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Paediatrics > Gastrointestinal II > Flashcards

Gastrointestinal II Flashcards

1
Q

When should GORD be suspected in an infant (up to 1 year old)?

A

Regurgitation + at least one of:
- Distressed behaviour whilst feeding (arched back, unusual neck postures)
- Hoarseness and/ or chronic cough
- Single episode of pneumonia
- Unexplained feeding difficulties (refusing to feed, gagging, choking etc)
- Faltering growth

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2
Q

What additional features of GORD may children >1 present with?

A
  • Heartburn
  • Retrosternal pain
  • Epigastric pain
  • Episodic torticollis
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3
Q

What are the risk factors for developing GORD in children?

A
  • Premature birth
  • Parental history of heartburn or regurgitation
  • Obesity
  • Hiatus hernia
  • Hx of congenital diaphragmatic hernia
  • Hx of congenital oesophageal atresia
  • Neurodisability (such as cerebral palsy)
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4
Q

What are the complications of GORD in children?

A
  • Reflux oesophagitis
  • Recurrent aspiration pneumonia
  • Recurrent acute otitis media (>3 episodes in 6 months)
  • Dental erosion in a child with neurodisability
  • Apnoea or apparent life-threatening events (rare)

Complications from GORD are rare

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5
Q

When is the typical onset of GORD symptoms in children?

A

Before 8 weeks, typically resolving before the child is 1

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6
Q

What is a normal level of vomiting/ regurgitation for an infant?

A

Effortless spitting up of one to two mouthfuls

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7
Q

What examinations should be done in suspected GORD?

A
  • Chest examination for respiratory complications
  • Temperature
  • Abdominal palpatoion
  • Growth assessment using centile charts
  • Review of head circumference to exclude alternative explanation of vomiting
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8
Q

What differentiates CMPI from GORD?

A
  • Dermatological features eg. eczema
  • Chronic diarrhoea
  • Patient has/ is at high risk of atopy
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9
Q

What differentiates pyloric stenosis from GORD?

A

Frequent, forceful vomiting and the child is very hungy and keen to feed

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10
Q

What differentiates intestinal obstruction from GORD?

A
  • Bile-stained vomit
  • Abdominal distention, tenderness or palpable mass
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11
Q

What differentiates raised ICP from GORD?

A
  • Bulging fontanelle or altered responsiveness
  • Rapidly increasing head circumference, vomiting in the morning
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12
Q

When should same-day admission be arranged for a child with suspected GORD?

A
  • Haematemesis (not caused by ingested blood)
  • Melaenia
  • Dysphagia
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13
Q

When should a specialist assessment be arranged for a child with suspected GORD?

A
  • Uncertain diagnosis/ red flag sx suggesting a more serious condition
  • Persistent, faltering growth
  • Unexplained distress in children with communication difficulties
  • Sx not responding to treatment
  • Feeding aversion + hx of regurgitation
  • Unexplained iron deficiency anaemia
  • No improvement in sx after 1 year of age
  • Suspected Sandifer’s syndrome (episodic torticollis)
  • Complications from GORD
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14
Q

How should breastfed infants with frequent regurgitation be managed in primary care?

A

Conservative:
- Breastfeeding techniques
- Positioning after feeds (30 degree head-up)

Medical:
- 1-2 weeks alginate therapy
- If sx improve, continue with treatment, stop at regular intervals (eg. every 2 weeks) to see if sx have improved and whether it’s possible to stop tx

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15
Q

How should formula fed infants with GORD be treated in primary care?

A

Conservative:
- Review feeding hx
- Reduce volumes of feeds if they’ve excessive for the child’s weight
- Reduce volume but increase frequency of feeds (trial 1-2 weeks)
- If unsuccessful, offer 1-2 weeks of feed thickeners/ pre-thickened formula

Medical:
- If all else unsuccessful, 1-2 weeks of alginate (should not be used at the same time as thickening agents)

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16
Q

What is the managment of breast or formula fed infants with GORD for whom alginate therapy has been unsuccessful?

A

4-week PPI eg. omeprazole suspension or histamine-2 receptor antagonist (H2RA)

Should only be considered if there is:
- Unexplained feeding difficulties
- Distressed behaviour
- Faltering growth

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17
Q

What is the management for children 1-2 years who have persitent heartburn, retrosternal or epigastric pain?

A

4 week trial of PPI or H2RA

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18
Q

What is intussusception?

A

The telescoping of a segment of the bowel inside another segment, most commonly in the ileo-caecal region

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19
Q

What is the peak age incidence of intussusception?

A

6-36 months

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20
Q

What are the risk factors associated with intussusception?

A
  • Age (6-36 months)
  • Sex (males 2:1)
  • Anatomical lead points: polyps, Meckel’s diverticulum, tumours or other structural abnormalities
  • Infections: lymphoid hyperplasia (lymphoid tissue in Peyer’s patches is particularly sensitive to viral infections)
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21
Q

What is the triad of intussusception?

A
  • Colicky abdominal pain
  • Vomiting
  • Red ‘currant jelly’ stools

Complete triad is rarely present

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22
Q

What are the signs and sx of intussusception?

A
  • Intermittent severe, crampy abdo pain (worse during peristalsis), may lead to children drawing knees up
  • Lethargy/ altered consciousness
  • Vomiting: initially non-bilious but can progress to bilious as obstruction worsens
  • Palpable abdominal mass: RUQ/ mid-abdomen
  • Diarrhoea/ constipation
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23
Q

What are the investigations for suspected intussusception?

A
  • Abdominal USS (first line): target sign
  • Abdominal x-ray: may show signs of bowel obstruction or soft tissue mass (normal x-ray doesn’t rule out intussusception)
  • Contrast enema: ‘coiled spring’/ ‘crescent’ sign
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24
Q

In which patient groups with suspected intussusception should contrast enemas not be performed in?

A

Patients that are unstable with signs of perforation or peritonitis

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25
Q

What is the non-operative management for intussusception?

A

Air/ liquid enema under fluoroscopic/ ultrasound guidance

Should only be performed in stable patients without signs of perforation, ischaemia or peritonitis

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26
Q

What is the surgical intervention for intussusception?

A

Performed if non-operative reduction is unsuccessful, contraindicated or the patient presents with complications requiring emergency surgery

  • Manual reduction or bowel resection if non-viable bowel segments are identified
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27
Q

What is the supportive care for intussusception?

A
  • IV fluids
  • Electrolyte management
  • Pain control
28
Q

What are the complications of intussusception?

A
  • Bowel ischaemia/ necrosis
  • Bowel perforation
  • Recurrence (10%, most within 24-48 hours)
  • Short bowel syndrome in cases with extensive bowel resection
29
Q

Which factors increase the risk of recurrence of intussusception?

A
  • Younger age
  • Shorter duration of sx
  • Presence of anatomical lead points
30
Q

What is mesenteric adenitis?

A

An inflammatory condition primarily involving mesenteric lymph nodes of the abdomen and a common mimic of appendicitis

31
Q

Which patient groups does mesenteric adenitis commonly affect?

A

Children and adolescents, typically following URTI

32
Q

Which viruses are commonly associated with mesenteric adenitis?

A
  • EBV (most common viral trigger)
  • Adenoviruses
  • Enteroviruses
33
Q

Which bacteria are most commonly associated with mesenteric adenitis?

A
  • Yersinia enterocolitica (contaminated food or water)
  • Yersinia pseudotuberculosis (contaminated food or water)
  • Campylobacter (uncooked poultry or unpasteurised milk)
34
Q

What is the typical pattern of mesenteric adenitis occurance?

A
  1. Infection (usually URTI)
  2. Infection clears
  3. Mesenteric adenitis develops - indicating a reactive process rather than ongoing infection of mesenteric lymph nodes themselves
35
Q

How does mesenteric adenitis present?

A
  • Diffuse abdominal pain (often mistaken for appendicitis)
  • Low-grade fever
  • Generalised abdominal tenderness
  • Pharyngitis/ sore throat
35
Q

What are the investigations for mesenteric adenitis?

A
  • FBC: typically normal
  • US abdomen: enlarged mesenteric lymph nodes and normal appendix
36
Q

What is the management of mesenteric adenitis?

A
  • Observation and reassurance (usually self limiting)
  • Surgical intervention if appendicitis absolutely can’t be ruled out
37
Q

Which areas are most commonly affected in necrotising enterocolitis?

A
  • Terminal ileum
  • Colon
38
Q

What is the pathophysiology of necrotising enterocolitis?

A

Unknown, but in preterm infants theroised:
- Immature GI tract (impaired intercellular junction integrity and mucosal barriers)
- Triggering event leading to normal intestinal microbiome dysbiosis
- Increased pathogenic bacterial growth
- Exaggerated immune response
- Tissue injury –> necrosis

Term infants:
- Underlying condition

39
Q

What are the risk factors for necrotising enterocolitis?

A
  • Prematurity <32 weeks
  • Low birth weight
  • Dysbiosis contributing interventions (abx, acid-reducing agents, bovine milk formula)
  • Infection
  • Underlying conditions (fetal growth restriction, GI disorders etc)
40
Q

What are the compliactions of necrotising enterocolitis?

A
  • Bowel perforation: sepsis, ileus, respiratory failure, coagulopathy
  • Increased risk of neurodevelopmental impairment (systemic inflammation)
  • Death
41
Q

What are the signs and symptoms of necrotising enterocolitis?

A
  • Feeding intolerance
  • Abdominal distension, tenderness
  • Vomiting (often bilious), bilious drainage from enteral feeding tubes
  • Hematochezia
  • Non-specific findings: temperature instability, lethargy, apnea
42
Q

What are the investigations and results for necrotising enterocolitis?

A

Bedside
- Abdominal examination

Bloods
- Blood cultures: positive
- Thrombocytopaenia
- Anaemia
- DIC
- Increased serum lactate

Imaging
- Abdominal x-ray (supine, first line imaging)
- Abdominal ultrasound

43
Q

What is seen on x-ray in necrotising enterocolitis?

A
  • Dilated bowel loops
  • Bowel wall oedema
  • Pneumatosis intestinalis (gas in the bowel wall)
  • Portal venous gas
  • Pneumoperitoneum (gas in the peritoneum)
  • Rigler sign (air inside and outside the bowel wall)
  • Air outlining the falciform ligament (football sign)
44
Q

What’s the management of necrotising enterocolitis?

A

Medical
- Supportive
- Cessation of oral feeding
- Broad spectrum abx
- Gastric aspiration (NG decompression)
- Total parenteral nutrition

Surgical
- Resection of necrotic bowel and creation of proximal enterostomy
- Re-anastamosis delayed until the infant has recovered

45
Q

What are the indications for surgery in necrotising enterocolitis?

A
  • Bowel perforation
  • Portal venous gas
  • Fixed dilated loop on serial x-rays
  • Abdominal wall erythema
  • Rapid deterioration
46
Q

When can oral feeds be re-started in necrotising enterocolitis?

A

7-10 days after pneumatosis clears

47
Q

What are the complications of surgery in necrotising enterocolitis?

A
  • Short bowel syndrome
  • Strictires
  • Stoma related complications
  • Infection (abscess)
48
Q

What is biliary atresia?

A

Obliteration of discontinuity within the extrahepatic biliary system, resulting in obstruction of the flow of bile

49
Q

What is the pathogenesis of biliary atresia?

A

Unclear, however theorised:
- Infectious agents causing inflammation
- Congenital malformation
- Retained toxins within the bile

50
Q

What is the epidemiology of biliary atresia?

A
  • Females > males
  • Neonates
  • 1/10-15,000 births
51
Q

What are the types of biliary atresia?

A
  • Type 1: proximal ducts are patent, common duct is obliterated
  • Type 2: atresia of the cycstic duct and cystic structures are found in the porta hepatis
  • Type 3: atresia of the left and right ducts to the level of the porta hepatis (>90% biliary atresia)
52
Q

How does biliary atresia present?

A

First few weeks of life:
- Jaundice (extending beyond physiological 2 weeks)
- Dark urine, pale stools (obstructive)
- Appetite and growth disturbances

53
Q

What are the signs of biliary atresia?

A
  • Jaundice
  • Hepatomegaly with splenomegaly
  • Abnormal growth
54
Q

What are the investigations and results for biliary atresia?

A

Bedside
- Abdominal examination

Bloods
- Serum bilirubin (including conjucated and total): total may be normal, conjugated will be high
- LFTs: usually raised (can’t differentiate between biliary atresia and other causes of neonatal cholestasis)
- Serum alpha 1-antitrypsin: deficiency can cause neonatal cholestasis
- Sweat chloride test: CF often involves biliary tract

Imaging
- USS biliary tree and liver: distention and tract abdnormalities
- Percutaneous liver biopsy with intraoperative cholangioscopy

55
Q

What is the managment of biliary atresia?

A

Definitive
- Surgical intervention (Kasai procedure): removal of defective ducts and anastamosis of small intestine segment to liver, creating path from bile to small intestine

Medical
- Abx coverage
- Bile enhancers

56
Q

What are the complications of biliary atresia?

A
  • Progressive liver disease (whilst surgery will increase bile drainage, 80% patients will need a liver transplant by 20 years old)
  • Unsuccessful anastamosis formation
  • Cirrhosis with eventual hepatocellular carcinoma
57
Q

What’s the prognosis of biliary atresia?

A
  • Generally good if the surgery is successful - 80% of patients need liver transplant by 20
  • In failed surgery, liver transplant might be required by 2 years old
58
Q

At what age does pyloric stenosis usually present?

A

In the 2nd - 4th week of life as babies are born with a normal pylorus

Rarely may present later at up to 4 months

59
Q

What is the pathophysiology of pyloric stenosis?

A

Hypertrophy and hyperplasia of the circular muscles of the pylorus

60
Q

What is the epidemiology of pyloric stenosis?

A
  • 4/1,000 live births
  • 4x more common in males
  • 10-15% positive family history
  • First borns more commonly affected
  • Has been associated with exposure to macrolide abx
61
Q

What are the features of pyloric stenosis?

A
  • Projectile non-biliouis vomiting, typically 30 mins after feeding
  • Child is extremely hungry and eager to feed
  • Constipation and dehydration
  • Palpable mass in RUQ (olive shaped)
  • Hypochloraemic, hypokalaemic alkalosis
  • Visible peristalsis (hypertrophy of the walls of the stomach)
62
Q

Why is a hypochloraemic, hypokalaemic alkalosis present?

A
  • Persistent vomiting leads to loss of HCl (hypochloraemia)
  • Dehydration leads to retention of Na+ and excretion of K+ (hypokalaemia)
  • Hypokalaemia leads to intracellular shift of H+ and extracellular release of K+ (alkalosis)
63
Q

What is the diagnostic investigation for pyloric stenosis?

A

Abdominal ultrasound

64
Q

What is the management of pyloric stenosis?

A

Ramstedt’s pyloromyotomy

Paediatrics (16 decks)

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