Paediatrics- GI + Liver Flashcards
What are the differences between ‘Posseting’, ‘Regurgitation’, and ‘Vomiting’?
Posseting is the small amounts of milk that accompany the return of swallowed air (wind)- happens in nearly all babies
Regurgitation describes larger, more frequent losses and may indicate GORD
Vomiting is forceful ejection of gastric contents
What are the causes of vomiting in children?
1) Gastro-oesophageal reflux
2) Feeding problems
3) Infection (GE, urinary tract, meningitis, pertussis, resp tract etc.)
4) Food allergy/intolerance
5) Intestinal obstruction (pyloric stenosis etc.)
6) Inborn errors of metabolism
7) Congenital adrenal hyperplasia
8) Renal failure
What are the causes of vomiting in preschool children?
1) GE
2) Infection (meningitis, pertussis, resp tract, urinary tract etc.)
3) Appendicitis
4) Intestinal obstruction
5) Raised ICP
6) Coeliac
7) Renal failure
8) Inborn errors of metabolism
9) Testicular torsion
What are the causes of vomiting in school age and adolescent children?
1) GE + Infection (pyelonephritis, septicaemia)
2) Peptic ulcer + H. Pylori infection
3) Appendicitis
4) Migraine
5) Raised ICP
6) Coeliac disease
7) Renal failure
8) Diabetic ketoacidosis
9) Alcohol/drug ingestion or meds
10) Cyclical vomiting syndrome
11) Bulimia/anorexia nervosa
12) Pregnancy
13) Testicular torsion
What are the red flags in the vomiting child?
1) Bile-stained vomit (obstruction)
2) Haematemesis (ulcer)
3) Projectile vomiting (pyloric stenosis)
4) Vomiting at end of cough (whooping cough)
5) Abdominal tenderness/pain on movement
6) Hepatosplenomegaly (chronic liver disease, metabolism problems)
7) Blood in stool (infection, obstruction)
8) Severe dehydration/shock (severe GE, systemic infection, ketoacidosis)
9) Bulging fontanelle/seizures (raised ICP)
10) Faltering growth (GORD, coeliac)
Gastro-oesophageal reflux is more common in what type of children?
1) Cerebral palsy or other neurodevelopmental disorders
2) Preterm infants (esp. bronchopulmonary dysplasia)
3) Following surgery for oesophageal atresia or diaphragmatic hernia
What are the complications of gastro-oesophageal reflux?
1) Faltering growth
2) Oesophagitis
3) Recurrent pulmonary aspiration
4) Dystonic neck posturing (Sandifer syndrome)
5) Apparent life-threatening events
How is gastro-oesophageal reflux investigated?
Usually clinically diagnosed- investigations indicated if atypical history, complications, or failure to respond to treatment
1) 24 hour oesophageal monitoring
2) 24 hour impedance monitoring
3) Endoscopy with oesophageal biopsies
How is gastro-oesophageal reflux managed?
Uncomplicated: good prognosis, managed by parental reassurance, thickening agents to feeds, making feeds smaller + more frequent
Significant reflux: ranitidine or omeprazole
Complicated + doesn’t respond to treatment/oesophageal stricture: Nissen fundoplication
What is pyloric stenosis?
Hypertrophy of the pyloric muscle causing gastric outlet obstruction. It presents at 2-8 weeks of age. More common in boys.
What is the presentation of pyloric stenosis?
Vomiting- increases in frequency/forcefulness until projectile
Hunger after vomiting until dehydration leads to loss of interest in feeding
Weight loss (if delayed presentation)
Hypochloraemic metabolic alkalosis w/ a low plasma sodium + potassium
How is pyloric stenosis diagnosed?
1) Test feed: give milk feed, gastric peristalsis is seen moving from left to right across abdomen. Pyloric mass feels like an olive and is usually palpable in the RUQ
2) USS to confirm diagnosis if in doubt
How is pyloric stenosis managed?
1) Correct fluid + electrolyte imbalance with IV fluids
2) Pyloromyotomy (division of hypertrophied pyloric muscle down to the mucosa)
Name some extra-abdominal causes of acute abdominal pain:
1) URTI
2) Lower lobe pneumonia
3) Testicular torsion
4) Hip and spine
Name some intra-abdominal (medical) causes of acute abdominal pain:
1) GE
2) Urinary tract (UTI etc.)
3) Henoch-Schonlein purpura
4) Diabetic ketoacidosis
5) Sickle cell disease
6) Hepatitis
7) IBD
8) Constipation
9) Recurrent abdominal pain of childhood
10) Gynaecological
11) other (psychological, lead poisoning, acute porphyria)
12) Non-specific abdominal pain
Name some intra-abdominal (surgical) causes of acute abdominal pain:
1) Acute appendicitis
2) Intestinal obstruction
3) Inguinal hernia
4) Peritonitis
5) Inflamed Meckel diverticulum
6) Pancreatitis)
7) Trauma
What are the symptoms of acute appendicitis?
1) Anorexia
2) Vomiting
3) Abdominal pain (initially central + colicky –> localises to the RIF
What are the signs of acute appendicitis?
1) Flushed face with oral fetor
2) Low grade fever
3) Abdominal pain aggravated by movement)
4) Persistent tenderness with guarding in the RIF (McBurney’s point)
5) If retrocaecal there may be no guarding. If pelvic there may be few abdominal signs
How is acute appendicitis investigated?
1) Diagnosis made by repeat observation and clinical review. Avoid delay and unnecessary laparotomy.
2) USS- may support clinical diagnosis and demonstrate complications (perforation, abscess etc.).
How is acute appendicitis managed?
Uncomplicated: appendicectomy
Perforation: fluid resus + IV antibiotics given prior to laparotomy
Palpable mass w/ no signs of generalised peritonitis: IV antibiotics with surgery a few weeks later. If symptoms progress, do laparotomy
What is non-specific abdominal pain and mesenteric adenitis?
NSAP: abdominal pain which resolves in 24-48 hours.
Mesenteric adenitis: diagnosed in children who have large mesenteric nodes on laproscopy and whose appendix is normal.
How do you distinguish between non-specific abdominal pain and appendicitis?
The pain is less severe than appendicitis
Tenderness in the RIF is variable
Often accompanied with an URTI with cervical lymphadenopathy
What is intussusception and where does it normally happen?
Invagination of proximal bowel into a distal segment
Most commonly involves ileum passing into the caecum through the ileocaecal valve
When does intussusception tend to present?
Peak presentation is between 3 months and 2 years of age
What are the complications of intussusception?
Stretching and constriction of the mesentery –> results in venous obstruction –> causes engorgement and bleeding from the bowel mucosa, fluid loss, and subsequently bowel perforation, peritonitis, and gut necrosis
How does intussusception present?
1) Redcurrant jelly stool comprising blood stained mucus (CHARACTERISTIC)
2) Paroxysmal, severe colicky pain with pallor (becoming increasingly lethargic)
3) Sausage-shaped mass (often palpable in abdomen)
4) Abdominal distension and shock
How is intussusception investigated?
1) X-ray of abdomen: distended small bowel and absence of gas in distal colon or rectum
2) Abdominal USS: useful to confirm diagnosis and check response to treatment
How is intussuception managed?
1) Immediate IV fluid resus
2) If no signs of peritonitis: reduction of the intussusception by rectal air insufflation
3) If this fails, surgery is required
What is Meckel Diverticulum?
An ileal remnant of the vitello-intestinal duct which contains ectopic gastric mucosa or pancreatic tissue
What is the presentation of Meckel Diverticulum?
1) Most are asymptomatic
2) May present with severe rectal bleeding (neither bright red nor true melaena)
3) Other forms of presentation include intussusception, volvulus, or diverticulitis
How is Meckel Diverticulum investigated?
1) Usually an acute reduction in haemoglobin
2) A technetium scan will demonstrate increased uptake by ectopic gastric mucosa (in 70% of cases)
How is Meckel Diverticulum managed?
Surgical resection
What is the pathology of malrotation?
During rotation of the small bowel in foetal life, if the mesentery is not fixed at the duodenojejunal flexure or in the ileocaecal region its base is shorter than normal and is predisposed to volvulus
Ladd bands are peritoneal bands which may cross the duodenum, often anteriorly. They obstruct the duodenum or volvulus
What are the two ways in which malrotation presents?
Obstruction
Obstruction with a compromised blood supply: emergency
What are the presenting features of malrotation?
Bilious vomiting (often first few days of life)
Abdominal pain and tenderness (from peritonitis or ischaemic bowel)
How is malrotation investigated?
Urgent upper GI contrast study to assess intestinal rotation (always do when bilious vomiting)
If compromised blood supply: urgent laparotomy
How is malrotation treated?
Urgent surgical correction
Appendix is generally removed to avoid diagnostic confusion
What is the definition of recurrent abdominal pain?
Pain sufficient to interrupt normal activities that lasts over 3 months
How does recurrent abdominal pain present?
Characteristic peri-umbilical pain
Children are otherwise entirely well
What are the causes of recurrent abdominal pain?
IBS, Constipation, dyspepsia, abdominal migraine, gastric/peptic ulceration, eosinophilic oesophagitis, IBD, malrotation
Gynaecological
Psychological
Hepatobiliary (hepatitis, gallstones, pancreatitis)
Urinary tract (UTI, PUJ obstruction)
How is recurrent abdominal pain managed/investigated?
1) Full history + thorough examination (check growth)
2) Urine microscopy and culture
3) USS to exclude gallstones and PUJ obstruction
4) Coeliac antibodies and TFTs
What is the prognosis of recurrent abdominal pain?
50%: rapidly become free of symptoms
25%: symptoms take months to resolve
25%: symptoms continue or return in adulthood as migraine, IBS, or functional dyspepsia
Abdominal Migraine: Definition
Often associated with abdominal pain in addition to headaches, and in some children the abdominal pain predominates
Abdominal Migraine: Epidemiology
Usually a personal or FH of migraine
Abdominal Migraine: Presentation
Characteristic history with long periods of no symptoms and then a shorter period (12-48 hours) of non-specific abdominal pain and pallor, with or without vomiting
The attacks of pain are midline, associated with abdominal pain and facial pallor
Abdominal Migraine: Management
Treatment with anti-migraine medication may be beneficial if the problem causes school absence
IBS: Pathology
Associated with altered GI motility and an abnormal sensation of intra-abdominal events
Symptoms may be precipitated by a GI infection
Often a positive FH
IBS: Presentation
Non-specific abdominal pain, may be worse before or relieved by defecation
Explosive, loose, or mucus stools
Bloating
Feeling of incomplete defecation
Constipation (often alternating with normal or loose stools)
Peptic ulceration/Gastritis/Functional Dyspepsia: Causes
H. Pylori infection is a strong predisposing factor
Peptic ulceration/Gastritis/Functional Dyspepsia: Presentation
Ulcers: epigastric pain that wakes them up at night, and radiates to the back
Gastritis: abdominal pain + nausea
Functional Dyspepsia: peptic ulcer symptoms + early satiety, bloating, post-prandial vomiting, delayed gastric emptying
Peptic ulceration/Gastritis/Functional Dyspepsia: Investigations
1) Gastric antral biopsies (H. Pylori produces urease)
2) 13C breath test
3) Stool antigen may be positive for H.Pylori
Peptic ulceration/Gastritis/Functional Dyspepsia: Management
Peptic ulceration: PPI (omeprazole) + clarithromycin/metronidazole + amoxicillin.
If they fail to respond do upper GI endscopy
If normal, then functional dyspepsia is diagnosed (some children respond to a hypoallergenic diet)
Eosinophilic Oesophagitis: Definition
Inflammatory condition affecting the oesophagus caused by activation of eosinophils in the mucosa and submucosa
Eosinophilic Oesophagitis: Presentation
1) Vomiting
2) Discomfort on swallowing
3) Bolus dysphagia (food ‘sticks’ in the upper chest)
Eosinophilic Oesophagitis: Investigations
Endoscopy
Eosinophilic Oesophagitis: Management
Oral corticosteroids (fluticasone or viscous budesonide)
Gastroenteritis: Causes
Virus: rotavirus (also adenovirus, norovirus, coronavirus)
Bacterial (less common- blood in stool): campylobacter jejuni, shigella, salmonella, cholera, enterotoxigenic E.Coli)
Protozoan parasite (giardia, cryptosporidium
How is degree of dehydration assessed and what are the degrees?
Body weight
1) No clinically detectable dehydration (<5% loss of body weight)
2) Clinical dehydration (5-10% loss of body weight)
3) Shock (>10% loss of body weight)
What is post-gastroenteritis syndrome?
Following an episode of GE, the introduction of a normal diet causes a return of watery diarrhoea –> Return to the use of ORT
In what 3 ways do disorders affecting digestion or absorption of nutrients present?
1) Abnormal stools
2) Poor weight gain/faltering growth
3) Specific nutrient deficiencies (single or combination)
Coeliac Disease: Pathology
1) An enteropathy in which the gliadin fraction of gluten provokes a damaging immunological response in the proximal small intestinal mucosa
2) As a result, enterocytes start moving up the villi at a higher rate but it isn’t enough to compensate for increased cell loss from villous tips
3) Villi become progressively shortened and then absent, leaving a flat villi
Coeliac Disease: Presentation
1) Faltering growth
2) Abdominal distension
3) Buttock wasting
4) Abnormal stools
5) General irritability
Other (anaemia, short stature, mild + non-specific GI symptoms)
Coeliac Disease: Investigations
1) Serology (IgA tissue transglutaminase and endomysial antibodies)
2) Endoscopy w/ biopsy: confirmation depends on mucosal changes (increased intraepithelial lymphocytes, villous atrophy and crypt hypertrophy, with catch-up growth on gluten withdrawal)
Coeliac Disease: Management
Gluten-free diet
Other than coeliac disease, name 6 other (uncommon) causes of nutrient malabsorption:
1) Short bowel syndrome
2) Exocrine pancreatic dysfunction (CF)
3) Small-intestinal mucosal disease
4) Lymphatic leakage or obstruction
5) Loss of terminal ileal function (Crohn’s)
6) Cholestatic liver disease or biliary atresia
What is the most common cause of persistent loose stools in preschool children?
Chronic Non-specific Diarrhoea (previously known as Toddler diarrhoea)
Crohn’s Disease: How does it present in children and adolescents?
1) General ill health (fever, lethargy, weight loss)
2) Growth failure
3) Delayed puberty
4) Classic presentation: abdominal pain, diarrhoea, weight loss
5) Extra-intestinal manifestation: oral lesions (or perianal skin tags), uveitis, arthralgia, erythema nodusum
Crohn’s Disease: How is it investigated?
Endoscopy with biopsy (non-caseating epithelioid granulomata)
May also have raised ESR, CRP, platelet count
May have iron deficiency anaemia and low serum albumin
Crohn’s Disease: How is it managed?
1) Remission is induced with nutritional therapy or steroids
2) Relapse: immunosuppressants (azathioprine, mercaptopurine, or methotrexate). Anti-TNF (infliximab or adalimumab)
3) Surgery for complications
Ulcerative colitis: presentation
1) Rectal bleeding, diarrhoea, and colicky pain
2) Weight loss and growth failure (less common than Crohn’s)
3) Extraintestinal (erythema nodusum, arthritis)
Ulcerative colitis: diagnosis
1) endoscopy w/ biopsy (mucusal inflammation, crypt damage
2) exclude infection
3) small bowel imaging to check that extra-colonic inflammation suggestive of Crohn’s is not present
Ulcerative colitis: management
Mild disease: aminosalicylates (balsalazide and mesalazine)
More aggressive disease: systemic steroids for exacerbations and immunomodulatory therapy (azathioprine) to maintain remission
Surgery for severe disease
Name 7 causes of constipation
1) Idiopathic
2) Hirschsprung disease
3) Lower spinal cord problems
4) Anorectal abnormalities
5) Hypothyroidism
6) Coeliac disease
7) Hypercalcaemia
What is the presentation of constipation in children?
1) Abdominal pain, which changes with passage of stool or overflow soiling
2) Constipation may be precipitated by dehydration or anal fissure
3) Older children: problems with toilet training, anxieties about opening bowels in unfamiliar toilets
4) Soft faecal mass in lower abdomen on examination
What are the red flags of constipation in children?
1) Failure to pass meconium in first 24 hours (Hirschsprung)
2) Faltering growth/growth failure (hypothyroid/coeliac)
3) Abdominal distension
4) Abnormal lower limb neurology or deformity
5) Sacral dimple over natal cleft (spina bifida occulta)
6) Abnormal appearance/position/patency of anus (anormal anorectal anatomy)
7) Signs of sexual abuse
8) Perianal fistulae, abscesses, or fissures
How is constipation investigated?
History and clinical findings (do not do DRE)
What can occur in longstanding constipation and how should this be explained to the child and parents?
The rectum becomes distended, with a loss of the need to defecate. Involuntary soiling may occur as contractions of the full rectum inhibit the internal sphincter, leading to overflow.
Explain that the soiling is involuntary and that recovery of normal rectum size and sensation can be achieved but may take a long time
What is the general aim of constipation management?
Evacuate the overloaded rectum completely. This is done using a disimpaction regime of stool softeners, followed by maintenance treatment to unsure ongoing regular pain-free defecation.
What is Hirschsprung Disease?
The absence of ganglion cells from the large bowel, resulting in a narrow contracted segment. The abnormal bowel extends from the rectum proximally, ending in a normally innervated, dilated colon
Hirschsprung Disease: Presentation
1) Usually presents in neonatal period
2) Intestinal obstruction with failure to pass meconium in first 24 hours
3) Followed by abdominal distension and bile-stained vomiting
4) Rectal exam: narrow segment, withdrawal of finger releases gush of liquid stool and flatus
5) In later childhood: profound chronic constipation, abdominal distension, growth failure
Hirschsprung Disease: Diagnosis
Suction rectal biopsy is diagnostic (demonstrates absence of ganglion cells and presence of large, acetylcholinesterase-positive nerve trunks
Hirschsprung Disease: Management
Surgical: initial colostomy followed by anastomosing normally innervated bowel to the anus
What is the most common presentation of liver disease in the neonatal period?
Prolonged (persistent) neonatal jaundice
At what point is physiological jaundice in newborns considered prolonged?
If the jaundice doesn’t subside after 2 weeks (3 if premature)
Why must prolonged neonatal jaundice be investigated promptly?
To distinguish between unconjugated hyperbilirubinaemia (resolves spontaneously) and conjugated (sign of liver disease)
What are the causes of prolonged neonatal jaundice?
Unconjugated: breastmilk jaundice, infection (UTI), haemolytic anaemia, hypothyroidism, Crigler-Najjar syndrome
Conjugated: bile duct obstruction (biliary atresia, choledochal cyst), neonatal hepatitis syndrome, intrahepatic biliary hypoplasia
What is the characteristic appearance of prolonged neonatal jaundice?
Raised conjugated bilirubin (>20) accompanied by:
1) Pale stools
2) Dark urine
3) Bleeding tendency
4) Failure to thrive
What is biliary atresia?
Progressive fibrosis and obliteration of the extrahepatic and intrahepatic biliary tree
Leads to chronic liver failure and death within 2 years unless treated
What is the presentation of biliary atresia?
1) Mild jaundice
2) Pale stools (increasingly pale as disease progresses)
3) Normal birthweight followed by faltering growth
4) Hepatomegaly initially, then splenomegaly due to portal hypertension
How is biliary atresia investigated?
1) ERCP is diagnostic
2) Raised conjugated bilirubin
3) Fasting abdominal USS: may show contracted or absent gallbladder
4) Liver biopsy: extrahepatic biliary obstruction
5) LFTs abnormal but of little value to diagnosis
How is biliary atresia managed?
1) Kasai hepatoportoenterostomy
2) If surgery fails: liver transplant
(nutrition and fat-soluble vitamin supplementation is essential)
Choledochal cysts: pathology
cystic dilatations of the extrahepatic biliary system
Choledochal cysts: presentation
Abdominal pain, palpable mass, jaundice, or cholangitis
Choledochal cysts: investigations and management
Investigate: USS or MRCP
Manage: surgical removal of cyst
Neonatal hepatitis syndrome: pathology
Prolonged neonatal jaundice and hepatic inflammation
Neonatal hepatitis: presentation
1) Low birthweight + faltering growth
2) Jaundice may be severe
A1AT Deficiency: pathology
Inherited autosomal recessive disorder –> accumulation of protein in hepatocytes –> lack of circulating A1AT results in emphysema in adults
A1AT Deficiency: presentation
1) Prolonged neonatal jaundice
2) Bleeding (vit K deficiency)
3) Hepatosplenomegaly
A1AT Deficiency: Investigation and management
Investigation: estimating the level of A1AT in plasma and identify protein phenotype
Management: 50% good prognosis, rest develop liver disease and may require transplant
What are the clinical features of acute viral hepatitis?
1) Nausea and vomiting
2) Abdominal pain
3) Lethargy
4) Jaundice
5) Large, tender liver
