Paediatric Gastro Flashcards
signs of dehydration in babies?
- sunken fontenelles
- dry mucus membranes
- reduced skin turgor
- prolonged CRT
- reduced urine output/wet nappies
- tachycardia and tachypnoea (non specific)
what is the typical abnormality seen on blood gas analysis in pyloric stenosis?
metabolic alkalosis
non bilious vomiting = only stomach acid juices are lost so
hypo cl- and hypo k+
and more HCO3-
history:
1 year old pulling up knees since this morning and screaming for the last 20 minutes (inconsolable)
looks white
vomiting green x3 with blood and BNO
decreased oral intake
what are you thinking for bilious vomiting and BNO?
what if it were a newborn?
lower bowel obstruction
likely intussusception
newborn: suggestive of congenital obstructive GI malformations, such as duodenal/jejunal atresias, malrotation with midgut volvulus, meconium ileus or plugs, and Hirschsprung disease.
what is pyloric stenosis and how does it classically present?
what clinical signs might you see?
what imaging might you do?
what kind of emergency is it?
Pyloric stenosis is the hypertrophy of the pyloric muscles at the outlet of the stomach.
NEWBORN
classic presentation: projectile, non-bilious vomiting immediately following feeds that presents in the first few weeks of life.
Infants are classically firstborn males with a positive family history of pyloric stenosis, and may have visible abdominal peristalsis or a palpable olive-shaped mass near the umbilicus.
Abdominal ultrasound is the modality of choice to assess for suspected pyloric stenosis.
It is considered a medical (and surgical) emergency due to the risk of severe electrolyte disturbances – classically, a hypochloremic hypokalemic metabolic alkalosis.
what is duodenal atresia?
how does it classically present?
what clinical signs are there?
what might you see on abdo x ray?
Duodenal atresia is the congenital absence of a portion of the first part of the small bowel.
Symptoms typically present shortly after birth. They may present with either bilious or non-bilious vomiting, depending whether the atresia is distal or proximal to the ampulla of Vater, the site where bile and pancreatic enzymes are released into the duodenum from the common bile duct.
It typically does not present with abdominal distension.
A classical x-ray finding associated with duodenal atresia is the ‘double bubble sign.’
what is malrotation?
what does it present as?
what type of emergency is it treated as?
intestinal malrotation - congenital anomaly in rotation of the midgut as it forms
presents as intermittent bilious vomiting, usually with significant abdominal distension. It may be associated with severe abdominal pain if associated with midgut volvulus causing bowel ischemia. Since the bowel obstruction is often intermittent, the timing of presentation can be variable.
Bilious or bile-stained vomiting should be treated as a potential surgical emergency.
Gastro-esophageal reflux (GER) is extremely common in infants, describe a classical presentation of it.
how is it different from GERD?
and typically presents in infants between 1-3 months of age.
characterized by frequent small volume regurgitation of a milky substance, irritability with feeds or when lying supine, or back arching with feeds. Many infants are asymptomatic.
Gastro-esophageal reflux is a normal physiologic process in infants and must be distinguished from gastro-esophageal reflux disease (GERD), which is associated with esophagitis, failure to thrive and recurrent aspiration.
what is intussusception and how does it normally present?
involves invagination of a portion of the small bowel into another portion of bowel (telescoping)
It is the most common cause of intestinal obstruction in children six to 36 months of age.
In addition to vomiting, the classic triad of features includes intermittent, progressive abdominal pain with screaming and drawing up of legs,
palpable sausage-like abdominal mass.
red currant jelly stools (late sign)
what are ‘red current jelly stools’ associated with?
intussusception
what 3 worrying features should you always ask about in a child presenting with vomiting, which will help to narrow down ddx?
bilious vs non bilious - is it green/yellow?
bloody/non bloody - red/brown
projectile/non projectile? - where does the sick go? hits the wall? - pyloric stenosis
First, it should be categorized as bilious or non-bilious. Bilious vomit has a greenish appearance due to the presence of bile and is indicative of obstruction distal to the ampulla of Vater, the opening of the common bile duct into the duodenum. Thus, determining whether vomit is bilious or non-bilious helps to localize GI problems within the GI tract.
Second, it should be categorized as bloody or non-bloody. Blood in the vomit indicates inflammation or damage to the GI mucosa and may indicate need for endoscopy to rule out acute upper GI bleed.
Third, the vomit should be identified as projectile or non-projectile, as projectile vomiting may point to a specific diagnosis – namely, pyloric stenosis. True expulsive vomiting should be distinguished!
run through the most common causes of vomiting based on the age of a child?
newborn
infancy
child
adolescent
The most common causes of vomiting in the neonatal period include gastroenteritis, malrotation, pyloric stenosis, TEF and necrotizing enterocolitis (esp if prem), duodenal atresia
In infancy, common causes are GERD, gastroenteritis, bowel obstruction, milk protein allergy and UTI.
In children, one must think of gastroenteritis, UTI, DKA, post-tussive vomiting and increased intracranial pressure.
In adolescents, consider gastroenteritis, appendicitis, DKA and increased intracranial pressure on the differential.
to help distinguish between infection causing vomiting or a non infective aetiology, one should ask about?
what infections might cause vomiting in children?
fevers
actual gastroenteritis
- pyelonephritis
- meningitis
what advice should be given to the parents of a baby with Gastro oesophageal reflux?
nurse upright where possible - positioning
encourage papoose slings
small but frequent feeds
add infant gaviscon to bottle fed babies
can get a powder that’s mixed with formula to thicken it or use a pre-thickened formula milk or change feeds
if these don’t work we can give you some drugs, such as antacids, H2 blocker or PPI
what types of children have an increased incidence of GORD?
cerebral palsy
chronic lung disease of prematurity
down syndrome
how do babies with GORD present?
The main sign of gastro-oesophageal reflux is frequent spitting up or regurgitation after feeds.
This is often accompanied by abdominal pain or general crankiness in the hours after feeding.
Over time, babies with reflux may not gain weight as expected (failure to thrive) and may have frequent chest infections due to aspirating (breathing in) stomach contents into the windpipe and lungs.
What is GORD caused by?
When is it common and when should it improve?
Gastro-oesophageal reflux is very common in the first few weeks and months of life, as the sphincter (ring of muscle) at the base of the oesophagus has not matured yet.
Many babies with reflux gradually improve as they grow, particularly when they start to eat more solid food and feed in an upright position in a high chair for instance (6-8 months).
If a child has severe gastro-oesophageal reflux which is not controlled with medication or is causing significant complications what can be done? and what tests would be done before this decision is made?
your doctor may recommend an operation called a fundoplication to prevent reflux.
Before reaching this decision, the severity of the child’s reflux will usually be assessed with:
pH impedance study (24 oesophageal probe)
upper GI contrast study
what medications can be used to treat reflux if conservative measures, such as thickening milk and repositioning fail?
infant gaviscon
ranitidine (H2 antagonist = less acid) - for screamers
domperidone (prokinetic = increased gastric emptying) - - for vomiters
how does gastroenteritis normally present in babies/children?
sudden change to more than 2 watery stools or 2 vomits a day +/- fever, abdominal pain
what most commonly causes gastroenteritis children/babies?
which cause can cause a life threatening illness?
MOST ARE VIRAL SO ABX DO NOT PLAY A PART IN THIS
viruses- rotavirus(less so now after vaccinations), adenovirus
less commonly bacterial - salmonella, campylobacter, e.coli 0157
ecoli 0157 have to worry about as it can cause HUS - haemolytic uraemic syndrome as it releases the shiga toxin
what tests should you do in suspected haemolytic uraemic syndrome and what will they show?
FBC and blood film
AND U+E
FBC will show low platelets and low haemoglobin
film will show fragmented red cells (schistocytes)
U+E will show acute renal failure
what is the pathophysiology in haemolytic uraemic syndrome?
ecoli 0157 releases shiga toxin
shiga toxin causes endothelial damage in microvasculature of renal circulation
activation of coagulation cascase and microvascular thrombosis in the renal syndrome
this causes
- platelet aggregation in kidney = consumption thrombocytopenia
- fibrin/platelet mesh causes partial occupation of the microcirculation = acute renal failure
- mesh shreds encirculating red cells giving fragmented red cells on film = microangiopathic haemolytic anaemia
how do you manage gastroenteritis?
most cases are self limiting and should be managed at home with oral fluid (diarolyte)
more severe cases leading to dehydration may need admission for rehydration with NG fluids or IV fluids
stool samples can be sent to help isolate the organism if required
when you see/feel an olive shaped mass under the right upper quadrant want condition are you thinking of?
pyloric stenosis
what investigations would you do for pyloric stenosis?
surgical emergency but also potential medical emergency
- test feed - observe feed, watch for hyper peristalsis, palpate for pyloric mass, witness projectile vomit
- cap gas - METABOLIC ALKALOSIS IS A MEDICAL EMERGENCY
- ultrasound- thickened and lengthened pyloric muscle (but if not seen it doesn’t rule it out because intraobserver differences)
U+E might show raised sodium, urea, creatinine (dehydrated) and low potassium and chloride (from vomiting)
what is the preferred imaging for suspected intussusception ?
abdo US
management for intussusception?
ABC
C = IV access, fluid resus, reassessment
Diagnosis = ultrasound abdo
treatment = air reduction enema or surgery
how might coeliac disease present in a small child?
short stature - failure to thrive - due to malabsorption
increased loose stools per day
distended abdomen
thin skin with loss of subcut fat
wasted buttocks with reduced muscle bulk
pallor (due to anaemia)
what is coeliac disease?
autoimmune disease triggered by gluten in cereals/wheat products
what is the pathophysiology in coeliac disease?
undiagnosed, what can it lead to?
immune response to gliadin leads to progressive flattening of the small bowel mucosa leading to malabsorption (can lead to steatorrhoea - fatty poos)
faltering growth
iron deficiency anaemia
osteopaenia
how can you confirm a diagnosis of coeliac disease?
anti tissue transglutaminase antibodies (anti ttg)
and total IgA
normal IgA + increased anti TTG = coeliac
(if both low then anti- TTG is less useful as may suggest Ig deficiency anyway)
confirmatory EMA antibody testing (/and human leukocyte antigen (HLA)-DQ2/-DQ8 testing.)
If both anti ttg and EMA are positive, celiac disease may be diagnosed without a small intestinal biopsy - IN CHILDREN
vs whilst adults - they should have a biopsy to confirm (showing villus atrophy)
how do you diagnosis coeliac on biopsy if the blood test results aren’t conclusive?
from where?
what do you see?
how are the changes classified?
duodenal
intraepithelial lymphocytes should be increased (lymphocytic infiltrate)
and the villous-to-crypt ratio decreased (due to subtotal villous atrophy)
Marsh classification 0-4
What conditions are associated with coeliac disease?
downs syndrome
dermatitis herpetiformis (itchy vesicles)
vitiligo
pernicious anaemia
hashimoto’s (hypothyroidism)
T1DM - they will have a screening tests for coeliac antibodies
HLA B8
how is coeliac disease managed in paediatrics?
life long gluten free diet!
refer to paediatric dieticians
gluten rechallenge can be done if diagnosed before 2 years/diagnostic uncertainty
A child previously well starts having episodes bloating, stomach pain and flatulence after drinking milk
you find out they had gastroenteritis about 10 days ago
what is the diagnosis?
transient lactose intolerance post gastroenteritis
temporary lactose intolerance can happen after some illnesses, such as gastroenteritis, when the body’s stores of lactase are temporarily reduced. Inflammation of the bowel as a result of intolerance to other foods, infection or bowel surgery can also result in lactose intolerance.
What symptoms can a cow’s milk allergy (CMA) cause?
Cows’ milk allergy can cause a wide range of symptoms, including:
skin reactions – such as a red itchy rash or swelling of the lips, face and around the eyes
digestive problems – such as stomach ache, vomiting, colic, diarrhoea or constipation
hay fever-like symptoms – such as a runny or blocked nose
eczema that does not improve with treatment
Occasionally CMA can cause severe allergic symptoms that come on suddenly, such as swelling in the mouth or throat, wheezing, cough, shortness of breath, and difficult, noisy breathing - anaphylaxis
what are the different types cow’s milk allergy (CMA)?
IgE mediated - reacts faster (mins - hours)
might see anaphylaxis in this type
non- IgE mediated where there is a delayed reaction from 2 hours - 1 week and there is no test for it
mixed reaction
how can a baby with CMA that is exclusively breast fed react?
and how do you treat them?
in very sensitive babies with CMA they can still react to the cows milk consumed by their mother
treat by having the mother exclude all cows milk product from her diet
when will a baby with cows milk allergy typically present?
between 3-6 months of life, when they’re beginning to have either cows milk mixed in with formula feeds or solid foods
they will not present after 12 months
what is protective against developing cows milk allergy?
breast feeding
what formulas are given to babies who are allergic to cows milk?
what are the differences between them?
AAF - amino acid formula - this has never seen any cows milk before, but is really expensive
EHF - extensively hydrolysed formula, which is cheaper but will contain some small amounts of cows milk protein as it has been hydrolysed
BUT 90% will tolerate EHF, and those who need AAF can often tolerate a step down of EHF after while
what should you monitor in children with CMA?
height and weight for age because low height and weight for age are complications of cows milk allergy
which form of IBD is more common in children?
crohns is more common that UC
what ages do children normally present with IBD?
12-17
IBD symptoms
how long does a child have to be having IBD symptoms before a diagnosis can be made?
bloody/mucus stools with increased frequency
particularly during the night time
tenesmus (feeling of not fully emptying)
mouth ulcers in crohns
abdo pain
> 4 weeks
what are the two methods of inducing remission in children with crohns? which is preferred and why?
steroids
OR
6-8 weeks of dietary remission with exclusive liquid/enteral/elemental nutrition = NO SOLIDS
- EEN is preferred, as it supports mucosal healing and can be as affective as the steroids but without the side effects such as increased risk of infections etc
what are the problems with using exclusive enteral nutrition to induce remission in children with crohns?
- it’s expensive
- hard to ensure compliance/adherence
- can be embarrassing for them
- some will dislike the taste
what problems do children with IBD experience?
reduced nutritional intake due to malabsorption =
weight loss/failure to thrive
vitamin D deficiency
iron deficiency
what is the key inflammatory marker seen in IBD?
faecal calprotectin
although ESR and CRP can also be raised
how do you induce remission in children with UC, not crohns?
there is no evidence for EEN to induce remission in UC therefore must use drug therapy - steroids
what is the main differences between UC and crohns?
Crohns - ‘gum to bum’ affected, and is transmucosal, non-caseating granulomas, discontinuous - skip lesions, often see rectal sparing, perianal disease is common
UC - colon and rectum only affected and is mucosal only. no rectal sparing, no granuloma, IS associated with primary sclerosing cholangitis (PSC)
what drugs are used in the maintenance of IBD?
Aminosalicylates (also known as 5-ASAs) such as sulfasalazine and mesalazine
Immunosuppressants, such as azathioprine
Biologics, such as infliximab and adalimumab
whats the difference between GOR and GORD?
reflux vs the reflux disease
only have the disease when there are complications from it or symptoms persist up to 2 years
complications can include: faltering growth oesophagitis apneoa aspiration, wheezing, hoarseness iron deficiency anaemia seizure like events - torticolis
what test can you use to check for GOR/D?
PPI test
if symptoms improve with PPI and get worse without PPI then they have GOR
difference between intolerance and allergy
allergy is immune mediated whilst intolerance is not immune mediated and is related to metabolism
what condition is cows milk protein allergy associated with?
atopy - eczema, asthma and hay fever
how can you test for food allergies?
elimination diet - 4-6 weeks removal from diet if symptoms improve its likely that (and can try re-introduction check)
what is Hirschsprung’s disease? and who does it present?
how do you definitively diagnose it?
A congenital condition characterised by partial or complete colonic functional obstruction associated with the absence of ganglion cells. Because of the aganglionosis, the lumen is tonically contracted, causing a functional obstruction.
- presents with obstruction/constipation type symptoms, bowel distention
may present with delayed passage of meconium in the first 24 hours of life
definitive diagnosis: rectal biopsy
when does Hirschsprung’s present?
The vast majority of patients present in the newborn period up to 1 year of age.
what complication can Hirschsprung’s lead to?
complication: enterocolitis
what condition is Hirschsprung’s associated with?
associated with downs syndrome
what are the complications of long term constipation?
acquired megacolon, anal fissures, overflow incontinence, behavioural problems
when examining a child presenting with diarrhoea or vomiting what must you examine?
hydration status
what are the extra intestinal features of IBD?
uveitis, arthritis, erythema nodosum
primary sclerosing cholangitis (PSC) - in UC only
