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 Bone infections
Osteomyelitis Septic arthritis
Part II Degenerative bone disorders: OA Metabolic bone disorders

Osteoporosis Pagets dse Osteomalacia Gout and gouty arthritis
Disorders of foot
Hallux valgus (bunions) Mortons neuroma (plantar neuroma) Hammer toe
Spinal column deformities

Scoliosis Kyphosis Lordosis
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Muscular disorders
Muscular dystrophy Rhabdomyolysis
2 Maria Carmela L. Domocmat, RN, MSN
Bone infections
Osteomyelitis Septic arthritis
Maria Carmela L. Domocmat, RN, MSN
8/24/2011
Bone infections: Osteomyelitis
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Osteomyelitis
is an acute or chronic bone infection or inflammatory process of the bone and its structures secondary to infection with pyogenic organisms.
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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 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.
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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
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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 foot Osteomyelitis of T10 secondary to streptococcal disease.
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Osteomyelitis
Osteomyelitis of the great toe Osteomyelitis of index finger metacarpal head secondary to clenched fist injury
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Osteomyelitis
Osteomyelitis of index finger metacarpal head secondary to clenched fist injury. Osteomyelitis of the elbow.
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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
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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
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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.
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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.
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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.
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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.
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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 thirdgeneration 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)
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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 Gresistant 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 gramnegative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms; arrests bacterial growth by binding to one or more penicillinbinding proteins. Note: Administer with a penicillinase-resistant synthetic penicillin, when treating osteomyelitis.
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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.
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Antibiotics
Ciprofloxacin (Cipro)
Fluoroquinolone with activity against pseudomonads, streptococci, MRSA, Staphylococcus epidermidis, and most gramnegative 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.
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Antibiotics
Ceftazidime (Fortaz, Ceptaz)
Third-generation cephalosporin with broad-spectrum gramnegative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms; arrests bacterial growth by binding to one or more penicillinbinding proteins.
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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.
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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 penicillinallergic 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 lifethreatening or urgent conditions. Linezolid may increase serotonin CNS levels as a result of MAO-A inhibition, increasing the risk of serotonin syndrome.[14]
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(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
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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
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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.
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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.
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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/
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Bone infections: Septic arthritis
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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 diseasecausing 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
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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.
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Symptoms
Symptoms usually come on quickly. Fever joint swelling - usually just one joint. intense joint pain- gets worse with movement.
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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
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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
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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
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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.
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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.
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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.
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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).
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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/236299medication#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.
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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.
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(Prognosis) Outlook (Prognosis)

Recovery is good with prompt antibiotic treatment. If treatment is delayed, permanent joint damage may result.
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Possible Complications
Joint degeneration (arthritis)
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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.
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Prevention
Treat any infection promptly to lessen the chance of bloodstream invasion. decreasing the incidence of underlying infections best prevents reactive arthritis
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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 290. 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 http://emedicine.medscape.com/article/236299medication#showall
Disorders of foot
Hallux valgus (bunions) Mortons neuroma (plantar neuroma) Hammer toe
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http://familyfootcarenj.com/web/images/layout/conditions_map.jpg
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Disorders of foot : Hallux valgus (bunions)
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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.
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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 malpositioned joint. A bunion deformity is always progressive. It will always get worse over time.
http://www.footankleinstitute.com/hallux-valgus-bunion-surgery/
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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.
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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.
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Etiology
Biomechanical instability Arthritic/metabolic conditions Structural deformity Neuromuscular disease Traumatic compromise
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Etiology
Biomechanical instability
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.
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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.
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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 Gouty arthritis Rheumatoid arthritis Psoriatic arthritis Connective tissue disorders such as EhlersDanlos syndrome, Marfan syndrome, Down syndrome, and ligamentous laxity
Structural deformity
Malalignment of articular surface or metatarsal shaft Abnormal metatarsal length Metatarsus primus elevatus External tibial torsion Genu varum or valgum Femoral retrotorsion
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Etiology
Neuromuscular disease Traumatic compromise
Multiple sclerosis Charcot-Marie-Tooth disease Cerebral palsy
Malunions Intra-articular damage Soft-tissue sprains Dislocations
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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
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Types of Hallux valgus

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

Degree 3 Degree 4
Malpositioning between 30 and 50 degrees. Regular pain. Increasing restraints on activities. Pronounced malpositioning!
Severest form with malpositionings over 50 degrees and painful restraints on the activities of everyday life. Surgical treatment
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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
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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.
85 Maria Carmela L. Domocmat, RN, MSN http://www.concordortho.com/patient-education/topic-detailpopup.aspx?topicID=a5cea3a8a6d8093483657c959125dbaf 8/24/2011
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
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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
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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 degenerative joint disease.

http://emedicine.medscape.com/article/1232902-treatment#showall
Postoperative radiograph obtained after resectional arthroplasty and total joint implant placement. 8/24/2011
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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 radiograph shows arthrodesis.

Postoperative radiograph show arthrodesis.

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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 hypermobile first ray.

Postoperative radiograph shows arthrodesis of the first metatarsocuneiform.
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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 wellchosen 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
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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
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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
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pectus carinatum
pectus excavatum
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EhlersGenetics 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 EhlersDanlos 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 hypermobility is less intense than with other conditions.
Patient with Ehlers-Danlos syndrome. Note the abnormal 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
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Type
Inheritance Previous Major Diagnostic Minor Diagnostic Nomenclature Criteria Criteria

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

Autosomal Types I and II dominant Skin hyperextensibility,
Minor Diagnostic Criteria
Hypermobilit Autosomal Type III y dominant Vascular Autosomal Type IV dominant
Smooth, velvety skin; easy bruising; 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) Skin involvement (soft, smooth and Recurrent joint dislocation; chronic velvety), joint hypermobility joint pain, limb pain, or both; positive family history Thin, translucent skin; Acrogeria, 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
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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
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Disorders of foot : Mortons neuroma (plantar neuroma
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Neuromas
are non-cancerous growths of the nerve tissue that develop in different parts of the body.
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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.
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http://www.footdoc.ca/www.FootDoc.ca/Website _Neuroma.gif
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Neuroma and adherent fibrofatty tissue.
http://emedicine.medscape.com/article/308284-clinical#showall
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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.
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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]
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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.
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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.
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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.
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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.
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http://orthoinfo.aaos.org/topic.cfm?topic=a00158
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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 antiinflammatory medication, custom foot orthoses and cortisone injections provide relief in over 80 percent of people with Morton's Neuroma.
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http://orthoinfo.aaos.org/topic.cfm?topic=a00158
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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
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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.
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Maria Carmela L. Domocmat, RN, MSN Neurectomy: deeper dissection.
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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.
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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.
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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.
Maria Carmela L. Domocmat, RN, MSN 8/24/2011
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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.
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SerotoninSerotonin-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
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Disorders of foot : Hammer toe
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Hammer toe
is a deformity of the toe, in which the end of the toe is bent downward.
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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.
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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
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http://www.myfootshop.com/images/medical/ortho/hammer_toe_differences_mod.jpg
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http://www.familyfoot.com/images/hammer_toe_whatis.jpg
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Treatment
Mild hammer toe in children can be treated by manipulating and splinting the affected toe.
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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
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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.
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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.
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Prevention and Cure of Hammer Toes with Products

Hammer Toe Regulator Hammer Toe Cushion Foam Toe Tubes Gel Toe Cap Toe Spreader Silicone Toe Crest Toe Spacer Cushion Digital Toe Pad Yoga Toes Toe Stretcher
Toe Rings Toe Brace Toe Alignment Splint Toe Trainers Hammer Toe Straightener
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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
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http://mdbuyinggroup.com/products/sites/default/files/productimages/pedifix%20budin%20hammer %20toe%20regulator.jpg
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Hammer Toe Correction Bandage

Price $14.95
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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Prevention
Avoid wearing shoes that are too short or narrow. Check children's shoe sizes often, especially during periods of fast growth.
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(prognosis) Expectations (prognosis)

If the condition is treated early, you can often avoid surgery. Treatment will reduce pain and walking difficulty.
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Complications
Foot deformity Posture changes caused by difficulty in walking
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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/
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Muscular disorders: Muscular dystrophy
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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
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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
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http://www.humanillnesses.com/original/images/hdc_0001_0002_0_img0181.jpg
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Muscular Dystrophies (MD)

characterized by progressive weakness and degeneration of the skeletal muscles that control movement. Some forms seen in infancy or childhoodothers 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
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Etiology
are a group of inherited conditions Its 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/
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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/musculardystrophy/DS00200/DSECTION=symptoms
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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 Xchromosome. 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.
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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
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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.
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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
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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.
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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
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Duchenne muscular dystrophy
http://www.checkorphan.org/grid/iwishes/duchenne-muscular-dystrophy
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Duchenne muscular dystrophy
http://trialx.com/curetalk/wpcontent/blogs.dir/7/files/2011/05/diseases/Muscular_Dystrophy_Duchenne-3.jpg
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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/
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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.
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Facioscapulohumeral muscular dystrophy

Also known as Landouzy-Dejerine dystrophy involves progressive muscle weakness involving:
Face Shoulders Abdomen Feet Upper arms Pelvic area Lower arms
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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.
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Myotonic MD
Aka: Steinerts 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
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Maria Carmela L. Domocmat, RN, MSN 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
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http://www.websters-onlinedictionary.org/images/wiki/wikipedia/commons/thumb/e/e1/Autodominant.jpg/180px-Autodominant.jpg
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http://www.websters-onlinedictionary.org/images/wiki/wikipedia/commons/thumb/e/e1/Autodominant.jpg/180px-Autodominant.jpg Maria Carmela L. Domocmat, RN, MSN
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.
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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.
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Myotonic MD
Maria Carmela L. Domocmat, RN, MSN 182 http://blog.thirdeyehealth.com/images/muscular-dystrophy-1.jpg
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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
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LimbLimb-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.
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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
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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.
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Congenital myotonic dystrophy

Signs in infants may include:
Severe muscle weakness Difficulty sucking and swallowing Difficulty breathing Cognitive impairment
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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.
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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.
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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
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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.
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EmeryEmery-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.
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EmeryEmery-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.
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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)
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195
http://healthmedcare.com/muscular-dystrophy-types-symptoms-of-each-form/ Maria Carmela L. Domocmat, RN, MSN
8/24/2011
Clinical manifestations
Progressive muscular weakness Delayed meeting of motor milestones Waddling gait Walking on toes Frequent falls Gowers 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 musclesprimarily 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
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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
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http://www.wrongdiagnosis.com/symptoms/walking_symptoms/book-causes-16g.htm
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.
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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.
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Gowers sign
to stand, affected children press their hands against their ankles, knees and thighs
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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-LacSt-Jean regions, where one person out of 500 is estimated to carry the disease.
http://pathologyproject.wordpress.com/2011/04/24/muscular-dystrophy/
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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
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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
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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
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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.
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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.
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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.
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References
http://www.mdausa.org/ http://www.mayoclinic.com/health/musculardystrophy/DS00200/DSECTION=treatments-and-drugs
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Muscular disorders: Rhabdomyolysis
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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
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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
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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.
Maria Carmela L. Domocmat, RN, MSN 215 http://www.emedicinehealth.com/rhabdomyolysis/page2_em.htm 8/24/2011
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.
Maria 216 Medscpae Carmela L. Domocmat, RN, MSN 8/24/2011
Incidence
United States
Rhabdomyolysis accounts for an estimated 8-15% of cases of acute renal failure.
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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.
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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
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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.
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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]
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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
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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.
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Symptoms
Abnormal urine color (dark, red, or cola colored) General weakness Muscle stiffness or aching (myalgia) Muscle tenderness Weakness of the affected muscles
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Symptoms
Additional symptoms that may be associated with this disease include the following:
Fatigue Joint pain Seizures Weight gain (unintentional)
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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.
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Assess ABCs and support as needed. Treat any underlying conditions, such as trauma, infection, or toxins. General recommendations for the treatment of rhabdomyolysis include
fluid resuscitation prevention of end-organ complications
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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.

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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.
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http://emedicine.medscape.com/article/827738-clinical#showall Maria Carmela L. Domocmat, RN, MSN
8/24/2011
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.
8/24/2011
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.
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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.
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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.
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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.
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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.
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Loop diuretics
Class Summary
These agents elicit a loss of free water, increasing diuresis.
Furosemide (Lasix)
Increases water excretion by interfering with the chloridebinding 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
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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
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Further Inpatient Care

In patients with no apparent precipitating factors for rhabdomyolysis
consider inherited disorders of carbohydrate or lipid metabolism and myopathies.
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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)
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(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.
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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.
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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.
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References
In: Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 114. http://www.nlm.nih.gov/medlineplus/ency/article/00047 3.htm http://emedicine.medscape.com/article/827738clinical#showall
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Musculoskeletal Disorders Part 1

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Musculoskeletal Disorders Part 1

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Musculoskeletal Disorders Part I

Part II Degenerative bone disorders: OA Metabolic bone disorders

Spinal column deformities

Maria Carmela L. Domocmat, RN, MSN

Bone infections: Osteomyelitis

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

Causes, incidence, and risk factors

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

Emergency Department Care

Maria Carmela L. Domocmat, RN, MSN

Emergency Department Care

Maria Carmela L. Domocmat, RN, MSN

Antibiotics are given to destroy the bacteria causing the infection.

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

osteomyelitis due to trauma

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

(prognosis) Expectations (prognosis)

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

Bone infections: Septic arthritis

Maria Carmela L. Domocmat, RN, MSN

chronic septic arthritis

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

Symptoms in newborns or infants:

Maria Carmela L. Domocmat, RN, MSN

Symptoms in children and adults:

Maria Carmela L. Domocmat, RN, MSN

Exams and Tests

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

Medical management of infective arthritis focuses

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

Joint Immobilization and Physical Therapy

Synovial Fluid Drainage

Maria Carmela L. Domocmat, RN, MSN

Surgical Intervention in Prosthetic Joint Infection

Maria Carmela L. Domocmat, RN, MSN

(Prognosis) Outlook (Prognosis)

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN

Maria Carmela L. Domocmat, RN, MSN