This document provides guidance on evaluating and treating a child presenting with vomiting. It begins with definitions of related terms like nausea, retching, and regurgitation. It then reviews the major neurophysiological pathways that can induce vomiting. Etiologies are discussed including central, infectious, metabolic, and peripheral causes. An approach is outlined involving obtaining a thorough history and physical exam to determine potential causes and guide testing. Common etiologies are reviewed for different age groups. Complications, treatment principles targeting the underlying cause, and sick day management for diabetes are also summarized.

1. Approach to the
Child with Vomiting
By
Dr. C. Kannan,
1st year PG, Pediatrics Department, MGMCRI

2. 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.
Retching
muscular activity of the abdomen and thorax, often voluntarily
leading to forced inspiration against a closed mouth and glottis
without oral discharge of gastric contents
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.
Rumination
Food that is regurgitated in the postprandial period, re-chewed and then
re-swallowed (psychological)

3. NEUROPHYSIOLOGY
There are four major pathways by which nausea and vomiting are induced,
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 over distension, food
poisoning, mucosal irritation, cytotoxic drugs, and radiation.
Area postrema
 Chemotrigger receptor zone
Vestibular system
It involved in the emetic response to motion
Exacerbated by visual sensations, Irritation or labyrinthine inflammation.
Amygdala

4. ETIOLOGY OF VOMITTING
Central
Vestibular - motion sickness and vertigo
Infectious - gastroenteritis, septicemia, non-GI infections
Cortical - pain, strong emotions, smell, taste
Drugs - chemotherapy, opiates
Metabolic - acidosis, uremia, hyperthyroidism, hypercalcemia,
adrenal disorders
Peripheral
Pharyngeal stimulation
Gastric mucosal irritation
Gastric and intestinal obstruction/dilation

5. INTRODUCTION TO APPROACH
A standardized approach is not recommended
Vomiting may be caused by many pathologic states involving several
systems including
Gastrointestinal,
Neurologic,
Renal, and
Psychiatric
The best course of action should be dictated by the medical history.

6. History of presenting illness
Characteristics of vomitus
Smell
Quantity
Colour
Blood - Bright red/dark red/coffee-ground
Bilious
Timing - Onset, Duration, Frequency and Time of day
Triggers / Associated symptoms
Diarrhoea
Fever
Abdominal pain/distension
Anorexia
Stool frequency
Urinary output
Headache
Vertigo
Lethargy
Stiff neck
Cough
Sore throat

7. Past medical history
Chronic illnesses like Diabetes
Travel history (infectious gastroenteritis)
Recent head trauma
Toxin exposure
Medications
Allergies

8. Few important interpretations of history
Undigested Achalasia
Bilious Post ampullary obstruction
Blood or coffee ground Gastritis , Ulcer
Bloody after forceful vomiting Mallory wiess tear
Malodorous Stasis with bacterial overgrowth
Feculent Obstruction
Force of vomiting
Forceless Regurgitation , gastroesophagial reflux
Projectile Pyloric stenosis, obstruction, metabolic disease

9. Temporal associations of chronic or recurrent vomitting
Temporal associations Diagnosis
Time of day
Early morning increased ICP, sinusitis with postnasal mucous, pregnancy, uremia
(headache, papilledema, sinus tenderness, secondary amenorrhea)
During or after meals peptic ulcer disease, reflux(epigastric pain, heart burn)
for specific foods(Heredetary fructose intolerance,
galactocemia, metabolic inborn error, cows milk intolerance, etc.,
After fasting
food vomitted gastric obstruction
food not vomitted metabolic disease

10. Other precipitants
Cough posttussive
Infections metabolic, reccurent gastroenteritis
Vestibular stimulation motion sickness, menetrriers disease
Hyperhydration uretropelvic junction obstruction
Menses dysmenorrhea associated vomitting, acute intermittent porphyria
Medications and toxins medication side effects – pancreatitis, hepatitis, AIP
steroid withdrawal – Addisons disease
poisonings – NSAIDS
Episodic / cyclic
Abdominal migraine, abdominal epilepsy, pheochromocytoma, pophyria, familial
dysautonomia, metabolic inborn error, FMF, self induced, cyclical vomitting

11. Food associations
Cow milk, soy, gluten - Protein intolerance
Multiple food exacerbants - Esinophilic gastroenteritis, fructose
intolerance
Periodicity of vomiting
Paroxysmal, cyclic
- cyclic vomiting syndrome, porphyria, carcinoid, pheochromocytoma, familial
dysautonomia
Neurological symptoms
Headache, vertigo, visual changes - Metabolic, toxin, CNS disease
Fundoscopic evidence of increased ICP - CNS mass

12. Others
Lack of nausea CNS mass
Esophagial pain Esophagitis
Diarrhea Infectious enteritis
Abdominal peristaltis Obstruction, pyloric stenosis
Peritoneal signs Surgical abdomen, perforated appendicitis
Jaundice Hepatobiliary etiology or urinary tract infection in a neonate
Surgical scars Obstruction secondaryto adhesions
Early morning vomiting Pregnancy and CNS mass
Vomiting with meals
Peptic ulcer disease,
Psychogenic disease,
Disproportionate hypotention,
Hyperkalemia,
Adrenal crisis

13. Prolonged vomiting
>12 hours in a neonate,
>24 hours in children younger than two years of age, or
>48 hours in older children should not be ignored.
Screening laboratory tests should include
Complete blood count
Electrolytes,
Blood urea nitrogen,
Amylase, lipase,
Liver function tests,
Urinalysis, urine culture, and stool studies for occult blood
Leukocytes, and parasites.
Additional testing should be based upon the history and physical
examination

14. Clues on physical examination
Certain physical findings may offer diagnostic clues
Which aids in narrowing the differential diagnosis:
 A tense, bulging fontanel in a neonate or young infant
Increases the level of suspicion for meningitis.
 Projectile vomiting in an infant three to six weeks of age suggests
Pyloric stenosis
 Ambiguous genitalia and/or hyperkalemia suggest the possibility of
Adrenal crisis (usually due to congenital adrenal hyperplasia).

15.  An unusual odor emanating from the patient should prompt an investigation for
Metabolic causes of vomiting.
 Marked distension, visible bowel loops, absent bowel sounds, green or yellow bile, or
increased "rumbling" bowel sounds should raise suspicion for
Intestinal obstruction.
 Enlarged parotid glands in an adolescent should raise suspicion for
Bulimia
 Vomiting in association with trauma should prompt imaging studies
To rule out intracranial or intra abdominal injury.
 Hypotension disproportionate to the apparent illness and/or hyperkalemia suggests
The possibility of adrenal crisis
Headache, positional triggers for vomiting, lack of nausea on awakening should suggests
The possibility of intracranial hypertension

16. Most common causes of vomiting in Neonates
 Physiologic reflux or GERD
 Pyloric stenosis
 Necrotising enterocolitis
 Malrotation with midgut volvulus
 Gastroenteritis
 Hirshprung disease
 Congenital atresias, stenosis, web
 Metabolic disorders
 Feeding intolerance

17. Common causes of vomitting in Infants (1 month to 1 year)
Acute
 Gastroenteritis
 Pyloric stenosis
 Hirschsprung’s disease
 Acutely evolving surgical abdomen
 Congenital atresias and stenosis
 Malrotation
 Intussusception
 Sepsis and non-GI infection
 Metabolic disorders
Chronic
 Gastroesophageal reflux disease
 Food intolerance
 Congenital atresias and stenosis
 Malrotation
 Intussusception

18. Children and
Adolescents
ACUTE
Gastroenteritis
Appendicitis
Sepsis and non-GI
infection
Metabolic disorders
Toxic ingestion
CHRONIC
Gastroesophageal
reflux disease
Gastritis
Food intolerance
Cyclic vomiting
Intracranial
hypertension
Inborn errors of
metabolism
Eating disorders

19. COMPLICATIONS OF VOMITTING
Nutrition Adults - weight loss, kids - Failure to gain weight/grow
Cutaneous Petechia, Purpura
Oropharyngeal Dental erosion, sore throat)
Esophageal Esophagitis / hematoma
GE junction M-W tears, rupture of esophagus (Borhaeve’s)
Metabolic Electrolyte, acid-base, water imbalance
Renal Pre-renal azotemia, ATN, hypokalemic nephropathy
Infection Spread of infection to close contacts and caregivers
(H. pylori, GI viruses)

20. TREATMENT
Treatment should be directed towards the underlying etiology.
Electrolyte abnormalities, metabolic abnormalities, and 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 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.

21. Instead, antiemetics are most useful for motion sickness, postoperative vomiting, cyclic
vomiting syndrome, and gastrointestinal motility disorders .
A single dose ondensetran may facilitate oral rehydration in children with gastroenteritis
who are unable to tolerate oral intake.

22. GUIDELINES FOR SICK DAY MANAGEMENT
Urine ketones Insulin
(rapid acting)
Frequency of
monitoring
Comments
Negative/small Q2H Q2H
if CBG >250 mg/dl
Check ketones
every other void
Moderate to large Q1H Q1H
if CBG >250 mg/dl
Check ketones on
each void

23. THANK YOU !!