Paeds - Gastro Flashcards

1
Q

4 surgical causes of abdominal pain

A

Appendicitis causes central abdominal pain spreading to the right iliac fossa

Intussusception causes colicky non-specific abdominal pain with redcurrant jelly stools

Bowel obstruction causes pain, distention, absolute constipation and vomiting

Testicular torsion causes sudden onset, unilateral testicular pain, nausea and vomiting

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2
Q

Abdominal pain is a very common presentation in children. These can be split into non-organic causes, medical causes and surgical causes. Non-organic or functional abdominal pain is very common in children over 5 years. This is where no disease process can be found to explain the pain.

What are the red flag symptoms that suggest serious Abdominal pain

A

Persistent or bilious vomiting
Severe chronic diarrhoea
Fever
Rectal bleeding
Weight loss or faltering growth
Dysphagia (difficulty swallowing)
Nighttime pain
Abdominal tenderness

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3
Q

What do the following investigations findings indicate in someone with abdominal pain?

Initial investigations that may indicate the pathology pathology:

Anaemia
Raised inflammatory markers (ESR and CRP)
Raised anti-TTG or anti-EMA antibodies
Raised faecal calprotectin
Positive urine dipstick

A

Anaemia can indicate inflammatory bowel disease or coeliac disease
Raised inflammatory markers (ESR and CRP) can indicate inflammatory bowel disease
Raised anti-TTG or anti-EMA antibodies indicates coeliac disease
Raised faecal calprotectin indicates inflammatory bowel disease
Positive urine dipstick indicates a urinary tract infection

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4
Q

What causes recurrent abdominal pain and how is it managed?

A

A diagnosis of recurrent abdominal pain is made when a child presents with repeated episodes of abdominal pain without an identifiable underlying cause. The pain is described as non-organic or functional. This is common and can lead to psychosocial problems, such as missed days at school and parental anxiety. There is overlap between the diagnoses of recurrent abdominal pain, abdominal migraine, irritable bowel syndrome and functional abdominal pain.

Recurrent abdominal pain often corresponds to stressful life events, such as loss of a relative or bullying. The leading theory for the cause is increased sensitivity and inappropriate pain signals from the visceral nerves (the nerves in the gut) in response to normal stimuli.

Management involves careful explanation and reassurance. Measures that can help manage the pain are:

Distracting the child from the pain with other activities or interests
Encourage parents not to ask about or focus on the pain
Advice about sleep, regular meals, healthy balanced diet, staying hydrated, exercise and reducing stress
Probiotic supplements may help symptoms of irritable bowel syndrome
Avoid NSAIDs such as ibuprofen
Address psychosocial triggers and exacerbating factors
Support from a school counsellor or child psychologist

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5
Q

A 5 year child expieriences recurrent episodes of central abdominal pain, naseu and vomitting. Typically these episodes last a few hours. What is the likely cause?

Management?

prophalaxis medication?

A

Abdominal Migraine

Children are more likely than adults to suffer with a condition called abdominal migraine. This may occur in young children before they develop traditional migraines as they get older. Abdominal migraine presents with episodes of central abdominal pain lasting more than 1 hour. Examination will be normal.

There may be associated:

Nausea and vomiting
Anorexia
Pallor
Headache
Photophobia
Aura

Treating the acute attack - same as adult migraine:

Low stimulus environment (quiet, dark room)
Paracetamol
Ibuprofen
Sumatriptan

Prophalaxis
- Pizotifen - a seotnin antagonist

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6
Q

Constipation in children is a very common problem in paediatrics.

How often someone opens their bowels varies between individuals. This is even more variable in breast-fed babies, which can have as little as one stool a week. Someone opening their bowels daily may be constipated, whereas someone opening their bowels twice a week may not, if that is normal for them.

What are some of the Typical features in the history and examination that suggest constipation?

A

Less than 3 stools a week
Hard stools that are difficult to pass
Rabbit dropping stools
Straining and painful passages of stools
Abdominal pain
Holding an abnormal posture, referred to as retentive posturing
Rectal bleeding associated with hard stools
Faecal impaction causing overflow soiling, with incontinence of particularly loose smelly stools
Hard stools may be palpable in abdomen
Loss of the sensation of the need to open the bowels

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7
Q

What is encopresis

A

Encopresis is the term for faecal incontinence. This is not considered pathological until 4 years of age. It is usually a sign of chronic constipation where the rectum becomes stretched and looses sensation. Large hard stools remain in the rectum (faecal impaction) and only loose stools are able to bypass the blockage and leak out, causing soiling.

Other rarer causes of encopresis include:

Spina bifida
Hirschprung’s disease
Cerebral palsy
Learning disability
Psychosocial stress
Abuse

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8
Q

KEY

What is the most common cause of constipation?

Red flag symptoms for secondary causes - likely diagnosis?:
Not passing meconium within 48 hours of birth
Neurological signs or symptoms
Vomiting
Ribbon stool
Abnormal anus
Abnormal lower back or buttocks
Failure to thrive
Acute severe abdominal pain and bloating**

A

Most cases of constipation can be described as idiopathic constipation or functional constipation, meaning there is not a significant underlying cause other than simple lifestyle factors. It is important to think about possible secondary causes of constipation, such as Hirschsprung’s disease, cystic fibrosis or hypothyroidism.

There are a number of lifestyle factors that can contribute to the development and continuation of constipation:

Habitually not opening the bowels
Low fibre diet
Poor fluid intake and dehydration
Sedentary lifestyle
Psychosocial problems such as a difficult home or school environment (always keep safeguarding in mind)

Secondary Causes:
Not passing meconium within 48 hours of birth (cystic fibrosis or Hirschsprung’s disease)
Neurological signs or symptoms, particularly in the lower limbs (cerebral palsy or spinal cord lesion)
Vomiting (intestinal obstruction or Hirschsprung’s disease)
Ribbon stool (anal stenosis)
Abnormal anus (anal stenosis, inflammatory bowel disease or sexual abuse)
Abnormal lower back or buttocks (spina bifida, spinal cord lesion or sacral agenesis)
Failure to thrive (coeliac disease, hypothyroidism or safeguarding)
Acute severe abdominal pain and bloating (obstruction or intussusception)

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9
Q

Key - management of idiopathic constipation?

A

NICE clinical knowledge summaries recommend:

Correct any reversible contributing factors, recommend a high fibre diet and good hydration

Start laxatives (movicol is first line (macrogol same as laxido))

NOTE - ADULTS BULK FORMING THEN OSMOTIC, KIDS JUST MOVICOL FIRST LINE

Faecal impaction may require a disimpaction regimen with high doses of laxatives at first

Encourage and praise visiting the toilet. This could involve scheduling visits, a bowel diary and star charts.

Laxatives should be continued long term and slowly weaned off as the child develops a normal, regular bowel habit.

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10
Q

Gastro-oesophageal reflux is where contents from the stomach reflux through the lower oesophageal sphincter into the oesophagus, throat and mouth.

In babies there is immaturity of the lower oesophageal sphincter, allowing stomach contents to easily reflux into the oesophagus. It is normal for a baby to reflux feeds, and provided there is normal growth and the baby is otherwise well this is not a problem, however it can be upsetting for parents. This usually improves as they grow and 90% of infants stop having reflux by 1 year.

When is reflux in infants concerning?

How does reflux present in older children?

A

It is normal for babies to have some reflux after larger feeds. It becomes more troublesome when this causes them to become distressed. Signs of problematic reflux include:

Chronic cough
Hoarse cry
Distress, crying or unsettled after feeding
Reluctance to feed
Pneumonia
Poor weight gain

Children over one year may experience similar symptoms to adults, with heartburn, acid regurgitation, retrosternal or epigastric pain, bloating and nocturnal cough.

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11
Q

Vomiting is very non-specific and is often not indicative of underlying pathology.

List some some of the possible causes of vomiting?

What do the following red flag of vomitting indicate?
- not keeping down any food
- projectile/forceful vomitting
- bile stained
- haematemesis
- ahdominal distention
- reduced conciousness, bulging fontanele or neurological signs
- respiratory symptoms
- signs of infection
- rash, angioedma
- apnoeas

A

Some of the possible causes of vomiting include:

Overfeeding
Gastro-oesophageal reflux
Pyloric stenosis (projective vomiting)
Gastritis or gastroenteritis
Appendicitis
Infections such as UTI, tonsillitis or meningitis
Intestinal obstruction
Bulimia

Certain features in the history should make you think about serious underlying problems:

Not keeping down any feed (pyloric stenosis or intestinal obstruction)
Projectile or forceful vomiting (pyloric stenosis or intestinal obstruction)
Bile stained vomit (intestinal obstruction)
Haematemesis or melaena (peptic ulcer, oesophagitis or varices)
Abdominal distention (intestinal obstruction)
Reduced consciousness, bulging fontanelle or neurological signs (meningitis or raised intracranial pressure)
Respiratory symptoms (aspiration and infection)
Blood in the stools (gastroenteritis or cows milk protein allergy)
Signs of infection (pneumonia, UTI, tonsillitis, otitis or meningitis)
Rash, angioedema and other signs of allergy (cows milk protein allergy)
Apnoeas are a concerning feature and may indicate serious underlying pathology and need urgent assessment

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12
Q

How is GORD managed in children, including babies

Ix?

A
  • for simple cases - lifestyle advice (small frequent meals, burping to settle milk, keeping upright after feeding)
  • Gaviscon (alginate - form a layer) mixed with feeds
  • Thickened milk or formula (specific anti-reflux formulas are available)
  • Omeprazole - if required

Rarely in severe cases they may need further investigation with a barium meal and endoscopy. Surgical fundoplication can be considered in very severe cases, however this is very rarely required or performed.

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13
Q

What is sandifer’s syndrome - rare

A

This is a rare condition causing brief episodes of abnormal movements associated with gastro-oesophageal reflux in infants. The infants are usually neurologically normal. The key features are:

Torticollis: forceful contraction of the neck muscles causing twisting of the neck
Dystonia: abnormal muscle contractions causing twisting movements, arching of the back or unusual postures
The condition tends to resolve as the reflux is treated or improves. Generally the outcome is good. It is worth referring patients with these symptoms to a specialist for assessment, as the differential diagnosis includes more serious conditions such as infantile spasms (West syndrome) and seizures.

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14
Q

A two week old neonate presents with fialure to thrive (not putting on weight) and projectile vomiting. On examination you feel a firm round mass in the upper abdomen.

Diagnosis?

What does blood gas show?

Investigation?

Management?

A

Pyloric stenosis

Pyloric stenosis typically presents in the first few weeks of life, with a hungry baby that is thin, pale and generally failing to thrive. The classic description of vomiting you should remember for your exams is “projectile vomiting”.

The pyloric sphincter is a ring of smooth muscle the forms the canal between the stomach and the duodenum. Hypertrophy (thickening) and therefore narrowing of the pylorus is called pyloric stenosis. This prevents food traveling from the stomach to the duodenum as normal.

After feeding, there is increasingly powerful peristalsis in the stomach as it tries to push food into the duodenum. Eventually it becomes so powerful that it ejects the food into the oesophagus, out of the mouth and across the room. This is called “projectile vomiting”.

If examined after feeding, often the peristalsis can be seen by observing the abdomen. A firm, round mass can be felt in the upper abdomen that “feels like a large olive”. This is caused by the hypertrophic muscle of the pylorus.

Blood gas analysis will show a hypochloric (low chloride) metabolic alkalosis as the baby is vomiting the hydrochloric acid from the stomach. This is a common data interpretation question in exams, so worth remembering.

Ix - abdominal ultrasound to visualise the thickened pylorus.

Treatment involves a laparoscopic pyloromyotomy (known as “Ramstedt’s operation“). An incision is made in the smooth muscle of the pylorus to widen the canal allowing that food to pass from the stomach to the duodenum as normal. Prognosis is excellent following the operation.

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15
Q

What is Hirshprung’s disease - pathophysiology?

A

Hirschsprung’s disease is a congenital condition where parasympathetic ganglion cells of the myenteric plexus are absent in the distal bowel and rectum.

The length of colon without innervation varies between patients from a small area to the entire colon. When the entire colon is affected this is called total colonic aganglionosis.

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 - THIS WAS TESTED (KINDA) THE BOWEL IS DISTENDED, then constrited distally.

Family history is signifcant. Associated with down’s syndrome, neurofribmatosis, waardenburg syndrome and multiple endocrine neoplasia type ii - i would bother learning this…

Background:
The myenteric plexus, also known as Auerbach’s plexus, forms the enteric nervous system. 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.

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.

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16
Q

How does Hirschprung’s disease present?

What is Hirschprung’s associated enterocolitis?

Hirschprung’s - Ix and Management?

A

The severity of the presentation and the age at diagnosis varies significantly depending on the individual and the extent of the bowel that is affected. It can present with acute intestinal obstruction shortly after birth or more gradually developing symptoms:

Delay in passing meconium (more than 24 hours)
Chronic constipation since birth
Abdominal pain and distention (essenitally it is bowel obstruction, like ileus)
Vomiting
Poor weight gain and failure to thrive

Hirschsprung-associated enterocolitis (HAEC) is inflammation and obstruction of the intestine occurring in around 20% of neonates with Hirschsprung’s disease. It typically presents within 2-4 weeks of birth with fever, abdominal distention, diarrhoea (often with blood) and features of sepsis. It is life threatening and can lead to toxic megacolon and perforation of the bowel. It requires urgent antibiotics, fluid resuscitation and decompression of the obstructed bowel.

Ix:
1st line - Abdominal xray can be helpful in diagnosing intestinal obstruction and demonstrating features of HAEC.

Gold standard - rectal biopsy, histology shows an abscence of ganglionic cells

Management:
- fluid resuicitation
- definative management - surgical removal of the aganglionic section of bowel. Risk of incontinence.

17
Q

Differentials for Failure to pass meconium - 6

A

Differential diagnoses include:
Meconium Ileus: Distal small bowel is impacted by meconium leading to abdominal distension and failure to pass meconium.Can be differentiated by radiograph, barium enema or water-soluble contrast enema.
CF is the main cause!!! Meconium ileus: Failure to pass meconium, abdominal distension, bilious vomiting. A key feature is the thickened, sticky meconium causing small bowel obstruction. Contrast enema: Microcolon due to underuse and dilated proximal bowel.

Hirshprungs: Failure to pass meconium within 48 hours.
Progressive abdominal distension, vomiting (non-bilious or bilious), and reluctance to feed. Contrast enema: Transition zone between dilated proximal bowel and narrow aganglionic segment.

Meconium Plug Syndrome: Leads to failure to pass meconium but symptoms should resolve after passage of plug. Can be differentiated by barium enema or water-soluble contrast enema (water soluble preferred as less risk of perforation) - shows the plug, symptoms improve after the plug passes

Intestinal atresia: Congenital malformation of any part of the intestine resulting in complete obstruction. The presentation will depend on the site of the blockage but will usually involve abdominal distension and failure to pass meconium. Investigations: Abdominal X-ray: Double bubble sign (duodenal atresia) or multiple air-fluid levels.

Intestinal malrotation: This is caused by a congenital anomaly in the rotation of the midgut during embryological development. This can result in midgut volvulus presenting with bilious vomiting and abdominal distension. Contrast - abnormal position of the duodenojejunal junction and corkscrew appearance in volvulus.

Anorectal malformation (anal stenosis, imperforate anus): Congenital abnormalities in development of the lower colon can present with failure to pass meconium and abdominal distension. Can be differentiated by physical examination of the rectum that reveals malformation.

Constipation: Difficulty in passing stools. This is a diagnosis of exclusion.

18
Q

What is bilary atresia?

Presentation?

Initial Ix

Conjugated or uncojugated billirubin?

Management? - THIS

A

Atresia - closed or abscent, stenosis just means narrowed

Billiary atresia - a congenital condition where a section of the bile duct is closed or absent. This results in cholestasis, where the bile cannot be transported from the liver to the bowel.

Conjugated bilirubin is excreted in the bile, therefore biliary atresia prevents the excretion of conjugated bilirubin.

Biliary atresia presents shortly after birth with significant jaundice due to high conjugated bilirubin levels. Suspect biliary atresia in babies with a persistent jaundice, lasting more than 14 days in term babies and 21 days in premature babies.

**Ix - conjugated and unconjugated bilirubin.
**
a high proportion of conjugated bilirubin suggests the liver is processing the bilirubin for excretion (by conjugating it), but it is not able to excrete the conjugated bilirubin because it cannot flow through the biliary duct into the bowel.

**Remember that in normal neonatal jaundice - less develop liver funtion and high red blood cells turn over to high unconjugated billirubin. **

There are many causes of jaundice in the neonate. The majority of cases are benign (e.g. breast milk jaundice), however more serious causes such as biliary atresia need to be excluded by measuring the conjugated bilirubin level.

Management - surgery. The “Kasai portoenterostomy” involves attaching a section of the small intestine to the opening of the liver, where the bile duct normally attaches. This is somewhat successful and can clear the jaundice and prolong survival. Often patients require a full liver transplant to resolve the condition.

19
Q

What is coeliac disease?

Antibodies? What do the lead to and in what section of the bowels?

Presentation?

Linked condition?

A

Coeliac disease is an autoimmune condition where exposure to gluten causes an immune reaction that creates inflammation in the small intestine. It usually develops in early childhood but can start at any age.

In coeliac disease autoantibodies are created in response to exposure to gluten. These autoantibodies target the epithelial cells of the intestine and lead to inflammation. There are two antibodies to remember: anti-tissue transglutaminase (anti-TTG) and anti-endomysial (anti-EMA). These antibodies correlate with disease activity and will rise with more active disease and may disappear with effective treatment.

Inflammation affects the small bowel, particularly the jejunum. It causes atrophy of the intestinal villi. The intestinal cells have villi on them that help with absorbing nutrients from the food passing through the intestine. The inflammation causes malabsorption of nutrients and disease related symptoms.

Presentation:
Coeliac disease is often asymptomatic, so have a low threshold for testing for coeliac disease in patients where it is suspected. Symptoms can include:

Failure to thrive in young children
Diarrhoea
Fatigue
Weight loss
Mouth ulcers
Anaemia secondary to iron, B12 or folate deficiency
Dermatitis herpetiformis is an itchy blistering skin rash that typically appears on the abdomen
Rarely coeliac disease can present with neurological symptoms:

Peripheral neuropathy
Cerebellar ataxia
Epilepsy
TOM TIP: Remember that we test all patients with a new diagnosis of type 1 diabetes for coeliac disease, even if they don’t have symptom, because the conditions are often linked.

20
Q

Coeliacs disease:
- Ix with results?
- management?
- complications of not treating?

A

Investigations must be carried out whilst the patient remains on a diet containing gluten otherwise it may not be possible to detect the antibodies or inflammation in the bowel.

Check total immunoglobulin A levels to exclude IgA deficiency before checking for coeliac disease specific antibodies:

Raised anti-TTG antibodies (first choice)
Raised anti-endomysial antibodies

TOM TIP: Anti-TTG and anti-EMA antibodies are IgA. Some patients have an IgA deficiency. When you test for these antibodies, it is important to test for total Immunoglobulin A levels because if total IgA is low the coeliac test will be negative even when they have the condition. In this circumstance you can test for the IgG version of the anti-TTG or anti-EMA antibodies or do an endoscopy with biopsies.

Endoscopy and intestinal biopsy show:

“Crypt hyperplasia”
“Villous atrophy”

Treatment

A lifelong gluten free diet is essentially curative. Relapse will occur on consuming gluten again. Checking coeliac antibodies can be helpful in monitoring the disease.

Complications
- vitamin deficeincy and anemia
- osteoperosis
- enetropathy
- LYMPHOMA - Enteropathy-associated T-cell lymphoma (EATL) of the intestine and Non-Hodgkin lymphoma (NHL) - if inflammation is not controlled.

21
Q

Inflammatory bowel disease is the umbrella term for the two main diseases that cause inflammation of the GI tract: ulcerative colitis and Crohn’s disease. They both involve inflammation of the walls of the GI tract and are associated with periods of remission and exacerbation.

Key Sx

Crohns vs Ulcerative collitis?:
- Portion of GI tract affect
- Nature of inflammation
- Blood or mucus present
- effect of smoking
- Key endoscopy/Histology findings
- which one has goblet cells?

A

Suspect inflammatory bowel disease in children and teenagers presenting with perfuse diarrhoea, abdominal pain, bleeding, weight loss or anaemia. They may be systemically unwell during flares, with fevers, malaise and dehydration.

Crohns’:
- entired GI tract, most commonly the terminal illeum
- **transmural inflation,
skip legions** and cobblestoning
- less common to see blood or mucus
- smoking exercerbates sx- don’t set the crohn’s nest on fire
- endoscopy findings - deep ulcerations, cobblestoning and granlumatous regeneration
- histology - Goblet cells are preserved
- transmural so fistulas and strictures can occour (muscle hypertrophy

UC:
- limmmited to large bowel and rectum
- superficial inflammation, that is continouos

- blood or mucus is often present
- smoking is protective
- Associated with Primary sclerosing cholangitis.

22
Q

Inflammatory Bowel Disease:
- key investigations?
- Management? Crohns and UC, Including Surgical?

A

General - Blood tests for anaemia, infection, thyroid, kidney and liver function. A raised CRP indicates active inflammation.

Faecal calprotectin is released by the intestines when inflamed. It is a useful screening test and is more than 90% sensitive and specific for IBD in adults.

Endoscopy (OGD and colonoscopy) with biopsy is the gold standard investigation for diagnosis of IBD.

Imaging with ultrasound, CT and MRI can be used to look for complications such as fistulas, abscesses and strictures.

Management:

Crohn’s
Inducing remission
1st line - steroids (prednisalone or iv hydrocortisone)
2nd line - any of the five immunosupressants for maintaining remission

Maintianing remission
- perfectly reasonable not to take any medications
- 1st line- azathioprine or mercaptopurine
- 2nds line - Methotrexate, infliximab, adalimumab

If the disease only affects the distal ileum then surgical resection can be helpful

Ulcerative Colitis:
First line: aminosalicylate (e.g. mesalazine oral or rectal)
Second line: corticosteroids (e.g. prednisolone)
Third line - ciclosporin (immunosupressant)

Maintaining remission
Mesalzine (or or rectal)

Azathiprine or mercaptopurine

Panproctocolectomy is curative (removal of the colon and rectum) - ileostomy or a J-pouch -> anus.

23
Q
  • Bilious vomitting
  • abdominal pain
  • tinkling bowel sounds or absent bowel sounds
  • absolute constopation - stools or wind

Dx?
Causes?
Ix - shows?
Mx

A

Intestinal obstruction is where a physical obstruction prevents the flow of faeces through the intestines. This blockage will lead to a back-pressure through the gastrointestinal system, causing vomiting. It also causes absolute constipation, where the patient is unable to pass stools or wind.

Causes of Intestinal Obstruction

Meconium ileus
Hirschsprung’s disease
Oesophageal atresia
Duodenal atresia (double bubble sign on X-ray)
Intussusception
Imperforate anus
Malrotation of the intestines with a volvulus
Strangulated hernia

1st line- abdominal Xray - may show dilated looks of bowel proximal to the abstruction and collapsed loops distal to the obstruction

Drip and Suck- IV fluids, NG tibe to drain the stomach
Emergency surgery is often required

24
Q

What is intussuscpetion and which age group get it?

Key presentation details?

Ix?

Management - options?

A

Intussusception is a condition where the bowel “invaginates” or “telescopes” into itself. Picture the bowel folding inwards. This thickens the overall size of the bowel and narrows the lumen at the folded area, leading to a palpable mass in the abdomen and obstruction to the passage of faeces through the bowel. It typically occurs in infants 6 months to 2 years and is more common in boys.

It has many associated conditons including concurrent viral illness

Presentation:
- redcurrant jelly stool and sausage-shaped right upper squadrant mass on palpation. These are pathognomonic
- severe colickly abdominal pain
- vomiting and intestinal obstruction

TOM TIP: Look out for the “redcurrant jelly stool” in your exams as this indicates intussusception as a diagnosis. The other classic feature is the sausage-shaped mass in the abdomen. The typical child in the exam will have had a viral upper respiratory tract infection preceding the illness and will have features of intestinal obstruction (vomiting, absolute constipation and abdominal distention). Ultrasound is the initial investigation of choice.

Management:
Diagnosis is made mainly by ultrasound scan or contrast enema.

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.

Surgical reduction may be necessary if enemas do not work.

If the bowel becomes gangrenous (due to a disruption of the blood supply) or the bowel is perforated, then surgical resection is required.

Complications- not for memory
Obstruction
Gangrenous bowel
Perforation
Death

25
Q

What causes appendicitis?

Peak incidence?

Presentation? What two signs indicate peritonitis?

A

Appendicitis is inflammation of the appendix. The appendix is a small, thin tube sprouting from the caecum. The appendix becomes inflamed due to infection trapped in the appendix by obstruction at the point where the appendix meets the bowel. The inflammation can quickly proceed to gangrene and rupture. The appendix can rupture and release faecal content and infective material into the abdomen. This leads to peritonitis, which is inflammation of the peritoneal contents.

The peak incidence of appendicitis is in patients aged 10 to 20 years.

The key presenting feature of appendicitis is abdominal pain. This typically starts as central abdominal pain, that moves down to the right iliac fossa (RIF) over time and eventually becomes localised in the RIF. On palpation of the abdomen there is tenderness in McBurney’s point. This is a localised area one third the distance from the anterior superior iliac spine (ASIS) to the umbilicus.

Other classic features are:

Loss of appetite (anorexia)
Nausea and vomiting
Rovsing’s sign (palpation of the left iliac fossa causes pain in the RIF)
Guarding on abdominal palpation
Rebound tenderness is increased pain when quickly releasing pressure on the right iliac fossa
Percussion tenderness is pain and tenderness when percussing the abdomen

Rebound tenderness and percussion tenderness suggest peritonitis, caused by a ruptured appendix.

26
Q

Appendicitis:

  • diagnosis?
  • management?
A

Diagnosis is based on the clinical presentation and raised inflammatory markers

Ultrasound should be the preferred imaging modality in children

When a patient has a clinical presentation suggestive of appendicitis but investigations are negative, the next step is to perform a diagnostic laparoscopy to visualise the appendix directly. The surgeon can then proceed to an appendicectomy during the same procedure if indicated.

Management:
Removal of the inflamed appendix (appendicectomy) is the definitive management for acute appendicitis.

27
Q

What is mesenteric adenitis?

presentation?

Ix?

management?

A

Mesenteric adenitis, also known as mesenteric lymphadenitis, is inflammation of lymph nodes found in the mesentery, usually around the terminal ileum. The cause for this lymphadenopathy is usually not found in primary mesenteric adenitis (1) but it is thought to occur after a recent viral or bacterial infection.

It presents with abdominal pain, vommiting, fever, bowel habbit change. The clinical presentation of mesenteric adenitis is very similar to other conditions, such as appendicitis.

Ultrasound abdomen can help differentiate between mesenteric adenitis and appendicitis.

Management - self limmiting. Paractamol and Ibuprofen

28
Q

Cow’s milk protein allergy:
- what is it?
- how does it present?
- management?

A

Cow’s milk protein allergy is a condition typically affecting infants and young children under 3 years. It involves hypersensitivity to the protein in cow’s milk. This may be IgE mediated, in which case there is a rapid reaction to cow’s milk, occurring within 2 hours of ingestion. It can also be non-IgE medicated, with reactions occurring slowly over several days.

This is different to lactose intolerance and cow’s milk intolerance. People with cow’s milk protein allergy do not have an allergy to lactose. Lactose is a sugar, not a protein. Cow’s milk intolerance is not an allergic process and does not involve the immune system.

Cow’s milk protein allergy is more common in formula fed babies and those with a personal or family history of other atopic conditions.

Presentation:
Cow’s milk protein allergy usually presents before 1 year of age. It may become apparent when weaned from breast milk to formula milk or food containing milk. It can present in breastfed babies when the mother is consuming dairy products.

Gastrointestinal symptoms:

Bloating and wind
Abdominal pain
Diarrhoea
Vomiting
General allergic symptoms in response to the cow’s milk protein:

Urticarial rash (hives)
Angio-oedema (facial swelling)
Cough or wheeze
Sneezing
Watery eyes
Eczema
Rarely in severe cases anaphylaxis can occur.

MANAGEMENT
- clinical diagnosis, skin prick testing can be helpful
- avoiding cow’s milk should helo fully resolve the symptoms - Breast feeding mothers should avoid dairy, and if using formula milk replace it with hydralysed formulas
- most children outgrow cow’s milk protein allergy by age 3 or sooner
- every 6 months or so children are tried on the first step of the milk lader (malted milk buiscuit) and then progress up the laddder until they develop symptoms.

29
Q

Cow’s Milk Intolerance versus Cow’s Milk Allergy

A

Cow’s milk intolerance is different from cow’s milk protein allergy. It is important not to get these mixed up. Cow’s milk intolerance presents with the same gastrointestinal symptoms as cow’s milk allergy (bloating, wind, diarrhoea and vomiting), however** it does not give the allergic features **(rash, angio-oedema, sneezing and coughing).

Infants with cow’s milk allergy will not be able to tolerate cow’s milk at all, as it causes an allergic reaction, whereas infants with cow’s milk intolerance will be able to tolerate and continue to grow and develop, but will suffer with gastrointestinal symptoms whilst having cow’s milk.

Infants with cow’s milk intolerance will grow out of it by 2 – 3 years. They can be fed with breast milk, hydrolysed formulas and weaned to foods not containing cow’s milk. After one year of age they can be started on the milk ladder.

30
Q

What is a meckel’s diverticulum and what are the 3 complications you need to be aware of?

A

Meckel’s diverticulum is a malformation of the distal ileum that occurs in around 2% of the population. It is usually asymptomatic, however it can bleed (because it releases acid), become inflamed, rupture or cause a volvulus or intussusception. They are often removed prophylactically if identified incidentally during other abdominal operations.

If they cause problems they are treated with surgical removal.

31
Q

What is infantile Colic?

A

Infantile colic is defined as excessive crying in the first few months of life. The pathophysiology is unknown but it is thought to be due to increased gas production in the gut and abdomnal gut motility.

**It is self-limmiting and must resolve by 5 months of age
**
Infant colic is defined by the following clinical diagnostic criteria:
The infant is less than 5 months of age when the symptoms start AND stop.
There are recurrent and prolonged periods of infant crying, fussing, or irritability reported by caregivers that occur without obvious cause and cannot be prevented or resolved by caregivers.
There is no evidence of faltering growth, fever, or illness.
Additional clinical signs of infantile colic may include:
Crying which most often occurs in the late afternoon or evening.
Drawing the knees up to the abdomen or arching the back when crying.
Clenching of the fists.

32
Q

What level of intial weight loss in babies is acceptable and what causes excessive weightloss

A

It is acceptable for breast fed babies to loose up to 10% and formula fed babies to loose up to 5% of their body weight by day 5 of life. They should be back at their birth weight by day 10. If they loose more weight than this or do not regain their birth weight by two weeks, they need admission to hospital and assessment for possible causes.

The most common cause of excessive weight loss or not regaining weight is dehydration due to under feeding, even when they do not clinically look dehydrated. The most reliable sign of dehydration in babies is weight loss.

33
Q

What is failure to thrive?

Causes?

Ix?

Management?

A

Failure to thrive refers to poor physical growth and development in a child. Faltering growth is defined in the 2017 NICE guidelines on faltering growth in children as a fall in weight across:

One or more centile spaces if their birthweight was below the 9th centile
Two or more centile spaces if their birthweight was between the 9th and 91st centile
Three or more centile spaces if their birthweight was above the 91st centile
Centile spaces are the distance between two centile lines on a growth chart. The distance between the 75th and 50th centile lines is a centile space. A weight that falls this distance is a drop across one centile space. For example, if the initial weight of a child is plotted halfway between the 9th and 25th centile lines and several months later is plotted halfway between the 2nd and 9th centile lines, they have dropped a full centile space.

Causes:
- inadequete nutrition - maternal malabsortion when breastfeeding, poverty
- difficulty feeding - pyloric stenosis, poor suck
- malabsorbtion - Cystic Fibrosis, Cow’s Milk PA, IBD, coeliac
- increased energy requirements - cystic fibrosis, CHD, malignancy, hyperthyroidism
- metabolic diseases and T1DM

Ix:
BMI calcultation
Mid-parental height

Outcomes from the assessment that would suggest inadequate nutrition or a growth disorder are:

Height more than 2 centile spaces below the mid-parental height centile
BMI below the 2nd centile

NICE guidelines from 2017 on faltering growth recommend the following initial investigations:

Urine dipstick, for urinary tract infection
Coeliac screen (anti-TTG or anti-EMA antibodies)

Focussed investigaitons if indicated - pyloric stenosis, cystic fibrosis

//

Management:
- dietician review
- nutritional supplement drinks, advice more energy dense food and less milk consumption
- lactation consultants where difficulty with breastfeeding is the cause
- **enteral tube feeding ** if serious

34
Q

Causes of difficulty with feeding in infants

A

Poor suck, for example due to cerebral palsy

Cleft lip or palate

Genetic conditions with an abnormal facial structure

Pyloric stenosis

im gonna say poor maternal technique but that isnt on a list

There are other things like causes of malabsorbtion (cystic fibrosis, coelics, cows milk intolerance…), hyperthryodism, congenital heart disease, HIV, malignancy, type 1 diabetes

35
Q

Low yield: kwashiorkor vs marasmus

A

Both are forms of malnutriton

Kwashiorkor:
Inadequete protein intake but sufficient total calorie intake. This leads to the lower liver protein synthesis -> oedema -> ascites. (African kids with huge bellies)

Needs gradual refeeding - not to overwhelme the liver.

Marasmus:
Inadequete calorie and protein intake. It is typically characterized by muscle wasting, fat depletion, and impaired function of the organs. (Wasting with large boney face, and rib cage, no distended abdomen)

36
Q

What is toddler’s diarrhoea?

Management?

A

Toddler’s diarrhoea is a commonn chronic non-specific diarrhoea seen in small children, between about one and four years.

The history of this condition is of
- frequent, poorly formed brown and slightly offensive stools
- food material easily recognisable in the stools is a hallmark feature
- otherwise the child is well, active and has normal growth, with normal appeptide

Need to rule out:
-ceoliac
- chronic infective gastroenteritis

The Management
- no treatement
- increasing dietary fat intake to 4g/kg/day is usually sufficient. Basically just swapping skimmed for whole milk
- 4Fs - Fibres (make sure normal), fruit juice (cut down), fat (increase), fluids (decrease if high)

37
Q

What is a choledocal cyst

A

Choledochal cysts are very rare. They are swellings in your bile ducts and are usually found in young children. They are part of a group of conditions called fibrocystic liver conditions, and form during foetal development.

The present a bit like acute cholangitis (blockage of common duct with gallstone) - jaundice and pain.

I think diagnosis is US or MRCP

Surgical management (laproscopy). If not treated they can lead to liver damage or gallstones.

38
Q

What is malrotation of the bowel?

Pathophysiology, how does it present?

How is it managed?

A

Intestinal malrotation is a condition that is congenital (present at birth) and results from a problem in the normal formation of the fetal intestines. There is a disruption in the usual steps that the intestines follow to arrive at the correct position within the abdomen. Malrotation causes the parts of the intestine to settle in the wrong part of the abdomen, which predisposes them to twisting (volvulus) and becoming obstructed.

Most children with malrotation develop symptoms within the first year of life, but some may not have symptoms until adolescence or adulthood. Signs include not feeding well, sudden bouts of crying, and pulling the legs into the body.

A complication of malrotation is volvulus, which occurs when the intestines twist, causing a blockage and cutting off blood supply. Volvulus is a medical emergency that requires immediate surgery

Twisting in the bowel leads to a closed-loop bowel obstruction, where a section of bowel is isolated by obstruction on either side. The blood vessels that supply the bowel can be involved, cutting off the blood supply to the bowel, which leads to bowel ischaemia. Ischaemia leads to death of the bowel tissue (necrosis), and bowel perforation.

Ix - A barium X-ray or enema can show if the intestines are blocked or twisted

Surgical managent includes straiging out the bowel (Ladd’s procedure - for the volvulus) and resection of any ischemic bowel. The malroatation is also corrected in the same opertaution ussually

NOTE - red currant jelly stools are a classic feature of intussusception, not volvulus