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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2867_Библиотеки_им_академика_М_И_Перельмана.pdf
Contents
xiii
Part IX Nephrology
46 Apolipoprotein C-II Amyloidosis Misdiagnosed
as Light Chain Amyloidosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 339
Shashwat Shrivastava
47 Phyllodes Tumor Misdiagnosed as Benign Prostatic Hypertrophy
and a Cyst . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 345
Shashwat Shrivastava
48 Large Calcified Renal Artery Aneurysm Misdiagnosed
as Intrapelvic Calculus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 351
Shashwat Shrivastava
49 Anastomosing Hemangioma Misdiagnosed as Renal Cell Cancer . . . 357
Rupanshu
50 Urethritis Associated Hematuria Misdiagnosed
as C1q Nephropathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 363
Shashwat Shrivastava
51 Primary Mucinous Adenocarcinoma of Renal Pelvis
Misdiagnosed as Calculus Pyonephrosis . . . . . . . . . . . . . . . . . . . . . . . . 369
Maria Mohammed Javed Shaikh
52 Kidney Inflammatory Myofibroblastic Tumor Misdiagnosed
as a Metastatic Malignancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 375
Maria Mohammed Javed Shaikh
Part X Neurology
53 Guillain–Barré Syndrome Misdiagnosed as Posterior Circulation
Stroke . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 383
John Michael Baratta
54 Stroke Misdiagnosed as Benign Positional Paroxysmal Vertigo . . . . . 389
John Michael Baratta
55 Primary Amoebic Meningoencephalitis Misdiagnosed
as Pyogenic Meningitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 395
Sathish Venugopal
56 Cotard Syndrome Misdiagnosed as Major Depressive Disorder . . . . 407
Sathish Venugopal
Part XI Oncology
57 Colonic Cancer Misdiagnosed as Hemorrhoids . . . . . . . . . . . . . . . . . . 419
Junaid Hassan and Safeera Khan
xiv
Contents
58 Malignant Melanoma Misdiagnosed as Diabetic Foot Ulcer . . . . . . . 427
Junaid Hassan and Safeera Khan
59 Multiple Myeloma Misdiagnosed as Rheumatoid Arthritis . . . . . . . . 433
Safeera Khan and Junaid Hassan
Part XII Psychiatry
60 Bipolar Disorder Misdiagnosed as Major Depressive Disorder . . . . . 443
Aemil Palm and Carla Rodriguez
61 Schizoaffective Disorder Bipolar Type Misdiagnosed as Bipolar
I with Psychotic Features . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 451
Jonathan Seok
62 Borderline Personality Disorder Misdiagnosed as Bipolar
Disorder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 459
Aemil Palm and Carla Rodriguez
63 Generalized Anxiety Disorder Misdiagnosed as Nonspecific
Physical Pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 465
Jonathan Seok
Part XIII Pulmonology
64 Chronic Beryllium Disease Misdiagnosed as Sarcoidosis . . . . . . . . . . 473
Abdulla Khan and Jose Luis Ferrero
65 Idiopathic Pulmonary Fibrosis Misdiagnosed
as Sputum-Negative Tuberculosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 479
Abdulla Khan and Jose Luis Ferrero
Part XIV Rheumatology
66 How to Differentiate Chronic Widespread Pain in Order
to Reduce Misdiagnosis of Fibromyalgia . . . . . . . . . . . . . . . . . . . . . . . 491
Kosha Geslaghi and Brandon Krout
67 Rheumatoid Arthritis Misdiagnosed as Gout . . . . . . . . . . . . . . . . . . . . 499
Kosha Geslaghi and Brandon Krout
68 Spondyloarthritis: Gender-Based Symptomatology in Order
to Reduce Misdiagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 505
Kosha Geslaghi and Brandon Krout
Contents
xv
Part XV Legal
69 Legal Consequences of the Misdiagnosed Patient . . . . . . . . . . . . . . . . 515
James M. Ringer
Part XVI An Editor’s Perspective
70 Strategies to Avoid a Misdiagnosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 533
Hassaan Tohid
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 539
Contributors
AkhilAnsary St. Martinus University Faculty of Medicine, Willemstad, Curacao
Fatima Anwer, MD PGY-1, Internal Medicine, Harlem Hospital, New
York, NY, USA
Anthony V. Baratta Jr., MD Gastroenterology Associates of Rochester,
Rochester, NY, USA
John Michael Baratta, MD, MBA Department of Physical Medicine and
Rehabilitation, Medical Director of Stroke Rehabilitation, University of North
Carolina School of Medicine, Chapel Hill, NC, USA
Adedamola Bello, MD St. Martinus University Faculty of Medicine,
Willemstad, Curacao
PushpaBhatt, MBBS, DDV, MPH St. Martinus University Faculty of Medicine,
Willemstad, Curacao
Ivan Cancarevic, MD Icahn School of Medicine at Mount Sinai, New
York, NY, USA
Jose Luis Ferrero, MD St. Martinus University Faculty of Medicine,
Willemstad, Curacao
AllisonFoster, MD Icahn School of Medicine at Mount Sinai, New York, NY, USA
KoshaGeslaghi St. Martinus University Faculty of Medicine, Willemstad, Curacao
Mohammad J. Ghosheh, MBBS Al-Faisal University College of Medicine,
Riyadh, Saudi Arabia
Momina Shahid Hameed, MBBS, MRCGP Partner GP, Strathmore Medical
Practice, Wrexham, Wales
JunaidHassan, MBBS, FCPS M. Islam Medical & Dental College, Gujranwala,
Pakistan
Department of Surgery, M. Islam Medical & Dental College, Gujranwala, Pakistan
xvii
xviii
Contributors
KatarzynaKarpinska-Leydier, MD Internal Medicine, Florida State UniversityCape Coral Hospital, Cape Coral, FL, USA
Sirving Keli, MD, PhD St. Martinus University Faculty of Medicine,
Willemstad, Curacao
AbdullaKhan St. Martinus University Faculty of Medicine, Willemstad, Curacao
Safeera Khan, MBBS California Institute of Behavioral Neurosciences and
Psychology, Faireld, CA, USA
Arseni Khorochkov, MD California Institute of Behavioral Neurosciences and
Psychology, Faireld, CA, USA
Brandon Krout, MD St. Martinus University Faculty of Medicine,
Willemstad, Curacao
Bilal Haider Malik, MBBS, MRCP Dermatology, Betsi Cadwaladr University
Health Board, Mold, Wales
Mohammed Mohammed, MBBS, MD St. Martinus University Faculty of
Medicine, Willemstad, Curacao
Revathi Myneni, MD St. Martinus University Faculty of Medicine,
Willemstad, Curacao
AemilPalm St. Martinus University Faculty of Medicine, Willemstad, Curacao
JamesM.Ringer, Esq. Meister Seelig & Fein LLP, New York, NY, USA
Carla Rodriguez, MD St. Martinus University Faculty of Medicine,
Willemstad, Curacao
Rupanshu St. Martinus University Faculty of Medicine, Willemstad, Curacao
JonathanSeok St. Martinus University Faculty of Medicine, Willemstad, Curacao
Prakrut Nishamanish Sethi St. Martinus University Faculty of Medicine,
Willemstad, Curacao
SrushtiShahi St. Martinus University Faculty of Medicine, Willemstad, Curacao
Maria Mohammed Javed Shaikh, MD St. Martinus University Faculty of
Medicine, Willemstad, Curacao
AkshayK.Shetty St. Martinus University Faculty of Medicine, Willemstad, Curacao
Shashwat Shrivastava, MD St. Martinus University Faculty of Medicine,
Willemstad, Curacao
Shitij Shrivastava, MD PGY-1, Internal Medicine, BronxCare Health System,
Bronx, NY, USA
St. Martinus University Faculty of Medicine, Willemstad, Curacao
Contributors
xix
Danna Soria, MD, MSc St. Martinus University Faculty of Medicine,
Willemstad, Curacao
Hassaan Tohid, MBBS, SUDCC, CCATP California Institute of Behavioral
Neurosciences and Psychology, Faireld, CA, USA
Alluri Vasu, MD, Dip Card St. Martinus University Faculty of Medicine,
Willemstad, Curacao
Sathish Venugopal, MD St. Martinus University Faculty of Medicine,
Willemstad, Curacao
Ravi Vintha, MBBS, MD St. Martinus University Faculty of Medicine,
Willemstad, Curacao
Part I
Allergy and Immunology
Chapter 1
Allergic Bronchopulmonary Aspergillosis
Masquerading asRecurrent Bacterial
Pneumonia
KatarzynaKarpinska-Leydier
Learning Objectives
By the end of this presentation, the clinician will be able to:
1. Assess the overlapping features between allergic bronchopulmonary aspergillo-
sis and the two most common differentials: bacterial pneumonia and pulmonary
tuberculosis.
2. Recall allergic bronchopulmonary aspergillosis as a differential for common
presenting pulmonary symptoms.
3. Choose appropriate testing to best manage patients presenting with respiratory
complaints regardless of geographic region.
4. Minimize the time needed for accurate diagnosis and treatment of allergic bron-
chopulmonary aspergillosis.
5. Apply the knowledge gained from this and similar cases where appropriate in
future clinical settings.
Introduction
The clinical presentation of allergic bronchopulmonary aspergillosis (ABPA) is
indistinguishable from other infectious pulmonary conditions [1]. Aspergillus
fumigatus through airborne conidia is the most common pathogen, although colonization is dependent on the host’s immune system competence [2]. Similarly, there is
a distinction between colonization, the benign isolation of Aspergillus from the
lower respiratory tract, and disease as per clinical judgment [3]. Interactions between
the host and fungus are unfavorable in conditions where patients are
K. Karpinska-Leydier (*)
Internal Medicine, Florida State University - Cape Coral Hospital,
Cape Coral, FL, USA
© 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_1
3
4
K. Kar pinska-Leydier
immunocompromised, critically ill, on steroids, or with underlying lung conditions
[3]. Furthermore, ABPA is relatively uncommon compared with bacterial pneumonia and pulmonary tuberculosis (TB), depending on the geographic region [4].
Cystic bronchiectasis and mucus plugs are frequently overlapping features
between ABPA and cavitating pulmonary TB, which are seen on chest computed
tomography (CT.) [4, 5] Asthma and cystic brosis (CF) patients are predisposed to
ABPA if Aspergillus exposure occurs and results in hypersensitivity to Aspergillus
antigens, involving eosinophilic inltration of the bronchial wall, mucoid impaction, or granulomatous inammation [4, 6]. Patients with asthma and ABPA often
have hemoptysis, fever, malaise, and eosinophilia, which mimic TB; it is common
for misdiagnosed ABPA patients to receive anti-TB therapy even with smearnegative testing [4, 6, 7]. Productive cough and a suggestive chest X-ray (CXR) are
common manifestations of bacterial pneumonia and may show temporary clinical
improvement with antibiotic therapy; however, suspicion for ABPA and evaluation
for eosinophilia are needed to avoid potential misdiagnosis [1].
Patients with an extensive history of asthma complicated by misdiagnosis and
poor respiratory function are more likely to exhibit acute exacerbations [8].
However, treatment with glucocorticoids and antifungal agents may prolong eventfree periods [8]. Contributing factors to the misdiagnosis of ABPA include atypical
presentations, interference of tumor markers in diagnostic testing, misunderstandings of screening indicators, and signicant overlap with other pulmonary pathologies [9]. The high misdiagnosis rate of ABPA and lack of standardized treatment
contribute to diagnostic delays and suboptimal prognosis [10].
Clinical Case Presentation
A man aged 74years sought medical attention for a cough and was found to have a
chest X-ray (CXR) showing right perihilar airspace opacities 4 months ago. His past
medical history includes hypertension, allergic rhinitis, and diabetes mellitus. He is
a nonsmoker and denies alcohol. He was treated for bacterial pneumonia, improving
his cough and CXR by day 30 and almost normal by 3 months. Successively, he was
admitted due to a 10-day history of productive cough with viscous, white-cloudy
sputum. His initial presentation in the emergency department was with dyspnea and
fatigue. Physical exam was signicant for tachycardia, respiratory rate of 28/min,
temperature of 37 °C, and peripheral capillary oxygen saturation (Sp2) of 88%
breathing room air. A pulmonary exam revealed scattered rhonchi and the use of
accessory respiratory muscles. On workup, eosinophilia was 3400/mm3, and blood
glucose was 336 mg/ml. Bilateral perihilar airspace opacities were present on
admission. Serologic tests and direct fecal smear ruled out parasitic infections on
day +1. Acid-fast bacilli (AFB) testing was negative in three consecutive sputum
samples; however, Klebsiella pneumoniae (2.106cfu/ml) was positive on hospital
day +3. He started antibiotic therapy for the presumed diagnosis of bacterial pneumonia. Evaluation of the total serum IgE level revealed 5110 IU/m, and serum
1 Allergic Bronchopulmonary Aspergillosis Masquerading as Recurrent Bacterial…
5
level- specic IgG to Aspergillus was 1000U/ml. Skin prick testing with a standard
Aspergillus mix was negative despite the elevated serum IgE specic to Aspergillus
spp. (38LU). On hospital day +6, high-resolution contrast-enhanced chest computed tomography (CT) showed scattered nodules and halo signs without bronchiectasis. However, mucus plugs occluding the central bronchi contained inltrated
eosinophils on bronchoscopy. 30% of the cell count was eosinophil on bronchoalveolar lavage (BAL). AFB testing of BAL uid was negative, but it was positive for
Aspergillus sp.; therefore, serologic allergic bronchopulmonary aspergillosis
(ABPA-S) was conrmed.
Further spirometry showed respiratory function compatible with asthma. The
patient was managed with inhaled corticosteroids (ICS) using a combination of salmeterol/uticasone 25/250 with a dose of uticasone of 1000 micrograms daily.
Within 1 month, the eosinophil count was 206/mm3, and his CXR showed the disappearance of air space opacities, achieving remission at 1 year.
Differential Diagnosis
1. Allergic Bronchopulmonary Aspergillosis – ABPA is a syndrome caused by a
type 1 hypersensitivity to Aspergillus species. Features include asthma, eosino-
philia, bronchiectasis, and recurrent bronchopulmonary inltrates. Patients with
an atopic history or lung disease are at increased risk, particularly those aficted
with asthma, hyper-IgE syndrome, or cystic brosis. Patients may present with
chronic asthma, productive cough, hemoptysis, or fatigue. Chest CT is necessary
to assess for central bronchiectasis or mucoid impaction. Skin prick testing is
helpful for diagnosis of ABPA; however, it may be negative in serologic ABPA,
and further lab testing for total and specic IGE and eosinophil count is necessary.
2. Bacterial Pneumonia– Bacterial pneumonia is a pulmonary parenchymal infec-
tion of the lower respiratory tract. Patients at risk may have an underlying lung
disease such as COPD or other compromising conditions, including smoking,
alcohol consumption, aspiration, or diabetes. The most common implicated bacterial organism is Streptococcus pneumoniae. Presenting symptoms may include
fatigue, dyspnea, pleuritic chest pain, and cough, which may be either productive or nonproductive. Diagnosis is supported by imaging or sputum culture.
Empiric antibiotics are rst-line therapy.
3. Pulmonary Tuberculosis– Mycobacterium tuberculosis is the agent responsible
for pulmonary tuberculosis. Patients at risk are in close contact with Tb patients
or patients with immunosuppression. Presenting symptoms are productive or
nonproductive cough, hemoptysis, fever, anorexia, night sweats, and weight
loss. Chest imaging is useful in identifying lobar consolidation, but cavitary
lesions or hilar adenopathy may also be seen. Sputum is positive for acid-fast
bacilli. Treatment is with a regimen of rifampin, isoniazid, and ethambutol.
4. Bronchial Asthma– Bronchial asthma is characterized by inammation causing
a reversible and intermittent obstructive respiratory disease of the small airways.