Paediatric Gastroenterology Flashcards

1
Q

Acute Abdomen

A

In half of children admitted, pain resolves undiagnosed; Appendicitis is far most common of surgical causes; Important to also look for Testes, Hernial Orifices and Hip Joints
• Important Medical Causes include – Lower Lobe Pneumonia, Primary Peritonitis (in patients with ascites), Diabetic Ketoacidosis, UTI (check Dipstick) and Pancreatitis (check Lipase)

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2
Q

Surgical Causes of Acute Abdominal Pain

A
Acute appendicitis
Intestinal obstruction including intussusception 
Inguinal Hernia 
Peritonitis
Inflamed Meckel Diverticulum 
Pancreatitis 
Trauma
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3
Q

Medical Causes of Acute Abdominal Pain

A
Non specific abdominal pain 
Gastroenteritis 
Urinary Tract: UTI, acute pyelonephritis, hydronephrosis, renal calculus 
Diabetic Ketoacidosis
SCD
Hepatitis 
IBD
Constipation 
Recurrent Abdominal pain of childhood
Gynaecological in pubertal females
Psychological 
Lead poisoning 
Unknown
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4
Q

Extraabdominal causes of Acute Abdomen

A

URTI
Lower lobe pneumonia
Torsion of testes
Hip and Spine

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5
Q

Uncomplicated Acute Appendicitis: Presentation

A

Uncommon under 3 years
Uncomplicated: Anorexia, vomiting, characteristic abdominal pain (central then colicky due to midgut colic then localising to RIF)

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6
Q

Complicated Acute Appendicitis: Presentation

A

Presence of Mass, Abscess or Perforation

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7
Q

Diagnosing Acute Appendicitis

A

Fever, Abdominal Pain aggravated by movement, Persistent Tenderness with RIF Guarding over McBurney’s Point; NB: If Pelvic Appendix, might have few abdominal signs
o Diagnosis more difficult in younger children, especially if early; Faecoliths more common and can be seen of AXR; Perforation more rapid as Omental is less developed, and signs are easy to underestimate
• Repeated observation and clinical review every few hours;
No laboratory investigation or imaging is consistently helpful in making diagnosis
o Neutrophilia not always present; Pyuria not uncommon due to proximity
o Ultrasound may support clinical diagnosis – Thickened, non-compressible Appendix, increased blood flow; Identify complications such as Abscess, Perforation or Mass
• Laparoscopy for diagnosis in some centres;

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8
Q

Management of Appendicitis

A

Appendectomy is uncomplicated in appendicitis
• Perforation – Fluid resuscitation and Abx given prior to Laparotomy
• If palpable mass in RIF and no signs of Generalised Peritonitis, for Conservative Management with IV Abx and Appendectomy performed after several weeks; Laparotomy if persistent

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9
Q

Non specific Abdominal Pain

A

Abdominal Pain which resolves in 24-48hrs; Pain less severe than Appendicitis, and RIF tenderness is variable; Often accompanied with UTRI with Cervical LNA
o In some children, Abdominal signs do not resolve and Appendectomy performed

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10
Q

Mesenteric Adenitis

A

Large Mesenteric LN seen on Laparoscopy, and Appendix normal; Although unsure if true diagnostic entity

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11
Q

Intussusception

A

Invagination of the Proximal Bowel into Distal Segment; Most commonly Ileum into Caecum through Ileocaecal valve; Peak age 3/12 – 2yrs;
o Most common cause of Obstruction in infants after Neonatal period

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12
Q

Complications of Intussusception

A

Most serious complication is Vascular Compromise; Stretching and constriction of Mesentery leading to Venous Obstruction; Engorgement and Bleeding from Bowel Mucosa
o Leads to Bowel Perforation, Peritonitis and Gut Necrosis

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13
Q

Presentation of Intussusception

A

Presents with Paroxysmal, Severe Colicky Pain with Pallor (especially Perioral); Recovery between episodes but eventual Lethargy; Anorexia, Vomit (might be Biliary), Sausage-shaped Mass often palpable; Redcurrant stool (Blood stained mucous; Characteristic, but tends to occur later and after PR examination); Distention and Shock

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14
Q

Causes of Intussusception

A

Usually, no underlying cause found; Some evidence that viral illness leading to Peyer Hypertrophy related to Intussusception
o Identifiable lead points, such as Merkel’s Diverticulum or Polyp more likely if >2yrs

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15
Q

Investigating Intussusception

A

AXR shows distended Small Bowel and absence of gas in Distal Colon or Rectum
• Ultrasound useful for diagnosis (Target/Donut sign) and check response to treatment`

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16
Q

Management of Intussusception

A

Managed by Rectal Air Insufflation if no Peritonitis signs; 75% success rate; Performed by radiologist in presence of paediatric surgeon in case of need for laparotomy
o Remaining 25% for Operative reduction; Overall Recurrence less than 5%
o Peritonism – Severe pain, Generalised Guarding/Rigidity, Rebound Tenderness

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17
Q

Merkel’s Diverticulum

A

Rule of twos: 2% of individuals have Ileal Remnant of Vitello-Intestinal Duct; 2 inches long, 2 feet from Ileocaecal valve, 2/3s contain ectopic tissue (Gastric or Panc), 2% symptomatic

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18
Q

Presentation of Merkels Diverticulum

A

o Most asymptomatic, but can present with severe rectal bleeding; Acute ↓Hb
o Classically described as neither bright red, nor true Melaena
• Can also present as Intussusception, Volvulus or Diverticulitis (Mimics Appendicitis)

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19
Q

Management of Merkel’s Diverticulum

A

o Tc scan – Increased uptake by ectopic gastric mucosa in 70% of cases
o Treatment by Surgical Resection

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20
Q

Malrotation

A

incomplete rotation of the bowel during foetal development leading to the formation of Ladd’s bands
There can be associated bowel infarction alongside obstruction

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21
Q

Presentation of Malrotated Gut

A

Obstruction with Bilious vomiting is usual presentation in first few days of life; Requires urgent Upper GI Contrast study

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22
Q

Management of Malrotation

A

Unless signs of vascular compromise = Urgent Laparotomy (Very unwell, Severe Abdominal Pain, Peritonism); Volvulus – SMA supply compromised, possibly leading to infarction
• Operative management – Volvulus resolved, Duodenum mobilised to Duodenojejunal Flexure; Caecum and Appendix placed into the left; This broadens the Mesentery
o Appendix generally removed if symptoms suggestive of appendicitis

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23
Q

Inguinal Hernia

A

Common; 5% of boys, even more common in premature babies; Persistent Patent Processus Vaginalis; Emerges from Deep Inguinal Ring through Inguinal Canal = Indirect
o In Premature babies, Direct hernias more likely than in older children

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24
Q

How does an inguinal hernia present?

A

Presents as Lump in Groin, that may extend into Scrotum or Labia
o Typically, Asymptomatic; May be Intermittent, visible only during straining
o Often with Palpable lump, or thickened cord structures

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25
Q

Management of Inguinal Hernia

A

Most can be reduced by gentle compression along line of Inguinal Canal, with good Analgesia
Irreducible Hernia = Incarcerated; Causing Pain, Intestinal Obstruction, or Testicular damage
o Tender lump, Irritable Infant, Vomiting; Risk of Incarceration higher in infants than older children; If reduction impossible, Emergency surgery required
• Surgery – Ligation and Division of Processus Vaginalis (=Herniotomy); C/f adults, Herniorrhaphy (Reinforcement of Inguinal Abdominal Wall e.g. Mesh

26
Q

Umbilical Hernia

A

Hernia through Transversalis Fascia Umbilical ring; Size of base of herniated tissue inversely related to risk of strangulation
• 3% of live-births; More common Afro-Carib, Down and Congenital Hypothyroidism
o Surgical repair rarely needed (3 in 1000); at 3yrs spontaneous resolution

27
Q

Paraumbilical Hernia

A

Herniation above or below Umbilicus; Crescent-shaping of Umbilicus
o Only half of hernia fundus covered by umbilicus; Is an acquired defect
• Neck of sac is narrow; Always requires surgery (Mayo repair)

28
Q

Gastroschisis

A

Protrusion of Abdominal Contents through defect in Anterior Abdominal Wall right of the Umbilicus; Protruding bowel covered by thin ‘peel’
o Cautious Fluid Resuscitation followed by Prompt surgical repair
o 4% associated with Congenital Heart Defects

29
Q

Exomphalos (Omphacocoele)

A

Associated with other defects (Anencephaly, Cardiac, Hydrocephalus, Spinal Bifida); Abdominal contents outside of abdomen, covered by Peritoneum, Wharton’s Jelly and Amnion
Less urgent repair than Gastroschisis due to protective membranes
o Challenging repair – Need to fit organs into small abdominal cavity, without vascular or pulmonary compromise

30
Q

Posseting

A

small amounts of milk that come with return of swallowed air

31
Q

Regurgitation

A

larger, more frequent losses

32
Q

Vomiting

A

Forceful ejection of gastric contents

33
Q

Red Flags in Vomiting

A

Bile-stained, Haematemesis, Projectile Vomiting, Vomiting on Paroxysmal cough, Distention, Hepatosplenomegaly, Blood in stool, Severe dehydration/shock, Bulging Fontanelle or Focal Neurology, Faltering growth

34
Q

Main causes of vomiting in the infant

A

Reflux, Infections (Gastroenteritis, URTI, Whooping cough, UTI, Meningitis), Food Allergies, Intolerance, Intestinal Obstruction (Pyloric Stenosis, Atresia, Intussusception, Malrotation, Volvulus, Strangulated Inguinal Hernia, Hirschsprung’s Disease)

35
Q

Main causes of vomiting in preschool child

A

Infection, Appendicitis, Obstruction, Coeliac disease, Testicular Torsion

36
Q

Main causes of school-aged child

A

Infection, Peptic Ulceration, Appendicitis, Migraine, Coeliac disease, DKA, Drugs/ETOH, Cyclical Vomiting Syndrome, Eating Disorders, Pregnancy, Testicular Torsion

37
Q

GOR

A

Involuntary passage of gastric contents into the oesophagus; Extremely common in infancy due to inappropriate LOS relaxation due to functional immaturity
o Predominantly fluid diet, mainly horizontal posture, short intra-abdominal length
o Common in first year; nearly all symptomatic reflux resolves by 12/12 as sphincter matures, upright posture adopted and new diet
• Many infants with GOR have recurrent regurgitation/vomiting, but put on weight normally and otherwise well; usually benign, self-limiting condition

38
Q

When does GOR become GORD

A

Significant if it develops into Gastro-oesophageal Reflux Disease (GORD); More commonly in CP patients or with other neurodevelopmental disorders, pre-term infants, or following surgery for Oesophageal Atresia or CDH
o GOR becomes GORD if Faltering Growth, Oesophagitis (Haematemesis, Heartburn, IDA), Recurrent Pulmonary Aspiration, Dystonic Neck Posturing (Sandifer Syndrome

39
Q

Investigation of GORD

A

Clinical diagnosis, no investigations required
Atypical history or no response to treatment:
24h Oesophageal pH monitoring, 24H Impedance monitoring, Endoscopy with Oesophageal Biopsies; Contrast studies not sensitive nor specific for GORD

40
Q

Managing GORD

A

Parental reassurance, Inert thickening agents, feeding in smaller, more frequently
• H2 Antagonists, Proton-Pump Inhibitors; poor evidence for drugs that increase gastric emptying (e.g. Domperidone); Consider cow’s milk protein allergy if non-responsive
• Surgery if unresponsive to intensive medical therapy, or if Oesophageal Stricture
o Nissen Fundoplication either open or laparoscopically

41
Q

Pyloric Stenosis

A

Hypertrophy of Pylorus leading to Gastric Outlet Obstruction; Presents about 2-8/52 of age regardless of gestational age
o 4× more common in boys; Particularly first-born; FMHx

42
Q

Presentation of Pyloric Stenosis

A

Presents with Vomiting (Increasing Frequency and Forcefulness over time), Hunger after vomiting, Anorexia following Dehydration, Weight loss if delayed presentation
o Excessive vomiting leads to Hypochloraemic Metabolic Alkalosis; May also be accompanied by Hyponatraemia, Hypokalaemia

43
Q

Management of Pyloric Stenosis

A

Correction of Fluid and Electrolyte Disturbances with IV fluids
• Definitive Pyloromyotomy once Hydrated, Acid Base and Electrolytes balanced
o Division of Hypertrophied muscles down to mucosa; Either open procedure via Periumbilical incision, or Laparoscopic
• Feeding can start within 6hrs post-op, Discharged within 2 days

44
Q

Malabsorption in the child

A

Manifest as Abnormal stools (difficult to flush, foul odour), Poor weight gain/Faltering growth in most cases, or Specific Nutrient deficiencies
o Some disorders affect small intestine or pancreas lead to pan-malabsorption, while other conditions are more specific e.g. Fat malabsorption with Biliary disorders

45
Q

Coeliac Disease

A

Enteropathy caused by Gliadin (derived from Gluten and related Prolamines) provoking a damaging immune response against proximal Small Intestinal Mucosa; 1% population;

46
Q

Risk Factors for Coeliac Disease

A

Higher risk if T1DM, Autoimmune Thyroid disease, Down syndrome, FMHx

47
Q

Clinical Symptoms of Coeliac

A

Profound malabsorption 8/12 to 2yrs; Faltering growth, Distention, Buttock Wasting, Abnormal Stools and Irritability
o Now more common to present as less acute in later childhood

48
Q

Diagnosis of Coeliac

A

Positive serology (IgA Anti tTG, Anti EMA); Confirmation by Biopsy (Increased Intraepithelial Lymphocytes, Villous Atrophy, Crypt Hyperplasia), and resolution of symptoms following dietary change

49
Q

Management of Coeliac

A

Removal of Wheat, Rye, Barley products from diet, under supervision of Dietitian; Gluten challenge in later childhood if initial biopsy or response to treatment doubtful
o Non-adherence risks development of micronutrient deficiency, Osteopaenia, and small increased risk of malignancy (especially Small Bowel Lymphoma)

50
Q

IBD in Children

A

25% present in childhood or adolescence; In children, Crohn’s is more common than UC (Opposite in adulthood)
• IBD may result in poor general health, restricted growth and psychological adverse effects;
Requires specialist MDT care

51
Q

Presentation of Crohn’s

A

Classic presentation of Abdominal Pain, Diarrhoea and Weight Loss; Febrile Lethargy, Oral lesions and Peri-anal Skin tags; Non-GI signs include Uveitis, Arthralgia and Erythema Nodosum; Can present without GI symptoms
o Mistaken as psychological problems, anorexia nervosa
Presence of Raised Inflammatory Markers (Platelets, ESR. CRP), Iron-
deficiency Anaemia, and low Serum Albumin
Transmural, Focal, Subacute or Chronic; Most commonly Terminal Ileum and Proximal Colon
o Initially acutely inflamed, thickened bowel; Subsequently Strictures and Fistulae

52
Q

Diagnosis of Crohn’s

A

Endoscopy + Biopsy; Upper GI endoscopy, Colonoscopy and Small Bowel Imaging required (Crohn’s can affect any part of the GI tract)
o Histology: Presence of Non-Caseating Epithelioid Cell Granulomata; although not present with 30% of patients initially
o Imaging of Small Bowel might show Narrowing, Fissuring, Mucosal abnormalities and Bowel Wall Thickening

53
Q

Management of Crohn’s

A

Remission through Nutritional Therapy (Whole Protein Modular Feeds) for 6 – 8/52; Effective in 75% of cases; Systemic steroids if ineffective
o Relapse is common – Steroid-sparing agents (Immunosuppressants) e.g. Azathioprine, Mercaptopurine or Methotrexate to maintain remission
o Anti TNFa Mabs e.g. Infliximab, Adalimumab when conventional therapy fails
o Long term enteric supplementation (e.g. Overnight feeds) help correct growth
• Surgery – Obstruction, Fistulae, Abscess Formation, Severe resistant and localised disease

54
Q

Ulcerative Colitis

A

Recurrent, Inflammatory and Ulcerating disease of the Colon Mucosa; Classic presentation of Rectal Bleeding, Diarrhoea and Colicky Pain; Weight Loss and Growth Failure may occur, although less frequently than in Crohn’s disease
o Extra-intestinal complications include Erythema Nodosum and Arthritis

55
Q

Diagnosis of UC

A

Endoscopy and Histology, to rule out infective causes
o Confluent Colitis extended from Rectum proximally for variable length; 90% of children have Pancolitis (C/f adults, disease typically confined distally)
o Histology: Mucosal Inflammation, Crypt damage, Ulceration
o Small Bowel Imaging to rule out Crohn’s disease

56
Q

Management of mild UC

A

Aminosalicylates (e.g. Mesalazine) for Induction and Maintenance
o If only confined distally (rare in children) – Topical steroids

57
Q

Management of more severe UC

A

Systemic Steroids for Acute Exacerbations, Immunosuppressants for Remission; Anti TNFa Mabs for resistant disease; If ineffective, Surgery should not be delayed
• Severe Fulminating disease can progress to Toxic Megacolon; Medical emergency requiring IV fluids and Steroids; if remission still not achieved, Ciclosporin can be used
• Surgery – Colectomy with Ileostomy, or Ileorectal Pouch
• Increased incidence of Adenocarcinoma (0.5%/yr); Regular Colonoscopic screening 10yrs from diagnosis

58
Q

Hirschsprung Disease

A

Absence of Ganglion cells from Myenteric and Submucosal Plexuses of part of the Large Bowel leads to Narrow, Contracted Segment
o Extends from Rectum for variable distance proximally; Ending in normally innervated and dilated colon
o 75% confined to Rectosigmoid, but 10% have entire colon involvement

59
Q

Presentation of Hirschsprung Disease

A

Intestinal obstruction in Neonatal period, Failure to pass Meconium within first 24hrs
o Abdominal distention, Bilious Vomiting
o PR exam – Narrowed segment; Withdrawal of finger often leads to gush of liquid stool and flatus; Temporarily improves the obstruction
• Can present as Severe, Life-threatening Hirschsprung Enterocolitis; In later childhood, might present as Chronic Constipation, Abdominal Distention; Growth failure might be present

60
Q

Diagnosis of Hirschsprung’s

A

Suction Rectal Biopsy – Absence of Ganglion cells and ACh-positive Nerve trunks; Anorectal Manometry and Barium studies unreliable for diagnosis but useful for surgical planning
o Surgical management – Initial Colostomy, followed by Anastomosis of normally innervated bowel to anus