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)