Abdominal Pain and Vomiting

What are the common causes of abdominal pain and vomiting in young children?
How can the history and physical examination help distinguish between these causes?
Investigations? Management? Parental advice?

Acute abdominal pain

1. Common causes/probability diagnosis:
o infant colic
o gastroenteritis (all ages)
o viral syndrome
o mesenteric adenitis
2. Serious causes, not to be missed:
o intussusception (peaks at 6-9
months)
o acute appendicitis (mainly 5-15
years)
o bowel obstruction (volvulus,
intussusception, or adhesions)
o pyloric stenosis
3. Pitfalls:
o child abuse
o constipation
o torsion of testes
o lactose intolerance
o peptic ulcer
o infections: mumps, tonsillitis, pneumonia
(especially right lower lobe), EBM, UTI
o adnexal disorders in females (e.g. ovarian)
4. Rarities:
o Meckel diverticulitis
o Henoch-Schönlein purpura
o sickle crisis
o lead poisoning
5. Seven masquerades checklist:
o diabetes mellitus
o drugs
o UTI
6. Psychogenic consideration:
o important cause

VOMITING
Approach
 consider: infection, inflammation, mechanical obstruction,
motility disorders, others (e.g. eating disorder)
 Non GI causes: CNS, UTI, systemic infections, others
Assessment
 history
• age of onset, duration, severity
 • quality: bilious, bloody, regurgitation
• associated symptoms e.g. fever, abdominal pain
• effect on growth and development, concurrent disease
 physical exam: assess hydration
 lab investigation
• bloody emesis: investigate for causes of upper GI bleed
• bilious emesis: rule out obstruction (upper GI series, U/S)
• regurgitation: evaluate for reflux (barium swallow with fluoroscopy, 24 hour oesophageal pH probe)
 useful tests (based on history and physical exam)
• CBC, lytes, BUN, Cr, ESR
• urine, blood, stool C&S
• amylase, lipase
• arterial blood gases
• abdominal x-ray, ultrasound, contrast radiology
• endoscopy
 management
• treat the underlying cause
• rehydration
VOMITING IN THE NEWBORN
 congenital anomalies are a frequent cause, e.g. atresia, Hirshprung’s
 differential diagnosis: gastroenteritis, gastroesophageal reflux, overfeeding, food allergy, milk protein
intolerance, meconium ileus (CF)
Tracheoesophageal Fistula
 incidence: 1:3000-1:4500
 clinical features vary with type
• vomiting, coughing and gagging
• cyanosis with feeds
• respiratory distress
• may have history of maternal polyhydramnios
• associated anomalies: VATER = Vertebral anomalies, Anal atresia, TEF and Renal disease plus cardiac
abnormalities and radial defects of the upper limb
 x-ray —> plain and contrast studies show anatomic abnormality, NG tube curled in pouch
 treatment: early repair to prevent lung damage and maintain nutrition
 complications
• pneumonia, lung damage, chronic reactive airways
• stenosis and strictures at repair site
• gastroesophageal reflux and poor swallowing following repair
Duodenal Atresia
 clinical features
• bile-stained vomiting if distal to bile duct
• abdominal distention, peristaltic waves
• dehydration
• associated with Down syndrome
• may have history of maternal polyhydramnios
 abdominal x-ray —> air-fluid levels on upright film
• "double bubble" sign (dilated stomach and duodenum)
 differential diagnosis: annular pancreas, aberrant mesenteric
• vessels, pyloric stenosis
 treatment → decompress with NG tube, correct metabolic, surgery
Pyloric Stenosis
 incidence: most common in first-born males, often family history
• M:F = 5:1
 More common whites of N Europe, less in blacks, rare in Asians
 Higher risk if maternal positive
• 20% males, 10% female child positive
 Possibly associated with maternal macrolides, or neonatal erythromycin
 Usually not present at birth, develops after

 clinical features
• non-bilious projectile vomiting that occurs after feeding
 Vomiting is from loss of gastric fluid (water and HCl)
• usually starts at 2-6 weeks of age
• 20% intermitted emesis straight after birth
• infant hungry and alert, will re-feed after vomit
• FTT, wasting
• dehydration, may lead to prolonged jaundice
• Leads to loss of fluid, hydrogen ion and chloride

 Hypochloeremic metabolic alkalosis
 ↑ pH  ↓potassium
 ↓bicarbonate  ↓ or normal sodium
 ↓chloride  Normal or ↑ creatinine/urea
• gastric peristalsis goes from LUQ to epigastrium
• “olive sign” (olive-shaped mass on right at margin of rectus abdominis muscle)
 Firm, movable, ~2cm length, olive shaped, hard
 Above and right to epigastrium especially after vomiting
• Hyperbilirubinamia common clinical association
 Icteropyloric syndrome
 More unconjugates bilirubin, consider ddx if more conjugated
 lab: hypochloremic metabolic alkalosis
 diagnosis: clinical, abdominal ultrasound to confirm, barium studies
 treatment: pyloromyotomy lapracopic using Ramstedt procedure – curative
• Pyloric mass cut longitudinally to submucosa with blunt dissection
 relieves the constriction and allows normal passage of stomach contents into the duodenum
• Laparoscopic technique equally successful
 lower incidence of postoperative emesis and a shorter hospital stay
 Pre-op
• Correct fluid, acid-base, electrolyte loss
• Nasogastric suction occasionally reqd.
• Delay surgery until corrected
• Correct alkalosis, associated with post-operative apnea
• Inappropriate rehydration with low-sodium-containing fluid can lead to cerebeal odema
• 0.45% saline (1/2 normal) with 5% dextrose
 Add potassium once baby passing urine
• If baby weight known prior to onset symptoms, 100mL/kg per 24hrs for maintenance.
 Post-op
• 50% vomiting, oedema of pylorus at incision site
• Feed 12-24hrs
• Maintain oral feedings within 36-48hrs
• If persistent vomiting
 Consider incomplete pylomytomty (endoscopic balloon dilatation), gastritis, GORD, obstruction
• Possible complications
 duodenal perforation
 GORD
 wound infection
VOMITING AFTER THE NEWBORN PERIOD
 distinguish from regurgitation (passive ejection of gastric contents secondary to reflux)
Infectious
 GI causes: gastroenteritis, peritonitis, appendicitis, hepatitis, ulcers, pancreatitis
 non-GI causes: UTI, otitis media, CNS infection, raised ICP, almost any infection, drugs, foreign body
Anatomic
 GI tract obstruction
 • intussusception
• foreign body e.g. bezoar
 gastroesophageal reflux
• usually temporary relaxation of lower esophageal sphincter —> decreased gastric emptying
• presents with recurrent vomiting after feeds and FTT
• most outgrow reflux by 18 months of age
• conservative management: thickened feeds, elevate bed to 30 degrees
• esophagograms may miss, pH studies are preferred
• treat only if symptomatic or poor weight gain
• medication e.g. cisapride, H2 blockers
• if unresponsive to medication: surgery - Nissen fundoplication
• complications: aspiration, esophageal bleeding, stricture formation, apnea
Central Nervous System
 increased ICP
• hydrocephalus
• neoplasm
 drugs/intoxicants
 migraine
 meningitis, encephalitis
Other
 metabolic/endocrine e.g. DKA, inborn errors, liver failure
 poisons/drugs: e.g. lead, digoxin, erythromycin, theophylline
 psychogenic: e.g. rumination syndrome, bulimia, anorexia, cyclic vomiting
 food allergy
 regurgitation, overfeeding

Neurological basis of abdo pain

 Pain receptors in the abdomen include visceral receptors (located on serosal surfaces, within the mesentery,
and within the walls of hollow viscera) and mucosal receptors
 Visceral receptors respond to mechanical and chemical stimuli whereas mucosal receptors respond primarily
to chemical stimuli.
 Visceral pain is usually poorly localized
o Most visceral digestive tract pain is perceived in the midline because of bilaterally symmetric
innervation. In some conditions, such as appendicitis, precise localization of the pain may develop
once the overlying parietal peritoneum (which is somatically innervated) becomes inflamed.
 Pain originating in the viscera may sometimes be perceived as originating from a site distant from the
affected organ → Referred pain usually is located in the cutaneous dermatomes sharing the same spinal cord
level as the visceral inputs.

LIFE-THREATENING CAUSES OF ABDO PAIN

Trauma 
 Motor vehicle collisions, motor vehicle pedestrian collisions, falls, and child abuse
 must be carefully evaluated for intra-abdominal injuries
 Such as solid organ laceration or perforated viscus
 Mortality
o <20% isolated liver, spleen, kidney, or pancreatic trauma
 o 20% if GIT tract involved
o 50% if major vessels are injured
 Children are more vulnerable to abdominal injury caused by blunt forces than are adults
o compact torsos with smaller anterior-posterior diameters
o relatively larger viscera, less overlying fat, and weaker abdominal musculature
 Important to understand mechanism of injury in evaluation
 address life-threatening injuries that compromise airway, breathing, and circulation first
o Assessment for abdominal injury should take place as part of the secondary survey
 Children with abdominal trauma and hemodynamic instability unresponsive to crystalloid infusion and blood
transfusion should undergo immediate emergent laparotomy
 Abdomen signs
o ecchymoses (particularly of the umbilical or flank regions); abrasions; tire-tracks; seat-belt marks;
abdominal distension, tenderness, rigidity, or masses; pain in the left shoulder induced by palpation of
the left upper quadrant (Kehr's sign); or prolonged ileus (greater than four hours)
 Repeated, serial examinations are necessary in children with abdominal trauma because life-threatening
abdominal injury may not be apparent upon the initial examination
 Diagnostic evaluation
o FBC, blood type and crossmatch
o For baseline
 prothrombin time (PT), partial thromboplastin time (PTT), serum electrolytes, glucose, amylase,
lipase, transaminases (alanine aminotransferase [ALT], aspartate aminotransferase [AST]).
o CT with IV contrast of abdomen awaiting lab results
o Urinalysis
 screening test for genitourinary trauma and to assess the need for imaging
o FAST U/S
o Diagnostic peritoneal lavage is rarely indicated in children
 Pancreatitis → peritonitis or a pseudocyst if a large duct is transected
 Liver
o >90% non-operative
 Spleen
o CT-contrast if best diagnosis
o Manage by clinical course and presence or absence of an arterial blush
o >90% non-operative
o Consider repair or partial splenectomy to save the spleen
o Manage post-splenctomy accordingly
Appendicitis 
 most common inflammatory bowel disorder and reason for surgery from 5 years on, peaks at 15-30
 Obstruction of the appendix by fecalith (25%) is a common predisposing factor. Parasites may rarely cause
obstruction (especially ascarids) and most of the remaining cases are idiopathic
 degree of inflammation and different anatomic variants of appendix determine treatment and clinical features
o retroperitoneal has back pain and peritonitis may not occur
o Pelvic → may be only vague suprapubic tenderness.
 Clinical Features:
o 3 most predictive clinical features of appendicitis are:
 pain in the right iliac fossa with guarding
 abdominal wall rigidity
 migration of periumbilical pain to the right lower quadrant.
 at least one of these manifestations is frequently absent, particularly in younger children
o Other features:
 low grade fever
 anorexia
 nausea, vomiting (after onset of pain and is often bilious)
 peritoneal signs
 diarrhoea (not common)
 generalized peritonitis
 Consider the diagnosis of appendicitis in all cases of previously healthy children who have a history of abdominal
pain and vomiting, with or without fever or focal abdominal tenderness.
 Lab: ↑WBC count (<15,000) and ↑CRP
o 92% PPV
 Diagnosis: clinical, ultrasound (noncompressible, thickened appendix in 93% of cases)
o Enlarged mesenteric lymph nodes are a nondiagnostic finding
o DO not perform rectal exam in children
o Difficult <4yrs old
 Treatment → surgical laparoscopic preferred or laparotomy if perforated or gangrenous → antibiotics
o The mortality rate is less than 1% during childhood
 Complications → perforation, abcess, sepsis, peritonitis
o The incidence of perforation is high in childhood (40%), especially <2yrs age
 DDX
o Pneumonia, pleural effusion, urinary tract infection, right-sided kidney stone, cholecystitis, perihepatitis,
and pelvic inflammatory disease may all mimic appendicitis
o Mesenteric adenitis (diagnosis of exclusion, caused by viral)

Intussusception 
 invagination of a part of the intestine into itself, causing obstruction
 typically 2months to 2 years of age
o most frequent cause of intestinal obstruction in the first 2 years of life
o M:F 3:1
 90% idiopathic, children with CF and celiac disease at significantly at risk due to bulk
of stool in the terminal ileum
o Possible causes may be swollen Peyer's patches, Meckel's diverticulum,
polyp, malignancy in older child
o Rotavirus vaccines were implicated as a potential risk factor for
intussusception, not proven
 telescoping of segment of bowel into distal segment —> ischemia and necrosis
o usual site: ileocecal junction
 Clinical
o characteristic pain that develops suddenly, is intermittent, severe periumbilical pain
o classically accompanied by inconsolable crying with drawing up of the legs toward the abdomen
o Bilious emesis and diarrhoea may develop as the obstruction progresses.-90%
o Between the painful episodes, the child may behave normally
o rectal bleeding (“red currant jelly” stools)
o sausage-shaped mass → central, beneath the rectus abdominis on the right side, difficult to feel often
o shock and dehydration
o “classic triad” of abdominal pain, palpable sausage-shaped mass and red currant jelly stools only in 10-
15% of patients
o May be febrile
o abdomen is tender and often distended
o Lethargy or altered consciousness can be the primary symptom of intussusception, especially in infants.
o Presentations may be variable, however, with some children having no apparent pain or blood in the
stool
o can persist for several days if obstruction is not complete, and patients may present with intermittent
attacks of enterocolitis
o In older children, sudden attacks of abdominal pain may be related to chronic recurrent intussusception
with spontaneous reduction.
 Initial symptoms can be confused with gastroenteritis
 Lab: Most children have gross or occult blood in the stool.
o Contrast air enema —> see reverse "E" sign
o Contraindications:
 peritonitis, significant dehydration or established bowel obstruction
o U/S to confirm
 An infant with suspected intussusception requires urgent surgical assessment and radiological investigations
for diagnosis and treatment.
 Treatment:
o reduction under hydrostatic pressure, contrast barium and air enema
o surgery rarely needed, but team should be available at a tertiary centre
 Mortality rate with treatment is 1–2%.

Malrotation and volvulus

 Green bile-stained vomiting → no obvious septic cause → urgent surgical consultation for intestinal
Malrotation and lethal complications of midgut volvulus
 Abdominal distension is not usually seen in the early stages of presentation
 Neonates may have emesis (bilious or nonbilious) with apparent abdominal discomfort as the result of midgut
volvulus
 50% are <1 month age
o Chronic patterns of episodic vomiting and abdominal pain in
older children
o 80% experience symptoms in first 2 months of life
o 10% of neonatal obstructions
 Pathophys
o intestinal nonrotation or incomplete rotation around the
superior mesenteric artery (SMA)
o The midgut extends from the duodenojejunal junction to the
mid transverse colon. It is supplied by the SMA, which runs in the root of the mesentery. During
gestation, the midgut elongates into the umbilical sac, returning to an intra-abdominal position during
the 10th week of gestation. The root of the mesentery rotates in a counterclockwise direction during
retraction causing the colon to cross the abdominal cavity ventrally. The cecum moves from the left to
the right lower quadrant, and the duodenum crosses dorsally becoming partly retroperitoneal. When
rotation is incomplete, the dorsal fixation of the mesentery is defective and shortened, so that the bowel
from the ligament of Treitz to the mid transverse colon may rotate around its narrow mesenteric root
and occlude the SMA (volvulus).
o It involves anomalies of intestinal fixation as well
 Occur during fetal development by disruption of normal embryological development and
rotation
 Most commonly in midgut volvulus → can result in short bowel syndrome or death
 3 presentations: recurrent vomiting (bilious intermittently); FTT with vomiting; sudden onset abdominal pain and
then shock
 if vomiting with bilious material, malrotation with volvulus until proven otherwise
 clinical features
o distended abdomen
o vomiting due to volvulus and bands across duodenum
o cecum free
 Physical exam depend on type of rotational defect
o Acute midgut volvulus
 Abdominal distention is frequently present, and the infant appears in acute pain + GUARDING
 intraluminal bleeding may occur, which leads to blood per rectum and sometimes hematemesis.
 May develop signs of shock, including poor perfusion, decreased urine output, and hypotension.
 Signs of peritonitis, including abdominal tenderness and discoloration of the skin.
o Chronic midgut volvulus
 May be normal if not obstructed at the tome, and signs of acute if twisted partially at the time
 signs include intermittent intestinal obstruction, malabsorption, protein-losing enteropathy, or
diarrhea
 chronic GI symptoms of nausea, vomiting, diarrhea, abdominal pain, dyspepsia, bloating, and
early satiety
o Acute duodenal obstruction
 Abdominal distention and gastric waves may be present.
 Passage of meconium or stool can be present.
  Usually do not have signs of peritonitis or shock unless volvulus is also present
o Chronic duodenal obstruction
 may be completely normal at the time of presentation.
 Diagnosis is usually made by history and enough suspicion to obtain radiologic studies; physical
examination findings are very unreliable.
o Internal herniation
 diagnosis is made by radiologic studies and index of suspicion only.
 Patients with left mesentericoparietal hernias may have findings related to venous obstruction,
such as hematochezia, hemorrhoids, and dilated anterior abdominal veins.
 If the bowel of the patient is obstructed at the time of presentation, abdominal tenderness and
guarding may be present, and a soft globular mass may be palpated at the location of the hernia.
 diagnosed by Barium upper Gl studies: duodenum not fixed, spiral jejenum, mobile cecum (may not be in RLQ)
o malrotation can be further confirmed by barium enema, which may demonstrate a mobile cecum
located in the midline, right upper quadrant, or left abdomen
o Plain films of the abdomen in the newborn period may show a "double-bubble" sign, resulting in a
misdiagnosis of duodenal atresia
o "whirlpool sign" denoting midgut volvulus or reversal of the normal position of the SMA on CT or US
 treatment: surgical Ladd procedure
o duodenum is mobilized, the short mesenteric root is extended, and the bowel is then fixed in a more
normal distribution
o surgical repair is usually recommended, even in asymptomatic children
o usually laparotomy
o Midgut volvulus is one of the most common indications for small bowel transplant in children

Incarcerated inguinal hernia 

 usually irritable and crying
 Vomiting and abdominal distention may develop
o Depending on if intestinal obstruction has occurred
 On physical examination, a firm, discrete inguinal mass, which may extend to the scrotum or labia majora

Adhesions with intestinal obstruction 

 abdominal pain and/or vomiting who have had previous abdominal surgery → small bowel obstruction (SBO) →
result of adhesions
 Shock (from hypovolemia and/or sepsis) can develop as the result of ischemic bowel injury
 1-2% children with abdo surgery → adhesions within 5 yrs
o Factors: multiple procedures, peritonitis, and surgery on the ileum.

Necrotizing enterocolitis (NEC)
 Newborn syndrome of intestinal necrosis → more in premature
 vomiting, abdominal distention, and tenderness
 Systemic signs include apnea, respiratory failure, lethargy, poor feeding, temperature instability, or hypotension
resulting from septic shock in the most severe

Peptic ulcer disease 

 If complicated by severe hemorrhage or perforation is an uncommon cause of life-threatening abdominal pain
among children.
 Vomiting, hemorrhage, and perforation are more commonly seen in young children
 PUD related to Helicobacter pylori is relatively uncommon in children
o often due to medications (corticosteroids or NSAIDs) or major stresses in 6-10 yr olds, most idiopathic
Ectopic pregnancy 
 must be considered in the diagnosis of abdominal pain for postmenarchal girls
 Abdominal pain, amenorrhea, and vaginal bleeding are the classic symptoms
 typically appear six to eight weeks after a missed menstrual period
 Risk factors include previous genital infection and previous ectopic pregnancy.

Uncommon life-threatening causes 

 Diabetic ketoacidosis (DKA)
o Usually presents with polyuria, polydipsia, and glycosuria, but may also present with abdominal pain and
vomiting, especially in young children.
 Hirschsprung associated enterocolitis (HAEC)
o uncommon, fulminant complication of Hirschsprung disease
o explosive diarrhea, fever, and abdominal pain
 Hemolytic uremic syndrome (HUS)
o after an infection with Shiga toxin-producing enterohemorrhagic E. coli (EHEC) or Shigella
o associated with pneumococcal infection, HIV, and genetic factors
o bloody diarrhea, hemolytic anemia, thrombocytopenia, and acute renal injury due to ↑BUN
 Primary bacterial peritonitis
o usually caused by Streptococcus pneumoniae or E. coli
o life-threatening infectious complication of nephrotic syndrome and occasionally other conditions that
cause ascites (eg, cirrhosis of the liver).
 Myocarditis
o passive hepatic congestion from heart failure → abdominal pain
o Pericarditis may cause referred abdominal pain.

COMMON CAUSES
Constipation 
 can present with rectal impaction and, at times, severe lower, colicky abdominal pain
 Usually most common cause of acute abdominal pain (~50%)
o About 2% of healthy primary school children have chronic retentive constipation.
 Most constipation in childhood is a result of voluntary or involuntary retentive behavior (chronic retentive
constipation).
 painful defecation; skeletal muscle weakness; psychological issues, especially those relating to
control and authority; modesty and distaste for school bathrooms; medications
 Drugs, abuse, under-nutrition, lack of bulk,
o organic causes is much rarer
 structural defects in GI tract, smooth muscle disease (sclerodema, SLE), abnormalities of
myenteric ganglion cells (Hirschsprung disease), Hypo- and hyperganglionosis, spinal cord
defects, metabolic and endocrine( hypothyroidism, diabetes insipidus, hypercalcemia),
cerebreal palsy of muscular dystrophy
 The ratio of males to females may be as high as 4:1.
 likely if:
o <3 stools weekly
o fecal incontinence (usually related to encopresis)
o large stools palpable in the rectum or through the abdominal wall
o retentive posturing
o passage of stool so large that it obstructs the toilet
o painful defecation
 Clinical
o <3 months: grunt, strain, and turn red in the face while passing normal stools
o develop the ability to ignore the sensation of rectal fullness and retain stool
 Treatment:
o ↑ high-residue foods and ↑fluid intake
o Medications: Barley malt extract, polyethylene glycol solution
 Stool softeners, laxatives (senna fruit), Dis-impaction if encopresis is present
o Psychiatric consultation
Acute infectious gastroenteritis
 Most common cause is rotavirus infection, season peak in autumn and winter in Australia
o Up-to 2/3 of cases requiring hospital admission
 Reducing due to Rotavirus vaccine
o Children <5 years of age with rotavirus-positive gastroenteritis are unlikely to have another pathogen
isolated from their faeces.
 o adenovirus infection causes between 7–17% of cases
o Bacterial gastroenteritis (5-15%)
 Salmonella spp., Campylobacter jejuni, Yersinia enterocolitica and Escherichia coli
 Most bacterial causes of diarrhoea are self-limiting and do not usually require antibiotic therapy,
even if blood or mucus is present.
o Parasites, such as Cryptosporidium, are also a known cause of acute gastroenteritis
 unusual to find a protozoal parasite in the setting of acute diarrhoea
o Repeat stool investigations are not helpful except in patients with chronic diarrhoea, suspected
Salmonella carriage or parasitic infection.
o The cause of infectious diarrhoea can often be identified by simple laboratory studies but rarely alters
management.
o Nosocomial infection is common.
 Pathophysiology
o changes in the small bowel are typically noninflammatory while the ones in the large bowel are
inflammatory
o Transmission may occur due to improperly prepared foods, contaminated water or close contact with
those who are infectious.
 Exclude other causes → adequate assessment + treatment of dehydration
 Differential diagnoses of vomiting and diarrhoea
o Appendicitis.
o Urinary tract infection.
o Other sepsis (including meningitis).
o Other surgical conditions including intussusception, enterocolitis associated with Hirschsprung disease
and malrotation of the bowel.
o Haemolytic uraemic syndrome.
 Clinical
o Usually fever, severe cramping abdominal pain, and diffuse abdominal tenderness before diarrhea
begins
o poor feeding, vomiting and fever, followed by diarrhoea
o Stools are frequent and watery in consistency
o Onset of diarrhea generally helps rule out other causes (eg. Appendicitis)
o Yersinia enterocolitica gastroenteritis can cause focal right lower quadrant pain and peritoneal signs that
are clinically indistinguishable from appendicitis
o Bacterial gastroenteritis is suggested by a history of frequent small-volume stools with passage of blood
and mucus, and abdominal pain
o is essential that all children with acute onset of vomiting, diarrhoea and fever are re-evaluated regularly
so as to confirm the diagnosis of acute gastroenteritis and adequacy of rehydration therapy
 Management
o Hydration
 rapid enteral rehydration over 4–6 h
 except children with significant neurological or biochemical disturbance (hyper- and
hyponatraemic)
 Most rehydrated using oral rehydration solutions (ORS)-Hydralyte at home, Gastrolyte in
hospital
 NG administration if oral not tolerated →Vomiting is not a contraindication to NG tube
 use the principle of glucose-facilitated sodium transport in the small intestine
 Parent education is vital, especially in the outpatient management of children
 Drink fluid more often, in small volumes frequently→ if too much, child will vomit
 Home-made solutions and ORS should be carefully prepared according to instructions
 PULL IV fluids back when starting oral
o Nutritional management
 Early re-feeding (after rehydration) has been shown to enhance mucosal recovery in children/
infants with acute gastroenteritis and reduces the duration of diarrhoea
 Breast-feeding should continue through rehydration and maintenance phases of treatment
 Formula-fed infants and children should re-start oral age appropriate formula or food intake
after completion of rehydration
  Children can have complex carbohydrates (e.g. rice, wheat, bread and cereals), yoghurt, fruit and
vegetables once rehydration is complete
 Transient lactase deficiency may occur but is not common in infants <6months
 Lactose-free diets are infrequently required after, consider if persistent diarrhoea after
re-introduction of feeds
o Admission to hospital
 moderate or severe dehydration
 young age (<6 months) with a high frequency of diarrhoea (8 per 24 h) and vomiting (>4 /24 h)
 High-risk infants/children (e.g. ileostomy, short gut, cyanotic heart disease, chronic renal
disease, metabolic disorders and malnutrition).
 Infants/children whose parents and carers are thought to be unable to manage at home
 If the diagnosis is in doubt.
o Biochemical investigations
 Glucose, electrolyte and acid–base studies are required in children with:
 A history of prolonged diarrhoea with severe dehydration.
 Altered conscious state.
 Convulsions.
 Short-bowel syndrome, ileostomy, chronic cardiac, renal and metabolic disorders.
 Infants <6 months of age who are judged as being dehydrated.
o Pharmacotherapy
 Infants and children should not be treated with antidiarrhoeal agents
 Most bacterial infections do not require antibiotics
 Salmonella or Campylobacter gastroenteritis may require antibiotic treatment
 Shigella dysentery requires antibiotic treatment.
 Antibiotics should be considered for the immunocompromised and neonates.
 Complications
o Hypernatraemic dehydration (sodium >150 mmol/L)
 Results from severe water and sodium depletion with greater loss of water. This can lead to
severe neurological sequelae if rehydration is not carried out appropriately.
 Oral rehydration therapy is preferred to i.v. rehydration. If the patient is in shock, give a bolus of
normal saline 20 mL/kg i.v., repeat until organ perfusion is restored.
 Following this, ‘slow ORT’ aiming to complete rehydration over 12 h is required, followed by
maintenance fluids
 Serum electrolytes should be monitored on a 4 hourly basis. As a guideline, serum sodium
should not fall by >0.5 mmol/L per hour.
 Consult with ICU
o Hyponatraemic dehydration (serum sodium <130 mmol/L)
 Can cause seizures and coma, and requires consultation with an ICU
 Be aware of iatrogenic hyponatraemia due to fluid (hypotonic) overload.
o Others: Repeat infections in areas of poor sanitation → malnutrition, stunted growth and development
 Reactive arthritis in 1%, Guillian Barre syndrome (HUS) occurs in 0.1% (associated with Shiga
producing toxins from E.Coli or Shigella)
o Temporary lactose intolerance from ↓brush border enzymes
 TEMPORARY, lactose-free diet for 3-4 weeks
 overdiagnosed

Specific Causes:
Rotavirus
 Incubation period: illness usually begins 12 h–4 days after exposure.
 Infectious period: most children shed the virus in the stools for up to 10 days; however, about 1/3 with severe
primary rotavirus infection continue shedding for >21 days.
 Clinical features
 o Major cause of severe diarrhoea in children causing over 50% of hospitalisations for acute gastroenteritis
in children <5 years. Also a common cause of nosocomial infection.
o Annual peak period of infection occurs in the winter–spring period. Presents with diarrhoea, vomiting
(may precede diarrhoea) and fever lasting for up to 1 week. Respiratory symptoms are common. May be
complicated by dehydration, electrolyte imbalance and acidosis.
 Diagnosis: enzyme immunoassay and latex agglutination assay.
 Treatment: supportive, with particular attention to hydration.
 Vaccine

Adenovirus
 Similar presentation to rotavirus, but there is no seasonality.
 It is more common under 12 months of age.
 Diarrhoea and vomiting may last longer and high fever is less common.

Salmonella (non typhi)

 Clinical features
o Broad spectrum of clinical syndromes including asymptomatic carriage, gastroenteritis, bacteraemia
and focal infections (e.g. bone and joint).
o Age-specific attack rates are highest in children <5 years of age (peak at <1 year of age) and the
elderly.
o Invasive infections and mortality are more common in infants, the elderly and those with underlying
diseases.
 Diagnosis
o Does not usually alter management, but serology and PCR are available.
 Treatment
o Antibiotic treatment is not usually indicated for uncomplicated gastroenteritis as it may prolong
excretion.
o Antibiotic treatment is indicated for bacteraemia, systemic involvement or infection in infants <3
months of age, those with underlying disease (e.g. immunocompromised) and elderly people.
 Cefotaxime
Campylobacter jejuni
 More common >5 years of age.
 Causes diarrhoea with visible or occult blood, abdominal pain, malaise and fever.
 Antibiotic treatment is not usually necessary, except in special circumstances where the elimination of the
carrier state is important, such as infection in food handlers.
Giardia intestinalis (lamblia)
 Transmission
o The most common parasite identified in stool specimens from children.
o More common in children (and staff) in childcare centres and returned travellers.
o The major reservoir and means of spread is contaminated water and, to a lesser extent, food.
o Person-to-person spread also occurs.
 Clinical features
o most common are: diarrhoea (usually persistent), abdominal distension, flatulence, abdominal
cramps and weight loss/ failure to thrive.
 Diagnosis
o Confirmed by microscopy of stool specimens. These do not usually contain blood, mucus or
leucocytes. Repeat specimens may be necessary.
 Treatment
o Metronidazole 3 days or tinidazole one dose

Escherichia coli
 There are at least 5 categories of diarrhoea-producing E. coli:
• Enterohaemorrhagic E. coli (EHEC): haemolytic uraemic syndrome (HUS), haemorrhagic colitis.
• Enteropathogenic E. coli (EPEC): watery diarrhoea in children <2 years of age in developing
countries.
• Enterotoxigenic E. coli (ETEC): the major cause of traveller’s diarrhoea (usually self-limiting).
 • Enteroinvasive E. coli (EIEC): usually watery diarrhoea, but may cause dysentery.
• Enteroaggregative E. coli (EAEC): chronic diarrhoea in infants and young children.
 Antibiotic treatment is not usually indicated for diarrhoea caused by E. coli and may be associated with
increased rates of HUS in EHEC infection.
Clostridium difficile
• Transmission
 Acquired from the environment or by faecal–oral transmission from a colonised host.
 Up to 50% of healthy neonates and infants <2 years of age are colonised, in contrast to 5% of those >2
years of age.
• Clinical features
 Rare cause of diarrhoea in those <12 months of age.
 Only clinically significant diarrhoea or colitis should be considered to be caused by Clostridium difficile.
 Pseudomembranous colitis usually occurs in patients on antibiotics (particularly penicillins, clindamycin
and cephalosporins).
o Metrandizole treatment

Gastro-oesophageal reflux (GORD)

 Oesophageal reflux of gastric contents occurs normally and is more frequent after meals
o pathological if associated with frequent regurgitation, or if it results in clinically significant adverse
sequelae
 normally greater in infants than in older children
 Reflux of gastric acid with heartburn may result in episodic irritability, but this is usually associated with
obvious regurgitation and is rarely ‘silent’
 may cause infant distress
 Both infant distress and frequent regurgitation are common in the first 6 months of life
 consider other possible causes
 Investigations such as 24 h oesophageal pH monitoring can be useful to correlate any episodes of reflux with
irritability
 Complications
o Peptic oesophagitis
o Peptic strictures → dysphagia and failure to thrive.
o Failure to thrive
o Pulmonary complications → recurrent or persistent cough and wheeze
 Management
o Regurgitation of gastric contents is common in infancy. In most cases this ‘possetting’ does not result
in any adverse sequelae and the most appropriate therapy is parental reassurance.
 ‘Physiological’ gastro-oesophageal refl ux with regurgitation usually resolves by the age of
9–15 months.
o In the absence of signs of significant oesophagitis, aspiration or growth failure, the following should
be suggested:
 Avoid excessive handling.
 Posture after feeds: placed in a cot in the head-up position at or near 30°.
 Thicken feeds: use a proprietary thickening agent or a prethickened formula if formula-fed.
o Medications are not indicated in otherwise healthy, thriving infants with frequent regurgitation.
 Mylanta, ranitidine, PPI
o Surgery - Fundoplication

Colic 
 Condition of a healthy baby in which it shows periods of intense, unexplained fussing/crying lasting more than 3
hours a day, more than 3 days a week for more than 3 weeks
 Possible causes:
 o Stomach gas (due to poor burping or milk flow issues), intestinal gas (pocketed in the intestinal tract),
neurological overload (the overwhelmed and overstimulated baby that becomes exhausted) and
muscular type of colic (perhaps due to muscle spasm and birth trauma).
 may appear to have abdominal pain
 Other clinical features that suggest the diagnosis of colic include:
o A typical pattern of paroxysmal crying
o Crying usually in the evening
o Crying relieved with the passage of flatus or stool
o Normal feeding
o No associated symptoms
o Normal physical examination

Urinary tract infections 

 Abdominal pain and fever are the most common presenting symptoms with 2-5 year olds
 dysuria, frequency, and/or flank discomfort more likely >5years
Streptococcal pharyngitis 
 group A beta hemolytic streptococcal (GABHS) pharyngitis, but also other causes
 abdominal pain in addition to fever and exudative pharyngitis
Pneumonia 
 particularly in the lower lobes
Viral illnesses 
 other than gastroenteritis (such as viral pharyngitis and URTI) are also associated with abdominal pain
Pelvic inflammatory disease 
 acute infection of the upper female genital tract in sexually active girls
Mesenteric lymphadenitis
 inflammatory condition of the mesenteric lymph nodes that can present with acute or chronic abdominal
pain
o usually in the right lower quadrant, mesenteric lymphadenitis sometimes mimics appendicitis
 diagnosed by an ultrasound that shows abdominal lymph nodes greater than 10 mm, does not exclude
appendicitis
 Etiologies of mesenteric lymphadenitis include viral and bacterial gastroenteritis (eg, Yersinia enterocolitica),
Group A Streptococcal pharyngitis, inflammatory bowel disease, and lymphoma; viral infection is most
common.
Ruptured ovarian cyst 
 Acute severe pain simulating appendicitis or peritonitis may result from rupture of an ovarian cyst. Usually,
the patient is stable. Rarely, life-threatening hemorrhage develops
 Mittelshemterz also considered (mid-cycle pain)
Foreign body ingestion 
 usually eliminated without difficulty once they have passed through the pylorus
 particularly objects that are sharp (which may perforate the bowel) or >5 cm in length (which may cause
obstruction), multiple magnets (which may lead to entrapment of a piece of bowel wall between two
magnets that are attracted to each other), or button batteries (which may release caustic material) warrant
emergent evaluation for obstruction or perforation.

OTHER CAUSES
Gastrointestinal
 Inflammatory bowel disease (more often Crohn disease than ulcerative colitis)
 Acute cholecystitis typically causes pain in the right upper quadrant or epigastrium.
 Intraabdominal abscess
o typically febrile and may have histories of prior intraabdominal disease or abdominal surgery.
 Dietary protein allergy
 Malabsorption (such as occurs with celiac disease and carbohydrate malabsorption)
 Pancreatitis generally
o Causes acute upper abdominal pain (usually in the mid-epigastrium or right upper quadrant) at the
onset, which may radiate to the back. Vomiting (that may be bilious) and fever also occur commonly.
 o Causes of pancreatitis among children include trauma, infection, structural anomalies, and some
medications (such as tetracycline, L-asparaginase, valproic acid, and steroids)
 Meckel's diverticulum usually presents with painless rectal bleeding.
 Abdominal migraine (included in childhood periodic syndromes)
 Wandering spleen refers to acquired laxity or congenital underdevelopment or absence of the primary
ligamentous attachments of the spleen in the left upper quadrant

Non-gastrointestinal
 Henoch-Schönlein purpura (HSP)
o systemic vasculitis affecting small vessels in skin, gut, and glomeruli
 Hepatitis
o typically causes jaundice, mild abdominal pain, and fever, but young children in particular may be
afebrile and/or anicteric. Vaccines
 Sickle cell syndromes
 Malignant solid tumors
o Wilms' tumor and neuroblastoma occur more commonly in infants, whereas leukemic or
lymphomatous involvement of the liver, spleen, or retroperitoneal lymph nodes occurs more often
in older children.
 Urolithiasis
o Nonspecific abdominal pain
 Testicular torsion
o Scrotal pain that may radiate to the abdomen. Patients may have associated nausea, vomiting, and
fever. The affected testis usually is tender, swollen, and slightly elevated because of shortening of
the cord from twisting.
 Ovarian torsion
 Toxins
o Associated with abdominal pain include lead and iron.
 Acute porphyrias
 Familial Mediterranean fever

Recurrent abdominal pain

 10% of school-age children
o definition: three or more episodes of pain severe enough to affect activities, occurring over a period
of 3 months
 usually no specific identifiable cause
o may be a result of dysmotility of the bowel
o Can me from emotional problem
o Organic (<10%) → chronic infection, constipation, IBS, anatomic anomalies, peptic ulcers,
 Also consider genitourinary disease, gynaecological, cardiovascular, neoplastic causes

Hirschsprung's Disease (congenital aganglionic megacolon)

 resulting from an absence of ganglion cells in the colon → loss of rectosphincteric reflex → mechanical
obstruction causes by reduced motility in colon
 rectosigmoid in 75% of cases →→→ DIAGNOSED AT BIRTH MOSTLY
 associated with Down syndrome, genetic factors (autosomal dominant)
 clinical features
o no meconium within first 24 hours
o palpable stool on abdominal exam with empty rectum on DRE
o intermittent diarrhea, BM only with rectal stimulation
o constipation, Abdominal distention, vomiting, FTT
 complications → enterocolitis (possibly fatal), toxic megacolon and perforation
 diagnosis → barium enema: proximal dilatation due to functional obstruction, rectal biopsy for definative
 treatment → surgery if not short segment → colostomy and re-anastomosis
How do we assess hydration status?
 Dehyrdration is caused by a negative fluid balance resulting from decreased intake, increased output (renal, GI,
or insensible losses from the skin or respiratory tract), or from systemic responses to specific disease states such
as burns or sepsis
 Most common sites for extracellular fluid loss :
o Gastrointestinal tract (eg, diarrhea, vomiting,
bleeding)
o Skin (eg, fever, burns)
o Urine (eg, glucosuria, diuretic therapy, diabetes
insipidus)
o prolonged inadequate intake without excessive
losses.
 Children are susceptible because:
o dependent on caretakers to provide oral fluids and therefore cannot regulate their intake
o increased fluid requirements and increased fluid losses in young children
o Rapidly growing infants have an extremely high basal metabolic rate and require a relatively high
number of calories relative to their body weight
 metabolism requires a correspondingly large amount of water
o The daily turnover of free water in infants is up to three to four times that in adults
o Water loss through urination accounts for approximately 50% of daily fluid requirements and is the
predominant cause of sensible losses; because infants have a decreased ability to concentrate urine
o larger percentage of young infants' total body water is contained in the extravascular space in
comparison with older children and adults → greater risk for cardiovascular compromise when
confronted with sudden fluid losses
o There is a higher frequency of gastroenteritis (diarrhea and vomiting) in children compared to adults.
o Children, especially young children, have a higher surface area-to-volume ratio with proportionally
higher insensible losses that are accentuated in disease states (eg, fever or burns).
o Volume depletion reduces the effective circulating volume (ECV), compromising tissue and organ
perfusion. If severe hypovolemia is not corrected in a timely fashion, ischemic end-organ damage occurs,
leading to serious morbidity and, in patients in shock, death.
 This problem is more common in the hot summer months and has been associated with severe dehydration,
brain damage, and death.
 Hypermetabolic states increase the need for free water
o Commonly FEVER (↑requirement by 12% per degree over normal)
 In relation to sodium
o Isonatremic dehydration (sodium level of 130 to 150 mEq/L)
 most common form of dehydration, eg. diarrheal
 occurs when the fluid sodium losses are proportionate in the ICF and ECF compartments
o hyponatremic dehydration (sodium level of <130 mEq/L)
 occurs when fluid that is lost contains proportionately more sodium than blood, which leads to
osmotic shifts of free water from the ICF to the ECF compartments
 tissue perfusion is more significantly impaired for a given degree of hyponatremic dehydration
than for a comparable degree of isotonic or hypertonic dehydration.
 does not occur directly, as losses such as diarrhea are not hypertonic to plasma. Rather, solute
and water are lost in proportion, and water is taken in and retained (because hypovolemia-
induced secretion of ADH limits water excretion), lowering the serum sodium concentration
o hypernatremic dehydration (sodium level of >150 mEq/L)
 occurs when the fluid lost contains less sodium than the blood, which causes ECF free water to
move into the ICF space.
 insensible fluid losses and losses in states of urinary concentrating defects (diabetes insipidus
 associated increase in serum osmolality from the hypernatremia pulls water out of the cells,
which initially minimizes the degree of extracellular fluid volume loss. This also minimizes some
of the physical findings that are associated with isotonic extracellular fluid loss.
 also apply to children with diabetes mellitus with significant hyperglycemia, which causes a
hyperosmolar state that pulls water out of the cells, thereby minimizing the degree of
extracellular hypovolemia.
Dehydration is not synonymous with hypovolemia
  Volume depletion refers to any condition in which the effective circulating volume is reduced. It can be
produced by salt and water loss (as with vomiting, diarrhea, diuretics, bleeding, or third space sequestration)
or by water loss alone (as with insensible water losses or diabetes insipidus).
 Dehydration refers to water loss alone. The clinical manifestation of dehydration is often hypernatremia. The
elevation in serum sodium concentration, and therefore serum osmolality, pulls water out of the cells into
the extracellular fluid.
 Both are used interchangeably
 Severe hypovolemia requires immediate aggressive isotonic fluid resuscitation to restore the ECV and
prevent ischemic tissue injury.

CLINICAL EVALUATION
 FOCUS ON:
o composition and volume of fluid intake
o frequency and amount of vomiting, diarrhoea, and urine output
o degree and duration of fever
o nature of any administered medications
o the existence of underlying medical conditions
 A recently recorded weight, if known, can be very helpful in calculating the magnitude of dehydration
 Clinical features:
o capillary refill time
o postural blood pressure
o heart rate changes
o dryness of the lips and mucous membranes
o lack of tears
o lack of external jugular venous filling when supine
o sunken fontanelle in an infant
o oliguria
o altered mental status or seizures
o listlessness, lethargy, and decreased tone
o scaphoid or distended abdomen
o Mottled skin
o decreased elastic recoil of the skin
 Children generally respond to a decrease in circulating volume with a compensatory increase in pulse rate and
may maintain their blood pressure in the face of severe dehydration
o A low or falling blood pressure is, therefore, a late sign of shock in children, and when present should
prompt emergent treatment
History
 environment in which symptoms developed
 symptoms of the illness
 prior treatment
 Quantify the child's intake and output
 Ask about intake—the amount, frequency, and types of fluids taken (including orally, via gastrostomy tube,
or parenterally)
o For breastfed infants, ask if the infant is feeding or merely sucking.
o For bottle-fed infants, ask how formula is prepared (e.g., premixed or powdered formula) and
whether other types of liquids have been substituted, such as water, tea, or juices, because
consumption of the latter fluids can lead to electrolyte abnormalities.
 amount of tear production, occurrence of drooling, and presence or absence of sweating
 Ask about level of activity and mental status, skin color (pallor, cyanosis, mottling), and temperature, and, in
infants, whether parents or other caretakers have noticed a sunken fontanelle
Give special consideration to hydration status in any child with an underlying disease for which fluid requirements
and losses are unique, such as diabetes, cystic fibrosis, thyroid disease, neurologic diseases, tumor, pituitary
dysfunction, diabetes insipidus, adrenal diseases affecting mineralocorticoid production, metabolic diseases, chronic
GI illnesses, heart disease, burns, and trauma.

 Lab features:
o high urine specific gravity (in the absence of an underlying renal concentrating defect as seen in diabetes
insipidus or chronic obstructive or reflux nephropathy)
o relatively greater elevation in blood urea nitrogen than in serum creatinine
o low urinary [Na+] excretion (< 20 mEq/L)
o elevated hematocrit or serum albumin level secondary to hemoconcentration

LABORATORY TESTING
 often reveals normal electrolytes and acid base balance in children with mild dehydration
o measurement of serum electrolytes is typically limited to children who require intravenous fluid
repletion
 Laboratory testing is less useful for assessing the degree of volume depletion
 Serum bicarbonate is the most useful test to assess degree of dehydration in children
 the serum sodium concentration in a child with hypovolemia varies with the relative loss of solute to water.
o Does lay an important role in deciding the type and speed of fluid repletion therapy
 Secretion of ADH
o ADH secretion promotes the retention of free water in the distal nephron and is stimulated by
hyperosmolality or moderate to severe hypovolemia
o In children with hypernatremia and associated hyperosmolality, ADH secretion and avid water
reabsorption by the kidney decreases urinary water loss and tends to prevent a further increase in
serum sodium.
 Serum potassium — Either hypokalemia or hyperkalemia can occur in hypovolemic patients
o Hypokalemia is more common, as children with gastroenteritis lose potassium in diarrheal stool
o the serum potassium concentration may be higher than expected or even elevated if a marked
acidosis is present
o The effects of hypovolemia upon potassium balance are reversed with correction of the acidosis
o children with borderline potassium reserves, this fall can result in hypokalemic symptoms, such as
muscle weakness, intestinal ileus, flattening of the T waves and the development of U waves on ECG,
and potentially lethal arrhythmias
 Serum bicarbonate
o low serum bicarbonate concentration (less than 17 meq/L) may be useful in assessing the degree of
hypovolemia
 almost always represents metabolic acidosis
 Gastroenteritis→acidosis is because of the loss of bicarbonate in the stool.
o Other causes of acidosis associated with diarrheal losses include:
 Increased acid production from shock (lactic acidosis) or from enhanced fat breakdown (eg,
starvation or fasting ketosis) or ↓ acid excretion by the kidney caused by ↓ renal perfusion
  Urine sodium
o In hypovolemia, the urine sodium concentration in a random void should be less than 25 meq/L and
may actually become non-detectable.
 Because kidney is trying to conserve sodium and water to restore the ECV.
o Does not exclude hypovomeia if negative because there may be high rate of water reabsorption
from the renal filtrate.
 Urine osmolality and specific gravity
o In hypovolemic states, the urine should be concentrated with an osmolality exceeding 450
mosmol/kg
 May be impaired by renal disease, an osmotic diuresis, the administration of diuretics, or
central or nephrogenic diabetes insipidus
o a high urine osmolality is consistent with hypovolemia, but a relatively isosmotic value does not
exclude hypovolemia.
o specific gravity also can assess urinary concentration
 less accurate than the osmolality
 dependent upon the size as well as the number of solute particles in the urine
 should be used only if the osmolality cannot be measured

Clinical Scoring Systems

 gold standard is pre-illness and post-illness weight
 WHO
o Mild dehydration (<5%),
o Some dehydration (5% to 10%)
o Severe dehydration (>10%

Emergency IV therapy for severe

 Indicated when evidence of compromised perfusion (inadequate capillary refill, tachycardia, poor color,
oliguria, or hypotension)
 Initially rapidly expand plasma volume and to prevent circulatory collapse → 20-mL/kg bolus of isotonic
fluid over 5 to 10 minutes repetitively until hemodynamics stabilize
o Give a minimum of 60 mL/kg or more in the first hour, unless contraindicated based on the patient's
disease
o Either colloid (5% albumin) or crystalloid (normal saline or Ringer lactate) may be used
o Colloid is particularly useful in hypernatremic patients in shock, in malnourished infants, and in
neonates
 o If no intravenous site is available, fluid may be administered intraosseously through the marrow
space of the tibia
 If adequate perfusion is not restored after 40 mL/kg of isotonic fluids, other pathologic processes must be
considered such as sepsis, occult hemorrhage, or cardiogenic shock
 Isotonic dehydration may be treated by providing half of the remaining fluid deficit over 8 hours and the
second half over the ensuing 16 hours in the form of 5% dextrose with 0.2–0.45% saline containing 20 mEq/L
of KCl.
o In the presence of metabolic acidosis, potassium acetate may be considered

Oral Rehydration
 with mild to moderate dehydration
 Clear liquid beverages found in the home, such as broth, soda, juice, and tea, are inappropriate for the
treatment of dehydration
 Frequent small aliquots (5–15 mL) should be given to provide approximately 50 mL/kg over 4 hours for mild
dehydration and up to 100 mL/kg over 6 hours for moderate dehydration
 Oral rehydration is contraindicated in children with altered levels of consciousness or respiratory distress
who cannot drink freely, acute surgical abdomen; in infants with greater than 10% volume depletion; in
children with hemodynamic instability; and in the setting of severe hyponatremia ([Na+] < 120 mEq/L) or
hypernatremia ([Na+] > 160 mEq/L)

MAINTENANCE FLUID AND ELECTROLYTE REQUIREMENTS

The primary formula for daily fluid requirements in children is as follows:
 For the first 10 kg: 100 mL/kg/d
 For the second 10 kg: 50 mL/kg/d
 For each kg >20 kg: 20 mL/kg/d
How can urine be collected in children, does the method of urine collection alter the interpretation of
results and if so, how are they altered?

 Children who are toilet trained can provide clean voided urine samples
 If not, options are:
o "clean voided" bag samples
o Invasive:
 suprapubic bladder aspiration (SPA)
 transurethral bladder catheterization (TUBC)
 only valid ways to collect urine for culture in febrile young infants under 2 months of age
and older infants and children with unexplained fever who are younger than 2 years of age
and ill enough to merit immediate antimicrobial therapy

CLEAN VOIDED BAG SAMPLES 

 Non-invasive
 should not be used to obtain urine samples for culture
 Requires proper cleansing, rinsing, and drying of the perineum before application of the bag, immediate
removal of the bag after urine is voided, and prompt processing of the urine.
 Cultures of urine specimens obtained by clean voided bag have an unacceptably high rate of false positive
results compared with catheterized specimens → adverse treatment outcomes
 acceptable for urinalysis in infants and children between two months and two years of age who have
unexplained fever and do not appear ill enough to require immediate antimicrobial therapy
 An infant or young child should never receive antibiotics on the basis of a urinalysis from a clean voided bag
urine specimen → invasive measure undertaken if:
o Positive leukocyte esterase or nitrite test
o Greater than 5 white blood cells per high-power field (spun urine)
o Presence of bacteria on Gram stained urine (unspun urine)
 negative urinalysis does not exclude a UTI→ continue monitoring

SUPRAPUBIC BLADDER ASPIRATION (SPA)

 safe and effective method for obtaining urine specimens in infants and young
children (usually not performed in children who are older than 2 years)
 The distended bladder, which extends above the level of the pubic symphysis into
the lower abdomen, is easy to access percutaneously
o more likely if the bladder can be visualized by portable ultrasonography, percussed, or palpated and the
child has not emptied the bladder in the 60 minutes before the procedure
o Percussion or palpation of the bladder may stimulate urination in some children.
 represents the gold standard in the diagnosis of UTI → high positive predictive value, and high negative
predictive value
 Steps:
1. child is restrained in the supine and frog leg position
2. site for needle insertion, in the midline, approximately one to two centimeters above the pubic
symphysis, is widely prepared with povidone-iodine solution
3. may be locally anesthetized with lidocaine → sometimes more painful
4. urethral opening should be occluded just before needle insertion because the procedure will stimulate
urination in many children
5. 1.5 inch, 22-gauge needle attached to a 3 or 5 mL syringe is inserted one to two centimeters above the
pubic symphysis. The needle should be angled 10 to 20 degrees cephalad and advanced under negative
pressure until urine returns
6. Urine is not likely to be obtained after the third attempt → transurethral bladder catheterization
 Complications
o microscopic hematuria is common
o gross hematuria and anterior abdominal wall abscess, are rare
 o Intestinal perforation can occur if a loop of bowel overlies the bladder, but the small puncture rarely
leads to peritonitis
TRANSURETHRAL BLADDER CATHETERIZATION (TUBC) 
 catheterization of the urethra is another safe and effective method for obtaining urine samples for culture in
most infants and children who are not toilet trained
 Specimen contamination may occur in up to 15 percent of children under two years of age and is more
common in uncircumcised boys, infants under six months of age, and children in whom the urethra is not
well visualized or who require several attempts to pass the catheter
 latex allergy must be determined
 steps
1. child is restrained in the supine and frog leg position (stabilizes pelvis)
2. anterior urethra is cleansed thoroughly with povidone-iodine solution
3. Sterile lubricant jelly is applied to the end of an appropriately sized catheter (5 French for children
younger than six months; 8 French for those between six months and adolescence, and 10 French
for adolescents).
4. Boys:
a. foreskin of the glans is retracted gently to permit complete visualization of the urethral
meatus if the boy is uncircumcised
b. repositioned after the procedure to prevent paraphimosis
c. catheter is inserted with the dominant hand until urine returns
d. Resistance may be encountered near the base of the penis due to contraction of the
external bladder sphincte
5. Girls:
a. An assistant often is needed to retract the labia majora
b. catheter is inserted into the urethral meatus until urine returns
c. first few drops of urine obtained should be discarded to prevent contamination of the urine
with urethral organisms or cells
 Complications
o include urethral trauma and microscopic hematuria and iatrogenic infection (extremely low risk)