Trauma Flashcards
What is the continuation of the artery supply the lower limb?
Common iliac > external iliac - femoral once passed under inguinal ligament - popliteal artery once enters posterior compartment of thigh > terminal branches: anterior and posterior tibial arteries
What are the branches off the femoral artery?
Superficial epigastric artery
Superficial circumflex iliac artery
Superficial external pundendal artery
Deep external pudendal artery
Profunda femoris
Descending genicular artery
What is the arterial supply in the thigh and gluteal region?
Common iliac > external iliac > femoral
Profunda femoris artery PFA from femoral
PFA branches: perforating branches, lateral and medial femoral circumflex
Common iliac > internal iliac > obturator artery > anterior and posterior branch
Internal iliac > superior and inferior gluteal arteries
What is the arterial supply of the leg?
Popliteal artery divides into anterior tibial artery and tibioperoneal trunk
Tibioperoneal trunk bifurcates: posterior tibial and fibular artery
Anterior tibial artery runs down into the foot and becomes the dorsalis pedis artery
What is the arterial supply of the foot?
Supplied via two arteries:
Dorsalis pedis > anastomoses with lateral plantar artery and forms deep plantar arch
Posterior tibial > splits into lateral and medial plantar arteries > deep plantar arch
What is a crush injury?
Compression of part of the body that causes muscle swelling/neurological disturbances
What is crush syndrome?
Crush injury with systematic manifestations
Systemic manifestations caused by traumatic rhabdomylolysis (destruction of skeletal muscle) due to muscle repurfusion injury when compressive forces are released
Cause local tissue injury, organ dysfunction, metabolic abnormalities - acidosis, hyperkalemia, hypocalcaemia
What is the pathophysiology of crush syndrome?
After prolonged compression on muscle tissue
- Ischaemia reperfusion (pressure relieved) causes traumatic rhabdomyolysis
- Muscle cell rupture releases large quantities of potassium, phosphate, myoglobin, CK, LDH and urate > enter circulation
- Excess myoglobin filtered by kidneys - precipitates in DCT causes obstruction when renal threshold is exceeded. Vasoconstriction of afferent vessels due to myoglobin metabolic products > tubular destruction
- NO system is activated and further leads to vasodilation and hypotension
What is crush syndrome characterised by?
Hypovolemic shock - due to sequestration of water in injured muscle cells
Hyperkalaemia - due to release from injured muscle cells
Can lead to:
- Metabolic acidosis: release of cellular phosphate and sulphate by injured cells
- Acute kidney injury: from excess myoglobin filtered
- Disseminated intravascular coagulation: due to release of thromboplastin and prothrombin from muscle cells
How does rhabdomyolysis cause metabolic acidosis?
Excessive cell breakdown releases uric acid
Hypovolemia and poor tissue perfusion can cause release of lactic acid
How does rhabdomyolysis cause hyperphosphatemia?
Leukocytes move into damaged muscle cells upon reperfusion and cause release of muscle breakdown products into bloodstream including phosphate
How does rhabdomyolysis cause hyperkalaemia?
Leukocytes move into damaged muscle cells upon reperfusion and cause release of muscle breakdown products into bloodstream including potassium
How does rhabdomyolysis affect calcium?
Initial hypocalemia:
Muscle injury causes influx of calcium and sodium. Hyperphosphatemia causes deposition of calcium phosphate in destroyed muscle cells and other tissue.
Later hypercalemia:
Calcium leaks out of myocyte after cell lysis
What is the clinical presentation of crush syndrome?
Crushing of large muscle mass
Sensory and motor disturbances in compressed limb - become tense and swollen - limb may become pulseless
Myoglobinuria and haemoglobinuria may make urine brown
Oligouria with hypovolemic shock
Nausea, vomiting, confusion, agitation
Elevated urea, creatinine, uric acid, postassium, phosphate, CK
Hypo/hypercalcemia
How does rhabdomyolysis cause hypovolemic shock?
Muscle cell injury > influx of sodium and calcium
Water is drawn into the cell with sodium > cell swelling and disruption of membranes
Massive fluid shift from extracellular fluid and blood into cells.
Pre-shock: compensatory mechanisms - increased sympathetic tone - increased HR, cardiac contractility, peripheral vasoconstriction.
Continued volume decrease > shock state: fall in systolic BP, tachycardia, oliguria
Tissue hypoperfusion, hypoxia - switch to anaerobic respiration > lactic acidosis
What blood tests should be ordered for crush syndrome?
- U&Es:
- Creatinine
- Calcium
- Phosphate
- Creatinine kinase
- Uric acid
- FBC and clotting studies
- LFTs
- Blood gases
How may a patient with a crush injury be treated?
- Primary survey ABC
- IV access and fluid resuscitation prior to releasing crushed extremity
- Short term use of tourniquet if required
- Acute limb amputation should be avoided until extrication is impossible
- Aggressive hydration to combat hypotension
- Haemodialysis
- Monitor for cardiac arrhythmia
What will be checked before amputation surgery?
- Physical examination
- X-ray
- CT scan
- Medication history
What will be undertaken on the day of the surgery before operating?
- Pulse monitored
- BP taken
- Cannulation
- Anaesthesia
- Surgery
What will be undertaken post-surgery?
- Continuous BP and pulse
- IV drip
- Healing of wound
- Oxygen
- Pain relief
- Physical therapy
What is the ascending tract that transmits pain perception?
Spinothalamic tract:
Stimulus activates cytokine release
This activates an action potential in sensory nerve fibres and carry impulses to the dorsal horn of the spinal cord
Synapse with secondary neurons at the dorsal horn
Secondary neuron runs up the spinothalamic tract contralaterally and synapse at the thalamus
Tertiary neurons relays information to the somatosensory cortex
What is the descending pathway involved in pain modulation?
- Neurons arise from periaqueductal grey matter in the spinal cord and come down to synapse at the nucleus raphe magnus
- Secondary neuron can control the conduction of the ascending pathway within the substantia gelatinosa
What is the idea of gate control theory?
Proposed by Melzack and Wall
The gate is a machnism where pain can be let through if open. It can also be closed.
If the gate is closed, the pain signals will be restricted travelling up to the brain, and the perception of pain won’t be perceived
Application of a non-noxious stimulus e.g. light rubbing may reduce the pain.
What is the proposed mechanism of the gate control theory?
Deep touch activates pacinian corpuscules in the dermis of the skin e.g. rubbing skin
Signal is transmitted by the DCML ascending ipsilaterally to the MO
Decussates in the medial leminiscus in the MO
The DCML can activate inhibitory neurons which can release enkephalin which bind to opioid receptors in the post synaptic membrane of the neuron
Causes closure of calcium channels, which reduces excitatory neurone e.g. glutamate and substance P release from primary neuron
Reduced excitation of secondary neurones, depolarisation and reduced firing of APs sent to the brain
What are the theories of phantom limb pain?
Cortical reorginsation: Area of the somatosensory cortex still responds to signals from the missing limb due to stimulation of other neurons nearby
Nerve damage: damage to peripheral nerves during amputation leads to abnormal signalling resulting in perception of pain in the missing limb
Psychological factors: cognitive factors may exacerbating or alleviate phantom pain. Retaining memories of pain experiences which can persist even after the cause of the pain is removed
What is the pharmacology of morphine?
Primary targets: mu, kappa and delta receptors which are GPCRs. Modulate calcium channel activity
Secondary target: Lymphocyte antigen 96 (pharmacolohical effect unknown)W
What is the physiology of morphine?
Morphine binds to opioid receptors: mu, kappa, delta
Causes inhibition of pain signals
Normally excitatory NTs are released e.g. glutamate, substance P and CGRP which promote pain signalling by exciting second-order neurons in the dorsal horn which cause excitation, propagating signals
Activation of opioid receptors causes closing of Ca2+ channels in presynaptic neuron, decreases release of NTs, cause K+ efflux
What are the side effects of morphine?
Nausea: stimulation of CRT in MO
Constipation, light-headedness, dizziness
Respiratory depression
What are the types of fractures? 9
Avulsion: small fragments puled away by tendons/ligaments
Comminuted: break into multiple fragments
Compound: open, bone penetrates the skin
Greenstick: incomplete break, bone bends
Impacted: one end of broken bone is driven into interior of other fragment
Linear: straight line across the bone
Oblique: diagonal break across bone
Spiral: spiralling break along length of bone
Transverse: break perpendicular to axis of bone
How can fractures be repaired?
Closed reduction and immobilisation: manipulating bones from outside before using cast/brace/splint
Open reduction and internal fixation: open surgery to reposition bone to correct position to place plates, rods, screws to fix position
External fixation: metal pins or screws into bone and connecting them externally to a rigid frame
Traction: applying force using a system of weights and pulleys to align bone - temporary before treatment
Functional bracing: brace to support fracture, allows some movement
Intramedullary nailing: long metal rod inserted into medullary canal of long bone
