Paed GI Flashcards

1
Q

Examples of GI issues

A

-Acute abdomen
-Cows milk protein intolerance
-Gastroesophageal reflux
-IBD
-Coeliac
-Pyloric stenosis
-Intussusception
-Hernia/ hydrocele

-Constipation
-Diarrhoea
-Vomiting
-Feeding problems
-Jaundice

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2
Q

Causes of abdominal pain

A

-Abdominal conditions
=Colic
=Intussusception
=Mesenteric adenitis
=Constipation
=Inflammatory bowel disease
=Coeliac disease
=Appendicitis

-Extra-abdominal conditions
=Migraine
=Diabetic ketoacidosis
=Infection elsewhere (e.g. throat)
=Pneumonia
=Urinary tract infection
=Stress

-Some causes are rare but serious enough not to be forgotten:
=Malignancy: Neuroblastoma, Wilms tumour
=Testicular torsion
=Bowel obstruction: Incarcerated hernia, Malrotation, Meckel’s diverticulum (bilious vomit green bile, not wanting to eat, severe pain worse on movement)

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3
Q

History of abdominal pain

A

-An acute or chronic condition
-A medical or surgical problem
-A sign of something serious
-Recent illness

-Easy to miss conditions:
=Urinary tract infection
=Obstruction
=Appendicitis
=Inflammatory bowel disease

-Rare but serious conditions:
=Neuroblastoma
=Wilms tumour

-Causes of acute pain – hours to days:
=Urinary tract infection
=Diabetic ketoacidosis (excessive thirst and polyuria)
=Surgical problems

-Causes of chronic pain – weeks or longer:
=Constipation
=Inflammatory bowel disease
=Malignancy
=Growth (faltering), potential stress

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4
Q

Red flags in GI history

A

-Life restriction
-Anorexia, early satiety
-Weight loss; decreased height velocity; pubertal delay; slowed pubertal progress
-Family history (e.g. IBD, coeliac)
-Diarrhoea, urgency, tenesmus
-Nocturnal pain
-Blood in stools
-Nocturnal stooling

A weak, abnormally high-pitched, or continuous cry is a red flag which may indicate potentially serious illness.
Other red flags include fever, apnoeic episodes, cyanosis, abnormal breathing pattern, bilious or projectile vomiting, weight loss or faltering growth, and blood in the stool.

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5
Q

Abdo exam

A

-General observations – what is the child’s behaviour:
=Whilst lying down?
=Whilst climbing on and off the couch?
=Walking and moving comfortably?

-Physiological observations – are there signs of dehydration or sepsis:
=Fever
=Capillary refill
=Heart rate
=Respiratory rate- lower lobe pneumonia can present as abdo pain

-Gather the child’s trust:
=Use distraction techniques
=Ask the child to show you where it hurts
=Away from or near the umbilicus?

-Examine the abdomen for:
=Tenderness
=Guarding
=Peritonism
=Masses (LIF constipation)
=Organomegaly

-Perform urinalysis for:
=Infection
=Glucose
=Ketones

Examine genitalia in all boys, rectal exam considered by surgeon

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6
Q

Abdominal red flags

A

-Peritonitis
-Intussusception
-Abdominal mass
-Vomiting bile
-Torsion of testis

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7
Q

Abdo emergencies

A

-Gastrointestinal – severe IBD; coeliac crisis; severe GI bleed
-Hepatological – Acute liver failure; portal hypertensive bleeding
-Nutritional – Severe undernutrition needing refeeding protocol
-Procedural – Bleeding; foreign bodies especially button batteries

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8
Q

Symptoms of malabsorption and maldigestion

A

-Diarrhoea
-Smelly, floaty stools (fat)
-Watery, explosive stools +/- perianal excoriation +/- distension (CHO)
-Short stature, faltering height growth, weight loss
-Vomiting
-Anorexia, early satiety
-Oedema (hypoalbuminaemia); specific nutrient signs (scurvy, rickets)

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9
Q

Overview of peritonitis

A

-Severe inflammation of peritoneal cavity
-Look for guarding, dehydration, sepsis
-Most common: perforated appendix

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10
Q

Overview of appendicitis in children

A

-Appendicitis is one of the most common acute surgical problems facing children. Diagnosis is often made difficult by a presentation which is far from the classically history of:
=central abdominal pain which later radiates to the right iliac fossa
=low-grade pyrexia
=minimal vomiting

-Children who are younger or have a retrocaecal/pelvic appendix are more likely to present in an atypical way

-Appendicitis is uncommon in children under 4 years old but in this group often presents with perforation

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11
Q

Overview of intussusception

A

-Infants and toddlers; invagination of intestine into lumen of adjacent bowel (collapsible telescope): bowel obstruction. Most commonly around ileo-caecal region (proximal or at level of)
-Infants between 6-18 months, boys x2

-P: Signs of extra-abdominal infection (tonsillitis, otitis media, lead point in Peyer’s patches lymph node swelling, vomiting and diarrhoea)
-Bouts of colicky pain, settled in between (intermittent severe crampy progressive abdo pain)
-Inconsolable crying
-During paroxysm the infant will characteristically draw their knees up and turn pale
-Blood stained stool (red currant jelly late sign)
-A right sided mass (sausage shaped in RUQ)
-Anticipate dehydration (IV fluids)

-I: USS (target like mass)

-M: the majority of children can be treated with reduction by air insufflation under radiological control, which is now widely used first-line compared to the traditional barium enema
=if this fails, or the child has signs of peritonitis, surgery is performed

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12
Q

Overview of abdominal mass

A

-Neuroblastoma
-Wilms tumour
-Appendix abscess
-Constipation

-Diagnosed late

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13
Q

Overview of Meckel’s diverticulum

A

-Congenital diverticulum of the small intestine
-Occurs in 2% of the population, 2 feet from the ileocaecal valve, 2 inches long

-P: usually asymptomatic, abdominal pain mimicking appendicitis, rectal bleeding (most common cause of painless massive GI bleeding requiring a transfusion in children between the ages of 1 and 2 years), intestinal obstruction
secondary to an omphalomesenteric band (most commonly), volvulus and intussusception

-I: if the child is haemodynamically stable with less severe or intermittent bleeding then a ‘Meckel’s scan’ should be considered, mesenteric arteriography may also be used in more severe cases e.g. transfusion is required

-M: removal if narrow neck or symptomatic
options are between wedge excision or formal small bowel resection and anastomosis

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14
Q

Overview of Mesenteric adenitis

A

Mesenteric adenitis is inflamed lymph nodes within the mesentery. It can cause similar symptoms to appendicitis and can be difficult to distinguish between the two. It often follows a recent viral infection and needs no treatment

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15
Q

Overview of vomiting bile

A

-Bilious vomiting is intestinal obstruction until proven otherwise:
=Green colour
=Empty stomach?

-Investigate by
=Abdominal X-ray
=Blood tests

-Consider a surgical opinion

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16
Q

Overview of pyloric stenosis

A

-Pyloric stenosis typically presents in the second to fourth weeks of life with vomiting, although rarely may present later at up to four months. It is caused by hypertrophy of the circular muscles of the pylorus.
-Epidemiology: incidence of 4 per 1,000 live births, 4 times more common in male,10-15% of infants have a positive family history, first-borns are more commonly affected

-P: ‘projectile’ vomiting (non bile stained), typically 30 minutes after a feed, constipation and dehydration may also be present, a palpable mass may be present in the upper abdomen, hypochloraemic, hypokalaemia alkalosis due to persistent vomiting

-I: USS, test feed

-M: Ramstedt pyloromyotomy (open or laparoscopic)

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17
Q

Overview of testis torsion

A

-Symptoms of testicular torsion include:
=Testicular pain – usually
=Abdominal pain – occasionally
=Crying & being unsettled in infants
=More common in 12 and above

-Check scrotum for
=Swelling
=Tenderness
=Discolouration

-Have a low threshold for urgent referral to surgeons- operation within 6 hours
= Fertility in the testicle concerned may be lost within 4 to 6 hours of interrupted blood flow to the organ

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18
Q

Overview of necrotising enterocolitis

A

Necrotising enterocolitis is one of the leading causes of death among premature infants.

-P: Initial symptoms can include feeding intolerance, abdominal distension and bloody stools, which can quickly progress to abdominal discolouration, perforation and peritonitis.

Abdominal x-rays are useful when diagnosing necrotising enterocolitis, as they can show:
=dilated bowel loops (often asymmetrical in distribution)
=bowel wall oedema
=pneumatosis intestinalis (intramural gas)
=portal venous gas
=pneumoperitoneum resulting from perforation
=air both inside and outside of the bowel wall (Rigler sign)
=air outlining the falciform ligament (football sign)

M: Increased risk when empirical antibiotics are given to infants beyond 5 days
Treatment is with total gut rest and TPN, babies with perforations will require laparotomy

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19
Q

Overview of coeliac disease in children

A

-Sensitivity to the protein gluten.
-Repeated exposure leads to villous atrophy which in turn causes malabsorption.
-Children normally present before the age of 3 years, following the introduction of cereals into the diet
-Genetics, incidence of around 1:100, it is strongly associated with HLA-DQ2 (95% of patients) and HLA-DQ8 (80%)

-P: Features may coincide with the introduction of cereals (i.e. gluten): failure to thrive, diarrhoea, abdominal distension, older children may present with anaemia, many cases are not diagnosed to adulthood

-I: jejunal biopsy showing subtotal villous atrophy
anti-endomysial and anti-gliadin antibodies are useful screening tests

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20
Q

Overview of IBD

A

-Paed: Incidence 12/100,000, increasing prevalence and incidence

-CD – granulomatous, transmural inflammation with skip lesions
-UC – mucosal inflammation, continuous and starts in rectum
-IBD unclassified (U) - mucosal inflammation , limited to the colon

-I: height and weight, oral, Abdo and peri-anal exam, EIM’s, stool and blood tests

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21
Q

History and exam findings in PIBD

A

-Abdominal pain
-Diarrhoea with or without blood
-Pyrexia
-Arthritis
-Rash
-FH

-Abdominal tenderness, mass
-Finger clubbing
-Erythema nodosum (very rarely pyoderma gangrenosum)
-Growth problems: reduced height velocity, height centile/ z-score out with that expected for parental height. Mean final height 2.4cm below target height

-Crohns: perianal exam (abscess, fistula, deep fissures, large inflamed skin tags), perioral (mucogingivitis, buccal tagging, deep ulceration, perioral erythema)

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22
Q

Diagnostic pathways in Crohn’s

A

-Blood inflammatory markers (ESR/CRP)
-FBC
-Albumin and liver function
-Faecal calprotectin (bowel inflammation)

-Upper GI endoscopy and ileocolonoscopic with histology
-Small bowel imaging (MRE or VCE)
-Immune workup?

23
Q

IBD Management

A

-Exclusive Nutrition (Steroids for failures)
-Early use of Azathioprine (MP): used for severe disease at presentation or nutrition/ steroid dependency
-Methotrexate for Aza failures: s/c, steroid sparing/ growth promoting effect
-Anti- TNF for non-responsive disease
-Surgical Resection for localised disease

-Combination of Azithromycin and Metronidazole shown to be effective intreating active luminal CD
-Azithromycin 7.5mg/kg once daily 5 days for 4 weeks then 3 days for 4weeks
-Metronidazole 10mg/kg per dose twice daily

-Anti-TNF therapy is recommended for inducing and maintaining remission in children with chronically active luminal CD despite prior optimised immunomodulator therapy (EL2)
-Anti-TNF therapy is recommended for inducing remission in children with active steroid-refractory disease (EL2)

24
Q

Toxicity of corticosteroids

A

-Osteoporosis/osteonecrosis
-Serious infections
-Cushing syndrome
-Cataracts
-GROWTH DELAY
-Behavioural changes
-Diabetes
-Cardiovascular complications

25
Q

Overview of GORD

A

-Commonest cause of vomiting in infancy. Around 40% of infants regurgitate their feeds to a certain extent so there is a degree of overlap with normal physiological processes.

-RF: preterm delivery, neurological disorders

-P: typically develops before 8 weeks, vomiting/regurgitation, milky vomits after feeds, may occur after being laid flat, excessive crying, especially while feeding

-I: clinical

-M:
=advise regarding position during feeds - 30 degree head-up
=infants should sleep on their backs as per standard guidance to reduce the risk of cot death
ensure infant is not being overfed (as per their weight) and consider a trial of smaller and more frequent feeds
=a trial of thickened formula (for example, containing rice starch, cornstarch, locust bean gum or carob bean gum)
=a trial of alginate therapy e.g. Gaviscon. Alginates should not be used at the same time as thickening agents
=NICE do not recommend a proton pump inhibitor (PPI) to treat overt regurgitation in infants and children occurring as an isolated symptom. A trial of one of these agents should be considered if 1 or more of the following apply:
==unexplained feeding difficulties (for example, refusing feeds, gagging or choking)
==distressed behaviour
==faltering growth
=prokinetic agents e.g. metoclopramide should only be used with specialist advice

-Complications: distress, failure to thrive, aspiration, frequent otitis media, in older children dental erosion may occur
=If there are severe complications (e.g. failure to thrive) and medical treatment is ineffective then fundoplication may be considered

26
Q

Overview of eosinophilic oesophagitis

A

-Increasingly common

-P: similar to GORD but children older, can be co-existent atopy, dysphagia and food bolus obstruction more common. Feeding difficulties (3 yr.), vomiting/GERD (5), abdominal pain (9), dysphagia (11), food impaction and oesophageal stricture

-I: GI endoscopy, increased eosinophils in biopsies (>15)

-M: omeprazole, steroids (liquids, Budesonide), immunosuppression in difficult cases, oesophageal dilatation if stricture, dairy exclusion/ 6 food elimination diet/ elemental feeds

27
Q

Overview of IBS

A

-10-15% school children get abdo pain, 90% no organic pathology
-Functional Abdominal pain (FAP): functional dyspepsia, IBS, abdominal migraine

-P: pain, bloating, tired, occasional diarrhoea, anxiety and parental attention can make it worse. >3 episodes/ month for min 2 months, pain often related to defecation, >3 yrs., daily activities affected, can be associated with sleep disturbance or headache

-I: assess dietary triggers (irregular patterns, overeating, high fat, sugar, caffeine, carbonated drinks, milk), physical triggers (recent viral illness, intolerances, chronic illness, low activity levels, overt fatigue), psychosocial (problems at school, home, anxiety, life events, social media, school avoidance)

-M: familial acceptance/ supporting coping skills, reassurance and education, focus on improvement of functioning rather than pain resolution. Peppermint oil, antispasmodics (Mebeverine), PPI (omeprazole), laxatives (Movicol), amitriptyline (severe)

28
Q

What is acute liver failure?

A

-No underlying chronic liver condition
-INR >2.0/PT >20
-Encephalopathy – prime factor in adult ALF; hard to determine in infants and toddlers
-INR 1.5-1.9/PT >15 with encephalopathy <8 weeks after onset of jaundice
=Hyperacute (<7 days)
=Acute/sub-acute (>28 days)
-Death – infection; bleeding; encephalopathy; MOF

29
Q

Clinical presentation of ALF

A

-Lethargy
-Jaundice
-Hypoglycaemia
-History of viral infection (coryza)/paracetamol ingestion
-Coagulopathy
-Encephalopathy

30
Q

Acute management of ALF

A

-Support ABCs; treat cause; check PT, glucose, albumin, NH3
-IV Vitamin K (infants 5mg, children 10mg)
-Specific:
=Paracetamol – NAC
=Metabolic – diet, substrate
=Infectious – e.g. Aciclovir in HSV
=Autoimmune – steroids
=Infection: low threshold for empirical antibiotics (e.g. Tazocin/Gentamicin)

31
Q

Overview of biliary atresia

A

-Section of the bile duct is either narrowed or absent.
=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.

-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.
-Jaundice extending beyond physiological 2 weeks, dark urine and pale stools, appetite and growth disturbance, hepatomegaly with splenomegaly, abnormal growth

-I: 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.
=Serum bilirubin including differentiation into conjugated and total bilirubin: Total bilirubin may be normal, whereas conjugated bilirubin is abnormally high
=Liver function tests (LFTs) including serum bile acids and aminotransferases are usually raised but cannot differentiate between biliary atresia and other causes of neonatal cholestasis
=Serum alpha 1-antitrypsin: Deficiency may be a cause of neonatal cholestasis
=Sweat chloride test: Cystic fibrosis often involves the biliary tract
=Ultrasound of the biliary tree and liver: May show distension and tract abnormalities
=Percutaneous liver biopsy with intraoperative cholangioscopy

-Jaundice > 14 days
-Increased conjugated bilirubin
-Urgent Kasai procedure: portoenterostomy, involves attaching a section of the small intestine to the opening of the liver, where the bile duct normally attaches

32
Q

Overview of meconium ileus

A

-Usually delayed passage of meconium and abdominal distension
-The majority have cystic fibrosis
-X-Rays will not show a fluid level as the meconium is viscid, PR contrast studies may dislodge meconium plugs and be therapeutic
-Infants who do not respond to PR contrast and NG N-acetyl cysteine will require surgery to remove the plugs

33
Q

Overview of Oesophageal atresia

A

-Associated with tracheo-oesophageal fistula and polyhydramnios
-May present with choking and cyanotic spells following aspiration
-VACTERL associations

34
Q

Overview of intestinal malrotation

A

-High caecum at the midline
-Feature in exomphalos, congenital diaphragmatic hernia, intrinsic duodenal atresia
-May be complicated by the development of volvulus, an infant with volvulus may have bile stained vomiting
-Diagnosis is made by upper GI contrast study and USS
-Treatment is by laparotomy, if volvulus is present (or at high risk of occurring then a Ladd’s procedure is performed (includes division of Ladd bands and widening of the base of the mesentery)

35
Q

Clinical manifestations of Upper GI haemorrhage

A

-Relatively rare in children, mortality <10%
-Haematemesis
-Abdominal pain
-Melaena
-Fresh PR bleed (if large/rapid)
-Pallor
-Cardiovascular compromise

-Portal hypertension bleeding
=Splenomegaly +/- hepatomegaly
=Thrombocytopenia +/- leukopenia
=Visible ectatic abdominal wall veins: caput medusa
=Variceal haemorrhage may be the first presentation of portal hypertension/liver disease (~50%)

36
Q

Causes of upper GI bleed in children

A

-New-born
=Swallowed maternal blood
=Vit K deficiency
=Stress gastritis or ulcer
=Acid-peptic disease
=Vascular anomaly
=Coagulopathy
=Milk-protein sensitivity

-Infant
=Stress gastritis or ulcer
=Acid-peptic disease
=Mallory Weiss tear
=Vascular anomaly
=GI duplications
=Varices
=Duodenal/ gastric webs
=Bowel obstruction

-Child/adolescent
=Mallory Weiss tear
=Acid-peptic disease
=Varices
=Caustic ingestion
=Vasculitis (Henoch Schonlein purpura)
=Crohns
=Bowel obstruction

37
Q

Management of upper GI bleed

A

-Assessment – major haemorrhage protocol
-Resuscitation – don’t overdo transfusions
-Re-evaluation
-Identification of the cause/source of bleeding
-PPI; octreotide; antibiotics
-Appropriate definitive therapy

38
Q

Diagnosis of constipation in children (2 or more of following)

A

Child <1 year
-Stool pattern: Fewer than 3 complete stools per week (type 3 or 4 on Bristol Stool Form Scale) (this does not apply to exclusively breastfed babies after 6 weeks
of age)/ Hard large stool/ ‘Rabbit droppings’ (type 1)
-Symptoms associated with defecation: Distress on passing stool/ Bleeding associated with hard stool/ Straining
-History: Previous episode(s) of constipation/ Previous or current anal fissure

Child >1 year
-Stool pattern: Fewer than 3 complete stools per week (type 3 or 4)/ Overflow soiling (commonly very loose, very smelly, stool passed without sensation)/ ‘Rabbit droppings’ (type 1)/ Large, infrequent stools that can block the toilet
-Symptoms associated with defecation: Poor appetite that improves with passage of large stool/ Waxing and waning of abdominal pain with passage of stool/ Evidence of retentive posturing: typical straight-legged, tiptoed, back arching
posture/ Straining/ Anal pain
-History: Previous episode(s) of constipation/ Previous or current anal fissure/ Painful bowel movements and bleeding associated with hard stools

39
Q

Causes of constipation in children

A

-Idiopathic
-Dehydration
-Low-fibre diet
-Medications: e.g. Opiates
-Anal fissure
-Over-enthusiastic potty training
-Hypothyroidism
-Hirschsprung’s disease
-Hypercalcaemia
-Learning disabilities

40
Q

Indications for idiopathic constipation

A

-Starts after a few weeks of life
-Obvious precipitating factors coinciding with the start of symptoms: fissure, change of diet, timing of potty/toilet training or acute events such as infections, moving house, starting nursery/school, fears and phobias, major change in family, taking medicines
-Passage of meconium: <48 hours
-Growth generally well, weight and height within normal limits, fit and active
-No neurological problems in legs, normal locomotor development
-Changes in infant formula, weaning, insufficient fluid intake or poor diet

41
Q

Red flags suggesting underlying disorder in constipation

A

-Reported from birth or first few weeks of life
-Passage of meconium: >48 hours
-Ribbon stools
-Faltering growth (amber flag)
-Previously unknown or undiagnosed weakness in legs, locomotor delay
-Distended abdomen
-Disclosure or evidence that raises concerns over possibility of child maltreatment (amber)

42
Q

Factors suggesting faecal impaction

A

-Symptoms of severe constipation
-Overflow soiling
-Faecal mass palpable in the abdomen (digital rectal examination should only be carried out by a specialist)

43
Q

Management of faecal impaction

A

-Polyethylene glycol 3350 + electrolytes (Movicol Paediatric Plain) using an escalating dose regimen as the first-line treatment
-Add a stimulant laxative if Movicol Paediatric Plain does not lead to disimpaction after 2 weeks
-Substitute a stimulant laxative singly or in combination with an osmotic laxative such as lactulose if Movicol Paediatric Plain is not tolerated
-Inform families that disimpaction treatment can initially increase symptoms of soiling and abdominal pain

44
Q

Maintenance therapy for constipation

A

-Very similar to the faecal impaction, with obvious adjustments to the starting dose, i.e.
-First-line: Movicol Paediatric Plain
-Add a stimulant laxative if no response
-Substitute a stimulant laxative if Movicol Paediatric Plain is not tolerated. Add another laxative such as lactulose or docusate if stools are hard
-Continue medication at maintenance dose for several weeks after regular bowel habit is established, then reduce the dose gradually

General points
=do not use dietary interventions alone as first-line treatment although ensure the child is having adequate fluid and fibre intake
=consider regular toileting and non-punitive behavioural interventions
=for all children consider asking the Health Visitor or Paediatric Continence Advisor to help support the parents.

-Infants not yet weaned (usually < 6 months)
=bottle-fed infants: give extra water in between feeds. Try gentle abdominal massage and bicycling the infant’s legs
=breast-fed infants: constipation is unusual and organic causes should be considered

-Infants who have or are being weaned
=offer extra water, diluted fruit juice and fruits
=if not effective consider adding lactulose

45
Q

Overview of Hirschsprung’s Disease

A

-Hirschsprung’s disease is caused by an aganglionic segment of bowel due to a developmental failure of the parasympathetic Auerbach and Meissner plexuses (Absence of ganglion cells from myenteric and submucosal plexuses). Although rare (occurring in 1 in 5,000 births) it is an important differential diagnosis in childhood constipation.

-Pathophysiology
=parasympathetic neuroblasts fail to migrate from the neural crest to the distal colon → developmental failure of the parasympathetic Auerbach and Meissner plexuses → uncoordinated peristalsis → functional obstruction

-Associations
=3 times more common in males
=Down’s syndrome

-Presentations
=neonatal period e.g. failure or delay to pass meconium
=older children: constipation, abdominal distension

-Investigations
=abdominal x-ray
=rectal biopsy: gold standard for diagnosis (full thickness)

-Management
=initially: rectal washouts/bowel irrigation
=definitive management: surgery to affected segment of the colon (anorectal pull through procedure)

46
Q

Overview of cow’s milk protein intolerance/ allergy

A

-3-6% of all children
-Typically presents in the first 3 months of life in formula-fed infants, although rarely it is seen in exclusively breastfed infants.
-Both immediate (IgE mediated) and delayed (non-IgE mediated) reactions are seen. The term CMPA is usually used for immediate reactions and CMPI for mild-moderate delayed reactions.

-P: regurgitation and vomiting, diarrhoea, urticaria, atopic eczema, ‘colic’ symptoms: irritability, crying
wheeze, chronic cough, rarely angioedema and anaphylaxis may occur. Persistent/ severe treatment resistant GORD atopic eczema
IgE: diarrhoea vomit, colicky pain angio-oedema
Non IgE: pain/discomfort, constipation, blood in stool food refusal, faltering growth

-D: clinical (e.g. improvement with cow’s milk protein elimination), skin prick/patch testing, total IgE and specific IgE (RAST) for cow’s milk protein

-M: If the symptoms are severe (e.g. failure to thrive) refer to a paediatrician.
=Formula-fed: extensive hydrolysed formula (eHF) milk is the first-line replacement formula for infants with mild-moderate symptoms, amino acid-based formula (AAF) in infants with severe CMPA or if no response to eHF, around 10% of infants are also intolerant to soya milk
=Breastfed: continue breastfeeding, eliminate cow’s milk protein from maternal diet. Consider prescribing calcium supplements for breastfeeding mothers whose babies have, or are suspected to have, CMPI, to prevent deficiency whilst they exclude dairy from their diet, use eHF milk when breastfeeding stops, until 12 months of age and at least for 6 months

-Prognosis:
=CMPI usually resolves in most children
=in children with IgE mediated intolerance around 55% will be milk tolerant by the age of 5 years
=in children with non-IgE mediated intolerance most children will be milk tolerant by the age of 3 years
=a challenge is often performed in the hospital setting as anaphylaxis can occur.

47
Q

Causes of diarrhoea

A

-Gastroenteritis
=main risk is severe dehydration
=most common cause is rotavirus - typically accompanied by fever and vomiting for the first 2 days. The diarrhoea may last up to a week
treatment is rehydration
=diarrhoea usually lasts for 5-7 days and stops within 2 weeks, vomiting usually lasts for 1-2 days and stops within 3 days

-Chronic diarrhoea in Infants
=most common cause in the developed world is cows’ milk intolerance
=toddler diarrhoea: stools vary in consistency, often contain undigested food
=coeliac disease
=post-gastroenteritis lactose intolerance

48
Q

When to do stool culture in diarrhoea

A

-You suspect septicaemia or
-There is blood and/or mucus in the stool or
-The child is immunocompromised

-You should consider doing a stool culture if:
=the child has recently been abroad or
=the diarrhoea has not improved by day 7 or
=you are uncertain about the diagnosis of gastroenteritis

49
Q

Hernias in children

A

Inguinal hernias are a common disorder in children. They are commoner in males as the testis migrates from its location on the posterior abdominal wall, down through the inguinal canal. A patent processus vaginalis may persist and be the site of subsequent hernia development.

Children presenting in the first few months of life are at the highest risk of strangulation and the hernia should be repaired urgently. Children over 1 year of age are at lower risk and surgery may be performed electively. For paediatric hernias a herniotomy without implantation of mesh is sufficient. Most cases are performed as day cases, neonates and premature infants are kept in hospital overnight as there is a recognised increased risk of post operative apnoea.

50
Q

Overview of hydrocele

A

-A hydrocele describes the accumulation of fluid within the tunica vaginalis. They can be divided into communicating and non-communicating:
communicating: caused by patency of the processus vaginalis allowing peritoneal fluid to drain down into the scrotum.
-Communicating hydroceles are common in new-born males (clinically apparent in 5-10%) and usually resolve within the first few months of life
non-communicating: caused by excessive fluid production within the tunica vaginalis

-Hydroceles may develop secondary to:
=epididymo-orchitis
=testicular torsion
=testicular tumours

-Features
=soft, non-tender swelling of the hemi-scrotum. Usually anterior to and below the testicle
=The swelling is confined to the scrotum, you can get ‘above’ the mass on examination
=transilluminates with a pen torch
=the testis may be difficult to palpate if the hydrocele is large

-Diagnosis may be clinical but ultrasound is required if there is any doubt about the diagnosis or if the underlying testis cannot be palpated.

-Management
=infantile hydroceles are generally repaired if they do not resolve spontaneously by the age of 1-2 years
=in adults a conservative approach may be taken depending on the severity of the presentation. Further investigation (e.g. ultrasound) is usually warranted however to exclude any underlying cause such as a tumour

51
Q

CF GI disease

A

-Malabsorption
=Managed with Creon pancreatic enzyme replacement
=Supplementation of fat-soluble vit
-Poor growth
-GORD
-Meconium ileus (10-15%)
-Constipation
-Distal intestinal obstruction syndrome (DIOS)
-Rectal prolapse

52
Q

Overview of undescended testis

A

Undescended testis occurs in around 2-3% of term male infants, but is much more common if the baby is preterm. Around 25% of cases are bilateral.

-Complications of undescended testis
=infertility
=torsion
=testicular cancer
=psychological

-Management
=Unilateral undescended testis
==NICE CKS now recommend referral should be considered from around 3 months of age, with the baby ideally seeing a urological surgeon before 6 months of age
==Orchidopexy: Surgical practices vary although the majority of procedures are performed at around 1 year of age
=Bilateral undescended testes
==Should be reviewed by a senior paediatrician within 24hours as the child may need urgent endocrine or genetic investigation

53
Q

Overview of infantile colic

A

Infantile colic describes a relatively common and benign set of symptoms seen in young infants. It typically occurs in infants less than 3 months old and is characterised by bouts of excessive crying and pulling-up of the legs, often worse in the evening. Increases in the early weeks of life and peaks around 6-8 weeks of age and usually improves by 3-4 months of age

Infantile colic occurs in up to 20% of infants. The cause of infantile colic is unknown.

NICE do not recommend the use of simeticone (such as Infacolµ) or lactase (such as Coliefµ) drops.