Northeast Florida Medicine, Spring 2016

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Northeast Florida Medicine

Vol. 67, No. 1 2016

Palliative Care

Nausea and Vomiting

Nausea and vomiting are other causes for acute emer-

gency department visits in the palliative care population

and significantly affect quality of life. Identifying the eti-

ology andpotentially reversible conditions shouldfirst be

explored. Once initiating treatment, understanding the

cause of symptoms greatly influences any pharmacologic

intervention. Basic understanding of the emetic pathway

is vital in providing targeted therapy. Simply, the central

vomiting center receives input fromboth central (cortex,

vestibular, chemoreceptor trigger zone) and peripheral

afferentpathways.Emetogenicneurotransmitters include

dopamine, serotonin, histamine and acetylcholine.

Centrally, the chemoreceptor trigger zone (CTZ)

mediates the most frequent causes for nausea. Given its

location on the floor of the fourth ventricle, where the

blood brain barrier is porous, toxins, metabolites, and

drugs (opioids and chemotherapeutic agents) can be

highly provoking.The CTZ then stimulates the central

vomiting center via dopamine and serotonin. Initial

therapy targeting this area should be addressed using

dopamine antagonists (metoclopramide, prochlorper-

azine and haloperidol). Secondarily, ondansetron can

be added. In the palliative population, ondansertron

is generally reserved for intractable symptoms, save

those related to chemotherapy/opioid induced nausea

and vomiting.

Peripherally, GI tract causes of vomiting are me-

diated by both vagal and splanchnic afferents from

mechano/chemo receptors. Serotonin and dopamine

are the primary neurotransmitters involved.Typically,

a first line agent, after ruling out bowel obstruction, is

metoclopramide given its dual central and peripheral

actions on serotonin and dopamine. Prochlorperazine

and haloperidol are alternatives. Again, ondansetron

is a viable and safe option but effects are limited to

serotonin antagonism only.

Initiate therapy with attempts to target the apparent

provoking receptor. If response is only partially effec-

tive, consider adding new therapy targeting alternate

neurotransmitter pathways, rather than changing the

agent. If a patient presents and is already established

on anti-emetic therapy, apply a second and different

class of anti-emetic to augment and address symptoms

given the mechanistic interplay.

Acknowledge major

side effect profiles and drug interactions as there

are many. Fortunately, the role of the EDP is acute

symptom management and many of the long term

drug effects can be scrutinized further once comfort

has been provided.

In this advanced illness population, common pal-

liative causes, associated neurotransmitters and drug

suggestions can be abridged using the AVOMIT

mnemonic (Table 2).

Table 2: Nausea and Vomiting in Palliative Care

Cause

Receptor

Drug

nxiety/Anticipate

Central

Benzodiazepines

estibular (Meds/Mets)

AcH, H1

Promethazine, Meclizine,

Diphenhydramine

bstruction (bowel,

constipation, visceral,

metastases)

AcH, H1,

D2, 5HT3/4

Metoclopramide, Prochlorperazine,

Haldol, ondansetron

Do not use metoclopramide

in complete obstruction

edication/Metabolic (CTZ)

D2, 5HT3

Metoclopramide, Haloperidol,

Ondansetron

nfection/Inflammation

AcH, H1, 5HT Prochlorperazine, Promethazine,

Ondansetron

umor/Toxins

D2, 5HT3

Haloperidol, Metoclopramide,

Ondansetron, Prochlorperazine,