ELDER TIP Primary osteoarthritis is strongly associated with aging, and indeed aging may predispose to the cartilage degeneration common in persons with osteoarthritis.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Psoriatic arthritis:
Causes
(Professional Guide to Diseases (Eighth Edition))
Evidence suggests that predisposition to psoriatic arthritis is hereditary; 20% to 50% of patients are human leukocyte antigen-B27 positive. However, onset is usually precipitated by streptococcal infection or trauma.
About 5% to 7% of patients with psoriasis develop psoriatic arthritis. It occurs in up to 1% of the general population.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Rheumatoid arthritis:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
RA occurs worldwide, striking three times more females than males. Although it can occur at any age, it begins most often between ages 25 and 55. This disease affects more than 7 million people in the United States alone.
What causes the chronic inflammation characteristic of RA isn’t known, but various theories point to infectious, genetic, and endocrine factors. Currently, it’s believed that a genetically susceptible individual develops abnormal or altered immunoglobulin (Ig) G antibodies when exposed to an antigen. This altered IgG antibody isn’t recognized as “self,” and the individual forms an antibody against it — an antibody known as RF. By aggregating into complexes, RF generates inflammation. Eventually, cartilage damage by inflammation triggers additional immune responses, including activation of complement. This in turn attracts polymorphonuclear leukocytes and stimulates release of inflammatory mediators, which enhance joint destruction.
Much more is known about the pathogenesis of RA than about its causes. If unarrested, the inflammatory process within the joints occurs in four stages. First, synovitis develops from congestion and edema of the synovial membrane and joint capsule. Formation of pannus — thickened layers of granulation tissue — marks the second stage’s onset. Pannus covers and invades cartilage and eventually destroys the joint capsule and bone. Progression to the third stage is characterized by fibrous ankylosis — fibrous invasion of the pannus and scar formation that occludes the joint space. Bone atrophy and malalignment cause visible deformities and disrupt the articulation of opposing bones, causing muscle atrophy and imbalance and, possibly, partial dislocations or subluxations. In the fourth stage, fibrous tissue calcifies, resulting in bony ankylosis and total immobility.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Juvenile rheumatoid arthritis:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
The cause of JRA remains puzzling. Research continues to test several theories, such as those linking the disease to genetic factors or to an abnormal immune response. Viral or bacterial (particularly streptococcal) infection, trauma, and emotional stress may be precipitating factors, but their relationship to JRA remains unclear.
Considered the major chronic rheumatic disorder of childhood, JRA affects an estimated 150,000 to 250,000 children in the United States; overall incidence is twice as high in females, with variation among the types of JRA.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Septic arthritis:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
In most cases of septic arthritis, bacteria spread from a primary site of infection — usually in adjacent bone or soft tissue — through the bloodstream to the joint. Common infecting organisms in children are group B Streptococcus and Haemophilus influenzae. Adults are usually infected by Staphylococcus, Streptococcus (pneumonia), and group B Streptococcus, whereas chronic septic arthritis is caused by Mycobacterium tuberculosis and Candida albicans.
Various factors can predispose a person to septic arthritis. Any concurrent bacterial infection (of the genitourinary or the upper respiratory tract, for example) or serious chronic illness (such as malignancy, renal failure, rheumatoid arthritis, systemic lupus erythematosus, diabetes, or cirrhosis) heightens susceptibility. Consequently, elderly people and those who abuse I.V. drugs run a higher risk of developing septic arthritis. Of course, diseases that depress the immune system and immunosuppressive therapy increase susceptibility. Other predisposing factors include recent articular trauma, joint arthroscopy or other surgery, intra-articular injections, and local joint abnormalities.
Septic arthritis may be seen at any age in children, but it occurs most often in children younger than age 3. It’s uncommon from age 3 until adolescence, at which time the incidence increases again.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Hypothyroidism in adults:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Hypothyroidism results from inadequate production of thyroid hormone — usually because of dysfunction of the thyroid gland due to surgery (thyroidectomy), irradiation therapy (particularly with 131I), inflammation, chronic autoimmune thyroiditis (Hashimoto’s disease) or, rarely, conditions such as amyloidosis and sarcoidosis. It may also result from pituitary failure to produce thyroid-stimulating hormone (TSH), hypothalamic failure to produce thyrotropin-releasing hormone, inborn errors of thyroid hormone synthesis, the inability to synthesize thyroid hormone because of iodine deficiency (usually dietary), or the use of antithyroid medications such as propylthiouracil. In patients with hypothyroidism, infection, exposure to cold, and sedatives may precipitate myxedema coma.
Hypothyroidism is more prevalent in females than males, and frequency increases with age; in the United States, incidence is rising significantly in people ages 40 to 50.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Splenomegaly:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Amyloidosis
Marked splenomegaly may occur with this disorder from excessive protein deposits in the spleen. Associated signs and symptoms vary, depending on which other organs are involved. The patient may display signs of renal failure, such as oliguria and anuria, and signs of heart failure, such as dyspnea, crackles, and tachycardia. GI effects may include constipation or diarrhea and a stiff, enlarged tongue, resulting in dysarthria.
Brucellosis
With severe cases of this rare infection, splenomegaly is a major sign. Typically, brucellosis begins insidiously with fatigue, headache, backache, anorexia, arthralgia, fever, chills, sweating, and malaise. Later, it may cause hepatomegaly, lymphadenopathy, weight loss, and vertebral or peripheral nerve pain on pressure.
Cirrhosis
About one-third of patients with advanced cirrhosis develop moderate to marked splenomegaly. Among other late findings are jaundice, hepatomegaly, leg edema, hematemesis, and ascites. Signs of hepatic encephalopathy—such as asterixis, fetor hepaticus, slurred speech, and decreased level of consciousness that may progress to coma—are also common. Besides jaundice, skin effects may include severe pruritus, poor tissue turgor, spider angiomas, palmar erythema, pallor, and signs of bleeding tendencies. Endocrine effects may include menstrual irregularities or testicular atrophy, gynecomastia, and loss of chest and axillary hair. The patient may also develop fever and right-upper-abdominal pain that’s aggravated by sitting up or leaning forward.
Endocarditis (subacute infective)
This infection usually causes an enlarged, but nontender, spleen. Its classic sign, however, is a suddenly changing murmur or the discovery of a new murmur in the presence of fever. Other features include anorexia, pallor, weakness, fever, night sweats, fatigue, tachycardia, weight loss, arthralgia, petechiae, hematuria and, in chronic cases, clubbing. If embolization occurs, the patient may develop chest, abdominal, or limb pain; paralysis; hematuria; and blindness. Endocarditis may produce Osler’s nodes (tender, raised, subcutaneous lesions on the fingers or toes), Roth’s spots (hemorrhagic areas with white centers on the retina), and Janeway lesions (purplish macules on the palms or soles).
Felty’s syndrome
Splenomegaly is characteristic in this syndrome that occurs with chronic rheumatoid arthritis. Associated findings are joint pain and deformity, sensory or motor loss, rheumatoid nodules, palmar erythema, lymphadenopathy, and leg ulcers.
Hepatitis
Splenomegaly may occur with this disorder. More characteristic findings include hepatomegaly, vomiting, jaundice, and fatigue.
Histoplasmosis
Acute disseminated histoplasmosis commonly produces splenomegaly and hepatomegaly. It may also cause lymphadenopathy, jaundice, fever, anorexia, emaciation, and signs and symptoms of anemia, such as weakness, fatigue, pallor, and malaise. Occasionally, the patient’s tongue, palate, epiglottis, and larynx become ulcerated, resulting in pain, hoarseness, and dysphagia.
Hypersplenism (primary)
With this syndrome, splenomegaly accompanies signs of pancytopenia—anemia, neutropenia, or thrombocytopenia. If the patient has anemia, findings may include weakness, fatigue, malaise, and pallor. If he has severe neutropenia, frequent bacterial infections are likely. If he has severe thrombocytopenia, easy bruising or spontaneous, widespread hemorrhage may occur. The patient also experiences left-sided abdominal pain, and a feeling of fullness after eating a small amount of food.
Leukemia
Moderate to severe splenomegaly is an early sign of both acute and chronic leukemia. With chronic granulocytic leukemia, splenomegaly is sometimes painful. Accompanying it may be hepatomegaly, lymphadenopathy, fatigue, malaise, pallor, fever, gum swelling, bleeding tendencies, weight loss, anorexia, and abdominal, bone, and joint pain. At times, acute leukemia also causes dyspnea, tachycardia, and palpitations. With advanced disease, the patient may display confusion, headache, vomiting, seizures, papilledema, and nuchal rigidity.
Lymphoma
Moderate to massive splenomegaly is a late sign and may be accompanied by hepatomegaly, painless lymphadenopathy, scaly dermatitis with pruritus, fever, fatigue, weight loss, and malaise.
Malaria
A common sign of malaria, splenomegaly is typically preceded by the malarial paroxysm of chills, followed by high fever and then diaphoresis. Related effects include headache, muscle pain, and hepatomegaly. With benign malaria, these paroxysms alternate with periods of well-being. With severe malaria, however, the patient may develop a persistent high fever, orthostatic hypotension, seizures, delirium, coma, coughing (with possible hemoptysis), vomiting, abdominal pain, diarrhea, melena, oliguria or anuria and, possibly, hemiplegia.
Mononucleosis (infectious)
A common sign of this disorder, splenomegaly is most pronounced during the second and third weeks of illness. Typically, it’s accompanied by a triad of signs and symptoms: sore throat, cervical lymphadenopathy, and fluctuating temperature with an evening peak of 101° to 102° F (38.3° to 38.9° C). Occasionally, hepatomegaly, jaundice, and a maculopapular rash may also occur.
Pancreatic cancer
This cancer may cause moderate to severe splenomegaly if tumor growth compresses the splenic vein. Other characteristic findings include abdominal or back pain, anorexia, nausea and vomiting, weight loss, GI bleeding, jaundice, pruritus, skin lesions, emotional lability, weakness, and fatigue. Palpation may reveal a tender abdominal mass and hepatomegaly; auscultation reveals a bruit in the periumbilical area and left upper quadrant.
Polycythemia vera
Late in this disorder, the spleen may become markedly enlarged, resulting in easy satiety, abdominal fullness, and left-upper-quadrant or pleuritic chest pain. Signs and symptoms accompanying splenomegaly are widespread and numerous. The patient may exhibit deep, purplish red oral mucous membranes, headache, dyspnea, dizziness, vertigo, weakness, and fatigue. He may also develop finger and toe paresthesia, impaired mentation, tinnitus, blurred or double vision, scotoma, increased blood pressure, and intermittent claudication. Other signs and symptoms include pruritus, urticaria, ruddy cyanosis, epigastric distress, weight loss, hepatomegaly, and bleeding tendencies.
Sarcoidosis
This granulomatous disorder may produce splenomegaly and hepatomegaly, possibly accompanied by vague abdominal discomfort. Its other signs and symptoms vary with the affected body system but may include nonproductive cough, dyspnea, malaise, fatigue, arthralgia, myalgia, weight loss, skin lesions, lymphadenopathy, irregular pulse, impaired vision, dysphagia, and seizures.
Splenic rupture
Splenomegaly may result from massive hemorrhage with this disorder. The patient may also experience left-upper-quadrant pain, abdominal rigidity, and Kehr’s sign.
Thrombotic thrombocytopenic purpura
This disorder may produce splenomegaly and hepatomegaly accompanied by fever, generalized purpura, jaundice, pallor, vaginal bleeding, and hematuria. Other effects include fatigue, weakness, headache, pallor, abdominal pain, and arthralgias. Eventually, the patient develops signs of neurologic deterioration and of renal failure.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Arthritis/Dermatitis:
Differential Overview
(Field Guide to Bedside Diagnosis)
❑Lyme disease
❑Erythema nodosum
❑Rheumatoid arthritis
❑Systemic lupus erythematosus
❑Psoriatic arthritis
❑Disseminated gonococcemia
❑Sarcoidosis
❑Scleroderma
❑Dermatomyositis
❑Reiter syndrome
❑Rheumatic fever
❑Behçet syndrome
❑Still disease
❑Hypersensitivity vasculitis
Clinical Findings
Lyme disease Erythema migrans, a rapidly expanding annular rash with a clearing center, is the key early finding. The site of the ixodid tick bite at the center of the lesion is usually intensely indurated, vesicular, or necrotic. The arthritis is an asymmetric oligoarthritis that usually occurs after the rash has resolved.
Erythema nodosum A prodromal syndrome of fever, chills, malaise, and polyarthralgia is followed by the development of lesions that are discrete, tender, slightly raised subcutaneous nodules on the shins or ankles. They represent a hypersensitivity reaction to group A streptococcal infection, tuberculosis, sarcoidosis, inflammatory bowel disease, or drugs such as oral contraceptives and sulfonamides.
Rheumatoid arthritis Symmetric polyarticular arthritis with synovial proliferation, especially of the wrist, and morning stiffness lasting more than 1 hour characterize the early joint involvement. Rheumatoid nodules appear over extensor surfaces. Vasculitic lesions are frequently found on the digits, appearing as small red or purpuric macules that progress to painful nodules or ulcers.
Systemic lupus erythematosus A classic butterfly rash occurs in 40% and is exacerbated by sun exposure. A diffuse maculopapular rash in areas exposed to the sun heralds disease flares. Discoid lesions and scaling plaques that range in color from red to violaceous, with central atrophy and telangiectasias, occur in 20%. Vasculitis, in the form of painful ulcers on the extremities, palpable purpura, or lupus profundus (firm nodules in the subcutaneous fat on the forehead, cheeks, buttocks, and upper arms) are found. The arthritis is typically one of symmetric fusiform swelling of the proximal interphalangeal and metacarpophalangeal joints, diffuse puffiness of the hands, and tenosynovitis.
Psoriatic arthritis Psoriatic plaques, erythematous with a silvery scale, are critical to diagnosis, but may be hidden in the scalp, umbilicus, or gluteal folds. Nail changes such as pitting or yellow discoloration of the nail plate are other clues. The arthritis typically involves the proximal interphalangeal and distal interphalangeal joints, creating sausage digits. The arthritis may become erosive, leading to telescoping of the hands. One-fourth of patients have axial skeletal arthritis.
Disseminated gonococcemia Acral lesions are typically hemorrhagic pustules, but petechiae, hemorrhagic papules, or hemorrhagic bullae can occur. Fever, rigor, tenosynovitis, and polyarthritis are other findings.
Sarcoidosis Transient maculopapular eruptions of the trunk, face, and extremities are often accompanied by uveitis, adenopathy, and parotid enlargement. Translucent reddish-brown to purple indolent plaques may develop on the face (lupus pernio), buttocks, or extremities. Joint symptoms consist of migratory transient arthralgias.
Scleroderma Early findings are primarily Raynaud phenomenon and puffy fingers. Later findings include sclerodactyly (smooth, shiny, tapered fingers with taut, bound-down skin); contractures with “claw hand” deformity; expressionless face (with thin lips, a beak-like nose, and sunken cheeks); microstomia; mat telangiectasias on the nail folds, face, lips, oral mucosa, or trunk; and calcinosis with leathery crepitation over the joints.
Dermatomyositis The classic skin manifestation is a lilac-colored heliotrope rash on the eyelids and in a butterfly distribution. Gottron papules are violaceous, scaly, flat lesions on the extensor aspect of the interphalangeal joints, elbows, knees, and medial malleoli; these occur as a late manifestation. Proximal muscle aching/weakness, not arthritis, is prominent. The patient is unable to reach overhead or arise from a chair. Neck flexors are more involved than extensors.
Reiter syndrome Arthritis, urethritis, conjunctivitis, and mucocutaneous ulcers are found. The arthritis is asymmetric, usually involving the lower extremity joints. Solitary sausage digits may be seen. Tendinitis and fasciitis are common. The mucocutaneous lesions are eroded red vesicles or papules of the corona and glans, which when confluent are called circinate balanitis. Pustules may change into thick hyperkeratotic plaques on the palms and soles, keratoderma blennorrhagicum.
Rheumatic fever There is an acute migratory polyarthritis with fever. Subcutaneous nodules appear over the bony prominences of the elbows, knuckles, ankles, scapulae, and occiput. They are associated with carditis. Erythema marginatum, appearing as evanescent pink lesions with serpiginous borders, is also associated with carditis.
Behçet syndrome The classic triad is arthritis, iritis, and oral and genital ulcerations. Recurrent aphthous ulcers are a sine qua non. They begin as macular erythema that develops into superficial gray ulcers. Scrotal or labial ulcerations are also found. Hypopyon uveitis, a hallmark, is a rare finding. The arthritis is primarily of the knees and ankles.
Still disease Skin lesions are red, flat, and less than 1 cm in diameter. Lesions are evanescent, occurring with fever spikes. A migratory polyarthralgia occurs.
Hypersensitivity vasculitis After an upper respiratory infection, young adults may develop palpable purpura over the extensor surfaces and buttocks. Arthritis, edema, and colicky abdominal pain, followed by bloody stools, suggests the diagnosis.
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Source: Field Guide to Bedside Diagnosis, 2007
Acute Monoarticular Arthritis:
Differential Overview
(Field Guide to Bedside Diagnosis)
❑ Injury
❑ Gout
❑ Osteoarthritis
❑ Lyme disease
❑ Gonococcal arthritis
❑ Seronegative spondyloarthropathy
❑ Septic arthritis
❑ Pseudogout
❑ Septic bursitis
❑ Avascular necrosis
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Source: Field Guide to Bedside Diagnosis, 2007
Polyarticular Arthritis:
Differential Overview
(Field Guide to Bedside Diagnosis)
❑ Osteoarthritis
❑ Rheumatoid arthritis
❑ Lyme arthritis
❑ Systemic lupus erythematosus
❑ Psoriatic arthritis
❑ Polyarticular gout
❑ Viral arthritis
❑ Scleroderma
❑ Reiter syndrome
❑ Inflammatory bowel disease
❑ Gonococcal arthritis
❑ Ankylosing spondylitis
❑ Systemic vasculitis
❑ Sarcoidosis
❑ Pseudogout (CPPD)
❑ Acute rheumatic fever
❑ Still disease
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Source: Field Guide to Bedside Diagnosis, 2007
Osteoarthritis:
Causes
(Handbook of Diseases)
Osteoarthritis is widespread, occurring equally in both sexes until age 55. After age 55, incidence is higher in women. Incidence is after age 40; its earliest symptoms generally begin in middle age and may progress with advancing age.
The degree of disability depends on the site and severity of involvement; it can range from minor limitation of the fingers to severe disability in persons with hip or knee involvement. The rate of progression varies, and joints may remain stable for years in an early stage of deterioration.
Primary osteoarthritis, a normal part of aging, results from many things, including metabolic, genetic, chemical, and mechanical factors. Secondary osteoarthritis usually follows an identifiable predisposing event — most commonly trauma, congenital deformity, or obesity — and leads to degenerative changes.
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Source: Handbook of Diseases, 2003
Psoriatic arthritis:
Causes
(Handbook of Diseases)
Evidence suggests that predisposition to psoriatic arthritis is hereditary; 20% to 50% of patients are human leukocyte antigen-B27-positive. However, its onset may be precipitated by streptococcal infection or trauma.
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Source: Handbook of Diseases, 2003
Rheumatoid arthritis:
Causes
(Handbook of Diseases)
What causes the chronic inflammation characteristic of RA isn’t known. One theory states that abnormal immune activation (occurring in a genetically susceptible individual) leads to inflammation, complement activation, and cell proliferation within joints and tendon sheaths. Although no single environmental factor has been found to be a consistent and reproducible cause of this response, infection (viral or bacterial), hormonal factors, and lifestyle factors may all influence disease onset.
Some RA patients develop an immunoglobulin (Ig) M antibody against their body’s own IgG, which is called RF. Increased production of this antibody may also play a role in genetic inflammation.
Pathogenesis
Much more is known about the pathogenesis of RA than about its causes. If unarrested, the inflammatory process within the joints occurs in four stages.
In the first stage, synovitis develops from congestion and edema of the synovial membrane and joint capsule. Infiltration by lymphocytes, macro-phages, and neutrophils perpetuates the local inflammatory response. These cells, as well as fibroblast-like synovial cells, produce enzymes that help to degrade bone and cartilage.
Formation of pannus — thickened layers of granulation tissue — marks the onset of the second stage. Pannus covers and invades cartilage and eventually destroys the joint capsule and bone.
Progression to the third stage is characterized by fibrous ankylosis — fibrous invasion of the pannus and scar formation that occludes the joint space. Bone atrophy and malalignment cause visible deformities and disrupt the articulation of opposing bones, causing muscle atrophy and imbalance and, possibly, partial dislocations or subluxations.
In the fourth stage, fibrous tissue calcifies, resulting in bony ankylosis and total immobility.
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Source: Handbook of Diseases, 2003
Juvenile rheumatoid arthritis:
Causes
(Handbook of Diseases)
JRA is thought to be an autoimmune disorder. Research has linked causation to genetic and immune factors. Viral or bacterial (particularly streptococcal) infection, trauma, and emotional stress have been identified as precipitating factors.
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Source: Handbook of Diseases, 2003
Septic arthritis:
Causes
(Handbook of Diseases)
In most cases of septic arthritis, bacteria spread from a primary site of infection, usually in adjacent bone or soft tissue, through the bloodstream to the joint.
Common infecting organisms include four strains of gram-positive cocci — Staphylococcus aureus, Streptococcus pyogenes, Streptococcus pneumoniae, and Streptococcus viridans — and two strains of gram-negative cocci — Neisseria gonorrhoeae and Haemophilus influenzae. Various gram-negative bacilli — Escherichia coli, Salmonella, and Pseudomonas, for example — also cause infection.
Anaerobic organisms such as gram-positive cocci usually infect adults and children older than age 2. H. influenzae most often infects children younger than age 2.
Risk factors
Various factors can predispose a person to septic arthritis. Any concurrent bacterial infection (of the genitourinary or the upper respiratory tract, for example) or serious chronic illness (such as cancer, renal failure, rheumatoid arthritis, systemic lupus erythematosus, diabetes, or cirrhosis) heightens susceptibility. Consequently, alcoholics and elderly people run a higher risk of developing septic arthritis.
Of course, susceptibility increases with diseases that depress the autoimmune system or with prior immunosuppressant therapy. I.V. drug abuse (by heroin addicts, for example) can also cause septic arthritis.
Other predisposing factors include recent articular trauma, joint surgery, intra-articular injections, and local joint abnormalities.
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Source: Handbook of Diseases, 2003
Hypothyroidism in adults:
Causes
(Handbook of Diseases)
Hypothyroidism results from inadequate production of thyroid hormone, usually because of dysfunction of the thyroid gland due to surgery (thyroidectomy), radiation therapy (particularly with 131I), inflammation, chronic autoimmune thyroiditis (Hashimoto’s disease) or, rarely, conditions such as amyloidosis and sarcoidosis. It may also result from pituitary failure to produce thyroid-stimulating hormone (TSH), hypothalamic failure to produce thyrotropin-releasing hormone, inborn errors of thyroid hormone synthesis, inability to synthesize thyroid hormone because of iodine deficiency (usually dietary), or the use of antithyroid medications such as propylthiouracil.
In patients with hypothyroidism, infection, exposure to cold, and sedatives may precipitate myxedema coma.
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Source: Handbook of Diseases, 2003
Splenomegaly:
Medical causes
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)
Amyloidosis
Marked splenomegaly may occur with amyloidosis from excessive protein deposits in the spleen. Associated signs and symptoms vary, depending on which other organs are involved. The patient may display signs of renal failure, such as oliguria and anuria, and signs of heart failure, such as dyspnea, crackles, and tachycardia. GI effects may include constipation or diarrhea and a stiff, enlarged tongue, resulting in dysarthria.
Brucellosis
With severe cases of brucellosis, splenomegaly is a major sign. Typically, this rare infection begins insidiously with fatigue, headache, backache, anorexia, arthralgia, fever, chills, sweating, and malaise. Later, it may cause hepatomegaly, lymphadenopathy, weight loss, and vertebral or peripheral nerve pain on pressure.
Cirrhosis
About one-third of patients with advanced cirrhosis develop moderate to marked splenomegaly. Among other late findings are jaundice, hepatomegaly, leg edema, hematemesis, and ascites. Signs of hepatic encephalopathy — such as asterixis, fetor hepaticus, slurred speech, and a decreased level of consciousness that may progress to coma — are also common. Besides jaundice, skin effects may include severe pruritus, poor tissue turgor, spider angiomas, palmar erythema, pallor, and signs of bleeding tendencies. Endocrine effects may include menstrual irregularities or testicular atrophy, gynecomastia, and the loss of chest and axillary hair. The patient may also develop fever and right upper abdominal pain that’s aggravated by sitting up or leaning forward.
Endocarditis (subacute infective)
Endocarditis usually causes an enlarged, but nontender, spleen. Its classic sign, however, is a suddenly changing murmur or the discovery of a new murmur in the presence of fever. Other features include anorexia, pallor, weakness, fever, night sweats, fatigue, tachycardia, weight loss, arthralgia, petechiae, hematuria and, in chronic cases, clubbing. If embolization occurs, the patient may develop chest, abdominal, or limb pain accompanied by paralysis, hematuria, and blindness. Endocarditis may produce Osler’s nodes (tender, raised, subcutaneous lesions on the fingers or toes), Roth’s spots (hemorrhagic areas with white centers on the retina), and Janeway lesions (purplish macules on the palms or soles).
Felty’s syndrome
Splenomegaly is characteristic in Felty’s syndrome that occurs with chronic rheumatoid arthritis. Associated findings are joint pain and deformity, sensory or motor loss, rheumatoid nodules, palmar erythema, lymphadenopathy, and leg ulcers.
Hepatitis
Splenomegaly may occur with hepatitis. More characteristic findings include hepatomegaly, vomiting, jaundice, and fatigue.
Histoplasmosis
Acute disseminated histoplasmosis commonly produces splenomegaly and hepatomegaly. It may also cause lymphadenopathy, jaundice, fever, anorexia, emaciation, and signs and symptoms of anemia, such as weakness, fatigue, pallor, and malaise. Occasionally, the patient’s tongue, palate, epiglottis, and larynx become ulcerated, resulting in pain, hoarseness, and dysphagia.
Hypersplenism (primary)
With hypersplenism, splenomegaly accompanies signs of pancytopenia — anemia, neutropenia, or thrombocytopenia. If the patient has anemia, findings may include weakness, fatigue, malaise, and pallor. If he has severe neutropenia, frequent bacterial infections are likely. If he has severe thrombocytopenia, easy bruising or spontaneous, widespread hemorrhage may occur. The patient also experiences left-sided abdominal pain and a feeling of fullness after eating a small amount of food.
Leukemia
Moderate to severe splenomegaly is an early sign of acute and chronic leukemia. With chronic granulocytic leukemia, splenomegaly is sometimes painful. Accompanying it may be hepatomegaly, lymphadenopathy, fatigue, malaise, pallor, fever, gum swelling, bleeding tendencies, weight loss, anorexia, and abdominal, bone, and joint pain. At times, acute leukemia also causes dyspnea, tachycardia, and palpitations. With advanced disease, the patient may display confusion, headache, vomiting, seizures, papilledema, and nuchal rigidity.
Lymphoma
Moderate to massive splenomegaly is a late sign and may be accompanied by hepatomegaly, painless lymphadenopathy, scaly dermatitis with pruritus, fever, fatigue, weight loss, and malaise.
Malaria
A common sign of malaria, splenomegaly is typically preceded by the malarial paroxysm of chills, followed by high fever and then diaphoresis. Related effects include headache, muscle pain, and hepatomegaly. With benign malaria, these paroxysms alternate with periods of well-being. With severe malaria, however, the patient may develop a persistent high fever, orthostatic hypotension, seizures, delirium, coma, coughing (with possible hemoptysis), vomiting, abdominal pain, diarrhea, melena, oliguria or anuria and, possibly, hemiplegia.
Mononucleosis (infectious)
A common sign of infectious mononucleosis, splenomegaly is most pronounced during the second and third weeks of illness. Typically, it’s accompanied by a triad of signs and symptoms: sore throat, cervical lymphadenopathy, and fluctuating temperature with an evening peak of 101° to 102° F (38.3° to 38.9° C). Occasionally, hepatomegaly, jaundice, and a maculopapular rash may also occur.
Pancreatic cancer
Cancer of the pancreas may cause moderate to severe splenomegaly if tumor growth compresses the splenic vein. Other characteristic findings include abdominal or back pain, anorexia, nausea and vomiting, weight loss, GI bleeding, jaundice, pruritus, skin lesions, emotional lability, weakness, and fatigue. Palpation may reveal a tender abdominal mass and hepatomegaly; auscultation reveals a bruit in the periumbilical area and left upper quadrant.
Polycythemia vera
Late in polycythemia vera, the spleen may become markedly enlarged, resulting in easy satiety, abdominal fullness, and left upper quadrant or pleuritic chest pain. Signs and symptoms accompanying splenomegaly are widespread and numerous. The patient may exhibit deep, purplish red oral mucous membranes, headache, dyspnea, dizziness, vertigo, weakness, and fatigue. He may also develop finger and toe paresthesia, impaired mentation, tinnitus, blurred or double vision, scotoma, increased blood pressure, and intermittent claudication. Other signs and symptoms include pruritus, urticaria, ruddy cyanosis, epigastric distress, weight loss, hepatomegaly, and bleeding tendencies.
Sarcoidosis
A granulomatous disorder, sarcoidosis may produce splenomegaly and hepatomegaly, possibly accompanied by vague abdominal discomfort. Its other signs and symptoms vary with the affected body system, but may include nonproductive cough, dyspnea, malaise, fatigue, arthralgia, myalgia, weight loss, lymphadenopathy, skin lesions, irregular pulse, impaired vision, dysphagia, and seizures.
Splenic rupture
Splenomegaly may result from massive hemorrhage. The patient may also experience left upper quadrant pain, abdominal rigidity, and Kehr’s sign.
Thrombotic thrombocytopenic purpura
Thrombotic thrombocytopenic purpura may produce splenomegaly and hepatomegaly accompanied by fever, generalized purpura, jaundice, pallor, vaginal bleeding, and hematuria. Other effects include fatigue, weakness, headache, pallor, abdominal pain, and arthralgias. Eventually, the patient develops signs of neurologic deterioration and renal failure.
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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007
Splenomegaly:
Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Cirrhosis
About one-third of patients with advanced cirrhosis develop moderate to marked splenomegaly. Among other late findings are jaundice, hepatomegaly, leg edema, hematemesis, and ascites. Signs of hepatic encephalopathy — such as asterixis, fetor hepaticus, slurred speech, and decreased level of consciousness that may progress to coma — are also common. Besides jaundice, skin effects may include severe pruritus, poor tissue turgor, spider angiomas, palmar erythema, pallor, and signs of bleeding tendencies. Endocrine effects may include menstrual irregularities or testicular atrophy, gynecomastia, and loss of chest and axillary hair. The patient may also develop fever and right-upper-abdominal pain that’s aggravated by sitting up or leaning forward.
Endocarditis (subacute infective)
Endocarditis usually causes an enlarged, but nontender, spleen. Its classic sign, however, is a suddenly changing murmur or the discovery of a new murmur in the presence of fever. Other features include anorexia, pallor, weakness, fever, night sweats, fatigue, tachycardia, weight loss, arthralgia, petechiae, hematuria and, in chronic cases, clubbing. If embolization occurs, the patient may develop chest, abdominal, or limb pain; paralysis; hematuria; and blindness. Endocarditis may produce Osler’s nodes (tender, raised, subcutaneous lesions on the fingers or toes), Roth’s spots (hemorrhagic areas with white centers on the retina), and Janeway lesions (purplish macules on the palms or soles).
Hepatitis
Splenomegaly may occur with hepatitis. More characteristic findings include dark urine, clay-colored stools, anorexia, malaise, pruritus, hepatomegaly, vomiting, jaundice, and fatigue.
Histoplasmosis
Acute disseminated histoplasmosis commonly produces splenomegaly and hepatomegaly. It may also cause lymphadenopathy, jaundice, fever, anorexia, emaciation, and signs and symptoms of anemia, such as weakness, fatigue, pallor, and malaise. Occasionally, the patient’s tongue, palate, epiglottis, and larynx become ulcerated, resulting in pain, hoarseness, and dysphagia.
CULTURAL CUE:Histoplasmosis occurs worldwide, especially in the temperate areas of Asia, Africa, Europe, and North and South America. In the United States, it’s most prevalent in the central and eastern states, especially in the Mississippi and Ohio River Valleys.
Hypersplenism (primary)
With hypersplenism, splenomegaly accompanies signs of pancytopenia — anemia, neutropenia, or thrombocytopenia. If the patient has anemia, findings may include weakness, fatigue, malaise, and pallor. If he has severe neutropenia, frequent bacterial infections are likely. If he has severe thrombocytopenia, easy bruising or spontaneous, widespread hemorrhage may occur. The patient also experiences left-sided abdominal pain, and a feeling of fullness after eating a small amount of food.
Leukemia
Moderate to severe splenomegaly is an early sign of acute and chronic leukemia. With chronic granulocytic leukemia, splenomegaly is sometimes painful. Accompanying it may be hepatomegaly, lymphadenopathy, fatigue, malaise, pallor, fever, gum swelling, bleeding tendencies, weight loss, anorexia, and abdominal, bone, and joint pain. At times, acute leukemia also causes dyspnea, tachycardia, and palpitations. With advanced disease, the patient may display confusion, headache, vomiting, seizures, papilledema, and nuchal rigidity.
Lymphoma
Moderate to massive splenomegaly is a late sign of lymphoma and may be accompanied by hepatomegaly, painless lymphadenopathy, scaly dermatitis with pruritus, night sweats, fever, fatigue, weight loss, and malaise. Scaly rashes and pruritus may develop.
Mononucleosis (infectious)
A common sign of mononucleosis, splenomegaly is most pronounced during the second and third weeks of illness. Typically, it’s accompanied by a triad of signs and symptoms: sore throat, cervical lymphadenopathy, and fluctuating temperature with an evening peak of 101° to 102° F (38.3° to 38.9° C). Occasionally, hepatomegaly, jaundice, and a maculopapular rash may also occur.
Pancreatic cancer
Pancreatic cancer may cause moderate to severe splenomegaly if tumor growth compresses the splenic vein. Other characteristic findings include abdominal or back pain, anorexia, nausea and vomiting, weight loss, GI bleeding, jaundice, pruritus, skin lesions, emotional lability, weakness, and fatigue. Palpation may reveal a tender abdominal mass and hepatomegaly; auscultation reveals a bruit in the periumbilical area and left upper quadrant.
Polycythemia vera
Late in polycythemia vera, the spleen may become markedly enlarged, resulting in easy satiety, abdominal fullness, and left-upper-quadrant or pleuritic chest pain. Signs and symptoms accompanying splenomegaly are widespread and numerous. The patient may exhibit deep, purplish red oral mucous membranes, headache, dyspnea, dizziness, vertigo, weakness, and fatigue. He may also develop finger and toe paresthesia, impaired mentation, tinnitus, blurred or double vision, scotoma, increased blood pressure, and intermittent claudication. Other signs and symptoms include pruritus, urticaria, ruddy cyanosis, epigastric distress, weight loss, hepatomegaly, and bleeding tendencies.
Splenic rupture
Splenomegaly may result from massive hemorrhage with splenic rupture. The patient may also experience left-upper-quadrant pain, abdominal rigidity, and Kehr’s sign. Signs and symptoms of shock may also occur.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Splenomegaly:
Principal Causes of Splenomegaly
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
- Infection
- Viral
- Bacterial
- Fungal
- Rickettsial
- Parasitic
- Hemolytic anemia
- Cardiac failure
- Trauma
- Neoplasia
- Portal hypertension
- Metabolic disorders
- Other
» READ BOOK EXCERPT ONLINE »
Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Splenomegaly:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
Brucellosis.With severe cases of brucellosis, splenomegaly is a major sign. Typically, brucellosis begins insidiously with fatigue, headache, backache, anorexia, arthralgia, fever, chills, sweating, and malaise. Later, it may cause hepatomegaly, lymphadenopathy, weight loss, and vertebral or peripheral nerve pain on pressure.
Cirrhosis.About one-third of patients with advanced cirrhosis develop moderate to marked splenomegaly. Among other late findings are jaundice, hepatomegaly, leg edema, hematemesis, and ascites. Signs of hepatic encephalopathy—such as asterixis, fetor hepaticus, slurred speech, and decreased level of consciousness that may progress to coma—are also common. Besides jaundice, skin effects may include severe pruritus, poor tissue turgor, spider angiomas, palmar erythema, pallor, and signs of bleeding tendencies. Endocrine effects may include menstrual irregularities or testicular atrophy, gynecomastia, and a loss of chest and axillary hair. The patient may also develop a fever and right upper abdominal pain that's aggravated by sitting up or leaning forward.
Felty's syndrome.Splenomegaly is characteristic in Felty's syndrome. Associated findings are joint pain and deformity, sensory or motor loss, rheumatoid nodules, palmar erythema, lymphadenopathy, and leg ulcers.
Histoplasmosis.Acute disseminated histoplasmosis commonly produces splenomegaly and hepatomegaly. It may also cause lymphadenopathy, jaundice, fever, anorexia, emaciation, and signs and symptoms of anemia, such as weakness, fatigue, pallor, and malaise. Occasionally, the patient's tongue, palate, epiglottis, and larynx become ulcerated, resulting in pain, hoarseness, and dysphagia.
Leukemia.Moderateto severe splenomegaly is an early sign of acute and chronic leukemia. With chronic granulocytic leukemia, splenomegaly is sometimes painful. Accompanying it may be hepatomegaly, lymphadenopathy, fatigue, malaise, pallor, fever, gum swelling, bleeding tendencies, weight loss, anorexia, and abdominal, bone, and joint pain. At times, acute leukemia also causes dyspnea, tachycardia, and palpitations. With advanced disease, the patient may display confusion, headache, vomiting, seizures, papilledema, and nuchal rigidity.
Mononucleosis (infectious).A common sign of mononucleosis, splenomegaly is most pronounced during the second and third weeks of the illness. Typically, it's accompanied by a triad of signs and symptoms: a sore throat, cervical lymphadenopathy, and fluctuating temperature with an evening peak of 101° to 102° F (38.3° to 38.9° C). Occasionally, hepatomegaly, jaundice, and a maculopapular rash may also occur.
Pancreatic cancer.Pancreatic cancer may cause moderate to severe splenomegaly if tumor growth compresses the splenic vein. Other characteristic findings include abdominal or back pain, anorexia, nausea and vomiting, weight loss, GI bleeding, jaundice, pruritus, skin lesions, emotional lability, weakness, and fatigue. Palpation may reveal a tender abdominal mass and hepatomegaly; auscultation reveals a bruit in the periumbilical area and left upper quadrant.
Polycythemia vera.Late in polycythemia vera, the spleen may become markedly enlarged, resulting in easy satiety, abdominal fullness, and left upper quadrant or pleuritic chest pain. Signs and symptoms accompanying splenomegaly are widespread and numerous. The patient may exhibit deep, purplish red oral mucous membranes, headache, dyspnea, dizziness, vertigo, weakness, and fatigue. He may also develop finger and toe paresthesia, impaired mentation, tinnitus, blurred or double vision, scotoma, increased blood pressure, and intermittent claudication. Other signs and symptoms include pruritus, urticaria, ruddy cyanosis, epigastric distress, weight loss, hepatomegaly, and bleeding tendencies.
Sarcoidosis.Sarcoidosis may produce splenomegaly and hepatomegaly, possibly accompanied by vague abdominal discomfort. Its other signs and symptoms vary with the affected body system, but may include a nonproductive cough, dyspnea, malaise, fatigue, arthralgia, myalgia, weight loss, lymphadenopathy, skin lesions, an irregular pulse, impaired vision, dysphagia, and seizures.
Splenic rupture.Splenomegaly may result from massive hemorrhage with splenic rupture. The patient may also experience left upper quadrant pain, abdominal rigidity, and Kehr's sign.
Thrombotic thrombocytopenic purpura.Thrombotic thrombocytopenic purpura may produce splenomegaly and hepatomegaly accompanied by fever, generalized purpura, jaundice, pallor, vaginal bleeding, and hematuria. Other effects include fatigue, weakness, headache, pallor, abdominal pain, and arthralgia. Eventually, the patient develops signs of neurologic deterioration and renal failure.
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
Septic Arthritis:
Septic Arthritis - pathophysiology
(The 5-Minute Pediatric Consult)
- Entry of bacteria into joint space:
- Hematogenous spread
- Direct inoculation (penetrating trauma)
- Extension from bone infection (mainly in children <1 year old when vessels cross from metaphysis to epiphysis)
- Influx of inflammatory cells within the joint capsule
- Rapid destruction of cartilaginous structures within the joint by bacterial and lysosomal enzymes:
- If untreated, may progress to necrosis of the intra-articular epiphysis
Septic Arthritis - etiology
- Bacteria:
- Staphylococcus aureus most common etiology outside of perinatal period (Methicillin-sensitive and Methicillin-resistant)
- Streptococci
- Kingella kingae
- Haemophilus influenzae
- Salmonella
- N. gonorrhoeae
- Neisseria meningitidis
- Borrielia burgdorfderi (Lyme)
- Aseptic arthritis:
- Rubella
- Parvovirus
- Hepatitis B or C
- Mumps
- Herpesviruses (Epstein-Barr virus, cytomegalovirus, herpes simplex virus, varicella zoster virus)
- Epstein-Barr virus
- Varicella
- Candida albicans (neonatal)
>
» READ BOOK EXCERPT ONLINE »
Source: The 5-Minute Pediatric Consult, 2008
Splenomegaly:
Splenomegaly - pathophysiology
(The 5-Minute Pediatric Consult)
- The spleen is an hematopoietic organ with 2 main parts:
- White pulp is the lymphoid tissue.
- Red pulp is the red cell mass.
- Splenic sinusoids are lined with macrophages that destroy abnormal red cells.
- The spleen also serves as a reservoir for platelets. A normal-sized spleen can hold 1/3 of the circulating platelets; an enlarged spleen can hold up to 90% of the circulating platelet mass.
» READ BOOK EXCERPT ONLINE »
Source: The 5-Minute Pediatric Consult, 2008
Fever and Neutropenia:
Patient Afebrile within the First 3 to 5 Days of Treatment, Etiology Found
(Pediatric Infectious Disease)
If a responsible pathogen is isolated, the antibiotics can be changed to give
optimal treatment to the specific pathogen. Antibiotic treatment should be
continued for a minimum of 7 days; many specialists continue treatment for at
least 10 to 14 days if an isolate is recovered in blood culture. Often,
antibiotics are continued until there is evidence of bone marrow recovery
(i.e., neutrophil count
> 500/m3). In cases in which neutropenia is predicted to be prolonged, afebrile patients
may have antibiotics stopped and are closely observed.
Patient Afebrile, No Etiology Found
The management of these patients is difficult because no infectious disease
process has been documented. Patients who are afebrile and who have an absolute
neutrophil count of more than 500/m
3 may have their antibiotics discontinued. In persistently neutropenic children,
there has been an effort to divide patients into low-risk and high-risk
categories. Children are considered at low risk if they lack ongoing signs of
sepsis, chills, hypotension, severe mucositis, and have a neutrophil count of
more than 100/m
3. In these children, antibiotics may be stopped when the child is afebrile for
about 1 week. A small number of studies have suggested that the antibiotic can
be changed to oral cefixime and the child monitored closely. It should be noted
that these studies involving the use of oral antibiotics often took place with
the patients remaining as inpatients for close monitoring. Children who are
labeled at high risk (i.e., those with continued absolute neutropenia or
mucositis, or in whom follow-up cannot be guaranteed) are continued on
intravenous antibiotics until the resolution of neutropenia.
Continued Fever without Etiology
Patients who continue to have fever without obvious etiology present the most
difficult management dilemma. The most important management principal in these
patients is continued evaluation with physical examination, blood cultures, and
radiographic studies. Because systemic fungal infections can be associated with
negative blood cultures and may present with progressive intracranial, sinus,
or pulmonary disease, these areas should be closely monitored. Examination of
the oropharynx for viral lesions caused by either herpes simplex virus or
cytomegalovirus is important. Children with persistent fever and neutropenia
are often treated for 2 weeks, with a complete reevaluation at that time. In
certain situations, it has been suggested that if the patient remains
clinically stable with no evidence of progressive infectious disease,
antibiotics may be discontinued under close observation.
» READ BOOK EXCERPT ONLINE »
Source: Pediatric Infectious Disease, 2004
Osteomyelitis and Septic Arthritis:
Etiology
(Pediatric Infectious Disease)
Children are colonized with a variety of bacteria; a culture of the nasopharynx
of an asymptomatic child could yield any number of bacteria, including
Staphylococcus aureus and Streptococcus pneumoniae. Usually, these organisms reside on body surfaces with no ill effects. However,
by a process not always well defined, these colonizing bacteria enter the
bloodstream.
Once the bacteria enter the bloodstream, numerous things can occur (Fig. 2.1).
Bacteremia can be transient and resolve without sequelae; this is often the
case with viridans streptococci. Bacteremia, by its very presence in the
systemic circulation, can cause overwhelming sepsis, as is often the case with
Neisseria meningitidis. Bacteria can also be deposited in secondary sites, such as the cerebrospinal
fluid or bone.
The bones are a frequent site of secondary infection because the blood supply
takes a hairpin turn at the metaphyses of long bones, increasing the chance of
the bacteria being deposited. This secondary seeding of bones from the blood is
the major mechanism of pediatric osteomyelitis. This is in contrast to adults,
who usually acquire osteomyelitis from direct inoculation following trauma or
surgical procedures.
Pyogenic arthritis develops in a fashion similar to osteomyelitis, whereby
blood-borne organisms are deposited in the synovium of the joint space. Similar
to the long bones of children, the joint space is highly vascularized and is an
area where bacteremic organisms are readily deposited. Bacterial arthritis can
also spread from a contiguous osteomyelitis; blood vessels can deposit
infection from the metaphysis into the joint space. The organisms of septic
arthritis are similar to those of osteomyelitis.
S. aureus is the most common organisms, followed by S. pneumoniae, Kingella kingae, and group A streptococcus.
» READ BOOK EXCERPT ONLINE »
Source: Pediatric Infectious Disease, 2004
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