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inhibitors [MAOIs] and SSRIs). Fentanyl is emerging as a useful alternative to morphine, with a
lesser tendency to cause haemodynamic instability (Shapiro et al, 1995). It has a short duration
of action after a single dose due to redistribution, but its long elimination half‐life suggests
that it may accumulate when given in high doses for long periods.
The newer opioids, alfentanil and remifentanil, have potentially favourable kinetics for use in
patients with organ dysfunction. Alfentanil combined with propofol led to shorter time to
extubation and ICU discharge compared with a morphine and midazolam combination (Manley
et al, 1997 Level II). Remifentanil exhibits rapid clearance that is independent of renal function
(Cohen & Royston, 2001; Breen et al, 2004) while remifentanil acid, a weak active metabolite, may
accumulate in the presence of renal impairment (Pitsiu et al, 2004 Level IV). This has no clinical
consequences (Breen et al, 2004 Level IV). When titrated carefully against a sedation scale,
remifentanil did not reduce the need for supplementary sedation or the time to extubation
after cessation compared with fentanyl (Muellejans et al, 2004 Level II). The use of remifentanil
in postsurgical ICU patients provided superior analgesia and an accelerated extubation time
compared with morphine (Dahaba et al, 2004 Level II). The combination of morphine and
remifentanil provided better analgesia and sedation than morphine alone, with a lower
incidence of side effects and a similar haemodynamic profile and patient satisfaction (Carrer et
al, 2007 Level II). In a comparison between a remifentanil‐based sedation regimen titrated to
response before the addition of midazolam for further sedation, or a midazolam‐based
sedation regimen with fentanyl or morphine added for analgesia, remifentanil‐based sedation
reduced the duration of mechanical ventilation, improved the weaning process, and decreased
overall sedative doses required in ICU patients requiring long‐term ventilation (Breen et al, 2005
Level II).
Dexmedetomidine is a highly selective alpha‐2 agonist sedative, with anxiolytic and analgesic
properties. It has the advantage of providing titratable sedation with minimal respiratory
depression (Martin et al, 2003 Level II). It can cause a temporary increase in blood pressure
during administration, but the subsequent reductions in heart rate and blood pressure are
more noticeable, especially in haemodynamically labile individuals. It has been introduced into
intensive care practice as an aid to increase tolerance of intubation and mechanical ventilation
and to smooth the transition to spontaneous respiration and extubation. After coronary artery
CHAPTER 9 sedation but significantly lower morphine requirements and fewer ventricular arrhythmias
surgery, dexmedetomidine was associated with similar ventilation times to propofol‐based

(Herr et al, 2003 Level II). These findings were contradicted by a retrospective review in general
ICU patients, where adjunctive dexmedetomidine reduced sedative requirements but did not
alter analgesic requirements. (MacLaren et al, 2007 Level III‐2).
In ventilated patients, the spread of thoracic epidural block increased with positive pressure
ventilation (Visser et al, 2006 Level II).

9.8.4 Guillain-Barre syndrome
Patients with Guillain‐Barre syndrome commonly need treatment in an ICU. They may report
significant pain including painful paraesthesiae, backache, sciatica, meningism, muscle and
joint pain. The distal to proximal distribution of pain that characterises peripheral
neuropathies is not usually seen (Khatri & Pearlstein, 1997).
Early treatment of pain with carbamazepine improved analgesia and reduced requirements
for pethidine and sedation in patients with Guillain‐Barre syndrome (Tripathi & Kaushik, 2000
Level II). Gabapentin (Pandey et al, 2002 Level II) and ketamine infusions (Parisod, 2002) also
improved pain relief. Gabapentin was more effective than carbamazepine for the treatment
of pain in patients with Guillain‐Barre syndrome admitted to ICU for mechanical ventilation

288 Acute Pain Management: Scientific Evidence