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- •Preface
- •Contents
- •Introduction
- •Prevention
- •Harm Reduction
- •Decision-Making/Differential Diagnosis
- •Screening
- •Health Maintenance
- •References
- •Physical Exam
- •Vaccinations
- •Introduction
- •Symptoms
- •Other History
- •Physical Exam
- •Lab Tests
- •Differential Diagnosis
- •Treatment
- •Prevention
- •Long Covid
- •References
- •Introduction
- •Provider Perspectives
- •Portable Medical Summary
- •Education
- •Employment
- •Specialist-Dominated Care
- •Internist-Dominated Care
- •Condition-Specific Medical Knowledge
- •Medication Reconciliation/Polypharmacy
- •Secondary Medical Conditions
- •Behavioral Health
- •Health Maintenance
- •Sexual Health
- •Sexual Abuse
- •Contraception
- •Cervical Cancer Screening
- •Health Disparities
- •Ethical Considerations
- •Conclusion
- •References
- •Introduction
- •Outpatient Assessment
- •Social History
- •Medications
- •Functional Assessment
- •Geriatric Syndromes
- •Delirium
- •Confusion Assessment Method (CAM): Short version [14]
- •Delirium Evaluation
- •Depression
- •Medication Management
- •Preventing Future Falls
- •Polypharmacy
- •Sensory Loss
- •Vision
- •Hearing Loss
- •Osteoporosis
- •Sleep Disorders
- •Advanced Care Planning
- •Home Care
- •References
- •History
- •Palliative Care/Hospice Care
- •Constipation
- •Nausea/Vomiting
- •Pain
- •Conclusion
- •References
- •Introduction
- •Definitions
- •Decision-Making
- •Identification
- •Key History
- •Workup
- •Management
- •Risky or Unhealthy Alcohol Use
- •Risky Opioid Use or OUD
- •References
- •Introduction
- •History
- •Physical Exam
- •Type 1 Diabetes
- •Type 2 Diabetes
- •Lifestyle Changes
- •Metformin
- •GLP-1 Receptor Agonists (Exenatide, Liraglutide, Dulaglutide, Lixisenatide)
- •DPP-4 Inhibitors (Sitagliptin, Saxagliptin, Linagliptin, Alogliptin)
- •SGLT-2 Inhibitors (Canagliflozin, Dapagliflozin, Empagliflozin, Ertugliflozin)
- •Thiazolidinediones (Pioglitazone)
- •Alpha-Glucosidase Inhibitors (AGIs) (Acarbose, Miglitol)
- •Insulin
- •References
- •Subclinical Hypothyroidism
- •Treatment Challenges
- •Hyperthyroidism
- •Brief Introduction
- •Key H&P
- •Decision-Making/Differential Diagnosis
- •Treatment
- •Graves’ Disease
- •Hypothyroidism
- •Brief Introduction
- •Key H&P
- •Decision-Making/Diagnosis
- •Treatment
- •Overt Hypothyroidism
- •Radioactive Iodine (RAI)
- •Surgery
- •Treatment: Subclinical Hyperthyroidism
- •Thyroid Nodules
- •Brief Introduction
- •Key H&P
- •Decision-Making/Differential Diagnosis
- •Treatment
- •References
- •Introduction
- •History
- •Medical History
- •Family History
- •Social History
- •Physical Exam
- •Decision-Making/Differential Diagnosis
- •Screening Population
- •Testing Lipid Levels: Fasting vs. Non-fasting
- •Treatment
- •Treatment Strategies
- •Lifestyle Modification
- •Statins
- •Fibrates
- •Fish Oil
- •Other Non-statin Medications
- •Monitoring After Initiating Therapy
- •References
- •Introduction
- •History
- •Who Should Lose Weight?
- •Treatment
- •Diet
- •Physical Activity
- •Pharmacotherapy
- •Long-Term Follow-Up After Uncomplicated Bariatric Surgery
- •References
- •Brief Introduction
- •Decision-Making/Differential Diagnosis
- •Acute Cough
- •Subacute Cough
- •Chronic Cough
- •Evaluation/Investigation
- •Disease-Specific Features
- •Acute Cough
- •Subacute Cough
- •Chronic Cough
- •Treatment
- •References
- •Introduction
- •Sudden-Onset Dyspnea
- •Acute-Onset Dyspnea
- •Episodic Dyspnea
- •Chronic Dyspnea
- •Treatment
- •References
- •Introduction
- •Acute Sinusitis
- •Chronic/Recurrent Sinusitis
- •Physical Findings
- •Diagnosis
- •Diagnostic Tests
- •Additional Evaluation
- •References
- •Introduction
- •Decision-Making/Differential Diagnosis
- •Key H&P
- •Rapid Antigen Detection Tests
- •Treatment
- •Symptomatic Treatment
- •References
- •Introduction
- •ICSD3 Classifies Sleep Disorders into Seven Major Categories [4]
- •Prevalence
- •Sleep History
- •STOP-Bang Questionnaire
- •Understanding ESS Score
- •Focused Physical Exam
- •Definition
- •Risk Factors
- •Pathophysiology
- •Diagnosis
- •Treatment: OSAHS/SDB (Usual Therapy)
- •References
- •Brief Introduction
- •Decision-Making/Differential Diagnoses
- •Physical Examination
- •Measuring Blood Pressure
- •Diagnostic Studies
- •Clinical Quality Measure
- •Assessment
- •Treatment
- •Lifestyle Management
- •Pharmacological Interventions
- •Refractory or Resistant Hypertension
- •References
- •Chest Pain
- •History
- •Physical Exam
- •Differential Diagnosis
- •Potentially Life-Threatening
- •Acute Coronary Syndromes
- •Aortic Dissection
- •Pulmonary Embolism
- •Pneumothorax
- •Non-Life-Threatening Causes
- •Gastroesophageal Reflux Disease
- •Pleuritic Chest Pain
- •Cervical Angina
- •Pericarditis
- •Chronic Angina
- •Herpes Zoster
- •Muscular Pain
- •Rib Fracture
- •Costochondritis
- •Esophageal Spasm
- •Diagnostic Testing
- •Electrocardiogram
- •Blood Testing
- •Imaging
- •Chest X-Ray
- •X-Ray C-Spine
- •Transthoracic Echocardiogram
- •References
- •Introduction
- •Laboratory Evaluation
- •Hypoproliferative Anemias
- •Microcytic Anemia
- •Differential Diagnosis
- •Iron Deficiency Anemia
- •Epidemiology
- •Pathophysiology
- •Key History
- •Physical Exam
- •Laboratory Evaluation
- •Diagnosis
- •Treatment
- •Normocytic Anemia
- •Differential Diagnosis [6]
- •Epidemiology
- •Pathophysiology
- •Laboratory Evaluation
- •Diagnosis
- •Treatment
- •Macrocytic Anemia
- •Differential Diagnosis [2]
- •Megaloblastic Anemia
- •Vitamin B12 Deficiency
- •Epidemiology
- •Pathophysiology
- •Laboratory Evaluation
- •Diagnosis
- •Folic Acid Deficiency
- •Hyperproliferative Anemia
- •Hemolytic Anemia
- •Intrinsic Hemolytic Anemia
- •Sickle Cell Anemia
- •Epidemiology
- •Pathophysiology
- •Laboratory Evaluation
- •Diagnosis
- •Treatment
- •Thalassemia
- •Epidemiology
- •Pathophysiology
- •Laboratory Evaluation
- •Hereditary Spherocytosis (HS)
- •Epidemiology
- •Pathophysiology
- •Laboratory Evaluation
- •Glucose-6-Phosphate Dehydrogenase Deficiency (G6PD Deficiency)
- •Epidemiology
- •Pathophysiology
- •History Physical Exam
- •Laboratory Evaluation
- •Extrinsic Hemolytic Anemia
- •Autoimmune Hemolytic Anemia
- •Warm Autoimmune Hemolytic Anemia (WAHA)
- •Epidemiology
- •Pathophysiology
- •Laboratory Evaluation
- •Cold Autoimmune Hemolytic Anemia
- •Epidemiology
- •Pathophysiology
- •Laboratory Assessment
- •Conclusion
- •References
- •Introduction
- •Differential Diagnosis
- •Decision-Making/Treatment
- •References
- •Introduction
- •Decision-Making/Differential Diagnosis
- •Papulosquamous
- •Psoriasiform
- •Pityriasiform
- •Lichenoid
- •Erythroderma
- •Eczematous
- •Dermal
- •Vascular
- •Vesiculobullous
- •Infectious
- •Autoimmune, Intraepidermal
- •Autoimmune, Subepidermal
- •Noninflammatory
- •References
- •Introduction
- •Decision-Making/Differential Diagnosis
- •Non-scarring Alopecias
- •Androgenetic Alopecia
- •Focal Hair Loss
- •Diffuse Hair Loss
- •Scarring Alopecia
- •Lymphocytic
- •Acne Keloidalis
- •Neutrophilic
- •References
- •Introduction
- •Key H&P
- •History
- •Medications
- •Social History
- •Physical Examination
- •Differential Diagnosis
- •Decision-Making
- •Treatment
- •References
- •Introduction
- •Key H&P
- •History
- •Physical Examination
- •Differential Diagnosis
- •Intrinsic Shoulder Pain
- •Decision-Making
- •Treatment
- •Rotator Cuff Injury
- •Adhesive Capsulitis
- •References
- •Introduction
- •Key H&P
- •History
- •Medications
- •Social History
- •Physical Examination
- •Differential Diagnosis
- •Decision-Making
- •Treatment
- •Pharmacotherapy
- •Non-pharmacotherapy
- •References
- •Introduction
- •Decision-Making/Differential Diagnosis
- •Vertigo
- •Central vs. Peripheral Vertigo
- •BPPV
- •Meniere’s Disease
- •Labyrinthitis/Vestibular Neuritis
- •Migrainous Vertigo
- •Presyncope
- •Disequilibrium
- •Lightheadedness
- •Dix-Hallpike Maneuver
- •Nystagmus
- •Hearing Evaluation
- •Romberg Testing
- •Other Diagnostic Testing
- •Treatment
- •BPPV
- •Vestibular Neuritis/Labyrinthitis
- •Meniere’s Disease
- •Disequilibrium
- •Presyncope
- •Lightheadedness
- •References
- •Introduction
- •History

482
M. Kinjo
axial low back pain. Short-term treatment within 4 weeks’
duration is recommended—ibuprofen 400–600mg four times
daily or naproxen 250–500mg twice daily and taper as tolerated. Recent evidence concluded that acetaminophen showed
no benefit compared to placebo in acute low back pain [16];
thus, only selected patients with contraindication to NSAIDs
can be recommended for the use of acetaminophen.
Non-benzodiazepine muscle relaxants may be effective in
patients with acute low back pain who are refractory to initial
pharmacotherapy [17]. Cyclobenzaprine is a reasonable choice.
Benzodiazepine muscle relaxant should not be used due to
physical dependence. Tramadol may be effective for acute and
chronic low back pain [18]. For radicular pain, gabapentinoid
could be used as add-on analgesics or stand-alone therapy.
In chronic axial pain, the use of simple analgesics such as
acetaminophen or tramadol in combination with an antidepressant appears to be efficacious [19]. Tricyclic antidepressants or duloxetine can be tried if chronic low back pain is
refractory.
Non-pharmacotherapy
Patients with acute low back pain should be advised against
bed rest. We encourage patients returning to activities or
work as soon as possible. In patients with acute low back
pain, exercise does not improve outcomes. For patients with
subacute (4–12weeks) or chronic (12weeks or longer) nonspecific low back pain, exercise should be encouraged for
those who were already active. Referral to physical therapy to
strengthen abdominal muscle by increasing lumbar flexion
and reducing lumbar lordosis may prevent recurrence of low
back pain. Aerobic exercise is recommended to all patients
for chronic back pain.
Clinical Pearls
• Only a small proportion of patients with inflammatory
back pain will have spondyloarthritis. Not all patients with
spondyloarthritis have inflammatory back pain.

Chapter 24. Back Pain
483
• Osteoporotic compression fracture should not guide you
away from malignancy-related vertebral compression frac-
ture. Always look for any signs of malignancy or infection
even when the history is highly suggestive of osteoporotic
fracture.
Do Not Miss
• Cauda equina syndrome secondary to malignancy or mid-
line intervertebral disc herniation should not be missed as
it could become irreversible in neurological deficit.
• Aortic dissection and anterior spinal artery infarction are
life-threatening conditions.
References
1. Deyo RA, Weinstein JN. Low back pain. N Engl J Med.
2001;344:363–70.
2. Hooten WM, Cohen SP. Evaluation and treatment of low Back
pain: a clinically focused review for primary care specialists.
Mayo Clin Proc. 2015;90:1699–718.
3. Gardner A, Gardner E, Morley T. Cauda equina syndrome: a
review of the current clinical and medico-legal position. Eur
spine J. 2011;20:690–7.
4. Sieper J, van der Heijde D, Landewe R, etal. New criteria for
inflammatory back pain in patients with chronic back pain:
a real patient exercise by experts from the assessment of
SpondyloArthritis international society (ASAS). Ann Rheum
Dis. 2009;68:784–8.
5. Depalma MJ, Ketchum JM, Trussell BS, etal. Does the location
of low back pain predict its source? PM R. 2011;3:33–9.
6. Michel F, Decavel P, Toussirot E, et al. Piriformis muscle syndrome: diagnostic criteria and treatment of a monocentric series
of 250 patients. Ann Phys Rehabil Med. 2013;56:371–83.
7. Suri P, Rainville J, Kalichman L, etal. Does this older adult with
lower extremity pain have the clinical syndrome of lumbar spinal
stenosis? JAMA. 2010;304:2628–36.
8. Leone A, Cianfoni A, Cerase A, etal. Lumbar spondylolysis: a
review. Skelet Radiol. 2011;40:683–700.
9. Matsui H, Maeda A, Tsuji H, etal. Risk indicators of low back
pain among workers in Japan. Association of familial and physi-

484
M. Kinjo
cal factors with low back pain. Spine. 1976;1997(22):1242–7. discussion 8
10. Hoy D, Brooks P, Blyth F, etal. The epidemiology of low back
pain. Best Pract Res Clin Rheumatol. 2010;24:769–81.
11. Vroomen PC, de Krom MC, Knottnerus JA. Diagnostic value
of history and physical examination in patients suspected of
sciatica due to disc herniation: a systematic review. J Neurol.
1999;246:899–906.
12. Katz JN, Harris MB.Clinical practice. Lumbar spinal stenosis. N
Engl J Med. 2008;358:818–25.
13. Katz JN, Dalgas M, Stucki G, etal. Degenerative lumbar spinal
stenosis. Diagnostic value of the history and physical examination. Arthritis Rheum. 1995;38:1236–41.
14. Szadek KM, van der Wurff P, van Tulder MW, etal. Diagnostic
validity of criteria for sacroiliac joint pain: a systematic review. J
Pain. 2009;10:354–68.
15. Chou R, Deyo RA, Jarvik JG. Appropriate use of lumbar
imaging for evaluation of low back pain. Radiol Clin N Am.
2012;50:569–85.
16. Saragiotto BT, Machado GC, Ferreira ML, etal. Paracetamol for
low back pain. Cochrane Database Syst Rev. 2016;2016:CD012230.
1 7. van Tulder MW, Touray T, Furlan AD, etal. Muscle relaxants
for non-specific low back pain. Cochrane Database Syst Rev.
2003;2003:CD004252.
18. Ruoff GE, Rosenthal N, Jordan D, et al. Tramadol/acetaminophen combination tablets for the treatment of chronic lower
back pain: a multicenter, randomized, double-blind, placebocontrolled outpatient study. Clin Ther. 2003;25:1123–41.
19. Malanga G, Wolff E.Evidence-informed management of chronic
low back pain with nonsteroidal anti-inflammatory drugs, muscle
relaxants, and simple analgesics. Spine J. 2008;8:173–84.

Part VII
Neurologic

Chapter 25
Dizziness
RobertKennedy Jr
Introduction
A dizzy patient presenting to a busy clinician poses a unique
diagnostic challenge. Fortunately, a focused, structured evaluation can guide a provider through the most common differentials in order to establish a clear diagnosis and develop
an effective treatment plan. It should be noted that about
5% of primary care visits deal with a chief complaint of dizziness and more than 50% of patients with dizziness seek
help from their primary care clinician [1]. The causes of dizziness remain constant across a wide spectrum of practice
settings [2].
Dizziness can be classified into four main categories: vertigo, presyncope, disequilibrium, and lightheadedness. Making
a diagnosis can initially seem challenging due to the often
vague, nonspecific, or inconsistent nature of the patients’
reporting. In addition, some causes of dizziness can share
similar features and precipitants. A broad differential consisting of both malignant and benign causes coupled with nonspecific patient descriptors can lead to diagnostic frustration.
R. Kennedy Jr (*)
University of Maryland Upper Chesapeake Medical Center,
Bel Air, MD, USA
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2022
E. Sydney et al. (eds.), Handbook of Outpatient Medicine,
https://doi.org/10.1007/978-3-031-15353-2_25
487

488
R. Kennedy Jr
Despite these barriers, the cause of the dizziness is revealed
by the patient’s history in more than 50% of cases [3].
The patient’s initial, raw, unguided description of their
symptoms is the most important step in determining the
cause of their dizziness. For this reason, it is imperative to
obtain an unguided, pure description of what the patient is
actually experiencing. This can be achieved by starting with
open-ended, non-leading questions such as: “Without using
the word ‘dizzy’ tell me what you are feeling” or “When you
say you feel dizzy, what exactly do you mean?” After the provider has cast the net widely, wait and listen as the diagnostic
clues come to the surface.
Patients with vertigo tend to report a spinning sensation or
fictitious sense of motion. If such a patient also has migraine
symptoms (photophobia, phonophobia, aura, or typical headache), vertiginous migraine should also be considered, affecting 3% of the population and 10% of migraineurs [1]. Patients
with presyncope may report a feeling of pending loss of consciousness or “blackout.” Patients with disequilibrium may
report being “off-balance” and “feeling wobbly” or describe
other perturbations in balance and coordination. Feelings of
lightheadedness are often very vague, imprecise, and difficult
for patients to articulate without using the word “dizzy.” They
may describe feeling disconnected from the environment, a
sense of floating or giddiness; it is this abstract nature of
symptom reporting that in itself is actually diagnostic. It
should be noted that psychiatric causes can be identified in
many of these patients as well [4] (Fig.25.1).

sN
Chapter 25. Dizziness
489
Dizzy patient
Open ended history
Treat
disorder
underlying
If non diagnostic...
syncope evaluation.
Perform presyncope/
EKGExam concerning for
Presyncope
physical exam
Category specific
Review
medications
psychiatirc disorder
Hyperventilation test
Screen for underlying
signs?
+ Orthostatic vital
deficits
Assess for
oNseY
multiple sensory
Migraine
symptoms?
Treat underlying
No Yes
No
Ye s
cause
Treat for
Hearing
Teach
Ye o
Evaluation
Corrects with
migraine
loss
breathing
controlled
for
syncope
volume
replacement?
oNseY
Episodic
exercises
No
Ye s
symptoms?
Cosider
behavioral
Review med list
Suspect
Ye sNoYe sNo
health
referral
dysfunction
Consider autonomic
orthostatic
presyncope
neuritis
Vestibular
BPPV
Vertigo Disequilibrium Lightheadedness
central vertigo?
Labyrinthitis
Episodic
symptoms?
MRI
Urgent eval
if present
Treat for stroke
Menier’s
disease
F . Approach to patient with dizziness

490
R. Kennedy Jr
Decision-Making/Differential Diagnosis
Vertigo
Vestibular dysfunction accounts for more than 40% of dizzy
episodes. Here the subtypes include benign paroxysmal positional vertigo (BPPV), vestibular neuritis (viral infection that
involves the vestibular nerve), labyrinthitis (postinfectious
inflammation of the labyrinthine organs), and Meniere’s disease (increased endolymphatic fluid in the inner ear). Central
vertigo (brainstem stroke, posterior circulation insufficiency)
and migrainous vertigo, as previously noted, are also important diagnostic considerations. Vertigo can be caused by disturbance of the peripheral vestibular system (vestibular
portion of the eighth cranial nerve and vestibular labyrinth)
or by lesions within the central nervous system (brainstem or
cerebellum). Nausea and vomiting are typical with acute vertigo, but can be mild or short lived in BPPV. Interestingly,
peripheral vertigo tends to cause more severe nausea and
vomiting than central causes. Movement worsens all types of
vertigo, and even though patients with peripheral vertigo may
not want to move, they are usually able to walk. In comparison, patients with central vertigo experience greater impairment in gait and posture and are often very ataxic and unable
to walk [5].
Most patients have benign disorders of the peripheral vestibular system and dysfunction of either the vestibular nerve
(vestibular neuritis) or the labyrinth (labyrinthitis). A few
(less than 5%) may have serious strokes of the cerebellum or
brainstem, which may rapidly cause coma and death from
acute hydrocephalus or brainstem compression. For this reason, it is imperative to make a clinical distinction between
central and peripheral vertigo [6].

Chapter 25. Dizziness
491
Central vs. Peripheral Vertigo
Severe vertigo may occur in the setting of acute peripheral
and central lesions. However, there are some clinical clues
that favor a central cause over a peripheral cause. An acute
vertebrobasilar stroke is almost always accompanied by other
signs and symptoms of brainstem ischemia such as diplopia,
dysphagia, weakness, or numbness. A history of atherosclerotic cardiovascular disease and associated risk factors should
heighten a clinician’s concern for vertebrobasilar ischemia.
Findings on the physical exam that suggest stroke in dizzy
patients include normal bilateral vestibulo-ocular reflexes
(noted on head impulse test), skew deviation, (described later
in the chapter), abnormal visual tracking (saccadic pursuit),
and direction-changing nystagmus. Visual fixation can suppress nystagmus from the peripheral lesion but not from a
central cause. In peripheral lesions, the predominant direction of nystagmus remains the same in all directions of gaze;
nystagmus that changes direction with gaze shifting is suggestive of a central abnormality. Other features that suggest a
peripheral cause include falling in the opposite direction to
nystagmus and horizontal/torsional nystagmus. In summation, the probability of stroke is increased in the setting of
severe truncal ataxia, normal vestibulo-ocular reflex, skew
deviation, saccadic pursuit, direction-changing nystagmus,
and nystagmus that is not suppressed with visual fixation (see
Table25.1) [5].
T . Findings concerning for central vertigo
Severe ataxia
Direction-changing nystagmus
Nystagmus not affected by fixation
Saccadic pursuit
Skew deviation
Nystagmus does not fatigue with repeated dix-Hallpike
maneuver

492
R. Kennedy Jr
BPPV
BPPV is the most common form of peripheral vertigo and
tends to occur when the patient moves the head in a particular position as in turning over in bed, looking up, getting up,
or lying down in bed. It is believed to be caused by calcium
debris within the posterior semicircular canal (canalithiasis).
The semicircular canals detect angular head accelerations.
Debris in the canal causes inappropriate movement of the
endolymph causing the erroneous sensation of spinning when
the head shifts with respect to gravity. Most causes of BPPV
are idiopathic or related to minor head injury; however, many
different precipitants have been proposed. Patients tend to
experience recurrent episodes of vertigo that last 1min or
less. Associated symptoms include nausea and vomiting.
Hearing loss is usually absent and patients have no other
neurologic complaints. Episodes may recur for weeks without
therapy. Provoking symptoms and nystagmus with maneuvers
such as the Dix-Hallpike maneuver support the diagnosis.
With this maneuver, nystagmus and vertigo usually last less
than 30s; after it stops and the patient sits up, the nystagmus
will recur but in the opposite direction. Repeating the maneuver on the same side will diminish the intensity of the nystagmus. Further testing is not indicated in typical BPPV, and
neuroimaging is reserved for patients with symptoms that are
not typical or those who present with other red flags [7].
Meniere’s Disease
Meniere’s disease is believed to be caused by abnormal fluid
balance in the inner ear and associated with episodic vertigo
(rotational nystagmus with episodes lasting up to 24h), tinnitus (low pitch), and sensorineural hearing loss. It is unclear
why fluid builds up in the endolymphatic spaces of the inner
ear. The diagnosis is made based on clinical features as no
specific testing is confirmatory. Audiometry should be performed in all patients with suspected disease. Brain MRI is
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