1 / 45

IMMOBILIZATION

IMMOBILIZATION. SUSANTI DHARMMIKA, dr. SpKFR SISTEM DERMATOMUSKULOSKELETAL FAKULTAS KEDOKTERAN UNISBA 2012. IMMOBILIZATION. IS THE PHYSICAL RESTRICTION OF MOVEMENT INVOLVING A BODY SEGMENT OR THE ENTIRE BODY. DECONDITIONING.

jsacco
Download Presentation

IMMOBILIZATION

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. IMMOBILIZATION SUSANTI DHARMMIKA, dr. SpKFR SISTEM DERMATOMUSKULOSKELETAL FAKULTAS KEDOKTERAN UNISBA 2012

  2. IMMOBILIZATION IS THE PHYSICAL RESTRICTION OF MOVEMENT INVOLVING A BODY SEGMENT OR THE ENTIRE BODY

  3. DECONDITIONING • THE SEVERITY OF THE DECONDITIONING IS DEPENDENT ON THE DEGREE AND DURATION OF IMMOBILIZATION • THE PREVENTION OF IMMOBILIZATION IS MUCH MORE COSTEFFECTIVE AND IS PREFERABLE TO TREATMENT

  4. THE ADVERSE CLINICAL MANISFESTATIONS OF PROLONGED IMMOBILZATION

  5. I. MUSCULOSKELETAL CHANGES

  6. 1. CONTRACTURE • IS THE LACK OF FULL ACTIVE OR PASSIVE RANGE OF MOTION (ROM) DUE TO A JOINT, SOFT TISSUE, OR MUSCLE LIMITATION • CONDITIONS PRODUCING LIMITED JOINT ROM: • PAIN (E.G. TRAUMA, INFLAMMATION, INFECTION, JOINT DEGENERATION, ISCHEMIA, AND HEMORRHAGE) • MUSCLE IMBALANCE (E.G. PARALYSIS AND SPASTICITY) • CAPSULAR OR PERIARTICULAR TISSUE FOBROSIS • PRIMARY MUSCLE DAMAGE (E.G. POLYMYOSITIS, MUSCULAR DYSTROPHY) • MECHANICAL FACTORS (E.G. IMPROPER BED POSITIONING, CASTING/ SPLINTING IN FORESHORTENED POSITION)

  7. CONTRACTURE… • THE MUSCLE FIBRES & CONNECTIVE TISSUE • IN SHORTENED POSTION (3 – 5 DAYS) • ↓ • CONTRACTION OF COLLAGEN FIBERS DECREASE IN MUSCLE FIBERS • ↓ • ≥ 3 WEEKS • THE LOOSE OF CONNECTIVE TISSUE IN MUSCLES & AROUND JOINT  DENSE CONNECTIVE TISSUE • ↓ • CONTRACTURE MOST COMMONLY AT: • LOWER LIMB ( BIARTICULAR MUSCLE) IN THE HIPS, KNEES, ANKLES • UPPER LIMB : THE SHOULDER, ELBOWS,WRISTS, FINGERS

  8. CONTRACTURE… • PREVENTION: • - PROPER POSITIONING • (USING PILLOWS, TROCHANTER ROLLS, HAND ROLLS, RESTING SPLINTS) • - ACTIVE/PASSIVE ROM EXERCISE • - EARLY MOBILIZATION AND AMBULATION

  9. 2. MUSCLE WEAKNESS AND ATROPHY • SEEN IN THE ANTIGRAVITY MUSCLES OF THE LOWER LIMBS • TOTAL INACTIVITY  ↓ISOMETRIC MUSCLE STRENGTH: • 10-20%/WEEK (1-3%/DAY) • 50% IN 2- 5 WEEKS • STREGTH THAT LOST IN1 WEEK MAY TAKE 4 WEEKS FOR REGAIN EVEN WITH MAXIMAL STREGTHENING PROGRAM

  10. MUSCLE WEAKNESS AND ATROPHY… • PREVENTION: • MUSCLE MUST EXERT 20-30% OF ITS MAXIMAL CAPACITY FOR SEVERAL SECOND EACH DAY • MUSCLE EXERTION AT 50% MAXIMUM CAPACITY ( 1 SEC/DAY)  MORE EFFECTIVE • NEUROMUSCULAR ELECTRICAL STIMULATION (NMES) FOR DENERVATED MUSCLE • PROPRIOCEPTIVE NEUROMUSCULAR FACILITATION

  11. 3. DISUSE OSTEOPOROSIS • IMMOBILIZATION • ↓ • LACK OF STIMULUS • (E.G. WEIGHT BEARING, GRAVITY, AND MUSCLE ACTIVITY) • ↓ • ↑URINARY EXCRETION OF CALCIUM & HYDROXYPROLINE • ↑ EXCRETION OF THE CALCIUM IN THE STOOL • ↓ • INCREASED OF BONE RESORPTION • ↓ • LOST OF THE BONE DENSITY • ↓ • DISUSE OSTEOPOROSIS

  12. DISUSE OSTEOPOROSIS… • MORE MARKED IN SUBPERIOSTEAL REGION • INITIALLY INVOLVES THE CANCELLOUS BONE AT THE METAPHYSIS & EPIPHYSIS EXTENDS TO DIAPHYSIS • ↓ BONE DENSITY : • 40-45% AFTER 12 WEEKS OF BED REST • > 50% AFTER 13TH WEEKS • SENSITIVE TO MINOR TRAUMA  FRACTURE

  13. DISUSE OSTEOPOROSIS… • PREVENTION: • WEIGHT BEARING STANDING • STANDING FRAME OR TILT TABLE  IF UNABLE TO STAND UNSUPPORTED : • 30 DEGREE 1 MINUTE • ↑10 DEGREES EVERY 3-5 DAYS • UNTIL 70 DEGREES (30 MINUTES) • STANDING IN PARALLEL BAR • AMBULATION • GENERAL EXERCISE PROGRAM (STRENGTHENING, ENDURANCE, COORDINATION, ADL)

  14. II. CARDIOVASCULAR CHANGES

  15. 1. ORTHOSTATIC (POSTURAL) HYPOTENSION • IS DUE TO THE IMPAIRED ABILITY OF THE CIRCULATORY SYSTEM TO ADJUST TO THE UPRIGHT POSITION • AS THE PERSON STANDS  BLOOD POOLS IN THE LOWER LIMBS CAUSING AN IMMEDIATE DROP IN VENOUS RETURN  ↓ STROKE VOLUME &↓ CARDIAC OUTPUT • NORMALLY: IMMEDIATE VASOCONSTRICTION AND ↑ HEART RATE (HR)& SYSTOLIC BLOOD PRESSURE (SBP) • IN PROLONGED BED REST: LOSE THIS ADAPTATION : TINGLING, BURNING IN THE LOWER LIMBS, DIZZINESS, LIGHTHEADEDNESS, FAINTING, VERTIGO, ↑ HR (> 20 X/MINUTE), ↓ SBP (> 20 mmHg), ↓ PULSE PRESSURE

  16. ORTHOSTATIC (POSTURAL) HYPOTENSION… • TREATMENT: • EARLY MOBILIZATION (ROM EXERCISES, STRENGTHENING EXC., AMBULATION, CALISTHENICS) • ABDOMINAL STRENGTHENING AND ISOTONIC-ISOMETRIC EXERCISE OF THE LEGS ( TO REVERSE VENOUS STASIS AND POOLING) • PROVIDING THE WHEELCHAIR WITH ELEVATING LEG RESTS AND RECLINING BACK • TILT TABLE (GRADUAL TILT UP TO 70 DEGREES F0R 20 MINUTES) • BANDAGE WRAPS, FULL LENGTH ELASTIC STOCKINGS, ABDOMINAL BINDERS • SYMPATHOMIMETIC PRESSOR AGENTS • MINERALOCORTICOID  TO MAINTAIN BP < ADEQUATE SALT & FLUID INTAKE TO PREVENT FURTHER BLOOD VOLUME CONTRACTION AND WORSENING HYPOTENSION

  17. 2. CHANGES DUE TO CARDIAC DECONDITIONING • AT REST: • ↑RESTING HR • ↓ RESTING STROKE VOLUME  RELATED TO ↓ BLOOD VOLUME • ↓ CARDIAC SIZE • ↓ LEFT VENTRICULAR & DIASTOLIC VOLUME • REMAINS UNCHANGED : RESTING SYSTOLIC & MEAN BP, O2 UPTAKE AT REST, ARTERIOVENOUS O2 DIFFERENCE

  18. 2. CHANGES DUE TO CARDIAC DECONDITIONING • WITH EXERCISE: • ↑HR RESPONSE TO SUBMAXIMAL EXERCISE (MAXIMAL HR REMAINS UNCHANGED OR SLIGHTLY ↑) • ↓STROKE VOLUME AT SUBMAXIMAL & MAXIMAL EXERCISE • ↑ CO • ↓ MAXIMUM O2 UPTAKE (VO2 MAX) • ARTERIOVENOUS O2 DIFFERENCE AT SUBMAXIMAL EXERCISE

  19. 3. CHANGED IN FLUID BALANCE • IN THE RECUMBENT POSITION: • ↑ CO • ↑ CARDIAC WORK • SHIFT OF 700 ML OF BLOOD VOLUME TO THE THORAX • DELAYED SHIFT OF EXTRAVASCULAR FLUID INTO THE CIRCULATION • COMPENSATORY DIURESIS ( ↓PLASMA VOLUME WITH SUBSEQUENT LOSS OF PLASMA MINERAL AND PROTEIN  ↓HYDROSTATIC BP, ↓ ADH

  20. CHANGED IN FLUID BALANCE… • TREATMENT: • ISOTONIC EXERCISE IS ALMOST TWICE AS EFFECTIVE AS ISOMETRIC • EXERCISE IN PREVENTING PLASMA VOLUME REDUCTION

  21. 3. VENOUS THROMBOEMBOLISM • DUE TO VENOUS STASIS INCREASED BLOOD VICOSITY AND HYPERCOAGULABILITY (↓ PLASMA VOLUME, RED BLOOD MASS UNCHANGED) • PREVENTIVE: • ACTIVE EXERCISE (E.G. CALF OR ANKLE PUMPING EXERCISE AND WALING • ELASTIC STOCKINGS (KNEE OR THIGH HIGH)/ ELASTIC WRAPS • LOW MOLECULAR/UNFRACTIONED HEPARIN • PROPER POSITIONING (LEGS ELEVATED)

  22. III. RESPIRATORY CHANGES

  23. RESPIRATORY CHANGES… • BED REST • ↓ • ↓ ROM OF THE COSTOVERTEBRAL & COSTOCHONDRAL JOINT • ↓ • ↓ CHEST EXCURSION • ↓ • MECHANICAL RESTRICTION OF BREATHING • ↓ • RAPID, SHALLOW BREATHING • ↓ • ↓ PULMONARY FUNCTION PARAMETERS (↓ TIDAL VOLUME, MINUTE VOLUME, VITAL CAPACITY, MAXIMUM VOLUNTARY VENTILATION)

  24. RESPIRATORY CHANGES… • IN THE SUPINE POSITION: • THE MUCOCILIARY MECHANISM INEFFECTIVE IN CLEARING SECRETIONS • ↓ • MUCUS SECRETIONS ACCUMULATE IN THE DEPENDENT RESPIRATORY SEGMENT (POSTERIOR SEGMENT) • ↓ • IN THE NON DEPENDENT RESPIRATORY SEGMENTS ( ANTERIOR SEGMENT) DRY

  25. RESPIRATORY CHANGES… • IN THE SUPINE POSITION: • THE CILIARY MALFUNCTION • WEAKNESS OF THE ABDOMINAL MUSCLES • ↓ • IMPAIRED COUGH

  26. RESPIRATORY CHANGES… • IN THE SUPINE POSITION: • THE DEPENDENT RESPIRATORY SEGMENT BECOME POORLY VENTILATED & OVERPERFUSED • ↓ • REGIONAL CHANGES IN THE VENTILATION-PERFUSION RATIO • ↓ • SIGNIFICANT ARTERIOVENOUS SHUNTING • ↓ • LOWER ARTERIAL OXIGENATION • ↓ • IF METABOLIC DEMAND IS INCREASED • ↓ • HYPOXIA • ↓ • ATELECTASIS & HYPOSTATIC PNEUMONIA

  27. RESPIRATORY CHANGES… • PREVENTION: • EARLY MOBILIZATION • FREQUENT CHANGE IN POSITION • CHEST PHYSICAL THERAPY ( DEEP BREATHING, INCENTIVE SPIROMETRY, ASSISTED COUGH, AND/OR CHEST PERCUSSION AND VIBRATTION) • ADEQUATE PULMONARY HYGIENE

  28. IV. SKIN CHANGES

  29. SKIN CHANGES … • PRESSURE ULCERS • DEPENDENT EDEMA  PREDISPOSE TO CELLULITIS (PREVENTION: ADEQUATE MOBILIZATION AND ELEVATION, USE OF STOCKING/ GLOVES, PRESSURE GRADIENT COMPRESSION, AND MASSAGE) • SUBCUTANEOUS BURSITIS (B ECAUSE OF EXCESSIVE PRESSURE ON THE BURSAE (USUALLY PREPATELLAR OR ELBOW BURSAE)  PREVENTION: NSAID, PERCUTANEOUS DRAINAGE, CORTICOSTEROID INJECTIONS, SURGERY IN REFRACTORY CASE)

  30. V. GASTROINTESTINAL CHANGES

  31. GASTROINTESTINAL CHANGES… • ↓ APPETITE • ↓ GASTRIC SECRETION • ATROPHY OF INTESTINAL MUCOSA AND GLANDS • SLOWER RATE OF ABSORPTION • DISTATE FOR PROTEIN RICH FOOD ( LEADS TO NUTRITIONAL HYPOPROTEINEMIA) • REDUCING OF DESIRE TO DEFECATE • CONSTIPATION DUE TO DECREASED GASTRIC AND INTESTINAL MOTILITY  AGGRAVATED BY THE LOSS OF PLASMA VOLUME AND DEHYDRATION • TREATMENT  LAXATIVES, ENEMAS, MANUAL EXTRACTION, OR SURGICAL • PREVENTION  ADEQUATE FLUID INTAKE & FIBER RICH DIET, USE SOFTENERS AND BULK FORMING AGENT, AVOIDANCE OF NARCOTICS, LIMITED USE OF HYPEROSMOTIC (E.G. GLYCERIN) OR PERISTALTIS-STIMULATING (E.G. BISACODYL) SUPPOSITORIES COMBINED WITH REGULARLY-TIMED BOWEL PROGRAM

  32. VI. GENITOURINARY CHANGES

  33. GENITOURINARY CHANGES… • INCREASED DIURESIS AND MINERAL SECRETION • URINARY STAGNATION & HYPERCALCIURIA  STONE FORMATION • URINARY TRACT INFECTION • DECREASED GLOMERULAR FILTRATION RATE AND DECREASED ABILITY TO CONCENTRATE URINE • DECREASED OF SPERMATOGENESIS AND ANDROGENESIS

  34. GENITOURINARY CHANGES… PREVENTION : • ADEQUATE FLUID INTAKE • USE OF THE UPRIGHT POSITION FOR VOIDING • STRICT AVOIDANCE OF BLADDER CONTAMINATION DURING INSTRUMENTATION • PATIENT WITH HIGH POST VOID RESIDUAL  CONDOM CATHETERIZATION OR INTERMITTENT CATHETERIZAT ION • FOR UTI ANTIBIOTICS , ACIDIFICATION ( VITAMIN C) TO PREVENT THE GROWTH OF PROTEUS ORGANISM, URINARY ANTISEPTICS • HIGH RISK OF STONE FORMATION  UREASE INHIBITOR • TREATMENT FOR STONE FORMATION  SURGICAL REMOVAL OR LITHOTRIPSY

  35. VII. METABOLIC & NUTRITIONAL CHANGES

  36. METABOLIC & NUTRITIONAL CHANGES… • ↓ LEAN BODY MASS • ↑ BODY FAT • DISSORDER OF NITROGEN BALANCE • MINERAL & ELECTROLYTES LOSSES • HYPERCALCEMIA DUE TO IMMOBILIZATION  ASSOCIATED WITH OSTEOPOROSIS  ESPECIALLY IN ADULT MALES WITH TRAUMATIC INJURY  TREATMENT : ADEQUATE CALCIUM EXCREATION THROUGH HYDRATION (SALINE 0,9% OR 0,45 %) AND DIURESIS WITH FUROSEMIDE

  37. VIII. ENDOCRINE CHANGES

  38. ENDOCRINE CHANGES… • DUE TO ALTERED RESPONSIVENESS OF HORMONES AND ENZYMES : • GLUCOSE INTOLERANCE (NOTED 8 WEEKS AFTER IMMOBILITY )  DUE TO REDUCED INSULIN-BINDING SITES DECREASED SENSITIVITY OF PERIPHERAL MUSCLE TO CIRCULATING INSULIN)  IMPROVED BY ISOTONIC EXERCISES OF THE LARGE MUSCLE GROUPS IN THE LEGS • ALTERED CIRCADIAN RHYTHM • ALTERED TEMPERATURE AND SWEATING RESPONSES • ALTERED REGULATION OF PARATHYROID HORMONE (PTH), THYROID HORMONE,, ANDROGENS , ADRENAL HORMONES, PITUITARY HORMONES, GROWTH HORMONES AND PLASMA RENIN ACTIVITY

  39. IX. NEUROLOGICAL, EMOTIONAL, AND INTELLECTUAL CHANGES

  40. NEUROLOGICAL, EMOTIONAL, AND INTELLECTUAL CHANGES … • THE EFFECTS OF SENSORY DEPRIVATION ( ↓ ATTENTION SPAN, CONFUSION AND DISORIENTATION TO TIME AND SPACE, ↓ HAND – TO – EYE COORDINATION) • ↓ INTELLECTUAL CAPACITY • EMOTIONAL & BEHAVIORAL DISTURBANCES (ANXIETY, DEPRESSION, AUTONOMIC LABILITY, RESTLESNESS, ↓ PAIN TOLERANCE, IRRITABILITY, HOSTILITY, INSOMNIA, AND LACK OF MOTIVATION) • ↑ AUDITORY THRESHOLD • ↓ VISUAL ACUITY • IMPAIRED BALANCE AND COORDINATION (PROBALY DUE TO NEURAL FACTORS RATHER THAN MUSCLE WEAKNESS) • COMPRESSIONS NEUROPATHIES

  41. NEUROLOGICAL, EMOTIONAL, AND INTELLECTUAL CHANGES … PREVENTION: • ENCOURAGING THE PATIENT TO INTERACT WITH STAFF, OTHER PATIENTS, AND FAMILY MEMBERS • RECREATIONAL THERAPY FOR PSYCHOSOCIAL INTERAGRATION, RESOCIALIZATION, AND ADJUSTMENT TO INDEPENDENT FUNCTIONING • NERVE COMPRESSION CAN BE PREVENTED BY PROPER POSITIONING TO RELIEVE PRESSURE FROM THE NERVE

  42. REFFERENCE • PRACTICAL MANUAL OF PHYSICAL MEDICINE AND REHABILITATION: DIAGNOSTICS, THERAPEUTICS AND BASIC PROBLEMS, JACKSON TAN, MOSBY, 1998

  43. THANKYOU

More Related