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Yr 4 - Paediatrics > GI: Intussusception, Mesenteric Adenitis & Functional Abdo Pain & Diarrhoea > Flashcards

GI: Intussusception, Mesenteric Adenitis & Functional Abdo Pain & Diarrhoea Flashcards

1
Q

What is intussusception?

A

A potentially life-threatening condition in which a segment of the intestine telescopes into an adjacent segment, causing bowel obstruction and potentially compromised blood flow.

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2
Q

What is the most common cause of intestinal obstruction in infants and young children?

A

Intussusception

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3
Q

Peak age incidence of intussusception?

A

6 months - 36 months

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4
Q

Causes of intussusception?

A

Majority of cases of idiopathic.

Some risk factors:
- Age
- Male sex
- Anatomical lead points e.g. polyps, Meckel’s diverticulum, tumours etc
- Infection e.g. viral or bacterial gastroenteritis

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5
Q

How can viral or bacterial gastroenteritis increase risk of intussusception?

A

Due to the enlargement of lymphoid tissue in the bowel wall.

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6
Q

What is the classic triad of features of intussusception?

A

1) Colicky abdo pain
2) Vomiting
3) ‘Redcurrant jelly’ stools (due to presence of blood and mucus)

Note - this complete triad is present in only a minority of cases.

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7
Q

Signs and symptoms of intussusception?

A
  • Colicky abdominal pain
  • Vomiting
  • Red ‘currant jelly’ stools
  • Lethargy or altered level of consciousness
  • Palpable abdominal mass
  • Diarrhoea or constipation
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8
Q

How may children react during pain episodes in intussusception?

A

Children may draw their knees up to their chest during pain episodes.

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9
Q

How does vomiting progress in intussuception?

A

Initially non-bilious, which can progress to bilious as the obstruction worsens.

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10
Q

What may be felt in the abdomen in intussusception?

A

A sausage-shaped mass may be palpable in the RUQ or mid-abdomen.

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11
Q

1st line imaging investigation in suspected intussuception?

A

Abdo US

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12
Q

What can an abdo US show in intussuception?

A

Characteristic ‘target sign’ or ‘doughnut sign,’ representing the telescoping bowel segments.

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13
Q

Management of intussusception?

A

Depends on the patient’s clinical stability and the presence of complications.

Options:

1) Non-operative reduction
2) Surgical intervention
3) Supportive care

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14
Q

When may non-operative reduction be indicated in intussusception?

A

In stable patients without signs of bowel perforation, ischemia, or peritonitis.

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15
Q

What happens in non-operative reduction of intussusception?

A

Therapeutic enemas can be used to try to reduce the intussusception. Contrast, water or air are pumped into the colon to force the folded bowel out of the bowel and into the normal position.

Can be both diagnostic and therapeutic, achieving a reduction of the intussusception in the majority of cases.

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16
Q

When is surgical intervention indicated in intussuception?

A
  • If non-operative reduction is unsuccessful or contraindicated
  • If patient presents with complications (e.g., perforation, peritonitis)
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17
Q

What are some key complications of intussusception (if delay in diagnosis and intervention)?

A
  • Bowel ischaemia and necrosis
  • Bowel perforation (and sepsis)
  • Recurrence
  • Short bowel syndrome
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18
Q

What is short bowel syndrome?

A

In cases requiring extensive bowel resection, short bowel syndrome can develop, leading to long-term nutritional and digestive issues.

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19
Q

What conditions is intussusception associated with?

A
  • Concurrent viral illness
  • Henoch-Schonlein purpura
  • Cystic fibrosis
  • Intestinal polyps
  • Meckel diverticulum
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20
Q

What is mesenteric adenitis?

A

inflamed lymph nodes within the mesentery.

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21
Q

What can mesenteric adenitis cause similar symptoms to?

A

Appendicitis

22
Q

What does mesenteric adenitis typically follow?

A

Viral infection

23
Q

management of mesenteric adenitis?

A

No treatment needed

24
Q

Presentation of mesenteric adenitis?

A

RLQ pain

25
Q

What is functional abdominal pain (FAP)?

A

Persistent stomach pain that does not resolve with usual therapeutic treatment.

The pain may be constant or may come and go.

26
Q

Who is FAP more common in?

A

Children and young people

27
Q

A child with functional abdominal pain may also suffer from multiple, interrelated problems.

What are some examples?

A

1) heightened sensitivity to light, sound, or diet

2) fatigue or sleep disorders

3) anxiety and depression

4) headaches

5) nausea

6) joint pain

28
Q

Symptoms of FAP?

A
  • diarrhoea or constipation or both
  • abdo pain
  • indigestion
  • abdominal pain with bowel movements
  • feeling full after eating a small amount of food
  • N&V
29
Q

Give some causes of diarrhoea in children

A

Acute:
- gastroenteritis

Chronic:
- cow’s milk intolerance
- toddler diarrhoea
- coeliac disease
- post-gastroenteritis lactose intolerance

30
Q

What is the most common cause of chronic diarrhoea in infants in the developed world?

A

Cow’s milk intolerance

31
Q

Describe stools in toddler diarrhoea

A

Stools vary in consistency, often contain undigested food

32
Q

What are the ‘four F’s’ for Toddler diarrhoea?

A

Fat –> Children should NOT eat a low fat diet. Fat slows the digestion in the gut (good).

Fruit juices –> The immature gut cannot absorb fructose easily (can irritate gut).

Fibre –> Increase fibre intake.

Fluid –> Increase fluid intake and reduce sugary drinks.

33
Q

What is Hirschsprung’s disease?

A

A congenital condition where nerve cells of the myenteric plexus are absent in the distal bowel and rectum.

The myenteric plexus, also known as Auerbach’s plexus, forms the enteric nervous system. It is the brain of the gut.

34
Q

What is the myenteric plexus?

A

This nerve plexus runs all the way along the bowel in the bowel wall, and is a complex web of neurones, ganglion cells, receptors, synapses and neurotransmitters.

It is responsible for STIMULATING PERISTALSIS of the large bowel.

Without this stimulation the bowel looses it’s motility and stops being able to pass food along its length.

35
Q

What is the key pathophysiology in Hirschsprung’s disease?

A

The absence of parasympathetic ganglion cells.

During fetal development these cells start higher in the GI tract and gradually migrate down to the distal colon and rectum.

Hirschsprung’s occurs when the parasympathetic ganglion cells do not travel all the way down the colon, and a section of colon at the END is left without these parasympathetic ganglion cells.

The aganglionic section of colon does not relax, causing it to becomes constricted.

This leads to loss of movement of faeces and obstruction in the bowel. Proximal to the obstruction the bowel becomes distended and full.

36
Q

The length of colon without innervation in Hirschsprung’s varies between patients from a small area to the entire colon.

What is it called when the entire colon is affected?

A

Total colonic aganglionosis.

37
Q

What is a key symptom of Hirschsprung’s?

A

Constipation

38
Q

Hirschsprung’s disease usually occurs in isolation, however it is associated with a number of other syndromes.

What are some examples?

A
  • Downs syndrome
  • Neurofibromatosis
  • Waardenburg syndrome
  • Multiple endocrine neoplasia type II
39
Q

What is Waardenburg syndrome?

A

a genetic condition causing pale blue eyes, hearing loss and patches of white skin and hair

40
Q

Presentation of Hirschsprung’s?

A
  • Delay in passing meconium (more than 24 hours)
  • Chronic constipation since birth
  • Abdominal pain and distention
  • Vomiting
  • Poor weight gain and failure to thrive
41
Q

What is Hirschsprung-associated enterocolitis (HAEC)?

A

Inflammation and obstruction of the intestine occurring in around 20% of neonates with Hirschsprung’s.

This is life threatening as can lead to toxic megacolon and perforation of the bowel.

42
Q

When does HAEC typically present?

A

Within 2-4 weeks of birth

43
Q

How does HAEC typically present?

A
  • fever
  • abdo distension
  • diarrhoea (often with blood)
  • features of sepsis
44
Q

What can HAEC lead to?

A

Toxic megacolon and perforation of the bowel.

45
Q

Management of HAEC?

A

Urgent Abx, fluid resuscitation and decompression of the obstructed bowel

46
Q

How does Hirschsprung’s typically present in the neonatal period?

A

failure or delay to pass meconium

47
Q

What are 2 key investigations in Hirschsprung’s?

A

1) AXR

2) Rectal biopsy

48
Q

What is the gold standard for diagnosis of Hirschsprung’s?

A

Rectal biopsy

The bowel histology will demonstrates an absence of ganglionic cells.

49
Q

Management of Hirschsprung’s?

A
  • Initially; rectal washouts/bowel irrigation
  • Definitive; surgery to affected segment of the colon
  • Fluid resuscitation in unwell children and those with enterocolitis
  • Management of the intestinal obstruction
  • IV Abx required in HAEC
50
Q

What is the definitive management of Hirschsprung’s?

A

surgical removal of the aganglionic section of bowel.

51
Q
A

Yr 4 - Paediatrics (78 decks)

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