Dr Muhammad Sajjad

Dr Muhammad Sajjad Welcome to Dr Muhammad Sajjad’s Medical Case Forum
Daily real-life medical cases, clinical insights, and practical management tips.

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Ultrasound of appendicitis 1. Clinical CorrelationBefore scanning, note:Age and s*xDuration of painMigration of pain (pe...
28/07/2026

Ultrasound of appendicitis

1. Clinical Correlation
Before scanning, note:
Age and s*x
Duration of pain
Migration of pain (periumbilical → right iliac fossa)
Fever, vomiting, anorexia
WBC count, neutrophilia, CRP
Pregnancy status in females
Previous abdominal surgery
2. Ultrasound Technique
Probe selection
High-frequency linear probe (7–15 MHz): first choice in thin patients and children.
Curvilinear probe (3–5 MHz): obese patients or deep appendix.
Scanning method
Start at the point of maximum tenderness.
Use graded compression technique (Puylaert technique) to displace bowel gas.
Follow the ascending colon to the cecum and identify the appendiceal base.
Scan in both transverse and longitudinal planes.
Apply Color Doppler.
3. Identification of the Appendix
A normal appendix is:
Blind-ending tubular structure
Arises from the cecum
Compressible
Diameter

Approach to a baby with history of fits
28/07/2026

Approach to a baby with history of fits

Needle-stick Injury Protocol (Healthcare Workers)A needle-stick injury is a medical emergency because early management r...
24/07/2026

Needle-stick Injury Protocol (Healthcare Workers)
A needle-stick injury is a medical emergency because early management reduces the risk of infection.
Immediate First Aid (Within Minutes)
Wash the wound immediately with soap and running water.
Do not squeeze the wound or scrub aggressively.
If eyes or mouth are exposed, irrigate thoroughly with clean water or normal saline.
Report the incident immediately to the infection control team or supervisor.
Assess the Exposure
Determine:
Type of injury (deep vs superficial)
Hollow-bore needle or solid needle
Visible blood on the device
Source patient status (HBsAg, Anti-HCV/HCV RNA, HIV Ag/Ab)
Obtain baseline tests from the exposed person:
HIV Ag/Ab
HBsAg and Anti-HBs (vaccination/immunity status)
Anti-HCV (± HCV RNA if indicated)
Hepatitis B (HBV)
If vaccinated and Anti-HBs ≥10 mIU/mL
No treatment required.
If vaccinated but antibody status unknown
Check Anti-HBs.
If

Thyroid Ultrasonography
19/07/2026

Thyroid Ultrasonography

Basic Ultrasonography of thyroid gland 1- patient's position 2- probe selection 3- orientation of probes 4- Transverse v...
19/07/2026

Basic Ultrasonography of thyroid gland
1- patient's position
2- probe selection
3- orientation of probes
4- Transverse vs Longitudinal view
5- Normal Thyroid measurements

A consultant rheumatologist approaches gout systematically—confirming the diagnosis, treating the acute attack effective...
19/07/2026

A consultant rheumatologist approaches gout systematically—confirming the diagnosis, treating the acute attack effectively, identifying the cause of hyperuricemia, and preventing future flares.
1. Confirm the diagnosis
History
Sudden onset of severe pain (often overnight)
Red, hot, swollen joint
First MTP joint (podagra) is classic
Previous attacks
Alcohol intake, red meat, seafood, fructose-rich drinks
Drugs: thiazides, loop diuretics, low-dose aspirin
CKD, hypertension, diabetes, obesity, metabolic syndrome
Family history
Examination
Warm, erythematous, exquisitely tender joint
Monoarthritis is most common
Look for:
Tophi (ears, elbows, fingers, Achilles tendon)
Polyarticular involvement in chronic disease
Fever (consider septic arthritis)
2. Exclude septic arthritis (most important differential)
If there is:
Fever
Immunocompromised patient
Prosthetic joint
First attack with marked inflammation
Diagnostic uncertainty
→ Perform urgent joint aspiration before assuming gout.
Synovial fluid
Cell count
Gram stain
Culture
Crystal analysis
Monosodium urate crystals
Needle-shaped
Strong negative birefringence under polarized microscopy
This remains the gold standard for diagnosis.
3. Investigations
Blood tests
CBC
ESR/CRP
Serum uric acid
Urea, creatinine, eGFR
LFTs
Blood glucose/HbA1c
Lipid profile
Remember: Serum uric acid can be normal during an acute attack.
Imaging
X-ray (chronic disease)
"Punched-out" erosions with overhanging edges
Ultrasound
Double contour sign
Tophi
Dual-energy CT if diagnosis remains uncertain
4. Treat the acute attack
NSAIDs (if no contraindication)
Examples:
Naproxen 500 mg twice daily
Indomethacin 50 mg three times daily
Etoricoxib 120 mg daily (short course)
Avoid in:
CKD
Peptic ulcer disease
Heart failure
Significant ischemic heart disease (use caution)
Colchicine (best if started within 24 hours)
Low-dose regimen
1.2 mg immediately
Then 0.6 mg after 1 hour
Then 0.6 mg once or twice daily until attack settles
Reduce dose in CKD.
Corticosteroids
Oral:
Prednisolone 30–40 mg daily for 5–7 days (or taper)
Intra-articular steroid:
Excellent for monoarthritis after septic arthritis is excluded.
IL-1 inhibitors
Reserved for refractory or contraindicated cases:
Anakinra
Canakinumab
5. Decide whether urate-lowering therapy (ULT) is indicated
Indications:
≥2 attacks/year
Tophi
CKD stage ≥3
Uric acid stones
Radiographic damage
Very high serum urate (>9 mg/dL)
6. Long-term urate-lowering therapy
First line: Allopurinol
Start low:
100 mg/day
50 mg/day if CKD
Increase every 2–5 weeks
Target serum urate:

Management of knee osteoarthritis (OA) depends on the severity of symptoms, functional limitation, comorbidities, and ra...
14/07/2026

Management of knee osteoarthritis (OA) depends on the severity of symptoms, functional limitation, comorbidities, and radiographic changes. Most patients benefit from a combination of non-pharmacological and pharmacological treatment.
1. Non-pharmacological management (First-line for all patients)
Patient education about the chronic nature of OA.
Weight reduction if overweight (even 5–10% weight loss significantly improves symptoms).
Exercise therapy
Quadriceps strengthening
Range-of-motion exercises
Low-impact aerobic exercise (walking, cycling, swimming)
Physiotherapy
Knee brace or patellar taping (selected patients)
Walking aids (cane in the opposite hand if needed)
Avoid prolonged squatting, kneeling, and stair climbing where possible.
2. Pharmacological management
A. Topical therapy (preferred for mild to moderate OA)
Topical NSAIDs (e.g., diclofenac gel) 3–4 times daily
Capsaicin cream (less commonly used)
B. Oral analgesics
Paracetamol
500–1000 mg every 6–8 hours as needed
Maximum 3 g/day in older adults
NSAIDs (if no contraindications)
Naproxen
Celecoxib
Diclofenac
Etoricoxib
Lowest effective dose for the shortest duration
Consider a proton pump inhibitor (PPI) in high-risk patients
C. Duloxetine
Useful if chronic pain persists despite NSAIDs or if central pain sensitization is suspected.
Start 30 mg daily, increase to 60 mg daily if tolerated.
D. Intra-articular injections
Corticosteroid injection
Good for acute flare with effusion
Provides relief for several weeks
Avoid frequent injections (generally no more than 3–4/year)
Hyaluronic acid
May benefit selected patients, though evidence is mixed.
3. Supplements
Chondroitin sulfate
Some patients report symptom relief, but evidence is mixed.
Glucosamine
Routine use is not recommended by many international guidelines because benefits are inconsistent.
4. Advanced disease
Refer to orthopedics when:
Severe pain despite optimal medical treatment
Significant limitation of daily activities
Marked deformity
Advanced radiographic OA
Options include:
Osteotomy (selected younger patients)
Unicompartmental knee replacement
Total knee replacement (TKR)
Suggested stepwise approach for a GP
Lifestyle modification + exercise + weight loss.
Topical diclofenac gel.
Add oral NSAID (if appropriate) ± PPI.
Consider duloxetine for persistent chronic pain.
Intra-articular corticosteroid injection for painful flares.
Refer for orthopedic evaluation if symptoms remain disabling.
Red flags requiring further evaluation
Fever with a hot, swollen joint (consider septic arthritis)
Rapid onset of severe swelling (crystal arthritis or infection)
Significant trauma
Night pain or unexplained weight loss (consider malignancy)
For a typical adult with symptomatic knee OA and no contraindications, a practical regimen is:
Quadriceps strengthening exercises daily
Weight reduction if overweight
Topical diclofenac gel 3–4 times/day
Naproxen 250–500 mg twice daily (or celecoxib 200 mg/day if GI risk is a concern) with a PPI when indicated
Consider chondroitin sulfate 800–1200 mg/day for a trial of 3–6 months, stopping if there is no meaningful improvement.

25/06/2026
✅ Correct Answer: D. Ramsay Hunt Syndrome💡 Why this is correct:• Severe ear pain (otalgia) with a vesicular rash on the ...
25/06/2026

✅ Correct Answer: D. Ramsay Hunt Syndrome

💡 Why this is correct:

• Severe ear pain (otalgia) with a vesicular rash on the external ear is classic for herpes zoster oticus.
• Ipsilateral facial weakness/paralysis indicates involvement of the facial nerve (CN VII).
• Ramsay Hunt syndrome results from reactivation of Varicella-Zoster Virus (VZV) in the geniculate ganglion.
• The triad of ear pain + vesicular ear rash + facial palsy is highly characteristic.

❌ Why not the others?

A. Bell's Palsy
• Causes acute facial nerve palsy but does not produce vesicular lesions of the ear.

B. Otitis Media
• May cause ear pain and fever but does not typically present with vesicular rash and facial paralysis.

C. Cellulitis
• Causes diffuse skin redness, warmth, and swelling rather than grouped vesicular lesions with facial nerve involvement.

🔥 Exam Pearl

🧠 Painful vesicular rash on the ear + ipsilateral facial paralysis = Ramsay Hunt Syndrome (Herpes Zoster Oticus).

✅ Correct Answer: D. Campylobacter enteritis💡 Why this is correct:• Fever + bloody diarrhea + abdominal pain/tenderness ...
23/06/2026

✅ Correct Answer: D. Campylobacter enteritis

💡 Why this is correct:

• Fever + bloody diarrhea + abdominal pain/tenderness are classic features of Campylobacter jejuni infection.
• Often associated with outdoor activities, contaminated water, or undercooked poultry during camping trips.
• Causes inflammatory diarrhea that may be bloody.

❌ Why not the others?

A. Cholera – Causes profuse watery "rice-water" diarrhea, not bloody diarrhea.

B. Viral gastroenteritis – Usually causes watery diarrhea and vomiting, rarely bloody stools.

C. IBS – Does not cause fever or bloody diarrhea.

🔥 Exam Pearl

🧠 Camping trip + fever + bloody diarrhea + abdominal cramps/tenderness = Campylobacter enteritis.

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