Approach to
Vomiting
Dr Vivek Jha
Definition
Nausea: The unpleasant sensation of the imminent need
to vomit, usually referred to the throat or epigastrium; a
sensation that may or may not ultimately lead to the act
of vomiting.
Vomiting: Forceful oral expulsion of gastric contents
associated with contraction of the abdominal and
chest wall musculature.
Regurgitation: The act by which food is brought back
into the mouth without the abdominal and
diaphragmatic muscular activity that characterizes
vomiting.
Five classes of stimuli provoke nausea and vomiting:
(1)toxic substances within the lumen of the gastrointestinal tract, which
initiate release of mediators by enteroendocrine cells (including 5-
hydroxytryptamine, substance P, and cholecystokinin [CCK]);
(2)absorbed or parenterally administered toxins, which act directly on the
area postrema (also referred to as the chemoreceptor trigger zone—a major
lower brainstem center for coordination of drug-induced vomiting);
(3)pathologic processes in viscera (eg, gastrointestinal dilation or
inflammation, renal failure);
(4)central nervous system (CNS) stimuli (eg, fear, anticipatory nausea, raised
intracranial pressure);
(5)vestibular stimuli (eg, motion sickness) that result in nausea and vomiting
by
Neurophysiology
Nausea and vomiting are innate responses
that induce a learned and conditioned
aversion to ingested toxins
There are four major pathways by which nausea and
vomiting are induced.
Vagal afferents
Area postrema
Vestibular
system
Amygdala
Vagal
Afferents
Abdominal vagal afferents are involved in the
emetic response.
Can be evoked by either mechanical or
chemo- sensory sensations.
Examples of sensations that trigger this
pathway include overdistension, food
poisoning, mucosal irritation, cytotoxic drugs,
and radiation.
Area
Postrema
It’s a chemoreceptor trigger
zone. Anatomically, this region
is located at the caudal
extremity of the floor of the
fourth ventricle.
It’s a permeable blood-brain
barrier region in which
systemic chemicals act to
induce emesis can reach
This area contains receptors A diagram summarizing the pathways
for neuroactive compounds involved in emesis. Rache: Nucleus
such as dopamine, morphine, Rache, AP: area postrema, IV: 4 th
ventricle, 5-HT: 5-hydroxytryptamine
acetylcholine, endorphin,
(serotonin), EC: enterochromaffin cell, GI:
and many others gastrointestinal.
Vestibular
System
It involved in the emetic response to
motion
Exacerbated by visual sensations, Irritation or
labyrinthine inflammation.
Somatomotor
Events
The diaphragm descends and the
intercostal muscles contract while
the glottis is closed.
The abdominal muscles contract
and the gastric contents are forced
into upper gastric vault and lower
esophagus.
The abdominal muscle relaxes
and the esophageal refluxate
empties back into the gastric
vault.
Several cycles of retching, each
more rhythmical and forceful in
nature, occur, with shorter intervals
in between.
Abdominal contraction associated
with elevation of diaphragms results
Infancy/Early childhood -
Congenital
•Regurgitation — gastro esophageal reflux
•Atresia— stenosis (tracheoesophageal fistula, antral web, intestinal atresia,
annular pancreas)
• Gastrointestinal tract duplication
•Volvulus (secondary to an error in rotation and fixation or to
Meckel diverticulum)
•Congenital bands
• Meconium ileus (cystic fibrosis), meconium plug
• Hirsch sprung disease
Infancy/Early childhood -
Acquired
• Acute infectious gastroenteritis
• Food allergy, cow milk protein intolerance, eosinophilic gastroenteritis
• Eosinophilic esophagitis
• Pyloric stenosis
• Intussusception
• Celiac disease
• Incarcerated hernia—inguinal, internal secondary to old adhesions
• Postviral gastroparesis
• Adynamic ileus—the mediator for many nongastrointestinal causes of
vomiting
• Neonatal necrotizing enterocolitis
• Chronic granulomatous disease with gastric outlet obstruction
Infancy/Early childhood -
Nongastrointestinal
•Infectious—otitis, UTI, Pneumonia, URTI, Sepsis, Meningitis
•Metabolic— Aminoaciduria And Organic Aciduria,
Galactosemia, Fructosemia, Adrenogenital Syndrome,
Renal Tubular Acidosis, Hyperammonemia, Disorders Of
Fatty Acid Oxidation(eg, Medium-chain Acyl Coenzyme A
Dehydrogenase Deficiency), Mitochondrial Disease
•Central Nervous System — Trauma, Tumor, Infection,
Increased Intracranial Pressure, Ventriculo-peritoneal
Shunt Failure, Autonomic Responses (Pain, Shock).
Childhood/Adolscenes
-
Gastrointestinal
•Appendicitis
• Food poisoning (staphylococcal, clostridial)
• Peptic disease—ulcer, gastritis, duodenitis, Helicobacter pylori infection
• Trauma—duodenal hematoma, traumatic pancreatitis, perforated
bowel
•Pancreatitis—viral, trauma, drug induced, cystic fibrosis,
hyperparathyroidism, hyperlipidemia, hereditary
pancreatitis,
•Gallbladder—cholelithiasis, choledochal cyst
• Crohn disease
• Adhesions—congenital or secondary to previous
abdominal surgery
• Visceral neuropathy or myopathy.
Childhood/Adolscenes-
NonGastrointestinal
•Medications— anticholinergics, Alcohol, Idiosyncratic Reaction (Eg,
Codeine), Chemotherapy, Radiation Therapy, Overdose(especially
Aspirin Or Acetaminophen)
• Central Nervous System—cyclic Vomiting, Migraine, Anorexia
Nervosa, Bulimia Nervosa
•Motion Sickness
•Metabolic—diabetic Ketoacidosis, Acute Intermittent Porphyria
•Pregnancy
Histor
y
Age of pt.
Duration/Frequency.
Onset
Associated with food intake.
Instantly : esophageal obstruction.
After a while : stomach or duodenal
obstruction.
Nature (projectile/non-projectile)
Color & contents
Non digested – proximal obstruction.
Semi digested – distal obstruction.
Billious content – distal to 2nd part of duodenum
Fecal material – large intestinal obstruction.
Histor
y
RS : cough, chest discomfort.
Urinary : dysuria, hematuria.
CNS : irritability, altered sensorium, neck stiffness, headache, visual
disturbance.
Past history :
Any known medical illness like IEM, cerebral palsy, down syndrome.
Drug & allergy history
Birth history
Nutritional history : recently changed to cow’s milk, food allergy.
Other history : recent travelling/eating outside, family members or
friends having similar complaints.
Examination
General condition
Weight comparison before & after onset of
illness.
Consciousness – GCS.
Hydration status.
Abdominal examination :
Distension/visible peristalsis.
Tenderness/hepatosplenomegaly.
Palpable mass.
Bowel sounds,
Examination
CNS ex. :
Tone, power, reflexes.
Change in vision.
Respiratory ex.
Otoscopy &
fundoscopy.
Investigations
TC, DC – Leukocytosis (infections)
S.electrolytes, urea, s.creatinine – effect of vomiting on electrolytes.
RBS – DKA
ABG –
Acidosis – organic acidemias.
Alkalosis- pyloric stenosis.
Urine C/S.
Imaging : CXR, abdominal xray, barium meal, barium follow-
through, Cranial CT. Upper endoscopy.
Esophageal ph monitoring.
Metabolic workup in suspected IEM.
Managemen
t
Asses the severity of
dehydration.
Rehydrate accordingly.
Correct electrolyte imbalances.
Encourage oral intake.
Treat underlying cause.
Treatment should be directed toward the underlying
etiology.
Electrolyte abnormalities, metabolic abnormalities, or nutritional deficiencies
should be corrected.
Cognitive-behavioral interventions are useful for vomiting associated with
functional
dyspepsia, adolescent rumination syndrome, and bulimia.
Prokinetic medications such as metoclopramide, domperidone (where available),
and erythromycin are beneficial when there are abnormalities in esophago-
gastric motility.
Antiemetics, which are useful in persistent vomiting to avoid electrolyte
abnormalities or nutritional sequelae, typically have not been recommended in
the case of vomiting of unknown etiology. These agents are contraindicated in
infants .
Likewise, they are not indicated for anatomic abnormalities or surgical abdomen
Complications
Dehydration and electrolyte imbalance, especially when the vomiting
is persistent.
Aspiration pneumonia.
A tear at the gastro-esophageal junction (Mallory-Weiss
syndrome)
Rupture of the esophagus (very uncommon in children).
Feeding refusal may follow persistent vomiting.
