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Musculoskeletal & IntegumentaryDisorders

University of San Francisco

Dr. M. Maag©2003 Margaret Maag

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Class 3 ObjectivesUpon completion of this lesson, the student will be able to

• explain the etiological differences of OA, RA, osteoporosis,osteomyelitis and bone fracture.

• recognize common skin lesions, and determine the nurse’srole in the prevention of skin breakdown.

• differentiate between acute and chronic pain, and describe thepathophysiologic consequences of pain gone untreated.

• state the different types of burns and clinical manifestations.• identify ways that children and elders respond to changes in

environmental temperature.• investigate the biologic basis for sleep, vision, hearing, and

taste disorders across the lifespan.

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Osteoporosisl A multifactorial disorder involving < bone mass and

> bone fragility as a result of a disequilibrium ofosteoblastic and osteoclastic activity

l Epidemiology: Affects 25 million females in the US

l Etiology: Low bone density & genetically determinedrapid rate of bone loss

l African Americans have denser bones

l Hyperparathyroidism: bone resorption isstimulated = high serum calcium levels.

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Osteoporosisß Factors promoting bone loss:

l Family history, white race, femalel cigarette smoking; ETOH abuse; lack of exercisel > amount of caffeine; > corticoidsteroids; < estrogen levels; agingl Dx: Dual photon absorptiometry and CT scans

ß Clinical manifestations:l Fracture is the first sign; compression fractures of the spine and

“kyphosis” & loss of heightl Pain and bone deformity

ß Prevention: > dietary intake of Ca+ ( 1 g for young women; 1.5 g PM)l vitamin D; wt. bearing exercise; HRT; Fosimax; Calcitonin;

Raloxifene

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Infectious Osteomyelitisß An acute infection of the bone

l “hematogenous”: spread of a bloodborne pathogens• Spread from bone to adjacent soft tissues• Found in infants, children, and elderly

l “exogenous”: spread via compound fractures, puncture wound,human or animal bites, IM injection sites,and surgical sites

• Spread from soft tissue to adjacent bone

l organisms: Staph aureas; Streptococci, Pseudomonas, H-flul local “Brodie” abscesses may develop

ß Elderly, children; diabetics & SCD are at > riskß S&S: Adult:fever, fatigue, malaise, wt. loss, pain

l Child: fever, chills, reluctance to move a limb

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Fracturesß A break in the continuity of bone

l Open: damage to the tissue in addition to the fracture

l Closed: no penetration of the skin or soft tissues

l Comminuted: bone fragments are completely separated

ßRisk factors:l sport injuries; falls; MVAs; drugs & alcohol; immaturity;

osteoporosis; primary or metastatic bone tumors

ßVelocity: an > force greater then the bone can withstand

l dense bone requires more force (e.g. femur)

l weak ( “swiss cheese”) bone requires less force

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Common Fracturesß Pathological: any disease process that weakens bone

l low velocity impact: tumors, osteoporosis, infections

ß Fatigue: d/t abnormal stress or torque to a bone of normalability to deform and recover (e.g. joggers, dancers)

ß Insufficiency: a stress fracture that occur in bones lackingnormal ability to deform and recover (e.g. normal WB)

ß Pelvis & Femur High-energy trauma r/t MVA or sports injuriesß Hip: falls; osteoporosis; elderlyß Tx: reduction (closed vs. open) followed by immobilization

l traction; surgical intervention with hardwareß Outcome: most fractures heal with appropriate treatment

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Bone Fracture Repair

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Osteoarthritis (OA)ß Joint damage & inflammation caused by a biochemical alteration

of the cartilage in one or a few jointsl Women > 55; hand, wrist, neck, lower back joints, hip, knee, feet

l postmenopausal females at highest risk; or athletes

ß Articular cartilage is completely destroyed and underlying bone isexposed leading to stress on the bone

l results in bony overgrowth; formation of bone spurs; cysts

ß S & S: joint pain, stiffness in the morning, crepitus, &limitation of movement; Heberden’s or Bouchard’s nodules

ß Tx: REST; ROM; acetaminophen; isometric exercises

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Rheumatoid Arthritis (RA)

ßA chronic systemic autoimmune disorderassociated with chronic inflammation of connectivetissue.

• Genetic predisposition: HLA subtypes (DR4 & DRB1)

• Epstein Barr virus may be implicated as the antigen

• Synovitis: inflammation of the synovial membrane is present

• Ankylosis: fusion of the joint which causes immobilization

l Fingers, feet, wrists, elbows, ankles, and knees areaffected

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Rheumatoid Arthritis (RA)

ßSigns and symptoms:l First: Fatigue, weakness, poor appetite, low

grade fever, anemia and ESRl Diagnostic criteria established by the American

Rheumatism Association• Morning stiffness, joint pain or tenderness, swelling

of at least two joints, structural changes upon x-rayand subcutaneous nodules

• Positive rheumatoid factor agglutination test• Ulnar deviation, Swan-Neck or Boutonniere deformity

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Integumentary Disorders& Burns

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CellulitisßA diffuse inflammation of the dermis & subcutaneous

tissuel Generally in the extremities, but can occur other places

l Cause: bacterial infection of the skinl Staph aureas or Beta-hemolytic strepl Predisposing factors:

• Problems with venous or lymphatic drainage• Previous injury to the limb (trauma, break in skin, surgery)• Athletes foot, obesity, pregnancy, diabetes, alcoholism

l Inflammation fails to contain the infecting organism

ßManifestations: redness, swelling, warmth, drainage

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Pressure Ulcersß Ischemic ulcers as a result of shearing force

and/or pressureß Factors:

l Immobilized elders in SNF are @ > riskl Incontinence, lying on an O.R. table for long

periodsl > length of hospital stay, spinal cord injuries

ß Stages:l One = nonblanchable erythema of intact skinl Two = partial-thickness skin loss (epidermis and/or dermis)l Three = full-thickness skin loss involving damage or

necrosis of subcutaneous tissuel Four = full-thickness skin loss with extensive destruction,

tissue necrosis, damage to muscle, bone, or supportingstructures

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Skin Cancer

ß Most common:l basal cell & squamous cell : high cure ratel malignant melanoma: most lethal skin cancer

ß Risk factors: UVB light; scarring; ulcerationsß Squamous cell may metastasize

l Firm, elevated, granular-appearing tumorsthat bleed easily

ß Malignant mealnoma: malignant neoplasm frommelanocytes

l “ABCD” criteria

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Skin CancerTreatment

ßBasal Cell: simple excision

ßSquamous Cell: excision & possiblyradiation therapy

ßMalignant Melanoma: excision, surgicalremoval of surrounding tissue, & lymphnode biopsy.

l Radiation, chemotherapy, or immunetherapy may be used.

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Karposi Sarcoma

ßHHV-8 is the viral infection underlying thedevelopment of Karposi Sarcoma (KS)

l Pathogenesis is complex and involves the processof infection with HHV-8 and the production ofinflammatory cytokines, as well as the process ofangiogenesis

l The use of antiangiogenesis compounds mayprevent Karposi Sarcoma

l Interferon may work by inhibiting angiogenesis

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Burnsß An injury to the skin & possibly to deeper tissues d/t direct

contact with heat, chemicals, electricity, radiation

l 1.25 million people/ year in the US

l At risk: elderly; handicapped; children; occupational hazard

ß Thermal: exposed skin or mucous membranes to direct flame,hot liquids, or radiant energy

ß Chemical: skin or mucous membranes have direct contact withchemical spills or inhalation of toxic gases

ß Electrical: passage of electrical current through the body to theground

• lightning; high-voltage sources; electrical devices

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BurnsßLocal & Systemic Responses:

l minor burns heal with inflammatory response

l larger wounds heal with scar tissue formation

l loss of normal skin function; stress response;release of > cytokines; dysrhythmias (v-fib);damage to the alveolar -capillary membraned/t inhalation of toxins; all body systems areaffected

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Burn Classification

Sensory neuronsare destroyed

Dermis isdestroyed but

hair follicles willgrow back

2nd: Deep partialthickness

Looks like a3rd degree

No paingenerally

Muscle, bone,and internal

tissues

Fourth

WhiteCherryBlack

No pain presentif nerves areburned

Extend throughdermis, epidermis& subcutaneous

layer

Third

Full thickness

Barrierfunction islost in both

types ofsecond degree

burns

Extreme pain

Blisters immed.

Epidermis &partial dermis

2nd: Superficial

Partial thickness

SunburnErythemaEpidermal cells

onlyFirst

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Burnsß Fluid Imbalances: during post-burn period the

capillaries reach their maximal dilation and permeabilityd/t release of histamine, prostaglandins, and kinins

ß Intravascular fluid shifts into interstitial spacel fluids are loss through evaporation 10 times normal rate

ßHypovolemic shock (“burn shock”) resultsl manifests as < cardiac output, hypotension, tachycardia,

oliguria, massive edema ( watch out for airway !)

l treat with large doses of isotonic fluid (Ringer’s Lactate)

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Burns

ßPrevention: Smoke detectors in homes & publicbuildings; educate the elderly and children

ßTreatment: fluid resuscitation is immediate priority inmajor burns; titrate fluids according to cardiac output &urine output once the capillaries have sealed off

ßRenal function may need support of dialysis

ßBurn wound will require cleaning & debridement

ß“Rule of Nines:” assessment tool to assist withestimation of total burn surface area.

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References

ß Hansen, M. (1998). Pathophysiology:Foundations of disease and clinical intervention.Philadelphia: Saunders.

ß Huether, S. E., & McCance, K. L. (2002).Pathophysiology. St. Louis: Mosby.