Some basic rheumatology cases & common mistakes for beginners
Assistant Prof. Ahmed Yehia Ismaeel
🎯 Objectives
By the end of this lecture, you should be able to:
Recognize common rheumatology emergencies
Identify red flags
Know when to refer urgently
🚨 Why this matters?
Missing these =
high morbidity & mortality
Rheumatology patients may present with
Life-threatening complications
Drug-related emergencies
Pregnancy-related risks
Goal
The goal of the musculoskeletal evaluation is to formulate a D.D. that leads to an accurate diagnosis & timely therapy, while avoiding excessive diagnostic testing & unnecessary treatment.
1st , back to basics……
Entheseopathy/itis
So , don’t request an investigation unless
Case
A 4-year-old girl presents with 2 months history of bilateral knee & right wrist arthritis.
What’s the best next step?
Put a differential diagnosis to guide diagnosis plan.
Differential diagnosis �of childhood arthritis.
Mostly no.
Duration (chronic > 6 weeks)
Echocardiography: normal
Is this rheumatic fever?
ASOT
600 🡪 800 (Rising)
Is this juvenile idiopathic arthritis(JIA)?
All were non-significant.
So, we requested
ESR, CRP, ANA (IF) with titre, rheumatoid factor, TSH, calcium, s. 25 OH vitamin D.
JIA is a diagnosis of exclusion.
Approach to arthritis can be classified into 8 steps :�
Jones criteria for diagnosis of acute rheumatic fever
ASOT is one of the most badly used labs in Egypt.
So, this a case of JIA
Per ILAR criteria, JIA is a diagnosis of exclusion.
JIA is the commonest cause of chronic arthritis in children.
Case
A 16-year-old girl presents to the emergency department with
History
Examination
Ill-looking, febrile
Right knee
No
Initial Investigations
WBC
ESR/CRP
ASOT
Jones criteria for diagnosis of acute rheumatic fever
So, she fulfilled the ARF criteria.
SO, THE PHYSICIAN DIAGNOSED HER AS ARF.
SHE GAVE HER HIGH DOSE ASPIRIN & DISCHARGED HER.
Monoarthritis
Acute
Septic until proven otherwise
An essential rule
it will lead unfortunately to
irreversible damage
lifelong disability
if not death from disseminated infection.
If a septic monoarticular joint was not diagnosed & treated properly,
Then what is the best first step in acute monoarthritis?
The first step is
Joint aspiration
This is to be treated as a rheumatological emergency.
Acute Monoarthritis
High value care (HVC) RECOMMENDATION
Joint aspiration is usually the most effective means of diagnosing the underlying cause of acute monoarthritis.
Case
A 22-year-old male with known�Hemophilia A
presents with:
No trauma history
Etiology of monoarthritis
Acute
Inflammatory
Non-inflammatory
Chronic
Inflammatory
Non-inflammatory
Etiology of monoarthritis
Acute
Inflammatory
Septic
Crystal
Early rheumatic disease
Non-inflammatory
Trauma
Hemarthrosis
AVN
Chronic
Inflammatory
Chronic infectious
Fungal
Mycobacterial
Borrelia burgdorferi
Rheumatic diseasses
Non-inflammatory
OA
AVN
Differential diagnosis of acute monoarthritis
I. Septic arthritis
2. Crystal arthropathies
3. Haemorrhagic arthropathies
4. Miscellaneous: Palendromic rheumatism, others
5.Monoarticular onset of chronic inflammatory arthritis (frequently seen in psoriatic arthritis, may occur in RA and seronegative inflammatory arthritides)
Case
The differential diagnosis of heel pain is extensive, but a mechanical etiology is the most common. The specific anatomic location of the pain can help guide diagnosis.
The most common diagnosis is plantar fasciitis.
Case
Not gout.
Still plantar fasciitis
Hyperuricemia is a necessary but not sufficient precondition for the development of urate crystal deposition disease & should be distinguished from gout, the clinical syndrome.
2018 updated EULAR evidence-based recommendations for the diagnosis of gout
4. The diagnosis of gout should not be made on the presence of hyperuricemia alone. (2a B)
Gout is
a clinical syndrome
having specific criteria
not a laboratory diagnosis
i.e. not hyperuricemia
Can serum urate levels be used to diagnose gout?
Serum urate levels are elevated (>6.8 mg/dL) at some time in almost all gout patients
Serum concentrations are normal at the time of an acute flare in upto one-third (false-negative results). This may be due to interleukin (IL)-6 (uricosuric).
Many individuals may have hyperuricemia without gout (false-positive results).
Alone cannot
Case
A 25-year-old female with SLE presents with
Fever (39°C)
Joint pains
Fatigue
How to approach diagnosis & management?
This is straightforward. Lupus is active. Fever & joint affection are of the classification & activity criteria.
SLEDAI-2K
Activity assessment
Labs
CRP
+ve, 96 mg/l
WBC
12.000
Red Flags for Infection
Very high fever
Neutrophilia
CRP very high
On steroids/immunosuppressants
But with no shift to the left
But steroids can cause neutrophilia.
Educational Message
Wrong diagnosis=
In rheumatology patients,
As increasing immunosuppressives to control flare
Shift to the left
CASE: Acute Shortness of Breath in SLE
A 30-year-old woman with SLE
Causes of dyspnea in SLE?
What causes dyspnea in SLE patients?
No. Causes of dyspnea in SLE patient
Causes of dyspnea in SLE patient
SLE-specific causes
Pulmonary affection
Lupus pneumonitis
Pleural effusion
Shrinking lung syndrome
Cardiac affection
myocarditis
SLE-non-specific
Infection
Pulmonary embolism (PE)
Others
Further history
She gives history of right lower limb DVT 1 year ago. What to ask about this DVT?
Was it provoked?
No
Exam
SaO2: 96%
BP: 110/80
RR: 22
HR: 110 bpm
T: 37.3oC
🧪 Investigations
D-dimer
CT pulmonary angiography
What to choose?
Well’s score for PE
Pulmonary embolism
What is next?
RT LL acute DVT
Duplex
CTPA
Red Flags for PE
Sudden onset
Tachycardia
Risk factors (APS)
Management
Start anticoagulation if high suspicion
💡 Educational Message
Think as
lupus-specific causes
lupus-non-specific causes
“SLE + dyspnea =
Don’t attribute all the symptoms to the original disease.
CASE
A pregnant woman (28 weeks) with SLE presents with
Headache
High BP
Her urine shows
3+ protein.
What are the major considerations?
Preeclampsia
Lupus Nephritis flare
How to differentiate?
Feature | Lupus Nephritis (LN flare) | Preeclampsia |
Underlying condition | Flare of Systemic lupus erythematosus | Placental vascular disorder |
Timing | Any time in pregnancy | Usually, >20 weeks gestation |
Blood pressure | May be normal or elevated | Always elevated |
Proteinuria | Present (may be heavy) | Present (≥300 mg/day or significant) |
Urine sediment | Active (RBCs, dysmorphic RBCs, RBC casts) | Blunt/inactive (no casts) (Acellular) |
Hematuria | Common | Rare |
Serum creatinine | May rise | May rise |
Feature | Lupus Nephritis (LN flare) | Preeclampsia |
Complement levels (C3, C4) | Usually Low (consumption) | Normal |
Anti-dsDNA | Usually Elevated (active disease) | Normal |
Platelets | Usually normal (↓ only if severe lupus) | May be Low (in severe disease/HELLP) |
Liver enzymes | Usually normal | May be Elevated (especially in HELLP) |
Uric acid | Normal or mildly ↑ | Elevated |
Edema | Can occur | Common |
Other lupus features | Rash, arthritis, serositis | Absent |
Fetal effects | Variable (depends on disease activity) | Growth restriction, placental insufficiency |
Response to steroids | Improves | No effect |
Definite management | Immunosuppression (e.g., steroids) | Delivery |
Management
Justification
Preeclampsia is life-threatening to mother & fetus
Treat as preeclampsia until proven otherwise
CASE
A 30-years-old female with SLE patient on hydroxychloroquine, prednisolone & methotrexate presented with
The oral lesions are atypical.
This is oral mucositis mostly MTX toxicity.
This is lupus activity.
Common causes of MTX toxicity
⚠️ 1. Dosing Errors (Most common cause)
Daily instead of weekly dosing
Misunderstanding prescription instructions
Elderly patients at higher risk �
💊 2. Drug Interactions
Medications that increase MTX levels or reduce its clearance
NSAIDs (reduce renal perfusion → ↓ MTX excretion)
Trimethoprim-sulfamethoxazole (antifolate effect → severe BM suppression)
Penicillins (↓ renal clearance)
Proton pump inhibitors (e.g., omeprazole) ↑MTX
Salicylates
3. Renal Impairment
MTX is primarily renally excreted
Even mild renal dysfunction
💧 4. Dehydration
Reduces renal perfusion
Leads to increased MTX concentration
5. Lack of Folic Acid Supplementation
MTX inhibits folate metabolism
Absence of folic acid → ↑ risk of
Management
Stop drug
1
Give folinic acid
2
Admit if severe
3
🧠 GENERAL RULE (TAKE AWAYS) FOR GP & non-rheumatology specialists
Ask yourself 3 key questions
Is this disease activity?
Is this disease complication?
Is this infection?
Is this drug complication?
Is this pregnancy-related issue?
Is this other coincidental event?
Don’t attribute all the symptoms to the original disease.
Thank You