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Postoperative nausea and vomiting


It is estimated that up to 80% of patients experience postoperative nausea and vomiting (PONV) within the first 24 h after surgery. If risk factors are identified and acted upon, PONV can be easily managed, but for a small, high-risk cohort of patients, symptoms can be extremely distressing and disabling. Fortunately, the aetiology of PONV is multifactorial; therefore a variety of different treatments and interventions can be used to minimise the risk of developing PONV. Prevention, along with prompt and effective treatment, decreases adverse effects, limits the length of inpatient stay and reduces hospital costs. Importantly, successful prevention of PONV greatly improves patient satisfaction.

Definitions

Nausea is derived from the Greek word naus, meaning ‘ship’ and was used originally to describe the feeling of seasickness. Nausea is an unpleasant sensation caused by afferent signals emanating from the upper gastrointestinal (GI) tract and pharynx. It is associated with dizziness and the 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 often underestimated. Retching is the involuntary process of unproductive vomiting. It is characterised 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 GI, 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, nausea and vomiting also occur in response to a wide range of pathological and environmental triggers including sight, smell, motion and GI disturbances. Other important triggers include pregnancy, migraine, head injury, vestibular problems and severe pain. 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. 7.1 ). 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 coordinated via autonomic, sensory and motor nerves into a highly complex series of neuronal signals known as the ‘vomiting reflex’.

Fig. 7.1, Schematic diagram of the vomiting reflex. See text for details. CB, Cannabinoid; CTZ, chemoreceptor trigger zone; D 2 , dopaminergic 2; receptors; GABA A , γ-aminobutyric acid A; H1, histaminergic 1; 5-HT 3 , 5-hydroxytryptamine 3; M 1 , muscarinic-1; NK 1 , neurokinin 1.

Chemoreceptor trigger zone

The chemoreceptor trigger zone (CTZ) 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 and generous blood supply allows it to ‘sense’ chemicals not only within cerebrospinal fluid but also within peripheral blood. In other words, the highly vascularised CTZ uses its defective blood–brain barrier to detect potentially harmful substances present within the circulation. The CTZ contains an abundance of cholinergic (muscarinic M 1 ), dopaminergic (D 2 ), histaminergic (H 1 ), serotonergic (5-HT 3 ) and opioid (mainly µ) and neurokinin (NK 1 ) receptors which send afferent projections to the vomiting centre. Stimulation of the CTZ contributes significantly to the nausea and vomiting experienced by surgical patients; therefore pharmacological manipulation within the CTZ forms an important strategy in the prevention and treatment of PONV.

Stimulation of the vomiting centre

Fig. 7.1 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; therefore blocking afferent or efferent signalling in this area will potentially have an antiemetic effect. Alternatives include direct stimulation of cannabinoid (CB 1 ) receptors within the vomiting centre using synthetic cannabinoid derivatives (e.g. nabilone), or NK 1 receptor antagonists (e.g. aprepitant), which antagonise substance P at NK 1 receptors. These agents decrease chemotherapy-induced vomiting (CIV), although their use in the perioperative period is currently under review. Other important causes of emesis are described later.

Gastrointestinal tract

The normal functioning of the GI tract is dependent on fully integrated neural feedback mechanisms. As part of this dynamic process, numerous mechano- and chemoreceptors send information to the central nervous system via vagal nerve afferents. Any threat to the integrity of the GI system, such as gastric distension, irritation, damage, drugs or toxins, triggers an increase in ascending vagal activity which relays directly or indirectly to the vomiting centre. For example, delayed gastric emptying and reduced lower oesophageal sphincter tone induced by hormonal changes, compounded by increased intra-abdominal pressure, significantly increase the risk of nausea and vomiting during pregnancy. Cholinergic M 1 , serotoninergic 5-HT 3 and dopaminergic D 2 receptors are the principal mediators of signal transduction within the gut mucosa. Stimulation of one or all of these receptors initiates a key step in the vomiting reflex; therefore pharmacological antagonism at these sites is a logical approach to managing symptoms.

Vestibular system

Motion sickness is an unpleasant consequence of 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 males. The neurophysiological mechanisms responsible for motion sickness are largely unknown, but it is likely that an imbalance in 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 later).

Cardiovascular system

Anaesthetists should recognise that nausea may represent an important sign of underlying hypotension, particularly in patients undergoing regional anaesthesia. Myocardial ischaemia and infarction are also associated with nausea and vomiting. It is likely that retrograde autonomic signalling to the brainstem is responsible for these early warning signs of cardiovascular compromise. Similarly, autonomic disturbances may contribute to the nausea and emesis in patients presenting with severe pain.

Cortical inputs

Higher cortical centres and the limbic system are intimately involved with initiation and modification of the vomiting reflex. For example, unpleasant sights, sounds or smells, fear or emotional stress can induce nausea. In this context, cholinergic M 1 antagonists (e.g. hyoscine) or γ-aminobutyric acid A (GABA A ) receptor potentiators (e.g. benzodiazepines) may be useful, with or without behaviour-modifying techniques.

Gag reflex

The gag reflex reduces the risk of ingestion of noxious material and airway obstruction. 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 after oral insertion of airway adjuncts in semiconscious patients.

Neural and muscular coordination during nausea and vomiting

Nausea usually precedes vomiting and consists of several symptoms, including pallor, salivation, shivering and the urge to vomit. The synchronised neuromuscular events mediating the vomiting reflex are divided into two distinct phases: retching and expulsion. Retching is associated with rhythmic contraction of the abdominal, intercostal and diaphragmatic muscles, whereas expulsion occurs when abdominal muscle contraction causes intragastric pressure to exceed lower and upper oesophageal pressure. Complex neuromuscular coordination using motor, sensory and autonomic nerves ensures the glottis is closed during the ejection phase to prevent aspiration of gastric contents into the trachea and lungs.

Adverse effects of PONV

Some clinicians dismiss PONV as an inevitable consequence of anaesthesia and surgery, but from the patient's perspective, PONV is almost always associated with distress and dissatisfaction. Importantly, if nausea or vomiting persist, there is a risk of potentially serious perioperative morbidity ( Box 7.1 ). Intact laryngeal reflexes ensure glottic closure during vomiting, but in the immediate postoperative phase, laryngeal reflexes may be obtunded because of residual effects of general anaesthesia and centrally acting analgesics, resulting in aspiration of gastric contents if the upper airway is not protected. The physical act of vomiting may lead to pain, wound dehiscence, haemorrhage, haematoma or possibly oesophageal rupture (Boerhaave's syndrome). If PONV persists, dehydration, reduced oral intake, electrolyte imbalance and delayed mobilisation can result in significant morbidity and increased healthcare costs associated with delayed discharge and unplanned admissions.

Box 7.1
Adverse effects of PONV

  • Patient distress and dissatisfaction

  • Pulmonary aspiration

  • Postoperative pain

  • Wound dehiscence/haemorrhage

  • Dehydration, electrolyte disturbance and/or requirement for intravenous fluids

  • Delayed oral intake of fluids, nutrition and drugs

  • Delayed mobilisation

  • Delayed discharge

Identifying patients at risk

Many different approaches have been used to stratify patients according to their individual risk of PONV. Risk stratification allows clinicians to optimise prevention and treatment for patients at moderate or high risk of PONV whilst minimising indiscriminate prescribing and adverse drug reactions in patients at lower risk.

Patient factors

Although it is impossible to identify every patient at risk of PONV, several factors contribute ( Box 7.2 ). Numerous studies report that non-smoking habits, female sex and a history of PONV or motion sickness are all strong independent predictors for PONV. Anxiety and obesity may increase the risk; however, the evidence for these associations is weaker. Children older than 3 years and young adults are also at high risk, but the incidence decreases in later life. Vomiting, rather than nausea, is often used as an outcome measure in paediatric studies because of the difficulties in assessing and quantifying nausea in young children.

Box 7.2
Risk factors for PONV

Patient

  • Female sex

  • Non-smoker

  • History of PONV or motion sickness

  • Children (age >3 years) and young adults

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