U11W2: Trauma - Limb amputation Flashcards
What is the process of direct bone healing from a fracture?
Where there is no motion at fracture site due to hairline fracture of surgical fixation.
1) appositional healing - cutting cones can directly across the fracture line, osteoclasts create longitudinal cavities which are filled by osteoblasts depositing new bone matrix and proliferate to form new osteons or by the bone marrow or blood vessels. Mature by direct remodelling into lamellar bone
2)Gap healing - small soft callus formation with mesenchymal stem cells causing a small cartilage matrix deposition and woven bone formation, however this is perpednicular to the long axis of the bone, must undergo secondary remodelling where cutting cones osteoclasts restore longitudinal cavity for marrow and osteoblasts deposit osteoid and regenerate osteons.
What is the process of indirect bone healing from a fracture?
1) Homeostasis - blood vessel damage in injury - vasoconstriction of blood vessels followed by coagulation to prevent further blood loss - haematoma forms from blood cells and platelets collected around the necrotic areas of the bone - stabilises the fracture.
2) Inflammation - DAMPs release from damaged bone and potential PAMPS if infected (open fracture) activate PRRs - leads to release of pro-inflammatory mediators, macrophages phagocytose and remove necrotic material. Resolution of inflammation - macrophages produce growth factors. Granulation tissue forms as angiogenesis and fibroblasts are activated.
3) Soft callus formation - periosteum is a source of mesenchymal stem cells differentiate into chondroblasts and then chondrocytes which form a primitive cartilage matrix. Fibroblasts deposit collagen. A fibrocartilaginous matrix forms and starts to be invaded by blood vessels. Acts as a model for bone remodelling.
4) Hypoxia activates HIF expression in immune cells - results in VEGF release from platelets, macrophages etc - results in angiogenesis - restore blood supply to the bone (temporal overlap with stage 3)
5) Hard callus formation - cutting cones are activated, osteoclasts degrade organic bone matrix, osteoblasts deposit new bone matrix, the cartilage model is gradually degraded and calcified, replaced by unorganised bone matrix - this is woven bone
6) osteoclasts create longitudinal cavities to hold bone marrow and the woven bone is remodelled into the lamellar bone with a regular osteon structure, mineralised and with mature vasculature.
How do we decide where to amputate?
Extent of damage - removal all necoritic material, if risk of infection may remove just above evident infection to ensure no spread
Blood supply: compromised blood supply region should be removed or will eventually become necrotic
Aim to preserve as much function and quality of life as possible
Amputate in a way that is suitable for a prosthetic
Consider patient wishes, lifestyle and expectations.
Why might we amputate a limb?
Severe infection (gangrene)
Severe trauma
Diabetic complication
Poor blood circulation
Limb deformities
Tumour
Chronic pain
IN general: poor blood supply and necrosis.
Where do we amputate?
Forequarter amputation
Hind quarter amputation
Shoulder/elbow/wrist/hip/knee/ankle disarticulation (thorugh the joint)
Tranhumeral (above elbow)
Transradial (bleow elbow)
Transfemoral (above knee)
Transtibial (below knee)
Transmetacarpal (mid foot)
What elavluation is needed before an amputation?
General systems review - particular cardiovascular and respiratory
Nutritional status
Strength and condition of healthy limb - may require physio
Psychological and social support assessment - to determine if will have mental stability and ability to meet post-surgery rehabilitation goals
What is the procedure of amputation?
- Anesthesia - general or epidural
- nerve management - cauterisation, ligation, burying nerve in bone, forming a nerve loop - handled in a way to prevent neuroma
- Blood vessel management - haemostasis by ligation or cauterisation to prevent blood loss
- Bone tissue - removed by surgical saw such as Charriere saw, smoothen the stump, take care to cover in soft tissue for a better fit of prosthetic and weight bearing
- Muscle and tendon removal: muscle stabilisation is often reattached to distal bone (myodesis) or each other (myoplasty) - in an arrangement to ensure stability and functionality of stump
- Skin closure - sewn together under tension, broad-based flaps to maintain blood supply, drain system may be used to remove excess fluid, may adjust location of scar to avoid rupture or further complications when weight bearing/prosthetic wearing.
What care may be required after an amputation?
Pain evaluation and pain medication
Physiotherapy to strengthen limb and increase range of motion, may practise transfer processes and positioning, prevent pressure sores.
Wound monitoring and dressing to prevent infection
Psychologist - emotional support and coping
What is phantom limb pain?
The perception of pain or discomfort in a limb that is no longer there
How common in phantom limb pain?
80% of amputees experience phantom limb pain up to two years after the amputation
What are the different causes of phantom limb pain?
Peripheral Nerve Changes
Spinal Cord changes
Brain Changes
Pyschogenic changes
What are the different types of trauma?
Penetrating trauma - foreign object pierces the skin - such as stab wound - has a high risk of hypovolemic shock
Blunt trauma - dull object force striking the body commonly in a car crash targeting the abdomen
Deceleration trauma - when a person moving forward comes to an abrupt halt and the brain within the skull still has forward momentum causing it to hit the inner surface of the skull - concusion.
Describe how peripheral nerve changes may cause phantom limb pain.
Significant nerve and tissue trauma.
Damage nerves may develop neuromas - this disorganised growth structure has more sodium channels hence is hyper-excitable and can cause spontaneous discharges.
This nerve still projects in the spinal cord and the brain - mapping in the brain still connects the nerve to the missing limb.
Suggest how spinal cord changes can lead to phantom limb pain.
There is an increase in NDMA receptors in the dorsal horn leading to higher sensitivity on neurones to substance P, neurokinin etc - this is termed central sensitisation - an increase in activatory signals.
This change in dorsal horn structure can also cause inhibitory neurons to loose their target - decreased in inhibitory signals
This change means that any incoming sensation can cause a disproportionately large response may also be described as a lower threshold for sensory input - causing conscious perception
This is more common in chronic pain syndrome rather then phantom pain
What brain changes may cause phantom limb pain?
Cortical reorganisation - can occur in a sensory deprived brain, this results in a change in the mapping pattern of the brain so that stimuli activate different parts of the cortex than they originally do (change to projection patterns of neurons).
Areas of the cortex that represent the amputated area are taken over by neighbouring regions in the primary somatosensory cortex,
This explains why sensation on/near the stump is often felt in teh amputated limb.
The degree of cortical reaorgansiation is also proportional to the degree of phantom pain felt.
How do psychogenic factors cause phantom limb pain?
Chronic pain is multi-factorial
Depression, anxiety and increased stress can trigger phantom limb pain and increase the risk of developing into chronic pain syndrome.
This may be due to dysregulation in serotonin and norepinephrine - which regulate both mood and pain.
Also opening of the pain gate - lower the threshold for painful sensations from the amputated limb.
What are the pharmacological treatments for phantom limb pain?
NSAIDs
Opiods
Antidepressants (amitriptyline) - 1st line
Anticonvulsants
NMDA receptor antagonists
What are some non-pharmacological treatments for phantom limb pain?
TENS - gate theory - low frequency and high intensity is most effective for PLP
CBT including Mirror therapy
Spinal cord stimulation
How does mirror therapy treat phantom limb pain?
Mirror positions so opposing limb reflextion appears in place of the hidden amputated limb.
Can help reverse cortical reorganisation
Mirror image of the normal body part helps reorganise and integrate the mismatch between proprioception and sensation and the visual feedback of the removed body part - brain preferences visual over sensory feedback.
Brain feels pain but see’s an uninjured limb - reorganise to correct this.
May also activate mirror motor neurons - by seeing a movement of sensation - stimulates the region of the brain previously responsible for this - brain does not become hyposensitised prevents cortical reorganisation.
How does spinal cord stimulation treat phantom limb pain?
Implanted device - sends low levels of electrical activity directly into the spinal cord to relieve pain.
Can be activated in times of pain
Older device - paresthesia - replace with tingling sensation
Newer devices - replace with sub-perception
What is the arterial supply to the arm?
Subclavian artery
Axillary Artery
Brachial artery (with a depp artery branch)
Spilts into the ulnar and radial artery
Deep artery with converge back with the radial artery
The Ulnar artery has a common interosseous which then branches into the Ant and Post interosseus
The radial adn ulnar artery anastomose int he superficial adn deep dorsal arch with the radial contributing more to the deep adn the ulnar the superficial
What is the venous drainge of the upper limb?**
Drains into the subclavian vein
Axillary Vein
Deep: mimic arterial supply, however veins travel in pairs in the forearm (ulnar and radial veins)
Superficial: the cephalic (into axillary) and basilic vein (merge with brachial to continue as axillary) - linked by the median cubital vein or the median antebrachial vein
What is the arterial supply of the lower limb**
External iliac artery
Femoral Artery
Profunda femoral artery (anterior thigh) has perforating branches in medial adn posterior thigh, lateral and medial femoral circumflex artery.
Femoral artery is renamed the popliteal artery as it leaves the abdcutor hiatus and travels through the popliteal fossa.
In the leg this branches into the anterior tibial artery (which becomes the dorsalis pedis artery in the foot) and the tibiopernoneal trunk which then becomes the posterior tibial and the fibular artery.
Internal illiac artery - Obturator artery, superior and inferior gluteal artery.
What is the venous drainage of the lower limb?**
Deep veins - dorsal venous arch, posterior tibial vein/posterior tibial and fibular vein - popliteal vein - femoral vein (joined by the profundis femoral vein) - external iliac
Inferior and superior gluteal veins drain into the internal iliac vein
Superficial veins-
Long saphenous vein - from dorsal venous arch up the medial aspect of the leg into the femoral vein
Small saphenous vein - dorsal venous arch of the foot, moves up posterior aspect of the leg into the popliteal vein.
What happens when arterial supply to a limb is cut off?
Ischemic necrosis - lack of oxygen supply to tissue
Anaerobic respiration - increase in lactic acid
Build up in waste products such as CO2, Urea etc
Results in tissue death (skeletal muscle within 60-90 minutes) - this are that has died by necrosis is termed infarcation.
Presents as: Pallor, paralysis, pain, pulselessness, paraesthesia, polar
What is crush syndrome?
Extensive compression force on body parts - complication of trauma.
Often results in arterial occlusion, and nerve compression leading to extensive muscle and tissue ischemia then necrosis.
When circulation is restored to the area there is a massive release of waste/cellular content into circulation -
this includes myoglobin and potassium.
What is compartment syndrome?
When the pressure within a confined fascial compartment increases beyond a critical level
Results in decreased perfusion pressure.
The injured tissue expands due to oedema, haemorrhage and inflammation, the limited space within the fascial compartment causes intracompartmental pressure to rise - vascular occlusion, ischemic and necrotic muscle - eventually becomes permanent contracture or fibrotic.
What are the potential complications of crush syndrome?
Hyperkalemia - cardiac arrhythmias, muscle weakness or paralysis.
Hyperphosphatemia - which can lead to hypocalcemia
Rhabdomyolysis - muscle breakdown - the release of large quantities of myoglobinuria - leads to renal tubular obstruction and then failure due to acute renal tubular necrosis.
Acidosis - due to generation of lactic acid in anerobic metabolism
