musculoskeletal disorders part 3 muscular disorders

8/2/2019 Musculoskeletal Disorders Part 3 Muscular Disorders

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Maria Carmela L. Domocmat, RN,MSNInstructor, Curative and Rehabilitative Nursing CareManagement II

School of NursingNorthern Luzon Adventist CollegeArtacho, Sison, Pangasinan


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Part 1: Degenerative & Metabolic bonedisorders:

Part 2: Bone infections

Part 3: Muscular disordersPart 3: Muscular disordersPart 3: Muscular disordersPart 3: Muscular disorders

RhabdomyolysisRhabdomyolysisRhabdomyolysisRhabdomyolysis

Part 4: Disorders of the hand

Part 5: Spinal column deformities

Part 6 : Disorders of foot

Part 7: Sports Injuries

3/5/2012Maria Carmela L. Domocmat, RN,

MSN 2


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MSN 3


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The word "dystrophy" comes originally from theGreek "dys," which means "difficult" or "faulty,"

and "trophe," meaning "nourishment." This word was chosen many years ago because it

was at first believed that poor nourishment of the

dystrophy. Today we know that muscle wasting in the

disorder is caused by defective genes rather than

poor nutrition.


MSN 4

http://www.humanillnesses.com/original/Men-Os/Muscular-Dystrophy.html


5/112

refers to a group of more than 30 inheriteddiseases that cause muscle weakness and muscle

loss. Some forms of MD appear in infancy or

childhood, while others may not appear until.

The different muscular dystrophies vary in whothey affect and the symptoms.

All forms of MD grow worse as the person's

muscles get weaker. Most people with MD eventually lose the ability to

walk.


MSN 5

http://www.nlm.nih.gov/medlineplus/musculardystrophy.html


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MSN 6

http://www.humanillnesses.com/original/images/hdc_0001_0002_0_img0181.jpg


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characterized by progressive weakness anddegeneration

of the skeletal muscles that control movement.

Some forms seen in infancy or childhood-others may not appear until middle a e or later.

differ in terms of the distribution and extent of muscle weakness

(some forms of MD also affect cardiac muscle)

age of onset

rate of progression, and

pattern of inheritance


MSN 7

http://www.ninds.nih.gov/disorders/md/md.htm


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are a group of inheritedconditions

caused by incorrect ormissing genetic informationthat prevents the body frommaking the proteins needed

healthy muscles. Many cases of MD occur

from spontaneous mutationsthat are not found in thegenes of either parent, andthis defect can be passed tothe next generation.


MSN 8

http://pathologyproject.wordpress.com/2011/04/24/muscular-dystrophy/


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is a general term for a group of inheriteddiseases involving a defective gene.

Each form of muscular dystrophy is caused bya genetic mutation that's particular to that

.

The most common types of musculardystrophy appear to be due to a geneticdeficiency of the muscle protein dystrophin


MSN 9

http://www.mayoclinic.com/health/muscular-dystrophy/DS00200/DSECTION=symptoms


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Duchenne's and Becker's musculardystrophies - passed from mother to son

through one of the mother's genes in apattern called X-linked recessive inheritance.

Boys inherit an X chromosome from their

mothers and a Y chromosome from theirfathers. The X-Y combination makes themmale. Girls inherit two X chromosomes, onefrom their mothers and one from their

fathers. The X-X combination determines thatthey are female.


MSN 10



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The defective gene that causes Duchenne'sand Becker's muscular dystrophies is locatedon the X-chromosome.

Women who have only one X-chromosome

muscular dystrophies are carriers andsometimes develop heart muscle problems(cardiomyopathy) and mild muscle weakness.


MSN 11



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The disease can skip a generation untilanother son inherits the defective gene onthe X-chromosome.

In some cases of Duchenne's and Becker's,

a new mutation in a gene rather than from aninherited defective gene.


MSN 12



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Women can pass down X-linked recessive disorderssuch as Duchenne's

muscular dystrophy. A woman who is a carrier

of an X-linked recessivedisorder has a 25 percent

unaffected son, a 25percent chance of havingan affected son, a 25percent chance of havingan unaffected daughter

and a 25 percent chanceof having a daughter whoalso is a carrier.


MSN 13

http://www.mayoclinic.com/health/medical/IM02723


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MyotonicMyotonicMyotonicMyotonic dystrophydystrophydystrophydystrophy and most MFMs -passedalong in a pattern called autosomal dominantautosomal dominantautosomal dominantautosomal dominantinheritanceinheritanceinheritanceinheritance.

If either parent carries the defective gene for',

chance the disorder will be passed along to achild.


MSN 14



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Some of the less common types of musculardystrophy are passed along in the sameinheritance pattern that marks Duchenne'sand Becker's muscular dystrophies.

passed on from generation to generation andaffect males and females equally. Still othersrequire a defective gene from both parents.


MSN 15



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In an autosomal dominantdisorder, the mutated gene isa dominant gene located on

one of the nonsexchromosomes (autosomes).You need only one mutatedgene to be affected by thistype of disorder. A person

disorder in this case, thefather has a 50 percentchance of having an affectedchild with one mutated gene(dominant gene) and a 50percent chance of having anunaffected child with twonormal genes (recessivegenes).


MSN 16

http://www.mayoclinic.com/health/medical/IM00991


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most common form of MD

primarily affects boys.

caused by the absence of dystrophin, aprotein involved in maintaining the integrity of muscle.

Progresses rapidly. Most boys are unable to walk by age 12, and later need a

respirator to breathe.

Girls in these families have a 50percent chance ofinheriting

and passing the defective gene to their children.


MSN 17



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a group of genetic disorders that affect the use ofmuscles in the body.

inherited as an X-linked disorder. This is whyDuchenne MD primarily affects boys. Girls can inheritthe gene for DMD but not have any symptoms of thedisease.

,

births. There are thousands of new cases every year. affects children of all ethnic backgrounds. causes an absence of dystrophin, a protein that helps

keep muscle cells intact. This means that muscle cells are easily damaged and

become weak over time.


MSN 18

http://www.checkorphan.org/grid/iwishes/duchenne-muscular-dystrophy


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MSN 19

http://www.checkorphan.org/grid/iwishes/duchenne-muscular-dystrophy


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MSN 20

http://trialx.com/curetalk/wp-content/blogs.dir/7/files/2011/05/diseases/Muscular_Dystrophy_Duchenne-3.jpg


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similar to Duchenne but the symptoms aremilder and can appear till 25 years of age.

Boys with BeckerBeckerBeckerBecker MD have faulty or not enough dystrophi

life and are also able to walk but they havesome heart problems and is present only inmales.


MSN 21

http://healthmedcare.com/muscular-dystrophy-types-symptoms-of-each-form/



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usually begins in the teenage years. causes progressive weakness in muscles of th

eface, arms, legs, and around the shoulders and chest.

affects both males and femalesprogresses slowly and can vary in symptoms from mild to disabling.

about half of the sufferers are able to walkthroughout their life and almost all thepatients live a normal life span.


MSN 22




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Also known as LandouzyLandouzyLandouzyLandouzy----DejerineDejerineDejerineDejerine dystrophydystrophydystrophydystrophy

involves progressive muscle weaknessinvolving: Face

Abdomen Feet

Upper arms

Pelvic area Lower arms


MSN 23



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When someone with facioscapulohumeral MDraises his or her arms, the shoulder bladesmay stick out like wings. Progression of thisform is slow, with some spurts of rapidly

.

during the teen to early adult years.


MSN 24



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Aka: Steinerts disease the disorder's most common adult form

produces stiffness of muscles and an inability torelax muscles at will (myotonia), as well as themuscle weakness of the other forms of musculardystrophy.

typified by prolonged muscle spasms, cataracts,cardiac abnormalities, and endocrine disturbances.

Individuals with myotonic MD have

long, thin faces drooping eyelids a swan-like neck


MSN 25




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CauseCauseCauseCause A repeated section of DNA on either chromosome

19 or chromosome 3.

OnsetOnsetOnsetOnset Con enital form a ears at birth.

More common form may begin in teen or adultyears.


MSN 26

http://www.mda.org/disease/dm.html


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MSN 27

http://www.websters-online-

dictionary.org/images/wiki/wikipedia/commons/thumb/e/e1/Autodominant.jpg/180px-Autodominant.jpg

http://www.websters-online-dictionary.org/images/wiki/wikipedia/commons/thumb/e/e1/Autodominant.jpg/180px-Autodominant.jpg


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SymptomsSymptomsSymptomsSymptoms Generalized weakness and muscle wasting first

affecting the face, lower legs, forearms, hands andneck, with delayed relaxation of muscles aftercontraction common.

system, vision, heart or respiration. Learning disabilities occur in some cases. Congenital myotonic dystrophy is the more severe

form.

Men with myotonic muscular dystrophy havebaldness on their foreheads.


MSN 28



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ProgressionProgressionProgressionProgression Progression is slow, sometimes spanning 50 to 60

years.

InheritanceInheritanceInheritanceInheritance Autosomal dominant the disease ma be inherited

through either the father or the mother.


MSN 29



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MSN 30http://blog.thirdeyehealth.com/images/muscular-dystrophy-1.jpg


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The other major types of muscular dystrophyinclude: Limb-girdle muscular dystrophy

Congenital muscular dystrophy

Oculo har n eal muscular d stro h

Distal muscular dystrophy Emery-Dreifuss muscular dystrophy

Myofibrillar myopathies


MSN 31



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the type which affects from teenage years toadulthood

is present in both males and females.

As the name indicates, in this type the

and then reaches to the shoulders ( pectoralpectoralpectoralpectoralgirdlegirdlegirdlegirdle ) and later legs and arms are alsoaffected,

sufferers are unable to walk and mostpatients live past mid adulthood.


MSN 32



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the form which is present at the time of birth

rare

cause the loss of muscles

The term "congenital muscular dystrophy"re ers o a group o n er e muscu ardystrophies. Signs of these disorders mayinclude: General muscle weakness

Joint deformities


MSN 33




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is apparent at birth or becomes evidentbefore age 2.

The course of this disorder variessignificantly depending on the type.

cause only mild disability, while others progressrapidly and cause severe impairment.


MSN 34



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Signs in infants may include: Severe muscle weakness

Difficulty sucking and swallowing Difficulty breathing

Co nitive im airment


MSN 35



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affects primarily the muscles of eyes andthroat which occur around 40s to onward

ages symptoms include the weakness of eyes and

dysphagia - predisposes the patients topneumonia and choking.


MSN 36



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The first sign of this type of musculardystrophy is usually drooping of the eyelids

followed by weakness of the muscles of theeye, face and throat, resulting in difficulty

. .

Signs and symptoms first appear inadulthood, usually in a person's 40s or 50s.


MSN 37



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very rare

mildest

affects the muscles of fore arms to hands andmuscles of lower legs to feet

very s ow y progress ng

not very severe


MSN 38



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This group involves the muscles farthest awayfrom the center of the body (distal muscles)

those of the hands, forearms, feet andlower legs. The severity is generally less than

,

progress slowly. Distal MD generally begins inadulthood between the ages of 40 and 60.


MSN 39



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the type which affects from childhood to teenyears

present only in the males

affects the muscles of pectoral region to

with that patients have extreme heartextreme heartextreme heartextreme heartproblemsproblemsproblemsproblems that are usually fatal.

This is the type which also affects the carriers

(females) but the symptoms are not verysevere.


MSN 40



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This form of muscular dystrophy usuallybegins in the muscles of the: Shoulders Upper arms

Shins

Cardiac arrhythmias, stiffness of the spineand muscle contractures are other features ofEmery-Dreifuss MD. Emery-Dreifuss MD

usually begins in the childhood to early teenyears and progresses slowly.


MSN 41



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Though in some cases the MFMs affect onlythe muscles closest to the center of the body

(proximal muscles) such as the shoulderand hip muscles the distal muscles also are

.

disorders also is commonly associated with: Stiffness of the spine

Muscle contractures

Nerve damage (peripheral neuropathy) Thickening and stiffening of the heart muscle

(cardiomyopathy)


MSN 42



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MSN 43



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Progressive muscular weakness

Delayed meeting of motor milestones

Waddling gait Walking on toes

Frequent falls

Gowers signGowers signGowers signGowers sign Hyperthrophied calf muscles

Poor balance

Scoliosis of the spine

Fracture of long bones Inability to walk (late stages)


MSN 44


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Waddling gait, a distinctive ducklike walk, is animportant sign of muscular dystrophy, spinal

muscle atrophy or, rarely, congenital hipdisplacement.

The ait results from deterioration of the pelvic

girdle musclesprimarily the gluteus medius, hipflexors, and hip extensors. Weakness in thesemuscles hinders stabilization of the weight-bearing hip during walking, causing the opposite

hip to drop and the trunk to lean toward that sidein an attempt to maintain balance.


MSN 45

http://www.wrongdiagnosis.com/bookimages/8/2591.1.png


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Typically, the legs assume a wide stance andthe trunk is thrown back to further improve

stability, exaggerating lordosis andabdominal protrusion. In severe cases, leg

equinovarus deformity of the foot combinedwith circumduction or bowing of the legs.


MSN 46

http://www.wrongdiagnosis.com/bookimages/8/2591.1.png


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With Duchenne's musculardystrophy, waddling gait becomes clinically

evident between ages 3 and 5. The gaitworsens as the disease progresses, until the

use of a wheelchair, usually between ages 10and 12. Early signs are usually subtle: a delayin learning to walk, frequent falls, gait or

posture abnormalities, and intermittent calfpain


MSN 47

http://www.wrongdiagnosis.com/symptoms/walking_symptoms/book-causes-16g.htm


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With Becker's muscular dystrophy, waddlinggait typically becomes apparent in late

adolescence, slowly worsens during the thirddecade, and culminates in total loss ofambulation. Muscle weakness first appears int e pe v c an upper arm musc es.Progressive wasting with selected musclehypertrophy produces lordosis withabdominal protrusion, poor balance, a

positive Gowers'sign and, possibly, mentalretardation.


MSN 48



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With facioscapulohumeral musculardystrophy, which usually occurs late in

childhood and during adolescence, waddlinggait appears after muscle wasting has spread

to the pelvic girdle and legs. Earlier effectsinclude progressive weakness and atrophy offacial, shoulder, and arm muscles; slight

lordosis; and pelvic instability.


MSN 49



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to stand, affected children press their handsagainst their ankles, knees and thighs


MSN 50


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MSN 51


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Morbidity and mortality rates depend on thetype of congenital muscular dystrophy.

Its incidence varies, as some forms are morecommon than others.

3300 live male births.


MSN 52



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Myotonic muscular dystrophy is the mostfrequent form of muscular dystrophy among

adults. Its prevalence is estimated at one casefor every 10,000 people in most countries.

,

the Charlevoix and Saguenay-Lac-St-Jeanregions, where one person out of 500 isestimated to carry the disease.


MSN 53



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Careful review of family's history of muscledisease

medical history review and physical examination Blood testsBlood testsBlood testsBlood tests

Dama ed muscles release enz mes such as creatinekinase (CK), into blood. High blood levels of CK suggesta muscle disease, such as muscular dystrophy.

ElectromyographyElectromyographyElectromyographyElectromyography

UltrasonographyUltrasonographyUltrasonographyUltrasonography

Muscle biopsyMuscle biopsyMuscle biopsyMuscle biopsy


MSN 54

http://www.mayoclinic.com/health/muscular-dystrophy/DS00200/DSECTION=treatments-and-drugs


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Genetic testing.Genetic testing.Genetic testing.Genetic testing. Blood samples are examined for mutations in some of

the genes that cause different types of muscular

dystrophy. For Duchenne's and Becker's muscular dystrophies,

standard tests examine just the portions of thedystrophindystrophindystrophindystrophin genegenegenegene responsible for most cases of thesetypes of MD. These tests identify deletions or

duplications on the dystrophin gene in more than two-thirds of people with Duchenne's and Becker's MDs. The genetic defects responsible for Duchenne's and

Becker's muscular dystrophies are harder to identify inother cases of those affected, but new tests that

examine the entire dystrophin gene are making itpossible to pinpoint tiny, less common mutations.


MSN 55



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There is no cure for muscular dystrophyno cure for muscular dystrophyno cure for muscular dystrophyno cure for muscular dystrophy.

Current treatment is designed to help prevent

or reduce deformities in the joints and thespine and to allow people with MD to remain

.


MSN 56



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Treatments include Physical and speech therapy

Orthopedic devices Surgery Medications

ome peop e w muscu ar ys rop y ave

mild cases that worsen slowly. Other casesare disabling and severe.

Research into gene therapy may eventually

provide treatment to stop the progression ofsome types of muscular dystrophy.


MSN 57



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As muscular dystrophy progresses and musclesweaken, fixations (contractures) can develop in

joints. Tendons can shorten, restricting the flexibility

and mobility of joints. Contractures are uncomfortable and may affect

the joints of your hands, feet, elbows, knees and

hips. One goal of physical therapy is to provide regular

range-of-motion exercises to keep joints asflexible as possible, delaying the progression of

contractures, and reducing or delaying curvatureof your spine. Using hot baths (hydrotherapy)also can help maintain range of motion in joints.


MSN 58



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In some cases, doctors may prescribemedications to slow the progression and

manage signs and symptoms of musculardystrophy: ,,,,

((((myotoniamyotoniamyotoniamyotonia).).).).Medications that may be used to helpmanage myotonia associated with MD includemexiletine (Mexitil), phenytoin (Dilantin, Phenytek),baclofen (Lioresal), dantrolene (Dantrium) and

carbamazepine (Tegretol, Carbatrol).


MSN 59



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Muscle deterioration.Muscle deterioration.Muscle deterioration.Muscle deterioration. The anti-inflammatorycorticosteroid medication prednisone may help

improve muscle strength and delay the progressionof Duchenne's MD. The immunosuppressive drugscyclosporin and azathioprine also are sometimes

cells.


MSN 60



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Assistive devicesAssistive devicesAssistive devicesAssistive devicesBraces can both provide support for

weakened muscles of your hands and lowerlegs and help keep muscles and tendons

,

progression of contractures. Other devices,such as canes, walkers and wheelchairs, canhelp maintain mobility and independence. If

respiratory muscles become weakened, usinga ventilator may become necessary.


MSN 61



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SurgerySurgerySurgerySurgeryTo release the contractures that may develop

and that can position joints in painful ways,doctors can perform a tendon release

.

of your hip and knee and on the Achillestendon at the back of your foot. Surgery mayalso be needed to correct curvature of the

spine.


MSN 62



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Other treatmentsOther treatmentsOther treatmentsOther treatmentsBecause respiratory infections may become a

problem in later stages of musculardystrophy, it's important to be vaccinated for

influenza shots.


MSN 63



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Perform passive and active muscle-stretchingexercises to the arms and legs.

Encourage the patient to walk at least 3 hourseach day (with leg braces, if necessary) to

,

contractures, and delay further gaitdeterioration, if possible.


MSN 64



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Stay near the patient during ambulation, toprovide support if necessary.

Provide a balanced diet to maintain energylevels and prevent obesity.

with muscular dystrophy and spinal muscleatrophy, provide emotional support for thepatient and his family.


MSN 65



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Caution the patient about long, unbrokenperiods of bed rest, which accelerate muscle

deterioration. Refer the patient to a local Muscular

, .

Suggest genetic counseling for parents, ifthey're considering having more children.


MSN 66



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On the cover: AndyVladimir, of CoconutGrove, Fla., had MMDand used a wheelchair,but that barely slowed

businessman, textbookauthor, world travelerand travel writer,including for MDA's

Quest magazine, Andylived to age 76.


MSN 67


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http://www.mdausa.org/

http://www.mayoclinic.com/health/muscular

-dystrophy/DS00200/DSECTION=treatments-

-


MSN 68


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MSN 69


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a condition that may occur when muscletissue is damaged due to an injury in which

muscle in the body is damaged rhabdomyo=skeletal muscle + lysis= rapid


MSN 70

http://www.emedicinehealth.com/rhabdomyolysis/page2_em.htm


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There are a three of types of muscle in thebody, including:

skeletal muscles that move the body; cardiac muscle located in the heart; and

smooth muscle that lines blood vesselsgastrointestinal tract, bronchi in the lung, and thebladder and uterus. This type of muscle is notunder conscious control.

Rhabdomyolysis occurs when there is damage

to the skeletal muscle.


MSN 71



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is the breakdown of muscle fibers withleakage of potentially toxic cellular contents

into the systemic circulation. The final common pathway of rhabdomyolysis

homeostasis

3/5/2012Maria Carmela L. Domocmat, RN,MSN 72


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The injured muscle cell leaks myoglobin (aprotein) into the blood stream.

Myoglobin can be directly toxic to kidneycells, and it can impair and clog the filtration

.

Both mechanisms can lead to kidneyfailure (the major complication ofrhabdomyolysis).


http://www.emedicinehealth.com/rhabdomyolysis/page2_

em.htm


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Significant muscle injury can cause fluidand electrolyte shifts from the bloodstream

into the damaged muscle cells, and in theother direction (from the damaged musclecells into the bloodstream).

As a result, dehydration may occur. Elevated

levels of potassium in the bloodstream(hyperkalemia) may be associated with heartrhythm disturbances and sudden cardiac

death due to ventriculartachycardia and ventricular fibrillation.


http://www.emedicinehealth.com/rhabdomyolysis/page2_

em.htm


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When muscles are damaged, especially due toa crush injury, swelling within the muscle can

occur, causing compartment syndrome. If this occurs in an area where the muscle is

membrane), the pressure inside the musclecompartment can increase to the point atwhich blood supply to the muscle is

compromised and muscle cells begin to die.


Medscpae


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Rhabdomyolysis was first appreciated as asignificant complication from crush and blast

injuries sustained in a volcano eruption inItaly, in 1908.

and second World Wars help furtherunderstand the relationship between massivemuscle damage and kidney failure.


Medscpae


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United StatesUnited StatesUnited StatesUnited States Rhabdomyolysis accounts for an estimated 8-15%

of cases of acute renal failure.



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When muscle is damaged myoglobin (protein pigment) - released into the

bloodstream and filtered out of the body by thekidneys.

Myoglobin breaks down into potentially harmfulcompounds.

It may block the structures of the kidney, causingdamage such as acute tubular necrosis or kidneyfailure.



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Dead muscle tissue may cause a largeamount of fluid to move from the blood into

the muscle, reducing the fluid volume of thebody and leading to shock and reduced blood

.

The disorder may be caused by any conditionthat results in damage to skeletal muscle,especially trauma.



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The etiologies may be subdivided into Traumatic

exercise induced toxicologic

Environmental

Metabolic

Infectious

Immunologic

inherited classifications


http://emedicine.medscape.com/article/827738-clinical#showall


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Major blunt trauma and crush injury

Electrocution

Lightening strikes Major burns

Excessive exercise, or examp e, running a

marathon or excessive weight lifting Patients in status epilepticus, in which

the seizure lasts for a prolonged period of

time and muscles involuntarily contract




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Prolonged immobilization patients who have been lying in one position for a

prolonged period of time due to adebilitating stroke, alcohol or drug overdose,

or those who have remained unconscious for aprolonged period of time for other reasons

The weight of the body is enough to crush themuscles that are pushed up against a hard surfacesuch as the floor.




83/112

Dystonic reactions cause muscles to spasm,and if left untreated can damage muscle

Cholesterol lowering medications [forexample, statins prescribed to treat highcholesterol (particularly when combined withother cholesterol lowering medications such

as fibrates) Antidepressant medications

[for example selective serotonin reuptake inhibitors(SSRIs) antidepressants may cause a serotoninsyndrome characterized by agitation, fever, andmuscle spasm]


MSN 83



84/112

Some anesthetics can cause malignanthyperthermia syndrome with high fever and

muscle rigidity A variety of drugs of abuse [for

, , ,

(PCP), and amphetamines] Hyperthermia and hypothermia (high and low

body temperature, respectively)


MSN 84



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Complications from a variety of infectionscaused by bacteria, viruses, and fungi

Association with other diseases such as sicklecell disease, polymyositis,

Complications from the venom from snakebites and black widow spider bites


MSN 85



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Alcoholism (with subsequent muscle tremors)

Certain inherited or genetic syndromes

Crush Injuries Heat intolerance

Heatstro e

Ischemia or necrosis of the muscles (as mayoccur with arterial occlusion, deep venousthrombosis, or other conditions)


MSN 86


87/112

Low phosphate levels

Seizures

Severe exertion such as marathon running orcalisthenics

a ng c s

Trauma Use or overdose of drugs, especially cocaine,

amphetamines, statins, heroin, or PCP


MSN 87


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Melli et al reviewed 475 patients withrhabdomyolysis hospitalized at Johns

Hopkins Hospital and found that the mostcommon risk factors were exogenous toxinsexogenous toxinsexogenous toxinsexogenous toxins,

illicit drugs, alcohol, and prescription medicationsresponsible in 46% of patients.


MSN 88



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Abnormal urine color (dark, red, or colacolored)

General weakness Muscle stiffness or aching (myalgia)

usc e en erness

Weakness of the affected muscles


MSN 89


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Additional symptoms that may be associatedwith this disease include the following:

Fatigue Joint pain

Seizures

Weight gain (unintentional)


MSN 90


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An examination reveals tender or damagedskeletal muscles.

CPK is very high. Serum myoglobin test is positive.

Serum otassium ma be ver hi h

Urinalysis may reveal casts and be positivefor hemoglobin without evidence of red blood cellson microscopic examination.

Urine myoglobin test is positive.


MSN 91


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This disease may also alter the results of thefollowing tests:

CPK isoenzymes Urine creatinine

Serum creatinine

3/5/2012

Maria Carmela L. Domocmat, RN,

MSN 92


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Vigorous hydration with isotonic crystalloidVigorous hydration with isotonic crystalloidVigorous hydration with isotonic crystalloidVigorous hydration with isotonic crystalloid the cornerstone of therapy for rhabdomyolysis.

Support of the intravascular volume increases theglomerular filtration rate (GFR) and oxygen deliveryand dilutes myoglobin and other renal tubulartoxins.

Immediately obtain intravenous access with a large-bore catheter.

Administer isotonic crystalloid 500 mL/h and thentitrate to maintain a urine output of 200-300 mL/h.

3/5/2012


MSN 93



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Because injured myocytes can sequester largevolumes of extracellular fluid, crystalloid

requirements may be surprisingly large.

3/5/2012


MSN 94



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Assess ABCs and support as needed.

Treat any underlying conditions, such as

trauma, infection, or toxins. General recommendations for the treatment

fluid resuscitation prevention of end-organ complications

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MSN 95



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Patients with CK elevation in excess of 2-3 timesthe reference range, appropriate clinical history,and risk factors should be suspected of having

rhabdomyolysis. Administer isotonic crystalloid 500 mL/h and

titrate to maintain a urine output of 200-300m .

Consider central venous pressures or Swan-Ganzcatheterization in patients with cardiac or renaldisease. These invasive studies can assist in the assessment of

the intravascular volume.

Repeat CK assay every 6-12 hours in order todetermine peak CK level.

3/5/2012


MSN 96



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Acute renal failureAcute renal failureAcute renal failureAcute renal failure develops in 30-40% ofpatients with rhabdomyolysis.

Suggested mechanisms include precipitation of myoglobin and uric acid crystals

decreased glomerular perfusion, and

the nephrotoxic effect of ferrihemate (formed upondissociation of myoglobin in the acidic environmentof the renal parenchyma). I

To prevent renal failure, many authorities advocateurine alkalinizationalkalinizationalkalinizationalkalinization, mannitol, and loop diuretics, mannitol, and loop diuretics, mannitol, and loop diuretics, mannitol, and loop diuretics.

3/5/2012


MSN 97

http://emedicine.medscape.com/article/827738-

clinical#showall


98/112

UrinaryUrinaryUrinaryUrinary alkalinizationalkalinizationalkalinizationalkalinization recommended for patients with rhabdomyolysis and

CK levels in excess of 6000 IU/L. should be considered earlier in patients with

acidemia, dehydration, or underlying renal disease..

ampule of sodium bicarbonate administered at 100

mL/h and titrated to a urine pH higher than 7. After establishing an adequate intravascular

volume, mannitol may be administered to enhancerenal perfusion. Loop diuretics may be used to

enhance urinary output in oliguric patients, despiteadequate intravascular volume.

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MSN 98



99/112

Treatment of hyperkalemiahyperkalemiahyperkalemiahyperkalemia consists of intravenous sodium bicarbonate, glucose, and

insulin; oral or rectal sodium polystyrene sulfonate

(Kayexalate); and

hemodialysis.

Administer intravenous calcium chloride forpatients who are hemodynamically compromisedand hyperkalemic.

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MSN 99


d f


100/112

HypocalcemiaHypocalcemiaHypocalcemiaHypocalcemia is noted early in the course ofrhabdomyolysis and generally is not of clinicalsignificance. Calcium supplementation is not recommended.

Compartment syndromeCompartment syndromeCompartment syndromeCompartment syndrome

fasciotomy.

DICDICDICDIC fresh frozen plasma, cryoprecipitate, and platelet

transfusions.

Hyperuricemia and hyperphosphatemiaHyperuricemia and hyperphosphatemiaHyperuricemia and hyperphosphatemiaHyperuricemia and hyperphosphatemia rarely are of clinical significance and rarely require

treatment.

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MSN

10

0



101/112

Medical therapy for rhabdomyolysis focuseson

restoring adequate intravascular volume usingisotonic crystalloid.

Adjunctive measures that may decrease theincidence of acute myoglobinuric renal failure

include urinary alkalinization and osmotic and loopdiuresis.

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MSN

10

1


llll


102/112

Class SummaryClass SummaryClass SummaryClass Summary Sodium bicarbonate is administered IV to alkalinize

urine in patients with rhabdomyolysis. This mayprevent toxicity caused by the presence ofmyoglobin in acidic urine and crystallization of uricaci .

Sodium bicarbonate (Sodium bicarbonate (Sodium bicarbonate (Sodium bicarbonate (NeutNeutNeutNeut)))) Useful in alkalization of urine to prevent acute

myoglobinuric renal failure. Titrate dose to increasepH to >7.

3/5/2012


MSN

10

2


Class SummaryClass SummaryClass SummaryClass Summary


103/112

Class SummaryClass SummaryClass SummaryClass Summary These agents increase osmolarity of glomerular filtrate

and induce diuresis. They hinder tubular reabsorption ofwater, causing sodium and chloride excretion toincrease.

Mannitol (Mannitol (Mannitol (Mannitol (OsmitrolOsmitrolOsmitrolOsmitrol))))

inadequate despite aggressive fluid therapy.

Initially assess for adequate renal function in adults byadministering a test dose of 200 mg/kg IV over 3-5 min.Should produce a urine flow of at least 30-50 mL/h over2-3 h.

In children, assess for adequate renal function by

administering a test dose of 200 mg/kg IV over 3-5 min.It should produce a urine flow of at least 1 mL/h over 1-3 h.

3/5/2012


MSN

10

3


Class S mmarCl SCl SClass S mmar


104/112

Class SummaryClass SummaryClass SummaryClass Summary These agents elicit a loss of free water, increasing

diuresis.

Furosemide (Lasix)Furosemide (Lasix)Furosemide (Lasix)Furosemide (Lasix) Increases water excretion by interfering with the

- ,inhibition of sodium and chloride reabsorption inthe ascending loop of Henle and distal renal tubule.

Individualize doses. Depending on response,administer at increments of 20-40 mg q6-8h untildesired diuresis occurs. When treating infants,titrate with 1-mg/kg/dose increments until asatisfactory effect is achieved

3/5/2012


MSN

10

4


continued volume support and urinarycontinued volume support and urinarycontinued volume support and urinarycontinued volume support and urinary


105/112

continued volume support and urinarycontinued volume support and urinarycontinued volume support and urinarycontinued volume support and urinaryalkalinizationalkalinizationalkalinizationalkalinization

Obtain serial CK measurementsCK measurementsCK measurementsCK measurements to verify thatvalues have peaked and are returning toreference range.

Serial physical examinations and laboratory

studies are indicated to monitor for compartment syndrome Hyperkalemia acute oliguric or nonoliguric renal failure DIC

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MSN

10

5


In patients with no apparent precipitating


106/112

In patients with no apparent precipitatingfactors for rhabdomyolysis

consider inherited disorders of carbohydrate orlipid metabolism and myopathies.

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MSN

10

6


Death from hyperkalemia or renal failure


107/112

Death from hyperkalemia or renal failure

Compartment syndrome

Disseminated intravascular coagulation (DIC) Hepatic insufficiency

Hypovo emia sequestration o p asma water

within injured myocytes)

3/5/2012


MSN

10

7


Hyperkalemia (release of cellular potassium


108/112

Hyperkalemia (release of cellular potassiuminto the systemic circulation)

Metabolic acidosis (release of cellularphosphate and sulfate)

Acute renal failure (nephrotoxic effects ofliberated myocyte components)

3/5/2012


MSN

10

8


The prognosis depends on the underlying


109/112

The prognosis depends on the underlyingetiology and any existing comorbidities.

Acute kidney failure occurs in many patients.

rea men soon a er r a omyo ys s eg ns

will reduce the risk of chronic kidney damage. People with milder cases may return to

normal activity within a few weeks to a month

or more. However, some continue to haveproblems with fatigue and muscle pain.

3/5/2012


MSN

10

9


Advise patients with rhabdomyolysis caused


110/112

Advise patients with rhabdomyolysis causedby hyperthermia and/or inordinate exertion

to exercise in moderation with carefulattention to hydration and external methods.

Advise patients with rhabdomyolysis relatedto ethanol, recreational drugs, or prescriptionmedications to discontinue use of theoffending agent and refer them to a

rehabilitation program.

3/5/2012


MSN

11

0


Drink plenty of fluids after strenuous exercise


111/112

Drink plenty of fluids after strenuous exerciseto dilute the urine and flush the myoglobin

out of the kidney. Proper hydration is also necessary after any

to skeletal muscle.

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MSN

11

1


112/112

musculoskeletal disorders part 3 muscular disorders

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