Lesson 1 Flashcards
Indications for Amputation
Peripheral vascular disease Diabetic limb disease necrotising fascitis trauma infection tumors nerve injury congenital anomalies
extended foot plate:
extended carbon fiber foot plate
includes incorporation of a steel shank into the sole of shoe to allownormal toe off ambulation
What does spring steel shank do?
reproduces the action of longitudinal arch offoot during ambulation
toe filler:
custom molded foam pad or lamb’s wool can fill the distal empty toeportion of the shoe
rigid rocker bottom sole
What does a Chopart amputation remove and save?
remove: forefoot and midfoot
save: talus and calcaneus
Benefit’s of Syme’s amputation:
Distal Weight Bearing Longer limb=less energy loss Can ambulate without prosthesis Proprioception Preservation of distal growth plate in children
Negative of Syme’s amputation:
Wound healing
Compliance
Heel pad instability
Tibial length not feasible for fitting:
3.5 inches
Myoplasty suturing
Opposing Muscle sutured together
Muscle to soft tissue
Soft tissue to soft tissue
Transtibial amputation preferred
Main advantage of thru knee amputation:
creation of endbearing stump and preservation of distal femoral physes
long active lever arm
Suction socket:
provide suspension by means of negative pressure vacuuming.
achieved by forcing air out of the socket through a one-way valve when donning and using the prosthesis
Myodesis:
suturing of muscle bone
Myoplasty:
muscle is sutured to muscle and then placed over the end of the bone before closing the wound
patients with poor vascular health, the myoplasty technique is preferred
PFFD’s: Proximal Focal Femoral Deficits
Congenital defect of the proximal femur
Congenital defect of the proximal femur
absent hip
femoral neck pseudoarthrosis
absent femur
shortened femur
transradial optimum level:
junction prox 2/3 and distal 1/3
Transradial shortest level:
3cm below biceps insertion
Transhumeral optimum level:
middle third
Transhumeral shortest level
4cm below axillary fold
Transfemoral optimum level
middle third
Transfemoral shortest level
8cm below pubic ramus
Transtibial optimum level
8cm for every metre of height(12cm
transtibial shortest level
7.5cm below knee joint
Transradial longest level
5cm above wrist joint
Transhumeral longest level
10cm above olecranon
Transfemoral longest level
15cm above knee joint
Krukenberg procedure
Separate radial and ulna rays distally
forming radial and ulna pincers capable of strong prehension and excellent manipulative ability
What are the three parts of the peripheral vascular system?
Arterial System
Venous System
Lymphatic System
Function of arterial system:
Carry oxygenated blood to the capillaries of the body organs.
Tunica Intima
endothelium, CT, basement membrane
Tunica Media
smooth muscle. The strength of the artery
Tunica Adventitia
elastic and collagenous fibers
Where is blood pressure greatest?
Muscular smaller arteries expand only slightly regardless of the pressure.
Lymphatics
facilitates movement of fluid between bloodstream (veins and arteries) and interstitium to remove wastes, extra fluid and proteins
Peripheral vasculature:
arterial
venous
lymphatics
Arteriosclerosis
hardening of arterial walls
Atherosclerosis
common form of arteriosclerosis, often plaque deposits on endothelial lining
Arteriosclerosis obliterans
atherosclerosis manifested peripherally (usually LE)
Thromboangiitis obliterans (Buerger’s disease)-
Specific arterial disease with tissue ischemia in young men who smoke
Raynaud’s disease-
disease which causes constriction in the small arteries
Risk factors for arterial disease
Smoking Cardiac disease (and its related risk factors) Diabetes High blood pressure Kidney disease
Function of lymphatic system:
Transport interstitial fluids back to blood
Transport absorbed fat from small intestine
Lymphocytes provide immunological defenses
Tunics of lymphatic system:
Three layers, similar to veins
Close-ended tubes
Inner layer forming valves which prevent backflow of lymph.
Movement of lymph
Peristaltic motion and valvular closure
PVD Signs and Symptoms (arterial)
sharp pain relieved by rest chronic cramping w/exercises, heaviness, leg fatigue diminished or absent pulse absent edema cool or cold skin dry, shiny, scaling, thin skin hairless cyanotic
PVD Signs and Symptoms (venous)
aching, deep muscle pain relieved by activity or elevation intermittent claudication pulses present edema increases at end of day warm skin, thick, toughened dark pigmentation varicose veins/ulcers
Aterial Occlusive
4 major risk factors
Smoking
Diabetes
High-fat diet
Hypertension
Symptoms – The Five P’s
Pain Pallor Paralysis Parasthesia Pulselessness
Peripheral arterial disease (atherosclerosis)
Pathology:
Slow progression
Initial injury to vessel from HTN or trauma
Fatty deposits line artery wall at injury site.
Leads to vessel narrowing and blockage followed by ischemia and tissue necrosis
Symptoms of Chronic Arterial Disease
intermittent claudication
diminished/absent pulses
trophic changes
wound formation
Buerger’s Disease
Similar to Acute Arterial Occlusive Disease but it occurs predominantly in young men (under age 40) who are heavy smokers
Inflammatory process in the small vessels of the feet and hands that is directly related to nicotine use
Leads to thrombus formation
Starts distally and progresses proximally
Cold extremities, pain, trophic changes, ischemia, necrosis
Smoking cessation arrests the disease
What subjective clues will your patient give you about arterial disease during the evaluation
Cramping with walking (intermittent claudication)
Rest pain, relieved by dependency
Wounds may have no history of trauma
Arterial disease: objective Signs
Trophic skin changes-loss of hair growth, abnormal nails, dry skin
Cool skin
Decreased pulses
Vasculitis
inflammation of the vessel wall resulting from immune complex deposition or cell-mediated immune reactions directed against the vessel wall
cause unknown
Varicose veins
Abnormally dilated veins resulting from intrinsic vessel wall weakness and chronic valvular insufficiency
Increased risk of thrombosis and chronic venous insufficiency
Venous disease
Deep Vein Thrombosis (DVT)
Venous insufficiency-inadequate drainage of venous blood (also called venous hypertension)
Chronic venous insufficiency
Risk factors for venous disease
Aging Pregnancy Obesity Long hours of standing/sitting Lack of regular activity Family history
What venous disease “sounds” like (subjective information)
Aching, heavy legs
Sometimes relieved by elevation
Wounds may have no history of trauma
What venous disease “looks” like- objective information
Swelling (unilateral or bilateral)
Skin changes: hemosiderin deposits, fibrosis (hardening) of the skin
Pulses present
Wounds with drainage
Symptoms of chronic venous insufficiency;
Dilated veins, leg pain, edema, and cutaneous changes (stasis dermatitis)
Causes of chronic venous insufficiency:
Venous occlusion
Valvular defects
Problems with muscle pump
Medical Management of CVI
Surgical
Angioplasty
Stenting
Amputation
Arterial wound presentation:
Present anywhere distal to the ankle, often the foot/toes Dry appearance Pale tissue Painful No pulses
Venous wound presentation:
Present most often on the medial malleolus and lower leg Large amounts of drainage Red or dark granulation Not always painful Hyperpigmentation Pulses
Arterial wound characteristics:
Anywhere on leg or foot; bony prominences
Painful esp. with LE elevation
Pulses poor or absent
Minimal drainage
Blanched wound base
Well-circumscribed or “punched-out” borders
Venous wound characteristics:
Usually on medial aspect of distal 1/3 of leg Not often painful Normal pulses Moderate to heavy drainage Red wound base Irregular borders and dark pigmentation
Primary lymphatic dysfunction
Primary
Congenital – Failure of complete formation of lymph vessels
Secondary lymphatic dysfunction
Secondary
Caused by trauma, surgery, parasitic infection, radiation, etc
Pathophysiology of lymphatic dysfunction:
Capillaries become more permeable
Damaged lymphatic system can’t keep up
Edema develops
Can lead to soft tissue fibrosis
Risk factors for lymphedema
Hereditary/congenital factors Breast cancer (and other cancers) with surgical and radiation therapy procedures Long standing edema Paralysis Damage during surgical procedures Filariasis
What lymphedema “sounds like”- subjective information
Feelings of fullness and heaviness
Numbness/tingling
What lymphedema “looks” like- objective information
Swelling, not usually improved with elevation Pitting non pitting edema with fibrosis Dermal changes: cysts, hyperkeratosis Decreased ROM Lymph leakage
Neuropathy Risk Factors:
Diabetes Spina bifida Lupus HIV/AIDS Chemotherapy MS Vascular disease
What neuropathy looks like-
subjective information
Gradual onset with tingling, numbness
Acute onset with significant pain sensory loss
What neuropathy looks like-
objective information
Loss of protective sensation Skin changes Inflammation Ulceration Infection Foot deformity Pulses may or may not be present
Neuropathic wounds
Typically pain free
Often on the plantar aspect of the foot
Punched out appearance
Calloused edges
Charcot’s Joint
Joint breakdown
Feet sensory, motor, and anatomic issues
Process of Charcot’s joint:
Bone decalcification on joint surfaces
Boney overgrowth about the margins
P usually absent – some exceptions
Deformity & instability characteristic
Physiology of Wound Healing
Inflammatory phase
Proliferative phase
Maturation phase
Inflammatory phase
Vasodilatation, migration of leukocytes, histamine release (redness, heat, swelling, pain)
Platelet-derived growth factors facilitate migration of granulocytes and macrophages
Proliferative phase
Formation of granulation tissue (collagen + vascular network), wound contraction, re-epithelialization
Maturation phase
Day nine up to two years
Remodeling of new skin
Collagen re-organized & tensile strength increases
Continues even after wound closure (overlap with proliferation phase)
PT wound intervention at this stage
Pressure Ulcer:
ocalized area of tissue necrosis as a result of pressure - Also called decubitus ulcers
Venous Stasis Ulcer:
Wounds that arise on the lower leg as a result of venous insufficiency
Arterial Ulcer:
Wounds that arise on the lower leg or foot as a result of arterial insufficiency, or lack of blood flow to the tissue
Neuropathic Ulcer:
Wounds that arise in diabetic individuals as a result of insensate extremity
Also occur in persons with Hansen’s disease
Pressure Ulcer Etiology:
mechanical injury (pressure, friction, shear) or moisture/Chemical damage
Venous Ulcer Etiology:
Venous insufficiency
Edema/swollen leg
Stasis
Micro trauma
Arterial Ulcer Etiology:
Lack of blood flow
Peripheral vascular disease
Neuropathic Ulcer Etiology:
Diabetes/Hansen’s Disease
Peripheral Neuropathy
Insensate Extremity
Pressure
Stage 1 Pressure Ulcer:
Skin intact; Involves epidermis - hyperemic response; Can’t blanche skin
Stage 2 Pressure Ulcer:
Skin is broken; Involves dermis; Superficial; May appear as blisters
Stage 3 Pressure Ulcer:
Full thickness loss into subcutaneous fat; May have necrotic tissue, tunneling, exudate and/or infections.
Stage 4 Pressure Ulcer:
Full thickness - extends into muscle and/or bone or tendons
Venous Stasis Ulcer Appearance/Location:
Pain is mild and relieved by elevation
Proximal to medial malleolus or gaiter area of leg
Shallow with irregular shape, granular base, oozing
Stasis dermatitis, hyperpigmentation, palpable pulses
Arterial Ulcer appearance/location:
Pain is severe, exacerbated by elevation
Distal to medial malleolus, on dorsum of foot and toes
Irregular edge, poor granulation tissue, little bleeding
Trophic skin changes, absent pulses
Neuropathic Ulcer appearance/location:
Pain Free
Along pressure points of foot, first or fifth metatarsal head
Punched out, callous edges, deep sinus, brisk bleeding
Neuropathy, warmth, variable pulses
Risk factor for pressure ulcer:
Decreased Mobility Lack of Sensation Impaired Nutrition/Low Body Weight Incontinence Impaired Hydration Decreased Cognitive Status Obesity Decreased Diastolic BP Medical Co-morbidity Ischemia Anemia Age Infection Polypharmacy
Venous Stasis ulcer risk factor:
Lymphoedema
Obesity
Pregnancy
Cancer hx
Arterial ulcer risk factor:
PVD
Diabetes
CAD
Stroke
Neuropathic ulcer:
Any dx with sensory loss but motor sparing
Pressure ulcer treatment
Remove necrotic tissue Manage exudate Eliminate infection Maintain a moist wound environment Eliminate Pressure E-stim Patient Education Mobility Training
Venous stasis ulcer treatment
Remove necrotic tissue Manage exudate Eliminate infection Maintain a moist wound environment Edema control - bandaging/compression Patient Education
Arterial ulcer treatment
Remove necrotic tissue Manage exudate Eliminate infection Surgical Consult Patient Education Increase circulation (US/PSWD/E-stim)
Neuropathic ulcer treatment
Remove necrotic tissue Manage exudate Eliminate infection Maintain a moist wound environment Pressure Relief - casting Patient Education E-stim
