Gastroenterology Flashcards

1
Q

What is the most common cause of loose stool in preschool children?

A

Toddler’s diarrhoea or chronic non-specific diarrhoea

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2
Q

What age does chronic non-specific diarrhoea usually affect?

A

1-4 yrs

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3
Q

What is the aetiology of chronic non-specific diarrhoea?

A

Aetiology thought to be due to imbalance of fluid, fibre and undigested sugars that reach large bowel causing excessive fluid to be passed out into stools

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4
Q

What can chronic non-specific diarrhoea result from?

A
  • Undiagnosed coealiac disease
  • Excessive ingestion of fruit juice (esp. apple juice)
  • Cows milk allergy following gastroenteritis (trial may be helpful)
    *
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5
Q

What are the clinical features of chronic non-specific diarrhoea?

A

o Typically >2 watery stools per day (can be up to 8-10/day)
o Stools: vary in consistency, smelly, pale, contain undigested vegetables e.g. sweetcorn, carrots
o May have associated mild pain o Well and thriving child

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6
Q

How do we manage chronic non-specific diarrhoea?

A
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7
Q

How should we think about chronic diarrhoea?

A

o Infant with faltering growth→consider coeliac disease and cow’s milk protein allergy
o Following bowel resection, cholestatic liver disease or exocrine pancreatic deficiency→consider malabsorption
o In otherwise well toddler with undigested vegetables in stool→consider chronic non-specific diarrhoea

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8
Q

Define Hirschsprung’s disease.

A

Hirschsprung disease is characterised by the absence of ganglion cells from the myenteric and submucosal plexuses of the large bowel, resulting in a narrow and contracted segment of the large bowel.

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9
Q

Where does the abnormal bowel extend in Hirschsprung’s disease?

A

The region of abnormal bowel extends from the rectum for a variable distance proximally, ending in a normally innervated, dilated colon

In 75% of cases, lesion is confined to the rectosigmoid

In 10% of cases, the entire colon is affected

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10
Q

What is Hirschsprung’s disease associated with?

A

Down’s Syndrome

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11
Q

How common is Hirschsprung’s disease?

A

1 in 5000 births

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12
Q

Describe the pathophysiology of Hirschsprung’s disease.

A

• Within gut muscle, nerve plexuses can be found (networks of nerves) within which there are ganglia (groups of individual nerves) which help co-ordinate peristalsis

o Myenteric plexus (Auerbach’s plexus): causes smooth muscle relaxation

o Submucous plexus (Meissner’s plexus): helps control blood flow, absorption and secretion

These plexuses are key for normal bowel function

In HD, these plexuses are absent

This occurs due to abnormal fetal development causing lack of migration and/or development of neural crest cells

No nerves→no peristalsis→blocks movement of faeces

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13
Q

How does Hirschsprung’s disease present?

A

• Presents usually in the NEONATAL PERIOD with intestinal obstruction (CONSTIPATION)
o Manifests as failure to pass meconium within first 24 hours of life
o Later on, abdominal distension and bile-stained vomiting will develop

Rectal examination may reveal a narrowed segment and withdrawal of the examining finger often releases a gush of liquid stool and flatus

o Temporary improvement in the obstruction following the dilation caused by the rectal examination can lead to a delay in diagnosis

Occasionally, infants may present with severe, life-threatening HIRSCHSPRUNG ENTEROCOLITITS during first few weeks of life

o This is sometimes due to C difficile infection

In later childhood

o Chronic constipation

o Abdominal distension

o Growth failure

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14
Q

How do we investigate Hirschsprung’s disease? What is the Gold Standard?

A

First line

o Plain abdominal X-ray

▪ This is a non-specific investigation as it is difficult to differentiate between a distended colon and the small bowel in a newborn

▪ A normal film does not exclude HD possibility but without evidence of distended colon, it is unlikely to be this disease

o Contrast enema

▪ Most valuable screening diagnostic test

▪ Shows contracted distal bowel and dilated proximal bowel

Gold-standard: rectal suction biopsy

o This allows definitive diagnosis
o Must extract both mucosa and submucosa
o Demonstrates absence of ganglion cells, along with presence of large acetylcholinesterase-positive nerve trunks on a suction full thickness rectal biopsy

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15
Q

How do we manage Hirschsprung’s disease?

A

Surgical: BMJ Best Practice:

If without enterocolitis

o First line: Bowel irrigation
▪ To manage abdominal distension prior to proceeding with surgery

o Plus: definitive surgery

▪ Three techniques exist, which all involve the removal of the distal aganglionic segment with pull-through of the proximal normal ganglionic bowel (i.e. initial colostomy followed by anastomosing normally innervated bowel to the anus)

▪ Procedure is called an ANORECTAL PULL-THROUGH

If with enterocolitis

o 1st line: bowel irrigation + IV fluids + antibiotics
o Adjunct: decompression by colostomy or ileostomy

o Plus: definitive surgery

If total colonic aganglionosis

o 1st line: ileostomy – as irrigations do not often work in these causes because it is difficult to reach the dilated small bowel
o Plus: definitive surgery – involves a straight ileorectal anastomosis

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16
Q

What is the most common cause of intestinal obstruction in infants after the neonatal period?

A

Intussusception

17
Q

Define intussusception.

A

Intussusception is the invagination of proximal bowel into a distal segment

Most commonly involves ileum passing into the caecum through the ileocaecal valve

18
Q

Define intussusception.

A

Intussusception is the invagination of proximal bowel into a distal segment

Most commonly involves ileum passing into the caecum through the ileocaecal valve

19
Q

What is the peak age of incidence of intussusception?

A

3 months to 2 years

20
Q

What is a complication of intussusception?

A

Most serious complication: stretching and constriction of the mesentery resulting in venous obstruction, causing engorgement and bleeding from the bowel mucosa, fluid loss and subsequently bowel perforation, peritonitis and gut necrosis.

21
Q

Describe the pathophysiology of intussusception.

A

One portion of the intestine telescopes into the lumen of the intestine immediately distal to it causing OBSTRUCTION

Usually affects ileo-caecal region of intestines – almost all intussusceptions happen when the ileum folds into the cecum

The mesentery is dragged alongside the proximal bowel wall into the distal lumen resulting in obstruction of venous return →oedema, mucosal bleeding, increased pressure

If arterial flow becomes compromised→ ischaemia, necrosis, perforation can occur

Ischaemic and infarcted tissue leads to sloughing off of intestinal mucosa, blood and mucus into the gut→can result in red-currant jelly stool

22
Q

What causes intussusception?

A

Usually no underlying cause for the intussusception is found

There is some evidence that viral infection leading to enlargement of Peyer’s patches (lymphoid hyperplasia) may form the lead point of intussusception in children (peristalsis then drags the lead point across)

An identifiable lead point such as a Meckel diverticulum (outpouching of GI tissue which usually sticks out into the peritoneal cavity, and can invert and stick back into the intestine dragging the ileum into the caecum), polyp, inflamed appendix, neoplastic lesion and ileal duplication is more likely to be present in children over 2 years of age

23
Q

What are the suggested RFs of intussusception?

A

o Henoch-Schonlein purpura→intestinal wall haematoma (lead point)

o Cystic fibrosis→hypertrophied mucosal glands (lead point)
o Lymphoma (lead point)
o Well- developed lymphoid tissue
o Thin intestinal wall
o Narrow intestinal lumen
o Poor fixation of ileocaecal region

o Preceding respiratory infection or gastroenteritis
▪ Can lead to hypertrophied Peyer’s patches (enlarged mesenteric lymph nodes) which then act as a lead point

▪ Usually in younger patients

o Recent abdominal operation
o Previous intussusception increases risk of further

24
Q

What is the triad of features in intussusception?

A
  1. Vomiting
  2. Colicky pain
  3. Bloody stool
25
Q

What are the other clinical features of intussusception?

A

TRIAD: vomiting + colicky pain + bloody stool

Paroxysmal, severe colicky pain with pallor

o During the episodes of pain, child becomes PALE especially around mouth, and draws up legs

o Recovery between episodes but may become increasingly lethargic

Refusing feeds

Vomiting: may be bile-stained depending on location of the intussusception

Sausage-shaped mass palpable in abdomen (25%) - RUQ

Passage of redcurrant jelly stool comprising of blood-stained mucus

o This is a characteristic sign but tends to occur later in illness

o Occurs due to bleeding into the intestine

Abdominal distension and shock

Sepsis and fever can occasionally occur if there is intestinal tear causing release of bacteria

26
Q

What are the investigations of intussusception?

A

• AXR may show distended small bowel with no gas in the distal colon and rectum (paucity of gas),
o AXR is key to assess for free air in bowel → which suggests peritonitis
Abdominal ultrasound (investigation of choice) is useful to confirm the diagnosis and check the response to treatment (target/doughnut sign) – represents telescoped intestine

o May show free fluid indicating peritonitis
o If colour Doppler also done, may show if bowel is ischaemic

Air contrast enema

PR examination (only done by a specialist) would reveal blood on gloved finger

27
Q

How do we manage intussusception?

A
  • Rapid treatment key as there is potential for ischaemia (A-E approach)
  • IV fluid resuscitation is likely to be necessary immediately, as there is often pooling of fluid in the gut which can lead to hypovolaemic shock
  • NG tube insertion if child is repeatedly vomiting in face of obstruction
  • Urgent referral to paediatric surgeon
  • Unless there are signs of peritonitis, reduction of the intussusception by rectal air insufflation (with fluoroscopy guidance) is usually attempted by a radiologist
    • Success rate is75%
    • Remaining 25% require an operation
  • Clinically stable with no contraindications to contrast enema reduction
    • Fluid resuscitation
    • Contrast enema( air or contrast liquid e.g .Barium or Gastrograffin)
    • Contraindications
      • Peritonitis
      • Perforation
      • Hypovolaemic shock
    • Broad-spectrum antibiotics
      • Clindamycin + gentamicin OR tazocin OR cefoxitin + vancomycin
    • 2nd line: surgical reduction with broad-spectrum antibiotics
  • If recurrent intussusception - consider investigating for a pathological lead point (e.g. Meckel’s diverticulum)
28
Q

How should you counsel on Intussusception?

A