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et al, 2006 Level III‐3). In patients having radical prostatectomy, the addition of daily dronabinol
did not alter the analgesic requirement for piritramide (Seeling et al, 2006 Level II).
Although the number of clinical trials was small, cannabinoids were mildly effective in the
treatment of chronic neuropathic and multiple sclerosis‐related pain; the most common
adverse effect was dizziness (35% of patients) (Iskedjian et al, 2007 Level I).
In patients with a variety of causes for both peripheral and central neuropathic pain, smoking
cannabis (low and high dose) was significantly more effective than smoking placebo cigarettes
in reducing neuropathic pain; acute cognitive impairment, particularly of memory, was
significantly greater at higher cannabis doses, but psychoactive effects (‘feeling high’, ‘feeling
stoned’) with both high and low doses were minimal and well‐tolerated (Wilsey et al, 2008
Level II). Smoked cannabis was also more effective than placebo cigarettes in HIV‐associated
neuropathic pain (Abrams et al, 2007 Level II); the rate of responders (30% reduction in pain) in
one trial was 46% with cannabis and 18% with placebo (Ellis et al 2009 Level II). A cannabidiol/
THC oromucosal spray was more effective than a placebo spray for multiple sclerosis‐related
neuropathic pain (Rog et al, 2005 Level II). Compared with placebo, oromucosal administration
of both combined cannabidiol/THC and THC alone were effective for the relief of intractable
central neuropathic pain resulting from brachial plexus avulsion (Berman et al, 2004 Level II).
It should be noted that all clinical studies to date have design limitations, involve small
CHAPTER 4 The possible benefits from more selective agonists have yet to be investigated in the
numbers of patients and only used non‐selective highly lipophilic cannabinoid compounds.

clinical setting.

Key message
1. Current evidence does not support the use of cannabinoids in acute pain management (S)
but these drugs appear to be mildly effective when used in the treatment of chronic
neuropathic pain, including multiple sclerosis‐related pain (N) (Level I).
4.3.9 Glucocorticoids

Surgical tissue trauma leads to the conversion of arachidonic acid to prostaglandins and
leukotrienes. NSAIDs inhibit the formation of prostaglandins whereas glucocorticoids also
inhibit the production of prostaglandins, leukotrienes and cytokines (Gilron, 2004; Romundstad &
Stubhaug, 2007). Several randomised controlled studies have shown that the addition of
glucocorticoids reduces postoperative pain and analgesic requirement (see below). Additional
benefits include decreased PONV and fatigue (Romundstad et al, 2006; Kehlet, 2007).
However more information is still needed about dose‐finding, the effects of repeat dosing,
procedure‐specific effectiveness and safety (Kehlet, 2007). While good data regarding side
effects are still lacking, high doses have been used in elective and emergency surgical patients
without an increase in morbidity (Sauerland et al, 2000 Level I).
Earlier studies have shown benefit after oral surgery, tonsillectomy, lumbar disc surgery,
laparoscopic cholecystectomy, arthroscopic surgery and lung resection (Gilron, 2004;
Kehlet, 2007).
Studies looking at the effect of glucocorticoids after surgery include those where comparisons
have been made with placebo only and those where comparisons have been made with other
analgesics +/‐ placebo.
Preoperative administration of dexamethasone in patients undergoing total hip arthroplasty
led to better dynamic pain relief than placebo, but there were no differences in pain at rest,
PCA morphine requirements, wound complications or infection at one month after surgery

94 Acute Pain Management: Scientific Evidence