1. PHYSIOLOGY OF NAUSEA AND
VOMITING , VOMITING IN
ANESTHESIA , PREVENTATION
AND MANAGEMENT
DR. SHIRISH ACHARYA
2. VOMITING
• Vomiting is the means by which the upper gastrointestinal tract rids
itself of its contents when almost any part of the upper tract becomes
excessively irritated, overdistended, or even overexcitable.
• Excessive distention or irritation of the duodenum provides an
especially strong stimulus for vomiting.
3. PHYSIOLOGY OF VOMITING
• Sensory signals that initiate vomiting originate mainly from the
pharynx, esophagus, stomach, and upper portions of the small
intestines.
• the nerve impulses are transmitted by both vagal and sympathetic
afferent nerve fibers to multiple distributed nuclei in the brain stem,
especially the area postrema, that all together are called the
“vomiting center.”
4. • From here, motor impulses that cause the actual vomiting are
transmitted from the vomiting center by way of the fifth, seventh,
ninth, tenth, and twelfth cranial nerves to the upper gastrointestinal
tract, through vagal and sympathetic nerves to the lower tract, and
through spinal nerves to the diaphragm and abdominal muscles.
6. ANTIPERISTALSIS, THE PRELUDE TO VOMITING
• In the early stages of excessive gastrointestinal irritation or
overdistention, antiperistalsis begins to occur, often many minutes
before vomiting appears.
• This process can actually push a large share of the lower small
intestine contents all the way back to the duodenum and stomach
within 3 to 5 minutes.
• Then, as these upper portions of the gastrointestinal tract, especially
the duodenum, become overly distended, this distention becomes
the exciting factor that initiates the actual vomiting act
7. • At the onset of vomiting, strong intrinsic contractions occur in both
the duodenum and the stomach, along with partial relaxation of the
esophageal-stomach sphincter, thus allowing vomitus to begin
moving from the stomach into the esophagus.
• From here, a specific vomiting act involving the abdominal muscles
takes over and expels the vomitus to the exterior.
8. VOMITING ACT
• Once the vomiting center has been sufficiently stimulated and the
vomiting act has been instituted, the first effects are :
(1) a deep breath
(2) raising of the hyoid bone and larynx to pull the upper esophageal sphincter
open
(3) closing of the glottis to prevent vomitus flow into the lungs, and
(4) lifting of the soft palate to close the posterior nares.
9. • After this there occurs a strong downward contraction of the
diaphragm along with simultaneous contraction of all the abdominal
wall muscles, which squeezes the stomach between the diaphragm
and the abdominal muscles, building the intragastric pressure to a
high level.
• Finally, the lower esophageal sphincter relaxes completely, allowing
expulsion of the gastric contents upward through the esophagus
10. CHEMORECEPTOR “TRIGGER ZONE” IN THE BRAIN
MEDULLA FOR INITIATION OF VOMITING BY DRUGS
OR BY MOTION SICKNESS
• This mechanism is true for a small area called the chemoreceptor
trigger zone for vomiting, located in the area postrema on the lateral
walls of the fourth ventricle.
• Electrical stimulation of this area can initiate vomiting, but more
importantly, administration of certain drugs, including apomorphine,
morphine, and some digitalis derivatives, can directly stimulate this
chemoreceptor trigger zone and initiate vomiting.
11. • Rapidly changing direction or rhythm of motion of the body can cause
certain people to vomit.
• The motion stimulates receptors in the vestibular labyrinth of the
inner ear.
• From here impulses are transmitted mainly by way of the brain stem
vestibular nuclei into the cerebellum
• then to the chemoreceptor trigger zone, and finally to the vomiting
center to cause vomiting.
12. NAUSEA
• The sensation of nausea is often a prodrome of vomiting.
• Nausea is the conscious recognition of subconscious excitation in an
area of the medulla closely associated with or part of the vomiting
center.
13. • It can be caused by
(1) irritative impulses coming from the gastrointestinal tract,
(2) impulses that originate in the lower brain associated with motion sickness,
or
(3) impulses from the cerebral cortex to initiate vomiting.
14. • Vomiting occasionally occurs without the prodromal sensation of
nausea, which indicates that only certain portions of the vomiting
center are associated with the sensation of nausea.
17. CAUSES OF VOMITING
• Patient factors
(a) Full stomach
· Emergency surgery
· Inadequate fasting time
· Gastrointestinal obstruction
(b) Delayed gastric emptying
· Systemic diseases, including diabetes
mellitus and chronic kidney disease
· Recent trauma
· Opioids
· Raised intra-cranial pressure
· Previous gastrointestinal surgery
· Pregnancy (including active labour)
(c) Incompetent lower oesophageal
sphincter
· Hiatus hernia
· Recurrent regurgitation
· Dyspepsia
· Previous upper gastrointestinal
surgery
· Pregnancy
(d) Oesophageal diseases
· Previous gastrointestinal surgery
· Morbid obesity
18. • Surgical factors
· Upper gastrointestinal surgery
· Lithotomy or head down position
· Laparoscopy
· Choleocystectomy
Anaesthetic factors
· Light anaesthesia
· Supra-glottic airways
· Positive pressure ventilation
· Length of surgery > 2 h
· Difficult airway
Device factors
· First-generation supra-glottic
airway devices
19. RISK FACTORS FOR POST OPERATIVE NAUSEA
AND VOMITING
PATIENT RELATED
• female patients
• Non-smoking status
• history of motion sickness, PONV,
or both
• PONV decreasing as patients age
• Low ASA physical status (I – II)
• history of migraine
• preoperative anxiety
ANAESTHESIA-RELATED
• use of volatile anaesthetics
• intraoperative and postoperative
opioid use
• duration of anaesthesia
• general anaesthesia
20. SURGERY-RELATED
• There is much controversy over the impact of type of surgery on
PONV.
• Some studies have shown that gynaecological, ophthalmological,
otological,laproscopic and thyroid surgery can each increase the risk
of PONV.
• Duration of surgery 60 min increases the risk of PONV
• In children, strabismus surgery was identified as an independent risk
factor for POV.
22. PREVENTION
Reducing gastric volume
Preoperative fasting
Nasogastric aspiration
Prokinetic premedication
Avoidance of general anaesthetic Regional anaesthesia
Reducing pH of gastric contents
Antacids
H2 histamine antagonists
Proton pump inhibitors
Airway protection
Tracheal intubation
Second-generation supra-glottic airway devices
Prevent regurgitation
Cricoid pressure
Rapid sequence induction
Extubation
Awake after return of airway reflexes
Position (lateral, head down or upright)
23. Experienced anaesthesia assistance available to all times
Intubate all emergency cases
Apply appropriate cricoid pressure with all inductions using neuromuscular blocking agents
Intubate/seriously consider intubation in the following:
Delayed gastric emptying (pregnancy, opioids, diabetes mellitus, renal failure)
Increased intra-abdominal pressure (obesity, ascites, masses)
27. ANTIEMETIC DRUGS
• Serotonin antagonists:
Ondasetron, granisetron, dolasetron, tropisetron
• DOC: prophylaxis and treatment of chemotherapy and radiation therapy
induced nausea and vomiting, PONV
28. • PROKINETICS/ Dopamine antagonist:
Metoclopramide, Domperidone, Cisapride
• Motility modulating drugs by increases lower esophageal sphincter tone, Enhancing
peristaltic contractions and accelerating the rate of gastric emptying
• USES
Preoperative decrease of gastric fluid, Production of an antiemetic
effect, Treatment of gastroparesis: in DM, Symptomatic treatment of
gastroesophageal reflux:
29. • NEUROLEPTICS(D2 receptor antagonist)
Haloperidol, chlorpromazine, prochlorperazine
• Neurotoxic and causes brain atrophy on long term use
30. • Histamine antagonists/ H1 receptor antagonist:
Promethazine, Diphenhydramine and dimenhydrinate
• Effective H1 antagonist against motion sickness and PONV with
anticholinergic property
32. • Neurokinin antagonists
Aprepitant: 1st drug approved for clinical use
200mg reduces incidence of PONV
Substance P is a regulatory peptide that binds to neurokinin 1 (NK 1)
receptors found in vagal afferents in GIT
Highly effective against a wide range of emetics
More superior for preventing vomiting than nausea.
33. • Adjuvants
DEXAMETHASONE
• Central antiemetic action through an activation of the glucocorticoid
receptors in the bilateral nuclei tractus solitarius in the medulla
• Effective antiemetics when combined with other antiemetic for refractory
nausea and vomiting
• Efficacy similar to ondansetron or droperidol
CANNABINOIDS: it acts at the higher centres/ at vomiting centres.
36. Combination and multimodal therapy
• Combination of dexamethasone, ondansetron and droperidol
• Synergistic combination for positive result
• Patient with high risk mostly benefited.
Antiperistalsis means peristalsis up the digestive tract rather than downward. Antiperistalsis may begin as far down in the intestinal tract as the ileum, and the antiperistaltic wave travels backward up the intestine at a rate of 2 to 3 cm/sec; this process can actually push a large share of the lower small intestine contents all the way back to the duodenum and stomach within 3 to 5 minutes.
Thus, the vomiting act results from a squeezing action of the muscles of the abdomen associated with simultaneous contraction of the stomach wall and opening of the esophageal sphincters so that the gastric contents can be expelled.
Destruction of this area blocks this type of vomiting but does not block vomiting resulting from irritative stimuli in the gastrointestinal tract itself.
Pathophysiology of nausea and vomiting. Vomiting is caused by noxious stimulation of the vomiting center directly or indirectly via 1 or more of 4 additional sites: the gastrointestinal (GI) tract, the vestibular system, the chemoreceptor trigger zone, and higher centers in the cortex and thalamus. Once receptors are activated, neural pathways lead to the vomiting center, where emesis is initiated. Neural traffic originating in the GI tract travels along afferent fibers of cranial nerves IX (glossopharyngeal) and X (vagal). Antiemetic targets for drug interventions are predicated on their ability to block the illustrated receptor sites. Receptors illustrated along with their conventional ligands are as follows: H1 histamine, M1 acetylcholine, 5-HT3 serotonin, DA2 dopamine, NK1 (neurokinin) substance P, and mu/kappa opioids. Transmitter mediators in the cerebral cortex and thalamus are poorly understood, although cortical cannabinoid (CB1) pathways have been characterized.