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Key messages
1. Parenteral corticosteroids appear to reduce the duration of analgesia requirements and
length of hospital stay, without major side effects, during sickle cell crises (S) (Level I
[Cochrane Review]).
2. There is insufficient evidence to suggest that fluid replacement therapy reduces pain
associated with sickle cell crises (N) (Level I [Cochrane Review]).
3. Hydroxyurea is effective in decreasing the frequency of acute crises, life‐threatening
complications and transfusion requirements in sickle cell disease (U) (Level I).
4. Intravenous opioid loading optimises analgesia in the early stages of an acute sickle cell
crisis. Effective analgesia may be continued with intravenous opioid therapy, optimally as
PCA (U) (Level II).
5. Oxygen supplementation does not decrease pain during a sickle cell crisis (U) (Level II).
The following tick box represents conclusions based on clinical experience and expert
opinion.
Pethidine should be avoided for the treatment of acute pain in sickle cell disease or acute
porphyria, with increased seizure risk being a potential problem (U).
9.6.5 Acute headache
Headaches are a common cause of acute pain. There are many causes of acute headache,
some of which involve structures other than the head (eg the neck). Before treating acute
headache, it is vital to rule out serious cranial pathologies such as tumour, infection,
cerebrovascular abnormalities, acute glaucoma and temporal arteritis (Silberstein, 2000; Steiner
& Fontebasso, 2002).
The most frequent causes of acute headache are episodic tension‐type headache (TTH) and
migraine (Headache Classification Subcommittee of the IHS, 2004). Less frequent causes include
trigeminal autonomic cephalalgias (episodic cluster headache, episodic paroxysmal hemicrania
and Short‐lasting Unilateral Neuralgiform headache attacks with Conjunctival injection and
CHAPTER 9 Tearing [SUNCT]) or ‘secondary headaches’, such as acute post‐traumatic headache, postdural
puncture headache (PDPH), headache attributed to substance use or its withdrawal and
cervicogenic headache (Headache Classification Subcommittee of the IHS, 2004).
Comprehensive guidelines for the evaluation and treatment of acute headaches including
migraine have been promulgated (Edlow et al, 2008; Steiner et al, 2007; Evers et al, 2006), including
for children and adolescents (Lewis et al, 2004).
Episodic tension-type headache
TTHs may be episodic (frequent or infrequent) or chronic in nature. The lifetime prevalence of
TTH in the general population is between 30% and 78%. Episodic TTH is usually bilateral and is
often described as a mild to moderate ‘pressing’ or ‘tight pain’ (sometimes with pericranial
tenderness), not worsened by movement and not associated with nausea. Photophobia or
phonophobia may occasionally be present (Headache Classification Subcommittee of the IHS, 2004).
The symptoms and pathogenesis of TTH may overlap with migraine, chronic daily headache,
medication overuse headache and cervicogenic headache (Goadsby, 2003). Psychological,
physical and environmental factors are important in TTH and should be addressed during
assessment and treatment (Holroyd, 2002).
260 Acute Pain Management: Scientific Evidence
