Pathophysiology

• Phantom Limb Pain (peripheral nerve changes).

  Limbs full of sensory neurons, most pathways remain after amputation

  At site of amputation there are severed nerve endings -> endings can thicken & become more sensitive -> transmit distress signals (even in response to mild pressure) - normally inhibited by dorsal horn

  In somatosensory cortex, representation of amputated is still present -> increased representation (phantom limb pain)

  Overtime area of cortex representing amputated limb may shrink & pain stops
• What is compartment syndrome?

  Increased pressure within a muscle compartment leading to reduced blood flow and tissue damage.
• What is reperfusion injury?

  Can be called ischaemia reperfusion injury (IRI)

  Tissue damage caused when blood supply returns to tissue after a period of ischemia or lack of O2

  Return of O2 & inflammatory cells may lead to free radical generation -> further damages myocytes
• What are the damaging substances produced from anaerobic respiration?

  Histamine

  Lactic acid

  NO

  Potassium

  Thromboplastin
• What is released into systemic circulation in crush syndrome?

  Myoglobin

  Creatine kinase

  Potassium

  Magnesium

  Phosphorus

  Uric acid
• How is histamine damaging (related to crush syndrome)?

  Vasodilator = exacerbates hypovolaemic shock

  Bronchoconstriction = exacerbates hypoxaemia
• What is crush syndrome?

  Significant metabolic derangement

  Develops when crushed extremities or body parts remain trapped for prolonged period

  Can lead to renal failure & death

  When body part is released, floods with toxins
• How can potassium be damaging when released in excess?

  Hyperkalaemia -> arrthymia
• What is phantom limb pain?

  Ongoing painful sensations that seem to be coming from part of limb that is no longer there

  Limb is gone, pain is real
• What is a major complication of crush syndrome?

  Compartment syndrome
• How is lactic acid damaging?

  Metabolic acidosis
• When is the onset of phantom limb pain most often?

  Soon after surgery
• Crush injuries

  Trauma to blood vessels -> transudation of fluid, interstitial bleeding -> ischaemia & hypoxia

  Cells no longer able to maintain metabolic function -> oedema & third spacing of fluid

  If oedema occurs in a closed space -> increased pressure will collapse microcirculation, eliminate O2 transfer across capillary endothelium & further contribute to hypoxic insult
• What are the 4 theories behind phantom limb pain?

  Not fully understood

  • Peripheral nerve changes
  • Spinal cord changes
  • Brain changes
  • Psychogenetic changes
• Phantom limb pain (spinal cord changes)

  Central sensitisation - increase in DNMA receptor expression in dorsal horn

  Any incoming sensation can drive a disproportionate response -> conscious perception
• Phantom limb pain (brain changes).

  Cortical reorganisation - areas of cortex that previously represented the amputated limb become invaded by neighbouring somatosensory & motor cortex

  Signals are still being sent & received to & from that are of cortex that belonged to missing limb