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addition, showed a reduction in the incidence of PONV. Later studies, where continuous
ketamine infusions were used for 48 hours after abdominal surgery, have shown similar
results. One reported significantly reduced pain scores, PCA morphine consumption, nausea
and vomiting, with no ketamine‐related adverse effects, compared with placebo (Zakine et al,
2008 Level II). The other also reported lower PCA morphine requirements, better pain scores at
rest and with movement, as well as less sedation; there were no differences in trail‐making
test times and errors, dreams or hallucinations (Webb et al, 2007 Level II). A 24‐hour
postoperative infusion of 83 mcg/kg/hr but not 42 mcg/kg/hr in addition to PCA fentanyl after
cervical spine surgery was opioid‐sparing and improved pain relief (Yamauchi et al, 2008 Level II).
While concurrent administration of ketamine reduced PCA opioid requirements and the
incidence of nausea and vomiting (Bell et al, 2006 Level I), there is conflicting evidence regarding
the benefit derived from adding ketamine to the PCA opioid solution. In six studies where
ketamine was added to the PCA opioid, results were mixed; pain was reduced in four of these
studies and morphine consumption in three (Bell et al, 2006 Level I). Three more recent studies
showed a lack of benefit after gynaecological (Aubrun et al, 2008 Level II) and orthopaedic
surgery (Sveticic et al, 2008 Level II), or uterine artery embolisation (Jensen et al, 2008 Level II). In
another, however, the addition of ketamine to morphine PCA reduced pain scores and the
incidence of nausea and vomiting, was opioid‐sparing, and led to shorter duration of use of
PCA compared with PCA morphine alone (Kollender et al, 2008 Level II). In a study of post‐
CHAPTER 4 thoracotomy patients, the addition of ketamine to morphine for PCA was opioid‐sparing but
failed to improve analgesia; however patients in the ketamine group had better respiratory
parameters (Michelet et al, 2007 Level II).
Use of a low‐dose IV ketamine infusion postoperatively significantly reduced acute pain in
patients receiving epidural ropivacaine and morphine analgesia following thoracotomy (Suzuki
et al, 2006 Level II).
Other outcomes have also been investigated. Parenteral ketamine improved rehabilitation
after total knee arthroplasty (Adam et al, 2005 Level II). There was no significant difference in
postoperative morphine consumption or area of stump allodynia between patients who
received either a ketamine or saline infusion for 3 days after leg amputation; interestingly, the
incidence of acute stump pain was significantly increased in the ketamine group (Hayes et al,
2004 Level II).
Based on these data, the ‘routine’ use of IV perioperative ketamine is not indicated and the
place of ketamine in the treatment of chronic pain and the effects of long‐term use remains
unclear (Visser & Schug, 2006).
Bolus dose ketamine (0.25 mg/kg) was an effective ‘rescue analgesic’ in patients with acute
postoperative pain that was poorly responsive to morphine (Weinbroum, 2003 Level II). In
contrast, in a later study, the addition of bolus dose ketamine (0.25 mg/kg) to morphine for
rescue analgesia in the recovery room failed to improve analgesia or reduce the incidence of
nausea or vomiting (Gillies et al, 2007 Level II).
In the emergency department, ketamine used to treat severe trauma pain had a significant
morphine‐sparing effect without a change in pain scores (Galinski et al, 2007 Level II). A low‐dose
SC ketamine infusion provided better analgesia for acute musculoskeletal trauma pain with
less nausea, vomiting and sedation, and improved respiratory function, than intermittent SC
morphine injections (Gurnani et al, 1996 Level II). Ketamine‐midazolam mixtures used for
fracture reductions in paediatric patients in the emergency department were associated with
less distress and fewer airway interventions than fentanyl‐midazolam or propofol‐fentanyl
combinations (Migita et al, 2006 Level I).

84 Acute Pain Management: Scientific Evidence