Musculoskeletal disorders part 1

Musculoskeletal Disorders Part I

Maria Carmela L. Domocmat, RN,MSN
Instructor, Curative and Rehabilitative Nursing Care Management II
School of Nursing
Northern Luzon Adventist College
Artacho, Sison, Pangasinan

Overview
Part I Part II
Bone infections Degenerative bone disorders:
Osteomyelitis OA
Septic arthritis Metabolic bone disorders
Disorders of foot Osteoporosis
Hallux valgus (bunions) Paget’s dse
Morton’s neuroma (plantar Osteomalacia
neuroma) Gout and gouty arthritis
Hammer toe Spinal column deformities
Muscular disorders Scoliosis
Muscular dystrophy Kyphosis
Rhabdomyolysis Lordosis

2 Maria Carmela L. Domocmat, RN, MSN 8/24/2011

Bone infections
Osteomyelitis
Septic arthritis


Bone infections:
Osteomyelitis


Osteomyelitis
is an acute or chronic bone infection or inflammatory process
of the bone and its structures secondary to infection with
pyogenic organisms.


Osteomyelitis

Osteomyelitis is infection in the bones. Often, the
original site of infection is elsewhere in the body, and
spreads to the bone by the blood. Bacteria or fungus
6
may sometimes be responsible for osteomyelitis.
Maria Carmela L. Domocmat, RN, MSN 8/24/2011

Causes, incidence, and risk factors
Bone infection can be caused by bacteria (more common) or fungi
(less common).
Infection may spread to a bone from infected skin, muscles, or
tendons next to the bone, as in osteomyelitis that occurs under a
chronic skin ulcer (sore).
The infection that causes osteomyelitis can also start in another
part of the body and spread to the bone through the blood.
A current or past injury may have made the affected bone more
likely to develop the infection. A bone infection can also start after
bone surgery, especially if the surgery is done after an injury or if
metal rods or plates are placed in the bone.
In children, the long bones are usually affected. In adults, the feet,
spine bones (vertebrae), and the hips (pelvis) are most commonly
affected.


Risk factors
Diabetes
Hemodialysis
Injected drug use
Poor blood supply
Recent trauma
People who have had their spleen removed are also at higher
risk for osteomyelitis


Symptoms
Bone pain
Fever
General discomfort, uneasiness, or ill-feeling (malaise)
Local swelling, redness, and warmth
Other symptoms that may occur with this disease:
Chills
Excessive sweating
Low back pain
Swelling of the ankles, feet, and legs


Osteomyelitis
Osteomyelitis of diabetic Osteomyelitis of T10
foot secondary to streptococcal
disease.


Osteomyelitis
Osteomyelitis of the great Osteomyelitis of index
toe finger metacarpal head
secondary to clenched fist
injury


Osteomyelitis
Osteomyelitis of index Osteomyelitis of the elbow.
finger metacarpal head
secondary to clenched fist
injury.


Dx tests
A physical examination shows bone tenderness and possibly
swelling and redness.
Tests may include:
Blood cultures
Bone biopsy (which is then cultured)
Bone scan
Bone x-ray
Complete blood count (CBC)
C-reactive protein (CRP)
Erythrocyte sedimentation rate (ESR)
MRI of the bone
Needle aspiration of the area around affected bones


Dx tests
Diagnosis requires 2 of the 4 following criteria:
Purulent material on aspiration of affected bone
Positive findings of bone tissue or blood culture
Localized classic physical findings of bony tenderness, with
overlying soft-tissue erythema or edema
Positive radiological imaging study

http://emedicine.medscape.com/article/785020-treatment


Emergency Department Care
rarely requires emergent stabilization or resuscitation.
The primary challenge for ED physicians is considering the
appropriate diagnosis in the face of subtle signs or symptoms.
Treatment for osteomyelitis involves the following:
Initiation of intravenous antibiotics that penetrate bone and
joint cavities
Referral of the patient to an orthopedist or general surgeon
Possible medical infectious disease consultation



Select the appropriate antibiotics using direct culture results
in samples from the infected site, whenever possible.
Empiric therapy is often initiated on the basis of the patient's
age and the clinical presentation.
Empiric therapy should always include coverage for S
aureus and consideration of CA-MRSA.
Further surgical management may involve removal of the
nidus of infection, implantation of antibiotic beads or pumps,
hyperbaric oxygen therapy, or other modalities.



Treatment
goal of treatment
get rid of the infection
reduce damage to the bone and surrounding tissues.
Antibiotics are given to destroy the bacteria causing the
infection.
may receive more than one antibiotic at a time.
Often, the antibiotics are given through an IV (intravenously,
meaning through a vein) rather than by mouth.
Antibiotics are taken for at least 4 - 6 weeks, sometimes longer.


Treatment
Surgery
to remove dead bone tissue if have an infection that does not go away.
If there are metal plates near the infection, they may need to be
removed.
The open space left by the removed bone tissue may be filled
with bone graft or packing material that promotes the growth of new
bone tissue.
Infection of an orthopedic prosthesis, such as an artificial joint,
may need surgery to remove the prosthesis and infected tissue
around the area.
If have diabetes- need to be well controlled.
If problems with blood supply to the infected area, such as the
foot, surgery to improve blood flow may be needed.


Medication Summary
The primary treatment for osteomyelitis
is parenteral antibiotics that penetrate bone and joint cavities.
for at least 4-6 weeks.
After intravenous antibiotics are initiated on an inpatient basis,
therapy may be continued with intravenous or oral antibiotics,
depending on the type and location of the infection, on an
outpatient basis.


Medication Summary
The following are recommendations for the initiation of empiric
antibiotic treatment based on the age of the patient and
mechanism of infection:
hematogenous osteomyelitis (newborn to adult),
infectious agents include S aureus, Enterobacteriaceae organisms,
group A and BStreptococcus species, and H influenzae.
Primary treatment - combination of penicillinase-resistant
synthetic penicillin and a third-generation cephalosporin.
Alternate therapy - vancomycin or clindamycin and a third-
generation cephalosporin, particularly if methicillin-resistant S
aureus (MRSA)
Linezolid
ciprofloxacin and rifampin


Medication Summary
with sickle cell anemia and osteomyelitis
primary bacterial causes are S aureus and Salmonellae species.
primary choice for treatment - fluoroquinolone antibiotic
(not in children).
alternative choice - a third-generation cephalosporin (eg,
ceftriaxone)


Medication Summary

nail puncture through an athletic shoe
the infecting agents may include S aureus and Pseudomonas
aeruginosa.
primary antibiotics - ceftazidime or cefepime.
alternative treatment - Ciprofloxacin
osteomyelitis due to trauma
infecting agents include S aureus, coliform bacilli,
and Pseudomonas aeruginosa.
Primary antibiotics - nafcillin and ciprofloxacin.
Alternatives - vancomycin and a third-generation cephalosporin
with antipseudomonal activity.


Antibiotics
Nafcillin (Nafcil, Unipen)
Initial therapy for suspected penicillin G–resistant
streptococcal or staphylococcal infections.
Use parenteral therapy initially in severe infections. Change to
oral therapy as condition warrants.
Because of thrombophlebitis, particularly in elderly patients,
administer parenterally for only the short term (1-2 d).
Change to PO route as clinically indicated.
Note: Administer in combination with a third-generation
cephalosporin to treat osteomyelitis.
Do not admix with aminoglycosides for IV administration.


Antibiotics
Ceftriaxone (Rocephin)
Third-generation cephalosporin with broad-spectrum gram-
negative activity;
lower efficacy against gram-positive organisms;
higher efficacy against resistant organisms;
arrests bacterial growth by binding to one or more penicillin-
binding proteins.
Note: Administer with a penicillinase-resistant synthetic
penicillin, when treating osteomyelitis.


Antibiotics
Cefazolin (Ancef)
First-generation semisynthetic cephalosporin that arrests
bacterial cell wall synthesis, inhibiting bacterial growth;
primarily active against skin flora, including S aureus;
typically used alone for skin and skin-structure coverage.


Antibiotics
Ciprofloxacin (Cipro)
Fluoroquinolone with activity against pseudomonads,
streptococci, MRSA, Staphylococcus epidermidis, and most gram-
negative organisms,
but no activity against anaerobes.
Inhibits bacterial DNA synthesis and, consequently, growth.
Continue treatment for at least 2 d (typical treatment, 7-14 d)
after signs and symptoms disappear.


Antibiotics
Ceftazidime (Fortaz, Ceptaz)
Third-generation cephalosporin with broad-spectrum gram-
negative activity;
lower efficacy against gram-positive organisms;
higher efficacy against resistant organisms;
arrests bacterial growth by binding to one or more penicillin-
binding proteins.


Antibiotics
Clindamycin (Cleocin)
Lincosamide for the treatment of serious skin and soft-tissue
staphylococcal infections;
also effective against aerobic and anaerobic streptococci (except
enterococci);
inhibits bacterial growth, possibly by blocking dissociation of
peptidyl t-RNA from ribosomes, arresting RNA-dependent
protein synthesis.


Antibiotics
Vancomycin (Vancocin)
Potent antibiotic directed against gram-positive organisms and active
againstEnterococcus species. Useful in the treatment of septicemia and
skin structure infections. Indicated for patients who can not receive
or have failed to respond to penicillins and cephalosporins or have
infections with resistant staphylococci. For abdominal penetrating
injuries, it is combined with an agent active against enteric flora
and/or anaerobes.
To avoid toxicity, current recommendation is to assay vancomycin
trough levels after third dose drawn 0.5 h prior to next dosing. Use
creatinine clearance to adjust dose in patients with renal impairment.
Used in conjunction with gentamicin for prophylaxis in penicillin-
allergic patients undergoing gastrointestinal or genitourinary
procedures.


Antibiotics
Linezolid (Zyvox)
Prevents formation of functional 70S initiation complex, which
is essential for bacterial translation process. Bacteriostatic
against staphylococci.
The FDA warns against the concurrent use of linezolid with
serotonergic psychiatric drugs, unless indicated for life-
threatening or urgent conditions. Linezolid may increase
serotonin CNS levels as a result of MAO-A inhibition,
increasing the risk of serotonin syndrome.[14]


(prognosis)
Expectations (prognosis)
The prognosis for osteomyelitis varies but is markedly
improved with timely diagnosis and aggressive therapeutic
intervention.
The outlook is worse for those with long-term (chronic)
osteomyelitis, even with surgery. Amputation may be needed,
especially in those with diabetes or poor blood circulation.
The outlook for those with an infection of an orthopedic
prosthesis depends, in part, on:
The patient's health
The type of infection
Whether the infected prosthesis can be safely removed


Complications
When the bone is infected, pus is produced in the bone,
which may result in an abscess. The abscess steals the bone's
blood supply. The lost blood supply can result in a
complication called chronic osteomyelitis. This chronic
infection can cause symptoms that come and go for years.
Other complications include:
Need for amputation
Reduced limb or joint function
Spread of infection to surrounding tissues or the bloodstream


Complications
Complications of osteomyelitis may include the following:
Bone abscess
Paravertebral/epidural abscess
Bacteremia
Fracture
Loosening of the prosthetic implant
Overlying soft-tissue cellulitis
Draining soft-tissue sinus tracts


Prevention
Prompt and complete treatment of infections is helpful.
People who are at high risk or who have a compromised
immune system should see a health care provider promptly if
they have signs of an infection anywhere in the body.


Deterrence/Prevention
Acute hematogenous osteomyelitis can potentially be avoided
by preventing bacterial seeding of bone from a remote site.
This involves the appropriate diagnosis and treatment of
primary bacterial infections.
Direct inoculation osteomyelitis can best be prevented with
appropriate wound management and consideration of
prophylactic antibiotic use at the time of injury.


References
Espinoza LR. Infections of bursae, joints, and bones. In:
Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed.
Philadelphia, Pa: Saunders Elsevier; 2007:chap 293.
Gutierrez KM. Osteomyelitis. In: Long SS, ed. Principles and
Practice of Pediatric Infectious Diseases. 3rd ed. Philadelphia, Pa:
Elsevier Churchill Livingstone; 2008:chap 80.
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH000147
3/


Bone infections:
Septic arthritis


Septic arthritis
Septic arthritis is inflammation of a joint due to a bacterial or
fungal infection.
AKA:
infectious arthritis
Bacterial arthritis
Non-gonococcal bacterial arthritis
Reactive arthritis
a sterile inflammatory process that usually results from an
extra-articular infectious process.
Bacteria are the most significant pathogens because of their
rapidly destructive nature.


Causes
Septic arthritis develops when bacteria or other tiny disease-
causing organisms (microorganisms) spread through the
bloodstream to a joint. It may also occur when the joint is directly
infected with a microorganism from an injury or during surgery.
most common sites - knee and hip.
acute septic arthritis
bacteria such as staphylococcus or streptococcus.
chronic septic arthritis –
less common
caused by organisms such as Mycobacterium tuberculosisand Candida
albicans.


Risk factors
Artificial joint implants
Bacterial infection somewhere else in your body
Chronic illness or disease (such as diabetes, rheumatoid
arthritis, and sickle cell disease)
Intravenous (IV) or injection drug use
Medications that suppress your immune system
Recent joint injury
Recent joint arthroscopy or other surgery


Risk factors
seen at any age.
Children
occurs most often in those younger than 3 years.
The hip is often the site of infection in infants.
uncommon from age 3 to adolescence.
Children - more likely than adults infected with Group B
streptococcus or Haemophilus influenza, if they have not been
vaccinated.


Symptoms
Symptoms usually come on quickly.
Fever
joint swelling - usually just one joint.
intense joint pain- gets worse with movement.


Symptoms in newborns or infants:
Cries when infected joint is moved (example: diaper change
causes crying if hip joint is infected)
Fever
Inability to move the limb with the infected joint
(pseudoparalysis)
Irritability


Symptoms in children and adults:
Inability to move the limb with the infected joint
(pseudoparalysis)
Intense joint pain
Joint swelling
Joint redness
Low fever
Chills may occur, but are uncommon


Exams and Tests
Aspiration of joint fluid for cell count, examination of
crystals under the microscope, gram stain, and culture
Blood culture
X-ray of affected joint


Treatment
Antibiotics are used to treat the infection.
Resting, keeping the joint still, raising the joint, and using
cool compresses may help relieve pain. Exercising the
affected joint helps the recovery process.
If synovial fluid builds up quickly due to the infection, a
needle may be inserted into the joint often to aspirate the
fluid.
Severe cases may need surgery to drain the infected joint
fluid.


Medical management of infective arthritis focuses
adequate and timely drainage of the infected synovial fluid,
administration of appropriate antimicrobial therapy
immobilization of the joint to control pain.


Antibiotic Therapy
In native joint infections, parenteralantibiotics - at least 2 weeks.
Infection with either methicillin-resistant S aureus (MRSA) or
methicillin-susceptible S aureus (MSSA) - at least 4 full weeks IV
antibiotic therapy.
Orally administered antimicrobial agents are almost never
indicated in the treatment of S aureus infections.
Gram-negative native joint infections with a pathogen that is
sensitive to quinolones can be treated with oral ciprofloxacin for
the final 1-2 weeks of treatment.
As a rule, a 2-week course of intravenous antibiotics is sufficient to
treat gonococcal arthritis.


Antibiotics
linezolid with or without rifampin - for staphylococcal
prosthetic joint infection (PJI).
Ceftriaxone (Rocephin)
drug of choice (DOC) against N gonorrhoeae.
This agent is effective against gram-negative enteric rods.
Monitor sensitivity data.
Ciprofloxacin (Cipro)
alternative antibiotic to ceftriaxone to treat N gonorrhoeae and
gram-negative enteric rods.


Antibiotics
Cefixime (Suprax)
a third-generation oral cephalosporin with broad activity against
gram-negative bacteria.
Oral cefixime is used as a follow-up to intravenous (IV)
ceftriaxone to treat N gonorrhoeae.
Oxacillin
useful against methicillin-sensitive S aureus (MSSA).


Antibiotics
Vancomycin (Vancocin)
anti-infective agent used against methicillin-sensitive S aureus
(MSSA), methicillin-resistant coagulase-negative S aureus
(CONS), and ampicillin-resistant enterococci in patients
allergic to penicillin.
Linezolid (Zyvox)
an alternative antibiotic that is used in patients allergic to
vancomycin and for the treatment of vancomycin-resistant
enterococci.

http://emedicine.medscape.com/article/236299-
medication#showall

Joint Immobilization and Physical
Therapy
Usually, immobilization of the infected joint to control pain is
not necessary after the first few days. If the patient's
condition responds adequately after 5 days of treatment,
begin gentle mobilization of the infected joint. Most patients
require aggressive physical therapy to allow maximum
postinfection functioning of the joint.
Initial physical therapy consists of maintaining the joint in its
functional position and providing passive range-of-motion
exercises. The joint should bear no weight until the clinical
signs and symptoms of synovitis have resolved. Aggressive
physical therapy is often required to achieve maximum
therapy benefit.


Synovial Fluid Drainage
The choice of the type of drainage, whether percutaneous or surgical, has not
been resolved completely.[19, 25] In general, use a needle aspirate initially,
repeating joint taps frequently enough to prevent significant reaccumulation of
fluid. Aspirating the joint 2-3 times a day may be necessary during the first few
days. If frequent drainage is necessary, surgical drainage becomes more
attractive.
Gonococcal-infected joints rarely require surgical drainage.
Surgical drainage is indicated when one or more of the following occur:
The appropriate choice of antibiotic and vigorous percutaneous drainage fails to
clear the infection after 5-7 days
The infected joints are difficult to aspirate (eg, hip)
Adjacent soft tissue is infected
Routine arthroscopic lavage is rarely indicated. However, drainage through the
arthroscope is replacing open surgical drainage. With arthroscopic drainage, the
operator can visualize the interior of the joint and can drain pus, debride, and
lyse adhesions.


Surgical Intervention in Prosthetic Joint
Infection
In cases of prosthetic joint infection (PJI) that require surgery for cure,
successful treatment requires appropriate antibiotic therapy combined with
removal of the hardware. Despite appropriate antibiotic use, the success rate has
been only about 20% if the prosthesis is left in place. In recent years, evidence
has shown that debridement alone could yield a cure rate of 74.5% of patients
with a prosthetic joint infection and a C-reactive protein (CRP) level of 15
mg/dL or less who are treated with a fluoroquinolone.[26] For the time being, a
2-stage approach should be regarded as the most effective technique.
First, remove the prosthesis and follow with 6 weeks of antibiotic therapy.
Then, place the new joint, impregnating the methylmethacrylate cement with
an anti-infective agent (ie, gentamicin, tobramycin). Antibiotic diffusion into
the surrounding tissues is the goal. The success rate for this approach is
approximately 95% for both hip and knee joints.
An intermediate method is to exchange the new joint for the infected joint in a
1-stage surgical procedure with concomitant antibiotic therapy. This method,
with concurrent use of antibiotic cement, succeeds in 70-90% of cases.


(Prognosis)
Outlook (Prognosis)
Recovery is good with prompt antibiotic treatment. If
treatment is delayed, permanent joint damage may result.


Possible Complications
Joint degeneration (arthritis)


Prevention
Strictly adhere to sterile procedures whenever the joint space
is invaded (eg, in aspiration or arthroscopic procedures).
Antibiotic prophylaxis
with an antistaphylococcal antibiotic has been demonstrated to
reduce wound infections in joint replacement surgery.
Polymethylmethacrylate cement impregnated with antibiotics
may decrease perioperative infections.


Prevention
Treat any infection promptly to lessen the chance of
bloodstream invasion.
decreasing the incidence of underlying infections best
prevents reactive arthritis


References
Espinoza LR. Infections of bursae, joints, and bones. In:
Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed.
Ohl CA. Infectious arthritis of native joints. In: Mandell GL,
Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett's
Principles and Practice of Infectious Disease. 7th ed. Philadelphia,
Pa: Saunders Elsevier; 2009:chap 102.
http://www.nlm.nih.gov/medlineplus/ency/article/00043
0.htm
medication#showall


Disorders of foot
Hallux valgus (bunions)
Morton’s neuroma (plantar neuroma)
Hammer toe


64 Maria Carmela L. Domocmat, RN, MSN
http://familyfootcarenj.com/web/images/layout/conditions_map.jpg 8/24/2011

Disorders of foot :
Hallux valgus (bunions)


Hallux valgus
is a condition that affects the joint at the base of the big toe.
The condition is commonly called a bunion.
bunion - refers to the bump that grows on the side of the first
metatarsophalangeal (MTP) joint.


Hallux valgus (bunion)
The deformity involves the big toe and the long bone behind the big toe, the 1st
metatarsal.
Over time, the 1st metatarsal will begin to move towards the other foot
(medial) while the big toe will move out of joint towards the 2nd toe (lateral).
As the end of the 1st metatarsal bone begins to stick out, it will be under
pressure from shoes and the ground.
this constant pressure and friction will cause extra bone formation, leading to
the bump that is seen on the side of the foot.
The big toe will continue to shift towards the second toe causing an unbalanced
big toe joint. Over time arthritis can develop in the joint due to the mal-
positioned joint.
A bunion deformity is always progressive. It will always get worse over time.

http://www.footankleinstitute.com/hallux-valgus-bunion-surgery/


term hallux valgus actually describes what happens to the big
toe.
Hallux - medical term for big toe
Valgus - anatomic term that means the deformity goes in a
direction away from the midline of the body.
hallux valgus - big toe begins to point towards the outside of
the foot.
As this condition worsens, other changes occur in the foot that
increase the problem.


Changes include:
bone just above the big toe, the first metatarsal
usually develops too much of an angle in the other direction.
This condition is called metatarsus primus varus.
Metatarsus primus -means first metatarsal
varus - medical term that means the deformity goes in a direction
towards the midline of the body.
This creates a situation where the first metatarsal and the big toe now
form an angle with the point sticking out at the inside edge of the ball
of the foot. The bunion that develops is actually a response to the
pressure from the shoe on the point of this angle. At first the bump is
made up of irritated, swollen tissue that is constantly caught between
the shoe and the bone beneath the skin. As time goes on, the constant
pressure may cause the bone to thicken as well, creating an even
larger lump to rub against the shoe.


Etiology
Contrary to common belief,
high-heeled shoes with a small toe box or tight-fitting shoes do
not cause hallux valgus.
such footwear does keep the hallux in an abducted position if
hallux valgus is present, causing mechanical stretch and
deviation of the medial soft tissue.
In addition, tight shoes can cause medial bump pain and nerve
entrapment.


Etiology
Biomechanical instability
Arthritic/metabolic conditions
Structural deformity
Neuromuscular disease
Traumatic compromise


Etiology
most common yet most difficult to understand etiology
Contributing factors, if present, include
gastrocnemius or gastrocsoleus equinus,
flexible or rigid pes plano valgus,
rigid or flexible forefoot varus,
dorsiflexed first ray,
hypermobility, or
short first metatarsal.
Most often, excessive pronation at the midtarsal and subtalar joints
compensates for these factors throughout the gait cycle.


Etiology
Some pronation must occur in gait to absorb ground-reactive
forces. However, excessive pronation produces too much
midfoot mobility, which decreases stability and prevents
resupination and creation of a rigid lever arm; these effects
make propulsion difficult.


Etiology
During normal propulsion
approximately 65° of dorsiflexion is necessary at the first
metatarsophalangeal joint,
only 20-30° is available from hallux dorsiflexion.
Therefore, the first metatarsal must plantarflex at the sesamoid complex to
gain the additional 40° of motion needed.
Failure to attain the full 65° because of jamming of the joint during pronation
subjects the first metatarsophalangeal to intense forces from which hallux
valgus develops.
If the foot is sufficiently hypermobile as a result of excessive
pronation, the metatarsal tends to drift medially and the hallux drifts
laterally, producing hallux valgus. If no hypermobility is present,
hallux rigidus develops instead.


Etiology
Arthritic/metabolic
conditions Structural deformity
Gouty arthritis Malalignment of articular
Rheumatoid arthritis surface or metatarsal shaft
Psoriatic arthritis Abnormal metatarsal
Connective tissue length
disorders such as Ehlers- Metatarsus primus elevatus
Danlos syndrome, Marfan
syndrome, Down External tibial torsion
syndrome, and Genu varum or valgum
ligamentous laxity Femoral retrotorsion


Etiology
Neuromuscular disease Traumatic compromise
Multiple sclerosis Malunions
Charcot-Marie-Tooth Intra-articular damage
disease Soft-tissue sprains
Cerebral palsy Dislocations


Symptoms
Symptoms of Hallux valgus depending on the
degree of severity:
Aesthetic problem.
Formation of calluses, chronic irritation of the skin and
bursa.
Increasing pain under load and when moving.
Progressive arthrosis and stiffening in the base joint of the
toe.
Corollary deformities such as hammer and claw toe.

http://www.hallufix.org/english/hallux_valgus.html


Types of Hallux valgus
Degree 1 Degree 2
Toe malpositioning below Malpositioning between 20
20 degrees. No symptoms. and 30 degrees. Occasional
pain.


Types of Hallux valgus
Degree 3 Degree 4
Malpositioning between 30 Severest form with
and 50 degrees. Regular malpositionings over 50
pain. Increasing restraints degrees and painful
on activities. Pronounced restraints on the activities
malpositioning! of everyday life.
Surgical treatment


Treatment
Medical Therapy
Adapting footwear
Pharmacologic or physical therapy
Functional orthotic therapy
Surgical Therapy
Capsulotendon balancing or exostectomy
Osteotomy
Resectional arthroplasty
Resectional arthroplasty with implant
First metatarsophalangeal joint arthrodesis
First metatarsocuneiform joint arthrodesis


Bunionectomy
remove the bump that makes up the bunion.
performed through a small incision on the side of the foot immediately over the
area of the bunion.
Once the skin is opened the bump is removed using a special surgical saw or
chisel.
The bone is smoothed of all rough edges and the skin incision is closed with
small stitches.
It is more likely that realignment of the big toe will also be necessary. The major
decision that must be made is whether or not the metatarsal bone will need to
be cut and realigned as well. The angle made between the first metatarsal and
the second metatarsal is used to make this decision. The normal angle is around
nine or ten degrees. If the angle is 13 degrees or more, the metatarsal will
probably need to be cut and realigned.
When a surgeon cuts and repositions a bone, it is referred to as an osteotomy.
There are two basic techniques used to perform an osteotomy to realign the
first metatarsal.

http://www.concordortho.com/patient-education/topic-detail- 8/24/2011
popup.aspx?topicID=a5cea3a8a6d8093483657c959125dbaf

Distal Osteotomy
the far end of the bone is cut and moved laterally
This effectively reduces the angle between the first and
second metatarsal bones.
usually requires one or two small incisions in the foot.
Once the surgeon is satisfied with the position of the bones,
the osteotomy is held in the desired position with one, or
several,metal pins.
Once the bone heals, the pin is removed. The metal pins are
usually removed between three and six weeks following
surgery.


Proximal Osteotomy
the first metatarsal is cut at the near end of the bone
usually requires two or three small incisions in the foot.
Once the skin is opened the surgeon performs the osteotomy. The bone
is then realigned and held in place with metal pins until it heals. Again,
this reduces the angle between the first and second metatarsal bones.
Realignment of the big toe is then done by releasing the tight structures
on the lateral, or outer, side of the first MTP joint. This includes the
tight joint capsule and the tendon of the adductor hallucis muscle. This
muscle tends to pull the big toe inward. By releasing the tendon, the toe
is no longer pulled out of alignment. The toe is realigned and the joint
capsule on the side of the big toe closest to the other toe is tightened to
keep the toe straight, or balanced.
Once the surgeon is satisfied that the toe is straight and well balanced,
the skin incisions are closed with small stitches. A bulky bandage is
applied to the foot before you are returned to the recovery room.


Good footwear is often all that is needed
Wearing good footwear does not cure the deformity but may ease
symptoms of pain and discomfort. Ideally, get advice about footwear
from a podiatrist or chiropodist.
Advice may include:
Wear shoes, trainers or slippers that fit well and are roomy.
Don't wear high-heeled, pointed or tight shoes.
You might find that shoes with laces or straps are best, as they can be
adjusted to the width of your foot.
Padding over the bunion may help, as may ice packs.
Devices which help to straighten the toe (orthoses) are still occasionally
recommended, although trials investigating their use have not found
them much better than no treatment at all.
http://www.patient.co.uk/health/Bunions-(Hallux-Valgus).htm


Resectional arthroplasty
is a joint-destructive procedure
most commonly is reserved for elderly patients with advanced
degenerative joint disease and significant limitation of motion.
The typical resectional arthroplasty that is performed is known as
a Keller procedure.
It is performed when morbidity might be increased with the more
aggressive osteotomy that would otherwise be selected. The
procedure includes resection of the base of the proximal phalanx
with reapproximation of the abductor and adductor tendon
groups. The technique is inherently unstable and should be used
judiciously. The postoperative course includes limited-to-full
weight bearing in a surgical shoe immediately after the procedure.
http://emedicine.medscape.com/article/1232902-treatment#showall


Resectional arthroplasty with implant
is the same procedure as the resectional arthroplasty, with
similar indications, but stability is markedly improved with
the addition of the total implant.

Preoperative radiograph shows
Postoperative radiograph
degenerative joint disease.
obtained after resectional
arthroplasty and total joint
http://emedicine.medscape.com/article/1232902-treatment#showall
implant placement.


First metatarsophalangeal joint
arthrodesis
First metatarsophalangeal joint arthrodesis (see images
below) is a joint-destructive procedure that offers a higher
degree of stability and functionality. It is considered the
definitive procedure for degenerative joint disease. It results
in complete loss of motion at the first metatarsophalangeal
joint and is reserved for patients with high activity levels and
functional demands.

Preoperative
Postoperative
radiograph
radiograph
shows
show
arthrodesis.
arthrodesis.

First metatarsocuneiform joint
arthrodesis
Significant and/or hypermobile hallux abductovalgus may be
reduced with arthrodesis of the first metatarsocuneiform
joint (see images below). Indications include metatarsus
primus varus, hypermobility of the first ray, metatarsalgia of
the lesser metatarsals, and degenerative joint disease of the
metatarsocuneiform joint.

Preoperative radiograph shows a Postoperative radiograph shows
hypermobile first ray. arthrodesis of the first
92 Maria Carmela L. Domocmat, RN, MSN metatarsocuneiform. 8/24/2011

How to Choose Shoes
1. Know your foot.
Take a look at your old shoes. Look at what areas the most worn out shoes. A well-
chosen shoes will help to endure the physical stress well. One way to determine your
foot's shape is to do a "wet test"--- wet your foot, step on a piece of brown paper and
trace your footprint. Or just look at where your last pair of shoes shows the most wear.
2. Don't buy uncomfortable shoes even if they are hot!
3. Ideally, you should avoid wearing heels
4. Don't make shoes multitask.
5. Knowing your foot's particular quirks is key to selecting the right pair of shoes.
6.You must find shoes with well cushioned soles and ideally, some type of soft arch-support.
7. Measure your foot frequently. Foot size changes as we get older.
8.You should not buy shoes in the morning. The size of our feet at night more than in the
morning. Feet swell over the course of the day; they also expand while you run or walk,
so shoes should fit your feet when they're at their largest.

http://hallux-valgus-rigidus.com/index.php?option=com_content&view=article&id=74&Itemid=88


How to Choose Shoes
9. Always buy shoes to fit the larger or wider foot.
Buy well-fitting shoes with a wide toe box.
10. Use bunion shields, bunion pads or bunion cushions to protect
the bunion when wearing shoes. A bunion sleeve can be especially
effective at relieving shoe pressure when walking with a hallux
valgus.
11. Utilize an orthotic device or insert, such as a bunion splint or
bunion brace, to redistribute the pressure along the arch and ball
of the foot and control the separation of the bones. These devices
help support your foot and reduce the tendency toward hallux
valgus formation.
12. Use a bunion regulator to stretch tight tendons and toe muscles
overnight – especially if you want to avoid surgery.

http://hallux-valgus-rigidus.com/index.php?option=com_content&view=article&id=74&Itemid=88


Marfan syndrome (MFS)
is a spectrum disorder caused by a heritable genetic defect of connective tissue
that has an autosomal dominant mode of transmission
The defect itself has been isolated to the FBN1 gene on chromosome 15, which
codes for the connective tissue protein fibrillin.
Abnormalities in this protein cause a myriad of distinct clinical problems, of
which the musculoskeletal, cardiac, and ocular system problems predominate.
The skeleton of patients with MFS typically displays multiple deformities
including arachnodactyly (ie, abnormally long and thin digits),
dolichostenomelia (ie, long limbs relative to trunk length), pectus deformities
(ie, pectus excavatum and pectus carinatum), and thoracolumbar scoliosis
In the cardiovascular system, aortic dilatation, aortic regurgitation, and
aneurysms are the most worrisome clinical findings. Mitral valve prolapse that
requires valve replacement can occur as well. Ocular findings
include myopia,cataracts, retinal detachment and superior dislocation of the
lens


pectus carinatum pectus excavatum


Ehlers-
Genetics of Ehlers-Danlos Syndrome
Ehlers-Danlos family of disorders is a group of related
conditions that share a common decrease in the tensile
strength and integrity of the skin, joints, and other
connective tissues.
The first detailed clinical description of the syndrome is
attributed to Tschernogobow in 1892. The syndrome derives
its name from reports by Edward Ehlers, a Danish
dermatologist, in 1901 and by Henri-Alexandre Danlos, a
French physician with expertise in chemistry of skin
disorders, in 1908. These 2 physicians combined the
pertinent features of the condition and accurately delineated
the phenotype of this group of disorders.


The amazing, almost unnatural, contortions that some
patients with Ehlers-Danlos syndrome can perform often
arouse curiosity. Historically, some patients with Ehlers-
Danlos syndrome displayed the maneuvers publically in
circuses, shows, and performance tours. Some achieved
modest degrees of fame and bore titles such as "The India
Rubber Man," "The Elastic Lady," and "The Human
Pretzel." Such clinical features also raise suspicion of the
diagnosis when identified upon physical examination.
Unfortunately, patients often go many years before being
diagnosed


Patient with Ehlers-Danlos
syndrome mitis. Joint Patient with Ehlers-Danlos
hypermobility is less intense than syndrome. Note the abnormal
with other conditions. ability to elevate the right toe.

Girl with Ehlers-Danlos syndrome.
Dorsiflexion of all the fingers is easy
and absolutely painless.


All forms of Ehlers-Danlos syndrome share the following
primary features to varying degrees:
Skin hyperextensibility
Joint hypermobility and excessive dislocations
Tissue fragility
Poor wound healing, leading to wide thin scars: The classic
description of abnormal scar formation in Ehlers-Danlos
syndrome is "cigarette paper scars."
Easy bruising


Type Inheritance Previous Major Diagnostic Minor Diagnostic
Nomenclature Criteria Criteria
Kyphoscol Autosomal Type VI – lysyl Joint laxity, severe Tissue fragility,
iosis recessive hydroxylase hypotonia at birth, easy bruising, arterial rupture,
deficiency scoliosis, progressive marfanoid,
scleral fragility or microcornea,
rupture of globe osteopenia,
positive family
history (affected sibling)
Arthrocha Autosomal
ArthrochaAutosomal Type VII A, B Congenital bilateral Skin hyperextensibility,
lasia dominant dislocated hips, tissue fragility with atrophic
severe joint scars, muscle hypotonia,
hypermobility, easy bruising,
recurrent subluxations kyphoscoliosis, mild osteopenia
Dermatos Autosomal Type VII C Severe skin fragility; Soft, doughy skin;
paraxis recessive saggy, redundant skin easy bruising; premature
rupture of membranes; hernias
(umbilical and inguinal)


Type Inheritanc Previous Major Diagnostic Criteria Minor Diagnostic Criteria
e Nomenclature
Classic Autosomal Types I and II Skin hyperextensibility, Smooth, velvety skin; easy bruising;
dominant molluscoid pseudotumors;
subcutaneous spheroids; joint
hypermobility; muscle hypotonia;
wide atrophic scars, joint postoperative complication
hypermobility (eg, hernia); positive family history;
manifestations of tissue fragility (eg,
hernia, prolapse)
Hypermobilit Autosomal Type III Skin involvement (soft, smooth and Recurrent joint dislocation; chronic
y dominant velvety), joint hypermobility joint pain, limb pain, or both;
positive family history
Vascular Autosomal Type IV Thin, translucent skin; Acrogeria,
dominant arterial/intestinal fragility or hypermobile small joints;
rupture; extensive bruising; tendon/muscle rupture; clubfoot;
characteristic facial appearance early onset varicose veins;
arteriovenous, carotid-cavernous
sinus fistula;
pneumothorax;
gingival recession; positive family
history; sudden death in close
relative


Down syndrome
Down syndrome is by far the most common and best
known chromosomal disorder in humans and the most
common cause of intellectual disability.[3]
Mental retardation, dysmorphic facial features, and other
distinctive phenotypic traits characterize the syndrome


Disorders of foot :
Morton’s neuroma (plantar neuroma


Neuromas
are non-cancerous growths of the nerve tissue that develop in
different parts of the body.


Mortons Neuroma
affects a nerve in the foot, often times the nerve between the
third and fourth toe.
thickens the tissue around the nerves that lead to the toes,
causing sharp, burning sensations in the ball of the foot, as
well as a numbing or stinging feeling.
AKA: plantar neuroma or intermetatarsal neuroma.


http://www.footdoc.ca/www.FootDoc.ca/Website
_Neuroma.gif


Neuroma and adherent fibrofatty tissue.

http://emedicine.medscape.com/article/308284-clinical#showall


Sex
The female-to-male ratio for Morton's neuroma is 5:1.

Age
The highest prevalence of Morton's neuroma is found in
patients aged 15-50 years, but the condition may occur in any
ambulatory patient.



Causes
Various factors have been implicated in the precipitation of Morton's neuroma.
Morton's neuroma is known to develop as a result of chronic nerve stress and
irritation, particularly with excessive toe dorsiflexion.
Poorly fitting and constricting shoes (ie, small toe box) or shoes with heel lifts
often contribute to Morton's neuroma. Women who wear high-heeled shoes for
a number of years or men who are required to wear constrictive shoe gear are
at risk.
A biomechanical theory of causation involves the mechanics of the foot and
ankle. For instance, individuals with tight gastrocnemius-soleus muscles or who
excessively pronate the foot may compensate by dorsiflexion of the metatarsals
subsequently irritating of the interdigital nerve.
Certain activities carry increased risk of excessive toe dorsiflexion, such as
prolonged walking, running, squatting, and demi-pointe position in ballet.[4]



Manifestations
Obtaining an accurate history is important to making the diagnosis of Morton's
neuroma. Possible reported findings provided by the patient with Morton's
neuroma include the following:
The most common presenting complaints include pain and dysesthesias in the
forefoot and corresponding toes adjacent to the neuroma.
Pain is described as sharp and burning, and it may be associated with cramping.
Numbness often is observed in the toes adjacent to the neuroma and seems to
occur along with episodes of pain.
Pain typically is intermittent, as episodes often occur for minutes to hours at a
time and have long intervals (ie, weeks to months) between a single or small
group of multiple attacks.
Some patients describe the sensation as "walking on a marble."
Massage of the affected area offers significant relief.
Narrow tight high-heeled shoes aggravate the symptoms.
Night pain is reported but is rare.


Dx tests
palpable mass or a "click" between the bones.
Doctor put pressure on the spaces between the toe bones to
try to replicate the pain and look for calluses or evidence of
stress fractures in the bones that might be the cause of the
pain.
Range of motion tests will rule out arthritis or joint
inflammations.
X-rays may be required to rule out a stress fracture or
arthritis of the joints that join the toes to the foot.



Treatment
Rehabilitation Program
Physical Therapy
Treatment strategies for Morton's neuroma range from conservative to surgical
management. The conservative approach to treating Morton's neuroma may benefit from
the involvement of a physical therapist. The physical therapist can assist the physician in
decisions regarding the modification of footwear, which is the first treatment step.
Recommend soft-soled shoes with a wide toe box and low heel (eg, an athletic shoe).
High-heeled, narrow, nonpadded shoes should not be worn, because they aggravate the
condition.
The next step in conservative management is to alter alignment of the metatarsal heads.
One recommended action is to elevate the metatarsal head medial and adjacent to the
neuroma, thereby preventing compression and irritation of the digital nerve. A plantar
pad is used most often for elevation. Have the patient insert a felt or gel pad into the
shoe to achieve the desired elevation of the above metatarsal head.
Other possible physical therapy treatment ideas for patients with Morton's neuroma
include cryotherapy, ultrasonography, deep tissue massage, and stretching exercises. Ice
is beneficial to decrease the associated inflammation. Phonophoresis also can be used,
rather than just ultrasonography, to further decrease pain and inflammation.


Treatment
Initial therapies are nonsurgical and relatively simple. They
can involve one or more of the following treatments:
Changes in footwear. Avoid high heels or tight shoes, and
wear wider shoes with lower heels and a soft sole. This enables
the bones to spread out and may reduce pressure on the nerve,
giving it time to heal.
Orthoses. Custom shoe inserts and pads also help relieve
irritation by lifting and separating the bones, reducing the
pressure on the nerve.

http://orthoinfo.aaos.org/topic.cfm?topic=a00158

Treatment
Injection. One or more injections of a corticosteroid
medication can reduce the swelling and inflammation of the
nerve, bringing some relief.
Combination
Several studies have shown that a combination of roomier,
more comfortable shoes, nonsteroidal anti-
inflammatory medication, custom foot orthoses and
cortisone injections provide relief in over 80 percent of
people with Morton's Neuroma.

http://orthoinfo.aaos.org/topic.cfm?topic=a00158

Surgical Intervention
When conservative measures for Morton's neuroma are
unsuccessful, surgical excision of the area of fibrosis in
the common digital nerve may be curative.
Common adverse outcomes include
dysesthesias radiating from a painful nerve stump. Dysesthesias
may be treated as any other dysesthetic pain.
Surgical options include the following:
Neurectomy with nerve burial
Transverse intermetatarsal ligament release, with or
without neurolysis
Endoscopic decompression of the transverse
metatarsal ligament


Other Treatment
Perform injection into the dorsal aspect of the foot, 1-2 cm proximal to the
webspace, in line with the MTP joints.
Advance the needle through the midwebspace into the plantar aspect of the foot
until the needle gently tents the skin. Then withdraw it about 1 cm to where the
tip of the neuroma is located.
Inject a corticosteroid/anesthetic mix. A reasonable volume is 1 mL of
corticosteroid and 2 mL of anesthetic. T
he anesthetic used should not contain epinephrine, as necrosis may result. Care
also should be taken not to inject into the plantar pad.
Adverse outcomes include plantar fat pad necrosis. Transient numbness of the
toes also may occur. Although many practitioners use multiple injections, the
likelihood of benefit from subsequent injections, after failure to achieve relief
from the initial injection, is negligible.
An Australian investigation using a single, ultrasonographically guided
corticosteroid injection for Morton's neuroma found that 9 months after
treatment, complete pain relief had occurred in 11 of the 39 neuromas studied.


Neurectomy: typical incision location. Neurectomy: superficial exposure.

Neurectomy: deeper dissection. Neuroma and adherent fibrofatty tissue.
8/24/2011

Medication Summary
Dysesthesias may be treated as any other dysesthetic pain.
Tricyclic antidepressants, such as amitriptyline at 10-25 mg
PO qhs, may be tried. If this approach is unsuccessful,
anticonvulsants (eg, gabapentin, carbamazepine) often are
effective.


Tricyclic Antidepressants
Class Summary
A complex group of drugs that have central and peripheral
anticholinergic effects, as well as sedative effects. They have
central effects on pain transmission, and they block the active
re-uptake of norepinephrine and serotonin.
Amitriptyline (Elavil)
Analgesic for certain chronic and neuropathic pain. Low doses,
10-25 mg qhs, may provide pain relief from burning and
tingling occurring at rest but function only as an adjunct to
definitive treatment.


Anticonvulsants
Class Summary
Use of certain antiepileptic drugs (AEDs), such as the GABA
analogue Neurontin (gabapentin), has proven helpful in some cases of
neuropathic pain. Thus, although unstudied, a trial of such an agent
might conceivably provide analgesia for symptomatic neuropathy.
Used for dysesthesias not controlled with definitive treatment plus
tricyclic antidepressants (or in patients unable to take tricyclic
antidepressants).
Gabapentin (Neurontin)
Neuromembrane stabilizer useful in pain reduction with dysesthetic
pain. Has antineuralgic effects; however, exact mechanism of action is
unknown. Structurally related to GABA, but does not interact with
GABA receptors.


Anticonvulsants
Pregabalin (Lyrica)
Structural derivative of GABA. Mechanism of action unknown.
Binds with high affinity to alpha2-delta site (a calcium channel
subunit). In vitro, reduces calcium-dependent release of several
neurotransmitters, possibly by modulating calcium channel
function. FDA approved for neuropathic pain associated with
diabetic peripheral neuropathy or postherpetic neuralgia and as
adjunctive therapy in partial-onset seizures.


Serotonin-
Serotonin-Norepinephrine Reuptake
Inhibitors
Class Summary
These agents inhibit neuronal serotonin and norepinephrine
reuptake.
Duloxetine (Cymbalta)
Description Indicated for diabetic peripheral neuropathic pain.
Potent inhibitor of neuronal serotonin and norepinephrine
reuptake


Disorders of foot :
Hammer toe


Hammer toe
is a deformity of the toe, in which the end of the toe is bent
downward.


Causes, incidence, and risk factors
Hammer toe usually affects the second toe. However, it may also
affect the other toes. The toe moves into a claw-like position.
The most common cause of hammer toe is wearing short, narrow
shoes that are too tight. The toe is forced into a bent position.
Muscles and tendons in the toe tighten and become shorter.
Hammer toe is more likely to occur in:
Women who wear shoes that do not fit well or have high heels
Children who keep wearing shoes they have outgrown
The condition may be present at birth (congenital) or develop
over time.
In rare cases, all of the toes are affected. This may be caused by a
problem with the nerves or spinal cord.


Symptoms
The middle joint of the toe is bent. The end part of the toe
bends down into a claw-like deformity. At first, you may be
able to move and straighten the toe. Over time, you will no
longer be able to move the toe.
A corn often forms on the top of the toe. A callus is found on
the sole of the foot.
Walking or wearing shoes can be painful.


Dx tests
physical examination of the foot
decreased and painful movement in the toes.

http://www.nlm.nih.gov/medlineplus/ency/images/ency/fullsize/9360.jpg


http://www.myfootshop.com/images/medical/ortho/hammer_toe_differences_mod.jpg

http://www.family-
foot.com/images/hammer_toe_whatis.jpg


Treatment
Mild hammer toe in children can be treated by manipulating
and splinting the affected toe.


Treatment
The following changes in footwear may help relieve
symptoms:
Wear the right size shoes or shoes with wide toe boxes for
comfort, and to avoid making hammer toe worse.
Avoid high heels as much as possible.
Wear soft insoles to relieve pressure on the toe.
Protect the joint that is sticking out with corn pads or felt pads


Treatment
A foot doctor can make foot devices called hammer toe
regulators or straighteners for you, or you can buy them at
the store.
Exercises may be helpful.
You can try gentle stretching exercises if the toe is not already
in a fixed position.
Picking up a towel with your toes can help stretch and
straighten the small muscles in the foot.


Treatment
For severe hammer toe, you will need an operation to
straighten the joint.
The surgery often involves cutting or moving tendons and
ligaments.
Sometimes the bones on each side of the joint need to be
connected (fussed) together.
Most of the time, you will go home on the same day as the
surgery. The toe may still be stiff afterward, and it may be
shorter.


Prevention and Cure of Hammer Toes
with Products
Hammer Toe Regulator Toe Rings
Hammer Toe Cushion Toe Brace
Foam Toe Tubes Toe Alignment Splint
Gel Toe Cap Toe Trainers
Toe Spreader Hammer Toe Straightener
Silicone Toe Crest
Toe Spacer Cushion
Digital Toe Pad
Yoga Toes Toe Stretcher


Pedifix Budin Hammer Toe Regulator,
Single Loop
Hammer Toe Splint aligns crooked, overlapping or hammer
toes. Effective post-op splint. Encourages flexion and
extension of flexible digits. Soft, durable, cotton covered.
One size fits all.
Price: $3.40


http://mdbuyinggroup.com/products/sites/default/files/productimages/pedifix%20budin%20hammer
%20toe%20regulator.jpg

Hammer Toe Correction Bandage
Price $14.95


Hammer Toe Regulator
Toe regulator efficiently
integrates the middle joint of toe
with other joints. It reduces the
pressure and irritation at toe tips
and region over the toes. The toe
regulator straightens the joint of
hammer toes (or) claw toes with
a slight and smooth pressure.
Toe regulator is effective for pain
relief and proper alignment of
hammer toes.


Hammer Toe Cushion
Hammer Toe Cushion provides ease feel
over the contracted part and comforts
Hammer toe with enough support. It
assists for a stress free movement and aid
in lifting the toe to normal position.
Hammer toe cushion minimizes pressure
at the top and tip of toes with a spongy
effect.
Toe cushion is provided with an adjustable
toe loop for comfortable and secure fit.


Foam Toe Tubes
The soft foam present in the tube safeguard toes from rash
rubbing against footwear. Foam toe tube is easy to wear for
getting effective pain relief from hammer toes. It reduce the
pressure and swelling over Hammer toes for trouble free
walks.


Gel Toe Cap
Gel Toe Cap softens the Hammer toes giving excellent
cushioning to the painful deformed toes. It also relieves
extreme pain at the top and tip of toes effectively.
Gel maintains the spongy comfort and reduces pressure all
over the hammer toe.


Silicone Toe Crest
The reinforced loop with elastic
fabric of the toe crest holds the toe
perfectly straight. The toe crest
provides soft feel under three toes
excluding the big and little toe. It
relieves the pain caused by hammer
toe. It adds strength to the toe and
gives extra smoothness to the
affected spot.
Silicone soothes the toe for ease
feel.
Toe crest is durable and can be
worn comfortably with a snug fit.


Toe Alignment Splint
Toe alignment splint reduces the
pressure and pain caused by Hammer
toes and Bunions. It specifically aligns
the toe placing it in correct position.
The smooth cotton band with elastic
property gives secure fit around the
foot. Its thin straps can be placed over
affected toes and the rigidity is
adjustable using hook-and loop strap.
Unique T-strap of the splint reduces
the pain of bunion and prevents the
big toe to slant over hammer toes (or)
crooked toes.
Toe alignment splint is comfortable to
wear with casual shoes.


Toe Trainers

Toe trainer comforts flexible
hammer toes. It gives better
relief against the pain and
irritation. Toe trainer
separates the toes and aligns
them to look straight. It is an
effective item to cure slightly
movable Hammer toes.
The cotton-covered foam
provides secure feel to the
crooked toes.
Toe trainer is easy to wear
and fits snugly for efficient
correction of hammer toes.


Hammer Toe Straightener

The toe Straightener perfectly aligns
Hammer toes with little pressure. Its
cotton-covered loop with elasticity holds the
toe firmly in proper place and it can be
easily adjusted for stress free movements.
The smooth foam pad molds accordingly
with the foot shape and renders superior
cushioning at the bottom of the feet. It also
stops the pain caused by hammer toes. The
hook closure present in the toe straightener
pulls down and aligns the deformed toes to
keep you always smiling.
Hammer toe Straightener assists for healthy
feet by strengthening the toes and forefoot
muscles.


Prevention
Avoid wearing shoes that are too short or narrow.
Check children's shoe sizes often, especially during periods of
fast growth.


(prognosis)
Expectations (prognosis)
If the condition is treated early, you can often avoid surgery.
Treatment will reduce pain and walking difficulty.


Complications
Foot deformity
Posture changes caused by difficulty in walking


References
Krug RJ, Lee EH, Dugan S, Mashey K. Hammer toe. In:
FronteraWR, Silver JK, Rizzo TD Jr., eds. Essentials of
Physical Medicine and Rehabilitation. 2nd ed. Philadelphia, Pa:
Saunders Elsevier;2008:chap 82.
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH000221
5/


Muscular disorders:
Muscular dystrophy


The word "dystrophy" comes originally from the Greek
"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 muscles was in some way to blame for muscular
dystrophy. Today we know that muscle wasting in the
disorder is caused by defective genes rather than poor
nutrition.

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


Muscular dystrophy(MD)
refers to a group of more than 30 inherited diseases that
cause muscle weakness and muscle loss.
Some forms of MD appear in infancy or childhood, while
others may not appear until middle age or later.
The different muscular dystrophies vary in who they 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.

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


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


Muscular Dystrophies (MD)
characterized by progressive weakness and degeneration
of the skeletal muscles that control movement.
Some forms seen in infancy or childhood-
others may not appear until middle age 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

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


Etiology
are a group of inherited conditions
It’s caused by incorrect or missing
genetic information that prevents the
body from making the proteins
needed to build and maintain healthy
muscles.
Many cases of MD occur from
spontaneous mutations that are not
found in the genes of either parent,
and this defect can be passed to the
next generation.

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


Muscular dystrophy is a general term for a group of inherited
diseases involving a defective gene. Each form of muscular
dystrophy is caused by a genetic mutation that's particular to
that type of the disease. The most common types of muscular
dystrophy appear to be due to a genetic deficiency of the
muscle protein dystrophin

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


Inheriting Duchenne's or Becker's MD
Duchenne's and Becker's muscular dystrophies - passed from mother to son through one
of the mother's genes in a pattern called X-linked recessive inheritance.
Boys inherit an X chromosome from their mothers and a Y chromosome from their
fathers. The X-Y combination makes them male. Girls inherit two X chromosomes, one
from their mothers and one from their fathers. The X-X combination determines that
they are female.
The defective gene that causes Duchenne's and Becker's muscular dystrophies is located
on the X-chromosome.
Women who have only one X-chromosome with the defective gene that causes these
muscular dystrophies are carriers and sometimes develop heart muscle problems
(cardiomyopathy) and mild muscle weakness.
The disease can skip a generation until another son inherits the defective gene on the X-
chromosome.
In some cases of Duchenne's and Becker's muscular dystrophies, the disease arises from a
new mutation in a gene rather than from an inherited defective gene.



X-linked recessive inheritance pattern
with carrier mother
Women can pass down X-linked
recessive disorders such as
Duchenne's muscular dystrophy.
A woman who is a carrier of an
X-linked recessive disorder has a
25 percent chance of having an
unaffected son, a 25 percent
chance of having an affected son,
a 25 percent chance of having an
unaffected daughter and a 25
percent chance of having a
daughter who also is a carrier.
http://www.mayoclinic.com/health/medical/IM02723


Patterns differ for other types of MD
Myotonic dystrophy and most MFMs -passed along in a pattern
called autosomal dominant inheritance.
If either parent carries the defective gene for myotonic dystrophy,
there's a 50 percent chance the disorder will be passed along to a
child.
Some of the less common types of muscular dystrophy are passed
along in the same inheritance pattern that marks Duchenne's and
Becker's muscular dystrophies.
Other types of muscular dystrophy can be passed on from
generation to generation and affect males and females equally. Still
others require a defective gene from both parents.


In an autosomal dominant disorder, the mutated gene is a
dominant gene located on one of the nonsex chromosomes
(autosomes).You need only one mutated gene to be affected
by this type of disorder. A person with an autosomal
dominant disorder — in this case, the father — has a 50
percent chance of having an affected child with one mutated
gene (dominant gene) and a 50 percent chance of having an
unaffected child with two normal genes (recessive genes).

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


Duchenne MD
most common form of MD
primarily affects boys.
caused by the absence of dystrophin, aprotein involved in mai
ntaining the integrity of muscle.
Onset is between 3 and 5 years
Progresses rapidly.
Most boys are unable to walk by age 12, and later need a respira
tor to breathe.
Girls in these families have a 50percent chance of inheriting
and passing the defective gene to their children.


Duchenne muscular dystrophy (DMD)
a group of genetic disorders that affect the use of muscles in the
body.
inherited as an X-linked disorder. This is why Duchenne MD
primarily affects boys. Girls can inherit the gene for DMD but not
have any symptoms of the disease.
affects approximately 1 in every 3,500 live male 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.

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


Duchenne muscular dystrophy

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


Duchenne muscular dystrophy

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


Becker Muscular Dystrophy
similar to Duchenne but the symptoms are milder and can
appear till 25 years of age.
Boys with Becker MD have faulty or not enough dystrophi
Usually the affected people can live and enjoy life and are also
able to walk but they have some heart problems and is
present only in males.

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



Facioscapulohumeral MD
usually begins in the teenage years.
causes progressive weakness in muscles of the
face, arms, legs, and around the shoulders and chest.
affects both males and females
progresses slowly and can vary in symptoms from mild to
disabling.
about half of the sufferers are able to walk throughout their
life and almost all the patients live a normal life span.




Facioscapulohumeral muscular
dystrophy
Also known as Landouzy-Dejerine dystrophy
involves progressive muscle weakness involving:
Face
Shoulders
Abdomen
Feet
Upper arms
Pelvic area
Lower arms



When someone with facioscapulohumeral MD raises his or
her arms, the shoulder blades may stick out like wings.
Progression of this form is slow, with some spurts of rapidly
increasing weakness. Onset usually occurs during the teen to
early adult years.



Myotonic MD
Aka: Steinert’s disease
the disorder's most common adult form
produces stiffness of muscles and an inability to relax muscles
at will (myotonia), as well as the muscle weakness of the
other forms of muscular dystrophy.
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

http://www.ninds.nih.gov/disorders/md/md.htm 8/24/2011

Myotonic MD
Cause
A repeated section of DNA on either chromosome 19 or
chromosome 3.
Onset
Congenital form appears at birth.
More common form may begin in teen or adult years.

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


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
8/24/2011

Myotonic MD
Symptoms
Generalized weakness and muscle wasting first affecting the
face, lower legs, forearms, hands and neck, with delayed
relaxation of muscles after contraction common.
Other symptoms involve the gastrointestinal system, vision,
heart or respiration.
Learning disabilities occur in some cases.
Congenital myotonic dystrophy is the more severe form.
Men with myotonic muscular dystrophy have baldness on their
foreheads.



Myotonic MD
Progression
Progression is slow, sometimes spanning 50 to 60 years.
Inheritance
Autosomal dominant; the disease may be inherited through
either the father or the mother.



Myotonic MD

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

Other major types of muscular
dystrophy
The other major types of muscular dystrophy include:
Limb-girdle muscular dystrophy
Congenital muscular dystrophy
Oculopharyngeal muscular dystrophy
Distal muscular dystrophy
Emery-Dreifuss muscular dystrophy
Myofibrillar myopathies



Limb-
Limb-Girdle
the type which affects from teenage years to adulthood
is present in both males and females.
As the name indicates, in this type the problem starts from
hip (pelvic girdle) region and then reaches to the shoulders
( pectoral girdle ) and later legs and arms are also affected,
sufferers are unable to walk and most patients live past mid
adulthood.



Congenital Muscular Dystrophy
the form which is present at the time of birth
rare
cause the loss of muscles
The term "congenital muscular dystrophy" refers to a group
of inherited muscular dystrophies. Signs of these disorders
may include:
General muscle weakness
Joint deformities




Congenital Muscular Dystrophy
is apparent at birth or becomes evident before age 2.
The course of this disorder varies significantly depending on
the type.
Some forms of congenital MD progress slowly and cause only
mild disability, while others progress rapidly and cause severe
impairment.



Congenital myotonic dystrophy
Signs in infants may include:
Severe muscle weakness
Difficulty sucking and swallowing
Difficulty breathing
Cognitive impairment



Oculophyrangeal Muscular Dystrophy
affects primarily the muscles of eyes and throat which occur
around 40s to onward ages
symptoms include the weakness of eyes and facial muscles
which could later cause dysphagia - predisposes the patients
to pneumonia and choking.



Oculopharyngeal muscular dystrophy
The first sign of this type of muscular dystrophy is usually
drooping of the eyelids
followed by weakness of the muscles of the eye, face and
throat, resulting in difficulty swallowing. Progression is slow.
Signs and symptoms first appear in adulthood, usually in a
person's 40s or 50s.



Distal MD
very rare
mildest
affects the muscles of fore arms to hands and muscles of
lower legs to feet
very slowly progressing
not very severe



Distal muscular dystrophy
This group involves the muscles farthest away from the
center of the body (distal muscles) — those of the hands,
forearms, feet and lower legs. The severity is generally less
than for other forms of MD, and this form tends to progress
slowly. Distal MD generally begins in adulthood between the
ages of 40 and 60.



Emery-
Emery-Dreifuss
the type which affects from childhood to teen years
present only in the males
affects the muscles of pectoral region to upper arms and
lower parts of legs and along with that patients
have extreme heart problems that are usually fatal.
This is the type which also affects the carriers (females) but
the symptoms are not very severe.



Emery-
Emery-Dreifuss muscular dystrophy
This form of muscular dystrophy usually begins in the
muscles of the:
Shoulders
Upper arms
Shins
Cardiac arrhythmias, stiffness of the spine and muscle
contractures are other features of Emery-Dreifuss MD.
Emery-Dreifuss MD usually begins in the childhood to early
teen years and progresses slowly.



Myofibrillar myopathies(MFMs)
(MFMs)
Though in some cases the MFMs affect only the muscles
closest to the center of the body (proximal muscles) — such
as the shoulder and hip muscles — the distal muscles also are
usually involved. This group of muscle disorders also is
commonly associated with:
Stiffness of the spine
Muscle contractures
Nerve damage (peripheral neuropathy)
Thickening and stiffening of the heart muscle (cardiomyopathy)



Maria Carmela L. Domocmat, RN, MSN
195 8/24/2011

Clinical manifestations
Progressive muscular weakness
Delayed meeting of motor milestones
Waddling gait
Walking on toes
Frequent falls
Gower’s sign
Hyperthrophied calf muscles
Poor balance
Scoliosis of the spine
Fracture of long bones
Inability to walk (late stages)


Waddling gait, a distinctive ducklike walk, is an important
sign of muscular dystrophy, spinal muscle atrophy or, rarely,
congenital hip displacement.
The gait results from deterioration of the pelvic girdle
muscles—primarily the gluteus medius, hip flexors, and hip
extensors. Weakness in these muscles hinders stabilization of
the weight-bearing hip during walking, causing the opposite
hip to drop and the trunk to lean toward that side in an
attempt to maintain balance. (

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


Typically, the legs assume a wide stance and the trunk is
thrown back to further improve stability, exaggerating
lordosis and abdominal protrusion. In severe cases, leg and
foot muscle contractures may cause equinovarus deformity of
the foot combined with circumduction or bowing of the legs.

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


With Duchenne's muscular dystrophy, waddling gait becomes
clinically evident between ages 3 and 5. The gait worsens as the
disease progresses, until the child loses the ability to walk and
requires the use of a wheelchair, usually between ages 10 and 12.
Early signs are usually subtle: a delay in learning to walk, frequent
falls, gait or posture abnormalities, and intermittent calf pain
With Becker's muscular dystrophy, waddling gait typically becomes
apparent in late adolescence, slowly worsens during the third
decade, and culminates in total loss of ambulation. Muscle
weakness first appears in the pelvic and upper arm muscles.
Progressive wasting with selected muscle hypertrophy produces
lordosis with abdominal protrusion, poor balance, a positive
Gowers'sign and, possibly, mental retardation.
http://www.wrongdiagnosis.com/symptoms/walking_symptoms/book-causes-16g.htm


With facioscapulohumeral muscular dystrophy, which usually
occurs late in childhood and during adolescence, waddling
gait appears after muscle wasting has spread downward from
the face and shoulder girdle to the pelvic girdle and legs.
Earlier effects include progressive weakness and atrophy of
facial, shoulder, and arm muscles; slight lordosis; and pelvic
instability.



Gower’s sign
to stand, affected children press their hands against their
ankles, knees and thighs


Incidence and Mortality
Morbidity and mortality rates depend on the type of congenital
muscular dystrophy.
Its incidence varies, as some forms are more common than
others.
Duchenne muscular dystrophy affects one in 3300 live male births.
Myotonic muscular dystrophy is the most frequent form of
muscular dystrophy among adults. Its prevalence is estimated at
one case for every 10,000 people in most countries. However, this
frequency is 20 times higher in the Charlevoix and Saguenay-Lac-
St-Jean regions, where one person out of 500 is estimated to carry
the disease. http://pathologyproject.wordpress.com/2011/04/24/muscular-dystrophy/


Diagnostic tests
A careful review of your family's history of muscle disease can help your doctor reach a diagnosis. In addition to a
medical history review and physical examination, your doctor may rely on the following in diagnosing muscular
dystrophy:
Blood tests. Damaged muscles release enzymes, such as creatine kinase (CK), into your blood. High blood levels
of CK suggest a muscle disease, such as muscular dystrophy.
Electromyography. A thin-needle electrode is inserted through your skin into the muscle to be tested.
Electrical activity is measured as you relax and as you gently tighten the muscle. Changes in the pattern of
electrical activity can confirm a muscle disease. The distribution of the disease can be determined by testing
different muscles.
Ultrasonography. High-frequency sound waves are used to produce precise images of tissues and structures
within your body. An ultrasound is a noninvasive way of detecting certain muscle abnormalities, even in the early
stages of the disease.
Muscle biopsy. A small piece of muscle is taken for laboratory analysis. The analysis distinguishes muscular
dystrophies from other muscle diseases. Special tests can identify dystrophin and other markers associated with
specific forms of muscular dystrophy.
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 the dystrophin gene responsible for most cases of these types 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 in other cases
of those affected, but new tests that examine the entire dystrophin gene are making it possible to pinpoint tiny,
less common mutations.
http://www.mayoclinic.com/health/muscular-dystrophy/DS00200/DSECTION=treatments-and-drugs


Treatment
There is no cure for muscular dystrophy.
Treatments include
Physical and speech therapy
Orthopedic devices
Surgery
Medications
Some people with muscular dystrophy have mild cases that
worsen slowly. Other cases are disabling and severe.

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


There's currently no cure for any form of muscular dystrophy. Research into gene therapy may eventually provide treatment to stop the progression of some
types of muscular dystrophy. Current treatment is designed to help prevent or reduce deformities in the joints and the spine and to allow people with MD to
remain mobile as long as possible. Treatments may include various types of physical therapy, medications, assistive devices and surgery.
Physical therapy
As muscular dystrophy progresses and muscles weaken, 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 your joints as flexible as possible, delaying the progression of contractures,
and reducing or delaying curvature of your spine. Using hot baths (hydrotherapy) also can help maintain range of motion in joints.
Medications
In some cases, doctors may prescribe medications to slow the progression and manage signs and symptoms of muscular dystrophy:
Muscle spasms, stiffness and weakness (myotonia).Medications that may be used to help manage myotonia associated with MD include mexiletine
(Mexitil), phenytoin (Dilantin, Phenytek), baclofen (Lioresal), dantrolene (Dantrium) and carbamazepine (Tegretol, Carbatrol).
Muscle deterioration. The anti-inflammatory corticosteroid medication prednisone may help improve muscle strength and delay the progression of
Duchenne's MD. The immunosuppressive drugs cyclosporin and azathioprine also are sometimes prescribed to delay some damage to dying muscle cells.
Assistive devices
Braces can both provide support for weakened muscles of your hands and lower legs and help keep muscles and tendons stretched and flexible, slowing the
progression of contractures. Other devices, such as canes, walkers and wheelchairs, can help maintain mobility and independence. If respiratory muscles
become weakened, using a ventilator may become necessary.
Surgery
To release the contractures that may develop and that can position joints in painful ways, doctors can perform a tendon release surgery. This may be done to
relieve tendons of your hip and knee and on the Achilles tendon at the back of your foot. Surgery may also be needed to correct curvature of the spine.
Other treatments
Because respiratory infections may become a problem in later stages of muscular dystrophy, it's important to be vaccinated for pneumonia and to keep up to
date with influenza shots.

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


Nursing considerations
▪ Perform passive and active muscle-stretching exercises to the
arms and legs.
▪ Encourage the patient to walk at least 3 hours each day (with leg
braces, if necessary) to maintain muscle strength, reduce
contractures, and delay further gait deterioration, if possible.
▪ Stay near the patient during ambulation, to provide support if
necessary.
▪ Provide a balanced diet to maintain energy levels and prevent
obesity.
▪ Because of the grim prognosis associated with muscular
dystrophy and spinal muscle atrophy, provide emotional support
for the patient and his family.


Patient teaching
▪ Caution the patient about long, unbroken periods of bed
rest, which accelerate muscle deterioration.
▪ Refer the patient to a local Muscular Dystrophy Association
chapter, as indicated.
▪ Suggest genetic counseling for parents, if they're
considering having more children.



On the cover: Andy Vladimir,
of Coconut Grove, Fla., had
MMD and used a wheelchair,
but that barely slowed him
down. A successful
businessman, textbook author,
world traveler and travel
writer, including for MDA's
Quest magazine, Andy lived to
age 76.


References
http://www.mdausa.org/
dystrophy/DS00200/DSECTION=treatments-and-drugs


Muscular disorders:
Rhabdomyolysis


Rhabdomyolysis
a condition that may occur when muscle tissue is damaged
due to an injury in which muscle in the body is damaged
rhabdomyo=skeletal muscle + lysis= rapid breakdown
There are a three of types of muscle in the body, including:
skeletal muscles that move the body;
cardiac muscle located in the heart; and
smooth muscle that lines blood vessels, gastrointestinal tract,
bronchi in the lung, and the bladder and uterus. This type of
muscle is not under conscious control.
Rhabdomyolysis occurs when there is damage to the skeletal
muscle.
http://www.emedicinehealth.com/rhabdomyolysis/page2_em.htm


Rhabdomyolysis
is the breakdown of muscle fibers with leakage of potentially
toxic cellular contents into the systemic circulation.
The final common pathway of rhabdomyolysis may be a
disturbance in myocyte calcium homeostasis


Rhabdomyolysis
The injured muscle cell leaks myoglobin (a protein) into the blood
stream.
Myoglobin can be directly toxic to kidney cells, and it can impair
and clog the filtration system of the kidney.
Both mechanisms can lead to kidney failure (the major
complication of rhabdomyolysis).
Significant muscle injury can cause fluid and electrolyte shifts from
the bloodstream into the damaged muscle cells, and in the other
direction (from the damaged muscle cells into the bloodstream).
As a result, dehydration may occur. Elevated levels of potassium in
the bloodstream (hyperkalemia) may be associated with heart
rhythm disturbances and sudden cardiac death due to ventricular
tachycardia and ventricular fibrillation.

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

When muscles are damaged, especially due to a crush injury,
swelling within the muscle can occur, causing compartment
syndrome.
If this occurs in an area where the muscle is bound by fascia (a
tough fibrous tissue membrane), the pressure inside the muscle
compartment can increase to the point at which blood supply to
the muscle is compromised and muscle cells begin to die.
Rhabdomyolysis was first appreciated as a significant complication
from crush and blast injuries sustained in a volcano eruption in
Italy, in 1908. Victims of the blast injuries during the first and
second World Wars help further understand the relationship
between massive muscle damage and kidney failure.

216 Medscpae Carmela L. Domocmat, RN, MSN
Maria 8/24/2011

Incidence
United States
Rhabdomyolysis accounts for an estimated 8-15% of cases of
acute renal failure.


Causes
When muscle is damaged
myoglobin (protein pigment) - released into the bloodstream
and filtered out of the body by the kidneys.
Myoglobin breaks down into potentially harmful compounds.
It may block the structures of the kidney, causing damage such
as acute tubular necrosis or kidney failure.
Dead muscle tissue may cause a large amount of fluid to
move from the blood into the muscle, reducing the fluid
volume of the body and leading to shock and reduced blood
flow to the kidneys.
The disorder may be caused by any condition that results in
damage to skeletal muscle, especially trauma.


Causes
The etiologies may be subdivided into
Traumatic
exercise induced
toxicologic
Environmental
Metabolic
Infectious
Immunologic
inherited classifications.



Causes
Major blunt trauma and crush injury
Electrocution
Lightening strikes
Major burns
Excessive exercise, for example, 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



Causes
Prolonged immobilization
(for example, patients who have been lying in one position for a
prolonged period of time due to a debilitating stroke, alcohol
or drug overdose,
or those who have remained unconscious for a prolonged
period of time for other reasons).
The weight of the body is enough to crush the muscles that are
pushed up against a hard surface such as the floor.



Causes
Dystonic reactions cause muscles to spasm, and if left
untreated can damage muscle
Cholesterol lowering medications [for example, statins
prescribed to treat high cholesterol (particularly when
combined with other cholesterol lowering medications such
as fibrates)
Antidepressant medications
[for example selective serotonin reuptake inhibitors (SSRIs)
antidepressants may cause a serotonin syndrome characterized
by agitation, fever, and muscle spasm]


Causes
Some anesthetics can cause malignant hyperthermia syndrome
with high fever and muscle rigidity
A variety of drugs of abuse [for example, cocaine, heroin,
phencyclidine (PCP), and amphetamines]
Hyperthermia and hypothermia (high and low body temperature,
respectively)
Complications from a variety of infections caused by bacteria,
viruses, and fungi
Association with other diseases such as sickle cell
disease, polymyositis, and dermatomyositis
Complications from the venom from snake bites and black widow
spider bites


Risk factors
Alcoholism (with subsequent muscle tremors)
Certain inherited or genetic syndromes
Crush Injuries
Heat intolerance
Heatstroke
Ischemia or necrosis of the muscles (as may occur with arterial occlusion, deep
venous thrombosis, or other conditions)
Low phosphate levels
Seizures
Severe exertion such as marathon running or calisthenics
Shaking chills
Trauma
Use or overdose of drugs, especially cocaine, amphetamines, statins, heroin, or
PCP


Risk factors
Melli et al reviewed 475 patients with rhabdomyolysis
hospitalized at Johns Hopkins Hospital and found that the
most common risk factors were exogenous toxins, with
illicit drugs, alcohol, and prescription medications responsible
in 46% of patients.



Symptoms
Abnormal urine color (dark, red, or cola colored)
General weakness
Muscle stiffness or aching (myalgia)
Muscle tenderness
Weakness of the affected muscles


Symptoms
Additional symptoms that may be associated with this disease
include the following:
Fatigue
Joint pain
Seizures
Weight gain (unintentional)


Diagnostic Exams
An examination reveals tender or damaged skeletal muscles.
CPK is very high.
Serum myoglobin test is positive.
Serum potassium may be very high
Urinalysis may reveal casts and be positive for hemoglobin without
evidence of red blood cells on microscopic examination.
Urine myoglobin test is positive.
This disease may also alter the results of the following tests:
CPK isoenzymes
Urine creatinine
Serum creatinine


Prehospital Care
Vigorous hydration with isotonic crystalloid
the cornerstone of therapy for rhabdomyolysis.
Support of the intravascular volume increases the glomerular
filtration rate (GFR) and oxygen delivery and dilutes myoglobin
and other renal tubular toxins.
Immediately obtain intravenous access with a large-bore
catheter.
Administer isotonic crystalloid 500 mL/h and then titrate to
maintain a urine output of 200-300 mL/h.
Because injured myocytes can sequester large volumes of
extracellular fluid, crystalloid requirements may be
surprisingly large.

Assess ABCs and support as needed.
Treat any underlying conditions, such as trauma, infection, or
toxins.
General recommendations for the treatment of
rhabdomyolysis include
fluid resuscitation
prevention of end-organ complications



Patients with CK elevation in excess of 2-3 times the
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 200-300 mL/h.
Consider central venous pressures or Swan-Ganz
catheterization in patients with cardiac or renal disease.
These invasive studies can assist in the assessment of the
intravascular volume.
Repeat CK assay every 6-12 hours in order to determine
peak CK level.


Acute renal failure develops in 30-40% of patients with
rhabdomyolysis.
Suggested mechanisms include
precipitation of myoglobin and uric acid crystals within renal
tubules,
decreased glomerular perfusion, and
the nephrotoxic effect of ferrihemate (formed upon dissociation
of myoglobin in the acidic environment of the renal
parenchyma). I
To prevent renal failure, many authorities advocate urine
alkalinization, mannitol, and loop diuretics.

232

Urinary alkalinization
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.
0.5 isotonic sodium chloride solution with one 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 enhance renal perfusion. Loop diuretics
may be used to enhance urinary output in oliguric patients,
despite adequate intravascular volume.


Treatment of hyperkalemia consists of
intravenous sodium bicarbonate, glucose, and insulin;
oral or rectal sodium polystyrene sulfonate (Kayexalate); and
hemodialysis.
Administer intravenous calcium chloride for patients who are
hemodynamically compromised and hyperkalemic.



Hypocalcemia is noted early in the course of
rhabdomyolysis and generally is not of clinical significance.
Calcium supplementation is not recommended.
Compartment syndrome
requires immediate orthopedic consultation for fasciotomy.
DIC
fresh frozen plasma, cryoprecipitate, and platelet transfusions.
Hyperuricemia and hyperphosphatemia
rarely are of clinical significance and rarely require treatment.



Medication Summary
Medical therapy for rhabdomyolysis focuses on
restoring adequate intravascular volume using isotonic
crystalloid.
Adjunctive measures that may decrease the incidence of acute
myoglobinuric renal failure include urinary alkalinization and
osmotic and loop diuresis.



Alkalinizing agents
Class Summary
Sodium bicarbonate is administered IV to alkalinize urine in
patients with rhabdomyolysis. This may prevent toxicity caused
by the presence of myoglobin in acidic urine and crystallization
of uric acid.
Sodium bicarbonate (Neut)
Useful in alkalization of urine to prevent acute myoglobinuric
renal failure. Titrate dose to increase pH to >7.



Osmotic diuretics
Class Summary
These agents increase osmolarity of glomerular filtrate and induce
diuresis. They hinder tubular reabsorption of water, causing sodium
and chloride excretion to increase.
Mannitol (Osmitrol)
Alternative diuretic used when urine output is inadequate despite
aggressive fluid therapy.
Initially assess for adequate renal function in adults by administering a
test dose of 200 mg/kg IV over 3-5 min. Should produce a urine flow
of at least 30-50 mL/h over 2-3 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.


Loop diuretics
Class Summary
These agents elicit a loss of free water, increasing diuresis.
Furosemide (Lasix)
Increases water excretion by interfering with the chloride-
binding cotransport system, resulting in inhibition of sodium
and chloride reabsorption in the ascending loop of Henle and
distal renal tubule.
Individualize doses. Depending on response, administer at
increments of 20-40 mg q6-8h until desired diuresis occurs.
When treating infants, titrate with 1-mg/kg/dose increments
until a satisfactory effect is achieved


Further Inpatient Care
continued volume support and urinary
alkalinization.
Obtain serial CK measurements to verify that values have
peaked and are returning to reference range.
Serial physical examinations and laboratory studies are
indicated to monitor for
compartment syndrome
Hyperkalemia
acute oliguric or nonoliguric renal failure
DIC


Further Inpatient Care
In patients with no apparent precipitating factors for
rhabdomyolysis
consider inherited disorders of carbohydrate or lipid
metabolism and myopathies.


Complications
Death from hyperkalemia or renal failure
Compartment syndrome
Disseminated intravascular coagulation (DIC)
Hepatic insufficiency
Hypovolemia (sequestration of plasma water within injured
myocytes)
Hyperkalemia (release of cellular potassium into the systemic
circulation)
Metabolic acidosis (release of cellular phosphate and sulfate)
Acute tubular necrosis (ATN)
Acute renal failure (nephrotoxic effects of liberated myocyte
components)


(Prognosis)
Outlook (Prognosis)
The prognosis depends on the underlying etiology and any
existing comorbidities.

Acute kidney failure occurs in many patients.
Treatment soon after rhabdomyolysis begins 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 have problems with fatigue and muscle pain.


Patient Education
Advise patients with rhabdomyolysis caused by hyperthermia
and/or inordinate exertion to exercise in moderation with
careful attention to hydration and external methods of
cooling.
Advise patients with rhabdomyolysis related to ethanol,
recreational drugs, or prescription medications to
discontinue use of the offending agent and refer them to a
rehabilitation program.



Prevention

Drink plenty of fluids after strenuous exercise to dilute the
urine and flush the myoglobin out of the kidney.
Proper hydration is also necessary after any condition or
event that may involve damage to skeletal muscle.


References
In: Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed.
http://www.nlm.nih.gov/medlineplus/ency/article/00047
3.htm
clinical#showall


Musculoskeletal disorders part 1

More Related Content

What's hot

Similar to Musculoskeletal disorders part 1

More from Carmela Domocmat

Recently uploaded

Musculoskeletal disorders part 1