Abdominal Flashcards

1
Q

What are the Ix for neonatal jaundice?

A

Bedside: Full neonatal examination, Set of basic observations + generation of PEWS score
Weigh the baby
Urine dip

Bloods:
Measure bilirubin:
Measure using transcutaneous bilirubinometer if:
>35 GA
Jaundice develops after first 24h

Measure serum bilirubin if:
TCB is >250 mmol/L
<35 GA
Jaundice develops before first 24h
Plot bili on NICE treatment threshold graph and monitor

Assess risk of kernicterus
Increased if serum bili >340 mmol/L in babies >37 GA, rapidly rising of >8.5 mmol/L per hour or clinical feature of encephalopathy
Measure every 6 hours until it drops below Tx threshold

Investigate underlying cause
FBC - Heamatocrit (<45% indicates haemolytic anaemia)
G&S of mother and baby - did she receive anti D
Blood film
G6P levels
LFTs for congenital infection
Cultures of blood/urine/CSF

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2
Q

What is the Mx for neonatal jaundice?

A

Treatment - bili can enter the brain at this level so is important to treat
Admit if:
Features of encephalopathy (via 999 ambulance if in primary care)
Jaundice within less than 24 hours of age (within 2 hours)
Within 6 hours:
First appears at more than 7 days of age
Unwell neonate (lethargy, fever, vomiting)
GA <35 weeks
Prolonged jaundice. GA < 37 and 21 days or GA > 37 and 14 days
Poor feeding/weight loss >10%
Pale stools, dark urine
1) IV fluids and Abx
2) Phototherapy - dependent on NICE treatment threshold chart. special blue light that shines on the skin and changes the bilirubin into a product that baby will be able to break down easily.
3) Exchange transfusion - type of blood transfusion where a small amount of baby’s blood would be replaced from a matching donor through a thin plastic tube.

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3
Q

What are the causes of neonatal jaundice and how would you distinguish between them?

A

<24 hours life: PATHOLOGICAL
Haemolysis
Rh haemolytic disease - usually identified antenatally, if severe will be anaemic, hepatosplenomegaly and hydrops
ABO incompatibility - less severe, no hepatosplenomegaly, positive DAT/Coombs test
G6PD deficiency - common in Greece, certain medications and food groups to be avoided
Hereditary spherocytosis
Pyruvate kinase deficiency
Congenital infection - TORCH (esp CMV)

2 days - 2 weeks:
Physiological - no underlying cause
Breast milk jaundice - unconjugated
Dehydration - unconjugated
Infection - unconjugated, poor intake, haemolysis, deranged LFTs, increase in enterohepatic circulation (UTI, GBS)
Polycythaemia/bruising (esp after ventouse)
Crigler-Najjar syndrome (deficient or absent UGT enzyme)

>2 weeks
Upper GI obstruction e.g pyloric stenosis (conjugated)
Bile duct obstruction e.g. biliary atresia (conjugated)
Infection e.g. neonatal hepatitis (conjugated)
Congenital hypothyroidism

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4
Q

What are the Ix for Coeliac disease?

A

Bedside: Abdo Exam: Distended abdomen, buttock wasting, No tenderness, masses, or other signs
Examine shins
Height and weight - BMI
Bloods: FBC – microcytic anaemia, Bone chemistry –
B12, Folate + iron studies, (Anti-gliadin antibodies, anti-endomysial antibodies), and anti-TTG antibodies
IgA tissue transglutaminase (TTG) serological test of choice
Imaging/special: If positive anti- TTG demonstrate flat mucosa on jejunal biopsy on endoscopy
to confirm diagnosis

Other: Must have clinical improvement on dietary gluten withdrawal and exhibit catch-up growth for full diagnosis

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5
Q

What is the Mx for Coeliac disease?

A

1) Gluten-free diet for life (reduces symptoms and malignancy risk) -> ‘free from’ -> some patients able to get staple products on prescription
2) Contact GP. MDT approach with support from specialist paediatrician, dietician, GP, school.
3) Lifelong follow-up to monitor for associated conditions - malnutrition - BMI. Annual GP reviews.
AI disorders e.g. thyroid disease, pernicious anaemia
Small bowel malignancy (esp. lymphoma)
Osteoporosis - DEXA scan
4) Patient education - signpost leaflets and NHS choices website

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6
Q

What are the Ix for intussception?

A

Bedside: Abdominal examination - RUQ sausage-shaped mass, distended abdomen, findings of peritonitis, Obs + PEWS
Bloods: FBC - Hb check for anaemia, WBC to rule out gastroenteritis
Imaging: Abdominal X-ray
Abdominal US - donut - target sign present

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7
Q

What are the Mx for intussception?

A

A - airways
B - breathing
C - circulation
D - disability
E - exposure

1) Admit + Notify surgical team early + involve seniors
2) Fluid resuscitation
3) Air contract enema + radiological sir insufflation (if failure/bowel perforation/peritonitis/shock -> surgery)

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8
Q

What are the signs and sx of intussception?

A

Most commonly occurs in infants 5-12 months of age.
The “classical triad” of symptoms include vomiting, (red-currant jelly) bloody stools and abdominal pain (colic). Bloody stools are rather a late symptom and vomiting can be absent.

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9
Q

What are other differentials for intussception?

A

Coeliac disease
Gastroenteritis
Appendicitis

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10
Q

What are differentials for a chronic abdominal pain with bloody diarrhoea picture?

A

Crohn’s disease
Coeliac disease
Gastritis/peptic ulcer disease
UC?
UTI

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11
Q

What are the extra-intestinal manifestations of crohn’s disease?

A
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12
Q

What investigations would you like to do in a child with chronic abdominal pain and bloody diarrhoea?

A

Bloods: FBC, CRP, Check the serum immunoglobulin (Ig)A tissue transglutaminase antibody (tTGA) and total IgA first-line (coeliac), faecal calprotectin, stool MC&S for H. pylori

Imaging: Abdominal X-ray - dilated loops of bowel with strictures (crohn’s)

Other: colonoscopy with biopsy (crohn’s: inflammed bowel with strictures, skip lesions); endoscopy for coeliac disease, ask height, weight and plot on growth chart to find out how growth has been affected

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13
Q

How would you manage a child with Crohn’s disease?

A

Lifestyle: Nutritional therapy - whole protein modular feeds for 6-8/52 (if fails give steroids)

Medications: Immunosuppressants - Azathioprine, 5-mercaptopurine, methotrexate, mesalazine/sulphalazine, anti-TNF (infliximab, adalimumab, golimumab, certozimumab, etanercept)

Consider enteral feeding if growth failure persists

Regular follow up monitoring - once monthly and management using and MDT approach - paediatrician, IBD nurse, dietician, psychologist

Support groups

Involve my seniors and check guidelines

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14
Q

What are the complications of crohn’s disease?

A

Bowel obstruction, fistulae, abscess, severe local disease requiring surgery (carries it’s own risks - short bowel syndrome, malodourous diarrhoea, vitamin and mineral malabsorption)

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15
Q

When a child is in remission with crohn’s what would monitor them for?

A

Once monthly monitoring - looking at Thiopurine methyl transferase (TPMT) before giving azathioprine and neutropenia in those taking azathioprine/mercaptopurine (bone marrow suppression)

Monitor bloods for anaemia

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16
Q

What are some specific investigations to do when cows milk protein intolerance/allergy is suspected?

A

Diagnosis is often clinical (e.g. improvement with cow’s milk protein elimination). Investigations include:

skin prick/patch testing

total IgE and specific IgE (RAST) for cow’s milk protein

Plotting height and weight on a growth chart and tracking centiles

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17
Q

What is the management for CMPI/A in a formula fed infant?

A

Management if formula-fed

extensive hydrolysed formula (eHF) milk is the first-line replacement formula for infants with mild-moderate symptoms

amino acid-based formula (AAF) in infants with severe CMPA or if no response to eHF

around 10% of infants are also intolerant to soya milk

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18
Q

What is the management for CMPI/A in a breastfed infant?

A

continue breastfeeding

eliminate cow’s milk protein from maternal diet. Consider prescribing calcium supplements for breastfeeding mothers whose babies have, or are suspected to have, CMPI, to prevent deficiency whilst they exclude dairy from their diet

use eHF milk when breastfeeding stops, until 12 months of age and at least for 6 months

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19
Q

When would you refer a child to a specialist paediatrician with CMPI/A?

A

If it is extremely severe

If there is evidence of failure to thrive

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20
Q

What is the prognosis of CMPI/A?

A

IgE mediated - 55% tolerant by 1 year

Non-IgE mediated most children tolerated by 3 yrs

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21
Q

How may CMPI/A present?

A

Features

regurgitation and vomiting, particularly after feeds

diarrhoea

urticaria, atopic eczema

‘colic’ symptoms: irritability, crying, drawing up legs

wheeze, chronic cough

rarely angioedema and anaphylaxis may occur

22
Q

What is the difference in the management of exomphalos and gastroschisis?

A

Exomphalos should have a gradual repair to prevent respiratory complications. Gastroschisis requires urgent correction

23
Q

What is exomphalos?

A

Exomphalos is a congenital defect of the abdominal wall resulting in intestinal herniation from the abdominal cavity. There is a peritoneal membrane around the herniated intestines. There are 2 types: Major (opening is greater than 4cm and/or with the liver inside the cord) and Minor (opening is less than 4cm and only containing the intestine).

24
Q

What is omphalocele?

A

Omphalocele (pronounced uhm-fa-lo-seal) is a birth defect of the abdominal (belly) wall. The infant’s intestines, liver, or other organs stick outside of the belly through the belly button. There is a thin membranous sac around the herniated abdominla contents.

25
Q

What is gastroschisis?

A

Gastroschisis is a defect of the abdominal wall that occurs in utero, can be detected antenatally using fetal ultrasonography, and results in herniation of abdominal contents.

In contrast to omphalocele, there is no sac covering the intestines in gastroschisis.

26
Q

How is gastroschisis managed?

A

Potential for vaginal birth

Herniated contents are wrapped in cling-flim

Immediate surgical repair - call paediatric surgical team immediately

27
Q

How is exomphalos managed?

A

Caesarian section

Transfer to specialist centre i.e. GOSH/specialist ward

Gradual staged repair if large herniation to prevent respiratory distress (increased abdominal pressure)

GOSH website advice:

Exomphalos is a serious condition so needs prompt treatment soon after birth. Children born with exomphalos are usually transferred to Great Ormond Street Hospital (GOSH) within a few hours of birth.

Immediately after birth, if the membrane covering the intestines is intact, the child will be kept warm and hydrated until they are transferred to GOSH, either to our intensive care unit or another of our specialist wards.

Depending on the size of the exomphalos, the infant may need to have it repaired in one operation or in several stages. If the exomphalos is small and the child is stable, they may have an operation soon after transfer, where the surgeon replaces the contents back inside the abdomen and closes up the base of the umbilical cord.

If the exomphalos is larger, contains the liver and/or the child needs to be stabilised, doctors may place a silo or pouch over the intestines, which is closed over a period of days to weeks, to allow the child to grow so that there is room inside the abdomen.

28
Q

How may exomphalos/gastroschisis/omphalocele be diagnosed?

A

Prenatal ultrasound scanning - this is good as it allows for the birth to be planned appropriately

29
Q

What does this picture show?

A

This is an micturating cystourethrogram showing vesicoureteric reflux. We see gross dilatation of the ureter, pelvis and calyces with ureteral tortuosity.

30
Q
A
31
Q

What is necrotising enterocolitis?

A

Inflammation of the bowel wall, progressing to necrosis and perforation.

Presents in infants with bloody stools and abdominal distension

32
Q

What is the Ix of choice for necrotising enterocolitis and what is the key feature on it?

A

Abdominal X-ray

Intramural air

33
Q

When do the nephrons begin to develop in the fetus?

A

From week 6

The baby then starts to produce urine from week 10 and full complement from week 36

34
Q

When is functional maturity of GFR reached?

A

2 years of age

35
Q

How much in a % is total body water of an adult, term neonate and premature neonate?

A

Adult - 60%

Term neonate - 75%

Premature neonate - 85%

36
Q

Why should you not start K+ requirements infusion in neonate if they are unable to produce urine?

A

Risk of hypernatraemia

37
Q

What additional factor must you always take into account when you want to use a NICE treatment threshold chart for neonatal jaundice?

A

The babies age as term and premature baby treatment thresholds vary significantly

38
Q

What is kernicterus?

A

It is a bilirubin encephalopathy which has long term neurological sequelae

39
Q
A
40
Q

How may Hirschprung’s present in a child?

A

Hirschsprung’s disease can present at birth with:

a delay in passing meconium (>48 hours)

a distended abdomen

forceful evacuation of meconium after digital rectal examination

It is also common for children with this condition to present later in childhood with a chronic history of constipation with poor response to movicol disimpaction regimens and poor weight gain.

41
Q

What is the pathophysiology of malrotation?

A

The resulting bowel obstruction in malrotation causes a buildup of gut contents, which results in profuse vomiting as nothing can get past the obstruction. As the obstruction is past the Sphincter of Oddi, the bowel contents are full of green bile and so the vomit is dark green.

42
Q

How is malrotation diagnosed?

A

Upper gastrointestinal contrast study

43
Q

How does meconium ileus present?

A

Meconium ileus presents as a delay in passing meconium (>48 hours until the baby’s first poo) and can present with signs of obstruction (bilious green vomiting).

44
Q

How is meconium ileus diagnosed?

A

Abdominal X-ray

Meconium ileus is diagnosed with abdominal X-ray, which shows characteristic findings of a ‘bubbly’ appearance of the intestines with a lack of air-fluid levels.

45
Q

How is meconium ileus managed?

A

Meconium ileus is managed with ‘drip and suck’ (stomach drainage with an NG ryles tube, and IV fluids), along with enemas to remove the sticky meconium. In severe cases, surgery may be necessary.

46
Q
A
47
Q

Define oesophageal atresia

A

Oesophageal atresia describes a blind-ending oesophagus. It is more common in trisomies – Downs/Pataus/Edwards

48
Q

Define GORD/GERD

A

Gastro-oesophageal reflux (GOR) is the passage of gastric contents into the oesophagus. It is considered physiological in infants when symptoms are absent or not troublesome.

GORD is the pathological version when symptoms are present and troublesome.

49
Q

What is the management of GORD?

A

Management of GORD in infants can be conservative (advice on keeping baby upright and burping after feeds, put their cot on a slight incline for sleeping), medical (infant gaviscon, omeprazole) and even surgical in severe cases (fundoplication).

50
Q

What rash is associated with coeliac disease?

A

Dermatitis herpetiformis

51
Q

Define coeliac disease

A

Coeliac disease is an autoimmune condition in which the immune system reacts to protein component of gluten (gliadin) and attacks the small bowel.

52
Q

When is a child classed as overweight or obese?

A

Overweight: >91st centile for BMI

Obese: >98th centile for BMI