Emesis
Background
protective mechanism rids the body of ingested toxins and poisons before dangerous amounts can be absorbed
However, sometimes it is an inappropriate response or not desirable (surgical procedures, chemotherapy, motion sickness) Protracted N&V can cause dehydration, malnutrition and metabolic disturbances
Retching - consists of rhythmic, labored, spasmodic movements, involving the diaphragm, chest wall, and abdominal muscles
Pathophysiology
Vomiting Center (VC)- located in dorsal portion of the lateral reticular formation in the medulla
coordinates the respiratory, GI and abdominal muscles vomiting can be induced by electrical stimulus of the VC the final common pathway that mediates vomiting from all causes
Pathophysiology
Vomiting can also be induced by stimulation of the chemoreceptor trigger zone (CTZ), the GI tract, and the vestibular apparatus CTZ- located in area postrema on the floor of the fourth ventricle
accessible to blood and cerebrospinal fluid (CSF) may not be as important to vomiting induction as previously felt
Pathophysiology
CTZ- important in N&V, however
when CTZ is surgically ablated can still have vomiting in response to certain toxins
Some feel that GI tract may be important initiator of emesis as well Multiple neurotransmitters involved in N&V
Dopamine, opiate, serotonin, acetylcholine, histamine found in CTZ (see table 8-2) Dopamine and serotonin found in GI tract as well N&V associated w/distension or GI tract dysfunction-responds best to metoclopramide
Pathophysiology
Input to Vomiting Center (VC) also occurs from higher cortical centers
e.g. patient experiences N&V in response to terror, also, in cancer patients who have conditioned response and have emesis even at sight of hospital
Disturbance in vestibular function -> stimulate cranial nerve VIII -> stimulates the VC.
e.g. motion sickness- main neurotransmitters involved - acetylcholine and histamine (dopamine and serotonin not involved)
Pharmacotherapy
First - In order to determine treatment,
get history to determine the cause, onset and duration, precipitating factors, recent ingestion (medication, food, liquids), medical conditions e.g. acute onset of emesis in pt with large ingestion of alcohol, may not need antiemetic tx at all
mild to moderate N&V for <48hrs in absence of more severe symptoms -> monitor hydration status ->OTC products may help (e.g. carbohydrate solution-emetrol, calmX, nausetrol) or pepto-bismo
Pharmacotherapy
N&V accompanied by more serious signs, require more intervention
blood in vomitus, abdominal pain or distension, fever, severe headache, recent trauma, diabetes
Section 1
What is potential cause for motion sickness? Do children grow out of motion sickness? What are drugs of choice for moderate motion sickness? (see Table 8-5) Is there a role for sympathomimetics in motion sickness? What is relative efficacy of dimenhydrinate compared to scopolamine patch?
Section 1 (cont)
When is scopolamine patch applied? What are adverse effects of scopolamine patch? See table 8-6
Section 3
What is the incidence of Postoperative nausea and vomiting (PONV) What factors determine risk for PONV?
Section 4
Which cranial nerve may have influence on emesis? Which agents are used for PONV? Table 87 Between droperidol and ondansetron
Which is more efficacious? Which is more costly? Which can affect QT more?
Section 5
How often does prophylaxis of PONV work? How long does PONV usually last after surgical procedure? What 2 agents are usually avoided in pediatric population due to concern about extrapyramidal side effects
Nonpharmacologic Therapies
What is a TENS unit? What is NST (ReliefBand)? How does the ReliefBand work? How does a TENS unit work?
Cannabis
How effective is Delta-9-terahydrocannabinol (THC) relative to prochlorperazine? How often was marijuana effective (in decreasing N&V) when used for cancer chemotherapy in patients non-responsive to standard treatments?