Anaphylaxis

Also known as: Anaphylactic shock, Severe allergic reaction

Acute, severe, potentially life-threatening systemic hypersensitivity reaction (typically IgE-mediated, type I hypersensitivity), causing widespread mast cell/basophil degranulation with release of histamine and other mediators, resulting in vasodilation, increased vascular permeability, bronchospasm, and smooth muscle contraction.

Onset typically within minutes to 2 hours of exposure (faster with IV/parenteral triggers, slower with oral).

Common triggers: foods (peanuts, tree nuts, shellfish, eggs, milk), drugs (antibiotics — especially beta-lactams, NSAIDs, contrast media, neuromuscular blocking agents), insect stings, latex, exercise-induced, idiopathic.

Diagnostic criteria (any ONE of the following, per international consensus):

Acute onset illness (minutes-hours) with skin/mucosal involvement PLUS respiratory compromise OR hypotension/end-organ dysfunction
Two or more of the following occurring rapidly after LIKELY allergen exposure: skin/mucosal involvement, respiratory compromise, hypotension, persistent GI symptoms
Hypotension after exposure to a KNOWN allergen for that patient (even without other features)

Features by system:

Skin/mucosal: urticaria, flushing, pruritus, angioedema (lips, tongue, periorbital)
Respiratory: dyspnea, wheeze, stridor (upper airway edema — ominous sign), hoarseness, throat tightness, chest tightness
Cardiovascular: hypotension, tachycardia, dizziness, syncope, collapse
GI: nausea, vomiting, abdominal cramping, diarrhea
Sense of impending doom, anxiety
Biphasic reaction risk: recurrence of symptoms hours after apparent resolution (typically within 8-12 hours, rarely up to 72h) without re-exposure — necessitates observation period

Primarily clinical, based on rapid symptom onset and pattern following exposure — treatment must NOT be delayed for confirmatory testing.

Serum tryptase: can support retrospective diagnosis if drawn appropriately timed (ideally within 1-2 hours of symptom onset, second sample at baseline/24h for comparison) — most useful when diagnosis uncertain or for allergy referral, not needed to guide acute treatment
Post-event allergy workup (NOT acute phase): skin prick testing, specific IgE testing, referral to allergy/immunology

Differentials: vasovagal syncope (pallor, bradycardia rather than tachycardia, no urticaria/respiratory symptoms), asthma exacerbation alone, panic attack, scombroid poisoning, hereditary angioedema (no urticaria, doesn't respond to adrenaline/antihistamines).

Adrenaline (epinephrine) IM is the first-line, life-saving treatment — give IMMEDIATELY, do not delay for IV access or further assessment.

IM adrenaline 1:1000, anterolateral thigh:

Adult: 0.5mg (0.5mL of 1:1000)
Child 6-12 years: 0.3mg
Child 6 months-6 years: 0.15mg
Auto-injector doses: 0.3mg adult, 0.15mg pediatric

Repeat every 5 minutes if no improvement — most patients respond to 1-2 doses
Do NOT delay adrenaline for antihistamines/steroids — these are adjuncts only, not substitutes

Concurrent management:

Remove/stop trigger if identifiable and ongoing
Position: lie flat with legs elevated unless respiratory distress makes this intolerable — avoid sudden standing/sitting (risk of cardiovascular collapse)
High-flow oxygen
IV access, large-bore — IV fluid bolus (crystalloid 500-1000mL rapidly, repeat as needed) for hypotension not responding to adrenaline alone
Continuous monitoring: ECG, BP, SpO2

Refractory anaphylaxis (not responding to 2-3 IM adrenaline doses):

IV adrenaline infusion (dilute, titrated carefully — specialist/critical care setting)
Additional IV fluid boluses
Nebulized bronchodilators for persistent bronchospasm
Nebulized adrenaline for upper airway edema/stridor as an adjunct
Consider glucagon 1-2mg IV/IM if patient on beta-blockers
Early anesthetic/airway team involvement if any stridor — low threshold for early intubation before edema progresses

Adjunct therapy (secondary, do not delay adrenaline for these):

Antihistamine: for cutaneous symptom relief only, no effect on airway/cardiovascular compromise
Corticosteroid: evidence for preventing biphasic reaction is weak, but remains commonly used adjunctively

Observation: minimum 6-8 hours post-resolution for most reactions, extend to 24 hours for severe reactions, refractory/biphasic course, asthma history, or poor access to emergency care.

Discharge planning (essential, often overlooked): prescribe adrenaline auto-injector (2 devices) with training, written anaphylaxis action plan, allergy/immunology referral, medical alert bracelet, avoidance advice.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Osteoarthritis

Degenerative joint disease characterized by progressive cartilage loss, subchondral bone remodeling, osteophyte formation, and low-grade synovial inflammation, resulting from an imbalance between cartilage breakdown and repair. Most common form of arthritis, leading cause of disability in older adults.

Risk factors: age, obesity (mechanical load + metabolic/inflammatory contribution), female sex, joint malalignment, previous joint injury/trauma, occupational/repetitive joint loading, genetic predisposition, prior inflammatory arthritis.

Classified by:

Primary (idiopathic): no identifiable underlying cause, associated with aging/wear
Secondary: due to identifiable cause ; post-traumatic, inflammatory arthritis sequelae, metabolic (hemochromatosis, ochronosis), congenital/developmental joint abnormality, avascular necrosis
Commonly affected joints: knees, hips, hands (DIP/PIP joints, first CMC joint), spine (facet joints), first MTP joint

Joint pain: mechanical pattern ; worse with activity/weight-bearing, relieved by rest (distinguishes from inflammatory arthritis where rest worsens/morning stiffness prolonged)
Morning stiffness: typically brief, <30 minutes (contrast with rheumatoid arthritis where morning stiffness >1 hour is characteristic)
Reduced range of motion, crepitus on joint movement
Joint examination findings:
Bony swelling/enlargement (not soft/boggy synovitis as in inflammatory arthritis)
Heberden's nodes (DIP joints), Bouchard's nodes (PIP joints) ; hand OA
Fixed flexion deformity, varus/valgus deformity (knee OA)
Reduced internal rotation (early sign, hip OA)
Mild joint effusion possible but marked warmth/erythema atypical (suggests alternative/superimposed inflammatory process, e.g., crystal arthropathy)
Functional impact: difficulty with stairs, walking distance, rising from chairs, fine motor tasks (hand OA)
Progressive course, though pain severity does not always correlate with radiographic severity

Primarily clinical for typical presentation (age >45, activity-related pain, no/brief morning stiffness); imaging not always required to confirm diagnosis in classic cases (per NICE clinical diagnosis criteria).

Plain radiographs (weight-bearing views for knee/hip): joint space narrowing, osteophytes, subchondral sclerosis, subchondral cysts; classic findings but severity doesn't always correlate with symptoms; useful to exclude other pathology or when diagnosis uncertain, or pre-surgical planning
Blood tests: NOT required for diagnosis, generally normal (ESR/CRP normal or mildly elevated) ; used to exclude inflammatory arthritis if diagnostic uncertainty (rheumatoid factor, anti-CCP, ANA if inflammatory features present)
Joint aspiration: if effusion present and diagnostic uncertainty : synovial fluid analysis (non-inflammatory, WCC <2000/mm³ typical in OA) helps exclude septic arthritis, crystal arthropathy (gout, pseudogout)
MRI: not routine, reserved for specific indications (suspected meniscal/ligamentous injury, avascular necrosis, atypical presentation)

Differentials: rheumatoid arthritis and other inflammatory arthropathies (prolonged morning stiffness, symmetric small joint involvement, systemic symptoms, elevated inflammatory markers), gout/pseudogout (acute, monoarticular, marked erythema/warmth), septic arthritis (acute, hot, systemically unwell — exclude urgently if acute monoarticular presentation), avascular necrosis, referred pain (hip OA can present as knee pain).

Core/first-line (all patients):

Patient education: nature of condition, self-management expectations
Weight loss if overweight/obese (significant impact on symptom burden and disease progression, especially weight-bearing joints)
Exercise: strengthening (particularly quadriceps for knee OA) and aerobic exercise ; improves pain and function, does NOT accelerate joint damage (address common patient misconception)
Physiotherapy referral for individualized exercise program, gait aids assessment (cane, walking aids)

Pharmacological (symptom control, does not modify disease progression):

Topical NSAIDs (diclofenac gel); first-line for knee/hand OA, particularly favored in older patients (fewer systemic effects)
Oral NSAIDs: first-line if topical insufficient ; use lowest effective dose, shortest duration, with gastroprotection (PPI co-prescription) if risk factors (age, GI history, concurrent anticoagulant/steroid); caution in cardiovascular disease, renal impairment
Paracetamol: modest efficacy alone per current evidence, may be used as adjunct but no longer considered strongly effective as monotherapy in current guidelines
Topical capsaicin: adjunct option for localized joint pain
Intra-articular corticosteroid injection: short-term symptom relief (weeks-months) for flares, particularly knee OA ; avoid frequent repeated injections (cartilage toxicity concern with excessive use)
Intra-articular hyaluronic acid: evidence mixed/weak, not routinely recommended by major guidelines (e.g., NICE, AAOS) though used in some practice
Duloxetine: option for chronic OA pain, particularly with central sensitization component
Opioids: NOT recommended for routine use given poor risk-benefit in chronic non-cancer pain ; reserved for short-term severe flares awaiting definitive treatment, avoid long-term use

Surgical management (for severe disease refractory to conservative management, significant functional limitation/quality of life impact):

Joint replacement (arthroplasty) ; knee/hip most common, highly effective for pain relief and function restoration
Osteotomy: selected younger patients with malalignment, joint-preserving option
Arthroscopic debridement/meniscectomy: limited role, not recommended for pure OA management (evidence does not support benefit over sham/conservative management in absence of mechanical locking symptoms)

Referral: orthopedics for surgical assessment when conservative management fails and significant functional impairment/pain persists; rheumatology if diagnostic uncertainty or inflammatory features present.

Anaphylaxis

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management