Gastrointestinal II Flashcards
When should GORD be suspected in an infant (up to 1 year old)?
Regurgitation + at least one of:
- Distressed behaviour whilst feeding (arched back, unusual neck postures)
- Hoarseness and/ or chronic cough
- Single episode of pneumonia
- Unexplained feeding difficulties (refusing to feed, gagging, choking etc)
- Faltering growth
What additional features of GORD may children >1 present with?
- Heartburn
- Retrosternal pain
- Epigastric pain
- Episodic torticollis
What are the risk factors for developing GORD in children?
- Premature birth
- Parental history of heartburn or regurgitation
- Obesity
- Hiatus hernia
- Hx of congenital diaphragmatic hernia
- Hx of congenital oesophageal atresia
- Neurodisability (such as cerebral palsy)
What are the complications of GORD in children?
- Reflux oesophagitis
- Recurrent aspiration pneumonia
- Recurrent acute otitis media (>3 episodes in 6 months)
- Dental erosion in a child with neurodisability
- Apnoea or apparent life-threatening events (rare)
Complications from GORD are rare
When is the typical onset of GORD symptoms in children?
Before 8 weeks, typically resolving before the child is 1
What is a normal level of vomiting/ regurgitation for an infant?
Effortless spitting up of one to two mouthfuls
What examinations should be done in suspected GORD?
- Chest examination for respiratory complications
- Temperature
- Abdominal palpatoion
- Growth assessment using centile charts
- Review of head circumference to exclude alternative explanation of vomiting
What differentiates CMPI from GORD?
- Dermatological features eg. eczema
- Chronic diarrhoea
- Patient has/ is at high risk of atopy
What differentiates pyloric stenosis from GORD?
Frequent, forceful vomiting and the child is very hungy and keen to feed
What differentiates intestinal obstruction from GORD?
- Bile-stained vomit
- Abdominal distention, tenderness or palpable mass
What differentiates raised ICP from GORD?
- Bulging fontanelle or altered responsiveness
- Rapidly increasing head circumference, vomiting in the morning
When should same-day admission be arranged for a child with suspected GORD?
- Haematemesis (not caused by ingested blood)
- Melaenia
- Dysphagia
When should a specialist assessment be arranged for a child with suspected GORD?
- Uncertain diagnosis/ red flag sx suggesting a more serious condition
- Persistent, faltering growth
- Unexplained distress in children with communication difficulties
- Sx not responding to treatment
- Feeding aversion + hx of regurgitation
- Unexplained iron deficiency anaemia
- No improvement in sx after 1 year of age
- Suspected Sandifer’s syndrome (episodic torticollis)
- Complications from GORD
How should breastfed infants with frequent regurgitation be managed in primary care?
Conservative:
- Breastfeeding techniques
- Positioning after feeds (30 degree head-up)
Medical:
- 1-2 weeks alginate therapy
- If sx improve, continue with treatment, stop at regular intervals (eg. every 2 weeks) to see if sx have improved and whether it’s possible to stop tx
How should formula fed infants with GORD be treated in primary care?
Conservative:
- Review feeding hx
- Reduce volumes of feeds if they’ve excessive for the child’s weight
- Reduce volume but increase frequency of feeds (trial 1-2 weeks)
- If unsuccessful, offer 1-2 weeks of feed thickeners/ pre-thickened formula
Medical:
- If all else unsuccessful, 1-2 weeks of alginate (should not be used at the same time as thickening agents)
What is the managment of breast or formula fed infants with GORD for whom alginate therapy has been unsuccessful?
4-week PPI eg. omeprazole suspension or histamine-2 receptor antagonist (H2RA)
Should only be considered if there is:
- Unexplained feeding difficulties
- Distressed behaviour
- Faltering growth
What is the management for children 1-2 years who have persitent heartburn, retrosternal or epigastric pain?
4 week trial of PPI or H2RA
What is intussusception?
The telescoping of a segment of the bowel inside another segment, most commonly in the ileo-caecal region
What is the peak age incidence of intussusception?
6-36 months
What are the risk factors associated with intussusception?
- Age (6-36 months)
- Sex (males 2:1)
- Anatomical lead points: polyps, Meckel’s diverticulum, tumours or other structural abnormalities
- Infections: lymphoid hyperplasia (lymphoid tissue in Peyer’s patches is particularly sensitive to viral infections)
What is the triad of intussusception?
- Colicky abdominal pain
- Vomiting
- Red ‘currant jelly’ stools
Complete triad is rarely present
What are the signs and sx of intussusception?
- Intermittent severe, crampy abdo pain (worse during peristalsis), may lead to children drawing knees up
- Lethargy/ altered consciousness
- Vomiting: initially non-bilious but can progress to bilious as obstruction worsens
- Palpable abdominal mass: RUQ/ mid-abdomen
- Diarrhoea/ constipation
What are the investigations for suspected intussusception?
- Abdominal USS (first line): target sign
- Abdominal x-ray: may show signs of bowel obstruction or soft tissue mass (normal x-ray doesn’t rule out intussusception)
- Contrast enema: ‘coiled spring’/ ‘crescent’ sign
In which patient groups with suspected intussusception should contrast enemas not be performed in?
Patients that are unstable with signs of perforation or peritonitis
What is the non-operative management for intussusception?
Air/ liquid enema under fluoroscopic/ ultrasound guidance
Should only be performed in stable patients without signs of perforation, ischaemia or peritonitis
What is the surgical intervention for intussusception?
Performed if non-operative reduction is unsuccessful, contraindicated or the patient presents with complications requiring emergency surgery
- Manual reduction or bowel resection if non-viable bowel segments are identified
What is the supportive care for intussusception?
- IV fluids
- Electrolyte management
- Pain control
What are the complications of intussusception?
- Bowel ischaemia/ necrosis
- Bowel perforation
- Recurrence (10%, most within 24-48 hours)
- Short bowel syndrome in cases with extensive bowel resection
Which factors increase the risk of recurrence of intussusception?
- Younger age
- Shorter duration of sx
- Presence of anatomical lead points
What is mesenteric adenitis?
An inflammatory condition primarily involving mesenteric lymph nodes of the abdomen and a common mimic of appendicitis
Which patient groups does mesenteric adenitis commonly affect?
Children and adolescents, typically following URTI
Which viruses are commonly associated with mesenteric adenitis?
- EBV (most common viral trigger)
- Adenoviruses
- Enteroviruses
Which bacteria are most commonly associated with mesenteric adenitis?
- Yersinia enterocolitica (contaminated food or water)
- Yersinia pseudotuberculosis (contaminated food or water)
- Campylobacter (uncooked poultry or unpasteurised milk)
What is the typical pattern of mesenteric adenitis occurance?
- Infection (usually URTI)
- Infection clears
- Mesenteric adenitis develops - indicating a reactive process rather than ongoing infection of mesenteric lymph nodes themselves
How does mesenteric adenitis present?
- Diffuse abdominal pain (often mistaken for appendicitis)
- Low-grade fever
- Generalised abdominal tenderness
- Pharyngitis/ sore throat
What are the investigations for mesenteric adenitis?
- FBC: typically normal
- US abdomen: enlarged mesenteric lymph nodes and normal appendix
What is the management of mesenteric adenitis?
- Observation and reassurance (usually self limiting)
- Surgical intervention if appendicitis absolutely can’t be ruled out
Which areas are most commonly affected in necrotising enterocolitis?
- Terminal ileum
- Colon
What is the pathophysiology of necrotising enterocolitis?
Unknown, but in preterm infants theroised:
- Immature GI tract (impaired intercellular junction integrity and mucosal barriers)
- Triggering event leading to normal intestinal microbiome dysbiosis
- Increased pathogenic bacterial growth
- Exaggerated immune response
- Tissue injury –> necrosis
Term infants:
- Underlying condition
What are the risk factors for necrotising enterocolitis?
- Prematurity <32 weeks
- Low birth weight
- Dysbiosis contributing interventions (abx, acid-reducing agents, bovine milk formula)
- Infection
- Underlying conditions (fetal growth restriction, GI disorders etc)
What are the compliactions of necrotising enterocolitis?
- Bowel perforation: sepsis, ileus, respiratory failure, coagulopathy
- Increased risk of neurodevelopmental impairment (systemic inflammation)
- Death
What are the signs and symptoms of necrotising enterocolitis?
- Feeding intolerance
- Abdominal distension, tenderness
- Vomiting (often bilious), bilious drainage from enteral feeding tubes
- Hematochezia
- Non-specific findings: temperature instability, lethargy, apnea
What are the investigations and results for necrotising enterocolitis?
Bedside
- Abdominal examination
Bloods
- Blood cultures: positive
- Thrombocytopaenia
- Anaemia
- DIC
- Increased serum lactate
Imaging
- Abdominal x-ray (supine, first line imaging)
- Abdominal ultrasound
What is seen on x-ray in necrotising enterocolitis?
- Dilated bowel loops
- Bowel wall oedema
- Pneumatosis intestinalis (gas in the bowel wall)
- Portal venous gas
- Pneumoperitoneum (gas in the peritoneum)
- Rigler sign (air inside and outside the bowel wall)
- Air outlining the falciform ligament (football sign)
What’s the management of necrotising enterocolitis?
Medical
- Supportive
- Cessation of oral feeding
- Broad spectrum abx
- Gastric aspiration (NG decompression)
- Total parenteral nutrition
Surgical
- Resection of necrotic bowel and creation of proximal enterostomy
- Re-anastamosis delayed until the infant has recovered
What are the indications for surgery in necrotising enterocolitis?
- Bowel perforation
- Portal venous gas
- Fixed dilated loop on serial x-rays
- Abdominal wall erythema
- Rapid deterioration
When can oral feeds be re-started in necrotising enterocolitis?
7-10 days after pneumatosis clears
What are the complications of surgery in necrotising enterocolitis?
- Short bowel syndrome
- Strictires
- Stoma related complications
- Infection (abscess)
What is biliary atresia?
Obliteration of discontinuity within the extrahepatic biliary system, resulting in obstruction of the flow of bile
What is the pathogenesis of biliary atresia?
Unclear, however theorised:
- Infectious agents causing inflammation
- Congenital malformation
- Retained toxins within the bile
What is the epidemiology of biliary atresia?
- Females > males
- Neonates
- 1/10-15,000 births
What are the types of biliary atresia?
- Type 1: proximal ducts are patent, common duct is obliterated
- Type 2: atresia of the cycstic duct and cystic structures are found in the porta hepatis
- Type 3: atresia of the left and right ducts to the level of the porta hepatis (>90% biliary atresia)
How does biliary atresia present?
First few weeks of life:
- Jaundice (extending beyond physiological 2 weeks)
- Dark urine, pale stools (obstructive)
- Appetite and growth disturbances
What are the signs of biliary atresia?
- Jaundice
- Hepatomegaly with splenomegaly
- Abnormal growth
What are the investigations and results for biliary atresia?
Bedside
- Abdominal examination
Bloods
- Serum bilirubin (including conjucated and total): total may be normal, conjugated will be high
- LFTs: usually raised (can’t differentiate between biliary atresia and other causes of neonatal cholestasis)
- Serum alpha 1-antitrypsin: deficiency can cause neonatal cholestasis
- Sweat chloride test: CF often involves biliary tract
Imaging
- USS biliary tree and liver: distention and tract abdnormalities
- Percutaneous liver biopsy with intraoperative cholangioscopy
What is the managment of biliary atresia?
Definitive
- Surgical intervention (Kasai procedure): removal of defective ducts and anastamosis of small intestine segment to liver, creating path from bile to small intestine
Medical
- Abx coverage
- Bile enhancers
What are the complications of biliary atresia?
- Progressive liver disease (whilst surgery will increase bile drainage, 80% patients will need a liver transplant by 20 years old)
- Unsuccessful anastamosis formation
- Cirrhosis with eventual hepatocellular carcinoma
What’s the prognosis of biliary atresia?
- Generally good if the surgery is successful - 80% of patients need liver transplant by 20
- In failed surgery, liver transplant might be required by 2 years old
At what age does pyloric stenosis usually present?
In the 2nd - 4th week of life as babies are born with a normal pylorus
Rarely may present later at up to 4 months
What is the pathophysiology of pyloric stenosis?
Hypertrophy and hyperplasia of the circular muscles of the pylorus
What is the epidemiology of pyloric stenosis?
- 4/1,000 live births
- 4x more common in males
- 10-15% positive family history
- First borns more commonly affected
- Has been associated with exposure to macrolide abx
What are the features of pyloric stenosis?
- Projectile non-biliouis vomiting, typically 30 mins after feeding
- Child is extremely hungry and eager to feed
- Constipation and dehydration
- Palpable mass in RUQ (olive shaped)
- Hypochloraemic, hypokalaemic alkalosis
- Visible peristalsis (hypertrophy of the walls of the stomach)
Why is a hypochloraemic, hypokalaemic alkalosis present?
- Persistent vomiting leads to loss of HCl (hypochloraemia)
- Dehydration leads to retention of Na+ and excretion of K+ (hypokalaemia)
- Hypokalaemia leads to intracellular shift of H+ and extracellular release of K+ (alkalosis)
What is the diagnostic investigation for pyloric stenosis?
Abdominal ultrasound
What is the management of pyloric stenosis?
Ramstedt’s pyloromyotomy
