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Anesthesia Pharm I > antiemetics > Flashcards

antiemetics Flashcards

1
Q

what are the top three reasons for unplanned admissions in outpatient procedures?

A
  • pain
  • bleeding
  • PONV
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2
Q

what percentage of patients may PDNV affect and how long?

A
  • 35-50%
  • may last up to 5 days
  • partly d/t ride home, especially if hypovolemic
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3
Q

what are complications of PONV?

A
  • surgical wound dehiscence (especially with abdominal or hernia repair; gagging increases pressure)
  • esophageal damage
  • aspiration
  • dehydration
  • alkalosis (vomiting out stomach acid)
  • hypokalemia
  • intraocular hemorrhage (eye surgery)
  • increased ICP (craniotomy)
  • myocardial ischemia
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4
Q

what may result from PONV?

A
  • delayed discharge from PACU
  • delayed discharge from hospital (increased cost and inconvenience)
  • electrolyte imbalance: hypochlorema, hyponatremia, alkalosis
  • increased postsurgical bleeding (hypertension)
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5
Q

what are positive risk factors for PONV in adults?

A
  • female
  • hx of PONV or motion sickness
  • nonsmoking
  • younger age (after age 3)
  • general vs. regional anesthesia
  • use of volatile agents and N2O
  • postop opioids
  • duration of anesthesia
  • type of surgery (cholecystectomy, laparoscopic, gyn, middle ear, thoracic, eye, abd)
  • ketamine, etomidate
  • full stomach (food, gas) (blood: tonsillectomy, adenoidectomy)
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6
Q

what are possible risk factors for PONV in adults?

A
  • ASA physical status (higher, higher risk)
  • menstrual cycle
  • level of anesthetist’s experience
  • muscle relaxant antagonists (neostigmine)
  • fear or anxiety
  • obesity
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7
Q

describe risk scores for PONV

A
  • each risk factor present (female, nonsmoker, hx PONV, postop opioids) gives 1 point
  • 4 points is an 80% risk of PONV
  • 3 points: 60%
  • 2 risks 40%
  • 1 risk: 20%
  • 0 risks: 10%
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8
Q

what are medical causes for N/V?

A
  • hypoxia
  • hypotension
  • MI
  • DKA
  • increased ICP
  • abd inflammation
  • early pregnancy
  • systemic infections
  • Reye’s syndrome
  • adrenal crisis
  • dig toxicity
  • estrogen
  • aminophylline
  • L-dopa
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9
Q

describe risk scores for PDNV

A
  • each risk gives 1 point (female, hx PONV, age <50, nausea in PACU, opioids in PACU)
  • 5 risks: 80% risk of PDNV
  • 4 risks: 60%
  • 3 risks: 50%
  • 2 risks: 30%
  • 1 risk: 20%
  • 0 risks: 10%
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10
Q

describe POV risk in children

A

similar to adults with following differences:

  • vomiting 2x more than adults
  • risk increases with age over 3 and declines after puberty
  • gender doesn’t make a difference before puberty
  • risk increases more with specific operations (eye, ears, tonsils, adenoids, etc.)
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11
Q

how can risk factors be reduced?

A
  • avoid general anesthesia by use of regional
  • use propofol for induction and maintenance
  • avoid N2O
  • avoid volatile agents
  • minimize intraop and postop opioids (local anesthetic, blocks, NSAIDS)
  • adequate hydration
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12
Q

how should treatment be approached with each risk level of PONV?

A
  • low risk: wait and see
  • medium risk: 1 or 2 interventions
  • high risk: > 2 interventions; multimodal approach
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13
Q

when should droperidol be used in children?

A

only if other treatment has failed and being admitted to the hospital
*Haldol for adults only

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14
Q

what are options if prophylaxis fails?

A
  • use a different drug
  • redose after 6 hrs
  • don’t redose scopolamine or dexamethasone
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15
Q

what are indications for TIVA with propofol?

A
  • risk for malignant hyperthermia
  • high risk for PONV
  • propofol may also be used as a rescue drug on onset of PONV in small dose
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16
Q

what is affected in the brain to cause PONV?

A

-brainstem vomiting center located in the lateral medullary reticular formation
-receptors include:
muscarinic
histamine H1
serotonin 5-HT3
neurokinin-1

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17
Q

what causes afferent input into the vomiting center?

A
  • chemoreceptor trigger zone (4th ventricle): dopamine, serotonin 5-HT3, opioid receptors
  • vestibular system (motion sickness): muscarinic, H1 receptors
  • irritation of the pharynx (vagus nerve): gag and retch response
  • vagal and enteric afferents (mucosa of the GI tract: 5-HT3 receptors activated by serotonin released by the mucosa, then stimulate vagal input to CTZ and vomiting center
  • CNS: stress and anticipatory vomiting (midazolam helps)
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18
Q

what causes visceral afferents to signal the vomiting center?

A

disease of:

  • heart
  • digestive tract
  • biliary tract
  • GU tract
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19
Q

what causes stimulation of the CTZ that then signals the vomiting center?

A
  • motion leads to vestibular labyrinth which signals the cerebellum then CTZ
  • drugs
  • radiation
  • metabolic disturbances
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20
Q

what causes cortical afferents to signal the vomiting center?

A
  • hypoxia
  • pain
  • increased ICP
  • smell, sight, taste
  • psychotropic factors
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21
Q

how do benzodiazepines help with PONV?

A
  • decrease dopamine input at the CTZ as well as anxiolysis
  • may also decrease adenosine reuptake leading to decreased synthesis, release, and postsynaptic action of dopamine at the CTZ
  • anxiolysis from anticipatory vomiting
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22
Q

how do antihistamines work?

A
  • anticholinergic effect (muscarinic receptors)

- histamine receptor blockade (H1 receptors)

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23
Q

what antihistamines are used with PONV?

A
  • diphenhydramine (Benadryl), meclizine (Bonine), dimenhydrinate (Dramamine)
  • phenothiazines
  • prochlorperazine (Compazine)
  • promethazine (Phenergan)
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24
Q

describe diphenhydramine, meclizine, and dimenhydrinate use in PONV

A
  • weak effect except specific to MOTION SICKNESS
  • good if pts. are “stuffy” and PONV tx may be a bonus
  • give towards beginning of case to allow sedation to wear off
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25
Q

what are limitations of use of diphenhydramine, meclizine, and dimenhydrinate?

A
  • sedation
  • dizziness
  • confusion
  • dry mouth
  • urinary retention
  • anticholinergic effects
26
Q

describe phenothiazine class use in PONV

A
  • inhibition of dopamine muscarinic, and histamine receptors

- marked sedation potentiates effect of postop narcotics

27
Q

what are limitations of phenothiazine class use?

A
  • sedation (anticholinergic effect)
  • extrapyramidal effects (dopamine blocked)
  • pseudoparkinson’s (dopamine blocked)
  • lowers seizure threshold
  • hypotension (alpha blockade)
28
Q

what is the dose of prochlorperazine (Compazine)?

A

2.5-10 mg IV

29
Q

what is the dose of promethazine (Phenergan)?

A

25 mg IV

30
Q

what is the MOA of scopolamine?

A

antimuscarinic (vestibular system)

-antagonizes histamine and serotonin

31
Q

describe scopolamine

A
  • lipid soluble: crosses BBB, transdermal absorption (patich)
  • apply 60 minutes prior to induction
  • can provide adequate drug levels 48-72 hrs
32
Q

what is the dose of a scopolamine patch?

A

1.5 mg patch releases 1 mg dose

33
Q

what are limitations of scopolamine?

A
  • ocular effects (caution with glaucoma pts.)
  • restlessness
  • delirium
  • sedation (not typically a lot)
  • dry mouth
  • tachycardia (uncommon)
  • caution pts. on touching patch and rubbing eyes
34
Q

describe butyrophenones (droperidol, Inapsine)

A
  • dopamine blockade (alpha blockade)
  • extremely sedating, dissociative state
  • causes vasodilation d/t peripheral alpha blockade (decreased in BP)
  • give up front so dissociative state wears off before emergence
35
Q

what is the dose of butyrophenones (droperidol, Inapsine)?

A

0.625-1.25 mg IV (0.05 mg/kg)

36
Q

what are limitations of butyrophenones (droperidol, Inapsine)?

A
  • prolonged QT interval (DOSE 25mg)(torsade de pointes)
  • extrapyramidal effects (avoid in Parkinson’s and elderly)
  • hypotension
  • sedation
37
Q

describe metoclopramide

A
  • dopamine blockade in the CTZ
  • gastrokinetic: moves everything forward (aspiration prophylaxis)
  • if used with phenothiazines or droperidol, increases incidence of extrapyramidal effects (restlessness, dystonias, parkinsonian)
38
Q

what is the dose of metoclopramide?

A

10-20 mg IV

39
Q

when should metoclopramide be avoided?

A

intestinal obstruction (increased pressure may cause perforation)

Parkinson’s

40
Q

describe serotonin

A
  • serotonin is an endogenous vasoactive substance and neurotransmitter (emesis and pain), cerebral stimulant
  • 90% stored in the enterochromaffin cells of the GI tract
41
Q

describe 5-HT receptors

A

1: cerebral vasoconstriction (cause migraines)
2: coronary artery and pulmonary vessel vasoconstriction
3: PNS-visceral pain; CNS- emesis, appetite, addiction, pain, and anxiety
4: gastrokinesis (constipation, IBS)

42
Q

how do 5-HT3 receptor antagonists work?

A
  • block peripheral receptors on the intestinal vagal afferents and central receptors in the vomiting center, CTZ (vagal stimulation)
  • no effect on dopamine, histamine, adrenergic, or muscarinic receptors (no parkinsonian, restlessness, hypotension, or sedation)
  • *minimal side effects
  • *good for chemotherapy induced NV, PONV (not motion sickness)
43
Q

what are side effect of 5-HT receptor antagonists?

A

headache, constipation, theoretically cardiac arrhythmias (Anzemet)

44
Q

what are limitation of 5-HT receptor antagonists?

A
  • cost
  • prolonged QT interval (caution if QT interval already prolonged)
  • effectiveness of droperidol
  • propofol induction and maintenance
45
Q

what is the dose of ondansetron (Zofran)?

A

4-8 mg (0.15 mg/kg) IV

46
Q

what is the dose of dolasetron (Anzemet)?

A

12.5 mg IV

47
Q

what is the dose of granisetron (Kytril)?

A

1 mg (0.01 mg/kg) IV

48
Q

what is the dose of palonosetron (Aloxil)?

A

0.075 mg IV

49
Q

describe corticosteroid use in PONV

A
  • unknown mechanism
  • enhances the effectiveness of 5-HT3 antagonists (6-10mg)
  • increases blood sugar (caution with diabetics)
  • give at beginning of case
50
Q

what is the dose of dexamethasone (Decadron)?

A

0.5 mg/kg (4-8 mg)

pediatrics up to 6 mg

51
Q

what are the limitations of dexamethasone?

A

with chronic therapy: interference with healing, immune suppression, avascular necrosis (?)

52
Q

what drugs antagonize the dopamine receptors at the CTZ?

A
  • droperidol

- metoclopramide

53
Q

what drugs antagonize the ACh receptors at the CTZ?

A
  • scopolamine; atropine

- diphenhydramine

54
Q

what drugs antagonize the histamine 1 receptors at the CTZ?

A
  • diphenhydramine

- promethazine

55
Q

what drugs antagonize the 5-HT3 receptors at the CTZ?

A
  • ondansetron

- high dose metoclopramide

56
Q

describe guidelines for PONV prophylaxis and treatment

A
  • identify pts. at high risk
  • reduce baseline risks of PONV
  • use prophylaxis with high risk and moderate risk (5-HT antagonist + 2nd agent like decadron or scopolamine if history of motion sickness)
  • use appropriate rescue treatment
57
Q

what are appropriate rescue treatment guidelines?

A
  • if not previously given, give 5-HT3 antagonist (Zofran)
  • do not repeat initial therapy
  • if within 6 hrs., don’t redose 5-HT3 antagonist
  • if after 6 hrs., repeat 5-HT3 antagonist dose and second agent from a different class
58
Q

what is neurokinin (NK1) or substance P

A

the natural ligand of the neurokinin receptor found in the area postrema, nucleus of the solitary tract and afferent fibers of the vagus nerve

59
Q

how does aprepitant (Emend) work?

A

antagonist of the NK1 receptor

-approved for PONV prophylaxis

60
Q

what is the dose of Emend?

A

40 mg po one hour prior

61
Q

what are alternative treatments for PONV?

A
  • acupressure: relief band or inject D50 between flexor tendons, 3 finger widths below hand-wrist crease
  • hypnosis
  • propofol: 0.5 mg/kg
  • ephedrine: IM dose 0.5 mg/kg
  • ephedrine equal to droperidol IV and increases BP
62
Q

explain PONV prevention algorithm

A

low risk: prophylaxis either none or use drug A + (drug B or TIVA); treatment if no prophylaxis 1) drug B 2) drug C if prophylaxis used then 1) drug C 2) drug D
medium risk: prophylaxis drug A + (drug B or TIVA); treatment 1) drug C 2) drug D
high risk: prophylaxis drug A + drug B + TIVA; treatment 1)drug C 2)drug D
-drug A: dexamethasone 4 mg
-drug B: ondansetron 4 mg
-drug C: droperidol 1 mg
-drug D: dimenhydrinate 1 mg/kg

Anesthesia Pharm I (28 decks)

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