Surgery

Question 1

What are the usual causes of appendicitis?

Answer 1

Direct luminal obstruction usually secondary to a faecolith, lymphoid hyperplasia or impacted stool

Question 2

What are the clinical features of appendicitis?

Answer 2

Abdominal pain - initially peri-umbilical and later migrates to RIF

Nausea and vomiting, anorexia, diarrhoea, constipation

Rebound tenderness, guarding

Question 3

What is Rovsing’s sign?

Answer 3

RIF pain on palpation of the LIF

Question 4

What is psoas sign?

Answer 4

RIF pain with extension of the right hip

Question 5

What are some differentials of appendicitis in children?

Answer 5

UTI, pyelonephritis, IBD, Meckel’s diverticulum, testicular torsion, epididymo-orchitis, acute mesenteric adenitis, gastroenteritis, constipation, intussusception

Question 6

What are some risk factors for pyloric stenosis?

Answer 6

Male gender (4x risk)
Family history

Question 7

What is pyloric stenosis?

Answer 7

Progressive hypertrophy of the pyloric muscle causing gastric outlet obstruction

Question 8

What are the clinical features of pyloric stenosis?

Answer 8

Presents around 4-6 weeks

Non-bilious vomiting after every feed, usually projectile

Weight loss and dehydration

Visible peristalsis

Palpable olive-sized pyloric mass

Question 9

What are some differentials of pyloric stenosis?

Answer 9

Gastroenteritis, GORD, overfeeding, sepsis, UTI, food allergy

Question 10

How is pyloric stenosis investigated?

Answer 10

Test feed with an NG tube in situ and the stomach aspirated. Whilst the child is feeding, the examiner should palpate for a pyloric mass and observe for visible peristalsis

Ultrasound of the pylorus - wall thickness >3mm, length >15mm and diameter >11mm

Blood gases - hypokalaemia, hypochloraemic metabolic alkalosis

Question 11

What does the blood gas typically show in a baby with pyloric stenosis and why?

Answer 11

Hypokalaemic, hypochloraemic metabolic alkalosis

Due to loss of Hal with vomiting causing a chloraemia and metabolic alkalosis

Kidneys then change potassium to retain protons as a compensation, leading to hypokalaemia

Question 12

How is pyloric stenosis managed?

Answer 12

Preoperatively - correct underlying metabolic abnormalities

Fluid boluses

Rehydration at 150ml/kg/day

Ramstedt’s pyloromyotomy (babies can resume feeding after 6 hours)

Question 13

What are some complications of pyloric stenosis?

Answer 13

Hypovolaemia, apnoea secondary to hypoventilation associated with metabolic acidosis

Complications post op:

Wound dehiscence
Infection
Bleeding
Perforation
Incomplete myotome

Question 14

What is Hirschsprung’s disease?

Answer 14

A congenital disease in which ganglionic cells fail to develop in the large intestine

Question 15

What is the classical triad that 25% of patients with Hirschsprung’s disease have?

Answer 15

Failure to pass meconium, abdominal distension and bilious vomiting

Question 16

What is the median age of presentation of Hirschsprung’s?

Answer 16

2 days old

Question 17

What are the most common clinical features of Hirschsprung’s?

Answer 17

Failure to pass meconium in the first 48 hours, bilious vomiting and abdominal distension

Question 18

What gene is strongly associated with Hirschsprung’s?

Answer 18

Receptor tyrosine kinase (RET) gene - a proto-oncogene on chromosome 10q11

Question 19

What are the three main subtypes of Hirschsprung’s?

Answer 19

Short segment, long segment and total colonic agangliosis disease

Short term is the most common (85% of cases) - restricted to rectosigmoid portion of colon

Question 20

What is the pathophysiology of Hirschsprung’s?

Answer 20

Arrest of the neuroblast, derived from neural crest cell migration in fetal development between week 8 and 12

Or normal cell migration occurs but the neuroblast fails to develop properly due to apoptosis, improper differentiation or failure in proliferation

The aganglionic segment remains in a tonic state - failure in peristalsis and bowel movements

Question 21

What are the risk factors of Hirschsprung’s?

Answer 21

Male (4x risk), chromosomal abnormalities, family history

Question 22

What are some differentials of Hirchsprung’s?

Answer 22

Meconium plug syndrome, meconium ileus, intestinal atresia, intestinal malrotation, anorectal malformation, constipation

Question 23

How is Hirschsprung’s investigated?

Answer 23

Plain AXR

Contrast enema - short transition zone between proximal end of colon and narrow distal end of colon

Gold standard - rectal suction biopsy (submucosa tested for ganglionic cells) - biopsy stained for acetylcholinesterase

Question 24

How is Hirschsprung’s managed?

Answer 24

IV antibiotics, NG insertion, bowel decompression

Surgery - resecting the ganglionic section of bowel and connecting the unaffected bowel to the dentate line

Question 25

What are some complications of Hirschsprung's?

Answer 25

Hirschsprung associated enterocolitis - stasis of faeces leads to bacterial overgrowth (C diff, staph aureus and anaerobes) - presents as fever, vomiting, diarrhoea, tenderness, sepsis Complications of surgery - constipation, enterocolitis, perianal abscess, faecal soiling and adhesions

Question 26

What are the terms used to describe the proximal bowel segment and distal bowel segment in intussusception?

Answer 26

Proximal = intussusceptum Distal = intussucipiens

Question 27

What is intussusception?

Answer 27

Movement or telescoping of one part of the bowel into another - 90% of cases are ileo-colic whereby the distal ileum passes into the caecum through the ileocaecal valve

Question 28

When is the peak incidence of intussusception?

Answer 28

Between 5-7 months of age Rare after 2 years

Question 29

What are some risk factors for intussusception?

Answer 29

Rotaviruses, Meckel's diverticulum, polyps, Henoch-Schonlein purpura, lymphoma, post op

Question 30

What are the clinical features of intussusception?

Answer 30

Sudden onset inconsolable crying episodes Drawing up legs to a alleviate pain Pallor Red-current stools due to presence of blood and mucus Sausage shaped abdominal mass in RUQ

Question 31

What are the differentials of intussusception?

Answer 31

Colic, testicular torsion, appendicitis, gastroenteritis, volvulus

Question 32

How is intussusception investigated?

Answer 32

Abdominal ultrasound - doughnut/target sign AXR (low sensitivity) - distended small bowel loops, may have Rigler's sign if perforated Contrast enema - contraindicated if peritonitis or perforation

Question 33

How is intussusception managed?

Answer 33

Fluid resuscitation if shock or dehydration, NG tube insertion Non operative reduction - air or contrast enema to reduce the intussuscepted bowel Surgical reduction

Question 34

What are some complications of intussusception?

Answer 34

Obstruction, perforation, dehydration and shock

Question 35

What is cryptorchidism?

Answer 35

Failure of testicular descent into the scrotum

Question 36

What are some risk factors for cryptorchidism?

Answer 36

Prematurity, low birth weight, genital abnormalities eg hypospadias, family history

Question 37

What is the management of cryptorchidism?

Answer 37

At birth - review at 6-8 weeks At 6-8 weeks - if unilateral, re examine at 3 months At 3 months - if undescended, refer to paediatric surgery for definitive intervention ideally occurring at 6-12 months Definitive intervention - open orchidopexy

Question 38

What are some complications of cryptorchidism?

Answer 38

Impaired fertility, testicular cancer, torsion