Allison Kliewer December 19, 2012
Allison KliewerDecember 19, 2012
› Introduction
› Patient Profile
› Disease background
› Admission
› Nutrition Care Process
› Summary and Reflection
› Exertional rhabdomyolysis is a muscle injury the results in the lysis of skeletal muscle and the release of celllularcomponents 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)
› 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
› 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
› 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
› 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)
› Breakdown of skeletal muscle resulting in the release of intracellular contents
› Leakage of contents can become severe and life threatening
(Khan, 2009)
› Illicit drug use, alcohol abuse, muscle disease, trauma, seizures and immobility
› Sporadic strenuous exercise can cause exertional rhabdomyolysis
› Excess heat increases risk
› Hypokalemia
› Hyponatremia
› 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)
› Low levels of intracellular Ca allows for increased actin-myosin muscle contraction
› Na/K-ATPase pump and Ca-ATPasepump
› Every electrochemical pump requires ATP
› ATP depletion = Pump dysfunction resulting in rhabdomyolysis
› Destruction of myocytes
› Dysfunction of the electrochemical pumps located in the sacrolemmamembrane
› Altered ATP = Na in cytoplasm = intracellular Ca
› Proteases and phospholipases activate = destruction of myofibrillar cytoskeletalmembrane proteins
(Bosch, 2009 and Khan 2009)
› Muscle cell breaks down, K, aldolase, phosphorus, myoglobin, creatinekinase, 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)
› 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
› Hypovolaemia: fluid into necrotic muscle
› Compartment syndrome: ischemia and swelling
› Hepatic dysfunction
› Lactic acidosis
› Acute Renal Failure ~ 33% of rhabdomyolysis
› Depends on underlying cause
› If treated early and aggressively, good prognosis
› 80% have recovered renal function
› 1,500 die of rhabdomyolysis per year
› Pt initial diagnosis was heat exhaustion with cramps, then later the primary diagnosis changed to Rhabdomyolysiswith Acute Renal Failure
› Pt was hospitalized for 10 days
› Pt expressed a lack of understanding related to his condition
› Pt experienced exertionalrhabdomyolysis after playing a soccer tournament
› Weightlifting, sprinting, contact practices, noncontact practices, running and swimming
› Good physical shape
› Outside and in air conditioned environments
Total Daily Calories: 1,210
Sodium: 2,988
Fat: 61
Protein: 77
CHO: 76
Calories: 2,560 - 2,985
Sodium:
Fat:
Protein: 102 – 136g (1.2-1.6 g/kg)
CHO: 385 – 682g (4.5 –8 g/kg)
ESTIMATED DAILY NEEDS
Calories: 1,210
Sodium: 2,988
Fat: 61
Protein: 77g
CHO: 76g
ESTIMATED DAILY INTAKE
› Facilitates rehydration
› Sustains the thirst drive
› Promotes retention of fluids
› More rapidly restores lost plasma volume during rehydration
› Water intoxication
› < 135 mEq/L of sodium in the blood
› Excessive water intake
› Osmotic imbalance
› 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)
› 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)
› Higher average energy deficit = higher body fat percentage
› rate of protein catabolism
› ↓ immune function
(Deutz et al, 2000 and Maughan, 2002)
› 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)
› 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)
› risk of opportunistic infections
› Damaged tissues caused by free radicals after exercise can lead to incomplete recovery
(Maughan, 2002)
› 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)