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- •Preface
- •Contents
- •Contributors
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Diagnostic Approach Toward Fixed Drug Eruptions
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Hypereosinophilic Syndrome Treatment Options
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Differential Diagnosis
- •Clinical Case Presentation
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Discussion
- •Differential Diagnosis
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Alternative Diagnosis/Potential Misdiagnosis
- •Note
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Alternative Diagnosis/Potential Misdiagnosis
- •Note
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Alternative Diagnosis Considered/Potential Misdiagnosis
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Alternative Diagnoses
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Alternative Diagnoses
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Plan of Action, the Points Clinician Should Consider, Pitfalls to Avoid, and Pearls of Knowledge to Consider
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnoses
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Plan of Action, the Points Clinician Should Consider, Pitfalls to Avoid, and Pearls of Knowledge to Consider
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Case 1
- •Case 2
- •Differential Diagnosis
- •Discussion
- •Plan of Action, the Points Clinician Should Consider, Pitfalls to Avoid, and Pearls of Knowledge to Consider
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Plan of Action, the Points Clinician Should Consider, Pitfalls to Avoid, and Pearls of Knowledge to Consider
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Plan of Action, the Points Clinician Should Consider, Pitfalls to Avoid, and Pearls of Knowledge to Consider
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •The Plan of Action, Points to Consider, Pitfalls to Avoid, and Pearls of Knowledge
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Clinical Case Presentation
- •Differential Diagnosis
- •Discussion
- •Conclusion
- •References
- •Introduction
- •The Lawyers Are Watching
- •Misdiagnosis Versus Missed Diagnosis
- •Prostate Cancer Misdiagnosis
- •Breast Cancer Misdiagnosis
- •Exemplar Cases
- •Cardiac Misdiagnosis
- •COVID Misdiagnosis
- •References
- •Introduction
- •Conclusion
- •References

66 How to Differentiate Chronic Widespread Pain in Order to Reduce Misdiagnosis…
495
must be explored to ensure that the medication’s adverse effect is not the cause of
the pain complaint. Medications that should be considered include lipid-lowering
agents in statins, aromatase inhibitors, bisphosphonates, and paradoxically even
opioids. Therefore a history of current medication use is obligatory. Physical examination: A physical examination is required specically to examine for evidence of
structural joint abnormality, muscle weakness, neurological abnormality, or evidence of endocrine disease. The physical examination should be within normal
limits for the patient’s age. Clues that may point to a diagnosis of FM are soft tissue
and generalized body tenderness. Although the tender point examination was used
in the past to establish a diagnosis of FM, this nding is no longer incorporated into
the physical examination because of poor validity and poor reproducibility. Some
patients may demonstrate dysesthesia on light touch, myofascial induration, or
joint hypermobility. Additional testing: No conrmatory blood tests, imaging, or
histological analysis is available for FM.A limited number of laboratory tests will
allow for screening for medical conditions that can mimic FM symptoms. The
2016 criteria require a widespread pain index (WPI) of between four (2011 required
three) and six pain sites and symptom severity (SS) score of ≥9. In addition, generalized pain, as dened by pain occurring in at least four of ve body regions
except for the face and the abdomen, should be present [19]. The Fibromyalgia
Survey Questionnaire (also called polysymptomatic distress scale, PSD) capturing
the 2011 (21) and 2016 (21) diagnostic criteria of FM can be completed by the
patient to further complement the clinical assessment and can be used to give some
indication of the severity of the condition. In most cases, a denite diagnosis can
be effectively established based on the history, a physical examination that demonstrates general tenderness, the absence of some other pathology that could explain
pain and fatigue, and normal basic laboratory tests. The standards of good medical
practice state that the physician must always consider a differential diagnosis for
any patient presenting with a diffuse pain complaint. This has been covered in the
section on misdiagnosis of FM. FM may coexist with other pain syndromes.
Patients diagnosed with FM may also experience other painful conditions that are
mostly distinct from FM and are generally classied as overlapping pain conditions. Notably, the 2011 [20] and 2016 [20] criteria include headache and abdomi-
nal pain in the somatic symptom score, increasing the probability that patients with
migraine or tension headaches or irritable bowel syndrome will meet FM criteria.
Even when the ACR 1990 classication criteria [21] are used for diagnosis, many
patients with FM meet the criteria of some other function. Recent studies have
demonstrated that treatment of visceral pain comorbidities (endometriosis, IBS,
primary dysmenorrhea) reduced FM pain [14–16]. Therefore, FM patients should
be screened for other pain syndromes, and a questionnaire that captures somatic
symptom burden, such as the Patient Health Questionnaire (PHQ) [15, 18–20]. The
coexistence of FM with some other medical condition that could act as a pain generator may inuence the outcome of the other condition in particular and the global
health outcome in general. There are two considerations when FM coexists with
some other condition: rstly, the underlying condition should be treated according
to best practice, e.g., for osteoarthritis or mechanical back pain; secondly, there

496
K. Geslaghi and B. Krout
must be an appreciation that concomitant FM may affect the outcome of the underlying condition. This has been shown for a surgical outcome that is less favorable
for patients with osteoarthritis of the knee and comorbid FM [20]. FM may coexist
with mental health disorders. Depression is another FM symptom identied in the
somatic symptom scale of the Fibromyalgia Symptom Questionnaire. Depending
on the clinical setting, up to 80% of FM patients meet the criteria of depressive and
anxiety disorder. FM’s severity (number and intensity of symptoms and degree of
disability) is substantially determined by comorbid mental disorders [5]. A screening of FM patients for psychological distress either by questions such as “Over the
last 2 weeks, how often have you been feeling down, depressed, or hopeless” and
“Feeling nervous, anxious or on edge” or questionnaires (e.g., PHQ 4) [21] is recommended by some FM guidelines. Severe comorbid mental disorders require the
inclusion of a mental health specialist in the management of FM [19]. The severity
of FM as a chronic disorder for patients with the full expression of FM are at the
end of a continuum of multiple pain sites and other somatic and psychological
symptoms [20]. As for other diseases dened by continuous variables, such as
hypertension, diabetes, or depression, there is currently no absolute point dening
where FM begins. Cutoff points for diagnosing continuum disorders are dened by
expert consensus and based on clinical studies. The higher the cutoff point for a
diagnosis, the lower the prevalence. The 2016 diagnostic criteria for FM [21]
increased the requirements needed to meet the widespread pain criterion compared
to the 2011 diagnostic criteria [21]. Thus, potential FM cases in the general German
population decreased from 2.1% [21] to 1.9% (Wolfe 2018, submitted). In addition, longitudinal studies of patients with CWP and/or bromyalgia have demonstrated that some patients report uctuation in symptoms over time and thus
oscillate around the cutoff points, at times being FM positive or FM negative [19–
21]. FM’s waxing and waning nature might explain some discrepancies between
the prevalence of criteria identied FM and clinical FM.There is no internationally
accepted grading of the severity of FM, but clinical wisdom requires the treating
physician to assess severity to direct treatment options [4]. Most gradings suggest
a distinction between mild, moderate, and severe forms of FM based on the intensity of symptoms and the degree of limitation in daily functioning. It, therefore,
follows that a stepwise management approach can be based on the severity of
FM. Mild forms require primarily education and advice (regular physical and
social activities) with perhaps the occasional use of drug therapy for episodes of
exacerbation and can be managed in primary care. More severe forms require multicomponent (exercise, psychological therapies, drugs) and multidisciplinary therapies [12, 18]. Therefore, for the follow-up of patients diagnosed with FM, a
“continuum” assessment, e.g., by questions about general well-being (e.g., on a
0–10 scale or a Likert scale of “the same,” “better,” or “worse”) or by symptom
questionnaires such as the PSD [20] or the PHQ 15 [21], might be more appropriate
[19] than the determination of whether a patient meets FMS criteria or not at a
particular time point [21].

66 How to Differentiate Chronic Widespread Pain in Order to Reduce Misdiagnosis…
497
Plan ofAction, Pitfalls toAvoid, andPearls ofKnowledge
toConsider
1. Know all the clinical manifestations of FM.
2. Incorporate a multisystemic approach when diagnosing FM.
3. Create a plan of action when doing an examination of a new patient.
4. Avoid coming into the examination with an idea of diagnosis.
5. Review current up-to-date criteria for diagnosing FM.
6. Have the patient ll appropriate questionnaires when there is CWP.
7. Consider mental distress as a possible indicator of FM not just CWP.
Conclusion
Fibromyalgia syndrome (FM) is an enigma. Even with the gradual acceptance of the
validity of FM, it has continued to be misdiagnosed by clinicians. Evidence-based
interdisciplinary guidelines have presented a comprehensive clinical assessment to
avoid misdiagnosis. A patient with chronic pain should be screened for CWP.Those
with CWP should be examined for presence of additional major symptoms of FM:
unrefreshed sleep and fatigue. A complete medical history and complete physical
examination are mandatory in the evaluation of a patient with CWP in order to conclude the diagnosis of FM.Mild and limited simple laboratory testing is recommended to screen for possible other diseases. When taking into consideration of the
differential diagnosis of FM, special attention should be paid to the presence of
other chronic pain that is overlapping conditions and of mental disorders. FM on its
own as a diagnosis is rare, as almost all patients with FM meet criteria for other
overlapping pain conditions or mental disorders. The intensity of FM should be
assessed in order to direct treatment approaches and help inform the likely outcome
for an individual patient.
References
1. Häuser W, Fitzcharles MA. Facts and myths pertaining to bromyalgia. Dialogues Clin
Neurosci. 2018;20:53–62.
2. Talotta R, Bazzichi L, DI Franco M etal. One year in review 2017: bromyalgia. Clin Exp Rh.
3. Wolfe F.Fibromyalgia wars. J Rheumatol. 2009;36:671–8.
4. Wolfe F.Criteria for bromyalgia? What is bromyalgia? Limitations to current concepts of
bromyalgia and bromyalgia criteria. Clin Exp Rheumatol. 2017;35(Suppl 105):S3–5.
5. Agarwal A, Oparin Y, Glick L, et al. Attitudes toward and management of bromyalgia: a
National Survey of Canadian rheumatologists and critical appraisal of guidelines. J Clin
Rheumatol. 2018;24:243–9.

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6. Häuser W, Ablin J, Fitzcharles MA, etal. Fibromyalgia. Nat Rev Dis Primers. 2015;1:15022.
7. Shir Y, Fitzcharles MA. Should rheumatologists retain ownership of bromyalgia? J
Rheumatol. 2009;36:667–70.
8. Perrot S, Choy E, Petersel D, Ginovker A, Kramer E.Survey of physician experiences and
perceptions about the diagnosis and treatment of bromyalgia. BMC Health Serv Res.
2012;12:356.
9. Briones-Vozmediano E, Vives-Cases C, Ronda-Pérez E, Gil-González D.Patients’ and professionals’ views on managing bromyalgia. Pain Res Manag. 2013;18:10–24
10. Choy E, Perrot S, Leon T, etal. A patient survey of the impact of bromyalgia and the journey
to diagnosis. BMC Health Serv Res. 2010;10:102.
11. Häuser W, Zimmer C, Felde E, Köllner V.What are the key symptoms of bromyalgia? Results
of a survey of the German Fibromyalgia Association. Schmerz. 2008;22:176–83.
12. Petzke F, Brückle W, Eidmann U, et al. General treatment principles, coordination of care
and patient education in bromyalgia syndrome: Updated guidelines 2017 and overview of
systematic review articles. Schmerz. 2017;31:246–54.
13. Fitzcharles MA, Esdaile JM. The overdiagnosis of bromyalgia syndrome. Am J Med.
1997;103:44–50.
14. Fitzcharles MA.BOULOS P: inaccuracy in the diagnosis of bromyalgia syndrome: analysis
of referrals. Rheumatology (Oxford). 2003;42:263–7.
15. di Franco M, Iannuccelli C, Bazzichi L et al. Misdiagnosis in bromyalgia: a multicentre
study. Clin Ex.
16. Walitt B, Katz RS, Bergman MJ, Wolfe F.Three-quarters of persons in the US population
reporting a clinical diagnosis of bromyalgia do not satisfy bromyalgia criteria: the 2012
National Health Interview Survey. PLoS One. 2016;11:e0157235.
17. Album D, Johannessen LEF, Rasmussen EB.Stability and change in disease prestige: a comparative analysis of three surveys spanning a quarter of a century. Soc Sci Med. 2017;180:45–51.
18. Fitzcharles MA, Ste-Marie PA, Goldenberg DL, etal. Canadian Pain Society and Canadian
rheumatology association recommendations for rational care of persons with bromyalgia: a
summary report. J Rheumatol. 2013;40:1388–93.
19. MacFarlane GJ, Kronisch C, Atzeni F, et al. EULAR recommendations for management of
bromyalgia. Ann Rheum Dis. 2017;76:e54.
20. Nakamura I, Nishioka K, Usui C, etal. An epidemiologic internet survey of bromyalgia and
chronic pain in Japan. Arthritis Care Res (Hoboken). 2014;66:1093–101.
21. Marschall U, Arnold B, Häuser W.Treatment and healthcare costs of bromyalgia syndrome
in Germany: analysis of the data of the Barmer health insurance (BEK) from 2008-2009.
Schmerz. 2011;25(402–4):406–10.
K. Geslaghi and B. Krout

Chapter 67
Rheumatoid Arthritis Misdiagnosed
asGout
KoshaGeslaghi andBrandonKrout
Learning Objectives
By the end of this presentation, the clinician should be able to:
1. Correctly differentiate between gout and rheumatoid arthritis.
2. Discuss how to correctly identify radiographic images of gout in patients.
3. Explain the symptomatology of gout and rheumatoid arthritis.
4. Summarize the effects of diuretics in patients who may be presenting with the
same clinical manifestations of gout.
Introduction
Rheumatoid arthritis (RA) is a chronic inammatory disease with an etiology that is
not well understood. RA is characterized by symmetric polyarthritis, the most common form being chronic and inammatory [1, 2, 4, 6–8]. Since active RA often ends
in articular cartilage and bone destruction and functional disability, it is crucial to
diagnose and treat this disease early before damage ensues [1, 2, 4, 9]. As RA is a
systemic disease, if left untreated, it may also lead to a variety of articular symptoms
and subcutaneous nodules, including fatigue, lung involvement, peripheral neuropathy, pericarditis, vasculitis, and hematologic abnormalities [1, 2, 4, 5].
A different, metabolic disease that is often a cause for misdiagnosis in RA
patients is gout. The most prevalent demographic for patients with gout and RA
overlap which can lead to misdiagnosis, i.e., a middle-aged to elderly males or
K. Geslaghi (*) · B. Krout
St. Martinus University Faculty of Medicine, Willemstad, Curacao
e-mail: kosha.geslaghi@martinus.edu; brandon.krout@martinus.edu
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
H. Tohid et al. (eds.), The Misdiagnosis Casebook in Clinical Medicine,
https://doi.org/10.1007/978-3-031-28296-6_67
499

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K. Geslaghi and B. Krout
postmenopausal females. Gout is a metabolic disease with a main demographic of
middle- aged to elderly men and postmenopausal women. Gout results from an
increase of urate with hyperuricemia [1, 2, 4]. It is identied by episodic acute
arthritis or chronic arthritis caused by deposition of monosodium urate crystals in
joints and connective tissue tophi [2, 4]. There is the risk for deposition of monosodium urate crystals in kidney interstitium or uric acid nephrolithiasis [1, 2, 4].
In recent years, the atypical presentation of gout in the elderly has started to be
acknowledged in greater frequency [1, 2]. Gout observed in older patients is often a
subacute, symmetric polyarthritis missing in classic podagra [1–4]. Early development of tophi in a patient with symmetric gouty arthritis can lead to the misdiagnosis
of rheumatoid arthritis with rheumatoid nodules; this results in inappropriate management of a condition that is generally treated with very positive results [1, 2]. The
crystals found in gout are that of a buildup of uric acid which crystallizes in the synovial uid; however, RA being an autoimmune disorder, there is a buildup of granulated tissue in the synovial spaces. The following case will demonstrate these points
as well as the challenging clinical problems frequently encapsulating the effective
diagnosis and treatment of gout in the most common demographic: that of the elderly.
Clinical Case Presentation
A 74-year-old elderly woman arrived into the emergency room after 10days of
weakness, diarrhea, and anorexia. She described 4years of arthritis, occurring rst
in her ankles and later progressing to knees and hands, with the development of
deformities and soft tissue nodules [1, 2]. There were no signs of morning stiffness
and acute attacks of arthritis. The patient’s past medical history was signicant for
hypertension, two myocardial infarctions, and renal insufciency [10–13]. A diagnosis of rheumatoid arthritis had been made [1, 2]. Treatment with nonsteroidal
anti-inammatory agents (NSAIDS) was initiated. Two weeks prior to admission,
she noted increasing pain in all joints, swelling of hands and knees, and resultant
inability to ambulate [1, 2]. Her medications included prazosin, diltiazem, furosemide, indomethacin, and acetaminophen with codeine. System review revealed no
cough, chest pain, or fever. She did note recent weight gain.
On examination the patient was fully oriented, with BP 200/100mm Hg, pulse
104, respirations 28, and temperature 102F.Soft tissue nodules were present on the
ngers and were prominent around the proximal and distal interphalangeal joints.
Cardiopulmonary exam showed a diffuse ventricular impulse and lowered breath
sounds with left basilar egophony [1, 2]. No evident nodules were present on the
olecranon or pinnae. Joint exam revealed warm knees with a 3+ effusion on the right
limiting exion and a 1+ effusion on the left with crepitance [1, 2]. Destruction of the
metacarpophalangeal joint and proximal interphalangeal joints had caused a right
hand exion contracture and an asymmetric left hand deformity with ulnar deviation
(Fig. 67.1). Bilateral hallux valgus deformities of the rst metacarpophalangeal
joints were present. Laboratory exam revealed Hgb 8.5g/dL, WBC 11,500/mm3,

67 Rheumatoid Arthritis Misdiagnosed asGout
Fig. 67.1 Hands of a 74-year-old woman in full extension, asymmetric deformities of proximal
interphalangeal and metacarpophalangeal joints, ulnar deviation, and exion contractures on
the right
501
Fig. 67.2 Radiographs of patient’s left hand in Fig.67.1: preserved joint space in noninvolved
joints and characteristic para-articular gout erosion with overhanging margin in the middle proximal interphalangeal
BUN 58mg/dL, creatinine 3.0mg/dL, uric acid 9.4mg/dL, rheumatoid factor 1: l O
by latex xation, normal cardiac isoenzymes, age-indeterminate infarction by ECG,
cardiomegaly with cephalization of blood ow, and a predominant left lower lobe
inltrate on chest X-ray [1, 2]. Echocardiogram revealed a hypokinetic left ventricle
with ejection fraction of 13%. On knee radiographs, changes of the patellofemoral
compartment and a right knee effusion were present, without overt chondrocalcinosis or erosions. On left hand lm, a soft tissue deformity and eccentric cortical erosion with overhanging margins of the involved proximal interphalangeal joint were
present (Fig.67.2) [1, 2]. Arthrocentesis of the right knee yielded copious opalescent
uid with a thick slurry of visible white particles [1, 2]. Polarizing microscopy

502
revealed a mass of needle-shaped crystals with both negative and positive birefringence. Intracellular crystals were present. When diluted 10× the synovial uid
revealed concentrations of uric acid 13.1mg/dL, calcium 1.2 mg/dL, and glucose
10mg/dL, conrming the predominant presence of monosodium urate crystals. The
patient was treated on admission for congestive failure, hypertension, azotemia, and
suspected pneumonia using erythromycin, prazosin, diltiazem, and azotemia; oral
colchicine was begun without loading.
The diagnosis of gout rests on the identication of negatively birefringent intracellular crystals from synovial uid or tophi [1, 2]. Supporting evidence, as in this
case, may also include asymmetric joint involvement, soft tissue tophi, and periarticular osteolysis or classical marginal erosions outside the joint capsule.
K. Geslaghi and B. Krout
Differential Diagnosis
1. Septic Arthritis—A joint infection that causes severe pain, swelling, erythema,
warmth, and loss of function of the affected joint. Also frequently causes systemic signs such as fever. This condition is marked by its trademark fever prior
to the onset of arthritis.
2. Osteoarthritis—A condition characterized by degeneration of the articular carti-
lage and the underlying bone as a result of chronic wear and tear. Usually occurs
in the elderly but can be accelerated in patients with an underlying joint pathology and increased or abnormal biomechanical forces on the joint, including
elevated body mass index. While this condition appears to be the same as RA,
the risk factors of obesity differ from that of RA.
3. Psoriatic Arthritis—A seronegative inammatory arthritis found in patients with
psoriasis. In 60–80% of patients, psoriasis precedes the arthritis; in 15–20% of
patients, arthritis appears before psoriasis. Other common symptoms include
enthesitis particularly where the Achilles tendon attaches to the calcaneus, dactylitis, and nail changes.
4. Pseudogout—The acute form of calcium pyrophosphate crystal deposition dis-
ease. Manifests similarly to an acute gout are, with sporadic episodes of monoarticular synovitis affecting large joints. Unlike gout, it can last for months and
may be associated with systemic symptoms.
What WasMisdiagnosed inThis Case andWhy?
Diuretic gout was misdiagnosed as RA.The reason for this misdiagnosis was the
diagnosing physician did not consider the effects of diuretics in patients with hypertension; the side effects of the aforementioned diuretic lead to accumulation of uid
in the proximal interphalangeal joints leading medical professionals to believe that
it was RA caused by an autoimmune etiology.

67 Rheumatoid Arthritis Misdiagnosed asGout
503
Discussion
RA is known as a chronic inammatory disease and its etiology is unknown. RA is
characterized by polyarthritis and is the most prevalent form of inammatory arthritis. Gout, however, causes arthritis-like pain but it is not an inammatory disease.
Gout occurs in response to the presence of monosodium urate (MSU) crystals in
the joints.
The prole of the elderly gout patient has been classied as a thin 75-year-old
woman with Heberden’s nodes who is a teetotaler and uses diuretics [12, 13].
Accompanying this new prole for gout is the clinical history of a polyarticular
arthritis involving both the upper and lower extremities, with subacute or no acute
attacks [10, 11]. Gout in the elderly is strongly associated with diuretic use; the
association reaches levels of 85%, 95%, and 100% in reports on gout in elderly
women. All women were on diuretics and presented after the fth decade with subacute attacks and often exuberant tophi, warranting the new label of diuretic-induced
gout. A study emphasized renal insufciency in 90% of all elderly gout patients,
underscoring decrease in urate excretion as the cause of their gout [12]. Polyarticular
gout in the setting of mild renal insufciency and diuretic use may be the predominant form of gout in women. Early tophi are a unique characteristic of diuretic gout,
often occurring within the rst or second year of disease [1, 2, 13]. Urate deposition
in the elderly shows a predilection for the sites of osteoarthritis in hand interphalangeal (IP) joints known as Heberden’s and Bouchard’s nodes. Several authors have
demonstrated by crystal analysis that attacks of previously classied “inammatory
osteoarthritis,” with clinical inammation and erosive changes, are actually episodes of gouty arthritis in osteoarthritic IP joints. Development of tophi at osteoarthritic IP joints or in the soft tissue of the distal ngerpad may predate all attacks of
gouty arthritis. It is therefore critical for the diagnosing physician to consider the
side effects of medication on the patient population as the source for the current
pathophysiology. This knowledge, combined with a focused physical exam, imaging, and synovial uid analysis, is needed for a comprehensive medical workup of
the presenting patient.
Plan ofAction, thePoints Clinician Should Consider, Pitfalls
toAvoid, andPearls ofKnowledge toConsider
1. Create a framework when meeting new or referred patients.
2. Know all possible side effects of medication of patients, especially long-term
medications.
3. Always refer to radiographic images before making diagnosis as well as clinical
manifestations.
4. Running tests to conrm diagnosis may be invasive, but it would save the
patient’s time and energy in early diagnosis.

504
K. Geslaghi and B. Krout
Conclusion
Rheumatoid arthritis is a very common diagnosis in the elderly patient population.
As such, there are chances for error in assuming that a presenting patient who is
elderly with symmetric polyarticular joint pain and nodules is suffering from rheumatoid or systemic arthritis. There must be a consideration of medication side
effects, especially diuretics, for the proper patient workup. Diuretics can potentially
lead to an increase of monosodium urate crystals in the kidneys and joint spaces,
with resulting tophi formation and pain. A complete workup should include a
detailed history, including medication review, physical examination, imaging, and
serum studies. By using the various modalities offered to modern physicians, the
misdiagnosis of gout can be signicantly limited.
References
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