Postoperative Nausea and Vomiting

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Postoperative Nausea and Vomiting

It is estimated that up to 80% of patients experience postoperative nausea and/or vomiting (PONV) within the first 24 h after surgery. For most, PONV is easily manageable but for a smaller, ‘high risk’ cohort, symptoms can be distressing and disabling and, in some cases, have been described as worse than the pain of surgery. It is a common misconception that general anaesthetics are solely responsible for PONV because it is often forgotten that surgical procedures under anaesthesia involve not only a pharmacological but also a physical ‘assault’ on the patient. Fortunately, the multifactorial aetiology of PONV lends itself to interventions using a variety of different treatment options. Prevention, along with prompt and effective treatment of PONV, decreases the risk of adverse effects, limits the length of inpatient stay and reduces hospital costs. More importantly, successful prevention of PONV greatly improves patient satisfaction.

DEFINITIONS

Nausea is derived from the Greek word naus denoting ‘ship’ and was used originally to describe the feeling of seasickness. Nausea is an unpleasant sensation referred to the upper gastrointestinal tract and pharynx. It is associated with dizziness and a strong urge to vomit. Assessment of nausea is extremely difficult because symptoms are subjective, entirely patient-dependent and often difficult to quantify. For this reason, the incidence of postoperative nausea is frequently underestimated. Retching is the involuntary process of ‘unproductive vomiting’. It is characterized by the synchronous contraction of diaphragmatic and abdominal muscles against a closed mouth and glottis. Retching is extremely distressing and is usually accompanied by feelings of intense nausea. Vomiting represents the final common pathway of a highly coordinated sequence of events involving gastrointestinal, abdominal, respiratory and pharyngeal muscles which results in the active and rapid expulsion of contents from the stomach and upper intestine. In contrast to the rather subjective assessment of nausea, vomiting is easily identifiable and measurable!

MECHANISMS OF NAUSEA AND VOMITING

Vomiting Centre

The vomiting reflex probably developed as an evolutionary protective mechanism against ingestion of harmful substances or toxins. However, vomiting also occurs in response to a wide range of pathological and environmental triggers including sight, smell, motion and gastrointestinal disturbances. Afferent signals mediated by the vagus, vestibular and higher cortical nerves are carried to discrete areas within the brainstem collectively known as the ‘vomiting centre’ (Fig. 42.1). Traditionally, the vomiting centre was thought to be a single anatomical entity but there is increasing evidence that it is made up of a disparate group of interconnected cells and nuclei located in the lateral reticular formation of the medulla and the nucleus tractus solitarius (NTS). All information entering the vomiting centre is processed and co-ordinated (via autonomic and motor nerves) into a highly complex series of neuronal signals to initiate the three phases of the vomiting reflex.

FIGURE 42.1 Schematic diagram of the vomiting reflex. See text for details.

Chemoreceptor Trigger Zone (CTZ)

The so-called ‘chemoreceptor trigger zone’ consists of several nuclei found within the area postrema at the caudal end of the fourth ventricle. Although the CTZ is anatomically located within the central nervous system, its unusual pattern of endothelial fenestrations allows it to ‘sense’ chemicals not only within cerebrospinal fluid, but also within circulating peripheral blood. In simple terms, the highly vascularized CTZ utilizes its defective blood brain barrier to detect potentially harmful substances present within the circulation. The CTZ contains an abundance of cholinergic, dopaminergic, histaminergic, serotinergic (5-HT) and opioid receptors which send afferent projections to the vomiting centre. Stimulation of the CTZ contributes significantly to the nausea and vomiting experienced by surgical patients, and pharmacological antagonism of receptor signalling within this important area represents a key strategy in the prevention and treatment of PONV.

Stimulation of the Vomiting Centre

Figure 42.1 outlines the various triggers and neural connections involved in the initiation of the vomiting reflex. The vomiting centre acts as the final processor for all sensory information received from central and peripheral receptors. Although the majority of afferent information from the periphery is relayed through the CTZ, other important causes of emesis are described below.

Gastrointestinal Tract

The normal functioning of the gastrointestinal (GI) tract is dependent on fully integrated neural feedback mechanisms. As part of this dynamic process, numerous mechano- and chemo-receptors send information to the central nervous system via the vagal nerve afferents. Any threat to the integrity of the GI system, e.g. gastric distension, irritation, damage or toxins, triggers an increase in ascending vagal activity which relays directly or indirectly to the vomiting centre. Cholinergic M₁, serotoninergic 5-HT₃ and dopaminergic D₂ receptors are the principal mediators of signal transduction within the gut mucosa. Stimulation of one or all of these key receptors initiates a key step in the vomiting reflex and pharmacological antagonism at these sites represents a logical approach in the management of nausea and vomiting.

Vestibular System

Motion sickness is an unpleasant side-effect induced by aberrant vestibular or visual activity. Susceptible individuals develop motion sickness in childhood, with the incidence peaking during early adolescence. Fortunately, symptoms diminish with advancing age. Numerous studies report that females are more prone to motion sickness than men. The neurophysiological mechanisms responsible for motion sickness are largely unknown but it is likely that an imbalance between the vestibular-cerebellar-visual axis together with stimulation of higher autonomic nerves triggers activation of the vomiting reflex. Therefore, female patients with a history of motion sickness have two independent predictors of PONV (see below).

Cardiovascular System

Most anaesthetists recognize that nausea may represent an important sign of underlying hypotension, particularly in patients who have just received regional nerve blockade. Myocardial ischaemia leading to infarction is also associated with a high incidence of vomiting. It is likely that retrograde autonomic signalling to the brainstem is responsible for these early warning signs of cardiovascular compromise.

Cortical Inputs

Higher cortical centres (e.g. the limbic system) are intimately involved with initiation and modification of the vomiting reflex. For example, unpleasant sights, sounds or smells induce emetic responses. In this context, cholinergic M₁ antagonists (e.g. hyoscine) may provide some relief. Patients with preconceived expectations or anxiety can be encouraged to modify their behaviour to reduce the incidence of nausea or vomiting. In cases involving anticipatory symptoms (e.g. protracted chemotherapy-induced nausea), anxiolytics may be beneficial.

Gag Reflex

The gag reflex reduces the risk of upper airway obstruction and ingestion of noxious material. The glossopharyngeal nerve (cranial nerve IX) mediates the afferent limb of this reflex, synapsing directly within the nucleus solitarius in the brainstem. The efferent limb is coordinated by the vagus nerve (cranial nerve X). This primitive reflex is one of the strongest triggers of emesis and is particularly active following insertion of oral airway adjuncts in semiconscious patients.

Neural and Muscular Co-ordination During Vomiting

The synchronized events mediating the vomiting reflex are divided into three phases: pre-ejection, ejection and post-ejection.

Pre-Ejection Phase

Nausea (not a prerequisite to vomiting).

Gastric smooth muscle relaxes and retrograde peristalsis begins.

Deep inspiration.

Glottis closes (to avoid aspiration).

Ejection Phase

Abdominal and diaphragmatic muscles contract.

Lower and upper oesophageal sphincters relax.

Intra-abdominal pressure increases.

Mouth opens and gastric contents are forcefully expelled.

Post-Ejection Phase

Autonomic and visceral nerves ‘recalibrate’

Lethargy and weakness.

Increased autonomic activity results in salivation, pallor and tachycardia throughout all phases of the vomiting reflex.

ADVERSE EFFECTS

Some clinicians dismiss PONV as an inevitable consequence of surgery but from the patients perspective PONV is almost always associated with distress and dissatisfaction. Importantly, if nausea or vomiting persist there is a risk of rare, but potentially serious, perioperative morbidity. These complications are summarized in Table 42.1.

TABLE 42.1

Adverse Affects of PONV

Patient distress and dissatisfaction

Pulmonary aspiration

Postoperative pain

Wound dehiscence/haemorrhage

Eyes

Head and neck

Oesophageal

Abdominal

Dehydration, electrolyte disturbance and/or requirement for intravenous fluids

Delayed oral input

Drugs

Nutrition

Fluids

Delayed mobilization

Delayed discharge

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