prevention of PONV include 5-HT3 antagonists, dexamethasone,
antagonists; therefore, the costs of the different agents should be
taken into consideration when selecting therapy.52,60 Droperidol
has long been used for PONV, but concerns have been raised
Medications for Prevention and Treatment of Postoperative Nausea and Vomiting (PONV) in Adults
Medication Prophylactic Dose Treatment or Rescue Dose
Aprepitant 40 mg PO within 3 hours before induction of anesthesia None
Dexamethasone 4–10 mg at the start of induction of anesthesia 2–4 mg IV
Dolasetron 12.5 mg IV at end of surgery 12.5 mg IV
Droperidol 0.625–1.25 mg IV at end of surgery 0.625–1.25 mg IV or IM every 4–6 hours
Metoclopramide 10–20 mg IV at end of surgery 10–20 mg IV or IM every 6 hours
Granisetron 0.35–1 mg IV at end of surgery 0.1 mg
Ondansetron 4–8 mg IV at end of surgery 1 mg IV every 8 hours
Palonosetron 0.075 mg IV immediately prior to induction of anesthesia None
Prochlorperazine 5–10 mg IV at end of surgery 5–10 mg IV or IM every 4–6 hours
Promethazine 12.5–25 mg IV at induction or end of surgery 12.5–25 mg IV or IM every 4–6 hours
Scopolamine 1.5 mg TOP evening before surgery or at least 4 hours
IM, intramuscular; IV, intravenous; PO, oral; TOP, topical patch.
111Nausea and Vomiting Chapter 6
about the rare occurrence of QT prolongation and torsades de
for adults).53,61,62 The mechanism by which dexamethasone
protects against PONV is unclear, but its efficacy has been shown
Aprepitant has been studied in the prevention of PONV.29,52,53
Studies have shown the activity of aprepitant and indicate similar
activity compared with ondansetron.29,52,53 Aprepitant, however,
and are highly effective.52,53,57,59,62 Transdermal scopolamine is
antagonists and droperidol seem to be more effective when given
at the end of surgery. Corticosteroids are best given before the
Several methods for nonpharmacologic techniques for the
prevention of PONV have been studied and have been shown to
be effective, at least in some patient populations. These include
acupuncture, transcutaneous nerve stimulation, acupressure at
the P6 wrist point, hypnosis, and aromatherapy with isopropyl
alcohol. Ginger remedies were not found to be more effective
Even with appropriate prophylaxis for PONV, some patients
will experience breakthrough symptoms and require rescue
therapy.52 Patients who have not received prophylaxis with a
5-HT3 antagonist can be offered a low dose of a 5-HT3 antagonist
for rescue. For rescue, only about one-quarter of the prophylaxis
pharmacologic class than the agents used for prophylaxis.52,54,59
A full list of references for this chapter can be found at
http://thepoint.lww.com/AT10e.Below are the key references
American Society of Clinical Oncology et al. American Society of
Clinical Oncology guideline for antiemetics in oncology: update
2006 [published correction appears in J Clin Oncol. 2006;24:5341].
J Clin Oncol. 2006;24:2932. (12)
Feyer P et al. Radiotherapy-induced nausea and vomiting (RINV):
MASCC/ESMO guideline for antiemetics in radiotherapy: update
2009. Support Care Cancer. 2010 Aug 10 [Epub ahead of print].
Gan TJ et al. Society for Ambulatory Anesthesia guidelines for
the management of postoperative nausea and vomiting. Anesth
Golding JF, Gresty MA. Motion sickness. Curr Opin Neurol. 2005;
Roila F et al. Guideline update for MASCC and ESMO in the
prevention of chemotherapy- and radiotherapy-induced nausea
and vomiting: results of the Perugia consensus conference. Ann
Oncol. 2010;21(Suppl 5):v232. (13)
Ettinger DS et al. Antiemesis: clinical practice guidelines
in oncology. V2.2010. http://www.nccn.org/professionals/
physician gls/pdf/antiemesis.pdf. Accessed September 30,
Priesol AJ. Motion sickness. Up To Date. http://www.upto
date.com/contents/motion-sickness?source=search result&
selectedTitle=1%7E51. Accessed September 27, 2010. (2)
Lee A. Kral and Virginia L. Ghafoor
1 Pain is an unpleasant sensory and emotional experience associated with actual or
potential tissue damage. The perception of pain is individualized and affected by
other comorbidities such as depression and anxiety. It is characterized as
musculoskeletal, neuropathic, or visceral.
2 Pain management is complex and requires multimodal therapies, both pharmacologic
and nonpharmacologic. Many factors affect analgesic selection, including
comorbidities, available routes of administration, and cost. Multimodal therapy,
especially with medications, requires monitoring for efficacy and adverse effects.
3 Fibromyalgia and myofascial pain both present with musculoskeletal pain, but
fibromyalgia is a syndrome of central neurotransmitter imbalance. Myofascial pain is a
localized chronic pain at the neuromuscular junction. Muscle relaxants have shown
minimal benefit for chronic pain.
4 Anticonvulsants and antidepressants are the analgesics of choice for treating
peripheral neuropathic pain either as monotherapy or combination therapy. Opioids
and topical agents may also be used. Therapy is chosen depending on whether the
pain is localized or more generalized in presentation.
5 Elderly patients and patients with multiple comorbidities are at high risk for adverse
effects. Pharmacokinetic and pharmacodynamic drug interactions must be considered
with use of antineuralgics and antidepressants.
6 Neuropathic pain may be caused by injury to peripheral nerves or to the central
nervous system. Central neuropathic pain may present with peripheral symptoms that
are localized or generalized. Pharmacotherapy has minimal effectiveness.
Interventional therapies may serve an adjunctive role for pain relief to facilitate the
primary goal of physical functional rehabilitation.
7 Pain is the most common symptom of osteoarthritis in older adults. There are several
guidelines addressing osteoarthritis, and pain management is a balance between pain
relief and prevention of side effects. Acetaminophen, nonsteroidal anti-inflammatory
drugs, and opioids are beneficial in the treatment of pain but have unwanted side
effects. Topical agents may be an alternative to systemic therapies in patients at risk
for adverse gastrointestinal and renal effects.
8 Abdominal pain is mediated by the enteric nervous system and does not always have
a typical presentation. Pharmacologic therapy is often ineffective. Antidepressants in
conjunction with cognitive behavioral pain management are recommended for
management of functional abdominal pain syndrome.
9 Opioid therapy requires effective risk assessment to avoid medication abuse, misuse,
and diversion. Monitoring recommendations should include use of written opioid
agreements, urine drug testing, opioid risk screening tools, and electronic
prescription monitoring program records.
113Pain and Its Management Chapter 7
10 Cancer pain may result from one or more causes related to direct tumor involvement,
cancer therapy, and psychological factors. Pain management involves assessment of
the patient to determine the etiology of pain and development of a care plan to
address pain and symptom management.
11 Transdermal fentanyl and methadone are potent opioids commonly used in cancer
pain management. Opioid conversion tables for fentanyl and methadone are different
due to differences in pharmacokinetics in cancer patients. Treatment of incident,
spontaneous, and end-of-dose pain should be part of the cancer pain management
plan. Supplemental doses of short-acting opioids are recommended for breakthrough
12 Medication adverse effects including sedation, constipation, nausea, vomiting,
itching, and respiratory depression should be addressed in the pain management
plan. Risk of QTc prolongation should be periodically evaluated with methadone.
Complimentary and alternative medicine therapies are widely used by patients in the
management of cancer pain, dyspnea, and nausea and vomiting. Neuraxial opioid
administration may be appropriate for patients with intolerable pain who cannot
tolerate systemic opioid therapy.
described in terms of such damage.”1 The ability to experience
pain is critical for survival because it informs the body of real
or potential injury (e.g., touching a hot stove). The body is then
able to respond to the threat and protect itself from further injury
(e.g., refraining from touching or removing the hand from the
most common types of pain include low back pain, headache,
and joint pain.2 Many people think that pain is a natural part of
growing older, and up to 60% of people believe that pain is just
something you have to live with.3 Chronic pain is reported more
often in women than men, and in non-Hispanic white patients
compared with other races and ethnicities.2 Chronic pain is also
more common in those whose income is two times less than
the level of poverty. Pain is more complex than just physiology.
It is a subjective experience, and sometimes the amount of pain
Recall of previous pain experiences
FIGURE 7-1 Factors affecting chronic
cultural, spiritual, and cognitive factors. Unrelieved chronic pain
ones. About one-third of people with chronic pain describe it as
“disabling,” with the Centers for Disease Control and Prevention
reporting that chronic pain is the leading cause of disability in the
United States and that the cost of chronic pain was estimated in
1998 to be $100 billion annually.4 Pain is also the second leading
cause of health-related work absenteeism, with at least 50 million
Gureje et al. investigated an international population of
chronic pain patients in the primary care setting.6 They found
factors, cognitive factors, and emotional factors (Fig. 7-1). All
are interrelated and illustrate the complex nature of chronic
FIGURE 7-2 Pain pathways. 5-HT, serotonin; NE, norepinephrine.
Nociception, or the sensation of pain, is composed of four basic
(free nerve endings located throughout the skin, muscle, joints,
fascia, and viscera). Normal sensory stimuli do not activate the
pain signal, but if the stimulus is powerful enough to surpass the
(crushing or pressure), chemical (endogenous or exogenous), or
thermal (hot or cold) stimuli. Some nociceptors are polymodal,
transducing more than one type of stimuli. One of these types
of nociceptors is called the transient receptor potential (TRP).
This family has a large number of members that are activated by
the whole spectrum of thermal stimuli (very hot to very cold),
as well as some mechanical and various chemical stimuli. Other
receptors are “silent,” but are recruited if the stimulus is more
After stimulation of nociceptors, several processes occur.
Proinflammatory mediators, including histamine, substance P,
prostaglandins, bradykinins, and serotonin, are released at the
site of injury. Immune mediators are also released, including
tumor necrosis factor, nerve growth factors, interleukins, and
interferons. These mediators sensitize the nociceptors, lowering
Transmission is the propagation of the electrical signal along
primary afferent nerves, through the dorsal horn of the spinal
cord to the central nervous system (CNS). Painful impulses are
generated at the nociceptor, with voltage-gated sodium channels
initiating the action potentials. Voltage-gated calcium channels
are responsible for allowing calcium influx to the presynaptic
terminal, causing neurotransmitter release. The message is then
transmitted to the spinal cord via two primary afferent nerve
types: myelinated A fibers and unmyelinated C fibers. The Aδ
fibers are responsible for rapidly conducting impulses associated
with thermal and mechanical stimuli. Transmission of signals
along Aδ fibers results in sharp or stabbing sensations that alert
the patient to an injury (also called “first pain”). This produces
reflex signals, such as musculoskeletal withdrawal, to prevent
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