GI Illness Flashcards

1
Q

How common is constipation in children?

A

Constipation in children is a very common problem in paediatrics. 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.

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2
Q

How does constipation present?

A

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.

Typical features in the history and examination that suggest constipation are:

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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3
Q

What is encopresis and what causes it?

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 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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4
Q

Which lifestyle factors can contribute to the development of constipation?

A

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)
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5
Q

What is desensitisation of the rectum and how does this cause problems?

A

Often patients develop a habit of not opening their bowels when they need to and ignoring the sensation of a full rectum. Over time they loose the sensation of needing to open their bowels, and they open their bowels even less frequently. They start to retain faeces in their rectum. This leads to faecal impaction, which is where a large, hard stool blocks the rectum. Over time the rectum stretches as it fills with more and more faeces. This leads to further desensitisation of the rectum. The longer this goes on, the more difficult it is to treat the constipation and reverse the problem.

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6
Q

Name some secondary causes of constipation.

A
Hirschsprung’s disease
Cystic fibrosis (particularly meconium ileus)
Hypothyroidism
Spinal cord lesions
Sexual abuse
Intestinal obstruction
Anal stenosis
Cows milk intolerance
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7
Q

Which features would make you suspect a more serious cause of constipation?

A

Red flags are things in the history or examination that should make you think about serious underlying conditions that may be causing the constipation. These should prompt further investigations and referral to a specialist:

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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8
Q

What complications arise from constipation?

A
Pain
Reduced sensation
Anal fissures
Haemorrhoids
Overflow and soiling
Psychosocial morbidity
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9
Q

How can constipation be managed?

A

A diagnosis of idiopathic constipation can be made without investigations, provided red flags are considered. It is important to provide adequate explanation of the diagnosis and management as well as reassure parents about the absence of concerning underlying causes. Explain that treating constipation can be a prolonged process, potentially lasting months.

NICE clinical knowledge summaries recommend:

Correct any reversible contributing factors, recommend a high fibre diet and good hydration
Start laxatives (movicol is 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

How does the pyloric sphincter work?

A

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”.

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11
Q

How does pyloric stenosis present?

A

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”.

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.

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12
Q

How is pyloric stenosis managed?

A

Diagnosis is made using an 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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13
Q

What is gastroenteritis?

A

Acute gastritis is inflammation of the stomach and presents with nausea and vomiting. Enteritis is inflammation of the intestines and presents with diarrhoea. Gastroenteritis is inflammation all the way from the stomach to the intestines and presents with nausea, vomiting and diarrhoea.

Gastroenteritis is a very common condition in children. The most common cause of gastroenteritis is viral. It is very easily spread and patients presenting with gastroenteritis often have an affected family member or contact.

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14
Q

What is important to remember in gastroenteritis?

A

It is essential to isolate the patient in any healthcare environment, such as a paediatric assessment unit or hospital ward, as they can easily spread it to other patients.

Dehydration is the main concern. The key to management is establishing whether they are able to keep themselves hydrated or whether they need admission for IV fluids. Antibiotics are generally not recommended or required. Most children make a full recovery with simple supportive management, but beware gastroenteritis can potentially be fatal, especially in very young or vulnerable children with other health conditions.

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15
Q

What differentials other than gastroenteritis would you consider in diarrheoa cases?

A

Loose stools are a common complaint and not all cases are caused by gastroenteritis. Stools from normal babies can vary from loose stools several times a day to one stool per week. Steatorrhoea means greasy stools with excessive fat content. This suggests a problem with digesting fats, such as pancreatic insufficiency (think about cystic fibrosis).

Key conditions to think about in patients with loose stools are:

Infection (gastroenteritis)
Inflammatory bowel disease
Lactose intolerance
Coeliac disease
Cystic fibrosis
Toddler’s diarrhoea
Irritable bowel syndrome
Medications (e.g. antibiotics)
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16
Q

What are the common causes of viral gastroenteritis?

A

Viral gastroenteritis is common. It is highly contagious. Common causes are:

Rotavirus
Norovirus

Adenovirus is a less common cause and presents with a more subacute diarrhoea.

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17
Q

How does e.coli cause gastroenteritis?

A

Escherichia coli (E. coli) is a normal intestinal bacteria. Only certain strains cause gastroenteritis. It is spread through contact with infected faeces, unwashed salads or contaminated water.

E. coli 0157 produces the Shiga toxin. This causes abdominal cramps, bloody diarrhoea and vomiting. The Shiga toxin destroys blood cells and leads to haemolytic uraemic syndrome (HUS).

The use of antibiotics increases the risk of haemolytic uraemic syndrome, therefore antibiotics should be avoided if E. coli gastroenteritis is considered.

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18
Q

How does campylobacter cause gastroenteritis?

A

Campylobacter is a common cause of travellers diarrhoea. It is the most common bacterial cause of gastroenteritis worldwide. Campylobacter means “curved bacteria”. It is a gram negative bacteria that has a curved or spiral shape. It is spread by:

Raw or improperly cooked poultry
Untreated water
Unpasteurised milk
Incubation is usually 2 to 5 days. Symptoms resolve after 3 to 6 days. Symptoms are:

Abdominal cramps
Diarrhoea often with blood
Vomiting
Fever
Antibiotics can be considered after isolating the organism where patients have severe symptoms or other risk factors such as HIV or heart failure. Popular antibiotic choices are azithromycin or ciprofloxacin.
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19
Q

How does shigella cause gastroenteritis?

A

Shigella is spread by faeces contaminating drinking water, swimming pools and food. The incubation period is 1 to 2 days and symptoms usually resolve within 1 week without treatment. It causes bloody diarrhoea, abdominal cramps and fever. Shigella can produce the Shiga toxin and cause haemolytic uraemic syndrome. Treatment of severe cases is with azithromycin or ciprofloxacin.

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20
Q

How does salmonella cause gastroenteritis?

A

Salmonella is spread by eating raw eggs or poultry, or food contaminated with the infected faeces of small animals. Incubation is 12 hours to 3 days and symptoms usually resolve within 1 week. Symptoms are watery diarrhoea that can be associated with mucus or blood, abdominal pain and vomiting. Antibiotics are only necessary in severe cases and should be guided by stool culture and sensitivities.

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21
Q

How does bacillus cereus cause gastroenteritis?

A

Bacillus cereus is a gram positive rod spread through inadequately cooked food. It grows well on food not immediately refrigerated after cooking. The typical food is fried rice left out at room temperature.

Whilst growing on food it produces a toxin called cereulide. This toxin causes abdominal cramping and vomiting within 5 hours of ingestion. When it arrives in the intestines it produces different toxins that cause a watery diarrhoea. This occurs more than 8 hours after ingestion. All of the symptoms usually resolves within 24 hours.

The typical course is vomiting within 5 hours, then diarrhoea after 8 hours, then resolution within 24 hours.

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22
Q

How does giardia cause gastroenteritis?

A

Giardia lamblia is a type of microscopic parasite. It lives in the small intestines of mammals. These mammals may be pets, farmyard animals or humans. It releases cysts in the stools of infected mammals. The cysts contaminate food or water and are eaten, infecting a new host. This is called faecal-oral transmission.

Infection may not cause any symptoms, or it may cause chronic diarrhoea. Diagnosis is made by stool microscopy. Treatment is with metronidazole.

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23
Q

How is gastroenteritis managed?

A

Good hygiene helps prevent gastroenteritis. When patients develop symptoms they should immediately be isolated to prevent spread. Barrier nursing and rigorous infection control is important for patients in hospital to prevent spread to other patients. Children need to stay off school until 48 hours after the symptoms have completely resolved.

A sample of the faeces can be tested with microscopy, culture and sensitivities to establish the causative organism and antibiotic sensitivities.

The key to managing gastroenteritis is to ensure they remain hydrated whilst waiting for the diarrhoea and vomiting to settle. Attempt a fluid challenge. Each hospital will have a policy for this. It involves recording a small volume of fluid given orally every 5-10 minutes to ensure they can tolerate it. If they are able to tolerate oral fluid and are adequately hydrated they can usually be managed at home. Rehydration solutions (e.g. dioralyte) can be used if tolerated. Dehydrated children or those that fail the fluid challenge may require IV fluids.

Once oral intake is tolerated a light diet can be slowly reintroduced. Dry foods such as toast may be better tolerated.

Antidiarrhoeal medication such as loperamide and antiemetic medication such as metoclopramide are generally not recommended. Antidiarrhoeal medications are particularly avoided in e. coli 0157 and shigella infections, and where there is bloody diarrhoea or high fever.

Antibiotics should only be given in patients that are at risk of complications once the causative organism is confirmed.

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24
Q

Which post-gastroenteritis complications may occur?

A

The are possible post-gastroenteritis complications:

Lactose intolerance
Irritable bowel syndrome
Reactive arthritis
Guillain–Barré syndrome

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25
Q

What is coeliac disease?

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.

26
Q

How does coeliac disease present?

A

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

27
Q

Which genes are associated with coeliac disease?

A

HLA-DQ2 gene (90%)

HLA-DQ8 gene

28
Q

Which auto-antibodies are associated with coeliac disease?

A

Tissue transglutaminase antibodies (anti-TTG)
Endomysial antibodies (EMAs)
Deaminated gliadin peptides antibodies (anti-DGPs)

If total IgA is low, TTG and EMA may be negative.

29
Q

How is coeliac disease diagnosed?

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
Endoscopy and intestinal biopsy show:

“Crypt hypertrophy”
“Villous atrophy”

30
Q

Which conditions are associated with coeliac disease?

A

Coeliac disease is associated with many other conditions:

Type 1 diabetes
Thyroid disease
Autoimmune hepatitis
Primary biliary cirrhosis
Primary sclerosing cholangitis
Down’s syndrome
31
Q

What are the complications of untreated coeliac disease?

A
Vitamin deficiency
Anaemia
Osteoporosis
Ulcerative jejunitis
Enteropathy-associated T-cell lymphoma (EATL) of the intestine
Non-Hodgkin lymphoma (NHL)
Small bowel adenocarcinoma (rare)
32
Q

How is coeliac disease treated?

A

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.

33
Q

What is inflammatory bowel disease?

A

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.

34
Q

Which features can be used to differentiate between Crohn’s amd UC?

A

Crohn’s and ulcerative colitis have features that are distinct from each other. These features are often tested in exams.

Crohn’s (crows NESTS)

N – No blood or mucus (these are less common in Crohns.)
E – Entire GI tract
S – “Skip lesions” on endoscopy
T – Terminal ileum most affected and Transmural (full thickness) inflammation
S – Smoking is a risk factor (don’t set the nest on fire)
Crohn’s is also associated with weight loss, strictures and fistulas.

Ulcerative Colitis (remember U – C – CLOSEUP)

C – Continuous inflammation
L – Limited to colon and rectum
O – Only superficial mucosa affected
S – Smoking is protective
E – Excrete blood and mucus
U – Use aminosalicylates
P – Primary sclerosing cholangitis
35
Q

How does inflammatory bowel disease present?

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.

Patients with inflammatory bowel disease can develop signs outside the gastrointestinal system that examiners like to test. It is worth remembering these extra-intestinal manifestations:

Finger clubbing
Erythema nodosum
Pyoderma gangrenosum
Episcleritis and iritis
Inflammatory arthritis
Primary sclerosing cholangitis (ulcerative colitis)
36
Q

How do you test for IBD?

A

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.

37
Q

How is IBD managed in general?

A

Any child presenting with symptoms suggestive of inflammatory bowel disease should be referred to secondary care for specialist assessment and management. They will be closely followed up by the multi-disciplinary team. This team includes paediatricians, specialist nurses, pharmacists, dieticians and surgeons if necessary.

It is essential to monitor the growth and pubertal development in children with inflammatory bowel disease, particularly when they are having exacerbations or being treated with steroids.

Management involves a combination of inducing remission during flares and maintaining remission when well. It is essential to monitor and supporting growth and development, and patients are likely to need input from a dietician.

38
Q

How is Crohn’s managed?

A

This section is based on NICE guidelines last updated May 2019. Please see the full guidelines and talk to seniors before treating patients.

Inducing Remission

First line are steroids (e.g. oral prednisolone or IV hydrocortisone).

If steroids alone don’t work, consider adding immunosuppressant medication under specialist guidance:

Azathioprine
Mercaptopurine
Methotrexate
Infliximab
Adalimumab

Maintaining Remission

Treatment is tailored to individual patients based on risks, side effects, nature of the disease and patient preference. It is reasonable not to take any medications whilst well.

First line:

Azathioprine
Mercaptopurine
Alternatives:

Methotrexate
Infliximab
Adalimumab

Surgery

When the disease only affects the distal ileum it is possible to surgically resect this area to prevent further flares. Crohn’s typically involves the entire GI tract. Surgery can also be used to treat strictures and fistulas secondary to Crohn’s disease.

39
Q

How is ulcerative colitis managed?

A

This section is based on NICE guidelines last updated May 2019. Please see the full guidelines and talk to seniors before treating patients.

Inducing Remission

Mild to moderate disease

First line: aminosalicylate (e.g. mesalazine oral or rectal)
Second line: corticosteroids (e.g. prednisolone)
Severe disease

First line: IV corticosteroids (e.g. hydrocortisone)
Second line: IV ciclosporin

Maintaining Remission

Aminosalicylate (e.g. mesalazine oral or rectal)
Azathioprine
Mercaptopurine

Surgery

Ulcerative colitis usually only affects the colon and rectum. Therefore, removing the colon and rectum (panproctocolectomy) will remove the disease. The patient is then left with either a permanent ileostomy or something called an ileo-anal anastomosis (J-pouch). This is where the ileum is folded back on itself and fashioned into a larger pouch that functions like a rectum. This “J-pouch” is then attached to the anus and collects stools prior to the person passing a motion.

40
Q

What is biliary atresia?

A

Biliary atresia is a congenital condition where a section of the bile duct is either narrowed 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. The initial investigation for possible biliary atresia is 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.

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.

41
Q

How is biliary atresia managed?

A

Management of biliary atresia is with 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.

42
Q

What is intestinal obstruction?

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.

43
Q

What can cause intestinal obstruction?

A
Meconium ileus
Hirschsprung’s disease
Oesophageal atresia
Duodenal atresia
Intussusception
Imperforate anus
Malrotation of the intestines with a volvulus
Strangulated hernia
44
Q

How does intestinal obstruction present?

A

Persistent vomiting. This may be bilious, containing bright green bile.
Abdominal pain and distention
Failure to pass stools or wind
Abnormal bowel sounds. These can be high pitched and “tinkling” early in the obstruction and absent later.

45
Q

How is intestinal obstruction diagnosed?

A

The initial investigation of choice is an abdominal xray. This may show dilated loops of bowel proximal to the obstruction and collapsed loops of bowel distal to the obstruction. There will also be absence of air in the rectum.

46
Q

How is intestinal obstruction managed?

A

Patients presenting with intestinal obstruction need to be referred to a paediatric surgical unit as an emergency. Initial management involves making them nil by mouth and inserting a nasogastric tube to help drain the stomach and stop the vomiting. They will also require IV fluids to correct any dehydration and electrolyte imbalances, and keep them hydrated while waiting for definitive management of the underlying cause.

47
Q

What is Hirschsprung’s disease?

A

Hirschsprung’s disease is 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.

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.

The key pathophysiology in Hirschsprung’s disease is 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 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.

48
Q

Which syndromes is Hirschsprung’s sometimes a part of?

A

There are a number of genes on various chromosomes that may have a modifying effect to increase the risk of Hirschsprung’s. A family history of Hirschsprung’s greatly increases the risk. Therefore where you are considering a diagnosis of Hirschsprung’s always take a careful family history.

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

Downs syndrome
Neurofibromatosis
Waardenburg syndrome (a genetic condition causing pale blue eyes, hearing loss and patches of white skin and hair)
Multiple endocrine neoplasia type II

49
Q

How does Hirschsprung’s present?

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
Vomiting
Poor weight gain and failure to thrive
50
Q

What is Hirschsprung-associated enterocolitis?

A

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.

51
Q

How is Hirschsprung’s disease managed?

A

Abdominal xray can be helpful in diagnosing intestinal obstruction and demonstrating features of HAEC.

Rectal biopsy is used to confirm the diagnosis. The bowel histology will demonstrates an absence of ganglionic cells.

Unwell children and those with enterocolitis will require initial fluid resuscitation and management of the intestinal obstruction. IV antibiotics are required in HAEC.

Definitive management is by surgical removal of the aganglionic section of bowel. Most patients will live a normal life after corrective surgery, although they can have long term disturbances in bowel function and may be left with some degree of incontinence.

52
Q

What is intersusception?

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.

53
Q

Which conditions are associated with intersusception?

A

It is associated with various conditions:

Concurrent viral illness
Henoch-Schonlein purpura
Cystic fibrosis
Intestinal polyps
Meckel diverticulum
54
Q

How does intersusception present?

A
Severe, colicky abdominal pain
Pale, lethargic and unwell child
“Redcurrant jelly stool”
Right upper quadrant mass on palpation. This is described as “sausage-shaped”
Vomiting
Intestinal obstruction
55
Q

How is intersusception managed?

A

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

56
Q

What are the possible complications with intersusception?

A

Obstruction
Gangrenous bowel
Perforation
Death

57
Q

What is appendicits?

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.

58
Q

How does appendicits present?

A

he 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.

59
Q

How is appendicits diagnosed?

A

Diagnosis is based on the clinical presentation and raised inflammatory markers. Performing a CT scan can be useful in confirming the diagnosis, particularly where another diagnosis is more likely. An ultrasound scan is often used in female patients to exclude ovarian and gynaecological pathology.

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.

60
Q

What other differentials should be considered in a patient with suspected appendicitis?

A

Ectopic Pregnancy

Consider ectopic pregnancy in girls of childbearing age. This is a gynaecological emergency with a relatively high mortality if mismanaged. A serum or urine bHCG (pregnancy test) to exclude pregnancy is essential in adolescent girls.

Ovarian Cysts

Ovarian cysts can cause pelvic and iliac fossa pain, particularly with rupture or torsion.

Meckel’s Diverticulum

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, become inflamed, rupture or cause a volvulus or intussusception. They are often removed prophylactically if identified incidentally during other abdominal operations.

Mesenteric Adenitis

Mesenteric adenitis describes inflamed abdominal lymph nodes. This presents with abdominal pain, usually in younger children. This is often associated with tonsillitis or an upper respiratory tract infection. No specific treatment is required.

Appendix Mass

An appendix mass occurs when the omentum surrounds and sticks to the inflamed appendix, forming a mass in the right iliac fossa. This is typically managed conservatively with supportive treatment and antibiotics, followed by appendicectomy once the acute condition has resolved.

61
Q

How is appendicitis managed?

A

Patients with suspected appendicitis need emergency admission to hospital under the surgical team. Older children, for example those aged above 10 years, can often be managed by adult general surgical teams at local hospitals, provided there is a paediatric department in the hospital. Younger children will need to be admitted under paediatric surgeons.

Removal of the inflamed appendix (appendicectomy) is the definitive management for acute appendicitis. Laparoscopic surgery is associated with fewer risks and faster recovery compared to open surgery (laparotomy).

62
Q

What are the possible complications of appendectomy?

A

Complications of Appendicectomy

Bleeding, infection, pain and scars
Damage to bowel, bladder or other organs
Removal of a normal appendix
Anaesthetic risks
Venous thromboembolism (deep vein thrombosis or pulmonary embolism)