Who Isn't Sick of PONV?

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Patients fear it and staff would rather dedicate their resources elsewhere. Can post-op sickness be avoided?


There's no worse feeling than being on the verge of vomiting. That awful sensation occurs more often than your patients — and you — would like. But advancements in medications, anesthesia techniques and the use of multi-modal therapy seem to be making progress in treating post-operative nausea and vomiting. Here's how to identify high-risk patients and tailor care regimens to their needs.

Who's at risk?
We want to minimize, if not eliminate, post-op nausea and vomiting. While some patients are at a higher risk for PONV than others, some studies report that 30 percent to 35 percent of all patients will suffer PONV. Patients identified as high risk for PONV have a 70-percent chance of feeling queasy after surgery.

Who's at high risk? Patients who are young, female or obese; non-smokers; patients with a history of motion sickness or PONV; anxious patients and those given opioids during or after surgery. The type and length of the procedure also plays a role in the development of PONV. High-risk procedures include GYN, ENT, ocular, breast, laparoscopy, laparotomy and craniotomy cases.

While we can't expect complete PONV prevention, we have several medications and modalities at our disposal to help lower the risk. By altering your anesthetic technique, you may be able to minimize the effects of anesthesia on the vomiting center and the chemoreceptor trigger zone (CTZ). You can:

  • limit the use of opioids by adding ketorolac or COX-2 inhibitors;
  • eliminate nitrous oxide during general anesthesia;
  • avoid inhalational agents by using total intravenous anesthesia and propofol (which has been shown to have anti-nausea properties) for induction and maintenance;
  • know that desflurane may have a higher incidence of PONV than sevoflurane or isoflurane;
  • maintain adequate hydration;
  • time the administration of muscle relaxants so reversal isn't required; and
  • employ orogastric or nasogastric tubes that maintain an empty stomach during procedures.

Multi-modal therapy
Upwards of 40 neurotransmitters are involved in the initiation of PONV. However, acetylcholine and histamine have been identified as the major players. Other important neurotransmitters include dopamine, serotonin 5-HT3, norepinephrine, epinephrine and Substance P. Since the CTZ resides outside the blood-brain barrier, medications and neurotransmitters are able to interact with the CTZ directly to initiate PONV. Medications designed to antagonize these neurotransmitters at their receptor sites are therefore the mechanisms by which anti-nausea and anti-emetic medications are formulated.

Various medications continue to be the mainstay of the multi-modal treatment of PONV, although none are 100-percent effective. The medications act as antagonists at the receptor sites for the previously mentioned neurotransmitters. The following play integral parts in multi-modal therapy protocols.

  • Anticholinergics. They act directly on the vomiting center, making them effective for patients with a history of motion sickness or vertigo. They also seem to be effective against PONV caused by opioid use. The tendency for producing sedation, dry mouth, blurred vision and urinary retention has limited their use. Anticholinergics can increase intraocular pressure, making them contraindicated in patients with closed-angle glaucoma.
  • Antihistamines. Like the anticholinergics, antihistamines act directly on the vomiting center. Their sedative effects can cause oversedation following general anesthesia, which may offset their use.
  • Dopamine antagonists. These medications act at the CTZ. Low-dose droperidol was widely used as an anti-emetic until it received a "black box warning" from the FDA in 2001. It was determined that several patients suffered an adverse cardiac dysrhythmia after receiving doses several times higher than what is typically used for PONV. As a result, some surgical facilities have dropped droperidol from their formulary. Metoclopramide acts on the CTZ, promotes gastric emptying and increases the tone of the gastroesophageal sphincter. Its side effects include extra-pyramidal symptoms and neuroleptic malignant syndrome.

  • Serotonin 5-HT3 antagonists. The newest class of medications used to treat PONV at the level of the CTZ. After widespread use in treating vomiting associated with chemotherapeutic agents administered during cancer treatments, ondansetron is now also popular in the perioperatve setting. The 5-HT3 antagonists are the most expensive medications available for PONV prevention. The action of dexamethasone appears to have a synergistic effect when used in combination with a 5-HT3 antagonist. It has also shown effectiveness when used alone.
  • Acupuncture and acupressure. Several studies support the use of both acupuncture and acupressure for several surgical-related issues, especially PONV. Random controlled studies have shown that stimulation of the PC6 acupressure point, located three finger-widths from the wrist and between the radius and ulna bones, decreases the incidence of PONV by as much as 35 percent to 40 percent as compared to a placebo. Patients can wear a wristband apparatus that stimulates the PC6 acupressure point before, during and after procedures.

Many anesthesia providers advocate the multi-modal approach in combating PONV. Resorting to the use of more cost-effective medications such as antihistamines or dexamethasone as a first choice may be all that is necessary. If PONV persists, providers may add a 5-HT3 receptor antagonist or dopamine antagonist. Studies indicate that once the 5-HT3 receptors are blocked there is no additional benefit of repeating the dose. The 5-HT3 antagonists are the most expensive of the antagonists. Repeat-ing a dose of this medication only serves to increase overall case costs.

Using different antagonists that block several receptors, altering one's anesthetic technique (such as eliminating nitrous oxide and using propofol as the induction agent), limiting the use of opioids and using other pain medications such as ketorolac or the COX-2 inhibitors may all add up to a reduction of PONV. While the use of an orogastric tube is controversial in its efficacy in reducing PONV, the multi-modal approach does use the orogastric tube.

Costly concern
PONV is a common anxiety among surgical patients, some of whom rate their PONV concerns higher than their fear of post-op pain. It can prove costly in terms of delayed discharge, unplanned hospital admission and increased personnel requirements to care for the patient. While the concern of many, the responsibility of managing PONV ultimately lies with the anesthesia provider.

Physiology of PONV

Several neuronal pathways lead to an area in the brain called the vomiting center. This center, located in the hindbrain or medulla, is the end of the road for signals that initiate nausea and vomiting. The physiology of nausea and vomiting is complex and involves mechanical and chemical receptors located along the gastrointestinal tract (especially the vagus nerve), in the area of the brain involved in motion sickness, the vestibular system and in poorly localized areas of the main brain or cerebral cortex.

Additionally, various drugs and neurotransmitters arrive and interact with the vomiting center in a discrete, specialized, highly vascular area of the brain's fourth ventricle. This area is called the chemoreceptor trigger zone (CTZ). Stimulation of the vomiting center and the CTZ by a noxious event initiates a chain of events leading to dreaded queasiness. The mouth starts salivating, the stomach begins feeling uneasy and sweat begins to form on clammy skin.

The act of vomiting is the result of the interaction of several physiological and mechanical processes. A noxious signal arrives at the vomiting center. The vomiting center then sends signals to initiate the vomiting process. Nerve impulses travel along the vagus nerve and to the nerves that control the abdominal muscles. Respirations become deep; contents from the small bowel located just beyond the duodenum reverse direction and re-enter the stomach; salivary glands increase secretions, and the opening to the airway closes to prevent gastric contents from entering the airway.

The vomiting center then signals the breathing center in the medulla to hold the breath while the esophagus and gastroesophageal sphincter relax. The abdominal and chest wall muscles contract and the diaphragm forcefully descends, greatly increasing the pressure within the abdomen. Finally, the gastric contents are forced into the esophagus and exit through the mouth.

— Mark Green, CRNA, MSN

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