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9.1.2 Acute postamputation pain syndromes
Following amputation of a limb, and also breast, tongue, teeth, genitalia and even inner
organs such as the rectum, or a deafferentiation injury such as brachial plexus avulsion (Bates
& Stewart, 1991; Boas et al, 1993; Dijkstra et al, 2007), a number of phenomena can develop. These
require differentiation.
• Stump pain is pain localised to the site of amputation. It can be acute (usually nociceptive)
or chronic (usually neuropathic) and is most common in the immediate postoperative
period (Jensen et al, 1985; Nikolajsen & Jensen, 2001). The overall incidence of stump pain is
uncertain but the risk of early stump pain is increased by the presence of severe
preamputation pain (Nikolajsen et al, 1997).
• Phantom sensation is defined as any sensory perception of the missing body part with the
exclusion of pain. Almost all patients who have undergone amputation experience
phantom sensations (Jensen et al, 1983). These sensations range from a vague awareness of
the presence of the organ via associated paraesthesia, to complete sensation including
size, shape, position, temperature and movement.
• Phantom limb pain is defined as any noxious sensory phenomenon in the missing limb or
organ. The incidence of phantom limb pain is estimated to be 30% to 85% after limb
amputation and occurs usually in the distal portion of the missing limb (Jensen et al, 1985;
Perkins & Kehlet, 2000; Nikolajsen & Jensen, 2001). Pain can be immediate — 75% of patients
will report phantom pain within the first few days after amputation (Nikolajsen et al, 1997)
— or delayed in onset. The pain is typically intermittent and diminishes with time after
amputation. Factors that may be predictive of postamputation phantom pain are the
severity of preamputation pain, the degree of postoperative stump pain and
chemotherapy (see Section 1.3). If preamputation pain was present, phantom pain may
resemble that pain in character and localisation (Katz & Melzack, 1990). Intensity of
preamputation pain and acute postoperative pain were strong predictors of intensity of
chronic pain after amputation (Hanley et al, 2007 Level III‐3). Preoperative passive coping
strategies, in particular catastrophising, were other strong predictors of phantom limb pain
6 months later (Richardson et al, 2007 Level III‐3).
CHAPTER 9 inter‐related (Jensen et al, 1983; Kooijman et al, 2000). All three of the above phenomena can
There is a strong correlation between phantom limb and stump or site pain and they may be
coexist (Nikolajsen et al, 1997).
A survey identified the high incidence of these pain syndromes after amputation in
537 amputees; only 14.8% were pain free, 74.5% had phantom limb pain, 45.2% stump
pain and 35.5% a combination of both (Kern et al, 2009 Level IV).
Prevention
Evidence for the benefit of epidural analgesia in the prevention of all phantom limb pain is
inconclusive (Halbert et al, 2002 Level I). However, an analysis of studies on phantom limb pain
prophylaxis showed that perioperative (pre, intra and postoperative) epidural analgesia
reduced the incidence of severe phantom limb pain (NNT 5.8) (Gehling & Tryba, 2003 Level III‐2).
A small observational study found that while the overall incidence of long‐term phantom limb
pain was similar in patients given ketamine (bolus dose followed by an infusion, started prior
to skin incision and continued for 72 hours postoperatively) compared with no ketamine, the
incidence of severe phantom limb pain was reduced in the ketamine group (Dertwinkel et al,
2002 Level III‐3). Another study looking at the effects of ketamine reported a numerical but
not statistically significant difference in the incidence of phantom limb pain at 6 months after
amputation (47% in the ketamine group and 71% in the control group) (Hayes et al, 2004
234 Acute Pain Management: Scientific Evidence

