Paediatric Surgery Flashcards
Some relevant phase 1 stuff on appendicitis
What is the appendix?
narrow blind-ended tube that is attached to the posteromedial end of the cecum (large intestine).
Some relevant phase 1 stuff on appendicitis
Emrbyologically, where is the appendix derived from?
Embryologic midgut
Some relevant phase 1 stuff on appendicitis
For the appendix, what is the:
1. Arterial supply?
2. Venous drainage?
3. Innervation?
Note: Blood supply comes from the superior mesenteric vessels
1. Appendicular artery - which is a branch of the ileocolic artery
2. Appendicular vein
3. Sympathetic and parasympathetic branches of the autonomic NS (which are branches of the superior mesenteric plexus)
Some relevant phase 1 stuff on appendicitis
With understanding of the innervation of the appendix, explain why appendicitis pain is intially felt centrally in the abdomen
Sympathetic afferent fibres of the appendix come from level T10 of the spinal cord. So, early pain is central in the abdomen - where the T10 dermatome is.
What are causes of appendicitis?
Very young children = increased lymphoid tissue size which occludes the lumen
When older and into adulthood = blocked appendix due to faecolith (a mass of compacted faeces) - see picture
Main age of children to present with appendicitis?
10 - 20.
(rarely younger than 4 - if they do present, they usually already have perforation)
What are clinical features of appendicitis?
symptoms and signs
- Initially - dull, peri-umbilical, diffuse pain
- migrates to RIF - sharp, well-localised pain.
- vomiting (after pain starts)
- nausea
- anorexia
- fever
- constipation (more common than diarrhoea)
On examination:
* rebound tenderness on palpation and percussion pain of McBurney’s point, guarding (if perforated)
* pain in RIF when LIF is palpated (Rovsing’s sign)
* RIF pain with extension of right hip (Psoas sign)
* features of sepsis may be present - hypotensive, tachycardia
Differential diagnosis for presentation of appendicitis?
Gynaecological:
* ovarian cyst rupture,
* ectopic pregnancy,
* pelvic inflammatory disease
Renal:
* ureteric stones,
* UTI - common in children
* pyelonephritis
Gastrointestinal:
* acute mesenteric adenitis - common in children
* gastroenteritis - common in children
* constipation - common in children
* intussuseption - common in children
* inflammatory bowel disease
* Meckel’s diverticulum
Urological:
* testicular torsion
* epididymo-orchitis
What investigations would you do for suspected appendicitis?
Bedside:
* VBG = check lactate
* Urine dip - stones, or pregnancy (if post-pubertal female). Can also show increased leukocytes in appendicitis
Labratory:
* FBC = white cell count
* U+Es = check renal function and dehydration
* G+S = ready for theatre
* LFTs and amylase = if need to rule out biliary differentials
* clotting screen
* blood cultures = if septic.
Imaging:
* usually not needed
* erect CXR (only after excluding pregnancy) = to look for perforation
* USS - minimise radiation in children and good to rule out gynae causes
* CT scan - for appendicitis, urological and gastrointestinal causes
How is appendicitis managed?
Definitive = laparoscopic appendicectomy (below 10 years = paeds team. 10+ = adult surgical team)
Prophylactic IV abx
Sepsis 6 if necessary
If perforation = need copious abdominal lavage
What features on examination would lean towards a ruptured appendix with peritonitis?
Rebound tenderness on palpation
Percussion tenderness
What are benefits of laprascopic appendectomy over open surgery?
Faster recovery
Fewer risks
What are complications of appendectomy?
Complications of Appendicectomy
- Bleeding, infection, pain and scars
- Damage to bowel, bladder or other organs
- Removal of a normal appendix
- Anaesthetic risks
- Venous thromboembolism (deep vein thrombosis or pulmonary embolism)
What are complications of appendicitis?
- Pelvic abscess
- Surgical site infection
- Perforation
- Appendix mass
What is biliary atresia?
- congenital condition
- section of bile duct is narrowed (due to fibrosis) or absent
- resulting in obstruction in the flow of bile = cholestasis
- therefore bile can’t be transported from the liver to the bowel
- Usually, conjugated bilirubin is excreted in bile - so biliary atresia prevents excretion of conj bilirubin = get conjugated hyperbilirubinaemia.
What is the epidemiology of biliary atresia?
- extrahepatic biliary atresia is more common in females than males
- in neonatal children (i.e. presenting in first 28days of life)
- 1 in every 10,000 live births
What are the types of biliary atresia?
I think just know there are three types - but just in case:
Type 1 = proximal ducts are patent but common duct is obliterated
Type 2 = atresia of the cystic duct and cystic structures are found in porta hepatis
Type 3 = atresia of left and right ducts to the level of the porta hepatis (most common - > 90% cases)
How does biliary atresia present?
signs and symptoms
- in first few weeks of life
- prolonged jaundice (for more than 14 DAYS in term babies, for more than 21 DAYS in premature babies)
- dark urine
- pale stools - chalky white.
- appetite and growth disturbance
Signs:
* jaundice
* heaptomegaly with splenomegaly
* abnormal growth
* cardiac murmers - if have associated cardiac abnormalities
What investigations would you do for suspected biliary atresia?
- 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 will be deranged - 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 (echogenic fibrosis)
- Percutaneous liver biopsy with intraoperative cholangioscopy
- Definitive diagnosis of biliary atresia is confirmed with cholangiography, which will fail to show normal architecture of the biliary tree
- Hepatic scintigraphy radioisotope scan - will highlight liver (as it takes up the isotope) but poor excretion into the bowel (as bile ducts connecting the liver and gut will have been destroyed)
How is biliary atresia managed?
- surgery is needed = Kasai procedure which is hepatoportoenterostomy –> this creates a new pathway from the liver to the gut, to bypass the fibrosed ducts.
- ful liver transplant to resolve the condition.
- medical management = antibiotics and bile acid enhancers.
What are complications of biliary atresia?
- unsuccessful anastomosis formation from surgery
- progressive liver disese (bile build up in liver)
- cirrohsis with eventual hepatocellular carcinoma
- Kernicterus- Bilirubin is neurotoxic - high levels of unconjugated accumulate in the CNS gray matter causing irreversible neurological damage.
What is prognosis of biliary atresia?
Good if surgery is successful
where surgery fails - need liver transplant in first 2 years of life
Phase 1 recap of bilirubin excretion
How is bilirubin usually excreted?
- What is epididymitis?
- What is orchitis?
- Inflammation of the epididymis
- Inflammation of the testes
epidid and orch can occur together - will group them for rest of cards
What age group commonly get epididymitis?
Bimodal age distribiution:
15-30 years old
>60 years old
Phase 1 recap
Label this diagram
What are infective causes of epididymo-orchitis?
- Escherichia coli
- Chlamydia trachomatis
- Neisseria gonorrhoea
- Mumps (pts with this cause will have parotid gland swelling and orchitis, usually sparing the epididymis)
How does epididymo-orchitis present?
- acute
- unilateral testicular pain and swelling
- urethral discharge (sometimes - older children = gonorrhea or chlamydia)
- dragging or heavy sensation
- tenderness on palpation - particularly over epididymis
- systemic symptoms - fever, rigors and sepsis
What are differentials of epididymo-orchitis?
MAIN ONE - testicular torsion
Testicular trauma
Testicular abscess
Epididymal cyst
Hydrocele
Testicular tumour
Why is it important to rule out testicular torison in pt presenting with symptoms of epididymo-orchitis?
It is a urological emergency
Needs rapid treatment to avoid ischaemia of testicle
If in doubt of Dx - treat as testicular torsion until proven otherwise.
What investigations would you do in suspected epididymo-orchitis?
Think of how you would test for each cause as well as differentials
- urine dip - have low threshold to send off for M,C&S
- first void urine - collected and sent for Nucleic Acid Amplification Test (NAAT) = test for N.gonorrhoeae, C.trachomatis, and M.genitalium
- FBC and CRP = assess infective cause
- Blood cultures = if have systemic infection/sepsis
- Saliva swab for PCR testing of Mumps, if suspected
- Serum antibodies for mumps - IgM if acute infection, IgG if previously infected or have vaccine
- USS Doppler of testes to look for torsion or tumours
What is the pathophysiology of Hirschprung’s disease?
long and wordy answer but read step by step!
- Normally, parasympathetic ganglion cells start higher in GI tract and migrate down towards the distal colon and rectum.
- In Hirschprung’s disease, during fetal development, parasympathetic neuroblasts (ganglion cells) fail to migrate from the neural crest all the way down to the distal colon
- This means there has been a developmental failure of the parasympathetic Auerbach and Meissner plexuses, whereby there is a section of colon without these cells (see pics).
- This mysenteric plexus is needed throughout the GI tract to aid peristalisis. Without it, there is uncoordinated peristalsis
- This leads to an aganglionic colon whichis shrunken and can not distend properly. Because of this, there is back pressure of stool trapped in the proximal colon (see pics). This leads to functional obstruction.
How does Hirschprung’s disease present?
- Failure or delay to pass meconium within 48hrs of birth
- Chronic constipation since birth
- Adbo pain and distension
- Vomiting
- Poor weight gain and failure to thrive
Describe the pathophysiology of an indirect inguinal hernia
- Abdo contents protrude through the deep inguinal ring into the inguinal canal AND throigh the superficial inguinal ring into the groin
- WHY? Due to incomplete closure of the processus vaginalis (an outpouching of peritoneum) after the descent of the testes in utero
What is the anatomical difference between a direct inguinal hernia and an indirect inguinal hernia?
Direct:
* in adults,
* due to a weakness in the posterior wall of the inguinal canal (Hesselbach’s triangle) - hernia goes through this –> then through superficial inguinal ring
* medial to the inferior epigastric vessels
Indirect:
* children,
* hernia is due to failure to close processus vaginalis
* goes through deep and superficial ring
* lateral to the inferior epigastric vessels
What are boundaries of Hesselbach’s triangle?
R.I.P
Rectus abdominus muscle - medial border
Inferior epigastric vessels - superior/lateral border
Poupart’s ligament aka inguinal ligament - inferior border
What is an omphalocoele?
From phase 1: Persistence of the physiological herniation of midgut
From TMPaeds: a congenital, abdominal wall defect at the insertion of the umbilical cord. Abdominal contents herniates outside the abdomen within a membranous sac consisting of the peritoneum and amnion
What is gastroschisis?
Phase 1: failure of closeure of abdo wall during lateral folding of the embryo
TMPaeds: full-thickness abdominal wall defect - fetal abdominal organs protrude outside the abdomen with no protective membrane covering them. Direct intestinal exposure to amniotic fluid in utero leads to chemical reactions, creating a thick inflammatory film or peel over the bowel.
How does gastroschisis present?
- visible at birth or at 20 week scan
- abdo organs herniated out of abdo cavity, usually on right of the umbilical cord.
- no membrane covering abdo contents
- intestines lok swollen, inflamed, thickend and short.
- see thick fibrous peel over contents (due to amniotic fluid exposure)
