Paediatric Surgery Flashcards

1
Q

Some relevant phase 1 stuff on appendicitis

What is the appendix?

A

narrow blind-ended tube that is attached to the posteromedial end of the cecum (large intestine).

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2
Q

Some relevant phase 1 stuff on appendicitis

Emrbyologically, where is the appendix derived from?

A

Embryologic midgut

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3
Q

Some relevant phase 1 stuff on appendicitis

For the appendix, what is the:
1. Arterial supply?
2. Venous drainage?
3. Innervation?

A

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)

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4
Q

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

A

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.

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5
Q

What are causes of appendicitis?

A

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

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6
Q

Main age of children to present with appendicitis?

A

10 - 20.
(rarely younger than 4 - if they do present, they usually already have perforation)

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7
Q

What are clinical features of appendicitis?

symptoms and signs

A
  • 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

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8
Q

Differential diagnosis for presentation of appendicitis?

A

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

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9
Q

What investigations would you do for suspected appendicitis?

A

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

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10
Q

How is appendicitis managed?

A

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

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11
Q

What features on examination would lean towards a ruptured appendix with peritonitis?

A

Rebound tenderness on palpation
Percussion tenderness

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12
Q

What are benefits of laprascopic appendectomy over open surgery?

A

Faster recovery
Fewer risks

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13
Q

What are complications of appendectomy?

A

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)
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14
Q

What are complications of appendicitis?

A
  • Pelvic abscess
  • Surgical site infection
  • Perforation
  • Appendix mass
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15
Q

What is biliary atresia?

A
  • 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.
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16
Q

What is the epidemiology of biliary atresia?

A
  • 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
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17
Q

What are the types of biliary atresia?

A

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)

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18
Q

How does biliary atresia present?

signs and symptoms

A
  • 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

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19
Q

What investigations would you do for suspected biliary atresia?

A
  • 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)
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20
Q

How is biliary atresia managed?

A
  • 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.
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21
Q

What are complications of biliary atresia?

A
  • 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.
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22
Q

What is prognosis of biliary atresia?

A

Good if surgery is successful
where surgery fails - need liver transplant in first 2 years of life

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23
Q

Phase 1 recap of bilirubin excretion

How is bilirubin usually excreted?

A
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24
Q
  1. What is epididymitis?
  2. What is orchitis?
A
  1. Inflammation of the epididymis
  2. Inflammation of the testes

epidid and orch can occur together - will group them for rest of cards

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25
What age group commonly get epididymitis?
Bimodal age distribiution: 15-30 years old >60 years old
26
# Phase 1 recap Label this diagram
27
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)
28
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
29
What are differentials of epididymo-orchitis?
MAIN ONE - testicular torsion Testicular trauma Testicular abscess Epididymal cyst Hydrocele Testicular tumour
30
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.
31
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
32
How is epididymo-orchitis managed?
If acutely unwell / septic * admit to hospital for IV abx If STI related * urgent referral to GUM for assessment and treatment * if organism unknown = ceftriaxone 500mg IM single dose, plus doxycycline 100mg PO BD for 10-14 days If caused by E coli (an enteric organism) * give Ofloxacin for 14 days or Levofloxacin for 10 days or Co-amoxiclav for 10 days if quinines are contraindcated. * also send MSU off. Additional measures: * Analgesia for pain * Supportive underwear * Reduce physical activity * Abstain from intercourse + use barrier protection
33
What are two main side effects to remember when prescribing Quinolone antibiotics? | (ofloxacin, levofloxacin and ciprofloxacin )
* Tendon damage and tendon rupture --> Achilles tendon rupture is common * Lower seiure threshold --> so caution in pts with epilepsy
34
What are complications of epididymo-orchitis?
* reactive hydrocele formation * chronic pain * chronic epididymitis * testicular atrophy (rare) * sub-fertility or infertility * scrotal absccess (rare)
35
What is Hirschprung's disease?
Hirschsprung’s disease is a congenital condition where **ganglionic cells** of the myenteric plexus are **absent/fail to develop** in the **distal bowel and rectum**
36
What is the epidemiology of Hirschprung's disease?
* present in neonatal period - usually 2 days old * Males:females = 4:1
37
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.
38
What syndromes is Hirschprung's disease associated to?
* Downs syndrome * Neurofibromatosis * Waardenburg syndrome (a genetic condition causing pale blue eyes, hearing loss and patches of white skin and hair) * Multiple endocrine neoplasia type II
39
RF for Hirschprung's disease?
FHx - genetic mutations in RET gene Being male Downs syndrome Neurofibromatosis Waardenburg syndrome Multiple endocrine neoplasia type II
40
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
41
What are ddx for Hirschprung's disease?
* meconium plug syndrome * meconium ileus * intestinal atresia * intestinal malrotation * anorectal malformation * constipation - a diagnosis of exclusion
42
What investigations would you do for suspected Hirschprung's disease?
* inital investigation = plain abdominal XR / radiograph * gold standard for diagnosis = **rectal suction biopsy** --> this allows the submucosa to be tested for ganglionic cells (absence of them in this condition) * **contrast enema** (contraindicated if you suspect a perforation). Classical finding is a short transition zone between the proximal end of the colon and the narrow distal end of the colon.
43
How is Hirschprung's disease managed?
Initially = rectal washouts/bowel irrigation, IV abx, nasogatric tube insertion, bowel decompression Definitive management = surgical removal of the aganglionic section of bowel and then connect unaffected bowel to below the dentate line.
44
What are complications of Hirschprung's disease?
* Hirschsprung associated enterocolitis = main cause of mortality in these patients. * Enterocolitis | more qu on these in detail
45
What are complications of **having surgery** for Hirschsprung's disease?
Constipation Enterocolitis Perianal abscess Faecal soiling Adhesions
46
What is pathophysiology of Hirschsprung associated enterocolitis (HAEC)?
Have stasis of faeces This leads to bacterial overgrowth (Clostridium difficile, Staph aureus, and anaerobes) in colon - leading to infection
47
For Hirschsprung associated enterocolitis (HAEC): 1. How does it present? 2. What investigations are done? 3. How is it managed?
1. fever, vomiting, diarrhoea, abdo tenderness, sepsis if not picked up early. 2. stool culture and abdo XR 3. Need emergency treatment for suspected enterocolitis with fluid resuscitation, bowel decompression and broad spectrum IV abx.
48
After surgery for Hirschprung's disease, how is enterocolitis prevented?
Prophylactic abx after surgery Colon irrigation
49
What is a hernia?
the protrusion of viscus through a defect of the walls of its containing cavity. Example: In the case of an inguinal hernia, the viscus is intra-abdominal contents (i.e. bowel), the containing cavity is the abdomen, and the protrusion is into the inguinal canal.
50
What is the most common form of hernia in children?
Indirect inguinal hernia
51
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
52
What are risk factors for indirect inguinal hernias?
* premature baby * male sex (8M:1F) * FHx
53
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
54
How does an inguinal hernia present? | symptoms and on examination.
Groin lump/swelling * superior and medial to the pubic tubercle * 70% are right sided Associated symptoms: (could indicate obstruction) * nausea * vomiting * constipation * abdo pain/discomfort ^ could also indicate strangulation - but this is rare. On examination: * inguinal mass that you can not get above * lump is reducible when lying flat * not transilluminate * positive cough reflex
55
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
56
What specific finding will help differentiate between indirect inguinal hernia and a direct inguinal hernia? | Dr Tom
When an indirect hernia is reduced and pressure is applied (with two fingertips) to the deep inguinal ring (at the mid-way point from the ASIS to the pubic tubercle), the hernia will remain reduced. this is not the case for direct.
57
What are contents of the inguinal canal?
Ilioinguinal nerve Genital branch of the genitofemoral nerve Females: round ligament of the uterus Males: spermatic cord
58
# Phase 1 recap for inguinal hernia What are contents of spermatic cord?
Although the contents are complex, a simple way to remember them is by using the ‘rule of 3’: 3 fascial layers: * external spermatic fascia, * cremasteric fascia/ muscle, * internal spermatic fascia 3 arteries: * artery to vas (ductus) deferens, * cremasteric artery, * testicular artery 3 nerves: * ilioinguinal nerve, * genital branch of genitofemoral, sympathetic * visceral afferent nerve fibres 3 other: * pampiniform plexus, * vas deferens, * testicular lymphatics
59
What are differential diagnosises for indirect inguinal hernia presentation?
Hydrocele = can get 'above' it, transilluminates, non-tender Varicocele = scrotal heaviness, non-tender, bag of worms, sensation on palpation
60
What investigations would you do for suspected indirect inguinal hernia?
Usually clinical basis If uncertain/ need more info: * USS * CT scan * MRI - rarely used
61
What is management for inguinal hernia?
Definitive management - surgical repair of hernia (herniotomy) = performed on all full term male infants with asymptomatic reducible inguinal hernias * involves mesh repair If irreducible = emergency surgery to prevent bowel and testicular ischaemia
62
What are complications of inguinal hernia (and complication of having surgery)?
Recurrence Strangulation Incarceration Bowel obstruction Surgery: bruising, wound infection, chronic pain, recurrance
63
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
64
Describe the pathophysiology of an omphalocele | (Describe what happens nomally then in this condition)
* During normal development - midgut starts to elongate at 6weeks gestation. * at the same time - liver and stomach are growing - so not enough room in the abdomen to accommodate the midgut * so midgut herniates through the umbilical ring out of the abdomen into the umbilical cord (physiological umbilical herniation). * By 10th week - the midgut should return back to abdomen (baby now big enough to house all of midgut and liver) In omphalocele: * failure of normal intestinal migration back into abdo cavity * have persistence of physiological umbilical herniation.
65
What are RF for omphalocele?
Maternal smoking Maternal age >40
66
What are the conditions/ associations to omphalocele?
Trisomy 13, 18, 21 Turner syndrome Klinefelter syndrome Triploidy Beckwith-Wiedemann syndrome Cardiac malformations Kidney malformations
67
What are differential diagnosis of omphalocele?
* Gastroschisis * Cloacal exstrophy * physiological gut herniation * Hernia of the cord
68
How is omphalocele managed?
* Found in antenatal USS - so discuss w/ families re birth plan. * C section indicated to reduce risk of sac rupture * After delivery - fluid resus, maintain temperature, insert NG tube --> NICU * Surgery needed to reduce bowel into abdo cavity and closure of skin and fascia - this is a staged closure, starting immediately and completed by 6-12 months
69
Complications of omphalocele?
Ruptured omphalocele - needs to be treated like gastroschisis Abdo compartmental syndrome
70
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.
71
RF for gastroschisis?
* maternal smoking * maternal age < 20 years olf * environmental exposure - e.g. to nitrosamines * maternal cox inhibitor use - aspirin and ibuprofen
72
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)
73
DDx for gastroschisis?
Omphalocoele Cloacal exstrophy Physiological gut herniation
74
What is management of gastroschisis?
* mother induced at 37weeks for immediate neonatal and surgical care * immediate fluid resus, maintain temp. * Sterile clear covering over herniated bowel = protects it, prevents evaporation, heat loss and infection * surgery to reduce organs and close abdo wall defect. * NG tube to help decompress bowel
75
Complications of gastroschisis?
Abdominal Compartmental Syndrome Persistent bowel dysfunction Wound infection Necrotizing Enterocolitis Short gut syndrome
76
Brain dump differneces between gastroschisis and omphalocoele
They are both congenital visceral malformations Gastroschisis = no peritoneum covering abdominal viscera so more probelms with GI development. Omphalocele = peritoneum IS covering abdo viscera so is protected and intestines fully develop. Gastroschisis vs Omphalocele mortality = 1: 8 * why? --> omphalocele is associated to other genetic problems = so higher mortality
77
What is an umbilical hernia?
hernia around the umbilicus due to a defect in the muscle around it.
78
How are umbilical hernias managed?
No treatment Typically resolve by 3 years old
79
What are associations of umbilical hernias?
* Afro-Caribbean infants * Down's syndrome * Mucopolysaccharide storage diseases