Paediatric GI Flashcards
GORD IN CHILDREN
MC cause of what in infancy?
Risk factors
vomiting
infants regurgitate their feeds.
preterm delivery
neurological disorders
features of GORD in children
before 8 weeks
vomiting/regurgitation - milk vomits after feeds and could be after laid flat.
excessive crying - esp whilst feeding
diagnosis of GORD in children
clinical
mx of GORD in kids
30 degree head up during feed.
sleep on back - reduce cot death risk
ensure not overfed , trial smaller feed
trial thickened formula eg:
- rich starch
- cornstarch
-locust bean gum
-carob bean gum
- trial alginate therapy - gaviscon. not at same time as thickened formula.
NO PPI.
prokinetic if specialist: metoclopramide
when could you give a ppi in gord in kids
1 or more of:
- unexplained feeding difficulties like refusing, gagging/choking
- distressed behaviour
- faltering growth
complications of gord in kids
distress
failure to thrive
aspiration
frequent otitis media
in older kids dental erosion.
GORD kid has severe comp like failure to thrive what to do?
if med tx ineffective do fundoplication
adults: indications for upper gi endoscopy
over 55
sx over 4 weeks or persistent sx despite tx
dysphagia
relapsing sx
weight loss
what to do in gord suspected adult if endoscopy negative
24hr oesophageal ph monitoring (gold standard)
adults: mx of gord
endoscopy proven oesophagitis
endoscopically negative reflux disease
proven:
- full dose ppi 1-2 mths
- if response, low dose tx when needed
- if not double dose ppi 1 month
negative:
- full dose ppi 1 mth
- response: low dose tx, when needed
- if no response: H2RA (famotidine) or prokinetic 1 mth
stop nsaids
antacids like gavison - short term
complications adult gord
oesophagitis
ulcers
anaemia
benign strictures
barrett’s oesophagus
oesophageal carcinoma
what is GORD?
acid from stomach flow through lower oesophageal sphincter and into oesophagus
irritates lining and causes sx.
why does the acid affect oesophagus more than stomach?
squamous epithilial lining in oesophagus more sensitive to acid than columnar epithelial lining in stomach.
causes of gord in adults
greasy spicy foods
coffe tea
alcohol
nsaids
stress
smoking
obesity
hiatus hernia
how does gord present in adults
dyspepsia :
- heart burn
- acid regurg
-bloating
-nocturnal cough
-hoarse voice - retrosternal/epigastric pain
red flags with GORD - adults
2 week wait referral.
- urgent direct-acess endoscopy.
dysphagia - any age - 2 week wait refer
- over 55
-weight loss
-upper abdo pain
-reflux - tx-resistant dyspepsia
-n+v - upper abdo mass on palpation
-low hb (anaemia) - raised platelet count.
what is a oesophago-gastro-duodenoscopy?
assess for what?
camera through mouth down to oesophagus, stomach and duodenum.
used to assess:
- gastritis
-peptic ulcers
-upper gi bleed
-oesopageal varices (liver cirrhosis) - barrets oesophagus
- oesophageal stricture
- malignancy of oesophagus/stomach
pt comes in with upper gi bleeding ie melaena or coffee ground vomiting what to do ?
admission
urgent endoscopy
what is fundoplication?
laparoscopic fundoplication - tie the fundus of the stomach around lower oesophagus to narrow LOS.
What is a hiatus hernia?
4 types?
1- sliding
2- rolling
3 - combo of sliding and rolling
4- large opening with additional abdo organs entering thorax
hernation of stomach through diaphragm.
- normally diaphragm opening at los level and fixed.
- narrow opening helps maintain the sphincter and stop acid and stomach contents refluxing up.
- when its wider, stomach enters through diaphragm and contents reflux up.
how can a hiatus hernia be seen?
ix
cxr
ct
endoscopy
barium swallow
explain
sliding hiatus hernia
rolling hiatus hernia
type 4
- sliding:
- stomach slides up through diaphragm, gastro-oesopageal junction pass up into thorax.
- rolling:
- seperate portion of stomach folds around and enters through diaphragm opening alongside oeso.
4:
- large hernia
- bowel pancreas or omentum pass up through diaphragm.
What is pyloric stenosis caused by ?
when does it present and how?
2nd to 4th week of life - projectile vomiting - 30 mins after feed.
rarely upto 4 months.
cause: hypertrophy of circular muscles of pylorus.
epidemiology of pyloric stenosis
males : 4* more
10-15% infants positive fhx
1st borns - more affected.
features of pyloric stenosis
projectile vomiting - 30 mins after feed
constipation and dehydration
palpable mass - upper abdomen - poss (hypertrophic muscle of pylorus)
- hypochloraemic, hypokalaemic alkalosis due to persistent vomiting.
how would you diagnose pyloric stenosis?
how would you manage pyloric stenosis?
uss - thickened pylorus
ramstedt pyloromyotomy. - laparoscopic pyloromyotomy :
- incision into smooth muscle of pylorus
- widen canal allowing food to pass from stomach to duodenum as normal.
blood gas: hypochloric (low chloride) met alkalosis. - baby vomits the hcl from stomach.
presentation of pyloric stenosis pt
1st few weeks of life
hungry baby thin pale failing to thrive.
projectile vomiting.
what is the pyloric sphincter?
ring of smooth muscle forms canal between stomach and duodenum.
hypertrophy and narrowing of pylorus causes the stenosis.
food cant travel.
then you get powerful peristalsis in stomach as it tries to push food into duodenum but it cant so goes other way: oeseophagus - projective vomit.
What is zollinger ellison syndrome?
what is gastrin?
sx
gastrinoma associated with?
rare condition.
duodenal or pancreatic tumour secretes excessive quantities of gastrin.
gastrin: hormone stimulates acid secretion in stomach.
=
severe dyspepsia
diarrhoea
peptic ulces
gastrin-secreting tumours - gastrinomas associated with MEN1 - autosomal dominant. - can cause parathyroid and pituitary tumours
What is hirschsprung’s disease?
CONGENITAL
caused by aganglionic segment of bowel due to developmental failure or parasympathetic (MYENTERIC) auerback and meissner plexuses.
RARE.
important for childhood constipation!!
associations of hirschsprungs disease
3 times mc in males
downs syndrome
neurofibromatosis
MEN type II
Waardenburg syndrome: pale blue eyes, hearing loss and patches of white skin and hair)
pathophysiology of hirschsprungs disease
parasympathetic neuroblasts fail to migrate from neural crest to the distal colon and rectum. - section at end of colon left without parasympathetic ganglion cells.
therefore : developmental failure of parasympathetic auerback and miessner plexuses
therefore uncoordinated peristalsis
therefore functional obstruction
aganglionic section doesnt relax - constriction. - loss of movement of faeces and obstruction in bowel.
possible presentation of hirschsprungs disease
neonatal period: failure or delay to pass meconium more than 24 hrs.
chronic constipation since birth
vomiting
poor weight gain/failure to thrive
older children:
constipation
abdo distention
ix for hirschsprungs disease
abdo x ray
rectal biopsy - gold : bowel histology: abscence of ganglionic cells.
mx of hirschsprungs
initially: rectal washouts/bowel irrigation
fluid resus
definitive: surgery to affected segment of colon
RELEVANCE OF myenteric plexus in hirschprungs disease
the myenteric plexus or the auerbachs forms the enteric nervous system - brain of gut.
its not there for hirschsprungs.
this nerve plexus run along bowel in bowel wall.
- stimulates peristalsis of large bowel. - without it the bowel loses mobility and cant pass food along length.
what is hirschsprung - associated entercolitis?
presentation
lead to what?
tx?
inflammation and obstruction of intestine.
2-4 weeks of birth with :
- fever
-abdo distention
-diarrhoea(often with blood)
- features of sepsis
life threatening.
lead to : - toxic megacolon an perforation of the bowel.
tx:
- abx
-fluid resus
-decompression of obstructed bowel
What is biliary atresia?
CONGENITAL
obliteration or discontinuity within extrahepatic biliary system : obstruction in bile flow.
3 types of biliary atresia
1: proximal ducts patent, common duct obliterated
2: atresia of cystic duct and cystic structures found in porta hepatis
3: atresia of left and right ducts to level of porta hepatis.
pt presenting with biliary atresia?
1st few weeks of life
jaundice - extending beyond phsyiological 2 weeks.
darkin urine and pale stools.
appetite and growth disturbance. - could be normal in some
signs of biliary atresia
jaundice
hepatomegaly with splenomegaly
abnormal growth
cardiac murmurs if associated cardiac abnormalities present.
ix of biliary atresia
Serum Billirubin : conjugated and total. conjugated high total normal
LFT: serum bile acids, aminotransferases raised.
serum alpha 1 antitrypsin: deficiency
sweat chloride test: CF involves biliary tract
uss of biliary tree and liver: poss distention and tract abnormalities
percutaneous liver biopsy with intraoperative cholangioscopy
mx of biliary atresia
surgery only definitive: dissection of abnormalities into distinct ducts and anastomosis creation.
medical: abx and bile acid enhancers after surgery
KASAI PROTOENTEROSTOMY: attack section of SI to liver opening where bile ducts normally attaches.
complications of biliary atresia
unsuccessful anastomosis formation
progressive liver disease
cirrhosis with eventual HCC
prognosis of biliary atresia
good if surgery successful
if fails: liver transplant needed in 1st 2 yrs of life
What is marasmus?
Severe malnutrition caused by an overall deficiency in caloric intake (protein and energy). Usually kids under 5, in developing countries.
Results in extreme fat and muscle loss, causing stunted growth, severe weight loss and immunodeficiency.
Common in areas of famine or severe malnutrition
presentation of marasmus
Severe weight loss
Emaciation
Prominent bones, sunken eyes, thin, dry skin
Irritability
Growth failure
Weakness
Mx of marasmus
Rehydration
Gradual intro of calories
Micronutrient supplementation
Long term nutritional rehabilitation and infection management
comps of marasmus
Immunodeficiency leading to severe infection
Electrolyte imbalance (hypokalaemia)
Hypoglycaemia
Growth retardation
What is kwashiorkor?
Severe protein malnutrition that occurs despite sufficient caloric intake. Often areas where diet is primarily starchy or carbohydrate heavy with little protein.
Children often appear puffy due to generalised oedema (hypoalbuminaemia), especially in legs and face.
Presentation of Kwashiorkor
Oedema (legs, face)
Moon face
Depigmented hair
Enlarged, fatty liver
RF of kwashiorkor
Sudden breastfeeding cessation
Poverty
Insufficient protein, high carbohydrate
Food insecurity/scarcity
comps of kwashiorkor
High mortality if untreated
Heart failure (due to severe oedema)
Sepsis
Severe diarrhoea
Refeeding syndrome if not treated properly
mx of kwashiorkor
Electrolyte and fluid imbalance correction (slow, prevent osmotic demyelination syndrome)
Gradual nutritional rehabilitation, protein rich etc
What is neonatal hepatitis syndrome?
Inflammation of liver of newborns usually in first months of life. Can be due to viral infection, genetic disorders, or may be idiopathic.
Inflammation leads to impaired bile flow, damaging liver
Causes of neonatal hepatitis syndrome
Viral (cytomegalovirus, hepatitis B)
Metabolic disease (galactosemia, tyrosinaemia)
Genetic disorders (alpha 1 antitrypsin deficiency)
Family history and prematurity are RF
How does neonatal hepatitis syndrome present
Jaundice >first 2 weeks, prolonged
Hepatomegaly
Dark urine and pale stools
Poor feeding, failure to thrive
Management of NH Syndrome
Treatment of underlying cause
Fat soluble vitamin supplementation (ADEK)
Ursodeoxycholic acid to aid bile flow
Liver transplant if severe
What is meckel’s diverticulum?
Congenital diverticulum of the small intestine. Remnant of omphalomesenteric duct and contains ectopic ileal, gastric or pancreatic mucosa
Usually asymptomatic but can present with abdominal (RLQ) pain, rectal bleeding or intestinal obstruction. It is the biggest cause of painless massive GI bleeding between 1 and 2y.
How is meckel’s diverticulum ix and mx?
Meckels scan
- 99m Technetium pertechnetate scan, which has an affinity for gastric mucosa
Managed
- Laparoscopic surgery or diverticulectomy.
- Small bowel resection and anastomosis.
rule of 2’s
meckels diverticulum
Meckel’s diverticulum
- 2% of population
- 2 inches long
- 2 feet from ileocaecal valve
- 2x as likely in boys
- 2yo when it causes GI bleed
- 2 types of ectopic tissue (pancreatic and gastric (susceptible to ulcer))
possible causes of intestinal obstruction
Meconium ileus
Hirschprung’s disease
Oesophageal/duodenal atresia
Intussusception
Intestinal malrotation
presentation of intestinal obstruction
Persistent vomiting
Abdominal pain/distention
Failure to pass stool/wind
Bowel sounds (tinkling early and absent later)
ix in bowel obstruction
Abdominal X ray
- Dilated loops of bowel proximal to obstruction and collapsed distal.
- Absence of air in rectum
mx of bowel obstruction
NBM
NG Tube and draingage
IV fluids
Surgical definitive
What is toddlers diarrhoea?
Chronic, non specific diarrhoea, between 1 and 4 years of age. Is a diagnosis of exclusion
features of toddlers diarhoea?
Frequent, poorly formed, offensive stools
Food material easily recognisable
Child is normally well, active and has unimpaired growth. Normal appetite and normal/increased fluid intake.
No positive findings on examination or lab investigations
Mx of toddlers diarhoea
Paternal reassurance, avoidance of full strength fruit juice.
Faeces normally becomes firm when child is toilet trained or by 3 years
What is failure to thrive?
Poor physical growth and development
Faltering growth if they fall in centile spaces (e.g. distance between 75th and 50th centile)
1 if birthweight <9th centile
2 if birthweight 9-91st centile
3 if birthweight above 91st centile
causes of failure to thrive
Inadequate intake
- Maternal absorption
- Neglect
- Poverty
Difficulty feeding
- Poor suck (cerebral palsy)
- Cleft lip/palate
- Pyloric stenosis
Malabsorption
Increased energy requirements
- Hyperthyroid
- Cystic fibrosis, heart disease
- Chronic infection
Inability to process nutrition
how do BMI and MID parental height suggest inadequate growth?
Height more than 2 centiles below mid parental height centile
BMI below 2nd centile
What is cows milk protein allergy/intolerance?
Usually seen in the first 3 months of formula fed children,
can rarely be seen in exclusively breastfed infants.
CMPA for immediate (<2 hours, IgE mediated)
CMPI if mild/moderate and delayed (several days, non IgE mediated)
features of cows milk protein intolerance/allergy
Occurs in first 3 months of life:
- Regurgitation and vomiting
- Diarrhoea
- Urticaria
- Colic symptoms (crying, irritability)
- Wheeze, chronic cough
- Rarely anaphylaxis
Cows milk protein intolerance has the bloating, wind, diarrhoea and vomiting, but no rash, angio-oedema, sneezing or coughing.
How is cows milk protein intolerance/allergy ix?
skin prick/patch testing
total IgE and specific IgE (RAST) for Cows milk protein
Avoiding cows milk should fully resolve issues
mx of cows milk protein intolerance/allergy
Avoid cow’s milk
If formula fed
- Extensive hydrolysed formula first line replacement
- If intolerance, can be started on milk ladder
Breast feeding
- Breast feeding mother should avoid dairy products
- May need maternal calcium supplements
- Hydrolysed formula milk when breastfeeding stops until 12 months, for at least 6 months
What is coeliac disease?
A sensitivity to the gluten protein. Repeated exposure leads to villous atrophy causing malabsorption. Children normally present before 3yo. Normally affects small bowel, particularly the jejunum
How does coeliac present?
Often asymptomatic, low threshold for testing
- Failure to thrive
- Diarrhoea
- Abdominal distention
- Anaemia
- Mouth ulcers
Dermatitis herpetiformis - itchy, blistering skin rash that typically appears on the abdomen
genetic association with coeliac disease
HLA-DQ2 (90%)
HLA-DQ8
Ix for coeliac
Antibodies
- Anti-TTG and Endomysial antibodies (IgA - undetectable if IgA deficiency)
- Anti-DGPs (Deaminated Gliadin Peptides)
Endoscopy and intestinal
- Crypt hyperplasia
- Villous atrophy
- Increased intraepithelial lymphocytes
- Lamina propia infiltration
Gluten free diet trial
tx of coeliac
gluten free diet
disease associations with coeliac
Autoimmune
- T1DM
- Thyroid disease
- Autoimmune hepatitis
- PBC/PSC
- Down’s
Possible complications of untreated coeliac
Malnutrition/vitamin deficiency
Anaemia
Osteoporosis
Non hodgkins lymphoma
Small bowel adenocarcinoma
What is irritable bowel syndrome, how does it present and how long should symptoms last?
Abdominal pain or
Bloating or
Change in bowel habit and stool constitution (watery, loose, hard, mucus)
Pain relieved with defecation.
> 6 months.
Diagnosed through exclusion and if
- Altered stool passage
- Abdominal bloating
- Symptoms made worse by eating
- Passage of mucus
Red flags in bloody diarrhoea
Rectal bleeding
Unexplained weight loss
FH of bowel or ovarian cancer
> 60y onset
Ix in ibs, including cancers that mimic it (not necessarily in kids)
FBC (check anaemia)
Inflammatory markers
Coeliac serology
Faecal calprotectin
CA125 (ovarian cancer) CA19/9 (pancreatic)
*Ovarian presents similar, just much older. E.g. 50yo woman with bloating, abdo pain. Non specific
non medical mx of ibs
Lifestyle advice
- Fluids
- Regular small meals
- Low FODMAP diet
- Limit caffeine, alcohol, fatty foods
- Reduce stress
- Change fibre depending if constipation or diarrhoea
CBT may be used
Medical management of IBS
Loperamide for diarrhoea (slows down bowel)
Linaclotide for constipation (laxative)
What is bowel intussusception, what age does it normally affect?
When a portion of the bowel invaginates into the lumen on the adjacent bowel, most commonly around the ileo-caecal region. This increases bowel size and narrows lumen, causing ostruction.
Usually affects infants 6-24 months. Boys 2x as often
Presentation of intussuception. what does the infant do during attacks?
Intermittent severe crampy progressive abdo pain
Inconsolable crying
During attack the infant will raise knees up and turn pale
Vomiting
Bloodstained stools “red-currant jelly” late sign
Sausage shaped mass in upper right quadrant
May present with viral URTI preceding illness
Ix and Mx of bowel intussusception
Ultrasound is investigation of choice - target like mass
Managed with reduction by air insufflation.
OR Barium enema
comps of intussusception
obstruction
gangrene
perforation
death
Pathophys of appendicits
Appendix sits at end of caecum. Trapped stool or other obstruction causes infection and inflammation, which quickly causes gangrene and rupture. Rupture releases contents into abdomen, causing peritonitis and possibly sepsis.
How does appendicitis present?
Severe central abdominal pain that moves to RIF over time.
Tenderness in McBurney’s point (2/3 of the distance from belly button to ASIS (Anterior Superior Iliac Spine))
Rovsing’s sign (palpation of left iliac fossa causes pain in RIF)
Guarding
Rebound tenderness and percussion tenderness if progression to peritonitis
How is appendicitis diagnosed?
Usually made clinically:
- Pain moving centrally to RIF
- low grade pyrexia
- minimal vomiting
CT GOLD Standard
Ultrasound in women (rule out ovarian cancer and gynae pathology)
Diagnostic laparoscopy if negative, with appendectomy in same procedure
key appendicitis differentials
Ectopic pregnancy - bHCG will be raised (test to rule out)
Ovarian cysts - Pelvic and IF pain, not always right, can rupture or torsion
Meckels diverticulum - Malformation of distal ileum, usually asymptomatic but can inflame, rupture, bleed, volvulus, intussusception.
Mesenteric adenitis - Inflamed lymph nodes. Often associated with tonsilitis or URTI
Appendix mass - Omentum surrounds and sticks to inflamed appendix. Treated with abx and supportively. Appendectomy once acute infection resolves
Complications of appendectomy
Bleeding, infection, pain scars
Bowel adhesions, causing obstruction
Damage to nearby organs
Veneous thromboembolism
What is chrons
Chronic inflammation of the entire GI tract (mouth to anus). Terminal ileum and colon most commonly affected. Affects white people more
rf of chrons
Family history
Smoking
White people
OCP
Diet low in fibre
NSAID
Genetic association with chrons
NOD2/CARD15 gene mutation
Inflammatory pattern of chrons
Transmural inflammation with areas of healthy bowel in between known as skip lesions, giving a cobblestone appearance.
Signs and symptoms of Crohns
Aphthous mouth ulcers
Abdominal tenderness and diarrhoea
Perianal lesions- skin tages, fissures, abscesses, ulcers, etc
Weight loss and failure to thrive
Extra intestinal manifestations of chrons
Skin
- Perianal/mouth ulcers
- Erythema nodosum
- Pyoderma gangrenosum
MSK
- Arthritis
- Seronegative spondyloarthropathy
- Clubbing
Eyes:
- Conjunctivitis
- Iritis
Ix in chrons
Faecal calprotectin raised
Serology
- pANCA Negative (more in UC)
- ASCA positive (more in Crohns)
Endoscopy + Biopsy
- Endoscopy: Skip lesions, cobblestoning, strictures
- Biopsy: Transmural inflammation, non caseating granulomas, goblet cells present
Small bowel enema
- High sensitivity/specificity for examination of terminal ileum
- Stricturs (Kantor’s string sign)
- Proximal bowel dilation
- Rose thorn ulcers
- Fistulae
Tx in chrons
Stop smoking, NSAID
Induce remission
- Glucocorticoids: Budesonide (mild), prednisolone (moderate), IV hydrocortisone (very severe)
- Immunosuppressant: Azathioprine or methotrexate
- AntiTNF (infliximab)
Maintain remission:
- Azathioprine
indications for surgery in chrons
80% of patients
- Sticturing terminal ileus disease (ileocaecal resection)
- Perianal fistulae (Diagnosed with MRI, treated surgically and draining seton left in to prevent abscess formation)
- Perianal abscess (Surgical incision and drainage)
comps of chrons
Small bowel cancer
Colorectal cancer
Osteoporosis
Perianal fissure/fistula/abscess
Anaemia/malnutrition
define uc
Relapsing and remitting bowel disease that usually involves rectum and can extend up large bowel, up to ileocaecal valve (does not affect anus).
3X more common in non smokers (smoking protective)
rf for uc
Family History
HLAB27
NSAIDs
Infections
Not smoking
Chronic stress/depression
UC Pattern of inflammation, what course does it follow, and how does damage lead to one of its characteristic features
Continuous inflammation affecting only the mucosal layers. Usually starts at rectum, working its way proximally, never past the ileocaecal valve.
Relapsing remitting course (flares with new damage, followed by healing)
Regenerating mucosa forms a scar that looks like polyps (pseudopolyps)
sign of uc
LLQ and tenesmus
Bloody, mucusy diarrhoea
Abdominal pain, urgency, weight loss and malnutrition
Extraintestinal manifestations
- Uveitis
- Colorectal cancer
- Erythema nodosum
- Pyoderma gangrenosum
- Arthritis
- PSC!
ix in uc
Colonoscopy
- Avoid colonoscopy if severe (perforation risk)
- Red, raw mucosa
- Continuous inflammation
- Loss of haustrations
Biopsy
- Pseudopolyps, crypt abscesses, goblet cell depletion, inflammation limited to mucosal layers
What is the most common extra-intestinal manifestation of Crohns and UC
Arthritis
PSC and uveitis more common in UC
classification of uc
Mild <4 stools/day, small amount of blood
Moderate 4-6 stools/day, varying amounts of blood
Severe 6+ bloody stools/day
mx of uc
Induce remission
Rectal (topical) aminosalicylate - mesalazine/sulfasalazine. Add high dose oral aminosalicylate, and then oral corticosteroid, if extensive or if remission not achieved in 4 weeks.
Maintain remission
Aminosalicylate + azathioprine.
If severe/non responsive,
Colectomy is curative
comps of uc
PSC
Bowel perforation
Toxic megacolon
Colonic adenocarcinoma
Strictures and bowel obstruction
What if fulminant uc and what is its treatment?
Sudden, acute, severe UC flareup
> 10 bowel movements
Continuous bleeding
Abdominal tenderness
Toxicity
Colonic dilation
Managed in hospital
- IV corticosteroid
- IV ciclosporin or infliximab
Consider colectomy
Rf of hiatus hernia
Obesity
Increased abdo pressure - ascites or multiparty
Investigations for hiatus hernia
Barium swallow
Endoscopy 1st line for the sx then you find incidentally
Sx of hiatus hernia
Dysphagia
Heart burn
Regurgitation
Chest pain
Mx of hiatus hernia
Weight loss
Ppi - omeprazole
Surgery only if para oesophageal hernia
