Definition: any nausea, retching, or vomiting occurring during the first 24–48 h after surgery in inpatients (1).

Physiology: the physiology of PONV is complex and not perfectly understood. According to our current model, the brain structures involved in the pathophysiology of vomiting are distributed throughout the medulla oblongata of the brainstem, not centralized in an anatomically defined 'vomiting centre' (2). PONV can be triggered by several perioperative stimuli, including opioids, volatile anaesthetics, anxiety, adverse drug reactions, and motion. Multiple neurotransmitter pathways are implicated in the physiology of nausea and vomiting. Enterochromaffin cells in the gastrointestinal tract release serotonin, and the vagus nerve communicates with the chemoreceptor trigger zone (CRTZ) via 5-HT₃ receptors. The CRTZ communicates with the NTS primarily via dopamine-2 (D2) receptors. The vestibular system, which detects changes in equilibrium, communicates with the NTS via histamine-1 (H1) and acetylcholine (mACh). Anticipatory or anxiety-induced nausea and vomiting appears to originate in the cerebral cortex, which communicates directly with the NTS via several types of neuroreceptors. Therefore, antiemetic drugs have been developed that are effective against 5-HT3, D2, NK1, H1, and mACh receptors. However, no antiemetic can reduce the incidence of PONV to zero (1).

Epidemiology:

• incidence: 30% in all post-surgical patients and up to 80% in high-risk patients (1).
• risk factors (1):
• in adults:
  
• patient-related:
• Female gender (female patients are—on average—three times more likely than men to suffer from PONV).
• Non-smoking status (roughly doubles the patient's risk of PONV).
• A history of motion sickness, PONV, or both (roughly doubles the patient's risk of PONV and indicates a general susceptibility to PONV).
• Potential risk factors: low ASA physical status (I–II), history of migraine, and preoperative anxiety have all been associated with an increased risk of PONV, although the strength of association varies from study to study.
• anesthesia-related:
• The use of volatile anaesthetics is associated with a two-fold increase in the risk of PONV, with risk increasing in a dose-dependent manner, and no significant difference in incidence with different volatile anaesthetics. In fact, the use of volatile anaesthetics is the single most important factor for predicting emesis in the first 2 postoperative hours.
• Intraoperative and postoperative opioid use increases the risk of PONV in a dose-dependent manner. Opioids reduce muscle tone and peristaltic activity, thereby delaying gastric emptying, inducing distension, and triggering the vomiting reflex.
• The duration of anaesthesia, which is closely linked to the duration of surgery, can help predict the patient's risk of PONV, since the duration of anaesthesia describes the patient's exposure to emetogenic stimuli like volatile anaesthetics and intraoperative opioids.
• in children:
• patient-related: children >3 yr have been shown to have an increased risk of PONV.
• surgery-related: strabismus surgery was identified as an independent risk factor for PONV.

Measurements:

• in adults the risk score consists of four predictors: female gender, history of motion sickness or PONV, nonsmoking, and the use of postoperative opioids. If none, one, two, three, or four of these risk factors were present, the incidences of PONV were 10%, 21%, 39%, 61% and 79% (3).
• in children the postoperative vomiting in children (POVOC) score is a simplified risk score considering the following clinical risk factors: duration of surgery ≥30 min, age ≥3 yr, strabismus surgery, and a positive history of postoperative vomiting in the child, or history of PONV in parents or siblings. Depending on the presence of none, 1, 2, 3, or 4 risk factors the estimated incidence for PV in the pediatric patient is 9, 10, 30, 55, and 70%, respectively (4).
  

Treatment: only 20–30% of the patients will respond to any currently available antiemetic. If possible, use loco-regional anaesthesia instead of general anaesthesia. If general anaesthesia is required, total i.v. anaesthesia with propofol and nitrogen reduces the incidence of PONV by 30%, making this intervention as effective as an antiemetic drug. (1).

• in adults:

• No risk/low risk (<10%): no prophylaxis, rescue with ondansetron 4 mg or dolasetron 12.5 mg (6).
• Mild-moderate risk (10-30%): prophylaxis with droperidol 0.625-1.25 mg near the end of surgery, rescue with ondansetron 4 mg or dolasetron 12.5 mg (5,6).
• High risk (30-60%): prophylaxis with steroid at induction and droperidol 0.625-1.25 mg near the end of surgery, rescue with ondansetron 4 mg or dolasetron 12.5 mg (1,5,6).
• Extremely high risk (>60%): prophylaxis with steroid at induction and droperidol 0.625-1.25 mg near the end of surgery, rescue with ondansetron 4 mg or dolasetron 12.5 mg, metoclopramide, phenothiazine other antiemetic (1,5,6).
  
• in children: prophylaxis with ondansetron 50–100 μg/kg iv near the end of surgery (5).
• for ENT-operations (7): immer bei HNO-Eingriffen die potentiellbluten: droperidol 10-20 mcg/kg, ondansetron 0,1 mg/kg, resp. 4 oder 8 mg iv, dexamethason 0,1mg/kg,resp. 4 oder 8mgzu OP-Beginn, ausser bei Kindern <40kg.

If patients experience breakthrough PONV despite prophylaxis, they should be treated with a drug from a group other than the one used for prophylaxis (e.g., metoclopramide) (5).

Complications: suture dehiscence, aspiration of gastric contents, oesophageal rupture (1).