Gastro Flashcards
How does malrotation present? Ivx?
• 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)
How is malrotation managed?
- Urgent laparotomy – Ladd’s procedure if signs of vascular compromise
- Untwist volvulus, mobilize duodenum, place bowel in non-rotated position and remove necrotic bowel
What is IBS? How does it present?
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
How could we ivx IBS?
FBC - normal
Tests to rule out other dfx:
Fecal occult blood - normal. Positive in IBD or CC
Etc
How is IBS treated?
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
What is the variation in presentation of gastroenteritis based on pathogen of aetiology?
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)
What is the presentation of gastroenteritis?
Diarrhoea plus or minus vomiting
Define acute diarrhoea?
3+ stools in 24 hours
Lasts for up to 2 weeks
Stools liquid or semi liquid
How do we manage gastroenteritis?
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!
How may coeliac disease present in kids?
• 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
How do we ivx coeliac in kids?
• 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
How do we Mx coeliac in kids?
• 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
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?
Toddler diarrhoea
Relieve symptoms with increased fiber and fat in diet – whole milk, yoghurts, cheeses
• Avoid fruit juice and squash
How does ulcerative colitis present and how is it ivx?
- 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
How we Mx coeliac? Complications?
- 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
How does Hirschsprung disease present?
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!!
What is the aetiology of Hirschsprung?
complications ?
• 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
How is Hirschsprung ivx?
- 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
How is Hirschsprung managed?
prognosis?
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%
What is the aetiology of necrotising enterocolitis?
Unknown but risk factors include: premature, LBW
Most common surgical emergency in newborn babies
How does necrotising enterocolitis present? What will ivx show?
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
How is necrotising enterocolitis Mx? Complications?
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
What condition is clinically indistinguishable from appendicitis? Mx?
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
What is the staging system for necrotising enterocolitis? What are the signs and sx in each stage?
And what do ivx show?
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
What is NEC?
Inflammation of the bowel that may lead to bowel damage to the extent where parts of the bowel dies.
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
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
How do we manage Chrons in kids?
- 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
- • 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
- Surgery
- If disease limited to distal ileum
• Surgery for complications – obstruction, fistula, abscess, severe localized disease unresponsive to Tx
• SUPPORT→www.chronsandcolitis.org.uk
Chrons and UC are examples of?
Inflammatory bowel disease
Define ulcerative colitis
• Recurrent, inflammatory and ulcerating disease involving the mucosa of the colon
How does ULCERATIVE COLITIS present?
- Classic presentation is rectal bleeding, diarrhea, abdo pain
- weight loss and growth failure +/- erythema nodusum, arthritis
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
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
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
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
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):
- 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
- 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
What is ENCOPRESIS? Rx?
Involuntary passing of stools into clothes
Usually fluid overflow on background of constipation
Just as with constipation
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
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
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
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
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.
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
How does LACTOSE INTOLERANCE present?
• Wind, diarrhea, bloating with lactose ingestion, abdo rumblings and pain
Failure to thrive, tiredness, eczema
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)
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
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
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
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
What are the cause of NEONATAL JAUNDICE by time of presentation?
What is the definition?
Definition: bilirubin > 85 micromol/L
- Physiological: unconjugated aka indirect hyperbilirubinaemia
- 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
- 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)
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
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;
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)
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
- 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
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
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)
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
What is the most common cause of prolonged (>2weeks) unconjugated hyperbilirubinaemia in kids?
Breast milk jaundice
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
How would we manage conjugated hyperbilirubinaemia?
Treat the cause directly
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)
