Gastro Flashcards
1
Q
How does malrotation present? Ivx?
A
• May be asymptomatic but will present with obstruction once the duodenum twists ± compromised blood supply → no stools, cramps, crying and pulling legs up
- Classically first few days of life – obstruction with bilious vomiting
- Can present at any age with volvulus
- Look for bilious vomiting + signs of dehydration
IX:
• Urgent upper GI contrast study - gold standard
(AXR) to assess intestinal rotation in any child with dark green vomiting
• Abdominal xray:
- bird-beak cut-off of duodenum (volvulus);
- corkscrew of duodenum (volvulus)
• FBC - anaemiia, polycythaemia
can do - ABG: metabolic acidosis with respiratory alkalosis (bcos reduced bowel perfusion -> lactic acidosis)
2
Q
How is malrotation managed?
A
- Urgent laparotomy – Ladd’s procedure if signs of vascular compromise
- Untwist volvulus, mobilize duodenum, place bowel in non-rotated position and remove necrotic bowel
3
Q
What is IBS? How does it present?
A
Irritable bowel syndrome (IBS) is a chronic condition characterised by abdominal pain associated with bowel dysfunction.
The pain is often relieved by defecation and is sometimes accompanied by abdominal bloating.
There are no structural abnormalities to explain the pain. IBS occurs in about 15% of the adult population.
May have: passage of mucus with stool urgency of defecation Tenesmus Constipation Explosive loose stools
4
Q
How could we ivx IBS?
A
FBC - normal
Tests to rule out other dfx:
Fecal occult blood - normal. Positive in IBD or CC
Etc
5
Q
How is IBS treated?
A
Depends if diarrhoea or constipation predominant
Both need lifestyle advice: food to avoid that make diarrhoea or constipation worse
Adjuncts - loperamide for diarrhoea and laxatives for constipation
6
Q
What is the variation in presentation of gastroenteritis based on pathogen of aetiology?
A
Most commonly rotavirus – 60% in <2y
• Campylobacter jejuni (+ abdo pain)
• Shigella/salmonella (+blood and pus in stool, tenesmus)
• Cholera/E. coli (profuse, rapidly dehydrating diarrhea)
7
Q
What is the presentation of gastroenteritis?
A
Diarrhoea plus or minus vomiting
8
Q
Define acute diarrhoea?
A
3+ stools in 24 hours
Lasts for up to 2 weeks
Stools liquid or semi liquid
9
Q
How do we manage gastroenteritis?
A
Advice eg more fluid intake
if in shock
Give IV fluid bolus THEN maintenance therapy
1st - try oral fluids
If cant tolerate eg vomiting then 2nd - IV fluids
• ABX if – suspected sepsis, extra-intestinal
spread, salmonella (<6m, malnourished, for specific organisms eg. C diff, giardiasis, shigella, cholera) - post stool culture
- SAFETY NET:
- Diarrhoea: usually 5-7d, most stop within 2 weeks
- Vomiting: usually 1-2d, most stop within 3 days
Assessing dehydration
• Weight loss is the most accurate marker
• Can use clinical signs to estimate degree of dehydration
Consider admission if dehydrated, shock etc
- No clinically detectable dehydration (<5% loss of body weight)
- Clinical dehydration (5-10%)
- Shock (>10%)
Anti diarrhoeal and anti emetic drugs are NOT recommended for kids!
10
Q
How may coeliac disease present in kids?
A
• Profound malabsorption syndrome at 8-24m after introduction of wheat-containing weaning foods → failure to thrive, abdo distension:
Classic sx:
bloated tummy
irritability
diarrhoea, constipation and other gut symptoms
faltering growth or a change in growth pattern.
Most common cause of malabsorption in kids?
• May present later in childhood with non-specific GI symptoms, anemia, iron or folate def, growth failure
Recurrent mouth ulcers Blood deficiencies Autoimmune conditions eg diabetes Elevated tea Sami ashes FH Unexplained depression or anxiety
dermatitis herpetiformis - with red, raised patches often with blisters -> not everyone gets this
11
Q
How do we ivx coeliac in kids?
A
• Assess for malnutrition – weight, height, BMI
IX: super sensitive and specific serological screening tests – TTG- IgA tissue transglutamase antibodies and endomysial antibodies
FBC - usually anaemic due to malabsorption Inflammaotry markers (CRP, ESR) - normal
12
Q
How do we Mx coeliac in kids?
A
• Gluten free diet – remove all products containing wheat, rye, barley from the diet • Refer to dietician for supervision • Life long • Yearly check-up, monitor growth and development
• If presenting <2y then gluten challenge later in
childhood to demonstrate continuing susceptibility – and check serology
13
Q
Parent complains her toddler is having episodes of loose stools. The Child is well and thriving – no precipitating dietary factors and normal examination. What is the Dfx? Mx?
A
Toddler diarrhoea
Relieve symptoms with increased fiber and fat in diet – whole milk, yoghurts, cheeses
• Avoid fruit juice and squash
14
Q
How does ulcerative colitis present and how is it ivx?
A
- Classic presentation is rectal bleeding, diarrhea, abdo pain
- weight loss and growth failure +/- erythema nodusum, arthritis
Ix:
- FBC – Hb,WCC, Platelets
- Anaemia, raised wcc + platelets - Stool microbiology investigation
- Raised faecal calprotectin = presence of inflammation in IBD (not accurate/used if <18)
- rule out infectious colitis - Endoscopy + Biopsy:
- histological features
- Continuous colitis extending from rectum proximally
- In children, 90% have pancolitis
- Histology → mucosal inflammation, crypt damage (abscesses, loss, architectural distortion) and ulceration
- small bowel imaging to check extra-colonic inflammation (Crohn’s) is not present
15
Q
How we Mx coeliac? Complications?
A
- Aminosalicylates (mesalazine or balsalazide) for induction and maintenance
- +/- topical steroids if confined to rectum/sigmoid
• If extensive or aggressive→add systemic
steroids and immunomodulatory therapy
(azathioprine)
• If severe fulminating disease→consider
colectomy with ileostomy or ileorectal pouch
- Increased risk of adenocarcinoma of colon
- Increased risk of toxic megacolon
• Regular colonoscopy screening from 10y post
diagnosis
16
Q
How does Hirschsprung disease present?
A
Clinically:
• Presents in the neonatal period with intestinal obstruction, failure to pass meconium within first 24h of life (basically they pass it AFTER 48h)
Normally, 90% of babies pass their first meconium within 24 hours, and 99% within 48 hours.
• Leads to development of abdo distension, bile-
stained vomiting
• Classically explosive passage of liquid and foul
stools (particularly after rectal examination)
• May present later in life with severe, life-
threatening Hirschsprung enterocolitis during
first few weeks (commonly Clostridium difficile)
• Or later with chronic CONSTIPATION and abdo
distension
• RF: Down syndrome Male!!
17
Q
What is the aetiology of Hirschsprung?
complications ?
A
• Most commonly diagnosed in first year of life
• Absence of ganglion cells from myenteric (Auerbach) and submucosal plexus (miessner's) of the distal/large bowel
→ this means loss of parasympathetic/motor innervation to the segment so absence of peristalsis
causes a narrow-contracted segment of bowel
- Extends from the rectum for a variable distance proximally, ends in dilated colon
- 75% is rectosigmoid only
complications: megacolon, bowel obstruction, intestinal perforation
18
Q
How is Hirschsprung ivx?
A
- AXR used initially, but is non-specific → can ID if colon or small bowel (will see dilated loops of bowel and constricted segments too)
- Contrast enema → contracted distal bowel and dilated proximal bowel with demonstration of transition zone in between
• Definitive diagnosis with Punch biopsy/ suction rectal biopsy!!!
→ confirms diagnosis → demonstrate absence of ganglion cells with presence of large acetylcholinesterase positive nerve trunks
19
Q
How is Hirschsprung managed?
prognosis?
A
First do -> • Initially, bowel irrigation aka rectal washout; with saline
- is the short term rx for constipation
• Definitive management is surgical:
- Anorectal pull-through
- affected loop of bowel is pulled out and bowel is anastomosed
- can be done if child is well or newborn - Initial stoma/colostomy
- done if child is too unwell for surgery
- once they stabilise / feel better, corrective surgery can be arranged
• IV fluids and ABX (Metronidazole) if presence of
enterocolitis
prognosis: ongoing constipation in 7%
20
Q
What is the aetiology of necrotising enterocolitis?
A
Unknown but risk factors include: premature, LBW
Most common surgical emergency in newborn babies
21
Q
How does necrotising enterocolitis present? What will ivx show?
A
Preterm neonates in the first 2 weeks of life!!!
• Feeding difficulties • Abdo distension, altered stool pattern • Bloody stool and bile-stained vomiting Abdominal erythema/ discolouration- if perforation Failure to thrive
• Palpable abdo mass or ascites
See staging card for more signs/ sx
Late finding:
• Associated → bradycardia, lethargy, shock, apnoea, respiratory distress
Lactate can rise if severe
Ix:
- Clinical diagnosis
- Dx confirmed by AXR, the finding that is seen will determine the STAGE
- Arterial blood gas and bloods (coagulation panel) will help with staging too when signs of compromise eg if DIC seen
22
Q
How is necrotising enterocolitis Mx? Complications?
A
Decompress bowel with NG tube
• IV fluids, nil by mouth
TPN - orogastric tube, IV Abx for 10-14d using local guidelines:
vancomycin and tazocin (g+- cover) - NICU
o Ampicillin/Gentamicin or Cefotaxmine + Metronidazole/Clindamycin - notes
Note if not severe, abx + nbm can resolve it
If patchy, they try not to use surgical methods.
• If they do not respond, or if perforation or necrotic bowel is suspected (free air in AXR) → surgical intervention (needed in 20-40%), open laparotomy
+ resection of necrotic bowel + creation of stoma
Complications: multi organ failure and death
23
Q
What condition is clinically indistinguishable from appendicitis? Mx?
A
Mesenteric adenitis - often preceded by sore throat. Usual organism - Yersinia enterocolitica. Not just RIF
DX can only be made definitively when large mesenteric lymph nodes are seen at laparoscopy (w/ normal appendix)
Do bloods to differentiate
Mx:
Pain relief, will go in few days
Sometimes can use abx
24
Q
What is the staging system for necrotising enterocolitis? What are the signs and sx in each stage?
And what do ivx show?
A
Bells staging
Stage 1:
Mild intestinal signs inc haematochezia and possibly abdominal distension, emesis.
systemic disease
Normal or non specific radiological signs - distension, mild ileus.
Stage 2:
Moderate intestinal signs inc absent bowel sounds, ileus, pneumatosis intestinalis (bowel wall gas)
AXR: portal venous gas
Lab tests: thrombocytopenia, metabolic acidosis
Stage 3:
3a - bowel intact, Hypotension, bradycardia, apnoea, peritonitis. AXR - portal venous gas.
3b - bowel peroration. AXR - Pneumoperitoneum (extraluminal gas)
Neutropaenia Metabolic (and respiratory) acidosis and DIC
25
What is NEC?
Inflammation of the bowel that may lead to bowel damage to the extent where parts of the bowel dies.
26
How does Chrons present in kids?
complications?
• Affects any part of the GI tract mouth → anus
Will find skip lesions; areas of healthy bowel separating diseased bowel
• Transmural and most commonly affects the terminal ileum and proximal colon.
Clinically:
Likely lots of psychological problems/worries
May mimic anorexia nervosa
• Abdo pain, diarrhea, weight loss
• May see growth failure, delayed puberty, fever,
lethargy, weight loss, oral lesions, perianal skin tags
• Uveitis, arthralgia, erythema nodosum
• Complications → inflamed thickened bowel is susceptible to strictures and fistulae
27
How do we ivx CHRONS in kids?
* FBC: raised inflammatory markers;↑ platelets, ↑ CRP/ESR, Iron deficiency anaemia
* Decreased albumin
• Dx: endoscopy /ileocolonoscopy or AXR + histology findings on biopsy
Hallmark on histology→ non-caseating epithelioid cell granulomata
Imaging/AXR - narrowing, fissuring, bowel wall thickening
* This is done under general anaesthesia in young children, and using heavy sedation in older children
* Consider: faecal calprotectin testing – to confirm diagnosis
28
How do we manage Chrons in kids?
1. Nutrition + Steroids:
1a. Induce remission with Enteral nutritional therapy:
Replace diet with whole protein modular feeds/polymeric diet – excessively liquid, for 6-8 weeks
▪ This is effective in 75%
▪ Products are easily digested and provide all nutrients needed to replace lost weight, can get form pharmacy, lots of different flavors so palatable
1b. STEROIDs - eg prednisolone
2. • Maintain remission with immunosuppressants
o Azathioprine, 6-mercaptopurine or methotrexate
o Anti TNF (infliximab, adalimumab) can be added
o +/- long term supplemental enteral nutrition to correct growth failure
3. Surgery
- If disease limited to distal ileum
• Surgery for complications – obstruction, fistula, abscess, severe localized disease unresponsive to Tx
• SUPPORT→www.chronsandcolitis.org.uk
29
Chrons and UC are examples of?
Inflammatory bowel disease
30
Define ulcerative colitis
• Recurrent, inflammatory and ulcerating disease involving the mucosa of the colon
31
How does ULCERATIVE COLITIS present?
* Classic presentation is rectal bleeding, diarrhea, abdo pain
* + weight loss and growth failure +/- erythema nodusum, arthritis
32
How is UC diagnosed?
• Dx by endoscopy and biopsy for histological features
o Confluent colitis extending from rectum
proximally
o In children, 90% have pancolitis
* Histology→mucosal inflammation, crypt damage (abscesses, loss, architectural distortion) and ulceration
* + small bowel imaging to check extra-colonic inflammation (Crohn’s) is not present
33
How is UC managed? Complications?
• Aminosalicylates (mesalazine or balsalazide) for induction and maintenance
• +/- topical (rectal) steroids if confined to rectum/sigmoid
• If extensive or aggressive→add systemic
steroids and immunomodulatory therapy
(azathioprine)
• If severe fulminating disease→consider
colectomy with ileostomy or ileorectal pouch - remove bowel and make stoma
Complications
• Increased risk of adenocarcinoma of colon
• Increased risk of toxic megacolon
• Regular colonoscopy screening from 10y post
diagnosis
34
How does constipation with overflow present?
Aetiology?
What are the risks?
Aetiology:
Poor diet, picky eater
Hypothyroid, neurological, psychogenic
• Intermittent cramping abdo pain, avoiding going
to the toilet
• Some liquid leak ± blood
• Children get trapped in a cycle
o Pain on passing stool = avoids going to the toilet = try and hold it in = do not go until told to or forced to sit on the toilet = suddenly comes out all at once (school) = ↑pain ↑embarrassment = next time will try harder not to poo and cycle ensues
• Risk of megacolon with ↑ dilatation of the colon and build up of stool – dilatation leads to gradual loss of innervation and control
35
How might we ivx constipation in kids?
• Usually clinical diagnosis with no real investigations
• But some investigations could be implicated in certain settings
o XR – if you need to prove constipation o Allergies may cause constipation too, consider allergy testing if +++ atopy or other signs
o Can also do bloods (hypothyroid) → also consider psychogenic cause
o Exclude neuro cause → look at back,ask about leg weakness, exam leg power and reflexes
• DON’T DO A PR in children – at most, can pull
cheek apart but no indication for PR and its too
traumatic
36
How do we mx CHRONIC constipation in kids?
First line: Disimpaction regime
1 -> Osmotic laxative / stool softener
- movicol aka polythene glycol 3350 (or macrogol)
- 2-12 sachets/day. 200ml water with each (divide into 3-4 drinks pd) see PACES sheet
- best to start on low dose and increase according to response
- After 48 hours reduce to maintenance dose (2 macrogol sachet pd)
- Continue until: stools are soft, no hard lumps, light brown, inoffensive
note, 12 is max dose in age 5+ with constipation complications eg faecal impaction, abdo mass, soiling. 8 max if under 5.
Note - use a paediatric macrogol
After disimpaction - Maintenance (only needed if disimpaction was required):
2. Stimulant laxative - 2nd line
- senna
- if movicol fails after 2 weeks.
- as maintenance dose. Take even when the stool becomes normal for 3-6months -> as LT constipation causes changes to rectum + to encourage full emptying of bowel
- Warn the parent that there can be accidents with increased laxatives
May take weeks-months to be effective
3. Diet and lifestyle advice
- more fruit and fibre and more water
- increased exercise
- reward system with positive toilet usage
- Put them on toilet in a set routine every
day eg before bed → this trains the child and the gut
- Bowel habit diary – timing and Bristol stool chart : stool frequency
37
What is ENCOPRESIS? Rx?
Involuntary passing of stools into clothes
Usually fluid overflow on background of constipation
Just as with constipation
38
How is ANAL FISSURE managed?
* Reduce constipation (stool softener, DIET, ↑fluid)
* Warm bath to soothe pain ± topical anaesthesia
* Keep area as clear as possible to aid healing
• Prevention By managing constipation
• Safety net → return if fissure unhealed in 2 weeks or
increased pain
• Support → national charity – Education and Resources for
Improving Childhood Continence (ERIC; www.eric.org.uk ) has a range of leaflets on constipation and soiling and runs a helpline
39
What is the aetiology of INDIRECT INGUINAL HERNIA?
Patent processus vaginalis:
When children develop in the womb, the testicles develop inside the abdomen
* Towards the end of the pregnancy, each testicle creates a passage (processesus vaginalis) as it travels into the scrotum
* Failure of this passage to close → remains wide → the abdominal lining and bowel can protrude through it, causing a lump to form in the groin
* More commonly on right (60%) due to delayed descent of right testicle
40
What are risk factors and complications of hernia?
Can result in portion of the lining and bowel dying, resulting in serious infection and bowel disorders
• RF: male, prematurity, connective tissue disorders
41
How might you examine or investigate a patient with inguinal hernia?
* Scrotal sac is enlarged, contains palpable loops of bowel, fluid (does not always transilluminate)
* ±pain
* Swelling or bulge may be intermittent, and can appear on crying or straining
Ix:
• Dx is clinical
• Examine supine and standing, try to reduce it
• If spontaneously reducing → increase abdo pressure by lifting arms, provoking crying, cough, blow a balloon
• If incarcerated → tender, firm mass + vomiting,
obstruction (unable to pass stool), poor feeding, erythematous/discoloured skin
42
How do we Mx hernias?
Inguinal - Surgical correction (lap or open), elective herniorrhaphy due to risk of strangulation/incarceration
UMBILICAL → may not need treatment as tends to close after baby is born, if persistent at 3yo, surgical repair
EPIGASTRIC → surgical repair if causing discomfort or affecting activities of daily living
FEMORAL → can be very difficult to differentiate from indirect. Location is below the inguinal canal, through femoral canal. Differentiation often only made during operation once anatomy and relationship to inguinal ligament is visualized. Signs and symptoms are same as for indirect inguinal hernias.
43
What is the aetiology and risk factors for LACTOSE INTOLERANCE.
Digestive system is unable to digest lactose (natural sugar in cow’s milk) → ferments in the gut, ↑ waste gas, leading to pain and bloating.
Primary (70%) → body does not produce enough lactase enzyme, most common in east Asian. African, Hispanics. There is an age related decline in lactase expression. Varies from one person to another.
Secondary → damage to gut lining, temporary lactase deficiency (seen with gastroenteritis, Crohn’s, coeliac, alcoholism)
Congenital (autosomal recessive) and developmental (premature borns) forms exist too.
RF: FH, ethnicity
44
How does LACTOSE INTOLERANCE present?
• Wind, diarrhea, bloating with lactose ingestion, abdo rumblings and pain
Failure to thrive, tiredness, eczema
45
How can we ivx lactose intolerance?
Dietary lactose elimination
If inconclusive: lactose tolerance test:
• Bloods measuring glucose before/after lactose
to monitor level of digestion
• FBC to rule out 2ndary disease (anemia, ↑
WCC)
46
How do we Mx lactose intolerance?
For primary
• Experiment with diet – different with each child, need to discover individual lactose threshold
• Life long intolerance but over time will find a diet that suits them
• Avoid → cows/goat milk, soft/cottage cheese, yoghurt, ice cream
• Alternatives → soya/coconut/oat milks For secondary
• Cut out dairy and allow gut time to heal May need Ca and Vit D supplements
Lactase enzymes→ can be taken in capsule or liquid before eating a meal containing lactose. Will help child’s digestion of lactose on special occasions but shouldn’t be taken every day
Developmental
• In preterm infants <34w → rapidly improves as the intestinal mucosa matures
Recommend that premature infants are breastfed/given lactose- containing formulas
Those who develop symptoms of lactose intolerance may be fed with lactase supplements alongside feeds for a few weeks – 2 months
Congenital
Management → complete avoidance of lactose
o 1st line → diarrhea management
(rehydrate and replace electrolytes), can be life threatening
o Then complete avoidance of lactose from birth – substitute with lactose free formula and nutritionist consultation
47
Define acute liver failure?
Acute liver failure (ALF) is a rapid decline in hepatic function characterised by jaundice, coagulopathy (INR >1.5), and hepatic encephalopathy in patients with no evidence of prior liver disease
48
What might ivx show on ALF?
LFTS, PT, INR
ABG - metabolic acidosis if paracetamol OD
Paracetamol levels
Lactate - prognostic in paracetamol OD
U&Es - Renal failure is a known complication of ALF
Bilirubin can be normal early
• ↑ AST and ALT, ↑ ALP, abnormal coagulation
Increased NH3
49
How do we Mx acute liver failure?
Depends on cause, hepatitis? Paracetamol OD?
• IV dextrose to maintain blood glucose
• Prevent sepsis with broad-spectrum ABX,
antifungals
• IV vitamin K, FFP or cryoprecipitate to prevent
haemorrhage
• PPI or H2 blockers to prevent GI tract bleeding
• Fluid restrict and mannitol diuresis if cerebral
oedema develops
• Urgent transfer to specialist liver unit
Nacetyl cysteine
50
What are the cause of NEONATAL JAUNDICE by time of presentation?
What is the definition?
Definition: bilirubin > 85 micromol/L
1. Physiological: unconjugated aka indirect hyperbilirubinaemia
2. If under 2 days old (1st 24 hrs of life) - always pathological
• Severe haemolysis
1 - ABO or Rh incompatibility
2- G6PD deficiency/ Hereditary spherocytosis
3• Sepsis – increased reticulocyte turnover
4- Congenital infection eg CMV
-> needs action
3. 2 days – 2 weeks = CAN BE NORMAL = INVESTIGATE
• Physiological jaundice – enzyme glucoronyl transferase
• Breastmilk jaundice – inhibition of glucoronyl transferase
- Dehydration
• Gilbert’s disease – usually triggered by infection
• Haemolysis – G6PD (X-linked), spherocytosis (dominant)
• Infection – UTI
• Congeital Hypothyroidism
All are unconjugated – can cross BBB as are fat soluble – damage basal ganglia -> Kernicterus. Note: conjugated bilirubin cannot do this
```
4. Over 2 weeks = NEEDS ACTION = JAUNDICE SCREEN
• Any of the above but ongoing
• Biliary atresia
• Congenital hepatitis
• Cystic fibrosis
```
Last 3 are conjugated – dark urine, pale stool = liver disease
In times of priority of treatment
Rule out abo, rhesus and sepsis first
The for prolonged jaundice screen (2+ weeks)
51
What are the causes of congenital and physiological jaundice?
Congenital:
- Haemolysis
- infection eg CMV
• Jaundice at birth can be due to congenital infection
• Bilirubin is conjugated and infants have other abnormal clinical signs
Physiological jaundice;
• Have higher haematocrit (more Hb)
+ red cells have higher turnover = more prone to jaundice
-> RBCs have shorter lifespan - 70 days
- Less efficient herpatic biliruibin metabolism;
UGT1A1 enzyme production is just increasing so hepatic conjugation of bilirubin is slow
• Can only be used once all other causes have been ruled out
52
What questions must your skin a neonatal jaundice case?
• Obstetric history; mother’s Rh status and blood group;
GA;
FHX (G6PD), thyroid, autoimmune conditions
• Jaundice in neonate – cephalocaudal progression
Mum:
Has your milk come in?
Child;
Feeding, stools, voiding, mental status
Are they exclusively breastfed? Are they latching?
Number of feeds in past 24hrs? Length of time feeding at breast?
Wet diapers in 24hrs? Colour of stool (yellow)
Are they waking up to feed? They hungry?
signs of illness (fever, vomiting, weight loss);
dark urine/pale stool
```
Examination:
Weight
Skin, sclera - jaundice
Head - cephalohaematoma
Abdo- organomegaly
Neuro - focus on suck and tone
assess state of hydration;
```
53
How do we ivx neonatal jaundice?
• total Serum bilirubin level AND conjugated/direct bilirubin level - best test -
every 6 hours
- ivx further if above 205
only total level needed initially/ to decide treatment
Do conjugated if jaundice after 2 weeks as it then becomes more relevant!
• Transcutaneous bilirubin
if jaundice >24hrs - 2 weeks
not most sensitive but less invasive
do serum bili if above 250
• FBC, blood film;
look for sepsis,
low haematocrit/hb with haemolytic anaemia,
increased reticulocytes with haemolysis
• Blood group – mother and baby for ABO and rhesus incompatibility
Blood film - hereditary spherocytosis
* DAT (Coombe’s test) – for ABO or Rhesus isoimmunization
* LFTs – look for congenital infection or neonatal hepatitis
TSH - congential hypothyroid
• G6PD activity
• +/- microbio culture of blood, urine, CSF if
infection is suspected to look for source of sepsis
Liver US; signs of cirrhosis (indications for transplant)
54
How do we Mx NEONATAL JAUNDICE?
Physiologica - reassure and observe - resolves in 2 weeks
Emergency admission:
• If features of bilirubin encephalopathy – sleepiness, poor feeding, irritability
• Refer to neonatal unit if under 24h old
USE threshold graph -
between the 2 lines = option 1
above top line; option 2
1. Phototherapy
- if bilirubin above 350
- second line if encephalopathy
- measure bilirubin every 6 hours
- stop when bili is 50umol below threshold 1
1b. IV fluids to rehydrate if needed
2a. IVIG
2b. Exchange transfusion
- infants blood is exchanged. measure bili every 2 hrs
- 1st line if signs of hepatic encephalopathy or risk of kernicterus
- or if phototherapy didn’t work.
- still do phototherapy as well
Mum - if rhesus sensitised -> Anti D 500 IU
55
How does kernicterus present? Risk factors?Complications?
```
• Severe jaundice
• Bulging fontanelle
• Seizures
• Hypotonia → then hypertonia
• Opisthotonos – hyperextension of spine causing backward arching of neck and back
• High pitched cry
Lethargy
Fever
Poor suck
```
• Later – sensory hearing loss,
intellectual disability, muscle rigidity, speech difficulties, seizures, movement disorder, eye movement/ gaze abnormalities
Irreversible brain damage
• Increased risk if: prematurity, rhesus incompatibility, family hx of G6PD deficiency or spherocytosis
56
What is breast feeding jaundice? How does it present?
| How can we treat it?
• it is an Extension of physiological jaundice → unconjugated jaundice - so no dark urine n pale stools
Aetiology:
-both promote the enterohepatic circulation
It is thought that Breast milk contains a steroid which inhibits hepatic glucuronyl transferase - UGT1A1 (breast milk jaundice)
OR that inadequate feeding due to poor milk supply causes lower clearance of bilirubin
* Most common cause – affecting upto 15% of healthy breast fed infants
* Jaundice gradually fades and disappears by 4- 5 weeks of age – can sometimes last for 12 weeks
* Diagnosis can be made in healthy, breastfed infants with good weight gain in whom other pathological causes are ruled out by clinical or lab study
If bilirubin above 200 can’t just be breast milk jaundice ??
Stop breastfeeding for 1-2 days if phototherapy indicated?? - BMJ
3rd line is exchange transfusion
mothers should be encouraged to continue with breast feeding as the condition resolves spontaneously. - Lissaeur
Jaundice can occur due to poor feeding-> dehydration too
• No treatment needed if serum total bilirubin level remains below that recommended for phototherapy (350)
57
What are normal bilirubin levels in neonates?
at least two thirds of all breastfed infants will have serum bilirubin concentrations in the third week of life that are significantly higher than the adult normal value is an important foundation for diagnosis
58
What is the most common cause of prolonged (>2weeks) unconjugated hyperbilirubinaemia in kids?
Breast milk jaundice
59
How can you tell the difference between un/conjugated hyperbilirubinaemia?
conjugated/direct hyperbilirubinaemia - presents with pale stools, dark urine (never normal, always investigate)
In blood tests:
-order the total bilirubin levels - direct serum bilirubin = unconjugated fraction
60
How would we manage conjugated hyperbilirubinaemia?
Treat the cause directly
61
What is ABO incompatibility and how do we test for it?
• Most ABO antibodies are IGM and do not
cross placenta but some group O women have IgG anti-A-haemolysin in blood which can cross placenta and haemolyse RCs of group A infant
* Occasionally, group B infants are affected by anti-B haemolysis
* Antibody mediated so positive DAT (Coombe’s test)
62
How do we treat HAEMOLYTIC DISEASE?
Jaundice - phototherapy
IVIG as adjunct
Severe:
Resus eg IV fluids etc
Blood transfusions - O negative
If seen in utero → transfuse with O neg packed cells cross-matched with maternal blood, ideally at 18 weeks, IV transfusion across umbilical vein with US guidance
Deliver at 37-38weeks
63
What is biliary atresia? Complications?
A fibro-obliterative obstruction of the extrahepatic biliary tree progressing to intrahepatic ducts, which can develop in utero or during the neonatal period.
inflammation and resulting fibrosis ) → leads to biliary obstruction, chronic liver failure and death (needs urgent surgical intervention
growth failure or FTT , portal hypertension, cholangitis, and ascites
This condition is fatal without surgery and is the leading indication for paediatric liver transplantation. At least 70% of children with biliary atresia will undergo liver transplantation, 50% of them by age 2 years.
64
How does BILIARY ATRESIA present?
• Failure to thrive (↓ absorption of long-chain fats and catabolic state)
• Mild jaundice (conjugated) >14d
• Pale urine, dark stools (after normal
meconium)
• Hepatomegaly ± splenomegaly and portal HTN
65
List some risk factors for BILIARY ATRESIA
genetic predisposition - HLA B12
viral infection
environmental or behavioural exposures
immune dysregulation
66
How do we ivx BILIARY ATRESIA?
• Radioisotope scan → hepatobiliary scintigraphy, technetium-99m, shows good uptake by liver but no excretion into bowel
• Definitive diagnosis - liver biopsy (percutaneous)
o Shows features of extrahepatic biliary obstruction
• LFTs non specific but – abnormal with ↑↑GGT
-serum total and direct or conjugated bilirubin
* Fasting abdo US shows contracted/absent gall bladder
* ERCP to visualize the biliary tract if the dx is unclear, technically difficult in infants, use confined to large centers
67
How do we Mx BILIARY ATRESIA?
Urgent action required
1st line •-> Surgical bypass of fibrotic ducts with Kasai procedure (hepatoportoenterostomy - HPE)
• Loop of jejunum anastomosed to the cut surface of porta hepatis to allow drainage
* Best results if surgery performed before 8w of age
* Success of procedure drops with increased time
Adjunct post surgery:
3o Ursodeoxycholic acid to encourage bile flow
o Fat soluble vitamins and nutritional supplements
2o ABX to prevent cholangitis
- 1st year of life
• Even when successful, few will still progress to cirrhosis and portal HTN → need liver transplant
68
What is the aetiology of cleft palates?
Unilateral or bilateral
Results from failure of fusion of the frontonasal and maxillary processes
Most inherited as polygenes, but may be form of syndrome –
chromosomal abnormalities
Some associated with maternal anticonvulsant therapy
69
Mum is asking why cleft palates in her child was missed. What do you say? Risks?
75% are detected on antenatal US – 20w anomaly
| Infants have increased risk of otitis media
70
How do we manage CLEFT PALATES?
• MDT
o NHS Cleft Team (GOSH): plastics, ENT surgeons, paed orthodontist, audiologist, SALT, clinical nurse specialists, psych
* Surgical repair of lip at 3-4 months
* Palate repair at 8-12 months
* Some can feed normally
* If needed, can offer special teats or feeding devices
* + orthodontic advice, dental prosthesis
• Support groups – CLAPA (cleft lip and palate association)
* Vast majority have successful surgery and live normal lives
* Further issues (speech, language) can be managed by MDT
71
What is the aetiology of DIAPHRAGMATIC HERNIA? How is it diagnosed?
* 6-8 weeks of pregnancy – diaphragm does not form correctly
* Part of intestine moves through chest area – stops lungs from developing properly (Bochdalek hernia)
• Usually L sided
• Diagnosed on routine antenatal US or after
delivery with respiratory issues (cyanosis; increased RR, increased HR, chest asymmetry, bowel sounds in chest, absent breath sounds on one side)
72
How do we ivx DIAPHRAGMATIC HERNIA?
* CXR – retrocardiac air bubble or normal or organs in chest area
* O2 sats for resp function
* Blood gas, U&Es, US for other abnormalities
73
What are the complications of DIAPHRAGMATIC HERNIA?
Increased risk of GORD,
further resp problems,
delays in milestones
74
What is the management of DIAPHRAGMATIC HERNIA?
1. Admit after birth, NG tube to release excess air (stomach or intestine) and relieve pressure on lungs
1b. May need intubation and ventilator or ECMO to stabilise + intensive care support
DEFINITIVE:
1. Immediate Surgical repair under GA + stabilisation of infant within first week of life
• Keyhole or open, patch
- TPN until intestines recover + dietician input
2. If bowel necrosis - loop resection
75
What is a OESOPHAGEAL ATRESIA & TRACHEOOESOPHAGEAL FISTULA?
* OA – malformation of oesophagus so it does not connect to stomach
* TOF – part of oesophagus joined to trachea
• Both rare, TOF tends to occur alongside OA
76
list some risk factors for OA and TOF?
Trisomy 18 and 21
FH - Feingold's syndrome
MUM - Polyhydramnios
77
what is the presenting hx of OA and TOF?
1. history of polyhydramnios
2. large amount of pharyngeal secretions present after birth (cannot tolerate his or her own secretions or feed)
3. inability to pass an orogastric or nasogastric tube is diagnostic - check on XRAY
```
Others;
Laboured breathing
Coughing, choking
VACTERL association - other developmental deformities
Cyanosis - uncommon
```
78
what is VACTERL association?
```
VACTERL association:
vertebral defects,
anorectal anomalies,
cardiac defects,
tracheo-oesophageal abnormalities,
radial and renal abnormalities, and
limb anomalies.
```
79
how do we ivx OA and TOF?
1. Routine antenatal screening
polyhydramnios and a small or no stomach bubble
polyhydramnios - high sensitivty for OA-TOF
If polyhydramnios, do fetal MRI !!
2. Fetal MRI
oesophageal pouch and small stomach
3. chest + abdo x-ray:
diagnostic with an indwelling orogastric tube curled in the upper oesophageal pouch
80
how is OA-TOF managed?
Depends on the type, ie if OA alone or OA-TOF
But its mostly just the following;
1. Suction catheter in the upper oesophageal pouch which should limit secretions entering the trachea.
2. Surgery should take place in the first 24 to 48 hours of life
GA – either keyhole or open
• Will need intensive care and ventilator support after
81
what is SMALL BOWEL ATRESIA?
aetiology?
Congenital malformation of the GIT (duodenum, jejunum, ileum) resulting in absence or complete closure of a part of its lumen
• Unknown aetiology, possible failure of recanalization of duodenum during embryonic core stage
- vascular accident in utero that leads to decreased intestinal perfusion and ischemia of the respective segment of bowel
82
what are the risk factors of SMALL BOWEL ATRESIA?
Polyhydramnios,
Down’s syndrome - particularly Duodenal atresia
Downs - Duodenal atresia
Congenital cardiac abnormalities
Familial multiple intestinal atresia
83
What is the presentation of SMALL BOWEL ATRESIA?
vomiting (in first few days of life) and abdo distension,
vomiting is usually bile stained in jejunal (most common) or ileal atresia,
can be non-billous in other forms of duodenal atresia
failure to pass meconium - sometimes
Jaundice - sometimes
There can be malrotation and absence of mesenteric arteries in Type 3b
84
what is the ivx for SMALL BOWEL ATRESIA?
* Bloods – FBC, LFT, bilirubin (total + conjugated), INR, plasma, serum amino acids
* Urinary – organic acids, succinyl acetone, bile acids, lactate:pyruvate ratio
* Imaging – US, CXR, cholangiogram, Tc 99m scan
Abdo XRAY - Radiograph with double bubble sign indicating duodenal atresia; dilated loops of small bowel separated by stricture
-
• Liver biopsy Management
85
How do we manage SMALL BOWEL ATRESIA?
1. IV fluid hydration
2. nasogastric or orogastric tube may be used to aspirate the contents of the stomach
3. Surgery - Laparotomy;
- Remove segments of affected bowel e gduodenotomy
o Need to examine entire bowel to exclude other multiple atretic segments
o Primary anastomosis
or Ladd procedure if malrotation present ; untwisting bowels
4. Post-op TPN - until bowel can assume normal functoin
86
what are the complications of SMALL BOWEL ATRESIA?
If the atresia is not treated, the bowel may become perforated or ischemic.
This can lead to abdominal tenderness and meconium peritonitis, which can be fatal
Pulmonary aspiration,
anastomotic complications (stenosis or leak), proximal bowel may have abnormal peristalsis
87
what conditions does CAKUT "congenital anomalies of the kidney and urinary tract" involve?
Non-Renal;
- Vesicoureteral reflux (VUR)
- Bladder outlet obstruction
- Pelvi-ureteric junction obstruction
Renal;
- Dysplastic or hypoplastic kidneys (kidneys do not fully develop while fetus is in the womb)
- Multicystic dysplastic kidneys (abnormal kidney development while fetus is in the womb
- Hydronephrosis
88
What is the presentation of CAKUT "congenital anomalies of the kidney and urinary tract"?
• Antenatally: oligohydramnios + decreased foetal urine output
• Postnatally: irritability
• Present as
o Decreased foetal urine output,
intra- abdo mass, haematuria, renal calculi, renal failure, HTN, hepatosplenomegaly
Mild forms of the disease can result in:
recurring UTIs or a blockage of urine, which can damage the kidneys or other structures.
A severe case can result in:
kidney failure and End stage RF.
89
what is the aetiology of CAKUT "congenital anomalies of the kidney and urinary tract"?
associated with many different chromosomal loci +
| PAX 2 gene mutation
90
what is the management of CAKUT "congenital anomalies of the kidney and urinary tract"?
• General – antenatal counselling and screening for other associated anomalies
```
• Surgical – treat cause eg. nephrectomy,
hypospadias correction (Snodgrass correction),
```
b. open/lap pyeloplasty for PUJ obstruction - fix strictures at renal pelvis
c. Ureterocoele puncturing
```
• Medical –
- meds to help with voiding
- catheterisation to help with voiding
ABX prophylaxis (UTI),
Dialysis/ renal transplant if renal failure
```
others; symptom control (HTN), calcium supplements, phosphate binders,
91
how do we ivx CAKUT "congenital anomalies of the kidney and urinary tract"?
US KUB
CT KUB
Tests to assess voiding; bladder scans, voiding cystourethrogram (VCUG)
92
what are complications of CAKUT "congenital anomalies of the kidney and urinary tract"?
* HTN, renal osteodystrophy, UTI and calculi
* Most renal lead to end-stage renal failure
* Prognosis good if non-renal are treated
93
what are the forms of ANORECTAL MALFORMATIONS?
* Low anorectal anomaly – anus closed over, in a different position or narrower than usual + fistula to skin
* High anorectal anomaly – bowel has closed end at high level, does not connect with anus, usually associated with bladder/urethral/vaginal fistula
3:
No anal (bottom) opening at all
An ectopic anus (small opening in the wrong place)
Anal stenosis (narrowed opening of the bottom)
94
what is the presentation of ANORECTAL MALFORMATIONS?
* May not pass meconium at all – swollen abdomen, vomiting
* If fistula – may pass stool from abnormal area; urine or vagina + abdo swelling and vomiting
Rare - 1 in 5000 babies
95
how do we ivx ANORECTAL MALFORMATIONS?
• Dx on examination + X-ray, US, MRI
96
how do we mx ANORECTAL MALFORMATIONS?
NG tube inserted
IV fluids given
• Surgical correction depending on anomaly
Low;
1• Anoplasty
A few days later it will be necessary to start passing a dilator (small plastic rod) on a daily basis into the new opening to prevent it narrowing. On the first occasion this may need to be done under an anaesthetic.
High:
- Colostomy/ stoma -baby will pass stool into a bag rather than through the anus.
- For several weeks/months until a more complicated operation is performed to create a new bottom for your baby.
• All ops usually complete by 9 months
97
what are complications of ANORECTAL MALFORMATIONS?
risks - perforated bowel and subsequent infection/peritonitis
UTIs if fistula to urinary tract
98
ANORECTAL MALFORMATIONS are associated with what?
VACTERL association - or VATER syndrome
99
what is CRYPTORCHIDISM and list some risk factors and prevalence
• Undescended testis - when one or both testes are not present within the dependent portion of the scrotal sac.
Risks - premature infants (30% prevalence)
3% Prevalence in normal population
100
what is the presentation of CRYPTORCHIDISM
testicle(s) cannot be felt in scrotal sac
70-80%:
palpable within the upper portion of the scrotum or inguinal canal
20-30% :
intra-abdominal location, testicular nubbin, or anorchia.
101
how do we ivx CRYPTORCHIDISM
Clinical diagnosis really;
Physical exam:
testicle(s) cannot be felt in scrotal sac
1. Laparoscopy; diagnostic and therapeutic
- under aneasthetic
others that are not recommended:
MRI - very good
US
102
how do we mx CRYPTORCHIDISM
• If bilateral → refer to senior paeds for urgent endocrine/genetic investigation
Review at 6 weeks and 3 months - looking for descent
• If not descended by 6 months;
Refer to paeds for surgery to be seen by 6 months → orchidopexy by 1yo via inguinal approach (if testes palpable),
if not palpaple - examine under anaesthesia, if you feel testes -> orchidopexy
if not -> surgical exploration
ideally done between age 1-1.5 years
POST-PUBERTY:
Straight orchidectomy, + consider orchiectomy
103
what are complications of CRYPTORCHIDISM?
Later life - low sperm counts and infertility
increased risk testicular cancer
104
male presents with CRYPTORCHIDISM and hypospadias, what do you do?
Karyoptype to screen for disorder of sexual development
105
what is PHIMOSIS and list some risk factors and prevalence
• Inability to retract foreskin, “tight” foreskin
Physiological OR Pathological:
• At birth, foreskin is non-retractable and phimosis is physiological because it's still attached to the glans.
• By 1y – 50% have a non-rectractable foreskin but by 4y only 10% and by 16y only 1%
Common from age 2-6 years
106
what is the presentation of PHIMOSIS
• Can present with haematuria, painful erections, recurrent UTI, weak urinary stream, swelling, redness, tenderness
* If persistent to puberty – increased risk of infection and can cause problems with urination
* Can lead to ballooning on micturition which is physiological
poor hygiene can lead to infection or trauma
glans is sore and inflamed, - balanitis (inflammation of the head of the penis).
There may also be a thick discharge underneath the foreskin. If both the glans and foreskin are inflamed, it's known as balanoposthitis.
107
how do we ivx PHIMOSIS
clinical diagnosis
108
how do we mx PHIMOSIS
Hygiene tips - withdraw foreskin from glans and clean with mild soap
- Urine can irritate the glans
balanoposthitis - MAY need anti fungal cream/ antibiotics
Topical steroids - makes skin easier to retract
Severe/persistent:
Circumcision
or surgery to remove adhesions
109
what are complications of PHIMOSIS?
risks of infections
recurrent UTI
110
what is Paraphimosis ?
its where the foreskin cannot be returned to its original position after being retracted.
111
what is HYPOSPADIAS?
urinary Meatus is wrongly positioned – ventral urethral meatus
can have some foreskin abnormalities
• Spectrum with varying presentation
112
what is the presentation of HYPOSPADIAS?
Incorrectly positioned urethral meatus
Ambiguous genitalia - in these cases allow them to grow up a bit before decision to change genitals unless urinary obstruction.
May be solely cosmetic concern
• May have functional issues eg. inability to micturate in a normal direction and erectile deformity
113
HYPOSPADIAS?
Corrective surgery often undertaken 2 years of age – reposition terminal urethral meatus and enable a straight erection and normal looking penis
• Affected infants must not be circumcised as foreskin is often needed for later reconstructive surgery
114
how does Balanoposthitis present and what is the mx ?
prognosis?
* Single attacks common
* Redness and inflammation of foreskin and purulent discharge
• Usually responds well to warm baths, good hygeine
broad spectrum ABX
• Recurrent attacks are uncommon, circumcision occasionally indicated
115
what are the complications of PARAPHIMOSIS?
• Restricted blood flow to head of penis – penis turns dark purple – urological emergency
116
how do we mx PARAPHIMOSIS? prognosis?
* Adequate analgesia needed and then attempt to reduce foreskin – gentle compression with saline soaked swab, usually successful
* Problem not recurrent
* If simple measures fail – refer to urologist
117
what is TESTICULAR TORSION ?
epidemiology? RFs?
* Torsion of the spermatic cord
* Causes occlusion of testicular blood vessels, and viability of testis is compromised
* Lax tissues surround the testis enables them to move around the scrotum
* Hence a twisting may occur
RFs: genetic and anatomical factors
• Any age, commonly 11-30y, mean age 16y
118
what is the presentation of TESTICULAR TORSION ?
* Sudden onset pain in ONE testis
* Makes walking uncomfortable ± abdo pain ± Nausea, vomiting
* Often hx of previous, brief episodes of similar pain (due to torsion which has self-resolved)
* Need to recognise before cardinal signs + symptoms as prompt surgery saves testes
119
how do we ivx TESTICULAR TORSION ?
Physical exam;
• Tender, hot, swollen testes – may lie high and transversely
• Lifting the testis over symphysis = increases pain
(in epididymitis this relieves pain)
US:
1. Greyscale US - presence of fluid and the whirlpool sign (the swirling appearance of the spermatic cord from torsion)
2.Colour doppler -absent or decreased blood flow in the affected testicle
120
how do we mx TESTICULAR TORSION ?
Refer to Urology
Emergency Scrotal exploration within 6 hours of symptoms ideally:
Orchidectomy or Orchidopexy - drs decision
- detort the testes
• If testis is found to be necrotic, orchidectomy
121
what are the complications and Prognosis
| of TESTICULAR TORSION ?
* Testicular infarction + atrophy - will lose a testicle
* Impaired fertility
Prognosis
• If surgery performed in <6h – salvage rate is 90-100%
• If >24h then 0-10%
122
what is the pathophysiology of kernicterus?
deposition of UNCONJUGATED bilirubin in the
Basal ganglia, Brainstem nuclei
123
what parameters would warn you of high risk of kernicterus?
Very high serum bilirubin:
- above 340 umol/L
Rapidly rising bilirubin
- above above 8.5 mol/hour
presence of clinical features of kernicterus
124
what is pyloric stenosis?
what is the aetiology?
hypertrophy of the pyloric sphincter results in narrowing of the pyloric canal. It is the most common cause of gastric outlet obstruction in the 2- to 12-week-old age group.
Pyloric stenosis leads to progressive and projectile vomiting
Aetiology:
• Hypertrophy of pyloric muscle because mechanisms:
- repeated contractions
- poor neuronal innervation to muscle
- NO synthase deficiency = less SM relaxation
125
how does pyloric stenosis present?
Non-billous vomiting – increased frequency,
increased forcefulness, progressing to projectile
• Hunger after vomiting until dehydration leads to
loss of interest in feeding
• Weight loss/FTT if presentation delayed
may include a history of feeding intolerance with multiple formula changes - parents think it’s formular intolerance
Signs of being unwell
Present at approx age 3-6 weeks old
• More common in boys and first born, RF if FHx
Upper abdominal mass
126
how doe we invx PYLORIC STENOSIS?
Physical exam:
• Palpable ‘olive’ mass in RUQ,
1st:
A. Check U/E - decreased K and decreased Na
Capillary Blood gas; to check for Hypochloraemic metabolic alkalosis
B. US if required - Gold standard
(pylori muscle thickness >4mm, pyloric canal
length >17mm) – sensitivity 97%
Test feed, observe for gastric peristalsis
127
How is PYLORIC STENOSIS managed ?
1. IV fluid resus
• at 1.5x maintenance rate
(0.45% saline, 5% dextrose)
No K+ until urine output is stable then can add KCl)
2• Surgery - Pyloromyotomy (lap)
- once stable / once HCO3- is <28 & Cl >95
128
what is GASTRO- OESOPHAGEAL REFLUX GOR in a child?
Gastro-oesophageal reflux (GOR) is the passage of gastric contents into the oesophagus. It is a common physiological event that can happen at all ages from infancy to old age, and is often asymptomatic.
It occurs more frequently after feeds/meals. In many infants, GOR is associated with a tendency to 'overt regurgitation' – the visible regurgitation of feeds.
129
what does the term GORD mean in kids?
Gastro-oesophageal reflux disease (GORD) refers to gastro-oesophageal reflux that causes symptoms (for example, discomfort or pain) severe enough to merit medical treatment,
OR to gastro-oesophageal reflux-associated complications (such as oesophagitis or pulmonary aspiration).
It only happens in a small proportion of infants.
130
How may GOR present in kids?
prognosis? complications?
Common (40%) in 1st year of life, 90% resolve
by 1 year old
• Recurrent regurgitation or vomiting
these are also possible:
heartburn, retrosternal pain, epigastric pain
• Complications (GORD)→
failure to thrive, oesophagitis,
pulmonary aspiration,
frequent otitis media (3+ episodes in 6 months)
sandifer syndrome (dystonic neck posturing, torticolis, neck extension and rotation)
131
How do we ivx GOR?
Clinical diagnosis no ivx needed
Can consider:
1. Trial of hypoallergenic feed
- excludes cows. milk protein allergy
2. 24hr Esophogeal PH if:
patients with severe symptoms, or who have failed to improve with anti-reflux medication
132
How do we manage GOR?
1. Reassure
Give advice about GOR and reassure parents and carers that in well infants, regurgitation of feeds:
is very common (it affects at least 40% of infants)
• usually begins before the infant is 8 weeks old
• may be frequent (5% of those affected have 6 or more episodes each day)
• usually becomes less frequent with time (it resolves in 90% of affected infants before they are 1 year old)
• does not usually need further investigation or treatment.
2. Safety net
Advise them to return for review if any of the following occur:
• the regurgitation becomes persistently projectile
• there is bile-stained (green or yellow-green) vomiting or haematemesis (blood in vomit)
• there are new concerns, such as signs of marked distress, feeding difficulties or faltering growth
• there is persistent, frequent regurgitation beyond the first year of life.
Also:
1- If breastfed - trained professional to conduct breastfeeding assessment
2- Formula fed; reduce amount if excessive
- recommend 150ml/kg body weight over 24h (MUST know how to calculate if baby over feeding)
- try smaller, more frequent feeds +/- Gaviscon (antacid) if <1yr
- Try a thickened formula (eg Enfamil)
3 -Upright positioning after feeds (not with sleep) – 30deg
- Paeds referral
- Admit if haematemesis, dysphagia, melaena
PPIs or H2 antagonists (NICE 2021):
- Don't give if Reflux is only symptom
- Give if unable to tell you about their symptoms eg baby/disabled
- Give if the following are present:
A. unexplained feeding difficulties (for example, refusing feeds, gagging or choking)
B. distressed behaviour
C. faltering growth
Surgical:
Nissens Fundoplication - in cases where there is a hiatus hernia
133
what could the following red flags in a regurgitating child mean and what are the next steps:
Onset of regurgitation and/or vomiting after 6 months old or persisting after 1 year old
Late onset suggests a cause other than reflux, for example a urinary tract infection
Next:
Urine microbiology investigation
Specialist referral
134
what could the following red flags in a regurgitating child mean and what are the next steps:
Blood in stool /haematochezia
May suggest a variety of conditions, including
bacterial gastroenteritis - salmo, campy
infant cows' milk protein allergy
Intussusception (red current jelly/ mucus stool)
Meckle's diverticulum (fresh painless PR bleed)
Next:
Stool microbiology investigation
Specialist referral
135
what could the following red flags in a regurgitating child mean and what are the next steps:
Abdominal distension, tenderness or palpable mass
May suggest intestinal obstruction or another acute surgical condition
Next:
Paediatric surgery referral
136
what could the following red flags in a regurgitating child mean and what are the next steps:
Chronic diarrhoea
May suggest cows' milk protein allergy
next :
specialist referral
137
what could the following red flags in a regurgitating child mean and what are the next steps:
Bile-stained (green or yellow-green) vomit
Intestinal obstruction
Next:
Paediatric surgery referral
138
what could the following red flags in a regurgitating child mean and what are the next steps:
Vomiting at end of paroxysmal coughing
whooping cough
139
what could the following red flags in a regurgitating child mean and what are the next steps:
Haematemesis
Oesophagitis, peptic ulcer
140
what are the risk factors for GOR?
* premature birth
* parental history of heartburn or acid regurgitation
* obesity (advise weight loss)
* hiatus hernia
* history of congenital diaphragmatic hernia (repaired)
* history of congenital oesophageal atresia (repaired)
* a neurodisability.
141
what is infant colic ? presentation?
Episodes of crying for more than 3 hours pay day
for more than 3 days a week, for 3 weeks in an otherwise healthy child.
Usually occurs in the evening and in First few months of life
• Affects up to 40% of babies
• Paroxysmal (sudden attack/outburst), inconsolable, drawing up of the knees and flushed face, clenched hands (XS flatus??)
142
what is the cause of infant colic?
unknown
Thought to be multi-factorial
possibly gastrointestinal discomfort like intestinal cramping
Fewer than 5% of infants with excess crying have an underlying organic disease eg constipation of lactose intolerance
143
what are the effects of Infant Colic?
The crying can result in:
- frustration of the parents,
- depression following delivery,
- excess visits to the doctor,
- child abuse - shaken baby syndrome
144
how do we manage infant colic?
Reassure, common problem which should resolve by 6m of age:
- average baby cries just over two hours a day
Calming measures may be used:
soothing motions, limiting stimulation, pacifier use, and carrying the baby around in a carrier.
optimal winding technique,
encourage patients to look after themselves
- no evidence that these work
Breastfeeding mums:
1. Try hypoallergenic diet:
- No milk or dairy products or nuts
- best evidence of efficacy compared to everything
Formula fed mums:
o Consider 2 week trial of whey
hydrolysate formula
Medications:
2 week trial of anti-reflux tx - no evidence for these
• If persistent → consider cow’s milk protein allergy or reflux
• Support
o Self-help support group Cry-sis for families with excessive crying or sleepless children
www.cry-sis.org.uk and runs a national telephone hotline
o Get support from health visitor
o Ask family and friends for support, try
meet other parents
145
in an infant presenting with colic, which red flags should you look out for to investigate further?
Vomiting (vomit that is green or yellow, bloody or occurring more than five times a day)
Change in stool (constipation or diarrhea, especially with blood or mucous)
Abnormal temperature
Irritability (crying all day with few calm periods in between)
Lethargy (excess sleepiness, lack of smiles or interested gaze, weak sucking lasting over six hours)
Poor weight gain (gaining less than 15 grams a day)
146
What is the aetiology of coeliac?
Autoimmune disorder that primarily affects the small intestine.
Coeliac disease is caused by a reaction to gluten
causing inflammatorry response that causes the damage
This often begins between six months and two years of age.
147
what sign may be seen on Abdominal USS for Intussusception?
target or doughnut sign
148
what is gold standard ivx for Meckles diverticulum?
Technitium scan
149
define prolonged jaundice?
>14 days in term baby
| >21 days preterm
150
what is the purpose of phototherapy in neonatal jaundice?
helps convert unconjugated bilirubin into an isomer that is easily excreted
151
heinz bodies on blood film may be seen in which condition?
G6PD deficiency
152
what are some trtiggers for jaundice in G6PD to tell parents?
anti-malarias
antibiotics like sulphonamides
153
still to do
meckle diverticulum
| intussuception
154
How is Ulcerative Colitis managed?
Mild UC:
1 - Oral 5-ASA
o Continue as maintenance if no relapse
1B - Relapse = use oral prednisolone and taper
§ If they relapse with steroids, then it is called steroid dependent disease
• Moderate UC:
1 - Oral prednisolone for 2-4wks and taper
1B - If good response -> Oral 5-ASA for maintenance
o If relapse frequent, then steroid dependent disease ->
Steroid dependent disease:
o #1: Thiopurine or infliximab
o If successful continue with medication as maintenance
-> if not surgery
• Severe UC - Medical emergency
o High dose IV Methylprednisolone
o Antibiotics + Parenteral nutrition until improvement or surgery
