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46. Schroder DM, Lathrop JC, Lloyd LR, Coccaccio JE, Hawasli A. Laparoscopic appendectomy for acute appendicitis: is there really any benet? Am Surg. 1993;59(8):541-547; discussion 547-548. 47. Kollias J, Harries RH, Otto G, Hamilton DW, Cox JS, Gallery RM. Laparoscopic versus open appendectomy for suspected appendicitis: a prospective study. Aust N Z J Surg. 1994;64(12):830-835. 48. Buschard K, Kjaeldfaard A. Investigation and analysis of the position, xation, length, and embryology of the vermiform appendix. Acta Chir Scand. 1973;139(3):293-298. 49. Bjerke K, Brantzaeg P, Rognum TO. Distribution of immunoglobulin producing cells is different in normal human appendix and colon mucosa [abstract]. Gut. 1986;27(6):667. 50. Lin J, Bleiweiss U, Mendelson MH. Cytomegalovirus-associated appendicitis in a patient with the acquired immunodeciency syndrome. Am J Med. 1990;89(3):377-379. 51. Lopez-Navidad A, Domingo P, Cadafalch J. Acute appendicitis complicating infectious mononucleosis: case report and review. Rev Infect Dis. 1990;12(2):297-302. 52. Nadler S, Cappell MS, Bhatt B. Appendiceal infection by Entamoeba histolytica and Strongyloides stercoralis presenting like acute appendicitis. Dig Dis Sci. 1990;35(5):603-608. 53. Hennington MH, Tinsley EJ, Proctor HJ. Acute appendicitis following blunt abdominal trauma: incidence or coincidence? Am Surg. 1991; 214(1):61-63. 54. Houghton A, Aston N. Appendicitis complicating colonoscopy. Gastrointest Endosc. 1988;34(6):489. 55. Barr D, van Heerden JA, Mucha PJ. The diagnostic challenge of postoperative acute appendicitis. World J Surg. 1991;15(4):526-528. 56. Schrock TR. Acute appendicitis. In: Sleisinger MH, Fortran JS, eds. Gastrointestinal Disease: Pathophysiology, Diagnosis, Management. Philadelphia, PA: WB Saunders Co; 1996:1339-1347. 57. Poole GV. Anatomic basis for delayed diagnosis of appendicitis [abstract]. South Med J. 1990;83(7):771-773. 58. Shen GK, Wong R, Daller J, et al. Does the retrocecal position of the vermiform appendix alter the clinical course of acute appendicitis? a prospective analysis [abstract]. Arch Surg. 1991;126(5):569-570. 59. Maxwell JM, Ragland JJ. Appendicitis: improvements in diagnosis and treatment. Am Surg. 1991;57(5):282-285. 60. Silen W. Copes Early Diagnosis of the Acute Abdomen. New York, NY: Oxford University Press Inc; 1987:1-290. 61. De Dombal FT. Diagnosis of Acute Abdominal Pain. New York, NY: Churchill Livingstone Inc; 1991:1-259. 62. Staniland JR, Ditchburn J, De Dombal ET. Clinical presentation of acute abdomen: study of 600 patients. BMJ. 1972;3(5823):393-398. 63. Brewer RJ, Golden OT, Hitch DC, Rudolf LE, Wangensteen SL. Abdominal pain: an analysis of 1000 consecutive cases in a university hospital emergency room. Am J Surg. 1976;131:219-223. 64. Nauta RI, Magnant C. Observation versus operation for abdominal pain in the right lower quadrant: roles of the clinical examination and the leukocyte count. Am J Surg. 1986;151(6):746-748. 65. Liddington MI, Thomson WHF. Rebound tenderness test. Br J Surg. 1991;78(7):795-796. 66. Izbicki JR, Wolfram TK, Dietmar KW, et al. Accurate diagnosis of acute appendicitis: a retrospective and prospective analysis of 686 patients. Eur J Surg. 1992;158(4):227-231. 67. Eskelinen M, Ikonen J, Lipponen P. Acute appendicitis in patients over the age of 65 years: comparison of clinical and computer based decision making. Int J Biomed Comput. 1994;36:239-249. 68. Eskelinen M, Ikonen J, Lipponen P. The value of history-taking, physical examination, and computer assistance in the diagnosis of acute appendicitis in patients more than 50 years old. Scand J Gastroenterol. 1995;30(4):349355. 69. Wilson DH, Wilson PD, Walmsley RG, Horrocks JC, De Dombal FT. Diagnosis of acute abdominal pain in the accident and emergency department. Br J Surg. 1977;64(4):250-254. 70. Nardone DA, Lucas LM, Palac DM. Physical examination: a revered skill under scrutiny. South Med J. 1988;81(6):770-773. 71. Sackett KL, Haynes RB, Guyatt GH, Tugwell P. Clinical Epidemiology: A Basic Science for Clinical Medicine. Boston, MA: Little Brown & Co; 1991:173-186. 72. Simel DL, Samsa GP, Matchar DB. Likelihood ratios with condence: sample size estimation for diagnostic test studies. J Clin Epidemiol. 1991;44(8):763-770.

UPDATED SUMMARY ON LOW BACK PAIN Original Review
Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA. 1992;268(6):760-765.
We initially sought articles including the keywords back pain, herniated disk, or sciatica and specicity using the Clinical Query mechanism in MEDLINE. In addition, we ltered for human, English-language articles, resulting in 190 citations from 1992 to August 2004. We performed an additional search including the various forms and combinations of the terms intervertebral disk displacement, characteristic, feature, nding, marker, predictor, sign, test, variable, physical, exam, and sensitivity. This search added 28 unique citations to our article pool. We also searched bibliographies and personal les for additional articles. Two reviewers independently examined the abstracts of the articles retrieved by
No new ndings substantially changed the results of those originally reported in the Rational Clinical Examination series. 83
Table 7-4 Estimated Accuracy of Ipsilateral Straight-leg Raise Test for Lumbar Disk Herniation Source, Patient Population Jonsson and Stromqvist,4 surgical seriesa (n = 300 patients) van den Hoogen et al,2 surgical series (n = 7 studies) Deville et al,1 surgical series (n = 10 studies) LR+ (95% CI) or Range 2.0 (1.7-2.4) 0.99-1.8 1.1 (1.0-1.1) LR (95% CI) or Range 0.21 (0.12-0.36) 0.04-0.54 0.34 (0.28-0.40)
The reference standard for a herniated disk causing radiculopathy continues to be surgical ndings or the combination of clinical ndings, imaging results, electrophysiology, and clinical course. No major new diagnostic techniques have been introduced. However, as suggested in the synthesis of literature of SLR, the choice of reference standard (imaging vs surgical ndings) may inuence estimates of test performance.
Abbreviations: CI, condence interval; LR+, positive likelihood ratio; LR, negative likelihood ratio. a Patients with herniated disk were compared with patients with lateral or central stenosis.
RESULTS OF LITERATURE REVIEW Univariate Results of Tests for Herniated Lumbar Disk
The methods used in studying low back pain continue to be poor, leading to ambiguous results. As indicated in previous reviews, a clinical diagnosis is generally reached from multiple items of medical history and physical examination, with no single test sensitive and specic enough to make a denitive diagnosis. Since the original Rational Clinical Examination article on back pain, 1 systematic review and a new surgical series have addressed the sensitivity and specicity of the SLR and crossed straight leg raise (CSLR) tests. These studies result in estimates close to those cited in the original Rational Clinical Examination article (Tables 7-4 and 7-5). The review article suggests a somewhat higher sensitivity of the SLR test (close to 0.90 rather than 0.80), whereas the surgical series reported somewhat greater specicity for the CSLR test (0.96 vs 0.90). The sit-to-stand test is the most reliable test ( = 0.85) for detecting quadriceps weakness, and it may discriminate those with an L3 to L4 herniation from those with an L5 to S1 lesion.6 To perform the single-leg sit-to-stand test, the patient attempts to rise from a chair by using only 1 leg. The patient is allowed to place his or her hand in the examiners for aid with balance, and a negative nding/normal result is recorded if the patient is able to rise successfully (LR+, 26 [95% CI, 1.7-413]; LR, 0.35 [95% CI, 0.22-0.56]) (Table 7-6). With regard to reexes, a large study assessed whether absent Achilles reexes occur in seemingly normal older patients (Table 7-7). The absence of an ankle reex becomes increasingly common in individuals older than 60 years, suggesting that this nding is most meaningful at younger ages.

Standard assessment of the Phalen and Tinel signs. The ick sign was obtained by asking the patients how they relieved the discomfort in their hands and wrists when they were experiencing severe symptoms. Patients who demonstrated that they ick their hands (like shaking down a mercury thermometer) were considered positive. The criterion standard was standard electrodiagnostic testing, performed after the clinical evaluation. It is not clear whether the same examiner did the clinical examination and the electrodiagnostic testing. However, the electrodiagnostic testing was based on the quantitative output nerve latency.
CITATION Muscle Nerve. 2001;24(1):107-111. TITLE Lack of Predictive Power of the Tethered Median Stress Test in Suspected Carpal Tunnel Syndrome. AUTHORS Kaul MP, Pagel KJ, Dryden JD. CITATION Arch Phys Med Rehabil. 2000;81(7):348-350. QUESTION Does a physical examination maneuver meant to provoke symptoms predict patients who will have abnormal electrodiagnostic testing? Each study in this summary reports a different maneuver. DESIGN Prospective, consecutive.

Electrodiagnosis of CTS.

SETTING Electrodiagnostic laboratory of a Veterans Affairs medical center, Portland, Oregon. PATIENTS In each study, patients had median nerve symptoms, no previous surgery for carpal tunnel syndrome, and no proximal neuropathy on the affected side.
One hundred forty-two patients were studied, of whom 95 had electrodiagnostic testing of CTS.
Table 10-8 Likelihood Ratios of Provocation Tests for Carpal Tunnel Syndrome Test (n) Pressure provocation (134) Carpal compression (135) Lumbrical (st) provocation (96) Tethered median nerve stretch (112) Abnormal Electrodiagnostic Study Result Sensitivity 0.55 0.52 0.37 0.50 Specicity 0.68 0.56 0.71 0.59 LR+ (95% CI) 1.7 (1.1-2.7) 1.4 (0.94-2.1) 1.3 (0.73-2.3) 1.2 (0.8-1.9) LR (95% CI) 0.66 (0.49-0.90) 0.77 (0.56-1.0) 0.88 (0.66-1.2) 0.85 (0.59-1.2)
Positive test results induce or exacerbate the median nerve symptoms. The lumbrical provocation test is performed by having the patient hold a st for 1 minute. (The lumbricales are the 4 small muscles of the palm of the hand that ex the proximal phalanx and extend the 2 distal phalanges of each nger.) The tethered median nerve test creates a stretch of the median nerve by the examiners passively hyperextending the wrist and distal interphalangeal joint of the index nger. The carpal compression test is performed by applying moderate pressure with both thumbs over the transverse carpal ligament. The pressure provocation test uses a 2.5-cm-wide pressure cuff applied to the patients wrist. The cuff is inated to 50 mm Hg, and then direct pressure is applied to bring the sphygmomanometer reading to 150 mm Hg. The electrodiagnostic studies were performed immediately after the provocation tests. When the provocation test result was positive, the patient was allowed to have the symptoms return to baseline before the electrodiagnostic studies.

Given high random variation, how well does the nding of a single elevated BP predict later denite hypertension? Casual BP, particularly SBP at 1 visit, is predictive of later BP elevation in young men,118 medical students,119 adults,13 and children.120 (Tracking correlations vary widely, eg, r = 0.2-0.7, depending on the population, technique, and follow-up interval.) In a large prospective study,DBP reading of 90 mm Hg or higher predicted a later denite diagnosis of hypertension in 69% of men and 49% of women; any BP elevation warrants careful follow-up. Looked at the other way, however, about one-third to one-half of subjects with initially elevated BP will ultimately prove not to have hypertension. In practice, regression to the mean guarantees that many individuals with initially elevated BP are actually normotensive.75 For example, among subjects with 4 DBP measurements at 2 entry visits averaging between 95 and 104 mm Hg in a mild hypertension trial in Australia,122 28% proved to have an average DBP of less than 90 mm Hg during the next 4 years while receiving placebo. In a careful screening program, similar DBP reductions were observed in the 105 to 114 mm Hg stratum from the rst to second screen, and approximately 10% of subjects with DBP greater than or equal to 115 mm Hg were normotensive (< 90 mm Hg) at the next visit.116 Therefore, using the mean of several visits BP readings improves the ability to predict not only future hypertension120 but also CVD sequelae.13 Because he may be normotensive, the patient in our case scenario should not be told that he is hypertensive at this initial visit,4 but he should be carefully followed up.

Other Ways to Measure BP

If you cannot hear properly, both SBP and DBP can be determined by palpation to within about 10 mm Hg.133 Palpated SBP is about 7 mm Hg lower than the auscultatory value.134
Is a High BP Value Ever Normal?
In normotensive subjects, aerobic exercise, which is generally accepted to be good for health, causes SBP to increase moderately, whereas DBP changes little.123,124 Because increased BP forms part of the ght or ight response, pain (eg, a lacerated nger) and other stresses (eg, pulmonary edema) predictably increase BP, sometimes to extreme values. These reactive elevations of BP do not indicate the presence of hypertension if the BP returns to normal levels at rest.

Pediatrics practitioners often elicit historical points from adult caregivers instead of directly from the patient. When assessing volume status in infants, physicians may ask about number of wet diapers (surrogate for urine output), presence or absence of vomiting and diarrhea, and amount and type of oral intake. Caregivers also frequently report their interpretation of examination signs by clarifying whether the child is active, whether the eyes appear sunken, and whether the child drinks vigorously. Clinicians should ask parents whether they have given a successful trial of clear uids at home, whether the child has been treated by another medical practitioner during the illness, and the date and value of the childs most recent weight measurement.1,13 The ability to elicit some examination signs is impaired when pediatric patients are crying and uncooperative. Therefore, assessment of hydration status should progress from the least to the most invasive maneuvers. The examination should begin with the child across the room in a position of comfort (eg, in the parents lap). Overall appearance, activity, and response of the child to stimulation should be observed. Evaluating the respiratory pattern is important for assessment of dehydration and all other acute illnesses. Respiratory rate should be measured for 60 seconds by observing chest wall movements. The precise measurement requires a quiet and comfortable child. The rate should be compared with age-based norms.14 In a potentially dehydrated child, the examiner should specically look for hyperpnea (deep, rapid breathing without other signs of respiratory distress), suggestive of an acidosis.1 Other vital signs, including temperature, pulse, and blood pressure, should also be evaluated while the child is comfortable.1
Anatomic/Physiologic Origins of Dehydration Signs
Many signs in pediatric assessment are attributed to the uid and electrolyte shifts caused by dehydration. Early work to 330
CHAPTER 25 Next, the clinician should assess skin turgor and capillary rell time. Skin turgor has been used to diagnose dehydration for more than 50 years and, when abnormal, is also called tenting or inelastic skin.15,16 To elicit the sign, the examiner should use the thumb and index nger to pinch a small skin fold on the lateral abdominal wall at the level of the umbilicus.15 The fold should be promptly released, and then the time is measured for the skin folds return to normal form.15 Clear norms for this time have not been published, and most clinicians simply qualify skin turgor as immediate, slightly delayed, or prolonged. Excess subcutaneous fat and hypernatremia may falsely normalize the turgor in dehydrated children, whereas malnutrition may falsely prolong the recoil time.15,17-21 Primary skin disorders complicate the interpretation of skin turgor.19 To assess capillary rell time, the examiner compresses a supercial capillary bed and estimates the time it takes for normal color to return after the pressure is released. Capillary rell time varies as a function of ambient temperature, site of application, lighting, medications, and primary (eg, reex sympathetic dystrophy) or secondary (eg, cardiogenic shock) autonomic changes.16,18,22-24 Extremes in patient temperature may also affect the capillary rell time; for example, capillary rell times are markedly prolonged after cold immersion.25 However, Gorelick et al22 found that fever did not affect the test characteristics in children with vomiting, diarrhea, or poor oral intake. According to the available studies, and to standardize examination techniques, we recommend assessing capillary rell time on a nger with the arm at the level of the heart in a warm ambient temperature. Pressure should be gradually increased on the palmar surface of the distal ngertip and then released immediately after the capillary bed blanches. The time elapsed until restoration of normal color should be estimated. Although many practitioners use other sites to measure capillary rell time, most

The studies presented used varying denitions for fever, ranging from 37.8C to 38.5C (Table 26-1). We dened fever as present or absent according to the individual articles denition. Feverishness was reported by the patient and could have been based on either a temperature taken at home or a subjective sense of having an elevated temperature. The sensitivity, specicity, positive LR, negative LR, and diagnostic OR for clinical variables evaluated in at least 2 of the 5 studies are reported in Tables 26-2 and 26-3. Summary estimates are also presented. Eleven of the 13 clinical factors had heterogeneous diagnostic ORs (all with P <.05). The patients sense of feverishness and vaccination history provided homogeneous results across studies. Despite the heterogeneity, the studies we reviewed seem representative of the universe of patients with inuenza, and most of the differences in estimates created by the statistical heterogeneity were small. The heterogeneity, expressed in the CIs, never moved a nding from useless (LR approaching 1) to obviously useful (LR so different from 1 that it would make inuenza extremely likely or extremely unlikely). Therefore, we present the summary LRs and diagnostic ORs as an efcient way of conveying the relative diagnostic effect of the symptoms and signs.

The Diagnostic OR

The diagnostic OR is a single indicator of diagnostic test performance, reecting its accuracy.27 The diagnostic OR can also be viewed as presenting the odds (likelihood) of the symptom or nding among individuals with disease (ie, the positive LR) compared with the odds of the symptom or nding among those not having the disease (ie, the negative LR). The diagnostic OR should always be assessed in comparison with the paired sensitivity and specicity because the same diagnostic OR can be associated with different pairs. The value of the diagnostic OR ranges from 0 to innity, with higher values indicating better test performance. Values less than 1 indicate more negative test results among individuals with disease. The diagnostic OR can also be used to develop summary estimates in meta-analyses. 346
Table 26-1 Studies of the Diagnostic Performance of Clinical Findings in Diagnosing Inuenza No. of Age Patients Range, y 533 60-90 Grade of Evidencea A Prevalence of Inuenza, % 8
Source, y Nicholson et al,25 1997
Study Period Winters of 1992-1993 and 19931994
Location Leicestershire, England
Design Prospective cohort

Table 36-2 Studies Used to Determine the Accuracy of Clinical Examination for Diagnosing Osteoporosis Source Setting and Country Methodologic Prevalence of Osteoporosis, % Qualitya Inclusion Criteria No. of Patients Mean Age, y Diagnosis Used

Sanila et al23

Outpatients, Finland

Level 3

Dargent-Molina et al47
Volunteers for prospective, multicenter trial, France (EPIDOS)

Level 1

Michaelsson et al44 Outpatients, Sweden Dargent-Molina et al47 Bedogni et al51 Volunteers for prospective, multicenter trial, France (EPIDOS) Community, Italy

Level 1 Level 1

Height Loss Women aged 55-70 y with rheumatoid arthritis, able to walk White women aged 75 y, general population, without past fractures Weight Random sample of women aged 28-74 y, no exclusions White women aged 75 y, general population, without past fractures Women aged 18 y without disease
BMD-diagnosed osteoporosis lumbar BMD < 0.9 on Lunar machine BMD-diagnosed osteoporosis T score < 3.5 SD

175 4638

BMD-diagnosed osteoporosis T score < 2.5 BMD-diagnosed osteoporosis T score < 3.5 SD BMD-diagnosed osteoporosis T score < 2.5
Not reported (range, 49-77)

Ettinger et al28

Outpatients, California

Kantoret al53

Outpatients, Ohio

Di Monaco et al33

Outpatients, Italy
Foley et al34 Dargent-Molina et al47
Outpatients, Ohio Volunteers for prospective, multicenter trial, France (EPIDOS) Outpatients, California
Orme and Belchetz20 Earnshaw et al60

Inagaki et al64

Outpatients in multicenter alendronate trial, United Kingdom, United States, and Denmark Outpatients, Japan
Kyphosis Consecutive sample of women aged 65-91 y Self-reported Humped Back 10 White women aged 18 y referred for bone density scan Grip Strength 34 Consecutive postmenopausal, white female volunteers 18 Older, independent adults in the community 50 White women aged 75 y, general population, without past fractures Hand Skinfold 63 Consecutive women in osteoporosis clinic Tooth Count 33 White postmenopausal women aged 45-59 y 10

CASE 2 This elderly patient has a high pretest probability
96 (90-99) 45 (40-49) 1.7 (1.5-1.9) 0.09 (0.04-0.11) Organon Teknika latex immunoassay(81-96) 45.1 (39-51) 1.6 (1.4-1.8) 0.22 (0.11-0.44) Vidas Rapid ELISA assay46 SimpliRED 84.8 (79-89) 68.4 (65-71) 2.7 (2.4-3.0) 0.22 (0.16-0.3) D-dimer assay43
Abbreviations: CI, condence interval; ELISA, enzyme-linked immunosorbent assay; LR, likelihood ratio.
for pulmonary embolism (approximately 65%) with the simplied Wells rule because of the combination of immobilization, tachycardia, previous deep vein thrombosis/pulmonary embolism, and the absence of an alternate diagnosis as likely as or more likely than pulmonary embolism. This combination of ndings results in a score of 7, which falls into the category of a high pretest probability. In combination with a negative whole-blood red blood cell agglutination D-dimer assay result (LR, 0.22),43 the revised pretest probability is approximately 30%. A ventilation/perfusion scan is reported as intermediate probability (LR, 1.2)48; therefore, his posttest
probability of pulmonary embolism is about 33% and pulmonary embolism has not been ruled out. Further testing with compression ultrasonography and, if the nding is normal, pulmonary angiography should be considered.
PhD, and Marieke J. H. A. Kruip, MD, for providing clarication of data.
1. Anderson FA Jr, Wheeler HB, Goldberg RJ, et al. A population-based perspective of the hospital incidence and case fatality rate of deep vein thrombosis and pulmonary embolism: the Worcester DVT study. Arch Intern Med. 1991;151:933-938. 2. Silverstein MD, Heit JA, Mohr DN, Petterson TM, OFallon WM, Melton LJ III. Trends in the incidence of deep vein thrombosis and pulmonary embolism: a 25-year population based study. Arch Intern Med. 1998;158(6):585593. 3. Barritt DW, Jordan SC. Anticoagulant drugs in the treatment of pulmonary embolism: a controlled trial. Lancet. 1960;1(7138):1309-1312. 4. Goldhaber SZ, Visani L, De Rosa M. Acute pulmonary embolism: clinical outcomes in the International Cooperative Pulmonary Embolism Registry (ICOPER). Lancet. 1999;353(9162):1386-1389. 5. PIOPED Investigators. Value of the ventilation/perfusion scan in acute pulmonary embolism: results of the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED). JAMA. 1990;263(20):2753-2759. 6. Stein PD, Wills PW, DeMets DL. History and physical examination in acute pulmonary embolism in patients without pre-existing cardiac or pulmonary disease. Am J Cardiol. 1981;47:218-223. 7. Hoellerich VL, Wigton RS. Diagnosing pulmonary embolism using clinical ndings. Arch Intern Med. 1986;146(9):1699-1704. 8. Heit JA, Mohr DN, Silverstein MD, Petterson TM, OFallon WM, Melton LJ III. Risk factors for deep vein thrombosis and pulmonary embolism: a population-based case control study. Arch Intern Med. 2000;160(6):809-815. 9. Grady D, Wenger NK, Herrington D, et al. Postmenopausal hormone replacement therapy increases the risk of venous thromboembolic disease: the Heart and Estrogen/Progestin Replacement Study. Ann Intern Med. 2000;132(9):689-696. 10. Douketis JD, Ginsberg JS, Holbrook A, Crowther M, Duku EK, Burrows RF. A reevaluation of the risk for venous thromboembolism with the use of oral contraceptives and hormone replacement therapy. Arch Intern Med. 1997;157(14):1522-1530. 11. Goldhaber SZ. Pulmonary embolism. N Engl J Med. 1998;339(2):93-104. 12. Hampson NB. Pulmonary embolism: difculties in the clinical diagnosis. Semin Respir Infect. 1995;10(3):123-130. 13. Moser KM, Fedullo PF, LitteJohn JK, Crawford R. Frequent asymptomatic pulmonary embolism in patients with deep vein thrombosis. JAMA. 1994;271(3):223-225. 14. Wells PS, Ginsberg JS, Anderson D, et al. Use of a clinical model for safe management of patients with suspected pulmonary embolism. Ann Intern Med. 1998;129(12):997-1005. 15. Wells PS, Hirsh J, Anderson DR, et al. Accuracy of clinical assessment of deep vein thrombosis. Lancet. 1995;345(8961):1326-1333. 16. Anand SS, Wells PS, Hunt DH, Brill-Edwards P, Cook D, Ginsberg JS. The rational clinical examination: does this patient have deep vein thrombosis? JAMA. 1998;279(14):1094-1099. 17. Kearon C, Ginsberg JS, Crowther M, Brill-Edwards P, Weitz JI, Hirsh J. Management of suspected deep vein thrombosis in outpatients by using clinical assessment and D-dimer testing. Ann Intern Med. 2001;135(2): 108-111. 18. Bates SM, Kearon C, Crowther M, et al. A diagnostic strategy involving a quantitative latex D-dimer assay reliably excludes deep venous thrombosis. Ann Intern Med. 2003;138(10):787-794. 19. Becker DM, Philbrick JT, Bachhuber T, Humphries JE. D-dimer testing and acute venous thromboembolism: shortcut to diagnosis? Arch Intern Med. 1996;156(9):939-945. 20. Stein PD, Athanasoulis C, Alavi A, et al. Complications and validity of pulmonary angiography in acute pulmonary embolism. Circulation. 1992;85(2):462-468. 21. Hull RD, Hirsh J, Carter CJ, et al. Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan. Ann Intern Med. 1983;98 (6):891-899. 22. Kruit WHJ, De Boer AC, Sing AK, Van Roon F. The signicance of venography in the management of patients with clinically suspected pulmonary embolism. J Intern Med. 1991;230(4):333-339.

28%, even if percussion and palpation results were negative. On the other hand, when a positive bedside examination result was dened as both percussion and palpation results being positive, the high test specicity of 97% signicantly increased the likelihood of splenic enlargement to 60% or more.
IS SPLENOMEGALY RESULT EVER NORMAL?
About 3% of otherwise healthy students entering a US college were found to have unexplained palpable spleens1 and, on incomplete follow-up, appeared to fare none the worse20; similarly, 12% of otherwise healthy postpartum women at a Canadian hospital had palpable spleens.21
Guidelines for examining for splenic enlargement are summarized in Table 46-3. 1. Splenomegaly is uncommon but occurs in a wide variety of conditions. Given the low sensitivity of the clinical examination, it can be argued that the routine examination for splenomegaly cannot denitively rule in or rule out splenomegaly in normal, asymptomatic patients when the prevalence is less than 10% and additional imaging tests will be required. Rather, the examination for splenomegaly is most useful to rule in the diagnosis of splenomegaly among patients in whom there is a clinical suspicion of at least 10%. 2. The bedside examination of the spleen should start with percussion. If percussion is not dull, there is no need to palpate because the results of palpation will not effectively rule in or rule out splenic enlargement. If the possibility of missing splenic enlargement remains an important clinical concern, then ultrasonography or scintigraphy is indicated. In the presence of percussion dullness, palpation should follow. If both test results are positive, the diagnosis of splenomegaly is established (providing that the clinical suspicion 609
The Rational Clinical Examination sity and Henderson General Hospital, Hamilton, Ontario, Canada (Dr Sackett).
Table 46-3 Guidelines for Examining for Splenic Enlargement Recommendations and Rationale Clinical Suspicion (Prior Probability) of Splenic Enlargement Less than 10% Percussion or palpation for splenomegaly of limited usefulness Maneuvers are not sufficiently sensitive to rule out splenomegaly Given the low pretest probability of splenomegaly, test specificity of clinical examinations is not sufficiently high to rule in splenic enlargement, even if both test results are positive 10% Or more Percussion and palpation can be used to rule in splenomegaly if both results are positive Percuss first, and if result is positive, then palpate If percussion result is negative but your clinical suspicion remains high, order ultrasonography because palpation in the presence of abdominal tympany is not specific enough to rule in splenomegaly If percussion result is positive but palpation result is negative, then ultrasonography is also needed to confidently evaluate spleen size To condently rule out splenomegaly, a radiologic procedure is necessary because of the limited sensitivity of bedside examination

CHAPTER 48 The screen was evaluated prospectively on all noncomatose, nontrauma patients with neurologic complaints compatible with stroke, who were transported by emergency medical technicians to a single hospital. The relevant neurologic signs were altered consciousness, focal neurologic signs, seizure, syncope, head pain, or a cluster category of weakness/dizziness/sick. The criteria for an in-the-eld stroke diagnosis by the emergency medical technician were met when the patients were older than 45 years, had no seizure history, had symptoms for fewer than 24 hours, were not wheelchair bound or bedridden, had a blood glucose level between 60 and 400 mg/dL (3.3 and 22 mmol/L), and a unilateral decit in one of the 3 ndings previously listed. A reviewer, masked to the emergency medical personnels evaluation, determined the nal discharge diagnosis according to the emergency department chart. Compared with the nal diagnosis, the LAPSS had a sensitivity of 91% (95% CI, 76%-98%), specicity of 97% (95% CI, 93%99%), LR+ of 31 (95% CI, 13-75), and LR of 0.09 (95% CI 0.03-0.27) for patients with possible stroke (Table 48-4). An analysis that included all ambulance runs showed even better specicity (and therefore a much higher LR+), with only a slight decrement in sensitivity, attributed to 2 stroke patients who were not correctly identied in the eld as having a possible stroke, of 1092 total ambulance runs (0.19%). Among all patients with neurologically relevant signs, the prevalence of stroke was 10%, which represents a useful anchor for prior probability estimates (Figure 48-1).

Reliability

Table 48-3 Comparison of Physician Assessment With That of Emergency Medicine Personnela,b No. of Findings Present Stroke Nonstroke Diagnosis LR (95% CI)
Physician Assessment c Emergency Medical Personnel d 63 476
14 (1.6-121) 4.2 (1.4-13) 5.2 (2.6-11) 0.39 (0.25-0.61) 7.0 (3.3-14) 7.6 (3.7-16) 4.4 (3.0-6.4) 0.46 (0.38-0.56)
Abbreviations: CI, condence interval; LR, likelihood ratio. a Based on data from Kothari et al.18 b Collapsing data into a table yields an LR of 1 nding = 5.5; 95% CI, 3.3-9.1. c Data represent unique patients and stratum-specic LR. d Data represent 4 examinations for each patient.
Table 48-4 Performance of Emergency Medicine Technicians on Stroke Assessment in the Fielda Stroke Frequency/All Patients LR+ (95% CI) Ambulance runs for patients with target symptoms for possible strokeb All patients transported by ambulance 34/(13-75)
LR (95% CI) 0.09 (0.03-0.27)
The data assessing the CPSS compare emergency medical personnel with physicians for examinations performed in a controlled hospital setting rather than in the eld.18 The intraclass correlation coefcient (Pearson r) for the total score was 0.89 (95% CI, 0.87-0.92) among the prehospital care personnel and 0.92 (95% CI, 0.89-0.93) between the physician and the prehospital personnel. The greatest agreement was for arm drift (Pearson r = 0.91; 95% CI, 0.89-0.93), followed by abnormal speech (Pearson r = 0.87; 95% CI, 0.34-0.90) and facial palsy (Pearson r = 0.78; 95% CI, 0.74-0.83).

UPDATED SUMMARY ON TEMPORAL ARTERITIS Original Review
Smetana GW, Shmerling RH. Does this patient have temporal arteritis? JAMA. 2002;287(1):92-101.
We performed an updated MEDLINE literature search from January 2000 to August 2004, using the same search strategy as in our original publication. After reviewing the titles and abstracts, we identied 48 potential new relevant articles. We included studies with an emphasis on commonly available laboratory tests because the interpretation of the results is always tightly coupled to the clinical evaluation for temporal arteritis. We then applied the inclusion and exclusion criteria of our original review. After a detailed review of each retrieved article, 5 articles met the inclusion criteria. Most excluded studies contained no detailed clinical information about historical or physical examination features or failed to require that at least 90% of patients in the temporal arteritis group have a positive temporal artery biopsy result. An additional 10 articles did
Update ment of patients suspected of having temporal arteritis. We identied 3 such studies7-9 through our literature search. Not surprisingly, using different assumptions, these authors developed differing predictive models. Each study modeled empiric treatment strategies, treatment guided by biopsy results, and treatment of all patients irrespective of biopsy results. The model results changed with differing estimated prior probability of disease. None of these studies, however, estimated the inuence of particular clinical or laboratory features on the likelihood of positive biopsy results. Therefore, these provide a complementary analysis but do not add to the information in our review or update on The Rational Clinical Examination.
Table 49-7 Summary Likelihood Ratios of Symptoms, Signs, and the Erythrocyte Sedimentation Rate for Temporal Arteritis Finding (No. of Studies) Jaw claudication (17) Diplopia (5) Scalp tenderness (8) Any headache (19) Any vision symptoms (19) Abnormal ESRa (7) ESR > 100 (4) ESR 50-100 (5) ESR < 50 (5) LR+ (95% CI) 4.3 (3.0-6.1) 3.5 (1.8-6.8) 1.7 (1.1-2.4) 1.7 (1.5-1.9) 1.1 (0.94-1.3) 1.1 (1.0-1.2) 1.9 (1.1-3.3) 1.1 (0.87-1.5) 0.55 (0.38-0.80) LR (95% CI) 0.72 (0.66-0.79) 0.96 (0.93-0.99) 0.73 (0.66-0.82) 0.67 (0.56-0.80) 0.97 (0.92-1.0) 0.2 (0.08-0.51)
Abbreviations: CI, condence interval; ESR, erythrocyte sedimentation rate; LR+, positive likelihood ratio; LR, negative likelihood ratio. a An abnormal ESR was dened by the laboratory analyses of the individual studies. From these data, a normal ESR has a likelihood ratio of 0.2 for temporal arteritis.
New data allowed us to rene our summary estimates for the LRs of clinical features for temporal arteritis. None of the estimates changed appreciably, although the new data generally led to narrower CIs and, therefore, more condence in the role of each nding.

CHAPTER 51 the lowest possible posttest probability of disease, a woman must still present with at least 1 symptom. If she presents with frequency (LR, 1.8) with no dysuria (LR, 0.5) and no back pain (LR, 0.8) (the only 2 negative symptoms other than vaginal symptoms), a negative dipstick result (LR, 0.3), and no other positive symptoms, her posttest probability of disease is still 18%, which is considerably higher than the prevalence of asymptomatic bacteriuria in the population (5%). Although we do not address the optimum treatment of such patients, we believe that the relatively high probability of UTI (~20%) warrants a urine culture (Figure 51-1), an approach that has been supported by others.10 Clinicians may also want to consider performing a pelvic examination, especially in patients at high risk for sexually transmitted disease or if the urine culture result is negative and symptoms persist. As noted, it is theoretically possible to rule out UTI in women who present with vaginal discharge, in which the lowest possible posttest probability of disease is 6% (if they also have no dysuria, no back pain, a negative dipstick result, and no other positive symptoms). We recommend that clinicians consider obtaining a urine culture in patients with at least 1 urinary symptom and vaginal discharge because the posttest probability of disease will only rarely reach this lowest possible 6%. If the medical history and physical examination are neither strongly positive nor negative, a positive dipstick result still results in a high posttest probability of disease (approximately 80%), and empirical therapy should again be considered without urine culture. In all of the scenarios in the algorithm, urine culture may be indicated, without regard to the posttest probabilities, if the patient has experienced recurrent infection and antibiotic resistance is suspected. Older guidelines for the evaluation of patients with suspected UTI recommend urine culture in all patients, even in those found to have a high probability of UTI after the medical history and physical examination.29,44 More recent reviews and management strategies suggest that a diagnosis of UTI can be established in women who present with typical symptoms and are found to have a positive dipstick or urinalysis result (without obtaining a urine culture).10,45-48 Unlike these treatment recommendations, our proposed algorithm (Figure 51-1) suggests that, in selected patients with mostly positive symptoms, the probability of UTI is so high (~90%) that empirical treatment may be considered without dipstick testing or urinalysis. A similar strategy was recently evaluated in a randomized trial comparing management via telephone with ofce evaluation in 72 women with suspected UTI.49 The investigators found no difference in symptom scores or patient satisfaction with the 2 strategies. Previous studies examining the effect of symptom-based treatment of patients with suspected UTI (after a telephone call or ofce visit to a health care provider) have shown that empirical therapy decreases costs without increasing adverse outcomes.50,51 However, the main purposes of the current algorithm are to dene the posttest probabilities of disease from specic clinical scenarios and to allow clinicians to make informed testing and treatment decisions based on their clinical judgment. Further research is needed to determine clinical

U P D A T E : Vertigo

Prepared by David L. Simel, MD, MHS Reviewed by David A. Froehling, MD, and Richard Bedlack, MD, PhD
A 58-year-old healthy man presents with dizziness. One week ago, he had an upper respiratory illness consisting of a slight fever, cough, and rhinorrhea. During the previous 2 days, he has had 3 episodes of extreme unbalance lasting less than 3 to 4 minutes, when he felt as if he were drunk. During these episodes, he felt nauseated, which caused him to lie down and close his eyes until the symptoms resolved. He has had no hearing loss. Your neurologic examination reveals no focal ndings in the cranial or peripheral nerves.
clinical population, using a patient questionnaire for diagnosing vertigo.
The response to the Dix-Hallpike maneuver serves as a reasonable reference standard for benign positional vertigo because it identies patients who will respond to canalith repositioning maneuvers. Hearing loss, part of the examination of the dizzy patient, has been reviewed in The Rational Clinical Examination series and can be assessed with the whispered voice test.3
Froehling DA, Silverstein MD, Mohr DN, Beatty CW. Does this dizzy patient have a serious form of vertigo? JAMA. 1994;271(5):385-388.
Patients with dizziness may have a variety of disorders so that diagnosing benign positional vertigo requires an understanding of its overall incidence in relation to other etiologies. Peripheral vestibular disorders are the most common causes for dizziness (about 40% of patients with dizziness), of which benign positional vertigo and vestibular neuronitis are the most frequent diagnoses. Retrospective studies tend to nd a higher incidence of benign positional vertigo than those that enroll dizzy patients prospectively. Clinicians (and patients) may be overly concerned with brain tumors when there is a new symptom of vertigo, but the likelihood that a dizzy patient without hearing loss will have a cerebellopontine angle mass responsible for the symptoms is low (probability, 1 104).4 Among patients with dizziness associated with asymmetric hearing loss, a clinician would need to perform 638 scans to detect 1 cerebellopontine angle mass (compared with 9307 scans for dizzy patients without hearing loss). Thus, the approach to clinical diagnosis should more appropriately focus on attempts to rule in less serious causes of vertigo (eg, benign positional vertigo), rather than an initial effort to rule out serious causes such as tumors. We found a systematic review1 that identied 2 retrospective studies suggesting that the clinical history alone allows proper diagnosis of 69% to 76% of dizzy patients. We also found a prospective study in a small group of patients referred to an otolaryngologist where patient history was collected through a questionnaire.5 The questionnaire directs the clinician to the more common causes of vertigo and would have allowed correct 715