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Quiz 3 Study Guide
Skin Lesions: External Clues to Internal Problem Box 9.8 p. 157
Many systemic conditions or disorders may present congenital external clues that are apparent on
physical examination. The following are a few examples of cutaneous markers that may signal
underlying disease. A thorough evaluation is necessary, although some clues may be isolated
findings and may require no intervention, follow-up, or treatment.
• Faun tail nevus: Tuft of hair overlying the spinal column at birth, usually in the lumbosacral area;
may be associated with spina bifida occulta.
• Café au lait macules: Flat, evenly pigmented spots varying in color from light brown to dark brown
or black in darker skin; larger than 5 mm in diameter; present at birth or shortly thereafter; may be
associated with neurofibromatosis or miscellaneous other conditions including pulmonary stenosis,
temporal lobe dysrhythmia, and tuberous sclerosis.
• Freckling in the axillary or inguinal area: Multiple flat pigmented macules associated with
neurofibromatosis; may occur in conjunction with café au lait macules.
• Facial port-wine stain: Usually at least one eyelid and/or the forehead of one side of the face are
affected. It may be associated with ocular defects, most notably glaucoma; or may be accompanied
by angiomatous malformation of the meninges (Sturge-Weber syndrome), resulting in atrophy and
calcification of the adjacent cerebral cortex.
• Port-wine stain of limb and/or trunk: When accompanied by varicosities and hypertrophy of
underlying soft tissues and bones, may be associated with orthopedic problems (Klippel-TrenaunayWeber syndrome).
• Supernumerary nipples: Congenital accessory nipples with or without glandular tissue, located
along the mammary ridge (see Chapter 17); may be associated with renal abnormalities, especially
in the presence of other minor anomalies.
• “Hair collar” sign: A ring of long, dark, coarse hair surrounding a midline scalp nodule in infants is
usually an isolated cutaneous anomaly that may indicate neural tube closure defects of the scalp.
Abnormalities Skin, Hair Nails Page 163-170
Eczematous Dermatitis
Most common inflammatory skin disorder; several forms, including irritant contact dermatitis, allergic
contact dermatitis, and atopic dermatitis.
Pathophysiology
• Common factor of the various forms are intercellular edema and epidermal breakdown.
• Eczematous dermatitis has three stages: acute, subacute, and chronic.
• Itch-scratch cycle perpetuates the rash.
• Excoriation from scratching predisposes to infection and causes crust formation (Fig. 9.44).
Subjective Data
• Itching is typically present.
• Those with atopic dermatitis often report allergy history (allergic rhinitis, asthma).
• For irritant or allergic contact, exposure history is important.
Objective Data
• Acute phase characterized by erythematous, pruritic, weeping vesicles
• Subacute eczema characterized by erythema and scaling
• Chronic stage characterized by thick, lichenified, pruritic plaques
• Atopic dermatitis: during childhood, lesions involve flexures, the nape, and the dorsal aspects of
the limbs; in adolescence and adulthood, lichenified plaques affect the flexures, head, and neck2
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Folliculitis
Inflammation and infection of the hair follicle and surrounding dermis.
Pathophysiology
• Presence of inflammatory cells within the wall and ostia of the hair follicle creates a follicular-based
pustule.
• Inflammation can be either superficial or deep; deep folliculitis can result from chronic lesions of
superficial folliculitis or from lesions that are manipulated.
• Persistent or recurrent lesions may result in scarring and permanent hair loss.
• Sometimes due to a bacterial (e.g. staphylococcus) or yeast infection.
Subjective Data
• Acute onset of papules and pustules associated with pruritus or mild discomfort; may have pain
with deep folliculitis
• Risk factors: frequent shaving, immunosuppression, hot tubs without adequate chlorine, preexisting
dermatoses, long-term antibiotic use, occlusive clothing and/or occlusive dressings, exposure to hot
humid temperatures, diabetes mellitus, obesity, and use of EGFR (epithelial growth factor receptor)
inhibitor medications
Objective Data
• Primary lesion is a small pustule 1–2 cm in diameter that is located over a pilosebaceous orifice
and may be perforated by a hair.
• Pustule may be surrounded by inflammation or nodular lesions; after the pustule ruptures, a crust
forms (Fig. 9.45).
• May have suppurative drainage with deep folliculitis.
• Any hair-bearing site can be affected; the sites most often involved are the face, scalp, thighs,
axilla, and inguinal area.
Furuncle (Boil)
A deep-seated infection of the pilosebaceous unit.
Pathophysiology
• Staphylococcus aureus is the most common organism.
• Initially, a small perifollicular abscess that spreads to the surrounding dermis and subcutaneous
tissue.
• May occur singly or in multiples; when infection involves several adjacent follicles, a coalescent
purulent mass or carbuncle forms.
Subjective Data
• Acute onset of tender red nodule with center filled with pus.
Objective Data
• Skin is red, hot, and tender.
• Center of the lesion is purulent and forms a core that may rupture spontaneously or require surgical
incision (Fig. 9.46).
• Sites commonly involved are the face and neck, arms, axillae, breasts, thighs, and buttocks.
Cellulitis
Diffuse, acute, infection of the skin and subcutaneous tissue.3
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Pathophysiology
• Majority of cases caused by Streptococcus pyogenes or Staphylococcus aureus.
Subjective Data
• Break in the skin, such as a fissure, cut, laceration, insect bite, or puncture wound
• Pain and swelling at the site
• May have fever
Objective Data
• Skin is red, hot, tender, and indurated; borders are not well demarcated (Fig. 9.47).
• Lymphangitic streaks and regional lymphadenopathy may be present.
• Rare to have bilateral cellulitis.
Tinea (Dermatophytosis)
Group of noncandidal fungal infections that involve the stratum corneum, nails, or hair.
Pathophysiology
• Infection by dermatophytes, typically acquired by direct contact with infected humans or animals;
invade the skin and survive on dead keratin.
• Lesions are usually classified according to anatomic location and can occur on nonhairy parts of
the body (tinea corporis), on the groin and inner thigh (tinea cruris), on the scalp (tinea capitis), on
the feet (tinea pedis), and on the nails (tinea unguium).
Subjective Data
• May report pruritus.
• May report hair breaking.
• Nail changes accompany onychomycosis.
Objective Data
• While often annular, lesions can vary in appearance and may be papular, pustular, vesicular,
erythematous, or scaling (Fig. 9.48).
• Secondary bacterial infection may be present.
• Microscopic examination of skin scraping with potassium hydroxide (KOH) solution shows
presence of hyphae.
• Infected nails are yellow and thick and may separate from the nail bed.
Pityriasis Rosea
Self-limiting inflammation of unknown cause.
Pathophysiology
• Possible infectious etiology (Drago et al., 2015), likely herpesvirus (HHV)-6 or HHV-7
• Not contagious
Subjective Data
• Sudden onset with occurrence of a primary (herald) oval or round plaque.
• Herald lesion is often missed.
• Eruption occurs 1–3 weeks later and lasts for several weeks.
• Pruritus may be present with the generalized eruption.
• Often occurs in young adults during the spring time.
Objective Data4
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• Lesions are usually oval, pale, erythematous, flat-topped papules and plaques with fine scaling
(Fig. 9.49).
• Lesions develop on the extremities and trunk; palms and soles are not involved, and facial
involvement is rare.
• Trunk lesions are characteristically distributed in parallel alignment following the skin tension lines
in a Christmas tree–like pattern.
Psoriasis
Chronic and recurrent disease of keratinocyte proliferation.
Pathophysiology
• Multifactorial origin with genetic component and immune regulation
• Characterized by increased epidermal cell turnover, increased numbers of epidermal stem cells,
and abnormal differentiation of keratin expression leading to thickened skin with copious scale
• Related to tumor necrosis factor (TNF)-alpha
Subjective Data
• May have pruritus
• Concerns about appearance
• Does not typically get superinfected
Objective Data
• Characterized by well-circumscribed, dry, silvery, scaling papules and plaques (Fig. 9.50).
• Lesions commonly occur on the back, buttocks, extensor surfaces of the extremities, and the scalp.
• Can be associated with psoriatic arthritis in up to 30% of patients.
• May have pitting nail involvement.
Rosacea
Chronic inflammatory skin disorder.
Pathophysiology
• Cause unknown; occurs most often in persons with a fair complexion
• Lasts for years, with episodes of activity followed by quiescent periods of variable length
Subjective Data
• Itching is absent.
• Many patients report a stinging pain associated with flushing episodes.
• Common triggers are exposure to the sun, cold weather, sudden emotion (e.g., laughter or
embarrassment), hot beverages, spicy foods, and alcohol consumption.
Objective Data
• Eruptions appear on the forehead, cheeks, nose, and occasionally about the eyes.
• Characterized by telangiectasia, erythema, papules, and pustules that occur particularly in the
central area of the face (Fig. 9.51).
• Although rosacea resembles acne, comedones are not present.
• Tissue hypertrophy of the nose (rhinophyma) may occur, characterized by sebaceous hyperplasia,
redness, prominent vascularity, and swelling of the skin of the nose (Fig. 9.52).
Herpes Zoster (Shingles)
Varicella-zoster viral (VZV) infection.5
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Pathophysiology
• VZV morphologically and antigenically identical to the virus causing varicella (chickenpox)
• Dormant viral particles (since the original episode of varicella) in the posterior spinal ganglia or
cranial sensory ganglia become activated and spread along the nerve
Subjective Data
• Pain, itching, or burning of the dermatome area usually precedes eruption by 4–5 days.
• After eruption resolves, there may be persistent pain called postherpetic neuralgia.
Objective Data
• Single dermatome that consists of red, swollen plaques or vesicles that become filled with purulent
fluid (Fig. 9.53)
• Does not cross midline
• Can still occur in immunized patients
• Disseminated lesions in immunosuppressed or older adults
Herpes Simplex
Infection by herpes simplex virus (HSV).
Pathophysiology
• Two virus types cause the infection: type 1, usually associated with oral infection, and type 2, with
genital infection.
• Crossover infections are becoming common.
Subjective Data
• Tenderness, pain, paresthesia, or mild burning at the infected site before onset of the lesions
Objective Data
• Grouped vesicles appear on an erythematous base and then erode, forming a crust (Fig. 9.54).
• Lesions last 2–6 weeks.
• Can occur anywhere on the body.
Lyme Disease
A tick-borne disease that can lead to multisystemic infection.
Pathophysiology
• Spirochetal infection caused by Borrelia burgdorferi
• Most common tick-borne disease in the United States
• The spirochete deposited by the tick into the skin rather than directly into the bloodstream.
• Three phases of the disease are recognized: early localized, early disseminated, and late disease.
• The objective clinical manifestations are thought to be due to an inflammatory response to live
spirochetes or to their antigens.
Subjective Data
• Exposure to ticks
• Constitutional symptoms of fatigue, anorexia, and headache may develop.
• Expanding rash
Objective Data6
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• Early localized infection typically manifested by a single erythema migrans skin lesion, a flat to
slightly raised, erythematous skin lesion (usually ≥5 cm in diameter) that is round or oval in shape,
with central clearing (Fig. 9.55) (classic target or bull’s-eye appearance).
• Early disseminated infection is usually manifested by multiple erythema migrans skin lesions, by
neurologic symptoms such as facial palsy, meningitis, or encephalitis, or by symptoms of carditis
such as lightheadedness, palpitations, dyspnea, chest pain, or syncope.
• Late disease usually manifested by arthritis atrophicans or atrophic dermatitis.
Skin: Malignant/Neoplastic Abnormalities Page 171-172
Basal Cell Carcinoma
The most common form of skin cancer.
Pathophysiology
• Arises from the basal layer of the epidermis
• Occurs in various clinical forms including nodular, pigmented, cystic, sclerosing, and superficial
• Occurs most frequently on exposed parts of the body—the face, ears, neck, scalp, shoulders
Subjective Data
• Persistent sore or lesion that has not healed
• May have crusting
• May itch
Objective Data
• Shiny nodule that is pearly or translucent; may be pink, red, or white, tan, black, or brown (Fig.
9.58)
• Open sore; may have crusting; may bleed
• Reddish patch or irritated area, frequently occurring on the face, chest, shoulders, arms, or legs
• Pink growth with a slightly elevated rolled border and a crusted indentation in the center; as the
growth slowly enlarges, tiny blood vessels may develop on the surface.
• Scar-like area that is white, yellow, or waxy and often has poorly defined borders; the skin appears
shiny and taut.
Squamous Cell Carcinoma
Second most common form of skin cancer.
Pathophysiology
• This malignant tumor arises in the epithelium and has squamous differentiation.
• Lesions occur most commonly in sun-exposed areas, particularly the scalp, back of hands, lower
lip, and ear; the rim of the ear and the lower lip are especially vulnerable.
Subjective Data
• Persistent sore or lesion that has not healed or that has grown in size
• May have crusting and/or bleeding
Objective Data
• Elevated growth with volcano-type pattern (Fig. 9.59)
• Wartlike growth; may have crusting, may bleed
• Scaly red patch with irregular borders may have crusting and may bleed
• Open sore; may have crusting
Malignant Melanoma7
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Lethal form of skin cancer that develops from melanocytes.
Pathophysiology
• Melanocytes migrate into the skin, eye, central nervous system, and mucous membrane during
fetal development.
• Less than half of the melanomas develop from nevi; the majority arise de novo from melanocytes.
• The exact cause of malignancy is not known; heredity, hormonal factors, ultraviolet light exposure,
or an autoimmunologic effect may contribute to causation.
Subjective Data
• New nevus or preexisting nevus that has changed or is changing
• New pigmented lesion that has irregularities (Fig. 9.60)
• History of melanoma
• History of atypical nevi
• Family history of melanoma (first-degree relative)
• Significant sunlight or tanning bed use
Objective Data
• ABCDE changes in nevi (Fig. 9.61)
• A Asymmetry of lesion: one-half of a nevus or birthmark does not match the other
• B Borders: edges are irregular, ragged, notched, or blurred. Pigment may be streaming from the
border.
• C Color: the color is not the same all over and may have differing shades of brown or black,
sometimes with patches of red, white, or blue.
• D Diameter: the diameter is 6 mm (about the size of a pencil eraser) or is growing larger.
• E Evolution: changes seen in existing pigmented lesions, particularly in a nonuniform, asymmetric
manner.
Actinic Keratosis p 187
Atypical squamous cells confined to the upper layers of epidermis
Pathophysiology
• Occurs secondary to chronic sun damage
• Most lesions remain superficial; lesions can progress into squamous cell carcinoma over time.
Subjective Data
• History of chronic sun exposure
• Increasing number of lesions with age
Objective Data
• Raised, gritty, erythematous lesion that is usually with an irregular, rough surface
• Lesion is most common on the dorsal surface of the hands, arms, neck, and face (Fig. 9.88).
Lymph nodes Page 190-191
Lymph nodes are discrete structures surrounded by a capsule composed of connective tissue and a
few elastic fibrils. Lymph nodes usually occur in groups. Superficial nodes are located in
subcutaneous connective tissues, and deeper nodes lie beneath the fascia of muscles and within the
various body cavities. The nodes are numerous and tiny, but some of them may have diameters as
large as 0.5 to 1 cm. They defend against the invasion of microorganisms and other particles with
filtration and phagocytosis, and they aid in the maturation of lymphocytes and monocytes.8
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Lymphatic system Abnormalities 200-207
Acute Lymphangitis
Inflammation of one or more lymphatic vessels
Pathophysiology
• Pathogenic organisms enter the lymphatic vessels directly through a wound or as a complication of
infection and produce a local inflammatory response.
• Inflammation or infection then extends proximally toward regional lymph nodes.
Subjective Data
• Enlarged lymph node
• Pain, malaise, possibly fever
• Minor trauma to the skin distal to the area of infection
Objective Data
• Red streaks in the skin after the course of the lymphatic collecting duct
• Appears as a tracing of rather fine lines streaking up the extremity
• Sometimes indurated and palpable to gentle touch
• Look distal to the inflammation for sites of infection, particularly between digits
Acute Suppurative Lymphadenitis
Infection and inflammation of a lymph node; may affect a single or localized group of nodes
Pathophysiology
• Most commonly caused by group A beta-hemolytic streptococci and coagulase-positive
staphylococcal infection
• Other pathogens may include actinomycotic adenitis as a result of dental disease; mycobacterial
lymphadenitis in the presence of the tuberculosis organism; Pasteurella multocida infection at the
site of a scratch or bite from a dog or cat
• Lymph nodes enlarged because of the cellular infiltration and edema
• Nodes tender because of distention of the capsule
• Acute lymphadenitis most often seen in the cervical region due to microbial drainage from
infections of the teeth or tonsils and in the axillary or inguinal regions secondary to infections in the
extremities
• Systemic viral infections (particularly in children) and bacteremia often produce generalized
lymphadenopathy.10
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Subjective Data
• Enlarged lymph nodes
• Pain from enlarged lymph nodes
Objective Data
• Involved node usually firm and tender
• Overlying tissue edematous; skin appears erythematous, usually within 72 hours
• When abscess formation is extensive, nodes fluctuant
• Mycobacterial adenitis characterized by an inflammation without warmth that may or may not be
slightly tender
Lymphedema
Edematous swelling due to excess accumulation of lymph fluid in tissues caused by inadequate
lymph drainage
Pathophysiology
• Result of protein-rich interstitial volume overload, secondary to lymph drainage failure
• Four major physiologic mechanisms: increased blood capillary hydrostatic pressure, decreased
plasma protein concentration, increased blood permeability, and blockage of lymph return
• Primary lymphedema: hypoplasia and maldevelopment of the lymphatic system; can manifest in
infants or later; termed praecox in adolescence and tarda in patients approaching 40 years of age
• Secondary: acquired damage to regional lymph nodes—pressure from tumors, scar tissue after
radiation, or surgical removal of lymph nodes
Subjective Data
• Painless swelling of a limb; unilateral or bilateral
• Onset usually gradual
• History of trauma, surgery, or radiation to a regional area
• Travel to areas where filariasis is common
• Family history of leg swelling
Objective Data
• Swelling and often grotesque distortion of the extremities (Fig. 10.23)
• Lymphedema may or may not pit.
• Overlying skin eventually thickens and feels tougher than usual
• Primary lymphedema often apparent at birth and most often involves the legs, particularly the
dorsum of the foot; the degree varies with the severity and distribution of the abnormality and may
not appear until young adulthood
Lymphangioma/Cystic Hygroma
Congenital malformation of dilated lymphatics
Pathophysiology
• Results from a failure of complete development and subsequent obstruction of the lymphatic
system; commonly found in the neck
Subjective Data
• Painless cystic masses
• Usually manifest during the first year of life and often enlarged after an upper respiratory infection
• Asymptomatic when in the posterior triangle of the neck, but if found anteriorly, may cause airway
or swallowing problems11
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Objective Data
• Soft, non-tender, and easily compressible spongy fluid-containing mass without discrete margins
• Most present at birth and apparent early in life, usually in the neck or axilla, less commonly in the
chest or extremities
• May be large enough to distort face and neck
• Diagnosis through physical examination and imaging studies (ultrasound, computed tomography,
or magnetic resonance imaging), which show a thin-walled, multiloculated cystic mass
Lymphatic Filariasis (Elephantiasis)
Massive accumulation of lymphedema throughout the body; the most common cause of secondary
lymphedema worldwide
Pathophysiology
• Results from widespread inflammation and obstruction of the lymphatics by the filarial worms
Wuchereria bancrofti or Brugia malayi; transmitted by mosquitoes
• Adequate drainage is prevented, and the patient becomes more susceptible to infection, cellulitis,
and fibrosis
• The term elephantiasis often incorrectly used to describe the result of any obstruction, congenital or
acquired.
Subjective Data
• Swelling of limb or body area
• Travel to infected areas: Asia, Africa, the Western Pacific, India, Philippines
• Many patients are asymptomatic, but some may develop fever with lymphangitis and
lymphadenitis, chronic pulmonary infection, and progressive lymphedema
Objective Data
• Lymphedema of the entire arm or leg; the genital regions (vulva, scrotum, breasts)
• Diagnosis can be made by identification of microfilariae microscopically in blood
Non-Hodgkin Lymphoma
Malignant neoplasm of the lymphatic system and the reticuloendothelial tissues
Pathophysiology
• Non-Hodgkin lymphomas occur most often in lymph nodes in the chest, neck, abdomen, tonsils,
and skin; they may also develop in sites other than lymph nodes such as the digestive tract, central
nervous system, and around the tonsils.
• Most arise in B cells; the rest occur in T cells
• Histologically, their cells are often undifferentiated but resemble lymphocytes, histiocytes, or
plasma cells.
Subjective Data
• Painless enlarged lymph node(s)
• Fever, weight loss, night sweats, abdominal pain, or fullness
• Family history of non-Hodgkin lymphomas
Objective Data
• Nodes may be localized in the posterior cervical triangle or may become matted, crossing into the
anterior triangle.
• Nodes usually well defined and solid12
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• Cannot distinguish the findings of these conditions from those in Hodgkin lymphoma through
physical examination alone
Hodgkin Lymphoma
Malignant lymphoma
Pathophysiology
• Unknown etiology, several subtypes
• Starts in a single node or chain and spreads to contiguous lymph nodes, spleen, liver, and bone
marrow
• Neoplastic giant cells release factors that induce the accumulation of reactive lymphocytes,
macrophages, and granulocytes.
• Occurs in all races, generally in late adolescence and young adulthood, although it also occurs in
people older than 50 years; most often, Hodgkin lymphoma starts in B-cell lymphocytes located in
lymph nodes in the neck area, although any lymph node may be the site of initial disease.
Subjective Data
• Painless enlarged lymph nodes
• May have abdominal pain, sometimes fever
• May have history of infectious mononucleosis
Objective Data
• Clinical presentation variable
• Most commonly, painless enlargement of the cervical lymph nodes, often in the posterior triangle,
that is generally asymmetric and progressive (Fig. 10.24)
• Nodes sometimes matted and firm, almost rubbery
• Usually asymmetric; may occasionally be enlarged in similar patterns on both sides of the body
• Nodal size may fluctuate
Epstein-Barr Virus Mononucleosis
Infectious mononucleosis
Pathophysiology
• Initially infects oral epithelial cells; after intracellular viral replication and cell lysis with release of
new virions, virus spreads to contiguous structures such as the salivary glands, with eventual
viremia and infection of the entire lymphoreticular system, including the liver and spleen
• Incubation period of infectious mononucleosis in adolescents is 30–50 days
Subjective Data
• Malaise, fatigue, acute or prolonged (longer than 1 week) fever, headache, sore throat, nausea,
abdominal pain, and myalgia
• Prodromal period may last 1–2 weeks
Objective Data
• Generalized lymphadenopathy most commonly in the anterior and posterior cervical nodes and the
submandibular lymph nodes and less commonly in the axillary and inguinal lymph nodes
• Epitrochlear lymphadenopathy is particularly suggestive of infectious mononucleosis
• Hepatomegaly; symptomatic hepatitis or jaundice is uncommon, but elevated liver enzymes are
common.
• Splenomegaly to 2–3 cm below the costal margin is typical; massive enlargement is uncommon
• Moderate to severe pharyngitis with tonsillar enlargement, occasionally with exudates13
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• Petechiae at the junction of the hard and soft palate frequently seen
• Diagnosis with mononucleosis spot test
Toxoplasmosis
Zoonosis, caused by the parasite Toxoplasma gondii
Pathophysiology
• Ingestion or inhalation of oocysts in soil/fomites, undercooked meat, or raw eggs; cat feces or litter
• Infection persists for life without signs of disease.
• In immunosuppressed persons, quiescent parasites multiply, resulting in neurologic disease or
other organ manifestations.
• May cause serious congenital infection if exposed during pregnancy, particularly in the first
trimester; transmitted directly from pregnant mother to fetus
Subjective Data
• No significant symptoms
• History of eating raw or rare meat or uncooked eggs
• History of direct contact with cat feces, cleaning the litter box, gardening in feces-contaminated soil
Objective Data
• Single node, chronically enlarged and non-tender
• Node is usually in the posterior cervical chain
Roseola Infantum (HHV-6)
Infection by human herpes virus 6
Pathophysiology
• Common in infancy with peak age of acquisition 2 years
• Virus present in the saliva of most adults and is readily transmitted by oral secretions
• Latency permits persistence of the virus in the presence of a fully developed immune response and
allows lifelong infection of the host.
• Through periodic reactivation of latent virus and the production of recurrent infection; virus
shedding occurs at intervals throughout life, allowing the virus to be spread to new susceptible hosts
Subjective Data
• Fever—usually high grade and persistent over 3–4 days
• Sometimes associated with a mild respiratory illness and lymphadenopathy
Objective Data
• Adenopathy, discrete and not tender, involves the occipital and postauricular chains and may last
for some time
• When the fever diminishes, a morbilliform fine maculopapular rash occurs, spreading from the trunk
to the extremities; the child begins feeling much better
Herpes Simplex (HSV)
Infection by human herpes virus 1 (HSV-1) or human herpes virus 2 (HSV-2)
Pathophysiology
• Transmitted by oral secretions, genital secretions, and close contact
• HSV causes lytic infection of fibroblasts and epithelial cells, and establishes latent infection in
neurons; HSV-1 has predilection for oropharyngeal infection and HSV-2 for genital infection;14
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although both viruses can infect and produce latent infection at either site, reactivation of each is
most common at the preferred site.
Subjective Data
• Burning, itching lesions
• May report enlarged lymph nodes
Objective Data
• Discrete labial and gingival vesicles or ulcers (Fig. 10.25)
• May have enlargement of the anterior cervical and submandibular nodes
• These nodes tend to be somewhat firm, quite discrete, movable, and tender; the frequency of this
condition and the symptoms are generally sufficient to establish the diagnosis; a viral culture can be
obtained if necessary
Cat Scratch Disease
A common cause of subacute or chronic lymphadenitis in children
Pathophysiology
• Caused mainly by Bartonella henselae and Bartonella clarridgeiae; usually follows a bite, scratch,
or other penetrating injury from a kitten or cat; the organisms, however, rarely cause illness in the cat
Subjective Data
• Bite, scratch, or wound from cat or kitten
• Inoculation lesion: a papule or pustule lasts 3–5 days and then becomes vesicular and crusts in 2–
3 days
• Painful enlarged lymph nodes
Objective Data
• Inoculation lesion; may be healing
• Lymphadenopathy develops in 1–2 weeks in the region that drains the primary lesion.
• Single lymph node most often, but multiple nodes are involved occasionally
• Tender nodes commonly in head, neck, and axillae; the accessible nodal areas in the arms and
legs are less often involved.
• Nodes can be very large—up to several centimeters; often red and tender and occasionally
suppurate
• Diagnosis can be made in the presence of a nodal enlargement lasting longer than 3 weeks,
accompanied by an inoculation lesion of the skin and after an interaction with a cat, a cat scratch, or
cat lick on a break in the skin.
• Lymphadenopathy can last for 2–4 months or even longer
Human Immunodeficiency Virus/Acquired Immune Deficiency Syndrome (HIV/AIDS)
Viral infection that attacks the body’s immune system
Pathophysiology
• Characterized by the dysfunction of cell-mediated immunity
• HIV seropositivity (HIV+): antibodies to HIV present, but sequelae of recurrent infections and
neoplastic disease has not yet occurred
• AIDS manifested clinically as the development of recurrent, often severe, opportunistic infections
• Common life-threatening diseases associated with full-blown AIDS include Kaposi sarcoma,
Pneumocystis jiroveci pneumonia, pulmonary tuberculosis, recurrent pneumonia, invasive cervical15
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cancer, a parotid enlargement simulating mumps, anemia and thrombocytopenia, chronic diarrhea,
and recurrent infections
Subjective Data
• Enlarged lymph nodes
• Initial symptoms include severe fatigue, malaise, weakness, persistent unexplained weight loss,
fevers, arthralgias, and persistent diarrhea
Objective Data
• Generalized lymphadenopathy
• In children there may be a prolonged clinical latent period, but initial signs may include
neurodevelopmental problems with loss of developmental milestones
• Progressive infection characterized by decreasing CD4+ T-lymphocyte count and increasing viral
load level
Serum Sickness (Type III Hypersensitivity Reaction)
An immune complex disease
Pathophysiology
• Systemic type III hypersensitivity reaction in response to antigens
• Mediated by the tissue deposition of circulating immune complexes, the activation of complement,
and the ensuing inflammatory response
• Patient can react similarly to repeated exposure to the stimuli; subsequent reactions may be more
severe and even fatal
Subjective Data
• Enlarged lymph nodes
• Pain, pruritus, and erythematous swelling at the injection site
• Urticaria, other rashes, lymphadenopathy, joint pain, fever, and at times facial edema
• Medications: beta-lactam antibiotics (especially cefaclor), sulfonamide antibiotics, minocycline
• Organ transplant
Objective Data
• Findings become apparent about 7–10 days after administration of the provoking substance
• Urticaria, maculopapular or purpuric lesions
• Lymphadenopathy most prominent in the area draining the injection site; can be generalized
• Facial and neck edema
• Symptoms subside slowly, recurring at times over several weeks
Latex Allergy Type IV Dermatitis
Delayed hypersensitivity reaction
Pathophysiology
• T cell–mediated, delayed response
• Allergic contact dermatitis that involves the immune system and is caused by the chemicals used in
latex products
Subjective Data
• Exposure to latex products
• Rash at area of contact16
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Objective Data
• Skin reaction usually begins 48–72 hours after contact
• Vesicular lesions, erythema localized to area of contact
• Reaction may progress to oozing skin blisters
Latex Allergy Type I Reaction
True allergic reaction caused by protein antibodies
Pathophysiology
• Immunoglobulin E antibodies form as a result of interaction between a foreign protein and the
body’s immune system.
• Antigen-antibody reaction causes release of histamine, leukotrienes, prostaglandins, and kinins
Subjective Data
• Exposure to latex
• Allergy to cross-sensitizing foods (e.g., banana, avocado, potato, tomato, kiwi)
Objective Data
• Local: urticaria (skin wheals)
• Systemic: generalized urticaria with angioedema (tissue swelling), asthma, eye/nose itching and
gastrointestinal symptoms, anaphylaxis (cardiovascular collapse)
Lymph Node Inspection and Palpation 195-197
Disorders of the lymph system present with three possible physical signs: enlarged lymph nodes
(lymphadenopathy), red streaks on the overlying skin (lymphangitis), or lymphedema (Box 10.2).
Inspect each area of the body for apparent lymph nodes, edema, erythema, red streaks, and skin
lesions. Using the pads of the second, third, and fourth fingers, gently palpate for superficial lymph
nodes (see Box 10.1 and Fig. 10.14). Try to detect any hidden enlargement, and note the
consistency, mobility, tenderness, size, and warmth of the nodes. In areas where the skin is more
mobile, move the skin over the area of the nodes. Press lightly at first, then gradually increase
pressure. Heavier pressure alone can displace nodes before you have had a chance to recognize
their presence. Superficial nodes are accessible to palpation but in healthy adults are not large or
firm enough to be felt. You may detect small, movable, discrete, “shotty” nodes (small, multiple
nodes that feel like BBs under the skin) less than 1 cm in diameter that move under your fingers.
Shotty nodes are generally of no clinical consequence and usually represent transient enlargement
of the lymph nodes after viral infection. However, even shotty nodes in the epitrochlear or
supraclavicular regions require additional evaluation. A node fixed to surrounding tissues is cause
for concern.17
Quiz 3 Study Guide
Special Procedures for Assessment of the Musculoskeletal System
22.2 page 560
Knee Assessment 563-565
Ballottement is used to determine the presence of an effusion in the knee from excess fluid. With the
knee extended, apply downward pressure on the suprapatellar pouch with the web or the thumb and
forefinger of one hand, and then push the patella quickly downward against the femur with a finger of
your other hand. If an effusion is present, a tapping or clicking will be sensed when the patella is
pushed against the femur. Release the pressure against the patella, but keep your finger lightly
touching it. If an effusion is present, the patella will float out as if a fluid wave were pushing it (Fig.
22.47).
Examination for the bulge sign is also used to determine the presence of excess fluid in the knee.
With the patient’s knee extended, milk the medial aspect of the knee upward two or three times, and
then milk the lateral side of the patella. Observe for a bulge of returning fluid to the hollow area
medial to the patella (Fig. 22.48).
The McMurray test is used to detect a torn medial or lateral meniscus. Have the patient lie supine
and flex one knee. Position your thumb and fingers on either side of the joint space. Hold the heel
with your other hand, fully flexing the knee, and rotate the foot and knee outward (valgus stress) to a
lateral position. Extend and then flex the patient’s knee. Any palpable or audible click, pain, or limited
extension of the knee is a positive sign of a torn medial meniscus. Repeat the procedure, rotating
the foot and knee inward (varus stress) (Fig. 22.49). A palpable or audible click, pain, or lack of
extension is a positive sign of a torn lateral meniscus.
The anterior and posterior drawer test is used to identify instability of the anterior and posterior
cruciate ligaments. Have the patient lie supine and flex the knee 45 to 90 degrees, placing the foot
flat on the table. Place both hands on the lower leg with the thumbs on the ridge of the anterior tibia
just distal to the tibial tuberosity. Draw the tibia forward, forcing the tibia to slide forward of the femur.
Then push the tibia backward (Fig. 22.50). Anterior or posterior movement of the knee greater than 5
mm in either direction is an unexpected finding.18
Quiz 3 Study Guide
The Lachman test is used to evaluate anterior cruciate ligament integrity. With the patient supine,
flex the knee 10 to 15 degrees with the heel on the table. Place one hand above the knee to stabilize
the femur and place the other hand around the proximal tibia. While stabilizing the femur, pull the
tibia anteriorly. Attempt to have the patient relax the hamstring muscles for an optimal test.
Increased laxity, greater than 5 mm compared with the uninjured side, indicates injury to the
ligament.
The varus (abduction) and valgus (adduction) stress tests are used to identify instability in the lateral
and medial collateral ligaments. Have the patient lie supine and extend the knee. Stabilize the femur
with one hand and hold the ankle with your other hand. Apply varus force against the ankle (toward
the midline) and internal rotation. Excessive laxity is felt as joint opening. Laxity in this position
indicates injury to the lateral collateral ligament. Then apply valgus force against the ankle (away
from the midline) and external rotation. Laxity in this position indicates injury to the medial collateral
ligament (Fig. 22.51). Repeat the movements with the patient’s knee flexed to 30 degrees. No
excessive medial or lateral movement of the knee is expected.
Hand and Wrist assessment p. 560-562
Several procedures are used to evaluate the integrity of the median nerve, which innervates the
palm of the hand and the palmar surface of the thumb, index and middle fingers, and half of the ring
finger. Ask the patient to mark the specific locations of pain, numbness, and tingling on the Katz
hand diagram (Fig. 22.41). Certain patterns of pain, numbness, and tingling are associated with
carpal tunnel syndrome.
The thumb abduction test isolates the strength of the abductor pollicis brevis muscle, innervated only
by the median nerve. Have the patient place the hand palm up and raise the thumb perpendicular to
it. Apply downward pressure on the thumb to test muscle strength (Fig. 22.42A). Full resistance to
this pressure is expected. Weakness is associated with carpal tunnel syndrome.
To perform the Phalen test, ask the patient to hold both wrists in a fully palmar-flexed position with
the dorsal surfaces pressed together for 1 minute (Fig. 22.42B). Numbness and paresthesia in the
distribution of the median nerve are suggestive of carpal tunnel syndrome. The reverse Phalen test
is performed by placing the palms and fingers together with full wrist extension. The Tinel sign is
tested by striking the patient’s wrist with your index or middle finger where the median nerve passes
under the flexor retinaculum and volar carpal ligament (Fig. 22.42C). A tingling sensation radiating
from the wrist to the hand in the distribution of the median nerve is a positive Tinel sign and can
indicate carpal tunnel syndrome.
Musculoskeletal abnormalities Page 571-577
Ankylosing Spondylitis
A chronic inflammatory disease of the spine, ankylosing spondylitis has a genetic predisposition
associated with human leukocyte antigen (HLA)-B27 and may affect the cervical, thoracic, and
lumbar spine along with the sacroiliac joints (Fig. 22.66)
Pathophysiology
• Inflamed intervertebral disks and longitudinal ligaments ossification
• Leads to eventual fusion and severe deformity of the vertebral column
Subjective Data
• Develops predominantly in men between 20 and 40 years of age19
Quiz 3 Study Guide
• Begins insidiously with inflammatory low back and buttock pain, also involving hips and shoulders
• Buttock pain can fluctuate from one side to the other
Objective Data
• Restriction in the lumbar flexion of the patient
• Limited range of motion of the shoulders, chest wall, hips, and knees may develop
• Uveitis may be present
Lumbosacral Radiculopathy (Herniated Lumbar Disk)
Herniation of a lumbar disk that irritates the corresponding spinal nerve root
Pathophysiology
• Generally caused by degenerative changes of the disk
• Most commonly occurring at the L4, L5, and S1 nerve roots
• Greatest incidence occurs between 31 and 50 years of age
Subjective Data
• Can be associated with lifting heavy objects
• Common symptoms include low back pain with radiation to the buttocks and posterior thigh or
down the leg in the distribution of the dermatome of the nerve root
• Pain relief is often achieved by lying down
Objective Data
• Spasm and tenderness over the paraspinal musculature may be present
• Potential difficulty with heel walking (L4 and L5) or toe walking (S1)
• Numbness, tingling, or weakness in the involved extremity (Fig. 22.67)
Lumbar Stenosis
Narrowing of the spinal canal
Pathophysiology
• Canal narrowing from bone and ligament hypertrophy may lead to entrapment of the spinal cord as
it traverses the spinal canal
Subjective Data
• Pain with walking or standing upright that often seems to originate in the buttocks and may then
radiate down the legs
• Pain relief may occur with sitting or bending forward
• Pain may be worsened by prolonged standing, walking, or hyperextending the back
Objective Data
• In the early stages, the neurologic examination is frequently normal
• With progression, the examination may show lower extremity weakness and sensory loss
• A stooped forward gait may be present
Carpal Tunnel Syndrome
Compression on the median nerve (see Fig. 22.41)
Pathophysiology
• Compression of the nerve within its flexor tendon sheath due to microtrauma, local edema or
inflammation, repetitive motion, or vibration of the hands20
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• Associated with rheumatoid arthritis, gout, acromegaly, hypothyroidism, and the hormonal changes
of pregnancy
Subjective Data
• Numbness, burning, and tingling in the hands often occur at night
• Can also be elicited by flexion/extension movements of the wrist
• Pain may radiate to the arms
Objective Data
• Weakness of the thumb and flattening of the thenar eminence of the palm
• Reproduction of symptoms with provocation of the Tinel and Phalen maneuvers
Gout
A form of arthritis resulting from chronically elevated serum uric acid
Pathophysiology
• Monosodium urate crystal deposition in joints and surrounding tissues results in acute inflammatory
attacks
Subjective Data
• Sudden onset of a hot, swollen joint; exquisite pain; limited range of motion
• Primarily affects men older than 40 years and women of postmenopausal age
• Usually affects the proximal phalanx of the great toe, although the wrists, hands, ankles, and knees
may be involved
Objective Data
• The skin over the swollen joint may be shiny and red or purple
• Uric acid crystals may form as tophi under the skin with chronic gout (Fig. 22.68)
Temporomandibular Joint Syndrome
Painful jaw movement
Pathophysiology
• Caused by congenital anomalies, malocclusion, trauma, arthritis, and other joint diseases
Subjective Data
• Unilateral facial pain that usually worsens with joint movement
• May be referred to any point on the face or neck
Objective Data
• Most patients have a muscle spasm, and many have clicking, popping, or crepitus in the affected
joint
Osteomyelitis
An infection in the bone
Pathophysiology
• Usually results from an open wound or systemic infection
• Purulent matter spreads through the cortex of the bone and into the soft tissue
• Decreased blood flow to the affected bone may lead to bone necrosis21
Quiz 3 Study Guide
Subjective Data
• Dull pain develops insidiously at the involved site and progresses over days to weeks
• Limp or decreased movement in infants and children
Objective Data
• Signs of infection include edema, erythema, and warmth at the site
• Tenderness to palpation, pain with movement, and signs of inflammation such as fevers
Bursitis
Inflammation of the bursa
Pathophysiology
• Due to repetitive movement and excessive pressure on the bursa
• Can also be due to infection or gout
Subjective Data
• Common sites include the shoulder, elbow, hip, and knee, with pain and stiffness surrounding the
joint around the inflamed bursa
• The pain is usually worse during activity
Objective Data
• Limitation of motion caused by swelling; pain on movement; point tenderness; and an
erythematous, warm site (Fig. 22.69)
• Soreness may radiate to tendons at the site
Paget Disease of the Bone (Osteitis Deformans)
A focal metabolic disorder of the bone
Pathophysiology
• Appears in persons older than 45 years
• Excessive bone resorption and bone formation produce a mosaic pattern of lamellar bone
Subjective Data
• Vertigo and headache as a result of skull involvement
• Progressive deafness from involvement of the ossicles or neural elements may develop
Objective Data
• Bowed tibias, misshapen pelvis, or prominent skull forehead may be evident
• Frequent fractures may occur
Osteoarthritis
The deterioration of the articular cartilage covering the ends of bone in synovial joints
Pathophysiology
• As a result of cartilage abrasion, pitting, and thinning, the bone surfaces are eventually exposed,
with bone rubbing against bone
• Separately there can be remodeling of the bone surface and formation of bone spurs
Subjective Data
• Pain in hands, feet, hips, knees, and cervical or lumbar spine (most commonly)22
Quiz 3 Study Guide
• Onset usually begins after 40 years of age and develops slowly over many years with nearly 100%
of people older than 75 years affected
Objective Data
• The joints may be enlarged due to bone growths (osteophytes) (see Fig. 22.18B)
• May have crepitus and limited, painful range of motion
Rheumatoid Arthritis
A chronic systemic inflammatory disorder of the synovial tissue surrounding the joints
Pathophysiology
• Cause is unknown
• Within the inflamed synovial tissue and fluid, polymorphonuclear leukocytes aggregate
• Multiple inflammatory cytokines and enzymes are released that can result in subsequent damage
to bone, cartilage, and other tissues
Subjective Data
• Joint pain and stiffness, especially in the morning or after periods of inactivity
• Constitutional symptoms of fatigue, myalgias, weight loss, and low-grade fever are common
Objective Data
• Involved joints include the hands, wrists, feet, and ankles, as well as the hips, knees, and cervical
spine
• Synovitis, with soft tissue swelling and effusions, is present on examination
• Nodules and characteristic deformities can develop (see Fig. 22.16)
Heberden nodes vs Bouchard nodes p 547
Bony overgrowths in the distal interphalangeal joints, which are felt as hard, non-tender nodules
usually 2 to 3 mm in diameter but sometimes encompassing the entire joint, are associated with
osteoarthritis. When located along the distal interphalangeal joints, they are called Heberden nodes;
those along the proximal interphalangeal joints are called Bouchard nodes. Painful swelling of the
proximal interphalangeal joints causes spindle-shaped fingers, which are associated with the acute
stage of rheumatoid arthritis (Fig. 22.18). Cystic, round, non-tender swellings along tendon sheaths
or joint capsules that are more prominent with flexion may indicate ganglia
Sports injuries 576-577
Muscle Strain
Pathophysiology
• Can be due to excessive stretching or forceful contraction beyond the muscle’s functional capacity
• Often associated with improper exercise warm-up, fatigue, or previous injury
Subjective Data
• Muscle pain
• Severity ranges from a mild intrafibrous tear to a total rupture of a single muscle
Objective Data
• Temporary muscle weakness, spasm, pain, and contusion23
Quiz 3 Study Guide
Dislocation
Complete separation of the contact between two bones in a joint
Pathophysiology
• Often caused by pressure or force pushing the bone out of the joint; usually occurs in the setting of
acute trauma
Subjective Data
• Can occur more easily in patients with hyperextensibility conditions (e.g., Marfan, Ehlers-Danlos)
Objective Data
• Deformity and inability to use the extremity or joint as usual
Fracture
Partial or complete break in the continuity of a bone
Pathophysiology
• From trauma (direct, indirect, twisting, or crushing)
Subjective Data
• Pain, limited movement, cannot bear weight, swelling
• Felt a pop or snap with injury
• Can occur more easily in patients with bone disorders (e.g., osteogenesis imperfecta, osteoporosis,
bone metastasis)
Objective Data
• Deformity, edema, pain, loss of function, color changes, and paresthesia
Tenosynovitis (Tendonitis)
Inflammation of the synovium-lined sheath around a tendon
Pathophysiology
• Seen with repetitive actions associated with occupational or sports activities
• Can occur in inflammatory conditions like rheumatoid arthritis
Subjective Data
• Pain with movement of such common sites as the shoulder, knee, heel, and wrist
Objective Data
• Point tenderness over the involved tendon
• Pain with active movement and some limitation of movement in the affected joint
Rotator Cuff Tear
Microtrauma and tearing of the rotator cuff muscles, most often the supraspinatus
Pathophysiology
• Usually due to degeneration of the muscle and tendon from repeated overhead lifting and
compression under the acromion
• An acute tear may also result from a fall on an outstretched arm24
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Subjective Data
• Pain in the shoulder and deltoid area is common. This can awaken the patient at night
Objective Data
• Inability to maintain a lateral raised arm against resistance may develop due to pain
• Tenderness over the acromioclavicular joint
• Grating sound on movement, crepitus, and weakness in external shoulder rotation
Infant and Children 577-579
Clubfoot (Talipes Equinovarus)
Fixed congenital defect of the ankle and foot
Pathophysiology
• Causes include genetic factors and external influences in the final trimester, such as intrauterine
compression
Subjective Data
• Diagnosis is usually obvious at birth with the characteristic deformity
Objective Data
• Most common combination of position deformities includes inversion of the foot at the ankle and
plantar flexion, with the toes lower than the heel (Fig. 22.70)
Metatarsus Adductus (Metatarsus Varus)
The most common congenital foot deformity; can be either fixed or flexible
Pathophysiology
• Defect is caused by intrauterine positioning
• Medial adduction of the toes and forefoot results from angulation at the tarsometatarsal joint
Subjective Data
• Diagnosis is usually obvious at birth with the characteristic deformity
• The heel and ankle are uninvolved (Fig. 22.71)
Objective Data
• The lateral border of the foot is convex
• A crease is sometimes apparent on the medial border of the foot
Legg-Calvé-Perthes Disease
Avascular necrosis of the femoral head
Pathophysiology
• Results from a decreased blood supply to the femoral head
Subjective Data
• Most commonly seen in boys between 3 and 11 years of age
• Pain is often referred to the medial thigh, knee, or groin
• Bilateral involvement may occur in 10% of cases25
Quiz 3 Study Guide
Objective Data
• Child may have a limp that is painless or antalgic (painful limp with shortened time on extremity)
• Loss of internal rotation; abduction and decreased range of motion on the affected side are seen
• Muscle weakness of the upper leg may be present if symptoms have been present for a prolonged
period
Osgood-Schlatter Disease
A traction apophysitis (inflammation of a bony outgrowth) of the anterior aspect of the tibial tubercle
Pathophysiology
• Inflammation of a bony outgrowth of the anterior aspect of the tibial tubercle
• Develops in association with inflammation of the anterior patellar tendon
• This self-limiting disorder is most common in boys between 9 and 15 years of age
Subjective Data
• The child may walk with a limp
• Often describes knee pain (especially with activity)
Objective Data
• Knee swelling that is aggravated by strenuous activity
• Pain especially prominent with activity involving the quadriceps muscle
• Pain with palpation over the tibial tuberosity
Slipped Capital Femoral Epiphysis
Disorder in which the capital femoral epiphysis slips over the neck of the femur
Pathophysiology
• Most common between 8 and 16 years of age, although affected girls are often younger than
affected boys
• Majority of cases (75%) are unilateral; left side is involved more often than the right
• More common in overweight and obese patients
Subjective Data
• The child or adolescent presents with knee pain and a limp
Objective Data
• The affected child has leg weakness and reduced internal hip rotation
• Characteristic plain radiograph shows slippage of femoral head
Muscular Dystrophy
A group of genetic disorders involving gradual degeneration of the muscle fibers
Pathophysiology
• Progressive symmetric weakness and muscle atrophy or pseudohypertrophy from fatty muscle
infiltrates
• Skeletal muscles and the heart may be involved.
• Some forms result in only mild disability, and these patients can expect a normal life span.
• Other types produce severe disability, deformity, and death
Subjective Data
• Early signs may include clumsiness, difficulty climbing stairs, and frequent falls26
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Objective Data
• Muscle atrophy and weakness with a waddling gait
• A positive Gower sign (see Fig. 22.64)
• Progressive loss of function, including ability to walk
Scoliosis
Physical deformity of the spine
Pathophysiology
• A curvature of the vertebral bodies such that when viewed from the rear, the spine may look more
like an “S” or a “C” rather than a straight line
• Structural scoliosis most commonly affects girls and progresses during early adolescence.
• There is no known cause
Subjective Data
• May lead to back discomfort and is often associated with a leg length discrepancy
Objective Data
• Lateral curvature of the spine, rib hump as the child flexes forward to touch the toes
• Scoliometer reading of greater than or equal to 7 degrees is a positive screening test
• In severe deformities, the patient has uneven shoulder and hip levels; may have a crease on one
side at the waist
• Physiologic alterations occur in the spine, chest, and pelvis (Fig. 22.72)
Radial Head Subluxation (Nursemaid’s Elbow)
A dislocation injury
Pathophysiology
• Caused by jerking the arm upward while the elbow is extended
• The jerking pulls apart the elbow joint and tears the margin of the annular ligament around the
radial head into the joint
• Common in children 1 to 4 years of age
Subjective Data
• Child complains of pain in the elbow and wrist and/or refuses to move the arm
Objective Data
• Child holds the arm slightly flexed and pronated
• Supination motion is resisted
Infants 566-567
Genetic disorders and fetal conditions can produce musculoskeletal anomalies. The fetus may
experience various postural pressures leading to reduced extension of the extremities and torsions
of various bones.
Fully undress the infant and observe the posture and spontaneous generalized movements. Use a
warming table when examining a newborn. No localized or generalized muscular twitching is
expected. Inspect the lower back for tufts of hair, dimples, discolorations, cysts, or masses near the
spine. A mass near the spine is likely to be a meningocele or myelomeningocele.27
Quiz 3 Study Guide
From about age 2 months, the infant should be able to lift the head and trunk from the prone
position, giving you an indication of forearm strength. Assess the curvature of the spine and the
strength of the paravertebral muscles with the infant in a sitting position. Kyphosis of the thoracic
and lumbar spine will be apparent in the sitting position until the infant can sit without support (Fig.
22.53).
Inspect the extremities, noting symmetric flexion of arms and legs. The axillary, gluteal, femoral, and
popliteal creases should be symmetric, and the limbs should move freely. No unusual proportions or
asymmetry of limb length or circumference, constricted annular bands, or other deformities should
be noted.
Place the newborn in a fetal position to observe how that may have contributed to any asymmetry of
flexion, position, or shape of the extremities. Newborns have some resistance to full extension of the
elbows, hips, and knees. Movements should be symmetric.
All infants are flat-footed, and many newborns have a slight varus curvature of the tibias (tibial
torsion) or forefoot adduction (metatarsus adductus) from fetal positioning. The midline of the foot
may bisect the third and fourth toes rather than the second and third toes. The forefoot should be
flexible, straightening with abduction. It is necessary to follow tibial torsion and metatarsus adductus
variations carefully, but they seldom require intervention. As growth and development take place, the
expected body habitus is usually achieved.
The hands should open periodically with the fingers fully extended. Observe the palmar and
phalangeal creases on each hand. A single crease extending across the entire palm is frequently
associated with Down syndrome and other genetic conditions, but it may also be seen in healthy
individuals. Count the fingers and toes, noting polydactyly (six or more digits on an extremity) or
syndactyly (two or more digits fused together) (Fig. 22.54).
Palpate the clavicles and long bones for fractures, dislocations, crepitus, masses, and tenderness.
One of the most easily missed findings in the newborn is a fractured clavicle. This may be evident by
a lump on the collarbone caused by the callus that forms on the healing clavicle noted in the first
weeks after birth.
Position the baby with the trunk flexed and palpate each spinal process. Feel the shape of each,
noting whether it is thin and well-formed, as expected, or whether it is split, possibly indicating a bifid
defect (Fig. 22.55).
Range of Motion and Muscle tone p. 547
Examine both the active and passive range of motion for each major joint and its related muscle
groups. Muscle tone is often evaluated simultaneously. Allow adequate space for the patient to
move each muscle group and joint through its full range. Instruct the patient to move each joint
through its range of motion as detailed in specific joint and muscle sections. Pain, limitation of
motion, spastic movement, joint instability, deformity, or contracture may suggest a problem with the
joint, related muscle group, or nerve supply.
Ask the patient to relax and allow you to passively move the same joints until the end of the range of
motion is felt. Do not force the joint if there is pain or muscle spasm. Muscle tone may be assessed
by feeling the resistance to passive stretch. During passive range of motion, the muscles should
have slight tension. Passive range of motion often exceeds active range of motion by 5 degrees. The28
Quiz 3 Study Guide
range of motion with active and passive maneuvers should be equal between contralateral joints.
Discrepancies between active and passive ranges of motion may indicate true muscle weakness or
a joint disorder. No crepitation or tenderness with movement should be apparent. Note the specific
location of tenderness when present. Spastic muscles are harder to put through the range of motion.
Measurements may vary if the muscle tested relaxes with gentle persistence.
When a joint appears to have an increase or limitation in its range of motion, a goniometer (see
Chapter 3) can be used to precisely measure the angle. Begin with the joint in the fully extended or
neutral position, and then flex the joint as far as possible. Measure the angles of greatest flexion and
extension, comparing these with the expected joint flexion and extension values (Fig. 22.13).
Evaluating the strength of each muscle group is an important part of the neurologic examination.
However, it is usually integrated with the examination of the associated joint for range of motion. Ask
the patient first to contract the muscle you indicate by extending or flexing the joint and then to resist
as you apply force against that muscle contraction (Fig. 22.14). Alternatively, tell the patient to push
against your hand to feel the resistance. Compare the muscle strength bilaterally. Expect muscle
strength to be bilaterally symmetric with full resistance to opposition. Full muscle strength requires a
complete active range of motion.
Variations in muscle strength are graded from no voluntary contraction to full muscle strength, using
the scale in Table 22.1. When muscle strength is grade 3 or less, disability is present; activity cannot
be accomplished in a gravity field, and external support is necessary to perform movements.
Weakness may result from an underlying muscle disorder, pain, fatigue, or overstretching.