Case of the Month #39: Post Amputation Pain by Dr Fiona Sweeney

Published: 06/06/2024

Assessment

Differential diagnoses

Phantom limb syndrome
Persistent stump pain1
  • Infection
  • Stump neuroma
  • Wound breakdown
  • Osteomyelitis
  • Bone spur
  • Haematoma
  • Insufficient myoplasty covering
  • Opioid induced hyperalgesia

Ms A was apyrexial with stable observations and a normal white cell count, CRP, blood and wound cultures. She had been reviewed by the surgeons who had ruled out a surgical reason for her sudden onset pain. She was diagnosed with opioid induced hyperalgesia, a mixed nociceptive and neuropathic persistent stump pain and phantom limb pain. Ms A was also awaiting psychological assessment for increasing anxiety and negative thoughts.

How do you diagnose phantom limb syndrome?

Phantom limb syndrome is a clinical diagnosis and a common sequela of amputation, occurring in up to 80% of patients1-6, with an onset in the early postoperative period of 75% of cases6. It is characterized by stump pain, phantom limb pain and phantom sensations.

The phantom limb pain is typically felt in the distal extremity of the absent limb. Pain characteristics vary but are often described as being episodic, occurring in short bouts (a few seconds to many hours) and cramping, burning or shooting in nature1,3,6. A minority of patients have severe and unremitting phantom pain1.

Telescoping can occur and is where sensation from the missing limb migrates in perceived position towards the stump1.

Phantom sensations are non-painful phenomenon. These are normal and dealt with via reassurance.

Risk factors for developing phantom limb syndrome
  • Severe preoperative pain
  • Bilateral amputation
  • Lower limb amputation
  • Loss of dominant upper limb
  • Repeated limb surgeries
  • Presence of stump pain
  • Increasing age
  • Depression
Pathophysiology

Initial transection of peripheral nerves during surgery causes histamine, bradykinin and prostaglandin release: ‘a sensitising soup’. A lowered threshold potential and increased expression of sodium channels through this peripheral sensitisation further increases the rate of neuronal impulse transmission. As axons are transected, sprouting of the ventral terminal’s large, myelinated axons occurs, allowing the sensory axons to terminate in lamina II so that ‘wrong’ connections are made. For example, the sensory neurons responsible for touch might connect with interneurons that normally receive input from nociceptors.

The increased neuronal activity leads to a central sensitisation or ‘wind-up phenomenon’, with the final factor: cortical re-organization, producing persistent postoperative pain and phantom pain and sensations1-6. The cortical changes after amputation are complex but thought not unique to phantom pain and share similar functional MRI scanning results as that of lower back pain and complex regional pain syndrome1. The degree of cortical reorganization correlates with the severity of phantom limb pain.

Not all painful sensations after amputation are related to phantom pain and can be due to amputation residual limb pain. This can develop from wound healing disorders, structural changes in the stump, mechanical stress and adapting unfavourable movement patterns eg piriformis syndrome, myofascial trigger points, radiculopathy, lower back pain or hip osteoarthritis.