NLE Musculoskeletal Nursing — Degenerative, Inflammatory and Metabolic Bone DisordersDetailed Explanation

Osteoarthritis (OA) — Degenerative Joint Disease

Osteoarthritis is the most common form of arthritis and is classified as a DEGENERATIVE, non-inflammatory (or minimally inflammatory) disorder. Think of it as 'wear and tear' — like the worn-out soles of old rubber shoes. Over time, the articular cartilage (the smooth cushion covering the ends of bones inside a joint) progressively breaks down. Without this protective cartilage, bone rubs directly against bone, causing pain, osteophyte (bone spur) formation, and narrowing of the joint space. OA predominantly affects WEIGHT-BEARING JOINTS such as the knees, hips, and spine, as well as the distal finger joints. It is typically ASYMMETRIC — meaning it may affect the right knee more than the left, unlike RA which is symmetric. Key risk factors include advanced age (most common in people over 50), obesity (increases load on weight-bearing joints), female sex, repetitive joint use (occupational risk), and previous joint injury. CLINICAL FEATURES to remember for the NLE: • PAIN that is WORSE with ACTIVITY and RELIEVED by REST — this is opposite to RA where rest can worsen stiffness. • MORNING STIFFNESS lasting LESS THAN 30 MINUTES (brief stiffness after inactivity, sometimes called 'gelling'). • HEBERDEN'S NODES: bony swellings at the DISTAL interphalangeal (DIP) joints of the fingers. • BOUCHARD'S NODES: bony swellings at the PROXIMAL interphalangeal (PIP) joints of the fingers. • NO systemic symptoms — no fever, no fatigue, no weight loss. This is a local joint problem, not a whole-body disease. • Crepitus (a grating or crackling sound/sensation in the joint during movement). NURSING MANAGEMENT: Using the nursing process, the priority nursing diagnosis for OA is Chronic Pain related to cartilage deterioration and bone-on-bone friction. Nursing interventions include: • PHARMACOLOGIC: ACETAMINOPHEN (paracetamol) is the FIRST-LINE analgesic for OA — safer for long-term use in older adults because it does not cause GI irritation like NSAIDs. NSAIDs (like ibuprofen, naproxen) are added if acetaminophen is insufficient. Topical NSAIDs (diclofenac gel) are useful for knee OA with less systemic risk. • NON-PHARMACOLOGIC: Apply HEAT for stiffness (before exercise) and COLD PACKS for acute pain or after activity. Teach the patient to alternate these. • WEIGHT REDUCTION: Every kilogram of body weight loss reduces knee joint load by approximately 4 kg. This is significant for Filipino patients with OA of the knee. • LOW-IMPACT EXERCISE: Swimming, walking, and cycling strengthen muscles around the joint without excessive loading. Discourage high-impact activities like running or jumping. • JOINT PROTECTION TECHNIQUES: Use assistive devices (cane, walker), avoid prolonged standing or kneeling, and use proper body mechanics. • PATIENT EDUCATION: Teach realistic expectations — OA cannot be reversed, but symptoms can be managed. Emphasize weight management and regular low-impact exercise.

Rheumatoid Arthritis (RA) — Autoimmune Inflammatory Arthritis

Rheumatoid Arthritis is fundamentally different from OA — it is a CHRONIC, SYSTEMIC, AUTOIMMUNE, INFLAMMATORY disease. The immune system mistakenly attacks the body's own synovial membrane (the lining of joint capsules), causing SYNOVITIS (inflammation of the synovium). This inflamed synovium thickens and forms a destructive tissue called PANNUS, which erodes the cartilage and eventually the underlying bone, causing joint destruction and deformity. RA affects SMALL JOINTS FIRST — the metacarpophalangeal (MCP) joints, proximal interphalangeal (PIP) joints of the hands, and the wrists and feet are the classic initial sites. Crucially, RA involvement is SYMMETRIC — if the right wrist is affected, the left wrist is also affected. This systemic, bilateral pattern is a hallmark NLE differentiator. CLINICAL FEATURES: • MORNING STIFFNESS lasting MORE THAN 1 HOUR — this is the most important distinguishing feature from OA. The stiffness is prolonged because the inflamed synovium takes time to 'warm up.' Patients often describe difficulty making a fist or gripping objects in the morning. • SYSTEMIC SYMPTOMS: low-grade fever, fatigue, malaise, anorexia, and weight loss — because RA is a whole-body autoimmune disease, not just a joint problem. • SYMMETRIC joint involvement: bilateral hands, wrists, feet, elbows, knees, and ankles. • Joint DEFORMITIES in advanced disease: - ULNAR DEVIATION: fingers deviate toward the little finger side - SWAN-NECK DEFORMITY: PIP joint hyperextends, DIP joint flexes - BOUTONNIERE DEFORMITY: PIP joint flexes, DIP joint hyperextends • RHEUMATOID NODULES: firm, nontender subcutaneous nodules, often at pressure points like the elbows. • Extra-articular (outside the joints) manifestations: pleuritis, pericarditis, vasculitis, Sjogren's syndrome, anemia of chronic disease. DIAGNOSTIC LABS: • POSITIVE RHEUMATOID FACTOR (RF): an autoantibody — positive in about 70-80% of RA patients • POSITIVE ANTI-CCP (anti-cyclic citrullinated peptide) antibodies: more SPECIFIC for RA than RF • ELEVATED ESR (erythrocyte sedimentation rate) and CRP (C-reactive protein): markers of systemic inflammation • CBC: may show normocytic normochromic ANEMIA (anemia of chronic disease) NURSING MANAGEMENT: Priority nursing diagnoses include: Chronic Pain, Impaired Physical Mobility, Fatigue, Risk for Situational Low Self-Esteem (body image changes from deformities), and Deficient Knowledge. Interventions: • BALANCE REST AND ACTIVITY: Rest during flares (acute inflammation) and resume activity during remission. Complete bed rest is NOT recommended. • JOINT PROTECTION: Use splints to maintain joint alignment and prevent deformity. Teach energy conservation techniques — do important tasks when energy levels are highest (usually midday after morning stiffness resolves). • HEAT AND COLD: Warm soaks or paraffin baths for morning stiffness; cold packs for acute inflamed joints. • PHARMACOLOGY (CRITICAL FOR NLE): 1. NSAIDs (ibuprofen, naproxen): Reduce pain and inflammation. NOT disease-modifying — they do not stop joint destruction. 2. CORTICOSTEROIDS (prednisone): Potent anti-inflammatory, used for acute flares or as a bridge while waiting for DMARDs to take effect. Long-term use causes osteoporosis, Cushingoid features, immunosuppression. 3. DMARDs (Disease-Modifying Antirheumatic Drugs): These SLOW or STOP disease progression by modifying the immune response. - METHOTREXATE: The ANCHOR DMARD and FIRST-LINE choice for RA. It is a folic acid antagonist. CRITICAL NURSING POINTS: * Give FOLIC ACID (folate) to reduce side effects (mouth sores, nausea) * Monitor for HEPATOTOXICITY (liver enzymes, LFTs) and BONE MARROW SUPPRESSION (CBC) * It is a TERATOGEN — counsel female patients of childbearing age about CONTRACEPTION * Given WEEKLY, not daily (common error) - Hydroxychloroquine (Plaquenil): Monitor for RETINAL TOXICITY (ophthalmologic exams) - Sulfasalazine: monitor CBC and urinalysis 4. BIOLOGIC AGENTS (e.g., etanercept, adalimumab — TNF inhibitors): Highly effective but increase risk of SERIOUS INFECTIONS including reactivation of TUBERCULOSIS (important in the Philippine context where TB is endemic). Screen for TB before starting biologics.

Gout — Metabolic Disorder of Purine Metabolism

Gout is a metabolic disorder caused by a defect in PURINE METABOLISM resulting in HYPERURICEMIA (elevated uric acid in the blood). When uric acid levels become too high, MONOSODIUM URATE CRYSTALS deposit in joints and surrounding tissues, triggering an intense acute inflammatory response. Understanding the pathophysiology helps you remember the management: • PURINES (from certain foods and cell turnover) → broken down to URIC ACID → normally excreted by the kidneys • In gout: too much uric acid is produced, or not enough is excreted → HYPERURICEMIA • Uric acid crystallizes as MONOSODIUM URATE → deposits in joints → acute INFLAMMATORY ARTHRITIS CLASSIC PRESENTATION: • PODAGRA: the most classic presentation — acute, intensely painful inflammation of the GREAT TOE (first metatarsophalangeal joint). The joint is red (erythema), hot, swollen, and exquisitely tender — even the weight of a bed sheet causes pain. • Attacks are SUDDEN in onset, often waking the patient at night. • Other joints affected: ankles, knees, wrists, elbows (can affect any joint). • Between attacks: the joint returns to normal (asymptomatic interval). • CHRONIC GOUT: leads to TOPHI — chalky-white deposits of urate crystals under the skin at pressure points (ears, elbows, fingers). Also increases risk of URATE KIDNEY STONES (urolithiasis). DIET IN GOUT (HIGH-YIELD NLE CONTENT): High-purine foods must be AVOIDED: • ORGAN MEATS: liver, kidney, brain, heart (common in Filipino cuisine — e.g., goto, dinuguan) • SHELLFISH: shrimp, crab, lobster, mussels (talaba, tahong — commonly eaten in the Philippines) • SARDINES and ANCHOVIES (bagoong, tuyo — very common in Filipino diet!) • RED MEATS: beef, pork (in large quantities) • ALCOHOL: especially BEER (beer contains high purines from brewer's yeast and also inhibits uric acid excretion) • Avoid CRASH DIETING — rapid weight loss increases uric acid levels due to cell breakdown FOODS ENCOURAGED: • Increased fluid intake: 2–3 liters per day of WATER to flush uric acid and prevent kidney stones • Low-fat dairy products (may lower uric acid) • Complex carbohydrates (rice, vegetables, fruits) • Cherries (may lower uric acid levels — emerging evidence) PHARMACOLOGY — CRITICAL NLE DISTINCTION: ACUTE ATTACK MANAGEMENT: 1. COLCHICINE: Specifically for acute gout. Mechanism: prevents urate crystal-induced inflammation by inhibiting neutrophil migration. Side effects: NAUSEA, VOMITING, DIARRHEA (GI toxicity is the most common sign of toxicity — STOP the drug if severe diarrhea occurs). 2. NSAIDs (indomethacin, naproxen, ibuprofen): Effective for acute pain and swelling. Avoid in patients with renal impairment. 3. CORTICOSTEROIDS: Used when colchicine and NSAIDs are contraindicated. CHRONIC URATE-LOWERING THERAPY: 1. ALLOPURINOL: XANTHINE OXIDASE INHIBITOR — it REDUCES THE PRODUCTION of uric acid. This is the primary long-term medication for gout prevention. - KEY NLE POINT: DO NOT START ALLOPURINOL DURING AN ACUTE ATTACK — it can paradoxically worsen the attack by mobilizing urate crystals. Start only after the acute attack has resolved. - Encourage increased fluid intake while on allopurinol. - Monitor for hypersensitivity rash (can rarely be severe — Stevens-Johnson syndrome). - Avoid aspirin (raises uric acid levels). 2. PROBENECID: Uricosuric agent — increases RENAL EXCRETION of uric acid. Requires adequate fluid intake and is avoided in patients with kidney stones or renal impairment. MEMORY AID: 'ACUTE attack = Colchicine; CHRONIC prevention = Allopurinol. Never start Allopurinol during an Acute attack.' NURSING CARE DURING AN ACUTE ATTACK: • REST and ELEVATE the affected joint (usually the foot) • Apply COLD PACKS to reduce inflammation (NOT heat — heat increases vasodilation and inflammation) • Use a BED CRADLE to keep bed linens off the hypersensitive joint • Administer prescribed colchicine or NSAIDs • PUSH FLUIDS: at least 2–3 L of water daily • Monitor urine output and renal function • Educate about dietary modifications and alcohol avoidance

Osteoporosis — Metabolic Bone Disease

Osteoporosis is a METABOLIC BONE DISEASE characterized by decreased bone mass and deterioration of bone tissue, resulting in FRAGILE, POROUS BONES that are highly susceptible to fractures. The word itself means 'porous bone' (osteo = bone, porosis = porous). Think of it like a sponge — healthy bone has a solid structure, but in osteoporosis, the internal 'scaffolding' becomes thin, weak, and full of holes. PATHOPHYSIOLOGY: Bone is a dynamic living tissue constantly being broken down (RESORPTION by osteoclasts) and rebuilt (FORMATION by osteoblasts). Osteoporosis occurs when BONE RESORPTION OUTPACES BONE FORMATION — the skeleton loses density faster than it can be replaced. In postmenopausal women, the loss of ESTROGEN is a critical trigger because estrogen normally suppresses osteoclast activity. Without estrogen, osteoclasts become overactive, accelerating bone loss. RISK FACTORS (Remember 'FRACTURED'): • Female sex • Race (White and Asian women at highest risk — Filipino women are at risk!) • Age (advanced age) • Calcium and Vitamin D deficiency • Thin/small frame and low body weight • Underactive lifestyle (sedentary) • Reproductive factors (early menopause, estrogen loss) • Estrogen loss (postmenopausal) • Drugs (long-term CORTICOSTEROIDS, proton pump inhibitors, anticonvulsants) Additional risk factors: smoking, excess alcohol consumption, family history. CLINICAL PRESENTATION: • SILENT until a FRACTURE occurs — osteoporosis has NO PAIN until the bone breaks. This is why it is called the 'silent thief.' • Classic FRACTURE SITES: 1. VERTEBRAL (spine): Most common type; compression fractures cause loss of HEIGHT, KYPHOSIS ('dowager's hump' or 'humpo'), and back pain. 2. HIP: The most serious and life-threatening — high mortality in elderly patients. 3. WRIST (COLLES' FRACTURE): Falls on an outstretched hand. • Back pain that worsens with prolonged standing or activity. DIAGNOSIS: • DEXA SCAN (Dual-Energy X-ray Absorptiometry): The GOLD STANDARD for measuring bone mineral density (BMD). - T-SCORE INTERPRETATION (memorize this for NLE): * T-score ABOVE -1.0 = NORMAL * T-score -1.0 to -2.5 = OSTEOPENIA (low bone mass, precursor to osteoporosis) * T-score AT OR BELOW -2.5 = OSTEOPOROSIS * T-score at or below -2.5 WITH a fragility fracture = SEVERE OSTEOPOROSIS MANAGEMENT: 1. CALCIUM SUPPLEMENTATION: • Adults 19-50: 1000 mg/day; Adults over 50: 1200 mg/day • Dietary sources: milk, cheese, yogurt, sardines with bones, leafy greens, tofu • Take supplements in divided doses — calcium is better absorbed in smaller amounts (500 mg at a time) 2. VITAMIN D: • 800-1000 IU/day recommended • Needed for calcium ABSORPTION from the gut • Sources: sunlight exposure, fatty fish, fortified foods, supplements 3. WEIGHT-BEARING EXERCISE: • Walking, jogging, dancing, stair climbing • Stimulates OSTEOBLAST activity and bone formation • Muscle strengthening also reduces fall risk 4. BISPHOSPHONATES (Most important drug class for NLE): • Examples: ALENDRONATE (Fosamax), RISEDRONATE (Actonel), IBANDRONATE • Mechanism: Inhibit OSTEOCLASTIC bone resorption (reduce bone breakdown) • CRITICAL NURSING TEACHING — this is heavily tested on NLE: * Take on an EMPTY STOMACH in the MORNING (before any food, drink, or other medications) * Take with a FULL GLASS (180-240 mL) of PLAIN WATER only * REMAIN UPRIGHT (sitting or standing) for at LEAST 30 MINUTES after taking — this prevents the tablet from sitting in the esophagus and causing ESOPHAGITIS, ESOPHAGEAL ULCERATION, or ESOPHAGEAL EROSION * Do NOT lie down after taking * Do NOT crush or chew the tablet 5. FALL PREVENTION (Priority safety intervention): • Remove environmental hazards: loose rugs, electrical cords, cluttered floors • Ensure adequate lighting (especially at night) • Use non-slip footwear and non-slip mats in bathrooms • Install grab bars in bathrooms and along staircases • Recommend assistive devices if needed (cane, walker) • Advise caution with medications that cause dizziness or orthostatic hypotension

Osteomyelitis — Bone Infection

Osteomyelitis is an INFECTION OF THE BONE, usually bacterial in origin. The most common causative organism is STAPHYLOCOCCUS AUREUS — remember this for the NLE. The infection can reach the bone through THREE ROUTES: 1. HEMATOGENOUS (blood-borne): Bacteria from another infection site (e.g., skin infection, UTI, dental abscess) travel through the bloodstream and seed the bone. This is most common in CHILDREN (affects the metaphysis of long bones like the tibia and femur) and in immunocompromised adults. 2. CONTIGUOUS SPREAD: Infection spreads from adjacent infected tissue (e.g., diabetic foot ulcer, pressure injury, soft tissue abscess). 3. DIRECT INOCULATION: Bacteria introduced directly into bone via OPEN FRACTURE, orthopedic surgery, or penetrating trauma. In the Philippine context, diabetic foot osteomyelitis (contiguous spread) is very common, given the high prevalence of diabetes mellitus in the Filipino population. CLINICAL MANIFESTATIONS: • BONE PAIN: Deep, aching, localized pain at the site of infection — the most consistent symptom • FEVER and CHILLS: Signs of systemic infection • LOCAL SIGNS: Warmth, swelling, erythema (redness), and tenderness over the affected bone • SINUS TRACT FORMATION: In chronic osteomyelitis, a pathway from the infected bone to the skin surface develops, draining purulent material (pus). This is a sign of chronic, poorly treated infection. • SYSTEMIC SIGNS: Malaise, fatigue, irritability (especially in children) DIAGNOSTIC FINDINGS: • ELEVATED WBC (leukocytosis): Indicates infection/inflammatory response • ELEVATED ESR and CRP: Markers of systemic inflammation — also useful for monitoring treatment response • BLOOD CULTURES: To identify the causative organism before starting antibiotics • BONE BIOPSY: The DEFINITIVE DIAGNOSIS — confirms the organism and guides antibiotic selection • IMAGING: - X-ray: May be normal early in the disease (bone changes appear only after 10-21 days of infection) - MRI: Most sensitive for early detection of osteomyelitis - Bone scan (radionuclide scan): Detects increased bone activity early MANAGEMENT — NURSING PRIORITIES: PHARMACOLOGIC: • PROLONGED ANTIBIOTIC THERAPY: Typically 4–6 WEEKS or LONGER of IV antibiotics. This is the cornerstone of treatment. The antibiotic must penetrate bone tissue, which requires high doses and extended duration. • IV antibiotics are started after cultures are obtained, usually empirically with an anti-staphylococcal agent (e.g., oxacillin, nafcillin, or vancomycin for MRSA). • Many patients transition to OUTPATIENT IV ANTIBIOTIC THERAPY through a PICC (peripherally inserted central catheter) line or CVAD after initial hospital stabilization — the nurse plays a crucial role in patient and family teaching for home IV antibiotic administration. SURGICAL: • DEBRIDEMENT: Surgical removal of necrotic (dead) bone and tissue to allow antibiotics to reach the viable bone. • SEQUESTRUM: Dead, avascular bone that has separated from living bone — a sequestrum cannot be reached by antibiotics and must be surgically removed. • BONE GRAFTING: May be needed after debridement to fill bone defects. NURSING CARE: 1. IMMOBILIZE and ELEVATE the affected limb: Reduces pain, promotes drainage, and prevents pathologic fracture (the infected, weakened bone is vulnerable to breaking). 2. HANDLE THE AFFECTED LIMB GENTLY: Risk of PATHOLOGIC FRACTURE — always support the limb above and below the affected area when moving or repositioning. 3. PAIN MANAGEMENT: Assess pain regularly, administer analgesics as prescribed, and use non-pharmacologic measures (positioning, distraction). 4. WOUND CARE with STRICT ASEPTIC TECHNIQUE: Especially if a sinus tract is draining — prevent cross-contamination and nosocomial infection. 5. MONITOR IV ANTIBIOTIC ADMINISTRATION: Check IV site for signs of phlebitis, infiltration; monitor for antibiotic side effects (nephrotoxicity with aminoglycosides, ototoxicity with vancomycin). 6. NUTRITIONAL SUPPORT: HIGH PROTEIN and VITAMIN C intake to support immune function and tissue healing. Malnutrition impairs the body's ability to fight infection and heal bone. 7. PATIENT AND FAMILY TEACHING for home IV antibiotic therapy: Emphasize completing the FULL COURSE — premature discontinuation leads to treatment failure, chronic osteomyelitis, and antibiotic resistance. 8. PSYCHOLOGICAL SUPPORT: A prolonged illness requiring weeks of IV antibiotics is emotionally and financially draining — acknowledge the patient's coping challenges and involve social services if needed.

Total Joint Replacement and Hip Precautions

Total Joint Replacement (Arthroplasty) is a surgical procedure in which the damaged joint surfaces are replaced with prosthetic components made of metal, plastic, or ceramic. The most common procedures are TOTAL HIP REPLACEMENT (THR) and TOTAL KNEE REPLACEMENT (TKR). The primary indication is end-stage osteoarthritis or rheumatoid arthritis that has not responded to conservative management. For the NLE, the most tested content is the set of TOTAL HIP PRECAUTIONS and the prevention of PROSTHESIS DISLOCATION — the most feared early complication of THR. WHY HIP PRECAUTIONS MATTER: The prosthetic hip joint is secured in place while the surrounding soft tissues (capsule, muscles) heal. During this healing period (usually 6–12 weeks post-surgery), the prosthesis can be DISLOCATED if the hip is placed in certain positions. The new joint does not yet have the same stability as a natural hip — the anterior or posterior capsule may be compromised during surgery, creating a vulnerable period. TOTAL HIP PRECAUTIONS (Memorize ALL THREE — the NLE may test any of them): 1. NO HIP FLEXION BEYOND 90 DEGREES: • The hip must not be bent more than 90 degrees (a right angle) • Avoid: LOW chairs (patient sinks below 90°), TOILET SEATS (standard toilets are too low — use a RAISED TOILET SEAT), bending forward to put on shoes or socks, reaching the floor, riding in the back seat of a car (confined space forces hip flexion) • Solution: Use RAISED TOILET SEAT, elevated chairs, long-handled shoe horn and sock aid, elevated bed level 2. NO ADDUCTION PAST THE MIDLINE: • The operated leg must NOT cross the body's midline • Avoid: CROSSING THE LEGS, crossing ankles, lying on affected side without pillow support • Solution: Place an ABDUCTION PILLOW (triangular wedge pillow) between the legs at ALL TIMES — when lying down, when being transported, and when turning. This keeps the hip in proper alignment and prevents the prosthesis from slipping out of the acetabulum. • When turning in bed: ALWAYS turn toward the UNAFFECTED SIDE with the abduction pillow between the legs 3. NO INTERNAL ROTATION: • The foot and toes of the operated leg must NOT turn INWARD • Keep the TOES POINTING UPWARD or slightly outward when lying in bed • Avoid: Pivoting on the affected leg, sitting with feet turned inward SIGNS OF HIP DISLOCATION (Report IMMEDIATELY — this is a surgical emergency): • SUDDEN, SEVERE HIP PAIN (usually described as a 'pop' followed by intense pain) • SHORTENED LIMB: The operated leg appears SHORTER than the other leg • ABNORMAL ROTATION: The foot turns INWARD (internal rotation) or OUTWARD (external rotation) — depends on the surgical approach • INABILITY TO MOVE or BEAR WEIGHT on the affected leg • If dislocation is suspected: IMMOBILIZE the patient, do NOT attempt to move the joint, notify the surgeon IMMEDIATELY GENERAL POSTOPERATIVE CARE FOR THR AND TKR: 1. DVT/PE PREVENTION — CRITICAL: • Venous thromboembolism (DVT/PE) is a major life-threatening complication of joint replacement surgery • ANTICOAGULANTS: Warfarin, low-molecular-weight heparin (enoxaparin), or direct oral anticoagulants (rivaroxaban) — follow prescribed protocol • SEQUENTIAL COMPRESSION DEVICES (SCDs): Applied to the lower legs to promote venous return • EARLY AMBULATION: Begin walking with physical therapy assistance as early as the day of surgery or postoperative day 1 • Teach ANKLE PUMPING exercises: dorsiflexion and plantarflexion of the feet — stimulates venous blood flow in the legs 2. WOUND AND DRAIN MANAGEMENT: • Monitor surgical wound for signs of infection (increasing redness, warmth, purulent drainage, fever) • If a HEMOVAC or JACKSON-PRATT drain is in place, monitor output, maintain suction, and document 3. PAIN MANAGEMENT: • PCA (patient-controlled analgesia) or scheduled analgesics in the immediate postoperative period • Adequate pain control facilitates early ambulation, which is essential for recovery 4. TOTAL KNEE REPLACEMENT — SPECIFIC: • CONTINUOUS PASSIVE MOTION (CPM) MACHINE: A device that passively moves the knee through a range of motion while the patient lies in bed — maintains joint flexibility and prevents scar tissue formation. Start with low degrees of flexion (10-20°) and gradually increase as tolerated. • Elevate the limb and apply ice to reduce swelling • Hip precautions DO NOT apply to TKR — this is a different procedure with different precautions 5. PATIENT EDUCATION before discharge: • Reinforce hip precautions (for THR) — often continue for 6-12 weeks • Home modifications: raised toilet seat, shower chair, firm chair with armrests, removal of rugs and hazards • Activity progression: walk with walker → cane → independent ambulation as directed by PT • Sexual activity guidelines: usually acceptable after 6-8 weeks with modifications to avoid prohibited positions

Low Back Pain (LBP) — Mechanical and Disc-Related

Low Back Pain (LBP) is one of the MOST COMMON HEALTH COMPLAINTS worldwide and in the Philippines. It is a leading cause of disability and work absenteeism. Most cases are ACUTE AND SELF-LIMITING, resolving within 4–6 weeks. However, some cases become chronic or signal serious underlying conditions. CLASSIFICATION: 1. MECHANICAL LBP: The most common type — caused by muscle strain, ligament sprain, degenerative disc disease (OA of the spine), poor posture, or obesity. Pain is localized to the lower back without nerve involvement. 2. HERNIATED INTERVERTEBRAL DISC (Slipped Disc): The soft inner core (nucleus pulposus) of an intervertebral disc protrudes through its outer casing (annulus fibrosus) and compresses adjacent nerve roots, causing RADICULOPATHY (radiating nerve pain). HERNIATED DISC — CLINICAL FEATURES: • SCIATICA: Shooting, radiating pain that travels from the lower back down the BUTTOCK, POSTERIOR THIGH, and into the LEG and FOOT — follows the distribution of the sciatic nerve. This is the hallmark of L4-L5 or L5-S1 disc herniation. • NUMBNESS and TINGLING (paresthesia) in the affected leg or foot • MUSCLE WEAKNESS in the leg • POSITIVE STRAIGHT LEG RAISE TEST (Lasegue's test): With the patient lying flat, raising the leg to 30-70° while keeping the knee straight reproduces radicular leg pain — confirms nerve root irritation from disc herniation. RED FLAGS IN LOW BACK PAIN (Requires Urgent Evaluation — Possible Surgical Emergency): • NEW BLADDER OR BOWEL INCONTINENCE (loss of control) • SADDLE ANESTHESIA: Numbness in the perineum, inner thighs, and genitalia (the area that would contact a saddle) • PROGRESSIVE LEG WEAKNESS (rapid worsening neurologic deficit) • These three together suggest CAUDA EQUINA SYNDROME — compression of the cauda equina nerve roots. This is a SURGICAL EMERGENCY requiring immediate decompressive surgery to prevent permanent neurologic deficit (paralysis, permanent incontinence). • Other red flags: fever + back pain (possible spinal infection or osteomyelitis), unexplained weight loss (possible malignancy), history of cancer with new back pain (metastatic compression). CONSERVATIVE MANAGEMENT (First-Line for Most Cases): • ACTIVITY MODIFICATION: A short period (1-2 days) of activity modification — NOT prolonged bed rest. The current evidence shows that PROLONGED BED REST (more than 2 days) WORSENS outcomes for mechanical LBP by causing deconditioning. • NSAIDs (ibuprofen, naproxen): First-line pharmacologic treatment — reduce inflammation and pain. • MUSCLE RELAXANTS (cyclobenzaprine, methocarbamol): For muscle spasm component — note that these cause drowsiness, advise caution with driving. • HEAT OR COLD APPLICATION: Cold for acute injury (first 24-48 hours to reduce swelling); Heat for chronic/subacute LBP (relaxes muscles, reduces stiffness). • PHYSICAL THERAPY: Core strengthening exercises, stretching, posture training. PROPER BODY MECHANICS (KEY PATIENT EDUCATION — NLE HIGH YIELD): • BEND AT THE KNEES, NOT AT THE WAIST — the most important principle. When picking up objects from the floor, squat down by bending the knees (keeping the back straight and spine in neutral), not by bending the waist forward. • Keep objects CLOSE TO THE BODY when lifting — reduces the moment arm and stress on the lumbar spine. • AVOID TWISTING while lifting — combine lifting and turning as two separate movements. • PUSH RATHER THAN PULL heavy objects. • MAINTAIN PROPER POSTURE: Sit in chairs with lumbar support; keep ears, shoulders, and hips aligned when standing. • SLEEP ON A FIRM MATTRESS — too soft a mattress does not support the lumbar curve. • STRENGTHEN CORE MUSCLES: Abdominal and paraspinal muscles support and protect the spine. • MAINTAIN HEALTHY WEIGHT: Obesity increases mechanical load on the lumbar spine. SURGICAL MANAGEMENT (When Conservative Care Fails or Red Flags Present): • DISCECTOMY: Surgical removal of the herniated disc material compressing the nerve root. • LAMINECTOMY: Surgical removal of the lamina (bony arch of the vertebra) to decompress the spinal canal. • SPINAL FUSION: May be added to stabilize the spine after decompression. POST-SPINAL SURGERY NURSING CARE: • LOG ROLLING: When turning or repositioning the patient post-spinal surgery, use the LOG ROLL TECHNIQUE — maintain the spine in a straight line (neutral alignment) by turning the head, shoulders, trunk, and pelvis simultaneously as ONE UNIT. No twisting of the spine. • ASSESS FOR CSF LEAK: A complication of spinal surgery — look for CLEAR DRAINAGE on the wound dressing. Test with HALO TEST (glucose-positive halo on a paper towel around the drainage) — CSF is glucose-positive. If CSF leak is suspected, notify the surgeon immediately. • MONITOR FOR NEUROLOGIC CHANGES: Any NEW or WORSENING weakness, numbness, or loss of bladder/bowel control post-operatively must be reported IMMEDIATELY — may indicate spinal hematoma, edema, or other surgical complication. • Assess motor and sensory function regularly in the lower extremities.

The key features identifying RA: (1) bilateral (symmetric) hand involvement, (2) morning stiffness OVER 1 HOUR (2 hours in this case), (3) systemic symptoms (fatigue, weight loss), (4) elevated ESR and POSITIVE RF. Methotrexate is the first-line DMARD for RA. Nursing priorities: administer folic acid alongside methotrexate, monitor LFTs and CBC regularly, and counsel the patient about teratogenicity if she is of childbearing age.

Allopurinol is a xanthine oxidase inhibitor that lowers uric acid levels for long-term prevention. However, when uric acid levels drop suddenly (as allopurinol begins to work), urate crystals can mobilize from deposits into joint fluid, WORSENING or precipitating an acute attack. Allopurinol should be initiated only AFTER the acute attack has completely resolved. During the acute attack, colchicine and/or NSAIDs are the appropriate treatments. Clarifying potentially harmful medication orders is within the nurse's professional responsibility under RA 9173.

The T-score of -3.1 confirms osteoporosis (at or below -2.5). Alendronate is a bisphosphonate that is poorly absorbed (only about 1% bioavailability) and highly irritating to the esophageal mucosa. Lying down after taking it allows the tablet to remain in contact with the esophageal wall, causing esophagitis, erosions, and ulcers. Taking it with food or other beverages significantly reduces absorption. These three instructions are the most frequently tested bisphosphonate nursing points on the NLE.

Total hip precautions must be strictly followed for 6-12 weeks post-surgery. NO hip flexion beyond 90° is one of the three cardinal precautions. A standard low chair forces the hip into acute flexion, risking dislocation of the prosthetic femoral head from the acetabular component. Always use: elevated chairs, raised toilet seats, and chairs with armrests (to assist standing up without bending the hip excessively). The preceptor role includes supervising student nurses and ensuring patient safety — consistent with the professional standards defined in RA 9173.

A CSF leak after spinal surgery can lead to meningitis, spinal headache (positional headache that worsens upright and improves lying down), and other neurologic complications. The nurse should NOT remove or change the dressing independently — mark the borders of the drainage on the dressing to monitor progression, and notify the surgeon urgently. CSF can be differentiated from other wound drainage by the HALO TEST: if the fluid placed on a white cloth creates a clear 'halo' ring around a bloody center, CSF is likely. CSF is also glucose-positive on dipstick testing. This is a patient safety issue requiring immediate escalation.

This question contextualizes gout dietary management within Filipino food culture, which is critical for NLE scenarios. Filipino traditional foods that are high in purines include shellfish (alimango, hipon, talaba, tahong), organ meats (goto, dinuguan, pork liver), dried fish (tuyo, danggit, dilis), and alcohol (beer, lambanog). The nurse should help the patient identify safe alternative foods: fresh vegetables, rice, low-fat dairy products, eggs, fruits, and chicken (in moderate amounts). Encouraging 2-3 liters of water daily to flush uric acid is essential.