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P1: Trim: 8.375in × 10.875in Top: 0.373in Gutter: 0.

664in
LWBK915-06 LWW-KodaKimble-educational November 17, 2011 16:23

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CHAPTER CASES

POSTOPERATIVE NAUSEA AND VOMITING

Chapter 6
1 The risk of postoperative nausea and vomiting depends on several patient, surgical Case 6-4 (Question 1),
and anesthetic factors. The antiemetic regimen should be proportional to the risk Table 6-6
factors.

2 The most active agents in preventing postoperative nausea and vomiting are 5-HT3 Case 6-4 (Question 1),

Nausea and Vomiting


antagonists. For patients at moderate to high risk, a 5-HT3 antagonist should be Table 6-6
combined with dexamethasone or droperidol. Antiemetics used for rescue therapy
should be of a different class than the prophylaxis agents used.

DEFINITION ing signals from other parts of the brain and the GI tract and then
coordinates the emetic response by sending signals to the effector
Nausea and vomiting are unpleasant symptoms caused by self- organs. The VC is located in the medulla oblongata of the brain,
limiting disorders or serious conditions such as cancer. These near the nucleus tractus solitarius (NTS). The VC is stimulated
symptoms can range from mild, short-lived nausea to contin- by neurotransmitters released from the chemoreceptor trigger
uing severe emesis and retching. The emetic response can be zone (CTZ), the GI tract, the cerebral cortex, the limbic system,
described in three phases: nausea, vomiting, and retching. Nau- and the vestibular system (Fig. 6-1). The major neurotransmitter
sea is the subjective feeling of the need to vomit. It includes an receptors associated with the emetic response include sero-
unpleasant sensation in the mouth and stomach and can be asso- tonin (the 5-hydroxytryptamine type 3, [5-HT3 ]) receptors, neu-
ciated with salivation, sweating, dizziness, and tachycardia. Vom- rokinin 1 (NK1) receptors, and dopamine receptors. Other recep-
iting is the forceful expulsion of the stomach contents through tors involved include corticosteroid, acetylcholine, histamine,
the mouth, but is preceded by the relaxation of the esophageal cannabinoid, gabaminergic, and opiate receptors. Many of these
sphincter, contraction of the abdominal muscles, and temporary receptors are targets for antiemetic therapy.
suspension of breathing. Retching is the rhythmic contraction of In the CNS, the CTZ is located in the area postrema on the
the abdominal muscles without actual emesis. It can accompany floor of the fourth ventricle in the brainstem; it lies outside the
nausea, or occur before or after emesis. blood–brain barrier. When the CTZ senses toxins and noxious
substances in the blood or cerebrospinal fluid, it triggers the
emetic response by releasing neurotransmitters that travel to
the VC and the NTS. The major neurotransmitter receptors
EPIDEMIOLOGY AND CLINICAL include serotonin, dopamine, and neurokinin 1.
PRESENTATION The GI system also plays a large part in the initiation of the
emetic response. The GI tract contains enterochromaffin cells in
Nausea and vomiting are caused by many disorders. Central ner- the GI mucosa. When these cells are damaged by chemother-
vous system (CNS) causes include increased intracranial pres- apy, radiation, anesthetics, or mechanical irritation, serotonin is
sure, migraine headaches, brain metastases, vestibular dysfunc- released, which can stimulate the vagal afferents as well as directly
tion, alcohol intoxication, and anxiety. Infectious disease causes stimulate the VC and NTS. The vomiting center then initiates
include viral gastroenteritis, food poisoning, peritonitis, menin- the emetic response.
gitis, and urinary tract infections. Metabolic causes include The cerebral cortex and limbic system can stimulate the
hypercalcemia, uremia, hyperglycemia, and hyponatremia. Gas- emetic center in response to emotional states such as anxiety,
trointestinal disorders, such as gastroparesis, bowel obstruction, pain, and conditioned responses (anticipatory nausea and vomit-
distension, and mechanical irritation, can cause nausea and vom- ing). The neurotransmitters involved in this pathway are less well
iting. Among the many medications that can cause nausea and understood. Disorders of the vestibular system, such as vertigo
vomiting are cancer chemotherapy, antibiotics, antifungals, and and motion sickness, stimulate the VC through acetylcholine and
opiate analgesics. histamine release.
In addition to the suffering involved, uncontrolled vomiting
can lead to dehydration, electrolyte imbalances, malnutrition,
aspiration pneumonia, and esophageal tears. Nausea and vom- DIAGNOSIS
iting often reduces food intake and can impair a person’s ability
to care for himself or herself. Significant reductions in quality- The initial evaluation of the patient with nausea and vomiting
of-life scores have been demonstrated in cancer patients with should include the onset of symptoms, the severity and dura-
chemotherapy-induced nausea and vomiting compared with tion of symptoms, hydration status, precipitating factors, current
patients who did not have those symptoms.1 medical conditions and medications, and food and infectious con-
tacts. The etiology of the nausea and vomiting should be deter-
mined, if possible, so that underlying conditions can be treated
specifically. Supportive treatment should be initiated, if needed,
PATHOPHYSIOLOGY including fluid and electrolyte replacement. If the nausea and
vomiting is mild and self-limited, antiemetic therapy may not be
The CNS, the peripheral nervous system, and the gastrointestinal required. For others, however, the appropriate antiemetic ther-
(GI) tract are all involved in initiating and coordinating the emetic apy will depend on the patient and the etiology of the nausea
response. In the CNS, the vomiting center (VC) receives incom- and vomiting.

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