Damaged tissues caused by free
radicals after exercise can lead to
incomplete recovery
(Maughan, 2002)
30. › Adequate dietary CHO before exercise
and regular CHO ingestion during
exercise to minimize stress hormones
that have negative effect on immunity
› Maintaining adequate dietary CHO
intake is a priority
(Maughan, 2002)
