A 48-year-old man presents with acute onset of severe low back pain after moving furniture. His pain radiates down his legs but he has no neurological deficits or systemic symptoms. His examination shows tenderness but normal strength and reflexes. He is diagnosed with an acute lumbar sacral strain from overexertion. Conservative treatment with rest, NSAIDs, and muscle relaxants is recommended initially without imaging.

1. Musculoskeletal Case
Presentations
Dr. Kamau David

2. Case Presentation - 1
• A 58-year-old man with a long history of treated
essential hypertension and mild renal insufficiency
presents to the urgent care clinic complaining of pain in
the right knee.
• His primary care provider saw him one week ago and
added a thiazide diuretic to improve his blood pressure
control.
• He had been feeling well until the night before the clinic
visit, when he noted some redness and slight swelling of
his knee.
• He went to sleep and was awakened early by significant
swelling and pain.
• He was able to walk only with assistance.
• He has no history of knee trauma.

3. Case Presentation - 1
• The physical examination confirmed the
presence of a swollen right knee, which was
erythematous and warm.
• Joint aspiration recovered copious dark yellow,
cloudy synovial fluid.
• A microscopic analysis demonstrated 30,000
leukocytes/µL, a negative Gram stain, and many
needle-like, negatively birefringent crystals
consistent with acute gout.

4. Case Presentation: Questions
A. What factors may have precipitated this gout flare?
• Gout flares are typically precipitated by a combination of
metabolic and physical stressors in the setting of either
urate underexcretion, seen in the vast majority of cases,
or urate overproduction.
• The mild renal insufficiency may be associated with a
decreased glomerular filtration rate and thus poor urate
excretion.
• The recent addition of a diuretic further exacerbated this
underlying impairment.

5. Case Presentation: Questions
B. Describe the inflammatory pathways involved in acute gout.
• Multiple inflammatory pathways are invoked by the negatively
charged urate crystals.
• For example, they activate the classic complement pathway whose
cleavage products serve as effective neutrophil chemoattractants.
• The kinin system is stimulated by crystals as well, contributing to the
inflammatory signs seen on examination, such as tenderness and
erythema from local vasodilation.
• In addition, macrophages phagocytose urate crystals, initiating the
release of pro-inflammatory cytokines (eg, IL-1, TNF1β, TNFα, IL-8,
PGE2), which activate the vascular endothelium, encouraging
neutrophil adhesion and migration.
• Neutrophils are able to simulate their own recruitment by releasing
leukotriene B4 in response to urate crystal phagocytosis.

6. Case Presentation: Questions
C. What agents should the urgent care physician consider in treating this gout
flare? What are their mechanisms of action?
• Therapy for an acute gouty attack should target the pro-inflammatory
mediators described previously.
• NSAIDs such as ibuprofen reduce prostaglandin synthesis; colchicine impairs
the migration of neutrophils into the joints; and corticosteroids deactivate
myelomonocytic cells responsible for crystal phagocytosis and subsequent
cytokine release.
• Because gouty flares are typically self-limited events, treatment is offered to
alleviate symptoms and reduce the duration of the flare.
• On the other hand, probenecid (which is a uricosuric agent, inhibiting renal
tubular urate resorption), allopurinol and febuxostat (which are xanthine
oxidase inhibitors, interfering with the conversion of hypoxanthine and
xanthine to uric acid), and pegloticase, (which converts uric acid to allantoin,
an inactive and soluble metabolite readily excreted by the kidneys) are
typically reserved for the prevention of future attacks.

7. Case Presentation - 2

8. Case Presentation - 2
• A 47-year-old woman presents to the clinic with a four-week history of
fatigue, bilateral hand pain and stiffness, and hand and wrist joint swelling.
• About a month before presentation, she noticed that her hands were stiffer
in the morning but thought that it was due to too much typing.
• However, the stiffness has worsened, and she now needs about an hour each
morning to “loosen up” her hands.
• As the day goes on, the stiffness improves, although it does not go away
entirely.
• She has also noticed that her knuckles and wrists are swollen and feel
somewhat warm.
• The physical examination reveals warm, erythematous wrists and metacarpal
joints bilaterally.
• Hand x-ray films show periarticular demineralization and erosions, and blood
test results are significant for a mild anemia, elevated sedimentation rate,
and a positive rheumatoid factor.
• The patient is diagnosed with rheumatoid arthritis.

9. Questions
A. What is the basic pathogenic process in rheumatoid
arthritis?
• The pathophysiology of rheumatoid arthritis is centered
around the synovial linings of joints.
• The normal synovium is 1–3 cell layers thick.
• In rheumatoid arthritis, the synovium is markedly
thickened and contains inflammatory cells in the
interstitium, including T cells, B cells, and macrophages.
• This inflammatory tissue can invade adjacent bone and
cartilage, accounting for the bony erosions and joint
destruction.

10. Questions
B. Describe the interplay between genetic and environmental factors
that leads to the pathogenic process.
• Rheumatoid arthritis is thought to arise when an environmental factor
(such as an infection) triggers an autoimmune response to antigens
present in the synovium and elsewhere in the body.
• However, the specifics have not been identified.
• No definite infectious agents have been identified as causal agents in
rheumatoid arthritis.
• The autoimmune mechanisms involved in triggering and maintaining
the rheumatoid inflammatory response have also not been definitively
identified, although TNF plays a central role.
• Genetic factors have been found, arising from the observation that
identical twins have a 15–35% concordance rate of developing
rheumatoid arthritis.
• A specific subset of MHC class II alleles has been found that determine
disease development and severity.

11. Questions
C. How are novel treatments being used to treat this condition?
• For many years, the mainstay of treatment for rheumatoid
arthritis involved nonspecific immunosuppressant agents.
• More recently, biologic modifiers of defined pathogenic pathways
have been used successfully to treat disease.
• TNFα inhibitors were the first to be developed, and they function
by sequestering TNFα so that it cannot maintain the inflammatory
response.
• They are either soluble TNFα receptors or monoclonal antibodies
that bind the free TNFα and clear it from the body.
• Similar therapeutic strategies have been used to block the
inflammatory effects of IL-1β and IL-6, and new agents are being
developed for still other RA-associated cytokines.

12. Case Presentation - 3

13. Case Presentation - 3
• A 22-year-old African American woman with a
family history of SLE reports intermittent knee
arthralgias.
• She denies any facial rash, photosensitivity,
chest pain, and shortness of breath.
• She is convinced she has lupus and requests
confirmatory blood tests.

14. Case Presentation – 3: Questions
A. What additional history may be helpful in supporting the diagnosis of lupus as the cause of
this patient’s arthralgias?
• This patient’s suspicion that her arthralgias may be explained by lupus is supported by a high
prevalence of systemic lupus erythematosus (SLE) among African American women—
approximately 1 in 250—as well as her family history of this disorder.
• The symptoms are highly variable but tend to be stereotyped in a given individual (ie, the
prominent clinical features often remain constant over years).
• Since SLE can affect many organs, it is important to do a thorough review of systems.
• Skin symptoms such as photosensitivity and a variety of SLE-specific skin rashes (including a
rash over the malar region, discoid pigmentary changes to the external ear, and erythema over
the dorsum of fingers) are common.
• Like those with other immune complex–mediated diseases, patients with SLE may manifest a
nonerosive symmetric polyarthritis.
• Renal disease, which takes the form of a spectrum of glomerulonephritides, can present with
hematuria or symptoms of renal failure.
• Patients may manifest a variety of hematologic disturbances (including hemolytic anemia,
thrombocytopenia, and leukopenia), inflammation of serosal surfaces (including pleuritis,
pericarditis, and peritonitis), as well as several neurologic syndromes (eg, seizures, organic
brain syndrome).

15. Case Presentation – 3: Questions
B. Why is it essential to elicit a medication history when
considering this diagnosis?
• Several environmental exposures have been
definitively associated with disease initiation in SLE.
• These include sunlight exposure (associated with both
disease onset and flares), viral infection (Epstein–Barr
virus exposure is strongly associated with SLE in
children), and certain drugs.
• These are agents to which humans are commonly
exposed, suggesting that individuals who develop SLE
have underlying abnormalities that render them
particularly susceptible to disease initiation.

16. Case Presentation – 3: Questions
C. Describe three possible mechanisms of
autoantibody-induced tissue injury in SLE.
• These mechanisms include:
① Subendothelial deposition of immune complexes, in
which antigens are derived from damaged or dying
cells
② Autoantibody binding to extracellular molecules in
the target organs (eg, skin, joints, kidneys, blood
elements), which activates inflammatory effector
functions and induces damage at that site
③ The induction of cell death by autoantibodies.

17. Case Presentation – 3: Questions
D. Describe the natural history of the disease. Which stimuli
have been implicated in the exacerbations that punctuate its
course?
• The natural history of SLE is characterized by a relapsing,
remitting course.
• Flares reflect immunologic memory, sparked by rechallenge
of a primed immune system with antigen.
• Numerous stimuli such as viral infections, ultraviolet light
exposure, and endometrial and breast epithelial involution
may induce apoptosis, which resupplies immune-inciting
antigens.
• Despite this course, 10-year survival rates commonly exceed
85%.

18. Case Presentation -4

19. Case Presentation -4
• A previously healthy 48-year-old man presents to his
primary care office with severe low back pain that began the
previous day after he helped his daughter move into her
college dorm.
• He denies any trauma or previous back injury. He describes
the pain as generally “achy” and sometimes characterized as
being “sharp” when he moves suddenly.
• The pain is located in his lower back and radiates down the
back of both legs to the middle of his posterior thighs.
• He denies any bladder or bowel incontinence or weakness in
his legs.

20. Case Presentation -4
• He denies fever, chills, weight loss, or malaise.
• He finds it very difficult to stand for prolonged periods of
time because he cannot find a comfortable position.
• He states that this is the worst back pain he has ever
experienced.
• It has not been relieved with acetaminophen or
ibuprofen.
• His past medical history is significant for hypertension,
and his only medication is lisinopril daily.
• He does not smoke or use illicit drugs and only drinks
alcohol on occasion..

21. Case Presentation -4
• On physical examination, he is well developed,
overweight, and in moderate discomfort.
• His vitals are within normal limits.
• On neuromuscular examination, he has moderate
tenderness bilaterally in his lumbar paraspinous muscles,
and his lumbar flexion and extension are limited by pain.
• Strength and sensation are within normal limits and are
symmetrical bilaterally.
• He has normal and symmetric knee and ankle deep
tendon reflexes.
• Straight leg raise testing is negative bilaterally, and gait is
within normal limits.

22. Summary:
• A 48-year-old man presents with
• Acute onset of low back pain after strenuous activity
• Previously healthy status
• Appears overweight, unremarkable neurologic examination
• Denial of any systemic complaints
• Past medical history significant for hypertension, with his only
medication being lisinopril daily

23. Case Presentation -4: Questions
• What is the most likely diagnosis?
• Most likely diagnosis: Acute low back pain,
lumbar sacral strain.

24. Case Presentation -4: Questions
• What is the most appropriate workup?
• Most appropriate workup: No formal workup is
required unless symptoms persist after
conservative treatment for at least 1 month.

25. Case Presentation -4
• What is the best treatment plan?
• Best treatment plan: Relative rest (but not bed
rest), nonsteroidal anti-inflammatory drugs
(NSAIDs) or acetaminophen, and muscle
relaxants.

26. Analysis
Objectives
• Develop a differential diagnosis for acute low back
pain.
• List the “red flag” symptoms of low back pain and
how to investigate them.
• Describe effective treatments for musculoskeletal
back pain.

27. Considerations
• Acute low back pain is the one of the most
common diagnoses in primary care practices.
• Approximately 90% of patients with acute low back
pain will fully recover within 4 to 6 weeks of
symptom onset.
• Since the differential diagnosis of low back pain is
broad, the role of the clinician is to determine if
the pain is caused by a self-limited condition, an
acute neurological compromise, or a systemic
disease and to consider psychosocial factors that
may lead to chronic back pain and complicate the
recovery or efficacy of treatment.

28. Considerations
• This patient’s history includes pertinent positive findings of a recent
history of repetitive lifting and twisting associated with lumbar sacral
strain.
• His signs, symptoms, and physical examination are all consistent with
a localized musculoskeletal condition.
• His lack of acute neurologic or systemic symptoms is a pertinent
negative finding.
• He denies a history of depression and substance abuse.
• This clinical scenario is best managed by symptomatic therapies for 4
to 6 weeks without imaging and with close follow-up if symptoms do
not resolve.
• In the majority of patients with acute back pain in the absence of red
flag symptoms, laboratory tests and imaging studies are not required.
• Education in proper lifting techniques and exercise therapy to improve
core and lumbar sacral strength and flexibility may help to prevent
future strain and injury.

29. THANK YOU