Myalgia (Muscle Pain): Complete Clinical Guide — Causes, Types & Treatment

Myalgia (Muscle Pain) — Complete Clinical Guide (Definition, Pathogenesis, Tests, Medicines with Dosing, Nutrition, Rehab, Prognosis)

Myalgia (Muscle Pain) — Complete Clinical Guide

Full clinical coverage: differential diagnosis, detailed investigations, medicine dosing (adult & pediatric), rehabilitation, nutrition, prevention, and linked resources for deeper reading.

Contents — Jump to

  1. Definition & classification
  2. Epidemiology & clinical significance
  3. Causes (detailed)
  4. Pathogenesis & pathology
  5. Clinical features & red flags
  6. Differential diagnosis & important mimics
  7. Investigations — bedside, lab, imaging, special tests
  8. Management — algorithmic & medicines with dosing
  9. Inflammatory myopathies & immunosuppressive therapy
  10. Rehabilitation & physiotherapy
  11. Nutrition & supplements
  12. Complications, prognosis & follow-up
  13. When to refer / red flags
  14. Internal links — related posts
  15. References & disclaimer

Definition & classification

Myalgia = subjective muscle pain. It is a symptom, not a diagnosis. It can be classified by duration (acute < 2–4 weeks; subacute 4–12 weeks; chronic >12 weeks), distribution (localized vs generalized), and mechanism (inflammatory, metabolic, infectious, drug-induced, traumatic).

Note: Myalgia may coexist with true muscle weakness — always document whether weakness (objective) is present, because that differentiates neuropathic/neuromuscular pathology from simple muscle pain.

Epidemiology & clinical importance

Myalgia is extremely common: seen in viral illnesses (influenza, COVID-19), statin therapy adverse effects, electrolyte disturbances, and systemic inflammatory disorders. While most cases are benign and self-limiting, some indicate serious disease (rhabdomyolysis, polymyositis, dermatomyositis, electrolyte emergencies) and require urgent work-up.

Causes — comprehensive list with examples

1. Infectious

  • Viral: Influenza, COVID-19, Dengue, Enteroviruses, HIV seroconversion.
  • Bacterial: Sepsis-related myalgias, pyomyositis (Staph aureus), Lyme disease.
  • Parasitic: Trichinosis, malaria (with myositis).

2. Inflammatory / autoimmune

  • Polymyositis, Dermatomyositis, Inclusion body myositis, SLE-associated myositis.

3. Drug & toxin induced

  • Statins (myopathy/rhabdomyolysis), fibrates (esp. with statin combo), colchicine, antimalarials (chloroquine), certain antipsychotics, alcohol, illicit drugs.

4. Metabolic / endocrine

  • Hypothyroidism (myalgic pain, cramps), hypocalcemia (tetany, cramp), hypokalemia (weakness/cramps), vitamin D deficiency.

5. Traumatic / Overuse

  • Delayed onset muscle soreness (DOMS), traumatic tears, compartment syndrome.

6. Neuromuscular junction & neuropathic causes

  • Myasthenia gravis (fatigue > pain), peripheral neuropathies can present with aching pain.

7. Functional / central sensitization

  • Fibromyalgia (widespread myalgia with tender points), chronic fatigue syndrome.

Medication-induced myalgias are common — review drug list (statins, antivirals, immunomodulators). For statin-related muscle symptoms see baseline CK and consider switching agent or dose adjustment.

Pathogenesis & pathology

Pathways for pain generation:

  • Peripheral nociception: muscle injury/inflammation → prostaglandins, bradykinin, cytokines activate nociceptors.
  • Ischemic pain: intracompartmental pressure or vascular insufficiency.
  • Metabolic derangements: electrolyte abnormalities disturb membrane potentials, causing cramps/pain.
  • Immune-mediated: T-cell mediated muscle fiber injury (polymyositis) with MHC upregulation and complement activation (dermatomyositis).

Pathology findings (biopsy/histology)

  • Polymyositis: endomysial lymphocytic infiltrate, fiber necrosis, MHC-I upregulation.
  • Dermatomyositis: perivascular/perimysial inflammation, perifascicular atrophy, complement-mediated microangiopathy.
  • Rhabdomyolysis: muscle fiber necrosis, myoglobin release — risk of acute tubular necrosis.

Clinical features — history & examination

History tips

  • Onset: sudden vs gradual. Relation to exercise, trauma, new drug, infection.
  • Distribution: proximal (shoulder/hip girdle → think inflammatory myopathy) vs distal vs focal (pyomyositis/tennis injury).
  • Systemic symptoms: fever, rashes (heliotrope rash → dermatomyositis), weight loss.
  • Medication history: statins, antivirals, antimalarials, fibrates, steroids.

Examination

  • Inspection: swelling, erythema, rash (Gottron papules, heliotrope).
  • Palpation: focal tenderness, warmth (infective), crepitus (trauma).
  • Power testing: objective weakness (MRC grading) — differentiates myositis from simple myalgia.
  • Neuro exam: reflexes, sensory signs to exclude neuropathy.

Red flags (seek urgent care)

  • Severe muscle pain with dark urine (myoglobinuria) → rhabdomyolysis risk
  • Acute compartment syndrome (severe pain out of proportion, tense swelling)
  • Fever with focal muscle swelling/overlying erythema → pyomyositis/abscess
  • Rapidly progressive weakness, respiratory muscle involvement

Differential diagnosis — brief

  • Fibromyalgia (widespread pain, tender points, normal CK)
  • Polymyalgia rheumatica (older adults: proximal stiffness, elevated ESR)
  • Polymyositis / Dermatomyositis (objective weakness, high CK)
  • Rhabdomyolysis (very high CK, myoglobinuria)
  • Hypothyroid myopathy (TSH high, CK may be moderately elevated)
  • Statin myopathy (temporal relation to statin)

Investigations — algorithm & interpretation

Start with baseline basic tests and escalate guided by red flags.

Immediate / bedside

  • Vitals, pulse oximetry
  • Urine dipstick for blood (if red → check myoglobin & send CK)
  • Point-of-care glucose (hypoglycaemia can mimic weakness)

Laboratory panel

TestWhy & Interpretation
CBCInfection (leucocytosis), anemia contributing to fatigue
CK (Creatine Kinase)Marker of muscle injury — markedly raised in rhabdomyolysis/myositis
CRP, ESRInflammation (elevated in inflammatory myopathies, infection)
Electrolytes (Na, K, Ca, Mg)Electrolyte disturbances cause cramps/weakness (treat promptly)
LFT, RFTAssess hepatic/renal function (important before medications & for rhabdomyolysis management)
Thyroid function tests (TSH, FT4)Hypothyroidism causes myalgic symptoms
Autoimmune serology (ANA, myositis panel, Anti-Jo-1)If suspicion of inflammatory myopathy
Urine myoglobinRhabdomyolysis indicator (may be negative early)
Viral serology (HIV, Hep B/C)If clinical indication

Imaging & speciality tests

  • Chest X-ray/ultrasound if focal infection suspected
  • MRI muscle — sensitive for myositis (muscle edema pattern)
  • Electromyography (EMG) — distinguish neuropathic vs myopathic process
  • Muscle biopsy — gold standard for inflammatory myopathies and certain metabolic myopathies

When to measure CK & how often?

In suspected myositis or rhabdomyolysis: baseline CK and repeat every 6–24 h depending on severity. CK >5–10×ULN suggests significant injury; CK >10,000 U/L raises strong concern for rhabdomyolysis and renal risk.

Management — algorithmic approach

Management depends on cause and severity. Below is a practical stepwise algorithm.

Step 1 — Immediate stabilization

  • Airway/breathing/circulation if severe weakness/respiratory involvement
  • Stop offending drug (e.g., statin) and potential interactants (fibrates, macrolides, azoles)
  • Analgesia and symptomatic care (rest, heat/ice as appropriate)

Step 2 — Investigate & treat reversible causes

  • Correct electrolytes (give calcium gluconate for symptomatic hypocalcemia — see Calcium Gluconate guide)
  • Treat infection — targeted antibiotics for pyomyositis (IV flucloxacillin/cephalosporin) or antivirals for certain conditions if indicated
  • Hydration & urine alkalinization in rhabdomyolysis to protect kidneys

Step 3 — Analgesics & anti-inflammatory therapy (common medicines & dosing)

Below are commonly used medicines with typical adult doses. Adjust for renal/hepatic impairment, age and local guidelines.

DrugTypical Adult DoseComments / Precautions
Paracetamol500–1000 mg PO q6–8h PRN (max 3–4 g/day)Preferred first-line for mild-moderate pain; check liver function for chronic/high-dose use
Ibuprofen200–400 mg PO q6–8h (max 1200–2400 mg/day depending on guideline)GI/renal caution; take with food
Diclofenac50 mg PO BDGI/CV/renal risk — avoid long-term
Topical NSAIDs (diclofenac gel)Apply as per product 3–4 times/dayUseful for localized pain with less systemic exposure
Muscle relaxant (e.g., cyclobenzaprine / tizanidine)Cyclobenzaprine 5–10 mg at night; tizanidine 2–4 mg PRNSedation; avoid with other CNS depressants
Opioids (short-term severe pain)Use as rescue: e.g., tramadol 50–100 mg PRN, or short course of weak opioidUse minimal duration; monitor for dependence
Antihistamine (for allergy-associated symptoms)Chlorpheniramine 4 mg PO q4–6h PRNSedating; caution driving
If signs of severe inflammation (confirmed inflammatory myopathy) — systemic corticosteroids often indicated (see immuno section).

Step 4 — Specific therapy for important conditions

  • Rhabdomyolysis: Aggressive IV fluids (isotonic saline), monitor urine output, serum CK, electrolytes; consider bicarbonate & mannitol in selected cases; urgent nephrology if rising creatinine or hyperkalemia. See emergency protocols.
  • Pyomyositis/Abscess: IV antibiotics (cover Staph aureus; e.g., flucloxacillin/cefazolin) and surgical drainage if abscess.
  • Polymyalgia rheumatica: low-dose oral corticosteroids (e.g., prednisolone 15–20 mg/day) with rheumatology follow-up.
  • Inflammatory myositis: High-dose corticosteroids ± steroid-sparing agents (see below).

Inflammatory myopathies — diagnosis & immunosuppressive therapy

If inflammatory myopathy suspected (proximal weakness, high CK, MRI/EMG & biopsy supportive):

  1. Start high-dose corticosteroids: Prednisolone 0.5–1 mg/kg/day (typical adult 40–60 mg/day) — monitor response and taper gradually.
  2. If severe or steroid-refractory: add steroid-sparing agents — Methotrexate 15–25 mg weekly (with folic acid), Azathioprine 1–3 mg/kg/day, Mycophenolate mofetil 1–2 g/day.
  3. IVIG (2 g/kg divided over 2–5 days) for severe or refractory dermatomyositis or necrotizing autoimmune myopathy.
  4. Biologics (rituximab) occasionally used for refractory cases — specialist care.

Baseline TB/HBV/HCV screening prior to starting potent immunosuppression. Monitor CBC, LFTs, and for drug-specific adverse effects.

Rehabilitation & physiotherapy

Rehab is essential for recovery and prevention of chronicity.

  • Acute phase: relative rest, pain control, avoid aggressive exercises during active inflammation.
  • Recovery phase: graded active exercises, range-of-motion, strengthening (under physio guidance).
  • Pain management techniques: heat, cold packs, TENS, stretching.
  • Occupational therapy for ADL support in severe weakness.

Nutrition & supplements — supportive evidence-based guidance

Nutrition supports healing and reduces complications. Key points:

  • Ensure adequate protein intake (1.0–1.5 g/kg/day) for muscle repair — dietary sources: dairy, eggs, fish, pulses. See detailed protein guide: Protein — role & sources.
  • Correct vitamin D deficiency — test 25-OH D and supplement guided by level.
  • Consider multivitamin support in malnutrition / chronic alcohol use — e.g., Alamin M Forte.
  • Electrolyte repletion: potassium, magnesium and calcium if deficient; symptomatic hypocalcemia treat with IV Calcium Gluconate in emergent cases.
  • Anti-inflammatory dietary components: omega-3 fatty acids (fatty fish, flaxseeds), antioxidants (fruits like guava, banana, anjeer), and phytochemicals (onion/allium benefits: Onion).
Avoid high alcohol intake and extreme fasting during recovery as they impair muscle repair and interact with drugs (eg. acetaminophen, statins).

Complications, prognosis & follow-up

Complications

  • Rhabdomyolysis → Acute kidney injury
  • Chronic disability & contractures (if severe prolonged myositis)
  • Secondary infections (pyomyositis)

Prognosis

Depends on underlying cause: viral/DOMS → excellent recovery; inflammatory myopathies → variable (often chronic but treatable); rhabdomyolysis → recovery if renal complications prevented.

Follow-up schedule (practical)

  • Acute benign myalgia: review in 1–2 weeks if unresolved
  • Elevated CK / suspected myositis: follow CK every 1–2 weeks until trending down; rheumatology referral
  • On immunosuppression: regular CBC, LFT, and specialist monitoring as per agent

When to refer — red flags for specialty care

  • Rapidly progressive weakness / respiratory muscle involvement — refer to neurology/intensive care
  • CK markedly elevated (>5000–10,000 U/L) or myoglobinuria — nephrology consult for rhabdomyolysis
  • Suspected inflammatory myopathy — early rheumatology/neuromuscular referral
  • Focal abscess / pyomyositis — surgical/orthopaedic referral

References & disclaimer

  1. Clinical textbooks: Harrison’s Principles of Internal Medicine; Current Rheumatology and Neurology guidelines.
  2. Guidelines for rhabdomyolysis & inflammatory myopathies (ACR/EULAR guidance).
  3. Local formularies & product labels for dosing and contraindications.

Disclaimer: This page provides educational clinical information. Always individualize treatment and dosing based on patient weight, comorbidity, renal/hepatic function and local protocols. For prescription-level decisions consult specialist guidance.

Author: Mahfooz Ansari — Mahfooz Medical Health • Last updated: 29 Aug 2025

Post a Comment (0)
Previous Post Next Post