17.07.25

1. Patient education about OA as a chronic degenerative condition
2. Encourage weight loss if overweight
3. Begin physical therapy to strengthen muscles around the joint
4. Advise on activity modification and joint protection

• Initiate topical or oral NSAIDs (consider GI/cardiac/renal risk)
• Consider paracetamol if NSAIDs are contraindicated
• Use assistive devices (e.g., cane, brace)
• Consider intra-articular corticosteroid injection for flares

• Refer to orthopedic surgery for joint evaluation (e.g., knee or hip replacement)

The most likely mechanism of osteoarthritis (OA) involves mechanical and biochemical cartilage breakdown. Key processes include:

1. Mechanical Stress & Joint Overload: Repetitive use, obesity, or joint misalignment leads to excess load on the cartilage.
2. Cartilage Matrix Degradation: Chondrocytes respond to stress by producing matrix metalloproteinases (MMPs) and aggrecanases, which degrade collagen and proteoglycans.
3. Failed Repair Response: The cartilage attempts to regenerate, but the repair is imperfect and inefficient, leading to fibrillation, softening, and loss of cartilage.
4. Subchondral Bone Remodeling: As cartilage thins, subchondral bone thickens and becomes sclerotic, with osteophytes forming at joint margins.
5. Low-grade Synovial Inflammation: Cartilage debris triggers a mild inflammatory response in the synovium, worsening joint damage.

Osteoarthritis is primarily a mechanical wear-and-tear disease, amplified by a failed chondrocyte repair response, leading to:

• Progressive cartilage loss
• Subchondral bone changes
• Low-grade inflammation

Obesity is a major risk factor for knee and hip osteoarthritis due to mechanical overload and the presence of inflammatory adipokines.

Certain occupations that involve repetitive joint use or heavy physical labor, such as farming or mining, increase the risk of developing osteoarthritis.

Muscle weakness, particularly around the quadriceps, leads to poor joint support, increasing the risk of osteoarthritis.

Physical inactivity contributes to weaker muscles and joint stiffness, which can increase the risk of osteoarthritis.

Metabolic syndrome and diabetes are associated with systemic low-grade inflammation and cartilage degradation, increasing the risk of osteoarthritis.

Chronic joint pain is a complication of osteoarthritis that leads to persistent pain, especially with activity, which limits mobility.

• Bony overgrowth and misalignment (e.g. varus/valgus knee)
• Reduced range of motion due to cartilage loss and osteophyte formation
• Joint instability caused by weak muscles and ligament damage
• Muscle wasting (disuse atrophy) from inactivity or pain-avoidance behavior
• Gait abnormalities due to pain and joint damage (e.g. limping, use of cane)

• Disability: Difficulty performing daily activities (e.g. stairs, dressing)
• Loss of independence: Particularly in elderly patients with bilateral hip or knee OA
• Social isolation: Resulting from limited mobility and chronic pain
• Depression/anxiety: Common in patients experiencing chronic pain and functional decline

• GI bleeding
• Peptic ulcers
• Kidney injury
• Cardiovascular risk

• Risk of joint infection
• Cartilage damage if overused

• Infection
• Thrombosis
• Prosthesis failure
• Revision surgery

• Worsening of coexisting conditions (e.g. diabetes, hypertension due to inactivity)
• Falls and fractures due to reduced balance and joint instability
• Secondary osteoarthritis in other joints due to compensation

The main goals of therapy for Osteoarthritis (OA) are to relieve pain, improve function, slow progression, and enhance quality of life.

The first-line therapy recommended for managing Osteoarthritis is Non-Pharmacologic Therapy, which includes interventions such as:

1. Weight loss - Reduces joint load (especially knees/hips) and pain.
2. Physical therapy / Exercise - Strengthens muscles, improves mobility and stability.
3. Patient education - Improves adherence and empowers self-care.
4. Occupational therapy - Teaches joint protection techniques and assistive device training.
5. Assistive devices - Includes cane, walker, knee brace to reduce joint stress.

Weight loss in the management of Osteoarthritis has the following benefits:

• Reduces joint load, particularly in the knees and hips.
• Decreases pain associated with joint stress.

Physical therapy contributes to the management of Osteoarthritis by:

• Strengthening muscles around the affected joints.
• Improving mobility and stability, which can help reduce pain and enhance function.

Patient education plays a crucial role in the management of Osteoarthritis by:

• Improving adherence to treatment plans.
• Empowering self-care, allowing patients to take an active role in their management.

The purpose of occupational therapy in Osteoarthritis management is to:

• Teach joint protection techniques.
• Provide assistive device training to help patients manage daily activities while minimizing joint stress.

Recommended assistive devices for Osteoarthritis patients include:

• Cane
• Walker
• Knee brace These devices help to reduce joint stress and improve mobility.

Topical NSAIDs (e.g., diclofenac gel) are the first-line treatment for knee and hand osteoarthritis due to their fewer systemic effects.

Total joint replacement is indicated for severe osteoarthritis with intractable pain and disability.

Duloxetine is used for chronic osteoarthritis pain, especially when there is a central pain component.

Intra-articular corticosteroid injections provide short-term pain relief during severe flares.

Glucosamine/chondroitin is not recommended due to conflicting evidence, and long-term opioids should be avoided due to dependence and side effects.

The core criteria for diagnosing Osteoarthritis include:

History:

• Joint pain that worsens with activity and improves with rest
• Morning stiffness lasting less than 30 minutes
• Gradual onset of symptoms
• Joint-specific pain, commonly in the knee, hip, hands, or spine

Physical Exam:

• Tenderness over the joint line
• Bony enlargement, such as Heberden's and Bouchard's nodes in the hands
• Crepitus with movement
• Reduced range of motion
• Absence of systemic inflammation (no fever, weight loss, or marked swelling)

The typical X-ray findings for Osteoarthritis include:

1. Joint space narrowing (asymmetric)
2. Osteophyte formation
3. Subchondral sclerosis
4. Subchondral cysts

Optional tests to exclude other diseases in Osteoarthritis include:

• Blood tests (usually normal in OA):

  • ESR, CRP → Normal (used to rule out RA, gout, etc.)
  • Rheumatoid factor (RF), anti-CCP → Negative

• Synovial fluid analysis (if joint effusion or atypical presentation):

  • Non-inflammatory profile:
    • WBC < 2,000/mm³
    • Clear/yellow fluid
    • No crystals or bacteria

The severity of findings on X-ray does not always match the severity of symptoms in Osteoarthritis, indicating that radiographic changes may not correlate directly with the patient's experience of pain or dysfunction.

The ACR clinical criteria for Hand Osteoarthritis require 3 out of the following 4 criteria:

1. Hard tissue enlargement of ≥2 of 10 selected joints
2. Hard tissue enlargement of ≥2 DIP joints
3. Fewer than 3 swollen MCP joints
4. Deformity of at least 1 selected joint

An acute adrenal crisis (or Addisonian crisis) is a life-threatening emergency caused by a severe deficiency of cortisol, and sometimes aldosterone. It can result from primary, secondary, or tertiary adrenal insufficiency, leading to hemodynamic instability and metabolic derangements.

In primary adrenal insufficiency (Addison's disease), the adrenal cortex fails, resulting in:

• Decreased cortisol
• Decreased aldosterone

In secondary adrenal insufficiency, the pituitary gland fails, leading to:

• Decreased ACTH
• Decreased cortisol (with aldosterone usually remaining normal)

In tertiary adrenal insufficiency, there is hypothalamic dysfunction leading to decreased CRH (Corticotropin-Releasing Hormone), which results in decreased ACTH (Adrenocorticotropic Hormone) and subsequently decreased cortisol levels.

Common triggers for adrenal crisis include:

1. Infection (most common)
2. Trauma or surgery
3. Sudden withdrawal of steroids
4. Gastrointestinal illness with vomiting or diarrhea leading to volume depletion
5. Acute illness in individuals with undiagnosed adrenal insufficiency

Laboratory findings indicative of adrenal insufficiency include:

• Decreased serum cortisol
• Increased ACTH in primary adrenal insufficiency, decreased ACTH in secondary/tertiary adrenal insufficiency
• Hyponatremia and hyperkalemia (only in primary)
• Hypoglycemia
• Metabolic acidosis
• Pre-renal acute kidney injury (increased urea/creatinine)
• Eosinophilia

The clinical signs include hypotension, vomiting, abdominal pain, and a history of steroid use or known adrenal insufficiency (AI).

Baseline labs should include cortisol, ACTH, glucose, and electrolytes.

Immediate management includes:

1. IV Hydrocortisone: 100 mg IV bolus, then 200 mg/24h (continuous or q6h)
2. IV Fluids: NSS 1-3 liters within the first few hours
3. Correct hypoglycemia: Administer dextrose if needed.

Supportive measures include:

• Treating the precipitating illness (e.g., administering antibiotics)
• Correcting electrolyte imbalances.

Monitoring should include blood pressure, glucose levels, electrolytes, and urine output.

Preventive measures include:

• Educating patients on stress-dose steroids
• Providing a steroid card or medical alert bracelet
• Avoiding abrupt withdrawal of corticosteroids.

1. Give IV Hydrocortisone Immediately:

   • Hydrocortisone 100 mg IV bolus
   • Then continuous infusion of 200 mg over 24 hours or 50 mg IV every 6 hours

2. Start IV Fluids Immediately:

   • Normal Saline (0.9% NaCl) rapid infusion (1-3 L in first few hours)
   • Add 5% dextrose if hypoglycemia is present

3. Draw Labs Before Steroids (if possible):

   • Serum cortisol
   • ACTH level
   • Electrolytes, glucose, BUN/creatinine, CBC
   • Blood cultures (if infection suspected)

4. Correct Hypoglycemia (if present):

   • Dextrose 50% (D50) IV push, then D5NS

5. Identify and Treat the Underlying Cause:

   • E.g., antibiotics for infection, surgery for trauma

6. Monitor Closely:

   • BP, heart rate, electrolytes, glucose, mental status, urine output

The core mechanism is an acute deficiency of cortisol (± aldosterone) during stress.

Mechanism: Destruction of the adrenal cortex leading to decreased cortisol and aldosterone production.

Common causes:

• Autoimmune conditions
• Tuberculosis (TB)
• Metastases
• Adrenal hemorrhage

Result:

• Decreased cortisol results in poor stress response, hypotension, and hypoglycemia.
• Decreased aldosterone leads to sodium loss, potassium retention, resulting in hyponatremia, hyperkalemia, and hypovolemia.

Mechanism: Pituitary failure results in decreased ACTH, leading to decreased cortisol production while aldosterone remains intact.

Common causes:

• Pituitary tumors
• Sheehan syndrome
• Chronic steroid use

Result:

• Cortisol deficiency only, leading to hypotension, weakness, and hypoglycemia.
• No hyperkalemia since aldosterone levels are normal.

Mechanism: Hypothalamic failure or sudden steroid withdrawal leads to decreased CRH, which results in decreased ACTH and subsequently decreased cortisol production.

Common cause: Chronic steroid therapy with abrupt cessation.

Result: Same as secondary adrenal insufficiency: cortisol deficiency without any aldosterone problem.

The primary consequences include:

• Hypotension
• Electrolyte imbalance
• Hypoglycemia
• Shock

These conditions worsen under physiological stress when cortisol demand increases and the body cannot mount a response.

The risk factors for acute adrenal crisis include:

• Underlying adrenal insufficiency
• Sudden withdrawal of steroids
• Increased physiological stress

The major risk factors for adrenal insufficiency include:

1. Known Adrenal Insufficiency:

   • Primary AI (Addison's disease) due to autoimmune destruction, TB, HIV, or metastatic cancer.
   • Secondary AI caused by pituitary adenoma or Sheehan syndrome.
   • Tertiary AI from chronic exogenous steroid use with abrupt withdrawal.

2. Glucocorticoid Use:

   • Sudden discontinuation of corticosteroids after prolonged therapy.
   • Inadequate "stress-dose" steroids during illness or surgery.

3. Severe Physiological Stress:

   • Infection (especially sepsis, pneumonia, UTI, gastroenteritis).
   • Surgery or trauma.
   • Major burns.
   • Dehydration, vomiting, diarrhea leading to volume depletion.

4. Adrenal Damage or Bleeding:

   • Adrenal hemorrhage (e.g., Waterhouse-Friderichsen syndrome).
   • Bilateral adrenalectomy.
   • Infiltrative disease (e.g., amyloidosis, metastases).

Acute adrenal crisis is a medical emergency that can lead to severe complications and death if not recognized and treated promptly.

Hypovolemic shock is a condition caused by aldosterone and cortisol deficiency leading to sodium and water loss, resulting in hypotension. If not rapidly corrected, it can progress to multi-organ failure.

Severe electrolyte imbalances can lead to:

• Hyponatremia: confusion, seizures, coma
• Hyperkalemia: life-threatening arrhythmias
• Hypoglycemia: seizures, altered mental status, coma

Acute kidney injury (AKI) can occur from volume depletion and hypotension, leading to either pre-renal AKI or ischemic acute tubular necrosis (ATN).

A hypoglycemic crisis is a severe drop in blood sugar levels that can lead to loss of consciousness or seizures. It is especially common in children or patients with infection or fasting.

Cardiac arrhythmias can occur as a secondary effect of electrolyte disturbances, particularly due to hyperkalemia and acidosis, which can be life-threatening.

Neurological complications can include confusion, delirium, lethargy, or coma. These complications may arise due to conditions such as hypoglycemia, hyponatremia, or hypotension-related cerebral hypoperfusion.

Secondary infections can occur in an immunosuppressed state, particularly if the patient is under-treated. These infections can worsen or trigger another adrenal crisis.

If untreated or misdiagnosed, an adrenal crisis can rapidly progress to refractory shock and death, especially in vulnerable populations such as the elderly, septic, or surgical patients.

Long-term complications from recurrent adrenal crises may include:

1. Cognitive impairment (from repeated hypoglycemia or hyponatremia)
2. Reduced quality of life
3. Adrenal atrophy (with prolonged exogenous steroids)
4. Dependence on lifelong steroid replacement

Hydrocortisone is the drug of choice because it has both glucocorticoid and some mineralocorticoid activity.

1. Hydrocortisone 100 mg IV bolus immediately.

2. Then 200 mg IV over 24 hours, either:

   • Continuous IV infusion, or
   • 50 mg IV every 6 hours.

Switch to oral hydrocortisone (e.g., 20 mg in the morning + 10 mg in the afternoon) once the patient stabilizes and can tolerate PO.

• Normal Saline (0.9% NaCl) — 1–3 L in the first 24 hours to rapidly correct hypotension and volume depletion.

Administer 50 mL of D50 IV push followed by a D5NS infusion if hypoglycemia is present.

Monitor and treat hyperkalemia, hyponatremia, and metabolic acidosis.

Treat underlying causes with:

1. Antibiotics for infection
2. Surgery for hemorrhage or trauma
3. GI care for vomiting/diarrhea

Monitor the following parameters:

• Vitals (BP, HR)
• Urine output
• Glucose and electrolytes (Na+, K+)
• Mental status
• Daily weight and fluid balance

Maintenance therapy includes:

• Hydrocortisone: 15-25 mg/day orally, split doses
• Fludrocortisone: 0.05-0.2 mg/day if primary adrenal insufficiency is present

During stress situations such as fever, surgery, or trauma, the steroid dose should be increased:

• Double or triple the maintenance dose as needed

Acute adrenal crisis is a clinical diagnosis that requires immediate treatment. Diagnosis should not be delayed to confirm it. However, once stabilized, underlying adrenal insufficiency can be confirmed through lab tests.

The essential first step is clinical suspicion. Diagnosis is suspected in any patient with symptoms indicative of adrenal crisis.

• Hypotension unresponsive to fluids
• Nausea, vomiting, abdominal pain
• Hyponatremia, hyperkalemia, hypoglycemia
• History of adrenal insufficiency or steroid use
• Stressful triggers such as infection, surgery, or trauma

• Serum Cortisol:

  • <3 µg/dL (83 nmol/L) → strongly suggests adrenal insufficiency

  • 18 µg/dL (500 nmol/L) → unlikely adrenal insufficiency

• Plasma ACTH:

  • ↑ ACTH + low cortisol → Primary adrenal insufficiency
  • ↓ ACTH + low cortisol → Secondary or tertiary adrenal insufficiency

• Electrolytes: Hyponatremia, hyperkalemia (in primary)

• Glucose: Low

• Urea/Creatinine: May be elevated due to dehydration

• CBC: May show eosinophilia

• Blood cultures: If sepsis is suspected

• The ACTH (Cosyntropin) Stimulation Test is the gold standard for diagnosing adrenal insufficiency but is not used in acute settings to avoid delaying treatment.

How it works:

1. Administer 250 µg synthetic ACTH IV/IM.
2. Measure serum cortisol at 0, 30, and 60 minutes.

Interpretation:

• Normal response: cortisol rises to >18-20 µg/dL (500-550 nmol/L)

A blunted or absent rise in cortisol levels confirms adrenal insufficiency.

Starting hydrocortisone immediately is crucial because delaying treatment for lab confirmation can be life-threatening in cases of adrenal crisis.

Testing for adrenal insufficiency should be performed after stabilization, or blood should be drawn before steroid administration if feasible.

Osteoarthritis is a chronic, progressive degenerative joint disease characterized by the breakdown of articular cartilage, subchondral bone remodeling, and synovial inflammation, leading to joint pain, stiffness, and functional limitation.

• Most common form of arthritis
• Affects >10% of people over age 60
• More common in females (especially after menopause)
• Commonly affects: knees, hips, hands, and spine

• Cartilage degradation due to mechanical stress and biochemical factors (cytokines like IL-1, TNF-alpha)
• Subchondral bone sclerosis and osteophyte formation
• Synovial inflammation (low-grade)
• Joint space narrowing on imaging
• Unlike RA, it is non-inflammatory (or mildly inflammatory)

The modifiable risk factors for osteoarthritis include:

1. Obesity: Increases mechanical load on joints.
2. Joint overuse/trauma: Repetitive stress or injury can lead to osteoarthritis.
3. Sedentary lifestyle: Lack of physical activity can contribute to joint issues.
4. Muscle weakness: Weak muscles can lead to joint instability and increased risk.

The clinical features of osteoarthritis include:

• Joint pain: Worsens with activity and improves with rest.
• Morning stiffness: Lasts less than 30 minutes.
• Crepitus: A grinding sensation in the joints.
• Decreased range of motion: Limited movement in affected joints.
• Bony enlargement: Includes Heberden's nodes (DIP) and Bouchard's nodes (PIP).
• Asymmetry: Symptoms are usually asymmetric between joints.

In osteoarthritis, laboratory findings are typically normal, including:

• Inflammatory markers: CRP and ESR are usually normal.
• Synovial fluid analysis: Non-inflammatory with WBC count less than 2,000/mm³.

The key X-ray findings that indicate osteoarthritis include:

• Joint space narrowing
• Osteophytes (bone spurs)
• Subchondral sclerosis
• Subchondral cysts

The first-line non-pharmacologic management strategies for osteoarthritis include:

1. Weight loss
2. Physical therapy / exercise
3. Assistive devices (e.g. cane)
4. Patient education

The first-line pharmacologic treatments for hand and knee osteoarthritis include:

• Topical NSAIDs
• Oral NSAIDs (e.g. ibuprofen, naproxen)
• Paracetamol (less effective, used if NSAIDs are contraindicated)
• Intra-articular corticosteroids (for short-term relief)

• Chronic disability
• Loss of joint function
• Reduced quality of life
• Dependency on pain medications

The next step in management for osteoarthritis (OA) depends on the stage of disease and current symptoms. A stepwise approach should be followed based on the patient's specific condition.