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liquid-based Pap smears include less artifact, a lower number of unsatisfactory specimens,
and the ability to perform HPV DNA testing on a single sample.
1. The American Cancer Society, American Society for Colposcopy and Cervical Pathology,
and American Society for Clinical Pathology released updated consensus guidelines for
cervical cancer screening in 2012 (8). They state that:
a. women should begin screening at 21 years of age with only Pap smears every 3 years.
b. At age 30, women should receive either a Pap smear alone every 3 years, or a Pap smear
combined with molecular screening for high-risk HPV every 5 years.
c. Those older than 65 with either three negative Pap smears or two negative high-risk
HPV assays in the preceeding 10 years may discontinue screening.
d. Women who are status-post hysterectomy for benign reasons are exempt from testing.
e. Current recommendations for women who have received the HPV vaccine are not
different from that listed above.
IV. PAP SMEAR DIAGNOSES AND MANAGEMENT. It is important to remember that the Pap
test is for screening only; the definitive diagnosis of preinvasive and invasive neoplastic lesions
can only be made histologically. The purpose of the Pap smear is to identify abnormalities in
exfoliated ecto- and endocervical cells that suggest underlying neoplastic lesions and signify
the need for additional testing. The 2001 Bethesda System delineates uniform terminology for
cervical cytopathology reporting. This allows for standardization of follow-up and treatment.
The common cytopathologic diagnoses with typical follow-up for each are as follows (9):
A. Atypical Squamous Cells of Undetermined Significance. This represents abnormal
squamous cells that do not meet morphologic criteria for higher grade lesions. According to
2006 ASCCP guidelines, women <30 years of age can be followed with a repeat Pap smear
in 4 to 6 months or proceed to diagnostic colposcopy, depending on the clinical situation.
Those older than 30 years of age are typically managed according to the high-risk HPV
DNA status: if positive, colposcopy should be performed. If negative, the patient can be
followed with a repeat Pap smear in 1 year.
B. Atypical Squamous Cells (Cannot Exclude High-Grade Squamous Intraepithelial
Lesion [ASC-H]).
Because 30% to 40% of patients with ASC-H demonstrate high-grade
dysplasia and a very high prevalence of high-risk HPV DNA (approaching 85%), these
patients should all have colposcopic evaluation and biopsies.
C. Atypical Glandular Cells (AGCs). This diagnosis should include a comment by the
pathologist regarding the probable source of the AGCs. Patients with AGC favored to be
endometrial in origin should undergo endometrial and endocervical sampling with col-
poscopy afterward if no endometrial pathology is noted. All other ACG diagnoses warrant
immediate colposcopy with HPV testing and the addition of endometrial sampling if the
patient is >35 years of age.
D. Low-Grade Squamous Intraepithelial Lesion (LGSIL). All patients with LGSIL
results on a Pap smear should undergo colposcopy with a recommendation for endocer-
vical curettage in non-pregnant, premenopausal patients or those with an unsatisfactory
colposcopic examination. HPV DNA testing is only performed if moderate- or high-grade
squamous dysplasia (CIN 2-3) is discovered on colposcopic biopsies. Pregnant women with
LGSIL may defer colposcopy until at least 6 weeks following delivery.
E. High-Grade Squamous Epithelial Lesion (HGSIL). Most guidelines recommend that
patients of any age with HSIL should undergo immediate colposcopy. If high-grade squa-
mous dysplasia is noted on biopsy, definitive excisional therapy (such as loop electrosurgic
excision) is warranted. HPV testing is not appropriate in this setting.
V. COLPOSCOPY. Colposcopy uses magnification to identify the abnormal areas of the uterine
cervix. After a Pap smear is performed, the cervix is painted with a solution of 3% to 5% acetic
acid, allowing for the visualization of abnormally staining areas to direct subsequent biopsy.
The examination is considered satisfactory only if the entire transformation zone can be visual-
ized and the most abnormal areas can be biopsied. A simultaneous endocervical curettage is
usually performed to ensure adequate sampling of the transformation zone and to evaluate the
258
glandular cells in the endocervical canal. If colposcopy is inadequate, there is an abnormality
in the endocervical canal, or there is a suspicion of invasive cancer; further diagnostic testing
should include either a conization of the cervix or a loop electrosurgical excision procedure
(LEEP) to complete the workup.
REFERENCES
1. Siegel R, Naishadham D, Jemal A. Cancer statistics 2012. CA Cancer J Clin 2011;61:69.
2. Mahdavi A, Monk BJ. Vaccines against human papillomavirus and cervical cancer: promises and chal-
lenges. Oncologist 2005;10:528.
3. Holoway P, Miller AB, Rohan T, et al. Natural history of dysplasia of the uterine cervix. J Natl Cancer
Inst 1999;91:252.
4. Ho GY, Bierman R, Beardsley L, et al. Natural history of cervicovaginal papillomavirus infection in
young women. N Engl J Med 1998;338:423–428.
5. Kahn JA. HPV vaccination for the prevention of cervical intraepitheial neoplasia. N Engl J Med
2009;361:271.
6. Winer RL, Lee SK, Hughes JP, et al. Genital human papillomavirus infection: incidence and risk fac-
tors in a cohort of female university students. Am J Epidemiol 2003;157:218.
7. Östor AG. Natural history of cervical intraepithelial neoplasia: a critical review. Int J Gynecol Pathol
1993;12:186–192.
8. U.S. Preventive Services Task Force. Screening for cervical cancer: recommendations and rationale, http://
www.ahrq.gov/clinic/uspstf/uspscerv.htm, accessed January 20, 2003.
9. Wright TC, Massad LS, Dunton CJ, et al. 2006 consensus guidelines for the management of women
with abnormal cervical cancer screening tests. Am J Obstet Gynecol 2007;197:346–355.
11.9
Postmenopausal
Bleeding
Naureen Raq
I. BACKGROUND. Postmenopausal bleeding or PMB is defined as vaginal bleeding that occurs
in a woman who has had amenorrhea for a year or more.
II. PATHOPHYSIOLOGY
A. Etiology.
Any vaginal bleeding in a postmenopausal woman requires the clinician to
strongly consider the possibility of endometrial malignancy. Women on cyclic hormone
replacement therapy (HRT) are expected to have uterine bleeding; however, irregular or
excessive bleeding in these patients requires investigation (Table 11.9.1).
B. Epidemiology. Abnormal vaginal bleeding is a common outpatient problem, occurring in
10% of women older than 55 years of age (1) and accounting for 70% of gynecologic visits
during the perimenopausal and postmenopausal years (2).
III. EVALUATION
A. History
1. Pattern of bleeding. The amount of bleeding should be estimated to help assess
whether and what type of intervention may be required in order to avoid anemia or
hypovolemia. Vaginal and endometrial atrophy and endometrial polyps are common
causes of PMB. Association of bleeding with bowel movements or urination suggests a
nongenital source.
2. Current medications. Any use of hormonal therapy, including estrogen, proges-
terone, tamoxifen, thyroid replacement, or corticosteroids should be quantified and
recorded.
259
a. Acyclic bleeding is common in the first 3–4 months on continuous estrogen–progestin
therapy and usually does not indicate pathology. Bleeding that is excessive, persists
after months of therapy, or occurs after amenorrhea has been established on these
regimens should be evaluated.
b. The rate of endometrial cancer in women taking tamoxifen or unopposed estrogen is
six to seven times the rate for untreated women. The frequency of endometrial polyps
is also increased (3, 4).
c. Exogenous corticosteroids or thyroid abnormalities can lead to menstrual irregularities
and PMB.
d. Anticoagulant therapy may cause uterine bleeding in postmenopausal women.
e. Endometritis is an uncommon cause of bleeding in postmenopausal women, but
endometrial tuberculosis in developing countries may present with PMB (5–7).
3. Past medical history. Nulliparity, early menarche, late menopause, and history of
chronic anovulation are risk factors for endometrial hyperplasia and carcinoma. Obesity,
hypertension, diabetes, and liver disease are commonly associated with estrogen excess
and can also increase risk. Past use of oral contraceptives is associated with a decreased
risk of endometrial carcinoma.
4. Family history. A strong family history of endometrial, breast, or colon cancer is a risk
factor for endometrial cancer.
B. Physical examination
1. Vital signs. Blood pressure and pulse can indicate the degree and acuity of blood loss;
orthostatic changes can be evidence of significant volume depletion. Fever suggests infec-
tion as a potential cause (Chapter 2.6).
2. Abdomen. Tenderness or guarding suggests an infectious or inflammatory cause.
Malignancy may also present with an abdominal mass.
3. Pelvis. It is necessary to examine the external genitalia, vagina, and cervix for lesions
that could be the source of bleeding. The uterus and ovaries are palpated to assess for
enlargement, masses, and tenderness.
4. Rectum. Rectal examination and anoscopy may be warranted to rule out hemorrhoids
or other intestinal sources of bleeding (Chapter 9.11).
C. Testing
1. Office laboratory testing. Urinalysis, stool guaiac testing, or both can be useful to assess
for nongenital sources of blood. A complete blood count may be helpful in assessing the
TABLE 11.9.1 Etiology of Postmenopausal Bleeding
Gynecologic Causes Non-gynecologic causes
Atrophic uterus Hormone replacement therapy
Cervical and endometrial polyp Thyroid replacement therapy
Endometrial hyperplasia Corticosteroids
Uterine fibroids Anticoagulants
Endometrial, cervical, ovarian, or Fallopian
tube cancers
Obesity
Hydrometra Dramatic weight loss
Pyometra Infections in adjacent organs like diverticulitis
leading to endometritis
Hematometra Stress
Diabetes, hypertension, and liver disease
260
degree of blood loss or elevated white count due to infection. Testing for gonorrhea and
chlamydia may be warranted.
2. Papanicolaou (Pap) smear. Many sources recommend a Pap smear as part of the evalu-
ation, although the diagnostic yield is generally low. Cervical lesions or friability raise
the possibility of a source of cervical bleeding. Endometrial cells or abnormal glandular
cells of unknown significance found on the Pap smear of a postmenopausal woman not
on HRT warrants further evaluation of the endometrium.
3. Biopsy
a. Visible lesions of the vulva, vagina, or cervix should be sent for biopsy.
b. In the absence of a clear nonuterine source of bleeding, endometrial biopsy is recom-
mended. Office-based endometrial biopsy is less invasive and more cost-effective than
dilation and curettage (D & C), with comparable sensitivity and specificity (8). There
is excellent correlation between the histopathology of specimens taken by office biopsy
and D & C (9). Blind sampling of either type is most effective when pathology is
global, rather than focal.
c. If there is persistent bleeding after a normal biopsy result, further assessment is neces-
sary. This may include a repeat biopsy, D & C, and/or imaging.
4. Diagnostic imaging. Several methods are available; there is little evidence-based consen-
sus on when each method should be used (1, 10).
a. Transvaginal ultrasound (TVUS) is gaining popularity as an alternative or adjunct to
endometrial biopsy. A clearly identifiable, homogeneous endometrial stripe ≤4 mm
in thickness is highly unlikely to contain hyperplasia or carcinoma, and biopsy may
not be necessary (8). TVUS is better tolerated than endometrial biopsy, with similar
detection rates for endometrial abnormalities (1, 9). However, women with persistent
bleeding warrant further investigation. TVUS should not be used in place of biopsy
among women taking tamoxifen or women on HRT (Table 11.9.2).
b. Saline infusion sonohysterography (SIS; ultrasound evaluation after the instillation
of fluid into the endometrial cavity) allows the architectural evaluation of the uterine
cavity to detect small lesions that may be missed by endometrial biopsy or TVUS. The
disadvantage of this method is the absence of tissue diagnosis, so if a lesion is found,
hysteroscopy is then necessary for directed biopsy.
c. Hysteroscopy is becoming the “gold standard” against which other methods of endo-
metrial assessment are compared. This provides direct visualization of the endometrial
cavity, allowing targeted biopsy or excision of lesions. However, it is more costly and
requires more special expertise than most other modalities. Because lesions are occa-
sionally missed even with this method, some recommend performing D & C along
with hysteroscopy (9).
d. Magnetic resonance imaging is occasionally helpful in determining the presence of
fibroids when sonography is not definitive.
e. Palpable adnexal abnormalities should be evaluated by ultrasound or other imaging as
appropriate.
D. Genetics. Genetic testing is not helpful in the evaluation of PMB. Women with a family
history of gynecologic malignancy are at high risk and should be evaluated thoroughly.
IV. DIAGNOSIS
A. Differential diagnosis.
Causes of PMB have been reported as atrophy (59%), polyp
(12%), endometrial cancer (10%), endometrial hyperplasia (9.8%), hormonal effect (7%),
cervical cancer (<1%), and other (2%) (8).
TABLE 11.9.2 Endometrial Thickness
<3 mm with or without endo-
metrial fluid
3–5 mm with endometrial
fluid
5 mm with bleeding or
11mm without bleeding
No further studies Further studies Further studies
261
B. Clinical manifestations. Initial clinical evaluation may identify a nonuterine source.
Postcoital spotting in conjunction with vaginal atrophy or cervical friability suggests cervical
or vaginal mucosal bleeding. If no other source is identified, the key to diagnosis is imaging
and tissue sampling of the endometrium. A thin endometrial stripe in a woman in a low-
risk category suggests endometrial atrophy. If neither biopsy nor TVUS provides sufficient
information, SIS and/or hysteroscopy with directed biopsy may be used. D & C should be
reserved for cases in which other methods are unsuccessful or unavailable.
REFERENCES
1. Goldstein RB, Bree RL, Benson CB, et al. Evaluation of the woman with postmenopausal bleeding:
society of radiologists in ultrasound-sponsored consensus conference statement. J Ultrasound Med
2001;20:1025–1036.
2. Clark TJ, Mann CH, Shah N, et al. Accuracy of outpatient endometrial biopsy in the diagnosis of
endometrial cancer: a systematic quantitative review. BJOG 2002;109:313–321.
3. Fisher B, Costantino JP, Redmond CK, et al. Endometrial cancer in tamoxifen-treated breast cancer
patients: findings from the National Surgical Adjuvant Breast and Bowel Project (NSABP) B-14. J
Natl Cancer Inst 1994;86:527.
4. Chalas E, Costantino JP, Wickerham DL, et al. Benign gynecologic conditions among participants in
the Breast Cancer Prevention Trial. Am J Obstet Gynecol 2005;192:1230.
5. Sabadell J, Castellví J, Baró F. Tuberculous endometritis presenting as postmenopausal bleeding. Int
J Gynaecol Obstet 2007;96:203.
6. Mengistu Z, Engh V, Melby KK, et al. Postmenopausal vaginal bleeding caused by endometrial
tuberculosis. Acta Obstet Gynecol Scand 2007;86:631.
7. Güngördük K, Ulker V, Sahbaz A, et al. Postmenopausal tuberculosis endometritis. Infect Dis Obstet
Gynecol 2007;2007:27028.
8. Goodman A. Evaluation and management of uterine bleeding in postmenopausal women. Accessed at
UpToDate online (www.uptodate.com) on July 2005, last update October 2004.
9. Feldman S. Diagnostic evaluation of the endometrium in women with abnormal uterine bleeding.
Accessed at UpToDate (www.uptodate.com) on July 2005, last update January 2005.
10. Clark TJ, Voit D, Gupta JK, et al. Accuracy of hysteroscopy in the diagnosis of endometrial cancer
and hyperplasia: a systematic quantitative review. JAMA 2002;288(13):1610–1621.
11.10
I. BACKGROUND. Vaginal discharge can be physiologic or pathologic. When pathologic, it is
reported that 90% of affected women have bacterial vaginosis (BV), vulvovaginal candidiasis
(VVC), or trichomoniasis (1–3). Other pathologic causes include vaginal infections such as
chlamydia and gonorrhea, malignancies, and allergic conditions.
II. PATHOPHYSIOLOGY. BV is not a sexually transmitted disease. It is characterized by a reduc-
tion in the number of vaginal Lactobacillus species with subsequent overgrowth of Gardnerella
vaginalis, Mobiluncus species, Mycoplasma hominis, or anaerobic Gram-negative rods. This
disruption of the normal vaginal microflora has been associated with multiple or new sex part-
ners, antimicrobial use, douching, smoking, or pregnancy. These predisposing factors have been
reported in up to 33% of women suffering from BV (4).
Candida species are a part of the normal vaginal flora among many healthy asymptomatic
females. Vulvovaginitis is most commonly due to Candida albicans. Less commonly, it may
be due to C. glabrata or C. parapsilosis. The exact mechanism by which it causes symptom-
atic disease is complex and involves host inflammatory responses and virulence factors in the
Vaginal Discharge
Sanjeev Sharma
262
organism. Risk factors for vaginal candidiasis include diabetes mellitus, antibiotic use, and
immunosuppression.
Trichomoniasis vaginalis is a flagellated protozoan parasite contracted almost exclusively
through sexual contact. Trichomoniasis is responsible for 10–25% of vaginal infections (4).
In the United States, infection with Chlamydia trachomatis is prevalent. Between 5 and 15%
of pregnant women may be infected with this organism (5). Neisseria gonorrhoeae is the second
most commonly reported bacterial sexually transmitted infection (STI) (6). N. gonorrhoeae and
C. trachomatis infections both present with cervicitis, although N. gonorrhoeae typically presents
more acutely. Other common causes of vaginal discharge include noninfectious causes such as
atrophy and allergies, chemical irritation (2), neoplasia, and foreign bodies such as retained
tampons (5) or intrauterine devices.
III. EVALUATION
A. History.
A good clinical history is helpful in clarifying the cause of vaginal discharge.
Many women take over-the-counter medications before presenting to the physician, and
this may affect patient presentation or subsequent evaluation. The history should focus
on the age of the patient, relationship status, sexual history, number and gender of sexual
partners, menstrual history, vaginal hygiene practices including douching, recent medica-
tion, instrumentation or surgery, current health and smoking, contraceptive history, and the
characteristics of the discharge.
Young women, especially those younger than 30 years, may be at increased risk for STIs
(7, 8). In elderly patients, a persistent vaginal discharge may indicate atrophy or neoplasia.
The patient’s general health status is important; frequent problems with discharge, par-
ticularly recurrent candidiasis, may suggest the presence of a systemic illness such as diabetes
or human immunodeficiency virus.
B. Discharge Characteristics. Physiologic discharge is most commonly described as being clear
and thin. Typically, the amount of discharge varies with the menstrual cycle. Pathologic dis-
charge is more frequently described as copious, having a particular color and may have an odor.
The discharge of BV is classically a homogenous white, noninflammatory discharge
that smoothly coats the vaginal walls. The discharge can be fishy or musty before or after
the addition of potassium hydroxide (KOH; a positive “whiff” test); see Section III.C (3).
The discharge of VVC is often thick, clumpy, white, and odorless, and it can be associ-
ated with vaginal pruritus, erythema, and edema. The discharge of trichomoniasis may be
diffuse, malodorous, and yellow-green, with vulvar irritation (3).
C. Associated Symptoms. These can include itching, soreness, dysuria, or postcoital bleed-
ing, lower abdominal pain, pelvic pain, and dyspareunia.
D. Physical Examination. A complete physical examination should be considered if the
patient appears to be acutely ill, has signs of systemic illness, including abdominal pain, rash,
fever, or other complaints. When preparing to examine the genitalia, care must be given
to patient comfort, privacy, and the sensitive nature of the lithotomy position. Attention
should be given to the presence of cervical or vulvar inflammation and the presence of cervi-
cal motion tenderness.
E. Testing. (Refer Table 11.10.1.) Office laboratory testing is easy and usually available in
the outpatient clinical setting. KOH test, pH, and microscopic examination of the vaginal
discharge can determine the cause of vaginal discharge in most cases.
IV. DIAGNOSIS. BV is commonly diagnosed by using Amsel’s criteria. These include the presence
of a characteristic discharge, the presence of clue cells on microscopic examination, discharge
pH > 4.5, and a positive “whiff” test. Diagnosis of vaginal trichomoniasis is usually made by
microscopic examination of a wet mount of the discharge. However, the sensitivity of micro-
scopic exam has been reported to be only 60–70% , and a fresh specimen yields better results
(8). Culture is a sensitive method of diagnosing trichomoniasis. A polymerase chain reaction
assay for the detection of gonorrhea and chlamydia is widely available.
If all laboratory tests are negative and signs of local inflammation are present, noninfectious
causes of vaginitis should be considered. These include mechanical friction, as well as chemical
irritation (often seen with the use of douching) or allergic causes, often seen among those using
certain soaps, scented menstrual pads, or fabric softeners.
263
REFERENCES
1. Egan ME, Lipsky MS. Diagnosis of vaginitis. Am Fam Physician 2000;62(5):1095–1104.
2. Miller KE, Ruiz DE, Graves JC. Update on the prevention and treatment of sexually transmitted
diseases. Am Fam Physician 2003;67(9):1915–1922.
3. Accessed at http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5106a1.htm on August 11, 2012.
4. Accessed at www.infopoems.com on May 11, 2012.
5. Mitchell H. Vaginal discharge—causes, diagnosis and treatment. BMJ 2004;328:1306–1308.
6. Mejeroni U. Screening and treatment for sexually transmitted infections in pregnancy. Am Fam
Physician 2007;76:265–270.
7. Diseases characterized by vaginal discharge. Treatment guideline. Accessed at www.cdc.gov/std/tricho-
monas/treatment.htm on August 12, 2012.
8. Department of Health and Human Services. Centers for Disease Control and Prevention. Morbidity
and mortality weekly report: recommendations and reports. Sexually transmitted diseases treatment guide-
lines, 2006. August 4, 2006, Volume 55, Number RR-1.
TABLE 11.10.1 Differential Diagnosis and Clinical Manifestations in Vaginal
Discharge
Bacterial vaginosis Vulvovaginal candidiasis Trichomoniasis
Discharge
character-
istics
Homogenous, white,
noninflammatory
Thick, white, cottage
cheese-like
Yellow-green copious,
watery, pooling,
frothy (4)
Odor Fishy before and after
KOH + “whiff” test
Not typical Malodorous (10%)
Physical exam-
ination
Discharge coats
vaginal wall
Excoriation edema,
erythema
Strawberry cervix (2% of
patients) (4)
Precipitating
factors
Changes to vaginal
flora, pregnancy,
condoms, douching,
new or multiple
partners (1)
Antibiotics, systemic
illness, medication,
immunocompromise
Sexually transmitted
infection
pH
>4.5 Normally <4.5 >4.5 in 90%
Microscopy/
Gram stain
Amsel’s diagnostic
criteria
a
Budding yeast or hyphae
after 10% KOH
60–70% sensitive
Culture most
sensitive(3)
Presence of clue cells
highly sugges-
tive (1)
Moving flagellae (2)
Associated
symptoms
May be asymptomatic Pruritus, vaginal irritation,
dysuria (1)
Vulvar irritation and
dysuria, lower
abdominal pain; may
be asymptomatic (4)
a
Thin homogenous discharge, positive “whiff test,” clue cells, vaginal pH >4.5—three out of four is
highly suggestive of BV (1).
264
CHAPTER 12
Musculoskeletal Problems
Allison M. Cullan
12.1
I. BACKGROUND. Arthralgia means joint pain. It is a symptom, not a diagnosis. Arthralgia
may affect a single joint or several joints. The symptom may arise from bones or periarticular
structures (such as muscle, ligament, or tendon). Arthralgia is sometimes equated with “arthri-
tis,” although the terms are not synonymous. Arthritis typically causes arthralgia, but not all
arthralgia is caused by arthritis (1).
II. PATHOPHYSIOLOGY. Arthralgia can be a manifestation of a variety of causes, including
mechanical trauma to a joint, degenerative joint disease (DJD)/osteoarthritis, infection, and
local or systemic inflammation. Twenty percent of all primary care visits worldwide are related
to joint and muscle pains. In the elderly, the most common cause of arthralgia is DJD, affecting
about one-third of those over age 65 years; in middle-aged patients, inflammatory conditions
(various arthritides) predominate; in the young, systemic conditions, such as viral infections,
are more likely (2–4).
III. EVALUATION. The differential diagnosis is broad; thus, it is useful to target the history and
examination upon several key elements: duration of arthralgia, the presence or absence of signs
of joint inflammation, distribution of affected joints, systemic symptoms, patient gender/age/
medical history (5). The consideration of these factors can substantially narrow the range of
possible diagnoses and help establish the cause. Laboratory testing and imaging may be neces-
sary in some instances to clarify or confirm a final diagnosis.
A. Duration of Arthralgia (5, 6)
1. Abrupt onset of significant pain in a single joint immediately following trauma highlights
the probable cause.
2. Acute onset of pain, with signs of inflammation and fever, points to an infectious or
perhaps crystal-induced arthropathy.
3. Indolent onset of arthralgia in several joints over weeks or months would make infection
or crystal-induced disease improbable.
4. Acute onset may reflect an acute, self-limited process or simply the first recognition of
what will become a chronic condition.
B. Presence or Absence of Inflammation (5, 6)
1. Warm, swollen, erythematous, tender joints point to “arthritis” as a result of bacterial or
viral infection, crystal arthropathy, or connective tissue disease and would be less likely
to represent osteoarthritis.
2. Morning stiffness, especially that lasting for over 30 minutes, would support a diagnosis
of rheumatoid arthritis.
Arthralgia
Richard H. Rutkowski
265
C. Distribution of Joints (5, 6)
1. Symmetric involvement of the metacarpophalangeal (MCP) joints would suggest consid-
eration of rheumatoid arthritis.
2. Symptoms in weight-bearing joints such as the knees and hips raise suspicion of DJD.
3. Symptoms in the first metatarsophalangeal (MTP) joint with signs of local inflammation
support a diagnosis of
gout.
D. Systemic Symptoms (5, 6)
1. Current symptoms of upper respiratory infection or recent history of measles mumps
rubella vaccine and polyarthralgia point to reactive arthralgia.
2. Urethritis, conjunctivitis, and large lower extremity joint involvement in a young male
raises the likelihood of Reiter’s syndrome or perhaps gonococcal infection.
3. Associations with fatigue, myalgias, and sleep disturbance may indicate a diagnosis of
fibromyalgia, depression, hypothyroidism, or hypercalcemia.
E. Age/Gender/Family History (5)
1. Most connective tissue diseases are more prevalent in females.
2. Gout is more common in males and uncommon in premenopausal females.
3. Osteoarthritis (DJD) is the most common cause of arthralgia in the elderly population.
Polymyalgia rheumatica may present with arthralgias, particularly in the axial skeleton
in individuals over the age of 50 years.
4. Multiple joint inflammation in a female with a malar rash and a family history of sys-
temic lupus erythematosus (SLE) would suggest a likely diagnosis of SLE.
F. Physical Examination—Some Helpful Findings (5, 6)
1. Vital signs/general: weight loss, fever, lymphadenopathy.
2. Head, eyes, ears, nose, throat: conjunctivitis, decreased tears/saliva, thyroid enlargement.
3. Skin: psoriatic plaques, malar rash, “viral” exanthem, erythema chronicum migrans,
thickening of the skin, erythema infectiosum.
4. Cardiovascular: new heart murmur.
5. Joint examination: warmth, tenderness, joint effusion, deformity, range of motion,
crepitus.
6. Tenderness in periarticular structures or trigger points in soft tissue.
G. Testing. Careful history and examination may be sufficient to confidently establish a
diagnosis. However, some cases of arthralgia may require laboratory testing and/or imaging
to evaluate for or confirm the presence of inflammation, infection, crystal-induced disease,
or systemic conditions. Several examples include
1. Laboratory Tests (5–8)
a. Complete blood count, erythrocyte sedimentation rate, and C-reactive protein are
nonspecific tests but may support or refute inflammatory conditions.
b. Analysis of synovial fluid can confirm bacterial infection, inflammation, trauma, or
crystal-induced disease.
c. Antinuclear antibody is positive in 90% of SLE cases.
d. Rheumatoid factor or anti-citrullinated protein antibody could support a diagnosis of
rheumatoid arthritis or some other autoimmune diseases.
e. Human leukocyte antigen-B27 (HLA-B27) is often present in ankylosing spondylitis,
Reiter’s disease, and enteropathic arthritis.
f. Positive rapid test for influenza supports reactive arthralgia.
g. Positive Lyme serology in the proper context favors Lyme arthritis.
2. Imaging (5, 8)
a. Plain radiographs, especially in cases of trauma or suspected DJD.
b. Computed tomography and magnetic resonance imaging may be useful for suspected
traumatic injury, possible metastatic disease, or intraarticular derangements.
IV. DIAGNOSIS. The differential diagnosis of arthralgia, highlighting the types more commonly
encountered in a primary care setting, and classified by usual presentation as monoarticular or
polyarticular (or both), is presented in Table 12.1.1.
266
Taylor’s DifferenTial Diagnosis Manual
REFERENCES
1. Hardin JG. Arthralgia. In: Walker HK, Hall WD, Hurst JW, eds. Clinical methods: the history, physical,
and laboratory examinations, 3rd ed. Boston, MA: Butterworths, 1990:Chapter 160.
2. Morris D. Osteoarthritis. Prim care Update 2005;3(1):20–26.
3. Lawrence RC, Felson DT, Helmick CG, et al. Estimates of the prevalence of arthritis and other rheu-
matic conditions in the United States. Part II. Arthritis Rheum 2008;58(1):26–35.
4. Dillon CF, Rasch EK, Gu Q, Hirsch R. Prevalence of knee osteoarthritis in the United States: arthritis
data from the Third National Health and Nutrition Examination Survey 1991-1994. J Rheumatol
2006;33(11):2271–2279.
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2003;68(6):1151–1160.
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TABLE 12.1.1 Differential Diagnosis of Arthralgia, by Usual Presentation (5, 6, 8)
Monoarticular Polyarticular
Trauma
Overuse injury
DJD/osteoarthritis
Septic arthritis/osteomyelitis
Crystal-induced arthropathy (e.g., gout)
Lyme disease
Hemoglobinopathy (e.g., sickle cell)
Metastatic tumor
Stress fracture
DJD/osteoarthritis
Fibromyalgia
Rheumatoid arthritis
Psoriatic arthritis
Reiter’s syndrome
Viral reactive arthritis (e.g., parvovirus)
Lyme disease
Systemic lupus erythematosus and other
connective tissue diseases
Adverse drug reaction
DJD, degenerative joint disease.
12.2
Calf Pain
Michael J. Bryan
I. BACKGROUND. Calf pain is a common problem that can result from an array of causes that
range from benign to life threatening.
II. PATHOPHYSIOLOGY. A number of conditions can result in calf pain (see Table 12.2.1).
Musculoskeletal causes account for 40% of calf pain (1). Pain can be referred from the back,
such as an S1–S2 radiculopathy. Deep vein thrombosis (DVT) is one of the most serious causes
Chapter 12 • Musculoskeletal Problems
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